DIP Episode 274 - USMLE Step 2CK Rapid Review Series 45

Okay, welcome. On Inns Divine, this is episode 274 of the Divine Intervention podcast. And in this podcast, I'll be continuing our Rapid Review series for the USMELIS Dev 2 CK exam. In this series, I'll be going over a bunch of high-yield vignettes that relate to commonly tested things on the USMELIS. I'll also spend some time describing the mechanisms behind that alertnesses, because that's something that has started popping up quite a bit on exams. And it's just something that is really not described in many resources. And this should be a Rapid Review series number 45. So let's get going. So what if they give you a question about a 25-year-old male? And they tell you that he's an immigrant that he recently immigrated to the United States about a year ago. And that, you know, over the last nine or so months, he's been having like cyclical abdominal pain. And then they tell you something about him having like just constant fatigue. And then they tell you that over a fecal-alcohol blood test is positive. What should you be thinking about? Well, I would really hope that you're thinking that that person potentially has like some warm infection. So typically, what they were doing on your test is they will give you that the person has a very high eosinophilic count. So you see a lot of eosinophilia that tells you to do a warm infection. And then they may even give you like a CBC. And you'll notice that, wow, this person's hemoglobin is like nine.

And the MCB is like somewhere in the 60s, right, or 70s. Telling you that, oh, this is a micrositic anemia of some sort. I would hope in those circumstances that you're thinking about iron deficiency anemia. So this person, so if you see a person with iron deficiency anemia, that has eosinophilia. Then you want to be thinking about some kind of GI bleed from a warm infection. So what are those ones? You know, for the most part, it's going to be a hookworm infection. So it can be something like necator or anselostoma. So those things, they basically suck blood literally from you. So you're chronically losing blood, right? It's almost like menstruating through the GI tract. If that happens, right, you're going to become iron deficient. And remember, when a person has iron deficiency anemia, the first thing you're going to notice is the iron stores will be depleted. Right? So the afferating will be low. And then in addition to the afferating being low, if the body is like, wow, I don't have iron stores where your body is going to send out all its little food soldiers to try to crawl iron from anywhere possible. So your TIBC is going to go up, right? And then your transferring is not going to be very saturated because you literally have no iron. So your transferring saturation is going to be diminished.

So if you see a person that has a micrositic anemia in the presence of a parasitic infection, then you want to think about a hookworm infection of some sort with, again, Nikita or Anselostema. But if they give you a question about a person that has an anemia and it's macrositic and they have a parasitic infection, then I want you to think about Diffy Lobotrium Lada. Remember, that's that bug that loves to consume B12. It's one of those bugs that can cause a B12 deficiency. And B12 deficiency obviously does not cause a micrositic anemia. On NBM exams, it causes a micrositic, if it want to be more specific, it's going to be a mechanoblastic anemia. And remember, when people have a B12 deficiency, their homocysteine levels is going to be very high, right? But then in addition to that, they're going to have an increase in their methamalonic acid levels. They're going to have a methamalonic acidemia as a result of that. And many of these warm infections, especially the hookworm infections, you can treat them with a bandazole. So like, arbondazole, mebondazole, firebondazole, things like that. Now, what did they give you a question about a patient? And they tell you that this is a 26 year old male, has a history of FSGS, and that he had a renal transplant, like three weeks ago. And then they notice that since he got the renal transplant, he's creatinine for over the past week or something. Let's see, he's been going for regular checkups.

His creatinine has jumped from like 1.5 to 3.7. And they tell you that he has been having like skin hyperpigmentation and all those things. What should you be thinking about? And they tell you that he's on a bunch of immunosuppressants. So they give like a ton of immunosuppressants, and then you have to figure out which one is causing the problem. Well, what should you be thinking about? I'll really hope you're thinking about cyclosporin. And then, the number of cyclosporin is kind of a weird thing. It loves to cause kidney problems, right? So that's why whenever this is actually a higher concept to know. Whenever a person is having a transplant problem, especially if it's a kidney transplant, they love to do this because they know people find it hard to tease apart. Whenever you see a person that has like a transplant problem, and the transplanted organ doesn't seem to be working well, you need to biopsy that transplant. Because without biopsy in that transplant, you can't see for sure what's going on. You can't see for sure if it's the immunosuppressant that's causing problems or if it's the transplanted organ that actually has problems. So you always always need to take some kind of biopsy. So in this case, especially for the person where they got a renal transplant three weeks ago, so you're wondering, is this a acute rejection or is this cyclosporin toxicity? So you need, you need biopsy results to be able to make those claims, right?

