DIP Episode 324 - USMLE Step 2CK Rapid Review Series 60 (+ 2CK/3 Course Reminder)

Okay, welcome. My name is Devine. This is episode 324 of the Divine Intervention Podcasts. And in this podcast, I'll be continuing the Rapid Review series for the US Emily Step 2 CK and Slash Step 3 exam. And this is going to be series 60. And just want to say a few quick things before I get started here. The first one is about organization. Again, I think I've said this quite a number of times, but the best way to organize the website content for yourself is when you go to the website, Devine Intervention Podcasts.com, I would encourage you to go to the top of the page that says exam topics list. Now lead you to a spreadsheet. When you click on that spreadsheet, it's a Google sheets document which only me can edit. I only make myself edit it so people don't mess it up. So if you click on it, it has a column that says step one and then it has a column that says step 2ck slash step three. If you're studying for step one, I literally break down the podcasts by topic. So if you want to study embryology, there's a section for that. If you want to study GI, there's a section for that. If you want to study neuro, there's a section for that. If you want to study cardio, there's a section for that. Basically whenever I make a new podcast, I essentially use that as a kind of a filing system that tells you all, this is exactly where you need to go. Right? And then there's a step 2ck step three column.

There's an internal medicine section, there's a family medicine section, there's a surgery section, there's a pete section, there's a psych section. So just literally study the things that are suggested on their each section and you will get a very good third review for that section, especially for step 2ck step three. So I use that as a filing system like for example, when I'm done making this podcast, which is our rapid review podcast, our gondas step 2ck step three and literally put it under the rapid review section with the podcast episode. So you're not going in blind because one common complaint afraid is, oh, divine, your website is very unorganized. Well, that filing system is in place. I feel like many people have just not really taking time. Like really going like, oh, this website that I use every day, what is on it? How is it organized? That's a great, that's like an easy way because again, you should also realize that I have tons of commitments. Right? So I wish I could build like a ginormous, amazing website, which will probably come in the future, right? But again, this website is being kept free. Right? And again, I have all the commitments. So use that example picks less page, at least in the meantime, I feel like it's a pretty great way. Once you see that, well, I want to listen to a particular episode, just go to like episode 12 or episode 21, pviatrix.

Just do it during the search box, going the search box on the website, type in the episode number and the topic. And I will just pop right up for you. Right? So I think that's a way to go about that. So that's one, too. For those that are in America, I want to wish you a happy Fourth of July, a happy independence day to this country. This country is a great country. And there's definitely been a been a big blessing to me. And then the third thing I want to say is for those of you that are taking step to seek is that three. I know a lot of people are going to be taking step to seek is that three over the next few weeks here. I do have an NV Me testing and strategy scores taking place on the 14th of this month. That's next week from two to four 30 p.m. Pacific standard time. And then I have a very comprehensive step to seek is the three review course, which takes place from the 15th of this month to the 17th of this month. So that's from a Thursday to Saturday. So the testing and strategy scores is on Wednesday. So if that's something you're interested in, just ship me an email through the website. And I'll give you some more information. I've had tons of people take these courses. Even people taking complex level two and three. And they've done extremely well on the exams. I get many, in fact, Wednesdays, probably like my happiest days of the week, although actually, really love Sundays. Actually, I take that back. Sundays are my happiest day of the week.

But Wednesdays are probably a pretty close second there because I get lots of emails from people that have taken the course and then they go higher on their exam than they did on any practice exam. In fact, I've literally had people take the course like a day or two just before their test. And that the course ends up coming through in a big way for them. And again, I'm not just seeing this based on a sample of five, 10 people. No, I've had hundreds of people take this course that have been really successful with it. So again, if you're studying, we know how competitive the the era's process is, your scores are very big component of how well you do with your interviews and with your application season. So if you're interested in this course, you should be an email through the website. And I'll give you some more information. So let's just get ready into it. So what if they give you a question about a patient and they tell you that it's a it's a seven year old male and they tell you that for the past two months, so this is our first vignette. So it's a seven year old male, they tell you for the past two months, he has been having, you know, he has been having really bad headaches when he gets up in the morning and then they tell you that on physical exam, he has extensive e-taxia and they then tell you that they obtain an MRI of the brain and spine and you find a mass in the Serbilla vermus, right?

