DIP Episode 351 - USMLE Step 2CK/3 Rapid Review Series 66

Okay, welcome. My name is Divine. This is episode 351 of the Divine intervention podcasts. And into these podcasts we're going to be continuing the Rapid Review series for the USM Listep 2 CK slash step 3 exams. And this is going to be series 66. And as a reminder, if you're taking the USM Listep 2 CK or step 3 exams or complex level tour 3 exams in December or January of December of this year or January of 2022, you may be interested in the MBME Testikin Strategies course I have taken place on the 6th of December from 2 to 4 30 PM Mountain Standard Time which is 4 to 6 30 PM Eastern Time. And you'll also potentially be interested in the 24 hour course I'm offering. That starts on the 7th of December and around still the 10th. We'll be meeting from 10 a.m. to 4 p.m. Mountain Time which is essentially known to 6 p.m. Eastern Time on all four of those days. So 24 hour course again you'll learn a ton. We'll talk about PEED surgery internal medicine OBGYN psych neural biostatistics ethics multi-system processes and disorders communications professionalism. We'll be talking about so many things that are tested on the USM List. And again, you'll be in a case-based format. So as you know, I'm not a big fan of not a big fan of these classic lecture formats. I'm of like integrated things together use cases use vignettes and things like that. So that's almost exclusively what we'll be doing for all parts of the course.

And you know, we'll spend about one six of the total time taking an answering people's questions. So again, most people again end up having about 130 pages of notes from the course. So if you're interested, just feel free to shoot me an email through the website and I can show you how to reserve your spot and things like that. Okay. So let's just jump right into this. So what do they give you a question about a patient? They tell you that he had an upper respiratory infection two weeks ago. But that now he's having a lot of trouble with walking that he has noticed that he cannot get out of bed in the morning. And then that he has also noticed that he's hand muscles are getting weak. If you see this, what should you be thinking about? I really hope you're saying oh divine. It sounds like this guy has Guillembury syndrome. Right. So remember Guillembury syndrome. It has an association with any kind of mucosa l'infection. It can be a GI infection. But the thing is our friends at the MBM is realized that most people have memorized that bloody diarrhea, Campylo-Bacteria, J.J. business. Right. So these days they just give you any mucosa l'infection. So if you see a person having like paralysis that started in the lower extremities and is going upwards after any kind of mucosa l'infection. So it can be like a GI infection. It can be a respiratory infection. It can be a GI infection. I really want you to think about Guillembury syndrome. Right.

Remember Guillembury syndrome in general, if you were to perform a lumber puncture on these people, right. You would find this again, Albuminous cytologic dissociation where you notice now, wow. The CSF in the protein is markedly increased where you notice that wow. The number of cells in white blood cells in that CSF is very, very little. Right. When you see stuff like that, you absolutely want to think about Guillembury syndrome. Right. Albuminous cytologic dissociation obviously means referring to protein cytologic referring to cells because many times when the number of white blood cells in your CSF is up and your CSF protein will be up. So seeing elevated CSF proteins usually a surrogate, but your CSF white blood cells are increased. But if you notice that wow, the CSF protein is really high. But I'm only seeing again like zero to three white blood cells per high power field or whatever. And you really want to think about Guillembury syndrome in those circumstances. Now remember Guillembury syndrome, these people, if they start crushing and burning from a respiratory perspective, you're going to start looking towards some kind of endotracheal intubation. Right. And then those people usually want to try IVIG or something along those lines for them to get them well. Right. Remember, it can be a respiratory emergency because it can involve it can involve the diaphragm. Right.

Now, what if they give you a question about a three-year old and they tell you that this three-year old for the last, you know, one week has been having a lot of nose bleeds, has been having a lot of bleeding gums when she brushes her teeth. And they tell you that she had an upper respiratory infection like two, two, you know, like 10 days ago or something like that. Right. And then they give you some labs. You notice that the hemoglobin is fine, it's like 11, the white blood cell count is like 5,000. So that's normal. And they notice the platelet count is 1,000. If you see this, what do you want to think about? But I really hope you're saying, oh, the vine looks like this kid has ITP, right. Immune thrombocytopenic pepper. Right. Remember, ITP is associated. It's an autoimmune disease. Literally, you may go to antibodies against your platelet protein GP2 B3 A. Right. So you basically clobber your protein count. And when you clobber your protein count, I mean, sorry, you clobber your protein platelet. You clobber your platelet count and the person is going to have an incidence of bleeding, nose bleeds, right. So like epistaxis, they'll have all these problems. Right. And remember, these kids will typically treat them first off. We're going to try steroids. That's first line. Stairs don't work. Then the second thing will try is IVIG. If IVIG doesn't work, then the final thing will try for these kids is a spleenectomy, right.