Because cyclosporin tends to cause problems with the afrin material. It causes a constriction of the afrin material. And remember, cyclosporin toxicity is not just new kin, the kidneys can also do all that stuff, right? Like it can cause gingivol hyperplasia. So the person's gingivol gets really big. So if you see a person where it's like, man, this person's gingivol is like way bigger than the person's teeth. Then you want to think about, you want to think about cyclosporin toxicity. And then you can also cause skin hyperpigmentation and like her sutism. So those are all things you should come to associate with cyclosporin on an MDM exam. In terms of some of these other immunosuppressants and their classic side effects, right? So don't forget like myromanab. Myromanab sometimes you may see it on exams referred to as OET3. Remember, it's basically something that attacks the CD3 receptor that we find on T cells. The thing about myromanab is the first time you get it, that first attack of the CD3 receptor may actually cause like a cytokine store. So it's almost like a first dose effect. Whenever a drug has a first dose effect, your friends at the MDM love to test those. So you can get a first dose effect with myromanab. Because again, ultimately it will knock down your T cell population, it will take CD3 out of circulation. But that first attack may not be as pleasant. Your T cells may think it's some kind of stimulation.

And then you release a lot of cytokines that can cause a really bad like febral like reaction, like septic like reaction. But after a while it kind of goes away. So usually when you start people on myromanab, it's probably not the worst idea in the world to maybe keep them in the hospital for like a day or two. Watch them, make sure they're doing well before you send them home. And then don't forget cyclophosphamide, right? It's also used as an immunosuppresent cyclophosphamide loves to torch people's blood. Big, big, big thing what cyclophosphamide is the bladder, right? It likes to cause hemorrhagic cystitis. So you can be a person in immunosuppressive therapy having a lot of blood clots like fresh blood in your urine. You only think about hemorrhagic cystitis. You'll have like lower abdominal pain because obviously that's where your bladder is. And remember you can prevent that by giving mesna. Mesna binds up the acroline, which is a metabolite of cyclophosphamide that causes all those problems. But nothing that they love to test on NV Me exams because they know most people have memorized this mesna mesna business. One thing should maybe keep at the back of your mind is this whole concept valve. Hydration. So people that take cyclophosphamide, they actually get a lot of, especially when you're studying like a fruit like newly, they tend to get a ton of ivy fluid hydration. They tend to get a little bladder irrigation.

So you're literally like squirting water into these people's blooders so that the acroline does not attach to the blood epithelium for too long. And then don't forget that cyclophosphamide is also a risk factor for bladder cancer. It's also a risk factor for bladder cancer. And then don't forget is a thioprin. That's another classically used immunosuppresent. The big thing what is a thioprin is, if you have gout, you better know what you're doing. At least usually when people have gout and they're taking a lupurinol of a buxostat, those xanthin oxidis inhibitors, typically what is done is you're going to give a much lower dose of six-megaphthupurin or it's derivative is a thioprin. Because remember those drugs, those immunosuppressants, are broken down by xanthin oxidis. So if you're thinking of xanthin oxidis inhibitor, those drugs can increase in amount, they can increase in quantity, they can hang around for longer, and can begin to see a lot of toxicity. So that's something you want to keep at the back of your mind on exams. And then what if they give you a question about a patient and they tell you that this patient was recently started on chemotherapy for some hematologic malignancy. And then the patient has been having a lot of epistaxis, a lot of bleeding gums, and they then show you some lups. And notice that the patient's bleeding time is increased and the PT and PTT are both increased.

