DIP Episode 553 - USMLE Step 2/3 Rapid Review Series 117

Welcome to episode 553 of the Divine Intervention Podcasts. Into this podcast we're going to be continuing the Rapid Review series for the USMLE Step 2 Secans Step 3 exams. This is going to be series 117. Let's get right into it. So what if they give you a question about 59 year old male and you're told that for the last four weeks he has noticed swelling of his abdomen and he tells you that he has to keep turning from side to side because he feels like whenever it especially at night when he's sleeping because whenever he sleeps on one side for a long time he notices like his abdomen is getting even bigger in that direction. And you're told that he has clear ligtres, he has some jaundice and you're giving that his BMI is 45 kilograms per meter squared and then you're told that he has no history of alcohol consumption and that he recovered from hebe infection. You know he had a hebe infection 20 years ago that he recovered from and then you're given hebe laps and you're told that his hebe surface antibodies are positive and his anti hebe core antibodies are positive. And then they say you know what is the most likely finding with organ biopsy in this patient. So first things first what does this person have? Well I hope you're seeing the wine sounds like this person has cirrhosis. Divine how did you get there? Well let's explain. First this guy has a side is again this whole concept of a fluid wave.

If the MBME is present that to you then that's wonderful you should be thinking God with that. But again the more recent exams these these are more descriptive so they may not go in that direction. They may just say oh you lay down on one side and your belly seems to be expanding the direction of your lay. And you see that that's a fluid wave that person has a side is right there. I remember why would a person have a side is in cirrhosis? Well they'll have a side is because the liver is one of the primary organs that makes albuming. If you can make albuming then there goes you on cortic pressures and if you don't have on cortic pressures you'll not be able to retain fluid in your vasculatory. So you can have a little fluidic transition from your mesenteric vessels and that's going to cause you to have a side is all right. So that's number one. Now number two what's the thing that's causing these guys? What's the most likely cause of this guy cirrhosis before we answer the main question that I posed? Well the most likely cause of this guy cirrhosis is probably the otter is non-alcoholic fat-eliver disease although these days they call it metabolism associated fat-eliver disease. So you may wonder divine how do you know that? Why can't you say it's hepatitis? I mean dude like this guy has like hepatitis. No so this guy had acute hebi. He actually does not have ongoing hebi infection. How do I know that? Well look at the labs I gave you.

I told you that these hebi surface antibodies are positive. I'm going to tell you this right now for presence hebi surface antibodies are positive. They don't have hebi infection. You may be wondering divine why is this person's antihibic or antibody positive? Well it's positive because it means that the person probably got hebi in the part is not probably. The person got hebi in the past and the person recovered from it. So you may be wondering divine okay how do I not know that this person got vaccinated? Well this person we know that he didn't get vaccinated. Like it was not a vaccine that we know that he's had a troll hebi why? Because he's anti hebi quarantine bodies are positive because the thing is hebi the bug has the hebi quarantine. So if your immune system sees it, it make antibodies against it. But the actual hebi vaccine doesn't contain the quarantine. So if your method of your immune system developing hebi surface antibodies anti HPS is the person getting vaccinated then your hebi quarantine bodies will not be your anti hebi quarantine bodies will not be positive. That's actually kind of high yield to know for you. Okay so again this guy does not have chronic hebi leading to his cirrhosis. He's not an alcoholic right? And I don't give you any of the thing in this question that should guide you in this direction right?

