Okay, so medicine review, okay? So we have 70 keywords today. We'll try to spend 90 seconds on last per slide I will encourage you again try to follow along you'll get the most from this review if you you try to capture most of what we talk about okay and then just review those notes over and over again and i will encourage you to do the i mean you're probably familiar with my other reviews from back in the day i used to do a medicine review in the past with like material but i stopped basically changed from that because I feel like this format is a lot more comprehensive.
We'll cover like a lot more material than I do at my regular reviews. And I will encourage you to do the four practice MBMEs, right? They are the most reasonable approximation of the real test.
It costs $20 a pop. You're already in, I mean. Tons and tons of debt already.
$80 would not like, I mean, it's like nothing, right? I mean, you probably spend that much on coffee every month. And it's really not, like I said, it's not a big departure from step one. Many people call this like step 1.5, okay? So, any questions before I start?
Good? Okay. First one. So, opening snap with diastolic rumble at the left fourth interspace.
What kind of murmur is this? So left fourth interspace right here. Remember like the apartment M mnemonic.
So A, P, T, M. What's here? Tricuspid. And it's a diastolic murmur. So what is that? Stenosis.
Very good. So this is a tricuspid stenosis. And why are the jugular venous A waves tall? right?
So the atria, remember on your jugular venous pulsation wave, the A wave represents atrial contraction, right? So if your atria are contracting against increased resistance, that A wave will be bigger. Does that make sense? Okay.
And what What can we do to increase the intensity of this murmur? Will an increase in preload make this murmur sound louder or softer? Louder, right?
Because again, by bringing more blood to the heart, right? So if you do like the leg raise or you give this person an infusion of fluid, fluid or you inspire, because this is a right-sided heart murmur, right? So inspiration will increase venous return.
When you have that, you're increasing preload, and that will increase the intensity of the murmur. Real quick, what would an increase in afterload do to this murmur? It will decrease the murmur, right?
Because you have less flow across that stenotic valve. Does that make sense? Any questions on this slide? Okay, good.
Now, elevated AST and ALT and blistering lesions on the dorsum of the hands and severe hirsutism. What's your diagnosis? Anyone here interested in dermatology?
So hirsutism, right? So the person is like hairy like a lot. They have elevated liver enzymes. And they will tell you that the person sweats like a ton.
What is this? It's a derm condition. Think of that heme synthesis pathway.
Very good. This is porphyria cortina tarda. And what's the deficient enzyme?
Very good. UROD. Okay. Uropoferinogen decarboxylase.
Do you think they test derm on the medicine shelf? Oh yeah, they do. Very good. Do you think they test ophthalmology on the medicine shelf?
They do. Very good. Okay. So this is porphyria cutanea tarda. Okay.
So UROD deficiency. And how do you treat this? What do you do to them?
phlebotomy very good you literally like bleed out these patients i mean you don't like bleed out your patients but you in a gentle manner try to extract blood from them okay that's how this is treated uh what's the other liver condition uh that's also treated with phlebotomy it also causes like a restrictive cardiomyopathy hemochromatosis very good okay any questions on this Good? Good. Okay. Now, this is an annoying triad.
You know my feelings about this triad. So hypoglycemia, hypoglycemic symptoms, and resolution with glucose administration. What is this?
What's this triad called? Whipple's triad. Very good. What's the pancreatic tumor that has an association with Whipple's triad?
An insulinoma, very good, an insulinoma. And if a person has an insulinoma, what will be true of their insulin levels? It'll be high, good. How about C-peptide?
It'll be high because that's endogenous insulin secretion. Okay. Now, let's assume one of you is injecting insulin because you're like, I don't want to work this night shift. I just want to, like, be hypoglycemic so they send me home. What will be true of your insulin levels?
It'll be high, good. What will be true of your C-peptide? It'll be low because the insulin they sell on the street, not on the street, in the pharmacy. The insulin they sell in the pharmacy does not have C-peptide.
But let's assume some of you are a little wiser. If they see low C-peptide, they think I'm injecting insulin. And you start taking a sulfonylurea instead to fake your symptoms so you don't work your night shift. What would be true of your insulin levels?
High. How about C-peptide? It would be high as well. Because if you remember from step one, for those of you that have taken it already, your sulfonylureas, they block that potassium channel. at the beta cells in the islets of longer hands, right?
So you basically, by blocking those potassium channels, the cell depolarizes and you squared out insulin, okay, at some point, okay? So because sulfonylureas work that way and you're increasing endogenous insulin release, your insulin levels go up and your C-peptide levels go up. So how do you differentiate between taking a sulfonylurea factitiously and an insulinoma on labs?
There's a screen. You guys know what it is? It's a secretagogue screen.
They also call it the sulfonylurea screen. So let me get my... So it's called the secretagogue screen. or the sulfonylurea screen. It's basically a test to detect sulfonylureas in your blood.
So that's how you tell those things apart. And if a person has hypoglycemia, and they're like circling the drain, how do you treat them? You can give glucagon.
Very good. Remember, glucagon raises your blood glucose levels. So it's actually the quickest way to acutely raise a person's blood glucose levels. It does it within seconds. OK, but if glucagon is not an answer choice, what do you do on your exam?
Give what? Juice, right? So you give like a sugar drip.
Okay. Does this make sense? And what's the classic buzzword for the skin association for glucagonoma? Very good.
Necrolytic migratory erythema. It will come up in a later question. Okay.
Any questions on this slide? Okay, now let's do some quick micro, okay? And if you notice, I sort of, I'm going to try to spread the knowledge around.
I'm not just going to do like 10 micro, 10 heme, 10 no, because your exam would not be like in neatly divided sections, right? So I try to spread the wealth around. So if a person has diarrhea and they consumed pork, what is that? No. T-solium classically does not cause diarrhea on exams.
Not in the real world, on exams. No. It starts with a Y. Yersinia enterocolitica.
Very good. Okay. Now, undercooked shellfish with diarrhea. Very good.
Vibrio, right? So your vibrio species, right? So like vibrio volnificus or vibrio parahemolyticus.
And what's, of these two vibrio species, what's the one that has this, like, pretty bad prognosis if a person has pre-existing liver disease? Vulnificus. Very good. Vulnificus. Okay.
Now, severe rice water stools in a developing country? Cholera. Very good.
Vibrio cholera. Okay. And how do you treat most vibrio species in general? Oral rehydration, good. So that's one thing you should do.
What's another thing you could do if you wanted to give them a drug? What class of protein synthesis inhibitors? Your tetracyclines.
Okay, your tetracyclines cover Vibrio pretty well. Okay. Now, bloody diarrhea with a super small inoculum? Shigella? Good.
Shigella? Good. Now, bloody diarrhea after consuming eggs or poultry?
Salmonella. Very good. Okay. Salmonella. Now watery diarrhea two hours after consuming potato salad.
Staph aureus. Awesome. Okay. Never eat potato salad.
It's usually a bad idea. I'm just kidding. Okay. Now bloody diarrhea with low platelets, unconjugated hyperbilirubinemia, and elevated creatinine. That's EHEK.
Very good. E. coli 0157H7.
Okay. So this is potentially like hemolytic uremic syndrome. Okay. Remember your thrombocytopenia, right? Hemolytic anemia and acute renal failure.
Okay. So this is HUS. Any questions on these slides? Good.
And in general, I would just say that if a person has a diarrhea, usually supportive care is all that's warranted. But if they are trying to get you to pick a drug on exams, probably go more with your fluoroquinolones or your macrolides. Yeah, your macrolides or your fluoroquinolones.
They tend to treat most causes of diarrhea pretty well. But I'll say in general, on exams, go with fluoroquinolones like ciprofloxacin, moxifloxacin, levofloxacin, the works. Let's do some more.
Now, you go to Mexico, come back to the U.S., diarrhea. What is that? ETEC, very good.
Enterotoxigenic E. coli, okay? That's your Montezuma's revenge, if that's what floats your boat.
Now, foul-smelling watery diarrhea after recent treatment for an anaerobic bacterial pneumonia. CDEF, right? You probably saw this on the wards, right? So remember, if you ever see a question where a person gets an antibiotic, and then afterwards they get diarrhea. Okay, usually foul-smelling.
Think about C. diff. And how do you prevent C. diff? Very good, hand-washing.
Okay, you would probably see preventive medicine questions on your exam. Okay, let me say like, Oh, which of the following interventions would have decreased the risk of transmission of this bug? Okay, C. diff, it's hand-washing.
And how do you treat C. diff? Metronidazole, if that doesn't work.
Orovancomycin, very good, if that doesn't work. Fidaxomycin, very good. Fidaxomycin.
And if that does not work, fecal transplant, very good. A fecal transplant. Okay, I know, it's kind of gross, right? So, crampy abdominal pain after consumption of home-canned veggies. That's botulism.
Very good. That's botulism. So many people have come to expect the flaccid paralysis. They are beginning to shy away from that on MBMEs. And then they just put like, oh, a kid with abdominal pain and diarrhea.
Think about botulism. Especially if you see the consumption of canned foods in the question. Think about botulism.
Now, puppy owner, bloody diarrhea with ascending paralysis. Very good. This is CJ Junai.
Okay. Campylobacter Junai. What's the ascending paralysis talking about?
Guillain-Barre syndrome. Very good. Okay. Now, what are you dire after eating fried rice at a Chinese restaurant? Very good.
Be serious. Bacillus serious. Okay.
It has a toxin. It's known as serolite. Serolite causes a lot of nausea and vomiting. Okay. So it's a pretty nasty diarrhea.
I believe I've actually had this in the past. And actually I did in fact, but it was not Chinese fried rice this time. It was Nigerian fried rice that actually cooked. And then I got into trouble.
It was, it's just, it's the worst feeling. It's the worst feeling. Trust me.
Okay. So, Prussian blue staining of a bone marrow smear reveals basophilic inclusions around the nucleus in a 75-year-old male that lives in a home built in the 1930s. What is this?
Very good, right? Cideroblastic anemia, lead poisoning. Okay. Now, what would be true of your ferritin in lead poisoning?
High or low? It'll be high, right? So let's talk about this real quick, right?