Like in the middle of the Serbilla or a par, you know, like a par, a vermus mass and then they tell you that they find diffuse lesions all throughout the spinal cord or the spinal canal. If you see that, what should you think about? I really hope you're seeing what the vine, this shot has a medallule blastoma. This shot has a medallule blastoma. Again, that medallule blastoma, the big thing with it is it loves to grow in the Serbilla. It loves to grow in the Serbilla. In fact, I would say on the mbim exams, the test medallule blastomas a lot more than Pynocytic Astrocytomas. Even if Pynocytic Astrocytomas are the most common, you know, brain masses and kids, but they love to test medallule blastomas. Now, one thing that you can test on your exam is what is the mechanism behind that medallule blastoma? Methastasizing to the spinal cord. When I want you to think about drop metastasis, basically that medallule blastoma loves to go through CSF pathways and it goes down those pathways from the ventricles all the way to the central canal of the spinal cord. That's how it spreads because the thing is most brain malignancies do not spread because brain malignancies almost feel like they are like, we're gonna kill you regardless. We don't need to bother spreading. I'm not gonna deal with that extra stress of metastasizing, right?

So the thing is whenever a person has a brain malignancy, most times he does he doesn't spread, but one very notable exception to that role is a medallule blastoma. It has this again concept of drop metastasis. So because of those drop metastasis, he can settle down into the presence, you know, going to the ventricles because again, remember your Serbilla almost has almost like a very direct contact with ventricles. So it goes into the ventricles, spreads through the spinal, the CSF pathways to the central canal of the spinal cord and then causes problems. And then the next thing that wants us to go into is what if they give you a question about a 19 year old male, they tell you has a history of HIV, they tell it that his most recent CD4 count was 25 and that he started on highly active antiretroviral therapy and that in addition is also studied on a appropriate prophylactic therapy. And then you'll notice that he has like a profound bone marrow suppression, like a few weeks after that therapy started. And then they ask, what is your next best step in management? Well, I hope you're saying, oh, divine, I'm gonna go ahead and give this guy a look of worry. Remember, this guy having a CD4 count of 25, I would imagine that he has gotten some of the HIV prophylaxis, I mean, in addition to being studied on highly active antiretroviral therapy, he must also have been started on HIV prophylaxis, right?

So having a CD4 count of 25 should hopefully tell you that, oh, okay, well, if you see for count is 25, you probably need to have been started on trimethylperensofonethoxazone to prophylaxis against Neumocystisioverzine and you also need to have been prophylaxed against Toxoplasmagondii because your CD4 count again is less than a hundred. Also, it's trimethylperensofonethoxazone. And then remember, if you are on highly active antiretroviral therapy, you're no longer, right? So this is very high, you know, you're no longer need prophylaxis against micro-bacterium-ivium complex release, it's through my cell. But in general, if a person has a CD4 count less than 50, which this person does, and they are not on highly active antiretroviral therapy, then you should put those people on easy thromising for mac prophylaxis. But if they're CD4 counts are less than 50, and they are not on highly active antiretroviral therapy, you should not put them on easy thromising for mac prophylaxis. So the thing is trimethylperensofonethoxazone in this patient calls the big time-borne marrow suppression. That big time-borne marrow suppression, you could essentially, it arises because again, TMPSMX, right, is a full-it synthesis inhibitor. Remember trimethylperensofonethoxazone in hybrids that hydropterate synthetase. So if you inhibit those enzymes, you're going to inhibit full-it production.