And the patient has like some weird liver labovnamalitis, like the ASTLT is a little elevated. If you see this, I hope you're thinking about acute bromylocytic leukemia. Remember I could bromylocytic leukemia, that's the one that's associated with the 15-17 translocation, where you have those our, those our roads can trigger the IC. So if you see the IC in the setting of treatment for some kind of hematologic malignancy, I want you to absolutely, absolutely think about acute bromylocytic leukemia. Now how do we treat acute bromylocytic leukemia? Well, we use all trans-retinoic acid, right? But again, your friends at the end of the year are smart. They probably won't put atra. Again, atra is blasted over every on-key deck known to them. So they may put retinoic acid derivative, they may put vitamin E derivative as an answer choice. So if I keep bromylocytic leukemia, you give those people all trans-retinoic acid. Well, why does that help? The thing is, because acute bromylocytic leukemia is an acute leukemia, it's a blast cell problem. So because it's a blast cell problem, if you can give those blast cells something that will cause them a work on the genetic level, right? Remember, all trans-retinoic acid, it's binds to an intracellular receptor that goes on binds to, you know, it dimerizes and then you bind to response element on DNA.

All those things when it smashes those, when it smashes that receptor that response element on DNA, it will then cause those blast cells to differentiate towards a terminal cell. Because blast cells, they have the ability to divide. That's why acute leukemias are bad, right? But it basically takes you from like some cell that, oh, can divide, divide, divide to some cell that cannot divide. Well, if you differentiate a cell to a cell that cannot divide, or guess what? That cancer is pretty much cured, right? Because those terminal cells, decently forever, they will die after a while, and then the cancer, the cancer goes away. The cancer goes away. Now, next thing I want to talk about here, what if they give you a question about a patient and they tell you that this patient has a history of scleroderma, like chris-chloroderma, so they give you all the findings, you know, the caustonosis, they tell you when the pressing goes out in the cold, the fingers on blue, they become cyanotic. And then they tell you that over the last six months, this patient has been having profound shortness or breath, having a lot of exercise intolerance. And then they tell you that they give you like this stack of numbers, especially for the right side of the heart and the left side of the heart. I notice that man, this person's rifle and trickler pressures are really, really high. What should you be thinking about in those circumstances?

I would really hope that you're thinking about the person having a pulmonary arterial hypertension. Remember, people that have chris-chloroderma, they can get pulmonary hypertension. In fact, that's one of the most common causes of death in insulin-chloroderma. So those people, they can get pulmonary arterial hypertension, but you want to be careful about the differences between the pulmonary arterial hypertension and people who have chris-chloroderma versus people that have the diffuse, cutaneous systemic sclerosis. So people that have chris-chloroderma, the pulmonary hypertension is a pulmonary arterial hypertension. The alongs are for the most part fine, where the pulmonary arteries are not. So that fibrosis and all that badness, collagen deposition happens in the pulmonary arteries. So because they have a pulmonary arterial hypertension, then they go into right-sided heart failure and then they get into trouble. People that have the diffuse sclerosis, the thing that happens with them is they have intestinal lung disease. They have intestinal lung disease and then that intestinal lung disease would then ultimately give rise to a pulmonary hypertension. So the essentially going into right heart failure because they are actual lung pyroenchamysol messed up. So they put corpomonalis as an answer.

Basically whenever you see a person having pulmonary hypertension or right-sided heart failure because of a long process, then the right answer should be picking as the cause of their problem or their shortness or breath or whatever is going to be corpomonalis. Corpomonalis happens, that's the mechanism behind the right-sided heart failure, for example in a person that has COPD. Although don't forget that primary pulmonary hypertension. It's something that happens when you have, it will be like in a young female, and should be having shortness or breath, and should have very innovative, you tell you about like, oh, this float, some kind of swan-gans catheter, and her right-sided heart pressure is really high, her pulmonary arterial pressure is really high. If you see that, you definitely want to think about primary pulmonary hypertension from that BNPR-2 mutation, right? I think it's like the bone morphogenic protein receptor-2 mutation. And remember, for those people that have this primary, a terropromary hypertension, you can try to give them pulmonary viso-diilators, right? So you want to give them something like a phosphodiester is 5 in a better, so something like cell-denafil, vardenafil, or you can give them like a prostaglandin analog, right? So something like ipoprostinol or like iloprost, or you can also give them an endothelian receptor antagonist, so something like amber-centan or bocentan, those things can help in those circumstances.

