DIP Episode 299 - USMLE Step 2CK Rapid Review Series 53

Okay, welcome. My name is Divine. This is episode 299 of the Divine Intervention podcasts. And in this podcast, I'll be continuing the Rapid Review series for the US Emily Step 2 CK exam. This is going to be series 53. So let's just jump right into it. So what if they give you a question about like a 52-year-old male and he tells you that, you know, he has just been feeling, he has not been feeling well for the past like two weeks, right? And they tell you that he is pass medical history is notable for like hypertension and that, you know, he has been having low back pain for the last like month or whatever and he started taking like an approximate every day. And then you notice that he has like some mouth-flank pain and you know they give you a bunch of labs and you notice that you know his potassium is a little high, his creatinine is like 2.3 and his BUN is elevated. What should you be thinking about? Lord, hope you're thinking about some kind of kidney injury, right? From the answer that he's taken, right? So remember, insides are very bad with causing a lot of kidney injuries, right? I mean, what exactly do they do? Because again, friends at the MBM, they've had this renewed focus in recent times on testing issues that relates to step one, right? So bringing step one material all the way down to step two, CK step three. The thing you want to keep think about is that insides, right? Remember, the inhibit cycloxygenase.

So if you inhibit cycloxygenase, the thing that's going to happen is you're going to have less in the world of first agglendants. I remember that first agglendants are very powerful viso-diilators, right? So if the viso-diilator that viso-diilator effect is gone, you're going to have a net viso-construction of the afren material, right? And when you constrict the afren material, you're going to have less profusion of the kidneys. You're going to have less hydrostatic pressures in the glomerular capillaries. And that's going to bring down obviously the hydrostatic pressures go down. Your GFR is going to go down. So your creatinine is going to go up, right? And remember, the reason that your potassium gets high in kidney disease is that people that have kidney disease of some sort, the potassium will not be able to be excreted. Remember, your kidneys are one of the primary excretory organs for potassium, right? So obviously in that case. And also remember, other than the afren at afren at your early effects, NSAI Ds also have like a direct toxic effect on the tubules, on the renal tubules, right? So they can cause problems in those circumstances. Now, what if they give you a question about like, ah, 16-year-old, you know, immigrant from Vietnam, right? And they tell you that this person, you know, has these episodes where he's like very short of breath. And then they give you like some labs and you notice that his hemoglobin is eight, right? 8 grams per deciliter, right?

Obviously that's low. And then they also give you some story in the question about how this person's MCV is like 75, right? And then they ask, oh, what should we throw the EPO levels in this patient? Right? So obviously this person from Vietnam with a low hemoglobin and a low MCV, an MCV that's less than 80, you know, micrositic anemia. Obviously has thalacymia, right? So remember, if a person has thalacymia, right? Again, they usually have that problem because they have issues with the synthesis, at least less you were dealing with like beta thalacymia, for example. They have issues with the synthesis of beta globin, right? So because they have issues with the synthesis of beta globin, right? They're not going to be able to make hemoglobin, right? Because again, that's why the hemoglobin is low. Because remember, hemoglobin literally includes hem and globin, right? So if you have a globin deficiency, then there's nothing for him to marry for you to form him or globin, right? So those people, right? Like their red blood cells will be hemolized very commonly, right? They'll be exploding all the time. And if you keep exploding, those people's red blood cells, right? Like the way the body will try to respond is to say, you know what? Let's try to, let's try to see if we can make newer and newer and newer red blood cells, right? Because those people are going to be chronically hypoxic from having the low hemoglobin.

Remember, hemoglobin that is when hemoglobin is low, that will reduce the oxygen content of your blood, right? And when the oxygen content of your blood goes down, the thing that's going to, because again, remember, that equation for hemoglobin is like your hemoglobin times your SEO2, right? Plus 1.34 males, right? Times your P little AO2, right? So like your amount of hemoglobin your SEO2 and your P little AO2, those things are going to the oxygen content equation for your blood, right? So if the person's oxygen content of blood is low, right? That's going to trigger the release of Epo, right? Epo from the kidneys. And as they release more, Epo from the kidneys, that's what's going to try to drive the bone marrow to produce more red blood cells. Although if you really think about it, right? If you really think about it, a person, whenever a person has an anemia, right? Whenever a person has an anemia, it's actually very high to know that because I think this is one thing that people kind of mess up on the exams and they kind of screw them over. So let me maybe backtrack a little, right? Many people, you know, they try to memorize specific disorders and the effect on the reticuloside count, right? But that's where you need to be careful. You don't even have to really memorize a lot of stuff. The thing is, reticulosides are immature red blood cells, right? So the thing is, you will make immature red blood cells.