And that can cause bone marrow suppression because full-it is needed in any rapidly dividing cell line, so that those cells are produced, because you literally need full-it to make DNA. Remember that step where you go from the oxy-oridin monophosphate to the oxy-finidin monophosphate. You literally make finidin because full-it is there. So if you inhibit the synthesis of full-it, that can cause a bone marrow suppression. That bone marrow suppression is something that you can rescue those people from with a drug known as lukovorin. Lukovorin is an analog of folenic acid, not folic acid, folenic acid. That's very important to know, because folenic acid is way more reactive than folic acid. It's essentially like a biologically active form of folic acid, folenic acid, lukovorin. That's how you rescue people from TMPSMX bone marrow suppression. Remember that TMPSMX bone marrow suppression is also something that's here with any sulfonamide. So they can give you a question about a person being treated for toxoplasmosis with pyramid amin and sulfodizing. That's a full-it synthesis inhibitor combination that can also cause bone marrow suppression. So those are things you want to keep in mind on and one of the few other key things I would say to keep in mind on mbim exams with bacteria, or try to prevent sulfonamethoxysol, are things like how TMPSMX inhibits a C2 C9. So because inhibits C2 C9, you're going to have a build-up of warfreak.

Remember C2 C9 is a big, big, big cyclone P450 enzyme that brings down warfreak. So if you're not able to bring down warfreak and warfreak is still metabolically active, you're going to have a super therapeutic ionar. So that's why you really need to be careful about giving bacteria to people that are warfreak. And then, another thing about trimethropromesophyrmethoxysol that they love to test on imbim exams is how it can be problematic in patients that have glucose 6-4-5 dehydrogenase deficiency. Because TMPSMX is a powerful oxidizing compound. I mean, literally look at it's sophyrmethoxysol. Sophyr is in group 6 of the periodic table, is in the same group as oxygen. So it's a powerful oxidizing agent. So if you're present in TMPSMX or some kind of sulfonamide, and then you'll notice that they have like an indirect hyperburebinemia, that I want you to think about those people having a G6 PD deficiency. Because that TMPSMX has caused a lot of oxidative stress, and if you're like G6 PD, EK8 glucose 6-5 dehydrogenase, you're not going to be able to deal with that oxidative stress. If you can deal with that oxidative stress, the unfortunate thing that's going to happen is that your rib blood cells are going to start hemolizing, and they'll release all the ahimoglobin into the bloodstream, right? And obviously that's going to bring down your HAPTO Globin. But in addition to that, you're going to make a lot of indirect bilirubin.

That'll be an example of a COOMPS-negative hemolytic anemia. I'll see that again. G6 PD deficiency is an example of a COOMPS-negative hemolytic anemia. Because that hemolosis is not being mediated by your immune system. It's just your rib blood cells being hemolized because they cannot deal with oxidative stress. And then another thing you could also see with trimethoprimsofamethoxazole. And remember by the way, G6 PD deficiency has excellent recessive inheritance, right? So it will not be in a boy, it will not be in a girl, sorry, on an inbeaming exam, it's going to be in a boy, on an inbeaming exam. Now another key thing you want to keep at the back of your mind with trimethoprimsofamethoxazole is that TMPSMX can cause hyper-kilemia. They love to test that thin on exams. TMPSMX has the ability to cause hyper-kilemia. The reason it can cause hyper-kilemia is that it's a potassium-sparing diuretic in a sense. How exactly is that? Well, if you go back to reno-physiology, at the principal cell of the collecting duct, we have an innexional that brings in sodium. And as that sodium is being brought in, that's going to cause the wrong key channel to extrude potassium into the person's urine. So the thing is, whenever you're absorbing that sodium through the innexional, you're getting rid of potassium. So the thing is, trimethoprimsofamethoxazole is a blocker of that innexional that we find at the level of the principal cell of the collecting duct.

It basically works like amylo-ride or triumtering. If you block that innexional, then you're not going to be able to get rid of potassium through that wrong key channel. So potassium will build up in you when you're going to get hyper-kilemia. It's very, very high-yield on exams to know the mechanism behind the hyper-kilemia in a person that is sticking trimethoprimsofamethoxazole. So that's something you want to keep at the back of your mind again for tests. And then, so they can give you a drug interaction question about a person that develops like a fiddle hyper-kilemia from being started on like an esenhibitor and arb with trimethoprimsofamethoxazole. So again, the uses and the complications, as a sujite, will trimethoprimsofamethoxazole. They are very, very important to know for exams. Now the next thing I want to talk about is, so vignette number three is how do you different sheets between a person like what is that? Let me put it this way. What is the classic signature on an ambimexam for a person that has a defect in the oxidation of fatty acids? Right? A fatty acid oxidation defect. Well, the key thing I would say is look for the presence of ketosis. If a person has ketosis, they don't have a fatty acid oxidation defect. If a person does not have ketosis, they do have a, especially in the presence of hypo glycemia. They do have fatty acid oxidation defect. Well, what could be here for a second? So think about it.

