DIP Episode 167 - USMLE Step 2CK Rapid Review Series 21 (Cardio)

Okay, welcome. My name is Divine, I'm a resident. This is episode 167 of the Divine Intervention Podcast. And in this podcast I'll be continuing our Rapid Review series for the US Emily Step 2 CK exam, but I'll be focusing on cardiology. So let's get right into it. So what if you get a question about a 75-year-old guy that passes out while he's mowing his lawn? What's your diagnosis? That's a Yodic stenosis, right? That'll be Yodic stenosis. And what is your next best step in management when diagnosis? Let's see maybe they tell you that on our school tradition of the chest. You hear like you hear like a systolic ejection murmur that's radiating to the carodid. Right? So you know, obviously a dealing with the Yodic stenosis, but if this is a voivola problem, what diagnostic step would you consider your test? Well, I hope you're saying that you consider an echocardiogram, right? So I mean again, like I said, this guy clearly has a Yodic stenosis. And there are some key high-year things your friends at the MBME expect you to know about the Yodic stenosis. First thing you want to know is where is it heard best? Right? It's heard best at the right or personal border. Know that name for the right or personal border is essentially like the second intercostal space, okay? Right by the sternum, right? So Yodic stenosis, the thing is also your friends at the MBME, they want you to know the Boswatt pathophysiology behind the Yodic stenosis, right?

Where you have like a calcification of the valve, right? Remember you want to be able to compare and contrast that with the Boswatt pathophysiology for my trovov prolapse, which is make some others degeneration. And then you also want to compare that with the Boswatt pathophysiology for Yodic dissection, which is cystic mediodigeneeration or some key times you see referred to as a cystic medionicosis. So when a person has a Yodic stenosis, right? Again, it's calcification of the valve. And one high-year thing you want to keep at the back of your mind is that prior to the age of 70, most people that have Yodic stenosis have it because they have a bicospidiodic valve. Okay? But past the age of 70, you just have like just regular good old calcification of the valve. So prior to the age of 70, you have calcification of a bicospid valve being one of the more common causes of Yodic stenosis, right? And one thing your friends at the MBME again want you to be able to do is they want you to be able to differentiate between Yodic stenosis and hypertrophic obstructive cardiomyopathy. Both of these of those conditions have some very similar features, right? They kind of sound similar, but they have some very key high-yield subtle differences you want to keep at the back of your mind. The first one is more of a test-taking thing, but that's just looking at the age of the person, right? Yodic stenosis will almost certainly be an old person on an MBME exam.

Hypertrophic obstructive cardiomyopathy will almost certainly be a young person on the MBME exam. Now, so let's talk about some key differences and compare them side by side, right? So Yodic stenosis already served it's heard best at the right of personal border. Well, hypertrophic obstructive cardiomyopathy is different. It's actually heard best at the left low strinal border, okay? That's why. Second thing is that Yodic stenosis, the murmur tends to be a systolic ejection murmur. That is actually the same thing with hypertrophic, like hookum. Hookum is also a systolic ejection murmur, but unlike Yodic stenosis that radiates to the carodid, the murmur of hookum does not radiate to the carodid. That's a very important subtle difference to keep in mind. The murmur of hookum does not radiate to the carodid. And the thing is you probably remember the, I think it's like maybe Greek or Latin, right? That's used to describe Ayodic stenosis as like pulsus pervasy tardis, right? So the tardis, right? Tardis means tardy, tardy means lit, right? So whenever a person has Yodic stenosis, right? You obviously have trouble getting blood out of the left ventricle. So if you feel like the PMI and then you feel their carodid pulse, you notice like man, just if you try it on yourself right now, your PMI and your carodid pulse, they kind of like arrive at the same time. But if you notice that it's like your PMI, you can see, feel your heart beating.

And then it takes a couple of seconds for you to feel like your carodid pulse. That's something called, that means your carodid pulse is arriving in lit. So it's arriving tardily, right? That's why that's called pulsus pervasy tardis. The thing is, pulsus pervasy tardis is not observed in hookum. Hookum goes along the lines of something called pulsus bicepheriens. Pulsus bicepheriens, the bicepheriens just means that you have a bifid carodid pulse. So what do I mean by bifid carodid pulse? Essentially, you have a small carodid pulse like pulse and then it's followed up by a bigger one. Okay? That's the classic characteristic of hookum. And then hookum, one key thing to know about it is that hookum tends to be like knowing what physical examiner ver is modulated to what. So the thing is in aortic stenosis, if you increase preload, right? So let's say you squat, right? Or you go from a standing to a supine position, that will increase preload. If you increase preload, you put more blood in the left ventricle. If you put more blood in the left ventricle, there will be more blood to eject through the stenotic aortic valve. So you have a louder murmur. So increasing any maneuver that increases preload will make the murmur of aortic stenosis louder. That's different for hookum. The thing is in hookum, right? And again, I've talked about this adenosing in many other podcasts. I'm not really going to go into a ton of detail here.

