DIP Episode 595 - USMLE Step 2/3 Rapid Review Series 121

Welcome, my name is Divine. This is episode 595 of the Divine Intervention Podcasts. In today's podcast, we're going to be continuing the Rapid Review series for the US Emily Step 2 CK Step 3 exam. This is going to be Series 1-21. I'm again, I just want to sound a quick note. For those of you that are studying for Step 2, Step 3, I will strongly encourage you if you can to take the Step 1-3-120. Just add it to the list of practice exams you're taking. And then please listen to the series I have on it. I have made podcasts on questions 1-105. I only have to make podcasts on the remaining 15 questions and God willing, I'm going to finish that pretty soon within the next few days here. But there's just very important bits of information. I think I want to pass across in this podcast. So I figured let's make this one and then we'll jump right back into the Step 1-3-120. All right. So first things first, what if they give you a question about a lady and they tell you that she has a history of bipolar disorder and that she delivers a newborn and this newborn has signs and symptoms of heart failure. You know, you're told that she was diagnosed with bipolar disorder two years ago and was started on pharmacotherapy. Let me ask you this. What should be your diagnosis here? What's the cause of the heart failure symptoms in her child? I'd really hope you're thinking about Epstein's anomaly. So this child has Epstein's anomaly.

Remember, in Epstein's anomaly, we typically see it in association with lithium. So mom has bipolar disorder. Lithium is a very good mood stabilizer. The thing is one problem lithium can cause. Although it's not very common, but it certainly is associated with lithium use. Is that lithium can cause a downward displacement of the tricospid valve leaflets. Then in addition to that, you're going to have the right ventricle does not develop as well as it should. So they can have a lot of issues with tricospid regurgitation and things like that. All right. So those are very common things we see in Epstein's anomaly. Right. And sometimes our friends at the USMLE, they'll ask you, oh, which of the following additional cardiac abnormalities will be found with further evaluation of this patient? You want to pick the answer that talks about an atroceptal defect or a patent for immunovale. This is very, very high to know for the USMLE exams. AS Ds and PF Os have a very strong association, very, very strong association with Epstein's anomaly. Okay. So again, whenever there is a disorder and it has a congenital cardiac association, that's usually pretty high to know for purposes of your exams. Right. AS Ds and PF Os have a strong association in fact about half of the kids that have Epstein's anomaly. Well, have an ASD. Well, have a PFO. Please make sure you know that for your exams. Right. Make sure you know that for your exams. And let's think of some other disorders, right?

Like de-jorge syndrome, where you're third and your fourth-firing geopartis do not form. So you have no thymus, you have no profyreglanz. What has, what cardiac issues are associated? Don't forget, shrunk osateriosis and tetralogy of phyllo. Strongest arterialysis, tetralogy of phyllo. They have very strong associations with de-jorge syndrome. Right. Okay. How about Down syndrome? What's the strong cardiac association with Down syndrome? Well, the strong cardiac association with Down syndrome is an endocardial cushion defect. Right. It's an endocardial cushion defect. Sometimes on exams, they call it an atroventricular canal defect. An atroventricular canal defect. An atroventricular canal defect. Right. How about phyllo alcohol syndrome? What's the cardiac association to know? Phyllo alcohol syndrome is associated with a VSD, right? A ventricular septal defect. VS Ds have a very, very strong association with phyllo alcohol syndrome, with phyllo alcohol syndrome, right? With phyllo alcohol syndrome. How about Marfan? So remember Marfan has a very strong association with mitral valve prolapse. Remember Marfan is an urusomodominant disorder, chromosome 15, fibrelingin defect. Right. It has a very strong association with mitral valve prolapse. And it also has a very strong association with aneurysms of de-jorge. Right.