So like I think same thing like burns diabetes or whatever and I've talked about this extensively in the iron story podcast very high yield podcast on herodicure hemocromatosis he doesn't have a phone antitripsine deficiency. So we should probably be shooting for metabolism associated with liver disease. So that's what's causing this person's problem. So now what are you going to find on biopsy if a person has cirrhosis? Well if a person has cirrhosis you're pretty much going to have a fibroetic liver. I like to think of it as fibroetic liver disease. Again, I know some of you may think that all step two, step three days, no way they'll be testing these organ biopsy findings. Trust me, that will be a very unwise thing to keep in mind. In fact, in many of my review classes I go over some of these are classic basic science organ biopsy findings. They love to test them on exams. So for a person who has cirrhosis you're going to see diffuse fibrosis of your liver. In addition to that you're going to see like all these nodules. If you're going to see like a nodular appearance and those nodules will pretty much be outlined by fibrosis. We'll pretty much be outlined by fibrosis. You see those things absolutely keep up think of cirrhosis on your exams. Okay, now what if they give you a question about a 25 year old male?

They tell you that oh he just returned from a foreign country for one week vacation and you're told that he tasted many different local foods and he had a wonderful time but I didn't have intercourse with anybody on this sexual intercourse with anybody. But then you also told a few more things. You're told that right now he has like right upper cordon pain. He's not able to keep anything down. He's been vomiting and you're told that this guy has usually smokes two packs of cigarettes every day. He's done that for the past 10 years. And you're told that for the past three days he has not taken a single cigarette. And then they ask what is the most likely mechanism of transmission of this patient's illness? And you know, he has jaundice on all these things. And I'll hope you're saying you're picking the answer that says a fecal oral. They will try to trick you on your exam and put something about like sexual transmission, IV drug use, ja ja ja ja ja ja ja ja ja. But no, pick the answer that says fecal oral transmission. So what in the world am I talking about here? I'll hope you're saying oh divine. This is hip A infection. This is hip A infection. This is hip A infection. Remember hip A what are the key things to know about hip A? Number one is transmits hip by the fecal oral route. Right? So basically you're going to find this if a person is returning from like a country that doesn't have the best sanitary practices. Right? Or please that's just a ton of people.

So they can actually give you a hip A outbreak question like in a military bark. Again, you know the US semilies they have this big focus these days on returning service men and women. So they can absolutely focus on that like in a military bark or in a college dorm or whatever. So something you want to keep out the back of your mind, right? So basically you consume contaminated water, you consume contaminated food. So the kind of weird thing that's a zero hip A infection is shellfish. When you see those associations, I absolutely want you to think about hip A infection on your exams. And I give you the classic symptoms, you know, right? A proconjuan pain, anorexia, you know, vomiting, nausea. But actually one kind of high old thing to keep out the back of your mind for your exams is a person that is a smoker not wanting to smoke. When you see that with the right context, so don't say divine said that a person that smokes doesn't want to smoke anymore. Or this must be hip, this must be hip A infection. They can present it as another pathology. That's why context matters a lot on the US semilies. Look at the overall context of the question before you start jumping to those kinds of conclusions. But that desire to not smoke when you're regular smoker is actually a feature of hip A infection. It's actually a feature of hip A infection. So just make sure you kind of keep that at the back of your mind as you study for the US MLA exams, right?

And most of these people pretty much all they need is supportive care. They're going to be fine. All right. Now again, just to make sure that I emphasize this, let me ask you this. Actually, let me frame this as a vignette. What did they give you a question about a, let's say, 26 year old female and they tell you that she comes for her first prenatal visit. And you're told that you're given a bunch of, you told that you know, prenatal, you know, 10 week visit, they get a bunch of labs, HIV, whatever is negative, hip C RNA, negative, HIV RNA, negative. And then they say, a heavy quarantine, buddy. Sorry. They said the heavy surface antigen is positive. They say the anti-heb, quarantine body is positive, but the heavy surface antibodies are negative. And then they say, which of the following lab findings is, and you know, they say, you know, better he sees his positive, you know, cause he's pregnant. And then they say which of the following additional lab findings is most strongly associated with vertical transmission of this patient's infection to her fetus. And I would, you know, they put a bunch of answers that include a bunch of like random things, they put a bunch of heavy difference analogies. So which one do you want to pick? I hope you're thinking of about the hip BE antigen, the heavy antigen. Again, our friends at the MBM is these days. They like to ask these prognostic based questions on the USMLA exams.

