DIP Episode 290 - USMLE Step 2CK Rapid Review Series 50

Okay, welcome. My name is Divine. This is a piece of 290 of the Divine intervention podcast. In this podcast, I'll be going over the USM List.Juicy Keeer Rapid Review series. This will be series 50. Yeah, this will be series 50 actually. And we'll be going over again a grab bag of things that are again very high yield to know for purposes of the USM List.Juicy Keeer and step 3 exams. In fact, I'll just say this. Whenever you see me make a podcast for the step juicy Keeer exam, assume that it's something you should also study for step 3. I think that's kind of like one of the big things here. Okay, so let's just go ahead and jump right into it. So what if they give you a question about a patient and they tell you that, you know, this patient presented to the emergency room or was brought to the emergency room by their family, right? And the patient, he was noticed that this, you know, this patient is like hypotensive. Has been having a productive cough. And, you know, they are giving this patient fluids, the fluids and antibiotics and the patient is not still not doing well. And they have to initiate a presser, right? To maintain the presence of central venous pressure, which again, as you know, is the rightytropressure or the pulmonary capillary which pressure, which as you know, is the leftytropressure. Well, what are we thinking about here? Or I hope you are saying that, okay, this guy has septic shock, right?

So again, kind of keeping with our theme of risk factors, most common causes, prognostic factors for things. If you ever see a person having septic shock, what is going to be the most likely cause? Well, I hope that you're telling me that, oh, it's, it's a gram positive is gram positive bacteria, right? Gram positive, but having a gram positive bacterial infection is actually the most common cause of septic shock, right? And again, when a person has septic shock, what are some parameters you should expect? Well, we know that in sepsis or in septic shock, people release all these inflammatory mediators, right? These inflammatory mediators, the decreased systemic vascular resistance and the also increased vascular permeability. So when that happens, right? As you lower the SVR, that's going to bring down the person's blood pressure, right? So the SVR will be low. And if the SVR is low, if you really think about it, that means it will be easier for blood to escape from the heart. So the cardiac output goes up, right? The cardiac output goes up. And because the cardiac output is up, then blood is not backing up in the heart. So the pulmonary capillary wedge pressure, which again is a surrogate for left atrial pressure. And the central vnos pressure, CVP, which is a surrogate for right atrial pressure, are both decreased. Now, one thing that people always mention is, but divine, how about early septic shock, how about late septic shock? Yes, don't get me wrong.

Those things are important distinctions, but those are important distinctions when you're caring for patients. That is not something that you routinely go after on NV Me exams, right? So like, these values that I'm giving you apply to early septic shock, and that's what you really should focus on more for purposes of the USML exams, right? So all this early septic shock, because I know some cue banks and stuff they like to go into the fine details. Those fine details in general, I'm not useful at all on step 2, CK or step 3. Now, what if they give you a question about, for the one-year-old guy, and they tell you that, oh, you know, here recently immigrated from some South American or Central American country. And then they tell you that over the last like three, four weeks, he's been having like heart failure symptoms, you know, the orthopnea, paroxysymal, noxional dyspnea, and all those things, you know, fluid in the lungs. Well, if you see that, I really hope you're thinking about Chagas disease, right? Remember, Chagas disease is caused by tripe on a somarchruzii, right? In fact, the most common cause of death in people that have t-chruziia infection is actually myocarditis, right? So they can get a myocarditis, and remember whenever people get a myocarditis, they ultimately end up getting heart failure, right? Because it's like some kind of diluted cardiomyopathy. So those people can go into heart failure, right?

And in fact, if you even think about people that have t-chrux troughs, remember another name for t-chrux troughs is, you see, nophilic granolomatosis with polyangitis. The most common cause of death in those people as well is also myocarditis, that again, ultimately only to heart disease. Again, whenever a person has myocarditis, always think of them having some kind of diluted cardiomyopathy, some kind of systolic heart failure, right? So they will ultimately have a heart failure with reduced ejection fraction, right? And again, remember how those troughs troughs present? Trucks troughs present with, excuse me, they'll have very highucinophils, they'll have a lot of weird peripheral neuropathy. And then they'll also have something that I call a lead diagnosis of asthma, right? Like just a diagnosis of asthma that's really weird, right? Like most people that get asthma, they get it as kids, right? And then, but if you're chilling till your lead thirties, forties to get that first diagnosis of asthma, there's something kind of weird going on there, especially when you see like a lot of peripheral neuropathy and very highucinophilic, sometimes very high IgE. If you see that, you want to think about trough troughs, right? So the most common cause of death in trough troughs is myocarditis, you know, essentially again, pulling those people towards heart disease. And also, again, in people that have t-chruziia infection, excuse me, right?

