DIP Episode 621 - USMLE Step 2/3 Rapid Review Series 129

Welcome. My name is Divine. This is episode 621 of the Divine Intervention Podcast. Into this podcast we're going to be continuing the Rapid Review series for the US Emily Step 2, CKN Step 3 exams. And this is going to be series 129. Let's jump into it. So, when if they give you a question about a, we're told that we have this two-year-old child and this child for the last week has had very high fevers, very, very high fevers. They tell you that this child has become more and more lethargic and then they tell you that on the child's skin you see a lot of PTKI, proper echimosis and they give you a bunch of labs. You notice that this child's white count is pretty high and with that high white count you see a, you know, a lot of lymphocytes, you see the pleated leg counts is extremely low, right? And then they tell you that you know the child has a pardomagaly, this also has pleated legally and that the child has a diffuser lymphatic anopathy. When you see this, they then ask a, without treatment, you know, without treatment what may happen to this child within the next few weeks. I'm really hoping you're picking the answer that says death. So what does this child have? So this child has ALL, right? This child has ALL. ALL is really bad, right? And it's one of the more common pediatric hematologic hematolognesies, right? And I think there is something I want to emphasize here that can really draw some knowledge out that can really help you on your exams.

The thing is many people do not believe this, but these acute leukemias you can die from them quickly. In my experience, they tend to have good treatment. Like if you treat them, you recover from them. But if you don't treat them from when your symptoms begin to death is usually pretty short, you know, pretty short. Sometimes you can be dead within a couple of weeks, right? So this child has ALL. So how does ALL classically present on the US Emily exams? ALL is going to present on the US Emily exams with the following. Number one is going to be in a little child, right? It's going to be a little child on your test, right? And then number two, they're going to have diffuser lymphatic anopathy. Their spleen's may also be big. Their liver's may be big. And typically they will have a lucosytosis that is predominantly lymphocytosis, right? Predominantly lymphocytosis. And you may notice that there are other cell lines, they are platelets, they are red cells may be reduced. In fact, typically you may notice that they may have an antecedents of low levels of those of the blood elements, right? Like for example, you see me talking about these PTKI and proper any chemoses on this child's skin. Those are signs of thrombocytopenia, right? So ALL has to be treated. If you don't treat it quickly, the child is going to die, right? So these acute leukemias, they tend to have pretty sudden presentations, right?

Like even AML in adults, AML in adults is something that has to be treated and treated fast. If you don't treat it fast, the adult may not survive. That's something that's very important to know for your for your exams, right? Like for example, many of you are probably familiar with acute pro-mylocytic leukemia with those 15, 17 translocations. Typically, you know, they can present with the DIC presentation, right? Because, you know, those blast cells in acute leukemias, they can make tissue factor, right? And that can trigger the coagulation cascade, right? So those things have to be treated quickly. If you don't treat them quickly, the person may not make it, right? If you don't treat them quickly, the person may not make it. And then, ALL, what are some other high-ill things you want to make sure you know about ALL? Well, some other high-ill things you want to make sure you know about ALL is number one. If a child has ALL, don't be afraid to give them chemo therapy, you know, you're going to give them chemo. But don't be afraid as well to potentially give them, what am I trying to get at here? Don't be afraid to give them the treatment quickly. I think that's what I'm trying to emphasize here. Don't be afraid to give them the treatment quickly because the thing is, ALL sometimes they can make it into an ethics question. And with that ethics question, you notice that, oh, the parents want to try something like some kind of alternative medicine therapy.

The thing is, that's not the way to go, right? You have to override those parents because that kid is going to die quick, right? So in those circumstances, you need to override the parents either get the courts to come and decide in your favor, right? But that child needs to get treated, right? Any other alternative medical, whatever that the parents want to try, that's not going to fly on the USMLA exams, right? And then don't forget that ALL, people that have Down Syndrome, people that have Down Syndrome, Down Syndrome actually has a pretty solid association with ALL, right? Don't forget that association between Down Syndrome and ALL, right? Okay, let's go ahead and move on to something else. So what if they give you a question about a patient and they tell you that this patient is a 35 year old African American male and it comes to the physician because, you know, he's, he noticed that a health fear that his blood pressure has been elevated and we're told that at the health fears, blood pressure was found to be like 165 over 105. So that, you know, over the last few days, he has been checking his blood pressure at home with an over the counter purchased blood pressure monitor and you, you know, they give you a list of his blood pressures, right? The USMLA is they kind of get, you know, kind of cheesy and corny like this. They'll give you a list of their home blood pressures, you know, measured over like a week or two weeks or something.