We're basically with hookum, you have something known as Sam, right? Sam just means a systolic anterior motion of the mitral of like it's like systolic motion of the anterior mitral valve leaflet, right? So the thing is whenever you end that anterior mitral valve leaflet, when it moves forward, it tends to occlude the left ventricle valve flow tract, right? And now make the murmur of hookum sound louder. But one way we can prevent the anterior leaflet of the mitral valve from occluding the LVUT, okay? The left ventricle valve flow tract is to put more blood in the left ventricle, okay? So the key thing you want because maybe put in to get confused by this, any maneuver that puts more blood in the left ventricle will make the murmur of hookum sound softer. So essentially, if you have a situation where you have increased preload or increased afterload, now we'll make the murmur of the, sorry, of hookum sound softer because increased preload will put more blood in the left ventricle, increased after load will prevent blood from being ejected from the left ventricle, right? So that's why the murmur will sound softer under those circumstances. So again, those are all high-yield things to know versus think about it if a person has increased afterload, then there is less of a gradient for flow across the valve in erotic stenosis. So the murmur actually becomes softer.

So again, our summarize, increased preload makes the murmur of AS louder, the murmur of hookum softer, increased afterload, mixed the murmur of AS softer and the murmur of hookum softer. Very high yield to understand that. Now, how do we treat erotic stenosis, right? For the most part, you need to go ahead and replace the valve, right? Because remember, if people start having like, anginous symptoms or like, syncopal episodes or like heart failure symptoms, those people are knocking on death's door, right? They may die soon. Obviously, the one that's the worst is having heart failure symptoms versus having like syncopal symptoms versus having anginous symptoms, right? So you go ahead and you replace the valve. For hookum, in general, right, you can, you know, you can implant a defibrillator, right? So they don't get like nasty ventricular tachyritmias that can kill them. But another thing you also do is to give them drugs that are negative vinyl tropes like beta blockers, because when you give a person a beta blocker, that will slow down the heart rate. And if you slow down the heart rate, the heart will spend more time in the astaly. And if the heart spends more time in the astaly, that means the live ventricle will feel a blood more, right? So you're essentially, again, preventing that dynamic LVOT obstruction by that anterior leaflet of the mitral valve. So in those circumstances, you can relieve those people's symptoms. So beta blockers are great.

They are first, they are the first line medications for the management of hookum. Now, remember, right, you're all the classic murmurs, right, like the buzzword descriptions, like mitral stenosis, right? Obviously, that's like the dastolic murmur, right? Dastolic murmur heard best at the apex, right? Remember that other things you may see with mitral stenosis on your exam is like rheumatic fever. Remember, the biggest risk factor for mitral stenosis is rheumatic fever. And then remember that mitral stenosis, right? Tens to also be the biggest. So rheumatic fever is the biggest risk factor for mitral stenosis. Mitral stenosis in and of itself is the biggest risk factor for for a thin because when a person has mitral stenosis, the left atrium has to contract against increased resistance. So that makes the left atrial wall dilute. And if the left atrial wall dilute, right, that can begin to create opportunities for a fit. And remember that as the left atrial wall dilutes, that can compress the esophagus. And that can cause this phisia. That is one weird how you think you want to keep at the back of your mind, for example. And then mitral regurg, right? Mitral regurg, remember that'll be a holosistolic murmur heard best at the apex, okay? Redete into the axilla, right? And remember that mitral regurg, right? Again, heard best at the apex. That's pretty much all you need to know about that. And then mitral off prolapse, right?

Will be like the mit, uh, murmur heard best at the apex with a mit systolic click. Um, classically, you'll find that in people would like connective tissue disorders, like morphans, burles, danlos, adp, kd. So like, ozomo dominant, polycystic kidney disease, right? And again, you'll have that mit systolic click, right? And again, any, the key principle you want to remember because mitral valve prolapse and mitral regurg are a little different. They are both regurgitant murmurs, but maneuvers do different things to them, right? So in mitral regurg, if you increase preload, right? You put more blood in the left ventricle. So there'll be more blood available to regurgitate. So the murmur will actually sound louder. Now, if you increased afterload, right? Again, there'll be more blood left behind in the left ventricle. And when there is more blood left behind in the left ventricle, there'll be more blood available to regurgitate. So that'll make the murmur sound louder. On the other hand, in mitral valve prolapse, the prolapse develops, right? It's the prolapse of the valves that gives rise to the murmur. So if you can unprol apps the valves, then you decrease the chance of the person having a murmur. And the key principle, because again, there are many ways the people go with this and then they get confused and then they see it's hard to memorize. But here's the one principle you want to remember. Anything that puts more blood in the left ventricle will unprolapse the valve.