So remember, if a wedding is to actually happen, you need the two people to sort of shop for the wedding, right? So basically, with lead poisoning, you have problems where ultimately you're trying to make heat. That's the wedding that's supposed to happen. But instead, you have an iron shop for the wedding, but you don't have protocol for it for that wedding because the heat is in the...
doesn't start away, it's all screwed up, okay? If that happens, iron sort of hangs around, like just hanging out, chilling, chilling, chilling. So all that iron that's hanging out like in the bone marrow, okay, that raises your ferritin because you're storing more and more iron, but you're not necessarily using it, okay?
So your ferritin goes up in lead poisoning. What happens to your TIBC? It goes down, okay?
So hopefully you remember from pathoma, that inverse relationship between ferritin and TIBC. If your ferritin goes up, your TIBC goes down, okay? And how do you treat this? How do you treat lead poisoning? Soxhimer, what else?
EDTA, very good. What else? British antiloacite.
Wow, that's pretty specific. Yes, that's correct. What else? DMSA, okay, DMSA, right? So DMSA, Soxhimer, British Antimoacite, EDTA, DMSA, I've talked about that already, okay?
And is there a vitamin you could introduce to supplement and treat, like I said, aeroblastic anemia? B6, very good. Okay, remember the rate limiting enzyme of heme synthesis is ALA synthase that uses vitamin B6 as a cofactor. Does that make sense? Good.
Now, chest x-ray showing, bless you, so chest x-ray showing diffuse bilateral ground glass infiltrates in a febrile patient taking high dose immunosuppressants. What's the bug? Very good, pneumocystis gervetzi.
Pneumocystis gervetzi. And what is this positive for? What do you stain PCP pneumonia with?
Silver. Very good. Okay.
So if you get an exam question about bronchial alveolar lavage revealing silver stain positive organisms, think about pneumocystis gervetzi. Okay. And how do you prophylax against this bug? Back trim, right?
So TMP-SMX. Okay. What else?
Dapsone. Very good. What else?
Sorry? Etovoquine. Yes.
What else? Clenda. Yes.
What else? There's another one I've seen on exams. That's with a P.
No? Pentamidine. Very good.
Okay. So let me read out those things. The big ones on exams. Trimethoprim, sulfamethoxazole, TMP-SMX, Bactrim. Okay.
aerosolized pentamidine that's another one okay dapsone is the third one they occasionally test does that make sense so those are the big ones you can use the exotic stuff as well like atova corn you can use clindamycin but i'll say the first three are probably the big ones you should remember tmpsmx dapsone and aerosolized pentamidine okay and um I mean, obviously, you also treat this with TMP-SMX. But real quick, what's the magic CD4 count where you have to begin to prophylax against this stuff? 200. Very good.
That's the magic number you want to remember. And who should get steroids? That's not one of the criteria. There are like three high-yield things you need to know, like criteria. Like, oh, this person has PCP pneumonia.
We should put this person on steroids as well. What's the oxygen saturation cutoff? No.
So if your SAO2 is less than 92%, but what's the oxygen partial pressure thing? 70. Very good. Okay.
And what's the AA gradient criteria? What's one half of 70? 35, very good.
If your A gradient is greater than 35, okay, if you meet any of those criteria, in addition to TMP-SMX, those patients should be placed on steroids, okay, because they actually report of people that by treating the PCP pneumonia, you get rid of the infection, but the massive inflammatory reaction just kills off the lungs, and those people end up needing a lung transplant, okay? So if you meet any of these criteria on exams, and trust me, I've seen this tested quite often. go ahead and place those people on steroids. And how do you diagnose PCP pneumonia?
A BAL, very good. A bronchial alveolar lavage, okay? And what's classically elevated in the pulmonary fluid? LDH, very good. If you ever see LDH elevated pulmonary fluid, stop reading the question.
That's PCP pneumonia, end of story, okay? Now, flunk pain with gross hematuria, what's the big diagnosis you're thinking of? Kidney stones, right? So the $5 term is nephrolithiasis, right? So let's be a little more medical here.
Envelope-shaped stones, what is that? calcium oxalate very good right so you will get it in one of many ways right so you could say oh you know what i want to commit suicide by drinking uh what do they call this thing uh ethylene glycol right so like antifreeze that's one another way to get this is if a person has crohn's disease they actually have increased reabsorption of oxalate in the terminal ileum okay so they can get uh calcium oxalate stones in fact uh what's the most common kind of kidney stone calcium mock select. Very good. Now, coffin-shaped stones, what are those? Struvite stones, okay?
So don't forget your magnesium, ammonium, phosphate stones. What's the big bug risk factor for that? Proteus, very good. Because remember proteus is urase positive, so it can make your urine alkaline, okay?
So acetazolamide will probably be contraindicated in those kinds of people because it can make your urine even more basic and precipitate those stones some more, okay? But the big one you want to remember, the urase positive bug, proteus mirabilis. Which one is radiolucent? Very good. The uric acid stones.
Remember the U in radiolucent for the U in uric acid stone. Now shaped like a hexagon, so like a benzene ring. Cysteine.
Very good. Remember cysteine sounds like six team. Okay.
So six members to the ring. Okay. And how do people get cysteine stones? What's like the genetic defect? Chola.
Very good. So chola transport a problem, right? What does the C stand for?
What does the O stand for? L stand for? I see.
Very good. These are all basic amino acids. What does the A stand for?
Arginine. Very good. Whenever people have this transporter defect, it's a transporter you find both in the GI tract and in the proximal tubule of the nephron. If they have that transporter defect, they do not reabsorb cysteine, and it shows up in the urine. Now, is there a particular diuretic that could be used to treat that transporter defect?
Because cysteine stones are acidic stones, so what kind of diuretic would you want to give those people? Acetazolamide, very good. Because it will make the urine basic and solubilize those cysteine stones. Does that make sense?
Okay, and I guess I'll just add this as a question. That transporter defect, let's assume you have like other transporter defects at the proximal tubule. What kind of RTA will that be? That'll be a type 2, okay? Remember, your proximal RTAs are your type 2 RTAs.
And how do you diagnose kidney stones? What's the imaging test you go for? A CT scan, okay?
A helical CT scan. Do you want to do that in a pregnant female? No, very good.
Just no. Never get CT scans, pregnant women, big no-no. But if a lady's pregnant, what do you do? ultrasound very good okay and how do you treat kidney stones fluids what else so fluids tamsulosin right how does tamsulosin work it's an alpha one antagonist okay so it opens up those urinary sphincters it dilates your ureters as well so you can pass that stone better and this person is in intractable pain what do you do Give them some pain meds, right? That's probably what you should do first after fluids.
But if it's like a huge stone, right, like a struvite stone, what do you need to do? Right? You need to place a nephrostomy tube to drain that distended kidney, okay?
But those people also have to go to surgery. So call your friendly urologist to sort of make that surgery happen. But you could also do shockwave lithotripsy for bigger stones, okay? but the Struvite stones in general surgery plus nephrostomy drainage, okay?
But if it's like a big-ish stone that will probably not pass on its own, you probably go ahead with shockwave lithotripsy for that, okay? Does that make sense? So quick review.
IV fluids, a ton of pain control, okay? You can give Tamsulosin, that's an alpha-1 antagonist, to open up the urinary sphincters and also relax the ureters. You can actually Should also give my fed a pin. That's a dihydropyridine calcium channel blocker.
That also works for that. And then you could also explore the surgical things like shockwave lithotripsy, or you can go ahead and do a nephrostomy plus surgery, okay? Especially for the struvite stones.
Does that make sense? Any questions? Good.
Now, 24-year-old male presents with a painless, palpable, bony mass on the left knee. A knee x-ray reveals a contiguous mushroom-shaped mass. What is this?
It's an osteochondroma. Very good. Okay.
So osteosarcoma, in general on exams, will show up in kids, not in adults. Okay. Could this show up in an adult?
Yes. But I'll say almost always osteosarcoma is a kid disease on MBMEs. Okay? So this is an osteochondroma.
Classically, they will show you like an image where you see something like this. A lot of green. out from bone, okay? That's an osteochondroma, okay? Don't confuse this with an osteoid osteoma.
Osteoid osteoma, again, that's probably not for a medicine shelf. It's probably for a peach shelf, okay? It's that pain in the leg in like a kid that's relieved with analgesics, okay?
If you see that presentation, that's an osteoid osteoma, okay? But osteochondroma, it's usually painless. It's palpable like on the skin. The only time it hurts is if it's like irritating surrounding tissue okay Does this make sense?
Good. Now, 66 year old female is found unconscious at home by her daughter in December. So pay attention to the timing. Physical exam is notable for a cherry red appearance of the skin. What's the next best step in diagnosis?
Not management, diagnosis. Blood, uh, what, what are we looking for exactly? Carb.
Carbon monoxide poisoning. Very good. Okay.
So I want to go ahead and check the carboxyhemoglobin levels. Okay. And right. So December, probably using a space heater, who knows, right?
Or a chimney or some kind of, what's, what are like fireplaces at homes? Okay. And how do you treat this high flow oxygen, right? Or like hyperbaric oxygen. Okay.
And how does that work? Like, what does it do to the half-life of carbon monoxide binding to hemoglobin? It decreases it.
Very good. Okay. And what happens to your oxyhemoglobin dissociation curve with carbon monoxide poisoning, left or right shift?
It's actually a left shift. So this is why carbon monoxide poisoning is bad. One thing it does is it occupies spots on hemoglobin where oxygen should hang out.
And then the second thing it does is whatever oxygen you have bound to hemoglobin, it prevents it from hanging out. Prevent you from releasing them. So that's really, really bad.
That's why this is something you sort of pay attention to and sort of try to treat quickly. Because it could be pretty fatal. And how do people classically present on exams with carbon monoxide poisoning?
Headache. Very good. Altered mental status.
What else? Like cherry. Very good. Cherry red lips.
Very good. And remember your associations, right? So like winter, space heaters, garage suicide. So a person is trying to like hook up something to their car, turn off the blinds and like try to kill themselves. Think of carbon monoxide poisoning, okay?