And you notice that all those pressures are high, you know, they're still like in the 160s, systolic, some in the 170s, many in the 100s that are stolic, right? And then they tell you that the blood pressure in that these results are also confirmed in the office and they are asked which of the following is the most appropriate, you know, and they give you some, you know, some other labs, you know, you notice that his creatinine is completely fine, his A1 C is totally good. And then they ask you which of the following is the most appropriate next best step in management? And I really hope that you're picking some answer that released to either a thazide diuretic or calcium channel blocker, a dihydroperidine calcium channel blocker, right? The thing is many people kind of screw this up on the exams. So I want to kind of spend a little bit of time talking about this, right? So if you notice this vignette I gave was an African American, right? Was an African American. The thing is when people are African Americans and they have high blood pressure, you have to start them on a thazide or a dihydroperidine calcium channel blocker as first line. I'm going to say that again, when a person is an African American and they have high blood pressure, if you're starting them on an anti-hypertensive, the first line anti-hypertensive in this population is a dihydroperidine calcium channel blocker like I'm low-deep pain or thazide diuretic, right?

Like hydrochlorothiazide, chlorothali, don't on things like that. ACE inhibitors and arms are not indicated as first line for hypertension in African Americans if they don't have a secondary need for it. I'm going to say that again, ACE inhibitors and arms are not indicated as first line for the management of hypertension in African Americans if they do not have a secondary need for it. So what do I mean by a secondary need? A secondary need is going to be something like diabetes, right? Because remember ACE inhibitors and arms are renauprotective in a person that has diabetes, right? Because remember they dilute your effrayin arterial. When they dilute those effrayin arterials, they're going to reduce the hydrostatic pressures within your glomerular capillaries, right? So that's going to reduce intraglomerular hypertension. That's going to prevent hyper filtration injury because that's going to prevent hyper filtration injury because as we know, when you have diabetes, you have no enzymatic glycosylation of your effrayin arterial. So when that happens, that's going to raise, that's going to basically cause a constriction of your effrayin arterials. And when that happens, when that happens, you're going to raise the blood pressures within your glomerular line. And that's going to raise your GFR transiently, right? Until your kidneys basically die, right? And that rising GFR can cause injury known as hyper filtration injury. That hyper filtration injury, right?

Too much filtration. I can damage the glomerular eye over time, right? You have all those chemo steel whale syn modules and all those problems, right? So ACE inhibitors and arms help with that process by diluting the effrayin arterial. That's going to pull out away from the glomerular capillaries. That's going to reduce the hydrostatic pressure within those glomerular capillaries. And that's going to be very, very helpful, right? So now, so if you have diabetes, right? Or let's say you have heart failure because remember ACE inhibitors, arms, they improve survival in heart failure. Then yes, in those circumstances, you can start an ACE inhibitor and arm for high blood pressure in an African American. But if they don't have those secondary indications, you really should not on your exams. This is one of those things many resources don't cover, but it's actually very, very high you to know for your tests. The thing is, there has been some studies that have shown that ACE inhibitors and arms, they're not as effective in African Americans for high blood pressure compared to other populations, right? So there's something you want to keep at the back of your mind for your exams, right? And then what are some unique quirks you want to know about some of these anti-hypertensives, right? I just kind of want to hit on a few that are commonly tested on the US exams, right? So remember, if a person is pregnant, you want to be aware of the heterogeneous anti-hypertensives.

