Transcript for:
Nephrology Overview

all right we move on to Reno the complete Reno review for the US Emily and shelf now if you struggle with Nephrology then this video is absolutely amazing for you because I covered everything you need to know in a really fun way let's begin here we have the heart and here we have the kidney it's actually kind of cool seeing them side by side like this they're actually the same height about five inches tall but that's not why I brought them both here the reason why I brought them both here is to make the following point the heart supplies blood to the kidney and as you can probably recall from your Nephrology teacher Kitty gets about 20 percent of cardiac output yes indeed the kidney gets 20 of cardiac output meaning the heart pumps out five liters of blood every minute and the kidneys get one of those leaders but this does not mean that GFR is a liter a minute the nephrons are of course not filtering a liter a minute of blood this merely means that the kidneys are supplied a liter of blood but they're actually only filtering 0.12 liters of blood a minute or 120 milliliters of blood a minute and this is what GFR is I hope we didn't insult our Nephrology teacher with this information let's tell him two Nephrology jokes to make him happy what do nephrologists say to non-compliant patients you're in trouble what happens to nephrologists who smoke marijuana they get kidney stoned with that introduction let us begin with acute kidney injury question one a 72 year old lady is brought to the Ed for lethargy and reduced appetite a few days after enduring a URI here are her lab values urine sodium Ob La less than 20 or more than 20. well let's take a look at the important lab values ethergy temperature and hypotension fever lethargy and hypotension equals sepsis and what happens in sepsis reduce perfusion to the kidneys that's a consequence of sepsis and when there's reduced perfusion to the kidneys that's a pre-renal Aki State and therefore sodium will be less than 20 and let's explain why in pre-renal Aki the urine sodium is less than 20 because the kidneys recognize the reduced perfusion activating the retinin Angiotensin aldosterone system then aldosterone acts to increase serum sodium thereby decreasing urinary sodium so again in pre-renal Aki aldosterone is released which leads to increased serum sodium now this is really important because in pre-renal Aki the kidneys are able to do this they're able to retain sodium because the tubules themselves at least at this point in time are not damaged this is in contrast to so as we'll see intrinsic renal Aki so again low perfusion sodium reabsorbed what will the osmolality of the urine be well as sodium comes out water comes along with it and therefore urine osmolality will actually be high so urine will have a low sodium because sodium is reabsorbed but it will have high osmolality question two what will appear in her urine again she has a pre-renal Aki red blood cell casts moneycasts or hyaline casts so remember in pre-renal Aki the tubules are intact and therefore there will not be any pathologic casts there will be hyaline casts which are normally seen in the urine and so she's happy red blood cell casts are a sign of glomerular injury Mighty casts are a sign of acute tubular necrosis but hyaline tests are normal maybe we'll name the lady in our scene harleen because she has hylene casts because again she had a pre-renal Aki they're composed of aggregated th proteins which we don't care about these hylene casts can be elevated in a person with a pre-renal azotemia so so far what do we have about pre-renal azotemia urine sodium less than 20 because of aldosterone urine osmolality High because as sodium comes out water also comes out and in the urine we'll see hyaline casts which are not necessarily pathologic question three what is her bun to creatinine ratio again in a pre-renal Aki more than 20 to 1 or less than 15 to 1 well as we recall there's low perfusion in pre-renal Aki and sodium is reabsorbed and Bon is also reabsorbed primarily in the PCT creatinine however cannot be reabsorbed it goes into the toilet so Bon is being reabsorbed just like sodium and creatinine is going out therefore the bun to creatinine ratio will be elevated bun to C bunk is elevated that's why I like to imagine a bunk bed on her head bunk bed for buen to creatinine her name was harleen because she has hylene casts I.E non-pathologic casts and in a toilet there's low urine sodium so the toilet's happy because he doesn't like salt in pre-reading like AI sodium is retained and here is the hippo I guess harleen likes hippos just kidding this hippo represents what we're talking about hypovolemia that in a hypovolemic State all these conditions are true question four what is the treatment for pre-renal azote besides treating the underlying problem such as antibiotics for pneumonia crystallite solution or amicasin and the answer is crystalloid solution crystallite solution is just a fancy way of saying saline or lactate ringers that's what it is fluids fluids that mimic or closely mimic the body's osmolality amacasin no way Jose that's an aminoglycoside that can cause an acute tubular necrosis that would not treat a pre-renal azotemia question 5 an 18 year old woman is in the Ed due to