DIP Episode 178 - USMLE Step 1 Cardiology Review Series 7 (Vascular Pathology)

Okay, welcome. My name is Divine. This is episode 178 of the Divine intervention podcast. In this podcast, I'll be going into the US Emily Step 1 cardiology review. This will be Series 7 and in this podcast, I'll be talking about cardiovascular pathology. Although I will spend more time on the vascular part of cardio vascular. I think it's imperative that I discuss, you know, the vascular issues and, you know, kind of put everything hopefully together and you'll find this to be useful for for your exam. Yeah, just cardio is just a very broad, expansive subject and again, I want to hopefully try to do a decent job in terms of getting everything together. So the very first thing I want to go ahead and start with, let's just talk about what, like if you're looking at a blood vessel, especially like an artery, right, what are the three major parts of an artery, right? So the three major parts of an artery, right? There's the intima, there's the media, and then there's the adventition, right? There's the intima that's usually thin. It's lined by embulfial cells, okay? And then we have the media and the media is made of smoke muscle, right?

And hopefully you remember that the media is kind of like limited by like right after the intima, you have the internal elastic lamina and then you have the media and then after that you have the external elastic lamina and then after that you have the adventition, remember, the adventition contains like nerves, contains blood vessels, those blood vessels tend to be known as the viso visor, which as you see later is attacked by syphilis, especially like in the other, right? These say in the other and the euric arch, so that those are all high-yield fins to keep at the back of your mind. And again, the thing is, right, if you're sort of going from the heart, we have the yoder and then you know, you form all these like smaller muscularis and then after that you form an arterial and then you have a capillary and then you have a venial. Well, the thing is the primary, this is a very high-yield to know for step one, but the primary means of control of blood pressure happens at the level of the arterial, okay? The arterial is where blood, like arterial is our resistance vessels, that's where blood pressure control is primarily regulated. And then if you want to keep this at the back of your mind like venial, it's like your veins, they are capacitance vessels, they have the ability to hold blood, they can hold large amounts of blood because they are very distensible, they have a lot of compliance. And if you want that to integrate this with pharmacology, right?

If they were to ask you on the USML step one about the mechanism behind the peripheral edema that's observed in people that have, that are taking a dihydroperidine calcium channel blocker, like I'm low-depine or fellow-depine. And the mechanism there is that those drugs are dilethose of pre-capillary arterials, right? So the dilipric capillary arterials, if you dilipric capillary arterials, if you think about it's the hydrostatic pressures within the capillaries will increase and that will cause fluid extroversation and that will ultimately cause a dima. So the corollary to that is that you can actually treat the peripheral edema associated with taking a dihydroperidine calcium channel blocker by dilating the post capillary venials. And you do that with an ACE inhibitor or an ARB. So if you dilate those post capillary venials, you'll decrease the capillary hydrostatic pressures and that will help with that peripheral edema. So that's a nice way of friends that the MD love to integrate this. Integrate this stuff. Now the thing is one big topic that they love to test on the MD is revolves around this process of atherosclerosis, right? So this process of atherosclerosis. So the thing is it's actually a process you want to make sure you actually understand from beginning to end, like how it's sort of like progresses, right? So the thing is, atherosclerosis for the most part starts when you have a fatty streak on a blood vessel, right? You have a fatty streak on a blood vessel.

If you know people that are pretty young that have you know relatively clean blood vessels, they're pretty healthy, they may have like a few fatty streaks here and they're in your blood vessels. But as people get older and especially again if you're very unhealthy, right? You can begin to get into a lot of trouble with atherosclerosis. So the thing that happens is that these are fatty streaks, right? For you know for the most part we contain like LDL cholesterol and all that badness. And the thing is if you have, if you then partner up that the presence of that fatty streak with some kind of endothelial dysfunction, so what do I mean by endothelial dysfunction? So things like certain toxins that's found in like cigarette smoke, right? Or anything that for whatever reason causes like dysfunction of like the endothelial surface, well that endothelial surface is exposed to that fatty streak. That fatty streak can begin to go from the intima and go into the media, right? And the thing is even while it's a fatty streak, right? It can be oxidized, right? You have like oxidized LDL in a sense. It goes into the media and then when you have that endothelial injury, right? A lot of things are released like like certain like hemotactic factors and whatnot that attract macrophages. When those macrophages show up, well macrophages, they are main job in life is to eat things. They eat that oxidized LDL and if they eat that oxidized LDL, they become something known as a form cell, okay?

They form something known as a form cell and those form cells, right? The thing that can happen is again you can begin to release factors like plethora, direct-grid factor and all that stuff that can then tell some of those smooth muscle cells that are in the media to start laying a lot of like fibros tissue, right? And that's what ultimately forms the fibroscap that underlies an atheroma, okay? An atheroma is just almost like an inward distinction of a blood vessel because the media has in addition to the smooth muscles you already have in media, the media has already been taken over by those macrophages, sometimes they call those macrophages that eat up the LDL cholesterol, the unknown has a form cells, right? So it's all stable and everything in that region. So you found that atheroma but the thing is that atheroma, I mean if it's big enough, it can begin to occlude blood vessel and that can begin to cause symptoms, right? So say for example if you have this in the coronary vessels, if an atheroma is already occluding like 70% of the diameter of a blood vessel, then that's gonna cause angina, right? You generally need about 70% stenosis to begin to cause angina. Now one high-year thing you wanna keep at the back of your mind is that if you decrease the diameter of the radius, let's say the radius, if you decrease the radius of a blood vessel by one half, you actually increase the resistance in that blood vessel by a factor of eight, okay?

That's a very high-year relationship, you definitely want to make sure that you know on your exam. Now what are some things that contribute to the stability of an atheroma? This is something they love to test on exams, right? One big one you wanna keep at the back of your mind is the thickness or the strength of the fibroscap, okay? Because if something has like a thick fibroscap, like a very strong fibroscap, then it's unlikely to rupture because the thing is if an atheroma ruptures, then you have the release of substances that can trigger primary hemostasis and secondary hemostasis and if you form a thrombos at that level, at the level of the atheroma, then that's one of the things that can cause like an acute vascular syndrome, right? So, see for example, a person has like a heast of like like an angina, like you know they're like, oh I have chest pain when I work, when I participate in any kind of activity and then it kind of gets better with rest, right? That's an angina and like I said, that typically happens when you have like an atheroma that's occluding you know like a pretty big chunk, like 70% or more of the of the lumen of a blood vessel, like a coronary artery, right? So, the thing that happens is if you get into a situation where the atheroma sort of like explodes, you form a thrombos that can cause like an acute coronary syndrome like like an endstemy or stem, right?

So, that's typically how that kind of progresses and one high-yield thing kind of unusual that your friends at the NVME kind of expect you to know is that when like one thing that can contribute to the degeneration of the fiber scap and ultimate like pretty much like explosion of an atheroma for like an acute thrombos to form, one big thing that can play a role in that is an increase the expression of something known as a matrix metalloproteinies, okay? A matrix metalloproteinies, that's actually something high you want to keep in mind, you love to test that on example, for whatever visual reason you don't tend to find that in too many study resources and I mean obviously what are the things that can, what are the lifestyle habits that can contribute to the formation of an atheroma? Well, I mean all the bad things you can think about like hyperalipidemia, you smoke, smoking causes in the failure of dysfunction, hypertension, hypertension also causes in the failure of dysfunction, if you're obese, if you've got diabetes, right? All these things and kind of cause a lot of trouble and you may say okay, divine, how do I deal with this so that I don't develop all these atheromas all over my body? Well, just do the things that you hear on the news all the time that can maintain good health, right? Exercise regularly, right? 30 minutes at least five days a week, right? And then also try to reduce how much you consume, right?

There's actually been a lot of studies that show that the only I think the only thing that has been shown to improve like a presence longevity is coloric restriction, right? So coloric, I'm not saying becoming an aerotic, right? But you know, eat within reason, you don't need to eat 3000 calories at every meal kind of deal. And actually, if you big, if you exercise a lot and you eat healthy, if you already have an atheroma, you can actually regress over time, you can actually regress over time, that's a thing something high you ought to know. Now, one thing that your friends at the MB&E love to test occasionally is what if they give you a question about a person, you know, this person had an MI and then they tell you that this person like two days they went for cardiac catheterization and stent placement. And then they tell you that this person's creatinine has been rising. And this person's toes look blue and they look almost like gangrenos like necrotic in a sense. And the person is having like severe, like lower extremity pain. Well, I would hope you're really you're thinking about a cholesterol, under those circumstances, you're thinking about something known as a cholesterol embolization syndrome. The thing that typically happens to cause cholesterol embolization syndrome is that in the process of cardiac catheterization, you know, as you're like margin, margin, margin at the vessel, you can square off some cholesterol emboli.