That myocarditis can give rise to heart failure, right? So that's the most common cause of death in those people. And again, remember, t-chruziia doesn't cause small problems, right? Cause these big, big, big problems. So you can cause a bigger suffergosis. Remember, it's one of those microbial causes of ecalysia, right? In addition to being one of those microbial causes of ecalysia, it's also a cause of a dilithet. So again, big, biggest suffergosis, right? Ecalysia, big heart, right? Dilithet cardiomyopathy from the myocarditis causes. And then it can also cause a big GI tract, right? Especially a big colon, right? Remember, it can cause a toxic... It can cause a hersperum's disease, right? It can cause hersperum's disease, because again, it can consume the myenteric nerve plexi. Now, you'll find in the colon, right? So you can cause hersperum's disease. And remember, hersperum's disease can actually be a presentation of toxic mega-colon on your exams, right? Because if you have e-peristolsis of a part of the GI tract, well, bugs can begin to grow, multiply, or those things in that region of the GI tract. And then the pressing gets in trouble, right? Pressing gets in trouble. And then they can get toxic mega-colon. And remember, how do we diagnose toxic mega-colon? We essentially take an abdominal x-ray, and then they'll tell you in the custem. Usually, they don't always do this, though.

They'll tell you in the custem that, oh, the transverse colon is more than six centimeters in diameter. If the transverse colon is six or more centimeters in diameter, in a person that has, again, the commensurate symptoms. They very likely have toxic mega-colon, right? So toxic mega-colon can be a presentation of hersperum's disease. And remember, hersperum's is something we also find in people that have Down syndrome, right? Toxic mega-colon can also be a presentation in a person that has ulcerative colitis, right? But the thing is, some people may see it divine. How do I differentiate ulcerative colitis itself from toxic mega-colon? The way you make that differentiation is, in toxic mega-colon, you'll be an acute worsening of symptoms, right? You'll be an acute worsening of symptoms. People will not have toxic mega-colon for weeks and be alive. No. You're very likely to be dead, right? So pay attention to the way things move in questions, right? You'll be a person that has diarrhea, diarrhea, diarrhea. It's very likely going to be blood. It's very likely going to be a guy, right? Because it's usually guys that get UC on MB Ms. Not saying women can't, they can, but almost like 98, 99% of UC questions I've seen on MB Ms are in the male demographic. Right? So they'll have diarrhea, diarrhea, diarrhea for a couple weeks. And then you'll notice that, man, over 24 hours, over 48 hours, these people start crashing and burning, CV abdominal pain.

They may have signs that almost look like parotonitis, right? Raybomb, guardians, stuff like that. If you see that, that acute worsening of symptoms. I want you to think about toxic mega-colon. And again, toxic mega-colon is not something that is just found in herchprom disease or found in all three difficulties. You can also find it in C-DeF. Remember, that's one of the most dangerous complications of CV infection, right? Toxic mega-colon, right? Toxic mega-colon. Now, since I guess I cannot talk about Down Syndrome, well, what is one other thing we should maybe keep in mind with regards to Down Syndrome? What's the thing that is the most important predictor? What is the most important predictor of prognosis in a kid with Down Syndrome? Is actually the presence of all these cardiac defects, right? The presence of all these cardiac defects, right? So in kids that have Down Syndrome, if they don't have cardiac defects associated with it, the ultimately thing to do better than kids that have associated cardiac defects, right? And again, remember the most common cardiac defect in a kid that has Down Syndrome is an endocardial cushion defect, right? Sometimes on in-beam exams, just to mess with your head, they'll call it an AV canal defect, an atroving, trickle-a-canal defect, right? And remember, the biggest risk factor for Down Syndrome is actually having, like, increased maternal age, right?