pneumonia now she has sepsis she's got IV fluids vasopressors and antibiotics such as Gentamicin she has stabilized but a few days later Serum cratin is elevated and Uranus shows epithelial cell casts epithelial cell casts are another way of saying muddy casts and they're a sign that the tubes themselves got damaged steel creatinine is of course elevated because the nephron is damaged so it's not doing its job properly and Gentamicin is an amino glycoside which is probably the cause of the Nephron damage here because you know glycoside can cause nephrogenic acute tubular necrosis so the tubules got damaged remember there are two types of acute tubular necrosis such as ischemic example due to an MI or nephrogenic causes such as drugs aminoglycosides Vancomycin ethylene glycol along with contrast now how long does it take for the patient to recover from acute tubular necrosis without considering severe complications the answer is about two to three weeks that's how long it takes for the tubular cells to regenerate and now that we've spoken about acute tubular necrosis we could compare pre-renal states which we've spoken about already with intra-renal states such as acute tubular necrosis and the lab values are the exact opposite whereas in pre-renal States urine sodium is low in intramenal States urine sodium is high because the tubes are damaged and they can't absorb sodium anymore and if we move down these are the red blood cell casts the white ones the muddy ones and the fat ones question six a 37 year old man comes in blah blah blah blah blah blah blah and urine shows white blood cell casts what is a diagnosis so white blood cell casts are seen in acute interstitial nephritis when I was in glomerular notified as we see red blood cell casts in acute tubular necrosis we see muddy casts eosinophils may also be found in the urine in acute interstitial nephritis but they're not always found now the same thing acute interstitial nephitis would have been the right answer I had the question said a man comes in with a fever rash and kidney injury what is a diagnosis acute interstitial nephritis acute interstellation nephritis is a hypersensitivity reaction which affects the interstitium and the tubules and it improves the cessation of the drug drugs which can cause an acute interstellation arthritis include penicillin sulfur drugs allopurinolphenitine quinolones and NSAIDs the same drugs which cause Stephen Johnson syndrome in addition to Lamotrigine and it makes sense both conditions cause a Type 4 hypersensitivity reaction ah how is acute interstellations diagnosed clinically but kidney biopsy is the gold standard we just usually don't need it how is acute interstitutional right is treated stop the offending agent and if there's no response then we give steroids so so far we've discussed tubular diseases now let's talk about glomerular diseases nephrotax and syndrome which involves loss of protein and ephritic syndrome which primarily involves glomerular inflammation question 7 which value is increased in a product syndrome albumin anti phenomen gamma globulins or lipids and the answer is lipids are elevated in nephrotic syndrome albumin is lost in the urine proteinuria that's the definition of nephrotic syndrome more than 3.5 grams a day of protein that's lost and that's why they get edema because there's a lot of cloud of pressure antithrombin 3 that's what leads to hypercoagulability and gamma globulins those are also lost in the urine that's why patients with the hemphotic syndrome are more prone to infections that's why patients with nephrotic syndrome require pneumococcal vaccinations lipids those will be elevated and the reason is because the liver produces lipids and cholesterol in response to low circulating proteins that's why in nephrotic syndrome patients are more prone to accelerated atherosclerosis because they have so much lipids in their body they need to be put on statins now how do you minimize proteinuria in nephrotic syndrome ACE inhibitors how do you minimize lipids and nephrotic syndrome statins how do you minimize edema and nephrotic syndrome Loop Diuretics what cheese is made backwards Adam cheese right because if you spell the letters backwards Adam cheese that's just a joke all right question seven a patient with nephratic syndrome now has flank pain and hematuria this was most likely caused by if they have flank pain and hematuria it's likely caused by reduced anticoagulant because now they have a renal vein thrombosis causing the flank pain and hematuria hematuria and red blood cell casts in the urine is a sign of nephritic or nephrotic syndrome but usually this is associated with nephritic syndrome here's acute mnemonic nephritic syndrome involves proteinur hematory acetamine red blood cell gas algoria and hypertension and here we just see the differences between nephritic and nephrotic syndrome in a cute little cartoon I actually put this Cola can over here this Cola can reminds us of the cola colored urine in nephritic syndrome question 9 which type of renal tubular acidosis causes hyperkalemia one two three or four so if you don't know renal tubular acidose as well welcome to the club as for the ants sorry oh it's not type three because there is no type three at least not that I'm aware of it's type 4. here's a cute