If you have the feet stuck, that is necessary for you to make those red blood cells, right? But the thing is, if you... So there are certain anemias where you have enough to make red blood cells. The only reason you're anemic is because you are destroying the red blood cells at an accelerated rate. So for example, if a person has a kind of hemolytic anemia, right? So see, for example, a person has like hair-ditchrysphere cytosis, right? Or a person has an autoimmune hemolytic anemia, right? In those circumstances, you are able to bump off as many red blood cells as you want. The only problem is that those red blood cells are being destroyed at an accelerated rate. And also, I guess, in a person that has paroxysm or noxinal hemoglobinuria, right? Those people all have anemias, but the reason that they have those anemias is because those red blood cells are being destroyed at an accelerated rate. So those people, because their body is like, oh, wow, these red blood cells, they're supposed to survive for 120 days, but because they can leave that long, let's go ahead and make more red blood cells. They have the feet stuck, everything is great. So those people's reticuloside count will be high, right? Because the body is like, let's try to replenish these red blood cells, right? So they are pumping, pumping, pumping, right? So they don't have enough time to do like adequate amounts of quality control. So they produce all these reticulosides, right?

So in those circumstances, whenever you have an anemia from increased destruction, your retic count is going to be high, right? But if you have an anemia because you have decreased production of red blood cells, your reticuloside count is going to be low, right? So for example, in thalacemia, if you really think about it, remember, a person, remember like in red blood cells, we have hemoglobin. We said in thalacemia, right? In all the thalacemias, you have a decrease in globin synthesis. So if you're looking at again, hemoglobin has been made up of hem plus globin. If your globin is down, then your hemoglobin will be down. That's a decreased production anemia. So in thalacemia, the reticuloside count is going to be low. That's a common misnomer amongst many medical students. They're like, oh, in thalacemia, the reticuloside count is high. No, it's not. In thalacemia, the reticuloside count is actually low. That's something that's floridly high yo to know for the purposes of your exam. And then another classic thing, right? That's all the classic things that cause the luridic count, right? Again, think about things like iron deficiency anemia. Again, if you think about it, if you actually want to make a hemoglobin, right? Again, if you boil it down to this equation, you'll be pretty set for the most part. Again, if you're making hemoglobin, hemoglobin is made from what? From hem and globin. I mean, literally the name hemoglobin, right? So hem and globin.

And we know that he is made from iron and prolobe offering, right? So when a person has, when a person has iron deficiency anemia, the thing that happens in people that have an inefficiency anemia is they literally have an iron deficiency, right? So if you have an iron deficiency, you're not going to be able to make him. If you're not able to make him, there is no marriage partner for globin. So you're going to have decreased hemoglobin synthesis. So those people are going to have a low retic count. Think about a person that has lead poisoning. For person has lead poisoning. Remember, those people led inhibits early synthase and ferroquilates, right? And those are key enzymes that are necessary for the synthesis of him. So again, if you cannot make him, that you cannot make himoglobin. So your hemoglobin is low. So in lead poisoning, the retic count will be low. Or think about a person that has any of these hem path-wease synthesis disorders, right? Like, although these are more, you know, like, prefer cutinia tarda or acute intermithent pufferia. Again, membrane acute intermithent pufferia, you have a deficiency of the enzyme that I like to call peanut butter and jelly, the amines, right? Pofoblinogen, the amines, right? For prefer cutinia tarda, you have a deficiency of valve of, what's the name of this thing? Europe, right? Europe, preferienogen, decarboxylase, right? If you have a deficiency of those things, again, you're not going to be able to make him.