So when women are in their late 30s and they are having kids, then there's a higher than normal chance that those kids will have Down Syndrome, right? Because the thing is, as a woman gets older, you know, she'll be some, unfortunately, in some women, it's not common, right? But it definitely happens. In some women, they begin to have, like, you know, a lot of stuff happen at the genetic level, like maternal non-disjunction. Sometimes, they may have this, uh, rubric, sony, and translocations, right? And then, when the sperm comes, right? So the woman will be, like, essentially, you know, she has her, she forms a zygote and egg that contains, you know, two chromosome 21s. And then when she fuse this with a sperm, that house one chromosome 21, then you get three chromosome 21s, and then unfortunately, it'll be, kind of, gets, gets in trouble, right? On an end-beam exam, though, if they want to get cute, if they give you a question about a, uh, a child having two chromosome 21s, well, then you'll notice that the child has a downspinotype, and they ask you about the mechanism behind the child having Down syndrome. Then you want to think about our, our, our, our Sonya and translocation, right? So it may be like, wow, I'm only seeing two chromosome 21s. But the thing is, what do we then do is, do we show you chromosome 14? How do you notice that, man? This chromosome 14 is longer than a normal control chromosome 14. The thing is chromosome 14 is an acrocentric chromosome, right?

So it's just these, these are chromosomes that, you know, they tend to have, like, one very long arm, very short arm. So they can break. So the thing is, one chromosome 21, we have each that right on that chromosome 14. So you may be looking, we're like, wow, this child has only two chromosome 21s. Why do you have in the Downspinotype? Well, they have two chromosome 21s, and then we have the genes that control many of these, you know, essentially like, like some part of, of acromosome 21 on acromosome 14, right? So that's why you're seeing that, wow, they have a normal number of chromosomes, but they have those things, right? Because at the end of the day, they have like three copies of the relevant genes on chromosome 21, right? So that's why those kids have a Down syndrome, right? So never see that specific situation again. You may be like, divine, this is something I would never see on stuicycist, three, think again, right? Think again. Those are things that your friends at the end of the evening could absolutely throw on an exam, right? So again, the genetic principles you want to remember, as the path of physiology behind Down syndrome is one, think about maternal non-disjunction, that is the most common genetic mechanism on endbimies, or two, another one you want to think about, it's rare, but it happens and it pops up on exams, is a rebertsonian translocation.

And again, I've kind of given you how to me, ward that in a question where the person you're like, dude, I got 46 chromosomes. Or because a person that has Down syndrome, right, tries to be 21, is supposed to have 47. So if you see a person that has tried to be 21, with 47 chromosomes, then you want to think about maternal non-disjunction as the mechanism of disease. But if you see a person that has Down syndrome and they have 46 chromosomes, maybe like you have 46, how are you having a try-son, 21 phenotype? Well, they have two chromosome, 21s, but they have a third chromosome, 21, or at least part of it that has hitched a ride on an acro-saintry chromosome, usually chromosome 14. That's a rebertsonian translocation for you on endbimie exams. Again, I kind of took my time there to explain that, but make sure you understand it. Again, as I think I've said many times, one of the greatest, unfortunate things that is happening in medicine now is many people, they learn information, and they have no understanding of said information. Folks, it's not to your benefit, I'm telling you. Before you start memorizing things, committing things to memory and all that stuff, just try to understand. When you understand things, you'll be able to answer questions more successfully. Even if you've memorized it like because many, you see many people.

There is a reason why you see many people they have, they've done these memorization tools, but it doesn't end up reflecting in higher than normal scores, right? It's because the understanding is not there, especially on the newer exams. Again, forgive me for going on the soapbox for a while, but the thing is, the newer MBME exams are reasoning-based exams. Don't get me wrong, you do still need to memorize what you need to memorize, right? But the thing is people will do like, man, I've done 10,000 flashcards or 50,000 flashcards. I've done 7,000 questions, but at this exam, I felt like I was guessing all through. Let me tell you this. The understanding makes a big difference, because the thing is when you understand something. Even if the present is in a slightly different way from what you're used to, you'll be able to see right through it and pick out the right answer. Because the MBME, yes, don't get me wrong, there's a lot of new things. They've been tested since, you know, November of last year, that's November of 2020. But many of the things they still test are the same things they've always tested. They just find a different way to test it, right? Or find an unusual way to test it, right? So they know that in some deck that exists out there, maternal non-disjunction, Robert Sonia and translocation, are both worse people have remembered, right? So they won't just make it a straightforward question. Maybe back in the day, they'll do that.