little mnemonic from Dirty medicine 214 Lolo more in type 2 will be low in type one it will be low but in Type 4 potassium will be elevated if on test day there's hyperkalemia you know it's type four if on test day there are kidney stones or the urine pH is elevated or there's calcium you know it's type 1. question 10 when a person has a low blood volume for example due to vomiting what will happen to the nephron efferent arterial well remember Angiotensin II has various functions and when a person has a low blood volume Angiotensin II does its job for example it constricts the efferent arterial so therefore since we have low blood volume in our question the arterial will constrict remember Angiotensin 1 is converted to Angiotensin II through ACE and Angiotensin 1 itself used to be angiotensinogen until renin came along that's what renin does question 11 does metformin cause kidney damage and the answer is no metformin does not cause kidney damage it just increases lactic acidosis that's why we hold it in hospitalized patients especially in a patient with renal insufficiency because we don't want lactic acidosis to build up which can increase creatinine and the answer is BPH fiber might be able to reduce creatinine but BPH could lead to an increase in creatinine here we see the BPH causing an obstructive neuropathy this leads to a slow Rising creatinine but if you see a question the person who has BPH and they have proteinuria you know it's probably not because of the obstruction because BPH cannot lead to an increase in proteinuria question 10 I'm not sure we got to question 10 we've already done question 12 but anyway secondary nocturnal anti-resistance in children is usually developmental or due to some cause and the answer is it due to some medical or psychological condition remember primary means since birth and secondary means they've gone at least six months with bladder control so secondary anuresis would be due to Medical psychological condition whereas primary would be developmental in both cases the child is over five in both cases we get a linear analysis to assess for example UTI or proteinuria and remember newborns are supposed to have at least one wet diaper per day of life so if a neonate has a single wet diaper in the first two days of life we need to get for example a renal and bladder ultrasound to assess for any congenital anomalies question 11 what is the main cause of death in patients with Scleroderma renal failure or lung disease and the answer is lung disease it used to be renal failure before the 1980s by now it's lung the disease and what is the mechanism of sclerodermal renal crisis it occurs due to collagen deposition and endothelial injury in the renal blood vessels question 12 splanchnic vasodilation that leads to kidney injury which does not improve with fluids this is hepato renal syndrome a very life-threatening condition what is the treatment for hepatoreenal syndrome well really it's liver transplant but until then albumin and renal vasoconstructors because again the problem is vasodilation and you can just take a look at my video online of hepato renal syndrome question 13 a 48 year old woman with a recent UTI nighthouse right side of flank pain fever but no bacteria or red blood cells are found what is the diagnosis so this is renal abscess remember renal axis shows up after UTI with flank pain and fever we may or may not see bacteria or proteinuria and here we just have a picture of the renal abscess question 14 a 47 year old woman got a renal transplant now has decreased renal function her medications include prednisone tacromis among others what caused the kidney injury so remember that chromos or tacroilimus is nephrotoxic and it causes a pre-renal condition that is calcium Inhibitors cause vasoconstriction the Aki is through a pre-renal mechanism it's quite interesting tacrolamus is used in kidney transplants to prevent rejection but it's nephrogenic and note diuretics such as furosemide also leads to pre-renal azotemia but through a different mechanism that is they lower blood volume so there's lower cardiac output so there's lower perfusion to the kidney question 15 how does cardio renal syndrome damage the kidneys this is not hepatitarino is cardiorenal and cardiorenal syndrome there's increased central venous pressure heart failure leading to volume overload and venous pressure and congestion damaging the kidneys question 16 what is the mechanism of nsaid-induced kidney injury so NSAIDs lead to either social inflammation as we mentioned before in acute interstitial arthritis but we usually refer to the prostaglandin inhibition by inhibiting the prostaglandins which dilate the efferent arterial and says effectively constrict afferent and here we just have a comparison of NSAIDs and Aces and arbs remember NSAIDs constrict the afferent and ACE inhibitors effectively dilate the efferent question 17 50 of patients with rhabdo develop acute kidney injury 50 that's why we have to check their CK levels and the mechanism of injuries that myoglobin causes damage to the kidney tubules question 18 how to prevent contrast induced kidney injury and the answer is not by holding a metformin remember metformin is not nephrogenic it's by giving contrast with fluid for example 0.9 saline we also want to give the