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As we prepare for the challenges ahead, let us remember that we rise by lifting others, and that true success is measured not by what we achieve alone, but by how we empower others to achieve their goals. Let us flock together, not as individuals, but as a team, bound by a common purpose and a spirit of collaboration, and reach new heights of success. \n\n## PDF version: 27th April'2023 https://t.me/usmleinnercircle Step 2 CK Notes \n\n# Step 2 CK Notes \n\n Important Update \n\n Read these instruction first \n\n Change-log \n\n Renal \n\n Pulmonary \n\n CVS \n\n Endocrine \n\n Gynae & Reproductive Health \n\n Obs \n\n GIT \n\n Blood & Oncology \n\n Musculoskeletal \n\n Dermatology \n\n CNS, Eye, Ear \n\n Psychiatry & Substance Abuse \n\n Short Subjects \n\n General Paeds \n\n Public Health \n\n Ethics & Communication \n\n1https://t.me/usmleinnercircle USMLE Inner Circle \n\n# USMLE \n\nINNER CIRCLE COMMUNITY \n\n-------Step 2 CK Notes Disclaimer \n\nAll the copyrights goes to Uworld,LLC. The distribution and/or reproduction of these notes is intended for educational, non-commercial use only. The information provided in these notes is NOT intended as a replacement for Uworld Qbank, but only as a review resource intended to facilitate quick revision of the topics covered in Uworld Qbank. If the copyright owners have any issues, please drop me an email on sidmalhotra0118@gmail.com and Ill take down the link immediately. \n\n2https://t.me/usmleinnercircle Important Update \n\n# Important Update \n\nHey, thankyou all of you for writing to me over mail ! When I started my Step 2 prep I did not find any good resource like First Aid for Step 2. I found that while Uworld is a Gold standard resource for preparing for Step 2, there wasn't a good way to review and re-read information (creating Visuospatial memory) while solving the questions. So, I began creating my own coloured notes. After sharing these notes with friends and others, I discovered that many people had the same issue that I initially faced during my preparation. I was encouraged by the positive feedback I received and it became clear that these notes were helping others as well. As a result of indirectly assisting others through my notes, I was also able to establish mutually beneficial connections with other medical students. These connections led to opportunities such as a research paper and an observership for me. I have created the initial version of this rapid review resource, but it needs to be frequently updated to stay current. Therefore, I am inviting all interested medical students preparing for the USMLE to join and collaborate with me to produce the highest quality community-generated notes .Additionally I believe that as we all strive towards the same goal, we can greatly benefit from supporting and assisting each other with study strategies, research experience, mental health support and clinical experience. With this in mind, I have decided to create a Telegram group called \" The USMLE Inner Circle \" to facilitate these connections and collaborations. \n\n I will be uploading the PDF (when it is completed) and all future updates in this group itself. As the links to these notes may change in the future, I strongly encourage you to join the group to stay updated on the latest version and links. \n\nThe USMLE Inner Circle \n\nYou can view and join @usmleinnercircle right away. \n\nhttps://t.me/usmleinnercircle \n\n3https://t.me/usmleinnercircle USMLE Inner Circle Read these instruction first \n\n# Read these instruction first \n\n1. These are notes that I am made with the help of Tzanki Deck and solving UWorld questions. 2. The notes Include major tables and concepts from Step 2 uworld which I believe are new additions to Step 1 knowledge. I am skipping repeated Step 1 tables, if theres nothing new. Suggest you to keep your step 1 first aid handy for reviewing repeated step 1 concepts. 3. Have any other questions? Feel free to join our telegram group and ask. \n\n Things that I find interesting while doing NBME forms are in these yellow boxes \n\n Things I find interesting listening to Divine podcasts are in these orange boxes \n\n These are general highlighted points. \n\nMy Personal Progress \n\n Uworld Percentage Complete: 100% \n\nUworld Percentage Correct: 75% Assessments: \n\n21/03/23: NBME 10: 259 (36 incorrects) \n\n24/03/23: NBME 9: 257 (40 incorrects) \n\n28/03/23: UWSA 1: 265 (84%) + New Free 120 (106/120) \n\n31/03/23: NBME 11: 256 (40 incorrects) \n\n03/04/23: NBME 12: 261 (36 incorrects) \n\n08/04/23: UWSA 2: 263 (83%) + Old Free 120: (104/120) \n\n13th April 2023: D-DAY Predicted Score: 262 +- 12 Actual Score: 267 !!! \n\n4https://t.me/usmleinnercircle Renal \n\n# Renal Metabolic Abnormalities Metabolic Acidosis RTA Metabolic Alkalosis Electrolyte Disturbances Hypercalcemia Hypocalcemia Hypernatremia Hyponatremia Hyperkalemia Hypokalemia Hypophosphatemia Renal Cysts Fibromuscular Dysplasia Acute Kidney Injury Contrast Induced AKI Rhabdomyolysis Analgesic Nephropathy Hemodialysis Calcific Uremic Arteriolopathy CardioRenal Syndrome Renal Stones Pyelonephritis Asymptomatic Bacteriuria Recurrent UTI Renal Abscess Nephrotic Syndrome HIV-associated nephropathy Glomerulonephritis Bladder Interstitial cystitis (painful bladder syndrome) Urinary Incontinence Renal Artery Stenosis Renal Vein Thrombosis Renal Cancers Miscellaneous Peripheral Edema Hematuria Renal Osteodystrophy Renal Drugs Paeds Renal Hematuria Neonatal AKI Nocturnal Enuresis Vesicoureteral Reflux UTI \n\n5https://t.me/usmleinnercircle USMLE Inner Circle Renal Metabolic Abnormalities Benign Proteinuria Renal Surgery Genitourinary trauma Kidney Injury Bladder Ureter Injury Urethral Injury Post Operative Urinary Retention Urethral Strictures \n\n6https://t.me/usmleinnercircle \n\n# iCD \n\nCheck arterial pH \n\npH< 7.35 pH> 7.45 \n\n( I 1\n\nAcidemia Alkalemia \n\nPea, > 44 mm Hg ~ - ' I<, C, \n\n> 12 mE q/L v>,,J \n\n( _____.,_ { ---\n\n!Anion gap \n\nGOLDMARK :Gl yc ols (eth ylene gl yc ol, pr op l ye ne gl ycol) Oxop rolin e !toxic metabolite of acetaminophen) L-l ac tate Uac tic acidos is) D-la ctate !exogenous lactic acid )Me th an ol l and other alcohols) .Awrin(l ate effect) \n\nRenal failur e\n\nKeytones !d iab etic, alcoholic, sta ~ )\n\nV\n\nNormal anion gap \n\nHARDASS r\" '- c..-~.t:.,. t~c~ Hype rch lo rem ia/h vperal imentat ion Addison dis ease ~\n\nRen al tubylarJ idosiS \"TtN \n\nDiarrhea \n\nAcetazo lamide ~ ,,. ... -411c..; \n\nSpj ro nola ctone -,,, c-w~f-a.. \n\nSa line infusion \n\nCl i.,.,.;~ \n\nl, - .,_ \n\n,j;.v7.1, the relatively small benefits of sodium bicarbonate do not typically outweigh the risks. \n\nRTA \n\n What is the likely diagnosis in an elderly diabetic with non-anion gap metabolic acidosis, hyperkalemia, and mild renal insufficiency? \n\nType 4 (hyperkalemic) renal tubular acidosis \n\nmost common in elderly patients with poorly controlled diabetes (damage to the juxtaglomerular apparatus results in hyporeninemic, hypoaldosteronism) \n\n Top 3 differentials for Non-AG metabolic acidosis is diarrhea , RTA , and Addisons !T/t: \n\n8https://t.me/usmleinnercircle \n\n> Renal tubular acidosis Type 1 (Distal) 2 (Proximal) 4Primary Poor hydrogen secretion Poor bicarbonate Aldosterone\n> defect into urine resorption resistance\n> Ur ine pH ~5.5 <5.5 <5.5\n> Serum Low-normal Low-normal High\n> potassium\n> Genetic disorders Fanconi syndrome Obstructive Medication toxicity (glucosuria , uropathy\n> Causes phosphaturia , Congenital Autoimmune disorders aminoaciduria) (eg, Sjogren syndrome, ad renal rheumatoid arthritis) hyperplasia\n\nRenal Type 1: Alkali Therapy : Sodium Bicarbonate, Sodium Citrate \n\n Type 2: Alkali Therapy: Potassium citrate \n\n Type 4: Furosemide , Mineralocorticoid replacement \n\n Renal tubular acidosis in infants commonly presents with failure to thrive in the setting of normal anion gap metabolic acidosis .\n\n Causes of elevated urine pH (pH > 5.5) \n\nType I RTA , UTI with a urease (+) bug (proteus mirabilis) (magnesium-ammonium phosphate stones) \n\nMetabolic Alkalosis \n\n9https://t.me/usmleinnercircle USMLE Inner Circle \n\nClinical features of metabolic alkalosis Saline -responsive \n\n Vomiting Gastric suc tioning Diuretics \n\nCauses Laxative abuse Decreased oral fluid intake (volume d ep letion) Sali ne-resistan t Primary hyperaldosteronism Cushing's syndrome Severe hypokalemia (<2 mE q/ l ) Vo lume depletion: Easy fatigabi lity, postu ra ldizziness, mu sc le cramps Clinical Hypokalemia: Muscle weakness, arrhyth mias \n\npresentation \n\n Urine chloride: <20 mEq/L (saline-responsive), >20 mEq/L (saline-resistant) \n\n T real underlying cause to reverse gene ration \n\nTreatment phase in all cases Saline-responsive Also give normal saline to correct maintenance phase \n\nDifferential diagnosis of metabolic alkalosis \n\nMetabolic alkalosis pH >7.45 & HCO, >24 mEq/L L ow urine chloride (<20 mEq/L) Hypovolemic H ig h urine chloride (>20 mEq/L) Hypervolem,c Vomijing/nasogastric aspi ra t io n Bartte r& Gitelman syndromes \n\nExcess mineralocorticoid ac ti vity \n\n Prima ry hyperaldosteron ism Diuretic overuse* Cush in g disease Ectopic ACTH production Sa line respons ive Saline unresponsive \n\nUfine chloride v.il be high if natriuresis \n\nBlocks ADH water reabsorption Natriuresis --> volume depletion --> metabolic alkalosis \n\n What is the likely etiology of hypercalcemia in a patient that develops symptoms 4 weeks after a severe motor vehicle accident left the patient a quadriplegic? \n\nImmobilisation \n\ndue to increased osteoclastic bone resorption , especially in individuals with a high baseline rate of turnover (e.g. young individuals, Paget's disease patients); characterised by high Ca2+ and low PTH \n\nT/t: Bisphosphonates Hemodialysis is an effective treatment for hypercalcemia. However, it is typically reserved for patients with renal \n\ninsufficiency or heart failure in whom aggressive hydration cannot be administered safely \n\n12 https://t.me/usmleinnercircle \n\n> Management of hypercalcemia Short-term (immediate) treatment Severe\n\n# . Normal saline hydration plus calcitonin \n\n> (calcium >14 mg /dl) Avoid loop diuretics unless volume overload (heart failure) exists\n> or symptomatic Long-term treatment\n\n# . Bisphosphonate (zoledronic acid) \n\n> Moderate\n\n# . Usually no immediate treatment required unless symptomatic \n\n> (calcium 12-14 mg/dl) Treatment is similar to that for severe hypercalcemia\n> Asymptomatic or mild\n\n# . No immediate tr eatmen t required (calcium <12 mg/dl) Avoid thiazide diuretics, lithium, volume depletion & prolonged bed rest Renal What is the drug class of choice for stabilising bony metastatic lesions and preventing hypercalcemia of malignancy ?\n\nBisphosphonates \n\n Hypercalcemia of malignancy and hypervitaminosis D secondary to granulomatous disease both present with similar calcium lab panels ( increased Ca, increased PO4, decreased PTH ). What lab test can be ordered to discern between the two? \n\n1,25-Vitamin D levels (to confirm hypervitaminosis); or PTH-rp levels (to confirm paraneoplastic syndrome) \n\nIf you're asked this, use the history to discern which one you need (i.e. history suggestive of sarcoid/TB vs. a lung mass) \n\nHypocalcemia In hypercalcemia due to malignancy, serum calcium is typically much higher (often >14 mg/dL )\n\n13 https://t.me/usmleinnercircle USMLE Inner Circle \n\nMilk-alkali syndrome Excessi ve intake of calc ium & absorbab le alkali Path ophysiology Re nal vasoconstri ct ion & decreased GFR Renal lo ss of sodium & water . reabsorption of bicarbonate Nausea, vo mi ti ng , constipation \n\nS ymptoms Polyuria. po lydipsia Neuropsychiatric symptoms Hypercalcemia \n\nLaboratory Metabolic alkalosis findings Acute kidney injury Suppressed PTH Treatment Di scont inuation of causative agent \n\n Isotonic sa li ne followed by furosemide \n\nHypercalcemia of malignancy Ca use Tumor type Mecha nism Diagnostic Squamous ce ll j PT HPTHrP\" Renal & bl adder PTHm imic Breast & ovarian l PTHrP \n\nBreast ! PTH & PTHrP \n\nBone metast ases T Ost eo lys is \n\nMult iple mye loma l Vitamin D\n\n1, 25-d ihydroxyvitamin D Lymphoma T Ca lcium absorption j PT H\n\nTVitamin D\n\n PTHrP causes approxima tely 80% of ma li gnancy-associa ted hypercalce mia PTH = par at hyro id hormone ; PT HrP = parathyroid hor _mon __ e-_rel _a _t_ ed _ p ~ro _t _e_ in __________ _Renal What formula is used to calculate the \" corrected Ca2+ \" in a patient with low albumin? \n\nSerum Calcium + 0.8(4 - serum albumin) \n\nLevel of Total Ca 2+ is decreased, however, ionized Ca2+ remains stable and thus patients remain asymptomatic \n\n What electrolyte abnormality is typically the cause of hypocalcemia in an alcoholic patient? \n\nSevere hypomagnesemia \n\nhypomagnesemia causes decreased PTH release and resistance to PTH , resulting in hypoparathyroidism with low Ca2+ and low phosphorus (vs other causes of hypoparathyroidism) \n\nHypocalcemia due to hypomagnesemia is typically refractory to treatment with calcium unless magnesium is replaced as well. Although PTH levels increase rapidly after magnesium replacement, hypocalcemia takes longer to improve because PTH resistance persists despite improvement in magnesium levels. \n\n14 https://t.me/usmleinnercircle \n\nAcute hypocalcemia \n\n## . Neck surgery (parathyroidectomy) \n\n## . Pancreatitis \n\nCauses . Sepsis \n\n## . Tumor lysis syndrome \n\n## . Acute alkalosis \n\n## . Chelation: blood (c itrate) transfusion, EDTA, foscarnet \n\n## . Muscle cramps \n\n## . Chvostek & Trousseau signs \n\nClinical features . Paresthesias \n\n## . Hyperreflexiai tetany \n\n## . Seizures \n\nTreatment . IV calcium gluconate /chloride \n\nEDTA = ethylenediaminetetraacetic acid; IV= intravenous. \n\nApproach to hypocalcemia \n\nLow serum calcium Confirm with repeat measurement Correct for serum albumin or measure ionized calcium (if needed) Low magnesium level? Is rt due to a drug? Recent blood transfusion (l crtrate, volume)? \n\nNo Normal or low PTH \n\nT real underlying cause Replete magnesium Intravenous calcium for severe symptoms \n\nHypoparathyroidism \n\nSurgical: Parathyroidectomy, thyroidectomy, radical neck surgery \n\nMetabolic: Vrtamin D deficiency, chronic kidney disease \n\nAutoimmune: Polyglandular \n\nauto immune syndrome Infiltrative disease: Metastatic cancer, Wilson disease, hemochromatosis \n\nGenetic: PT H gene or calcium sensing receptor gene mutations \n\n> UWortd\n\nInflammatory: Pancreatitis, sepsis \n\nOncology: Tumor lysis syndrome \n\nPTH resistance: Pse udo-\n\nhypoparathyroidism Renal Hypernatremia \n\n What is the fluid of choice for initial resuscitation of severe hypovolemic hypernatremia in an infant ?\n\nIsotonic solutions (e.g. normal saline, lactated Ringer's) \n\nusing hypotonic solutions initially may lower the sodium too rapidly \n\nHyponatremia \n\n15 https://t.me/usmleinnercircle USMLE Inner Circle \n\n S IA DH \n\nHypernatrem ia \n\nEuvolemic Hypovolem ic jSymptomatic INo \n\ni\n\nHypotonic solution \n\n(eg , 5% dextrose) 'Tach ycardia , decreased blood pr essure dry mucous membranes , de lay ed ca pd la ry refill \n\nEvaluation of hyponatremia \n\nYes Isotonic solution \n\n(eg, 0 . 9% saline) until euvolemic \n\nWV\\lort(j \n\nHypovolemic hyponatremia \n\nSerum osmolality > 290 mOsm / kg Marked hyperglycemia Advanced renal failure No No Urine osmolality <100 mOsm/ kg No Urine sodium <25 mEq/L Yes Primary polydipsia Malnutritio n (beer drinker 's potomania) Volume depletion \n\n Serum sodium < 13 5 m q/L \n\n Symptoms/signs of hypovolemia: Intake & output of water , orthostatic lightheadedness, dry mucous membranes, poor skin turgor, tachycardia, orthostatic hypotension \n\nxtrarenal losses Diarrhea, vomiting Bums (urine sodium S:20 m q /l) Pancreatitis Renal losses Diuretics (urine sodium >20 m qi ) Mineralooortlcoid deficiency \n\n Adrenal insufficiency Congestive heart failure \n\n Hypothyroidism Cirrhosis Decreased effective CHF \n\n UWorld circulating volum Cirrhosis CHF = congestive he J1 f 1lure .Renal Why would a patient with hyperosmolar hyperglycemic state have hyponatremia? \n\nPseudohyponatremia due to hyperglycemia need to correct \n\n(Na+ + (2 mEq/L for each 100 mg/dL that glucose is above 100 )) \n\nNa+ = 128 Glucose = 800 \n\nActual Na+: (128 + (7 x 2)) = 142 mEq/L \n\n What is the likely diagnosis in a young female with orthostatic hypotension, hyponatremia, and hypokalemia with high urine Na+ and K+? \n\nDiuretic abuse \n\nnormally dehydrated patients with hyponatremia and hypokalemia will have reduced urine Na+/K+ \n\n16 https://t.me/usmleinnercircle \n\nHyponatremia Serum ECV Urine findings Cause osmolality \n\nUNa <40 mEq/ L . Nonrenal salt loss (eg, vomiting, diarrhea, dehydration) Hypovolemic \n\nUNa >40 mEq/L . Renal salt loss (eg, diuretics, primary adrenal insufficiency) \n\n# . Psychogenic polydipsia Low Uosm <100 mOsm/kg . Beer potomania (<275 mOsm/kg) Euvolemic \n\nUosm > 100 mOsm/kg & UNa >40 . SIADH (rule out hypothyroidism, secondary adrenal mEq/L insufficiency) Hypervolemic Variable . CHF , hepat ic failure , nephrotic syndrome Normal . Pseudohyponatremia (eg, paraproteinemia, hyperlipidemia) High Variable . Hyperglycemia (>295 mOsm/kg) . Exogenous solutes (eg, mannitol) \n\nCHF =congestive heart failure; ECV =extracellular volume ; SIADH =syndrome of inappropriate antidiuretic hormone; UNa =urine sodium; Uosm =urine osmolality. \n\n> Iatrogenic hyponatremia\n> Hypotonic fluid hydration\n> Risk factors Children , premenopausal women, elderly Hypoxia Central nervous system disorders Headache\n> Clinical presentation Nausea/vomiting Encephalopathy (eg , mental status changes, seizure) Hypertonic (3%) saline\n> Management Serial measurement of electrolytes Increase serum sodium 6-8 mEq/L in first 24 hrs\n\nRenal Correction of serum sodium (both hypo- and hyper-natremia) should not exceed a rate of 0.5 mEq/L/hr. \n\nand thus should not exceed 12 mEq/L/24 hours \n\n Adaptations to normalize brain volume (eg, extrusion of osmolytes from brain cells) typically take ~48 hours. \n\nAcute hyponatremia (present for <48 hr ) is poorly tolerated, and patients are at high risk of brain herniation. Therefore, patients with serum sodium of <130 mEq/L with any symptoms of elevated intracranial pressure should be treated with hypertonic 3% saline boluses to rapidly correct serum sodium. Because neural adaptations have not occurred, patients are at relatively low risk of osmotic demyelination syndrome (ODS). \n\nChronic hyponatremia (present for 48 hr ) is typically better tolerated; therefore, hypertonic saline \n\nis often reserved for those with severe hyponatremia (<120 mEq/ L) , severe symptoms (eg, seizure) , or concurrent intracranial pathology (eg, masses, hemorrhagic stroke). \n\n Symptoms of hyponatremia are dependent on the severity of depletion and the acuity of onset. Acute onset leads to more severe symptoms, such as seizure and coma, while chronic onset generally has milder symptoms, such as nausea, vomiting, fatigue, and confusion. Diuretics \n\nare a common cause of symptomatic hyponatremia, and, thus, patients should have sodium concentrations monitored after initiation. If hyponatremia develops, the diuretic should be discontinued .\n\nHyperkalemia \n\n17 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nPotassium shifts SHIFTS K' INTO CE LL (CAUSING HYPOKALEMIA) \n\nl-l ypo-osmolarity Alkalosis p-adrenergic agonist (t Na /K - ATPase) \n\n~ 1 (t Na /K - ATPa se) In sulin shifts K in to ce ll s\n\nSHIFTS K OUT Of CELL (CAUSING HYPERKALEMIA )\n\nO igoxi , (bloc ks Na ' /K+ ATPase) l-l yperOsmolarity Ly sis of cells (eg, crush in ju ry, rhabdom yo lys is, tumor l ys is syn dr ome) Ac idosi s\n\nP-blocker \n\nHigh blood Sugar ( in su li n de fi ciens y) \n\nSuccinylcholine ( r isk in hnrns/nmscle t ra11ma Hyp erkalemia? DO LAPSS Renal IV calcium infusion (e.g. calcium gluconate or calcium chloride )18 https://t.me/usmleinnercircle \n\nCommon medications that cause hyperkalemia Medication Mechanism ACE inhibitor, ARB Decreases aldosterone secretion (inhibition of AT II/AT II receptor)+ inhibits ENaC \n\nCyclosporine Blocks aldosterone activity \n\nDigitalis Inhibits Na1K-ATPase \n\nHeparin Blocks aldosterone production \n\nNonselective 13-adrenergic blocker Interferes with 13 2 -mediated intracellular potassium uptake \n\nNSAID Decreases renal perfusion ----, decreased potassium delivery to the collecting ducts \n\nPotassium-sparing diuretic Inhibits ENaC or aldosterone receptor \n\nSuccinylcholine Causes extracellular leakage of potassium through acetylcholine receptors \n\nTrimethoprim Inhibits ENaC \n\nARB= angiotensin II receptor blocker; AT= angiotensin; ENaC = epithelial sodium channel; Na1K-ATPase =sodium-potassium pump; NSAID = nonsteroidal anti-inflammatory drug. \n\nResult of blood sample K > smEq/l Etiology Pseudohyperkalemia \n\nArising from \n\nHemoiysis Leukocytosis Thrombocytosis Repeat the blood sample Renal failure - Acute or chronic Low aldosterone state - ACE inhibitors/ARBs - RTAIV - Drugs - Addison disease \n\nClinical features of hyperka l emia \n\nIncreased release from tissues Cell lysis Low insulin Acidosis Drugs - Beta blockers - Digoxin - Heparin Ta ll peaked T waves with shortened QT interval \n\nSequence of ECG changes Cardiac membrane stabilization Rapidly acting treatment options Removal of potassium from the body (s low-acting) \n\nTall peaked Twave \n\n# !\n\n PR prolongation & QRS widening \n\n Di sa ppearance of P wave Conduction bl ocks, ectopy, or sine wave pattern Calcium infusion In sul in wi th glucose Beta-2 adrenergic agonists Sodium bica rb onate Diuretics Calion exchange resins Hemo di al ysis Hyperkalemia Tall peaked Twave \n\n## !\n\nWidened ORS \n\n(sine wave pattern) AV node block Fascicle & BB blocks \n\nK6 to 7 mEq/L \n\n# - K7 to 8 mEq/L \n\n# - K >B mEq/L Renal If patient has CAD, beta-2 agonists are contraindicated because they can cause tachycardia and precipitate angina. Calcium gluconate or insulin with glucose is typically reserved for hyperkalemia in patients with ECG changes , K+ > 6.5 mEq , or rapidly rising K+ .\n\nHypokalemia \n\n What is the likely diagnosis in a patient that presents with muscle cramps /weakness and hyporeflexia with broad, flat T waves on EKG? \n\nHypokalemia \n\n ECG changes: T-wave flattening, ST depression, Presence of U Waves \n\n What is the likely underlying cause of refractory hypokalemia in an alcoholic patient? \n\nHypomagnesemia \n\n(intracellular Mg2+ typically inhibits potassium secretion by renal outer medullary potassium \n\n(ROMK) channels) \n\nHypophosphatemia \n\n19 https://t.me/usmleinnercircle USMLE Inner Circle \n\nHypokalemia \" U'' .w av e,s. (1 j H~,: p O: kalem a\n\nt;.14 .-\n\n# . Diuretic therapy ( eg , thiazides) \n\n## . Vom iting/dia rr hea \n\nEtiologies . Hypomagnesemia \n\n## . Hyperaldosteron ism \n\n## . Increased beta-adrenergic activity (eg , albuterol ) \n\n## . Muscle weakness & cramps \n\nClinical . Hyporeflexia \n\nfeatures . Rhabdomyolysis \n\n## . Cardiac palpita ti ons/arrhythmias LJ: : uECG . Broad, flat T waves \n\nfindings . Prominent U waves \n\nTreatment . Potassium replacement \n\nCauses of hypophosphatemia \n\n# . Increased insulin secretion (especially refeeding malnourished \n\nInternal pat ients) \n\nredistribution . Acute respiratory alka losis (stimulates glycolysi s) \n\n# . Hungry bone syndrome (after parathyroidectomy) \n\nDecreased . Chron ic poor intake \n\nintestinal . Aluminum - or magnesium-conta ining antacids (bind phosphate) \n\nabsorption . Ste atorrhea or chronic diarrhea \n\n# . Primary & secondary hyperparath yro idism \n\nIncreased . Vitamin D defi ci ency(! GI absorpt ion , f ur i nary excretion) \n\nurinary . Primary renal phosphate wasting syndromes \n\nexcretion . Fanconi syndrome Renal Renal Cysts \n\n What are the common extra-renal complications of AD-Polycystic Kidney Disease? 1. Hepatic cysts \n\n2. Berry aneurysm : routine screening is not recommended 3. MVP \n\n4. Arterial hypertension (\"morning headaches\") \n\n20 https://t.me/usmleinnercircle \n\nCharacteristics of renal cysts Simple renal cyst Malignant cystic mass \n\nThin, smooth, regular wall Thick, irregular wall \n\nUnilocular Multilocular No septae Multiple septae, occasionally thick & calcified Homogeneous content Heterogeneous content (solid & cystic) Absence of contrast enhancement on CT/MRI Presence of contrast enhancement on CT/MRI Usually asymptomatic May cause pain, hematuria, or hypertension No follow-up needed Requires follow-up imaging & urological evaluation for malignancy \n\nAutosomal dominant polycystic kidney disease \n\n Most patients asymptomatic until age 30-40 \n\n# . Flank pain, hematuria \n\nClinical . Hypertension \n\npresentation Palpable abdominal masses (us ually bilateral) .. Chronic kidney disease (CKD) \n\n# . Cerebral aneurysms \n\n# . Hepatic & pancreatic cysts \n\nExtrarenal . Mitral valve prolapse, aortic regurgitation \n\nfeatures . Colonic diverticulosis \n\n# . Ventral & inguinal hernias \n\nDiagnosis . Ultrasonography showing multiple renal cysts \n\n# . Aggressive control of risk fac tors for CV & CKD \n\nManagement . ACE inhibitors preferred for hypertension \n\n# . Hemodialysis, renal transplant for ESRD \n\nCV = ca rdi ovascular; ESRD = e nd -stage renal disease. Renal ADPKD can also produce hypertension through activation of RAAS. \n\n(Can present with pain and hematuria and be mistaken for stones) \n\n What is the preferred medication for hypertension associated with autosomal dominant PKD? \n\nACE inhibitors \n\n## Fibromuscular Dysplasia \n\n Non-inflammatory and non-atherosclerotic condition that commonly involves the renal , carotid ,and vertebral arteries \n\n What is the gender disparity of fibromuscular dysplasia in children? \n\nMales = females ( vs. adults 8:1 female:male )Clinical features? Renal Secondary Hypertension - Due to Secondary Hyperaldosteronism Abdominal bruit at costovertebral angle \n\nCKD symptoms \n\nCerebrovascular (involves carotids) \n\nHeadache , pulsatile tinnitus, TIA \n\nSubauricular Bruit Diagnostics? Duplex ultrasound and/or CT angio (Non-invasive imaging) \n\nInitial for renal: Duplex U/S and/or CT angio \n\nCerebrovascular FMD: CT angio Gold standard: Digital Subtraction Angiography (string of beads) \n\n21 https://t.me/usmleinnercircle USMLE Inner Circle \n\n00000Fibrom us cula r dyspl asia 90% wome n (in adu lts) Internal carotid artery stenosis \n\no Rec u rrent headache \n\no Pulsatile tinnitus Clin ic al pr es enta tio n o Transient ischemic attack \n\no Stroke Renal artery st enos is \n\no Secondary hypertensi on \n\no Fl ank pai nPhysical ex amina ti on Subauricular sys to lic bru it Abdom inal b ru it Diag nosi s Imaging preferred (eg, duplex US, CTA , MRA) Catheter-based arteriography \n\n Antihyperten si ves (AC E in hi bitors or ARBs 1st ti ne) \n\nTrea tme nt PTA \n\n Surgery (if PTA uns uccessful) ARB = angiotensin II receptor bl oc ker; CTA = CT angiography; MRA = MR angiography; PTA = percutaneous translumi na langioplasty; US = ultrasonography. Renal Acute Kidney Injury Give a trial of IV fluids first if evidence of volume depletion else go for UA \n\n22 https://t.me/usmleinnercircle \n\nClinical features of FMD \n\nWomen age <50 with 1 of the following: Severe or resistant hypertension \n\nPatients to Onset of hypertension before age 35 Sudden increase in blood pressure from baseline \n\nscreen Increase in creatinine (;:>,0.5-1 mg/dl) after starting angiotensin-converting enzyme inhibitor or angiotensin receptor blocker & without significant effect on blood pressure Systolic-diastolic epigastric bruit Resistant hypertension from renal artery involvement Cerebrovascular FMD with symptoms of brain ischemia (eg, amaurosis fugax, Homer's \n\nClinical syndrome, transient ischemic attack, stroke) \n\npresentation Nonspecific symptoms (eg, headache, pulsatile tinnitus, dizziness) from carotid or vertebral artery involvement Can also involve iliac, subclavian & visceral arteries Noninvasive testing preferred (eg, computed tomography angiography, duplex ultrasound) \n\nDiagnosis & Catheter-based digital subtraction arteriography for patients with inconclusive noninvasive testing \n\nfollow-up Medically treated patients need follow-up blood pressure & creatinine every 3-4 months & renal ultrasound every 6-12 months \n\nFMD = fibromuscular dysplasia. \n\nEval ua ti on of acute kidney injury \n\nEvidence of volume depletion? ]\n\nr--Yes No 7\n\nImprovement -- No - Urinalysis with microscopy with IV fluids? IYes jMonit or to resolution Hematuria \n\n\n\nproteinu ri aEvaluate for glomeruloneph ri tis \n\nRenal ultrasonography, Sterile pyuria jEvaluate for AIN \n\nAI N = acute intersti ti al nephritis; ATN = acute tubular necrosis. IV = Intravenous. Normal Granul ar casts &/or ep ithelial cells Evaluate for ATN Exclude urinary obstruction .. \n\ni0UWorld Renal What is the next step in evaluation of acute kidney injury in an elderly patient with BPH who presents with rising creatinine and urinary urgency without hematuria, weight loss, or elevated PSA? \n\nRenal ultrasound: helps assess for hydronephrosis and other causes of obstruction What is the likely diagnosis in an afebrile elderly male with BPH who experiences agitation and lower \n\nabdominal tenderness 2 days after surgery? \n\nAcute urinary retention : diagnosis is confirmed by bladder ultrasound ( > 300 mL of urine ) ;treatment is insertion of a Foley catheter \n\n ACE inhibitors (eg, lisinopril) are used with caution in acute kidney injury because of the risk of exacerbating hyperkalemia . Acute tubular necrosis : characterised by muddy brown casts; distinguishing features from pre-renal AKI include BUN:creatinine ratio < 20:1, urine Na+ > 40 mEq/L, and FeNA > 2% Normal Postvoid residual 150 mL in women, 50 mL in men IV normal saline : need to restore renal perfusion and prevent development of acute tubular necrosis Also excessive vitamin C \n\n23 https://t.me/usmleinnercircle USMLE Inner Circle \n\nEtiol ogy Clinical features Treatment \n\nManagement of acute oliguria History & physical examination \n\n(eg, assess for benign prostatic hyperplasia) \n\nSerum&urine \n\nbiochemistry \n\n:timaging \n\nNo signific an t\n\nurine \n\nretention Bedside bl adder \n\n- ------f scan to assess for I-----< \n\nurinary retention \n\nSignificant \n\nurine re tention Urethral catheter to decompress b ladder \n\nPre-renal cause s: Renal ca uses: Serum & urine \n\nHypovolemia Acute tubu lar necrosis biochemistry Sepsis Interstitial nephritis imaging \n\nLow cardiac output Glomerular disease \n\n(eg, heart failure) \n\n## ! Treat under l ying cause (eg, benign Fluid administration if Treat under lying cause prostatic hyperplasia, appropriate or treat malignancy) with underlying cause urologic cons ultat io n\n\nPrerenal acute kidn ey in ju ry Clinical features of crystal-induc ed ac ute kidney injury Decr eased re nal pe rfusion o True volume depletion \n\no Decreased EA BV (eg, heart failure, cirrhosis) \n\no Displacement of intrav a scular fluid (eg, se psis , pancreatitis) \n\no Renal artery stenosis o Afferent arteriole vasocons triction (eg, N SAIOs) \n\n Acyclo vir \n\n Sulfonamides \n\nCommon Methotrexate \n\net iol og ies Ethylene glycol Protease inhibitors Increase in serum crea tinlne (eg, 50% from baseline) Usually asymptomatic \n\nDe cr ease d urin e output \n\nBk>od urea nitrogen/creatinine ratio >20:1 Fraction al ex cr e ti on of sod ium <1% Clinical Elevated creatinine within 1-7 days of starting drug \n\npres en tation Urinalysis can show hematuria, pyuria & crystals \n\n l Risk with underlying volume depletion, chronic \n\nUnrem a ri20:1) \n\n Most cases of renal failure result in hypocalcemia due to reduced renal phosphorus excretion ;because phosphorous combines with calcium to form calcium phosphate salts, serum calcium levels usually decline. Patients who have acute renal failure and hyper calcemia often have an underlying malignancy \n\nthat is driving calcium release. This is most often seen in the setting of multiple myeloma \n\nContrast Induced AKI \n\n Metformin is typically held before administering contrast to patients at risk for CA-AKI. done in order to prevent metformin accumulation (eg, lactic acidosis ) from reduced renal elimination. It does not reduce the risk for CA-AKI itself. \n\nRhabdomyolysis \n\n24 https://t.me/usmleinnercircle \n\nAcute kidney injury Prerenal Acute tubular necrosis BUN/creatinine ratio Typically >20 Typically normal (~10-15) \n\nUrine sodium <20 mEq/L >40 mEq /L \n\nFractional excretion of sodium <1% >2% Urine osmolality >500 mOsm/kg ~300 mOsm / kg \n\nUrine specific gravity >1.020 <1.020 \n\nMicroscopy Bland Muddy brown casts Contrast-associated acute kidney injury \n\n# . Creatinine elevation 24-48 hr after arterial contrast administration \n\nPresentation . Gradual return to baseline within 3-7 days . Chronic kidney disease (particularly diabetic nephropathy) . High contrast load \n\nRisk factors \n\n Hypovolemia . NSAID use . Prerenal vasoconstriction \n\nPathophysiology Direct tubular cytotoxicity .. Clinical diagnosis (ie, biopsy usually not needed) \n\nDiagnosis . Fe Na < 1% & muddy brown, granular casts . Patchy necrosis of renal tubular cells on biopsy . Optimize renal perfusion (eg , 0.9% saline) \n\nPrevention . Hold NSAIDs . Use lowest volume of contrast agent possible \n\nFeNa = fractional excretion of sodium ; NSAID = nonsteroidal anti-inflammatory drug. Renal Other laboratory abnormalities indicative of rhabdomyolysis include: \n\nHyperkalemia and hyperphosphatemia , which result from the release of these electrolytes from lysed muscle cells into the bloodstream. \n\nHypocalcemia , which is often present due to deposition of calcium in damaged muscle tissue. Moderate transaminase elevations, which characteristically show greater elevation in aspartate aminotransferase (AST) than alanine aminotransferase (ALT) due to relatively higher levels of AST in skeletal muscle. The intravascular volume depletion causes an initial prerenal insult, which is followed by a subsequent insult from direct tubular toxicity of heme (pigment nephropathy) .\n\n Affected muscle groups must be monitored closely because the initial tissue damage and subsequent volume replacement create a risk for acute compartment syndrome. \n\n What is the likely diagnosis in a patient who overdosed on cocaine and presents with elevated K+ and creatine phosphokinase (CPK)? Rhabdomyolysis \n\n Statins can cause many adverse effects on skeletal muscle (eg, asymptomatic inflammation, myopathy, rhabdomyolysis), possibly by impairing regulatory proteins (eg, coenzyme Q). Colchicine inhibits microtubule function, leading to myocyte waste product accumulation. Synergistic toxicity can lead to widespread skeletal muscle necrosis . Creatine phosphokinase is a marker of skeletal muscle damage, and serum elevation >1,000 U/L \n\nconfirms the diagnosis in the appropriate clinical setting. Opioids and other CNS depressants (eg, ethanol, benzodiazepines) can cause rhabdomyolysis by inducing impaired consciousness with prolonged immobilization and ischemic compression of dependent areas of skeletal muscle (eg, mottled skin over back, buttocks, and posterior thighs). \n\nAnalgesic Nephropathy \n\n25 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDrug-induced rhabdomyolysis Rhabdomyolysis Major mechanism Examples Skeletal muscle lysis/necrosis due to: \n\n## . Stalins, fibrates \n\n## . Colchicine Direct myotoxicity . Ethanol \n\n## . Cocaine \n\n Crush injury or prolonged immobilization \n\nEtiology Intense muscle activity (eg, seizure, exertion) \n\n# . Drug/medication toxicity (eg, statins) \n\n## . Cocaine Vasoconstrictive ischemia . Amphetamines \n\n# . Muscle pain & weakness \n\n Dark urine (myoglobinuria/pigmenturia) \n\n## . Ethanol Prolonged immobilization . Opioids (compression ischemia) . Benzodiazepines \n\nClinical features + Blood on urinalysis & no RBCs on microscopy \n\n j Serum K & P0 4, ! serum Ca, j AST> ALT \n\n Acute kidney injury \n\n Serum crealine kinase >1,000 U/L Diagnosis \n\n Consistent clinical features \n\nManagement Aggressive intravenous fluid resuscitation Sodium bicarbonate in some cases \n\nALT= alanine aminotransferase ; AST= aspartate aminotransferase; RBCs = red blood cells .Renal NSAID-induced acute kidney injury: \n\nPatients with intravascular volume depletion (eg, vomiting, diarrhea) normally have increased renal prostaglandin production to dilate the afferent arteriole and maintain the glomerular filtration rate. Nonsteroidal anti-inflammatory drugs inhibit prostaglandin synthesis , which can cause prerenal azotemia. \n\ne.g: Cirrhosis : Which is a state of reduced intravascular volume \n\nHemodialysis \n\n What is the most common cause of death in dialysis and renal transplant patients? \n\nCardiovascular disease : accounts for approximately 50% of all deaths in dialysis patients oxidative stress; resulting in accelerated atherogenesis and inhibition of nitric oxide synthesis. \n\n26 https://t.me/usmleinnercircle \n\nAnalgesic nephropathy \n\n# . Prolonged use of combination analgesics \n\nPathophysiology o Acetaminophen: direct oxidative renal toxicity o Aspirin/NSAIDs: depletion of glutathione impairs deactivation of reactive acetaminophen metabolites \n\n## . Manifests as chronic interstitial nephritis papillary necrosis \n\n## . History of chronic pain (eg , headaches, lower back pain) \n\n## . Often asymptomatic, may have malaise, fatigue, flank pain \n\nClinical presentation . Urinalysis: WBCs & WBC casts mild proteinuria \n\n## . Hematuria & urine RBCs if papillary necrosis is present \n\n## . Imaging: small kidneys papillary calcification & irregular contours \n\nNSAIDs = nonsteroidal anti-inflammatory drugs; RBCs = red blood cells ; WBCs = white blood cells. \n\nIndications for urgent dialysis (AEIOUl \n\n## . Metabolic acidosis \n\nAcidosis pH <7.1 refractory to medical therapy 0. Symptomatic hyperkalemia \n\nl;lectrolyte abnormalities 0 ECG changes or ventricular arrhythmias \n\n## . Severe hyperkalemia \n\n> 0\n\nPotassium >6.5 mEq/L refractory to medical therapy \n\n Toxic alcohols (methanol, ethylene glycol) \n\nIngestion . Salicylate \n\n## . Lithium \n\n## . Sodium valproate, carbamazepine \n\nQverload Volume overload refractory to diuretics \n\n## . Symptomatic: \n\n.Y_remia 0 Encephalopathy \n\n> 0\n\nPericarditis \n\n> 0\n\nBleeding \n\nCardiovascular risk factors in ESRD patients \n\n Hypertension, diabetes mellitus & dyslipidemia \n\nTraditional risk factors Left ventricular hypertrophy Advanced age & low physical activity Anemia of chronic kidney disease \n\nESRD-specific risk factors Vascular calcifications (t phosphorus, t calcium) Oxidative stress related to uremia and dialysis \n\nESRD = end-stage renal disease. Renal Patients with chronic renal failure are prone to volume overload , hyperkalemia ,\n\nhyperphosphatemia , metabolic acidosis , hyperparathyroidism , osteodystrophy , and \n\nanemia .These patients should minimize their intake of fluids, potassium and phosphate \n\nCalcific Uremic Arteriolopathy \n\n Calciphylaxis is most common in areas of adiposity (eg, trunk, thighs) and, in contrast to atherosclerotic ischemia, usually presents with intact peripheral pulses . Laboratory studies can show high serum parathyroid hormone and hyperphosphatemia (which is common in patients with ESRD due to reduced renal clearance of phosphate). \n\nAlthough hypercalcemia (not hypocalcemia) is also a risk factor, normal serum calcium levels do not rule out calciphylaxis because tissue calcium concentrations may be much higher due to local inflammatory changes \n\nCardioRenal Syndrome Vitamin K promotes synthesis of matrix proteins that prevent vascular calcification and reduce the risk of calciphylaxis. Therefore, patients with vitamin K deficiency or who are taking vitamin K inhibitors (eg, warfarin) are at increased risk of developing calciphylaxis. \n\n27 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCalcific uremic arteriolopathy (calciphylaxis) \n\n Arteriolar & soft tissue calcification \n\nPathophysiology Local tissue ischemia & necrosis End-stage renal disease \n\nRisk factors Hypercalcemia, hyperphosphatemia Hyperparathyroidism Oral anticoagulants (eg , warfarin) Painful nodules & ulcers \n\nClinical manifestations Soft tissue calcification on imaging Diagnosis requires skin biopsy: arteriolar calcification/occlusion , subintimal fibrosis Analgesia & wound care \n\nManagement Treatment of risk factors (eg, high phosphorus, high calcium) Optimization of dialysis \n\nl Central venous &renal venous pressure Venous congestion \n\n! Glomerular capillary filtration gradient \n\nCardiorenal syndrome \n\nLV & RV failure Vasoconstriction &\n\nl Na & H2O reabsorption RAAS activation Reduced forward flow ! Cardiac output \n\n1 Renal artery perfusion Renal Diuretics are usually the most effective therapy for AKI due to cardiorenal syndrome; the resulting \n\nreduction in renal venous pressure restores the glomerular capillary filtration gradient and improves GFR. \n\n## Renal Stones \n\n Uric acid stones : radiolucent therefore must be evaluated by abdominal CT , ultrasound , or IV pyelography (not X-ray) \n\n Be careful! Do not choose CT with contrast! For test purposes, don't pick U/A --> presence of hematuria is nonspecific An intravenous pyelogram (IVP ) uses IV contrast and plain x-ray to visualize the urinary system. IVP was previously the test of choice for diagnosing urinary stones. However, due to the risk of contrast administration (eg, allergy, acute kidney injury), non-contrast CT is now preferred. \n\n What is the likely diagnosis in a patient with intermittent flank pain, low-volume voids, and occasional episodes of high-volume voids ?\n\nObstructive uropathy \n\ne.g. due to renal calculi; high-volume voids occur due to large volume of retained urine overcoming the obstruction ( post -obstructive diuresis )\n\nExcessive diuresis may lead to potassium wasting and dehydration , both of which can cause weakness Pain Control: morphine (narcotic) and ketolorac (NSAID) Children may present with Painless Hematuria \n\n28 https://t.me/usmleinnercircle \n\nManagement of symptomatic ureteral stones \n\n> Initial symptom control: Analgesia Antiemetics IV fl ui ds Assess for the following: Urinary infection Acute kidney injury Complete obstruction (anuria) In tractable pain, nausea, vomiting Inpat ient admission Urgent urology consultation IV medications (analgesics, fluids antibiotics) Alpha blocker if stone >5 mm and s10 mm Strain urine\n> C)UWorld\n> Outpatient management\n> Pain control Oral hydration Alpha blocker if stone >5 mm and s10 mm Strain ur ine\n> Outpatient urology consultation for: Stone >10 mm No stone passage in 4--6 weeks Persistent pain\n\nHematuria, Colicky Flank Pain Radiating to the Groin, Nausea / Vomiting Consider Something Else (Highly Sensitive) Pass Stone Analyze Stone NOW \n\n# 24-hr Urine >6 weeks later Renal Pyelonephritis \n\n When is imaging indicated with pyelonephritis ?Not indicated unless complicated ( obstruction, sepsis ) or no response to antibiotics after 48-72 hours \n\n What is the next step in management for a patient with pyelonephritis that has clinically resolved after two days of IV ceftriaxone? Urine culture reveals E. coli sensitive to ceftriaxone and TMP-SMX. \n\nSwitch to oral TMP-SMX \n\nmost hospitalized patients can be transitioned to culture-guided oral antibiotics if symptoms are \n\nimproved at 48 hours \n\n29 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPrevention of recurrent nephrolithiasis \n\n Increase fluids (produce >2 L urine/day) Reduce sodium (< 1 00 mEq /d L) \n\nDietary Reduce prote in N orma l calcium in take (1200 mg/day) \n\nmeasures Increase citrate (f r uits & v egetab l es) Reduced-oxalate diet for oxa l ate st ones (dark roughage , vitami n C) \n\nDrug Thiazide diuretic \n\ntherapy Urine alkalinization (potassium citrate / bicarbonate salt) Allopurinol (for h yperu ri cosuria- r ela t ed sto n es) \n\nTreatment of urinary tract infection in nonpregnant women \n\n Nitrofurantoin \n\nUncomplicated Trimethoprim-sulfamethoxazole . Fosfomycin (single dose) \n\nUTI . Fluoroquinolones only if previous options cannot be used . Urine culture only if initial treatment fails \n\nComplicated Outpatient: fluoroquinolones . Inpatient: ceftriaxone , piperacillin-tazobactam, carbapenems (eg , imipenem) \n\nUTI* Culture obtained prior to therapy, with adjustment of antibiotic as needed *Infection above the bladder (eg, pyelonephritis), pelvic pain in men, other signs or symptoms of systemic illness. \n\nTreatment of acute cystitis & pyelonephritis in nonpregnant women Nitrofuranto in for 5 days (avoid in suspected pyelonephritis or creatinine clearance <60 mUmin) \n\nUncomplicated Trimethoprim-sulfamethoxazole for 3 days (avoid if local resistance rate >20%) \n\ncystitis Fosfomycin single dose Fluoroqui no lones only if above options cannot be used Urine culture needed only if initial treatment fa ils \n\nComplicated Fluoroquinolones (5-14 days ), extended-spectrum antibiotic (eg, ampicillin/gentamicin) \n\ncystitis' for more severe cases Obtain sample for urine culture prior to initiating therapy & adjust antibiotic as needed \n\nOutpatient: Fluoroquinolones (eg , ciprofloxaci n, levofloxacin) \n\nPyelonephritis Inpatient: Intravenous antibiotics (eg, fiuoroquinolone, aminoglycoside ampicillin) Obtain sample for urine culture pr ior to initiating therapy & adjust antibiotic as needed 'Associat ed wi th di abetes , pregnancy , renal fa ilu re , u ri nary tract obstruct ion, indwell ing catheter , urinary procedur e (eg ,cystoscopy ), l mmunos uppress ion & hospita l-acqu ired .\n\n oo not use fluoroqu inolo nes in pregnancy , Cons ider cefpodox ime , cepha lexin , amox icill in-c lavulanate & fosfomycin .Renal What is the treatment of choice in a pregnant patient with pyelonephritis ?\n\nHospitalize + ceftriaxone \n\n UTI prophylaxis for rest of the pregnancy if pregnant female has pyelonephritis \n\nAsymptomatic Bacteriuria Recurrent UTI Increase risk of pyelonephritis , preterm birth, and low birth weight. \n\n30 https://t.me/usmleinnercircle \n\nPyeloneph ri tis in pregnancy \n\n Asymptomatic bacteriuria \n\nRisk factors . Diabetes mellitus Age <20 Escherichia coli (most c o mm on) Common . Klebsief/a \n\npathogens . Ent e robact er \n\n# . Grou e B Stre e_ to coc cus \n\n# . P re term labor \n\nComplications . L ow birth we ight \n\n A cute r espi r atory d is tr ess sy n drome \n\n# . Intravenous antibiotics \n\nTreatment . S u pportive the r apy \n\nAsymptomatic bacteriuria in pregnancy \n\nDefinition . ~100,000 CFU/ml bac ter ia \n\n## . Pregestational diabet es mellitus \n\nRi sk . History of urin ary t ra ct fa cto rs infection \n\n## . Multi pa rity \n\n## . Escherichia coli (mo st Common common) \n\n## . Klebsie fl a\n\np at hogens Enterobact er .. Group B Streptococcus \n\nPotenti al Acute pyelonephritis compli ca ti on s . Preterm l ab or & delivery \n\n## . Cefpodoxime Treat m e nt . Fosfomycin \n\n Amoxicillin-clavulanate \n\n## . Nitrofurantoin* \n\nAvo id ed in first & third trimest ers .CFU = colo ny-fo rming uni ts .Renal Renal Abscess \n\n Renal and perinephric abscesses manifest with insidious onset of flank pain and systemic symptoms \n\n(eg, fever, weight loss), typically in patients with a history of urinary tract infection or extrarenal infection (eg, bacteremia) in the prior 1-2 months .In most cases, the urinalysis demonstrates pyuria , bacteriuria , and proteinuria , but it may remain normal if the abscess is not in contact with the collecting ducts. \n\n## Nephrotic Syndrome Same for recurrent cystitis \n\n31 https://t.me/usmleinnercircle USMLE Inner Circle \n\nRecurrent u ri nary tract infection \n\n# . ;,2 infections in 6 mo nths \n\nDefinition \n\n ;,3 infections in 1 ~ear \n\n History of cystitis at age :5 15 \n\n# . Spermicide use \n\nRisk factors \n\n New sexual partner Postmenopausal status \n\n# . Urinalysis \n\nEvaluation \n\n Urine culture Behavior modification \n\nPrevention Postcoital or daily antibiotic prophylaxis Topical vaginal estrogen for postmenopausal pati en ts \n\nRenal ab scess Renal What is the earliest renal abnormality in patients with diabetic nephropathy? \n\nGlomerular hyper-filtration (elevation in GFR) - First change that can be quantitated is thickening of GBM --> mesangial expansion --> nodular sclerosis \n\n- The pathologic hallmark of diabetic nephropathy is nodular glomerulosclerosis (with Kimmelstiel-Wilson nodules), but diffuse glomerulosclerosis is more common. Which type of nephrotic syndrome is most commonly associated with renal vein thrombosis &\n\nMalignancy ?\n\nMembranous nephropathy \n\nmay present acutely with abdominal pain , fever , and hematuria or gradually as worsening renal function and proteinuria in an asymptomatic patient (more common) Also, patients with SLE can get membranous nephropathy, making them even more hypercoagulable \n\nLook for proteinuria, hyperlipidemia, hypoalbuminemia, and edema in a patient with cancer. \n\nHIV-associated nephropathy \n\n Usually advanced HIV but can also occur with normal CD-4 count. Can develop relatively quickly and typically presents with heavy proteinuria and rapidly progressive renal failure .\n\nEdema , hematuria , and hypertension may also occur. The diagnosis is confirmed with renal biopsy that demonstrates collapsing focal segmental glomerulosclerosis ; tubuloreticular inclusions are usually visible on electron microscopy. \n\nAntiretroviral therapy (ART) may help kidney recovery and should be initiated in patients who develop HIVAN and are not already on therapy Patients with nephrotic syndrome are at risk of developing atherosclerosis due to the loss of albumin, which triggers a compensatory increase in hepatic synthesis of cholesterol/triglyceride levels. \n\n32 https://t.me/usmleinnercircle \n\n> tLiver protein &\n> lipid synthesis\n\n## !I Hyper1ipidemia I \n\n> Nephrotic syndrome\n> Glomerular injury\n> tGlomerularpermeability\n\n## ! \n\n> fAldosterone &\n> tADH secretion\n\n## ! \n\n> IBlood flow to\n> the kidneys\n\n## !I Edema 1~ Na & water retention t Ren in \n\n# L tHydrostaticpressure - Vasoco} stfiction \n\n> ADH =antidiietic hormone\n> 10 UW0<1d\n\nRenal prognosis for HIVAN is poor \n\n## Glomerulonephritis \n\n What diseases will have a low C3 ?\n\nPSGN, SLE, MPGN, Bacterial endocarditis \n\n MPGN is classically associated with cryoglobulinemic small-vessel vasculitis (eg, palpable purpura , arthralgia ) Glomerulonephritis general key points: the differential for the type of glomerulonephritis is extensive \n\nRBC casts are typical of GN Definitive diagnosis is via biopsy \n\n33 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nGlomerulonephritis serologic evaluation \n\nGl ome rul ar hematuria ( dysmo rphic ery throc ytes erythr ocyte casts )Serum complement L ow \n\n+\n\nImmune complex m ed iated\" Norma l\n\n+\n\nAn tibo dy med iated Lupus nephr itis: A NA , an ti- gross . Gross > microscopic Glomerulonephritis . Nephrolithiasis \n\no Poststreptococcal . Cancer (eg, renal, prostate) \n\nCommon etiologies o lgA nephropathy . Po lycystic kidney disease Basement memb ra ne dis or der . Inf ection (eg, cystitis) \n\no Alpert syndrome . Papillary necrosis \n\nClinical pr ese ntation Nonspecific or no symptoms . Dysuria Nephritic sy nd rome . Uri na ry obstruction \n\nUrinalysis Blood & protein . Blood but no prote in RBC casts, dysmorphic RBCs . Normal-appea ri ng RBCs \n\nC)l.1Wof1d Renal Important to rule out nephrotic syndrome with UA spot test or 24 hr urine collection \n\n Presence of hematuria and pulmonary edema helps distinguish nephritic syndrome from other causes of edema (e.g. hypoalbuminemia, cirrhosis, heart failure) What is the likely diagnosis in a young male with hemoptysis and hematuria without history of sinusitis? \n\nGoodpasture's disease \n\ngranulomatosis with polyangiitis can cause hemoptysis and hematuria with upper airway involvement (e.g. sinusitis, otitis media, etc.) \n\n## Bladder \n\nInterstitial cystitis (painful bladder syndrome) \n\n Chronic, noninfectious cystitis with unknown etiology Pain can be exacerbated with sexual intercourse (dyspareunia) \n\nUrinary Incontinence \n\n34 https://t.me/usmleinnercircle \n\n\n\nInterstitia l cystitis (p ai nf ul bladder syndrome) E pi demiology More common in women Associated wi th psych iatric disorde rs (a nxiety) & pain syndromes (fibromyalgia) \n\n Bladder pain wi th fi lli ng , reli ef wi th voidi ng \n\nCl inical presentation Frequency, urgency Dyspareunia \n\nDiag nosis Bladder pain wi th no other attributable cause for ;>:6 weeks Normal urinalysis Not curative; focus is on qua li ty of life \n\nT re atm en t Behavioral modifica ti on & trigger avoidance \n\n Am itripty li ne Analgesics for exacerbations \n\nDifferential diagnosis of urinary incontinence Etiology Symptoms Stress l Urethral sphincter tone Leakage with coughing , lifting , sneezing Urethral hypermobility \n\nUrge Detrusor hyperactivity Sudden, overwhelming urge lo urinate \n\nOverflow Impaired delrusor contractility Incomplete emptying & persistent involuntary dribbling Bladder outlet obstruction Renal Key idea: Neurogenic bladder can range from bladder atony to spastic bladder , but importantly these patients would have a clear neurological insult on NBME (Multiple sclerosis, stroke, etc.) Initial evaluation of mixed incontinence includes a voiding diary , which tracks fluid intake, urine output, and leaking episodes in order to classify the predominant type of urinary incontinence and \n\ndetermine optimal treatment .All patients with mixed incontinence generally require bladder training with lifestyle changes (eg, weight loss, smoking cessation, decreased alcohol and caffeine intake) and pelvic floor muscle exercises (eg, Kegels). What type of catheterization is recommended for patients with neurogenic bladder to reduce the risk of catheter-associated UTI ?\n\nClean intermittent catheterization \n\ni.e. insertion/removal of a clean urinary catheter every 4 - 6 hours; can be performed by patient or caregiver \n\n What is the next best step in management of a patient with acute urinary incontinence ? The patient has a history of dementia and has been less active and sleeping more for the past week. Vitals are First-line treatment for any type of urinary incontinence includes bladder training and pelvic floor muscle (Kegel) exercises \n\n35 https://t.me/usmleinnercircle USMLE Inner Circle \n\nUrinary incontinence Type Symptoms Treatment \n\n Lifestyle modifications \n\nStress Leakage with Valsalva Pelvic floor exercises (coughing , sneezing , laughing) Pessary Pelvic floor surgery Sudden , overwhelming , or frequent Lifestyle modifications \n\nUrgency need to void Bladder training Antimuscarinic drugs \n\nMixed Features of stress & urgency Variable treatment depending on predominant incontinence symptoms Constant involuntary dribbling & Identify & correct underlying cause \n\nOverflow Cholinergic agonists incomplete emptying Intermittent self-catheterization \n\nCauses of urinary incontinence in the elderly \n\n## . t Detrusor contractility, detrusor overactivity \n\nGenitourinary . Bladder or urethral obstruction (eg , tumor, BPH) \n\n## . Urethral sphincter or pelvic floor weakness \n\n## . Urogenital fistula \n\n## . Multiple sclerosis \n\nNeurologic . Dementia (eg , Parkinson, Alzheimer, normal pressure hydrocephalus) \n\n## . Spinal cord injury, disc herniation \n\n## . Delirium \n\n## . Infection (eg, UT I) \n\n Atrophic urethritis/vaginitis \n\nPotentially reversible . Pharmaceuticals (eg, alpha blockers, diuretics) \n\n## . Psychological (eg, depression) \n\n## . Excessive urine output (eg, diabetes mellitus, CHF) \n\n## . Restricted mobility (eg, postsurgery) \n\n## . Stool impaction \n\nBPH = benign prostatic hyperplasia ; CHF = congestive heart failure ; UTI = urinary tract infection . Renal normal. \n\nUrine analysis with culture \n\nMost common cause of UI in elderly patients are UTI's . Elderly patients often lack typical \n\nsymptoms of UTI (like dysuria , fever ). Patient may have delirium secondary to a UTI. \n\nOnce infection is excluded, additional testing can be done to rule out other causes. \n\n A continence pessary is used to treat stress urinary incontinence (SUI) and symptomatic pelvic organ prolapse (eg, anterior vaginal wall bulge); it works by stabilising the pelvic floor in its anatomic position and compressing the urethra against the pubic symphysis. \n\nMidurethral sling procedures are performed for SUI due to urethral hyper-mobility or when pessary fails. \n\n Vaginal estrogen therapy is used in patients with genitourinary syndrome of menopause (eg, vaginal dryness, atrophy) due to estrogen deficiency. In postmenopausal patients, localized estrogen can relieve urinary symptoms (eg, stress and/or urge incontinence) related to atrophy .\n\n Postmenopausal estrogen deficiency usually causes Urge Incontinence . Stress urinary incontinence is often associated with urethral hyper-mobility. \n\ncharacterized by urethral angle of > 30 degrees from horizontal with an increase in abdominal pressure ( Q-tip test ); SUI may also be caused by decreased urethral sphincter tone \n\n Postpartum SUI increases the risk of chronic SUI, but most cases are self-limited because the pelvic floor muscles and pudendal nerve heal after delivery; therefore, patients <6 weeks postpartum are managed with observation and reassurance and encouraged to perform Kegel exercises to strengthen pelvic floor muscles. \n\n36 https://t.me/usmleinnercircle \n\n> Resung\n> Re1bng\n> NO RMAi.\n> ST RESS URIN ARY\n> INCO NTI NEN CE\n\nRenal Renal Artery Stenosis \n\n RAS causes Secondary Hyper Aldosteronism \n\n A systolic-diastolic abdominal bruit lateralizing to one side can be heard in ~40% of patients; this finding has very high specificity(99%) for RAS. \n\nTreatment: \n\n1. ACE, ARB - 1st Line; Nephroprotective -there is a higher risk of AKI ; therefore, renal function should be monitored closely. \n\n-Given for both unilateral and bilateral RAS ( continued if the creatine rise remains acceptable ie, <30% ). \n\n2. Revascularisation with stenting or angioplasty done only for refractory cases \n\n Transplant RAS typically occurs in the first 2 years after kidney transplantation. \n\n## Renal Vein Thrombosis Dx: Renal USG with Doppler \n\n37 https://t.me/usmleinnercircle USMLE Inner Circle \n\nClinical clues to renovascular disease \n\n## . Resistant HTN (uncontrolled despite 3-drug regimen) \n\n## . Malignant HT N (with end-organ damage) \n\nHTN-relat ed sy mp toms . Onset of severe HT N (>180/ 120 mm Hg) after age 55 \n\n## . Severe HTN with diffuse atherosclerosis \n\n## . Recurrent flash pulmonary edema with severe HTN \n\nPhysical exa minati on \n\n# . Asymmetric renal size (>1.5 cm) \n\n## . Abdominal bruit \n\nSupportive evide nce La bo ratory results \n\n# . Unexplained rise in serum creatinine (>30%) after starting ACE inhibitors or ARBs \n\nIma gi ng r es ults \n\n# . Unexplained atrophic kidney \n\nARB s = angiotensin II receptor blockers; HTN = hypertension. \n\nRenal vein th rombosis \n\n# . Hypercoagulability \n\n0 Nephrotic syndrome (particularly membranous nephropathy) \n\nCau ses 0 Malignancy (particularly renal cell) \n\n0 Ot her (eg, inherited thrombophilia, oral contraceptive pills) \n\n Tra um a\n\nClinical features Acute: renal infarction symptoms (flank pain, hematuria, 1 LD H, 1 kidney si ze on imaging) \n\n# . Chronic: renal symptoms typically absent (may cause pulmonary embolus) \n\n# . CT scan or MR angiography \n\nDiagnosis . Renal venography \n\nTreat ment Anticoagulation \n\n# . Local thrombolysi s/ thrombectomy (if AK I present) \n\nAKI = ac ute kidney injury; LOH = l ac tat e dehydrogen ase .Renal Renal Cancers \n\n Renal cell carcinoma and hepatocellular carcinoma : Secrete EPO (causing polycythemia vera) Patients age > 35 with gross hematuria should be evaluated for urological neoplasms with CT urogram (diagnostic imaging) and cystoscopy. \n\n In a patient with with unexplained hematuria and risk factors for bladder cancer , cystoscopy is the preferred next step to examine the bladder and urethral linings. \n\nEg. patient with BPH has gross and microscopic hematuria with extensive smoking history \n\nCystoscopy should be obtained to rule out bladder cancer \n\n What is the most common malignancy associated with painless hematuria in adults? \n\nBladder tumors \n\nespecially patients age > 35 with a smoking history \n\n What is the current recommended screening regimen for bladder cancer ?\n\nNot recommended , even in patients with significant smoking and family histories bladder cancer screening does not provide survival benefit , even among high-risk populations. This is likely due to the following: Current screening tests such as dipstick urinalysis (for hematuria), cytology of urine sediment, and urinary tumor biomarkers have relatively low sensitivity/specificity , leading to missed cases (low sensitivity) or unnecessary workup (false-positive testing). Most bladder cancers are detected at an early stage, progress slowly , and are associated with relatively high rates of 5-year survival ; therefore, earlier detection (via screening) \n\n38 https://t.me/usmleinnercircle \n\nIndications for cystoscopy \n\n> Gross hematuria with no evidence of glomerular disease or infection Microscopic hematuria with no evidence of glomerular disease or infection but increased risk for malignancy Recurrent urinary tract infections refractory to antibiotic therapy Obstructive symptoms with suspicion for stricture, stone Irritative symptoms without urinary infection Abnormal bladder imaging or urine cytology\n\nBladder cancer \n\n## . >90% urothelial carcinoma \n\nEpidemiology j Risk with smokers & exposure to industrial carcinogens .\n\n## . Painless hematuria throughout micturition \n\nManifestations . Irritative voiding symptoms (eg , frequency, urgency, dysuria) \n\n## . Regional pain \n\nDiagnosis . Flexible cystoscopy with biopsy (gold standard) \n\n## . Urine cytology \n\n## . TURBT \n\nStaging Upper urinary tract imaging (eg , IVP, MRI , CT) .\n\n## . No muscle invasion: TURBT & intravesical immunotherapy \n\nTreatment . Muscle invasion: radical cystectomy & systemic chemotherapy \n\n## . Metastatic: systemic chemotherapy & immunotherapy \n\n> IVP\n\n= intravenous pyelogram; TURBT = transurethral resection of bladder tumor. Renal provides minimal mortality benefit. \n\n## Miscellaneous \n\nPeripheral Edema Hematuria \n\n39 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDisease characteristics Patient characteristics Test characteristics Program characteristics Primary mechanism Increased capillary hydrostatic pressure Decreased capillary oncotic pressure (hypoalbuminemia) Increased capillary permeability Lymphatic obstruction/increased interstitial oncotic pressure \n\n~3 RBC \n\nEvaluation of red urine \n\nRed/brown urine, heme-positive dipstick Urinalysis 0- 2 RBC I\n\nIdeal screening program \n\n Common Serious \n\n## . Long asymptomatic phase \n\n Correctable if identified early High prevalence in screened population Appropriate age range & gender \n\n## . Low cost relative to disease severity \n\n## . High sensitivity & specificity Acceptable to broad range of patients \n\n## . Identifies population to be screened Avoids \"overdiagnosis\" (detects benign/indolent disease) Avoids \"lead-time\" bias (detects disease early but does not alter ultimate prognosis) Improves outcomes of screened vs nonscreened population \n\nCauses of peripheral edema Clinical examples \n\n Heart failu re (left ventricular & cor pulmonale) \n\n Primary renal sodium retention (renal disease & drugs) \n\n Venous obstruction (eg , cirrhosis & venous insufficiency) \n\n Protein loss (eg , nephrotic syndrome & protein-losing enteropathy) \n\n Decreased albumin synthesis (eg , cirrhosis & malnutrition) \n\n Burns, trauma & sepsis \n\n Allergic reactions \n\n Acute respiratory distress syndrome \n\n Malignant ascites \n\n Malignant ascites \n\n Hypothyroidism \n\n Lymph node dissection \n\nHematuria th roughout urinary stream : \n\n Renal mass (benig n/malignant) Glome ru lonephri ti s Urolithiasis Polycystic kidney disease Pyelonephrit is Urotheli al cancer Trauma \n\nUpper collecti ng system He maturia ] He mo g lo bi nuria My ogl ob in uri a lntravascular \n\nhemol ys is \n\n J. Hemoglobin &haptoglobin CK = creat,ne kinase; RBC = red blood cells. Rh abdomyo lysis t CK \n\nC)I.JWl>r ld Renal Initial hematuria is characterised by blood at the beginning of the voiding cycle and often reflects a urethral source. \n\nTotal hematuria is characterised by blood during the entire voiding cycle and can reflect bleeding from anywhere in the urinary tract (eg, bladder, kidneys). \n\nTerminal hematuria is characterised by blood at the end of voiding cycle and often suggests bleeding from the prostate, bladder neck or trigone, or posterior urethra. Significant exertion (eg, long-distance running ) can lead to dark urine due to the following: \n\nMyoglobinuria from skeletal muscle injury (ie, rhabdomyolysis) \n\nMarch hemoglobinuria (Exertional hemoglobinuria) (eg, mechanical red blood cell (RBC) damage/hemolysis in the vasculature of the plantar surface vasculature of the feet) (rare) \n\nBenign hematuria from bladder due to traumatic injury to the bladder mucosa Dx: clinical , T/t: Self Limited \n\nRenal Osteodystrophy \n\n## Renal Drugs \n\n40 https://t.me/usmleinnercircle \n\nTe r mi nal he maturia : Urothelial cancer Urolithiasis Benign pr ostatic hyperplasia Prostate cancer Init ial he maturi a: Ure th ritis Trauma (eg, catheterization) \n\nRenal osteodystrophy \n\nChronic kidne y disease ( GF R) )\n\n## ,,.,so,\"\"\"\"\"A\"\" n \n\n.1 Calcium t Phosphorus \n\n# yT PTH \n\n(secondary hyperparathyroidism) \n\nInadequate treatm 7 Optima l Latment ~ cessi ve treatment \n\nOste1t1s fibrosa cystica High PTH, high bone turnover .1 Mi neralizati on with fibrosis, T fracture risk Adynam1c bone disease Low PTH, low bone turnover .1 Cellularity & min er alization, T fracture risk Normal bo ne turnover ) \n\n> \"Trea tment invol ves dietary pt,ospha te restriction .t phOSpha te binders\n\nOnce phO sphOrus is normaliz ed , vrtamin \n\nD can be giv en (while d osely moni tOfi ng fOf hypercalce mia ). \n\n> GFR\n\n= glomerular filtration rate; PT H = parathy roid hOmlone. CtMl odd \n\n> UWorld\n\nRenal Acute nitrofurantoin-induced pulmonary injury is due to a hypersensitivity that can present with \n\nfevers , shortness of breath , dry cough , and erythematous rash .Symptoms usually begin 3-9 days from medication initiation. Bilateral basilar opacities and pleural \n\neffusions are common. Treatment involves cessation of nitrofurantoin. \n\n## Paeds Renal \n\n In utero hydronephrosis : if sufficient amniotic fluid is present, dont do anything. \n\nif there is oligohydramnios, you can try in utero surgical diversion of kidneys. (only in severe cases though) \n\nHematuria \n\n41 https://t.me/usmleinnercircle USMLE Inner Circle \n\nGlomerular \n\nCreat111 ,ne, \n\ncomplement levels. CBC Diuretic effects on tota l body electrolyte levels \n\nNa K+ Ca 2+ Uric \n\nDiuretic type HCO a- acid \n\nLoop U! u\n\n(eg, furosemide) it ! tThiazide (eg, HCTZ , metolazone) u ! t t t\n\nPotassium sparing ! t ! - -(eg, spironolactone, amiloride) Carbonic anhydrase inhibitor ! ! ! ! -(eg, acetazolamide) \n\nHCTZ = hydrochlorothiazide. \n\nEvaluation of hematuria in children \n\nTrauma history abdomen \n\nCTscan ~\n\nHematuna J \n\n(2:3RBC) \n\nNonglomerular Symptomatic U ri nary tract Perineal/meatal \n\ninfection Kldney stones \n\n(dysuna pyuie) imtatoon ( fl- pain, aystals) \n\n!\n\nUrine culture, Reassurance J Renal Janbbtotics ultrasound \n\n'Fonding, cl QlomeNI ose .. ,,_ t,ro,m ume, edema t,ypenens,on prc1e,nuna, end RBC cnlS l:a: Cr caloum to creai,rw,e ra1>0 , CBC ~ blOOcl count; RBC r..t blood 011 \n\nAsymptomabc \n\nConsider Renal ultrasound Urine cuhure Urine Ca Cr Renal Young children are more likely to have stones located in the kidney, which are painless and cause an \n\natypical presentation of gross hematuria alone, The preferred imaging study for evaluation of nephrolithiasis in children is a renal and bladder ultrasound , which can detect some stones and ureteral obstruction while avoiding radiation \n\nexposure. \n\nCT scan of the abdomen without contrast is more sensitive, particularly for identifying small calculi, and may be required if the ultrasound is nondiagnostic \n\n Glomerular disease should be suspected with any of the following: Red blood cell casts (pathognomonic) Proteinuria Hypertension Edema Brown, cola-colored urine (in contrast to red/pink urine with lower urinary tract bleeding) \n\nNeonatal AKI \n\nAll neonates with oliguria require further evaluation with the following: \n\nHistory and physical examination to evaluate for possible risk factors (eg, nephrotoxins, family history, renal anomaly) and volume status (volume overload vs hypovolemia) \n\nRenal and bladder ultrasound (RBUS), which documents the number, shape, and size of the kidney(s) and detects vascular abnormalities or congenital anomalies. \n\nNocturnal Enuresis \n\n42 https://t.me/usmleinnercircle \n\n\n\nCommon causes of neonatal acute kidney injury \n\n# . Hypovolemia \n\n> Prerenal disease\n\n Cardiac disease \n\n# . Sepsis \n\n> Acute tubul ar necrosis (eg, ischemic injury)\n\n# . Nephrotoxins (eg, maternal NSAID use , aminogly cos ides) \n\n> Intrinsic renal\n\n Renal vascul ar disease ( eg , renal vein thrombosis) \n\n> disease\n\n# . Gl omerular & cystic disease (eg, polycystic kidne y disease) Congenital anomalies (eg, renal agenesis) \n\n> Postrenal\n\n Obstructive uropathy (eg , posterior urethral v alves ) \n\n> disease NSAID =nonsteroidal anti-inflammatory drug .\n\nRenal Constipation is commonly associated with bladder dysfunction and should be considered in any patient with enuresis. Because of the close proximity of the bladder to the rectum, fecal retention can lead to a \n\ndecreased functional bladder capacity and instability of the detrusor muscle of the bladder. Although often mistaken as diarrhoea, encopresis (ie, fecal incontinence) is usually a sign of \n\nconstipation and is characterised by leakage around impacted stool .\n\nLeft-sided firmness , or a palpable fecal mass, on abdominal examination further supports the diagnosis of constipation. Family history of bed wetting is the greatest risk factor. Secondary nocturnal enuresis is more likely to be due to a medical condition \n\n43 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPrimary nocturnal enuresis Causes of secondary enuresis Definition Nighttime urinary incontinence age ~5 \n\n No prior prolonged period of overnight dryness \n\nEtiology Associated symptoms \n\nPsychological stress Behavior regression , mood !ability Delayed maturation of bladder control \n\nPathogenesis f Nocturnal urine output (eg , f evening fluids , ! ADH) Urinary tract infection Dysuria, hesitancy, urgency, abdominal pain \n\n ! Bladder capacity Diabetes mellitus Polyuria, polydipsia , polyphagia, weight loss, lethargy, candidiasis \n\nRisk factors Family history Boys age 5-8 Diabetes insipidus Polyuria, polydipsia Obstructive sleep apnea Snoring , dry mouth , fatigue , hyperactivity, irritability \n\nEvaluation Urinalysis (to exclude other causes) Voiding diary Treatment of comorbid conditions (eg, constipation) \n\nManagement Behavioral modifications (eg, restrict evening fluids) Enuresis alarm Desmopressin therapy \n\nADH = antidiuretic hormone. \n\nMedical conditions causing enuresis Etiology Symptoms Findings Constipation* . Infrequent & hard stools Palpable stool mass \n\n## . Encopresis \n\n## . Daytime incontinence \n\nBladder dysfunction* Weak stream , urgency, straining Recurrent urinary tract infections \n\n## . Dysuria, urgency, frequency \n\nUrinary tract infection . Positive urine culture Abdominal pain \n\nChronic kidney disease . Daytime incontinence . Hypertension Weight loss, fatigue . Proteinuria, hematuria \n\n## . Polyuria, polydipsia, polyphagia \n\nDiabetes mellitus Glucosuria Weight loss, fatigue \n\nDiabetes insipidus . Polyuria, polydipsia . Low urine specific gravity \n\nObstructive sleep apnea Snoring Adenotonsillar hypertrophy \n\n## . Hyperactivity, inattention \n\n*Often a clinical diagnosis. Renal CKD in children is most commonly due to a congenital urinary tract abnormality such as posterior urethral valves (PUV) . PUV is an obstructive uropathy that prevents the outflow of urine from the bladder, causing symptoms of bladder dysfunction such as urinary incontinence (during the day and night ) and a weak stream. Urinary stasis and associated vesicoureteral reflux from the distended bladder into the ureters can cause damage to the kidneys and predispose patients to recurrent UTIs ,which further contribute to renal scarring. \n\nFatigue , poor growth, and hypertension in a child, in addition to urinary symptoms, should also raise suspicion for CKD. Proteinuria (and/or hematuria) on urinalysis may be present and cause edema if in the nephrotic range (typically 3+). The next step in evaluation of CKD is to check a serum creatinine level as an indicator of renal function. Imaging with renal ultrasound and voiding cystourethrogram may also be considered. \n\n The first step in evaluation of all patients with nocturnal enuresis (both primary and secondary) is a urinalysis (UA). \n\nVesicoureteral Reflux \n\nSymptoms ? Recurrent UTI's in neonate/child Diagnosis ?UA, urine culture \n\nU/S Contrast voiding cystourethrogram (t est of choice for definitive diagnosis) indicated in: \n\n>2 episodes of febrile UTIs Renal anomaly detected on U/S Findings: retrograde reflux of contrast into ureters during micturition is diagnostic of VUR. \n\n44 https://t.me/usmleinnercircle \n\n\n\n> 00\n\n\n\nEvaluation of bladder dysfunction in children \n\n> Bladder dysfu nction Nighttime symptoms only Manage nocturnal\n> enuresis\n> in children Urinalysis\n\nI- Positive ---+ Treat underlyi ng cause \n\n> ,(eg, UTI , diabetes mellitus) INegative Yes\n\n+ \n\n> Daytime symptoms Red flags for spin al cord anomaly? Neurologic deficits Cutaneous lumbosacral abnorma li ty No\n\n+ \n\n> Obtain spinal MRI for spinal dysraphism Consider VUR, constipation, behavioral etiologies\n> UTI =urinary tract infection ;VUR =vesico ureteral reflux.\n> Lower extremity we akness ,hypotonl a, hypo< efle xi aCIUWofld\n\nRenal Cystourethrogram : contrast instilled into bladder through foley --> images obtained via fluoroscopy while child is voiding \n\n Renal scintigraphy with dimercaptosuccinic acid is the preferred modality for long-term evaluation for renal scarring. \n\nUTI Spontaneous resolution of VUR by age 5 is common due to growth of the intravesical ureteral segment \n\n45 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPrimary vesicoureteral reflux in children Pathogenesis . Retrograde urine flow through a short intravesical ureter \n\nPresentation . Febrile urinary tract infection \n\n# . Renal ultrasonography: hydronephrosis \n\nDiagnosis Voiding cystourethrography: ureteral filling dilated collecting system Mild (grade 1-11) *: observation prophylactic antibiotics \n\nManagement Severe (grade Ill-IV) *: prophylactic antibiotics surgery \n\n# . Mild : spontaneous resolution with growth \n\nPrognosis Severe (without intervention): renal scarring and chronic kidney disease *Plus screening/treatment of concomitant bladder & bowel dysfunction (eg , stool softeners/laxatives). Normal \n\nGrade \n\nIII \n\nIll \n\nIV VVesicoureteral reflux \n\nGrade I Grade II Grade Ill Grade IV GradeV \n\nDescription \n\nInto a nondilated ureter Into the pelvis & calyces wi thout dilation Mild to moderate dilation of the ureter, renal pelvis & calyces , with minimal blunting of the fornices Moderate ureteral tortuosity & dilation of the pelvis & calyces Gross dilation of the ureter, pelvis & calyces; loss of papillary impressio ns ; ureteral tortuosity \n\nIndications for renal & bladder ultrasound \n\nInfants and children age< 24 months with a first febrile UT IRecurrent febrile UTls in children of any age UTI in a child of any age with a family history of renal or urologic disease , hypertension, or poor growth Child r en who do not respond to appropriate antibiotic treatment Renal Ciprofloxacin is reserved for treatment of UTIs caused by Pseudomonas aeruginosa , which typically occur in patients with an indwelling catheter \n\nUTI's in Children \n\n1. Urine analysis and urine culture 2. Renal and bladder U/S \n\na. 2-24 mo w/ febrile UTI b. Recurrent UTI's (any age) 3. Voiding cystourethrography \n\na. <1 mo. b. <2 years with recurrent UTI's ( >2 episodes of febrile UTIs) \n\nc. Organism other than E. coli \n\nd. if any anomaly seen in U/S What is the next step in management for a 12-month-old girl with a confirmed E. coli UTI that is resolving after initiation of antibiotics? \n\nRenal and bladder ultrasound \n\n What is the first step of diagnosis of a UTI in infants in diapers? \n\nStraight catheterization to obtain sterile specimen sample for UA and urine culture \n\nclean-catch specimens are unreliable in diapered patients due to high likelihood of contamination with stool or skin flora Recurrent UTI= 2 episodes. \n\n46 https://t.me/usmleinnercircle \n\nUrinary tract infection (UTI) in children \n\n## . Female sex Risk factors . Unc ir cumcised ma le in fa nts . Urologic abnormalities (eg, vesicoureteral reflux) \n\n## . Bowel/ bladder dysfunction (eg, ~Q St i '2a1iQD) \n\n> Clinical features\n\n## . Infants: fever, fussiness, poor feeding \n\n## . Older children: dysuria, suprapubic/flank pain Laboratory findings . Urinalysis: leukocyte esterase, nitrites, WBCs \n\n## . Urine culture: bacteriuria \n\n## . Antibiotics (eg, cephalosporin ) \n\n## . First febrile UTI : Management 0 Age <2: RBUS, followed by VCUG if abnonmal \n\n> 0Age :?:2: obse,vation alone\n\n# . Recurrent febrile UTls: RBUS & VCUG RBUS = renal & bladder ultrasound; VCUG = voiding cystourethrogram; WBCs = white blood cells. Renal The presentation of UTI in infants is nonspecific and can include fever , fussiness , and poor feeding. \n\nBenign Proteinuria \n\n What is the next step in management for a child that is found to have isolated proteinuria on urine dipstick? \n\nRepeat dipstick testing on two subsequent occasions \n\nif subsequent tests are negative, the diagnosis is transient proteinuria; if subsequent tests reveal continued proteinuria, further workup is warranted \n\n## Renal Surgery \n\nGenitourinary trauma \n\nGross hematuria following blunt trauma suggests an injury to what structures? \n\nKidney or bladder \n\n1. Thus, need to first do a CT scan to identify any renal trauma \n\n2. Injury to the bladder can be determined by either a retrograde cystogram or CT cystogram \n\n3. Blood at the urethral meatus suggests urethral injury -- perform retrograde urethrogram \n\n Ability to insert a Foley catheter helps distinguish Bladder Injury from urethral injury \n\nKidney Injury \n\n Evaluation of kidney injury in blunt genitourinary trauma should include urinalysis and contrast-enhanced CT of abdomen/pelvis in hemodynamically stable patients with evidence of flank pain and ecchymosis, costovertebral area tenderness, and hematuria. \n\nmay warrant retrograde cystourethrogram if patients have gross hematuria , difficulty urinating ,\n\nblood at the meatus , or suprapubic pain \n\nBladder Most common cause of proteinuria in children \n\n47 https://t.me/usmleinnercircle USMLE Inner Circle \n\nBenign proteinuria \n\n Defined as isolated proteinuria < 3.5 g/day i;:::l \n\n Important , benign differential diagnosis in the evaluation of proteinuria Very common; mostly affects younger individuals i;:::l \n\n Types of benign proteinuria \n\n Orthostatic proteinuria (postural proteinuria): increased protein excretion only in the upright position \n\n Transient proteinuria Most common cause of isolated proteinuria in children \n\nCauses: Heavy exertion / stress Fever Exposure to cold temperatures A dipstick test should be repeated to exclude underlying disease. No treatment necessary; excellent prognosis Renal Rupture of the dome of the bladder can cause urine to leak into the peritoneal cavity and can lead to chemical peritonitis .\n\nIrritation of peritoneal lining of right or left hemidiaphragm may cause referred pain to shoulder (\"Kehr sign\") \n\nRetrograde cystography , in which the bladder is passively filled (eg, via Foley catheter) with \n\nwater-soluble contrast and then imaged (eg, CT scan ), can confirm the diagnosis \n\nUreter Injury \n\n Usually due to gynae procedures Spl Hysterectomy \n\n Ureter obstruction Hydronephrosis nonradiating back pain and costovertebral angle tenderness \n\n Only 1 ureter involved usually Creatinine normal \n\n Dx: Renal USG Unilateral ureteral laceration, during hysterectomy, may present with Intrabdominal Urine Collection \n\nand abdominal distention. \n\nmight overflow through vaginal sutures as vaginal discharge. \n\nUrethral Injury \n\n What imaging modality is used to diagnose urethral injury ?\n\nRetrograde urethrogram Extravasation of contrast from the urethra is diagnostic of urethral injury. \n\n48 https://t.me/usmleinnercircle \n\nUrethral injuries \n\n> The goal is to maintain urinary continence and sexual function . Place suprapubic catheter to decompress bladder (diverts urine from the healing urethra and anastomosis) Anterior urethral injury\n> Partial injury: place Foley catheter for healing by secondary intention Penetrating injury: surgical exploration with debridement and defect repair with a direct anastomosis over a catheter Posterior urethral injury\n> Endoscopic approach: early realignment (within 1 week) with combined transurethral and percutaneous transvesical approach Surgical approach: place suprapubic catheter .... delayed urethroplasty (6-12 weeks after initial injury)\n\nRenal Any of the following should prompt evaluation for urethral injury: \n\nBlood at the urethral meatus Hematuria (eg, pinkish-red urine) \n\nDifficulty voiding (due to disruption of urethral continuity) Are most cases of Posterior urethral injury treated with immediate or delayed surgical repair ?\n\nDelayed \n\ntypically treated with temporary urinary diversion by suprapubic catheter , followed by delayed repair \n\n Anterior urethral injuries (eg, penile fracture, straddle injury) are typically repaired urgently (eg, within 24 hours ) Foley catheter NOT recommended for patients with suspected urethral injury \n\nPost Operative Urinary Retention \n\n Urinary retention is a common postoperative complication. Factors associated with an increased risk of POUR include: \n\nPatient factors: increasing age and male sex (eg, prostatic enlargement) \n\nType of surgery: hernia repair , joint arthroplasty , or anorectal operations Anesthetic factors: prolonged anesthetic duration, excessive fluid administration, and use of medications (eg, opioids, anticholinergics) that impair bladder emptying Dx: Suprapubic Fullness , USG (>300ml urine) \n\nUrethral Strictures Commonly Idiopathic \n\n49 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nUrethral stricture \n\n## . Male > female Etiology . Urethral trauma (eg, catheterization) \n\n## . Urethritis \n\n# . Radiotherapy \n\n## . Weak or spraying stream Symptoms . Incomplete emptying \n\n## . Irritative voiding (eg, dysuria, frequency) \n\n# . Acute urine retent ion Complications . Recurrent urinary tract infection \n\n## . Bladder stones \n\n## . Postvoid residual, uroflowmetry \n\nDiagnosis . Urethrography \n\n## . Cystourethroscopy \n\n## . Dilation Management Urethroplasty .Pulmonary \n\n# Pulmonary Physiology Ventilator Pulmonary Function Tests Capnography PIP DLCO Hypoxemia Methemoglobinemia Cyanide Toxicity CO Poisoning Hemoptysis Head, Neck & Nose Stridor Laryngomalacia Torus Palatinus URI Epiglottitis Retropharyngeal Abscess Peritonsillar Abscess Sinusitis Tracheitis Laryngeal Papillomatosis Rhinitis Septal Hematoma Neck Masses Mediastinum Masses Acute Mediastinitis Obstructive Acute Bronchitis COPD Treatment Asthma Status Asthmaticus Occupational Asthma Exercise Induced Treatment Bronchiectasis Allergic Bronchopulmonary Aspergillosis Restrictive Interstitial Lung Disease Hypersensitivity Pneumonitis Sarcoidosis Pulmonary Hypertension Pneumonia \n\n50 https://t.me/usmleinnercircle Pulmonary Physiology VAP Aspiration Pneumonia Treatment Pleural Effusion Lung Abscess Pneumothorax Spontaneous Pneumomediastinum Pulmonary Embolism DVT Air embolism ARDS Lung Cancer Pancoast Tumor Lung Carcinoid Tumour Head and Neck Cancer Nasopharyngeal Carcinoma Oral Leukoplakia Miscellaneous Chronic Cough Hyperventilation Syndrome Acute Chest Syndrome Decompression Sickness High Altitude Sickness Diffuse Alveolar Hemorrhage Pulmonary Paeds Choanal Atresia CHARGE Syndrome Foreign Body Aspiration Nasal Foreign Body NRDS Persistent Pulmonary Hypertension of Newborn OSA Breath holding spells Sudden Infant Death Syndrome Drowning Pulmonary Surgery Post-operative Atelectasis Flail Chest Blunt Chest Trauma Hemothorax Tracheobronchial Injury Pulmonary Contusion Diaphragmatic Rupture Diaphragmatic Paralysis \n\n51 https://t.me/usmleinnercircle USMLE Inner Circle Pulmonary 52 https://t.me/usmleinnercircle \n\nTopography of the lungs Lower border of Midclavicular Midaxillary Paravertebral pleura line line line Lungs (& visceral pleura) 6th rib 8th rib 10th rib 10th rib Right - upper \n\nParietal pleura 8th rib border 12th rib \n\nCell type Alveolar macrophage Type1 pneumocyte Type2 pneumocyte Ciliated airway epithelial cell Club cell Goblet cell Fibroblast \n\nLeft - lower border \n\nLung cells & functions Normal function(s) \n\n## . Clearance of alveolar debris \n\n(surfactant, pathogens, inhaled \n\nparticulate matter) \n\n## . Alveolar epithelial lining for gas \n\nexchange \n\n## . Surfactant production \n\n## . Stem cell reservoir for type 1 pneumocytes \n\n## . Mucociliary escalator \n\n## . Salt, water & moisture homeostasis \n\n## . Protection & repair of distal airway \n\n## . Secretion of mucins \n\n Maintenance of interstitial lung tissue Example disease association(s) \n\n## . PAP: impaired macrophage \n\nclearance of surfactant \n\n## . ARDS due to inhalational injury \n\n## . Hyaline membrane disease \n\nof prematurity \n\n## . Ciliary dyskinesia (Kartagener syndrome) \n\n## . Cystic fibrosis: airway desiccation \n\n## . COPD: tobacco smoke \n\ndetoxification \n\n## . COPD & asthma: goblet cell \n\nmetaplasia & mucus hypersecretion \n\n IPF: increased fibroblast activity \n\n Emph ysema: decreased \n\nfibroblast activity \n\nARDS = acute respiratory distress syndrome; COPD = chronic obstructive pulmonary disease; IPF = idiopathic pulmonary fibrosis; PAP = pulmonary alveolar proteinosis. Pulmonary Ventilator \n\n When using a ventilator, the goal is to keep -SpO2 between 88 - 95%. -PaO2 between 55 - 80 mmHg \n\n When using a ventilator, prolonged FiO2 levels > 60% are associated with oxygen toxicity. \n\nthus it is usually preferable to increase PEEP to allow for lower levels of FiO2 if oxygenation needs to be increased. \n\n 02 is changed with altering FiO2 or PEEP .\n\nCO2 is changed with tidal volume or respiratory rate (preferred) \n\n In general, tidal volumes in mechanically ventilated patients should be about 6-8 ml/kg of ideal body weight. \n\n70kg patient = tidal volume of ~420 \n\n53 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSpectrum of ventilation/perfusion (V/Q) mismatch Intrapulmonary shunt \n\nPerfusion wi tho ut ventilation (V=O) \n\nUV \n\nDiffuse pulmonary \n\nedema ,\n\nARDS \n\n!V \n\nLobar pneumonia, localized atelectasis \n\n# ~Consolidated Normally \n\nregions ventilated \n\n0\n\n\">\n\nii \n\n0\n\n~\n\n0\n\nV/Q ratio Normal \n\nV&Q matched NormalV/Q \n\n# Li__ 0 1\n\nV/Q ratio Dead-space ventilation \n\nVentilation without perfusion (Q =O) \n\nIQ \n\nSegmental PE 0Normally perfused \n\n11 0\n\nMassive PE, R-to-L shunt, severe PAH Unperfused \n\nregions V/Q ratio ARDS = acute respi rat ory distress syndrome ; PAH = pulmonary arterial hyperten sio n; PE = pulmonary embo lism . ~Pulmonary Complications of PEEP :\n\nBarotrauma ; typically involves worsening SOB after PEEP has been given to the pt \n\nPneumothorax ; suspect this if the patient becomes hypotensive and mediastinal shift/tracheal deviation ; diagnosed with CXR; treatment with needle decompression; can be secondary to barotrauma. \n\n Somnolent patient or coma : inability to protect airway = Intubation \n\n Positive pressure mechanical ventilation causes an acute increase in intrathoracic pressure. \n\nin the setting of decreased CVP (e.g. hypovolemic shock), this can cause acute loss of right ventricular preload with resultant sudden cardiac death \n\n Continuous positive airway pressure (CPAP) predisposes users to recurrent epistaxis because of its \n\ndrying effect on the nasal mucosa .\n\nHumidification is often effective in preventing CPAP-associated epistaxis .\n\n54 https://t.me/usmleinnercircle \n\n\n\n Positive end-expiratory pressure (PEEP): \n\nalveolar collapse during mechanical ventilation \n\n Definition: Positive pressure (- 5 cm H 2 O) c;;:::i \n\nin the lung is maintained over the entire inhalation and expiration phases. c;;:::i \n\n Mechanism of action \n\nPEEP j alveolar pressure and alveolar \n\nvolume -+ collapsed or unstable alveoli reopen -+ improves ventilation/ perfusion relation Provides an adequate arterial ~?_9 2 at a low and safe concentration of oxygen (< \n\n60%) -+ reduces the risk of oxygen toxicity \n\n Advantages \n\nAvoidance of atelectasis \n\nj Oxygenation \n\ni Gas exchange area \n\nj Functional _ residual _ capacity \n\nj Pulmonary compliance \n\nNoninvasive positive pressure ventilation \n\n## . COPD (severe exacerbation , prevent extubation failure) \n\n## . Cardiogenic pulmonary edema \n\nIndications . Acute respiratory failure \n\n(strongest evidence) 0 Postoperative hypoxemic respiratory failure \n\n> 0\n\nlmmunosuppressed patients \n\n## . Facilitate early extubation \n\nMedical instability \n\n## . Cardiac or respiratory arrest (or impending arrest) \n\n## . Severe acidosis ( pH <7.1 ) \n\n## . Acute respiratory distress syndrome \n\n## . Nonrespiratory organ failure \n\n> 0\n\nUnstable cardiac arrhythmia/hemodynamic instability \n\n> 0\n\nEncephalopathy (Glasgow Coma Score <10) \n\nContraindications 0 Gastrointestinal bleed \n\nInability to protect airway \n\n## . Uncooperative or agitated \n\n## . Inability to clear secretions/high aspiration risk \n\nMechanical issues \n\n## . Recent esophageal anastomosis \n\n## . Facial or neurologic surgery, deformity, or trauma \n\n## . Upper airway obstruction \n\nCOPD = chronic obstructive pulmonary disease. Pulmonary An endotracheal tube that is advanced too far will preferentially enter into the right mainstem bronchus. \n\ncauses asymmetric chest expansion and markedly decreased breath sounds on the left side. \n\nIdeal Position: 2-6 cm above Carina \n\n The initial criteria for extubation readiness include: \n\npH >7.25 \n\nAdequate oxygenation (eg, PaO 60 mm Hg ) on minimal support (ie, fraction of inspired oxygen \n\n[FiO] 40% and positive end-expiratory pressure [PEEP] 5 cm HO) Intact inspiratory effort and sufficient mental alertness to protect the airway Because there is short-term risk of recurrent respiratory failure requiring reintubation, most patients who meet the above criteria should undergo a spontaneous breathing trial (SBT) to help confirm readiness for extubation. During an SBT, patients remain intubated but ventilatory support is turned off Candidacy for successful extubation may be further assessed during an SBT using the rapid shallow breathing index (RSBI) , which is calculated by dividing respiratory rate (per minute) by tidal volume (liters). \n\nPatients with a high RSBI (eg, >105) are breathing fast and shallow and are unlikely to do well without continued ventilatory support. Major Mortality Benefit \n\n55 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nEffects of positive pressure ventilation in cardiogenic pulmonary edema \n\nt lntrathoracic pressure \n\n! RV preload t RV afterload ! MAP ! LV transmural (I Central (Pulmonary capillary \n\nve nous return) compression) \n\n# L ! LV preload J l pressure gradient \n\n! LV afterload J Displaces interstitial lung wa t er \n\nt LV peLmance d':~~;;::t,n t L,(I mproved st ro ke volume ----------+ (! Intrapulmonary \n\n& diastolic filling) \n\n+t CO \n\nI\n\n## !t End-organ O, delivery & survival \n\nAortic compression triggers ba rorecept or reflex to lower blood pressure. CO = cardiac output; LV = left ventricle; MAP = mean arterial pressure; Pa0 2 = art erial partial pressure of oxygen; PVR = pulmonary vascu lar resistance ; RV = rig ht ve nt ri de . QUWorld Pulmonary Because an endotracheal tube can cause damage to the larynx and upper trachea over time (eg, tracheal stenosis), tracheostomy is indicated when prolonged intubation (eg, >7-10 days) is required. \n\n Mechanical ventilation can lead to respiratory muscle atrophy and insufficiency .Exercises such as physiotherapy , coughing , repositioning (sitting) , and moving can improve respiratory sufficiency after mechanical ventilation. \n\nPulmonary Function Tests \n\n56 https://t.me/usmleinnercircle \n\nPulmonary function tests in chronic lung disease Asthma COPD Interstitial lung Pulmonary arterial Restrictive chest diseases hypertension TLC Normal/-1 i 1 Normal \n\nFEV1/FVC 1* 1 Normal Normal \n\nDLCO Normal/j 1t 1 1\n\nCOPD = chronic obstructive pulmonary disease; DLCO = diffusing capacity for carbon monoxide; TLC = total lung capacity. *With positive bronchodilator response. \n\ntNormal in early COPD. \n\nPulmonary auscultation examination findings \n\nCondi tion Breath sounds Tactile Percussion Mediastinal fremitus shift Bronchovesicular N orma l lung (hilar), vesicular Normal Resonance None (peripheral) Consolidation Increased (eg , l obar (crackl es & Incr eased Dullness None pne umon ia) ego phony present) Pleural Decreased or Away from effusion absent Dec reased Dullness effusion (if large) Decreased or Away from Pneumothorax absent Decreased Hype rr esonant tension pneumothorax Emphy se ma Decreased Dec reased Hyperresonant None Atelectasis Dec reased or Towa rd (eg , mucus absent Decreased Dullness atelectasis plugging) (if large) \n\nwall disease \n\n1\n\nNormal Normal Pulmonary FVC is the gold standard for assessing ventilation ; decline in FVC (especially < 20 mL/kg )indicates impending respiratory failure \n\nCapnography \n\nA normal capnogram has a characteristic rectangular waveform with 4 phases. A flat waveform \n\nindicates that the sensor (located at the hub of the ETT) is not detecting CO2. This most commonly reflects 2 situations: Because CO is not produced in the stomach or esophagus, esophageal intubations are classically represented by a flat line. An uncuffed ETT can easily become displaced during transport and move the relatively short distance from the trachea to the esophagus. \n\n(Uncuffed ETTs are commonly used in children because they are thought to be associated with less mucosal injury.) \n\nIn prolonged cardiac arrest (production of CO has ceased), a flat waveform can occur. \n\n57 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\n0\n\n\n\nDiagnostic pulmonary tests Test Indications Disadvantages \n\nGold standard in evaluating May be difficult to perform in \n\nSpirometry pulmonary function (eg, FVC , forced expiratory volume in 1 second) unstable patients \n\nPeak flow Assessment of airflow out of the Less accurate than spirometry \n\nmeter lungs (peak expiratory flow rate) \n\nChest First-line imaging of tracheal Insensitive for small tumors & position, lung fields, bones & heart pulmonary embolus; no \n\nx-ray size with relatively low radiation information about lung function Rapid & detailed visualization of Significant radiation exposure; \n\nChest CT tracheal position , lung fields, bones no information about lung & heart size function \n\nPulse Rapid assessment of oxygenation at Inaccurate if the extremity is cold, calloused , or moving; \n\noximeter fingertip, earlobe, or foot (infant) cannot assess ventilation \n\nArterial Quantitative measurement of arterial Slight risk of bleeding , infection pH , oxygen/carbon dioxide/ \n\nblood gas bicarbonate levels & base deficit & radial artery thrombosis \n\nCommon capnography waveforms \n\n# !~ Inspirat ion Anatomical dead space Anatomical a lv eolar dead space Alveolar plateau \n\nt t\n\nInspiration Expiration \n\nHyperventilation Bronchospasm \n\nLoss of a angle phases 2 and 3 \n\n!\n\nCPR \n\nETCO 2 = end- ti dal CO 2.Increase of ETCO 2 base li ne \n\nHypoventilation \n\ni Increased --------------------------------------- ETC0 2 __ _\n\nTube displacement \n\nSudden loss in all phases or reduction of ETCO 2\n\n!\n\nAbsence of phases 0, 1, 2, 3 \n\nUWorld Pulmonary PIP \n\n The peak airway pressure (the maximum pressure measured as the tidal volume is being delivered) equals the sum of the resistive pressure (flow x resistance) and the plateau pressure. \n\n The plateau pressure is measured during an inspiratory hold maneuver, when pulmonary airflow and thus resistive pressure are both 0. It is determined by the compliance of the lung. \n\ni.e. if there is a problem with compliance , plateau pressure will rise. ( increased plateau pressure = decreased compliance.) \n\nElastic pressure is inversely related to compliance, so decreased compliance causes a higher elastic pressure \n\n The alveolar end-expiratory pressure is typically equal to the atmospheric pressure . In obstructive lung disease, however, the alveoli cannot empty completely, resulting in higher than normal end-expiratory pressures. This is called intrinsic, or auto-PEEP . The end-expiration hold maneuver measures auto-PEEP. \n\nDLCO \n\n58 https://t.me/usmleinnercircle \n\nPeak ai rway pres su re = res is ti ve pre ss ure + plat ea u pres sur e\n\nPlateau pressure = elastic pressure + PEEP In creased peak pressure \n\nf Peak pressure Normal plateau pressure Bronchospasm Mucus plug Biting ET tube \n\nf Plateau pressu re Pneumotho rax Pulmonary edema Pneu moni aAtelectasis Right mainstem i ntubatio nPEEP PIP IResistance f low \n\n> Pplal\n> Auto-PEEP\n\nPulmonary Hypoxemia Methemoglobinemia \n\n Standard pulse oximetry is unable to detect methemoglobin, thus creating a falsely low oxygen saturation (versus co-oximetry , which can detect hemoglobin, methemoglobin, and carboxyhemoglobin) Arterial blood gas ( ABG ) detects free , unbound O2 , which is not affected by methemoglobin. \n\nCyanide Toxicity \n\n59 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDifferential diagnosis based on carbon monoxide diffusi ng capacity of the lung Obstructive Rest ri ctive pattern pattern (FEV1 /FVC >70% Normal spirometry (FEV1/FVC <70% predicte d, FVC pred ic ted) <80% predicted) \n\n Interstitial lung diseases Anemia \n\nLow Sarcoidosis Pulmonary embolism \n\nDLCO Emphysema Asbestosis Pulmonary hypertensi on Heart failure Chronic Musculoskeletal \n\nNormal bronchitis deformity \n\nDLCO Neuromuscular Asthma disease \n\nIncreased Morbid obesity Pulmonary hemorrhage \n\nDLCO Asthma Polycythemia \n\nauses o ypoxem1a Example A-a Corrects with gradient supplemental 02? Reduced Pi0 2 High altitude Normal Yes \n\nHypoventilation CNS depression, neuromuscular Normal Yes weakness \n\nDead-space ventilation Pulmonary embolism Increased Yes \n\n(V/Q=oo) Diffusion Emphysema, ILD Increased Yes \n\nlimitation Intrapulmonary Pneumonia , pulmonary edema, \n\nshunt Increased No \n\n(V/Q=O) atelectasis \n\nlntracardiac shunt Tetralogy of Fallot, Eisenmenger Increased No (right to left) syndrome \n\nClinical presentation of methemoglobinemia History Exposure to oxidizing substances (eg, dapsone , nitrites, local/topical anesthetic) Cyanosis \n\nClinical examination Pulse oximetry saturation -85% \n\n Dark chocolate-colored blood \n\nlaboratory findings Saturation gap (>5% difference between oxygen saturation on pulse oximetry & ABG) \n\n Normal Pa02 Pulmonary Risk factors for cyanide toxicity due to nitroprusside include prolonged infusion (> 24 hours) and high rates (5-10 g/kg/min) , as well as chronic kidney disease \n\n To prevent cardiorespiratory arrest and permanent neurologic disability, victims of smoke inhalation should be treated empirically for cyanide toxicity .\n\nCO Poisoning \n\n60 https://t.me/usmleinnercircle \n\nCyanide poisoning \n\n# . St ruct ur e fires (eg, combustion of plastics) Common etiologies . Oc cupational exposure (eg, mining) \n\n# . Cyanide-containing medications (eg, sodium nitroprusside) \n\n# . Inhib it s oxidative phosphorylation & forces anaerobic metabolism \n\nPathophysiology Rapidly lethal if untre ated .. H yp ertension, tachycardia, tac hypnea - circulatory coll apse , death \n\n# . He adache, con fu sion, an xiety - seizures, coma Clinical features . Cherry-red skin \n\n# . Elevated anion gap metabolic acidosis with t lactic acid \n\n# . Decontamination \n\nManagement . Supportive care (eg, 100% oxygen, intraven ous fluids, vasopressors) \n\n# . Em piric treatment w ith hydroxocobalamin sodium thiosulfate* *S od ium nitr ite+ sodium thiosulfa te is an a lt ernate tr eatment but is contrai nd icated in carbon mo no xide poisoning . \n\nTrea tment overv iew fo r suspected cyanide poisoning \n\nDermal exposure Removal of clot hing Sk in decon tam ination Ingestion Ac tiv ated charcoal Dec ont ami nat ion All exp osures \n\n Antidote o Hydroxocobalamin preferred \n\no Sodium thi osu lphate a s a lt ernate t he rapy A ntid ote n ot ava ilab le o Ni tr ites to in duce meth emo globinemia Resp i ratory No mouth-to-mouth resuscitation Su ppl ementa l oxygen \n\nsupp ort A irw ay pro t ectio n (intubation) Cardiovascular Intr ave n ous flui ds fo r h ypotens ion \n\nsupp ort Pulmonary Diagnosis is confirmed by measuring \n\ncarboxyhemoglobin levels ( > 3% in non-smokers ; > \n\n10% in smokers )\n\n A standard pulse oxymetry is unreliable and may appear normal because it cannot differentiate carboxyhemoglobin from oxyhemoglobin What is the most likely diagnosis in a patient with headache for 2 months with a recent decline in his performance in school? He lives in the basement of his house. Labs show a Hb 19.6 .\n\nCerebral hypoxia secondary to carbon monoxide \n\nCO binds to Hb 240x stronger than O2 and prevents normal O2 delivery to cells, leading to a chronic hypoxic state --> stimulation of EPO production \n\n Carbon monoxide (CO) poisoning induced myocardial infarction \n\nchest pain, ECG changes , elevated troponin , and bilateral radiographic infiltrates no acute coronary occlusion \n\nHemoptysis \n\n61 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCarbon monoxide poisoning Carbon monoxide poisoning \n\n# . Smoke inhalation \n\nEpidemiology . Defec t ive heat ing systems \n\n# . Gas mot ors operating in poorly ventilated areas Mild-moderate \n\n# . Headache , confus ion \n\n# . Malaise , dizziness , nausea \n\nManifestations Severe \n\n# . Seizure , syncope, coma \n\n# . Myocardial ischemia , arrhythmias \n\n# . ABG : carboxyhemoglobin level \n\nDiagnosis ECG cardiac enzymes \n\n# . High-flow 100% oxygen \n\nTreatment . ln tubation/ hyperbaric oxyge n (severe) \n\nABG = arterial b lo od gas. \n\nInhalation injury Pathophysiology . Upp er airway thermal inju ry lower airway chemical injury \n\n# . Concomitant CO & cyanide poisoning common \n\nConcerning . Historical: smoke exposure in enclosed space \n\nfeatures . Physical: singed hair, facial bums, carbonaceous sputum, wheezing \n\nStrong indicators . Oropharyngeal blistering or edema \n\nof airway injury . Retractions, respiratory distress, hy poxia \n\n# . 100% oxygen to displace CO \n\nManagement . Stable patients with concerning features but no strong indicators: bedside fiberoptic laryngoscopy \n\n# . Unstable patients or patients with strong indicators: endotracheal intubation \n\nCO = carbon monoxide .Pulmonary What position should a patient with massive hemoptysis be placed? \n\n1. Put patient in dependent positioning (lateral position) (on side of bleeding) to avoid blood collection in the airways of the opposite lung. \n\n2. Secure airway 3. Stabilize 4. Stop bleeding ( bronchoscopy , embolization )\n\n## Head, Neck & Nose \n\n Adenoid hypertrophy is hyperplasia of the pharyngeal tonsils and is the most common cause of nasal obstruction in children. \n\nStridor \n\n62 https://t.me/usmleinnercircle \n\nPulmonary Cardiac Infectious Hematologic Vascular Systemic disease Other Causes of hemoptysis \n\n Bronchitis \n\n Lung cancer \n\n Bronchiectasis \n\n Mitral stenosis/acute pulmonary edema \n\n Tuberculosis \n\n Lung abscess \n\n Bacterial pneumonia \n\n Aspergillosis \n\n Coagulopathy \n\n Pulmonary embolism \n\n Arteriovenous malformation \n\n Granulomatosis with polyangiitis \n\n Goodpasture syndrome \n\n Trauma \n\n Cocaine use (inhalation) \n\n> History & physica l t o rule out ot her causes (eg, oropharynx, gastrointestinal) Mild/moderate Massive\n> (>600 ml /24 hr\n\nOR 100 ml/hr) \n\n> Chest\n\nx-ray, CBC, coagulation studies, renal function, urinal ysis ,rheuma to logic workup if suspected CT scan bronchoscopy (dependent on imaging result & if intervention is needed) Treat cause; persistent bleeding treated via bronchoscopic intervent ions, embolization, or resection \n\n> Bleeding Secure airway,\n> stops br ea thing\n\n& circu lation \n\n> Bleeding continues\n\nPulmonary Tracheal stenosis (ie, rigid narrowing) or tracheomalacia (ie, weakness and collapsibility) are complications of prolonged endotracheal intubation, and can cause dyspnea and noisy breathing. Tracheal stenosis is associated with prolonged (>2 weeks) mechanical ventilation , presents with slowly progressive (rather than episodic) dyspnea, and is potentially accompanied by expiratory stridor .\n\n Adolescent boy with VACTERL presenting with subacute cough accompanied by \n\nexpiratory stridor, forced vital capacity < slow vital capacity and a scooped-out flow-volume loop , all of which are associated with tracheal collapse Key idea: FORCED vital capacity (amount of air that can be FORCEfully expired) is almost always about equal to SLOW vital capacity (amount of air expired in passive breathe), with one exception being tracheal collapse because forceful expiration leads to obstruction > less air expired \n\n Vocal cord dysfunction (ie, paradoxical closure during inspiration) can present with intermittent dyspnea and noisy breathing (ie, inspiratory stridor ) triggered by exercise or psychosocial stress . It is more common in young women. Dx: Laryngoscopy showing vocal cord adduction during inspiration T/t: Acute episodes : sniff or pant , which activates the posterior cricoarytenoid to abduct the vocal cords, noninvasive positive-pressure ventilation Endotracheal intubation ideally should be avoided Long-term treatment: primarily consists of education and therapy with a speech-language pathologist. \n\n Velopharyngeal insufficiency (VPI) is a common sequela of cleft palate, with or without surgical repair. VPI is defined as an inability to properly close the velopharyngeal port separating the nasopharynx and oropharynx during the production of speech, which is frequently caused by a shortened palate or persistent palatal defects. VPI can lead to high-pitched , hypernasal , or whistling speech with reduced intelligibility .\n\nLaryngomalacia \n\n63 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCauses of stridor in infants & toddlers Acute \n\n# . Parainfluenza vi rus , most cases in fall /winter Croup lnspiratory or biphasic stridor, \"barky\" cough, infectio us symptoms .\n\n# . Choking episode \n\nForeign body aspiration lnspiratory stridor &/or wheeze , focally diminished breath sounds . Chronic \n\n## . \"Floppy\" supraglottis, prominent age 4-8 months \n\nLaryngomalacia lnspiratory stridor wo rsens when feeding, CcY ing, or su ~ine; improves when prone .. Great vessels encircle & compress trachea Vascular ring Biphasic stridor that improves with neck extension .\n\nAirway hemangioma . Hemangiomas enlarge in the first few weeks of life . Worsening biphasic stridor, concurrent skin hemangiomas (\"beard distribution\") Pulmonary Laryngomalacia is characterized by floppy supraglottic structures that collapse during inspiration due to laryngeal hypotonia (possibly from delayed maturation). However, it presents in infancy and typically resolves by age 18 months. \n\n What imaging test/study may be used to confirm the diagnosis of laryngomalacia ?\n\nFibrooptic laryngoscopy \n\nTorus Palatinus \n\n What is the most likely diagnosis for a hard , immobile mass on the hard palate of a young individual ?\n\nTorus palatinus (benign bony growth) \n\ncan increase in size throughout life; \n\nno medical or surgical therapy is required unless the growth becomes sympatomatic \n\n It can be congenital or develop later in life \n\nURI \n\n64 https://t.me/usmleinnercircle \n\nLaryngomalacia Pathophysiology . Collapse of supraglottic tissues on inspiration \n\nClinical . lnspiratory stridor that worsens when supine \n\npresentation . Peak at age 4-8 months \n\nDiagnosis . Laryngoscopy (eg , omega-shaped [OJ epiglottis) \n\n# . Reassurance with close follow-up ( concurrent GER \n\nManagement treatment) for most cases \n\n# . Supraglottoplasty for severe symptoms \n\n> GER\n\n= gastroesophageal reflux. Start of inspiration \n\n> Thoracic\n> cavityo\n> expands\n> Laryngomalacia Mid-inspiration\n\nPulmonary because the risk of rheumatic fever is high, negative results should be confirmed with throat culture in kids Penicillin allergy ? Macrolides ; or Clindamycin 65 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDistinguishing features of common upper respiratory illnesses Viral upper respiratory syndrome Influenza Streptococcal pharyngitis Onset of symptoms Slow, stepwise, migratory, or evolving Abrup t & often drama ti c Variable \n\nUpper respiratory Rhinorrhea, coryza , sneezing, mild Usually mild Predominantly pharyngeal symptoms \n\nsymptoms pharyngitis \n\nSystemic Usually mild Prominent with possible high feve r, Variable with possible fever &\n\nsymptoms myalgias , headache myalgias \n\nExamination Nasal edema with normal or slightly Pharyngeal erythema , tonsillar Variable but often unremarkable hypertrophy & exudate s, tender \n\nfindings erythematous pharynx cervical lymph nodes \n\nImportant respiratory tract infections in children Clinical illness Presentation Common etiologic agents \n\n## . Rhinovirus \n\nNasopharyngitis Nasal congestion & discharge, sneezing, . Influenza virus \n\n(common cold) cough & sore throat . Coronavirus \n\nLaryngotracheitis Upper respiratory tract symptoms . Pa rainfluenza \n\n(croup) followed by hoarseness, barking cough , virus strider & respiratory distress Sore throat, cervical lymphadenopathy, . Corynebacterium \n\nDiphtheria coal es cing pseudomembrane diphtheriae \n\nSore throat, dy sphagi a, drooling & . Haemophilus \n\nEpiglottitis respiratory distress influenzae \n\nUpper respiratory tract symptoms . Re spiratory \n\nBronchiolitis followed by whee zi ng, cough & respi ratory distress syncytial virus \n\nKey respiratory tract infections in children Diagnosis Classic pathogen Presentation Laryngotracheitis (croup) . Parainfluenza virus Age 6 months to 3 years Barking cough , strider, hoarseness \n\nEpiglottitis . Haemophi/us influenzae \n\nBronchiolitis . Respiratory syncytial virus \n\nEvaluation of acute pha ryngitis in children \n\nVira l symptoms present (eg , cough , conj un ctivitis, ora l ulce rs) \n\nViral pharyngitis \n\nYes Negat iv eNo Rapid streptococcal antigen testing Negative Positive Positive Throat cultu re ---- Streptococcal pharyngitis \n\n## .. Unvaccinated children \n\n## . Sore throat, dysphagia, drooling, tripod position \n\n Age <2 \n\n Wheezing, coughi ng \n\nEvaluation & management of pharyngitis Centor criteria \n\n Fever by history Tender anterior cervical lymphadenopathy Tonsillar exudates Absence of cough 0-1 present No testing/treatment for streptococcal infection 2-3 present )lRapid streptococca l antigen test 4 present ) \n\n# ~Empiric penicillin or amoxicillin \n\nI Supportive care Oral pen icillin or amoxicillin \n\nC UWood \n\nCuwld \n\nPenicillin or amoxicillin for positive results Pulmonary What is the next step in management for a child that presents with fever , pharyngitis with tonsillar exudates , and tender anterior cervical lymphadenopathy ?\n\nRapid streptococcal antigen testing \n\nGAS pharyngitis in children should always be confirmed by rapid streptococcal antigen testing or throat culture prior to initiation of antibiotics (versus adults, who can be treated empirically if they meet all Centor criteria) \n\nEpiglottitis \n\n66 https://t.me/usmleinnercircle \n\nInfectious epiglottitis \n\n# . Streptococcus pneumoniae, Haemophilus influenzae \n\nEpidemiology Risk reduced with H influenzae vaccination .. Rapidly progressive & life-threatening . Fever, sore throat, drooling, muffled voice \n\nClinical . Airway obstruction (stridor, dyspnea) . Pooled oropharynx secretions . Laryngotracheal tenderness . Direct visualization \n\nDiagnosis Imaging (lateral neck x-ray) .. Early artificial airway (if needed) \n\nTreatment . Intravenous antibiotics (ceftriaxone plus vancomycin ) \n\nEpiglottitis nfl amed and sw oll en eplg k> tlis ; most commonly caused by Haemophi/us influenzae C)UWo12 weeks ) What is the treatment of sinusitis ?\n\nSupportive (usually viral) \n\nAntibiotics indicated if ( Amoxicillin +/- Clavulanic acid )\n\n>10 days Fever >39, facial pain \"Double-worsening\" -- initially better then gets worse \n\nHard to distinguish viral vs bacterial sinusitis \n\nViral rhinosinusitis generally improves by days 7-10 \n\n Both endotracheal tubes and nasogastric tubes can cause acute sinusitis in critically ill patients as a result of impaired sinus drainage. Symptoms include fever, cough, headache, and purulent nasal drainage. Diagnosis is made with CT scan of the sinuses , which will show opacification of the sinuses, and culture of the sinus fluid . Management is with antibiotic therapy and removal of the obstruction , although operative sinus drainage may also be required. \n\nTracheitis Most common predisposing factor: Viral URI or sometimes \n\nallergic rhinitis \n\n70 https://t.me/usmleinnercircle \n\n\n\nAcute rhinosinusitis in children Acute bacterial rhinosinusitis \n\n## . Nasal congestion &/or purulent drainage . Cough, nasal discharge \n\n> Clinical features\n\n## . Facial pressure/pain Clinical features . Fever . Fever, cough, headache, loss of smell, ear pain . Face pain/headache \n\n## . Viral \n\n> 0No fever or early resolution of fever\n> 0Mild symptoms (eg, well-appearing, mild facial pain)\n> Diagnostic criteria\n\n## . Persistent symptoms :?:10 days without improvement \n\n> (1 of 3)\n\n## . Severe onset (fever ~39 C [102.2 F] + drainage) ~3 days Worsening symptoms following initial improvement \n\n> Etiology 0Improvement & resolution by day 5-1 o\n\n## . Bacterial \n\n> Treatment Amoxicillin clavulanate\n> 0Fever ~3 days OR\n> 0New/recurrent fever after initial improvement OR\n> 0Persistent symptoms ~1\n\nO days \n\n> Treatment\n\n## . Intranasal saline, saline irrigation, NSAIDs \n\n## . Antibiotics if bacterial \n\n> NSAIDs =nonsteroidal anti-inflammatory drugs .\n\n\n\n> 000\n\nPulmonary What is the organism is most likely in a patient that presents with fever and croup-like symptoms that do not resolve with racemic-epi ?\n\nS. aureus (tracheitis) \n\nWork-up requires? Endoscopy ( laryngoscopy or bronchoscopy ) with tracheal culture \n\nPath: S. aureus most common following viral prodrome Presentation? ~4 years Follows viral prodrome \n\nCroup that does not resolve Toxic (sick as shit) \n\nDiagnosis? \n\nEndoscopy ( laryngoscopy or bronchoscopy ) with Tracheal culture \n\nImaging: steeple sign (just like Croup so not sensitive/specific )No improvement with racemic epi ( i.e. it is not Croup )Treatment? \n\nMaintenance of airway IV Antibiotics \n\nLaryngeal Papillomatosis \n\n Vertical transmission of human papillomavirus subtypes 6 and 11 can cause recurrent respiratory \n\npapillomatosis , which results in hoarseness due to finger-shaped growths on the true vocal cords .T/t: Surgical Debridement \n\nRhinitis \n\n71 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\n\n\n\n\n\n\n\n\nNormal vocal cords Recurrent respiratory papillomat osis Pulmonary During peak allergy seasons, patients can experience systemic (eg, fever ) or neuropsychiatric (eg, \n\nfatigue , irritability ) symptoms. Patients with NAR typically lack the sneezing and allergic conjunctivitis (eg, itchy eyes, injected conjunctivae) that classically accompany allergic rhinitis. Be careful with decongestants (sympathomimmetics like phenylephrine) -- do not use for more than 3days as hey can produce rebound congestion (rhinitis medicamentosa) \n\nPhysical examination often shows beefy-red nasal mucosa as opposed to the edematous, pale mucosa often seen in allergic rhinitis. T/t: Cessation of medication ; Nasal Glucocorticoids \n\nSeptal Hematoma can also have thick , green nasal discharge Transverse nasal crease \n\n72 https://t.me/usmleinnercircle \n\nAllergic rhinitis \n\n# . Rhinorrhea, nasal congestion, sneezing, nasal itching \n\nSymptoms . Cough secondary to postnasal drip \n\n## . Ocular itching & tearing . \"Allergic shiners\" (infraorbital edema & darkening) . \"Allergic salute\" (transverse nasal crease) \n\nPhysical examination . Pale, bluish, enlarged turbinates . Pharyngeal cobblestoning \n\n## . \"Allergic facies\" (high-arched palate, open-mouth breathing) \n\nTreatment . Allergen avoidance \n\n## . Intranasal corticosteroids \n\nNonallergic rhinitis Allergic rhinitis \n\n# . Nasal congestion, rh inorrhea, sneezing, postnasal . Watery rh inorrhea, sneezing, eye symptoms drainage Earli er age of onset .. Later onset (age >20) common \n\nClinical . Identifiable allergen or seasonal pattern \n\n# . No obvious allergic trigger \n\nfeatures . Pale/bluish nasal mucosa \n\n# . Perennial symptoms (may worsen with season . Associated with other allergic disorders (eg, eczema, changes) asthma, eustachian tube dysfunction) \n\n# . Erythematous nasal mucosa \n\n# . Mild: intranasal antihistamine or glucocorticoids . Intranasal glucocorticoids \n\nTreatment . Moderate to severe: combination therapy . Antihistamines Pulmonary A septal hematoma presents after nasal trauma as fluctuant swelling of the nasal septum. It should be recognized and promptly drained to avoid complications of infection, septal perforation, and nasal deformities. If a patient develops a whistling noise during respiration following rhinoplasty, what is likely the diagnosis? \n\nNasal septal perforation \n\nlikely resulting from a septal hematoma (more common) or septal abscess (less common) \n\nNeck Masses \n\n73 https://t.me/usmleinnercircle USMLE Inner Circle \n\nThyroglossal duct cyst Der mo id cyst Branchial cleft cyst Reac tive adenopathy \n\nMycobacterium av ium \n\nlymphadenitis Cystic hygroma Septa l hematoma Soft fluctuan t _____ _\n\nswelling \n\n## .\n\nMidline ...\n\nMidline ...\n\nLateral \n\n## ..Lateral ..\n\nLateral ..\n\nPosterio r .\n\nPediatric neck mas ses Hematoma pre ven ts jdiffusio n of nut rients from pe richondrium to the septa! carti lage .T ract between fo ramen cecum & base of a nt e ri or neck Cystic, moves with swallowing or tongue p rot rusion Often eresen ts after uee er reseirato~ tract infec tio n\n\nCystic mass with trapped epithelial debris Occurs along embryologic fusion planes \n\nNo displacement with to ngue protrusio n\n\nTract may extend to the ton si llar Iossa (2nd branchial arch) or pyriform recess (3 rd branchial arch) \n\nAnterior to the sternocleidomastoid muscle \n\nFirm, often tender Multiple nodules Necrotic lymph node \n\nViolaceous discoloration of skin Fr equent fistula formation \n\nDilated lymphatic vessels Pulmonary Similar to a thyroglossal duct cyst (TDC) , which is also formed from incomplete involution of an embryologic remnant, a BCC is often detected when it becomes secondarily infected after an upper respiratory tract infection ( URI ), leading to erythema, tenderness, and sometimes drainage of fluid from a sinus tract. \n\n## Mediastinum \n\nMasses \n\n1) Anterior mediastinum: 4 T's \n\n-- Thymoma -- Thyroid neoplasm -- Teratoma -- Terrible lymphoma \n\n3) Posterior mediastinum \n\n-- Neurogenic tumors ( neurofibroma, schwannoma )-- Meningocele -- Enteric cyst \n\n74 https://t.me/usmleinnercircle \n\n> Branchial cleft cyst Thyroglossal duct cyst Cystic hygroma\n\nThyroglossal duct cyst Embryology . Forms along path of thyroid descent . Foramen cecum (base of tongue) to base of anterior neck \n\n# . Midline cystic neck mass . Moves superiorly with swallowing or tongue protrusion \n\nClinical presentation Often present after upper respiratory tract infection (secondary infection) .. Associated with ectopic thyroid tissue \n\n# . Confirm presence of normal thyroid tissue \n\nManagement Surgical resection of cyst, associated tract & central portion of hyoid bone .\n\n Pulmonary 2) Middle mediastinum \n\n-- Bronchogenic cyst -- Tracheal tumor -- Pericardial cyst -- Lymphoma -- Lymph node enlargement -- Aortic arch aneurysm -- Lymphoma -- Diaphragmatic hernia -- Esophageal tumor -- Aortic aneurysm A large thymic silhouette is a normal finding on frontal CXR in children < 3 years \n\nIn question stems, if you find this missing in a young person, consider things like DiGeorge or SCID !\n\n75 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nCUWorld \n\n\n\nMediastinal Compartments , Structures , & Masses Compartment Structures Anterior Thymus Lymph nodes Lymph nodes' Pe ricardi um Heart & great ves sels T rac hea & main bronchi Esophagus N eura l tissue Vertebrae Lymph nodes \n\nMasses \n\n Thymic ne oplasms (eg , thymoma } Lymphoma Germ cell tumors Teratomas Seminomas , nonseminomas \n\n Thyroid tissue {eg, ectopic , subs ternal goiter} Lymphadenopathy {eg, sarcoidosis, lung cancer} . lymphoma Ben i gn cyst ic masses ( eg , pericardia I cys t, bronchogenic cyst} Vascular masses Esophageal tumors Neurogen ic tumors (eg , schwannoma ,ne urofib roma} , meningocele Sp inal masses (eg , metastases} Lymphoma 'Lymph nodes , from which lymphoma may ar i se , are present in all 3 compartments .\n\n\"Some sources define the midd le & poste ri or compartments based on their relationship to the posterior pericardia! surface rather tha n the posterior thoracic wa ll .\n\nCUWorld \n\nNormal thymus in a neonate Pulmonary The thymus normally atrophies and is replaced by fat after puberty , when it has completed the production of T lymphocytes. Therefore, adults with mediastinal opacities on x-ray should undergo further work-up for a \n\npathologic cause (eg, lymphoma, germ cell tumor). \n\nAcute Mediastinitis \n\n What is the treatment for post-operative acute mediastinitis ?\n\ndrainage, debridement, and antibiotics \n\nsymptoms include fever , chest pain , leukocytosis , and mediastinal widening on CXR \n\n## Obstructive \n\n The presence of digital clubbing in patients with COPD should prompt a search for occult malignancy ( i.e. chest CT ).\n\nCOPD itself, with or without hypoxemia, does NOT cause clubbing \n\nAcute Bronchitis \n\n76 https://t.me/usmleinnercircle \n\nConditions commonly associated with digital clubbing Br onchogenic carcin oma lntrathoracic Me tastatic ca ncers neoplasms Ma lignant mesothelioma Lym phoma Lung abscess Empyema lntrathoracic Bronchiectas is suppurative d is eases Cys tic fi bros is C hron ic cavitary infections \n\n(eg, fungal, mycobacterial) \n\n> Idi opa thic pu lmonary fibrosis Lung disease Asbestosis\n> Pulmonary arteri o-ve nous ma lformations\n\nCardiovascular disease Cya n otic conge nital heart disease \n\nAsthma vs COPD Asthma COPD Late-stage COPD FVC Normal/! Normal/! !I!! \n\nFEV1 ! ! !! \n\nFEV1/FVC ! ! !! \n\nBronchodilator Partially reversible/ Usually Reversible response nonreversible nonreversible \n\nChest x-ray Normal Normal Hyperinflation, loss of lung markings \n\nDLCO Normal/t Normal/! !\n\nCOPD :;; chronic obstructive pulmonary disease; DLCO :;; diffusion capacity of the lung for carbon monoxide. Pulmonary Sputum production occurs in roughly half of patients; the typical yellow/purulent sputum is due to \n\nepithelial sloughing and is not a sign of bacterial infection. Small amounts of blood in the sputum can occur due to inflammation and epithelial damage D/D: Pneumonia which has systemic signs of inflammation \n\nCOPD \n\n Jugular venous distention may be observed on physical examination of acute COPD exacerbation during expiration due to increased intrathoracic pressure. -Phys. exam often shows wheezing, tachypnea, prolonged expiration, and use of accessory respiratory muscles \n\n-M/C Trigger : Upper respiratory infection (URI) \n\n When should intubation be considered in patients with COPD/Asthma exacerbation ?\n\nProfound acidemia (pH <7.1), poor mental status ( somnolence, lack of cooperation ), hemodynamic instability \n\nOtherwise, begin with initiation of noninvasive positive-pressure ventilation in patients with respiratory failure. Endotracheal intubation with mechanical ventilation is recommended for patients who fail a trial of NPPV .Systemic Glucocorticoids: IV or Oral ! NOT INHALED \n\n77 https://t.me/usmleinnercircle USMLE Inner Circle \n\nAcute bronchitis Etiology . Preceding respiratory illness (90% viral) \n\n## . Cough for >5 days to 3 weeks ( purulent sputum) \n\nClinical presentation . Absent systemic findings (eg, fever , chills) \n\n## . Wheezing or rhonchi, c hest wall tenderness \n\n## . Clinical diagnosis, CXR only when pneumonia suspected \n\nDiagnosis & treatment . Symptomatic treatment (eg, NSAIDs &/or bronchodilators) \n\n## . Antibiotics not recommended \n\nCXR;;; chest x-ray; NSAID s:;;; nonsteroidal anti-inflammatory drugs .\n\nAcute exacerbation of chronic obstructive pulmonary disease \n\n## . Infectious (70%): respiratory viruses (eg, rhinovirus) & commensal bacteria (eg, nontypable \n\nPrecipitants Haemophilus influenzae) \n\n# . Noninfectious (30% ): sterile inflammation (underl~ in 9 disease), pulmonary embolism, inhaled irritants \n\n# . Bronchial inflammation: systemic response (eg, fever, leukocytosis) usually absent \n\nPathophysiology & Cardinal symptoms: t dyspnea, t sputum volume, t sputum purulence .presentation t WOB (hyperinflation) & impaired gas exchange (hypoxemia [l V/Q], hypercapnia [tV 0 ]) .. Maximize expiratory flow: inhaled bronchodilators \n\n# . Reduce airway inflammation: systemic glucocorticoids \n\nManagement . Treat underlying triggers : antibiotics &/or antivirals (influenza, COVID-19) \n\n# . Maintain adequate oxygenation: SpO 2 target 88%-92% \n\n# . Maintain adequate ventilation: NIPPV or invasive mechanical ventilation *A ntibiotics generally indicated if: (1) increased sp utum p urulence+ loss of CO2 \n\nCOPD will have respiratory acidosis and widespread wheezing. \n\nPulmonary embolism is acute onset \n\n High CO2 and Respiratory Acidosis help differentiate from CHF exacerbation , which causes \n\nLow CO2 and Respiratory Alkalosis \n\n What CXR finding may be found on patient with COPD ?\n\nHyperinflation with flattening of diaphragm; >8 ribs counted = hyperinflation \n\nWhat physical exam finding does this produce? \n\nDistant heart sounds ( listen at subxiphoid process )\n\n Patients with an acute exacerbation of chronic obstructive pulmonary disease are at risk for \n\nSymptomatic Hypercapnia and should be promptly investigated with arterial blood gas analysis. \n\nClinical manifestations are predominantly neurologic and include headache and hypersomnolence \n\nwith mild to moderate hypercapnia ; higher levels of hypercapnia (eg, PaCO2 >75-80 mm Hg) can cause confusion , lethargy , and eventually coma (CO2 narcosis ) or seizures .\n\n Severe COPD is commonly accompanied by pulmonary cachexia , which is characterized by \n\nloss of lean muscle mass due to energy imbalance and systemic inflammation. \n\nTreatment \n\n78 https://t.me/usmleinnercircle \n\nChronic obstructive pulmonary disease \n\n> )\\)World Normal chest x-ray Chronic obstructive pulmonary disease\n\nPulmonary What are the ( 2) interventions to improve mortality and delay progression of disease in COPD? \n\n1. Smoking cessation 2. Long-term oxygen therapy ( PO2 <55 or O2 Sat <88 )\n\nIf O2 sat is fine, then O2 is not indicated \n\nSurvival benefits of home oxygen therapy are significant when it is used for 15 hours a day \n\nMTB says pneumococcal and influenza vaccines decrease mortality, UWorld says they just decrease the rate of COPD exacerbations. \n\n The primary long-term intervention for COPD is a daily long-acting anticholinergic inhaler. \n\ne.g. ipratropium, tiotropium; may be combined with a SABA for greater symptom relief \n\ninhaled steroids and LABA can be used for patients with more severe COPD (vs Oral/IV steroids for Acute exacerbation) \n\n79 https://t.me/usmleinnercircle USMLE Inner Circle \n\n0 2 use: \n\np0 2 <55/sat :S 88% \n\n with pulmonary HTN, high HCT, or cardlomyopathy: \n\np0 2 <6 0/sat s90% \n\nInhal ed antlchollnerglc agents are most e ff ec tiv ein COPD. \n\nTreatment Improves Mortality and Delays Progression of Disease \n\n Smoking cessation Oxygen therapy for those with p0 2 S:55 or sat ur ation S88%; mortality benefit is d irectly proportional to th e number of hours that the oxygen is used. Influenza and pneumococcal vaccinations \n\nDefinitely Improves Symptoms (But Does Not Decrease Disease Progression or Mortality) \n\n Short-acting beta agonists (e .g., albuterol) Anticholinergic agents: tiotropium, ipratropium Steroids Long-acting beta agonists (e.g., salmeterol) Pulmonary rehabilitation \n\n TIP \n\nAsthmatics not controlled with albuterol --+ inhaled steroid COPD not controlled with albuterol --+ anticholinergic (e.g., tiotroplum) \n\n--+ inhal ed steroid 1. Resting arterial oxygen tension (PaO 2) :SSS mm Hg or pulse oxygen saturation (SaO 2)\n\n:S88% on room air 2. PaO 2 ~59 mm Hg or SaO 2 ~89% in patients with cor pulmonale, evidence of right heart failure, or hematocrit >55% Pulmonary Asthma \n\n The diagnosis of asthma can be made in patients with normal or increased DLCO & a >12% increase in FEV1 following bronchodilator administration. \n\npatients with COPD typically have a decreased DLCO and < 12% increase in FEV1 after bronchodilators \n\n What is the likely diagnosis in an inmate who smokes and presents with rapidly worsening shortness of breath , tachycardia, tachypnea, and 87% O2 sat? He is poorly adherent to his asthma medications and began taking ibuprofen for shoulder pain the previous night. Urticarial rash is seen over the trunk and extremities. \n\nAnaphylaxis ( laryngeal edema )\n\n80 https://t.me/usmleinnercircle \n\nSelection of initial bronchodilator for stable COPD \n\nGroup E Exacerbations in prior year \n\n~1 requiri ng hospitalization \n\nLABA+ LAMA :I: 1cs OR \n\n~2 requiring outpatient systemic corticosteroids \n\n., C: \n\n~\n\n## 1wGroup ABronchodilator \n\n(eg, SAMA as needed) Group B\n\nNone requiring hospitalization \n\nLABA+ LAMA &\n\n<2 requiring outpatient systemic cortiocosteriods Low er -== ===---- .. Higher .. \n\nSymptoms 1cs recommended if penpheral blood eoslnophllla {> 300/mm 3) Is present but avoided If recurrent pneumonia is present Assess us ing validated onl/ument such as COPD Assessment Test (CAT ) or standard dyspnea scale \n\nHigher symptom severity = dyspnea causing slower walking or worse. COPD = chronic obstructive pulmonary disease; tCS = Inhaled corticosteroid, LABA = long.acting fl2 agoni st ;\n\nLAMA = long-acti ng muscarinic antago ro st. SAMA = short-acting muscarinic antagonis \n\nEvaluation of suspected asthma In te rmittent respiratory symptoms \n\n(cough, dyspnea, wheezing , chest tightness) Obstruction (FEV1/FVC <70% )Spirometry Normal Inhaled bronchodilator \n\n(SABA) \n\nMethacholine bronchoprovocat1on test \n\nReversible Nonreversible Negative Positive \n\nAsthma \n\nconfirmed \n\nAsthma \n\nunlikely \n\nAsthma possible \n\nSeek alternate diagnosis \n\n(eg . CHF, PH , VCD) \n\nReversible: A t least 12% and 200 ml increase FEV1 or FVC , with postbronchodilator FEV1/FVC rise to ~70% \n\nCHF = congestive heart failure : PH = pulmonary hypertension: COPD = chron ic obstructive pulmonary disease: SABA = short-acting beta agonist (albuterol): VCD = vocal cord dysfunction. OUWo11<1 Pulmonary Anaphylaxis may be confused with an asthma exacerbation if skin involvement is minimal or missed by the clinician. \n\nNSAIDs can worsen anaphylaxis \n\n Mechanisms by which GERD exacerbates Asthma \n\n1) Increased vagal tone 2) Heightened bronchial reactivity 3) Microaspiration of gastric contents into the upper airway \n\n-Patient with asthma has several clues in their history suggesting comorbid GERD, including sore throat , morning hoarseness , worsening cough only at night , and increased need for her albuterol inhaler following meals. \n\n-Proton-pump inhibitor (PPI) therapy has been shown to improve both asthma symptoms and peak expiratory flow rate in asthma patients with evidence of comorbid GERD \n\nStatus Asthmaticus \n\n A dditional bronchodilation with one-time infusion of IV magnesium sulfate may be added if no improvement appreciated after an hour. Upper Airway Obstruction (e.g. laryngeal edema): \n\nCharacterized by flattening of the top and bottom of the curve due to limited airflow during both inspiration and expiration Scooped out pattern in Asthma \n\n81 https://t.me/usmleinnercircle USMLE Inner Circle \n\nFlow (L /sec) 8 Flow (Lisee) Lu ng volume (L) Lung volume (L) UWorld \n\nFeatures of respiratory failure in acute asthma \n\n AbsenUminimal wheezing (poor air movement-> silent chest) \n\nClinical features Accessory muscle use Altered mental status ABG*: poor ventilation (i PaCO 2 & ! pH), poor oxygenation (! PaO 2 )\n\nLaboratory findings Lactate: transient j due to muscle WOB (type A) &/or J3-agonist-induced (type B) . K+ : transient ! due to J3-agonist &/or respiratory alkalosis Nebulized albuterol & ipratropium , IV corticosteroids IV magnesium \n\nManagement Short trial (<2 hr) of NIPPV Low threshold for intubation & invasive mechanical ventilation \n\n*Impending respiratory failure : it respiratory effort to maintain normal/borderline PaCO 2 & pH .\n\nABG = arterial blood gases; IV= intravenous; NIPPV = noninvasive positive pressure ventilati on ; WOB = work of breathi ng .Pulmonary What is the next step in management for a patient with severe asthma exacerbation with an elevated PaCO2 ?\n\nEndotracheal intubation \n\nPatients with asthma exacerbation often have tachypnea , which should lead to low CO2 --a normal or elevated PaCO2 suggests impending respiratory failure (inability to meet increased respiratory demands) \n\n Systemic glucocorticoids (eg, oral prednisone , dexamethasone) reduce late-phase inflammation in Status Asthamaticus. \n\nBecause the anti-inflammatory activity of glucocorticoids is delayed by several hours (due to the time required to change nuclear gene expression), they are often given with bronchodilators in the emergency department. (B agonsist + anticholi ) Corticosteroids are continued at home (eg, prednisone 40-60 mg daily for 5-7 days) to prevent relapse and decrease the need for hospitalization \n\nOccupational Asthma \n\n Diagnosis requires a detailed occupational history, careful symptom timeline, and 2-step confirmatory testing: First, asthma must be confirmed (eg, reversible obstruction on spirometry). For patients with normal baseline spirometry, bronchoprovocation (eg, methacholine) is performed to confirm bronchial hyperresponsiveness. Next, an occupational relationship is established by confirming workplace-specific worsening of airflow obstruction. This can be accomplished with serial peak expiratory flow rate (PEFR) measurements using a portable peak flow meter. \n\n82 https://t.me/usmleinnercircle \n\nFatal asthma: risk factors Patient history . Prior respiratory failure : N1PPV , intubation , ICU admission \n\n## . Poor asthma control: j inhaler use , frequent oral corticosteroids or acute care visits Clinical status (impending respiratory . Examination: respirations >30/min , Sa0 2 S90% , accessory muscle use, AMS , \"silent chest\" \n\n> failure)\n\n## . ABG : 1 or inappropriately normal PaCO 2 relative to WOB \n\n## . Peak flow: S50% of baseline ABG = arterial blood gas ; AMS = altered mental status ; ICU = intensi ve care unit ; NIPPV = nonin vasi ve positi ve pressure ventilation ; SaO 2 = arterial saturation of oxygen ; WOB = work of breathing .Occupational asthma Pathogenesis Workplace antigens ----, inflammation (lgE-dependent or independent) ----, bronchoconstriction \n\n& high-risk Classic antigens: animal proteins (eg, animal workers, seafood processors), grain \n\noccupations carbohydrates (eg, bakers), isocyanates (eg , painters), metals (eg , welders) Latency (months/years) due to gradual sensitization \n\n# . Initially, symptoms clearly exacerbated at workplace & relieved at home \n\nClinical Over time, symptoms persist throughout week & subside only after sustained work absence \n\nfeatures . Diagnosis: confirm asthma or BHR (eg, methacholine bronchoprovocation)----, confirm workplace-specific worsening of obstruction (eg, serial PEFR at home & work) Antigen avoidance (change of workplace if possible) or reduction (eg, respirator, shift rotation) \n\nManagement . Bronchodilators & inhaled corticosteroids \n\n# . Desensitization (immunotherapy) \n\n> BHR\n\n= bronchial hyperresponsiveness; PEFR = peak expiratory flow rate .\n\nPulmonary Patients record their PEFR at home and at work (along with their symptoms): a PEFR decline by 20% at the workplace relative to at home is consistent with occupational asthma. \n\nExercise Induced \n\n What is the first-line treatment for patients with exercise-induced bronchoconstriction who exercise daily? \n\nInhaled corticosteroids or anti-leukotriene agents 10-20 minutes before exercise \n\nuse short-acting -agonists if only needed a few times per week \n\nTreatment \n\n83 https://t.me/usmleinnercircle USMLE Inner Circle \n\nExercise-induced bronchoconstriction \n\n## . Hyperventilation ----, incomplete heating & humidification of inspired air----, cooler, dry air \n\nPathophysiology triggers mast cell degranulation & bronchospasm Can occur in isolation or in underlying asthma \n\n## . t Exercise tolerance; asthma symptoms appear within 5-10 min & improve* after 20 min of exercise \n\nClinical features Diagnosis: \n\n& diagnosis o Supportive: empiric response to preexercise bronchodilator o Confirmatory: bronchoprovocation testing (eg, spirometry before & after exercise) showing ~15% decline in FEV 1. Improve control of underlying asthma (ie, step-up therapy) \n\nManagement . Premedicate before exercise: ICS-formoterol (10 min prior) preferred over SABA , LTRA (2 hr prior) Daily ICS-beta agonist or LTRA may be needed for frequent, prolonged exercise Refractory period U preformed mast cell mediators & j inhibitory prostaglandins). \n\nICS = inhaled corticosteroid; LTRA = leukotriene receptor antagonist; SABA= short-acting beta agonist. \n\nAsthma severity for patients not on controller medication Asthma severity Symptom frequency/ Nighttime awakenings I nd icated therapy initiatio n SABA use lntenmittent S2 days a wee k S2 times a m on th Step 1 \n\nMild pers istent >2 da ys a week but no t da ily 3-4 ti mes a mo nt h Step 2 \n\nModerate persistent Da ily >1 ti me a week but not nightly Step 3 \n\nSevere persistent Throug hout the day 4-7 times a week Step 4 or 5 Pulmonary You cannot give LABA without an ICS/steroids. That will increase mortality and is always the wrong answer. If the patient is on a LABA, they must be on steroids . NEVER USE LABA FIRST OR ALONE. \n\n What is the likely cause of leukocytosis with neutrophilic predominance in a patient being treated for asthma exacerbation ?\n\nGlucocorticoid side effect \n\n The primary long-term intervention for persistent asthma is daily inhaled corticosteroids. \n\nversus a long-acting anticholinergic inhaler (COPD) \n\nBronchiectasis \n\n84 https://t.me/usmleinnercircle \n\nLocal Systemic* \n\nLess than daily \n\nSteps 1* & 2\n\nICS-formoterol PRN \n\nStep-up strategy for asthma treatment (adults) \n\nMost days Wa king with asthma \n\nStep 3 \n\nICS-formoterol daily \n\n(low-dose ICS) Daily symptoms Wa king with asthma Decreased FEV 1\n\nStep 4 \n\nICS-formoterol daily (medium- to high-dose ICS) \n\nReliever = IC S- formoterol PRN Still uncontrolled after Step 4\n\nFrequent need for OCS \n\nStep 5 \n\nICS-formoterol daily (high-dose ICS) \n\n+LAMA \n\nConsider biologic therapy: Anti-lgE or Anti-lL5/5R mAb \n\nAdjunctive controller therapies = LTRA , allergy i mmun o th erapy \n\nst ep 1: Alternatively, ICS + SABA may be used PRN ,ICS = inhaled corticosteroid: LAMA = k>ng -ac ting musearin ic antagonist LTRA = teukotriene receptor an tagon tSt: \n\nmAb monocolon al antibody; O CS oral corticosteroid; PRN as needed: SABA .. short-acting beta-2 agonisl. \n\nAdverse effects of inhaled corticosteroids \n\nCCIJWo1 wk) \n\n## Restrictive \n\nInterstitial Lung Disease \n\n Inspiratory \"Velcro\" (eg, fine, dry) crackles are sensitive for interstitial fibrosis, which is present in many forms of ILD Early into disease progression, interstitial lung abnormalities may not be seen on CXR . Therefore, patients with suspected ILD should undergo high-resolution computed tomography (HRCT), a thin-slice (usually 1 mm) CT scan protocol developed to visualize subtle interstitial lung features (eg, reticulation, honeycombing). \n\n In ILD , hypoxemia , especially with exertion, is more characteristically observed than \n\nhypercapnia . (vs COPD) \n\nHypersensitivity Pneumonitis \n\n86 https://t.me/usmleinnercircle \n\nAllergic bronchopulmonary aspergillosis Risk factors & . Structural airway disease (eg, asthma, cystic fibrosis) \n\npathogenesis . Fungal spore colonization --+ Th2-based sensitization --+ allergic inflammation \n\n# . Difficult-to-control asthma , thick sputum \n\n# . Chest imaging : fleeting infiltrates, bronchiectasis, bronchial mucoid impaction \n\nClinical features Aspergillus sensitization: & diagnosis 0 Elevated serum lgE (usually >1,000 IU / ml) \n\n> 0\n\nPositive Aspergillus skin test &/or lgE \n\n> 0\n\nSuggestive: eosinophilia, positive Aspergillus lgG \n\n# . Systemic glucocorticoids --+ t allergic inflammation \n\nTreatment . Antifungal drugs (eg , voriconazole) --+ t spore burden \n\n# . Treatment of underlying asthma (eg , bronchodilators) \n\nInterstitial lung disease \n\n# . Sarcoidosis, amyloidosis, alveolar proteinosis \n\n## . Vasculitis (eg, granulomatosis with polyangiitis) Common etiologies . Infection (eg, fungal , tuberculosis, viral pneumonia) \n\n# . Environmental exposure (eg, silicosis, HP) \n\n# . Connective tissue disease (eg, SLE, scleroderma) \n\n# . IPF , cryptogenic organizing pneumonia \n\n# . Progressive exertional dyspnea, dry cough Clinical presentation . >50% of patients have significant smoking history \n\n# . Fine inspiratory crackles digital clubbing \n\n# . Chest x-ray: reticulonodular interstitial opacities Diagnosis . HRCT: fibrosis, honeycombing, traction bronchiectasis \n\n# . PFT: restrictive pattern with J DLCO DLCO = diffusion capacity of the lung for carbon monoxide; HP = hypersensitivity pneumonitis ; HRCT = high resolution CT scan ; IPF = idiopathic pulmonary fibrosis ; PFT = pulmonary function testing; SLE = systemic lupus erythematosus. Pulmonary Acute symptoms recur and resolve within 1-2 days (vs other infectious causes like Pneumonia) \n\nSarcoidosis \n\nSarcoidosis key points: common in young, AA, females presents as SOBOE with occasional fine rales on exam; no wheezing can be associated with erythema nodosum and lymphadenopathy ; if present, the diagnosis is likely best initial test: CXR (hilar adenopathy seen in > 95% of cases) \n\n87 https://t.me/usmleinnercircle USMLE Inner Circle \n\nHypersensitivity pneumonitis \n\nEtiology . Immunologic response to inhaled antigen (eg, mold, animal protein) Acute \n\n## . Abrupt-onset fever, chills, cough, dyspnea, fatigue, leukocytosis \n\n## . Episodes often recurrent and self-resolving Clinical . Chest x- ray : scattered micronodular interstitial opacities presentation Chronic \n\n## . Progressive cough, dyspnea, fatigue , weight loss \n\n## . Hypoxemia that worsens with exertion \n\n## . Chest x-ray: diffuse reticular interstitial opacities \n\n## . PFT : restrictive pattern , J DLCO (chronic only) Diagnosis . BAL : high relative lymphocyte count \n\n## . Lung biopsy: lymphocytic infiltrate, poorly formed noncaseating granulomas, interstitial inflammation or fibrosis (chronic only) \n\nTreatment . Remove antigen exposure (resolves acute disease) \n\n## . Glucocorticoids and/or lung transplantation (chronic only) BAL = bronchoalveolar la vage; DLCO = diffusion capacity of the lung for carbon monoxide; PFT = pulmonary function testing. \n\nManifestations of sarcoidosis Sarcoidosis with mediastinal and hilar lymphadenopathy Hilar lymphadenopathy *\n\nPulmonary Interstitial infiltrates Papules , nodules & plaques \n\nCutaneous \n\n Erythema nodosum* \n\nOphthalmologic Anterior & posterior uveitis Keratoconjunctivitis sicca Facial nerve palsy \n\nNeurologic Central diabetes insipidus Hypogonadotropic hypogonadism \n\n AV block \n\nCardiovascular \n\n Dilated or restrictive cardiomyopathy Hepatosplenomegaly \n\nGastrointestinal Asymptomatic LFT abnormalities Hypercalcemia Peripheral lymphadenopathy \n\nOther Parotid gland swelling Polyarthritis* Constitutional symptoms (fever*, malaise) *Manifestations of Lofgren syndrome . \n\nAV =atrioventricular; LFT =liver function test. Pulmonary most accurate test: lymph node biopsy to look for noncaseating granulomas \n\ntreatment is prednisone ; if asymptomatic, do not treat \n\n Although lung involvement (eg, hilar lymphadenopathy) is common in sarcoidosis, it is often (>50%) asymptomatic , and patients may present with extrapulmonary disease. \n\n -osis : causes restrictive disease of some organ e.g: Sarcoidosis = restrictive lung disease, restrictive heart disease possible Patient with sarcoidosis who presents with RUQ pain \n\nLiver involvement (granulomas in liver) \n\nPulmonary Hypertension \n\n## Pneumonia \n\n88 https://t.me/usmleinnercircle \n\n\n\nManagement of pulmonary hypertension \n\n## . Evaluate for autoimmune CTD, toxins (eg , amphetamines), HIV, \n\nGroup 1 schistosomiasis, etc. PAH . Pulmonary vasodilator therapy, treat underlying (eg , autoimmune) cause \n\nGroup 2 . Echocardiography ( RHC if diagnosis unclear) Left-sided Optimize left ventricular function (eg, heart failure therapy), treat significant valve heart disease disease \n\nGroup 3 . Pulmonary function tests, chest imaging, polysomnography Lung disease &/or Treat underlying respiratory condition (eg, obstructive sleep apnea) chronic hypoxemia \n\nGroup 4 V/Q scan, pulmonary angiography CTEPH . Pulmonary thromboendarterectomy surgery (curative), anticoagulation \n\n## . Refer to accredited PH center \n\nGeneral . Maintain normoxia, euvolemia & sinus rhythm \n\nmeasures Contraceptive counseling, immunization, cardiac rehabilitation \n\n## . Refractory PH : bilateral lung transplant \n\nCTD =connective tissue disease (eg, scleroderma); CTEPH =chronic thromboembolic pulmonary hypertension; PAH =pulmonary arterial hypertension; PH =pulmonary hypertension; RHC =right-sided heart catheterization; V/Q =ventilation-perfusion. \n\n## . ! Cardiac output: exertional syncope/presyncope, fatigue , weakness \n\nSymptoms . i PA pressure : chest tightness , hemoptysis (rare) . RV demand ischemia: exertional angina/tightness \n\n## . Venous congestion: abdominal distension (bowel edema), early satiety \n\n## . Precordial heave due to RV hypertrophy \n\nSigns . Loud P2, right-sided S3 &/ or S4 \n\n## . Holosystolic murmur of tricuspid regurgitation \n\n## . JVD , ascites, peripheral edema, hepatomegaly Pulmonary According to the most recent guidelines published by the Infectious Diseases Society of America, pneumonia is classified as follows: Community-acquired develops in a nonhospitalized setting (M/C: S. Pneumoniae) \n\nHospital-acquired develops 48 hours after admission to the hospital \n\nVentilator-acquired develops 48 hours after endotracheal intubation \n\n Patients with HIV are at increased risk for community-acquired pneumonia (CAP) \n\n \"Rusty sputum\" is classic for pneumococcal pneumonia but may not always be present. Can present with Clear Sputum (Only select if there are no viral options in question) \n\n Immunocompromised Patients with CAP may have no alveolar infiltrate on initial chest x-ray d/t less cytokine response. DO a CT scan if CAP in suspected in such patients and X-ray is Normal. \n\n89 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nEtiology .\n\n## .Clinical .features .\n\n## .Treatment \n\nFev er + Cough + Sput um Bronc hitis Amoxici ll in Cephalosporin Fl uoroQuin \n\nTvpica/ Sxs \n\nStrep Pneumo \n\n3\"' Gen Cephalo ( if C AP )\n\nVancomycin \n\n(i fllAP )\n\nAt yp ic al Sxs \n\nSomething El se Macrolid es ( if C AP ) No Zosyn (i f HAP )l&D \n\nC li nda Ye sPCP Risk Bronchoalvcol ar Lavage \n\nBac trim \n\nSteroids \n\nCommunity-acquired pneumonia in school-aged children Lobar Bilateral \n\n# . Mycop/asma pneumoniae Streptococcus pneumoniae . Chlamydia pneumoniae \n\n# . Viruses (rare) Abrupt onset of fever, cough, chest pain . Fever, malaise, headache, sore throat \n\n# . Prolonged, gradually worsening cough Increased work of breathing . Patient can often continue normal activities \n\nFocal crackles . Bilateral crackles, wheezing Oral amoxicillin (outpatient) or intravenous ampicillin Macrolide (eg, azithromycin) .or ceftriaxone (if hospitalized) Pulmonary What imaging modality is typically used to diagnose pneumonia ?\n\nChest X-ray \n\ndiagnosis requires presence of lobar , interstitial , or cavitary infiltrate on imaging; CXR should be ** acquired before administering empiric antibiotics** \n\nWhat test/imaging study should be ordered first to evaluate an older patient with a 30 pack-year smoking history and recurrent episodes of pneumonia in the same anatomic location ?\n\nCT scan of chest \n\nin patients > 50 with significant smoking history (> 30 pack-years), it is essential to evaluate for lung malignancy; CT scan has better sensitivity than CXR \n\n Recurrent pneumonia in the same anatomic location is a red flag for lung cancer . What is the pathophysiologic mechanism underlying worsening hypoxemia when a patient with lobar pneumonia lies on the affected side ?\n\nIncreased intrapulmonary shunting \n\nlying on the affected side increases blood flow (Q) to this area due to gravity, where ventilation (V) is poor due to pneumonia, thus worsening the V/Q ratio \n\n90 https://t.me/usmleinnercircle \n\n> Same lung lobe* Different lung lobes\n\nCommon causes of recurrent pneumonia Bronchial obstruction \n\n> Extrinsic: neoplasm, adenopathy Intrinsic: bronchiectasis, foreign body\n> Recurrent aspiration\n> Altered consciousness: seizure, sedatives, antipsychotics, alcohol, illicit drugs Dysphagia: neurologic disorder, esophageal motility issue Poor dental hygiene Gastroesophageal reflux Immunodeficiency: HIV, leukemia, CVID Sinopulmonary disease: cystic fibrosis, immotile cilia Noninfectious: vasculitis, BOOP *Recurrent aspiration can lead to pneumonia in different dependent regions of the lung depending on the position of the patient during the aspiration event.\n> BOOP =bronchiolitis obliterans with organizing pneumonia; CVID =common variable immunodeficiency.\n\nPulmonary What is the likely diagnosis in a patient with pneumonia that presents with continued symptoms despite adequate antibiotic coverage and loculation on CXR ?\n\nComplicated parapneumonic effusion \n\nDo chest X-ray to Dx; requires drainage in addition to antibiotics \n\n Pneumonia unresponsive to treatment despite adequate Antibiotic coverage; evaluate for complications like Effusion , Abscess \n\n Both conditions can cause fever , leukocytosis , hypoxemia , and bilateral lung crackles. \n\nVAP \n\n91 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nEffects of positioning in a patient with pneumonia \n\nPneumonia down \n\nt perfusion of poorly ventilated region \n\nl\n\nt V/Q mismatch & \n\nworsened hypoxemia \n\nPneumonia up \n\n! perfusion of poorly ventilated region \n\nl\n\n! V/Q mismatch &\n\nimproved hypoxemia Characteristics of high-altitude pulmonary edema versus multifocal pneumonia High-altitude pulmonary edema Multifocal pneumonia \n\nRecent arrival at high altitude (<1 week) Persistent stay at high altitude Absent or mild leukocytosis . Leukocytes >15,000 mm 3 with bands Procalcitonin normal Procalcitonin elevated Marked early improvement with 0 2 Minimal early improvement with 0 2Pulmonary Ventilator-associated pneumonia is a type of hospital-acquired pneumonia that develops after more than 48 hours of mechanical ventilation ( intubation ). \n\nPresentation ? Pulmonary infiltrates with one or more of the following: \n\nfever, purulent secretions, leukocytosis, difficulty with ventilation \n\nAspiration Pneumonia \n\n92 https://t.me/usmleinnercircle \n\nEvaluation of suspected ve nt il ator-assoc iated pneumonia Suspected V AP \n\n Abnormal chest x-ray Lower respiratory tr act endotracheal tube sample Cu lture Microscopy \n\nEmpiric antibiotics \n\n Gram-positive coverage Positive cultures w ith clinical improvement Negative cultures \n\nDiscontinue an tibio tics &evaluate f or other causes Antipseudomonal & gram-negative coverage Cons ider MRSA coverage Narrow antibiotics accord ing to cu lture results \n\nPositive cultures wit hout clini cal improvement Like ly VAP Consider chang in g an tibiotics Assess for VA P complications (eg , abscess , empyema ) Consi der evaluat in g for ot her causes MRSA met tJc:1ffin- empinccowrage depends on drug-resistance pattern at insbtu1ion,\n\nMajor risk factors for ventilator-associated pneumonia \n\n## . Acid suppression (eg , PPI , H2R block er , antacid) \n\n## . Supine position \n\n## . Pooled subglottic secretions \n\n## . Paralysis & excessive sedation \n\n## . Excessive patient movement while intubated \n\n# . Frequent ventilat or circuit changes \n\nH2R = hista min e-2 receptor; PPI = pro ton p ump inhi bi tor. \n\nCl UWor1d \n\nPredisposing cond itions for aspiration pneumonia Conditions associated with aspiration pneumonia \n\n Altered consc i ousness impairing cough reflex/glottic closure (eg , dement ia , drug intoxicatio n ) Dysphagia due to neuro l og ic deficits (eg , stroke ,neurodegenerative disease) Upper gastrointestinal tract d i sor d ers (eg , G ER D ) Mechanica l compromise of aspiration defenses (eg , nasogas t ric & endotrachea l tubes) Protracted vom iting Large-volume tube feed ings in recumbent positio n\n\nTrigger Reduced consciousness Dysphagia Pharyngeal or glottal dysfunction Dental issues Related conditions \n\n Sedatives or antipsychotics Illicit drugs or alcohol Anesthesia Generalized seizure Neurologic disorders Esophageal motility defects Protracted vomiting Gastroesophageal reflux Tracheostomy Intubation Nasogastric feeding Gingivitis Poor dental hygiene Pulmonary Most patients have foul-smelling sputum and symptoms that progress over 1-2 weeks \n\n Aspiration pneumonia prophylaxis can include oral care, diet modification for patients with dysphagia, and elevating the head of the bed to 30-45 degrees. \n\n Also can benefit from Thickened Liquids. \n\nNormal swallowing involves a complex sequence of voluntary and reflexive processes that move food from the mouth to the esophagus while preventing it from entering the airway (ie, aspiration). Three main airway-protective movements occur during normal swallowing: \n\nDisplacement of the larynx superiorly and anteriorly under the base of tongue, which allows food to be directed into the more posteriorly located esophagus \n\nTilting of the epiglottis to block the airway Closing of the glottis by adduction of the vocal folds \n\nBecause of the complexity of swallowing, patients who sustain strokes often have persistent dysphagia and/or aspiration . If a neurologic deficit cannot be corrected, behavioral modifications can sometimes improve the safety of swallowing. A chin-tuck maneuver (ie, flexion of the head and neck during swallowing) sometimes helps. The maneuver seems to decrease the distance from the hyoid bone to the \n\n93 https://t.me/usmleinnercircle USMLE Inner Circle \n\nBacterial aspiration pneumonia \n\n# . Orop haryngeal/gast ri c mi crobes asp ira ted int o l ungs --+ host defenses overwhelmed due to \n\nPathophysiology l arge inoculum si ze \n\n# . Reduced co nsciousness (eg, anesthesia) \n\n# . Dysphagia (eg, neuromuscular disorder) \n\nMajor risk factors . Im paired glottic closu re (eg, intubation) \n\n# . Protracted vomiting \n\n# . Poor dental hygiene \n\n# . Fe ve r & cough foul-smelling sputum \n\nClinical features . Infiltrate in dependent portions of lu ng \n\n# . Aerob ic + anaerobic pathogens on sputum studies \n\n# . No empyema or lung abscess: treat for community-acquired pneumonia \n\nManagement . E mpyema or l ung abscess present: ex t end coverage to inc lude anaerobes (eg, ampicillin-sulbactam) \n\nStrategies to prevent aspiration pneumonia in hospitalized patients Recommended Not recommended \n\n# . Elevation of head of bed to 30-45 degrees . Prokjnejjc agent s\n\n# . Enteral feeding Gastrostomy tube or naso g astric tube \n\n# . Speech & swallow evaluation . Gastric volume measu r ement \n\n# . Dra inage of subglottal secretions . Probiotic medications \n\n# . D econtamination of oro 11 ha !) nx/di gestive tract* \n\n*In intubated patients. \n\n\n\nPulmonary larynx ( simulating elevation of the larynx ), as well as to narrow the distance of the laryngeal entrance, leading to decreased aspiration. \n\nTreatment \n\nHAP: Vancomycin + Piperacillin -Tazobactam \n\n Fluoroquinolones (eg, levofloxacin, moxifloxacin) that target respiratory tract organisms can also be used for CAP in the inpatient setting, this class of medication is generally avoided (when possible) in elderly patients due to increased risk of Clostridium difficile infection , tendon rupture , and aortic dissection. \n\n Empiric treatment of pneumonia in a young child with cystic fibrosis should include coverage against methicillin-resistant S. aureus .\n\ne.g. IV vancomycin M/C Cause: S. Pneumoniae \n\n94 https://t.me/usmleinnercircle \n\nEmpiric treatment of CAP \n\n Macrolide or doxycycline (health y) \n\nOutpatient Fluoroquinolone or beta-lactam + macrolide (co morbidities) \n\nInpatient Fluoroquinolon e (I V} \n\n(non-ICU) Beta-l actam + macrolide (I V} \n\nInpatient Beta-lactam + macrol ide (I V} \n\n(ICU) Beta-l ac tam + fluor oq uinolone (I V) \n\n> *Respiratory fluoroquinolones\n\n(eg, levofloxacin, moxifloxacin) are required. CAP = commu nity -acquired pneumonia; ICU = in tP.n sive care unit; IV = intravenous. \n\nOutpatient treatment of community-acquired pneumonia \n\nCan tolerate penicillins I\n\nNo \n\n## l\n\n Amox icillin or amoxicillin-clavulanate \n\n- Yes- PLUS Macrolide (preferred) or doxycycline Can tolerate cephalosporins - Yes -\n\n Third generation cephalosponn PLUS Macrolide (preferred) or doxycycline \n\nNo \n\n Respiratory fluoroqu,nolone \n\n use amoXJcilh n-davulanate when nsk factors for severe disease are presen t (eg ,\n\nsmokmg , age >65. recent an tibiotics, major c:omorbiditles . alcohol use disorder). CUWorld \n\nCURB-65 to determine hospitalization \n\n1 point for eaeh of the following Confusion Urea >20 mg /dl Respirations .e30/min B lood pressure \n\n(Systolic blood pressure <90 mm Hg or diastolic <60 mm Hg ) Age .e 65 \n\n# TL ow mortality Outpatient treatment \n\n# TIntermediate morta li ty likely inpati ent treatment \n\n# THigh mortali ty Urgent inpatient adm i ss ion; possi bly ICU if score >4 Pulmonary Pleural Effusion \n\n Positive gram stain & culture helps distinguish empyema from complicated pleural effusion ; both are managed with antibiotics and drainage \n\n An uncomplicated parapneumonic effusion forms when lung interstitial fluid increases during pneumonia and moves across the adjacent visceral pleural membrane. The pleural fluid is characterized by \"exudative\" chemistries and an influx of neutrophils into the pleural space. \n\n A complicated parapneumonic effusion develops when there is bacterial invasion of the pleural space. Bacterial invasion typically leads to an increased number of neutrophils and the development of pleural fluid acidosis , which results from anaerobic utilisation of glucose by the neutrophils and bacteria. In addition, lysis of neutrophils increases the LDH concentration in the pleural fluid to values often in excess of 1000 IU/L. \n\n Normal pleural fluid pH is 7.60 ;\n\n95 https://t.me/usmleinnercircle USMLE Inner Circle \n\nRates of bacterial colonization in cystic fibrosis based on age \n\nEtiology \n\nPleural fluid analysis Pleural fluid Gram stain & culture Treatment \n\nouw\"\"\" \n\nParapneumonic effusions Uncomplicated Ster il e exudate in pleural space \n\n pH >7.2 \n\n Glucose >60 mg/dl WBC <50,000/mm 3\n\n<2 10 15 Complicated \n\n20 \n\nAge ( year s) Bacterial in vasion of pleural space \n\n pH <7.2 \n\n Glucose <60 mg/dl W BC >50,000/mm 3*Gram stain & culture is typically a false negative due to low bacterial count. Both are typically positive in empyema. \n\nWBC = white blood cells. Parameter Uncomplicated parapneumonic effusion Inflammatory fluid from pneumonia --+ \n\nEtiology pl eural space \n\nPleural fluid analysis pH = 7 .20, )/ normal glucose, LDH ratio >0.6 \n\nPleural fluid Gram stain &\n\nculture Negative LOH = lactate de hy drogen ase .25 30 35 40 >45 \n\nManagement of Parapneumonic Effusions No respiratory distress or hypoxia Respiratory dis tr ess \n\nOR \n\nHypoxia Oral antib io ti cs Close monitoring \n\nll) lJWorld \n\nComplicated parapneumonic effusion Bacterial invasion into ple ural fluid \n\nEmpyema \n\nUltra so und IV antibio ti cs Drainage Bacterial colonization --+ \n\npurulent fluid pH <7.20, j glucose, LDH ratio pH <7.20, j glucose, LDH ratio >0.6 >0.6 Can be positive or negative Positive Pulmonary -Exudative effusions typically have lower pH (7.30 - 7.45) \n\n-Transudative effusions typically have higher pH (7.40 - 7.55) \n\n What is the next step in management for a smoker with progressive dyspnea , weight loss , and evidence of pleural effusion on CXR ?\n\nDiagnostic thoracentesis \n\nundiagnosed pleural effusion is best evaluated with thoracentesis to determine if the fluid is transudative or exudative; \n\n exception : in patients with evidence of CHF (e.g. weight gain, pedal edema, bibasilar crackles), the first step is a trial of diuretics. Can quickly determine CHF by BNP level (>500 = CHF) \n\n What are the etiologies for pleural effusion with high lymphocytic count (>50%)? \n\nCancer, Tuberculosis, Fungus \n\n High lymphocyte count with high ADA ? Tuberculosis \n\n96 https://t.me/usmleinnercircle \n\nLight 's criteria Phy s ica l appearance \n\nSpeci fic grav ity \n\nGlucose l;I \n\nCholesterol Total prote in \n\nPleural flu id protein : serum prote in rat io Transudate Does not froth or lorn, clots \n\n,: 1.016 \n\n~ 60mg/dL \n\n<60mg/dL \n\n,: 30g/l \n\ns 0.5 \n\nPleural fluid LOH : serum LOH s 0.6 \n\nratio \n\nPleural fluid LOH (lactate \n\ndehydrogenase) \n\n< ~ the upper lim it of normal \n\nserum LOH Pl eu ral flu id with a bloody appearance suggests a mali9\"ant etiology! \n\nExudate \n\nStraw--colored fluid (may rarety be hemorrhagic), wh ic h fro th s on shak ng and forms clots oo standing still \n\n> >\n\n1. 016 \n\n 3~9 mg/d L: suggests ma lignant effusion, tuberculous pleurisy, empyemo, pneumo ni a, esophageal \n\nrupture, or lupus pleuritis - \n\n < 3o fflg1d l: suggests rheumatoid pleuri sy or empyema \n\n> ~\n\n60 mg/dL (strongly elevated in chylothor ax )\n\n> 30gll \n\n> 0.5 \n\n> 0.6 l;J \n\nPleural fluid LOH > ; the uppe, lim~ of normal serum LO H 1;J \n\nExudative effusions \n\n## . Pleural protein/serum protein ratio >0.5 Pleural fluid analysis . Pleural LOH/serum LDH >0.6 \n\n## . Pleural LDH > 213 upper limit of normal for serum LDH \n\n## . Empyema (purulent fluid , neutrophil-predominant, + gram stain/culture) Etiologies . Chylothorax (milky white fluid , j triglycerides) \n\n## . Malignancy (abnormal cytology) \n\n Tuberculosis(+ acid-fast bacterium stain/culture) LOH = lactate dehydrogenase. Pulmonary A pancreaticopleural fistula (between the pancreatic duct and the pleural space) resulting in an \n\namylase-rich exudative pleural effusion occurs most commonly as a result of acute or chronic \n\npancreatitis .Management includes bowel rest to promote fistula closure ; endoscopic retrograde cholangiopancreatography with sphinceterotomy may be required to drain pancreatic fluid through ampulla of vater rather than fistula. D/D: Boerhaave Syndrome ; pleural fluid ph is very low (<6) \n\nLung Abscess \n\nLung Abscess key points: abscesses don't just form out of nowhere; these patients typically have an aspiration risk \n\nempiric treatment with Ampicillin-sulbactum is recommended (again, due to the aspiration risk; most lung abscesses involve anaerobes) aspiration risk is typically secondary to seizure, alcoholism, MS or stroke give proper treatment once culture and sensitivity return. Ceftrixone + Vancomycin/ Clindamycin \n\n97 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPediatric empyema \n\n## . Bacterial in vas ion of pl eural space Etiology resulting in fibrinopurulent co nso lidation Common organisms . Streptococcus pneumoniae \n\n## . Staphylococcus aureus (eg, MRSA) \n\n## . Pneumonia symptoms \n\n(eg, fever, dyspnea, pl eur itic chest pain) \n\n## . No improvement wi th Clinical features routine pneumonia treat ment \n\n# . Signs of pleural effusion (eg, dullness to percussion) \n\n## . Laboratory eviden ce of i nflammation \n\n(eg, leukocytosis, thrombocytosis) \n\n## . Supportive care Management . Empiric antibiotics + drainage \n\n(ie, chest tube or su rg ical) .lntrapleural fibrinolyti cs may aid drainage MRSA = methici llin -res ista nt Staphylococcus aure us .\n\nLung abscess \n\n Aspiration of oropharyngeal/gingival anaerobes \n\nPathophysiology . Risk factors: dysphagia, substance abuse, seiz ur es \n\n# . Pneumonitis -, pneumonia -, abscess/empyema Subacute fever, night sweats, weight loss \n\nManifestations . Cough with putrid sputum Cavitary infiltrates with air-fluid levels \n\nDiagnosis Cultures rarely useful .. Ampicillin-sulbactam, imipenem, meropenem \n\nTreatment . Alternate: clindamycin Pulmonary Pneumothorax \n\n98 https://t.me/usmleinnercircle \n\nAir f uid ievel \n\nsuggests abscess \n\nAssociated featu res Signs &\n\nsymptoms Imaging Management Lung abscess Pneumothorax Spontaneous pneumothorax \n\n Primary: No preceding event or lung disease; thin, young men Secondary: Underlying lung disease (eg, COPD) Chest pain , dyspnea . ! Breath sounds, jchest movement lpsilateral hyperresonance to percussion Absent lung markings Visceral pleural line Small (:Q cm): Observation & oxygen Large & stable: Needle aspiration or chest lube COPD = chronic obstruc ti ve pulmonary disease. \n\nTension pneumothorax \n\n Life-threatening \n\n Often due to trauma or mechanical ventilation Same as spontaneous with: Hemodynamic instability \n\n Tracheal deviation away from affected side Same as spontaneous with: \n\nseparating \n\nand lower I\n\n Contralaleral mediastinal shift \n\n lpsilateral hemidiaphragm flattening Urgent needle decompression or chest tube placement Pulmonary What is the likely diagnosis in a patient on a ventilator who develops hypotension , tachycardia ,and unilateral absence of breath sounds ?\n\nPneumothorax \n\n What is the diagnosis in Premature infant with unilateral absence of breath sounds, heart sounds on right, increased transillumination on left side of the chest? Tension Pneumothorax on left side Illumination test can be used in infants to diagnose it quickly, or Chest X-ray can be used if not sure. Pneumothorax on left pushed the heart to the right Urgently Needle Decompression \n\nneeded \n\n Meconium aspiration syndrome (most common in post-mature neonates ) is associated with \n\npneumothorax because meconium plugging of airways traps distal gas, promoting alveolar overdistension and rupture. \n\n Key idea: Intubation is CONTRAINDICATED in a patient with a pneumothorax \n\nPut a tube or needle first \n\nSpontaneous Pneumomediastinum \n\n99 https://t.me/usmleinnercircle USMLE Inner Circle \n\nLeft pneumothorax Spontaneous pneumomediastinum \n\n Asthma exacerbation \n\nRisk factors . Respiratory infection \n\n Tall, thin, adolescent boy \n\n Acute chest pain, shortness of breath, cough \n\nClinical features . Subcutaneous emphysema \n\n# . Hamman sign (crunching sound over heart) \n\nDiagnosis . Mediastinal gas on chest x-ray \n\n# . Rest, analgesics \n\nTreatment Avoid Valsalva maneuvers Pulmonary Pulmonary Embolism \n\n If there is no contraindication to anticoagulation, it should precede diagnostic imaging in patients with likely PE, especially when in moderate distress \n\n PE inhospital mortality Risk Factor: AGE & Obstructive Shock \n\n What is the test of choice to diagnose pulmonary embolism in clinically stable patients with a high likelihood of PE (modified Wells > 4)? \n\nCT angiography \n\n100 https://t.me/usmleinnercircle \n\nPneumomediastinum & pneumopericardium Approach to patient with suspected pulmonary embolism \n\nStabilize patient wi th oxygen & IV fluids Evaluate for absolute contraindications to anticoagulation Yes No Obtain diagnostic test to evaluate for PE Assess clinical suspicion of PE with modified Wells criteria Negative for PE PE unlikely Consider IVCfilter No further Consider anticoagulation, especially if patient has: IV = intravenous; IVC = inferior vena cava ; PE ;;; pulmonary embolism . \n\n> CD UWorkt\n\n No relative contraindications Moderate to severe distress I Positive for PE I\n\ni\n\nStart or continue anticoagulation; consider surgery or thrombolytics if indicated Negative for PE Stop anticoagulation \n\nDiagnostic strategy in suspected pulmonary embolism \n\nClinical assessmen t for pulmonary embolism Modified Wells criteria PE unlikely } PE likely t\n\nD-dimer assay ) j\n\nssoo ng / ml ) > 500 ng/ml J------. CT pulmonary angiography ] \n\nI\n\nt\n\nPE excluded ) \n\n, PE excluded ] PE confirmed ) \n\n> PE\n\n= pulmonary embolism . eUV\\lolld Pulmonary in patients with low likelihood of PE (modified Wells < 4), D-dimer testing can help rule out PE due to high negative predictive value \n\n A patient is thought to have a pulmonary embolism but cannot tolerate IV contrast due to severe renal disease . What other diagnostic test can be ordered to help in the workup? \n\nV/Q scan \n\nAlso done in Pregnant patients to avoid fetal radiation >4 = likely = immediate anticoagulation -> CT Angiography \n\n<4 = D- dimer > 500 --> CT Angiography only if +ve, reassurance if -ve \n\n What is the likely diagnosis in a post-operative patient with hypotension , JVD , and new-onset right bundle branch block ?\n\nMassive pulmonary embolism \n\n-massive PE is defined as PE complicated by hypotension and/or acute right heart strain (e.g. JVD, RBBB) \n\n Acute pulmonary embolism (PE) may present with syncope due to right ventricular dysfunction , cardiac arrhythmia, or vasovagal response to PE. Can also present with mild atelactesis and bloody pleural effusion. \n\n It may be difficult to differentiate PE from RV myocardial infarction [MI], which can also cause RV dysfunction; however, RVMI is less likely to cause dyspnea or syncope and more likely to cause bradycardia or arrhythmias). Patients with acute massive PE can present with syncope and hemodynamic collapse \n\n101 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPathophysiology of submassive/massive pulmonary embolism \n\nMassive PE RV outflow obstruction 1--------~ \n\nt RV pressure \n\n! RV cardi ac output &septal deviation to wa rd LV t RV wall tension +RV myocardial \n\n02 demand \n\n! LV preload &cardiac output \n\n! Coronary perfusion &\n\n! RV myocardial supply \n\nModified Wells criteria for pretest probability of pulmonary embolism \n\n Clinical signs of DVT \n\n+3 points Alternate diagnos is l ess likely than PE \n\n Previous PE or DVT \n\n+1.5 points Heart rate > 100 Re cent surgery or i mmob ilizati on \n\n+1 point Hemoptysis Cancer S4 = PE unlikely \n\nTotal score >4 = PE li ke ly \n\nDVT = deep vein thrombosis; PE = pulmona ry embolism. Pulmonary Chest CT scan showing a wedge-shaped infarction (red arrows) is virtually pathognomonic for PE ( Hamptons Hump )102 https://t.me/usmleinnercircle \n\nHampton hump (from pulmonary embolism) lpsilateral pleural effusion -----+ \n\nFleischner sign of pulmonary embolism Pulmonary Sometimes, chest x-ray shows nonspecific findings that may be associated with PE (eg, \n\natelectasis , pleural effusion )\n\n Patients with PE commonly develop small pleural effusions due to hemorrhage or inflammation. The effusions tend to be exudative and grossly bloody , and they can be associated with pain due to pleural irritation. Leukocytosis and/or peripheral neutrophilia may be seen, as with any acute inflammatory process. What ECG findings are classically associated with pulmonary embolism ?\n\n\"S1Q3T3\" \n\nOr right heart strain - ST depression and T wave inversion in the right leads (aVR, II, V5 and V6). This is rarely seen (sinus tachy is the most common!) \"S1-Q3-T3\" prominent S in lead I \n\nQ wave in lead III \n\nT-wave inversion in lead III indicative of R heart strain \n\n Common Symptoms: Acute-onset dyspnea , Pleuritic chest pain, Atrial fibrillation ( due to atrial dilation ) \n\n103 https://t.me/usmleinnercircle USMLE Inner Circle \n\nWestermark sign Pulmonary DVT \n\n What is the diagnostic test of choice for a patient with moderate -high probability of DVT (modified Wells > 2)? \n\nCompression ultrasonography \n\nmay use D-dimer in patients with low pretest probability; diagnosis of DVT should be confirmed before anticoagulation is started \n\n In Upper arm DVT, Catheter site is clean with swelling of arm. \n\n Patients who inject drugs into the femoral vein can develop DVT due to iliofemoral venous wall trauma, chemical irritation, and/or infection. \n\n104 https://t.me/usmleinnercircle \n\nModified Wells criteria for pretest probability Upper extremity deep venous thrombosis of deep venous thrombosis . Central venous catheters \n\n## . Previously documented DVT \n\n Active cancer Risk factors . Repetitive arm motions (eg, baseball pitching) . Weight lifting \n\n## . Recent immobilization of the legs . Malignancy \n\nScore 1 point for . Recently bedridden >3 days each feature . Localized tenderness along vein distribution present Swollen le g\n\n## . Calf swellin g >3 cm compared to other leg . Acute amn edema, heaviness, pain & erythema \n\nManifestations . Dilated subcutaneous collateral veins in chest/upper extremity . Pulmonary embolism \n\n## . Pitting edema \n\n## . Collateral superficial nonvaricose veins \n\nDiagnosis . Duplex or doppler ultrasonography \n\n Alternate diagnosis more likely (-2 points) \n\nTotal score for 0 points = Low probability \n\nTreatment . 3 months of anticoagulation \n\n## . Thrombolysis (non---<:atheter-related) \n\nclinical probability . 1 or 2 points = Moderate probability \n\n ~3 points = High probability DVT = deep venous thrombosis. \n\nManagement of lower extremity proximal DVT \n\nNo \n\nt\n\nLower extremity proximal DVT (ie, above the knee} \n\nLimb -threatening DVT \n\n Compartment syndrome Phlegmasia ceru lea dotens Yes \n\nAnticoagulation contraindicated \n\n Adive/difficull-to-treat major bleeding \n\n> I\n\nntracranial h emo1Thage Yes \n\n+\n\nIVCfilt er .. \n\n(retrievable prefefTed) \n\nNo \n\n+\n\nAntlcoagulat :J Thrombolysis or thrombe c torny Systemic or catheter-directed thrornbolysis Percutaneous or surgical thrombectomy \n\nLarge occlusive iliofemoral OVT - venous limb ischemia & gangrene (cyanosis, bullae, massive edema, extreme pain) \n\n.. Lesser (re la tive) i nd ications clot propagation despite anticoagclatioo. J l cardiopulmonary reserve (eg . impending rig ht ventricular failure). DVT = deep vein tl'Yombosis; IVC = inferior vena cava C)UWo,ld Pulmonary What is the most common source of symptomatic pulmonary embolism ?\n\nProximal deep leg veins (e.g. femoral, popliteal, iliac) \n\nDistal veins (e.g. calf veins) are less likely to embolize \n\nWhat underlying cause of DVT must be ruled out in an older patient with their first episode of DVT and no history of immobilization, surgery, or provocative medications? \n\nMalignancy \n\ne.g. age-appropriate cancer screening (colonsocopy, mammogram) and CXR; more detailed testing may be indicated depending on the patient's symptoms Test for inherited causes (eg. protein c deficiency) if <45 , multiple sites , or family history \n\nAir embolism \n\n A small VAE often causes minimal sequelae, traveling to the pulmonary capillaries where it can diffuse into the alveoli without consequence. However, a large VAE (eg, >50 mL) can lodge in the right ventricle to cause right ventricular outflow tract obstruction or lodge within the pulmonary arterioles to obstruct pulmonary blood flow. \n\n105 https://t.me/usmleinnercircle USMLE Inner Circle \n\nTreatment of acute deep venous thrombosis/pulmonary embolism O ra l factor Xa inhibitors Wa rfa rin Mechanism of ac tion Direct factor Xa inhibition Vitamin K antagonism \n\nTherapeutic on se t 2-4 hours 5-7 days \n\nOv er la p n ee ded? No Yes , overlap with UFH or LMWH for - 5 days \n\nLa bo ratory monitoring No Prot hr ombin time/lNR \n\nVenous air embolism \n\n Trauma, ce rt ain surgeries {eg, ne urosurgical) \n\nEtiologies . Central venous catheter manipulation \n\n# . Barotrauma {eg, positive-pressure ventilation) \n\n# . Sudden-onset respiratory distress \n\nClinical manifestations . Hypoxemia, obstructive shock, cardiac arrest \n\n# . Left lateral decubitus positioning \n\nManagement High-flow or hyperbaric oxygen .Pulmonary Manifestations of arterial air embolism include stroke and myocardial infarction. \n\nPatients with suspected arterial air embolism should be placed in supine positioning , as it helps prevent the embolism from traveling to the brain and causing a stroke .\n\n## ARDS Traps the VAE on the lateral wall of the right ventricle, preventing RVOT obstruction \n\n106 https://t.me/usmleinnercircle \n\nLeft lateral decubi tus posi tion ing for venous air embolism \n\nRisk factors &\n\npathogenesis Pathophysiology Diagnosis \n\nRight ventricular outflow tract \n\nAcute respiratory distress syndrome: pathogenesis & diagnosis \n\nC> UWortd \n\n Direct (eg, pneumonia, inhalation) or indirect (eg, sepsis, pancreatitis, trauma) lung injury \n\n## . Inflammatory cell activation & j permeability .... fluid & cytokine leakage into alveoli \n\n t Lung compliance (alveolar flooding) --+ j work of breathing Severe V/Q mismatch (intrapulmonary shunt) --+ severe hypoxemia j Hypoxic pulmonary vasoconstriction --+ j RV afterload & acute PHTN New bilateral alveolar opacities within 1 week of inciting insult Edema not explained by cardiac failure or volume overload Hypoxemia with PaO 2/FiO 2 :5300 \n\nPHTN =pulmonary hypertension; RV =right ventricular; V/Q =ventilation/perfusion. \n\nAcute respiratory distress syndrome: management & prognosis \n\n## . Lung protection: limit alveolar distending volume (VT 6 ml/kg ) & pressure (Pplat \n\n:530cm H2O) \n\nMechanical ventilation Ventilation: tolerate permissive hypercapnia (ie, j PaCO 2 & t pH acceptable) to avoid excessive VT \n\n Oxygenation: set lowest feasible FiO 2 (goal SpO 2 92%-96%) to avoid 0 2 toxicity Treat underlying etiology: source control (eg, sepsis) \n\nSupportive care . Prevent iatrogenic harm: negative fluid balance, timely extubation (eg, minimize sedation) \n\n Corticosteroids: select patients with moderate-to-severe early ARDS \n\n## . Mortality rate: 40% in hospital, death mostly due to multiorgan failure \n\nPrognosis . Morbidity rate: 50% with chronic cognitive impairment & physical debility, 25% with chronic pulmonary dysfunction (restriction & t DLCO) \n\nARDS =acute re spiratory distress syndrome; DLCO =diffusion capacity of lung for carbon monoxide; Pplat =plateau pressure; \n\nSpO 2 =oxygen saturation as measured by pulse oximetry; Vy= tidal volume. Pulmonary What is the PaO2/FiO2 ratio ?Clinical indicator of hypoxemia Ratio of O2 tension (O2 in blood ) to fraction of inspired O2 (fraction O2 in inspired air, usually .21 (21%) )\n\nNormal vs. ARDS ?\n\nNormal = 300-500, <300 = ARDS (100 = severe ARDS) \n\n Mechanical ventilation in patients with ARDS should use low tidal volumes and high PEEP. \n\nIn ARDS, a significant number of the alveoli remain collapsed despite positive airway pressure, and any tidal volume delivered by the ventilator is distributed to those remaining open (functional \"baby lung\"). LTV prevents overdistension of these alveoli and improves mortality (PEEP 10 cm H2O) \n\n Prone positioning distributes the ventilation from the ventral to the dorsal (dependent) lung regions, where the majority of alveoli are located. This improves the homogeneity of ventilation throughout the lungs and decreases mortality in patients with ARDS \n\n107 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nAcute respiratory distress syndrome: Initial ventilator management In itial ventilator settings \n\n Oxygenation: FiO, = 100% & PEEP = 5 cm H,O Ventilation: V, = 6 mllkg IBW & RR = 14-18/min \n\nAdjust oxygenation J Adjust ventilation \n\nPaO, >90 mm Hg {hyperoxia) PaO, <60 mm Hg (hypoxia) ftPaCO , & pH <7.25 \n\n1RR \n\nrv , as last resort i PaCO, & pH ~7.45 \n\nN , \n\n!RR \n\nrSedation as last resort \n\nEnsure lung-protective ventilation {avoid alveolar overd istension) \n\nEvaluate lu ng compliance: measure Pplat with inspiratory ho ld \n\nGoal Pplat ;;30 cm H,O: N , &lor adju st P EE PPause venblator briefly after tidal volume is delivered and measure pressure required to hold the lungs at distension on cu rr ent settings. \n\nABG :: artenal blood gas; ET :: endotracheal ; FiO 2 :: fraction of inspired oxygen; IBW = ideal body weight; Pplat = plateau pressure; PEEP = positive end-expiratory pressure; RR = respiratory rate; V, = tidal volume uwor ld Pulmonary Fluid balance refers to the net sum of all fluid intake and output from the time of admission. Patients with ARDS often have an initial positive fluid balance (eg, volume resuscitation for sepsis, blood transfusion for trauma). During hospitalization, a conservative fluid strategy aimed at achieving a neutral or negative fluid balance accelerates recovery from ARDS, with a trend toward improved survival rate (\"dry lungs = happy lungs\"). This goal is accomplished by: \n\nMinimizing intake: avoiding unnecessary fluid boluses, concentrating intravenous drips \n\nPromoting removal: diuretics, renal replacement therapy Patients with refractory hypotension (eg, septic shock) should be assessed for fluid-responsiveness prior to blind volume loading (eg, via passive leg raise to simulate a fluid bolus). Vasopressors (eg, norepinephrine) may be required to support hemodynamics to permit volume removal. \n\n## Lung Cancer \n\n A lobectomy is the standard approach to surgical management of lung cancers and can be tolerated if the FEV1 >1.5L and DLCO >60% .\n\n FEV1 and DLCO , obtained by preoperative pulmonary function testing, are the best predictors of postoperative outcomes following lung resection surgery. If a solid lesion revealed on prior imaging is stable in size for >2 years , malignancy is effectively ruled out and \n\n108 https://t.me/usmleinnercircle \n\nType of tumor Adenocar ci noma Squamou s cell carcinoma Small cell \n\ncarcino ma \n\nLarge ce ll \n\ncarcino ma ISe rial CT sca ns IInc idence Locat i on Clinical associations Clubbing \n\n40% - 50% Peripheral Hypertrophic osteoarthropathy \n\n Central \n\n20%-25% Necrosis & Hypercalcemia cavitation Cus hing sy ndr ome \n\n10%-15% SI AD H Central L am bert -Ea t on syn dr ome \n\n5%- 10% Peripheral Gynecomas tia Galac t orrhea So litary p ulmon ary nodule on routine ch est x- ray Previous chestx -r ay No pr evio us im agi ng or possible no dul e g rowt hInd ete rmin ate or su spic ious for malignan cy Further inv es tigation with bi ops y or PET \n\nStable lesion \n\n 60 Smoking sta tus Never sm oked Current Current Smoking > 15 5-15 <5 cessa t ion (yr) Nodul e ma rg in Smooth Sca lloped Corona radiate c hara cterist i cs or spiculated \n\nSolitary pulmonary nodule High malllJna ncy risk Low to Intermediate malignancy risk \n\nSurgie<~exc isioo I~ \n\n# ~ ~\n\n# -~- F~-~.! ~malglancy for malignancy \n\nLow \n\nISurgical excision I Serial CT scans I No follow up Pulmonary Pancoast Tumor Lung Carcinoid Tumour Head and Neck Cancer \n\n What is the best initial test in a patient found to have a cervical lymph node with metastatic squamous cell carcinoma ?\n\nPanendoscopy ( esophagoscopy, bronchoscopy, laryngoscopy )\n\nhelps detect the primary tumor, which can then be biopsied to determine further management no further testing is necessary \n\n109 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSquamous cell carcinoma of the lung Clinical presentation of Pancoast tumors \n\n Sho uld er pain (most common) Homer syndrome (ipsil ate ral ptosis, miosis, enophthalmos & anhidrosis) from involvement of paravertebral sympa th etic chain & inferior cervical ganglion C8-T2 neurological involvement o Weakness &/or atrophy of intrinsic hand muscles o P ain & paresthesias of 4th & 5th digit s, medial arm & forearm Supraclavicular lymph node en largement Weight lo ss \n\nBronchial carcinoid tumor \n\n## . Most common lung cancer in adolescents/young adults \n\nEpidemiology . Neuroendocrine tumor derived from bronchial Kulchitsky cells \n\n## . Proximal airway obstruction (eg, dyspnea, wheezing , cough) \n\n## . Recurrent pneumonia distal to obstruction \n\nManifestations . Hemoptysis Carcinoid syndrome less common than with midgut carcinoid \n\nDiagnosis Chest imaging: contrast enhanced (vascular) tumor with endobronchial component \n\n## . Bronchoscopy with biopsy Pulmonary Head and neck cancer can present with Cervical LN enlargement or Referred Otalgia \n\n An enlarged , ulcerated tonsil with ipsilateral cervical adenopathy is likely oropharyngeal (head and neck) squamous cell carcinoma. \n\nHuman papillomavirus is the likely etiology in the absence of traditional risk factors (smoking, alcohol) in younger patients. A laryngeal ulcer in a smoker is likely squamous cell carcinoma .\n\nPersistent hoarseness should always be evaluated by laryngoscopy to ensure no delay in diagnosis of possible cancer. \n\nNasopharyngeal Carcinoma Oral Leukoplakia \n\n110 https://t.me/usmleinnercircle \n\n> CIUWortd\n\n# .Epidemiology ...Manifestations ..\n\nDiagnosis ..Treatment .Referred otalgia \n\n> -Vagus nerve (CN X)\n> Poster ior pharyngeal wall tumor\n\nNasopharyngeal carcinoma \n\nEndemic to Asia \n\nLinked with Epstein-Barr virus reactivation Risk factors: Diet (salty fish), smoking , genetics Obstruction: Nasal congestion , epistaxis , headache Mass effect: Cranial nerve palsy, otitis media Spread: Neck mass (cervical lymphadenopathy) Endoscope-guided biopsy Radiation therapy Chemotherapy Pulmonary D/D: Oral hairy leukoplakia typically presents as multiple white lesions on the lateral tongue with a distinct corrugated appearance which cannot be scrapped off. Caused by EBV \n\nBecause it occurs almost exclusively in patients with significant immunodeficiency , HIV testing \n\nshould be performed, especially in patients with signs of systemic illness. \n\nNOT premalignant and can occur in young people (vs Oral Leukoplakia )\n\n## Miscellaneous \n\nChronic Cough \n\n What is the next step in management for a young patient who presents with chronic nocturnal dry cough with a sensation of liquid dripping into the back of the throat? \n\n111 https://t.me/usmleinnercircle USMLE Inner Circle \n\nOral leukoplakia Risk factors . Tobacco & alcohol use \n\nClinical features . Painless white mucosal patch \n\n## . Cannot be wiped off \n\n## . Nonhomogeneous gross appearance \n\nIncreased risk of cancer . Large size (>4 cm) \n\n## . Dysplasia seen on biopsy \n\n## . Biopsy (at diagnosis & if appearance changes) \n\nManagement . Risk factor modification (eg, tobacco cessation) \n\n## . Close monitoring \n\n## . Surgical excision \n\nCommon etiologies of chronic cough Upper airway . Upper airway cough syndrome (postnasal drip) \n\ndisorders . Chronic sinusitis \n\n## . Asthma \n\nLower airway & . Post-respiratory tract infection \n\n## . Chronic bronchitis \n\nparenchymal . Bronchiectasis \n\ndisorders . Lung cancer \n\n## . Nonasthmatic eosinophilic bronchitis \n\nOther causes . Gastroesophageal reflux \n\n## . ACE inhibitors \n\nEvaluation of subacute (3-8 weeks) or chronic (>8 weeks) cough \n\nSus pe cted eti ol ogy on H & P\n\nEvaluate & t reat as Ind icated \n\nACEinhib it ors - StopA CE UACS - First-generation H lb locker Asthma - PFTs GE RD Empi ric PPI \n\nt\n\nNo im pro ve ment after intervention \n\nI\n\nChest x-ray Parenchymaldisease Purule ntsp utum /immunocompromised No specific etiology \n\nGERO= gastroesophageal reflux disease; H & P = history& physica l; PFTs = pulmonaryfunction tests; PPI = proton pump inhibit or; UACS = upperairwaycoughsyndrome. Pulmonary Oral first-generation H1 blocker \n\nthis patient likely has upper-airway cough syndrome (post-nasal drip) and should be treated empirically \n\nHyperventilation Syndrome \n\nHyperventilation syndrome , a diagnosis of exclusion characterized by intermittent episodes of hyperventilation without any obvious cardiac or pulmonary etiology. Neurologic symptoms, including paresthesias, headache, lightheadedness, and carpopedal spasms, are often present and may be related to cerebral vasoconstriction or alkalosis-induced hypocalcemia \n\nand hypophosphatemia .If the episode does not improve with breathing retraining , a small dose (not a high dose) of a short-acting benzodiazepine (eg, lorazepam ) is appropriate second-line therapy. \n\n Breathing into a paper bag was previously recommended to improve hypocarbia by rebreathing CO2; however, this can also result in hypoxia and therefore should not be done \n\nAcute Chest Syndrome \n\n Acute chest syndrome is a life-threatening complication of sickle cell disease caused by vasoocclusion of pulmonary microvasculature. The most common trigger in adults is acute vasoocclusive pain causing \n\nfat embolism and/or hypoventilation. \n\nDecompression Sickness \n\n112 https://t.me/usmleinnercircle \n\nPathophysiology of acute chest syndrome \n\n> Acute vasoocclusive pain Pulmonary in fecti on , asthma exacerbation Fat embolus (from bone marrow necrosis) Atelectasis (from splinting/pain) Pu lmonary infarction/inflammation ]Regional alveolar hypoxia\n\n# L \n\n> RBC =red blood cell .\n\n## lTT RBC sickling & vasoocclusion in pulmonary vasculature Acute chest syndrome \n\n> \"New pulmonary dens ity on chest im ag ing with fever, chest pa on, &/or respiratory symptoms. QuWorld\n\nPulmonary Symptoms usually begin within 12 hours of surfacing. Small air bubbles in the venous bloodstream can lodge in the capillaries of the skin to cause pruritus or \n\nmottling and cyanosis of the extremities. The air bubbles can also lodge in the pulmonary capillaries to cause respiratory distress and localized ischemia, with resulting pulmonary edema . A relatively large volume of coalesced air (eg, 50 mL) can lodge in the right ventricular outflow tract and cause obstructive \n\nshock . Air can also pass into the arterial circulation by overwhelming the pulmonary capillary filtering capacity or via a right-to-left-shunt (eg, patent foramen ovale). Small air bubbles in the arterial circulation can travel to the brain to cause confusion , gait ataxia , and dysarthria . A small volume (eg, 1-2 mL) of coalesced air can cause localized stroke (eg, left arm weakness) or myocardial infarction . Emergency treatment: IV hydration , Trendelenburg positioning , administration of 100% oxygen .Optimal management is with hyperbaric oxygen therapy. \n\nHigh Altitude Sickness Diffuse Alveolar Hemorrhage \n\n113 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDecompres si on sickness \n\nPathophysiology . Abrupt l in ambient pressure causes formation of nitrogen gas bubbles within the body \n\n## . Rapid ascent to surface foll ow ing deep dive \n\nRisk factors . Obesity (nitrogen is f at soluble), male sex \n\n## . Air travel soon after diving (may f urt her reduce ambient pressure) \n\nPresentation . Type 1 (mild illness): musculoskeletal (the bends ), cutaneous & lymphatic \n\n## . Type 2 (severe): neurologic (the staggers) & pulmonary (the chokes) \n\nTreatment . Intravenous fluids & 100% oxygen \n\n# . Hyperbaric oxygen therapy as soon as possible \n\nHigh-altitude illness \n\nPathogenesis . Reduced Pi0 2 at high altitude (>2,500 m [-8 ,000 ft]) \n\n## . AMS \n\n> 0\n\nHeadache, fatigue, nausea \n\n## . HAGE Complications 0 l Pa0 2 - i cerebral blood flow \n\n> 0\n\nLethargy, confusion, at axia \n\n## . HAPE \n\n0 Uneven h yp oxic vasoconstriction \n\n> 0\n\nDyspnea, c ough hemoptysis, respiratory distress \n\n## . Supplemental oxygen Treatment . Acetazolamide for AMS, dexamethasone for HAGE \n\n## . Descent to lower altitude (definitive treatment for all HAI) AMS = acute mountain sickness; HACE = high-altitude cerebral edema; HAI = high -a ltitude illness; HAPE = high-altitude pulmonary edema; Pi02 =partial pressure of inspired oxygen. Pulmonary Pulmonary Paeds \n\nChoanal Atresia coloboma [missing eye tissue] \n\n114 https://t.me/usmleinnercircle \n\nDiffuse alveolar hemorrhage \n\n# . Pulmonary capillariti s: ANCA vasculitis, SLE, antiphospholipid antibodies \n\nEtiology & pathogenesis . Bland hemorrhage: mitral stenosis, anticoagulation Alveolar damage : viral pneumonitis, ARDS, drug-induced (eg, cocaine, amiodarone) . Dyspnea, hypoxemia, hemoptysis (absent in ~50%) & blood loss anemia \n\nClinical presentation & diagnosis . CXR or CT: diffuse ground-glass opacities \n\n# . Bronchoscopy: progressive blood on serial lavage \n\nManagement Treat underlying (eg, rheumatologic, infectious) cause . Supportive care: oxygen , mechanical ventilation; avoid anticoagulation \n\nANCA = antineutrophil cytoplasmic antibody; ARDS = acute respiratory distress syndrome; CXR = chest x-ray; SLE = systemic lupus erythematosus. \n\nDiffuse airspace opacification Definition: Alveolar filling processes that can involve multiple lobes Fluid Transudative edema: card i ogenic \n\n Exudative edema: noncardiogenic (ARDS) \n\n Neutrophils (pus): i nfectious pneumonia \n\nCells Lymphocytes & macrophages: hypersensitivity pneumonitis . Eosinoph ils: acute eos i nophi l ic pneumonia Malignant cells: carcinomatosis \n\nBlood Diffuse al veolar hemorrhage \n\n Aspirated nonalveolar hemorrhage \n\nOthers Fat: lipoid pneumonia (eg, vap in g oi l s) . P r otein : pu l monary alveolar proteinosis \n\nARDS = acute respiratory distress syndrome .\n\nChoanal atresia \n\n## . Unilateral (most common) \n\n> 0\n\nChronic nasal discharge \n\n> 0\n\nSymptomatic during ch il dhood \n\n## . Bilateral \n\nClinical findings 0 Cyanosis that worsens with feeding & improves with crying \n\n> 0\n\nNoisy breathing (stertor) \n\n> 0\n\nSymptomatic shortly after birth \n\n## . May be associated with CHARGE syndrome \n\nDiagnosis . Inability to pass catheter past nasopharynx \n\n## . Confirmation with CT scan or nasal endoscopy \n\nTreatment . Oral airway \n\n## . Surgical repair \n\nCHARGE = Coloborna , Heart defe cts, Atresia c hoanae, g rowth Retardation , Genital and Ear abnormalitie s. Pulmonary What is the likely diagnosis in a generally healthy newborn that presents with cyanosis that worsens with feeding and is relieved with crying despite a normal cardiac and respiratory exam? \n\nChoanal atresia \n\nfailure to pass a catheter through the nose into the oropharynx is suggestive of this diagnosis; CT scan confirms the diagnosis \n\n Because neonates are obligate nasal breathers (ie, preferentially breathe through the nose), the complete obstruction of bilateral choanal atresia causes intermittent cyanosis, even at rest \n\nCHARGE Syndrome \n\nForeign Body Aspiration \n\n115 https://t.me/usmleinnercircle USMLE Inner Circle \n\nChoanal atresia \n\nNormal anatomy \n\n UWorkl \n\nCHARGE syndrome \n\n## . Qoloboma \n\n# . _tj_eart defects (eg , TOF, VSD) \n\nCharacteristic . Atresia choanae \n\nfeatures . Retardation of growth/development \n\n## . ~enitourinary anomalies . !;_ar abnormalities (eg, hearing loss) . Anosmia \n\nAdditional key findings . Cleft lip/palate . Hypotonia \n\n## . Clinical \n\nDiagnosis CHD7 gene testing .TOF = tetralogy of Fallot; VSD = ventricular septal defect. \n\nBony or membranous obstruction \n\n# L\n\nChoanal atresia Pulmonary Wheezing and decreased breath sounds on the affected side are characteristic, and hyperresonance to percussion can occur over the hyperexpanded lung. What is the next step in management for a child in respiratory distress due to foreign body aspiration ?\n\nBronchoscopy \n\ncharacterized by sudden-onset respiratory distress; most aspirated foreign bodies end up in the right mainstem bronchus \n\n Normal radiograph does not rule out FB aspiration because at least 30% of radiographs are normal , particularly if a radiolucent FB (eg, food) is lodged in a small airway. Therefore, if clinical suspicion remains high, bronchoscopy is indicated to confirm the diagnosis and remove the aspirated object. Sometimes, CT Scan can also be used if Xray is normal in asymptomatic child. \n\nNasal Foreign Body \n\nNRDS \n\n116 https://t.me/usmleinnercircle \n\nForeign body aspiration \n\n History of choking event with sudden-onset cough Symptoms depend on location \n\nClinical features a Trachea/main bronchus: acute respiratory distress, cyanosis, stridor (trachea), hemoptysis (bronchial) 0 Lower airway: chronic/recurrent cough \n\nExamination . Focal, unilateral, and/or monophonic wheeze \n\nfindings . Focal area of diminished breath sounds \n\n# . Hyperinflation of affected side mediastinal shift toward unaffected side \n\nX-ray findings Atelectasis if complete obstruction Foreign body \n\n# . Recurrent pneumonia \n\nComplications . Bronchiectasis \n\nManagement . Bronchoscopic removal \n\nNasal foreign body \n\n## . Inorganic substance (eg , toy ): mild pain/discomfort \n\nClinical manifestations . Organic substance (eg , food): unilateral, foul-smelling , purulent, bloody discharge \n\n## . Button battery: epistaxis, purulent or black discharge . Positive pressure expulsion (eg , forceful exhalation with unaffected naris occluded) \n\nTreatment . Mechanical extraction \n\n## . Local irritation \n\nComplications . Infection (eg, sinusitis) \n\n## . Aspiration \n\n## . Nasal septa! perforation (eg, button battery, multiple magnets) Pulmonary What is the treatment ?