If you're not able to make him, you're not going to be able to make himoglobin, right? So that's a reduced production anemia. So the thing that's going to happen in those circumstances is that your retic count is going to be low, right? So again, hopefully this kind of clears things up for people because again, I feel like many people struggle with this retic count, but you don't have to struggle with it. If you just can understand this pathway that, oh, him comes from iron plus poroproferin, and then that him plus globin makes himoglobin. If you have anything that is low along that pathway, that's going to crush your hemoglobin synthesis. Well, if you're not able to make himoglobin, guess what? You're not going to be able to make red blood cells, right? And you're going to be able to make red blood cells. But again, many people, unfortunately, will then say, oh, divine. Okay, okay, okay. I like what you're saying right now. So that means any anemia that is associated with a lower retic count, right? Maybe associated with a low ferritin. Well, guess what folks? That's not true. Again, that's why many times on these exams, right? Again, that's that's one of the unfortunate things that I've had that has happened with this increased emphasis of the current generation on just memorizing things and not necessarily understanding them, right? The thing is they then make like these, oh, you see them, they know all these things, they can tell you every factor known to man.

But then you throw like a generic NVME question in front of them and they're knowledge base completely falls apart, right? The reason that knowledge base is completely falling apart is guess what? You don't have an actual understanding of pathophysiology, right? Because the thing is if a person looks at iron deficiency anemia, iron deficiency anemia, right? The retic count is low. And we know why the retic count is low. Because again, you have low levels of iron. So you're not able to make him because there's nothing to bind to proto-portfering to make him, right? So an iron deficiency anemia, obviously your iron stores will be low. So your ferritin is going to be low. If your ferritin is low, your TIBC is going to be high, right? And again, because you literally have an iron deficiency, your transfer and saturation is going to be low, right? But the thing is if you look at lead poisoning, lead, yes, it inhibits early dehydrates, it inhibits ferroquilates, so you're not able to make proto-portfering. And if because you're not able to make proto-portfering, there is no marriage partner for iron for to form him. So because of that, the retic count is low. But the thing is if you really understand lead poisoning, you see that, oh, it's proto-portfering synthesis that is impaired. There's nothing wrong with iron synthesis. So I mean with iron, right? So guess what? Those people is almost like an iron overload state.

Lead poisoning to be honest with you is almost like an iron overload state. So if you that have lead poisoning, guess what? Their ferritin is actually high. The TIBC is actually low and their transfer and saturation is actually high. Because they have a lot of iron around, but it's kind of like iron showed up for the wedding, but there's no proto-portfering for iron to get married to for it to form him, right? So again, it's very high yield. Again, like that's the thing with these iron laps. Himatology is something that's there for many people. But he is actually a relatively simple subject. If you just understand like what in the world is going on? And to be honest with you, I did not plan to talk about all the stuff with iron and hema or whatever, but I'm just kind of like, yeah, this is probably something interesting to kind of kind of talk about, right? That can, you know, kind of clear things up for for people again, a lot of this stuff is in the understanding, not necessarily in how much you memorize. So again, don't get me wrong for these USML exams. Memorization is key, right? It's very important. But one thing you need to keep at the back of your mind is you also need to to that memorization add on the standing, right? To that memorization, you need to add on the standing. I mean, there's a reason why people use this term knowledge, understanding and wisdom, right? When you memorize the fact you're getting knowledge, right?

But the thing is you got to understand that because remember wisdom is like when you practically apply the knowledge that you have on the stoop, right? So if you memorize the knowledge is there, but if there's no understanding, there's almost like a brick in the pathway to wisdom, because you may not necessarily be able to, again, you can, you can press all those threes in on key or you want. But if you don't have the understanding, again, the enemy does just needs to write a bunch of questions, especially with the newer exams that will just make your knowledge base completely fall apart, right? And you absolutely do not want to be in those kinds of circumstances, right? So since we're kind of talking about thalacymia, let's kind of talk about one thing I want to mention, right? So I don't know, I feel like today I'm just addressing many mismommers that people have from like Met School or whatever or from their studying and then he ends up like hosting them on MDM exams, right? So one thing that kind of came to mind with thalacymians, right? So remember like alpha, that's was beta thalacymians, right? Remember those are examples of hemoglobin opathies, right? So many times people that have, you know, many people take away this blanket statement that, oh, whenever a person has a hemoglobin opathy, usually the smart thing to do for those people in terms of diagnostic testing is to do hemoglobin electrophoresis. That's true for the most part, but guess what?