lowest possible dose of contrast possible question 19 what study should be done in a patient diagnosed with membranous nephropathy and the answer is Hepatitis B serology Because membranous nephropathy is associated with hepatitis B as well as C I like this mnemonic I made over here another Pharaoh remember the froggy reminds me of membranous nephropathy Arrow here is really scared because of the froggy he had been in the middle of putting a deposit near a Subway so Subway deposit for sub epithelial deposit or deposition and it's associated with Hep B and C because the story of pharaoh occurred in BC before the year zero and it's also associated with SLE malignancies and NSAIDs question 20 what type of castes are seen in renal disease associated with hanakshanley purpura remember IGA nephropathy is associated with hanax online some consider them different manifestation of the same disease but anyway they have red blood cell casts because it's a glomerulonephritis remember IGA deposits in the mesangium leading to inflammation but we do not see any changes in complement because complement is not involved in IGA nephropathy and then headaches online there's a low range proteinuria and I just wrote a reminder over here not that this is a new question but chronic hcd can also cause mixed cryoglobular anemia which is a small vessel vasculitis that presents with palpable purpura glomerularis joint pain and peripheral neuropathy here's the real question 21 a six-year-old boy comes in with hematoria and C3 levels that are low protein is one plus what is the diagnosis so here we see C3 levels are low so we're not we know it's not IGA nephropathy this is post-strap glomerulonephritis in focal segmental comedosclerosis we would see protein three plus or four plus in the nephrotic range again an idea nephropathy C3 levels will be normal host drip glamophytus this involves immune complex deposition so C3 levels will be low C4 levels may also be low and remember to see a kid with periorbital or general edema with color colored urine a little bit after having group a strap think of post-regular menonephritis and here we just compare hygiene nephropathy and poster at glomerulophytus Remember by the way both conditions may be asymptomatic but in both serum creatinine is elevated question 22 creatinine increases in pregnancy or diabetic kidney disease and the answer is in diabetic kidney disease because in pregnancy it actually goes down due to hyperfiltration so if you have a pregnant patient with elevated creatinine start thinking about kidney disease for example diabetes because pregnancy can actually worsen a diabetic nephropathy besides ACE inhibitors and Loop Diuretics how is an obese patient with focal segmental glamarosclerosis managed with steroids or weight loss and the answer is with weight loss steroids are only helpful in primary focal segmental glandifitis and weight loss is helpful in secondary for example due to heroin HIV or infection so I mentioned obese in our question which on exam day is associated with secondary focal segmental glomerular sclerosis I have another question 22 glomerulonephritis and low complement and positive serum cryoglobulins this is seen in membranoproductive glomerulonephritis in lupus nephritis we see a positive Ana which is the most sensitive test or anti-dna or anti-smith which are more specific but not so sensitive cytopenia is not just associated with malignancy it's also seen in conditions for example in lupus and here we just have the thick capillary wall seen in memoroplanative glomerulonephritis by the way both focal segmental glomerular sclerosis and minimal change disease both involve protocyte effacement so if you see podocyte effacement on examine I think of these two conditions minimal change disease more often in children question 23 a 15 year old boy has hematoria dysuria and pyuria I.E white blood cells in the urine but no flank pain what's the next step so we want to give antibiotics because we're dealing with a UTI renal ultrasound that would be for Seneca Stone which would cause pain question 24 3 year old girl has few Day history of periorbital edema and Labs four plus proteinuria so we know this in that post replica is so what's the next step so here we want to give steroids because it's most likely mineral change disease which shows up in children and steroids are very effective for this condition but the condition does recur question 25 how do you treat uric acid kidney stones and the answer is increase the pH of the urine for example with potassium citrate this causes uric acid to be more soluble and promotes Stone disillusion furosemide doesn't treat uric acid Stones it can contribute to the development of calcium Stones because furosemite dumps calcium into the nephron and here we just have associations of the various Stones definitely remember this because this is super high yield for example calcium oxalate stones are seen especially in Crohn's patients because in Crohn's patients they can't reabsorb fat so the fat binds with calcium so oxalate is reabsorbed and then dumped into the kidney leading to calcium oxalate zones the treatment for calcium oxalate zones are thiazides of course we also give hydration ammonium Magnesium phosphate think of the gram-negative bugs Proteus and klebsiella