Now, let me take a small segue and describe the, and I'll be done with this podcast, so since it's a rapid review podcast. So I'm going to go ahead and describe some of these mechanisms behind that electasis, because one thing the MBM is doing these days is, they will give you a question about a person that has that electasis, and then they will give you like many different answers, where they're like, man, these are, they ask like, which is the most likely mechanism behind this patient's presentation, right? And then they'll put many different things, right? So let's go through some of these mechanisms, because literally the put answer choices where it's literally the mechanism that they are described, they are putting as an answer, and they'll be like, what are we doing these are circumstances, right? So what do you do with these? The first thing you want to recognize is, you want to recognize that the different kinds of electasis, right? So like the first one, you put an answer that says, resultative adelectasis, and other name for resultative adelectasis is actually obstructive adelectasis. So what's the mechanism? Why does the lung collapse in the circumstance? The reason the lung collapses is, first and first, you're going to completely occlude an earway. So say for example, a person, let's say like in a kid, it can be like a foreign body ingestion problem, right?

Or it can be a person that has a really bad mucus plug, let's say because they have asthma or because they've been on an ventilator. So the thing is whenever you completely obstruct an earway, then basically the portion of lung that is supplied by that earway does not get any oxygen, right? Now, whatever air is in that part of lung before the obstruction, well remember, the ordinary capillaries going all around the lungs. So the blood that's flowing through those pulmonary capillaries, it's going to pick up a lot of that air, it's going to pick up a lot of that oxygen. So as you're picking up that air, picking up that air, picking up that air and there's no air coming into replenishing it. And obviously that part of lung is going to collapse. That is resortive adelectasis, right? That is resortive adelectasis. And classically, on any of these exams, if you see like, you know, a patient coming out, patient basis, let's say like an older male or older female smoker. And they have, you notice that man, on this person, you get a chest x-ray notice that one complete lung has collapsed or one complete lung lobe has collapsed. Oh, that's not good. You need to send them for a CT scan because they likely have some kind of lung cancer that's obstructing like a bronchus or something like that. That's actually a pretty classic, not just on inbimis, but also in real life.

If I'm taking care of a patient and a patient has like big time adelectasis of one lung lobe and you're like an older person. I'm not going to think twice about getting a chest CT because they likely have lung cancer. Now, another classic mechanism behind the electasis that shows up on exams is this whole concept of relaxation adelectasis. Sometimes it's called passive adelectasis. This is something that you'd classically see whenever there's something between like your visceral plurra and your parietal plurra. Remember, the visceral plurra is the part that is juxtaposed to the lung itself and then the parietal plurra is the one that juxtaposed to the chest wall. The thing is, if there is something that comes between those two bodies, let's say fluid, let's say a person has a really bad parietal fusion or air. A person has a really bad hemothorax. That thing can basically rip apart the visceral plurra and then the visceral plurra will just basically keep pressing and pressing on the lung parankama and the person will have adelectasis, the lung buculaps in those circumstances. Another classic one you may also see is something called compressive adelectasis. Usually this happens when you have some kind of lesion. Let's say a person has an adenocarcinoma, like a big mass or a large cell carcinoma of the lungs, that's kind of green in the periphery. The thing that can do is it's literally a mass. That mass is growing.

If someone is growing, that means someone else is going to be shrinking. The thing that's going to be shrinking is the structure that has less density. In this case, there's going to be a lung with the air in it. That mass can literally physically compress on the lung parankama and then the person ultimately gets in trouble. Those are the three big ones that you want to keep at the back of your mind on exams. They love love love to test these things. It's just one of these things again. You won't see this costs in many places, but it's something that you want to make sure you know and you understand. I'm trying to think, do I want to cover a new topic now? Let's cover one more topic. I just want to try to keep this on the 20 minutes since it's a rapid review. Let's talk about one more mechanism actually. A classic thing you hear, you read about a menu of being in text or you see a menu of being in exams or you see menu of being in resources, is how having some kind of infection during pregnancy. It's like pilot arthritis or is symptomatic bacteria area or bacteria, vaginosis or whatever. They'll tell you that man, this thing increases the patient's risk for XYZ and usually it increases the patient's risk for pretermly-brand delivery. So it's not some of you may be wondering, why is that the case? Why will the risk of pretermly-brand delivery be increased when a patient has an infection? Think about it.