And those things can begin to occlude small vessels. Okay, it can be, it can occlude renal vessels so that can cause like a, like an acute kidney injury, it can also occlude small vessels, especially in the lower extremities. And that can cause like digital or like distal ischemia. So you may see riddles that cholesterol come from well, the cholesterol comes from the atheroma. Okay, the cholesterol comes from the atheroma because if you actually look on locationally on the end being, they may give you like histology images, uh, opus, I guess, pictures. So they can show you like a histology picture. And you may look at a blood vessel and be like, I'm seeing all these white lines within the blood vessel. Well, those are things known as cholesterol clefts. Okay, those are things known as cholesterol clefts. Uh, those are pattern of money for an atheroma. If you see those in the walls of a blood vessel, just a lot of like longitudinal white spaces pretty much, uh, that tells you that you're dealing with a, you're dealing with an atheroma. So you want to make sure that you can actually identify, uh, you can actually identify that on an endemic exam, right? And again, like I said, those macrophages, they consume those, consume the oxidized LDL cholesterol, right?

And then the, those macrophages, the secret all these cytokines like again, like pleatlet derived root factor that then causes the smoke muscle cells in the media to differentiate into almost like fibroblast and this that secret in like all these weird stuff and then they form the fibroscab that they're ultimately leads to the formation of the atheroma. So again, I know you may say, oh, divine, you know, you've kind of said this a lot of times. Again, I'm not seeing this because I, uh, because I love to hear myself speak, um, seeing this because this is something that is tested frequently, but people seem to not pay attention to, um, people get the stuff wrong all the time. So again, you don't want to, hopefully you don't want to be one of those, uh, you don't want to be one of those people. Now, what if they give you a question about a patient that? So what if you get a question about, uh, uh, yeah, what if you get a question about like a 25 year old guy, they tell you that you know, he goes, uh, like, uh, underwater dive in. And then about 15 minutes after it comes up to the surface, he starts complaining of like severe chest pain. And then he suddenly becomes comatose and dags. What are you thinking about under those circumstances? Well, I'll really hope you're thinking about something called a case on disease. Okay. So people call it the bends. But basically the thing that happens, right?

If you remember, I think from undergrad, because again, I tell people in chemistry, there's this thing known as hair is low, right? And in hair is low, basically as you exert more pressure over fluid surface, right? You can dissolve more gas in that fluid. So here's the deal. When you descend to very high pressures, right? As you go lower in the water, right? The pressures increase. So things like nitrogen, right, can actually dissolve in your blood. So things that normally don't dissolve in your blood, right? Because again, remember, under increased pressure, solubility increases, right? So on the normal circumstances, things that will ordinarily not be able to dissolve in your blood, actually become able to be dissolved in your blood like nitrogen. So if that happens, and then you come up to the surface very quickly without giving enough time for equilibration, then that nitrogen can undissolve because we are reducing pressures, that nitrogen can undissolve out of your circulation. And that can begin to occlude vessels. You can occlude coronary vessels, causing my massive heart rate infarction. It can occlude coronary vessels. It can cause like a pomerian ballast, right? So those are things you all want to keep at the back of your mind. And the thing is your friends at the MBM, they know that, oh, the only situation people seem to think about where this stuff is, oh, just think about the bend, think about the sun's disease.

One thing you also want to keep at the back of your mind is that these things can also happen in people that, like, they can literally give you a very similar presentation in a person that's getting some kind of line placed in them, either like an arterial line, although, say on MBM exams, probably one that's probably a little more common is like a central venous, like a CVCS central venous catheter, right? Those things can introduce air, those things can introduce air into the blood vessels. And when you introduce air into the blood vessels, that can ultimately go ahead and cause occlusion of things and the person can get ischemia from that. So that's again a higher presentation. You want to keep your mind now. Okay, so what if you get a question about 55 year old female? Has a history of breast cancer? She has had an acetylene phenodysection and she complains of she's been complaining of like arm swelling and unpaying. What's your diagnosis for that patient? Well, I'll hope you're saying that this person's got a lymphedema. Okay, lymphedema. Lymphedema is a fairly common complication of lymph node dissection. And classically on MBM is they tend to test that in the context of a person that has had an acetylene phenodysection for breast cancer. Now, what if they then tell you that, oh, this woman, you know, she has had this lymphedema for a long period of time.

And then all of a sudden, like over like a three month period, she starts having like profound weight loss, massive swelling of that extremity. And like the extremity begins to appear like edemodus and necrotic. What are you thinking about? Well, I would hope you're thinking about some kind of malignant degeneration. The thing is when a person has chronic lymphedema, it can degenerate to form some kind of sarcoma. It can either become like an lymphangio sarcoma, right? Which is probably the most common thing you'll find on exams. Remember, lymphangio sarcoma is just essentially an angiosarcoma of a lymphatic channel, right? So, and again, the the prognosis is terrible, terrible, terrible. Now, what other angiosarcoma are you familiar with in the body that's tested on the USMV exams? Well, I would hope you're thinking about like angiosarcomas in the in the liver. Remember, those are pretty common in people that have been exposed to PVC. So, like polyvaino chloride. That's actually again, something that your friends at the NBME love to test. And again, these angiosarcomas, they have a terrible prognosis. People that have angiosarcomas, they they let's just say they don't do very well. It's it's not something that a person you would wish on anyone. It's a terrible, terrible thing to have. Now, what do they give you a question about a patient? And this patient, you know, is a long-term IV drug user. And then they give you some labs. And this person, C.D. Fort County, is like 20.

And then they tell you that this person has been having a has been having like a bloody bowel movements, right? And then they tell you that, oh, they perform like an EGD or they perform some kind of colonoscopy. And they tell you, they will likely go after the EGD on the exam. They tell you that you know an EGD was performed. And they see like multiple like red and purple nodules in the persons are lining the persons gastric mucosa. One of those circumstances, what's your diagnosis? I would actually hope you're thinking about Kaposi Sorkoma. Remember Kaposi Sorkoma is an AIDS defining illness. And the classic presentation, right, you can either present on the skin or it can present in visceral organs, right? You can present on the skin, you can present in visceral organs, right? So they'll basically describe a person that has all these like red or like purple nodules on their skin or in their GI tract. That's Kaposi Sorkoma for you. And hopefully you want to remember that couple. And I mean, the reason it's red and purple red is that you know, the tumor in general, like the lesions in general contain a ton of blood vessels, right? So that's why they tend to have that color. And remember that Kaposi Sorkoma has an association with what bug? Well, I was hoping you're saying HHV8, right? So like, sometimes it's called KSHV Kaposi Sorkoma Repi virus. So HHV8 has a different association with Kaposi Sorkoma.

And remember that in general, I mean, you can treat Kaposi Sorkoma with chemotherapy. But for the most part Kaposi Sorkoma is something that if a person's CD4 count is adequate, then they should not have Kaposi Sorkoma in the first place. In fact, there are some people that they have Kaposi Sorkoma, you study them on an anti-retro viral, like highly active anti-retro viral therapy. And they get a lot better. And then they don't, the Kaposi Sorkoma just kind of like disappear pretty much. So that's one thing you want to keep at the back of your mind. Now, what if you get a question about a patient that you know, IV drug user has multiple sexual partners. And they tell you that he appears to be a kektic. And he came into the hospital, complaining of like severe chest pain, radiating to the back. What are you thinking about under those circumstances? Well, I would really hope that you're thinking about like syphilis, right? Again, IV drug user, multiple sexual partners, the person probably has some antecedents of tertiary syphilis, right? And in this case, the person, I mean, presenting like the severe chest pain, radiating to the back, they probably have an eortic dissection, right? Because remember, syphilis, right? If you remember very early in this podcast, I talked about the three parts of a blood vessel where they said we can have the intima, we can have the media, and we can have the adventition.

And I said that the adventition can contain certain blood vessels known as the viso visorum, right? And syphilis loves to infect the viso visor, and when it infects the viso visor, it can cause a schemia of the eortic wall, and that can cause an eortic wall dilution, right? But the person can have a eortic root dilution. So syphilis can actually lead to a eortic because the eortic root is all diluted, that's one. Another thing that syphilis can cause, that is, it can cause the eortic dissection, because again, you are weakening the walls of the eortic root, because by killing off the viso visor, then you're not having enough blood flow to the media, right? And that can kind of weaken that muscular wall, right? And then another thing that syphilis can cause is just a thoracic eortic aneurysm, right? Because again, when you have a schemia, right? A schemia is typically followed by dilution of an organ or a blood vessel. I mean, if you think about the heart, if a person has a big myocardial infarction, almost all those people ultimately progress to getting some kind of a diluted cardiomyopathy. So that's like a big thing you want to keep at the back of your mind with syphilis. And remember that this eorticrist that's associated with syphilis is something that you find as a part of tertiary syphilis. And one high-ealthy emission on the test is pathologically, when a person has syphilitiki or titis, there is typically like this tree bark appearance of the person's aorta, okay?