it can cause stack or colliculus which has rapid growth and it's associated with UTIs treatment of ammonia Magnesium phosphate zones are surgical under the stone antibiotics and possible nephrectomy uric acid Stones remember these are the ones not seen on x-ray because they're radio Lucent and as you mentioned treatment is potassium citrate and cysteine zones are rare their most common in children and they could also present with sagorn colliculi and treatment is with hydration and alkanelization of the urine question 26 kidney and Bone cysts are seen in amyloidosis due to dialysis the beta-2 microglobulin cannot be adequately eliminated resulting in carpal tunnel syndrome shoulder pain and Bone cysts and these could actually result in fracture question 27 elevated creatinine small kidneys no red blood cells Trace proteinuria is due to high blood pressure and high blood pressure there is chronic stress on the renal vasculature so there's ischemia and fibrosis as opposed to an amyloidosis we see large kidneys and nephrotic syndrome I.E lots of proteinuria question 28 AA amyloidosis in a patient with for example rheumatoid arthritis was commonly manifests with renal problems that's why we're talking about in the renal section 90 of patients with a amyloidosis have renal problems and diagnosed with biopsy which shows amorphous material unstaining with Congo red is it just me or do you think of this guy when you think of Congo red maybe it's just me but anyway Congo red amyloidosis renal problems versus Al amlodosis seen in multiple myeloma question 29 sickle cell trait does which of the following all the above it provides military protection confers an increased risk to DVD and converts an increase risk to renal papillary necrosis and this happens especially under physiological stress such as dehydration acidosis because sickling can occur question 30 atherosclerosis and severe hypertension and pulmonary edema for example with crackle's jvd but no low extremity edema so we know we're dealing with a pulmonary edema this is due to renal artery stenosis we get a Doppler ultrasound and by the way just a reminder that this condition may be seen a few years after a patient's had a kidney transplant that the renal artery from the Canadian transplant could lead to a stenosis as I mentioned already renal artery stenosis causes risen hypertension and which kidney releases renin only the kidney involved only the kidney that has the stenosis if it's bilateral it will be bilateral question 31 a patient comes in with severe flank pain CT reveals a four millimeter Stone there are no signs of infection or impaired kidney function what's the next step and the answer is hydration and a strainer what I mean by a strainer is like a tea strainer to catch the stone so we can assess the stone composition hospitalization is not necessary because most Stones pass when they're less than five millimeters question 32 what is seen in chronic renal failure and the answer is we see easy bruising the mechanism is as follows as Yuri arises Arginine and its precursors are shunted to produce nitric oxide nitric oxide levels build up which disrupts primary hemostasis so we don't have proper platelets and this is what's seen in chronic renal failure we don't need to know this mechanism just recognize in a chronic renal failure there may be easy bruising but there's not hypercalcemia and hypokalemia we have the opposite we have hyperkalemia because we can't excrete potassium question 33 kidney failure leads to Bone damage due to all of the above elevated pH levels because pth is released in response to low calcium and pth leads to bone resorption as we mentioned we have low vitamin D levels so we can't mineralize new bone and metabolic acidosis produces an environment of low ph and that inhibits bone mineralization so if you see a patient with osteoporosis come in with a history of CKD the first thing to order is a pth level maybe there's low calcium leading to elevated pth and that leads to bone resorption question 34 sudden death in these patients what do we see polycystic kidney disease is from cerebral aneurysm well subarachnoid hemorrhage now how do you treat autosomal dominant polycystic kidney disease hypertension because these patients have hypertension and you treat it with ACE inhibitors and the reason is because in autosomal dominant polyester kidney disease what happens is there's a localized ischemia secondary to assist enlargement and this local ischemia leads to an elevated rash that's why we give ACE inhibitors to depress or suppress the RAS system the most common cause of death in these patients is not cerebral aneurysm it's a renal failure and we treat this with tallaptim this delays progression but it doesn't stop it completely and that's why these patients often need long-term dialysis question 36 patients in their 30s with hypertension hematoria and flank pain this is polycystic kidney disease remember patients often present in their 30s and 40s with polycystic kidney disease question 37 kidney disease and mitral valve prolapse this is polycystic kidney disease remember in this condition they're floppy everywhere in the kidneys in the heart in the liver leading to cysts in the intestines that's why they get Diverticulitis and brain vessels that's why they got