What are those heterogeneous anti-hypertensives, right? Your ACE inhibitors and your arms, they can cause a lot of renal problems in the fetus. That is not ideal. You don't want that for a fetus, right? So typically on the US semily exams, what are you going to do for those kids? The thing you're going to do for those kids is that you're going to give them, you're going to give them, I mean, for those pregnant women, you're going to give them something like hydrozene, right? Or methyldopa or labidolol on hyphenipine, okay? So those are the drugs you're going to use to control blood pressure in pregnancy, right? There's this nomonic called a hypotensive mom's love, my fetipine. Hypertensive mom's love, my fetipine, right? So hydrozene, methyldopa, labidolol, under my fetipine. You can use any of those. And those drugs also happen to be the drugs you can use to manage hypertensive emergencies in pregnancy, like helps syndrome, right? Or preeclampsia or things of that nature, right? So that's something you want to keep at the back of your mind for your exams. And then if a person has high blood pressure, right? And the person has BPH, right? In that case, you want to give those people an awful one blocker, right? It's going to kill those two birds. It's going to help them with their high blood pressure, but it's also going to help open up the bladder neck and that's going to help them pee better, right? And then what if a person has a histro of a nephrolothiasis?

What kind of anti-hypertensive would you recommend for these people? But I hope you're saying, oh, divine, I'm going to recommend a thazide diuretic. Why? Because thazides, they actually cause you to soak up more calcium from your urine, to reabsorb more calcium from your urine. If that happens, that's going to reduce the amount of calcium that you have in your urine. And that's going to be very, very helpful if you have a histro of nephrolothiasis, right? So they basically, because remember, you know, you probably memorize this demonic that loops loose calcium, but thazides retain calcium, right? So thazides, they cause calcium retention. So because they cause calcium retention, they can cause you to have hypokalcyuria, which is good, which is advantageous if you have a histro of nephrolothiasis. But again, loop diuretics, although we technically don't use loop diuretics for hypertension, but loop diuretics are not a good idea if you have a histro of nephrolothiasis, because loops, because you don't more calcium in your urine. If you don't more calcium in your urine, that's going to cause more problems for you. It's going to cause more problems for you. Very, very high yield to know this stuff for your exams, right? And then remember thazides are also helpful if a person has osteoporosis, right? If you've got hypertension and you have osteoporosis, thazides are really good because again, they raise your blood calcium levels.

So because they raise your blood calcium levels, they are very, very, very good for helping with osteoporosis, right? Because they're kind of like spursing up your blood calcium, they're kind of spursing up your blood calcium. And then another weird thing that is actually pretty high yield to know with thazidei redics is that our friends at the MBM Es can ask you about, so you know, if a person has been on thazide therapy for a few weeks, so which of the following will be expected with your parathyrate hormone response? Well, I'll really hope you're saying that the PTH, the endogenous PTH should fall, okay? The endogenous PTH should fall. Why? Because again, you're literally raising the blood calcium levels. You're literally raising the blood calcium levels, right? You're literally raising the blood calcium levels, right? And then don't forget that your thazidei redics also have a few more problems with them. The thing is thazides are one of these classic, you know, when people say, oh, step two, step three, they're testing a bunch of basic sciences. Thazidei redics are like a very classic for that, right? So remember thazidei redics, they can give you a question about a person that was, you know, has a history of diabetes and the person was placed on a thazidei diuretic for their hypertension. And then the notice that for the next few weeks after the therapy has been started, that their blood glucose is having poly-controlled, right?

You know, or not necessarily poly-controlled, but that their blood glucose is have been more elevated than is normal, since they started their thazidei redic. If you see something like this, our friends at the MBM Es can ask you about the mechanism behind it. I wanted to pick the answer that talks about some kind of drug interaction. Okay, so let's, let's kind of talk about this. Why is it that a thiazide me mess up your blood glucose control if you're diabetic? The thing is thiazides, you know, we know that they work at the distal convoluted tubule, the inhibit that sodium chloride is simpler that causes a utero-absorbed sodium and chlorine at the proximal, I mean, at the distal convoluted tubule, right? But the thing is thiazides, they also have this secondary mechanism of action. They can actually open up potassium channels. When you open up potassium channels, that's actually kind of beneficial because you can get a viso-dilitary effect from thiazide diuretics. But the thing is, can you think of any other part of your body that contains potassium channels? You know, anything kind of linked with insulin? Is there anything in your mind that kind of like insulin? Potassium channels? I would hope you're thinking about those beta cells, right? So those beta cells in the eyelids or longer hunts, right? Remember, for them to secret insulin, you know, the following snapshot process happens. Again, I'm not going to go into the deep mechanism. This is not a step one review.