Because really, it's those spleenect macrophages that are binding to the IGG antibodies that are bound to GP2 B3 A. That's causing the damage. Right. So if you take away the person's spleen, you will largely take away the person's problem. Right. Again, remember, ITP is an autoimmune disease. You make autoantibodies against the platelet protein GP2 B3 A. Right. Please do not confuse ITP with glansmone thrombostemia. We're in glansmone thrombostemia. Right. You have an actual deficiency, it's an autozomer recessive disease. You have an actual deficiency of GP2 B3 A. Now, what if they give you a question about a patient and they tell you that this patient, you know, has, you know, for the, for the last, let's say she's a 12-year-old female. And for the last two weeks, she has been having like just a lot of joint pain and the joint pain, like, you know, starting the knees. He started in the knees, but now it's gone to the elbows, going to the thigh, going to the hips, stuff like that. Right. And they tell you that, oh, she had an operation with her infection like six weeks ago. If you see something like this, what should you be thinking about? Well, I would really, really hope. You're thinking about a rheumatic fever, right. Rheumatic fever. Remember, rheumatic fever is very high, you know, for the USML exams. In fact, maybe let's start off with how does this operator's vitro infection relate?

Well, if you think about it, this operator's vitro infection was probably like strep foreign gyroidest, right. Group B strep infection. And then that group B strep infection, the thing is, maybe one principle to know, one genetic principle to keep in mind for stucychistep 3 is this whole concept of molecular mimicry, right. Molecular mimicry. So the thing is the body, when you see certain strains of group B strep, makes antibodies against it. But the thing is, those anti, some of the antigens that group A strep expresses look like similar antigens in the body. So the thing is when the body makes antibodies against group B strep, those antigens that group B strep is presenting to it. They can also make antibodies against things like the bizzle ganglia. That's how people get, like, sitting ham scorri and all these problems. Or you make these antibodies attack like myocardial proteins, that's how you get a rheumatic fever and all those things, right. So that's very high utonore. So this person has rheumatic fever. I remember rheumatic fever, right. Like many times it can thrash the persons that might throw off, right. In fact, the biggest risk factor for microstomosis, as we know, is rheumatic fever. So how do we treat rheumatic fever on NVM exams? Well, don't forget, you're going to go ahead and give these people penicillin, you're going to give them an answer.

You're going to give them penicillin, even if they don't seem to have any antecedents of infection, because you want to clear everything that's going wrong with those people. Okay. And remember again, if you were to biopsy the persons like heart or whatever, or like a tissue that's affected with, especially the heart, it's affected in the person that has rheumatic fever, the key key thing I'll see you find, you'll find those ashove bodies, right. Ashove bodies. That's actually very high utonore for the purposes of the exam. Now, what if they give you a question about a patient, you know, they tell you that this patient is on chemotherapy, and especially in goes into DIC, right. Some kind of hematologic malignancy and they're on chemo, and they're going to DIC. If you see this, what kind of malignancy do they have? Well, this is easy, right. This person has acute pro myelocytic leukemia. Remember, acute pro myelocytic leukemia is pretty much the only kind of AML that you need to know for your exam, right. It's like the M3 type of AML. But for the most part, if you're testing AML on your exam, is acute pro myelocytic leukemia, they're going to test, right. In fact, sometimes the MBM is don't even bother putting an acute pro myelocytic leukemia. They just put AML as an answer, right. So, remember, AML is, you know, acute pro myelocytic leukemia rises from a 15, 17 translocation, right.

So, because of that, you're going to form, you know, your blood cells are going to perform for rate, cause a lot of problems, right. And remember, many times, you're going to treat these people by giving them atra, all trans-rich noioc acid. Again, instead of putting all trans-rich noiocacid as an answer, they can put rate noioc acid as an answer, they can put vitamin E derivative as an answer, right. These are always the contestous exact same thing. Now, by giving all trans-rich noioc acid, you're basically going to make those blood cells different sheet to terminal cells that cannot divide. And in so doing, pretty much fixed malignancy. Now, it's very high you to know that in acute pro myelocytic leukemia, these are our rods, right. These are our rods can absolutely positively cause the IC, right. They can trigger the IC. In fact, to be honest with you, I would strongly encourage you to be able to identify our rods on a blood smear, okay. Be able to identify our rods on a blood smear. It can trigger the coagulation cascade, and that can cause the IC. Now, what if they tell you that this person has been on all trans-rich noiocacid, and let's see, it's a woman. And, you know, she's been on this therapy for like a few weeks, and now she has like morning headaches, she has like blurry vision, and all those things. If you see that, what should you be thinking about? Well, I would really hope you're saying, divine.