And remember when you have a hebee infection and you have the hebee antigen that's positive, it indicates high transmissibility. And maybe wondering why does that mean high transmissibility? Well the thing is that the antigen is heavily expressed when he bee is replicating like crazy. So if you see a lot of like the hebee antigen is positive, that indicates high transmissibility. But again, they know that most people that have the job description medical student know, you know, if you're a hebee antigen is positive, if you have high transmissibility, right? They know that all of you know that stuff. So what are you going to do on the exam? They're going to put it in a pregnant woman scenario. It's the same concept, literally nothing different, literally. The same concept, just in a somewhat novel situation that you've not really thought about. So that's something that's actually pretty high you also know for your exams. If your hebee antigen is positive, then there's a pretty high risk of you giving that infection, that chronic hebee infection you have to your fetus. So kind of keep that at the back of your mind as you study for your tests. And one thing I want to say about this is a friend at the MBM is another prognostic question they can kind of throw in your exams is they can say they can give you like a side by side vignette of a person that has, you know, they can in fact, you know, if they want to kind of throw this on the exam, they'll make this a two part question.

The first part will be some easy question about some person where you have to make the diagnosis that they have acute hebee infection and you'll be in an adult. That'll be the first part of the question. Because I'm sure many of you know these questions where you have to answer the first one hits of mid before you can answer the second part of the series. And then in the second part of the series, so you know, you answer the first question like, yay, this is pretty easy, you know, classic hebeena, the agnocent acute hebee infection and adult, you know, the end. And then they'll give the second part of the question that involves vertical transmission of hebee to the fetus, to a fetus in a woman that is pregnant. And then you'll ask which of the following, compared to the patient from the previous question, which of the following has the highest risk of progression to chronic hebe infection. They'll give you the, you know, they'll say adult, you know, fetus, yada yada yada. So which answer should you pick? Well, if you're thinking in terms of prognosis, I would hope you want to pick the one involving the child. Here's the thing. This is something that is floridly, floridly, floridly, excessively, ridiculously high to know for your exams. See, whenever an adult contracts hebe infection, the risk of proceeding to the patient to chronic infection is very, very low.

In fact, I'll tell you this, more than 95% of adults that have acute hebee infection have a complete resolution of that infection. Have a complete resolution of that infection. It is extremely rare for an adult that gets acute hebee to proceed to chronic hebee. All right. Is that the same thing with kids? Nada. No. No. Whenever a child, a fetus gets hebee infection, vertical transmission from mom, they have a very, very, very high risk of progression to chronic hebee infection. Keep that in mind. Why me that makes sense instead of just blindly memorizing something? I don't know. As a kid, do you have much of an immune system? Probably not. Probably not. Right? So it's pretty high you to know that for your test. Okay. It's pretty high you to know that for your test. Know those differences in prognosis. Prognosis. Prognosis. This is something I spent so much time testing in class talking about how to answer questions involving a prognosis. Make sure you know these things for your exams. In fact, I feel like there's one more thing I want to say about hebee. That's kind of high yield. Just with some of these almost like tongue twister questions you don't think about until you see it on a test. So between hebee infection and hebee infection, which one is more likely to be acquired by sexual contact. But I hope you're saying the vine needs hebee infection. Again, you'll try to trick you at hepsy. Don't get me wrong. You get hepsy with sexual contact. Absolutely. Absolutely.