When are you going to be doing beta oxidation of fatty acids? What are you going to be doing that when you're in the fasting state? When you're in a hypo glycemia state where you're long glucose? So the thing is, if you're doing beta oxidation, then you're generating a syrucoye that can be used as feedstock in the production of ketone bodies. So the thing is, if your fatty acid oxidation is not working. So let's say you have a problem with a beta oxidation of some sort, then you're not going to be able to get all the way down to that a syrucoye. And if you can get down to a syrucoye, you're going to run into a lot of problems, right? So those people are going to be hypo ketotic and they're going to have hypo glycemia. Many times hypo glycemia is associated with being hyper-ketotic. So many times when you're hypo glycemic, you begin to build up ketone bodies, and those things are acidic, so they will bring down your bicarb. So the normal response is that you get acedotic when you're hypo glycemic. And also you also get acedotic when you're hypo glycemic for many, many other different reasons. But people that have people that have a fatty acid oxidation defect, they're not able to make those ketone bodies, so they're not able to become acedotic, so they don't really lower their bicarb by much. So whenever you say a person having a hypo ketotic hypo glycemia, I want you to think of those people potentially having some kind of fatty acid oxidation defect.

And then the thought we need I want to talk about is one thing that many people tend to confuse on exams, which is basically being able to differentiate between two sequelae of group a strap infection. One is Cidenham's Korea, and then the other one is something called pandas. Pandas is a disorder that is, you know, the phoning is a pediatric autoimmune neuropsych disorder associated with group a strap infection. So how do you differentiate between those two pathologies? Because the thing is those two pathologies, they both cause choreoform movements, they both cause Korea. So how do you differentiate between those two things on exams? One of the weird differentiate between them is the first key thing I'll say will help you differentiate is many times when people have pandas, you're going to have Korea, but in addition to that Korea, they're going to have a lot of neuropsych problems. That's very important to know. In addition to the Korea, they're going to have lots and lots and lots of neuropsych problems. So you're going to see a lot of psychiatric related issues in that patient. That's why it's called pediatric autoimmune neuropsych disorder, as well as the group a strap infection. Cidenham's Korea for the most part, they will just have those choreoform movements. But many times they're not going to have neuropsych issues. That's one very good differentiating factor. Now a second differentiating factor that is a little weaker is timeline.

Many times when people have seen in ham's career, they usually have it and are right around the same time as when they have that groupie strap infection. Many times when people have pandas, they have it weeks or months or years after the groupie strap infection. So that timing information can help you differentiate between pandas and Cidenham's Korea on an MD exam. Now the next thing I want to talk about is just being able to differentiate between renal and actually maybe let me see something about pandas. So some of you may wonder, okay, divine. What is the pathophysiology behind pandas? Right, what is the pathophysiology behind pandas? Well, the thing is many times when your body makes antibodies against groupie strap. Some of those antigens that are on groupie strap also look like antigens that are expressed by just momo cells in other parts of our bodies. Like in the heart, that's why many times people can develop endocraditis after a groupie strap infection. Or in the brain, especially in the bizoganglia, there are antigens in the bizoganglia that look like similar antigens that we find on groupie strap. So those antibodies that your body makes against groupie strap are going to begin to attack your bizoganglia. And obviously if you attack the person's bizoganglia, that's going to cause a lot of movement problems. That's one of the reasons why it's basically like an autoimmune attack of bizoganglia cells of antigens in the bizoganglia.