And if you unprolapse the valve, you will decrease the regurgitation. And if you decrease the regurgitation, the murmur will sound softer. So if you increase preload, they'll put more blood in the left ventricle, though unprolapse the valve and the murmur will sound softer. If you increase afterload, it will be difficult for blood to be ejected from the left ventricle. So more blood will stain the left ventricle. That will also again unprolapse the valve and make the murmur sound softer. So I hope you understand that. And then Eodich regurgitation, right? Remember Eodich regurg tends to occur in people that have, you know, like Marfan's, right? That's like a classic presentation. When for person again has like a thoracic Eodich aneurysm, like a Marfan's percent and Elisdandlus percent, that Takayaso at a right is percent, a person that has like syphilis, remember tertiary syphilis tends to cause like an inflammation of the viso visorum of the Eodich arch. So that can cause an Eodich aneurysm and that can cause a mitral regurg. I mean, sorry, Eodich regurg. Remember that Eodich regurg, right? He's generally associated with a white pulse pressure. It's also kind of like the scene you would be seen in Dr. Satyrioosis also has a white pulse pressure. If you see a white pulse pressure, there's only two things you really should think about on your MBM exam. Think about in terms of murmurs, think about a PDA, and that'll be a pediatric question, or think about Eodich regurg.

And remember that in Eodich regurg, the blood, the Eodich regurg, right, is the dastolic murmur, right? dastolic, blue murmur, heard best of the left-leur external border, right? And it has like these weird things like the quinky pulse, head bob in sine, right? Water hammer pulse, all that stuff. Okay? And remember that Eodich regurg, right? Because the blood is regurgitating back into the left ventricle, you essentially have an chronic volume overload of the left ventricle. And when you have chronic volume overload of the left ventricle, that will, you know, sort of change the wall tension properties of the left ventricle. And that will cause a volume overload. That volume overload will give rise to eccentric hypertrophy, right? Where you add sacomers in series. And whenever you have eccentric hypertrophy, you begin to introduce a stolic dysfunction. So a person that has chronic Eodich regurgitation will ultimately have heart failure with reduced ejection fraction. Contrast this with a person that has Eodich stenosis, right? That will cause more of a pressure overload and pressure overload. It gives rise to the addition of sacomers in parallel. Sacomers are added in parallel. And when you add sacomers in parallel, right? That decreases the luminal size of the left ventricle. So that causes the astolic dysfunction. So under those circumstances of concentric hypertrophy, the person will ultimately have heart failure with preserved ejection fraction.

So again, those are all high-yield things. You want to keep at the back of your mind with those murmurs. Now, what if they give you a question about a patient that has severe chest pain, right? Like severe sodium onset chest pain. And then they tell you that the chest pain is radiating to the person's back. What's your diagnosis? Only those circumstances. That's theortic dissection, right? The thing is, I just give you the classic presentation, but there are some other classic presentations. Your friends at the MBME love to present, right? So they may give you a question about a patient that has like sodium onset chest pain. And this patient has like differences in blood pressures between the arms. Whenever you see that, think about theortic dissection. Or if we show you an image and you see that the media's sign name is wider than normal, think about theortic dissection. Or they can describe a person that has like severe chest pain. And then they tell you that the on image in the patient has a unilateral plural of fusion. If you see that, you can think about theortic dissection. And almost always again, this is not always true. But I'll say like 80 to 90% of the time it's true. Whenever you get an aortic dissection question, question on the MBME exams, the person's blood pressure will be markedly elevated. Okay? It'll be markedly elevated. So how do you diagnose aortic dissection? The patient is hemodynamically stable. Set them for CT and geography, right?

But if the patient is like hemodynamically unstable, you can do like a TTE. You do some kind of echocardiogram. You can do like a transdoracic. Or if you are particularly facile, you can do a transness of a geocardiogram. But really for the most part, transdoracic will do. Right? And the thing is, once you visualize the dissection, you essentially want to break it up into one of two things. Is it a type A dissection? So is it a Stanford type A dissection? Or is it a Stanford type B dissection? The reasoning behind that is if you have a Stanford type, basically the thing that delineates those two groupings is involvement of the ascending yore. Your decision tree basically should be, does this dissection involve the ascending yore? If it does, it's a type B dissection. Your job is done. Okay? Your job is done. Remember the A in Stanford type A for the A in ascending yore, right? But if the dissection does not involve the ascending yore, then it has to be a type B. Okay? So just ask yourself the simple question, does it involve the ascending yore? If yes, it's a type A. If no, it's a type B. And the reason you need to know those differences is that it helps you apportion your treatment appropriately because when a person has a type A, aortic dissection, right? You need to, I mean for every aortic dissection, B type B, type B, you need to start first with a beta blocker. Okay? You start with a beta blocker.