And this is not for this shelf, but for people taking the newer shelf in the future. It's just a specific association you want to know. Carbon monoxide poisoning on imaging. You can find like...
like hyper intense lesions in the globus pallidus okay not for this shelf but it's a bonus for your neural shelf in the future okay now elevated creatinine 24 hours after getting a ct scan what is this god contrast induced nephropathy very good now how could you have prevented this ton of hydration what else N-acetylcysteine. Very good. Okay, N-acetylcysteine. What if a person gets skin fibrosis after getting a brain MRI? That's NSF.
What were they exposed to? Gadolinium. Very good.
So gadolinium toxicity. So it's called nephrogenic systemic fibrosis or nephrogenic systemic sclerosis, whatever floats your boat. and if a person has diabetes what should you hold before like doing anything that can affect the kidneys.
Hold metformin. Why? Lactic acidosis.
Okay. We talked about the mechanism behind the lactic acidosis from metformin at the farm reviews. Okay.
Now, what are the other things that N-acidosis team could be used for besides preventing contrast nephropathy? Tylenol overdose, right? So I said aminophene overdose.
Good. What else? Right?
So if a patient has cystic fibrosis, remember from GTS, you probably learned about how N-acetylcysteine breaks disulfide bonds, okay, to cause CF patient to cough up all that nasty goopy stuff. And then an unusual scenario is hemorrhagic cystitis with cyclophosphamide. You could actually prevent that as well with N-acetylcysteine, okay?
Although on your exam, what is the first thing you're going for with that? Cyclophosph... Mesna.
Very good. Mesna. Okay.
Remember, cyclophosphamide has this nasty metabolite known as what? It starts with an A. Acro...
Acrolein. Okay. So that metabolite basically messes up the bladder.
Okay. So you can bind up that metabolite with mesna. Okay. To prevent the hemorrhagic cystitis with cyclophosphamide.
And while we're talking about hemorrhagic cystitis, what's the virus that causes hemorrhagic cystitis? Adenovirus. Very good.
And let's assume a person has hemorrhagic cystitis and they're from Egypt. That's schistosomiasis. Very good.
Schistosomahematobium. Awesome. Now, a common lower extremity side effect associated with hydralazine and your, I guess, dihydropyridine calcium channel blockers.
What's the big side effect? Peripheral edema. Okay. Now, what's the mechanism behind that?
Okay. So, let's talk about it. So, let's assume a series of What are the blood vessels that feed capillaries? Arterials, very good.
Arterials feed capillaries. So these are arterials. These are capillaries. Now, what are the blood vessels that drain capillaries? Very good.
So, we know that hydralazine and your dihydropidine calcium channel blockers cause vasodilation. The thing they dilate are your precapillary arterioles. The arterioles are precapillaries.
So if you dilate those precapillary arterioles, what happens to the hydrostatic pressures in capillaries? Those up. And if hydrostatic pressures go up, what happens to fluid extravasation? So, how will you potentially relieve the cardiac pressures?
What do you want to do to these venules? You want to dilate them. So you want to dilate these post-capillary venules.
So what are the classic drugs that dilate post-capillary venules? Your urine and your tensile and aldosterone system. Okay. Now, HIV patient with a three-day history of fever. Presents with targetoid skin lesions, lip and mouth ulcerations, and visual impairment.
A physical exam is notable for skin sloughing, so like 8% body surface area. Nikolsky sign is positive. He was placed on allopurinol, that's the trigger.
Allopurinol 10 days ago for chronic gout. What is this? Sorry?
Is it SJS or TEN? It's SJS. Very good.
What's the percent body surface area caught up for SJS? 10%. If it's more than 30%, that's TEN. Okay. So toxic epidermal necrolysis.
Okay. But this is SJS. Does that make sense? And how do you treat this?
What do you do first? Stop the drug. Very good. And maybe call your friendly derma resident or attendant.
Probably the resident that will come, not the attendant. Okay, good. Now, 30-year-old female presents with a three-day history of polydipsia and polyuria.
Her blood glucose is 650 and her bicarb is 21, pH is 7.35. What is this? That's what they want you to choose on exams.
What should you choose on the exam? HHS, very good. What do you need for you to make that diagnosis of DKA? You need ketosis, right?
And would a person have a pH of 7.35 in DKA? No. Very good.
No. Okay. It's usually pretty low. Okay. This is almost normal.
Okay. So this patient has HHNS. Okay. So what triggers HHNS?
This is not a step one review, so I'm not going to belabor this issue. But basically, you get stressed with like infection or you're studying for a medicine shelf. Right.
So you get stressed. You release a ton of cortisol. What does cortisol do to your blood glucose levels?
It increases it, right? And you have a relative insulin deficiency with type 2 diabetes, so you cannot utilize that increased blood glucose, okay? So that can tip you over the edge, okay?
Actually, real quick, why do patients with type 2 diabetes not have ketosis? Because they have some insulin, and what is that insulin doing to glucagon? It's inhibiting glucagon, right?
So remember from your endocrine lectures, right? So the beta cells are in the middle of the islets. The alpha cells that secrete glucagon are on the outside.
So as you secrete that insulin on its way out, it inhibits glucagon. So those people don't have lipolysis. That's why they don't have the ketosis, okay?
And how do you treat HHNS? Fluids and... Insulin. Very good. Fluids and insulin.
What's true of their sodium balance? So low sodium, right? What kind of hyponatremia is that?
Is it hyper? So real quick, is it a hyper, hypo, or isoosmolar hyponatremia? Hyperosmolar, okay? Because they have a ton of glucose, so it's pulling water out of cells, okay?
So that artificially lowers their blood glucose, I mean, their blood sodium levels. And how do you correct for that? what's like the formula right so let's use an easy example let's assume your sodium is 129 600 uh how many hundreds are you above 100 five so you basically take that number and multiply by one 126. Come back to 129. A person's sodium is 137. So you take the number of hundreds, above a hundred, multiply by 1.6, add that to the sodium, end of story. What's true of their total body potassium?
Total body potassium. It's low. But what may be true of their potassium measured on a lab valley? It'll be like high or normal, okay? So don't be fooled by artificially high potassium in a patient with like DKA or HHNS.
You want to supplement potassium. And let's assume you're like a very happy 30. You're like, yes, I want to rapidly lower their blood glucose levels. And then the patient becomes like comatose and like they die. What happened?
So let's say their blood glucose was 650 like at 2 p.m. And by 4 p.m., because of your gangbusters work, their blood glucose is now 150, like perfect. I heard someone say it. Cerebral edema.
Very good. Okay. You never want to fix anything too quickly in the body. Okay. So remember your sodium mnemonic from step one, right?
So like from low to high, what happens to the pons? It dies. Good. And from high to low, what happens?
right the brain blows okay so just sort of take that hypernatremia mantra and extend it to hyperglycemia okay from high to low sodium the brain will blow from high to low glucose too quickly the brain will blow as well okay so you never correct glucose too quickly this will probably also show up on your peach shelf they love that stuff for kids with dka when you lower the glucose too quickly Okay, 49-year-old female, any questions so far? Are we good? Okay, you guys are eerily quiet tonight. All good?
Don't worry, I know I'm the thin standing between you on your good weekend, supposedly, but anyhow. Okay, so 49-year-old female presents with wheezing and flushing. Physical exam is positive for murmurs consistent with tricuspid regurg and pulmonic stenosis. What does she have? Carcinoid syndrome.
Very good. Okay. So remember your mnemonic for carcinoid, right? So BFDR, right?
So what does the B stand for? So like bronchospasm. Very good. What does the F stand for?
Flushing. Good. What does the D stand for? Diarrhea.
Very good. And how about the R? Good.
Right-sided heart problems, right? So right-sided heart lesions. Now, why do they get problems on the right side of the heart?
What can the lungs do to the serotonin? They can metabolize them. Very good. In fact, if you have a cross-moid tumor that's in the GI tract, like in the headaches, for example, the liver can be symptoms. Once it spreads to the liver, then it can go to the right side of the heart.
Never get left-sided problems, because the lungs have the ability to metabolize that serotonin, right? So remember, the lungs have a lot of metabolic activity, right? And this is just something you need to memorize, but the classic...
Murmurs, like the right-sided heart problems that are found in these people, is tricuspid regurg and pulmonic stenosis. Does anyone know the mnemonic for remembering that? Tips?
Like, tips? Tricuspid insufficiency? Pulmonic stenosis? That's how you remember the valvular lesions in carcinoid.
Now, how do you diagnose carcinoid syndrome? What's your first test? What do you check first? Urine for what?
5-HIAA. 5-HIAA in the urine. That's a metabolite of serotonin. And then, after you see elevated levels of 5-HIAA, what do you do next? What's the classic scan everyone gets in the ED?
CT scan. Very good. CT scan.
Well, let's assume you get an exam question and you're like, hmm, CT scan is not showing this tumor. What can you do? What kind of nuclear medicine test?
Very good. Octreotite scintigraphy. octreotide scintigraphy, right?
And the reason behind that is many cells that secrete serotonin are responsive to somatostatin, okay? In fact, that's why you can treat carcinoid syndrome with octreotide, okay? Octreotide decreases the synthesis of serotonin.
And I've talked about the symptoms by location, like based on like meds to liver and whatnot. Now, why would a person on Crash Nights Syndrome Half Pelagra. Niacin deficiency.
How does that work? Very good. Okay. Very good, right?
So tryptophan can be used to make niacin and serotonin, right? In fact, that's why serotonin is called 5-HT, 5-hydroxytryptophan, okay? So if you divert all your tryptophan to making serotonin because of carcinoid syndrome, then you have a relative niacin deficiency, okay?
And the person could get pellagra with that. And what are the four Ds of pellagra? Diarrhea. Dermatitis, dementia, and what's the big bad one? Death.
Very good. Okay. And real quick, is there a particular tumor of the thyroid gland that could present with diarrhea as well? This is one of those bizarre things they love to test.
Most people get this thing wrong. Medullary thyroid cancer, why is that? Very good. Calcitonin actually causes diarrhea.
So, medullary thyroid cancer, remember if you see like apple grain birefringence in the thyroid gland, that's medullary thyroid cancer. Calcitonin is the tumor marker. We'll talk about that in a later slide.
Now, 61-year-old male presents with exertional dyspnea. CBC is notable for hematocrit of 27%. What is the next best step in management?
Old person with ion deficiency anemia. Colonoscopy. Very good. Okay. So they have an ion deficiency because what are you worried about?