This person, it sounds like they have a idiopathic intracranial hypertension, right. Idiopathic intracranial hypertension. Remember, that's what we affectionately refer to, you know, back in the day, as pseudo-tumorsary brine. Remember, this vitamin A derivatives, right. Like isotret knowing, and all those things, these walk me, you know, associated with pseudo-tumorsary brine. Again, all trans-ret noiocacid is a vitamin A derivative, right. So, you can certainly cause a very similar, very similar problems, right. So, again, that's kind of high-youtu-no, for exams, right. Again, remember, pseudo-tumorsary brine, most times, there's no real obstruction to CSF flow, right. So, this is actually an example of a communicating hydrocephalus. There's no real obstruction. The problem is more with CSF absorption, right. At the level of the arachnoid granulations, you know, before you start going into the, into the drool folds. So, that's very high-youtu-no, for exams, right. So, how do we diagnose pseudo-tumorsary brine? Well, that's easy. All you need to do is perform that lumbar puncture, right. And when you perform that lumbar puncture, you notice that, wow, the CSF pressure is a crazy high, right. Like, 200 to 50 kind of deal. Most times, it was going to be above 200 on the USMEL exams, which is obviously insane. That's insane. Me, right. And remember, these people, they may have like papula dima on fondoscopic exam, right. Again, just from those increasing trocranial pressures.

Now, the one thing I'm going to go ahead and see here is, once you diagnose, be also pseudo-tumorsary brine, right. One thing, certainly are many different treatments you can consider, right. Like you can try acetyzolomide. Remember, acetyzolomide is a carbonic and hydrase inhibitor. So, because it inhibits carbonic and hydrase, right, it would decrease the production of CSF, because the thing is, carbonic and hydrase is one of these enzymes that I need therefore, CSF production. So, if you decrease the amount of CSF that's made, that could potentially help those patients, right. So, that's one thing you can do. And another thing you can potentially do for these people, right, is to go ahead and again, do like serial lumbar punctures, just to drain off some of that CSF, right. So, that it doesn't build up and cause those symptoms. Now, one thing you can try, let's say we have having like very disabling eye symptoms, and those symptoms just do not seem to be responding to acetyzolomide or serial L Ps. Then one thing you can consider on MBME exams is something called optic nerve-sheath sheath fenestration, right. Optic nerve-sheath fenestration, right. Optic nerve-sheath fenestration. That's something that can decrease those intracular pressure so that the person doesn't get in, get in hot water.

Now, one thing I guess I want to go ahead and say with acetyzolomide is, again, whether you like it or not, so the thing people see this question on SDN ready all the time, like, oh, you know, how much step one material to do test on step two? So, the thing is they won't test it directly, they're going to test it indirectly. That's a very big thing. They're going to test it indirectly, indirectly, right. So, they can talk about a person that will start it on acetyzolomide, right, for pseudo-tomorcerybri. And then ask which of the following will be the most likely electrolyte abnormally caused as a result of this drug. In fact, to be honest with you, they will very likely make this an art like a series of hours. Well, let's examine that. Well, the thing is acetyzolomide, as we said, inhibits cabonic and hydrates. So, the thing is, cabonic and hydrates is a big, big, big, big time enzyme that works at the level of the proximal convoluted tubule. Well, if it's not working, then you're not going to be able to reabsorb by carb in the nephron. And if you cannot reabsorb by carb in the nephron, you're going to pee it out. So, you're literally going to be peen out a ton of bees, right, a ton of bees. So, think about what kind of acetyzolomide would you get? Well, that's easy. You're going to get a metabolic acidosis, right, because you're peen out bees. You're going to get a metabolic acidosis. So, with more specific, you're going to get a normal anion gap metabolic acidosis.