It can be like per per an all, basically anything that's a beta blocker, even a beta long is acceptable for use on the NV Me exams. But the thing you do beyond that depends is based on the type of aortic dissection you have. So if you have a type A dissection, in addition to giving the beta blocker, you need to proceed to surgery. But if you have a type B dissection, then you do not proceed to surgery. You can manage that medically. Okay? You can manage that medically. Now, when a person has aortic dissection, right? Again, remember the boss phrase I give you, right? The boss phrase pathophysiology is the cystic medial necrosis or in some circles is described as cystic medial degeneration. And what is the biggest risk factor for aortic dissection? That's hypertension. Hypertension is actually the biggest risk factor for aortic dissection. Now, one classic thing your friends on the NV Me love to do is that they like to give you questions about aortic dissection and try to get you to choose like hydrozina statement. Do not choose hydrozina. The thing is when a person has aortic dissection, you want to try to avoid increased heart rates because increased heart rates will place more shear stress on the aortic wall and worse in the dissection. So if you give a person hydrozina, hydrozina is an atti-riola dileter. When you dilute those arterios, that will decrease systemic vascular resistance and that will cause your borough receptors to cause a compensatory reflex tachycardia.

And that reflex tachycardia again will cause more shear stress on the aortic wall and that will worsen the dissection. So you don't want that. Okay? So that's why you give a beta blocker. Remember beta blockers and negative ionotrips so they slow the heart rate down. So I think those are all the high yield things I want to say about aortic dissection. Now what if they give you a question about an IV drug user? And this IV drug user for the last couple of weeks has been having like relatively high fever like 101. And this person has lost like 10 pounds of weight and then they tell you that when you're oscultating this person's chest, you actually hear a murmur at the left lowest turn on border. Okay? You hear a murmur like a holosistolic murmur at the left lowest turn on border. What are you thinking about under those circumstances? So think about this. IV drug user chronic high fever's new murmur. What is that? That's endocraditis. Right? That's endocraditis. The thing is endocraditis is a very high subject, high yield subject. That's tested on the USML exams. So it's something you definitely won't know and know pretty well. Right? And the thing is if you suspect endocraditis, what is always your first step in diagnosis? You want to get a blood culture, right? You want to get a blood culture first, right? Typically you don't also obtain an echocardiogram. But if you had to pick one diagnostic test on the your USML exam, go ahead and pick a blood culture initially.

And then those patients needs to be on IV antibiotics. You do the blood cultures, right? And then they need to be on IV antibiotics for a prolonged period of time. It's usually six weeks in the real world. So now let's talk about some on ways they can present endocraditis to you. Right? So what if they give you a question about endocraditis in an IV drug user? What kind of book should you be thinking about? Well, I hope you're telling me stuff. Warriors, right? Staff Warriors is the most common cause, very high yield is the most common cause of endocraditis in an IV drug user. Right? And this stuff, Warriors endocraditis and an IV drug user will obviously affect the track of speed valve. Right? Usually does that. It usually affects the track of speed valve. Usually we track cost speed regurgitation. And you may see divine. What is it that track of speed valve that is affected? Well, if you think about it, if you're an IV drug user, that means you're injecting the drugs into I Vs into veins, okay? And veins drink to the right side of the heart. So the first valve that will be encountered by the bugs you're injecting because you're injecting drugs with the track of speed valve. That is why the track of speed valve is the most commonly involved valve in endocraditis in people that have in people that IV drug users. Now, what if they give you a question about a patient that has endocraditis, right? And they mentioned that this patient recently had a dental procedure.

What book should you be considering? Well, I hope you're thinking about shrubberry dance on the little circumstances. Remember, shrubberry dance tends to cause like a subacute endocraditis, especially if you have that is already already has like preexisting issues. That places you at very high risk for endocraditis with a shrubberry dance. And typically the way you preferlaxis, you can give the patient like like a more like oral amoxicillin, right? I mean, I think amoxicillin is only in the oral formulation. And pysillin is the ibif formulation of amoxicillin. So you give amoxicillin like a few hours before the procedure commences, okay? As anti-bioreca perphylaxis. Now, what if they give you a question about a patient? And this patient has culture negative, like they tell you that this patient has endocraditis. What you notice that blood cultures don't seem to be growing squat. One thing should maybe try to think about on your exam is something called a coxiela. So coxiela per nadi is beginning to become a fairly common cause of endocraditis, especially when the blood cultures are negative. So that's just something to keep on the back of your mind. Now, what if they give you a question about a patient and they tell you that this patient, you know, has like autoimmune hemolytic anemia or ITP or has like a Miller rush on the face and they have endocraditis. What should you be thinking about?

I would really hope that under those circumstances, you're thinking about lupus and the libman-saxon endocraditis. Remember the nomonic that SLE causes LSE, right? That will help you keep that straight on exams. Now, what if you get a question about a patient and they tell you that this patient has endocraditis and you get blood cultures. And you notice that the blood cultures are growing strebobovis. What is your next step in management? Well, I will hope you are considering obtaining a colonoscopy, right? Because remember, strebobis bacteria has a very strong association with the co-existence of a colonic malignancy, right? So you need to do a perform a colonoscopy under those circumstances. Now, what if you get a question about a patient and this patient recently had a valve replacement? And on this person's valve, especially like, you know, like 70 days after the valve was they have like, you know, signs and symptoms of endocraditis. What book are you thinking about? Well, I hope you're seeing stuff epidermidious, right? Remember stuff epidermidious? Mix biofilm, that's like a step one concept, then we still pop up on the other USMLA exams. But stuff epidermidious in mixed biofilm and that biofilm is very adherent to plastic surfaces. So that's why prosthetic valve endocraditis is usually caused on MBME exams by staff epidermidious. And then, what if they give you a question about a patient that has endocraditis?