Colon cancer. Very good. Now, what would the ion studies dictate for this patient?
What would be true of the ferritin? It would be low. Good.
What would be true of the TIBC? It would be high. What would be true of the transferrin saturation?
You'll be low. Very good. Okay.
So don't forget your hematologic markers, right? So if you're iron deficient, you have low iron stores. So your, uh, your ferritin will be low.
Okay. If you remember the pathoma inverse relationship, if your ferritin is low, your TIBC will be high. Okay. Uh, because think about it, right?
So let's assume one of you is a mob boss. Okay. And you're running low on cash. What do you do to your enforcers?
You send them to go and like start calling all your debts back, right? So your binding capacity for money, goes up. Okay.
So your TIBC goes up and your transferring saturation is a measure of how much iron is being held by transferring. Because you're iron deficient, it's low. So your transferring saturation is low. Okay.
Now, so colon cancer. Now, when should you transfuse? Someone should tell me the answer. The someone knows himself should tell me the answer to this question. When should you transfuse a person?
Hemoglobin of? Of seven. Very good.
I'll be very concerned if you got that wrong. Okay. Now, if a patient had this same presentation, right? So like low hematocrit and they had difficulty swallowing.
Okay. What would your diagnosis be? Plummer-Vincent syndrome.
Okay. Remember that triad? What's the triad?
right so esophageal webs iron deficiency anemia okay and the beefy red tongue right so like plumber vincent syndrome plumber vincent This is not just for step one, okay? Believe it or not, it's for step two as well. And for your medicine shop, that's why it's here. Okay, now, 29-year-old female with a recent trip to India, ate local foods, okay?
She returned two weeks ago. No offense to the Indian people here, I apologize. I promise I'm not racist, it's just... Blame the NBMA, I know.
They're already nodding their heads at me. I'll just cover my head in shape. So, 29-year-old female with a recent trip to India, ate local foods.
She returned two weeks ago and initially had fevers for one week. So, high fevers for one week. Now, she presents with severe abdominal pain and distension and physical exam is notable for salmon-colored circular lesions on the trunk. What is this? That's Salmonella.
Very good. Salmonella typhi. Remember the rose spots on the abdomen?
But, well, any reasonable question writer saying, oh, patient presents with high fever, blah, blah, blah. And physical exam shows rose spots on the abdomen. No. No one, I mean, even you, you'll never do that.
Okay? So, this is Salmonella typhi. This is typhoid fever.
And how do you treat this? Fluoroquinolone, very good. Okay, so like Cipro or Levofloxacin or like Moxifloxacin. Okay, remember those are your topoisomerase inhibitors. Now, septic arthritis, right?
So I'm going to give you different scenarios. You tell me what the bug is. So most common cause of septic arthritis, Staph aureus, good. Sickle cell patient, Salmonella, good.
Okay, young female with purpuric skin lesions. That's gonorrhea. Very good. Niceregonorrhea.
And if a person presents with septic arthritis, what's your first step in diagnosis? Tap that joint. Very good.
Do you literally like tap the joint? What do you actually do? athrocentesis very good that's the five dollar word right that's why i went to med school to learn the big word athrocentesis okay um and what would you see like what will your white cum be like in the joint fluid greater than greater than 50 000 very good and how do you treat like gonococcal septic arthritis so actually let me ask you a question how do you treat septic arthritis in general Surgery. So you try to wash out the joint and what else?
Antibiotics. Okay now for gonococcal septic arthritis, that's an exception. In general, you do not need to wash out the joint you just give ceftriaxone and what else?
And doxy or ceftriaxone and what else? Starts with an A. Azithromycin.
Okay, so let me just erase this real quick. Can I get rid of this? So, in general, for septic arthritis, joint washout, okay, plus antibiotics for like many, many weeks. Or, for gonococcal septic arthritis, you can give ceftriaxone plus doxy. What does the doxy help you cover?
Chlamydia. Good. You could also give azithromycin. Remember, azithromycin is a macrolid.
It also covers chlamydia. And it also decreases resistance to nyserial species. And if a person has chlamydia, what do you treat them with? You can give doxy or azithro. Do you also treat empirically for nyseria?
You don't. Exactly. Right. So this is a high yield thing to know for exams.
If you detect my Syria, you have to treat for chlamydia at the same time. Okay. If you detect chlamydia, you do not have to treat for my Syria at the same time.
It's only if they tell you. oh, we found chlamydia and Neisseria, then you treat both. Okay.
But if you see only chlamydia, treat only chlamydia. If you see only Neisseria, treat Neisseria and chlamydia. Does that make sense? I promise it's very hard to know this. If you've done your world, you probably have been dinged by this kind of a scenario.
Okay. Now, subconjunctival hemorrhage in a patient with nasty coughing episodes. Pertussis.
Very good. So this is the way they will test pertussis on your exam. If you are a person that coughs so hard, they have subconjunctival hemorrhage, or they cough so hard, they vomit after they cough.
If you see any of those scenarios, stop reading the question. It's pertussis. And how do you treat pertussis? A macrolid, okay, like erythromycin or azithromycin. And if a person is a close contact, how do you, how do you prophylax?
Same thing. Very good. You also prophylax with a macrolid.
Okay. Now, and just one quick thing I'll just also tell you that should lead you towards pertussis on your exam. It's a bacterial infection. And for most bacterial infections, what goes up in your blood? PMNs.
Very good. Neutrophils. But what is different about pertussis? It's lymphocytes. Okay.
So it's a bacterial infection with a reactive lymphocytosis. Okay. The white count could go to like 80,000 in some of these patients. Okay. And what would your next step in management be in a person that recently started Ramipro for the treatment of hypertension and then they have a cough?
Stop the Ramipro and switch to an Arblike. Like Losartan. Okay. Any Sartan.
Good. Now, quick drive-by for the first, second, and third degree V blocks. So, I'll just describe the EKG finding. You tell me the kind of block. Okay.
Now, the PP intervals are the same. The RR intervals are the same. But there is no relationship between the P waves and the QRS complexes? Third degree. Good.
Now, There are no dropped beats, but the PR interval is prolonged. That's first degree. Now, there are dropped beats.
But prior to the dropped beats, the PR interval is prolonged, but it's fixed. It doesn't keep changing. That's a Mobitz 2. Okay?
And I'll mention all of these again. But what if you see a drop beat, the PR interval is prolonged, and it keeps prolonging? What is that?
That's a Mobitz 1. Okay? So, real quick overview. First, the Gravy block. You only have anomaly on the PR interval.
There are no drop beats. On Mobitz 2, the PR interval is prolonged, and it keeps prolonging. Okay? until the QRS complex does not show up anymore, so it drops. This mnemonic from DIT is like longer, longer, longer, something, winky, bump.
So, if you're studying for step one, you will run that mnemonic. But Mobitz 2, that's where the PR interval is prolonged, but it's fixed. It's like a fixed length, but you still drop a beat. Okay?
And then third degree is PP interval same, RR interval same, but there's really no relationship between the P's and the QRS's. And real quick, how do you treat a Mobitz 1 or first degree V block? Nothing.
Good. You only treat if symptomatic. If they're symptomatic, you treat. But no symptoms, like if you just discovered an EKG, no treatment. Now, how about Mobitsu and a third degree V block?
Pacemaker. Very good. What if they're acutely decompensating?
What do you do? You can do, you can pace them, right? So you can do something called like a transvenous or transcutaneous pacemaking.
Okay. What's the drug you can give? Atropine. Very good.
Okay? Because remember, atropine is a muscarinic receptor antagonist. Very good. So it speeds conduction down the AV node.
Okay? Speeds conduction down the AV node. Now, would you want to give a person a hard block like beta blocker? No.
Good. Why? Very good. It slows the conduction through the AV node even more.
Do you want to give them like deltiazem? No. Okay, remember your non-dihydropyridine, calcium channel blockers, your class 4 antiarrhythmics. Yeah. They also slow conduction down the AV node.
Do you want to give the Juxin? No. Good.
The Juxin has a muscarinic receptor agonist activity, so it also slows conduction down your AV node. Good. Okay. Now, reduced EF in a patient with coarse facial features and enlarging fingers.
What is this? This is acromegaly. Okay. In fact, what's the most common cause of death in acromegaly?
Heart failure. Heart failure. Okay. And how do you... So this is an endocrine question, obviously.
What do you check first? IGF-1. Okay.
IGF-1 is elevated. Okay. So you find that. What do you do next? The glucose suppression test.
Very good. So you check IGF-1 first. Okay.
If that is elevated... Your next step is to do the glucose suppression test. So, if you load people with a ton of glucose, what should happen to their growth hormone levels?
It should go down. It should suppress. So, failure to suppress is indicative of acromegaly.
So, what do you now do after that? Imaging. Very good.
So, you send them to radiology. They look at their brains with an MRI. They find the pituitary adenoma.
How do you treat this? What's like first-line treatment for acromegaly? From a pituitary adenoma? Surgery.
Surgery. Okay? Surgery. So this is different from a prolactinoma. For a prolactinoma, you always, always treat with a dopamine agonist.
Okay, for a pituitary adenoma that's secreting growth hormone, your first line treatment is surgery. If surgery is not an answer choice, or they say prior to surgery, which of the following should be given? Then you can give octreotype, or you can give a dopamine receptor agonist.
What are the highly-yield dopamine agonists to know? Bromocriptin, what else? Cabergoline, very good.
Now there's this fancy drug that blocks growth hormone receptors that could also work. Do you guys remember? Pegvisomant, very good.
Believe it or not, I have seen this tested. Pegvisomant is a growth hormone receptor antagonist that can be used to treat acromegaly. Does this make sense? So, peg-vi-so-mant. PEGVISOMANT for those of you that are going to be taking step 1 soon don't worry you'll know this like you know your name in a few months so IGF-1 glucose suppression and then brain MRI now dysphagia to solids and liquids in a patient with thick and thin blood smears sort of Gimsa stain, basically.
Revealing what appears to be motile parasites. What is this? This is Chagas disease.
Okay. Trypanosoma cruzii. Okay.
Remember, it's one of those Gimsa positive organisms. Okay. Now, what does this person have specifically? Oh.
They have a calesia. Very good. So, what do you do to diagnose a calesia? Barium swallow. And what do you see on imaging?