So if you see sodium onset severe chest pain in a person that is very tall on you exams, besides thinking of anemothorax, because remembering may be found in tall, thin, young males, also think of Marfan's, think of Marfan's with aortic dissection of the rupture of an aortic aneurysm. Okay. Again, many of you are used to aortic dissections with Marfan's, but I kid you not, they can absolutely positively just give you a thoracic aortic rupture question for a person that has Marfan's and they may not give you aortic dissection. Okay. So please keep that at the back of your mind as you prepare for your test. And remember, those people, they need immediate surgery if not the risk of death is extremely high. Right. In fact, this is one of the reasons why people that have Marfan's, they get, you know, fairly regular screening, uh, echocardiograms just to look at their hearts and also to look at the aortic wall. And also don't forget, another disorder that is associated with mitral valve prolapse is autosomal dominant polycystic kidney disease ADPKD. Remember, people that have ADPKD, they have a cluster of problems. People with ADPKD, they have a cluster of problems. Right. They're going to have cysts in the liver. Right. So they can get signs and symptoms of liver failure. They can have cysts in the kidneys. And remember, some of those cysts, unfortunately, can transform and become a renal cell carcinoma. Right. But you can also have mitral valve prolapse.

They can also have mitral valve prolapse. And also don't forget, just like people that have Marfan's, they can have aneurysms in the circle of Willis. Right. And those aneurysms can pop, they can rupture and the person can have a brain bleed. Okay. The person can have a brain bleed. The person can have a brain bleed. So please make sure you know that stuff for your exams. All right. Now, what if they give you a question about a 57 year old male and they tell you that he has smoked two packs of cigarettes daily for the past 30 years. And then we're told that this man, this man has a already appearance to his skin. And you're told that he's hematocrit. His hematocrit is 63%. Obviously, this person has really bad polycythemia. And then they ask you, what is the mechanism behind this person's polycythemia? I would really hope you're saying, oh, divine, this person has polycythemia because of hypoxemia induced, hypocycretia, hypoxemia induced, erythropoetine secretion, right? Hypoxemia induced, hypocycretion. Remember, when a person has COPD, right? Say for example, in Fezima, that's probably the most common one that is tested on exams. You have a lot of proteases that are chewing up your lung parankama. And as those proteases drop your lung parankama, you're losing surface area. And when you have surface area loss, you will have issues with diffusion.

Remember, the fusibility of a gas is directly related to the area, the surface area available, and inversely related to the thickness of the wall, separating that diffusion, the barrier wall between the gases that are diffusing, right? So in the case of COPD, the mechanism behind the hypoxemia is a decrease in the surface area available for diffusion. So because the surface area for diffusion has decreased, you don't have proper equilibration of oxygen between the lumens of the alveoli and your pulmonary vessels. So that person develops hypoxia. Whenever hypoxia develops, then remember, remember, that that will cause the kidneys to produce erythropoetine, and that erythropoetine can cause polycythemia, that erythropoetine can cause polycythemia. Remember, we can see the exact same problem in a patient that has cystic fibrosis, right? These people, they cannot clear their respiratory secretions very well, right? So since they can clear their respiratory secretions very well, over time they can develop pulmonary hypertension, they can develop pulmonary problems, they can have a lot of hypoxia. That hypoxia can lead to the development of polycythemia, from increased ipo production. Now, what is one very clever thing that our friends at the NBM is can do to mess you up with polycythemia in a smoker. This is where you have to be abundantly cautious and careful on your exams. Polycythemia in a smoker on the USMLE is probably going to be caused by the hypoxemia, right?

From chronic obstructive pulmonary disease. But one other thing in a smoker that can cause polycythemia is renal cell carcinoma, okay? Is renal cell carcinoma? Is renal cell carcinoma? Is renal cell carcinoma? Divine, where is that relationship coming from? Well, let me ask you this, what is the biggest risk factor for renal cell carcinoma? The biggest risk factor for renal cell carcinoma is smoking, right? So what's the link between renal cell carcinoma and polycythemia? Well, the link is that renal cell carcinoma can produce ipo in a perinoplastic fashion, okay? It can produce a rethru poetin in a perinoplastic fashion and that can absolutely positively cause polycythemia, right? So what are some other causes of polycythemia on the exams, especially from a malignancy perspective? Well, don't forget hepato cellula carcinoma, right? HCC can make ipo in a perinoplastic fashion. Don't forget hemanguoblastoma. Hemanguoblastomas, right? Remember, those have a very strong association with one hipo-lindel disease and remember the key associations to know there, right? If a person has hemanguoblastomas, it's going to show up as a posterior for some us. It's going to have calcifications. It's going to have like a myronodial, right? Basically, it's going to have like an intra-luminar calcification, right? Those things can make ipo in a perinoplastic fashion, right? In fact, what is another unusual cause of polycythemia that you mission you exams?