But the risk is pretty low compared to hebee. But hebee, you can absolutely, positively get it through sexual contact with a person that has an infection. So again, please, these different like little things here and there that I'm saying about these hepatitis viruses. Don't ignore them. If not, you're just ignoring that your own risk. I'm telling you, ignore to your own peril. I kid you not. This stuff is pretty high yield to know for your exams. If this is not clear to you, go back and listen to it because I've given a pretty clear series of explanations. Go back and listen. Right? Again, don't don't miss exam points. It may be two questions you answer right from this podcast. There'll be the difference between you being in the two forties on your exams and being in the two fifties. I've seen this so many times. All right. So what if they give you a question about a five year old boy and you're told that this boy is parents say that for the last one week, they've noticed that his face has been very, very swollen. But they tell you that he has really not had any symptoms and you know, you're told that you know, the physician decides to, you know, as a beta pediatrician. This has to check his weight in the office and he has gained seven pounds compared to his last visit two months ago. And then they tell you that, oh, what is the next best step in the, you know, in diagnosis. I hope you're saying, let's go ahead and get a urinalysis. Why? Why?

And they'll give you another answer that says to do a kidney biopsy. Come on, please don't do that first. Mix zero cents. No, you should get a urinalysis first. What's going on with this kid? I hope you're saying divine sounds like this kid has a minimal chain disease, right? Probably has nephrodisiac syndrome. I mean, wonder, oh, divine, but couldn't they say, pick, trap the caca, glomerular nephritis? Or, um, what is the other one? I gene a frappathy. Uh, no, it's not because guess what? I didn't say anything about a respiratory infection. They see jack about a skin infection. So don't think in those directions. Don't think in those directions. Think of minimal chain disease. Remember, minimal chain disease is the most common cause of nephrodisiac syndrome in kids. And in minimal chain disease, obviously, you're going to have hypopubinemia. Why? Because T cells are literally damaging your putocyte food processes, right? This is a T cell problem. It's not an antibody problem. This is a T cell problem is not an antibody problem. In fact, this is a classic folder on the USMELY exams for basic science questions, like what kinds of basic science questions? Number one, they can ask, what is the immune cell that is most strongly implicated in whatever issue? It's going to be T cells, okay? It's going to be T cells. They're going to damage your putocyte food processes. They're going to damage your negative charge barrier in your glomerular basement membrane.

And that's going to cause you to have selective protein area, selective protein area. So what in the world do I mean by selective protein area? By that, I mean that you're going to be losing mostly opiumin. Pro-opiumin has a pretty big negative charge, right? So if you lose a negative charge barrier, you lose those repulsive forces that should keep opiumin inside your glomerular. So you lose all that opiumin, you have low opiumin, you have low oncotic pressures. So you're going to have a demon, things like that because of increased fluid extraversation. So the person is going to have a big time protein area, mostly opiumin, okay? And this is actually kind of a key feature. And this is part of why minimal chain diseases is not as bad. And I'm going to talk about a few more basic science things here. But this one is not as bad because what you're damaging the putocyte food processes, you're losing that negative charge barrier. So you're just losing opiumin. For the most part, you don't lose much of any other kind of protein if you have minimal chain disease. You really don't. Versus other kinds of nephotic syndrome where the destruction and the damage, especially by antibodies, leads you, you know, you have this antigen antibody complexes leads you to having like nonselective protein area. So you're not just losing things like opiumin. You're losing things like anti thrombin three, which is an anti-quagulant protein. So you become hyperquagulable, right?

So just kind of keep that in mind. That's actually one thing that kind of shows you how minimal chain disease is not as bad because you're just losing opiumin versus losing opiumin and other stuff that you see on the recording, other kinds of nephotic syndrome. So again, it's the T cells that do the damage. So what are you going to see on like my crosscappy in a person that has been a machine disease? Well, the answer is going to be nothing. Okay. What are you going to see on immunofluorescence? Well, does this damage involve antibodies? Did I say anything about antibodies here? No, I did not. I said it's T cells. So guess what? Immune fluorescence is going to be absolutely negative. Okay. Now, so how are you going to see this putocyte food processing facement in a person that has minimal chain disease? Well, the simple straightforward thing to do is what? Electrome microscopy, right? Electrome microscopy. You're going to see that putocyte food process, if facement. Okay. So please, in minimal chain disease, light microscopy is normal. Immune fluorescence is normal. But electron microscopy will absolutely show you that putocyte food process, if facement. And you know, if they are trying to extract a treatment, commitment, out of your exam, you can have big steroids. You can give these kids steroids. But again, these kids are going to do well. They're going to proceed to end stage, uh, renal disease or anything crazy like that. Okay.