When you have an infection in pregnancy, that brings an inflammatory state to the body. When you have inflammation, the things that will be produced will be things like luchotrines and things like prostaglandins. If you remember, prostaglandins, they are very powerful contractors of the uterus. They can induce the maymetrum to begin to contract. So when you have those inflammatory states, those prostaglandins that are released can cause the uterus to begin to contract and can take the woman into pretermly-brand. So that's really the mechanism behind all those states. And then another thing, that's why you want to be quite aggressive with the treatment of infections the woman has during pregnancy. Another mechanistic thing that helps with understanding is, some people may say, why do people, why do fetuses have variable decals when the umbilical cord is compressed? I believe I've been describing in another podcast, but if I've not, I'll go ahead and describe it right now. So the thing that happens is when you compress the umbilical cord, you are literally squishing on the umbilical blood vessels. And when you squish on the umbilical blood vessels, what do you think that's going to do to the child's blood pressure? That's going to raise the child's blood pressure. And remember, fetuses have bar receptor as well. So the bar receptors are on their carotids and things like that will sense, oh blood pressure is really, really high.

And since the blood pressure is really, really high from that compression because again, fetuses, those umbilical blood vessels are probably the biggest blood vessels that exist in said fetus. So you squish on those, you raise the blood pressure, bar receptors that freaking out. So the body responds by sending out the parasympathetic discharge. And that parasympathetic discharge can slow conduction down the EV node. If you slow conduction down the EV node, that's going to cause a pretty cardio. That's what manifests as a deceleration on the fetal heart rate monitor. So those are things that I think are important mechanisms to understand, especially in the context of some NV Me questions I've seen a relatively recently. So thank you for listening. Please subscribe to the podcast. I have this an Apple podcast on Google podcasts of Spotify and then also have a You Tube channel, the one intervention USM. Any podcast and videos. And then um, if you want to get like an alert when I make a new podcast or upload a new podcast, just feel free to go ahead and subscribe to the website. The vinyne intervention podcast.com. So I will see you in the next podcast. Have a wonderful rest of your day and wish you all the best of your era cycle. God bless you. Thank you.

Microcytic anemia, low ferritin/iron stores, high TIBC, and diminished transferrin saturation.

Elevated homocysteine levels AND elevated methylmalonic acid (MMA).

Hemorrhagic cystitis. Prevention involves administering Mesna or aggressive hydration/bladder irrigation.

Mycophenolate Mofetil (MMF).

1. Obstructive/Restrictive (Airway occlusion); 2. Relaxation/Passive (Fluid between visceral/parietal pleura); 3. Compressive (External mass).

Compression increases fetal blood pressure $\rightarrow$ Baroreceptors trigger parasympathetic discharge $\rightarrow$ Slow conduction through the AV node, causing bradycardia/deceleration.

t(15;17) translocation. Treated with All-trans retinoic acid (ATRA).

Xanthine Oxidase Inhibitors (e.g., Allopurinol, Febuxostat), as they can increase the concentration and toxicity of the immunosuppressant.

CREST causes PAH due to vascular fibrosis within the pulmonary arteries; Diffuse Sclerosis causes PH due to Interstitial Lung Disease (ILD).

The inflammatory state releases prostaglandins, which are powerful uterine contractors.

1. Obstructive/Restrictive (Cause: Foreign body or mucus plug); 2. Relaxation/Passive (Cause: Fluid between visceral/parietal pleura, e.g., hemothorax); 3. Compressive (Cause: External mass, e.g., lung adenocarcinoma).

B12 deficiency causes elevated methylmalonic acid (MMA) and homocysteine; Folate deficiency only elevates homocysteine.

t(15;17) translocation. Treated with All-trans retinoic acid (ATRA).

Xanthine Oxidase Inhibitors (e.g., Allopurinol, Febuxostat), as they can increase the concentration and toxicity of the immunosuppressant.

CREST causes PAH due to vascular fibrosis within the pulmonary arteries; Diffuse Sclerosis causes PH due to Interstitial Lung Disease (ILD).

The inflammatory state releases prostaglandins, which are powerful uterine contractors.

1. Obstructive/Restrictive (Cause: Foreign body or mucus plug); 2. Relaxation/Passive (Cause: Fluid between visceral/parietal pleura, e.g., hemothorax); 3. Compressive (Cause: External mass, e.g., lung adenocarcinoma).

B12 deficiency causes elevated methylmalonic acid (MMA) and homocysteine; Folate deficiency only elevates homocysteine.