But these days, they can just give you like a carry-o-type, literally a picture of a carry-o-type, and then you count. And you notice that this person has Down Syndrome. I'm counting for these extramosomes. What's going on here? And then they'll put all these different answers. And again, because they're smart, they'll put them a turn on non-disjunction as an answer. They'll put Robert Sonia in translocation as an answer, right? And then you know that people, they'll again, they don't have that understanding. But then all that information, they've memorized. It then just ends up not being helpful in the end, right? So I will encourage you, memorization is good. But get the understanding first. After you've understood, then begin to memorize. When you do that, your memorization will be more effective. And you do a lot better on exams. I'm telling you this. There are people that don't remember as much as a person that has memorized, there are these like 50,000 different facts. But you notice that, man, these people, they are working on limited information. But they are still getting in the 260s, the 270s, the 280s. Let me tell you this. The thing that helps those people is, they are very good test-takers. And they also just very good at abstracting the relevant information in a question, right? And they're able to abstract that relevant information because they have the understanding. And I guess these are almost like a life lesson within the podcast.

But I guess since rapid review, let's just get right back to it. All right? So what if the, give you a question about a patient that, you know, again, over like two days, they develop like this sudden swelling of the abdomen, fluid wave, epatomegally, blah, blah, blah, blah. If you see that, what should you be thinking about? Well, I hope you're thinking about vodka or syndrome, right? Now, what is the most common cause of vodka or syndrome? I hope you're telling me police. I think me out there, right? Again, don't forget. Remember, police, I think me out there is one of those my look proliferative disorders. And again, you want to be careful. Many people for some reason on NBM exams. And again, I won't be seeing this if I haven't seen this. Many people for some bizarre reason on NBM exams, they, the confuse, I guess, conflict. My look proliferative disorders with my low dysplastic syndrome. Those are not the same thing at all, right? My look proliferative disorders are your jack-to-muteation disorders, right? Like, police, I think me a Vera essential thrombocyphemia primary my low fibrosis, right? And in P Vera, specifically, right, you know, it's a jack-to-muteation. And these people have a very high hematocrate, very high hemoglobin, right? Yeah, hemoglobin will be like 18, 19, 20 on a test. And sometimes these people usually they'll be men on an exam. They'll have like a rhodi appearance, right? So rhodi, r-u, w-d-y, it kind of sounds like a dog's name.

But they'll have a rhodi appearance, they'll be red. They can have a cajenne preridus, right? So they'll say, oh, whenever they take a hot shower, they begin to eat a ton, right? And these people may even have like spleen omega-lea and all those stents, right? And they may have like these chronic headaches because you know, their blood is like sludge, right? Their blood is sludge, right? Because their blood is so thick with hemoglobin, right? So their blood is sludge and all those things do that thick hemoglobin can begin to cause strokes, right? And again, these people, they can have a hypertrophic cardiomyopathy, right? And you may be like, no, I'm divine. Why would you have a hypertrophic cardiomyopathy? Well, again, let's think about this for a second. If you remember the equation that details the factors that control systemic vascular resistance, one of those things is viscosity, right? So if the viscosity of your blood is high, which it will be, and a person that has polycythemia there, right? If the blood viscosity is high, and the systemic vascular resistance is going to be increased. If that systemic vascular resistance is increased, that means that afterload is increased. And when the afterload is increased, right? The heart is basically working against bigger resistance chronically. It's almost like having like a mini-eiotic stenosis, right? But the heart is working against resistance chronically, right? To pump blood out of the heart, right?

So you'll undergo that concentric hypertrophy, and that can lead to a gastolic dysfunction, right? Contrast this with a person that has just straight-up anemia. And again, I promise I'll get to the myelodisplastic business. But contrast this with a person that has straight-up anemia, right? Again, just kind of making being able to meet these dichotomies. A person with polycythemia there, we said, can develop a hypertrophy cardiomyopathy. Because the blood is viscous, systemic vascular resistance is high, afterload is high. Compared to the person that has really bad chronic anemia, a person has really bad chronic anemia. That means their blood is not very viscous, right? And if the blood is not very viscous, that causes like a functional decrease in systemic vascular resistance, right? So because the SVR is always low, because there's so little blood to pump, the heart is always working at elevated cardiac outputs, over time, that can lead to high output heart failure, right? That can lead to high output heart failure. Because the thing is, you need to present the heart with some resistance so that the heart kind of slows down a bit like, oh, you know, some resistance, some resistance. I mean, not too much resistance with blood that is too viscous, right? You know, that causes hypertrophy cardiomyopathy, right? But not too little resistance to read the heart, the SVR is so low, that the heart is always like, wu, wu, wu, wu, wu, wu, pumping out blood at high rates, right?