They're not going to proceed to end stage renal disease. So please keep that in the back of your mind. Then again, why did I say we should do your analysis first? Well, I literally said we should do your analysis first because it's going to show you the protein. It's going to show you protein, Nure. It's going to show you protein, Nure. Okay. It's literally going to show you protein, Nure. Right? So you don't, you maybe start with something that is not as invasive first before you start going for something that is super, super invasive like a renal biopsy, right? When you do your analysis and it shows you something worrisome, then you can proceed to do your renal biopsy. To be honest with you, I almost never worry about, um, doing renal biopsy for minimal chain disease on USMLE exams. You know, I would only do renal biopsy if I'm dealing with like legit, I'm not saying minimal chain disease knowledge yet. But like, come on, don't turn to renal biopsy for in a child for minimal chain disease. That doesn't make any sense. It's just one of those things where I'm like, you pick that answer on the exam. It's the wrong answer you're picking, but we're going to let that, let that go. Okay. Now, um, let's maybe consider one or two more vignettes and then I think we'll go ahead and kind of, kind of wrap this up.

So what if they give you a question about a 49 year old female, they tell you that, you know, for the past three months, she's been losing some weight, she has jaundice, uh, and that she, it's a lot and that each in is really bad, especially at night. Um, what's going to be a diagnosis here? Well, I hope you're saying, ooh, divine this. And then they give you like, you know, bunch of labs, you see the elk forces elevated, you know, the GGT's elevated, the gamma glutamol transfer is elevated. And then they show you that the anti-minor control antibodies are positive. So what is this? That's easier, right? Right? Remember, back in the day, this is called a primary bilayer is seroses, but now in the day, these days, they call it primary bilayer equal and triad, it's the, that's a newer term, right? Remember, basically, it's an autoimmune disease. It's an autoimmune disease. So what are you going to see there? They're going to give you a destruction of, of, of stuff, right? Like your intradiparty bowel ducts. Uh, you pretty much destroy your intradiparty bowel ducts with these antibodies. When you destroy those, you're obviously going to have issues secreting bile into your bilayer tree. And if you have those issues, then that bile is going to complete in your bloodstream, it's going to cause you to have priders, you're going to have jaundice, uh, because it's pretty much like an obstructive liver pathology. Obviously, you're going to have an increase in your direct bilayer.

So the primary hyperb bilayer, you have is a direct hyperb bilayer. In academia, you're going to have an increase in your outfoss, you're going to have an increase in your GG team. In addition to that, um, you know, again, you're going to have these positive anti-matter control antibodies. And remember, when people have PVC, what will be the, will be trove their urine? All their urine is going to be dark, uh, because remember, direct bilayer rubin is water soluble. And what is a big component of your urine? Water, right? So because direct bilayer rubin is water soluble, can be filtered at the kidneys. So those are going to have dark urine. But what's going to be trove the color of those people's tools? They're going to have pale acolytic stones because again, they cannot secret biline to the abillary tree. So you cannot get into the GI tract. So they cannot form this thing called sterco biline. So since you can form sterco biline, you'll not be able to colorize your stool. So whenever you see this pattern of jaundice, increase the direct bilayer rubin, um, acolytic stones. In fact, they may skip the direct bilayer rubin part because that kind of makes it too easy. So you see a person that has jaundice, has pale acolytic stones, but has dark urine. That should be a very, very strong indicator on your exams that you're dealing with. What with obstructive liver disease? You're dealing with obstructive liver disease. And how do we treat PVC?