There is a tree bark appearance of the person's aorta. That is a boss phrase you absolutely want to make sure you remember for purposes of your exam. And I mean, obviously what causes syphilis, right? Well, hopefully, again, let me try to integrate some micro here for you. Remember that syphilis is classically caused by trapponimapalida, okay? Remember, it's a spirochet. I'll tell you this that there are two high-ealth spirochetes you want to know for the purposes of the USML exams. Trapponimapalida is one. And then the second one is Borrelia Borgdophry, the bug that causes lung disease. Those are two very high-ealth spirochetes that show up all the time on exams, right? So what are some high-ealth things you want to keep at the back of your mind with Trapponimapalida, right? You want to remember like the diagnostic testing, right? You want to remember that especially if a person has like primary syphilis with a painless shanker, you can actually do dark-filled microscopy to see the bug, right? It's like a cox-screw-shaped organism. And then you can also do like a screening test, they're called a non-trapponimaltest, right? Like the RPR test, RPR stands for like Rapid Plasma Regain Test, or you can do the VDRL. I think it's like the venereal disease research lab or something like that, right? Those are the non-trapponimaltest, right? They're good screening tests.

What do you think is remember for every screening test, this is a concept that I know pathoma that causes quite extensively. For every screening test, you always want to follow it up with some kind of confirmatory test, right? So if a person has syphilis, right? And you know, the VDRL RPR is positive because those things are not very sensitive because like the RPR test, for example, is like a test that attacks like anti-cardiolipin antibodies. Anti-cardiolipin antibodies are found in many diseases, right? So you cannot say, oh, your RPR is positive, so that means you've got syphilis. No, you cannot say that with any degree of certainty. So you typically want to follow it up with a test, a confirmatory test that is more specific, right? And those confirmatory tests are like treponimaltest. Remember RPR, VDRL? Those are non-trapponimaltest, but these are the tests like MHATP, right? So like it's like a microhemaglotininase, again, so treponimapaledom. That's an example of a confirmatory test for syphilis, or there's this other one known as FTAEBS. It's like a fluorescent something antibody test for syphilis. So FTAEBS, MHATP, those are tests that those are confirmatory tests for the diagnosis of syphilis. And remember, again, like I said, primary syphilis is the painless shanker. Terture syphilis is like the otitis, the tibis dorsalis, where you scrub the dorsal columns, right?

And when you think of secondary syphilis, you want to think about the russian and the poms and souls, or you want to think about condiloma ladder, right? Those are all big things that tend to go with secondary syphilis for purposes of the USML exams. Now, what if you get a question about 65-year-old guy? And this guy comes in, he says that, oh, doc, for the last like two months, I've been having pretty significant leg pain, whenever I walk like a block, it begins to hurt a ton. And this person has maybe smoked like two packs of cigarettes every day for the past 40 years. What's your diagnosis? Well, I hope you're seeing that this person has peripheral arterial disease, right? If they ask for your next step in management on the exam, you want to go ahead and perform an ankle-break healing index, right? So, you want to go ahead and get an ABI and you'll typically be less than 0.9 and you're like, oh, crap, this person's got a PED. And one thing they may ask on your exam is, what do you do for treatment, right? Typically for treatment, you can consider doing things like a supervised walking program, right? That's one thing you can consider. If a supervised walking program doesn't pan out so well, you can give this drug known as selloztazol. Selloztazol is a phosphodistory, phosphodistory is inhibitor. It's an anti-plitility gene, actually, believe it or not. But it's also a very good viso-diiliter. So, you can use it to pharmacologically help a person that has PED.

But the thing is, if all that is not working and the person is having like leg pain at rest, they are very high, they are very high risk for like, like gangrene and like permanent ischemia of the extremities. So, under those circumstances, you need to consider placing like a graft, like you can place like an endovascular graft on like a stent to relieve the obstruction and improve profusion to their extremities. And, again, the biggest risk factor for peripheral arterial disease on NBME exams is smoking, okay? The biggest risk factor for peripheral arterial disease is smoking. Now, what if they give you a question about a pregnant woman, you know, she delivers a baby and then they tell you that within three, like three hours after she's delivered the baby, she becomes completely unresponsive, becomes comatose and she's not, you know, like, the physicians cannot get anything from her and then they give you like a blood pressure, like 40 over poppable and she's like super, super, super high-boxic. What's your diagnosis on that or circumstances? Well, I hope you're thinking about like an amniotic fluid embolism, okay? This is the classic presentation of an amniotic fluid embolism on NBME exams. Basically, the thing that happens is whenever a woman is about to deliver a baby, right? You know, she's been pregnant for a while and then the water breaks, right? So the amniotic sac breaks.

That amniotic sac when it breaks, you know, typically, the amniotic fluid just goes out the vagina, right? But in some unfortunate cases, that amniotic fluid can actually gain entry into the vasculatory and then go to like a pulmonary artery, for example. Amniotic fluid, believe it or not, it can actually embol, like that embolic process, right, is what's known as amniotic fluid embolism, okay? So amniotic fluid can actually occlude vessels, like you can occlude the pulmonary vessels and it can cause like a sudden death, like a, from like a very nasty, like, it's almost, it's essentially like the same pathophysiology as a pulmonary embolism. It's just that the thing that's embolizing in this case is amniotic fluid. That's why it's known as amniotic fluid embolism. That's the classic presentation and that's something you actually want to keep at the back of your mind, for example. Now, what if they give you like a similar presentation, but they tell you that, oh, this person, you know, is a patient that has recently undergone like orthopedic surgery and again, the person has like, this person is becoming confused, having PTKI on the skin, complaining of severe shortness of breath and they show you like some labs and you notice that the person's O2 sat is like, I don't know, like, 50, right? So obviously the person is hypersic. What are you thinking about under those circumstances? Well, I hope you're thinking about fat embolism, okay? Think about fat embolism.

The classic presentation is a person that has like a recent orthopedic surgery because the thing is think about it. Think about it. If a person has like recent orthopedic surgery or they have like a, like a bone fracture, remember your bone contains bone marrow, right? And there's a certain part of your bone marrow that's known as yellow marrow that literally contains fat. So that fat again can embolize and occlude the person's like pulmonary vessels and that can cause something called fat embolism syndrome. Now the thing is your friends at the MBM, they realize that every human being that's a met student has, you know, very effectively memorized this whole bone, long bone fracture orthopedic surgery association. So these days they're beginning to put some, you know, a little more exotic things that can cause fat embolism syndrome. So if a person has like a history of like fatty liver disease or a person is like a burn patient, those are really things that can precipitate fat embolism syndrome because really anything that just makes you have a ton of fat running around in your circulation can absolutely cause fat embolism syndrome. So those are some unusual presentations. You actually want to keep at the back of your mind that may actually show up on an MBM exam. Okay. Now what if you get a question about about, you know, like a 65 year old guy, he's BMI is like 40 and he smokes a ton and they tell you that he comes in with, you know, like chest pain, right?

Rediting to the job blah, blah, blah. What's your diagnosis for this guy? This is a stem, right? That's an easy one to stem it. And how do you treat stem is in general? Well, the first thing you want to give that patient is aspirin, right? You give that patient aspirin and then there's some other medications you can give, well, that's more for the purposes of step two CK. So I'm going to skip that. But for the most part, you give aspirin and remember that the most commonly occluded vessel in a person that has a myocardial infarction is actually the LED, okay, the left anterior descending artery. And you also want to know that whenever a person has like an RCA infarct, those people, the way you actually treat an RCA infarct, at least initially before you take them for percutaneous or coronary intervention, is actually to consider giving them fluids, okay? I mean, you don't give them a crap ton of fluids, we give them fluids, right? And you want to remember that in those people, nitrates actually contraindicated because those nitrates, right? They are venodilators. So that will decrease the preload. And when you have an RC infarct, you become very, very preload dependent. I'm almost starting to have described the mechanism behind this in some other cardiology podcasts. So I'm going to keep moving, right? So in general, the primary treatment for an MI is percutaneous or coronary intervention.

The only time you use a thrombolytic is when you're like more than two hours away from a hospital or a center that is capable of a percutaneous or coronary intervention. So when you do a PCI, right? One high yield thing your friends at the MBM kind of expect you to remember is that when you do a percutaneous coronary intervention, you typically place a kind of stent known as a drug eluding stent, right? A drug eluding stent. So it's a stent that, essentially, the walls of the stent are impregnated pretty much with an mTOR inhibitor, like serolimus, right? Or you can actually also impregnate those walls with, although this is less commonly done with microchipulin inhibitor like your pachyletaxel and stuff like that, right? Because the thing is by putting these drugs, right, cells lose the ability to proliferate so that you don't have like smooth muscle cells and all these inflammatory cells coming and essentially like clogging of the stent you just placed. That is actually a very nice way that your friends at the MBM can integrate immunology with cardiology, right? So that's something you actually want to keep at the back of your mind, for example. Now, what if you get a question about this is just I guess a concept you want to be able to keep in mind, but remember, if you ever see PTKI on a person's skin, if you ever see PTKI on a person's skin, what is the very first thing that should come to your mind on MBM exams?