And again, also obviously for persons anemic, they're hypoxic, the body's tissues need oxygen, right? So those tissues will be like, heart, we need oxygen, we need oxygen, we need oxygen, we need oxygen. So the heart has to keep pumping, pumping, pumping blood at elevated rates, right? So if it does that, over time, those people will go into high output heart failure. Because again, remember, the heart is a muscle, it can pump that well forever. At some point, it will give up, right? And it will pretty much not work, right? So that's how people get into high output heart failure, right? So I almost think of it as a number line, right? It is a concept that encourages you to be attention here. There is a nice midpoint of systemic vascular resistance where the heart is like, mmm, great, it's not a problem. But then if you go too far in the systemic vascular resistance column, you're like, ooh, go too far in SVR with like very viscous blood, right? P-vera, for example, you can get hypertrophy cardiomyopathy. If you go too little on the SVR, then the heart's cardiac output is going to be very, very, very, very, very, very high all the time, right? So the heart doesn't have time to take a breather. Again, if you have really bad anemia, your blood is less viscous. And again, whenever your oxygen capacity in the blood decreases, cardiac output increases commensurically to try to keep up so that the tissues get an awful oxygen, right?

Back and forth, that's heart-on-the-stits of high output, right? Pressing goes into high output heart failure, right? So again, just going to keep those two things at the back of your mind, right? So P-vera, remember, because these people's hemoglobin hematocryl is really high, they're going to have a decrease, they're going to have a decrease in Epo. They're going to have a decrease in Epo on the test, okay? They're going to have an Epo decrease. And again, we treat these people full of bottom, right? They're going to have a decrease in Epo, right? And again, they're going to have a decrease in Epo. And again, they're going to have a decrease in Epo. And again, they're going to have a decrease in Epo. And again, they're going to have a decrease in Epo. And again, they're going to have a decrease in Epo. And again, they're going to have a decrease in Epo. And again, they're going to have a decrease in Epo. And again, they're going to have a decrease in Epo. And again, they're going to have a decrease in Epo. And again, they're going to have a decrease in Epo. And again, they're going to have a decrease in Epo. And again, they're going to have a decrease in Epo. And you notice that, well, the calcium is really high. And it's in an outpatient setting. What do you want to think about there? But I hope you're thinking about primary hyperparaphrotisism, right? Remember, the most common cause of hypercalcemia in an outpatient setting is primary hyperparaphrotisism, right?

But in an inpatient setting, it's going to be cancer, right? Like, scrimal cell lung cancer. In general, scrimal cell cancer is tend to be the ones that have the strongest association with hypercalcemia. Although, don't forget that multiple myeloma, right? Because remember those plasma cells, they're releasing, they're looking one, which we can also call osteoclast activity in factor. Those tends cause bonds to be resorbed, right? And then the person gets hypercalcemia. So, maybe one thing I think I should mention here is, let me go back to this myelotusplastic syndrome. Then I just remember that I said I'll talk about it, my apologies. So, don't conflict myeloperlyphritidous orders with myelotusplastic syndrome, right? Myeloperlyphritidous orders, that's polysylthemia vera, essential thrombocythemia, primary myelofibrosis, right? And also, CM Ls, technically, myeloperlyphritidous order. But CML is from the 922 translocation BCR able. The other three that I mentioned, though, have those jahto mutations. And remember, in primary myelofibrosis, right? They will usually have that red blood cell morphology where you see like the tear drop-shape red blood cell because the marrow is all fibrosis. Sometimes those are called dachrocytes on exams. Now, a myelotusplastic syndrome is a particular kind of bone marrow failure, right? The big thing you want to know there is if you usually give you some blood smear, and then you'll show you like a neutrophil that's wearing glasses, right?