Well, I mean, if you want to curate, you deserve a new lever, but um, your levers are kind of hard to combine. So what can you do to improve survival? You can give also dial or so dial. Remember, another name for also dial, you may see on your exams is also the oxycolic acid, okay? Also the oxycolic acid. Remember, that drug will also use it to treat the intra hepatic holostasis of pregnancy, okay? Intradepatic holostasis of pregnancy. So please just kind of keep this at the back of your mind. And remember, people that have PVC, um, they can actually give you a lab. They can show you that their turocholesterol is very elevated. And then they ask, what is the most likely mechanism behind this person's hypercholestrolymia? Again, it's because of decreased excru, because remember, what is one of the, actually, one of the primary ways your liver gets rid of cholesterol in the body is secreted into a bio. A big component of bio is cholesterol. But if you have obstructive liver disease, literally, especially if it's a chronic issue like PVC, you may be able to secret the cholesterol into the bio. So that cholesterol is going to build up in your bloodstream. So those people can actually have things like zanctomas or zanctelasmas, zanctomas or zanctelasmas. So don't think that zanctomas and zanctelasmas are found only in people that have, um, familial hypercholestrolymia. You can absolutely find it in people that have PVC. All right.

Again, all these different nooks and crun, like not some boasts things I'm discussing. You may think that these things are low yield for your exams. Please, I'm begging you, they're not low yield. They're absolutely not low yield. You're going to heavily regret it. If you don't put in the time and attention to actually like mastering these concepts. Okay. Now I'm telling you the USMLE's, I'm again, I have a lot of experience with these exams, not just old experience, but like recent experience, like I literally like teach classes and prep people for these exams like very frequently, right? Even on an individual basis, I prep people for these exams. So I have a very strong temperature on these exams. So please, I'm not saying this to be proud. I'm just saying they should probably be a, you know, pay attention. Okay. What if they give you a question about a patient that is 25 years old? And they tell you that, you know, for the last two days, he has had very significant abdomen open, very, very significant abdomen open. And you know, they tell you that his abdomen on physical exam is extremely distended and his temperature is like 103.1 and his blood pressure is like 75 over 40. You know, they tell you that he has a long history of chronic abdomen open and bloody diarrhea. And then they ask, what is the next best step in in management? Well, I would hope that the first thing you're doing is to go ahead and get a plain film extra of the abdomen.

When I get it, go ahead and get an abdominal X-ray. What are we worried about here? Well, sounds like this guy has an ulcerative colitis. And what is this bad thing that he seems to have going on for him right now? Sounds like toxic maker colon, toxic maker colon, toxic maker colon is actually really bad. But basically, you're going to see a person that has like a history of like ulcerative colitis and they will have like severe abdominal pain, severe distension, right? Blodded area, very high fivers. These are going to be very, very unstable. And again, you want to get that plain film X-ray. And you're going to see that their transverse colon is huge. This is actually one of those classic abdominal films you want to be able to recognize on you exams. I want to make sure you can recognize that on you exams. You're going to see that transverse colon is going to be pretty big. And I think usually for you to, you know, if it's more than six centimeters, you want to start worrying about these, these folks, you know, again, sometimes you can just do like conservative management for these people who fluids and whatnot. But if they're having signs of parietanitis or signs that they're like crush and burning, you should consider this person going for some kind of surgical procedure. And actually, what kind of testing is contraindicated in these folks? What kind of testing is contraindicated in these folks?