Think of a sanotic congenital heart defect, right? The thing is, again, that is one backhand way our friends at the NBM Es can test sanotic congenital heart defects, right? So things like tetralogy or phallone or things like truncocacteriosis or things like transposition of the grid vessels or things like total anomalous pulmonary venous return. All those things are sanotic congenital heart defects. That sanosis can trigger the production of ipo and that ipo that is produced, right? That ipo that is produced, that ipo that is produced can cause polycythemia, right? So please make sure you can make all these integrations as you prepare for your exams. And I guess since I'm kind of talking about this, what is the most common cause of polycythemia? Let me ask you this, what is the most common cause of polycythemia? In general, the most common cause of polycythemia is hypoxemia caused by pulmonary disease. I'm going to say that again, the most common cause of polycythemia in general is hypoxemia caused by pulmonary disease, is hypoxemia caused by pulmonary disease, hypoxemia caused by pulmonary disease, right? And I guess since we're talking about this polycythemia business, let's talk about a few more things that are related to polycythemia, right? Because again, many of you are probably familiar with polycythemia there, right? Polycythemia there, polycythemia there. We know that polycythemia there is one of these myeloproliferative disorders, right?

Is one of these myeloproliferative disorders, is one of these myeloproliferative disorders, right? From a jaqtum mutation. So your red blood cell precursors, the proliferate in an ipo-independent fashion. In fact, let me tell you this. Our friends on the NBM Es, sometimes instead of writing polycythemia there as an answer, they will write ipo-independent red blood cell proliferation as the answer instead of p-vera. Again, if you remember from many of my podcasts, I have talked about the concept of a derivative. What's a derivative, right? If you're a person that has experience in the financial markets, a derivative is something that derives its value from something else. For example, an options contract is a very simple derivative, right? So say for example, you get call options. Let's say you believe that, oh, ililili is going to make great headwind in the future. Because of these anti-obstitial drugs that they're making, you can say, you know what? I'm going to express my views, not by buying ililili stock. And again, please, none of this is financial advice. I'm just giving an example, right? I'm going to buy call options on ililili, right? Those call options, they change in value based on how well ililili does, right? So if the ililili stock does well, then the derivative, the call option will rise in value as well. Many times these call options give you like very significant leverage. But again, that's a different discussion.

The divine is not trying to teach about options here. But the thing that's going to happen is the USMLE is the employee that seems strategy, right? They know that many people have anchored x-policythemia vera, jack-to-mutee-shon-yada-yada-yada-yada-yada. So what do they do these days on exams? They take what you know and they address it in a somewhat different way, right? So remember, another thing you may see for policythemia vera on your exams is ipo-independent red blood cell proliferation, right? Because again, if you notice, I've given so many examples of how policythemia may arise. What I give those examples of policythemia from elevated ipo. But policythemia vera is a cause of policythemia that is not associated with an elevation in ipo. If anything is associated with a decrease in ipo. So the thing that is causing your red blood cells to proliferate like crazy is not ipo, it's the jack-to-mutee-shon, it's an ipo-independent red blood cell proliferation, it's an ipo-independent red blood cell proliferation, right? ipo-independent red blood cell proliferation, right? And again, remember people that have policythemia vera, they can have a bunch of problems, right? They can have a lot of thrombosis. You may wonder, why do they have a lot of thrombosis? They have a lot of thrombosis because they have increased blood viscosity, increased blood viscosity, increased blood viscosity, right? Because remember, these people have policythemia, so their hematocrate is elevated.