Bird's beak sign. Very good. Bird's beak sign. Okay.
And after you do the barium swallow, what do you do next? Manometry. Very good.
In fact, just anyone here like a BME major? Like biomedical engineering? Oh yeah, all the smart people, I'm just kidding.
Okay, so BME. So BME, so you do the barium swallow first, okay? And then you do the manometry. So BME. And then you do an endoscopy.
Because Echolesia may also be a presentation of cancer, okay? So before you treat, barium swallow first, manometry second, and then upper jaw endoscopy, okay? Now, and on imaging, what do you find?
on a barium swallow, bird's beak, okay? So real quick, let's talk about t-cruzii, right? So t-cruzii can cause big problems.
I've discussed this mnemonic many times, okay? It can cause big esophagus, okay, achillesia. What can it do to your heart?
What's the big heart problem? Dilated cardiomyopathy. Very good. Now what can you do to your GI tract like big colon?
Toxic megacolon because it can cause Hirschsprungs. Okay remember it can destroy like your Albach's and your Meissner's plexi. Okay so you destroy those neural networks in the GI tract you can get Hirschsprung's disease and then your tummy gets big. So it can cause achalasia, big esophagus, dilated cardiomyopathy, big heart, Hirschsprung's disease, big GI tract. And how could you treat achalasia?
There are many options. So what are they? Pyloro, no, not pyloromyotomy.
You can give Botox. Remember, pyloral myotomy is pyloric stenosis. So you can give Botox. Good.
What else? The haloromyotomy. Very good, right?
So you can just look for myotomy on your exam, but don't pick pyloral myotomy. That would definitely be wrong. Okay, what else could you do?
You would give a calcium channel blocker, okay? A dihydropyridine calcium channel blocker, okay? Now, is there something else you could do to the esophagus?
Think of like blowing air into a person's esophagus. What are you trying to do? Balloon dilation. Okay.
Now, what if you did that, right? And then the patient becomes unresponsive. What did you just do? You popped the esophagus, right? So you've basically given them Birchhoff syndrome.
Okay. So pneumatic dilation is almost always the wrong answer for a calesia. Okay.
Usually the answer is a myotomy. Okay. Or you can inject Botox or you can give a dihydropyridine calcium channel blocker. Okay?
Does that make sense? Good. Now, reduced MCV in a patient with a long history of untreated rheumatoid arthritis.
What is this? Anemia of chronic disease. Very good.
Now, ferritin. High. Good.
Ferritin is high. Okay. Because you're storing iron, but you've thrown away the key. Okay.
The thing that throws away the key is hepcidin. Okay. But that's too detailed for your shelf.
That's more step one territory. Okay. So this is anemia of chronic disease. So ferritin is high. How about your TIBC?
It's low. Good. Now what we draw of your transferring saturation? It's actually low. So in anemia of chronic disease, your transferring saturation is low.
There is another pathology I think is coming up in a later slide where it's basically similar values, where your transferring saturation is actually elevated. In fact, I will say in lead poisoning, your ferritin is high, like we discussed. Your TIBC is low. But your transferring saturation is typically high in... Lead poisoning.
There's another disease where that's a more classic finding. We'll talk about that later. Okay.
But in anemia of chronic disease, low ferritin. No, no, no, no. High ferritin, low TIBC, low transferrin saturation. Okay. Low transferrin saturation.
Does that make sense? Any questions? You guys all seem quiet.
Did I say something wrong, maybe? If I say something wrong, remember, I can still claim this. I'm a fourth-year medical student, not a doctor, okay? So I could say a wrong thing.
So call me out if I say the wrong thing, okay? Sorry. But not yet.
I'm still a fourth year medical student. I'll claim that for as long as I can. Because I'm going to lose my safety net pretty soon.
That's kind of scary. Okay. So back to this. Now, 25 year old male with nasal packing presents with a blood pressure of 65 over 40. Just never use nasal packing. It's almost always a bad idea.
So blood pressure 65 over 40, elevated creatinine, respiratory distress, high fever, marginally elevated troponins. What is this? Toxic shock syndrome. Okay.
We're not going to belabor the pathophysiology here, but this is where you have some infection, you release toxin, and a lot of badness happens. Okay. Now, what are the two bugs that classically cause TSS? Staph aureus and strep pyogenes.
Okay. And how do you treat this? It's a kind of shock. So what do you do?
Fluids. antibiotics right and send them to the ICU okay this should never be managed on a medicine floor ICU level care let's see there's one more thing I wanted to see here I forgot it oh well okay now CKD so chronic kidney disease do you get a metabolic acidosis or metabolic alkalosis acidosis very good okay because You're retaining more protons, right? So remember that. Proton pump at the alpha-intercalated cell doesn't work anymore because your kidneys are like bye-bye, okay? So you retain protons, so you get a metabolic acidosis.
What happens to your potassium in kidney disease? It's high, okay? Because that ROMK channel at the principal cell doesn't work, okay?
What happens to your calcium? It's low, right? Because 1-alpha-hydroxylase does not work.
If it doesn't work, you do not make active vitamin D. If you don't make active vitamin D, you cannot reabsorb calcium or phosphate in the gut, okay? Now, what happens to your phosphate levels in kidney disease? It's high. Why?
So many people said the right thing. So your PTH goes up in kidney disease because you're hypocalcemic. And if PTH is a phosphate trashing hormone, what should happen to your phosphate in kidney disease? It should go down, but does it go down? No.
Why? You cannot excrete it. Your kidney is your primary excretory organ for phosphate. So this will be an example of a secondary hyperparathyroidism. So here's an evil question that we'll throw to you on the exam.
So let's assume a patient has... Let's assume we have two patients. They give you these values, so they give you arrows on your test. And so calcium, phosphate, PTH. Find them both.
And phosphate is high here, low here. Your calcium is low here, low here. So liver disease, kidney disease, those are your options.
Which of these ones? So patient A or patient B? Patient has secondary hyperparathyroidism from kidney disease.
Okay, very good. Because again, you cannot trash phosphate, even if your PTH is high. Which one is from liver disease? Very good, because if you have liver disease, right, remember, when you consume vitamin D, it doesn't do squat for you.
That vitamin D has to be converted to calcidiol in the liver, okay? If you have liver disease, you don't make calcidiol. If you don't make calcidiol, you have a vitamin D deficiency. So, with that, your calcium and phosphate will go down, and that will upregulate the release of PT. Because your kidneys are functional, you don't have kidney disease.
Your prostate will be appropriately scratched. Okay? Your prostate will be loved. And your cancer will also be loved. Bless you.
So those are two causes of secondary hyperparathyroidism. Okay. Now, uremia. What are the big things they love to test on exams with uremia? Pericarditis.
What else? Encephalopathy? What else?
Quaglopathy, right? So they can bleed. How do you treat the quaglopathy from kidney disease? Desmopressin.
Very good. You give desmopressin. Okay, we'll talk about that in a later slide. Now, what happens to your hemoglobin if a person has kidney disease?
Why? Not making EPO. Okay?
Not making EPO. So that can be a cause of a normocytic anemia. Okay?
Now, CKD, right? So how do you try to treat the hyperphosphatemia? You want to give a phosphate binder, like...
So they probably won't put Foslo on your exam. There is a drug they're actually looking for. It starts with an S.
I think that's Foslo, actually. Sevelamer. I don't know how to pronounce that thing. I'll just spell it out. S-E-V-E-L-A-M-E-R.
Sevelamer. Now, how do you treat their calcium problems? Vitamin D. Do you give them calcidio or calcitriol?
Calcitriol, very good. Because if you give them calcidiol, they don't have kidneys to convert it to calcitriol. Okay, so you give calcitriol and you could potentially give EPO. And if a person has diabetes and they have some albumin in their urine, how do you slow that process down?
ACE inhibitor. Okay, remember ACE inhibitors, if you remember from GTS renal, they decrease intraglomerular blood pressures. Okay, so you don't have hyperfiltration injury. Okay, and what are the indications for dialysis?
What's the A? Acidosis, the E. Electrolyte problems, the I. Ingestion, good, the O.
Overload of fluid and the U. Uremia, very good. Any questions on this slide? Should I go faster?
Some people are saying no. Okay, most people are saying no. Okay, good.
Now, if a person, so an RB gene mutation, Paget's disease, and the administration of teriparatide increase the risk of what primary bone malignancy? Osteosarcoma, very good. Okay, remember, RBG mutation, it can cause retinoblastoma.
So if they describe a kid with a white reflex when they're born and they say, oh, what are they most at most increased risk of in the future? Okay, that's an osteosarcoma. Remember, Paget's disease can also increase a person's risk of osteosarcoma. And teriparatide, how does teriparatide work?
It's an analog of what? of PTH. So if you give PTH in a pulsatile fashion, you can actually cause bone growth versus a continuous fashion where you cause bone resorption. So if you're giving a stimulating factor for a bone, you could potentially imagine a person having cancer with that. And what do you see on imaging?
Sunburst pattern. What else? Codman's triangle. Very good.
Now, Aspirin-exacerbated respiratory disease. So before, the name you probably memorized was aspirin-induced asthma. They've changed the name now. It's now AERD, aspirin-exacerbated respiratory disease. Now, how does this usually show up on exams?
Asthma and what? Nasopolyps, okay? Asthma and nasopolyps, right? So if you see nasopolyps on your exam, this is AERD.
So this is ARD. So asthma plus nasal polyps, that's ARD. And the potential pathophysiology.
Membrane phospholipids, you can convert it to arachidonic acid with some enzyme, phospholipase A2, whatever. We don't care about that for this. But, arachidonic acid can be converted to prostaglandins or leukotrienes. What's the enzyme that does this?
Tox. What's the enzyme that does this? Tox. Good. Like oxygenics.
If a person is taking aspirin, how does aspirin work? It kills coughs. Good.
So it kills coughs. So all the flux through this pathway is down this way. Okay? And these things can cause, like, bronchoconstriction, increased vascular permeability, blah, blah, blah.
Okay? So you can have asthma symptoms. So that's why people think that's a potential pathophysiology behind AERD.
So if you know that this is the pathophysiology, what do you want to do to this pathway? Okay, so you could potentially kill this enzyme or you could kill the receptor. It's the cis-LT1 receptor. You have to test this factory for some bizarre reason.