\n\nNasal CPAP with PEEP of 3-8 cm H2O ( prevents collapse )Administration of artificial surfactant within 2 hours postpartum. \n\nDDx: Transient tachypnea of the newborn (wet lung disease) Full-term neonates born by cesarean section (lungs full of fluid) Therapy should focus on supportive care \n\n Meconium Aspiration Syndrome :\n\nPost-term neonates with meconium aspiration Unresponsive neonate and green amniotic fluid establish diagnosis \n\nEmergency intubation \n\nOthers: Congenital Diaphragmatic hernia, Pneumothorax, Neonatal pneumonia, Sepsis, Lung hypoplasia \n\n117 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nDiagnosis Pathophysiology Clinical features Chestx-ray \n\n\n\nManagement of neonatal respiratory distress syndrome \n\nNeonate with respi ra tory distress syndrome Apnea or gasping? )Yes \n\n# 'Bag valve mask ventilation ) \n\n# iContinued apnea ] - No___. Noninvasive posi ti ve ai rway pressure (eg CPAP\") \n\n. Consider surfactant \n\nI\n\nYes \n\n# 'Intubate Chest compressions Consider surfactant \n\ncPAP = conti nu ous positive airway pressu re Common causes of neonatal respiratory distress Transient tachypnea Respiratory distress of the newborn syndrome \n\n Inadequate alveolar fluid Surfactant deficiency Alveolar collapse & diffuse clearance at birth atelectasis Tachypnea shortly after Prematurity birth Severe respiratory distress Resolves by day 2 of life & cyanosis Bilateral , perihilar linear Diffuse, ground-glass streaking appearance with low lung Fluid within interlobar volumes fissures Air bronchograms \n\nCUWor ld \n\nPersistent pulmonary hypertension \n\n High pulmonary vascular resistance Right-to-left shunt Tachypnea & severe cyanosis Clear lungs with decreased pulmonary vascularity Pulmonary D/D for Early Differential Cyanosis: \n\n1. PDA with RDS 2. Persistent Pulmonary Hypertension What is the next step in management for a newborn with respiratory distress and hypoxia secondary to a suspected congenital diaphragmatic hernia? \n\nEndotracheal intubation \n\nABCs take precedence over diagnostic studies; a gastric tube should be placed immediately after to decompress the stomach and bowel \n\n Infant 2 hours after birth has elevated hematocrit >65%, respiratory distress, hypoglycemia, cyanosis, and plethora .This is likely due to intrauterine hypoxia .Risk factors? Smoking, maternal diabetes, small or large for gestational age Prominent interlobar fissure \n\n118 https://t.me/usmleinnercircle \n\nBronchopulmonary dysplasia \n\n# . Premature arrest of pulmonary development \n\nPathogenesis Alveolar hypoplasia with t septation . Impaired vasculogenesis . Premature infant with continued supplemental oxygen requirement \n\nClinical diagnosis .:28 days from birth* \n\nChest x-ray Mild: diffuse hazy infiltrates, low/normal lung volumes Severe: fibroct stic changes, hyperinflation \n\nTreatment Supportive (eg, oxygen, nutrition, fluid restriction/diuretics) . Pulmonary artery hypertension \n\nComplications Cardiovascular disease (eg , hypertension) . Recurrent respiratory infections some definitions include an oxygen requirement at 36 weeks postmenstrual age (ie, gestational + chronologic age). \n\nTransient tachypnea of the newborn Pulmonary Persistent Pulmonary Hypertension of Newborn \n\nOSA \n\n The mechanism of enuresis is unclear, but it may be related to the elevated levels of B-type natriuretic peptide seen with OSA, possibly due to intermittent obstruction causing increased cardiac volume and pressure. \n\nBreath holding spells \n\n119 https://t.me/usmleinnercircle USMLE Inner Circle \n\nRespiratory distress syndrome \n\nDiffuse alveolar collapse (atelectasis) due to surfactant deficiency UWor ld \n\nPersistent pulmonary hypertension of the newborn \n\n Abnormal persistence of elevated fetal pulmonary vascular \n\nPathogenesis resistance \n\n# . Right-to-left shunting across ductus arteriosus \n\n# . Lung hypoplasia (eg, congenital diaphragmatic hernia) \n\nRisk factors . Meconium aspiration syndrome \n\n# . Infection (eg, neonatal pneumonia) \n\n# . J Postductal relative to preductal oxygen saturation \n\nExamination . Respiratory distress & cyanosis \n\n# . Prominent S2 \n\n# . Oxygenation & ventilation \n\nTreatment . Inhaled nitric oxide (pulmonary vasodilator) \n\nPediatric obstructive sleep apnea Pathophysiology Adenotonsillar hypertrophy Night symptoms \n\no Loud snoring , pauses in breathing, gaspi ng \n\no Enuresis, parasomnias (eg, sleepwalking, sleep terrors) \n\nClinical manifestations Day symptoms \n\no Inappropriate naps or falling asleep during school \n\no Irritability, inattention, learning problems, behavioral problems \n\no Mouth breathing, nasal speech Poor growth (ie, failure to thrive) \n\nComplications Poor school performance Cardiopulmonary (eg, hypertension, structural heart changes) \n\nManagement Tonsillectomy & adenoidectomy Pulmonary What is the next step in management for an infant that experienced a breath-holding spell ?\n\nReassurance; no further testing \n\nbreath-holding spells are considered normal development ( Resolution by 5 Years age) \n\nscreening for associated IDA is recommended because iron-deficient patients typically experience \n\nimprovement in BHS frequency with iron therapy. \n\n No murmur and very brief cyanosis (vs TOF which has left upper sternal murmur and improvement in cyanosis with squatting) \n\nSudden Infant Death Syndrome \n\n Impaired cardiovascular reflexes (eg, increased heart rate due to hypercarbia) and diminished arousal responses may account for elevated risk with Smoke Exposure. \n\n Sudden infant death syndrome is the leading cause of mortality in infants age 1 month to 1 year in the United States \n\nDrowning \n\n120 https://t.me/usmleinnercircle \n\nBreath-holding spell (BHS) vs seizure Cyanolic BHS Pallid BHS Seizure \n\n Age 6 months to 2 years Any age \n\nEpidemiology j Risk with iron deficiency anemia . j Risk with history of febrile seizure or \n\n## . developmental delay \n\n## . Minor trauma . Often unprovoked \n\nTriggers . Crying/frustration Pain or fear Sleep deprivation . .\n\n Apnea & cyanosis - . Bradycardia, apnea & pallor -\n\nClinical LOC LOC . LOC - tonic-clonic movements \n\nfeatures . Rapid return to Brief (<5 min) confusion or . Prolonged (>5 min) postictal confusion baseline sleepiness \n\n> LOC\n\n= loss of consciousness. \n\nRisk factors for sudden infant death syndrome \n\n# . Substance use (eg , cigarettes, \n\nMaternal/antenatal alcohol , recreational drugs) \n\n## . Maternal age <20 . Inconsistent prenatal care \n\n## . Prematurity or low birth weight . Sleep environment \n\n> 0\n\nProne-/side-sleep position \n\nInfant 0 Soft sleep surface, loose bedding \n\n> 0\n\nBed sharing . Smoke exposure Pulmonary A patient with purposeful movements demonstrates good functional neurologic ability and indicates a good prognosis. (basically shows less hypoxic damage to brain) \n\n Even if the fluid is coughed out quickly and normal ventilation is restored, the fluid may have already caused damage capable of resulting in delayed pulmonary complications. This damage may include: \n\nDirect tissue injury from chemicals or contaminants in the fluid, leading to inflammation Washout of alveolar surfactant , leading to alveolar collapse Disruption of the osmotic gradient of the alveolar-capillary membrane, leading to increased fluid permeability \n\nTogether, these insults can progressively impair oxygen exchange and cause atelectasis , decreased lung compliance, and non-cardiogenic pulmonary edema .\n\n## Pulmonary Surgery \n\n121 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nDrowning injuries \n\n# . Ch ildren age <5 & males age 15-25 \n\nRisk factors . Inabili ty to swim &/or inadequate supervision \n\n# . Concomitant drug/alcohol use . Acute respiratory distress syndrome \n\nComplications . Cerebral edema [M .... ... ~ ;,._ l\n\n# . Arrhythmia I~\n\n# . Subme rsion time >5 min \n\n# . Del ay in initiation of ca rdiopulmonary resuscitation \n\nPoor prognostic Indicators . Prolonged resuscitative efforts . Age >14 . Arterial blood pH <7.1 \n\nManagement of drowning Ac ut e inte rv e nt ions \n\n Adm inister rescue breaths first, then chest \n\ncompressions for cardi ac arrest \n\n Remove wet clothing to improve hypothermia Transport to emergency department \n\n# lEmergency department care Symptomatic Asymptomatic \n\n# l lObserve (~8 hours) II Maintain oxygenation & ventilation Continuous cardiopulmonary monitoring Supportive care as needed (eg, supplemental oxygen, bronchodilators, NIV, intubation) Continu ous cardiopulmonary monitoring Evaluate CXR ECG ABG, CBC , electrolytes Drug screen (in adolescents/adults) Monitor for signs of ARDS (eg, dyspnea, wheeze) Evaluate CXR at end of observation (to assess for pulmonary edema) ABG, CBC, electrolytes, drug screen \n\nAB G =arterial blood ga s analys is; CBC =complete blood count ; C XR =chest x-ray ; NI V =noninvas iv e venb1a tion . OUWo'1d Pulmonary In all patients anticipating elective surgery, immediate smoking cessation is recommended as those who quit smoking >4-8 weeks prior to surgery substantially decrease their postoperative pulmonary risk. \n\nLesser durations of preoperative smoking cessation do not reduce the risk, likely because the airway inflammation and increased bronchial mucus production induced by smoking requires some time to improve. \n\n Uncontrolled postoperative pain often presents with patient discomfort, tachycardia ,\n\ntachypnea , hypertension , and respiratory splinting , particularly for thoracic and upper abdominal incisions. \n\nAdequate pain control following a surgical procedure is necessary to decrease the risk of postoperative complications, such as pneumonia .\n\nPatient-controlled analgesia is a frequently used option to provide opioid-based pain relief to patients after surgery. \n\nPost-operative Atelectasis \n\n Atelectasis commonly occurs post-operatively due to shallow breathing and weak cough secondary to pain. Typically manifest on post-operative day 2 and 3 \n\nshallow breathing causes hypoxia with resultant tachypnea and low CO2 (respiratory alkalosis) \n\n What breathing instrument is useful for preventing post-operative atelectasis ?\n\nIncentive spirometer \n\nAn incentive spirometer is a device that teaches patients how to take slow, deep breaths, which opens up airways and prevents collapse \n\n122 https://t.me/usmleinnercircle \n\n> Postoperative pulmonary complications Complications Atelectasis, bronchospasm, pneumonia\n\n Prolonged ventilator requirement \n\n> Risk Age >50, active smoking\n\n Underlying heart failure or obstructive lung disease \n\n> factors\n\n Emergency surgery or surgery duration >3 hr Smoking cessation >4-8 weeks prior to surgery \n\n> Perioperative Symptomatic control of underlying lung disease\n\nprevention Pain control, deep-breathing exercises, incentive spirometry Pulmonary Once atelectasis develops, it can be treated with continuous positive airway pressure (CPAP) \n\nto help open collapsed alveoli \n\n CPAP may stent the airways open, but if this is not sufficient to promote ventilation, escalation to BiPAP or invasive positive pressure ventilation may be required. \n\n Incentive Spirometry also helps to prevent Post op Pneumonia \n\nFlail Chest \n\n How does the flail chest segment move with inspiration? \n\nMoves inward (paradoxical chest wall motion) \n\n123 https://t.me/usmleinnercircle USMLE Inner Circle \n\nFlail chest Pathophysiology ;,, 3 contiguous ribs fractured in ;,, 2 locations \n\n- flail chest segment Paradoxical chest wall motion with respiration \n\nFindings Chest pain, tachypnea , rapid shallow breaths CXR: Rib fractures +/- contusion/hemothorax \n\nManagement Pain control, supplemental oxygen PPV ( +/- chest tube) if respiratory failure CXR = chest x-ray; PPV = positive pressure ven tilation. \n\nFlail chest Pulmonary due to negative intrathoracic pressure \n\n What is the most essential part of management for an uncomplicated rib fracture (e.g. no hypotension, pneumothorax, etc.)? \n\nPain control \n\nessential to maintain deep breathing and adequate cough , which helps prevent atelectasis and \n\npneumonia \n\n The extreme blunt force required to create flail chest typically injures the underlying lung resulting in \n\npulmonary contusion (eg, seen on x-ray as infiltrates underlying patient's rib fractures) decreases \n\noxygen diffusion (due to alveolar hemorrhage and edema). As a result, patients must breathe harder to maintain oxygenation. The combination of increased work of breathing and decreased oxygenation causes many patients to fatigue and develop \n\nrespiratory failure , requiring mechanical ventilation. \n\nBlunt Chest Trauma Hemothorax \n\n What is the underlying cause of hemorrhagic shock in a patient with decreased breath sounds , tracheal deviation , and dullness to percussion ?\n\nHemothorax \n\neach hemithorax is capable of holding up to 50% of circulating blood volume! \n\n What is the treatment of a hemothorax ?1. Chest tube insertion (thoraco stomy )2. Thoracotomy indicated if >1500 mL or >200 mL/hr for >2 hours or Continuous need for transfusion to maintain hemodynamic stability. \n\n124 https://t.me/usmleinnercircle \n\n> Hemodynamically unstable\n\n# ! \n\n> Resuscitat ion and eva luation\n> eFAST Chest x-ray ECG +/ -stabilizing in tervention\n> (eg, chest tube) if indicated\n\n# !\n\n> Hemodynamic stability achieved/maintained?\n\nI\n\nNo \n\n# lOR thoracctomy \n\nBlunt chest trauma \n\n> +-----Yes-----\n> Additional tests (eg ,CT chest) Hemodynamically stable\n\n# ! \n\n> High-risk mechanism or\n> serious injury on examination\n\nINo \n\n# l\n\n> Abnormal findings on evaluation, chest x-ray, ECG\n\nI\n\nNo \n\n# lPossible discharge \n\n> or observation eFAS T=extended Focused Assessment with Sonography for Tral.fTia ;OR =operating room .CUWo Clinical features Tachypnea, tachycardia, hypoxia\n\n# . Rales or decreased breath sounds \n\n> Diagnosis CT scan (most sensitive) or CXR with patchy, alveolar infiltrate not restricted by anatomical borders\n\n Pain control \n\n> Management\n\n# . Pulmonary hygiene (eg, incentive spirometry, chest PT) \n\n> Supplemental oxygen\n\n& ventilatory support \n\n> CXR =chest x-ray; PT =physiotherapy.\n\nPulmonary contusion Pulmonary Look for NG tube in the pulmonary cavity -other signs include deviation of mediastinal contents to opposite side and elevation of the hemidiaphragm \n\n Some patients (especially children) with traumatic diaphragmatic injury may initially have no symptoms and can present months to years later after progressive expansion of the diaphragmatic defect. \n\nDiaphragmatic Paralysis \n\n127 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDiaphragmatic rupture Unilateral diaphragmatic paralysis \n\n# . Phrenic nerve injury (eg , cardiac surgery, trauma, radiation therapy, compressive tumor) \n\nEtiology . Viral infection (eg , herpes zoster, poliomyelitis) \n\n# . Systemic neurologic disease (eg , A LS, GBS) \n\n# . Idiopathic \n\nClinical . Typically asymptomatic at rest \n\n# . Dyspnea on exertion \n\nfeatures . Orthopnea \n\nDiagnosis . Fluoroscopic \"sniff' test (earadoxical movement of the diaphragm seen during i;l ri ~ in i;! i [ s! l i Q l\n\nALS = amyotrophic lateral sclerosis; GBS = Guillain-Barre syndrome. \n\n--CVS \n\n# CVS Hypertension Infective Endocarditis Rheumatic Heart Disease Cholesterol Aorta Aortic Trauma Aortic Dissection Aortic Aneurysm Coarctation of Aorta Aortoiliac Occlusion (Leriche Syndrome) Carotid Artery Carotid Artery Dissection MI Post MI Complications Angina CAD Stress Test Perfusion Test Murmur & Valvular Defects Mitral Regurgitation Mitral Stenosis Aortic Regurgitation Aortic Stenosis Pulmonary Regurgitation Pulmonary Stenosis ECG Tracings PSVT Atrial Fibrillation PAC MAT WPW Ventricular PVC Monomorphic Ventricular Tachycardia Torsade de Pointes Bradycardia Tachyarrythemia and Cardiac Arrest Heart Block 1st Degree 2nd Degree Complete Heart Block Sick Sinus Syndrome Heart Failure Systolic failure Diastolic Failure \n\n128 https://t.me/usmleinnercircle CVS Hypertension \n\nIn the absence of end-organ damage, the diagnosis of hypertension must be confirmed by one of the following: \n\nAmbulatory BP readings , as measured by an automatic device worn continuously by the patient for \n\n24-48 hours . The device monitors BP at regular intervals (eg, 15-60 min). Cor Pulmonale High Output Heart Failure Cardiomyopathy Takotsubo cardiomyopathy HOCM Carditis Acute Pericarditis Constrictive Pericarditis Myocarditis Cardiac Tamponade Peripheral Vascular Diseases Venous Insufficiency Acute Limb Ischemia Shock Anaphylactic Hypovolemic & Hemorrhagic Shock Fluid Replacement Obstructive Shock CVS Drugs Anti-Arrhythmic Miscellaneous Syncope Pulsus Paradoxus Stent JVP Prosthetic Valve Prosthetic Valve Thrombosis Hereditary Hemorrhagic Telangiectasia Exercise Induced Postural Hypotension Paeds CVS VSD Tricuspid Atresia Persistent Pulmonary Hypertension of the Newborn Hypoplastic Left Heart Syndrome CVS Surgery CABG Postpericardiotomy Syndrome Sternal Dehiscence Preoperative Cardiac Other Tests Vascular Trauma Blunt Cardiac Injury Myocardial Contusion \n\n129 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCVS If continuous ambulatory BP monitoring is not available, an acceptable alternative is home BP monitoring done twice a day (morning and evening) for a week .If home BP monitoring is not possible, 3 office readings (preferably by an automated machine while the patient is alone) at least a week apart are needed. Urinalysis: for occult hematuria and urine protein/creatinine ratio \n\n130 https://t.me/usmleinnercircle \n\n\n\n\n\noi 120 \n\n> I\n\nE\n\n.. \n\ni 100 \n\n[\n\n> 0\n\ni: \n\n> ~\n\n80 -Determi nants of blood pressure \n\nPulse pressure \n\nIncreases with i SV or \n\n! aortic compliance Diastolic blood pressure (DBP) Increases with i SVR or l arterial blood volume SV == s tr oke volume; SVR systemic vascular resistance. \n\nLaboratory evaluation of hypertension Choice of antihypertensive drug Renal function tests Endocrine tests Cardiac tests Other tests for comorbid conditions \n\n Serum electrolytes (Na, K, Ca) Serum creatinine Urinalysis Urine albumin/creatinine ratio (optional) \n\n## . Angina pectoris: 13 -blocker. CCB \n\nCoronary . Post-myocardial infarction: ACE inhibit or or ARB ,\n\natherosclerosis 13 -bloc ker \n\nHeart failure \n\n Fasting glucose or hemoglobin A 1c . ACE inhibitor or ARB , 13-blocker, diuretic, \n\nwith reduced \n\n Lipid profile ejection fraction aldosterone antagonist TSH \n\nAtrial fibrillation \n\n ECG or flutter . 13-Blocker, nondihydropyridine CCB Echocardiography (optional) Complete blood count \n\nChronic kidney ACE inhibitor or ARB .disease \n\n Uric acid (optional) Gout . Losartan , other ARB , CCB (avoid diuretics) \n\nOsteoporosis . Thiazide diuretic \n\nMi raine . 13 - Blo cker, CCB \n\nARB= ang iote ns in II re ce ptor blo ck er; CCB = cal ci um chann el blo ck er. \n\nJoint National Comm i ttee 8 recommenda ti ons for tr eating hypertens i on Initiate Rx Goa l bl ood pr ess ur eAg e 2::60 ~150 mm Hg systolic BP or <150/90 mm Hg >90 mm Hg diastolic BP \n\nAg e <60 ,ch ronic ki dn ey ~140 mm Hg systolic BP or <140/90 mm Hg \n\ndi se as e, >90 mm Hg diastolic BP \n\ndi ab etes \n\nTh iazide diuretic or CC B, Black alone or in combina ti on (ACEI/ARB, not fi rst- li ne) \n\nIni t ia l t re atm en t Other ethn icities Thiazide di uretic, AC EI , ARB, or CCB , \n\nchoice al on e or in combi na ti on All ethn ici ti es with AC EI or ARB, chronic kidney disease alone or in combi na tion wi th other drug classes \n\nACEI =ACE inhibitor; ARB = angiotensin II receptor blocker; B P= blood pressure; CC B =calcium channel blocker. CVS Renovascular HTN is common cause of secondary HTN in peds patients, dx using Renal USG with Doppler \n\nT/t : CCB Renal Artery Stenting/ Angioplasty. \n\n Hyperparathyroidism is a cause of secondary hypertension and should be suspected in patients who have hypertension associated with hypercalcemia , renal stones , abdominal \n\npain , or neuropsychiatric symptoms. \n\n Hypertension can be induced by both hyperthyroidism (predominantly systolic \n\nhypertension ) and hypothyroidism (predominantly diastolic hypertension ). \n\nDistractor: Smoking cessation (not shown to significantly reduce blood pressure but should be recommended to reduce overall risk of cardivascular complications) \n\n ARBs provide the greatest reduction in LVH of all first-line antihypertensive agents \n\n131 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSecondary causes of hypertension Condition Clinical clues/features Renal parenchymal disease . Elevated creatinine level . Abnormal urinalysis (proteinuria, red blood cell casts) . Recurrent flash pulmonary edema \n\nRenovascular disease . Elevated creatinine le ve l (particularly with ACE inhibitor use) . Abdominal bruit \n\nPrimary hyperaldosteronism . Hypokalemia (spontaneous or thiazide induced) . Metabolic alkalosis \n\nObstructive sleep apnea . Daytime somnolence . Increased neck circumference \n\nPheochromocytoma . Paroxysmal hypertension & tachycardia . Headaches, palpitations, diaphoresis \n\nCushing syndrome . Cushingoid body habitus & proximal muscle atrophy . Hyperglycemia \n\nThyroid disease . Hyperthyroidism: anxiety, heat intolerance, weight loss, tachycardia . Hypothyroidism: fatigue , cold intolerance, weight gain, bradycardia \n\nPrimary hyperparathyroidism . Mild hypercalcemia symptoms (eg, constipation) \n\n## . Kidney stones \n\nCoarctation of the aorta . Upper extremity hypertension with brachial-femoral pulse delay (common) . Lateralizing hypertension (less common) \n\nLifestyle interventions for hypertension Modification Recommended plan Approximate !\n\nsystolic BP (mm Hg) \n\nDASH diet Diet high in fruits & vegetab le s & l ow in saturated & total fats 11 \n\nWeight loss Reduction of BMI to <25 kg/m 2 6 per 10-kg loss \n\nAerobic exercise 30 minutes/ day for 5+ days/week 7\n\nDietary sodium <1.5-2.3 g/ day (response varies) 5-8 \n\nAlcohol limitation S2 drinks/day in me n, S1 drink/day in women 5\n\nDASH = Dietary Appr oaches to Stop Hypertension . CVS What is the next step in management for a patient with extensive alcohol use and hypertension that is not well controlled on two medications? \n\nCounsel for reduction in alcohol intake \n\nwhile adding a third medication is a reasonable option, counseling to reduce alcohol intake should be attempted first \n\n What is the likely physiologic cause of isolated systolic hypertension in an elderly patient? \n\nIncreased stiffness of the arterial wall \n\nassociated with increased CV morbidity and mortality and should be managed in the same way as primary hypertension \n\n Isolated Systolic BP : \n\n1. Aortic Stiffening in old age 2. Aortic Valve insufficiency ( Aortic Regurgitation ) \n\n## Infective Endocarditis Oral meds in Urgency, IV drugs in emergency. \n\n132 https://t.me/usmleinnercircle \n\nHypertensive complications Hypertensive Severe hypertension (us ually ;>:180/120 mm Hg) with no \n\nurgency symptoms or acute end-organ damage Severe hypertension with acute, life -t hreatening, end-organ complications \n\nHypertensive Ma li gnant hypertension: Severe hypertension with retinal \n\nemergency hemorrhages, exudates , or papilledema \n\n Hypertensive encep halopathy: Severe hypertension with cerebral edema & non-localizing neurologic symptoms & signs \n\nComplications of infective endocarditis Infective endocarditis \n\n## . Congenital heart disease or prosthetic valve Valvular insufficiency - common cause of death . Previous endocarditis \n\nRisk factors Card iac Perivalvular abscess . lntravascular catheters Conduction abnormalities . Intravenous drug use Mycotic aneurysm . New regurgitant murmur \n\n## . Skin: Janeway lesions, Osler nodes Embolic stroke Physical examination . Roth spots (eyes), splinter hemorrhages (nails) Cerebral hemorrhage \n\nNeurologic Brain abscess . Splenomegaly \n\n## . Signs of embolic phenomenon Acute encephalopathy or meningoencephalitis . Hematuria/proteinuria (glomerulonephritis) \n\nDiagnostic testing . Positive blood cultures Renal infarction . TEE > TTE for detecting vegetation \n\nRenal Glomerulonephritis Drug-induced acute interstitial nephritis from therapy Treatment . Acute: Empiric treatment with vancomycin \n\n## . Subacut e: Treatment based on culture results Vertebral osteomyelitis TEE= transesophageal echocardiogram; TTE = transthoracic echocardiogram .\n\nMusculoskeletal Septic arthritis Musculoskeletal abscess \n\n> C> UWorid\n\nCVS Evaluation begins with blood cultures from 3 different venipuncture sites. First Culture \n\nthen Antibiotics \n\n Perivalvular abscess should be suspected with the development of conduction abnormalities in patients with infective endocarditis. \n\nPerivalvular abscess: extends into adjacent cardiac conduction tissues, leading to heart block \n\nWhat valve is most commonly involved? Aortic valve \n\n What is the common vascular phenomena seen in right-sided endocarditis (S. aureus IVDU )? \n\nSeptic pulmonary emboli \n\nmultiple nodular, peripheral opacities , often with cavitation seen on CT splinter hemorrhages, Janeway lesions not produced in right-sided \n\n Most Viridans group streptococci are highly susceptible to penicillin and should be treated with IV aqueous penicillin G (NOT ORAL) or IV ceftriaxone x 4 weeks (preferred) Oral antibiotics are generally not recommended as initial therapy in pt. With IE \n\nCeftriaxone is preferred due to daily dosing versus 4-6x per day for penicillin Roth Spots \n\n133 https://t.me/usmleinnercircle USMLE Inner Circle \n\nInfective en docardi ti s with intravenous drug use \n\n## . Inj ected pa rt icles cause microdama ge to ri gh t-s id ed Pa thogenesis valv es before be ing filtered out by the lungs . Microdamage facilitates bacterial a tt ac hm ent \n\n## . Increased risk with HIV \n\n## . Tr ic usp id valve most commonly affect ed \n\n## . Staphylococcus aureus is the most common organism \n\n## . Septic pulmonary emboli present in up to 75% of cases Cl inical features . Aud ibl e murmu r may be absen t in 50% of cases \n\n## . Few peripheral man ifestations \n\n(eg, sp lin ter hemorrhages, Janeway lesions) \n\n## . Heart failure uncommon Septic emboli CVS Overall, the risk of IE following dental procedures in patients with acquired valvular defects due to rheumatic fever is low , and antibiotic prophylaxis is not indicated. However, prophylaxis is \n\nindicated in patients with a history of IE. \n\n134 https://t.me/usmleinnercircle \n\nPrevention of infective endocarditis with antimicrobial prophylaxis* \n\n Gingival/apical tooth manipulation (amoxicillin} \n\nHigh-risk procedures Respiratory mucosa incision (amoxicillin) (Prophylaxis needed} Surgery on infected skin or muscle (vancomycin) GI or GU procedure in setting of active infection (ampicillin ) \n\nLow-risk procedures GI or GU endoscopy/procedure in absence of infection (No prophylaxis) Most vaginal/caesarian deliveries \"Indicated for high-ri sk patients ( eg , prosthetic heart val ve, previous infective endocarditis, certain congenital cyanotic heart diseases). \n\nGI =gastrointestinal; GU =ge nitourinary. \n\nHigh-risk conditions for infective endocarditis Common surgical indications in infectious endocarditis \n\n Prosthetic heart valve Acute heart failure (eg , aortic/mitral valve regurgitation) \n\n Previous infective endocarditis Extension of infection (eg , abscess , fistula, heart bloc k} \n\n Structural valve abnormality in transplanted heart Difficult-to-eradicate organism (eg , fungus, M DR pathogen )\n\n Unrepaired cyanotic congenital heart disease Persistent bacteremia on antibiotics \n\n Repaired congenital heart disease with residual defect Large vegetation/persistent septic emboli \n\nMDR = multidrug-resistant. \n\nInfective endocarditis-modified Duke criteria Major criteria \n\n Blood culture positive for typical microorganism (eg , Staphylococcus aureus, Enterococcus, \n\nviridans streptococci) Echocardiogram showing valvular vegetation \n\nMinor criteria \n\n Predisposing cardiac lesion \n\nDiagnostic criteria for Intravenous drug use IE Temperature >38 C (100.4 F) \n\n. Embolic phenomena Immunologic phenomena (eg , glomerulonephritis) Positive blood culture not meeting above criteria \n\nDefinite IE 2 major OR 1 major + 3 minor criteria \n\nPossible IE \n\n. 1 major + 1 minor OR 3 minor criteria \n\n. Fever (>90%) \n\n. Heart murmur (85%) \n\n. Petechiae (s50%) \n\nClinical findings Subungual splinter hemorrhages (<50%) \n\n(frequency) Osler nodes, Janeway lesions (<50%) Neurologic phenomena (embolic) (\"40%) \n\n Splenomegaly (s30%) \n\n Roth spots (retinal hemorrhage) (<5%) IE = infective endocarditis. CVS Gram-negative HACEK organisms can produce subacute endocarditis and are seen in patients with poor dental hygiene and/or periodontal infection .\n\nHaemophilus Aggregatibacter actinomycetemcomitans Cardiobacterium hominis \n\nEikenella corrodes \n\nKingella \n\n Rheumatoid factor: may be elevated in patients with infective endocarditis \n\nrheumatoid factor is a non-specific finding; don't let it throw you off the diagnosis if symptoms otherwise point to infective endocarditis! \n\n## Rheumatic Heart Disease \n\n What is the likely diagnosis in an immigrant with progressive dyspnea , orthopnea , palpitations , and an elevated left main bronchus on CXR? \n\nRheumatic heart disease \n\n135 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCulture-positive infective endocarditis \n\n## . Prosthetic valves \n\n## . lntravascular catheters \n\nStaphylococcus aureus Implanted devices (eg , pa cemaker/defibrillator) .. Intravenous drug users Viridans streptococci . Gingival manipulation \n\n## . Respiratory tract incision or biopsy \n\n## . Prosthetic valves \n\nStaphylococcus epidermidis . lntravascular catheters \n\n## . Implanted devices Enterococci . Nosocomial urinary tract infections \n\nStreptococcus gallolyticus . Colon carcinoma (formerly S bovis) . Inflammatory bowel disease Fungi . lmmunocompromised host \n\n## . lntravascular catheters (eg , Candida) Prolonged antibiotic therapy .\n\nNonbacterial thrombotic endocarditis \n\n## . Hypercoagulable state due primarily to underlying malignancy (80%) or SLE \n\nEtiology . Noninfectious thrombi form on healthy valve \n\n## . Usually asymptomatic until embolism to kidney, spleen , skin , extremities, or brain occurs \n\nManifestations . Uncommon: fever, leukocytosis, significant valve insufficiency (eg, murmur) \n\n## . Blood cultures: no growth \n\nDiagnosis . Echocardiography: small, mobile vegetations on aortic/mitral valves \n\n## . Evaluate for hypercoagulable state &/or malignancy \n\nTreatment Anticoagulation \n\nSLE = systemic lupus erythematosus. CVS mitral stenosis results in left atrial enlargement, predisposing to arrhythmia (palpitations) and elevation of the left main bronchus \n\nTreatment/prevention ?\n\nOral penicillin V to prevent ARF ARF should still be treated with long-acting IM benzathine pencillin G until adulthood Can acute rheumatic fever be prevented with treatment of Streptococcal pharyngitis (e.g. oral penicillin)? \n\nYes \n\nversus PSGN, which can occur with or without treatment 2 Major Jones criteria or 1 Major and 2 minor criteria Erythema Marginatum \n\n136 https://t.me/usmleinnercircle \n\nAcute rheumatic fever Epidemiology Peak incidence: Age 5-15 Twice as common in girls \n\n Joints (m igratory arthritis) ., (Carditis) \n\nMajor No du le s (subcutaneous) Erythe ma marginatum Sydenham chorea Clinical \n\nfeatures Fever Arthralgias \n\nMinor Elevated erythrocyte sedimentation rate/ C-reactive prote in Prolonged PR interval \n\nLate Mitral regurgitation/stenosis \n\nsequelae Prevention Penicillin for group A streptococcal \n\n(Streptococcus pyogenes) pharyngitis \n\n\n\n\n\nAntibiotic prophylaxis for secondary prevention of rheumatic fever Severity Duration of therapy following last attack \n\nUncomplicated rheumatic fever 5 years or until age 21* With carditis but no valvular disease 10 years or until age 21* With carditis & valvular disease 10 years or until age 40 **Whichever duration is longer. Intramuscular penicillin G benzathine every 3-4 weeks is preferred. CVS Cholesterol \n\n Cholesterol emboli may result in skin complications, such as livedo reticularis and blue toe syndrome. \n\n Treatment is supportive and involves statin therapy to prevent recurrent cholesterol embolism \n\n137 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSydenham chorea \n\n# . Preceding GAS infection \n\nPathophysiology Molecular mimicry between anti-GAS antibodies & neuronal antigens in basal ganglia .. Involuntary, jerky movements (worse while awake & with ac tion) \n\n# . Hypotonia \n\nClinical features . Emotional !ability, obsessive-compulsive behaviors \n\n# . Symptoms of acute rheumatic fever \n\n# . GAS testing: throat culture, ASO & anti-DNAse B titers \n\nEvaluation . Cardiac testing: echocardiography, ECG \n\n# . Chronic antibiotics ( eg , penicillin G) \n\nTreatment . Symptomatic (antidopaminergics (eg, haloperidol)) \n\n# . Spontaneous remission Prognosis . Recurrence common \n\n# . t Risk of rheumatic heart disease \n\nanti-ONAse = antideoxyribonuclease ; ASO = antistrepto ly sin O; GAS= group A Str ep toco ccus .\n\nCholesterol crystal embolism (atheroembolism) Risk Comor!Jid conditions (hypercholesterolemia, \n\nfactors hypertension, type 2 diabetes melli tus} Cardiac catheterization or vascular procedure \n\n Dermatologic (livedo reticularis , ulcers, gangrene, blue toe syndrome} Clinical Renal (acute or subacute ki dney injury} features Centr al nervous sys tem (stroke, amaurosis fugax} Ocular involvement (Hollenhorst plaques} \n\n Gastrointestinal (i nt estinal ischemia, pancreatitis} Laboratory findings o El evated se rum crea tinine , eosinophilia, \n\nhypocomplementemia \n\no Ur inalysis - typically beni gn with few cells or \n\nDiagnosis casts, may have eosinophiluria Sk in or renal biopsy \n\no Biconv ex , needle-sh aped clefts within occlud ed vessels \n\no Perivascular inflammation with eosi nophi ls CVS NBME question had 2+ proteinuria, Blood, RBC and granular casts in UA of Cholesterol emboli syndrome. \n\n ALL (40-75) diabetic patients should be started on statin therapy, regardless of other risk factors \n\n Hypercholesterolemia is commonly asymptomatic and increases risk for significant cardiovascular and cerebrovascular disease. Therapeutic options include dietary modifications , weight reduction , increased physical activity , and lipid- lowering pharmacotherapy .\n\n The normal Optimal range for LDL cholesterol levels is less than 100 mg/dL (BEWARE THEY MENTION NORMAL LEVEL <160 IN THEIR LAB VALUES SECTION BUT THEY WANT YOU TO KEEP IT BELOW 100 IN CMS FORMS) \n\nThose who develop rhabdomyolysis , a rare side effect of severe statin-induced myopathy, should \n\ndiscontinue statin use entirely .However, most muscle toxicity is mild (eg, myalgias) , and the majority of patients can tolerate a different statin . ( Prefer moderate intensity) Rosuvastatin (high intensity), Pravastatin , pitavastatin , and fluvastatin (moderate intensity) \n\n138 https://t.me/usmleinnercircle \n\nGuidelines for statin therapy I nd i ca tion Recommen de d th erap yClinically sig nificant A SCVD \n\n> Ac ute co ron ary sy ndrome Ag e,;75: High-intensity st atin St ab le angina Ag e >75: Mod er ate-intensi ty statin Art er ial r ev asc ularization ( eg , CABG) St roke, TIA, PAD LDL 2:190 mg /dl High-intensi ty statin\n> Age 40 -75 with diabetes 10-year ASCVD risk .e7 .5% :High-intensity statin 10-year ASCVD ri sk <7. 5% : Moderate-i nt en si ty statin\n> Estimated 10-year ASCVD risk 2: 7.5% Moderate- to high-int en sity statin*\n> (p oo led coho rt equations)\n\nCVS Aorta \n\nAortic Trauma \n\n What is the initial screening test for blunt aortic trauma ?\n\nChest X-ray \n\nshould be ruled out in patients with blunt deceleration trauma (MVA or fall from > 10 feet )\n\nconfirm via CT Scan or TTE \n\n139 https://t.me/usmleinnercircle USMLE Inner Circle \n\nTriglycerides General measures Specific measures \n\n# !\n\nTreatment of hypertriglyceridemia \n\nHypertriglycendemia \n\n# !Eva luate for secondary causes 1150-500 mg/d l >1 ,000 mgldl \n\n Lifestyle modifications Initial goal is pancreal.lt1s prevention \n\no Weig ht loss o Fibrates \n\no Moderate alcohol intake o Fish oi l \n\no Increased exercise o Abstinence from alcohol ... Known card10vascular disease or high risk \n\no StaM therapy \n\n# t On ce leve ls ssoo mg/dl \n\nTreatment of hypertriglyceridemia 150-499 mgldl 500-999 mg/dl \n\nLimit dietary sugar/tight glycemic control in diabetes Limit saturated fat Regular aerobic exercise \n\n Weight loss of 5%-10% of body weight \n\n Treat with statins based on ASCVD risk \n\n Abstain from alcohol . Limit alcohol intake \n\n0-3 acids if high risk of ASCVD . 0-3 acids or fibrates, depending on . ASCVD risk \n\n~1 ,000 mgldl \n\n Abstain from alcohol \n\n Fibrates to reduce pancreatitis risk ASCVD = atherosclerotic cardiovascular disease ; n-3 acids = omega-3 fatty acids. \n\nTriglyceride-induced pancreatitis Triglyceride levels (mg/ dl) <500: minimal risk 500-999: mild risk \n\nRisk \n\n 1,000-1,999: moderate risk ~2,000: high risk Other risk factors : pregnancy, alcoholism, obesity, uncontrolled diabetes \n\n Acute epigastric pain radiating to back \n\nClinical features Fever, nausea, vomiting Elevated serum lipase (>3 times upper limit of normal) Intravenous fluid hydration, pain control \n\nManagement Triglycerides ~500 mg/dl: consider insulin infusion \n\n Triglycerides >1,000 mg/dL or severe pancreatitis (eg, lactic acidosis, hypocalcemia): consider apheresis (therapeutic plasma exchange) CVS What is the most sensitive finding indicative of blunt aortic trauma ?\n\nMediastinal widening \n\ncommon symptoms include anxiety , tachycardia , and hypertension ;\n\nCXR may also show left-sided effusion due to hemothorax \n\n In hypotensive patients, systolic blood pressure is generally kept at <100 mm Hg to prevent \n\ninjury extension and rebleeding while awaiting emergent operative repair. \n\nAortic Dissection \n\n Involvement of the subclavian or iliac arteries can result in asymmetry of pulses or blood pressure (pulses and blood pressure are typically symmetric if these arterial branches are not involved). \n\n140 https://t.me/usmleinnercircle \n\nThorac ic aortic injury Normal chest x-ray Widened mediastinum: supi ne chest x- ray >8 cm; upright chest x- ray >6 cm \n\n(i) UWo20 mm Hg \n\n## . Hypertension usually present \n\n## . ECG: normal or nonspecific ST-segment & T-wave changes \n\nDiagnosis . Chest x-ray: mediastinal widening \n\n## . CT angiography or TEE for definitive diagnosis \n\n## . Pain co nt ro l (eg, morphine) \n\nTreatment . Intravenous beta blockers (eg, esmolol) \n\n## . Sodium nitroprusside (if SBP >120 mm Hg) \n\n## . Emergency surgical repair for ascending dissection s trongest overall risk factor. ** Hypotension on presentation suggests aortic rupture or ot h er complication (eg, cardiac tamponade, acute aortic regurgitation). \n\nSBP =systolic blood pressure; T EE =transesophageal echocardiography. CVS Aortic regurgitation may result in sudden onset worsening chest pain, hypotension, and pulmonary edema Cardiac tamponade can occur as a complication as well, but those patients with clear lung fields \n\n Chronic systemic hypertension is the most important predisposing risk factor for aortic dissection. \n\nMarfan is common cause for dissection in younger patients <40 (vs HTN >60 )\n\nPulse deficit or differential blood pressure (>20 mm Hg difference) in the upper extremities is noted in only 20%-30% of the patients and its absence should not be used to exclude the diagnosis. \n\n What is the work-up of a stable and unstable aortic dissection ?1) Initial: CXR ( mediastinal widening , tracheal deviation )2) Stable: CT angiography \n\n3) Unstable/contrast allergy/renal dysfunction : TEE (reveals intimal flap )\n\n141 https://t.me/usmleinnercircle USMLE Inner Circle \n\nComplications due to extension of acute aortic dissection \n\n# . Stroke (carotid artery) \n\n# . Horner syndrome (carotid sympathetic plexus) \n\n Acute aortic regurgitation (aortic rooUvalve) \n\n# . Myocardial ischemia/infarction (coronary artery ostia ) \n\nComplication Pericardia! effusion/tamponade (pericardium) .(involved structure) . Hemothorax (pleural cavity) \n\n# . Renal infarction (renal arteries) \n\n# . Intestinal ischemia (mesenteric arteries) \n\n# . Lower extremity paralysis (spinal arteries) \n\nDiagnostic approach for suspected aortic dissection Suspected aort ic dissectio n\n\nRisk factors (eg, Marfan syndrome, connective tissue disease, hypertension) Tearing chest/abdominal pain radiating to the back Perfusion deficit s (eg, pulse deficit, >20 mm Hg b l ood pressure difference between right & left arm, aortic regurgitation murmur) Chest x- r ay or ECG suggest ing other diagnoses? \n\nNo \n\nNormal serum creat ini ne \n\n& no contrast allergy No Yes Evaluate &\n\ntreat appropriately TEE preferred Im aging based on availa bili t y TEE UWorld Chest CT with contrast MR I (on ly if nonemergency \n\n& pat ie nt can lie st ill) CVS CXR shows widened mediastinum, aortic knob \n\n TEE noninvasive, performed at bedside \n\n CT Angiography : invasive, but best test for determining extent of dissection for surgery \n\nAortic Aneurysm \n\n AAA rupture usually occurs posteriorly into the retroperitoneum , which can delay the onset of hemodynamic instability (eg, 1 h of symptoms in a patient); \n\nhowever, rupture may occur anteriorly with direct leakage into the peritoneum and rapid onset of \n\nhemodynamic instability and shock \n\n142 https://t.me/usmleinnercircle \n\nAbdominal aortic aneurysm \n\n## . Advanced age (eg, >60) \n\nRisk factors . Smoking, male sex, hypertension \n\n## . His tory of atherosclerosis or CTD \n\n## . Mostly asymptomatic \n\n## . Rapid expansion \n\n> 0\n\nDull abdominal/back pain \n\nClinical presentation 0 Distal embolization \n\n## . Rupture \n\n> 0\n\nSudden, severe abdominal/back pain shock \n\n> 0\n\nUmbilical/flank hematoma \n\n## . Smoking cessation \n\nManagement . Elective repair for size >5.5 cm (asymptomatic) \n\n## . Urgent repa ir for symptomatic & HD stable patients \n\n## . Emergency repair for symptomatic & HD unstable patients \n\n> CTD\n\n=con nective tissue disease; HD =hemodynamically. CVS Other clues to the diagnosis of AAA include a pulsatile abdominal mass (present in slightly over half of patients) and prevertebral aortic calcification on plain x-ray, consistent with extensive atherosclerosis. \n\n What is the likely diagnosis in a male smoker with chest discomfort and the CXR findings below ?\n\nThoracic aortic aneurysm \n\nSuggestive findings include a widened mediastinum, increased aortic knob, and tracheal deviation Initial test: CXR \n\nBest confirmatory test: CT with contrast \n\n What is the imaging modality of choice for diagnosis and follow-up of abdominal aortic aneurysms ?\n\nAbdominal ultrasound \n\ncheap and does not require contrast (vs. CT and MRI) Ruptured AAA \n\n143 https://t.me/usmleinnercircle USMLE Inner Circle \n\nEvaluation of suspected unstable abdominal aortic aneurysm Symptoms suggesting unstable AAA \n\n abdominal/flank/groin pain pulsatile mass flank ecchymosis limb ischemia \n\nHemodynamically stable \n\nrYes \n\nI\n\nObt ain CT of abdomen Known AAA AAA identifi ed \n\nJYes Medical optimization \n\nand repair \n\nAAA \"' abdominal aonic aneurysm .\n\n0UWOrld \n\nExplore oth er diagnoses \n\nNo Yes \n\nObtain focused \n\na bdominal ultrasound \n\nAAA identified \n\nYes l\n\nEmergency \n\nrepair CVS The strongest predictors of abdominal aortic aneurysm rupture are large aneurysm diameter(> 5.5 cm) , rapid rate of expansion ( > 1 cm per year) , and current cigarette smoking .\n\n Active smoking is the strongest modifiable influence for AAA development and progression. \n\n What is the recommended screening protocol for abdominal aortic aneurysm ?\n\nOne-time abdominal ultrasound for male active or former smokers aged 65-75 years \n\n What abdominal aortic aneurysm repair complication results in progressive abdominal pain and bloody diarrhea ?\n\nBowel ischemia/infarction \n\ndue to inadequate perfusion after loss of IMA during aortic graft placement \n\n What are the most common peripheral artery aneurysms ?\n\nPopliteal (#1) and Femoral (#2) \n\nfrequently associated with abdominal aortic aneurysms \n\nCoarctation of Aorta \n\n Left ventricular hypertrophy (LVH) signs: \n\nhigh-voltage QRS complexes , lateral ST segment depression , lateral T wave inversion often presents a couple days after birth when the ductus arteriosus closes \n\n144 https://t.me/usmleinnercircle \n\n> Coarctat ion of the aorta\n> Etiology Congenital Acquired (rare) (eg, Takayasu arteritis) Upper body\n> oWell developed\n> oHypertension (headaches, epistaxis) Lower extremities Clini ca lfeatur es oUnderdeveloped\n> oClaudi cat ion Brachial-femoral pul se de lay Upper &lower extremity blood pressure differential Left interscapular s~stolic or continuous murmur ECG: Left ventricular hypertrophy Chest x-ray Diagnostic studies oInferior notching of the 3rd to 8th ribs\n> o\"3\" sign due to aortic indentation Echocardiography: Diagnostic confirmation\n> Treatment Balloon ang ioplasty stent placement Surgery\n\nCVS Increased LV afterload \n\n Continuous murmur at the back due to collaterals Patients with suspected severe aortic coarctation should immediately receive prostaglandin E1 to maintain patency of the DA .This allows blood from the pulmonary artery to supply the descending aorta (right-to-left shunting) , restoring distal perfusion. \n\nAortoiliac Occlusion (Leriche Syndrome) \n\nAortoiliac occlusion (Leriche syndrome ) is characterized by a triad of 1. bilateral hip , thigh , and buttock claudication ,2. impotence , and 3. symmetric atrophy of the bilateral lower extremities. \n\n## Carotid Artery \n\n145 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCoarctation of the aorta Pathology Thickening of tunica media of aortic arch Can be associated with Turner syndrome or bicuspid aortic valve \n\n j BP & strong pulses in upper extremities \n\n ! BP & weak pulses in lower extremities Neonates* (severe narrowing) o Heart failure (eg, poor feeding , diaphoresis) \n\nClinical features o Cardiogenic shock Children/adults (mild narrowing) o Lower extremity claudication o Palpable pulsations of intercostal vessels (collaterals) o Secondary hypertension (upper arms) \n\nComplications Aortic aneurysm, dissection & rupture Cerebral aneurysm & subarachnoid hemorrhage \n\nTreatment . Prostaglandin E1 for neonates with severe narrowing Surgical repair *After closure of ductus arteriosus. \n\nBP= blood pressure. Patent ductus Left common Aortic coarctation Closed ductus CVS Patients with stenosis <80% should receive periodic (eg, annual) carotid duplex \n\nsurveillance to detect any progression. \n\nCarotid Artery Dissection \n\n What is the likely diagnosis in a child that presents with hemiparesis and aphasia hours after falling down with an object in their mouth ?\n\ninternal carotid artery dissection or thrombus formation \n\n146 https://t.me/usmleinnercircle \n\n<50% \n\nNo benefit of CEA \n\nManagement of carotid atherosclerotic disease \n\n# l\n\nAsymptomatic )\n\n50-79% \n\nCEA typically not recommended-Intensive medical therapy Aspirin Stalin Blood pressure control +Evaluation for carotid revascularlzation lSymptomatic j\n\n# l j\n\n80-99% <50% 50-6 9% \n\nCEA No benefit CEA recommended recommended of CEA in select patients-\n\n\"Degree or stenos.s \n\nMay be recommended ., se lect pabents with low perioperat 1v e risk (eg, <3%). \n\n Men likely benefit from CEA, whereas women likely benefit from intensive medical therapy only \n\nCEA = carotid endarterectomy, TIA = IJ'8ns ient 1schemJC attad< .\n\nCarotid artery dissection \n\n# . Trauma; spontaneous occurrence Etiology Underlying contributors: HTN, smoking, CTD .. Unilateral head & neck pain, t ransient vision los s\n\n# . lpsilateral partial Horner syndrome \n\nClinical presentation 0 Ptosis & miosis without anhidrosis \n\n# . Signs of cerebral ischemia (eg, focal weakness) \n\nDiagnosis . Neurovascular imaging (eg, CT angiograp h y) \n\n# . T hrombolysis (if $4 5 hr after Smptam aosel) \n\nTreatment \n\n# l70-99% \n\nCEA recommended \n\nCuw ld \n\n# . Antiplatelet therapy (eg, aspirin) anticoagulation \n\nCTD;;; conne ct ive tissue disease; HTN :;;; hypertens ion. CVS What is the next best step in a young woman who runs a marathon and complains of neck pain, headache, right-sided weakness, and vision loss? She recently completed a marathon. CT scan is normal and duplex ultrasound shows absence of flow in the internal carotid artery .\n\nHeparin and oral anticoagulation for 3-6 mo. \n\nAlso can do with antiplatelet agents for 1 year Treatment should be initiated after an intracerebral hemorrhage has been ruled out .\n\n## MI \n\n Perioperative MI is common in patients undergoing noncardiac surgery; \n\nintraoperative hemorrhage requiring blood transfusion increases the risk (likely due to reduced oxygen delivery to the myocardium). Patients with perioperative MI often lack chest pain , possibly due to receipt of postoperative pain control (eg, morphine). \n\n147 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPenetrating or blunt posterior pharyngeal trauma Traumatic carotid injuries Mechanism Presentation Diagnosis \n\n Penetrati ng trauma Fall with obJect in mouth (eg, toothbr ush , pencil) Neck m an ipulation (eg , yoga , sports) Grad ua l--0nset hemiplegia Aphasia Neck pain \"T hu nd erclap\" headache CT or MR angiography \n\nInitial stabilization of acute ST-segment elevation Ml \n\n Supplemental oxygen (i f SaO 2 <90% or dyspnea) Aspi rin 3 25 mg P2Y12 in hibitor (eg, clopidogrel) Nitrates (sublingual) Beta blocker (unless hypotension , bradycardia, acute heart fa ilure, heart block) High-dose statin (eg, atorvastatin 80 mg) Anticoagulation (drug depends on planned revascu larization) Persistent pa in, hypertension, or heart failure \n\nIV nitroglycerin \n\n(not if hyootension, \n\nri ght ventricular infarct, or severe aortic stenosis is presen t) IPersistent severe pain \n\nIV morphine Repertusjon: \n\nUnstable si nus bradycardia \n\n## !\n\nIV atropine \n\n PCI within 90 min preferred T hr ombolysis (i f PCI not available within 120 min) Pulmonary edema \n\n## !\n\nIV furosemide \n\n(not if patient is hypotensive or \n\nhyoovolemic) \n\nIIV = intr ave nous ; Ml = myocard ial infarcbon ; PC. I = percutaneo us coronary interven ti on . C,UWortd \n\nInternal carotid Tearing in tunica int i ma results in arte ry dissecti on CVS What pharmaceutical treatment should be avoided in patients with MI that present with CHF or bradycardia ?\n\nBeta blockers \n\n What is the recommended reperfusion therapy for patients with NSTEMI that present within 12 hours of symptom onset but cannot undergo PCI ?\n\nFibrinolysis \n\nfibrinolysis is associated with higher rates of recurrent MI, intracranial hemorrhage, and mortality compared to PCI \n\n Percutaneous coronary intervention (PCI) is recommended for patients with acute STEMI within 12 hours of symptom onset and within 90 minutes from first medical contact to device time at a PCI-capable facility. \n\nor 120 minutes from first medical contact to device time at a non-PCI-capable facility (to allow time for transport). \n\n What is the most important factor for survival in a patient with an out-of-hospital sudden cardiac arrest ?\n\nElapsed time to effective resuscitation \n\ne.g. adequate bystander CPR , prompt rhythm analysis , and defibrillation in patients found to be in ventricular fibrillation \n\n What is the initial management for hypotension in a patient with a right ventricular MI that has low-normal JVP ?\n\nIV saline bolus ( Nitrates should be avoided ) \n\n148 https://t.me/usmleinnercircle \n\nAcute management of acute coronary syndrome (STEMI, NSTEMI, or unstable angina) \n\nNitrates . Rapid chest pain relief \n\n## . Caution with hypotension (eg, RV infarction) . Cardioselective (eg, metoprolol, atenolol) \n\nBeta blocker . Decreases myocardial 0 2 demand to limit infarct size \n\n## . Contraindicated in cardiogenic shock & bradycardia \n\nAntiplatelet therapy . Aspirin+ P2Y 12 inhibitor (eg, prasugrel, clopidogrel)* \n\n## . Reduces platelet activity Anticoagulation . Unfractionated heparin, bivalirudin, or enoxaparin \n\n## . Limits thrombus expansion \n\nStalin therapy . High potency (eg, atorvastatin, rosuvastatin) \n\n## . Stabilizes atherosclerotic plaque STEMI \n\n## . PCI <90 min f rom 1st medical contact \n\nCoronary reperfusion . Fibrinolytics (eg, alteplase) if PCI is unavailable NSTEMI or unstable angina \n\n## . Coronary angiography often within 24 hr \n\n> *In patients wi th NSTEMI or unstable angina, P2Y 12 inhibitor therapy is often held until after coronary angiography in case the atherosclerotic coronary anatomy indicates the need for co ronary artery bypass grafting. NSTEMI =non-ST-segment elevation myocardial infarction; PCI = percutaneous coronary intervention; RV= right ve ntricula r; STEMI = ST-segment elevation myocardial infarction.\n\nCVS RVMI often creates high sensitivity to intravascular volume depletion; hypotension with low JVP suggests inadequate RV preload \n\n Marked hypotension is a characteristic feature of RVMI AV Block because RCA supplies AV node, hence bradycardia \n\n149 https://t.me/usmleinnercircle USMLE Inner Circle \n\nMyocardial infarction location based on coronary vessel involvement Involved Blocked ECG leads involved myocardium vessel Anterior Ml LAD Some or all of leads V1-V6 \n\nInferior Ml RCA ST elevation in leads II , Ill & aVF orLCX LCX ST depression in leads V1-V3 \n\nPosterior Ml or RCA ST elevation in leads I & aVL (LCX) ST depression in leads I & aVL (RCA) \n\nLateral Ml LCX, ST elevation in leads I, aVL, V5 & V6 diagon al ST depression in leads II , Ill & aVF \n\nRight ventricle Ml \n\n(occu rs in of RCA ST elevation in leads V4-V6R inferior Ml) \n\nPosteroinferior ST-elevation myocardial infarction (STEMI) \n\nn~~ ~ ~I aV R V I V4 \n\nV I \n\nPathophysiology \n\nMost commonly due to RCA occlusion Less commonly due to LC x oc cl usion \n\nKey features \n\nST elevation in II, Ill, & aVF (inferior wall STEMI) ST depression in V1 & V2 (posterior wall STEMI) Reciprocal ST depression 2:1 AV block (every other P wave not conducted) AV = atrioventricular; LCx = le ft circu mflex artery; RCA = ri ght coronary artery uwo r ld CVS The failing RV becomes reliant on hydrostatic pressure to force blood through the pulmonary circulation and is highly sensitive to a reduction in preload \n\n Whenever inferior wall MI is suspected based on ischemic changes in the inferior ECG leads, RV involvement should be evaluated using a Right-sided precordial ECG , which is obtained via precordial lead placement in a mirror image on the right side of the chest. \n\nST-segment elevation in lead V4R is highly accurate in confirming RVMI. \n\n Use of NSAIDs increases the risk for Acute Coronary Syndrome and MI \n\nPost MI Complications \n\n150 https://t.me/usmleinnercircle \n\nComparison of left ventricular & right ventricular myocardial infarction Left ventricular Ml Right ventricular Ml Clinical features Pulmonary edema Clear lungs & JVD S3 & S4 Marked hypotension lschemic changes in anterior, lateral, Inferior ischemic changes \n\nECG findings or inferior leads ST-segment elevation in V 4 R Bradyarrhythmias \n\nHemodynamic findings t LV & RV preload t RV preload, ! LV preload \n\n t SVR t SVR Fluid restriction Fluid resuscitation \n\nManagement Preload & afterload reduction Avoid preload reduction Reperfusion therapy Reperfusion therapy \n\nJVD =jugular venous distension ; LV =left ventricular; Ml =myocardial infarction; RV= right ventricular; SVR =systemic vascular resistance. \n\nOptimal medical management following myocardial infarction Medication Indication Dual anti platelet therapy All patients (regardless of stent placement) (low-dose aspirin+ P2Y 12 inhibitor) Low-dose aspirin continued indefinitely P2Y 12 inhibitor continued for 12 months \n\nBeta blocker All patients, continued indefinitely (eg , metoprolol, carvedilol) Reduces myocardial oxygen demand, decreases arrhythmia risk & inhibits remodeling \n\nACE inhibitor or angiotensin II receptor All patients, continued indefinitely for reduced LVEF \n\nblocker Inhibits post-Ml remodeling \n\nHigh-intensity statin All patients, continued indefinitely (ie, atorvastatin, rosuvastatin) Stabilizes atherosclerotic plaque & reduces recurrent Ml \n\nMineralocorticoid antagonist Reduced LVEF with symptoms or comorbid DM (eg , spironolactone) Inhibits post-Ml remodeling \n\nDM =diabetes mellitus; LVEF =left ventricular ejection fraction; Ml =myocardial infarction. CVS What are the complications ?\n\nHeart failure, arrhythmias, mitral regurgitation (distortion of LV geometry results in papillary muscle dysfunction ), mural thrombus \n\n151 https://t.me/usmleinnercircle USMLE Inner Circle \n\nMechanical complications of acute myocardial infarction Complication Time course Involved coronary artery Clinical findings Echocardiography findings \n\n. Severe pulmonary edema, \n\nPapillary muscle Acute or within 3-5 respiratory distress \n\nrupture/ RCA . New early systolic murmur Severe MR dysfunction days . Hypotension/cardiogenic shock \n\n. Chest pain \n\nlnterventricular Acute or within 3-5 LAD (apical septal ) or RC A . New holosystolic murmur Left-to-right ventricular \n\nseptum rupture days (basal septal) . Hypotension/cardiogenic shunt shock \n\n## . Chest pain Within 5 days or up . Distant heart sounds Pericardia! effusion with \n\nFree wall rupture LAD to 2 weeks . Shock, rapid progression to tamponade cardiac arrest \n\n. Heart failure \n\nLeft ventricular Up to several Thin & dyskinetic LAD . Angina \n\naneurysm months . Ventricular arrhythmias myocardial wall ' 50 % occur within 5 days. \n\n' *Right heart catheterization shows step up in Oz concentration from right atrium to right ventricle. \n\nLAD = left anterior descending ; MR= mitral regurgitation ; RCA= ri ght coronary artery. \n\nLeft ventricular aneurysm Etiology . Scar tissue deposition following transmural Ml \n\n# . Several months following Ml \n\n# . Heart failure & angina \n\nClinical presentation Ventricular arrhythmia (eg, ventricular tachycardia) \n\n# . Systemic embolization ( eg, stroke) \n\n# . ECG : Persistent ST elevation , deep Q waves \n\nDiagnosis Echocardiograph: Thin and dyskinetic myocardial wall .\n\nMl = myocardial infarction. \n\nLeft ventricular aneurysm Pathophysiology \n\n Fibrous scarring of myocardial wall following transmural (ST-elevation) myocardial infarction Most commonly affects the LAD territory \n\nLAD = left anterior descending artery. \n\nKey features \n\n Deep Q waves & persistent ST elevation in leads corresponding with previous myocardial infarction UW orl dCVS What is the most common cause of sudden cardiac arrest in the immediate post-infarction period in patients with acute MI? \n\nRe-entrant ventricular arrhythmias (e.g. ventricular fibrillation) \n\n Middle-aged man with ST-elevation MI complicated by extensive anterolateral akinesis \n\nwho on day 5 of hospitalization develops bilateral lower extremity pain/paresthesias, cyanosis, hypotension, and weak upper extremity pulses with absent lower extremity pulses , most consistent with aortic embolism. \n\nAngina \n\n What is the likely diagnosis in a male with a history of SLE that presents with epigastric burning provoked by exertion and relieved by rest ?\n\nAtypical angina \n\n152 https://t.me/usmleinnercircle \n\n> LV dilation\n\nPost-myocardial infarction ACE inhibition \n\n> Infarct\n\nl ACE inhibitor \n\n~ Angiotensin II remodeling ~\n\n+ (over weeks to months) + \n\n> Reduced LV dilation Reduced contractile function More preserved contractile function LV= left ventricle U Wo rld\n\nClassification of angina \n\n Typical location (eg, substernal), quality & duration \n\nClassic . Provoked by exercise or emotional stress \n\n# . Relieved by rest or nitroglycerin \n\nAtypical . 2 of the 3 characteristics of classic angina \n\nNonanginal <2 of the 3 characteristics of classic angina CVS Propanolol is a -blocker that may exacerbate vasospasm in Vasospastic (Prinzmetal) angina. \n\n What two drugs/drug classes are used for dual anti-platelet therapy ?\n\naspirin and P2y12 receptor blockers (e.g. clopidogrel) \n\nuseful for treatment of acute coronary syndromes and prevention of coronary events after stent placement (Use for atleast 12 months )\n\n The Mediterranean diet is high in fresh fruits , vegetables , and legumes . It is proven to reduce cardiovascular morbidity and mortality in patients both with and without established coronary artery disease. \n\nCAD \n\n153 https://t.me/usmleinnercircle USMLE Inner Circle \n\nVasospastic angina Pa thogenes is Hyperreactivi ty of coron ary smooth muscle Young patients (age <50) Smok ing (minimal other CAD risk factors) \n\nCl in ica l pres en ta ti on Recurrent chest discomf ort \n\no Occurs at rest or during sleep \n\no Spcntaneous resolution S15 minutes \n\nDi agnosi s Ambulatory ECG: ST elevation Coronary angiography: No CAD \n\nTr ea tm ent , Ca lcium channel blocker (preventive) Sublingual nitroglycerin (aborti ve) \n\nTreatment of chronic stable angina Beta bl ockers , First-line t herap y\n\n ! Myocard i al contractility & heart rate \n\nNondihydropyridine CCBs . Al te rna tiv e to beta bloc k er \n\n. ! Myocard i al contract ility & heart rate Added to beta blocker when needed \n\nDihydropyridine CCBs Coronary artery vasod i lation ! Afte rl oad by systemic vasodilation \n\nNitrates Long-ac ti ng added for pers istent angina ! Preload by dilation of capacitance veins \n\nRanolazlne Alternative therapy for refractory angina ! Myocard ial calcium influx Pretest probability of coronary artery diseas eLow Asymptomatic people of all ages \n\n(< 10%) Atypical chest pain in women age <5 0\n\nIntermediate Atypical angina in men of all age s\n\n(20 %-80 %) Atypical angina m women age ;,50 \n\n Typical angina in women age 30-50 \n\nHig h Typical angina in men age ;, 40 \n\n(> 90 %) Typical angina in women age ;,60 CVS Patients with risk factors for coronary artery disease and new symptoms such as angina or \n\nexertional dyspnea should be assessed for the presence of obstructive coronary disease by means of a stress test .For patients with a normal resting ECG who are able to exercise, an exercise stress test is preferred. For those unable to exercise or with abnormal ECGs, a pharmacologic nuclear stress test is frequently used What is the recommended diagnostic test for patients with chest pain that have low-risk for CAD ?\n\nNo further testing for CAD. (explore other pathologies) a positive stress test in low-risk patients is likely to be a false positive \n\n What is the recommended diagnostic test for patients with chest pain that have high-risk for CAD ?\n\nCoronary angiography \n\n154 https://t.me/usmleinnercircle \n\nLow No additional diagnostic testing , UWorld Evaluation of chest pain Pretest probability of coronary artery disease Intermediate Able to exercise Yes No \n\nHi gh \n\nStart phannacologic \n\n> therapy for CA D\n\nPham1acologic stress I Expert evaluation ] imaging test \n\nNo \n\nExercise imaging test Coronary ang iography Positive Ev aluation of chest pain in the emergency depar tment \n\nSTEMI \n\n> Treat wi th\n\nemergency catherization or thrombolysis Foc used his tory &physical exami nat io n Assess vi tal signs \n\n Ob t ai n venous access Stable patient Unstable patient \n\n Obtain ECG & chest x-ray Stabilize hemoclynamics \n\n Administer aspirin if the \n\nrisk for aortic dissection \n\nis low \n\n> Check for underlying ca uses\n> ECG\n\nconsistent with ACS? \n\nNSTEMI \n\n> Treat with appropriate\n\nanticoagulation \n\n# T T A ssess fo r pulmonary embolism Check ca rdiac markers & risk stratify for ACS Assess for pericarditis Assess for aortic dis sec ti on CVS Aspirin: reduces the rate of myocardial infarction and overall mortality in patients with ACS \n\n What is the best initial test for chest pain ?\n\nECG \n\n What is the likely underlying etiology of chest pain for > 1 hour , unrelated to activity in a young patient with normal cardiac and pulmonary exam? \n\nEsophageal disease (e.g. GERD) \n\nfeatures suggestive of esophageal origin include episodes lasting > 1 hour, post-prandial symptoms, associated heartburn, and relief by anti-reflux therapy \n\n Pain radiation is a less reliable distinguishing factor. Pain fibers from the esophagus and heart (visceral afferents) overlap at multiple different spinal cord levels, where they converge with somatic nerves. Therefore, chest pain caused by esophageal or cardiac pathology can be referred to the arms , jaw , neck , and/or back .\n\n155 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDifferential diagnosis & features of chest pain \n\n# . Substernal Coronary artery Precipitated by exertion .disease . Relieved by rest or nitroglycerin \n\nPulmonary/pleuritic . Sharp/stabbing pain (pleuris y, pneumonia, Worse with inspiration pericarditis, PE) . Pericarditis: worse when lying flat Aortic Abrupt (maximal at onset ), severe \"tearing\" pain (dissection, . May radiate to back intramural hematoma) . Hypertensi on and/or inherited aortopat hy \n\n# . Substernal, may refer to neck \n\nEsophageal Associated with regurgitation \n\n# . Provoked by recumbent position \n\n# . Nonexertional, relieved by antacids \n\n# . Persistent pain \n\nChest wall/ musculoskeletal Worse with movement or change in position \n\n# . Often follows repetitive activity PE = pulmonary embolism. CVS In patients with suspected ACS who go on to have acute myocardial infarction, the initial ECG (ideally obtained within 10 min of emergency department arrival) is often normal or nondiagnostic. Regardless of cardiac biomarker (eg, troponin) levels, changes (eg, ST-segment elevation, depression) on subsequent ECGs can develop quickly and may significantly affect patient management. \n\nStress Test Atypical symptoms associated with MI are more common in women , the elderly , and diabetics .\n\n156 https://t.me/usmleinnercircle \n\nEvaluation of suspected acute coronary syndrome in the emergency department Initial assessment: \n\n ECG \n\n Tropon in ST elevation Ml or new LBBB Other ischemic changes or elevated troponin Negati ve findings Serial ECG and troponin \n\nUrgent reperfusion \n\n## !Positive \n\nAdm;t to , furtho, ~\n\nmanagement \n\nL BBB =left bundle branch block; Ml =myocardial infarction . \n\n UWOt1d \n\nI\n\n## lNegative \n\n## lNoninvasive stress test Relative frequency of selected Acute Coronary Syndrome \n\n~\n\n## ~ ------,-1 -v_ e _s _S_T_e _l_ e_ v_at-i o-n -,I I_ N_ o_S _T _ e-le _v_ a-ti _o_ n ~I \n\n# I I Ca,d;,c Lma,kora I\n\n\\ ST elevation Ml I... ,-N-o-n-_S_T_e _l --' e~\"\"\"a -~-io_ n_M _l _,1,....1-u \"'\" n-st_ a_ b_ le _a _n _g-in _a_,j \n\nFigure 3.2: Acute Coronary Syndromes Diagnosis Algorithm \n\nType of stress Mechanism Best for Exercise ECG test t HR Patients able lo reach \n\n t BP tHR ( tH R = 85% of 220 - age) \n\nPharmacologic stress Nonselective adenosi ne LBBB \n\ntest with adenosine or agonist Pacemaker \n\ndipyridamole Dilates coronary arteries Patients unable to reach without t HR or BP tHR \n\nDobutamine stress B-1 agonist Reactive airway disease \n\nechocardiography t HR BP , Patients unable to reach tHR \n\npresenti ng symptoms in acute coronary syndrome \n\nChest pain 80%-85% Dyspnea 70%-75% Na usea 40%-55% Vom iting 15%-20% Epigast ri c pain 10%-15% \n\nNot for \n\n LBBB Pacemaker \n\n, Patien ts unable to reach !HR Reactive airway disease \n\n Patien ts on dipyridamole or theophylline Tachyarrhythm ias CVS What classes of medications (3) should be held for 48 hours prior to cardiac stress testing ?\n\nbeta blockers, calcium channel blockers, and nitrates \n\nexception: continue these medications in patients with known CAD undergoing stress testing to assess the efficacy of anti-anginal medication \n\nPerfusion Test \n\n Technetium-99-labeled ( Tc-99m ) perfusion agents (sestamibi or tetrofosmin) have a half-life of 6 hours, passively diffuse into perfused myocardial cells, have minimal redistribution afterward, and can provide an assessment of both myocardial function and perfusion \n\nAny differences between rest and stress images can help identify ischemia. Patients with normal tracer uptake at both rest and exercise have a low likelihood of ischemia with an excellent prognosis and <1% annual risk of coronary artery disease (CAD). A decreased tracer uptake both at rest and with exercise (fixed defect ) indicates likely scar tissue with decreased perfusion and CAD. A decreased tracer uptake with stress but normal uptake at rest (reversible defect )indicates inducible ischemia and likely CAD . What is preferred treatment to prevent coronary artery disease in a patient with inducible ischemia ?\n\nAnti-platelet therapy (e.g. aspirin), B-Blocker and risk factor modification \n\n## Murmur & Valvular Defects \n\n157 https://t.me/usmleinnercircle USMLE Inner Circle \n\nMedications to wit hh old prior to cardiac str ess testi ng Hold for 48 hours Beta blo c kers , ca lci um channel blockers, nitrates Ho ld for 48 hours prior to Dipyridamole vasodila to r stress test Ho ld for 12 hours prior to Caffeine-containing food or drinks vasodila to r stress test Angiotensin-converting enzyme in hi bitor s, Continue angiotensin rece pto r blockers, digoxin, stat ins, diur eti cs \n\nReversible myocardial perfusion defect \n\nI_IF ll lE \n\nt.:.f-F \n\n# ' \\ *\n\n# \\, *\n\n# ' *\n\n# 'I ,., e I L\"\" T\n\n# ' 'BASE \n\nSTRfSSIRH C(G) \n\n# ;ue \";.E P l A.T \n\n# ,, , f 'I '1 1 n1 E: ><: :.E \n\nRfST_IRllC \n\n'I perfusion (I tracer uplake) during slress testing (top row) but not at rest (bottom row) CUWorld \n\nCVS Common innocent murmurs include the following: \n\nStill's murmur : systolic, vibratory , best heard over left lower sternal border , intensity when supine \n\nPulmonic flow murmur : systolic ejection , best heard over left upper sternal border , may radiate to axilla \n\nVenous hum: continuous , best heard over the supra- or infraclavicular area , intensity with neck rotation \n\n In peds world, if musical qualities to murmur dont worry thats benign you don't need to investigate it \n\n158 https://t.me/usmleinnercircle \n\n\n\n\n\nSplitting of 52 \n\nInspiration Expiration \n\nPathologic \n\nWde ned splitting A2 f' \n\nIWidened s pl itting A2 P2 f' \n\nDelayed P2 \n\n P ulmon ic ste nos is Pulmonary HTN \n\n ASD\", RBBB Or early A2 \n\n VSD \n\nf = Split is audibly discernible. \n\n> wdened splitting\n\nis fixed throughOut respi ratory cycle .Phys i ologic A2 P2 7f' \n\n~\n\nA2 P2 I I Pathologic Narrowed sp litting Paradoxical splitting Delayed A2 \n\n Aortic stenosis System ic HTN LBBB, HCM ASD = atrial septet defect; HC M = hypertrophic card]omyopathy; HTN = hypertension; LBBB : left bi.ndle-branch block; RBBB ,. right bundle-branch block; VSD : ventricular septal defect \n\n> C l.l'Ni:wld\n\nBenign vs pathologic murmurs Benign Pathologic \n\n# . Infants: poor weight gain, Asymptomatic respiratory distress, difficulty \n\n# . feeding \n\nHistory . Normal growth Older children: exertional fatigue, No significant family history .. chest pain, syncope \n\n# . Family history of SCD or CHO \n\n# . Early or midsystolic . Holosystolic or diastolic \n\n# . Musical or vibratory . Harsh \n\nMurmur characteristics* . Grade 1-2 intensity . Grade ;;,3 intensity \n\n# . Decreases or disappears with . Intensity persists with standing & standing & Valsalva maneuver** Valsalva maneuver Normal vital signs . Central cyanosis \n\nOther . Loud , fixed , or single S2 .. Normal S1 & S2 \n\nfindings Symmetric pulses . Weak femoral eulses \n\n# . Hepatomegaly .\n\nManagement . Reassurance . ECG & echocardiography *An y sing le pathologic feature warrants evaluation. \n\n> 0\n\nVenous hum is a benign murmur exception that increases with standing. \n\nCHO = co ngenital heart defect; SCD = sudden cardiac death .CVS What is the next step in management for an asymptomatic adult with an early diastolic murmur at the left sternal border that is best heard with expiration ?\n\nTransthoracic echocardiogram \n\ndiastolic and continuous murmurs are usually due to an underlying pathologic cause and their presence should prompt further evaluation \n\n What abnormal heart sound is often heard during the acute phase of myocardial infarction ?\n\nS4 (atrial gallop) \n\ndue to left ventricular stiffening and ischemia-induced myocardial dysfunction \n\n S4 : often referred to as \" ten-nes-see \" a sound, which corresponds to S4-S1-S2 S3: often referred to as \" ken-tuc-ky \" a sound, which corresponds to S1-S2-S3 \n\n159 https://t.me/usmleinnercircle USMLE Inner Circle \n\nExtra (gallop) heart sounds Featu res A ss oc iate d pathol ogy *\n\n Hea rd j ust after S2 Heart failure with reduced EF \n\nS3 Caused by reverberant sound as blood fills an enlarged LV High-output states ( eg , thyrotoxicosis) cavity du ring passive diastolic filling Mitral or aortic regurgitation Hea rd just before S 1 Concentric LV hypertrophy \n\nS4 Caused by blood striking a stiff LV wall during atr ial Restrictive ca rdiomyopathy contraction Acute myocardial infarc ti on s3 can be normal in children, young adults & duri ng pregnancy. S4 can be normal in the elde rl y ( eg , age >70 ). \n\nEF = ejection fraction; LV = left ventricular. \n\nNormal \n\n100 Aortic valve \n\n\"' opens :,: \n\nE \\.. Aorta \n\n~ 50 \n\n~\n\n'\" Mit ral .., valve 0\n\nJI closes m\n\n-- -- --;>- Left ven tncle T ime CVS Mitral Regurgitation \n\n What is the most common cause of mitral regurgitation in developed countries? \n\nMitral valve prolapse \n\nusually causes mild MR with a mid-systolic click and mid-to-late systolic murmur but can develop into severe MR with a holosystolic murmur on examination \n\n What are the ( 3) causes of acute mitral regurgitation post-MI? \n\nIschemic papillary muscle displacement (immediate )\n\nPapillary muscle rupture (days )\n\nLV aneurysm (days-weeks )Murmur max at max pressure gradient \n\n160 https://t.me/usmleinnercircle \n\n> 150\n\nci \n\n> J:\n> E\n> .5. 100\n\n## I[\n\n> 'C\n> 0\n\n-2 50 \n\n> ID\n> <0 UWorld\n\n~\n\n> E\n\ng\n\ne \n\n> 100\n> ~50\n\n[\n\n> 'C\n> 00\n\niii \n\n\n\n\n\nAortic regurgitation \n\n> Time\n\nMi tr a! regu rg itati on \n\n> Time Aorta Left atrium\n> Left ventricle\n> 150\n\nci \n\n> J:\n> E\n> .5. 100\n\n## I[\n\n> 'C\n> 0\n\n-2 50 \n\n> ID\n> UWorld\n> 100\n\n~\n\n> E\n\ng\n\ne \n\n> :50\n\n[\n\n> 'C\n> 00\n\niii \n\nAortic stenosis \n\n> Time\n\nMi tra! stenosis Hemodynamic changes in mitral regurgitation Acute MR Compensated Decompensated chronic MR chronic MR Preload it t t\n\nAfterload t No change t\n\nContractile function No change No change t\n\nEjection fraction it t t\n\nForward stroke volume t No change t\n\nMR = mitr al regurgitatio n. Aorta Left atrium CVS Mitral Stenosis \n\n What is the likely diagnosis in a young patient from a developing country that presents with dyspnea ,\n\nhemoptysis , and occasional palpitations ?\n\nMitral stenosis (from rheumatic heart disease) \n\nAortic Regurgitation \n\n AR murmur due to Root Dilation : RUSB \n\n AR murmur (vulvur) : Left Sternal Border \n\n Prominent capillary pulsations in the fingertips or nail beds can be seen with aortic regurgitation (AR) as a result of widened pulse pressure. Left lateral decubitus position brings the enlarged LV closer to the chest wall, increasing awareness of the heartbeat (Pounding Heart) \n\n161 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSurgical indications for severe chronic mitral valve regurgitation \n\n## . Surgery if LVEF 30%-60% (r ega rdl ess of sy mptoms }\n\n## . Consider surgery if successful valve repair* is highly likely: \n\nPrimary MR A symptomatic & LVEF >60% 00 Symptomatic & LVEF <30% \n\nSecondary MR . Medical management , valve surgery rarely indicated *When possible, durable valve repair is favored over replacement because replacement necessitates lifelong anticoagulation & re peat re pla cement is often ne eded after -10 yr. \n\nLVEF = left ventricular ejection fraction ; MR = mitral regurgitation. \n\n## .Etiology ..Clinical presentation ...Diagnosis .\n\nTreatment .\n\nMitral stenosis in adults Rheumatic heart disease (vast majority of cases) Age-related calcification, radiation induced Exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, hemoptysis Pulmonary edema right-sided heart failure (eg, lower extremity edema) Atrial fibrillation , j risk for s ystemic embolization Opening snap with middiastolic rumble at the apex Echocardiography: f transmitral flow velocity Percutaneous valvotomy or surgical repair/replacement Clinical features Phys ica lexamination Mitral stenosis Dyspnea , orthopnea, PNO, hemoptysis Atrial fibrillation , system ic thromboembolism Voice hoarseness from recurrent laryngeal nerve comp ress ion due to LAE (Ortn er syndrome) Mitral f ac i es (pi nk ish-purple patches on cheeks) Loud 51 , loud P2 rf pulmonary hypertension Opening snap (h igh-frequency ea rl y diastolic sou nd) Mid-diastolic rumble (best heard at cardiac apex) CXR: Pu lm onary blood flow redi st ri bution to up per lobes, dilated pulmonary vessels , LAE, fl attened left heart bo rde rDiagnosis ECG : \"P mitrale\" (broad & notched P waves), atrial \n\ntachyarrllythmias, RVH (tall R waves in V1 & V2) TTE : MV thickening/calcification/ ! mobility, coexisting MR \n\nChronic aortic regurgitation \n\n# . Congenital bicuspid aortic valve \n\nCommon etiologies . Postinflammatory (eg, rheumatic heart disease, endocarditis) \n\n Aortic root dilation (eg , Marian s :i: ndrome , syphilis) \n\n# . Backflow from aorta into LV -> j LV end-diastolic volume \n\nPathophysiology . LV initially compensates with eccentric hypertrophy --+ i SV & CO \n\n# . Eventual LV dysfunction --+ t SV & CO --+ heart failure \n\n# . Decrescendo diastolic murmur \n\nClinical Widened pulse pressure (i SBP & LDBP) \n\nfindings . Rapid rise-rapid fall (\"water-hammer\") pulsation \n\n Abrupt carotid distension & collapse, \"pistol-shot\" femoral pulses \n\nCO = cardiac output; DBP =diastolic blood pressure; LV =left ventricle ; SBP =systolic blood pressure; SV =stroke volume .CVS What is the likely underlying cause of an early decrescendo diastolic murmur in a young patient in the U.S. with a family history of heart disease? \n\nCongenital bicuspid aortic valve \n\nthe murmur is typically best heard while the patient is sitting up , leaning forward , and holding a breath in full expiration \n\n What is the likely underlying cause of a harsh systolic murmur (right second intercostal space) with radiation to the carotid arteries in a young patient in the U.S.? \n\nBicuspid aortic valve \n\nbicuspid aortic valve is the cause of aortic stenosis in the majority of patients under 70 years old In young patients, it can lead to Aortic Regurgitation and in older patients can lead to aortic stenosis \n\nAortic Stenosis \n\n What is the likely diagnosis in a young patient with exertional chest pain , a systolic murmur at the first right intercostal space, and a palpable thrill in the suprasternal notch? \n\nSupravalvular aortic stenosis \n\nUsually refers to congenital LV outflow tract obstruction; LV hypertrophy develops overtime and increased myocardial O2 demand causing exertional angina. Can be associated with Williams Syndrome (hypersociability, elfin facies) \n\nOther findings :\n\nSuprasternal notch thrills Right arm > left arm BP (high pressure jet in ascending aorta ), \n\nUnequal carotid pulses \n\nCan also have coronary artery stenosis as an associated anomaly. Causes a systolic murmur similar to that seen with valvular AS; however, the murmur is usually best heard at the first right intercostal space , higher than where the valvular AS murmur is best heard. \n\n162 https://t.me/usmleinnercircle \n\n\n\n\n\nDiscrete supravalvar aortic stenosis in a patient with Williams syndrome . This catheter CVS Atenolol is a cardioselective -adrenergic blocker. It may exacerbate symptoms of heart failure in patients with aortic stenosis by reducing ejection fraction. Physical examination findings suggestive of severe AS include: diminished and delayed carotid pulses (\" pulsus parvus et tardus \") \n\nlate-peaking , crescendo-decrescendo systolic murmur \n\nsoft and single S2 during inspiration \n\n D/D: Angina d/t CAD but first rule out AS in old patients with Echo .\n\nTreadmill Test is C/I for Severe AS \n\n163 https://t.me/usmleinnercircle USMLE Inner Circle \n\nAortic stenosis \n\n# . Calcific disease (most common, age >70) Causes . Congenital bicuspid valve (younger patients) . Rheumatic heart disease (common worldwide but rare in developed cou ntries) . Dyspnea on exertion , decreased exercise tolera nce \n\nCl ini ca l Angina pectoris (severe AS) manifestation s . Syncope (severe AS) \n\n# . Heart failure (severe AS) . Crescendo-decrescendo systolic murmur best heard at RUSB wi th radiation to carotids &\n\nPhysical axillae examina ti on . Slow-risi ng (delayed) & weak carotid pulse \n\nManagement Aortic valve replacement for severe AS causi ng symptoms or LV systolic dysfunction AS = aortic stenosis ; LV = left ventricula r; RUSB = right upper sternal bor der .\n\nValve replacement in aortic stenosis \n\n Ao rtic jet velocity 1'4.0 m/sec, or Severe AS c ri teria . Mean tra nsvalvu l ar pressure gradient 1'40 mm Hg \n\n Valve ar ea usually :S1 .0 cm 2 but not required Severe A S & 1'1 of the following: . Onset of symptoms (eg, angina, syncope) \n\nInd ications for valve replacement L eft ve nt ricul ar ejection fraction <50% .. Undergoing other cardiac surgery (eg, CAB G) AS = aortic stenos is; CABG = coronary artery bypass grafting .\n\n\n\nPhysical examination features of LVOT obstruction due to aortic stenosis & hypertrophic cardiomyopathy \n\nAort ic stenosis Hy pert r ophic cardiomyopath yDecreased preload* ! Murmur intensity T Murmur intensity \n\n(eg , Valsalva strain phase) Increased afterload (eg, handgrip) ! Murmur intensity ! Murmur intensity \n\n54 Often present Often present Ejection click* Usually present Absent Carotid pulses* Soft & delayed Brisk *Distinguishing feature. LV OT = left ventricular outflow tract. CVS Complications :1. AR 2. Stroke (due to embolization of native valve calcification) \n\nPulmonary Regurgitation Pulmonary Stenosis \n\n## ECG Tracings For severe Aortic Stenosis \n\n164 https://t.me/usmleinnercircle \n\nPositioning \n\nEtiologies \n\n\n\nPa thophy siology ..Clin ic al fi ndings ...Treatment .\n\nTr anscat h eter aortic val ve i mplan tat ion \n\nExpansion & placement Function Chronic pulmonic regurgitation \n\nCorrection of pulmonic stenosis or RVOT obstruction (iatrogenic)* Rheumatic heart disease, infective endocarditis Progressive RV vo lume overload __. RV dilation & eventual failure Decrescendo, diastolic murmur at L SB , j with inspiration Soft (or sometimes absent) P2 Dyspnea & prominent parasternal impulse (once RV dilation develops) Serial echocardiography Valve replacement once symptoms or RV dysfunction develops \n\n* Mo st co mmon ca use of severe pulm on ic regurgitati on. LSB =left sternal border, RV =right ventric ul ar, RVOT =right ventricular outflow trac t. \n\nPulmonic valve stenosis Etiology . Congenital (usually i so lated defect) \n\n## . Rarely acquired (eg, carcinoid) \n\n# . Severe: Right-sided heart failure in childhood \n\nClinical presentation . Mild: Symptoms (eg, dyspnea) in early adulth oo d\n\n# . Crescendo-decres ce ndo murmur (i on inspiration) \n\n## . Systo li c ejection click & widened split of S2 \n\nDiagnosis . Echocardio gr aphy \n\nTreatment . Percutaneous balloon valvulotomy (preferred) \n\n# . Surgi ca l repair in some cases CVS PSVT \n\n Paroxymal supraventricular tachycardia ( PSVT ) is a type of arrhythmia arising from a defect in the atrioventricular conduction that causes the heart to sporadically beat faster .\n\nAVNRT = dysfunctional AV node that contains two electrical pathways --> leads to circulating electrical impulses \n\nAVRT = tachy caused by accessory pathway between atria and ventricles (WPW) Atrial tachy = atria respond to impulses from outside of SA node \n\nAFib and Aflutter = types of supraventricular tachy \n\n165 https://t.me/usmleinnercircle USMLE Inner Circle \n\nV5 AV nodal re-entry tachycardia (AVNRT) Atrial flutter \n\n.. / iOOllatioo {'\"\"'tiple at,ial wa,e lots) \n\n## - ~ ~(f' ~ Alria l lachyca 150 \n\n166 https://t.me/usmleinnercircle \n\nAtrioventricular nodal reentrant tachycardia Pathophysiology \n\n Dual AV node conduction pathways (fast & slow) creating a reentrant circuit Triggered by a premature atrial contraction \n\nConditions associated with atrial fibrillation \n\n Hypertensive heart disease (most common) Coronary artery disease RheumaticN alvular heart disease (eg, mitral stenosis, mitral regurgitation) \n\nCardiac Congestive heart failure Hypertrophic cardiomyopalhy Congenital heart disease (eg, atrial septal defect) Post cardiac surgery Obstructive sleep apnea \n\nPulmonary Pulmonary embolism Chronic obstructive pulmonary disease Acute hypoxia (eg , pneumonia) Obesity \n\nMiscellaneous Endocrine (eg , hyperthyroidism, diabetes) Alcohol abuse Drugs (eg, amphetamines, cocaine, theophylline) \n\nKey features \n\n 120-180 bpm Regular R-R intervals P waves buried within the QRS complexes Narrow QRS complexes \n\nPharmacologic rate control of atrial fibrillation \n\nStart beta blocker or nondihydropyridine ccs \n\n(eg , verapam il, d il tiazem) IAdditional rate control needed? \n\nt\n\n Add another first-line drug of different class Consider digoxin in patients with HFrEF IAdequate rate control still not achieved? \n\nt\n\n Add amiodarone 0\n\n Consider other measures (eg, ablation procedure) No ndihydropyridine CCBs contraindicated in HFrEF \" Amiodarone relatively contraindica ted in COPD & other chronic lung disease \n\n> AV =at riov en tricula r; CCB\n\n= calcium channel blocker; COPD = chronic obstructive pulmonary disease; HFrEF = heart fa il ure with reduced ejection fraction. \n\n> @UWorld\n\nCVS Patients with new-onset AF should have TSH and free T4 levels measured. \n\n What is the initial therapy for patients with atrial fibrillation due to hyperthyroidism ?\n\nBeta blockers \n\nhelps control heart rate and hyperadrenergic symptoms; should be continued until the patient becomes euthyroid with thionamides, radioiodine, and/or surgery \n\n167 https://t.me/usmleinnercircle USMLE Inner Circle \n\nComorbidities that encourage atrial fibrillation . Advanced age . Systemic hypertension (1\"1..t '\"'1'..1-\"\"-) \n\nPrecipitants of atrial dilation &lor conduction . Mitral valve dysfunction . Left ventricular failure remodeling Coronary artery disease & related factors (eg, DM , smoking) .. Obesity & obstructive sleep apnea . Chronic hypoxic lung disease (eg , C OPD ). H :z:e erth :z: roidism \n\n# . Excessive alcohol use \n\n----\n\nTriggers of increased automaticity . Increased sympathetic tone \n\n0 Acute illness (eg, sepsis, PE, Ml) \n\n0 Cardiac surgery . Sympathomimetic drugs (eg, cocaine ) COPD = chronic obstructive pulmonary disease; DM = diabetes mellitus; Ml = myocardial infarction; PE = pulmonary embolism. \n\nLong-term management of atrial fibrillation Rate-control strategy* Rhythm-control strategy* \n\n# . Atrioventricular node blockade . Electrical cardioversion \n\n0 Beta blockers . Phamnacologic antiarrhythmics \n\n0 Nondihydropyridine CCBs 0 Flecainide , amiodarone \n\n0 Digox in . Radiofrequency ablation . Anticoagulation usually indicated . Anticoagulation often indicated *Clin ical ou tco mes for each strategy are roug hl y equivale nt. Choice of strategy is typically based on case pa rticulars (eg, dura ti on of atr ia l fibrill ati on ) & patient preferen ce. CCBs = ca l ci um cha nn el blocker s. CVS Valvular Atrial Fibrillation: Warfarin ; regardless of any score \n\nPAC \n\n Also known as a PAC or Atrial Premature Beat, these occur when part of the atria sends out a depolarisation wave a little too early. \n\nClues include: 1. The P wave of the PAC looks different from the other P waves, since it starts at a diff location in the atria 2. The P wave and subsequent QRS complex come earlier than would be expected. 3. The QRS and T wave are followed by a relative pause before the SA node repolarises and initiates a normal beat. Hence, the Normal, Short, Long pattern. \n\n What is the recommended management for a patient with a smoking/drinking history and atrial premature beats discovered on routine ECG (asymptomatic)? \n\nAvoid alcohol and tobacco \n\nthis is a benign arrhythmia that doesn't require treatment, however reversible risk factors should be avoided Oral Anticoagulation: Warfarin or Dabigatran , Rivaroxaban , Apixaban \n\n168 https://t.me/usmleinnercircle \n\nCHA 2DS 2-VASc score for thromboembolic risk in nonvalvular atrial fibrillation \n\n> Risk criteria Points\n\nC Congestive heart failure 1 \n\n> HHypertension\n\n1 \n\n> A2 Age ~75\n\n2 \n\n> DDiabetes mellitus\n\n1 \n\n> S2 Stroke or TIA\n\n2 \n\n> VVascular disease (eg, PAD, prior Ml)\n\n1A Age 65-74 1Sc Sex category female 1 \n\n> Maximum score 9\n\nTotal score Generalized stroke risk Antithrombotic therapy Male Female** \n\n0 0 Low None \n\n1 2 Moderate None or oral anticoagulant \n\n~2 ~3 High Oral anticoagulant *Patients are assigned to 1 of the 2 age categories. \n\n> **Different cutoffs are used for males &females. Female sex is considered a risk modifier that adds to the CHA2DS2-VASc score only if other nonsex risk factors are present (female patients cannot have a total score of 1). Ml = myocardial infarction; PAD = peripheral artery disease; TIA= transient ischemic attack.\n\nPremature atrial contractions (PACs) \n\nIrregul ar rhythm PAC CVS If symptomatic, beta-blockers may be helpful. \n\nMAT \n\n Multifocal atrial tachycardia (MAT) is a supraventricular tachyarrhythmia that likely occurs due to atrial conduction abnormalities triggered by disturbances such as right atrial enlargement , catecholamine \n\nsurge (eg, sepsis), or electrolyte imbalance . It is most commonly seen in elderly (age >70) patients with an acute exacerbation of underlying pulmonary disease. \n\nThe best treatment is appropriate management of the inciting disturbance ; the administration of \n\nbronchodilators , systemic corticosteroids , and supplemental oxygen/ventilatory support for patient's acute exacerbation of COPD can lead to resolution of the MAT. (Tachycardia itself is Asymptomatic) \n\nWPW \n\n Acute treatment of AF in patients with WPW is aimed at prompt control of ventricular response and termination of AF as follows: \n\nHemodynamically unstable patients require immediate electrical cardioversion \n\nFor stable patients, rhythm control with anti-arrhythmic drugs such as intravenous ibutilide or \n\nprocainamide is preferred Curative: Catheter radiofrequency ablation \n\n AV nodal blocking agents such as adenosine , beta blockers , CCB (especially verapamil), and \n\ndigoxin should not be used for AF in WPW \n\nmay promote conduction across the accessory pathway and lead to degeneration of AF into VF. \n\nVentricular \n\nPVC \n\n169 https://t.me/usmleinnercircle USMLE Inner Circle \n\nMultifocal atrial tachycardia \n\n# nII \n\nPathophysiology Key features \n\n Ectopic atrial foci driven by acute illness Atrial rate >100/min Most commonly seen in COPD exacerbation ~3 different P wave morphologies Irregular R-R intervals CVS The beat marked by the letter Y in this patient is a premature ventricular contraction (PVC), recognized by a wide QRS complex, opposite-facing T wave, and brief ensuing sinus pause (ie, delayed P wave). PVCs may result from increased ventricular automaticity leading to spontaneous ventricular depolarization. Occasional PVCs are normal and considered benign. \n\nWhen a PVC occurs, it interrupts diastolic filling of the left ventricle, resulting in decreased end-diastolic volume (EDV) compared to the previous normal beat ( beat X > Y ). The sinus pause that occurs after a PVC allows for longer-than-normal filling time before the next ventricular contraction (ie, prolonged ventricular diastole), which creates increased EDV at the time of the post-PVC beat (beat Z > X ). The greater-than-normal EDV causes a large-stroke volume ventricular ejection, which may be responsible for the palpitations that some patients experience with PVCs. \n\nMonomorphic Ventricular Tachycardia \n\n170 https://t.me/usmleinnercircle \n\nDuration of ventricular diastole prior to each beat yMonomorphic nonsustained ventricular tachycardia Identification 2:3 consecutive ventricular beats (wide QRS complex) \n\n Rate >100/min & duration <30 sec \n\n Heart failure with reduced ejection fraction \n\nPredisposing conditions . lschemic heart disease \n\n Other cardiomyopathy (eg, HCM) \n\n Serum electrolyte abnormalities (eg, t K, t Mg) \n\nPrecipitating factors Hypoxemia or acute myocardial ischemia \n\n Elevated sympathetic tone (eg, sepsis) \n\nManagement Address precipitating factors (eg, replace electrolytes ) \n\n Consider adding (or increasing dose of) beta blockade \n\n> HCM =\n\nhypertrophic cardiomyopathy. \n\nTypes of beats in monomorphic ventricular tachycardia Vent ri cula r beat Fus ion beat (rare) Capture beat (rare) \n\n> UWofld\n\nECG \n\n> morphology\n\n# A\n\n# ~\n\n# -4 \n\nPhys i ology Ventricles fully depola ri zed by ventricular impulse Upward transmissi on blocked by AV node P waves created by sinoatrial rhythm are obscured Ventricles depolarized partially by vent ri cular impulse & partially by sinoatrial impulse Preceding P wave usually visible (a rrow) Confirms the presence of 2 separate rhythms Ventricles fully depolarized by sinoatrial node impulse Preceding P wave usually visible (a rrow) \n\nMonomorphic nonsustained ventricular tachycardia Pathophysiology \n\n Underlying predisposing condition (eg , cardiomyopathy, ischemic disease) Precipitating factor (eg , hypokalemia , increased sympathetic drive) \n\nKey features \n\n ~3 ventricular beats (regular, wide-complex) Rate >100/min & duration <30 seconds Spontaneous return to baseline rhythm CVS Torsade de Pointes \n\n What is the first-line therapy for conscious and stable patients with torsades de pointes ?\n\nIV magnesium \n\nif patient is hemodynamically unstable, immediate defibrillation is indicated \n\n When possible, patients receiving intravenous haloperidol or other QT-prolonging medications, particularly individuals at increased risk for arrhythmia, should undergo ECG testing prior to administration . The medication must be withheld if the baseline-corrected QT interval is prolonged (eg, \n\n>450 msec ). Treatment for patients with prolonged QT intervals includes beta blocker therapy and pacemaker placement. \n\n171 https://t.me/usmleinnercircle USMLE Inner Circle \n\nMonomorphic ventricular tachycardia \n\n# nVl \n\nPathophysiology \n\n Aberrant conduction focus within the ventricles \n\nKey features \n\n 100-240 bpm Regular R-R intervals Typically seen with cardiomyopathy or ischemia P waves usually obscured by QRS complexes Wide QRS complexes (>120 ms/3 small boxes) Fusion beats may be occasionally seen \n\nTorsade de pointes (polymorphic ventricular tachycardia) \n\n# n\n\nPathophysiology \n\n Long QT interval creates a prolonged \"vulnerable period\" during which a PVC can trigger arrhythmia Ventricular depolarization varies in a cyclical fashion \n\nKey features \n\n Rate 200-250/min Wide QRS complexes with cyclical variation in morphology P waves obscured by QRS complexes Irregular R-R intervals \n\nPVC = premature ventricular contraction . UWorld \n\nCauses of QT prolongation \n\n Hypocalcemia \n\nElectrolyte derangements Hypokalemia Hypomagnesemia Antibiotics (eg, macrolide, fluoroquinolones) \n\nAcquired Psychotropics (eg , antipsychotics, TCAs , SSRls} \n\nMedication-induced Opioids (eg, methadone, oxycodone) Antiemetics (eg , ondansetron , granisetron) Antiarrhythmics (eg, quinidine, procainamide, flecainide , amiodarone, sotalol} \n\nInherited Jervell & Lange-Nielsen syndrome (autosomal recessive) Romano-Ward syndrome (autosomal dominant) CVS beta blockers limit extertional heart rate and shorten the QT interval; additional management should also include avoidance of electrolyte derangements, vigorous exercise, and medications that block K+ channels \n\nBradycardia \n\n What is the initial treatment for symptomatic sinus bradycardia ?\n\nIV atropine \n\nTachyarrythemia and Cardiac Arrest \n\n172 https://t.me/usmleinnercircle \n\nManagement of symptomatic sinus bradycardia \n\nPulse IV\n\n=intravenous: Ml =myocardial infarction. C,UWo< td \n\nSinus bradycardia \n\n~-------------------- ---------------------1 \n\n# n__ ---.,t,-- t tII \n\nPathophysiology \n\n Slow generation of impulses within the sinoatrial node Common causes include sick sinus syndrome & medication adverse effect \n\nKey features \n\n <60 bpm Regular rate and rhythm P wave precedes each QRS complex CVS Synchronized cardioversion \n\nUsed for all wide- or narrow-based tachyarrhythmias --unstable A-Fib, A-Flutter, atrial tachy, and SVT's \n\n173 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSinus Tachy ca rdia P waves usually before QRS complex Ventricular rate ~ 100 beats/ min P waves are usually upright in leads I, ll, a VF , V3-V6 Maximal heart rate in sinus tachycardia can be determined (beats/ min = 220 - age) Management of adult tachycardia with a pulse (ACLS guidelines) Sustained rapid tachyarrhythmia )\n\niNo \n\n+\n\n# l Airway management & supplemental 0 2 as needed Assess cardi ac rhythm l Seek underlying \n\nSinus tachycardia? -Yes -+ cause & treat I .....::: :::::::::::::::::::=::::::::.. .J \n\nNo \n\n+\n\nINo \n\n+\n\n\\l\\,ldened ORS complexes \n\n~ (>0. 12sec)? ~\n\nNo --------~ Yes \n\n+ +\n\niNo \n\n+\n\nLikely Afib or Aflutter Non-Afib SVT (eg , AVNRT) Afib with aberrancy, \n\nPreexcited Afib , or PMVT Likely monomorphic VT \n\n Rate control agents 2\n\n Vagal maneuvers &/or adenos1ne Expert consultation Rhythm-specific therapy' \n\n1 Hemodynamic Instability usually OCCU'S only with heart rate >150/min \n\n, Beta blocker or nondlhydropyridine caldllTl channel blocker \n\n, Rate control tor Afib with abe5 min) \n\n Absence of vital signs \n\n Advanced age History of cardiac disease .!:2 Chronic illnesses \n\n Persistent coma after CPR \n\n Need for intubation or vasopressors \n\n Pneumonia or renal failure after CPR \n\n Sepsis, cerebrovascular accident, or class Ill or IV heart failure \n\nCPR= cardiopulmonary resuscitation . \n\nAtrioventricular block Clinical presentation ECG features Management First degree Asymptomatic PR interval prolongation Observation Observation \n\nMobitz type I second Usually asymptomatic Progressive PR interval lengthening followed by dropped (rarely PPM \n\ndegree ORS complex placement) \n\nMobitz type II second Fatigue, lightheadedness, Constant PR interval with randomly dropped ORS PPM placement \n\ndegree syncope complexes \n\nThird degree (complete) Fatigue, lightheadedness, Complete dissociation of P waves & ORS complexes PPM placement syncope \n\nPPM = permanent pacemaker .First-degree atrioventricular (AV) block \n\n~~I ~--11 \n\n## n.,,_,.~~ ... .../~~ ........ -~~........,,~'--',,_,.~~.....,'--''\"~~~~........,~'--' .... ~~~-~~.....,'\"'~~~-~.....,~~ H\n\nPathophysiology \n\n Slowed conduction through the AV node Common causes include enhanced vagal tone and pharmacologic AV node blockade \n\nKey features \n\n Constant P-P intervals with P wave preceding each QRS Prolonged PR interval >0.2 sec (one large box) Regular rhythm with constant R-R interval CVS In type 1 , The block usually is located within the AV node , and causes include elevated vagal tone \n\n(eg, highly trained athletes), excessive pharmacologic AV nodal blockade (eg, beta blockers), \n\nischemia , and age-related degeneration of the conduction system \n\nT/t: Observation and correction of reversible causes \n\nComplete Heart Block \n\n What is the management in a stable patient with dizziness , weakness , and the ECG findings below ?\n\nComplete heart block should be managed with a temporary pacemaker \n\nManage with a temporary pacemaker while undergoing further evaluation to identify and correct reversible causes. Per AMBOSS, unstable patients should be given atropine .a permanent pacemaker is indicated if no reversible causes of heart block are found on further evaluation \n\n176 https://t.me/usmleinnercircle \n\nSecond-degree AV block :Distinguishing features of Mobitz type I & type II AV block \n\n> Mobi tz type\n\nI Mob itz type II \n\n> Level of block Usually AV node Below the level of AV node\n> {eg, bundle of His) Progressive prol'onged PR PR interval rema ins constant interval leads to a\n> ECG findings nooconducted P wave with intermittent\n> (\"group be .ating\") nonconducted P waves QRS comple,c Narrow arrow or wide\n> Exerc ise or Improves type I AV block Worsens\n\ntype 11 AV block \n\n> atropine\n> Vagal maneuvers Paradoxically improves\n\ntype II (carot id sinus Worsens type I AV block \n\n> massage)\n\nAV blook \n\n> Risk of complete\n\nLow risk Higher risk , indication for \n\n> heart block\n\npacemake Mobitz type I second degree AV block (Wenckebach) \n\n1---------------+-------I \n\nPathophysiology Key features \n\n Disrupted conducti on , usually within the AV node Constant P-P interval Causes include enhanced vagal tone, pharmacologic AV node blockade, ischemia, age-related conduction degenerati on Progressive PR interval lengthening followed by Slight progressive RR interval shortening Usually narrow QRS complexes \n\nThird degree (complete) AV block \n\nR1++fft Lf ft-LU..l p wave-QRS complex dissociation u I\n\n.. t i ; l ~ ---f - - - ~ -- - f -- - - - - f - -- - - -1 P waves (atrial rhythm) 1'i ii1 \n\n## fl.-..JL-JI-\"\\ II \n\n> UWorld\n\nI -- -- -- - - ~ - -- - -- -- f - -- -- --- ~ QRS complexes Uunctional escape rhythm) I II I I I I I I I I ~CVS Sudden onset results in asystole , which may lead to Stokes-Adams Attacks ( sudden loss of consciousness )\n\nSick Sinus Syndrome \n\n## Heart Failure \n\nSystolic failure \n\n ICD placement is recommended in patients with symptomatic heart failure and LV ejection fraction 35% , regardless of MI history. \n\n177 https://t.me/usmleinnercircle USMLE Inner Circle \n\nEKG findings in complete AV block There is a complete failure of atrial impulses (p waves) to capture the ventricles (ORS) Unless an escape rhythm is initiated, ventricular asystole (syncope/death) will occur The escape rhythm (ORS) can be narrow uunctional escape) or wide (ventricular escape) The p waves have no relation to ORS complexes (complete AV dissociation) Ventricular rate is always slower than the atrial rate and is usually < 50 \n\nSick sinus syndrome \n\n# . Elderly patients . Bradycardia \n\nClinical features o Fatig ue , dyspnea, dizziness, syncope . Bradycardia-tachycardia syndrome \n\no Atrial arrhythmias (eg , atrial fibrillation) 0 Palpitations . Sinus bradycardia \n\nECG findings . Sinus pauses (delayed P waves) . Sinoatrial nodal exit block (dropped P waves) \n\n# . Pacemaker \n\nTreatment . +/- Rate-control medication (iftachyarrhythmias) \n\nClinical findings for heart failure Poor prognost ic factors in systolic heart failure Sensitivity Specificity Higher NYHA functional class Resting tachycardia \n\nDyspnea High Low Presence of S3 gallop \n\nClinical Elevated jugular venous pressure \n\nSerum BNP >100 pg/ml High Moderate Low blood pre ssure(< 100/60 mm H g) Moderate to severe mitral regurgitation \n\nLower extremity edema Moderate Moderate Low maximal oxygen consumpt ion (peak V0 2) Hyponatremia \n\nJugular venous distension Moderate Moderate Laboratory Elevated pro-B NP levels Renal insufficiency \n\nPulmonary crackles Moderate Moderate \n\nOrthopnea Moderate High \n\nElectrocardiography QRS duration >120 msec Left bundle branch block pattern Severe L V dysfunction \n\nAudible S3 Low High Echocardiography Concomitant diastolic dysfunction Reduced right ventricular function \n\nBNP = brain natriuretic pept i de . Pulmonary hypertension \n\nAssociated Anemia \n\nconditions Atrial fibrillation Diabetes mellitus CVS BNP level can be falsely low in patients with heart failure and obesity because BNP undergoes increased clearance by fat cells Chronic hyponatremia is common in patients with HFrEF; it parallels disease severity and is an \n\nindependent predictor of mortality . Patients with HFrEF and serum sodium <130 mEq/L have an estimated 1-year survival as low as 15%. \n\nIt likely results primarily from ongoing and profound nonosmotic stimulation for antidiuretic hormone secretion in the setting of reduced renal perfusion. \n\n Flash pulmonary edema is a form of acute decompensated heart failure in which acute increases in LV diastolic pressure cause accumulation in the pulmonary interstitium. Treatment? Furosemide \n\nIn acute decompensated heart failure, this is the most important intervention \n\n Treatment of acute pulmonary congestion: \n\nLMNOP (Lasix, morphine, nitrates, oxygen, upright position) Do not use if patient is hypotensive or hypovolemic \n\n Inotropes only in patients with cardiogenic shock (ie, severe hypotension causing end-organ dysfunction \n\n178 https://t.me/usmleinnercircle \n\nInitial management of acute decompensated heart failure \n\n> Recogn ize clln lcal presentation Dyspnea, orthopnea, S3, JVD , lung crackles, LE edema Diagnos ti c studies: chest x-ray, BNP\n\n# lEvaluate clin ical stab i lity Respiratory fai lure .... \n\n> supplemental 0 2 ,NIPPY, intubation Cardiogenic shock \n> inotropes (dobutamine, milrinone)\n\n# jImprove symptoms (reduce preload) Intravenous diuretics ( eg , furosemide) \n\n ven od il ator (eg, ni troglycer in ) Balanced vasodilator (eg, nitroprusside) if afterload red uction also needed \n\n# lInvestigate precipitating factors \n\n> E CG & troponln (ischemia, arrhythmia) Bedside echocardiogram (valvular dysfunction)\n> BNP\n\n= bra in na triu re tl c pep ti de ; JVD = j ugu lar veno us dist ens i on ; LE = lower extre mi ty ; NIPPV = non in vas i ve po si ti ve pr essu re ven til ati on . UWOfld CVS What is the initial management for a patient with pulmonary hypertension that presents with JVD , peripheral edema , bibasilar crackles , and an ejection fraction of 30% ?\n\nLoop diuretics and ACE inhibitors (or ARBs) \n\nthe pulmonary hypertension is due to LV systolic dysfunction and thus treatment involves addressing the underlying cause; \n\nbeta-blockers and occasionally aldosterone antagonists may be used as well \n\n Patients with slowly progressive decompensation may have minimal or no pulmonary edema .\n\nPulmonary lymphatics can gradually increase fluid outflow rate up to 10 times the baseline when needed, effectively offloading fluid from the pulmonary venous system to the central venous system and allowing evidence of elevated central venous pressure (eg, JVD, peripheral edema) to be present despite minimal or no pulmonary edema. \n\nDiastolic Failure \n\n179 https://t.me/usmleinnercircle USMLE Inner Circle \n\nClinical features of acute decompensated heart failure \n\n Acute dyspnea, orthopnea, paroxysmal nocturnal dyspnea Clinical Hype rt ension common; hypotension suggests severe disease Accessory muscle use, tachycardia, tachypnea presentation Diffuse crackles with possible w heezes (cardiac asthma) Possible S3, jugular venous distention, peripheral edema Norma l or elevated blood pressure with adequate end-organ perfusion Supplemental oxygen Intravenous loop diure ti c (eg, furosemide) Treatment Consider intravenous vasodilator (eg , nitroglycerin) Hypotension or signs of shock Suppleme nt al oxygen Intravenous loop diure ti c (eg, furosemide) as appropriate In trave nous vasopressor (eg, norepin ep hrine) \n\nHeart failure with preserved ejection fraction Causes of heart failure with preserved Etiology . LV diastolic dysfunction due to impaired relaxation left ventricular function \n\n# . Chronic hypertension (concentric LV hypertrophy) H ype rt ension with left ven tricu l ar Risk factors . Obesity & sedentary lifestyle (myocardial interstitial fibrosis) hypertrophy . CAD & related risk factors (eg, diabetes mellitus) . Specific therapies to reduce hoseitalization & eossibl J'.: mortali !r \n\n Restrictive cardiomyopa thy \n\nDiastolic heart Infiltrative cardiomyopathy failure (eg , sarco idosis) \n\n0 MRAs (eg , spironolactone) \n\n0 SGLT2 inhibitors (eg, dapagliflozin) Management . Loop diuretics as needed to treat volume overload H ype rtr oph ic cardiomyopathy Occ ult coronary art ery di sease . Additional antihypertensives PRN to reduce afterload . Treatment of exacerbating conditions (eg, CAD, OSA, A-fib) Valvular heart Aortic st enos is or regurgitation disease Mitral stenosis or regurgi ta tion . Exercise training/cardiac rehabilitation A-fib = atrial fibrillation; CAD = coronary artery disease; LV = left ventricular; Pericardia! Cons trictive pericarditis MRAs = mineralocorticoid antagonists; OSA = obstructive sleep apnea; PRN = as needed; disease Cardi ac tampo nade SGLT2 = sodium-glucose cotransporter 2. \n\nSystemic disorders Thyrotoxicosis (high-output Seve re an em ia cardiac conditions) CVS Cor Pulmonale High Output Heart Failure \n\n What is the likely diagnosis in a patient with a history of a stab wound that develops progressive weakness and exertional dyspnea with widened pulse pressure , tachycardia , and brisk carotid upstroke ?\n\nHigh-output heart failure (secondary to AV fistula formation) \n\n180 https://t.me/usmleinnercircle \n\nPhysical fitness and the risk of developing heart failure \n\nHeart failure \n\n# A\n\nwith reduced EF (HFrEF) Heart failure with preserved EF (HFpEF) Physical activity level & fat mass r ed uc ti on \n\nEF = e,ection fraction. \n\nCor pulmonale Pathophysiology . Right-sided heart failure due to primary pulmonary disorder \n\n Absence of left-sided heart disease \n\n## . Parenchymal disease/chronic hypoxia o COPD (most common) \n\nCommon o Cystic fibrosis \n\netiologies 0 Interstitial lung disease o Obstructive sleep apnea \n\n## . Pulmonary vascular disease: pulmonary embolism \n\n## . Dyspnea & fatigue on exertion \n\nSymptoms . Exertional angina (due to j cardiac demand) \n\n## . Exertional syncope (due to t cardiac output) Jugular venous distension \n\nExamination . Peripheral edema \n\n## . Palpable RV heave , loud P2, tricuspid re gurgitation murmur \n\n## . Hepatomegaly with pulsatile liver \n\n## . Electrocardiography \n\n> 0\n\nIncomplete/complete right bundle branch block \n\nDiagnostic 0 Right axis deviation, RV hypertrophy, RA enlargement \n\nevaluation . Echocardiography \n\n> C)UWo 0\n\nPulmonary hypertension, RV dilation/dysfunction, tricuspid regurgitation \n\n Catheterization (gold standard ) \n\n> 0\n\nElevated filling pressures, decreased cardiac output, pulmonary hypertension \n\nCOPD =chronic obstructive pulmonary disease ; RA =right atr i al ; RV =right ventricular. \n\nCommon mechanisms of high-output heart failure Increased quantity . Morbid obesity \n\nof peripheral vessels . Paget disease \n\nBypass of systemic Acquired AV fistula (eg , trauma , HD) \n\narteriolar resistance . Congenital AV malformation \n\nVasodilation due to unmet . Hyperthyroidism \n\nmetabolic demand in tissues . Severe anemia Thiamine deficiency (wet beriberi) \n\nAV = arteriovenous; HD = hemodialysis. CVS results in increased preload , decreased afterload , and increased cardiac output ;\n\nDoppler US is the preferred test for diagnosis and surgical therapy may be warranted \n\n## Cardiomyopathy \n\n What is the mainstay of therapy to improve/normalize heart function in patients with alcoholic cardiomyopathy ?\n\nAbstinence from alcohol \n\nalcoholic cardiomyopathy is suggested by CHF in the presence of heavy alcohol consumption, macrocytic anemia, >2:1 AST:ALT ratio, and no evidence of CAD/valvular defects \n\n What is the initial treatment for tachycardia-mediated cardiomyopathy ?\n\nRate or rhythm control \n\npresents with progressive dyspnea, decreased exercise tolerance, and LV systolic dysfunction \n\nsecondary to chronic tachycardia (e.g. chronic A-fib) An elevation in ventricular contraction rate (eg, >100/min) that is sustained for weeks or more can cause left ventricular dilation \n\n Peripartum cardiomyopathy typically causes rapid-onset systolic heart failure at last month of pregnancy or within 5 months following delivery \n\ne.g. fatigue, dyspnea, cough, pedal edema \n\nTakotsubo cardiomyopathy HOCM \n\n181 https://t.me/usmleinnercircle USMLE Inner Circle \n\nStress-induced (takotsubo) cardiomyopathy \n\n Postmenopausal woman \n\nRisk factors \n\n Recent physical or emotional stressor C hest pain mimicking myocardial infarction Decompensated heart failure \n\nClinical features \n\n Moderate troponin elevation ECG: ischemic changes in precordial leads Catheterization: no obstructive CAD \n\nDiagnosis Echo: LV apical hypokinesis, basilar hyperkinesis .\n\nTreatment Resolves in several weeks with supportive care \n\nCAD = coronary artery disease: LV = left ventricu lar. CVS S yncope in HOCM is multifactorial and can be due to outflow obstruction (interventricular septal hypertrophy), arrhythmia , ischemia , or a ventricular baroreceptor response that inappropriately causes vasodilation. \n\n182 https://t.me/usmleinnercircle \n\nNormal heart Hypertrophic cardiomyopathy \n\n Genetic mutations affecting cardiac sarcomere proteins \n\nPathophysiology Autosomal dominant inheritance Variable phenotypic penetrance Many patients are asymptomatic \n\n## . Exertional dyspnea, fatigue, angina, light-headedness, syncope \n\nClinical features Systolic ejection murmur accentuated by t LV blood volume Diastolic dysfunction with audible S4 \n\n## . j Risk for atrial fibrillation & ventricular tachycard ia \n\n## . ECG: left axis deviation, abnormalities of depolarization (eg , Q waves) or repolarization \n\nDiagnosis (eg, inverted T waves) \n\n## . Echocardiography: septal LV hypertrophy, dynamic LVOT obstruction, LA dilation Beta blocker or nondihydropyridine CCB (facilitate j LV blood volume) \n\nManagement Avoidance of dehydration & vasodilators (avoid t LV blood volume) \n\n## . ICD placement for increased risk for SCD Septal ablation, cardiac transplantation \n\nCCB =calcium channel blocker; ICD =implantable cardiac defibrillator; LA =left atrial; LV =left ventricular; LVOT =left ventricular outflow tract; SCD =sudden cardiac death. \n\nHypertrophlc cardiomyo pa thy Management of hypertrophic cardiomyopathy \n\nAsymptomatic ) ------------+ R o~~~~i~ ~t\n\n## l ~\n\nSymptomatic (e g, dyspnea, ang ina) Beta blocker or n ond ihydropyridi ne CC BRefractory symptoms High risk for SCD (eg, prior syncope or ---+ ICD placement }\n\nsustain ed VT, fa mily history) At ria l fibrillation } ------. \n\nSignificant LVOT obstruction \n\n_j Nonobstructi ve \n\n# ' ~-\n\nRate or rhythm control &antico ag ulation Septal ablation or su rgical myecotomy Cardiac transplantation CC B = calcium channel blocker, ICO = implantable cardiac defibrillator; LVOT = left ventricular outflow tract \n\n> SC D\n\n= sudden cardiac death: VT = ventricular tachycardia. CUWot1d CVS Additional ECG findings that can be seen include increased QRS voltage and J point elevation; \n\nisolated T-wave inversion in V1 is relatively common in the general population, including in athletes. \n\nvs T-wave inversions in 2 contiguous leads in HOCM. \n\n## Carditis \n\nAcute Pericarditis \n\n183 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDistinguishing hypertrophic cardiomyopathy from athlete's heart \n\nHypertrophic cardiomyopathy Athlete's heart Family Common Usually unremarkable history LVH criteria+ depolarization &/or repolarization LVH criteria without other ECG findings abnormalities* abnormalities Left atrial Enlarged Normal \n\nsize \n\nLV cavity Usually decreased Slightly enlarged \n\nsize \n\nLVwall ~15mm < 15mm \n\nthickness \n\nFocal septal Yes No hypertrophy \n\nLV diastolic Impaired Normal \n\nfunction \n\n*Common depolarization abnormalities include prominent Q waves; common repolarization abnormalities include T-wave inversions \n\nLV = left ventricular; LVH = left ventricular hypertrophy \n\nHypertrophic cardiomyopathy \n\n Left ventricular hypertrophy: Tall R wave in aVL + Deep S wave in V3 (Cornell criteria) Repolarization changes in anlerolaleral leads (I , aVL, V4 , VS , V6) \n\nI\n\nUWortd CVS Auscultation at the left sternal border typically indicates a triphasic pericardial friction rub (heard in atrial systole, ventricular systole, and early ventricular diastole). Initial ECG typically shows subtle (diffuse) PR depression and diffuse ST elevation that eventually evolves to diffuse T wave inversion \n\n What is the treatment of choice for peri-infarction pericarditis (Post infarction fibrinous pericarditis)? \n\nSupportive (best prevented by early coronary reperfusion therapy) \n\nNSAIDs are typically avoided (versus Dressler syndrome ) for at least 7 days due to a possible increased risk of free wall rupture. \n\nAnticoagulation should be avoided in Dressler syndrome to prevent development of hemorrhagic pericardial effusion. \n\n All patients suspected of having PIP should undergo echocardiography , which allows for characterization of any associated pericardial effusion and helps rule out other post-MI complications (eg, free wall rupture). Uremic pericarditis does not show typical ECG changes like ST-segment elevation (lack of inflammation invading the myocardium in uremic pericarditis) \n\n>50% of cases are accompanied by pericardial effusion ,\n\ncardiac tamponade should be ruled out prior to dialysis initiation. Corticosteroids (eg, prednisone) are used in patients with a contraindication to NSAIDs (eg, renal insufficiency) or failure of combination NSAID/colchicine therapy. \n\n184 https://t.me/usmleinnercircle \n\nAcute pericarditis \n\n## . Viral or id iopathic \n\n## . Autoimmune disease (eg, SLE) \n\n## . Uremia (acute or chronic renal failure )Etiology Post myocardial infarct ion . 0 Early: pe ri-infarction pericarditis \n\n> 0Late: Dressler syndrome\n\n# . Pleuritic chest pain(! when sitting) fever \n\n> Clinical features\n\n## . Pericardia! friction rub (highly specific) \n\n> &diagnosis\n\n## . ECG: diffuse ST-segment elevation & PR-segment depression \n\n## . Ec hoca rd iog raphy: pericardia! effusion Treatment . NSAIDs & colchicine for viral or idiopathic etiology . Variable for other etiologies \n\n> NSAIDs =non steroidal anti-inflamma tory drugs: SLE =systemic lupus erythematosus.\n\nCVS Young women with recent viral illness (sore throat, runny nose) who now presents with \n\npleuritic chest pain but otherwise normal exam and labs most consistent with a diagnosis of \n\nviral pleurisy \n\nPleurisy is basically analogous to a post-viral pericarditis, and therefore is also managed with an NSAID \n\nKey idea: Pleuritic chest pain > Pneumothorax , Pleurisy , Pericarditis , Pulmonary embolism \n\nKey idea: Recurrent ulcers + Pleurisy may also be pointing to a diagnosis of pleuritis in the setting of lupus \n\nConstrictive Pericarditis \n\n What is the most common causes of constrictive pericarditis in the United States? \n\nViral or idiopathic (>40%) \n\nother common causes include radiation therapy (30%), cardiac surgery (10%), uremia , and connective tissue disorders \n\nTuberculosis common in developing countries( India, China) \n\nTreatment: surgical removal of the stiff and fibrotic pericardium (ie, pericardiectomy ) to restore ventricular diastolic function. \n\nD/D: Cardiac Amyloidosis: May manifest as Restrictive Cardiomyopathy, LV is thicked and will not have pericardial calcification \n\nMyocarditis Pericardial knock (mid-diastolic sound); occurs due to filling ventricles hitting thickened pericardium \n\n185 https://t.me/usmleinnercircle USMLE Inner Circle \n\nFeatures of constrictive pericarditis \n\n## . Recurrent idiopathic or viral pericarditis \n\nEtiology . Cardiac surgery or radiation therapy \n\n## . Tuberculous pericardilis (where endemic) \n\n## . Fatigue, dyspnea on exertion . Peripheral edema, ascites, hepatic congestion ( ll>10 mm Hg during inspiration . ECG: low-voltage ORS complex, electrical alternans \n\nDiagnosis . Chest x-ray: enlarged cardiac silhouette , clear lungs . Echocardiography: right atrial & ventricular collapse, I VC plethora \n\n## . Intravenous fluids to increase right-sided preload \n\nTreatment . Drainage via pericardiocentesis or p ericardia! window subacute but not acute tamponade .IVC = infe ri or vena cava; JVD = j ugu lar venous di stension; LV = left ven tri cular; SBP = systo l ic bl ood pressure. Characteristics of cardiac tamponade Acute Subacute Rapidity of fluid accumulation \n\nMinutes to hours Days to weeks \n\nClinical signs Bec k triad: hypotension, JVD, muffled heart sounds Pulsus paradoxus (>10 mm Hg decrease in SBP with inspiration) \n\nEffusion volume 100-200 ml 1-2 L \n\nChest x-ray findings Normal cardi ac silhouette Enlarged, globular cardiac silhouette \n\nJVD = jugular venous distension ; SBP = systolic blood pressure .Purulent pericardia! effusion \n\n# . Hematogenous or direct intrathoracic spread \n\nEt iology . Risk factors: immunosuppression, hemodialysis, recent thoracic surgery/trauma \n\no Organisms: Staphylococcus aureus (most common), Streptococcus pneumoniae, Salmonella, Candida \n\nClinical Acute presentation, patients often appear severely ill . Fevers, chills, chest pain (pleuritic or nonpleuritic) \n\nfeatures . Can be rapidly fatal . ECG: tachycardia, diffuse ST-segment elevation, low-voltage ORS complexes \n\n# . CXR: enlarged cardiac silhouette & clear lung fields I' Diagnosis . Echocardiography : pericardia! effusion Cytology: turbid fluid with t WBCs (neutrophil predominant), t protein, ! glucose 1:\n\n# .\n\nTreatment . Intravenous antibiotics + pericardia! drainage \n\nCXR = chest x-ray; WBCs = white blood cells. CVS What is the likely diagnosis in a patient with an aortic dissection that develops hypotension , JVD ,and pulsus paradoxus ?\n\nCardiac tamponade \n\nElectrical alterans with sinus tachycardia is highly specific for large pericardial effusion, which may result in cardiac tamponade. \n\n188 https://t.me/usmleinnercircle \n\nMalignant pericardia! effusion Etiology . Common primary tumors: lung, breast, GI tract, lymphoma, melanoma \n\n## . May be initial manifestation of malignancy or recurrence . Progressive dyspnea , chest fullness, fatigue \n\nClinical . ECG: l QRS voltage electrical alternans \n\nfeatures . CXR: enlarged cardiac silhouette & clear lung fields . Echo: large effusion signs oftamponade (eg, right atrial collapse) \n\nTreatment . Acute management: pericardiocentesis, cytologic fluid analysis \n\n## . Prevention of recurrence : prolonged drainage (eg, catheter, pericardia! window) \n\nCXR =chest x-ray; echo =echocardiography; GI =gastrointestinal. \n\nElectrical alternans \n\n UWorld \n\n1 week ago Today \n\n UW011d CVS What is the likely diagnosis in a patient on post-op day 1 status-post CABG that presents with hypotension , tachycardia , and the findings below: \n\nRight atrium : 20 mmHg \n\nRight ventricle : 35/20 mmHg \n\nPCWP : 20 mmHg \n\nCardiac tamponade \n\nequilibrated intracardiac diastolic pressures suggests cardiac tamponade \n\n## Peripheral Vascular Diseases \n\n Patients with PAD and intermittent claudication have an estimated 20% 5-year risk of non-fatal MI and stoke and a 15-30% risk of death due to cardiovascular causes. \n\n What is the recommended pharmaceutical therapy to reduce overall cardiovascular mortality in patients with peripheral arterial disease ?\n\nAntiplatelet Agent (e.g. aspirin) and a Statin \n\nStatin recommended in all patients with ASCVD \n\n What is the best initial therapy for peripheral vascular disease? \n\nMost important: Stop smoking and exercise (promotes circulation )\n\nAspirin, cilostazol (Most effective) Appear on CXR as an enlarged and globular cardiac silhouette with clear lung fields \n\n189 https://t.me/usmleinnercircle USMLE Inner Circle \n\nAnkle-brachia! index \n\nABI ; SBP of dorsalis eedis or eosterior tibia l arte ~ + SBP of brachia! arterv \n\n~0 .9 Diagnostic of peripheral artery disease \n\n0.91-1 .3 Normal \n\n>1 .3 Suggests calcified & uncompressible vessels* *Other testing should be considered . \n\nABI = ankle-brachia! index; SBP = systolic blood pressure .CVS Percutaneous or surgical revascularization is generally reserved for patients who have persistent symptoms despite initial exercise and/or pharmacologic therapy. \n\nCilostazol can also be considered with persistent claudication. \n\n Smoking cessation is a first-line intervention for peripheral arterial disease. What is the most useful intervention to improve functional capacity and reduce symptomatic claudication in patients with peripheral artery disease? \n\nSupervised graded exercise program \n\n What is the likely diagnosis in a hypotensive patient requiring IV fluids /pressors to maintain BP that develops cool extremities and the skin findings below? \n\nPressor-induced vasospasm (e.g. norepinephrine) \n\ndiagnosis is suggested by symmetric duskiness and coolness of all finger tips \n\nCan also negatively impact the intestines \n\n(causing mesenteric ischemia ) and/or kidneys \n\n(causing renal failure ). \n\nVenous Insufficiency \n\n What is the most common cause of lower extremity edema ?\n\nVenous insufficiency (valvular incompetence) \n\nclassically worsens throughout the day and resolves overnight \n\n What is the initial treatment for chronic venous insufficiency ?\n\nConservation measures (e.g. leg elevation, exercise, compression therapy) \n\npatients who do not respond to conservative measures should have diagnosis of CVI confirmed by identification of venous reflux in the deep venous system on duplex ultrasound \n\n190 https://t.me/usmleinnercircle CVS Approximately 50% of patients with acute DVT develop postthrombotic syndrome within 2 years due to \n\nvenous hypertension distal to the site of previous thrombus. \n\nThis is thought to arise due to venous valve damage from the release of inflammatory mediators and venous lumen stenosis due to wall remodeling. \n\n D/D: Recurrent DVT : Do Venous Ultrasonography to rule it out first \n\nAcute Limb Ischemia Stasis Dermatitis \n\n191 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPostthrombotic syndrome \n\n Chronic venous insufficiency following acute \n\nEpidemiology DVT Most cases arise within 2 years of thrombus Leg edema , fatigue, pain , superficial venous \n\nManifestations dilation, venous stasis ulcers Often worse at the end of the day \n\nTreatment Exercise (eg, ankle flexion , walking) Compression (eg , bandages, stockings) \n\nDVT = deep vein thrombosis. CVS What is the initial management for a patient with suspected acute limb ischemia ?\n\nAnticoagulation (e.g. IV heparin) \n\nShould be initiated empirically, prior to further evaluation with other imaging studies \n\nDiagnostics : Arterial and venous Doppler confirmed with Angiography (digital subtraction angio is the modality of choice) \n\nTreatment :Non-threatened limb > angiography with revascularization .If limb is threatened, undergo emergent revascularization (catheter directed thrombosis is and/or thromboembolectomy) Non-viable = amputation \n\n Presence of gangrene requires amputation \n\n What imaging study should be considered in a patient with acute limb ischemia after an MI ?\n\nTransthoracic echocardiogram \n\nto screen for LV thrombus and evaluate LV function; patients also require immediate anticoagulation and vascular surgery consult \n\n In patients with PAD, atherosclerosis of peripheral arteries (eg, popliteal artery) may be complicated by \n\nplaque disruption .This can lead to thrombosis and acute-on-chronic limb ischemia \n\nDue to preexisting collateral circulation , acute limb ischemia in the setting of chronic peripheral artery disease (PAD) often presents less dramatically than in patients without PAD. \n\nEmergency intervention is still necessary. \n\n## Shock \n\nAnaphylactic \n\n192 https://t.me/usmleinnercircle \n\nAcute limb ischemia \n\n# . Cardiac/arterial embolus (eg, AF , LV thrombus, IE) \n\n> Etiology\n\n Arterial thrombosis (eg, PAD) Iatrogenic/blunt trauma \n\n> 6Ps of acute limb ischemia\n\n Pain \n\nClinical Pallor \n\n# . Paresthesia \n\n> features\n\n# . Pulselessness \n\n# . Poikilothermia (cool extremity) \n\n# . Paraly sis (late) \n\n# . Anticoagulation (eg, heparin) \n\n> Management Thrombolysis vs surgery\n\n# . \n\n> AF ;atrial fibrillation; IE ;in fective endocarditis; LV ;left ventricu la r; PAD ;peripheral artery disease.\n\nCVS At the time of discharge, all patients should be prescribed epinephrine auto-injector and instructions on how to use it. \n\n Hymenoptera Venom Immunotherapy is recommended for patients who have severe systemic reactions to bee stings to decrease the risk of future reactions. Anti-venom IgG antibodies, or \" blocking\" antibodies are created , and upon re-exposure, block the interaction between the allergen and preformed lgE antibodies on the surface of mast cells and basophils to prevent degranulation. IV epinephrine is indicated for patients with anaphylaxis who do not respond to initial IM epinephrine \n\n193 https://t.me/usmleinnercircle USMLE Inner Circle \n\nAnaphylaxis Diagnostic challenges in anaphylaxis \n\nTriggers Foo d (eg, nu ts, shellfish) Medications (eg, ~-lactam an tibiotics) Insect stings \n\nNonclassic . No prior allergic reactions (ie, first episode) \n\npresentation . Absence of hypotension, respiratory symptoms, or cutaneous signs \n\n## . Protracted or biphasic presentation Ca rd iovascul ar \n\no Vasod ilation - hypotension & tissue edema \n\no Tachycardia Respiratory \n\nChallenging . Preexisting conditions with similar symptoms (eg , asthma, COPD) \n\nclinical situations . Ongoing physiologic shifts (eg , childbirth, hemodialysis) \n\n## . Impaired communication (eg , sedation, severe psychiatric illness) Clinical manifestations o Upper aiiway edema - strider & hoarseness \n\no Bronchospasm - wheezing Cutaneous \n\nMedication . Directly activate mast cells (eg , opiates, NSAIDs) \n\neffects . Interfere with epinephrine effect (eg , ~-blockers, \n\na-adrenergic blockers) \n\no U rt icaria! rash , pru ritus, flush in g Gastrointestinal COPD = chronic obstruc ti ve pulmonary disease; NSAIDs = nonsteroidal anti-inflammatory drugs. \n\no Nausea , vomiting, abdominal pain Intramuscular epinephrine Treat ment Airway management & volu me resuscitation Ad junc tive therapy (eg, antihistamines, glucocorticoids} \n\nDiagnostic criteria for anaphylaxis \n\nAnaphylaxis is likely if there is rapid symptom onset & any 1 of the following criteria: \n\n1 Skin/mucosa involvement (eg, hives, lip/tongue swelling) & either hypotension or respiratory distress Involvement of ~2 organ systems after exposure ta a likely allergen . Skin/mucosa (eg , hives, lip/tongue swelling) \n\n2 . Respiratory (eg , wheezing , strider, dyspnea) \n\n## . Cardiovascular (eg , hypotension, tachycardia, syncope) \n\n## . Gastrointestinal (eg, abdominal pain , vomiting , diarrhea) \n\n3 Hypotension after exposure ta a known allergen \n\nManagement of anaphylaxis \n\n Epinephrine (mast important): \n\n0 IM preferred , may be repeated (eg , 3 doses) \n\nImmediate 0 IV in severe/refractory cases \n\nmanagement . IV crystalloid & Trendelenburg positioning for hypatensian Albuterol for bronchospasm Early intubation for upper airway obstruction H1/H 2 antihistamines Glucocarticaids \n\nAdjunct Glucagon for patients an beta blockers (reversal) \n\nmanagement Hospital admission for severe initial presentation (eg, shack) or ongoing symptoms despite treatment \n\nIM =intramuscular; IV =intravenous. CVS When intravenous access cannot be obtained in emergency cases, intraosseous (IO) access should be attempted immediately. M/C: Proximal Tibia Contraindications: \n\n1. Infection (eg, cellulitis) overlying the access site, 2. Fracture or previous IO attempts in the chosen extremity, or 3. Bone fragility (eg, osteogenesis imperfecta). \n\nHypovolemic & Hemorrhagic Shock \n\n Balanced resuscitation (aka, damage-control resuscitation) is used; it includes the following measures: \n\nLimiting use of crystalloids (eg, 1 L ), which dilute existing coagulation (eg, clotting) factors and platelets, thereby increasing coagulopathy Replacing lost intravascular volume with blood products (rather than crystalloids), transfused in a ratio similar to that of whole blood (eg, 1:1:1 ratio of packed red blood cells /plasma /platelets )\n\nPermitting hypotension (ie, permissive hypotension ) to limit ongoing hemorrhage and/or prevent clot disruption and rebleeding With balanced resuscitation, blood products are administered only as needed to maintain a blood pressure (eg, mean arterial pressure ~65 mm Hg ) sufficient for tissue perfusion, until definitive hemorrhage control (eg, surgical intervention) can be achieved. Adjunct therapies for hemorrhagic shock include tranexamic acid (antifibrinolytic agent) , which is effective in a subset of patients with acute life-threatening hemorrhage if administered within the first 3 hours of injury, and topical hemostatic agents (eg, kaolin-impregnated sponge, fibrin sealant dressing), which are applied to control external hemorrhage. In such situations, group O, Rh D-negative blood should be administered unless type-specific blood is immediately available. Spl to women of childbearing age and to young girls .In men and in women past childbearing age , O Rh D-positive blood can be given. \n\n194 https://t.me/usmleinnercircle \n\n\n\nManagement of hemorrhage due to trauma \n\n# . Control bleeding from any compressible site \n\n> Control\n\n# . Early t ransfer to locat ion (t rauma center , operating r oom , ang iography sui te) f or definitive care & \n\n> bleeding co ntrol of hemorrhage\n> Give blood\n\n# . Tr ansfu se bl ood produ cts early in res usc ita ti on \n\n> products early\n\n# . Massive transfusion protocol*: ratio of 1:1:1 F FP / pRBCs /platelets to minimize ri sk of coagul opathy \n\n# . Limit to -1 L if patient is hypotensive Limit use of crystalloids Switch to bl ood products as soon as avai l ab le . \n\n> *Massive transfusion protocol likely required in patients with 2'2 of the following: SBP S90 mm Hg, pulse 2'120/mi n, positive FAST examination, and penetrating mechanism of injury.\n> FAST = Focused Assessment with Sonography for Trauma; FFP =fresh frozen plasma; pRBCs =packed red blood cells; SBP =systolic blood pressure.\n\nCVS What is the next step in management for a patient that needs emergency fluid resuscitation and peripheral IV access cannot be obtained? \n\nAttempt intraosseous access \n\nrequires less skill and practice than central line placement and is safer and faster \n\n Hemorrhagic shock is the most common type of shock in the trauma setting, particular attention is given during trauma survey to areas where large blood loss can occur (\"blood on the floor and 4 more\"): \n\nExternal bleeding (\"the floor\"): up to the entire blood volume \n\nChest : up to 40% of the blood volume/hemithorax \n\nAbdomen (ie, peritoneal cavity): up to the entire blood volume \n\nPelvis : up to the entire blood volume; blood loss often hidden within the retroperitoneum \n\nDo pelvic X ray to rule out (retroperitoneal fluid can be missed in FAST) \n\nThigh : up to 1-2 L/thigh \n\nFluid Replacement \n\n 25kg child with burns over 40% of her body. What is fluid of choice ( and why )? \n\nLactated Ringer (closely resembles physiologic EC fluid and lactate reduces metabolic acidosis incidence) \n\nDo not use normal saline -- not suitable for fluid loss replacement in burn patients \n\n Calculate fluid regimen for next 24 hours :\n\nParkland + Maintenance = Total Parkland Formula: 4 mL x BSA x weight (kg) \n\n4 x 40 x 25 = 4000 mL = 4 L Maintenance Fluid: 4-2-1 formula \n\n4 ml/kg/hr for first 10kg = 40 ml 2 ml/kg/hr for next 10kg = 20 ml 1 ml/kg/hr for remaining = 5 ml 65 ml/kg/hr = 1560 ml per 24 hr = 1.5L \n\n4 + 1.5 = 5.5 L Lactated Ringer \n\nAdults only requires Parkland formula \n\n What imaging modality should be used to confirm placement of a central venous catheter tip ?\n\nChest X-ray \n\nthis step may be omitted in the setting of an uncomplicated ultrasound-guided CVC placement \n\n Ideal placement for a central venous catheter tip? Lower superior vena cava \n\n195 https://t.me/usmleinnercircle USMLE Inner Circle \n\n000000CVS Tip placement in smaller veins (eg, subclavian, jugular, azygous) predisposes to venous perforation .In addition, inappropriately placed catheter tips may cause lung puncture, leading to pneumothorax , or myocardial perforation, leading to pericardial tamponade .\n\n Adequate fluid resuscitation is an essential component of managing severe sepsis and septic \n\nshock .Patients with hypotension or evidence of impaired perfusion should receive immediate fluid resuscitation. If pt is on is on diuretics, they should be stopped .\n\nObstructive Shock \n\n The expected hemodynamic parameters in obstructive shock include elevated central venous pressure (CVP) and low cardiac output ; however, pulmonary capillary wedge pressure (PCWP), an estimate of left atrial pressure and representation of left-sided preload, can vary depending on the location of the obstruction. \n\nPrepulmonary obstructive shock (due to massive PE or tension pneumothorax) is most common and results from obstruction involving the right atrium, right ventricle, or pulmonary arteries. Because blood is unable to pass from the right side of the heart to the left side, PCWP is low or normal. \n\nPostpulmonary obstructive shock typically involves obstruction within the left side of the heart or \n\naorta ; PCWP is elevated , making the hemodynamic parameters the same as those expected in \n\ncardiogenic shock. (e.g: Aortic Stenosis, Aortic Dissection) \n\n## CVS Drugs \n\n What anti-hypertensive medication is commonly associated with peripheral edema as an adverse effect? \n\nDihydropyridine Ca2+-channel blockers \n\ndue to preferential dilation of precapillary vessels (arteriolar dilation), which increases capillary hydrostatic pressure \n\n What drug classes are useful for reducing Ca2+ channel blocker-induced peripheral edema ?\n\nACE inhibitors and ARBs \n\n196 https://t.me/usmleinnercircle \n\nCVS the combination of CCB and ACE inhibitors was associated with a significantly lower risk of CCB-associated peripheral edema compared with CCB monotherapy. \n\n The combination of atrial tachycardia with AV block is fairly specific for digitalis toxicity. \n\ndigitalis causes both an increased ectopy in the atria or ventricles (atrial tachycardia) and an increased vagal tone (AV block) \n\n Angioedema is s/e of both ACE inhibitor and ARNI not when ARB is used without Nephrilysin inhibitor \n\nAnti-Arrhythmic \n\n Enhanced effect at faster heart rates is known as use dependence. Prolonged PR intervals at faster heart rates: Class IV (CCBs) \n\nProlonged QRS durations at faster heart rates: Class I (especially class IC) \n\nIt is the primary mechanism behind their efficacy against supraventricular arrhythmias. \n\n197 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSymptoms of digoxin toxicity Cardiac . Life-threatening arrhythmias \n\n## . Anorexia \n\nGastrointestinal . Nausea & vomiting \n\n## . Abdominal pain \n\n## . Fatigue \n\n## . Confusion \n\nNeurologic Weakness .. Color vision alterations \n\n\n\nThyroid effects of amiodarone Disorder Features Treatment \n\n t T4 None needed \n\nDecreased T4-T3 conversion ! T3 Normal/t TSH \n\nInhibition of thyroid hormone synthesis t TSH Levothyroxine \n\n ! T4 \n\nAITtype 1 ! TSH Antithyroid drugs \n\n(iodine-induced increase t T3 & T4 \n\nin thyroid hormone synthesis) ! RAIU Increased vascularity on ultrasound \n\n ! TSH Glucocorticoids \n\nAITtype 2 t T3 & T4 \n\n(destructive thyroiditis) Undetectable RAIU Decreased vascularity on ultrasound \n\nAIT =amiodarone-induced thyrotoxicosis; RAIU =radioactive iodine uptake. CVS Miscellaneous \n\nSyncope \n\n What is the most likely underlying etiology in a patient who passes out at home suddenly without any warning signs? Clonic jerks were noted while he was unconscious . His past medical history is significant for hypertension and previous myocardial infarction . Patient appears comfortable with no symptoms at time of examination. \n\nArrhythmia \n\nClonic jerks can occur during any syncopal episode that is prolonged and associated with cerebral hypoxia, regardless of etiology. Patients with arrhythmic cause of syncope usually have underlying structural heart disease and may not have any prodromal symptoms -- versus vasovagal or neurocardiogenic syncope, which have aura and notable triggers \n\nIf this was a seizure, look for trigger stimuli (stress, lack of sleep, flashing lights) with prodromal aura , tongue laceration, and prolonged postictal phase .\n\n Evidence of lateral tongue biting is the most reliable finding to differentiate epileptic seizure and syncope. It has low sensitivity (33%) but high specificity (96%) for epileptic seizure. \n\n198 https://t.me/usmleinnercircle \n\nMajor side effects of amiodarone \n\n# . Sinus bradycardia, heart block \n\nCardiac . Risk of proarrhythmias: QT prolongation & risk of torsade de pointes Chronic interstitial pneumonitis (cough, fever, dyspnea, \n\nPulmonary pulmonary infiltrates) most common . Hypothyroidism \n\nEndocrine . Hyperthyroidism \n\nGastrointestinal/ . Elevated transaminases, hepatitis \n\nhepatic \n\n# . Corneal microdeposits \n\nOcular . Optic neuropathy \n\nDermatologic Blue-gray skin discoloration \n\nNeurologic . Peripheral neuropathy \n\nSeizure Vasovagal syncope \n\n# . Lack of sleep . Flashing light . Prolonged standing Triggers . Emotional stress . Physical /emotional stress \n\n# . Alcohol withdrawal . Heat . Idiopathic . Preceding aura (eg , olfactory hallucinations) . Preceding lightheadedness (ie , presyncope) . Can occur with sleeping / sitting . Unlikely to occur while sleeping/sitting Clinical . Tonic / clonic movements . Uncommon to have clonic jerks (can occur with prolonged cerebral clues . Rapid, strong pulses hypoperfusion) . Tongue biting . Weak, slow pulses \n\n# . Incontinence . Pallor & diaphoresis Sequelae . Delayed return to baseline (postictal drowsiness or Immediate return to baseline confusion) .CVS Continuous ECG monitoring can evaluate for transient arrhythmia (eg, ventricular tachycardia ) that may not be detected on initial ECG. like Ambulatory ECG monitoring (eg, Holter monitor , insertable cardiac monitor )\n\n Tilt-table testing can help distinguish between orthostatic and vasovagal \n\nsyncope if the etiology is unclear (+ve in Vasovagal) \n\n199 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSyncope Likely eti ology Clinical clues to di agnosis \n\nVasovagal or Triggers: Prolonged standing or emotional distress, painf ul stimuli neurally mediated syncope Prodromal symptoms: nau sea , warmth , diaphoresis \n\nSituational syncope Triggers: Cough, micturition, defecati on Orthostatic syncope Postural changes in heart rate/blood pressure after standing suddenly Aortic stenosis, HCM , Syncope wi th exertion or during exercise anomalous coronary arteries \n\nVentricular arrhythmias Pr ior history of CAD, M l, card iomyopathy, or j EF Sick sinus syndrome, bradyarrhythm ias, atrioventricular Sinus pauses, t PR or t ORS duration \n\nblock \n\nTorsades de pointes Hypokalemia, hypomagnesemia, medications causing t QT interval \n\n(acquired long QT syndrome) Congenital long QT syndrome Family history of sudden death, t QT interva l, syncope with triggers (eg ,exerci se , startle, sleeping) \n\nMedication-induced orthostasis Diagnosis of orthostatic hypotension Mechanism Examples \n\n## . Terazosin, prazosin, doxazosin With in 2-5 min of standing . .e20 mm Hg ) in systol ic blood pressure OR \n\nfrom a supine position . .e 10 mm Hg j in diastolic bl ood pr essure \n\na1 blockade-mediated vasodilation . Antipsychotics (eg, risperidone) \n\n## . Antihistamines, TCAs \n\n## . ACE inhibitors & ARBs \n\n## . Dihydropyridine CCBs \n\nOther vasodilation . Hydralazine, nitrates . Phosphodiesterase inhibitors \n\n## . Diuretics \n\nVolume depletion SGL T-2 inhibitors .. Beta blo ckers \n\nSympathetic blockade . Clonidine \n\nARBs = angiotensin II receptor blockers; CCBs = calcium channel blockers; \n\nSGLT = sodium-glucose cotransporter; TCAs = tricyclic antidepressants. \n\nVasovagal & situational syncope Cardiac syncope \n\nTriggers . Pain,* anxiety,* emotional stress, heat, prolonged standing \n\n## . Situational: cough ,* micturition,* defecation , eating, hair-combing* \n\nEtiology Clues to diagnosis \n\nClinical . Prodrome (eg, warmth , pallor, nausea, diaphoresis) presentation . Rapid recovery of consciousness (eg , <1-2 min) Aortic stenosis or HCM . Exertional syncope \n\n## . Systoli c murmur o n ex amination Diagnosis . Mainly based on clinical history of event \n\n## . Upright tilt table testing sometimes indicated in uncertain cases Ventricular tachycardia . No preceding symptoms \n\n## . Cardiom~oeath~ or e re vious Ml Treatment . Reassurance & avoidance of triggers \n\n## . Counterpressure techniques for recurrent episodes Sick sinus syndrome . Preceding fatigue or dizziness \n\n## . Sinus pauses on ECG *Particularly common triggers in the pediatric population. Advanced AV blo ck . Bifascicular block or t PR interval on ECG \n\n## . Dropped ORS complexes on ECG \n\n## . No preceding symptoms Torsades de pointes . Medications that prolong QT interval \n\n## . Hypokalemia or hypomagnesemia AV = atrioventricular; HCM = hypertrophic ca rdiomyopath y; Ml = myocardi al infarction. CVS AV block can be intermittent and thus may not be present on ECG at the time of testing. \n\n Vasovagal Pathogenesis: Over-activation of vagus nerve (for whatever reason ) leads to bradycardia (cardioinhibitory ) and hypotension (vasodepressor ) fall in BP syncope For patients with recurrent syncope, management consists of advice to avoid triggers and to assume a supine position with leg raising at the onset of symptoms. \n\nPhysical counterpressure maneuvers : Leg crossing with tensing of muscles, handgrip and tensing of arm muscles with clenched fists (improves venous return and cardiac output) aborting prodromal symptoms. \n\nPulsus Paradoxus \n\nPulsus paradoxus (C ardiac tamponade, Asthma, COPD ): fall in systolic pressure > 10 mmHg during inspiration \n\nStent \n\n What is the likely cause of LAD artery occlusion (V1-V3) in a patient with recent stent placement in the LAD artery? \n\nStent thrombosis (likely due to medication non-compliance) \n\npremature discontinuation of antiplatelet therapy is the strongest predictor of stent thrombosis after intracoronary stent implantation \n\n200 https://t.me/usmleinnercircle \n\n# \"'lilJVJJJJ r 120 \n\n# t ,,. t 1 (111 \n\nI .. \n\n.. ~ =------=~~~~~ CVS If stent was placed in LAD and now ST elevations are seen in lateral (ie, I, aVL, V5-V6) or inferior (ie, II, III, aVF) leads, this would suggest new atherosclerotic plaque rupture. (not stent thrombosis) \n\nJVP \n\n Cannon A waves are intermittent, prominent A waves caused by the surge in jugular venous pressure that occurs due to right atrial contraction against a closed tricuspid valve; these waves can be seen with any arrhythmia involving atrioventricular dissociation , such as ventricular tachycardia ,which is characterized by self-propagation within the ventricles without communication with the atria. Other arrhythmias in which cannon A waves are commonly seen include complete atrioventricular block and frequent premature ventricular contractions . Patients may sometimes report symptoms associated with cannon A waves, including headache, jaw pain, and sensation of neck pulsation. \n\n201 https://t.me/usmleinnercircle USMLE Inner Circle \n\nBare metal stent Shorter thrombotic nsk penod Higher nsk of restenosis \n\nt\n\nEarly endothe li alization Drug-eluting stent Longer thrombot ic nsk penod Lower risk of restenos1s Late endothe lialization \n\nEstimating central venous pressure (CVP) \n\nCVP = Jugular venous pressure (JVP) + Depth to right atrium (5 cm) \n\nNormal CVP (6-8 cm H20) Elevated CVP (>8 cm H 2O) CVS What physical exam manuever is useful for distinguishing between cardiac- and liver disease-related causes of lower extremity edema? \n\nHepatojugular reflux (distension of neck veins by pressure on liver with hand) \n\npositive reflux is suggestive of cardiac causes (e.g. heart failure) \n\nProsthetic Valve \n\nProsthetic Valve Thrombosis \n\nMost common presentations of PVT include: \n\nThromboembolism : left-sided (ie, mitral or aortic) PVT can present as TIA , stroke , MI , bowel \n\nischemia , and limb ischemia ; by contrast, right-sided (eg, tricuspid) PVT may cause pulmonary \n\nembolism .\n\nProsthetic valve dysfunction : usually manifesting as obstruction (stenosis) or, rarely, \n\nregurgitation . Patients may have a new murmur or signs and symptoms of heart failure. \n\nDx: Transthoracic echocardiography \n\n202 https://t.me/usmleinnercircle \n\nHepatojugular reflux to differentiate between cardiac and liver disease \n\nRight ventricular failure (hepatojugular reflux present) Liver cirrhosis (hepatojugular reflux absent) \n\n> \n\nt Hydrostat ic pr ess ur eLower extremity edema Lowe r ex t re mi ty edema \n\n> RUQ =right upper quadrant.\n\n(d ue to hypoalbumine mi a &ili ac vein com pression by ascites) \n\n> @UWorld\n\nProsthetic valve dysfunction \n\n## . Transvalvular regurgitation (cusp \n\nTypes & causes degeneration) \n\n## . Paravalvular leak (annular degeneration , IE) \n\n## . Valvular obstruction/stenosis (valve thrombus) \n\nClinical . New murmur (regurgitant or stenotic) \n\nmanifestations . Macroangiopathic hemolytic anemia \n\n## . Heart failure sy mptoms , thromboembolism \n\nDiagnosis . Echocardiography IE = infec ti ve en docarditis .CVS Mechanical prosthetic valves: are more thrombogenic and require anticoagulation .\n\nBioprosthetic valves: are less thrombogenic and typically require only aspirin therapy \n\nHereditary Hemorrhagic Telangiectasia \n\n In patients with symptomatic, bleeding pulmonary AVMs (hemoptysis), management involves \n\npulmonary angiography followed by embolization. \n\nExercise Induced Postural Hypotension \n\n## Paeds CVS \n\n203 https://t.me/usmleinnercircle USMLE Inner Circle \n\nHereditary hemorrhagic telangiectasia (Osler-Weber-Rendu) Vascular bed Sequelae \n\nCNS . Hemorrhagic CVA \n\n## . Brain abscess: Raradoxical bacterial embolization across eulmona !}'. AVM \n\nMucocutaneous . Oral & cutaneous telangiectasia \n\n## . Recurrent epistaxis Lung . Pulmonary AVM : hemoptysis \n\n## . PAH : right-sided heart failure \n\n## . Chronic GI bleed GI . Liver: portal hypertension, high-output heart failure \n\nAVM = arteriovenous malformation; CVA = cerebrovascu lar acciden t; GI = gastrointestinal; PAH = pulmonary art erial hypertension .Exercise-associated postural hypotension \n\n# . Cessation of exercise results in sudden \n\nPathophysiology decrease in veno us return to the heart (p reload) \n\n# . Athlete collae ses immediatell after cessat i on of exercise \n\n----Manifestations . No loss of consciousness \n\n# . Dizziness or lightheadedness \n\n# . Normal to minima lly elevated core temperature \n\n# . Trendelenburg positioning (ie, feet i nc lined \n\nManagement above the head) \n\n# . Ora l hydration CVS What is the next step in management for a newborn with cyanosis that does not improve with 100% O2 and a continuous machine-like murmur on auscultation? \n\nAdminister prostaglandin E1 \n\ncyanosis that fails to improve with 100% O2 is indicative of a possible congenital heart defect; maintaining the patency of the PDA can be life-saving This patient is cyanotic -- PDA are not cyanotic at birth, thus do not give endomethacin! Hyperoxia test for Central Cyanosis \n\n204 https://t.me/usmleinnercircle \n\nApproach to neonatal cyanosis \n\nNeonatal cyanosis ]\n\nIDistal extremi ties & lips Normal Sp0 2Mucosal or diffuse Low Sp0 2Per ipheral cyanosis: Central cyanosis: Reassuran ce Administ er 0 2Sp0 2 unchanged OR Hemodynamic instability Cardiac pathology: Administer prostaglandin \n\ni\n\nSp0 2 increased ]\n\nPulmonary pathology: Provide respiratory support (eg, intubation, ven ti lation) \n\n> consider persistent pulmonary hypertension of the newborn, partJclJa r1 yif diff erentJal cyanosis is present.\n\nSp0 2 = oxygen satura ti on measured by pu lse oxlmetry ()UWor ld \n\nCongenital heart disease Cause Clinical features Examples \n\nLeft-to-right Tachypnea Ventricular septal defect shunting Poor weight gain Atrial septal defect Sweating with feeds Isolated patent ductus arteriosus Transposition of the great vessels Right-to -left Tetralogy of Fallot shunting Cyanosis Tricuspid atresia Anomalous pulmonary venous return Truncus arteriosus Interrupted Pallor or shock Coarctation of the aorta left ventricular Severe acidosis Hypoplastic left heart syndrome output CVS VSD \n\n What is the likely diagnosis in a young child that presents with failure to thrive and easy fatigability with a grade II holosystolic murmur best heard over the left sternal border with a diastolic rumble over the cardiac apex? \n\nLarge ventricular septal defect (VSD) \n\nlarger VSDs tend to be quieter (grade II) due to less turbulence; the diastolic rumble is heard due to increased flow across the mitral valve \n\nTricuspid Atresia \n\n205 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCyanotic hea rt di sease in newborns Diagnosis Examination X-ray find ings Transposition of Single S2 \"Egg-on-a-string\" heart \n\nthe great vessels +/- VSD murmur (narrow mediastinum) \n\nTetralogy of Harsh pulmonic \"Boot-shaped\" heart stenosis murmur (right ventricular \n\nFallot VSD murmur hypertrophy) \n\nTricuspid atresia Single S2 Minimal pulmonary VSD murmur blood flow Single S2 \n\nTruncus Systolic ejection Increased pulmonary \n\narteriosus murmur (increased flow blood flow, edema through truncal valve) \n\nTotal anomalous Pulmonary edema, \n\npulmonary Severe cyanosis \"snowman sign \n\nvenous re turn Respiratory distress (enlarged supracardiac \n\nwith obstructi on veins & SVC) \n\nVentricular septal defect Small Moderate to large Clinical Asymptomatic . Respiratory distress, poor feeding , poor growth (due to \n\n## . pulmonary overcirculation & high-output LV failure ) \n\nfeatures . Loud, harsh, holosystolic murmur at LLSB . Holosystolic murmur at LLSB; loud S2 \n\nChest x-ray Normal . Cardiomegaly \n\n## . . Increased pulmonary markings \n\n## . Serial echocardiography . Diuretics \n\nManagement . Most spontaneously close at age <2 . Surgical closure \n\nLLSB =lower le ft sternal border; LV =left v en tri cular. CVS What is the likely diagnosis in a newborn that becomes cyanotic with left axis deviation on ECG and decreased pulmonary markings on CXR? \n\nTricuspid valve atresia \n\nleft axis deviation is seen as up-going R wave in lead I and down-going R wave in lead avF ; lack of blood flow to the RV results in underdevelopment of the pulmonary valve and/or artery; ASD and VSD are necessary for survival (hence LVH and left axis deviation )\n\n Absent tricuspid valve : No flow from right atrium (RA) to right ventricle (RV) results in enlarged RA \n\n(ie, tall, peaked P waves ) and hypoplastic RV \n\n206 https://t.me/usmleinnercircle \n\nTricuspid atresia \n\nPu lmonary \n\n___ __ ,( artery \n\nLeft ventricle \n\n> AS\n\n= atrial septal defect; PFO = patent forame n ovale; VSD = ventricular septa l defect \n\nTricuspid atresia \n\n@ UWorld \n\n# n, ,__ a:rrrr1TITI1 ~; n;m,1Rwa,e, '\"-LLLLI \n\nLehaxis ~:r ~[J ~r :] deviation Ta ll , peaked 1LLU Pwaves Minimal R wave: \n\n1AA jAA \n\n# IA,. I/\\,. \n\nII a L :rrrn~sl v r -, 1-, CVS ECG in a newborn normally shows physiologic right axis deviation. \n\nPersistent Pulmonary Hypertension of the Newborn Hypoplastic Left Heart Syndrome \n\n Present with tachypnea , cyanosis , no murmur , and a single S2 ; presentation is typically delayed until a few days after birth when the ductus arteriosus closes. \n\n## CVS Surgery also known as persistent fetal circulation \n\n207 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDetermine axis \n\n1. Look at the QRS complex in leads I a nd aVF 2. If both are mainly positi ve , then the axis is n or ma l. 3. If mainly positive in le ad I a nd mainly negati ve in aV F, the axis is deviated to the le ft. 4. If mainly negative in lead I a nd mainly pos it ive in a VF, the axis is deviated to the right. 5. If mainly negati ve in both I a nd a VF, then there is extreme rig ht axis deviation. \n\nPersistent pulmonary hypertension of the newborn Pathogenesis Risk factors Examination Treatment Normal heart \n\n Abnormal persistence of elevated fetal pulmonary vascular resistance Right-to-left shunting across ductus arteriosus Lung hypoplasia (eg, congenital diaphragmatic hernia) Meconium aspiration syndrome Infection (eg, neonatal pneumonia) \n\n l Postductal relative to preductal oxygen saturation Respiratory distress & cyanosis Prominent S2 Oxygenation & ventilation Inhaled nitric oxide (pulmonary vasodilator) \n\nHypoplastic left heart syndrome Narro w\n\nascending \n\nao rt a\n\nAtrial septal defect Underdeveloped \n\nleft ve ntr icl e UWor1d CVS Management of small AVFs involves observation (sometimes resulting in spontaneous closure) or \n\nultrasound-guided compression .Large AVFs typically require surgical repair. \n\n Femoral artery aneurysms often present with vascular claudication and a pulsatile groin mass . Complications include acute limb ischemia, rupture, or distal embolism. Risk factors include male sex, older age, tobacco use, hypertension, hyperlipidemia, and coronary artery disease. Diagnosis is most frequently made with duplex ultrasonography or CT angiography .Treatment of symptomatic or large ( 3 cm) aneurysms consists of surgical arterial repair. \n\n Inadequate post-procedural arterial compression is the strongest risk factor for \n\npseudoaneurysm development. The diagnosis should be confirmed by ultrasound .\n\nCABG \n\n Atrial fibrillation commonly (up to 15%40%) occurs within a few days after CABG and is usually self-limited , with resolution in <24 hours .Rate control with beta-blockers or amiodarone is best \n\n Acute mediastinitis can occur following cardiac surgery and present with fever , chest pain ,leukocytosis, and mediastinal widening on chest x-ray .\n\n208 https://t.me/usmleinnercircle \n\n> Primary survey in Advanced Trauma Life Support\n> Airway with cervical spine protection Breathing &ventilation Circulation with hemorrhage control Disability (basic neurologic assessment) Exposure &environmental control Local vascular complications of cardiac catheterization\n> Hematoma Pseudoaneurysm Arteriovenous fistula\n> Mass Bulg ing ,pulsatile mass No mass\n> Nobruit Systolic bruit Continuous bruit\n\n\"\"\"\"\" CVS It is a serious condition that requires drainage , surgical debridement , and prolonged antibiotic therapy. \n\n Pleural effusions occur in almost half of patients who undergo coronary artery bypass graft surgery \n\nPostcardiac surgery effusions that meet the following criteria can be managed conservatively \n\nwith observation only: \n\nSmall to moderate in size and not enlarging \n\nEarly onset (postoperative day 1 or 2) Not associated with respiratory symptoms \n\nPostpericardiotomy Syndrome \n\n What is the likely diagnosis in an infant that presents with distant heart sounds and hypotension with cardiomegaly on X-ray one week after having cardiac surgery? \n\nPostpericardiotomy syndrome (pericardial effusion after cardiac surgery) \n\nIt presents 1-6 weeks after cardiothoracy surgery with fever, chest pain, tachy, and pericardial friction rub , and is often associated with pericardial effusion (that may develop into cardiac tamponade )\n\nSternal Dehiscence \n\n Sternal dehiscence is a complication of cardiac surgery characterized by separation of the bony edges of the sternum. Patients may report mild pain or sensation of chest wall instability and \" clicking \" with chest movement. The diagnosis can be made radiographically (eg, displaced sternal wire) or clinically ; palpable rocking or clicking of the sternum confirms the diagnosis. \n\nManagement involves urgent surgical exploration and repair. \n\n Soft tissue dehiscence occurs when only the superficial tissues (eg, skin, muscle) separate. There are no signs of sternal instability or systemic illness; \n\nlocal wound care or debridement followed by primary closure is indicated. \n\n209 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nPost-cardiac injury syndrome \n\n# . Myocardial infarction (ie, Dressler syndrome) \n\nCauses . Cardiac surgery or trauma \n\n# . Percutaneous coronary intervention \n\n# . Lat ent period of several weeks to months \n\nClinical . Pl eur itic ch es t eain, fever, leukoc~ osis \n\nfeatures . Chest x-ray: pleural effusion enlarged cardiac silhouette \n\n# . Echocardiography: pericardia! effusion \n\n# . NSAID (usually high-dose aspirin) colchicine \n\nTreatme nt . Corticosteroids in refractory disease \n\n# . Usually self-limited disease course \n\nPrognosis May cause chronic/recurrent disease leading to constrictive pericarditis .\n\nN SA ID = nonsteroidal anti-inflammatory drug .CVS A high-mortality complication of dehiscence is deep tissue infection (mediastinitis) , due to either contiguous spread of superficial infection or intraoperative deep tissue contamination. Although it classically presents with systemic symptoms (eg, fever, tachycardia), chest pain, chest wall edema/crepitus, and purulent wound discharge, atypical presentations can occur; therefore, any patient with significant sternal wound drainage should be evaluated with chest and sternal imaging (eg, mediastinal fluid collections or pneumomediastinum on CT scan ). Management includes emergency surgical debridement , tissue cultures , and empiric intravenous antibiotics. \n\nPreoperative Cardiac \n\n Perioperative cardiovascular complications, referred to as major adverse cardiovascular and cerebrovascular events (MACCE) are a significant cause of morbidity and mortality in non-cardiac surgical cases. Anesthesia and surgery place the body under tremendous physiological stress. which can lead to myocardial ischemia, infarction and potential cardiac death. \n\n210 https://t.me/usmleinnercircle \n\nRevised Cardiac Risk Index (RCRI) (cardiovascular risk of noncardiac surgery) \n\n# . Hi gh -r isk surgery (eg, vascu la r, in tra th oracic) \n\n# . lschemic heart diseas e\n\n# . Hi story of congestive heart failure 6 risk pr ed i ctors H istory of ce re br ov asc ular di sease (stroke or TIA ).. Diabetes mellitus treated with insulin \n\n# . Pr eo perat ive creatinine >2 mg / dl Risk of cardiac deat h, 0 -1 factor: low risk* .nonfatal cardiac arrest, --. ~2 factors: elevated ri sk \n\nor nonfatal Ml \n\n> *RCRI sco re of 0-1 originally reported as S1\n\n% a nd still accepted as l ow ri sk . Slightly high er eve nt rat es of l ate r studi es pr obably d ue to using troponins (T sensitivity) and including additional outcomes (eg, all-ca u se mortality). Ml = myocardial infarction; TIA = transi ent ischemic a tt ac k. \n\nCardiac risk * of selected Estimated cardiac functional capacity noncardiac surgical procedures by activity (METs*) Ri sk level Surgery type . Eat, dress, use toil et Ao rt ic or other major vascular High . lntrathoracic \n\n# . Open intraperitoneal \n\n# . Walk indoors in the house \n\n<4 METs Do li ght housework . (eg, vacu um ing) Head and nec k leg , thyr oid ecto my )\n\n# . Climb a flig ht of stairs \n\n# . Ru n a short dist ance In termedi ate . Orthopedic \n\n Ews.lale.. i!:4METs . Do yardwork (eg, raking l ea ves) \n\n# . Partic ipa te in go lf , tennis, \n\n# . Bmasi..(eg, lum pec tomy, mastect omy) or dancing L ow . Endoscop ic procedure *1 M ET (m etabo lic equivalent) :;:; volume of oxy gen \n\n# . Catar act ext raction co nsu med at rest (3.5 ml 0 2 uptake/kg/min). *Ca rd i ac deat h, nonfatal ca rdiac arrest, or nonfatal m yo ca rdia l in far ct ion. CVS Other Tests \n\n211 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPreoperative evaluation of ischemic heart disease for noncardiac surgery \n\nEmergency procedure ) ---- Yes ----+ Proceed to surgery )\n\nI\n\nNo \n\nt\n\nAcute coronary syndrome .. \n\nINo \n\nt\n\nLow risk for MACE: S1 RCR Ior < 1% risk calculator \n\nI\n\nNo \n\nt\n\n----Yes----+ Postpone surgery: manage per guidelines Functional capacity .:4 METs ) ----Yes-------~ \n\nI\n\nNo \n\nt\n\nCardiac evaluation will impact management \n\nI\n\nYes \n\nt\n\nProceed to surgery Pharmacologic stress test J---Negati ve-----------~ \n\nI\n\nPositive \n\nt\n\nCoronary revascularization \n\n\"Emergency procedu re . <6 holn to avoid lo ss or life~lmb .\n\n.. Acute corona ry syndrome. acute or rece nt (<60 da ys) my oca rdial i nf arction or uns ta ble angina. MACE = major adverse cardiac ev e nt , MET = metabolic equivalen t; RCRI = Revised Card iac Risk Index. \n\nValvular heart disease management before noncardiac surgery \n\nValve dysfuncti on )Mild Low Moderate/severe \n\ni\n\nSymptom s ]\n\nNo i\n\nSurgical ri sk ]\n\nIntermediate or high \n\nt\n\nValve-specific criteria ... \n\n( eg , normal EF & no significant PHTN )Yes No \n\n.j, .j, \n\nYes Noncardiac surgery ) Valve intervention before surgery \" AR/AS= nonna l EF. MS= no significant PHTN, M R= normal EF & no significant PH TN. AR = aortic reg urgitati on ; AS = aortic stenosis; EF = ejection fraction; MR = m1tral regurgitation; \n\nMS = mitral stenosis, PHTN = pu lmonary hypertension. CIJINorld \n\nCl!No,ld CVS Vascular Trauma \n\n Signs of distal ischemia (eg, absent pulses , cool extremities )\n\nBlunt Cardiac Injury \n\n212 https://t.me/usmleinnercircle \n\nIndications for select preoperative tests \n\n# . History of coronary artery disease or arrhythmia \n\nECG . Asymptomatic patients with risk of MACE ~1 %\n\n# . History of cardiopulmonary disease \n\nChest radiograph Undergoing upper abdominal/thoracic surgery .\n\n# . History of anemia, significant expected blood loss \n\nHemoglobin Undergoing major surgery .\n\n# . History of abnormal bleeding , anticoagulant use \n\nCoagulation & platelets Liver disease, malignancy, planned spinal anesthesia .\n\n# . History of kidney disease, cardiovascular risk calculation \n\nCreatinine & electrolytes Predisposing medications (eg, diuretic, ACE inhibitor, ARB) .\n\nACE = angiotensin-converting enzyme; ARB = angiotensin receptor blocker; MACE = major adverse cardiovascular event. Extremity vascular trauma Hard signs \n\n## . Observed pulsatile bleedin g\n\n## . Presence of bruiUthrill over inj ury \n\n## . Expanding hematoma \n\n## . Signs of distal ischemia Clinical manifestations Soft signs \n\n## . History of hemorrhage \n\n## . Diminished pulses \n\n## . Bony injury \n\n## . Neurologic abnormality If hard signs or hemodynamic instability \n\n## . Surgical exploration Evaluation Otherwise \n\n## . Injured extremity index \n\n## . CT scan or conventional angiography \n\n## . Duplex Doppler ultrasonography CVS Patients with findings concerning for BCI require 24-48 hours of continuous cardiac monitoring because most life-threatening arrythmias occur during that time. Blunt cardiac injury can lead to Obstructive Shock or Cardiogenic Shock \n\nMyocardial Contusion \n\nWhat is the likely diagnosis in a hemodynamically unstable patient that presents following a motor vehicle accident with an elevated PCWP that worsens after administration of IV fluids ?\n\nMyocardial contusion \n\nAn elevated PCWP at baseline should raise suspicion of myocardial contusion (hypovolemic shock would have a low PCWP); urgent echocardigram is required for further evaluation \n\nCardiac contusion results in cardiac dysfunction with poor cardiac output Cardiac contusion : arrhythmia ( palpitations ), hypotension and tachycardia that do not respond to fluid resuscitation (hypotension and tachy in trauma pt due to hemorrhage, however contusion should be suspected if tachycardia persists despite fluid resuscitation) \n\n Might as well have mild increase in troponins \n\n213 https://t.me/usmleinnercircle USMLE Inner Circle \n\nHemodynamically unstable \n\n# !\n\nResuscitation and evaluation eFAST Chest x-ray \n\n ECG \n\n+/ - stabilizing in tervention (eg , chest tube) if indicated \n\n# !\n\nHemodynamic stability achieved/ ma intained? I\n\nNo \n\n# lOR thoracotomy \n\nBlunt chest trauma \n\n- ----Yes-----\n\nAdditional tests (eg, CT chest) Hemodynamically stable \n\n# !\n\nHigh-risk mechanism or serious injury on examination INo \n\n## l\n\nAbnormal findings on evaluation, chest x-ray, ECG I\n\nNo \n\n# lPossible discharge or observation eFA ST = extended Focused Assessment wi th Sonography tor Tralma . OR = opera li ng room. \n\nBlunt cardiac injury \n\nPathophysiology . Rapid deceleration or direct blow to the precordium - shearing, compression, abrupt pressure change Arrythmia r anging from asymptomatic (eg , PVCs ) to fatal (eg , VFib) \n\nClinical Acute coronary syndrome from coronary dissection or thrombosis \n\n# . Myocardial dysfunction (\"myocardial contusion\") \n\nspectrum Ruptured valv e , septum, or ventricular wall . Cardiac tamponade \n\nConfirmatory . ECG \n\ntesting . Echocardiogram PVCs = premature ventricular contractions; VFib = ventricular fibrillation. CVS 214 https://t.me/usmleinnercircle Endocrine \n\n# Endocrine \n\n## Pituitary \n\nHyperPituitarism Pituitary HyperPituitarism SIADH HypoPituitarism Thyroid Hyperthyroidism Hypothyroidism Euthyroid Sick Syndrome Parathyroid Gland Hyperparathyroidism Adrenal Gland Adrenal Excess Conn Syndrome Cushing Adrenal Insufficiency Pancreas Diabetes Screening DKA Treatment Diabetic Nephropathy Metabolic Syndrome Hypoglycemia Endocrine Tumor VIPoma Zollinger Ellison Neuroblastoma MEN Pheochromocytoma Endocrine Drugs Miscellaneous Milk Alkali Syndrome Hypoglycemia associated autonomic failure Endocrine Paeds Neonatal Thyrotoxicosis Congenital hypothyroidism Congenital Adrenal Hyperplasias \n\n215 https://t.me/usmleinnercircle USMLE Inner Circle Endocrine What is the preferred imaging modality for evaluation of pituitary tumors ?\n\nMRI \n\nrecommended for patients with elevated prolactin, mass-effect symptoms, very low testosterone levels, or disruptions in other pituitary hormones \n\n A prolactin level > 200 ng/mL is virtually diagnostic of prolactinoma. \n\n As a general rule in endocrinology, imaging is performed after the biochemical diagnosis of a disorder is made. \n\n216 https://t.me/usmleinnercircle \n\nManagement of hyperprolactinemia in premenopausal women \n\n Detai l ed cl inical evaluation Ru le out secondary causes (eg, pregnancy) \n\nMRI of pituitary gland J\n\nAsymptomatic microprolactinoma (<1 0mm ) Macroprolactinoma (~10 mm) Risk or presence of neurol og ic symptoms Hypogonadism Galactorrhea No treatment ] Dopamine agon ists Cabergoline \n\n> (C)UWor ld\n\n Bromoc ri pt ine Persistent hyperprolactinem ia Persistent symptoms No decrease in tumor size Intolerance to medication Consider surgical resection Clin ical suspicion of acromegaly \n\n## !IGF-1 level \n\nNor:r ~ evated \n\nR ul es o ut acromegaly \n\n# L O ral glucose suppression test AdequateGH sup pr ess,on Inadequate GH suppressi on MRI of brain Pituitary mass No rm al pituitary Su rgical versus Evaluate for extrapituitary medical management cause of acromega ly (eg , ectopic GH -& GHRH-secret in g tumors) \n\n> GH =growth hormone; GHRH\n\n= growth hormone-releasing hormone; KiF -1 = insulin-like growth factor 1 \n\n> UWorld\n\nEndocrine SIADH \n\n Intranasal Desmopressin use for DI can cause Secondary SIADH. \n\nHypoPituitarism \n\nSerum Na+ < 137 mEq/L with dilute urine favours primary polydipsia and excludes diabetes insipidus \n\n Central DI usually has significant hypernatremia (>150 mEq/L) due to an impaired thirst mechanism. Patients with nephrogenic DI usually have an intact thirst mechanism and adequate water intake; they usually compensate for renal water loss and may have a normal sodium level. \n\n217 https://t.me/usmleinnercircle USMLE Inner Circle \n\nClinical features of acromegaly local tumor effect Headache, visual field defects, cranial nerve defects \n\nMusculoskeletal Gigantism, frontal bossing , malocclusion of jaw , macrognathia, arthritis, carpal tunnel syndrome , enlargement of hands/feet \n\nSkin Skin thickening, hyperhidrosis (odor), skin tags \n\nCardiovascular Cardiomyopathy, hypertension , heart failure \n\nRespiratory Sleep apnea \n\nGastrointestinal Colon polyps/canc er , diverticulosis \n\nEndocrine Galactorrhea, hypogonadism, diabetes mellitus, hypertriglyceridemia \n\nAdditional features Enlarged tongue, thyroid , salivary glands, liver, spleen, kidney, prostate \n\nStimuli for secretion of antidiuretic hormone Osmotic Serum osmolality > -285 mOsm/kg H 2O Nausea \n\n## . Pain Physical or emotional stress \n\nNonosmotic . Hypotension \n\n## . Hypovolemia \n\n## . Hypoxia \n\n## . Hypoglycemia \n\nADH-related causes of polyuria & polydipsia Primary Central DI Nephrogenic DI \n\npolydipsia Defect I Water in take I ADH release from ADH resistance in pituitary kidney Idiopathic Chro ni c l ith iu m u se An tipsychotics Tra um aEtiology Anxious , Pituitary surgery Hypercalcemia middle-age Hereditary \n\nwomen lsc hem ic (AVPR2 mutations) encephalopathy \n\nClinical Low serum Na High serum Na Normal serum Na \n\nfeatures Endocrine Low Urine osmolality and specific gravity (<1.006) = DI \n\nHigh Urine osmolality and specific gravity (>1.006) = DM \n\n What is the likely diagnosis in a patient that presents with constipation , cold intolerance , low libido ,and hypoglycemia with eosinophilia on laboratory exam? \n\nHypopituitarism \n\npatient is experiencing secondary hypothyroidism, secondary adrenal insufficiency, and hypogonadotropic hypogonadism \n\nEosinophilia secondary to central adrenal insufficiency \n\n Remember : Aldosterone levels will be Normal \n\n## Thyroid \n\n What is the diagnostic test for thyroglossal duct cyst and why is it done?: \n\nU/S to evaluate cyst and confirm location of thyroid, screen TSH ;\n\n218 https://t.me/usmleinnercircle \n\n\n\nEvaluation of suspected polyuria \n\nComplete 24-ho u r u ri ne co ll ect ion \n\n## l l\n\nUrine output> 3L : Urine output < 3L :Polyuria present N ot true polyuri a ; worl< up causes of urina ry fr eq uen cy \n\n# !\n\nDilute urine : water diures is Primary polydipsia , d iabetes i nsipidus \n\n# l\n\nConcentrated urine : Osmot ic diure sj s\n\nI ncreased solute excretion (glu co se , ur ea , saline} \n\n~----------' - ---\n\nCl in ical features of hypopituitarism Pi tu i tary causes \n\n> o\n\nPrima ry (eg , ad e nom a) or metastat ic m ass Infiltration (eg, h emoc hroma tos is, lymphocytic hy pophysitis) Hemorrhage (pi tu itary apoplexy) or infarction (Sheehan syndrome} \n\nEtiology Hypothalamic causes \n\n> o\n\nM ass lesi ons \n\n> o\n\nRadiation therapy \n\n> o\n\nInfiltration (sa rcoid os is} \n\n> o\n\nTra um a to sku ll base Infections (tub ercu los is meningitis) ACTH deficiency (secondary adrena l i nsuffic ienc y) \n\nCuw..ld \n\n> o\n\nPostural hypo tension, tachycardia, fati gue , we igh t loss, hypoglycemia, eosi no philia \n\nHypothyroidism (central) \n\nCli nical presentation o Fatigue, co ld intolerance, co nstipat io n, d ry skin, bradycardia, sl ow ed deep tendon reflexes Go n adot r op ins \n\n> o\n\nWom en: Amenorrhea, inf ertility \n\n M en : Infertility, l oss of libi do Endocrine surgical excision \n\nNeed to make sure this is not the patients only functioning thyroid tissue and need to prevent postop hypothyroidism \n\nHyperthyroidism \n\n219 https://t.me/usmleinnercircle USMLE Inner Circle \n\n0Yes Evaluation of hyperthyroidism Measure TSH , free T3 & T4 \n\n..------~----, .-----\n\nPrimary hyperthyroidism \n\nTSH low Free T3 & T4 high Signs of Graves disease (goiter+ ophthalmopathy)? No \n\nSecondary hyperthyroidism \n\n TSHhigh Free T3 & T4 high MRI of pituitary gland \n\nRad ioactive iodine uptake (+ scan) High Low \n\n+Measure serum Diffuse pattern l Nodularpattem lthyroglobulin IHigh i i low \n\nIGraves disease I Toxi cadenoma Thyroiditis IExogenous hormone I Multinodulargoiter Iodide exposure Normal or elevated TSH \n\nEvaluation of thyroid nodules \n\nTSH level & thyroid US LowTSH Radioactive iodine scintigraphy Hypofunctional (\"cold \") or indeterminate nodule Hyperfunctional (\"hot\") nodule Consider FNA based on size & US findings Treat hyperthyroidism \n\nFNA =fine-needle aspiration ; us =ul trasonography . @UWorld \n\nManagement of postpartum thyroiditis Confirm diagnosis \n\n T4 and T3; ! TSH Thyroglobulin RAIU 0 T PO antibody; 0 TRAb \n\nHyperthyroid phase \n\n T4 and T3 ; ! TSH \n\nHypothyroid phase \n\n T4 and T3; tTSH \n\nEulhyroid phase \n\n Normal T4 ,T3, and TSH \n\n- Beta blocker for symptom control Breastfeedi ng or attempting pregnancy? Hypothyroid symptoms? TSH > 6 months \n\n- Levothyroxine \n\n_ Wean off Levothyroxine (as tolerated) Annual TSH measurement \n\nRAIU =radioiodi ne uptake; TPO =thyroid peroxidase; TRAb =thyrotropin receptor antibody. CUWor1d \n\nHyperthyroid bone disease \n\nE xcess thyroid h ormone \n\nI Renal ca lcium reabsorption ~\n\n Hypercalciuria \n\n Net calcium wasting PTH = parathyroid hormone Conversion 25-0 H-vitamin Dto 1,25- 0H-vitam in D Catabolism 1,25-0H -vitamin D \n\n I Gastrointestinal calcium absorption \n\n I Renal ca lcium reabsorption Endocrine Radioactive iodine \n\ncontraindicated in patients with severe ophthalmopathy (due to increased thyroid-stimulating immunoglobulin titers); glucocorticoids and antithyroid drugs may be given initially to minimize side effects of RAI in patients with mild ophthalmopathy \n\n What is a common complication of radioactive iodine when treating Graves disease ?\n\nPermanent hypothyroidism \n\nthe dose needed for treatment, as well the diffuse uptake of iodine in Graves disease, results in permanent hypothyroidism in >90% of patients \n\nIn contrast, when RAI is used to treat toxic nodular goiter and toxic adenoma , the radioisotope is taken up only by the autonomous thyroid tissue, and the function of the remaining normal tissue is usually adequate to prevent permanent hypothyroidism. Painless thyroiditis is associated with thyroid peroxidase autoantibodies and is considered a variant of chronic lymphocytic (Hashimoto) thyroiditis .\n\n220 https://t.me/usmleinnercircle \n\n## I Choice of treatment in Graves \n\n## Ihypenhyroid i sm \n\n# ! !Antithyroid drugs Radioactive iod i ne Thyroidectomy \n\n. Mild hyperthyroidi sm . Moderate to severe . Very large goiter \n\n. Older age with limited hyperthyroidism . Suspicion of thyroid with/Without mi ld life expectancy ophthalmopathy cancer \n\n. Preparation for . Patient preference in . Coex isti ng primary \n\nradioactive iodine or mild hyperthyroidism hyperparathyroidi sm \n\nthyroideotomy . Pregnant patients who \n\n# . Pregnancy (PTU in 1st cannot tolerate \n\ntrimester) thionamides \n\n. Severe \n\nophthalmopathy . Retrostemal goiter with obslructive \n\n> rop)'fthiouracil. PTU = p\n\nUWo rl dsymptoms \n\nClinical features of thyroid storm Precipitating Thyroid or nonthyroidal surgery \n\nfactors Acute illness (eg, trauma, infection), childbirth Acute iodine load (eg, iodine contrast) \n\n## . High fever Tachycardia, hypertension , congestive heart failure, cardiac arrhythmias (eg , atrial \n\nClinical fibrillation) \n\npresentation Agitation , delirium , seizure, coma Goiter, lid lag, tremor Nausea , vomiting, diarrhea , jaundice \n\nThyrotoxicosis with normal or j RAIU Thyrotoxicosis with t RAIU \n\n Painless (silent) thyroiditis \n\n Subacute (de Quervain) thyroiditis \n\n Graves disease Amiodarone-induced thyroiditis Toxic multinodular goiter . Excessive dose (or surreptitious intake) of levothyroxine Toxic nodule Struma ovarii \n\n## . Iodine-induced Extensive thyroid cancer metastasis \n\nRAIU = radioactive iodine uptake. Endocrine What is the likely diagnosis in a patient that develops post-operative high fever , tachycardia , hypertension , and lid lag with no muscle rigidity? Serum creatinine kinase is slightly elevated. \n\nThyroid storm \n\ntypically triggered by a specific event in patients with undiagnosed or inadequately treated hyperthyroidism (e.g. surgery, trauma, infection, CT scan with contrast due to acute iodine load) \n\n Also on the differential is pheochromocytoma , but will have no fever; episodes of pheochromocytoma can be precipitated by medications, especially anesthetic agents, and surgical procedures \n\n Also malignant hyperthermia -- look for similar symptoms but with elevated CK, hyperkalemia, and muscle rigidity \n\nHypothyroidism \n\nPainless thyroiditis is often a self-limited hyperthyroid phase of Hashimoto thyroiditis (hence the anti-TPO AB) \n\n221 https://t.me/usmleinnercircle USMLE Inner Circle \n\nClinical manifestations of Graves disease General Heat in to lerance, weight lo ss , sweating Eyes Lid lag, proptosis, diplopia \n\nSkin Hair loss, infiltrative dermopathy (pretibial myxedema) \n\nCardiovascular Tachycardia , hypertens ion, atria l fibr illa tion Nails Onycholysis, clubbing (acropachy) \n\nEndocrine Hyperglycem ia , hyp erca lcem ia , bone loss , me nst rua l irreg ula rities Gastrointestinal Diarrhea Neurology Tr emors, hyperreflexia, pro xi ma l muscle weak ness Thyroiditis Clinical featur es Diagnostic testing \n\nChro ni c au to immune thyroiditis Pr ed omin ant hypothyroid features Pos it ive TPO a ntibody (H as hi mo to th yro iditi s) Diffuse goit er Vari ab le radioiodi ne up take \n\nVa ri an t of c hron ic autoimmune thyro iditis Positive TPO antib ody \n\nPainless thyroiditis Mild, brief hyperthyroid phase Low radioiodi ne u ptake {s il ent thyroiditis) Sma ll, nontender goiter Sponta ne o us recovery Likely p ostv iral infla mm at ory process Elevat ed ESR & CRP \n\nSubac ut e thy roiditis Prom i ne nt f eve r & hyperthyroid sy mp toms Low radioiodi ne u ptake (de Quervain thy ro idi tis ) Painful/ten der goiter Endocrine What is the likely diagnosis in a patient with a long history of Hashimoto thyroiditis that develops a rapidly enlarging , firm goiter with dysphagia , hoarseness , and fever ?\n\nThyroid lymphoma \n\nmay also have facial plethora and cyanosis when raising the arms above the head due to compression of the subclavian vein and IJV between the clavicle and thyroid (Pemberton sign) \n\n What pregnancy complication is associated with subclinical hypothyroidism ?\n\nMiscarriage \n\ndue to high titers of anti-thyroid peroxidase antibodies ; increased risk in both euthyroid and hypothyroid women \n\n Subclinical hypothyroidism refers to a normal T4 level with mild elevation in TSH -- the elevated TSH is able to keep thyroid hormones at a normal level, hence subclinical ie no symptoms of hypothyroidism. Treat with levothyroxine , even if they do not have symptoms. \n\nEuthyroid Sick Syndrome \n\n Low T3 is thought to be the result of decreased peripheral conversion of T4 to T3. \n\nESS represents a mild, transient central hypothyroid state that functions to minimize maladaptive catabolism in severe illness. Factors that suppress conversion of T4 to T3 include: \n\nCaloric deprivation \n\nIncreased glucocorticoid and inflammatory cytokine (eg, tumor necrosis factor, interferon alpha) levels Elevated free fatty acid levels \n\n## Parathyroid Gland \n\n Treatment of chronic hypoparathyroidism is with calcium and vitamin D , but calcium and phosphorus levels must be closely monitored. A calcium-phosphorus product (serum calcium serum phosphorus) >55 increases the risk of soft tissue calcification .Calcification in the basal ganglia can cause extrapyramidal manifestations. \n\n222 https://t.me/usmleinnercircle \n\n> Euthyroid sick syndrome Early/mild Prolonged/severe T3\n\nt t \n\n> T4 Normal\n\nt \n\n> TSH Normal\n\nt \n\n> Reverse T3\n\nt t\n\nEndocrine Hyperparathyroidism \n\n What tests help localize the involved gland in hyperparathyroidism ?\n\nU/S and nuclear imaging ( 99-m technetium sestamibi scan below ) are most used \n\n What is the likely diagnosis in a patient with an elevated serum PTH/Ca2+ and normal urine Ca2+/Cr clearance ratio (> 0.02) ?\n\nPrimary hyperparathyroidism \n\ndifferentiated from familial hypocalciuric hypercalcemia by increased urine Ca2+ excretion (> 0.02) \n\n Newborn boy presents three days after delivery with tachypnea, tachycardia, spasms, seizures . Labs show PTH, Ca++. The remainder of exam shows no abnormalities. Most likely cause ?\n\nMaternal familial hypocalciuric hypercalcemia \n\nAsymptomatic so may go undiagnosed \n\nMaternal hyperCa++ causes hyperCa++ in fetus suppression of parathyroid glands \n\nAfter delivery, fetus presents with hypoparathyroidism and hypocalcemia \n\nDdx: DiGeorge will have CATCH features as well \n\n In patients with long-standing CKD , especially those with end-stage renal disease (ESRD), chronic parathyroid stimulation can lead to parathyroid hyperplasia . This is associated with autonomous PTH secretion (ie, not suppressed by rising calcium levels) due to downregulation of calcium-sensing receptor and vitamin D receptor in the parathyroid glands. The net effect, termed tertiary hyperparathyroidism , is characterized by: \n\nExtremely high serum PTH levels Hypercalcemia due to mobilization from bone \n\nHyperphosphatemia due to renal phosphate retention \n\n## Adrenal Gland \n\n223 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\n\n\n\n\n\n\nPrimary hyperparathyroidism \n\n Parathyroid adenoma (most common), hyperplasia, \n\nEtiology carcinoma Increased risk in MEN types 1 & 2A Asymptomatic (most common) \n\nSymptoms Mild , nonspecific symptoms (eg , fatigue , constipation) Abdominal pain, renal stones, bone pain , neuropsychiatric symptoms \n\nDiagnostic Hypercalcemia findings Elevated or inappropriately normal PTH \n\n Elevated 24-hour urinary calcium excretion Age <50 Symptomatic hypercalcemia \n\nIndications for Complications: Osteoporosis (T-score <-2 .5, fragility \n\nparathyroidectomy fracture) , nephrolithiasis/calcinosis, CKD (GFR <60 ml/min) Elevated risk of complications: Calcium ;:,,1 mg/dl above normal , urinary calcium excretion >400 mg/day \n\nCKD =chronic kidney disease; GFR =glomerular filtration rate ; MEN =multiple endocrine neoplasia ; PTH = parathyroid hormone .Endocrine Adrenal Excess \n\nConn Syndrome \n\n224 https://t.me/usmleinnercircle \n\nFunctional adrenal masses Clinical features Hormone levels \n\n# . Central obesity , moon facies, enlarged \n\nCortisol-producing dorsocervical fat pad . Elevated cortisol (urine, salivary) \n\nadenoma . Hypertension . Decreased ACTH & DHEAS \n\n(most common) . Proximal muscle weakness . No suppression by dexamethasone \n\n# . Hyperglycemia, hypokalemia \n\nAldosterone-producing . Hypertension . Elevated plasma aldosterone-to-plasma renin \n\nadenoma . Hypokalemia (muscle cramps, weakness) activity ratio . Elevated urine metanephrines &\n\n# . Paroxysmal tachycardia, headache , tremor \n\nPheochromocytoma catecholamines Hypertension . . Elevated plasma metanephrines \n\nCHEAS = dehydroepiandrosterone sulfate. \n\nPrimary hyperaldosteronism (Conn syndrome) \n\n## . Bilateral adrenal hyperplasia (-60%) or unilateral adenoma \n\nClinical features . Difficult-to-control hypertension \n\n## . Hypokalemia & metabolic alkalosis* \n\n## . No extravascular volume overload (aldosterone escape) \n\n## . Elevated plasma aldosterone & low plasma renin (ratio >20) \n\nDiagnosis . Absence of aldosterone suppression with oral saline load \n\n## . CT scan of adrenal glands to determine bilateral h ~e erelasia vs adenoma \n\nTreatment . Bilateral adrenal hyperplasia: MRA (eg , spironolactone) \n\n## . Unilateral adenoma: surgical resection preferred * In some patients, the characteristic electrolyte abnomialities are apparent only after a thiazide is initiated for blood pressure management. MRA = mineralocorticoid receptor antagonist. \n\nEvaluation of suspected hyperaldosteronism \n\nf PRA, f PAC ,PAC/PR A rat io - 10 \n\nSe condary hyp eraldost e roni sm Diuretic u se Cirrhos is or congestive h ea rt failure Renovascular hyp erten sio nRenin-secreting tumo rMalig nant hypertension Coarctation of aorta \n\n UWorld \n\nHypertension & hypokalemia Measu re plasma renin activity &pl asma aldosterone concentration \n\n! PRA, f PAC, \n\nPAC/PRA ratio ~20 \n\nAND \n\nPAC> 15 ng/dl \n\nPrimary hyperaldosteronism Adrenal computed tomography to determine etiology \n\n# TOth er ca uses of hyp e rt ens ion &hypokal emia Congenital adrenal hyperpl asia Glucocort icoid resistance Ex og enous mineralocorticoid Cushing's sy ndr ome Altered aldosterone metabolism Endocrine What is the likely diagnosis in a young patient with hypertension that develops \n\nsevere weakness and muscle cramps after beginning a low-dose thiazide diuretic? \n\nPrimary hyperaldosteronism \n\npatients with mild primary hyperaldosteronism are prone to developing diuretic-induced hypokalemia ; other findings include metabolic alkalosis and mild hypernatremia \n\n Adrenal vein sampling : aldosterone:renin ratio be 4x in unilateral adenoma on side of the tumor No difference between two sides in patients with bilateral \n\nCushing Adrenal suppression testing usually involves salt loading and documenting inability to suppress serum aldosterone. vs Morning cortisol levels check in Adrenal insufficiency \n\n225 https://t.me/usmleinnercircle USMLE Inner Circle \n\nHypertension & hypoka lemia Plasma aldosterone/ renin ratio Evaluate f or other ca u ses Eva lu ate for other ca u ses \n\n~ Adrenal imaging Unilatera l adeno ma or hyperplasia Consider s ur gery \n\nI Consider surgery I\n\nIMedical therapy I\n\nFeatures of Cushing syndrome \n\n# . Central obesity \n\n# . Skin atrophy & wide, purplish striae \n\n# . Proximal muscle weakness \n\nClinical . Hypertension \n\nmanifestations \n\n Glucose intolerance \n\n# . Skin hyperpigmentation (if due to ACTH excess) . Depression, anxiety \n\n# . 24-hour urinary cortisol excretion \n\nDiagnosis Late-night salivary cortisol assay . Low-dose dexamethasone suppression test Endocrine Hyperandrogenism (e.g Hirsutism) can be seen in Cushing syndrome due to ACTH -induced \n\nadrenal androgen production or co-secretion of cortisol and testosterone by an adrenal \n\ntumor. \n\nAdrenal Insufficiency \n\n What is the likely diagnosis in a patient with tuberculosis who presents with hyponatremia, hyperkalemia, and eosinophilia? \n\nPrimary adrenal insufficiency \n\nMost common cause world-wide is TB Peripheral eosinophilia, nonspecific finding sometimes seen with adrenal insufficiency, as cortisol normally facilitates eosinophil migration from the bloodstream into the tissues. \n\n Primary adrenal insufficiency is associated with increased levels of ADH. \n\nin response to volume depletion and increased corticotropin-releasing hormone; leads to dilutional hyponatremia \n\n In women with AI, features of hypogonadism (eg, loss of libido, decreased pubic hair) can be seen due to decreased adrenal androgen production; however, men with AI do not develop these findings as androgens are primarily produced in the testes. \n\n What anaesthetic is associated with adrenal insufficiency , especially in elderly and critically ill patients? \n\nEtomidate \n\ndue to inhibition of 11-hydroxylase \n\n226 https://t.me/usmleinnercircle \n\nPrimary adrenal insufficiency \n\n# . Autoimmune adrenalitis (most common) \n\n> Etiology\n\n# . Infection (eg, tuberculosis) \n\n# . Metastatic infiltration \n\n## . Fatigue, weakness, anorexia/weight loss \n\n> Clinical\n\n## . Nausea, vomiting , abdominal pain features . Salt craving, postural hypotension \n\n## . Hyperpigmentation \n\n## . Acute adrenal crisis: confusion , hypotensi on /shock \n\n> Laboratory\n\n## . Hyponatremia, hyperkalemia, eosinophilia \n\n> findings\n\n## . Lo w morni ng cortisol, hi gh ACTH \n\n> Treatment\n\n## . Glucocorticoids (eg, hydrocortisone, prednisone) \n\n## . Mineralocorticoids (eg, fludrocortisone) \n\n> ACTH =adreno co rt icotro pi chormone.\n\nEndocrine What is the most specific test of adrenal function ?\n\nCosyntropin test ( ACTH stimulation test )\n\nCosyntropin is synthetic ACTH analogue \n\n Because the ACTH assay can take several days, an ACTH stimulation test (cosyntropin test) is usually performed concurrently to rapidly confirm the diagnosis. Infusion of a 250-g bolus of cosyntropin normally triggers a rapid increase in serum cortisol. In contrast, patients with PAI will not have a significant rise. \n\nIn addition, most patients with central adrenal insufficiency have a blunted (minimal or suboptimal) response due to adrenal atrophy from chronically low ACTH. If results are indeterminate, further pituitary function testing can be considered. \n\n In patients with underlying chronic adrenal insufficiency, acute stressors (eg, procedure, illness, trauma) can trigger adrenal crisis , which presents with hypoglycemia and severe hypotension often refractory to initial volume resuscitation. \n\n## Pancreas \n\n227 https://t.me/usmleinnercircle USMLE Inner Circle \n\nIndeterminate Further testing to assess pituitary function \n\n UWorld \n\nSymptoms &/ or signs of adrena l insufficiency 250 g cosyntropin stimulation test with cortisol & ACTH levels Basal cortisol low, Basa l cortisol low, \n\nACTH high ACTH low \n\nMinimal co rti so l Minimal or subopt imal response to cortisol response to cosyntropin cosyntropi n \n\n## !\n\nPrimary adrenal Secondary or tertiary insufficiency adrenal in suffi cie ncy Normal response (cortisol l eve l> 20 g/ dl 30-60 min after cosyn tropin) Unlikely to be adren al insufficiency; investigate other ca uses \n\nAcute adrenal insufficiency (adrenal crisis) \n\n## . Adrenal hemorrhage or infarction \n\nEtiology . Illness/injury/surgery in patient with chronic Al \n\n## . Pituitary apoplexy \n\n## . Hypotension & shock Clinical features . Naus ea, vomiting, abdominal pain \n\n## . Fever, generalized weakness \n\nTreatment . Hydrocortisone or dexamethasone \n\n## . Rapid intravenous volume repletion \n\nAl = adrenal insufficiency. Endocrine Diabetes \n\n Glucosuria is not sufficient to establish diagnosis of DM \n\n What is the likely diagnosis in an insulin-dependent diabetic patient with anorexia , nausea /vomiting , early satiety , and post-prandial hypoglycemia without heartburn or epigastric pain? \n\nDiabetic gastroparesis \n\nhypoglycemic episodes due to insulin administration prior to meals followed by impaired gastric emptying and delayed absorption \n\n Monofilament testing is useful for determing the presence of peripheral neuropathy .\n\nTests pressure sensation with a 10g monofilament. Patients with neuropathy have a higher pressure threshold and loss of monofilament sensation, which are associated with increased risk of foot ulceration \n\n-Checked annually \n\n Insulin resistance is a fundamental response to injury/stress and is a well-known phenomenon in the post-op and post-trauma patient. \n\n Key idea: If a young patient develops diabetes, do NOT assume they have type 1 diabetes because a lot of children (especially now with high rates of obesity) are at risk for developing type 2 diabetes \n\nScreening \n\n228 https://t.me/usmleinnercircle \n\nClinical features of diabetic autonomic neuropathy Tachycardia, impaired exercise tolerance Ca rdi ovas cular Postural hypotension with loss of diurnal blood pressure variation Dry skin, pruritus, callus formation P er iph eral Foot ulcers & poor wound healing nerve s Charcot arthropathy (increased fracture risk with resultant secondary ulceration) Gastroparesis with delayed gastric emptying Gastro i nt es tinal Esophageal dysmotility with possible dyspepsia Intestinal invotvement with possible diarrhea, constipation, or fecal incontinence Er ectile dysfunction & retrograde ejaculation in men, decreased libido & dyspareunia in women Decreased ability to sense full bladder leading Genitourinary to i nco mple te emptying & decreased urination Eventual recurrent urinary tract infections &/or overflow incontinence ( eg , dribbling, poor urinary stream) Monofilament test Endocrine What test should be used to screen for diabetes mellitus in patients with polycystic ovarian syndrome ?\n\n229 https://t.me/usmleinnercircle USMLE Inner Circle \n\nIndications for testing 124 112 5 1\n\nThe indications listed below are consistent with the 2023 ADA guidelines. The 2021 USPS TF guideline recommends screening in adults aged 35-70 years with overweight or obesity. i;:l [2 6][24]1251 ~ 35 years of age History of prediabetes or gestational diabetes Patients < 35 years of age with both i;:J \n\no Overweight or obesity i;:l \n\no AND~ 1 additional risk factor for T2DM Presence of risk-enhancing comorbidities, including: \n\no HIV infection o Cystic fibros is o Post organ transplantation Consider in women who are planning pregnancy with any risk factor for T2DM (e.g., overweight or obesity). See \"Gestational diabetes\" for testing indications during pregnancy. If results are normal, repeat testing in asymptomatic patients at least every three \n\n0 years. Patients with prediabetes should be tested at least annually to detect progression to diabetes. [ 25 1\n\nScreening tests for diabetes mellltus Test Interpretat ion \n\n Preferred tes t m nonfasti ng state \n\nAt e ~ .5% = Diab@les mlilh l us \n\n 5. -6. 4% = ll ncmaSQd ~isk tor diabetes \n\n <5.7% = No~mal \n\n No caloric i ntake for >8 hours \n\nFasting blood :::126 mg / dl = Di abetes mellitus \n\ngl ue015,e . 100-125 mg/dl = Inc re ased risk for di ab etes \n\n <100 mg/dl = Normal \n\n :::200 mg / dl wi th symptoms of hype ~gl ycemia = Diabetes \n\nRa ,ndom glucose mellitus \n\nleve ls . 140a 199 mg/dl = lncrEJ 0\n\nLater: altered mentation, hyperventilation, abdominal pain I\n\n## . t Glucose (typically 300-800 mg/dl) \n\n## . Metabolic acidosis (b icarbonate < 18 mEq/L) Diagnosis t Anion gap . Positive serum ketones . High-flow IV fluids (normal saline) \n\nTreatment . IV insulin . Follow & replace potassium \n\nIV = intravenous. \n\nManagement of diabetic ketoacidosis \n\n## . Initial: give isotonic intravenous fluids \n\n## . Subsequent: \n\nFluids . Continue isotonic fl uids if serum Na <135 mEq/L \n\n## . Switch to half normal saline if serum Na ;,,135 mEq /L \n\n## . Add dextrose when serum glucose <200 mg/ dl \n\n## . Reduce insulin infusion rate when serum glucose <200 mg/dl \n\nInsulin . Hold insulin infusion if serum K+ <3.3 mEq/L \n\n# . Switch to subcutaneous insulin on OKA resolution Potassium . Give replacement when serum K+ <5.3 mEq/L .. \n\nBicarbonate . Consider replacement for severe OKA with blood pH S6.9 \n\n*Nonnalization of anion gap & patient able to eat. ** Due to total body potassium depletion and risk of insulininduced hypokalemia. DKA = diabetic ketoacidosis. Endocrine Treatment \n\n What type of insulin therapy is indicated in type 2 diabetic patients with persistently elevated A1C levels despite oral antidiabetic regimen ( i.e. failed dual therapy )? \n\nBasal supported oral therapy ( long-acting insulin i.e. glargine (Lantus) before bed time combined with oral antidiabetic drug )\n\n What is the next step in management for a diabetic patient taking metformin and nightly insulin glargine that presents with an elevated hemoglobin A1c despite normal fasting glucose levels ?\n\nAdd rapid-acting mealtime insulin \n\nthis patient likely has postprandial hyperglycemia pt. with elevated HbA1c despite good control of fasting glucose may have post-prandial hyperglycemia . A combined regimen of long-acting basal insulin (glargine) to control baseline fasting glucose and rapid-acting mealtime insulin (aspart) to control postprandial glucose excursions may be needed to provide optimal control \n\n The indications for insulin therapy in diabetes is a newly diagnosed patient with an A1C >8.5% or symptomatic diabetes, pregestational and gestational diabetes, and end-stage renal failure .\n\nAlso, if patient has insufficient glycemic control ( target A1c not reached ) over a 3-month period with metform + other antidiabetic drug --> initial basal insulin \n\n Oral antidiabetic drugs are contraindicated in renal failure. Should also be avoided in patients undergoing surgery or with severe illness. \n\nWhat should be used instead? Insulin therapy \n\n Recommended add-on therapy (ie, in addition to metformin, which remains the first-line agent for type 2 diabetes mellitus) for patients with established cardiovascular disease, includes the following: \n\nSGLT-2 inhibitors (eg, canagliflozin, empagliflozin) cause increased urinary glucose excretion. These agents induce weight loss (due to urinary glucose loss) and decrease the risk for atherosclerotic \n\n231 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nProgressive therapeutic intensification in type 2 diabetes mellitus \n\n UWortd Metformin (preferred initial therapy) Metformin + oral antidiabetic agents, GLP-1 analogue, or basal insulin Basal-bolus insulin therapy Endocrine cardiovascular disease and heart failurerelated mortalities . They also slow progression of albuminuria in diabetic nephropathy. \n\nGlucagon-like peptide-1 (GLP-1) receptor agonists (eg, semaglutide, liraglutide) regulate glucose by slowing gastric emptying, suppressing glucagon secretion, and increasing glucose-dependent insulin release, making them less likely to cause hypoglycemia. Similar to SGLT-2 inhibitors, GLP-1 agonists induce weight loss and reduce mortality associated with atherosclerotic cardiovascular disease .\n\nMorning glucose is dependant on how much long acting insulin you gave at night. \n\n Giving a basal-bolus regimen involves giving basal insulin 1-2 times daily + a bolus injection 30-45 minutes before meals \n\nBolus injection needs to be adjusted to preprandial blood glucose measurements \n\n 1 unit of insulin lowers the blood glucose by 30-40 mg/dL. \n\n232 https://t.me/usmleinnercircle \n\n\n\nType 2 diabetes and comorbid cardiovascular disease Lifestyle . Smoking cessation , re gular exercise \n\n# . Reduced saturated fat refined sugar intake \n\nCardioprotective antidiabetic agents . GLP-1 receptor agonists (eg, liraglutide) \n\n# . SGLT-2 inhibitors (eg, empagliflozin) \n\n# . Stalins \n\nLipid/anti platelet therapy Low-dose aspirin .