If your hematocrate is elevated, that is going to cause bloodstasis. There is a very big difference between the way that water flows and the way that grease flows. I'm going to say that again, there's a big difference between the way water flows and the way grease flows, right? Water is almost like a less viscous fluid, so it can flow very easily. But grease is a more viscous fluid, so it doesn't flow as easily. If something doesn't flow easily, that thing has stasis. And if you remember, vera-coastriate of hypercwaagulability, right? Remember, there is the shinomonic for its stasis, it's the s. Hypercwaagulability is the h, and endothelial dysfunction is the e. That blood stasis arises in policythemia vera because they have increased blood viscosity. So because their blood is static, the clotting factors have more time to hang out together. Think about it. Whenever things slow down, more interactions can happen. More interactions can happen between your clotting factors. If that happens, then you're going to have a lot of thrombosis, you can have things like, for example, like a hepatic vein thrombosis, botchiaris syndrome, this is why botchiaris syndrome is quite common in policythemia vera. Because of that, blood stasis leads to hypercwaagulability, again, do not forget vera-coastriate. All these people live on having high blood pressure. The high blood pressure makes a lot of sense. Why does it arise? Again, their blood is very viscous because they have policythemia.

When your blood is viscous, that actually raises your total peripheral resistance. Why did I establish this relationship? When it all goes back to a fancy principle, you probably remember learning as you were studying for step one. And that's known as Poiseus Law. In Poiseus Law, remember, viscosity is directly related to the total peripheral resistance. What is Poiseus Law? Basically, the radius of the vessel is inversely related to the total peripheral resistance, that's to the fourth power. And then the viscosity is directly related to the total peripheral resistance, and the length of the vessel is also directly related to the total peripheral resistance. Because these people have very viscous blood, the total peripheral resistance increases. And if the total peripheral resistance increases, that's going to cause you to have hypertension. In fact, they can give you a question about an S-4 heart sound in a person that has policythemia vera. Or they can give you a question about a person that died from policythemia vera. And then they provide a pathological image on your exams that shows concentric hypertrophy. And they can ask you what is the mechanism behind the findings seen on autopsy evaluation of the patient. Pick the answer that says, increase levventricular afterload. Increase levventricular afterload. Again, what is the link? Remember, hypertension increases afterload. Hypertension increases afterload. You may wonder why?

Or the thing is, if your blood pressure is very, very high, it's going to make it so that your left ventricle has to generate a lot of pressure to overcome the pressure in your yoder to push blood out. Because remember, flow happens from high pressure to low pressure. If you want blood to come out of your heart and to produce your systemic vessels, the pressure within the left ventricle, the systolic pressure within the left ventricle has to overcome, has to be more than the systolic pressures that exist in your peripheral vessels. So if you have high blood pressure already, let's say your blood pressure is like 1.80 over 120. Then your left ventricle has to generate pressures, has to generate systolic pressures that are higher than 180 millimeters of mercury to push blood out. If that happens, that's pressure overload, that's a chronic pressure overload on the left ventricle. What will that lead to? That will lead to the development of concentric hypertrophy. Because you are laying down your sacramir in parallel, that will ultimately cause the systolic dysfunction of the heart. That will cause a heart failure with preserved ejection fraction. Although many times, those people will have decreased ejection fraction. It will not be as profoundly decreased as the person that has a stolic heart failure. But it will be decreased nonetheless. They will have again the stolic heart failure. They will have the stolic heart failure. They will have issues with ventricular failure.

The left ventricle wall will be very thick, big and biffy. As you have blood striking the walls of that big biffy left ventricle, that is going to cause you to have that S4 heart sound. Again, please, these integrations I'm talking about, you may be like, wow, divine. You're going to ham on basic sciences today. I promise you this stuff may sound like basic sciences, but it sounds an awful lot like the things that pop up on the USMLE Step 2 and Step 3 exams these days. Do not sleep on these things I'm discussing. Make sure that you understand these mechanisms. That's why I'm trying to be very systematic. I'm trying to be very slow in going through these things. I'm trying to be very methodical in going through these things. I promise you is going to be for your best benefit on your exams. It's going to be for your best benefit on your exams. In fact, let's mix some more integrations with this. Let's use police I think they are there. I love pver because there are so many different topics you can touch on with pver. There are so many different topics you can touch on with pver. For example, they can ask people to have pver. They tend to have a lot of bleeding. What's the mechanism behind the bleeding in the presence of the hospitalist? The reason behind that is that they have an acquired from Willibrand Factor deficiency. Divine. What? Acquired from Willibrand Factor deficiency. What do you mean? Well, again, let's go back to what we have discussed.