Cis-LT1, that's the leukotriene receptor. So what are the drugs that block the leukotriene receptor? Very good. So like, you can give those.
You could also inhibit this enzyme with a drug called xyluton. Generally, do not just jump to xyluton. Just do it. Do whatever.
Okay? So, I don't talk sick. Let's put it that way. But it's not a clean drop, basically.
Okay? So, you give the Lucas first. If that doesn't work or it's not an answer choice, you can give the liver-exploding agent, like xyluton.
Okay? Now, this is just a slide I'll let you go over on your own. The big thing I'll just say here is... You need to know your classification of asthma. That's one.
I think I got this from the AFP like website. But the big thing you want to know is in terms of the gradation of treatment, they love to test it a lot. What does every asthma patient start with?
Arbuterol, inhaled beta agonist. If that's not controlling symptoms, what do you add? an inhaled corticosteroid, okay. If that doesn't work, what do you add next?
A LABA, okay. A long-acting beta agonist like salmeterol or famotero. If that doesn't work, what do you add finally? Oral, oral steroids, okay. Oral steroids.
So, Saba, inhaled corticosteroid, LABA, then oral steroids. Okay? Oral steroids.
Oh, okay. Repeating myself again. Sorry about that.
Moving on. Now, SVT. How does an SVT present, right? So, regular or irregular? Regular.
Wide or narrow complex? Narrow. Good. Right.
So this is a narrow complex regular tachyarrhythmia. Okay. So it's narrow complex because it's coming above the ventricles.
Okay. And usually SVTs are regular. So the spaces between the QRS complexes are usually the same.
Now. How do you manage an SVT? So let's assume the patient comes in.
They're not super symptomatic. They're just like, you just see it on an EKG. What do you do first?
Very good, right? So you do the VEGO maneuvers, right? So you can massage the carotid, okay?
I can tell them to blow into a straw. They love to do that in the ED a lot. Like dunk their heads in cold water. You can gently... submerge their heads in cold water.
Okay? If that does not work, what do you give next? Adenosine.
Okay. You give three doses. You give six makes. Doesn't work, give 12 makes.
Doesn't work, give 12 makes. So six, 12, and 12. Okay. Now, if that does...
Okay, let's assume that works. Okay? How do you maintain them out of the arrhythmia? What are the two drug classes you give? I want to slow down the heart.
Beta blocker, good, or your non-dihydropyridine calcium channel blockers, okay? So your class 2 or 4 antiarrhythmics, okay? But if you describe a patient, you see that EKG, and your blood pressure is very low, or they're altered, or they have Lyme, they're just looking pretty bad.
What do you do? Talk then, okay? Now, on your exam, you need to watch out for the wording.
You want to do a synchronized cardioversion or an unsynchronized cardioversion. Unsynchronized cardioversion is defibrillation. Only do that for two kinds of rhythms.
What are they? VFib and pulseless VTAC. If a patient has VTAC with a pulse, you do not defibrillate them. So VFib and pulseless VTAC are the only rhythms we defibrillate or give unsynchronized cardioversion. But if a patient is hemodynamically unstable and they have an SVT, go with a synchronized cardioversion.
Now, if a patient has a PE, what is the most common finding? Is it S1Q3T3? No. What is it?
Sinus tachycardia. Very good. Sinus tachycardia.
That's a classic MDMA exam question. Okay. Now, 18-year-old female presents with scaly erythematous upper extremity lesions.
She has a long history of allergic rhinitis. What's your diagnosis? eczema, right?
Or if you're a dermatologist in the making, atopic dermatitis, okay? That's the $5 term. Now, how do you treat eczema? Topical steroids.
Very good. Topical steroids. Now, what if you saw like this kind of lesion, where you saw umbilicated vesicles? What is that? Eczema So, umbilicated vesicles on top of these kinds of lesions.
Eczema herpeticum. Very good. Eczema herpeticum. Eczema herpeticum.
And how would you treat eczema herpeticum? How do you treat herpes? Acyclovir.
It's basically a herpes super infection on top of atopic dermatitis. And what is classically elevated in CBCs with a patient that has like eosinophils? Okay. That's a differential diagnosis for eosinophilia is... floridly high yield for your shelf okay I promise you you need to like that Canada P or DN triple ACP blah blah blah mnemonic you need to memorize it okay if you've done any sort of preparation with questions for this shelf you're taking on Monday I am sure you have encountered it severely in at least 10 questions okay it's very high yield if you've not encountered it you've probably not done the practice.
tests, okay? So you need to know your differential diagnosis. Okay, now a patient presents with the classic stones, bones, groans, psychic overtones, and you find skin tension.
What's your first step in management? Fluids. Very good. Fluids. If a patient ever has hypercalcemia, fluids are your first step in management.
And real quick, calcium pharmacology. So, bless you. If a patient has Paget's disease, or they have a hypercalcemia of malignancy, what do you give those people?
Phosphonate. What do you need to do if you take a bisphosphonate? What do you need to do for 30 minutes?
Hit up or stand, right? Because you don't want to burn your esophagus, okay? Let's see, there's one more thing we use this phosphonate for, right? So if a patient has to be on steroids for like three months or more... Also need to prophylax against osteoporosis with a bisphosphonate, okay?
Because remember that steroids can cause osteoporosis. If a patient also has osteoporosis, you place them on a bisphosphonate. And what's the T-score caught up for osteoporosis?
Minus 2.5. Very good. Okay, minus 2.5.
Let's see. This is the big pharmacology I want to mention. There's more stuff coming up, but it will come up in a bit.
And real quick, what can bisphosphonates do to the jaw? Jaw necrosis. Very good.
They can cause osteonecrosis of the jaw. Okay? In general, for your exams, steroids cause hip osteonecrosis.
Bisphosphonates cause jaw osteonecrosis. Okay? So jaw osteonecrosis, bisphosphonates, hip osteonecrosis, steroids.
Okay. Any questions so far? Good?
Okay. Now how do you test for H. pylori?
So you can do the breath test. What else? 2-Lantigen.
What else? You can check for antibodies in the serum. What else?
You can biopsy that thing. Very good. Okay.
Now, how do you treat H. pylori? Tripotherapy. The mnemonic there is CAP. What does the C stand for?
Clarithromycin. Good. What does the A stand for? Amoxicillin.
What does the P stand for? PPI. Okay. If that does not work, you could try quadruple therapy. What does the M stand for?
Metronidazole, what does the B stand for? Bismuth, right? Bismuth subsalicylate. What does the T stand for?
Tetracycline. And the P? PPI. Very good.
In fact, if a patient is going to be tested for H. pylori, right? You usually want to discontinue the PPI for like two weeks before the test.
Because PPIs can suppress H. pylori. Okay, now what are the big risk factors for peptic ulcer disease?
H. pylori is one of them. Any other things?
Chronic NSAIDs, right? So the classic presentation is epigastric pain in a patient that has osteoarthritis. If you see that, think about H.
pylori. I mean, think about PUD from chronic NSAID use. Okay, good on this question. Okay?
Now, alpha... I know, this slide is annoying. It's a lot of stuff.
Okay. This will take a while. Okay. So alpha thalassemia.
How many alpha genes do you have? Four. So let's do this real quick. If you have a deficiency of one, do we care? No.
Two, do we care? No. Good.
Three, do we care? Yes, we do. So what's the kind of disease that happens with...
when you lose three alpha genes hemoglobin hemoglobin h disease very good so hemoglobin h disease and what is hemoglobin h so you have beta 4 So you have four beta subunits coming together, okay? Now, so we've talked about if you lose two, you lose one, we don't care. I mean, we care, but it's not clinically relevant for our discussion.
If you lose three, you have a lot of problems, okay? Now, if you lose four, are you ever... born no what is that called hemoglobin BART good hemoglobin BART that's gamma four okay so hemoglobin BART so that's alpha thalassemia in a nutshell now beta thalassemia if you lose how many genes do you have total if you lose one do we care Not much, but we should care for the exam.
Okay? That's called beta-thalminer. What's classically elevated in beta-thalminer on hemoglobin and electrophoresis?
Hemoglobin. Hemoglobin. A2. Very good.
Hemoglobin A2. Now hemoglobin A2 is alpha what something what? Alpha 2 something 2. Delta. Very good. If you see elevated alpha 2 delta 2, you should have a very strong reason for not picking beta-thal on your exam.
So, you'll find elevated hemoglobin A2 in beta-thal minor and major. Because in beta-thal major, you have no beta-globines at all. So you'll see alpha-2, delta-2.
But you'll also see inhibitions in hemoglobin F. Okay, that's alpha 2, gamma 2. Let's see. Now, when does alpha thalassemia classically show up? Does it show up at birth, or does it show up six months after birth? Alpha thalassemia.
At birth, why? At birth, what kind of mood loving do you have? F, which is alpha 2 gamma 2. There are alpha chains in hemoglobin F.
It doesn't show up very early. But, in a thalassemia, hemoglobin F persists for like six months. Usually, the episodes begin to show up after six months.
And I've talked about hemoglobin H disease and hemoglobin BART. What do you usually find on blood-span thalassemias? Target cells. Good. Now, hemolytic anemias, what do you usually find on CBC?
So what's true of the... Haptoglobin. Low.
Low. Good. Because haptoglobin binds up that hemoglobin.
What is true of... Do you get a direct or an indirect type of bilirubinemia? Indirect.
Okay. Because remember, hemoglobin is broken down to bilirubin. Okay. Now, if a patient has hemolytic anemia, what could happen with their gallbladders? Stones.
Good. Gallstones. Because what do gallstones contain a ton of? Bilirubin. Very good.
Bilirubin. Okay. Now, these patients, they had increased risk of aplastic crisis with what bug?
Harvard B19. Remember, it's the only high yield, at least that you need to know for any exam, single-stranded DNA virus. And real quick, do thalassemias present as a microcytic, normocytic, or microcytic anemia? Microcytic. And what's usually true of the red cell distribution width in a thalassemia?
Is it normal or increased? It's normal. It's high in what kind of anemia?
In iron deficiency anemia. Very good. So RDW is high in iron deficiency anemia, but normal in thalassemias. I've seen this concept tested before.