the cerebral aneurysms question 38 what is very concerning a patient with kidney stone and the answer is fever and CVA fever and CVA tenderness are signs of infection for example pyelonephritis and so it can progress to sepsis dilation of the ureter is not turning because that scene with all Stones question 39 what gynologic condition can result in cyclic hematuria the answer is endometriosis because the implants can be in the bladder leading to cyclic hematuria they get it when they have their periods question 40 stones that are between 5 millimeters and 10 millimeters are treated with Alpha antagonists such as tamsulosin because the blocking Alpha leads to smooth muscle relaxation and so the stone passes surgeries when it's 10 or more some say seven or eight or more but the point is for you know the purposes of exams if it's 10 or more that's when I go with surgery question 41 which does not prevent calcium oxalate kidney stones and the answer is protein protein actually increases the risk of a stone because there's increased oxalate and oxalate binds with calcium to produce the stone and you can take a look at the other conditions that we have over here why they could prevent calcium oxalate kidney stones question 42 what are the most common bugs implicated in dialysis related infections staphorase and staph epidermis seen in both hemodialysis and peritonitis related to peritoneal dialysis so in both forms of dialysis we have these bugs we grab I'm staying in culture the peritoneal fluid question 43 a 20 year old woman with recarn headaches hypertension and renal artery stenosis this is fibromuscular dysplasia where you see this picture it's always this picture when it comes to fibromuscular dysplasia where we see the string of beads appearance inside the renal vasculature it is kind of like what we see in primary sclerosing cholangitis what we see in the biliary ducts this is what we see in fibromuscular dysplasia by the renal vasculature all right the headaches in this condition are due to the internal carotid stenosis first line hypertensives for fibromuscular dysplasia are Aces and arbs definitive treatment is with percutaneous transluminal angioplasty or surgery question 44 what is the management for simple renal cysts reassurance concerns for malignancy are when they are irregular walls multilocular contrast enhancement and they cause pain or hematuria question 45 patients such as a baby with that but if the reflux is only mild antibiotics may not even be needed question 46 a patient is older than 50 unintentional weight loss smoking hard flank Mass we know this this is renal cell carcinoma but the mass may be found incidentally for example in an asymptomatic patient don't think that in renal cell carcinoma there's always flank pain or that there's always hematuria question 47 besides behavior modification what's the best treatment for nocturnal antaresis the answer is desmopressa not immobreen that is a TCA a tricyclic antidepressant that has lots of side effects so it's of course not first line for example could cause cardiotoxicity question 48 what's the test for a patient with suspected urethral injury the answer is retrograde erythrography involves an x-ray of the urethral tract an extravatization of contrast to denotes urethral injury question 49 flank pain and wedge shape cortical infarction of CAT scan that's a relay infarction it has a wedge shape remember ischemia produces wedge shape just like just like it does in the lungs in pulmonary embolism and for example renal infarction could be due to an infectious endocarditis question 50 bladder cancer screening is never never ever ever even though it's at increased risk question 51 first step in suspected bladder cancer is cystoscopy this allows direct visualization I meant to write visualization of the bladder wall and we biopsy anything suspicious we get a CAT scan just for staging question 52 the most common cause of bladder distention in newborn boys is posterior urethral valves this can lead to a powder sequence When In Utero you get a renal and bladder ultrasound and a sister urethrography question 53 renal cell carcinoma and hemangioblastomas we know this it's an autosomal dominant condition where there's a vhl tumor on Gene 3 leading to hemangioblastomas field cross anatomas renal cell carcinoma and we treat it with tumor resection question 54 the most common renal malignancy in children is Wilms tumor associated with wagger and with bws in Wagner we see Williams aniridia gu and mental retardation now known as intellectual disability question 56 and Adolescent new develop survocacy all should be reassured generally adolescents should be reassured because it's probably primary and we can test it out if it decompresses when supine as opposed to in children varicoceles are concerning usually secondary and it persists in the Supine position so we get an abdominal ultrasound 57 child with hearing loss and hematuria alport syndrome alport syndrome is involves splitting of the glomerular basement membrane and it's an x-linked disorder 50 57 early 57 a child with recurrent episodes of simple cystitis with no fever flank pain may have constipation recant UTI would cause pyelonephritis not simple cystitis constipation can lead to cystitis and and the treatment is stop holding it