I'm not going to go into the deep mechanism, but basically potassium channels are going to close. They're going to close under the action of ATP. ATP closes those channels. And then when you close those channels with ATP, the cell potassium is not going to leak out of it anymore. It's going to cause the cell to depolarize. If that cell depolarizes, then voltage-gated calcium channels are going to open. Calcium is going to come in and then insulin is going to be secreted, right? That's how this will insulin secretion process works. So ATP blocks a potassium channel. Potassium cannot leak out of beta cell anymore. Potassium is a positively charged ion. So the cell is going to depolarize. As a depolarize, voltage-gated calcium channels open because the voltage is changing because the cell is depolarizing. And then insulin is exosite toast. End of story, right? End of story. That's how things happen. Insulin and CPAPTIT are exosite toast. So that potassium channel can be opened by thiazides, right? They can literally be opened by thiazides. So if you open up that potassium channel with a thiazide diuretic, the cell is not going to depolarize. Those voltage-gated calcium channels are not going to open. If they don't open, then you're not going to secret insulin. If you don't secret insulin, you're going to have poor blood glucose control. You're going to have an impaired insulin response, right?

So that's why you know, you probably memorize this back in the day that, oh thiazide diuretic calls a hypergluc. Yes, that G, that's the mechanism behind the hyperglycemia. You may get it with a thiazide diuretic because they can raise your blood glucose levels because they suppress insulin production, right? And then remember thiazides, they're also not the greatest if you have a history of a gout. Why? Because they compete for the exact same transporters that you used to excrete uric acid, right? In the kidneys. So if you're taking, if you have a history of hyperglycemia and then you take a thiazide diuretic, you're going to have decreased excretion of uric acid. If you have decreased excretion of uric acid, then you're going to build up your serum uric acid levels and that can put you in trouble with a gout, right? So they can give you a question about a person, right? That, you know, they, you know, our friends at the MBM is, they may even be smart enough to not tell you that the person has a history of gout, right? But they just tell you that the person was started on an anti-hypertensive. And then they tell you that over a few weeks after the anti-hypertensive is began, the patient presents acutely to the emergency room or the physician's office with like very severe, like acute joint pain. Well, that severe acute joint pain is gout, right? And then they can ask you about the mechanism behind the person's gout. It's going to be from hyperglycemia, right?

It's going to be from more specifically, it's going to be from decreased uric acid excretion. Again, the thing is on the USML is these days and this is something I elaborate on in many of my review classes. The USML is these days, they test mechanisms, mechanisms, mechanisms, right? It's one of the more effective ways to combat blind memorization, right? It's honestly, it's actually pretty genius. Just like, hey, why put the actual disease or, you know, straight up answer that people are familiar with when I can just like put a mechanism answer instead, right? So that's something that they do all the time these days on the exam. So again, this one, standing these mechanisms is very helpful, right? So we've kind of hit thousands from the perspective of hyperglycemia. We've talked about how they cause hyper uricemia. Again, they cause you to increase the reabsorption of calcium from your urine, right? So they cause hypercalcemia, which again is beneficial if you have a history of a nephrodisiases. And then you heard me say hypergluc, right? So the L, what does the L stand for? The L stands for hyperlipidemia, right? So phyasides can cause hyperlipidemia. How can they cause hyperlipidemia? Again, it's from that same anti-insulin effect, right? This suppress insulin production. Remember, one of the things that insulin does is that it causes you to put more lipids inside your adipocytes, right?

So if you're not making insulin, you'll not be able to put lipids inside your adipocytes. So your serum lipid levels are going to rise, right? Your serum lipid levels are going to rise, right? Again, that's pretty high yield to know for your exams. All right, so I think I've hit phyasidiretics strongly enough. So let's go on to like, you know, two or three other concepts that I want to review. And then we'll go ahead and wrap this rapid review up. Again, please, all these things I'm talking about, you may think that they will never show up on your exams until they show up on your exams. All right, so now let's talk about what if they give you a question about a person and they tell you that this person is a HIV patient and that, you know, this HIV patient, you know, comes to the physician's office because he has noticed bilateral legs swelling, right? And then they tell you that on physical exam, he has like three plus billion a dim of the bilateral or extremities, right? And then they provide your analysis and then they tell you that, you know, they give you like the urine sample and you notice that this person has like five plus proteinuria. But then they also tell you that this person has, you know, that a lot of shaped lipid structures are found in the person's urine. And then they ask you which of the following is the underlying mechanism behind those are shaped lipid structures or behind the lipid casts that we find in this person's urine?