\n\nBlood pressure control . Goal BP <130-140/80-90 mm Hg \n\n ACE inhibitor/ARB preferred \n\nACE= angiotensin converting enzyme; ARB= angiotensin receptor blocker; BP= blood pressure; GLP-1 =glucagon-like peptide-1 ; SGLT-2 \n\n=sodium-glucose cotransporter-2. \n\nSGLT-2 inhibitors* Mechanism of action . Increased urinary glucose excretion (block proximal tubule glucose reabsorption) \n\n## . Reduced progression of nephropathy & albuminuria \n\nPossible benefits . Reduced cardiovascular morbidity & mortality \n\n## . Reduced hospitalizations for heart failure Weight loss \n\nAdverse effects . Euglycemic ketoacidosis \n\n## . Increased risk of genitourinary infections Type 1 OM \n\nContraindications . History of OKA \n\n## . Impaired renal function (eGFR <30-45 mUmin/1.73 m 2)*For example, canagliflozin & empagliflozin. \n\nDKA = diabetic ketoacidosis; DM = diabetes mellitus; eGFR = estimated glomerular filtration rate; SGLT-2 =sodium-glucose cotransporter 2. Endocrine What drug should be discontinued in an acutely ill patient with sepsis and acute renal failure taking low-dose aspirin, atorvastatin, metformin, and sitagliptin? \n\nMetformin : Contraindicated in CHF , CKD , and liver disease (risk of lactic acidosis )\n\ndue to less metformin excretion; not recommended with creatinine >1.4 \n\nNephrotoxins, such as NSAIDs and metformin , should NOT be given to patients with acute renal failure or sepsis; low-dose aspirin has not been shown to precipitate or worsen renal failure \n\n How should patients with T1DM manage their insulin when exercising? Exercise increases insulin sensitivity \n\nDecrease insulin dosage by 1-2 units per 20-30 minutes of physical activity \n\nMonitor glucose before, during, after exercise Eat slowly absorbed carbs after exercise to prevent delayed hypoglycemia \n\nDiabetic Nephropathy \n\n Random urine albumin-to-creatinine ratio testing is the most sensitive test to detect early elevations in albumin excretion. Perform annually. \n\n What is the most beneficial therapy for reducing the progression of diabetic nephropathy ?\n\nStrict blood pressure control \n\n233 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nProblems: early-morning hyperglycemia \n\n Dawn phenomenon \n\n A common problem (especially in young type 1 diabetic patients) Definition: early-morning hyperglycemia occurs because of the physiological increase of growth hormone levels in the early morning hours, which stimulates hepatic gluconeogenesis. The subsequent increase in insulin demand cannot be met in diabetic insulin-dependent patients, resulting in elevated blood glucose levels in the morning . \n\n Treatment : measurement of nocturnal blood glucose levels before initiating insulin therapy. The long-acting \n\ninsulin dose may be given later (around 11 p.m.) or increased under careful glycemic control. Treatment with an insulin pump may be considered in children. Somogyi effect \n\n Rare Definition: early-morning hyperglycemia i;:J because of a counterregulatory secretion of hormones i;:J that is triggered by nocturnal hypoglycemia secondary to an evening insulin injection Treatment : reduction of the evening dose of the long-acting insulin \n\nDiabetic kidney disease \n\n## . Persistent albuminuria (>3 months apart) \n\nClinical findings . Initial hyperfiltration followed by progressive decline in GFR \n\n## . Hypertension usually present \n\n## . Screen at the time of diagnosis in type 2 OM \n\n## . Screen 5 years after the diagnosis in type 1 OM \n\nEvaluation . Serum creatinine \n\n## . Urine spot albumin to creatinine ratio (or 24-hour urine protein) \n\n## . Urinalysis/urine microscopy (to exclude other causes) \n\n## . Intensive glycemic control o Target hemoglobin A1c S7% (for most patients) \n\n0 SGLT2 inhibitor preferred ; G LP-1 agonist \n\n## . Blood pressure control \n\nManagement/prevention o Target blood pressure <130180 mm Hg o ACE inhibitor preferred (or angiotensin II receptor blocker) \n\n## . General cardiovascular risk management \n\n0 Smoki ng cessation \n\n0 Lipid management \n\nOM= diab etes mellitus; GFR =glomerular filtration rate ; GLP-1 =glucagon-li ke peptide-1 ; SGLT2 =sodium-glu cos e c ot r ans po rter-2 .Endocrine Intensive glycemic control (HbA1c < 7) is important, but intensive BP control is the primary intervention proven to slow the decline in GFR \n\n A patient's diabetes is considered well controlled if the HbA1c is < 7.0 % Tight glycemic control in patients with diabetes decreases the risk of micro -vascular complications such as retinopathy and nephropathy .\n\nHas uncertain effect on macrovascular complications (MI, stroke) and all-cause mortality. \n\nACCORD trial showed that very intensive glycemic targets (ie, A1c between 6.0% and 6.5% )appear to increase risk of all-cause and cardiac mortality. \n\nMetabolic Syndrome \n\nMetabolic syndrome is diagnosed when at least 3 of the 5 following criteria are met: 1. Abdominal obesity (waist circumference > 40 inches in males, > 35 inches in females) 2. Fasting glucose (> 100-110 mg/dL) 3. Blood pressure (> 130/80 mmHg) 4. Triglycerides (> 150 mg/dL) 5. HDL cholesterol (< 40 mg/dL in men, < 50 mg/dL in women) \n\nA major pathogenic factor underlying metabolic syndrome is insulin resistance. \n\nHypoglycemia \n\n234 https://t.me/usmleinnercircle \n\n> Effect of intensive glycemic control in type 2 diabetes Macrovascular complications No change (short-term) (eg , acute myocardial infarction, stroke)\n> Microvascular complications Improve (eg , nephropathy, retinopathy)\n> Mortality No change or increased\n> Hypoglycemia in patients without diabetes mellitus\n> Drugs: quinolones, quinine, beta blockers Alcohol (usually with prolonged starvation) Sepsis/critical illness Adrenal insufficiency lnsulinoma Surreptitious insulin , sulfonylurea, or meglitinide use Depleted glycogen stores (anorexia nervosa) Severe hepatic failure\n\nEndocrine It can occur in those with sepsis or other critical illnesses due to increased use of glucose in the \n\ntissues , which is promoted by inflammatory cytokines .Sepsis may also lead to suppression of gluconeogenesis in the liver. \n\n## Endocrine Tumor \n\n Post-operative adjuvant therapies for papillary thyroid carcinoma may include radioiodine ablation and/or suppressive doses of thyroid hormone. \n\nthyroid hormone suppresses TSH, which can stimulate growth of occult residual or metastatic disease; adjuvant therapy is usually for patients with increased risk of recurrence \n\n Serum thyroglobulin measurements are used as a tumor marker once the normally functioning thyroid tissue is removed. Medullary thyroid cancer arises from the calcitonin -secreting parafollicular C cells .\n\nSerum calcitonin levels correlate with the risk of metastasis and recurrence , and are measured serially following surgery .\n\nVIPoma \n\n Facial flushing present in 20% \n\nTreatment: \n\n1. IV volume repletion ,2. octreotide to decrease diarrhea, watery diarrhea (can be tea coloured and odourless), \n\n235 https://t.me/usmleinnercircle USMLE Inner Circle \n\nHypoglycemia in insulin ther ap yRi sk fa ct ors . Long-standing type 1 diabetes \n\n## . Pancreatogenic diabetes \n\nManifestations . Mild to moderate (neurogenic symptoms): anxiety, tremor, palpit at ions, sweati ng \n\n## . Severe (neuroglycopenic symptoms ): confusion, seizure, loss of consciousness \n\n## . Query pat ients regarding hypoglycemic symptoms \n\nManagement . I nd ividualized glycemic targets \n\ns tr a te gies . Flexible insulin dosing regimen \n\n## . Emergency glucagon kits \n\nClinical features of VI Poma \n\n Watery diar rhea C linical Hypo- or achlorhydria due to ! gastric acid secretion \n\npre se nta tio n Associated flushing, lethargy, nau sea, vomiting, \n\nmusc le wea kn ess/cramps \n\n Hypokalemia (t int est inal potassium sec retion) Hypercalcemia (increased bone resorption} \n\nLaboratory Hyperglycemia due to increased glycogenolysis \n\nfi ndings Stool studies show secretory diarrhea with t sodium & os molal gap <50 mOsml kg Wa tery diarrhea wi th VIP level >75 pg/ml \n\nDiag no sis Ab dom inal CT or MRI to localize t umo r in pancreas (usually in pancreatic tail} Endocrine 3. and possible hepatic resection in patients with metastasis to the liver \n\n Carcinoid syndrome can cause flushing, diarrhea, and bronchospasm, but occurs in the small intestine (not the pancreas) \n\nZollinger Ellison \n\n Why can Zollinger-Ellison Syndrome present with diarrhea and steatorrhea? \n\nIncreased gastric acid secretion decreases the pH of intestinal contents, inactivating pancreatic enzymes \n\nInterferes with emulsfication of fat by bile acids and damages epithelial cells and villi --> malabsorption \n\n Ulcers distal to the duodenum in the jejunum suggest excess gastric acid that cannot be fully neutralized in the duodenum \n\nNeuroblastoma \n\n236 https://t.me/usmleinnercircle \n\nZollinger-Ellison syndrome \n\n## . Age 20-50 \n\nEpidemiology 80 % Sporadic/20% MEN1 .\n\n## . Multiple & refractory peptic ulcers \n\nClinical features . Ulcers distal to duodenum \n\n## . Chronic diarrhea \n\nDiagnosis . Markedly elevated serum gastrin (>1,000 pg/ml ) in the presence of normal gastric acid (pH <4) \n\n## . Endoscopy \n\nWorkup CT scan/MRI & somatostatin receptor scintigraphy for tumor localization . \n\n> MEN1\n\n= multiple e nd oc rin e n eo plasia type 1. \n\nNo gastrinoma UWorld \n\nNegative \n\nSuspected gastrinoma Endoscopy shows multiple stomach ulcers & thickened gastric folds Check serum gastrin level off PPI therapy for 1 week \n\n110-1000 pg / ml Secretin stimulation test Check gastric pH off PPI therapy for 1 week Further testing to localize gastrinoma No gastrinoma Endocrine Calcifications and/or hemorrhages may be seen on X-ray \n\n Tumor involvement in the cervical paravertebral sympathetic chain can lead to ipsilateral Horner Syndrome \n\nMEN Pheochromocytoma \n\n## Endocrine Drugs \n\nWhat should be suspected in a patient taking PTU or methimazole that presents with fever and sore throat ?Raccoon Eyes \n\n237 https://t.me/usmleinnercircle USMLE Inner Circle \n\nNeuroblastoma Pathogenesis . Neural crest origin \n\n## . Involves adrenal medulla, st meathetic chain \n\n## . Median age <2 \n\n## . Abdominal mass \n\nClinical features . Periorbital ecchymoses (orbital metastases) \n\n## . Spinal cord compressio n from epidural invasion (\"dumbbell tumor\") \n\n## . O 12 soclonus-m:ioclonus S:indrome \n\n## . Elevated catecholamine metabolites \n\nDiagnostic findings . Small , round blue cells on histology \n\n## . N-myc gene amplification \n\nMultiple endocrine neoplasia type 1 Manifestation Clinical features Pituitary adenomas Secretion of prolactin, growth hormone, ACTH (or \"nonfunctioning\" (10 %-20%) tumors) Mass effects (eg, headache, visual field defects) \n\nPrimary hyperparathyroidism Multiple parathyroid adenomas or parathyroid hyperplasia Hypercalcemia (eg, polyuria, kidney stones, decreased bone (>90%) density) Gastrinoma - recurrent peptic ulcers \n\nPancreatic/gastrointestinal lnsulinoma - hypoglycemia \n\nneuroendocrine tumors VIPoma - secretory diarrhea, hypokalemia, hypochlorhydria (60%-70%) Glucagonoma - weight loss, necrolytic migratory erythema, hyperglycemia \n\nPheochromocytoma \n\n# . Classic triad : episodic headache, sweating & tachycardia \n\nIndications for testing Resistant HTN or HTN accompanied by unexplained j glucose \n\n# . Family history or fam ilial syndrome (eg , MEN2, NF1 , VHL) \n\n# . Urine or plasma metanephrine levels \n\nDiagnostic approach Confirmatory abdominal imaging for j metanephrines \n\nNotable features 10% bilatera l, 10% extraadrenal , 10% malignant Preoperative alpha blockade prior to beta blockade \n\nManagement Laparoscopic or open surgical resection .\n\nHTN = hypertension; MEN2 = multiple endocrine neoplasia type 2; NF1 = neurofi bromatosis type 1; VHL = von Hippel-Lindau syndrome. Endocrine Agranulocytosis \n\nwarrants discontinuation of the drug and WBC count measurement \n\n A total WBC count less than 1,000/cubic mm warrants permanent discontinuation of the drug. If the total WBC count is more than 1,500 per cubic mm, antithyroid drug toxicity is unlikely to be the cause of the sore throat and fever. \n\n Routine monitoring of the granulocyte count is not cost effective and not advocated \n\n## Miscellaneous \n\nMilk Alkali Syndrome Hypoglycemia associated autonomic failure \n\n238 https://t.me/usmleinnercircle \n\nMajor drug interactions of levothyrox ine \n\nBile acid bindi ng agents (eg, cholestyrami ne )\n\nLevothyroxine absorption Ir on, ca lci um , aluminum hydroxide P roton pu mp in hi bitors, sucralfate \n\nTBG concentration Estrogen (oral), t amo xifen, ra loxifene Heroin, methadone Androgens, glucoco rti coids \n\nTBG concentration An abo l ic steroids Slow-release ni cot inic ac id Rifampin \n\nThyroid hormone metaboli sm Phenytoin Carbamazepine \n\nTBG = thyroxine-binding globulin . \n\nMilk-alkali syndrome \n\n Exce ssive intake of calcium & absorbable alkali Pathophysiology Renal vasoconstriction & decreased GFR Renal loss of sodium & wate r, reabsorption of bicarbonate Na usea, vom iting, constipation \n\nSymptoms Polyuria , polydipsia \n\n# . Neuropsychiatric symptoms Hypercalcemia \n\nLaboratory Metabolic alkalosis \n\nfind ings Acute kidney injury \n\n# . Suppressed PT H Discontinuation of ca usativ e agent \n\nTreatment . Isotonic saline followed by furosemide \n\nGFR = glomerul ar filtration rate; PTH = parathyro id hormone. Endocrine Hypoglycemia normally prompts a catecholamine (eg, epinephrine) surge, which increases hepatic glucose production and triggers hypoglycemic symptoms. Recurrent or severe hypoglycemia in patients with long-standing diabetes reduces the glucose-raising effects of epinephrine and suppresses the symptoms related to the catecholamine surge, increasing the risk for progressively worsening hypoglycemic episodes. \n\n Those with long-standing diabetes (ie, >5 yr) often also have alpha cell failure , which can lead to decreased glucagon secretion and exacerbate hypoglycemia. \n\n## Endocrine Paeds \n\n Fetal goiters can be caused by inborn errors of thyroid hormone metabolism , developmental \n\nabnormalities of the thyroid , iodine excess or deficiency , transplacental passage of maternal thyroid-stimulating antibodies , or transplacental passage of antithyroid drugs such as propylthiouracil. \n\nLarge goiters can compress the esophagus, leading to polyhydramnios , or the airway , leading to \n\nrespiratory distress at birth .\n\nNeonatal Thyrotoxicosis Congenital hypothyroidism \n\n239 https://t.me/usmleinnercircle USMLE Inner Circle \n\nHypoglycemia-associated autonomic failure \n\nNormal response Hypoglycemia Epineph ri ne release Lo ng-stan ding diabetes Hypoglycemia Epineph ri ne release Hypoglycemic awareness Hypoglycemic awareness Behavioral response \n\nCVWortd \n\n## .Pathophysiology ...Clinical features ..\n\nDiagnosis ..Treatment .\n\nHepatic glucose producti on \n\nCorrectio n of hypoglycemia \n\nBehavioral response \n\nNeonatal thyrotoxicosis \n\nHepatic glucose producti on \n\nRisk for seve re hypoglycemia \n\nTrans pl acental passage of maternal anti-TSH receptor antibodies Antibodies bind to inf ant 's TSH receptors & cause excessive thyroid hormone release Warm , moist skin Tachycardia Poor feed ing , irritability, poor weight gain Low bi rth weight or preterm birth Maternal anti-TSH receptor antibodies 2:500% normal Self resolves within 3 months (disappearance of maternal antibody) Methimazole plus j3 blocker Endocrine Neonate with umbilical hernia, jaundice, hypotonia, decreased activity, poor feeding, macroglossia \n\nInfants usually appear normal due to presence of maternal hormones \n\nCretinism -- impaired development of brain, skeleton \n\n What is the most common cause of congenital hypothyroidism worldwide? \n\nThyroid dysgenesis \n\ne.g. aplasia, hypoplasia, ectopic gland \n\nT/t: Levothyroxine ( necessary to prevent neurodevelopmental injury) \n\n Delayed passage of meconium (first stool at >48 hr of life) - CF - Hirchsprung - Congenital Hypothyroidism \n\nCongenital Adrenal Hyperplasias \n\nAll receive glucocorticoid therapy \n\n17-: Spironolactone , Na+ intake, estrogen therapy for females] 21-: lifelong fludrocortisone (aldosterone substitute )11-B: Spironolactone , Na+ intake Partial deficiency of 21-hydroxylase. Basically similar to 21 alpha deficiency but with normal gluco and mineralocorticoids \n\n240 https://t.me/usmleinnercircle \n\nCongenital hypothyroidism \n\n> Usually asymptomatic at birth (rarely causes delayed meconium passage) After maternal thyroxine wanes (weeks to months)\n> oLethargy, poor feeding\n\nClinical o Enlarged fontanelle \n\nmanifestations o Protruding tongue, puffy face, umbilical hernia \n\n> oConstipation\n> oProlonged jaundice\n> oDry skin\n\nDiagnosis t TSH & ! free thyroxine levels Newborn screening \n\nTreatment Levothyroxine *\n\nPrognosis No deficits if treatment started in neonatal period Untreated disease is associated with neurocognitive dysfunction (eg , ! intelligence quotient) \n\n> Avoid coadministration with soy products, iron , or calcium.\n\nNonclassic congenital adrenal hyperplasia \n\n Autosomal recessive \n\nPathophysiology ! 21-hydroxylase activity Normal gluco- & mineralocorticoids j Androgens Early pubic/axillary hair growth Severe acne \n\nClinical features Hirsutism & oligomenorrhea in girls j Growth velocity & bone age j 17-hydroxyprogesterone level \n\nTreatment Hydrocortisone Endocrine 241 https://t.me/usmleinnercircle USMLE Inner Circle \n\nAdrenal steroids and congenital adrenal hyperplasias \n\n~ Ketoconazole /blocks several ste ps mstero1do qeneS1s )\n\n# ! ~ Ch oles terol [v,a SIA R' ) \n\n-l Anastrozole , le t rozole , exemestane 17 0. h vdrox las e\n\nPrea nenotone \n\n# l\n\n1~\n\n17 -hydro, yp regn enolone --ft Dehydroep ,androstero ne [ DHEA \n\n# lde hvd ro J ri c '\"' \n\nProges terone 17a-hy drox ylase \n\n## @~~ _J __ ____,.J_ __ _J \n\n11 - deoxycorticoste rone Cor t icoste rone \n\n# j\n\nAldosterone \n\nAngiotensin II 1l deoxycor t1 sol \n\nMety rapone \n\nCortiso l\n\n# 11-0-Gl ycyrrheti ni c aci dCor t isone ZONA FASCICULATA Glucocorticoids \n\n# j\n\nTestosterone ZONA RETICULARIS Androgens Ar omatase 5 -reductase \n\n# 1Estr adiol \n\nDihy drotestoste rone \n\n[ DH TI \n\nFinas ter ide \n\nPeriphera l tissue \n\nV\n\nVGynae & Reproductive Health \n\n# Gynae & Reproductive Health Gynaecology Physiology Physiologic Leukorrhea PMS Dysmenorrhea Menopause Infertility Ovarian Hyperstimulation Syndrome Amenorrhea Craniopharyngioma vs Kallmann's Hematocolpos Hirsutism Hyperandrogenism Ovarian Hyperthecosis Abdominal Pain PID Mid Cycle Pain PCOS Obesity and Anovulation Breast Nipple Discharge Lactation Uterus Fibroid Endometriosis Abnormal Menstrual Bleeding Adenomyosis Uterine Polyp Endometrial Cancer Cervix Cervicitis Pap Smear CIN Cervical Cancer Ovary Cyst Torsion Ovarian Cancer Vulva Labial Adhesion Bartholin Cyst Lichen Sclerosus Vulvar Lichen Planus Vulval Cancer Vagina \n\n242 https://t.me/usmleinnercircle Gynae & Reproductive Health Gynaecology \n\nPhysiology Vaginismus Cancer Miscellaneous Urethral Diverticulum Disorders of Sex Development Turner Syndrome Aromatase Deficiency Mullerian Agenesis 5-Alpha Reductase Male Gynecomastia Male Breast Cancer Hypogonadism Urethritis Scrotum Varicocele Hydrocele Prostate Prostatitis Prostate Cancer & BPH Penis Erectile Dysfunction Balanitis Penis Fracture Peyronie Disease Phimosis Testes Cryptorchidism Cancer Repro Paeds Precocious Puberty Neonatal Withdrawal Bleeding Drugs Progesterone OCP & IUD Emergency Contraceptive SERM PDE-5 Inhibitors \n\n243 https://t.me/usmleinnercircle USMLE Inner Circle Gynae & Reproductive Health What is typically the first sign of puberty in girls ?\n\nBreast development (thelarche) \n\nremembered with the mnemonic \" boobs , pubes , grow , flow \"\n\nPhysiologic Leukorrhea \n\n Cervical mucus just prior to ovulation is profuse, clear, thin, and corresponds with an LH surge .\n\nNot an indication of infection. \n\nPhysiologic leukorrhea is a white , odourless, cervical discharge composed of cervical mucus, normal vaginal flora, and vaginal squamous epithelium. \n\nNo signs of infection like pruritis, pain, fever, few PMN cells Occurs mid cycle due to Estrogen surge \n\nPMS \n\n Do not recommend treatment without first confirming the diagnosis using a menstrual diary \n\nover 2 menstrual periods !\n\nDysmenorrhea Symptoms typically occur 1-2 weeks before menses (luteal phase) and resolve after menses (follicular phase) \n\n244 https://t.me/usmleinnercircle \n\n> Norma l pubertal gro wt h in girls I\n\nIPeak height \n\n> ~elocity\n\n# -r 'J\n\n,, V \\\n\n# - ..,,,,, \n\n## \\\\\n\n\\ \n\n> Bre ~st Menarche\n\n## \\develo bment \n\n'I \\\n\nI \n\n> 10 11 12 13 14 15 16 17 18\n> Age (years)\n> --Averagemat1.1' 8b0n\n\nPremenstrual syndrome and premenstrual dysphoric disorder \n\n Symptoms occur during luteal phase \n\nClinical . Physical: bloating, fatigue , headaches, hot flashes , breast tenderness \n\nfeatures Affective: anxiety, irritability, mood swings, decreased interest; more severe in premenstrual dysphoric disorder \n\nEvaluation . Symptom/menstrual diary \n\nTreatment Selective serotonin reuptake inhibitor Gynae & Reproductive Health The features of primary dysmenorrhea includes pain before/during menstruation , most likely due to endometrial PGF2 (prostaglandin) production causing vasoconstriction/ischemia and stronger uterine contractions. Also causes Nausea , Vomiting , Diarrhoea \n\nThe treatment includes NSAIDs ( first-line ) and OCP's ( refractory ).\n\nOCP's decrease PG levels by suppressing ovulation \n\n Patients with any of the following clinical features should be evaluated for secondary causes of dysmenorrhea :Symptom onset at age >25 Unilateral (non-midline) pelvic pain \n\nNo systemic symptoms (eg, fatigue, nausea) during menses \n\nAbnormal uterine bleeding (eg, intermenstrual bleeding, postcoital spotting) \n\nMenopause \n\n In women with regular menstrual cycles, infertility can occur due to diminished ovarian reserve ,characterized by decreased oocyte number and quality .vs pain throughout the cycle in endometriosis \n\n245 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDiagnosis Primary dysmenorrhea Endometriosis Fibroids Adenomyosis Pelvic congestion \n\n\n\nDifferential diagnosis of dysmenorrhea Primary dysmenorrhea Clinical features Etiology . Excessive prostaglandin production Crampy lower abdomen &/ back pain during menses Age <30 Normal examination . BMI <20 kg/m 2 Tobacco use Pain peaks before menses Dyspareunia \n\nRisk factors . Menarche at age <12 Infertility Heavy/long menstrual periods \n\n# . Sexual abuse Heavy menses wi th clots Constipati on , urinary frequency, pelvic pain/heaviness . Pain first 2-3 days of menses Enlarged uterus on examinati on Clinical features . Nausea, vomiting, diarrhea Dysmenorr hea , pelvic pain Normal pelvic examination Menorrhagia Bulky, globular & tender uterus . Nonsteroidal anti-inflammatory drugs \n\nManagement \n\n Combination oral contraceptive pills Dull & ill-defined pelvic ache that worsens wi th stand i ng Dyspareunia \n\nFollicle number Ovarian reserve with aging \n\n1,000,000 Optimal fertility 100,000 10,000 Decreased fertility End of fertility Irregular cycles 1, QQQ ~-+--~ l -'--1 _1_ .,__ I ~I _1_ ~1 ~1_ 1~ 1 ~l ~ l -'--1 +-' - -'-I ~1 _ 1 _ 1 ~l~ l ~----' ~ ----'-'---'-----'--+----'-----+ - -'--1 _,_ I -+----'-I ~I--'-----+ -' \n\n UWor ld 0Birth 18 37 \n\nAge (yrs) \n\n41 45 51 \n\nMenopause Gynae & Reproductive Health Regular menstrual periods still occur due to continuing ovulation, but fecundability (ie, conception rate ) decreases due to diminished oocyte quality. \n\n Increased FSH , as more FSH is needed for ovulation of those last left eggs. \n\n Vaginal atrophy can also develop in postpartum females due to low estrogen levels secondary to Lactational Amennorhea \n\n Hormone replacement therapy is only indicated for the treatment of vasomotor symptoms in women age < 60 who have undergone menopause within the past 10 years. \n\ne.g. hot flashes, sleep disturbances; \n\nnot indicated for chronic disease prevention (e.g. osteoporosis, coronary heart disease) \n\n Menopausal women with vasomotor symptoms and contraindications to HRT are typically managed with non-hormonal therapy, such as SSRIs .\n\ncontraindications include history of coronary heart disease, thromboembolism ,\n\nTIA/stroke, breast cancer , or endometrial cancer \n\n What is the effect of low estrogen levels on vaginal pH ?\n\nIncreased pH (> 5) \n\nthus increased pH with normal urinalysis may indicate a hypoestrogenic state (e.g. atrophic vaginitis )\n\n What is the next step in diagnosis for a middle-aged woman that presents with \"night sweats \", insomnia , and irregular menses ? Pregnancy test is negative. Very high levels of FSH is characteristic of menopause. Dx Clinically ; Estrogen/ FSH levels NOT measured \n\n246 https://t.me/usmleinnercircle \n\n> Menopause Genitourinary syndrome of menopause\n> Vasomotor symptoms\n\n# . Vulvovaginal dryness, irritation, pruritus \n\n> Oligomenorrhea/amenorrhea\n\n# . Dyspareunia Sleep disturbances Symptoms . Vaginal bleeding \n\n> Clinical features Decreased libido\n\n# . Urinary incontinence, recurrent urinary tract infection Depression . Pelvic pressure Cognitive decline Vaginal atrophy . Narrowed introitus Clinical manifestations \n\n> Diagnosis\n\n i FSH \n\n# . Pale mucosa, ! elasticity, ! rugae \n\n> Physical examination\n\n# . Petechiae, fissures \n\n# . Loss of labial volume \n\n> Treatment Topical vaginal estrogen\n> Systemic hormone replacement therapy\n\n# . Vaginal moisturizer & lubricant \n\n> Treatment Topical vaginal estrogen\n\n# .\n\nGynae & Reproductive Health Measure serum TSH and FSH \n\nthese symptoms could be due to menopause or hyperthyroidism , thus both should be evaluated \n\n Bilateral salpingo-oophorectomy in postmenopausal women may result in re-emergence of menopausal symptoms due to an abrupt decrease in circulating androgens .\n\nwhile postmenopausal ovaries no longer produce estrogen, they continue to produce androgens ,which are peripherally converted to estrone and estradiol \n\n Female sexual interest/arousal disorder is a sexual dysfunction commonly seen in \n\npostmenopausal women . It can cause significant distress and should not be assumed to be a normal consequence of aging. Substance-induced and medical causes, including vaginal atrophy and dyspareunia, must be ruled out when making the diagnosis. \n\nInfertility \n\n Infertility in patients age < 35 is defined as the failure to achieve pregnancy after 12 months of regular, unprotected sexual intercourse. Evaluate Men first \n\n247 https://t.me/usmleinnercircle USMLE Inner Circle \n\nTreatment of menopause \n\nVasomotor symptoms \n\nM~era te/ se vere \n\nBehavioral modifications Contraindications to estrogen* Nonhormonal therapy (eg , SSRI) Intact uterus Estrogen &progestin \n\nContraindications to estrogen: Breast cancer, coronary heart disease, endometr ia1 cancer, liver disease, thromboemboli sm .SSRI = setective serotonin reuptake inh ib it or .\n\nCU \\l\\bf1d \n\nInfertility \n\nEstrogen only \n\nEtiology Diagnostic test Male factor . Semen analysis \n\nOvulatory function . Midluteal phase ( day 21) progesterone level \n\n## . Day 3 FSH & estradiol levels \n\nOvarian reserve . Clomiphene citrate challenge test \n\n## . Antral follicle count . Antimullerian hormone \n\nFallopian tube patency . Hysterosalpingogram \n\nUterine cavity evaluation . Sonohysterogram Gynae & Reproductive Health for women age > 35 , infertility evaluation can begin after 6 months \n\nWhat is the likely diagnosis in a 38-year-old woman that presents with infertility despite a regular menstrual cycle and normal physical exam? \n\nDecreased ovarian reserve \n\ncharacterized by decreased oocyte number and quality; sharp decline in conception is notable after age 37 \n\nOvarian Hyperstimulation Syndrome \n\nAmenorrhea Rare but life-threatening complication of ovulation induction First Step: Pelvic USG to check for Uterus \n\n248 https://t.me/usmleinnercircle \n\nOvarian hyperstimulation syndrome Pathophysiology i hCG enhances ovarian vascular permeability Acute fluid shift to extravascular space Ascites Respiratory distress Hemoconcentration \n\nClinical features Hypercoagulability Electrolyte imbalances Multiorgan failure (eg, renal failure) Disseminated intravascular coagulation Fluid balance monitoring Serial CBC, electrolytes Serum hCG \n\nEvaluation Pelvic ultrasound Chest x-ray Echocardiography Correct electrolyte imbalances \n\nManagement Paracentesis &/or thoracentesis Thromboembolism prophylaxis \n\nCBC = complete blood count. \n\nPrimary amenorrhea evaluation \n\nUterus Present FSH Low Absent Karyotype (46, XY [Al), 46,XX [m ullerian agenesis)) Normal High T SH , prolactin Karyotype \n\n,------~ I ,---__ ___, \n\nt TSH \n\nt Prolactin Normal TSH \n\nt Prolactin Hypothyroidi sm } Prolactinoma j\n\nNormal lmperforate hymen \n\n> Al =and rogen insensitivity ;FHA =fun ctional hypoth ala mic amenorrhea .POI =primary ov aria nInsufficiency .\n\nTurner syndrome Gynae & Reproductive Health FSH karyotyping (Turner's) FSH MRI ( Craniopharyngioma , Kallmann's ) Lack of menses is considered normal at age < 15 if development of secondary sex characteristics has been appropriate. \n\ntypically occurs around Tanner stage 4 \n\n Primary amenorrhea is not diagnosed until age > 15 with normal secondary sex characteristics (age > 13 without ) Patients with FHA have decreased estrogen levels but no vasomotor symptoms (eg, hot flashes, night sweats) or vaginal atrophy due to low basal levels of estrogen produced by the normal (yet unstimulated) ovaries. Patients with amenorrhea , vasomotor symptoms , and vaginal atrophy are more likely to have \n\nprimary ovarian insufficiency. The pathogenesis of hypogonadotropic hypogonadism involves loss of pulsatile GnRH secretion. \n\n249 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nPathophysiology of functional hypothalamic amenorrhea \n\nExcessive physi cal tra ining Ve ry -low-calor ie dieVstarvation Weight loss Ch ronic i ll ness Stress & depressi on Anorexia nervosa \n\nl Ghre lin , NPY , CRH , GABA & !3- endorph ins \n\nLeptin \n\ni\n\nHypot hal amus )\n\ni J GnRH \n\n, Pi tu it ary gland )\n\ni J LH , FSH Ovaries )\n\ni J Es tr oge nAmenorrhea , low estrogen state , bone loss ]CRH = corticotropi n- UW orid\n\nHormones normal \n\nPrior uterine procedure Asherman syndrome PCO~ Hypothyroidis~ \n\nAUB & secondary amenorrhea evaluation \n\nAUB / secondary amenorrhea Age< 45 ) Age2'45 J\n\nRou ti ne evaluation with FSH , TSH, \n\nprolactin \n\n> AUB =abnormal uterine bl eeding.\n\nPregnan t J \n\n> ~secondary amenorrhea = no men ses >3 months with pri or reg ular me nses OR\n\nno menses > months wi th onor in;eou iar menses No routine evaluation indicated. TSH , prolactin in \n\nsel ectca ~\n\n> IIUWorld\n\nGynae & Reproductive Health A patient with secondary amenorrhea with a negative progesterone challenge and negative E/P challenge is indicative of outflow tract obstruction/scarring ( Asherman's ).Next best step? Hysterosalpingogram to ID lesion \n\nTreatment? Hysteroscopic resection of adhesions \n\nWith Asherman's, pt. will still have cyclic abdominal pain , but no bleeding because blood is obstructed. Look for history of D&C. \n\nCraniopharyngioma vs Kallmann's \n\nPath: Kallmann's: loss of GnRH FSH/LH E/P + anosmia \n\nCraniopharyngioma: AP tumor FSH/LH E/P + bitemporal hemianopsia \n\nPresentation? \n\nPrimary Amenorrhea + Uterus secondary sex characteristics (breast, pubic hair) Diagnosis? \n\nCranial MRI mass = craniopharyngioma (\"calcified cyst on CT\") \n\nLow FSH/LH (Turner's = FSH/LH = karyotype )\n\nHematocolpos \n\n251 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCIU W0!1d \n\n\n\n0\n\n\n\n0\n\n\n\n\n\nProgesterone withdrawal test High estrogen \n\nProgesterone administered \n\nPathogenesis Clinical features Management \n\n# .......\n\n~\n\nQ) \n\n~\n\n0\n\n\n\n(0 \n\n;:; \n\nQ) \n\nE0\n\n'O \n\nC: \n\nw\n\nlmperforate hymen Low estrogen \n\nProgesterone administered \n\nnme \n\nNo withdrawa l bleeding Incomplete degeneration of hymen Cyclic lower abdominal pain Bulk symptoms (defecatory & urinary dysfunction) \n\nPrimary amenorrhea \n\nSuprapubic mass (uterus) Blue-tinged vaginal mass Hymenal incision & drainage Gynae & Reproductive Health The enlarging blood collection with each menstrual period causes increasing pressure on the surrounding pelvic organs, resulting in lower back pain , pelvic pressure , or defecatory rectal pain. \n\nPelvic examination typically reveals a blue , bulging vaginal mass or membrane that swells with \n\nincreased intra-abdominal pressure (eg, Valsalva). \n\nHirsutism \n\n Cushing syndrome may be similar in presentation to PCOS (obesity, hirsutism, amenorrhea), but PCOS does not cause muscle weakness nor easy bruisability \n\nHyperandrogenism \n\n Signs of Virilization: Deepening Voice , Cliteromegaly , Inc Muscle Bulk , Male Pattern baldness \n\nThe primary ovarian androgens are testosterone , androstenedione , and dehydroepiandrosterone \n\n(DHEA ). The adrenals also produce these androgens as well as DHEA sulfate (DHEAS) . Therefore, women with a suspected androgen-producing tumor should be evaluated with serum testosterone and DHEAS levels :Rapid Hirsutism < 1 Year = Tumor \n\n252 https://t.me/usmleinnercircle \n\nCauses of hirsutism in women Etiology Clinical features Polycystic ovary syndrome . Oligomenorrhea, hyperandrogenism, obesity \n\n Associated with type 2 diabetes, dyslipidemia, hypertension \n\n## . Normal menstruation \n\nIdiopathic hirsutism . Normal serum androgens \n\nNonclassic . Similar to polycystic ovary syndrome \n\n21-hydroxylase deficiency . Elevated serum 17-hydroxyprogesterone \n\n## . More common in postmenopausal women \n\nAndrogen-secreting ovarian tumors, ovarian . Rapidly progressive hirsutism with virilization \n\nhyperthecosis Very high serum androgens \n\nCushing syndrome . Obesity (usually of the face , neck, trunk, abdomen) \n\n## . Increased libido, virilization, irregular menses \n\nCauses of hyperandrogenism in women Diagnosis Clinical features \n\nOligo-ovulation, clinical or biochemical \n\nPCOS hyperandrogenemia, polycystic ovaries on imaging, no evidence of another diagnosis \n\nNonclassic CAH Oligo-ovulation, hyperandrogenemia, \n\nt 17-hydroxyprogesterone levels \n\nOvarian/adrenal Older age, rapidly progressive symptoms, \n\ntumors t androgen levels (>3 times upper limit of normal) \n\nHyperprolactinemia Amenorrhea, galactorrhea, t prolactin levels Cushingoid features, nonsuppressible \n\nCushing syndrome dexamethasone suppression test, t 24-hour urinary free cortisol \n\nAcromegaly Excessive growth, t GH & IGF-1 levels \n\nCAH = congenital adrenal hyperplasia; GH = growth hormone; \n\nIGF-1 = insulin-like growth factor 1; PCOS = polycystic ovary syndrome. Gynae & Reproductive Health Elevated testosterone levels with normal DHEAS levels suggest an ovarian source (more common). \n\nElevated DHEAS levels suggest an adrenal tumor (far less common). \n\n What is the recommended management for a pregnant woman with a suspected theca lutein cyst secondary to a complete molar pregnancy? \n\nSuction curettage of the hydatidiform mole \n\ntheca luteum cysts typically resolve following removal of the hydatidiform mole \n\n What is the recommended management for a pregnant woman with a suspected luteoma ?\n\nObservation and expectant management \n\nmasses typically regress spontaneously after delivery; luteomas are occasionally complicated by ovarian torsion or symptoms related to mass effect (e.g. hydronephrosis) \n\n What is the likely diagnosis in an African-American woman at 20 weeks gestation that presents with new-onset hirsutism and acne ? Pelvic ultrasound reveals an intrauterine gestation consistent with dates and bilateral 8-cm solid ovarian masses .\n\nLuteoma \n\nversus theca luteum cysts , which typically arise due to high hCG levels (e.g. molar pregnancy or multiple gestation) \n\n If surgical removal of an ovarian tumor is indicated during pregnancy , when should surgery take place? \n\nAfter 10 weeks \n\nSecretion of progesterone by corpus luteum is essential to maintain pregnancy Placenta takes over this function by 10th week \n\nOvarian Hyperthecosis \n\n Ovarian hyperthecosis is a cause of virilization but is typically diagnosed in postmenopausal women .Pregnancy luteomas are rare, nonneoplastic lesions of the ovary thought to be caused by the hormonal effects of pregnancy \n\n253 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nCauses of hyperandrogenism in pregnancy Diagnosis Clinical features Placental . No ovarian mass aromatase . High maternal & fetal virilization risk deficiency B~sc l11ticc cf wa1~ca l s:i,::wgtcws after de livery \n\n. Solid, unilateral/bilateral ovarian masses \n\nLuteoma . Moderate maternal virilization risk; high fetal virilization risk \n\n. Spontaneous regression of masses after deliv ery \n\n. Cystic, bilateral ovarian masses \n\nTheca lutein . Moderate maternal virilization risk; low fetal virilization risk \n\ncyst . Spontaneous regression of masses after delivery \n\n. Solid unilateral ovarian mass \n\nSertoli-Leydig . High maternal & fetal virilization risk \n\ntumor . Surgery required (2nd trimester or postpartum) Gynae & Reproductive Health Patients with this condition also typically have signs of insulin resistance (eg, hyperglycemia, acanthosis nigricans) and low/normal LH and FSH levels .Typical ultrasound findings are solid-appearing , enlarged ovaries. \n\nAbdominal Pain \n\nOvarian Torsion: laparoscopic cystectomy and detorsion \n\n Absence of free pelvic fluid helps differentiate ovarian torsion from a ruptured cyst \n\n What is the recommended treatment for a hemodynamically stable patient with a ruptured ovarian cyst ?\n\nSupportive (e.g. analgesics) \n\nhemodynamically unstable patients require urgent surgical intervention \n\n Cyst could be Follicular (Unruptured mature follicle) or Corpus Luteum Cyst (these can be hemorrhagic) What is the next step in management for a young woman that presents with diffuse periumbilical abdominal pain that then localizes to the right lower quadrant ? Her LMP was 25 days ago. \n\nPregnancy test \n\nshould be administered to any woman of childbearing age before performing any diagnostic tests (e.g. X-ray, CT scan) \n\nPID \n\n254 https://t.me/usmleinnercircle \n\n> Acute abdominal/pelvic pain in women Diagnosis Clinical presentation Ultrasound findings\n\n Recurrent mild & unilateral mid-cycle pain prior to ovulation \n\n> Mittelschmerz Not indicated\n\n Pain lasts hours to da :z: s \n\n> Ectopic pregnancy Amenorrhea, abdominal/pelvic pain &vaginal bleeding No intrauterine pregnancy\n\n Positive 13-hCG \n\n Sudden-onset, severe, unilateral lower abdominal pain; nausea & vomiting Enlarged ovary with decreased or \n\n> Ovarian torsion\n\n Unilateral, tender adnexal mas s on examination absent blood flow \n\n> Ruptured ovarian\n\n Sudden-onset, severe, unilateral lower abdominal pain immediately Pelvic free fluid \n\n> cyst following strenuous or sexual activity\n> Pelvic inflammatory\n\n Fever/chills, vaginal discharge, lower abdominal pain & cervical motion Tuboovarian abscess \n\n> disease tenderness\n\nGynae & Reproductive Health 25 y.o. sexually active female with cervical motion tenderness, fever, and pleuritic RUQ pain. \n\nPID + Fitz-Hugh-Curtis (perihepatitis) \n\ninflammation of the liver capsule with adhesion formation resulting in right upper quadrant pain What is the recommended initial test/imaging study to evaluate infertility in a patient with a history of pelvic inflammatory disease ?\n\nHysterosalpingogram \n\nminimally invasive way to detect fallopian tube patency and/or uterine cavity anomalies \n\n Tubal occlusion occurs causing infertility due to immune response to the infection, despite antibiotic treatment.. What is the likely diagnosis in a woman that presents with fever and RLQ abdominal pain with a \n\nlarge multiloculated adnexal mass on ultrasound? CA-125 is elevated. Tubo-ovarian abscess \n\nsevere complication of pelvic inflammatory disease \n\nFever , leukocytosis , and elevated CA-125 suggest infection rather than malignancy \n\nMid Cycle Pain \n\n Mittelschmerz pain , caused by peritoneal inflammation from ovarian follicle rupture ( physiologic corpus luteum cyst ) , occurs during ovulation, approximately 2 weeks prior to menses. diagnosis can be confirmed by ultrasound , which typically reveals a simple-appearing ovarian cyst \n\n(a large cyst with several smaller cysts) with normal Doppler flow .Treatment: NSAIDs, Observe & Repeat Examination in 6 weeks \n\nPCOS \n\n255 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPelvic inflammatory disease Symptoms Lower abdominal pain Abnormal bleeding Cervical motion tenderness \n\nPhysical examination . Fever >38.3 C (>100.9 F) Mucopurulent cervical discharge Third-generation cephalosporin \n\nTreatment plus \n\n Azithromycin or doxycycline Tuba-ovarian abscess \n\nComplications . Infertility Ectopic pregnancy Perihepatitis \n\nIndications for hospitalization for pelvic inflammatory disease \n\n Pregnancy Failed outpatient treatment Inability to tolerate oral medications Noncompliant with therapy Severe presentation (eg , high fever, vomiting) Complications (eg , tuba-ovarian abscess, perihepatitis) Gynae & Reproductive Health Ovulation Induction : Now Letrozole is used, earlier Clomiphene was used. Although many patients with PCOS have biochemical evidence of hyperandrogenism with elevated serum levels of total testosterone , these laboratory values may be normal in some due to decreased levels of sex hormone -binding globulin , with elevated free testosterone levels instead. Therefore, the diagnosis requires either clinical or biochemical evidence of hyperandrogenism .\n\n (Elevated LH/FSH are NOT required for diagnosis!) \n\nObesity and Anovulation \n\nExcess adipose tissue affects the hypothalamic-pituitary-ovarian axis by 2 major mechanisms: Obesity causes increased insulin resistance and hyperglycemia , which decrease the production of sex hormonebinding globulin, causing elevated free androgen (eg, androstenedione) levels. The increased free androgens are aromatized in the adipose tissue to estrone (a type of estrogen), which leads to persistently elevated estrone levels. High estrone levels affect GnRH pulses lack of LH surge Anovulation \n\n Overall LH/FSH concentration change is minimal \n\nBreast \n\n256 https://t.me/usmleinnercircle \n\n\n\n\n\n## ..Clinical features ...Pathophysiology ....Comorbidities ...Treatment options ..\n\nAromatase \n\n> Androstenedione -\n> CU Wortd\n> Polycystic ovary syndrome Androgen excess (eg , acne, male pattern baldnes s, hirsutism) Oligoovulation or anovulation (eg , menstrual irregularities)\n> Obesity\n> Polycystic ovaries on ultrasound\n\nt Testosterone levels t Estrogen levels LH/FSH imbalance Metabolic syndrome (eg , diabetes, hypertension) Obstructive sleep apnea Nonalcoholic steatohepatitis Endometri al hyperplasia/cancer Weight loss (first-line) Oral contraceptives for menstrual regulation Letrozole for ovulation induction \n\nObesity & anovulation \n\n> Hypothalamus\n> ( 4 GnRH) Anterior pituitary\n\n( 4 FSH , LH) \n\n# - Ovary \n\n( 4 Estradiol) \n\n# !Anovulation Amenorrhea Gynae & Reproductive Health USG in <35y women acc to NBME. \n\n In an adolescent with a \n\nsuspected fibroadenoma ,\n\nreassurance and reexamination \n\nafter the next menstrual cycle may be appropriate. \n\n Breast cancer , the most common non-dermatologic malignancy in women, may present with a palpable breast mass. In patients over age 30 years mammography should be the first step in diagnosis. Regardless of imaging findings, biopsy should occur if the physical examination is highly concerning for breast cancer (specially in older women like in 50s or 60s where incidence of breast cancer is very high) . Fine-needle aspiration is an appropriate initial biopsy technique , but it is associated with a low sensitivity . Those patients with suspicious masses but normal fine-needle aspiration results should therefore undergo excisional biopsy to confirm the diagnosis . What is the next step in management for an afebrile woman that experiences relief of symptoms following aspiration of clear fluid from a simple breast cyst ?The diagnosis of a palpable breast mass can only be confirmed with a biopsy .Patients with cyclical pain and no masses: Supportive Bra ,\n\nNSAIDS. \n\n257 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPalpable breast mass \n\n## ~Age <30 \n\n## lUltrasonogram \n\n mammogram \n\n# ~Simple cyst Complex cyst/mass (solid mass) \n\n# lNeedle aspirati on (if patient desires) \n\n## 1Image-guided core biopsy Age 30y) increase with exposure to estrogen. \n\ne.g. with pregnancy, prior to menstruation \n\n Fat Necrosis: the presence of calcifications on mammography and a fixed mass on physical exam can mimic breast cancer \n\nExcise mass and reassure Breast cyst are SOFT vs Fibroadenoma which is HARD \n\n258 https://t.me/usmleinnercircle \n\nBenign breast disease Fibroadenoma Diagnosis Clinical features Epidemiology Age <30 \n\nBreast cyst Solitary, well-circumscribed , mobile mass +/- Tenderness \n\nClinical Single, unilateral , mobile, well-circumscribed mass \n\nfeatures . Pain &/or size prior to menses \n\nFibrocystic Multiple, diffuse nodulocystic masses \n\nchanges Cyclic premenstrual tenderness \n\nManagement Observation & reassurance (adolescent) Ultrasound for a persistent mass or older patient \n\nFibroadenoma Solitary, well-circumscribed , mobile mass Cyclic premenstrual tenderness lntraductal papilloma \n\n Post-trauma/surgery Pathology . Benign papillary tumor arising from breast duct lining \n\nFat necrosis Firm , irregul ar mass +/- Ecchymosis, skin/nipple retraction Clinical features . Unilateral bloody nipple discharge (can be nonbloody) \n\n## . No associated breast mass or ll'. mehadenoeath l'. \n\n## . Mammography & ultrasound \n\nManagement Biopsy excision .\n\nBreast cancer warning signs Clinical finding Pathophysiology Nipple retraction Invasion of lactiferous ducts \n\nNipple scaling or ulceration Epidermal infiltration by neoplastic cells \n\nNipple discharge lntraductal tumor growth necrosis \n\nSkin retraction Invasion of suspensory (Cooper) ligaments \n\nPeau d'orange Obstruction of dermal lymphatics \n\nFixed breast mass Invasion into adjacent breast tissue \n\nAxillary lymphadenopathy Lymphatic spread to regional lymph nodes Gynae & Reproductive Health Alcohol consumption is a dose-dependent risk factor for breast cancer. \n\n The risk of developing breast cancer is directly correlated with lifetime exposure to estrogen .\n\n The most common risk factor is increasing age , primarily due to increasing probability for spontaneous genetic mutations \n\n What is the single most important prognostic consideration in the treatment of patients with breast cancer ?\n\nTumor burden (based on TNM staging) \n\n What is the likely diagnosis in an afebrile middle-aged woman that presents with unilateral breast warmth , erythema , and swelling refractory to antibiotics? \n\nInflammatory breast carcinoma \n\nlack of fever and no response to antibiotics help distinguish inflammatory breast cancer from \n\nmastitis ;other distinguishing features include axillary lymphadenopathy and a peau d'orange appearance \n\nNipple Discharge screening mammography beginning at age > 50 every 2years due to invasion of lymphatic spaces \n\n259 https://t.me/usmleinnercircle USMLE Inner Circle \n\nBreast cancer risk factors Inflammatory breast cancer \n\n Hormone replacement therapy \n\nModifiable Nulliparity Increased age at first live birth Alcohol consumption Genetic mutation or breast cancer in first-degree relatives \n\nNon- White race \n\nmodifiable Increasing age Early menarche or later menopause Retracted nipple Gynae & Reproductive Health The most common cause of physiologic galactorrhea is hyperprolactinemia .\n\nDischarge can be milky, yellow, brown, gray, or green! \n\nLactation \n\n Nipple pain that worsens and persists between feedings is commonly due to nipple injury caused by \n\npoor infant positioning and improper latch-on technique .On examination, patients can have open, linear areolar abrasions that cause a bloody-appearing nipple discharge ; bruising, cracking, and blistering may also be present. \n\nBreast engorgement , with bilateral, diffusely tender, and engorged breasts, can also develop because nipple pain limits breastfeeding. Initial management is with the observation of breastfeeding and patient education .\n\n Galactocele can be both painful and painless Breast engorgement \n\n260 https://t.me/usmleinnercircle \n\nDiagnosis Engorgement Nipple in jury Plugged duct Galactocele Mastitis Abscess Evaluation of nipple discharge Unilateral breast \n\nNipple discharge 1---------------------, \n\n> Color of discharge .,._ __\n\nB_loody __ o r_s_e_ro_u_s_d_is_c_h_a_rg_e _ _\n\nPath ologic dis charge Milky, nonbloody discharge \n\nPalpable lump or skin changes \n\nNo Likely physiologic d isc harge \n\n> Pregnancy test Guaiac\n\ntest \n\n> Serum prolactin, TSH Consider MRI of pituitary TSH Thyroicktim Age <30\n\nUltrasound mammogram \n\nCommon problems related to lactation Clinical features \n\nBilateral, symmetric fullness, tenderness & warmth Breast ultrasound Mammography (if age .?30) \n\nYes \n\n> I\n\nPathologic Age 30- 39 Age ,?40 \n\nMammogram Mammogram ultrasound + ult ra sound Proper breastfeeding l at c h Abrasion , bruising , cracking &/or blistering from poor latch Focal tenderness & firmness &/or erythema; no fever Subareolar, mobile, well-circumscribed , nontender mass; no fever Tenderness/erythema + fever Symptoms of mastitis + fluctuant mass Gynae & Reproductive Health common 3-5 days after delivery when colostrum is replaced by milk; improves with breastfeeding \n\n Methods for lactation suppression include a supportive bra , avoidance of nipple stimulation ,application of ice packs to the breast, and administration of NSAIDs .\n\nNSAIDs are used to reduce pain and inflammation; medications are not recommended to suppress lactation (e.g. dopamine agonists) \n\n What is the likely diagnosis in a breastfeeding woman that presents with fever and localized breast erythema /tenderness with a palpable, fluctuant mass on physical exam? \n\nBreast abscess \n\npersistent mastitis can result in a collection of pus, thus causing an abscess \n\n What is the likely diagnosis in a breastfeeding mother with bilateral red , shiny , painful nipples ?\n\nCandidiasis of the nipple \n\nmastitis is not typically associated with intense nipple pain \n\nUterus \n\n What is the recommended treatment for an elderly patient with severe pelvic organ prolapse ?\n\nColpocleisis \n\ni.e. closure of the vagina; used for elderly women who are not good surgical candidates and no longer sexually active (colpocleisis can be performed without general anesthesia) \n\nFibroid \n\n261 https://t.me/usmleinnercircle USMLE Inner Circle \n\nLactational mastitis Breast abscess Pathogenesis Skin flora (eg , Staphylococcus aureus) enters ducts through nipple & multiplies in stagnant milk . Maternal age >30 \n\nRisk factors . First pregnancy History of mastitis . Tobacco use Engorgement & inadequate milk drainage due to: o Sudden increase in sleep duration . Fever o Replacing nursing with formula or pumped breast Clinical features . Focal inflammation \n\nRisk factors milk . Fluctuant, tender mass o Weaning o Pressure on the duct (tight bra or clothing , prone Diagnosis . Breast ultrasound sleeping) o Cracked or clogged nipple pore . Antibiotics \n\nManagement Drainage .o Poor latch Fever \n\nClinical presentation Firm, red, tender , swollen quadrant of unilateral breast Myalgia, chills , malaise Analgesia \n\nTreatment Frequent breastfeeding or pumping Antibiotics Gynae & Reproductive Health Patients with symptomatic submucosal fibroids who desire future fertility are treated with \n\nhysteroscopic myomectomy \n\n What type(s) of fibroids are most associated with heavy menstrual bleeding and/or recurrent pregnancy loss ?\n\nSubmucosal and Intracavitary fibroids (leiomyomata) \n\n What type(s) of fibroids are most associated with bulk-related symptoms and irregular uterine enlargement ?\n\nSubserosal and Pedunculated fibroids (leiomyomata) \n\ne.g. constipation, incomplete voiding, pelvic pressure \n\n What is the likely diagnosis in a woman that presents with \"labor pains\" despite recently having her period? Pelvic examination reveals an irregularly enlarged uterus and a dilated cervix with a firm mass visible through the external os. \n\nProlapsing uterine fibroid \n\ntypically occur when a submucosal or intracavitary fibroid prolapses through the cervical os, resulting in labor pains and cervical dilation \n\n Uterine Sarcoma is Indistinguishable from fibroid but it should be suspected in \n\nPostmenopausal women . (Usually solitary mass with Necrosis and Haemorrhage) \n\n What medical therapy may be used for short-term treatment of symptomatic fibroids refractory to OCPs and NSAIDs? \n\nGnRH agonists (e.g. leuprolide) \n\nnot recommended for more than 3 - 6 months ; typically used before a hysterectomy or to \n\nbridge a woman close to menopause \n\n Leiomyomata uteri can outgrow their blood supply and degenerate during pregnancy because myometrial blood flow shifts toward the developing fetus and placenta. Dx: USG \n\n262 https://t.me/usmleinnercircle \n\n> Uterine fibroids Prolapsing uterine fibroid\n> Pedunculated\n> CLI Wor1d\n\nGynae & Reproductive Health An infarcted , degenerating uterine fibroid can cause severe abdominal pain ; uterine tenderness ; a \n\npalpable , firm , and tender mass ; and signs of inflammation (eg, leukocytosis). \n\n A highly sensitive test for the evaluation of submucosal fibroids is sonohysterography , a form of transvaginal ultrasonography that infuses saline into the uterine cavity for improved detection of intrauterine pathology (eg, fibroid, polyp). \n\nEndometriosis \n\n The \"three D's\" of endometriosis are dysmenorrhea , deep dyspareunia , and dyschezia. \n\n What is the recommended management for an asymptomatic patient with incidentally discovered endometriosis during an unrelated surgery? \n\nObservation laparoscopy is reserved for treatment failure , adnexal mass , or infertility \n\n263 https://t.me/usmleinnercircle USMLE Inner Circle \n\nEndometriosis Pathogenesis . Ectopic implantation of endometrial glands . Dyspareunia . Dysmenorrhea \n\nClinical features . Chronic pelvic pain . Infertility . Dyschezia \n\n. Cyclic dysuria, hematuria \n\n. Immobile uterus . Cervical motion tenderness \n\nPhysical examination . Adnexal mass . Rectovaginal septum, posterior cul-de-sac, uterosacral ligament nodules \n\nDiagnosis . Direct visualization & surgical biopsy \n\nTreatment . Medical (oral contraceptives, NSAIDs) . Surgical resection \n\nNSAIDs = nonsteroidal anti-inflammatory drugs. \n\nManagement of endometriosis \n\nSuspected endometriosis Chronic pelvic pain \n\nDysmenorrtiea \n\nDeep dyspareunia Dyschezia Contraindications to medical therapy? Need for definitive diagnosis? History of infertility? Concern for malignancy or adnexal mass? \n\nYes \n\noral contraceptives ILaparoscopy I\n\nNSAIDs = nonsteroidal anti-inflammatory drugs. Gynae & Reproductive Health intraoperative findings may include adhesions , powder-burn lesions , and \" chocolate cysts \"; asymptomatic patients do not require any treatment \n\n What is the definitive treatment for endometriosis ?\n\nHysterectomy and oophorectomy \n\ntypically done in symptomatic women who have completed childbearing \n\n What is the likely diagnosis in a young woman that presents with chronic pelvic pain , especially with exercise , and a homogenous cystic ovarian mass on ultrasound? \n\nOvarian endometrioma (secondary to endometriosis) \n\nPatients with uterine or pelvic sidewall implants may have worsening pain with exercise or intercourse (ie, dyspareunia ), as well as adhesion formation that can cause tubal infertility .\n\nAbnormal Menstrual Bleeding \n\n What is the pathogenesis of abnormal uterine bleeding in an adolescent? \n\nImmature HPA axis (leads to heavy, irregular bleeding ) What is the treatment for AUB in a hemodynamically stable adolescent \n\nProgesterone only pills or Combined Oral Contraceptives \n\nEstrogen triggers rapid growth of endometrium --> stops sudden, heavy bleeding from uterine surface \n\nProgestins stabilize endometrial lining \n\n For hemodynamically unstable patient: Dilatation & Curettage can be done to quickly scrape thick endometrial lining causing acute bleeding along with Packed red cell transfusion. homogenous, hypoechoic ovarian cyst with a ground-glass appearance. \n\n264 https://t.me/usmleinnercircle \n\n> Endometriomas on pelvic ultrasound\n> Cuworld\n\nGynae & Reproductive Health Adenomyosis \n\n Adenomyosis typically causes dysmenorrhea and heavy menstrual bleeding in multiparous women > 40 years of age. The continued accumulation of endometrial tissue within the myometrium causes an increase in the endometrial cavity surface area (resulting in heavy menstrual bleeding ) and progression to chronic pelvic pain .\n\nnew-onset dysmenorrhea in later reproductive years is classic \n\n265 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCauses of heavy menstrual bleeding Diagnosis Clinical features \n\n## . Heavy, regular menses \n\nAdenomyosis . Dysmenorrhea, pelvic pain \n\n## . Uniformly enlarged (globular) , tender uterus \n\n## . Irregular, intermenstrual, heavy, or postmenopausal bleeding \n\nEndometrial cancer/hyperplasia . History of unopposed estrogen (eg , obesity, nulliparity, chronic anovulation) \n\n## . Nontender uterus ( enlarged) \n\n## . Uncommon cause of heavy menses \n\nEndometriosis . Dysmenorrhea, pelvic pain, dyspareunia \n\n## . Fixed uterus, adnexal mass (endometrioma), rectovaginal nodularity \n\n## . Heavy, regular menses \n\nUterine leiomyomas (fibroids) . Bulk symptoms (eg , pelvic pressure/pain, constipation) \n\n## . Irregularly enlarged uterus with uneven contour \n\n## . Heavy, regular menses \n\nCoagulopathy (eg, von Willebrand disease) . Bruising , mucocutaneous bleeding (eg, gums) TVUS endometrium \n\n## . Normal uterus \n\nApproach to postmenopausal bleeding \n\nPostmenopausal bleeding \n\n# / ~>4 mm Endometrial biopsy \n\n## Bemg / ~ :~~asia \n\nObservation Progesti ns ,surgery \n\nTVUS = tr a nsva gin al ul trasou nd .\n\nC\\J Vl,l:, rld \n\nAdenomyosis Pathogenesis Abnormal endometrial tissue within the uterine myometrium \n\n Age >40 \n\nRisk factors . Multiparity \n\n## . Prior uterine surge ry (eg , myomectomy) \n\n## . Dysmenorrhea \n\n## . Heavy menstrual bleeding \n\nClinical features . Chronic pelvic pain \n\n## . Diffuse uterine enlargement (eg, globular uterus) \n\n## . Uterine tenderness \n\n## . Clinical presentation \n\nDiagnosis . MRI & ultrasound: Thickened myometrium \n\n## . Confirmation via pathology \n\nTreatment . Hysterectomy Gynae & Reproductive Health Uterine Polyp \n\n Endometrial polyps are common, well-vascularized , hyperplastic endometrial gland growths that extend into the uterine cavity Develop around 30-40 age \n\n Symptoms: Intermenstrual AUB with normal regular monthly painless menses \n\n Intracavitary therefore, small , mobile , non-tender uterus \n\n T/t: Polypectomy \n\nEndometrial Cancer \n\n What is the typical presentation ?\n\nPrimarily postmenopausal with vaginal bleeding Old + obese or HRT/SERM Young + PCOS Granulosa-Theca HNPCC (Lynch) \n\n266 https://t.me/usmleinnercircle \n\nEndometrial polyps \n\n> UWo~d\n\nEndometrial hyperplasia/cancer \n\nExcess estrogen . Obesity \n\n## . Chronic anovulation/PCOS \n\nRisk factors . Nulliparity \n\n## . Early menarche or late menopause \n\n Tamoxifen use \n\nClinical . Heavy, prolonged , intermenstrual &/or postmenopausal \n\nfeatures bleeding \n\nEvaluation . Endometrial biopsy (gold standard) . Pelvic ultrasound (postmenopausal women) \n\nTreatment . Hyperplasia: progestin therapy or hysterectomy . Cancer: hysterectomy \n\n> PCOS\n\n= polycystic ovary syndrome .Gynae & Reproductive Health Endometrial biopsy is indicated to evaluate for endometrial cancer in women with \n\npostmenopausal bleeding and an endometrial lining >4 mm on ultrasound .\n\n If the Biopsy is non Diagnostic, Dilatation & Curettage or Hysteroscopy can be done. \n\nCervix \n\nCervicitis \n\n What is the likely diagnosis in a sexually active woman that presents with postcoital bleeding and mucopurulent discharge with a friable cervix on pelvic examination? \n\nAcute cervicitis \n\nless common symptoms include dysuria, dyspareunia, and vulvovaginal pruritus \n\n Pregnant patients with cervicitis often have no cervical motion tenderness (a sign of ascending upper reproductive tract infection) because the gravid uterus is sealed from the lower reproductive tract to maintain uterine sterility via the mucus plug. \n\n Fever is important differential for PID , which will have fever \n\nPID : Fever \n\nCervicitis : No fever \n\n267 https://t.me/usmleinnercircle USMLE Inner Circle \n\nEndometrial biopsy indications \n\n# . Abnormal uterine bleeding \n\nAge ,\"_45 Postmenopausal bleeding .Abnormal uterine bleeding PLUS: . Unopposed estrog en (obesity, anovulation) \n\nAge <45 Failed medical management .. Lynch syndrome (hereditary nonpolyposis colorectal cancer) \n\nAge ,,._35 . Atypical glandular cells on Pap test \n\nCervicitis Acute cervicitis Etiology . Infectious: Chlamydia trachomatis, Neisseria gonorrhoeae \n\n## . Noninfectious: foreign object, latex, douching \n\n## . Asymptomatic \n\nClinical presentation . Mucopurulent discharge . Postcoital/intermenstrual bleeding . Friable cervix \n\nEvaluation . Nucleic acid amplification testing \n\n## . Wet mount microscopy \n\nManagement . Empir ic treatment: ceftriaxone + doxycycline \n\n* Ceftriaxone + azithromy cin in pregnancy. Gynae & Reproductive Health What is the most likely diagnosis in a patient who presents in the third trimester with pelvic pain? She states the she recently began having sex and examination shows cervical bruising and tenderness with no signs of active bleeding. \n\nCervical trauma ( cervix becomes hyper-vascular during pregnancy )\n\nPap Smear \n\n Evaluation of atypical glandular cells on Pap test in women > 35 years old includes colposcopy , endocervical curettage , and endometrial biopsy . What is the next step in management for a pregnant patient with high-grade squamous intraepithelial lesion discovered on Pap testing? \n\nColposcopy and biopsy (safe during pregnancy) \n\n Pap smears without HPV co-testing are repeated every 3 years beginning at age 21 .\n\nbegin at age 21 regardless of age of onset of sexual activity in immunocompetent patients; \n\nPap smears with HPV co-testing are repeated every 5 years beginning at age 30. Acetic acid is used to help visualize abnormal cervical tissue (e.g. aceto-white changes )\n\n268 https://t.me/usmleinnercircle \n\nColposcopy Normal cervix \n\nCervical cancer screening Age <21 . No screening \n\n> Age 21-29\n\n## . Cytology every 3 years \n\n## . Cytology every 3 years OR \n\n> Age 30-65\n\n## . Cytology plus HPV testing every 5 years OR \n\n## . Primary HPV testing every 5 years \n\n> Age >65\n\n## . No screening if negative pri or screens & low risk \n\n> Hysterectomy\n\n## . No screening if negative pri or screens & low risk \n\n> (with cervix removed)\n\n## . Onset of sexua l jntercourse or time of HIV diagnosis (whichever is first) \n\n> HIV Annually until lmmunosuppressed\n\n## . Onset of sexual intercourse \n\n> (eg, SLE, organ transplant) Annual Pap test with HPV cotesting\n> HPV\n\n=human papillomavirus; SLE =systemic lupus erythematosus. Gynae & Reproductive Health Patients with cervical cancer risk factors (e.g. immunosuppression, tobacco use, DES exposure, high-risk sexual activity) may need continued Pap testing \n\n If a patient has a history of CIN 2 or higher , Pap testing should continue for another 20 years after detection. In women age <45 , endometrial cells are not reported on Pap test results because this is a common, benign finding , particularly during the first 10 days of the menstrual cycle .In women age 45 , endometrial cells are reported because this finding is more concerning for endometrial hyperplasia or cancer ,\n\nCIN \n\nCervical Stenosis: 1. May impede menstrual flow & cause sec \n\namenorrhea or dysmenorrhea \n\n2. Infertility d/t impaired sperm entry \n\n269 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nWhen to stop Pap testing \n\n Age 65 or hysterectomy PLUS No history of cervical intraepithelial neoplasia 2 or higher AND 3 consecutive negative Pap tests OR 2 consecutive negative co-testing results \n\nPap smear results requiring endometrial evaluation Result Group requiring endometrial sampling \n\nBenign-appearing endometrial cells Atypical glandular cell s Atypical glandular cells, favor neoplastic \n\nManagement of CIN3 CIN3 \n\n## lAge >25 Not currently pregnant \n\n## l LEEP Cold knife conization Cryoablation lPap test with HPV 1 and 2 years postprocedure \n\n\"CIN3 =cervical inlraepithelial neoplasia 3; LEEP =loop eleclrosurgical excision procedure ; HPV = human papillomavirus. Premenopausal women wi th: \n\no Abnormal uterine bleeding OR \n\n0 Risk fo r endometrial h~e erelasia \n\n Postmenopausal women \n\n Women age ~35 OR at risk for endometrial hyperplasia \n\n All women \n\nCervical conization Indications Cerv ical intraepithelial neoplasia grades 2 & 3* \n\n Cerv ical stenosis \n\n Preterm birth \n\nComplications Preterm premature rupture of membranes Second trimester pregnancy loss *Observation preferred for cervical intraepithe li al neoplasia 2 in young women. Gynae & Reproductive Health Cervical Cancer \n\n Cervical lesions suspicious for cancer require cervical biopsy , which can be performed safely during pregnancy \n\n Patients with invasive lesions must undergo Hysterectomy \n\nOvary \n\nCyst \n\n What is the next step in management in asymptomatic, young patient with small, smooth walled ovarian cyst ?\n\nFollow up exam to monitor growth \n\nTorsion \n\n270 https://t.me/usmleinnercircle \n\nCervical cone biopsy LEEP cervical biopsy \n\n> Uterus Uterus Normal tissue Normal tissue zone Vagina Vagina\n> WW ortd ~Wort d\n\nRisk factors for cervical cancer \n\n# . Infection with high-risk HPV strains (eg , 16, 18) . History of sexually transmitted diseases Early onset of sexual activity Multiple or high-risk sexual partners . lmmunosuppression Oral contraceptive use Low socioeconomic status Tobacco use \n\nHPV= human papillomavirus. Gynae & Reproductive Health Patients may initially have partial torsion , which occurs due to oscillation between the twisted and \n\nuntwisted positions (ie, causing pain, nausea, and vomiting when twisted and relief when untwisted). Can also cause Vaginal Bleeding from adnexal edema and necrosis Complete torsion usually triggered by physical activity like walking. \n\n Remember: it is a CLINICAL DIAGNOSIS & medical emergency; Doppler USG can support the Dx but is NOT required \n\nOvarian Cancer \n\n BRCA -positive individuals are recommended to have a prophylactic bilateral salpingo-oophorectomy to decrease incidence of ovarian cancer .\n\nrecommended as soon as childbearing is complete \n\n What is the recommended screening for asymptomatic patients at average-risk of ovarian cancer ?\n\nNo screening recommended Pain in unilateral and NOT radiating \n\n271 https://t.me/usmleinnercircle USMLE Inner Circle \n\nOvarian torsion \n\n# . Ovarian mass \n\nRisk factors . Women of reproductive age \n\n# . Infertility treatment with ovulation induction \n\n# . Sudden-onset unilateral pelvic pain \n\nClinical presentation . Nausea & vomiting \n\n# . Palpable adnexal mass \n\nUltrasound . Adnexal mass with absent Doppler flow to ovary \n\n# . Laparoscopy with detorsion \n\nTreatment . Ovarian cystectomy \n\n# . Oophorectomy if necrosis or malignancy \n\nBRCA mutations & ovarian cancer \n\n BRCA 1 & BRCA2 mutations \n\nGene tic s Autosomal dominant inheritance Ashkenazi Jewish ancestry Premenopausal epithelial ovarian cancer Fallopian tube cancer \n\nCancer risks Primary peritoneal cancer Breast cancer at age < 50 Breast cancer in male Bilateral salpingo-oophorectomy \n\nRisk Oral contraceptive use Age < 30 at first live birth \n\nmodification Breastfeeding Tubal ligation Gynae & Reproductive Health Ovarian cancer typically presents with vague symptoms and is usually discovered at an advanced stage. The first-line therapy recommendation is surgical resection followed by \n\nsystemic chemotherapy , preferably with a platinum-based agent. \n\n272 https://t.me/usmleinnercircle \n\nRisk-based ovarian cancer screening & management \n\nFamily history ) -Low/ave rage risk-+ No screening indicated IHigh risk : ~1 of the following l Multiple members on 1 side of the family with breast or ovarian cancer Male breast cancer Bilateral breast cancer Breast cancer diagnosed age <50 Ashkenazi Jewish ancestry ~3 relatives with a Lynch syndrome-assoc,ated cancer \n\n# !Hereditary cancer syndrome testing (eg, BRCA1 , BRCA2, Lynch syndrome) \n\n! Pos itive \n\n Concurrent TYUS and CA-125 every 6 months beginning at age 30 \n\nNegative \n\n# 7 No screening OCPs for pre-menopausal women rrBSO upon completion of childbearing rrBSO in postmenopausal women, particularly at time of hysterectomy for benign reasons OCP = oral contracepbve pill; rrBSO = risk reducing belateral sa lplng~horectomy ,\n\nTVUS = transvaginal ultra sol.W'ld .\n\nLynch syndrome genetic screening criteria \n\n Colorectal cancer \n\nPatient-based criteria Endometrial cancer age < 60 \n\n> @ UWotld\n\n First-degree relative with MMRIEPCAM gene mutation \n\n @UWorld\n\nGynae & Reproductive Health What is the next step in management for a postmenopausal woman with an incidentally discovered ovarian cyst on ultrasound? \n\nMeasure CA-125 levels \n\nan elevated CA-125 level in a postmenopausal patient is suspicious for malignancy, even if the ultrasound findings seem benign \n\n Postmenopausal women with ultrasound findings suspicious for ovarian cancer and/or elevated CA-125 should undergo further imaging (e.g. CT, MRI) prior to surgical exploration. \n\nhelps assess for the presence of metastatic disease which can guide surgical exploration \n\n What is the first step in the work-up of an adnexal mass ?\n\nTransvaginal U/S \n\n What features indicate a malignant ovarian mass? \n\nIrregularly thickened septa, indistinct borders \n\n What work up is absolutely contraindicated ?\n\nFine needle aspiration cytology risk of spreading tumor cells to peritoneum Biopsy is Contradicted \n\n273 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPremenopausal adnexal mass evaluation \n\nAdnexal mass J\n\n# !Pregnancy test &pelvic ultrasound \n\n# tMaligna nt features \n\nYes_LNo 7\n\n# tRule out ectopic pregnancy Conservative management: NSAIDs +/. narcotics \n\n# !Repeat ultrasound -every \n\n6 weeks until resolution \n\neg mplex sotld com pon ent s se plal lons calc ifi ca ti ons incr eas ed vasculari ty . C) UWorld \n\nEpithelial ovarian carcinoma \n\n# . Acut e: shortness of breath, obstipation/constipation with vomiting, abdominal distension \n\nClinical . Subac ut e: pelvic/abdominal pain, bloating, early satiety \n\npr esentation Asymptomatic adnexal mass \n\nLaboratory t CA-125 .findin gs \n\n# . Solid mass \n\nUltrasound . Thick septations \n\nfindin gs A sc ites .\n\nMan age me nt . Exploratory laparotomy Gynae & Reproductive Health Epithelial ovarian carcinoma refers to a malignancy involving the ovary , fallopian tube , and \n\nperitoneum .Histologically, abnormalities can begin at any of these sites and present with the hallmark large ovarian mass and widespread pelvic and abdominal metastasis regardless of primary origin. \n\n Testosterone inhibits hypothalamic GnRH and pituitary FSH/LH release, resulting in low estrogen \n\n What is the likely diagnosis in a young girl with breast development and a white , odorless vaginal \n\ndischarge with an ovarian mass on ultrasound? \n\nGranulosa cell tumor \n\n White , odorless vaginal discharge is indicative of estrogen stimulation \n\n What is the recommended treatment for advanced ovarian cancer ?\n\nExploratory laparotomy followed by chemotherapy (e.g. cisplatin + paclitaxel) \n\nthe ovaries, uterus, omentum, and any visible cancerous lesion are removed and pelvic/aortic lymph nodes are dissected \n\nVulva \n\nLabial Adhesion \n\n274 https://t.me/usmleinnercircle \n\n> Sertoli-Leydig cell tumor Granulosa cell tumor\n\n## . Sex cord- stromal tumor \n\n> Pathogenesis\n\nt Testosterone . o Sex cord-s tromal tumor \n\n> Pathogenesis\n\n# . j Estradiol . Rapid-onset virilization j lnhibin 0 Voice deepening 0 Male-pattern baldi ng \n\n> Clinical Increased mus cle mass 0\n> features Clitoromegaly 0\n\n# . Oligomenorrhea Complex ovarian mass Juvenile subtype \n\n> 0Precoci ous puberty\n> Clinical features\n\n Adult subtype . Unilateral, solid adnexal mass 0 Breast tenderness o Abnonmal uterine bleeding \n\n> Management\n\n## . Surgery (tumor staging) o Postmenopausal bleeding \n\n> Histopathology Call-Exner bodies (cells in rosette pattern)\n\n# . Endometrial biopsy (endometrial ca ncer) \n\n> Management Surgery (tumor stagin g)\n\nGynae & Reproductive Health Labial adhesions, or fused labia minora, typically affect prepubertal girls (with a peak incidence at age 2-3 due to low estrogen production .Can also lead to Pruritis \n\nT/t: Observation ; Estrogen cream if symptomatic \n\nBartholin Cyst \n\n Idiopathic or sec to Trauma , Edema . 4 o clock or 8 o clock position \n\nvs Skene Gland cyst which are lateral to Urethral meatus \n\n Asymptomatic Cyst: Observation only ; self resolve \n\n Symptomatic Cyst/Abscess: Incision & Drainage + Word Catheter to reduce recurrence \n\n Recurrent Cyst: Marsupialization procedure , which creates another point of drainage for the Bartholin gland. \n\n275 https://t.me/usmleinnercircle USMLE Inner Circle \n\nNormal Labial adhesion Bartholin gland cyst/abscess \n\n-- Norm al Bartholin gland Gynae & Reproductive Health Lichen Sclerosus \n\n In severe cases, normal anatomic structures may be obliterated or atrophied , leading to loss of the labia minora and clitoral hood retraction , which can result in dyspareunia. \n\n Does NOT affect the vaginal mucosa , which is an important distinguishing feature from \n\natrophic vaginitis and Lichen Planus \n\n Biopsy is recommended only in ADULTS not children \n\n276 https://t.me/usmleinnercircle \n\nWord catheter Epidemiology Clinical features Workup Treatment Bartholin gland marsupialization 1. Incise & drain cyst or abscess \n\nVulvar lichen sclerosus \n\n# . Prepubertal girls & perimenopausal or postmenopausal women \n\n Thin, white, wrinkled skin over the labia majora/minora; atrophic changes that may extend over the perineum & around the anus \n\n# . Excoriations, erosions, fissures from severe pruritus \n\n# . Dysuria, dyspareunia, painful defecation \n\n# . Punch biopsy of adult-onset lesions to exclude malignancy \n\n# . Superpotent corticosteroid ointment \n\nVulvar lichen sclerosus \n\n> 2. Evert edges of cyst or abcess & suture to mucosal edge\n\nGynae & Reproductive Health Vulvar Lichen Planus \n\nAcute vaginal inflammation that causes friable vaginal mucosa and a serosanguinous vaginal discharge ; chronic inflammation can eventually result in stenosis of the vaginal introitus. \n\nVulval Cancer \n\nVagina \n\n Patients with cytology results that show bacterial vaginosis on Pap testing should be asked about \n\nsymptoms (eg, malodorous vaginal discharge). \n\nSymptomatic patients are screened (eg, wet mount microscopy , potassium hydroxide whiff testing ) and treated if the diagnosis is confirmed. \n\nAsymptomatic patients do not require treatment. \n\n Speculum examination should not be performed in a prepubertal girl .\n\n277 https://t.me/usmleinnercircle USMLE Inner Circle \n\nVulvar lichen planus \n\n# . Women age 50-60 \n\n# . Vulvar pain or pruritus \n\n# . Dyspareunia \n\n# . Erosive variant (most common): \n\nClinical features 0 Erosive, glazed lesions with white border \n\n0 Vaginal involveme nt stenosis \n\n0 Associated oral ulcers Papulosquamous variant: \n\n0 Small pruritic papules wit h purple hue \n\nDiagnosis Vulvar biopsy \n\nTreatment High-potency topical corticosteroids \n\nVulvar cancer \n\n# . Persistent HPV infection \n\nEtiology Chronic inflammation .\n\n Tobac co use \n\n Vulv ar lic hen sclerosus \n\nRisk factors . Immunodeficiency \n\n# . Prior cervical cancer \n\n Vulvar/cervical intraep it hel ial neoplasia \n\n Vul var pruritus \n\nClinical features Vul var plaque/ulcer Abnormal bleeding Diagnosis . Biopsy HPV = human papillomavirus. \n\nVaginal foreign bodies in children \n\n# . Usually prepubertal girls \n\nEpidemiology Toilet paper most commonly retained object .\n\n Vaginal spotting \n\nClinical features Malodorous vaginal discharge No signs of trauma (eg, lacerations) \n\n# . Topical anesthetic & warmed fluid irrigation \n\nManagement If necessary, vaginoscopy under anesthesia .Gynae & Reproductive Health It can result in significant discomfort and trauma due to the narrow vaginal introitus and sensitive hymenal tissue from a low estrogen level at this age. Even when under anesthesia , prepubertal girls should be evaluated with vaginoscopy , not speculum examination. \n\n Vulvovaginitis in a prepubertal child presents with vaginal itching and erythema , as well as foul odor or vaginal discharge based on the cause. Causes include poor hygiene, foreign bodies, occlusive clothing, exposure to irritants, and infection. Children presenting with vulvovaginitis should be carefully evaluated for signs and symptoms of physical or sexual abuse .Treatment of nonspecific vulvovaginitis is initially conservative , with recommendations to \n\nimprove hygiene and limit exposure to irritants such as bubble baths or synthetic materials. \n\nVaginismus \n\n What is the likely diagnosis in a premenopausal woman with aversion to sexual intercourse due to muscle spasm /pain with penetration ? External pelvic examination is unremarkable. \n\nGenito-pelvic pain/penetration disorder (vaginismus) \n\ntreatment is aimed at relaxing the vaginal muscles (e.g. desensitization therapy, Kegel exercises); \n\nDifferentiated from vulvodynia by absence of pain to superficial touch of the vaginal vestibule \n\nCancer \n\n278 https://t.me/usmleinnercircle \n\nGenito-pelvic pain/penetration disorder \n\n Sexual trauma \n\nRisk factors Lack of sexual knowledge History of abuse Pain with vaginal penetration \n\nClinical features Distress/anxiety over symptoms No other medical cause \n\nTreatment Desensitization therapy Kegel exercises \n\n> Vaginal cancer Sarcoma botryoides Type Squamous ce ll Clear cell adenocarcinoma Ep idem iology Age > 60 Age <20 HPV16or18 In utero exposure to\n> Risk factors History of cervical dysplasia diethylstilbestrol or cancer Cigarette use\n> Location of Upper 1/3 of the posterior Upper 1/3 of anterior\n> cancer vaginal wall vaginal wall\n> Cl in ical Malodorous vaginal discharge\n> features Postmenopausal or postcoital vaginal bleeding Irregular mass, plaque, or ulcer on vagina\n> Diagnosis Biopsy\n\nGynae & Reproductive Health The most significant risk factors for vaginal squamous cell carcinoma are smoking and HPV infection .\n\nsimilar to the risk factors for cervical cancer \n\n## Miscellaneous \n\nUrethral Diverticulum \n\n Urethral diverticulum , an abnormal localized outpouching of the urethral mucosa into surrounding tissues. A urethral diverticulum typically arises from recurrent periurethral gland infections, which can develop into an abscess that can eventually breach the urethral mucosa. The persistent infection, inflammation, and increased tissue tension in the area causes a tender anterior vaginal wall mass that may present as dyspareunia or a palpable mass on pelvic examination. In addition, the diverticulum may collect urine and debris, resulting in a purulent discharge, dysuria, or postvoid dribbling .\n\nMRI is used to confirm the diagnosis of a urethral diverticulum; patients are treated via surgical excision. \n\n279 https://t.me/usmleinnercircle USMLE Inner Circle \n\nUrethral diverticulum \n\nUrethral diverticulum \n\n Urethral mucosa herniated \n\nDefinition into surrounding tissue \n\n Dysuria \n\n Postvoid dribbling \n\nClinical features \n\n Dyspareunia \n\n Anterior vaginal wall mass \n\n Urinalysis \n\n Urine culture \n\nDiagnostic testing MRI of the pelvis Transvaginal ultrasound Gynae & Reproductive Health Disorders of Sex Development \n\nTurner Syndrome Occurs in Prepubertal girls \n\n280 https://t.me/usmleinnercircle \n\nUrethral prolapse Normal \n\nDiso r ders of sexual development Breast Reproductive Axillary Diagnosis Cause development & pubic Karyotype organs hair Complete Absent uterus \n\nandrogen X-linked mutation & upper Minimal \n\ninsensitivity of androgen Yes vagina; to 46 ,XY \n\nsyndrome receptor cryptorchid absent testes \n\nMiillerian agenesis Absent or (Mayer- Hypoplastic or rudimentary uterus &Rokitansky- absent mullerian Yes upper vagina ; Normal 46 ,XX Kuster- ductal system normal Hauser ovaries syndrome) Normal \n\nTransverse Malformation of uterus, \n\nvaginal urogenital sinus Yes abnormal Normal 46 ,XX vagina; \n\nseptum & MOllerian ducts normal ovaries Complete/partial Variable Normal uterus \n\nTurner (depending \n\nsyndrome absence of 1 on ovarian & vagina ; Normal 45 ,X X chromosome function) streak ovaries \n\nComorbidity screening in Turner syndrome \n\n# . Congenital heart defect s*: 4-extremity B P, ECG , echocardiogram \n\nCardiovascular . Aortic dilatation/dissection**: TIE or cardiac MRI \n\n# . Metabolic syndrome: BP , HbA1c , lipid panel, LFT \n\nRenal . H orseshoe kidney: r enal ultrasound \n\nMusculoskeletal . Osteoporosis: 25-hydroxyvitamin D level, D XA scan \n\nVision & hearing . S trabismus , myopia : o phthalmology evaluation \n\n# . Recurrent otitis media , hearing loss: a udiology testing \n\nAutoimmune . Celiac disease : tissue transglutaminase antibodies \n\n# . Hypothyroidism : TSH, free T4 *Aortic coarctation, bicuspid aortic valve. **High risk in pregnancy. \n\nBP =blood pressure; HbA 1c =glycosylated hemoglobin; LFT =liver function test; TTE =transthoracic echocardiogram. Gynae & Reproductive Health All patients with Turners require screening for cardiac disease with 4-extremity blood pressures ,\n\nECG , and imaging (eg, echocardiography , cardiac MRI). If aortic dilatation is detected, beta blockers and aggressive blood pressure control are indicated ;surgical repair may be considered based on aortic size and risk factors. \n\nAromatase Deficiency \n\n What is the likely diagnosis in an adolescent girl with delayed puberty , clitoromegaly ,and osteoporosis ? Laboratory exam reveals undetectable estrogen and elevated testosterone levels. \n\nAromatase deficiency \n\nMullerian Agenesis \n\n281 https://t.me/usmleinnercircle USMLE Inner Circle \n\nTurner syndrome Coarctation of aorta Broad chest with widely spaced nipples ~--.. ~~ \n\nBicuspid aortic valve Aortic dissection Streak ovaries Horseshoe kidney (amenorrhea , infertility) Congenital lymphedema Aromatase deficiency \n\n Karyotype : 46 XX or 46 XY (normal sex development) Pathophysiology: Mutations in the CYP19Al gene which encodes for the enzyme _a_~~ -ri:i~ _t_ a_~_E!_ i;:l -+ i serum ~-~!~~9.~!1. \n\nand l serum testosterone Clinical features \n\n Females (46 XX) _Birth : Ambiguous genitalia despite normal internal genital organs Puberty Impaired maturation of secondary sexual characteristics Primary amenorrhea o \n\n:-{(~i _l!~_ a_!\\CJ _t! (e.g. , -~(~~~ -t!~ _f!l_ , severe _ acne) Both males and females Childhood Tall stature Osteoporosis (e.g., fractures following minimal trauma) \n\n Mothers of affected children may experience virilization during pregnancy (may start at 12 weeks' gestation and typically disappear after delivery) Treatment \n\n Estrogen and p rogesterone replacement therapy Calcium and vitamin D supplementation \n\n Surgical correction of ambiguous genitalia Gynae & Reproductive Health 5-Alpha Reductase \n\n## Male \n\nGynecomastia Dx: elevated testosterone/DHT ratio. \n\n282 https://t.me/usmleinnercircle \n\nMiillerian agenesis \n\n# . MOllerian duct system defect \n\nPathogenesis Abnormal development of uterus, cervix & upper third of vag ina .. Primary amenorrhea \n\n# . Normal female external genitalia \n\nClinical features Blind vaginal pouch \n\n# . Absent or rudimentary uterus \n\n# . Bilateral functioning ovaries (normal FSH) \n\n# . Evaluate for renal tract abnormalities (eg, renal ultrasonography) \n\nManagement . Vaginal dilation (surgical or nonsurgical) \n\n5-a reductase deficiency \n\n 46,XY genotype \n\n# . Impaired co nversion of testosterone to DHT \n\nPathogenesis Impaired virilization during embryogenesis \n\n# . Normal male testosterone & estrogen levels \n\n# . Male internal genitalia (eg, testes, vas deferens) Female external genitalia (eg, blind-ending vagina) \n\n# . Phenotypically female at birth \n\nClinical features Virilization at puberty (t testosterone) o Clitoromegaly \n\n> 0\n\nIncreased muscle mass \n\n> 0\n\nMale pattern hair development \n\n> 0\n\nNodulocystic acne DHT = dihydrotestosterone. \n\n- -Gynae & Reproductive Health What should you tell a pubertal boy (12-14 years) with gynecomastia ?\n\nReassurance \n\nPersistence will require work up Occurs in 2/3 of boys and is normal, Due to conversion of testosterone to estrogen \n\nMale Breast Cancer \n\n283 https://t.me/usmleinnercircle USMLE Inner Circle \n\nEva luati on of gynecomastia \n\nEnlargement of breast tissue in a male patient \n\n# !Discrete enlargement of glandular breast tissue \n\n# !Rule out toxic exposure (herbal s up plements, anabohc ster 01ds, cannabinoids) \n\n## 1Indistinct fatty enlargement, obese habitus \n\n# !\n\nNo discrete glandular tissue \n\nPseudogynecomastia Measure hormone levels (hCG, LH, testosterone, estradiol) \n\nthCG l or normal LH \n\nl Testosterone tLH \n\nl Testosterone fLH \n\nf Testosterone 1 Estradiol Testicular or gonad al germ-cell tumor Central hypogonadism (eg, pituitary tumor) Primary hypogonadism (eg, Klinefelter syndrome) Possible thyrotoxicosis Testicular or adrenal tumor h CG = Human chorio ni c gonadotropin, LH = Luteinizing hormone C)UW ld \n\nCommon pathological causes of gynecomastia \n\n Testicular, adrenal, or hu m an chorionic gonadotropin-secreting tumors \n\nIncreased estrogen Cirrhosis or malnutrition \n\nproduction or Thyrotoxicosis \n\nperipheral Congenital excessive aromatase activity \n\nconversion Androgen use Drugs (eg , spironolactone, cimet id ine), herbal products (eg, tea tree oil, lavender oil) Pri mary or secondary male hypogonad ism \n\nAndrogen (eg, Kli nefelter syndrome, testicular damage) \n\ndeficiency Hyperprolactine mi a Renal fa il ure \n\nPubertal gynecomastia \n\n# . Imbalance of estrogens & androgens duri ng midpuberty \n\nEtiology (Tanner stages 3-4) \n\nClinical . Small (<4 cm) firm , u ni lateral or bilateral, subareolar mass . No pathologic features ( eg , nipple discharg e, axillary \n\nfeatures lymphadenopathy, systemic illness) . Reassurance & observation \n\nManagement Resolution within a year .Gynae & Reproductive Health Gynecomastia can have variable density but is typically symmetric , is centrally located with respect to the nipple, and may have an indistinct margin with surrounding fat. \n\nBreast cancer is more likely eccentric to the nipple, has well -defined or spiculated margins , and may contain calcifications .\n\nHypogonadism \n\n Opioids suppress GnRH and LH secretion, leading to reduced Leydig cell testosterone synthesis, decreased spermatogenesis, and testicular atrophy. \n\nUrethritis \n\n The diagnosis of infectious urethritis is made when 1 of the following are present: Breast enlargement in secondary hypogonadism is less prominent. (vs Primary) First-line empiric treatment awaiting results: Single dose of intramuscular ceftriaxone plus a 7-day course of oral doxycycline \n\n284 https://t.me/usmleinnercircle \n\nMale breast cancer Risk factors . Family history; BRCA 1/ 2 \n\n# . Abnormal estrogen/androgen rati o: Klinefelter s ;r: ndrome, obesity, cirrhosis, mari juana use . Subareolar mass \n\nPresentation . Skin & nipple dimpling , induration , ulceration \n\n# . Often detected at advanced stage \n\nDiagnosis . Mammography \n\n# . Biopsy: invasive ductal carcinoma (hormone receptor-positive) most common \n\nMale secondary hypogonadism \n\n Fatigue, decreased libido \n\nClinical features Testicular atrophy Laboratory: low testosterone, low/normal LH Pituitary tumors, hyperprolactinemia Medications: opioids, glucocorticoids, exogenous androgens (withdrawal phase) \n\nCommon causes Infiltrative disease (eg, hemochromatosis) Chronic/severe illness Eating disorders, severe weight loss \n\nInfectious urethritis in men \n\n Neisseria gonorrhoeae \n\nEtiology Chlamydia trachomatis \n\n Mycoplasma genitalium Trichomonas vagina/is \n\nManifestations Dysuria Discharge Gram stain & culture \n\nDiagnosis Nucleic acid amplification testing GU alone: ceftriaxone \n\nTreatment GU + Chlamydia*: ceftriaxone + doxycycline \n\nChlamydia/Mycoplasma: azithromycin Trichomonas: metronidazole \n\n> *GU +uncertain Chlamydia status is also treated with ceftriaxone +doxycycline. GU =gonococcal urethritis.\n\nGynae & Reproductive Health Purulent or mucopurulent penile discharge \n\n2 leukocytes per field on urethral swab Gram stain Positive leukocytes on urine dipstick or 10 leukocytes/hpf on urinalysis \n\n Trichomoniasis is usually asymptomatic in men and is an uncommon cause of urethritis. \n\nScrotum \n\nVaricocele \n\n Left sided and Bilateral are common ; Right sided should raise the suspicion for \n\nMalignancy \n\nHydrocele \n\n285 https://t.me/usmleinnercircle USMLE Inner Circle \n\nVaricocele \n\nPrimary Secondary \n\n# . Compression of left renal vein between SMA and . Extrinsic compression (renal or re t ro peritoneal mass) of \n\nPathophysiology aorta IVC . Incompetent venous valves . Venous thrombus . \"Bag of worms\" mass . \"Bag of worms\" mass . Pubertal onset . Prepubertal onset \n\nClinical features . Left-sided . Right-sided . Decompresses when supine . Persists when supine \n\nInitial . Reassurance and observation . Abdominal ultrasound management \n\nIVC = inferior vena cava; SMA = superior mesenteric artery. \n\nVaricocele \n\n# . Soft scrotal mass (\"bag of worms\") Clinical 0 ! In supine position \n\n0 j With standingNalsalva maneuvers presentation Subfertility .. Testicular atrophy Ultrasound . Retrograde venous flow findings . Tortuous, anechoic tubules adjacent to testis . Dilation of pampiniform plexus veins . Gonadal vein ligation (boys & young men with \n\nTreatment testicular atrophy) . Scrotal support & NSAIDs (older men who do not desire additional children) NSAIDs = nonsteroidal anti-inflammatory drugs. Gynae & Reproductive Health Transillumination helps differentiate scrotal masses, as hydroceles are cystic and transmit light \n\nwhereas inguinal hernias contain bowel that does not typically transilluminate. Most hydroceles , both communicating and noncommunicating, should spontaneously resolve by \n\nage 1 year and can be safely observed during that period. \n\nProstate \n\nProstatitis \n\n Cystoscopy and urethral catheterization should generally be avoided in patients with Acute Bacterial \n\nProstatitis because passage of instruments through the urethra can cause septic shock (due to release of bacteria from prostate) or prostatic rupture .Patients who develop acute urinary retention due to prostatic swelling from ABP often require \n\nsuprapubic (not urethral) catheterization .\n\n286 https://t.me/usmleinnercircle \n\nClinical p re sentation Di ag nosis Treatment \n\nDuc tu sdef ere ns Cl osed Normal anato my Noncommunicating hydrocele Abdom ina l\n\n/ cavity \n\nCommunicating hydrocele vag inalis \n\nOverview of prostatitis Acute Chro ni c\n\nFever, chill s, malaise, myalgia . Dysuria and urinary frequency Pelvic pain, cloudy u ri ne . No sym ptoms of acute prostatitis \n\n. Recurrent urinary tract infection Pyuri a, tender prostate . Pyuria with possible ten der prostate Urine culture p os iti ve (usual ly Escherichia . Urine culture p os itive ( us uallyEscherichia coil) \n\nco/ 1)\n\n TM P- SMX or fluoroquinolones . Fluoroq ui nolones \n\nChronic prostatitis/chronic pelvic pain syndrome Chronic bacterial prostatitis \n\n## . Pain in pelvis, perineum, genitalia \n\nSymptoms . Irritative voiding symptoms (eg, urgency, hesitancy) \n\n## . Young & middle-aged men \n\nEpidemiology l Ri sk with diabetes, smoking , urinary tract procedure .. Hematospermi a, pain with ejaculation \n\n## . No or mild prostate tenderness \n\nDiagnosis Sterile urine culture . . Col iforms enter from urethra via intraprostatic reflux \n\nPathogens Escherichia coli causes >75 % of cases .\n\n# . Recurrent urinary tract infection (with the same organism) \n\n Alpha blockers (eg, tamsulosin) \n\nManagement An ti biotics (eg , ciprofloxacin), espe ci ally if history of UTI \n\n## . +/- Prostatic tenderness & swelling (often absent) \n\nPresentation . Pain with ejaculation \n\n## . 5-alpha-reductase inhibitors (eg, finasteride) . History of antibiotic treat ment --+ transient improvement \n\nUTI = uri na ry tract inf ecti on. \n\nDiagnosis . Pyuria and bacteriuria on urinalysis \n\n## . Bacteria in prostatic fluid > bacteria in urine \n\nTreatment . Fluoroquinolones (eg, ciprofloxacin) for 6 weeks Gynae & Reproductive Health What is the most likely diagnosis in an elderly male with 3-month history of perinatal and scrotal pain , pain during ejaculation , and a mildly tender prostate? Vitals are within normal limits. Urine analysis shows: Positive WBC, Urine Culture Negative .\n\nChronic Pelvic Pain Syndrome \n\nDiagnosis of exclusion. Patients present with persistent pelvic pain, irritation urological complains, and painful ejaculation \n\nProstate Cancer & BPH \n\n What is the most appropriate pain management for a patient with advanced prostate cancer with bony metastasis , status-post orchiectomy ?\n\nRadiation therapy \n\nbisphosphonates are useful for controlling chronic pain, but radiation is more acute; anti-androgen therapy is not needed in patients that have undergone orchiectomy \n\n What are the current recommendations regarding PSA screening in asymptomatic patients? \n\nControversial; should be determined on a case-by-case basis by the physician and patient \n\n What is the best next step in a male with nocturia, increased urinary urgency, and frequency ? Vitals are normal. Rectal exam shows a diffusely enlarged and non-tender prostate with a smooth surface. \n\nUrine analysis \n\nPatients with lower urinary tract symptoms should have a urine analysis to evaluate for \n\nhematuria (bladder cancer, stones) and infection .\n\n What is the preferred initial treatment for uncomplicated benign prostatic hyperplasia (BPH)? \n\nAlpha-1 blockers (e.g. terazosin, tamsulosin) \n\n287 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCompar i son of benign prostatic hyperplasia & prostate c ancer BPH Pr os ta te c an cer Risk factors Age >50 Age >4 0, African American & family history \n\nA ff ected part Ce nt ral portion (transitional zone) Us ua lly periph er a l zone of prostate but can be anywhere \n\nExam ination Symmetri ca lly enlarged & smooth prostate Asymmet ri ca lly enlarged, nodules & firm prostate Can have elevated PS A Markedly elevated PS A\n\nMedical therapy for benign prostatic hyperplasia Alpha-adrenergic Relax smoot h muscle in bladder neck , prostate capsule \n\nantagonists & prosta tic ure t hr a(eg, terazos in, Usual first-line therapy tamsulosin) Sid e effect s: Orthostatic hypotension, di zzi ness \n\n5-alpha-reductase Inhibit conversion of te s to s terone to dihyd rot esto sterone \n\ninhibitors Red uce prostate gl and size (eg, finasteride, Effectiveness may take 6- 12 months dutasteride) Side effects : Dec reased libido, erectile dy sfunction \n\nAntimuscarinics Used to treat overactive bladder (urinary fr equency ,urgency & incontin en ce) (eg , to lterodin e) Side effect s: Urine retention, dry mouth Gynae & Reproductive Health 5-alpha-reductase inhibitors can be used as an alternative or in addition to alpha blockers but have a slower onset of action \n\n Patients can have re-growth of BPH after TURP .\n\nPenis \n\n Which anti-depressant medication is associated with priapism ?\n\nTrazodone \n\nhowever the most common drug that causes priapism is prazosin \n\nErectile Dysfunction \n\n Lack of nocturnal erections suggests an organic etiology of erectile dysfunction , such as neurogenic or vascular .\n\nNormal testing suggests psychogenic etiology. \n\nBalanitis \n\n288 https://t.me/usmleinnercircle \n\nHypospadias Normal urethral opening Hypospadias \n\nCommon causes of erectile dysfunction Clinical features Vascular . Cardiovascular risk factors (eg, hypertension, smoking, diabetes) \n\n Abnormal vascular examination (eg , bruits, decreased pulses) \n\nNeurologic . Neurologic comorbidity (eg, diabetic neuropathy, multiple sclerosis, spinal injury/surgery) \n\n# . Gradual onset, loss of bulbocavernosus reflex \n\n# . Sudden onset \n\nPsychogenic . Situational (eg , ED with partner, normal erection during masturbation) \n\n# . Normal nonsexual nocturnal erections \n\nEndocrine Additional symptoms due to underlying disorder Abnormal hormone levels (eg, TSH , prolactin) \n\nMedications . Onset related to starting medication Antihypertensives, SSRls, antiandrogenic medications \n\n# . Gradual onset \n\nHypogonadism . Decreased libido, gynecomastia, testicular atrophy \n\n# . Low serum testosterone \n\nED= erectile dysfunction ; SSRls = selective serotonin reuptake inhibitors. Gynae & Reproductive Health Penis Fracture \n\n Are penile fractures typically managed medically or surgically? \n\nSurgically \n\nmedical management of PF has a higher rate of complications \n\nPeyronie Disease \n\nArises due to repetitive blunt trauma to the penis during sexual intercourse with subsequent aberrant wound healing. It is characterized by the formation of fibrous plaques (due to transforming growth factor-1 up-regulation) in the tunica albuginea. Manifestations generally include penile pain , curvature , and dorsal nodules or plaques .Dx: Clinical or USG \n\nT/t: Spontaneous resolution or progressive PD often require NSAIDs drugs for pain; pentoxifylline to reduce fibrosis; and/or intralesional injections of collagenase . Surgery may be indicated in refractory \n\n289 https://t.me/usmleinnercircle USMLE Inner Circle \n\nBalanitis & balanoposthitis \n\n# . Balanitis: inflammation of the glans pen is \n\nDefinition . Ba lan oposthi ti s: in flam ma tion of the glans pe nis + fore ski n\n\n## . Irritat io n ( eg , poor h yg iene, contact dermatitis) \n\nEtiologies . Infection (eg, Candida albicans, bacterial flora, STls) \n\n## . Trauma (e g, ag gressi ve for es kin retrac ti on) \n\n# . Consider KOH m ic ro scopy for suspected Candida infection (e g, th ick, whi te discharg e) *\n\nEvaluation . S TI scr ee n if urethral discharge er es ent \n\n## . Foreskin hy gi ene, sitz bath s\n\nManagement . Topical tr ea tment ( ie , antifungal or antibiotic) \n\n## . DM screen for Candida infection without risk fa ctor (e g, diaeer dermatitis, re ce nt antibiotic us e) \n\n* Em pi ric tr ea tm e nt ap pro pri ate wi th co nc urr ent diaper derma ti tis. OM = diabetes mellit us; KOH = pot a ss ium hyd roxi de; STI = sex ua ll y trans mi tte d inf ec ti on. Clinical features \n\n Cracking, snapping, or popping sound caused by rupturing of the tunica albuginea and soft tissue Immediate detumescence (loss of erection) Pain; varies in intensity depending on severity of the injury Pronounced soft tissue swelling , curving , and hematoma of the penis (\"eggplant \" appearance) i;:J \n\n Blood at the urethral meatus in concomitant urethral injury \n\nReferences: [ 11\n\n, .. Your notes Diagnostics Differential diagnoses Treatment \n\n Surgical procedure i;:J \n\n Exploration of the penis with evacuation of hematoma Repair of possible urethral injury with insertion of a catheter for stenting purposes Suture of rupture in the tunica albuginea Postoperative measures \n\n Pain medication ; prophylactic oral antibiotics Light compression dressing \n\n Feedbac 4 weeks of sexual abstinence (suppression of spontaneous erections with diazepam or stilboestrol may be considered) \n\n# I\n\n Follow-up with retrograde urethrography in patients with urethral reconstruction upon removal of the urethral catheter after 2 weeks Penile fracture is a urological emergency and requires immediate surgical treatment to restore functionality and minimize risk of long-term complications! Gynae & Reproductive Health cases. \n\nPhimosis \n\n Pathologic phimosis is the inability to retract the foreskin due to scarring and fibrosis (eg, secondary to balanoposthitis) of the prepuce. \n\nTopical corticosteroids are used in these cases \n\nTestes \n\nCryptorchidism \n\n290 https://t.me/usmleinnercircle \n\nPhimosis \n\nUncircumcised penis Phimosis Physiologic in children Paraphimosis Urologic emergency \n\nC>UWorld \n\nPhimosis, or the inability to retract the prepuce (foreskin) in an uncircumcised male patient, is usually considered physiologic in infants and young children . Forced manipulation of the prepuce may result in paraphimosis, the retraction and entrapment of the prepuce. Due to decreased lymphatic and venous blood flow to the distal penis, the presentation of paraphimosis includes edema and significant tenderness of the glans penis and prepuce. Initially, the glans may appear pink and soft. Without intervention, however, arterial blood flow may be compromised , leading to ischemia and penile tissue firmness and darkening (blue to black). Management of paraphimosis is emergency reduction , either manually or surgically, to maintain vascular flow to the glans penis. Circumcision is a definitive treatment option for preventing the recurrence of paraphimosis but may be unnecessary for an isolated episode that is easily resolved by reduction . \n\nManagement of cryptorchidism in infants \n\nUndescended testicle (testicle not present in scrot um ) Bilateral nonpalpable testicles Hypospad,as \n\n# ~_1_:::L.o, sex development' \n\nAge <6 months Age ~6 months Karyotype Pelvic ultrasound Adrenal/gonadal hormones Monitor for spontaneous descent Refer for orchiopexy \n\neg, congenita l adrenal hyperpfasla , hypogonad otrophic hypogonad lsm .androgen inse nsmvi ty , gonada l dysg enesis . C UWorld Gynae & Reproductive Health Cancer \n\n Patients with testicular cancer may present with low back pain due to para-aortic (retroperitoneal ) lymphadenopathy. \n\n Scrotal ultrasound solid , hypoechoic lesion (seminoma ) or a lesion with cystic areas and calcifications (nonseminomatous germ cell tumor [NSGCT]) \n\n If AFP is elevated, it excludes seminoma \n\n What is the next best step in a patient with a hard mass in the left testicle and ultrasound evidence likely for a testicular tumor? Inguinal Radical Orchiectomy \n\nDo not cut the scrotum, may spread the disease. Likewise, do not perform needle biopsy. There is a high cure rate, even if there is metastasis. Kill first, investigate later biopsy can be done with the orchiectomy. \n\n291 https://t.me/usmleinnercircle USMLE Inner Circle \n\nTesticular cancer Epidemiology Age 15-35 \n\n Risk factors: Family history, cryptorchidism Unilateral, painlesstesticularnodule Manifestations Dull lower abdominal ache Metastatic symptoms (eg , dyspnea, neck mass , low back pain) Examination: Firm, ovoid mass Diagnosis Tumor markers (AFP , 13-hCG) \n\n Scrotalultrasound \n\n Screening imaging (CT scan, chest x-ray) Radical orchiectomy Treatment Chemotherapy Cure rate -95% \n\nMalignant testicular neoplasms \n\nSeminoma . Retain features of spermatogenesis \n\nGerm cell . ~-hCG, AFP usually negative (95%) . 2:1 partially differentiated cells: yolk sac , embryonal carcinoma, teratoma, and/or choriocarcinoma Nonseminoma . ~-hCG , AFP usually positive Leydig . Often produces excessive estrogen (gynecomastia) or testosterone (acne ) \n\nStromal . Can cause precocious puberty (5%) . Rare Sertoli . Occasionally associated with excessive estrogen secretion (eg, gynecomastia) \n\nAFP = alpha-fetoprotein . GERM CELL ISE MINO MA---------------1---------NO N-SEM IN OMA \n\nP-HCG* I1-------------1--------1----------1--------1 CHORIOCARCINOMA YOLK SAC EMBRYONAL TERATOMA \n\np-HCG AFP AFP + p-HCG No marker I I\n\n------------1--------\n\nTERATOCARCINO MA AFP + p-HCG \n\nSeminoma \n\nIncidence Most common \n\nElevated AFP levels 0\n\nElevated BCG levels Rare \n\nRadical inguinal orchiectomy Yes \n\nRadiation therapy Radiosensitive \n\nChemotherapy Yes \n\nRetroperitoneal lymph node 0\n\ndissection \n\nonseminoma \n\nLess common Common Common \n\nYes \n\not radiosensitive Yes Yes (many patients) Gynae & Reproductive Health FNAC and trans royal biopsy are contraindicated because of risk of spillage of cancer cells. \n\n## Repro Paeds \n\n What is thelarche ?\n\nOnset of breast development as a result of release of estrogen \n\n Adrenarche ?\n\nOnset of pubic or axillary hair development in female as a result of release of adrenal androgens \n\n Breast buds are usually the first sign of puberty in females (15% is pubic hair). \n\nFirm , Retroareolar Mass , might be slightly Tender \n\n What is the first sign of puberty in a male? \n\nTesticular enlargement \n\nPrecocious Puberty \n\n What is the treatment of premature thelarche and premature adrenarche ?\n\nNone - Very common and benign in 1st 2 years of life \n\n292 https://t.me/usmleinnercircle \n\n> Tanner stages\n> Tanner 1 Tanner 2 (age 10-11 .5) Tanner 3 (age 11 .5-13) Tanner4 (age 13-15) Tanner 5 (age >15)\n\nGynae & Reproductive Health What are the ( 4) components of the work-up for central precocious puberty ?1. FSH, LH, sex steroids 2. GnRH stimulation test ( inc. in LH )\n\n3. MRI (r/o CNS lesions ) - prior to starting GnRH agonist therapy 4. Thyroid ( r/o hypothyroidism ) What is the mechanism of treatment of central precocious puberty ?\n\nGnRH agonists (leuprolide) \n\n What is the likely diagnosis in an obese young girl that presents with pubic hair , acne , and normal bone age ?\n\nPremature adrenarche \n\nadiposity can trigger excess insulin production, which stimulates the adrenal glands to produce sex hormones ; associated with an increased risk of PCOS in adolescence \n\n What is the likely diagnosis in a young girl that presents with precocious puberty with an advanced bone age , high FSH/LH levels , and a normal MRI ?\n\nIdiopathic precocious puberty \n\nt/t: Continuous GnRH agonist therapy (e.g. leuprolide) \n\nprevents premature epiphyseal plate fusion and maximizes adult height potential \n\n What is the likely diagnosis in a young boy that presents with advanced bone age , coarse pubic hair ,and severe cystic acne with low basal LH levels and normal testicular exam? \n\nLate-onset (non-classic) congenital adrenal hyperplasia \n\ndue to 21-hydroxylase deficiency; excessive adrenal androgen production leads to peripheral precocious puberty Central: Idiopathic, Tumor; Peripheral: CAH, Exogenous, McCune Albright \n\n293 https://t.me/usmleinnercircle USMLE Inner Circle \n\nEvaluation of precocious puberty \n\nEarly secondary sexual development* Advanced bone age Normal bone age Low basa l LH High basa l LH \n\n# nGaRH stim\"lalioo lest ~\n\n,-,H l H,gh LH jIsolated breast development \n\nPeripheral precocious puberty Central Premature precocious puberty thelarche \n\nSecondary sexu al development in gi~ s age <8 or boys age <9 \n\nIsolated pubic hair development j\n\nPremature adrenarche Gynae & Reproductive Health Neonatal Withdrawal Bleeding \n\n What are consequences of intrauterine estrogen exposure ?\n\nBreast bud development is normal in infants of either gender \n\nNewborn girls have bloody or mucoid vaginal discharge (most common cause of vaginal bleeding in neonate )\n\n## Drugs \n\n GnRH agonists are not recommended for adolescents due to decreased bone mineral density caused by prolonged use. \n\nProgesterone girls typically have premature vaginal bleeding and breast development \n\n294 https://t.me/usmleinnercircle \n\nMcCune-Albright syndrome \n\n Mutation GNAS gene \n\nPathogenesis Constant G protein activation \n\n## . Hormone overproduction Peripheral precocious puberty \n\nClinical features . Irregular cafe-au-lait macules Polyostotic fibrous dysplasia Thyrotoxicosis \n\nComplications Acromegaly Cushing syndrome \n\nNeonatal withdrawal bleeding \n\n# . In utero: maternal estrogen stimulates fetal endometrial proliferation \n\nPhysiology . After delivery: withdrawal of maternal hormones --+ endometrial sloughing in neonate \n\n# . Light vaginal bleeding in first 2 weeks of life \n\n# . Additional signs of maternal estrogen exposure: \n\nClinical features 0 Physiologic leukorrhea \n\n> 0\n\nLabial swelling \n\n> 0\n\nBreast hypertrophy galactorrhea \n\n# . Clinical diagnosis \n\nDiagnosis & management . Reassurance for parents Resolves on its own within days \n\nClinical features of androgen abuse \n\n# . Exogenous (eg, testosterone replacement therapy) \n\nTypes of androgens . Synthetic (eg, stanozolol , nandrolone) \n\n Androgen precursors (eg, DHEA) \n\n# . Reproductive \n\n> 0\n\nMen: decreased testicular function & sperm production, gynecomastia \n\nSide effects/ o Women: acne, hirsutism, voice deepening, menstrual irregularities \n\nclinical presentation . Cardiovascular: left ventricular hypertrophy, possible t HDL & j LDL \n\n# . Psychiatric: aggressive behavior (men), mood disturbances \n\n# . Hematologic: polycythemia , possible hypercoagulability \n\nDHEA = dehydroepiandrostenedione. Gynae & Reproductive Health Adolescents with irregular menstrual bleeding due to anovulatory cycles may benefit from progesterone therapy. \n\nprogesterone, which is normally secreted by the corpus luteum during ovulatory cycles, causes differentiation of the proliferative endometrium into secretory endometrium; withdrawal causes menstruation \n\n Common side effects of the injectable medroxyprogesterone contraceptive are vaginal bleeding /spotting and weight gain. \n\n The progestin-releasing subdermal implant is a long-acting (ie, up to 3 years ), reversible contraceptive that reduces menstrual bleeding in 50% of patients and causes amenorrhea in 20% of patients Useful for patients where estrogen is contraindicated \n\nOCP & IUD \n\n Hypertension: due to increased angiotensinogen synthesis by estrogen during first-pass metabolism; discontinuing use can correct the hypertension in most patients Should not be used in women age > 35 that use tobacco due to risk of myocardial infarction and stroke \n\n295 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCombined estrogen/progestin oral contraceptive pills \n\n# . Irregular, unscheduled bleeding \n\n# . Breast tenderness , nausea, bloating \n\n Amenorrhea \n\nAdverse effects \n\n(most due to estrogen component) . Hypertension \n\n Venous thromboembolic disease \n\n# . Liver disorders (eg, hepatic adenoma) \n\n# . j Serum triglycerides \n\n# . Pregnancy prevention \n\nBenefits . Menstrual cycle regulation \n\n# . i Dysmenorrhea \n\n# . t Hyperandrogenism (eg, acne, hirsutism) \n\n# . t Risk of ovarian & endometrial cancer (if ever used) \n\nRisk augmentation j Risk of cervical cancer (only if currently or recently used) .\n\nSide effects & risks of combination oral contraceptives Absolute contraindications \n\n Breakthrough bleeding to combined hormonal contraceptives \n\n Breast tenderness, nausea, bloating Amenorrhea Migraine with aura Hypertension .=:'..15 cigarettes/day PLUS age .=:'..35 \n\n Venous thromboembolic disease Hypertension .=:'..160/100 mm Hg Decreased risk of ovarian & endometrial cancer Heart disease Increased risk of cervical cancer Diabetes mellitus with end-organ damage Liver disorders (eg, hepatic adenoma) History of thromboembolic disease Increased triglycerides (due to estrogen component) Antiphospholipid-antibody syndrome History of stroke \n\n Breast cancer Cirrhosis & liver cancer Major surgery with prolonged immobilization Use <3 weeks postpartum Gynae & Reproductive Health Weight gain is NOT a side effect of OCP What is the preferred method of contraception for patients with breast cancer ?\n\nCopper IUD \n\nall hormone-containing contraceptives are contraindicated in patients with breast cancer \n\n(both estrogen and progesterone may have a proliferative effect on breast tissue) \n\n What is the recommended contraceptive for a woman with a history of anemia and medication non-compliance ?\n\nLevonorgestrel IUD \n\ntypically causes amenorrhea , which is beneficial in patients with anemia (versus the copper IUD ,which can cause heavy menstrual bleeding ); \n\nAlso the progestin-releasing IUD does not affect thromboembolic risk. \n\nless common side effects include mood changes , breast tenderness , and headache \n\n Age and parity are not contraindications to IUD insertion \n\n In postpartum patients who are breastfeeding , progestin-only contraception methods (eg, \n\nsubdermal progestin-releasing implant , progestin-releasing IUD ) are preferred. \n\nEstrogen containing contraceptive avoided due to risk of thromboembolism \n\nEmergency Contraceptive \n\n296 https://t.me/usmleinnercircle \n\nContraindications to IUD placement \n\n## . Pregnan cy \n\n## . Endome tr ial or cervical ca n ce r \n\n> Copper IUD &\n\n## . Unexplained vaginal bleeding \n\n> progestin IUD\n\n## . G es ta ti onal trophoblastic disease \n\n## . Severe uterine cavity distortion . Active pelvic infection (eg , PIO, cerviciti s) \n\n## . Active liver disease \n\n> Progestin IUD Current breast cancer\n\n## . II \n\n> Copper IUD\n\n# . Wilson disease IUD = intraut er ine device; PID = pelv ic inflammatory disease. Gynae & Reproductive Health IUD contraindicated if the patient has acute cervicitis or PID \n\nSERM \n\n Selective estrogen receptor modulators increase the risk for venous thromboembolism by increasing protein C resistance. \n\ndue to estrogen agonist activity In addition, they increase 2/7/8/10 , decrease antithrombin 3 , and decrease protein S \n\n What is the most common side effect of tamoxifen ?\n\nHot flashes (80%) \n\ndue to anti-estrogenic activity in the CNS which causes thermoregulatory dysfunction in the anterior hypothalamus \n\n Tamoxifen decreases the blood cholesterol level and may protect against coronary artery \n\ndisease. \n\nPDE-5 Inhibitors \n\n297 https://t.me/usmleinnercircle USMLE Inner Circle \n\nEmergency contraception Method Timing after Efficacy Contraindications intercourse \n\n# . Wilson disease \n\nCopper-containing 0-120 hr >99% Active pelvic infection \n\nintrauterine device .. Severe uterine cavity distortion . Breast cancer \n\nProgestin-releasing 0-120 hr >99% Active pelvic infection .intrauterine device . Severe uterine cavity distortion \n\nUlipristal 0-120 hr 98%-99% . None \n\n---\n\nOral levonorgestrel 0-72 hr 92%-98% . None \n\nOral contraceptives* 0-72 hr 75%-89% . None *Combined estrogen/progestin oral contraceptive pills containing levonorgestrel or norgestrel. \n\nSelective estrogen receptor modulators \n\n# . Tamoxifen \n\nDrugs Raloxifene .. Competitive inhibitor of estrogen binding \n\nMechanism of action . Mixed agonisVantagonist action \n\n# . Prevention of breast cancer in high-risk patients \n\nIndications . Tamoxifen: adjuvant treatment of breast cancer \n\n# . Ralox~ene: postmenopausal osteoporosis \n\n# . Hot flashes \n\n# . Venous thromboembolism \n\nAdverse effects . Endometrial hyperplasia & carcinoma (tamoxifen only) \n\n# . Uterine sarcoma (tamoxifen only) Gynae & Reproductive Health What is the first-line treatment for most patients with erectile dysfunction ?\n\nPDE-5 inhibitors (e.g. sildenafil) \n\nIf patient has CAD and is on beta-blockers , which may be associated with ED, do not stop these medications unless patients are completely intolerant or experience severe side effects \n\n PDE-5 inhibitors are contraindicated in patients who take nitrates and used cautiously in patients who take alpha blockers due to the risk of hypotension. use minimum doses of alpha blockers and sildenafil at least 4 hours apart \n\n298 https://t.me/usmleinnercircle \n\n> Adverse effects of phosphodiesterase-5 inhibitors\n> Cardiovascular Hypot ensi o n {especially with nitrates, alpha blocker s) Ocular Blue discoloration of vision Nonarteritic anterior ischemic optic neuropathy Genitourinary Pr iapism Flushing\n> Other Headache Hearing loss\n\nObs \n\n# Obs Physiology Physiologic Hydronephrosis of Pregnancy Exercise Vaccines RhD & ABO incompatibility Hormone Amniotic Fluids Polyhydramnios Oligohydramnios Fetus Gestational Age Fetal Surveillance Fetal Heart Rate Prenatal Testing & Screening Congenital Infections Group B Strep Syphilis Rubella HSV Hepatitis HIV IUGR Twins Demise Hydrops Fetalis Hypertension Preeclampsia Eclampsia HELLP Gestational Diabetes Pregnancy Preterm Labour Labour Breech External Cephalic Version Internal Podalic Version Shoulder Dystocia Post Term 3rd Trimester Bleeding Placenta Previa Vasa Previa Uterine Rupture Placental Abruption PROM Chorioamnionitis \n\n299 https://t.me/usmleinnercircle USMLE Inner Circle Obs Physiology \n\n Fall in sodium concentration during pregnancy closely correlates with i nc. production of hCG Fall below 130 should prompt evaluation for pathologic causes of hyponatremia Miscarriage/ Abortion Recurrent Pregnancy Loss Ectopic Pregnancy Hydatidiform Mole Choriocarcinoma Vomiting Hyperemesis Gravidarum Postpartum PPH Uterine Inversion Placenta Accreta Sheehan Syndrome Perineal Laceration Fistula Pubic Symphysis Diastasis Septic Pelvic Thrombophlebitis Postpartum Endometritis Urinary Retention Miscellaneous Back Pain Round Ligament Pain Liver Disorders of Pregnancy Pseudocyesis Drugs Uterotonic \n\n300 https://t.me/usmleinnercircle \n\nNormal physiological changes during pregnancy System Clinical finding Mechani sm \n\nt Glomerular fi ltration rate & t Ca rdiac ou tpu t & renal blood renal siz e, l blood urea flow due to progesterone, nitrogen & serum creatinine w it h t re nal excretion \n\nRenal / Urinary Urinary frequency, nocturia t Urine output & sodium excretion Hormones reset thres hold to Mild hyponatremia t ADH release from pituita ry Di lutional an emia t Pl as ma vol ume & red blood ce ll m ass \n\nHeme Hormone-mediated l in tot al protein S Proth r ombotic state antigen & activity; t in fibrinogen &coag ulation fac tors \n\nCardiovascular t Cardiac output & heart rate t Blood vo lume, l systemic vascular resis tan ce Chronic respiratory alkalosis Progesterone dir ec t ly stimulates centra l \n\nPulmonary with metabolic compensation, respiratory cente rs to t tida l vo lume &\n\nt PaO 2 & l PaCO 2 minute ventilation Obs fibrinogen low/normal fibrinogen in pregnancy may be sign of DIC \n\n When should folic acid supplementation ideally begin for pregnancy? 4 weeks prior to pregnancy \n\nConsequences of deficiency ?\n\nNeural tube defects (anencephaly, meningomyelocele) (look for inc. AFP) If patient with previous NTD pregnancy is on prenatal vitamins already, she still requires extra folic acid! \n\nPhysiologic Hydronephrosis of Pregnancy \n\nDue to 1. Increase blood volume Increased filtration \n\n2. High Progesterone Ureteral Dilatation \n\n3. Uterine Compression Dilatation of Proximal Ureters and Bilateral Hydronephrosis No management needed \n\n Renal pelvis and ureter dilation during pregnancy occurs more commonly on the right side \n\ndue to cushioning provided by the sigmoid colon on the left \n\nExercise \n\n What exercise regimen is recommended for healthy women with uncomplicated pregnancies ?\n\n20 - 30 minutes of moderate-intensity exercise on most or all days of the week \n\ncontact sports and activities with high fall risk should be avoided; women with risk for preterm delivery, preeclampsia, or severe cardiopulmonary disease should also avoid exercise \n\n301 https://t.me/usmleinnercircle USMLE Inner Circle \n\nWeight gain in pregnancy Prepregnancy Ideal weight gain Complications BMI (kg/m 2)\n\n< 18 .5 12.7-18.1 kg (28-40 lb) Inadequate weight gain Low birth weight 18.5-24.9 11 .3-1 5.9 kg (25-35 lb) Preterm delivery 25-29.9 6.8-11.3 kg (15-25 lb) Excessive weight gain Gestational diabetes mellitus \n\n2'30 5-9 kg (11-20 lb) . Fetal macrosomia \n\n# . Cesarean delivery \n\nShort interpregnancy interval Definition . <6-18 months from delivery to next pregnancy \n\n# . Maternal anemia \n\n# . PPROM \n\nComplications Preterm delivery .. Low birth weight \n\nPPROM = preterm prelabor rupture of membranes. Obs Prior cesarean delivery is NOT a contraindication to exercise .\n\nVaccines \n\n Tdap: Given >26 weeks (in every pregnancy) If there is wound injury, give Tdap regardless of gestational age on the basis of standard wound management guidelines (e.g if not received in last 10 years) What is the recommended management for a pregnant woman that is rubella-nonimmune ?\n\nImmediate postpartum vaccination (e.g. MMR) \n\ncontraindicated during pregnancy but safe during breastfeeding \n\n The inactivated influenza vaccine is safe during every trimester of pregnancy and while breastfeeding. \n\nRhD & ABO incompatibility \n\n302 https://t.me/usmleinnercircle \n\nPregnancy & exercise \n\n Amniotic fluid leak Cervical incompetence \n\nAbsolute Multiple gestation \n\ncontraindications Placenta abruption or previa Premature labor Preeclampsia/gestational hypertension Severe heart or lung disease Contact sports (eg, basketball, ice hockey, soccer) \n\nUnsafe High fall risk (eg, downhill skiing, \n\nactivities gymnastics, horseback riding) Scuba diving Hot yoga \n\nVaccines during pregnancy \n\n Tdap \n\nRecommended Inactivated influenza Rho(D) immunoglobulin Hepatitis B Hepatitis A \n\nIndicated for high-risk patients Pneumococcus Haemophilus influenzae \n\n Meningococcus Varicella-zoster immunoglobulin HPV \n\nContraindicated MMR Live attenuated influenza Varicella Obs What screening test is used to determine if an Rh(D)- pregnant woman has already alloimmunized ?\n\nAntibody screen (indirect Coombs test) \n\ndetects the presence of any RBC antibodies; \n\nRh(D)- women with a negative antibody screen should still receive anti-D immune globulin at 28 - 32 weeks gestation IgM at first exposure, cant cross placenta. IgG seroconversion by the time of second pregnancy \n\n303 https://t.me/usmleinnercircle USMLE Inner Circle \n\nIndications for prophylactic administration of anti-D immune globulin for Rh(D)-negative patients* \n\n At 28-32 weeks gestation <72 hours after delivery of Rh(D)-positive infant <72 hours after spontaneous abortion Ectopic pregnancy Threatened abortion Hydatidiform mole Chorionic villus sampling, amniocentesis Abdominal trauma 2nd- & 3rd-trimester bleeding External cephalic version *Antepartum prophylaxis is not indicated if the father is Rh(D) negative. \n\nPreg na ncy 1 Pregnancy 2 RBCs = red blood cells . \n\nRh alloimmunization \n\nFetal \n\nRh RBCs \n\n# RBCs enter mate rn al blood stream & generate maternal anti-D antibodies \n\n# \n\nMatemal anti-Rh(D) \n\n# MU: \\;-~ \n\nAnti-Rh(O} antibodies cross placenta & cause lysis offe tal RBCs Hemolytic disease of the fetus/newborn \n\nHydrops fetalis \n\nPericardia! effusion Obs Administration of RhD immune globulin is ineffective in a patient who has already developed RhD antibodies What does \"unsensitised\" mean? \n\nRh negative mother with no antibodies to Rh \n\nNext step? Give RhoGAM (anti-D Rh Ig) if: Any maternal-fetal mixing (any gyn operation, delivery, abortion , C/S) \n\nUnsensitized at 28 weeks Within 72 hours of Delivery if baby is Rh-positive The Kleihauer-Betke test may be used to determine if a higher dose of anti-D immune globulin is needed after a procedure or delivery. \n\nthe standard dose (300 mg) is enough to neutralize 30 mL of fetal blood; this test is typically used when there is an increased risk of fetal blood cells entering the maternal circulation (e.g. placental \n\nabruption , amniocentesis )\n\n Antibodies against A and B are hemolytic . However, in addition to red blood cells, A and B antigens are present on the cells of all other fetal tissues . The reaction of the anti-A and anti-B antibodies with the antigens on these other cells neutralizes the antibody response, leading to a much milder form of hemolytic disease. Non-invasive diagnosis of fetal anemia may be made by middle cerebral artery peak systolic velocity on Doppler ultrasound \n\nuseful for fetuses at risk of anemia due to red cell alloimmunization If unsensitized re-screen at 28 weeks and delivery and give RhoGAM as indicated \n\n304 https://t.me/usmleinnercircle \n\nRh Antibody Screening -----------\n\n._______,.__~ -------- \n\n> Rh negative\n> Antibody titer \"--\n\n## ~- \"-,. \n\n~---~ ~-----~ \n\n> Sensitized Further Monitoring Unsensitized Repeat at 28 weeks and give Rhogam as indicated\n> ABO hemolytic disease\n> ~-----~\n> Rh positive\n> No further screening\n> Risk factors Infants with blood types A or B born to a mother with blood type 0 Jaundice within 24 hours of birth Anemia\n> Clinical features jReticulocyte count Hyperbilirubinemia Positive Coombs test\n> Management Serial bilirubin levels, oral hydration &phototherapy for most neonates Exchange transfusion for severe anemia/hyperbilirubinemia\n\nObs Hormone \n\n Evaluation of hyperthyroidism in pregnancy starts with measuring Free T4 levels (it is the only reliable marker in pregnancy) \n\n What is the treatment of hypo/hyperthyroidism in pregnancy? \n\nHyper thyroidism: PTU (1st trimester), Methimazole (2nd/3rd trimester) Hypo thyroidism: Levothyroxine \n\nMonitor q4 weeks as pregnancy TBG, which will increase L-thyroxine requirements \n\n What is the recommended management for a woman with medically-managed hypothyroidism that desires to get pregnant in the near future? \n\nIncrease levothyroxine dose at the time pregnancy is detected \n\nAmniotic Fluids \n\n Polyhydramnios is characterized by an amniotic fluid index > 24 cm or a single deepest pocket > 8 cm. \n\n Oligohydramnios is characterized by an amniotic fluid index < 5 cm or a single deepest pocket < 2 cm. \n\nPolyhydramnios \n\nManagement is based on severity, maternal symptoms, and gestational age: Patients with severe or symptomatic polyhydramnios at preterm gestation are at increased risk for obstetric complications, including preterm labor and preterm prelabor rupture of membranes. \n\n305 https://t.me/usmleinnercircle USMLE Inner Circle \n\nMaternal thyroid testing in pregnancy, first trimester Hormone Change Mechanism Total T4 Increased [3 -hCG stimulates thyroid hormone production in first trimester Unchanged or Estrogen stimulates TBG ; thyroid \n\nFree T4 increases hormone production to mildly increased maintain steady free T4 levels \n\nTSH Decreased Increased [3 -hCG & thyroid hormone suppress TSH secretion \n\n11 - hCG = ~human chorionic gonadotropin; TBG = thyroxine-binding globulin .\n\n\n\n0Amniotic fluid index Oligohydramnios (AFI <5 cm) Polyhydramnios (AFI ~24 cm) \n\n Preeclampsia Esophageal/duodenal atresia \n\n Abruptio placentae . Anencephaly \n\nCauses Uteroplacental insufficiency Multiple gestation \n\n# . Renal anomalies . Congenital infection \n\n NSAIDs Diabetes mellitus \n\n# . Fetal malpresentation \n\n Meconium aspiration \n\n Umbilical cord prolapse \n\nComplications . Preterm delive [ll . Preterm labor \n\n Umbilical cord compression \n\n Preterm prelabor rupture of membranes \n\nAFI =amniotic fluid index; NSAIDs =nonsteroidal anti-inflammatory drugs .Obs Therefore, these patients may benefit from amnioreduction (ie, amniotic fluid removal by amniocentesis) Patients with mild , asymptomatic polyhydramnios at term gestation , can undergo expectant management because obstetric outcomes are unchanged by increased antenatal fetal surveillance or intervention. \n\nOligohydramnios \n\nThe etiology of oligohydramnios can vary with gestational age: \n\nEarly-gestation oligohydramnios is concerning for fetal etiologies (eg, aneuploidy, renal agenesis, posterior urethral valves) because amniotic fluid volume is dependent on normal fetal urine production. \n\nSecond- and third-trimester causes of oligohydramnios are typically due to uteroplacental insufficiency (with concomitant fetal growth restriction ) or maternal causes, such as dehydration \n\nor rupture of membranes (with normal fetal growth ). \n\n## Fetus \n\nGestational Age \n\n What is the most accurate way to determine estimated gestational age ?\n\nUltrasound crown-rump measurement in the first trimester \n\nlast menstrual period may be used to estimate gestational age if the patient has normal menses and a reliable LMP \n\n After 20 weeks gestation, fundal height in centimeters should directly correlate to gestational age in weeks with a small variation (eg, 2-3 cm) \n\n306 https://t.me/usmleinnercircle \n\n \n\n> Ultrasound assessment of gestational age Measuring fundal height\n> Ultrasound Gestational age Accuracy parameter (weeks) (days) Gestational sac 4. 5----6 +/-5---7\n> diameter /\"\\.-P~ 2'-\"'---+-t--Xiphoid process 7- 10 +/- 3\n> Crown-rump length 11 - 14 +/- 5 14- 20 +/- 7\n> Bi parietal diameter, head 21 - 30 +/- 14\n> circumference, Umb il icus\n> femur length\n> >30 +/-21 - 28\n> CUWorld\n\nObs Fetal Surveillance \n\n Management? \n\n0-4: fetal hypoxia --> urgent delivery ~6 : repeat in 24 hours 8-10: normal and rules out fetal hypoxia What is the recommended management for a pregnant woman at 32 weeks gestation with gestational hypertension and a biophysical profile score of 6 at today's visit? \n\nRepeat biophysical profile in 24 hours \n\npregnant women with gestational hypertension need weekly BPPs starting at 32 weeks \n\ngestation; a BPP of 6/10 is equivocal and should be repeated in 24 hours \n\n What is the next step in management for a pregnant woman at 34 weeks gestation that presents with decreased fetal movement ? Non-stress testing reveals a normal FHR but is non-reactive despite vibroacoustic stimulation. \n\n307 https://t.me/usmleinnercircle USMLE Inner Circle \n\nTest Nonstress test Biophysical profile Contraction stress test Doppler sonography of the umbilical artery \n\n\n\n\n\nAntepartum fetal surveillance Description Normal result Abnormal result \n\n Nonreactive: Reactive: <2 accelerations External fetal heart rate monitoring for 20-40 2'2 accelerations Recurrent variable or late minutes 2 points decelerations 0 points Nonstress test plus ultrasound assessment of the fo ll owing: \n\no Amnioti c fiuid volume \n\no Fetal breathing movement Equivocal: 6 points \n\no Fetal movement 8 or 10 points Abnormal : 0 , 2, or 4 points \n\no Fetal tone Oligohydramnios 2 points per category if normal (maximum 10/10) 0 points per category if abnonmal External fetal heart rate monitoring during No late or Late decelerations with >50% spontaneous or induced (eg, oxytocin, nipple recurrent variable of contractions stimulation) uterine contractions decelerations Evaluation of umbilical artery fiow in fetal High-velocity diastolic Decreased, absent, or intrauterine growth restriction only fiow in umbilical artery reversed end-diasto li c fiow \n\nBiophysical profile* Component Normal finding \n\n1. Nonstress test Reactive fetal heart rate monitoring 2. Amniotic fluid volume Single fluid pocket ;:-: 2 x 1 cm or amniotic fluid index >5 3. Fetal movements ;:-: 3 general body movements 4 . Fetal tone ;:-: 1 episodes of flexion/extension of fetal limbs or spine 5. Fetal breathing ;:-: 1 breathing episode for ;:-: 30 seconds movements Maximum score = 1O; 0 = abnonmal; 2 = normal for each component \"Performed continuous observa ti on for 2'30 minutes Obs Biophysical profile or Contraction stress test \n\nchoice of test depends on resources available and contraindications (e.g. contraction stress test is contraindicated if there are contraindications to labor, such as placenta previa or prior myomectomy) \n\n Normal fetal movements: 10 movements in 2 hours \n\n What is the next step in management for a pregnant woman at 32 weeks gestation that presents with decreased fetal movement ? Heart tones are heard by Doppler. \n\nNon-stress test \n\ni.e. recording the fetal heart rate while monitoring for spontaneous perceived fetal movements \n\n What is the most common cause of a non-reactive non-stress test ?\n\nFetal sleep cycle \n\nvibroacoustic stimulation may be used to awaken the fetus; sleep cycles can last as long as 40 minutes therefore a non-reactive test should be extended to 40 - 120 minutes \n\n What is a normal (reactive) nonstress test ?\n\nDue to fetal sympathetic nervous system activity, which develops around 26 - 28 weeks (no reactivity before 28 weeks) \n\n NST Non-reactive Vibroacoustic Test/BPP Still Non reactive/ equivoval or low score Contraction Stress Test \n\n Can a reactive non-stress test effectively rule out fetal acidemia ?\n\nYes \n\na reactive NST has a high negative predictive value for fetal acidemia \n\nNon-reactive NST has a low positive predictive value for fetal acidemia ( high rate of false positives )\n\n Late- and post-term pregnancies require antenatal fetal surveillance beginning at 41 weeks with a biophysical profile to screen for fetal hypoxia. \n\nlate- and post-term pregnancies are at risk for uteroplacental insufficiency (e.g. oligohydramnios ,late decelerations) \n\n308 https://t.me/usmleinnercircle \n\n> Nonstress test\n> Baseline of 110-160/min\n> Reactive Moderate variability (6-25/min) 2:2 accelerations in 20 minutes, each peaking 2'15/min above baseline & lasting 2'15 seconds\n> Nonreactive Does not meet criteria for reactivity\n\nObs aging placentas may have decreased fetal perfusion, which causes decreased renal perfusion and urinary output \n\nFetal Heart Rate \n\nOccurs when the umbilical cord delivers through the cervix ahead of the presenting fetal part. \n\nRisk factors: \n\n Malpresentation Polyhydramnios \n\n Cord Compression: Variable deceleration & return to baseline (Dec in amniotic fluid after rupture of membranes cause cord compression and decompression) Cord Prolapse: Abrupt , prolonged deceleration with no return to baseline \n\n Which type(s) of decelerations may be indicative of fetal hypoxia and/or acidosis ?\n\nlate and recurrent variable decelerations \n\n309 https://t.me/usmleinnercircle USMLE Inner Circle \n\nEarly Late \n\nVar i ab le \n\nLate-term and postterm pregnancy complications Fetal Maternal \n\n Oligohydramnios Cesarean delivery Meconium aspiration Infection Stillbirth Postpartum hemorrhage Macrosomia Perinea! trauma Convulsions \n\nlntrapartum fetal heart rate monitori ng Relationsh ip to cont ra cti on \n\n Symmetric to contraction Nadir of deceleration corresponds to peak of contraction Gradual ( 2: 30 sec from onset to nadir) \n\nEtiology \n\n Fetal head compression Can be normal fetal tracing \n\nRelationsh ip to cont ra ction \n\n Delayed compared to contraction Nadir of deceleration occurs after peak of contraction Gradual ( 2: 30 sec from onset to nadir) \n\nEtiology \n\n Uteroplacental insufficiency \n\nRelationsh ip to contracti on \n\n Can be but not necessarily associated with contractions Abrupt (<30 sec from onset to nadir) Decrease 2: 15/min; duration 2: 15 sec but <2 min \n\nEtiology \n\n Cord compression Oligohydramnios Cord prolapse Onset :\n\nI7Jo i Recovery \n\n+ sec j ! '\n\n## ~1 Nadir !\n\nI Contracti on l ,\n\n~ I\n\ni l\n\nOnset i\n\nI ~ l Recovery \n\n+ sec : !\n\n~\n\n: t :: :\n\ni Nadir i\n\n: :\n\nConi action I\n\n~\n\ni ~\n\n_ :\n\n<30 : Recovery \n\nsec i /\n\n~ I\n\nr a, ir \n\nContraction \n\n~\n\nC)t.JINotld \n\nUmbilical cord prolapse \n\n~.r-- ,--- Ruptured \n\nmembranes Obs Variable decelerations Cord compression /prolapse Treatment: Intermittent: <50% contrations no treatment Recurrent (>50% contractions) : Intrauterine resuscitation ( O2 , reposition mom ) delivery if fails Late decelerations (onset occurs after peaks of uterine contractions )\n\nTreatment: Intrauterine resuscitation ( O2 ,\n\nreposition mom ) if failure amnioinfusion or C-section \n\n Cord Prolapse - Urgent C Section \n\n What is the first-line intervention for a woman in first stage of labor with recurrent variable decelerations and moderate variability on fetal heart tracing? \n\nMaternal repositioning (e.g. left lateral decubitus, all fours) \n\namnioinfusion (instillation of saline in intrauterine cavity) is a possible second-line intervention; assisted vaginal delivery could be indicated if the patient was fully dilated \n\n Amnioinfusion is contraindicated in a patient with a history of uterine surgery. \n\n Fetal scalp stimulation is performed to evaluate fetal acidosis in patients who have no accelerations \n\non FHR monitoring \n\n310 https://t.me/usmleinnercircle \n\n \n\n> 00Fetal heart rate variability Absent: undetectable amplitude Minimal : S5 bpm\n> 180 150\n> 120\n> Moderate: 6-25 bpm Marked : >25 bpm CNS =central nervous system ,Clinical significance Abnormal or intermediate pattern\n> Etiology: CNS depressants (narcotics, alcohol , recrea tional drugs) Temporary fetal sleep Prematurity Fetal hypoxia\n> Normal pattern Unclear significance\n\nObs Not performed in patients with decelerations \n\nPrenatal Testing & Screening Cesarean Section for category 3 Fetal anemia typically presents with a sinusoidal fetal heart tracing \n\n311 https://t.me/usmleinnercircle USMLE Inner Circle \n\nBaseline fetal heart rate \n\n# . Maternal fever (eg , intraamniotic infection) \n\nFetal tachycardia . Medication side effect (eg , beta agonists) \n\n(>160/min) . Fetal hyperthyroidism . Fetal tachyarrhythmia . Maternal hypothermia \n\nFetal bradycardia . Medication side effect (eg , beta blockers) \n\n(<110/min) . Fetal hypothyroidism . Fetal heart block (eg, anti-Ro/SSA, anti-La/SSB) \n\nFetal heart rate tracing patterns \n\nRequires all the following criteria: Baseline 110-160/min \n\nCategory I Moderate variability (6-25/min) No late/variable decelerations Early decelerations Accelerations \n\nCategory II Not category I or Ill (indeterminate pattern) \n\n~1 of the following characteristics: Absent variability + recurrent late decelerations \n\nCategory Ill Absent variability + recurrent variable decelerations Absent variability + bradycardia Sinusoidal patte rn Sinusoidal fetal heart rate \n\nContractio ns UA OmmHg Obs An indirect antiglobulin (Coombs) test can be used to determine whether an Rh-negative patient has developed anti-Rh antibodies and is an important component of early prenatal care, especially in patients with previous pregnancies. \n\n Prenatal visits are recommended every 4 weeks until 28 weeks of gestation, every 2 weeks from 28 to 36 weeks of gestation and then every week until delivery .100g 3-hour OGT to confirm ! \n\n312 https://t.me/usmleinnercircle \n\nRoutine prenatal laboratory tests \n\nRh(D) type & antibody screen Hemogl ob in /hematocrit, MCV, ferritin HIV , VDRURPR, HBsAg , anti-HGV Ab \n\nInitial prenatal visit Rubella & varicella immunity Urine culture Ur in e dipstick for protein Chlamyd ia PCR (if risk factors are present) Pap test (if screening indicated) Hem og lob in /hematocrit \n\n24-28 weeks An tibody screen if Rh (D)-negative 1-hr 50-9 GC T\n\n36-38 weeks Gro up B Streptococcus rectovaginal cult ure anti - HCV Ab = hepatitis C an tibody; GCT = glucose challenge t est ; HBsAg = hepa ti tis B surface ant ige n ; MCV = mean corpuscul ar vol um e; PCR =pol yme rase cha in reaction; RPR = r ap id plasma reagin. \n\nHigh-risk sexually transmitted infection screening in pregnancy \n\n Age <25 \n\nHigh-risk patients Prior sexually tran sm itted infection \n\n# . High-risk sexua l act ivity (eg , multiple partners, commercial sex work) \n\n Perf or med at initial prenatal vis it & 3rd trimester: \n\n> 0\n\nHIV \n\n> 0\n\nSyphilis \n\nRequired screening 0 Hepatitis B & C vi ru se s \n\n> 0\n\nGonorrh ea \n\n> 0\n\nChlamydia \n\nPrenatal testing \n\nTest Timing Advantages Disadvantages \n\n(weeks) \n\nFirst-trimester 9-13 Early screen ing Not diagnostic combined test* Cell-fre e fetal DNA ~10 High sensitivity & specificity for aneuploidy N ot diagnostic Chorionic villus 10-13 Definitive karyotypic diagnosis Invasive ; risk of spontaneous abortion sampling Second-trimester Screens for neural tube defects & 15-22 N ot diagnostic quadruple s creen ** aneuploidy Amnioc entesis 15-20 De fi nitive karyotypic diag nosis Invasive ; risk of membrane rupture, fetal injury & pregnancy loss Second-trimester 18-20 Measures fetal growth, evaluates fetal Cannot identify all abnormalities; some ultrasound anatomy, confirms placenta positi on findings are of uncertain significance *Pregnancy-associated plasma protein , 13 -hCG, nuchal translucency. \n\n> \"Materna l serum o-fetoprotein , estriol , f3 -hCG , inhibin A\n\n1st trimester screening Trisomy p-hCG \n\n21 t\n\n18 I\n\n13 I\n\n2nd trimester screening Trisomy P-hCG lnhibinA \n\n21 t t\n\n18 J- - or !. \n\n13 - ~ -\n\nPAPP-A \n\nI\n\nI\n\nI\n\nEstriol AFP \n\n.!- I\n\nI_ J.. \n\n- -Obs When is cell-free DNA testing (cffDNA) indicated? Test used in 10 weeks gestation onwards to identify chromosomal aberrations (high specificity and sensitivity for aneuplodies); not diagnostic (must confirm with CVS or amniocentesis) \n\n Cell free DNA is also used to screen for heritable disorders . In white patients these include \n\nCystic Fibrosis , Tay Sachs , Spinal Muscular Atrophy. \n\n What is the next step in management for a pregnant woman at 12 weeks gestation with an abnormally elevated beta-hCG level and increased nuchal thickness on ultrasound? \n\nChorionic villous sampling (CVS) \n\nthis patient has a positive first-trimester combined test; diagnosis is made via CVS or \n\namniocentesis depending on gestational age \n\nCongenital Infections \n\n Zika : Intracranial calcifications + Microcephaly \n\n Toxoplasma: Intracranial calcifications + Microcephaly/ Macrocephaly (hydrocephalous) VZV: limb hypoplasia , cataracts and skin scars CMV periventricular calcifications \n\n313 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCell-free fetal DNA testing \n\nMaternal age ~35 \n\n Abnormal maternal serum screening test \n\nIndications Sonographic findings associated with fetal aneuploidy Previous pregnancy with fetal aneuploidy Parental-balanced Robertsonian translocation \n\nApplications Screening for trisomy 21 , 18, 13 & sex-chromosome aneuploidies Fetal sex determination \n\nClinical findings of congenit al infections \n\n Intrauterine growth restriction All Hepatosplenomegaly Jaundice Blueberry muffin spots Cytomegalovirus Periventricular calcifications Diffuse intracerebral calcifications Toxoplasmosis Severe chorioretinilis Rhinorrhea Syphilis Abnormal long-bone radiographs Desquamaling or bullous rash Rubella Cataracts Heart defects (eg, PDA) Obs Congenital CMV infection is the most common cause of nonhereditary sensorineural hearing loss in children. The infection is frequently asymptomatic in infants but can cause progressive or delayed-onset, unilateral or bilateral hearing loss later in childhood. \n\nGroup B Strep \n\n Intrapartum antibiotic prophylaxis (IAP) is not necessary for planned cesarean delivery \n\nwithout labor or rupture of membranes because GBS transmission is low in such settings. In patients with mild Penicillin allergy(e.g just rash) Cephalosporin Intrapartum = During Labour !! Screen early but give penicillin only during labour ! \n\n314 https://t.me/usmleinnercircle \n\n> Chorioretinitis\n\nPreventing neonatal group B Streptococcus infection Antenatal screening Rectovaginal culture at 36-38 weeks gestation \n\n GBS bacteriuria or GBS urinary tract infection in current pregnancy (regardless of treatment) \n\n GBS-positive rectovaginal culture in current pregnancy \n\n Unknown GBS status PLUS any of the following: \n\nIndications for intrapartum prophylaxis o <37 weeks gestation 0 lntrapartum fever \n\n> o\n\nRupture of membranes for ~18 hours \n\n Prior infant with early-onset neonatal GBS infection \n\nlntrapartum prophylaxis . Intravenous penicillin \n\n> GBS =group BStreptococcus.\n\nObs Syphilis \n\n Which TORCH infections are routinely screened for in pregnant women during their first prenatal visit? \n\nRubella and Syphilis \n\nother routinely screened infections include HIV , Hepatitis B , and Chlamydia trachomatis Desensitize if penicillin allergic \n\n315 https://t.me/usmleinnercircle USMLE Inner Circle \n\nNeonatal group B Streptococcus infection \n\n## . Most common cause of neonatal sepsis , pneumonia & meningitis \n\n## . Early onset (age <1 week) \n\nPathogenesis 0 Usually exposure to bacteria in maternal genital tract \n\n## . Late onset (age >1 week) \n\n0 Usually exposure to colonized contacts \n\n## . Sepsis, pneumonia , men ingitis: \n\n0 Temperature instabili ty (eg, fever, hypothermia) \n\n0 Irritability, lethargy, poor feeding \n\nClinical findings 0 Tachycardia, hypotension \n\n0 Respiratory distress (eg, tachypnea , grunting) \n\n## . Focal infection (late onset) : \n\n0 Septic arthritis \n\n0 Cellulitis \n\nPrevention . lntrapartum antibiotic prophylaxis for mothers with positive screening GBS culture at 36 weeks \n\nGBS = group B Streptococcus. \n\nSyphilis in pregnancy Screening Universal at first prenatal visit Third trimester & delivery (if high risk) \n\nSerologic tests Nontreponemal (RPR, VDRL) Treponemal (FTA-ABS) \n\nTreatment Intramuscular benzathine penicillin G \n\nPregnancy effects Intrauterine fetal demise Preterm labor Hepatic (hepatomegaly, jaundice) \n\nFetal effects Hematologic (hemolytic anemia, L platelets) Musculoskeletal ( long bone abnormalities) Failure to thrive \n\nFTA-ABS = fluorescent treponemal antibody absorption; RPR = rapid plasma reagin. \n\nCongenital syphilis Early* \n\n# . Snuffles: copi ous clear, purulent, or serosanguineous rhinorrhea . Maculopapular rash \n\nClinical . 0 Palms , soles, buttocks, legs usually involved \n\nfeatures 0 Desquamation & hyperpigmentation \n\n## . Long bone abnormalities (eg , metaphyseal lucencies) \n\nLate \n\n## . Saddle nose, notched (Hutchinson) teeth , saber shins, sensorineural hearing loss \n\nDiagnosis . Serologic testing : VDRL , RPR \n\n## . Darkfield microscopy: Treponema pallidum in infectious material (eg, nasal discharge, skin lesions, placenta) \n\nTreatment . Penicillin \n\nPrevention . First-trimester maternal screening; repeat if high risk (eg, other prenatal STI) \n\n## . Prenatal penicillin *Nonspecific findings : jaundice, hepatosplenomegaly, growth restriction , \"blueberry muffin\" spots. \n\nRPR = rapid plasma reagin ; STI = sexually transmitted infection. Obs Rubella \n\n What is the treatment for a mother with rubella who is at 21 weeks gestation ?\n\nReassurance \n\nInfection from 1-11 weeks is associated wtih 90% risk After 20 weeks there is very low risk \n\n Triad is NOT always present. \n\nHSV \n\n316 https://t.me/usmleinnercircle \n\nSaber shins Hutchinson teeth Diagnosis Newborn and pregnant women PCR for rubella RNA (throat swab, CSF) Serology (lgM antibodies , lgG antibodies in abnormally high or persistent concentrations) Viral culture (nasopharynx, blood) Fetus \n\nlgM antibody serology (chorionic villi, amniotic fluid) PCR for rubella RNA (chorionic villi, amniotic fluid) Treatment \n\n Intrauterine rubella infection \n\n< 16 weeks: counsel to terminate pregnancy > 16 weeks : reassurance Congenital rubella syndrome : supportive care (based on individual disease manifestations) and surveillance (including monitoring for late-term complications) Prevention \n\nImmunization of seronegative women before pregnancy Nationally notifiable condition : Suspected congenital rubella syndrome should be reported to the local or state health department .\n\nJliii) Triad congenital rubella syndrome : CCC= Cataracts , Cochlear defect, \n\n\\ ( Cardiac abnormality Obs Hepatitis \n\n What is the risk of a neonate developing chronic hepatitis B if mother has active Hep B infection? \n\n90% \n\nTreatment of newborn? HB vaccine + HBIG \n\nThese should be administered within 12 hours of birth, regardless of the infant's birth weight or clinical condition. \n\nHIV \n\n317 https://t.me/usmleinnercircle USMLE Inner Circle \n\nRisk factors for neonatal herpes simplex virus i nf ection \n\n Primary maternal infection Longer duration of rupture of membranes Vaginal delivery with active lesions Impaired skin barrier (eg, fetal scalp electrode) Preterm birth \n\nPregnancy management in patients with HSV \n\nPrior HSV infecti on Yes Antiviral suppression beg i nn ing at 36 weeks jLesion/prodromal symptoms during labor No Yes No Vaginal delivery \n\nHSV = herpes simplex vi ru s. Cesarean delivery \n\nCU Wor1d \n\nRoutine prenatal care \n\nPerinatal hepatitis B virus infection Hepatitis C in pregnancy \n\n# . 90% risk of vertical transmission without prophylaxis \n\nEpidemiology . <2% risk after prophylaxis . Chronic infection in 90 % of perinatally infected infants Gestational diabetes \n\nPotential Cholestasis of pregnancy \n\ncompl ications \n\n Preterm delivery . High maternal viral load \n\nRisk factors . Maternal HBeAg+ Ribavirin is teratogenic & should be avoided . Perinatal exposure to genital secretions (most common ) \n\nTransmission . Transplacental (rare) \n\nMaternal No indication for barrier protection in \n\nmanagement serodiscordant, monogamous couples . Not transmitted by breastfeeding Hepatitis A & B vaccination \n\n## . HBV vaccine (active immunization) \n\nPrevention AND Vertical transmission strongly associated with maternal viral load . HBIG (passive immunization) Prevention of Cesarean delivery not protective \n\nvertical \n\nHBIG = hepatitis B i mmune globulin ; HBV = he patiti s B vaccine . transmission Scalp electrodes should be avoided Breastfeeding should be encouraged unless maternal blood present (eg, nipple injury) Obs What is the recommended treatment for an infant born to a mother with an HIV viral load > 1000 copies/mL ?\n\nMulti-drug ART for > 6 weeks \n\n What is the recommended antepartum treatment for a pregnant woman with HIV ?\n\nCombined anti-retroviral therapy (cART) \n\ne.g. two NRTIs and an NNRTI or protease inhibitor \n\nHow can you reduce risk of transmission of HIV in pregnancy? cART (combined antiretroviral therapy ) is recommended throughout pregnancy \n\nCesarean delivery if viral load > 1,000 \n\nHIV post-exposure ppx (neonatal zidovudine )Avoid breastfeeding \n\nRisk of transmission w/ treatment = <2% \n\nViral load <1,000 + cART -- may consider vaginal delivery + HIV post-exposure PPX \n\n Antibody testing is not performed at age <18 months as maternal antibodies may cause \n\nfalse positives Selective loss of CD4+ T lymphocytes, however absolute lymphocyte count is normal (versus SCID ); diagnosis is confirmed with PCR reaction testing \n\n318 https://t.me/usmleinnercircle \n\nHIV management during pregnancy \n\n HIV RNA viral load at initial visit, every 2-4 weeks after initiation or change of therapy, monthly until undetectable, then every 3 months \n\nAntepartum CD4 cell count every 3-6 months Resistance testing if not previously performed ART initiation as early as possible \n\n Avoid amniocentesis unless viral load s1 ,000 copies/ml Avoid artificial ROM , fetal scalp electrode, operative vaginal delivery \n\nlntrapartum Viral load s1 ,000 copies/ml: ART+ vaginal delivery Viral load >1 ,000 copies/ml: ART+ zidovudine + cesarean delivery Mother: Continue ART \n\nPostpartum Infant (maternal viral load s1 ,000 copies/ml): Zidovudine Infant (maternal viral load >1 ,000 copies/ml): Multi-drug ART \n\n> ART\n\n=antiretroviral therapy; ROM =rupture of membranes .\n\n\n\nHIV in infancy Risk factors High maternal viral load (eg, insufficient prenatal care, lack of antiretroviral therapy) Breastfeeding by infected mother Failure to thrive Chronic diarrhea \n\nClinical features lymphadenopathy , hepatosplenomegaly Pneumocystis pneumonia Prolonged/refractory candidiasis \n\nDiagnosis HIV DNA or RNA PCR \n\nTreatment Combination antiretroviral therapy Obs Infants have high baseline levels of CD4 cells due to amplified thymic activity in the months after birth. Therefore, they frequently develop immunocompromised state from HIV at relatively high CD4 counts (eg, 1,000-1,200/mm3 )\n\n D/D: SCID: Decreased absolute lymphocyte count and absence of lympoid tissue (vs Lympadenopathy in HIV) \n\nIUGR \n\n FGR can be a complication of maternal vascular disease (eg, type 1 diabetes mellitus, chronic hypertension), which causes chronic placental vasoconstriction and ischemia with resultant \n\nuteroplacental insufficiency \n\nPatients with FGR have a high risk for intrauterine fetal demise and require an immediate umbilical artery Doppler ultrasound to assess placental perfusion \n\n Bicornuate uterus with two separate endometrial cavities has less room for appropriate egg implantation, placental development, and fetal growth. Patients with this abnormality are also at increased risk for preterm delivery , fetal growth restriction , and malpresentation .\n\n319 https://t.me/usmleinnercircle USMLE Inner Circle \n\nFetal growth restriction Definition Weight <10th percentile for gestational age Maternal hypertension \n\nRisk factors Pregestational diabetes mellitus Genetic abnormalities Congenital infection Large anterior fontanel Thin umbilical cord \n\nAppearance Loose, peeling skin Minimal subcutaneous fat \n\nEvaluation Placenta histopathology Consider karyotype, urine toxicology, serology Polycythemia \n\nNeonatal complications Hypoglycemia Hypocalcemia Poor thermoregulation \n\nFetal growth restriction Symmetric Asymmetric Definition Ultrasound estimated fetal weight <10th percentile for gestational age \n\nOnset 1st trimester 2nd/3rd trimester Chromosomal abnormalities Utero-placental insufficiency \n\nEtiology Congenital infection Maternal malnutrition \n\nClinical features Global growth lag \"Head-sparing\" growth lag Weekly biophysical profiles \n\nManagement Serial umbilical artery Doppler sonography Serial growth ultrasounds \n\n Monitor/treat complications (eg, hypoglycemia, hypothermia, polycythemia) \n\n Hypoglycemi a: frequent screening and frequent feedings \n\nManagement Hypothermia: skin to skin with mother, examinations in incubator \n\n Polycythemia and hypocalcemia: screen if symptoms develop (eg , poor feeding, vomiting , jitteriness) Obs Fetal constitutional smallness is associated with short maternal stature, low prepregnancy weight , and fetal female sex . Constitutional smallness presents with an ultrasound-estimated fetal weight <10% for gestational age, normal umbilical artery Doppler evaluation , and appropriate interval growth .Constitutionally small infants have normal long-term outcomes. \n\nTwins \n\n The risk of preterm labor during a multiple gestation pregnancy may be reduced with adequate \n\nearly weight gain \n\n320 https://t.me/usmleinnercircle \n\nTypes Maternal complications Fetal complications Twin pregnancy \n\n Monochorionic, monoamniotic \n\n> o\n\n1 placenta, 1 amniotic sac Monochorionic, diamniotic \n\n> o\n\n1 placenta , 2 amniotic sacs \n\n> o\n\n\"T-sign\" at intertwin membrane Dichorionic, diamniotic \n\n> o\n\n2 placentas , 2 amniotic sacs \n\n> o\n\n\"Lambda sign\" at intertwin membrane Hyperemesis gravidarum Preeclampsia Gestational diabetes mellitus Iron-deficiency anemia Congenital anomalies Fetal growth restriction Preterm delivery (r'lt) \n\n Malpresentation (eg, breech) Monochorionic twins \n\n> o\n\nTwin-twin transfusion syndrome Monoamniotic twins \n\n> o\n\nConjoined twins \n\n> o\n\nCord entanglement \n\nLambda sign for twins Oi chorionic diamniotic \n\n> Two placentas\n\nObs Monochorionic monoamniotic twins are typically managed inpatient beginning at 28 weeks gestation with frequent fetal monitoring (eg, nonstress test) and antenatal corticosteroid administration. Patients are delivered preterm (32-34 weeks gestation ) via cesarean delivery .\n\nDemise \n\n321 https://t.me/usmleinnercircle USMLE Inner Circle \n\nT sign for twins Monochorionic diamniotic \n\nSingle placenta Obs Kleihauer-Betke: A maternal blood smear is exposed to acid, and stained afterwards. Adult hemoglobin is removed by the acid, whereas fetal hemoglobin (HbF) is not, resulting in pink color cells that indicate fetal hemoglobin on a positive test. \n\n Women with unexplained late term still birth , should undergo weekly non-stress testing in the \n\nthird trimester starting at 32 weeks gestation \n\n Even after thorough evaluation, up to half of IUFDs have no identifiable cause . Therefore, patients should be counselled in advance that testing may be negative. \n\n Development of DIC requires urgent delivery \n\nof the fetus, via vaginal or cesarean delivery. \n\n What is the recommended management for a pregnant woman at 28 weeks gestation that presents in \n\nlabor for a fetus diagnosed with anhydramnios and anencephaly ? The fetus is in breech presentation. \n\nAllow spontaneous vaginal delivery Induce vaginal delivery when mother is ready \n\n322 https://t.me/usmleinnercircle \n\nIntrauterine fetal demise Definition Absent fetal cardiac activity at 2:20 weeks gestation \n\n## . Aneuploidy . Fetal or placental anomalies \n\n## . Fetal growth restricti on \n\nRisk factors . Congenital infecti on . Substance use (eg , tobacco, cocaine) . Maternal conditions (eg , hypertension , diabetes mellitus) Fetal \n\n Autopsy \n\n## . Gross & microscopic examination of placenta &\n\numbilical cord \n\nEvaluation . Karyotype/genetic studies Maternal \n\n## . Kleihauer-Betke test \n\n## . Antiphospholipid antibodies \n\n## . Coagulation studies* \n\nIntrauterine fetal demise Delivery planning for a nonviable fetus Defin ition Fetal death at ~ 20 weeks Anencephaly Bilateral renal agenesis \n\nDiagnosis Absence of fetal cardiac activity on ultrasound 20-23 weeks \n\nFetal diagnosis Holoprosencephaly Acardia Dilation & evacuation Thanatophoric dwarfism \n\nManagement OR Vaginal de livery* Intrauterine fetal demise \n\n~24 weeks Vaginal delivery* Obstetric management Vaginal delivery No fetal monitoring \n\nComplication Coagulopathy after several weeks of fetal retention \n\nNeonatal management Palliative care if not stillborn *Cesarean delivery by maternal choice if history of prior classical cesareanlmyomectomy Obs the priority for patients with lethal fetal anomalies (e.g. anecephaly) is to minimize maternal morbidity /mortality ; C-section has an increased risk of maternal complications A breech presentation in lethal anomalies does not require a C-section (vaginal delivery preferred due to increased risk of maternal complications associated with C-section) \n\n What is the next step in management for a pregnant woman at 25 weeks gestation that presents after feeling no fetal movement for the past two days? Fetal heart sounds are not heard on Doppler. \n\nTransabdominal ultrasound \n\nthe patient likely has intrauterine fetal demise (fetal death at > 20 weeks), which must be confirmed by the absence of fetal cardiac activity on ultrasound \n\n Because parents may blame themselves for the baby's death, it is important for the physician to respond with a clear statement that it is not their fault and there is nothing they could have done to prevent the loss. The physician should also avoid prematurely changing the focus of discussion to medical management and reassurance about future pregnancies. Referring to the fetus as their \" baby \" and avoiding medical terminology (eg, fetal demise) are helpful. \n\nHydrops Fetalis \n\n## Hypertension High output heart failure \n\n323 https://t.me/usmleinnercircle USMLE Inner Circle \n\nFetal hydrops Hydrops fetalis \n\nPathogenesis . f cardiac output demand causing heart failure \n\n## . f flu id movement into interstitial spaces (thi rd spacing) \n\n## . Pericardia! effusion \n\n## . Pleural effusion \n\n## . Ascites \n\nClinical features . Skin edema \n\n## . Placental edema \n\n## . Polyhydramnios \n\n## . Immune \n\n> 0\n\nRh(D) alloimmunization \n\n## . Non immune \n\nEtiology 0 Parvov ir us B 19 infection \n\n> 0\n\nFetal aneuploidy \n\n> 0\n\nCardiovascular abnormalities 0 Thalassemia (eg , hemoglobin Barts) Obs Preeclampsia \n\n High-risk patients also require a 24-hour urine collection for total protein at the initial prenatal visit to establish a baseline (prepregnancy) proteinuria assessment. Elevated blood pressure must be seen on 2 separate measurements taken at least 4 hours apart \n\n324 https://t.me/usmleinnercircle \n\nHypertensive disorders of pregnancy Chronic hypertension Systolic pressure _::,_140 mm Hg &/or diastolic pressure _::,_go mm Hg prior to conception or 20 weeks gestation \n\nGestational hypertension New-onset elevated blood pressure at _::,_20 weeks gestation No proteinuria or end-organ damage New-onset elevated blood pressure at _::,_20 weeks gestation \n\nPreeclampsia AND \n\n Proteinuria OR signs of end-organ damage Preeclampsia \n\nEclampsia AND \n\n New-onset grand mal seizures \n\nChronic hypertension with Chronic hypertension AND 1 of the following : \n\nsuperimposed New-onset proteinuria or worsening of existing proteinuria at _::,_20 weeks gestation \n\npreeclampsia Sudden worsening of hypertension Signs of end-organ damage \n\nObstetric complications of hypertension Antihypertensive medications in pregnancy \n\n Superimposed preeclampsia First-line (safe) Second-li ne Contraindicated \n\n# . Cesarean delivery \n\nMaternal Abruptio placentae Methyldopa Thiazide diuretics ACE inhibitors Postpartum hemorrhage Maternal mortality Beta blockers Clonidine Angioten sin rece ptor \n\n(l abetalol ) blockers Hydralazine Aldo sterone blockers Fetal growth restriction oligohydramnios Preterm delivery \n\nFetal \n\n Calcium channel Direct renin inhibitors blockers (nifedipine) Furos emide Intrauterine fetal demise Perinatal morta li ty \n\nPreeclampsia Preeclampsia prevention \n\n Nulliparity Definition New-on set hyperten sion & p roteinur ia &/ or Obesity end -o rg an dama ge at >20 wee ks gestation \n\nRisk factors Preexisting medical condition (eg , SLE , chronic hypertension) Pr io r pr eecl am psi a Multiple gestation Chronic kidney disease Advanced maternal age High risk Chronic hypertension Diabetes mellitus New-onset hypertension* (SBP 1.1 mg/dl or 2x normal Elevated transaminases >2x upper limit of normal Pulmonary edem a Vision or cerebral symptoms (eg , headache) <37 weeks & no severe featur es : expectant 0.3) \n\n Patients with preeclampsia are at increased risk of hemorrhagic and ischemic stroke due to acute elevations in cerebral perfusion pressure and intracerebral vessel rupture (hemorrhagic ), as well as preeclampsia-mediated vascular endothelial damage and microthrombi formation ( ischemic ). \n\nNOT Subarachnoid Haemorrhage \n\n Preeclampsia can present upto 6 weeks after delivery. \n\n What is the likely diagnosis in a pregnant woman with preeclampsia that develops sudden-onset dyspnea , hypoxia , and crackles ?\n\nPulmonary edema \n\nrare but life-threatening complication of severe preeclampsia Preeclamptic patients have generalized arterial vasospasm leading to increased systemic vascular resistance and high cardiac afterload -- the heart becomes hyperdynamic to try to overcome the systemic hypertension. \n\n In patients with Myasthenia Gravis and Preeclampsia, magnesium sulfate is contraindicated because it may trigger a myasthenic crisis. \n\nIn these patients, seizure prophylaxis is with valproic acid. \n\n What are the first-line agents (3) for maternal hypertensive crisis ?\n\nnifedipine, hydralazine, or labetalol \n\nBe careful with labetalol -- if patient has bradycardia(<60 bpm) or asthma, do not give! Nifedipine is oral , thus patient may not be able to tolerate if they have emesis! \n\nEclampsia \n\n325 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPathophysiology of pulmonary edema in preeclampsia/eclampsia \n\nGeneralized arterial vasospasm (systemic hypertension) \n\n Afterload against which the heart is pumping \n\n Pulmonary capillary pressure \n\n~ IPulmonary edema I~ ~ Renal function I\n\n Vascular permeability USMLEWortd, LL C\n\nTreatment of preeclampsia Drug Indication \n\nHydralazine IV, labetalol IV, Lower blood pressure acutely to or nifedipine PO decrease stroke risk Magnesium sulfate IV or IM Prevent or treat eclamptic seizures Obs HELLP \n\n Delivery should occur at > 34 weeks gestation or with deteriorating maternal /fetal status \n\n## Gestational Diabetes Patients with risk factors (e.g. obesity , previous GDM ) should be \n\nscreened earlier and re-screened at 24-28 weeks if negative \n\n326 https://t.me/usmleinnercircle \n\nEclampsia (preeclampsia + new-onset seizure) \n\n# . Hypertension, typically severe (ie, SBP ~160 or DBP ~110 mm Hg) . Seizure, typically tonic-clonic with postictal phase \n\n Severe headache \n\nClinical features Visual disturbances (ie, scotoma) . Hyperreflexia . Proteinuria \n\nDiagnosis . Mainly clinical . Bilateral frontal lobe edema on CT scan of the head . Magnesium sulfate infusion \n\nManagement Antihypertensive agen t for severe hypertension . Delivery \n\nDBP = diastolic blood pressure; SBP = systolic blood pressure. \n\nHELLP syndrome Clinical Preeclamp sia \n\nfeatures Nau sea/vomiting R ight upper quadrant abdominal pain \n\nLaboratory Microangiopathic hemolyt ic anemia \n\nfindings Elevated liver enzymes Low platelet count Delivery \n\nTreatment Magnesium for seizure prophylaxis Ant ihypertensive drugs \n\nGestational diabetes mellitus 2-stepapproach forscreening & diagnosing gestational diabetes mellitus Pathophysiology . Human placental lactogen secretion . 24-28 weeks gestation \n\nScreening . 1-hr 50-g GCT \n\n## . 3-hr 100-g GTT \n\n## . 1st line: diet \n\nManagement 2nd line: insulin, glyburide, metformin \n\n## . Fasting: S95 mg/dl \n\nTarget blood glucose goals . 1-hr postprandial: S140 mg/dl 2-hr postprandial: S120 mg/d l\n\nPostpartum management . Fasting glucose at 24-72 hr \n\n 2-hr 75-g GTT at 6- to 12-week visit \n\nGCT =glucose challenge test ; GIT =glucose tolerance test. 24-28 weeks gestation \n\nStep 1 \n\n Administer 50-g oral glucose load Check serum glucose 1 hr later \n\nBlood glucose .:140mg/dL Step2 \n\n Administer 100-g oral glucose load Check fasting serum glucose each hour afterward for 3 hr Blood glucose <140mg/dL \n\nDiagnos is of gestational diabetes mellitus (.:2 abnormal values) Blood glucose level Carpenter & Coustan NOOR \n\nFasting 1 of the follow,ng : prior GD M, prior macrosomte infant, \n\nfam ily history (fi rst degree} , paycysbc ovary syl'laome 1 age i!:.40 \n\nGD M ges tat ional diabetes me lhtus CIUWor ld \n\nInfant of mother with diabetes mellitus: complications \n\nMaternal hyperglycemia \n\nFirst trimester \n\n Congenital heart disease Neural tube defects Small left colon syndrome Spontaneous abortion \n\ni Metabolic demand \n\niFetal hypoxemia \n\nii Erythropolesis \n\ni\n\nPolycythem ia \n\nCU'Norld \n\nOrganomega ly Second & third \n\ntri mesters \n\nFetal hyperglycemia & hyperinsu li nemia \n\nNeonatal hypoglycemia \n\nMacrosom ia \n\nShoulder \n\ndystocia \n\n## l\n\n Brachi a! plexopathy C lavicle fractur e\n\n Pe rin ata l asphy xi a\n\n1 Glycogen \n\nsynt hes is \n\n## lGlycogen deposition in \n\ninterventricu lar septum \n\n## l\n\nHypertrophic cardiomyopathy Obs The pathophysiology of hypocalcemia in infants of diabetic mothera relates to maternal \n\nhypomagnesemia , which is caused by osmotic diuresis in the setting of poorly controlled gestational diabetes. Low fetal magnesium concentrations, which reflect maternal levels, lead to PTH suppression and \n\nlow calcium levels in the neonate. \n\n Symptomatic hypocalcemia can present with jitteriness \n\n What maternal pathology is associated with increased risk for neonatal respiratory distress syndrome ?\n\nMaternal diabetes \n\nmaternal diabetes results in fetal hyperinsulinism, which antagonizes cortisol and blocks \n\nmaturation of sphingomyelin .other risk factors include Prematurity, male sex, perinatal asphyxia and C-section \n\n## Pregnancy \n\n328 https://t.me/usmleinnercircle \n\nNeonatal complications of diabetes during pregnancy \n\n# . Maternal hyperglycemia - fetal hyperglycemia - P-cell hyperplasia &\n\nPathogenesis hyperinsulinemia \n\n# . 1 Fetal fat & glycogen stores \n\n# . 1 Fetal metabolic demand \n\n# . Prematurity \n\n## . Congenital anomalies (eg , caudal regression syndrome) \n\nAssociated . Macrosomia & associated complications (eg, brachia! plexus injury, \n\nrisks clavicle fracture) \n\n# . Respiratory distress syndrome \n\n# . Hypertrophic cardiomyopathy \n\n# . Hypoglycemia \n\nLaboratory . Polycythemia, low iron \n\nfindings . Hypocalcemia & hypomagnesemia \n\n# . Hyperbilinubinemia \n\nHypertrophic cardiomyopathy in infants of diabetic mothers \n\n# . Maternal hyperglycemia - fetal hyperglycemia & hyperinsulinemia \n\nPathogenesis i Glycogen & fat deposition in interventricular septum - dynam ic LVOT obstruction .. Oft en asymptomatic \n\nClinical findings . May have respiratory distress and/or hypotension \n\n## . Systolic ejection murmur \n\nImaging . Chest x-ray: cardiomegaly \n\n## . Echocardiogram: j thickness of interventricular septum, L LV chamber s iz e\n\nTreatment . Intravenous fluids & beta blockers to increase LV blood volume \n\nPrognosis . Spontaneous regression by age 1\n\nLVOT = left ve ntricular outfl ow tract. Obs Preterm Labour \n\n A negative fetal fibronectin test prior to term is an indicator of low risk for preterm delivery. \n\nhigh negative predictive value ; fetal fibronectin levels are high until 20 weeks gestation and thus are not a reliable marker of preterm delivery in early pregnancy Pregnancy contraindicated UNLESS the condition is fixed first. Strongest : preterm delivery in a prior pregnancy Risk factor for Cervical insufficiency \n\n329 https://t.me/usmleinnercircle USMLE Inner Circle \n\nAbsolute contraindications to pregnancy \n\n# . Pulmonary arterial hypertension \n\n# . Peripartum cardiomyopathy with re sidual LV dysfunction . Heart failure with LVEF <30% \n\nConditions in which pregnancy is contraindicated . Severe coarctation . Severe mitral stenosis . Severe symptomatic aortic stenosis . Severe aortic dilation (eg, Marian syndrome) . Recommend against pregnancy at preconception counseling visit Management If pregnant, discuss abortio n; if abortion declined, regular cardiology follow-up .\n\nLV = left vent ricle; LVEF = left ventricular ejection fraction. \n\nRisk facto rs Screen ing \n\n&\n\nprevention Preterm labor Cervical cone biopsy Prior spontaneous preterm delivery Multiple gestation Short cervical length Cervical surgery (eg, cold knife conization) Cigarette use Cervical length measurement by TVUS Progesterone administration Cerclage placement \n\nPreterm birth prevention \n\nPri or preterm delivery? \n\nr-- No \n\n2nd-trimester TYUS for cervical length \n\nNorma l ce rvical length \n\nRoutine care \n\nIn cidental short cervix \n\n(S2 .5 cm at <24 weeks) \n\n Vagin al pr ogesterone \n\nYes----i \n\nPrior preterm de livery associa t ed with pain fu lcontr actions? \n\nr- No_J_Yes 7\n\nCervical ins ufficiency \n\n Prophylactic cerclage \n\nPrior preterm labor \n\n Progesterone \n\n(IM or vaginal) \n\n.. Preterm la bor= regula r contractions causing cervical change al <37 weeks gestation wi th intact membranes. \n\nIM = in tramuscu lar; TVUS = transvaginal ultrasound. \n\nOUWorld Obs What is the first step in evaluating risk of preterm delivery in a patient with a history of cervical surgery (e.g. cold knife conization)? \n\nTransvaginal ultrasound measurement of cervical length in the 2nd trimester \n\n What is the recommended management for a pregnant patient with no history of preterm labor and a short cervix (< 2 cm) on TVUS? \n\nVaginal progesterone \n\nprogesterone maintains uterine quiescence and protects against premature rupture of membranes \n\n In patients who have bulging or prolapsing amniotic membranes , a rescue cerclage is not \n\ntypically recommended due to the high risk of membrane rupture, complications (eg, intraamniotic infection, cervical trauma), and likely imminent delivery. \n\n Tocolytics: Indomethacin (preferred if given with magnesium), nifedipine, Terbutaline. visible cervical dilation and no uterine contractions Magnesium sulfate given <32 weeks for neuroprotection if birth is indicated. ( Decreases risk for Cerebral Palsy )\n\n330 https://t.me/usmleinnercircle \n\nRisk factors Clinical features Management Cervical insufficiency Normal cervix Cerclage Incompetent cervix \n\n# .......\n\nCollagen defects Uterine abnormalities Cervical conization Obstetric injury \n\n~2 prior painless, 2nd-trimester losses Painless cervical dilation Cerclage placement \n\n<32 weeks (very preterm) Antenatal corticosteroids Penici ll in if GBS+ or unknown Tocolysis: indomethacin Magnesium sulfate Long ,closed cervix \n\nPreterm labor management \n\nPreterm labo r Mate rn al mstability, Short, Amniotic sac dilated cervix bulging at os intrauterine infection, - Yes_. Immediate delivery fetal distress/demise I\n\nNo \n\n32 -34 weeks \n\n(moderate preterm) Antenatal corticosteroids Pen icill in if GBS+ or unknown Tocolysis: nifedipine \n\n34-37 weeks \n\n(late preterm) \n\n Antenatal corticosteroids Penicill in if GBS+ or unknown \n\n> Pretenn labor = r99ular oonlraclions causing cervical change at <37 weeks gestation with in tac tmembranes .\n> GBS\n\n= group B Streptococcus . @UWorld \n\n> Cerclage\n> Sutures\n\nObs Indomethacin C/I after 32 weeks due to risk of premature Fetal Ductus Arteriosus Closure. It can also cause Decreased renal perfusion and fetal oliguria can result in oligohydramnios. Hence not given for more than 48 hours. \n\n 30 year old female that has gone into preterm labor (32 weeks). The patient was given a drug to attempt to slow down the labor WHILE she is given appropriate pharmacotherapy to promote fetal lung development. An hour to 2 hours later the heart rate of the woman increases significantly. Mechanism? \n\nNifedipine causing arterial dilation > reflex tachycardia \n\nLabour \n\nLabour has three stages: \n\nThe first stage is when the neck of the womb (cervix) opens to 10cm dilated. The second stage is when the baby moves down through the vagina and is born. The third stage is when the placenta (afterbirth) is delivered. \n\nStages of Normal Labor Stage 1 Latent : 0-6 cm ; <20 hr (nulli), <14 hr (multi) \n\nStage 1 Active : 6-10cm Stage II : 10cm delivery; 3 hr (n), 2 hr (m) Stage III : Fetus placental expulsion; < 30 min \n\nFalse labor: characterized by mild , irregular contractions (Braxton Hicks contractions) that cause no cervical change \n\n What is the recommended management for patients that present in false labor ?\n\nExpectant management \n\n331 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nFalse labor versus latent labor Contractions False labor Lat ent labor \n\nTiming Irregular, Regular, increasing frequency infrequent Strength Weak Increasing intensity Pain None to Yes mild Cervical No Yes change \n\nDisorders of the active phase of labor Diagnosis Clinical features Treatment \n\n Cervical change slower than expected \n\nProtraction Oxytocin Inadequate contractions \n\n# . No cervical change for ~4 hours with adequate contractions \n\nArrest OR Cesarean delivery No cervical change for ~6 hours with inadequate contractions Obs The active stage of labor typically begins at > 6 cm dilation ( 1 cm dilation every 2 hour) \n\nProtraction: 1 cm dilation in 2 hours \n\n Adequate contractions are defined as generation of > 200 Montevideo units (MVUs) \n\nin 10 minutes. \n\nmeasured via an intrauterine pressure catheter \n\n In order to Operative Vaginal delivery to occur, fetal head must be fully engaged i.e at 0station \n\n Neuraxial anesthesia (eg, epidural) can lengthen the second stage of labor NOT first. \n\n What is the most common cause of second stage arrest of labor ?\n\nFetal malposition (e.g. occiput transverse) \n\nthe optimal fetal position is Occiput anterior \n\n332 https://t.me/usmleinnercircle \n\n> Second stage arrest of labor\n> Insufficient fetal descent after pushing for:\n> Definition ~3 hours if nulliparous ~2 hours if multiparous Maternal obesity\n> Risk factors Excessive pregnancy weight gain Diabetes mellitus Cephalopelvic disproportion\n> Etiology Mal position Inadequate contractions Maternal exhaustion\n> Management Operative vaginal delivery Cesarean delivery\n\nLeft occiput transverse position \n\n> Occiput anterior position Occiput posterior position\n> (0 UWor1d\n\nObs Rupture of membranes when there is no palpable presenting fetal body part or there is fetal malpresentation carries a high risk for umbilical cord prolapse , which can lead to cord compression and fetal hypoxia. What is the recommended management for a patient at 28 weeks gestation with the fetus in transverse lie position ? The patient desires a vaginal delivery. \n\nExpectant management \n\nmost fetuses in transverse lie spontaneously convert to vertex presentation prior to term; persistent malpresentation may require external cephalic version or C-section \n\n Digital cervical examination is used to determine cervical dilation and fetal presentation (ie, the fetal part [eg, head, buttocks] directly overlying the pelvic inlet) \n\n333 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSagittal suture \n\nLeft occiput anterior \n\nTransverse lie \n\nOcciput anterior positions \n\nPubic symphysis I\n\nOcciput anterior \n\n UWorld \n\nUterine surgical history & vaginal birth Right occiput anterior Surgery Trial of labor contraindicated? \n\nLow transverse cesarean de li very {horizontal incision) No Classical cesarean delivery (vertical incision ) Yes Abdominal myomectomy with uterine cavity entry Yes Abdominal myomectomy without uterine cavity entry No Palpable bulging bag Obs If fetal presentation (eg, cephalic, breech) is uncertain on digital cervical examination, a \n\ntransabdominal ultrasound should be performed to confirm fetal presentation and determine the safest route of delivery. \n\n Amniotomy / Iatrogenic Rupture of Membranes are NO longer done. \n\n The most commonly injured nerves in the lithotomy position (with feet in stirrups) are the \n\nfemoral nerve and the peroneal nerve . The femoral nerve can be compressed under the inguinal ligament when the hip is flexed greater than 90 degrees, which can lead to numbness of the anterior and medial aspects of the thigh, as well as weakness of the quadriceps muscle. \n\nPeroneal nerve injuries typically are caused by compression at the fibular head against the stirrup, leading to foot drop and numbness over the dorsal foot and lateral lower extremity \n\nBreech \n\n Frank, Complete: Can try Vaginal \n\n Incomplete, Footling: Vaginal Contraindicated \n\n What is the recommended management for a pregnant woman at 35 weeks gestation that presents in preterm labor with the fetus in breech presentation on ultrasound? \n\n334 https://t.me/usmleinnercircle \n\n> Breech presentation\n\n## . Frank: hips flexed & knees \n\n> Breech extended (buttock presenting)\n\n## . Complete: hips & knees flexed \n\n> types Incomplete: 1 or both hips not\n\n## . flexed (feet presenting) \n\n## . Advanced maternal age (~35) \n\n## . Multiparity \n\n## . Uterine didelphys, septate uterus \n\n> Risk\n\n## . Uterine leiomyomas \n\n> factors\n\n## . Fetal anomalies (eg , anencephaly) \n\n## . Preterm (<37 weeks gestation) \n\n## . Oligohydramnios/polyhydramnios \n\n## . Placenta previa \n\n> Management\n\n## . External cephalic version \n\n## . Cesarean delivery \n\n> Breech Presentation Types\n> Frank Incomplete Complete Single Footling Double Footling\n\nObs Cesarean delivery \n\nbetamethasone +/- penicillin may be administered as well \n\n If vertex presentation on ultrasound? \n\nExpectant management \n\n Active labor is a contraindication for external cephalic version \n\n What is the management of Breech presentation/Transverse Lie :\n\n< 37 weeks = no intervention as most fetuses spontaneously convert to cephalic \n\nExternal cephalic version = >37 weeks, no active labor, no fetal distress C-section if fails \n\nExternal Cephalic Version \n\n What is the next step in management for a healthy pregnant woman at 37 weeks gestation that desires a vaginal delivery ? Ultrasound reveals the fetus is in a frank breech presentation .\n\nExternal cephalic version \n\ncan be attempted in women with breech pregnancies at > 37 weeks of gestational age if there's no contraindications to vaginal delivery and the fetus is in good health \n\nInternal Podalic Version Active Labour \n\n335 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nProcedure Indications Absolute contraindications Complications External cephalic version Contraindications to external cephalic version \n\n# . Manual rotation of fetus to cephalic presentation \n\n# . Decreases cesarean delivery rate Indications for cesarean delivery regardless of fetal lie (eg , failure to progress during labor, non-reassuring fetal status) \n\n# . Breech/transverse presentation \n\n# . ~37 weeks gestation Placental abnormalities (eg , placenta previa or abruption) Oligohydramnios \n\n# . Contraindication to vaginal delivery Ruptured membranes \n\n0 Prior classical cesarean delivery Hyperextended fetal head \n\n0 Prior extensive uterine myomectomy \n\n0 Placenta previa Fetal or uterine anomaly Multiple gestation \n\n Abruptio placentae \n\n# . Intrauterine fetal demise \n\nExternal cephalic version \n\nForward ro ll \n\ny yObs Shoulder Dystocia \n\n336 https://t.me/usmleinnercircle \n\nDefinition \n\nRisk \n\nfactors \n\nWarning \n\nsigns Breech extraction of the second twin \n\nPlace hand in uterus, grab fetal foot Deliver baby, feet first \n\nShoulder dystocia \n\nFa ilure of usual obstetric maneuvers to deliver fetal shoulders Fetal macrosomia Maternal obesity Excessive pregnancy weight gain Gestational diabetes Postterm pregnancy >42 Weeks Protracted labor \n\nRetraction of fetal head into the per in eum after delivery (turtle sign) Complications of shoulder dystocia \n\n# . Clavicular crepitus/bony irregularity \n\nFractured clavicle . ! Moro reflex due to pain on affected side \n\n# . Intact biceps & grasp reflexes \n\n# . Upper arm crepitu s/ bony irregularity \n\nFractured humerus . ! Moro reflex due to pain on affected side \n\n# . Intact biceps & grasp reflexes \n\n# . ! Moro & biceps reflexes on affected side Waiter's tip \n\n> 0\n\nExtended elbow \n\nErb-Duchenne palsy 0 Pronated forearm \n\n> 0\n\nFlexed wrist & fingers \n\n# . Intact grasp reflex \n\n## . Clawhand \n\n> 0\n\nExtended wrist \n\n> 0\n\nHyperextended metacarpophalangeal joints \n\nKlumpke palsy 0 Flexed interphalangeal joints o Absent grasp reflex \n\n# . Homer syndrome (ptosis, miosis) \n\n# . Intact Moro & bice2s refle xes Shoulder dystocia \n\n1. McRoberts maneuver Legs flexed onto abdomen causes rotation of pelvis, alignment of sacrum & opening of birth canal \n\n2. Suprapub lc pressure Applied to fetal anterior shoulder Variable presentation depending on duration of hypo xi a\n\nPerinatal asphyxia Altered mental status (eg, irritability, lethargy), respiratory or feeding difficulties, p oor tone, seizure Obs In Erb & Klumpke Palsy, Management involves observation alone because most infants recover arm function spontaneously within a few months. \n\nPost Term \n\n337 https://t.me/usmleinnercircle USMLE Inner Circle \n\nB\n\nE\n\nCA\n\nL\n\nMManagement of shoulder dystocia (BE CALM) \n\nBreathe; do not push Elevate legs & flex hips, thighs against abdomen (McRoberts) \n\nCall for help Apply suprapubic pressure \n\nEnlarge vaginal opening with episiotomy Maneuvers: Deliver posterior arm Rotate posterior shoulder (Woods screw) - apply pressure to anterior aspect of the posterior shoulder Adduct posterior fetal shoulder (Rubin) - apply pressure to the posterior aspect of the posterior shoulder Mother on hands & knees - \"all fours\" (Gaskin) \n\n Replace fetal head into pelvis for cesarean delivery (Zavanelli) Definition Risk factors Complications Management Nuchal cord reduction \n\nLoop of umbilical cord wrapped around neck \n\n# I\n\nReducing the nuchal cord Late- & post-term pregnancy \n\n# . Late-term : FHR; fetal heart rate ;ROM ;rupture of membranes.\n\nObs Uterine Rupture \n\n What is most important risk factor for uterine rupture ?\n\nPrevious C-section or myomectomy (scar becomes weakest point of uterus )Presentation? \n\nPainful 3rd trimester bleeding, sudden abdominal pain during labour Loss of fetal station (presenting fetal part retracts )Palpable fetal parts on abdominal exam \n\nFetal heart decels (bradycardia) \n\nLaboring patients at high risk of uterine rupture require urgent laparotomy and delivery \n\nPlacental Abruption \n\n Regular, High frequency contractions (vs irregular and decreasing in Uterine Rupture )\n\n Occurs after 20 weeks gestation. Progressively decreasing contraction amplitude: Staircase Sign Painful Bleeding which may be concealed \n\n339 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nFetal heart rate \n\nBaseline: 130 bpm Variability ; moderate Accelerations : none UA O mmH~ \n\nUterine rupture Abruptio placentae \n\n12 10 \n\nDefinition Placental detachment from the uterus before fetal delivery Hypertension, preeclampsia Abdominal trauma \n\nRisk factors Prior abruptio placentae Cocaine & tobacco use Sudden-onset vaginal bleeding \n\nClinical presentation Abdominal or back pain High-frequency, low-intensity contractions Rigid , tender uterus Clinical \n\nDiagnosis Ultrasound: Retroplacental hematoma \n\nComplications Fetal hypoxia, preterm birth , mortality Maternal hemorrhage, disseminated intravascular coagulation \n\nFHR 240 \n\n210 \n\n# nln Obs Uterine tachysystole (eg, >5 contractions in a 10 minute period ). What is the initial management for a hemodynamically unstable pregnant patient that presents with abruptio placentae following a motor vehicle accident? \n\nIV fluid resuscitation and left lateral decubitus positioning \n\nleft lateral decubitus position displaces the uterus off the aortocaval vessels and maximizes cardiac output \n\nPROM \n\n Rupture of membranes before onset of uterine contractions AND before <37 weeks \n\n Tocolysis is NOT indicated in PROM. It is only used to preterm labour if membranes have not yet ruptured. \n\n340 https://t.me/usmleinnercircle \n\nPreterm prelabor rupture of membranes (PPROM) Definition . Membrane rupture at < 37 weeks prior to labor onset \n\n# . PriorPPROM \n\nRisk factors . Genitourinary infection (eg, ASB, BV) . Antepartum bleeding \n\n# . Vaginal pooling or fluid from cervix \n\nDiagnosis . Nitrazine-positive (blue) fluid . Ferning on microscopy \n\n# . <34 weeks (reassuring): latency antibiotics, corticosteroids \n\nManagement . <34 weeks (nonreassuring): delivery . :<34 weeks: delivery \n\n# . Preterm labor \n\n# . lntraamniotic infection \n\nComplications Placental abruption .. Umbilical cord prolapse \n\nASB = as ymptomati c bacteriur ia; BV = ba cterial vag inos is; PPROM = preterm prelabor ruptur e of membranes. Management of preterm prelabor ROM \n\nRuptu re of membranes <34 weeks IUncomplicated l Expectant management Latency antibiotics (eg , ampicillin & azithromycin) Corticosteroids Fetal surveillance Infection, fetal/maternal \n\ncomprom ise \n\n## l\n\n Delivery IAI treatment (eg, ampicillin & gentamicin) Corticosteroids Magnesium if <32 weeks \n\nGBS = group B stre ptococcal : IAI = intr aam nio ti c inf ection : RO M = rupuxe of membranes .\n\n34 to <3 7 weeks lDelivery GBS prophylaxis (eg, penicillin G) \n\n ccrticcsteroids \n\n> CUWorld\n\nObs What are the risk factors for premature and premature/preterm rupture of membranes ?\n\nAscending infection (GBS) Smoking \n\nMultiple Pregnancies Previous PPROM \n\n Although membrane rupture typically presents as a sudden gush of fluid, patients can have a subclinical presentation with slow leakage occurring over days, with increased clear vaginal discharge . What is the likely diagnosis in an obese, multiparous pregnant woman at 34 weeks gestation that presents with intermittent leakage of clear fluid and a negative nitrazine/fern test? Stress urinary incontinence \n\nA small pool of urine in the posterior vagina may be seen on speculum examination because urine can become trapped in the vagina (ie, retrograde vaginal voiding ) during pregnancy \n\ndifferentiated from rupture of membranes by negative nitrazine/fern tests and absence of vaginal pooling \n\nChorioamnionitis \n\n341 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\n\n\nTe st Nitraz in e test Fluid from vaginal exam placed \n\non strip of nitrazine paper Paper turns blue in presence of alkaline (pH> 7.1) amniotic fluid \n\n Fe rn t est \n\n Fluid from vaginal exam placed on slide and allowed to dry Amniotic flu id narrow fern vs. cervical mucus broad fern Obs A low amniotic fluid glucose is an indicator of intra-amniotic infection \n\n Management? \n\nIV ampicillin + gentamicin (+ Clindamycin for C/S) Immediate delivery via augmentation of labour C/S generally not indicated unless of obstetrical complications (non-reassuring tracings, breech) What is the next step in management for a pregnant woman at 38 weeks gestation with chorioamnionitis after administration of antibiotics ? Fetal heart tracing reveals tachycardia but is otherwise reassuring. \n\nInduction of labor \n\ncesarean delivery is reserved for standard obstetric indications (e.g. prior uterine surgeries, breech presentation, non-reassuring fetal heart tracing) \n\n What is the likely diagnosis in an intrapartum patient that presents after >18 hours of membrane rupture and prolonged labor with fever and tachycardia ? Fetal heart tracing demonstrates fetal tachycardia. \n\nChorioamnionitis (intra-amniotic infection) \n\nintra-amniotic infection caused by migration of vaginal or enteric flora through the cervix, typically in a patient with premature or prolonged rupture of membranes; intrapartum fever is a distinguishing feature \n\nMiscarriage/ Abortion \n\nSpontaneous abortion = loss < 20 weeks Stillbirth (intrauterine fetal demise ) = loss after 20 weeks Deliver regardless of age \n\n342 https://t.me/usmleinnercircle \n\n> lntraamniotic infection (chorioamnionitis)\n\n# . Prolong ed rueture of membranes (>18 hours) Preterm prelabor rupture of membranes \n\n# . Prolong ed labor \n\n> Risk factors\n\n Internal fetal/uterine monitoring devices Reeetitive vaginal examinations \n\n# . Presence of genital tract eathogens Maternal fever PLUS ;,1 of the following: Fetal tachycardia (>160/min) \n\n> Diagnosis Maternal leukocytosis\n\n Purulent amniotic fluid \n\n# . Broad-spectrum antibiotics \n\n> Management\n\n Delivery \n\n# . Maternal: postpartum hemorrhage, endometritis \n\n> Complications Neonatal: preterm birth, pneumonia, encephalopathy\n\nObs Missed Abortion \n\nPatients are typically asymptomatic or have loss of pregnancy symptoms (e.g. nausea , breast tenderness ) with decreasing beta-hCG levels \n\nUSG findings : No Cardiac activity , empty gestational sac without a fetal pole Complete Abortion \n\nother findings include Unilateral Ovarian Cyst (Corpus luteum ) and some fluid in the pelvis. \n\nB-HCG can take 6 weeks to go undetectable \n\n343 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDefinition Risk factors Treatment options Additional management Complications \n\nMissed No vaginal bleeding Closed cervical OS No fetal cardiac activity or empty sac \n\nIncomplete \n\nVaginal bleeding Dilated cervical os \n\nTypes of Miscarriages \n\nThreatened Vaginal bleeding Closed cervical os Fetal cardiac activity Inevitable Vaginal bleeding Dilated cervical os Products of conception may be seen or fell at or above cervical os Some products of conception expelled & some remain \n\nComplete \n\nVaginal bleeding Closed cervical OS Products of conception completely expelled \n\nOOWorld \n\nSpontaneous abortion Septic abortion \n\nPregnancy loss <20 weeks Retained POC from: Risk factors . Elective abortion with nonsterile technigue Advanced maternal age . Missed or incomplete abortion (rare) Previous spontaneous abortion . Fever, chills, abdominal pain Substance use disorder Expectant Clinical presentation . Sanguinopurulent vaginal discharge \n\n## . Boggy, tender uterus; dilated cervix Medical induction (misoprostol) . Pelvic ultrasound: retained POC, thick endometrial stripe Suction curettage if infection or hemodynamic instability . Intravenous fluids Management . Broad-spectrum antibiotics Rho(D) immunoglobulin . Suction curettage Pathology examination POC = products of conception. Hemorrhage Retained products of conception Septic abortion Uterine perforation Intrauterine adhesions Obs Spontaneous abortion is most often due to chromosomal trisomies , especially trisomy 16 \n\n What is the recommended treatment for patients with septic abortion ?\n\nBroad-spectrum antibiotics and suction curettage \n\nmedical emergency; urgent treatment required to reduce risk of sepsis \n\nRecurrent Pregnancy Loss \n\nEctopic Pregnancy \n\n What is the likely diagnosis in a hemodynamically unstable patient with a gestational sac in the uterine cornu and free fluid in the posterior cul-de-sac on transvaginal ultrasound? \n\nRuptured ectopic pregnancy \n\ni.e. a cornual or interstitial ectopic pregnancy; often presents as abdominal pain and vaginal bleeding \n\n344 https://t.me/usmleinnercircle \n\nCauses of recurrent pregnancy loss \n\n Uterine: fibroids, adhesions, polyps \n\nStructural \n\n Cervical insufficiency \n\n Aneuploidy \n\nChromosomal Translocations/rearrangements Mosaicism \n\nImmunologic/ Hypercoagulable disorders (eg, antiphospholipid syndrome) \n\nHematologic Alloimmune intolerance Thyroid disease Polycystic ovary syndrome \n\nEndocrine \n\n Diabetes mellitus Hyperprolactinemia \n\n Advancing maternal age Defective endometrial receptivity \n\nOther \n\n Decreased ovarian reserve Celiac disease I \n\n> Ectopic pregnancy\n\nEctopic pregnancy locations \n\n> Tubal (most common) Previous ectopic pregnancy\n> Risk factors Previous pelvic/tubal surgery Pelvic inflammatory disease Abdominal pain, amenorrhea, vaginal bleeding\n> Clinical features Hypovolemic shock in ruptured ectopic pregnancy Cervical motion, adnexal &/or abdominal tenderness\n\n Palpable adnexal mass Positive hCG \n\n> Diagnosis Transvaginal ultrasound revealing adnexal mass, empty uterus\n> Management Stable: Methotrexate Unstable: Surgery\n\nObs Early but viable intrauterine pregnancies : 35%-50% rise in -hCG every 48 hours. \n\nCompleted spontaneous abortions : -hCG levels decrease \n\nEctopic and nonviable intrauterine pregnancie s : <35% rise \n\n To distinguish between an ectopic pregnancy and nonviable intrauterine pregnancy, patients may undergo diagnostic dilation and curettage , a procedure that samples tissue within the endometrial cavity. The procedure confirms the abnormal pregnancy's location based on the postprocedure -hCG level :\n\nA negative or decreased -hCG leve l confirms that the patient had a nonviable intrauterine pregnancy; these patients require reassurance and observation only because the products of conception have been removed by the dilation and curettage. \n\nA persistent rise in -hCG level after dilation and curettage is diagnostic for an ectopic pregnancy (ie, the uterus has been evacuated but an extrauterine pregnancy continues to produce -hCG). These patients require additional management. (Methotrexate) \n\n A progesterone level < 5 ng/mL suggests an abnormal or extrauterine pregnancy >25 ng/mL suggests a healthy intrauterine pregnancy \n\nHydatidiform Mole Mx: Methotrexate \n\n345 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nManagement of suspected ectopic pregnancy \n\nHemodynamically stable \n\nPositive urine hCG, lower abdominal pain, \n\n&for vaginal bleeding Hemodynamically unstable Immediate surgical consultation Adnexal mass ) Intrauterine pregnancy ) Nondiagnostic }\n\nTreat ectopic pregnancy TVUS = tran svaginal ultrasound Serum B-hCG level ]\n\nRepeat B-hCG level +\n\nTVUSin ~ s\n\nI\n\nRepeat 11--hCG level in 2 days \n\nC)tMtotld Obs Choriocarcinoma \n\n What is the likely diagnosis in a 6-month postpartum woman that presents with irregular vaginal bleeding , an enlarged uterus , and dyspnea with multiple infiltrates on CXR? \n\nChoriocarcinoma \n\nclassically occurs after a complete hydatidiform mole, but can occur after normal pregnancy or \n\nspontaneous abortion \n\nVomiting \n\n Nausea and vomiting during pregnancy affects many women in the first trimester and is relatively mild with no associated weight loss, hypovolemia, or electrolyte abnormalities. What is the pharmacological treatment (1st and 2nd line ) of nausea and vomiting in pregnancy (\" morning sickness \")? \n\nAvoid triggers, consume fluids 30 minutes before or after solid meals \n\n1st line : ginger, pyridoxine (B6) 2nd line : add doxylamine \n\n Some cases of nausea and vomiting during pregnancy can mask an underlying eating disorder , with potential concerning findings , including: Choriocarcinoma \n\n346 https://t.me/usmleinnercircle \n\n\n\nHydatidiform mole \n\n Abnormal vaginal bleeding hydropic tissue Uterine enlargement > gestational age Abnormally elevated 13-hCG levels \n\nClinical presentation Theca lutein ovarian cysts Hyperemesis gravidarum Preeclampsia with severe features Hyperthyroidism \n\nRisk factors Extremes of maternal age History of hydatidiform mole \"Snowstorm\" appearance on ultrasound \n\nDiagnosis Quantitative serum 13-hCG \n\n Histologic evaluation of uterine contents Dilation & suction curettage \n\nManagement Serial serum 13-hCG post evacuation Contraception for 6 months \n\nManagement of hydatidiform mole \n\nSuction curettage \n\n## lWeekly 13-hCG levels until undetectable \n\n> Decreasing\n\n## l\n\nMont hl y 13-hC G\n\nlevels x 6 months \n\n> 13-hCG\n\n## lundetectable Surveillance complete Can attempt preg nancy Increasing/ plateauing Diagnosis of gestational trophoblastic neoplasia \n\n> !3-hCG becomes detectable\n\nObs Weight loss with an already relatively low BMI \n\nUnpredictable appetite (suggesting dysregulated eating habits) with skipping meals (suggesting possible caloric restriction) followed by episodes of overeating (suggesting possible binge eating) \n\nDistorted view of body weight and shape , evidenced by the perception of \"looking pregnant\" despite early gestational age (when the uterus is still below the pubic symphysis) and switch to maternity clothing despite weight loss Evaluate for Disordered Eating behaviour \n\nHyperemesis Gravidarum \n\n Patients with HG can develop prolonged hypoglycemia due to inadequate oral intake ; this can lead to ketoacidosis and ketones on urinalysis .\n\nKetonuria suggests more severe disease and is an indication for hospital admission \n\n With appropriate treatment, there are rarely any adverse fetal effects. \n\n## Postpartum \n\n347 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nHyperemesis gravidarum \n\n## . Hydat idifor m mole \n\nRisk factors . Mu ltifetal gestation \n\n# . History of hyperemesis grav i darum \n\n# . Severe , persistent vom iti ng \n\nClinical features . >5% loss of prepregnancy weigh t\n\n# . Dehydration \n\n# . Orthostatic hypotension \n\n# . Ketonuria \n\nLaboratory abnormalities . Hypochl oremic metabolic alkalosis \n\n## . Hypokalemia \n\n# . Hemoconcentrati on \n\nTreatment . Admission to hospital \n\n# . Antiemetics & intravenous fluids \n\nPostpartum period \n\n# . Transient rigors/chills \n\n# . Per ipheral e dema \n\nNormal . Lochia rubra \n\nfindings Uter ine contraction & involution .. Breast engorgement \n\n# . Rooming-in/lac ta tion support \n\n# . Serial examination for uterine atony/bleeding \n\nRoutine . Peri neal care care . Voiding trial \n\n# . Pain management Obs Lochia Rubra : upto 1 Week ; Bright Red blood with small clots (<1 pads per hour) \n\n Patients often have concerns about postpartum bleeding because it is heavier and more prolonged than normal menses. These patients should be evaluated for features concerning for delayed postpartum hemorrhage, including the following: Passage of large blood clots Increased pad counts (eg, saturation of 1 pad/hr for 2 consecutive hours )Signs and symptoms of anemia (eg, dizziness, chest pain) due to acute blood loss \n\nPPH \n\nUterine atony unresponsive to medical management may respond to a B-lynch compression suture during exploratory laparotomy. What are the ( 4) etiologies of postpartum hemorrhage ?\n\n'Absent': Uterine inversion 'Soft and boggy': Uterine atony (most common) Oxytocin is a first-line agent; other agents, such as methylergonovine and carboprost may be administered if \n\noxytocin fails \n\n348 https://t.me/usmleinnercircle \n\n\n\nNormal postpartum lochia Expected duration Description Lochia . Dark or bright red (blood ); odor similar to that of menstrual blood ; occasional small \n\nrubra . Birth to 3-4 days postpartum clot s ; quantity decreasing each day \n\nLochia . 4th postpartum day to 10th or 14th . Serosanguineous (pink ); brownish (old blood) ; quantity gradually decreasing in \n\nserosa postpartum day amount \n\nLochia . 11th postpartum day to 6 weeks \n\nalba postpartum . Wh i te/yello w ; c reamy ; lig ht quantity lochia may increase in quantity after breastfeeding (suckli ng releases oxytocin & causes uterus to contract) & 7-14 days postpartum , when scabbing on the placental site sloughs off (heavier bleeding for <2 hr); lochia may also feel increased after lying down & then standing (due to blood pooling in vagina) .