I hope you are saying that this person likely has some kind of thrombocytopenia going on, okay? Whenever you see PTKI on your MBM exams, the first thing you want to think about is thrombocytopenia. Now, what if you get a question about a patient? You know, this patient is like four foot, five inches tall and she has like a low posterior hairline and she has like a had neck kind of looks, you know, she's kind of swollen and they tell you that, oh, she has a history of horseshoe kidney. What are you thinking about on the other circumstances? Well, I would hope you're thinking about Turner syndrome. If you notice, for this cardiac pathology podcast, I'm focusing a lot on clinical vignettes because I think that's a very effective way to cover at least the bulk of the high-end material with cardiac path. So I'm just going to keep doing that pretty much. So this person, right? You know, it's got Turner syndrome, right? And Turner syndrome has a lot of cardiovascular associations that your friends at the MBM kind of expect you to know, okay? So one is that you want to remember that these people can have a bicozopidiotic valves, okay? Bicozopidiotic valves are pretty common in people that have Turner syndrome and that can increase the risk of having like thoracic eodic aneurysms and having an eodic dissection.

So if you see a chest pain and a patient that has a history of Turner syndrome, you really, really want to think about like a eodic dissection or some acute eodic syndrome, right? That's complicating the clinical course. And remember that this Turner syndrome rate is 45xO, right? So don't mix that up on your test. Now, quick question for you. What's causing the person's neck to be enlarged and swollen? I hope you're seeing that that's a cystic hygroma. The thing is, the reason I'm mentioning this, right? Again, this is a vascular pathology podcast I'm talking about like diseases of arteries, or veins and of capillaries. The thing is your friends at the NBM realize that every human being has memorized the term cystic hygroma. So they are beginning to you know get a little more effective, admitting with people's heads by changing the name, right? Because the thing is, cystic hygroma is actually an example of lymphedema. Believe it or not, it's actually an example of a congenital lymphedema because I mean it's not like a tumor, anything like that, you're like, oh, hygroma, so it won't be a mass. No, it's not a real mass. For the most part is just problems with the proper development of the lymphatic channels in the neck, right? And that's what causes that problem in people that have in people that have a Turner syndrome, okay? And remember, again, Turner syndrome is 45xO. Very high you to know that for purposes of exams.

So now, what if you get a question about a child and it's like a three-month old child and experience coming to you're worried because this child has like a red-raised lesion like on the face or on the back or in the lower extremities, what are you thinking about on that those circumstances? Well, I hope you're telling me that this person likely has a capillary hygroma, right? The thing is, there are some unique questions that your friends at the MBM love to test in the context of these capillary hymengeomas. They may ask you that what's the most likely clinical course of a capillary hymengeoma? Well, the most likely clinical courses it may rapidly expand and then you'll regress, almost all of them regress as the child gets older, right? So those are lesions that you generally do not do anything for, okay? The lesions you generally do not do anything for. Okay, now, so what if you get a question about a 40-year-old guy and he's getting like a CVC, right? So like a central venous catheter placed and then they tell you that 10 minutes after the CVC was placed, I remember a CVC, right? Central venous. Whenever you see the term central venous, just think of it as a five-dollar word for right each among you, exactly. You're just literally placed at a catheter in the person's right at the right each. Okay, that's where it's supposed to be, right?

So they tell you that you know 10 minutes after placing the CVC, the patient starts complaining of severe chest pain and it becomes profoundly hypoxic and your blood pressure goes down a ton. What's your diagnosis on those circumstances? Well, I would really hope you're thinking about a pneumothorax. Okay, remember in the placement of again lines in the chest, right? You can puncture the lung and give rise to a pneumothorax. Again, that's just again a higher presentation. You want to keep in mind. So all your next step in management beyond those circumstances, well, you want to go ahead right then do a knee-to-deep compression, right? You want to go ahead and do a knee-to-deep compression. You can do it like in the fifth second intercostal space in the mid-clavicular line, right? Or you can do it in the fifth intercostal space in the mid-accelerated line. And then after you've done when you do the knee-to-deep compression, that will convert the tension pneumothorax to an open pneumothorax and then after that you place a chest tube. After that you place a chest tube. Now, what if they give you a question about a patient that you know has been on a long car ride? And this patient has like, it's complete of like severe leg pain and swelling, like let's say it's just one leg that is swollen, it's tender, it's, and this patient has been on like a 20-hour car ride or something like that.

And then they tell you that, oh, this person recently had like two days ago, had like brain surgery and that brain surgery was complicated by a bleed and he also had like a history of GI bleeding like three months ago. What your next step in management beyond those circumstances? I mean, obviously this person's got a DVT, right? Would you want to study them on like anti-coagulation? Probably not, right? For a person that's had like recent like neuro surgery, like a brain bleed or like a GI bleed, those are in general on NV Me exams, are contraindications to anti-coagulation. So under those circumstances your next step in management will actually be to placing an IVC filter, okay? Those IVC filters they essentially prevent, at least they can prevent a large clot from going from the leg because the DVT is very likely not going to kill you, but a PE is very likely to kill you, right? So under those circumstances, the thing that happens on NV Me is you place an IVC filter and that IVC filter will prevent the propagation of the clot, at least if it propagates, at least it will not get into, it will not get into the person's pulmonary vasculature and cause a massive PE. Now, what if they give you a question about a 45-year-old let's say she's like gravita 4 par 3, so she has had like multiple pregnancies, unless she just went, it's like super, super obese and then she comes in and says that for the last six months she has, we have it a lot of leg pain, okay?

And she says that she notices that by the end of the day her leg is swollen and is both legs, both legs, what's your diagnosis? Well, I hope under those circumstances you're thinking about chronic venous insufficiency, sometimes those are known as varicose veins, whether some key things you want to keep in mind with the NV Mes. Well, you want to remember that those things associated with the pathophysiology, right? Is when a person has incompetence of the valves that line the veins of the lower extremities, okay? That's a higher thing you want to know. And then you want to know like, again, some key treatment options that you could explain these patients, right? So you may see the one you're going very clinical today. Again, I know I'm going very clinical, but that is the direction that the USML is taking these days with step one, right? Like, they're still testing a lot of basic science concepts, but they are now beginning to test it in like clinical contexts or not even, they may not even necessarily be like going after like a clinical, clinical sounding answer. What a thing is they may present the information to you in a very clinical way. So I want to essentially train you with these kinds of podcasts to recognize those things in the first place, because if you can recognize it, then the step one example becomes very easy. And one area that they love to do this clinical mumbo jumbo, classically, is with cardiology, right?

So that's where I'm again, really hitting that stuff hard. So the thing is, in general for treatment, right? You can do things like you'll tell them to, you know, like, elevate their legs, because that will encourage drainage back towards the heart, so that the fluid doesn't hang out in the veins. And then you can also use something known as an una but it's like you double NA, like an una but that really helps with their symptoms. And the thing is, if these people were to develop an ulcer, like an ulcer on their lower extremities, where would they most likely develop that ulcer on the NV Me exams? Well, I hope you're telling me that they will develop that ulcer above the medial maliolus. Well, even if it's not above the medial maliolus, at least it's going to be on the medial side of their lower extremities, okay? But classic neon NV Me exams, it's almost always above the medial maliolus. And again, remember that these people, they can have like a dermatitis that arises from this chronic venous insufficiency, because if you think about it, right? Because the valves are not working, blood is collecting in their lower extremities. And as that blood collects in their lower extremities, that will cause extroversition of like, like, like, there will like raise hydrostatic pressures in those veins. And you can have like extroversition of red blood cells.

And as those red blood cells are broken down, you begin to have like these like deposits of hemocidurine in the persons like, like the layers of the person's skin. And that can cause something called as stasis dermatitis, right? So the person's skin kind of looks like reddish brown, but it tends to look like edemadas, okay? And unfortunately, these things are very, very, very, very hard to treat. Now, one thing that your friends at the NV Me can test in relation to these things is they can say, what is a, what is a likely infectious complication of a person having like stasis dermatitis or having like chronic venous insufficiency? What you want to think about the good old cellulitis, cellulitis is a relatively common complication of having a prolonged history of stasis dermatitis or chronic venous insufficiency. And I guess one last thing I'll mention with chronic venous insufficiency is that you can actually make the diagnosis by, you can actually make the diagnosis by doing like a Doppler ultrasound of the lower extremity. And in this day and age, where your friends at the NV Me care a lot about risk factors, they may ask, they may give you a question like you, they may describe like you know, like a classic patient. And then they can say, oh, which of the following historic risk factors in this patient increases the risk for this presentation? Well, here are some key things you want to know.