That is not entirely true. That is absolutely not entirely true, right? For example, if a person has beta thalacymia, well, if you look at the different kinds of hemoglobin, right? Remember, there's hemoglobin, there's hemoglobin A, you know, the regular hemoglobin in humans, that's alpha two, beta two. There's hemoglobin A2, right? Which is alpha two, delta two. There's hemoglobin F, which is alpha two, gamma two, right? So those are like the major hemoglobin that you find in human beings. Well, guess what? All those hemoglobin, there is at least one, actually, there's two that do not contain beta globin chains, right? So like hemoglobin F, which I said is alpha two, gamma two, and hemoglobin A2, which is alpha two, delta two. So guess what? If a person has a beta thalacymia, which is a decrease in beta globin gene synthesis, it would make sense that those other hemoglobin that do not contain beta chains would increase, right? So because it's like, oh, wow, one kind of hemoglobin would decrease, in this case, hemoglobin A, that's alpha two, beta two. But another kind of hemoglobin would increase, in this case, hemoglobin F, that's alpha two, gamma two, and hemoglobin A2, that's alpha two, delta two, right? You can observe those relative differences on hemoglobin electrophoresis. But think about it. If a person has alpha thalacymia, look at all the hemoglobin's logistics, I just literally run them down, right?

Hemoglobin A, alpha two beta two, hemoglobin A2, alpha two, delta two, hemoglobin F, alpha two, gamma two. Guess what? All those hemoglobin's, at least the major hemoglobin's, that we talk about in the human world, right? All contain alpha chains. So if all of them contain alpha chains, all of them will reduce proportionally in a person that has alpha thalacymia. So guess what? Alpha thalacymia cannot be diagnosed with hemoglobin electrophoresis. If a person has hemoglobin electrophoresis, if a person has alpha thalacymia, you examine, you choose hemoglobin electrophoresis as a diagnostic test, you will get the question wrong, right? You will get the question wrong. And again, it's not like some strange random concept I'm explaining. It actually makes a lot of sense if you just really, really understand the path of physiology, right? So hemoglobin electrophoresis is something you use when like there's a differential between the different kinds of hemoglobin that you can observe clinically, right? So again, if there's no differential, as you see in alpha thalacymia, then hemoglobin electrophoresis is absolutely not the right thing to do, right? Now, what are the questions that your friends at the MD Mikudasco and examines? What is the biggest risk factor for diastolic heart failure, right? What is the biggest risk factor for diastolic heart failure, right? Again, let's kind of work our way backwards here.

We know that diastolic heart failure is the heart failure that is classically called heart failure with preserved ejection fraction. And let me say this because again, some people can take that name as gospel and then they begin to run into some, you know, sad unpleasant circumstances on MDM exams. That preserved ejection fraction. Think of it, Mars, an ejection fraction that is 40% or higher. So I'll see this. A person can have an ejection fraction of 45% on an MDM exam and still have heart failure with preserved ejection fraction. Again, I know many people cannot fall for that, but again, you don't need to fall for that. If you're paying attention with all I'm saying in this podcast, right? So remember in the acetylchart failure, right? Those people again, they have a preserved ejection fraction. Again, my definition that I will say you should take away from this podcast for MD Mikudasco is an EF of 40% or higher, right? And again, there will be many other parts of the question that will lead you towards that, right? So the acetylchart failure, heart failure, preserved ejection fraction, that's something that usually happens to people that have a long term history of an increased pressure overload on the left ventricle, right? So again, if you put a lot of pressure on, if the left ventricle has to contract against a lot of resistance, you'll say you know what? For me to be able to generate adequate amounts of contractility, let me go ahead and get bigger and beefier, right?