And let's say six months ago, this patient immigrated from some kind of foreign developing country. And they tell you that this person had like an operator infection two years ago that resolved without treatment. What should you be thinking about under those circumstances? Well, I hope you're thinking about like, rheumatic fever causing endocraditis, right? And remember that rheumatic fever is associated with group A-stripping infection, right? So, strep pyrogenics. So I think if you understand all these different permutations I just talked about, you should be good in from an endocraditis perspective. Now, what if they give you a question about a 75-year-old guy? And let's say this guy has smoked two packs of cigarettes every day for the last 50 years. And then this patient has been presenting with pain that is severe when he's walking to the YMCA that is about a block from where he lives. What that does he should you be thinking about under those circumstances? Well, I hope you're thinking about PAD, okay? I hope you're thinking about peripheral arterial disease, right? And then if your friends at the MBME ask you for your next best step in diagnosis or in management, what would you want to do? Well, you want to go ahead and obtain an ankle-breaked index, right? You want to go ahead and obtain an EBI. The thing is that EBI, the number you're looking for is a number less than 0.9.

If you measure a presence EBI, so the ankle-breaked index and it's less than 0.9, that tells you that you're dealing with peripheral arterial disease. And once you come from that a person has peripheral arterial disease, really the next thing you want to do is to put them on a supervised walking program, okay? That really does improve walking distance in a lot of people. But if for example that does not cut it, your next step in management on the exam is to add a drug, okay? You want to add a drug that has anti-plichlytic activity, but it's also a potent visual dileter. And this is the drug cellosterzone. Cellosterzone is a phosphodisteris inhibitor. Remember when you inhibit phosphodisteris, that increases the amount of cyclic ampine in smoke muscle. And increase the amounts of cyclic ampine in smoke muscle, make the smoke muscle relax, okay? So that is why cellosterzone is good because it can dilute the vessels that feed the lower extremities. Now, if for example that is not cutting it, then you need to consider performing some kind of bypass. But the thing is before you perform the bypass, you need to do a vascular study to actually prove for sure that you know this person has legit PED, right? So typically for that you perform something called an arteriography, okay? You perform something called an arteriography, and then you go ahead and send the patient for bypass surgery.

Now, remember that it's, you know, like if you have like a conclusion of like many people that have peripheral arterial disease, they have a conclusion of like the femoral arteries or the apopleety arteries, okay? When people have femoral artery occlusions, they tend to have more of the pain in the thigh. When people have popleety artery occlusions, they tend to have more of the pain in the leg, okay? Contrast this with lyrish syndrome, right? So lyrish syndrome will be a person that has like a lot of bottled pain, okay? And they'll tell you that this patient is important, having like marital problems because he cannot get it up with his wife. Under those circumstances, think about a variant of PED known as lyrish syndrome. In lyrish syndrome, you essentially have PED of your other and like the iliac branches like external iliac and internal iliac. Again, these are all higher things you need to know for your, for your exam. And then, what is the biggest risk factor for peripheral arterial disease? What is the biggest risk factor for peripheral arterial disease? Well, I would really hope you're telling me that it's smoking, okay? Smoking is the biggest risk factor for peripheral arterial disease, okay? Smoking is the biggest risk factor for peripheral arterial disease. Again, that is something high out your friends at the MBME expect you to know for exams.

And then one last thing I want to go ahead and for some people when you measure their, when you measure their EBI, you're like, man, this person's EBI is like 1.5. When you see that, usually that's in a person that has a history of diabetes, okay? Now, being a person that has a history of diabetes, that condition is known as Monkerback. So M-O-N-C-K-E-B-E-R-G, that's what's known as Monkerberg atherosclerosis. Typically, your next step in management for those people is to measure something known as the Toe Brickial Index, okay? You measure the Toe Brickial Index. And you measure the Toe Brickial Index, that gives you a more accurate measure, right? Because the thing is people that have diabetes, they may have calcified their blood vessels, so that gives you a falsely elevated EBI. Again, that's something very high out you want to keep at the back of your mind, for exams. Now, what if they give you a question about a patient, you know, that has spoke for a long period of time, and then this patient has been complaining like over the last 30 minutes, he's been having like severe back pain and abdominal pain, and then they tell you that his blood pressure is really low, and his abdomen is distended, and you can feel a pulsatile mass. What's your diagnosis? Well, I would really hope that you're thinking about a ruptured triple A, okay? I would really hope that you're thinking about a ruptured triple A, right?