I'm out hope you're saying divine, you know what for these folks is maybe not a very smart idea to do anything like, come on divine, think, you don't want to do a barium, animal, barium, bad, bad, bad idea in these people colonoscopy, bad, bad, bad idea in these people, you know why? Because you can explode the colon. You can prefer the colon doing stuff like that. So please don't do stuff like that on your exams. And remember, what are some other things? Let's talk about some weird, not some both things like kind of like I did for the hepatitis viruses. Both slot that in here for UCPSC and all these things. So number one, what, let's see, how do I put this? How do I put this? What are some other things that can increase your risk of toxic mega-colour? Well, don't forget to see death. See death can cause toxic mega-colour on your exams. It's not only those really difficult ideas that causes toxic mega-colour. And then, you know, our friends at the MDM Es occasionally like to kind of throw out screening guidelines with this stuff on the test. So remember, if you have, so let's kind of break this down. If you have O3 DF colitis, just straight up O3 DF colitis. Each to 10 years after that UC has been diagnosed, you should get a colonoscopy. You should get a colonoscopy. And then what's the screening interval after that is everyone to two years. But what if your diagnosis with primary sclerosis in colongitis?

Or if you're diagnosed with PSE, which has a strongest role on O3 DF colitis? Remember, you're going to start that colonoscopy at the time of diagnosis. At the time of diagnosis. And in addition to doing that, then what's the screening interval? Every five years afterwards, you deserve screening colonoscopies. Although, don't forget that if you have primary sclerosis in colongitis, in addition to O3 DF colitis, then again, you should get that screening colonoscopy at the time of diagnosis. But if you have PSE and UC together an IBD of any sort with PSE, then the screening interval is actually everyone to two years. So let me just summarize this for you. If you have inflammatory bowel disease and no PSE, eight to 10 years after the diagnosis, get a colonoscopy, screen every one to two years afterwards. If you have any kind of IBD literally, especially also difficult colitis. But when a person has PSE, if they just have only PSE with no IBD, start screening at the time of diagnosis. And then every five years afterwards, colonoscopy. But if they have PSE and IBD and inflammatory bowel disease, start screening at the time of diagnosis, you colonoscopy, and then do it every what, one to two years afterwards. OK, what's another weird, not some bolts things, not some bolts things you're going to keep at the back of your mind, for example? Let's talk prognosis. You're probably going to be here in the vine, say more and more about prognosis going forward.

I'm telling you, it's one of the biggest things that they love to test on the USM Ls these days. And these things, again, they are certain guidelines to prepare for these, and also just certain nuts and bolts you just kind of got to prepare for. You know, stuff like this is something that if you've not learned it, then you probably never know it. So you never get it right, sadly. So again, try to make sure you kind of keep these things at the back of your mind. So what are some things to keep at the back of your mind here, for exams? Well, what if they give you a question involving prognosis that involves a person that has... Australia's colitis, you know, some kind of inflammatory bowel disease, versus a person that just has like... So a person that has IBD, UC, whatever, that develops colorectal cancer, versus a person that just... Has colorectal cancer that develops, you know, just sporadically like a regular colorectal cancer. What are some weird prognosis things they can ask you? Okay, first things first. Um, who is more likely to be diagnosed with colorectal cancer at a younger age? Is it the person that has IBD or the person that has proide colorectal cancer? It's gonna be a person that has IBD. IBD actually has a lot of prognosis associations. Number one, you're more likely to be diagnosed with colorectal cancer at a very, very young age. That's very important to know.

And let me ask you this, between these two people developing colorectal cancer, who is more likely to have the more aggressive disease? It's gonna be the person that has IBD. The person that has IBD, if they have colorectal cancer, they tend to have more aggressive cancers, higher grade cancers, very high you to know that for exams. And which one is more likely to be associated with development of cancer from polyps? It's gonna be the sporadic colorectal cancer. People that have IBD, they vary on your exams, they may not develop colorectal cancer from any kind of polyp. It may just be some kind of flat lesion that gives rise to colorectal cancer in those people. And then, let me ask you this, who is more likely to have lesion spread throughout the colon? Well, I hope you're thinking of a person that has IBD. People that have IBD, they are more likely to have multi-focal lesions. For instance, a person that has sporadic colorectal cancer, that is more likely to have lesions that are localized and not multi-focal. Please, these different things I said about prognosis, they have very, very high you to know for your exams. So I think I'm personally gonna go ahead and stop here. This stuff is pretty high yield. And again, if you're interested in, if you love the way I teach, you're gonna love my classes. They're all over Zoom. And I have a series of classes for Step 1 to Step 3 starting next week.