In fact, if you want to be even more specific, you're going to be getting a type 2 RTA as your cause of a normal anion gap metabolic acidosis. And it is very, very high urtunoil, you're getting rid of bees, you're literally losing bees, by carb in your urine, right. So, people that are on acetyzolomide, they essentially get an a type 2 RTA that's induced by your drug, right. So, this you are going to get a type 2 RT, it's going to cause them to have a normal anion gap metabolic acidosis, right. Now, let me ask you this, are these people going to have hyperkelimia or hypokelimia? Well, I hope you're seeing, oh, they're going to have hypokelimia, because many of you have probably learned this that, oh, many times, you know, especially with the diuretics, if you have a metabolic acidosis, hypokelimia is coming, coming into, right, like literally hypokelimia metabolic acidosis. You see people almost saying it like a prayer, hypokelimia metabolic acidosis, hypokelimia metabolic acidosis. Yes, that's true, right. But that's not always true, especially for acidosolomide. Acidosolomide, our friends at the MVM is love this drug, because in addition to causing the metabolic acidosis, it causes hypokelimia. So, it's almost like it picks from, it's like double-deepen, right. We know why it causes the metabolic acidosis, because it prevents you from reabsorbing bicarbine in your nephron, at the level of the proximal convoluted chibio.

But another thing that it does is it's a diuretic, right, because that bicarb sodium is going to follow it, water is going to follow it, so it's going to make you volume down. If you're volume down, what's going to happen to the activity of the reigning and jutezine adostroent system, when it's going to go up, right. And we know that one of the things adostroent does is to make you reneed potassium, right. So, if you reneed that potassium, you're going to have serum hypokelimia, okay. You're going to have serum hypokelimia. Again, that's very high yield to know for purposes of your exams. Okay. Now, acidosolomide, though, I guess the last thing I would say about acidosolomide, with regards to MBM exams, right. Again, you don't only use it for pseudo-tomo cerebride. Remember, you can easily find increase in chocryneopressures, you can easily find glaucoma, right. Because again, as it so happens, the monocanhydrate is necessary for ectosumor production, right. So, again, those are just all high yield things you need to keep in mind. Keep at the back of your mind with acidosolomide. Now, what if they give you a question about, you know, like a four-year-old African-American male, the tell you that he comes into the, he's brought to the emergency room because he has been having like very high fevers for the last two days, like, you know, like teeth-shattering fevers, like terrible, terrible, terrible fevers.

His temperature is like 103, the tell you that he has like a pulmonary infiltrate on a chest x-ray, and then the tell you that they get blood cultures, and they get a blood smear, and you know, the C gram positive, the block oxide, right. And his white count is like 25,000, like some crazy high number, right. And he asks, oh, what is the most likely mechanism behind this patient's findings? Okay, well, what do you want to think about there? I really hope you're saying, oh, divine. This kid has sickle cell disease, right. African-American, right. So why do they have this problem? Why do they have this nasty, nasty, nasty infection? Well, our friends at the NBM Es, they would really want you to think of this child having no spleen, right. A classic thing they can literally write down as an answer is auto-splinectomy, right. So literally this child's spleen is gone, right. Literally this child's spleen is gone, right. So remember, these kids, they're going to have like an ischemic, you know, destruction ultimately of their spleen, right. You have an auto-splinectomy, right. And remember when you have no spleen, well, you're going to have a lot of problems with encapsulated organisms, right. Strep pneumo, HL fluencer, nice, sermeninjaididis, things like that, right. So this child has pneumocococcus sepsis from strep pneumo infection, again, because this child has no spleen, right.

And many times in these circumstances, you're going to at least give like a third generation sephalosporine as broad coverage, right. You can give like seph traaxone, sephal taxine to help them under those circumstances, right. This child has a pneumococcus pneumonia, right. This child has a pneumococcus pneumonia. Okay. Now, what if they give you a question about a, what if they give you a question about a six-year-old girl, right. At the TV that she has like ten or five breasts, right. And the TV that she has like, nexel mass. If you see this, what should you be thinking about? Maybe like, huh, divine six-year-old female, ten or five breasts, that doesn't sound right. Yeah, that absolutely does not sound right. Right. Then you see on the nexel mass, what are you thinking about under those circumstances? I really hope you're saying, oh, divine, this, because think about it, right. This child has precocious puberty, obviously, right. Remember, if you're female, and you're under the age of eight, and you're having these super advanced secondary sexual characteristics, you have precocious puberty, right. Now, to be honest, with you, this is actually one of those unique causes of peripheral precocious puberty, right. So, but let's address this a little bit more. Why would this person have precocious puberty and have an nexel mass? Well, the thing is, if a lady is having precocious puberty, then that means she's being exposed to a ton of estrogen. Okay.