\n\nPostpartum hemorrhage Management of postpartum hemorrhage due to uterine atony Definition >500 ml after vaginal delivery >1 , 000 ml after cesarean delivery Prolonged or induced labor Chorioamnionitis \n\nRisk factors Multiple gestation Polyhydramnios Grand multiparity Operative delivery Uterine atony (most common) Retained placenta \n\nCauses Genital tract laceration Uterine rupture Coagulopathy Bimanual uterine massage, oxytocin Intravenous fluids , oxygen \n\nTreatment Uterotonics (methylergonovine, carboprost, misoprostol) Intrauterine balloon tamponade Uterine artery embolization Hysterectomy Postpartum hemorrhage & soft, boggy u te rus Step 1: Uterine massage & high-dose oxytocin Step 2: Tranexam ic acid Step 3: S eco nd-line uterotonic agents: Methylergonovine (Cl : hypertension) Carboprost tromethamine (Cl : a st hma) Misoprostol Step 4: Intrauterine balloon tamponade Step 5: laparotomy Estimated blood loss ~, ,000 mL Of bleeding + hypovolemia. \n\n> Cl\n\n= contraindication. CUWork! Obs 'Firm': Placental retention or incomplete seperation Normal/Firm: Trauma/laceration/DIC \n\n Because the vagina is supplied by branches of the uterine artery (which receives 30% of maternal cardiac output at delivery), patients with a vaginal laceration/hematoma can have profuse bleeding. \n\n Vulval Hematoma caused by damage to Pudendal Artery. Secondary = >24 hours after Delivery \n\n349 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nDifferential diagnosis of postpartum hemorrhage Diagnosis Risk factors Examination Management \n\n## . Prolonged labor . Enlarged, boggy uterus . Bimanual uterine \n\n## . Chorioamnionitis massage \n\nUterine atony Uterine overdistension (multiples, fetal Uterotonic . .macrosomia, polyhydramnios) medications \n\n## . Succenturiate placenta . Enlarged, boggy uterus . Manual extraction \n\nRetained products of . Manual extraction of placenta . Placenta missing cotyledons \n\nconception . History of previous uterine surgery . Retained placental fragments on ultrasound \n\nGenital tract trauma . Operative vag inal delivery . Laceration of cervix or vagina . Laceration repair \n\n## . Enlarging hematoma \n\n## . History of abnormal bleeding in patient or family . Continued bleeding despite . Correction of \n\nInherited coagulopathy members contracted uterus coagulopathy \n\nVaginal hematoma \n\n Operative vaginal delivery \n\n# . Infant 2:4000 g (8.8 lb) \n\nRisk factors \n\n Nulliparity Prolonged 2nd stage of labor \n\nClinical Vaginal mass Rectal or vaginal pressure \n\nfeatures . hypovolemic shock Nonexpanding: observation \n\nTreatment \n\n Expanding: embolization , surgery \n\nSecondary (late) postpartum hemorrhage Cause Clinical features Management Retained POCs . Heavy bleeding Dilation & curettage .. Uterine atony \n\nPlacental site subinvolution . H eavy bleeding Uterotonics (eg, oxytocin, methylergonovine, carboprost) .. Uterine atony \n\n## . Feve r \n\nPostpartum endometritis . Uterine tenderness . Broad-spectrum IV antibiotics (eg, cl indamycin & gentamicin) \n\n## . Purulent lochia \n\nPOCs = products of conception; IV= intravenous. Obs Delayed placental delivery occurs when the placenta does not deliver within 30 minutes .A common risk factor is extreme preterm delivery (eg, <26 weeks gestation) because these deliveries typically require prolonged oxytocin administration and are often complicated by intraamniotic infection, stillbirth , and placental disorders (eg, preeclampsia, placenta accreta). In addition, the prolonged oxytocin administration can cause a paradoxical decrease in myometrial contractility, thereby inhibiting placental expulsion. Intrauterine inflammation (eg, from intrauterine fetal demise) can also increase placental adhesion to the uterine wall. Patients with a retained placenta usually have profuse postpartum bleeding , which may be immediate or delayed. Initial management includes gentle downward cord traction and oxytocin administration to promote placental separation and expulsion. If the placenta does not deliver with these measures, manual placental extraction or dilation and curettage are indicated. What is the next step in management for a mother with post-partum hemorrhage following a forceps-assisted vaginal delivery? The patient is afebrile and the uterus is normal-sized and firm. \n\nGenital tract inspection \n\ngenital tract injury is a common cause of PPH after operative vaginal deliveries \n\n Post -cesarean delivery patients with hemorrhagic shock and no signs of uterine atony most likely have intraabdominal bleeding from uterine artery injury. a rare but life-threatening cause of postpartum hemorrhage that typically presents with no incisional bleeding and minimal abdominal or back pain \n\nHemodynamically unstable patients with a suspected retroperitoneal hematoma require \n\nemergency laparotomy. \n\nUterine Inversion \n\n350 https://t.me/usmleinnercircle \n\n> Operative vaginal delivery (vacuum/forceps) Bimanual uterine massage\n> Protracted 2nd stage of labor\n> Indications Fetal heart rate abnormalities Maternal contraindications to pushing Laceration Cephalohematoma\n> Fetal complications Facial nerve palsy lntracranial hemorrhage Shoulder dystocia Genitourinary tract injury\n> Maternal complications Urinary retention Hemorrhage\n\nObs Neurogenic shock , due to the traction effect on the surrounding peritoneum, may also occur, resulting in a paradoxical bradycardia. \n\nPlacenta Accreta \n\n What is the likely diagnosis of a \" firm uterus\" in the setting of a post-partum hemorrhage ?\n\nPlacenta accreta \n\nMost important risk factor? Previous C-section \n\nPresents with delayed placental detachment and massive PPH at the time of attempted manual separation of the placenta \n\n Antenatally diagnosed placenta accreta is delivered by planned cesarean hysterectomy .\n\nSheehan Syndrome \n\n T/t: Replace the hormones individually. Cant do anything else \n\nPerineal Laceration \n\n351 https://t.me/usmleinnercircle USMLE Inner Circle \n\nUterine inversion Pathophysiology Excessive fundal pressure Excessive umbilical cord traction Lower abdominal pain \n\nPresentation Round mass protruding through cervix Uterine fundus not palpable transabdominally Hemorrhage shock Aggressive fluid replacement \n\nManagement Manual replacement of the uterus Placental removal & uterotonic drugs after uterine replacement \n\nPlacenta accreta Definition Morbidly adherent placental attachment to the myometrium \n\nRisk factors Placenta previa + prior uterine surgery (eg, cesarean delivery, D&C , m l omectom l )\n\nClinical features Prenatal diagnosis: US with placenta previa, numerous placental lacunae, myometrial thinning Postpartum diagnosis: adherent placenta, postpartum hemorrhage \n\nManagement Cesarean h l sterectom l with placenta in situ \n\nD&C = di lation & curettage; US = ul t rasound. \n\nSheehan syndrome Pathogenesis Obstetric hemorrhage complicated by hypotension Postpartum pituitary infarction Lactation failure(! prolactin) \n\nClinical Amenorrhea , hot flashes , vaginal atrophy( ! FSH , LH) \n\nfeatures Fatigue, bradycardia (! TSH) Anorexia , weight loss , hypotension (! ACTH) Decreased lean body mass( ! growth hormone) Obs Fistula \n\n Rectovaginal fistula may occur after obstetric trauma and presents with incontinence of flatus and feces through the vagina. \n\n\"Red, velvety (rectal) mucosa\" may be seen on posterior vaginal wall \n\n What is the likely diagnosis in a patient that presents with foul-smelling brown discharge from the posterior vaginal wall two weeks after a vaginal delivery complicated by third-degree laceration? \n\nRectovaginal fistula \n\n352 https://t.me/usmleinnercircle \n\nPerinea! lacerations \n\n> First-degree Second-degree Third-degree Fourth-degree\n> CI UWorkl\n\nRectovaginal fistula \n\n# . Pelvic radiation \n\n## . Obstetric trauma \n\n## . Pelvic surgery \n\nRisk factors . Colon cancer \n\n## . Diverticulitis \n\n## . Crohn disease \n\nClinical features . Uncontrollable passage of gas &/or feces from the vagina . Physic al examination \n\n## . Fistulography \n\nDiagnostic studies Magnetic resonance imaging .. Endosonography \n\nVesicovaginal fistula \n\n Pelvic surgery \n\nRisk factors Pelvic irradiation Prolonged labor/childbirth trauma Genitourinary malignancy \n\nClinical features Painless, continuous urine leakage from the vagina Physical examination \n\nDiagnostic studies Dye test Cystourethroscopy Obs Takes some days to form and no bladder distention (vs Bladder atony sec to epidural )\n\nPubic Symphysis Diastasis Septic Pelvic Thrombophlebitis Pelvic examination typically shows vaginal pooling of urine, a visible defect, or an area of raised, red granulation tissue on the anterior vaginal wall. typically resolves within the first 4 weeks postpartum \n\n353 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCatheter - \\\n\nC>U Wor1d \n\nTampon - Syringe (with dye) \n\nPubic symphysis diastasis \n\n## . Fetal macrosomia \n\nRisk factors . Multiparity \n\n## . Precipitous labor Operative vaginal delivery \n\n## . Difficulty ambulating \n\n## . Radiating suprapubic pain \n\nPresentation . Pubic symphysis tenderness . Intact neurologic examination Conservative \n\n## . Nonsteroidal anti-inflammatory drugs \n\nManagement . Physical therapy \n\n## . Pelvic support \n\nSeptic pelvic thrombophlebitis \n\n# . Cesarean delivery . Pelvic surgery . Endometritis \n\nRisk factors . Pelvic inflammatory disease . Pregnancy . Malignancy . Hypercoagulability . Pelvic venous dilation \n\nPathophysiology Vascular trauma . Infection . Fever unresponsive to antibiotics \n\nPresentation . No localizing signs/symptoms . Negative infectious evaluation . Diagnosis of exclusion \n\nTreatment . Anticoagulation . Broad-spectrum antibiotics Bladder dye test Vesicovaginal Blue dye fistula on tampon Obs Diagnosis of exclusion ; due to an infected thrombosis of the deep pelvic or ovarian veins \n\nPostpartum Endometritis \n\n Neither blood nor endometrial cultures are required for diagnosis, but further evaluation is indicated if there is no clinical improvement after 48 hours of antibiotic therapy Clindamycin covers: Gram +ve and Anaerobes Gentamycin (Aminoglycoside ) covers Gram -\n\n Postpartum endometritis is 5-10x more common in patients with Cesarean delivery \n\n Because of the risk for puerperal sepsis following cesarean delivery, women typically receive a \n\nprophylactic dose of antibiotics at the time of surgery. \n\n Chronic endometritis shows Plasma Cells on biopsy. \n\nUrinary Retention \n\n What is the most likely diagnosis in a post-partum patient unable to void since delivery and is experiencing urine dribbling? \n\nOverflow incontinence secondary to bladder atony \n\nSuspect if patient hasn't voided in 6 hours after delivery (2/2 epidural) Infection of Endometrium lining \n\n354 https://t.me/usmleinnercircle \n\n> Postpartum endometritis\n> Cesarean delivery lntraamniotic infection\n> Risk factors\n\n. Group B Streptococcus colonization \n\n. Prolonged rupture of membranes Operative vaginal delivery \n\n. Fever >24 hr postpartum \n\n> Clinical Uterine f undal tenderness\n> features Purulent lochia\n> Etiology\n\n. Polymicrobial infection \n\n> Treatment\n\n. Clindamycin & gentamicin Obs Postpartum urinary retention often occurs due to the following: \n\nPerineal trauma from a prolonged second stage of labor and/or perineal laceration that results in a \n\npudendal nerve injury . Damage to the pudendal nerve can result in a decreased voiding sensation, thereby promoting urinary retention, and cause external urethral sphincter dysfunction. \n\nReduced sensory and motor sacral spinal cord impulses from regional neuraxial anesthesia (eg, \n\nepidural anesthesia ), which can suppress the micturition reflex and decrease detrusor tone ,resulting in bladder atony .Self limited: <1 week \n\n## Miscellaneous \n\nBack Pain \n\n What is the recommended management for a woman in the third trimester of pregnancy that presents with lower back pain that radiates down the legs, especially with activity? Physical exam is benign. \n\nReassurance and Conservative management \n\nThe management includes: \n\nReassurance and behavioral modifications \n\nLifestyle interventions (wear-low heeled shoes, good back support, heat/cold/massage to the painful area) \n\nRest with hip flexion Confirmed by > 150 mL of urine upon urethral catheterization \n\n355 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPostpartum urinary retention \n\n Primiparity Regional anesthesia \n\nRisk factors Operative vaginal delivery Perinea! injury Cesarean delivery \n\nClinical . Inability to void or small-volume voids \n\nfeatures . Incomplete bladder emptying Dribbling of urine Self-limited condition \n\nManagement Intermittent catheterization .\n\nLow back pain during pregnancy \n\n## . Enlarged uteru s --+ exaggerated lordosis \n\nEtiology Joint/ligament laxity fr om j progesterone/relaxin \n\n Weak abdominal muscles --+ decreased lumbar support \n\n## . Excessive weight gain \n\nRisk factors . Chronic back pain \n\n## . Back pain in prior pregnancy \n\n## . Multi parity \n\nImaging . Not indicated \n\n## . Behavioral modifications \n\nManagement . Heating pads Analgesics \n\n\n\n00Obs Exercise Medication: Short course analgesic acetaminophen has best safety profile in pregnancy \n\nRound Ligament Pain \n\n Round ligament pain develops when the ligament is stretched by the gravid uterus , usually in the late \n\nsecond trimester and the third trimester .It typically presents as a sharp unilateral pain that radiates to the vagina , is triggered by movement \n\n(ie, positional), and resolves without treatment .\n\nLiver Disorders of Pregnancy \n\n Normal BP (vs HELLP) \n\n AFLP is unique because it is an intrahepatic process due to microvesicular fatty infiltration \n\nof hepatocytes secondary to abnormal maternal-fetal fatty acid metabolism. Pregnancy, pruritis, elevated total bile acids, +/- elevated aminotransferases \n\nIntrahepatic cholestasis of pregnancy \n\nTreatment: ursodeoxycholic acid, typically resolves within weeks following delivery Immediate delivery irrespective of gestational age Cholecystectomy usually delayed until postpartum \n\n356 https://t.me/usmleinnercircle \n\n00Liver disorders unique to pregnancy Acute fatty liver of pregnancy Disorder Presentat ion Laboratory abnormalities . Nausea , vomiting \n\nClinical features Right upper quadranUepigastric pain Elevated bile acids . Fulminant liver failure \n\nICP Elevated levels of liver Intense pruritus aminotransferases . Profound hypoglycemia Diagnosis of exclusion j Aminotransferases (2 -3x normal) Preeclampsia Hemolysis Moderately elevated liver \n\nHELLP Right upper-quadrant pain aminotransferases Nausea/vomiting Thrombocytopenia \n\nLaboratory findings 1 Bilirubin \n\n Thrombocytopenia \n\n# . Disseminated in travascular coagulopathy Hypoglycemia Management . Immediate delivery Malaise Mildly elevated liver Righi upper-quadrant pain aminotransferases \n\nAFLP Nausea/vomiting Elevated bilirubin Sequelae of liver failure Possible disseminated intravascular coagulopathy \n\nlntrahepatic cholestasis of pregnancy Symptomatic cholelithiasis in pregnancy \n\n## . Development in 3rd trimester \n\nClinical . Generalized pruritus Pathophysiology j Biliary cholesterol excre ti on (estrogen) \n\n i Gallbladder motility (progesterone) \n\n## . Pruritus worse on hands & feet \n\nfeatures . No associated rash Clinical features Recurrent, postprandial epigastric/RUQ pain \n\n## . Right upper quadrant pain RUQ ultrasound with echogenic foci (stones or sludge) \n\nLaboratory . 1 Total bile acids (:?1 0 mol/L) \n\nabnormalities . i Liver transaminases (typically <2x normal , rarely >1000 U/L) Management Conservative (eg , pain control) \n\n Cholecystectomy (for complicated, recurrent cases) \n\n## . i Total & direct bilirubin RUQ = ri ght upper quadr ant. \n\n## . Intrauterine fetal demise \n\nObstetric . Preterm delivery \n\nrisks . Meconium-stai ned amniotic fluid \n\n## . Neonatal respiratory distress syndrome \n\n## . Ursodeoxycholic acid \n\nManagement Antihistamines \n\n## . Delivery at 37 weeks gestation Obs The risk of intrauterine fetal demise (IUFD) is particularly high when serum bile acids are 100 mol/L \n\nPseudocyesis \n\nWhat is pseudocyesis ?\"False pregnancy\" Women present with classic signs of pregnancy (e.g. morning sickness, amenorrhea, abdominal distention) despite it being ruled out with U/S and negative pregnancy test \n\n Pseudocyesis can occur when psychological pressures (eg, difficulty conceiving), social pressures, and the somatization of stress affect the hypothalamic-pituitary-ovarian axis, or when bodily changes (eg, weight gain, amenorrhea) are misinterpreted by the patient. The end result is a deeply held, nondelusional belief of being pregnant that may be strong enough to cause a patient to misread a negative home pregnancy test result as positive Because pseudocyesis is a form of somatization , management requires psychiatric evaluation \n\nand treatment. \n\n## Drugs \n\n Inhaled B agonist and inhaled corticosteroids are safe to use in pregnancy. Hypocalcemia due to temporary suppression of PTH \n\n Magnesium is solely excreted by the kidneys \n\nthus patients with renal insufficiency are at increased risk for toxicity Mg becomes toxic at concentrations > 8 mg/dL \n\n357 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nMagnesium toxicity \n\n. Mild: nausea, flushing , headache, hyporeflexia \n\nClinical features Moderate: areflexia, hypocalcemia, somnolence \n\n. Severe: respiratory paralysis, cardiac arr est \n\n. Stop magnesium therapy \n\nTreatment . Give IV calcium gluconate bolus Obs Uterotonic \n\nWhat are the ( 4) uterotonic agents? \n\nOxytocin Carboprost tromethamine (Hemabate ): PGF2 analog \n\nCI in asthma Methylergonovine (Methergine ): Ergot alkaloid \n\nCI in htn Misoprostol : Prostaglandin also used in abortions, cervical ripening, labor induction \n\n Oxytocin is not effective in stimulating uterine contractions or expelling retained products of conception during the first or second trimesters because few oxytocin receptors are in the uterus during early pregnancy. What are the ( 3) complications of oxytocin toxicity ?\n\nReleased from posterior pituitary with ADH a nd both have similar structure \n\nHyponatremia (seizures )Treat with hypertonic saline Hypotension Uterine Tachysystole ( >5 contractions in 10 minutes )\n\n358 https://t.me/usmleinnercircle \n\n> Illicit drug abuse in pregnancy\n> Adolescent pregnancy\n> Risk factors Late/noncompliant prenatal care Inadequate pregnancy weight gain Spontaneous abortion Preterm birth\n> Obstetric complications Preeclampsia Abruptio placentae Fetal growth restriction Intrauterine fetal demise\n\n\n\n> 0\n\n\n\n> 0\n\n\n\n> 0\n\nOxytocin Indications Induction or augmentation of labor Prevention & management of postpartum hemorrhage \n\n> Adverse Hyponatremia Hypotension\n> effects Tachysystole\n\n\n\n> 0\n\nGIT \n\n# GIT Salivary Gland Sialadenosis Suppurative Parotitis Esophagus Achalasia GERD Perforation Eosinophilic esophagitis Stomach Dyspepsia Vomiting & Diarrhea Factitious Diarrhea Chemotherapy-related diarrhea Bile Salt Diarrhea Constipation Gastroparesis Gastric Outlet Obstruction Liver Jaundice Acute Liver Failure Cirrhosis NAFLD Hepatic Encephalopathy HepatoPulmonary Syndrome HepatoRenal Syndrome Budd Chiari Liver Abscess Gall Bladder & Bile Duct Acalculous Cholecystitis Emphysematous Cholecystitis Acute Cholangitis Primary Sclerosing Cholangitis Primary Biliary Cholangitis Post-cholecystectomy syndrome Pancreas Severe Acute Pancreatitis Pancreatic Pseudocyst Pancreatic Cyst Chronic Pancreatitis Spleen Small Intestine D-Xylose Test IBS IBD Celiac Disease \n\n359 https://t.me/usmleinnercircle USMLE Inner Circle GIT SIBO Appendicitis Infectious ileocecitis (Pseudo-appendicitis) Obstruction Large Intestine & Rectum Hemorrhoids Diverticulitis & Diverticulosis Angiodysplasia Colovesical Fistula Toxic Megacolon Colonic Pseudo-obstruction (Ogilvie Syndrome) Volvulus Ischemic Colitis Microscopic Colitis Proctalgia Fugax Proctitis Rectal Prolapse Anal Fissure Anorectal Fistula Peritoneum & Mesentery Retroperitoneal Hematoma Mesenteric Ischemia Peritonitis Hernia Umbilical Hernia Incisional Hernia Rectus Abdominis Diastasis GIT Tumors Esophagus Stomach Pancreas Colon PJ Syndrome Liver MALToma Miscellaneous Abdominal Compartment Syndrome Paeds GIT Tracheoesophageal Fistula Foreign Body Ingestion Crying Infant Constipation Vomiting Cyclical Vomiting Syndrome Food Allergen Proctocolitis Breastfeeding Dehydration Midgut volvulus Pyloric Stenosis Neonatal Jaundice Bilirubin induced Neurologic Dysfunction Biliary Atresia 360 https://t.me/usmleinnercircle GIT Salivary Gland \n\n What is the pharmacologic treatment of sialadenitis ?\n\nClindamycin or nafcillin + metronidazole \n\nPoor response to 48 hours of antibiotics or abscess -- proceed to surgical drainage and \n\ndecompression \n\n What bacteria is the most common cause of acute bacterial parotitis ?\n\nStaphylococcus aureus \n\n What preventive measures are useful for preventing post-operative acute bacterial parotitis ?\n\nAdequate fluid hydration and Oral Hygiene \n\nSialadenosis \n\n Sialadenosis is a benign, non-inflammatory, painless enlargement of the salivary glands often seen in patients with dietary/nutritional disorders ( diabetes, bulimia ), chronic alcohol use or \n\nadvanced liver disease. \n\nSuppurative Parotitis Biliary cyst Intestinal Atresia Hirschsprung Intussusception Meckel's Diverticulum NEC Reye Syndrome Duodenal Hematoma GIT Surgery Bariatric Surgery Gastric Bypass Billroth 2 Nissens Fundoplication Pancreaticoduodenectomy Abdominal Trauma Pancreatic Injury Splenic Rupture Duodenum Perforation Rectus Sheath Hematoma Wound Dehiscence Pilonidal Sinus GI Bleed Variceal Bleeding Hemobilia \n\n361 https://t.me/usmleinnercircle USMLE Inner Circle GIT Esophagus \n\n Globus sensation is a diagnosis of exclusion and is characterized by the sensation of a lump \n\nin the back of the throat. It is a functional disorder and does not cause any abnormalities on barium esophagram. What is the likely diagnosis in a patient with GERD who complains of difficulty swallowing solid foods and has symmetric , circumferential narrowing on barium swallow? \n\nEsophageal stricture \n\nother causes of peptic strictures include radiation, systemic sclerosis, and caustic ingestion; biopsy is necessary to rule out malignancy (typically asymmetric narrowing) Strictures typically cause slowly progressive dysphagia to solid foods without anorexia or weight loss. As they progress, they can actually block reflux, leading to improvement of heartburn symptoms \n\n362 https://t.me/usmleinnercircle \n\nRisk factors Clinical presentation Management \n\n~\n\n~: A\\.s~+\"'~ ,1,..os \n\nL~JII...._\\.,. \n\nfL s.w -~ t..i ,.\\....t. .. t\n\n~.ju-c\\'4~ \n\nt>~, e,..;,.. __.., B,n!.s 3.,.1,. \n\n- '\"\"\"~-l.S dots\"\" ~\\co< \n\nSuppurative parotitis \n\n# . Elderly. dehydrated , postsurgical . Decreased oral intake (eg, NPO perioperatively) . Medications (eg , anticholinergics) \n\n## . Obstruction (eg, calcul i, neoplasm) . Firm, erythematous pre/postauricular swelling . Exquisite tenderness exacerbated by chewing and palpation . Trismus, systemic findings (eg, fever, chills) . Elevated serum amylase without pancreatitis . Ultrasound or CT scan (eg, ductal obstruction, ~ )\n\n# . Hydration, oral hygiene \n\n## . Antibiotics Massage (ie, milking pus out of gland) \n\n~\n\n~\n\n# . Sialagogues \n\n~---\" \"\"\"kpr-,,nssi~\"','l'\"t\" \n\nl'!!!!,_ , co11..,. cl.yalih,. 4;,..~ .-...,.1,aoo ... ~. \n\n.. 1 l.~ ...... ~ .. ch,,, \n\n> 0'1. , ~g:..,.J,,l-\n> E.~wllb\n\n\"\"\"\"\"\"\"\"t \n\n(~op\"\"<_ic...l~\"'l)l \n\n'Sd,.cd:z-'4~ g;'.'t) \n\n!'l!!h it-,i ~ C::,E j\"\"',.; ., \n\n~i_; SJ,.k\\..udjSpi,\";j\" \n\nt'r-y,.,,.;..,._ \n\n(l=oo.lS wi .. ) \n\nsop\\.~.,J Web~ \n\nl!,!!,;P\\.._.vi\"' \n\n.fi d' wl dwloo\"' F<' -\"'4 -li ,\n\n\"1lli.. \n\nc~-~) 1 .Lo..~ I f\"\"\\'1-I,,, \n\nt .... ~.,i\"\"'C---f'f.. \n\n> ~p\n\n~I h (r/, <\"-/p\"\"\"'..i,.1.) \n\n-Vs...ll~ ... ......t \n\nfL -~ Colc,...,;,,~__,r,~ Soi-'u1,lo, \n\nI~~~~ ~ ,J:.~ Tc:.~iufa.~d \n\n-~.-1,u<1..ilY (O~~r'i~ _. -~.._~\\_(, >S, (f .M\"0~6;-,\n\no..t. S\\.\\\"7<1/r.wi;-,ttf'O~St..,~ lit. \n\n,R.,i..-11 .. , C.E!> \n\nB. wh\",,,is..- -P 1 t:1<.o.N'ttM'-Q.. \n\n> D.\\cd-v,..,\n\n<1-?~,...t n~L \n\n1:>,ft.,;..~~.,....1-sp .. s,,, \n\nTulk 12,,wt\"\"' unho.<;.... ol' 11Sof'\"-:l-s \n\nfl. \"Nt\"---.. ts, +,oSto,w.t ci....t,o;,,, ,, ,-.,p,uv._~ \n\n..,/ cc/3 4..,/ ,. , /ralL~ \n\n~ /,, AC.S -~~, CJ:, \n\nisoi.. - \"Co,li.-=- E'\"'f& \"\n\n111~-Mvlbf\\@\"\"'+.ut,,\"'\"~'\"\"'\"\"\"'\"a \n\nI..G,D \n\nE:c..c.e \n\n> ~\n> ~;8a.'l\\\\lft,\\\n\n111...tnr-4'.,,.d-.,,.{LE.5 \n\n~.!!.!. \n\n> ~t::,;taho-..\n\n~\n\nM , \"~\"\" <, ..... w _..,A,,) \n\n1JS.:.1_.. \n\n> Ebl> ..... Ibx -s.c.'t\"UM .(..,,. Co.l\\Qr\n\nl.do ..... d,, .......... ,....., \n\n..M1~-~-~ ... v1 \n\n'5t.Kl,'\"9,L.fdl-S.u.v,,.,,,YJ \n\n.fL. t~ b.~t.o ~~S ,...,rGII.M. fL c.1.-_ ~ bEt.o ~sp'lt\"t);,,.., \n\n> ~\"9..-i,KJei i,M-/0$.1 w~M.\\ou\n\n~; s...;,..- ~ ,U-ft,../.J ~S, .!2.i 11.~-~ '= , fi-P \n\n.ti- l{...-:,-,-\") ~ \n\n> ~\n> ~t).\",.-.,t; E ~\n\nA\\.p~ .. -PNI' <.o\"\"- ~~..-.k-. \n\nof\\Giv,eZ...~ GIT What is the likely diagnosis in a patient with sudden-onset odynophagia and retrosternal pain with a discrete ulcer in the mid-esophagus? \n\nPill esophagitis \n\nmid-esophagus most common due to compression by the aortic arch or an enlarged left atrium \n\n Vascular ring is a congenital anomaly of the aortic arch . Esophageal compression causes dysphagia, vomiting, and food impaction, but not abdominal pain. Endoscopy shows an indentation at the site of the ring. (T3,T4) \n\nCan also compress trachea in infants Cyanosis \n\n Schatzki ring is a circumferential band of tissue that partially occludes the esophageal lumen and will appear as a thin , ringed defect on barium esophagography. Patients typically present with intermittent dysphagia to solids. \n\nAchalasia \n\nOropharyngeal dysphagia: Characterized by difficulty initiating a swallow ;underlying etiologies include stroke, NMS disorders, Zenker diverticulum, \n\n363 https://t.me/usmleinnercircle USMLE Inner Circle \n\nMedication-induced esophagitis Drug class Drug \n\nAntibiotics Te tracy clines Anti-inflammatory Aspirin & many nonsteroidal agents anti -inflammatory drugs Bisphosphonates Alendronate, risedronate Others Potassium chloride, iron \n\nEvaluation of dysphagia \n\nHistory of difficulty initiating \n\nswallowing wi th coug h, choking, or nasal regurgitation No \n\nDysphagia with \n\nsolids & liquids at \n\nonset Bari um sw al low followed \n\nby poss ible ma nometry \n\n USML EWo lid, LL C\n\nLikely oropharyngeal dysphagia \n\nVideofluoroscopic modified bari um swallow \n\nDysphagia with so lids \n\nprogress in g to liquids \n\nMechanical obstruction \n\nH istory of prior radiation, ca ustic injury, complex stricture, or surgery for esophageal/laryngeal cancer \n\nBari um swal low \n\nfollowed by possible endoscopy Upper endoscopy GIT Advanced Dementia \n\n Achalasia key points: \n\nBa swallow is the best initial test \n\nManometry follows here and offers more info \n\nEndoscopy must be done to rule out cancer treatment is preferred w/ Heller myotomy (balloon dilatation can cause perforation; botox \n\nis less effective) \n\n Pseudoachalasia is a narrowing of the distal esophagus secondary to causes other than denevervation (achalasia) , such as esophageal cancer .In this case, a endoscopy must be performed to exclude malignancy. \n\nLooks for clues such as weight loss, acute onset, and age >60 \n\nWhat test is most accurate for diagnosis of achalasia ?\n\nEsophageal manometry \n\nfindings include high LES resting pressure and incomplete LES relaxation ; barium esophagram is sometimes used as an initial test \n\nGERD \n\n364 https://t.me/usmleinnercircle \n\nOnce daily PPI f 0< \n\n> 2 months\n> Refr actory\n> symptoms\n\nSwitch to different PPI or \n\n> increase PP Ito twice daily\n\nSy mptoms consistent with GERD \n\n> Men age >5 0with\n> No symptoms for >5 years\n\nor ca nc er ri sk factors \n\nOR \n\nalarm symptoms \n\n> No esophagit is\n> Symptoms controlled Persis tent symptoms\n> Continue present\n> th erapy\n> *Alarm symptoms ,Melena\n> Persist ent vomiting\n> Hematemesis , Weight loss ,Anem ia Dysphagia/odynophagia\n\nConsider endoscopy \n\n> or esophageal pH\n\nmonitoring \n\nConsider further test ing for following diagnoses: \n\n Ach,1lasia \n\n> Gastroparesis\n\n, N onacid re fi ux di sease Nocturnal acid breakthrough Esophageal manometry Impedance testi ng \n\n> Gastric scintigraphy\n> Esophagit is\n\nTreat acco rding to diagnosis: \n\n> Pill esophagitis Autoimmune skin disease Zo llinger-Elli s.on synd rome\n\n, Eosi nophilic esophagit is \n\n> Barrett 's esophagus\n\nGIT Patient with GERD and failed PPI therapy (greater than 6 weeks ) --> go to EGD Person with a history of Barrett's Esophagus and symptoms worsening --> go to EGD \n\n Clear EGD? Still can have GERD 24-hour esophageal pH monitoring (Gold standard) \n\n Complications of GERD: \n\n1. Adenocarcinoma 2. Strictures 3. Ulcers \n\nPerforation \n\n365 https://t.me/usmleinnercircle USMLE Inner Circle \n\nManagement of gastroesophageal reflux disease (GERD) \n\nUpper gastrointestinal endoscopy \n\nAlarm features \n\n Oysphagia/odynophagia Iron deficiency anemia GI bleeding Unexplained weight loss Persistent vomiting Fami ly history of gastrointestinal cancer GERO symptoms (substemal burning, regurgitation) \n\n## !\n\nPresence of alarm features OR Multiple Barrett esophagus risk factors .. \n\nYes----~-- No --i \n\nSymptom severity Mi ld <2 days/Wk \n\nSevere \n\n~2 days/wk PPI Antacids (eg, calcium carbonate) or H2RA + lifestyle changes + lifestyle changes \n\n,. Ba rre tt esophagus ri sk factors Age >50 Male sex Smoking history GERO ~5 years Obesity Family history V\\nlite ethnicity Hiatal hernia \n\nGI= gast roi nt es tin al ; H2 RA = H2 receptor an tag oni st; PPI = proto n pum p i nh ibitor . C)UWor ld GIT What is the most common cause of esophageal rupture ?\n\nEndoscopy \n\n What is the diagnosis of Boerhaave Syndrome in a stable and unstable patient? Stable Gastrografin swallow ( water soluble )\n\nUnstable CT scan \n\nDo NOT start out with EGD (camera may go through perforation) \n\nDo NOT do barium swallow (non-water soluble barium enters mediastinum mediastinitis) \n\nEosinophilic esophagitis Pleural effusion is typically left-sided because the esophagus is positioned on the left anatomically \n\n366 https://t.me/usmleinnercircle \n\nEsophageal perforation \n\n# . Instrumentation (eg, endoscopy ), trauma \n\nEtiology . Effo rt rupture (Boerhaave syndrome) \n\n# . Esophagitis (infectious/pills/caustic) \n\n# . Chest/back &/or epigastric pain, systemic signs (eg, fever) \n\nClinical presentation . Crepitus, Hamman sign (c runching sound on auscultation) \n\n# . Pleural effusion with atypical (eg, green) fiuid \n\n# . Chest x-ray or CT scan: widened mediastinum, pneumomediastinum, pneumothorax, pleural effusion \n\nDiagnosis . CT scan: esophageal wall thickening, mediastinal fiuid collection \n\n# . Esophagography with water-soluble contrast: leak from perforation \n\n# . NPO, IV antibiotics & proton pump inhibitors \n\nManagement Emergency surgical consultation .\n\nCharacteristics of gastroesophageal mural injury Mallory-Weiss syndrome Boerhaave syndrome Etiology . Forceful retching . Forceful retching \n\n## . Mucosal tear . Transmural tear \n\n# . Submucosal venous or arterial plexus bleeding . Spillage of esophageal air/fluid into surrounding tissues \n\nClinical . Epigastric/back pain . Chest/back/epigastric pain \n\n## . Hematemesis {bright red or coffee-grou nd) . Crepitus, crunching sound (Hamman sign) \n\npresentation Possible hypovolemia Odynophagia, dyspnea, fever, sepsis . .. Chest x-ray: pneumothorax, pneumomediastinum , pleural \n\n# . Upper GI endoscopy confirms diagnosis (& can e ffu sion Studies tr eat persistent bleeding) . Esophagography or CT scan with water-soluble contrast \n\nconfirms diagnosis \n\nManagement . Acid suppression . Acid suppression, antibiotics, NPO \n\n## . Most heal spontaneously . Emergency surgical consultation GI = g as tro int es tinal. GIT Does eosinophilic esophagitis respond to GERD therapy (e.g. PPIs)? \n\nNo \n\nhowever, a 2-month trial of PPIs is part of the diagnostic evaluation; if there is no symptom improvement, an endoscopy with esophageal biopsy is warranted \n\n## Stomach \n\n What is the likely diagnosis in a patient with abdominal pain and hematemesis following recent use of alcohol , aspirin , and cocaine ?\n\nAcute erosive gastropathy \n\ncharacterized by development of severe hemorrhagic lesions after exposure to various injurious agents Hallmark is development of hemorrhagic and erosive lesions shortly after exposure of gastric mucosa to various substances or reduction in mucosal blood flow. Things like NSAIDs and alcohol (direct injury) or burns, sepsis, trauma (hypoxia of mucosa) cause loss of the protective barrier and permits acid and other substances to penetrate into the laminate propria. \n\nD/D: Mallory Weiss Tear but will have several episodes of nausea and vomiting before hematemesis happens, wont be hematemesis from first bout of vomiting itself. Stress ulceration is common in patients in the ICU and can cause occult or gross gastrointestinal \n\nbleeding .Risk factors include shock , sepsis , coagulopathy , mechanical ventilation , traumatic spinal \n\ncord /brain injury , burns , and high-dose corticosteroids. \n\nPainless bleeding (vs Peptic Ulcer) \n\nT/t: PPI \n\n Both NSAIDs and aspirin can cause gastritis and/or gastric ulcers leading to chronic gastrointestinal blood loss and depletion of iron stores (IDA). First-line treatment is dietary modification to avoid potential food triggers \n\n367 https://t.me/usmleinnercircle USMLE Inner Circle \n\nEosinophilic esophagitis in adults Pathogenesis & Th2-mediated inflammatory response triggered primarily by food antigen exposure \n\nepidemiology . Comorbid atopic disease (asthma, eczema, food allergies, allergic rhinitis) common \n\n. Dysphagia \n\nClinical . Heartburn & epigastric pain \n\nfeatures . Regurgitation \n\n. Food impaction \n\n. Endoscopy & esophageal biopsy (eosinophils: .?15/hpf} \n\nDiagnosis . Exclusion of alternate diagnoses (eg, achalasia, infection) \n\n. Elimination diet \n\nTreatment . Proton pump inhibitors Topical glucocorticoids \n\nTh2 = T-helper cell type 2. GIT Autoimmune atrophic gastritis is an autoimmune disorder resulting in the formation of antibodies toward parietal cells (resulting in hypochlorhydria and unchecked gastrin production) and intrinsic \n\nfactor (resulting in B12 deficiency ). Common manifestations include postprandial abdominal pain , bloating , elevated serum gastrin levels , and macrocytic anemia. \n\nDyspepsia \n\n Common symptoms of duodenal ulcers include nocturnal pain (due to circadian rhythm of gastric acid secretion), worsening of the pain with fasting, postprandial bloating, and nausea Biopsy of the gastric antrum during endoscopy can confirm infection. In a patient without occult bleeding, noninvasive diagnostic testing, including stool antigen studies and \n\nurea breath testing , can be employed. \n\n Serology cannot distinguish between active and cleared infection and is not preferred .\n\n Peptic ulcer disease can be complicated by perforation , which typically causes acute-onset, severe pain; a systemic inflammatory response (eg, fever, tachycardia); and peritonitis (Guarding, diffuse abdominal pain) \n\n368 https://t.me/usmleinnercircle \n\nDyspepsia \n\n# . Epigastric pain or burning \n\nSymptoms . Postprandial fullness , early satiety, bloating . :?:1 months . Functional/idiopathic (75%) \n\nEtiology . Malignancy (eg, gastric, esophageal) . Peptic ulcer (eg, Helicobacter pylori infection , NSAIDs) . Drug-induced (eg, NSAIDs, bisphosphonate) . Low malignancy risk (eg, age <60 & no alarm symptoms*) \n\nWork-up 0 Testing & treatment for H pylori \n\n# . High malignancy risk (eg, age >60 or alarm symptoms) \n\n> 0\n\nGastroenterology referral/upper endoscopy \n\nTreatment . Treatment of underlying cause . Trial of proton pump inhibitor if no cause found *G I bleeding, weight loss, iron deficiency anemia , lymphadenopathy , dysphagia, odynophagia, persistent vom iting , palpable mass, famil y history of upper GI cancer. \n\n> GERD\n\n= gastroesophageal reflux disease; GI = gastrointestinal; NSAIDs = nonsteroidal anti-inflammatory drugs. GIT Tripple Therapy: PPI + Clarithromycin + Amoxycillin/ Metronidazole Quadruple: PPI + Metronidazole + Tetracycline + Bismuth \n\nVomiting & Diarrhea \n\n Vomiting and diarrhea are conditions that can lead to a decrease in insulin demand \n\nVomiting and diarrhea lead to decreased glucose uptake, increasing the risk of hypoglycemia \n\nvs. acute stress reaction in illness and stress where there is increase in demand \n\n Is diarrhea that occurs during fasting /sleeping characteristic of secretory or osmotic diarrhea? \n\nSecretory \n\nEtiologies include chronic infection, microscopic colitis, bile acid diarrhea (Bowel Resection or Cholecystectomy), or a hormone-secreting tumor (eg, gastrinoma, VIPoma), Diabetes \n\n A low stool osmotic gap is indicative of secretory diarrhea .\n\n369 https://t.me/usmleinnercircle USMLE Inner Circle \n\nActive i nfect i on wi t h H . pylori \n\nAre ANY of the fo ll owing prese nt? \n\n Prior e x pos u re to macro li des fo r any reason \n\n loc al d a rith romycin resista n ce rates .!: 15 % or \n\neradication rates with cla.r ithromycin based \n\ntripl e t herapy ,:85% \n\nI\n\nYes lllo \n\n# Penci ll in a ll ergy p resent? \n\nYes No I Me tro nidazo le use within \n\nthe pas t few ye as ?\n\nClarithromy dn b ased tri ple th er a.py with a mox i ci llin .6 \n\nYes \n\nBism ut h qu adrn ple \n\nthera py1 \n\n# .\n\nNo \n\n# T r-eat with any one of the follow in g r eg imens: \n\n Cl arith romycin based t ri ple thera py with \n\nmet roni daz ole \n\n Bi smuth qu ad r u ple therapy Common causes of steatorrhea \n\nChronic pancreatitis due to alcohol abuse, cystic fibrosis, or autoimmune/hereditary pancreatitis \n\nPancreatic insufficiency Pancreatic cancer .. Small-bowel Crohn disease . Bacterial overgrowth \n\nBile salt-related . Primary biliary cirrhosis . Primary sclerosing cholangitis \n\n## . Surgical resection of ileum (at least 60-100 cm) . Celiac disease \n\nImpaired intestinal surface epithelium . AIDS enteropathy . Gia rd iasis . Whipple disease \n\nOther rar e causes . Zollinger-Ellison syndrome . Medication induced GIT < 50 mOsm/kg ; due to increased secretions of ions (e.g. bacterial/viral infection, congenital disorders of ion transport, postsurgical changes) \n\n A high stool osmotic gap is indicative of osmotic diarrhea. \n\n> 125 mOsm/kg ; due to non-absorbed and unmeasured osmotically active agents in the GI tract (e.g. lactose intolerance) \n\n Chronic diarrhea can be due to either a functional disorder (eg, irritable bowel syndrome) or an \n\norganic disorder (eg, inflammatory bowel disease [IBD], malabsorptive disease, chronic infection). An organic cause should be suspected when any of the following features are present: Age >50 \n\nNocturnal symptoms Systemic symptoms (eg, fever, weight loss )Rectal bleeding Laboratory abnormalities (eg, elevated inflammatory markers) Family history of colon cancer or IBD If a patient has weight loss and episodes of diarrhea overnight, she requires further work-up for organic pathology, including malabsorptive conditions (eg, celiac disease) and chronic infections ( usually parasitic \n\neg, Giardia , Cryptosporidium )\n\nFactitious Diarrhea \n\n What is the likely diagnosis in a female with frequent , watery , nocturnal diarrhea and melanosis coli on colonoscopy? \n\nFactitious diarrhea (laxative abuse) \n\ntypically in a healthcare worker ; diagnosis is supported by positive stool screen for laxatives \n\nother points: Metabloc Alkalosis, Hypokalemia, \n\nCheck history of no weight loss (vs celiac disease which has weight loss) \n\n Melanosis coli can develop within a few months of the onset of regular anthraquinone (eg, senna) laxative abuse and can similarly disappear if laxative use is discontinued. Melanosis coli \n\n370 https://t.me/usmleinnercircle \n\nSOG = plasma osmolalit y- 2 x ,( stool sodium + stool potass ium) \n\n---------GIT If melanosis coli is not seen on gross inspection, histological examination may demonstrate the \n\npigment in the macrophages of the lamina propria. \n\n Depending on the laxative abused, the SOG can be high (eg, lactulose ) or low (eg, senna ). Patients with factitious diarrhea purposely cause large , voluminous stools, most commonly by improper use of laxatives ; however, they can also create the appearance of diarrhea by adding fluid to the stool . Therefore, helpful tests in evaluating factitious diarrhea include: \n\nStool osmolality: Stool osmolality is in equilibrium with plasma osmolality and typically remains \n\nconstant (eg, 290 mOsm/kg) in organic gastrointestinal disease . Hypoosmolality suggests addition of water or other dilute fluid; hyperosmolality suggests addition of a concentrated fluid (eg, urine). \n\nStool electrolytes: Elevated stool magnesium or phosphate levels suggest overuse of saline osmotic (ie, magnesium- or phosphate-containing) laxatives. \n\nStool osmotic gap : Osmotic laxatives (eg, lactulose, polyethylene glycol) cause a high osmotic gap \n\ndiarrhea, whereas senna and bisacodyl produce a low osmotic gap secretory diarrhea .\n\nChemotherapy-related diarrhea \n\nSecretory diarrhea, which is voluminous , watery , and persistent despite periods of fasting (eg, nocturnal diarrhea). Treatment: Loperamide , diphenoxylate -atropine \n\n Chemotherapy is a risk factor for infection (particularly with C difficile ), all patients with persistent diarrhea should undergo laboratory evaluation (eg, complete blood count, serum chemistry) and stool testing (eg, C difficile stool studies, fecal occult blood) prior to a presumptive diagnosis of CRD. \n\nBile Salt Diarrhea \n\n Causes Fat soluble vitamins deficiency !\n\nConstipation \n\n371 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nBile acid diarrhea \n\n Unresorbed bile acids spill into the colon, resulting in mucosal irritation \n\nPathophysiology 0 Bile acid enters terminal ileum too rap idly & overwhelms resorptive capaci ty (eg, post cholecystectomy) \n\n> 0\n\nlleal disease imeairs bile abso~ tion (eg, Crohn disease, abdominal radiation damage) \n\n# . Secretory diarrhea (eg, fasting diarrhea, nocturnal episodes) \n\nClinical features . Bloating, abdominal cramps \n\n# . Unremarkable serum & stool studies \n\nTreatment . Bile acid-b inding resins (eg, cholestyramine, colestipol) GIT Fecal impaction is common in older patients with impaired mobility, inadequate fluid or dietary fiber intake, chronic constipation , or decreased sensation of stool in the rectal vault (eg, spinal cord injury, dementia). Obstruction of fecal flow in the rectum can cause backup of stool proximal to the impaction; passage of liquid stool around the impaction leads to incontinence. Urinary incontinence is also common due to pressure against the bladder. The diagnosis of fecal impaction is typically apparent on digital rectal examination , although impaction in the proximal rectum may be apparent only on abdominal x-ray .Initial management includes manual disimpaction to break up the hard stool followed by enemas \n\n(eg, tap water, mineral oil) to dislodge the fecal fragments. \n\nGastroparesis Gastric Outlet Obstruction \n\n Common causes of gastric outlet obstruction include gastric malignancy , peptic ulcer disease , Crohn \n\ndisease, strictures (with pyloric stenosis) secondary to ingestion of caustic agents , and gastric \n\nbezoars . The presence of an \" abdominal succussion splash \" suggests a diagnosis of gastric outlet obstruction .\n\nthe physician places the stethoscope over the upper abdomen and rocks the patient back and fourth at the hips; definitive diagnosis requires endoscopy \n\n What is the likely cause of gastric outlet obstruction in a patient with a history of acid ingestion ?\n\nPyloric stricture \n\ncharacterized by early satiety , nausea , non-bilious vomiting , weight loss , and abdominal succussion splash \n\n## Liver \n\nJaundice \n\n372 https://t.me/usmleinnercircle \n\n> Gastroparesis\n> Diabetes mellitus (autonomic neuropathy) Medications (eg, opioids, anticholinergic drugs)\n> Causes Traumatic/postsurgical injury (ie, vagus nerve injury) Neurologic (eg , multiple sclerosis, spinal cord injury) ldiopathic/postviral Nausea & vomiting, epigastric abdominal pain\n> Clinical features Early satiety, bloating , weight loss Labile glucose (diabetes mellitus) Epigastric distension & succussion splash\n> Diagnosis Exclude obstruction: upper endoscopy CT/MR enterography Assess motility: nuclear gastric-emptying study Frequent small meals (low fat, soluble fiber only)\n> Treatment Promotility drugs (eg, metoclopramide, erythromycin) Gastric electrical stimulation &/or jejunal feeding tube (refractory symptoms)\n\nGIT Presence of biliary dilatation is suggestive of extrahepatic cholestasis ; absence of biliary dilatation suggests intrahepatic \n\n Endoscopic retrograde cholangiopancreatogram (ERCP) is usually performed in patients when initial ultrasonography or CT scan suggests the presence of obstruction due to cholelithiasis or malignancy .ERCP in these settings can be both diagnostic and therapeutic by relieving obstruction and facilitating biliary drainage. What is the likely diagnosis in an elderly patient with conjugated hyperbilirubinemia , elevated alkaline phosphatase , and painless jaundice ?\n\nMalignant biliary obstruction Can cause painless jaundice \n\n373 https://t.me/usmleinnercircle USMLE Inner Circle \n\nApproach to hyperbilirubinemia in adults \n\nPredominantly \n\nMainly Hyperbilirubinemia \n\n----,----~ unconjugated \n\nMa inly \n\nconjugated \n\nEvaluate liver \n\nenzyme pattern elevated AST & ALT Nonmal AST, ALT, alkaline phosphatase \n\n Viral hepatitis Autoimmune hepatitis Dubin-Johnson syndrome Rotor syndrome Toxin/drug-related hepatitis \n\n Hemochromatosis \n\n lschemic hepatitis Alcoholic hepatitis \n\nALT al an ine transa min ase : AST a sp art ate tra ns am inase .\n\nClJWorld \n\nMalignant biliary obstruction \n\n## . Cholangiocarcinoma \n\nEtiologies . Pancreatic/hepatocellular carcinoma \n\n## . Metastasis (eg, colon, gastric) \n\n## . Jaundice , prur itus, acho li c stools , dark urin e\n\n## . Weight loss \n\nManifestations . RUQ pain \n\n## . RUQ mass or hepatomegaly \n\n## . t Direct bilirubin, ALP, GGT \n\n## . Serum tumor markers (CEA, CA - 19 , AFP) \n\nDiagnos is . Abdominal imaging (u lt rasound, CT scan) \n\n## . EUS or ERCP for tissue diagnosis if unclear Possible causes \n\nOverproduction (eg, hemo l ys i s) Reduced uptake (eg , drugs, portosystemic shunt) Con jugation defect ( eg , Gi lbert syndrome) \n\nPredominantly elevated alkaline phosphatase \n\nCholestasis of pregnancy Ma lignancy (eg, pancreas, ampullary) Cholangiocarcinoma Primary bili ary cholangitis Primary sc le rosing c ho langitis Choledocholithiasis Abdominal imaging (ultrasound or CT) Antimitochondrial an tibody \n\nAFP = alpha-fetopro tein ; ALP = alka line phosphatase ; CEA = carci noembryon ic a ntigen ; EUS = endoscopic ultrasound ; ERCP = endoscop ic re tr ograde cho langiopancreatography; GGT = gamma-glutamyl transferase; RUQ = rig ht upper quadrant. GIT Acute Liver Failure \n\n Drug-induced liver disease can also be broadly categorized according to morphology: 1. Cholestasis (eg, anabolic steroids), 2. Fatty liver (eg, valproate), 3. Hepatitis (eg Isoniazid) 4. Toxic or fulminant liver (eg, acetaminophen) 5. Granulomatous (eg, allopurinol) What is the likely diagnosis for a patient with an acute , massive increase in AST /ALT in the setting of hypotension ?\n\nIschemic hepatic injury (shock liver) \n\noften accompanied by modest elevations in total bilirubin and alkaline phosphatase; and dramatic increase in ALT/AST \n\n What is the next step in management for a patient with acetaminophen toxicity that develops worsening acute liver failure despite N-acetylcysteine treatment ?\n\nRefer to liver transplant center \n\nthis is an ethically complicated issue, however, if there is no history of psychiatric illness or previous suicide attempt, liver transplantation is typically pursued \n\n Chronic alcohol use is thought to potentiate acetaminophen hepatotoxicity by depleting glutathione levels and impairing the glucuronidation process. What AST:ALT ratio is typically seen in non-alcoholic fatty liver disease (NAFLD)? \n\n< 1 AST:ALT The presence of hepatic encephalopathy differentiates acute liver failure from acute hepatitis \n\n374 https://t.me/usmleinnercircle \n\n> Acute liver failure\n> Viral hepatitis (eg, HS V-CMV-heQ atitis AB O &E)\n\n~OTc. \n\n> Drug toxicity (eg, acetaminophen overdose, idiosyncratic)\n> Etiology lschemia (eg, shock liver, Budd-Chiari syndrome) Autoimmune hepatitis Wi lson disease Malignant infiltration Generalized symp tom s (eg, fatigue, lethargy, anorexia, nausea) Right upper quadrant abdominal pain\n> Clinical Pruritus &jaundice due to hyperbilirubinemia\n> presentation Renal insufficiency Thrombocytopenia HyQQglycemia\n> Diagnostic Severe acute liv er injury (ALT &AST often >1000 U/L)\n> requirements Signs of hepatic encephalopathy (eg, confusion, asterixis) Synthetic liver dysfunction (INR 2:1 .5)\n\nGIT useful distinguishing feature from alcoholic hepatitis , which is characterized by >2:1 AST:ALT ratio. The absolute values of AST and ALT in alcoholic hepatitis are almost always < 500 IU/L. \n\n Reye Syndrome will show micro-vesicular steatosis on liver biopsy. What produces the opposite finding? \n\nMacrovesicular = alcoholic hepatitis, NASH \n\nCirrhosis \n\nLiver also produces TBG , which binds thyroid hormones. Cirrhosis lowers total T3 and T4 but free T3 and T4 are unchanged, and thus TSH is normal. \n\n Most common infectious complication of cirrhosis? \n\nSBP (Spontaneous Bacterial Peritonitis). Prevent by Paracentesis &\n\nFluoroquinolones \n\n375 https://t.me/usmleinnercircle USMLE Inner Circle \n\nOverview of cirrhosis management Treat . HCV, HBV: antiviral therapy \n\nunderlying . NASH: weight loss \n\nliver disease Provide Avoid alcohol & hepatotoxic medications \n\npreventive Vaccinate for HAV & HBV (unless already immune) \n\ncare \n\n Screen for esophageal varices (endoscopy) \n\nManage Screen for HCC: ultrasound serum AFP every 6-12 months \n\ncomplications . Frequent clinical assessment for ascites and encephalopathy (prophylactic treatment not recommended) \n\nAFP = alpha fetoprotein; HAV = hepatitis A virus; HBV = hepatitis B virus; HCC = hepatocellular carcinoma; HCV = hepatitis Cvirus; NASH = nonalcoholic steatohepatitis. \n\nManagement of cirrhosis \n\nVariceaJ hemorrhage \n\nStart nonsetecllve beta blockers. \n\nrepeat EGO every year EGO = esophagogastroduodenoscopy. \n\n10UW0<1d \n\nPeriodic surveillance of liver \n\nfooctiontests \n\n(eg, INR, albumin, bilirubin) \n\nOecornpensated \n\nAssess cornplcalions \n\nAscites \n\nOi etaiy SOdium restriction, \n\n 100F (37.8C) warrants investigation \n\n The ascites bilirubin level is elevated in the setting of a perforated biliary duct or bowel \n\n Cytology should be performed for patients in whom there is a concern for underlying malignancy usually those with persistently bloody ascites and cachexia .SAAG <1.1 indicates hypoalbuminemia or malignancy (decreased oncotic pressure) \n\n376 https://t.me/usmleinnercircle \n\nAscites fluid characteristics Bloody: trauma , malignancy, TB (rarely) Color Milky: chylous Turbid: possible infection Straw color : likely more benign causes Neutrophils .?250/mm 3 : peritonitis (secondary or spontaneous bacterial) ~2.5 g/dl (high-protein ascites) Total protein o CHF, constrictive pericarditis, peritoneal carcinomatosis, TB, Budd-Chiari syndrome, fungal <2.5 g/dl (low-protein ascites) \n\n> oCirrhosis, nephrotic syndrome ~1.1 g/dl (indicates portal hypertension)\n> SAAG oCardiac ascites, cirrhosis , Budd-Chiari syndrome <1.1 g/dl (absence of portal hypertension)\n> oTB, peritoneal carcinomatosis, pancreatic ascites, nephrotic syndrome CHF =congestive heart failure; SAAG =serum-ascites albumin gradient; TB =tuberculosis.\n\nGIT ACE inhibitors , ARBs and NSAIDs are Avoided in Cirrhosis. Blunt RAAS effect and lead to organ hypoperfusion in these patients \n\nNAFLD \n\nHepatic Encephalopathy \n\n Common causes of asterixis include hepatic encephalopathy , uremic encephalopathy ,and hypercapnia. Neomycin may be used to treat HE in patients unresponsive to lactulose and unable to tolerate rifaximin \n\n377 https://t.me/usmleinnercircle USMLE Inner Circle \n\nManagement of ascites in cirrhosis \n\n# . Imaging for confirmation (eg, abdominal ultrasound) \n\nInitial evaluation . Diagnostic paracentesis to confirm etiology & ru le out infection 0 SAAG , cell count & differential, total protein \n\n# . Spironolactone with furosemide \n\nMedical therapy . Alcohol abstinence, sodium restriction \n\n# . Avoid ACE inhibitors, angiotensin receptor blockers, NSAIDs \n\n# . Large-volume paracentesis \n\nRefractory ascites Transjugular intrahepatic portosystemic shunt .\n\nNSAIDs =nonsteroidal anti-inflammatory drugs; SAAG =serum-ascites albumin gradient. \n\nNonalcoholic fatty liver disease \n\n# . Hepatic steatosis on imaging or biopsy \n\nDefinition . Exclusion of other etiologies (eg, alcohol, hepatitis C, glucocorticoids) \n\n# . Mostly asymptomatic \n\n# . Metabolic syndrome \n\nClinical features AST/ALT ratio <1 \n\n---. Hyperechoic texture on ultrasound examination \n\nTreatment Weight loss (eg, diet modification, exercise) \n\n# . Consider bariatric surgery if BMI ~35 \n\nPrognosis . Hepatic fibrosis associated with increased risk for cirrhosis & liver-related death \n\nALT = alanine aminotransferase; AST = aspartate aminotransferase. \n\nHepatic encephalopathy \n\n## . Drugs (eg, sedatives, narcotics) \n\n## . Hypovolemia (eg, diarrhea) \n\nPrecipitating factors . El ectrolyte changes (eg, hypokalemia) \n\n## . 1 Nitrogen load (eg, GI bleeding) \n\n## . ~ (eg, pneumonia, UTI, SBP) \n\n## . Portosystemic shunting (eg, TIPS) \n\n## . Sleep pattern changes \n\n## . Altered mental status \n\nClinical presentation Ataxia .. Asterixis \n\n## . Correct precipitating causes (eg , fluids, antibiotics) \n\nTreatment . l Blood ammonia concentration (eg, lactulose, rifaximin) GI = gastrointestinal; SBP = spontaneous bacterial peritonitis; TIPS = transjugular intrahepat ic portosystemic shunt; UTI = urinary tract infection. GIT Hypokalemia and metabolic alkalosis can precipitate hepatic encephalopathy , leading to lethargy, confusion, and asterixis. \n\n1. Be careful when giving diuretics , which can precipitate low intravascular volume and hypokalemia! 2. As a result, patients with HE and hypokalmiea require potassium repletion in addition to intravascular volume repletion \n\n What is the underlying etiology of a patient with black stools and progressive confusion ? He has a past medical history of hepatitis C and physical exam shows asterixis .\n\nHepatic encephalopathy secondary to gastrointestinal bleed \n\nHE is disorder of nervous system seen in patients with decompensated liver disease . Look for precipitating factors. \n\n Hepatic Encephalopathy vs SBP (Spontaneous Bacterial Peritonitis) \n\nHepatic Encephalopathy: NO abdominal pain, usually no ascites, forgetful/confused SBP Triad: Abdominal Pain , Ascites , Altered Mental Status (AMS) \n\nHepatoPulmonary Syndrome \n\nHepatopulmonary syndrome results from intrapulmonary vascular dilations (AV Shunting) in the setting of chronic liver disease. \n\nCondition characterized by hypothermia, intrapulmonary vasodilation, and portal htn in the presence of cirrhosis Patients may have with platypnea (dyspnea worse when moving from lying to sitting) \n\nOrthodeoxia (major clue): hypoxia upon sitting upright \n\nHepatoRenal Syndrome \n\nD/D: Hypovlemic AKI ; but it should improve with fluids unlike with Hepatorenal Intravenous colloid solutions (eg, albumin ) are used in the treatment of hepatorenal syndrome and \n\nspontaneous bacterial peritonitis. \n\nBudd Chiari \n\n378 https://t.me/usmleinnercircle \n\nHepatorenal syndrome Risk factors . Ad vanced cirrhosis with portal hypertension & edema \n\n. Reduced renal perfusion Precipitating factors . GI bleed, vomiting, seps is, excessive diuret ic use, SBP \n\n. Reduc ed glo mer ular pressure & GFR 0 NSAID use (constri cts affe re nt art erio le s) \n\n. Renal hypoperfusion \n\n. Fe Na <1% (or urine Na < 10 mEq/L) Dia gn osis . Absence of tubular injury \n\n. No RS C, pr otein , or granular casts in urine \n\n. No improvement in renal function with fluids \n\n. Address pr ec ipitating factors (eg, hypovolem ia , anem ia, infection) Treatment . Splanchnic vasoconstrictors (midodrine, octreotide, n orep inephrine) \n\n## . Liver transplantation FeNa = fractional excretion of sodium; GFR = glomerular filtration rate; GI = gastrointestinal; RBC = red blood cells; SBP = s po nta ne ous b ac terial peritonitis. GIT Liver Abscess \n\n Pyogenic liver abscesses typically present with fever , RUQ pain , hepatomegaly , leukocytosis , and \n\nelevated liver enzymes ; typically with greater increases in ALP and bilirubin than in aminotransferases. an associated right-sided pleural effusion may occur. Diagnosis requires abdominal imaging(CT, USG) , and management includes blood cultures, antibiotics, and drainage. CT scan classically demonstrates a well-defined, hypoattenuating, rounded lesion , often surrounded by a peripherally enhancing abscess membrane. T/t: Blood cultures , antibiotics , and percutaneous aspiration and drainage Amoebic Liver abscess is treated with Metronidazole (NOT drained); unless it fails to improve with medication or very large abscess. \n\n## Gall Bladder & Bile Duct Bacterial (Pyogenic) Liver Abscess \n\n379 https://t.me/usmleinnercircle USMLE Inner Circle \n\nBudd-Chiari syndrome \n\n# . Hepatic venous outflow obstruction \n\n# . Usually due to: \n\nEtiology 0 Myeloproliferative disorder (eg, PV) \n\n0 Malignancy (eg, hepatocellular carcinoma) \n\n0 Oral contraception use/pregnancy \n\n# . Acute \n\n0 Jaundice, hepatic encephalopathy, variceal bleeding \n\n0 Prolonged INR/PTT; elevated transaminases \n\nManifestations . Subacute/chronic \n\n0 Vague, progressive abdominal pain \n\n0 Hepatomegaly, splenomegaly, ascites \n\n0 Mild/moderate elevation in bilirubin, transaminases Abdominal Dopp ler ultrasound - t hepatic vein flow \n\nDiagnosis Investigation for underlying disorders (eg, JAK2 testing for PV) .\n\nINR = international normal iz ed ratio; PTT = partial thromboplastin ti me ; PV = polycythemia ve ra. Liver abscess GIT Alcohol raises GGT \n\n What are the differentials for air in the gallbladder ?\n\nEmphysematous cholecystitis (gb infected with gas-forming organisms like Clostridium )\n\nPneumobilia (air secondary to gallstone ileus )\n\n Features that distinguish biliary colic from cholecystitis are pain resolution within 4-6 hours and absence of abdominal tenderness, fever , and leukocytosis. \n\nAcalculous Cholecystitis \n\n380 https://t.me/usmleinnercircle \n\n\n\nEvaluation of elevated alkaline phosphatase \n\nAMApos~ive \n\nOR \n\nAbnormal hepatic parenchyma on \n\nuhrasound \n\nLiver biopsy Elevated senn1 \n\nalkaline phosphatase \n\nOleckGGT \n\nElevated GGT Alkaline phosphate \n\nlikely of boha,y ongon \n\nOleck RUQ ultrasound & AMA Both normal Consider liver btOpsy, \n\nERCP, observation \n\nNormal \n\nGGT Alkaline phosphat ase \n\nlikely of bone origin Dilated bile ducts \n\nAMA ; antmtochondrial antibody; ERCP ; endosa,picretrograde cholan9iopancreatooram ; GGT; gamma - glutamylransferase ; \n\n> RU Q\n\n=right upperquadr.ml \n\nCl> UWond \n\nManagement of gallstones Gallstones without symptoms . No treatment required in most patients \n\nGallstones with typical biliary colic symptoms . Elective laparoscopic cholecystectomy \n\n## . Possible u rsodeoxycholic acid in poor surgical candidates \n\nComplicated gallstone disease* . Cholecystectomy w ithin 72 hr Acute cholecyslitis, choledocholithiasis, gallstone pancreatitis. GIT Acalculous cholecystitis can present with unexplained fever and diffuse or right upper quadrant ( RUQ )abdominal pain \n\nEmphysematous Cholecystitis Acute Cholangitis \n\n381 https://t.me/usmleinnercircle USMLE Inner Circle \n\nAcalculous cholecystitis \n\n. Severe trauma or recent surgery \n\nRisk factors . Prolonged f ast ing or TPN \n\n. Critical ill ness (eg , seps is, I CU )\n\n. Fever , leuk ocytos is, i LFTs, RUQ pai n \n\nClinical pr esentation . Jaund ice & RUQ m ass less common \n\n. Abdom i na l ul tr aso u nd (preferred ) \n\nDiagnosis . HI DA or CT scan if needed \n\n. En te rt c an ti biot ic coverage \n\nTreat ment . Cholecystostomy for initial dra inage \n\n. Cholecystectomy once cli ni ca lly stab le \n\nEmphysematous cholecystitis \n\n# . Diabetes mellitus \n\nRisk factors . Vas cular co mpromi se \n\n# . lmmunosuppressi on Clinical presentation . Fever, right upper quadrant pain, nausea/vomiting \n\n# . Crepitus in abdominal wall adjacent to gallbladder \n\n# . Air-fluid levels in gallbladder, gas in gallbladder wall \n\nDiagnosis . Cultur es wit h gas-forming Clostridium, Escherichia coli \n\n## . Unconjugated hyperbilirubinemia, mildly elevated aminotransferases \n\nTreatment . Emergency cholecystectomy \n\n## . Broad-spectrum antibiotics with C/ostridium coverage (eg, piperacillin-tazobactam) \n\nEmphysematous cholecystitis GIT An anion gap metabolic acidosis commonly occurs from lactic acidosis with severe \n\nsepsis .\n\n Very high levels of ALP (vs Acute Cholecystitis) \n\n What surgical procedure is preferred for biliary drainage for patients with acute cholangitis ?\n\nERCP with sphincterotomy \n\nother options include percutaneous transhepatic cholangiography and open surgical decompression \n\nPrimary Sclerosing Cholangitis Common bile duct dilation in Acute cholangitis \n\n382 https://t.me/usmleinnercircle \n\nAcute cholangitis Etiology . Ascending infection due to biliary obstruction \n\nClinical presentation . Fever, jaundice, RUQ pain (Charcot triad ) . Hypotension, AMS (Reynolds pentad) . Cholestatic li ver function abnormalities \n\n> 0\n\nj Direct bilirubin, alkaline phosphatase \n\nDiagnosis 0 Mildly j aminotransferases . Biliary dilation on abdominal ultrasound or CT scan \n\nTreatment . Antibiotic coverage of enteric bacteria . Biliary drainage by ERCP within 24-48 hr \n\nAMS = altered mental status; ERCP = endoscopic retrograde cholangiopancreatography; RUQ = right upper quadrant. GIT What is the best diagnostic test for patients with primary sclerosing cholangitis ?\n\nMRCP ( magnetic resonance cholangiopancreatography )\n\nor ERCP; MRCP is imaging technique using MRI to visualize the biliary and pancreatic ducts Biopsy is not necessary for diagnosis but will show a \"onion-skin\" pattern. Biopsy will not be the answer \n\n What is the likely diagnosis in a 42 y.o. male with abdominal pain, bloody stools, and fatigue? Labs show elevated alkaline phosphatase .\n\nIBD ( Ulcerative colitis ) with primary sclerosing cholangitis \n\nPrimary Biliary Cholangitis Not curative: Liver Transplant \n\n383 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPrimary sclerosing cholangitis \n\n# . Asymptomatic \n\nClinical features . Fatigue & pruritus \n\n# . Associated with IBD, particularly UC (-90 % of patients) \n\n# . Cholestatic li ver injury (t alkaline phosphatase, t bilirubin) \n\nLaboratory/imaging . Multifocal stricturing/dilation of intrahepatic &/or extrahepatic bile ducts on cholangiography \n\nLiver biopsy . Fibrous obliteration of small bile ducts, with concentric replacement by connective tissue in onion-skin pattern \n\n# . Biliary stricture \n\nComplications . Cholangitis or cholelithiasis \n\n# . Cholangiocarcinoma, colon cancer, biliary cancer \n\n# . Cholestasis (eg , ! fat-soluble vitamins, osteoporosis) \n\nIBD = inflammatory bowel disease: UC = ulcerative co li tis. \n\nPrimary sclerosing cholangitis GIT PBC is commonly associated with severe hyperlipidemia (elevation of HDL out of proportion to LDL), hence the xanthelasmas \n\n The diagnosis primary biliary cholangitis requires 2 out of 3 of the following: 1. Positive anti-mitochondrial antibodies \n\n2. Elevated alk-phosphatase \n\n3. Liver biopsy revealing destruction of intrahepatic bile ducts \n\nPost-cholecystectomy syndrome \n\n Patients who complain of persistent abdominal pain after cholecystectomy should be evaluated for post-cholecystectomy syndrome. Metabolic bone disease seen in patients with PBC may be due to the inhibition of osteoblast activity by a retained toxin \n\nrather than vitamin D malabsorption \n\n384 https://t.me/usmleinnercircle \n\nPrimary biliary cholangitis Pathogenesis Autoimmune destruction of intrahepatic bile ducts Affects middle-age women \n\nClinical In sidious onset of fatigue & pruritus features Progressive jaundice, hepatomegaly, cirrhosis Cutaneous xant omas & xantf\\elasmas \n\n Cholesta ti c pattern of liver injury \n\nLaboratory ( t alkaline phosphatase, f aminotransferases) \n\nfindings Antimitochondrial antibody \n\n Seve re hypercfioleslerolemia \n\nTreatment Ursodeoxycholic acid (delays progression) Liver transplantation for advanced di sease Malabsorpti on , fat-soluble vitamin de fi ciencies \n\nComplications Metabolic bone disease (osteoporosi s, osteomalacia) Hepatocellular carcinoma \n\nComplications of cholecystectomy \n\n Injury to bile ducts or the hepatic artery (especially with acc idental incorrect clipping) Gallbladder fistulae Hemorrhage Subhepatic abscess \n\n Postcholecystectomy syndrome \n\n Description : persistent abdominal pain or new symptoms following gallbladder removal Frequency: 10-15% of patients \n\n Etiology: both biliary (e.g, biliary injury, retained cy stic duct, sphincter of Oddi dysfunction) and extrabiliary causes (e.g. , irritable bowel syndrome , pancreatitis) have been identified c;:i \n\n Clinical features : abdominal pain and upper GI tract (e .g ., dyspepsia) or lower GI tract (e .g ., diarrhea) symptoms Diagnosis: ultrasound or CT scan followed by ERCP (preferred test if intervention is planned) or MRCP Treatment : depends on the identified cause , but may involve endoscopic sphincterotomy (e.g ., in patients with sphincter of Oddi dysfunction) or transduodenal sphincteroplasty \n\nTable 15 .1 Postcholccystcctomy syndrome (PCS) Etio lo gy \n\n> Residual stone in CBD\n\nGailstone in cystic du ct stump Dysfunction of the biliary tree Other \n\nFeatures \n\nThis can 1 ead to pancrea ti tis, cbolangitis, or biliary obstruc ti on Patients with anatomically longer cystic ducts are at risk for retained gallstones Increased pressure at the sphincter of Oddi can l ead to impaired function of th e biliary tree \n\nGas tri tis, peptic ulcer disease GIT Diagnosis involves ultrasound or CT followed by ERCP .\n\nevaluated via abdominal imaging (e.g. ultrasound) followed by direct visualization (e.g. ERCP ,MRCP) to find the causative factor \n\n Sphincter of Oddi dysfunction (stenosis) produces recurrent , episodic pain in the right upper quadrant or epigastric region with elevations in AST/ALT. \n\nvisualization of a dilated common bile duct in the absence of stones favors this diagnosis \n\nDx: Sphincter of Oddi Manometry (Gold Standard) \n\n Opioid analgesics (e.g. morphine): precipitate symptoms of sphincter of Oddi dysfunction \n\n Biliary leakage should be suspected in patients with persistent abdominal pain , fever , and \n\nright upper quadrant tenderness 2-10 days after laparoscopic cholecystectomy .Laboratory studies often demonstrate elevated liver function tests (especially bilirubin), with \n\nnormal-appearing bile ducts (often with an intraabdominal fluid collection) on imaging. \n\n## Pancreas \n\n What is the first test or imaging study that should be ordered to diagnose pancreatitis in a patient with acute epigastric abdominal pain that radiates to the back ?\n\nSerum amylase and lipase \n\nif amylase or lipase is > 3x normal, may not need confirmatory imaging for diagnosis Order amylase and lipase to confirm diagnosis , then do imaging to identify the etiology (i.e. gallstones) \n\n What imaging modality is recommended to evaluate patients with suspected gallstone pancreatitis ?\n\nUltrasound (RUQ) \n\nCT is not as sensitive as US for detecting gallstones \n\n What imaging modality is preferred for the diagnosis of acalculous cholecystitis ?\n\nUltrasound \n\nabdominal CT scan or HIDA scans are more sensitive and specific; use of US is unclear \n\n What imaging modality is most useful for diagnosing acute pancreatitis if laboratory testing is unclear? \n\nContrast-enhanced CT scan \n\nnearly 30% of patients have an ileus with bowel gas that prevents ultrasound from fully visualizing the pancreas \n\n385 https://t.me/usmleinnercircle USMLE Inner Circle GIT Patient with RUQ pain radiating to back, hypertension controlled with thiazides. \n\nHypercalcemia causing pancreatitis \n\nHyperCa+ leads to secretory block in pancreatic duct \n\nHypercalcemia can cause pancreatitis but pancreatitis can cause hypocalcemia d/t saponificaiton, thus predisposing hypercalcemia may be missed \n\n Boy was riding bike and fell, high amylase/lipase traumatic pancreatitis \n\nNPO w/pain control and IV fluids Bad prognostic indications: increased BUN, low Ca , high WBC, low Hct, high LDH Diuretics , including thiazides (eg, hydrochlorothiazide) and most loop diuretics (eg, furosemide), are among the most common offenders. These drugs may trigger pancreatitis via hypersensitivity to the sulfonamide molecule, pancreatic ischemia due to reduced blood volume, and/or increased viscosity of pancreatic secretions. \n\n386 https://t.me/usmleinnercircle \n\nAcute pancreatitis \n\n# . Chronic alcohol use (-40%) \n\n# . Gallstones (-40%) \n\n# . Hypertriglyceridemia \n\nEtiology Drugs (eg, azathioprine , valproic acid , thiazides) .\n\n Infections (eg, C MV, Legionella, Aspergil/us) \n\n# . Iatrogenic (post-ERCP, ischemic/atheroembolic) \n\nDiagnosis (requires 2 of the follow) \n\n# . Acute epigastric pain radiating to the back \n\n# . Amylase or lipase >3 times normal limit \n\nClinical Abnormalities on imaging consistent with \n\npresentation pancreatitis \n\nOther findings \n\n# . A LT level >150 U/ L suggests gallstone pancreatitis \n\n# . Severe disease : fever, tachypnea , hypoxemia, hypotension \n\nALT= alanine aminotransferase; CMV = cytomegalovirus; ERCP = endoscopic retrograde cholangiopancreatography. \n\nDrugs associated with drug-induced pancreatitis Acute pancreatitis \n\n Acetaminophen \n\nAnalgesics Nonsteroidal anti-inflammatory drugs Mesalamine, sulfasalazine Opiates \n\n## . lsoniazid \n\nAntibiotics Tetracyclines Metronidazole Trimethoprim-sulfamethoxazole \n\nAntiepileptics Valproic acid Carbamazepine \n\nAnti hypertensives Thiazides, furosemide \n\n## . Enalapril, losartan Lamivudine \n\nAntivirals Didanosine \n\nlmmunosuppressants Azathioprine, mercaptopurine Corticosteroids \n\nOthers Asparaginase \n\n## . Estrogens GIT Acute pancreatitis from uncorrectable causes (eg, ischemia, atheroembolism) can be conservatively managed with analgesics and intravenous fluids. \n\nSevere Acute Pancreatitis \n\n What is the cause of hypotension in severe acute pancreatitis ?\n\nIncreased vascular permeability \n\nrelease of activated pancreatic enzymes and inflammatory mediators leads to widespread vasodilation and vascular permeability Acute pancreatitis can produce multiple organ dysfunction syndrome (MDOS)/SIRS/shock \n\nPancreatic Pseudocyst \n\n387 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSevere acute p ancreatiti sDe fi nition . Acute pancreatitis with organ failure (eg, respirato ry . cardiovascul ar, renal} persisting >48 hr . Patient factors: \n\n0 Older age (eg, age >55) \n\n0 Comorbiditi es, in clu ding obesity (BM I >30 kg /m 2 )\n\n## . Clinical findings: \n\n0 Altered mental status Pr edicto rs 0 SIRS (eg , leukocytes >12 ,000 / mm 3, temperature >38 C [100.4 F l) \n\n## . La boratory fi ndings of intravascular volume depletion: \n\n0 ) BUN (>20 mg /dL) and/or ) creatinine (>1.8 mg/dL) \n\n0 ) HCT (>44%) \n\n## . Rad iologic findi ngs :\n\n0 CXR: pulmonary infiltrates, pleural effusions \n\n0 Abdominal CT scan: severe pancreatic necrosis BUN ;;; blood urea nitrogen; CXR ;;; chest x-ray; HCT ;;; hematocrit; SIRS ;;; systemic inflammatory re sponse syndrome. \n\nClinical features of severe pancr ea titis \n\n. Fever, tachycardia, hypotension \n\n. Dyspnea, tachypnea &/or basil ar crackles \n\nClinical pr esentation . Abdominal tenderness &/or distension \n\n. Cullen sign: periumbilical bluish coloration indicating hemoperitoneum \n\n. Grey Turner sign: reddish-brown coloration around flanks indicating retroperitoneal bleed \n\n. Age >75 \n\n. Obesity \n\n. Alcoholism \n\nAssociated with j risk of severe . C-reactive protein >15 0 mg/dl at 48 hr after presentation \n\npa ncr eatitis . Rising blood urea nitrogen & creatinine in the first 48 hr \n\n. Chest x-ray with pulmonary infiltrates or pleural effusion \n\n. CT scan/magnetic resonance cholangiopancreatography with pancreatic necrosis & extra pancreatic inflammation \n\n. Pseudocyst \n\n. Peripancreatic fluid collection \n\n. Necrotizing pancreatitis \n\nComplications . Acute respiratory distress syndrome \n\n. Acute renal failure \n\n. Gastrointestinal bleeding GIT Pseudocysts are mature walled-off pancreatic fluid collections (usually no necrosis or solid material) surrounded by a thick fibrous capsule and containing enzyme-rich fluid, tissue, and debris. They can leak amylase-rich fluid i nto the circulation and increase serum amylase .Complications include spontaneous infection , duodenal or biliary obstruction ,\n\npseudoaneurysm (due to digestion of adjacent vessels), pancreatic ascites , and pleural \n\neffusion .T/t: Asymptomatic: expectant management (eg, symptomatic therapy, NPO). Symptomatic: Endoscopic drainage \n\nPancreatic Cyst \n\n Most pancreatic cysts are benign and can be managed conservatively (eg, surveillance imaging) Cysts with higher risk for malignancy :\n\nLarge size (3 cm) \n\nSolid components or calcifications Main pancreatic duct involvement (ie, ductal dilation) \n\nThickened or irregular cyst wall \n\nRequire further evaluation with endoscopic ultrasoundguided biopsy and possibly surgical resection. \n\nChronic Pancreatitis \n\n What is the likely diagnosis in a patient with a history of alcohol use and chronic , intermittent epigastric abdominal pain that is relieved by leaning forward ?\n\nChronic pancreatitis \n\nother common symptoms include steatorrhea , weight loss , and diabetes \n\n388 https://t.me/usmleinnercircle \n\n> Pancreatic pseudocyst\n\nGIT In patients with pancreatic insufficiency, pancreatic enzyme deficiency leads to the release of high volumes of CCK , resulting in a loop of pancreatic hyperstimulation .In association with pancreatic inflammation and ischemia , this results in the characteristic post-prandial abdominal pain common in patients with chronic pancreatitis. \n\nPancreatic enzyme supplementation , which typically contains lipase , protease , and amylase ,helps alleviate pain by reducing pancreatic hyperstimulation Pancreatic ascites is a rare complication of chronic pancreatitis that results from damage to the pancreatic duct, leading to leakage of pancreatic juice into the peritoneal space \n\nserosanguinous or straw-colored ascitic fluid with analysis showing high amylase (often >1000 U/L) \n\n## Spleen \n\n What is the likely diagnosis in a patient with recently diagnosed infective endocarditis that now presents with fever and left-sided chest /abdominal pain ? CT reveals a left-sided pleural effusion and splenomegaly with a splenic fluid collection. \n\nSplenic abscess (secondary to IE) The presence of pancreatic calcifications on abdominal imaging helps establish a diagnosis of chronic pancreatitis .\n\n389 https://t.me/usmleinnercircle USMLE Inner Circle \n\nOvervi ew of chronic pancreatitis \n\n Alcohol use \n\nEtiology Cys tic fibros is (common in chil dren) Ductal obs trucbon {eg , malignancy, stones) Autoimmune Chronic epigastric pain with intermittent Clinical pai n-free intervals presentation Malabsorption -steatorrhea , weight loss Diabetes mellitus Laboratory Amy lase/lipase can be normal & nondiagnostic results / imaging CT scan or MRCP ca n sh ow ca lcifications, dilated ducts & enlarged pancreas Pain manage me nt Treatment Alcohol & smok i ng cessa ti on Frequent, small meals Pancreatic enzyme supplements Clinical features of splenic abscess \n\n. Infection (eg, infective endocarditis) wi th hematogen ous spread \n\n. Hemoglobinopathy (eg, sickle cell disease) Risk factors . lmmunosuppression (eg, HIV) \n\n. Intravenous drug use \n\n## . Trauma \n\n. Class ic triad of fever, leukocytosis & left upper-quadrant abdominal pain \n\n## . Left-sided pleuritic chest pain wi th left pleural effusion co mm on ly seen Clinical presentation . Possible spl enomegaly \n\n. Most commonly due to Staphylococcus, Streptococcus & Salmo ne ll a\n\n## . Usually diagnosed by abdominal computed tomography scan Treatment . Combination of broad-spectrum antibiotics & splenectomy \n\n. Possible percutaneous drainage in poor surgical candi dat es GIT splenic abscess usually presents with a triad of fever , leukocytosis , and LUQ abdominal pain ;treatment is with antibiotics plus splenectomy \n\n## Small Intestine \n\nD-Xylose Test \n\nD-xylose is a monosaccharide that can be absorbed in the proximal small intestine without degradation by pancreatic or brush border enzymes. A false-positive D-xylose test (ie, low urinary D-xylose level despite normal mucosal absorption) can be seen in the following: Delayed gastric emptying Impaired glomerular filtration \n\nSmall intestinal bacterial overgrowth (SIBO), characterized by alterations in small intestinal flora (due to abnormal intestinal anatomy or motility), leading to bacterial fermentation of the D-xylose before it can be absorbed. \n\nIBS \n\n Due to Smooth Muscle Hypersensitivity to Cholecystokinin \n\n For IBS-C, fiber supplementation improves constipation and may reduce abdominal pain. IBS-D is usually treated with antidiarrheal agents such as loperamide .\n\n390 https://t.me/usmleinnercircle \n\n\n\nClinical features of irritable bowel syndrome \n\n> Recurrent\n\nabdominal pain/discomfort <=1 day/week for past 3 months & ;;>:2 of the \n\nRome IV diagnostic following : \n\ncriteria Related to defecation (improves or worsens) Change in stool frequency Change in stool form Older age of onset (;;>:50) Gastrointestinal bleeding Nocturnal diarrhea Worsening pain \n\nAlarm features Unintended weight loss Iron deficiency anemia Elevated C-reactive protein Positive fecal lactoferrin or cal protectin Family history of early colon cancer or IBD \n\n> IBD\n\n= inflammatory bowel disease. \n\n> IBS with diarrhea:\n> oStool cultures\n> oCeliac disease screening\n> o24-hr stool collection\n> Evaluation oColonoscopy or flexible sigmoidoscopy &biopsy IBS with constipation :\n> oRadiography\n> oFlexible sigmoidoscopy &colonoscopy\n\nGIT Patients with IBS-D should be screened for celiac disease because both disorders may present with abdominal pain, diarrhea, and bloating; screening is not indicated in IBS-C. \n\n Colonoscopy is recommended in patients with alarm features to evaluate for malignancy or inflammatory bowel disease \n\nIBD \n\n Smoking is a major risk factor that likely contributes to disease flare-ups in Crohns. \n\nMight be protective in UC. \n\n Use Glucocorticoids for immediate improvement of moderate to severe Crohns . Biological agents weeks to works. Pregnancy is a high-risk period for patients with UC due in part to placental cytokines that worsen colonic inflammation. Maternal complications include worsening UC disease activity , which can lead to severe hematochezia, anemia, and, in rare cases, toxic megacolon. Fetal risks include preterm delivery and small for gestational age . In addition, fertility rates are lower in those with active UC. Most medications used in the management of UC (eg, mesalamine , sulfasalazine , TNF- a inhibitors )are considered safe for continuation throughout pregnancy \n\ncan also be continued during breastfeeding (except salfasalazine) \n\nCeliac Disease \n\n391 https://t.me/usmleinnercircle USMLE Inner Circle \n\nClassification & management of mild ulcerative colitis \n\n <4 watery bowel movements per day \n\nClinical features \n\n Hematochezia is rare or intermittent No anem ia \n\nLaboratory findings Normal ESR & CRP 5-Aminosalicylic acid agents (eg, mesalamine, \n\nTreatment sulfasalazine) \n\nCRP =C-reactive protein; ESR =erythrocyte sedimentation rate. GIT The presence of IgA anti-endomysial and anti-tissue transglutaminase antibodies are highly predictive of celiac disease. \n\nabsence does not rule out celiac disease as many patients have concurrent selective IgA deficiency. In such cases use IgG antibodies for diagnosis. \n\n In children, a high degree of suspicion must be maintained because the main presenting sign of celiac disease may be growth delay (eg, weight loss, poor linear velocity). \n\nGrowth delay can occur in the absence of diarrhea , which is present in only two-thirds of patients. Patients with celiac disease commonly report fatigue and foul-smelling, greasy diarrhea. \n\n392 https://t.me/usmleinnercircle \n\nFeatures of malabsorption in celiac disease Nutrients Symptoms General Bulky, foul-smelling , floating stools \n\nFat & protein Loss of muscle mass, loss of subcutaneous fat, fatigue \n\nIron Pallor (anemia), fatigue \n\nCalcium & vitamin D Bone pain (osteomalacia), fracture (osteoporosis) \n\nVitamin K Easy bruising \n\nVitamin A Hyperkeratosis \n\nClinical manifestations of celiac disease \n\n# . Diarrhea, steatorrhea, weight loss \n\nGastrointestinal . Abdominal pain \n\n# . Flatulence/bloating \n\n# . Late manifestations: ulcerative jejunitis, enteropathy-associated T-cell lymphoma \n\nMucocutaneous . Dermatitis herpetiformis \n\n Atrophic glossitis \n\nEndocrine . Vitamin D deficiency . Secondary hyperparathyroidism \n\nBone disorders . Osteomalacia/osteoporosis (adults) \n\n# . Rickets (children) \n\nHematologic . Iron deficiency anemia \n\nNeuropsychiatric . Peripheral neuropathy \n\n# . Depression/anxiety \n\nCeliac disease \n\n# . First-degree relative with celiac disease \n\nRisk factors . Down syndrome Autoimmune disorders (eg , type 1 diabetes mellitus, autoimmune thyroiditis) \n\nClassic symptoms Abdominal pain, distension, bloating , diarrhea General: failure to thrive/weight loss, short stature,* delayed puberty/menarche* \n\nExtraintestinal Oral: enamel hypoplasia, atrophic glossitis . Dermatologic: dermatitis herpetiformis \n\nmanifestations . Hematologic: iron deficiency anemia (due to malabsorption) (may be sole . Neuropsychiatric: peripheral neuropathy, mood disorders (eg, anxiety, presentation) depression) . Musculoskeletal: arthritis, osteomalacia/rickets* (due to vitamin D malabsorption), . t Tissue transglutaminase lgA antibody \n\nDiagnosis . Proximal intestinal biopsy (villous atrophy, crypt hyperplasia, intraepithelial lymphocytosis) Gluten-free diet \n\nTreatment . Dapsone for dermatitis herpetiformis Pediatric findings. GIT In some patients, extraintestinal symptoms with no gastrointestinal features may be the sole presentation. \n\n Dermatitis herpetiformis is another extraintestinal manifestation and presents as grouped pruritic papules or vesicles (eg, fluid-filled) typically on extensor surfaces (eg, elbows, knees). Symptoms typically respond to a gluten-free diet; dapsone should also be given for acute management of dermatitis herpetiformis \n\nSIBO \n\n Do NOT consider SIBO in patients with regular bowel movement \n\n Carbohydrate breath test: a dose of fermentable carbohydrate (ie, lactulose, glucose) is taken orally, and breath samples for hydrogen and methane (produced by gut bacteria) are taken at regular intervals. Normally, colonic bacteria ferment any nonabsorbed substrate after 2-3 hours ; in contrast, an earlier rise in breath hydrogen (at <1.5 hours) suggests fermentation in the small bowel, indicating SIBO. \n\nAppendicitis \n\n What is the preferred imaging modality for diagnosis of acute appendicitis during pregnancy? \n\nUltrasound (graded compression technique) \n\nif ultrasound is non-diagnostic, MRI can be performed for further assessment \n\n393 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSmall intestinal bacterial overgrowth \n\n# . Anatomic abnormalities (eg, strictures, surgery, small bowel diverticulosis) \n\n# . Motility disorders (eg, diabetes mellitus, scleroderma, opioid use) \n\nRisk factors . Immunodeficiency (eg, lgA deficiency) \n\n# . Chronic pancreatitis Gastric hypochlorhydria, proton pump inhibitor use \n\n# . Bloating, flatulence \n\nClinical . Chronic watery diarrhea \n\nmanifestations Possible malabsorption \n\n# . i Vitamin 8 12 (bacterial consumption), j folate (bacterial synthesis) \n\n# . Carbohydrate breath testing (lactulose or glucose) \n\nDiagnosis Endoscopy with jejunal aspirate/culture .\n\nTreatment . Oral antibiotics (eg, rifaximin, ciprofloxacin, doxycycline) GIT During pregnancy, the appendix undergoes cephalad displacement by the gravid uterus; therefore, with increasing gestational age, patients may have an atypical presentation of pain in the right mid-to-upper quadrant or right flank .may mimic Cholecystitis pain What is the initial management for patients with an appendiceal abscess ?\n\nIV hydration, antibiotics, and bowel rest \n\nappendectomy should not be performed right away (may return in 6-8 weeks for elective appendectomy, though this is controversial) \n\n Infections are the most common complication of appendectomy , and risk of intra-abdominal abscess (e.g. Sub-phrenic Abscess) is significantly greater with laparoscopic appendectomy than laparotomy. Manifestations typically include recurrent fever and abdominal symptoms (eg, pain, vomiting) several days after an abdominal operation \n\n394 https://t.me/usmleinnercircle \n\nManagement of suspected appendicitis \n\nSuspected appendicitis (eg, modified Alvarado score ~4} \n\nPerform diagnostic imaging Child or pregnant female? No \n\n# ! I[ Abdominopelvic CT scan IEvaluate for other diagnoses \n\n> \"Modified A lvarado score\n\nNonvisualized appendix (ie, nondiagnostic} lManagement depends on specific modified Alvarado score Nonperforated \n\nappericitis \n\nAntibiotics & appendectomy \n\ns12 hr Yes \n\n## l\n\nUS MRI Perforated appendicitis \n\n## !\n\nAntibiotics & bowel rest; PCD (contained abscess} vs l &D with appendectomy (diffuse contamination} 1 point each: migratory RLQ pa in , anorexia, nausea or vomiting, RLQ rebound tenderness, fever >37 .5 C (99.5 F) .2 points each : RLQ tenderness, leukocytes >10,000/mm3. l& D = irrigation & drainage; PCD = percutaneous drainage; RLQ = right lower quadrant; u s = ultrasound. GIT Infectious ileocecitis (Pseudo-appendicitis) \n\nT/t: Amoxicillin ;l if severe \n\nD/D: \n\n1. Appendicitis : Mild diarrhoea vs Profuse and Mucoid. Presence of other sick contact 2. Cecal diverticulitis: Mild diarrhoea can occur, profuse or mucoid diarrhoea is not seen. In addition, diverticulitis is exceedingly rare in children \n\nObstruction \n\n395 https://t.me/usmleinnercircle USMLE Inner Circle \n\nExamination signs of appendicitis Sign Findings Si gn ificance Peritoneal signs \n\n# . Rebound tenderness . Acute i ncrease in pain after removing the hand from applying pressure Peritoneal ir rit at i on (rupture or \n\n# . Involuntary . Tensing of abdom inal wall muscles during palpation of abdomen impending rupture) guarding . Pers is tent tension of abdominal wall muscles \n\n## . Abdominal rigidity \n\nPsoas sign . RLQ pa in with extension of right thigh Abscess adjacent to psoas or retrocecal appendix \n\nObturator sign . RLQ pain with internal rotation of right thigh Pelvic appendix or abscess \n\nRovsing\"s sign . RLQ pain with LLQ palpation & retropul sion of colon ic contents Acute appendicitis \n\nRectal . Rig ht pelvic pain during rectal examinati on , especially with pressure on Pelvic appendix or abscess \n\ntenderness the right rectal wall \n\nCampy/obacter gastroenteritis Epidemiology . Most common ly transmitted via undercooked poultry \n\nClinical . Fever, abdominal pain, diarrhea (mucoid blood) \n\nfeatures . Pseudoappendicitis ( RLQ pain due to acute ileoceciti s) \n\nTreatment . Supportive care (symptoms usually self-limited <7 days) \n\n## . Antibiotics only in severe or high-risk cases \n\nComplications . Guillain-Barre syndrome \n\n## . Reactive arthritis \n\n\"'Duratio n > 7 da ys ; b loody st ools ; h igh feve rs ; pati e nts who are pregnan t, im munocompro mi se d, or el derly .\n\nRLQ = right lower quadrant. \n\nSmall bowel obstruction \n\n# . Colicky abdominal pain, vomiting Inability to pass flatus or stool if complete (no obs tip atio n if partial) \n\nClinical presentation Hyperactive - absent bowel sounds Dist ended & tympanitic abdomen Dil ated loops of bowel wit h air-fluid levels on plain fi lm or CT scan \n\nDiagnosis Partial: air in colon \n\n# . Complete: transition point (abrupt cutoff), no ai r in co l on lschemialnecrosis ( strangulation) \n\nComplications Bowel perforation .\n\n Bowel rest , nasogastric tube suctio n, intravenous fluids \n\nManagement Surgical exploration for s ign s of complications .GIT Can be a complication of Crohns Disease \n\n What is the initial step in the management of small-bowel obstruction that is complicated by fever , hypotension , and tachycardia ?\n\nUrgent surgical exploration \n\n What is the most common cause of small-bowel obstruction (SBO) in the U.S? \n\nAdhesions \n\ntypically result from abdominal operations or inflammatory processes \n\nCan be congenital (Ladd Bands) in children Is post-operative ileus characterized by a clear transition point on abdominal X-ray? \n\nNo \n\nboth small and large bowel dilation post-operative ileus \n\n396 https://t.me/usmleinnercircle \n\n> Small bowel obstruction vs ileus Small bowel obstruction lleus\n\n# . Recent surgery (hours to days) \n\n> Etiology\n\n# . Prior surgery (weeks to years) . Metabolic (eg, hypokalemia) \n\n# . Medication induced \n\n> Abdominal examination\n\n# . Distension . Possible distension \n\n# . Increased bowel so unds . Reduced/absent bowel sounds \n\n> Small bowel dilation Present Present\n> Large bowel dilation Absent Present\n\nGIT What class of analgesics may contribute to prolonged post-operative ileus ?\n\nOpiates \n\n Paralytic ileus is most commonly a complication of abdominal surgery but can also be seen in other conditions such as retroperitoneal/abdominal hemorrhage , intraabdominal inflammation (eg, pancreatitis), intestinal ischemia , and electrolyte abnormalities .\n\n## Large Intestine & Rectum \n\n What is the next step in management for an elderly patient with newly discovered iron deficiency anemia ?\n\ncolonoscopy and endoscopy \n\nnew IDA in an elderly patient is considered to be from GI blood loss until proven otherwise \n\n397 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSBOvs ileus \n\nSBO lieus \n\n# . Nausea, vomiting . Nausea vomiting \n\n# . Obstipation \n\nClinical features . No flatus Acute abdomen Abdominal distension \n\n# . Hyperactive or absent bowel sounds . Decreased or absent bowel sounds Air fluid levels . No transition point \n\nX-ray findings . Dilated proximal bowel, collapsed distal bowel . Dilated loops of bowel \n\n# . Little/ no air in colon/rectum Air in colon/rectum SBO = small bowel obstruction. \n\nEvaluation of minimal bright red blood per rectum \n\nAge <40 without red flags \n\ni\n\n# ~\n\nMinimal bright red blood \n\nper rectum \n\nAge 40-49 without red flags T~ ~ ISigmoidoscopy I--.-~ _ orcolonoscopy _Colonoscopy No further evaluation necessary \n\n10 UWorld \n\n\"Red flags = change ,n bowel hab~s . abdominal pain, weight \n\nloss , run deficiency anemia, fa-nity history of colo n cancer .GIT Hemorrhoids \n\n Infrared coagulation , rubber band ligation , and sclerotherapy are all used to treat symptomatic \n\nnonthrombosed internal hemorrhoids that fail conservative management. These techniques are avoided with external hemorrhoids because their location below the dentate is highly innervated and these procedures would cause severe pain. \n\n398 https://t.me/usmleinnercircle \n\nAnal & perianal masses Rectal prolapse . Erythematous mass with concentric ring s that occurs with Valsalva \n\n## . Mu cus discharge, mild abdominal pain , mass sensation \n\n## . Dusky/purple lump or polyp \n\nExternal hemorrhoid . Associated it ching, bleeding \n\n## . Th ro mbosi s: acute enlargement with pain Internal hemorrhoid . Intermittent itching , painle ss bleeding, leakage of stool \n\n## . Detected with digital rectal ex am or anoscopy (unless prolapsed) \n\n## . Fluctuant mass /sw elling with erythema Perianal abscess . Fever \n\n## . Gradual ons et \n\n## . Pink or flesh-colored papules, plaques , or cauliflower-shaped masses Anogenital wart . Chronic onset \n\n## . Mild itching, bleeding \n\n## . Squamous cell carcinoma most common Anorectal cancer . Bleeding, pain . Ulcerating , enlarging mass Skin tags . Small, flesh-colored papules \n\n## . May represent external terminu s of anal fis sure (sentinel tag )External hemorrhoids Pathophysiology . Hemorrhoidal venous plexus distension \n\n# . l nt ravascular inflamma ti on, wh ich leads to h emo rr hoid thrombosis \n\nRisk factors . Constipation, low-fiber diet , prolonged sitting \n\n# . Pregnancy, advanced age \n\n# . Anal pruritus, bleeding, discharge of mucus, f eca l incontinence, se nsation of full ness in anorectum \n\nPresentation . Thr om bo s is (severe anorectal pain) \n\n# . Purple or blue bulge on examination \n\n# . Conservative management: \n\n> 0\n\nHigh-fiber diet, stool softeners, sitz baths \n\n> 0\n\nTopical analgesics, ant i-inflammatories & ant ispasmodics ( eg , lidocaine, gl ucocorticoid \n\nManagement suppositories, nitrog ly cerin cream) \n\n# . Refractory or thrombosed hemorrhoids: \n\n> 0\n\nConservative measures when mild \n\n> 0\n\nHemo rrhoidectomy when severe \n\n> 0\n\nHemorrhoid incision with t hr o mbus removal for temporary rel ief \n\nInitial management of hemorrhoids \n\n## . Increased fluid intake \n\nDietary factors . Increased fiber i ntake (foods , fiber supplements) . Reduced fat intake \n\n## . Moderation of alcohol intake \n\n## . Limit ti me sitting on toilet (eg, 3 minutes) \n\nBehavioral factors . Limit defecation to once daily \n\n## . Avoid straini ng during defecation . A na l gesics (eg , be n zocai n e) \n\nTopical agents . A s trin ge nt s ( eg , wit c h h aze l) . H yd r ocortiso ne GIT Diverticulitis & Diverticulosis \n\n Other Signs: \n\n1. A palpable, tender mass (from focal inflammation) 2. Dysuria , or urinary urgency or frequency due to bladder irritation from an adjacent inflamed \n\nsigmoid colon . CT Scan: Focal bowel wall thickening and inflammatory signs (eg, stranding ) in pericolonic fat. \n\n What is the next step in management of a patient with diverticulitis complicated by an abscess > 4 cm ?\n\nCT-guided percutaneous drainage \n\nsurgical drainage can be attempted if percutaneous drainage fails \n\n Small abscesses (<4 cm) often respond to IV antibiotic therapy alone without drainage What is the most common cause of gross lower GI bleeding in adults ?\n\nDiverticulosis \n\n What dietary habits increase the risk of diverticulosis complications (e.g. hemorrhage, diverticulitis)? \n\n399 https://t.me/usmleinnercircle USMLE Inner Circle \n\nClinical featur es of acu te divert ic ulitis \n\n## . Abdominal pain \n\n# . Nausea/vomiting , alter ed bowel movements Clinical presentation . Fev er, leukocytosis \n\n# . Possible sterile pyuria Diagnos is . CT scan of the abdomen (oral & intravenous contrast) . Bo we l rest Management Antibiotics (eg, ciprofloxacin, metronidazole) \n\n# . Colonoscopy 6-8 weeks after resolution Complications . Abscess, obs tr uction, fistula, perforation \n\nAcute diverticulitis \n\n Acute (left) lower abdominal pain & tenderness CT scan: focal bowel wall thickening, visible diverticula No high -risk features or complications High risk features: \n\n Age >70 Compl i cations ]\n\nOu tpati ent management Oral fluids Oral antibiotics Close follow-up Comorbidities lmmunosuppression Sepsis/SIRS \n\n# l\n\nInpatient management Bowel rest IV fluids IV antibiotics \n\nAbscess \n\n# 1\n\nIV antibiotics \n\npercutaneous drainage Perforation, o bstruction , fistul a IV antibiotics Surgery IV = intravenous; SI RS = systemic Inflammatory response syndrome (le, signi fi cant fever, tachycardia, \n\ntachypnea, leukocytosis) GIT Heavy meat consumption, low fiber \n\nNSAIDs , obesity , and possibly smoking are also correlated with increased complications \n\nAngiodysplasia \n\n What is the likely diagnosis for an adult with episodic, painless dark maroon-colored stool ?\n\nAngiodysplasia \n\ntypically right-sided (versus diverticulosis, which is typically left-sided with passage of bright red blood(arterial); anemic patients may be treated with cautery \n\n Patients with angiodysplasia are more-likely to bleed if they have what other co-existing pathologies? \n\nEnd stage renal disease, vWD, Aortic stenosis \n\nPathogenesis ( low-yield but informative )? \n\nAortic stenosis/AV replacement --> shear stress cleaves vWF multimers --> platelet activation --> bleeding ( Heyde's Syndrome) \n\nvWF normally suppresses angiogenesis --> vWF = angiogenesis = angiodysplasia \n\nColovesical Fistula Toxic Megacolon \n\n400 https://t.me/usmleinnercircle \n\n \n\n> Clinical features of eolovesical fistula\n\n## . Diverticular disease (sigmoid most common ) \n\n> Etiology\n\n## . Cro hn disease \n\n## . Ma li gnancy (colon , bladder, pelvic organs) \n\n## . Pneumaturia (a ir in urine) \n\n> Clinical presentation\n\n## . Fecaluria (stoo l in ur in e) \n\n## . Re c ur re nt urin ary tract infections (m ixed flora) \n\n> Diagnosis\n\n## . CT scan of the abdomen with oral or rectal (not intr aveno us ) contrast \n\n## . Colonoscopy to exclude co l onic ma li gnancy GIT Usually watery diarrhea but CAN be bloody too ! \n\n Confirm via X-ray. \n\nDo not perform enema or colonoscopy due to risk of toxic perforation .\n\n Toxic megacolon is a medical emergency that requires nasogastric decompression , antibiotics ,\n\nIV fluids +/- steroids (if IBD associated ). \n\nMegacolon ie, colonic diameter >6 cm on abdominal x-ray, What IBD complication presents with colonic dilation on X-ray and fever , tachycardia , leukocytosis ,and/or anemia ?\n\nToxic megacolon \n\nmay also have severe bloody diarrhea; highest risk of developing toxic megacolon is early on in the disease Dx for Clostridium: Antigen Stool Test. The presence of C. difficile itself does not indicate infection as many individuals (8-15%) are asymptomatic carriers. \n\n401 https://t.me/usmleinnercircle USMLE Inner Circle \n\nClostridioides difficile colitis \n\n# . Recent antibiotic use or hospitalization Advanced age (>65) \n\nRisk factors Gastric acid suppression (eg , PPI , H 2 blocker) \n\n# . Underlying inflammatory bowel disease Chemotherapy \n\n# . Profuse watery diarrhea \n\nClinical Leukocytosis (-15,000/mm 3).presentation . Fulminant colitis or toxic megacolon Stool PCR for C difficile genes* \n\nDiagnosis Stool EIA for C difficile toxin & glutamate dehydrogenase antigen \n\n# . Hand hygiene with soap & water \n\nInfection Contact isolation \n\ncontrol Seoricidal disinfectants (eg, bleach) \n\n*Genes specific to toxigenic strains are assessed. EIA = enzyme immunoassay; H2 = histamine-2 receptor; PPI = proton pump inhibitor. \n\nToxic megacolon \n\n## . Colonic smooth muscle inflammation & paralysis \n\nPathophysiology . Complication of IBD or infectious colitis \n\n## . t Risk with use of antimotility agents (eg , loperamide) or opioids \n\nClinical features . Systemic toxicity (eg, fever, tachycard ia, hypotension ) . Abdominal pain & distension following diarrheal illness \n\nDiagnosis . Colonic dilation (>6 cm) on imaging . Bowel rest/decompression , antibiotics \n\nTreatment . Corticosteroids if IBD-associated . Surgery for perforation , peritonitis, clinical deterioration \n\nIBD = inflammatory bowel disease. GIT Colonic Pseudo-obstruction (Ogilvie Syndrome) Volvulus Not IV -- C. diff is one of the rare indications for ORAL vancomycin (in C. difficile infections, however, intravenous administration is ineffective, as vancomycin is hardly excreted into the colon (the main site of infection) \n\n402 https://t.me/usmleinnercircle \n\nManagement of C/ostridioides difficile infection \n\nNonsevere COi Classic symptoms: \n\nSevere COi Symptoms + either: Profuse watery diarrhea Leukocytes >15,000/mm' Abdominal pain Serum creatinine >1 .5 mg/dl Oral therapy Fidaxomicin \n\n Vancomycin \n\nFulminant COi Severe COi + either: Hypctension or shock lieus or megacolon lOral vancomycin .. and \n\nIV metronidazole lRefractory COi Consi de r fecal microbiota transplantation Cons ider surg ical intervention \n\nCOi = Clostridioides difficile infection ; IV = intravenous .\n\noral me tror uda zol e can be cons idered for nonsevere CDI if tidaxomicin and vancomycin are unavailable .\n\n.. ConSl dei addi ng vancx,myan enemas if ileus is present Acute colonic pseudoobstruction (Ogilvie syndrome) \n\n Major surgery, traumatic injury, severe infection Electrolyte derangement U K, ! Mg, ! Ca )\n\nEtiologies Medications (eg, opiates, anticholinergics) Neurologic disorders (eg, dementia, stroke) \n\nClinical Abdominal distension, pain, obstipation, vomiting Tympanic to percussion, ! bowel sounds \n\nfindings If perforation: guarding, rigidity, rebound tenderness \n\n> CUWorl d\n\n X-ray: colonic dilation, normal haustra, nondilated small bowel \n\nImaging \n\n CT scan: colonic dilation without anatomic obstruc ti on NPO, nasogastric/rectal tube decompression \n\nManagement Neostigmine if no improvement within 48 hr \n\nSigmoid volvulus \n\n# . Sigmoid co lon redundan cy (eg, dilation/elongation fr om chronic \n\nRisk factors constipati on) \n\n## . Co lonic d ys motility (eg, unde rlying n eu rologic disord er )\n\n## . Slowly progressive abdominal discomfort/distension obstructive \n\nPresentation symp toms (eg, nausea, emesis, obstipation) \n\n## . Abdomen distended & tympanitic to percussion \n\nImaging . X-ray: d ilated, inverted, U-shaped loop of colon (coffee b ea n sign) \n\n## . CT sca n: dilated sigmoid colon, mesenter ic twisting ( wh irl sign) \n\n# . Endoscopic detorsion (eg, flexible s ig mo idoscopy) & ele ct ive sigmoid \n\nManagement colectomy \n\n## . Emergency sigmoid co l ec tomy if perforation/ per itonitis present GIT Cecal volvulus forms a closed-loop obstruction . With continued gas formation by intraluminal bacteria, the lumen of the obstructed bowel loop gradually expands. This leads to slowly progressive (eg, over 2 days) abdominal distension. Sigmoid Volvulus \n\nM/c in old T/t: Endoscopic Detorsion : 1st line \n\nCaecal Volvulus \n\nYounger T/t: Emergency Laprotomy : 1st line \n\nIschemic Colitis \n\n403 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCecal volvulus \n\n# -Id Sigmoid volvulus GIT CT findings indicative of ischemic colitis include colonic wall thickening (edema) and fat stranding. \n\nalso may have air (pneumatosis) in the bowel wall \n\nMicroscopic Colitis Proctalgia Fugax \n\n404 https://t.me/usmleinnercircle \n\nColonic ischemia \n\n. Usually nonocclusive, \"watershed\" ischemia \n\nPathophysiology . Underlying atherosclerotic disease \n\n. State of low blood flow (eg, hypovolemia) \n\n. Moderate abdominal pain & tenderness \n\nClinical features . Hematochezia, di ar rhea \n\n. Leukocytosis, lactic acidosis \n\nDiagnosis . CT scan: Colonic wa ll th icken in g, fat stranding \n\n. Endosccpy: Edematous & friable mucosa Intravenous fl uids & bowel rest \n\nManagem en t . Antibiotics with enteric coverage \n\n. Colon ic resection if necrosis develops \n\nMicroscopic colitis Clinical Watery, nonbloody diarrhea ; feca l urgency & i ncontinence \n\nfindings Abdominal pain, fatigue , weight loss, arthralgias \n\nTriggers Smoking , medications (eg, N SAID s, PPl s, SSRl s) Colonoscopic biopsy with lymphocyt ic infiltration of lamina propria \n\nDiagnosis 0 Collagenous : thickened subepithelial collagen band \n\n> 0\n\nLymphocytic: hi gh levels of int raep ithelial lymphocytes R emove possible triggers \n\nManagement Antidiarrheal medications & budesonide \n\nNSAIDs = nonsteroidal anti-inflammatory drugs; PPls = proton pump inhibitor s; SSRls = select iv e ser ot onin r eu ptake inhibitor s. GIT Proctitis Rectal Prolapse \n\n405 https://t.me/usmleinnercircle USMLE Inner Circle \n\nProctalgia fugax Pathophysiology . Spastic contraction of the anal sphincter \n\n## . Pudenda! nerve compression \n\n## . Female sex Risk factors Other functional pathologies (eg, irritable bowel syndrome) \n\n## . Psychosocial stress, anxiety \n\n## . Recurrent rectal pain unrelated to defecation Manifestations . Episodes lasting seconds to minutes (S30 min) \n\n## . No pain between episodes Evaluation . Normal physical examination (eg, rectal , pelvic, prostate) \n\n## . No laboratory abnormalities \n\n## . Reassurance Management Nitroglycerin cream biofeedback therapy for refractory symptoms .\n\nRadiation proctitis Acute radiation proctitis Chronic radiation proctitis Postradiation onset . sa weeks . >3 months to years \n\n## . Obliterative endarteritis & chronic mucosal ischemia \n\nPathogenesis . Direct mucosal damage Submucosal fi brosis .\n\nManifestations . Diarrhea, mucus discharge, tenesmu s . Severe bleeding \n\n## . Minimal bleeding . Strictures with constipation & rectal pain \n\n## . Severe erythema . Multiple telangiectasias \n\nEndoscopic appearance Edema , ulcerations Mucosal pallor & friability . .\n\nManagement . Antidiarrheals (eg , loperamide} . Endoscopic thermal coagulation \n\n## . Butyrate enemas . Sucralfate or glucocorticoid enemas Rectal prolapse \n\n## . Women age >40 with history of vaginal deliveries/multiparity \n\n## . Prior pelvic surgery Risk factors . Chronic constipation, diarrhea, or straining \n\n## . Stroke, dementia \n\n## . Pelvic floor dysfunction or anatomic defects \n\n## . Abdominal discomfort Clinical . Straining or incomplete bowel evacuation, fecal incontinence \n\n## . Digital maneuvers possibly required for defecation presentation Erythematous mass extending through anus with concentric rings (full-thickness prolapse) or radial invaginations (non-full-. thickness prolapse) \n\n## . Medical \n\n0 Considered for non-full-thickness prolapse Management 0 Adequate fiber & fluid intake, pelvic floor muscle exercises \n\n0 Possible biofeedback therapy for fecal incontinence \n\n## . Surgical \n\n0 Preferred for full-thickness or debilitating symptoms ( eg , fecal incontinence, constipation , sensation of mass) GIT Anal Fissure Anorectal Fistula \n\n406 https://t.me/usmleinnercircle \n\nRectal prolapse Mucosal prolapse Full thickness prolapse \n\nAnal sphincter Protruding mucosa with radial invaginations Erythematous mass with concentric rings \n\nAnal fissures \n\n Local trauma (eg , constipation , prolonged diarrhea, anal sex) \n\nEtiology Inflammatory bowel disease (eg , Crohn disease) \n\n Malignancy \n\n Pain with bowel movements \n\nClinical Bright red blood on toilet paper or stool surface \n\npresentation Most common at posterior anal midline \n\n Chronic fissure may have skin tag at distal end \n\n High-fiber diet & adequate fluid intake \n\n Stool softeners \n\nTreatment \n\n Sitz baths \n\n Topical anesthetics & vasodilators (eg , nifedipine, nitroglycerin) \n\nAnorectal fistula (fistula in ano) \n\n Perianal abscess \n\n# . Crohn disease \n\nCauses \n\n Malignancy, radiation proctitis \n\n# . Infection (eg, lymphogranuloma venereum) Perirectal pain , discharge \n\nClinical manifestations . Inflammatory papule/pustule \n\n# . Palpable fistula tract \n\n Assess extent of fistula \n\n> 0\n\nGentle probe \n\nManagement Imaging (endosonography, fistulogram , MRI) 0. Surgery (eg , fistulotomy) GIT differentiated from Pilonidal tract disease by the presence of a true connection to the intestinal lumen. \n\n## Peritoneum & Mesentery \n\nRetroperitoneal Hematoma \n\n What is the likely diagnosis in a patient on warfarin who complains of weakness and back pain with new-onset anemia (CT below)? \n\nRetroperitoneal hematoma \n\n Diagnosis of a retroperitoneal hematoma is confirmed with non-contrast CT scan of abdomen/pelvis or abdominal ultrasound. \n\n407 https://t.me/usmleinnercircle USMLE Inner Circle \n\nRetroperitoneal abdominal organs \n\nAscending colon \n\n\"Secondarity retroperitoneal (devek>ped intrape ritoneal & migrated rettope ritoneal) .GIT Flank pain with suprainguinal tenderness in patient who had recent cardiac catheterization. Diagnosis? \n\nRetroperitoneal hemorrhage CT Scan \n\n What cardiac catheterization complication presents with sudden hemodynamic instability and ipsilateral flank /back pain ?\n\nRetroperitoneal hematoma \n\ntypically occurs within 12 hours of catheterization; treatment is supportive \n\nMesenteric Ischemia \n\nTreatment :Unstable or signs of peritonitis no imaging emergency lap Stable = endovascular approach (angioplasty, stent) AMI typically presents with sudden-onset , severe , poorly localized (visceral) midabdominal pain \n\naccompanied by nausea and vomiting. \n\n408 https://t.me/usmleinnercircle \n\nAcute mesenteric ischemia Chronic mesenteric ischemia \n\n Rapid onset of periumbilical pain (often severe) Etiology Atherosclerosis (smoking, dyslipidemia) \n\nPresentation Pain out of proportion to examination findings Hematochezia (late complication) Clinical Crampy, postprandial, epigastric pain features Food avers ion & weight loss Atherosclerosis (acute on chronic) \n\nRisk factors Embolic source (thrombus , vegetations) Hypercoagulable disorders \n\nDiagnosis Signs of malnutrition, abdominal bruit CT angiography (preferred), Dopp le r ultrasonography \n\nLaboratory Leukocytosis Elevated amylase & phosphate levels \n\nfindings Metabolic acidosis (elevated lactate) Management Risk reduction (eg , tobacco reduction), nutritional support Endovascular or open surgical revascularization Diagnosis CT (preferred) or MR angiography Mesenteric angiography , if diagnosis is unclear GIT Early in the course of illness, physical examination is typically unremarkable (eg, minimal , diffuse tenderness) despite the presence of severe pain ; this finding is classically referred to as \" pain out of proportion to the examination findings\" \n\nPeritonitis \n\n Hypotension and weakness in the setting of peritoneal dialysis are concerning for peritonitis and sepsis. \n\n## Hernia \n\nUmbilical Hernia Antibiotics AFTER paracentesis since AB therapy can cause negative ascites cultures \n\n409 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSpontaneous bacterial peritonitis \n\n# . Temperature ?_37.8 C (100 F) \n\n# . Abdominal pain/tenderness \n\nClinical presentation Altered mental status (abnormal connect-the- numbers test) .\n\n Hypotension, hypothermia, paraly1ic ileus with severe infection PMNs ?_250/mm 3\n\n# . Positive culture, often gram-negative organisms (eg, Escherichia coli, Klebsiella) \n\nDiagnosis from ascitic fluid Protein <1 g/dl \n\n# . SAAG ?_ 1.1 g/dl Empiric antibiotics - third-generation cephalosporins (eg, cefotaxime) \n\nTreatment . Fluoroquinolones for SBP prophylaxis \n\nPMN = polymorphonuclear leukocytes; SAAG = serum-ascites albumin gradient; SBP = spontaneous bacterial peritonitis. \n\nPeritoneal dialysis-related peritonitis \n\n# . Touch contamination of catheter lumen \n\nPathophysiology Extension of catheter site skin infection .. Abdominal pain fever & nausea \n\nClinical presentation . Diffuse abdominal tenderness rebound \n\n# . Cloudy peritoneal fluid \n\n# . Gram-positive bacteria (-65%) \n\nMicrobiology . Gram-negative bacteria (-30%) \n\n# . Fungal organism (~5%) \n\n# . Clinical presentation (ie, abdominal pain, cloudy fluid) \n\nDiagnosis . Relative neutrophilia on fluid analysis \n\n# . Positive fluid Gram stain or culture \n\nTreatment . lntraperitoneal antibiotics (eg, vancomycin + gentamicin)* *Empiric therapy should cover both gram-positive & gram-negative organisms. GIT Children with large or persistent defects are less likely to experience spontaneous closure and may undergo progressive enlargement of defect over time. \n\nIncisional Hernia Rectus Abdominis Diastasis \n\nRisk factors \n\n1. Chronic abdominal stretching (eg, pregnancy , multiparity), 2. Surgical weakening (eg, prior cesarean deliveries ), and 3. Increased intra abdominal pressure (eg, constipation )due to weakening of the linea alba \n\n410 https://t.me/usmleinnercircle \n\nCongenital umbilical hernia Pathophysiology . Incomplete closure of abdominal muscles \n\n## . Soft, nontender bulge at umbilicus \n\nClinical features . Protrudes with increased abdominal pressure \n\n## . Typically reducible \n\nManagement . Observe for spontaneous closure \n\n## . Elective surgery around age 5 \n\nlncisional hernia Pathogenesis . Breakdown of prior fascial closure \n\n## . Obes i ty \n\n## . Tobacco smoking \n\nRisk factors . Poor wound healing (eg, immunosuppression, malnutrition) \n\n## . Vertical or midline incision \n\n## . Surgical site infection \n\n## . Abdominal mass that enlarges with Valsalva \n\nClinical features . Palpable fascial edge s in nonobese patients . Possible delayed presentation (months-years) \n\n## . Clinical \n\nDiagnosis CT scan of abdomen .\n\nRectus abdominis diastasis \n\nCIU Wo~d GIT Unlike a true hernia, rectus abdominis diastasis has no associated fascial defect \n\nmanaged conservatively with observation and reassurance NOT palpable while supine ( vs Incisional Hernia )\n\n## GIT Tumors \n\n Microcytic (iron deficiency) anemia in an elderly patient is more likely due to colon or gastric \n\ncancer than to pancreatic cancer , which does not typically bleed into the gastrointestinal tract. \n\nEsophagus \n\n Patient with a history of Barrett's Esophagus and the patient has NO dysplasia :\n\nScreening/Surveillance EGDs every 3-5 years \n\n Patient with a history of Barrett's Esophagus and dysplasia present :\n\nScreening/Surveillance every 1-2 years (less than every 3 years) Man over age 50 with chronic GERD and other bad RF (smoking, obesity, high BMI) --> \n\nEGD screening/surveillance recommended \n\nStomach Pancreas imaging helps with disease staging , which determines prognosis and treatment options \n\n411 https://t.me/usmleinnercircle USMLE Inner Circle \n\nStaging of gastric adenocarcinoma \n\nInitial endoscopy/biopsy positive for adenocarcinoma CT abdomen and pelvis PET / CT , endoscopic ultrasound Laparoscopy, CT chest +/- Paracentesis/peritoneal lavage Surgical resection Chemotherapy +/- Palliative surgery \n\n UWorld GIT What imaging modality is preferred for detecting pancreatic tumors of the body /tail (e.g. non-jaundiced patients)? \n\nAbdominal CT scan \n\nultrasound is less sensitive for visualizing the pancreatic body/tail due to overlying bowel gas \n\n Pancreatic cancer classically presents with constant and/or gnawing epigastric pain that is worse at night .\n\nother classic signs include jaundice , anorexia with weight loss , and migratory thrombophlebitis \n\n Depression and associated anxiety may be prodromal features in more than one-third of patients with pancreatic cancer. Patients may describe nonspecific anxiety, a premonitory sensation (\"something bad is going to happen\"), and feeling \"low\" for no reason. \n\n Tumors in the body or tail of the pancreas may present with progressive, constant back pain \n\nthat is worse at night when lying supine. \n\n Pancreatic surgery C/I is tumor encasement in SMA artery .Tumor in head has better prognosis than in tail. \n\n Atypical DM (eg, DM presenting in a thin, older patient) should raise suspicion for pancreatic cancer What is the next step in management for an older patient with a significant smoking history that presents with painful , pruritic red streaks on the arm , with a similar episode two weeks prior on the chest that self-resolved, and mild epigastric pain ?\n\nAbdominal CT \n\nthis patient has migratory superficial thrombophlebitis ( Trousseau's syndrome ), which is associated with occult visceral malignancy ( pancreas , stomach, lung, prostate) Alcohol can cause chronic pancreatitis, which is associated with increase risk of pancreatic cancer, but it is not as significant as association bt. smoking and pancreatic cancer \n\n412 https://t.me/usmleinnercircle \n\n> Major risk factors for pancreatic cancer Pancreatic adeno carclnoma\n> First-degree relative with pancreatic ca ncer Smoking\n> Hereditary Hered ita ry pancreatitis\n> Gennli ne mutations (eg, BRCA1, BRCA2, Peutz-Jeghers syndrome)\n> Ri sk factors Hereditary pancreatitis No nh eredit ary chronic panc reatitis\n> Obesity & lack of physical activity Cigarette smo king (most significan t) Sys temic symp toms (eg, weight los s, anorexi a) (>85%)\n> Environmental Obesity, low physical activity Abdominal pa in /b a ck pain (80%) Nonhereditary ch ron ic pancreatitis Clin ic al Jaundice (56%)\n> presenta ti on Recent-o nset atypical diabetes mellitus\n> Une xplai ned migrat ory supe rficial thrombophlebi ti sHep atome galy & a sc ites w it hmet as ta sis\n> Laboratory Cho lestasis\n\n(f alkaline p hosp hatase & dir ec t bilirubin) \n\n> stud ies\n\n f Cancer -associ ated antigen 19-9 (not as a screening test) Abdominal ultrasound (if jaundiced) or CT scan (i f no jau ndice) GIT Presents with unexplained superficial venous thrombosis at unusual sites \n\n Advanced pancreatic adenocarcinoma , can obstruct the common bile duct (CBD) and cause extrahepatic cholestasis. Patients typically develop jaundice and pruritus due to direct (conjugated) hyperbilirubinemia and are at increased risk for cholangitis. Given the poor overall prognosis in surgically unresectable pancreatic cancer, palliative care is usually preferred. \n\nEndoscopic stent placement can effectively relieve CBD obstruction in most patients and is less invasive and less risky than surgery. \n\nSurgical bypass (eg, anastomosis between the gallbladder or CBD and jejunum) is sometimes considered as a second-line option in patients in whom stent placement would be technically challenging REMEMBER this, this is important ! \n\nColon \n\n413 https://t.me/usmleinnercircle USMLE Inner Circle \n\nTrousseau's Syndrome migratory thrombophlebitis (assoc ia t ed wi th panc rea ti c cance r) Colon cancer screening \n\n Start at age 45: \n\no Colonoscopy every 10 years \n\nPatients at o gFOBT or FIT every year \n\n0 FIT-DNA every 1-3 years \n\naverage risk o CT colonography every 5 years \n\n0 Flexible sigmoidoscopy every 5 years (or every 10 years with annual FIT) Colonoscopy at age 40 (or 10 years prior to age of diagnosis in \n\nPatients with FDR with CRC or high-risk FDR, whichever comes first) \n\nadenomatous polyp* . Repeat every 5 years (every 10 years if FDR diagnosed at age >60) \n\nPatients with ulcerative colitis Start screening 8-10 years after diagnosis Colonoscopy every 1-3 years Adenomatous polyp .e10 mm , high-grade dysplasia, villous elements (for example). \n\nCRC =colorectal cancer; FDR= first-degree relative; FIT= fecal immunochemical test; FIT-DNA= multitarget stool DNA test; \n\ngFOBT =guaiac-based fecal occult blood test. GIT For individuals with a history of abdominopelvic radiation treatment , colon cancer screening should commence at an earlier age (eg, age 30-40) than that recommended for average-risk patients (ie, age 45). Colonoscopy is preferred, although acceptable alternatives include fecal occult blood testing and fecal DNA testing. What characteristics (growth pattern, histology) of colonic adenomatous polyps suggest greater malignant potential ?\n\nsessile growth and villous histology \n\nother signs of malignant potential include large size (> 1 cm) and high number (> 3 concurrent adenomas) \n\n Due to their exceedingly high risk of CRC, patients with classic FAP (and sometimes attenuated FAP) need an elective total proctocolectomy in their late teens or early twenties . However, in younger patients (such as 9-year-old boy), surgery is usually delayed in favor of close surveillance with frequent colonoscopy until patients have completed puberty and matured both physically and emotionally. Urgent total proctocolectomy is performed no matter the patient's age in those with CRC or adenomas with high-grade dysplasia; other indications for colectomy include severe symptoms related to colonic neoplasia (eg, hemorrhage) and a significant increase in polyp number during the screening interval Regular aspirin or nonsteroidal anti-inflammatory drug use has been associated with reduced incidence of CRC in patients at average risk but does not influence the chances of developing CRC in FAP. Whenever possible, patients with adenocarcinoma of the colon should be offered surgical resection \n\nwith curative intent . When metastatic spread is confined to the liver, surgical resection of both the \n\n414 https://t.me/usmleinnercircle \n\nColon cancer screening in high-risk patients Family history of adenomatous Colonoscopy at age 40 or 10 years before polyps or CRC th e age of diagnosis in the relative (whichever comes first) First- Inflammatory bowel disease Begin 8 years po st diagnosis Ulcerative colitis (12-15 years if disease only in left colon) Crohn coli ti sColonoscopy with biopsies every 1-2 years\n> Familial adenomatous polyposis Begin at age 10-12 Colonoscopy every year Heredit ary nonpol yposis CRC Begin at age 20-25 (Lynch syndrome) Colonoscopy every 1-2 years\n\nRisk factors for colon cancer Lifestyle . Frequent consumption of red/processed meat \n\n> factors\n\n## . Tobacco, alcohol use \n\n## . Personal/family history of adenomatous polyps or colon cancer \n\n> Medical/family\n\n## . Inher ite d colon cancer syndromes (eg , familial adenomatous polyposis, Lynch syndrome) \n\n## . Ulcerative colitis \n\n> history Diabetes/obesity\n\n## .. Pr ior abdominopelvic radiation \n\n> Protective\n\n## . High-fiber diet \n\n> factors\n\n## . Aspirin/NSAID use \n\n> NSAID = nonsteroidal anti-inflammatory drug.\n\nGIT hepatic mass and the primary tumor can be curative , and often provides increased long-term (>5 yr) survival even when not curative. \n\nCombined chemotherapy and radiation are used for nonoperable rectal adenocarcinoma as well as anal squamous cell carcinoma; however, radiation therapy is typically avoided in tumors proximal to the rectum because the adverse effects (eg, radiation enteritis) can be severe. \n\nPJ Syndrome \n\nLiver \n\n Is needle biopsy recommended for a patient with a hepatic adenoma ?\n\nNo (due to risk of bleeding) \n\n415 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSurveillance after colon cancer resection Staging evaluation for rectal adenocarcinoma Stage I Colonoscopy in 1 yr & then every 3-5 yr Tumor markers Carcinoembryonic antigen \n\n Colonoscopy in 1 yr & then every 3-5 yr Imaging CT scan: chest, abdomen, pelvis \n\nStages II & Ill Periodic CEA testing \n\n Annual CT scan of the ches t, abdomen ( pelvis) Endoscopy/direct visualization Colonoscopy \n\n# . Individualize \n\nStage IV Consider stage 11/111 strategy but more frequent CT scans \n\nCEA = carcinoembryonic antigen. \n\nPeutz-Jeghers syndrome \n\n Autosomal dominant disorder \n\nEtiology Tumor suppressor gene mutation causes unregulated tissue growth \n\n## . Pigmented macules (eg, lips, buccal mucosa, palms/soles) . ~2 gastrointestinal hamartomatous polyps \n\no Abdominal pain due to obstruction or intussusception \n\nClinical features o Anemia due to acute/chronic bleeding 0 Rectal prolapse \n\n## . t Cancer risk (eg, gastrointestinal, breast, genital tract) \n\n## . Positive family history \n\nDiagnosis . Genetic testing \n\nManagement Annual anemia screening . Cancer screening (eg , upper/lower endoscopy) \n\nSolid liver masses Hepatic adenoma \n\n Associated with anomalous arteries \n\nFocal nodular hyperplasia Arterial flow & central scar on imaging \n\n## . Benign epithelial liver tumor \n\nEpidemiology Prima ri ly young women on oral contraception .\n\nHepatic adenoma Women on long-term oral contraceptives \n\n## . Possible hemorrhage or malignant transformation . Often asymptomatic (incidentally found) \n\nManifestations Regenerative nodules Acute or chronic liver injury (eg, cirrhosis) \n\n## . Episodic right upper quadrant pain . Systemic symptoms \n\nHepatocellular carcinoma . Chronic hepatitis or cirrhosis \n\n## . Solitary, solid lesion in right lobe of liver \n\nImaging Multiple lesions occasionally occur .\n\n# . Elevated a fetoprotein \n\nLiver metastasis . Single/multiple lesions \n\n## . Asymptomatic & <5 cm - stop oral contraception \n\nTreatment . Symptomatic or >5 cm - surgical resection . Known extrahepatic malignancy \n\n## . Malignant transformation (~10%) \n\nComplications . Rupture & hemorrhagic shock GIT surgical excision is preferred \n\n Hepatic adenoma can be seen in OCP use or Pregnancy \n\n AFP is elevated in ~50% of HCC cases ; therefore, it can serve as an important diagnostic clue (when elevated) but cannot be used to rule out the diagnosis \n\nMALToma \n\n 90% MALToma cases are ass with H. pylori. All patients with MALT lymphomas should be tested for H pylori infection, and patients with a positive result who have early-stage MALT lymphoma should undergo H pylori eradication therapy (eg, quadruple therapy). The majority of patients achieve complete remission with antibiotic treatment. Patients with more advanced malignancies or with H pylori -negative tumors should be considered for radiation therapy, immunotherapy (eg, rituximab), or single-agent chemotherapy. \n\n Pernicious anemia is related to an increased risk of gastric adenocarcinoma and gastric carcinoid tumors NOT MALToma \n\n## Miscellaneous \n\n416 https://t.me/usmleinnercircle \n\n> Areas of referred pain to the abdomen\n> Cholecystitis\n> WWor1d\n> Unintentional weight loss in elderly patients Definition >5% involuntary weight loss over 6-12 months Malignancy, depression Chronic end-organ disease (eg, CKD, COPD)\n> Causes Neurologic disease (eg, oropharyngeal dysphagia) Social factors (eg , poverty, isolation) Diminished smell &taste, poor dentition\n> CKD =chronic kidney disease; COPD =chronic obstructive pulmonary disease.\n\nGIT Advanced end-organ disease contributes to weight loss via components of both anorexia (ie, loss of appetite) and cachexia (ie, inflammatory loss of muscle mass). In such patients without findings to suggest malignancy (eg, blood in the stool, hypercalcemia, unexplained anemia), watchful waiting is typically most appropriate. This is especially true for \n\nelderly patients with limited life expectancy, and other explanations for weight loss (eg, CKD) because watchful waiting avoids diagnostic testing that is unlikely to improve quality of life or life expectancy .Furthermore, unnecessary diagnostic testing may increase patient anxiety, physical discomfort, and financial stress. In addition, such patients with evidence of malnutrition (eg, BMI <18.5 kg/m2) often benefit from nutritional supplementation (eg, high-calorie supplement drinks), which can help reverse cachexia progression (protein-energy wasting). \n\nAbdominal Compartment Syndrome \n\n Although reduced cardiac preload is typically reflected in a low CVP , the two are uncoupled in ACS, where CVP is increased (despite reduced preload) due to external compression rather than increased intravenous volume. Bladder pressure measurement can estimate intraabdominal pressure when abdominal compartment syndrome (ACS) is suspected. A patient develops hypotension, JVD, and distended abdomen 18 hours after abdominal surgery. He was transfused with 6 units of PBRC during surgery. Urine output is decreased . Labs show increased BUN:Cr . What is the treatment? \n\nAbdominal decompression by laparotomy with temporary closure (reopen abdomen and cover with plastic )\n\nAbdominal compartment syndrome leads to decreased preload and thus hypotension and hypoperfusion > AKI, tachycardia \n\n## Paeds GIT \n\n417 https://t.me/usmleinnercircle USMLE Inner Circle \n\nAbdominal compartment syndrome \n\n# . t lntraabdominal pressure causing organ dysfunction \n\nEtiology . Risk fa ctors: massive fluid resuscitation, major intraabdominal surgery or pathology \n\n## . Tense, distended abdomen \n\n## . t Ventilatory requirements (diaphragmatic elevation, t\n\nClinical intrathoracic pressure) \n\n## . t CVP (venous compression but L venous return & cardiac \n\nmanifestations preload) \n\n---. Hypotension, tachycardia (L venous return & cardiac output) \n\n## . L Urine output (L intraabdominal or 1i an perfusion) . Temporizing measures: \n\n> 0\n\nAvoid over resuscitation with fluids \n\nManagement 0 L lntraabdominal volume (eg, NG tube) \n\n> 0\n\nt Abdominal wall compliance (eg, sedation) \n\n## . Definitive man age ment: surgical decompression \n\nCVP :;;; ce ntral venous pressure ; NG := na sogastric. GIT Tracheoesophageal Fistula Foreign Body Ingestion \n\n What is the next step in management for a symptomatic child with evidence of a swallowed coin in the esophagus on X-ray ?\n\nFlexible endoscopy \n\nendoscopy is both diagnostic and therapeutic; asymptomatic children may be observed for 24 hours after ingestion (coins are not sharp and the metals used are not toxic) (vs Battery; \n\nnecessary to prevent further mucosal damage and esophageal ulceration; removal is necessary for both symptomatic and asymptomatic patients) \n\n What is the next step in management for a child that swallowed a battery that is located in the stomach on X-ray? \n\nObservation for 24 - 48 hours \n\nbatteries located distal to the esophagus typically pass uneventfully Trachea: Bronchoscopy ; Esophagus: Endoscopy \n\n418 https://t.me/usmleinnercircle \n\nTracheoesophageal fistula with esophageal atresia Pathogenesis . Defective division of foregut into esophagus & trachea \n\n## . Most commonly results in proximal esophageal pouch & fistula between distal trachea & esophagus \n\nClinical . Coughing, choking, vomiting with feeding . Excessive oral secretions \n\nfeatures . Commonly part of VACTERL association \n\nDiagnosis . Inability to pass enteric tube into stomach \n\n## . X-ray: enteric tube coiled in proximal esophagus \n\nManagement . Surgical correction . VACTERL screening: echocardiography, renal ultrasound \n\n> VACTERL =Vertebral, Anal ,Cardiac, TracheoEsophageal, Renal, Limb defects.\n\nGIT Sharp object (eg, needle, safety pin) in the esophagus, stomach, or proximal duodenum \n\nIf a sharp foreign body is distal to the proximal duodenum in an asymptomatic patient, observation with repeat x-ray in 12-24 hours may be appropriate because these objects are usually excreted uneventfully \n\nSymptoms of esophageal obstruction (eg, drooling, inability to swallow secretions) Symptoms of respiratory compromise Button battery in the esophagus (due to the risk of electrical and chemical injury) Magnets in the esophagus or stomach (due to the potential for bowel entrapment as a result of magnetic attraction across intestinal segments) \n\n In cases of high-risk esophageal foreign bodies, such as magnets, button batteries, and sharp objects (fish bone), immediate endoscopic removal is required to prevent complications. Ingestion of 2 magnets , especially if swallowed separately, can entrap bowel via attraction across varying intestinal segments and lead to necrosis , fistulae, or perforation . Therefore, magnets visualized in the esophagus or stomach on x-ray require immediate endoscopic removal even if patients are asymptomatic. \n\nIn case of single magnet ingestion; observation can be considered. \n\nCrying Infant \n\n419 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nSuspected foreign body ingestion \n\n# !PA & lateral x-rays (CT scan if object not visible on x-ray) \n\n# AHigh-risk features No high-risk features \n\n# ! !Endoscopic removal Serial x-rays \n\n# ANo transi t: Endoscopic \n\nremoval \n\nObject movi ng distally: \n\nPA = posteroanterior .\n\n\"Patient has respiratory or obstructive symptoms ;\n\nobject is a button battery , magne or sh arp item ,\n\nNo intervention \n\n UW Ol1d GIT Constipation Infantile Colic: benign; parents should be reassured and taught soothing/feeding techniques \n\n420 https://t.me/usmleinnercircle \n\nCrying in young infants Diagnosis Key features Normal . Intermittent, consolable, <3 hr/day \n\nColic 2:3 hr/day (usually evening), 2:3 days/week . Healthy infant age <3 months \n\nGastroesophageal . Frequent spit-up \n\nreflux disease Back-arching after feeding Acute otitis media: bulging tympanic membrane, fever \n\nInfection Meningitis: fever, lethargy, bulging fontanel Septic arthritis: fever, limited extremity movement . UTI : fever, vomiting , poor feeding . Episodic irritability with legs drawn to abdomen \n\nlntussusception Bilious emesis, bloody stools \n\nTorsion Testicular swelling or abdominal distension (ovarian) . Hair tourniquet: hair accidentally wrapped around digit \n\nTrauma Corneal abrasion : tearing, photophobia; + fluorescein test Abuse/fracture: bruising, laceration, asymmetric movements \n\nUTI = urinary tract infection. \n\nPediatric constipation Pathologic Functional \n\n# . Delayed meconium passage Solid food introduction \n\nRisk factors . Down syndrome (associated with HD Toilet training & intestinal atresia/stenosis) School entry . Poor weight gain or linear growth Absence of pathologic features . Narrow (ribbon) stools \n\nHistory . Painful , infrequent, large-. Blood mixed in stool . Bilious vomiting or fever caliber or pellet-like stools* . Fecal soiling (encopresis) . Displaced anus, t rectal tone, or Absence of pathologic sacral anomalies (eg , hair tuft) features \n\nExamination . Abnormal lower extremity neurologic . Mild abdominal distension findings (eg , weakness) Anal fissure ( rectal Severe abdominal distension bleeding) Work up for organic cause Age-appropriate toileting a Common (eg , celiac disease, plan . Dietary changes (t \n\nManagement hypothyroidism) fiber/water) 0 Urgent (eg , HD, CF, spinal . Laxatives (eg, polyethylene dysraphism) glycol) Benign features refractory to functional constipation management may also be pathologic. \n\nCF = cystic fibrosis; HD= Hirschsprung disease. GIT Initial management is dietary , including the addition of apple, prune, or pear juice/puree .These nondigestible, osmotically active carbohydrates (eg, sorbitol) pull water into the gastrointestinal tract, thereby softening stool. Pathogenesis of infant dyschezia involves the following: \n\nFailure to coordinate increased intraabdominal pressure with relaxation of the pelvic floor muscles \n\nInadequate abdominal muscle tone to produce an effective Valsalva maneuver These mechanisms result in characteristic findings of crying , turning red in the face , and straining for greater than 10 minutes, followed by passage of a soft, nonbloody stool. \n\nT/t: Reassurance only \n\nVomiting Recurrent cystitis ( UTI's ) (due to mass effect on the bladder, preventing voiding and leading to urinary stasis )\n\n421 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPediatric functional constipation \n\n Initiation of solid food & cow's milk \n\nRisk factors Toilet training School entry Painful/hard bowel movements \n\nClinical features Stool withholding Encopresis (fecal incontinence) Delayed passage of meconium Fever or vomiting \"Ribbon\" stools \n\nAlarm signs Poor growth Severe abdominal distension Abnormal examination findings (eg, displaced anus, tuft at gluteal cleft) Anal fissure \n\nComplications Hemorrhoids Enuresis/urinary tract infections \n\n j Dietary fiber & water intake Limit cow's milk (<24 oz/day) \n\nTreatment Laxatives (eg, polyethylene glycol) Age-appropriate toileting guidance Enemas/suppositories \n\nApproach to the straining infant \n\nStraining infant Ill-appearing or Well-appearing red flag s present i! ! l\n\nSerious organic cause Loose stools Normal stool Hard or Hirschsprung disease mucus & blood consistency pellet- li ke stools Cystic fibrosis \n\n## ! ! ! Spinal dysraphism Hypothyroidism Food induced Normal infant Functional protein enterocolitis dyschezia constipation \n\n( anal fi ssure if \n\nblood present) severe abdominal distention, abnormal rectal tone or sacral findings, de layed passage of meconium, failure to thrive @UW or ld \n\nGIT What is the next step in management for an infant with failure to thrive that spits up formula after each feed ?\n\nproton pump inhibitors and/or thickened feeds (e.g. adding oatmeal) \n\nfailure to thrive indicates that this is pathologic GERD (vs Adequate wt gain in physiologic) be careful with PPIs in infants loss of acidity predisposes to increased risk of infections \n\nCyclical Vomiting Syndrome Positional therapy (e.g. hold infant upright for 20-30 minutes after frequent, small-volume feeds) \n\n422 https://t.me/usmleinnercircle \n\nHistory Symptoms Differential diagnosis of regurgitation & vomiting in infants Diagnosis Clinical features Management \n\n## . Physiologic Reassurance .o Asymptomatic . Positioning therapy \n\n> 0\n\n\"Happy spitter\" \n\nGastroesophageal reflux . Pathologic (GERD) Thickened feeds \n\n> 0\n\nFailure to thrive Antacid therapy \n\n> 0\n\nSignificant irritability . If severe , esophageal pH probe monitoring \n\n> 0\n\nSandifer syndrome & upper endoscopy \n\n## . Regurgitation/vomiting \n\nMilk protein allergy . Eczema . Elimination of dairy & soy protein from diet \n\n## . Bloody stools \n\n## . Projectile nonbilious vomiting Abdominal ultrasonography \n\nPyloric stenosis . Olive-shaped abdominal mass Dehydration, weight loss . Pyloromyotomy \n\n## .\n\nGERD = gastroesophageal reflux disease. \n\n## ..\n\n## ..\n\n> C\\/World\n\nUnstable Free air Emergency laparotomy \n\nCyclic vomiting syndrome \n\nPersonal or family history of migraines Eva lua ti on of bili ou s emes is in t he neonate Bilious emesis J\n\nStable Abdominal x-ray J\n\n, Dilated loops of bowel J Normal \n\n# 'Increased rectal tone and/or delayed - No ~ Upper GI series passage of meconium Yes \n\n# 'Contrast enema Microcolon Meconium ileus Rectosigmoid transition zone Hirschsprung disease Right-sided ligament of Treitz Malrotation Double bubble sign ) \n\n## l\n\nDuodenal atresia \n\nDiagnostic criteria of cyclic vomiting syndrome \n\nEpisodes often have identifiable trigger (eg , infection, stress) ~3 episodes in a 6-month period Stereotypical vomiting episodes \n\no Acute onset of nausea, abdominal pain, headache, vomiting \n\n> 0\n\nSelf-limited, lasting 1-2 days Between episodes \n\n> 0\n\nUsually asymptomatic Easily recognizable to family (stereotypical) Lasts 1-10 days Vomiting ~4 times/hr at peak No symptoms in between vomiting episodes No under1ying condition can be identified \n\n> 0\n\nOften regular intervals (eg , 2-4 weeks) II GIT What is the likely diagnosis in a child that presents with self-limiting, recurrent nausea and vomiting at the same time each month with no symptoms in between episodes? \n\nCyclic vomiting syndrome \n\nTreatment: Abortive: Triptans \n\nSupportive: Anti-emetics \n\nFood Allergen Proctocolitis \n\n Symptoms suggestive of a different diagnosis include failure to thrive , profuse diarrhea ,and forceful vomiting \n\nBreastfeeding D/D: MECKEL but very rare in less than 6 months age \n\n423 https://t.me/usmleinnercircle USMLE Inner Circle \n\nM il k- or soy-protein-induced col itis Risk Family history of allergies, eczema , or asthma \n\nfactors \n\n Presents at age 2-8 weeks \n\nCl inical Regurgitation or vomiting \n\nfeatu res +/-Painless bloody stools +/- Eczema Elimination of milk & soy from maternal diet of \n\nT reatment exclusively breastfed infants Initiation of hydrolyzed formula in formula -fed infants \n\nPr ognos is Spontaneous resolution by age 1 year \n\nManagement of food protein-induced allergic proctocolitis (FPIAP) \n\nBreastfeeding J\n\nInfant with presumed FPIAP* Formula-feeding J\n\nEliminate common triggers from maternal diet (eg, dairy, soy) Switch to hypoalle rg enic (eg , hydrolyzed) formula FPIAP confirmed : Reintroduce offending protein around age 1 Symptom resolution? J\n\n# 1 Consider evaluation for \n\n+- Yes No---+ alternate diagnosis (eg , flexible sigmoidoscopy) \n\n'Well-appearing ,nfant age <6 months with blood-strea ked stools and nonlocal exam ination C\\/Wof1d \n\nlgE- & non-lgE-mediated food allergies Example Age Symptom onset Clinical features \n\n Urticaria Immediate \n\nlgE mediated Anaphylaxis Any (<1 hr) Vomiting , wheezing Angioedema, hypotension Food protein- Painless, bloody stools induced allergic <6 months Insidious proctocolitis Well appearing \n\nNon-lgE mediated Food protein- Profuse vomiting, diarrhea ( induced enterocolitis <12 months Within hours blood), dehydration, lethargy syndrome Ill appearing GIT Casual, moderate alcohol use is considered safe and not a contraindication to breastfeeding. Mothers with Hep B and Hep C can breast feed given their nipples are not cracked or bleeding. Neonates should breastfeed every 2 - 3 hours for > 10 - 20 minutes per breast during the first month of life \n\nor approximately 8 - 12 times per day \n\n Exclusive breastfeeding is recommended for the first 6 months of life. \n\n All exclusively breastfed infants should also be started on vitamin D supplementation, Iron supplementation for Premature babies <6 months and Vitamin B12 for babies with strict vegetarian mothers. \n\nDehydration \n\n424 https://t.me/usmleinnercircle \n\nBirth \n\nBreastfeeding benefits & contraindications Benefits Contraindications \n\n Active untreated tuberculosis \n\n(mothers may breastfeed after 2 More rapid uterine weeks of anti-tuberculin therapy) involution & decreased Maternal HIV infection (in postpartum bleeding developed countries where Faster return to prepartum formula is readily available) weight Herpetic breast lesions \n\nMaternal Improved child spacing Varicella infection <5 days prior Improved maternal -i nfant to or within 2 days of delivery bonding Specific maternal medications Reduced risk of breast Chemotherapy or ongoing \n\n& ovarian cancer radiation therapy Active abuse of street drugs or \n\nalcohol \n\n Improved immunity \n\n Improved gastrointestinal function Prevention of infectious diseases: \n\n> o\n\nOtitis media Infant o Gastroenteritis Galactosemia \n\n> o\n\nRespiratory illnesses \n\n> o\n\nUrinary tract infections Decreased risk of childhood cancer, type I diabetes mellitus &necrotizing enterocolitis \n\nTimeline of infant nutrition \n\n6 months 1 year Exclusive bre astfee ding Intro duct ion of pu reed foods In t r oduct i on of cow 's milk GIT Mild-moderate: Oral Rehydration Moderate-severe: IV bolus of isotonic solutions 20Ml/ Kg (e.g. normal saline, lactated Ringer's) \n\n Healthy infants may lose up to 7% of their birth weight in the first 5 days of life. \n\ndue to excretion of excess fluid acquired in utero and during labor; no treatment is required \n\n Approximately how many wet diapers should a 5-day-old newborn make per day? \n\n> 5 wet diapers/per day \n\nas a general rule, the number of wet diapers should equal age in days for the first week of life; after the first week, infants should have > 6 wet diapers per day \n\nMidgut volvulus \n\nSurgical emergency that classically presents in a neonate with congenital malrotation, manifesting as bilious vomiting and abdominal distention. \n\ndiagnosed using an upper GI series , which may show a \"corkscrew\" pattern; untreated volvulus can progress to bowel ischemia and perforation \n\n425 https://t.me/usmleinnercircle USMLE Inner Circle \n\nMild dehydration (3-5% volume loss) presents with a history of decreased intake or increased fluid loss with minimal or no clinical symptoms .Moderate dehydration (6-9% volume loss) presents with decreased skin turgor , dry mucus membranes ,tachycardia , irritability, a delayed capillary refill (2-3 seconds) , and decreased urine output. Severe dehydration (10-15% volume loss) presents with cool , clammy skin , a delayed capillary refill (>3 seconds}, cracked lips, dry mucous membranes , sunken eyes , sunken fontanelle (if st i ll present), tachycardia , lethargy, and minimal or no urine output. Patients can present with hypotension and signs of shock when severely dehydrated . \n\nEvaluation of neonatal hydration Neonatal weight trends \n\n Decreased wet diapers Absence of tears \n\nNatural Wei ght loss in first 5 days of life (eg, excretion of excess fluid , delayed \n\ncourse lactogenesis) \n\nSigns of Sunken fontanelle Weight regained (ie, back to birth we ight} by a ge 2 weeks \n\ndehydration Dry mucous membranes Decreased skin turgor S10% of birth weight lost Delayed capillary refill 0 Provi de reassurance & continue to monitor \n\n## . >10% of birth weight lost &/or signs of dehydration (eg, poor urine Continue exclusive breastfeeding < 7% Follow-up at age 10 - 14 days to check that infant has regai n ed birth weight \n\nManagement Management output, sunken fontanelle} \n\no Assess for breastfeeding complication s (eg, tongue-tie) 0 Measure weights daily \n\no Consider formula supplementation \n\nof weight loss Assess for oromotor dysfunction 0 Consider serum electrolytes & glucose measurements \n\n~ 7% Assess for lactation failure Daily weights Consider formula supplementation GIT For neonates with suspected volvulus (eg, bilious emesis, x-ray with dilated loops of bowel, normal rectal examination) who are hemodynamically stable, upper GI series (consisting of x-rays with contrast material for improved visualization) is the diagnostic gold standard .In contrast, in a neonate with bilious emesis who is hemodynamically unstable (eg, hypotension, tachycardia) or has peritoneal signs (eg, firm, distended, tender abdomen), the next step in management is exploratory laparotomy . Surgical exploration should not be delayed for diagnostic or repeat imaging due to increased risk of mortality \n\nPyloric Stenosis Acute Symptoms in Infants . Chronic in Older Children and adults .\n\n426 https://t.me/usmleinnercircle \n\nMalrotation with midgut volvulus \n\n# . Failure of normal embryonic gut rotation \n\n# . Narrow mesenteric base allows for j small bowel mobility \n\nPathogenesis Twisting of small bowel around superior mesenteric artery -> gut ischemia & necrosis \n\n# . Most common in infancy {usually age <1 month) \n\nClinical Acute: bilious emesis, abdominal distension \n\nfeatures Chronic: intermittent abdominal pain & vomiting , failure to thrive \n\n# . Untreated: hematochezia, peritonitis & shock Abdominal x-ray: dilated bowel , air-fluid levels, pneumoperitoneum \n\nDiagnosis . Upper gastrointestinal series {gold standard): li gament of Treitz on right; corkscrew, or bird's-beak duodenum \n\n# . Emergency laparotomy {to relieve volvulus) \n\nTreatment . Ladd procedure (to reposition malrotated bowel) \n\nVolvulus \n\n..... \\ ' r-... \n\n# --GIT Erythromycin : either through direct administraton or through breast milk; pyloric stenosis is also associated with formula feeds \n\n How soon after birth does pyloric stenosis typically present? \n\n~ 3 - 5 weeks \n\ntakes time for hypertrophy to develop; helps distinguish from intestinal atresia (bilious vomit within 1 - 2 days) \n\n What acid-base disturbance is associated with pyloric stenosis ?\n\nHypokalemic, hypochloremic metabolic alkalosis \n\nsecondary to vomiting of gastric acid and subsequent volume contraction; should be corrected prior to pyloromyotomy to reduce risk of post-operative apnea \n\nNeonatal Jaundice U/S can also detect pyloric muscle diameter and thickness \n\n427 https://t.me/usmleinnercircle USMLE Inner Circle \n\nInfantile hypertrophic pyloric stenosis \n\n First-born boy \n\nRisk factors Erythromycin Bottle feeding Projectile nonbilious emesis \n\nPresentation Poor weight gain Dehydration Olive-shaped abdominal mass Hypochloremic metabolic alkalosis \n\nDiagnostic studies Thickened pylorus on abdominal ultrasound \n\nTreatment Intravenous rehydration Pyloromyotomy \n\nManagement of neonatal unconjugated hyperbilirubinemia \n\nTotal bilirubin elevated for age J\n\nUnconjugated bilirubin >25 mg/dl J\n\nUncon jugated bilirubin above photothera py threshold for age \n\nNo ----'---- Yesl \n\nIncrease feed volume/frequency & monitor In itiate phototherapy 'eg, RhD lncomp abbd1t y. glucose-6- ph os pha tase deficiency, Unresponsi ve to therapy (eg , rapid rate of rise) In itiate exchange transfusi on Evaluate for \n\ni:iathol og ic causes \n\nCuwor ld GIT Most neonates with symptomatic congenital infections typically have other manifestations, such as growth restriction (eg, microcephaly) or hepatosplenomegaly. 428 https://t.me/usmleinnercircle \n\nNwvia; \n\nApproach to neonatal cholestasis \n\nNeonatal cholestasis j\n\nIAbdomi na l ultrasound j\n\nAbnorma l or Cystic dilation Isolated hepatomegaly or normal absent gallbladder of biliary tree Biliary atresia j Biliary cyst J\n\nInfectious evaluation J\n\n## l\n\nGenetic/metabolic evalua ti on CMV, toxoplasmosis, AAT deficiency HSV, UTl/sepsis Dubi n- Johnson syndrome Ga lactosemia Cystic fibrosis \n\n> 'Dark unne, acholic stools, conjugated hyperbolirubinemia.\n> AAT\n\n= atpha-1 antitryps,n; C MV = cytomegalovirus; HSV = herpes si mp lex virus; Ul t = urinary tract infection. IC>UW<>< ld \n\nNeonatal indirect hyperbilirubinemia Cause Examples \n\n## . Immune-mediated hemolysis (Coombs positive) \n\n> 0\n\nRh isoimmunization \n\n> 0\n\nABO incompatibility \n\ni Bilirubin . Nonimmune-mediated hemolysis (Coombs negative) \n\nproduction 0 RBC membrane defects (eg, spherocytosis) \n\n> 0\n\nRBC enzyme defects (eg, G6PD deficiency) \n\n## . Cephalohematoma \n\n## . Polycythemia \n\nL Bilirubin . Gilbert syndrome \n\nclearance . Crigler-Najjar syndrome \n\ni Enterohepatic . Lactation failure jaundice \n\ncirculation . Breastmilk jaundice \n\nG6PD = glucose-6-phophatase dehydrogenase; RBC = red blood cell. \n\n-/V\\osl- C.0\"\"\"\"'\"' c,..,5(. ,\\ P,.;.,lo~ \"'~ ,;... ~ ~ \n\n> 2./2.\n\nI--..~..-.. of IILF o.-' ,~ .... ~ ~.,+;,_ \"'-C,\\-\"\"\"\"' \n\n~e:- l~ B ii'ii ~- \\'.)ho\\.+~ 0\"''-a- .... , ~ l---------,.~ ~, 8 -, \"e--.,,,, - .,_. ~ a.. ~~ ~ '\":..i - \"\" ~- ~ .. ~(-.,., --- ~ -,., ~~--------------------~ ---c..., - ~ --.-~-ul ------u- l _s_ ~_\" _' _h _ 1t _,._. _\n\n---------------------------~ '\"~ co= -------------' B;I\", ----'------1 ~I I(. ~ l-\\1M \n\n11 ,,~i (~1) /' ;! ~ .1.~~--K\"\" ! l,\\0(0,\\J~ Scf>J~~ 1e\n\n----------------------,L-- / -1' ,._ '3si >--- ---: C'f\"..l -;-;-, o\"'-\"'rt -,-,-;,--: \"\"\"' -,-----------tll::, :,;;.: I r:,;; 31 i, (, --------, ~l;;.I ;\n\nt'<-t.'-t.lf!\"l:Sc:.-~'l..t-ul--..... 1..,..,_,\"\"'3.___,~s.,,._.,1o....,.,. \n\n-----~--r=-,..-.---= =--------'-(l e.:: ..i :::: , ='---~ ~ v_._..-d,f ',--------------t-----------------GIT What is the recommended management for infants with breastfeeding failure jaundice ?\n\nIncrease the frequency and duration of feeds \n\nif the bilirubin continues to rise (e.g. mother's milk supply is inadequate), formula supplementation may be necessary \n\n What is the initial treatment for rapidly rising hyperbilirubinemia in a newborn? \n\nnon-UV phototherapy (for kernicterus prevention) \n\nexchange transfusion is indicated for total bilirubin levels > 25 mg/dL \n\nBilirubin induced Neurologic Dysfunction \n\nBiliary Atresia Signs of dehydration include decreased urine/stool output and \"brick-red\" urate crystals in the diaper \n\n429 https://t.me/usmleinnercircle USMLE Inner Circle \n\nLactation failure jaundice vs breast milk jaundice Diagnosis Timing Pathophysiology Clinical features \n\nInsufficient intake of breast milk: . Suboptimal breastfeeding \n\nLactation failure jaundice Age <1 week . t Bilirubin elimination . Signs of dehydration . t Enterohepatic circulation Age >1 week t J,-glucuronidase in breast milk: Adequate breastfeeding .Breast milk jaundice . t Deconjugation of intestinal bilirubin (peaks at 2 weeks) . Well-hydrated . t Enterohepatic circulation \n\nBilirubin-induced neurologic dysfunction \n\n# . Excess levels of free , unconjugated bilirubin cross the blood-brain barrier \n\nPathophysiology . Deposition of bilirubin in basal ganglia & brainstem nuclei . Neuronal damage, necrosis & atrophy . Prematurity \n\nRisk factors . Hemolysis (eg, G6PD deficiency) . Birth trauma (eg, cephalohematoma) . Exclusive breastfeeding with excessive weight loss . Reversible (treatment: phototherapy, exchange transfusion) \n\nAcute . Clinical findings \n\nencephalopathy 0 Lethargy or inconsolability \n\n0 Hypotonia (early) or hypertonia (late ) o Apnea/respiratory failure, feeding difficulties, seizures . Irreversible . Clinical findings \n\nChronic 0 Developmental delay \n\nencephalopathy o Sensorineural hearing loss o Choreoathetoid movements \n\n0 Upward gaze palsy GIT What is the recommended management of patients with biliary atresia prior to a liver transplant? \n\nHepatoportoenterostomy (Kasai procedure) \n\nallows time for growth and reduces morbidity/mortality of liver transplant \n\nBiliary cyst \n\n Biliary cysts require surgical resection to relieve obstruction and prevent the development of cholangiocarcinoma . Acute complications: Pancreatitis, cholangitis, and stone formation \n\n430 https://t.me/usmleinnercircle \n\nBiliary atresia Pathogenesis . Extrahepatic bile duct fibrosis \n\n# . Asymptomatic at birth \n\nClinical . Infants age 2-8 weeks: \n\nfindings 0 Jaundice , acholic stools, dark urine \n\n> 0\n\nHepatomegaly \n\n# . Direct hyperbilirubinemia \n\n# . Ultrasound: \n\n> 0\n\nA bsenUabnormal gallbladder &/or CBD \n\n# . Liver biopsy: \n\nDiagnostic lntrahepatic bile duct proliferation 0\n\nevaluation 0 Portal tract inflammation & edema \n\n> 0\n\nFibrosis . lntraoperative cholangiography (gold standard): \n\n> 0\n\nBiliary obstruction \n\n# . Surgical hepatoportoenterostomy (Kasai procedure) \n\nTreatment . Liver transplant \n\nCBD = common bile duct. Biliary cysts \n\nBiliary cyst \n\n# . Cystic dilation of bili ary tree \n\nPathogenesis . Most common: si ngle , extrahepatic dilation of common bile duct (type I) \n\n# . May be incidental finding on imaging . Classic triad* in children/adults Norm,I Type I Type II \n\n> 0\n\nA bdominal pai n \n\nPresentation 0 RUQmass \n\n> 0\n\nJ aundice . Neonates : jaundice, acholic stools, dark urine, hepatomegaly . Nausea, vomiting \n\nDiagnosis . Ultrasound CT scan or MRCP Type Ill Type IV TypeV \n\n# . Cholangiocarcinoma . A cute cholangitis \n\nComplications Panc re at itis .. Stone formation . Cyst resection (to t risk for malignancy )\n\nTreatment . Roux-en-Y hepaticojejunostomy (to allow for biliary drainage) \n\n*Often, only two-thirds of findings are present. \n\nMRCP = MR cholangiopancreatography; RUQ =right upper quadrant. GIT There is still a small risk for developing cancer in the remaining bile ducts after surgery, and serial \n\nlaboratory testing with or without imaging is usually recommended postoperatively. \n\nIntestinal Atresia \n\n Atresia of the jejunum or ileum is thought to occur due to a vascular accident in utero that causes \n\nnecrosis and resorption of the fetal intestine, leaving behind blind proximal and distal ends of intestine .Risk factors include poor fetal gut perfusion from maternal use of vasoconstrictive medications or substances such as cocaine and tobacco .In contrast to duodenal atresia , jejunal and ileal atresia are not associated with chromosomal abnormalities. \n\nHirschsprung 99% of full-term infants stool within 48 hours of birth. \n\n431 https://t.me/usmleinnercircle USMLE Inner Circle \n\nJejunal atresia Duodenal atresia Delayed passage of meconium Hirschsprung disease Meconium ileus Pathophysiology . Failure of neural crest cell migration . Obstruction by inspissated stool \n\nLevel of obstruction . Rectosigmoid . Ileum . Increased tone . Normal tone \n\nRectal examination . Positive squirt sign* . Negative squirt sign* \n\nMeconium consistency . Normal . lnspissated . Dilated proximal colon small bowel . Dilated small bowel \n\nImaging Narrow rectosigmoid Microcolon . .\n\nAssociated disorder . Down syndrome . Cystic fibrosis *Expulsion of gas/stool on rectal examinati on .GIT Patients with a long segment of affected colon in Hirschsprung classically present in the newborn period with delayed passage of meconium. However, in patients with a short aganglionic colonic segment , symptoms often develop in infancy or early childhood and include chronic, refractory constipation and poor growth or failure to thrive. \n\nPatients do not respond to standard treatment of constipation. \n\nIntussusception T/t: Hyperosmolar Enema / Surgical Management \n\n432 https://t.me/usmleinnercircle \n\n> Meconium ileus\n> CUWor td\n\nHirschsprung disease ' Between narrow, aganglionic colon & dilated proximal colon. GIT U/S: best initial test --> Donut or Target sign \n\nBarium or air enema is both diagnostic and therapeutic Contrast enema using U/S or fluoroscopy best confirmatory test \n\n Laparotomy is indicated if enema reduction is ineffective, if a pathological lead point is identified, or if the patient has signs of perforation (eg, free air on x-ray, rigid abdomen). Most common age group: 6-36 months \n\n A pathologic lead point should be suspected in patients with intussusception and the following features: \n\nRecurrent episodes \n\nAtypical location (eg, small bowel into small bowel) Atypical age \n\nPersistent rectal bleeding despite reduction \n\nThe most common lead point is a Meckel diverticulum \n\nDx with Nuclear Scintigraphy M/C: Ileocaecal Junction ; invagination of the ileum into the colon causes the mass to be found in the RUQ instead of the \n\nRLQ \n\n433 https://t.me/usmleinnercircle USMLE Inner Circle \n\nlntussusception \n\n Recent viral illness or rotavirus vaccination Pathological lead point \n\no Congenital malformation of the intestines (eg , Meckel diverticulum) \n\nRisk factors o Henoch-Schonlein purpura \n\no Celiac disease \n\no Intestinal tumor \n\no Polyps Sudden , intermittent abdominal pain \n\nClinical \"Currant jelly\" stools \n\npresentation Sausage-shaped abdominal mass Lethargy or altered mental status \n\nDiagnosis \"Target sign \" on ultrasound Air or saline enema \n\nTreatment Surgery for removal of lead point \n\n\n\n\n\n\n\n\n\n\n\nlleocolic intussusception GIT Meckel's Diverticulum NEC \n\n434 https://t.me/usmleinnercircle \n\nlntussusception Meckel's diverticulum Rule of 2s \n\n 2% prevalence \n\nEpidemiology 2:1 male-to-female ratio 2% are symptomatic at age 2 Located within 2 feet of the ileocecal valve Asymptomatic incidental findi ng \n\nClinical Painless hematochezia \n\npresentation lntussusception Intestinal obstruction Volvulus \n\nDiagnosis Technetium-99m pertechnetate scan \n\nTreatment Surgery for symptomatic patients GIT Term infants with reduced mesenteric oxygen delivery from cyanotic congenital heart disease \n\nand/or hypotension are also at risk for intestinal ischemia and infarction. Given the risk of lethal septic shock, empiric broad-spectrum antibiotics should be started immediately. \n\nReye Syndrome Culture before antibiotics \n\n435 https://t.me/usmleinnercircle USMLE Inner Circle \n\nNecrotizing enterocolitis Pathogenesis Gut mucosal wall invasion by gas-producing bacteria \n\n# . Intestinal inflammation, necrosis \n\nRisk Prematurity \n\nfactors Very low birth weight (<1 .5 kg [3.3 lb]) Enteral feeding Nonspecific: apnea, lethargy, vital sign instability Gastrointestinal \n\nClinical findings o Abdominal distension \n\no Feeding intolerance, bilious emesis \n\no Bloody stools \n\nX-ray Pneumatosis intestinalis (air in bowel wall) \n\nfindings Pneumoperitoneum (free air under diaphragm) \n\nComplications Sepsis, disseminated intravascular coagulation Late: strictures, short-bowel syndrome \n\nManagement of necrotizing enterocolitis \n\n Discontinuation of enteral feeds \n\nImmediate Nasogastric decompression \n\ninterventions Blood cultures & empiric antibiotics Intravenous fluid repletion \n\nMonitoring Serial complete blood count & electrolytes Serial abdominal examinations & imaging \n\nIndications Bowel perforation (pneumoperitoneum) \n\nfor surgery Clinical deterioration despite medical management (suggestive of bowel necrosis) \n\nNecrotizing enterocolitis GIT Inc. ICP (secondary to hyperammonemia causing astrocyte edema (inc. opening pressure on LP) major cause of death in Reye \n\nDuodenal Hematoma \n\n Duodenal hematomas classically develop in pediatric patients 24 - 36 hours after an initial injury, causing epigastric pain and vomiting. \n\nsymptoms due to failure to pass gastric contents beyond the obstructing hematoma \n\nDx: Abdominal CT \n\n Management of a duodenal hematoma typically involves gastric decompression (NG tube) and possibly parenteral nutrition. \n\nsurgery or percutaneous drainage may be considered to evacuate hematoma if non-operative management fails \n\nif unstable and hypotensive \n\nAngiography with embolization (Often due to gastroduodenal artery) \n\n436 https://t.me/usmleinnercircle \n\nReye syndrome \n\n Aspirin use in children during viral infection (eg, influenza, varicella) \n\nPathophysiology Microvesicular fat deposits in the liver Cerebral edema \n\n# . Acute liver failure \n\n> 0\n\nHepatomegaly without jaundice \n\nClinical features \n\n Rapidly progressive encephalopathy II \n\n> 0\n\nVomiting, lethargy, seizure, coma Ii \n\n# . i AST, ALT, ammonia \n\n# . i PT, INR, PTT \n\nLaboratory findings . t Glucose \n\n# . Metabolic acidosis \n\n# . Normal bilirubin \n\nTreatment Supportive \n\n> ALT\n\n=alanine aminotransferase (SGPT); AST =aspartate am inotransferase (SGOT). GIT GIT Surgery \n\n Laparoscopic intraabdominal surgery (eg, cholecystectomy) requires insufflation of CO2 into the abdomen to create space for surgical maneuvering and visibility. The increased intraabdominal pressure stimulates stretch receptors on the peritoneum that respond by triggering an increase in vagal tone .Consequently, patients can develop severe bradycardia , atrioventricular block , and sometimes \n\nasystole .\n\nBariatric Surgery \n\n Weight-loss medication is indicated for patients with a BMI 30 kg/m2 (obese) and those with a BMI of \n\n25-29.9 kg/m2 (overweight) with weight-related complications \n\nGastric Bypass \n\n437 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDuodenal hematoma Preparation for bariatric surgery \n\n# . BMI 2'40 kg/m 2\n\nIndications . BMI ;,35 kg/m 2 with serious comorbidity (eg, T2DM, hypertension, OS A) . BMI ;,30 kg/m 2 with resistant T2DM or metabolic syndrome . Review previous attempts at weight loss, di et , exerci se habits \n\nIntake . Review psychiatr ic history, coping skills, readiness to change \n\nas sessment . Review risk for cardi ac (eg, CA D) and pulmonary (eg, OSA ) disease \n\nCAD = coronary artery disease; OSA = obstructive sleep apn ea; T2DM = type 2 diabetes mellitus. GIT Stomal (anastomotic) stenosis , is caused by progressive narrowing of the GJ anastomosis that leads to obstruction of gastric pouch outflow. This complication usually occurs within the first year after surgery, likely due to local tissue ischemia and ulceration. Patients typically have progressive symptoms including nausea, postprandial vomiting , gastroesophageal reflux , and dysphagia, to the point of not tolerating liquids. Diagnosis requires visualization of the GJ anastomosis via esophagogastroduodenoscopy (EGD) ,during which balloon dilation can be performed to open the narrowing. Patients sometimes require surgical revision if balloon dilation fails. Right upper quadrant ultrasound is useful in diagnosing cholelithiasis , which is a common complication after Roux-en-Y, especially in the setting of rapid weight loss. \n\n Anastomotic leak is a serious postoperative complication that can present with fever , abdominal pain ,\n\ntachypnea , and tachycardia , usually within the first week after bariatric surgery. The diagnosis is best confirmed by oral contrastenhanced imaging (either abdominal CT scan or \n\nupper gastrointestinal series ), and treatment requires urgent surgical repair. \n\n438 https://t.me/usmleinnercircle \n\nRoux-en-Y gastric bypass \n\n> Biliopancreatic limb Pa ncreatic enzymes & bile acids Jejunojejunal anastomosis Common l im b\n\nComplications of Roux-en-Y gastric bypass surgery Early Anastomotic leak (sep sis) Bowel is chemia ( diffuse abdominal pain) Anastomotic stricture ( dysphagia , bowel obstruction) Marginal ulcer ( abdominal pain , bleeding , peri - ana s tomotic \n\nLate perforation) Cholecystiti s (right upper quadrant pain) Dumping syndrome (diarrhea , crampy abdominal pain , vasomotor) Alimenta ry limb (Roux limb) \n\n## .Pathogenesis ..Etiology ..\n\nSymptoms ..\n\nTiming ...Management .. \n\n> Dista l stomach remn an t\n\nDumping syndrome \n\n> Destruction or bl,'.[! ass of the E!l,'. loric S[!hincter\n> Rapid emptying of hypertonic gastric contents Esophageal/gastric resection or reconstruction Vagal nerve injury (eg, Nissen fundoplication) Abdominal pain, diarrhea, nausea Hypotension/tachycardia Dizziness/confusion , fatigue, diaphoresis 15-30 min after meals Clinical diagnosis Small , frequent meals Replacement of simple sugars with complex carbohydrates Incorporation of high-fiber & protein-rich foods\n\nGIT Heart rate >120/min has been shown to be the most sensitive predictor of postoperative anastomotic leak. \n\nBillroth 2 \n\nPartial gastrectomy with gastrojejunostomy is most often performed to treat complicated peptic ulcer disease (eg, perforation, malignancy, gastric outlet obstruction) or ulcers refractory to medical management. In a Billroth II gastrojejunostomy, the gastric antrum is removed to decrease gastrin production and for histopathologic evaluation. A side-to-side anastomosis is then made between the jejunum and the gastric body, bypassing the duodenum and proximal jejunum. \n\nIron absorption occurs predominantly in the duodenum and proximal jejunum , and bypass of this segment of small bowel results in iron deficiency anemia . The post-surgical decrease in gastric acidity also diminishes iron absorption and may contribute to iron deficiency in these patients. Treatment is accomplished with pharmacologic iron supplementation , which allows for adequate iron absorption at secondary absorption sites in the distal small bowel. Deficiency involving thiamine, folate, vitamin B12, fat-soluble vitamins (especially vitamin D), and calcium is also common following gastrojejunostomy. \n\nNissens Fundoplication \n\n439 https://t.me/usmleinnercircle USMLE Inner Circle \n\nBillroth II \n\ne uwo11d GIT Pancreaticoduodenectomy \n\n What are the complications of pancreaticoduodenectomy (Whipple procedure )? \n\nAnastomotic leak : hyperchloremic acidosis and high levels of amylase in abdominal secretions \n\nLeakage of pancreatic secretions into abdominal cavity Hyperchloremic acidosis loss of HCO3- secretions in to the cavity; normal anion gap metabolic acidosis \n\nPancreatic fistula Prevention ? Octreotide before and after pancreatic surgery to minimize pancreatic secretions \n\nAbdominal Trauma \n\n440 https://t.me/usmleinnercircle \n\n\n\n00Postoperative complications of Nissen fundoplication \n\n## . Possibly caused by disruption of peristalsis due to tightening of the LES \n\nDysphagia . Symptoms develop within 12 weeks of surgery \n\n## . Diagnosed clinically & usually self-resolves \n\nGas-bloat . Likely caused by gastric air trapping due to tightening of the LES \n\nsyndrome . Symptoms include bloating & inability to belch \n\n## . Diagnosed clinically & usually resolves with conservative management \n\n## . Caused by inadvertent vagal nerve injury Gastroparesis . Symptoms: bloating, early satiety, postprandial emes is, food aversion, weight loss \n\n# . Diagnosed via gastric scintigraphy + EGD to rule out obstruction \n\n# . Managed with small, low-fat, low-fiber meals promotility agents .. \n\n*Includi ng simethicone & avoidance of carbonated beverages. \n\nMetociopramide typically first-lin e. EGO = esophagogastroduodenoscopy; LES = lower esophageal sphincter. \n\nNissen fundoplication for gastroesophageal reflux disease (GERD) \n\nGERO \n\nGastroesophageal junc tion (G EJ )Lower esophageal sphincter (L ES ) relaxation allows reflux \n\nBranches of the Vagus nerve may be injured during the procedure. Q UW,,,d GIT DPL is only used for blunt , NOT penetrating abdominal trauma evaluation (penetrating trauma warrants immediate surgical laparotomy) \n\n Any penetrating wound below the 4th intercostal space is considered to involve the abdomen. \n\nTherefore, suspicion of solid intraabdominal organ injury should prompt CT scan of the abdomen \n\n441 https://t.me/usmleinnercircle USMLE Inner Circle \n\nBlunt abdominal trauma Hemodynamlcally unstable Hemodynamlcally stable \n\nPeritonitis? + Free fluid on FAST? ++ - Of inconclusive \n\nLaparotomy I Consider CTAP (after Laparotomy resuscitation) or DPL. Consider CTA PEvaluate for other en rou te to OR sources of hemorrhage. CTAP = CT scan of th e abdome n & pet111s . CPL = di agnostic peri tonea l l avage .FAST = FOC UWortd \n\nIndication for immed iate laparotomy? \n\nHemodynamic instability \n\nPentonit1s \n\n# _J Evisceration Impalement \n\n1-\n\nPeritoneal penetration &\n\nsigni fi cant organ i njury (eg , based on imaging, local wound explorati on )? Close observation with serial abdominal examinations JRib fracture location & associated injuries Associated injuries \n\nSubclavian vessel s, brachia! plexus, mediastinal vessels (eg , aorta) Cardiovascular lntraabdominal: liver (right), spleen (left), kidney (posterior ribs 11 & 12) \n\nPulmonary ++Laparotomy IGIT Blunt abdominal trauma may result in damage to the mesenteric blood supply and bowel contusion, leading to subsequent necrosis and eventual GI perforation. \n\ncan occur acutely or several days after the initial event (versus penetrating trauma which presents only acutely )\n\n What is next step for blunt abdominal trauma with GI perforation identified on CT? \n\nExploratory laparotomy \n\n Which organs (2) are most commonly injured with blunt abdominal trauma ?\n\nliver and spleen \n\n Abdominal aortic injuries due to BAT are rare (<1%); most people die before reaching hospital. \n\n Pancreas is retroperitoneal ; it can injure in BAT but will NOT cause intraperitoneal fluid collection \n\nPancreatic Injury \n\n The development of the following symptoms and signs in patients with recent BAT should raise suspicion for undiagnosed pancreatic injury: \n\nPersistent abdominal discomfort /tenderness Persistent nausea /emesis \n\nIncreasing amylase over serial measurements \n\nPeripancreatic fluid collection (due to pancreatic duct injury) Ductal injury may require cholangiopancreatography for diagnosis Trauma to the RUQ , right lower rib cage (eg, right eighth and ninth ribs), or right flank should raise suspicion for hepatic injury. \n\n442 https://t.me/usmleinnercircle \n\n> Liver laceration\n> C)UWorld\n\nGIT Splenic Rupture \n\n Infectious mononucleosis , caused by Epstein-Barr virus, is associated with splenomegaly in up to 50% of cases, and splenic rupture within a month of symptom onset is a rare but serious complication. Because splenic rupture can occur even if the spleen is not initially palpable, activities that increase the risk of rupture (eg, contact sports) should be avoided for 3-4 weeks from the time of initial diagnosis. If a hemodynamically stable and alert patient with suspected splenic injury has a normal FAST exam despite high-risk features (e.g. guarding ), what is the next step? \n\nCT scan of abdomen \n\nDuodenum Perforation \n\nWhen viscus perforation occurs within the retroperitoneum (eg, duodenal tear) , classic symptoms and signs (eg, fever, diffuse abdominal pain) may be delayed .\n\nRetroperitoneal free air may be present on abdominal imaging. \n\nRectus Sheath Hematoma \n\n443 https://t.me/usmleinnercircle USMLE Inner Circle \n\nAtraumatic splenic rupture \n\n## . Hematologic malignancy (eg, leukemia, lymphoma) \n\n## . Infection (eg, CMV , E BV , malaria) \n\nRisk factors . lnfiammatory disease (eg, SLE, pancreatitis) \n\n## . Sp lenic congesti on (eg, cirrhosis , pregnancy) . Medications (eg, anticoagulation, G-CSF) . Diffuse or LUO abdominal pain, peritonitis \n\nClinical presentation . Referred l eft shoulder pain (Kehr sign) . Hemodynamic instabil ity . Acute anemia \n\nDiagnosis lntraperitoneal free fiuid on imaging .\n\n## . Catheter-based angioembolization (stable patients) \n\nTreatment . Emergency splenectomy (unstable patients) CMV = cytomegalovirus; EBV = Epstein-Barr virus; G-CSF = granulocyte-stimulating colony factor; LUQ = left upper quadrant; SLE = systemic lupus erythematosus. \n\nSplenic laceration GIT RSH typically occurs due to rupture of the inferior epigastric artery \n\n Manifestations include acute abdominal pain , often associated with rebound or guarding , and a \n\npalpable abdominal wall mass .The mass does not cross the midline and does not change with movement of the lower extremities (Fothergill sign). \n\nWound Dehiscence \n\n Postoperative abdominal wounds can be categorized based on fascial involvement: \n\nSuperficial wound dehiscences are separations of the skin and subcutaneous tissue with intact rectus fascia. These typically develop within the first postoperative week due to an abnormal subcutaneous fluid buildup (eg, seroma) and can often be managed conservatively with careful dressing changes. \n\nDeep (fascial) wound dehiscences involve the rectus fascia (ie, nonintact) and result in exposure of the intraabdominal organs to the external environment. T/t: Emergency Surgery \n\nPilonidal Sinus \n\n What disease often manifests in young males as a painful , fluctuant mass above the anus in the intergluteal region with associated discharge ? What is the treatment? \n\nPilonidal disease; treat with incision and drainage \n\n444 https://t.me/usmleinnercircle \n\n\n\nRectus sheath hematoma \n\n# . Abdominal trauma, forceful abdominal contractions (eg, coughing) \n\n> Risk factors\n\n# . Anticoagulation \n\n# . Older age, female sex \n\n# . Acute-onset abdominal pain with palpable abdominal mass Clinical . Blood loss anemia, leukocytosis \n\n> features\n\n# . Nausea, vomiting , fever \n\n# . Hemodynamically stable: serial monitoring of CBC , reverse anticoagulation and transfuse blood products when \n\n> Management appropriate\n\n# . Unstable: angiography with embolization, surgical ligation \n\n> CBC =complete blood count. Skin --------~ ::-..,_\n> Subcutaneous tissue\n> Peritoneum\n\n----. r.:allllr . \n\n> Omentum\n\n----, a\n\n> CIUWO, ..Ao. LeS\\in \n\nM;Nc,-.u.1\"\"'\"\"'\" \n\nD-&. , C..D \n\nT-: Q(..ty~O,L-;, .l.s,lo-,,J.. -.. ;, 1.1....A .f\\ 0 ..., ~ : E.C,.D (kll..-d. 11)..f;....1) \n\n- l>p\"' : V,. b .J-c-lol ix : ... \\o.\\.i... (IU~t.d-\n\nEw:t.ok-f'\\, baMJ l;tic:th\"' \n\n~~=v~~~t \n\nMll\"j - wu\" \n\nll.!\\. . o;.,,,..l\\ ..\\ -1.,, \n\n.. ~ /\\0,.U C. OSQ, \n\nli wt..c,U.J, ,...... .,x ..... on H.br.:lct.6.~\"'''-\n\nA---r ,.... f1.osluo.sti\"\"\"\"' {5t.A:,Q 1!1'1\\(1~,-o., \n\nl:lil:>. \n\nHrl\\. \" fjlfrll \n\nM~IO s\n\nc-\n\na ~\"' \n\n~ : ~D \n\n1l. Ei-,'Sl!),,.., , \n\n# .. ,\n\n~ ; EC..D 'St~e. f\"'i#,,,.,tl;.,,.,#c.v' _, .,. wd,o.,i..J,~1,lliuiot} \n\n2! l~ ~R. \n\n(.~ , :i\">IT>,,.{,. ( wol,,, --1) \n\nTu 5-\\.~ (.o,,,,ttul\\.t,A c-scn,o.lt've \n\ntf \n\n~\n\nfb_ : M&J.> ~ \\l....(,;k, \n\n&l<,,..l---->.,,.;,,, ,l>l<,./, ;kk \n\n~ . 1..., ,i.,.; .i 4<,-, .r ..J. co.J \n\nA~;~\"-'i \n\n&lh M\"' \n\n.ti:_ 'ilood o, -\\., , I~ I'S!\" fr S~ ~ d\"'\", ~,.f,a1t.., \n\n~0,,,,....tpn,ri-hs \n\nei: I bi,_../ \n\nAs'>IC. . w( 1-at. 1 E'SllO ,\n\n~o,.w1\\l..i,......n -l.D'\\.,Ac,,+:c. \n\n'Dz.- . ci;,.. -,uJ~ ~......J i.. ~- \n\n- DR.. \n\nT x 'S i ~'l.. 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Patients with upper (but not lower) GI bleeding often have an elevated blood urea nitrogen ( BUN ) and \n\nelevated BUN/creatinine ratio .Possible causes include increased urea production from intestinal breakdown of hemoglobin and \n\nincreased urea reabsorption in the proximal tubule due to associated hypovolemia. \n\nVariceal Bleeding \n\n What procedure should be done prior to endoscopic treatment in patients with an upper GI bleed who have a depressed level of consciousness and continued hematemesis? \n\nEndotracheal intubation \n\nthese patients are at high risk for aspiration and must have their airway protected before upper endoscopy \n\n446 https://t.me/usmleinnercircle \n\nAge-based evaluation of occult gastrointestinal bleeding \n\n> Occult gastrointestinal bleed\n\nj\n\n# lUpper endoscopy & colonoscopy ISource not found \n\nt \n\n> Small bowel bleed evaluation Adult Chi ld\n\ni i \n\n> Capsule endoscopy Angiodysplasia. neoplasia. ulcers Tc 99m pertechnetate scan\n> +-Source not found -Meckel d1verticulum\n\nISource not found \n\n*CT/MR enterography Malignancy/mass \n\n> BaJ loon -a ssiste denterosco py may als obe co nsidered if so urce remai ns u ni denti fi ed Tc 99 m=tech ne tium Tc 99m C U Wor ld\n\nGIT Hemobilia \n\n Hemobilia is a rare cause of upper gastrointestinal bleeding (UGIB) that usually occurs as a complication of hepatic or biliopancreatic interventions (eg, liver biopsy , cholecystectomy, endoscopic cholangiopancreatography); other etiologies include hepatobiliary tumors and blunt trauma .Patients typically present with RUQ pain , jaundice , and UGIB \n\n Massive hemobilia results in hemodynamic instability and UGIB that occurs immediately after the procedure; \n\nintraductal hematoma formation more commonly results in delayed UGIB until after dissolution of the clot (usually ~5 days post-procedure ). \n\nT/t: Usually self limited , managed conservatively Octreotide causes splanchnic vasoconstriction and reduces portal blood flow by inhibiting release of glucagon \n\n447 https://t.me/usmleinnercircle USMLE Inner Circle \n\nVariceal hemorrhage bleed algorithm \n\nSuspected variceal hemorrhage Place 2 large-bore IV catheters Volume resuscitation IV octreotide Antibiotics Urgent endoscopic therapy of esophageal varices No further bleeding Initiate secondary prophylaxis Beta blocker + endoscopic band ligation \n\n1-2 weeks later Continued bleeding Balloon tamponade (temporary) \n\nEarly rebleeding Repeat endoscopic therapy Recurrent hemorrhage \n\nITIPS or shunt surg e ry I\n\nIV = intravenous : TIPS = transjugula rl ntrahepatJc ponosystemic Shunt. Blood & Oncology \n\n# Blood & Oncology RBC Microcytic Anemia Macrocytic Anemia Hemolytic anemia G6PD PNH Sickle Cell Anemia Hereditary Spherocytosis Macroangiopathic Hemolytic Anemia Acute Intermittent Porphyria WBC Acute Leukemia Chronic Leukemia Hodgkin Lymphoma Plasma Cell Dyscarias Multiple Myeloma Platelets Hemostasis Vitamin K Deficiency ITP TTP HUS DIC Hemophilia Hereditory Thrombophilias Pseudothrombocytopenia Drugs Heparin EPO Tumour Blood Oncology Therapies Radiotherapy PET Scan Cancer Pain Miscellaneous Lymphangitis Idiopathic Anemia of Ageing Blood Transfusion Transfusion Overload Catheter Induced Septic Thrombophlebitis Paeds Blood Polycythemia Anemia of Prematurity Physiologic Anemia of Newborn \n\n448 https://t.me/usmleinnercircle Blood & Oncology RBC \n\nMicrocytic Anemia \n\n What is the most appropriate screening test in a preconception patient with a family history of thalassemia ?\n\nCBC \n\nIf there is anemia with a reduced MCV , then further testing is required ( Hb electrophoresis) \n\n What is the likely underlying cause of microcytic anemia in a patient with chronic kidney disease that recently began erythropoietin therapy ?\n\nIron deficiency \n\nthe erythropoietin-induced surge in RBC production can precipitate iron deficiency Remember, patients with CKD can develop anemia due to loss of EPO. When EPO is given, an iron deficiency anemia can develop due to depletion of iron stores during hematopoiesis after administration, especially if iron stores are already low. \n\n The treatment of choice for iron deficiency in patients on dialysis is intravenous iron. IDA Pancytopenia \n\n449 https://t.me/usmleinnercircle USMLE Inner Circle \n\nAnemia of chronic disease \n\n i inflammatory cytokines (eg, hepcidin) \n\n# . Inhibition of ferroportin on enterocytes and macrophages \n\nPathogenesis i iron absorption and i iron sequestration Reduced circulating iron --+ impaired erythropoiesis \n\n# . Malignancy \n\n# . Chronic infection Rheumatic disease \n\nCommon Etiologies Obesity .\n\n Diabetes mellitus Congestive heart failure \n\n# . Normocytic/slightly microcytic anemia i serum iron, iron-binding capacity, reticulocyte count \n\nLaboratory findings i bone marrow iron \n\n# . Lower than expected erythropoietin for degree of anemia \n\nTreatment . Treat underlying condition causing inflammation Blood & Oncology What is a useful way to tell Iron Deficiency Anemia from minor thalassemia on blood count from MCV and RBC count? \n\nMentzer index: MCV/RBC \n\n<13 is minor thalassaemia \n\n>13 is IDA This is useful if they are really vague with their question with limited information available \n\n IDA may be associated with reactive thrombocytosis (platelets >400,000/mm3) in response to low red blood cell count. This change is due to megakaryocytes and erythrocytes sharing a \n\ncommon progenitor cell. \n\nMacrocytic Anemia \n\n What is the most common cause of vitamin B12 deficiency ?\n\nPernicious anemia \n\n What is the likely underlying cause of anemia in a patient with a history of gastrectomy that presents with a shiny tongue , pale palmar creases , and laboratory evidence of hemolysis ? Labs show indirect hyperbilirubinemia and elevated LDH .RDW >20% in IDA \n\n450 https://t.me/usmleinnercircle \n\nParameter Iron deficiency a-thalassemia minor 13-thalassemia minor anemia MCV t t t\n\nRDW i Normal Normal \n\nRBCs t Normal Normal \n\nPeripheral smear Microcytosis, Target cells Target cells hypochromia \n\nSerum iron studies J Iron & ferritin Normal/j iron & ferritin (RBC Normal/j iron & ferritin (RBC \n\ni TIBC turnover) turnover) \n\nResponse to iron j Hemoglobin No improvement No improvement \n\nsupplementation Hemoglobin electrophoresis Normal Normal j Hemoglobin A2 \n\nMCV = mean corpuscular volume; RBCs = red blood cells ; RDW = red cell distribution width; TIBC = total iron-binding capacity. \n\nCommon causes of macrocytosis \n\n# . Hemolytic anemia \n\nIncreased reticulocytes Bone marrow recovery .\n\nImpaired RBC maturation Vitamin B 12 /folate deficiency \n\n# . Medications (eg, hydroxyurea, methotrexate) \n\n# . Myelodysplastic syndrome \n\nBone marrow disorders Sideroblastic anemia \n\n# . Multiple myeloma \n\n# . Liver disease \n\nLipid abnormalities Hypothyroidism . \n\n> RBC\n\n= red blood cell. Blood & Oncology Vitamin B12 deficiency ( impaired DNA synthesis )\n\ndeficiency due to loss of intrinsic factor ; high numbers of immature megaloblasts in the bone marrow results in increased intramedullary hemolysis, thus causing indirect hyperbilirubinemia and elevated LDH \n\nHemolytic anemia \n\nG6PD \n\n What is the likely diagnosis in an African-American patient that presents with dark urine that stains positive with Prussian blue after being treated for a urinary tract infection? \n\nG6PD deficiency \n\npositive stain indicates presence of hemosiderin in the urine due to hemolysis; hemolytic episodes are often precipitated by infection or medications ( increased oxidative stress )\n\n What is the likely diagnosis in an African-American male that develops dark urine , fatigue ,and jaundice after being treated with TMP-SMX? Peripheral smear reveals bite cells, but a G6PD activity assay is normal. \n\nG6PD deficiency \n\nmost erythrocytes with severe G6PD deficiency are hemolyzed early during the acute episodes, thus the G6PD assay may initially be abnormally normal; it is best to wait 3 months after the episode before re-testing \n\n Hemoglobinuria heme is excreted in the kidneys, which causes dark-colored urine and a \n\nfalse-positive urine dipstick for blood \n\nthe heme in hemoglobin causes a positive urine dipstick test, but no erythrocytes are seen on urine microscopy Triphalangeal thumbs in Diamond Blackfan \n\n451 https://t.me/usmleinnercircle USMLE Inner Circle Blood & Oncology PNH \n\n Reason for increase thrombosis : Venous thrombosis is caused by vasoconstriction and platelet aggregation as a result of free hemoglobin (due to hemolysis) scavenging serum nitric oxide (a vasodilator) and, according to the prevalent hypothesis, activating the endothelial lining of blood vessels. \n\nSickle Cell Anemia \n\n IV Opiates (e.g Morphine) are given for adequate Analgesia Parvovirus B19 infection can result in an aplastic crisis with no preceding viral symptoms. Blood transfusions are the mainstay of treatment. Pneumococcal Vaccine, Twice daily penicillin \n\n452 https://t.me/usmleinnercircle \n\nMedications that often trigger hemolysis in G6PD deficiency* \n\nDiaminodiphenyl su lf one (dapsone) lsobutyl nitrite \n\nAvoid Nitrofurantoin Rasburicase Primaquine Acetaminophen Acetylsalicylic acid (aspi ri n) Chloramphenicol Chloroquine Colchicine Diphenhydramine (Benadryl) \n\nUse with caution Glyburide lsoniazid L-Dopa Quinine Sulfamethoxazole Trimethoprim Vitamin K *This li st is not exhaustive ; it includes medications common ly used in the clinical setting . \n\nG6PD = glucose-6-phosphate dehydrogenase. \n\nClin ical features of paroxysmal nocturnal hemog1 lobinuria Clinical . Hemo lysis fatigu e \n\nman if estations Cytopenias (impaired hematopoiesis) Venous thrombosis (intraabdominal, cerebral veins) \n\n## . Complete blood count (hypoplastic/aplastic anemia, thrombocytopenia, le uko penia) \n\n## . Elevated lactate dehydrogenase & low haptoglobin \n\nWorkup (hemolysis) . Indirect hyperbilirubinemia \n\n## . Urinalysis (h emogl obin ur ia) \n\n# . F low cytometry (absence of CD55 & CD59 ') \n\n## . Iron & folate supplementation \n\nTreatment . Eculizumab (monoclonal antibody that inhibits complement activation) \n\n> Acute severe anemia in sickle cell disease\n\nManagement of sickle cell anemia Cause Reticulocytes Aplastic crisis Splenic sequestration crisis Key features \n\n> Transient arrest of erythropoiesis Secondary to infection (eg , parvovirus B19) Splenic vaso-occlusion ----+ rapidly enlarging spleen Occurs in children prior to autosplenectomy\n\n Vaccination \n\nMaintenance Penicillin (until age 5) Folic acid supplementation Hydroxyurea (for patients with recurrent vaso-occlusive crises) Hydration \n\nAcute pain crises Analgesia +/- Transfusion Blood & Oncology Transfusion should be administered cautiously (eg, half of normal volume) because RBCs in the spleen may return to circulation, resulting in a rapid increase in hemoglobin and complications such as \n\nhyperviscosity syndrome . Hyposthenuria is an impairment in the kidney's ability to concentrate urine producing nocturia in patients with sickle cell anemia and trait. \n\nHyperosmolar conditions of the renal medulla, red blood cells sickle in the vasa recta , impairing free water reabsorption and countercurrent exchange \n\nUrine osmolality is low ; however, normal serum sodium is maintained due to intact ADH \n\n In patients with sickle cell disease, chronic damage and autoinfarction typically causes functional asplenia by age 5.\n\n How long is risk of sepsis in patients with splenectomy ?\n\n>30 years \n\n What is the most common cause of sepsis in patients with sickle cell disease? \n\nStreptococcus pneumoniae \n\nBroad-spectrum empiric antibiotics ( ceftriaxone ) should be given to patients with SCD presenting with sepsis \n\n What is the likely diagnosis in a child with a history of sickle cell disease that presents with hypovolemic shock in the setting of LUQ tenderness and splenomegaly ?\n\nSplenic sequestration \n\nhypovolemic shock occurs due to pooling of RBCs within the spleen \n\n What is the most common complication of sickle cell trait ?\n\nPainless hematuria (microscopic or gross) \n\ndue to sickling in the renal medulla; isosthenuria (inability to concentrate urine) is common as well, and manifests as nocturia and polyuria Thrombocytopenia (as platelets are also trapped in the spleen) \n\n453 https://t.me/usmleinnercircle USMLE Inner Circle \n\nAcute splenic sequestration Infections in sickle cell disease \n\nPathophysiology . Complication of sickle cell disease seen in early childhood \n\n Vasoocclusion within spleen, causing trapping of red blood cells & platelets Infection Etiology Pneumonia . Streptococcus pneumoniae \n\n Abdominal pain Clinical features . Palpable splenomegaly Osteomyelitis/septic arthritis . Staphylococcus aureus \n\n. Salmonella species \n\n## . Signs of anemia (tachycardia, pallor, fatigue) \n\n## . Hypotensive shock Bacteremia/sepsis . Streptococcus pneumoniae \n\n. Haemophilus inffuenzae type B Laboratory Acute drop in hemoglobin findings . Reticulocytosis \n\n Thrombocytopenia Meningitis . Streptococcus pneumoniae \n\n## . Isotonic fluid resuscitation Treatment . Red blood cell transfusion \n\n## . Splenectomy Blood & Oncology Dactylitis presents at age 6 months to 4 years with an acute onset of pain and symmetric swelling of the hands and feet. \n\n454 https://t.me/usmleinnercircle \n\nElectrophoresis patterns in sickle cell syndromes HbA HbA2 HbF HbS HbC \n\nNormal ++++ + + None None Sickle cell trait +++ + + +++ None Sickle cell anemia (SCA) None + + ++++ None SCA on hydroxyurea None + ++ +++ None Hemoglobin SC disease None + + +++ +++ \n\nStroke in sickle cell disease \n\n# . lschemic stroke \n\n> 0\n\nIntimal hyperplasia & stenosis (vasculopathy) \n\no Adhesion of sickled red blood cells to vasculature \n\nPathogenesis . Hemorrhagic stroke \n\n> 0\n\nWeakened cerebral vessels \n\n> 0\n\nCerebral aneurysm rupture . Focal neurologic symptoms (eg , hemiparesis) \n\nPresentation . Seizure \n\n Altered mental status \n\nImaging . MRI of the head: ischemic stroke (large vessel region or watershed area) . CT scan of the head: hemorrhagic stroke \n\nTreatment . Exchange transfusion . Simple transfusion if exchange transfusion is unavailable \n\n Transcranial Doppler screening during childhood \n\nPrimary prevention . Hydroxyurea Chronic transfusions \n\nDifferential diagnosis of bone pain in sickle cell disease Cause Vaso-occlusive crisis Osteomyelitis Avascular necrosis \n\n Acute, severe pain Acute or subacute pain Pain ~1 site (eg, dactylitis) Focal pain at 1 site (eg , long Chronic, worsening pain (eg, \n\nClinical +/- Low-grade fever bone) femoral head) \n\nfeatures Erythema & warmth Prolonged fever Absence of fever May be preceded by trigger (eg, Erythema & warmth Absence of warmth or erythema dehydration) Positive blood culture Chronic dyspnea in sickle cell disease Cause Symptoms Diagnostic findings \n\n# . lntermittenUchronic wheezing Pulmonary function testing showing reversible \n\nAsthma May be worse at night or with exercise or upper .. airway obstruction \n\nreseirato~ infection \n\nPulmonary . Exertional dyspnea Tricuspid regurgitation on echocardiography . Signs of right-sided heart failure (eg , jugular venous . t Pulmonary arterial pressure on right-sided heart \n\nhypertension distension, edema) catheterization \n\nPulmonary Exertional dyspnea . Honeycomb patte rn on chest CT scan . Pulmonary function testing showing restrictive \n\nfibrosis Progressive .. pattern Blood & Oncology What are some complications of chronic hemolytic anemia in Sickle Cell patients? \n\nBaseline bilirubin increase Anemia Increase reticulocyte count ( except aplastic crisis )Folate deficiency Iron deficiency anemia \n\nHereditary Spherocytosis \n\n What is the likely diagnosis in a child with a family history of anemia that presents with Coombs-negative hemolytic anemia , jaundice , and splenomegaly ?\n\nHereditary Spherocytosis \n\nMacroangiopathic Hemolytic Anemia \n\n Mechanical aortic valves often cause mild, asymptomatic hemolysis. However, valve deterioration can trigger progressive symptomatic anemia (eg, fatigue, dyspnea with exertion) with signs of erythrocyte lysis (eg, jaundice, dark urine) and reticulocytosis .\n\nThrombocytopenia can also occur because platelets may be damaged as they pass through the rigid valve opening. Hepatosplenomegaly can develop as the fragmented erythrocytes are cleared in the macrophages and monocytes within the liver and spleen. Peripheral blood smear generally shows schistocytes .A transthoracic echocardiogram should be performed to visualize valve function and determine valvular pressure gradients. \n\nAcute Intermittent Porphyria Hypoplastic Thumb in Fanconi Anemia \n\n455 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSickle cell disease in pregnancy \n\nBaseline 24-hr ur ine collection/testing for total protein Baseline chemistry panel Serial urine cultures \n\nPrenatal care Pneumococca l vaccination \n\nFolic acid supplement Aspirin Serial fetal growth ultrasound examinations Spontaneous abortion \n\nObstetric complications Preeclampsia, eclampsia Abruptio placentae Antepartum bleeding Fetal growth restriction \n\nFetal complications Oligohydramnios Preterm birth Blood & Oncology Abdominal pain: Because the pain is neuropathic, it can be diffuse, although tenderness, rebound, and guarding are absent. Nausea/vomiting, hypoactive bowel sounds, and constipation may occur. \n\n Urobilinogen levels are typically elevated, and elevated urinary porphyrin levels confirm the diagnosis. \n\n## WBC \n\nAcute Leukemia Chronic Leukemia \n\n456 https://t.me/usmleinnercircle \n\nAcute intermittent porphyria Etiology Autosomal dominant disorder with low penetrance \n\n## . Reduced activity of porphobilinogen deaminase \n\n## . Medications (eg , cytochrome P-450 inducers, progesterone) \n\nExacerbating factors . Physiologic stress (eg , fasting , surgery, illness) \n\n Alcohol , tobacco \n\n Abdominal pain \n\n## . Peripheral neuropathy most pronounced in the proximal upper extremities \n\nManifestations Autonomic dysfunction (eg , tachycardia, diaphoresis, hypertension) \n\n## . Neuropsychiatric (eg, hallucinations, anxiety, psychosis) \n\n## . Red-tinged uri ne that oxidizes with light/air exposure \n\nLaboratory findings . Elevated serum & urinary PBG , ALA, porphyrins \n\n## . Hyponatremia, elevated transaminases \n\nManagement . Glucose & hemin (heme analogue) \n\nALA= aminolevulinic acid ; PBG = porphobilinogen .\n\nAcute lymphoblastic leukemia \n\n Most common childhood cancer \n\nEpidemiology Peak age: 2-5 years Nonspecific systemic symptoms (eg , fever, weight loss) Leukemic cells overcrowd bone marrow o Pallor/fatigue (anemia) o Easy bruising/petechiae (thrombocytopenia) o Bone pain \n\nClinical Extramedullary spread \n\nfeatures o Lymphadenopathy o Hepatosplenomegaly o Testicular enlargement Mediastinal mass (T cell lineage): airway compression &/or superior vena cava syndrome Leptomeningeal spread : neurologic symptoms (eg, cranial nerve deficits, meningismus) Complete blood count* \n\nEvaluation Bone marrow biopsy (>20% blasts is diagnostic) with \n\n& diagnosis flow cytometry Lumbar puncture to evaluate for CNS involvement \n\n;,2 cytopenias (leukocytes may be L or j), blasts on peripheral smear. Blood & Oncology Hodgkin Lymphoma \n\n What is the likely diagnosis in a patient with PMHx of Hodgkin lymphoma status-post chemotherapy /radiation who presents with cough , dyspnea , and chest pain ?\n\nSecondary malignancy \n\nthere is an 18.5-fold increased risk for developing a second cancer in HL patients compared to the general population (likely related to chemo- and/or radiation therapy at a young age); most common sites are lung , breast , thyroid , bone , and GI Hairy Cell \n\n457 https://t.me/usmleinnercircle USMLE Inner Circle \n\nLeukemoid reaction Chronic myeloid leukemia Leukocyte >50,000/mm 3 Elevated (often >100,000/mm 3)\n\ncount Caus e Severe infection BCR -ABL fusion \n\nLAP score High Low \n\nNeutrophil More mature Less ma ture precursors (metamyelocytes > myelocytes) (metamyelocytes < myelocytes) \n\nAbsolute Not present Present basophilia \n\nLAP c= leukocyte alkatne phosphatase .\n\nChronic lymphocytic leukemia \n\n Lymphadenopathy (cervical, supraclavicular, ax illary) \n\nClinical Hepatosplenomegaly \n\n Mild thrombocytopenia & anemia Often asymptomatic Severe lymphocytos is & s mudge cells Diagnostic Flo w cytom et rv \n\n Lymph node & bone marrow biopsy not generally needed Media n survival 10 years \n\n Wor se prognosis wit h: Prognostic o Multiple chain lymphadenopathy o Hepatosplenomegaly o Anemia & thrombocytopenia Infecti o n Complications Autoimmune hemolytic anemia \n\n Secondary ma lignancies (eg, Richt er transformation) \n\nHa iry cell leukemia \n\n. Clonal B-cell neopla sm Features . Mi dd le age/older adults \n\n. BRAF mutation \n\n. Pancytopenia due to bone marrow fibrosis Granulocytopenia (inf ect ions) \n\nManifestations Anemia (fatigue, weakness) Thrombocytopenia (b leeding, bruising) \n\n. Splenomegaly (early satiety) \n\n. Hepatomegaly/lymphadenopathy rare \n\n. Peripheral smear - \"hairy\" leukocyte ce ll sDiagnosis . Bone marrow biopsy with flow cytometry \n\n. Chemotherapy (for moderate/severe) \n\nTreatment . Life expectancy is often near-normal Blood & Oncology Patients with Hodgkin lymphoma (HL) are generally treated with combination chemotherapy and radiation therapy , which cures >75% of cases. However, these treatments are associated with serious \n\nlong-term complications , including: \n\nHL relapse (or recurrence) : The leading cause of death for the first 8-10 years after treatment is HL relapse. Relapses primarily occur in the first 2 years, but risk remains mildly elevated for life. \n\nSecondary malignancy : Radiation exposure increases the risk of solid organ (eg, breast, lung) malignancy, and chemotherapy increases the risk of hematologic malignancy. Most cases arise >5 years after treatment. Secondary malignancies are the leading cause of death in those who have been cured of HL. \n\nCardiovascular disease : Risk of coronary artery disease, valve damage, peripheral vascular disease, and cardiomyopathy are increased in those who have been treated for HL. Cardiovascular disease is the leading nonmalignant cause of death in long-term HL survivors. Other common treatment-related complications include pulmonary disease (eg, fibrosis, bronchiectasis) and hypothyroidism from chest radiation and neuropathy from chemotherapy. Patients with HL occasionally have severe pain in areas of lymphadenopathy (eg, chest) following exposure to small quantities of alcohol (eg, drinking a beer). \n\nThe etiology is unclear, but the pain may be due to alcohol-induced vasodilation within the lymph nodes, causing capsular distension. \n\n## Plasma Cell Dyscarias \n\nMultiple Myeloma \n\n458 https://t.me/usmleinnercircle \n\nSecond mallgna ric_?, \n\n# ---/ \n\n> /Recurrence 15 Years after treatment\n\nBlood & Oncology What screening tests would be useful for evaluating an elderly patient with chronic arm pain , anemia ,and back pain ?\n\nSerum/urine protein electrophoresis (best initial test ) or free light chain analysis \n\n A patient is diagnosed with multiple myeloma. What imaging should be performed? \n\nFull body XRay skeletal survey looking for lytic bone lesions/ pathological fractures \n\n Bone scans are not useful in the diagnosis of MM as they detect only osteoblastic activity \n\n## Platelets \n\n459 https://t.me/usmleinnercircle USMLE Inner Circle \n\nMultiple myeloma (MM) \n\n\"Moth-eaten\" appearance due to aggressive . irregLAa r bone marrow destruction (no nspecific for MM) c,uwonc \n\nWal denstriim Mu lti ple mye l oma macroglobul i nem ia Hype rv iscosity syndrome Osteo l yt ic lesions/fractures Maj or Neuropathy An e mi a\n\nmanifestations Bleeding Hypercalcem ia Hepatosplenomega ly Lymphad eno pathy Renal insufficiency Monoc l onal lgM lgG, lgA, light chains antib ody Per ipheral Rouleaux Rouleaux sme ar Bone ma rr ow > 10% clonal B cells > 10% clonal pl asma ce ll sbiopsy Blood & Oncology Hemostasis \n\n Normal plasma provides coagulation factors; therefore, it corrects prolonged PTT in the setting of coagulation factor deficiency but fails to correct prolonged PTT in the setting of a coagulation inhibitor. \n\nOne of the most common coagulation inhibitors is lupus anticoagulant (LA), a type of an \n\nantiphospholipid antibody . LA binds to the phospholipids used in most PTT tests and prevents them from inducing coagulation (thereby prolonging PTT). \n\n460 https://t.me/usmleinnercircle \n\nCommon causes of throm bocytopenia \n\nViral infections (eg, Epstein-Barr virus, hepatitis C. HIV} \n\nDecreased Chemotherapy \n\nplatelet Myelodysplasia (especially for age >60) \n\nproduction Alcohol use Congenita l (eg, Fanconi syndrome) Vi t amin Bl 2 or fo late deficiency Systemic lupus erythematosus \n\nIncreased Medications (eg, heparin) \n\nplatelet Idiopathic thrombocytopenic purpura, disseminated intravascular coagulation, thrombotic thrombocytopenic \n\ndestruction purpura-hemo lytic uremic syndrome Ant iphospho lipid syndrome \n\nOther Dilutional due to massive red blood cell transfusion Splenic sequestration \n\nBleeding disorders Type Symptoms Examples Laboratory results \n\n Hemarthrosis 1' Activated \n\nClotting defect Hemophilia A partial Deep tissue Hemophilia B thromboplastin hematomas time von Willebrand \n\nPlatelet disease Abnormal \n\naggregation defect Easy or Bernard-Soulier platelet prolonged function testing mucosa! syndrome bleeding Ecchymoses Idiopathic \n\nThrombocytopenia Petechiae thrombocytopenic -l-Platelet \n\npurpura count Leukemia Elevated PT &/or PTT 1:1 inhibitor mixing study Corrects, normal PT \n\n&/or PTT \n\nFactor deficiency, evaluate for individual factor assa ys UWorld Does not correct, abnormal PT &/or PTT \n\nInhibitor likely present, test for coagulation factor inhibitors Blood & Oncology This laboratory artifact is not improved with the addition of plasma (mixing test) but is resolved with the addition of phospholipids (which eventually overwhelm all the antibody binding sites). \n\nVitamin K Deficiency \n\n What is the likely diagnosis in an alcoholic patient that begins bleeding from an IV site on post-operative day 7 after having an emergency surgery? Laboratory exam reveals anemia with elevated PT/PTT and normal platelet counts. \n\nVitamin K deficiency \n\nacutely ill patients with underlying liver disease can become vitamin K deficient in 7 - 10 days, especially if they receive broad-spectrum antibiotics! PTT can be normal or elevated \n\nITP \n\n What two viruses should be tested for in an asymptomatic patient with idiopathic thrombocytopenic purpura ?