I have a test taking class on Monday, bio-stats class on Tuesday, social sciences, quality improvement, healthcare systems, ethics class on Wednesday. So all three of those classes are for Step 1 to Step 3. Then on Thursday, I have a last-minute review for Step 2 and Step 3. And then Friday, Saturday, Sunday, and the following Monday, I have a 20-hour step to Step 2 review. Again, if you're interested in any of these classes, just shoot me an email. I have a podcast I made where I talked about. Everything I'm gonna get from these are classes. Again, many people have taken these classes, found it to be extremely helpful. I've had people get, and this is not people that took the class like years ago, no, like old stories, no. Like people that literally took this class like last month. Got your results recently, got in the high 260s, at a 269 recently, I've had 270s. I've had very good results with this class because I try to make sure that I'm keeping in lockstep with the MBA me's every single time because the MBA me's changed. So you can not afford to be static with these classes. So if you're interested, just shoot me an email. You can register, it's over Zoom. And I think you're gonna find it to be very worth it for your exams. Especially with these newer exams that I get in tougher and tougher by today. And then I'll solve for one-on-one tutoring for the USMLA exams, also help with applications and things of that nature.

And I have this podcast on Apple Google and Spotify, of a You Tube channel, divine intervention, USMLA podcasts and videos you can check out. And then also have another website, call divineinterventionlifelessons.com. Many of you listening to this podcast, you know I'm a Christian. So every week, I post about one or two podcasts where from a biblical perspective, I address a life lesson, is literally titled divineinterventionlifelessons.com. There's almost 300 episodes on there. There's actually an Apple podcast, there's a deal with that, call the divine intervention life lessons podcast. Okay, so I'm gonna go ahead and stop here. Again, I hope you found this podcast to be helpful. Again, I'll just encourage you, I'll just encourage you, finish well. You know, today's the 9th of December. There's like 22 days left in this year, if you don't count today, putting your best. You may not have started well, you may have messed up your year so far. But you know what, you have 22 days to kind of start moving in the right direction. You may not make significant changes by the end of the year, but at least start taking steps in the right direction. So I will see you in episode 554. Thank you for listening to me. Have a wonderful first of your day. God bless you and bye for now. Thank you.

Non-alcoholic steatohepatitis (NASH) or Metabolic Associated Liver Disease (MASLD).

Dark urine (due to water-soluble direct bilirubin) and pale stools (due to lack of stercobilin formation).

In adults, acute HBV infection has a very low risk of progression to chronic infection (>95% resolution). In children or neonates, the risk is very high.

Electron microscopy (EM) will show podocyte foot process effacement; Immunofluorescence (IF) will be negative for immune deposits.

If the patient has IBD with PSC, colonoscopy should start at diagnosis and repeat every 1–2 years. If they only have IBD (without PSC), screen every 8–10 years.

Urinalysis, to rule out urinary tract issues before proceeding to invasive procedures like kidney biopsy.

Anti-mitochondrial antibodies (AMA).

Podocyte foot process effacement.

H BeAg (Hepatitis B surface antigen).

Selective proteinuria (loss primarily of albumin) because the negative charge barrier is lost, but other proteins are retained.

A markedly enlarged transverse colon on plain film X-ray.

Start at time of diagnosis and repeat every 1–2 years.

Anti-mitochondrial antibodies (AMA).

Podocyte foot process effacement.

H BeAg (Hepatitis B surface antigen).

Selective proteinuria (loss primarily of albumin) because the negative charge barrier is lost, but other proteins are retained.

A markedly enlarged transverse colon on plain film X-ray.

Start at time of diagnosis and repeat every 1–2 years.