Okay, so let's kind of unpack this question, right? Let's unpack this question. Let's unpack this question. So this stuff is actually pretty high out to know for your exams. So let's break it down. The first thing I want to say here is this. This is a very great question for the US families and this is something you should really try to make sure you understand the nooks and crannies I'm about to go into. So one of the nooks and crannies and begin, I'm about to go into number one is the following. Number one is the following. Do not ignore integrations on your exams. Do not do not ignore integrations on your exams. Number two, what does this patient have? This patient has nephrodite syndrome, right? What kind of nephrodite syndrome would you say this person has? I would hope you're saying FSGN, right? Focal segmental Gremelonephropathy. Remember, this is the most common cause. This is the most common cause of nephrodite syndrome in people that have HIV. Okay, number three. What is the most likely outcome of this person's nephrodite syndrome? Well, I want you to think chronic renophilia, right? Chronic renophilia. Remember, more than 50% of people that have FSGN, they're going to proceed to having nstidrenal disease, right? It's one of the worst prognostic. Again, prognosis is very, very high yield to know for the US families these days. It's one of the worst prognostic nephrodite syndrome. More than half of the people that have it proceed to nstidrenal disease.

All right, number four. What is the likely subtype of FSGN that will be found in this HIV patient? It's going to be the one called colapsin FSGN. Colapsin FSGN. Okay, colapsin FSGN. Colapsin FSGN is actually one of the worst prognosis FSG Ns and we find it in people that have HIV. Remember, FSGN means Focal segmental Gremelonephropathy. Another name is FSGN, Focal segmental Gremelose sclerosis. All right. Now, so obviously the prognosis is an ephrodite syndrome. But you may notice, like what's the, you see me asking, what's the mechanism behind the lipid casts? What's the mechanism behind the lipid casts? See, let me tell you something. The US families, when they're testing, when they do pull changes, right? Because this is something people are always freaked out about. People are always scared of, ooh, pull change, pull change, ooh, pull change, pull change, right? They're always freaking out. They're always flipping out about pull changes. See, when the US families do pull changes, there are two things they do for a pull change. Number one is that they bring in a few new concepts, right? The thing is, they generally test the same concepts from year to year. That's just a truth, right? So when they do a pull change, it may be 10% of the exam may be new concepts that, while you've never, you know, it's never popped up anywhere before, right?

Just like in over the last year or two, what you're doing, a ton of ethics, a lot of returning service men and women and all that fun stuff. But another mechanism behind a pull change on the US families is the following. Basically, what they do is this. What they do is this, right? They repurpose old concepts, right? They take these old concepts that you know and just test them in new ways. I'm telling you this, if you really set your mind to eight, you can actually like create multiple concepts from the same concept, right? Like for example, I bet many of you have never heard of what I'm about to describe, right? It's like, why is it that they're lipid casts in a person that has an euphrodite syndrome? Well, let me break it down for for you guys, right? So here's the thing that happens. We know that when you lose all this protein in your urine in an euphrodite syndrome, you're going to have a reduction in the oncotic pressure in your bloodstream. When you have that reduction in oncotic pressure, right? That's going to cause you to have a lot of fluidic extravacation, right? You're going to have a lot of a demon. So your body is like, man, I need to figure, I keep losing all this protein. I got to figure out a way to help my oncotic pressure issue. So how does your body fix that problem? One of the ways it fixes that problem is by your liver, generating a ton of lipid, a ton of lipid, right?