So you get bigger and beefier by adding saccombs in parallel. When you add saccombs in parallel, guess what? Yes, you'll be able to give like a very good squeeze for the blood in the left ventricle, right? But if you really think about it, as you get bigger and beefier, there's so much muscle in the way that the cavity size of the left ventricle goes down. So you're not able to feel with adequate amounts of blood. If you're not able to feel with adequate amounts of blood, the sad thing that's going to happen is that yes, you can contract well, but if you're contracting like 50% of like 100 meals instead of like 50% of like 500 meals as you did before, then obviously your stroke volume is going to go down. So your cardiac output is going to go down and the person is going to become symptomatic, right? So the big question then you can ask yourself what's the biggest risk factor for like chronic pressure overload on the left ventricle? It's going to be hypertension, right? So it actually makes sense that the biggest risk factor for the stolic heart failure, right? Or heart failure would preserve the ejection fraction is a history of chronic hypertension. So I want to try to keep this around 20 minutes. I'm going to go ahead and stop here. Again, as I do at the end of every podcast, I'd offer one or one two years from any exams. Step one, step two, CK, step three, pre clinical medical exams, 30th of the show of exams.

And again, if you also need a tutoring, if you're a medicine resident, I need tutoring for internal medicine, training exam, or you're internal medicine boards. I do offer tutoring for that as well. And then again, I have a step two CK class, step two CK slash step three class coming up from the 28th to the 20th of April to the 1st of May. Again, we're going to cover a ton of stuff that's extremely high yield for the exam that covers things that also include the new changes that started last year. And again, we're also going to cover a lot of bio stats, a lot of ethics, right? Again, it's very comprehensive. It's 20 hours, five hours each day. And then on the 27th of April, I have like an MBME test taking strategies class. Again, tons of people have taken that class out. They've found it to be extremely helpful. And then please subscribe to the website, divining intervention podcast.com. If I make a new podcast, you'll get an email notification. And then I have these podcasts on Apple podcasts on Google podcasts and on Spotify. So again, if you subscribe to those again, you can get those updates. And then also my videos are on my You Tube channel, Divine Intervention, USMLE podcast and videos, right? So if you want to sign off for any of these classes, just go ahead and shoot me an email through the website. And I'll be more than happy to give you some more information on on cost and times and all those things. And I'll be happy to point you in the right direction.

So thank you for listening to this podcast. I'll see you next time. God bless you and stay strong.

Inhibition of cyclooxygenase leads to decreased production of vasodilators (prostaglandins), causing afferent arteriolar vasoconstriction and reduced renal perfusion/GFR.

High reticulocyte count, because the body is actively trying to compensate for accelerated red blood cell destruction.

Lead poisoning results in a functional iron overload state (high ferritin, low TIBC, high transferrin saturation) because heme synthesis is impaired, not iron absorption.

Chronic hypertension, which causes chronic pressure overload on the left ventricle.

Because all major human hemoglobins contain alpha chains; therefore, any proportional reduction in alpha synthesis will affect all measured bands equally.

Decreased red blood cell production (hypoproliferative anemia), such as seen in thalassemia or iron deficiency.

Inhibition of COX $\rightarrow$ decreased vasodilators $\rightarrow$ afferent arteriolar vasoconstriction $\rightarrow$ reduced GFR.

Low (Hypoproliferative anemia).

Low ferritin, High TIBC, Low transferrin saturation.

High ferritin, Low TIBC, High transferrin saturation (Functional iron overload).

Chronic hypertension/Left ventricular pressure overload.

Because all major human hemoglobins contain alpha chains, and any proportional reduction in alpha synthesis affects all measured bands equally.

Inhibition of COX $\rightarrow$ decreased vasodilators $\rightarrow$ afferent arteriolar vasoconstriction $\rightarrow$ reduced GFR.

Low (Hypoproliferative anemia).

Low ferritin, High TIBC, Low transferrin saturation.

High ferritin, Low TIBC, High transferrin saturation (Functional iron overload).

Chronic hypertension/Left ventricular pressure overload.

Because all major human hemoglobins contain alpha chains, and any proportional reduction in alpha synthesis affects all measured bands equally.