That's the pathophysiology behind pandas. For some of you that still remember this from step one. This is one of those things that are known as molecular mimicry. So that's something that's very high to keep in mind on exams. If you notice today, I'm trying to do a lot of this versus that because again, on the new MBME exams, one thing people struggle with is being able to differentiate one pathology from another closely related pathology. So another thing I want to talk about in terms of pathophysies is being able to differentiate. So this will be my next vignette. So they'll give you a question about like some kind of young female that has been having a resistant hypertension. It doesn't seem to be responding to many anti-hypertensives. So they've tried and load the pain. They've tried a thiazide. They've tried a loop. They've tried many different things. Nothing seems to be working. Although by the way, you don't usually use loops to treat hypertension. You usually use loops to treat like a dematostate, like nephrodic syndrome or a person that is currently in some kind of CHF exacerbation. So the thing is when a person, when you see this person, young person, they have resistant hypertension and they have a flung brewery. I really, really want you on MBME exams to really consider thinking about fibromuscular dysplasia. Remember, people that have fibromuscular dysplasia, what part of their bodies are affected? You want to think about the renal arteries being affected.

But the thing is, one thing your friends at the MBME love to do is they love to go granular. And exactly what is affecting what the layer of the arterial wall is being affected. Because remember, arterial walls have many layers. They have the intema, which is the innermost layer, and then they have the media, which is the smooth muscle layer, and then they have the adventitia on the outside. So the thing is, when people have fibromuscular dysplasia, look at the name, fibromuscular dysplasia. It's a problem with the smooth muscle. It's a problem with the media of the arterial wall. That's very high you to know, for exams. On the flip side, if a person has renal arteries stenosis, which is the close cause, now being an older individual, renal arteries stenosis is going to be a problem in the intema. So again, they both have the same presentation, but you need to be able to tell these differences between these two pathologies. renal arteries stenosis is a problem with the intema. Fibromuscular dysplasia is a problem with the media. It's a problem with the smooth muscle layer of the arterial wall. So that's very high you to keep in mind for for exams. And remember, renal arteries stenosis because it's an atherosclerotic disease. Those people actually need high intensity statin therapy, because many of us studying for the US Meli exams, we know that, oh, many of us know the classic MI stroke as the things.

Oh, when we think of atherosclerotic cardiovascular disease, that's what we pretty much think about and say, oh, you know, none of these other, there's not really nothing else that falls on the other's preview. No, that could not be further from the truth. Other things that fall on that, that atherosclerotic cardiovascular disease category, a things like peripheral arterial disease, things like renal arteries stenosis. Those are people that also candidates for daily high intensity statin therapy. And that high intensity statin therapy is basically a tovers statin or a rezover statin. Although again, that level of detail many times, they don't go after that on NV Me exams. And then another thing I think that would be helpful to understand for NV Me exam purposes. So this is me pretty much going to my next vignette. Is they can give you a question about a boy, he's like seven years old, he's from Europe. And then they tell you that he has required blood transfusions twice in his life. And that now he's presenting with red upper corduroyntine. If you see this, I'll really hope you're saying, oh, divine. This person likely has hereditary spherocyteosis. Right, remember, it has that European association. So remember hereditary spherocyteosis. There's one of those topics that you can pretty much almost always guarantee. You're going to see tested in some iteration on your exam. So what are the key things you need to know about hereditary spherocyteosis for the USMEL exams?

First things first, and in a bit, I'm going to talk about why this child has red upper corduroyntine pain. But first things first, I want you to know is the fact that it's inherited in a horizontal dominant fashion. Okay, hereditary spherocyteosis is inherited in a horizontal dominant fashion. So what's the pathofysiology? The pathofysiology, right, is going to be that these people, they have a mutation in some key red blood cell membrane proteins. So things like spectring, things like anchoring, things like band 3.2. Sometimes you may see band 2.1, but basically spectrae and anchoring at the big ones you need to know for exams. If those things are not working, then you're going to have a depleted red blood cell membrane. The reason you have that depleted red blood cell membrane because for the most part, those things actually like silo skeletal proteins. They actually proteins that are important for the cytoskeleton, like the architecture of a red blood cell. So if that's cytoskeleton is not working well, then the membrane will be depleted and then those people will have smaller membranes. That's why many times when you do a blood smear for people that have hereditary spherocyteosis, you're going to notice that you're going to see spherocyte spherocyte are red blood cells that are completely filled in because most times red blood cells they have this region of central power in the middle.