Because at least lipids, they can exert some oncotic, some osmotic pressure in your bloodstream. But the thing is because you're now making so many excess lipids, some of those lipids can also begin to leak out into your urine. That's the mechanism behind people having lipid casts in their urine when they have an euphrodite syndrome. In fact, you may notice sometimes on the USML exams, instead of calling it an euphrodite syndrome, they may call it lipoid nephrosis, lipoid nephrosis, lipoid nephrosis. All right. So that's the mechanism behind the lipid cast we find in the urine in people that have an euphrodite syndrome. So let's go ahead and stop here. Again, if you know that you need to get your USML step two and step three scores, you know, in time for ERAS, then you want to take advantage of the classes I have this month. I actually have a class. This is like the last class I'm going to hold that you can take and get in the knowledge before you take your USML exams, your step two, step three exams, right? It's from the 27th to the 31st of this month. It's my 20-hour step two, step three review. If you know that, oh, I'm going to be taking my exams the first week in September, first 10 days in September, so I can get my scores back on time for September 24th. Then this class is what you want to take. Again, there's many people that I've taken this class and they've done really well, right?

They've gone from really poor scores and they've really elevated their scores, right? So I really encourage you, if you know you're taking your exams soon, these are the classes you want to take, right? The 20-hour step two step three review is going to help you tremendously. It's a very up-to-date class, right? And it covers a lot of the very high-yield information that the USML is love, right? And it's me that's going to teach the whole class. So if you love the way I teach, you love the way I break down information, you love the way I make integrations, to really prep you for MBME level exams and complex exams, then this is the class you want to take. If you're interested, shoot me an email. It starts from Wednesday this week to Sunday this week, right? So from the 27th to the 31st, you get that very high-yield review before you're running to your exams, right? Before you're running to your exams. And then I also have other review classes coming up in the month of September. Again, you can kind of check those out, I've made a podcast where I talk about those. I've talked about how those classes different from my, from my podcast because they are different. And then I also offer one or one tutoring for the USML and complex exams and I help with your application, smoke interviews, personal statements and all those things. And then I also have another website called divineinterventionlifelessons.com, divineinterventionlifelessons.com.

Every week I post like one or two podcasts where from a biblical perspective, address a life lesson, you know, many of you know I'm a Christian. So I do talk about these life lessons and many people have listened to them and found them to be helpful. I have like 360 episodes or something like that. There's actually an Apple podcast associated with that called the divineinterventionlifelessons podcast. So thank you for listening to me in this episode. I'll see you God willing in episode 622. So have a wonderful rest of your day. God bless you and bye for now. Thank you.

Pediatric patient with diffuse lymphadenopathy, lymphocytosis (predominantly lymphocytes), and signs of pancytopenia (e.g., petechiae).

Treatment must be initiated quickly; delay leads to rapid death.

Thiazide diuretics or Dihydropyridine Calcium Channel Blockers (CC Bs).

Only if the patient has a secondary indication, such as diabetes or heart failure.

Hydralazine, Methyldopa, Labetalol, Nifedipine. Mnemonic: "Hypertensive Mom's Love, My Fetipine."

Thiazide diuretics (they cause calcium retention/hypercalcemia).

Acute leukemia, especially ALL, is common in children and has a strong association with Down Syndrome.

They are not first-line unless secondary indications (like diabetes or heart failure) exist; they may be less effective than thiazides/CC Bs without these comorbidities.

Thiazides open potassium channels on pancreatic beta cells, preventing depolarization and blocking voltage-gated calcium channels, thereby impairing insulin secretion.

Alpha-blockers (e.g., Tamsulosin).

Focal Segmental Glomerulosclerosis (FSGN); it has a poor prognosis, with over 50% progressing to ESRD.

Loss of protein leads to reduced plasma oncotic pressure $\rightarrow$ systemic hyperlipidemia $\rightarrow$ excess lipids leak into the urinary filtrate.

Acute leukemia, especially ALL, is common in children and has a strong association with Down Syndrome.

They are not first-line unless secondary indications (like diabetes or heart failure) exist; they may be less effective than thiazides/CC Bs without these comorbidities.

Thiazides open potassium channels on pancreatic beta cells, preventing depolarization and blocking voltage-gated calcium channels, thereby impairing insulin secretion.

Alpha-blockers (e.g., Tamsulosin).

Focal Segmental Glomerulosclerosis (FSGN); it has a poor prognosis, with over 50% progressing to ESRD.

Loss of protein leads to reduced plasma oncotic pressure $\rightarrow$ systemic hyperlipidemia $\rightarrow$ excess lipids leak into the urinary filtrate.