We have said that people that have polycythemia there. They have a very high risk of thrombosis. When you have increased thrombosis, that's going to cause a consumptive coragulopathy. That's going to cause a consumptive coragulopathy because think about it. What are the raw materials that are necessary for the formation of a thrombus? The raw materials are things like for Willibrand Factor. Things like GP1 B. Things like GP2 B 3 A. These people are chronic problems they have. It's not like the polycythemia there. It's just self-resolve. No, it does not self-resolve. Because they are always in thrombosis land, thrombosis land. I explained the mechanism because of the increased blood viscosity. Because they are always in thrombosis land. They keep using of the Avon Willibrand Factor. They keep using of Avon Willibrand Factor. They keep using of the Avon Willibrand Factor. That causes them to develop like Avon Willibrand Factor deficiency. They may be forming a lot of thrombi but they may also be bleeding. They may be forming a lot of thrombi but they may also be bleeding. They may also be bleeding. They may also be bleeding. Please make sure you know that for your exams. All right. Now remember what if you see a person that has polycythemia there? And the person has you know like enlargement of their right and left or per-conscious. That's a parosplino megalith. It's because they have a lot of vascular conjection. A lot of vascular conjection.

That's going to be the mechanism behind that. Because again, remember these people have crazy high hematocrytes. Or what if they give you a question about sodium onset severe joint pain? That they develop very acutely. They develop very solidly. In a person that has polycythemia there, you want to think about gout. You want to think about gout. What is the mechanism behind that gout? Well remember remember remember whenever a lot of cells are being broken down, whenever a lot of cells are being broken down, they can release new click acid material into the circulation. If you think about it especially purines they can ultimately be converted to uric acid. They can ultimately be converted to uric acid. Diuric acid can lead to the development that hyper-urusymia can lead to development of gout. So these people can absolutely because think about it they have a lot of red blood cells. All these red blood cells are breaking down. Because these red blood cells are breaking down, you release a lot of cell stuff into the bloodstream. A lot of cell stuff into the bloodstream. That can be converted by zinc thin oxidies into uric acid. These people can have hyper-urusymia and they can have gout as a problem. Again, you never thought you could get all these stains from polycythemia vera. You absolutely can. In fact, when you see the USML is talk about this nebulos part of the example called multi-systems processes and disorders. This is precisely what they are talking about.

I'm going to say that again. When you hear our friends at the NBM is talking about multi-systems processes and disorders, they're literally talking about something like this where you can take one topic and create so many different integrations from it. Like literally, there's like 20 exam questions you can write. Like full-fledged multiple choice, long-thick questions you can write. Just from polycythemia vera. Just from polycythemia vera. Just from polycythemia vera. And don't forget, how do we treat polycythemia vera? We're going to do phlobotomy. We've got to reduce. Because if you notice, this increased blood viscosity, this polycythemia is causing so many of their problems. So blood lets these people in a controlled fashion. Do some phlobotomy. In addition to that, also give them aspirin. Also give them aspirin. You are basically taking advantage of its anti-thrombotic properties. It's anti-thrombotic properties. Because remember, aspirin is an irreversible inhibitor of Cox 1 and Cox 2. By doing that, it's going to reduce the synthesis of thromboxin A2. When you reduce the synthesis of thromboxin A2, you're going to help in shutting down completely the aggregation. So that's going to be very helpful. I feel like I've kind of slammed you guys with a lot of integrations, pathways, and stuff. Because this is a rapid review podcast, I think this is a very good place to stop. Again, if you love the way I teach, I think you will find a lot of benefit from my review classes.