Like a bilobneutrophil, sometimes it's called a hyposecmented neutrophilon exams, right? Remember, that's what's known as the pseudo-pelgrihuit anomaly, right? The pseudo-pelgrihuit anomaly, the pseudo-pelgrihuit HUET, right? Anomaly. So, you know, that anomalies is, again, you can be finding it in many of the other disorders. But on the main main thing, it seems, if you see it, thinking about myelotusplastic syndrome. And the thing is myelotusplastic syndrome, the bath in about it is it can progress to AML. In fact, that is the most dangerous complication of myelotusplastic syndrome, right? So, I think since this is a rapid review podcast, let me go ahead and pause here. So, again, don't confuse myeloprolypharative disorders to the different with myelotusplastic syndrome, right? And in myelotusplastic syndrome, maybe let me just see this one last thing. You love to make it a megaloblastic anemia-style question. You notice that a person's MCV is really high. But again, remember, when every see a person having a high MCV, you notice they have hyper-segmented neutrophils. They want to think about B12 of fully deficiency. When every see a person that has an elevated MCV, you know, more than 100, but they have high pool-segmented neutrophils, bi-lobe neutrophil. Neutrophil, that's pseudo-pelgricuit anomaly, then think about myelotusplastic syndrome. So, as you wrap up, again, if you're interested in the NBME step-to-seeking, you know, comprehensive course.

Again, the course is also for step three. It's 16.5 hours takes place from the 25th to the 27th of March. If you want to sign up, feel free to shoot me an email through the website. And then also the NBME Testic and Strategies class. It's from... It's on the 24th of March, right? So, it's 4 days total, right? The Testic and Strategies class is on the 24th. And then the comprehensive 16.5 hour classes on the 25th, 26th and 27th. If you're interested in those, just shoot me an email, and I'll be more than happy to through the website. And I can give you more information on the course than how to sign up. And then, you know, if you need one or one tutoring for the USMD exams, step one, step two, seek step three. Again, I've tutor tons of people for those. I've had people that have failed the exam. In fact, I had a pretty large cohort of people this past year, where, or actually, over the last two, three months, where these are people that have largely failed the exam the first time. And then I worked with them for a few weeks, in some cases, about just two weeks. And these people have all passed the exam. If I can remember, for sure, like, there's a bunch of people who have lost three months. They've all passed on their retake. So again, if you failed your exam, reach out to me, and I'll be happy to point you in the right direction. So you can pass on your next, on your next track. And then, I also tutor for pre-clear and comets with exams, 30-ish-off exams.

And I do a lot of application consulting, right? So in terms of preparing your application for a med school, for residency, preparing you for interviews. Again, I've been on a admissions committee for a year, and I've advised tons of people, worked with tons of people that are now residents. And some of these people had very tricky applications, like no research, failed a USMLE or multiple USML Es, have no completed all their rotations, or even have worked with tons of pre-med school graduates. So again, if you're following to any of these buckets, I can add a lot of value to your application, to your personal statements, to your recommendation letters, to your ERAS application, to your interview skills, to making your rank lists and all those things. So again, if that's something you need, feel free to reach out to me. And please don't forget to subscribe to the website, divininterventionpodcast.com, whenever I make a new podcast, I'll give you an alert if you're subscribed. And then, you know, these podcasts are also on Google podcasts, on Apple podcasts, on Spotify. So please subscribe, any bit of support definitely helps. And then, please also subscribe to the You Tube channel, the Vine Intervention USMLE podcast, and videos. And again, for people that are medicine residents, if you're studying for your medicine, training, exam, or your medicine boards, I'd offer one or one children for those as well. So thank you for listening. I'll see you in the next podcast.

God bless you. Have a wonderful day. Thank you.

Low SVR, decreased CVP/PAWP.

Gram-positive bacteria.

Myocarditis, leading to dilated cardiomyopathy and heart failure.

It increases SVR due to high blood viscosity, increasing afterload on the heart.

Primary hyperparathyroidism.

Robertsonian translocation (e.g., involving chromosome 14).

Toxic megacolon presents as an acute worsening of symptoms, whereas UC is typically a chronic condition.

Pseudo-Peligree anomaly (bi-lobed or hyposegmented neutrophils).

B12 deficiency.

Polycythemia Vera (PV), Essential Thrombocythemia (ET), and Primary Myelofibrosis (PMF).

Maternal non-disjunction.

Malignancy (e.g., squamous cell lung cancer) or Multiple Myeloma (via osteoclast activity).

Toxic megacolon presents as an acute worsening of symptoms, whereas UC is typically a chronic condition.

Pseudo-Peligree anomaly (bi-lobed or hyposegmented neutrophils).

B12 deficiency.

Polycythemia Vera (PV), Essential Thrombocythemia (ET), and Primary Myelofibrosis (PMF).

Maternal non-disjunction.

Malignancy (e.g., squamous cell lung cancer) or Multiple Myeloma (via osteoclast activity).