Well, so how does hyperestrogenism relate to said at nexel mass? Well, hyperestrogenism relates because she likely has a granulosa cell tumor of the ovaries, right. Remember, these granulosa cell tumors, they love to make estrogen. When they make estrogen, they can cause a lot of problems, right. That estrogen, remember, that unopposed estrogen can cause the, this girl to have like hyperplasia of the endometrium, but that high level of estrogen, right. And cause her to have these big large tanner stage five breasts, right. So it's very high to know this, right. So whenever you see a granulosa cell tumor, you'll usually present as a peripheral precocious puberty on an NBM exam, right. And if, again, you were to biopsy that tumor, remember, you're going to find these things we call the call x-ner buddies, right. The call x-ner buddies call being C A W L and then a hyphen x-ner, E X N E R, the call x-ner buddies, right. Again, you're going to see that with a granulosa cell tumor. Again, remember, in an elderly female, right, this is going to be more endometrial hyperplasia on cancer, right. Because remember, granulosis, again, granulosa cell tumors, they make a ton of estrogen. That estrogen is just going to cause the endometrium to proliferate like crazy, right. And that can certainly cause hyperplasia, that can certainly cause cancer. Okay. So I think I'm going to go ahead and stop here. Again, I really hope you found this podcast to be helpful.

Again, as I do, again, there's the step 2 C K step 3 course coming up from the seventh to the 10th of December. And the NBM testing and strategies course coming up on the 6th of December. Again, if you're interested, more details, signing up, registration, just should be an email through the website. I go for one or one to learn from any exams, step one, step 2 C K, step 3, pre-clean cool minutes, cool exams, 30-year shelf exams. And then if you need help with your ERAS application, mock interviews and stuff like that, again, should be an email. And I'll be happy to help. Again, I've worked with tons of people that are successful residents all over the country in many different specialties, in many different disciplines. And then I do have another website. I studied it recently, divineinterventionlifelessons.com. And again, many people have been like, oh, divine, I really love your life lessons. So I made a linear website just for that. And I just dressed like common problems that face humanity. So if you're listening to the, I think I have like 39 episodes right now, I put like two episodes of every week. So if you're interested, I even have the podcasts on Apple podcasts. It's called the divine intervention life lessons podcast. Again, just follow that podcast. Most of the podcasts are pretty sure they're about 10 minutes. You know, every now and then there'll be a topic that's so important that I need way more than 10 minutes, right? But those are few and far between.

And then these divine intervention podcasts itself, I have, I have them on Apple podcasts on Google podcasts on Spotify, at least the most recent 150. If you want everything from episode one, all the way to 351, you need to go to the website. And actually, if you subscribe to the website, divineinterventionpodcast.com, you'll get an email notification whenever I drop a new podcast. And then I also have a You Tube channel, divine intervention, USMD podcast and videos. And if you subscribe to that again, it will show up as your among your notifications in You Tube, because I've been making more videos in recent times. So thank you for listening today. Have a wonderful Monday. God bless you. I'll see you next time. Thank you.

Albuminocytologic dissociation (high protein, normal/low WBC count).

Steroids $\rightarrow$ IVIG $\rightarrow$ Splenectomy.

Aschoff bodies.

Acute Promyelocytic Leukemia (APL) / AML M3.

Idiopathic Intracranial Hypertension (IIH) or Pseudotumor Cerebri.

Type 2 RTA and Hypokalemia.

Albuminocytologic dissociation (high protein, low WBC).

Platelet protein GP2b3a.

Granulosa cell tumor of the ovary.

Inhibiting carbonic anhydrase in the proximal convoluted tubule, preventing $\text{HCO}_3^-$ reabsorption.

Auto-splenectomy leads to impaired filtration and clearance of these bacteria (e.g., S. pneumoniae).

Auer rods.

Albuminocytologic dissociation (high protein, low WBC).

Platelet protein GP2b3a.

Granulosa cell tumor of the ovary.

Inhibiting carbonic anhydrase in the proximal convoluted tubule, preventing $\text{HCO}_3^-$ reabsorption.

Auto-splenectomy leads to impaired filtration and clearance of these bacteria (e.g., S. pneumoniae).

Auer rods.