If for example a person has had multiple gestations, right, that can increase the person's risk of like varicose veins, right? Because again, if you have multiple gestations, you essentially leave extended periods of your life where the uterus is gravet, it's big, and it compresses on the IVC. And that can increase the hydrostatic pressures in of the veins that lie your low extremities and that can cause varicose veins. Another thing that can cause varicose veins and other risk factor is if a person just you know, works in a career that involves like standing at time, right? Let's say like you're rounding for hours and hours and hours, like 10 hours every day, for like years and years and years, that can actually increase the person's risk of varicose veins. And also the person is obese, obesity certainly can increase the person's risk of varicose veins, right? And then if a person is just old and frail, that can also increase the risk of varicose veins, right? Because think about it. The thing is the muscles of your low extremities, they as they contract, they actually push blood up towards the heart, okay? So they prevent blood from like hanging around in the person's veins, right? So it's almost like those muscles, they almost like massage your veins, right?

So the thing is as a person gets old and frail and they begin to have all this muscle atrophy, you lose that muscle contractile effect, I mean your muscles still contract if you are not going to be able to move, right? But you lose that muscle contractile effect and if you lose it, you're not able to like squish on those veins and send blood back to the heart and that can increase the person's risk of a, increase the person's risk of varicose veins. So again, these are all high-yield things you want to keep at the back of your mind. Now, what if you get a question about like a 35-year-old female, she comes in, she tells you that whenever she steps out into the cord, her fingers hurt a lot and her fingers turn blue, like it you know, it kind of like turns white and then it turns blue and then she says, well once she steps back into our apartment, her fingers kind of pinco up again, they become like red again. What's your diagnosis? Well, I would really hope you're thinking about like a renault phenomenon, right? A renault phenomenon, remember, it does not arise from atherosclerosis. It classically arises from like visospasm, right? It's a visospastic disease. Let me go ahead and mention this. There are two high-yield, I do this literally just dropped in my mind. There are two high-yield visospastic diseases you want to keep at the back of your mind for the USML exams. What you want to keep in mind is, is a renault phenomenon, that's the very first one.

But the second one you want to keep at the back of your mind is, Prince Metal Angina, okay? Prince Metal Angina, remember Prince Metal Angina, the name has actually changed, it's no longer known as Prince Metal Angina, it's no known as variant Angina, okay? Those are two visospastic diseases and they kind of have again, kind of similar pathophysiology where again, the person has a spasm of vessels. It's just in renault phenomena, people have like spasm of their digital arteries, in people that have variant Angina, they have spasm of their coronary vessels, okay? And these people in general, right? You can treat those people with a dihydroperidine calcium channel blocker, so like a lodipine, that can typically help with a visospasm and you just tell them to avoid the chord. Although for Prince Metal, the thing is, one way that your friends at the MBA may kind of sort of like stretch this concept, a little further, is you actually want to know that people that have these visospastic diseases, they should actually try to avoid viso-constricting drugs, you want to avoid drugs that can cause visospasid, right? So these people, right, or gotta mean derivatives and not a great idea in them, so much Riptan is not a great idea in these people, okay? Those are high-yield things that you want to know for purposes of the USML exam, and then what are the people that classically get renault phenomena on the USM Ls, right? So these are people that have like Crescleroderma, right?

Remember the Cresc, like the Cs for calciumoses, the R is for what? Guess what? Re-nault phenomenon, right? And then the E is for esophageal dysmortality, S is for sclerodactyl, and then T is for telangectages, right? These people tend to have renault phenomena, and remember that Cresc syndrome is associated with anti-centromere antibodies, right? And then renault phenomenon can also be found in people that have like Walden strums, macroglubulinemia, right? Like hyperviscocity syndrome. Those people also tend to have renault phenomenon on the USM Ls, and then just people that have like autoimmune diseases, autoimmune diseases, especially like lupus, increase of presence risk of having renault phenomenon on the USML exams. Now, okay. Now, what if you get a question about a patient, you know, that has a history of TB, and then they present with like hemoptysis, and they show you like imaging on the exam, and you notice that they have like this like CUB TB cavity, and you see like this rounded mass inside the cavity. And then they may give you like some labs, and the presence of white can maybe like 15,000, which is high, and then they will show you that the patient has like 10% of your synophiles. What are you thinking about on the other circumstances? Well, I hope you're thinking about as perjilus, right? Remember as perjilus loves to form these fungus balls, that's one, right?

But what am I talking about as perjilus in the context of, in the context of like cardiovascular pathology, well, the problem is as perjilus can actually infect blood vessels, you can actually invade blood vessels, you can invade the, in fact, typically this is why people that have like invisible as perjiluses have hemoptysis, you can actually invade the pulmonary vessels, right? And that can cause like fluid extroversation and all that badness, right? And then the person can get into trouble and begin to have hemoptysis. And the thing is these as perjilus hyphen, they can also actually like just literally occlude blood vessels chronically, and that can actually cause like pulmonary hypertension, right? Or you can cause like pulmonary embolus. So these are all complications of as perjiluses, you want to keep at the back of your mind, and you may ask, oh, divine, how do we treat as perjiluses? Well, if a person has like invisible as perjiluses, on your exam, one thing you can consider given is voreconazole, right? So you can give voreconazole or posaconazole, those are, those are very good drugs for children as perjiluses, but another one you may also consider is amphotericin B, right? Essentially, if you have any VC fungal infection, amphotericin B is almost always a good answer as to what you can consider giving the patient. So again, just key things you want to keep at the back of your mind, for example. Now, what if you get a question about a 25-year-old guy?

At this 25-year-old guy tells you that for the past six months, he had been having like, no, like, severe pain in his bilateral hands. I don't know if I've talked about this earlier, but I want to make sure I cover it because it's very high up to no. Like, you know, like severe pain in his bilateral hands, and he tells you that on a physical exam, his fingers look like black and this allered. What are you thinking about on the those circumstances? Well, I hope you're thinking about, and let's say, okay, this guy, let's say for the past 10 years, so let's see, you know, it's 25, what's starting at the age of 15, is that he's smoking like three packs of cigarettes every day. What's your diagnosis here? Well, this is burger's disease. I'll spell that out because you don't want to confuse this with burgers, or burger's, I don't know, but burgers disease, BUER, GER, okay, burgers disease, right? Classic presentation, smoker, right? You'll be a young male, that's a smoker, right? And has like gangrene also like necrotic-looking extremities, right? It's actually a kind of vasculitis, and for whatever reason, it also affects like medium-sized and small-sized arteries, okay? So it also affects like the radial arteries in the hands, and the TBL arteries in the lower extremities, okay? And the thing is, again, classic presentation, young male, heavy smoker, okay? And they will be completely not like pain in their fingers, they can even have like renault's phenomenon.

And really, the only treatment for these people is just tell them stop smoking, and they will get better, okay? They are literally people that this disease can almost entirely reverse, can almost entirely reverse if they stop smoking, right? And the thing is, if they don't stop, which unfortunately is the case for many patients that have this thing, they begin to develop like ulcers in their extremities, right? And then they can go into like gangrene, necrosis, and obviously they will lose that lamp, because they'll have to be unprotected, although sometimes you can actually, believe it or not, I've actually seen this clinically, I can, the treatment you can auto-unputate, you'll just kind of follow on its own from an necrosis, kind of grossed it. And one thing that your friends at the MDME, right, are beginning to do is, they know that people have memorized like the classic names of certain diseases, so they're beginning to like test the same thing, but you know, they just put different words that still describe the same disease, but are a little different from what you're used to, right? So, instead of seeing burgers, disease on your exam, they actually call this thing thrombone giitis obliterance, okay? Thromboc angiitis, so like THROMBOMGWITIS, okay? So thromboc angiitis obliterance, obliterance is like OBLITRANS, okay? So thromboc angiitis obliterance, that's again, classic, classic, classic, uh, burgers disease.

And the thing is, if you actually do like an angiogram of these people's extremities, you'll actually see like a coxcruelike pattern, that's classic for, that's classic for burgers disease. Now, what if they give you a question about a 30-year-old guy, he tells you that over the last like three weeks, he has been having a lot of like red urine, okay? And then he tells you that he has also been coughing a blood, so he's having him up to says, and then they tell you in the question that, oh, that he has like a saddo knows the formative, what are you thinking about on those circumstances? Oh, that's Wagner's, right? That's Wagner's, remember the name has changed from Wagner's, it's now called a GPA of Granulomatosis with poly angiitis. Remember the classic triad, right? Himoptysis, himaturia, the hematurias from nephritic syndrome. If you want to be a little more specific, they have a rapidly progressive pulmonary nephritis. And then they have sinusitis. But here is one thing you need to be careful of for purposes of the USMAD exams. Sinusitis can mean many different things on the USMA Ds because again, your friends at the MME realize that every human being has memorized that, oh, if you see a person with hematuria, hemoptysis, and like nasal polyps, or like sinusitis, bone, Wagner's. So they're beginning to expand their definition of what constitutes sinusitis.