I have a class actually taking place today. It's a biostatistics class. It's first step one of the way to step three. I have a social site. It's a four hour class. It's over Zoom. I have a social science, QI, healthcare systems, ethics class taking place tomorrow. Again, also for step one to step three. I have a test taking strategies class. That's going to be taking place next month in the month of May. Then I also have a last minute review for step two, step three, taking place this Friday. The next week I have a 20 hour step two step three review. Just imagine learning all these integrations, learning all this pathophysiology for 20 hours straight. Obviously, it's five hours each day, spread over four days. Again, it's something I'm going to find to be really helpful. Then next month, the first week of May, I have a 25 hour step one class. Remember, again, step two, step three, doing well on them depends on having a good basic science foundation. In fact, I'm having an increasing number of people taking step two, step three, taking that 25 hour step one class. It's a class you're going to find to be profoundly helpful. Also, there is this epic class taking place in the first two weeks of June. It's the 50 hour step two, step three review. Again, this class imagine, again, learning for 50 hours, learning integrations, learning test-ticking principles, learning pathophysiology, learning all the trips and traps that the NV Me set for you. That class is epic.

Again, listen to the podcasts I've made where I discussed these classes. I think it will give you a very good idea of how valuable it can be for your testing process. Then I also offer one on one tutoring for all the US ML Es and all the complex exams. I also help with applications, personal statements, more interviews and things of that nature. Then remember, I have this podcast on Apple Google and Spotify. Although if you want every episode from episode one, all the way to this episode, 595, you want to go to the website divineinterventionpodcasts.com. Divineinterventionpodcasts. Podcasts with an S at the end.com. Then I also have a You Tube channel, Divineintervention, US MLP podcasts and videos. I post the videos that I meet. Then many of you know I'm a Christian. I have another website called divineinterventionlifelessens.com. Divineinterventionlifelessens.com. Basically every week, I post two or three podcasts where from a biblical perspective, address a life lesson. There's actually more than 320 podcasts on there. Divineinterventionlifelessens.com. There is actually an Apple podcast associated with that called the Divineintervention Life Lessens Podcast. Thank you for listening to me today. If you're interested in any of these classes, shoot me an email. I can give you some more information. But again, please, I will really encourage you. This is one of those rapid review series that may be helpful for you to listen to again.

It's just so much good stuff packed in here that can be very helpful for your exams. I'm telling you this, many of these things will show up as questions on your on your test. All right, so thank you for listening to me today. I will see you in the next episode. God bless you. Have a wonderful day. Bye for now. Thank you.

Epstein's anomaly, specifically involving tricuspid valve defects and right ventricular hypoplasia.

Endocardial cushion defect (also called an atrioventricular canal defect).

Mitral valve prolapse and aortic aneurysms/dissection.

Hypoxemia due to decreased surface area available for gas diffusion in the alveoli.

Stasis, Hypercoagulability, and Endothelial dysfunction (Vera-costriate).

Polycythemia Vera (JAK2 mutation).

Hypoxemia caused by pulmonary disease.

Renal cell carcinoma (RCC), Hepatocellular Carcinoma (HCC), and Hemangioblastoma.

Tetralogy of Fallot and shrunken osateriosis.

Increased afterload causes pressure overload on the LV, resulting in concentric hypertrophy (due to parallel sarcomere laying down).

Phlebotomy (to reduce blood volume/viscosity) and Aspirin (anti-thrombotic agent).

Chronic, excessive clotting leads to a consumptive coagulopathy, depleting factors like von Willebrand factor.

Hypoxemia caused by pulmonary disease.

Renal cell carcinoma (RCC), Hepatocellular Carcinoma (HCC), and Hemangioblastoma.

Tetralogy of Fallot and shrunken osateriosis.

Increased afterload causes pressure overload on the LV, resulting in concentric hypertrophy (due to parallel sarcomere laying down).

Phlebotomy (to reduce blood volume/viscosity) and Aspirin (anti-thrombotic agent).

Chronic, excessive clotting leads to a consumptive coagulopathy, depleting factors like von Willebrand factor.