But if you notice that wow, they're giving me a slide on a USMLE exam, which they build by the way. And I'm not seeing any white species within the red blood cell. I'm just seeing just complete coverage with hemoglobin. Then those are spherocyte that they are trying to show you, right? Those are spherocyte that they're trying to show you. And one key lap that you need to keep at the back of your mind for in-beaming exams in hereditary spherocyteosis is the fact that the MCHC is elevated. So these people's MCH Cs tend to be elevated, right? So why is it elevated? Remember, MCHC means main coposcula hemoglobin concentration. So the concentration being high means that oh, because remember concentration is mass over volume. So in people that have hereditary spherocyteosis, there's nothing wrong with the mass of hemoglobin in the red blood cell. But the volume of hemoglobin in the red blood cell, the volume of the red blood cell itself, sorry, is going down because again, they have a membrane defect. So because the volume is going down, the thing that happens is again concentration being mass over volume as the, if the mass at the top is staying constant, but the volume is going down, then that means the concentration is going to go up because concentration on volume of that thing that contains the substance, right? Yeah, inversely related. So because the volume is going down, the concentration is going up. So the MCHC is going to increase as a result, right?

So how do we diagnose hereditary spherocyteosis? Well, you're going to do an osmotic fragility test because again, think about it. Those red blood cells are literally living on the edge, right? So they don't have enough membrane. So if you put that red blood cell in hypotonic solution, that solution is going to be a lot more dilute. So water is going to move into the red blood cell osmoticly and it's going to explode the red blood cell, right? So the red blood cells are much less resistant to hemoluses in a hypotonic solution. That is the basis of the osmotic fragility test. And then on that test, you can also use for hereditary spherocyteosis is the Eocene 5 malemite acid, the Eocene 5 malemite acid. That's another diagnostic test you can use in making that diagnosis of hereditary spherocyteosis. And then how do we treat hereditary spherocyteosis? Well, many times a key high-o thing to know is that those people can get us plenectomy because the thing is those red blood cells, even if they are not ideal, they actually work pretty well for the most part. So what the thing is, macrophages in the spleen, they love your red blood cells to look nice and pretty. So if for some reason your red blood cells don't look nice and pretty, like a spherocyte, then those plenect macrophages are going to destroy them. And when those plenect macrophages destroy those red blood cells, those red blood cells are no longer useful for you, right?

So it's very high-o to know that plenectomy is the treatment of choice for hereditary spherocyteosis on MBM exams, right? And the thing is, doing that plenectomy actually lowers the arrest of developing calling the thiocese. That's why the patient actually had red opal cordrum pain in the beginning. Because the thing is, when you keep himolizing your red blood cells, your spleen macrophages, so these are good examples of extravascular hemolysis. When your spleen macrophages keep just himolizing your red blood cells, the unfortunate thing that is going to happen is that you're going to start making all these pigmented gallstones. You're going to make all these pigmented gallstones. And those pigmented gallstones, they can collect in your gallbladder and cause colin viruses. So if they give you a European young boy, anemia, recurring red opal cordrum pain, that is especially worsened with males, I want you to think about colin lesiasis from pigmented gallstones. Spelectomy actually decreases the risk of colin lesiasis in people that have hereditary spherocyteosis. And then, remember also, people that have hereditary spherocyteosis or any kind of hemolytic anemia in general will have, so will have, they will need de-lypholite supplementation. Because those people, their red blood cells die like they live fast and they die young. Because remember, a normal red blood cell is supposed to live for about four months, for about 120 days.

In many of these hemolytic anemia, the red blood cells may live for like 17 days, 18 days, 20 days. So those people, they have a lot of red blood cell turnover, so they use folate very heavily, right? Just like think of a hospital, during COVID-19, you know, before COVID-19, hospitals may use like a few N95 masks a year. And then you now go to the phase we're here using a couple thousand N95 masks in a day, right? So the thing is, those people's red blood cells, because they keep pumping, pumping, pumping out reticulosites, right? Again, those are in matriolary blood cells, that you get increasing your bloodstream because you have increased destruction of red cells. Because they are making a ton of reticulosites, they just use up their folate quickly. So it's very easy for people that have hemolytic anemias, like hereditary scythosis or hereditary lyptocythosis or sickle cell disease to develop a folate deficiency. So those people need daily folate supplementation. So I think I'm going to go ahead and stop here. As I do at the end of every podcast, I do offer a one-on-one tutoring for many exams, you know, step one, step two, see case, step three, preclinical medical exams, 30-ish-off exams, and then I also offer review courses. That's the thing that probably works the best for people with my schedule. Because my schedule gets very busy and I get booked out for one-on-one tutoring for like weeks in advance sometimes. So actually, I'm training on any of my review courses.