Okay. High yield to know that. Now, 23-year-old male who recently returned from Tucson.
So pay attention. I'm not giving you Tucson because I love, I mean, I love Arizona. I'm actually going there in a few months.
But that's not the purpose here. So, return from Tucson, presents with a two-week history of fever, ankle and knee pain, chest pain, and a painful erythematous pre-tibial lesion. What is this?
Coccidio mycoses, right? So if I did not mention Tucson, I could have mentioned Houston, right? Or I could have mentioned, let's see, the applicable... Someone here from California. Oh, good.
So California. Or like West Texas, which would be me in this case. Okay?
So this is coccidio mycoses. Now what's the painful pre-tibial lesion they have? Erythema nodosum.
Okay? Erythema nodosum has a very powerful association with coccyx. Okay?
Now, African-American female with respiratory distress on that lesion, what is that? Sarcoidosis. Very good. Sarcoidosis. Okay.
Now, for COX-C, what do you see on microscopy? Spherules, okay? It's just one of those annoying things from step one you still want to remember, okay? Spherules.
For those of you that are taking step one, you definitely want to remember that, okay? And you want to be able to recognize it, okay? So, spherules.
And how do you treat cocci? Like an azole, right? Like itraconazole, okay? Remember, itraconazole, those azoles are the things that inhibit, I think it's like 14-alpha-D-methylase, okay?
So for those of you studying for step one, you'll learn that at some point in the future. Okay, now, perioperative edema, hematuria, and hypertension in a patient with a recent history of cellulitis. Good.
Post-infectious or post-treptococcal glomerulonephritis. Okay. Now, is this a kind of nephrotic or nephritic syndrome? Nephritic. Okay.
And basically, what are the antibodies that you may find elevated in the serum? ASO and anti... Anti-DNA is B. Very good. Anti-DNA is B.
In fact, anti-DNA is B is pretty specific for a strep skin infection. Okay? So, let's break this down. This will be relevant for your medicine shelf and for your peach shelf. If you have strep pharyngitis...
You get providing fever after that. Get PIGN after that. Get a strep skin infection. Can you get rheumatic fever after that? No.
Can you get PIGN after that? Yes. Yes, good.
Now, if you took antibiotics, can you decrease the incidence of rheumatic fever? Yes. Yes, can you decrease the incidence of PIGN?
No. No. Very good. Awesome.
And PIGN is what kind of hypersensitivity reaction? Type? Type 3, very good. Antigen antibody complex.
Okay, they go and deposit in the kidneys, activate complement and your kidneys explode. Okay, so it's a type 3 hypersensitivity reaction and your antibodies are ASO and anti-DNA is B. Okay, now, 1122 translocation, x-ray imaging reveals an onion skin-like periosteal reaction, and a bone biopsy with histology reveals small, round, blue cells. What is this? E-wings.
Very good. E-wings. Okay, E-wings sarcoma. And how do you treat E-wings sarcoma on exams? Usually it's surgery, but that's usually not the answer.
What's the drug they want you to pick? What's the drug that treats childhood cancers? acting out with actinomycin D.
Very good. Okay. Dactinomycin.
Very good. Those are bizarre things that sketchy may help you remember every now and then. Okay. Now, 922 translocation is what? Philadelphia chromosome in CML.
Very good. Don't worry. All those things are coming up. Now, okay, so this thing is extremely annoying, and there is a lot of conflicting information, but this stuff is very high yield. They love this stuff, okay?
I'm sure if you've done any kind of practice testing, this has tortured you quite significantly. So let's talk about it. I'll just write it up. Where is this?
Okay, so, those are the three things we want to talk about. I'll define what it means for scholars. They want to talk about a conflict.
They want to talk about an empyema. And we'll talk about three things. There's four things. We'll talk about the pH. We'll talk about the glucose in the pearl fluid. We'll talk about the LDH.
Then we'll talk about bugs. I promise it's super mega high yield for your exam. So, first things first. A paranemonic effusion is a pleural effusion in the setting of pneumonia.
Para-nemonic. Pneumonia, pleural effusion equals paranemonic effusion. First things first. Now.
The pH you want to remember here is 7.2. The glucose you want to remember here is 60. The LDH you want to remember is some phantom value. What's the phantom value? Let's call it 2 thirds upper limit of normal.
Then you want to know if there are bugs or no bugs. Now, in an uncomplicated parharmonic effusion, what is true of the pH? Is it less than or greater than 7.2? It's uncomplicated. Well, it's greater than 7.2.
The glucose is less than or greater than 60. 5, good, greater than 60. So LDH less than or greater than 2 thirds the upper limit of some phantom value we never know. Less, very good. So it's less than 1, 6, 7. You find bugs in the pleural fluid.
So, good. Let's talk about, I think, I feel it's easier to remember if you remember this. Remember this, and remember this evil guy in the middle. Okay? Now, empyema, what's from the pH?
Oh, good. It's like the opposite. How about this?
Oh, less than 60. How about this? Alright, good. Greater than .67. Find bugs? Absolutely.
Very good. So, remember this, remember this, you're good to go. In fact, just remember this.
Take the opposites, that's this one. Then, this one in the middle, the complicated one, it's too complex. Basically has all of this stuff. find any box. Less than 1.67, less than 60, less than 7.2, you won't find any box.
That's a complicated part of monochryon fusion. Good on that. I'm begging you, please. So you don't get questions wrong on your exam. You need to know this chart.
Now, how do you treat this one? Antibiotics. Very good. How do you treat these two?
Chest tube plus antibiotics. Now, if chest tube does not work, what do you do? That's very good. You call thoracic surgery. This is usually like a pretty smelly surgery.
You go in and pull out all the thrombosis stuff in the pleural fluid. Or you can also give like TPA. But most people progress surgery because TPA doesn't work as well.
Okay. So, any questions on this? Super high yield.
Okay. That took like five minutes. Can I move on?
Good. What is this? This is VTAC. Good. So VTAC.
Wide or narrow complex. Wide complex. Regular or irregular.
Regular or wide complex. So you have three decisions you need to make. First, the treatment.
Second, the treatment. If a patient has VTAC without a pulse, what do you do? You defibrillate them. Very good. And unsynchronize cardioversion.
So VTAC with no pulse equals defibrillation or unsynchronized cardioversion. Now, VTAC with a pulse but hemodynamically unstable. What kind of shock? A synchronized cardioversion. Okay, and I'll repeat all of this again.
Now, VTAC with a pulse, hemodynamically stable. I heard someone say it. Amururon.
Very good. Okay. So, it's super, super high.
You have to know this. VTAC, pulse, hemodynamically stable, amururon. T-tac, pulse, chemodynamically unstable, defined by hypotension, altered mental status, blah, blah, blah.
Synchronized from your version. T-tac, no pulse, breaks loose. Un-synchronized from your version. So that's defibrillation. Very, very, very, very high yield to know that.
Okay, and it's a white complex tachyarrhythmia. So, blah, blah, blah, blah, blah. Good.
So, we've talked about all this stuff. Now, what's the most common cause of death in the immediate period following an MI? What kind of arrhythmia?
VFib. Very good. They will try to put VTAC to trick you.
Don't pick VTAC. Okay? Remember Angry Divine saying don't pick VTAC.
Pick VFib. Okay? VFib.
And how do you treat VFib? Shock. Very good. Un-synchronized cardioversion. Okay, now oral mucosal ulcerations plus a positive Nikolsky sign, so like flaccid skin blisters, in a 45-year-old male.
What is this? Pemphigus vulgaris, okay? Pemphigus vulgaris is vulgar, so it exposes you all around because it's Nikolsky positive. That's a nice mnemonic to remember there. Now, what's the pathophysiology?
What are you making antibodies against? Desmosons, right? So if they want to be evil to you, well they'll probably be more evil on step one. You need to remember these buzzwords. You need to remember desmobiliae.
Those are desmoson problems. Antibodies against those things. Now, this is what kind of hypersensitivity reaction? Type 2, very good. Here's a trick I use to remember type 2 versus type 3. If you're making antibodies against a particular cell, that's a type 2 hypersensitivity reaction.
If you're making antibodies against something that is acellular, it's a type 3 hypersensitivity reaction. Not always accurate, but I'll say, like, it's overwhelmingly correct for exams. now how do you test for this disease?
Yes, but there's something you do. It's a little more exotic. Very good.
You do a direct skin immunofluorescence, right? And what would you find? They love to describe this in the exam question.
Would you find, like, a fluorescence? Sub epidermally or intrapithelial. Do you find intrapithelial? Or sub epidermal? Very good.
Any questions? Good? Okay. Now, lab differentiation between primary and secondary hyperaldosteronism. So, if a patient has primary hyperaldosteronism, aka Kahn's syndrome, what would be some of the levels of aldosterone?
Green. Oh, good, because if you have too much aldosterone on board... That Enech channel at the principal cell works too well. You absorb a ton of sodium and water, become hypertensive, and you appropriately suppress your renin-angiotensin-aldosterone system. Okay?
So your renin will be low, and what we drop your angiotensin, what is it? Those ones. Okay. But if you have secondary hyprodosteronism, so let's assume you get a question about a female, young female with abdominal bruise. What is that?
Fibromyalgia? Fibromyalgia. The fibromuscular dysplasia. What if it's an old guy with the same physical exam finding? Renal arteriosclerosis.
Very good. Those are causes of secondary hyperaldosteronism. So what will be your ringing?
I. And you can say one, two, and aldosterone. I. So, renin, angiotensin 1 and angiotensin 2 are low, with the aldosterone being high, the Kahn syndrome, that's primary, hyperaldosteronism.
But your renin, angiotensin 1 and 2, and aldosterone are all elevated in secondary hyperaldosteronism. And one thing you want to know is that... Your friends that write these exams, they are beginning to shy away from the abdominal bruioscopy. Here's a question about a person with resistant hypertension. You perform a fundoscopic exam and you burn arterial venous naked.
That buzzword, I don't see the bruise, that's pretty classic. It's like almost pathognomonic for renal artery stenosis. So, AV naked. If you see that plus resistant hypertension, think about renal artery stenosis if it's an old person or fibromuscular dysplasia if it's a young person.