\n\nHIV and hepatitis C \n\nSecondary ITP may be the initial presentation of HIV infection in 5-10% of patients \n\n461 https://t.me/usmleinnercircle USMLE Inner Circle \n\nInfantile vitamin K-deficient bleeding \n\n# . L ow v it a min K stores (poo r placental tr an sfer , sterile gut, low co n te nt in breast milk) \n\nPathophyslology In effic ient v it am in K u se by immatu re li ve r.. Classically pre sents on day 2-7 of lite \n\n# . Easy bruising \n\nClinical features . Umbili ca l, mucosal & gastrointestinal bleeding \n\n# . lntra cran ial hemorrhag e\n\n# . i PT \n\nLaboratory findings . i PTT (if severe) \n\n# . Nor ma l platel et co unt \n\nPrevention . In tramu scular vi tami n K at bi rth * Ca n occur up to age 6 months. Vitamin K deficiency \n\n## . Inadequate diet ary intake (eg, malnutrition) \n\n## . Disorde rs of fat malabso rpti on \n\n0 Cystic fibrosis \n\nRisk 0 Biliary atresia factors . Di sord e rs of int es tin al in fl a mm at ion \n\n0 Celiac disease \n\n0 Inflammatory bowel disease \n\n## . Decreased produ cti on by ba ct er ial flora (eg, frequent antibiotic use )Clinical . Easy br ui sin g\n\n# . Mucosal bl ee ding \n\nfeatures . Gast roi ntes tin al bl eeding Laboratory . 1 PT & I NR \n\nfindings . If severely deficient, 1 PTT Blood & Oncology Second-line therapies : Rituximab, thrombopoietin receptor agonists, and splenectomy \n\n Platelet transfusions are reserved for life-threatening hemorrhage in patients with ITP \n\nTTP \n\n TTP is life threatening and must be treated urgently with plasma exchange (PEX). PEX removes the patient's plasma and replaces it with donor plasma .This replenishes ADAMTS13 and removes the autoantibodies. Without emergent PEX, the mortality rate is approximately 90%. \n\nHUS Anti-D immune globulin (if Rh-positive and Coombs-negative) \n\n462 https://t.me/usmleinnercircle \n\nImmune thrombocytopenia \n\n Platelet autoantibodies \n\nEtiology Preceding viral infection \n\nClinical findings Petechiae, ecchymosis Mucosal bleeding (eg, epistaxis, hematuria) \n\nLaboratory findings Isolated thrombocytopenia <100,000/mm 3\n\n Few platelets (size normal to large) on peripheral smear Children \n\n> o\n\nObserve if cutaneous symptoms only \n\n> o\n\nGlucocorticoids, IVIG , or anti-D if bleeding \n\nTreatment Adults \n\n> o\n\nObservation if cutaneous symptoms AND platelets .:30,000/mm 3o Glucocorticoids, IVIG , or anti-D if bleeding or platelets <30,000/mm 3 \n\n> IVIG\n\n= intravenous immunoglobulin. \n\nThrombotic thrombocytopenic purpura \n\n l ADAMT513 level --+ uncleaved vWF multimers --+ platelet trapping & activation \n\nPathophysiology Acquired (autoantibody) or hereditary \n\n Hemolytic anemia (i LOH , l haptoglobin) with schistocytes \n\n Thrombocytopenia (i bleeding time, n ormal PT/PTT )Sometimes with: \n\nClinical features \n\n Renal failure \n\n Neurologic manifestations \n\n Fever \n\n Plasma exchange \n\nManagement Glucocorticoids \n\n Rituximab \n\nLDH = lactate dehydrogenase; vWF = von Willebrand factor. Blood & Oncology Treatment of the prodromal diarrhea with antibiotics or antimotility agents (eg, loperamide ), as in this case, can increase the risk of developing HUS and is NOT recommended. \n\nDIC Hemophilia \n\n What is the likely diagnosis in an adolescent with a history of hemophilia A that presents with gradually worsening pain and limited motion of his knee? \n\nHemophilic arthropathy \n\ndue to hemosiderin (iron) deposition leading to synovitis and fibrosis within the joint; risk is significantly reduced with prophylactic factor concentrates \n\n463 https://t.me/usmleinnercircle USMLE Inner Circle \n\nHemolytic uremic syndrome Pathogenesis Escherichia coli serotype 0157 :H? or Shigella dysenteriae \n\n Vascular damage & microthrombi formation Preceding bloody diarrhea \n\nClinical features Fatigue, pallor Bruising, petechiae Oliguria, edema Hemolytic anemia (schistocytes, j bilirubin) \n\nLaboratory findings Thrombocytopenia Acute kidney injury (i BUN, j creatinine) Fluid & electrolyte management \n\nTreatment Blood transfusions Dialysis \n\nBUN = blood urea nitrogen. \n\nAcute vs chronic disseminated intravascular coagulation (DIC) Acute DIC Chronic DIC \n\nSepsis \n\nCommon etiologies Severe trauma Malignancy (eg, pancreatic) Obstetric complications \n\nCoagulation studies Prolonged Often normal \n\nPlatelets Low Often normal \n\nFibrinogen Low Often normal \n\nD-dimer High High \n\nBleeding risk Very high Mildly increased \n\nThromboembolism risk Mildly increased Very high Blood & Oncology Inhibitor development occurs in approximately 25% of patients with severe hemophilia A (ie, frequent, spontaneous bleeds) as a complication of treatment. The immune system recognizes the infused factor as foreign, forming antibodies that interfere with factor function. \n\nTherefore, an inhibitor should be suspected when a patient with hemophilia A on factor replacement therapy develops increased bleeding frequency or has hemorrhage refractory to treatment. \n\nTreatment of an acute bleed in a patient with inhibitor development often involves bypassing products (eg, recombinant activated factor VII , activated prothrombin complex concentrates ); such agents work downstream in the coagulation cascade to promote clotting without the need for factor VIII. \n\nHereditory Thrombophilias Pseudothrombocytopenia \n\n464 https://t.me/usmleinnercircle \n\nNormal knee Hemophilic arthropathy Hereditary thrombophilias Factor V Most common in those of white ethnicity \n\n> Leiden Activated protein C resistance\n> Prothrombin 2nd most common in those of white ethnicity\n> mutation\n\n## . t Prothrombin levels \n\n> Antithrombin Inherited form is rare\n> deficiency Acquired : DIC, cirrhosis, nephrotic syndrome\n> Protein Cor jInactivation of factors Va &VIiia\n> S deficiency Warfarin-induced skin necrosis (protein C only)\n\nBlood & Oncology Pseudothrombocytopenia is a laboratory error caused by platelet aggregation in vitro .Most cases are due to incompletely mixed blood samples or the presence of serum antibodies to ethylenediaminetetraacetic acid (EDTA ), an anticoagulant used in hematologic testing. The error is generally identified when a patient with mild thrombocytopenia has peripheral blood smear evidence of large clumps of platelets \n\n## Drugs \n\nHeparin \n\n What is the recommended anticoagulation for pulmonary embolism in a patient with severe renal insufficiency (GFR < 30 mL/min/1.73m2)? \n\nUnfractionated heparin followed by warfarin \n\nWarfarin is preferred long-term oral anticoagulant in ESRD patients, but needs to be bridged first \n\n465 https://t.me/usmleinnercircle USMLE Inner Circle \n\n UWorld !Clumps of platelets I\n\nDrugs/supplements that affect warfarin metabolism (selected) \n\n Acetaminophen , NSAIDs \n\nCYP450 Antibiotics/antifungals (eg, metronidazole) \n\nInhibitors Amiodarone Cimetidine \n\nt Warfarin effect Cranberry juice, Ginkgo biloba, vitamin E Omeprazole ( bleeding risk) Thyroid hormone SSRls (eg, fluoxetine) \n\nCYP450 Carbamazepine, phenytoin \n\nInducers Ginseng, St. John's wort Oral contraceptives \n\nj Warfarin effect Phenobarbital \n\n(I in efficacy) Rifampin \n\nCYP450 = cytochrome P-450; NSAIDs = nonsteroidal anti-in fl ammatory drugs; \n\nSSRls = sel ect ive serotonin reuptake inhib~ors. \n\n UWo rl dBlood & Oncology LMWH and factor Xa inhibitors are not recommended in renal insufficiency because they are metabolized by the kidney \n\nEPO \n\n Up to 30% of patients receiving an ESA for CKD-induced anemia develop new or worsening \n\nhypertension , which typically occurs 2-8 weeks after treatment initiation. Hypertension is generally mild but can be severe. The mechanism by which ESAs cause hypertension appears to be independent of increased blood volume and likely involves systemic vasoconstriction caused by: Activation of erythropoietin receptors on vascular smooth muscle cells Heightened sensitivity of alpha receptors \n\nDepletion of endothelium-derived nitric oxide \n\nThe risk of ESA-induced hypertension is increased by large doses and a rapidly rising hemoglobin \n\nsoon after ESA administration. Following acute treatment of hypertension, subsequent ESA doses should be decreased with a goal of slowly increasing hemoglobin .\n\n## Tumour Blood \n\n The combination of a vascular tumor (e.g. hemangioma) and consumptive thrombocytopenia is indicative of Kasabach-Merritt syndrome. \n\nlarge or rapidly-growing tumors may trap platelets causing severe thrombocytopenia Lesion at Heparin injection site \n\n466 https://t.me/usmleinnercircle \n\nCl ini cal features of type 2 hepar in -ind uced thrombocytopenia \n\n> Suspected with heparin exposure >5 days &any of the following:\n> Clinical Platelet count redu ct ion >50% from baseline\n> si gns Arterial or venous thrombosis Necrotic skin lesions at heparin injection sites Acute systemic (anaphylactoi d) reactions after hepar in\n> Diagnostic Serotonin release assay: Gol d standard confirmatory te st\n> evaluation Start treatment in su spec ted cases prior to confirmatory tests St op ALL heparin products\n> Therapy Start a direct thrombin inhibitor (eg, argatroban) or fondaparinux (synthetic pentasaccharide)\n\nBlood & Oncology Oncology \n\n What is the recommended pharmacologic treatment for patients with cancer-related anorexia /cachexia syndrome (CACS)? \n\nProgesterone analogs (preferred) or corticosteroids \n\ne.g. megestrol acetate ;\n\nSynthetic cannibinoids are useful for HIV cachexia , but not as useful for CACS \n\n Baseline cardiac function should be assessed prior to initiating trastuzumab in patients with HER-2 positive breast cancer. Also routine echo is done during the therapy \n\nTherapies \n\n Salvage therapy is defined as treatment for a disease when standard therapy fails .\n\ni.e. radiation therapy for prostate-specific antigen recurrence after radical prostatectomy for prostate cancer \n\nAdjuvant therapy is defined as treatment given in addition to standard therapy \n\nInduction therapy is an initial dose of treatment to rapidly kill tumor cells and send the patient into remission (<5% tumor burden). A typical example is induction chemotherapy for acute leukemia. \n\n467 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSpecific cancer risk factors \n\n## . Tobacco smoke . Tobacco smoke \n\nPancreas Renal . Obesity \n\n## . Obesity . Hypertension \n\n## . Tobacco smoke . Dietary nitrates . Occupational exposures \n\nGastr ic . Alcohol & tobacco use Bladder (rubber, plastics, aromatic \n\n## . Helicobacter pylori amine-containing dyes, textiles, leather) \n\n## . Hepatitis B & C . Early menarche \n\n## . Li ver cirrhosis (any ca u se) . Late menopause \n\nLiver Breast \n\n## . H emochromatosis . Nulliparity \n\n## . Aflatoxin . BRCA mutations \n\n## . H ereditary CRC syndromes \n\n## . I nflammatory bowel disease . Increasing age \n\nColorect a l Prost ate \n\n## . Obesity . African American \n\n## . Charred or fried foods \n\nCRC = colorectal cancer. \n\nChemotherapy-induced cardioto xi city \n\n Associated with anthracycli nes \n\n Myocyte necrosis & destruction (fibrosis) Ty pe I Progression to overt clinical heart failure \n\n# . Less likely to be reversible \n\n Associated with tr astuzumab \n\n Myocardial stunning/hibernation without \n\nType II myocyte destruction \n\n Asymptoma ti c left ventricu l ar systolic dysfunction \n\n More likely to be reversible \n\nBlood & Oncology Consolidation therapy is typically given after induction therapy with multidrug regimens to further reduce tumor burden. An example is multidrug therapy after induction therapy for acute leukemia. \n\nMaintenance therapy is usually given after induction and consolidation therapies (or initial standard therapy) to kill any residual tumor cells and keep the patient in remission. An example is daily antiandrogen therapy for prostate cance \n\nNeoadjuvant therapy is defined as treatment given before the standard therapy for a particular disease. \n\nRadiotherapy \n\nRadiotherapy has applications as primary, adjuvant, or more commonly palliative therapy for many types of cancer. Tumor sensitivity to radiation depends on the rate of cell turnover, with rapidly growing tumors being more sensitive. In the same way, rapidly dividing normal body tissues such as blood cell precursors, epithelial surfaces in the skin, GI tract, and urinary tract, and the gonads (gametes) are also at risk for damage. \n\nFibrosis and strictures due to diffuse scarring of the damaged tissues often occurs as a late complication of radiotherapy for prostate cancer, and may lead to obstructive uropathy .Therapeutic ionizing radiation (eg, gamma rays, x-rays), commonly used to treat or palliate several types of cancer, can cause cell death through 2 major mechanisms: DNA double-strand breakage : Breakage of both strands is generally required, as single strand breaks are readily repaired by polymerases. Free radical formation: Reactive oxygen species are formed by ionization of water; oxygen free radicals are then able to cause cellular and DNA damage. The effect of radiation is most pronounced in malignant cells as they are rapidly dividing and consequently less able to repair DNA damage. Epithelial surfaces (eg, bowel mucosa, skin) are also severely affected because they are rapidly dividing. A characteristic cell death curve of exposure to radiation shows a nearly flat line on initial exposure, followed by a steep increase in cell death as the radiation dose increases. The steep portion is due to a sharp increase in double-stranded DNA strand fractures and oxygen free radicals. \n\n468 https://t.me/usmleinnercircle \n\nIN CREAS IN G RADIATI ON D OS EBlood & Oncology Most drugs exhibit a sigmoid-shaped dose response curve that shows no effect until a threshold concentration is exceeded. After this occurs, the effects increase with increasing drug concentration until a saturation threshold (ie, maximum effect) is reached. In contrast to this sigmoidal response, the risk of cancer following exposure to ionizing radiation shows a \n\nlinear doseresponse relationship (ie, risk increases proportionately with increased exposure). \n\nPET Scan \n\nPositron emission tomography (PET) scan with 18 fluorodeoxyglucose (FDG), an analog of glucose, is often the imaging test of choice for Lymphoma. Neoplastic cells have a high metabolic rate and readily take up radiotracer on PET scan. \n\nHowever, radiotracer also pools in healthy organs with high glucose requirements such as the \n\nbrain , kidneys , and liver ; excretion of radiotracer also leads to enhancement throughout the urinary collecting system. \n\nCancer Pain \n\n Can a patient with severe , acute pain refractory to NSAIDs and a history of IV drug abuse be given opioids for acute pain management? \n\nYes \n\nmanagement of acute pain is similar for all patients, regardless of substance abuse history \n\n469 https://t.me/usmleinnercircle USMLE Inner Circle \n\nLinear \n\n___ ..,.._ Sigmoid \n\nQ) \n\n1h \n\nC\n\ng_ \n\nVI \n\nQ) \n\n0:: \n\nDose \n\nCancer pain management \n\nChronic ca ncer-related pain ) Mild (eg, - 1-3/10 pain) Nonopioid Acetaminophen or NSAID adjuvant (eg, glucocorticoid, antidepressa nt , anticonvulsan t) \n\nIna deq ua te re lie r\n\n\"Short-act ing opioids for break through pa in should always be ava ,table .ER = extended-release ; NS AID = nonsteroidal anti-inflammatory drug \n\nModerate/severe (eg, - 4-10/ 10 pain) Short-acting opioid Oxycodone, mo r ph ine nonopioid ad juvant \n\nMu lti ple da il y d oses or sleep interruption \n\n+\n\nLong-acting opioid \n\n ER morphi ne , fenta n yl patch nono pi oi d ad juvant \n\nPLUS short-acting opioid for breakthrough pain \n\nClUWO 0Patients on maintenance may require higher doses 0Convert to oral as soon as possible with rapid taper to baseline 0Use for shortest period (3-5 days) if possible\n> NSAIDs ;nonstero idal anti-inflammato ry dru gs .\n\nLymphangitis Epidemiology . Cutan eo us inj ury - p at hogen invasion of lymphatics in deep de rmis \n\n## . Streptococcus pyogenes & MSSA \n\n## . Tender, erythematous streaks proximal to wound \n\nManifestations . Regional tender lymphadenopathy (lymphadenitis) \n\n## . Syst em ic sy mptoms (eg, fever, t ac hycardi a) \n\nTreatment . Cephalexin \n\n> MSSA =meth ici llin -sen sitive Staphylococcus aureus.\n\nBlood & Oncology Acute hemolytic transfusion reaction is distinguished from febrile non-hemolytic reaction by the presence of plasma free hemoglobin > 25 mg/dL. \n\nmay result in a \" pink \" appearing plasma ; plasma free hemoglobin is < 25 mg/dL in febrile non-hemolytic transfusion reactions \n\nT/t: Cessation of Blood product , IV Normal Saline for hydration \n\n471 https://t.me/usmleinnercircle USMLE Inner Circle \n\nIndications for specialized RBC treatments Transfusion reactions timeline Bone ma rr ow transplant (BMT) recipients \n\nIrradiated Acquired or congenital cellul ar immunodeficiency. \n\nIDelayed hemolytic I\n\n Blood components donated by first or second Febrile nonhemo1 ytic degree relatives TR ALI Chronically transfused patients CMV seronegative at-risk patients (e.g., AIDS, IAcute hemolyt ic I\n\nLeukoreduced transpla nt patients) \n\n Potential transplant recipients Previous febrile no nhemolytic transfusion reaction \n\nsecs-mins 1 hour 6 hours 2 days 10 days \n\n lgA deficiency Tim e {not to scale) Complement-24 hours to a month after transfusion Often asymptomatic \n\n# . Fatigue, dyspnea, tachycardia Jaundice \n\n# . Low-grade fever \n\n# . Hemolytic anemia 0 j indirect bilirubin , LOH, reticulocyte count 0 J hemoglobin, haptoglobin New positive direct antiglobulin (Coombs) test Supportive (eg, fluids ) Review transfusion history & pri or antibody screens \n\n Transfuse when necessary with extended-antigen cross-matched blood *Prior transfusion (eg , sickle cell disease patients), pregnancy, transplant. \n\nLOH= lactate dehydrogenase; RBC = red blood cell. Blood & Oncology Transfusion Overload \n\n inc BP (vs TRALI which has hypotension )\n\nCatheter Induced Septic Thrombophlebitis \n\n Catheter-related bloodstream Infections are a common cause of fever in hospitalised patients and can be complicated b catheter-associated septic thrombophlebitis. The infected thrombus serve as a nidus for microbial proliferation and presents with fever and signs and symptoms of bacteremia. The Involved vein may display erythema and induration and there may be purulent drainage from the catheter site. The diagnosis may be aided by duplex ultrasonography or with contrasted CT scan .\n\nTreatment : Infectious source control with removal of the catheter and surgical excIsion of the affected vein, Intravenous antibiotics \n\n## Paeds Blood \n\nPolycythemia \n\n473 https://t.me/usmleinnercircle USMLE Inner Circle \n\nTransfusion reactions Anaphylactic Urticarial \n\n# . Anti-lgA antibodies (lgG or lgE} in lgA-deficient patient . Preformed recipient lgE antibodies against soluble allergen \n\nMechanism against donor blood lgA in donated plasma \n\nOnset . Seconds to minutes . Hours . Respiratory distress/wheeze . Angioedema . Hives \n\nFindings Hypotension Itching . .. Hives \n\n## . Immediate cessation of transfusion . Immediate cessation of transfusion \n\nTreatment . Epinephrine Antihistamines \n\n## . Antihistamines, oxygen, fluids & vasopressors . Resume transfusion if patient is otherwise asymptomati cTransfusion-associated circulatory overload \n\n Age <3 and >60 \n\nRisk factors Underlying cardiac or renal condition Large transfusion volume or fast infusion rate Respiratory distress \n\nClinical features . i Heart rate ( <6 hr following . i Blood pressure transfusion initiati on ) Pulmonary edema (e g, rales) Respiratory support (eg, oxygen )\n\nManagement Diuresis (eg , f urosemide) I Blood & Oncology What is the recommended treatment for symptomatic neonates with polycythemia (e.g. respiratory distress, hypoglycemia)? \n\nPartial exchange transfusion \n\nblood is removed in exchange for normal saline to normalize the hematocrit; asymptomatic infants may be managed with rehydration (e.g. feeding, parenteral fluids) \n\nAnemia of Prematurity \n\n What hematologic pathology is characterized by normocytic anemia with a low reticulocyte count in preterm infants? \n\nAnemia of prematurity \n\nSuspect in premature infants with low RC and low Hb/Hct \n\ndue to impaired ability to produce adequate EPO, short RBC life span, and frequent phlebotomy in the NICU; diagnosis of exclusion \n\n474 https://t.me/usmleinnercircle \n\nNeonatal polycythemia Definition . Hematocrit >65% in term infants Increased erythropoiesis from intrauterine hypoxia: maternal diabetes, hypertension, or smoking; intrauteri ne growth \n\nCauses . restriction Erythrocyte transfusion: delayed cord clamping, twin-twin transfusion Genetic/metabolic disease: hypothyroidism/hyperthyroidis m, genetic trisomy (13, 18 , 21) \n\n Asymptomatic (most common) Ruddy skin \n\nClinical Hypoglycemia, hyperbilirubinemia \n\npresentation Respiratory distress, cyanosis, apnea \n\n Irritability, jitteriness \n\n Abdominal d is tension \n\n Intravenous fluids Treatment Glucose \n\n Partial exchange transfusion Anemia of prematurity \n\n# . t Oxygenation at birth - ! EPO production 0 Impaired transition from he patic to renal EPO \n\n# . Exacerbating factors in premature infants: \n\nPathogenesis ! RBC life span 00 Frequent blood draws 0 Iron de ~letion \n\n# . Often asymptomatic \n\nClinical features . Tachycardia, poor weight gain, apnea, hypoxia \n\nLaboratory findings . Normocytic , normochromic anemia \n\n# . Inadequate reticulocyte response \n\n# . RBC transfusion if severe or symptomatic \n\nManagement . Minimize exacerbating factors (eg, iron supplementation, limit blood draws) \n\n*Typically occurs in the 3rd trimester .EPO = erythropoietin; RBC = red blood ce ll. Blood & Oncology Normocytic anemia use reticulocyte counts to differentiate causes Low: ineffective or decreased RBC production (renal failure, aplastic anemia, anemia of prematurity) High: increased RBC destruction (hemolysis), blood loss \n\nPhysiologic Anemia of Newborn \n\nFindings suggestive of a pathologic cause of anemia ,\n\nHemoglobin <9 g/dL ,\n\nSigns of hemolysis (eg, elevated reticulocyte count), or \n\nMicrocytosis \n\nIDA \n\n What are causes of iron deficiency anemia in young children? \n\nExcessive intake of cow's milk (low in iron )\n\n>24 oz/day \n\nDelayed introduction of solids Cereal-rich diet ( low in iron but usually fortified )Treatment? Iron supplementation \n\n475 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nPhysiologic anemia of infancy Pathogenesis t Tissue oxygenation at birth ----, down-regulation of erythropoietin Asymptomatic term infant* age 2-3 months \n\nClinical features Normocytic anemia (hemoglobin 9-11 g/dL) Low to normal reticulocyte count Reassurance \n\nTreatment/prognosis Anemia resolves with t erythropoietin drive after age 3 months Prete rm infants h ave a lower nadir at a younger ag e (i e, anemia of prematurity) . \n\n\n\n\n\nIron deficiency anemia in young children \n\n## . Pr ematuri ty \n\n## . Le ad exposure \n\n## . Age <1 \n\n0 Delayed introduction of solids \n\nRisk factors (ie, exclusive breastfeeding after 6 months) \n\n0 Cow's, soy, or goat's milk \n\n## . Age >1 \n\n0 >24 oz/day cow's milk \n\n0 <3 servings/day iron-rich foods \n\nDiagnosis . Screening hemoglobin at age 1\n\n## . Hemoglobin <1 1 g/dL, ! MCV, t ROW \n\nTreatment . Em piric trial of iron supplementation \n\nMCV =mea n co rpu scu lar vo lum e; RDW =red bl ood cell dis t ribu ti on widt h. 0\n\n\n\nBlood & Oncology First do a trial of Iron , if it doesnt improve investigate other causes with Hb electropheresis etc. What hematologic pathology is more common in preterm infants within the first 4 - 6 months of life? \n\nIron deficiency anemia \n\nother risk factors for iron deficiency include maternal iron deficiency and introduction of cows milk before age 12 months full-term infants are born with adequate iron stores that prevent anemia in the first 4 - 6 months of life \n\nPancytopenia \n\n476 https://t.me/usmleinnercircle \n\nCommon pediatric causes of pancytopenia \n\n> Pancytopenia } Enhanced cell destruction )Impaired cell production }\n> Hypersplenism Immunologic (SLE)\n\nBone marrow Bone marrow aplasia Infiltration \n\n## ! \n\n> Inherited aplastic anemia\n\n Fanconi anemUI \n\n## l \n\n> Acquired aplastic anemia Idiopathic Drugs &toxins Infection ( HIV .EBV) Radiation Immunologic (SLE) Malnutrition\n\n# l Malignancy Storage disease (Gaucher disease) EBV = Epstein Barr-virus, SLE = systemic lupus erythematosus. CUWor ld Musculoskeletal \n\n# Musculoskeletal Arthritis Osteoarthritis Rheumatoid Arthritis Felty Syndrome Juvenile Idiopathic Arthritis Septic Arthritis Disseminated Gonoccocal Infection Seronegative Spondyloarthritis Gout SLE APLA Mixed Connective Tissue Disorder Sjogren Syndrome Scleroderma Temporomandibular Joint Upper Limb Carpal Tunnel Shoulder Adhesive Capsulitis Rotator Cuff Tear Dislocation Suprascapular Nerve Entrapment De Quervain Tendinopathy Elbow Dupuytren Contractures Lower Limb Trochanteric Bursitis Knee Patellar tendon rupture Patellar Dislocation ACL Injury Patellofemoral Pain Syndrome Popliteal Cyst Meniscal Tear Ankle & Foot Planter Fasciitis Achilles Tendinopathy Calcaneal Apophysitis Spine Spinal Spondylosis Cervical Radiculopathy Cervical Spondylotic Myelopathy Vertebral Compression Fracture Stenosis Spondylolisthesis \n\n477 https://t.me/usmleinnercircle USMLE Inner Circle Musculoskeletal Back Pain Lumber Radiculopathy Spine Trauma Bone Pathology Avascular Necrosis Osteomalacia Pagets Disease Osteoporosis Osteomyelitis Fracture Femur Scaphoid Clavicle Humerus Radius Stress Fracture Buckle & Greenstick Fracture Pelvic Fracture Bursitis Olecranon Bursitis Pes Anserine Bursitis Vasculitis Large Vessel GCA Takayasu Medium Vessel Kawasaki Polyarteritis Nodosa Buerger Disease Small Vessel Behcet Mixed Cryoglobulinemia Granulomatosis with polyangitis Churg Strauss Syndrome Henoch-Schonlein Purpura Myopathy Myasthenia Gravis Raynauds Phenomenon Drugs Bisphosphonate Osteonecrosis Tumors Osteoid Osteoma Osteosarcoma Ewings Sarcoma Miscellaneous Prosthetic Joint Compartment Syndrome Charcot Joint Complex Regional Pain Syndrome Amputation Langerhans Histiocytosis Myositis Ossificans 478 https://t.me/usmleinnercircle Musculoskeletal Arthritis \n\nOsteoarthritis Ganglion Cyst Peads Musculocutaneous Genu Varum Toddlers Fracture DDH Legg-Calve-Perthes Disease SCFE Clubfoot Growing Pains Congenital Muscular Torticolis Transient Synovitis Adolescent Idiopathic Scoliosis Strength Training \n\n479 https://t.me/usmleinnercircle USMLE Inner Circle \n\nRheumatologic diseases & commonly associated autoantibodies Sensitivity(%) Specificity (%) \n\nRheumatoid arthritis RF: 70-80 Anti-CCP: 95 \n\nSystemic lupus erythematosus ANA : 95 Anti-dsDNA/anti-Sm: 96 \n\nDrug-induced lupus ANA: 95 Antihistone : 95 \n\nDiffuse systemic sclerosis ANA : 95 Anti-Scl-70: 99 \n\nLimited systemic sclerosis ANA: 95 Anticentromere : 97 \n\nPolymyositis/dermatomyositis ANA : 75 Anti-Jo-1: 99 \n\nANA = antinuclear antibodies; anti-CCP = anti-cyclic citrullinated peptide; anti-dsDNA = anti-double-stranded DNA; anti-Scl-70 = anti-topoisomerase I; anti-Sm = anti-Smith; RF =rheumatoid factor. \n\nJoint fluid characteristics Normal Noninflammatory Inflammatory Septic joint \n\n(eg, OA) (eg , crystals , RA )Translucent or Appearance Clear Clear Opaque opaque \n\nWBCs(mm 3) <200 200-2,000 2,000-1 00,000 50,000-150,000 \n\nPMNs <2 5% 25% Often >50% >80%-90% \n\nOA = osteoarthritis; PMNs = polymorphonuclear leukocytes; RA = rheumatoid arthritis; WBCs = white blood cells. \n\nDifferential diagnosis for nontraumatic joint swelling Infectious lnflammatory/rheumatologic Neoplastic Onset Acute Subacute/chronic Subacute/chronic \n\nTiming of pain Constant Worse in morning Worse in evening/night \n\nAble to bear weight? No Yes Variable \n\nMultiple joints? Uncommon Common Variable \n\nLaboratory findings j WBCs/platelets j WBCs/platelets, l RBCs l WBCs/platelets \n\nj Inflammatory markers j Inflammatory markers RBC =red blood cell ; WBC =white blood cell. Musculoskeletal predominantly affects the second and third \n\nmetacarpophalangeal joints 480 https://t.me/usmleinnercircle \n\nRisk factors for osteoarthritis Modifiable Nonmodifiable \n\n# . Advanced age \n\n# . Sedentary lifestyle Female sex .. Obesity Family history .. Occupational joint loading Abnormal joint alignment .. Diabetes mellitus . Prior joint trauma \n\nHand osteoarthritis Osteoarthritis Age of onset >40 ; prevalence increases with age \n\n Knees \n\nJoint Hips \n\ninvolvement Distal interphalangeal joints \n\n 1st carpometacarpal joint \n\nMorning None/brief (<30 min) stiffness Systemic Absent symptoms Examination Hard, bony enlargement of joints \n\nfindings Reduced range of motion with crepitus Osteophyte Loss of joint space Hereditary hemochromatosis \n\nManagement of osteoarthritis Nonpharmacologic treatment \n\n(eg, exercise, weight loss) \n\n# 1Symptoms persi st Topical or oral NSAIDs as needed Consider duloxetine, topical capsaicin \n\n# 1\n\nSymptoms persi sV significant impairment Surgery (if possible) Chronic pa in management (nonsurgical candidates) \n\nNSAIDs = nonster Otda l anll-ln fl ammatocy drugs. @UW or ld Musculoskeletal OA develops within 10 years in most patients with anterior cruciate ligament injury Examination findings suggesting OA in the knee include: Periarticular bony hypertrophy and tenderness Limited range of motion with crepitus and pain Small joint effusion without erythema or warmth Varus or valgus angulation Popliteal (Baker) cyst behind Arthrocentesis shows clear fluid with few inflammatory cells and can be helpful in evaluating patients with acute symptoms the joint ESR , CRP and serologic (eg, rheumatoid factor ) markers are normal .\n\nRheumatoid Arthritis \n\n What musculoskeletal pathology is significantly more prevalent in patients with rheumatoid arthritis ?\n\nosteopenia/osteoporosis \n\ndue, in part, to increased levels of pro-inflammatory cytokines, corticosteroid therapy, and lack of physical activity \n\n Much of the Methotrexate toxicity, including hepatotoxicity and stomatitis, can be mitigated by concurrent administration of folic (or folinic) acid , which does not reduce the effectiveness of the drug. \n\n RA has prolonged morning stiffness >30 minutes Methotrexate side effect ( macrocytic anemia )\n\n481 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nExtraarticular manifestations of rheumatoid arthritis Disease-modifying antirheumatic drugs \n\n## . Fever Systemic . Weight loss Agent Mechanism Adverse effects \n\n## . Fatigue \n\n## . Fibrotic lung disease Hepatotoxicity Methotrexate Purine antimetabolite Stomatit is \n\n## . Pleural effusions Pulmonary . Lung nodules Cytopenias \n\n## . Pulmonary hypertension \n\n## . Atherosclerosis \n\nLeflunomide Pyrimidine Hepatotoxicity synthesis inhibitor Cytopenias \n\nCardiovascular . Vasculitis \n\nHydroxychloroquine TNF & IL-1 suppressor Retinopathy \n\nMusculoskeletal . Osteopenia/osteoporosis Dermatologic . Rheumatoid nodules Hepatotoxicity Sulfasalazine TNF & IL-1 suppressor Stomatitis \n\nHematologic . Anemia Hemolytic anemia \n\nNeuropsychiatric . De pression \n\n## . Neuropathy TNF inhibitors Infection Adalimumab Demyelination \n\n## . Sj6g ren s;z: ndrome Certolizumab Congestive heart fai lure \n\nOther . Raynaud phenomenon Etanercept Malignancy \n\n## . Scleritis , episcleritis Golimumab \n\n## . lnfliximab Musculoskeletal Before starting Methotrexate, Patients should be tested for hepatitis B and C . Methotrexate should not be used in patients who are pregnant or are planning to become pregnant in the near future and those with severe renal insufficiency , liver disease , or excessive alcohol intake. \n\n Patients treated with hydroxychloroquine should have a baseline ophthalmologic evaluation , with \n\nannual reassessment beginning after 5 years. \n\n Hoffman sign (flexion and adduction of the thumb when flicking the nail of the middle finger) suggests a \n\ncorticospinal tract lesion and supports the diagnosis of cervical myelopathy; however, it is nonspecific \n\nand may be seen in normal patients. \n\n482 https://t.me/usmleinnercircle \n\nMethotrexate-induced lung injury Pathogenesis . Idiosyncratic (ie, not dose dependent) hypersensitivity pneumonitis \n\n& risk factors . Risk factors : rheumatoid arthritis, parenchymal lung disease \n\n## . Onset 1-12 months : pneumonitis-> fibrosis (restrictive PFTs) \n\nClinical . CT scan with variable mix of patterns: inflammation (eg , GGO , consolidation) & fibrosis (eg , reticulation) \n\nfeatures . BAL : lymphocytosis; peripheral blood: eosinophilia \n\n## . Trial of MTX cessation is diagnostic & therapeutic \n\nBAL = bronchoalveolar lavage ; GGO = ground-glass opacities; MTX = methotrexate; PFTs = pulmonary function tests. Rheumatoid arthr iti s Rheumatoid arthritis of the hand Pe rs lstent symptoms fo r >6 months \n\nSwitch to alternate TNF inh ibitor \n\n& contin ue methotrex ate \n\n> TNF =tumor necrOSIS factof--a .\n\nSymptoms Signs Parallel therapy \n\nAdd another nonbiol og ic agent (eg , su~asalazl ne , hydroxychloroqul ne )\n\nClinical features of RA cervical myelopathy \n\n# . Neck pain radiating to occipital region \n\n## . Slowly progressive spastic quadriparesis \n\n## . Painless sensory deficits in hands or feet \n\n## . Respiratory dysfunction (eg , from vertebral artery compression) \n\n## . Protruding anterior arch of atlas \n\n## . Scoliosis with loss of cervical lordosis \n\n## . Upper motor neuron signs (eg, spastic paresis , hyperreflexia , Babinski sign) \n\n## . Hoffman sign \n\nRA = rheumatoid arthritis. Musculoskeletal Felty Syndrome \n\n Do not diagnose Felty in the absence of neutropenia! \n\nJuvenile Idiopathic Arthritis \n\n D/D: ARF but it has Migratory Polyarthritis and fever < 6 weeks (vs Systemic JIA) Joint swelling is present, but pain may be minimal \n\n483 https://t.me/usmleinnercircle USMLE Inner Circle \n\nFelty syndrome \n\n# . Rheumatoid arthritis \n\n0 Severe erosive joint disease & deformity \n\n0 Rheumatoid nodules \n\nClinical features o Vasculitis (mononeuritis multiplex, necrotizing skin lesions) \n\n# . Neutropenia (ANC <2000/L) \n\n# . Splenomegaly \n\n Anti-CCP & RF are positive in >90% of patients \n\nDiagnosis . Markedly elevated ESR, often >85 mm/hr \n\n# . Peripheral smear & bone marrow biopsy to rule out other causes of neutropenia \n\nANC = absolute neutrophil count; anti-CCP = anticyclic citrullinated peptide; ESR = erythrocyte sedimentation rate; RF= rheumatoid factor. \n\nJuvenile idiopathic arthritis \n\n Symmetric arthritis for at least 6 weeks \n\nClinical features o Polyarticular: ,\".5 joints involved \n\no Oligoarticular: <5 joints involved Elevated inflammatory markers (erythrocyte sedimentation rate, C-reactive protein) Hyperferritinemia \n\nLaboratory findings Hypergammaglobulinemia Thrombocytosis Anemia \n\nJuvenile idiopathic arthritis Subtype Frequency Age of onset Clinical features Sex ratio \n\n Arthritis in 2:1 joint for 2:6 weeks \n\n# . Quotidian fever \n\nSystemic 10% Age <18 for :2:2 weeks F=M \n\n# . Evanescent rash \n\n# . Hepatosplenomegaly \n\n# . Lymphadenopathy Age 2-5 Arthritis in 2:5 joints \n\nPolyarticular 40% . May be complicated F>M or 10-14 by uveitis \n\n Arthritis in <5 joints \n\nOligoarticular 50% Age 2-4 . May be complicated F>M by uveitis Musculoskeletal What fever pattern is seen in patients with systemic-onset juvenile idiopathic arthritis ?\n\nDaily fever spikes (Q uotidian Fever )\n\n Ophthalmologic screening examinations are performed regularly because untreated uveitis \n\nis often asymptomatic and can lead to irreversible vision loss .\n\nSeptic Arthritis \n\n484 https://t.me/usmleinnercircle \n\nln\\'ol\\'('fflffltoflcltlnN.\",\\11h,algus \n\n> ddormI)' o(\n\nkP.,l'f k\"R .and Rn.ion \n\n> coolr.Ktuwoll..r'IN' \n\n\"l'lliOR of p,0%1n\\JI intl'f}>hJL1ngcJI. \n\nm<'t.KdfJ><>ph.1LulR(.al. dnd \"'' t jomts \n\nin 1XNy.irtec:ul,1r onset disease. \n\nlmd,cmm1 usuall) S)mmc1ric, \n\nR('(('(f,ngc.hmrcwl1s from \n\nNf~ dosur(' ol m.1nd1bul~r \n\noss1l,u1ioncmtm,n \n\n> p,ogr<-SS1\\t.' d1it',Ut.'\n\nPathogenesis Clinical features Diagnosis Treatment Septic arthritis \n\n Abnormal joint: OA, RA, prosthetic joint, gout \n\nRisk Age >80 \n\nfactors Diabetes IV drug abuse, alcoholism .. Intra-articular glucocorticoid injections \n\nClinical Acute monoarthritis: hot, swollen, decreased ROM Fever \n\nfeatures Elevated ESR & CRP Blood cultures \n\nDiagnosis Synovial fluid analysis: leukocytosis \n\n(>50,000/mm\\ Gram stain, culture Gram-positive cocci : vancomycin \n\nInitial Gram-negative rod : third-generation cephalosporin \n\ntreatment Negative microscopy: vancomycin (+ third-generation cephalosporin if immunocompromised) CRP =C-reacti ve prote in; ESR =erythrocyte sedimentation rate ; IV = intra venous ;\n\nOA = osteoarthrit is ; RA = rheumato id arthritis; ROM = range of motion .\n\nPediatric septic arthritis \n\n## . Age <3 months: Staphylococcus aureus, group B Streptococcus, gram-negative bacilli \n\n Age .:3 months : Staphylococcus aureus, group A Streptococcus \n\n## . Acute-onset joint pain , swelling , limited motion \n\n## . Refusal to bear weight \n\n## . Fever .:38.5 C (101.3 F) \n\n## . i WBC , ESR , CRP \n\n## . Blood culture \n\n## . Joint aspiration (synovial WBC count of >50, 000/mm 3)\n\n## . Effusion on ultrasound/MRI \n\n## . Joint drainage & debridement \n\n## . IV antibiotics \n\n----\n\nCRP = C-reacti ve protein ; ESR = erythrocyte sedimentation rate; IV= intravenou s; WBC = white blood cell. Musculoskeletal What is the next step in management for a patient with a 3-day history of fever and increasing unilateral knee erythema , pain , and swelling ?\n\nSynovial fluid analysis (Arthrocentesis) both diagnostic and therapeutic any patient with possible septic arthritis should have urgent synovial fluid analysis; septic arthritis progressively worsens over a few days (versus gout which worsens over 12 - 24 hours). \n\n Underlying joint disorders (eg, gout, pseudogout, osteoarthritis) increase the risk for secondary joint infection . In patients with crystal-induced arthritis (eg, gout), the presence of crystals alone does not rule out septic arthritis as these can be present in synovial fluid between attacks. Lyme arthritis presents as an inflammatory monoarticular or asymmetric oligoarticular arthritis, most commonly in the knee .\n\nsynovial fluid analysis typically reveals ~25,000 WBCs/mm3 with negative gram stain /culture ;arthritis is the most common complication of late lyme disease. \n\nIn addition, fever is typically absent. \n\n In general, these wounds should be irrigated and left open due to the high risk of infection. \n\nDisseminated Gonoccocal Infection \n\n485 https://t.me/usmleinnercircle USMLE Inner Circle \n\nClenched-fist bite injury (\"fight bite\") \n\n# . Puncture through thin soft tissue overlying MCP joint \n\nMechanism . Enclosed bacterial proliferation under extensor tendon & within joint capsule \n\n# . Oral flora (eg, Eikenella corrodens, beta-la c tamas e-produc ing anaerobes )\n\nPathogens Skin flora (eg, streptococci , Staphylococcus aureus) .. Small puncture wound appears minor initially; delay in care common \n\nClinical features . Septic arthritis: joint pain, swelling, erythema /wa rmth, restricted /pai nful ROM \n\n# . Urgent surgical irrigation & debridement \n\nManagement . Antibiotics (eg, ampicillin-sulbactam [I V], amoxicillin-clavulanate [PO]) \n\nIV ; int rave nous; MCP ;;; metacarpophalangeal; PO ;;; orally; ROM ;;; range of motion. Disseminated gonococcal infection \n\nPuru lent monoarthritis Clinical &/OR presentation Tri ad of tenosynovitis, dermatitis (erythematous papul es & pustules), asymmetr ic mig ratory \n\npolyarthralgias \n\nBlood cu ltures (may be negative) \n\nDiagnosis Synovial fluid analysis: Inflammatory effusion with neutrophil predomi na n ce ; Gram stain & culture or NAA TCulture or NAA T of urethra, cervix, pharynx, rectum Intrave no us ceftri axone , sw itch to oral (cefixime) when clinically improved \n\nTreatment Em piric azi th romycin OR d oxycy cli ne for concomitant chlamydia! infection Jo int drai nage fo r purulent arthritis Musculoskeletal Seronegative Spondyloarthritis \n\n What is the most likely diagnosis in a young male with a history of back pain that is relieved with activity ? He endorses a history of diarrhea that is worse with NSAID use. \n\nInflammatory bowel disease ( complicated by spondylarthritis )\n\nFurther investigations would reveal sacroiliac joint inflammation ( ankylosing spondylitis ). \n\nNSAIDs are commonly used to treat the back symptoms, but will end up exacerbating the IBD. Chronic Back Pain \n\n486 https://t.me/usmleinnercircle \n\nSkin lesions in disseminated gonococcal infection \n\n> This woman developed a fever, several painful joints, and exquisitely tender necrotic acral pustules. A culture from her cervix grew Neisseria gonorrhoeae.\n\nAnkylosing spondylitis \n\n# . Insidious onset at age <40 \n\n# . Symptoms >3 months \n\nInflammatory back pain Relieved with exercise but not rest .. Nocturnal pain \n\n Arthritis (sacroiliitis) \n\n# . Reduced chest expansion & spinal mobility \n\nExamination findings Enthesitis (tenderness at tendon insertion sites) \n\n# . Dactylitis (swelling of fingers & toes) \n\n# . Uveitis \n\n# . Osteoporosis/vertebral fractures \n\nComplications Aortic regurgitation \n\n# . Cauda equina syndrome \n\n# . Elevated ESR & CRP \n\nLaboratory HLA-B27 association .\n\nImaging X-ray of sacroiliac joints \n\n# . MRI of sacroiliac joints \n\nCRP = C-reactive pr ote in; ESR = erythrocyte sedimentat ion rate. \n\nAnkylosing spondylitis Musculoskeletal What is the likely diagnosis in a young male with dyspnea on exertion accompanied by chronic lower back pain that is worse at night and improves with exercise ?\n\nAnkylosing spondylitis \n\n Patients with longstanding AS can develop osteopenia/osteoporosis due to increased osteoclast \n\nactivity in the setting of chronic inflammation (mediated by TNF- and interleukin-6 ). In addition, spinal rigidity in these patients can increase the risk of vertebral fracture , which often results from minimal trauma. afebrile and low leukocyte count (vs Septic Arthritis) Psoriatic arthritis \n\n487 https://t.me/usmleinnercircle USMLE Inner Circle \n\nTreatment of ankylosing spondylitis \n\n## . Exercise (postural exercises, ROM /stretching \n\nNonpharmacologic exercises) measures . Ph ysical therapy Initial treatment . NSAIDs (eg, ibuprofen, naproxen) \n\n## . COX-2 inhibitors (eg, celecoxib) \n\nTreatment failure/ \n\ndisease . TNF-a inhibitors (eg , etanercept, infliximab) progression . Anti-lL-17 antibodies (eg, secukinumab) COX-2 = cyclooxygenase-2; NSAIOs = nonsteroidal anti-inflammatory drugs; ROM = range of motion; TNF-a = tumor necrosis factor-alpha. \n\nReactive arthritis \n\n Genitourinary infection: Chlamydia trachomatis \n\nPreceding infection Enteritis: Salmonella, Shigella, Yersinia, Campylobacter, C/ostridioides (formerly \n\nC/ostridium) difficile \n\n Asymmetric oligoarthritis Musculoskeletal Enthesitis Dactylitis Ocular: conjunctivitis , anterior uveitis \n\n Gen ita l: urethritis, cervicitis , prostatitis \n\nExtraarticular symptoms Dermal: keratoderma blennorrhagicum, circinate balanitis O ral ulcers Ankylosing spondy li tis Healthy spine Affected spine Musculoskeletal Gout Losartan and CCB lower uric acid levels and likely reduce the risk of an attack. \n\n488 https://t.me/usmleinnercircle \n\nRisk factors for gout Prevention of future gout attacks \n\n Medications (eg , diuretics, low-dose aspirin} Weight loss to achieve BMI <25 kg/m 2 Surgery, trauma, recent hospitalization Low -fat diet Vo ll ume deplletion Decreased seafood & red meat i nt ake \n\nIncreased Di et: High-protein (meat, seafood), high -f at, Protein intake preferably from vegetable & low -fat dairy products \n\nrisk fructose or sweetened beverages Avoidance of or gan-rich foods (eg , liver & sweetbreads) Heavy alcohol consumption Avoidance of beer & disti ll ed spirits Underlying medical conditions (eg, hypertension, Avoidance of diuretics when possi bl eobesity, chronic kidney disease, organ transplant} \n\nDecreased Dairy product intake \n\nrisk Vitamin C (~1500 mg/day} Coffee intake (~6 cups/day) \n\nMedications associated with gout Tophaceous gout \n\n## . Diuretics ( eg , hydrochlorothia z id e, fur osemi de) \n\n## . Salicylates ( eg, low-dose aspirin) \n\nReduced uric acid excretion . ACE inhibito rs (e g, li sin opr il) \n\n## . Cycl os porine \n\nIncreased uric acid production . Cytotoxic chemot herapy agents (tumor lysis syndrom e) \n\n## . Xanthine oxi da se inhibitors (eg, allopurinol) \n\nRapid decline in uric acid levels . Uricosuric drugs (e g, probenecid) NOdu lar masses resUting from excessive monosodium urate crystal deposition .Musculoskeletal In patients with gout , synovial crystals may be seen between flares, so the presence of these crystals alone does not rule out septic arthritis .Septic arthritis can cause acute monoarticular arthritis, but it is typically associated with fever ,systemic manifestations (eg, chills ), and progressively worsening symptoms over a few days ,rather than the abrupt onset seen in gout. \n\n## SLE Characteristically show punched -out erosions with a rim of cortical bone \n\n489 https://t.me/usmleinnercircle USMLE Inner Circle \n\nGout Tophaceous gout \n\n\"EroSIOfls are commonly near (but not at ) the artio.Jar surface. CUWo,td Musculoskeletal Joint involvement in SLE tends to be symmetric , migratory , non-erosive , and associated with brief morning stiffness (versus RA )\n\n Lupus nephritis and subsequent renal failure is a major contributor to mortality in SLE. What test is imperative in investigating the severity of lupus nephropathy? \n\nBiopsy \n\nPerforming screening UA 's are imperative. If things are off, perform biopsy. \n\nOnly a biopsy will be able to tell us the severity of lupus nephropathy (i.e. nephritis, or glomerulosclerosis, or glomerular scarring). It also guides treatment (e.g. scarring is not treatable). Pancytopenia: Immune mediated destruction \n\n490 https://t.me/usmleinnercircle \n\nLurus Systemic lupus erythematosus \n\nPath: Autoimmune, Complex Formation Pt: Women > Men Blacks> Whites Pt: Dx: Tx: Malar Rash Discoid Rash Serositis Oral Ulcers Arthritis Photosensitivity \n\nl5 1 ANA \n\nThen: ds-DNA - Anti-smith Blood Renal Failure \n\nANA \n\nImmunologic Neurology - Anti-Histone (drug induce) Lupus Nephritis \n\n- U/ A -t Bx Kidney Flare Compliment Levels ! in flare \n\n- Compliment levels j in infection Reduce flares: Hydroxychloroquine Control symptoms: NSAIDs Flare: Prednisone Severe : Cyclophosphamide Nephritis: Cyclophosphamide \n\n> Pleuritis /\n\nFeatures of drug-induced lupus erythematosus \n\n> Acute onset of:\n\n## . Constitutional symptoms (eg, fever, malaise) \n\n> Clinical features\n\n## . Arthralgias \n\n## . Serositis (eg, pleuritis, pericarditis) \n\n## . Rash (less common compared with SLE) \n\n> Risk factors\n\n## . High drug dose, prolonged use (>3 months) \n\n## . Slow acetylator status \n\n> Laboratory findings\n\n## . Antihistone antibodies (>90%) . Antinuclear antibodies (>95%) \n\n> Implicated drugs\n\n## . Most common: procainamide, hydralazine, penicillamine \n\n## . Others: minocycline, TNF-a inhibitors (eg, etanercept, infliximab), isoniazid \n\n> *No minimum number of SLE criteria is needed for diagnosis.\n> SLE =systemic lupus erythematosus; TNF-a =tumor necrosis factor-alpha.\n\nSeizures Psychosis Cognitive dysfunction UWorld Musculoskeletal Systemic lupus erythematosus flare during pregnancy is distinguished from preeclampsia by the presence of RBC casts on urinalysis and classic symptoms of SLE (e.g. joint pain, malar rash). \n\nother findings consistent with SLE flare include decreased complement levels and increased ANA titers \n\nAPLA \n\n What is the recommended treatment for a pregnant woman with antiphospholipid syndrome ?\n\nAspirin and Heparin \n\nwarfarin is contraindicated during pregnancy \n\n Heparin prophylaxis is also given in pregnant patients with Factor 5 Leiden mutation (AD) \n\n## Mixed Connective Tissue Disorder Mx: Anticoagulation ( Heparin, Warfarin ) \n\n491 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSLE nephritis in pregnancy \n\n Edema \n\nClinical Presentation Malar rash Arthritis Hematuria Nephritic range proteinuria \n\nLaboratory findings Urinalysis with RBC & WBC casts \n\n J Complement levels \n\n i ANA titers \n\nDiagnosis Renal biopsy Preterm birth Cesarean delivery \n\nObstetric complications Preeclampsia Fetal growth restriction Fetal demise \n\nDiagnostic criteria for antiphosph ol ipid antibody syndrome (1 clinical & 1 laboratory cr it. er ion must. be met) Vasc u la r thrombosis \n\nArteria l/ venous throm bosis \n\nCl inical Pregnancy morbidity \n\n>-3 consecuti ve unexp lained fetal losses before 10th week \n\n>- 1 unexplained fetal loss after 10th wea k\n\n>- 1 premature bi rth of normal neona te before 34th wee,k d ue to preecl am psia, eclampsia, pl ac en tal insufficie ncy Lupus anllcoag ulan l \n\nLaborato ry Anti car\"d iolipin antibody (lgG/ lgM - medium or high tit er )Anti-b et a-2 glycoproteiin 1 anti body (lgGl lgM - high ti ter) Musculoskeletal Sjogren Syndrome \n\n What is the likely diagnosis in an elderly patient that presents with dry eyes and dry mouth ? ANA is negative. Age-related sicca syndrome \n\ndue to age-related exocrine gland atrophy ;\n\nSjogren syndrome typically presents in middle-aged patients with a positive ANA Exocrine output from lacrimal and salivary glands declines with age \n\nSjogren's Syndrome diagnosis key points: often a part of another autoimmune disease (esp SLE), but can be solo; diagnosis clinical but needs confirmation Best initial blood test is SS-A-Ro and SS-B-La testing Best initial overall test is the Schirmer tear production test with a fliter paper on the eye \n\nMost accurate test is a lip or parotid biopsy looking for the lymphocytic infiltration \n\n492 https://t.me/usmleinnercircle \n\nMixed connective tissue disease \n\n Autoimmune disorder with vari ab le features of : \n\n> 0\n\nSystemic lupus erythematosus \n\nDefiniti on 0 Systemic sclerosis \n\n> 0\n\nPolymyositis \n\n> 0\n\nRheumatoid arthritis \n\n# . Raynaud phenomenon \n\n# . Hand/finger swelling Arthritis/synovitis \n\nClinical fe atures . Inflammatory myopathy \n\n# . Pulmonary hypertension \n\n# . Malar or discoid rash \n\n# . Mild CNS &/or kidney disease Anti-U1 ribonucleoprotein Antinucl ear antibody \n\nLabora tory findings Rheumatoid factor, anti-cycl ic citrullinated peptide \n\n# . Elevated creatine kinase \n\n Anemia/cytopenia \n\nDiagnostic criteria. \n\nSjogren syndrome \n\n# . Kerat ocon ju nctiv itis si cca Exocr i ne \n\nfea tu res . Dry mouth, sa li vary hypertrophy . Xerosis . Raynaud phenomenon \n\n## . Cutaneous vasculitis \n\nExtraglandular Arth ra lgia/arthritis .fea tu res . Interstitial lung disease . Non-Hodgkin lymphoma . Objective signs of decreased lacrimation (eg , Schirmer test) \n\nDiagnostic . Positive anti-Ro (SSA) &/or an ti-La (SSB) \n\nfindi ng s . Salivary gland biopsy with focal lymphocytic sialoadenitis . Classification: primary if no associated CTD, secondary if comorbid CTD ( eg, SLE, RA, scleroderma) CTD = connective ti ssue disease; RA = rheumatoid arthritis; S LE = systemic lupus erythematosus; SS A/ SSB = Sj 6g ren sy ndrome (antibody) AJ B. \n\nMusculoskeletal Rose bengal staining reveals an abnormal corneal epithelium if performed Just a reminder that SS also cause: \n\nDental caries secondary to lack of saliva \n\nDyspareunia secondary to lack of vaginal secretions \n\n## Scleroderma \n\nTreatment: ACE inhibitors \n\nreduce RAAS activity and improve renal function and blood pressure Sclerosis of what organ is the most common cause of death in scleroderma ?\n\nLungs \n\ncauses interstitial fibrosis and pulmonary hypertension ;Second most common cause is kidney involvement ( sclerodermal renal crisis )\n\n## Temporomandibular Joint Upper Limb \n\n493 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nSystemic sclerosis can cause interstitial and perivascular fibrosis in the kidneys. The resultant arteriolar vasculitis and glomerulitis can cause scleroderma renal crisis, which manifests with: Sudden-onset hypertension Papilledema Azotemia Microangiopathic hemolytic anemia Hematuria, proteinuria \n\nTemporomandibular joint disorder Risk factors . Joint trauma (eg, injury, bruxism) . Psychiatric illness (eg , anxiety, history of abuse) . Facial pain (worsens with jaw motion) \n\nClinical . Ear pain , tinnitus \n\nmanifestations . Headache (unilateral , worse on awakening) . Jaw dysfunction . Clinical, imaging not typically needed . Tenderness of mastication muscles \n\nDiagnosis Tooth wear (evidence of bruxism) .. Crepitus or clicking with TMJ motion . Education (eg, avoidance of triggers, soft diet) \n\nManagement . Dental splints (if bruxism suspected) . NSAIDs (eg , naproxen) \n\nNSAIDs ; nonsteroidal anti-inflammatory drugs; TMJ ; temporomandibular joint. Musculoskeletal What is the typical prognosis for newborns with Erb-Duchenne or Klumpke palsy secondary to shoulder dystocia? \n\nSpontaneous resolution within 3 months (80%) \n\nrarely surgical intervention is considered for infants with no improvement by age 3 - 6 months \n\nCarpal Tunnel \n\n494 https://t.me/usmleinnercircle \n\n> Metacarpophalangeal\n> jointshyperextende &internally rotated lnterphalangeal Forearm joints flexed supinated\n\nRisk factors Clinical presentation Confirmatory test Treatment Cause Idiopathic/overuse Hypothyroidism Diabetes mellitus Rheumatoid arthritis Pregnancy End-stage renal disease Acromegaly Gout HD = hemodialysis. Wri st& \n\n> Normal arm fingers\n> nexe \"Claw hand\"\n\nErb-Duchenne palsy \n\n> \"Wa iter's tip\n\nCarpal tunnel syndrome \n\n## . Obesity \n\n# . Pregnancy \n\n# . Diabetes mellitus \n\n# . Hypothyroidism \n\n## . Rheumatoid arthritis \n\n# . End -stage renal disease/hemodialysis \n\n## . Pa in & pa resthesia in median nerve dist ri bution (first 3 digits) \n\n# . Pos iti ve Phalen, Tinel , or Durkan (carpal compression) test \n\n# . Severe disease: weakness of thumb abduction & opposition , atrophy of thenar eminence \n\n# . Nerve conduction studies \n\n# . Wrist splinting \n\n# . Glucocorticoid injection \n\n# . Surgery for severe or refractory symptoms \n\nPathophysiology of carpal tunnel syndrome Pathophysiologic features \n\n# . Swelling & fibrosis of tendons & soft tissue \n\n## . Soft tissue enlar gement (mucopolysaccharides) . Soft tissue enlar gement . Microvascu lar insufficiency & neovascularization \n\n## . Extrinsic compression from joint deformity . Edema/fluid accumulation \n\n## . Amyloid & calcium phosphate deposition \n\n## . Access related (bleeding, venous hypertension during HD , vascular steal) \n\n## . Tendon enlargement \n\n## . Synov ial edema \n\n## . Compression from tophi Musculoskeletal Shoulder \n\n Shoulder trauma can also cause acute subacromial (subdeltoid) bursitis , but the pain is usually aggravated by abduction or flexion with the arm internally rotated. Neer test : With the patient's shoulder internally rotated and forearm pronated , the examiner stabilizes the scapula and flexes the humerus .Reproduction of the pain is considered a positive test. Adduction of the arm across the body (ie, cross-body adduction test ), which compresses the AC joint , provokes pain in the AC joint in the superior shoulder in AC joint Sprain. \n\n Rotator Cuff Tear causes weakness with pain (vs Tendinopathy which causes only pain) Limited sensitivity and specificity \n\n495 https://t.me/usmleinnercircle USMLE Inner Circle \n\nProvocative tests for carpal tunnel syndrome Flexion of wr ist compresses nerve inside carpal tunnel Phalen test Tinel sign \n\nCommon causes of shoulder pain \n\n## . Pain with abduction , external rotation Rotator cuff impingement or tendinopathy . Subacromial tenderness \n\n## . Normal range of motion with positive impingement tests (eg, Neer, Hawkins) \n\n## . Similar to rotator cuff tendinopathy \n\nRotator cuff tear Weakness with abduction & external rotation \n\n Age >40 \n\nAdhesive capsulitis (frozen shoulder) . Decreased passive & active range of motion \n\n## . Stiffness pain \n\n Anterior shoulder pain \n\nBiceps tendinopathy or rupture . Pain with lifting, carrying , or overhead reaching \n\n Weakness (less common) \n\n## . Uncommon & usually caused by trauma Glenohumeral osteoarthritis . Gradual onset of anterior or deep shoulder pain \n\n## . Decreased active & passive abduction & external rotation \n\nAC joint sprain Pain over AC joint Passive shoulder adduction provokes pain Musculoskeletal Adhesive Capsulitis \n\n What is the likely diagnosis in a patient with two months of progressive left shoulder stiffness ? The patient has markedly decreased passive and active abduction, flexion, and rotation of the left shoulder. \n\nAdhesive capsulitis ( frozen shoulder )\n\nCharacterized by stiffness out of proportion to pain and reduction in both active and passive ROM \n\nDue to inflammation and fibrosis of the joint capsule DDX : Rotator cuff tendonitis is pain with abduction and external rotation + subacromial tenderness \n\nRotator Cuff Tear Popoye sign in Bicep tendon rupture \n\n496 https://t.me/usmleinnercircle \n\n\n\nAdhesive capsulitis \n\n# . Glenohumeral capsule contracture \n\nPathogenesis . Idiopathic or secondary to shoulder injury (eg, rotator cuff tear, surgery) \n\n# . Risk factors: diabetes mellitus, hypothyroidism \n\nClinical . Gradual onset, poorly localized shoulder pain & stiffness \n\npresentation . Decreased passive & active range of motion \n\n## . Clinical diagnosis \n\nDiagnosis X-ray, MRI , ultrasound to rule out other causes (eg, rotator cuff tendinitis, osteoarthritis) .. Range-of-motion exercises \n\n## . Nonsteroidal anti-inflammatory drugs \n\nTreatment . Corticosteroid injection \n\n## . Arthroscopic distension of joint capsule or surgical release \n\nNatural . Muscle atrophy of shoulder in advanced disease \n\nhistory . Pa in & stiffness may last years Musculoskeletal D/D: Axillary Nerve injury can mimic RCI with pain and weakness of abduction; however, the associated sensory loss over the lateral shoulder area differentiates it from RCI. \n\nDislocation \n\n497 https://t.me/usmleinnercircle USMLE Inner Circle \n\nAcute rotator cuff injury Risk factors . Age >40 \n\n## . Acute glenohumeral dislocation \n\n## . Lateral shoulder pain \n\nClinical presentation . Decreased active range of motion (eg , abduction) \n\n## . Positive drop arm test* \n\n## . MRI Diagnosis Ultrasound .\n\nManagement . Physical therapy \n\n## . Consider surgical repair *The arm is held in 90-degree abduction & released ; inability to hold the arm steady suggests a tear. \n\nDn!l p .i mi t l!S< t ( wp rra !;,,p\" ngJJ us mllS() le) \n\nPa tient is asfre4# to !1rn,w- !1:Je \n\narm slowly t:rom ' clbd'crctioo .\n\nRotator cuff tear \n\nShoulder dislocation Musculoskeletal What is the first choice treatment for anterior shoulder dislocation ?\n\nClosed reduction \n\nCheck for neurovascular (axillary) injuries BEFORE closed reduction is attempted \n\n Anterior Shoulder Dislocation is MOST common \n\nSuprascapular Nerve Entrapment \n\n498 https://t.me/usmleinnercircle \n\nNonnal shoulder Anterior glenohumeral dislocation Posterior shoulder dislocation \n\n## .Mechanism .of injury ..Clinical .features \n\n## .Management ..Complications ..\n\nAcute glenohumeral dislocation \n\nBlow to abducted/raised arm Fall on outstretched hand Violent muscle contraction (eg , seizure) \n\nAnterior dislocation: arm held in abduction/external rotation, anterior prominence of humeral head \n\nPosterior dislocation: arm held in adduction/internal rotation , loss of anterior contour , prominence of coracoid & \n\nacromion \n\nClosed reduction (uncomplicated), surgical repair Immobilization & progressive rehabilitation Fracture (glenoid, proximal humerus , clavicle) Rotator cuff injury Recurrent dislocation \n\nSuprascapular nerve entrapment \n\nSuprascapular \n\nne rv e\n\n# \\ Compression of nerve at \n\nSu perio r trans verse \n\nscapular ligament lnfraspinatus m. Musculoskeletal Clinical features suggestive of SNE at the suprascapular notch include: \n\nshoulder pain \n\nweakness of shoulder abduction (supraspinatus muscle) weakness of external rotation (infraspinatus muscle) Initial management includes NSAIDs and activity modification \n\nDe Quervain Tendinopathy Elbow Exclusively under 5 \n\n499 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nDe Quervain tendinopathy Pathogenesis . Myxoid degeneration of tendons/tendon sheaths \n\n## . Involves abductor pollicis longus & extensor pollicis brevis \n\nSymptoms . Lateral hand/wrist pain \n\n## . Provoked by lifting objects, thumb or wrist movement \n\n## . Based on clinical features (eg, positive provocative testing) \n\nDiagnosis . Tenderness at radial styloid \n\n## . Pain with thumb flexion + ulnar wrist deviation \n\n## . Thumb spica splint \n\nManagement . Nonsteroidal anti-inflammatory drugs \n\n## . Persistent/severe cases: corticosteroid injection \n\nDe Quervain tendinopathy \n\nExtensor retinaculum \n\n# I~ Thumb spica splint \n\n# fAbd,ctoc pollicis loog,s \n\nThickened tendon sheaths Extensor pollicis brevis \n\nRadial head subluxation (nursemaid's elbow) Mechanism Axial traction on forearm with elbow extended (child pulled , lifted , or swung by arm) \n\nPhysical findings Arm held extended & pronated No swelling , deformity, or focal tenderness Hyperpronation of forearm \n\nTreatment OR \n\n Supination of forearm & flexion of elbow Musculoskeletal Dupuytren Contractures \n\n## Lower Limb \n\n What should be suspected in a older patient with groin pain that is relieved with rest and worsens with activity? Examination shows pain on internal rotation of the leg. \n\nOsteoarthritis of the hip ( coxarthrosis )\n\n500 https://t.me/usmleinnercircle \n\nRisk factors Clinical presentation Treatment Dupuytren contracture \n\n# . Male sex , age >50, family history \n\n# . Diabetes mellitus \n\n Tobacco & alcohol use \n\n Thickening of palmar fascia at the 3rd, 4th & 5th digits \n\n# ......\n\nDiscrete nodules along flexor tendons near distal palmar crease Gradual decrease in extension of digits Modification of hand tools (eg, cushion tape, padded gloves) Needle aponeurotomy lntralesional glucocorticoid injection Surgery for contractures or advanced disease Location of pain for common hip disorders Joint pathology (eg, osteoarthritis) \n\nGreater trocha nteric \n\npain syndrome (bursitis, tendonitis) Meralgia paresthetica (late ra l femoral cutaneous nerve compression) \n\n> C)W>rtd\n\nDupuytren contracture Musculoskeletal Trochanteric Bursitis Knee \n\n501 https://t.me/usmleinnercircle USMLE Inner Circle \n\nMeralgia paresthetica \n\nLateral femoral cutaneous nerve entrapment or injury due to: \n\nEtiology . Compression (eg, tight clothing, obesity, pregnancy) . Iatrogenic injury (eg, total hip arthroplasty) \n\nClinical . Paresthesia & ! sensation at lateral thigh \n\nfeatures . Normal motor & reflex examination \n\n Avoidance of tight garments, weight loss . Nonopioid analgesics (eg, NSAIDs) \n\nManagement Anticonvulsants (eg , gabapentin), nerve block, or surgical release for refractory cases \n\nNSAIDs = nonsteroidal anti-inflammatory drugs. \n\nGreater trochanteric pain syndrome (trochanteric bursitis) \n\n## . Age ~50 \n\n## . Women> men \n\nRisk factors . Obesity \n\n## . L ow back & lower extremity disorders (eg , scoli os i s, osteoarthritis, plantar f asc iitis) \n\nSymptoms . Chronic lateral hip pain \n\n## . Pain worse with hip flexion or lying on affected side \n\n## . Focal tenderness over trochanter \n\nDiagnosis . X-ray to rule out hip joint pathology \n\n## . Ultrasound: degeneration of tendons, tendinosis \n\n## . Exercise, physical therapy, activity modification \n\nTreatment . Nonsteroidal anti-inflammatory drugs \n\n## . Corticosteroid injection \n\nSpecial tests for knee examination Valgus stress test MCL injury Stabilize lateral thigh with 1 hand . Place the other along medial leg & apply outward pressure. Laxity indicates MCL injury \n\nAnterior drawer test \n\n Patient supine with knee flexed Grip proximal tibia with both hands & pull anteriorly \n\nACL injury Lachman test \n\n Place knee at 30 degrees flexion Stabilize distal femur with 1 hand & pull proximal tibia anteriorly with the other Laxity of tibia indicates ACL injury \n\nThessaly test \n\n Patient stands on 1 leg with knee flexed 20 degrees Patient then internally & externally rotates on flexed knee \n\nMeniscal tear McMurray test \n\n Passive knee flexion & extension while holding the knee in internal or external rotation Pain , clicking, or catching indicates meniscal tear Musculoskeletal Injury to the popliteal artery is the most feared complication of any knee dislocation because the resulting lower leg ischemia can cause irreversible injury, requiring above-the-knee amputation. Management begins with immediate reduction of the dislocated knee . Given the risk of vascular injury, this should be followed by a meticulous vascular examination that includes: Palpation of the popliteal and distal pulses \n\nMeasurement of the ankle-brachial index (ABI) Duplex ultrasonography (if available) \n\nPatellar tendon rupture Patellofemoral associated with a sensation of instability or \" buckling \" at the knee. Osgood Schlatter \n\n502 https://t.me/usmleinnercircle \n\nDifferential diagnosis of anterior knee pain in the young patient Diagnosis Patellofemoral Patellar Osgood-Schlatter syndrome tendonitis disease \n\nYoung female Primarily Preadolescenl/ \n\nTypical athletes athletes adolescent at hl etes \n\npatient (\"jumper's Recent growth spurt knee\") Subacute to Episodic pain . t Pain with sports , chronic pain & tenderness relieved by rest I with sq uatt in g, at inferior Tenderness &\n\nClinical running , patella swelling at tibial \n\nfeatures prolonged sitt in g, tube rcl eusi ng stairs Pate ll ofemoral compression test Sa \n\nCommon overuse injuries of the knee Patellofemoral . Poorly localized anterior pain \n\nsyndrome . Pain with squatting \n\n## . Common in runners, more common in women \n\nlliotibial band . Poorly localized lateral pain \n\nsyndrome . Tenderness at lateral femoral epicondyle with flexion & extension \n\n## . Common in runners, cyclists \n\nPes anserine . Highly localized medial pain \n\nbursitis . Point tenderness at pes anserine bursa \n\n## . Common with osteoarthritis, diabetes mellitus \n\nPatellar . Localized pain in inferior patella \n\ntendinopathy . Tenderness at tendon insertion at inferior patellar margin \n\n## . Common in jumping sports (eg , basketball , volleyball) \n\nPre patellar . Anterior knee bogginess & tenderness \n\nbursitis . Propensity to secondary infection with Staphylococcus aureus \n\n## . Common in patients who work on their knees (\"housemaid's knee\") Musculoskeletal Risk factors include chronic kidney disease , hyperparathyroidism , fluoroquinolone antibiotics and \n\nanabolic steroid abuse .\n\nPatellar Dislocation \n\n503 https://t.me/usmleinnercircle USMLE Inner Circle \n\nQuadriceps tendon \n\nNormal \n\nPatella \\ z -\n\nPatellar tendon UWorld \n\nNormal knee Normal patella Patellar tendon rupture \n\nSwelling Ruptured patellar tendon \n\nPatellar tendon rupture Patellar tendon rupture Patella baja Musculoskeletal The quadriceps muscles normally exert a lateral force on the patella, especially during quadriceps contraction; therefore, in cases of patellar dislocation, lateral displacement with associated tear of the medial patellofemoral ligament (which normally provides an opposing medial force ) is most common. \n\nSuperior and medial dislocations are rare .T/t: Spontaneous Reduction or Closed Reduction \n\nACL Injury \n\n504 https://t.me/usmleinnercircle \n\nRisk factors Clinical presentation \n\nLaterally displaced patella (right knee) \n\n# I\n\n# \\\n\n## ...\n\n## .....\n\nPatellar dislocation \n\nJoint laxity Misaligned lower extremity Tight iliotibial band Patellar subluxation Competitive sports, dance, military training Quick, twisting motion around a flexed knee Feeling of knee giving way, severe pain, popping noise \n\nExamination : lateral dislocation of patella, decreased extension \n\nPatellar dislocation Normal \n\nQuadrice ps tendon Lateral patellofemoral ligament ligament \n\nDislocated patella Features of anterior cruciate ligament injury Tests for anterior cruciate ligament tear Anterior drawer test \n\nInjury . Rapid deceleration or direction changes \n\nmechanisms . Pivoting on lower extremity with foot planted \n\n# . Pain: sudden onset, severe \n\nSymptoms . Popping sensation at the time of injury \n\n# . Significant swelling (effusion/hemarthrosis) . Joint instability \n\nExamination . Anterior laxity of the tibia relative to the femur (anterior \n\nfindings drawer test, Lachman test) Lachman test . Plain x-rays usually normal, but fracture of tibial spine \n\nImaging or anterolateral tibial plateau suggests ACL tear \n\n# . MRI provides definitive diagnosis \n\nTreatment . RICE (Rest, Ice, Compression , Elevation) measures \n\n# . Surgery depending on age & activity level \n\nACL = anterior cruciate ligament. Musculoskeletal What is the likely diagnosis in an athlete that felt a \"popping sensation\" while playing soccer, followed by rapid pain /swelling ? Aspiration of the knee yields grossly bloody joint fluid. \n\nACL injury \n\na \"popping sensation\" with rapid-onset pain/swelling and hemarthrosis are characteristic of ACL injuries (versus slowly progressive or absent effusion in meniscal tears )\n\nPatellofemoral Pain Syndrome \n\n Atrophy or weakness of the quadriceps or hip abductors is common, and rotational or \n\nvarus /valgus malalignment may be noted. \n\n Dx: Provocation of pain during tonic contraction of the quadriceps with the knee flexed (eg, squatting, lunging); Imaging (eg, x-ray, MRI) is usually normal and needed only to exclude other disorders. Patellofemoral compression test : Extension of the knee while compressing the patella \n\n What is the initial pharmacologic therapy for treatment of patellofemoral pain syndrome ?\n\nNSAIDs \n\nadditional management includes activity modification and strengthening exercises \n\nPopliteal Cyst \n\n505 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPatellofemoral pain syndrome (PFPS) Anterior view Lateral view - - Femur \n\n UWond \n\nPopliteal (Baker) cyst Etiology . Extrusion of fluid from knee joint space into semimembranosus/gastrocnemius bursa \n\nRisk factors . Trauma (eg, meniscal tear) \n\n## . Underlying joint disease (eg, osteoarthritis, rheumatoid arthritis) \n\n## . Asymptomatic bulge behind knee that diminishes with flexion \n\nClinical presentation Posterior knee pain, swelling, stiffness .. Venous compression (leg/ankle swelling) \n\nComplications . Dissection into calf (erythema, edema, positive Homans si gn) \n\n## . Cyst rupture (acute calf eain, warmth, erythema, ecch~mosis~ Musculoskeletal What is the likely diagnosis in a patient that develops acute posterior calf pain /swelling while walking? Physical examination shows tenderness/induration at the medial head of the gastrocnemius and a crescent-shaped patch of ecchymosis at the medial malleolus. \n\nRuptured popliteal cyst \n\nmay resemble a DVT ; before rupture, popliteal cysts present as a painless bulge in the popliteal space \n\nMeniscal Tear \n\nAnkle & Foot Remember with L.I.M.E \n\n506 https://t.me/usmleinnercircle \n\n## .Etiology ..Symptoms ...Examination ..Diagnosis ...Management Meniscal tears Thessaly test for meniscal injury Younger patients : rotational force on planted foot Older patients: degeneration of meniscal cartilage Acute popping sensation Catch in g, locking, reduced range of motion Slow-onset joint effusion Joint line tenderness Pain or catching in provocative tests (Thessaly, McMurray) MRI Arthroscopy Surgery (knee arthroscopy): persistent symptoms &/or impaired activity Conservative management: Patient rotates body side to side with knee in 20\" flexion & foot planted \n\n> 0\n\nMild symptoms without impaired activity \n\n> 0\n\nOlder patients with degenerative tears \n\nMcMurray test for meniscal injury \n\n> @UWorld\n\nExam i ne r ma ximally flexes & exte n ds the kn ee w hile rotating the lower leg External rotation of tibia valgus force stresses medial men iscus Internal rotation of tibia varu s force st resses lateral meniscus Musculoskeletal What is the likely diagnosis in a young female that presents with foot pain? The patient experiences pain and a clicking sensation when the 3rd /4th metatarsal heads are squeezed together .\n\nMorton neuroma \n\nmechanically-induced degenerative neuropathy; Treatment is conservative (e.g. metatarsal support, padded shoe inserts) \n\nMulder sign: squeezing metatarsal joints will cause pain on the plantar surface of the foot along with crepitus between the third and fourth toes. \n\n507 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDifferential diagnosis of heel pain Plantar Maximal pai n on first stepping out of bed \n\nfasciitis Pain & tenderness at medial plantar heel, worse with toe dorsiflexion \n\nAchilles . Posterior pain \n\ntendinopathy . Swelling & tenderness 2-6 cm proximal to tendon insertion \n\n# . Pain that is worse with activity \n\nCalcaneal stress fracture . Pain reproduced by medial-lateral squeezing of the calcaneus \n\nTarsal tunnel Pain , paresthesia & numbness on the sole of the foot \n\nsyndrome Percussion tenderness over the posterior tibial nerve in the tarsal tunnel \n\noverview of runn ing injuries of the foot & ank le Injury Clinical features \n\n In sidious onset Stress Focal pain in navicular or metatarsals \n\nfracture Risk factor s: abrupt increase in intensity of training, poor running mechanics, female with eating disorder \n\nPlantar Plantar surface of the heel \n\nfasciitis Worse wh en initiating running or first steps of the d ay \n\nAchilles Burning pain or stiffness 2-6 cm above the \n\ntendinopathy posterior calcaneus \n\nMorton Numbness or pain between the 3 rd & 4th toes \n\nneuroma Clicking sensation when palpating space between 3rd & 4th toes while sq ueezing the metatarsal jo in ts \n\nTarsal tunnel Compression of the tibial nerve at the ankle \n\nsyndrome Burning, numbness & aching of the distal plantar surface of the fooVtoes \n\nOttawa ankle rules X-ray of the ankle is required if: Medial view Posterior margin or \n\nPa in at the malleolar zone and \n\n Tender at posterior margin/tip of m ed ial ma lleolus OR \n\n Tender at posterior margin/tip of lateral ma ll eo lu s OR \n\n Unable to b ea r weight 4 steps (2 on each fo ot) \n\nX-ray of the foot is requ ir ed if: tip of medial malleolus Lateral view Navicular \n\nI\n\nPain at the midfoot zone and \n\n Tender at the navi cu lar OR \n\n Tender at the base of the 5th metatar sa l OR Posterior margin or \n\n\\ tip of l ate ral malleolus \n\n Un a bl e to b ea r weight 4 steps (2 on each foot) \n\n'i> UW orid Musculoskeletal Use of a soft protective brace and early range of motion exercises through physical therapy is the next most appropriate step in management for this patient who most likely has an ankle sprain .Twisting injuries of the ankle are common and more frequently result from inversion injuries to the lateral ankle. The most important step in the evaluation of ankle injuries is to determine if the patient requires imaging to rule out a clinically significant fracture. \n\nPlanter Fasciitis Achilles Tendinopathy Pain at Anteromedial Heel \n\n508 https://t.me/usmleinnercircle \n\nRisk factors Symptoms Diagnosis Treatment \n\n> C)UWo,td\n\n# ...........\n\nPlantar fasciitis \n\nPes planus Obesity Working or exercising on hard surfaces Pain at plantar aspect of heel & hindfoot Worse with weight bearing (especially after prolonged rest) Tenderness at insertion of plantar fascia Pain with dorsiflexion of toes Presence of heel spurs on x-ray has low sensitivity & specificity Activity modification Stretching exercises Heel pads/orthotics \n\nPlantar fasciitis \n\n> Degeneration of plantar aponeurosis Calcaneus Heel pain with standing or wa lking\n\nMusculoskeletal Complete tendon rupture results in an impaired ability to walk on the tips of the toes because this movement requires the power of the gastrocnemius and soleus muscles \n\nCalcaneal Apophysitis Thompson Test: No Passive Planter Flexion on sqeezing Gastronemius \n\n509 https://t.me/usmleinnercircle USMLE Inner Circle \n\nRisk factors Achilles tendinopathy \n\n# . Athletic activity, increase in activity \n\nRisk factors . Systemic disorders: psoriasis, ankylosing spondylitis . Medicati ons : glucocorticoids, fluoroquinolones \n\nClinical . Swelling, warmth, pain at posterior heel \n\nfeatures . Tendon rupture: \"popping\" sensation & acute pain following rapid acceleration/direction change \n\nExamination . Swelling, tenderness 2-6 cm proxi ma l to tendon insertion \n\nfindings . Rupture: positive Thompson test* . Clinical findings \n\nDiagnosis . Ultrasound : swelling , neovascularization . MRI \n\n# . Acute: activity modification, ice, NSAIDs Management Chronic: eccentric resistance exercises .*With the patient prone and feet off the end of the table, squeeze the calf muscles; the absence of plantar flexion indicates tendon ru pture. \n\nNSAIDs = nonsteroidal anti-inflammatory drugs. Gastrocnemius muscle \n\nCI I.NVortd \n\nCalcaneal apophysitis (Sever disease) \n\n# . Running/jumping sports \n\n# . Growth spurts \n\nNormal Achilles tendon \n\nSoleus muscle Achilles tendon \n\n Athletic cleat use or footwear without heel padding \n\n# . Heel pain (50% bilateral) Calcaneal apophysitis \n\nClinical features . Pain with calcaneal palpation or compression \n\n# . Decreased gastrocnemius/soleus flexibility \n\nTreatment . Nonsteroidal anti-inflammatory drugs, ice \n\n Activity limitation Achilles tendon Growth plate ( apophysis) Musculoskeletal Diagnostic findings include tenderness with squeezing the heel (calcaneal compression test) and on palpation at the base of the heel over the apophysis. \n\n## Spine \n\n What is the likely diagnosis in a child with Down syndrome that presents with behavioural change , urinary incontinence , and upper motor neuron symptoms ?\n\nAtlantoaxial instability \n\ndue to compression of the spinal cord; treatment consists of surgical fusion of the first ( C1 ) and second ( C2 ) cervical vertebrae Excessive mobility between vertebrae C1 and C2, which may cause a subluxation of the cervical spine and spinal cord compression . Symptoms include pain , ataxia , incontinence , quadriparesis , and \n\nquadriplegia .\n\nSpinal Spondylosis \n\nCervical spondylosis is marked by cervical spine degeneration . It is generally associated with 2 clinical syndromes: \n\nCervical radiculopathy: Degeneration and osteophyte formation in the zygapophyseal (facet) and uncovertebral joints lead to intervertebral foramen narrowing and compressive nerve root symptoms. \n\nMost patients have progressive neck, shoulder, and/or arm pain plus weakness in a myotome and sensory loss in a dermatome. \n\n510 https://t.me/usmleinnercircle \n\nDifferential diagnosis of neck pain Condition Clinical clues \n\n> Strain\n\n## . Antecedent history of neck injury \n\n## . Pain/stiffness wit h neck movement \n\n## . Older individuals Facet osteoarthritis . Pain/stiffness worse with movement \n\n## . Relieved wi th rest \n\n## . Pain radiates to shoulder/ arm Radiculopathy . Dermatomal sensory/motor/reflex findings \n\n## . Positive Spurling test Spondylitic myelopathy . LE weakness, gait/bowel/bladder dysfunction \n\n## . Lhermitte sign \n\n## . Young men \n\n## . HLA-B27 Spondyloarthropathy Relieved with exerc is e.. Prolonged morning stiffness \n\n## . Constant pain Spinal metastasis . Worse at night \n\n## . Not responsive to position changes \n\n## . Focal tenderness Vertebral osteomyelitis . Fevers & night sweats \n\n## . IVDU, immune compromise, or recent infection \n\n> IVDU = intravenous drug use :LE = lower extremity.\n\nMusculoskeletal Compressive cervical myelopathy: Degeneration and thickening of the lateral vertebral bodies \n\nand posterior longitudinal ligament lead to spinal canal narrowing and subsequent spinal cord compression .This usually presents with neck pain, lower motor neuron signs in the upper extremities , upper motor neuron signs in the lower extremitie s, and bowel/bladder dysfunction. \n\n What is the likely diagnosis in an elderly patient with right-sided neck pain and sensory deficits over the posterior forearm ? Physical exam reveals limited neck rotation and lateral bending. \n\nCervical spondylosis \n\nlimited neck rotation and lateral bending is due to osteoarthritis with secondary muscle spasm; sensory deficit is due to osteophyte-induced radiculopathy \n\nCervical Radiculopathy \n\nRadiculopathy can occur due to 1. Disk Herniation: Abrupt onset 2. Spinal Spondylosis: subacute, progressive Dx: Clinical ; Imaging NOT required in mild symptoms T/t: NSAIDs and avoidance of provocative \n\n Shoulder abduction reduces tension on the impinged nerve root, and improvement of radicular symptoms when the hand is placed on the top of the head (ie, shoulder abduction relief test ) can be both diagnostic and therapeutic for short-term pain relief. \n\n MRI is recommended only for patients with severe , progressive , or bilateral neurologic deficits, or in those with high concern for malignancy or epidural abscess \n\nCervical Spondylotic Myelopathy \n\n511 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nFeatures of cervical radiculopathy \n\nNerve root Reflex affected Sensory loss* Weakness (disc space) \n\ncs . Shoulder abduction (deltoid) (C4-5) . Biceps . Lateral upper arm Elbow flexion (biceps) .. Elbow flexion (biceps) \n\nC6 . Biceps Thumb . Forearm pronation/supination (C5-6) . Brachioradialis . Index finger (brachioradialis) \n\n Wrist extension \n\nC7 Dorsal forearm . Elbow extension (triceps ) . Triceps Wrist flexion (C6-7 ) . Middle finger Finger extension .\n\nCB . Finger flexion & extension (C7-T1) . Finger flexors** . Ring & little fingers Thumb flexion & abduction \n\nT1 . Finger flexors** . Medial forearm . Finger abduction & adduction (T1-2) *In addition to neck/shoulder pain, radicular pain typically has a similar distribution to sensory loss. \n\n**Not typically evaluated clinically. Musculoskeletal An electric shocklike sensation down the spine with forward flexion of the neck ( Lhermitte sign ) is also commonly seen. MRI scan of the cervical spine is the first test of choice, but myelography is often require \n\n D/D: 1. ALS: but it has assymetric involvement 2. MS: but it doesnt cause LMN signs \n\nVertebral Compression Fracture Stenosis \n\n512 https://t.me/usmleinnercircle \n\nCervical myelopathy \n\n## . Age >55 \n\n## . Degenerative cervical spine/discs -> canal stenosis -> cord Epidemiology compression \n\n## . Gait dysfunction - usually first \n\n## . Extremity weakness & numbness \n\nManifestations . LMN signs (arms) - muscle atrophy, hyporeflexia \n\n## . UMN signs (legs) - Babinsk i, hyperreflexia \n\n## . ! Proprioception/vibration/pain sensation \n\n## . M RI of cervical spine \n\nDiagnosis . CT myelogram \n\n## . Nonsurgical - immobilization \n\nTreatment . Surgical decompression LMN =lower mot or neuron ; UMN =upper motor neuron .\n\nClinical features of vertebral compression fracture \n\n## . Trauma (often trivial) \n\n## . Osteoporosis, osteomalacia \n\nEtiologies . Bone metastases \n\n## . Metabolic (eg, hyperparathyroidism) \n\n## . Paget disease \n\nAcute \n\n## . Back pain & decreased spinal mobility \n\n## . Pain increasing with standing , walking , lying on back \n\nClinical . Referred pain to abdomen/flank \n\npresentation . Spinal tenderness at affected level \n\nChronic/gradual \n\n## . Painless \n\n## . Progressive kyphosis \n\n## . Loss of height \n\n## . Increased risk for future fractures \n\nComplications . Hyperkyphosis - protuberant abdomen, early satiety, weig ht loss, decreased \n\nreseirat0 !}'.: ca eaci~ Musculoskeletal Common causes of lumbar stenosis include vertebral osteoarthritis , degenerative disc disease ,and thickening of the ligamentum flavum. \n\nSpondylolisthesis \n\n What is the likely diagnosis in a child that presents with several months of back pain and recent urinary incontinence with a palpable \"step-off\" at the lumbosacral area on physical exam? \n\nSpondylolisthesis \n\ntypically caused by forward slip of the L5 vertebrae over S1 in preadolescent children \n\n513 https://t.me/usmleinnercircle USMLE Inner Circle \n\nNeurogenic & vascular claudication Neurogenic claudication (pseudoclaudication) Vascular claudication \n\n# . Posture-dependent pain \n\n## . Lumbar extension worsens pai n (eg , wa lking . Exertionally dependent pain downhill) . Pain rel ie ved wi th rest but not with bending Symptoms . Lumbar flexion relieves pain (eg, wal king while forNa rd whi le walk ing \n\nbent forward) . Lo wer extremity c ramping /t ightnes s\n\n## . Lower extremity numbness & ti ngling . No signifi cant l owe r extremity wea kness \n\n## . Lower extremity weakness . Possible buttoc k, thigh, calf, or foot pain \n\n## . Low back pain \n\n# . Decreased pu lses \n\n## . No rmal pulses Cool extrem iti es Examination . Freque ntly normal examination . Decreased hair growth \n\n# . Pallor with leg elevation Diagnosis . MRI of the spine Ankle-brachia! index Spondylolisthesis Pathophysiology . Bilateral pars interarticula ri s defects (eg, fractures) - anterior slippage of vertebral body \n\n## . Most co mm on: LS slips over S1 \n\nRisk factors . Repetitive back extension & rotation (eg, gymnasts, divers) \n\n# . Adolescent growth spurt \n\n## . Low ba ck pain that is worsened by extension \n\nClinical features . Radiculopathy as slippage progresses \n\n## . Palpable step-off m ay be present \n\nDiagnosis . Lumbar x-rays (typically visible on lateral views) \n\nManagement . Activity modification (avoid inciting sports), pain control \n\n## . Neurologic deficits or symptoms >90 days: obtain MRI of spine & surgical consultation Musculoskeletal Back Pain \n\n514 https://t.me/usmleinnercircle \n\nC)UW..ld \n\nSpondylolysis \n\nLS vertebra Fracture of pars interarticularis \n\nDlfferenti al l diagnosis of back pain Condition Cli nical clues \n\nDegenerative . Pos iti onal \n\nfosteoarthritis) . Relieved with rest Radlculopathy .Radiates to leg \n\n(eg , disc herniation) $em.cry & mot or fi 1ndin 9s \n\n## . Positive straight-leg raising test \n\nSpinal stenosis . Pain wi th standing (s pi na l extension) .Relieved by spinal fl exi on \n\n Young men \n\n# . HlA- B27 \n\nSponclyloarthrop at hy . Rel ie ve-d with exercise \n\n# .Prolonged mom s-. g s li lfness \n\n Constant pain \n\nSpinal me taet f Worse al night . Not responsi ve to pos ill M cMnges \n\nVertebra l . Focal tenderness \n\n## . Fever& & ni gh! sweats \n\nSpondylolisthesis spi nal nerve Spondylolysis \n\n- - ---,! --(Fracture of th epa rs in te rarticularis) \n\nosteom)'elltls . Reaml Infecti on , I1111,av enoua drug abuse , or rmrnune comprom ise Musculoskeletal What is the recommended next step in management for a patient with chronic low back pain despite intermittent use of acetaminophen and NSAIDs ?\n\nExercise therapy \n\nif pain persists after exercise therapy and intermittent acetaminophen/ NSAIDs, patients may benefit from TCAs or duloxetine ;\n\nback braces are not effective for prevention of treatment of lower back pain \n\n515 https://t.me/usmleinnercircle USMLE Inner Circle \n\nChronic back pain in adolescents Di agnosis Clini cal features Nocturnal pain Malignancy Systemic symptoms Neurologic findings if spinal cord is involved New-onset sco li osis Back/leg pain worse with activity \n\nTethered cord Neurol og ic findings (eg, weaknes s, hyporefl exi a) \n\n(spinal dysraphism) New-onset sco li osis Lumbosacral cutaneous abnormality \n\n. Nocturnal pain Chronic multifocal osteomyelitis Systemic symptoms \n\nSpondylosis & spondylolisthesis Occurren ce following repetitive trauma (eg, gymnastics) \n\n. Pain with extension \n\n. Morning st iffness Inflammatory arthritis . Pain worse at rest \n\n(eg, ankylosing spondylitis) Sacroiliac joint tenderness \n\nManagement of low back pain \n\n## . Maintain moderate activity Acute pain . NSAIDs or ace ta minophen Co nsi der : muscle relaxants, spinal manipulation, bri ef co urse of op ioi ds \n\n## . Intermittent use of NSAIDs or acetaminophen C hro nic . Exercise th erapy (stretching/s tr engthening, aerobic) pain Co nsi der : tricyclic antidepressants, du l oxe tine Se condary . Exercise therapy prevention . Education \n\nManagement of acute nonspecific back pain \n\n## . Ma intain normal, moderate activity \n\nNonpharmacologic measures . Education (eg, activi ty , prognosis) \n\n## . Consi der : ~ . massage, s~inal mani~ulation, ~,uguc,iuw \n\n## . NSAIDs (eg, naproxen, ibuprofen) \n\nFirst-line medication . Consi der acetaminophen Second-line medication . Nonbenzodiazepine muscle relaxant (eg, cycl ob enzaprine, tizanidine) \n\n## . Opioids, tramadol (not preferred; consider short course for severe, refracto !I eain) \n\nNSAIDs = nonsteroidal anti-inflammatory drugs. Musculoskeletal Lumber Radiculopathy Plain film x-rays have lower sensitivity for bone metastasis , but some guidelines suggest x-ray combined with inflammatory \n\nmarkers to increase sensitivity for patients with moderate clinical suspicion for malignancy. \n\n516 https://t.me/usmleinnercircle \n\nImaging in nontraumatic acute back pain \n\nAcu te bac k pain (<4-6 weeks) \n\nIndications for imaging in low back pain \n\nwithout history of trauma Osteoporosis/com pr ession fracture \n\ni X-ray Suspected malignancy \n\nSign ificant neurologic deficits Ankylosing spondylitis (eg , insid ious onset, nocturn al pai n, bett er \n\nwi th movement) Urinary retention/incontinence, saddle anesthesia (CES) -Yes--+ Emergency MRI I Sensory/motor deficits \n\n LE weakness invo lvi ng multiple nerve roots (cord compress ion )INo \n\n+\n\nSuspected infection Fe ver Sp inal tenderness IVDU/ immunosuppress ion INo \n\n+\n\nSuspected mal ignancy \n\n-Yes--+ MR I or consider x -ray + ESR/CRP \n\nMRI Radionuclide bone scan or \n\nCT scan \n\n Cauda equina syndrome (eg , urine retention, saddle anesthesia) Suspected epidural abscess/infection (eg, fever, intravenous drug abuse, con cu rrent infection, hemodialysis) In dica ti ons for M RI but patient n ot able to have M RI CurrenVrecent cancer hi story _ Yes --+ MRI + ESR/CRP J\n\n Systemic symp toms (eg , weight loss ) Mult iple cancer risk facto rs INo \n\n+\n\nUncomplicated bac k pain ]------+ No imag i ng needed , cont inue pa in ma nagement C ES = cauda 8QlJina syn dr ome : C RP = C-reactive protein: ESR = 8f'y ttvocyte sedimentation rate; IVOU = Intravenous drug use; LE= low er extremity \n\n> C)UWorld\n\nAcute lumbosacral radiculopathy \n\n# . Herniated intervertebral disc ( most common) \n\nCauses . Degenerative spondylosis \n\n# . Malignancy \n\n# . Epidural abscess \n\nSigns & . Pain in low back radiating down posterior leg to foot \n\n# . Positive straight-leg or crossed straight-leg raising test \n\nsymptoms Dermatomal sensory loss & myotomal weakness .. Diagnosis based primarily on clinical features \n\n# . MRI recommended for: \n\nEvaluation 0 Significant/progressive or bilateral neurologic deficits \n\n> 0\n\nEvidence of bladder/bowel dysfunction, saddle anesthesia \n\n> 0\n\nSuspected malignancy or eeidural abscess \n\n Activity modification (not bed rest) \n\n# . First 1-2 weeks: NSAIDs \n\nManagement After 2 weeks : consider physical therapy, oral glucocorticoids \n\n After 4-6 weeks: obtain MR I & assess for surgical indication \n\nNSAIDs = nonsteroidal anti-inflammatory drugs. Musculoskeletal Achilles tendon reflex decreases with age , and its absence is common in older individuals. \n\n(Normal finding) \n\n What is the next step in management for a patient that presents with suspected lumbosacral radiculopathy (sciatica ) after lifting a heavy box? Straight leg-test is positive and neurological exam is unremarkable. \n\nTrial of NSAIDs/acetaminophen \n\nImaging in herniation controversial as it doesn't change management. Therefore no MRI for just back pain + positive SLR alone .If severe/progressive neurological deficits, answer MRI .\n\nMost patients (80%) will experience spontaneous resolution \n\n Should a patient with disk herniation be recommended bed rest ?\n\nNo; maintain ordinary activities \n\nCommonly tested point -- do not do imaging studies in patients without focal neurological abnormalities or with simple lumbosacral strain \n\n What is the likely diagnosis in a patient that presents with back pain after carrying heavy packages? Physical exam reveals paravertebral tenderness . Straight leg-test is negative and neurological exam is unremarkable. \n\nLumbosacral strain \n\nmost common cause of acute back pain that does not radiate below the level of the knee \n\n517 https://t.me/usmleinnercircle USMLE Inner Circle \n\nFeatures of lumbosacral radiculopathy \n\nNerve Root Reflex affected Sensory loss* Weakness \n\n Anteromedial th igh . Hip flexion (iliopsoas) \n\nL2-L4** . Pate llar . Hip adduction \n\n## . Medial shin . Knee extension (quadriceps) Lateral shin . Foot dorsiflexion & inversion (tibialis anterior) \n\n## .LS . None . Foot eversion (peroneus) \n\n## . Dorsum of the foot Toe extension (extensor ha llucis & d igitorum) . Hip extension (gluteus ma xi mus) \n\n## . Posterior calf \n\nS1 Achilles . Knee flexion (hamstrings) \n\n## . Sole & lateral foot . Foot plantarflexion (gastrocnemius) \n\nS2-S4** Anocutaneous Perineum . Urinary o r fecal inc ontinence \n\n## . . Sexual dysfunction \n\nRadicular pain typically has a simil ar distribution to sensory lo ss. \n\n**Difficult to distinguish between individual nerve roots clinically. Musculoskeletal Spine Trauma \n\n What is the first step in the management of cervical spinal trauma ?\n\nSpine immobilization \n\n Cervical spine imaging should be performed whenever there is a high-energy mechanism of injury (eg, high-speed motor vehicle collision, fall 3 m [10 ft], trauma causing concomitant closed-head injury). According to NEXUS criteria, Cervical Spine imaging is necessary if any of the following is present: \n\nNeurologic deficit Spinal tenderness Altered mental status Intoxication Distracting injury (e.g long bone fracture) \n\nA CT scan of the CS without contrast is the preferred screening test to evaluate for CS injury If none of the NEXUS criteria are present, then imaging is not required ; a normal neurologic examination is sufficient to rule out CS injury and remove the collar. The presence of a single vertebral fracture (esp Cervical) in a patient with blunt trauma is an indication to image the entire spine .\n\nCT scan is the screening modality of choice because of its sensitivity and accuracy. \n\n## Bone Pathology \n\nAvascular Necrosis \n\n518 https://t.me/usmleinnercircle \n\nLumbosacral strain \n\n# . Strain of paraspinal muscles, tendons, interverlebral ligaments \n\nCauses Sudden or unbalanced muscle contraction (eg, lifting, twisting ) \n\n# . Risk factors: obesity, seinal deformity or degeneration, muscle weakness Pain in lumbar area; may radiate to buttocks, hips, thighs (above knee) \n\nClinical features . Paraspinal tenderness \n\n# . No neurologic deficits; negative straight-leg raising test \n\n# . Moderate activity \n\nManagement . Nonsteroidal anti-inflammatory drugs Nonbenzodiazepine muscle relaxants \n\nManagement of cervical spine trauma \n\n# . Spinal immobilization (eg, backboard, rigid cervical collar, lateral \n\nPrehospital head supports) . Careful helmet removal (eg, motorcycle helmet) \n\n## . Supplemental oxygenation \n\n## . Orotracheal intubation preferred unless significant facial trauma \n\nEmergency present \n\ndepartment . In-line cervical stabilization suggested unless it interferes with intubation \n\n## . CT of entire cervical spine Musculoskeletal Excessive alcohol use is a major risk factor, with the risk proportionate to the amount and \n\nduration of use. MRI: serpiginous low-intensity lines (T1 images) Crescent Sign on Advanced X-ray \n\n519 https://t.me/usmleinnercircle USMLE Inner Circle \n\nAvascular necrosis \n\n Steroid use \n\n Alcohol abuse Systemic lupus erythematosus \n\nEtiology Antiphospholipid syndrome \n\n# . Hemoglobinopathies (eg, sickle cell) \n\n# . Infectio ns (eg, osteomyelitis, HIV) \n\n# . Renal transplantation Decom 11 ression sickness Groin pain on weight bearing \n\nClini ca l manifestations Pain on hip abduction & internal rotation No erythema, swelling, or poi nt tenderness Normal white blood cell count \n\nLaboratory findings Normal ESR & CRP Crescent sign seen in advanced stage \n\nRadiologic imaging MR I is most sensitive modali ty \n\nCRP =C-reactive protein; ESR =erythrocyte sedimentation rate. \n\nOsteonecrosis (avascular necrosis) Musculoskeletal Initially X-ray and joint movement are NORMAL \n\n The femoral head has 2 main sources of blood - the ascending arteries and the foveal artery , which lies within the ligamentum teres. The foveal artery is patent early in life, but may become obliterated in older patients. For this reason, \n\naseptic necrosis of the femoral head is uncommon in children but the risk rises in older patients. \n\nOsteomalacia \n\n520 https://t.me/usmleinnercircle \n\nOsteonecrosis of the femoral head Clinical features of osteomalacia Rickets \n\n## . Malabsorption \n\n## . Intestinal bypass surgery \n\nCauses . Celiac disease \n\n## . Chronic liver disease \n\n## . Chronic kidney disease \n\n## . May be asymptomatic \n\nSymptoms/signs . Bone pain & muscle weakness \n\n## . Muscle cramps \n\n## . Difficulty walking, waddling gait \n\n## . t Alkaline phosphatase , t PTH \n\n## . ! Serum calcium & phosphorus, ! urinary calcium . ! 25(0H)D levels \n\nDiagnosis . Imaging 0 Cortical thinning & reduced bone density 0 Bilateral symmetric pseudofractures (Looser zones) \n\n25(0H)D = 25-hydroxycholecalciferol; PTH = parathyroid hormone. Musculoskeletal Pagets Disease Urine hydroxyproline reflects collagen breakdown \n\n521 https://t.me/usmleinnercircle USMLE Inner Circle \n\nClinical manifestations of rickets Enl arged -----,: \n\nepiph ys es Clinical features Pathogenesis Laboratory testi ng Imaging Treatment \n\nPseudofracture (osteomalacia) \n\nPaget disease of bone \n\nMost pa tients are asymptoma ti cBone pain & defo rm ity \n\no Skull : Headache, hea ri ng loss \n\no Spine : Spinal stenosis, radiculopathy \n\no Long bones: Bowi ng , fracture, arthri ti s of adjacent jo ints Giant cell tumor, osteosarcoma Osteoclast dy sf unction Increased bo ne turnover Eleva te d alka li ne phosphatase \n\nElevated bone turnover markers (eg, PINP, u ri ne hydroxyproli ne) Calcium & phosphorus a re usually n or m al \n\n X- ra y: Osteolytic or mixed lytic/sclerotic les io ns \n\nBone scan : Focal increase in uptake \n\nBisphosphonates PINP = procollagen type I N-termi nal propepti de . \n\nIMusculoskeletal Most common cause of an asymptomatic elevation of alkaline phosphatase in an elderly patient. \n\nOsteoporosis \n\n What is the recommended screening protocol for osteoporosis ?\n\nOne-time dual-energy x-ray absorptiometry (DEXA scan) for all women > 65 \n\nalso recommended for younger women who have an equivalent risk of osteoporotic fracture \n\n In patients with osteoporosis , the risk for fragility fracture is highest in those with a history of prior fragility fracture .\n\n Osteoporosis is often asymptomatic but increases the risk for fractures, most commonly involving the hip, vertebrae, and distal radius. Osteopenia can limit the detection of occult fractures on x-rays, and when they are suspected , advanced imaging with MRI or CT scan should be pursued. \n\nDEXA is not done when you suspect fracture. \n\n522 https://t.me/usmleinnercircle \n\nI\n\n24-5: A. Radiograph of the humerus in Paget di sease . Note the cortical thickening of the bone and the ragged appearing lytic areas throughout the bone matrix. B, Bone scan showing \" ho t spots in Paget disease . (A from Ka tz D, Math K. Grosk in S: Radiology Secrets, Philadelphia, Hanley & Belfus, 1998, p 311, Fig. 1: \n\nB from Bouloux P: Self-Assessment Picture Tests Medidne, \\.tJI. 4, London, Mosby-Wolfe, 1997 ,p 82, Fig. 163.) \n\n> Osteoporosis r isk facto rs\n> No nmod ifi ab le Modi fi ab le Adva nced age Smo king Post menopause Ex cessive al coho lintake Low body wei gh tSedentary lifestyle\n> Wh ite or As ia n ethnici ty Medi ca tions (eg, glucocorti co ids , anticonvulsants) Malabsorption disorders Vi tamin D de fi ci ency, inadequate ca lcium intake Hypercortisolism, hy perthyroidism, hy perpa ra thyroidi sm Estrogen deficiency (eg, pr emature menopause,\n> Inflammatory disorders ( eg , rheumatoid arthri ti s) hysterectomy/oophorectomy)\n> Chron ic liver or renal disease\n\nMusculoskeletal Osteomyelitis \n\n What is the next step in management for a patient with suspected vertebral osteomyelitis that has a significantly elevated ESR with normal spinal X-ray ?\n\nMRI \n\nfollowed by CT-guided bone biopsy if positive \n\n523 https://t.me/usmleinnercircle USMLE Inner Circle \n\nMedications asso ci at ed with osteopor ot ic fra ctures M edicati on Possi bl e me chanism \n\nAnticonvu lsants that induce cytochrome P450 T Vitamin D catabolism (phenobarbital, phenytoin, carbamazepine) Aromatase inhibitors \n\n! Estrogen Medroxyprogesterone GnR H agonists ! Testosterone & estrogen Proton pump in hibitors ! Calcium absorpt ion Glucocorticoids \n\n! Bone formation Unfractionated heparin \n\nClues to secondary causes of bone loss Sec onda ry c auses of osteopo ros is \n\n. Diarrhea, weight loss Malabsorption . ! 25- H yd roxyvita min D, ! urine calcium excretion Hyperthyroidism . Weig ht loss , h ea t int olerance, tr emo r\n\n## . Go it er \n\n## . Hyperthyroi dism \n\n## . Hyperparathyroidism Endocrin e Hypercortisolism .. Hypogonadism Hypercortisolism . Cen tral obesity/cushingoid habit us \n\n## . Hyperglycemia \n\nMetaboli c/ nu t ri ti ona l . Calcium &/or vitamin D deficiency \n\n. Eating disorder Hyperparathyroidism . H ype r ca lce mi a, hypercalciuria \n\n. Kidney stones \n\n## . Malabsorpti on (eg, ce li ac disease, Crohn disease) Ga st rointes tin a l/ hepatic Chronic liver disease .Inflammatory disorde r . Jo int pain, mo rning stiffn ess (eg, rh eu matoid arthriti s) . 1 ESR, C RP Re nal . Chronic kidn ey disease \n\n. Renal tubular acidosis \n\n## . ~ : ameno rrhea, weight loss/anor exia Hypogonadism . d: ! libi do , erectile dysfunction, loss of body ha ir \n\n. Glucocorticoids M edica t ions . Phenytoin , carbamazepine . Proton pump inhibitors \n\n. An em ia Multiple myeloma . H ype r ca lce mi a, i creatinine . Inflammatory disorder (eg, rheumatoid arthritis) CRP = C-reactive protein; ESR = erythrocyte sedimentation rate. Oth er . Multiple mye loma \n\n## . Alcohol use disorder \n\n. Immobilization Musculoskeletal MRI is the most sensitive diagnostic study in the work-up, but biopsy is the best confirmatory test \n\n What is the empiric treatment for osteomyelitis in adults ?\n\nIV vancomycin + antipseudomonals ( cephalosporins or fluoroquinolones )\n\n524 https://t.me/usmleinnercircle \n\nVertebral osteomyelitis \n\n# . Staphylococcus aureus most common \n\nPathogenesis . Hematogenous seeding (eg, distant infection, IVDU, intravenous catheter) \n\n# . Contiguous spread from local infection \n\n# . Penetrating injury, invasive procedure/iatrogenic \n\n# . Subacute-chronic pain & midline spinal tenderness \n\nClinical features . +/- Fever \n\n# . Possible radiculopathy, LE weakness \n\n# . Elevated CRP/ESR \n\nDiagnosis . MRI \n\n# . Blood culture, CT-guided bone biopsy/culture \n\nComplications Abscess/epidural extension/neuro logic deficits \n\n Vertebral collapse \n\n# . Intravenous antibiotics Management Drainage of any associated abscesses .\n\nEvalua t io n of v ert ebral osteo my eli tis Fever , back pa in & focat spinal tenderness \n\nBlood cultures \n\nESR/CRP \n\nPlain spinal x-rays \n\nf ESR/CRP but normal x-rays \n\n# TCT guided needle aspi rat ion / biopsy CRP = C-reactive protein ; ESR = erythrocyte sed imentation rate ; IVDU = intra venou s drug use; LE = lower ext remity .\n\nNuclear study \n\nScmt,graphy \n\n< 2weeks \n\n# iPat ien t MRI \n\nClinically suspected osteomyelitis \n\nOrder labs \n\nESRICRP, \\W Cs, \n\nblood cultures \n\nOnset of symptoms? \n\n+with meta~ \n\nimplant CT ,r MRI contramd,cated \n\nNo findings typical of \n\nosteomyel rtis \n\nTypical findings of osteomyel rtis \n\n. ~---Yes---\n\nStart empiric antibiotics \n\n> I\n\nSwrtch to \n\n+\n\nSpecific antibiotics \n\nt.tx,,, culture resu lt s\n\n# Osteomyelitis Bone biopsy feasible? \n\n> 2weeks \n\n# i\n\nX-ray Empiric antibiotics only :__ _________ ____ ____ Possible Surgery - - - - - - - --\n\nNo other imaging available \n\n'f \n\nUltrasound Musculoskeletal Treat after bone biopsy is done! \n\n What is the likely diagnosis in a patient with a recent UTI that presents with fever , back pain , focal tenderness over the L4-L5 vertebrae , and paravertebral muscle spasm ?\n\nVertebral osteomyelitis \n\nmost likely due to hematogenous spread of the UTI; initial workup includes CBC, blood cultures, ESR/CRP, and plain spinal X-rays A high index of suspicion for progenitor vertebral osteomyelitis should be present when examining patients with history of IV drug use or recent distant site infection ( UTI ). \n\n Fever and leukocytosis are unreliable findings! May be normal in vertebral osteomyelitis \n\n What is the likely causative organism in a patient that develops osteomyelitis after stepping on a rusty nail? The nail pierced the patient's shoes and pierced the heel. \n\nPseudomonas aeruginosa \n\nStaph aureus and Pseudomonas are responsible for most deep infections following puncture wounds; the sole of a shoe (warm, moist) is a hospitable environment for Pseudomonas \n\n Osteomyelitis in diabetic patients is typically preceded by a long-standing foot ulcer that spreads contiguously to bone, causing a poly-microbial infection. \n\nPatients almost always have polymicrobial infections with gram-positive, -negative, and anaerobic organisms Most likely due to contiguous spread from the overlying ulcer. \n\nHematogenous spread of osteomyelitis usually affects the vertebrae, pelvis, and hips \n\nT/t: IV Antibiotics \n\nFoot imaging (eg, x-ray, MRI ) is generally recommended for all diabetic foot ulcers to rule out Osteomyelitis that are: \n\ndeep (eg, exposed bone, positive probe-to-bone testing). \n\nlong-standing (eg, present >7-14 days). \n\nlarge (eg, 2 cm). associated with elevated ESR/CRP .associated with adjacent soft tissue infection .\n\n If you suspect Osteomyelitis in Diabetic Ulcer, Do a BIOPSY to confirm \n\n525 https://t.me/usmleinnercircle USMLE Inner Circle \n\nMusculoskeletal In children, osteomyelitis most often occurs in the metaphyses of bones (highly vascular) and develops secondary to hematogenous spread. \n\n## Fracture \n\n526 https://t.me/usmleinnercircle \n\nOsteomyelitis in children Patient population Most common organisms Empiric antibiotic therapy \n\n## . Low likelihood of MRSA \n\n> 0\n\nNafcillin/oxacillin OR cefazolin Healthy children . Staphylococcus aureus High likelihood of MRSA . 0 Clindamycin OR vancomycin \n\n As above .Children with sickle cell disease Salmonella spp PLUS \n\n## . Staphylococcus aureus Third-generation cephalosporin (ceftriaxone, cefotaxime) \n\nMRSA = meth icillin-resistant Staphylococcus aureus. \n\n## .Mechanisms ...Pathogens ...\n\nRisk factors ...\n\nClinical features ...\n\nDiagnosis ...Management .\n\nProgression of hematogenous osteomyelitis \n\nBacterial seeding results \n\nin focal bone marrow \n\ncellulitis \n\nInflammation within \n\nconfined space compromises blood flow ,\n\ncausing necrosis \n\nInfection forced through \n\nvascular channels into \n\nthe cortex and spreads along periosteum \n\nReactive bone \n\n(involucrum) \n\nsinus \n\nRetained, necrotic bone (sequestrum) \n\n UWorld Developmen t of chronic sequela \n\nChronic osteomyelitis \n\nHematogenous seeding Extension from infection in adjacent structure Direct inoculation (eg, compound fracture , bite wound) \n\nS taphylococcus aureus (most common) Coagulase-negative staphylococci Polymicrobial Surgical hardware/instrumentation Diabetes Impaired circulation or sensation in the limb Persistent pain, swelling, chronic wound Sinus tract formation Nonunion of fracture Positive probe-to-bone test Imaging: lytic lesion with loss of cortical & trabecular bone, surrounding sclerosis, periosteal thickening Bone biopsy for culture Surgical debridement Antibiotics (prolonged course) Musculoskeletal Injury to the growth plate can cause growth arrest and lead to persistent limb-length discrepancy. \n\nFemur \n\n527 https://t.me/usmleinnercircle USMLE Inner Circle \n\nNormal Tibia Growth plate \n\nCHJWorid \n\nType Ill \n\nGrowth plate \n\nand epiphys is \n\nPosterior glenohumeral dislocation Supracondylar \n\nhumerus fra cture \n\nOJ World \n\nUlnar styloid fracture \n\nSalter-Harris fracture classification Type I Ty pe II \n\nAcross growth plate Growth plate and metaphys is Type IV \n\nGrowth plate , metaphysis ,and ep iphys is TypeV Compress ion fracture of growth plate FOOSH : fall on an outstretched hand \n\nDistal rad ius (Calles) fracture Scapho id fracture Musculoskeletal When should older patients with hip fractures undergo definitive surgical correction ?\n\nAs soon as reasonably possible \n\nmay delay up to 72 hours to evaluate surgical risk and ensure medical stability (i.e. cardiac and pulmonary work up if needed )\n\nScaphoid \n\n How should non-displaced scaphoid fractures be managed? \n\nWrist immobilization with a cast \n\npatients should also be monitored with serial X-ray to rule out osteonecrosis of the proximal segment and non-union of the fracture \n\n If Displaced: should undergo ORIF (if >1mm) \n\n X-ray at the time of injury has low sensitivity for scaphoid fracture if initial x-rays are negative, CT scan or MRI of the wrist is recommended As an alternative, the wrist can be immobilized briefly in a thumb spica splint , followed by repeat imaging in 7-10 days .\n\nClavicle \n\n528 https://t.me/usmleinnercircle \n\nFemoral neck fracture Common types of hip fracture Femoral neck fracture lntertrochanteric hip fracture \n\nFemoral neck fracture \n\n# . Severe hip pain & inability to bear weight after a fall \n\nClinical presentation Risk factors: age >65, frailty, osteoporosis . Shortened , externally rotated leg \n\nExamination findings . Painful range of motion . Ecchymosis \n\n# . Disruption of cortical contour \n\n# . External rotation of distal fragment (prominence of lesser trochanter profile) \n\nX-ray findings Shortening of neck \n\n# . Lucency or hazy sclerosis at fracture plane \n\nManagement Open reduction/internal fixation or arthroplasty Musculoskeletal Are fractures of the middle-third of the clavicle typically treated operatively? \n\nNo \n\nusually treated non-operatively with a brace (figure of 8 splint) , rest , and ice ;careful neurovascular examination is required to rule out underlying brachial plexus and/or subclavian artery injury \n\nHumerus \n\n Can damage Median Nerve or Brachial Artery Clavicle Fractures in neonates heal fast 7-10 days, no splint necessary \n\n529 https://t.me/usmleinnercircle USMLE Inner Circle \n\nNeonatal displaced clavicular fracture \n\n# . Fetal macrosomia (maternal diabetes mellitus, postterm pregnancy) \n\nRisk factors . Instrumental delivery (vacuum or forceps) \n\n# . Shoulder d~stocia \n\n# . Crying/pain with passive motion of affected extremity \n\nClinical features . Crepitus over clavicle \n\n# . Asymmetric Moro reflex \n\nDiagnosis . X-ray \n\n# . Reassurance \n\nTreatment . Gentle handling \n\n# . Analgesics \n\n# . Place affected arm in a long-sleeved garment & pin sleeve to chest with elbow flexed at 90 degrees \n\nSupracondylar fracture \n\n Fall onto outstretched arm \n\nClinical features \n\n Pain , swelling, limited range of motion \n\nDiagnostic findings X-ray with posterior fat pad (occult), fracture line, or displacement of humerus Nondisplaced: long arm splint & sling \n\nTreatment \n\n Displaced : surgical reduction & pinning Neurovascular injury \n\nComplications Compartment syndrome \n\nSupracondylar humeral fracture Anterolateral displacement of proximal fragment \n\nAnteromedial displacement of proximal fragment \n\nHumerus \n\n(fractured) \n\nRadial nerve \n\n(injured) Lateral epicondyle \n\nUWond \n\nBrachial artery \n\nMedian nerve \n\nMedial epicondyle \n\nMedian nerve \n\n(injured) Musculoskeletal Open reduction and surgical exploration are indicated with 1. open fractures ,2. significant displacement (eg, arm shorteningt), 3. neurovascular compromise (eg, asymmetric radial pulses), 4. polytrauma , and pathologic fractures. \n\nRadius Stress Fracture \n\n Which metatarsal is most commonly injured by stress fractures ?\n\n2nd metatarsal \n\nsecond metatarsal is subjected to significant load during gait \n\nD/D: Medial Tibial Stress Syndrome (Shin Splints) : causes diffuse pain in anterior tibia (vs point tenderness) \n\n530 https://t.me/usmleinnercircle \n\n> Colles fracture\n\nColles fracture Dinner fork defonnity \n\nClinical features of stress fracture \n\n# . Repetitive activities (eg, running, military marching) \n\nRisk Abrupt increase in physical activity volume & intensity \n\nfactors . Low BMD from inadequate nutrition, malabsorption, estrogen deficiency in women (eg, functional hypothalamic amenorrhea) . Insidious, gradual worsening onset of localized pain \n\nClinical . Point tenderness at fracture site \n\npresentation Usually negative x-ray in the first 2-3 weeks \n\n Analgesia & reduced weight bearing \n\nManagement . Referral to orthopedic surgeon for high-risk fracture (eg , anterior tibial cortex, 5th metatarsal) \n\nBMD = bone mineral density. Musculoskeletal Buckle & Greenstick Fracture Pelvic Fracture \n\n Patients with severe pelvic fractures, such as open-book pelvic fracture (ie, pelvic ring disruption with anterior widening), are at risk for life-threatening hemorrhage .caused by the tearing of the thin-walled venous plexus (presacral, lumbar). Rapid, external stabilization with a pelvic binder should be performed as soon as possible in \n\nhemodynamically unstable patient ( this decreases pelvic volume and promotes tamponade of venous bleeding )\n\n531 https://t.me/usmleinnercircle USMLE Inner Circle \n\nBu ck le fracture Greenstick fracture (radius) \n\nOpen book pelvic fracture Musculoskeletal Bursitis \n\n During a joint or bursal aspiration or injection , introduction of skin flora may result in septic bursitis or septic arthritis, presenting as worsening pain several days following the procedure. \n\nDiagnostic aspiration of the joint or bursa is necessary to assess for infection. \n\nOlecranon Bursitis \n\n Aspiration only if infection is suspected \n\n532 https://t.me/usmleinnercircle \n\nSeptic bursitis Prepatellar bursitis \n\n Local cellulitis , abrasions, or penetrating trauma \n\nRisk factors . Bursal instrumentation/injection, prior bursal inflammation . lmmunocompromised state \n\n Painful, localized bursa l swelling with erythema & warmth \n\nPresentation . Fever, chills, myalgias \n\n Consider diagnostic aspiration of bursal fluid \n\nDiagnosis Consider x-ray (for suspected fracture , foreign body , or osteomyelitis) \n\n# . Systemic antibiotics \n\nTreatment \n\n Drainage in select cases \n\nOlecranon bursitis \n\n# . Chronic overus e/microtrauma \n\nEtiology A cute trauma/ hemorrhage \n\n Inflammatory (eg , gout , rheumatoid arthritis) \n\n Septic (eg , l'.)enetrating injury, spread from regional infection) \n\n# . Rounded swelling at posterior elbow , fluctuant on palpation \n\nClinical . Local pain (often absent if chronic) \n\npresentation Erythema, warmth, fever , or significant pain suggests infectious or inflammatory cause \n\n X-ray if fracture is suspected \n\nEvaluation . Bursal aspiration (eg, Gram stain, culture) in select cases \n\n# . Rest , ice, NSAID s, padding to reduce friction \n\nManagement . Septic : antistaphylococcal antibiotics, drainage \n\n Inflammatory: treat underlying gout , rheumatoid arthritis \n\nNSAIDs = nonsteroidal anti-inflammatory drugs. Musculoskeletal Gout can affect superficial bursae (eg, olecranon, prepatellar) in multiple ways: \n\nAcute bursitis in a gout flare, presenting with erythema , warmth , and swelling Chronic bursitis , presenting with a large , rounded, fluctuant effusion Bursal tophus , manifesting as a slowly enlarging, hard mass \n\nPes Anserine Bursitis \n\n What is the likely diagnosis in a young patient that presents with sharp, non-radiating pain on the medial side of the tibia just below the knee after falling one week ago? A valgus stress test has no effect on the pain. \n\nPes anserinus pain syndrome (anserine bursitis) \n\nno pain with valgus stress test indicates no MCL involvement \n\nPes anserine bursitis presents as a swelling over the upper medial tibial region . It is typically caused by overuse, obesity and poor knee mechanics. Treatment: \n\n1. NSAIDs 2. Quadriceps and Hamstring muscles exercise - to stablize knee When redness, warmth, and severe tenderness accompany bursal swelling, an aspiration should be done to rule out septic bursitis \n\n D/D: Osteoarthritis : progressive over years not months or weeks and involves crepitus / mild effusion \n\n## Vasculitis \n\nLarge Vessel Chronic Bursitis \n\n533 https://t.me/usmleinnercircle USMLE Inner Circle \n\nMusculoskeletal GCA \n\n AION : Fundoscopy shows a swollen pale disc with blurred margins . What aortic complication is associated with giant cell (temporal ) arteritis ?\n\nAortic aneurysm \n\nPatients should be followed with serial chest X-rays \n\nTakayasu \n\nMedium Vessel \n\nKawasaki \n\n534 https://t.me/usmleinnercircle \n\nGiant cell arteritis: clinical manifestations Systemic . Fever, fatigue , malaise, weight loss \n\nsymptoms \n\n## . Headaches: located in temporal areas \n\n## . Jaw claudication: most specific symptom of GCA \n\nLocalized . PMR symptoms . Arm claudication: associated bruits in subclavian or axillary areas \n\n Aortic wall thickening or aneurysms \n\n## . CNS : TIAs/stroke, vertigo, hearing loss \n\nVisual . Amaurosis fugax: transient vision field defect progressing to monocular blindness \n\nsymptoms AION: most common ocular manifestation .. Normochromic anemia \n\nLaboratory Elevated ESR & CRP .results . Temporal artery biopsy \n\n## . PMR onl y: low-dose oral glucocorticoids (eg, prednisone 10-20 mg daily) \n\n## . GCA : intermediate- to high-dose oral glucocorticoids (eg, prednisone 40-\n\nTreatment 60 mg daily) \n\n## . GCA with vision loss: pulse high-dose IV glucocorticoids (eg, methylprednisolone 1,000 mg daily) for 3 days followed by intermediate-to high-dose oral glucocorticoids \n\nAION =anterior ischemic optic neuropathy; CRP =C-reactive protein; ESR =erythrocyte sedimentation rate; GCA =giant cell arteritis; IV= intravenous; PMR =polymyalgia rheumatica; \n\nTIA =transient ischemic attack. \n\nTakayasu arteritis \n\n Female Risk factors Asian Age 10-40 Constitutional (eg, fever, weight loss) \n\nSymptoms Arterio-occlusive (eg, claudication , ulcers) in upper extremities Arthralgias/myalgias Blood pressure discrepancies \n\nExamination Pulse deficits \n\nfindings \n\n Arterial bruits Elevated inflammatory markers (eg , ESR, CRP) \n\nDiagnosis Chest x-ray: Aortic dilation, widened mediastinum CT/MRI : Wall thickening , narrowing of lumen \n\nTreatment Systemic glucocorticoids CRP = C-reactive protein ; ESR = erythrocyte sed i men tati on rate Musculoskeletal Echocardiography should be performed at the time of diagnosis and again 6 - 8 weeks later ;dilated arteries are prone to thrombotic occlusion, which may cause myocardial ischemia and/or infarction \n\n Pathophysiology of cardiac involvement relates to systemic inflammation leading to infiltration of \n\nlymphocytes and macrophages into cardiac tissues and vasculature. Complications include: \n\nCoronary artery aneurysm : severe dilatation can lead to stenosis/thrombosis and myocardial infarction \n\nVentricular dysfunction : systemic inflammation or lymphocytic myocarditis can cause poor contractility and heart failure Pericardial effusion : cardiac tamponade may result \n\nPolyarteritis Nodosa \n\n535 https://t.me/usmleinnercircle USMLE Inner Circle \n\nKawasaki disease \n\n## . Medium-vessel vasculitis \n\nPathophysiology & epidemiology . Usually affects children age <5 . t Incidence in East Asian ethnicity \n\n## . Fever ~5 days plus ~4 of the following : \n\n0 Conjunctivitis: bilateral, nonexudative \n\n0 Mucositis: injected/fissured lips or pharynx, strawberry tongue \n\nDiagnostic criteria 0 Cervical lymphadenopathy: ~1 node >1.5 cm \n\n0 Rash: perinea! erythema & desquamation; polymorphous, generalized \n\n0 Erythema & edema of the hands/feet, periungual desquamation . t Platelets & WBCs; ! hemoglobin . t Acute-phase reactants (eg, C-reactive protein) \n\nLaboratory findings . t AST & ALT . Sterile pyuria \n\nTreatment . Intravenous immunoglobulin & aspirin \n\nComplications . Coronary artery aneurysms . Ventricular dysfunction \n\nALT= alanine transaminase; AST= aspartate transaminase; WBCs = white blood cells. \n\nKawasaki disease \n\nMusculoskeletal Buerger Disease \n\n Although painful digital ulcers may occur with Raynauds , symmetric upper extremity involvement is more common. \n\nSmall Vessel \n\n536 https://t.me/usmleinnercircle \n\nPolyarteritis nodosa \n\n# . Correlation with underlying hepatitis B/C (immune complexes) \n\nPathophysiology . Fibrinoid necrosis of arterial wall --+ luminal narrowing & thrombosis --+ tissue ischemia \n\n# . Internal/external elastic lamina damage --+ microaneurysm formation --+ rupture & bleeding . Constitutional: fever, weight loss, malaise . Skin: nodules, livedo reticularis, ulcers, purpura \n\nClinical . Renal : hypertension, renal insufficiency, arterial aneurysms \n\nfeatures . Nervous: headache, seizures, mononeuritis multiplex . Gastrointestinal: mesenteric ischemia/infarction \n\n## . Musculoskeletal: myalgias, arthritis \n\n# . Negative ANCA & ANA \n\nDiagnosis . Angiography: microaneurysms & segmental/distal narrowing \n\n# . Tissue biopsy: nongranulomatous transmural inflammation \n\nANA= antinuclear antibodies ; ANCA = antineutrophil cytoplasmic antibodi es. \n\nThromboangiitis obliterans (Buerger disease) \n\n## . Age <45 \n\nClinical features . Ongoing or recent smoking history \n\n## . Distal limb ischemia, gangrene, ulceration due to nonatherosclerotic occlusion , thrombos is \n\nEvaluation . lschemia on vascular studies (eg , digital plethysmography) \n\n## . Segmental occlusion of small- & medium-sized vessels on angiography \n\nTreatment . Smoking cessation \n\nSmall Vessel Vasculitides ***** Musculoskeletal Behcet \n\n What vascular complication is a major cause of morbidity in patients with Behcet syndrome ?\n\nThrombosis \n\nboth venous and arterial thrombosis \n\nMixed Cryoglobulinemia \n\n What is the likely diagnosis in a hepatitis C patient with palpable purpura , hematuria , proteinuria ,\n\nPeripheral Neuropathy and low serum complement ?\n\nMixed cryoglobulinemia Pathergy \n\n537 https://t.me/usmleinnercircle USMLE Inner Circle \n\nBehcet disease Epidemiology Young adults Turkish , Middle Eastern , or Asian descent Recurrent, pa inful oral aphthous ulcers \n\n Genital ulcers \n\nClinical Eye lesions (eg, uveitis} \n\nfindings Skin lesions (eg, erythema nodosum, acneiform lesions} Thrombosis Pathergy - Exaggerated skin ulceration \n\nEvaluation with minor trauma (eg, needlestick} Biopsy - Nonspecific va sculitis of different-sized vessels \n\nCryoglobulinemia (immunoglobulins that precipitate at <37 C) Type I Mixe d= type II or Ill \n\nAssociated Plasma cell dyscrasias Chron ic viremia (eg, HGV, HIV) \n\ndiseases (eg, Waldenstrom, multiple myeloma) Autoimmunity (eg , SLE, Sjogren) \n\nPathogenesis: B-<:ell lineage malignancy: monoclonal B-<:ell hyperactivation: lgM RF' bound to \n\ncryoglobulin lgM polyclonal lgG Cryoprecipitates -> vascular occlusion Immune complexes-> va sc ulitis Clinical (eg, livedo reticularis, retiform purpura, (eg, palpable purpura, GN, arthralgia, \n\nfindings digital ischemia) neuropathy) High cryocrit -, hyperviscosity \n\n(eg, blurred vision, vertigo, ataxia) Vir al hepatrtis -, hepatomegaly \n\nLaboratory + Cryocrit, normal complement + Cryocrit, 1 C4 \n\n t Erythrocyte sedimentation rate + RF autoantibodies \n\nfindings + Monoclonal spike on SPEP + Viral or antinuclear antibodies *Monodo nal RF (type II) , polyclonal RF (ty pe Ill). \n\nGN = glomerulonephritis; HCV = hepatitis C virus; RF = rheumatoid factor; SLE = systemic lupus erythematosus; SPEP =serum protein electrophoresis. Musculoskeletal Meltzer's Triad of purpura, weakness, and arthralgia is present in 80% of patients. \n\nIn Mixed Cryoglobulinemia, the cryoglobin precipitation test becomes positive only after 72 hours. \n\nPatients can be RF positive (IgM in mixed cryo has activity of RF) \n\nGranulomatosis with polyangitis Churg Strauss Syndrome \n\n Person in their 40s-50s who, out of the blue, suddenly develops Asthma. On labs IgE significantly elevated. Patient also has cardiac issues, peripheral neuropathy. \n\nScreen for Churg-Strauss Syndrome \n\nHenoch-Schonlein Purpura The rash typically coalesces and darkens over days. \n\n538 https://t.me/usmleinnercircle \n\nGranulomatosis with polyangiitis \n\nUpper respiratory: sinusitis/otitis, saddle nose Clinical manifestations Lower respiratory: lung nodules/cavitation Renal: rapidly progressive GN Skin: livedo reticularis, nonhealing ulcers ANCA: PR3 (- 70%), MPO (-20%) Biopsy: \n\nDiagnosis o Skin (leukocytoclastic vasculitis) \n\n> o\n\nKidney (pauci-immune GN) \n\n> o\n\nLung (granulomatous vasculitis) \n\nManagement Corticosteroids & immunomodulators (eg, MTX, cyclophosphamide) ANCA ; antineutrophil cytop la smic antibody; GN ;;; g l omeru lonephritis; MPO :; myeloperoxidase; MTX = methotrexate; PR3 = proteinase-3. \n\nlgA vasculitis (Henoch-Schonlein purpura) \n\n# . Perivenular leukocytoclastic (neutrophils & monocytes) vasculitis \n\nPathogenesis Deposition of lgA, C3 & fibrin in small vessels .. Classic findi ngs' : \n\n> 0\n\nPa lp able purpura/pet ech iae on lo wer ex tremities Clinical 0 Arthritis/arthralgia \n\nmanifestations 0 Abdominal pain, intussusception \n\n> 0\n\nRenal disease (similar to lgA nephropathy) \n\n# . Other findings: scrotal pain & swelling \n\n# . No nma l platelet co unt & coagulat io n studies \n\nLaboratory Nonmal to t creatinine .findings Hematuria RBC cas ts &/or proteinuria .. Supportive ca re {hydration & NSAIDs) for most patients \n\nManagement Ho spitali za tion & systemic glucocorticoids for severe symptoms *Clinical diagnosis requir es purpuric rash plus 2: 2 additional cla ss ic findings. \n\nNSAIDs =nonsteroidal anti-inflammatory drugs; RBC =red blood cell. Musculoskeletal Renal disease in HSP may not be initially evident, with a normal urinalysis , but it can develop months \n\nafter symptom onset. Do Serial Urine Analysis \n\n Intussusception in HSP is usually confined to the small bowel (ileoileal). \n\nileoileal intussusceptions that do not reduce spontaneously often require surgical management. NOT treated with enema \n\n## Myopathy \n\n539 https://t.me/usmleinnercircle USMLE Inner Circle \n\nHenoch-Schonlein purpura \n\nArthralgias or arthritis \n\nC> UWoSO Polymyalgia . Systemic signs & symptoms . Elevated ESR, C-reactive protein rheumatica . Stiffness> pain in shoulders, hip girdle, neck . Rapid improvement with glucocorticoids \n\n## . Association with giant cell (temporal) arteritis \n\nANA= antinuclear antibody; AST = aspartate aminotransferas e; ESR = erythrocyte sedimentation rate. \n\nMyasthenia gravis Medications to avoid in myasthenia gravis \n\n# . Fluctuating & fatigable proximal muscle weakness: \n\nClinical 0 Ocular (eg, diplopia, ptosis) Magnesium sulfate \n\npresentation 0 Bulbar (eg, dysphagia, dysarthria) Fluoroquinolones, aminoglycosides \n\n0 Respiratory (myasthenic crisis) Neuromuscular blocking agents \n\n# . Medications: antibiotics (eg, fluoroquinolones, CNS depressants \n\nCauses of aminoglycosides), neuromuscular blocking agents, cardiac \n\nexacerbations medications (eg, BBs), MgS0 4 , penicillamine \n\n# . Physiologic stress: pregnancy/childbirth, surgery (especially thymectomy), infection \n\n Muscle relaxants \n\n Calcium channel blockers \n\n Beta blockers \n\n Opioids \n\nDiagnosis . Ice pack test (bedside), AChR-Ab (highly specific) \n\n# . CT scan of chest (thymoma) Stalins \n\n# . AChE inhibitors (eg , pyridostigmine) immunotherapy \n\nTreatment (eg, corticosteroids, azathioprine) \n\n# . Thymectomy \n\nAChE = acetylcholinesterase; AChR~Ab = acetylcholine receptor antibodies; BBs = beta blockers; MgS0 4 = magnesium sulfate. Musculoskeletal Fluoroquinolones (eg, moxifloxacin) are known to exacerbate myasthenia gravis (by blocking neuromuscular transmission) and should be avoided. Following intubation , acetylcholinesterase inhibitors (eg, pyridostigmine) used in the daily management of MG are temporarily held to reduce excess airway secretions and the risk of aspiration \n\n If a patient's ptosis is due to myasthenia gravis , application of an ice pack over the eyelids will result in improvement in ptosis. \n\ncold temperature inhibits the breakdown of acetylcholine in the NMJ; patients with a positive test should undergo confirmatory testing with acetylcholine receptor antibodies Edrophonium (AChE inhibitor) has a high-false positive rate so limited utility \n\n Lambert Eaton : Symptomatic therapy includes guanidine or 3,4-diaminopyridine to increase presynaptic acetylcholine levels. Refractory symptoms may respond to immunologic therapy with intravenous immunoglobulin or \n\noral immunosuppressants (eg, corticosteroids, azathioprine). \n\n542 https://t.me/usmleinnercircle \n\nMyasthenic crisis \n\n Infection or surgery \n\nPrecipitating Pregnancy or childbirth \n\nfactors Tapering of immunosuppressive drugs Medications (eg, aminoglycosides, beta blockers) \n\nSigns/symptoms j Generalized & oropharyngeal weakness Respiratory insufficiency/dyspnea \n\nTreatment Intubation for deteriorating respiratory status Plasmapheresis or IVIG as well as corticosteroids \n\n> IVIG\n\n= intravenous immunoglobulin. \n\n> Paraneoplastic Involved site Clinical features syndrome\n> Acetylcholine Fluctuating muscle weakness\n> Myasthenia receptor in Ocular (ptosis, diplopia)\n> gravis postsynaplic Bulbar (dysphagia, dysarthria) membrane Facial, neck &limb muscles Proximal muscle weakness Presynaptic Autonomic dysfunction (eg, dry mouth)\n> Lambert-Eaton membrane\n> syndrome voltage-gated Cranial nerve involvement (eg, ptosis) calcium channels Diminished or absent deep-tendon reflexes\n> Symmetrical &more proximal muscle weakness Interstitial lung disease, esophageal\n> Dermatomyositi s/ Muscle fiber dysmotility, Raynaud phenomenon\n> polymyositis injury Polyarthrilis Esophageal dysmotility Skin findings (eg , Gottron papules, heliotrope rash) in dermatomyositis\n\nMusculoskeletal Raynauds Phenomenon \n\n Workup for patients with suspected secondary RP may include: Complete blood count and metabolic panel Urinalysis \n\nAntinuclear antibody (ANA) and Rheumatoid factor \n\nErythrocyte sedimentation rate and complement levels (C3 and C4) If the ANA screen is positive, specific antibodies (eg, antitopoisomerase-1 for systemic sclerosis) may be obtained. \n\n## Drugs \n\n543 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nEtiology Clinical presentation Management \n\n## .\n\n# ...Differential diagnosis of neuromuscular weakness \n\nUpp er motor neurons \n\nLeukodystrophies Vascul itis Brain mass Vitamin 8 12 deficiency Amyotrophic lateral sclerosis \n\nAnterior horn cells Peripheral nerves \n\nHereditary primary motor se nsory neuropathy Guillain-Barre syndrome Diabetic neuropathy Amyloid neuropathy (myeloma) Lead poisoning \n\nNeuromuscular junction Myasthenia grav is Lambert-Eaton syndrome Organophosphate poisoning Botulism \n\nMuscle fibers \n\nSpinal muscular atrophy Amyotrophic lateral sclerosis Paraneoplastic syndromes Poliomyelitis Muscular dystrophies Polymyositis & derma tomyositis Hypothyroidism Corticosteroids HIV myopathy \n\nPrimary Raynaud Secondary Raynaud phenomenon phenomenon \n\n## . Connective tissue diseases \n\n## . Occlusive vascular conditions No underlying cause . Sympathomimetic drugs Vibrating tools .. Hyperviscosity syndromes \n\n## . Nicotine Usually women age <30 ~:)-..Ir,''-\n\n## . Usually men age > 40 As':),_,-~.t,..'c.. \n\n## . Symptoms of underlying disease No tissue injury Negative ANA & ESR . Tissue injury or digital ul cers Abnormal nail fold capillary examination \n\n## . Avoid aggravating factors Evaluate & treat underlying disorder \n\nCCB for persistent symptoms, aspirin for patients at risk .. CCB for persistent symptoms for digital ulceration \n\nANA= antinuclear antibody; CCB = calcium channel blocker; ESR = erythrocyte sedi mentation rate. Musculoskeletal Women with osteoporosis confirmed by DXA (ie, T-score 2.5) or with an osteoporotic fragility fracture warrant pharmacologic antiresorptive therapy . Antiresorptive therapy is also appropriate for patients with osteopenia (T-score between 1 and 2.5) who are at high risk for fragility fracture. Most experts recommend discontinuation after 5 years due to a risk of atypical fracture with prolonged use. \n\nBisphosphonate Osteonecrosis \n\n## Tumors \n\n A gradually enlarging, painless mass within an extremity should raise concern for the presence of a soft tissue sarcoma .After the pathologic diagnosis has been confirmed, imaging should be performed to investigate whether metastatic disease is present. This information aids in staging and treatment planning. \n\nOsteoid Osteoma \n\n544 https://t.me/usmleinnercircle \n\nMedications for osteoporosis \n\n First-line treatment for most patients \n\nBisphosphonates Taken with water on an empty stomach an hour before food & other medications (eg, alendronate, Not recommended for patients with renal impairment risedronate) Atypical fractures possible with prolonged use Oral & parenteral options available Risk of infection & skin reactions \n\nDenosumab Close monitoring for hypocalcemia needed \n\nAnabolic agents Useful in severe osteoporosis (eg, teriparatide) Monitor serum calcium , uric acid & renal function Modest reduction in fracture risk \n\nNasal calcitonin Reduces pain from fracture \n\nSelective estrogen Less effective than bisphosphonates \n\nreceptor modulators May lower risk of breast cancer (eg, raloxifene) Increased risk of DVT \n\n> DVT =deep vein thrombosis.\n\nBisphosphonate-related osteonecrosis of the jaw \n\n# . High-dose, parenteral bisphosphonates \n\nRisk . Dental procedures (eg , extractions , implants) \n\nfactors . Concurrent glucocorticoid use . Concurrent or previous malignancy \n\nClinical . Chronic, indolent symptoms \n\nfeatures . Mild pain, swelling \n\n# . Exposed bone, loosening of teeth, pathologic fractures \n\n# . Oral hygiene \n\nManagement . Antibacterial rinses \n\n# . Antibioti cs and debridement as needed Musculoskeletal Osteoid osteoma is a benign bone-forming tumor characterized by a small, radiolucent nidus. \n\nNidus produces high-levels of prostaglandins --> night-time pain and responds to NSAIDS \n\nT/t: NSAIDs with spontaneous resolution in few years; Surgery for refractory symptoms \n\nOsteosarcoma \n\n Most cases occur in a bimodal distribution, as follows: In children and adolescents, osteosarcoma usually develops at the metaphysis of long bones, where cellular turnover is high ( primary osteosarcoma ). In adults age >40, osteosarcoma usually develops at sites of damaged bone, particularly due to Paget disease of bone , irradiation , or prior benign bone tumor (secondary osteosarcoma ). \n\nEwings Sarcoma \n\n545 https://t.me/usmleinnercircle USMLE Inner Circle \n\nOsteosarcoma Musculoskeletal Moth Eaten: Ewings, Multiple Myeloma Codman: Ewings, Osteosarcoma Ewings Onion Skin \n\n546 https://t.me/usmleinnercircle \n\nEwing sarcoma Epidemiology . Second most common pediatric bony malignancy (after osteosarcoma) . White, adolescent boys . Chronic, localized pain & swelling \n\nClinical features . Long-bone diaphyses & axial skeleton (eg, pelvis) . Systemic findings (eg, fever, leukocytosis) . Early metastasis . Central lytic lesion . \"Onion skinning\" (l amellated periosteal reaction ) \n\nX-ray findings \"Moth-eaten\" appearance .. Periosteal elevation (Cadman triangle) \n\nEwing sarcoma Multiple myeloma \n\n> CUWorld\n\n~ Moth-eaten appearance clue to aggressive, Irregu lar bone matTOW destruction (nonspecific for MM) . C>UWo< ld \n\nGiant cell tumor of bone Musculoskeletal Miscellaneous \n\nProsthetic Joint \n\n What is the treatment of septic arthritis in an infected prosthetic joint ?\n\nRemove joint antibiotics reimplantation \n\n Infections due to less virulent organisms (eg, coagulase-negative staphylococci , Propionibacterium \n\nspecies), are likely to have a delayed onset (3-12 months) and present with chronic pain , implant loosening, gait impairment , or sinus tract formation .\n\nFever and leukocytosis are usually absent \n\nCompartment Syndrome \n\n What is the likely diagnosis in a child with a supracondylar humerus fracture that complains of increasing pain despite multiple analgesics? \n\nCompartment syndrome \n\n547 https://t.me/usmleinnercircle USMLE Inner Circle \n\nProsthetic joint infection Early onset Delayed onset Late onset Time to \n\nI II II I\n\nonset after <3 months 3-12 months >12 months \n\nsurgery \n\n Acute \n\n Acute pain symptoms in \n\n Wound Chronic joint pain previously \n\nPresentation infection or Implant loosening asymptomatic breakdown Sinus tract formation joint \n\n Fever Recent infection at distant site \n\n Staphylococcus Coagulase-negative Staphylococcus \n\nMost aureus staphylococci aureus \n\n Gram-negative \n\ncommon Gram-negative Propionibacterium rods \n\norganisms rods species Beta-hemolytic \n\n Anaerobes Enterococci streptococci \n\nAcute compartment syndrome of the extremity \n\n## . j Pressu re within enclosed fascial space Pathophysiology t Blood flow & tissue perfusion .\n\n## . Crush injury, long bone fracture, rhabdomyolysis \n\nCommon causes . Reperfusion after prolonged ischemia \n\n## . Massive fluid resuscitation \n\n## . Early: \n\n0 Progressive , severe pain \n\n0 Rapidly j & tense swelling \n\n0 j Pain with passive stretching \n\nClinical features 0 Paresthesia . Late : \n\n0 t Sensation \n\n0 Weakness (w ithin hours), paral ys is (late) \n\n0 Loss of pulses (uncommon) \n\nManagement . Compartment pressure measurement * can confirm diagnosis \n\n## . Emergency fasciotomy *Delta pressure (d ias t ol ic pressure - compartment pressure) S30 mm Hg is cons istent wi th compartment syndrome. Musculoskeletal Supracondylar humerus fracture classically occurs in a child after a fall on an outstretched hand; radiographs often reveal fat pads (lucency) anterior and posterior to the fracture \n\nHowever, brachial artery and median nerve injury are much more common than compartment syndrome , so be careful how the qeustion is phrased! \n\n Reperfusion of a limb following arterio-occlusive ischemia for longer than 4 - 6 hours can lead to intracellular and interstitial edema with possible compartment syndrome. \n\ncompartment syndrome is diagnosed when the pressure within a muscular fascial compartment rises above 30 mmHg \n\nExample: Cross-clamping during surgery may lead to ischemic endothelium, which leads to increased capillary permeability during surgery. Reperfusion then increases tissue damage and swelling due to oxidative stress and inflammation. \n\n A delta pressure (diastolic blood pressure compartment pressure) 30 mm Hg indicates inadequate tissue perfusion and is strongly suggestive of compartment syndrome. What is the most critical prognostic indicator for compartment syndrome ?\n\nTime to fasciotomy \n\nPrognosis depends on the amount of time that has elapsed prior to performing the facsiotomy: \n\n<6 hours = almost complete recovery \n\n6-12 = first necrosis; 68% chance of normal limb function returning \n\n>12 h = necrosis and normal limb function returns in 8% of cases \n\nCharcot Joint \n\n What is the likely diagnosis in a diabetic patient with a severely deformed foot ? X-ray shows large osteophytes and several extra-articular bone fragments. \n\nCharcot joint (neurogenic arthropathy) \n\nLoss of neurologic input results in trauma to weight-bearing joints, resulting in degenerative joint disease \n\n548 https://t.me/usmleinnercircle \n\n \n\n> Neuropathic (Charcot) arthropathy Pathophysiology Repetitive bone &joint trauma due to impaired sensation/ proprioception\n> &causes\n\n## . Diabetes mellitus (most common) \n\n## . Posterior column disease (eg, B 12 deficiency, tabes dorsalis) Acute \n\n## . Inflammatory erythema, warmth & edema of the foot \n\n> Clinical\n\n## . Minimal bone involvement (x-rays often normal) \n\n> manifestations Chronic\n\n## . Bone deformities (eg, subluxation, collapsed arch, stress fracture) \n\n## . Neuropathic ulcer s, ce llulitis, osteomyelitis \n\n> Acute\n> Management\n\n## . Foot cast to reduce edema & offload weight bearing \n\n> Chronic\n\n## . Orthotic footwea r, i nfection management , surgical realignment Musculoskeletal Claw toe and hammer toe deformities reflect an imbalance in strength and flexibility between the flexor and extensor muscle groups. In a patient with longstanding diabetes, these deformities may suggest underlying diabetic peripheral neuropathy. \n\nComplex Regional Pain Syndrome \n\n549 https://t.me/usmleinnercircle USMLE Inner Circle \n\nNeuropathic (Charcot) arthropathy \n\nAcute Inflammatory erythema, warmth, edema ;minimal physical deformities Chronic Minimal inflammatory fi ndings; significant physical deformities Hindfoot & m i dfoot Osseous fragmentation (1) Subluxation & dislocation (2) Midfoot arch collapse (3) N ew bone formation & sclerosis \n\nForefoot \n\n Metatarsals: resorption of heads (4) \n\n& osteopenia (5) Phalanges: osteolysis & subluxation Chronic neuropathic (Charcot) arthropathy \n\nHammer & claw toe deformities Hammer toe \n\nDorsal flexi on at DIP joint Plantar Hexion at PIP joi nt \n\nClaw toe \n\nPlantar flexi on at PIP & DIP joint DIP =distal interphalangeal; MTP =melatarsophalangeal; PIP =proximal interphalangeal. \n\nCUWor1d Musculoskeletal Amputation Langerhans Histiocytosis \n\n550 https://t.me/usmleinnercircle \n\nComplex regional pain syndrome \n\n# . Trauma: fracture, sprain \n\nTriggers Surge ry \n\n# . Pain: severe, region al (not dermatomal ), burning/slinging \n\n# . E dema , abnormal sweating \n\nClinical features \n\n Vasomotor changes, altered skin temperature \n\n# . Trophic skin, hair & nail change s\n\n# . Primarily based on clinical features \n\nDiagnosis . X-ray: p atchy demineralization Bone scintigraphy: j uptake in affected limb \n\n# . Physical & occupational therap y, exercise \n\nManagement Medications: NSAID s, antineuropathic medi ca tio ns (eg, pregabalin, TCA s ) \n\nNSAIDs = non steroida l anti-inflammatory drugs ; TCAs = tricycl ic ant idep ressan ts .Post-amputation pain \n\n# . Tissue & nerve injury \n\nAcute stump pain Severe pain last ing 1-3 weeks .. Swe lli ng , skin discoloration lschemic pain . Wound breakdow n\n\n# . ! Transcutaneous o x ygen t ens i on \n\n# . Weeks to months after amputa t ion \n\nP ost-traumatic neuroma . Focal tenderness , altered local sensatio n\n\n# . ! Pain with anesthetic injection \n\n# . Onset usually within 1 week Phantom limb pain . Inc reased risk in patients w i th se ve re a cut e pain \n\n# . In term i ttent cramping , burning felt in distal limb \n\nLangerhans cell histiocytosis \n\n# . Lytic bone lesions (eg, skull, jaw , femur )\n\n# . Skin lesions (purplish papules, eczematous rash) \n\nClinical findings . Lymphadenopathy, hepatosplenomegaly \n\n# . Pulmonary cysts/nodules \n\n# . Central diabetes insipidus \n\nDiagnosis . Langerhans cells on bone/skin biopsy \n\n# . Chemotherapy (prednisone vinblastine) \n\nTreatment . Desmopressin for diabetes insipid us Musculoskeletal Myositis Ossificans Ganglion Cyst \n\n551 https://t.me/usmleinnercircle USMLE Inner Circle \n\nMyositis ossificans Pathogenesis . Formation of lamellar bone in extraskeletal tissues \n\nCauses & . Traumatic: muscle injury, fracture , orthopedic surgery (eg, arthroplasty) \n\nrisk factors . Neurogenic: stroke, traumatic brain injury, spinal cord injury \n\nClinical . Intramuscular mass with pain, swelling/induration \n\npresentation . Days to weeks following injury \n\n## . Quadriceps & brachialis most common \n\nDiagnosis . Laboratory: elevated alkaline phosphatase, ESR, C-reactive protein \n\n## . X-ray: periosteal bone reaction , calcification with radiolucent center \n\nManagement . ROM exercise & NSAIDs (eg, indomethacin) \n\n## . Surgical excision \n\nESR =erythrocyte sedimentation rate ; NSAIDs =nonsteroidal anti-inflammatory drugs; ROM =range of motion. \n\nLangerhans cell histiocytosis \n\nMyositis ossificans Lytic l es ion with \"punched-out'' Musculoskeletal Peads Musculocutaneous \n\nGenu Varum \n\n Genu varum is normal up to age 2 , while genu valgus is normal between 4 and 8 .Treatment? \n\nReassurance and follow up; if bowlegs persist past 3 (Blount disease), Surgery can be done Characteristics of physiologic genu varum include: \n\nSymmetric bowing Normal stature \n\nNo leg length discrepancy No lateral thrust when walking \n\nToddlers Fracture \n\n Spiral fractures of the distal tibia can be seen in ambulatory children \n\nage 3 and are known as toddler's fractures .\n\n552 https://t.me/usmleinnercircle \n\n6 months Genu varum \n\nPathophysiology Presentation Treatment Prognosis Lower extremity alignment 2 years \n\nStraight legs \n\n> 4\n\nyears \n\nGenu valgum \n\n## .\n\n## ..\n\n## ..\n\n## .....\n\nGanglion cyst \n\nMucoid degeneration of periarticular tissue Herniation of connective tissue from joint capsule, tendon sheath, bursae Filled with clear/gelatinous fluid Wrist (most common), dorsal foot, knee Rubbery, round , well-circumscribed cystic nodule Transillumination positive Observation for asymptomatic cysts Needle aspiration (recurrence common) Surgical excision Most resolve spontaneously >7 years \n\nStraight legs \n\nWhen standing Lateral thrust \n\nKnee joint protrudes - - (,,\"'I ,r\n\nlaterally \n\nWhen walking Musculoskeletal These fractures typically result from a twisting injury during a low-impact fall in the early walking years. Treatment: Immobilisation with Reassurance \n\nSome bruises on knees and legs are also common in early walkers; \n\nDONOT confuse it with Osteogenesis Imperfecta \n\nDDH \n\n Treatment : Rigid brace (Pavlik harness) Screening done in Breech presentation upto 6 months of age a splint that holds the hip in flexion and abduction while \n\npreventing extension and adduction. \n\n553 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDevelopmental dysplasia of the hip \n\n# . Breech positioning \n\nRisk . Positive family history \n\nfactors . Excessively tight swaddling Red flags 0 Positive Ortolani test 0 Dislocated hip \n\nClinical 0 Limited hip abduction \n\nfeatures \n\n Supportive findings 0 Limb-length discrepancy \n\no Asymmetric gluteal/inguinal/thigh creases Red flags: refer to orthopedic surgery \n\n Supportive findings or risk factors \n\nManagement o Age <4 months: hip ultrasonography \n\no Age >4 months: hip radiography \n\nC> UWOl1d \n\nPosterior femoral displacement \n\nToddler's fracture Pavlik harness Galeazzi test Musculoskeletal Legg-Calve-Perthes Disease \n\n Idiopathic osteonecrosis of the femoral head that typically presents in boys age 4 - 10 years old; \n\ninitial X-rays may be negative \n\nSCFE \n\n554 https://t.me/usmleinnercircle \n\nBarlow & Ortolani maneuvers \n\nOrtolan i Maneuver: Abduction with anterior lifting of the hip Barlow Maneuver: Adduction with posterior pressure on the hip \n\nLegg-Calve-Perthes disease Pathogenesis Idiopathic avascular necrosis of the femur Boys age 3-12 \n\nClinical Insidious hip pain , limp \n\nfeatures Restricted hip abduction , internal rotation Positive Trendelenburg sign X-ray \n\n> 0\n\nEarly stages: May be normal \n\nDiagnosis 0 Later stages: Femoral head flattening, fragmentation, sclerosis MRI: Avascular/necrotic femoral head Non-weight bearing \n\nTreatment \n\n Splinting, possible surgical repair \n\n> Normal\n> C> UW0f1d\n\nDevelopmental dysplasia of the hip \n\n/ \n\n> Symmetric hip folds Asymmetric hip folds --+-------<\n> Extra fold on affected side\n> Abnormal\n\nMusculoskeletal D/D: Iliopsoas bursitis is inflammation within the bursa posterior to the iliopsoas muscle due to \n\noveruse or trauma .Patients have hip pain and limited range of motion , but a palpable click with manipulation of the hip is typically present \n\n Children with endocrinopathies(e.g hypothyroidism) often have SCFE at an earlier age (<10) and are more likely to develop bilateral disease. \n\nClubfoot Can be Bilateral too Surgery between 3-6 months of age This deformity is usually bilateral and occurs most frequently in first-born infants , likely due to the crowded positioning in a smaller, primigravid uterus .\n\n555 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSlipped capital femoral epiphysis Sl ipped capital femoral epiphysis Obesity \n\nRisk factors \n\n Adolescence Dull hip pain \n\nClinical Referred knee pain \n\npresentation Altered gait \n\n Limited internal rotation of hip \n\nDiagnosis Posteriorly displaced femoral head on x-ray Non-weight bearing \n\nTreatment \n\n Surgical pinning \n\n Avascular necrosis \n\nComplications Osteoarthritis \n\nMetatarsus adductus Congenital clubfoot \n\n Rigid positioning \n\nCl inical Flexible po si tioning Medial/upward deviation of \n\nfeatures Medial deviation of forefoot forefoot & hindfoot Neutral position of hindfoot Hyper-plantar flexion of foot \n\nTreatment Rea ss urance Serial manipulation & casting; surgery fo r refractory cases \n\nNormal foot Metatarsus add uctus Musculoskeletal Growing Pains Congenital Muscular Torticolis \n\n What is the likely diagnosis in an infant that presents with head tilting toward one side with a neck mass that does not transilluminate on ultrasound? \n\nCongenital muscular torticollis \n\nversus Cystic hygroma ,which does transilluminate on ultrasound \n\nTransient Synovitis \n\n What is the likely diagnosis in a child that presents with hip pain several days after a viral URI with normal physical exam, laboratory studies, and X-ray? \n\nTransient synovitis \n\nmost common cause of hip pain in children; \n\nX-ray is needed to assess for Legg-Calve-Perthes disease \n\nCan bear weight and negative trendelenburg sign (unlike LCPF) \n\n556 https://t.me/usmleinnercircle \n\nGrowing pains (idiopathic nocturnal pains of childhood) Epidemiology ..\n\nClinical features \n\n\n\n# ..Treatment \n\nCourse .\n\nCh i ld r en age 3-12 Episodic, bilateral lower extremity (eg , thighs, calves) pain \n\n> 0\n\nOccurs primarily at night \n\n> 0\n\nMore likely to occur after increased daytime physical exertion No systemic symptoms, joint involvement, or activity limitations Normal physical examination Parental education & reassurance Massage, heat, analgesics, or stretchi ng exercises May wax/wane for months to years Self-resolves by adolescence \n\nCongenital torticollis \n\nChin po int away from contracted musc le toward affected muscle Co ntracted SCM muscle Musculoskeletal What is the Kocher Criteria and what is it used for? \n\nSeptic arthritis vs. Transient synovitis \n\nSeptic arthritis if these are present: all four criteria \n\nWBC >12,000 Inability to bear weight Fever >38.5 (101.3) ESR > 40 \n\n When the diagnosis is unclear, bilateral hip ultrasound is performed. Joint effusion in septic arthritis is unilateral , whereas 25% of patients with transient synovitis have bilateral hip effusions (even with unilateral symptoms). If hip ultrasound shows a unilateral effusion , arthrocentesis is required to evaluate for septic arthritis. What is the recommended treatment for transient synovitis ?\n\nRest and NSAIDs \n\nResolves in 4 weeks \n\nAdolescent Idiopathic Scoliosis \n\n Risk factors at diagnosis associated with curve progression include: Female sex Age <12 Early pubertal status (eg, premenarchal) Skeletal immaturity Severe curvature (ie, Cobb angle 25 degrees) \n\n Management of scoliosis is based on the risk of curve progression . The greatest increase in curvature occurs during early adolescence at the time of the pubertal growth spurt, after which progression slows and subsequently stops once bone ossification is complete . First step: X-ray \n\n557 https://t.me/usmleinnercircle USMLE Inner Circle \n\nI Transient synovitis II Septic arthritis I\n\n Well-appearing Ill-appearing \n\nClinical Afebrile or low-grade Febrile \n\npresentation fever Non-weight -bearing \n\n Able to bear weight \n\n Normal or mildly Moderately elevated WBC ,elevated WBC , ESR , ESR, CRP CRP Positive blood culture \n\nDiagnosis Unilateral/bilateral Unilateral ultrasound effusion ultrasound effusion Synovial fluid WBC >50, \n\n Diagnosis of exclusion 000/mm 3I\n\nTreatment \n\nII \n\n Conservative I\n\n Joint drainage & antibiotics \n\nCRP = C-reactive protein; ESR = erythrocyte sedimentation rate ; WBC = white blood cell. \n\n\n\n0000\n\n\n\n\n\nMusculoskeletal Mild (10-30 degree): Monitor every 6 months \n\n Moderate (30-40): Thoracolumbosacral Spinal brace \n\n Severe (40-50) : Surgical Fixation \n\nStrength Training \n\n Children should engage in 1 hour of daily moderate to vigorous physical activity, which typically consists of aerobic exercise , such as hiking, running, jumping, or swimming. \n\nStrength training can also be combined with it. \n\nAvoid Bodybuilding due to risk of damage to growth plates >10 degrees is diagnostic \n\n558 https://t.me/usmleinnercircle \n\n> C> UWo Angle of trunk rotation\n\nScoliometry Measuring Cobb angle Most displaced upper vertebra ----+--- \n\n> C> UWoongiosis \n\nAcantboJysis \n\nAcanthosis \n\nInfection \n\nErysipelas CHARACTE RIS TI CS EXAMP LES \n\nAbnormal prematu re ke ra tiniza ti on t thi ckness of stra tu m c orneum \n\nS quamou s eel] c,u c inom -. 1 VPs or iasis, ca lluses \n\nRetentirn .u, nucl ei in s tratum corneu m Psoriasis. actin ic keratosis t thickne ss of st ra tum g rc. mul9sum Lichen planus E pi derma l acc um lJ la ti oo of ede m<-1t01 1s 01 1id in Ec ze mat ous d er m at itis intcr cd] u lar spaces \n\nSeparat ion of e pider mal cells Ec Jnphi gus vulgaris \n\nF.pidermal hyper plasia (I spin os um) Aca nth osis ni gricans, psoriasis \n\nCommon skin infections Organism Manifestations \n\n# . Superficial dermis & l ymphat ics \n\n# . Raised , sharply demarcated edges . Streptococc us pyogenes . Rapid spread & onset \n\n# . Fever ea rly in course \n\n# . Deep dermis & subcutaneous fat . .S pyogenes Flat edges with poor demarcation Cellulitis (nonpurulent) MSSA Indolent (over days) . .. Localized ( fever later in co ur se) \n\n# . Purulent drainage \n\n# . MSSA . Folliculitis: in fected h air fo llicle Cellulitis (purulent) MRSA Furuncles: folliculitis - dermis - abscess . .. Carbuncle: mu ltiple fur uncles MRSA = methicillin-resistant Staphylococcus aureus; MSSA = methicillin-sens itive S aureus. Dermatology Involvement of the external ear is particularly suggestive of erysipelas as this skin lacks a lower dermis level (making cellulitis, a deeper skin infection, unlikely). Patient presents with swollen, erythematous lower left leg that has sharpy defined borders .Physical exam reveals a red, hot, swollen lesion with erythematous streaks . He also complains of fever and chills . What is the most likely diagnosis? \n\nErysipelas \n\nthe red streaks are characteristic of ascending lymphadenitis known to be involved with the condition Impetigo \n\n562 https://t.me/usmleinnercircle \n\nImpetigo Type Nonbullous Microbiology . Staphylococcus aureus \n\n## . Group A Streptococcus (S pyogenes) \n\nClinical features . Papules & pustules with honey-crusted lesions \n\nTreatment . Limited: topical antibiotics (eg, mupirocin) \n\n## . Extensive: oral antibiotics (eg, cephalexin) \n\nSkin anatomy: Cellulitis, erysipelas, and skin abscess Cellul iti s Erysipelas Ab scess \n\n# lEp;denn;s \n\n> Dermis\n> Subcutaneous\n> tissue\n> Musde\n\nCellulitis and erysipelas manifest as areas of skin erythema, edema, and warmth; they develop as a result of bacterial entry via breaches in the skin barrier. Cellulitis involves the deeper dermis and subcutaneous fat; in contrast, erysipelas involves the upper dermis, and there is clear demarcation between involved and uninvolved tissue. A skin abscess is acollection of pus within the dermis or subcutaneous space. \n\nBullous \n\n# . S aureus-produci ng exfoliative toxin A\n\n## . Enlarging , flaccid bullae with yellow fluid \n\n## . Ruptured lesions with a collarette of scale at periphe ry \n\n## . Oral antibiotics (eg, cephalexin) Dermatology Tinea Pedis is one of the most common risk factors for lower extremity cellulitis .Dermatophytes are generally noninvasive but cause fissuring , erosions , and ulceration that allow bacterial entry into the tissue, particularly when the feet are chronically wet or occluded. Patients with immunosuppression (eg, uncontrolled diabetes ) are at particularly high risk of developing both severe TP and secondary cellulitis. \n\nLarge Local Reaction Erysipelas \n\n563 https://t.me/usmleinnercircle USMLE Inner Circle \n\nImpetigo \n\nRisk factors for cellulitis Bullous impetigo \n\n# . Diabetes mellitus \n\nImmune suppression . HIV infection \n\n# . Chronic glucocorticoid therapy \n\n# . Dry skin \n\nBreaches in . Chronic inflammation (eg, eczema, radiation therapy) \n\nskin barrier . Chronic wounds (eg, pressure ulcer, venous ulcer) \n\n# . Dermatophyte infection (eg , tinea pedis) . Postsurgical lymphedema (eg, lymph node dissection) \n\n# . Chronic venous insufficiency \n\nChronic edema . Congestive heart failure , chronic kidney disease . Prior cellulitis with lymphatic scarring \n\nOther . Obesity Dermatology D/D: Cellulitis but uncommon in insect bites and develop 3-5 days later NOT within 24 hours \n\nLudwig Angina \n\n What is the likely diagnosis in a patient that presents with fever , sore throat , drooling , and muffled voice ? The bilateral submandibular area is tender and indurated with palpable crepitus. \n\nLudwig angina \n\n D/D: Epiglotitis but wont have submandibular swelling or tenderness What is the most common source of infection causing Ludwig angina ?\n\nInfected mandibular molar ( dental infection )\n\nHiraadenitis Suppurativa Epinephrine if systemic anaphylactic reaction occurs May lead to Acute Airway Obstruction ; Intubate if exam findings are concerning for impending airway obstruction regardless of current O2 stats \n\n564 https://t.me/usmleinnercircle \n\n## .\n\nEpidemiology & pathophysiology .\n\nManifestations Treatment S ublln gual sp ace Mylohyo1 d\n\n> @UWorld\n\n## .\n\n# ....... \n\n> Normal sp ace\n\nLarge local reactions \n\nOften due to bites from Hymenoptera species (eg, bees, ants, wasps) Exaggerated, lgE-mediated, local allergic response (-10 % of stung individuals) Associated with possible increased risk for future systemic reactions Significant (-10 cm or more) localized swelling, erythema & warmth Swelling & erythema contiguous with site of the sting Develop within 24 hr, peak within 24-48 hr, resolve in 5-10 days Cold compresses Oral &/or topical steroids Antihistamines Anti-inflammatory medications \n\nLudwig angina Ludwig angina sublingual a nd subm a ndibu1 ar space Dermatology There is a strong association between tobacco use and HS .\n\nCandida \n\n Intetrigo is an erythematous plaque in the skin folds (inguinal, inframammary) that contains multiple \"satellite lesions \" near the primary infection .The most common cause of intertrigo is Candida albicans .\n\n565 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPathogenesis Clinical presentation Treatment Complications Diagnosis Pathogenesis Examination Treatment Hidradenltis suppurativa \n\n## . Disordered folliculopilosebaceous units: 0 Ductal keratinocyte proliferation --+ follicul ar occlusion --+ follicul ar rupture --+ inflammation \n\n## . Risk factors: smoking, metabolic syndr ome (obesity, diabetes mellitus) . Chr onic & re current lesions in intertriginous areas \n\n## . Mild: painful nodules, draining abscesses \n\n## . Moderate: sinus tracts & scarring . Severe: extensive sinus tracts, widespread disease \n\n## . Mild: topical clindamycin . Moderate: oral tetracycline \n\n## . Severe: tumor necrosis factor-a inhibitors (eg, adalimumab), surgical excision . Depression & suicide \n\n## . Squamous cell carcinoma of skin \n\nDiaper dermatitis Irritant contact dermatitis Candida dermatitis \n\n## . Skin breakdown from exposure to stool/urine . Yeast superinfection of irritant contact dermatitis \n\n## . Most common diaper rash . Second most common diaper rash Erythematous papule s, plaques . Beefy-red confluent plaques \n\n## . Involves skinfolds .. Spares skinfolds Satellite lesions .. Topical barrier (eg, petrolatum, zinc oxide) . Topical antifungal (eg, nystatin) \n\nDiaper dermatitis Irritant diaper dennatitls Cand ida! diaper dennatitls >Satellite \n\nlesions Dermatology Acrodermatitis enteropathica (ie, zinc deficiency ) is a rare cause of refractory diaper rash \n\nassociated with chronic diarrhea , perioral dermatitis , and alopecia .\n\nAnal Itching \n\n Pinworm ( Enterobius vermicularis ): itching worse at night Satellite lesions are smaller cutaneous lesions that surround a larger principal lesion. \n\n566 https://t.me/usmleinnercircle \n\nIrritant diaper dermatitis Candida intertrigo Perianal dermatoses Irritant contact Candida diaper Perianal Diagnosis diaper dermatitis dermatitis Streptococcus \n\n# . Most common diaper rash in . Second most common diaper . Infants through school-aged \n\nEpidemiology infants rash in inf ants ch il dren \n\n# . Erythematous papules, . Beefy-red, confluent plaques . Bright, sharply demarcated \n\nExamination plaques . Involves skinfolds erythema of perianal/perineal \n\n# . Spares skinfolds . Satellite lesions area \n\n# . Top ical barrier (eg , petrolatum, \n\nTreatment . Topical antifungal (eg, nystatin) . Oral antibiotics (eg , amoxicillin) zinc ox ide) Dermatology HPV \n\n What is the likely diagnosis in a young adult patient that presents with the foot rash above? The lesions are painful with walking and standing. \n\nPlantar warts; Cutaneous verrucae (due to HPV infection) \n\nHSV Herpetic Whitlow \n\n567 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPerianal streptococcal dermatitis Dermatology Molluscum Contagiosum \n\n The diagnosis of molluscum contagiosum is clinical , and symptoms typically self-resolve \n\nwithin 6-12 months. no biopsy required unless uncertain diagnosis \n\nTreatment is recommended in adults to prevent transmission to others and autoinoculation. \n\n Lesions in atypical regions, even the genital area , in children are typically due to \n\nautoinoculation and usually not sexual abuse \n\nTinea Versicolor \n\n The condition may first be noticed after sun exposure, when the surrounding skin becomes more darkly pigmented than the affected area. \n\nD/D: Vitiligo but does not cause scaling or itching .\n\nDermatophyte \n\n568 https://t.me/usmleinnercircle \n\nMolluscum contagiosum Children Adults \n\n. Trunk \n\nTypical . lntertriginous areas (eg , axillae) . Lower abdomen, genitals, upper thighs \n\nlocation . Face (including eyelids) \n\n. Clinical diagnosis (ie, firm , domed , papule . Clinical diagnosis \n\nEvaluation with central umbilication) . Genital lesions: STI testing \n\n. No further evaluation . Extensive lesions: HIV testing \n\n## . Cryotherapy \n\nTreatment . Reassurance . Curettage \n\n## . Topical therapy (eg, cantharidin, podophyllotoxin) \n\n> STI\n\n= sexually transm itted infection. \n\nTinea versicolor (pityriasis versicolor) Pathogenesis . Malassezia globosa skin flora grows in exposure to hot & humid weather \n\n## . Hypopigmented, hyperpigmented , or mildly \n\nClinical erythematous lesions (face in children , trunk & upper \n\nfeatures extremities in adolescents & adults) \n\n## . Fine scale \n\n## . Pruritus \n\nDiagnosis . KOH preparation shows hyphae & yeast cells in a\"spaghetti & meatballs\" pattern \n\nTreatment . Topical ketoconazole , terbinafine, or selenium sulfide \n\nKOH = potassium hydroxide. Dermatology Recurrent tinea cruris is common and suggests reexposure to an external source or autoinfection \n\nfrom a concurrent dermatophyte infection elsewhere on the body (eg, tinea pedis, tinea corporis, onychomycosis). Patients should have a thorough skin inspection , and any other sites of infection should be treated. Black dots \n\n569 https://t.me/usmleinnercircle USMLE Inner Circle \n\nTinea capitis \n\n# . Most common in African American children \n\nEpidemiology Transmission via direct contact or from fomite (eg, shared combs) .. Sca ly, erythematous patch with hair loss on scalp \n\nClinical features . Black dots in affected area . Tender lymphadenopathy \n\nManagement . Oral griseofulvin or terbinafine \n\nRisk factors for dermatophyte infection \n\n## . Wa rm, humid environments \n\nEnvironmental exposures . Direct contact with infected person, fomites, or public showers \n\n## . Contact with animals (eg, kittens) \n\n## . Concurrent dermatophyte infection (autoinoculation) \n\n## . Occlusive clothi ng \n\nPatient factors . Obesity \n\n## . Peripheral artery disease \n\n## . Diabetes mellitus \n\nImmune deficiency . HIV infecti on \n\n## . Systemic glucocorticoid therapy Dermatology Pigmented Skin Disorders \n\n Piebaldism is an autosomal dominant disorder characterized by patchy absence of melanocytes . It is usually noticed at birth and is confined to the head and trunk .\n\nSunburn \n\n570 https://t.me/usmleinnercircle \n\nEtiology .\n\nRisk factors ...Clinical features ..\n\nDiagnosis ...\n\nTreatment ..I\n\nRisk factor sExam in ation findings Di agnos is Tr eatment \n\nOny c homycos is \n\n Advanced age Tinea oedis \n\n## . ~\n\n Peripheral vascular disease Thick, brittle , discolored nails KOH, periodic acid-Schiff stain, culture Fir st li ne : terbinafine, itraconazole Sec ond line: griseofulvin, fluconazole, ciclopirox \n\nTinea pedis \n\nDermatophyte fungi (Trichophyton species mo st common) Barefoot walking in pu blic areas (eg, sw imming pools, athletic facilities) \n\nlnterdigital type: pruritus, erythema, erosions between toes \n\nMoccasin type: s ca les/fissures; ext en sion onto the sole, side, or dorsum of foot \n\nVe siculobultous type: painful bullae, erythema (lateral midfoot) Complications: secondary infec ti on , r ec urrence Clinical presentation \n\nPotassium hydroxide microscopy of skin scraping \n\nFirst line: topical antifungals (eg, miconazole, tolnaftate) \n\nSecond line: oral antifungals (eg, fluconazole) Keep feet dry & dispose of old footwear Dermatology Vitiligo \n\n571 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSunburn \n\n Symptoms begin hours after exposure, resolve by day 3-7 \n\nClinical manifestations Mild-moderate: Erythema, tenderness Severe: As above + blistering , systemic symptoms (eg , fever, vomiting , headache) Mild-moderate \n\no Topical: Cool compresses , calamine lotion, aloe vera \n\no Oral : Nonsteroidal anti-inflammatory drugs \n\nTreatment Severe \n\no Hospitalization \n\no Intravenous fluids & analgesia \n\no Wound care \n\nSun-protective measures \n\n## .Exposure Sun avoidance, especially age <6 months Reduce exposure 10:00 AM-4 :00 PM .. SPF .?30 \n\nSunscreen . Apply 15-30 minutes prior to sun exposure \n\n# . Reapply every 2 hours & after sw imming \n\nClothing . Long sleeve s, broad-brim hats \n\n## . Tight weave, dark color \n\nSPF = su n protection factor. \n\nVitiligo Cl inical Depigmented macules on acral areas & extensor \n\nmanifestations surfaces; face commonly affected Lesions may be symmetrical, dermatomal, or unilateral Most cases progress gradually \n\nClinical Repigmentation is spontaneous in 10%-20% of cases \n\ncourse Increased incidence of other autoimmune disorders (eg , lupus, thyroid disease, pernicious anemia, Addison disease) Lim ited disease: Topical corticosteroids \n\nTreatment Extensive/unresponsive disease: Oral corticosteroids, topical calcineurin inhibitors, PUVA PU VA = psoralen + ul tra violet A li ~ht. \n\nVITILIGO \n\nPath : Autoimmune disease P t: Shar pl y demarcated, sma ll patches of depigmented skin, often on face, hands and genitalia Dx: Wood 's Lamp shows NO pigment Biopsy = absence ofmelanocytes Tx: None Cosmetics - Bleaching to lighten uniformity \n\n- Dyes/makeup to darken uniformity \n\nVi tiligo Dermatology D/D: Tinea versicolor has partial depigmentation and usually present on chest (vs complete depigmentation here) \n\nDiscoid Lupus \n\n Discoid lupus erythematosus presents with scaly , erythematous plaques , leading to atrophy ,\n\nhypopigmentation , and scarring . It most commonly affects sun-exposed areas of the head and neck .DLE can occur independently , although systemic lupus erythematosus (SLE) eventually develops in up to 30% of patients. The rash often extends into the hair follicles, resulting in scarring alopecia .\n\n## Acne \n\n Topical retinoids inhibit comedogenesis by normalizing keratinization ; decreasing epithelial cohesiveness , which facilitates desquamation and prevents follicular plugging ; and increasing epithelial turnover , which facilitates the extrusion of comedones. \n\n572 https://t.me/usmleinnercircle \n\nTreatment of acne vulgaris Comedonal acne \n\n> Closed or open comedones on forehead , nose & chin May progress to inflammatory pustules or nodules Treatment:\n\nTopical retinoids ; salicylic, azelaic, or glycolic acid \n\nInflammatory acne \n\n> Inflamed papules (<5 mm ) & pustules; erythema Treatment: o Mild: Topical retinoids\n\n+ benzoyl peroxide o Moderate: Add topical antibiotics (eg , clindamycin, erythromycin) o Severe: Add oral antibiotics \n\nNodular (cystic) acne \n\n> Large (>5 mm ) nodules that can appear cystic Nodules\n\nmay merge to form sinus tracts with possible scarring Treatment: o Moderate: Topical retinoid + benzoyl peroxide + topica l ant ibi ot ics o Severe: Add oral antibi ot ics o Unresponsive severe: Oral isotretinoin \n\n> CUWo Triggers Rubber/latex Chemicals Leather dyes Acid/alkali Medications Primarily on exposed skin , well demarcated Commonly on hands\n> Appearance Erythema Erythema Papules/vesicles Fissures Chronic lichenification\n> Irritant contact dermatitis\n\nDermatology D/D: Contact dermatitis is characterized by erythematous papules and vesicles \n\n What is the recommended treatment for a patient that develops pruritus and multiple urticaria after taking amoxicillin for a sore throat? The lungs are clear to auscultation and there is no stridor. \n\nAntihistamines + discontinuation of amoxicillin \n\nthe patient is having a mild drug-induced type 1 hypersensitivity reaction and thus an antihistamine is appropriate \n\n Type-1 HS (true allergy) occurs rapidly , versus rash after Amoxycillin in IM which occurs after 5-9 days \n\n## Psoriasis \n\n577 https://t.me/usmleinnercircle USMLE Inner Circle \n\nAcute urticar ia \n\n## . Medications, insect stin gs \n\nEtiologies . Infections, rhe um ato logic diseases \n\n## . Ma ny cases are idiopathic \n\nPathophysiology . Mast cells rel eas e histamine _, dermal edema \n\n## . Prurit ic , erythematous pl aques (ie, wheals) \n\nClinical features . E ac h wheal lasts <24 hr, urticaria duration <6 weeks \n\n## . Diffuse or locali zed \n\n## . No workup for 1st episode \n\nEvaluation . Allergy testing if ll e~ifi~ trigg er (eg fQQ d) i Y Sll e~t !l d\n\n## . Laboratory testing/biopsy if systemic symptoms are present \n\nTrea tment & . 2nd-generation H1 antihistami nes \n\n## . A dd H2 antihistamines or systemic corticosteroids if severe \n\nprognosis Two -thirds of cases self-resolve .\n\nPlaque psoriasis Skin lesions . Well-defined, erythematous plaques with silvery scale \n\n# . Extensor surfaces (knees, elbows), hands, scalp, bac k, nail plat es \n\nExtradermal . Nail pitting \n\nmanifestations . Conjunctivitis, uveitis \n\n# . Psoriatic arthritis \n\n## . Topical: hi gh -potency glucocorticoids, vitamin D analogs, tar, retinoids, calcineurin inhibit or s, tazarotene \n\nTreatment . Ultraviolet lighVphototherapy \n\n# . Systemic: methotrexate, calcineurin inhibitors, retinoids, apremilast, biologic agents Dermatology Rosacea \n\n578 https://t.me/usmleinnercircle \n\nPalmar psoriasis Psoriatic nail disease Rosacea \n\n# . Persistent facial erythema/flushing \n\nErythemato-telangiectatic Telangiectasias .\n\nPapulopustular . Papules & pustules on central face . Conjunctiva! hyperemia \n\nOcular . Lid margin telangiectasias \n\n## . Avoidance of triggers (eg , alcohol , spicy foods) . Sun protection \n\nTreatment . Gentle cleansers & emollients . Topical metronidazole for papulopustular type \n\n## . Laser or topical brimonidine (vasoconstrictive a-2 agonist) for erythematotelangiectatic type Dermatology What are some triggers for rosacea ?\n\nIncrease body temperatures ( hot weather, hot drinks, spicy foods ), alcohol \n\n## Pityriasis Rosea \n\n579 https://t.me/usmleinnercircle USMLE Inner Circle \n\nTreatment of rosacea General measures . Avoidance of sun exposure, hoUspicy foods, alcohol \n\n## . Gentle cleansers & emollients \n\nErythematotelangiectatic rosacea . Topical brimonidine (flushing, erythema, telangiectasia) . Laser/intense pulsed light therapy \n\nPapulopustular rosacea . First line: topical metronidazole, azelaic acid , ivermectin (small papules & pustules) . Second line: oral tetracyclines \n\nPhymatous rosacea . Oral isotretinoin (irregular thickening of skin) . Laser therapy/surgery \n\nOcular rosacea . Lid scrubs & ocular lubricants (burning/foreign body sensations, blepharitis, keratitis, . Topical or systemic antibiotics (eg, metronidazole, macrolides) conjunctivitis, corneal ulcers) \n\nPityriasis rosea \n\n Viral prodrome \n\nClinical features Annular, pink herald patch on trunk Oval lesions in \"Christmas tree\" pattern Pruritus \n\nManagement Reassurance (spontaneous resolution) Treatment of pruritus (eg, antihistamines) Dermatology Seborrheic Dermatitis \n\n What is the likely diagnosis in a middle-aged patient that presents with a greasy-looking , yellowish , scaly facial rash (pictured below) and increased dandruff ?\n\nSeborrheic dermatitis \n\npredominantly affects the scalp and face, especially areas with numerous sebaceous glands \n\n Person who has a sudden breakout of seborrheic dermatitis: Screen for HIV \n\n580 https://t.me/usmleinnercircle \n\nPi ty riasis rosea \n\nIniti al s ig n\n\nHerald patch \n\nSecondary sign \n\nCh ri stmas tree rash \n\nSeborrheic dermatitis in adults \n\n# . Erythematous, pruritic plaques with greasy scales \n\nClinical features . Scalp, central face, ears, chest \n\n# . CNS disease (eg, Parkinson disease) \n\nRisk factors . HIV \n\n# . Topical antifungals (eg , selenium sulfi de , ketoconazole) \n\nTreatment . Topical glucocorticoids \n\n# . Topical calcineurin inhibitors (eg, pimecrolimus) \n\nSeborrheic dermatitis in infants \n\n# . Scalp (cradle cap), face (eg, eyebrows), retroauricu lar areas \n\n> 0\n\nYellow, greasy scales \n\nClinical features . lntertriginous regions (eg, neck folds, axillae, diaper area), umbilicus \n\n> 0\n\nG li stening, confluent erythema \n\n# . Mild pruritus; no systemic symptoms \n\nTreatment . F ir st-line: emollients, nonmedicated shampoos \n\n# . Second-line: topical antifungals or low-potency corticosteroids Seborrheic dermatitis distribution in an infant Dermatology Seborrheic Keratosis \n\n Main risk factor is Age. \n\n A 80 year old patient presents complaining of a pigmented lesion on his face. Physical exam reveals a large, brown, greasy-looking, and crusted pigmented lesion that appears stuck on the patients face. What is the most likely diagnosis? \n\nSeborrheic keratosis \n\n Itself is benign but rapid onset multiple SK could be a Sign of malignancy (Leser Trelat Sign) \n\n## Icthyosis Vulgaris \n\n581 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPath: Pt: Dx: Tx: f/u: \n\nSeborrheic dennatitis (cradle cap) \n\nSEBORRHEIC KERATOSIS \n\nLooks like cancer, but isn't Large, brown, greasy, \"stuck on\" lesions Elderly Clinical Leave it alone Biopsy if changing, if not changing, leave it alone. It could be cancer if it is changing. \n\nSeborrheic dennatitis Greasy yellow scaling \n\nove r erythema Dermatology What is the likely diagnosis in a patient that presents with diffusely rough , dry , and scaly skin ? The symptoms are worse in the winter, and symptoms of dry skin have been present for most of the patient's life. \n\nIchthyosis vulgaris \n\nchronic, inherited skin disorder characterized by diffuse dermal scaling \n\n## Erythema Nodosum \n\n582 https://t.me/usmleinnercircle \n\nlchthyosis vulgaris \n\n## . Loss of function in filaggrin gene \n\nPathophysiology 0 Impaired epidermal barrier \n\n> 0\n\nReduced skin moisturization \n\n## . Onset in infancy/early childhood \n\nClinical features . Diffuse, scaly skin with mild pruritus \n\n## . Worse on extensor extremities, spares intertriginous areas \n\nAssociated . Keratosis pilaris \n\nconditions . Palmar hyperlinearity \n\n## . Atopic disease \n\nDiagnosis . Clinical findings \n\n## . Biopsy if uncertain: reduced/absent granular layer in epidermis \n\n## . Long baths to remove scales \n\nTherapy . Moisturization \n\n## . Keratolytics (eg, urea, alpha-hydroxy acid, salicylic acid) \n\nHyperlinear palms Erythema nodosum Clinical features . Tender, indurated, erythematous nodules \n\n## . Most common on anterior legs \n\n## . Infections (eg , Streptococcus) \n\nEtiology . Inflammatory bowel disease \n\n## . Sarcoidosis \n\n## . Medications (eg, antibiotics, oral contraceptives) \n\nPathologic findings . Septal panniculitis without vasculitis \n\nNatural history . Spontaneous resolution (weeks) \n\n## . Residual hyperpigmentation Dermatology Other diseases associated with EN: endemic fungal infections (Coccidioides, Histoplasma) , Behcets \n\n What initial imaging study is recommended for patients with erythema nodosum ?\n\nChest X-ray \n\nuseful to evaluate for sarcoidosis and tuberculosis , which are both associated with EN; sarcoidosis patients may have no other symptoms \n\n The association between EN and IBD is well recognized and more commonly occurs in Crohn disease \n\nthan ulcerative colitis. EN mirrors IBD disease activity , meaning that it worsens during severe IBD flares and resolves as those flares improve. EN results from a delayed-type hypersensitivity reaction to antigen exposure. Biopsy of the nodules reveals septal panniculitis without vasculitis. \n\n## Lichen Planus Lymphedema Discontinue the offending medication Wickham Striae \n\n583 https://t.me/usmleinnercircle USMLE Inner Circle \n\nLichen planus Lichen planus \n\n## . 5 \"Ps\": pruritic, purple/pink, polygonal , papules & plaques \n\n## . Lacy, white network of lines (Wickham striae) \n\nClinical . Locations: \n\nfindings 0 Skin (eg, ankles, wr ists) \n\n0 Oral mucosa (white papules & plaques erythema, mucosa! atrophy, ulcers) \n\n0 Genitalia \n\nDisease . Hepatitis C \n\nassociations . Medications: ACE inhibitors, thiazide diuretics \n\nNatural . Chronic symptoms \n\nhistory . Formation of lesions at sites of trauma (Kobner phenomenon) \n\n## . Spontaneous resolution within 2 years \n\nTreatment . Topical high-potency glucocorticoids (eg , betamethasone) \n\n## . Widespread lesions: systemic glucocorticoids, phototherapy Dermatology Inability to lift the skin on the dorsum of the second toe is highly specific for lymphedema \n\ni.e. positive Stemmer sign ; typically occurs with advanced lymphedema, which causes firm , thickened , non-pitting edema secondary to deposition of collagen and adipose tissue Treat with manual compression therapy and weight loss/exercise \n\n## Dermatofibroma \n\n Dermatofibromas are nontender , firm, hyperpigmented nodules that are usually <1 cm in diameter. They are due to fibroblast proliferation and most commonly occur on the lower extremities. What is a key distinguishing feature of dermatofibroma on examination? \n\nCentral dimpling when pinched \n\n\"Buttonhole \" or \" Dimple \" sign. \n\n## Epidermal Inclusion Cyst \n\n584 https://t.me/usmleinnercircle \n\nLymphedema \n\n> Disruption of the lymphatic system\n> oObstruction (eg , malignancy)\n\nEtiology o Lymph node dissection \n\n> oChronic inflammation (eg , recurrent cellulitis)\n> oCongenital (eg , Turner syndrome)\n> oParasitic infection (eg, filariasis) Swelling , pain, heaviness\n\nClinical presentation Early: Soft skin , pitting edema Late: Firm & thickened skin, nonpitting edema Weight loss \n\nTreatment Limb elevation & compression Physiotherapy Dermatology What is the likely diagnosis in a patient with a firm , mobile nodule on the back? The nodule does not change shape when pinched at the edge. The patient had a similar bump in the same location months ago, which spontaneously resolved. \n\nEpidermal inclusion cyst \n\nbenign nodule containing squamous epithelium that produces keratin ; presents as a dome-shaped, firm, freely movable cyst or a nodule with a central punctum \n\n The lesion can remain stable or gradually increase in size but may produce a cheesy white discharge ; it usually resolves spontaneously .D/D: lipomas are usually soft to rubbery and irregular , and do not typically regress and recur. \n\n## Blistering Skin Disorders \n\nPemphigus Vulgaris Bullous Pemphigoid <60y age group \n\n585 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPemphigus vulgaris Autoantibody target Desmosomes (desmogleins 1 & 3) Flaccid bullae & ulcers \n\nClinical features Mucosa! erosions Separation of epidermis by light friction (Nikolsky sign) lntraepidermal cleavage \n\nHistopathology Acantholysis (detached keratinocytes) ''Tombstone cells\" along basal layer \n\nlmmunofluorescence Nellike intercellular lgG Systemic glucocorticoids \n\nTreatment Corticosteroid-sparing agents Aggressive wound care Dermatology Epidermolysis Bullosa \n\n Epidermolysis bullosa is a group of inherited disorders characterized by epithelial fragility (eg, bullae, erosions, ulcers) triggered by minor trauma .These conditions are caused by mutations of proteins involved in intraepidermal and \n\ndermoepidermal adhesion complexes in the basement membrane zone. There are four primary subtypes of EB ( simplex , junctional , dystrophic , Kindler syndrome ), with variable severity within subtypes. \n\n586 https://t.me/usmleinnercircle \n\nBullous pemphigoid \n\n## . Age >60 \n\nClinical . Pruritic, tense bullae \n\nfeatures . Rare mucosal involvement \n\n## . Prodrome of eczematous/urticaria-like rash \n\n## . Dementia \n\nAssociated . Parkinson disease \n\ndisorders . Depression, bipolar disorder \n\n## . Histology: subepidermal cleavage \n\nDiagnosis . lmmunofluorescence: li near lgG/C3 deposition along basement membrane \n\n## . Serology: autoantibodies to bullous pemphigoid antigens (hemidesmosomes) \n\nTreatment . Topical therapies : high-potency corticosteroids \n\n## . Systemic therapies: corticosteroid, doxycycline \n\nBullous pemphigoid Dermatology EB simplex , is the most common form, which is caused by mutations in keratin genes .EB simplex presents in children and young adults with friction-induced blisters at the palms and soles and other exposed areas. The lesions typically heal with no residual scarring, although patients may have chronic thickening of the skin of the feet .Infants with EB simplex may develop oral blisters with bottle-feeding , but mild cases often do not lead to definitive diagnostic testing. Suspected EB warrants biopsy of a fresh blister for immunofluorescence microscopy ; genetic testing is available for confirmation. Treatment primarily involves careful wound care and supportive measures. \n\nSJS Staph Scalded Skin Syndrome Mucositis \n\n587 https://t.me/usmleinnercircle USMLE Inner Circle \n\nStevens.Johnson syndrome & toxic epidermal necrolysis \n\n<10% of BSA: SJS \n\nNomenclature 10%-30%: SJSfTEN overlap >30%: TEN \n\n## . 4-28 days after exposure to trigger (2 days after repeat exposure ) \n\nClinical . Acute influenza-like prodrome \n\nfeatures . Rapid-onset erythematous macules, vesicles , bullae \n\n## . Necrosis & sloughing of epidermis \n\n## . Mucosal involvement \n\nDrugs \n\n## . Allopurinol \n\n## . Antibiotics (eg, sulfonamides) \n\n## . Anticonvulsants (eg , carbamazepine, lamotrigine, phenytoin) \n\nCommon . NSAIDs (eg , piroxicam) \n\ntriggers . Sulfasalazine \n\nOther \n\n## . Mycoplasma pneumoniae \n\n## . Vaccination . Graft versus host disease \n\nBSA = body surface area ; NSAIDs = nonsteroidal anti-inflammatory drugs; \n\nSJS = Stevens-Johnson syndrome; TEN = toxic epidermal necrolysis. Dermatology What is the likely diagnosis in a child that presents with generalized erythema , fever , and superficial flaccid bullae with a positive Nikolsky sign? \n\nStaphylococcal scalded skin syndrome \n\n## Porphyria Cutanea Tarda \n\n PCT is NOT inherited disorder (spontaneous inheritance pattern) \n\n## Hair \n\n Many chemotherapeutic agents preferentially target rapidly dividing cells, including hair follicle cells in the anagen phase .\n\n588 https://t.me/usmleinnercircle \n\nStaphylococcal scalded skin syndrome Pathogenesis . Staphylococcus aureus exfoliative toxin \n\nClinical . Feve r, irritability \n\nfeatures . Generalized erythema, blisters \n\n## . Epidermal shedding (Nikolsky sign) \n\n## . Antistaphylococcal antibiotic \n\nManagement (eg, nafcillin, vancomycin) \n\n## . Wound care \n\nPorphyria cutanea tarda Clinical Bllisters, bullae, scarring, hypopigrnentation/ hyperpigmentation \n\npresentation on sun-exposed skin (eg, back of hands, forearms , face) Scarring and calcification similar to scleroderma Hepatitis C \n\n HIV \n\nAssociated Excessive alcohol consumption \n\nconditions \n\n Estrogen use Srnoking1 \n\nDiagnostic Mildly elevated liver enzymes and iron overload \n\ntesting Ellevated plasma or urine porphyrin levels \n\nFemale & male pattern hair loss Etiology . Polygenetic inheritance . Hormonal factors (dihydrotestosterone) . Ch ronic, progressive thinning of hair \n\nClinical features . Men: vertex, frontal ha irline, temporal areas . Women: vertex, center of sca lp (sparing of hairline) \n\nManagement . Men: minoxidil, finasteri de \n\n## . Women: minoxidil Dermatology Impaired cellular reproduction in the anagen phase can lead to temporary , reversible cessation of hair growth and rapid shedding of hair shafts ( anagen effluvium )\n\nTelogen Effluvium \n\n What dermatologic pathology is characterized by widespread thinning of the hair with normal appearing scalp and hair shafts, typically after a stressful event ? Physical exam shows >20% of hair fibers are pulled out when pulled firmly. \n\nTelogen effluvium \n\ne.g. weight loss, pregnancy, major illness; characterized by a positive hair pull test ( >10% of fibers is diagnostic ). <10% is normal. Treatment is reassurance. Can occur with hypothyroidism, anabolic steroids, and pregnancy/childbirth (telegenic gravidarum) \n\nAlopecia Areata \n\n Associated with other autoimmune conditions (eg, vitiligo ,\n\nhypothyroidism )\n\n## Miscellaneous \n\nSenile Purpura exclamation point hair \n\n589 https://t.me/usmleinnercircle USMLE Inner Circle \n\nTelogen effluvium \n\n Acute, diffuse, noninflammatory hair loss \n\nClinical findings Scalp & hair fibers appear normal . Hair shafts easily pulled out (hair pull test) Severe illness, fever, surgery \n\nTriggers Pregnancy, childbirth Emotional distress Endocrine & nutritional disorders \n\nManagement Address underlying cause Reassurance (self-limited disorder) \n\nAlopecia areata \n\n# . Autoimmune attack on hair bulb cells \n\nPathogenesis Genetic predisposition .. Pa inless, patchy, nonscarring hair loss \n\nClinical presentation . Narrowing of hair shafts close to skin surface (exclamation point hairs) . Positive hair pull test (>5 -6 hairs extracted) \n\n## . Mild/moderate hair loss: topical or intralesional corticosteroids \n\nManagement Extensive hair loss: topical immunotherapy (eg, diphenylcyclopropenone), oral corticosteroids .Dermatology What is the likely diagnosis in an elderly patient with multiple ecchymoses on the hands and forearms ?The lesions are not itchy nor painful and laboratory studies are within normal limits. \n\nSenile purpura ( perivascular tissue atrophy )\n\ndue to age-related loss of elastic fibers in perivascular connective tissue \n\n Minor abrasions that would merely stretch the skin in younger patients can rupture superficial blood \n\nvessels in the elderly. The subsequent extravasation of blood leads to ecchymosis over vulnerable areas, such as the dorsum of the hands and forearms. Patients can have residual brownish discoloration from hemosiderin deposition. \n\nPseudofoliculitis Barbae \n\nPseudofolliculitis barbae presents with small , painful papules in the beard area .It is caused by penetration of the hair shaft into interfollicular skin , often due to shaving of tightly \n\ncurled hair .Complications include hyperpigmentation , secondary bacterial infection , and keloid formation .Management includes discontinuation of shaving or use of alternative shaving techniques .\n\nKeratosis Pilaris \n\n Keratosis pilaris is characterized by retained keratin plugs in the hair follicles . It occurs most commonly on the posterior surface of the upper arm and manifests as small , painless papules ; a \n\n590 https://t.me/usmleinnercircle Dermatology roughened skin texture ; and mottled, perifollicular erythema. Exacerbations are common in cold, dry weather. Treatment includes emollients and topical keratolytics (eg, salicylic acid, urea ). \n\nPyoderma Gangrenosum \n\n PG is diagnosed clinically after excluding other diagnoses (eg, infection , venous ulcers , cutaneous \n\ncancers ). \n\n591 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPyoderma gangrenosum \n\n## . Begins with small papule or pustule \n\nClinical features . Rapidly progressive, painful ulcer with purulent base & violaceous border \n\n## . Precipitation of ulceration at site of injury (pathergy) \n\n## . Peak onset age 40-60 \n\nEpidemiology . Women> men \n\n## . Association with inflammatory bowel disease, inflammatory (eg, rheumatoid) arthritis, malignancy \n\nDiagnosis . Exclusion of other causes of ulceration (eg, infection) . Skin biopsy: mixed inflammation (neutrophil predominant) \n\nTreatment . Local or systemic glucocorticoids \n\nPyoderma gangrenosum Dermatology Biopsy of ulcer margin in RECOMMENDED Surgical debridement is usually avoided due to the potential of inducing pathergy; \n\nInsect Bites \n\nScabies \n\n592 https://t.me/usmleinnercircle \n\nPathogenesis Clinical fe atures Diagnosis Tr eatment Common insect bites/infestation Insect Clinical features* \n\nBed bug Pruritic, sma ll puncta & maculopapul es in linear groups (\"breakfast, lunch, di nner\" pattern) on unclothed skin Pediculosis Widespread itching of hai r, body, or genitalia wit h visible louse \n\n# aScabies Pruritic burrows or hemorrhagic crusts in intertriginous areas Spider Tick Solitary papul e, pustule, or wheal +/- pruritus Painless red papule +/- pruritus during the spring & summer \n\n\"Some patients have no symptoms Scabies \n\n# . Sarcoptes scabi ei mite infestation \n\n## . Spread by d ir ect person-to-person contact \n\n## . Extremely pruritic, small, erythematous papules \n\n## . Di str ibution: interdigital we b spaces, flexor wrists , extensor elbows, axillae, fe et, umbilic us & genitalia \n\n## . Burrows {thin serpiginous lines) ma y not be visible but pathognomon ic if present \n\n# . Clinical \n\n## . Skin sc raping with mi cro sc op y is co nfirm at o !}'. \n\n## . Topica l 5% perrnethrin OR oral ivermectin \n\n## . Tr ea t household mem be rs & close per so nal co nta cts \n\n## . Environmental measures (eg, launder clothing/bedding) Dermatology Burns \n\n The first priorities of burn management are stabilization (eg, airway, breathing, circulation) and \n\nresuscitation (eg, intravenous fluids) patients with major burns (ie, >20% total body surface area [TBSA]) receive aggressive fluid resuscitation , which is usually begun based on a formula (eg, Parkland formula) and then titrated to maintain adequate urine output (goal: 0.5 mL/kg/hr) , a marker of organ perfusion. For accurate monitoring of urine output in these patients, a urethral catheter (eg, Foley catheter) is required. In patients who have genital burns and other burns covering a large TBSA, a catheter should be placed as soon as possible; delay can lead to edema that obstructs visualization and catheterization of the urethra. \n\n 50% of calculated fluid in 1st 8 hours and rest 50% in next 16 hours. \n\n Immediately after a severe burn , most infections are due to gram-positive organisms (Staph) \n\n After > 5 days following a severe burn , most infections are due to gram-negative organisms (Pseudomonas ) or fungi (Candida). \n\nDiagnosis requires quantitative wound culture (>105 bacteria/g of tissue) and biopsy for histopathology. \n\n Prophylactic Antibiotics are NOT indicated in burn patients. Change in appearance of a burn wound or loss of a viable skin graft is often the earliest sign of wound infection. \n\ne.g. partial-thickness injury turns into full-thickness injury \n\n 2 most common burn infection pathogens: Pseudomonas aeruginosa and Staphylococcus aureus \n\nT/t: Piperacillin -tazobactam or a carbapenem , in combination with vancomycin \n\n593 https://t.me/usmleinnercircle USMLE Inner Circle \n\nScabies Crusted scabies Dermatology Patients with severe burn injuries are at high risk for sepsis . Careful attention must be given to the following findings heralding the onset of burn wound sepsis: \n\nTemperature <36.5 C (97.7 F) or >39 C (102.2 F) \n\nVital sign changes , including progressive tachycardia (>90/min) or tachypnea (>30/min), or refractory hypotension (systolic blood pressure <90 mm Hg) Evolving laboratory abnormalities (eg, leukocytosis or leukopenia , thrombocytopenia )Evidence of organ hypoperfusion and/or dysfunction , such as oliguria or new-onset enteral feeding intolerance. \n\nT/t: Take blood and wound cultures and start empiric antibiotics \n\n Removal of eschar through early (eg, within 5 days of injury) wound excision and grafting reduces the risk of both noninvasive and invasive burn wound infections. In the operating room, layers of devitalized tissue are progressively removed until capillary bleeding is encountered (ie, tangential excision ). This is followed by application of split thickness skin grafts or, if graft donor sites are unavailable, other temporary coverage (eg, cadaveric skin, manufactured skin substitutes). Burn victims with oropharyngeal inflammation/blistering or carboxyhemoglobin levels > 10% should be intubated to prevent upper airway obstruction by edema. \n\nother indications for intubation include burns on the face , oropharyngeal carbon deposits , stridor ,and history of confinement in a burning building ;the supraglottic airway is very sensitive to direct thermal injury with subsequent edema/blistering, which can cause obstruction \n\n Circumferential , full-thickness burns can result in eschar formation that restricts venous/lymphatic drainage , leading to acute compartment syndrome. \n\nmay warrant surgical escharotomy to relieve pressure \n\nBurn Nutrition \n\n Enteral nutrition (EN) (ie, intestinal route) is preferred over parenteral (ie, intravenous) nutrition in patients with burn injuries because EN is associated with multiple clinical benefits , including the following: \n\n594 https://t.me/usmleinnercircle \n\n\n\nHypermetabolic response in burn injury Etiology . Moderate to severe bum injury (eg, inhalational, high-voltage electrical, TBSA >20%) \n\n# . r Inflammatory mediators, which result in r catecholamines, glucocorticoids & glucagon \n\n# . Hyperdynamic circulatory response: tachycard ia, hypertension \n\n> Clinical features\n\n# . r Gluconeogenesis & insulin resistance: hyperglycemia \n\n# . r Basal metabolic rate: r basal body temperature \n\n# . r Protein & lipid catabolism: r lean mu sc le wasting \n\n# . Early bum excision & grafting \n\n> Treatment\n\n# . Beta blockade (eg, propranolol) \n\n# . Glycemic control (eg, insulin) \n\n# . Nutritional support & anabolic steroid therapy (eg, oxandrolone) \n\n> TBSA =total body surface area.\n\nDermatology Trophic effect s on the intestinal mucosa and gut- and mucosa-associated lymphoid tissue, resulting in maintenance of gut integrity and decreased bacterial translocation Reduced rates of sepsis and other infectious complications (eg, pneumonia) \n\nDecreased mortality \n\nArousable patients may be able to eat; if not, a flexible, small-bore nasogastric feeding tube (eg, \n\nDobhoff tube) can be placed, even with facial burns. \n\n Initiated within 24 hours of the burn, beginning at a low rate (ie, trickle feeding) Given the increased protein catabolism in patients with moderate to severe burns, high-protein , high-calorie formulas are typically used. \n\n This is done not just burns but ALL critically ill patients \n\n Normal bowel sound s and/or evidence of bowel function (eg, passing flatus or stool) are \n\nNOT required for initiation of EN because they are indicative only of contractility rather than mucosal integrity and absorptive capacity. \n\nElectric Burns \n\n In patients with high-voltage electrical injuries , tissue damage occurs from both the direct injury \n\ncaused by electricity and from the secondary conversion of electrical energy to thermal energy . Because bone (with its high resistance to electrical current) generates the most heat as current passes through the body, thermal injury to internal tissues surrounding the bone (eg, skeletal muscle) often exceeds the visible injury to external tissues (eg, skin). Skeletal muscle necrosis in patients with high-voltage electrical injuries often leads to the following clinical features: \n\nAcute compartment syndrome from intracompartmental muscle swelling \n\nRhabdomyolysis , with leakage of muscle contents, including heme pigment, into the circulation Heme pigmentinduced acute kidney injury (eg, intratubular cast formation) Patients should be monitored for these conditions and should receive aggressive IV fluid resuscitation. Because of the risk of hyperkalemia from rhabdomyolysis, potassium -containing IV fluids should be avoided. \n\n## Vascular Tumors \n\nAngiosarcoma \n\n Secondary angiosarcoma is a malignant endothelial tumor that develops 4-8 years after breast cancer therapy .Risk factors include radiation therapy and chronic lymphedema .Typical lesions are red, bruise-like plaques and purple papules and nodules .Timely biopsy is recommended for diagnosis because the cancer readily metastasizes .\n\n595 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDermatology Pyogenic Granuloma \n\n Pyogenic granulomas (Lobar Capillary Hemangioma) are small vascular tumors composed of abnormal capillaries and granulation tissue. They typically present as friable , dome-shaped nodules on the hands, trunk, or oral mucosa/gingiva that can bleed with minor trauma. Pyogenic granulomas are common in pregnancy and usually regress postpartum .