So you may see things like a saddo knows the formative, with those other two members of the triad, that's still Wagner's. You may see things like otitis media with those other two members of the triad that's still Wagner's. You may see my stoiditis, right? So like pain behind the ear. Basically any infection like in the ear, knows throat in the setting of hemoptysis and hematuria is still Wagner's for purposes of your exams, right? And remember that Wagner's is positive for C-enka. Okay, it's positive for C-enka. Sometimes you may see that referred to an MBM is as anti-protein is 3-enka. Contrast this with P-enka that is positive in trx trouse, which is also known as EGPA, aka your synophilic granulomatosis with poly-engiaides, right? And also like microscopic poly-engiaides, those seem to be a pseudo-P-enka. Remember P-enka is anti-myloperoxidase, anka. Sometimes it's known as anti-MPO-enka. Okay, and really the way you treat Wagner's for the most part is you give those patients a steroids and a cyclophosphamide. Remember as you're giving those patients cyclophosphamide, you want to encourage like a lot of hydration, you want to give them mesna so that you can prevent the development of hemorrhagic cystitis. You want to prevent the development of hemorrhagic cystitis. And then remember that these posse immune, like these vasculities for the most part, the examples of type 3 hypersensitivity reactions. Okay, the examples of type 3 hypersensitivity reactions.

But there is a very, so you form like an antigen antibody complex blah blah blah. But there is actually one weird exception to that role. There's actually one weird exception to that role. And that's actually good posture syndrome. Okay, good posture syndrome is actually an example of a type 2 hypersensitivity reaction, right? So you make antibodies against the glomerular basement membrane, right? So those people tend to have hematuria, right? But in addition to that, you see the classic like linear pattern on immunofluorescence, right? But these people also tend to have hemoptysis. So if you again, if you see like a young male with just hematuria and hemoptysis, then think about good posture syndrome. They won't have any antecedents of sinusitis on NBM exams. Now, what if they give you a question about a patient? And this patient, you know, is like a 32-year-old female. She's been having like chronic abdominal pain. Occasionally, she has like bloody bowel movements. And then they tell you that, um, that you know, they obtain some kind of angiogram of like her GI vessels. And they notice all these like aneurysms forming. And you see like almost like this beads on a string pattern with a supermiss anterior card. What are you thinking about on that those circumstances? Well, I would really hope you're thinking about like polyadritis, nodosa. Okay, I'll really hope you're thinking about PE and polyadritis, nodosa.

The thing is with PE and it's actually very high you to remember that it tends to cause problems with like the mesenterid vessels, especially the superior mesenteric artery. In fact, let me just give you this testic in strategy. If you ask about a GI blood vessel and you don't like some pathology related to a GI blood vessel and you have no clue what's going on, you're completely blank out on your test. I will strongly encourage you to pick the superior mesenteric artery. Most GI pathologies that involve blood vessels in the GI tract is almost always linked in some way shape or form to the superior mesenteric artery. Okay, so that's one. Next thing is polyadritis, nodosa, again, like you have the classic beads on a string appearance on angiography. Another key thing with PE and is that it tends to not affect the lungs. It tends to not affect the lungs. That's what makes things to know. And then another final thing to know about, actually two final things to know about PE and is, PE tends to be uncann negative. Okay, so it's not positive for C and C or PE and C. And then finally, you want to remember that PE and has a very strong association with hepatitis B infection. Okay, no one really knows why or at least I haven't found a good enough explanation in the literature, but PE and has a very strong association with hepatitis B infection. Has a very strong association with hepatitis B infection.

Okay, now, what if you get a question and they're asking you about just the treatment of PE and really PE and the treatment is about the same as webinars. You actually can give those patients steroids plus a cyclophosphamide. And the thing is, you actually want to treat PE and when you don't treat it, you can actually increase the patient's risk of getting into a lot of serious trouble and a lot of serious trouble in the future. Okay, okay, now what if you get a question on the exam and you talk about like a 55-year-old female comes in, she says for the past like two days, she has been having like a severe headache on the right side of her forehead. And she tells you that like three weeks ago, she was having a pain as she was trying to true foot. What's your diagnosis? Well, this is giant cell arthritis, right? This is temporal arthritis. And one thing that we do on the exam is ask for your next best step in management. Your next best step in management for temporal arthritis is to strongly consider cortical steroids. They will try to treat you into doing like a temporal artery biopsy first. Don't do that, okay? Give steroids first and then do diagnostic testing later. You have up to like three days to do like a biopsy of the temporal artery to make a diagnosis, right? And remember that there are some other high-yield associations with temporal arthritis. Like I said, like trouble chewing, right? I like pain with chewing. That's something that's job-plotification, right?

That has an association with temporal arthritis or polymyajorromatica. That's another thing that also has an association where the person has like painful proximal extremities, okay? That's polymyajorromatica which for the most part tends to respond to low dose or cortical steroid treatment. Contrises with temporal arthritis that tends to respond more to high dose cortical steroid treatment, right? And the reason that you treat first and ask questions later is that in fact, I'll tell you this as a clinical pro. If you have a patient and you have any like with of temporal arthritis, even if you're not sure, like, you just have a headache blah, blah, blah. It doesn't matter. Treat first, like it's better to give people high dose cortical steroids and stave off like the inevitable blindness that can happen in a person that has a temporal arthritis and say, oh, you know, let's make sure and then they become blind, right? You don't want that. I want the course of like very heavy steroids is not going to kill a patient. It's probably going to save their vision, right? So what's temporal arthritis, right? It's the most common vasculitis, right? It's the most common vasculitis. And for whatever reason, the inflammation that causes this problem tends to occur in branches of the external curated artery, right? For the most part, it's usually the temporal artery, right?

So the patient will typically have like pain, like headache, like on one side of the forehead, like over their temples, basically, that's why it's called a temporal artery, right? But the thing is remember, they can actually have problems in any branch of the uterine, right? So like they can have problems like with the vertebral arteries, they can have problems with the ocurinary arteries, right? They can essentially have problems in any branch of the uterine, but classically, on MBM exams, they tend to have issues with with the temporal artery, okay? They tend to have issues with the temporal artery. And again, you want to treat so that they don't have occlusion of like, or like they don't have problems with an ophthalmic artery and then become a permanently blight. And again, remember that temporal artery, right? It will classically present in a person that is older than the age of 50 on MBM exams, older than the age of 50, and typically come on in females on exams. And the thing is, if a person has a normal erythrocyte sedimentation rate on MBM exams, they don't have temporal artery, okay? Yeah, having a high SR does not exclude it. I mean, having a normal ESR does not exclude the diagnosis, but I'll just tell you that I don't think I've ever seen an MBM equation on temporal artery, where the ESR was not markedly elevated, okay? So that's actually something you want to keep at the back of your mind for exams, right? And then the closed causing of Jansel artery, right?

Takayasu artery, this one on like Jansel artery, that tends to affect like, you know, like intracerebrovesalans, Takayasu artery, it tends to affect like, like legit branches of the order, right? So it tends to cause problems with like the subclavian artery, right? So that's why it's called like post-lest disease, remember your subclavian artery is the primary blood supply to your upper extremities, right? So if they give you a question about a patient, and this patient has like differential blood pressures in the arms, right? You want to think about, again, it will be a person that's less than 50, and it'll probably be a person that's of like some kind of Asian heritage, especially like, you know, so that's probably like Japanese, right? That's why it's called Takayasu, right? It's very common in Japan, right? So so that's like the classic presentation, and again, you know, they'll have like differential pulses and the extremities, or they may have like visual problems, believe it or not, or they can have pulmonary hypertension, because sometimes they can actually have involvement of the pulmonary arteries, my Takayasu, but again, woman less than 50, okay? Has a giant cellaritis style presentation, right?

And then they may show you like an angiogram, and we see like a big branch of the chronic artery, and that big branch, just you'll, they will typically like give contrast on the NV Mes, they will give contrast, and you'll see contrast, contrast, contrast, and then boom, you'll then see like clear space after a certain, after a while, under those circumstances, again, especially if it's a branch of the chronic artery, think about Takayasu and Raites on that those circumstances. And for the most part, you treat out with corticosterates as well, you treat out corticosterates. Now, as I round up this podcast, I guess there's some quick, quick hits I want to kind of like mention, right? So what if they give you a question about like a six foot seven inch guy that presents with like severe sodium onset ChSP, relating to the back? What are you thinking about under those circumstances? That's theotic dissection, right? That's theotic dissection. And the person in six foot seven inches tall, what do you think they have? I would hope you're telling me that they likely have marphans, right? Remember marphans, it's a connective tissue disorder, right? So these people tend to be like super super tall, right? And remember that marphans is an orosomo dominant, it's inherited in an orosomo dominant fashion. These people have like mutations in a fibrilline gene, right? Instead of putting fibrilline, they may put like FBN one as the gene that's mutated.