So what is the biggest first of what is the biggest risk factor for a triple A? Well, it's smoking, right? Smoking is the biggest risk factor for an abdominal eoreka, and your isn't, right? And the thing is with a triple A ruptures, that's bad, right? That's bad. The way you confirm the diagnosis of the rupturing, you can do again CT angiography, but you can also do an ultrasound at the bedside, right? And then go ahead and same the patient to surgery. Now, one thing your friends at the MDM may kind of care about with a triple A is one that you know the screening guidelines, right? Remember, if you're a man, so women are not screening for triple A, if you're a man, are you over the age of 65, and you have a history of smoking, then you deserve a one-time abdominal ultrasound to screen for a triple A. If you have a triple A, and the size is more than five and a half centimeters, and it is recommended that you go ahead and fix the problem. But if the size of the triple A is less than five and a half, then you watch and wait. You watch essentially like every six months or every year. If it grows by half a centimeter in six months or one centimeter in a year, then that person becomes eligible for repair. That's one high-yield thing to know. Second high-yield thing to know is that even if you've never smoked, if you have a family history of a triple A, then you deserve screening, especially if you're over the age of 50.

If you're over the age of 50, unless you have like a first degree relative that has had a triple A, then that actually buys you screening as well. Believe it or not, that's part of the guidelines. That is something that, again, the USMLA loves to test. Now, so, you know, a triple A, you fix it, but one thing your friends at the MBME kind of like you to know is to know the different complications that arise when you're trying to fix a triple A. So, one common one on the example is Renault failure. In fact, an EKI is probably one of the most common complications of fixing a triple A. EKI is probably one of the most common complications. Because, again, most triple A is arising the inferinally order. So, you're right around the Renault lottery. That then calls like like transient type of proficient of the of the Alfredo of the Renault lottery during the case. And that can ultimately lead to an acute kidney injury. That's what. Second one is that if a person is having a triple E repair, right? Remember that one thing that can happen is they can actually have problems with the spinal cord. They can infect the spinal cord during the case. Because the abdominal EKI order gives rise to an artery. There's this famous artery known as the artery of a dhamcoids. And the artery of a dhamcoids gives rise to the anterior spinal artery for many levels of the spinal cord.

So, if they give you a question about a patient that becomes paraplegic or like quadruplegic after a triple E repair, think about a anterior spinal artery syndrome. Essentially, in anterior spinal artery syndrome, all the pathways in the spinal cord are knocked out with the exception of the drossal column medial and miscus system. So, those people will have like, you know, they won't have any issues with like sense and fine touch, vibration and perception. But they will absolutely have issues with every other thing. Like pin and temperature from the upper and lower extremities. They'll have issues with with like open motor neuron and lower motor neuron like signs and like findings, right? For the spinal cord because everything has effectively been wiped out. And then one of the things you'll see on your exam is, they may describe a question about a patient that has had a triple E repair. And then they tell you that this patient over the last two, three months, you know, the hemoglobin has been dropping. And in addition to the hemoglobin dropping, they tell you that they have hemocort positive stones. If you see that, what are you thinking about on your exam? But I would really hope on that those circumstances you're thinking about the development of an E Odo enteric fistula. Okay? And E Odo enteric fistula. So, fistula is formed between the E Oder, the triple E that has been fixed and the GI tract, right? So, those people are chronically losing blood into the GI tract.

That's why they can have like an iron deficiency anemia. Now, last complication should know about a triple E, right? Especially if they tell you that, oh, you know, this person's triple E was fixed a few months ago or a few weeks ago. And they are noticing that, you know, they are doing like CT and geography. And they are seeing like contrasts go beyond the contours of the aneurysm that was just excluded. If you see that, think about a complication known as an endolique, okay? A complication known as an endolique. It just means that you did not properly exclude the aneurysm. So, things are still able to enter the aneurysm from the stents that you placed in the person's abdominal ear. So, again, that's something high you do want to keep at the back of your mind on exams. Now, what if they give you a question about a patient? And this patient, you know, maybe recently had like an orthopedic procedure or has been bedbound in the hospital for a long time for like whatever reason. If you see that, unless it is that complaint of like severe like like unilateral leg pain and swelling and tenderness and everything, one of those circumstances you really want to think about a DVT, right? And remember right, a DVT, the things that predispose you to DVT, a verkylstriad, right? Remember, a verkylstriad is best remembered by using the nomonic she. Right? So, remember that the S stands for the S stands for like stasis, right? So, being bedbound, the H stands for hypercognibility, right?

And then the S stands for endothelial dysfunction. So, whenever you have those situations, right? When a person is bedbound, then they can have those predisposing conditions that can increase their risk for having a DVT, right? And again, to diagnose a DVT, right? Obviously, you go ahead and do like a duplex scan of that person's lower extremity. And then after doing the duplex scan, you need to please the person on hepran, right? You need to please the person on hepran. If, for example, the person has like very high bleeding risk and you cannot give them hepran, then the thing you can consider doing on your NV Me exam is to place an IVC filter, right? Because that will protect the DVT from converting to a PE on that those circumstances. Now, I realize this is a rapid review podcast. Okay, let me just see some last, you know, real quick things and then I'll be done. What if they give you a question about a patient that has chest pain, right? A patient that has chest pain and then they tell you that, you know, you see an EKG ST elevations everywhere and then it's like radiating, they have like the chest pain, radiating to the jaw. Obviously, right? This person has a stem, right? So, this person obviously has one of the acute coronary syndromes. And remember that they have only three types of acute coronary syndromes on NV Me exams. The first one is unstable angina. Okay, the second one is an end stemmy and the third one is a stemmy.