There is pathophysiology there, but we do not have the time for that. Okay. And we'll be true of your plasma-aldosterone-to-renin ratio in Kahn syndrome. It'll be high. In fibromuscular dysplasia.
It will be low, so it will be less than 10. But for Kahn's syndrome, it will be greater than 20. How do you treat Kahn's syndrome? Let's say before you go for surgery, what do you do? You give an aldosterone blocker light. Spironolactone.
What if the guy says, oh, doc, I started taking spironolactone, and I have like big, you know what I'm talking about. What do you give? A plurinone. Remember, spironolactone, in addition to blocking aldosterone receptors, it also blocks androgen receptors.
But a plurinone does not. It's a pure aldosterone receptor antagonist. So you're trying to prevent the gynecomastia.
Nephron physiology, we don't have the time for that, so we're going to keep going. Now, the Rome criteria for irritable bowel syndrome. So who is the classic patient that gets IBS on exams?
Young female, okay. And what's the... buzzword, like buzz phrase description. She has abdominal pain that's relieved with defecation. If you see that, that is IBS, okay?
Young female, abdominal pain, relieved with defecation, bam, bam, bam, IBS, okay? And the Rome criteria, probably don't need to memorize those, but it's like changing like stool frequency, changing stool consistency, blah, blah, blah. I'll let you look that up on your own.
Now, are there any lab anomalies in IBS? No. Good.
There are no lab anomalies. Okay. And how do you classify IBS? What are the two big ones you need to know? IBS-C and D.
How do you treat IBS-C? Give something that causes like docolax or senna. What do those things cause?
Diarrhea. Okay. So if you have IBS-C, give something that causes diarrhea.
If you have IBS-D, give something that causes constipation, like loperamide, for example. Does that make sense? So IBS-C treated with a D, IBS-D treated with a C. Good?
Okay. So I promise by 8-10 will be done. Is that okay?
Sorry. Yes. Go ahead.
IBS constipation and IBS diarrhea. Yeah. Yeah. Does that make sense? Okay.
Good. Now, cold versus warm agglutinins is a cold agglutinin IgM or IGG. IGM. Okay, IgM.
Now, is a warm agglutinin IgM or IgG? IgG. Now, what's the classic bug associated with cold agglutinin disease?
Mycoplasma. Very good. And how do you treat warm agglutinin disease? What do you do to the spleen? You do a splenectomy.
Okay. Do you treat cold agglutinin disease with a splenectomy? No. How do you treat cold agglutinin disease? You could do plasmapheresis, but there's something else you do, like pharmacology-wise.
But hydrogen, on the other hand, can oxidize things. It gets to the spleen. It can be cleared by splenic macrophages.
So that's why, in general, splenectomy works for warm agglutinin disease. Now, what happens to your LDH if you have hemolytic anemia from these agglutinin diseases? It goes up. Good.
Because remember, red cells do only anaerobic metabolism. So they have high lactate dehydrogenase. What happens to bilirubin?
What kind of bilirubin? Indirect. How about haptoglobin?
Goes down. Good, because that binds up your hemoglobin. Now, 32-year-old Egyptian immigrant presents with a two-week history of abdominal pain, hepatosplenomegaly, and hematuria. He swam in the Nile two months ago.
What is this? Schistosoma hematobium. Very good.
How does this get into a human being? Just direct contact, right? So you may be swimming in the water like, oh, this is so much fun. And then it's just like dancing its way into your bladder.
Okay. And what would you see on a CBC? What's the blood cell that will be elevated?
Eosinophils. Very good. Okay. And what could happen with this down the line? Bladder cancer, what kind?
So they love to mess people up with this on exams. Would it be a bladder transitional cell cancer, or would it be a squamous cell cancer? It would be a squamous cell cancer. Most bladder cancers are transitional cell carcinomas, but there's a difference.
If it's from schistosoma hematobium, it's a bladder squamous cell cancer. Okay, and how do you treat schistosomiasis? This is like super low yield, but it may show up. Prairie Quantel. Wow, that's impressive.
Prairie Quantel. Good. Yeah, almost no one ever gets that right.
Awesome. Now, synpharyngitic glomerulonephritis. What am I referring to?
IgA nephropathy, right? So remember from GTS, two to six days versus two to six weeks, okay? So this is IgA nephropathy, okay?
Post-infectious glomerulonephritis shows up two to six weeks after an upper respiratory infection, okay? But IgA nephropathy shows up two to six days after an upper respiratory infection, okay? Now, what is true of your levels of complement in PIGN? Is it low or high?
It's low because the antibodies activate complement, okay, like IgG and IgM. They activate the classic complement cascade, okay? We'll be done in, what's the real time?
My watch is a little fast. 802. So once it's 809, someone just wave at me and I will just prepare to like abruptly stop talking, okay? And in general, these diseases, the treatment is pretty low yield, but you can give like steroids and ACE inhibitors, okay?
Steroids, ACE inhibitors. And in nephritic syndromes, what kinds of casts are found in the urine? Red cell casts, good.
And what's true of the proteinuria in nephritic syndromes? Less than... 3.5, very good. Less than 3.5 grams in 24 hours. Okay.
Now, 70-year-old male with leg pain that is worsened by a back-helding extension, but it's better when he goes to Walmart. Lumbar spinal stenosis. Very good.
Okay. Now, how do you diagnose lumbar spinal stenosis or any kind of spinal pathology? MRI.
Very good. MRI. Okay, so go to radiology.
Okay, and how do you treat this? Generally nothing. Good, right?
So like exercise, physical therapy, and pain control. But if that is not working, what do you then do? Surgery, right? So call your surgery.
They'll do something called like a laminectomy, like a spinal fusion. But that's not, that's for your surgery shelf, not for this one. Okay, now opening snap with a diastolic rumble, heard best in the forward intercostal space in the midclavicular line. What is this?
Opening snap. Mitrostenosis. Very good.
Mitrostenosis. So, for those of you that are just starting third year, I need to mention this. Okay. They love risk factors.
The MDMEs, they love risk factors for disease. The people that have like the biggest risk factor, like, oh, I love risk factors. Those are your OB-GYN people. They just go nuts with risk factors.
But for MDMEs in general, they love their risk factors. So what is the number one risk factor for mitral stenosis? Rheumatic fever. Very good, rheumatic fever. Okay.
And how do you diagnose any murmur? echocardiography and how do you treat this what do you do replace the valve replace the valve okay so remember it's a diastolic mirror because blood is going from the left atrium to the left ventricle in diastole and because you have the sternal valve you have that snap when that valve opens Yes, you can do a balloon valve vortomy, but you only do that if a person is a bad surgical candidate. If not, replace the valve. What is the valve lesion that is like balloon valve vortomy is generally like never the right answer? Aortic stenosis.
stenosis, you replace the valve. End of story. Okay.
But yes, for this, you can do a balloon valvotomy. But I have never seen that be the correct answer ever. It's almost always replace the valve.
Okay. Although maybe in your world, you may have seen that as an option, like, oh, like 80% surgery is too risky with all these comorbidities. Yes. But in general, for mitral stenosis, you replace the valve. And what's the most common arrhythmia in patients with mitral stenosis AFib.
Very good. They love this stuff. What's the most common arrhythmia in patients with Graves' disease?
AFib. Very good. Okay.
Hyperthyroidism, arrhythmia equals AFib. What's the time? 806. Okay.
I really want to get to 50. So no oral mucosal lesions, pruritus, and a negative Nikolsky sign. What is this? It looks like pemphigus vulgaris. So what is this?
Boulos pemphigoid, okay? So if you have a lesion, right, so if you're a dermatologist and you have a lesion, it looks like eczema, but it's not actually eczema, it's eczematoid, okay? So pemphigus vulgaris, this one looks like it, but it's really not.
So it's boulos pemphigoid, okay? So this is boulos pemphigoid. And what are you making autoantibodies again this time?
The hemidesmosomes. Very good. Okay.
And again, how do you diagnose this? Direct. Very good. Direct antibody immunofluorescence.
And what do you find? Do you find the fluorescence, like intraepithelial or subepidermal? Subepidermal. Because hemidesmosomes are below the epithelial cell layer.
And how do you treat this? Do you use, bless you, do you use oral steroids or? Topical steroids.
Topical. Okay. So topical steroids for the less severe disease.
Bullous pentagoy. Oral steroids for the more severe disease. Pentagos vulgaris.
Okay. It's very vulgar. So use the longer stuff. Oral steroids.
Okay. Now. Okay. Let's go to 50. We'll do 49 tomorrow. Okay.
This is a little over the top. Yeah, we can do this one. So, 69-year-old male with fever, leukocytosis, and left lower quadrant pain.
What is this? Diverticulitis. Very good.
What's the pathophysiology? Inflammation of what? For diverticula.
Good. Now, if a person comes in with diverticulitis, how do you confirm that? Very good.
Okay. Do you want to do a colonoscopy? No, right?
Don't do that, right? There'll be some lawyer that'll be happy to take away your medical license. So don't do that, okay? So that's a colonoscopy.
Don't do a colonoscopy. Do a CT scan. Now, how do you treat most GI infections? What's the online recommended cocktail?
So Cipra and what? And metronidazole or? amoxicillin, gentamicin, and metronidazole. Okay?
So just remember a mag. Metronidazole, amoxicillin, and gentamicin. Okay?
Peptazole is almost always the wrong answer on exams. Okay? It's too broad. It kills off too many things.
So, metronidazole, amoxicillin and gentamicin, or ciprofloxacin, a fluoroquinolone, plus metronidazole. Because the fluoroquinolone or the ampengene help you cover gram-negatives, and then the metro helps you cover anaerobes. Okay.
And now, let's assume the patient presents weeks later, and they have recurring UTIs, and you do a urinalysis. You see a ton of air in their urine, and you see feces in the urine. What is that?
That's a fistula. So they form the fistula from the colon to the bladder. Okay.
So that's a colovesicle fistula. And that's also diagnosed with a CT scan. Although you do like IV and oral, like oral and rectal contrast, but that's too much detail. Okay.
So CT scan, colovascular fistula. Okay. So we're stopping here today.
We'll pick up with 49 tomorrow and then we'll jump to 51. Okay. So any questions over anything we discussed? Are we all good?
So we'll meet here at nine tomorrow. Okay. So just give me one second.