So that's something you want to keep at the back of your mind. The thing is fibrilline, it helps with maintaining the integrity of collagen fibers. So when people have problems with fibrilline, they cannot maintain the integrity of like collagen fibers of elastic fibers and all that stuff. And that will begin to mess with things that contain a lot of collagen and elastic fibers, like the media of a person's blood vessels, right? And if the media becomes very weak, then that can certainly cause problems like erotic dissection. And you also want to remember that erotic dissection is not the only thing that happens in people's marphans, because think about it again. This fibrilline is very helpful for maintaining structural integrity, so things like the cordy tendony in the heart, things like the lens of the eye, they all depend on fibrilline for proper functioning. So if these things are not functioning properly, you can begin to have things like mitral valve prolapse, you can begin to have things like etopia lentis where the lens is dislocated upwards. That's a classic finding in marphans. These people can have like a thoracic erotic aneurysm, they can have a erotic regurg because thoracic erotic is like very diluted. These are all classic things you may find in a person that has marphans. And again, chromosome 15, fibrilline defect, and remember that people with marphans, they can also get aneurysms in the circle of willis, right?

So if a person with marphans comes in or sedic of their lives, yere yere yere, think about giving them a think about a rupture of like a very aneurysm classically from the anterior communicative artery that's leading to their symptoms. Now, there are two, let me take two side bars here that are very high for the example. The first side bar is differentiating marphans from homocystinuria, right? This is a common mistake that people make on exams, differentiating marphans from homocystinuria. Well, here's the deal. First thing, marphans, right? Those people have a marphanoid habitus, they are tall. Homocystinuria, they also have a marphanoid habitus, they are tall. That's what. Two, marphans is in herithetian and autosomodominant homocystinuria is in herithetian and autosomodominant recessive fashion. Three, a person that has marphans tends to have their lens dislocated upwards and a person that has homocystinuria tends to have their lens dislocated downwards. Four, marphans, the mutation is in February. In homocystinuria, the mutation is in an enzyme known as cystothionine beta synthase, so like CBS, alternatively it can be in an enzyme known as MTHFR, methylene tetrahhydrofolid reductase, sometimes they may call that enzyme methyonine synthase. And then the final difference is that people that have marphans tend to have normal intelligence. People that have homocystinuria tend to have intellectual disability. So those are very key but very high-eo differences.

You want to keep at the back of your mind for NV Me exams and people that have marphans. Kind of like differentiating it from homocystinuria. Now, second sidebar I want to take is more differentiating. But knowing some classic USMLE buzzwords for certain disorders and some key risk factors. So I will just reel these off. So if they ask you about the buzzword pathophysiology for like mitral valve prolapse, what are you thinking about? Well, I hope you're thinking about something known as mixometas degeneration. Now, what if they ask you for the buzzword pathophysiology behind the erotic stenosis? Well, I hope you're going to be telling me calcification of an erotic valve. So calcification of the valve. What if they ask you a question about erotic dissection? What's the buzzword pathophysiology? Well, the buzzword pathophys is something on an asistic medial degeneration. Sometimes you may see referred to as cystic medial necrosis. Okay, that's the buzzword pathophys behind erotic dissection. Now, what is the biggest risk factor for erotic dissection? It's hypertension. What is the biggest risk factor for a stroke? That's hypertension as well. What is the biggest risk factor for myocardial infraction? That's smoky. What is the biggest risk factor for an abdominal deerotic aneurysm? That's smoky as well. What is the biggest risk factor for peripheral arterial disease? That's smoky. What is the biggest risk factor for mitro stenosis? That's rheumatic fever.

What is the biggest risk factor for a fib? That's mitro stenosis. Okay, so notice, I just reeled out all these very high-yale things. Again, you see, you're divine. This is low yield for exams. You're the other, I promise you it's not low yield. Okay, these are things that are tested all the time on step one, step two, CK, step three. So that's why I'm trying to sit down and really hammer this into your head. So let's keep moving on because I want to go ahead and end this podcast as soon as I'm a leader. I've kind of popped about the erotic dissection already. Some big things you want to keep in mind right is erotic dissection. There are two types of erotic dissection. There's type A and there's type B. Basically, the way you do need those two is if a person has the erotic dissection of any sort and it involves the descending order. It doesn't matter if it also involves the descending order. No one cares. As long as an erotic dissection involves the ascending order, it's a type A dissection. Remember the A in type A for the A in ascending order. Okay, and then if a person has an erotic dissection and it only involves the descending order, that is a type B dissection. That is a type B dissection. Why is it important to know that stuff? It's important to know that stuff because for every erotic dissection, right, if you ask what's your first step in management, give a beta blocker, you always give a beta blocker.

You can give like propanolol, you can give me toprolol, you can give a beta law, it doesn't matter. But the thing is a type E dissection is treated with surgery. In addition to that medical therapy of a beta blocker, a type B dissection is treated exclusively medically. You just give the beta blocker and call it a day. That's a big thing you want to keep in my erotic dissection. Another high-yield thing with the erotic dissection is that it tends to, there are some complications that can happen. People can have a erotic rupture. That's obviously bad. Mortality is probably almost 70-80% for those people. Then, erotic dissection can also cause strokes because when you have like a retrograde dissection, where it begins to go back towards like the erotic root, that can cause a stroke because you can dissect and cut off blood supply to like a cerebral blood vessel. Another thing that can happen is that in the presence of erotic dissection, you can also dissect back and begin to cut off blood supply to coronary vessels. The most common coronary vessel to be impacted in a person that has an erotic dissection is the right coronary artery. That is a factoid you absolutely want to commit to memory for the purposes of your USMLA exams. Then, remember that, classically on imaging, people that have erotic dissection tend to have a widened media stina. People that get erotic dissection on exams. People that have hyper, like really severe hypertension. People that have morphans.

People that have erlos danlos syndrome. People that have turner syndrome. These are all people that have syphilis, like a syphilitic erotitis. Those things can all increase the presence risk of having erotic dissection. Some other things they may even put on exams with erotic dissections, they may say that all that on imaging, they see like two different lumens in the asendin or the descent in the order. If you see that boss phrase, think about erotic dissection. Think about erotic dissection. Again, erotic dissection, it's bad. You want to treat it because it can get back real fast. One other thing you want to keep in mind, what if they give you a question about like 65-year-old guy, he has smoked for like two packs a day, 40 years. Then he presents with like severe back pain. He tells you that on physical exam he has a pulse, a tal mass. What are you thinking about on those circumstances? I really hope you're thinking about an erotic aneurysm, like a triple A that has ruptured. I'm definitely erotic aneurysm. Remember that, abdominal erotic aneurysms is very high, you'll actually remember that. The arise below the erotic dissection is very high. The first factor for a triple A is smoking. Remember, when I talked about what is it called?

When I talked about like the rupture of an atheromatous plaque, I said that one thing that can increase a person's risk of rupture is if you have like increased expression of matrix metalo-pertinises or if you have like a very thin fibroscap, those are all risk factors for an increase, like essentially increased risk of rupture. The thing is also having increased expression of matrix metalo-pertinises increases a person's risk of rupture of an abdominal aortic aneurysm. And the classic presentation on endemic exam is the person who have like severe back pain because remember, your atheris, at least your descending ather, is retroperitoneal. So they may not have abdominal pain, they may have like back pain on an endemic exam. You see a person that has like long-term smoker, old guy, severe, sodden onset. It's not something that they'll say, well, we're having four weeks, doctor, no. You can have a rupture, three, four weeks, you know, a person will be long dead. So, the thing that happens is the sodden onset, severe back pain, low blood pressure, pulsatoma, some physical exam. When you see those things, think about and think about triply. And the thing is in general for a triply, like you want to typically screen people, you know, if a person has smoked for a long time, you typically want to like start screening them at the age of 65, you do like a one-time abdominal ultrasound.

If you notice that the abdominal ather, like the diameter is more than five and a half centimeters, that's typically an indication for repair. Okay, we want to go ahead and repair that. There's some other weird things they love to test there that I won't go into. Those are more step-to-seeking material. Well, there is one thing that's actually step one worthy material that they love to test with records to fix in a triple A. The thing is when you fix a person's triple A, one thing that can happen is you can actually during the process of like fixing the triple A, you can actually have something happen where you have a schemia of an artery known as the artery of a damn poet. Okay, you can have a schemia to an artery known as the artery of a damn poet. The artery of a damn poet arises from the, from the yoder. Okay, it arises from the yoder, arises from the yoder. And the artery of a damn poet gives rise to the anterior spinal artery for many levels actually in the spinal cord, like the thoracic spinal cord. And also actually some, if I'm not mistaken, so don't quote me on this, some parts of the lumbar cord as well. Right, so if you have that already, they give you a question about a person that just had a triple A repair and then they have like paraplegia after surgery, think about disruption or schemia to the artery of a damn poet's, okay, and that can ultimately cause an anterior spinal artery syndrome.