In unstable angina, you don't have like any ST elevations, you don't have any troponing elevations. In an end stemmy, you don't have any ST elevations, but you have troponing elevations. In a stemmy, you have ST segment elevations or like a new left bundle branch block and you have elevated troponins. Okay, that's how you differentiate between those three types of acute coronary syndromes. And the thing is, when a person has any kind of acute coronary syndrome, right? Your next step in management is always coronary and geography. Okay, I'll just go ahead and throw that out there. If a person has unstable angina, you absolutely have no business trying to do a stress test for those people. They are too high risk because the thing is, if a person has unstable angina and they have a negative stress test, you're still likely to want to post your coronary angiography under those circumstances because you cannot be sure. So that's why once you have an acute coronary syndrome, you've body yourself a coronary angiogram. On the other hand, if a person does not have an acute coronary syndrome, like stable angina, for example, then those people do not need to pursue the, those people do non-equinary angiography, stable angina, you can go ahead and get a stress test. Okay, and remember with your stress test, right? If a person has a preexisting ekeg abnormality, then you cannot do any kind of ekeg-b stress test. Your stress tests have to devolve into a echocardiogram of B stress test.

And remember, you can use exercise. If a person can exercise, they should exercise because that actually gives you a lot more information with regards to stress test. But obviously, if the person has like CV Ls to a throidist or the a CVL-O Bs and the cannot exercise, then you can consider pharmacology. Right? And for pharmacology, remember, you use adenosine derivatives like apadenosine, regadenosine, and things of that nature. You can also use dipyridamol, right? By essentially ticking advantage of the coronary steel principle under those circumstances, again, which I've explained at NOSEM in many podcasts. But remember, you cannot use the adenosine analogs if the patient has a histro-reactive airway disease. Right? So like bad asthma or bad COPD can do that under those circumstances. You can also do adenosine stress test, right? Adenosine stress test. Remember, adenosine is a beta-1 agonist. But remember that for a person has like a histro-reli-severe ventricular arrhythmias, then under those circumstances, doing adenosine-b stress test, beta-1 agonist is probably the smartest thing in the world. Okay. Now, what is the most common cause of death in the first 24 hours after an M-I? That's V-Fip, right? Remember that after an M-I, a person can also get paracoditis, right? They can get paracoditis within the first few days, which is known as Fibranosparicoditis, or remember that they can get paracoditis like, you know, a couple of weeks after the M-I episode, right?

That's an autoimmune phenomenon, right? Remember, that's what's known as dressler syndrome, okay? Dressler syndrome. So keep that at the back of your mind on exams. And remember, right? Obviously, for a person has paracoditis, the classic findings on E-TG would be the classic, um, diffuse like non-territorial ST-segment elevations, and then they will also have corresponding PR segment depressions, okay? So again, that's something high up to give out the back of your mind. And paracoditis, right? We'll obviously present as chest pain that is also in inspiration, right? Or the hotel is at the presence, chest pain is correspondingly lie back, or better when they sit up, right? If you see like chest pain that's better, when people sit up, right? Then you really want to think about paracoditis on those circumstances. And if a person has paracoditis, really, right? Like your first step in mind, it means you still give an exit, right? If the answer is not caught in, if you can add us, you can give us steroid. If the steroid is not caught in, you can give coaches in. Remember, if a person has renal failure, then your only option, the only option remaining to you is to give um steroids, okay? Because coaches in an NSAI Ds can torture persons kidneys relatively quickly, okay? So if a person has renal failure, you probably should consider not using any of those agents. Now, what if they give you a question about a patient?

You know, this patient has been having parpetitions 25-year-old guy, and then on EKG, you notice that the PR segment is short and the QRS complex is wide, and the person has a delta wave. What are you thinking about? I'll see on those circumstances, you're probably thinking about WPW, right? So Wolf Parkinson's white. Remember, the pathophysiology of WPW is that you have like this bundle of cancer that allows direct communication between the atria and the ventricles, okay? So direct communication between the atria and the ventricles through the bundle of cancer, right? And that can cause us some serious problems. So, under those circumstances, if a person has WPW, you know, they will try to trick you into giving like beta blockers or whatever you can do that. You cannot give an EV nodal blocking agents in a person that has WPW because that will actually like make things worse, right? So typically when a person has WPW, the drug of choice is a class 1 A, and Terry Smith known as Prokina Mide, okay? It's a class 1 A, and Terry Smith, right? Prokina Mide. I remember that Prokina Mide is also associated with drug induced lupus, right? With those fancy schmancy and he histone antibodies. So that's something you want to keep at the back of your mind, for exams. And yeah, WPW just as a row, short PR interval delta wave stuff like that, right? So again, all high oaths to keep your mind and you treat with Prokina Mide.