\n\nBacillary Angiomatosis \n\n596 https://t.me/usmleinnercircle \n\n> Secondary angiosarcoma due to radiation therapy Pyogenic granuloma\n\nDermatology The lesions stain positive with Warthin-Starry stain \n\nKaposi Sarcoma \n\n What is the likely diagnosis in a patient with poorly controlled HIV that develops multiple violaceous papules in the groin region? \n\nKaposi sarcoma \n\nmay require biopsy (lymphocytic infiltrate) to help differentiate from bacillary angiomatosis (neutrophilic infiltrate) \n\n## Skin Tumour Pedunculated /exophytic lesions and liver involvement \n\nare more typical of BA than Kaposi sarcoma \n\n597 https://t.me/usmleinnercircle USMLE Inner Circle \n\nBacillary angiomatosis \n\n Bartonella henselaelquintana \n\nEpidemiology Cat exposure or homelessness (lice) Severe immunocompromise o Advanced HIV (CD4 <100/mm 3) Vascular cutaneous lesions \n\n(papular, nodular, peduncular) \n\nManifestations Systemic symptoms \n\n(fever, nig ht sweats, fatigue) Organ involvement rarely (liver, bone, CNS) \n\nDiagnosis Lesional biopsy with microscopy/histopathology \n\nTreatment Doxycycline or erythromycin Antiretroviral therapy \n\nKaposi sarcoma \n\n# . Endothelial tumor caused by human herpesvirus 8 \n\nEtiology . Most common malignancy in patients with untreated HIV \n\n# . Endemic in certain African & Mediterranean regions \n\n# . Cutaneous lesions :\n\n0 Violaceous, red, or brown flat lesions grow into papules 0 Most common along skin folds 0 Pruritus. pain & friabili ty are rare \n\nManifestations 0 Lymphedema distal to lesions \n\n# . Visceral lesions: 0 Lungs & gastrointestinal tract most common 0 May cause life-threatening bleeding \n\n# . HIV-associated KS: 0 Antiretroviral therapy initiation \n\nTreatment 0 Local or systemic chemotherapy rarely required \n\n# . Endemic KS: 0 Surgery & local therapy are primary modalities \n\nKS = Kaposi sarcoma .Dermatology BCC \n\n In an excisional biopsy , the entirety of the visible lesion is removed, usually without excising a margin of surrounding skin. If the biopsy confirms BCC, additional excision with 4-mm margins is done with the goal of completely removing cancerous tissue \n\nSCC \n\n598 https://t.me/usmleinnercircle \n\nBasal cell carcinoma \n\n## . Sun/ultraviolet light \n\nRisk factors . Fa ir skin \n\n## . Ionizing radiation \n\nClinical . Skin-colored , pea~y nodule rolled borders \n\nfeatures . Telangiectatic vessels \n\n## . Central ulceration, local invasion \n\nDiagnosis . Shave , punch, or excisional biopsy \n\n## . First-line: \n\n> 0\n\nSurgical excision with 4-mm margins \n\nTreatment 0 Mohs micrographic surgery (face/high-risk tumors) \n\n## . Second-line: \n\n> 0\n\nTopical fluorouracil , topical imiquimod, C &E (low-risk tumors only) \n\nC&E ; curettage & electrodesiccation. \n\nSquamous cell carcinoma of skin \n\n## . Sun/ultraviolet, ionizing radiation exposure \n\nRisk factors . Chronic scars/wounds/burn in jur ies \n\n# . lmmunosu eeression \n\n## . Scaly plaques/nodules \n\nClinical features . Ulceration \n\n## . SCC in situ: well-demarcated patches/plaques \n\n## . Punch, shave, or excisional biopsy \n\nDiagnosis Dysplastic/anaplastic keratinocytes . sec in situ Invasive sec Excision with 4- to 6-mm margins . Excision with 4- to 6-mm margins \n\nTreatment . C&E .. Mohs micrographic surgery Cryotherapy .. Topical 5-FU, imiquimod \n\n5-FU ; 5-fluorouracil ; C&E ; curettage & electrodesiccation; sec ; squamous cell carcinoma. Dermatology SCC is the most common skin malignancy in immunocompromised patients ,\n\nBCC is more common in the general population \n\n In dark-skinned patients, SCC typically affects nonsun-exposed surfaces and areas with chronic \n\ninflammation (eg, venous stasis ulcers) or chronic scarring (eg, burn scars). In addition, high-risk human papillomavirus infection can cause genital and periungual SCC .\n\n Perineural invasion can cause local paresthesia . Metastatic disease should be suspected when regional lymphadenopathy is present. Which type of skin cancer is most likely to arise from chronically wounded , scarred , or inflamed skin ?\n\nSquamous cell carcinoma \n\nSCC arising in chronic wounds tends to be more aggressive NOT pruritic or painful. Limited to epidermis . Do BIOPSY \n\n599 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSquamous cell carcinoma in situ (Bowen disease) \n\nThickened, rough plaque with wrinkles. Squamous cell carcinoma \n\n,.. \\\n\nI \\\n\nI \\\n\nI \\\n\nI '-\n\nI \\I '\n\n\\. \n\n\\\n\n'- \\\\\n\n# - C)UWo< I\n\nCutaneous squamous cell carcinoma (poorly differentiated) Dermatology Marjolin's ulcer at the site of an old burn or continuously draining sinus is a risk factor for squamous cell carcinoma . Skin ulceration that fails to heal in the site of chronic burn wound. Biopsy is most likely to show what? \n\nSquamous cell carcinoma secondary to Marjolin Ulcer ( perform punch biopsy )\n\nSCC is most offen associated with ultraviolet exposure but can arise within chronic wounds, scars, or inflammed skin \n\nSCC arising within a burn wound is known as a Marjolin ulcer \n\nActinic Keratosis Keratoacanthoma \n\n Rapid growing, dome-shaped nodule with a central keratin-filled center \n\nKeratoacanthoma \n\nResembles SCC! \n\n600 https://t.me/usmleinnercircle \n\nActinic keratosis Clinical features . Erythematous, scaly papules; rough plaques \n\n## . Sun-exposed areas \n\nDiagnosis . Clinical appearance . Biopsy if flls! !U[ !l!:i Qf 12 2 !:i!:i ib l!l ::i!:.Q (eg , size ;?:1 cm , rapid growth, ulceration , tenderness) \n\n## . Chronic/persistent \n\nPrognosis . Progression to sec . Spontaneous resolution \n\nTreatment . Isolated lesion s: cryotherapy . Diffuse lesions: topical fluorouracil, imiquimod , tirbanibulin \n\n> SCC =\n\nsquamous cell carcinoma. \n\n> Actinic keratosis\n\nKeratoacanthoma \n\n# . Rapidly growing nodule wi th ulceration & keratin plug \n\nClinical features . Often shows spontaneous regression/resolution \n\nClinical significance . May resemble or progress to squamous cell carcinoma \n\nManagement . Excisional biopsy with complete removal of lesion Dermatology Melanoma \n\n What is the next step in a patient with no ABCDE features of melanoma but a positive \"ugly duckling sign\"? \n\nBiopsy (with initial margins of 1-3 mm) \n\n A mole may represent melanoma if it appears substantially different from others (\"ugly duckling sign\"), itches or bleeds , or develops nodularity . If melanoma is suspected, an excisional biopsy should be obtained. Regress spontaneously Most important prognostic indicator in malignant melanoma. \n\n601 https://t.me/usmleinnercircle USMLE Inner Circle \n\nABCDE criteria \n\n(~1-2 is suspicious) \n\n7-point checklist \n\n(~1 major or ~3 minor is suspicious) \n\nUgly duckling sign Nail melanoma with the Hutchinson sign Visual assessment of melanoma \n\n Asymmetry Border irregularity \n\n# . Color variati on (within lesion or compared to other lesions) Diameter ~6 mm Evolving appearance over time Major criteria: change in size, shape, or color Minor criteria : size ~7 mm , local inflammati on , crusting/bleeding , sensory symptoms \n\n# . One lesi on is significantly different from others on t he patient \n\nMelanoma depth of invasion \n\n0 -.. \n\n5 -.. \n\n Common drugs associated with photosensitivity reactions Antibiotics Tetrac lcline s\\eg, do xl cl cline )\n> Anti psychotics Chlorpromazine, prochlorperazine Diuretics Furosemide, hydrochlorothiazide\n> Others Amiodarone, promethazine, piroxicam\n\nDermatology Umbilical granuloma: soft , moist , pink , pedunculated lesion after the umbilical cord separation T/t: Silver nitrate \n\nNeonatal Rashes Erythema Toxicum Neonatorum Cephalic Pustulosis \n\n603 https://t.me/usmleinnercircle USMLE Inner Circle \n\nBenign neonatal rashes Diagnosis Onset Clinical features Management/resolution \n\n## . Pustules with \n\n## . Birth to erythematous . Observation Erythema toxicum age 3 base on trunk & Resolves within a .neonatorum days proximal ~\n\nextremities \n\n## . Observation Milia Birth . Firm . ~ Resolves within a . .papules on face month Any E!i! hematous, . Avoid overheating \n\n## . . (eg, cool age, papular rash on environment, Miliaria rubra ~ t ~ &\n\npresent intertriginous thin/cotton clothing) \n\n~\n\n## . If severe , topical \n\n~ corticosteroid . Nonerythematous \n\npustules ----+ \n\nevolve into . Observation hyperpigmented . Pustules resolve Neonatal pustular . Birth macules with within days melanosis collarette of scale . Hyperpigmentation . Diffuse , may may last months involve palms &\n\nsoles \n\n## . Observation \n\n## . Erythematous . Resolves in weeks to . Around Neonatal cephalic papules & months pustulosis age 3 pustules on face . If severe , topical weeks & scalp only corticosteroid or ketoconazole Dermatology Neonatal cephalic pustulosis presents with erythematous papules and pustules limited to the face and scalp around age 3 weeks .Management is typically limited to daily cleansing with gentle soap and water , and self-resolution \n\nwithout scarring is expected within weeks to months. \n\nMiliaria Rubra \n\n Miliaria (heat rash ) is due to blockage of the eccrine sweat ducts in the setting of increased heat or \n\nhumidity .It is most common in newborns and young children; manifestations can range from small , thin-walled \n\nvesicles to patches of erythematous papules or pustules .Management involves avoidance of overbundling and synthetic fabrics and switching to thin clothing made of breathable material (eg, cotton). \n\nCongenital Pigmented Lesions \n\n604 https://t.me/usmleinnercircle \n\n> Miliaria rubra (heat rash) Fine, erythematous papular rash\n\nDermatology Congenital dermal melanocytosis (Mongolian Spots) is commonly found in African, Asian, and Hispanic infants and presents as gray-blue macules , most commonly on the sacrum and buttocks .The spots usually fade spontaneously during childhood. CDM should be documented as these patches can be mistaken for bruises, potentially raising concern for coagulopathy or child abuse. \n\nVascular Lesions in Childhood dermal melanocytossis Melanocytic Nevus \n\n605 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCommon pigmented lesions in childhood \n\nCafe-au-la it spots Flat, hyperpigmented patches Associated with McCune-Albright syndrome or neurofibromatosis \n\n# -\n\nCon ge nital dermal melan ocy tos is Blue-gray patches More common in As ians & Africa n Americans Co ng enita l melan ocytic nev us Benign melanocyte proliferation \n\n t Density of hair follicles Dermatology Infantile Hemangioma Nevus sebaceous ; elevated lesion with surrounding alopecia nevus simplex \n\n606 https://t.me/usmleinnercircle \n\nCommon vascular lesions in childhood \n\nNevus flammeus (port-wine stain) Red to purple patches that do not r eg ress Respect midline Nev us simplex Blanching pink patches that fade with time Usually located on eyeli ds , glabella, and nape of neck Hemangioma Brighi red raised plaque Undergoes proliferation followed by involution Dermatology Propranolol acts by local vasoconstriction to limit further growth, promoting regression of the lesion. \n\n## Surgery \n\nNecrotising Fasciitis \n\n607 https://t.me/usmleinnercircle USMLE Inner Circle \n\nInfantile hemangioma \n\n## . Appears days to weeks after birth \n\nNatural history . Proliferation (age 0-6 months): growth of brig ht red , soft, raised plague . Involution (age >6 months): deep red/violet lesion that regresses in size . Clinical diagnosis \n\n## . Special considerations: \n\n0 .:5 cutaneous lesions --+ liver ultrasound \n\nEvaluation 0 Facial/segmental --+ echocardiography & MRI of the head (ie , PHAGE) \n\n0 Cervicofacial (beard distribution) --+ laryngoscopy \n\n0 Lumbosacral --+ spinal ultrasound . Observation for most lesions \n\n## . Beta-blocker therapy (eg , propranolol) for high-risk features: \n\nManagement 0 Large, facial, segmenta l, &/or rapidly growing (ulceration/scarring) \n\n0 Periorbital (visual impairment) \n\n0 Hepatic (high-output heart failure) \n\n0 Subglottic (airway obstruction) \n\nPHACE = posterior Iossa anomalies, hemangioma, arterial anomalies, cardiac anomalies, eye anomalies. Dermatology Vancomycin + Piperacillin-Tazobactum + Clindamycin \n\nSurgical Site Infection \n\n Necrotizing surgical site infections are usually poly -microbial .\n\nKey Points and Symptoms \n\n1. Pain, edema, erythema beyond surgical site 2. Systemic signs 3. Paresthesia at edges of wound \n\n608 https://t.me/usmleinnercircle \n\nFeatures of necrotizing fasciitis \n\n# . Streptococcus pyogenes (group A Streptococcus) \n\nMicrobiology . Staphylococcus aureus \n\n## . Clostridium perfringens \n\n# . Polymicr ob ial \n\n# . B ac teria spread r ap idly throu gh subcutaneous tissue & deep \n\nPathogenesis fascia, undermining the skin \n\n## . Mo st commo nly involves the extremities & per i nea ! region \n\n# . O ft en antecedent history of minor trauma \n\nClinical . Erythema of overlying sk in \n\nmanifestations . Swelling & edema \n\n# . Pain out of proportion to examination findings \n\n# . Systemic symptoms (eg, fever, hypotension) Treatment . Requires surgical debridement & broad-spectrum antibiotics \n\nRisk of surgical site in fec ti on \n\n# . Malnutrition/hypoalbuminemia, obes i ty \n\n# . Glucocorticoids, immunosuppressive drugs , chemotherapy , rad iation \n\n## . Smoking \n\nPatient factors . Un controlled diabetes , pe ripheral artery disease, venous ins ufficien cy \n\n# . Concurrent infection at anothe r site \n\n# . Advanced age \n\n## . E mergency surgery \n\nProcedural factors . Surgery fo r malignancy \n\n## . Open surgical approach \n\n# . Inadequate site preparation & antibi otic prophylaxis (as appropriate) \n\nPersonnel factors . Inadequate hand hygiene \n\n# . Inappropriate attire/gloving \n\nAntibiotics for 551 prevention Wound Pr oc edu re Typ ica lclassific at ion examples c on ta m inan ts Antibio tic pr op hylaxis \n\n1st -li ne : cefazolin \n\nClean Cardiac, neu rolo gical. ortho pedic Skin flora: Streptococcus, Staphylococcus Alternatives: vancomycin, vascular aureus & coagulase-negative staphy l ococc i clindamy ci n\n\nClean- Gastro intestinal, genitourinary, Sk in flora, gram -negative bacilli, enterococci Based on surgical site, contaminated ** gy neco logic/obstetric, h~ k, & endogenous flora of the viscus broader coverage often thoracic indicated \n\n---\n\n*Uninfected, uninflamed, the viscus is not entered .\n\n.. Viscus (~ . alimenta~ , 9enitourina~ . reseirato~ s~stems) is entered under con trolled conditions. SSI :: surgical site infection. Dermatology 4. Cloud-gray, purulent discharge (\" dishwater drainage \") 5. Subcutaneous gas or crepitus 6. Occur commonly in paients with diabetes and are usually polymicrobial \n\n7. Most important step is surgical exploration and debridement \n\n Surgical site infection is a relatively common complication of abdominal surgeries \n\nassociated with increased morbidity and mortality. Delayed primary closure is a wound management technique used for infected wound sites, such as those as a result of a traumatic injury or those with evidence of contamination. It involves leaving the wound open, often with \n\nnegative wound pressure therapy , to allow underling tissues to drain , which decreases the risk for surgical site infection. \n\nWound Dehiscence \n\nSuperficial wound dehiscence is a separation of the skin and subcutaneous tissue with an intact rectus fascia . It typically develops within the first postoperative week and occurs secondary to an abnormal subcutaneous fluid buildup ( eg, seroma ), resulting in a scant serosanguineous fluid drainage. T/t: Regular Dressing only Deep (fascial) wound dehiscence involves the rectus fascia (ie, nonintact) and results in exposure of the intraabdominal organs to the external environment. \n\n609 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\n0\n\n\n\n Tissue trauma Blood products Malignant hyperthermia Timeline of cause of postoperative fever Nosocomi al infections SSl'/catheter site infection Noninfectious (M l, PE, DVT) SSl 2/catheter site infection C/ostridioides \n\n(formerly C/ostridium) difficile \n\nD rug fever PE /D VT Viral infections SSI' \n\n0 6 hr 24 hr 1 wk >1 mo Immediate I Acute I Subacute I Delay ed SSI ' = Due to group A Streptococcus (GAS) or Clostridium perfringens \n\nSSI' = Due to other organisms (not GAS or C perfringens) \n\nSS I' = Due to indolent organisms \n\nDVT = deep venous th rombos is: Ml = myocard ial infarction : PE = pu lmonary embolism : SSI = surg ical si te infect ion .\n\n UWOl1d \n\nSuperficial dehiscence \n\nFasc ia (muscle aponeuroses) \n\nSkin------------:: ;....--:-.;; \n\nSubcutaneous tissue --Peritoneum --,---:,---:::--v':::al \n\nOmentum ----:---ii .. \n\nC>U World Dermatology T/t: Surgical Emergency \n\nUlcers \n\nDecubitus Ulcer \n\n A patient presents with a foot ulce. She had a stroke 3 months ago and now has residual hemiparesis .Current medical problems include hypertension, diabetes, hyperlipidemia, coronary artery disease, and dementia. What is the most likely cause of this patients ulcer? \n\nPressure (decubitus) ulcer \n\nWhile this patient is a vasculopath, they commonly present on the tips of the toes. \n\nApthous Ulcer Diabetic Ulcer \n\n610 https://t.me/usmleinnercircle \n\n> 0Aphthous ulcer\n\nDermatology Sensory neuropathy exposes the tissues to increased trauma (eg, friction from shoes due to decreased pain sensation) and pressure (eg, stomping feet due to decreased proprioception), and causes unawareness of tissue injury that can delay treatment. \n\nAutonomic neuropathy causes loss of autonomic tone in the arteriolar and capillary circulation, leading to shunting of blood from the arterioles to the veins and decreased tissue perfusion .\n\nMotor neuropathy can cause atrophy of the small intrinsic muscles of the feet, leading to unopposed action of the large lower leg muscles, and clawing of the toes with hyperextension at the metatarsal-phalangeal joints. As a result, pressure is redistributed to the metatarsal heads, increasing susceptibility to callus formation, skin breakdown, and ulcer formation .\n\n Dont forget to check for Osteomyelitis in Diabetic Ulcers by Imaging or Biopsy if you suspect it \n\n611 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDiabetic plantar ulcer CNS, Eye, Ear \n\n# CNS, Eye, Ear Physiology Speech Idiopathic Intracranial Hypertension Headache Raised ICP Thunderclap Headache Seizures Focal Seizure Absence Seizure Status Epilepticus Mental Examination GCS Movement Disorders Post Hypoxic Myoclonus Gait Disorders Stroke Cerebellar Hemorrhage Ischemic Stroke Subdural Hematoma Subarachnoid Lacunar Malignant Hemispheric Infarction Spinal Cord Compression Central Cord Syndrome Anterior Cord Syndrome Cauda Equina & Conus Medullaris UMN ALS Autonomic Dysreflexia Demyelinating Disorders Multiple Sclerosis Transverse Myelitis Neuromyelitis Optica GBS Miller Fisher Syndrome CIDP Neurodegenerative disease Dementia Parkinsons Multiple System Atrophy Progressive Supranuclear Palsy Alzheimer Disease FrontoTemporal Dementia Vascular Dementia \n\n612 https://t.me/usmleinnercircle CNS, Eye, Ear CJ Disease Adrenoleukodystrophy Alcohol Cerebellar Degeneration HIV Neurocognitive Dysfunction CNS Tumours Metastatic Brain Lesions Meningioma Schwannoma Choroid Plexus papilloma Neurocutaneous Disorders NF Tuberous Sclerosis VHL Sturge Weber Infection Meningitis Brain Abscess Spinal Epidural Abscess Brain Herniation Miscellaneous Ageing Tick Paralysis Skull Fracture CSF Rhinorrhea Venous Sinus Thrombosis Cavernous Sinus Syndrome Distal Symmetric Polyneuropathy Concussion Traumatic Brain Injury Paroxysmal Sympathetic Activity Coma Ventriculoperitoneal Shunt Diffuse Axonal Injury Facial Palsy Thermoregulation Failure CNS Drugs Anti-Epileptic Anesthesia Epidural Malignant Hyperthermia NeuroMuscular Blockers Paeds Spina Bifida Head Trauma Hydrocephalous Microcephaly Macrocephaly Cephalohematoma Stroke Hemiplegia Intraventricular Hemorrhage Paeds Seizures 613 https://t.me/usmleinnercircle USMLE Inner Circle CNS, Eye, Ear Physiology Infantile Spasms (West Syndrome) Lennox Gastaut Syndrome Febrile Seizures Cerebral Palsy EYE Ambylopia Glaucoma Closed Angle Corneal Abrasion Optic Nerve Injury Open Globe Injury Sympathetic Ophthalmia Orbital Compartmental Syndrome Hyphema Strabismus Retinoblastoma Photokeratitis Retinal Artery Occlusion Retinal Vein Occlusion Retinitis Pigmentosa Diabetic Retinopathy Infection Orbital Cellulitis Conjuctivitis Retinitis Endopthalmitis Keratitis Dacryocystitis Hordeolum/ Stye Blepharitis Uveitis Dacryostenosis Eye Drugs EAR Infection Otitis externa Malignant Otitis Externa Otitis Media Otitis Media with Effusion Chronic Suppurative Otitis Media Cholesteatoma Eustachian Tube Dysfunction Barotrauma Hearing Loss Vertigo Perilymphatic fistula Vestibulopathy Otosclerosis of Ear Auricular Hematoma \n\n614 https://t.me/usmleinnercircle CNS, Eye, Ear Speech Idiopathic Intracranial Hypertension \n\n What is a worrisome sequelae of pseudotumor cerebri if left untreated? \n\nBlindness \n\n Treatment for refractory pseudotumor cerebri may involve optic nerve sheath fenestration surgery or lumboperitoneal shunting. \n\nshort-term use of corticosteroids or serial lumbar puncture can serve as bridging therapy while awaiting surgical treatment > 200 mm H2O in a non-obese patient or > 250 mm H2O in an obese patient \n\n615 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCommon types of aphasia \n\nArcuate fasciculus Aphasia Spontaneous Comprehension Repetition Associated features syndrome speech Broca Sparse & Relatively Impaired Right hemiparesis nonfluent preserved (face & upper limb) Fluent & Greatly Right superior visual Wernicke voluminous but Impaired lacks meaning diminished field defect Conduction Fluent with Relatively phonemic errors preserved Very poor None \n\nIdiopathic intracranial hypertension \n\n Women of childbearing age \n\nRisk factors . Recent weight gain/obesity \n\n## . Medications (eg, retinoids/vitamin A, tetracyclines, growth hormone) \n\nPathophysiology . Impaired CSF resorption & intracranial venous hypertension \n\n## . Headache /nausea/vomiting \n\nClinical Visual changes (transient obscurations; vision loss; diplopia due to abducens nerve (CN VI] palsy) \n\nfeatures . Pulsatile tinnitus \n\n## . Retrobulbar pa in/n eck pa in/b ack pai n \n\n## . Papilledema & enlarged blind spots \n\n## . MRI to rule out mass lesions/hydrocephalus \n\nDiagnosis MR venography to rule out v enous thrombosis .. Lumbar puncture: elevated opening pressure \n\nTreatment Weight loss, including bariatric surgery \n\n Carbonic anhydrase inhibitor (acetazolamide, t opiramate )\n\nCSF = cerebrospinal fluid. CNS, Eye, Ear Headache \n\n Although overuse of any type of acute headache medication can lead to MOH , butalbital-containing products, acetaminophen , and opioids are the most commonly implicated drugs. \n\n616 https://t.me/usmleinnercircle \n\nEvaluation of suspected idiopathic intracranial hypertension Management of idiopathic intracranial hypertension \n\nHeadache + vision changes ]\n\nClinical assessment Headache quality (eg, positional) Weight c ha nges/~ !\n\n Neurolo9ic examination Suspected t ICP 1\n\nVisua l assessment Visual acuity \n\n-~ Fundusco py Papilledema 1\n\nEvaluate for mass lesions Urgent imagi ng (eg, CT/MRI) Consider venography (if concern fo rCVST )Negative imaging 1\n\nLumbar puncture Opening pressure >250 mm H201 No signs of infection Li kely idiopathic intracranial hypertensi on \n\nVision threatened J.-\n\nAcetazolam ide +\n\nconsider repeat LP or temporizing lumbar drain Surgery (eg, CSF shunt, optic nerve fenestration) We ight reduction counseling Evaluation of visual function: \n\n Visua l acu ity Visua l field testing \n\nNo immediate threat to vision Symptom burden: \n\n Headaches Dip lopia Ti nni tus Debilitating and/or progressive symptoms Tolerab le and stable symptoms \n\nAcetazolamide \n\n Surgery (eg, CSF shunt) Close follow-up : \n\n S ymptoms Visua l funct i on Continue weight reduction CSF =cerebrospinal Huid ; LP =lum ba r puncture. \\!:)UWorld \n\nCVST = cerebral venous si nus thrombosis ; ICP = i nt racran ial pr essure . e>uworld \n\nTypes of headache Migraine Cluster Tension Sex Female> male Male > female Female> male \n\npredilection Family Often present No No \n\nhistory Onset Variable During sleep Under stress \n\nLocation Often unilateral Behind one eye Band-like pattern around the head (bilateral) \n\nCharacter Pulsatile & throbbing Excruciating , sharp & steady Dull , tight & persistent \n\nDuration 4-72 hours 15-90 minutes 30 minutes to 7 days \n\nAssociated Auras , photophobia, Sweating , facial flushing , nasal congestion , Muscle tenderness in the head, \n\nsymptoms phonophobia & nausea lacrimation & pupillary changes neck, or shoulders \n\nCharacteristics of chronic headache Headache subtype Clinical presentation \n\n## . Female predominance \n\nMigraine . Un il ateral, throbbing \n\n## . Nausea/vomiting, photophobia \n\nTension-type . Gradual onset , bilateral pressure \n\n## . Mild to moderate without pericranial muscle tenderness \n\n## . Male predominance \n\n## . Un il ateral, trigeminal distribution with ipsilateral autonomic \n\nCluster symptoms \n\n## . Duration 15 min to 3 hr , circadian periodicity \n\n## . Improves with oxygen therapy \n\nMedication . Develops or worsens with daily medication use \n\noveruse . Similar pattern to chronic migraine or tension-type headache CNS, Eye, Ear Management involves cessation of the culprit drug with consideration of concomitant initiation of preventive therapy. The dx is made when patient experience headache atleast every other day and take pain medicine atleast every other day. Aura may include visual (eg, wavy lines, visual loss), sensory (eg, paresthesia, numbness), auditory \n\n(eg, sounds, hearing loss), and motor (eg, tremors, weakness) dysfunction. Women with migraine, particularly those associated with aura, are at increased risk of ischemic stroke \n\n Migraine aura is thought to involve sequential depolarisation of cortical neurons starting with the \n\noccipital cortex \n\n What is the likely diagnosis in an adolescent that presents with recurrent episodes of bifrontal headache accompanied by nausea and photophobia ?\n\nMigraine B Blockers preferred in pregnancy with lowest possible dose for prevention \n\n617 https://t.me/usmleinnercircle USMLE Inner Circle \n\nMigraine in children Epidemiology . Equal incidence in boys & girls until puberty \n\n## . j Risk in adolescent girls \n\n## . Pulsatile/throbbing headache lasting hours to days \n\n## . Bilateral* or unilateral \n\n. Associated symptoms \n\nClinical features 0 Photophobia & phonophobia \n\n0 Nausea/vomiting \n\n0 Autonomic symptoms* (eg , facial sweating, tearing, nasal congestion ) \n\n## . Preceding aura (eg, scintillating scotoma) \n\n. Normal ne urologic examination \n\n## . Acetaminophen , nonsteroidal anti-inflammatory drugs \n\nAbortive treatment . Triptans \n\n## . Antiemetics (eg, promethazine , prochlorperazine) \n\n## . Ergots (eg , dihydroergotamine) \n\n Not typ ica l of adult migr ai nes .\n\nManagement of migraines in pregnancy \n\nNonpharmacolog ic therapy: rest, hydrati on , heat \n\n## !Acetami nophen \n\n## !*An tiemetics ( eg , promethazine), codeine, caffei ne /butalbi tal **Nonsteroidal anti-inflammatory drugs ( eg , naproxen) Opioids ( eg , oxycodone) \n\nean be used m COflunctton wi th acetarrnnophen .\n\n-:2nd trimester only \n\nCUWorld \n\nMigraine therapies \n\n Triptans (eg , sumatriptan) NSAIDs (eg, naproxen) \n\nAbortives Acetaminophen Antiemetics (eg , metoclopramide, prochlorperazine) Ergots (eg, dihydroergotamine) Topiramate \n\nPreventives Divalproex sodium Tricyclic antidepressants Beta blockers (eg , propranolol) CNS, Eye, Ear migraines in children are often bifrontal and of shorter duration; first-line treatment in children includes acetaminophen or NSAIDs (triptans may be used as a second-line treatment) \n\n Coadministration of a triptan and an ergot derivative or an additional triptan after a first dose may result in prolonged vasospasm due to overactivation of serotonin receptors ,which can lead to severe elevations in blood pressure, myocardial infarction, or stroke. What is the next step in management for a patient that presents with bifrontal headaches upon \n\nawakening with associated nausea , vomiting , and blurry vision for the past month? \n\nMRI of the brain \n\nwarning signs that warrant early imaging include: \n\n Do tension headaches cause throbbing or constant pain? \n\nConstant/steady pain \n\nimportant distinguishing feature from migraines \n\nRaised ICP \n\n Symptoms of increased intracranial pressure include headache that is worse in the morning , nausea /vomiting , and mental status changes. \n\nthe headache classically worsens throughout the night (while lying supine), waking the patient up in his/her sleep \n\n Manoeuvres that increase intracranial pressure include leaning forward , Valsalva , and coughing .\n\nLook for patient with headache that gets worse when they lean forward (important D/D here is Sinusitis which they will try to trick you with so be careful!) \n\n Signs of Raised ICP: 1. Headache : Worse in morning, straining, bending forward 2. Transient Bilateral Vision Loss : Varies acc to Head position 3. Enlarged Physiologic Blind Spot \n\n Cushing triad is a poor prognostic sign of raised ICP and often indicates cerebral herniation is imminent. \n\n618 https://t.me/usmleinnercircle \n\n> Neurologic findings : Seizure, changes in consciousness, specific deficits Differences compared to prior headaches: Change in frequency, intensity, characteristics Other: New at age >40 , sudden onset, trauma , present on awakening\n\nCNS, Eye, Ear Fastest/Quickest way to decrease ICP --> HYPERVENTILATE patient \n\nThunderclap Headache \n\nSeizures \n\n What is the next best choice in management of choice in a patient that presents to the ED after an unprovoked first seizure who fell on the sidewalk? CBC, electrolytes, cervical spine imaging, and urine toxicology are all normal .\n\n619 https://t.me/usmleinnercircle USMLE Inner Circle \n\nInterventions to reduce intracranial pressure \n\n! Brain parenchymal . Osmotic therapy (eg, hypertonic saline, mannitol) to extract water \n\nvolume \n\nj Cerebral blood . Head elevation to j venous outflow \n\nvolume . Sedation to ! metabolic demand \n\n## . Hyperventilation to ! PaC0 2, resulting in vasoconstriction \n\nj CSF volume . CSF removal (eg, external ventricular drain) \n\ni Cranial volume . Decompressive craniectomy \n\nCSF = cerebrospinal fluid. \n\nThunderclap headache \n\n# . Sudden (maximum intensity <1 hr), severe headache \n\nClinical features Seizure neurologic deficits mental status abnormality \n\n# . Nausea/vomiting Most common: \n\n# . Subarachnoid hemorrhage: hypertension , neck stiffness \n\n# . RCVS: recurrent episodes over days to weeks Less common: \n\nEtiology . Pituitary apoplexy: ophthalmoplegia , visual field defects, adrenal insufficiency \n\n# . Cervical artery dissection : posterior headache, neck pain \n\n# . Cavernous sinus thrombosis: slower onset, proptosis, fever (if septic) \n\n# . Meningitis: slower onset, fever, neck pain & stiffness \n\n# . PRES: subacute headache, hypertensive crisis \n\n# . Immediate noncontrast CT scan of the head \n\nEvaluation . Lumbar puncture \n\n# . Expedited MRI of the head \n\nPRES = posterior reversible encephalopathy sy ndrom e; RCVS = reve rsib le ce rebral vasoconstriction sy ndrom e. \n\nPrognosis \n\n Mortality of ~ 20% (in adults with first occurrence of GCSE) \n\n## IStatus epilepticus is a life-threatening event! If not interrupted, it can lead to cerebral \n\n~ .e. rn _a. , a dangerous rise in body temperatur e, rhabdomyol ~~ i5. , and cerebral cardiovascular failure! \n\nGeneral complications of seizures and epilepsy \n\n Acute \n\n Hyperthermia, cardiorespiratory deficits, excitatory toxicity ~ potentially irreversible tissue damage (particularly to the CN~ , for example in the form of c: ort(cal !arnin,i_r \n\nnecrosis), which in turn may also result in further seizures Postictal tran sient anion gap metabolic acidosis with in creased lactic acid and \n\n;~ d ~~~d serum bic ;; b ~~ ; t; j:: ~~~ ~j jy -; ; ; ; l~ es spontaneously within 60-90 \n\nminutes after seizure activity stops Physical trauma (e.g., posterior disloc_ '!tion of the glenohumeral joint) \n\n Long-term Associated psychiatric disorders (e .g. , anxi ety, depression and risk of :'~i c: i_ ~': ,\n\ncognitive impairments) Psychosocial issues (e .g ., problems at the workplace) CNS, Eye, Ear CT head without contrast \n\nmust rule out acute neurologic problems (e.g. bleed); MRI is more sensitive for identifying structural causes of epilepsy and the imaging modality of choice in elective situations. Rule out structural brain lesions before EEG \n\nObviously, don't pick CT head with fuckin' contrast . That shit takes time and this patient fell, possibly hitting his head. \n\n What is the likely diagnosis in a patient with an adducted and internally rotated shoulder following an eclamptic seizure? \n\nPosterior shoulder dislocation \n\ntypically occurs with violent muscle contractions (e.g. seizure, electrocution) \n\n Generalized seizures may be differentiated from syncopal episodes by the presence of a post-ictal state. \n\n Discontinue anti-epileptic medications in someone with a history of unprovoked seizures if \n\nSeizure free for 2 years. \n\nFocal Seizure \n\n620 https://t.me/usmleinnercircle \n\nExclude an underlying condition \n\n> ECG: In every patient with loss of consciousness during an ictal event, cardiogenic causes (e .g ., cardiac arrhythmias resulting in cerebral hypoxia) should be ruled out .\n> CT /MRI (with and without contrast): structural lesions (e .g ., brain tumors) should be ruled out after a first seizure .\n\ni;:::l \n\n> Laboratory tests\n> Blood\n> Glucose Electrolytes\n> Prolactin\n\ni;:::l \n\n> Antiepileptic drug levels\n\ni;:::l \n\n> Toxicology screen\n> CBC ESR Rapid plasma reagin\n\ni;:::l \n\n> Creatine kinase\n\ni;:::l \n\n> Renal and liver function tests\n> Lumbar puncture : cerebrospinal fluid analysis (e .g ., if CNS infection is suspected)\n\n# I \n\n> The first focal seizure or the first focal seizure evolving into a generalized seizure in adults indicates a seizure of structural or metabolic origin and requires further evaluation!\n\nCNS, Eye, Ear Absence Seizure \n\n Absence seizures may be differentiated from inattentive staring spells by the presence of automatisms .\n\ne.g. lip smacking, eyelid fluttering \n\nStatus Epilepticus Absence seizures NOT associated with a post-ictal period \n\n621 https://t.me/usmleinnercircle USMLE Inner Circle \n\nFocal seizure Definition Originates from 1 cerebral hemisphere +/- Loss of consciousness Motor : Jacksonian march, turning of eyes/head/trunk \n\nTypes Sensory: Paresthesias, vertigo, visual phenomena Autonomic: Sweating, epigastric \"rising\" sensation Psychic: \"Deja vu,\" affective changes (eg, fear) \n\nAbsence seizures \n\n## . Sudden impairment of consciousness (staring spells) \n\n## . Preserved muscle tone \n\nClinical features . Unresponsive to tactile/verbal stimulation \n\n## . Short duration (<20 sec) \n\n## . Simple automatisms frequently present \n\n## . Easily provoked by hyperventilation \n\nDiagnosis . EEG: 3-Hz spike-wave discharges during episodes \n\nTreatment . Ethosuximide \n\nEEG = e le ctroencephalograp hy. \n\nClinical features of absence seizures & inattentive staring spells Absence seizures Inattentive staring spells \n\n Occurrence during all activities Occurrence primarily during Length <20 seconds \"boring\" activities Lack of response to vocal or Variable length, often >1 minute tactile stimulation Response to vocal or tactile Presence of automatisms stimulation Lack of automatisms CNS, Eye, Ear Status epilepticus is seizure activity for > 5 minutes (time), continuous or intermittent, without regaining consciousness. \n\ncan result in brain injury, recurrent seizures and possibly death \n\n A brain that has seized for >5 minutes (status epilepticus) is at increased risk for cortical laminar necrosis due to excitatory toxicity; appears as cortical hyperintensity on diffusion-weighted imaging. \n\nWhat is the treatment of status epilepticus ?\n\nBenzos and more benzos (Lorazepam): For seizure termination Anti-epileptics (e.g Phenytoin : to prevent recurrence. Failure Fosphenytoin Phenobarbital General Anesthesia \n\nFollowing drug therapy, patients with GCSE typically regain responsiveness in 10-20 minutes .Persistent unresponsive state , may be due to either: Sedation due to persistent effects of benzodiazepines or \n\nongoing seizure activity without physical manifestations (ie, nonconvulsive status epilepticus). Therefore, to differentiate between these 2 states, electroencephalography should be performed \n\nMental Examination \n\n622 https://t.me/usmleinnercircle \n\nGeneralized convulsive status epilepticus \n\n# . Nonadherence to AEDs \n\n# . Structural brain abnormalities (eg, brain tumor) \n\n> Risk factors\n\n# . Metabolic abnormalities \n\n# . Infection \n\n# . Drug withdrawal \n\n# . ~5 minutes of generalized convulsive seizure Diagnosis OR \n\n# . ;;?:2 generalized convulsive seizures without interval recovery of consciousness \n\n# . Stabilize circulation, airway & breathing \n\n# . Benzodiazepines (repeat administration until termination of seizure activity) \n\n> Treatment\n\n# . Begin antiepileptic drugs \n\n# . EEG monitoring for refractory status epilepticus or failure to regain consciousness AEDs = antiepileptic drugs ; EEG = electroencephalography. CNS, Eye, Ear What does an abnormal Reitan trail test (timed connect-the-numbers test) indicate? \n\nAltered mental status \n\nuseful for detecting subtle mental status changes \n\nGCS Movement Disorders \n\n623 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCauses of altered mental status \n\n# . Prescription drugs (eg, opioids, lithium, antipsychotics) \n\nDrugs/toxins Drugs of abuse (eg, ethanol, hallucinogens) \n\n Drug withdrawal (eg , ethanol , benzodiazepines) \n\n# . Sepsis, systemic infections \n\nInfections \n\n Meningitis, encephalitis, brain/epidural abscess \n\n# . Electrolyte disturbances \n\n# . Hypo-/hyperglycemia \n\n Endocrine (eg, hypo/hyperthyroid , pituitary, adrenal) \n\nMetabolic \n\n Hypoxemia, hypercarbia \n\n# . Nutritional (eg, thiamine, vitamin B 12 deficiency) \n\n Hepatic or renal failure \n\n Seizure, head injury \n\nCentral nervous system . Hypertensive encephalopathy \n\n Psychiatric disorders \n\nGlasgow Coma Scale \n\n4 - Spontaneous (open with blinking at baseline) 3 - To speech \n\n(E)ye opening 2 - To pain o nl y\n\n(Maximu m; 4) 1-None (C - Not assessable [eg , trauma , edema]) 5-0riented 4 - Confused (converses but confused, disoriented) \n\n(V)erbal response 3 - Inappropriate (i nappropriate words) (Maximum ; 5) 2 - Incomprehensible (sounds, no words) 1-None (T - Not assessable [intubated]) \n\n6 - Obeys commands for mo vement 5 - Loca lizes to pain (M)otor response 4 - Withdraws from pain \n\n(Maximum ; 6) 3 - Flex ion in respo nse to pain (decortica te posturing) 2 - Extensio n in response to pain (decerebra te posturing) \n\n1-None \n\n. Use best response for each category (range= 3-15). \n\n. Coma : Does not open eyes , does not follow commands , and does not utter understandable words ; Glasgow Coma Score (GCS) 3-8 .\n\n. Head injury classification : Mild , GCS 13-15; moderate, GCS 9-12; severe , GCS sa .CNS, Eye, Ear Functional (psychogenic) tremors often present abruptly with significant disability. They often decrease with distraction , have changeable or inconsistent features , and are not consistent with known tremor syndromes. \n\n624 https://t.me/usmleinnercircle \n\nMovement disorders \n\nDISORDER \n\nAkathisia Asterixis Athetosis Chorea Dystonia Essential tremor Intention tremor Rest ing tremor \n\nPRESENTATION \n\nR es tl ess n ess and in tense urge \n\n~\n\n-;: x t c11.sio11 o Grr ists causes \n\nuflappin g\" motion \n\nCHARACTERISTIC LESION \n\nSl ow, s~ e, wri l hi n Bas;1l ga 1 li a\n\n~ ; e :-. pcc1a ly seen i11 \n\nthe fin gers \n\nSudden, ~ purposeless Basa g,mg li a\n\nmoveme nt s\n\nSustained invo lu ntary muscle contractions when ~11ni o us \n\nSl ow, zig za g motion when pointing /ex tending toward a \n\nlargcl-\n\nU1 1co 11trollc( 111m c 111 cut of dista l a [> pcnda g c, (most noticeable in hand s); !:rs!.ll,l r\n\nallevj at ed bf i11t e 11ti o11al \n\n> lll0\\ 'C ll1 CJ-1\n\nCcrcbc ll F Weakness with spasticity Scissoring\n\n(myelopathy) Toes scrape the floor \n\n> Myopathic\n\n Waddling (myopathies, MG) Abnormal pelvic tilt (limb girdle weakness) \n\n> Magnetic Difficulty initiating steps\n\n(NPH) \n\n> Vestibular\n> (BPPV, Meniere disease)\n\n Stumbling or veering to one side (usually the affected side) \n\n> Cerebellar ataxia\n\n Wide based (stroke, drug toxicity, Stumbling, lurching alcohol, hereditary) May be one sided or bilateral depending on etiology \n\n> Sensory ataxia\n\n Wide based (sensory neuropathy, High stepping/stamping vitamin B 12 defi cie ncy) Wor se in the dark \n\n> BPPV\n\n=benign positional paroxysmal vertigo; DLB =dementia w ith Lewy bodies; MG =myasthenia gravis; MSA =multiple system atrophy; NPH =normal pressure hydrocephalus; PD =Parkinson disease; VD =vascular dementia. CNS, Eye, Ear A \" steppage gait \" secondary to foot drop is often caused by L5 radiculopathy and common peroneal neuropathy. \n\nboth pathologies result in weakness with dorsiflexion ;L5 radiculopathy also causes weak foot inversion and plantar flexion, as well as back pain radiating to the foot \n\n## Stroke \n\n What is the greatest risk factor for both ischemic and hemorrhagic stroke ?\n\nHypertension ( 4x risk of CVA compared to normotensive individuals )\n\nelevated shearing force on intracerebral vascular endothelium accelerates the atherosclerotic process other significant but less potent risk factors are hypercholesterolemia, DM, smoking, sedentary lifestyle. \n\n627 https://t.me/usmleinnercircle USMLE Inner Circle \n\nGait disorders Type of gait Description Associated signs Causes \n\n. Cerebellar degeneration Stroke \n\nCerebellar Ataxic: Staggering , wide-based Dysdiadochokinesia, dysmetria , Drug/alcohol .nystagmus, Romberg sign intoxication Vitamin B12 deficiency \n\n. Frontal lobe \n\nGait apraxia Magnetic (freezing): Dementia , incontinence, frontal lobe degeneration \n\n(frontal gait) Start & turn hesitation signs . Normal pressure hydrocephalus Bradykinesia, resting tremor, postural . Parkinson \n\nParkinsonian Short steps, shuffling instability, decreased arm swing disease \n\nFootdrop, excessive hip & knee flexion . Motor \n\nSteppage while walking , slapping quality, falls Distal sensory loss & weakness neuropathy Acute \n\nVestibular Unsteady, falling to one side Normal sensation , reflexes & motor labyrinthitis strength ; nausea, vertigo . Meniere disease \n\nModifiable risk factors for TIA & ischemic stroke Risk factor Estimated attributable risk \n\nHypertension 4x \n\nSmoking 2.5x \n\nDiabetes mellitus 2x \n\nHypercholesterolemia s2x \n\nAlcohol intake Variable/inconsistent effect Sedentary lifestyle, obesity Small effect \n\nTIA = transient ischemic attack. CNS, Eye, Ear MCA most commonly involved in Thromboembolic stroke \n\n628 https://t.me/usmleinnercircle \n\nStroke type lschemic (thrombotic) lschemic (embolic) \n\nlntracerebral hemorrhage Spontaneous subarachnoid hemorrhage \n\nlschemic stroke Clinical characteristics of major stroke subtypes Atherosclerotic risk factors (eg, uncontrolled hypertension, diabetes), history of transient ischemic attack Local in-situ obstruction of an artery Symptoms often fluctuate - stuttering progression with periods of improvement History of cardiac disease (eg, atrial fibrillation, endocarditis) or carotid atherosclerosis ( bruit )Onset of symptoms is abrupt & usually maximal at the start \n\nMultiple infarcts within different vascular territories History of uncontrolled hypertension, coagulopathy, i ll icit drug use (eg, amphetamines, cocaine) Symptoms progress over minutes to hours Focal neurologic symptoms appear early, followed by features of increased intracranial pressure (eg, vomiting & headache, bradycardia, reduced alertness) Rupture of an arterial saccular (\"berry\") aneurysm or from an arteriovenous malformation Severe headache at onset of neurologic symptoms Meningeal irritation (eg, neck stiffness) Focal deficits uncommon \n\nInitial management of stroke \n\nAcute stroke symptoms J\n\ni\n\nAssessment of ABCs Noncontrast CT scan of the head Laboratory studi es Hemorrhagic stroke Perm issive hypertension Possible systemic thrombolytics, endovascular thrombectomy BP control : goal systolic \n\n140-160 mm Hg Reverse anticoagulation Maintain normal ICP \n\nBP \" blood pressure; ICP \" lntracranlal pressure. \n\nClassical time course of strokes by etiology \n\n> C:\n> 0\n\niu. \n\n> CUWot ld\n> Embolic Maximum symptoms at onset Thrombotic Fluctuating symptoms Time Hemorrhagic\n\nworsening \n\n> symptoms\n> UW0< ld\n\nCNS, Eye, Ear Which lobes are most commonly involved in a spontaneous lobar hemorrhage secondary to cerebral amyloid angiopathy ?\n\nParietal and Occipital \n\noccurs due to beta-amyloid deposition in the walls of small- to medium-size cerebral arteries \n\n Carotid endarterectomy should be considered for symptomatic patients (e.g. TIA, stroke) with carotid stenosis between 70 - 99 % to reduce future stroke risk. \n\npatients with disabling neurologic deficits , 100% occlusion of the carotid artery , or life expectancy < 5 years are unlikely to benefit \n\nCerebellar Hemorrhage \n\n629 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSite-spec ifi c findings in in tracrani al hemorrhage Brain lesions & clinical presentations Site Neurologic fi nd i ng s Lesion C li nical presentation \n\n## . Contralateral hemiparesis & hemisensory loss Posterior limb of . Unilateral motor impairment \n\nBasal gangl ia . Homonymous hemianopsia internal capsule . No sensory or cortical deficits \n\n## . Gaze palsy (lacunar infarct) . No visual field abnormalities \n\n## . Usually no hemiparesis \n\nCerebellum . Facial weakness \n\n## . Ataxia & nystagmus . Occipital headache & neck stiffness \n\n# . Contralateral somatosensory & motor deficit (face , arm & leg) Midd le cerebral . Conjugate eye deviation toward side of infarct artery occlusion . Homonymous hemianopia \n\n## . Contralateral hemiparesis & hemisensory loss Aphasia (dominant hemisphere) \n\nThalamus . Nonreactive miotic pupils \n\n## . Upgaze palsy \n\n# . Hemineglect (nondominant hemisphere) \n\n## . Eyes deviate toward hemiparesis (l'o.!f'\\ . Contralateral somatosensory & motor deficit, . Contralateral hemiparesis (frontal lobe) \n\n## . Contralater al hemisensory loss (parietal lobe) \n\nCerebral lobe . Homonymous hemianopsia (occipital lobe) \n\n## . Eyes deviate away from hemiparesis (_fff) \n\nAnterior cerebral predominantly in lower extremity artery occlusion Abulia (lack of will or initiation) \n\n# . Dyspraxia , emotional disturbances, urinary incontinence . High incidence of seizures \n\nPons . Deep coma & total paralysis with in minutes \n\n## . Pinpoint reactive pupils Vertebrobasilar Alternate syndromes with contralateral system lesion hemiplegia & ipsi lateral cranial nerve involvement (supplying the brain . Possible ataxia stem) \n\nPatterns of intracranial hemorrhage by location Lob ar hemorrhage due to amyloid angiopathy \n\n# . Loba r: C AA (less common : AVM, tumor) \n\nlntraparenchymal hemorrhage . Basal ganglia, pons, thalamus: hypertension \n\n## . A ne urysm (80% of SA H) \n\nSubarachnoid hemorrhage . Trauma . AVM \n\nAVM =arteriovenous malformation; CAA= cerebral amyloid angiopathy; SAH =subarachnoid hemorrhage. CNS, Eye, Ear Ischemic Stroke a type of Intracerebral hemorrhage \n\n630 https://t.me/usmleinnercircle \n\nCerebellar hemorrhage \n\n# . H ypertension \n\nRisk factors Antithrombotic therapy (eg, warfarin, aspirin) \n\n# . Cerebral amyloid angiopathy \n\n# . Heada che, nausea , vomiting \n\nManifestations . lpsilateral ataxia, dysarthri a, vertigo , nystagmus \n\n# . Cranial neuropathies \n\n# . Reversal of anticoagulation \n\n# . Blood pressure managemen t\n\n# . ICP management (eg , head of bed elevation, manni to l) \n\nManagement . Surgical decompression indicated with: \n\n> 0\n\nHemorrhage >3 cm \n\n> 0\n\nN eurologic deterioratio n (eg, impaired conscious ness ) \n\n> 0\n\nBrainstem compression , obstructive hydrocephalus \n\nICP = intracranial pressure. \n\nClassic features of ischemic stroke subtypes Risk factors Time course Location Thrombotic Hypertension Stutter ing progression . Large cerebral vessels (due to plaque rupture) . . . Small perforating vessels (due to lipohyalinosis) \n\nEmbolic . Cardiac disease (eg , at ri al Symptoms maximal at onset . Multiple different vascular territories fibrillation, PFO) . (sy nchronous or metachronous) \n\nBorder Areas supp li ed by distal-most branches of . Systemic hypoperfusion (eg , . Delayed recognition due to cerebral arteries zone cardiac arrest, shock) critical illness Areas with high metabolic demand (eg ,(watershed) hi ppocampus) \n\nPFO = pa tent foram en ov al e. Initial management of ischemic stroke \n\nSymptoms & no ncontrast CT sca n of the head consistent with ischemic stroke ITime since symptom onset i~ ~4 .5 hr-24 hr ] ~\n\nAdminister thrombol ys is I INot eligible for (eg, tPA ) if eligible _ _ thrombolysis \n\n~~ ! ~\n\nObtain CTA of head & neck j\n\nLVO present LVO absent Not eligible for thrombolysis Mechanical thrombectomy Standard postischemic stroke management (eg , antiplatelet therapy, investigate for em bol ic source) \n\ner since las t observed at neuro!ogic basel ine .CTA = CT angiography ; LVO = lar ge vessel occlusion ; IPA = tissue plasminoge n activator . C)UWorld CNS, Eye, Ear Patients with suspected cerebellar stroke (vertigo, gait disturbance) are treated with \n\nthrombolysis even in the absence of classic stroke symptoms (eg, weakness, aphasia). What is the next step in management for a patient that develops a cardioembolic stroke secondary to bacterial endocarditis ?\n\nIV antibiotics and observation \n\nsurgery is indicated if patient develops CHF or r ecurrent infection/embolism \n\nDraw blood cultures before antibiotics! \n\nSubdural Hematoma \n\n631 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCriteria for thrombolytics in stroke Antiplatelet/antithrombotic therapy for ischem ic stroke lschernic stroke with measurable neurodeficils Inclusion criteria Symptom onset <3-4.5 ho ur s before treatment initiation Clini cal presentation Therapy Hemorr hage or mul ti lobar infarct involving >33% of cerebra l hemisphere on CT scan Stroke/head trauma in past 3 months Presen ta tion within 3.5-4 hours of Intraven ous alteplase symptom onset & no co ntr ai ndications \n\n History of intracrani al hemorrhage, neoplasm, or vascular malformation Strict exclusion Recent int racranial/spinal surgery Stroke with no prior antiplatelet therapy Aspirin criteria Active bleeding or arterial puncture in past 7 days at noncompressible site BP >185/110 mm Hg Stroke on aspirin therapy Aspirin + dipyrid amo le OR dopidogre l Platelets <100,000/mm3 or glucose <50 mg/dL Anticoagulan t use with IN R > 1. 7, PT >15 sec, or i aPTT Stroke on aspirin therapy & patient with Aspirin + clopidogrel intracranial large artery atherosclerosis Mi nor or rapidly improving neurodeficits Major surgery/trauma in the past 14 days Stroke with evidence of atrial fibrillation Long-term anticoag ulation (eg , warfarin , dab igatran, rivaroxaban) Relativ e Ml in the past 3 months exclusion criteria GU or GI bleeding in the past 21 days Seizure at stroke onset Pregnancy lschemic stroke Interventi on Blood pressure target Thrombolytics . Prjor to admjnjstratjon : lower BP to <185/ 110 mm Hg \n\nadministered . Afli:r ;ag ministr ;at i2 n: maintain BP < 180/105 mm Hg for 24 hr \n\nThrombolytlcs no t . Allow penmissive hypertension \n\nindicated* . Lower extreme h~2 ertensi on (SBP >220 mm Hg or DBP >120 mm Hg ) by 15% in first 24 hr \n\nit >4.5 hr si nce symp tom onset or contraindication present. \n\nBP = blood pressure ; DBP = di astolic bl ood pr ess ure ; SBP = systolic blood pressure .\n\nSubdural hematoma Pathogenesis . Rupture of bridging veins (head trauma) \n\n# . Elderly & alcoholic use disorder (cerebral atrophy, j fall risk) \n\nRisk factors . Infants (thin-walled vessels) \n\n# . Anticoagulant use \n\n# . Acute: gradual onset 1-2 days after injury \n\n0 Impaired consciousness (eg, coma), confusi on \n\nClinical 0 Headache, nausea & vomiting (i intracrani al pressure) \n\nfeatures Chronic; insidious onset weeks after injury \n\n0 Headache, somnolence , confusion, lightheadedness \n\n0 Focal neurologic deficits \n\n# . CT scan of th e head : crescent-shaped hyperdensity (acute) or \n\nDiagnosis hypodensity (chronic) crossing suture lines \n\n# . Reverse/discontinue anticoagulants \n\nTreatment . Surgical evacuation of symptomatic or large bleeds CNS, Eye, Ear What is the treatment in a elderly patient with a chronic subdural bleed from a recent fall who presents with headache, vomiting, and weakness? He is not oriented to time and place. \n\nSurgery ( craniotomy )\n\nPatients with subdural hematomas can be treated conservatively if there is no signs of herniation or <10mm .\n\nSubarachnoid CT showing hyperintense signal in subarachnoid spaces \n\n632 https://t.me/usmleinnercircle \n\nOverview of subarachnoid hemorrhage (SAH) \n\n## . Most commonly due to ruptured arterial saccular (\"berry\") Clinical aneurysm features . Severe headache at onset of neurologic symptoms \n\n## . Meningeal irritation (eg , neck stiffness) \n\n## . Focal deficits uncommon \n\n## . Rebleeding (first 24 hr) \n\n Vasospasm (after 3 days) Complications . Hydrocephalus/increased intracranial pressu re \n\n## . Seizures \n\n## . Hyponatremia (usually from synd rome of inappropriate antidiuretic hormone secretion) \n\n## . Noncontrast CT scan of the head is >90% sensitive \n\n## . Lumbar puncture required to definitely rule out SAH Diagnos is Xanthochromia in cerebrospinal fluid confirms diagnosis (usually seen 6 hr after onset) \n\n## . Cerebral angiography to identify bleeding source Angiographic procedure to stabilize aneurysm by coiling Treatment &/or stenting (endovascul ar therapy) \n\n## . Nimodipine & hyperdynamic therapy to reduce vasospasm \n\nTreatment Initial treatment \n\n Strict bedrest An algesia (acetaminophen) IV fluids for hydration a nd to avoid hyponatremia \n\n Reverse anticoagulation Control BP l;;J : maintain BP below 160 mm Hg to prevent rebleeding Prevent vasospasm in all patients -+ administer calcium channel blocker (es pecially oral nimodipine) \n\n Control t ICP: 30 head elevation , administer IV mannitol , \n\nhyperventila tio n in intubated patients , stool softeners l;;J \n\n Seizure prophylaxis with anticonvulsants: e.g., phenytoin for select cases l;;J \n\n Control blood glucose levels l;;J \n\nDefinitive treatment \n\n Surgical clipping l;;J (treatment of choice) and/or endovascular coiling \n\nl;;J (increasingly u sed alternative for poor surgical candidates) should be perform ed early to pr eve nt re bleeding If hydrocephalus is present-+ ventricular drain , serial LP s, or permanent ventri culoperi to neal shunt \n\n## I Use of nitrates shou ld be avoided since they may raise ICP! \n\n> \n\nRisk \n\nfactors \n\nSubarachnoid hemorrhage \n\n Hypertension Smoking Alcohol use Arteriovenous malformations \n\n ADPKD \n\n> i) UWorld\n\nSubarachnoid hemorrhage \n\nCollection of blood (hyperintense) in subarachnoid space CNS, Eye, Ear Hypertensive encephalopathy is characterized by marked blood pressure elevation with progressive headache, nausea/vomiting, and nonlocalizing neurologic symptoms (eg, confusion, restlessness) due to cerebral edema . Acute hemorrhage on CT scan of the head is not characteristic. \n\nLacunar \n\n Lacunar strokes often occur secondary to microatheroma formation and lipohyalinosis in the small penetrating arteries of the brain. \n\nultimately leads to thrombotic small-vessel occlusion; related to hypertension, diabetes, hyperlipidemia, and smoking \n\nMalignant Hemispheric Infarction \n\nA life-threatening condition that may occur when an ischemic stroke causes massive cerebral edema and/or hemorrhagic transformation: \n\nCerebral edema results from endothelial dysfunction and breakdown of the blood-brain barrier. The resulting mass effect and increase in intracranial pressure (ICP) can cause brain herniation. \n\nHemorrhagic transformation occurs when blood extravasates from injured cerebral vessels into the brain parenchyma. The larger the infarct, the greater the risk of hemorrhagic transformation. \n\n633 https://t.me/usmleinnercircle USMLE Inner Circle \n\nLacunar stroke Lacunar infarct Etiology Small penetrating a rt ery occlusion due to hypertensive arteriolar scleros is Basal ganglia \n\nAffected Subcortical white matter (eg, internal \n\nareas capsul e, corona ra diata) Pons \n\nRisk Hypertension factors Diabetes me ll itus, advanced age, t LDL, smoking Absence of cortical signs (eg, aphasia, ag nos1 a, neglect, apraxia, hemianop1 a), seizure, or mental status changes Common syndromes: \n\nC li nical o Pure motor hemiparesis \n\nfeatures (most frequent) \n\no Pure sensory stroke \n\no Ataxic hemiparesis \n\no Dysarth ria-clumsy hand Microatheroma Common lacunar stroke syndromes* Syndrome Typical location Clinical features Pure motor Posterior limb . Contralateral weakness (face, arm, leg) \n\nhemiparesis of internal capsule . No senSO !J: deficits \n\nAtaxic Posterior limb . Contralateral weakness & limb ataxia (leg > arm) \n\nhemiparesis of internal capsule . No senso !J: deficits \n\nPure sensory stroke Posterior thalamus . Contralateral hemisensory loss (face, arm, leg) \n\n## . No motor deficits \n\n## . Facial weakness & dysarthria \n\nDysarthria-clumsy hand syndrome Basis pontis . Contralateral hand weakness & clumsiness \n\n## . No senso !:l deficits *T hese syndromes typically lack cortical signs (eg , aphasia, agnosia, neglect, apraxia , hemianopia), seizures, and mental status changes . CNS, Eye, Ear Strokes that cause MHI typically are due to occlusion of a large vessel (eg, internal carotid, proximal middle cerebral artery) and initially present with severe deficits (eg, right-sided weakness, hemisensory loss, aphasia) due to the large affected area of the brain. Deterioration usually occurs in the first 48 hours but can be more gradual (up to a week). Patients with suspected MHI should have a noncontrast CT scan of the head performed emergently to determine the extent of edema and/or hemorrhage and guide further management. Decompressive hemicraniectomy is often necessary. What is the next step in management for a patient that presents one day after an ischemic stroke with signs of hemorrhagic transformation ?\n\nNon-contrast CT scan of the head \n\nrequired to confirm diagnosis of HT before urgent surgical decompression \n\n What is the likely diagnosis in a patient that presents with signs of increased intracranial pressure one day after a large ischemic stroke ?\n\nHemorrhagic transformation \n\nusually occurs within 48 hours of the stroke and manifests with deteriorating mental status \n\n## Spinal Cord \n\n In patients with traumatic spinal cord injury , urinary catheter placement can assess for urinary retention and prevent acute bladder distention /damage. \n\nCompression \n\n Down Syndrome patient with back pain, ataxia, incontinence, and quadriplegia .\n\nAtlantoaxial instability ( excessive mobility between C1 and C2 causing spinal cord compression )\n\nCentral Cord Syndrome \n\nCentral Cord Syndrome is a spinal cord injury that is commonly seen in the elderly following forced hyperextension of the neck (i.e. a rear-end collision). Glucocorticoids should be administered before MRI. Steroids are associated with improved outcomes. \n\n634 https://t.me/usmleinnercircle \n\n> Spinal cord compression Mechanical (eg , disc herniation, spinal stenosis) Causes Malignancy (eg , lung, breast, prostate cancers) Infection (eg , epidural abscess) Symptoms Gradually worsening , severe back pain Pain worse in recumbent position/ at night Early signs\n> oSymmetric extremity weakness\n> o\n\n! Deep tendon reflexes Physical examination Late signs \n\n> o\n\n! Rectal tone \n\n> o\n\nt Deep tendon reflexes , bilateral Babinski reflex \n\n> oParalysis Emergency MRI of the spine Management Emergency surgical radiation oncology consultation Intravenous glucocorticoids (eg , malignancy) or antibiotics (eg , infection)\n\nCNS, Eye, Ear Results in: Paralysis in the upper extremities Burning pain in the upper extremities Preservation of most functions in the lower extremities May be accompanied by localized deficit in pain and temperature sensation ;typically occurs with hyperextension injuries in elderly patients with pre-existing degenerative changes in the cervical spine \n\nT/t: Glucocorticoids / Surgery \n\n Because upper extremity CST motor fibers are located closer to the central part of the SC than lower extremity motor fibers, CCS is characterized by disproportionate upper extremity weakness \n\nD/D: Syringomyelia which is slowly progressive \n\nAnterior Cord Syndrome \n\nAnterior Cord Syndrome: burst fractures of vertebral bodies; distal paraplegia , bilateral loss of pain/temp ;preservation of vibration and position (dorsal column unaffected) \n\nCauda Equina & Conus Medullaris \n\n635 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nCentral cord syndrome \n\n- - - - - - - - - - - - - - - - - - - - - - - Cervical spine \n\nLa teral corticospinal tract Loss of pain and temperature sensation Weakness in upper limbs > lower limbs Anterior \n\ncommissure CNS, Eye, Ear Management of cauda equina syndrome involves emergent MRI and administration of glucocorticoids .\n\nSurgical Decompression in 24-48 hours needed to prevent permanent damage Does conus medullaris syndrome present with upper or lower motor neuron symptoms? \n\nBoth upper and lower \n\nhelpful distinguishing feature from cauda equina syndrome, which causes lower motor neuron symptoms only \n\nUMN \n\n What is the next step in management in a patient with tingling in her feet, pain down the back of her legs, hyperreflexia, and an up going plantar reflex? HbA1c is 7.6. \n\nMRI of the spine \n\nWhile this may look like diabetic neuropathy, the UMN symptoms are more concerning as diabetic neuropathy is strictly LMN. Thus, an MRI should be performed to evaluate for cord compression. \n\n Diabetic neuropathy strictly affects lower motor neurons. \n\n Patient stretches out and extends arm with palms up and closes their eyes. The left arm drifts downards and palm turns towards the floor . Where is the lesion? \n\nUMN lesion ( corticospinal or pyramidal tract )\n\nUMN lesions cause weakness in supinator > pronator muscles of upper limb, causing affected arm to drift downward and pronate \n\n636 https://t.me/usmleinnercircle \n\nConus medullaris syndrome Cauda equina syndrome Vertebral level . L1-L2 . L2-sacrum \n\nSpinal level . UMN: tracts of lumbosacral cord . LMN: lumbosacral spinal roots \n\n## . Severe low back pain . Mild or absent low back pain \n\nPresentation . Mild or absent radicular pain . Severe radicular pain \n\n## . Bowel/bladder dysfunction . Bowel/bladder dysfunction \n\n# . Motor weakness usually asymmetric \n\n# . Motor weakness usually symmetric Physical . Areflexia/hyporeflexia \n\n# . Hyperreflexia, UMN signs \n\nexamination . Asymmetric saddle numbness that may extend to . Symmetric perianal numbness the leg \n\n> LMN\n\n= lower motor neuron ; UMN = upper motor neuron. CNS, Eye, Ear ALS \n\n Early respiratory insufficiency may manifest as orthopnea and appear similar to obstructive sleep apnea (eg, daytime fatigue , morning headache )Suspicion of respiratory insufficiency should be confirmed with arterial blood gas analysis. \n\n Symptoms result from deterioration of UMNs (eg, corticospinal neurons located in the primary motor \n\ncortex ) and LMNs (eg, cranial nerves , anterior horn cells ). \n\nAutonomic Dysreflexia \n\n637 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPronator drift Amyotrophic lateral sclerosis \n\n## . Upper motor neuron signs \n\n0 Spasticity \n\n0 Hyperreflexia \n\n0 Pathologic reflexes (eg , jaw jerk , extensor plantar reflex) Clinical manifestations . Lower motor neuron signs \n\n0 Atrophy \n\n0 Fasciculations \n\n## . Bulbar symptoms \n\n0 Dysarthria \n\n0 Dysphagia \n\n## . Clinical evaluation Diagnosis . EMG \n\n## . MRI of brain & spinal cord (to exclude other causes) \n\n## . Riluzole \n\nTreatment . Respiratory support (eg, NIPPV) \n\n## . Nutritional support (eg, PEG tube) EMG = electromyography; NIPPV = noninvasive positive pressure ventilation ; PEG = percutaneous endoscopic gastrostomy. CNS, Eye, Ear Spinal cord injury above T6 can be complicated by autonomic dysreflexia, in which noxious stimuli below the injury level trigger an unregulated sympathetic response , leading to severe hypertension .A compensatory parasympathetic response above the lesion typically causes bradycardia .Management includes removing noxious stimuli and treating the hypertension. \n\n Lesions that arise above T1 also often cause neurogenic shock due to interruption of the descending \n\nsympathetic fibers , which results in unopposed parasympathetic stimulation of the vessels (hypotension ) and heart ( bradycardia ). \n\nHypothermia is also common due to a lack of peripheral vasoconstriction. \n\n## Demyelinating Disorders \n\nMultiple Sclerosis \n\n638 https://t.me/usmleinnercircle \n\nAutonomic dysreflexia \n\n> Compensatory parasympathetic response\n> slows heart rate lev el of spinal cord -.\n> injury\n\n= TS or above Descending inhibitory s i gn a ls blocked\" x \n\n> ReMJlts In ., unf'99Ulllled sympathetic responae dis la ~ , IH Wdespread\n> vasoconstrict io ncauses hypertension\n\nCNS, Eye, Ear Lumber Puncture is not required for MS diagnosis when clinical and MRI findings are definitive 639 https://t.me/usmleinnercircle USMLE Inner Circle \n\nEstablishing a diagnosis of multiple sclerosis \n\nSuspicious symptoms Optic neuritis Internuclear ophthalmoplegia Brainstem or cerebellar disorder Transverse myelitis Proof of DIT: >1 attack Need proof of DIS: 2 M RI lesions (different sites) Proof of DIS: >1 deficit \n\nNeed proof of DI T: Prior cl inical attack(s) Old MRI lesion \n\nNOT \n\nDI T or DIS Confirmed multiple sclerosis (start disease-modifying therapy) ] Clinically isolated syndrome ) DIS = disseminated ln space; DIT = disseminated in lime. CU\\Nor ld \n\nWorkup of multiple sclerosis Suspicious symptoms \n\n Optic neuritis Internuclear ophthalmoplegia Brainstem or cerebe ll ar disorder Transverse myelitis \n\nMRI with characteristic lesions (periventricular wh ite matter) IYes \n\ni\n\nDisseminated in t ime (\"Any New?\") Disseminated in space {\"An y Two?\") (Sympt oms or imag ing) IYes \n\ni\n\n- No } - L _u _m _b _a _r_ p_ u_ nc _t_ ur _e_w _it_ h..J \n\noligoclonal bands -No Yes Likely multiple sclerosis \n\ni I C)UWo Depression Antidepressant medication (eg, SSRI, SNR I)\n\n# . Physical therapy & stretching \n\n> Spasticity\n\n## . Massage therapy \n\n## . Baclofen or tizanidine \n\n## . Sleep hygiene, regular exercise \n\n> Fatigue Amantadine\n\n## . Stimul ant medication (eg, me thy lphenidate, modafinil) Neuropathic pain . Gabapentin or duloxetine Timed voiding Urge urinary in con tinence . Fluid r est riction (<2 Uda y) \n\n> Anticholinergic medication (eg, ox ybutynin, tol ter odi ne )SNRI = serotonin-no repinephrine reuptake inhibitor; SSRI =se lective serotonin reuptake inhibi tor .\n\nCNS, Eye, Ear Recently, autoantibodies against myelin oligodendrocyte glycoprotein (MOG) and \n\naquaporin-4 (AQP4) have been identified as a causative factor of some cases of optic neuritis. Patients who develop optic neuritis because of antibodies against MOG and AQP4 often have severe presentations but also have a decreased risk for subsequent MS compared with patients with optic neuritis who lack these autoantibodies Multiple sclerosis may present with transverse myelitis, which results in motor and sensory loss \n\nbelow the level of the lesion, often with bowel and bladder dysfunction. \n\ncauses flaccid paralysis initially (spinal shock) followed by spastic paralysis with hyperreflexia \n\nTransverse myelitis: cause is unknown, but affects the tracts that run across the horizontal aspect of the spinal cord at a given level. \n\nTransverse Myelitis Fundoscopy is normal ; inflammation is behind optic nerve head \n\n641 https://t.me/usmleinnercircle USMLE Inner Circle \n\nOptic neuritis \n\n Primarily in young women \n\nEpidemiology Associated with multiple sclerosis \n\n## . Immune-mediated demyelination Acute, peaks at 2 weeks Monocular vision loss Manifestations Eye pain with movement \"Washed-out\" color vision Afferent pupillary defect Diagnosis MRI of the orbits & brain \n\n## . Intravenous corticosteroids \n\nTreatment 35% of cases recur \n\nIdiopathic transverse myelitis \n\n# . Immune-mediated destruction of spinal cord \n\nPathophysiology Often postinfectious (molecular mimicry) Bilateral motor weakness, classically early flaccid (LMN) progressing to late spastic (UMN) \n\nClinical features Bilateral sensory dysfunction (all somatosensory systems) \n\n# . Distinct sensory level \n\n Autonomic dysfunction (bowel &/or bladder) \n\n# . MRI of spine: no compressive lesion, T2 hyperintensity \n\nDiagnosis Lumbar puncture: j WBCs, j lgG index High-dose intravenous glucocorticoids \n\nTreatment . Plasmapheresis \n\nLMN = lower motor neuron; UMN = upper motor neuron ; WBCs = white blood cells. CNS, Eye, Ear D/D: Spinal Epidural Abcess : but has fever and pain \n\nNeuromyelitis Optica \n\n Optic Neuritis + Transverse Myelitis + Intractable Hiccups. Finding: Aquaporin-2 autoantibodies in CSF T/t: Steroids , Plasma exchange \n\nGBS \n\n Acute HIV infection can also trigger GBS \n\nMiller Fisher Syndrome Inflammatory infiltrate leads to an increase in water content in the spinal cord \n\n642 https://t.me/usmleinnercircle \n\nTr an sverse mye li tis \n\nHypenntense on T2 MRI . cuw\"\"\" \n\nTransverse myelitis Guillain-Barre syndrome Motor . Earl :z: flaccid , late seastic earal :z: sis . Ascending paralysis \n\n## . If quadriplegia, weakness in LE = UE . Weakness in L E > UE in early di sease \n\nSensory Clearly identifiable sensory level . Mild sensory loss \n\n## . . No spinal cord level \n\nAutonomic . Bowel & bl adder dysfunction . Cardiovascular instability \n\nCranial nerves None . Oc u lomotor , g l ossop h aryngea l, or fac ial \n\n## . paralysis \n\nElectromyography/nerve . Mostly n orma l . Peripheral moto r &/or sensory NCV reduced \n\nconduction velocity \n\n## . Normal \n\nMRI . Focal enhanced area of T2 signal . E nhance m ent of an terior n erve roots o r cauda equina \n\nCerebrospinal fluid . Pleocytosis . Absence of pleocytosis \n\n## . Increased lgG index . Elevated protein \n\nLE = lower extremity; NCV = nerve co nd uc tion ve locity; UE = upper extremity. CNS, Eye, Ear Variant of GBS Path: Anti-GQ1b antibodies due to molecular mimicry Features: 1. Rapid-onset ophthalmoplegia \n\n2. Ataxia \n\n3. Arreflexia \n\n4. Paralysis is less common T/t and Dx similar to GBS \n\nCIDP \n\n CIDP responds to Steroids vs AIDP (GBS) which Does not \n\n## Neurodegenerative disease \n\nDementia \n\n What vitamin deficiency should always be screened for in patients with dementia ?\n\nVitamin B12 (cobalamin) Endocrine abnormality? Hypothyroidism \n\nImaging in all patients? n/c Ct or MRI to detect reversible causes of dementia \n\n643 https://t.me/usmleinnercircle USMLE Inner Circle \n\nChronic inflammatory demyelinating polyneuropathy \n\n# . Im m une-med iated demyeli nat ion of per ipheral nerves and nerve roots \n\nPathophysiology Non-length dependent .. Progr ess ion >8 weeks \n\nClinical features . Motor>> sensory \n\n# . Symmetric proximal & distal m uscle weakness \n\n# . LMN signs (eg, hyporeflexia, atrophy) \n\n# . CSF: t pro tein, normal wh ite blood ce lls Diagnosis . NCS : decreased conduction velocity (ie, demyelination) \n\n## . Nerve biopsy: segmental demyelination \n\n# . Glucocorticoids \n\nTreatment . Intrave no us immunoglobu li n\n\n# . Plasmaphere sis CSF = cerebrospinal fluid; LMN = l owe r motor neuron: N CS = nerv e condu ct i on studies. CNS, Eye, Ear What GI pathology is an irreversible cause of dementia ?\n\nWilson disease (hepatolenticular degeneration) \n\n Are patients with pseudodementia typically distressed by their memory impairment? \n\nYes \n\nhelpful distinguishing feature from Alzheimer's dementia, in which patients are relatively unconcerned \n\n Depressed patient with cognitive deficits have Acute onset and often answers I dont know and is aware of problems! (Vs. dementia patient confabulation and is unaware of problems )Many over-the-counter (OTC) allergy medications (eg, antihistamines ) have anticholinergic effects that can contribute to memory impairment , especially in older patients. \n\n644 https://t.me/usmleinnercircle \n\nInitial workup of suspected cognitive impairment Cognitive . MMSE (score <24/30 suggestive of MCI/dementia) \n\n## . Montreal Cognitive Assessment (score <26/30) \n\ntesting Mini-Cog (abnormal 3-word recall &/or clock-drawing test) .\n\nLaboratory . Routine: CBC , vitamin 8 12 , TSH, CMP \n\n## . Selective (specific risk factors ): folate, syphilis, vitamin D level \n\ntesting Atypical (early onset ): CSF .. Routine: CT scan or MRI of the brain \n\nImaging Atypical : E EG .\n\nCBC = complete blood count; CMP = complete metabolic panel; CSF = cerebrospinal fluid; EEG = electroencephalogram; MCI= mild cognitive impairment; MMSE = Mini-Mental State Examination. \n\nNormal aging Dementia (major cognitive disorder) \n\n# . Can provide details about incidents of forgetfulness . Cannot remember specific instances of forgetfulness \n\n## . Patient is concerned about memory loss . Family is more concerned than patient \n\nMemory loss . Recent memory for important events & . Has notable decline in memory for recent important conversations is intact events & conversations \n\nWord-finding Occasional (expressive aphasia) Frequent, with substitutions \n\ndifficulty . No receptive aphasia . Some receptive aphasia \n\n# . Maintains independence in ADLs . Becomes dependent on others for ADLs \n\n## . Is able to operate common appliances . Is unable to operate common appliances \n\nIndependence & Maintains interpersonal social skills Loses interest in social activities . .functioning Does not get lost in familiar territory (may have to Can get lost for hours in familiar territory while . .\n\npause briefly to reorient) driving or walking \n\nADL = activities of daily living .\n\nCognitive impairment in elderly patients Normal aging . Slight decrease in fluid intelligence (ability to process new information quickly) \n\n## . Normal functioning in all activities of da ily living \n\nMild neurocognitive disorder . Mild decline in ~1 cognitive doma i ns \n\n(mild cognitive impairment) . Nonmal functioning in all activities of daily living with compensation \n\n## . Significant decline in ~1 cognitive domains \n\nMajor neurocognitive disorder (dementia) . Irreversible global cognitive impairment \n\n## . Marked functional impairment \n\n## . Chronic & progressive, months to years \n\n## . Reversible mild-moderate cognitive impainment \n\nMajor depression . Features of depression (mood, interest, energy) \n\n## . Episodic, weeks to months CNS, Eye, Ear DO a careful review of medicines in workup if patient is taking any. Spl in the cases of abrupt onset memory impairement. \n\nParkinsons \n\nPatients with advanced Parkinson disease are at very high risk for aspiration due to difficulty forming a food bolus from lingual bradykinesia , impaired coordination of the muscles involved in swallowing due to autonomic dysfunction, and impaired cough reflex. As the disease progresses, swallowing evaluations \n\nare generally required so that modifications to diet (eg, thickened liquids) and eating position (eg, chin-tilt) can be made to reduce aspiration risk. Lewy Bodies: eosinophilic inclusions composed of -synuclein. Round Pick Bodies in Frontotemporal Dementia \n\n645 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDifferential diagnosis of dementia subtypes Common agents w i th antichol i nergic propert i es Alzheimer . Early , insidious short-term memory loss di s eas e . L angu a ge deficits & spatial di sor ientation \n\n## . L ater p erso nali!l'. chan9 es \n\nAn ti h is tam i ne s . Diphenhydrami ne , cyproheptadine, doxylami ne \n\n# . 1st generation: haloperidol \n\nPsychotropics . 2nd generation: clozapine \n\n# . TCAs: amitriptyline, clomipramine, doxepin \n\n## . Stepwise decline \n\nVascul ar . Early executive dysfunction Antiparkinson . Benztropi ne , trihexyphenidyl \n\ndementia . Ce rebra l in fa r ct ion &for deep w hite matter . lpratropium (bronchodilator} changes on ne u roimag i ng Antimu s car in ics . Oxybutynin, darifenacin (overactive bladder) \n\n# . Dicyclomine, hy o sc yamine (antispasmodics} \n\n## . Early personality changes . Scopolamine (antiemetic} \n\nFrontotempor al . Apat h y, d is inhibit ion & com p uls i ve Myd ri atics Atropine, cyclopentolate \n\ndementia behavior \n\n## . Frontotemporal atrophy on neuroimag ing . Musca ri nic mushroom s pe cies \n\nPl an t-ba se d . Jimsonweed \n\n## . Visual hallucinations . Nightshade species \n\nDementia with Lewy . Spontaneous parkinson ism TCA s = tri cyc lic antidepressant s. \n\nbodies . Fluctuating cognition \n\n## . Rapid eye movement behavior disorder \n\nNo rm al pressure . Ataxia early in disease \n\nhydrocephal us . Urinary incontinence \n\n## . Dilated ventricles on n euro i mag ing \n\n## . B ehavio ral cha n ges \n\nPr ion disease . Rapid progression \n\n## . Myoclonus &fo r seizures CNS, Eye, Ear Psychosis is common in Parkinson disease , occurring at a higher rate in those treated with dopamine agonists than in those treated with carbidopa-levodopa .Psychotic symptoms can be treated with antiparkinson medication dose reduction and/or the addition of a low-potency 2nd gen antipsychotic (eg, quetiapine , pimavanserin). \n\n Parkinson disease is associated with depression , which may lead to worsening of motor function and increased risk for suicide. Treatment is with selective serotonin reuptake inhibitors or atypical antidepressants, as well as cognitive behavioral therapy . The atypical antidepressant mirtazapine is particularly useful for patients with concomitant depression and insomnia \n\n646 https://t.me/usmleinnercircle \n\nClinical features of idiopathic Parkinson disease \n\n# . Bradykinesia \n\nPLUS Cardinal findings . 4- to 6- Hz resting tremor \n\nOR \n\n## . Cogwheel rigidity \n\n## . Unilateral onset \n\n# . Craniofacial (masked facial expression, decreased eyeblink rate, hypophonia) \n\n## . Visual (blurred vision , impaired upward gaze) \n\nSuggest diagnosis . Musculoskeletal (micrographia , dy stonia, myoclonus) \n\n## . Shuffling, stooped gait ; postural instability \n\n## . Autonomic dysfunction \n\n# . Neuropsychiatric (depression, psychosis, disturbed sleep, dementia) \n\nMajor depressive disorder vs Parkinson disease symptoms MDD Depressed mood \n\nAnhedonia \n\n(lacks pleasureflnterest) Affecti ve G uilt/worthlessness Suicidal ideation Neurovegetative Appetite/weight change Concentration deficits Fatigue lnsomnia/hypersomn ia Psychomot or Psychomotor slowing (bradykinesia) Blunted emotional expression (masked facies) \n\n> MOD =\n\nma jor depress ive di sorde r; PD = Patkinson di sease .PD Neutral mood \n\nApathy/abulia \n\n(lacks motivation) \n\n> CUINorl d\n\nCNS, Eye, Ear Severe sensitivity to antipsychotics (dopamine antagonists) is commonly seen in patients with DLB and is considered a supportive clinical feature \n\n A common cause of falls in patients with parkinsonism is postural instability , which can be confirmed by the pull test .Early-onset postural instability should raise concern for an atypical parkinsonian (ie, Parkinson-plus) syndrome (eg, dementia with Lewy bodies) because postural reflex dysfunction is typically a late finding (ie, >3 years) in idiopathic Parkinson disease. \n\nMultiple System Atrophy \n\n What neurological pathology manifests as Parkinsonism with orthostatic hypotension , impotence ,\n\nincontinence , or other autonomic dysfunction? \n\nMultiple system atrophy ( Shy-Drager syndrome )\n\nTriad of: \n\nmotor abnormalities (parkinsonian features), \n\nautonomic dysfunction (incontinence, orthostatic hypotension, erectile dysfunction), and \n\n647 https://t.me/usmleinnercircle USMLE Inner Circle \n\nParkinson-plus (atypical parkinsonism) syndromes* Characteristic \"plus\" features \n\n# . Early autonomic failure (eg, severe orthostasis, urinary incontinence) \n\nMultiple system atrophy . Early postural instability (eg, falls) . Cerebellar findings (eg, gait ataxia) . Vertical gaze palsy . Early postural instability (eg, falls) \n\nProgressive supranuclear palsy Akinesia (eg, early gait freezing) .. Progressive aphasia . Early dementia (executive dysfunction) . Visual hallucinations \n\nDementia with Lewy bodies Cognitive fluctuations .. REM sleep behavior disorder . Relatively rare . Myoclonus, dystonia \n\nCorticobasal degeneration Alien limb phenomenon (ie, has a will of its own) .. Cortical sensory loss important findings suggesting Parkinson -p lus syndromes instead of Parkinson disease include rapid progression, symme tric findings, a~ r &poor levodopa response. \n\nPull (retropulsion) test of postural instability* \n\n## . Patient in comfortab le stance, eyes open , with examine r behind \n\nProcedure . Sudden, brief pull on patient's shoulders (ready to catch patient, if needed) . Scoring = number of steps to recover balance \n\nNormal . 1-2 steps, recovers unai ded \n\nSlight . 3-5 steps, recovers unaided \n\nMild . >5 steps, recovers unaided \n\nModerate . Stands safely , falls during test if not caug ht by examine r\n\nSevere . Loses balance spontaneously \"From the Movement Disorder Society-Unified Parkinson's Disease Rating Scale. CNS, Eye, Ear cerebellar symptoms (ataxia) \n\nAnti-Parkinsonism drugs are generally ineffective ;treatment is aimed at intravascular volume expansion (e.g. fludrocortisone , salt supplements, Alpha agonists )\n\n Similar to NPH but no Dementia/ Cognitive Impairement \n\nProgressive Supranuclear Palsy \n\n What is the most likely diagnosis in an elderly female who presents with downward gaze palsy, postural intability, bradykinesia , and upper extremity rigidity ?\n\nProgressive supranuclear palsy \n\nMRI shows atrophy of midbrain structures with intact pons \n\n Associated with tau-positive neurofibrillary tangles in the basal ganglia , cortex, and brainstem \n\nAlzheimer Disease \n\nAddressing modifiable risk factors can reduce the likelihood of developing AD. Evidence shows that aggressive treatment of cardiovascular risk factors (eg, hypertension, diabetes, obesity/physical inactivity), especially in mid-life, can help reduce risk \n\nFrontoTemporal Dementia \n\n648 https://t.me/usmleinnercircle \n\n \n\n> Progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome)\n> Clinical features\n> Po~t11ral i11st,1bj1ity (leading to frequent falls) Frontal lobe abnormalities (e .g.,apathy, disinhibit ion, impaired reasoning) \\/ertical gaze palsy, especially downward gaze ,to complete external ophthalmoparesis\n\nl;l \n\n> Rigor Bradykinesi a,\n> Dysarthria, dysphagia Dementia Diagnosis\n\n M.~ !: \".1!1J.11'.'!!1 .i_ 11 ~~-i !_ ~__s _i_ g_11_\" showing ?,~~ CSF\n\n= cerebrospinal fluid; EEG = electroencephalogram; RT-QulC = real-time quaking-induced conversion. \n\nCreutzfeldt-Jakob disease Probable diagnosis: \n\n Rapidly progressive dementia 2 out of 4 clinical features : \n\no Myoclonus \n\no Akinetic mutism \n\no Cerebellar or visual disturbance \n\no Pyramidal/extrapyramidal dysfunction (hypokinesia) Periodic sharp wave complexes on EEG &/OR Positive 14-3-3 CSF assay \n\nDefinitive diagnosis includes above features in combination with \n\n Brain biopsy findings (gold standard) OR Demonstrated PRNP gene mutations CNS, Eye, Ear Pt: Young male, decreased vision, hearing, speaking with ataxia and male cousin with similar complaints. Hyperpigmentation (adrenal insufficiency). Low yield but treatment is supportive (diet and \"Lorenzo's oil\" -- lipid mix consisting of glycerol trioleate and glycerol trierucate in a ratio of 4:1) \n\nAlcohol Cerebellar Degeneration \n\n Other Signs: \n\n1. Hypotonia- Pendular Knee reflex (More than 4 swings abnormal) 2. Postural Tremors , Dysarthria , Diplopia \n\n Babinski Sign is NOT characteristic in Cerebellar disease \n\nHIV Neurocognitive Dysfunction \n\n MRI may also be helpful and usually reveals \n\ndiffuse brain atrophy , ventricular enlargement ,and increased white matter intensity. \n\n651 https://t.me/usmleinnercircle USMLE Inner Circle \n\nAlcoholic cerebellar degeneration Epidemiology . >10 years heavy alcohol use \n\n# . Degeneration of Purkinje cells (cerebellar vermls} \n\n# . Usually develops over weeks to months \n\nManifestations Wide-based gait \n\n# . lncoordinalion in legs \n\n# . Cognition usually intact \n\n# . Clin ic al: \n\n0 Impaired tandem wal ki ng/heel-knee-shin \n\nDiagnosis PreseNed finger-nose testing 0\n\n# . CT/MRI - cerebellar atrophy \n\n Alcohol cessation Treatment . Nutritional supplements \n\n Ambulatory assistance devices (eg, wa lker) HIV-associated neurocognitiv e disorders \n\n## . Impaired memory & attention/concentration \n\nManifestations . Personali~ & behavior chana es \n\n## . Motor symptoms (eg, ataxia, slowed movement) \n\n## . Asymptomatic neurocognitive imeairment \n\nSeverity . Mild neurocognitive disorder \n\n## . HIV-associated dementia \n\n---. Long-standing HIV disease \n\nRisk factors . Age ~50 \n\n## . CD4 count <200/mm 3\n\nDiagnosis . Clinical presentation \n\n## . Neuropsychological testing CNS, Eye, Ear CNS Tumours \n\n Brain tumors are often clinically silent until they grow large enough to compress neurologic structures or raise intracranial pressure (ICP). The most common symptom is a dull headache associated with >1 of the following: \n\nNausea and vomiting (due to increased ICP) \n\nFocal neurologic manifestations (due to tumor invasion or compression) MRI reveals a diffuse increase in intensity in the white matter. \n\n652 https://t.me/usmleinnercircle \n\nCauses Clinical presentation \n\n\n\nClinical features of sellar masses \n\n## . Benign tumors \n\n> 0\n\nPituitary adenoma (most common) \n\n> 0\n\nCraniopharyngioma (50% age >20) \n\n> 0\n\nMeningioma \n\n> 0\n\nPituicytoma (low-grade glioma) \n\n## . Malignant tumors \n\n> 0\n\nPrimary (eg, germ cell tumors , chordoma , lymphoma) \n\n> 0\n\nMetastatic (eg , breast, lung) \n\n## . Diplopia, bitemporal hemianopsia, vision loss \n\n## . Headache \n\n## . Hormonal deficiencies . Can be found incidentally on brain imaging \n\nPediatric brain tumor locations \n\nAstrocytoma ---------\n\nOptic glioma Supratentorial lnfratentorial (posterior fossa) Brainstem glioma \n\n> :)UWorld\n\nCraniopharyngioma CNS, Eye, Ear Symptoms worsening during the night or with positions that raise ICP (eg, bending, coughing Patients usually require MRI of the brain for further evaluation. \n\nMetastatic Brain Lesions \n\n Metastatic CNS tumors characteristically present as multiple, well-circumscribed lesions with vasogenic edema at the gray-white junction. \n\ntypically manifests as headache, focal neurologic dysfunction, cognitive change, or seizure \n\n Although pulmonary symptoms arise in the majority of patients with lung cancer, up to 30% of cases present with manifestations of metastatic brain disease , and may have no prominent pulmonary or systemic symptoms and an unremarkable cardiopulmonary examination. For patients with a single brain metastasis in a surgically accessible location and good performance status, surgical resection offers the best therapeutic option followed by stereotactic radiosurgery (SRS) or whole brain radiation therapy (WBRT) \n\nMeningioma \n\n653 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nClinical features of pineal gland masses \n\n# . Limited upward gaze \n\nParinaud syndrome . Upper eyelid retraction (Collier sign) \n\n# . Pupillary abnormalities (ie, reactive to accommodation but not to light) \n\nObstructive . Papilledema \n\nhydrocephalus . Headache, vomiting \n\n# . Ataxia Clinical features of metastatic brain cancer \n\nOrder of increased metastatic brain \n\nIncidence frequency: Lung > Breast > Unknown primary > Melanoma > Colon \n\nPrimari ly Breast \n\nsol itary brain Colon \n\nmetastases Renal cell carcinoma \n\nMultiple brain Lung cancer \n\nmetastases Malignant melanoma Prostate cancer \n\nRare brain Esophageal cancer \n\nmetastases Oropharyngeal cancer Hepatocellular carcinoma Non-melanoma skin cancers CNS, Eye, Ear Risk factors for meningioma include: Older age (as with many other tumors) \n\nFemale sex (also potentially exogenous estrogens, progestins, or antiandrogen medications) \n\nGenetic predisposition (eg, neurofibromatosis type 2, schwannomatosis )Exposure to ionizing radiation (Greatest Acquired Risk) \n\nSchwannoma Choroid Plexus papilloma Benign Tumor \n\n654 https://t.me/usmleinnercircle \n\nCervical spinal meni n gioma (MRI with contras t) \n\n\n\nVestibular schwannoma (acoustic neuroma) Epidemiology . Median age 50 \n\n## . Usually unilateral (bilateral associated with ne ur ofibromatosis type 2) \n\nClinical manifestations & pathophysiology . Sensorineural hearing loss & imbalance (CN VIII Schwann cell tumor) \n\n## . Facial numbness &/or paralysis (CN V & VII compression) \n\nDiagnostic studies . Audiogram \n\n## . MRI with contrast of internal auditory canal \n\n## . Observation (eg, small tumors, minimal symptoms older or infirm eatients) \n\nManagement . Surgery \n\n## . Radiation therapy CNS, Eye, Ear Most common in infants , CPP is a rare, slow-growing, benign overgrowth of the choroid plexus that results in increased CSF production causing Hydrocephalous. \n\nDx: MRI \n\nT/t: Resection \n\n## Neurocutaneous Disorders \n\n655 https://t.me/usmleinnercircle USMLE Inner Circle \n\nChoroid plexus papilloma \n\n0UVVorld CNS, Eye, Ear NF cafe-au-lait spots and cutaneous neurofibromas \n\n656 https://t.me/usmleinnercircle \n\n> Cafeaulait macules\n\nNeurofibromatosis type I \n\n> Lisch nodules Axillary&inguinal freckling\n\nCNS, Eye, Ear Yearly ophthalmologic examinations screen for Optic Glioma , and MRI of the brain and \n\norbits is required for any vision changes. \n\nTuberous Sclerosis \n\nTuberous sclerosis is a neurocutaneous disorder associated with ungual fibromas , which are flesh-colored lumps emerging from nail folds. \n\n657 https://t.me/usmleinnercircle USMLE Inner Circle \n\nNeurofibromatosis type II \n\n# . Autosomal dominant \n\nGenetics . NF2 gene on chromosome 22 encoding merlin (tumor suppressor) \n\n## . Variable expressivity, usually at age 20-30 \n\n## . Bilateral vestibular schwannomas \n\nClinical . lntracranial meningiomas \n\nmanifestations . Spinal tumors (eg, schwannomas , ependymomas) \n\n# . Cataracts \n\n## . Cutaneous tumors or skin plaques \n\nTumor . Audiogram \n\n## . Ophthalmologic evaluation \n\nsurveillance . MRI of the brain & spine \n\nTuberous sclerosis complex \n\n Mutation (inherited or de n ovo) in TSC1 or TSC2 gene \n\nPathophysiology Auto so mal domin ant Derma t ologi co Ash-leaf spots o Angiofibromas of the malar reg ion \n\n0 S hagreen patches Neurologic \n\nClinical features 0 CNS lesions (eg, subependymal tumors) \n\n0 Epilepsy (eg, i nfantile spasms) \n\n0 I ntellectual disability o Autism & behavioral disorders ( eg, h yperactivity) Cardiovascular: rhabdomyomas Renal : a ngiomyolipomas Tumor screening \n\n0 Regular skin & eye examinations \n\n0 S eria l M RI of the brain & kidney \n\nSurveillance 0 Ba se line e chocardiography & serial ECG Baseline electroencephalography \n\n# . Neuropsychiatric screening CNS, Eye, Ear VHL Sturge Weber Angiofibromas (adenoma sebaceum) Ash-leaf spots (hypopigmented macule) Shagreen patches (patches of localized leathery thickenings) \n\n658 https://t.me/usmleinnercircle \n\nTuberous sclerosis complex Von Hippel-Lindau disease Etiology . Mutation in the VHL tumor suppressor gene on chromosome 3 \n\n## . Autosomal dominant inheritance \n\n## . Cerebellar & retinal hemangioblastomas \n\nManifestations . Pheochromocytoma \n\n## . Renal cell carcinoma (clear cell subtype) \n\n## . Surveillance for associated malignancies \n\n> 0\n\nEye/retinal examination \n\nManagement 0 Plasma or urine metaneph ri nes \n\n> 0\n\nMRI of the brain & spine \n\n> 0\n\nMRI of the abdomen \n\n## . Tumor resection \n\nSturge-Weber syndrome Pathophysiology Mutation in GNAQ gene \n\n# . Port-wine stain (trigeminal nerve [CN V1N2] distribution) \n\n# . Leptomeningeal capillary-venous malformation Seizures hemiparesis \n\nClinical features \n\n Intellectual disability \n\n Visual field defects Glaucoma \n\nDiagnosis MRI of the brain with contrast \n\n# . Laser therapy \n\nManagement Antiepileptic drugs Intraocular pressure reduction CNS, Eye, Ear Infection \n\n Meningitis : Normal Cognition Encephalitis : Altered Mental Status Anti-NMDA receptor encephalitis is an autoimmune encephalitis syndrome characterized by \n\npsychiatric symptoms (eg, anxiety, psychosis), cognitive dysfunction (eg, memory impairment), \n\nseizure , autonomic instability, dystonia , and rigidity .It occurs most commonly in young women (median age of 21) and is associated with ovarian teratoma in >50% of cases. T/t: Tumor removal , Immunosuppressants \n\nMeningitis Port Wine \n\n659 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSturge-Weber syndrome \n\n*Due to venous congestion from the capillary-venous ma lformation . uworlc CNS, Eye, Ear often absent in patients age <1 year .What are the most common causes of viral meningitis ?\n\nNon-polio Enteroviruses ( Echo and Cox )\n\nRules of Thumb \n\nReally young (<1 month): Ampicillin (Listeria) and cefotaxime (prevent kernicterus) Kinda young to kinda old: Vancomycin + 3rd-gen cephalosporin (ceftriaxone )Old (>50): \" + \" + ampicillin (Listeria) Immunocompromised: look for option with cefepime (to cover pseudomonas) In neonates cefotaxime is preferred over ceftriaxone because ceftriaxone can displace bilirubin from albumin, increasing the risk of kernicterus Normal opening pressure: 20 cm H2O \n\n660 https://t.me/usmleinnercircle \n\nCerebrospinal fluid analysis WBC count Diagnosis (cells/L) Glucose (mg/dl) Normal 0-5 40-70 \n\nBacterial meningitis >1,000 <40 \n\nTuberculosis meningitis 5-1 ,000 <10 \n\nViral meningitis 100-1,000 40-70 \n\nGuillain-Barre 0-5 40-70 \n\nProtein (mg/dl) \n\n<40 >250 >250 <100 45-1,000 \n\nmd z1 ,\n\ni VE' flex i \n\nexion \n\nKe rn ,ig's '1ig11 . Patienl \n\nupin , wi lh hip fl d\n\n90\". Kn a11 no1 b ful ly \n\nex tended. \n\nbol 11 legs a nd thighs. \n\nBacteri al meningitis Risk group Common organisms Empiric antibiotics \n\nStreptococcus Vancomycin + a third-\n\nAge 2-50 pneumoniae , Neisseria meningitidis generation cephalosporin \n\nS pneumoniae , N Vancomycin + ampicillin +\n\nAge > 50 a third-generation \n\nmeningitidis, Listeria cephalosporin \n\nS pneumoniae , N Vancomycin + ampicillin +\n\nlmmunocompromised meningitidis, Listeria, cefepime gram-negative rods \n\nNeurosurgery/penetrating Gram-negative rods, MRSA, coagulase- Vancomycin + cefepime \n\nskull trauma negative staphylococci \n\n Third-generation cephalosporins: ceftriaxone or cefotaxime Alternatives to cefepime: ceftazidime or meropenem Alternative to ampicillin : trimethoprim-sulfamethoxazole for Listeria \n\n Poss ibly dexamethasone: only beneficial in some cases In adults: when pneumococcal meningitis is strongly suspected or confirmed In children : for suspected or confirmed HiB meningitis Doxycycline (during tick-bite season in endemic areas only!) \n\nCauses of meningitis in children \n\nGroup B Streptococcus \n\n<3 months Escherichia coli & other gram-negative bacteria Listeria monocytogenes \n\nHerpes simplex virus 3 months to 10 years Streptococcus pneumoniae Neisseria meningitidis \n\n~11 years Neisseria meningitidis CNS, Eye, Ear Do not perform a lumbar puncture if patient has any of the FAILS mnemonic: FND AMS Immunosuppressed/ICP Lesion at site of needle Seizures \n\nWant to make sure there is no increased ICP (eg, focal neurologic deficit, coma, papilledema) -> if there is, you can cause brain herniation and death \n\n Patients with an open anterior fontanelle have a natural pop-off valve to relieve elevated ICP, they are at very low risk for herniation and rarely require neuroimaging prior to LP What is the next best step in a patient with suspected bacterial meningitis and no signs of alarm symptoms? \n\n661 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nI\n\nNo \n\n+\n\nLumbar puncture Suspected meningitis Emergent blood cultures Any alarm symptoms? Signs of elevated ICP Focal neurologic deficits Impaired co nciousness or orientation Compromised immune system \n\nI\n\n# lEmpirical antibiotic treatment \n\n dexamethasone Empirical antibiotic treatment \n\n dexamethasone and hospitalization and hospitalization Cranial CT Lumbar puncture +--No- Signs ,';J;~evated \n\n## !Adjust when specific pathogens have been identified \n\nI\n\nYes \n\n\n\nContinue empirical treatment \n\n< 1 hour between administration and treatment \n\nManagement of bacterial meningitis in children age >1 month \n\nSuspected meni ng itis ]\n\nObtain blood cultures ]\n\n Rapid clinical deterioration? Neuroimagi ng required?* \n\nr-Yes \n\nAntibiotics dexamethasone ]\n\n CT scan of the head Lumbar puncture (if stable ¬ contraindicated) \n\nNo--i \n\nLumbar puncture Antibiotics dexamethasone 1n chcations fOf ne11oimag 1ng : dosed fontanelle with si gns of elevated intracranial press ure (eg, pa pi lledema, focal neurologi c deficits, coma ) CUWo r ld CNS, Eye, Ear Lumbar puncture before antibiotics \n\nOnly give antibiotics first if there is a contraindication to immediate lumbar puncture or meningococcal infection \n\n Although cerebrospinal fluid culture is diagnostic, treatment should not be delayed for lumbar puncture in patients with suspected meningococcal meningitis due to significantly increased mortality. \n\nlumbar puncture can be delayed , blood cultures should be obtained prior to antibiotic initiation Meningitis suspicion based on clinical features. Brain MRI shows parts of cortex next to the midbrain \n\nthat are WHITE . Dx? \n\nTemporal Lobe Meningitis/Encephalitis (due to Herpes) \n\n MRI preferred over CT for HSV encephalitis \n\n What is the most common neurologic sequelae of meningitis ?\n\nHearing loss --> all children with bacterial meningitis should have close developmental f/u and \n\naudiologic testing \n\nGive dexamethasone for children with Hib meningitis to avoid hearing loss \n\n662 https://t.me/usmleinnercircle \n\nBacterial meningitis \n\n Fever \n\nClinical Increased intracranial pressure (eg, vomiting, altered mental \n\nfeatures status , headache) \n\n Meningeal irritation (eg, nuchal rigidity) \n\n Hearing loss (most common) \n\nComplications Intellectual disability \n\n Cerebral palsy \n\n Epilepsy \n\nTuberculous meningitis \n\n# . Hematogenous spread of Mycobacterium tuberculosis to subarachnoid space \n\nPathophysiology Most commonly presents 2-6 months after primary infection .. Stage 1: several weeks of nonspecific fever, headache, drowsiness \n\nClinical . Stage 2: overt meningitis with lethargy, nuchal rigidity, vomiting , cranial nerve palsie s, or other focal neurologic signs \n\nmanifestations . Stage 3: coma, herniation, death \n\n# . CSF lymphocytic pleocytosis, t protein , t glucose \n\nDiagnosis . Positive acid-fast bacillus culture or PCR test from CSF \n\n Tuberculin skin testing or interferon-gamma release assay may be falsely negative \n\n# . Combina ti on antimycobacterial therapy \n\nTreatment . Glucocorticoids to reduce CNS swelling \n\nCSF = cerebrospinal fluid ; PCR = polymerase chain reaction . CNS, Eye, Ear Brain Abscess \n\n Diagnosis requires CT-guided aspiration or surgical biopsy to obtain tissue for Gram stain and culture \n\n663 https://t.me/usmleinnercircle USMLE Inner Circle \n\nTuberculous meningitis \n\n# . Occurs in ~5% of patients with disseminated TB \n\nEpidemiology j Risk with HIV, immunomodulatory medications, malnutrit i on, substance abuse .\n\n Subacute fever, vom iting, headache , lethargy \n\nManifestations . Cranial nerve palsy Stroke \n\n# . Imaging: basilar meningeal enhancement & hydrocephalus \n\nDiagnosis CSF: WBC count 100 - 500/mm 3, mildly j protein ,! glucose , j adenosine deaminase \n\n# . NMT or AFB CSF smear \n\nAFB = acid-fast bacillus; CSF = cerebrospinal fluid ; NAAT = nucleic acid amplification test; TB = tuberculosis; WBC = white blood cell. \n\nBrain abscess* \n\n Vi ri dans streptococci Microbiology Staphylococcus aureus \n\n Gram-negative organisms Direct from adjacent infecti on Pathogenesis (eg, sinusitis, otitis, dental infection) Hematogenous from distant infection (eg, endocarditis, osteomyelitis) Headache Fever (~50%) \n\nManifestations Focal neurologic deficits, seizure Brain imaging (CT scan, MRI): ~1 ring-enhancing lesion with central necrosis \n\nTreatment Prolonged antibiotic therapy Aspiration (or surgical drainage) \n\n'A single abscess usually indicates direct spread; multiple abscesses are usually hematogenous. \n\nRisk factors for brain abscess Predisposing problem Pathogenesis Affected area(s) \n\nOtitis media, mastoiditis Direct sp read Tempor al lobe, ce rebellum Frontal or ethmoid si nusitis Direct sp read Frontal lobe Den ta l infection Direct sp read Frontal lobe Bacteremia from other Mu ltiple abscesses along sites of infection, cyanotic Hematogenous distribution of middle sp rea d ce rebral a rt ery (gray-white heart disease matter junction) \n\nRisk factors for brain abscess \n\n(DUW011d CNS, Eye, Ear What is the likely diagnosis in a child with a history of tetralogy of Fallot and recurrent sinusitis that presents with a two-week history of worsening morning headaches , fever , and a recent first-time seizure ?\n\nBrain abscess \n\n Congenital heart disease and Recurrent sinusitis are important predisposing factors for brain abscess \n\nSpinal Epidural Abscess \n\n664 https://t.me/usmleinnercircle \n\n> Left temporal lobe brain abscess\n\nCNS, Eye, Ear Emergency surgical decompression: Laminectomy , which removes the roof of the spinal canal, and drainage of the suppurative fluid collection relieve pressure on the spinal cord. This may prevent permanent neurologic impairment when done early in the course of the illness (eg, \n\n<24 hr of onset of neurologic deficits ). \n\n Fever is most commonly absent , but patients often have other signs of infection (eg, leukocytosis , elevated ESR ) Trauma is a significant risk factor for SEA via development of a hematoma that may expand and become infected. \n\n665 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSpinal epidural abscess \n\n# . Staphylococcus aureus (65%) \n\n# . lmmunosuppression (HIV, diabetes, alcohol use , old age) \n\n# . Inoculating sources \n\nEpidemiology Distant infection (eg , cellulitis, joinUbone) 00 Spinal procedure (eg , epidural catheter) \n\n0 Injection drug use \n\n# . Classic tr iad \n\n0 Fever ( -50 %) \n\nManifestations 0 Focal/severe back pain \n\n0 Neurol 29 ic findin gs (eg, motor/sensory change, bowel/bladder dysfunction, paralysis) . j Erythrocyte sedimentation rate \n\nDiagnosis . MRI of the spine with contrast \n\n# . Blood & aspirate cultures \n\nTreatment . Broad-spectrum antibiotics (eg , vancomycin + ceftriaxone) \n\n# . Urgent aspiration/surgical decompression \n\nSpinal ep i dural abscess CNS, Eye, Ear If an SEA is suspected, lumbar puncture is contraindicated due to the risk of inoculating the cerebral spinal fluid during the procedure. \n\n## Brain Herniation Miscellaneous \n\nAgeing \n\n Normal aging includes a slow decline of executive functioning, attention span, and problem-solving after age 70 years. The central nervous system is affected greatly by the aging process, and there are characteristic findings consistent with normal aging that every physician should be familiar with. \n\n666 https://t.me/usmleinnercircle \n\nClinical features of brain herniation Herniation type Common features \n\n## . He rni ation of cingulate gyrus underneath falx cerebri \n\nSubfalci ne . No pu pi ll ary involvement, consciousness often preserved \n\n## . Contralateral leg weakness (ipsilateral ACA compression) \n\n## . He rni ation of un cus (medial temporal lobe) under tentorium cerebelli \n\n## . lps il ateral dilated & fixed pupil (i psilateral oculomotor nerve [CN Ill] compression) \n\nUncal . Early: contralateral hemiparesis (i psi lateral cerebral peduncle compression) \n\n## . Lat e: ipsilateral hemiparesis (contra lateral cerebral peduncle compression) \n\n## . Caudal displacement of diencephalon & brainstem \n\nCentral . Rupture of paramedian basilar artery branches \n\n## . Bi lateral m id position & fi xed pupils (loss of sympathetic & parasympathe ti c innervation) \n\n## . Decorticate (flexor) - decerebrate (extensor) posturing \n\nTonsillar . Herniation of cerebellar tonsil s through foramen magnu m \n\n## . Coma, loss of CN reflexes, flaccid paralysi s, respiratory arrest (b rai nstem compression) \n\nACA = anter ior ce reb ral artery; CN = cr anial nerve. Types of bra in herniati on \n\nEpidural \n\nhematoma CNS, Eye, Ear 1. One of the most common neurologic changes to occur is the loss of vibratory sensation , primarily in the distal extremities. 2. Decreased to absent deep tendon reflexes (DTR) (especially in the anKle). 3. Decreased pupillary response to light, presbyopia. and decreased hearing. \n\n4. As a patient ages, their gait often becomes broad-based and their stride shortens .\n\nTick Paralysis \n\n Tick-borne paralysis is characterized by rapidly progressive ascending paralysis , absence of fever \n\nand sensory abnormalities , and normal CSF exam. \n\nThe next best step is a meticulous search for a tick and removal of tick results in spontaneous improvement in most patients. \n\nGuillain-barre may be hard to distinguish but is usually not as rapid, is symmetric has CSF abnormalities, and autonomic dysfunction . A meticulous tick exam is easy to perform and should be done first. \n\n What is the likely diagnosis in a patient that develops asymmetric lower extremity weakness and diminished lower extremity DTRs , normal vitals, and normal CSF examination after returning from a hiking trip in the Northeast? \n\nTick-borne paralysis \n\ndue to neurotoxin release (requires 4-7 days of feeding); removal of the tick results in spontaneous improvement in most patients \n\nSkull Fracture \n\n Bilateral periorbital ecchymosis (\" raccoon eyes \") are associated with a anterior basilar skull fracture .\n\nPosterior basilar skull fracture will show Battle Sign \n\nCSF Rhinorrhea \n\n667 https://t.me/usmleinnercircle USMLE Inner Circle \n\nBasilar Skull Fracture \n\nh emotymponum Bott le ' s sign \n\nRaccoon eyes CNS, Eye, Ear CSF rhinorrhea can be evident immediately after the trauma or may have a delayed presentation (days to months) in which rhinorrhea is noted after acute edema resolves. \n\nVenous Sinus Thrombosis \n\nCavernous Sinus Syndrome \n\n668 https://t.me/usmleinnercircle \n\nCerebrospinal fluid rhinorrhea \n\n## . Accidental trauma (most common) \n\nEtiology . Surgical trauma (eg, sinus surgery) \n\n## . Nontraumatic (eg, elevat ed intracranial eressure) \n\nClinical . Unilateral watery rhinorrhea with salty or metallic taste presentation . Possible complication: meningitis \n\n## . Test for CSF-specific proteins (~-2 transferrin, ~-trace protein) Evaluation . Imaging (with intrathecal contrast) . Endoscopy ( intrathecal fiuorescein dye )\n\n## . Bed rest, head of bed elevation, avoidance of straining \n\nManagement . Lumbar drain placement \n\n## . Surgical repair CSF = cerebra l spinal fluid. \n\nCerebral vein & venous sinus thrombosis \n\n## . Thrombophilia (eg, fac to r V Leiden) \n\nRisk . Pregnancy & postpartum \n\nfactors . Oral contraceptive pills . Mali gnancy . Infection Clinical . Headache, t ICP (eg, vomiting, papilledema) features* . Focal neurologic symptoms, seizures \n\n## . Encephalopathy \n\n## . MRI of the head with MR venography (t sensitivity) Diagnosis . CT scan of the head with CT venography (rapid, t availability) \n\n## . Elevated D-dimer (supports diagnosis) Treatment . Anticoagulation (unfractionated heparin or LMWH acutely) *Presentation is highly variable & often mixed, dep endi ng on thrombus l ocat ion/distribution. ICP = intracranial pressure; LMWH = l ow molecul ar weight hepari n. \n\nThrombosis of cerebral veins and venous sinuses \n\nCortical veins Sup e rior sagittal sinus (cortical venous & CSF drainage) Motor defici ts , seizures, intracranial HTN Straight si nu s & great v ein (midbrain RAS venous & CSF drai nage )Motor deficits, encephalopathy Transverse & sigmo id sinuses (final CSF drainage into IJ vein) \n\nIsolated intracranial HTN Cavernous sinuses (ophthalmic venous & CSF drainage) Eye pa in , chemosis, proptosis, dip lopia, \n\ncranial nerve deficits (CNs Ill, IV, VI, V1 , V2) \n\n\"Due to compression as the cranial nerves pass through the cavernous sinus CSF = cerebrospinal fluid; HTN hypertension: RAS : reticular activating system. CNS, Eye, Ear The diagnosis of cerebral sinus thrombosis is confirmed with MRI with venography .\n\nCT scan often shows no abnormalities Treat with heparin first \n\n D/D: Orbital Cellulitis: No Palsies, loss of sensation A patient was bitten by a bug on his right cheek. Now, both of his eyes are swollen and he has a constant headache . Exam shows erythema and swelling of the right cheek and bilateral eyelid edema. Bilateral extraocular movements are restricted , and his forehead and midface are bilaterally tender. Vitals show fever and tachycardia. What is the most likely diagnosis? \n\nCavernous Sinus Thrombosis \n\nCN III, IV, V, and VI pass through cavernous sinus, which has anastomoses crossing midline --thus, unilateral symptoms can rapidly become bilateral \n\nDistal Symmetric Polyneuropathy \n\n HIV neuropathy is thought to occur due to the accumulation of HIV antigens (eg, gp120) on distal sensory nerve fibers , which triggers macrophage/T-cell infiltration, cytokine release, and subsequent axonal damage. Motor neurons are relatively spared, motor strength is usually intact . Treatment with antiretroviral therapy reduces the risk of progression. Gabapentin is first-line to help reduce sensory symptoms \n\n669 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDistal symmetr ic polyneuropathy \n\n Diabetes me llitus (diabetic neuropathy) Long-standing HIV infection Uremia \n\nTriggers Medications (eg, fluoroquinolones, metronidazole) Chemotherapy (eg, cisplatin, paclitaxel) \n\n Toxicity (eg, alcohol abuse, heavy metal expos ur e) \n\nPathophysiology Damage to distal sensory peripheral nerve axons Symptoms begin in toes/feet; progresses proximally over time Distal numbness, tingling, pins & needles sensation \n\nManifestations \n\n ! Pain, temperat ur e, touch & vibration sensation ! Ankle/Babinski reflexes \n\nTreatment Treat underlying cause Pa in management: gabapentinoid, tricyclic antidepressant, duloxetine &/or capsaicin cream CNS, Eye, Ear Vasculitic neuropathies typically occur when vasculitis affects the vasa nervorum , leading to nerve ischemia. It generally occurs in the setting of systemic vasculitis (eg, polyarteritis nodosa) and results in a patchy, asymmetric neuropathy that affects several nerves (ie, mononeuritis multiplex); severe pain is a prominent feature. In addition, systemic symptoms (eg, fever , fatigue ) are common. \n\n Chronic, gradual: Systemic diseases \n\nAcute: Medication , Toxin \n\nConcussion \n\n Atypical signs that should prompt further evaluation with a head CT scan. \n\n1. Focal neurologic deficits ,2. depressed or worsening mental status, \n\n3. or signs of possible skull fracture (eg, battle sign, temporal hematoma) are What is the likely diagnosis in a patient that develops persistent headache , confusion , difficulty concentrating , and poor sleep for the past month after hitting their head? \n\nPost-concussive syndrome \n\nother manifestations include amnesia , vertigo , and mood alterations ; symptoms typically resolve with symptomatic treatment within a few weeks to months. Celiac Disease \n\n670 https://t.me/usmleinnercircle \n\nCauses of peripheral neuropathy \n\n# . Diabetes mellitus \n\nMetabolic . Hypothyroidism Vitamin B12 deficiency \n\n Alcohol use \n\nToxic . Medications (eg, phenytoin, disulfiram, platinum chemotherapy) \n\n# . Heavy metals \n\n# . HIV \n\nInfectious . Lyme disease \n\n# . Charcot-Marie-Tooth \n\nHereditary Porphyria (eg, acute intermittent porphyria) .. Idiopathic \n\nOther . Plasma cell disorders (eg, multiple myeloma, MGUS) \n\n> MGUS =monoclonal gammopath y of undetennined significance.\n\nConcussion \n\n# . Transient neurologic disturbance (eg, dizziness, disorientation, amnesia) after mild TBI \n\nClinical features \n\n No structural intracranial injury Remove from same-day physical play \n\n# . Neurologic evaluation \n\n# . Rest for .e24 hr \n\nManagement Gradual return to normal activity if symptoms do not worsen . 0 Physical: light aerobic exercise --+ noncontact sports --+ contact sports \n\n> 0\n\nNeurocognitive: limited screen time, school accommodations (eg, frequent breaks, shortened days) \n\nTBI ; traumatic brain injury. CNS, Eye, Ear The predominant finding in patients with concussions is headache , which typically develops shortly after the head trauma and may be triggered by physical or cognitive exertion , as well as visual tasks (eg, rapid eye movement between two points). \n\nLight and/or noise sensitivity is also common and may worsen the headache. \n\nTraumatic Brain Injury \n\nParoxysmal Sympathetic Activity \n\n Traumatic brain injury can cause damage to cortical areas responsible for inhibiting lower sympathetic centers. \n\nThis disrupted inhibition may result in paroxysmal sympathetic hyperactivity , a syndrome characterized by rapid-onset episodes of tachycardia , hypertension , and tachypnea often accompanied by fever and diaphoresis .These episodes, which can last up to 20-30 minutes, are usually triggered by external stimuli (eg, bathing, repositioning) but may occur spontaneously. \n\nTreatment consists of supportive care (eg, avoiding triggers, treating fever) and medication (eg, \n\nopioids , GABA-agonists, 2-agonists) to abort and/or prevent episodes \n\nComa \n\n671 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPostconcussion syndrome \n\n# . Nonadherence to gradual return-to-play protocol after concussion \n\nRisk factors . History of multiple concussions \n\n# . Prolonged (>4 weeks) concussion symptoms after mild TBI: 0 Headac he 0 Dizziness Clinical features 0 Sleep disturbance 0 Mood changes 0 Cognitive impairment \n\n# . No structural intracranial injury \n\n# . Symptomatic care \n\nManagement Activity as tolerated \n\nTBI = traum atic brain injury. Management of traumatic brain injury Goal Interventions \n\n Maintain MAP: isotonic fluids, vasopressor therapy \n\nMaintain CPP \n\n Reduce ICP: head e lev ation, sedation, osmotic therapy (eg, hypertonic saline, mannitol), decompressive (= MAP- ICP) interventions (eg , CSF removal, craniectomy) \n\nPrevent ICH Antifibrinolytic therapy (ie, tranexamic acid) within first 3 hr Reversal of preexisting anticoagulation Prevent seizures (eg, levetiracetam, phenytoin) \n\nOther \n\n Control blood glucose (eg, insulin to target 140-180 mg/dl glucose) \n\nmeasures \n\n Maintain normothermia (eg, antipyretics, surface-cooling devi ces )\n\nCPP = cerebral perfusion pressur e; CSF = cerebrospinal fluid; ICH = intracranial hemorrhage; ICP = intracranial pressure; MAP = mean arterial pressure. CNS, Eye, Ear Additional test that can be used to confirm brain death: Cerebral Blood Flow Studies like CT Angiography \n\n Brain death constitutes legal and clinical death and mechanical ventilation may be withdrawn without the family's permission Can a patient be diagnosed with brain death if they have intact deep tendon reflexes ?\n\nYes \n\nbrain death is characterized by absent cortical and brain stem function; the spinal cord may still be functioning \n\nPersistent Vegetative State is similar to person having consciousness but LACKS Awareness Diagnosed after >12 months \n\nVentriculoperitoneal Shunt \n\n672 https://t.me/usmleinnercircle \n\nDiagnosis of brain death \n\n# . Known cause (eg, TBI, stroke} \n\n# . Evidence (eg, clinical, neuroimaging) of devastating CNS event \n\nClinical criteria . Exclusion of confounding conditions (eg, electrolyte abnormality, intoxication, paralytics) \n\n# . Core temperature >36 C (96.8 F), SBP >100 mm Hg \n\n# . Coma Absent brainstem reflexes: 0 Pupillary 0 Corneal 0 Oculocephalic, oculovestibular \n\nClinical examination 0 Jaw jerk 0 Cough 0 Gag \n\n# . Absent brain-originating motor responses (including decerebrate & decorticate posturing) Apnea test: no respiratory response to PaCO 2 >60 mm Hg \n\n> *Movements originating from the spinal cord (eg, deep tendon reflexes) may still be present. SBP =syst oli cblood pre ss ure ; TBI =traum ati cbr ain inj ury .\n\n@ Bring the case to the hospital ethics committee 45% \n\nWhen ther e is a difference of opinion between the family and th e medical team over life-sustaining mea sur es in a pa tient with established br ain d ea th , th e American Medical Associat i on Principles of M edical Ethics recommend seeking consult ation from an independe nt , objective medium, like an ethics committee. However, not e th at it is medica lly appropriate to di sco nt inue th erapy after br ain d ea th . Technically, t he physician does not n ee d to obtain the family's perm iss ion to remove lif e suppo rt . Neverthel ess , recommenda tion s mos tly advo ca te an empathetic approach, whi ch meets th e fa mily 's emo ti onal n ee ds and tri es to reach a mu tual understanding. CNS, Eye, Ear Diffuse Axonal Injury \n\n673 https://t.me/usmleinnercircle USMLE Inner Circle \n\nEtiology .\n\n\n\nClinical features \n\nTreatment \n\nApproach to suspected vent ri culoperitoneal shunt complications \n\n Increased ICP (eg, headache, vomiting , lethargy) Focal neurologic deficits Fever Abdominal pain (peritonitis) Shunt se ri es (x-rays) Neuroimaging (CT' )\n\n Abdom inal ultrasound (for localized pain) Abnormal Hydrocephalus Shunt discontinuity Abdominal cyst Norma l J\n\n# j Recently placed shunt (l Risk of CSF shunt tap J+-- Yes - - vent ri culitis in first 6 months) \n\nI Persistent fevers without a source O bstruction \n\nl Pressure or no flow _. replace shunt \n\nInfection \n\nl Cell counts, ( +) culture \n\n-, remove/externa li ze sh un t, s ta rt IV antibiotics \n\n May use ultrasound if fontanelle open .CS F = cerebrospinal fl uid; ICP -== lntraa an lal pressure: tv = intravenous. INo \n\n+\n\nEvaluate for \n\nalternate ca uses Ventriculope ri toneal shunt Diffuse Axonal Injury \n\nHead trauma \n\nC,U\\No,ld \n\nAcceleration-deceleration or rotational shearing forces on axons (eg , at gray-white matter junction) Severe neurologic impairment (eg , GCS <8) Impairment greater than imaging findings MRI findings: \n\n0 Punctate hemorrhages in white matter \n\n0 Blurring of gray-white matter junction Supportive care, ICP management \n\nGCS = Glasgow coma scale; ICP = intracrani al pressure; MRI = magnetic resonance imaging . CNS, Eye, Ear What brain injury typically occurs from traumatic acceleration/deceleration shearing forces ?\n\nDiffuse axonal injury \n\npatients typically have coma with head CT showing diffuse small bleeds at the gray-white junction \n\nFacial Palsy \n\n Involvement of forehead helps differentiate Bells Palsy from Stroke .Punctate Hemorrhages at grey white junction \n\n674 https://t.me/usmleinnercircle \n\nManagement of unilateral facial weakness \n\nUn ilateral facial weakness \n\nRed flags absent Red flags present ILikely Bell pa lsy (acute, idi opat h ic CN VII mononeuropathy) \n\n# ! Eye protection: lu brication drops. eyes taped closed at night High - dose glucocorticoids +/ - antivirals \n\nWorsen ing over 3week s or no improvement over 4 mon ths \n\nt\n\nFurther workup \n\n(eg, imaging) Sparing upper f ac e F ocal neurological deficits \n\n# !MR I brain to rlo stroke Lyme endemic Hearing loss exposure Imbalance/Vertigo EM rash l Flu-like illness \n\n## i\n\nLyme MRI sku ll base to serology r/o CPA tumor EM = erythema m,g rans , C PA = cerebellopontine ang le ; GB S = Guillain-Barr~ syndrome. L ower limb weakness I Deep tendon reflexes \n\n## i\n\nLumbar puncture to r/o GBS \n\nC)UWorld CNS, Eye, Ear Thermoregulation Failure \n\n vs heat exhaustion , which typically presents with lower-grade fever (< 104 F) and no altered mental status \n\n675 https://t.me/usmleinnercircle USMLE Inner Circle \n\nNonexertional (classic) heat stroke \n\n## . El derly, obesity, poor physi ca l fitness \n\nRisk factors . Alcohol, medications (eg, diuretics, beta blockers, anticholinergics, stimulants) \n\n## . Hi gh temperatures, high humidi ty, la ck of air conditioning \n\n## . Temperature ~40 C (104 F) with CNS dysfunction (eg, encephalopathy, seizure) \n\n## . Ta c hy cardia, tachypnea, hypotension \n\nManifestations . Flushing, diaphoresis \n\n## . End-organ d ysf unction (eg, DIC, pulmonary edema, renal/ he patic dysfunction) \n\n## . Hemoconcentration (t hemoglobin, leukocytes, platelets, BUN) \n\n## . Stabilization (ie, ai rway, breathing , circulation) \n\nManagement . Rapid cooling (evaporative techniques are best tolerated in the elderly) 0 Antipyretics/dantrolene are NOT indicated . Management of end-org an compli ca tions \n\nBUN = blood urea nitrogen; DIC = diffuse intravascular coagulation. Exertional heat stroke \n\n# . Strenuous activity during hot & humid weather . Dehydr at ion, poor acclimatization \n\nRisk factors . L ack of eh :z: si ca l fit ne ss, obesi !X \n\n## . Medications: anticholinergics, an tihistamines, phenothiazines, tri cyc li cs , antipsychotics \n\n# . Core temperature >40 C (104 F) with CNS \n\nClinical dysfunction ( eg , AMS, seiz ur e) \n\nmanifestations . Organ or tissue damage: renal or hepatic failure, disseminated intravascular coagulation, acute respiratory distress syndrome \n\n## . Rapid coo ling: ice water immersion preferred; ca nconsider high-flow cold water dousing, ice-wet \n\nManagement towe l rotation, evaporative cooling . Fluid resuscitation , electrolyte correction \n\n## . Management of end-organ complications . No role for antipyretic therapy \n\nAMS = altered mental status. \n\nHeat exhaustion \n\n# . St renuous activity during h ot & humid weather . Dehyd ration, poo r acclimatization \n\nRisk factors . La ck of physical fitness, obesity \n\n## . Acute illne ss \n\n## . Medications : anticho linergics , anti hi stamines, phenothiazines, tricyclics, antipsychotics . Hyperth ermia S40 C (104 F) with normal mental status \n\n# . Profuse sweating \n\nManifestations . Nausea/vomiting . Headache , dizziness . Tachycardia, hypoten sion . Cool patient (eg, a ir conditioning, coo l water showe r) \n\nManagement Sa lt-containing oral fluids .CNS, Eye, Ear Cystic fibrosis may predispose patients to heat-related illnesses due to higher rates of sodium and chloride lost in sweat. What is the recommended cooling technique for patients with non-exertional heat strokes ?\n\nEvaporative cooling (e.g. spraying lukewarm water while fans blow air on skin) \n\npresents similarly to exertional heat stroke but typically affects elderly patients in the absence of strenuous activity \n\n What is the recommended cooling technique for patients with exertional heat strokes ?\n\nIce-water immersion \n\n Also admit to Hospital for observation What is the recommended initial management of frostbite ?\n\nRapid rewarming with warm water \n\nhowever, rewarming should not be attempted if there is a possibility of refreezing before definitive care can be provided Patients often have hypothermia as well -- treatment of hypothermia should be prioritized !Bradycardia seen with hypothermia is often refractory to treatment with atropine/cardiac pacing, but improves with correction of hypothermia \n\n676 https://t.me/usmleinnercircle \n\nClinical features of hypothermia Class ificat i on Mild: 32-35 C (90-95 F) Tachycardia, tachypnea \n\n> Ataxia, dysarthria, i nc re as ed s hivering Mod e rate:\n\n28-32 C (82-90 F) Bradyca rd ia, lethargy, hypoven til ation, decre ased shivering, \n\natrial arrhythmias \n\n> Severe :\n\n<28 C (82 F) Coma, cardiovascular collapse, ventr icu lar arrhyt hmias Tr e atment General \n\n Warmed (42 C (107 Fl) crystalloid for hypotension Endotracheal intuba ti on in comatose patients Rew ar ming techniqu es \n\n> Mild hypot he rmia: Passive external warming (remove wet\n\nclothing, cover with blanket s) Mod era te hypoth e rm ia : Active external warming (warm \n\nblanket s, heating pads, warm bath s) Severe hypotherm ia : Active inte rn al rewarming (warmed pleu ral or pe rit oneal irri gation, warmed h um idified oxygen) Frostbite Clinical . S up erficial pallor & an es th es ia \n\nfindings . Blistering, esc har fo rmation \n\n# . Deep tissue necrosis & mummification \n\n# . Rapid rewarm ing in wa t er ba th at 37- 39 C (9 8.6 - 10 2.2 F) \n\nManagement . Analgesia & wou nd care \n\n## . Angiography or t echnetium-99m scan to ass e ss for thrombosis if r ewarming is unsuccessful \n\n## . Thrombolysis in severe, limb-threatening cases CNS, Eye, Ear Amputation is not typically performed until all possible salvage options (eg, angiography, thrombolysis) have been exhausted and the affected tissues have been given time (often weeks to months) to fully demarcate. \n\n## CNS Drugs \n\n Typical antipsychotics should not be used in patients with Lewy body dementia because they may exhibit neuroleptic hypersensitivity. \n\nneuroleptic administration can cause severe parkinsonism and impaired consciousness \n\n Treatment for facial nerve palsy may include corticosteroids and acyclovir .\n\nmost patients have a gradual recovery of function The role of viruses in the development of idiopathic facial palsy is not yet fully understood and the benefit of antiviral medication is unclear at present. However, administration of acyclovir is recommended as a precaution in severe cases. \n\nAnti-Epileptic \n\n Phenytoin is highly protein-bound and metabolized hepatically by the cytochrome p450 system; medications that inhibit cytochrome p450 (eg, trimethoprim-sulfamethoxazole, fluconazole) or that displace phenytoin from plasma proteins (eg, valproic acid) increase the risk of drug toxicity. Common symptoms of acute phenytoin toxicity include horizontal nystagmus , ataxia , hyper-reflexia and nausea/vomiting , and significant toxicity can result in altered mental status, coma, and death. Prevent adverse effect of Phenytoin: Folate , Calcium , Vit D supplementation \n\nAnesthesia \n\n What anesthetic is associated with neurotoxicity in patients with vitamin B12 deficiency ?\n\nNitrous oxide \n\nN2O inactivates vitamin B12, resulting in inhibition of methionine synthase \n\n Severe hypotension due to myocardial depression is a common adverse effect of propofol .\n\n677 https://t.me/usmleinnercircle USMLE Inner Circle \n\nD ru g Action Side effects \n\nLevodopa plus Dopamine Somnole n ce , confusion , hallucinations carbidopa precursor (older patients) Dyskinesia Trihexyphenidyl Anticholinergic Dry mouth , blurred vision, constipation, or benztropine nausea & urinary retention Amantadine Unclear Ankle edema & livedo reticularis mechanism Apomorphine ,bromocriptine, D opamine Somnolence , hypotension & confusion pramipexole, agonist Hallucinations (older patients) or ropinirole Entacapone COMT inhibitor Dyskinesia, hallucinations, confusion , or tolcapone nausea & orthostatic hypotension Selegiline MAO B inhibitor Insomnia & confusion (elderly patients) CNS, Eye, Ear Therefore, propofol should be avoided or used with extreme caution in patients with ventricular systolic dysfunction. Delayed emergence from anesthesia is defined as the failure to return to consciousness within the expected window of the last administration of an anesthetic or adjuvant agent (typically 30-60 minutes). The etiology is often multifactorial, however; the presence of respiratory failure (eg, low pH, elevated pCO2, low pO2), bradypnea , and bradycardia suggests prolonged medication effect \n\nresulting in hypoventilation .\n\nEpidural \n\n Hypotension is a common side effect of epidural anesthesia due to sympathetic blockade producing venous pooling , venodilation , and arterial vasodilation .\n\nL5 Sympathetic nerve fibers responsible for vascular tone in lower limbs are blocked, causing vasodilation (venous pooling), decreased venous return, and decreased CO. \n\nCan result in maternal hypotension and decreased placental perfusion, as evidenced by recurrent late fetal heart rate decelerations .Management is with left lateral patient positioning , I V fluid bolus , and vasopressors (eg, phenylephrine). High spinal or total spinal anesthesia can occur if the epidural catheter accidentally punctures the \n\ndura and anesthetic enters the subarachnoid (ie, intrathecal ) space. \n\n678 https://t.me/usmleinnercircle \n\nEmergence from anesthesia Normal . Transition from general anesthesia to consciousness \n\nemergence . Most patients fully awake within 15 min of extubation \n\n# . Delayed emergence: hypoactive state, somnolence persisting >30-60 min \n\n# . Emergence delirium: hyperactive state, usually manifests in the OR \n\nInadequate Reassure & reorient: most cases are temporary & due to anesthet jc effects .emergence Evaluate for serious underlying conditions (eg, oxygenation , metabolic, or neurologic factors) & causes of . discomfort (eg , acute pain, bladder distension) \n\nOR = operating room . Labor epidural analgesia Subarachnoid space \n\n> T10-L 1: blocks pain fibers during first stage of labor\n> L2 -L5 : blocks sympathetic fibers responsible for lower extremity blood vessel tone\n> S2-S4: blocks pain fibers during second stage of labor\n> uw orld\n> High spinal anesthesia\n> Subarachno id space Ep idural space Dura\n> C3-C5 :dysphag ia, resp iratory paralys is\n> Normal obs tet ric neurax ial anesthesia distribution :up to T10 (vaginal delivery) orT4 ( cesarea ndelivery)\n\nCNS, Eye, Ear Patients often have an exaggerated ascending paralysis with upper extremity weakness (eg, C5-C7 blockade) and respiratory paralysis due to blockade of the diaphragm (eg, C3-C5). Leakage of CSF after epidural placement may result in postural headaches , which are worse with sitting up and better with lying down .\n\noccurs if the dura is mistakenly punctured during epidural placement \n\n A 40 week gestation patient receives epidural with test dose of lidocaine and epinephrine . She immediately has tinnitus, perioral numbness and metallic taste in mouth . Pulse is 110, BP 140/100. What is the most likely cause ?\n\nSystemic toxicity of local anesthetic sec to inadvertant injection into blood vessel \n\nCan also cause Seizure \n\nT/t: Drug Cessation , Supportive care \n\n Spinal epidural hematoma is a potential complication of neuraxial anesthesia (eg, epidural block), lumbar puncture, or spinal surgery and is more common in older adults taking antithrombotic \n\nmedications .Manifestations include slowly progressive motor and sensory dysfunction and localized back pain ; bowel and bladder dysfunction may occur. Management includes an urgent MRI and neurosurgical decompression. \n\nMalignant Hyperthermia Hypercapnia (being the most reliable indicator) \n\n679 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPos td ural puncture headache \n\n After lumbar puncture or neuraxial anesthesia \n\n# . Positional (worse when upright, improves when supine) \n\nClinical features . Neck stiffness \n\n# . Photophobia, dip lo pia \n\n# . Hearing loss, tinnitus \n\nManagement Typically self-limited \n\n# . Epidural blood patch \n\nMalignant hyperthermia \n\n Genetic mutation alters cont ro l of intracellular calcium \n\nEpidemiology Triggered by volatile anesthetics, succinylcholine, excessive heat Masseter muscle/generalized rigidity Sinus tachycardia \n\nManifestations Hypercarbia resistant to increased minute ventilation Rhabdomyolysis Hyperkalemia Hyperthermia (late manifestation) Respiratory/ventilatory support \n\nTreatme nt Immediate cessation of causative anesthetic Dantrolene CNS, Eye, Ear Ass with significantly elevated CK (can reach >10,000-20,000 U/L )\n\n Neuroleptic malignant syndrome has a similar presentation to MH (eg, fever, muscle rigidity), it is triggered by neuroleptic agents (eg, haloperidol, promethazine) rather than anesthetics. In addition, it develops over the course of days, not minutes. \n\nNeuroMuscular Blockers \n\n What cardiac complication is associated with succinylcholine in patients with skeletal muscle trauma ?\n\nCardiac arrhythmia \n\nsecondary to hyperkalemia due to efflux of K+ ions following binding of succinylcholine to post-synaptic ACh receptors; also may occur in patients with burn injury and stroke \n\n## Paeds \n\n680 https://t.me/usmleinnercircle \n\nFused cor ona l\n\nLeft anterior plagiocephaly Types of plagiocephaly Normocephaly Right posterior plagiocephaly \n\nL_ Craniosy nostos is __J \n\nFrontal boss i ng \n\n/, \n\nPositional plagiocephaly \n\n> C) U-l d\n\nFetal alcohol syndrome \n\nMicrocephal) Sma ll pa lp ebra lfi ss ur es Smooth philtrum \n\n\"\"\"\"\"-.. - ~-----;-\" -,--'---- Th in \n\nvermilion border \n\nCommon causes of intellectual disability Syndrome Dysmorphic features Comorbid conditions \n\n## . Upslanting palpebral fissures Heart disease (eg, AV canal defect) Flat nasal bridge .Down syndrome . Short stature, obesity Epicanthal folds .. Hearing loss Single palmar crease ... Long face with prominent chin & forehead Self-injurious behavior (eg, hand biting) Large , protruding ears .Fragile X syndrome . Anxiety, autistic behaviors Macroorchidism .. . Tall stature . Macrocephaly \n\n## . Smooth philtrum Seizures .Fetal alcohol syndrome . Thin vermillion border . Growth restriction . Sma ll palpebral fissures \n\nAV = atr iov entricular. CNS, Eye, Ear Spina Bifida \n\n Spinal cord stretching leads to tethered cord syndrome: Back pain caused by spinal cord traction and exacerbated by activities that further stretch the cord (eg, bending forward ). Pain can radiate down the buttocks/legs. Lower extremity lower motor neuron signs (eg, hyporeflexia , weakness ) due to spinal dysfunction below T12/L1. Denervation and weakness can cause gait abnormalities and muscle atrophy .\n\nFoot deformities from peroneal muscle weakness (eg, pes cavus [high arch]) or tight foot ligaments (eg, hammer toe), as seen in this patient. \n\nBladder dysfunction (eg, urinary incontinence) due to detrusor underactivity and/or sphincter incompetence. \n\n681 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nClosed spinal dysraphism \n\n# . Failure of posterior vertebral arch fusion \n\nPathophysiology Spinal cord anomalies (eg, lipoma, cyst) . Stretch-induced distal spinal cord dysfunction (tethered cord) . May be asymptomatic . Cutaneous, lumbosacral anomalies (eg , hair tuft, mass) \n\nClinical features Tethered cord syndrome*: \n\n0 Neurologic: LMN signs (weakness, hyporeflexia) \n\n0 Urologic: incontinence/retention; recurrent UTI \n\n0 Orthopedic: back pain, scoliosis, foot deformities \n\nManagement . MRI of the spine . Surgical detethering of cord if symptomatic *Age of onset & organ system involvement are variable. \n\nLMN =lower motor neuron; UTI =urinary tract infection. \n\nSpina bifida \n\nNormal spine Spina bifida occulta Meningocele \n\nClosed sp inal dysraphism Common dermatologic manifestations of closed spinal dysraphism (spina bifida occulta) Dimple (>5 mm long & \n\n>2.5 cm above anus) Hair tuft Spinal process defect Myelomeningocele Myeloschisis \n\nOpen spinal dysraphism CNS, Eye, Ear Head Trauma \n\n What is the next step in management for a child that presents to the ED with signs of mild traumatic brain injury (TBI)? \n\nHead CT without contrast or observation for 4 - 6 hours \n\nsigns of mild TBI include GCS score of 13 - 15, loss of consciousness for < 5 minutes, headache, and vomiting \n\nHydrocephalous in those without these symptoms: Observation only \n\n682 https://t.me/usmleinnercircle \n\nChronic back pain in adolescents Diagnosis Clinical fea t ures Nocturnal pain Malignancy Systemic symptoms Neurologic findings if spinal cord is involved New-onset scoliosis Back/leg pa in worse with ac tivity Tethered cord Neurologic findings (eg, weakness, h yp oreflexia) \n\n(spinal dysraphism) New-onset scoliosis Lumbosacral cutaneous abnormality Chronic multifocal osteomyelitis Nocturnal pain Systemic symptoms Spondylosis & spondylolisthesis Occurrence following repetitive trauma (eg, gymnastics) Pain with extension Inflammatory arthritis Morning stiffness Pain worse at r es t\n\n(eg, ankylosing spondylitis) Sacroiliac joint tenderness \n\nPediatric traumatic brain injury (PECARN rule) \n\n Altered mental status (fussy behavior) \n\n# . Loss of co nsciousness \n\nHigh-risk features Severe mechanism of injury (fall >0.9 m (3 ft], high impact, MVC) .age <2 Nonfrontal scalp hematoma .. Palpable skull fracture \n\n## . Altered mental status (eg, somnolence, agitation) . Loss of co nsciousness \n\nHigh-risk features Severe mechanism of injury (fall >1.5 m (5 ft ], high impact, MVC) .age ~2-18 Vomiting, severe headache .. Basilar sk ull fracture signs (eg, CSF rhinorrhea) \n\nManagement . Head CT scan wi thout contrast \n\n1:\n\nCSF ;;; cerebrospinal fluid; MVC ;;; motor vehicle collision. II CNS, Eye, Ear While the cranial sutures are still open during infancy, hydrocephalus typically results in a rapidly enlarging HC and a full or bulging fontanelle. Once the anterior fontanelle closes, between age 12 and 15 months , children who develop hydrocephalus are more likely to present with signs/symptoms of increased intracranial pressure .\n\n Pressure on the midbrain may also cause upward gaze impairment (ie, persistent downward gaze). \n\nMicrocephaly \n\n683 https://t.me/usmleinnercircle USMLE Inner Circle \n\nHydrocephalus in children \n\n## . Impaired CSF circulation (obstructive, most common) \n\nCauses . Impaired CSF absorption \n\n# . Excessive CSF production \n\n## . Head examination \n\n0 Rapidly enlarging head circumference &/or macrocephaly \n\n0 Prominent scal p veins \n\n0 Full anterior fontanelle (if open) \n\nClinical manifestations . Behavioral changes &/or developmental delay \n\n## . Lower extremity weakness & spasticity \n\n# . Signs of increased ICP* \n\n0 Headache, vomiting \n\n0 Papilledema, impaired upward gaze \n\n0 Hypertension, bradycardia \n\n# . Neuroimagi ng \n\nEvaluation 0 Ultrasonography (if fontanelle is open) or ultrafast MRI \n\n0 CT scan for signs of acutely increased ICP *May not be present if the anterior fontanelle is open .\n\nCSF =cerebrosp in al fluid; ICP =intracranial pressure. Signs of increased intracranial pressure Wide, bulging fonta nelle ------Increased head \n\nci rcumfe rence - - '- _ ...... __ \n\nSevere hydrocephalus in a newborn \n\nUWorl d\n\nP rom inent \n\nscalp ve i ns CNS, Eye, Ear Findings consistent with benign microcephaly include: \n\nAbsence of dysmorphic features \n\nNormal head shape and neurologic examination Normal development \n\nAbsence of rapidly declining growth percentiles: 2 major percentiles \n\n MRI is preferred over CT scan because MRI lacks ionizing radiation and is more sensitive in identifying infarction or structural abnormalities. \n\nMacrocephaly \n\n Macrocephaly is defined as an HC >97th percentile for age and sex and may be the presenting sign of hydrocephalus Examination findings that are reassuring for benign macrocephaly include the following: Normal development No syndromic features No signs of increased intracranial pressure (eg, bulging fontanelle) No signs of infection (eg, fever, lethargy) USG can be done to rule out other causes of macrocephaly if suspected otherwise no workup needed \n\nCephalohematoma \n\n684 https://t.me/usmleinnercircle \n\n\n\n\n\n\n\n\n\n\n\n\n\nEvaluation of microcephaly \n\n> HC be low 3rd percentile\n\n## ! \n\n> Se ri al HC measurements across\n> ~2 dec li ning major percentiles OR N eu rologic symptoms (eg,\n> developmental ~ .h~\n> OR D ys morphic fea tures\n> r--No Yes --i\n> Measure &plot parents' HC s(benign familia l microcephaly) Order MRI of the brain (eg, perinatal stroke, co ngeni ta l malformation) Monitor growth &development Eva lu ate for congenital infection Order genetic testing (if dysmo rp hic features present)\n> For m,croceobalv on se tat bi rt hwith 'i: Ymme tcic orowth res triction .systemic features (eg ,hepatosplenomegaly) , h earing loss , or risk fadors (eg, maternal infection) .\n> HC :head a rcu mference CUWorld\n\nCNS, Eye, Ear What is the diagnosis with fluctuant scalp swelling that can move, cross suture lines , and expand for days after delivery? Associated with tachycardia and pallor secondary excessive blood loss? Subgaleal hemorrhage D/D: Infants who do not receive the routine intramuscular vitamin K injection at birth are at risk for bleeding between weeks 1 and 4 of life. Early-onset (<24 hr) bleeding due to vitamin K deficiency can occur with use of certain prenatal medications (eg, anticonvulsants ), that limit vitamin K action. \n\nStroke Both resolve spontaneously M/C: SCD \n\n685 https://t.me/usmleinnercircle USMLE Inner Circle \n\nLocation ...Clinical features ..\n\nPrognosis .\n\nCephalohematoma versus caput succedaneum \n\nSubperiosteal bleed that does not cross suture lines Edema/ hematoma above periosteum that crosses suture lines \n\nCephalohematoma Caput succedaneum \n\nNeonatal scalp swelling Caputsuccedaneum Cephalohematoma Subgaleal hemorrhage \n\nSubcutaneous . Subperiosteal (between skull & periosteum) . Between periosteum & gala aponeurotica Present at birth . Present hours after birth . Can expand over days Soft, boggy . Firm, nonfluctuant . Soft, fluctuant Crosses sutures . Does not cross sutures . Diffuse, crosses sutures Overlying skin is normal . Overlying skin is normal . Overlying bruising \n\n# . i Hyperbilirubinemia risk Self-resolves in days Can cause life-threatening blood loss \n\n# . Resorbs within a month \n\nCommon etiologies of pediatric stroke \n\n Sickle cell disease Prethrombotic disorders Congenital cardiac disease Bacterial meningitis Vasculitis Focal cerebral arteriopathy Head/neck trauma CNS, Eye, Ear In pediatric patient with suspected Acute Ischemic Stroke , MRI with MR angiography (MRA) should be urgently performed. \n\nDO NOT assume Todd Paralysis after seizures before ruling out AIS via MRA \n\nHemiplegia \n\n What is the likely diagnosis in a child that presents with unilateral hemiparesis that self-resolved within four hours following a seizure? \n\nTodd paralysis \n\nother causes of paralysis should be ruled out if there is no clear history of a preceding seizure (e.g. \n\nCT scan/MRI to evaluate for stroke )\n\nIntraventricular Hemorrhage \n\n686 https://t.me/usmleinnercircle \n\nHemorrhagic stroke in children \n\n Vascular malformations \n\nRisk factors o AVM (isolated or associated with HHT) o Aneurysm \n\n## . Hematologic abnormalities (eg, hemophilia, sickle cell disease) \n\n## . Headache , vomiting \n\n## . Seizure \n\nClinical features . Focal neurologic deficits \n\n Altered mental status \n\nImaging . Head CT scan: intraparenchymal , intraventricular, or subarachnoid hyperdense fluid collection \n\nManagement . Supportive (eg, antiepileptics) \n\n## . Reduction of intracranial pressure (eg , elevate head of bed, surgical decompression) AVM = arteriovenous malformation; HHT = hereditary hemorrhagic telangiecta si a. \n\nAcute causes of hemiplegia in children \n\nCause Historical clues Key findings \n\n## . Prothrombotic disorder (eg , ATIII deficiency) lschemic stroke . Cardiac disease (eg , PFO) . Focal infarct on brain imaging \n\n Vasculopathy (eg , S CD )\n\n## . Recent trauma lntracranial hemorrhage . Bleeding disorder (eg , hemophilia) . Hemorrhage on brain imaging \n\n# . Signs of i ICP (eg , vomiting , bradycardia) \n\nSeizure (Todd paralysis) . Symptoms preceded by limb jerking or loss of consciousness Symptoms self-resolve Presence of postictal confusion ... Onset in adolescence Hemiplegic migraine . Positive family history . Symptoms self-resolve \n\n## . History of h eadache with aura ATIII = antithrombin Ill; ICP = intracranial pressure ; PFC= patent foramen ovale; SCD = sickle cell disease. CNS, Eye, Ear Diagnosis? Cranial doppler ( up to one-half are clinically silent so routine U.S is performed in premature infants before 30-32 weeks )\n\nGenerally begins to involute around 28 weeks Neonatal intraventricular hemorrhage may be complicated by communicating hydrocephalus. The incidence of neonatal intraventricular hemorrhage may be reduced by preventing preterm labor and administering antenatal maternal corticosteroids . What is the next step in management for an infant that presents with poor feeding ,a bulging anterior fontanelle , and increasing head circumference ?\n\nCT scan of the head \n\nCT preferred in a symptomatic child; MRI is preferred if the patient is stable and asymptomatic to spare radiation exposure Per AMBOSS: < 6 mo = Ultrasound, > 6 mo = CT/MRI \n\nPaeds Seizures \n\nInfantile Spasms (West Syndrome) \n\nSymptoms? <1 yo with symmetrical limb jerking, not generalized, (-) fever \n\nDiagnosis? Interictal EEG with hypoarrhythmia \n\nTreatment? ACTH \n\nLennox Gastaut Syndrome \n\nAge? 3-5 years ( vs. <1 year in West Syndrome )\n\nPatient? Development delay or loss of milestones after onset of seizures Interictal EEG: a slow spike-and-wave pattern. \n\nTreatment: Anti-convulsant therapy, ketogenic diet \n\nFebrile Seizures \n\nWhat are the diagnostic requirements and treatment for simple febrile seizure ?Head USG \n\n687 https://t.me/usmleinnercircle USMLE Inner Circle CNS, Eye, Ear All 3 required : 1 in 24 hours, <15 min, generalized Lorazepam (benzo) to abort Acetaminophen (anti-pyretic )\n\nNo imaging required Complex ?Missing any of the above requirements \n\nBenzo to abort \n\nLP (r/o meningitis, encephalitis )\n\nEEG Imaging (CT/MRI )\n\nFollow-up ? Reassure parents low-risk of FND \n\n What is the next step in management for a child that presents to the ED after a transient simple febrile seizure ?\n\nReassurance \n\nCerebral Palsy \n\n688 https://t.me/usmleinnercircle \n\n\n\n000Febrile seizure Risk factors . Fever (typically wi th vi ral illness) . Family history of seizures \n\n Age 6 months to 5 years \n\nDiagnostic criteria . No previous afebrile seizure . No signs of CNS infection . No acute metabolic cause (eg, hypoglycemia) \n\n Abortive therapy (6 months) \n\nAbnormal tone \n\nInfants with CP may initially be hypotonic, but spasticity typically develops with time. Increased tone is accompanied by hyperreflexia and often clonus. What is the likely diagnosis in a non-dysmorphic infant that presents with bilateral lower extremity hypertonia and hyperreflexia with equinovarus deformities of both feet? \n\nCerebral palsy (Spastic Diplegia subtype) \n\nCP is a disorder of non-progressive motor dysfunction; other subtypes of cerebral palsy include dyskinetic and ataxic \n\n## EYE \n\n Argyll-Robertson pupil is a pupil that has a functional accommodation reflex , but no light reflex. Equinovarus \n\n689 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCerebral palsy Cerebral palsy \n\n Prematurity Etiology* Imaging findings Risk factors Low birth weight Intrauterine infection Prematurity/ . Periventricular leukomalacia \n\n Perinatal asphyxia low birth weight . lntraventricular hemorrhage Delayed motor milestones --, u..,-.1.lc. lro N>il ov.. \n\nClinical features Abnormal tone, hyperreflexia (_~-Col~)~ lJ..N I Ill~ \n\n Comorbidities: seizures, intellectual disability \n\nHypoxic-ischemic . Watershed injury \n\ninjury . Basal ganglia/thalamic lesions \n\nDiagnosis Clinical (usually by age 1-2) Brain MRI (eg~ ventricular leukomalacia, basal ganglia lesions) \n\nPerinatal stroke . Vascular distribution \n\nIntrauterine Prognosis Permanent, nonprogressive deficits I infection . Calcifications (eg, cytomegalovirus , toxoplasmosis) \n\nJ\n\nLo.OIi. Cl\\ C..r-is ~bili~ *Etiology is often multifactorial & the underlying cause may not be identified . \n\n,Jr Tit.. .wk c.b' I)~ '!>~'- ~_io~ P-><>~ , Ti~'\"'\"'~ \n\nJ, \n\nDeblA.o'(> ~[.c-~1 ~ , ~o-\\.(. \n\nJ, \n\n'1., {'fv.,J:;t..k ~V\\L c..n...t\" s.eo.'fu\"f ~.t~ \n\nCNS, Eye, Ear seen in neurosyphilis and diabetes \n\n What is the next step in management for a patient that woke up with a \"red eye\" (pictured below)? He does not complain of any symptoms. \n\nObservation \n\nspontaneous subconjunctival hemorrhages are benign and require no treatment \n\nCan also occur in neonates as they pass through the vaginal canal! \n\n Chemical burns to the eye are vision-threatening emergencies. The most important and urgent step in management is copious irrigation to normalize the pH. Marcus Gunn (RAPD) \n\n690 https://t.me/usmleinnercircle \n\nArgyll Robertson Pupil \n\n> While AR pupils are smalle than norm a l, they do not constrict when expose dto li ght\n> IV tube\n\nEye irrigation devices Nolight Normal Response to Light Positive \n\nRAPD of Right Eye /I \n\n> Mor gan lens\n> SU.nlotdMtdldne2S 9\n\nCNS, Eye, Ear Ambylopia Due to UV light exposure \n\n691 https://t.me/usmleinnercircle USMLE Inner Circle \n\nLens dislocation {ectopia lentis) \n\n# . Detachment of lens from ciliary body \n\nPathogenesis . Blunt ocular trauma (forceful projectile) \n\n# . Genetic condition (eg, Marfan syndrome) \n\n## . Painless vision loss \n\nClinical features . Tremulous iris with eye movement \n\n## . Lens displacement on slitla mp examination \n\n# . Glasses to correct refractive error \n\nManagement . Surgical correction \n\n# . Assessment for underl ::t ing condition if trauma is mild or absent \n\nMyopia (nearsightedness) \n\n# . Caused by increased axial length of eye (most common) or corneal protrusion \n\nPathophysiology Results in refracted image focused anteri or to retina .. New-onset incidence highest in adolescents \n\nEpidemiology . Severity typically stabilizes by early adulthood \n\n# . Risk factors: positive family history, East Asian descent \n\n# . Blurred distance vision \n\nClinical features . Normal near vision \n\nManagement . Prescription lenses with diverging (concave) lenses \n\n## . Retinal detachment \n\nComplications* Macular degeneration .\n\n*Associated with high myopia (ie, .?6 diopters of correction). CNS, Eye, Ear Glaucoma \n\n Topical glucocorticoid eyedrops and systemic glucocorticoids can raise intraocular pressure ( IOP ), leading to open-angle glaucoma (OAG) .OAG is usually characterized by insidious loss of peripheral vision , and some patients with steroid-induced OAG may develop central blurriness due to corneal edema .IOP can be measured with tonometry .\n\n692 https://t.me/usmleinnercircle \n\nAmb lyopia \n\n# . Functional reduction in visual a cui ty due to visual disturbances in ear ly childhood \n\nDefinition . Unilateral (most common): 2:2-line difference in vision between eyes (eg, 20 /3 0 & 2 0/ 50) . Bilateral: vis ion worse than 20/40 at age 2:4 \n\n# . Strabismus \n\nEtiology . Asymmetric refractive error . Visi on deprivation (eg , cataracts, ptosis) \n\n## . Corrective lenses . Encourage use of amblyopic eye \n\nManageme nt 0 Patching eye wi th better vision \n\n> 0\n\nCyclopl eg ic drops to bl ur normal eye \n\n## . Sur gery (eg, cataract r emova l) \n\nGlaucoma in children \n\n Optic neuropathy j IOP Causes: \n\n> 0\n\nImpaired drainage of intraocu lar fluid \n\nPathophysiology 0 Primary anato mic abnormali ty (eg, angle dysgenesis) \n\n> 0\n\nSturge-Weber syndrome \n\n> 0\n\nTu mor , t ra u ma , infection involving the angle \n\n> 0\n\nCorticosteroid-induced \n\n Tearing, pho to phobi a, bl ep harospasm Enlarged cornea and/ or globe \n\nKey features Optic nerve cupping \n\n Tonometry: i IOP Surgery \n\nManageme nt Pressure-reducing eye drops \n\nIOP = intraocular pressur e. Optic d isc in gl aucoma Normal Cup: di sc ra tio <0.5 Clear d isc rim Open-angle glaucoma Enl arged cup with cup:disc ra t io >0 .6 \n\nIncrease in cup size over time \n\nTh inn ing of d isc r im Pale disc (opt ic ne rve atrophy) \n\n1:CNS, Eye, Ear Glaucoma is associated with progressive peripheral visual field loss if untreated. \n\nversus macular degeneration , which causes progressive central visual field loss \n\nClosed Angle \n\nWalking into dark room can precipitate pain because of pupillary dilation causing loss of outflow \n\n Permanent cure is offered with laser peripheral iridotomy. \n\nCorneal Abrasion \n\n If initial pen light exam does not reveal any conjunctival and corneal abrasions or foreign bodies, proceed with fluorescein examination. \n\nFluorescein stains corneal basement membrane but not intact corneal epithelium Concentrated uptake of fluorescein with subsequent clearing in a waterfall pattern indicates full-thickness corneal laceration with Open Globe Injury. This, caused by washout from leaking aqueous humor, is known as Seidel sign and should prompt \n\nemergency ophthalmology consultation. \n\n Suspected OGI is a contraindication for Fluorescein Examination btw \n\n693 https://t.me/usmleinnercircle USMLE Inner Circle \n\nAngle-c lo sure glaucoma Clini ca l features . Symptoms: headache, oc ul ar pain, nausea, decreased visual acuity \n\n## . Sign s: conjunctival redness; corneal opacity; fixed, mid-dilated pupil \n\nDiagnosis . Tonometry (measures intraocul ar pressure) . Gonioscopy (measures corneal angle) \n\n## . Top ical therapy: multidrug topical therapy (eg, timolol, pi locarpine, apraclonidine) \n\nTreatment . Systemic the rapy: acetazolamide (consider mannitol) \n\n## . Laser iridotomy \n\nCorne al epithelial def ec ts \n\n## . Tr auma or foreign body \n\nEtiology . Contact l ens use \n\n## . Expos ure (eg, in comp lete lid clos ure) \n\n## . Severe eye pain \n\nCl i nic al f eatur es . Foreign body sensation, t tearing \n\n## . Photophobia, reluctance to open eye \n\n## . Penlight test: assess pupill ary sh ape & function, inspect f or foreign body \n\nEvaluation . Visual acui ty . Fluorescein examination after above tests: concent rated ue take indi ca t es corneal e e ithe lial de f ec tCNS, Eye, Ear Optic Nerve Injury Open Globe Injury \n\n694 https://t.me/usmleinnercircle \n\n# .Risk factors ...\n\nClinical features .....Management ...\n\nManagement of corneal abrasion \n\nTraumatic or foreign body abrasion \n\nManagement \n\nEye pain with foreign body sensation Ocular perforation? Corneal infiltrate (white spot, opacity)? Corneal ulcer? Yes \n\nIrregular pupi l? Foreign body not easily removed? \n\nNo \n\nContact lens abrasion \n\nManagement \n\nUrgent ophthalmology consultation Remove any foreign body by irrigation Topical antibiotic (eg, e ry thromycin , polymyxin/trimethoprim) Topical antipseudomonal antibiotic (eg , ofioxacin, ci profloxacin , tobramycin ) No eye patch due to infection risk Follow -u p not required for small (<3 mm) defects with improving symptoms, normal vision , & no foreign body Follow-up in 24 hr to ensure absence of cornea l infiltrate or ulcer \n\n> UWorld\n\nOptic nerve injury Mechanism . Indirect: shearing forces from facial trauma \n\n# . Direct: penetrating eye trauma \n\n## . Acute vision loss \n\nClinical features . Decreased color vision \n\n## . Afferent pupillary defect \n\nDiagnosis . CT scan of the orbit \n\nManagement . Urgent ophthalmology referral \n\n## . Surgical decompression \n\nOpen globe injury Eccentric or teardrop-shaped pup il Blunt force trauma (rupture) Penetrating trauma (laceration) Extrusion of vitreous (eg, \"gush\" of flu id) Eccentric or teardrop pupil Decreased visual acuity Relative afferent pupillary defect Decreased intraocular pressure Emergency ophthalmology consultati on Eye shield CT scan of eye Intravenous antibiotics Tetanus prophylaxis CNS, Eye, Ear Sympathetic Ophthalmia \n\n What is the likely diagnosis in a patient that presents with \" floating spots \" and blurred vision in the right eye? Several weeks ago, the patient had a penetrating injury to his left eye, causing vision loss. \n\nSympathetic ophthalmia (\"spared eye injury\") \n\ndue to an immunologic mechanism involving the recognition of \"hidden antigens\" Sympathetic ophthalmia : bilateral panuveitis after unilateral penetrating injury . It is caused by a delayed-hypersensitivity against hidden antigens in the injured eye that affects the healthy eye .\n\nOrbital Compartmental Syndrome Hyphema \n\n695 https://t.me/usmleinnercircle USMLE Inner Circle \n\nOrbital compartment syndrome Pathophysiology . f lntr ao rbital press ur e\n\n## . Ri sk fa ct ors: trauma, coagulopathy, infection, surge ry \n\nClinical features . Acute eye pain \n\n## . O iplo pia, vision loss \n\n## . Periorbital swelling, ecchymosis & tightness (eg, hard eyelid) \n\nExam i nation . Proptosis find ings . Diffu se subconjunctival hemorrhage \n\n## . Limited ex traocular m ove ments \n\n## . Afferent pupillary defect \n\nManagement . Em ergency surgical decompression Orbital decompression for orbital compartme nt syndrome Incision line Cut lateral can thu s (l ateral can th ot omy) Lateral cant hal tend on \n\n(inferior limb) \n\nC ut lat era l canthal tendon (cantholys is) CNS, Eye, Ear Hyphema , or the accumulation of blood in the anterior chamber, is common following blunt ocular trauma and may lead to significant vision loss as a result of ocular hypertension and \n\nglaucoma , corneal blood staining , and angle recession .While most patients may tolerate high intraocular pressure secondary to hyphema for up to 5 days before surgical washout becomes necessary, patients with sickle cell disease or trait are at much higher risk for anterior chamber and retinal vascular red blood cell sickling, which may lead to irreversible vision loss caused by retinal vascular occlusion .\n\nSurgical washout should be considered urgently for these patients if intraocular pressure is not controlled within 24 hours. \n\nStrabismus \n\n696 https://t.me/usmleinnercircle \n\n## .Mechanism ...Clinical presentation ....\n\nInitial management \n\n# ...Complications ..\n\nTraumatic hyphema \n\nBlunt ocular trauma (eg, baseball, airbag deployment) Penetrating trauma (less common) Vision loss Eye pain Photophobia Layering of blood in the anterior chamber Anisocoria (unequal pupils) Ophthalmology consultation \n\n> 0\n\nMonitor intraocular pressure \n\n> 0\n\nCycloplegic & glucocorticoid eye drops Eye shield Bed rest (elevate head) Re bleeding lntraocular hypertension -+ optic nerve atrophy (glaucoma) Permanent vision loss \n\nNormal eyes & strabismus Normal eyes \n\nRed reflexes & corneal light reflexes are equal. \n\nAsymmetric reflections \n\nIn strabismus, the red reflex is more in tense in the deviated eye. The corneal light reflexes are also asymmetric. UWorld Hyphema CNS, Eye, Ear Dilated funduscopic examination is performed to detect retinoblastoma , a life-threatening cause of strabismus. \n\n Screening for strabismus should be performed at every well child visit until age 5 because treatment outcomes are best when initiated while the visual cortex is most malleable. \n\nRetinoblastoma \n\n697 https://t.me/usmleinnercircle USMLE Inner Circle \n\n## ...Clinical findings ...\n\n## .\n\nTreatment ...Complications .\n\nStrabismus (ocular misalignment) Constant eye deviation at any age Intermittent eye deviation at age >4 months Eye deviation on cover test Asymmetric corneal light reflexes Asymmetric intensity of red reflexes Torticollis or head tilt Strengthen deviated eye (eg , patch unaffected eye, cycloplegic drops to blur unaffected eye) Correct refractive errors ( ie , prescription glasses) Surgery Amblyopia (reduced visual acuity) Diplopia \n\nNormal eyes & white reflex \n\nNormal eyes Red reflexes & corneal light reflexes are equal. Abs e nt reflex White reflex on abnormal eye can result from opacities of the lens (eg , cataract) or tumor (eg , retinoblastoma) . CNS, Eye, Ear Photokeratitis Retinal Artery Occlusion \n\nEtiology: \n\nRetinal artery : Release of thrombotic emboli 2/2 carotid artery atherosclerosis, thrombosis 2/2 atherosclerosis Clinical features: \n\nSudden loss of vision in >60 y.o. \n\nAmaurosis fugax : sudden, painless loss of vision that lasts for seconds to minutes followed by recovery \n\nTreatment: Ophthalmologic emergency! Occular massage , carbogen or hyperbaric oxygen therapy Carbogen: 5% CO2 , 95% O2 (Hypercapnea causes vasodilation, O2 improves oxygenation) \n\n698 https://t.me/usmleinnercircle \n\nReti nob las t oma Photokeratitis Etiology . UV light causes desquamation of corneal epithelium \n\n## . Ri sk factors: high altitud es , areas with increased UV light reflection (eg, ~ w~ snow )\n\n## . Severe, bilateral eye pain & photophobia 6-12 hr after exposure \n\nClinical . Foreign body sensation in the eye \n\nfeatures . Decreased vision \n\n# . Conjunctival erythema, chemosis, tearing \n\nDiagnosis . Punctate corneal staining with fluorescein dye \n\n## . Supportive (eg, oral analgesics, to pical antibio ti cs) \n\nManagement . Sym ptom resolution within 1-3 days \n\nPrev e nt ion . UV-protective eyewear UV = ultraviole t. 0CNS, Eye, Ear Retinal Vein Occlusion \n\n What is the likely diagnosis in an elderly patient with sudden loss of vision in the left eye? Funduscopic examination reveals swelling of the optic disk , retinal hemorrhages , dilated and tortuous veins , and \n\ncotton wool spots. Central retinal vein occlusion \n\n\"blood and thunde r\" appearance on funduscopy; CRVO is typically less acute than central retinal artery occlusion Fundoscopy typically reveals diffuse ischemic retinal whitening and cherry red spots \n\n699 https://t.me/usmleinnercircle USMLE Inner Circle \n\nIRetinal whitening \n\nCauses of acute, painless vision loss Diagnosis Symptoms Clinical findings Management Central retinal Severe vision loss with . Possible intraarterial thrombolytics \n\n## . temporal sparing . Pale fundus with cherry-red . Ocular massage \n\nartery spot Reduction of IOP (eg , an ter ior occlusion History of amaurosis fugax .. chamber paracentesis) \n\n## . Fundu s with retinal \n\nCentral retinal . Blurred vision to severe vision . Observation intravitreal injection vein occlusion loss hemorrhages & o ptic disc of VEGF inhibitors edema (\"blood & thunder\") \n\n## . Floaters, photopsia (flashing . Fundus with vitreous \n\nRetinal . Surgical correction (eg, retinopexy, \n\ndetachment lights) hemorrhage & marked vitrectomy) typically required \n\n## . Pr ogressive visua l field defect elevation of retina Ha zy vision red hue or vision . ! or absent red reflex . Bed rest, HOB elevation 30-45 \n\nVitreous . RBCs/floating debris in degrees .loss \n\nhemor rh age Floaters/shadows vitreous, obsc ur ed vi ew of . Photocoagulation or vitrectomy in \n\n## . fundus some cases HOB = head-of-bed; IOP = intraocular pressure; RBCs = red blood cells; VEGF = vascular endothelial growth factor. CNS, Eye, Ear T/t: Observation , VEGF inhibitor injection \n\nRetinitis Pigmentosa \n\n D/D: Vitamin A deficiency: also causes excessive dryness of the cornea and conjunctivae \n\nDiabetic Retinopathy \n\n700 https://t.me/usmleinnercircle \n\nFunduscopic findings in central retinal vein occlusion \n\n Venous dilati on & tortuosity due to venous occl us ion \n\n Scattered & di ffuse hemorrtlages due to backup of blood & increased resistance , leading to ischemic damage \n\n \"Blood & thunder' ' appearance due to di ffuse hemorrhages \n\n Cotton-woo l spots \n\n Di sc swelling OUVllor l~ \n\nRetinitis pigmentosa \n\n Genetic mutation causing loss of photoreceptors \n\nEtiology . Progressive retinal degeneration . Symptom onset from age 10 through adulthood . Night blindness \n\nClinical features . Progressive visual field loss (eg, midperiphery) . Decreased visual acuity (late finding) \n\nFunduscopic findings . Retinal vessel attenuation , optic disc pallor, abnormal retinal pigmentation \n\nPrognosis . Most are legally blind by age 40 CNS, Eye, Ear What is the likely diagnosis in a diabetic patient that presents with sudden-onset loss of vision in the right eye? Ophthalmoscopy reveals loss of fundus details , floating debris , and a dark red glow .\n\nVitreous hemorrhage \n\ntypically presents with sudden loss of vision and onset of floaters in a patient with diabetic retinopathy; \n\ndifferentiated from retinal detachment by loss of fundus details \n\n Vision loss in proliferative retinopathy may be due to Vitreous Hemorrhage or Retinal Detachment \n\n Floaters is associated with hemorrhage, which is not exclusive to diabetic retinopathy obviously (seen with retinal detachment, etc.). Floaters are secondary to injury to the retina , producing floating blood cells which create a perception of black moving spots )\n\n What is the suggested treatment to prevent complications of proliferative diabetic retinopathy ?\n\nArgon laser photocoagulation \n\nInfection \n\n701 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDiabetic retinopathy , nonproliferative CNS, Eye, Ear Orbital Cellulitis \n\n Severe complications include permanent visual impairment (eg, optic nerve involvement) and \n\nintracranial extension (eg, infection, cavernous sinus thrombosis). Orbital cellulitis is a more severe infection than preseptal cellulitis. \n\nperiorbital (preseptal) cellulitis is caused by infection anterior to the orbital septum ;most commonly a complication of bacterial rhinosinusitis Preseptal commonly results from a break in the periorbital \n\nskin (eg, abrasion , insect bite ), allowing cutaneous flora such as S.aureus or S. pyogenes to enter the preseptal space. \n\n702 https://t.me/usmleinnercircle \n\nOcular manifestations of HIV \n\n## . Loss of acuity, glare, halos around lights \n\nCataracts . Opacification of lens, loss of red reflex \n\n## . Surgery often required at early age . Unilatera l, acute/subacute loss of vision \n\nCytomegalovirus retinitis . Fluffy or granular retinal lesions . Decreased risk with HAART \n\nHerpes simplex keratitis . Acute unilateral ocular pain , redness, tearing \n\n## . Branching/dendritic corneal ulcers \n\n## . Pain, tearing, photophobia, decreased acuity \n\nUveitis . Hyperemia, constricted pupil, hypopyon \n\n## . Due to intraocular HIV replication or secondary infection \n\nNeuroophthalmic complications . Optic neuropathy \n\n## . Motor palsies \n\nHAART = highly active anti-retroviral therapy. \n\nOrbital cellulitis \n\n## . Local infection (eg, sinusitis, dental \n\nRisk factors in fection , skin infection) \n\n## . Orbital trauma \n\n## . Pa inful eye movements \n\nClinical signs . Ophthalmoplegia \n\n## . Proptosis \n\n## . Visual changes \n\n## . Clinical \n\nDiagnosis CT scan if diagnosis is uncertain .. Intravenous antibiotics \n\nTreatment . Surgical drainage for abscess \n\nPreseptal vs orbital cellulitis Orbital anatomy \n\nDiagnosis Preseptal Orbital cellulitis cellulitis \n\n# . Eyelid . Symptoms of preseptal cellulitis \n\nClinical erythema & PLUS features swelling . Pain with EOM , proptosis &/or \n\n# . Chemosis ophthalmoplegia with diplopia . Intravenous antibiotics \n\nTreatment . Oral antibiotics . Surgery \n\nEOM = extraocular movements. CNS, Eye, Ear orbital (postseptal) cellulitis is a posterior infection \n\n Diplopia , opthalmoplegia , and proptosis are typical features of orbital cellulitis , and do not occur in preseptal cellulitis \n\nConjuctivitis \n\n Most cases occur after direct contact with secretions of an infected individual. Adults: Staph Aueus \n\nChildren: Streptococcus pneumoniae, Haemophilus influenzae , Moraxella catarrhalis \n\n Atopic keratoconjunctivitis is a form of allergic conjunctivitis in which redness, pruritus, and tearing are common, but patients have chronic (not acute) symptoms , often with photophobia and a foreign \n\nbody sensation .Moreover, signs of chronic eyelid inflammation (eg, thickened, lichenified skin ) are typical. Olopatadine and azelastine , which are mast cell stabilizing agents and antihistamines, are indicated for treatment of allergic conjunctivitis. \n\n703 https://t.me/usmleinnercircle USMLE Inner Circle \n\nAcute conjunctivitis* Viral Bacterial Allergic Distribution Unilateral or bilateral Unilateral or bilateral Bilateral \n\nDischarge Watery/mucoid Purulent Watery \n\nConjunctiva! Diffuse injection; follicular Diffuse injection; nonfollicular Diffuse injection; follicular (\"bumpy\") \n\nappearance (\"bumpy\") \n\nAssociated Unremitting discharge (reaccumulates Ocular pruritus, history of atopy (eg, allergic \n\nfindings Viral prodrome within minutes) rhinitis , asthma) \n\nDuration 1-2 weeks 1-2 weeks <30 minutes (often sudden onset) to perennial \n\n*Red flags suggestive of alternate etiology: decreased visual acuity, photophobia, pain with extraocular movement & fixed/distorted pupil. \n\nConjunctivitis treatment \n\n## . Erythromycin ointment \n\nBacterial conjunctivitis . Polymyxin-trimethoprim drops . Azithromycin drops . Preferred agent in contact lens wearers : fluoroquinolone drops \n\nViral conjunctivitis . Warm or cold compresses . Antihistamine/decongestant drops \n\nAllergic conjunctivitis . Over-the-counter antihistamine/decongestant drops for intermittent symptoms . Mast cell stabilizer/antihistamine drops for frequent episodes CNS, Eye, Ear All infants, regardless of maternal screening results, should receive topical erythromycin prophylaxis shortly after birth to prevent gonococcal disease. What is the treatment/administration route of Chlamydial conjunctivitis ?\n\nOral erythromycin \n\nassume URT is also infected, so do systemic administration to prevent pneumonia Patients should be monitored for pyloric stenosis (S/E of macrolide) \n\n Trachoma , caused by Chlamydia trachomatis , is the leading infectious cause of blindness worldwide. Acute trachoma presents with follicular conjunctivitis (white follicles on upper tarsal conjuctiva) \n\nand inflammation of the tarsal conjunctivae .Repeated or chronic infection causes inversion of the eyelashes (trichiasis) and scarring of the cornea .\n\n704 https://t.me/usmleinnercircle \n\nOnset Type age \n\n## .Chemical <24 hr \n\n## .Gonococcal 2-5 days ..\n\n5-14 .Chlamydia! days . \n\n> IM =intramuscular .\n\nNeonatal conjunctivitis Findings \n\nMild conjunctival irritation & tearing after silver nitrate ophthalmic prophylaxis Marked eyelid swelling Profuse purulent discharge Corneal edema/ulceration Mild eyelid swelling Watery, serosanguineous, or mucopurulent eye discharge \n\nStages of trachoma Stage 1: Inflammation of th eupper tarsal conju nctiva Treatment \n\nEye lubricant Single IM dose of 3rd- generation cephalosporin Oral ery1hromycin \n\n> Stage 2: Scarring of the upper tarsal conjunctiva and trichiasis Stage 3: Corneal opacity and blindness\n> Cl UWorkt\n\nCNS, Eye, Ear Oral azithromycin is effective against C trachomatis and should be administered to the entire local population (eg, village, refugee camp) simultaneously. \n\nTrichiasis warrants eyelid surgery to preserve vision. \n\nRetinitis \n\n What is the likely diagnosis in a patient with a history of poorly controlled HIV that presents with eye pain , conjunctivitis , keratitis , and vision loss ? Funduscopy shows widespread, pale, peripheral retinal lesions and central necrosis of the retina. \n\nHSV retinitis \n\n\"acute retinal necrosis syndrome\"; HSV is painful and characterized by peripheral pale lesions and \n\ncentral retinal necrosis \n\n(vs CMV , which is painless and characterized by perivascular lesions )\n\nEndopthalmitis \n\n705 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCytomegalovirus (CMV) retinitis Bacte ri al endophthalmitis Etiology . Bacterial infection of the aqueous humor &for vitreous \n\n## . Ri sk factors: recent eye surgery (eg, catar ac t extraction) or trauma \n\n## . Decreased vision eye discomfort (eg, \"ache\") \n\nClinical features . Conjunc ti val injection & edema \n\n## . Purulent h az iness or layering of leukocytes (hypopyon) in anterior chamber \n\n## . Diagnosed clinically - ophthalmologic emergency \n\nDiagnosis Can confirm diagnosis with Gram stain & culture of vitreous .\n\nTreatment . lntravitreal injection of antibiotics \n\n## . Vitrectomy for severe cases CNS, Eye, Ear What is the likely diagnosis in a patient that presents with fever , decreased vision , and pain over the left eye for 12 hours? Physical examination reveals a swollen eyelid and exudates in the anterior chamber. She had a cataract extraction in her left eye one week ago. \n\nPost-operative endopthalmitis \n\nmost common cause of endophthalmitis ; causes pain and decreased visual acuity \n\n Most common etiology of endopthalmitis is after cataract surgery \n\n The organism replicates in the choroid and attacks the retina, leading to fluffy, yellow-white, mound-like lesions with indistinct borders. \n\nKeratitis \n\n706 https://t.me/usmleinnercircle \n\nPathogen Onset Symptom sSigns \n\nEpidemiology Manifestations Diagnosis Treatment \n\nAcute endophtha lmi tis Chronic en dophtha lmi tis Usually bacterial Usually fungal \n\n Les s virulent ba cteria \n\n Sudden (acut e) i;;::l In sidious \n\n Severe, deep-seated, dull oc ular pain O c ular pain is usually a b se n t/ appears la te . \n\n Acute loss of vision Gradually progressive loss of vision \n\n Features of sepsis may be present (in endogenous endophthalmiti s) . Flo aters {fungal end op hthalm it i s) Exogenous endophthalmitis , Conjunctival hyp eremia and che mo sls out of proportion to the surgical/traumatic In sult \n\nHa zy cornea (due to edema) Hazy aqueous chamber or hypopyon t;:J \n\n, Endogenous endophthalmiti s: The above signs do not develop/develop until late in the course of t he d isease i;;::l \n\n In bot h types Relative afferent pupillary defect Decreased visua l ac uity; in severe en dophthalmitis, on ly l igh t perception may be preserved .\n\nCandida endophthalmitis \n\n## . Tran sie nVpersistent fungemia --+ hematogenous dissemination to the ch oro id --+ in vas i on of the re tina & fluid chambers \n\n## . Risk factors: indwelling cen tr al catheter, TPN , broad-spectrum a ntibiotic use, gastrointestinal surgery &\n\nimmunocompromise \n\n## . Most cases ar ise in hose ita liz ed eatients or in those with recent e~e s ur ge !J: trau ma \n\n## . Usually unilateral floaters & progressive vision loss \n\n## . Pain rare until l ate in disease pr oce ss \n\n## . Fever may be absent & patient may ot herwise feel we ll \n\n## . Blood cult ur es (often negative) \n\n## . Vitreous fluid sampling & culture \n\n## . Systemic antifungal therapy \n\n## . Vitrectomy + vitreous inject io n (when fluid cha mber in vo lved) \n\nTPN = to tal parenteral nu t ritio n. CNS, Eye, Ear What is the likely diagnosis in a patient that wears contacts and presents with sudden-onset eye pain and discharge ? On examination, there is thick, globular yellow discharge . The cornea is hazy \n\nand ulcerated .\n\nContact lens-associated keratitis ( most commonly pseudomonas )\n\n What is the likely diagnosis in a young adult male that presents with pain , watering , and redness of the left eye for two days? Examination reveals vesicles and dendritic ulcers in the cornea of the left eye. He has had similar symptoms in the past. \n\nHerpes simplex keratitis \n\ncorneal vesicles and dendritic ulcers are characteristic Vs. Herpes Zoster ophthalmicus , which has a vesicular rash in the distribution of the cutaneous branch of the first divison of the trigeminal nerve (forehead, eye, etc.) \n\nDacryocystitis \n\nPatient presents with pain and swelling over the medial canthus (inner aspect of the eye ). Slight pressure causes expression of purulent material \n\ntypically caused by Staphylococcus aureus and Streptococcus pyogenes Central Round Infiltrate in Bacterial Keratitis \n\n707 https://t.me/usmleinnercircle USMLE Inner Circle \n\nInfectious keratitis Pathogen Risk factors Clinical features* \n\n## . Central, round ulcer Bacteria (eg , Staphylococcus aureus, . Improper contact lens use . Stromal abscess \n\nPseudomonas) . Corneal trauma , foreign body . Mucopurulent discharge \n\n## . Acute 12 resentation \n\n# . Branched dendritic ulcerations Herpes simplex virus lmmunocompromised, HIV . L Corneal sensation \n\n## . Watery discharge .. Recurrent episodes \n\n# . Ulcerations with feathery margins \n\n## . lmmunocompromised with corneal injury & satellite lesions Fungi (eg, Candida) involving contaminated soil (eg , gardening) Mucopurulent discharge .. Indolent course *Eye pain/redness, blurred vis ion & photophobia are features of all infectious keratitis. Herpetic keratitis, fluorescein CNS, Eye, Ear T/t: Systemic Antibiotic Therapy \n\nHordeolum/ Stye inflmmation of tear gland or eyelash follicles (Zeis or Meibomian glands) \n\n708 https://t.me/usmleinnercircle \n\nNasolacrimal anatomy Lacr imal \n\n> gland\n\nBlepharitis Chalazion Hordeolum Dacryocystitis \n\n## .....\n\nCommon inflammatory eyelid conditions Etiology \n\n## .Inflammation of the eyelid margin \n\n## .Granulomatous reaction to obstructed .meibomian gland External hordeolum (sty): focal infection of .Zeis gland Internal hordeolum: focal infection of meibomian gland \n\n## .Acute inflammation/infection of nasolacrimal sac \n\nAcute dacryocystitis Clinical findings \n\nRedness , swelling &/or scaling of lid margin, often with crusting of eyelashes Solitary, rubbery nodule deep to eyelid margin Usually painless, most common on upper eyelid Tender, erythematous nodule/pustule at lid margin (external hordeolum) or internal surface of eyelid (internal hord eolum) Painful swelling & redness around medial canthal region purulent discharge from punctum CNS, Eye, Ear What is the initial treatment for external hordeolum (stye)? \n\nWarm compresses \n\npersistent hordeolum (> 1-2 weeks) or large chalazions may be managed with incision and curettage \n\n What is the likely diagnosis in a patient that presents with a hard , painless bump on the eyelid ?\n\nChalazion \n\ntypically caused by granulomatous inflammation of the meibomian gland Usually a non-tender , chronic lesion that may present with heaviness of the eyelid. Hordeolum is painful \n\nBlepharitis \n\n What is the most likely diagnosis in a patient who presents with 3 months of waking up with both eyelids irritated , swollen, and covered with a dry crust ? Both eyes show erythema and irritation at the superior lid margin and there are flaes at the base of the lashes? \n\nBlepharitis \n\nCommon eyelid condition that presents as chronic and/or recurrent scaly inflammation of the eyelid margins \n\nCommon contributors include seborrheic dermatitis , rosacea , allergic disorders , bacterial infection , viral infection , and Demodex mite infestation .T/t: Lid hygeine and warm compresses \n\nRecurrent nature so practice good hygeine for long periods of time \n\nUveitis \n\n709 https://t.me/usmleinnercircle USMLE Inner Circle CNS, Eye, Ear Dacryostenosis Eye Drugs \n\n What is the most likely cause of a patient who with rheumatoid arthritis who complains of months of \"black spots \" in her vision? Fundoscopy below shows bilateral \" bull's eye macular lesions \". \n\nChloroquine toxicity \n\n## EAR \n\n Hearing loss in the elderly is common and may present with social isolation and cognitive decline .Careful history-taking and a whispered voice test should be conducted. \n\nAudiometric testing can help confirm the diagnosis and direct management. REMEMBER can be both infectious and autoimmune \n\n710 https://t.me/usmleinnercircle \n\nAnterior uveitis Anterior uveitis with hypopyon Presentation . Symptoms : ocular pain, photophobia, decreased acuity \n\n## . Examination : ciliary flush, pupill ary constriction, hypopyon \n\n## . Inf ections: herpesviruses, toxoplasmosis, syphilis \n\nCommon causes/ . Sarcoidosis \n\nassociations . Spondylarthritis (eg, ankylosing spondylitis, reactive arthritis) \n\n## . Inflammatory bowel disease \n\nEvaluation/testing . Slit-lamp examination \n\n## . As indicated: HLA-B27, pelvis/spine x-ray, chest x-ray , HIV, syphilis serology \n\nTreatment . Dilating eye drops (eg, cyclopento lat e) \n\n## . Topical glucocorticoids l ayering of inflammatory cells in anterior chamber cuw,.,, \n\nHLA-827 = human leukocyte antigen 827 .\n\nCongenital dacryostenosis Pathophysiology . ln co mel ete cana lization of distal nasola cr imal duct \n\n## . Increased tearing \n\nClinical features . Eyel ash cr usting \n\n## . Clear co nj un ct ivae \n\n## . Observation for spontaneous resolution \n\nManagement . La crimal sac m assa g es \n\n## . Probing of duct if pers ists >6 months \n\nComplications . Dacryo cystoce le \n\n## . Dacryo cystit is CNS, Eye, Ear Infection \n\nOtitis externa \n\n What is the likely diagnosis in a child that presents with ear pain , erythema , and discharge after swimming in an outdoor pool? \n\nOtitis externa (\"swimmers ear\") \n\nIt often occurs due to alterations in ear canal pH , loss of cerumen , skin maceration , and \n\nintroduction of bacteria . How do you differentiate between otitis media and externa based on symptoms? \n\nWith Otits Exterma, the pain is worse when you pull on pinna \n\nMalignant Otitis Externa Topical Fluoroquinolones are well tolerated by children. \n\n711 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDifferential diagnosis of otalgia Diagnosis Clinical features Acute otitis Middle ear effusion plus acute eardrum \n\nmedia inflammation ( eg , bulging eardrum , fever )\n\nOtitis media Middle ear effusion without \n\nw ith effusion acute inflammation \n\nBullous Serous liquid-filled blisters on the \n\nmyring itis tympanic membrane \n\nCerumen Liquid or hard wax in auditory canal \n\nimpaction obstruc ti ng eardrum visualization \n\nHemotympanum Purple or red eardrum +/- bulging \n\nOtitis Pain with tragal traction , erythematous &\n\nexterna swollen external auditory canal +/- otorrhea \n\nOtitis externa \n\n## . Water exposure \n\nRisk factors . Trauma (eg, cotton swabs, ear cand li ng) \n\n## . Foreign material (eg, hearing aid , headphones) \n\n## . Dermatologic conditions (eg, eczema, cont ac t dermati ti s) \n\nMicrobiology . Pseudomonas aeruginosa \n\n## . Staphylococcus aureus \n\n## . Otalgia, pruritus, discharge, hearing loss \n\nClinical . Pain with auricle manipulation \n\nmanifestations . Ear canal erythema, edema, debr is \n\n## . Tympanic membrane spared (clear, not inflamed, no middle ear fluid ) \n\n## . Remove debris \n\nTreatment . Topical antibiotic (eg, fluoroquinolone) \n\n## . Topical glucocorticoid \n\n## . Consider wick eiacement to facil itate medication delivery CNS, Eye, Ear Malignant otitis externa is typically seen in patients with diabetes ; treatment is surgical debridement + \n\nantipseudomonals .\n\nPatients may present with findings consistent with malignant otitis external, abnormal vitas (fever, tachy), and facial droop, indicating progression to osteomyelitis of the temporal bone with CN VII palsy. \n\n Presence of granulation tissue , elevated ESR , and severe pain distinguish MOE from typical otitis externa What is the next step in an elderly patient that presents with worsening severe left-sided ear pain with an edematous auditory canal and purulent discharge/granulation tissue visible on otoscopic exam? \n\nCT scan ( identify bone destruction )\n\nBiopsy can be done to distinguish between MOE from tumor and helps optimize treatment \n\nOtitis Media A life-threatening infection of the external auditory canal extending to the skull base ( osteomyelitis )\n\n712 https://t.me/usmleinnercircle \n\nNecrotizing (malignant) otitis externa \n\n## . Elderly (age >60) \n\nRisk factors . Diabetes mellitus \n\n## . Aural irrigation (cerumen removal) \n\nMicrobiology . Pseudomonas aeruginosa \n\n## . Severe, unremitting ear pain /worse at nig ht & with chewing) \n\nClinical . Deficits of lower cranial nerves (eg, facial [CN VII], g lossopharyngeal [CN IX] , vagus \n\nmanifestations (CN X]) \n\n## . Granulation tissue in the external auditory canal \n\n## . Elevated erythrocyte sedimentation rate \n\nTreatment . Intravenous antipseudomonal antibiotics (eg , ciprofloxacin) \n\n## . Surgical debridement \n\nAcute otitis media \n\n## . Streptococcus pneumoniae \n\nMicrobiology . Nontypeable Haemophilus influenzae \n\n## . Moraxella catarrhalis \n\n## . Age (6-18 months) \n\nRisk factors . Lack of breastfeeding \n\n## . Day care attendance \n\n## . Smoke exposure \n\nClinical . Bulging TM \n\nfeatures . Middle ear effusion plus TM inflammation (eg, fever , otalgia, erythema) \n\n## . Initial: amoxicillin \n\nTreatment . 2nd-line: amoxicillin-clavulanate \n\n## . Penicillin-allergic: clindamycin or azithromycin \n\n> TM =tympanic membrane\n\n## . TM perforation \n\nComplications . Conductive hearing loss \n\n## . Mastoidilis \n\n## . Meningitis \n\nTM = tympanic membrane. CNS, Eye, Ear Symptoms/Physical? \n\nRelief when pulling on pinna Loss of light reflex Bulging, red TM Child repeatedly touches affected ear \n\n Diagnosis? \n\nPneumatic Otoscopy: tense, rigid TM in response to insufflation (pressure changes) \n\n Treatment with oral antibiotics is recommended in specific situations: First-line therapy with amoxicillin is indicated for infants age <6 months and for children age 6 months with high fever (>39 C [102.2 F]), severe pain , or bilateral disease. \n\nSecond-line therapy with amoxicillin-clavulanate is indicated for refractory symptoms after 2-3 days of antibiotic therapy or recurrent AOM (within 30 days) after antibiotic therapy. \n\n Acute otitis media often follows an upper respiratory infection. \n\n Myringotomy with tympanostomy tube placement should be considered in children with > 3 episodes of acute otitis media in 6 months or > 4 episodes in 12 months. \n\n713 https://t.me/usmleinnercircle USMLE Inner Circle \n\nNormal ear Acute otitis media CNS, Eye, Ear What is the next best step in a child who presents with an fever and ear discharge ? Otoscopy shows a bulging tympanic membrane with pus . Physical shows postauricular tenderness .\n\nCT scan \n\nAntibiotics are always indicated in mastoiditis! Regimen always involves vancomycin but really depends on the course of the infection \n\nOtitis Media with Effusion \n\n Otitis media with effusion (OME) is defined by middle ear fluid without tympanic membrane (TM) inflammation (eg, bulging, erythema). Examination shows air-fluid levels and poor TM mobility .Management is observation with follow-up for resolution because chronic OME is associated with speech delay and long-term hearing loss. \n\nTympanostomy tube placement is warranted for chronic OME with associated hearing loss. What is the likely diagnosis in a patient with unilateral hearing loss with a dull , hypomobile tympanic \n\nmembrane on otoscopic exam? \n\nSerous otitis media (otitis media with effusion) \n\ni.e. middle ear effusion without signs of active infection Can be seen in patients with AIDS and lymphomas -- HIV lymphadenopathy and lymphomas obstruct the auditory tube \n\nChronic Suppurative Otitis Media \n\n714 https://t.me/usmleinnercircle \n\n> Mastoiditis\n\n# . Infection of the mastoid air cells \n\n> Pathophysiology\n\n# . Complication of acute otitis media \n\n# . Most commonly due to Streptococcus pneumoniae \n\n# . Fever & otalgia \n\n# . lnfiammation of mastoid \n\n> Clinical findings Protrusion of the auricle\n\n# .. Opacification of mastoid air cells on CT scan or MRI \n\n# . Intravenous antibiotics \n\n> Management Drainage of purulent material (eg, tympanostomy, mastoidectomy)\n\n# . \n\n> Complications\n\n# . Extracranial extension (subperiosteal abscess , facial nerve palsy, hearing loss, labyrinthitis) \n\n# . lntracranial extension (brain abscess, meningitis) Acute otitis media Otitis media with effusion \n\n> CI UWortcl\n\nCNS, Eye, Ear CSOM is most common in young children due to an increased incidence of acute otitis media , a major risk factor for CSOM. CSOM does not typically respond to oral antibiotics because the middle ear is poorly vascularized \n\ndue to chronic inflammation and scarring. \n\n Cholesteatoma can also cause chronic ear drainage , and should be considered when the condition does not respond to topical therapy for presumed CSOM. \n\nCholesteatoma \n\n What is the likely diagnosis in a child that presents with persistent ear discharge, despite antibiotic treatment, with granulation tissue and skin debris visible on otoscopic exam? \n\nCholesteatoma \n\nmay be complicated by hearing loss, cranial nerve palsies, vertigo, and/or infection \n\n715 https://t.me/usmleinnercircle USMLE Inner Circle \n\nChronic suppurative otitis media Perforated otitis media \n\n## . Often polymicrobial \n\nMicrobiology . Staphylococcus aureus & Pseudomonas aeruginosa \n\n## . Fungi (eg , Aspergillus) \n\n## . Chronic (>6 wk), purulent otorrhea \n\nSymptoms . Hearing loss \n\n## . Absence of ear pain \n\nExamination . Tympanic membrane perforation \n\n## . Otorrhea within normal-appeari ng external auditory canal \n\nTreatment . Ototopical fluoroquinolone drops (eg , ofloxacin) \n\nComplications . Infectious spread (eg, mastoiditis, meningitis, intracranial abscess) \n\n## . Permanent hearing loss \n\nCholesteatoma \n\nIOUWorkf CNS, Eye, Ear Cholesteatoma is a special form of chronic otitis media in which keratinizing squamous epithelium grows from the tympanic membrane or the auditory canal into the middle ear mucosa \n\nSurgery is ALWAYS indicated \n\nEustachian Tube Dysfunction \n\n Otoscopic examination reveals a retracted TM due to negative pressure within the middle ear. The Eustachian Tube connects the middle ear with the nasopharynx and drains middle ear secretions into the nasopharynx. Why are infants more prone to developing acute otitis media ?\n\nTube is short, wide, and horizontal, thus nasopharyngeal secretions easily reflux into middle ear \n\n Obstruction/blockage of ET --> lack of ventilate and drainage of middle ear --> accumulation and bacterial superinfection --> bulging tympanic membrane \n\nBarotrauma \n\n Barotrauma to the ear occurs most commonly after flying and can result in injury (eg, ear pain, hearing loss) to the tympanic membrane (TM). In severe cases, the TM can rupture , which rapidly equalizes the pressure difference and relieves the stretching; this relieves the pain but may also result in minor bleeding (eg, drop of blood on the finger) Most barotraumatic TM injuries heal spontaneously within a few weeks. \n\nHearing Loss \n\n716 https://t.me/usmleinnercircle \n\n> Eustachian tube dysfunction\n\n## . Eustachian tubes normally open and close to: \n\n> Physiology 0Equalize middle ear pressure\n> 0Drain middle ear\n> 0Prevent reflux of naso 12 ha !}'. ngeal secretions\n> Pathophysiology\n\n## . Inflammation (eg, infection, allergies, environmental irritation )-> tube obstruction \n\n## . Ear fullness/discomfort \n\n## . Tinnitus \n\n> Signs\n\n& symptoms Conductive hearing loss .. \"Popping\" sensation \n\n> Management\n\n## . Treat underlying cause (eg, antibiotics for acute bacterial rhinosinusitis) \n\n> Classification\n\n& features of hearing loss Type Sensorineural Conductive Cause Disorder involving inner ear, cochlea, or auditory Any cause that limits sound from gaining access to the inner nerve ear Presbycusis Otitis externa or media \n\n> Meniere disease Cholesteatoma\n> Examples Barotrauma Trauma Acoustic neuroma Cerumen Cerebrovascular ischemia Tympanic membrane perforation\n\nCNS, Eye, Ear Repeated ear infections can result in conductive hearing loss , which may be confused with certain pervasive and behavioral disorders of childhood. \n\nHearing tests should be routinely conducted in all children presenting with social or language deficits. \n\nVertigo \n\n VN is usually self-limited , patients can typically be managed symptomatically with vestibular \n\nsuppressants (eg, meclizine ) and antiemetics .\n\n VN combined with unilateral hearing loss is termed labyrinthitis \n\n Patient with vertigo undergoes the Dix-Hallpike Manuever . The head is extended and rotated to the right . Patient is placed in supine position , and nystagmus is seen. How do you interpret this? \n\n(+) for BPPV ( benign paroxysmal peripheral vertigo )Right-sided canal dyfunction ( dysfunction is present in ear turned downward )\n\nPerilymphatic fistula \n\n717 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCommon causes of vertigo \n\n## . Recurrent episodes lasting 20 minutes to several hours \n\nM&ni8re disease . Sensorineural hearing loss \n\n## . Tinnitus &/or feeling of fullness in the ear \n\nBPPV . Brief episodes triggered by head movement \n\n## . Dix-Hallpike maneuver causes nystagmus \n\n## . Acute, single episode that can last days \n\nVestibular neuritis . Often follows viral syndrome \n\n## . Abnormal head thrust test \n\nMigraine . Vertigo associated with headache or other migrainous phenomenon (eg, visual aura) \n\n## . Symptoms resolve completely between episodes \n\nBrainstem/ . Sudden-onset, persistent vertigo \n\ncerebellar stroke . Usually other neurologic symptoms \n\nBPPV = benign paro xy smal positional vertigo. \n\nPeripheral vertigo Central vertigo \n\n BPPV Stroke ( eg , cerebell ar )\n\nEtiologies Meniere disease Multi ple sclerosis Vestibular neuritis Migraine Never purely vertical May have any traje ct ory \n\nNystagmus Inhibited by fixation of gaze Not inhibited by fixation of gaze \n\ncharacteristics Fatigable (<1-min duration) Not fatigable (>1-min duration) Latency period (2-40 sec) No laten cy period Hearing loss/tinnitus absent Hearing loss/tinnitus may be present Severe postural instability \n\nOther possible \n\n Walking usually preserved Other CNS symptoms (eg, headache, diplopia, \n\nneurologic signs \n\n No other CNS symptoms weakness / numbness of face or limbs, dy sart hri a) often present \n\nBPPV = benign paroxysmal positional vertigo. CNS, Eye, Ear Perilymphatic fistulas are a rare, but debilitating, complication of head injury or barotrauma . They cause leakage of endolymph from the semicircular canals and cochlea into surrounding tissues, resulting in characteristic clinical features: \n\nProgressive sensorineural hearing loss caused by damage to cochlear hair cells from loss of endolymph. \n\nEpisodic vertigo with nystagmus triggered by pressure changes in the inner ear (eg, Valsalva maneuver, elevation changes [eg, riding in elevator]) due to acutely increased endolymph leakage. This can be demonstrated clinically by performing a loud clap (ie, pressure change due to sound conduction through the ossicles) near the patient's ear and observing for nystagmus ( Tullio phenomenon) .\n\nVestibulopathy \n\n Which class of antibiotics is associated with ototoxicity and/or vestibulopathy with an abnormal head thrust test? Aminoglycosides \n\nmay manifest as a sensation of objects moving around in the visual field when looking in any direction ( oscillopsia )Patients with vestibulopathy are unable to keep their eyes on a target. Vestibulopathy is due to gentamicin damage to motion-sensitive hair cells in the inner ear \n\n Aminoglycoside ototoxicity can damage hair cells in the cochlea (causing hearing loss ) and/or the \n\nvestibular system (causing imbalance ). Therefore, patients have varying clinical features, including the following: Bilateral, but not necessarily symmetric, hearing loss . Patients with a positive whisper test require a formal audiogram. \n\nImbalance and oscillopsia because bilateral vestibular systems are affected (rather than true vertigo, which generally occurs when 1 side is affected). A positive head thrust test (ie, inability to maintain visual fixation during forced, rapid head movement). This test evaluates the vestibuloocular reflex , which is affected by peripheral but not central vestibulopathies, as seen in this patient. \n\nOtosclerosis of Ear \n\n718 https://t.me/usmleinnercircle \n\n\n\n\n\n\n\n\n\n\n\n## Eii+iMifhi Patient focused on examiners nose \n\nfi =i/HMhfoi Patient focused on examiners nose After sharp turn to patient 's right, patient \n\n> remains focused on\n> ~<3>\n> ,examiners nose\n\n~ -\n\n# mw ~ CNS, Eye, Ear What is the most likely diagnosis in a pregnant female who complains of difficulty hearing on the right side? She was recently treated for acute pyelonephritis. Neurological exam shows BC > AC on the right side. When placed on the middle of her forehead, she feels the vibration better in the right ear . Audio entry shows low-frequency hearing loss. Which of the following is the most likely cause? \n\nOtosclerosis of the right ear \n\nFirstly, aminoglycosides can be used to treat pyelo and can cause ototoxicity. However, they wouldnt be given to a pregnant woman, and it produces sensineural hearing loss. Otosclerosis occurs in middle age, and symptoms can increase during pregnancy . It has conductive hearing loss and low-frequency hearing loss (hearing better in noisy environments) Compare this to presbycusis older people, high-frequency loss, and hearing is worse in noisy environments. \n\nAuricular Hematoma \n\n Prompt evacuation of the hematoma is required to avoid complications of infection , avascular necrosis , and permanent cauliflower ear deformity .\n\n719 https://t.me/usmleinnercircle USMLE Inner Circle \n\nOtosclerosls \n\n# . Youn ger (early to mid-30s) Caucas ian patients \n\nEpidemiology . More com mon in women \n\n## . Autosomal dominant wi th incomplete penetrance Pathophysiology . I mbalance of bone resorption & deposition - stiffening of stapes \n\n## . Pr ogressive conductive hearing los sClinical manifestations . Paradoxical impro ve ment in speech discrimination in noi sy en vironmen ts \n\n## . Reddish hue behind tympanic membrane \n\n## . Amplification (eg, hear ing aids) \n\nManagement Surgery (eg, stapes reconstruction) .\n\nAuricular hematoma Risk factors . Contact sports injury (eg, wrestling , martial arts) \n\nClinical fea tur es . Tender, fluctuant blood collection on anterior pinna \n\n## . Immediate incision & drainage \n\nTreatment . Pressure dressing \n\n## . Cauliflower ear (fibro ca rt ilage overgrowth) \n\nComplications . Bacterial superinfection \n\n## . Reaccumulation of hematoma CNS, Eye, Ear 720 https://t.me/usmleinnercircle \n\nNormal ear \n\nAuricular hematoma \n\nSwelling, erythema, & bruising within the posterior Iossa of the ear Normal ear \n\nCauliflower ear \n\nThinned-out ou ter ear Fibrous & cartilag in ous overgrowth leading to swelling & deformity Psychiatry & Substance Abuse \n\n# Psychiatry & Substance Abuse Ego Defence Delirium Amnesia Childhood Disorders Reactive Attachment disorder Oppositional Defiant Tourette Syndrome ADHD ASD Intermittent Explosive Disorder Gender Dysphoria Sleep Disorders REM Sleep Disorder Narcolepsy Sleep Terror Mood Disorder Depression Seasonal Affective Disorder Postpartum Dysthymia Bipolar Psychotic Disorder Psychosis Delusion Schizophrenia Suicide Homicide Anxiety disorders Phobia Social Anxiety Disorder Adjustment Disorder Generalised Anxiety Disorder Panic Disorder OCD Body Dysmorphic Disorder Acute Stress Disorder PTSD Dissociative Disorders Personality Disorders Eating Disorders Anorexia Nervosa Somatic Syndromes Somatic Symptom Disorder Factitious Disorder Miscellaneous \n\n721 https://t.me/usmleinnercircle USMLE Inner Circle Psychiatry & Substance Abuse Ego Defence Bereavement Catatonia Pyromania Psych Drugs & Therapies Anti Psychotics Tardive Dyskinesia Neuroleptic Malignant Syndrome Anti Depressants Serotonin Syndrome Anti Bipolar ECT Therapies Substance Abuse Urine Drug Test Neonatal Abstinence Symptoms Depressants Alcohol Benzodiazepines Opioid Inhalants Stimulants Amphetamines Cocaine Hallucinogens Marijuana MDMA/Ecstasy Poisoning & Toxicity Iron Beta Blocker Lithium Lead Magnesium Arsenic Caustic Ingestion Anti-Cholinergic Organophosphate Poisoning TCA overdose Acetaminophen Overdose Salicylate Toxicity Brown Recluse Spider Bite Snakebite \n\n722 https://t.me/usmleinnercircle Psychiatry & Substance Abuse Which ego defence is defined as involuntarily withholding an idea or feeling from conscious awareness ?\n\nRepression (immature defense) \n\ne.g. a 20-year-old does not remember going to counselling during his parents' divorce 10 years earlier \n\n Which ego defence is defined as largely unconscious assumption of the characteristics, qualities, or traits of another person or group ?\n\nIdentification (immature defense) \n\ne.g. a resident starts putting his stethoscope in his pocket like his favourite attending, instead of wearing it around his neck like before \n\n Which ego defence is defined as remaining at a more childish level of development ?\n\nFixation (immature defense) \n\ne.g. a surgeon throws a tantrum late in the operating room because the last case ran very late \n\n Which ego defence is defined as separating feelings from ideas and events ?