That is a very nice way of friends at the MB Mechaninative Grid Cardiology with neurology on on an exam, okay, so again very high yield to know the stuff. Now, I don't know why I'm having this business givings in my mind to talk about the other complications of triple E repair. I don't know, I have like this weird thought that it will shop on some persons, you are similarly step one exam, and then I'll feel terrible. Okay, let me just talk about it real quick. So this, I will say it right now, say it will out loud right now, this is probably low yield for step one, it's very high yield for step two, see, go step three, but I don't know, I have like this bad feeling in my mind that me shop on someone's desk, so let me talk about it. I've talked about the artery of a damn poet's business with a triple E repair. Another thing that can happen with a triple E repair is that those people can have, let's say they can give you a question about a person, you know, has had a triple E repair like three, four months ago, and in this person presents with like, you know, like shortness or breath, and you check their hemoglobin, it's like seven, and then let's see you, which is low, and then let's say you measure their, you know, you check their poop and their poop is hemocall positive. What are you thinking about on those circumstances? Well, I hope you're thinking about something known as an aodotentheric fistula, okay, an aodotentheric fistula.

Basically, the thing that has happened is in the process of fixing the triple E, you've led to like a, like a tract that has formed, and this person has like a tract that has formed between the aodotent and the GI tract, so the person is just chronically bleeding, and that can cause an iron deficiency and in a kind of situation. So an aodotentheric fistula is a relatively common complication. This is something that for whatever is in the lobe, like step two C, can the surgery shelf of fixing a triple A. Another triple A fix, what do I call this? Another triple A fix complication on the USMA exams is something called an an endolyq, an endolyq is just something that happens where the aneurysm you think you've excluded, you begin to have like communication of that excluded aneurysm of sac with the stent or the grafts that you've just placed. The classic without presenting is the metenary that, oh, you know, this person is having like full, like this person is completing of like some mild abdominal pain, and they have a history of like a triple A repair, and then the tell you that they perform like contrast and geography, or like contrast aotography, and you can see contrast going beyond the confines of the excluded aneurysm of sac. Whenever you see that think about an endolyq, there are many types of endolyqs, but that is beyond the scope of this discussion, so I'm going to move on.

Okay, so that's those are the high-yield complications of triple A repair, like you want to keep in mind, another complication is just renal failure, because again, remember, triple A is tend to be right around the renal artery, although they tend to be below the level of the renal artery, but in the process of fixing a triple A, you can inadvertently occlude the renal and cause like an acute kidney injury with that. Now, what if you get a question about a patient, and this patient has, you know, like peripheral arterial disease style symptoms, you know, like, oh, doc, I work, I walk one block, my legs start hurting, and it gets better when I kind of risk for a while, and then, you know, you do the ankle-break healing index, and you measure it, and you're like, it's like 1.4. Hmm, I like, wait, but you have, you have like what appears to be classic PAD, what is your ABI 1.4? Well, whenever you see that, I just want you to think of two associations. One is that the person is likely a diabetic, and then two is that the person likely has something known as Monkaburg, so spell that is M-O-N-C-K-E-B-E-R-G, Monkaburg calcific sclerosis, okay? Basically, this thing tends to happen in people that have diabetes, and for the most parts, they can have like calcification of the media of their blood vessels, right? So, they'll have like a falsely elevated and cubric healing index, okay?

Usually people that have Monkaburg calcific sclerosis usually tend to not have any like, you know, like significant like problems, but that can be one unusual cause of a falsely elevated and cubric healing index. So, they will tend to have like calcifications in the walls of their vessels, right? So, if they show you like, like a histology slice through that vessel, you see a lot of like blue within the media, think about, and they show you like, oh, the lumen of the vessel is relatively fine, like it's not super occluded. Think about a Monkaburg calcific sclerosis under those circumstances. It's very common in people that have a history of diabetes. And then I'm seeing that I really want to hopefully keep this podcast on there 90 minutes, although I've talked about again a ton of high-yield stuff here. So, I guess instead of just using venets, I'll just talk about the other key things I want to mention real quick. Remember this pathology, hyperplastic arteriolosclerosis, they tend to present this as a histology picture on the USML exams. You'll be a person that, we may show you like a person's blood vessel, right? And for the most part, the blood vessel will be occluded. And then you see that it actually looks like an onion skin, okay? Like, like an onion skin pattern to a person's blood vessel. If you see that, think about something called hyperplastic arteriolosclerosis, okay? Hyperplastic arteriolosclerosis.

Okay, so what are some other associations you want to keep in mind with hyperplastic arteriolosclerosis? You want to keep basically the biggest association, probably one of the memories, a person that has just bad, bad, bad, bad hypertension, like malignant hypertension kind of deal. A person having like a sclerodermarino crisis, stuff like that. Those things can cause an accelerated arteriolosclerosis, which again will have this onion skin pattern on a histology. And then another kind of arteriolosclerosis you want to keep at the back of your mind is a hyaline. So not hyperplastic hyaline arteriolosclerosis. Typically, the thing that will happen is that you know, you'll see like thickening of the person's arteriol walls. And again, it tends to be common in people that have like diabetes and people that have like hypertension. And for the most part, you tend to see these arteriol changes like in the kidneys and in the brain. And again, the classic thing is you'll see like a lot of thickening of the walls of the person's blood vessels. So personally, I think this podcast is maybe going on for a long enough. So let me go ahead and pause here. As I do at the end of every podcast, I do offer one or one tutoring for many exams, right? Step one, step two C case, step two C as step three, pre-cleaned school exams, 30-ish-elf exams.

I do this thing called longitudinal tutoring, where if you're first second or 30-year-old student, I tutor you for like your block exams or your shelf exams. But at the same time, I tutor you for your upcoming USML exams. And again, people have done this with they've been wildly successful. I'm also doing this thing called like a USML booster course, where I tutor you for it's like 10 hours for step two C case, step three, and 20 hours for step one. And it's good for a person that's at the end of the dedicated periods or a person that feels like the knowledge is good and they want someone in a Q&A format. Very rapid, it's a super rapid review to put things together for them like the most knows, the high yields for the exam. That's something I offer and again, a lot of people have found it to be extremely helpful. I'm probably one of my most popular courses with people right now. And then if you're a medicine resident and you need tutoring for the ABIM internal medicine board exam or the internal medicine training exam, also offer tutoring for that. And then if you have like a college buddy that needs tutoring for like the MCAT, general chemistry, organic chemistry, physics, biochemistry, histology, physiology, offer tutoring for all those things.

And then if you need like coaching or advice in for like if you're like a medicine or a plan to residency, so like an ERAS application or a college student applying to med school so an BCAS application, I offer like one or one advice in slash coaching for like you know like more kind of interviews, editing personal statements, rec letters, editing applications. Again, I've been on the admissions committee of a top two med school for like a year. Avert thousands of high quality applications. I've worked with tons of med students that have all much study of first choices. So in multiple specialties. And again, I've worked with a lot of international medical graduates. So again, if you need any of these things, feel free to reach out to me. So have a wonderful rest of your day. I am really glad the Lakers won their game last night as some of you may know I'm a big Lakers fan with like Anthony Dv's getting like 40 points and 20 rebounds in 31 minutes. I'm really excited for the Lakers this season. I really pray all the time that they remain healthy. But let me get off my soapbox for now. I'll see you in the next podcast. Thank you. God bless you.

Intima, Media, and Adventitia.

The adventitia.

At the level of the arterioles (resistance vessels).

Dilation of pre-capillary arterioles increases capillary hydrostatic pressure, causing fluid extravasation.

Cholesterol clefts (longitudinal white spaces).

Treponema pallidum (Syphilis) and Borrelia burgdorferi (Lyme disease).

Hemoptysis, hematuria, and sinusitis.

Type B dissection.

FTA-ABS or MAT (Microhemagglutination Test).

Recent orthopedic surgery, bone fracture, or trauma leading to pulmonary emboli.

Marfan syndrome (FBN1 gene defect).

Marfan $\rightarrow$ Ectopia Lentis upwards; Homocystinuria $\rightarrow$ Ectopia Lentis downwards.

Raynaud phenomenon and Prinzmetal (variant) angina.

"Beads on a string" appearance, typically affecting the superior mesenteric artery (SMA).

Diabetes and Monckeberg calcific sclerosis (falsely elevated reading).

FTA-ABS or MAT (Microhemagglutination Test).

Recent orthopedic surgery, bone fracture, or trauma leading to pulmonary emboli.

Marfan syndrome (FBN1 gene defect).

Marfan $\rightarrow$ Ectopia Lentis upwards; Homocystinuria $\rightarrow$ Ectopia Lentis downwards.

Raynaud phenomenon and Prinzmetal (variant) angina.

"Beads on a string" appearance, typically affecting the superior mesenteric artery (SMA).

Diabetes and Monckeberg calcific sclerosis (falsely elevated reading).