in and we may provide the child with laxatives 58 fibrotic narrowing of the urethra urethral stricture can be idiopathic quantized trauma and we treat with dilation or with surgery 59 first line treatment for stress urinary incontinence is kegels I just made up that word there's no such word kegels it's Kegel exercises Kegel exercises is first line for stress urinary incontinence and if the kegels don't work we may give a pessary and here we just compare the various types of urinary incontinence and I have a little mnemonic in case you have a hard time here we have the bladder who's very stressed he's very stressed and he has his cake Coco I give him the cake Coco to make him happy cake Coco for Kegel here we have something going on that's very urgent urgency or incontinence and there's this rocket flying away because an urgency and consonants there's a sudden overwhelming need to pay and what happens is there's this Ox over here trying to stop the rocket the ox oxybutynin this Ox over here actually has a mustache with an ants on it for anti-muscarinic because oxybutynin isn't antimascarinic so again the ox that's an antinoscriminic for oxybutynin is trying to stop the Urgent rocket flying away for urgency incontinence and here we have a lady who has overflow incontinence we see it's overflowing so her friend Beth gives her a call for bethena call epathetical is used to treat overflow incontinence question 60 what's the treatment for UTI in children the answer is we need E coli coverage and you can take a look at the other choices over here question 61 anticholinergic induced urinary tension is treated with a drug cessation reduction and intermittent catheterization for example in a patient taking amitriptyline of diphenhydramine and get urinary tension give them intermittent catheterization 62 lithium-educed nephron damage leads to low urine osmolality that does not improve with desmopressin remember if it improves with divers of Morrison we know it's Central diabetes insipidus but a nephrogenic it does not improve the desmopressin and high urine osmolality that would be seen in polydipsia question 63 thiazides lead to low levels of sodium and potassium that is thiazides increase renal excretion of sodium and potassium also we see low magnesium question 64 which tubulopathy is like being on a thiazide all the time that is they get hypokalemia and hyponatremia and Hyper magazemia and low blood pressure and the answer is ghetto man syndrome I like to imagine the gentle man wearing a tie gentleman for ghetto man and tie for thiazides you could think of getting him as being like a chronic thiazide state and we can contrast Skittle man with Liddell lidel there's high blood pressure now I like this because this is actually an ABC order barter ghetto man in Liddell meaning order affects the thick ascending lamb giggleman affects the distal tubule and Lydell affects the collecting duct and all cause hypokalemia my mnemonic is bagels are low in potassium bagels for butter get the Manila Dell lead to hypokalemia question 65 bulimia volume depletion is treated with normal saline flute your cortisone is for Primal adrenal insufficiency question 66 which electrolyte atom atom leads to Peak T waves and shorten QT and the answer is if you ever see the shortened QT think of the hypers and here it's hyperkalemia hyperkalemia and hypercalcemia both lead to Short QT as opposed to hypokalcemia and hypokalemia they lead to prolonged QT question 67 severe hypercalcemia is treated with hydration and calcitonin and of course not thia's eyes that would worsen hypercalcemia because it's calcium sparing question 68 lab show potassium levels eight which is really high and EKG shows peaked T waves so we see EKG changes associated with hyperkalemia what's the next step we don't repeat the potassium levels because we've already confirmed that there's a symptomatic patient here so we give calcium gluconate calcium protects the cardiac myocytes and we follow up with insulin and glucose 69 rapid correction of hyponatremia can result in osmotic demyelination I've never heard a medical student talk about osmotic demyelination or cerebral edema without using the following poem from low to high your ponds will die from high to low your brain will blow question 70 CKD hyperkalemia management includes zirconium or ACE inhibitors and the answer is zirconium K oxalate falling out of fever now it's zirconium and pateramer the way zirconium works is that it exchanges potassium for sodium that's why I like to spell it potassium sodium zirconium zirconium exchanges potassium for sodium so potassium dumps into the nephron and sodium is reabsorbed again also paterramer sodium for calcium question 71 tinnitus fever and technia so this is seen in aspirin overdose what metabolic status mix primary respiratory alkylosis and primary metabolic acidosis often showing normal pH 72 hypernatremia can be caused by to all of these diuresis dehydration diabetes insipidus diarrhea disease all cause diaper and atremia question 73 hyponatremia is defined as serum sodium less than 135. it may be asymptomatic patients may have confusion muscle cramps or nausea and the first step is the serum osmolality and here we just have workup for hyponatremia the purpose of the exams we focus on this one over here