\n\nIsolation of affect (immature defence) \n\ne.g. describing murder in graphic detail with no emotional response \n\n## Delirium \n\n723 https://t.me/usmleinnercircle USMLE Inner Circle \n\nKey defense mechanisms Immature (includes primitive & neurotic) \n\n Acting out: Expressing unacceptable feelings through actions Denial: Behaving as if an aspect of reality does not exist Displacement: Transferring feelings to a more acceptable object lntellectual iz ation: Using intellect to avoid uncomfortable feelings Passive aggression: Avoiding conflict by expressing hostility covertly ProJection: Attributing one 's own feelings to others Rationalization: Justifying behavior to avoid difficult truths Reaction formation: Responding in a manner opposite to one's actual feelings Regression: Reverting to earlier developmental stage Splitting: Seeing others as all bad or all good \n\nMature \n\n Sublimation: Channeling impulses into socially acceptable behaviors Suppression: Putting unwanted feelings aside to cope with reality Psychiatry & Substance Abuse The CAM assesses 4 fundamental features of delirium: 1. acute change (eg, hours to days) and fluctuating course (eg, intermittent) 2. inattention (eg, easy distractibility) 3. disorganised thinking (eg, confusion) 4. altered consciousness (eg, daytime somnolence) \n\n724 https://t.me/usmleinnercircle \n\n\n\nEvaluation of delirium Delirium: \n\nPositive CAM =Acute onseVfluctuating course + Inattention + (Disorganized thinking or altered consciousness) \n\n# l\n\n History: pain, trauma, substance use, dehydration, urinary retention Phys ic al examination: VS, cardiopulmonary, neurologic, skin Medications: opioids, benzodiazepines, anticholinergics Data: complete metabolic profile (including LFTs), C BC , ECG , UA Infectious Metabolic Neurologic Cultu re (urine, blood ): +UA Chest x- ray: hypoxia, crackles \n\n ABG: hypoxia, acidosis Ammonia: liver failure TSH: suggestive symptoms (hyper/hypo) CT scan/MRI: focal deficits, anticoagulation Lumbar puncture : mening is mus EEG: seizure history To xicologic screen: \n\nsuggestive history \n\nABG = art eria l blood gas; CAM = Confusion Assessment Method; CBC= complete bk>od coun t; EE G = el ectroencephaJogram , LFT = liver fu nction test , UA = urinalysis . VS = vital signs Management of hospital delirium \n\n> CUWorld\n\nReduce noise , imp rove room lighting, open window blinds during the day & avoid fr e q uent room chan g es Constant observation by a familiar person at the bedside , preferably a family member Nonpharmacologic sleep aids for insomnia Early mobilization & minimal use of physical rest raints \n\n Visual & hearing aids when appropriate Early volume repletion for dehydrated patients \n\n Adequate pain control Aggressive chronic disease management (eg , diabetes , COPD) Reduce polypharmacy Monitor & treat for metabolic disturbances, infec ti ons & drug toxicity \n\nCOPD = chronic obstructive pulmonary disease. \n\nDelirium symptom management Common complications of delirium \n\n# . Environment: noise reduction, intervention grouping \n\n# . Sleep facilitation: br i ght day / dim night lighting \n\nNonpharmacologic . Personal interaction: reassurance, physical touch \n\n## . Disorien tati on, fa ll s\n\n## . Immob ility , pressure ulcers Short term . Poor intake, deh ydra tion \n\n## . Aspir ation pn eumonia \n\n## . Constant observation: family, professional sitters . Prolonged hospita liza tion \n\n# . Mobilization: out of bed, restr aint avoidance \n\n# . Pa in management: nonopioid when possible \n\n## . Persistent del irium Long term Nursing home placement .\n\nPharmacologic . Antipsychotics: off-label indication \n\n# . Benzodiazepines: antips~chotic failure/withdrawal s~ ndromes Permanent . Cognitive decline /de menti a\n\n## . Death : ~2 0% mortality at 6 mon ths Definitive management is identification and treatment of t he underlyi ng cause(s). Psychiatry & Substance Abuse Delirium is typically worse at night ; however, fluctuation may allow patients to seem lucid during the day, resulting in under-diagnosis. \n\nHyperactivity (eg, agitation) is classic, although hypoactive delirium (eg, lethargy, somnolence) is more common in the elderly (often misdiagnosed as depression) D/D: Non-convulsive status epilepticus (NCSE) \n\ndescribes ongoing or intermittent seizures without convulsions. Both NCSE and delirium are more frequent in the setting of critical illness and present with fluctuating levels of consciousness. However, NCSE usually demonstrates additional symptoms (eg, catatonia , automatisms , eye deviation ), \n\n## Amnesia \n\nTransient global amnesia typically presents with an anterograde amnesia and is often precipitated by psychological stress. \n\nA typical feature is repeatedly asking the same questions, with identical intonation and choice of words, despite the absence or cessation of any stimulus (known as broken-record phenomenon or perseveration ). \n\n## Childhood Disorders \n\n Adolescents who develop significant changes in behaviour should be assessed for psychosocial \n\nstressors , trauma , substance abuse , and psychiatric disorders. \n\nHow should you first approach an adolescent? \n\nYoung patients often do not confide in adults they do not trust so develop a trusting physician-patient relationship \n\n Physicians should have high index of suspicion for physical/sexual abuse in children with sudden behavioural problems, stressful family environments, or parents with active drug/alcohol abuse. \n\n Children who are victims of physical abuse often avoid eye contact on exam According to the DSM-5, pathological encopresis cannot be diagnosed until the patient is at least 4-years-old (or equivalent developmental level). \n\nrepeated involuntary or intentional elimination of faeces inappropriate for developmental age (e.g., into clothes or on the floor) \n\n According to the DSM-5, pathological enuresis cannot be diagnosed until the patient is at least 5-years-old (or equivalent developmental level). \n\n725 https://t.me/usmleinnercircle USMLE Inner Circle Psychiatry & Substance Abuse Language Disorder is characterised by persistent difficulties in comprehension (receptive) and/or \n\nproduction (expression) of spoken and written language. It may involve the rules (grammar, syntax, morphology), content (vocabulary), and/or functional use of language. Typical symptoms include a markedly limited vocabulary , errors in tense , and difficulty producing \n\nsentences with developmentally appropriate length and complexity. A learning disorder is characterised by difficulty in acquiring and using core academic skills (eg, reading, writing, and/or mathematics), which typically manifests at school age but can worsen as academic expectations increase (eg, moving from kindergarten to first grade). Reading disorders manifest with difficulty in fluency , comprehension , and/or accuracy . A common learning disorder is dyslexia , which involves a pattern of difficulty with word recognition, decoding \n\n(ie, producing sound associated with letters or words), or spelling , affecting both reading and writing. This can affect the ability to follow directions and be associated with behavioural problems and reluctance to engage in learning due to negative self-concept. \n\n Learning disorder: Child has a problem acquiring and applying skills in reading , writing or \n\nmath , for e.g a child who has problems sounding out (reading) unfamiliar words \n\n Many environmental and social circumstances affect the behavioral development of a child. Family members with a history of significant behavioral issues (eg, illegal activities, incarceration, drugs use) do not necessarily lead to an increased inheritance risk for behavioral disorders in a child. \n\nReactive Attachment disorder \n\n726 https://t.me/usmleinnercircle \n\n> Parent management training Focus Parent interventions Antecedents\n\n# . Avoid (promote unwanted behavior): . Use (promote wanted behavior): (communication 0 nagging 0 clear instructions leadi ng to 0 threats 0 calm tones & supportive gestures wanted/unwanted 0 harsh comments \n\n> 0alternative choices behaviors) 0physical intimidation\n> Behaviors\n\n# . Shaping: . Role-play wanted behaviors: (practicing effective small behavioral goals adding to bigger artificial situations first 0 0parent-child changes build to realistic scenarios 0interactions) \n\n> Consequences Reinforce wanted behaviors: Manage unwanted behaviors:\n\n# . .(for wanted/ praise (verbal, nonverbal) extinction (eg, ignore, walk away) 0 0unwanted 0 token/point system rewards 0 mild punishment (eg, privilege loss) behaviors) Psychiatry & Substance Abuse Disinhibited social engagement disorder (DSED) is another possible outcome of severe neglect or abuse. Unlike RAD, where children are emotionally distant, children with DSED display overfamiliarity (even with adults they do not know) and a lack of appropriate boundary setting .\n\nOppositional Defiant \n\nD/D: Conduct disorder but it includes severe aggressive behaviour. \n\n A degree of rebellion against authority is normal (not complying with bedtime, questioning family rules) \n\nTourette Syndrome \n\n727 https://t.me/usmleinnercircle USMLE Inner Circle \n\nReactive attachment disorder \n\n# . Insufficient care (eg, neglect, abuse, inconsistent ca regiving) \n\nClinical features (some evidence . Does not seek or respond to comfort \n\n<5 years) . Poor social responsiveness, limited positive affect . Unexplained irritability/fear/sadness even during safe encounters \n\n## . Toileting & sleep difficulties \n\nAssociated features . Anxie!i'., a22 ression, hyeeracti vi !i'./imeulsivi!i'. \n\n# . Adjustment disorder, posttraumatic stress disorder . Global developmental delay , intellectual disability \n\nDifferential diagnosis . Autism spectrum disorder \n\n## . Anxiety disorders (eg, social anxiety disorder, selective mutism) . Depressive disorders \n\n## . Early intervent ion promoting: 0 safe, stable & enriching environment \n\nManagement consistent, responsive caregiving 0\n\n## . Psyc ho logical services (eg, parenting skills, individual/family counseling) \n\nOppositional defiant disorder \n\nPattern of angry/irritable mood, argumenta ti ve/defiant behavior, or vindictiveness for 2'6 months \n\n# . Argues with adults, defies authority figures, refuses to fo ll ow rules \n\nDiagnosi s . Deliberately annoys others \n\n## . Blames others for own mistakes or misbehavior \n\n## . Easily annoyed, ang ry , resentful, or vindictive \n\n# . Not due to ano th er mental disorder . Parent management training \n\nTreat men t . Psychotherapy (anger management, social skills training) \n\n# . No pharmacotherapy for ODD but assess for comorbid ADHD & treat if present \n\nADHD = attention deficit hyperactivity disorder; ODD = oppositional defiant di sorder. Psychiatry & Substance Abuse ADHD \n\n Attention-deficit hyperactivity disorder (ADHD) continues into adulthood in 50 % of cases Parents may be concerned about stimulant adverse effects in their children, they should be informed that stimulants are highly effective for ADHD and are generally well tolerated .Common adverse effects such as insomnia and appetite suppression can be managed strategically (eg, giving stimulants earlier in the day to prevent insomnia, large morning meals prior to administration to counteract decreased appetite). Methylphenidate is the first-line therapy for ADHD but should not be used in patients <6 years of age. \n\nBehavioural therapy is first-line therapy for pre-school aged children, and adjunct therapies for school-aged children and adults \n\n<6y: Behavioural Therapy >6y: Stimulants (First line), Atomoxetine \n\nASD \n\n728 https://t.me/usmleinnercircle \n\nTour ette syndrome \n\n## . Both multiple mot or & 2:1 vocal ti cs (not necessarily concurrent, >1 year) \n\n> 0\n\nMotor: facial grimacing, blinking, head/neck jerking, shoulder shrugging, \n\nClinical to ngue protrusion, sniffing \n\nfeatur es 0 Vocal: gr unt ing, snorting, throat clearing, ba rking, yelling, coprolalia (o bscenities) \n\n## . Onset age <18 \n\n## . Attention deficit hyperactivi ty disorder \n\nComorbidity Obsessive-compulsive disorder .. Education/watchful waiting if mild & nondisabling \n\n## . Behavioral therapy (habit reversal training) \n\nTreatment . Antidopaminergic agents \n\n> 0\n\nTetrabenazi ne (VMAT2 inhibitor) \n\n> 0\n\nAntipsychotics (receptor blockers) \n\n## . Alpha-2 adrenergic receptor agonists \n\nPrognos is . Severity peaks age 10 -1 2\n\n## . Ma jority resol ve or improve in adulthood; ti cs persist in 1/3 \n\nAtt ention deficit hyperact iv ity disorder \n\n# . Inattentive &/o r hyperactive/impulsive symptoms for 2:6 months 0 Ina tt entive symp t om s: difficulty focusing, distractible, does not listen or follow instructio ns , disorganized, forgetful, loses/misplaces objects \n\nClinical 0 Hyper ac tive/impul si ve symptoms: fidgety, unable to sit still, \"driven by a motor,\" hypertalkative, interrupts, blurts out \n\nfeature s answers \n\n# . Several symptoms present be for e age 12 \n\n# . Symptoms occur in at least 2 settings (home, school) & cau se functional impairment \n\n# . Subtypes: predominantly inattentive, predominantly hyperactive/impulsive, combined type . Stimu la nts (methylphenidat e, amphetamines) \n\nTr eat ment . Nonstimulants (atomoxetine, a-2 adrenergic agonists) . Behavioral the rapy Psychiatry & Substance Abuse Language delay without an attempt to compensate through nonverbal means of communication is characteristic of ASD. The diagnosis of ASD is a clinical one , but it should ideally involve a comprehensive evaluation ,including structured assessments of social, language, and intellectual development in addition to hearing, vision, and genetic (eg, fragile X syndrome) testing. Young children often prefer particular foods or food groups, which is consistent with normal development .However, when picky eating is accompanied by behavioural rigidity, poor growth, weight loss, or developmental delays, further evaluation is indicated. \n\nIntermittent Explosive Disorder \n\n Intermittent explosive disorder is characterised by recurrent episodes of impulsive verbal or physical aggression . Onset after age 6 \n\nThe aggressive behaviours are unplanned and out of proportion to the provocation and last <30 mins. \n\nf/b embarrassment/ remorse \n\nT/t: SSRI , Psychotherapy D/D: \n\n Mania ( symptoms last days or weeks) Disruptive Mood Dysregulation Disorder ( Person is constantly angry between episodes, onset before age 10 and not made after age 18 and before age 6) T/t: Stimulants , Anti-psychotic \n\nGender Dysphoria \n\n Gender identity is a person's internal sense of being male, female, a combination of both, or neither. Gender dysphoria is characterised by persistent distress due to a discrepancy between assigned gender and innately felt gender. early diagnosis and intervention is important to improve prognosis \n\n729 https://t.me/usmleinnercircle USMLE Inner Circle \n\nAutism spectrum disorder \n\n## . Deficits in social communication & interactions with onset in early childhood \n\n> 0\n\nImpaired social engagement (eg, back-and-forth conversation) \n\n> 0\n\nImpaired nonverba l comm11nicalion (eg, eye contacVgesturing) \n\n> 0\n\nDifficulty developing/understanding relationships (eg, inte res t in peers) Clinical features . Restricted, repetitive patterns of behavior \n\n> 0\n\nRe petitive movements or sp eech \n\n> 0\n\nInsistence on sameness/routines \n\n> 0\n\nIntense fixated interests \n\n> 0\n\nAdverse responses to sensory input (eg, textures) \n\n## . May occur with or without language & intellectual impairment \n\n## . Ear1y diagnosis & intervention Assessment & management . Comprehensive, multimodal treatment (eg, speech & behavioral therapy, educational principles services) \n\n## . Adjunctive pharmacotherapy for psychiatric comorbidities Psychiatry & Substance Abuse Gender expression is how a person chooses to express gender to the outside world. When gender identity or gender expression differ from social norms and/or expectations , it is referred to as gender variance or gender nonconformity .\n\n## Sleep Disorders \n\n What is the likely diagnosis in a patient that experiences sleep difficulties with normal bed times? The patient has no difficulty going to bed and waking up late ( e.g. sleeping from 4 am to 12 pm ). \n\nDelayed sleep phase syndrome Circadian rhythm disorder characterized by inability to fall asleep at \"normal\" bedtimes (\"night owls\") Advanced sleep phase syndrome , where patients cannot stay up late and have early morning insomnia (early birds) Treatment includes phototherapy in the evening. Poor sleep hygiene is a common cause of insomnia .Strategies to improve sleep hygiene include maintaining a regular sleep schedule and a quiet, dark, and comfortably cool bedroom; avoiding late afternoon naps and exposure to electronic devices \n\nbefore bedtime; and avoiding nicotine, caffeine, alcohol , and heavy meals in the evening .\n\n Poor sleeping habits displayed by patient: Sleeping late at night and smoking late at night (tobacco is a stimulant so basically equivalent of drinking coffee late at night) Key idea: First step in many problems associated with insomnia or difficulty sleeping is to educate patient about proper sleep hygiene \n\n 79 y.o. female complains of decreased total sleep time , earlier onset of sleep, nocturnal awakenings , reduced sleep during early-morning hours , and daytime napping. What is the most appropriate intervention ?\n\nReassurance \n\nThese are consistent with aging and no further workup is necessary if there is no significant impairment in activities of daily living or cognition \n\n Normal, age-related sleep changes include decreased total sleep time ; increased nighttime \n\nawakenings ; sleepiness earlier in the evening with early morning awakening ; and \n\nincreased daytime somnolence (napping). \n\n Depression is associated with increased total REM sleep. \n\nthus, these patients have decreased slow-wave sleep Also have DECREASED REM latency. \n\n Depression, normal aging, and narcolepsy are associated with decreased REM latency. \n\n730 https://t.me/usmleinnercircle Psychiatry & Substance Abuse however, depressed patients experience increased REM sleep, while normal aging results in decreased REM sleep \n\n Do patients with nightmare disorder have any memory of the scary dream? \n\nYes \n\noccurs during REM sleep ; important distinguishing feature from night terrors (N3 stage) \n\nREM Sleep Disorder \n\n Do patients remember their dreams in REM sleep behavior disorder ?\n\nYes \n\n In older patients, REM sleep behavior disorder may be a sign of neurodegeneration .\n\nNarcolepsy \n\n First-line treatment for diurnal sleepiness of narcolepsy involves daytime stimulants ( modafinil, amphetamines ).\n\nGeneral approach: ensure regular sleep periods, avoid meds that disturb sleep-wake rhythm (alcohol, antipsychotics, opiates) \n\nMedical therapy \n\nDiurnal sleepiness: Modafinil (CNS stimulant). Alternative: night-time sodium oxybate (never taken with alcohol or other CNS depressants may cause life-threatening respiratory depression) For cataplexy , sleep paralysis , and sleep hallucinations :Muscle atonia absent caused by decreased hypocretin (orexin ) production in the lateral hypothalamus. \n\n731 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\n00\n\n\n\nREM sleep behavior disorder \n\n REM _ sl eep arousal disorder (patient remembers the dream) \n\n Epi demiology Prevalence: (-0.5%) \n\nSex : d' > 50 years) \n\n Ri sk factors: associated with ~-~-~ ~~-1~-~~ Y. psychiatric me dications c;J , and neurodegenerative disorders c;J \n\n C li nical features \n\nActing out dreams during sleep c;J (sometimes leading to injury to self or others) Alert and orientated after awakening Trea tm ent \n\n Remove dangerous objects from the bedroom to re duce risk of self-injury If applicable, discontinue causative medications \n\n -~~ ~~ ?.~ ! ~ ~~P. !~ ~~ (e.g., ~!!? .':1 .~~~P.~.':i'.') \n\n Melatonin an al ogs \n\nNarcolepsy \n\n. Recurrent lapses into sleep or naps (2' 3 times/week for 3 months) \n\n. 2'1 of the following : \n\nDSM-5 diagnostic 0 Cataplexy: Brief loss of muscle tone precipitated by strong emotion (eg, laughter, \n\ncriteria excitement) \n\n> 0\n\nLow cerebrospinal fluid levels of hy po cretin-1 \n\n> 0\n\nShortened REM sleep latency \n\nAssociated features . Hypnagogic or hypnopompic hallucinations \n\n. Sleep paraly si sPsychiatry & Substance Abuse SSRIs or SNRIs \n\n Sleep paralysis , a manifestation of the atonia that primarily occurs during rapid eye movement (REM) sleep, happens during the transition from sleep to wakefulness at least once in most people's lives. After a single episode of sleep paralysis, reassurance is appropriate, but if sleep paralysis recurs, narcolepsy should be ruled out. \n\nSleep Terror \n\n Parents should be reassured that sleep terrors are not dangerous and usually resolve spontaneously \n\nwithin 1- 2 years. \n\n## Mood Disorder \n\nDepression \n\n Major depressive disorder is associated with increased levels of cortisol. \n\ndue to hyperactivity of the hypothalamic-pituitary-adrenal axis; results in increased early morning awakenings \n\n Other findings: 1. Decreased hippocampal and frontal lobe volumes \n\n2. Decreased REM latency \n\n3. Increased REM duration \n\n732 https://t.me/usmleinnercircle \n\n> 0\n\nSleep terrors \n\n# . Abrupt arousals from sl eep (pan i cked sc ream , terror , autonomic arousal, unrespons ive to \n\nFeatur es comfort) \n\n# . Little or no dream recall \n\n## . Amnesia for episodes \n\n## . Reassurance \n\nManagement . Administer low-dose benzodiazepine at bedtime if episodes are freq uen t. persistent & distressing \n\nDifferential diagnosis of depressed mood \n\n# . ~2weeks \n\nMajor depressive di sorder . ~5 of 9 symptoms: depressed mood & SIGECAPS \n\n## . Si gn ificant fun ctiona l im pa irm ent \n\n## . No lifetime history of mania \n\nPe rsis tent depre ss ive disorder . C hro ni c depressed m ood ~2 years (dysthymia) . ~2 of the following: appetite disturbance, sleep disturbance, low ener gy , low self-esteem, poor \n\nconce ntra tion, hopelessness \n\n## . Onset within 3 months of identifiable stressor \n\nAdjustment disorder with . Marked di st ress &/or f un ct io nal impairment depressed mood . Does not meet criteria for ano th er DSM-5 di so rde rNormal stress re sponse . N ot excess ive or out of pr oportio n to seve ri ty of stresso r\n\n## . No significant functional impairment \n\nSIGECAPS = Sl eep disturbance, loss of I ntere st, excessive Gu ilt , low Energy , im paired C oncentration , A ppetite dis turba nce, Psychomotor agitation/retardat ion , and Su icidal ideation .Psychiatry & Substance Abuse Patients with depression or anxiety often come to the office with headaches or other physical symptoms (eg, fatigue, insomnia , nonspecific aches and pains ) due to a lack of psychologic awareness or a perceived stigma around mental health issues. \n\n Pediatric depression often presents with symptoms of irritability rather than depressed mood. \n\n OSA frequently presents with depressive symptoms such as fatigue, sleep disturbance with multiple awakenings, impaired concentration , irritability , and low mood . Rule it out first, spl in obese males \n\n Possible etiologic factors for poststroke depression include inflammation, cerebrovascular dysregulation, altered neuroplasticity, and altered glutamate neurotransmission. \n\nSeasonal Affective Disorder \n\n What is the treatment in a patient with recurrent major depressive episodes with the onset in the fall and remission in the spring ?\n\nAntidepressants and bright-light therapy \n\nAlso known as seasonal affective disorder .Bright light therapy is administered with a 10,000-lux light box shortly after awakening. \n\nPostpartum \n\n Postpartum depression has a high incidence and is often underreported .Therefore, all women (regardless of prior psychiatric history) require screening for postpartum depression (eg, Edinburgh Postnatal Depression Scale). \n\nDysthymia \n\n733 https://t.me/usmleinnercircle USMLE Inner Circle \n\nMajor depressive disorder vs seasonal affective disorder* MDD SAD \n\n# . Recurrent m ajo r dep ressive epi sod es \n\n# . Si ng le or r ec urrent major d ep ress ive episodes . l!:2-y e ar pattern of seasonal recurren ce & remi ss ion (eg, \n\nClinical features (2:2 weeks of 2:5 of depressio n+ SI G- E -CA P S) win ter onset, sp ring re mi ssion) \n\n# . No seasonal pattern . No nonseasonal dep ressive epi sodes \n\n# . Li fet i me seasonal >>> nonseasonal depressive ep isodes \n\n# . Antidepr essa nt (eg, SSR I) + light therapy \n\n# . Antidepressant (eg, SSR I) . Psycho th e r apy (C BT )\n\nMan a gement . Psych ot her apy (C BT ) . Behav iora l (eg, ou tdoor wa lk s, aerobic exe rcise, sl eep \n\n# . Comb in ed t herapy hygien e) 'Seasonal affective disorder= major depressive disorder with seasonal pattern. \n\nCB T = cognitive-behavioral therapy; MOD = major depressive disorder; SAD = seasonal affective disorder; SIG-E- CAPS = Sleep, Interest, Guilt, Energy, Concentration, Appetite, Psychomotor changes, S ui ci dality; SSRI = selective serotonin reuptake inhibitor. Psychiatry & Substance Abuse Bipolar \n\n Genetic predisposition is the strongest predisposing risk factor for bipolar disorder \n\n Patients with bipolar I disorder may have psychotic symptoms (eg, delusions, hallucinations) when they experience severe manic and depressive episodes. The absence of psychotic symptoms outside of mood episodes , for eg in a patient who is only psychotic when he is manic, rules out primary psychotic disorders. \n\n Delusions in mania often involve grandiose themes in which patients believe that they have special abilities or powers or that others are jealous of them. Rapid Cycling Bipolar I disorder is a subtype of Bipolar I Disorder that involves at least 4 mood episodes in 12 months .\n\nTreatment with valproate \n\ne.g. cycle of MDE, mania, hypomania or mixed \n\n734 https://t.me/usmleinnercircle \n\nPersistent depressive disorder (dysthymia) \n\n Ch ron ic de pr essed mood l: 2 years (1 year in childr en /adolescents) No symptom-fr ee period for >2 months Presence of at least 2 of the following: \n\nDSM-5 o Poor appetite or overeating o Insomnia or hypersomnia o L ow energy or fatigue o Low se lf-esteem o Poor concentration or difficul ty making decisions o Feel in gs of hopelessness With pure dy sthymic syndrome: Criteria for major dep ressive episode never met \n\nSpecifiers With intermittent major depressi ve episodes With persistent major depressive episodes: Criteria for major depressive episode met throughout previous 2 years \n\nBipolar & related disorders Manic episode Hypomanic episode \n\n# . Symptoms more severe . Symptoms less severe \n\n# . 1 week unless hospitalized . 2:4 consecutive days \n\n# . Marked impairment in social or occupational functioning or . Unequivocal, observable change in functioning from pat ient's \n\nhospitalization necessary baseline \n\n# . May have psychotic features; makes episode manic by . Symptoms not severe enough to cause marked im pa irment or definition necessitate hospitalization \n\n# . No psychotic features Bipolar I. Manic episode(s) \n\n# . Depress ive episodes common but not required for diagnosis \n\nBipolar II . Hypomanic episode(s) \n\n# . ~1 major depressive episodes \n\nCyclothymic disorder \n\n# . 2:2 years of fluctuating, mild hy po manic & depressive symptoms that do not meet criteria for hypomanic or major depressive ep isodes Psychiatry & Substance Abuse Poor prognosis. \n\nDoes a patient with cyclothymia typically return to normal mood and functioning between episodes? \n\nNo \n\nminimal return to baseline ( < 2 months per 2 years )\n\n(vs Bipolar with normal mood between episodes) ADHD has a chronic (not episodic) course and presents with ongoing difficulties that begin in childhood. (vs acute in mania )\n\n Agitated, aggressive patient: Give Benzo \n\n## Psychotic Disorder \n\n735 https://t.me/usmleinnercircle USMLE Inner Circle \n\n Sy mp toms mu st last fo r at least 2 years Constant cy clin~i ni mal return to bas eli ne (< 2 mo per 2 yrs) Mood di so rde rs wi t h ps yc ho ti c features vs prima ry psychot ic d is o rders Major depre ss ive or bipolar di sorder wi th ps ychotic . Psychotic symptoms occur exclusively during mood episodes. features Schizophrenia . Mood symptoms, if present, are brief and not prominent. \n\n. Major depressive or manic episode occurs conc ur rent with symptoms of schizophrenia. Schizo affective di sorder . Lifetime history of delusions or hallucinations for .!:2 weeks outside of mood episode is present. \n\n. Mood episodes are prominent & recur throughout illness. Acute mania \n\n## . Elevated , i rr itable, labile mood C lin ica l . Increased energy & activity, decreased need for sleep f ea tu res . Pressured speech, racing thoughts, distractibility . Grandiosity, risky behavior . Marked impairment, may have psychotic symptoms . Antipsychotics (first- & second-generation) . Lithium (avoid in renal disease) Ma na ge ment . Valproate (avo id in liver disease) \n\n## . Combinations in severe mania (eg, antipsychotic plus lithium or valproate) \n\n## . Adjunctive benzodiazepines for insomnia 1 agitation Psychiatry & Substance Abuse High-dose glucocorticoids may cause glucocorticoid-induced psychosis (e.g. hypomania, confusion, hallucinations ). typically occur during the first week of glucocorticoid treatment but can occur at any time .Glucocorticoids can also cause manic or depressive symptoms. \n\n In general always rule out medication and substance abuse related symptoms first !\n\n New-onset behavioural changes in an older patient with no psychiatric history should prompt consideration of medical and substance-/medication-related causes . Indications for involuntary psychiatric hospitalisation including being a danger to self or others and/or grave disability (inability to care for self ) due to mental illness. Hospitalisation may be implemented on an involuntary basis if necessary. \n\nPsychosis \n\n736 https://t.me/usmleinnercircle \n\n> Differential diagnosis of DSM-5 psychotic disorders Brief psychotic ~1 days & <1 month , sudden onset, full return to function\n> disorder Schizophreniform ~1 months & <6 months, same symptoms as schizophrenia, functional decline not required\n> disorder Schizophrenia ~6 months (includes 2:1 months of active symptoms, can include prodromal & residual periods), requires functional decline\n> Schizoaffective Mood episode with concurrent active-phase symptoms of schizophrenia\n\n+ 2:2 weeks of delusions or hallucinations \n\n> disorder in the absence of prominent mood symptoms\n> Delusional ~1 delusions & ~1 months, no other psychotic symptoms, normal functioning apart from direct i mpact of\n> disorder delusions\n\nPsychiatry & Substance Abuse What is the most likely explanation for hallucinations in a young boy with fever, runny nose, and a cough who appears to be talking to someone in the room and says she can see her old cat ? The parents have tried OTC cough and cold medications for the past 36 hours. Labs are significant for fever of 101 F. \n\nMedication side effect due to antihistamines \n\nMost OTC preparations contain antihistamines but also have anticholinergic properties that can cause confusion and hallucinations .\n\nCough suppressant dextromethorphan can also cause dissociative symptoms and hallucinations \n\n To build rapport, it is important to acknowledge the patient's experience and distress without \n\nendorsing specific delusions or hallucinations. \n\nDelusion \n\nPersecutory (eg, being poisoned, harassed, plotted against) \n\nErotomanic (eg, false belief that someone of higher status is in love with the person) \n\nGrandiose (eg, great talent, insights, achievements) \n\nJealous (eg, unfaithful partners) \n\n737 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSecondary causes of acute-onset psychos is in ch il dren & adolescents Central nervous s ys tem Injury/dysfunction \n\n. Trauma \n\n. Space-occupying lesions \n\n. Infection \n\n. Stroke \n\n. Epilepsy \n\n. Cerebral hypoxia Metabolic/electrolyte disturbances Medical di sorde rs . Urea cycle disorders \n\n. Acute intermittent porphyria \n\n. Wilson disease \n\n. Renal/liver failure \n\n. Hypoglycemia \n\n. Sodium/calcium/magnesium disturbances Systemic disorders \n\n. Systemic lupus erythematosus \n\n. Thyroiditis \n\n. Hallucinogens (eg, PCP , L SD , ketamine) \n\n. Marijuana I lli cit subs tance use . Sympathomimetics (eg, cocaine , amphetamines) \n\n. Alcohol withdrawal \n\n. Bath salts Into x icat i on \n\n. Anticholine rg ics (eg, diphenhydramine, scopolamine) \n\n. Serotonin syndrome \n\n. Amoxicillin/erythromycin/clarithromycin \n\n. Anticonvulsants Medicat ion si de effec ts . Corticosteroids \n\n. lsoniazid Withdrawal \n\n. Baclofen \n\n. Benzodiazepines \n\nDelusional disorder \n\n## . 2: 1 de lu sions fo r 2:1 mo nths \n\nClinical features . Other es~chotic s~metoms absent or not erominent \n\n## . Behavior not obviously odd/bizarre; abi li ty to function apart from delusion's impact \n\n## . Subtypes: erotoma ni c, grandiose, jealou s, persecutory & somatic \n\nTreatment . An ti psychotics \n\n## . Cognitive -b ehavioral therapy \n\nPsychiatry & Substance Abuse Somatic (eg, bodily functions, sensations) (cannot be convinced of the possibility that they do not have the illness vs illness anxiety disorder )\n\n Delusions can be shared by individuals in close relationships; termed folie a deux. \n\nFormerly known as shared psychotic disorder now called Delusional symptoms in partner of individual with delusional disorder One persons delusion is transferred to another person \n\nAssess both individuals separately to determine degree of delusions in each \n\n Is functioning impaired in patients with delusional disorder ?\n\nNo \n\nBehaviour is not obviously bizarre or odd (vs Schizo )\n\nSchizophrenia \n\n Obstetric complications (hypoxia, haemorrhage, infection, preterm labor ) have been identified as an environmental risk factor for the later development of schizophrenia .\n\nAlso urban areas , birth in late winter-early spring , and advanced paternal age Urban areas is most likely due to loss of family structure and instability vs. rural areas that usually have more family support \n\n Schizophrenia presents earlier in men . What is the risk of developing schizophrenia in monozygotic twins? \n\n50% \n\n~10% if 1st degree relative \n\n~40% if both parents are affected Risk is 2% in general population \n\n Family therapy is an effective adjunct to antipsychotic medication in patients with schizophrenia and has been shown to reduce the risk of relapse. It focuses on educating the family about the symptoms, course, and treatment of the disorder, and it helps to promote a supportive family environment .\n\n## Suicide \n\n738 https://t.me/usmleinnercircle \n\n \n\n> Prognostic factors in schizophrenia Good Poor\n\n## . Later onset . Onset in childhood or adolescence . Female sex . Male sex \n\n## . Acute onset with precipitant . Gradual onset (prodrome), no precipitant \n\n## . Predominantly positive symptoms . Predominantly negative symptoms \n\n## . No family history . Family history of psychotic illness \n\n## . Short duration of active symptoms . Long duration of untreated psychosis Psychiatry & Substance Abuse A 17 y.o. teenager with active suicidal ideation must be hospitalized for safety and the parents must be informed. Is parental consent required ?\n\nIt is ideal, but not required. (You have to encourage the patient though) \n\nFurthermore, depending on the state, if a minor consents to inpatient psychiatric hospitalization, then confidentiality must be maintained, and protected health information cannot be released without the minor's consent \n\n In most jurisdictions, there is an exception that allows minors age 17 (age 16 in some states) to consent for themselves to inpatient psychiatric hospitalization \n\n Suicide-risk assessment in adolescents should include direct and nonjudgmental questions to determine the nature and intensity of suicidal thoughts. \n\nConfidentiality should not be promised because it cannot be maintained if the patient is at high risk for self-harm. \n\n739 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSuicide risk assessment: evaluate ideation, method, plan, intent Suicidal Wish to die, not wake up (passive) \n\nideation Thoughts of killing self (active) Thoughts of specific method (eg, weapons , pills) \n\nMethod/ Accessibility of method (eg, medication, gun access) \n\naccessibility Lethality of method (eg, gunshot to head, jumping from high floor, potentially lethal overdose of pills) \n\nPreparations/ Steps taken toward making a suicide attempt: collecting pills, obtaining a gun, giving valuables \n\nplanning away, writing a will or suicide note Specific planning of time, place, details \n\nIntent Strength of intention to act on suicidal thoughts Time frame (next 48 hr, weeks to months) \n\nManagement of suicidality Imminent risk of suicide (voiced intent, high number of unmanaged risk factors , collateral concerns raised) \n\n. Ensure safety: hospitalize immediately (involuntary if necessary) & start 1 :1 for constant observation \n\n## . Remove personal belongings & objects in room that may present self-harm risk \n\n## . Security may be required to hold against will \n\nManagement Nonimminent risk of suicide (no intent, strong social supports available , outpatient follow-up plan is reasonable) \n\n## . Create safety plan (eg, coping skills, social supports. crisis numbers) \n\n## . Ensure close follow-up (eg , psychiatry, therapy, intensive outpatient program) \n\n## . Plan to address modifiable risk factors (eg , depression, psychosis , substance use, pain) \n\n## . Ensure family or friends available to support patient \n\n## . Remove access to potential means (eg, secure firearms & medications) \n\nSuicide risk & protective factors \n\n. Psy chiatric disorders, prior suicide attempts \n\n. Hopelessness \n\n. Never married, divorced, separated \n\n. Living alone \n\nRisk factors . Unemployed or unskilled \n\n. Physical illness \n\n. Family history of suicide , family disco rd \n\n. Access to firearms \n\n. Substance abuse, impulsivity \n\n. Social support/family connectedness \n\nProtective factors . Pregnancy \n\n. Parenthood \n\n. Religion & participation in religious activities Psychiatry & Substance Abuse Patients age 18 - 24 have a slightly increased risk of becoming suicidal when initiating antidepressant treatment. \n\nslightly increased risk must be weighed against the benefits of antidepressants \n\n## Homicide \n\n What is the greatest risk factor for committing homicide in adolescents? \n\nAccess to firearms \n\n## Anxiety disorders \n\nPhobia \n\n What is the choice in pharmacotherapy for a patient with specific phobia who refuses CBT or if CBT is not available? \n\nBenzodiazepines ( i.e. lorazepam )\n\nCBT is the preferred first-line therapy \n\nShort-acting benzos are favorable. Take 30 minutes before boarding plane, for example. \n\nSocial Anxiety Disorder \n\n740 https://t.me/usmleinnercircle \n\nHomicide risk factors \n\n Young male Unemp l oyed Impove ri shed \n\n Access to firearms S ub stance abuse \n\n Ant isocial persona l it y diso r de r Hi story of viol ence or cr imin ality \n\n H is t ory of child hood ab use lm pu lsiv ity \n\nSpecific phobia \n\n# . Marked anxie ty about a specific object or situation ( th e ph ob ic stimulu s) f or >6 mon th s\n\nHistory & . Common types : fear of flying, heights, animals, injections, blood \n\nclinical features . Avo ida nce behavior (eg, avo iding bri dges & elevators, ref us ing work requ iring travel) \n\n# . Common (1 0% of p opu l at ion) . Usua lly d eve lops in childhood, often a fter tra um at ic eve nt \n\n# . Cognitive-behavioral therapy with exposure (first-line) \n\nTreatment . Short -acting benzodiazepines ( limit ed role, may help ac ut ely if the rap ist un avail ab le or in suff ici ent ti me) Psychiatry & Substance Abuse Individuals with performance-only social anxiety disorder do not fear nonperformance \n\nsocial situations and are not socially avoidant in general. \n\nAdjustment Disorder Generalised Anxiety Disorder \n\n Patients with GAD frequently seek medical attention in the primary care setting for physical symptoms related to muscle tension or for concerns about fatigue or poor sleep .\n\n741 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSocial anxiety dis or der (social ph ob ia) \n\n. Ma rk ed anxie ty a bo ut ?.1 s oc ial situations fo r ?.6 mon ths \n\n. F ea r of scrut i ny by others, humiliati on , embarrassme nt \n\nDiagnosis . S oci a l situations avo ide d or endu red with intense distress Ma rk ed i mpa i rment (soc ia l, academ i c, oc cupatio nal) \n\n. Subtype specifier: Pe rf ormance only \n\n. SSRI/SNR I\n\nTreatment . Cogn itive- beh av i ora l t herapy Be ta b l oc ke r or be nz od iazep ine for pe rf or ma nce-only subtype \n\nSNRI = sero t on in-n orep i nep hrine reuptake inhibito r; SSR I = se lecti ve serotonin reuptake inhibitor. \n\nAdjustment disorder \n\n## . Mood and behavioral symptom onset within 3 months of identifiable stressor Clinical features . Marked distress and/or functional impai rment \n\n## . Does not meet criteria for another DSM-5 disorder Differential . Normal stress response (not excessive, no significant impairment) \n\ndiagnosis . Acute stress disorder (traumatic event, intrusi ve re-experiencing) \n\n. Major depressive disorder (~2 weeks, 5/9 sy mptoms, depressed mood, SIGECAPS) \n\n## . Psychotherapy is the treatment of choice \n\nManagement . Adjuncti ve pharrnacotherapy (short term, reserved for rapid relief of impairing symptoms [eg, sleep aid, anxiolytic l) SIGECAPS = Sleep disturbance, loss of In terest, excessive Guilt , low En ergy , impaired Concentration, Appetite dis tu rbance, Psychomotor agitation/retardation, and Suicidal ideation. \n\nGeneralized anxiety disorder in children \n\n## . Excessive, uncontrollable worry (multiple issues) ~6 months \n\n## . ~1 of the fo ll owing symptoms: \n\n0 Restlessness; feeling on edge Clinical features 0 Fatigue \n\n0 Difficulty concentrating \n\n0 Irritability \n\n0 Muscle tension \n\n0 Sleep disturbance \n\n## . Physical symptoms: stoma cha ches heada ches \n\nAssociated features . f~[f~~ ti Q i W\n\nTreatment . Cognitive-behavioral therapy \n\n## . SSRls or SNRls \n\n## . Adjustment disorder (response to identifiable stressor) Differential diagnosis . Obsessive-compulsive disorder (intrusive thoughts; compulsive behaviors) \n\n## . Separation anxiety disorder (anxiety focused on separation fr om caregiver) \n\n## . Social anxiety disorder (fears of negative evaluation in social/performance situations) SNRl s = serotonin-norepinephrine reuptake inhibitor; SSRls = sel ec t ive serotonin re uptake inhibitor. Psychiatry & Substance Abuse Panic Disorder \n\n Benzodiazepines may be used to treat generalised anxiety disorder and panic disorder , until SSRIs and SNRIs take effect. \n\nNever used for long-term management increased risk of benzo dependence \n\n Increased sensitivity to lactate infusion is associated with panic attacks .\n\nAmygadala in brain responds to low pH and helps control our response to fear, so lactic acid infusion would make sense that it would induce panic attack \n\n Patients with panic attacks frequently develop agoraphobia , which is anxiety and avoidance of 2 situations in which it may be difficult to escape or get help (eg, being outside the home or in enclosed spaces, using transportation) in the event of a panic attack. Agoraphobia can also be diagnosed independently of panic disorder. Treatment includes SSRIs and CBT* . If pt is on SSRI and and agoraphobia is not adequately controlled , CBT would be treatment of choice (not adjusting her medication) \n\n D/D: Somatic Symptom Disorder where patients have persistent symptoms vs episodic in Panic Disorder \n\nOCD \n\n Person can have multiple OCDs too \n\n742 https://t.me/usmleinnercircle \n\nPanic di sorder \n\n# . Recurrent & unexpect ed panic attacks with 2: 4 of the foll ow ing: 0 Chest pain. palpitations, shortness of br eat h. chok ing 0 Trembling. sweating. nausea. chills \n\nClinical 0 Dizziness. paresthesia \n\nfe a tures 0 Derealizalion, de personalization 0 F ear of losing control or of dying \n\n# . Wor r:t. abo ut a dd it io nal attacks, avoidan ce behavi or \n\n# . First-lin e/ main te nance: SSRI/SNR I &/or cognitive-behavioral therapy \n\nTr e atment . Ac ut e distress: benzodiazepines \n\nSNRI = serotonin norepinephrine reuptake inhibitor; SSRI = se lective serotonin reuptake inhibitor. \n\n-\n\nObsessive-compulsive disorder \n\n## . Obsessions \n\n> 0Recurrent. intrusive. a nxiety-provoking tho ughts. ur ges, or images\n\nClinical features . Compulsi on s \n\n> 0Response to obsessions with repeat ed behaviors or me nt al acts\n> 0Behaviors not co nnected realistically with preventing feared event\n\n## . Time-consuming (>1 hr/d ay ) or causing signifi ca nt distress or imp ai rm ent \n\nTreatme nt . Se lective serotonin reuptake inhibitor \n\n## . Cognitiv e- behavioral ther a py (exposure & response preventi on )Psychiatry & Substance Abuse Disorder characterized by a persistent urge to keep items and accumulation of belongings , resulting in impairment in functioning and/or distress .\n\nHoarding disorder \n\nTreatment: CBT; trial of SSRI if CBT fails ( off-label use )\n\nPersistent urge = obsessive Accumulation of belongings = compulsive \n\n OCD can be differentiated from primary anxiety disorders by unwanted obsessions and associated rituals that are not realistically connected to each other and are clearly excessive (eg, spending hours unplugging appliances). (Ego-Dystronic) \n\nThey are recognised by patients as abnormal ( vs Illness Anxiety Disorder where person are unaware of their problematic behaviour) \n\nBody Dysmorphic Disorder \n\n Physicians should empathize with patients' efforts to cope with their condition and determine their level of insight by gently exploring their perceptions of how others see them. \n\nAcute Stress Disorder \n\n The best initial approach is to provide education on common physical and emotional responses to trauma (eg, avoidance, hypervigilance) and the course of ASD. \n\n743 https://t.me/usmleinnercircle USMLE Inner Circle \n\nBody dysmorphic disorder \n\n# . Preoccupation with 2'1 percei ved physical defects \n\n# . Defects not observable or appear slight to others \n\n# . R epet itive behavior performed in response to the preoccupation (eg, mirror checking, concealing, \n\nClinical features excessive grooming, skin picking) \n\n# . Significant distress or impairment Variable insight (good, poo r, absenVdelusional beliefs) \n\n# . Acknowledge distress; do not refer to perceived flaws as \"imagined\" Reassurance about normal appearance rarely helpful \n\nApproach to patient Focus on alleviating distress & functional impairment .. Avoid inappropriate cosmetic/medical/surgical treatments \n\n# . Antidepressants (selective serotonin reuptake inhibi to rs) \n\nTreatment . Cognitive-behavioral therapy \n\nAcute stress disorder \n\n## . Duration ~3 days & s 1 month \n\n# . Exposure to actual or threatened trauma \n\n## . Symptoms from following categories: \n\n> 0\n\nAvo idan ce of internal memories or externa l reminders Clinical features 0 Intrusion (eg, nightmares, flashbacks) \n\n> 0\n\nDissociation (eg , am ne sia for event, derealization) \n\n> 0\n\nArousal (eg, in so mnia, hypervigilance, startle) \n\n> 0\n\nNegative mood \n\n## . Tr auma-focused, brief CBT \n\nManagement . Consider med ication for ins omnia, inten se anxi ety \n\n## . Monitor for PTSD (symptom duration >1 month) \n\nCBT = cognitive-behavioral th erapy ; PTSD = posttrauma tic stress disorder .Psychiatry & Substance Abuse Normalizing the stress response, while explaining that symptoms may remit but can also cause persistent distress and impairment, would be helpful. \n\n First educate and then do Trauma focused CBT \n\nPTSD \n\n Posttraumatic stress disorder in children may present with distressing dreams with vague content \n\nand reenactment of traumatic themes in play , rather than clearly formulated memories. They often struggle with emotional regulation and may appear easily upset or angered with little provocation. \n\n Small Hippocampus Volume seen in PTSD \n\n Abnormal low cortisol and high catecholamines in urine due to a maladaptive hyperadrenergic response. Also exaggerated Dexamethasone suppression test \n\n## Dissociative Disorders \n\n Patients with DID commonly have chronic auditory hallucinations that have been present since childhood and are perceived as inside the patient's head. \n\n(as opposed to psychotic disorders , in which voices seem to come from outside the head ).\n\n744 https://t.me/usmleinnercircle \n\nPosttraumatic stress di so rder \n\n## . Exposure to life-threatening trauma \n\n## . Nightmares, flashbacks, intrusive memories \n\nClinical . Avoidance of reminders, dissociation \n\nfeatures . Emotional de tachment, negative mood, decreased interest in activities \n\n## . Sleep disturbance, hypervigilance, irritability . Duration >1 month \n\nTreatme nt . Trauma-focused cognitive-behavioral therapy \n\n## . Antidepressants (SSRls, SNRls) \n\nSNRls = serotonin-norepinephrine reuptake inhibitors; SSRls = selective serotonin reuptake inhibitors. \n\nDissociat iv e disorders \n\n# . Persistent or recurrent experiences of 1 or both: \n\nDepersonalization/derealization 0 Depersonalization (feelings of detachme nt from, or being an o ut side obse rver of, one's self) \n\ndisorder 0 Derealization (experienci ng surroundin gs as unreal) \n\n## . Intact reality testing \n\nDissociative amnesia . Inability to recall important personal information, usually of a traumatic or stressful nature \n\n# . Not explained by another disorder (eg, substance use, post-traumatic stress disorder) \n\n# . Marked discontinuity in identity & loss of personal agency with fragmentation in to 2:2 distinct \n\nDissociative identity disorder personality states \n\n# . Associated with severe tr auma/abuse Psychiatry & Substance Abuse Treatment consists of long-term, trauma-focused psychotherapy .\n\n DID is the only disorder that requires the presence of multiple personality states .\n\n## Personality Disorders \n\n Avoidant personality disorder and dependent personality disorder both cling to relationships, but avoidant PD are slow to get involved .\n\nDPD actively and aggressively seek relationships \n\n Personality disorders are not typically diagnosed in youth, during which personalities are still developing. Must be >18 years old \n\n745 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDSM-5 personality disorders Cluster A . Paranoid: suspicious, distrustful, hypervigilant Odd/eccentric . Schizoid: prefers to be a loner, detached, unemotional \n\n## . Schizotypal: unusual thoughts, perceptions & behavior \n\n# . Antisocial: disregard & violation of the rights of others \n\nCluster B . Borderline: chaotic relationships, abandonment fears, labile mood, impulsivity, inner emptiness, self-harm Dramatic/erratic . Histrionic: superficial, theatrical, attention-seeking \n\n## . Narcissistic: grandiosity, lack of empathy \n\nCluster C . Avoidant: avoidance due to fears of criticism & rejection Anxious/fearful . Dependent: submissive, clingy, needs to be taken care of \n\n## . Obsessive-compulsive: rigid, controlling, perfectionistic \n\nParanoid personality disorder \n\n# . Pervasive pattern of distrust & suspiciousness beginning in early adulthood & occurring in a variety of settings (no clear delusions) \n\n0 Believes being exploited & deceived by others \n\nClinical features 0 Interprets benign comments & events as threats; reacts angrily \n\n0 Bears grudges \n\n0 Questions loyalty of partner without justification Delusional disorder (delusions only) \n\nDifferential . Schizophrenia (delusions, hallucinations, disorganization, negative symptoms) \n\ndiagnosis Schizotypal personality disorder (eccentric behavior & thinking, unusual perceptual experiences) .Psychiatry & Substance Abuse In contrast to primary mood disorders , the mood shifts in BPD occur in response to situational stressors and typically last minutes to hours as opposed to the days or weeks required to diagnose manic and depressive episodes. A history of childhood trauma (eg, physical and sexual abuse, neglect) is common in patients with BPD \n\n## Eating Disorders \n\n Binges and inappropriate compensatory behaviours must occur at least once a week for 3 months for the diagnosis \n\nAnorexia Nervosa \n\n746 https://t.me/usmleinnercircle \n\nBorderline personality disorder \n\n# . Pervasive pattern of unstable relationships, self-image & affects & ma rked impulsivi ty , with ~ of the following features: 0 Frantic efforts to avoid abandonment 0 Unstable & intense interpersonal relationships 0 Markedly & persistently unstable self-image \n\nDiagnostic lmpulsivity in ~2 areas that are potentially self-damaging 0\n\ncriteria 0 Recurrent suicidal behaviors or threats of self-mutilation (eg, cutting) 0 Mood instability (marked mood reactivity) 0 Chron ic feelings of emptiness 0 Inappropriate & intense anger 0 Transient stress-related paranoia or dissociation . Primary treatment is psychotherapy (several types effective; best evidence for dialectical behavior ther apy) \n\n## . Adjunctive pharmacotherapy to target mood instability & transient psychos is (second-generation antipsychotics, \n\nTreatment mood stabilizer s) \n\n## . Antidepressants if comorbid mood or anxiety disorder \n\nHistrionic personality disorder \n\n# . Pattern of excessive emotionality & attention-seeking behavior since early adulthood \n\n# . Inappropriate, sexually seductive or provocative behavior; uses appearance to d raw attention \n\nClinical features . Shallow, shifting, dramatic emotions \n\n# . Impressionistic, vague speech \n\n# . Suggestible (easily influenced) \n\n# . Considers relationships more int i mate than they really are \n\nEating disorders \n\nDiagnosis Cl i nical features Treatment \n\n. BMI <18.5 kg/m 2 . Cognitive- be havioral t herapy Anorexia nervosa . Intense fear of weight gain . Nutritional rehabilitation \n\n. Distorted views of body weight & shape . Olanzapine if no response to first-line treatments \n\n. Recurrent episodes of binge eating . Cognitive- be havioral t herapy \n\n. Binge eating and inappropriate compensatory . Nutriti ona l rehabilitati on Bulimia nervosa behavior to prevent we ig ht gain . SSRI (fluoxetine), often in combination with fi rs t-\n\n## . E xcess ive worrying about body shape & we ight line treatments Recurrent episodes of binge eating . Cognitive-behavioral t herapy Binge eating . Behavioral weight loss therapy No inappropriate compensatory behaviors .disorder . SSRI .. Lack of co nt ro l dur i ng eating Lisdexamfetamine, topiramate .SSRI = selective serotonin reuptake inhibitor. Psychiatry & Substance Abuse What is the next step in management for a patient that presents with unstable vital signs and hypokalemia secondary to suspected anorexia nervosa? \n\nHospitalization for nutritional rehabilitation \n\n Patients with anorexia nervosa often have low T3 and/or T4 levels (also known as euthyroid-sick syndrome ) due to the body's adaption to chronic nutritional depletion \n\n## Somatic Syndromes \n\n \" la belle indifference \" is NOT required for the diagnosis of conversion disorder. \n\nThis sign is not specific or sensitive and was removed as a diagnostic criteria from DSM-5. Psychogenic nonepileptic seizure (PNES) is a type of conversion disorder commonly misdiagnosed as a seizure disorder. Features suggestive of PNES include forced eye closure, side-to-side head or body movements, memory recall of the event, and lack of postictal confusion. The gold standard for diagnosis of PNES is video-electroencephalogram of an event demonstrating lack of epileptiform activity. \n\n747 https://t.me/usmleinnercircle USMLE Inner Circle \n\nAnorexia nervosa \n\n## . Significantly low weight \n\nDiagnostic criteria . Fear of weight gain \n\n## . Distorted views of body weight & shape \n\n## . Cardiovascular: Myocardial atrophy, bradycardia, hypotension , arrhythmias \n\n## . Renal: Poor urinary concentration , dehydration \n\n## . Neurological: Seizures, cognitive impairment \n\nComplications . Dermatological : Dry skin , lanugo \n\n## . Gynecological : Amenorrhea , infertility \n\n## . Gastrointestinal : Gastroparesis, constipation \n\n## . Hematological: Cytopenia \n\n## . Other: Electrolyte depletion , osteopenia, hypercholesterolemia, hypercarotenemia \n\nAnorexia nervosa Clinical features . Underweight (BMI <18.5 kgim 2). Fear of we ight ga i n, distorted body image \n\n. Psychotherapy (individual, family, group) \n\nTreatment . Nutritional rehabilitation \n\n. Olanzapine if severe/refractory \n\n. Bradycardia (<40/min), dysrhythmia \n\n. Hypotension (<80/60 mm Hg ), orthostasis \n\nIndications for hospitalization . Hypothermia ( <35 C) \n\n. Electrolyte disturbance, marked dehydration \n\n. Organ compromise (renal , hepatic, cardiac) \n\n. <70 % expected weight (B MI <15 kg/m 2 )\n\nKey features of somatic symptom & related disorders Somatic symptom disorder 2:1 unexplained symptoms ; excessive thoughts , anxiety & behaviors in response to symptoms \n\nIllness anxiety disorder Minimal to no symptoms; preoccupation with idea of having a serious illness \n\nConversion disorder \n\n(functional neurologic Neurologic symptom(s) incompatible with anatomy or pathophysiology symptom disorder) \n\nFactitious disorder Falsification of symptoms/inducing injury in the absence of obvious external rewards \n\nMalingering Falsification of illness for obvious external rewards Psychiatry & Substance Abuse A psychiatric assessment is crucial as many patients with PNES have comorbid psychiatric disorders and/or a history of trauma . Dhat syndrome is a culture-bound syndrome of South Asia that manifests with psychological and \n\nsomatic symptoms that are attributed to loss of semen .When evaluating culture-bound syndromes, it is important to take a patient-centered approach and \n\nallow the patient to explain the cultural explanations, manifestations, and consequences of a given syndrome. \n\nSomatic Symptom Disorder \n\n Regularly scheduled visits that are not symptom driven (ie, do not require patients to develop worsening or new symptoms) are preferable. \n\n The most appropriate initial statement is to deliver the negative test results as good news \n\nthat a serious medical illness has been ruled out. \n\n What is the first-line pharmacotherapy for somatic symptom disorder? \n\nSSRI \n\nFirst-line is to regularly schedule visits and promote stress reduction .If that does not work, CBT and a trial of antidepressant medications (SSRI's) are warranted \n\n Also avoid diagnostic testing or therapies. Schedule individual psychotherapy. Do not hospitalize the patient. \n\nFactitious Disorder \n\n748 https://t.me/usmleinnercircle \n\n> Somatic symptom disorder\n\n## . Female \n\n## . Lower educational level \n\n> Risk factors\n\n## . Chronic childhood illness or family history chronic illness \n\n## . Sexual trauma \n\n## . 2:1 somatic symptoms causing distress/functional impairment \n\n> Key features\n\n## . Excessive thoughts, anxiety or behaviors (time & energy) related to symptoms \n\n## . 2:6-month duration \n\n> Associated\n\n## . High health care use /multip le providers \n\n> features\n\n## . Repeated testing rarely reassuring \n\n## . Regularly scheduled visits (not symptom driven) with same provider \n\n> Management\n\n## . Limit unnecessary workup & speciali st referrals \n\n## . Legitimize symptoms but focus on stress reduction & coping strategies \n\n## . Antidepressants, cognitive behavioral therapy if treatment resistant Psychiatry & Substance Abuse Management of these patients is difficult because they typically respond to confrontation with denial ,leading them to sign out against medical advice and seek treatment elsewhere . A confrontational approach also risks the patient becoming disruptive or physically threatening. Recommended management includes: Giving feedback in a supportive rather than a confrontational manner. Evaluating the patient for comorbid psychiatric disorders , psychosocial stressors , and self-harm \n\n(ie, further self-injurious behavior and/or suicidal ideation, intent, and plan). Patients with factitious illness and malingering have high rates of psychiatric comorbidity , including \n\ndepressive and anxiety disorders , substance use disorders , and personality disorders (eg, borderline personality disorder, antisocial personality disorder). \n\nPsychiatric consultation can also be obtained to assist in assessment and provide guidance on discussing the diagnosis and treatment recommendations with the patient. \n\n## Miscellaneous \n\nBereavement \n\n749 https://t.me/usmleinnercircle USMLE Inner Circle \n\nFactitious disorder (imposed on self) \n\n# . Intenti ona l falsificati on of illness: \n\n0 Fe igning illness \n\nBehavioral 0 Self-induced illness \n\ncharacteristics 0 Exacerbation of preexi st ing illness \n\n# . Motivation by internal factors rather than external ga in (eg, financial compensation) \n\n# . OverVdramatic sy mptoms \n\nClinical . Frequent visi ts for medical care \n\npresentation . Patient possibly refusi ng co n se nt to release recor ds or tampering with tes t sa mpl es \n\n# . More com mo n in health care workers \n\n# . Direct observation or discovery of medi ca l suppli es (eg, medi ca tions, sy ringes) \n\nDiagnostic Confirmatory testing (eg, sulfonylurea screen, stool laxative screen) .confirmation . Medical record review \n\nMajor depressive episode & g rief reaction Major de pressi ve ep isode Gri ef reaction (bereavement) \n\nFi ve of th e fo ll ow i ng 9 sy mptoms: Sl eep dist urba n ces , No rmal r eac tion to l oss appetite ch ange , l ow en er gy , psychomoto r changes , l ow Fe elings of l oss & emp tin ess m ood , anhed onia , g uilt, focus/conce nt ration difficulty, Sym pto ms revol ve ar ou nd the deceased suici da l i dea tion Fu nc tional de cline l ess seve re Low mood or an h edon ia m us t be present \"Waves\" of gri ef at rem inders May occur in respon se to a va riety of stressors, includi ng Wo rthlessness, se lf-loathing, gu ilt & suicidality less loss of l oved one comm on Du rat ion ?.2 wee ks Sad f ee lings are mo re spe cific to de c eased Social & occupa tion al dysfunc ti on Tho ughts of dy i ng i nvo lve jo ining the decease dSu ici da li ty relat ed to h ope l es s ness & wo rt hl ess ness I nt ensity de cr e as es ove r time ( we ek s to m on ths) Psychiatry & Substance Abuse Can a person with grief meet the criteria for major depressive episode ?\n\nYes \n\nstill considered major depressive episode and should be treated as such (e.g. CBT + SSRIs) ,even if they are grieving \n\n Persistent complex bereavement disorder is characterized by prolonged grief, difficulty accepting the death, persistent yearning for the deceased, and maladaptive ruminative thoughts and behaviors. \n\nPsychotherapy is the treatment of choice. \n\nCatatonia \n\n Catalonia is a syndrome that occurs in ill patients with mood disorders with psychotic features, \n\npsychotic disorders , autism spectrum \n\n A lorazepam challenge test (IV lorazepam 1-2 mg) resulting in partial, temporary relief within 5-10 minutes confirms the diagnosis \n\nPyromania \n\n750 https://t.me/usmleinnercircle \n\nBereavement \n\nBereavemen t is a norma l process that shares some symptoms with ma jo r depre ss ive di sorder and may also lead to depression. Bere ave ment Ma j or dep re ssive diso rd er Major complai nt is feeling of loss Major complaint is depressed mo od Normal se lf-esteem Feeling of worthlessness Negative feelings of pain and grief are mixed wi th positi ve memories/feeligns of .j ()~ ed one Fee lin gs predo mina ntly negati ve Generall y no suicida l_ ideation I;] \n\nDai ly function ing maintained Often su icidal ideati on Daily func t ion in g often impaired Catatonia \n\n## . Immobility or excessive purposeless activity \n\n## . Mutism, stupor (decreased alertness & response to stimul i) \n\nClinical features . Negativism (resistance to instructions & movement) \n\n## . Postu ri ng (assuming posi ti ons against gravity) \n\n## . Waxy flexibility (initial resistance, then maintenan ce of new posture) \n\n## . Echolalia, echopraxia (mimicking speech & movemen ts) \n\n## . Benzodiazepines (lorazepam) \n\nManagement Electroconvulsive therapy .\n\nPyromania \n\n# . Deliberate fire setting >1 occasion \n\n# . Fascinatio n w ith fire \n\nClinical features . Tension/arousal prior to act ; pleasure/relief when setting/witnessing fires \n\n# . No external motivation (eg, financial ga in, political st ateme nt , recognition) \n\n# . Conduct disorder, a n ti soc ial personal ity disorder \n\nDifferential diagnosis . Mania, psychosis \n\n# . Impaired judgmen t (eg, neurocognit ive disorder, substance intoxication) Psychiatry & Substance Abuse Psych Drugs & Therapies \n\n A patient with a recent hospitalization 1 month ago for a depressive episode with suicidal ideation develops a maculopapular rash over the patients left scapula. During that hospitalization, his episode remitted and a new medication regimen was initiated. What medication is the most likely cause of this patients condition? \n\nLamotrigine \n\nDiscontinue at first sign of rash. \n\nLamotrigine is an anti-convulsant that is also used as a mood stabilizer in bipolar disorder . A minor rash develops in 10% of patients, and 0.1% develop SJS and TEN. \n\n What is the most likely diagnosis in a patient who becomes agitated and confused shortly after taking his medications? Past medical history includes mild neurocognitive disorder, BPH, and anxiety. medications include terazosin and alprazolam .\n\nParadoxical agitation secondary to benzodiazepines \n\nCharacterized by increased agitation, confusion, aggression, and disinhibiton, typically within an hour of administration \n\nAnti Psychotics \n\nAcute psychotic episodes = short-acting (olanzapine) \n\nPoor adherence = first-generation depot \n\nTreatment resistance = clozapine \n\n Reduce dose before discontinuing only discontinue antipsychotic if reduction doesnt help Akathisia should be considered if a patient becomes agitated or restless when an antipsychotic is changed or the dosage is increased. it is dose dependant \n\n751 https://t.me/usmleinnercircle USMLE Inner Circle \n\nAntipsychotic extrapyramidal effects Pharmacotherapy \n\nAcute . Sudden, sustained contraction of the neck , mouth, . Benztropi ne \n\ndystonia tongue & eye muscles . Diphenhy dram ine . Beta blocker (propranolol) \n\nAkathi sia . Subjective restlessness, inability to s it still . Benzod iazepine (lor aze pam) . Benztropi ne \n\nParkinson ism Gradual-onset tremor , r ig id ity & bradykinesia . Benztropi ne \n\n. . Amantadi ne \n\nTardive . Gradual onset after prolo nge d therapy ( >6 Valbenazine .dyskinesia months): dyskinesia of the mouth , face , trun k & . Deutetrabenazine ext r em ities Management may include reducing th e dose or switching to another a ntipsychotic, depending on the cl inical scenario. Psychiatry & Substance Abuse Aripiprazole and quetiapine are atypical antipyschotics that are the least likely to produce \n\nhyperprolactinemia .\n\nRisperidone is most likely to cause it \n\n Antipsychotics may lower the seizure threshold and must be used with caution in patients who have seizure disorders . (Spl Clozapine) Require weekly CBC for first 6 months \n\n752 https://t.me/usmleinnercircle \n\nMedication-induced dystonia Precipitating medications . Antipsychotics (eg, haloperidol) (dopamine antagonists) . Antiemetics (eg, metoclopramide, prochlorperazine) \n\n## . Onset minutes to 24 hours after starting medication \n\n## . Sudden , sustained contraction of muscles , most often impacting the neck , mouth , tongue , &extraocular muscles Clinical features . Painful, distressing, often with tachycardia &for hypertension \n\n## . Preserved mental status \n\n## . Other extrapyramidal effects (eg, akathisia, parkinsonism, tardive dyskinesia) \n\nTreatment . Cessation (or ! dose) of offending medication(~ possibl e) \n\n## . Anticholinergics (eg, diphenhydramine, benztropine) \n\nAntipsychotic medication effects (dopamine antagonism) in dopamine pathways Second-generation antipsychotic side effects Pathway Effect Mesolimbic Antipsychotic efficacy \n\nWeight gain/ Extra pyramidal Prolonged metabolic syndrome side effects QTc Nigrostriatal Ex tra py ramidal sy mptoms : Acute dystonia ,akathis ia , parkinsonism Aripiprazole Low Low Low Tuberoinfundibular Hyperprolactinemia Clozapine Very high Low Medium Lurasidone Low Medium Low Clozapine treatment guidelines Olanzapine Very high Low Medium \n\n# . Treatment-resistant schizophrenia \n\nIndications . Schizophrenia associated with suicidality \n\nQuetiapine High Low Medium Risperidone High High Medium \n\n# . Agranulocytosis Ziprasidone Low Low High \n\n# . Seizures \n\nAdverse effects . Myocarditis \n\n# . Metabolic syndrome \n\nMetabolic effects of second-generation antipsychotics \n\n## . Weight gain \n\nMetabolic syndrome . Dyslipidemia \n\n## . Hyperglycemia (including new-onset diabetes) \n\nHighest-risk drugs . Clozapine . Olanzapine Baseline & regular follow-up . BMI Monitoring guidelines . Fasting glucose & lipids . Blood pressure \n\n## . Waist circumference Psychiatry & Substance Abuse Antipsychotic medication should be maintained indefinitely in patients with schizophrenia ,including those with a first episode of psychosis. Which antipsychotic medication occassionally causes hypothermia by disrupting thermoregulation and the body's shivering mechanism? \n\nFluphenazine \n\nPatients taking antipsychotics should be advised to avoid prolonged exposure to extreme temperatures. \n\n Which typical antipsychotic is associated with a purple grey metallic rash over sun-exposed areas and jaundice ?\n\nChlorpromazine \n\nTardive Dyskinesia \n\n The most likely atypical antipsychotic to cause tardive dyskinesia is risperidone , and the least likely is clozapine .\n\nIt is good management to replace an alternative antipsychotic with clozapine if tardive dyskinesia is present if antipsychotic dose reduction is not possible due to risk of worsening psychosis \n\n What is the likely underlying pathophysiologic mechanism of tardive dyskinesia ?\n\nD2 receptor upregulation and supersensitivity \n\nNeuroleptic Malignant Syndrome \n\n753 https://t.me/usmleinnercircle USMLE Inner Circle \n\nTardive dyskinesia \n\n## . Abnormal involuntary movements due to prolonged use of anti psychotics or metoclopramide \n\n## . Orofacial dyskinesia (tongue protrusion, lip smacking , grimacing) \n\nClinical features . Limb dyskinesia (dystonic postures, foot tapping , chorea) \n\n## . Trunk dyskinesia (rocking , thrusting , shoulder shrugging) \n\n## . Greater risk with first-generation antipsychotics \n\n## . Discontinue causative medication if feasible \n\nManagement . Switch to second-generation antipsychotic (quetiapine, clozapine) if continued antipsychotic is required \n\n## .Causative .agents ..Pathophysiology .\n\n# ..\n\nSigns/symptoms .....Treatment ... Treat with valbenazin e or deutetrabenazine \n\nNeuroleptic malignant syndrome \n\nAntipsychotic medicati on (eg, haloperidol) Antiemetic medications (eg , promethazine) Withdrawal of Parkinson medications Central dopaminergic receptor blockade (hyperthermia, dysautonomia) Disruption of nigrostriatal dopamine pathways (rigidity) Fever Altered mental status Generalized muscle rigidity (lead-pipe rig idity) Autonomic instability (abnormal vital signs, diaphoresis) Elevated creatine kinase renal failure Stop antipsychotics or restart dopamine agents Supportive care (hydration, cooling), intensive care unit Benzodiazepines Bromocriptine or dantrolene if refractory Autonomic instability ;Neuroleptic malignant syndrome \n\n'?? ?\n\nDiaphoresis - -l----4--1~ \n\nTachypnea Psychiatry & Substance Abuse Serotonin syndrome = similar to NMS but will also have shivering, hyperreflexia, myoclonus, ataxia Also it is acute (<24h) (vs days to week in NMS) \n\n Generalized lead-pipe rigidity is the hallmark of NMS \n\nAnti Depressants \n\n An adequate antidepressant trial is generally considered to be at least 4 - 6 weeks at a therapeutic dosage. \n\nif patient symptoms are not relieved after 4 - 6 weeks, then switching to another first-line antidepressant is be warranted \n\n What is the next step in management for a depressed patient with a partial response to SSRI therapy that complaints of fatigue and weight gain ?\n\nAdd buproprion \n\nin patients with a partial response, augmentation with another form of treatment is beneficial (versus non-responders, who would benefit from switching to another antidepressant) \n\n Major augmentation strategies include adding an antidepressant with a different mechanism of action , a second-generation antipsychotic (eg, aripiprazole), lithium ,\n\ntriiodothyronine , or psychotherapy . Antidepressants need to be tapered over 6-8 weeks to avoid antidepressant discontinuation syndrome , which may produce flu-like symptoms , headache , nausea , insomnia , and myalgias .\n\nOccurs in 20% of pt following sudden discontinuation of an antidepressant that has been taken for more than 6 weeks \n\nRestart drug and taper gradually over several weeks \n\n Antidepressants should be discontinued at least 2 weeks before initiating MAO-is due to risk of serotonin syndrome Fluoxetine should be discontinued at least 5 weeks before initiating MAO-is (d/t its longer half life) \n\n Patients with a single episode of major depressive disorder should continue antidepressants for an \n\nadditional 6 months following the acute response to decrease risk of relapse. \n\nversus patients with recurrent, chronic, or severe episodes, which require treatment for an additional 1- 3 years or indefinitely \n\n Prior history of episodes is the most consistently identified risk factor for future episodes. \n\nHence 2 episodes require 1-3 year drug therapy Idiosyncratic (NOT Dose dependant) \n\n754 https://t.me/usmleinnercircle Psychiatry & Substance Abuse Patients with 3 lifetime depressive episodes, severe episodes (eg, suicide attempts), or episodes lasting 2 years are candidates for lifelong antidepressant treatment. \n\n What is the treatment of choice in a depressed patient with poor appetite , weight loss , or insomnia ?\n\nMirtazapine \n\nIncreases appetite, weight gain, and sedation \n\n Patients taking monoamine oxidase inhibitors such as phenelzine should avoid foods rich in \n\ntyramine as the interaction of such food-drug combinations can result in hypertensive crisis .Tyramine may be present in aged cheeses , aged or cured meats , aged or fermented soy products, \n\noverripe fruits , and some alcoholic beverages . Activating effects (eg, anxiety , insomnia ) are possible early adverse effects of SSRI but frequently improve with time. Patients with anxiety disorders are more sensitive to activating adverse effects and may benefit from a temporary dose reduction or initiation at a lower-than-normal dose. The SNRI , venlafaxine is associated with dose-dependent hypertension due to increased norepinephrine reuptake inhibition at higher dose ranges. \n\nBlood pressure should be assessed before starting venlafaxine and regularly monitored \n\nthroughout treatment. SNRI (eg, duloxetine) have analgesic properties that can be helpful in treating patients with comorbid \n\ndepression and chronic neuropathic pain , including painful diabetic neuropathy .\n\nSerotonin Syndrome also Ondansetron \n\n755 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSerotonin syndrome \n\n. Serotonergic medications, especia lly in combination (eg, SSRI/SNR I, TCA, tramadol) \n\nCauses . Drug interactions: serotonergic medication & MAOI or linezolid \n\n## . Int entiona l overdose of serotonergic medications \n\n## . Serotonergic drugs of abuse (eg, MDMA) Clinical . Mental status changes (eg, anxiety, agitation, delirium) \n\nfeatures . Autonomic dysregulation (eg, diaphoresis, hypertension, tachycardia, hyperthermia, vomiting, diarrhea) \n\n## . Neuromuscular hyperactivity (eg, tremor, myoclonus, hyperreflexia) \n\n## . Discontinuation of all seroton erg ic medications \n\n## . Supporti ve care, seda ti on with benzodiazepines \n\nManagement . Serotonin antagonist (cyproheptadine) if supportive measures fail . Immediate sedation, paral ys is & tracheal intubation if t empe rat ur e >41 .1 C (106 F) \n\nMAOI = monoamine oxidase inhibitor; MOMA = 3 ,4-met hy lenedioxymethamphetamine; \n\nSNRI = serotonin-norepin ep hri ne reuptake inhibit or ; SSRI = selective serotonin reupta ke inhibitor; TCA = tricyclic antidepressant. Psychiatry & Substance Abuse Anti Bipolar \n\nAcute = Antipsychotics ( quetiapine and lurasidone) , lithium \n\nLong-term (maintenance) = lithium + valproate first line. \n\n Approximately 25% of patients treated with lithium will develop hypothyroidism , requiring that all patients have regular TSH monitoring every 6-12 months .Lithium-induced hypothyroidism is generally treated with T4 supplementation rather than discontinuation of lithium. \n\n Bipolar disorder is a highly recurrent illness . Lithium therapy should be maintained in patients whose condition is stable and who are tolerating the medication. What is the drug of choice in a bipolar patient who wishes to become pregnant? \n\nLamotrigine Also obtain B-hCG \n\n756 https://t.me/usmleinnercircle \n\n> Serotonin syndrome\n\nGuidelines for lithium therapy Indications . Acute mania, bipolar maintenance . Chronic kidney disease \n\nContraindications . Heart disease \n\n# . Hyponatremia or diuretic use \n\n# . Blood urea nitrogen, creatinine , calcium , urinalysis \n\nBaseline studies . Thyroid function tests . ECG in patients with coronary risk factors \n\nAcute \n\n# . Tremor, ataxia , weakness . Polyuria polydipsia \n\n# . Vomiting , diarrhea \n\nAdverse . Cognitive impairment \n\neffects Chronic \n\n# . Nephrogenic diabetes insipidus . Chronic kidney disease \n\n# . Thyroid dysfunction \n\n# . Hyperparathyroidism Psychiatry & Substance Abuse Has a favorable reproductive safety profile Treating during pregnancy is tricky because it depends on the severity. If possible, avoid during the first semester . If not, lamotrigine is the drug of choice .\n\nIn patients who switch to another medication, pregnancy should be delayed for 3-6 months to assess the efficacy of the medication. If affective stability is maintained with the new medication, pregnancy can be attempted. \n\n Lithium may be continued during pregnancy, including the first trimester, under specific circumstances in women with bipolar disorder. The risk for potential fetal abnormalities, in particular Ebstein anomaly, must be discussed with the patient and weighed against the potentially severe risks to both the mother and fetus associated with exacerbations of the psychiatric disorder. Most data suggest that lithium is safe during pregnancy after the first trimester . Lithium levels should be monitored carefully during pregnany and fetal cardiac ultrasonography \n\nshould be performed. \n\nECT \n\n ECT is appropriate for severely depressed geriatric patients who require rapid intervention; antidepressants + antipsychotics would take too long to be effective Common adverse effects of electroconvulsive therapy include temporary headache , disorientation ,and partial amnesia ; usually resolves within 6 months. \n\nCommonly includes anterograde and retrograde amnesia \n\nTherapies \n\n757 https://t.me/usmleinnercircle USMLE Inner Circle \n\nEle ct roconvu l si ve the r apy Cond iti ons t reat ed Un ipo lar & bi po lar depressi on Cata to nia Bi po l ar mania Specific i nd i cat i ons Treatment resistance Psyc hotic fea tures present I nd i cations Emergency conditi ons \n\no Refusal to eat or dr ink \n\no Imm inent risk for suicide Pharmacotherapy contraindicated due to comorbid m ed ical illness or poor tolerabili ty Pr egna ncy when pharmacotherapy is u nd es irable or ineffecti ve History of ECT re sponse No abso lute contrai nd icati ons Increased ri sk Safety o Severe car diovascular disease, r ece nt myocardial infar ct ion \n\no Space-occupyi ng brain lesion \n\no Recent stroke, unstable aneurysm Psychiatry & Substance Abuse Interpersonal psychotherapy is an evidence-based therapy primarily used for depression that focuses on the interplay between depressive symptoms and interpersonal stressors \n\n Biofeedback involves using signals from the body (ie, heart rate, muscle tension, skin temperature, blood pressure) as indicators of emotional distress .Patients are taught to identify and control their responses to various stimuli .\n\n## Substance Abuse \n\n758 https://t.me/usmleinnercircle \n\nModality Primary indications Features \n\n# . Depression \n\n# . Generalized anxiety disorder . Combines cognitive & behavioral therapy \n\nCognitive- . PTSD . Challenges maladapti ve cognitions \n\nbehavioral . Panic disorder . Targets avoidance w ith behavioral techniques (relaxation, \n\ntherapy . OCD \n\n# . Eating disorders exposure, behavior modification) \n\n# . Negative thought patterns \n\nInterpersonal . Links symptoms to current relationship conflicts &\n\n# . Depression \n\npsychotherapy interpersonal skill deficits \n\nSupportive . Lower functioning; psychotic disorders . Maintains hope; provides encouragement \n\npsychotherapy . Patients in crisis . Reinforces coping skills, adaptive defenses \n\n# . Builds insight into unconscious conflicts & past \n\nPsychodynamic . Higher functioning relationships \n\npsychotherapy . Personality disorders . Uses transference \n\n# . Breaks down maladaptive defenses \n\nMotivational . Nonjudgmental; acknowledges ambivalence & resistance \n\n# . Substance use disorders \n\ninterviewing . Enhances intrinsic motivation to change \n\nDialectical . Improves emotion regulation, distress tolerance, \n\nbehavioral . Borderline personality disorder mindfulness \n\ntherapy . Decreases self harm; builds skills \n\n# . Improves control over physiological reactions to emotional \n\nBiofeedback . Prominent physical symptoms; pain disorders stressors \n\nOCD = obsessive-compulsive disorder; PTSD = post-traumatic stress disorder. Psychiatry & Substance Abuse Alcohol, benzodiazepine withdrawal are associated with profound autonomic instability (vs Opioid withdrawal) \n\nUrine Drug Test \n\n Urine drug screening can be used in patients on long-term opioid therapy to detect recreational drug use , verify adherence to treatment, and identify possible medication diversion .However, false-positive and false-negative results can occur; unexpected results require confirmatory testing. \n\n For example, common over-the-counter medications (eg, dextromethorphan, diphenhydramine, ibuprofen), which patients often forget to disclose, can cause false-positive results for PCP .\n\n759 https://t.me/usmleinnercircle USMLE Inner Circle \n\nIntoxication syndromes in drugs of abuse \n\nDrug Clinical features \n\n## . Violent behavior \n\n## . Dissociation NMDA antagonists . Hallucinations (eg, PCP, ketamine) . Amnesia \n\n## . Nystagmus (horizontal or vertical) \n\n## . Ataxia \n\n## . Euph oria \n\n## . Tachycardia/hypertension \n\n## . Hyperthermia MDMA (ecstasy) . Serotonin syndrome \n\n## . H ypo natrem ia \n\n## . Seizures \n\n## . Mydriasis \n\n## . CNS depression \n\n## . Nonnal vital signs Benzodlazeplnes . Slurred speech \n\n## . Ataxia \n\n## . Coma \n\n## . Euphoria Opioid narcotics . Depressed mental status (eg, oxycodone) . Respiratory depression \n\n## . Miosis \n\n## . Constipation MOMA= 3,4-methylenedioxymethamphetamine; NMDA = N-methyl-0-aspartate; PCP = phencyclidine. Common withdrawal syndromes Substance Symptoms Examination findings \n\nAlcohol Tr emors, agitation, anxiety, delirium, psychosis Seizures, tachycardia, Tremors, anxiety, perceptual palpitations Benzodiazepines disturbances, psychosis, insomnia Nausea, vomiting, abdominal Dilated pupils, yawning, Op io ids cramping, diarrhea, muscle aches piloerection, lacrimation, hyperactive bowel sounds Stimulants Increased appetite, hypersomnia, (eg, cocaine, intense psychomotor retardation, amphetamines) severe depression (\"crash\") No significa nt findings Nicotine Dysphoria, irritability, anxiety, \n\nI/ increased appetite \n\nlrr itabili~ , anxiet~, deeressed Cannabis mood, insomn ia, decreased No significant findings appetite Psychiatry & Substance Abuse Even if recreational drug use is confirmed, physicians are legally prohibited from reporting it to authorities barring exceptional cases (eg, criminal investigations). \n\nNeonatal Abstinence Symptoms Depressants \n\nAlcohol \n\n Tremors are a hallmark of alcohol withdrawal. T/t: Long acting BZD: Diazepam , Chlordiazepoxide \n\n Hepatic disease (i.e. chronic alcoholic ) or in inpatient setting: Lorazepam \n\n Reduce Cravings: 1. Naltrexone : C/I Opioid use, Liver Failure 2. Acamprosate : C/I Renal Impairment \n\n760 https://t.me/usmleinnercircle \n\nNeonatal abstinence syndrome Pathophysiology . In utero exposure to maternal substances (primarily opioids) \n\n## . CNS: irritability, hypertonia, tremor, shortened sleep-wake \n\nClinical cycles, uncoordinated swallowing \n\nmanifestations . Autonomic nervous system: diaphoresis, sneezing, yawning \n\n## . Gastrointestinal: feeding difficulty, vomiting, diarrhea \n\n## . Primarily clinical \n\nDiagnosis Confirm: umbilical cord blood, urine, or meconium drug testing .. Mild withdrawal: nonpharrnacologic \n\n> 0\n\nMinimize environmental stimul i, swaddling, frequent small \n\n---Treatment feeds \n\n--. Moderate to severe withdrawal: pharrnacologic \n\n> 0\n\nMorphine, methadone \n\nAlcohol withdrawal syndrome Manifestations Symptoms/signs Onset since last drink (hr) Mild Anxiety, insomnia, tremors, diaphoresis, palpitations, gastrointestinal up set, intact 6-24 \n\nwithdrawal orientation Seizures Single or multiple generalized tonic-clonic 12-48 \n\nAlcoholic hallucinosis Visual, auditory, or tactile; intact orientation; stable vital signs 12-48 \n\nDelirium Confusion, agitation,~ . tach~cardia, h~pertension, diaehoresis, hallucinations \n\ntremens 48-96 Psychiatry & Substance Abuse Serum -glutamyltransferase (GGT) is a sensitive indicator of alcohol use. \n\nElevated in cholestasis and alcohol abuse (volume plays greater role than frequency) \n\n Alcohol use disorder refers to an addiction to alcohol that must meet at least two of the following criteria: 1. an inability to cut back on drinking, 2. drinking more than expected, 3. excessive time spent drinking, 4. alcohol cravings, 5. persistent drinking despite physical or mental problems related to drinking, 6. and persistent drinking despite negative social consequences .\n\n Recreational Alcohol use doesnt have dependance and negative consequences like falling grades. It is also NOT legal in adolescents though \n\n761 https://t.me/usmleinnercircle USMLE Inner Circle \n\nFeatures of commonly ingested alcohols Substance typically Major metabolite T Osmolal T Other clinical features ingested gap Ani on gap Ethanol Beer , wine , li quor Acetaldehyde ( minor tox ici ty) Yes Yes (if ketosis) Confusion \n\nMethanol Windshield was her fiuid, Formic acid (major Yes Yes Confus i on , vision deficits homemade li quor to xicity)* \n\nEthylene glycol Antif r eeze Glycolic & oxalic acids Yes Yes Confusion, calcium oxa la te (major t oxicity)* crystals (AK I, flank pain) \n\nlsopropyl alcohol Rubbing alcohol, hand Acetone (m ino r t oxicity) Yes No** Confusion sanitizer *T reatme nt of choice is fomepizole to i nhi bit production of toxic metabolites. \n\n.. No acidosis (anion gap or non-anion gap) is present with isopropyl alcohol ingestion. \n\nAKI = acute kidney injury. \n\nToxic alcohol ingestion (methanol or ethylene glycol) \n\n## . Methanol: windshield wiper fiuid, contaminated h omemade liquor Typ i cal sources . Ethyl ene glycol: automotive coo lanVanti fr eeze br ake fluid \n\n## . Industrial so l ven ts & deicing so lutions may contain either tox ic al coho l\n\n## . Early: C NS sedation & ine br iation, osmo lar gap \n\nClinical features . Late: anion gap metabolic ac ido sis, compe nsatory tachypnea 0 Ocular toxicity (methanol) 0 Urine oxalate crys ta ls. hypocalcemia, AKI (ethylene glycol) \n\n## . Fomepizole (inhibits AD Ha se) is preferred t he ra py Management . Ethanol solution (compe te s for ADHase) if f ome p iz o le una vai lable \n\n## . IV sodium bicarbonate for acidemia (eg, pH <7.3) \n\n## . Hemodialysis for severe cases (eg, acidosis, end-organ damage) ADHase = alcohol dehydrogenase; AKI = acute kidney injury; IV = intrav eno us .Psychiatry & Substance Abuse Benzodiazepines \n\n Benzodiazepine overdose leads to CNS depression , causing lethargy, somnolence, and hypo -\n\nreflexia . Benzodiazepine overdose can result in altered mental status , ataxia , and slurred speech .When vital sign derangements or respiratory depression are seen, co-ingestion with other sedative-hypnotics/central nervous system depressants should be suspected (e.g Alcohol ) What is the likely drug intoxication in a patient that presents with slurred speech , lethargy ,and difficulty walking ? Pupils are 5 mm and respiratory rate is 8/min. \n\nbenzodiazepine or alcohol overdose \n\n Lack of pupillary constriction and severe respiratory depression distinguishes \n\nbenzodiazepine overdose from opioid overdose Benzodiazepine use in the elderly may be associated with paradoxical agitation , which is characterized by confusion and aggression, typically within one hour of use. \n\nother major risks of benzodiazepine use in the elderly include increased cognitive impairment and \n\nfalls \n\nOpioid \n\n What is the next step in management for an unresponsive patient that presents with respiratory depression and decreased bowel sounds ? The patient smells of alcohol. Physical examination reveals 3 mm pupils bilaterally and a respiratory rate of 5/minute. Temperature is 93.2 F .\n\nNaloxone \n\nthis patient likely has opioid intoxication; Hypothermia will improve as OI is reversed \n\nBecause naloxone can precipitate sudden opioid withdrawal, it should be titrated to effect with \n\nsmaller doses to achieve restoration of ventilation , not resolution of all symptoms (eg, return of mental status to baseline). \n\n762 https://t.me/usmleinnercircle \n\nClinical features of acute opioid intoxication \n\n## . Subs tance ab use Risk factors . Chronic op ioid use \n\n## . Hospitalized patients (especially postoperative) \n\n## . Hepatic or renal insufficiency \n\n## . Somnol ence , AMS \n\n## . Pi npo i nt pupils (mi os is) \n\n> Cli nic al findings\n\n## . Shall ow breathing & l respiratory rate \n\n## . Bradycardia, hypothermia, l bowel sounds \n\n# . Respiratory acidosis on ABG \n\n## . Naloxone (may need repeated dosings) \n\n> Management\n\n# . Airway management & vent ilation \n\n# . Exclu de ot h er AMS caus es (eg, hypoglycemi a) \n\n> ABG = arteria lblood gas; AMS =altered me ntal sta tus .\n\nPsychiatry & Substance Abuse Decreased respiratory rate is the most reliable and predictive sign of OI; miosis may be absent! \n\n Naloxone has a short half-life and may need to be readministered if respiratory depression returns. Nalt Rexone = prevent Relapse in opioid use disorder but only in absence of acute withdrawal symptoms \n\nMethadone = Withdrawal Nal Oxone = Overdose Risk of prescription opioid misuse may be reduced by regular patient follow-up , random urine drug screens , and by reviewing the state's prescription drug-monitoring program data . \n\nrisk factors for misuse include age < 45, psychiatric disorder , and history of substance abuse or \n\nlegal history \n\n763 https://t.me/usmleinnercircle USMLE Inner Circle \n\nOpioid withdrawal Time course . 4 to 48 hr after opioid cessation \n\n## . Immediately after opioid antagonist (life-threatening) \n\n## . Gastrointestinal: nausea, vomiting, cramping, diarrhea , t bowel sounds \n\nClinical . Cardiac: t pulse, t blood pressure, diaphoresis \n\npresentation . Psychologic: insomnia, ya wning, dysphoric mood \n\n## . Other: myalgia, arthralgia , mydriasis, lacrimation, rhinorrhea, piloerection \n\nDiagnosis . History & examination alone (clinical diagnosis) \n\nManagement . Opioid agonist: methadone or buprenorphine \n\n## . Nonopioid: clonidine or adjunctive medications (antiemetics, antidiarrheals, benzodiazepines} \n\nPharmacotherapy for opioid use disorder Mechanism of action Characteristics \n\n# . Lower risk of respiratory suppression/lethal overdose \n\nBuprenorphine . Mu opioid receptor partial agonist . Lower risk of misuse \n\n# . Daily clinic dosing not required \n\n# . Greater risk of respiratory suppression/lethal overdose \n\nMethadone Mu opioid receptor full agonist . Greater risk of misuse \n\n## . Adverse effects: risk of hyperalgesia, hypogonadism, QTc prolongation .. Daily clinic dosing required \n\nOpioid prescribing best practices \n\n## . Scre en for risk fa ct ors for mi s use \n\nPrior to . Perf orm uri ne drug screeni ng \n\ninitiation . Que ry PDMP databa se \n\n## . Sign controlled substance agreement (eg , 1 p res cri ber , 2._ \n\nphar mac y) \n\nDuring . Follow up every 1-3 months \n\ntherapy . Query PDMP database before each refill \n\n## . Perform random urine drug screenings \n\nPOMP = prescription drug mo ni toring progra m. Psychiatry & Substance Abuse Naloxone should be offered to every patient who receives chronic opioid therapy , especially those at high risk for overdose (eg, high or escalating opioid dosage, concurrent benzodiazepine use). Prior to initiating chronic opioid therapy, both the patient and physician should sign a controlled substance agreement (informally referred to as a \"pain contract\"), which outlines the following: \n\nInformed consent for chronic opioid therapy, including the risks for dependence and addiction Prohibition of use that deviates from the dosage and purpose for which the opioid is prescribed Requirement of random urine drug screens and pill counts Designation of 1 prescriber and 1 pharmacy for all controlled substance prescriptions (barring exceptional circumstances) Statement that lost or stolen medications may not be replaced with an early refill \n\nInhalants \n\n Inhalant abuse usually occurs in boys age 14-17 and may involve multiple common household chemicals. Users may display characteristic perioral skin changes (\" glue sniffer's rash \"). Inhalant intoxication is characterized by a rapid onset and relatively short duration .\n\n Chronic abuse of nitrous oxide is associated with vitamin B12 deficiency and resultant \n\npolyneuropathy \n\n The rash involves Nasolabial folds (vs Malar rash in SLE which spares it) \n\nStimulants \n\n Caffeine is a stimulant that, when used in excessive amounts, can cause sympathetic hyperactivity ,leading to anxiety , jitteriness , insomnia , palpitations , and tremors .\n\nEnergy drinks typically contain large amounts of caffeine and should be considered as a cause of stimulant intoxication \n\nAmphetamines \n\n Compared to PCP , the effects of methamphetamine generally last longer .\n\nup to 20 hours (methamphetamine) vs < 8 hours (PCP) \n\n What is the likely diagnosis in a patient brought to the ED with severe agitation and combativeness ?Urine toxicology is negative. The patient is admitted and remained psychotic for one week before symptoms subsided. \n\nBath salts intoxication, Synthetic cathiones (synthetic amphetamine analogues) \n\nPCP and cocaine intoxication may present similarly but with shorter durations of effect ;additionally, PCP and cocaine are typically included in hospital urine toxicology screens \n\n764 https://t.me/usmleinnercircle \n\nPsychiatry & Substance Abuse Cocaine \n\n What is the treatment of choice for agitation in an NSTEMI patient with chest pain , agitation , dilated pupils , and normal cardiac enzymes? \n\nIV benzodiazepines \n\nthis patient likely is experiencing cocaine toxicity; IV benzodiazepines improve symptoms of agitation, reduce myocardial O2 demand, and alleviate cardiovascular symptoms Same for amphetamine overdose \n\n Several features of a patient's presentation that should raise suspicion for cocaine use as the underlying cause for brain hemorrhage: \n\nYoung age : Most patients who sustain stroke are age >60. \n\nAbsence of typical risk factors: Chronic hypertension , is the most common underlying cause of ICH. \n\nSympathetic activation : In addition to acute hypertension, a patient may have tachycardia, mydriasis, and hyperthermia (due to cocaine-induced vasoconstriction preventing heat dissipation). Diffuse alveolar hemorrhage (opacification) due to smoking Cocaine \n\n765 https://t.me/usmleinnercircle USMLE Inner Circle \n\nClinical features of cocaine use Clues to surreptitious cocaine use \n\n Sympathetic hyperactivity: tachycardia , hypertension, dilated pupils \n\nClinical presentation Chest pain due to coronary vasoconstriction . Personality & mood changes \n\n## . Psychomotor agitation, seizures Behavioral . Changes in sleep patterns Acute myocardial ischemia \n\nComplications Aortic dissection \n\nfeatures . Unexplained weight loss \n\n# . Financial difficulties \n\n## . ICH \n\n## . Benzodiazepines for blood pressure & anxiety Aspirin for inhibition of cocaine-induced platelet aggregation \n\n# . Chest pain \n\nReported Epistaxis, rhinitis (intranasal use) .symptoms Headaches .Management of chest pain . Nitroglycerin & calcium channel blockers for vasoconstrictive pain \n\n## . Immediate cardiac catheterization if indicated (eg, STEMI) Caution with : fibrinolysis (t risk of ICH), beta blockers (t risk of coronary vasoconstriction*) \n\nExamination . Hypertension , tachycardia \n\nsigns . Dilated pupils \n\n# . Psychomotor agitation Theoretical risk due to unopposed alpha stimulation. Mixed alpha/beta blockers are sometimes considered. ICH =intracranial hemorrhage; STEMI =ST-segment elevation myocardial infarction. . Seizures \n\nEmergent Acute myocardial ischemia \n\ncomplications Aortic dissection \n\n# . lntracranial hemorrhage Psychiatry & Substance Abuse Location : Cocaine-induced ICH is most commonly seen in subcortical locations (eg, thalamus) and has a higher risk of associated intraventricular hemorrhage. What drug intoxication presents as pupillary dilation , grandiosity , vasospasm , and paranoia that lasts for less than one hour ?\n\nCocaine \n\nimportant distinguishing feature from amphetamines , which have a longer duration \n\nHallucinogens \n\nMarijuana \n\n Dronabinol (medical marijuana) is used clinically as an appetite stimulant for AIDS patients. \n\n Cannabis is a hallucinogen that causes euphoria, paranoia, hallucinations, increased appetite, conjunctival injection, and cognitive slowing. Chronic cannabis use can lead to a disorder called cannabis hyperemesis syndrome , which is characterized by episodic vomiting associated with prolonged, frequent, and high-dose recreational cannabis use. Patients often find relief with hot-water bathing . It typically resolves after cannabis cessation. \n\nMDMA/Ecstasy \n\n Life-threatening effects of MDMA (ecstasy) include hyperthermia, serotonin syndrome and hyponatremia .\n\nalso may cause life-threatening hypertension and tachycardia; treat with normal saline and cooling \n\nDry mouth > thirst > increase water intake without electrolyte depletion > hyponatremia > seizures and life-threatening cerebral and pulmonary edema \n\n## Poisoning & Toxicity \n\nIron \n\n766 https://t.me/usmleinnercircle \n\n \n\n> Iron Poisoning\n> Within 30 minutes to 4 days: Abdominal pain Vomiting (eg , hematemesis)\n> Clinical Di arrhea (eg , melena)\n> features Hypotensive shock Metabolic acidosis Within 2 days: hepatic necrosis Within 2-8 weeks: pyloric stenosis\n> Diagnostic Anion gap metabolic acidosis\n> find ings Radiopaque pills Whole bowel irrigation\n> Treatment Deferoxamine Supportive care for circulation , airway and breathing\n\nPsychiatry & Substance Abuse Beta Blocker \n\n Treatment : Secure the airway and give isotonic fluid boluses and IV atropine for initial treatment of hypotension and bradycardia. In patients with refractory or profound hypotension, the next step is to administer IV glucagon \n\nother therapies that can be used simultaneously or in succession include IV calcium , catecholamine \n\nvasopressors (epinephrine or norepinephrine), high-dose insulin and glucose , and IV lipid emulsion therapy (used to manage poisoning in lipophilic medications such as beta blockers). \n\nLithium \n\n Cardiac abnormalities can also occur, mainly in the form of QT interval prolongation and \n\nbradycardia \n\nLead \n\n767 https://t.me/usmleinnercircle USMLE Inner Circle \n\nBeta blocker toxicity Symptom onset . 2-6 hr after ingestion \n\n## . Hypotension \n\n## . Bradycardia \n\nSigns and Bronchospasm .symptoms Altered mental status .. Seizures \n\nLaboratory findings . Hypoglycemia \n\nECG findings . Prolonged PR interval \n\n## . Bradycardia \n\n## . Secure airway \n\n## . GI decontamination \n\nManagement . IV fluid boluses \n\n## . IV atropine \n\n## . IV glucagon GI = gastrointestinal ; IV = intravenous. \n\nLithium toxicity \n\nAcute toxicity \n\n## . Intentional overdose \n\nEtiology Chronic toxicity \n\n## . Decreased renal perfusion U lithium clearance) \n\n0 Dehydration \n\n0 Thiazide diuretics, NSAIDs, ACE inhibitors Acute toxicity \n\n## . Gastrointestinal: nausea 1 vomiting 1 diarrhea \n\nClinical features . Late neurologic seguelae Chronic toxicity (neurologic) \n\n## . Letharg;t confusion agitation \n\n## . Ataxia , tremor/fasciculations, seizure \n\nTreatment . Intravenous hydration \n\n## . Hemodialysis (severe cases) \n\nNSAID = nonsteroidal anti-inflammatory drug. Psychiatry & Substance Abuse NO metabolic acidosis and no hematemesis (vs iron poisoning ) What is the next step in management for a child that has an elevated lead level on capillary blood testing? \n\nMeasure venous lead level \n\ncapillary blood testing is a good initial screen but false-positive results are common \n\nMagnesium \n\n768 https://t.me/usmleinnercircle \n\nLead poisoning \n\n## . Home built before 1978 \n\nRisk . Pica or mouthing behaviors (eg , infants, developmental delay) \n\nfactors . Sibling with lead poisoni ng \n\n## . Low socioeconomic status \n\n## . Immigrant or international adoptee \n\n## . May be asymptomatic \n\nClinical . Abdominal pain/constipation \n\nfeatures . Cognitive impairmenVbehavioral problems \n\n## . Encephalopathy \n\n## . Obtain venous sample (if screening performed by capillary sample) \n\n## . Environmental surveillance (identify & remove lead sources) \n\nManagement . Notify public health department \n\n## . Nutritional counseling \n\n## . Chelation therapy if lead level 2'45 g/dl \n\nApproach to childhood lead poisoning Does the child have the following risk factors? \n\n Home built before 1978 under renovation or with peeling paint Pica \n\n Sibling with lead poisoning Low socioeconomic status (eg , Medicaid) Immigrant or international adoptee II No further te sting I I Draw venous l ead level I\n\nI\n\nCauses \n\nUndetectable Mi ld: \n\n5--44 mcg /dL No medication, repeat level in <1 month Moderate: 45-69 mcg/dl Meso -2 ,3-Dimercapto-\n\nsuccinic \n\nacid (DMSA) \n\nMagnesium toxicity \n\n# . Renal impairment (ie , decreased Mg excretion) Severe: \n\n2' 70 mcg / dl Dimercapr ol (British Anti-Lewisite) plus ca l cium disodium edetate (EDTA) \n\n# . Increased Mg intake (eg , IV Mg sulfate , M g-based laxatives/enemas )\n\n# . Neuromuscular: ! reflexes , weakness , paralysis , respiratory failure \n\nClinical features . Cardiovascular: hypotensio n, bradycardia , conduction defects \n\n# . Electrolyte: hypocalcemia [Mf'f - fTl'l~J \n\n# . Discontinue Mg-containing medications \n\n# . IV fluids loop diuretics \n\nManagement IV calcium for neuromuscular & cardiac symptoms .. Hemodialysis in severe renal impairment \n\nIV = intravenous; Mg = magnesium. Psychiatry & Substance Abuse Arsenic \n\n Antique furniture builder presents with polyneuropathy, areas of hypo- and hyper-pigmentation on the neck, and tingling in his hands and feet. \n\nArsenic poisoning \n\n Mees lines (horizontal striation of fingernails) are characteristic \n\nCaustic Ingestion \n\n NBME doesn't recommend Gastric Lavage. DO NOT Consider it \n\n Esophageal strictures are the most common complication and occur weeks to months \n\nafter the ingestion. diagnosis is confirmed with elevated urine arsenic levels \n\n769 https://t.me/usmleinnercircle USMLE Inner Circle \n\nArsenic poisoning Mechanism . Binds to sulfhydryl groups \n\n## . Di srupts cellular respiration & gluconeogenesis \n\n# . Pe st icides/insecticides \n\nSources . Contaminated water (often from wells) \n\n# . Pressure -t reated wood \n\nManifestations . Acute: garlic breath , vomiting, watery diarrhea, QTc prolongation \n\n## . Chronic: hypo-/hyperpigmentation, hyperkeratosis, stocking-gl ove neuropathy \n\nTreatment . Dimercaprol (British anti-Lewisite) \n\n## . DMSA (ie, meso-2,3-dimercaptosuccinic acid, succimer) \n\nClinical features of caustic ingestion \n\n# . Chemical burn or liquefaction necrosis injury \n\nClinical . Affects lips, tongue, oral muc osa & esophagus \n\npresentation . Patients can develop chest & abdominal pain, vomiting with occasional hematemesis & dysphagia/odynophagia \n\nPrehospital \n\n# . Decontamination (eg, remove contaminated clothing, brush off visible chemi ca l, irrigate exposed skin) \n\n# . Do not indu ce vomiting or give charcoal \n\nEmergency department \n\n# . Confirm decontamination; chest & abdominal x-rays \n\nManagement . Endotracheal intubation for significant oropharyngeal inj ury \n\n# . Consider gastric lavage if nasogastric tube is placed \n\nInpatient \n\n# . Endoscopy within 12- 24 hr if hemodynamically stable & without respiratory distress or perforation \n\n# . Serial x-rays to rule out perforation \n\n# . Tube feedi ngs & surgi ca l int ervention for severe injury Psychiatry & Substance Abuse Many patients (approximately one-third) develop esophageal squamous cell carcinoma \n\nyears after the initial ingestion. What should you not do? \n\nInduce vomiting (avoid damage to esophagus), neutralize with weak acid \n\n What is the likely diagnosis in a patient that presents with heavy drooling , dysphagia , and a white tongue after being found next to an empty bottle of an unknown substance? \n\nCaustic ingestion \n\nin severe cases, perforation of the esophagus or stomach can occur, resulting in mediastinitis or peritonitis \n\n What is the diagnostic test of choice to evaluate the extent of injury following caustic ingestion ?\n\nUpper GI endoscopy \n\nshould be performed within 24 hours of ingestion if there is no evidence of perforation or severe respiratory distress Stabilize first! \n\nAcidic substances, causes coagulation necrosis (eg, protein denaturation) that results in an eschar, thereby preventing further acid penetration and injury. \n\nAlkaline substances (eg, many cleaning supplies), cause liquefactive necrosis (eg, cell membrane dissolution) that often leads to deeper penetration of tissues and therefore more severe injuries. \n\nAnti-Cholinergic \n\n What is the likely diagnosis in a patient that presents with confusion and blurry vision after overdosing on an unknown medication? Physical examination reveals dry mucous membranes, decreased bowel sounds, and 8 mm pupils bilaterally. \n\nAnticholinergic toxicity ( antimuscarinic, TCA's, antihistamines, etc. )\n\nmay be reversed with physostigmine (cholinesterase inhibitor) \n\n770 https://t.me/usmleinnercircle \n\n \n\n> Anticholine r gic toxicity Co mmon agents with antieholinergic properties Symptom Mec hanism Antihistamines\n\n## . Diphenhydramine, cyproheptadine \n\n> \"Hot as a hare\"\n\n! Sweating leads to ! heat dissipation \n\nt Body temperature . . 1st generation: chlorpromazine, haloperidol \n\n> Psycho tr opics\n\n## . 2nd generation : clozapine \"Dry as a bone \" . ! Glandular secretion & smooth muscle \n\n! Secre ti ons (eg, mucous contraction membra nes , sweat glands) \n\n## . Tricyclic antidepressants: amitriptyline , clomipramine Antiparklnson . Benztropine, trihexyphenidyl \n\n> \"Red as a beet \"Superficial vasodilation from T\n\nbody heat Fl ushed skin . \n\n> \"Blind as a bat\" Paralysis of ciliary muscle &iris sphincte rCycloptegia, mydriasis\n\n## .. lpratropium (bronchodilator) \n\n> An ti muscarinic\n\n## . Oxybutynin, darifenacin (overactive bladder) \n\n## . D icyclo mine, hyoscyam ine (a ntispasmodics )\n\n## . Scopolamine (antiemetic) \n\n> \"Mad as a hatter\"\n\n## . Permeates blood-brain barrier & affects CNS My drlatics . Atropine, cyclopentolate \n\n> Altered mental status pathways\n> \"Full as aflask \"\n\n## . ! Intestina l smooth muscle contraction Constipation , . ! Detrusor contraction & ! internal urethra lurinary retention sphincte r relaxation \n\n## . Muscarinic mushroom species Plant-based . Jimsonweed \n\n## . Nightshade species \n\n> \"Fast as a fiddle\"\n\n! Vagal tone at the si noatrial node Tachycardia .Psychiatry & Substance Abuse Organophosphate Poisoning TCA overdose \n\n Sodium bicarbonate likely improves cardiac toxicity through the following mechanisms: \n\nIncreasing serum pH makes the TCA less pharmacologically active, decreasing its avidity for sodium channels. \n\nIncreasing extracellular sodium concentration raises the electrochemical gradient across cardiac cell membranes, decreasing the impact of the TCA-induced sodium channel blockade. What is the most common cause of death in patients with TCA overdose ?\n\nCardiac toxicity (e.g. ventricular arrhythmias) \n\n What medication is administered to treat seizures in patients with suspected TCA toxicity ?\n\nBenzodiazepines \n\n Isolated overdose of SSRIs is usually well tolerated (aymptomatic/ mild CNS depression) .\n\nWhen a patient with SSRI overdose has altered mental status and abnormal physical examination findings, levels of common coingestants (eg, salicylates, ethanol) should be obtained .\n\nAcetaminophen Overdose \n\n771 https://t.me/usmleinnercircle USMLE Inner Circle \n\nOrganophosphate poisoning \n\n## . Pesticide: farmer/field worker, pediatric ingestion, suicide attempt \n\nCommon exposures . Nerve agent: multiple patients presenting with similar symptoms \n\n## . Muscarinic: \n\n0 Diarrhea/diaphores is \n\n0 Urination \n\n0 Mios is Manifestations 0 Bronchospasms, bronchorrhea, bradycardia \n\n0 Emesis \n\n0 Lacrimation \n\n0 Salivation \n\n## . Nicotinic: muscle weakness, paralysis, fasciculations \n\n# . Remove patient's clothes, irrigate skin \n\nManagement . Atropine reverses muscarinic symptoms \n\n# . Pralidoxime reverses nicotinic and muscarin ic symptoms (administer after atropine) \n\nClinical features & management of tricyclic antidepressant overdose CNS . Mental status changes (eg, drowsiness, delirium, coma) \n\n## . Seizures, respiratory depression \n\nClinical . Sinus tachycardia, hypotension \n\nCardiovascular . Prolonged PR/ORS/ QT intervals \n\npresentation . Arrhythmias (eg, ventricular tachycardia, fibrillation) \n\nAntichollnerglc . Dry mouth, blurred vision , dilated pupils \n\n## . Urinary retention, flushing , hyperthermia \n\n## . Supplemental oxygen, intubation \n\n# . Intravenous fluids \n\nManagement Supportive care & Activated charcoal for patients within 2 hours of ingestion (unless ileus present) .therapy Intravenous sodium bicarbonate for ORS interval widening or ventricular . arrhythmia Psychiatry & Substance Abuse Altered mental status is a contraindication to charcoal due to risk of aspiration. \n\nSalicylate Toxicity \n\n What is the likely ingested agent in a patient who overdosed and presents with fever , tinnitus , vertigo \n\nand tachypnea ?\n\nAspirin : causes mixed respiratory alkalosis and anion gap metabolic acidosis \n\nLook for normal pH in setting of mixed respiratory/metabolic disorder \n\nBrown Recluse Spider Bite \n\n772 https://t.me/usmleinnercircle \n\n# .Epidem iology ...\n\nMan ifestations .\n\n# ..\n\nDiagnosis ..Treatment ..\n\nActivated charcoal Acetaminophen intoxication \n\nSingle dose ~7.5 g (pediatric ~150 mg/kg) No {or indeterminate) \n\nYes \n\n:S: 4 hours since ingestion Chronic ingestion \n\nYes \n\nAdm in ister activated charcoal Yes \n\nCheck acetaminophen levels , ------~ \n\n Levels above treatment line in nomogram >10 g/mL if timing of ingestion unclear Any evidence of liver injury Administer N-acetylcysteine & monitor for liver injury \n\n UWorld \n\nSalicylate toxicity \n\nExcess ingestion of aspirin or o th er sa li cylates (eg , oil of wintergreen) Liver metabolism gets overwhelmed --+ sl ower renal excretion --+ prolonged elevated salicylate levels Nausea/vomit in g\n\nHypeiventilation \n\nHyperthermia Altered mental status Anion gap metabo li c ac idosis (elevated lactate) Serum salicylate level Activated charcoal (alert patients within 2 hr of ingestion) Intravenous sodium bicarbonate (enhances salicylate excre ti on) Hemodialysis (severe ingestions, pulmonary edema , renal fai lure) \n\nManagement of salicylate to xi city \n\n# . Binds salicylate in gastrointestinal tract and decreases systemic absorption . Give wit hi n 2 hr of acute ingestion (unlikely helpf ul in chronic ingestion) \n\n## . Avoid in confused or obtunded ea ti ents (risk of aspiration) \n\nIntravenous sodium . Alkalinizes urine a nd serum, enhanci ng salicylate excreti on \n\nbicarbonate . Requires large volumes of flu id to be adm in istered \n\n## . Inabili ty to tolerate large volumes of sodium bicarbonate: pulmonary edem a, acute or chr on ic renal \n\nIndications for failure \n\nhemodialysis . Persistent acidosis or worsening cli ni cal condit ion despite sodium bicarbonate therapy \n\n## . Severe ingestions: shock, seizures, CNS dysfunction , cerebral edema Psychiatry & Substance Abuse Snakebite \n\n773 https://t.me/usmleinnercircle USMLE Inner Circle \n\nBites from Loxosce/es rec/usa (brown recluse) \n\n## . Southwestern, southern, midwestern United States \n\nEp ide miology . Dry , warm areas (eg, attics, basements) \n\n## . Spider identificat ion rare (initial bite usually painless) \n\n## . Sma ll erythematous papule that se lf-resolves (most common) \n\n## . Burning pain --+ blister --+ eschar/necrosis \n\nMani fe statio ns 0 Expands over days, heals over weeks \n\n## . Systemic loxoscelism (eg, fever, hemo lysis, DIC) \n\n0 Uncommon ; not correlated with lesion size \n\n## . C leanse wound & apply ice (r educes phospholipase activity) \n\n## . No surgical debridement until lesion has stopped growing \n\nManagem e nt Supportive management for systemic loxoscelism .. Update tetanus \n\nDIC = disseminated intravascular coagu lation. Snakebite envenomation \n\n## . Effects due to venom toxins (may be delayed) \n\n## . Tissue injury (eg, progression to necrosis) \n\nClinical features . Myotoxici ty (eg, cardiovascular collapse) \n\n## . Neurotoxicity \n\n## . Coag ul opat hy \n\n## . Limb immob il ization & wound managem ent Management . Frequent coagulation studies \n\n## . Antivenom if indicated (not given in mild cases due to ri sk of life-threatening allergic reaction) \n\n## . Observation fo r 12-24 hr \n\n# . Unstable v it al signs (eg, hypotension, tachypnea) \n\nAntivenom indications . Rapidly progressing changes in wo und \n\n# . Abnormal coagulation studies Short Subjects \n\n# Short Subjects Biochemistry PKU Lesch Nyhan Glycogen Storage Disorder Vitamins and Minerals Niacin Vitamin D Vitamin C Genetics Autosomal Recessive Downs Edwards & Patau Cystic Fibrosis Marfan Osteogenesis Imperfecta Duchene Muscular Dystrophy Myotonic Dystrophy Prader Willi Fragile X Syndrome Rett Syndrome Immunology Spleen B & T Cell Disorders Transient Hypoglammaglobinemia of Infancy Bruton Agammalglobinemia CVID SCID IgA Deficiency Hyper IgE Leukocyte Adhesion Disorder Chronic Granulomatous Disease Hereditary Angioedema Amyloidosis Serum Sickness Immunosuppression Neutropenia Immunosuppressants Organ Transplant Post-Transplant Lymphoproliferative Disorder Microbiology Antibiotics Bacteria Strep Clostridium Diptheria \n\n774 https://t.me/usmleinnercircle Short Subjects Leprosy TB Gonococcal Meningococcal HiB Pertussis Legionella Pseudomonas E.Coli Vibrio Lyme Syphilis Mycoplasma Rickettsia Ehrlichiosis Tularemia Melioidosis Fusobacterium Fungus Histoplasmosis Blastomycosis Coccidioides Tinea Candida Aspergillus Cryptococcus Sporotrichosis Pneumocystis Parasite Giardia Malaria Babesiosis Trichinella Echinococcus Virus HSV Coxsackie Varicella EBV CMV Herpes Virus 6 HPV Hepatitis Parvovirus Rubella HIV Influenza Parainfluenza RSV Chickungunya Rabies Small Pox 775 https://t.me/usmleinnercircle USMLE Inner Circle Short Subjects Biochemistry \n\n Key idea: Main way to differentiate between classic galactosemia and hereditary fructose intolerance is based on age of patient (newborns will only be drinking breast milk and therefore will get classic galactosemia, whereas patients who develop symptoms at 6 months-1 year are more likely due to hereditary fructose. \n\nPKU \n\n What is the most likely diagnosis in a 4-month old boy who presents with seizures ? He was born at home. Physical exam shows light hair and blue eyes . His urine is noticable for a \"musty odor \". \n\nPhenylketonuria ( PKU )\n\nLesch Nyhan Systemic Sepsis Burns Toxic Shock Syndrome Diarrhea & Vomiting Genital Ulcers Lymphadenitis Animal Bite STD Infection Control Catheter Related Infection \n\n776 https://t.me/usmleinnercircle \n\nPhenylketonur ia . Autosomal recessive mutation in gene for ph enylalanine hydroxylase \n\nPathophysiology Impaired metabolism of phenylalanine to tyrosine -+ j phenylalanine causes neurologic injury .\n\nClinical features . Ne urologic: microcephaly, developmental delay, seizures, severe intellectual disability \n\n## . Nonneuro1ogic: musty body odor, hypopigmentation (eg, skin, hair, eyes), eczema . j Phenylalanine levels: Diag n os is 0 Universal newborn screening \n\n> 0\n\nSerum amino acid analysis Treatment . Phenylalanine-restricted diet (ie, avoidance of protein-rich foods) \n\n## . Dietary/supplemental tyrosine Prognosis . Preventable disease manifestati ons with early treatme nt \n\n## . Delayed diagnosis/treatme nt -+ irreversible neurologic injury Short Subjects Self mutilation also seen in Fragile X \n\nGlycogen Storage Disorder \n\n What is the likely diagnosis in a three-month-old that presents with severe hypoglycemia and lactic acidosis with a doll-like face and hepatomegaly ?\n\nvon Gierke disease (type I glycogen storage disease, glucose-6-phosphatase deficiency) \n\ntypically presents at age 3 - 4 months with hypoglycemia, lactic acidosis, hyperuricemia, and hyperlipidemia \n\nVitamins and Minerals \n\n777 https://t.me/usmleinnercircle USMLE Inner Circle \n\nLesch-Nyhan syndrome \n\n X-linked recessive \n\nPathophysiology . Deficiency of hypoxanthine-guanine phosphoribosyltransferase \n\n# . Hypoxanthine & uric acid accumulation \n\n# . Delayed milestones & hypotonia in infancy \n\n# . Early childhood 0 Intellectual disability \n\nClinical features 0 Extrapyramidal symptoms (eg, dystonia, chorea) \n\n0 Pyramidal symptoms (eg , spasticity, hyperreflexia) \n\n0 Self-mutilation \n\n Gouty arthritis in late, untreated disease Type of GSD Type I (Von Gierke's disease) Type II (Pompe's Type Ill (Cori's Type IV Type V (McArdle's disease) Relative frequency Deficient enzyme Role of the enyzme disease) Type la Type lb \n\n - 25% - 15% \n\n Glucose-6-phosphatase Glucose-6-phosphate translocase i;:::l Lysosomal acid \n\ni;:::i maltase deficiency \n\ni;:::i \n\n Hydrolysis of glucose-6-phosphate to glucose and inorganic phosphate Transport of glucose-6-phosphate into the Glycogenolysis endoplasmic_ reticulum where it is hydrolyzed by glucose-6-phosphatase within the lysosome \n\ndisease) (Andersen's disease) \n\n - 25% - 3% - 2% \n\n Glycogen Glycogen Muscle phosphorylase debrancher branching (myophosphorylase) enzyme Glycogenolysis Glycogenesis Glycogenolysis \n\nCharacteristic Hepatomegaly \n\nfeatures Severe fasting _ hypoglycemia, mild ketosis \n\n Hypertrophic cardiomyopathy \n\nand / or conduction blocks Generalized muscle weakness and / or cramps Proximal Generalized muscle weakness , Severe hyperlipidemia ---+ doll-like facies \n\n ,Hyperuricemia, \n\n Lactic _ acidosis \n\n Anemia Failure to thrive \n\n## .Composition ..Potential benefits ..Potential nutritional deficiencies .\n\n Proximal myopathy \n\n Macroglossia \n\n Failure to thrive \n\nVegan diet \n\n Hepatomegaly \n\n Possibly \n\n~irrh~_ ~i~ 1\n\n(ascitis , \n\n~plen<>megaly) \n\n Mild , fasting hypoglycemia and ketosis Hyperl_ ip_ idemia myopathy exercise intolerance (with a Hepatomegaly second wind phenomenon) i;:::1 ,\n\n Possibly Rhabdomyolysis and \n\n~irrhosis myoglobinuria \n\n(ascitis , \n\n~pl~n<>megal y) \n\nPlant-based foods: fruits, vegetables , legumes, grains No animal-derived foods (eg , meat , dairy , egg) L ower blood glucose & cholesterol levels Reduced risk for cardiovascular disease (eg , heart disease , stroke) Common : vitamin 8 12 , vitamin D, calcium Possible *: iron , zinc *Increased risk: children (rapid growth requires higher zinc/iron) & young women (menstrual blood loss requires higher iron). Short Subjects Risk factors for deficiency include malabsorption , bowel resection , poor nutritional intake , and \n\nparenteral nutrition \n\n Korsakoff syndrome is a potential complication of Wernicke encephalopathy that is characterized by \n\nretrograde and anterograde amnesia with preserved long-term memory, confabulation , lack of insight , and apathy .Korsakoff syndrome is caused by thiamine deficiency and develops more frequently in alcohol use disorder than in other malnourished states. It is irreversible unlike WE \n\nNiacin \n\nWhat type of diet will pre-dispose to niacin deficiency , and why? Corn based diets ( corn is deficient in tryptophan and niacin )\n\nWhat other causes are there ( 3)? \n\nHartnup disease (loss of tryptophan reabsorption )\n\nCarcinoid Syndrome (trytophan used to synthesize serotonin )\n\nIsoniazid (B6 deficiency )\n\n778 https://t.me/usmleinnercircle \n\nWater-soluble vitamins Vitamin Source Deficiency B1 (thiamine) Whole grains, meat, fortified cereal, nuts, . Beriberi (peripheral neuropathy, heart failure) legumes . Wernicke-Korsakoff syndrome \n\n## . Angular cheilosis, stomatitis, glossitis \n\nB 2 (riboflavin) Dairy, eggs, meat, green vegetables . Normocytic anemia \n\n## . Seborrheic dermatitis \n\nB 3 (niacin) Meat , whole grains, legumes . Pellagra (dermatitis, diarrhea, delusions/dementia, glossitis) \n\nB 6 (pyridoxine) Meat , whole grains, legumes, nuts . Cheilosis, stomatitis, glossitis , \n\n## . Irritability, confusion, depression \n\nB9 (folate, folic acid) Green leafy vegetables, fruit, meat, fortified . Megaloblastic anemia cereal/grains . Neural tube defects (fetus) \n\nB 12 (cobalamin) Meat , dairy . Megaloblastic anemia \n\n## . Neurologic deficits (confusion , paresthesias, ataxia) \n\nC (ascorbic acid) Citrus fruits, strawberries, tomatoes, . Scurvy (punctate hemorrhage, gingivitis, corkscrew potatoes, broccoli hair) \n\nClinical manifestations of trace mineral deficiencies Chromium Impaired glucose cont ro l in diabetics Brittle hair Sk in depigmentation \n\nCopper Neurologic dysfunction (eg , ataxia , peripheral n eu ropathy) Sideroblastic anemia Osteoporosis \n\nIron Microcytic anemia Thyroid dysf unction \n\nSelenium Cardiomyopalhy Immune dysfun ction Alopecia Pustular skin rash (perioral region & extremities) Zinc Hypogonadism Impaired wound healing Impaired taste Immune dy sfu nction \n\nShort Subjects Vitamin D Vitamin C \n\n Intramuscular or subperiosteal hemorrhages can occur, especially in the lower extremities due to gravity-dependent hydrostatic pressure within fragile capillaries. This results in pain and difficulty with ambulation , which may be the presenting symptoms in children \n\nGenetics \n\n779 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPellagra (niacin deficiency) \n\n Alcoholism \n\nAssociated Anorexia nervosa \n\nconditions Malabsorptive disease (eg, Grahn disease) Dietary niacin deficiency Diarrhea \n\nSymptoms Dermatitis (photosensitivity) Dementia, depression, distraction Death \n\nCauses of vitamin D deficiency \n\n## . Lactose intolerance or milk avoidance \n\nInadequate intake Vegan diet (without fortification) .\n\n## . Grahn disease \n\nMalabsorption . Celiac disease \n\n# . Bariatric surgery (eg , gastric bypass), gastrectomy . Extreme northern/southern latitudes \n\nInadequate sunlight exposure . Heavy skin pigmentation \n\n## . Sedentary/indoor lifestyle \n\nMetabolic disorders . Chronic kidney disease . Chronic liver disease \n\nIncreased catabolism . Drugs: anticonvulsants (eg, phenytoin , carbamazepine), isoniazid, rifampin \n\nVitamin C deficiency (scurvy) \n\n## . Insufficient dietary intake (lack of citrus fruits/vegetables) \n\nPathogenesis 0 Chronic alcohol/substance us e, severe malnutrition (eg , anorexia , restricted diet) \n\n## . Impaired collagen production \n\n## . Cutaneous: \n\n0 Coiled hair, perifollicular hemorrhage \n\n0 Petechiae , ecchymoses \n\nManifestations 0 Impaired wound healing \n\n## . Mucosal: gingivitis with bleeding \n\n## . Musculoskeletal (eg, periosteal hemorrhage): arthralgi a, limp \n\n## . Constitutional: malaise, depression, vasomotor instability \n\nLaboratory findings Anemia (normocytic or microcytic) \n\n## . Normal platelet count & coagulation studies \n\nTreatment . Oral/injectable vitamin C (improvement within days to weeks) \n\n Toxicity (eg , abdominal pain , diarrhea) with excessive supplementation Short Subjects Autosomal Recessive Downs \n\n Hypotonia is a prominent finding and can present with poor feeding due to a weak suck \n\n Atlantoaxial instability: compression of the spinal cord .Presentation can include weakness , gait changes, urinary/fecal incontinence , and vertebrobasilar \n\nsymptoms such as dizziness , vertigo , imbalance , and diplopia .\n\n780 https://t.me/usmleinnercircle \n\nSandal-toe deformity \n\nCommon medical conditions wi th polygenic inheritance \n\n Androgenetic alopecia Epilepsy Glaucoma Hypertension lschemic heart disease Schizophrenia Type II diabetes mellitus \n\nPrenata l screen i ng algorithm for autosomal recessive diseases \n\nNo additional testing Maternal genetic - Negative ---+ (mother not a carrier. low screening risk for disease in child) IPositive \n\nt\n\nPaternal genetic No additional testing \n\n- Negative ---+ (father not a carrier, low screening IPositive \n\nt\n\nDefin itive fetal testing (eg, CVS, amniocentesi s) risk for disease in child) \n\n> CVS :\n\nChOrion ic v,llus sampling. UW0< ld \n\nFeatures of Down syndrome \n\nEpicanthal folds Upslanting palpebral fissures mall, low-set ears - --- _..,, \n\nShort neck with excess skin Furrowed tongue \n\nDown syndrome comorbidities Neurologic . Intellectual disability \n\n# . Early-onset Alzheimer disease \n\n# . Complete atrioventricular septal defect \n\nCardiac . Ventricular septal defect \n\n Atrial septal defect \n\n# . Duodenal atresia \n\nGastrointestinal . Hirschsprung disease \n\n# . Hypothyroidism \n\nEndocrine . Type 1 diabetes mellitus \n\n# . Obesity \n\n# . Short stature \n\nOncologic Acute leukemia \n\nOrthopedic Atlantoaxial instability pal mar crease \n\n> <&> UWor1d\n\nShort Subjects On examination, upper motor neuron findings such as spasticity , hyperreflexia , and a Babinski sign (ie, upgoing big toe) are often present. \n\nEdwards & Patau Cystic Fibrosis \n\n Cefepime and Vancomycin both should be given emperically in CF. \n\nMarfan \n\n781 https://t.me/usmleinnercircle USMLE Inner Circle \n\nUWotld \n\nTrisomy 18 (Edwards syndrome) \n\nClenched hands with overlapping fingers \n\nTrisomy 13 (Patau syndrome) Primary ciliary dyskinesia versus cystic fibrosis Primary ciliary dyskinesia Cystic fibrosis \n\n Chronic sinopulmonary Chronic sinopulmonary infections infections \n\nRespiratory Nasal polyps Nasal polyps \n\ntract features Bronchiectasis Bronchiectasis Digital clubbing Digital clubbing Situs inversus Pancreatic insufficiency (50% of cases) \n\nExtrapulmonary . Infertility due to immotile Infertility due to absent vas \n\nfeatures spermatozoa deferens (azoospermia) Normal growth Failure to thrive Short Subjects Marfan requires close monitoring with echocardiography for the development of aneurysms, MVP and aortic arch dissection .\n\n Pt of Marfan Syn should never participate in Contact Sports d/t risk of Aortic Dissection. \n\nOsteogenesis Imperfecta \n\n Most fetuses either die in utero, during delivery due to trauma, or shortly after delivery due to \n\npulmonary hypoplasia (a complication of thoracic cavity hypoplasia ). Fibrillin-1 gene \n\n782 https://t.me/usmleinnercircle \n\nDifferential diagnosis of Marfanoid body habitus Diagnosis Overlapping features Distinguishing features \n\n# . Autosomal dominant . Pectus deformity . Normal intellect \n\nMarfan syndrome \n\n## . Tall stature . Aortic root dilation \n\n> 0\n\ni Arm : height ratio . Upward lens dislocation \n\n> 0\n\nl Upper: lower segment ratio . Autosomal recessive \n\n# . Arachnodactyly . Intellectual disability . Joint hyperlaxity . Thrombosis \n\nHomocystinuria . Skin hyperelasticity . Downward lens dislocation . Scoliosis . Megaloblastic anemia . Fair complexion \n\nClinical features of Ehlers-Danlos & Marfan syndromes Classic Ehlers-Danlos Marfan \n\n# . Transparent & hyperextensible \n\nSkin . Easy bruising , poor healing . No features other than striae . Velvety with atrophy & scarring . Joint hypermobility . Joint hypermobility . Pectus excavatum . Pectus excavatum or carinatum \n\nMusculoskeletal . Scoliosis . Scoliosis . High, arched palate . Tall with long extremities . Progressive aortic root dilation \n\nCardiac . Mitral valve prolapse . Mitral valve prolapse . Abdominal & inguinal hernias \n\nOther . Lens & retinal detachment . Uterine prolapse . Spontaneous pneumothorax . COL5A 1 & COL5A2 mutation . FBN1 mutation \n\nGenetics . Autosomal dominant . Autosomal dominant \n\nType II osteogenesis imperfecta \n\n Autosomal dominant \n\nPathophysiology Type 1 collagen defect Multiple fractures Short femur \n\nUltrasound findings Hypoplastic thoracic cavity Fetal growth restriction Intrauterine demise \n\nPrognosis Lethal Short Subjects Duchene Muscular Dystrophy \n\n A creatine kinase level is the initial screening tool used to assess for myopathy and is markedly elevated in children with DMD. As the disease progresses, the creatine kinase level drops as more muscle is replaced by fat and fibrosis \n\nMyotonic Dystrophy \n\n Myotonia is a characteristic feature and can be elicited by percussion of the thenar eminence , which results in thumb abduction followed by delayed relaxation (percussion myotonia ), or by sustained muscle contraction after the release of a handshake (grip myotonia )\n\nPrader Willi \n\n783 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDuche nne mu scular dy strophy \n\n## . Onset at age 2-3 \n\nClinical pr esentation . Pr oximal m usc le weakness (eg, Gower si gn , calf pseudohypertrophy) \n\n## . Dilated cardiomyopathy \n\n## . Scoliosis \n\n## . t Serum creatine kinase \n\nDiagnosis . Genet ic testing: dystrophin deletion \n\n## . Musc le bi opsy : fibrosis, fat , muscle degeneration \n\nTreatment . Glucocorticoids \n\n## . Wheelchair de pendent by ado lescence \n\nPro gnosis . Death at age 20-30 from respiratory/heart failure \n\nMyotonic dystrophy \n\n## . Autosomal domina nt CTG trinucleotide repeat expansi on \n\nPathogenesis Longer repeat length correlating with earlier & more severe disease .. Classic (adult ): myotonia & weakness (eg, face, hands, ankles) \n\nPresentation . Childhood: cognitive & behavioral diffic ulties (classic symptoms develop over ti me )\n\n# . Infantile: hypotonia, respiratory failur e, inverted V-shaped upper lip . Cardiac: arrhythmias, cardiomyopathy . Gastrointestinal: dysphagia, constipati on \n\nAssociated findings Resp ir atory: pharyngeal weakness, hypovent il a ti on .. No nm uscu la r: insu lin res istance, h ypogonadis m, cataracts, f rontal baldin g, excessive daytime sleepiness \n\n# . Genetic testing \n\nDiagnosis & trea tment Supportive management .\n\nCTG = cytosine-th ymine-gu a nine .Short Subjects Fragile X Syndrome Rett Syndrome \n\n## Immunology Patients with FXS have a normal life expectancy \n\n784 https://t.me/usmleinnercircle \n\nPrader-Willi syndrome \n\n## . Hypotonia \n\n## . Weak suck/feeding problems in infancy \n\n# . Hyperphag ia/ obes ity \n\n## . Short stature \n\nClinical features . H ypogonad ism \n\n## . Intellectual disability \n\n# . Dysmorphic facies 0 Narrow fo rehead \n\n> 0\n\nAlmond-shaped eyes 0 Downturned mou th \n\nDiagnosis . Lo ss of express ion on paterna l chromosome 15 (q11-q13) \n\n## . Sleep apnea (70%) \n\nComplications . Type 2 diabetes mellitus (25%) \n\n# . Gast r ic distension/rupture \n\n## . Death by choking (8 %) \n\nFragile X syndrome \n\n# . Trinucleotide (CGG) repeat expansion of FMR1 \n\nPathogenesis . Gene methylation silences FMR p rotein \n\n# . X-linked dominant inheritance \n\n# . De velop mental dela y\n\n## . Intelle ct ual disability \n\nNeuropsychiatric Attention deficit hyperactivity disorder features Autism spectrum disorder . Self-injurious behavior (eg, hand biting) \n\n Anxiety \n\n# . Long face with prominent forehead & chin . Large, protruding ears Examination \n\nfindings . Macroorchidism (age >8) \n\n# . Macrocephaly \n\n# . Joint hypermobility (eg, fingers, wrists) Diagnosis . FMR1 DNA analysis (PCR or Southern blot) FMR = fragile X mental retardation. Rett syndrome \n\n## . Rare neurodevelopmental disorder, greater incidence in girts, onset age 6-18 months \n\nKey . In itia ll y, norma l development followed by: features 0 Loss of speech \n\n> 0\n\nL oss of purposeful hand use , stereotypical movements \n\n> 0\n\nGait abnormalities . Microcephaly \n\n## . Se izures \n\nAdditional findings . Breathing abnormalities \n\n## . Sleep disturbance \n\n## . Autistic features \n\nEtiology . MECP2 gene mutations \n\nNeuropathology . Deceleration of brain growth \n\nPrognosis . Middle-aged life expectancy; reduced mobility, seizures, respiratory difficulties \n\n-Short Subjects Spleen \n\n What is the underlying pathophysiology leading to sepsis with gram-positive cocci in a patient with a history of extensive surgery for multiple gunshot wounds to the abdomen? \n\nImpaired antibody-mediated phagocytosis; Much of this is dependent on splenic macrophages and the generation of splenic opsonizing antibodies the patient likely had a splenectomy, making him/her more susceptible to encapsulated organisms (e.g. S. pneumoniae, H. influenza, N. meningitidis) \n\n What three vaccines should patients receive prior to undergoing splenectomy ?\n\nanti-pneumococcal, Haemophilus, and meningococcal vaccines; yearly influenza vaccine \n\ndue to risk of overwhelming sepsis; patients should also have daily oral penicillin prophylaxis until 5 years of age or for 3 - 5 years after splenectomy \n\n Patients who undergo splenectomy are prescribed an antibiotic to take immediately when they develop fever. Amoxicillin-clavulanate OR Levofloxacin \n\n Patients with splenectomy often have secondary thrombocytosis (Reactive Thrombocytosis) .Typically, platelet counts normalize after several weeks, but a minority of patients may have thrombocytosis for months or years after surgery. \n\nB & T Cell Disorders \n\n785 https://t.me/usmleinnercircle USMLE Inner Circle \n\nRecommended vaccines for asplenic adult patients \n\n## . PCV20 \n\nPneumococcus OR \n\n## . P CV15 followed by PPSV23 \n\nHaemophilus innuenzae . 1 dose Hib vac cine \n\nMeningococcus . Meningococcal quadrivalent vaccine & vaccine against serotype B \n\n## . Revaccinate every 5 years \n\nOther vaccines . Other vacci nes sh ou ld be give n according to age-appropriate guidelines \n\nHib = H influenzae type B; PCV15 = 15-valent pneumococcal conjugate vaccine; PCV20 = 20-valent pneumococcal conjugate vaccine; PPSV23 = 23-va lent pneumococca1 po lysaccharide vaccine. Short Subjects 786 https://t.me/usmleinnercircle \n\nCombined B & T-Cell Disorders B-Cell Disorders & DiGeorge Syndrome ***** Short Subjects Failure to thrive is usually present in T-cell disorders due to chronic diarrhea and increased metabolic needs from recurrent infections .\n\n Poor vaccine response usually involve B-cell Disorders. \n\n Young child presents with features of disseminated tuberculosis following administration of BCG vaccine. IL-12 receptor deficiency ( IFN-y )\n\nCommon pathogens: Intracellular -- salmonella and mycobacterial infections \n\nClinical features: Features of disseminated disease (esp. TB; i.e. following BCG vaccine administration, Fungal infections \n\nDiagnosis: IFN-y \n\n787 https://t.me/usmleinnercircle USMLE Inner Circle \n\nHumoral immunodeficiency syndromes Condi tion B cell lgG l gA lgM lgE count \n\nCD40 ligand deficien cy N orma l I I t I(hy pe r - lgM syndrome) Common variable N orma l I I I Iimmunodefic iency Job syndrome N orma l Normal N orma l Normal I(hyper - lgE syndrome) Selective lgA deficiency N orma l Normal I Normal N orma lX-linked agammaglobulinem ia I I I I I\n\nPrimary immunodeficiency syndromes Classifications Age of Key features Laboratory findings Examples onset \n\n## . Encapsulated Variable bacteria (recurrent \n\n8-cell . ! lg & vaccine . X-linked agammaglobulinemia \n\ndisorders (>4-6 sinopulmonary Common variable immunodeficiency months) infection) response .. Enterovirus* \n\nT-cell (& . Viral, bacterial & DiGeorge syndrome (T) Early fungal infections (eg, ! Leukocytes .combined 8- & . Severe combined immunodeficiency (B & T) .T-cell) (<4-6 Candida, . ! lg & vaccine Wiskott-Aldrich syndrome (B & T) months) Pneumocyst is) .\n\ndisorders response Ataxia-telangiectasia (B & T) .. Failure to thrive \n\n## . Skin & soft tissue infections . Normal lg \n\nPhagocyte Early Fungal infections Impaired oxidative . Chronic granulomatous disease \n\ndisorders (childhood) . . Leukocyte adhesion defect .. Catalase-positive burst** organisms** \n\nComplement Neisseria infections . ! CHS0 C1q deficiency . .Variable . Normal leukocytes & \n\ndisorders . Autoimmune disease . Terminal complement (C5-C9) deficiency lg *Only in X-linked agammaglobul inemi a. ** Only in c hronic granulomatous disease (eg , Staphylococcus aureus, Burkholderia, Se\"atia, Aspergillus , Nocardia). \n\nlg = immunoglobulin. Short Subjects Treatment: AB , IFN-y therapy \n\nTransient Hypoglammaglobinemia of Infancy \n\n What is the likely diagnosis in a 8-month-old infant with low serum IgG and normal serum IgM /IgA ?\n\nTransient hypogammaglobulinemia of infancy \n\ndue to decreased maternally derived IgG by 3 - 6 months; usually resolves by 12 months of age \n\nBruton Agammalglobinemia CVID \n\n788 https://t.me/usmleinnercircle \n\nTransient hypogammaglobulinemia of infancy lmmunoglobulin levels in infancy \n\n> 1,200\n\nPathophysiology . Prolonged ( age >6 months) physiologic lgG nadir \n\n## . May be asymptomatic 1,000 \n\nClinical features . Recurrent respiratory infections in infancy \n\n## . Atopy (eg , eczema, food allergies) 800 \n\n# . ! lgG ( ! lgAand/or lgM ) 600 \n\nLaboratory findings . Normal antibody response to vaccines \n\n## . Normal B and T ll mehoc~ es E 400 300 \n\nTreatment . Observation; self-resolution in early childhood C, \n\n> E200 150 125 100 75 50 25 008Bi rth 10 12\n> Mon th s\n> \"Ma ternal lgM does not cross placenta\n\nX-linked agammaglobulinemia \n\n# . BTK gene mutation resulting in defective \n\nPathophysiology Bruton tyrosine kinase \n\n## . Impaired B-cell maturation &\n\nimmunoglobulin production \n\n## . Recurrent sinopulmonary &\n\ngastrointestinal infections at age \n\nClinical >3-6 months \n\nmanifestations . Chronic enteroviral infection \n\n## . Small or absent lymphoid tissue (eg, tonsils, adenoids) \n\n## . ! lmmunoglobulins & antibody response \n\nLaboratory to vaccines \n\nfindings . Flow cytometry: ! co19+ B cells \n\n& normal T cells \n\nTreatment . lmmunoglobulin replacement therapy \n\n## . Prophylactic antibiotics if severe Short Subjects CVID should be suspected in adults with recurrent bacterial infections Versus other causes of immunodeficiency, which present in childhood \n\n Occurs in Adults (20-40 y) and adolescents (around puberty) \n\n What test is used to diagnose common variable immunodeficiency (CVID)? \n\nQuantitative measurement of serum immunoglobulins \n\n Which immunodeficiency is characterized by no B-cell maturation ?\n\nX-linked (Bruton) agammaglobulinemia \n\nversus CVID , which is caused by poor B-cell differentiation \n\nSCID \n\n What tests are used for the diagnosis of SCID ?\n\nQuantitative PCR : T-cell receptor expression cirlces (TRECs) Part of routine Newborn Screening \n\nAbsent T-cells \n\n789 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCommon variable immunodeficiency Pathophysiology . Abnormal differentiation of B cells into plasma cells -, \n\ndecreased immunoglobulin production \n\n## . Symptom onset classically age 20-40, as ea rly as puberty \n\n## . Recurrent respiratory infections ( eg , pneumonia, sinusitis, otitis) \n\n## . Recurrent GI infections ( eg , Salmonella, Cam pyl obacter, \n\nClinical Giardia ) \n\nmanifestations . Chronic disease: \n\n0 Autoimmune ( eg , RA, thyroid disease) \n\n0 Pulmonary (eg, bronchiectasis, fibrosis) \n\n0 GI (eg , chronic diarrhea, IBD-like conditions) \n\nDiagnosis . U lgG, L lgA/lgM \n\n## . No response to vaccination \n\nManagement . lmmunoglobulin replacement therapy \n\nGI = gastrointestinal ; IBD = inflammatory bowel disease; RA = rheumatoid arthritis. \n\nSevere combined immunodeficiency Etiology Gene defect leading to failure of T cell development \n\n## . B cell dysfunction due to absent T cells \n\nInherit ance X-linked recessive Autosomal recessive Recurrent, severe viral, fungal , or opportunistic \n\nClinical (ie, Pneumocystis) infections \n\nfeatures Failure to thrive Chronic diarrhea \n\nTr eatment Stem cell transplant \n\n0\n\nShort Subjects CXR: absence of thymic shadow Lymph node biopsy shows absence of germinal centeres \n\nIgA Deficiency \n\n Should receive blood products that are washed of residual plasma or from an IgA-deficient donor .\n\nHyper IgE Leukocyte Adhesion Disorder Chronic Granulomatous Disease \n\n790 https://t.me/usmleinnercircle \n\n\n\nSelective lgA deficiency Epidemiology . Most common primary immune deficiency \n\n# . Usually asymptomatic \n\n# . Recurrent sinopulmonary & gastrointestinal infections \n\nClinical features . Associated with autoimmune disease (eg, celiac) & atopy (eg , asthma, eczema) \n\n# . Anaphylaxis during transfusions Low or absent lgA \n\nDiagnosis Normal lgG , lgM leve ls, B cells .. Supportive care \n\nTreatment . Medical alert bracelet for transfusion reactions (for severe deficiency) \n\nHyper-lgE syndrome \n\n# . Autosomal dominant \n\nPathogenesis . Defective JAK-STAT signaling - impaired Th17 \n\n## . l Neutrophil proliferation/chemotaxis \n\n# . Severe, chronic eczema \n\nClinical . Noninflammatory (ie, cold) abscesses (eg, Staphylococcus, Candida) \n\nfeatures . Recurrent sinopulmonary infections \n\n# . Dysmorphic facies (eg, broad nose, prominent forehead) \n\n# . Retained primary teeth \n\n## . j lgE \n\nLaboratory Eosinophilia \n\nfindings .. Normal leukocyte count with l Th17 \n\n## . Supportive skin care \n\nManagement Antibiotic prophylaxis & treatment .\n\nTh17 = T-helper cell type 17 .\n\nLeukocyte adhesion deficiency \n\n# . Defect in CD18-containing integrins \n\nPathophysiology Impaired leukocyte adhesion & endothelial transmigration .. Skin & mucosal infections (eg, cellulitis, periodontitis) without pus formation \n\nClinical features . Impaired wound healing . Delayed umbilical cord separation ( age >3 weeks )\n\nLaboratory findings . Leukocytosis & neutrophilia Short Subjects Phagocytic cells filled with bacteria (due to ineffective intracellular killing) are a frequent finding on Gram stain. \n\n Live bacterial vaccines such as the BCG vaccine should be avoided in CGD because they can induce severe infection . Live viral vaccines , as well as inactivated vaccines , are safe. \n\n Patients also have impaired ability to degrade inflammatory cytokines, which predisposes them to \n\ninflammatory conditions (eg, IBD ) and diffuse granuloma formation , particularly in the gastrointestinal and genitourinary tract. In CGD-associated IBD, pigment-laden histiocytes are characteristically seen on histology and represent lipofuscin accumulation due to impaired lipolytic activity. To reduce risk of infection, patients are treated with antibacterial (eg, trimethoprim-sulfamethoxazole )and antifungal (eg, itraconazole ) prophylaxis; however, breakthrough infections may occur. Because breakthrough infection may involve resistant bacterial or fungal organisms, patients (unless they are critically ill) generally should undergo biopsy of areas of active infection prior to initiating empiric antimicrobial therapy .\n\nHereditary Angioedema \n\n791 https://t.me/usmleinnercircle USMLE Inner Circle \n\nChronic granulomatous disease \n\n## . X-linke d recessive mutation of NADPH oxidase \n\nPathogenesis Impa i red r espiratory burst & ! reactive oxygen species --+ inhibition of phagocytic intrace llular killing .. Recurrent in fections wit h catalase-pos iti ve bacteria & fungi \n\nClinical features . Lungs, skin, liver , lymph node involvement \n\n## . Diffuse granulomas (eg, gastrointestinal , genitourinary) \n\n## . Measurement of neu tr oph il superoxide production :\n\nDiagnosis 0 OHR flow cytometry (preferred) \n\n0 NBT testing \n\n## . Prophylaxis : TMP-SMX, itraconazole , i nterferon gamm a\n\nTreatment . Active infection : cu l ture-based , antimicrobial the rapy \n\n## . H ematopoietic cell transplant is curative \n\nstaphylococcus aureus, Burl 0\n\nAL: produced by clonal plasma cells \n\nEtiology 0 AA: secondary to chronic infla mm at ion \n\n> 0\n\nATTR: age-relat ed o r hereditary \n\n> 0\n\nAB2-m : dialysis-related \n\n# . Nephrotic syndrome (A L & AA) \n\n# . H epatomegaly wi th/ without sp lenomega ly (A L & AA) \n\nClinical . Restrictive cardiomyopathy ( AL & ATTR) prese nt atio n* . CTS, sca pulohu me ral periarthritis (AB2-m )\n\n# . Per ipheral/autonomic neuropathy \n\n# . Periorbital purpur a, waxy skin, macroglossia *Clini ca l presentation var ies depending on the ty pe of am y lo id present. AA = amy loid A; AB2-m = a myloid beta2 -mi crogl obu lin; AL = amy loid li gh t cha in; ATTR = am y loid transthyre t in ; CTS = carpa l tunne l syndr ome .\n\nCl inical man if estations of amyloidosis (primary & secondary) \n\n# . Heavy proteinuria with nephrotic sy ndr o me \n\nRenal . Periphera l edema \n\n# . Restrictive cardiomyopathy \n\nCardiac . Conduction defects , l ow voltage \n\n# . Peripheral &/ or auton om ic neuropathy \n\nCNS . Stroke \n\n# . Hepatomega ly \n\nGI . Dys moti l ity , ma labsorptio n \n\n# . GI bleeding due to vascular fragility \n\nPulmon ary . Pulmonary nodu l es , tra c heobronc h ia l infiltration, pleural e ff us i ons \n\nMusculoskeletal . Enlarged tongu e, shou lder pad enlargement \n\n# . Thickening of skin, sub c utaneous nod ules/ plaqu es \n\nSkin . Ecchymoses, periorbital purpura \n\nHeme Anemia , thrombocytopenia CNS = ce ntr al ne rv ous sy s tem ; GI = gas t ro int es ti na l. Short Subjects Other signs: 1. Diffuse Lymphadenopathy \n\n2. Mild Proteinuria \n\nImmunosuppression \n\nNeutropenia \n\nNeutropenia (<1500) Severe: (<500) Gram-ve: Pseudomonas \n\nGram+ve: S. Aureus, S. Epidermis \n\n Antifungal medications are recommended in high-risk neutropenic patients with persistent fever after 4-7 days of initial therapy in whom a source of infection is not identified. \n\n793 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSerum sickness & serum sickness-like reaction \n\nss SSLR Common Foreign proteins in antivenom, antitoxin, or monoclonal \n\ntriggers antibody Medications, particularly cefaclor, penicillin & T MP-SMX \n\nImmune High titer Mild or none \n\ncomplexes Complement Extensive Minimal or none \n\nactivation Onset 5-14 days after exposure 5-14 days after exposure \n\nFever High Low-grade \n\nArthralgia Yes Yes \n\nUrticaria Yes Yes \n\nResolution Spontaneous Spontaneous (discontinue drug if still receiving) \n\nSS == serum sickness; SSLR == serum sicknes~ike reaction; TMP-SMX ;;; trimethoprim-sulfamethoxazole . \n\nMedications associated with drug-induced neutropenia \n\n## . Methimazole Antithyroid . Propylthiouracil \n\n## . Sulfasalazine \n\nAnti-inflammatory . Methotrexate \n\nPsychotropic or . Clozapine . Carbamazepine \n\nanticonvulsant . Phenytoin \n\nCardiovascular . Antiarrhythm ic agents (eg, procainamide) \n\n## . Ticlopidine \n\n## . Trimethoprim-sulfamethoxazole \n\nAntimicrobial . Quinine \n\n## . Acyclovir \n\n Immune deficient FUO (neutropenic fever) \n\nNeutropenic patient with fever and a neutrophil count s 500/L (severe risk of bacterial infectio n) Neutropenic fever is often ~~-~. '!!~~~~~~eY.induced. c;:::i \n\n Other common causes: bacterial infections, ~~p~_ rg _i_ llo~! ~ ~~~~ -i~i~s!~, herpes virus \n\nManagement: Even without a determinant source of infection, broad-spectrum antibiotics must be administered without delay to avoid sepsis and life-th re atening complications. \n\nAn antiJ:1 .s.~~~~. '!!~!:' .~! B-lactam drug (c~ _fe(J i_ r:,:ie , T~ ~~p~~~ -~.. or pip_ e_ ~'.1~!1 .l ir,i ,i~?.~ ~~) .a. ~) that covers both gram-negative and gram-positive bacteria If fever persists, reassess for fungal or vi ral infection and adapt treatment accordingly. Short Subjects Immunosuppressants \n\n1. Cyclosporine and tacrolimus both cause nephrotoxicity . (d/t their vasoconstrictive property) \n\nCyclosporine causes hirsutism and gum hypertrophy, tacrolimus does not. \n\n Calcineurin inhibitors (eg, tacrolimus, cyclosporine) have a wide range of adverse effects, including nephrotoxicity , hypertension , neurotoxicity (eg, tremor ), and impaired glucose control. \n\n2. Azathioprine major side-effects are dose-related diarrhea , leukopenia , and hepatotoxicity .3. Major toxicity of mycophenolate is bone marrow suprression. \n\nOrgan Transplant \n\n What is the most likely diagnosis in a patient who presents with decreased urine output 2 weeks after a kidney transplant? Exam shows tenderness over the transplant area. Vitals reveal hypertension . Labs are significant for hyperkalemia and elevated BUN/Creatinine .\n\nAcute cellular rejection Key points Path: Occurs <6 months after transplant; allorecognition > T-cell induced cell-mediated and/or humoral immunity \n\nFindings: Pain in graft region ; in kidney transplants , elevation of BP and kidney function lab values and decreased Urine Output Diagnosis : Mononuclear/lymphocytic infiltrate. \n\nC4d staining +ve = humoral graft rejection ; C4d -ve = cellular rejection Treatment: Increase dosage of immunosuppressive therapy. \n\nFirst-line is high-dose corticosteroids (for cellular rejection). What prophylactic medications should be initiated in a patient who is beginning high-dose immunosuppression therapy following a renal transplant? \n\n794 https://t.me/usmleinnercircle \n\nLung transplant rejection Chronic Acute \n\n> (cell-mediated response) (mixed cell-mediated &antibody response)\n> Clinical\n\n## . :S6 months after transplant . Months to years after transplant \n\n> presentation\n\n## . Asymptomatic or fever, cough, . Progressive cough & dyspnea dyspnea . History of acute episodes BAL to rule out infection . Obstructive pattern on PFT \n\n## . . BAL to rule out infection \n\n> Diagnosis\n\n## . Biopsy: submucosal lymphocytic Biopsy: submucosal ly mphocytic infiltrate, perivascul ar inflammation . infiltrate, bronchiolitis obliterans \n\n> Management High-dose glucocorticoids\n\n# . Supportive management \n\n## . Possible repeat transplant . \n\n> BAL\n\n=bronchoalveolar lavage; PFT =pulmonary function testi ng. Short Subjects 1. TMP-SMX (for PCP) \n\n2. ganciclovir or valganclovir (for CMV) \n\nfungal prophylaxis may be required in other solid organ transplants (e.g. lung, liver); typically not needed for renal transplant \n\nShould also monitor blood for 12 months for CMV and EBV viral loads \n\n Most infections within the first month following liver transplantation are due to bacterial pathogens .\n\ndifferentiated from acute transplant rejection by the presence of significant leukocytosis and acute hemodynamic instability \n\nDDX: Acute cellular rejection can cause similar symptoms, except patients with bacterial infections will have rapid-onset hemodynamic instability , making bacterial infection more likely (also look for signs of sepsis) Infection etiology can be discerned based on time frame \n\n<1 month = bacterial infection and 1-6 month = opportunistic pathogens (CMV) \n\n Sudden onset liver pain and increased liver enzymes 4 weeks after liver transplant? Think \n\nHepatic Artery Thrombosis (Acute vs gradual in Transplant rejection) Most infections during months 1 - 6 following liver transplantation are due to opportunistic pathogens. \n\ndue to high-dose immunosuppressants; after 6 months, patients are primarily at risk for community-acquired pathogens \n\n Acute cellular rejection (ACR) can also present with respiratory dysfunction, new infiltrates, and fever. It cannot be excluded without histology. \n\nACR is often precipitated by infection (eg, CMV pneumonitis causing tissue damage and allosensitization to donor lung antigens). For this reason, ACR and infection may occur concurrently. Any lung transplant recipient with new infiltrates and fever should undergo a comprehensive workup for both ACR and infection , often with bronchoscopy and lung biopsy. \n\nPost-Transplant Lymphoproliferative Disorder \n\n795 https://t.me/usmleinnercircle USMLE Inner Circle \n\nMajor complications of solid organ transplantation \n\n# . Nosocomial infections (eg, h osp ital-acquired pneumonia) \n\nInfectious . Opportunistic pathogens (eg, CM V, PCP , Aspergillus) \n\n# . Hyperacute rejection: ABO mismat ch \n\nImmunologic . Acute rejection*: cell or antibody-mediated . Chronic rejection: fibrosis of graft structur es (eg, bronchiolitis ob lit erans of airways) . Surgical site: a nastomotic dehi sce nce \n\nPostoperative Primary graft dysfunction: ARDS, ATN .\n\n# . Drug toxicities: nephrotoxicity (calcineurin inhibitors), osteoporosis (corticosteroids} \n\nOther . Malignancy: posttransplant lymph op roliferative disorder (EBV) *A cu te cellular rejec ti on is th e most common type in th e first 90 days but can occur at an y time after transplant. \n\nARDS =acute res pi ratory distress syndrome; ATN =acute tubular ne cro sis; CMV =cytom eg alovirus; EBV =Epstein-Barr virus; PCP = Pneumocystis jirove ci pne umonia. Short Subjects Microbiology \n\nAntibiotics \n\n Antibiotic therapy prior to surgery: 1st generation cephalosporin (Cefazolin) Anaerobic coverage :\n\nClindamycin ,\n\nMetronidazole + Amoxicillin ,\n\nAmoxicillin -clavulanate \n\n Ceftrixone covers Gram -ve an +ve aerobes \n\n Clindamycin does not cover gram -ve \n\n Metronidazole covers Gram -ve an +ve anaerobes \n\nBacteria \n\nStrep \n\n796 https://t.me/usmleinnercircle \n\nPosttransplantation lymphoproliferative disorder \n\n# . lmmunosuppression following solid-organ or stem cell transplantation - suppressed cytotoxic T-cell immunosurveillance - unchecked viral replication - immortalized lymphocytes or plasma \n\nPathogenesis cells . Epstein-Barr viru s causes >95% of cases, but other human herpesviruses (eg, HHV8) can also trigger the disease . Fever . Lymphadenopathy & hepatosplenomegaly \n\nManifestations . Leukopenia . Masses in nonlymphatic tissue . High viral titers \n\nDiagnosis Biopsy evidence of lymphoid or plasma cell proliferation .. Reduce immunosuppression Treatment . B-cell immunotherapy (eg, rituximab} . Epstein-Barr virus titer monitoring \n\nCommon intracellular pathogens* \n\nChlamydia \n\nFrancisella tularensis \n\nLegionel/a \n\nListeria monocytogenes \n\nBacteria Mycobacterium Neisseria gonorrhoeae \n\nNocardia \n\nRickettsia \n\nSalmonella typhi \n\nYersinia pestis \n\nFungi Cryptococcus neoformans Histoplasma capsu/atum \n\nCryptosporidium parvum \n\nLeishmania \n\nProtozoa Plasmodium \n\nToxop/asma gondii \n\nTrypanosoma \n\n*Fa cultative intracellular pathogens are also included .\n\nShort Subjects Clostridium Sandpaper rash \n\n797 https://t.me/usmleinnercircle USMLE Inner Circle \n\nScarlet fever Etiology Streptococcus pyogenes \n\n Fever & pharyngitis Tonsillar erythema & exudates \n\nClinical features Strawberry tongue Tender anterior cervical nodes Sandpaper rash \n\nDiagnosis Rapid streptococcal antigen test Throat culture \n\nTreatment Penicillin (eg, amoxicillin) \n\nGroup B streptococcal infection in neonates & young infants Early onset (age <7 days) Late onset (age ~7 days) \n\n## . Vertical transmission in utero or during vaginal delivery Horizontal transmission from colonized .Pathogenesis . Reduced transmission with maternal intrapartum antibiotic individuals prophylaxis \n\nClinical Typically presents within 24 hours . Typically presents age 4-5 weeks \n\n## .features Sepsis, pneumonia, meningitis . Bacteremia, meningitis, focal infection (eg , \n\n## . cellulitis) \n\nDiagnosis . Gram-positive cocci in pairs/chains on culture of blood, CSF, or body fluid \n\n## . Early initiation of empiric antibiotics \n\nTreatment . Definitive therapy with penicillin G \n\nCSF = cerebrospinal fluid . Short Subjects Tetanus is a clinical diagnosis that should be suspected in a patient who has characteristic symptoms. (Dont do any toxin analysis) \n\n Giving infants horse serum can cause a severe allergic reaction \n\n For reducing hospital acquired C. Difficile infection: 1. Implementation of uniform (ie, standardized) cleaning and disinfection procedures that include the use of sporicidal agents (eg, bleach). Cleaning of all surfaces should be performed by a dedicated team \n\n2. Adherence to hand hygiene for all patients and contact isolation precautions , including use of gowns and gloves in patient rooms, for persons suspected to have C difficile . Soap and water are preferred for hand hygiene \n\nDiptheria \n\n What are the systemic side-effects of Diptheria and how do you diagnose? \n\nMyocarditis (arrhythmias) --> conduct multiple ECGs California , Pennsylvania , and Utah have the greatest concentration of soil botulism spores \n\n798 https://t.me/usmleinnercircle \n\nTetanus prophylaxis \n\nClean or minor wound Dirty or severe wound \n\nTetanus toxoid-containi ng vaccin e* Tetanus toxoid-containing vaccin e* \n\n?3 tetanus toxoid doses only if last dose ~10 years ago only if last dose ~5 years ago \n\nNo T IG No T IG \n\nUnimmunized, uncerta in, or <3 tetanus Tetanus toxoid-containi ng v acc in e* Tetanu s toxoid-containi ng vaccin e* only PLUS toxoid doses No T IG TIG \"Booster given as tetanus/diphthe ri a (Td) toxoids ad sorb ed or tetan us toxoid/red uced diphth er ia toxoid/ace ll ular pertussis (Tdap) \n\nTIG = tetanus immune g lobulin. Neonatal tetanus . Difficult feeding , trismus Clinical features . Spasms & hypertonicity: clenched hands, dorsiflexed feet, opisthotonus Treatment . Supportive care . Antibiotics & tetanus immunoglobulin . Vaccination Prevention . Hygienic delivery & cord care Differential diagnosis of flaccid paralysis Diagnosis Infant botulism Foodborne botulism Guillain-Barre syndrome Ingestion of Clostridium In gestion of preformed C Autoimmune peripheral neive \n\nPathogenesis botulinum spores from botulinum toxin demyelination environmental dust Presentation Descending flacc id paralysis Descending flaccid paralysis Ascend i ng flaccid paralysis Human-derived botulism immune Treatment Equine-derived botulism antitoxin Pooled human immune globulin globulin Short Subjects Leprosy TB \n\nMiliary tuberculosis is caused by lymphohematogenous dissemination of Mycobacterium tuberculosis \n\nfrom the lungs to other organs, resulting in micronodular lesions in the lungs, liver, and spleen. It is most common among infants and immunocompromised hosts with poor T-cell function and is often associated with false-negative tuberculosis test results. Hematogenous delivery of M tuberculosis back to the lungs results in the development of pulmonary micronodules that have the classic millet-seed appearance from which the term miliary TB is derived. The ineffective T-cell response in these patients means that interferon-based testing , such as interferon-gamma release assays and tuberculin skin testing, is often falsely negative . Definitive diagnosis requires culture of M tuberculosis from lungs, blood, or tissue biopsy. What is the classic chest x-ray sign for miliary tuberculosis? \n\nDiffuse, reticulonodular pattern (\" millet seed\" appearance )Bilateral Reticulonodular Opacities \n\n799 https://t.me/usmleinnercircle USMLE Inner Circle \n\nLeprosy \n\n Mycobacterium leprae \n\nEpidemiology . Primarily developing world (eg , Asia , Africa, South America) . Respiratory droplets/nine banded armadillo . Low infectivity \n\nManifestations . Macular, anesthetic skin lesions with raised borders \n\n# . Nodular, painful nearbl nerves with loss of sensory/motor function \n\nDiagnosis . Full thickness biopsy of skin lesion (active edge) M leprae is not culturable \n\nTreatment . Dapsone + rifampin Add clofazimine if severe (\"multibacillary\") \n\nMiliary tuberculosis Short Subjects Most common behavioural risk factor for TB in the United States is substance abuse \n\n Most TB cases in the United States (US) occur in foreign-born individuals who have recently emigrated from endemic areas (eg, Mexico, the Philippines, China, Vietnam, India, Dominican Republic, Haiti). Most of the cases represent reactivation of latent TB rather than a new infection acquired in the local community. Screening and treatment of latent TB is recommended for immigrants and refugees coming to the US. A patient presents with fever, cough, night sweats, weight loss and hemoptysis . He has risk factors for TB. You suspect TB. A CXR is positive. Follow-up AFB smear is also positive. What is the most appropriate next step in management? \n\nThis is a diagnosis of active TB; start RIPE therapy ( 2 months of RIPE + 4 months of isoniazid and rifampin )\n\n A patient presents with fever, cough, night sweats, weight loss and haemoptysis . He has risk factors for TB. You suspect TB. A CXR is positive. Follow-up AFB smear is negative. What is the most appropriate next step in management? \n\n800 https://t.me/usmleinnercircle \n\nPathog en esis of pulmonary tuberculosi s i nfe ction \n\n> Primary Inf ec tion\n\n## /Latent Inf e ction \n\nDormant bacteria \n\n> contained'Wlthin\n\nwalled-of! loo \n\n# !\n\n# 1--l\n\n# ~Bacteria spread 10 lymph nodes, \n\n> formng\n\nGhon comp6ex \n\n> Ruo lut lon Prog resstve primary\n> tuberculosis\n> Bacterial clearance Failed immune response\n> &\n\nscar formation resolls in progressive tung \n\n> consolida!lon &necrosis\n> Seconda ry tubercutosis Miliary tuberculosis\n> ReaclNated bactena spread\n> bronchogemcal ly &cause\n> extensrve cavitation\n> Hematogenous dissemination\n> of bacteria to multiple organs\n\nShort Subjects INH for 9 months \n\nCollect early morning sputum and get at least 3 cultures 8 hrs apart .To help ensure a true result, get 3 early morning sputum 24 hrs apart .Your last ditch effort if you have a very high suspicion of TB is nucleic acid assay .\n\n Chest x-ray during pregnancy is safe with appropriate shielding and should be pursued if it immediately affects management. Pregnant women should be evaluated for tuberculosis using the same diagnostic approach as nonpregnant patients In the US, an induration size of < 15 mm is considered negative in healthy patients with low likelihood of TB \n\n801 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPPD/TST induration \n\n..~5m m .....\n\n~10 mm ...\n\n~15 mm .\n\n'\\o hpo,urc \n\nR.I PI \n\nHIV-p os itive pa tients Recent contacts of known TB case \n\n1'1 H x9mo, \n\n86 \n\ne\n\nPatients to treat \n\nStop \n\nNodul ar or fibrotic changes on chest x-ray consistent with previ ous ly heal ed TB Organ transpl ant r ec ipients & oth er immun os up pr essed patients Recent i mm igran ts (<5 years) from TB-end em ic areas Inj ect ion drug users Res idents & employees of hi gh-r isk se ttings (eg, pr isons, nu rsing homes, hospital s, h ome less shelters) Mycobacteriol ogy laboratory personnel Hi ghe r risk fo r TB reactivation (eg, diabetes, prolonged corticosteroid therapy, leukemia, end-stage renal disease, chronic ma labsorption synd ro mes) Children age <4, or th ose ex po sed to adults in high-risk categories All of the above plus healthy individuals Short Subjects PPD may be false-negative in patients with CD4+ counts < 200/mm3 and CKD \n\nSome other labs of TB: Anemia , Monocytosis , Elevated total Protein , HypoAlbuminemia \n\n IGRA- interferon-gamma release assay \n\n1. More sensitive and specific than TST 2. Not affected by previous BCG vaccination 3. Minimal response to control antigens is most often seen with lymphocyte immunosuppression \n\ndue to HIV or the use of immunomodulatory medications (eg, glucocorticoids) \n\nRepeat when CD4 count improves or few weeks after discontinuing drug \n\n Most patients first exposed to TB have asymptomatic primary infection because the organism is rapidly contained within granulomas and can become \" latent \" if the body fails to clear the bacteria; they are at risk of secondary ( reactivation ) TB later in life. In contrast, ~10% of adults first exposed to TB develop symptomatic primary disease (\"progressive primary TB\"); risk factors for primary progression include impaired immunity due to comorbid conditions (eg, diabetes mellitus , renal disease, HIV), advanced age , or immunosuppressive medications. In contrast to reactivation TB (usually marked by cavitary infiltrates ), radiography in primary TB often shows a lobar infiltrate (due to unchecked mycobacterial replication) and significant ipsilateral hilar lymphadenopathy .\n\n802 https://t.me/usmleinnercircle \n\nPrimary pulmonary tuberculosis \n\n# . lmmunosuppression (eg, HIV} \n\n Travel from endemic area \n\nRisk factors . Exposure to infected household contact \n\n# . Resident/employee of prison, h ome less shelter, health care facility \n\n# . Chronic cough \n\nClinical . Prolonged fever \n\nmanifestations Weight loss, failure to thrive \n\n# . Positive screening PPD or interferon-y release assay \n\nDiagnosis . Chest x-ray: hilar adenopathy, effusion, consolidation , cavitation \n\n# . Positive AFB smear & mycobacterial culture \n\nTreatment . Multidrug therapy: isoniazid, rifampin, pyrazinamide, ethambutol \n\n> AFB ;;; acid-fast bacilli; PPD ;;; purified protein derivative.\n\nDiagnostic tests for pulmonary tuberculosis AFB smear . Low cost & rapid (minutes to hours) \n\n> microscopy\n\n## . Low sensitivity because high burden (>10,000/mL) of organisms required in sample \n\n## . Cannot differentiate TB from non-TB mycobacteria \n\n> Nucleic acid\n\n## . Higher cost & slightly less rapid (1-2 days) \n\namplification . Higher sensitivity (only-10 bacillUmL required for positive test) \n\n> testing\n\n## . Can differentiate TB from non-TB mycobacteria \n\nSputum . Gold standard, quantitative & allows for drug sensitivity testing \n\n> culture\n\n## . Slow: takes 3-8 weeks \n\n> AFB = acid-fast bacillus (stain); TB= tuberculosis.\n\nShort Subjects What is the next step in management for a patient being treated with RIPE therapy for TB for the past month that develops mild elevations in AST /ALT ?\n\nContinue with current treatment; monitor LFTs \n\nsubclinical hepatotoxicity is common within the first few weeks of isoniazid therapy; it is typically self-limited and resolves without intervention \n\n Severe INH hepatitis presents with clinical manifestations similar to those seen with viral hepatitis (eg, fatigue, nausea, flu-like symptoms, jaundice, aminotransferases >10 times upper limit of normal). \n\nsignificant hepatotoxicity warrants immediate discontinuation of drugs & switching to second line drugs \n\nGonococcal \n\n What is the likely diagnosis in a sex worker that presents with fever /chills , polyarthalgia , and pustules on the chest and extensor surfaces of the forearms ?\n\nDisseminated gonococcal infection \n\nthe patient is normotensive: rules out toxic shock syndrome \n\nhas no abnormal heart sounds: rules out infective endocarditis \n\nrash that spares the palms and soles: rules out secondary syphilis (rash is maculopapular) \n\n Patients with Neisseria gonorrhoeae are at high risk of simultaneous confection with several other pathogens, including Chlamydia trachomatis , HIV , syphilis , and hepatitis B .\n\n803 https://t.me/usmleinnercircle USMLE Inner Circle \n\nMycobacterium avium complex Epidemiology M avium , M infracel/u/are \n\nPatients with advanced AIDS (CD4 <50/mm 3)Fever & weight loss \n\nManifestations Abdominal pain & diarrhea LAD & (often) hepatosplenomegaly \n\no t Alkaline phosphatase \n\nDiagnosis Blood/lymph node culture - nontuberculous mycobacteria \n\nTreatment Ma crolide + ethambutol Primary prophylaxis (azithromycin) no longer r ec ommended \n\nLAD = lymp hadenopath y. \n\nDisseminated gonococcal infection \n\nPuru l ent monoarthritis Clinical &/ OR presentation Triad of tenosynovitis, dermatitis (erythematous papules & pustules), asymmetric mig ratory \n\npolyarthralgias \n\nBlood cultures (may be negative) \n\nDiagnosis Synovial fluid ana lysis: Inflammat ory effusion with neutrophil pred ominance ; Gram stain & culture orNAAT Cu lture or NAAT of urethra, cervix, pharynx, rectum Intraven ous ceft riaxone, sw itch to oral (cefixi me) when clinically im proved \n\nTreatment Empiric az it hromycin OR doxycyc line for concomitant chlamy dia! infection Jo int drai nage for purulent arthritis Short Subjects Gonococcal pharyngitis (non-exudative) occurs due to inoculation of the pharynx during orogenital contact . Patients typically have pharyngeal edema, erythema , and non tender cervical lymphadenopathy \n\nversus EBV , which typically causes tender cervical lymphadenopathy and exudative pharyngitis \n\nMeningococcal \n\n Other key features distinguishing meningococcal disease from more benign illnesses include: \n\nSevere myalgias (eg, diffuse leg pain) \n\nCold hands/feet Mottled skin or pallor \n\n Dx: Lumber puncture and CSF Culture \n\n Risk of transmission occurs from 7 days prior to symptom onset until 24 hours after initiating appropriate antibiotic therapy. \n\n804 https://t.me/usmleinnercircle \n\nGonococcal proctitis \n\n# . Receptive anal intercourse \n\nTransmission . Direct spread from the vagina \n\n# . Mucopurulent anal discharge, occasional rectal bleeding \n\nManifestations . Tenesmus, constipation . Pruritus, rectal pain, rectal fullness \n\nDiagnosis . Nucleic acid amplification test of rectal swab \n\nTreatment . Ceftriaxone + doxycycline (to cover Chlamydia) \n\nMeningococcal meningitis Epidemiology . Neisseria meningitidis \n\n## . Most common in young children & young adults \n\n## . Initial : nonspecific fever, headache , vomiting , myalgia, sore throat \n\nClinical features . Within 12-24 hr: petechiae/purpura , meningeal signs, AMS \n\nTreatment . Ceftriaxone \n\n## . Shock \n\nComplications . Disseminated intravascular coagulation \n\n## . Adrenal hemorrhage \n\nPrevention . Droplet precautions \n\n## . Chemoprophylaxis* for close contacts \n\n*Rifampin, ci profloxacin , or ceftriaxone. AMS = alte red mental status .\n\n\n\nNeisseria meningitidis postexposure prophylaxis \n\n Household members Roommates or intimate contacts Recommended Childcare center workers \n\npopulations Persons directly exposed to respiratory or oral secretions Person seated next to affected person for 2:8 hr (eg, airline traveler) \n\nProphylaxis Rifampin Ceftriaxone options Ciprofloxacin (adults only) \n\n*Regardless of vaccination status. Short Subjects HiB \n\n What is the initial treatment for a child with severe respiratory distress and signs of epiglottitis ?\n\nEndotracheal intubation \n\nPatients may require a surgical airway (eg, tracheotomy, needle cricothyrotomy) if attempts at intubation fail. \n\nbroad-spectrum antibiotics should be administered after the patient is stabilized \n\nPertussis \n\n The classic inspiratory whoop and posttussive emesis are often absent in adults , but cough can be severe and result in rib fractures , hernia , or subconjunctival hemorrhage. \n\n What is the recommended treatment for vaccinated close contacts of patients with pertussis? \n\n805 https://t.me/usmleinnercircle USMLE Inner Circle \n\nEp ig lotti ti sM ic robiology Haemophilus influenzae type b \n\n Distress (tripod position, sniffi ng position, strider) \n\nC lin ical features Dysphagia, dysphonia Drooling High fever \n\nX- ra y \"Thumbprint sign\" (enlarged ep iglottis) \n\nManagement End ot racheal i nt ubation Antibio ti cs \n\nPreventi on . Immunization \n\nPertussis Microbiology Bordetella pertussis (gram-negative coccobacilli) Catarrhal (weeks 1-2): mild cough , rhin itis \n\nClinical Paroxysmal (weeks 2-8): severe coughing spells \n\nphases o lnspiratory whoop, posttussive emesis, apnea/cyanosis (infants); posttussive syncope (older patients) Convalescent (weeks 8+ ): symptoms resolve gradually Clinical : cough + paroxysmal symptoms &/or pertussis exposure \n\nDiagnosis o Supportive findings: low-grade/no fever, leukocytosis with lymphocytosis, normal/nonspecific chest x-ray Confirmatory: pertussis PCR (sensitive) & culture (specific) \n\nTreatment Treat empirically with macrolide (eg, azithromycin) Droplet precautions Acellular pertussis vaccine \n\nPrevention Macrolides for close (home/health care) contacts regardless of vaccination status \n\nPertussis treatment & post-exposure prophylaxis Age <1 month Azithromycin x 5 days Azithromycin x 5 days OR \n\nAge :::1 mo nt h Clarithromycin x 7 days OR Erythromycin x 14 days Short Subjects Prophylactic macrolides \n\npatients who are not fully immunized also require pertussis vaccination in addition to antibiotic treatment \n\nLegionella Pseudomonas \n\nPseudomonas aeruginosa folliculitis (\"hot-tub\" folliculitis); Most cases develop within hours or a few days after swimming in an inadequately chlorinated swimming pool or hot tub. Self limited, no treatment required. \n\n M/C cause of folliculitis/purulent skin infections is S. Aureus \n\nE.Coli \n\n Why is empiric antibiotic therapy avoided in patients with suspected enterohemorrhagic E. coli (EHEC) infection? \n\nMay increase risk of HUS \n\n806 https://t.me/usmleinnercircle \n\nClues for increasing index of suspicion for Legionella pneumon ia Exposure to possibly contaminated water . Recent travel (especially cr ui se or hotel stay) within the previous 2 weeks . Contaminated potable wa ter in hospita ls /nursing homes . Fever >39 C (102.2 F) . Bradycardia rela ti ve to hi gh fever Cl inical clues . Neurologic symptoms (especially co nfusion) . Ga strointestinal symptoms (especially diarrhea) . Unrespo ns ive to ~-lactam & aminoglycoside antibiotics \n\n## . Hyponatremia Laboratory clues . Hepatic dysfunction . Hematu ria & pro teinuria \n\n# .Sputum Gram stain showi ng many neutro ph il s bu t few or no microorganisms Antibiotics effective against \n\nPseudomonas aeruginosa \n\nClass Dr ugs \n\nAnti-pseudomonal Ticarcillin penicillins Piperacillin Cephalosporins Ceftaz1dime (3rd generation) Cefepime (4th ge neration) Am ikacin \n\nAminoglycosid es Gentamicin Tobramycin Fluoroquinolones Ciprofloxacin Levofloxacin Monobaclams Aztreonam \n\nCart>apenems lm ipenem Meropenem Short Subjects Antibiotics eradicate the bacteria, which can lead to increased release of toxins that exacerbate course of disease \n\nVibrio Lyme \n\n What is the next step in management for a patient that notices a tick on the leg with surrounding erythema after spending the past day outside? \n\nRemove the tick with tweezers and reassure \n\nprophylaxis for Lyme disease is not required if the tick is attached for < 36 hours \n\nSyphilis \n\n807 https://t.me/usmleinnercircle USMLE Inner Circle \n\nVibrio vulnificus \n\n## . Gram-negative , free-living in marine environments \n\nEpidemiology . Ingestion (oysters) or wound in fection \n\n# . j Risk in those with liver disease* (cirrhosis , hepatitis) \n\n# . Rapidly progressive (often <12 hours )\n\nManifestations . Septicemia - septic shock , bullous l es i ons \n\n# . Cellulitis - hemorrhagic bullae , n ecrotizing fasciitis \n\nDiagnosis . Blood & wound cultures \n\n## . Empiric in those with lik e ly illn ess as highly fatal Treatment . Intravenous ceftriaxone + doxycycline *H ereditary hemochromatosis is particularly high risk as iron acts as a growth catalyst. \n\nLyme disease prevention Tick removal . Grasp with small forceps as close to skin as possible \n\n## . Pull firmly upwards without twisting \n\n## . lxodes scapularis (deer tick) identified \n\nProphylaxis criteria Tick attached for 2!:36 hours or engorged (must meet all 5) . Prophylaxis started within 72 hours of tick removal \n\n## . Local Borrelia burgdorferi infection rate 2!:20% (eg, New England) \n\n## . No contraindications to doxycycline (eg, pregnancy) \n\nAntimicrobial prophylaxis . Single-dose doxycycline \n\nSyphilis manifestations Neurosyphilis Primary Painless genital ulcer (chancre) Diffuse rash (palms & soles) Lymphadenopathy (epitrochlear) \n\nSecondary Condyloma latum Meningitis Ocular: uveitis & optic neuritis \n\nEarly Otologic: hearing loss & tinnitus Oral lesions Meningovascular: meningitis + ischemic stroke Hepatitis \n\nLatent Asymptomatic General paresis: progressive dementia \n\nLate \n\n CNS (tabes dorsalis, dementia) Tabes dorsalis: sensory ataxia & lancinating pains \n\nTertiary Cardiovascular (aortic aneurysm/insufficiency) Cutaneous (gummas) \n\nCNS = central nervous system .Short Subjects The middle cerebral artery is most often affected, and arteriography usually shows signs of vasculitis, such as focal segmental arterial narrowing .\n\n The presence of epitrochlear LAD is particularly characteristic of secondary syphilis \n\nAllergy = doxycycline \n\nAllergy + neurosyphilis/ or pregnancy = desensitization to penicillin \n\n808 https://t.me/usmleinnercircle \n\nTabes dorsal is \n\n## . Years ---+ decades after in itial infection Epidemiology Increased incidence/more rapid progression in those with HIV .\n\nPathogenesis . Treponema pallidum directly damages dorsal sensory roots \n\n## . Secondary degeneration of the dorsal columns \n\n## . Sensory ataxia \n\nClinical findings . Lancinating pains \n\n## . Neurogenic urinary incontinence \n\n## . Associated with Argyll Robertson pupils \n\nTreatment . 10-14 days of intravenous penicillin G \n\nSyphilis: diagnostic serology \n\n Antibody to cardioli ein-cholesterol-lecithin anti 11 en \n\nNontreponemal Quantitative (titers) \n\n(RPR, VDRL) Possible negative result in early infection Decrease in titers confirms treatment \n\n Ant ibody to treponemal antigens \n\nTreponemal Qualitative (reactive/nonreactive) \n\n(FTA-ABS, TP-EIA) Greater sensitivity in early infection Positive even after treatment \n\nFTA-ABS ; fluorescent treponemal antibody absorption; RPR ; rapid plasma reagin; \n\nTP-EIA ; Treponema pallidum enzyme immunoassay. \n\nSyphilis treatment \n\nStage First line Alternate Primary {chancre) Secondary (diffuse rash) Penicillin G IM x 1 Doxycycline x 14 days Earty latent (asymptomatic)* \n\nLate latent (asymptomatic)* \n\nPenicillin G IM x 3 Doxycycline x 28 days Tertiary (eg, CV, gummata) \n\nNeurosyphilrs Penicillin G IV x 10-14 days Cenriaxone IV x 14 days** \n\n(eg , meningitis, ocular) \n\n~Earty latent = asymptomatic with infection <1 year; Late latent = asymptomatic with unknown duration of infection or \n\nin fection >1 year. \n\n... Penici1fin desensitization followed by IV penicillin is preferred for those with penicillin allergy who have neurosyphitis; \n\nceftriaxone can be used in those unable to be desensitized CV = cardiovascular; IM = intramusrular; rv = intravenous Short Subjects Primary syphilis manifests with a painless papule that ulcerates over time (chancre). Syphilitic chancres are usually treated with antibiotics (penicillin) but otherwise resolve spontaneously within 3-6 weeks .\n\nvs a patient who had a penile ulcer for several months , making cancer more likely. \n\n All patients with syphilis require nontreponemal titers (eg, RPR) at the time of treatment and again at \n\n6-12 months to ensure adequate response (a 4-fold drop in titers). especially important for patients receiving alternate regimens because the risk of treatment failure is greater \n\nMycoplasma \n\n Unlike typical causes of CAP (eg, Streptococcus pneumoniae ), which cause lobar infiltrate on chest x-ray, patients with M pneumoniae usually have bilateral reticulonodular or patchy pulmonary infiltrates .\n\n Dry cough differential: Mycoplasma , Viruses , Coxiella , Pneumocystis , Chlamydia \n\nRickettsia \n\n809 https://t.me/usmleinnercircle USMLE Inner Circle \n\nJarisch-Herxheimer reaction Epidemiology 6-48 hours after initiating treatment for syphilis (most commonly primary or secondary) May also be seen with treatment of other spirochete diseases (eg, Lyme disease, leptospirosis) \n\nClinical presentation Acute onset of fever, chills, myalgias Rash progression in secondary syphilis \n\nTreatment Supportive (IV fluids , acetaminophen, NSAIDs) Typically self-limiting within 48 hours of onset \n\nIV = intrav e nous ; NSAIDs = nonsteroidal anti-inflamm a tory drugs .\n\nMycoplasma pneumonia \n\nRespiratory d ro plets \n\nEpidemiology Close quarters/ young (eg, school, mi litary) Fall or winter \n\nIndolent he ad ache, malaise, fever, pers istent dry cough Clinical Pharyngitis (nonexudative) Macular/vesicula r rash \n\nNorma l leukocyte count \n\nDiagnostic Subclinical hemolytic anemia (cold agglutinins) \n\nInterstitial infiltrate (chest x-ray) \n\nTreatment Usually emp iric \n\nMacrolide or respiratory fl uoroquinolone Short Subjects Ehrlichiosis \n\nLyme disease and Rocky Mountain spotted fever are less likely given the absence of rash; \n\nBabesiosis will have leukocytosis and is in Northeast \n\nTularemia \n\n Introduction of infected material into an eye (eg, splashing, rubbing with a contaminated hand) results in a less common clinical syndrome called oculoglandular disease .This form of tularemia usually presents with eye pain , photophobia , conjunctival erythema/purulence , and conjunctival ulcers .\n\n810 https://t.me/usmleinnercircle \n\nRocky Mountain spotted fever \n\n Rickettsia rickettsii infection \n\nEpidemiology Transmitted by tick bite . Peaks in summer \n\n Nonspecific fever, headache, myalgia, arthralgia \n\nClinical features Macular & petechial rash on wrists/ankles \n\n Can develop complications of encephalitis, pulmonary edema, bleeding, shock . t Platelets \n\nLaboratory findings t Sodium \n\n j AST&ALT . Rickettsia serology \n\nDiagnosis Skin biopsy .\n\nTreatment Doxycycline \n\nALT= alanine transaminase; AST= aspartate transaminase. Human monocytic ehrlichiosis Epidemiology T ra n sm itted by tick vector (lone star tick) Seen in so uth eastern & south cent ra l United Stat es Flu-li ke illness (high fever, he adache, myalgias, chi ll s) \n\nClinical Neurologic symptoms (confusion) \n\nmanifestations Rash is uncomm on (<30% in adults) (\"Rocky Mounta in spott ed fever without the spots\") \n\nLaboratory Leukopenia & thrombocytopenia findings El evated liver enzymes & lactate d eh ydroge na se \n\nDiagnosis lntracytoplasmic morulae in monocytes Po lymerase chain reaction testing for E chaffeensis/E ewingii \n\nTreatment Em piric doxycycline w hi le aw ai tin g confir ma to ry te sting \n\nTularemia \n\n# . Transmission: Epidemiology 0 Wild animal (eg , hare, rabbit) hunting/skinning \n\n> 0\n\nT ick or mosquito bite \n\n> 0\n\nBioterrorism agent \n\n# . Nonspecific systemic symptoms (fever, malaise) \n\n# . Ulceroglandular disease Common manifestations 0 Single papuloulcerative lesion (sometimes absent) \n\n> 0\n\nTender, suppurative regional lymphadenopathy \n\n# . Pneumonia \n\n# . Poorly staining , gram-negative coccobacillus Microbiology . Most strains require cysteine for growth \n\n# . Evades most immune defenses & replicates within macrophages/neutrophils Short Subjects Melioidosis \n\n Uncommon infection caused by the facultative intracellular gram-negative bacilli Burkholderia pseudomallei. \n\n Transmitted primarily when contaminated soil or water gets inoculated in subcutaneous tissue. Severe disease is rare in healthy individuals, but those with diabetes mellitus , excessive alcohol use , or chronic lung/kidney disease are at higher risk of fulminant infection. The following manifestations may occur: \n\nPneumonia is the most common manifestation and usually presents with high fever, cough, rigors, respiratory distress, and (sometimes) shock. Chest imaging typically shows bilateral opacities. \n\nSkin ulcers/abscesses occur in approximately 25% of cases and frequently appear as purple-colored lesions. Organ abscesses in the kidney, prostate, spleen , and liver occur in a minority of cases. Gram stain will reveal gram-negative rods that exhibit bipolar staining with a safety pin appearance. \n\nTreatment requires ceftazidime or a carbapenem for the acute infection followed by several months of \n\ntrimethoprim-sulfamethoxazole to eradicate the organism completely. \n\nFusobacterium \n\n Lemierre syndrome (LS) is caused by an oropharyngeal infection, usually pharyngitis or tonsillitis ,that leads to local invasion of the lateral pharyngeal wall and infection of the neurovascular bundle, especially the internal jugular vein .Thrombosis of this vein allows dissemination of septic emboli to distal sites particularly lungs. LS should be considered in any toxic-appearing patient with respiratory difficulties and significant neck swelling or tenderness in the week following an oropharyngeal infection. \n\nFungus \n\n811 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCommon causes of ulceroglandular syndrome Syndrome Transmission Manifestations \n\n# . Hunting/skinning wi ld animals (eg, hares, rabbits} . Single skin ulcer \n\nTularemia . Tick/mosquito bite . Regional suppurative lymphadenitis . Bioterrorism weapon . Fever \n\n# . Subacute/chronic Sporotrichosis Gardening or landscapi ng . Papuloulcerative lesion \n\n# . . New lesions up lymphatic chain \n\n# . No fever or purulence \n\n## . Feline scratch/bite . Papule in area of transmissi on Catscratch disease . Flea bite from infected feline . Prominent, tender regional lymphadenopathy \n\nShort Subjects Mississippi and Ohio River basins: Histoplasma and Blastomyces \n\nSouth-Western: Coccidioides \n\nLatin America: Paracoccidiodomycosis \n\nHistoplasmosis \n\n812 https://t.me/usmleinnercircle \n\nNew Hampshire Vermont \n\nBlastomycosls \n\n0 Ox:ddlofdomyco5 h\n\nHl nopta1 mosls \n\n> Cryptocc:us 9att/l\n> Connecticut New Jersey Delaware Maryland District of Columbia West Virginia U. S. Virgin Islands American Samoa\n\nEpidemiology and extrapulmonary clinical manifestations of endemic mycoses Syndrome Epidemiology Clinical clues \n\n## . Cutaneous plaques/ulcerations Mississippi/Ohio River Va ll ey . Bone lesions with sinus tracts Blastomycosis Midwestern Un ited States . Genitourinary involvement \n\n# . CNS involvement (very rare) \n\n# . Hilar/mediastinal lymphadenopathy Histoplasmosis Mississippi/Ohio River Va ll ey . Hepatosplenomegaly Central & South Ame ri ca . Pancytopenia \n\n# . Adrenal insufficiency \n\n## . Skin lesions Southern Arizona/California . Lymph node involvement Coccidioidomycosis Northern Mexico . Meningitis \n\n## . Osteoarticular infection Short Subjects What is the recommended treatment for patients with disseminated histoplasmosis ?\n\nIV Amphotericin B (1-2 weeks), followed by oral itraconazole (> 1 year) \n\nall patients with HIV who develop PDH should be considered for antiretroviral treatment (usually \n\n2 weeks after starting antifungal therapy ). \n\n Histoplasma most commonly has caseating granulomas but can have non-caseating \n\n Can also cause Erythema Nodosum \n\nBlastomycosis \n\n What systemic fungi can produce verrucous skin lesions when disseminated? \n\nBlastomyces \n\n813 https://t.me/usmleinnercircle USMLE Inner Circle \n\nDisseminated histoplasmosis \n\n## . Temperate regions worldwide \n\nEpidemiology . Soil contaminated by bird or bat droppings \n\n## . t Dose exposure or i mmunocompromised {eg, AIDS) . Systemic (fever, chills, malaise) \n\n Weight loss & cachexia \n\nSymptoms . Pulmonary (cough, dyspnea) \n\n## . Mucocutaneous lesions (papules, nodules) . Reticuloendothelial (HSM, LAD) \n\n## . Laboratory findings: \n\n0 Pancytopenia \n\n0 Transaminase elevation \n\n0 i LOH & ferriti n \n\nDiagnosis Chest x-ray (reticulonodular or interstitial infiltrate) .. Urine/serum histoplasma antigen (i sensitivity/rapid) . Serology \n\n## . Culture (takes 4-6 weeks) \n\nTreatment Amphotericin B (moderate to severe disease &/or HIV positive) \n\n## . ltraconazole (mild disease/maintenance) \n\nHSM = hepatosplenomegaly; LAD= lymphadenopathy; LOH= la ctate dehydrogenase. \n\nBlastomycosis \n\n## . South/South Central states, Mississippi & Ohio River valleys, Upper Midwest states, Great Lakes states & Canadian \n\nEpidemiology provinces \n\n## . Disseminated disease may occur even in immunocompetent patients \n\n## . Generally more severe in immunocompromised patients \n\n## . Lung: acute & chronic pneumonia (usually mild to moderate but may be severe) \n\nClinical . Skin: wart-like lesions, violaceous nodules, skin ulcers \n\nfeatures . Bone: osteomyelitis \n\n## . Genitourinary: prostatitis, epididymoorchitis \n\n## . CNS: meningitis, eeidural or brain abscesses \n\n## . Culture (blood, sputum, tissue specimens) \n\nDiagnosis . Microscopy (body fluids , sputum, tissue specimens) \n\n## . Antigen testing (urine, blood) \n\n## . Mild pulmonary disease in immunocompetent patients: m ay consider not treating \n\nTreatment . Mild-to-moderate pulmonary disease, mild disseminated disease: oral itraconazole \n\n## . Severe pulmonary disease, moderately se ve re to severe disseminated disease, immunocompromised patients: intravenous amphotericin B Short Subjects Coccidioides \n\n What is the likely diagnosis in an Army officer in Arizona that presents with pleuritic chest pain , fever , arthralgias , and erythematous , tender nodules on the bilateral shins? CXR shows a right lower lobe infiltrate. \n\nCoccidioides immitis infection \n\ncauses community-acquired pneumonia symptoms , often with arthralgias and erythema nodosum ; endemic to Southwestern U.S. \n\nTinea \n\n the only Tinea treatment that is oral \n\nCandida \n\n The presence of budding yeast in blood cultures should never be considered a contaminant; the following treatment is required: \n\nEmpiric antifungals : Echinocandins (eg, micafungin) are considered first-line, but the infectious diseases team should be consulted for antifungal selection/duration and assistance with work-up. \n\nRemoval of central venous catheter (when present): Source control typically requires removal of the central venous catheter because Candida produces a glycocalyx, which forms a protective, sticky biofilm that prevents eradication. \n\nEvaluation for metastatic infection : All patients with candidemia require ophthalmologic consultation to evaluate for endophthalmitis .\n\nEchocardiography is often required in those with persistent positive blood cultures to rule out \n\ninfective endocarditis \n\n Serum beta-D-glucan antigen can be used as a rapid indicator of possible infection \n\nAspergillus Avoid sharing combs and hats \n\n814 https://t.me/usmleinnercircle \n\n> Tinea capitis\n> Most common in African American children\n> Epidemiology Transmission via direct contact or from fomite (eg , shared combs)\n> Clinical Scaly erythematous patch with hair loss on scalp\n> features black dots in affected area tender lymphadenopathy\n> Management Oral griseofulvin or terbinafine\n\n\n\n> 0\n\nShort Subjects Cryptococcus \n\n C neoformans replicates in the central nervous system and clogs the arachnoid villi with yeast components and capsular polysaccharides, leading to CSF outflow obstruction and increased \n\nintracranial pressure (ICP) Patients also frequently have fever, malaise, and umbilicated skin lesions that resemble molluscum contagiosum (due to hematogenous dissemination to the skin). Brain imaging is usually normal but may show signs of increased ICP such as enlarged ventricles . The diagnosis is generally made with lumbar puncture (LP) , measurement of CSF pressure, analysis of CSF, and capsular polysaccharide antigen testing or India ink stain. Nodules with surrounding ground-glass opacities. \n\n815 https://t.me/usmleinnercircle USMLE Inner Circle \n\nInvasive aspergillosis Chronic pulmonary aspergillosis* Risk factors lmmunocompromise (neutropenia, glucocorticoids, HIV) Lung disease/damage (cavitary tuberculosis) Triad of fever , chest pain, hemoptysis >3 months: weight loss (>90%), cough , hemoptysis, \n\n Pulmonary nodules with halo sign fatigue \n\nManifestations Positive cultures Cavity lesion fungus ball \n\n Positive cell wall biomarkers (galactomannan, 13-D- Positive Aspergillus lgG serology glucan) \n\n Resect aspergilloma (if possible) \n\nManagement Voriconazole caspofungin Azole medication (voriconazole) \n\n Embolization (if severe hemoptysis) *Simple aspergilloma (fungus ball in preexisting lung cavity) is a form of chronic pulmonary aspergillosis but is usually quiescent with occasional hemoptysis. a, b. CT halo sign .a. Invasive as per gillo sis in a pat i ent w i th acute leukemia: CT image sh ow s halo sign (arrow s). b. Sun shine. \n\nCryptococcal meningoencephalitis \n\n Headache, fever & malaise \n\nPresentation Develops over 2 weeks (subacute) Can be more acute & severe in HIV \n\nCerebrospinal fl uid \n\n High opening pressure Low glucose, high protein \n\nDiagnosis White blood cells <50 / L with mononuclear predominance Transparent capsule seen with India ink stain Cryptococcal antigen positive Culture on Sabouraud agar \n\nInitial Treatment Amphotericin B with flucytosine \n\nMa intenance \n\n Fluconazole Short Subjects What is the likely diagnosis in a patient with poorly controlled HIV that presents with one week of worsening fatigue , headache , and fever ? Physical exam reveals bilateral papilledema . Brain MRI is normal. \n\nCryptococcal meningoencephalitis \n\nPapilledema and headache represent increased ICP Patients with HIV who have subacute -onset of low grade fever, headache, and signs of ICP ( papilledema, vomiting) should be avaluated for cryptococcal meningitis \n\nSporotrichosis \n\n Can present with no lymphadenopathy which helps rule out other diagnoses (e.g. cat scratch fever) \n\nPneumocystis Severe hypoxia and bilateral interstitial infiltrates in an HIV patient with CD4+ < 200/mm3 \n\n816 https://t.me/usmleinnercircle \n\nSporotrichosis \n\nSporothrix schenckii (d imorphic fungus )Ep idem io lo gy Decayi ng plant matter/ so il \n\nGardeners & landscapers Subacute/ ch ron ic \n\nSk in papule - ul ce rati on with nonpurul ent , odorless \n\nMani fest at ions drai nage \n\nProximal les ions al ong lymph at ic chai n Lymphadenopathy, deeper spread & systemic symptoms \n\nare r are Di ag nos is Cu ltures (aspirate fiuid or biopsy) \n\nTreatment 3-6 months of oral itraconazole \n\nPn eumocystis jirovecii pne umo nia Clin ical In do l ent {HI V) or acute r esp ira tory fail ure (i mm unocompromi sed) Fever, dry coug h, ! oxy ge n levels \n\nt LD H l eve l \n\n> Workup Diffu se re ti cu lar infiltrates on imag ing In du ced sp utu m or BAL (stai n)\n\nTrea tment TMP-SMX Predni so ne if ! oxygen levels \n\n> Prevention\n\nTMP-SMX Ant iretrovirals (in HIV ) Pati ents wi th HIV requi re proph ylax is to prevent Pneumocystis jirovecii pneumon ia with C0 4 counts <200/ mm 3.Short Subjects First test should be to get sample via induced sputum , but if unrevealing, then bronchoscopy \n\nwith bronchoalveolar lavage \n\nIf sputum is positive, no need for BAL \n\n When should steroids be added to Pneumocystic pneumonia ?Indications include: a PaO2 70 mm Hg \n\nan alveolar-arterial (A-a) gradient 35 mm Hg , or pulse oximetry <92% on room air. \n\nParasite \n\nGiardia \n\n817 https://t.me/usmleinnercircle USMLE Inner Circle \n\n)UWotld \n\n\n\nPneumocystis jiroveci pneumonia \n\nNormal chest x-ray Bilateral interstitial infiltrates Adverse effec ts of drug regimens for Pneu mo cysris \n\npneumonia Tr imethop r im-sulfame t hoxazole (IV for ac utety ill, oral for Pre ferr ed non-acutely ill patien ts) regimen Ra sh, neutropenia, hyperkalemia, elevated tr ansaminases Pe ntamid ine (IV) Nephrotoxicity, hy po tension, hypoglycemia, cardi ac arrhythmias, panc re atitis, elevated tr ans amina ses Atovaquone (oral )A lternate Gas tr ointestinal distr ess , rash r egimens Trimethoprim + dapsone {both oral) Dapsone: Hemolytic anemia (c he ck for G6 PD deficiency) Clindamycin {IV or o r al)+ primaquine (oral) Primaqu ine : Methemoglobinemia, hemolytic anemia (che ck for G6 PD deficiency) Add corticos teroid s if Pa(h !S70 mm Hg or A-a gradient i!:.35 mm Hg oo room air. \n\nA..a = alveolar-arterial; G6PO = gl ucose-6-phosphate dehydrogenase; IV = intravenous; \n\nPa(h = arterial partial pressure of oxygen. Short Subjects Malaria \n\nThe hallmark is cyclical fever Anemia and thrombocytopenia are classic. PBS gold standard. \n\n When should a patient visiting a malaria endemic country take chemoprophylactics (e.g. mefloquine)? \n\n> 2 weeks prior to travel, during the stay, and 4 weeks after returning \n\ne.g. Africa, Asia (including India), and Oceania (everywhere except parts of Carib and Central America basically) Chemoprophylaxis cannot prevent infection but suppresses course by killing parasite before it causes severe infection \n\n Babesiosis has similar presentation but seen in NE and Midwest U.S. \n\nBabesiosis \n\n B microti coinfection is often suspected when a patient with Lyme disease still has fever after \n\n48 hours of antimicrobial therapy and/or anemia , thrombocytopenia , or leukopenia .\n\n818 https://t.me/usmleinnercircle \n\nGiardiasis \n\n## . Contaminated food or wate r Risk factors . Fecal incontinence & crowding (eg, day care, nursing home) \n\n## . Immunodeficiency (eg, CVID lgA deficienc~ CF HIV} \n\nPathogenesis . Villous blunting, disruption of epithelial tight junctions, loss of brush border enzymes - malabsorption \n\n## . Subacute (<4 wee ks) or chronic (months) Clinical features . Loose, oily, nonbloody stools \n\n## . Bloating , fl atulence \n\n## . Weight loss, decreased line ar velocity (children), vitamin deficiencies Diagnosis . Stool antigen or PCR testing (1 sensitivity) \n\n## . Stool microscopy U sensitivity) \n\n## . First-line: tinidazole or nitazoxanide . Alternate : metronidazole (children) \n\nTreatment . Pregnancy (first trimester): paromomycin \n\n## . Refracto!l'./recurrent s~metoms: evaluation for immunodeficiency CF = cystic fibros is ; CVID = common variable immunodeficien cy. \n\nBabesiosis \n\n Babesia microti \n\nEpidemiology lxodes scapu/aris tick bite (Lyme disease & HGA) Northeastern United States Fever, fatigue, myalgias, headache (flu-like symptoms) \n\nManifestations If severe: ARDS, CHF , DIC , splenic rupture Anemia, thrombocytopenia , t bilirubin/LDH/LFTs \n\nDiagnosis Thin blood smear - intraerythrocytic rings (\"Maltese cross\") \n\nTreatment Atovaquone + azithromycin Quinine + clindamycin (if severe) ARDS = acute respiratory distress syndrome ; CHF = congestive heart failure; DI C = disseminated \n\nintravascular coagulation; HGA = human granulocytic anaplasmosis; LOH = lactate dehydrogenase; \n\n> LFT s\n\n= liv er function tests. Short Subjects What is the likely diagnosis in a patient that presents with flu-like symptoms without a rash after being bitten by a tick two weeks ago in the Northeast ? Laboratory exam reveals leukocytosis , thrombocytopenia , and signs of hemolytic anemia .