I have a step two, see case step three review course coming up next week. Just shoot me an email through the website and I'll be more than happy to give you some more information. And then I also work with people on the AERAS applications. So personal statements, recommendation letters, editing your AERAS application itself. I believe the AERAS application has actually opened. So it's going to be available for submission obviously on, you know, around, you know, some time in September. So if you're interested in any of those things, you have red flags in your application. If you just need help navigating a tricky application, again, shoot me an email through the website and I'll be more than happy to give you some more information on that. And then please subscribe to the website, divineinterventionpodcasts.com. Again, it contains tons and tons of podcasts that are very relevant for all the USML exams. And then also I have a You Tube channel, Divine Intervention, USML podcast and videos. So that You Tube channel, that's where I post my videos, so my shelf review videos. That's something I really recommend that if you're studying for step two, see case step three. The first thing you should start with are those shelf review videos. That's a thing that will really help you on your exams. Again, be out on the You Tube channel. Please subscribe and then also have these podcasts on Apple podcasts, Google podcasts and Spotify. So again, please do subscribe.

Any little bit of support definitely helps. And then many of you that listen to those podcasts, you know, that, you know, I'm a Christian. So I actually started a new podcast. It's called the Divine Intervention Life Lessons Podcast. I'm still going to be putting a few life lessons here and there in these podcasts that I make for this, for this, you know, this Divine Intervention Podcast. But the thing is I do meet like a separate website is literally Divine Intervention Life Lessons.com. So again, I'll see that Divine Intervention Life Lessons.com. And I have a life lessons podcast that I'm going to be posting there. And also this podcast, by the way, is right now also my poll podcast. So Divine Intervention Life Lessons. They are basically going to be podcasts that are 10 minutes or less long. Where most of them, I think pretty much all of them are less than 10 minutes long. And I basically talk about a life lesson. I use Bible Bees teaching to just describe life lessons that are useful for just key areas of our lives. So you can also exceed. You can all move forward. So thank you for listening to my podcast today. I'll see you in the next podcast. Thank you. God bless you. Amen.

PANDAS patients typically present with significant neuropsychiatric symptoms in addition to the choreiform movements.

Spread through cerebrospinal fluid (CSF) pathways, moving from the ventricles down to the central canal.

The media (the smooth muscle layer).

Hypoketotic hypoglycemia (low ketones and low blood sugar) during fasting.

Chronic hemolysis leads to increased bilirubin turnover, which can precipitate stones in the gallbladder.

It blocks the epithelial sodium channel (E NaC) in the collecting duct, preventing potassium excretion and leading to potassium retention.

Splenectomy, because splenic macrophages are responsible for destroying the abnormal spherocytes.

The mass of hemoglobin remains constant, but the volume of the RBC decreases due to membrane defects (Mass/Volume = High Concentration).

Osmotic fragility test.

PANDAS (Pediatric Autoimmune Neuropsychiatric Disorder associated with Strep infection).

Inhibition of CYP2 C9 by TMP-SMX leads to elevated levels of warfarin, increasing the risk of bleeding.

Any chronic hemolytic anemia (e.g., hereditary spherocytosis, sickle cell disease) due to high red blood cell turnover and increased reticulocyte production.

Splenectomy, because splenic macrophages are responsible for destroying the abnormal spherocytes.

The mass of hemoglobin remains constant, but the volume of the RBC decreases due to membrane defects (Mass/Volume = High Concentration).

Osmotic fragility test.

PANDAS (Pediatric Autoimmune Neuropsychiatric Disorder associated with Strep infection).

Inhibition of CYP2 C9 by TMP-SMX leads to elevated levels of warfarin, increasing the risk of bleeding.

Any chronic hemolytic anemia (e.g., hereditary spherocytosis, sickle cell disease) due to high red blood cell turnover and increased reticulocyte production.