very often that in hypotonic hyponatremia and the patient is uvulimic so we have to differentiate siadh from polydipsia what conditions can cause hypercalcemia and the answer is all of these hyperparathyism psychosis styzite all of these and malignancy as well as swim and cell carcinoma and multiple myeloma another question 74 a patient develops cramps and tetany after a thyroidectomy what happened parathidectomy remember parathidectomy can lead to a hypocalcemic state vision loss and optic disc hyperemia is seen in methanol toxicity ethylene vehicle leads to Stones methanol toxicity leads to vision changes question 76 kidney disease and Asthma Church Strauss syndrome the other two conditions involve kidney along kingly and lung but in wegeners we also see sinus question 77 man in his 20 says glomerular nephitis and Pulmonary Hemorrhage this is good syndrome which often shows up in men in their 20s there's no upper respiratory involvement and this is a very severe condition let's end off with pure Urology stuff fever and tender boggy prostate that's prostatitis treatment includes ciprofloxacin CPS and x and doxycycline hydroceles typically resolve in six to 12 months if not what's the treatment we take it out with surgery due to the risk of inguinal hernia remember hydroceles transaminate varicoceles do not testicular torsion should you first try to manually correct only if it will not delay surgery or surgery is unavailable remember this is a huge emergency you have to do with detergent in six hours or else 81 erection is mediated by parasympathetics remember point and shoot 82 nitrates cannot be combined with sildenafil pg5 Inhibitors can be taken dangerously lower blood pressure and affect the heart 83 best initial treatment for BPH is footlockers such as tamsulosin and terrazasin are great if the patient is also hypertensive what's the next best step five Alpha reductase Inhibitors such as finasteride severe transurethral resection or surgery take the prostate out by the way which zone is affected in btph the central zone and that's why not be felt on Dre 84 elevated PSA is seen in all of these prostate conditions and as we know it's controversial as a screening tool but it can detect a prostate carcinoma recurrence E5 the most common malignancy in men 15 to 34 years of age is testicular cancer question 85 the most common malignancy in men 15-34 is testicular cancer another 85 wellcopaxi should be done by six months remember inguinal hernia by five years but orcopexy by six months I like to call it orkyo six monkey orkyo six monkey reminds me that orkiopaxi should be done by six question 86 posterior testicular pain and swelling that improves with testicular elevation is seen in epididymitis all right and most common is chlamydia nyseria if the patient is less than 35 and equally after more than 35. less than 35 would give such a accident doxycycline question 87 if a wrestler has infertility and strong muscles what lab values are low probably taking anabolic steroids so gnrhlh and FSH low because the steroids inhibit GnRH released from the hypothalamus 88 after injection of phenylephrine a man's pre-opism improves what's the next step we want to get a CDC to assess for something like sickle cell that predisposes them to this condition but again pre-opism can be idiopathic 89 system leads infertility due to absence of acetapheres flagell motility that would be seen in Cartagena syndrome all right fast efforts may be the only feature in a patient with mild cystic fibrosis question 90 so the NFL can lead to all of these pre-apism flashing blue discoloration division optic neuropathy as well as headaches and by the way you don't take sildenafil with nitrates or I didn't mention this before alpha-1 blockers such as dexasin which is used to treat premature ejaculation peroxetine not or related topical lidocaine 92 after stabilization burn patients require aggressive fluids and urinary catheterization because they can't pay we need to get the PA out question 93 prostate tenderness your current UTI painful ejaculation this is chronic bacterial prostatitis all right we treat with six weeks for example alone 94 penile pain curvature and trouble with it of course this is Peyronie's disease I think that's how you pronounce it Peyronie's disease and we treat with pentoxophiline and collagenix injections and surgery if it's refractory 95 testicular Mass kind of capacity and elevated estrogen this is seen in latex cell tumors because of the increased estrogen levels they get gynecomastia all right this is not seen in for example sertoli 96 a common germ cell tumor that presents with a painless unilateral testicular Mass but usually no elevated lab values such as beta agency AFB this is the seminoma the most common of all the testicular cancers all right in the non-seminomas we have elevated lab values for example in beta HCG this is eating cardiocarcinoma in AFP that's the osac yolk Sac tumors 99 what's the greatest risk factor for peroxide's cancer Advanced age especially if they're over 70 and 100 a Boy comes in with suspected testicular torsion but it's not clear what the next step we want to get a Doppler ultrasound of the scrotum to assess alright at the end of this video I really hope you enjoyed stay tuned to the next video and take care foreign