\n\nBabesiosis \n\nLyme disease and Rocky Mountain spotted fever are less likely given the absence of rash; \n\nErlichiosis also presents without a rash (spotless RMSF), but not likely given the leukocytosis and signs of intravascular hemolysis (has leukopenia, thrombocytopenia )Ehrlichiosis has leukopenia and is in southeast \n\nTrichinella Echinococcus \n\n819 https://t.me/usmleinnercircle USMLE Inner Circle \n\nBabesiosis Clinical features of tr ichinellosis \n\n# . Ing es ti on of undercooked meat (usually pork) \n\n# . Mo re endemic in Mexico, China, Thailand, parts of central Europe & Argentina \n\nEp idemiology & life Gastric ac id releases larvae (with in 1st week of ingestion) th at invade the small intestine & develop into \n\ncycle worms \n\n# . Fema le worms release larvae (up to 4 weeks later) that migrate & encyst in striat ed muscle \n\nIntestinal stage (within a week of ingestion) \n\n Can be asymptomatic or include abdominal pain, nausea, vomiting & diarrh ea \n\nClinical presentation Muscle stage (up to 4 weeks after ingestion) \n\n# . Myositis \n\n# . Fever, subungual splinter hemorrhages \n\n# . Periorbital ede ma \n\n# . Eosinophilia (usually >20%) with possible elevated creatini ne kinase & leukocytosis Short Subjects What is the likely diagnosis in an afebrile farmer with RUQ pain and a smooth , round hepatic cyst with septations and eggshell calcifications on ultrasound? \n\nEchinococcus granulosus infection \n\nlack of fever and cystic lesion favor echinococcus rather than entamoeba histolytica (febrile with a smooth, cystic subcapsular mass) \n\nU/S shows hepatic cyst with daughter cysts (internal septations) \n\nVirus \n\nHSV \n\n Primary genital herpes is associated with high risk for recurrence, with less frequent recurrences over time in immunocompetent individuals. \n\ntreatment with antiviral medications (e.g. acyclovir) can speed resolution of outbreaks and decrease \n\nrecurrences Acute onset <1 week \n\n820 https://t.me/usmleinnercircle \n\nEchinococcus granulosus \n\n## . Dog tapeworm (sheep intermediate host) \n\nEpidemiology . Rural , developing countries (eg, South America , Middle East) \n\n## . Humans are incidental hosts (egg ingestion) \n\n## . Initially asymptomatic (often for years) \n\n## . Liver cyst (most common) \n\nManifestations 0 Mass effect: RUQ pain, nausea, vomiting, hepatomegaly \n\n> o~\n\nfever, eosinophilia \n\n## . Lung cyst: cough , chest pain, hemoptysis \n\nDiagnosis . Large, smooth hydatid cyst often with internal septations on imaging \n\n## . lgG E granulosus serology \n\n## . Albendazole \n\nTreatment . Percutaneous therapy (>5 cm or septations) \n\n## . Surgery (if rupture) \n\nRUQ = right upper quadrant. \n\nHerpes simplex virus (HSV) encephalitis Herpes encephalitis . Fever \n\n# . Headache \n\nClinical findings Seizure Altered mental status (eg, confusion, agitation) \n\n Focal neurologic findings (eg , hemiparesis, cranial nerve palsies, ataxia) CSF analysis: \n\no j WBCs (j lymphocytes), j RBCs \n\nDiagnostic findings o j Protein, normal glucose \n\no HSV DNA on PCR Brain MRI: temporal lobe hemorrhage/edema \n\nTreatment . Intravenous acyclovir \n\nCSF = cerebrospinal fluid ; WBCs = wh ite blood cells ; RBCs = red blood cells .Short Subjects Viral culture should be taken from the base of a vesicle that has just been deroofed , not the blister fluid. \n\nCoxsackie \n\nPleurodynia , also known as Bornholm disease, is an acute viral illness often caused by coxsackievirus group B, among other viruses. It presents with fever, headache, and characteristic, paroxysmal spasms \n\nof the muscles of the chest wall with pleuritic chest pain. \n\nPleurodynia tends to occur in epidemic outbreaks during the summer months. Patients may present with leukocytosis or increased serum concentrations of creatine kinase caused by muscle inflammation .The disease is usually self-limiting and resolves over several days to a week. \n\nVaricella Posterior oropharynx helps differentiate herpangina \n\n821 https://t.me/usmleinnercircle USMLE Inner Circle \n\nHerpangina vs herpetic gingivostomatitis Diagnosis Herpangina Herpetic gingivostomatitis Etiology Coxsackie A virus He rpes sim plex virus type 1 \n\nAge 1-7 years 6 months-5 years \n\nSeasonality Late summer/early fall None \n\n## . Fever \n\n## . Fever \n\nClinical features Pharyngitis . Pharyngitis \n\n## . Gray vesicles/ulcers on oropharynx . Erythematous gingiva \n\n## . Clusters of vesicles on anterior oral mucosa/lips .\n\nTreatment Supportive Oral acyclovir Herpangina \n\nHlerpes zost er (shingles) Pathog1 enesis . Reactiva ti on of varicella-zoster vii ru s from sensory nerve gangli on \n\n. Prodroma l phase: itching, tingling, b urning in dermatomal distribution \n\nClinical features . Rash: grouped papules & vesicles on e, ryth ema tous base; ulceration & cr usting; acute neuritic pain \n\n. Postherpetic neuralgi a: persisten t neu ri tic pa in >4 months after rash on se t\n\nTreatme nt . Antiviral therapy: acyc l ov ir, va lacyol ov ir, famd cl ov ir \n\n. Postherpetic neuralgia: t ri cyclic antidepressants, pr egaba li n, gabapentin Short Subjects Antiviral therapy (eg, valacyclovir) can shorten the course of acute shingles and reduce the risk of PHN. However, PHN is not associated with ongoing viral replication, and antiviral therapy has no benefits. \n\n Herpes zoster oticus (ie, Ramsay Hunt syndrome ): Ear pain Facial weakness Vesicular rash in the external auditory canal (EAC). The treatment includes topical ointments for pruritis such as calamine and pramoxine gel and acyclovir if immunosuppressed or unvaccinated. TCA C/I in Heart patients immunocompromised/ pregnant \n\n822 https://t.me/usmleinnercircle \n\n\n\nClassification of herpes zoster pain Pain Timeframe Treatment \n\nAcute herpetic neuralgia Persists S30 days from rash onset NSAIDs, analgesics Subacute herpetic neuralgia Persists >30 days but resolves within 4 months of NSAIDs, analgesics rash onset Postherpetic neuralgia Persists >4 months from rash onset Tricyclic antidepressants, gabapentin, pregabalin \n\n> NSAID\n\n= nonsteroidal anti-inflammatory drug .\n\nCh ickenpox (varicella) \n\n## . P ri mary infection with VZV \n\nEpidemiology . Transmission via direct contact or aerosol droplets \n\n## . High risk: adolescen ts , adults, immunocompromised individuals, pregnant women, newborns \n\n## . Prodrome (eg, fever, malaise) \n\nC li nical features . P ru ritic macules, papules & vesicles in successive crops at different stages \n\n## . Complications: skin infection, pneumonia, encephalitis \n\nDiagnosis . Clinical diagnosis \n\n## . VZV PCR in a!le ical cases \n\nTreatment . Supportive (eg, antihistamines) \n\n## . Ac i'. clovir for high-risk patien ts & com e li cated disease \n\nPrevention . 2 doses of VZV vaccine (age 1 & 4) \n\nVZ.V = varicella-zoster virus. Varice ll a post-exposure prophylaxis Hi sto ry of i mm unity {prior infection or 2 doses of vacci ne) \n\n# TIOb serva ti on I lmm unocom petent IVarice ll a vacci ne IVZI G = varicella-zoster immune globulin \n\n> UWo~d\n\nlmmunocompro mi sed Short Subjects Infants (age <1 year) outside the neonatal period are not eligible for VZV vaccine and do not \n\nrequire immunoglobulin as they are at lower risk than neonates or older children. \n\n While most cases of herpes zoster will be confined to a single dermatome, if a patient with zoster has >20 vesicles outside of primary dermatome, then they qualify as having \n\ndisseminated zoster Key idea: Patients with disseminated zoster need to be on airborne/contact precautions and should receive a chest x-ray and testing of LFTs because it most commonly involves the lungs and liver \n\nEBV \n\n823 https://t.me/usmleinnercircle USMLE Inner Circle \n\nVaricella (chickenpox) Primary varicella-zoster virus infection (chickenpox) \n\nVZI/ \n\nLesion stages Maculopaputar Vesicular Pustular Crusting Vesicular lesions in crops \n\nvzv varicella-zoster vi rus . & different 513 9 85 \n\nCI UWood \n\nNeonatal varicella-zoster infection \n\n# . Fever \n\nClinical features Vesicular eruption (chickenpox) \n\n# . Systemic involvement (eg, pneumonia , hepatitis , meningoencephalitis) \n\nTreatment Acyclovir \n\n# . Isolate infant from varicella contact \n\nPrevention Administer varicella-zoster immune globulin to infant if maternal infection developed 5 days before or 2 days after delivery Short Subjects What is the likely diagnosis in a young adult that presents with two-days of sore throat , enlarged /erythematous tonsils , lymphadenopathy , and splenomegaly ? Many variant forms of lymphocytes are seen on peripheral smear despite a negative heterophile antibody test. \n\nInfectious mononucleosis \n\nHeterophile antibodies may be falsely negative early in the illness; atypical lymphocytes are suggestive of infectious mononucleosis \n\n The heterophile antibody test is not accurate in children age <4 , for whom serum anti-EBV antibody testing is recommended instead. Infectious mononucleosis often presents with fever, exudative pharyngitis, and Tender lymphadenopathy, especially of the posterior cervical nodes. \n\nPharyngitis (viral, Group A Strep) may have anterior cervical LN \n\n What is the recommended treatment for a patient with infectious mononucleosis that presents with difficulty swallowing and laboured breathing ?\n\nIV corticosteroids \n\nacute airway obstruction is a rare but potentially fatal complication of infectious mononucleosis \n\nCMV Supportive Care Only. \n\n824 https://t.me/usmleinnercircle \n\n> Infectious mononucleosis Etiology\n\n# . Epstein-Barr virus most common Fever Tonsillitis/pharyngitis exudates Posterior or diffuse cervical lymphadenopathy \n\n> Clinical features\n\n# . Significant fatigue \n\n# . Hepatosplenomegaly \n\n# . Rash after amoxicillin Positive heterophile antibody (Monospot) test ( 25% false-negative rate during 1st week of illness) \n\n> Diagnostic findings\n\n# . Atypical lymphocytosis \n\n# . Transient hepatitis \n\n> Management\n\n Avoid sports for ;,3 weeks (contact sports ;,4 weeks) due to the risk of splenic rupture \n\n Acute airway obstruction \n\nComplications Autoimmune hemolytic anemia & thrombocytopenia \n\n Splenic rupture Short Subjects Zika: Intracerebral Calcifications \n\n Toxoplasma: Diffuse Parenchymal Calcification \n\nHerpes Virus 6 HPV \n\n825 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCongenital cytomegalovirus Cong enita l cyt omegalo virus infecti on Most common congenital infection \n\nEpidemiology Transmission: bodily fl uids (eg, urine, saliva) Main risk factor: caring for young children Growth restriction & microcephaly \n\n Periventricular calcifications \n\nClinical features \n\n Hepatosplenomegaly Thrombocytopenia PCR tes ti ng \n\nDiagnosis Viral culture of urine/saliva \n\nTreatment Antiviral therapy (eg , valganciclovir) if symptomatic \n\nRoseola infantum Microbiology . HHV -6 most common \n\nEpidemiology . Age <2 years \n\nClinical . 3-5 days of hi gh fever followed by \n\nfeatures blanching maculopapular rash \n\nTreatment . Supportive care \n\nHHV-o = human herpesvirus 6. \n\nGenit al warts (condylomata acuminata) Etiology HPV 6 & 11 \n\nClinical Multiple pink or skin-colored lesions \n\nfeatures Lesions ranging from smooth , flattened papules to exophytic/cauliflower-like growths Chemical : Podophyllin resin, trichloroacetic acid \n\nTreatment Immunologic: lmiquimod Surgical : Cryotherapy, laser therapy, excision \n\nPrevention Vaccination Barrier contraception Short Subjects What is the likely diagnosis in a young sexually active woman that presents with multiple papular lesions around the vagina? Some lesions bleed with manipulation .\n\nCondylomata acuminata (genital warts) \n\nIn contrast, condyloma lata (secondary syphilis) typically causes flat, velvety lesions \n\n HIV screening should be offered to patients with a new diagnosis of HPV. \n\n Perinatal HPV transmission can result in juvenile-onset respiratory papillomatosis , a rare complication in which condylomata acuminata form on a child's larynx and/or vocal cords, resulting in stridor, chronic hoarseness, or cough. However, cesarean delivery does not reduce the risk of vertical transmission and is therefore reserved for large condylomata that block the introitus or pose a bleeding risk with vaginal delivery. \n\nHepatitis \n\n Postexposure prophylaxis with hepatitis A vaccine or hepatitis A immune globulin should be considered in a number of groups, including: \n\nClose personal contacts (eg, sexual contacts , household contacts ) of hepatitis A-infected patients \n\nChild care center contacts (eg, staff and children) where staff, children, or household contacts of attendees have been infected \n\nFood preparation workers whose coworkers have been infected Prophylaxis should be given within 2 weeks of exposure ; in general, younger patients (age <40) should receive hepatitis A vaccine , whereas older patients (age >41 ) should receive hepatitis A immune globulin . Antiviral treatment for Chronic Hep- B \n\n1. Nucleoside/nucleotide analogs ( tenofovir #1) \n\n2. Pegylated interferon-A : contraindicated in pregnancy \n\n3. Liver transplant in cases of end-stage renal disease \n\nAcute: Supportive \n\n Hep B treatment: Emcitabine , Lamivudine , Tenofovir \n\n What is the recommended prophylaxis for an unvaccinated healthcare worker that is exposed to blood from a hepatitis B positive patient? \n\n3 doses hepatitis B vaccine and hepatitis B immune globulin \n\n826 https://t.me/usmleinnercircle \n\nShort Subjects Vaccinated + Ab response = no intervention \n\nVaccinated + no Ab response = Vaccine + Ig \n\nNot vaccinated = Vaccine + Ig \n\n The diagnosis of hepatitis C requires a 2-step process that requires both positive serologic antibody test and a confirmatory molecular test ( Hep C virus RNA PCR test ).\n\nTreatment with direct-acting antiviral agents (ledipasvir-sofosbuvir) should also be considered \n\n Patients who received blood transfusions before 1992 should be screened for hepatitis C. \n\nParvovirus \n\n What is the likely diagnosis in a patient with a one-week history of fatigue and bilateral joint pain/stiffness for 10 - 15 minutes upon awakening? Patient has also had fatigue and loose-bowel movements with skin-itching and patchy redness . She works at a day care center. Labs show a \n\nnormal ESR. Parvovirus B19 infection \n\nMay present similar to rheumatoid arthritis in adults, however, it is more transient and there is less joint swelling. RA and SLE usually correlate with inflammatory markers (eg ESR). RA and SLE are usually more chronic processes (vs. acute onset like this) Endocrine: increased risk for diabetes \n\n827 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nClinical features of chronic hepatitis C \n\n## . As ymptomatic or nons pecific symptoms (eg, fatigue, anorexia, arthralgialmyalgia) \n\n## . Hepatic manifestations: cirrhosis, hepatocellular carcinoma \n\nClinical . Extrahepatic manifestations \n\nmanifestations 0 Hematologic: mixed cryoglobulinemia , ITP, autoimmune hemolytic anemia \n\n0 Renal: membranoproliferative glomerulonephritis \n\n0 Dermatologic: porphyria cutanea tarda, lichen planus \n\n## . Anti-HGV lgG antibodies (screening): current or past infection . HGV RNA PGR (confirmatory/diagnostic): active infection \n\nLaboratory . Elevated AST , ALT \n\nfindings . Thrombocytopenia (c irrhosis or ITP) \n\n## . False-positive antinuclear antibodies & rheumatoid factor \n\n## . Liver biopsy: portal triad lymphocytic inflammation, lymphoid follicles, fibr osis & regenerative nodules (cirrh os is )\n\nALT = alanine aminotransferase; AST = aspartate aminotransferase; HCV = hepatitis C virus; ITP = immune thrombocytopenia . Parvovirus 819 infection \n\n# . Most patients are asymptomatic or have flulike symptoms \n\n# . Erythema infectiosum (fifth disease): Fever, nausea & \"slapped cheek\" rash (more common in children) \n\nSigns & symptoms Acute, symmetric arthralgia/arthritis: Hands, wrists, knees & feet (resembles RA ).. Transient pure red cell aplasia; aplast ic crisis in patients with underlying hematologic disease (eg, sickle cell) Acute infection 0 B 19 lgM antibodies in imm unocompete nt pat ients \n\nDiagnosis 0 NAAT for B19 DNA in immunocompromised patients \n\n# . Previous in fection: B19 lgG antibodi es (documents immunity) \n\n# . Reactivation of previous infection: NAAT for B19 DNA \n\nNAAT = nucleic acid amp lifi ca tion testing; RA = rh eumatoid arthriti s. Short Subjects Nearly 75% of adults develop non-specific rash, but <20% has the characteristic erythema infectiosum rash \n\nRubella HIV \n\n What testing should be offered to patient with fever , arthralgias , night-sweats, lymphadenopathy , prolonged diarrhea , and mucosal ulcerations ?\n\nHIV testing \n\n Diarrhea , oral ulcerations , and rash ( oval, pink/red macular lesions, Non-tender Lymphadenopathy, no tonsillar exudates will help differentiate from mononucleosis. \n\n Another common cause (apart from Enteroviruses ) of aseptic meningitis in young, sexually active adults is acute HIV infection \n\n828 https://t.me/usmleinnercircle \n\nRubella (German measles) \n\n Congenital: \n\n> o\n\nSensorineural hearing loss \n\n> o\n\nCataracts \n\n> o\n\nPatent ductus arteriosus \n\nClinical presentation Children: \n\n> o\n\nFever \n\n> o\n\nCephalocaudal spread of maculopapular rash Adolescents/Adults: \n\n> o\n\nSame as children + arthralgias/arthritis \n\nDiagnosis Serology \n\nPrevention Live attenuated rubella vaccine \n\nAcute HIV infection Ep idemiology Typically presents 2-4 weeks after exposure Mononucleos is -like syndrome (eg, fever, \n\nClinical lymphadenopathy, sore throat, arthralgias) \n\nfeatures Generalized macular rash Gastrointestinal symptoms Viral load is markedly elevated \n\n(>100,000 copies/ml) \n\nDiagnosis HIV antibody testing may be negative \n\n(not yet seroconverted) CD4 count may be normal Combination antiretroviral therapy \n\nManagement Partner notification , consider secondary prophylaxis Short Subjects What screening test(s) for STDs should be offered to an asymptomatic 22-year-old male that is not yet sexually active? \n\nHIV \n\ntesting for HSV, gonorrhea, syphilis, etc. is not needed in this sexually inactive, asymptomatic patient \n\n All patients with active CMV also require an ocular examination to rule out concurrent retinitis. \n\n What is the likely chief complaint in a patient diagnosed with Cryptosporidium parvum infection? \n\nProlonged, profuse, watery diarrhea (typically 10 - 14 days) \n\n What is the likely diagnosis in an HIV patient with a CD4+ count of 25/mm3 that presents with 3 weeks of fever , night sweats , abdominal pain , diarrhea , and weight loss ? CXR, CMV serology, and PPD are all negative. \n\nDisseminated Mycobacterium avium complex (MAC) infection Azithromycin for MAC NOT RECOMMENDED anymore \n\n829 https://t.me/usmleinnercircle USMLE Inner Circle \n\nHIV screening indications \n\n Age 15-65 (+ you nger or older if at ri sk) \n\nInitial screening Treatment for tuberculosis Treatment f or another STD IVDU + sex pa rtners MSM Annual Sex for money or drugs (or mo re frequent) Partner of HI V-positive screening Patient or partner has had >1 partner since last HI V test Homeless shelter li ving Correctional faci li ty in carcera ti on Pregnancy \n\nAdditional Occupational expos ur e to blood/body flu ids screening Any new STD symptoms Suggested: Prior to any new sexual relationship IVO U = intravenous drug use ; M SM = men who ha ve sex wi th men ; ST D= sexually transmitted di sease .\n\nCommon causes of diarrhea in patients with AIDS Opportunistic infections in HIV \n\nOrganism CD4 count Symptoms Infection CD4 cell count Prophylaxis \n\n## . Severe watery diarrhea Trimethoprim-sulfamethoxazole \n\nCryptosporidium <180/ mm 3 . Low-grade fever \n\n Weight loss \n\n## . <200/mm 3 0R Alternate therapies: \n\nPneumocystis . Oropharyngeal candidiasis OR . Dapsone \n\njirovecii . History of PCP infection . Atovaquone Watery diarrhea . Pentamidine \n\nMicrosporidiuml lsosporidium < 100 / mm 3 . Crampy abdominal pain Weight loss Trimethoprim-sulfamethoxazole \n\n## . Fever is rare Alternate therapies: \n\n Watery diarrhea \n\nToxoplasma <100/mm 3 & positive lgG antibody . Dapsone plus pyrimethamine plus \n\ngondii leucovorin \n\nMycobacterium av ium complex <50/ mm 3 . High fever (>39 C (102.2 Fl) . Atovaquone pyrimethamine plus Weight loss leucovorin \n\n## . Frequent, small-volume diarrhea Histoplasma <150/mm 3 & endemic area ltraconazole \n\n## . Hematochezia capsulatum \n\nCy1omegalovirus <50/ mm 3 Abdominal pain Close contact with person with \n\n## . Low-grade fever Weight loss vz:v chickenpox or shingles & no history VariZIG or IVIG administered within 4 of prior disease or negative days of exposure antibody to VZV IVIG = intravenous immune globulin; PCP = Pneumocystis jirovecii pneumonia; VariZIG = human varicella immune globulin; VZV = varicella-zoster virus. Short Subjects TB and CMV are less likely given the normal CXR, induration, and negative CMV IgG \n\n830 https://t.me/usmleinnercircle \n\nVaccines for adults with HIV infection Vaccine Indications HAV . All patients with out documented immunity to HAV \n\nHBV . All patients wi thout documented immunity to HBV \n\nHPV . All patients age 11-26 \n\n## . Consider with shared dec ision-mak ing in patients age 27-45 \n\nInfluenza . Annually for all patients (inactivated formu lation) \n\n## . All patients age 11-18 \n\nMeningococcus . La r ge groups living in close proximity (eg , college students, members of military \n\n(serogroups A, C, W, Y) serv i ces , incarcerated individuals) \n\n## . Asplen ia or complement defic i ency \n\n## . PCV20 \n\nPneumococcus OR . PCV15 followed by PPSV23 \n\nTetanus, diphtheria & pertussis . Tdap onc e (r epeat with each pregnancy in women) \n\n## . Td every 10 years Live vacc i nes (eg, MMR, var icella) are contraindicated if CD4 + cell count <200/mm 3\n\nHAV =hepatitis A virus; HBV =hepatitis B virus; HCV =hepatitis C vi rus ; HPV =human pap ill omavirus; MMR =measles, mumps & rubella; PCV15 =\n\n15-valent pneumococcal con jugate vaccine; PCV20 =20-valent pneumococcal conjugate vaccine; PPSV23 =23-valent pneumococcal polysacchari de vaccine; Td =tetanus-d iphtheria toxoi ds booster; Tdap =tetanus- reduced diphtheria-acellular pertussis. \n\nOccupational HIV postexposure prophylaxis Exposure of \n\n Mucous membrane, nonintact skin, or percutaneous exposure \n\nHigh-risk contact Exposure to \n\n(prophylaxis recommended) Blood, semen, vaginal secretions , or any body fluid with visible blood (uncertain risk : cerebrospinal fluid, pleural/pericardial fluid, synovial fluid, peritoneal fluid, amniotic fluid) Low-risk contact Exposure to \n\n(prophylaxis not Urine, feces , nasal secretions , saliva, sweat, tears recommended) (with no visible blood) Timing Initiate urgently, preferably in the first few hours \n\n Continue for 28 days \n\n~3-drug regimen recommended: \n\n Two nucleotide/nucleoside reverse transcriptase inhibitors (eg , tenofovir, emtricitabine) \n\nRegimen Plus \n\n lntegrase strand transfer inhibitor (eg , raltegravir) , \n\nprotease inhibitor, or non-nucleoside reverse transcriptase inhibitor Zidovudine Anemia Stavudine and didanosine Peripheral neuropathy and pancreatitis Abacavir (HLA B5701) Hypersensitivity, Stevens-Johnson reaction Protease inhibitors Hyperlipidemia, hyperglycemia lndinavir Nephrolithiasis Tenofovir Renal insufficiency Short Subjects Patients with HIV who present with an AIDS defining illness secondary to lack of anti-retroviral therapy should be initiated on HAART two weeks after treatment of the infection. \n\nto prevent immune reconstitution syndrome \n\n Immune reconstitution inflammatory syndrome occurs in patients with HIV within days or weeks of antiretroviral initiation. It is marked by a paradoxical worsening of concurrent infectious symptoms due to immune system improvement \n\n Patients with HIV actually have accelerated cardiovascular disease , even among patients on antiretroviral therapy, and therefore given that cardiovascular disease is the #1 cause of death in the general public it is easy to imagine that it would also be the #1 cause of death in patients with HIV. \n\nInfluenza \n\n What is the recommended treatment for a middle-aged patient that presents with symptoms related to influenza for 4 days? Nystatin is if you only see thrush! \n\n831 https://t.me/usmleinnercircle USMLE Inner Circle \n\nApproach to odynophagia & dysphagia in patients with HIV I\n\nSuspected esophagitis \n\n(dysphagia, odynophagia) \n\nMild symptoms, oral thrush \n\n Candida likely \n\n Empirk treatment (eg, fluconazole) Endoscopy for likely viral \n\n(eg. herpes simplex virus &cytomegalovirus) etiology \n\nI \"\"\"j I Large linear ulcers Candida likely Cytomegaloviruslikely \n\n Treatwithfluconazole Treat with ganciclovir \n\n UWortd \n\n EndOSCOP'f if no improvement \n\nwith treatment \n\n Herpes simplex virus likely \n\n Treat with acyclovir \n\nAdults at high risk for influenza complications \n\n Age ~65 \n\n Women who are pregnant & up to 2 weeks postpartum Symptomatic therapy \n\n Underlying chronic medical illness (eg , chronic pulmonary, cardiovascular, renal , hepatic) \n\n lmmunosuppressed \n\n Morbidly obese \n\n Residents of nursing homes or long-term care facilities Short Subjects Symptomatic treatment \n\ntreatment with anti-virals (e.g. oseltamivir ) is only recommended for those who present within 48 hours or those with other risk factors (age > 65, chronic medical conditions) \n\n Anti-viral treatment if reported within 48 hours OR high risk patient irrespective of symptom duration \n\n Pneumonia is the most common complication of influenza and is the result of either secondary bacterial infection (eg, Streptococcus pneumoniae ) or direct viral attack ( influenza pneumonia ). S pneumonia will cause lobar infilterates vs bilateral , diffuse interstitial infiltrates influenza pneumonia \n\nHospitalise , O2 support and antivirals / antibiotics \n\n What is the likely diagnosis in a college student with a recent viral URI that presents with high-grade fever , productive cough with hemoptysis , and leukopenia ? CXR reveals bilateral alveolar infiltrates and multiple cavitations. \n\nCommunity-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) infection \n\nCA-MRSA has a predilection for young patients with recent influenza \n\nCA-MRSA Causes necrotizing pneumonia with multiple cavitary lesions \n\n Streptococcus pneumoniae is the most common cause of influenza-related bacterial pneumonia but is rare in young individuals and less likely to cause cavitary lung lesions. \n\nParainfluenza \n\n The virus spreads from the nasopharyngeal mucosa to the larynx and trachea, causing edema and narrowing of proximal trachea (ie, subglottis). \"seal bark \" cough \n\n832 https://t.me/usmleinnercircle \n\n> Croup (laryngotracheitis) Pathogenesis Parainfluenza viral infection of the larynx & trachea\n> Epidemiology Age 6 months to 3 years Fall/early winter lnspiratory stridor\n> Clinical features Barking cough Hoarseness Mild (no stridor at rest): Humidified air corticosteroids\n> Treatment Moderate/severe (stridor at rest): Corticosteroids + nebulized epinephrine Handwashing\n> Prevention Decontamination of surfaces Ensure proper ventilation\n\nShort Subjects The symptoms of laryngotracheitis (croup ) often improve upon exposure to cold air. \n\nRSV \n\n833 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCroup \n\nBronchiolitis Epidemiology Age <2 year s\n\n# . RSV most common cause \n\nClinical Antecedent nasal congestion/discharge & cough \n\npresentation Wheezing/crackles & respiratory distress (eg, tachypnea, retractions, nasal flaring) \n\nTreatment . Supportive care \n\nComplications Apnea (especially age <2 months) . Respiratory failure Palivizumab for selected infants: \n\n# . <29 weeks gestation \n\nPrevention . Chronic lung disease of prematurity \n\n# . Hemodynamically significant congenital heart disease \n\nRSV = respiratory syncytial vir us .\n\nViral bronchiolitis (RSV) \n\n~sv = Respiratory syncyt1a1 virus . QUWor ld Short Subjects Treatment for bronchiolitis is supportive (eg, nasal suctioning, adequate hydration). Most patients can be treated as outpatients with close follow-up to ensure improvement of symptoms. \n\nDo not give: B-agonists, steroids, antibiotics \n\nChickungunya \n\n What is the likely diagnosis in a patient with recent travel to the Caribbean that presents with fever , polyarthralgias , and a diffuse maculopapular skin rash ? Laboratory exam reveals leukopenia and thrombocytopenia .\n\nChikungunya fever \n\npresentation is very similar to Dengue fever (unlikely to be required to differentiate the two in a question-- dengue has retro-orbital pain )Chikungunya exhibits similar sx to Dengue with an emphasis on bilateral polyarthralgia \n\nRabies \n\n If prophylaxis is required, what should it should include? Passive immunization: administer Human Rabies Ig \n\nActive: Vaccine in 3 IM doses \n\nIf previously immunized against rabies, only vaccine is required (2 doses) \n\nSmall Pox Hydrophobia and aerophobia are pathognomonic features of encephalitic rabies .\n\n834 https://t.me/usmleinnercircle \n\n0\n\nPa thogenesis Reservoir Clinical features Postexposure prophylaxis Prognosis \n\n\n\nChikungunya virus infection Epidemiology Tropical/subtropical parts of the Ca ri bbean region, Central/South America, Africa & Asia \n\n Vector: Aedes mosquitoes (also t ra nsmit dengue, yellow fever & Zika viruses) Incubation period : 3-7 days High fever & severe polyarthralgia (almost always present) \n\nManifestations \n\n Headache, myalgia, conjunctivitis, maculopapular rash Lymphopenia, thrombocytopenia, transaminitis \n\nManagement Supportive care ( in iti al symptoms usually resolve in 7-10 days) \n\n Chronic arthralgia/arthritis frequently occurs (may require methotrexate) \n\nHuman rabies Rabies PEP \n\nTransmission of rabies virus by bite from infected mammal Mammalian bite with possible rabies exposure (ie , broken skin or mucous membrane contact) United States: Bats (most common), raccoons , skunks, foxes Developing world: Dogs . Hydrophobia \n\nEncephalitic Aerophobia . Pharyngeal spasm , spastic paralysis Agitation \n\nParalytic Ascending flaccid paralysis Rabies immune globulin & rabies vaccine immediately after exposure to high-risk wild animal Coma , respiratory failure & death with in weeks \n\n> Low-risk wild animal\n> (eg , squirrel , chipmunk, mouse/rat, rabbit) Ye s Euthanize &test Start PEP if rabies test is positive\n> PEP =postex po sure prophyla xi s.\n> Pet Livestock or\n> (eg , dog, ca t, unknown ferret) wild animal Avai lable Contact public for quarantine? health department No Yes [ Start PEP ] Observe for 10 days No PEP if animal is healthy\n\nShort Subjects Smallpox is a viral illness caused by variola that is characterized by a febrile prodromal phase followed by a characteristic vesicular rash with lesions in the same stage of development and healing. Smallpox has been eradicated from the general population because of global vaccination using \n\nvaccinia , a live-attenuated poxvirus \n\nSystemic \n\nSepsis \n\n Baby < 28 days has a fever >100.4 is sepsis until proven other wise ( irritability, poor feeding, lethargy )Most common bugs? GBS, E. coli, Listeria \n\nEmpiric treatment? Ampicillin, gentamycin \n\n Neonates with sepsis are often brought in for evaluation due to poor feeding , inconsolability ,or lethargy . What is the likely diagnosis in a neonate that presents with hypothermia , hypotonia ,and leukopenia with bandemia? \n\nNeonatal sepsis \n\nsigns of neonatal sepsis are non-specific ; it may manifest with hypothermia, normothermia or \n\nhyperthermia , leukocytosis or leukopenia, etc. \n\n Unlike older children and adults, neonates with meningitis do not have nuchal rigidity or positive Kernig and Brudzinski signs. Instead, neonates are typically irritable , lethargic , and/or hypotonic (eg, weak suck, decreased muscle tone), often with a full fontanelle. \n\nBurns \n\n What organisms are common in burns ? Treatment? \n\nMRSA: (vancomycin) \n\n835 https://t.me/usmleinnercircle USMLE Inner Circle \n\nNeonatal sepsis \n\n## . Group B Streptococcus \n\nEtiology . Escherichia coli \n\n## . Listeria monocytogenes (age <7 days) \n\n## . Temperature instability (eg, fever, hypothermia) \n\n## . CNS signs (eg, letharg y, irritability, apnea) \n\nClinical features . Poor feeding \n\n## . Respiratory distress (eg, tachypnea, grunting) \n\n## . Jaundice \n\nEvaluation . Inflammatory markers (ie, CRP, ANC, procalcitonin) \n\n## . Blood, urine, CSF cultures* \n\nTreatment . Parenteral antibiotics (ampicillin & gentamicin) \n\n Limited evaluation (without CSF studies) & outpatient management may be considered in well-appearing, febrile neonates age >21 days. ANC = absolute neutrophil count; CRP = c-reactive protein , CSF = cerebrospinal fluid . Short Subjects Pseudomonas (cefepime )\n\nTreat empiracally if infection or sepsis occurs Immediately after = gram-positive organisms (S. aureus) >5 days = gram-negative (Pseudomonas) \n\nToxic Shock Syndrome \n\n Since there is no test for Toxic Shock Syndrome (S. aureus) and blood cultures are often negative , high index of clinical suspicion is important for diagnosis: \n\n1. High fever, Hypotension (shock) \n\n2. Diffuse maculopapular rash (covering palms and soles similar to sunburn) \n\n3. Multisystem involvement (thrombocytopenia, myalgias, vomiting/diarrhea, AMS, etc.) \n\nDiarrhea & Vomiting \n\n836 https://t.me/usmleinnercircle \n\n\n\nClinical features of toxic shock syndrome \n\n## . Feve r usua lly >38.9 C (102 F ) \n\n## . Hypotension with systo lic BP :S90 mm Hg \n\n## . Diffuse macular erythroderma \n\n## . Skin desquamation , including palms & soles, 1-2 weeks after i llness onset \n\n## . Multisystem involvement (3 or more systems) \n\n> 0\n\nGastro i ntestinal ( vom iti ng &/or diarrh ea) \n\n> 0\n\nM uscu la r ( seve re myalgias or elevated creatine ki nase) \n\n> 0\n\nM ucous membrane hyperemia \n\n> 0\n\nRenal (BUN or serum creatinine >1-2x upper limit of no r ma l) \n\n> 0\n\nHematologic (platelets <1 00 ,000/mm 3) \n\n> 0\n\nLi ver (ALT , AST & total bilirubin >2x upper limit of normal) \n\n> 0\n\nCentral nervous system (altered mentation without foca l neurologica l si gns) \n\nALT =alanine aminotransferase; AST = aspartate transaminase; BP =blood pressure; \n\nBUN = blood urea nitrogen . \n\nMajor pathologic mechanisms of foodborne illness Foodbome disease \n\nEn terotoxin Staphylococcus aureus Quick onset (1-6 hours) \n\ningested Bacillus cereus Vom iting predominant \n\nEn terotoxin Clostridium perfringens Delayed onset (>1 day) \n\nmade in ETEC/STEC \n\nintestine Vibrio cholerae Watery/bloody diarrhea Bacterial Campylobacter jejuni Variable onset \n\nepithelial Nontyphoidal salmonella Watery/bloody diarrhea invasion Listeria monocytogenes Fever \n\n Syst em ic ill ness (Listeria) \n\nVomiting predominant Staphylococcus aureus \n\n Bacillus cereus \n\n Noroviruses (eg , Norwalk) UWor1d Watery diarrhea predominant Clostridium perfringens \n\n Enteroto xic \n\nEscherichia coli \n\n Enteric viruses Cryptosporidium \n\n Cyc/ospora Intestinal tapeworms Inflammatory diarrhea predominant Salmonella (both typhi & non-typhi) Campylobacter \n\n Shiga toxin producing \n\nEscherichia coli \n\n Shigella \n\n Enterobacter \n\n Vibrio (usually \n\nparahaemolyticus) \n\n Yersinia \n\nNongastrointestinal symptoms Botulism (descending paralysis) Ciguatera toxin (paresthesia) Scombroid (flushing, urticaria) Listeria (meningitis) Vibrio vulnificus \n\n(cellulitis, sepsis) Hepatitis A (jaundice) Brucellosis (fever, arthralgias) Short Subjects 837 https://t.me/usmleinnercircle USMLE Inner Circle \n\nViral gastroenteritis \n\n## . Fecal-oral tr ansm i ss i on \n\nEpidemiology . Norovirus: most common among all ages \n\n## . Rotavirus : common in u nvaccinated age S2 \n\n## . Emesis &/or watery di arrhea \n\nClinical features . Abdominal pa in \n\n## . Fever \n\nDiagnosis . Cl inical* \n\n## . Fluid replet i on \n\n0 Oral for mild dehydration (eg , normal vital si gns , dry mucous membranes) \n\nTreatment 0 Intravenous for severe dehydration (eg , weak/rapid pulse, marked oliguria , j capillary refill time) \n\n## . R egular diet (with liwit~g fatia ai ia iw12 I~ 12 11 ga~) as tolerated *Consider bacterial/parasitic pathogens for the following : grossly bloody stools , persistent fever & exposures (eg, international travel, farm animals). \n\nOrgan ism \n\nBacillus cereus Staphylococcus aureus Clostridium difficile Clostridium perfringens \n\nCategory \n\nNoninflammatory \n\nInflammatory \n\nBacterial causes of diarrhea Features \n\n Diarmea, abdominal cramping Ingestion of preformed toxin in starchy foods such as rice \n\n Vomiting , abdominal pain Diarrtiea not typical but may occur Caused by preformed toxin with rapid onset of symptoms Abdomina l pai n, watery diarrhea , possible fever Bloody stools unusual Associated with antibiotic exposure Brief illness with watery diarrhea , cramps & fever \n\n Associated with undercooked or unrefrigerated food Acute infectious diarrhea \n\nClinical features &stool findings \n\n Usuallywatery No fecal RBCs or leukocytes Often bloody &/or mucoid + Fecal RBCsorleukocytes \n\nExamples of pathogens \n\n Viruses (most common) (eg, norovirus, rotavirus, adenovirus) \n\no Staphylococcus aureus* \n\no Baci l/usc ereus* \n\no Clostridium perfringens \n\no ETEC \n\no Vibrio cholerae \n\no Giardia \n\no Cryptosporidium \n\no Cyc/ospora \n\no Nontyphoidal Salmonella \n\no Campylobacter \n\no Shigella \n\no STEC \n\no Vibrio parahaemolyticus \n\no Entamoeba \n\n*Us ually vomiting-predominant ETEC =e nterotoxigen icEscher ichiaco/t, RBCs =redbloo dc ells; STEC =S higato xi n-produ cingEco/i. Watery diarrhea , fever, abdominal pain & vomiting \n\nSalmonella Associated wi th undercooked foods, especially poultry & eggs \n\n Antibiotic treatment needed only for severe disease or immunocompromised patients Vomiting, diarrhea & abdominal pain \n\nVibrio vulnificus Associated wi th raw or undercooked shellfish May cause invasive , life-threatening disease in immunocompromised patients or those with liver disease Watery diarrhea , may be bloody if associated with \n\nEscherichia enterohemorrtiagic (Shiga-toxin producing} strain \n\ncoli Associated wi th undercooked beef or foods contaminated with bovine feces Bloody diarrhea with fever & often bacteremia \n\nShigetta Associated with contaminated food or water, especially during \n\nCampytobacter \n\nspecies \n\ntravel outside the United States Abdominal pain, bloody diarrhea Highest incidence in children & young adults Associated with raw or undercooked meats \n\nApproach to suspected acute infectious diarrhea High-risk features \n\n Bloody stools or high-grade fever Severe disease (eg, ~ )\n\n Elderly, immunocompromised Diarrhea > 7 days \n\n# T---~----N o\n\nStool studies \n\n Fecal leukocytes Multiplex PCR testing Stool cult ur e\n\nInflammatory diarrhea \n\n Bloody stools (+)fecal leukocytes \n\nSTEC (via PCR) Non-STEC Noninflammatory diarrhea \n\n Avoid antibiotics due to HUS risk Intravenous voiuiiieexoaii sion Consider antibiotics fo r. Severe disease Elderly, immunocompromised Supportive care (ie, fluid replacement) only Pathogens with low infectious dose (eg, Shigella) \n\neonstde r ova & pa rasit e tes ti ng tgr repmt l@ vffl and/or Clootridioide s diffici f@ assa y for \n\nre awoti cs Orsottali zaroo \n\nHUS = hemolytic urem ic syndrome, STE C= Shiga toxin-producing Escherichia coli C)UWorld Short Subjects Shigella: high fever, cramping, stools that are initially watery before mucus and/or blood, tenesmus, Seizure, rectal prolapse (due to severe rectal inflammation) preferentially involves the rectosigmoid region (ie, left lower quadrant); \n\n Lack of fever is typical of infection with STEC/EHEC, although a minority of patients with STEC gastroenteritis may have low-grade fever, the presence of a temperature >38.5 C (101.3 F) suggests an alternate diagnosis. \n\n ETEC : Watery diarrhea within few days Giardia : Wattery/ foul smelling diarrhea after 1 week \n\n When infectious diarrhea is prolonged (2 weeks) , the causative pathogen is typically parasitic \n\nrather than bacterial or viral. \n\nGenital Ulcers In contrast to E coli O157:H7 diarrhea, in shigellosis , antibiotics do not increase the risk of HUS. \n\n838 https://t.me/usmleinnercircle \n\nInfectious bloody diarrhea Organism History Treatment Complications Shiga-toxin-producing Escherichia . Ingestion of undercooked beef Supportive care HUS \n\ncoli* Absence of high fever . .. Less . Ingestion of contaminated Supportive care commonly \n\nShigella food/water . HUS \n\n Antibiotics if severe . Outbreaks (eg , day care) . Seizure (in children) \n\nCampylobacter . Ingestion of raw or undercooked . Supportive care GBS .meat Antibiotics if severe \n\nSalmonella . Ingestion of undercooked chicken . Supportive care . Bacteremia (may be nonbloody) . Contact with reptiles Antibiotics if severe *For example, E coli 0157 :H7. \n\nGBS = Guillain-Barre syndrome; HUS = hemolytic uremic syndrome. \n\nProlonged (;?2 weeks) travelers' diarrhea Pathogen Clinical features \n\nEntamoeba . Bloody/mucoid diarrhea \n\nhistolytica . Extraintestinal disease: liver abscess . Watery/oily, foul-smelling stools \n\nGiardia . Bloating, fat malabsorption, weight loss \n\nCryptosporidium Watery diarrhea in immunosuppressed patients .or Cystoisospora . Watery diarrhea blood \n\nCyc/ospora . Waxing/waning symptoms IShort Subjects Haemophilus ducreyi: Bacterial culture HSV: PCR Testing; more sensitive and specific than Tzank \n\nLymphadenitis \n\nLymphadenitis: tender , enlarged , warm nodes \n\n What is the next step in management for an asymptomatic adolescent that presents with a soft , mobile , non-tender cervical lymph node measuring 1 cm in diameter? \n\nObservation \n\nfurther work-up is indicated if lymphadenopathy persists, the node enlarges, or if symptoms develop \n\n Palpable supraclavicular lymph node s should be considered pathologic until proved otherwise because they are associated with gastrointestinal, genitourinary, and pulmonary \n\nmalignancies .\n\n839 https://t.me/usmleinnercircle USMLE Inner Circle \n\nCharacteristics of ulcerative sexually transmitted diseases Initial lesion Disease Causative agent Features of primary lesion painful? \n\n# . Multiple & deep ulcers \n\n# . Base may have gray to yellow exudate Chancroid Haemophi/us ducreyi Yes \n\n# . Organisms often clump in long parallel strands (\"school of fish\") \n\n# . Multiple, small, grouped ulcers Herpes simplex virus . Shallow with erythematous base Genital herpes Yes 1&2 . Multinucleated giant cells & intranuclear inclusions (Cowdry type A) \n\n# . Extensive & progressive ulcerative lesions without Granuloma inguinale Klebsiel/a lymphadenopathy \n\n# . Base may have granulation-like tissue No (donovanosis) granulomatis . Deeply staining gram-negative intracytoplasmic cysts (Donovan bodies) \n\n## . Single, indurated, well-circumscribed ulcer \n\n# . Nonexudative base Syphilis Treponema pallidum . Painless inguinal lymphadenopathy No \n\n# . Thin, delicate, corkscrew-shaped organisms on dark-field microscopy \n\n# . Small & shallow ulcers \n\nChlamydia . Large, painful, coalesced inguinal lymph nodes (\"buboes\") Lymphogranuloma venereum No \n\ntrachomatis . lntracytoplasmic chlamydia! inclusion bodies in epithelial cells & leukocytes \n\n------ --- - -- - -- - -- - -- - - -- - -- - - - - - - - - - -\n\nLymph node features Reassuring Worrisome \n\n## . Soft . Firm or hard Palpation . Mobile . Immobile \n\n## . <2 cm (normal: <1 cm) . >2cm Location . Localized* . Generalized or supraclavicular Systemic symptoms** . Absent . Present *Exception: supraclavicular nodes. \n\n*\"Examples include fever & weight loss. Short Subjects Empiric antibiotic therapy for acute , unilateral lymphadenitis is typically with clindamycin or Amoxy-Clav \n\nhas activity against MRSA and Streptococcus pyogenes \n\nAnimal Bite \n\nWhat are common pathogens in bite wounds caused by animals? \n\nPasteurella multocida (cats ), Capnocytophaga canimorsus (dog ), anaerobes \n\nConsider rabies in dog bite Management? \n\nIrrigation and debridement Allow spontaneous closure (unless on face) Antibiotics: Augmentin / amoxicillin-clavulanate \n\nTetanus if indicated (last vaccine >5 years ago) \n\nSTD \n\n840 https://t.me/usmleinnercircle \n\nCervical lymphadenitis in children Pathogen Key clinical fi ndings \n\n## . Acute \n\nStaphylococcus aureus, . Most common \n\nStreptococcus pyogenes . Suppuration common Anaerobic bacteria . Acute (eg, Prevotel/a sppJ . History of periodontal disease or dental caries \n\nUnilateral . Acute \n\nFrancisella tularensis . History of contact with infected animal ( eg , rabbit) \n\nMycobacterium avium . ~\n\n## . Nontender, violaceous \n\nBartone/la hense/ae . ~\n\n## . Papule at site of cat scratch/bite \n\nfil!m!i!. Viral . ~ (eg , adenovirus) asso ci ated with self-limited URI \n\n## . Subacute/chronic (eg, EBV, CMV ) associated with mononucleosis symptoms \n\nCMV ; cyt om egaloviru s; EBV ; Ep st ein-Barr viru s; URI ; upper re spi rat ory infection. \n\nCat bi tes Microbiology Pasteurella multocida \n\n Anaerobic bacteria Copious irrigation & cleaning \n\nManagement Prophylactic amoxicillin/clavulanate Tetanus booster as indicated Avoid closure \n\nShort Subjects HPV screening is generally reserved for women (eg, cervical) or men who have sex with men (eg, anal) Routine screening in heterosexual men is not recommended. \n\n All patients with C trachomatis infection should inform current and recent sexual partners so they can get tested and treated ; otherwise, reinfection is common. Patients who test positive should receive antibiotics immediately and refrain from sexual intercourse \n\nuntil treatment is complete. All sexual partners from the preceding 2 months should also be tested and treated .\n\n Treat both partners with Trichomonas even if Asymptomatic and also screen for other STD in these patients. \n\n All sexually active women age <25 are recommended annual screening for C trachomatis \n\nand N gonorrhoeae , including those with low-risk sexual behavior (eg, monogamous, condom use). \n\nbecause these two have high prevalence and often asymptomatic \n\nInfection Control Also test for other STD in these pt. \n\n841 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSexually transmitted infection screening* \n\n. Neisseria gonorrhoeae (eg, NAAT) \n\n. Chlamydia trachomatis (eg, NAAT) \n\nAll patients . Syphilis (eg, RPR) \n\n. HIV (eg, 4th-generation antigen/antibody) \n\nAdditional testing for certain Wome n only: Trichomonas vagina /is (eg, wet mount) \n\n. Herpes simplex virus screening (eg, serology) only when history of characteristic \n\npopulations lesions *For patients with active sexually transmitted infection or those who request screen ing. \n\nNAAT = nucleic acid amplification testing; RPR = rapid plasma reagin. \n\nChlamydia & gonorrhea in women Risk factors . Age <25 \n\n## . High-risk sexual behavior \n\n## . Asymptomatic (most common) \n\n## . Cervicitis \n\nManifestations . Urethritis \n\n## . Perihepatitis (Fitz-Hugh-Curtis syndrome) \n\nDiagnosis . Nucleic acid amplification testing \n\n## . Empiric: ceftriaxone + doxycycline* \n\nTreatment . Confirmed chlamydia: doxycycline* \n\n## . Confirmed gonorrhea: ceftriaxone \n\n## . Pel vic inflammatory disease \n\nComplications . Ectopic pregnancy \n\n## . Infertility \n\n## . Pharyngitis \"Azithromycin in pregnancy. Short Subjects 5 microns: Droplet \n\n<5 microns: Airborne precautions (ie, negative-pressure rooms, N95) \n\n Unlike primary VZV, airborne isolation or contact precautions are not required for \n\nimmunocompetent patients who have secondary dermatomal VZV reactivation (ie, shingles/herpes zoster); for such patients, standard precautions are sufficient . What is the best initial step in the management of a hemodynamically stable patient with hemoptysis and a high clinical suspicion for tuberculosis ?\n\nRespiratory isolation \n\n Visual aids , such as signs on patient doors specifying isolation precautions, can increase adherence by doing the following: \n\nOptimizing environmental design (eg, sign outside patient's room conveys relevant information to health care worker immediately prior to patient contact) \n\nReducing reliance on memory (eg, sign specifies instructions needed for the protocol) Increasing attention through strategically placed alerts (eg, signs are brightly colored and placed selectively only where needed) \n\nCatheter Related Infection \n\n842 https://t.me/usmleinnercircle \n\nInfection control: isolation precautions Type Pathogen* Key requirements \n\n# . Bacterial: tuberculosis \n\n# . Viral: primary VZV (chickenpox ), disseminated VZV reactivation . Negative pressure room \n\nAirborne (shingles/zoster), dermatomal VZV reactivation (shingles/zoster) in . N95 respirator immunocompromised patients, COVID-19, measles \n\n# . Multidrug-resistant organism (eg, MRSA, VRE, ESBL producing) \n\n# . Bacterial: C/ostridioides diffici le , Escherichia coli 0157:H ? Gloves & gowns \n\nContact Viral: RSV, primary VZV (chickenpox), disseminated VZV reactivati on .. (shingles/zoster), dermatomal VZV reactivation (shingles/zoster) in . Single-use equipment (eg, stethoscope) immunocompromised patients \n\n# . Bact erial: Neisseria meningitidi s, Haemophilus influenzae type B, \n\nDroplet Mycoplasma pneumoniae . Mask within 1-2 m (3-6 ft) of patient \n\n# . Viral: influenza virus, adenovirus \n\n# . Hand hygiene \n\nStandard . Followed for all patients even when no infection is apparent . Gowns /gloves/masks when appropriate (eg, during procedures) *Precaution is started immediately w hen infection with pathogen is suspected. COVID-19 = coronavirus disease 2019 ; ESBL = extended-spectrum beta-lactamase; MRSA = m et hicillin-resista nt Staphylococcus aureus ; RSV =respiratory syncytial virus; VRE = vancomycin-resistant Enter ococcus ; VZ.V = varicella-zos ter v irus .Short Subjects Coagulase-negative staphylococci (CoNS) are the most common cause of catheter-related bloodstream infection. \n\ntypically occurs >48 hours after catheter insertion. Patients with suspected CRBSI should have 2 sets of blood cultures : 1 set from a peripheral site and 1 set from the catheter .This helps differentiate contamination (eg, 1 of 4 cultures is positive) from true infection (eg, 4 of 4 cultures are positive). \n\n Catheter-related bloodstream infections occur approximately once per year in patients with tunneled hemodialysis catheters .Most cases present with systemic signs of infection (eg, fever, malaise, chills) without localizing symptoms . The catheter site frequently appears normal. Initial therapy usually includes antibiotics , fluid resuscitation, and removal of the dialysis catheter. \n\n843 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPrevention of central line-associated bloodstream infections \n\n## . Hand hyg iene (Rrior to use of gloves) Catheter insertion . Full barrier precautions (eg, mask, sterile gloves, gown, drape} \n\n## . Preparation of sk in with chlorhexidine solution \n\n## . Procedure performed by experienced provider \n\n## . Use of Plees and tunneled catheters \n\nCatheter type and site For CVCs , use of subclavian and internal jugular vein sites over femoral vein .. Limit duration (eg, <6 days} for eves Catheter duration . Prompt removal of catheter when no longer needed \n\n## . Avoid routine replacement of eves CVC = central venous catheter; PICC = peripherally inserted central catheter. General Paeds \n\n# General Paeds \n\n Neonate : < 28 days By age 12 months, an infants weight should triple and height should increase by 50 %. \n\nweight should double by age 4 months \n\n Echocardiogram is indicated for a positive screen (<90% in either extremity, <95% in both upper and lower extremities, or >3% difference between upper and lower extremities). \n\n## Neonatal Resuscitation Neonatal Resuscitation Developmental Milestones Child Abuse Sexual Behaviour Motor Vehicle Restraints Injury Prevention Pre-ductal (right arm ) and post-ductal (either leg ) oxygen saturations \n\n844 https://t.me/usmleinnercircle \n\nRoutine newborn care \n\n# . Intramuscular vitamin K \n\nPreventive . Erythromycin eye ointment \n\n# . Hepatitis B vaccine \n\n# . Newborn screen (metabolic/genetic disorders) Hyperbilirubinemia \n\nScreening Hearing screen Pre- & post-ductal pulse oximetry (congenital heart disease) Hypoglycemia (select populations) General Paeds Routine newborn care (eg, vitamin K injection, erythromycin ophthalmic ointment) is typically postponed for 1 hour to allow for skin-to-skin contact. \n\n Diagnosing death in newborns requires a careful examination of cranial reflexes, apnea, lack of responsiveness, and may be supported by EEG. \n\nIn the setting of death in a nonviable , premature newborn (<22-23 weeks) , it is appropriate to \n\ndiscontinue resuscitative efforts. \n\n## Developmental Milestones \n\n Stranger anxiety typically starts at age 6 months, peaks at 8-9 months , and resolves by age 2 years .\n\n845 https://t.me/usmleinnercircle USMLE Inner Circle \n\nNeonatal resuscitation algorithm \n\n Term gestation Good tone Breathing or crying \n\n# r-No Yes 7Occurs in first minute afterb irth Provide warmth Improved Clear airway Routine care ( eg , skin-to-skin) \n\nAge \n\n(months) \n\n# .2\n\n# .4 .\n\n# ..6\n\n# .9\n\n# ..12 .\n\n Sttmulate Reevaluate \n\n# !HR <100 &/or ineffective respirations Initiate positive pressure ventilation \n\n# !Bradycardia &/or ineffective respira t ions Proceed to advanced resuscitation (eg , chest compress i ons , intubation) Developmental milestones of infants Gross motor Fine motor Language . Reacts to Lifts head when . Opens hands loud sound prone briefly . Makes noises . Brings hands Holds head steady to . Coos (\"coo\") \n\nPushes up on midline/mouth Turns to forearms . Holds toy if put voice in hand Rolls over . Reaches for . Blows Leans on hands to toy \"raspberries\" support seated . Puts things in . Squeals position mout h Transfers . Babbles Gets to sitting object between (\"ma mama\") unassisted hands Turns to Sits without support \"Raking\" grasp name \n\n# . Says \"mama\"or Pulls to stand . Pincer grasp \"dada\" Cruises . Understands \"no\" \n\nC UW ork:I \n\nSocial/cognitive . Social smile . Calms when spoken to \n\n Tracks past midline . Seeks attention (eg, smiles, makes sounds) . Enjoys looking at hands . Laughs . Recognizes familiar faces \n\n# . Stranger anxiety Separation anxiety \n\n# . Plays \"pat-a-cake\" \n\n# . Looks for hidden object General Paeds Children with stranger anxiety typically cry when an unfamiliar person approaches, even in the presence of the primary caregive (vs Separation Anxiety Disorder ) The next step in management for any patient with language delay is an audiology evaluation \n\nto assess for a hearing defect. Isolated speech delay is characterized by problems with: \n\narticulation (eg, mispronunciation) \n\nfluency (eg, stuttering) \n\nvocal quality (eg, abnormal volume or pitch) Speech should be 100% intelligible by age 4. If not, conduct a hearing test first ! \n\n Visual acuity testing is performed routinely at age 4 \n\n Having an imaginary friend , is a developmentally appropriate aspect of childhood. An imaginary friend may be human, animal, or a fantasized figure and is common in the preschool \n\nand early school-aged years, decreasing in frequency after age 6 \n\n846 https://t.me/usmleinnercircle \n\nDevelopmental milestones of toddlers Age Gross motor Fine motor Language Social/cognitive \n\n. Plays \"pat-a-\n\n12 . Pulls to stand . Says \"mama\" or \"dada\" cake\" months . Cruises . Pincer grasp . Understands \"no\" . Looks for \n\nhidden object \n\n. Follows 1-step \n\ncommand 15 months Takes a few steps . Stacks 2 blocks . Says 1-2 words (plus with gesture \n\n\"mama\" & \"dada\") . Points to get \n\nsomething \n\n. Shows affection \n\n. Follows 1-step \n\n18 Walks easily . Scribbles . Says ~3 words (plus command months . Climbs on/off chair . Feeds with fingers \"mama\" & \"dada\") without gesture \n\n. Imitates \n\n. Runs . Knows 2 2 years . Kicks ball . Uses spoon . Says 2-word phrases body parts \n\n Walks up stairs . Parallel play \n\n. Follows 2-\n\n. Removes clothes step \n\n2.5 years . Jumps . Says ~50 words command \n\n Turns pages . Knows 1 color \n\n. Knows \n\n Walks up stairs . Dresses with help Says ~3-word sentences age/sex 3years alternating feet . Uses fork .. Rides tricycle . Copies circle . Speech 75% intelligible . Plays with \n\nother children I\n\nDraws person with ~3 \n\nbody parts Comforts others \n\n4 Catches large ball Unbuttons clothes Says ~4-word se nt ences Avoids danger \n\nNames colors \n\nHolds pencil between Imaginative play fingers & thumb Speaks in full Buttons clothes sentences/tells story \n\n5 Hops on 1 foot Writes some letters Counts to 10 Follows ru les; takes turns \n\nNames letters \n\nGeneral Paeds Young children often engage in magical thinking , involving beliefs in the magical powers of objects and the existence of imaginary characters. It is a normal phase of cognitive development in children age 2-7. \n\n## Child Abuse \n\n Abuse must be ruled out in any child with abrupt onset of mood changes , bedwetting ,and/or academic difficulties .\n\n847 https://t.me/usmleinnercircle USMLE Inner Circle \n\nFeatures of possible child abuse Caregiver background \n\n. Young or single parents \n\n## . Lower education levels \n\n. Su bstance use disorder \n\n## . Psychiatric conditions (depression, impulse control disorders) \n\n. History of childhood abuse \n\nRisk Home environment factors . Unstable family situation (eg , divorce, conflict) \n\n. Financial difficulties, job loss \n\n. Lack of social su pport \n\n. Domestic violen ce Children \n\n. Physical, intellectual, or emotional disabilities \n\n. Unplanned pregnancy/unwanted child \n\n. Unexplained or implausible injuries Clinical . In juries in different stag es of healing presentation . Malnutrition \n\n. Sudden behavioral or scholastic chan~ es \n\nManagement . Document objective findings from evaluation \n\n. Report suspected abuse to child protective seivices \n\nNonaccidental trauma \n\n## . Injury inconsistent with developmental stage \n\nRed flags . Delay in seeking care \n\n## . Conflicting historical details \n\n## . Bruises: patterned appearance (eg, belt buckle), occurring in nonmobile child or over noninjury-prone area (eg, ear, trunk) \n\n## . Burns: linear, well demarcated \n\n## . Fractures: Clinical 0 Multiple & in various stages of healing features 0 Femur fracture in nonambulatory child \n\n0 Posterior rib fractures \n\n0 Metaphyseal corner fractures \n\n## . Head trauma: retinal & subdural hemorrhages Management . Disposition: ensure immediate safety of the child (eg, inpatient management, child protective services) \n\n## . Evaluation: skeletal survey, CT scan of the head, funduscopy General Paeds A spiral fracture occurs in response to a twisting force on the bone. \n\nHighly specific for child abuse if seen in a child with a suspicious history (in questions anyways, in real life it seems a little more controversial) \n\n## Sexual Behaviour \n\n848 https://t.me/usmleinnercircle \n\nInjury patterns in nonaccidental trauma \n\nCoup-contrecoup Long bone fractures Bruising on neck, torso, ear, buttoc ks \n\n> \"May be due to acddental trauma if child tS ambulatory\n\nSubdural &epidural hematomas Retinal hemorrhage lntraoral injuries on funduscopic (eg, frenulum tear)* examination \n\n> C)UWolJd\n\n<0UWOl1d \n\nS i gns of delibe rate scald injury \n\nSparing of flexural creases (\"zebra\" pattern) \n\nMetaphyseal corner fracture (humerus) \n\nfypically caused by a shaking or twisting fo rce (nonac ci dental trauma) Cl UWor1o General Paeds Anogenital trauma , coercive sex play , or repeated urinary tract infections with no medical cause should also raise concerns about possible sexual abuse. \n\n## Motor Vehicle Restraints \n\n The most common cause of death in teens and young adults is accidental death , frequently caused by motor vehicle collisions . All teens and young adults should therefore be encouraged to wear seat belts in vehicles to decrease their risk. Other health behaviors that should be encouraged in this patient population include exercise, maintaining a healthy weight, abstaining from tobacco use, and avoiding excessive alcohol use. \n\n## Injury Prevention \n\n849 https://t.me/usmleinnercircle USMLE Inner Circle \n\nSexual behavior in preadolescents Normal Abnormal Toddler \n\n# . Exploring one's own or others' genitals . Repeated insertion of \n\n## . Masturbatory movements objects into vagina or anus . Undressing self or others . Sex play involving genital-genital, oral-genital, or anal-\n\nSchool-age genital contact . Increased interest in se x . Use of force , threat s, or words & play bribes in sex play \n\n## . Asking questions about sex & . Age-inappropriate sexual reproduction knowledge . Masturbatory movements (may become more sophisticated) \n\nMotor vehicle restraints Age range Recommended safety device ** 0-4* \n\nR ear -fa cing car seat \n\n2-8 *\n\nF orward-f aci ng car seat \n\no r earlier, if child outgrows height OR weight limitation of safety device .\n\n.. All children age <13 should sit in back passenger row. \n\n5-12* \n\nB oos t er se at \n\n9-adult \n\nS eat b elt \n\n UWor1d General Paeds Foods that are choking hazards should be avoided in children age <4. \n\n850 https://t.me/usmleinnercircle \n\nInjury prevention in children \n\n# . Never leave child unattended around water Fence all 4 sides of pool & install self-locking, self-latching gate \n\nWater . Use life jackets \n\n Teach child to swim \n\n# . Install smoke detectors on every level of home \n\nFire . Test smoke detectors & change batteries regularly \n\n# . If present, store guns unloaded and locked \n\nGun . Store ammunition separately from guns \n\n# . Lock medications & toxic household products out of reach \n\n# . Remove dangling cords & cover power outlets \n\n# . Install safety gates on stairs \n\nHome . Set water heater to maximum temperature of 49 C (120 F) Mount furniture & TV to wall Avoid choking hazards (eg, whole grapes, raw vegetables, small objects) Public Health 1\n\n# Public Health \n\n250: HY Vaccines Podcast \n\n## Screening \n\n DO NOT SKIP UPSTF Screening Guidelines: \n\nhttps://www.uspreventiveservicestaskforce.org/uspstf/recommendation-topics/uspstf-a-and-b-recommendations The adolescent visit should include \n\ncontraceptive counseling and discussion of safe sex practices \n\n High Risk patients (e.g BRCA mutation) should undergo Annual Breast MRI Screening SPECIAL GENETIC DISEASES Familial Hypercholesterolemia Patients with MEN 2A or 2B BRCA Mutations Risky Sexual Group Children Miscellaneous Lung cancer Vaccine Adults Divine Ep \n\n851 https://t.me/usmleinnercircle USMLE Inner Circle \n\nScreening tests for patients at average risk* Routine adolescent screening Category Screening method* \n\nDisease Age Test & interval \n\nMental health . Validated depression questionnaire Breast cancer Women 50 - 75 Mammogram every 2 years . Confidential discussion about sexual activity \n\nSexual health . Gonorrhea & chlamydia testing if sexually active Cervica l cancer Women 21 - 65 Pap smear every 3 years . HIV testing (once at age <18) Co lon ca ncer 50 - 75 Fecal occ ult blood test yearly or colonoscopy every 10 years \n\nSubstance use . Confidential discussion about exposure, use, abuse \n\nDyslipidemia . Lipid panel once between age 17 & 21 HIV 15 - 65 HIV antibody screen 1 time . Inquiry about bullying \n\nSafety Inqui ry about seatbelt & helmet use .\n\nHyperlipidemia Men 35+ Lipid panel every 5 years *Annually, unless otherwise indi cated .Hypertension 18+ Blood pressure measureme nt every 2 years Osteoporosis Women65+ DEXA (interval uncerta in )* Optimum screen in g tests & intervals may vary for patients at increased risk or for those with abnorma l or near-abnorm al results. Public Health Universal lipid screening is recommended for children ages 9 - 11 and again between ages 17 - 21 .\n\nlipid levels typically remain stable prior to and after puberty; future lipid screening should begin again at age 35 (men) or age 45 (women) in 5-year intervals \n\nCan begin screen earlier if there is CAD \n\n What is the most appropriate first step for a patient that tests positive for HIV but does not want to tell his/her partner? \n\nEncourage the patient to tell the partner(s) & notify the local health department \n\npublic health laws require reporting HIV to the local public health department \n\n One-time screening for abdominal aortic aneurysm with an abdominal ultrasound is recommended for men age 65-75 who have ever smoked or have Family History. \n\n Screening for osteoporosis ?Women > 65 yo Women < 65 yo with risk factor (e.g. anorexia, prolonged steroid use) Smokers Premature Ovarian Failure FRAX > 9.3 T < -2.5 bisphosphonate \n\n Screening for prostate cancer \n\nShared decision-making \n\n> age 70 NOT recommended \n\n If DRE is done and nodule is found Do BIOPSY and imaging if pt has life expectancy of 10 years or more \n\n Women cancer incidence: Endometrial > Ovarian > Cervix \n\nPrognosis: C>E>O (Best to worst) \n\nCancer Incidence: Breast/Prostate > Lung > Colon (Lung MCC of Death) \n\nSPECIAL GENETIC DISEASES \n\nFamilial Hypercholesterolemia \n\nPeople get MI at age 25 People have LDL receptor mutation generally Remember rule of 3 Start checking LDL cholesterol at age of 3, 9 and 18y \n\n852 https://t.me/usmleinnercircle \n\n000Public Health o You will continue to screen but not tested on NBME \n\nPatients with MEN 2A or 2B \n\nIts not a matter of if but when will you get a medullary thyroid cancer You offer a prophylactic thyroidectomy!!! \n\nBRCA Mutations \n\nBreast cancer screening guidelines Between ages 25-29 you deserve an annual breast mammogram \n\nIf you are over the age of 30 you deserve o Annual breast MRI and annual mammography \n\nRisky Sexual Group \n\nIndividuals with HIV Men that have sex with men Sex workers IV drug users \n\nScreening guidelines \n\nIf you are between ages 15-64 You deserve annual HIV \n\nScreen for syphilis every three months \n\nScreen for Chlamydia and gonorrhea \n\no You only screen women, DO NOT SCREEN MEN! o You screen higher risk patients annually no matter the age o ALL patients (not only high risk) younger than 24 need annual testing o Non risky patients dont need to be screened for these two annually after age of 24 Screen for Hep B surface antigen every year \n\no Also screen the antivaxxers every year for hep b \n\nChildren \n\nPatients with Language difficulties: \n\nScreening hearing with audiometry \n\nAll kids between ages 3-5 years old \n\nScreen for amblyopia -> Lazy eye \n\nMiscellaneous \n\n Who needs to be screened for Hep B? \n\nNeed to be screened every year \n\n853 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPublic Health Patients who receive multiple blood transfusions or are constantly on dialysis \n\nLong term chemotherapy or long-term immunosuppressive therapy due to transplant. With hepatitis b surface antigen \n\n All people between ages Hep C: 18-79y once \n\nLung cancer \n\n## Vaccine \n\n In preterm infants, all vaccines should be administered according to chronologic age (age since birth). The first hepatitis B vaccine should be administered when the newborn weighs > 2 kg. \n\n2 kg = 4 lb 6 oz; this is the only exception to the rule that preterm infants should receive vaccines according to chronologic age \n\n854 https://t.me/usmleinnercircle \n\nRecommendations f or lung cancer screen ing Recommended . Low-dose CT scan of the chest tes tRe comm en ded interval . Yearly \n\nAge for 50-80 .screening \n\n## . ~20-pack-year history \n\n&\n\nEligibility Currently smoking or quit smoking within the past . 15 years . Patient successfully quit smoking fo r ~15 years \n\nTerm ination of OR \n\nscreening . Patient has medical conditions that significantly limit life expectancy Standard ped iatric imm u ni z ati on s in the Un i ted States \n\n. Polio Inactivated (killed) . Hepa titis A \n\n. Influen za (inj ect ion )Toxoid (inact i vated t oxin) . Diph the ria , tetanus \n\n. R otavirus \n\n. Me as les Live attenuated . Mumps \n\n. R ub ella \n\n. Varicella \n\n. He patitis B \n\n. Pertussis Subunit/conjugate . Haemophilus influenzae type B\n\n. Pneumococ ca1 \n\n. Men in gococca l\n\n. H uman pa pillom avirus Public Health Influenza vaccine given annually AFTER 6 months of age \n\n855 https://t.me/usmleinnercircle USMLE Inner Circle \n\nVaccine \n\nHepatitis B 1 (HepB) Rotav i rus 1 (RV) RVl (2-dose series); RVS (3-dose series) Diphtheria, tetanus, & acellular pertussis 1 (DTaP: <7 yrs) \n\nHaemophilus influenzaetype b4\n\n(Hibl Pneumococcat conjugate5 \n\n(PCV13J Inactivated poliovi rus 6\n\n(IPV:<18yrs) lnfluenza 7 (IIV) Meas les , mumps, rubella 8 (MMR) \n\nVaricella 9 (VAR) Hepatitis A10 (HepA) \n\nMeningococcal1 1 (H ib-MenCY \n\n2 6 weeks; MenACWY-D 29 mos; MenACWY-CRM .?:2 mos) Tetanus, diphtheria, & acellular pertussis 11 (Tdap:~7yrs) \n\nHuman papillomavirus 11 (HPV) Meningococcal B11 \n\nPneumococcal po lysaccharide5 \n\n(PPSV23) \n\nII Range of recommended \n\nl____J ages for all children \n\nHepB \n\n(protects against hepatitis B) \n\nDTaP (protects against dlphtherla, tetanus, pertussis) \n\nHib (protects agalnst ha emophilus inf lu enzae type b: may be 3 or 4 doses) \n\nIPV \n\n(p rotects against polio) \n\nRV (protects against rotavl ru s; may be 2 or3 doses) \n\nPCV13 (protects agalnst pneumococca1 di sease) \n\nFlu (prot ec ts against influenza) \n\nMMR (protects against measle s, mump s, rubella) \n\nVaricella \n\n(protects against varicella, also calledchickenpox) \n\nHepA \n\n(protects against hepatitis A) Birth 1 mo 2mos 4mos 6mos 9 mos 12 mos 15 mos 18 mos 19-23 2-3yrs 4-6yrs 7-lOyrs 11-12yrs 13-lSyrs 16yrs 17-18yrs l \" dose 2 nd dose \n\nl \" dose 2 nd dose See footnote2 l \" dose 2 nd dose 3rd dose 5th dose l \" dose 2 nd dose See footnote4 Il \" dose 2 nd dose 3' d dose 4t h dose Il \" dose 2 nd dose ,.. ------ 3rd dose ------ ..,: 4th dose I\n\nII Range of recommended ages \n\nl____J for catch-up immunization Annual vaccination (IIV) 1 or 2 doses I Annual vaccination (IIV) 1 dose onlv \n\nSeefootnote8 -- - - l\"dose 2nd dose \n\n ---1 \" dose 2nd dose \n\n - :l-dose series, See footnote 1O \n\nSee footnote 11 l\"dose Tdap \n\nL_seefootnote \n\nI n\n\nSee footnote 5\n\nII Range of recommended ages for non-high-risk \n\nl____Jgroups that may receive vaccine, subject to individual clinical decision making \n\n2 nd dose \n\nSee footnote 11 \n\nI\n\nLJ No recommendation Public Health An egg allergy is the most common contraindication to receiving the flu vaccine .The administration of multiple vaccinations at a single visit is safe , increases vaccine compliance, and optimizes protection at a young age. Live attenuated and inactivated vaccines may be given on the same day. \n\nBreastfed babies may receive live virus vaccines. Live virus vaccinations should not be administered to pregnant women due to the theoretical risk of fetal infection. Vaccines can be administered safely during minor illnesses (eg, upper respiratory infection, otitis media). They should be postponed until recovery from moderate or severe illnesse s (eg, high fever) because manifestations of the underlying illness can be incorrectly attributed to the vaccine or vice versa. Varicella (Chickenpox ) vaccination recommendations: \n\n1st dose: 1 year 2nd dose: 4-6 years Catch-up vacc : After 18 years in Individuals at high risk of exposure or close contact with immunocompromised/high-risk Before undergoing immunosuppressive therapy/organ transplant Endemic region , such as most of sub-Saharan Africa \n\nand Mecca \n\n856 https://t.me/usmleinnercircle \n\n\n\n \n\n> Rotavirus vaccine Indications\n\n## . Prevent most common cause of viral gastroenteritis worldwide \n\n## . Live attenuated oral vaccine Specifications Series administration between age 2 & 6 months .. Allergy to vaccine ingredients Contraindications . Severe combined immunodeficiency \n\n## . History of intussusception Meningococcal vaccination \n\n# . Age 11-12: primary vaccination \n\n> Routine schedule\n\n# . Age 16: booster \n\n# . Complement deficiency \n\n# . Asplenia \n\n> High-risk patients\n\n# . College students in residential housing (age S21) \n\n> (vaccinate if age .e2 months)\n\n# . Military recruits \n\n# . Travel to endemic area \n\n# . Exposure to community outbreaks \n\n\n\n\n\n\n\n> 0\n> 0\n\nPublic Health VZV vaccine rash is less contagious BUT Avoid contact with Immunocompromised patients &\n\npregnant patients \n\n What is the next step in management for a child that develops a fever and mild rash one week after receiving the MMR vaccine ?\n\nReassurance \n\na small fraction of patients develop a self-limiting mild rash and fever 1 - 3 weeks after vaccination; due to vaccine-strain live measles virus. Avoid contact with Immunocompromised patients \n\nrespiratory isolation is NOT required (vs Primary Measles infection where it is necessary) \n\n Patients with unstable neurologic disease or encephalopathy following vaccination should receive diphtheria and tetanus toxoids without pertussis \n\nAdults Occurs 1-3 weeks post vaccination In the setting of precautions, still give the vaccine as the benefit \n\noutweights the unlikely risk of significant side effects \n\n857 https://t.me/usmleinnercircle USMLE Inner Circle \n\nVaccine-strain versus wild-type varicella Vaccine strain Wild type \n\n <10 lesions >100 lesions Maculopapular &/or vesicular Vesicular in successive crops \n\n Mildly contagious Highly contagious \n\nDiphtheria-tetanus-acellular pertussis immunization Contraindications & precautions to \n\n# . Diphtheria toxoid diphtheria-, tetanus-, &/or pertussis-containing immunizations Components . Tetanus toxoid . Conjugated pertussis antigen (pertactin) \n\nVaccine Contraindications Precautions component \n\n Moderate or severe acute . 5 doses given at ages: illness +/- fever \n\nSchedule 0 2, 4 & 6 months \n\n0 15-18 months \n\n0 4-6 years Guillain-Barre syndrome within \n\nDiphtheria/ Anaphylaxis to vaccine 6 weeks of tetanus toxoid -\n\ntetanus ingredients containing vaccine Arthus-type hypersensitivity \n\nContraindications . Encephalopathy after previous dose . Anaphylaxis to vaccine component reaction following diphtheria- or tetanus toxoid--containing vaccine Moderate or severe acute Anaphylaxis to vaccine illness +/- fever ingredients Reactions to previous doses: Progressive neurologic Seizure within 3 days \n\nPe rtussis disorder (eg, uncontrolled Temperature N0 .5 C (105 epilepsy, infantile spasms) F) within 2 days Encephalopathy within a Hypotonic-hyporesponsive week of previous vaccine episode within 2 days dose Inconsolable, persistent crying within 2 days Public Health Herpes zoster (shingles ) vaccine recommended in all adults >60 years old \n\nTo prevent shingles and mitigate symptoms if shingles does occur \n\nDivine Ep 250: HY Vaccines Podcast \n\nTwo big types of vaccines \n\nLive attenuated \n\nBug that has been severely weakened, but retains ability to infect cells. Generates a T-Cell response \n\nNo real need to give boosters Ex \n\nMMR Varicella Intranasal influenza vaccine Killed/Inactivated vaccine \n\nDestroyed bug but you keep antigenic parts, which generates a response from immune system Generates Humoral response Need to give boosters Toxoid vaccine \n\n858 https://t.me/usmleinnercircle \n\n\n\n0\n\n\n\n\n\n\n\n0\n\n\n\n0Recommended vaccines for adults Age 19-64 Age ,!: 65 \n\nTd/Tdap T dap once as substitute for T d booster, then T d every 10 years \n\nInfluenza Annually \n\nPPSV23 alone Sequential PCV13 + PPSV23 \n\n Chronic heart, lung, or liver 1 dose of PCV13 followed disease by PPSV23 at a later time \n\n Diabete s, curren t smokers, alcoho li cs \n\nPneumococcus Sequential PCV13 + PPSV23 (very high risk patients) \n\n CSF leaks, coch lear implants Sickle cell disease, asplenia lmmunocompromised \n\n(eg , HIV, malignancy) Chronic kidney disease \n\n> CSF =cereb rospinal flui d; PCV13\n\n= 13-valent pneumococcal conjugate vaccine ; PPSV23 = 23-valent \n\n> pneumococcal polysaccharide vaccine ; Td\n\n= tetanus-diphtheria toxoid booster, Tdap = tetanus-diphtheria-pertussis Human papillomavirus \n\n Cervical cancer Vulvar & vaginal cancers Anal cancer \n\nDisease associations Penile cancer Oropharyngeal cancer Genital warts All girls & women* age 11-26 \n\nVaccine indications Boys & men age 9-21 (9-26 for men who have sex with men; individuals with HIV) *Including those with history of genital warts, abnormal cytology, or positive humanpapillomavirus DNA test. Public Health Toxin from bug that can act on receptors in the body to generate antibody response Child that receives rotavirus vaccine. Which of the following is the most dangerous complication? Intussusception If pt has had it in the past intussception Hx of meckels IgA nephropathy (or HSP) Two types of influenza Inactivated \n\nIntramuscular \n\nLive-attenuated \n\nIntranasal. Inhaled as mist PCV-13 and PPSV-23 PCV-13 \n\nConjugated. Pneumococcal Conjugated B + T cell response PPSV 23 Polysaccharide Humoral response (No T cells) \n\nPCV 13 always taken FIRST before 23 \n\nMnemonic aid: 13 comes before 23. PCV13 is taken by everybody! PPSV 23 Given for those > 65 y/o Those under 65 y/o that should have vaccine include (think of organs with chronic disease): Smoker Diabetes Cochlear implant Older person on test. Alport syndrome Chronic CSF Leak Immunodeficiency (HIV, Bruton, SCID, CVID) Those with no spleen Who does not get live attenuated vaccines? \n\n859 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\n\n\n0\n\n\n\n\n\n0\n\n\n\n0\n\n\n\n\n\n0\n\n\n\n\n\n0\n\n\n\n\n\n0\n\n\n\n00\n\n\n\n\n\n00\n\nPublic Health Pregnant women < 1 y/o ( exception: rotavirus) \n\nCD <200 (immunodeficiency) Vaccines in kids Approximate rule but works a lot: Most pediatric patients are at least 3 doses But not always true Most are given at 2, 4, 6 months of age. \n\nThose that dont follow this rule? Live attenuated vaccines! \n\nHep B vaccine \n\nNeed to get it before you leave the hospital. Three doses First dose at birth Second dose: within 2 months of birth Third dose is between 6-18 months of age Rotavirus vaccine obeys second rule 3 doses vaccines given at 2,4, and 6 months. \n\nDTap vaccine \n\n5 doses with extra information to know. 3 doses at 2, 4, and 6 months 4rth dose: ~ 15-18 months of age 5th dose: 4-6 y/o When youre older: TDap (Adolescent TD booster \n\nH. Flu Type B vaccine \n\n3 doses 1st dose: 2 months 2nd dose: 4 months 3rd dose: 12-15 months \n\nPCV-13 vaccine \n\n4 doses 1st dose: 2 months \n\n860 https://t.me/usmleinnercircle \n\n> 000\n\n\n\n> 0\n> \n\n\n\n> \n\n\n\n> 00\n> \n\n\n\n> 0\n> \n> 0\n> \n\n\n\n> \n\n\n\n> 0\n> \n\n\n\n> 0\n> \n\nPublic Health 2nd dose: 4 months 3rd dose: 6 months 4th dose: 12 - 15 months \n\nPolio vaccine \n\nFour doses 1st dose: 2 months 2nd dose: 4 months 3rd dose: 6 months 4rth dose: 4-6 y/o \n\nInfluenza vaccine \n\nEvery year. Less than a year old do NOT give intranasal. \n\nMMR and varicella \n\nGroup both together with the same vaccine schedule. Two doses 1st dose: 12-15 months \n\n2nd dose: 4-6 y/o Hep A vaccine \n\nTwo doses 1st dose within 2 y/o \n\n2nd dose: 6 month s after 1st dose Later given in adolescence \n\n10-18 y/o Meningococcal vaccine \n\nTwo doses First dose: 11-12 y/o \n\nSecond dose: 16 y/o \n\nHPV vaccine Can give starting from 9-26 y/o \n\nZoster vaccine Not the same as varicella Get zoster at age of 50 Two doses (6 months apart) \n\nPregnancy \n\n861 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\n0\n\n\n\n\n\n0\n\n\n\n0\n\n\n\n\n\n0\n\n\n\n\n\n\n\n0\n\n\n\n\n\n000\n\n\n\n0\n\n\n\n\n\n0Public Health Women supposed to get TDAP vaccine Within 27-36 weeks \n\nPt splenectomy (Sickle cell, trauma) \n\nPCV-13 and PPSV-23 , strep pneumo , Hib flu , and neisseria meningitidis \n\nTimeline between PCV-13 and PPSV-23 Wait between 2 months between both vaccines \n\nEgg allergy Avoid Yellow fever vaccine (Everything else is fine, yes - even MMR!!) \n\n NBME says Influenza Flu vaccine is not given in Egg allergy \n\n862 https://t.me/usmleinnercircle \n\n> \n\n0\n\n> \n> 0\n> \n> 0\n> \n\nEthics & Communication \n\n# Ethics & Communication Core Ethical Principles Medically Futile Treatment Consent Capacity Surrogate Leave Against Medical Advice Confidentiality Bad News Communication Interpreters Behaviour Interventions Motivational Interviewing Stages of Change Health Literacy Medication Medication Adherence Medication Non-adherence Adverse Drug Events Antibiotic Use Alternate Therapies Intimate Partner Violence Sexual Assault Pregnancy Adolescence Genetic Testing Geriatrics Falls Elder Abuse Medication Prescription Violent Patient Physician Impairment Quality Cross Culture Care Patient-Centered Care Home Health Care Rapid Response Teams Quality Improvement Processes PDSA Cycle Hospice Care Physician Assisted Suicide DNR Medical Errors Cognitive Errors Avoiding Errors Clinical Support Systems \n\n863 https://t.me/usmleinnercircle USMLE Inner Circle Ethics & Communication Core Ethical Principles \n\n Autonomy does not obligate the physician to provide nonindicated or inappropriate services ,regardless of patient request. The patient's autonomy to receive a requested medical treatment is always subject to the physician's medical judgment and discretion . When deciding whether to provide a requested treatment, the physician should consider the following: Whether the treatment is consistent with ethical and evidence-based scientific standards Whether the treatment potentially benefits the individual patient (ie, beneficence) Whether the treatment avoids unnecessary or excessive harm (ie, nonmaleficence) When counseling patients who request nonindicated services, physicians should empathetically explore patient motivations \n\n Patients with low back pain are less likely to request imaging studies when they believe the physician has performed a thorough physical examination that checks for serious pathology and they receive a specific explanation of their condition. Recommended practices include the following: Apply patient-centered (rather than paternalistic) approaches to build a patient-physician partnership and directly address patient concerns. Perform a detailed physical examination , giving special attention to areas that are concerning to the patient and providing ongoing commentary on what structures are being assessed and the significance of findings. Minimising Interruptions Healthcare Communication Error Reporting System Medical Error Analysis Root Cause Analysis Failure Mode & Effect Analysis Effective Teams Time Out & Site Verification Burnout Malpractice Defensive Medicine Insurance Pay for Performance System Research \n\n864 https://t.me/usmleinnercircle \n\n> Ethical principles in medicine Principle Duty Beneficence Promote good & act in the best medical int erests of the patient\n> Nonmaleficence Do no harm to the patient\n> Autonomy Protect & facilitate the patient's individual, informed de cisions\n> Justice Equally distribute health care resources & provide fa ir & equitable treatment\n> Proportionality Ensure that methods used to ac hieve a worthwhile goal are necessary, appropriate & not excessive\n\n\n\n\n\nEthics & Communication Patients have the right to refuse treatment except when doing so poses a serious threat to public health .In these cases, the physician is justified in restricting individual liberties until the public's health is no longer at risk. Physicians have an ethical and legal duty to treat patients with life-threatening conditions ,regardless of the patients' behavior. The physician's duty to treat comprises ethical and legal components. Physicians are ethically obligated to place patients' interests above their own and care for patients with potentially life-threatening conditions . In the emergency department setting, the legal duty to treat is further specified by the Emergency Medical Treatment and Active Labor Act (EMTALA). The emergency medicine provider (eg, physicians) must: Provide a screening examination \n\nAppropriately treat and stabilize the patient \n\nTransfer the patient (with limited exceptions) only after the patient is stabilized \n\n Key idea: Organ donation is primarily managed by organ procurement organizations rather than the hospitals themselves \n\nMedically Futile Treatment \n\n A medically futile treatment clearly offers no benefit (eg, physiologic improvement, reduction in suffering) and cannot accomplish intended goals. Medical futility can be defined as follows: \n\nPhysiologic futility: Treatment cannot improve physiologic condition or reach a physiologic goal (including promoting palliation or comfort). \n\nQualitative futility: Treatment offers marginal benefits that are substantially outweighed by the likelihood of significant pain and suffering. Physicians have no ethical obligation to administer futile treatments because doing so counters the ethical obligations of beneficence (ie, benefiting the patient) and nonmaleficence (ie, not harming the patient). When a patient (or surrogate decision-maker) requests a futile treatment, the physician should attempt to understand the reasons for the request (eg, distrust, concern for abandonment, overestimating treatment benefits) and empathetically explain why the treatment is futile. \n\nIn contrast, therapies that are high risk but offer some benefit (eg, prolongation of life via cardiopulmonary resuscitation in some patients without a terminal diagnosis) are not clearly futile. In such \n\n865 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nG See k permission fr om th e primary attend in g s ur geon to be th e ass istant surgeon in th e procedure 39% Al though there is no federal l aw t hat proh ib its physicians from treating or performing surgery on family members, t he \n\nAmerican Medical Association clearly advises against it becau se doing so rai ses et hi ca l issues of professional ob j ect iv ity, pa ti ent confid ent i al it y, and personal feelings that may cloud ju dgme nt . Exceptions t o t hi s recommendati on in clude medical emergencies in wh i ch no ot her qualified ph ysician is present and treatment of mi nor condit ions. In t his scenario, t he patient expli cit ly asks for his daughter to perform surgery on hi m. By asking t he pr imary attending surgeon if she may assist in t he procedure, the daughter manages to balance this ethical principle (avoiding treatment of fami ly members) w i th patient autonomy (honoring her fat her 's preferences) .Ethics & Communication cases, the physician should offer clear guidance but cannot refuse treatment if it is requested by an informed and competent patient or surrogate. \n\n Physicians should not feel pressured to order tests that are not medically indicated. Requests for additional testing should be declined in a nonjudgmental manner , accompanied by an \n\nexplanation of why the test is not in the patient's best interest. \n\n## Consent \n\n Informed refusal requires discussion of all the same elements (eg, diagnosis, proposed procedure, risks/benefits, alternatives, risks of refusal) required for informed consent. Important exceptions to informed consent: A life-saving procedure may be performed in an emergency where obtaining consent is not possible. Extension of a procedure is acceptable if an unexpected complication arises that requires immediate treatment (eg, unexpected ostomy creation is necessary because profound enteric spillage makes bowel repair unsafe). The additional procedure is typically related to the initial indication (eg, peritonitis) for treatment. \n\n866 https://t.me/usmleinnercircle \n\n \n\n> Elements of informed consent Preconditions\n\n## . Competency \n\n## . Voluntariness \n\n## . Diagnosis \n\n## . Proposed treatment or procedure \n\n## . Alternate treatment opti ons (medi ca l, surgical) \n\n> Disclosure of key facts\n\n## . Risks/ be nefits of proposed treatment & a lt ernatives 0 Co mmon complications 0 Rare but major complica ti ons \n\n## . Risks of refusing treatme nt \n\n## . Role of residents & medical stu de nts \n\n> Ot her disclosures if applicable\n\n## . Anti ci pated additional procedures \n\n## . Financial conflicts \n\n Disclose the student's ident ity and training status to the patient and ask for consent 76% \n\nBefore surgery, a patient (or their su rrogate) should be briefed about the risks, benefits, and alternatives to the procedure and authori ze the plan. A physician should ba lance their responsibility to train medical students wi th their ob li gation to provide optimal care (nonmaleficence) while upholding the rights of the patient (autonomy). If a student wishes to assist in surgery, the attending surgeon should inform the pati ent about the student's identi ty and lev e l of t rai ning, and the pati ent must give informed consent for participation. As w i th any other decision, the pati ent has the ri ght to refuse student involvement in their care at any time. \n\nEx ce ptions to sta ndard informed cons ent 128 1\n\n Lif e-thr eatening emergencies The patient lacks decision-ma kin g capacity, but their surrogate has authorized intervention. The patient decided to w aive the legal right of informed consent. Disclosing may pose a t hreat to the patient or affect their decision-making capacity (i.e., th erape utic privilege) .Ethics & Communication this exception does not cover procedures for unrelated issues that are not imminently life-threatening. (For e.g if you find a cancer incidentally that requires you gastrectomy, do not resect unless you have patient consent) \n\n Assent , defined as agreement with treatment , is ideally obtained from a minor but is not required to proceed with treatment. Parents cannot refuse life-saving treatment for their child in emergency situations. If a parent refuses medically necessary care for a child in such a situation, life-saving treatment should proceed without consent. \n\nThis exception applies only when treatment is clearly in the best interest of the patient (eg, may not apply in a child with terminal cancer). \n\n In a nonemergency situation in which a parent refuses potentially life-saving treatment for their child, the physician should seek a court order mandating treatment. A parental decision to decline routine immunization for an unvaccinated child is often tolerated as the risk of acquiring infection in a community with herd immunity is relatively low. In contrast to elective vaccination, if a patient is at high risk of tetanus infection from the deep puncture wound, administration of tetanus vaccination is urgent & should be done regardless of parental consent. \n\n In patients with divorced parents, only parents with custody may give consent for medical care. Parents with joint custody are each able to consent, but consent from only one parent is all that is necessary to \n\n867 https://t.me/usmleinnercircle USMLE Inner Circle \n\n0Exceptions to informed consent by parent/guardian in mi no rs \n\n# . Condition in which tr eat me nt delay \n\nEmergency care can cause serious impairment or death \n\n# . Parent \n\n# . Married \n\nEmancipated minor . Military service \n\n(adolescents) . Financially independent \n\n# . High sc h oo l graduate \n\n# . Homeless \n\n# . Sexually transmitted infection \n\nSpecific medical care . Substance use disorder (most states) \n\n(adolescents) . Pregnancy care (m ost states) \n\n# . Contraception \n\nC) Adm it t he patient and init iate appropriate treatment 74% A lth oug h pa rental consent is usually required before minors (children < 18 years of age in most US states) receive medical care, it does not apply in emergency situations in which there is a legal obligation to tre at in order to save a child's life or limb. Since severe neonatal hyperbilirubinemia has a very high risk of permanent brain damage and death, it is a life-th reatening medi ca l emergency and immediate the rapy is necessary. If the medical condition threatens t he child's life or limb and the effect ive t reatment can be delayed for a short while (e.g., early-stage cancer), a court order should be obtained if parents refu se the treatment, assuming all other measures to convince the parents have failed. Parental refusal to consent to t herapy is l ega lly permitted when there is no risk of serious harm to the minor (e.g., for most vaccination refusal s) or whe n the minor has a terminal condition that does not have any effective treatment (e.g., advanced metastatic cancer, certain high-grade brain tumors). Ethics & Communication proceed with treating the minor, especially when the decision is clearly in the child's best interests. In all cases, treatment is ideally discussed with both parents to reach an agreement that will help the child and facilitate cooperation between the treatment team and the parents. Obtaining informed consent from patients with mild intellectual disability may require Recruiting assistance from family members (eg, mother) to explain the information in familiar terms Explaining information in simple language (eg, \"gallbladder is sick and needs to be taken out\") Using visual aids (eg, illustration of gallbladder) Choosing a comfortable setting with minimal distractions (eg, quiet room) If, following further discussion, the patient demonstrates decision-making capacity and refuses surgery, that refusal should be honoured regardless of underlying intellectual disability if the patient does not demonstrate decision making capacity, ask the surrogate to make decision .\n\nCapacity \n\n Patients with psychotic illness do not necessarily lack decision-making capacity. If a patient's psychotic symptoms do not interfere with understanding or ability to communicate a choice regarding medical treatment, the patient has the right to refuse treatment , even if it would be lifesaving .e.g if patient has mild schizophrenic symptoms like hearing voices but is effectively communicating a choice with understanding, Respect that ! \n\n Competency is a legal determination (made by a judge) about a patient's global decision-making ability. In contrast, capacity is a clinical determination (made by a physician) about a patient's ability to make a specific medical decision at a specific moment in time. Irrespective of state laws, if a physician believes that a patient cannot drive safely , the physician must share their concerns with the patient and ask them to stop driving until they have been evaluated and \n\n868 https://t.me/usmleinnercircle \n\n \n\n> Assessment of decision-making capacity Criteri on Patient task Communicates a choice Patient ab le to clearly ind icate preferred treatment opt ion\n> Understands information provi ded Pati en t u nde rstands condition & t re atm ent op tions\n> Appreciates co nsequences Patient ack nowl edges hav ing co nd iti on & li ke ly consequences of tr eat ment options, inc luding no tr ea tme nt\n> Rationale gi ven fo r decision Patient ab le to weigh risks & benefits & offer reasons f or dec isi on\n\n\"I understand th at you want to go home but you have to stay at th e hospital for as long as you are intoxicated.\" SO %\n\nThis p at i ent is able to sta te his choice (no tre a tm ent), but his understandin g, appreciation of the rel eva nt facts, and ability to describe the reasoning for his decision are mo st likely impaired by acut e alcohol i ntoxication. As the patient curre nt ly does not have de ci sion -making capacity and discharge would seriously endanger his h ea lth , he should remain at the hos pit al until sober. If a patient's decision-making capacity is temporarily impaired (e .g., becau se of alcohol intoxication) and th eir condi tion is not lif e-t hr eatening but requires hospitali za tion , admission and reasse ss ment of the de ci sion when the impairment h as subsided are necessa ry .Ethics & Communication treated by a driver rehabilitation specialist. \n\nSurrogate \n\n Physicians can assist distressed surrogate decision-makers by guiding them in applying substituted judgment (ie, acting on what the patient would have wanted rather than the decision-maker's feelings or preferences). The following techniques may be helpful: \n\nRefocus the discussion on the patient, by asking what the patient was like before the illness. This step brings attention to the patient's goals and values and builds trust between the physician and surrogate. \n\nHelp surrogates apply their knowledge of the patient's goals to the current situation using objective clinical information (eg, prognosis, potential complications). \n\nEmphasize shared decision-making . The physician should offer close, empathetic guidance and make recommendations based on the patient's medical condition and information shared about the patient. This step can reduce the burden of decision-making for the surrogate and alleviate feelings of guilt. \n\nLeave Against Medical Advice \n\n869 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nHierarchy of substitute decision makers \n\nHigh.st authority Patient-designated proxy (eg, durable power of attorney) Co urt-appointed guardian., \n\nSpouse/partner Adult children Next of kin Parents (default surrogate) Adult siblings Other adult relatives \n\nLowest authority Unrelated friends \n\n Decisions guided by substituted judgment standard (ie, wh at the patient woutd have chosen ). \n\n.. Usualy appointed only~ the patient ts not compe tent to desiOnate a proxy. \n\nNext-of-kin surrogate decision maker \n\n## . Inabi li ty to communi ca te wishes regarding medical decision-making \n\nPatient selection . Advance di rective not available or applicable \n\n## . No previously des ignated surrogate decision maker \n\nSurrogate selection . Priority to patient's spouse \n\n## . Alternate: adult childr en , parents, adu lt siblings, other family members \n\nImplementation . Substituted judgment: what the patient, not family, would have wanted \n\n## . Decisions in the patient's best interest Ethics & Communication Confidentiality \n\nLimitations to adolescent confidentiality include determinations of imminent risk (eg, suicidality, homicidality) and threats to safety (eg, sexually abusive relationships, intoxicated driving). Additional risks to confidentiality should also be discussed with adolescent patients, including \n\nguardian access to information through the electronic medical record and patient portal, direct medical record requests , and insurance/billing statements. \n\nWhen confidentiality must be breached, it should be discussed first with the adolescent , who should be given the option to approach the topic with the guardian. \n\n Adolescent confidentiality regarding sensitive issues, including treatment for sexually transmitted infections, mental health concerns, and substance use, should be protected. When \n\ntransferring care , it is preferable to provide the medical record directly to the new provider \n\nrather than providing a copy to the parent. Physicians are ethically obligated to protect patient confidentiality .Unless a patient is at active risk of harm to self or others , physicians cannot disclose information to family members without the patient's consent. \n\n870 https://t.me/usmleinnercircle \n\nManagement of AMA discharges \n\n## . Financial concerns: involve social workers \n\nInvesti gat e/ addr ess Substance withdrawal: offer medication-assisted tr eatment .rea so ns for lea ving Care delay dissatisfaction: apologize for unmet expectations .. Determine t hat patient: \n\nEnsure/document p at ient's 0 H as ca pacity fo r medical decision-mak i ng \n\ninformed refusal 0 U nd erstandsb enefits of staying & risks of leaving \n\n> 0\n\nCommunicates reasoned basis for refusing treatment \n\n## . Document informed refusal in chart, inc luding signed AMA form \n\nPro vi de best possible . Offer appropriate treatments/prescripti ons \n\nalternative treatment . Offer assistance with follow-up care \n\n## . Offer to resume treat ment at an t ti me AMA = against medical advice. \n\nAdolescent nonsuicidal self-in ju ry \n\n## . Deliberate inju ry wit h no intent to die Fea tu re s . Methods: cutting, burning, scratching \n\n## . Typical onset: age 12 -1 4\n\n## . Regulate distressing emotions \n\nFunction/purpose . Punish se lf \n\n## . Elicit support or all ow for avoidance (eg, mi ss ing school) \n\n## . Psychotherapy \n\nManagement P syc hiatric eva l ua tion, me dications f or comorbid conditions .. Consider informing parents if any of the fo ll ow ing are present: \n\n> 0\n\nSuicidal ideation \n\nConfidentiality vs safety 0 Impairment, distress \n\n> 0\n\nMultiple episodes, escalating frequen cy \n\n> 0\n\nSingle episode with serious medical risks (eg, use of r azor , sut ures) Ethics & Communication Because vital details can influence the course of treatment, physicians are allowed to receive collateral information from concerned parties without obtaining patient consent, particularly in emergency situations (Choice E) . However, the physician's role must be limited to passive listening and the physician cannot reciprocate or engage in discussion of privileged information \n\n The Health Insurance Portability and Accountability Act (HIPAA) protects health information by requiring \n\nverbal or written authorization for release of information. Hospitals and physicians' offices frequently have additional policies requiring written forms for release of information and procedures to verify the identity of phone callers. It is important that health care providers be familiar with these rules and \n\ndisclose only the minimum necessary information .\n\n HIPPA does not require the provider to obtain proof of identity of phone callers. \n\n871 https://t.me/usmleinnercircle USMLE Inner Circle \n\n## --\n\nReceiving collateral information \n\n# 0Phys icia npassively liste ni ng to \n\n> CI.J'.\\,\\:)fld\n\n# IConcerned fam il y or friend Reciprocating information Ph ysicia n sh aring Co ncerned priv il eged information with fami ly or frie nd \n\nG Sending protected health information from a personal electronic mail address 83% Covered entities should only access or transmit electronic protected health information (ePHI) from a system that has \n\ntechnical safeguards to generate audit trails (i.e. , access logs to identify all individuals who int eract with ePHI) and prevent unauthorized access (e .g., password prot ection , automatic logoffs, encryption, secure network s). The transmi ss ion of PHI to or from a health care provider's personal electronic mail is a severe violation of the HIPAA Security Rule and may even result in the health care provider being charged with data theft because it leaves the PHI vulnerable to third parties. Other examples of HIPAA Security Rule violations include downloading PHI on an unauthorized device and leaving PHI in a place accessible to third parties. These violations are likely to occur when health care providers int eract with PHI in an unsecured system (e.g ., at home to complete patient notes, at a workstation that is accessib le to patients, discussing care with a colleague over texting applications). The HIPAA Security Rule al so requires covered entities to impleme nt administrative safeguards (e.g. , training personnel about HIPAA provisions) and physical safeguards (e.g. , locking cabinets or data servers with PHI, privacy filters for computer screens) to ensure that PHI is generated, stored, accessed, and transmitted securely. Violations of the HIPAA Privacy Rule include releasing PHI without patient authorization, after the expiry of the authorization time limit, or to unauthorized individuals (e.g ., health care providers not involved in the patient's care). The exceptions to the requirement for patient authorization include disclos ur es for treatment, payment (e.g ., claim reimbursement), and health care operations as we ll as disclosures mandated by law (e. g., notifiable diseases, elder or child abuse, organ or body donation). In these cases , the degree of disclosure must be limited based on the minimum necessary standard. \n\nG Reject the patient's request 81% Medical records are legal documents; the information provided should be complete and accurate. Intentional falsification of medical records may constitute misconduct and lead to se rious consequences for the physician, even if the medical care provided was appropriate. Th erefore, the physician should reject the patient 's request and r eass ure him that his records are treated confidentially. Under HIPAA, patients can request changes to their medical records if they consider them incomplete or inaccurate by placing a formal request to the covered entity. Th e covered entity should correct the medical record if the information is in complete or inadequate and when making changes, a strikethrough (i.e. , a line drawn through the text) should be applied to written and / or electronic notes but still remain legible to avoid ambiguit y. All amendments shou ld be dated and signed by the covered entity. Ethics & Communication Bad News \n\n When delivering bad news , a face-to-face visit in a comfortable private setting is preferred as it allows the physician to respond to nonverbal aspects of communication and provide empathy and emotional support as needed. It is also important to assess the patient's understanding of the condition and how much the patient actually wants to know. Patients have the right to know or to decline discussion of their diagnoses. When a patient declines, the physician should ask the patient to choose a family member with whom the diagnosis can be disclosed; doing so ensures continuity of information should the patient choose to be informed later. \n\n## Communication \n\n Decisions about whether to accept gifts from patients include the cost , type , and timing of the gift and the motivation behind giving it. Gifts should not be accepted from patients experiencing a mood episode potentially affecting their judgment. Gifts that are clearly extravagant , inappropriately intimate , or given to secure preferential treatment should not be accepted. The patient's motivation is the most important factor to consider because it is unethical to accept gifts motivated by the desire to influence the physician's behavior or by expectations of preferential or special treatment. The most appropriate response is to express appreciation for the gesture but decline the gift and assure the patient that he will continue to receive the same standard of care. \n\n872 https://t.me/usmleinnercircle \n\nSPIKES protocol for delivering serious news \n\n# . Arrange for a private, comfortable setting Set the stage . Introduce patient/family & team members \n\n# . Maintain eye contact & sit at the same level \n\n# . Schedule appropriate time interval & minimize interruptions Perception . Use open-ended questions to assess the patient's/family's perception of the medical situation Invitation . Ask patient/family how much information they would like to know \n\n# . Remain cognizant of cultural, educational & religious issues \n\n# . Warn the patient/family that serious news is coming Knowledge . Speak in simple & straightforward terms \n\n# . Stop & check for understanding Empathy . Express understanding & give support when responding to emotions Summary & strategy . Summarize & create follow-through plan, including end-of-life discussions if applicable \n\n> Counseling patients in clinical uncertainty Introduction\n\n# . Establish rapport & express conce rn \n\n# . Assess patient's knowledge & understanding of current facts \n\n# . Review established facts \n\n> Data revi ew\n\n## . Explain differential diagnosis (individualized) \n\n## . Clearly state level of uncertainty \n\n## . Recommend plan to c lar ify diagnosis (eg, tests, specialty consultation) \n\n> Plan of care\n\n## . Emphasize shared decision-making \n\n# . Arrange for follow-up Ethics & Communication Counseling a patient in the setting of clinical uncertainty should convey the potential seriousness of the situation and include an individualized discussion of differential diagnosis based on known facts of the case. The degree of uncertainty should be acknowledged . The discussion should also explain the need for further evaluation , include a clear plan for follow-up , and allow the patient an opportunity to ask questions .\n\nInterpreters \n\nUse qualified medical interpreters , either trained staff (ie, with training in interpreter ethics, skills, and medical terminology) or videoconference or telephonic systems. To optimize patient comfort and communication, providers should directly address the patient rather than the interpreter, maintain frequent eye contact with the patient, and speak in short sentences to allow for accurate translation. \n\nProvide translated written materials (eg, discharge or appointment summary) directly to patients when possible; such materials should accompany (ie, not substitute for) active patient counseling. Having bilingual family members translate English materials is not recommended due to potential for error; minor children should not be asked to interpret or translate in non-emergency situations. Use patient teach-back , in which patients describe their understanding of a treatment plan to the provider (eg, asking this patient to describe how she will take her new medication). This technique confirms patient understanding and allows clarification of miscommunicated information. Patients who participate in teach-back are more likely to use medications as prescribed and experience fewer medication errors. Ad hoc interpretation, referring to temporary interpretation by nonqualified individuals (eg, bilingual or partially fluent family members or medical staff), generally is not recommended due to error risk. However, ad hoc interpretation may be necessary in limited situations which meet the following conditions: the patient has an urgent medical need (ie, presenting with acute symptoms in urgent care setting) and appears ill (eg, restless, coughing, flushed) qualified interpreter services are not reasonably accessible (ie, system is inoperable) delaying care (eg, rescheduling the visit after services are restored) to access interpreter services may result in preventable patient harm (eg, undiagnosed illness leading to rapidly worsening symptoms). \n\n873 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\n@ \"I ca nnot accept yo ur i nv ita ti on becau se it would compromise your son's medi ca l ca re.\" 80% 0Third par ti es often make decisions that affect the patient's heal th and we lfare and are vulnerable to a physician's influence. Init i at ing a personal rel at ionship w it h a third party who is close to the pati ent (e.g. , pa rent, spouse, partner) an d plays an integral ro le in t he patient's medical decision-making process is therefore inappropri ate as it can compromi se t r ea tm ent (as we ll as au tono my and patient privacy in pat ient s w i th decision-maki ng capac it y and l ega lcompet ence). Such relationships ca n limit th e physician's objectivi ty , expl oit th e trust of t he t hird party , and negatively affect the patient 's wel l-being, wh ich is w hy t he invitat ion should be declined. Whil e roma nti c or sexual rela ti onships between physicians and curr ent patients are always unethi ca l, physicians (excluding psych iatr ist s) may engage in romantic or sexual relationships with patients if more than 1-2 years have passed since term ination of the patient-physician rela ti onship. Psychiatrists are in a special positi on of influence ov er their patient s and sh ould never engage in such relationships with current or former pa t ients. Ethics & Communication Behaviour Interventions \n\n Food deserts are identified as low-income communities that have limited access to healthy food. When addressing this barrier, communication should be nonjudgmental to foster collaboration, enhance patient motivation, and develop a practical treatment plan. \n\nHelpful information can be found within the USDA's Economic Research Service on both food deserts and food and nutrition assistance programs (eg, which may help address the patient's financial burden). \n\nMotivational Interviewing \n\n874 https://t.me/usmleinnercircle \n\nLifestyle modification \n\n## . Dietary improvements (eg, DASH diet) \n\nBehavioral changes . Regul ar exercise (eg, >150 min/week) \n\n## . Disease prevention & risk factor management \n\n## . Provide specific guidance rather than vague advice (eg, \"eat better\") \n\n## . Tailor counseling to the patient (eg, cultu ra lly preferred foods) \n\nClinician role . Apply motivational in terviewing & a partnership approach \n\n## . Assist patient in setting focused goals (ie, SM ART goals) \n\nDASH = Di etary App roaches to St op Hy pertension ; SMART = Sp ecific, Measurable , A ttai nab le, Relevant, Ti me bound. \n\nBehavioral interventions for weight loss \n\n## . Maintain stocks of easy-to-prepare, healthy fo ods \n\nStimulus control . Store healthy foods in prominent locatio ns \n\n# . Li mit stocks of less healthy foods \n\n## . Moderate-to-intense ae robic exercise \n\nPhysical activi ty . Resistance/strength training \n\n## . Lifestyle activity (eg, take stairs, reduce sitting time) Regular documentation of: \n\nSelf-monitoring . We ight . Food intake I\n\n## . Exercise \n\nAccountability/ . Provider visi ts , phone calls, Internet contacts \n\nfollow- up . Group participation sessions \n\nMotivational interviewing: components \n\n## . Start a nonjudgmental, open-ended conversation \n\nEngaging . Collaborate to se t the agenda \n\n## . Elicit patient strengt hs \n\nFocusing . Ask the patient to identify 1 or 2 behavior targets \n\n## . Elicit change ta lk to get the patient's: \n\nEvoking 0 Commitment 0 Rea so ns to change \n\n## . Guide the pati en t toward : \n\nPlanning 0 Identifying specific next steps \n\n> 0\n\nAnticipating obstacles \n\n> 0\n\nDe ciding how to meas ur e success Ethics & Communication In adolescents unable to change their eating behaviour, involving the parents to promote healthy eating habits at home is commonly beneficial. Regular Followup is also recommended \n\nStages of Change \n\n## Health Literacy Medication \n\nMedication Adherence \n\n875 https://t.me/usmleinnercircle USMLE Inner Circle \n\nStages of change model Stage Motivational intervie wi ng \n\n## . En co ur age patient to eva lu ate conse quences of \n\nNot ready to change: patient does not acknowledge c ur re nt behavior \n\nPrecontemplation negati ve co nseq uen ces Exp la in & pe rsonal iz e the ris k.. Recommending action is premature \n\nThinking of changing: patie nt acknowledges . Encourage eva luation of eros & cons of behavior \n\nContemplation consequences but is ambivalent ch ange \n\n## . Promote new, positive behaviors \n\nPreparation Ready to change: patient decides to change . Encourage small initial steps \n\n## . Re infor ce positive o utcom e expec tations \n\n## . He lp identify appropriate change strategies & en list \n\nAction Making change : patient makes specific, overt changes social su pport \n\n## . Prom ote self-efficacy for dealing w ith obstacl es \n\nMaintenance Changes integrated i nto patient 's lif e ; foc us on relap se . Follow-up support ; reinfor ce i nt rin sic r ewa r ds \n\n12 re vention . Develop relapse prevention strategies \n\nIdentification Behavior is automatic: changes incorporated int o . Pr aise chang es sense of se lf \n\nLow health literacy Definition & . Poor comp rehension of health information that impairs dec ision-making \n\nrisk factors . Affects all demographic groups; more common in low SES , elderly, minority groups \n\n## . Poor doctor -patient communication \n\n## . Inadequate preventive care \n\nAdverse . High eme rgency department use \n\noutcomes . Medication errors & nonadherence . Worse health stat us \n\n## . A sk ing few or no questions du ring the visit \n\nClinical . Asking to take materials home to read ove r with others \n\nclues . Inability to recall medication names, dosages, or indications \n\n## . Frequent missed appointments \n\nStrategies for . Use plain language & avoid excessive detail . Use visual aids & \"teach-back\" \n\nmanagement Use empat hetic communication, encourage questions .\n\nSES = socioeconomic status. \n\n- - - - - - - ------Ethics & Communication Medication Non-adherence Adverse Drug Events \n\n876 https://t.me/usmleinnercircle \n\nStrategies to promote medication adherence \n\n## . Include patient in de cisio ns (formulation, frequency, timing of dosing to match preferences/activiti es of daily living) \n\n## . Simplify regimen: \n\n> 0\n\nOnce daily dosing if feasible \n\n> 0\n\nUse fewest drugs possible \n\nPhysician Education/addressing barriers: \n\ninterventions . 0 Provide clear instructions, discuss perceived severity of illness, benefits of medication \n\n> 0\n\nAddress barriers such as misunderstanding, cost, adverse effects \n\n## . Nonjudgmental inquiry regarding adherence at follow-up visits \n\n## . Adherence aids: \n\n> 0\n\nElectronic reminders \n\nExternal 0 Pill boxes \n\nreinforcements 0 Pair with other activities (eg, breakfast) \n\n## . Family support \n\nMedication nonadherence \n\n# . Com plex treatment regimen \n\n## . Adverse drug effects \n\nRisk factors . Ex pe nsive drug regimen/limited patient financial resources . Little immediate or apparent benefit of medication \n\n# . Inadequate physician supervision & wr itten instruction . Integration into daily habits/schedule \n\n## . Pill organizers & dispensers \n\n# . Simplified treatment regimen \n\nInterventions to improve adherence . Automated reminders (eg, smartphone applications) \n\n# . Frequent telep ho ne contacts & interprofessional (eg, nurse, phar mac ist) follow-uo \n\n# . Motivational interviewing \n\n## . Consolidated refill schedule \n\nRecognizing medicat ion nonadherence \n\n Unexpected loss of d is e ase contro l\n\nSuggestive features Poor understanding of drug indication & schedule Frequent r eports of adverse drug effects Review schedule & dos i ng instruc tions \n\nPossible interventions Educate pat ient on purpose & how to take medicat ion Redu ce/conso lid ate medication l ist Increase fr eque n cy of follow-up \n\nAddressing barriers to adherence to anti hypertensive therapy \n\n# . Insight: provide education, shared decision- mak ing \n\nPatient . Cognitive cha ll enges (eg, depressi on ): diagnose & treat \n\n# . Side effects: change medication/dosing \n\n# . Lack of rapport: arrange for same provider, maintain communication \n\nPhysician . Complex regimen: prescribe fixed drug combination, once-a-day dosing \n\n## . Inadequate follow-up: make fo llow-ue aeeointments; reschedule missed visits \n\nHealth care . Expensive medications: prescribe generics & preferred formulary drugs \n\nsystem . High coinsurance: orde r routine tests yearly, be aware of costs Ethics & Communication Prescriptions should communicate plain-language instructions (eg, \"morning and before bed,\" rather than \"twice a day\"), intervals (eg, \"wait 1 hour before second dose\"), and limits (eg, \"maximum 2 pills per day\"). To prevent errors, multiple care team members should verify medications independently with the patient. This technique represents redundancy , a safety strategy used to reduce errors in complex, high-risk organizations (eg, health care, aviation). \n\nMedication reconciliation (ie, the process of reviewing and updating the current medication regimen) \n\nshould always involve direct conversation with the patient (when cognitively intact), address both prescription and nonprescription medications (including supplements), and include inspection of medication bottles if available. Other best practices for medication reconciliation include the following: \n\nInterprofessional review, including physicians, nurses, and pharmacists; each provider should review medications independently with the patient Brief, updated review by the ordering physician prior to placing or renewing medication orders \n\nAntibiotic Use \n\n## Alternate Therapies \n\n The initial response to a patient who requests an alternative approach is to explore the reasons for requesting a different treatment .Physicians must be prepared to discuss the risks and benefits of complementary and alternative approaches to treatment and be open to integrating modalities with proven safety and efficacy. When discussing a patient's use of nonstandard therapies that are known to be harmful, the physician should clearly explain the risks to the patient. \n\n877 https://t.me/usmleinnercircle USMLE Inner Circle \n\nPreventable adverse drug events Risk factors Sample corrective strategies \n\n## . Polypharmacy \n\n## . Low health literacy \n\nPatient . Very young or advanced age \n\n## . Communication barriers . Increased checkpoints in medication reconciliation \n\n# . Nonadherence/lack of follow-up (eg, multiple providers) Vague prescriptions . Plain-language medication counseling \n\n## . Patient \"teach-back\" (ie, patient describes .. Incorrect medication reconciliation Provider understanding of treatment in own words) \n\n## . Absence of counseling \n\n## . Illegible handwriting \n\nMedication . Look- or sound-alike drugs (eg, prednisone/prednisolone) \n\nReducing antibiotic use in URI & acute bronchitis Patient . Careful history & examination to rule out pneumonia & other serious illnesses assessment . Patient's understanding of causes & natural history of illness \n\nPatient . Expla in expected duration & self-limited course of illness education . Explain potential harm & lack of efficacy of antibiotics \n\n## . Refer to infection as a \"cold\" or \"chest cold\" \n\n## . Symptomatic treatment: OTC (eg, guaifenesin, tea with honey) & prescription (eg, benzonatate) options \n\nManagement . Consider delayed antibiotic prescription (ie, prescription to be filled only if no improvement occurs after predetermined lime) \n\nOTC= over-the-counter; URI = upper respiratory infection. Ethics & Communication If the patient insists on using such therapies, the physician should schedule close follow-up to strengthen the therapeutic alliance and monitor for toxicity. \n\n## Intimate Partner Violence \n\n The United States Preventive Services Task Force (USPSTF) recommends that screening be performed in all women of childbearing age. \n\n Also routine postpartum screening for IPV is required soon (eg, 3-6 weeks) after delivery. \n\n A high degree of clinical suspicion for IPV must be maintained. When somatic symptoms do occur, they are often nonspecific (eg, headaches, back pain, chronic abdominal or pelvic pain ). Additional clues may be present, such as resistance to being evaluated alone and multiple medical visits with varying health care providers (eg, emergency visits). Physical examination findings may include unexplained bruising on the head, neck, abdomen, or genitals; however, patients can have a normal examination. Patients with suspected IPV should undergo screening. Because this is a sensitive topic, providers should begin with a normalizing statement (eg, \"I sometimes see patients with similar pain that is caused by not feeling safe\") and proceed with both open-ended (eg, \"How safe do you feel in your relationship?\") and specific (eg, \"Have you ever been hit by your partner?\") questions to encourage disclosure. \n\n## Sexual Assault \n\n878 https://t.me/usmleinnercircle \n\nIntimate partner violence \n\n## . Routine annual examination Evaluation . Suspicious signs/symptoms (eg, bruising) \n\n# . Prenatal visits \n\n# . Homicide \n\n# . Mental health disorders (eg, PTSD) \n\n> Consequences\n\n# . Unintended pregnancy \n\n# . Pregnancy complications (eg, abruptio placentae) \n\n# . Sexually transmitted infections \n\n# . Safety planning (eg, local shelter referral) \n\nManagement Psychosocial counseling . \n\n> PTSD = posttraumatic stress disorder.\n\nSexual assault Postexposure prophylaxis for sexual assault \n\n## . Physical and forensic examination (eg, hair, semen) \n\nEvaluation . Psychologic assessment \n\nInfection Medication Chlamydia Doxycycline \n\n## . Mental health disorders (eg, PTSD) \n\nConsequences . Unintended pregnancy Gonorrhea Ceftriaxone \n\n## . Sexually transmitted infections \n\n## . Postexposure prophylaxis \n\nTrlchomonas Metronidazole \n\nvagina/is \n\nManagement . Emergency contraception \n\n## . Psychosocial counseling HIV Multidrug regimen (eg, tenofovir-emtricitabine with raltegravir) \n\n> PTSD =posttraumatic stress disorder .\n\nHepatitis B Hepatitis B vaccine hepatitis B immunoglobulin Ethics & Communication Patients who experience sexual assault are at high risk for developing PTSD , depression , and \n\nsuicidality .\n\n## Pregnancy \n\n Routine prenatal care should include an informed consent discussion that anticipates clinical complications necessitating a cesarean delivery .This process should include a clear description of indications , risks , and benefits as well as an opportunity to address the patient's specific concerns and questions. \n\n This is known as Preventive Ethics \n\n Can a pregnant woman with capacity refuse cesarean section if vaginal delivery would put the unborn child at risk? \n\nYes \n\na pregnant woman with capacity has the right to refuse treatment, regardless of risk to the unborn child \n\n When maternal and fetal interests conflict (which commonly occurs in pregnancy), medical decision-making is often based on prioritizing maternal health (ie, maternal beneficence) over fetal interests. Patients may desire a cesarean delivery in the absence of maternal or fetal indications. Physicians who are uncomfortable performing cesarean deliveries on maternal request should refer these patients to another obstetrician-gynecologist. \n\n## Adolescence \n\n Disclosure of an HIV diagnosis to a child with perinatally acquired infection should occur by adolescence to foster patient autonomy , increase medication adherence , and prevent transmission .The physician should respect the family's concerns and offer joint participation in establishing a timeline and plan for disclosure to the child. Emphasizing collaboration between the physician and family (eg, \"let's first talk\") is the most appropriate approach to best serve the child's health. Collaboration with the mother is needed to establish a detailed plan for disclosure , which should specify the timing, approach, and extent of information sharing, all while validating and respecting the mother's concerns. Having this collaborative discussion supports the parent by allowing her to rehearse a difficult discussion. Discussions regarding advance care planning for adolescents with chronic, life-limiting illnesses (eg, cystic fibrosis) should take a family-centered approach and involve the adolescent patient alongside the parents. \n\n879 https://t.me/usmleinnercircle USMLE Inner Circle Ethics & Communication Discussion should include information regarding prognosis, care options, and the patient's and family's preferences for end-of-life care. In pediatric populations, there is added complexity of integrating respect for parent authority with the obligation to be honest with patients. At times, parents request that information be withheld from their child, forcing the physician to balance obligations to the patient with parent wishes. However, the physician's primary duty is to the patient .In pediatric patients with a chronic or terminal illness and poor prognosis, the patient's understanding \n\nshould first be determined before making a detailed plan with parents for disclosure . Drug testing adolescents without their knowledge is inappropriate . Parents requesting surreptitious drug testing should be engaged to understand their specific concerns , educated about the limitations of drug testing , and informed about the need for private patient evaluation .\n\nGenetic Testing \n\n Testing in children is typically performed based on the onset of disease . Tests for genetic conditions with an early onset of disease (eg, cystic fibrosis, phenylketonuria) are performed because early diagnosis affects management in childhood. In contrast, genetic testing in children for an adult-onset condition (eg, breast cancer) is typically not recommended because it usually does not affect patient care (eg, frequency of monitoring) or prognosis. When there is no impact on the child's medical management or prognosis, genetic testing to predict future disease risk should be deferred until adulthood to ensure informed consent. \n\n## Geriatrics \n\nFalls \n\n880 https://t.me/usmleinnercircle \n\nFalls in older adults Overview . Leading cause of injury, morbidity, mortality \n\n## . History of fa ll \n\n> Risk factors\n\n# . Sensory & cognitive dis tur ba nce \n\n## . Chronic disease (eg, T2DM, arthritis, CVD) \n\n## . Medica ti ons (eg, neurol ept ics, antidepressants, vasodilators) \n\n# . Screening: musculoskeletal (eg, \"get up & go\" test*), vision, hearing, bone density, orthostasis \n\n> Outp atient prevention\n\n# . Medi ca ti on & home sa fe !}'. r ev iew \n\n## . Correction of vitamin D deficiency (in select patients) \n\n## . Su~ervised exercise ~rogram \n\n# . Assess fall risk & customize strategies to patient's specific risk factors \n\n## . Optimize environment (eg, minimize furniture, l ower the bed, place in direct vi ew of n ur ses if high risk) \n\n> Inpatient preve nt ion\n\n## . Perform frequent checks on high-risk patients \n\n## . Avoid restraints & overreliance on fall alert systems \n\n> *Ask the patient to rise from achair &walk briskly to the end of the room .nme\n\n& patient difficulty in this test predict the risk of falling. \n\n> CVO =cardiovascular disease; T2 0M =type 2 diabetes mellitus.\n\nEthics & Communication Supervised exercise training has been shown to significantly reduce fall risk and should be \n\nrecommended for all elderly patients who are at high risk for falls (or who have sustained a fall previously). \n\nElder Abuse Medication Prescription \n\n e.g: Ketorolac 0.5% solution, 1 drop in right eye, four times daily ( DO NOT use BD, OD etc) \n\n881 https://t.me/usmleinnercircle USMLE Inner Circle \n\nElder abuse \n\n## . Female \n\n## . Dementia, chron ic mental ill ness \n\nRisk factors . Functional impai rmen ts \n\n## . Social isolation \n\n## . Shared l iv ing environment \n\n## . Poor socioeconomic status/financial stress \n\nPhysical & sexual abuse \n\n## . A~e ical ab ra sions, lacerations, contusions, fra ct ur es \n\n## . Pain not consistent with repo rt ed et iol ogy \n\n## . Anogenital injuries \n\n## . Newll ac guir ed STI \n\nPsychological & verbal abuse \n\n## . Chan9e in behaviorteersona li ~\n\n## . De eression/anxie~ \n\nManifestations of abuse Neglect \n\n## . In ade quate nutrition or hydr at ion \n\n## . Pressure injuries \n\n## . Deterioration in comorbid conditions \n\nFinancial exploitation \n\n## . Failure to adhere to med ication regimen \n\n## . Mulliele missed appo intments \n\n## . Unpaid expen ses or rent payments STI = sexually transmitted infection. \n\nMedication prescribing in elderly patients \n\n## . Increased suscept ibil ity to ADEs \n\nMajor cons ider ations . Increased po l yp harmac y risk due to multiple chronic cond itions \n\n## . Susceptibility to harms from o vertre atmen t & u ndertreatment \n\n## . Limit the number of prescribers \n\nPrincipl es . Review criteria for geriatric populations (eg, Beers ,* START .. )\n\nof prescribing . Consider time to benefit for drug \n\n## . Tailor reg i men to the patient's goals & life expectancy \n\n## . Frequently reassess a p propriateness of medication \n\n* Be ers criteria: list of medications considered po tentially ina pp ro priate or to be used with caution in the elderly. \n\n'\"*STA RT criteria: used to identi fy potential harm of withholding specific drug in older patients. \n\nADEs = adverse drug events; START= Screening Tool to Alert to Right Treatment. Ethics & Communication Violent Patient \n\n When dealing with an angry patient , the most appropriate response is to remain nondefensive ,\n\nacknowledge that the patient is upset , and begin the discussion with an open-ended question. \n\nMay I ask what is upsetting you so I can help you? \n\n882 https://t.me/usmleinnercircle \n\n0 Penicillin V, 500 mg, orally, tw ice a day, for 10 days 88% This prescription is written in precise, simple, and common language and is, therefore, least likely to result in a medication error. First, the dr ug is named sp eci fically (\"Penicillin V\"). Second, the dosage (\" 500 mg \") describes the drug strength in cl earl y defined units and does not contain traili ng zer os. Third, the route (\"orally\"), fre quenc y (\"twice a day\"), and \n\ndu ration (\"for 10 days\") of administration are all written in plain English; Latin, abbreviations, and acronyms should be avoided because they can be misinterpreted. In addition, it is recommended to indicate the reason for the medication on the prescription (e.g. , \"Streptococcal pharyngitis\"), as this introduces an additional safety checkpoint and opportunity for counseling for pharmacists and collaborating providers, and reminds the patient of the drug's purpose. Other instructions typical ly provided on prescriptions include the number of medication units to be dispensed and the number of refills permitted before the patient 's next follow-up. \n\nBeers criteria \n\n# \n\nRisk factors \n\nWid ely used cr ite ri a developed to re du ce p ote ntia ll y ina pp ropriate prescribing a nd h armful po lyp harmac y in the ge ri atric population. !Delud es> 50 mer ications that should be avoided in eld er ly patients clu e to i efficacy a nd /or t risk of adverse even t s. E xa mp les: a -blo dc rs I ri sk of hn iotc nsion? TcA \n\n /\\ 11ticholincrgics nti clc prcss ant s, anti h ista mi 1c , opioicls (t risk of delirium , sed ation, falls, \n\n ry ret enti on )\n\nt risk of de lirium , sedation, fa lls) I b lee di ng, esp ec ia ll y with co n co mitant anticoagulati on ) PP!s (t risk of C di f{t cile in fection) \n\nAggressive patient in the emergency department \n\n. History of vio l en t behavior/antisocial personality disorder \n\n## . Psych iatr ic illness (eg, ps y cho sis, de lir ium , su ic ida l/homicidal ideation) \n\n## . S ubstan ce u se ; acute intoxication, withdrawal \n\n. Prolonged w ai t times \n\n. A ngry, irrit ab le de me an or \n\n## .Warning signs Lo ud , agg r ess ive speech , cu rs ing , verbal t hr eats Tense post ur e, clench ed fists, pacing .. Desk or wa ll pounding, throwing objects \n\n## . Maintain a distan ce of 2 arm lengths; avoid direct eye contact \n\n## . In terv iew with door open , clinician closer to the exit \n\n## . Verbal dees ca lat ion \n\n> 0\n\nUse calm voice , nonconfrontational approach \n\nManagement 0 Provide for basic nee ds (eg, offer food, drink , blanket) \n\n> 0\n\nListen attentively to clarify patient's wa nt s/ needs \n\n> 0\n\nSet clear expectations th at vio lence is un acceptable; re inf orce that patient will n ot be harmed \n\n> 0\n\nOffer choices if appropriate ( eg , ora l vs i nt ramuscular medications) \n\n## . Chemical & phys ical restraint when verbal deescalation fails & vi ole nce is imminent Ethics & Communication Patients with borderline personality disorder use the defense mechanism of splitting, which can result in polarized views of team members as \"good\" and \"bad\" and create division within the treatment team. Seeing the patient jointly as a team can help provide clear and consistent information and minimize the tendency for splitting to interfere with treatment. \n\n## Physician Impairment Quality \n\n883 https://t.me/usmleinnercircle USMLE Inner Circle \n\nG Reques t the presence of a chaperone 92 %\n\nAs part of the patient-physician re lat ionship, physicians should try to create a comfortable environment in order to build trust and fulfill t heir duty to provide opt i ma l care fo r their patients. Inappropriate patient behavi or can make fulfilling this duty challenging and should be addressed directly. In this scenario, telling the patient that his comment is inappropriate in a polite and direct manner (so as to n ot undermine the therapeutic alliance) and requesting the presence of a chaperone (i.e., an authori zed member of the care team, who can act as an imparti al observer and witness) can help create an environment in wh i ch all parties feel comfortable and respected. Fa mily members and other close contacts are not appropriate chaperones. Additional strategies to prevent inappropriate behavior include asking direct, close-ended questions and performing only medically necessary portions of the examination to minimize contact. \n\nPhysician impairment Definition . Impaired ability to practice medicine competently & safely due to psychiatric/medical illness, a~ . or drug dependency \n\n## . Lateness, unexplained absence s, inacc essibility \n\n## . Unusual rounding times \n\n## . Inappropriate orders , prescriptions errors , incorrect charting Recognit ion . Increased irritability , anger, conflicts with staff & colleagues \n\n## . Ov ert signs of substance misuse/abuse ( eg , excessive drinking at hospital functions, slurred speech, smell of alcohol, poor hygiene, needle marks) \n\n## . Increase in patient complaints \n\n## . Deterioration in clinical performance (usually a late sign) \n\nManagement . Report to PHP \n\n## . Refusal to comply with PHP recommendations may result in the provider being reported to the state medical board \n\nPHP = Physician Health Program. Dimensions of health care quality Dimension Description Safety Minimizes preventable errors \n\n# . Avoids harms from care \n\nEffectiveness . Adheres to scientific guidelines evidence \n\n# . Avoids umler:lraalrne t & overtreatment \n\nPatient-centeredness Identifies patient values, goals & preferences Tailors care delivery to expressed patient values \n\nTimeliness . fil'.QiQ!ii d!ills!lr'.!ii i Qs![!il , reduces wait times \n\nEfficiency Avoids wastin9 or overusin9 resources \n\nEquity . Provides quality care to all individuals regardless of demographic attributes (eg, ethnicity, age, gender) Ethics & Communication Hospital readmissions are used as a quality metric because they are often preventable through improved patient communication and follow-up. \n\nTelephone-based outreach shortly after discharge reduces readmissions rates by preventing loss to follow-up , increasing patient engagement (proactively identifying and addressing potentially serious concerns) and care coordination (effective transition between inpatient and outpatient care). High variation in care of medical conditions for which well-established practice guidelines exist is generally associated with unnecessary use (eg, overuse) of services and lower quality and lower value \n\n(ie, quality of care relative to costs) of care. Evidence suggests that differences in provider practice styles (ie, subjective decision-making, attitudes, and perceptions about treatment) is the leading contributor to variation in clinical performance. Provision of data-driven feedback on a physician's individual clinical performance (eg, cesarean delivery rates) compared to benchmarks and peers is effective in optimizing physician practice quality (eg, reducing unnecessary cesarean delivery). Increasing physician awareness of how their practice pattern differs from recognized standards can increase attentiveness in clinical decision-making and promote care that is better aligned with evidence-based guidelines. High-value health care optimizes quality while minimizing total costs and waste (ie, avoiding unnecessary treatment or complications). Value is defined as the ratio of quality to costs: \n\nQuality includes patient outcomes (eg, mortality, morbidity), safety (eg, adverse events), and patient care metrics (eg, patient satisfaction, wait times). Costs include the total costs (ie, not only short-term costs) of care per patient over the entire course of treatment. Costs may be assessed from the perspective of the patient, health care system, or society at large. \n\n Resource stewardship: Appropriate allocation of resources that leads to high-value, evidence-based care \n\nKey idea: If a patient has been bedridden for 3 years, so using an expensive, long-lasting stent to re-establish blood flow is likely not going to lead to any gains in function (i.e. use of the expensive stents is not high-value care) Timely (<4 weeks) primary care follow-up promotes completion of pending studies (eg, imaging, laboratory tests) and health management (eg, new medications, diagnoses). During the discharge process, patients should receive high-quality provider communication and counseling explaining the \n\n884 https://t.me/usmleinnercircle \n\n> Indicators used in quality measurement Structural\n\n## . Measure organizational structures, including human resources \n\n> indicators\n\n## . Example s: nurse-to-patient ratio, clinician knowledge \n\n> Process\n\n## . Measure health care worker compliance with a process, assess performance, detect variations \n\n> indicators\n\n## . Example: percentage of eligible patients screened for colon cancer \n\n> Outcome\n\n## . Measure changes in health status or outcomes \n\n> indicators\n\n## . Examples: blood pressure, mortality rate, nosocomial infection rate \n\n> Balancing\n\n## . Measure tradeoffs incurred as a result of systems change \n\n> indicators\n\n## . Example: increased documentation time after implementing a ne w safety protocol Ethics & Communication importance of follow-up, as this increases patient likelihood of attending primary care visits and completing follow-up recommendations. High-quality communication includes the following: \n\nFace-to-face discourse , allowing responses to nonverbal cues \n\nPatient-centered interaction tailored to the patient's current motivations, goals, and ability Interactive approaches for verifying patient understanding (eg, inviting questions, encouraging teach-back that summarizes patient understanding of the conversation) \n\n When systemic problems with health care quality are observed, the following approach should be used: communication with relevant stakeholders , coordinated efforts (eg, involving both inpatient and outpatient physicians), and team-based interventions to promote shared goals . Low adherence to well-established, evidence-based protocols can arise from suboptimal \n\norganizational and systems factors. Systems interventions are often prioritized as first steps. In certain situations where systems changes are insufficient, strengthening the organizational culture \n\nto promote individual accountability (known as \"just culture\") is useful. Examples of accountability-building interventions include incorporating hand hygiene compliance into physician evaluations and enforcing disciplinary measures when repeated hand hygiene transgressions occur (ie, warning note, remedial training). \n\n The Joint Commission Universal Protocol for Preventing Wrong Site, Wrong Procedure, Wrong Person Surgery was developed to reduce surgical errors and improve surgical reliability . Preprocedure actions include preoperative verification of the patient's identity, the procedure to be performed, and the surgical site. \n\n885 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\n Involve a social worker in discharge planning 77% The physician is responsib le for assessing whether to i nvo lve a multidisciplinary team of discharge planners (usua ll ysocial workers and/or nurses). Discharge planners can be especially helpful for patients who are at high risk for adverse events after discharge and require ongoing skilled care. Discharge planning should be in itiated as early as possible and includes a ps ycho social asse ss ment, discharge counse li ng, medication reconciliation, plann i ng of follow- up visits, and \n\ncoordina t ion of service s. The patient, their family, and future caregivers should be involved to establish a plan that meets the patient's medical needs and personal preferences. Effective discharge planning can increase patient satisfaction, reduce the duration of hospitalization, and decrease readmissi on rates. Home heal th care should be considered for patients who live at home and require complex ongoing care but are unable to travel. This form of rehabil i tat ion reduces costs while avoiding the risks associated with prolonged hospitalization (e.g. ,nosocomial infections). \n\nImproving hand hygiene compliance in health car e settings Reason for non co mpliance Exam ple solution \n\nIn effective placement of sinks and dispensers Place sinks/dispensers outside each pa tient's room Lack of accountability Build hand hygiene into provider evalua ti ons Lack of safety culture Create safety tea ms , prov ide real-time feedback on compliance Forgetfulness or lack of time Vis ua l cues (eg, signs, red arrows) near doorways Ethics & Communication Cross Culture Care \n\nCross-cultural care improves provider-patient communication and health outcomes, especially for minority populations that experience significant health disparities (eg, preventable differences in health linked to demographic attributes). Cross-cultural care reflects high-value care principles common to all populations, including: \n\nPatient-centeredness: identifying the patient's values and aligning care with the patient's priorities \n\nCultural sensitivity: exploring the patient's cultural beliefs and understanding how sociocultural background influences perceptions of health decisions \n\nEnhanced communication: addressing language barriers (eg, use of interpreter services) and tailoring communication styles (eg, adjusting eye contact, addressing family) to a patient's preferences Cross-cultural care emphasizes the importance of avoiding stereotyping , since minority groups (eg, Black) comprise a variety of subcultures (eg, Caribbean, African) and patients' preferences vary within groups \n\nPatient-Centered Care \n\n Patient-centered care incorporates patient preferences and values , with emphasis on measuring and monitoring outcomes prioritized by patients (eg, pain level, functional status). \n\nShared decision-making optimizes care in chronic conditions featuring multiple reasonable management strategies (eg, pain management, cancer treatment), promoting selection of treatments aligned with patient priorities. \n\nHome Health Care Rapid Response Teams \n\n886 https://t.me/usmleinnercircle \n\n \n\n> Patient-ce ntered care\n\n## . Incorporate patient values into medi ca l decisions \n\n> Overview\n\n## . Em phasize outcomes important to patients \n\n## . lmerove health care guali !l & eatient sa ti sfaction \n\n## . Shared decision-making be tween pa ti ent & physician \n\n> Examples\n\n## . Dec ision aids to assist patients in understanding options \n\n## . Ca re coordination to streamli ne chronic condition management \n\nHome health care Overview . Health services provided by skilled HCWs (eg, nursing, PT / OT , SW ) in t he home . Covered by Medicare if patient is homebound & h as sk ill ed hea lth needs . Medically stable fo r discharge but homebound & requiring intermittent mon itoring \n\nUses . High risk of adverse events (eg, fall risk, comp l ex medica ti on regimen) \n\n## . Skilled nursing needs (eg, wounds, physical rehabilitation) \n\n## . Promote patient menta l health, autonomy & independence \n\nBenefits . R educe risk of hospital readmission & length of hospitalization (eg, fewer nosocomial infections) \n\n## . Decrease health care spendi ng (ie, less expensive than skilled nursing fac ili ty ) \n\n> HCWs\n\n= health care workers; OT = occupational therapy; PT = physical therap y; SW = social work. Ethics & Communication Busy hospitals often experience delays in recognizing and responding to acute deterioration in patients' clinical status. Rapid response teams (RRTs) can provide early intervention in case of clinical decline, and their use is associated with improved patient outcomes (eg, reduced incidence of cardiac arrest and associated mortality). RRTs are characterized by the following: \n\nMultidisciplinary team: RRTs typically include practitioners from multiple health professions, including nurses, physicians, and respiratory therapists. \n\nPatient assessment: RRTs support primary care teams by regularly monitoring patients who are at high risk of clinical decline. RRTs can assess and immediately treat patients when signs of clinical deterioration appear, preventing serious sequelae. \n\nActivation criteria: RRTs are typically activated based on early clinical warning signs manifested by the patient (eg, sustained tachypnea, arrhythmia, uncontrolled pain). \n\nQuality Improvement Processes \n\nPDSA Cycle \n\n The Plan-Do-Study-Act (PDSA) and Plan-Do-Check-Act (PDCA) paradigms are quality improvement (QI) tools that involve cyclical processes with the goal of continual improvement. Once a QI issue is identified (eg, elevated rate of failed extubations among preterm infants), a 4-step process is put in place to address it, as follows: \n\nPlan: Identify any factors contributing to the issue (eg, lack of standardized extubation strategies), set an objective (eg, reduce failed extubation rate by 30%), and put a plan in place to carry out a cycle (eg, new protocol and checklist development, training in preparation for implementation). \n\nDo: Implement the plan (ie, new protocol) while making sure to collect data and document problems and unexpected observations. \n\nStudy (or Check): Using the data gathered, complete a data analysis that compares the results obtained to the objectives set (eg, evaluate variations in failed extubation rates). \n\nAct: Based on these data, identify changes that need to be made and lessons learned, and then begin work on the next cycle if needed to achieve the objective. \n\n887 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nQuality improvement processes \n\n## . Incremental c~cles of elannin9, eilotin9, assessin9 &\n\nModel for refining an intervention to achieve a se ec ific goal (ie, PDSA \n\nImprove me nt cycle) \n\n## . Example: testing a new check-in procedure with weekly tabulation of patient satisfaction surveys \n\n## . Identification & removal of inefficiency & waste in a workflow \n\nLean . Example: stream lining scheduling to reduce excess waiting time \n\n## . Near-elimination of defects through statistically driven \n\nSix Sigma process improvement \n\n## . Example: controlling annual incidence of w rong-s it e surgery to <0.00001 % thro ugh enhanced safety measur es \n\n## . Engaging person ne l to adopt innovation & implement \n\nChange or 9anizational chan9 es \n\nManagement . Example: identifying frontline early adopters to lead i mp lementation of a n ew EHR system \n\nEHR = el ect ronic health record; PDSA = Plan- Do -Study-Act. Ethics & Communication A run chart is a quality improvement tool that graphs a process performance outcome (eg, no-show rate) over time (eg, before and after a quality improvement intervention). Run charts allow visualization of trends (5 consecutive points with consistent directional change) and systematically determines effectiveness of a quality improvement intervention. \n\n## Hospice Care \n\n To qualify for hospice, patients must elect to discontinue curative or life-prolonging treatments ;however, they may continue palliative treatments (eg, surgery, palliative radiotherapy) that are primarily provided for control of symptoms. \n\n888 https://t.me/usmleinnercircle \n\nRun chart \n\nTime \n\nHome hospice c ar e\n\n## . Life expectanc~ S6 months \n\nPatie nt se lec tion . Agreement to fo rgo curative & life-sustaini ng treatment \n\n## . Fami ly/ private ca regiver available for daily needs \n\n## . Current s~m e; toms can be managed with home care \n\n## . Patient home \n\nLocati on of servi ces . Assisted l ivin g facil i~ \n\n## . Nursin g home \n\n## . Periodic home visits by experie nced personnel (eg, nurse) Typical s erv ices . Palliative medications {eg, analgesics, an tiemetics} \n\n## . Durable medical equipment (eg, hospital bed) \n\n## . Physical therapy (as well as ot her therapy modalities) \n\nCare philosophies at the end of life No escalation of treatment Time~imited trial Withdrawal of life support \n\n## . Sets upp er l im its on treatment (eg, no . Provides in tensive ca re for a p redefined . Focuses completell on comfort \n\nin vasive ventilation) interval le g. 2-3 days) measures onl y\n\n## . Avoids fu ti le interventions with greatest . May entail temporary escalation, even if futile . Withdrawing life support ;\n\nmorbidity \"withdrawing care\" \n\nCreates time to process impending loss Active dying soon follows & eases transition to withdrawal of li fe support Ethics & Communication In elderly patients with end-stage renal disease , especially those with advanced comorbidities and functional decline, chronic dialysis does not significantly extend life expectancy when compared to conservative kidney care; it is associated with increased hospitalizations and diminished quality of life .These factors should be discussed prior to initiation of dialysis. When patients elect to not initiate dialysis, the average life expectancy while on conservative kidney care is 6 months to 2 years. \n\n For patients with terminal illness (eg, advanced cancer), interventions that have adverse effects (eg, respiratory depression) are justified if they are given with the intention of promoting the patient's well-being or allowing for a comfortable death (ie, doctrine of double effect ). Voluntarily Stopping of Eating and Drinking is a decision by patients with terminal illness to cease all food and fluid intake, often as a symbolic acceptance of death. Physicians should verify that the patient has decision-making capacity and is acting voluntarily ,provide counseling regarding potential consequences (eg, discomfort), and record preferences for comfort (eg, oral swabbing) in case of thirst-induced cognitive impairment (eg, delirium). \n\nPhysician Assisted Suicide \n\n Physician-assisted suicide is the process by which a physician helps competent patients voluntarily end their lives when faced with end-of-life suffering. It involves providing medication, a prescription, or information to a patient with the understanding that the patient intends to use it to complete suicide .Although it is legal in a few states and in some countries, physician-assisted suicide is a controversial \n\narea of ethics. Physician-assisted suicide should be differentiated from euthanasia , in which a physician administers a lethal substance. In the United States, euthanasia is illegal and is considered unethical. When approached with such a request, the physician should respond with empathy and compassion and explore the reasons for the request . Reasons may include fears of loss of autonomy and dignity, fears of suffering (eg, uncontrolled pain, dyspnea) and poor quality of life, and feelings of not wanting to be a burden to others. Once the patient's concerns and fears are identified, the provider can optimize palliative care interventions to address specific issues and improve quality of life. \n\nDNR \n\n889 https://t.me/usmleinnercircle USMLE Inner Circle \n\nReframing personal goals in terminal illness \n\nExplore the patient's . Current symptoms & functional limitations understanding of the illness . Expected course & prognosis Clarify the patient's . Personal goals \n\n# . Fears & obstacles priorities & values Individual motivation & purpose .. Alternate means or schedule Reframe goals Current & possible help & support in realistic ways .. Avoid giving false hope Ethics & Communication A \"do not resuscitate\" (DNR) order specifically prohibits cardiopulmonary resuscitation (eg, chest compressions, defibrillation) in the event of cardiopulmonary arrest. However, it does not mean \"do not treat\" and does not prohibit other therapeutic interventions (eg, thrombolysis) that may be needed to address concurrent or newly presenting conditions as determined by standard practice. \n\n A patient's preferences for life prolonging measures would not apply in cases of brain death \n\nbecause brain death constitutes legal death and medical teams can legally withdraw care. \n\n Patients often fear that a do-not-resuscitate order may relegate them to a lower priority for the care team or otherwise compromise their care. To best understand the patients' wishes, code status should be addressed in a broader discussion regarding goals of care, using nonleading questions, avoiding euphemisms, and providing reassurance that their decisions will not otherwise alter their treatment or overall quality of care. \n\n## Medical Errors \n\n Continuity of care for medications at the time of transitions of care, between inpatient and outpatient facilities and within inpatient facilities, is a potential source of medical error. Interventions that target pharmacy personnel and high-risk patients appear to be the most effective in improving the quality of patient care. Near Miss : Unplanned event that doesnt cause harm but has potential to do so. Active failure is a medical error that is caused b a human error such as negligence, misinformation, incompetence or a technical mistake. and directly causes the patient harm. (Immediate Impact) e.g: Wrong site incision \n\n Latent conditions are systemic conditions that can lead to medical mistakes and patient harm. They are often caused by the organization or design of a system. (Accident waiting to happen) \n\n Adverse event is a medical error that reaches the patient and causes harm, such as giving the wrong medication to a patient. Sentinel event/ Never Event is a medical error that reaches a patient and leads to permanent disability or death .\n\n890 https://t.me/usmleinnercircle \n\n> Acti ve versus latent errors Active error Latent error\n\n. Proximal cause . Distal ca use \n\n. Invo lves actions of frontline . Involves organizational vul ne rabilities th at personnel influence actions of frontline personnel \n\n## . Occurs at interface of provider Occurs at level of system, process & policy with patient or system .. \"Sharp en d\" of the scalpel, tip . \"Accident waiting to happen,\" \"bl unt end\" of the of the iceberg scalpel, be low the su rf ace Ethics & Communication Examples would include performing an operation on the wrong patient or wrong site or administering a medication to which a patient was known to be allergic leading to anaphylaxis and/or death. \n\n Not every complication has a sentinel event, and not every sentinel event is caused by an error. Physicians have a duty to fully disclose significant complications , whether non-preventable or preventable, to patients. Full disclosure should include explanation of the following: \n\nDetails of the complication (ie, nature of injury) Potential causes and contributing factors (eg, complex anatomy, location of tumor) \n\nTreatment provided Expected prognosis and consequences (if any) \n\nPreventive strategies (if the complication was preventable) \n\n When a serious adverse event occurs during treatment, all physicians involved in the patient's care should collectively disclose the event to the patient and family. Patient discussions regarding treatment complications should ideally be conducted by the physician \n\nwho had primary responsibility for the initial intervention. If that physician is unavailable, a brief and honest explanation should be provided to the patient by the covering physician, with the assurance that a definitive answer will be provided once the matter has been fully discussed with the colleague. \n\n(This might be related to your recent procedure, let me discuss with your physician to give you a definite answer of why it happened.) \n\n891 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\n0 Speak t o the colleague who ordered t he initia l HIV test 44% W hen a physician is confronte d w ith t he possibil i ty that a colleague is responsible for a medical er ror , the physician must speak to the colleague privately in a non judgmental mann er and attempt t o fi nd out why the er ror o cc urred. If the pat i ent no lon ger has a pa t ie nt -p hysicia n rel atio ns hi p w it h t his individual, the physician should also seek the patient's permission to speak to the colleague (to prevent a HIPAA violat ion). Med i ca l errors are m uch more commonly caused by failures in health care systems t han by the act ive er ror of a health care prov ider. Moreover , there are a nu mber of patient factors \n\nt h at can cause adverse events (e .g., lack of access to heal th ca re due to economic inequi ties , failure to keep appoint ments) as we ll as ethically valid exceptions to full disclosure (e.g. , t herapeutic privilege, pati ent ref u sa l to recei ve in for m at io n) ; medical records might be incomplete or contain a mi srepresen tation of t he circu mstances for a particu l ar decision. Physician-physician comm un ication in a su p por ti ve setting hel ps t o prevent simil ar incidents from recurrin g. Afte r con fir ming t he cause of t he er ror , the physician in charge should in for m t he patient and advocate for changes to rectifv the issue. Ethics & Communication Cognitive Errors \n\n Metacognition , the process of understanding and self-monitoring potentially flawed cognitive patterns and biases, has been associated with reduced judgment errors .Metacognition can be promoted through morbidity and mortality conferences and practicing \n\ndiagnostic time-out (ie, critical reflection on the diagnostic thought process), particularly when caring for a complex patient. Triage cueing results when the diagnostic evaluation is overly influenced by the patient's triage category. For example, a physician may miss concerning signs in a patient who is triaged as low acuity by another staff member. \n\n892 https://t.me/usmleinnercircle \n\n0 Failure at the patient-telemetry device int erface 32% When humans interact w ith medical equipment, thr ee types of errors occur: human er rors, device er rors, and errors at the level of the device-human interface. Failure at the level of the device-human interface (e.g. , disconnection of the patient from or improper conn ect ion of the patient to the telemetry device) is the most common cause of inpatient cardiac telemetry-related errors (a pprox. 50% of cases) and typically occurs after patients are shifted (e.g. , for a test). Less common causes of inpa ti e nt cardiac t elemetry-related errors are equipment malfunction (25%), communication breakdown (20%), and alarm fatigue (5%). Cardiac telemetry-related e rror s rarely cause patients to be harmed, but when they do , the consequences are dire with death as the most frequent o ut come. Measures that can be taken to prevent such e rror s include checklists and standardi za t ion for inpa ti ent transfers, regul ar telemetry equ ipme nt checks, forcing functions that prevent alarms from being t urned down, and redirection of low-level alarms to telemetry t echnicians to prevent alarm fatigue in nurses. Common co gnit ive errors in medicine \n\nType of bias Defin iti on Example \n\n## . F ixa tin g on ini tia l im pressions to m ake a Bu rning th roa t pa in di ag n osed as acid refl ux di agnos is .\n\nAnchoring despite weight l oss \n\n## . Re la ted to confirmation bi as & premature Cor rect diagn os is is l un g maligna ncy .cl osure All owi ng recently seen or memorable ( hig h- . Dyspnea diagnosed as influenza during peak \n\n## .Ava ilability influenza season st akes) cases to swai'. d ia g nos is . Cor r ect di agnos is is p ul mo n ary e mb ol is m\n\n## . Em ehasizing ev idence that su e122 rts Burning throa t pa in afte r ea t ing sp icy f ood pr esumed d iag nos is & ove rl ooki ng i nfo r mation .\n\nC on fi rmation di ag n osed as ac id re fl ux despite we ig ht l oss that supports other diagnoses . Cor rect diagn os is is malignan cy \n\n## . Re lated to anc horing bi as \n\n## . Abdominal pain diagnosed as opioid Framing . Allowing di ag nost ic approach to be influenced withdrawal in patient desc ribed as drug by context & presentation of information seeking \n\n## . Correct di agnos is is bowel obstruction \n\n Commission bias 22% \n\nCommission bias is favoring action (e.g. , ordering a D-dimer test) over inaction when inaction w ill likely l ead to the same or a better outcome. This patient most likely has had a panic attack. His Wells score for pulmonary embolism (PE) indicates a l ow probability for PE and the pulmonary embolism rule-out criteria (total score of O points) indicate that no fur th er diagnostic testing is needed. Regardless of th ese facts, the physician h as ordered a D-dimer test most likely as a result of a sen se of obligation to the principle of beneficence. Commission bias is less common in health care than omission bias, which is the tendency to prefer inaction over action. Ethics & Communication Avoiding Errors \n\n Organizational goals of zero human errors are unrealistic .Instead, organizations should set goals of zero adverse events (ie, no harm to patients) \n\n893 https://t.me/usmleinnercircle USMLE Inner Circle \n\nImplicit bias Defini tion . Subconscious stereotypes about & attitudes t oward a specific group (eg, et hnic minority) \n\n# . Nondeliberate & unconscious ; distinct from intentional discrimination \n\nEff ects . I nfluences provider think i ng , communication & behavior (eg, affecting differential diagnosis , trea t ment )\n\n# . Contr i butes to hea lth dispar ities ( eg , suboptima l pa in management )\n\n# . Assess for presence of biases ( eg , using standardized testing tools*) \n\nM anagement . P romote individua l & group explo r ation ( eg , debriefing ) of bias & ste r eotypes \n\n# . Train providers to recognize & mon i tor thought processes (eg , metacognition) 'Examples include computerized, image-based sequential priming tests. \n\nSystems approach to error prevention \n\nOve rv iew . Address organizationa l environment & teams . Emulate high - re liability organization practices (eg, av iation) \n\n## . Culture of saf ety : prioritize safe ty -p romo ting resources \n\nCo mponents . Resilience: systems design to pr event errors \n\n## . Team -b ased vigilance: safety oversight by entire team \n\n## . Comprehensive anal ys is: avoid sim plistic ex pl anatio ns \n\n## . Human facto rs enginee ri ng: reduce human effort needed for safe actio n\n\nExamples Sw iss-cheese model: multiple overlapping l ayers to block errors (\" holes\" ).\n\nHuma n factors engi nee r ing strategies Re li abili ty Str at egy Descri pt ion & exam pl es \n\n## . Hard stops in de sign or process to eliminate risk of incorrect use \n\nForcing functions . Example: each an esthesia gas fits only one compatib le socket & is not in tercha n geable \n\nComputerized . Automated pr ocesses to r emove hum an effort & va r iat ions that cause er ro r Highest a ut o mati on Example: aq tQrnaled ~i ta l 5 i g s mc ilc[ i g.\n\nEnvironment & physical . Worksp ace design to facilitate correct action & minimize error \n\nlayout . Example: l ook -a like dru ~s s to ck ed in different locations \n\nStandardization & . Uniform p roc esses to minimize variation, co mp lexity & learning curve \n\nsimplification . Example: every hospital un it fo ll ows the same process for heparin adm in istration High Human-machine . Repetitive step to confirm correct action in an error-prone process \n\nredundancy . Example: ba r code scanni ng of med ications in addition to vi s ua l ins pe ction Medium Reminders, alerts & . Processes prompting providers to check actions to reduce errors \n\ndouble-checks . Examples: drug-drug interaction alerts; time-out before procedur es Human factors engineering seeks to reduce erro r risk by des igning sys tems based on expected human behavior s. Less reliable HFE strategi es include tr ainings, eo li c~ chanaes & education. \n\n Tes tin g th e new devices in th e opera tin g rooms using simulated surgeri es S8% Te stin g new devi ces be for e impleme nt at ion (usability testin g) under simulated or actual conditions can help identify unanticipated risks that may res ult in wo rkarounds, whi ch may l ea d to medi ca l error s. New devi ces can be evaluat ed based on wheth er they meet th e u se rs' requiremen ts (design validation) regarding th e intended purpose and usability. In t he action hierarchy of HFE, this method of e rror preve ntion is considered a \"stronger action ;' m ea ning th at it is more effective in pr eventing me di ca l errors sin ce it do es no t rely on hum an e ff ort for e rr or m iti gation compared t o \"w eaker action s\" such as training, double ch ec ks, warnin gs, and th e introducti on of new po li cies ( e.g., checking th e alarm volume hourly). Another exa mple of a \"st ronger act ion\" is th e impleme nt ation of a fo rcing fun ct ion, e.g., a d es ign f ea tur e th at swit ch es off th e elec tro ca ut e ry device if th e volume falls be low a ce rt ain leve l. Ethics & Communication Automation is appropriate for constant, predictable processes (eg, constant heparin infusion on a hospital floor) but is less suitable for dynamic processes requiring critical analysis and frequent adjustments (eg, administering heparin boluses in an operating room). The Swiss Cheese Model (SCM) is a strategy often used in health care organizations to increase safety. SCM recommends overlapping multiple barriers (visualized as slices of cheese) within a process to block hazards . Targeted hazards include both internal human error (eg, mistakes resulting from fatigue) and external threats (eg, infectious agents). \n\nClinical Support Systems \n\n Electronic decision support tools can optimize physician decision-making and reduce cognitive overload in busy, complex settings where risk of cognitive bias is highest. These tools are typically integrated in the electronic medical record and provide real-time, interactive feedback and guidance for physicians. They reduce diagnostic errors through the following: Reminding physicians of relevant patient information from previous encounters (eg, history of injection drug use as a risk factor for infection) Prompting physicians to perform specific actions during the history and physical examination to thoroughly assess risk (eg, asking about fever during evaluation of back pain) Providing quick access to evidence-based algorithms or clinical pathways that outline recommended steps in patient care (eg, ordering inflammatory markers, such as erythrocyte sedimentation rate, in patients with fever and back pain). \n\n894 https://t.me/usmleinnercircle \n\n\n\n> Purpose\n\nSw iss cheese model \n\n# enetrating \n\n> hazard Medical error Layers of defen se :Ph ys ica lenvir onment chang es Co mputerized aut omat ion Double-ch ec ks, Organizat io nal checkl ists traini ng , po li cies\n> uworld\n\nClinical decision support systems \n\n## . Assist providers in making clinical decisions based on patient data (eg, laboratory data) \n\n## . Usua ll y integrated into computerized provider order systems . Recommend actions to providers based on patient clinical information . Increase re li ab il ity of medical decision-making (ie, li miting potentia ll y harmful varia ti ons of care) \n\n> Potential benefits\n\n## . Detect and in tervene in cases of human error (eg , enter in g incorrect drug dose) \n\n## . Reduce medication prescripti on errors . Tool suggesting default drug dose and frequency based on patient weight \n\n> Examples\n\n## . Prompt recommending specific VT prophylaxis in a patient fo ll owing hig h-risk surgery \n\n## . Prompt recom mend in g specific diagnostic tests in a patient with suspected p ul monary embo li sm \n\n> DVT\n\n= deep ven ous thrombosis .Ethics & Communication Minimising Interruptions \n\n To maximize safety, interruptions should be managed as follows: \n\nMinimize task-switching: For nonemergency interruptions (eg, clarifying a routine order), the physician should complete the current, unfinished task and then address the new task. Unnecessary breaks in action (eg, stopping in the middle of order entry to listen to and resolve a nurse's question) should be avoided. \n\nMinimize multitasking: Whenever possible, the physician also should avoid performing multiple tasks simultaneously (eg, listening to a nurse's question while continuing to place orders). Retained surgical objects (eg, sponges, instruments) frequently occur even when surgical counts are thought to be reconciled. Interruptions increase the risk of counting error; holding a brief time-out (ie, a pause in activities to announce that the count is about to begin) can improve situational awareness (ie, group vigilance for safety concerns), reduce interruptions , and improve count quality. \n\nHealthcare Communication \n\n According to the Joint Commission, the most common root causes of sentinel events involve \n\nfailures in communication and teamwork .\n\n895 https://t.me/usmleinnercircle USMLE Inner Circle \n\nComputerized provider order entry 66% Paper-based systems, in which medication orders are handwritten, are prone to transcribing errors, which can result in the recipient of the o rd er not being able to properly read and interpret the prescription. In this case, as the physi ci an determined that the patient received ten times the prescribed dose, the transcribing er r or was most likely due to the misinterpretation of a trailing zero after a decimal point. Trailing zeros are part of the Joint Commission's \" Do Not Use\" list, wh i ch provides recommendations on information management. To prevent transcribing errors, most hosp it als have adopted computerized provider order entry (CPOE) systems , which also have the advantage of helping to prevent ordering errors because they are usually combined with a clinical decision support system . If a CPOE system has not been adopted and t he health care facil ity maintains a paper-based system, t he usage of standardized abbreviations/ writi ng styl es and having an interm ed iary (like a clinical pharmacist or a pharmacy technician) read and int erpret the prescriptions can also help to prevent transcribing errors. Str ategies to improve health care communication \n\nStrategy De sc rip t ion Benefit s\n\nStandardized Che cklist or other systemat ic process En su r es consisten cy and \n\nhandoff fram es provider -t o-prov ider discussion reliability. re du ces errors of during sign-out omiss ion \n\nClosed-loop Sender re l ays message to receiver, Min im izes erro rs of co mmuni ca tion/ receiver r epeats info rmation back to misi nter pretation and \n\n\"read-backs\" se nd er; sende r co n firms message is misunderstand in gco rrect Incr eases &ootiaYOY~ !eaw iag \n\nInterdisciplinary Team me mbers rep r esent multiple a nd co ll aborative overs ight of round s dis cipli nes (eg , nu rsing, pharmacy) patient's condition Red 11 ces bieracch ical barriers ,B ri ef , int erdi sc iplinary discus s io ns of \n\nTeam huddles encourag es sp eak ing up, \n\n& debriefing pa t ie nt concerns a nd risks; held prior pr omo t es shared team safety to , during, a nd /o r afte r clinical even t goa ls \n\nlm er oves com mun ication & \n\nTeam-based Tra in t eam membe rs t oge ther via collabo r at io n1 12 romotes gr oup training i nt eractive formats (eg , sim ul ation) learning, reduces h ie rarchical barriers Ethics & Communication Standardized sign-out templates represent the most effective intervention to improve sign-out safety. \n\nError Reporting System \n\n Error reporting systems (ERS; also known as incident reporting systems) are implemented in many hospitals as a way for staff to report observed errors (eg, medication administration error). ERS are more effective in improving quality of care when hospitals ensure structured mechanisms are present to respond to submissions , including systematic procedures to investigate reported incidents. The results of investigations should be communicated back to the reporting individual(s) to maintain transparency and increase confidence among personnel that their reports will result in positive organizational change. Other characteristics of effective ERS implementation include: Encouraging all front-line personnel who interact with patients (not only nurses and physicians) to submit reports. Establishing specific, clear criteria for which events should be reported (rather than relying on individual personnel judgment). For example, absence of clear criteria can lead to underreporting of near-miss events (ie, errors that were caught before causing patient harm) that should be reported in ERS. \n\nEliminating fear of retribution associated with reporting by maintaining confidentiality and anonymity and ensuring investigations primarily focus on systems factors rather than mistakes of individual personnel. \n\nSimplifying the reporting process to minimize the time and effort required to submit a report. \n\n896 https://t.me/usmleinnercircle \n\nErrors related to transfers of care Definition . Adverse patie nt outcom es due to changes in resp ons ibili ty of patient care \n\n## . Can occur in cli ni ca l se tt ing (eg, shift cha nge , transf er between departments) or post-discharge \n\n## . Suboptimal communication (omitted or vague information) between providers \n\nRoot causes . Excessi ve distractions d ur ing signout process \n\n## . Lack of standard iz ed si gno ut protocols \n\n## . Documentation errors ( eg , o ut dated medication list, no doc um entation of cross-cover events) \n\n## . I mp lement standardized signout communication (eg, checklists or mnemonics) \n\n## . Avoid va gue instr uct ions (eg, \"follow-u p x-ray\"); communicate specific action plans \n\nPreventive . Conduct signout communication in quiet environment \n\nstrategies . Add re dundancy (eg, separately documenting cross-coverage eve nt s in addition to verbal signout communication) \n\n## . E ns ure accu racy of in fo rm ation in w ri tten sig nout Re ducing errors i n pa tie nt handoffs \n\n## . Discuss highest-acuity (ie, \"sickest\") patients first \n\nOptimize Provide extra detail on critical patients .information . Avoid information overload . Follow template (eg, checklist )\n\nOptimize . Include oral & written communication \n\ncommunication . E ncourage questions throughout discussion . Use read-b ack se l ect i vely (eg, for to-do it ems )\n\nOp timi ze . Include follow-up items (eg , to-do list) \n\nactio ns . Provide anticip ate ~ 1i uidance (eg, \"if/then\" format) Ethics & Communication Medical Error Analysis \n\n Morbidity & mortality conferences minimise Cognitive Biases \n\nRoot Cause Analysis \n\nThe fishbone diagram (cause-and-effect diagram) is a visual tool used during team RCA discussions to organize the categories and causes of errors contributing to the problem. The diagram is analogous to a fish skeleton, displaying the following: The problem of concern (eg, prolonged wait times) is placed at the far right of the diagram, representing the \"head\" of the fish. \n\nCategories of factors (eg, staffing, organizational, operational, patient) that may be contributing to the problem are placed in diagonal spokes coming off the central spine, representing the \"ribs.\" Individual specific causes are listed under each respective main category, representing the \"scales.\" \n\n897 https://t.me/usmleinnercircle USMLE Inner Circle \n\n\n\nCommon tools used in error ana lys is Root ca us e analysis (event . Retrospective \n\nana lysis) . Ide ntifies all underll ing reasons (systems & personnel-related) that an error occurred \n\nFailure modes & effects . Prospective \n\nanalysis . Identifies the likelihood & potential sources of Sl stem failures before error occ ur s\n\nCommon cause ana lys is . Retrospective \n\n## . Identifies most common themes & trends present am ong multiple errors \n\nMorb idity & mortality . Retrospective \n\nconference . Identify system-level improvements to address an error throu gh confidential. interdisciplina ry standardized group discussion \n\n@) Morbidity and mortality review 52% \n\nMorbidity and mortality reviews (M&Ms) are department meetings in wh ich selected cases involving medical errors \n\n(including near misses and preventable or ameliorable adverse events) are confidentially presented, reviewed, and discussed among peers. The meetings should id eal ly follow a standardized format that includes analyzing medical errors \n\nand determining improvement measures to be followed up. M&Ms t ake place at regular int ervals, typically monthly. The goal of an M&M is not to punish individuals but to identi fy measures for individual improvement and increase situational awareness as well as collective responsibility among team members. Since M&Ms are a type of peer review activity, the meeting's proceedings, findin gs, and recommendations (as well as any documentation) are l ega lly protected and inadmissible in malpractice lawsuits. Category 2 (eg . teamwork) \n\nFishbone diagram Ca us e Effect \n\n# , ______,,____-------,-------\n\nSpe ci fic cau se ----~\n\n(eg, double-booking patients) Pr oblem \n\n(eg. long patient \n\nwa it tim es) \n\nCUWOr ld \n\nCatego ry 1(eg, sc heduling) Ethics & Communication Failure Mode & Effect Analysis \n\nFailure mode and effects analysis (FMEA) is a systematic, team-based approach that consists of identifying steps in a process and finding solutions to any problems that may arise, with the goal of ensuring safe outcomes. FMEA is a prospective process that can be performed before problems occur, \n\nEffective Teams \n\n Simulation training is a method of interactive group learning in which teams learn and practice skills together in simulated cases (eg, suspected Retained foreign objects during complex surgery). It improves teamwork and is used frequently in high-reliability organizations (ie, high risk industries with excellent safety records) to promote safety. Simulation-based training prepares teams to respond effectively and rapidly during high-risk clinical emergencies (eg, shoulder dystocia). This hands-on training can improve team performance ,refine technical skills, and reduce complications (eg, neonatal brachial plexus injury). \n\n898 https://t.me/usmleinnercircle \n\n0\n\nFailu re modes & effects analys is (FMEA) \n\n## . P rospective , sys tematic assessmen t for erro r prevention Ov e rv iew & us es . Ide ntifies potent ial i ssues before th ey occ ur \n\n## . Info rms deve lopment of new initi atives \n\n## . Form multidisc ipli nary tea m\n\n# . Defi ne process to be stud ied \n\nSteps in analysis . Cons t ruct fl owchart of process \n\n# . Ana lyze e rr or ri sks at each step \n\n## . Identify potential correc t ive act ions \n\n## . Impleme nt plan \n\nFeatures of effective teams* in health care Safe ty culture . Reso u rce commi t men t to safety \n\nCollaboration . Sh ared u nderstan di ng & prioritization of goa ls \n\n## . Disti nct rol es th at avoid a stee e hi erarc hy \n\nPs ycholog ical safety . Ask i ng ques tions & voicing concerns encouraged \n\n## . Avoiding bl ame or retal ia tion \n\nResponsive ness . Feedba ck rese ecte d & erom etl ~ acted ue on \n\nS it uational awar eness . Pe rsistent mind fuln ess & sa f ety vigil ance \n\n## . Cross -ch eck ing of each others' ac ti ons \n\nTransparency . Prom pt disc l os u re of errors & safety in fo rmation \n\n> Poor teamwork is aleading roo tcause of sentinel events; improved communication reduces medical errors\n\n& improves patient/c linica l ou tcomes. \n\n\"If we send the patient for echocardiography, his surgery w i ll be delayed by at least one day. Can you please explain to me why you think this patient requires this test?\" 71% This response is an example of collaboration ( conflict management strategy). The surgeon's genuine inquiry about the anesthetist's reasoning a ll ows an open discussion about the necessity of preoperati ve echocardiography and pote nt ial alternative courses of action. In collaborative negotiations, the participants should explore each other 's thought processes (appreciative in qu ir y) and aim to understand their own interests regarding the issue (self-reflection). The collaboration strategy, wh ich aims to solve problems in everyone's best interest (including the pati ent ' s), helps to maintain a good relationship between the conflicting parties and promotes mutual understanding, respect, and trust. A downside of this approach is that it is time-consuming and requires more effort and commi tment , which may be impractical in emergency situatio ns. Ethics & Communication Team safety debriefings are collaborative discussions encouraging expression of safety-related concerns and actions in a specific situation. They can occur before or after a clinical event. Debriefings are used by high-reliability organizations (organizations with excellent safety records despite high risk, such as aviation) to strengthen safety culture (shared commitment to safety goals) and continuous team learning. Attending team briefings can improve the student's psychological safety , confidence in safety culture, and familiarity with relevant communication skills, increasing likelihood of voicing his concerns during the procedure. Psychological safety refers to team members' comfort in taking actions (eg, openly voicing concerns, asking for help) for safe patient outcomes. Psychological safety is hindered by strict hierarchy or fear of retribution and can be promoted by organizational initiatives such as change management (ie, engaging front-line personnel in improving organizational culture). \n\nTime Out & Site Verification Burnout \n\n Physicians caring for critically ill and dying patients frequently experience grief and emotional distress, which can cause burnout .\n\nInterdisciplinary debriefing sessions dedicated to discussing psychosocial aspects of patient care are associated with improved physician well-being and ability to cope with distress. \n\nMalpractice \n\nTo determine whether medical malpractice occurred, all the following must be present: The physician has a duty to care for the patient (ie, a patient-physician relationship has been formally established). The physician's action deviated from standards of care , typically determined by current clinical guidelines. The deviation from standards of care directly caused damages to the patient, which may include physical injury, emotional suffering, and loss of wages. Damages need not be irreversible for malpractice to occur \n\n899 https://t.me/usmleinnercircle USMLE Inner Circle \n\nP ati ent saf ety pro ce du res in the surgical setting \n\n## . Patient identity, operative site, type of operation, & si de (verified/documented by ~2 providers) \n\nPreoperative verification . Performed in preoperative ho lding area \n\n## . Should involve patient (or surrogate) and 2 patient identifiers \n\n## . Mark (eg, \"YES\" + initials) on eac h operative site ( do not ma rk n ono perative sites) \n\nSite marking . Clearly mark using pe rrr anent marker \n\nSurgic al . Occurs immediately prior to skin incision time-out . Repeat verification of patient identit y, operative site & si de \n\n## . Entire surgical team participates & all concerns addressed Ethics & Communication Defensive Medicine \n\n Defensive medicine refers to provision of clinical services primarily to reduce physician liability without significant benefit to the patient. It can result in overuse (eg, unnecessary use of CT scans), with worse patient outcomes (eg, cumulative radiation exposure) and higher costs. Liability concerns are often effectively addressed by implementing clinical pathways or practice guidelines . These guidelines are typically established by major specialty societies (eg, American College of Radiology) and specify standardized, evidence-based recommendations for common conditions (eg, when CT scans are indicated in the evaluation of abdominal pain). Such guidelines serve as a broadly recognized standard of care ; therefore, physicians adhering to them are more likely to be protected from liability (because malpractice typically involves care that deviates from a reasonable clinical standard). \n\n## Insurance \n\n Insurance plans may deny coverage of medications that are less cost-effective or carry higher risk than the preferred medication choices. When a treating physician believes a denied medication is appropriate therapy for a patient, the \n\nphysician should request escalated review (eg, prior authorization) for coverage by the plan. \n\n EMTALA : Emergency departments that accept payments from Medicare must provide an \n\nappropriate examination/care to anyone seeking care regardless of ability to pay, insuarance, legal status or citizenship status. \n\n900 https://t.me/usmleinnercircle \n\n0 M isconduct 91% \n\nPhysician misconduct is any behavior that goes against the ethical principles of medical practice. In th is scenario, physician A leaves the hospital and puts patients at risk through his absence, which violat es the principles of nonmaleficence and beneficence. This behavi or is never acceptable regardless of whether it resu lt s in harm to a pat i ent or inc ur s l ega l consequences. Misconduct can al so occur outside the established physician- patient relationship and does not always co ns tit ute malpractice (e.g. , research malfeasance, fraudulent advertising). Other exampl es of misconduct include bu ll ying, making inappropriat e comments and/ or sexually harassing coll ea gues or pat ients, billing fraud, and receivi ng gifts from patients or pharmaceutical industry representatives. Colleagues w ho suspect a physician of misconduct shoul d report their concerns to the state medical board, and, if the misconduct implies any le ga l liability, to the approp ri ate legal authorities. \n\nDisability insurance \n\n## . Financial assistance for em ploy ees unab le to perform full j ob duties due to illness \n\nDefiniti on . May be short term (eg, <6 weeks) or lon g term \n\n## . Offered through private insurance or Social Security Administrati on \n\n## . Document findings related to medical condition \n\nClinici an 's role . Define severity & expected duration of condition \n\n## . Identify restrictions & job-related functional limitations \n\n## . Disability de finitions & certifi cat ion reg uirements va !:Y by erogram \n\nChallenges . Determin ing disability duration may requ ir e longitudinal & repeated eval ua tion \n\n## . Clinician assessment may co n fl ict with eatient ereferences Ethics & Communication Pay for Performance System \n\n Evidence suggests that practices serving affluent populations are more likely to achieve P4P quality metrics (eg, patients have more resources to afford recommended medications or follow-up tests). As a result, this large (ie, national) P4P network may preferentially reward more physicians in affluent regions, increasing gaps in resources and health outcomes between poor and high-income settings and failing to improve quality of health care for the overall population. Therefore, P4P systems are recommended to consider demographic characteristics of the patient (eg, insurance type, income level) and surrounding community (eg, status as a health professions shortage area) when determining amounts of incentive payments (eg, higher payments for quality achievements to practices located in a health professions shortage area). \n\n## Research \n\nRandomized controlled trials (RCTs) pose unique ethical risks to participating subjects because such research potentially has a significant chance (eg, 50% in a 2-arm RCT) of allocating participants to an inferior intervention (eg, placebo or harmful experimental treatment). Participants should be advised of this risk during the initial informed consent process; in addition, the study should include ongoing oversight of interim trial data by an external committee. \n\nData oversight should be performed by an independent data monitoring committee , consisting of biostatisticians and other experts. Committee personnel should be entirely external to the research team and study sponsor to avoid any bias or conflict of interest. The research team submits secured and de-identified data to the committee, which reviews the data in unblinded form to detect and report safety concerns, such as higher-than-expected incidence or severity of adverse events, treatment futility, and issues with data integrity that could compromise study results. The committee may recommend stopping an RCT early when interim data suggest that trial continuation poses an unnecessary risk to participants, as seen in the following circumstances: \n\nEvidence of benefit: Data reveal highly significant differences (eg, p < 0.0005) in outcomes in favor of the study intervention versus the control group. \n\n901 https://t.me/usmleinnercircle USMLE Inner Circle \n\n0 Perform a medical screening exam in at ion and provide stabilizing treatment if needed. 84% According to the Emergency Medical Treatment and Labor Act (EMTALA), any hospital w i th an emergency department is required to screen for emergency medical conditions if requested and, if such a condition exists, provide treatment until that condition is stabilized. Failure to diagnose and treat acute lower extrem it y ischemia places the patient at unacceptable ri sk for extremity infarction and, ultimately, loss of leg function. The EMTALA defines an emergency medical condit ion as a medical condit i on that manifests with acute symptoms (including pain and labor contractions) that are sufficiently severe to (i) place the health of the individual or unborn child in serious j eopardy, (ii) seriously impair bodily functions, or (iii) cause serious dysfunction of an organ or body part. \n\nPay-for-performance systems \n\n# . Incentive payments to providers (eg, physicians) are based on clinical performance \n\nDescription Payment is conditional on meeting eredefined guali!:i metrics .\n\n Optimizes health care spending while improving quality of care \n\nBenefits . Rewards improved outcomes & evidence-based use of resources \n\n# . Accountable care organization: network providers coordinate care & receive bonuses based on achievement of patient \n\nExamples metrics (eg, goal A1c%) Ethics & Communication Evidence of harm: Data reveal worse outcomes or unexpected, serious adverse events associated with the intervention. \n\nEvidence of futility: Data reveal that the study hypothesis is not provable for statistical reasons (eg, excessive drop-out rate, insufficient recruitment). The differences in outcomes between groups should pertain to clinically important endpoints (eg, myocardial infarction, mortality), be clinically significant, and meet a much stricter threshold (eg, p<0.0005 instead of p< 0.05) Conflict of interest (COI) in industry-funded research is increased when investigators have financial relationships with the sponsor (eg, consulting fees, stock ownership) or when industry sponsors are directly involved in research design and analysis. COI can compromise internal validity (eg, study is more likely to report favorable outcomes) and should be mitigated through independent oversight of the research process (including data analysis) and disclosure of COI in the final publication. Special protections apply to medical research subjects who are minors (ie, age <18). In particular, research protocols for studies involving minors must address the following: \n\nDegree of risk to participants, which may be minimal (eg, completing a survey) or substantial (eg, taking an experimental medication) \n\nRationale for including minors (eg, research is focused on a condition that affects children and will likely benefit affected children) Procedures to obtain informed consent from parents and guardians as well as age-appropriate assent (agreement) from minor participants \n\nAssent refers to agreement from a minor to participate in research. Assent is obtained directly from the minor as appropriate for age (eg, using oral script for minors age 7-11, and using written confirmation with signature for minors age 12). \n\n In some cases, if the research study will directly benefit (or potentially benefit) the minor participant, assent is not required . For example, a clinical trial that enrolls children with incurable bone cancer, in which subjects are given a new bone cancer drug to see if it is effective, would not require assent. \n\n902 https://t.me/usmleinnercircle \n\n\n\nEthical considerations for randomized controlled trials Appropriateness Intervention arms are at equipoise (ie, intervention is not alread :z: known to be sue enor to control) .ofRCT Appropriateness . Control is equivalent to the acce pted standard of care \n\n> of control\n\n# . Control does not pose unacceptable risks to part icipant \n\n## . Acceptable when effective standard of care is unc l ear or does not exist \n\n> Appropriateness OR\n> of inactive placebo When effective standard of care exists, but tem eoraril :z'. withholding such thera e:z'. would not harm the eart icie ant\n\n# . \n\n> Appropriateness Trial stopped when in !!;l rim g!!t!! !! nalysis shows clear, highly significant benefit or harm\n\n## .of stopping RCT RCT = randomized controlled trial. Ethics & Communication An institutional review board (IRB) is a committee with the authority to review, approve, disapprove, or require modifications in research activities involving human participants. The primary objective of any IRB is to protect the rights and welfare of human subjects involved in research; IRB review ensures that research with human subjects is conducted in accordance with all federal, institutional, and ethical guidelines. All research studies involving human participants, regardless of study design (eg, observational, secondary data analysis, no interaction with patients), must be submitted to an institutional review board for approval before study initiation. \n\n Research studies that use only secondary data (eg, medical charts) and that involve no more than minimal risk to participants do not require informed consent . (still requires IRB clearance) \n\n As a general rule: If research use Protected Health Information , you need clearance . If you are using some data where theres no way a patient can be identified, IRB can be exempted. \n\n Excessive compensation to research participants is inappropriate because it constitutes inducement (by incentivizing participants to overlook risks they may have otherwise considered as unacceptable), particularly for vulnerable (eg, low-income) populations. Compensation should be based only on the participants' actual time for study participation and \n\nassociated expenses .\n\n903 https://t.me/usmleinnercircle USMLE Inner Circle \n\nFederal regulations for research involving human participants \n\n# . Di sclose research procedures, risks & benefit s, alternatives \n\nInformed . Clarify differences in research vs clinical processes (eg, randomization, placebo) \n\nconsent . Generally re guired whenever research inv ol ves PHI . Ensure that research prot oc ol minimizes risks to participants \n\nIRB review . Ensure adequate i nf ormed consent, protection of PHI & equitable recruitment \n\n## . May be exempted or expedited in specific cases ( eg , minimal risks, no PHI collected) \n\nHIPAA . Requires researcher to obtain authorization from eatient to use PHI \n\n(privacy rule ) . Separate from informed consent \n\nIRB = institu ti ona l re vi ew boa rd; HIPAA = Health Insurance Portabi lity and Accou ntabil ity Ac t; PHI = prote cted health infonnatio n. \n\nG Re sea rch in a vu lnerable pop ul ation 66% \n\nVulnerable popula tio ns (e.g., preg nant women, neonat es, children, pri soners, ind ividuals w ith impaired decision-making capacity, economica lly or educationally disa dv anta ged individual s) are at increa se d risk of harm in cl in i ca l t ri als, and certain saf eg uards for protection of these populat ions are set in place by the Offic e of Human Re search Protection \n\n(OH RP). Befo re includin g ereg nant women in clinical tri al s, pr eclinical tr ials in pregna nt animals and clinical tri a ls in nonpr egnant individuals mu st have been conducted, a nd data regarding pote nt ial risks has to be avai la ble. Because t he proposed tr ial was preceded only by an animal tr ial in pregnant c himp s, it wo uld mo st like ly be rejected by an in s ti t ut ional review board. In addit i on to t he animal t rial, phase 0, I, 11 , and Ill clinical trials in nonpregnant women should be co nduct ed to ens ur e th e safety of the new dru g. Ethics & Communication 904 https://t.me/usmleinnercircle \n\n@ \"You can withdraw from your decision to participate in this study at any time.\" 94% Acknowledging this patient 's right to withdraw from the clinical trial at any time is the most appropriate response in th is case. According to regulations established by the Office for Human Research Protections (OH RP) of the U.S. Department of Health and Human Services, all subjects enrolled in a study have the right to discontinue their participation at any given time , for any or no reason , without incurring a penalty or loss of benefit which they were entitled to for participating in the study. The investigator cannot obtain any further informat ion without the subject's consent. If the study is not subject to Food and Drug Administration (FDA) review and the subject requests that the data already collected be destroyed, the investigator may honor the subject's requests depending on the protocol set up by the in st itutional review board. For studies subject to FDA review, the investigator cannot destroy this information or exclude it from analysis. For interventional studies, data regarding adverse events might be important to protect the safety of other research subjects, and the OHRP, therefore, recommends that the investigator clarify with the subject whether they wish to withdraw completely from the trial or only from the primary inte rventional component. If the subject wishes to withdraw only from the primary interventional component , follow-up data collection can cont inue after reobtaining the subject's consent.\n","transcriptionSegments",[],"notesText","title","flashcards","definitions","youtubeUrl","https://drive.google.com/file/d/1EEAFxtGwqkeAOIKtySS9au7Oyny2bI_u/view","emoji","noteLanguage","errorMessage","Error creating notes from the url","SUMMARIZING_FAILED","transcriptionRequestId","cloudflarePath","sessionId","9b241fff-fb37-4b65-9ca5-55792adb26c4","source","url","analyticsProperties",{"_70":71,"_74":75,"_76":77,"_68":69,"_78":79},"urlType","drive-pdf","appSource","web","urlSource","pickle","folderId","privacyStatus","PUBLIC","videoScriptId","podcastId","pickleId","studybee","classificationId","hasTimeline","server","root","routes/_user-details+/_dashboard+/_layout","routes/_user-details+/_dashboard+/_animated+/_layout","routes/_user-details+/_dashboard+/_animated+/notes.$id+/_index","actionData","errors"]