And then, what if you get a question about a patient, and this patient, you know, complains of like severe leg pain, she says it's worse at the end of the day, and it's better when she wakes up in the morning. And then they tell you that you'll notice that she has like a painless above-hamidial maliolus. What are you thinking about under those circumstances? Well, I would really hope that you're thinking about chronic venous insufficiency. Really, the way you make the diagnosis is, you know, you do like some kind of duplex kind of the extruder extremities. And the both-world pathophysiology you want to remember in your exam is incompetence of venous valves, okay? Incompetence of venous valves. That is the general path of physiology behind chronic venous insufficiency. Now, when the person has chronic venous insufficiency, right, it tends to get ulcers above the media maliolus, right? That's something very high oaths to remember and understand, okay? That's something very high oath to remember and understand. I mean that, and the thing is all that blood that's pulling those people's legs, right? That can cause like something called stasis dermatitis, okay? That can cause something called stasis dermatitis. And really, the way you treat the way you treat chronic venous insufficiency is just still the patient will leave their legs, right? Tell them to leave their legs.

And they can also be like compression, socks and compression but there are some buts una buts u double n a, okay? They work pretty well for the worker, you know, pretty well for treating for treating the condition. So again, those are all high oaths, you want to keep out the back of your mind on exams. And usually venous ulcers, right? So these like ulcers above the media maliolus, they tend to be non-purelent, okay? They tend to be non-purelent and they tend, actually they can be purely antig that back. The thing I wanted to say is that they tend to be not painful, okay? So venous ulcers are usually not painful on endemic exams. And then VTAC is the last thing I want to talk about, right? So they give you a question about a patient that has like a white complex regular attack your red mea. Obviously under those circumstances you want to think about VTAC. Remember that VTAC, the only three decisions you need to make on your exam, right? If a patient with VTAC has a pulse, you have two decisions to make. If a patient with VTAC has no pulse, well, you don't have many decisions to make. You just go ahead and activate, um, so a person has VTAC no pulse. You give the person on synchronized cardio version, also called defibrillation. But if the patient has a pulse and they have VTAC, the things you need to think about is um, adihimudynamically stable. If you're hymnudynamically stable, your next step release to give them a mutorun. But if you're hymnudynamically unstable, right?

Then your next step is to perform something called a synchronized cardio version. Remember your friends at the mbme, they have many names for synchronized cardio version, right? So things like direct current cardio version, direct current counter shock, those common one on the same thing. So again, all high yield things to keep at the back of your mind for exams. So, um, I think I'm gonna go ahead and stop here. I feel like I've gone on for long enough. This is almost 15 minutes. As I do at the end of every podcast, I do offer one on one tutoring for many exams. Step one, step two, CK, step three, step two, CS. Preclinical medical exams, 30-ish-off exams. If you're a medicine resident, I tutor for the IBI Mintraining exam and the board exam. Um, and then if you're a college student, I tutor like Genkame, O-Kame Physics, Bio-Kame, Histology and Physiology. And then also do this thing called longitudinal tutoring, where if you're a first second or 30 medical student, I tutor you for your class exams or like your, um, your shelf exams. And then at the same time, I tutor you for the upcoming USMEL exam you had. Again, I've done this with a lot of people, right? And many of the people that I've done this have found it to be like very successful for them. And then the final thing, I guess one of the final things I offer is like the USMEL booster course is 10 hours for step two, CK or step three, and 20 hours for step one.

It's something you do at the end of your dedicated period or when you feel like your, you know, your knowledge base is decent and you need someone to put everything together for you. Um, I do those booster courses to essentially, you know, integrate things together. You know, high yield format and talk about most of the, uh, high yield concepts that's likely to be tested on the exam. Okay? So that's what the road that served by those booster courses. And then if you're a medicine applying to, uh, if to residency or as well like an ERS application or a college student applying to like, um, uh, med school, right? So, okay, sorry, I said medicine applying to a med school. No, medicine applying to residency. So ERS application or college student applying to med school. So like an AMCA's application, I'd offer like one or one advice in coaching, consulting for that. So like personal statements, rec letters, editing applications, mocking interviews, I've worked with again tons and tons of people on that. And again, you've only majority of the people have worked with have much that their first choice. And I also have, uh, I mean, uh, experience right on the admissions committee of a top two med school for a long time. So I've again read thousands of high quality applications.

So if that's something you're interested in, if you're interested in any of these things, either reach out to me through the website or send me an email at divine intervention podcasts with an SAD end at gmail.com. So do have a wonderful rest of your day and congratulations to the WNBE champions, the Washington Mystics. They did a fantastic job. I was particularly impressed with, uh, De La Dona and my Belgian dynamite, M and Miss Smith. So, um, I do love basketball if you've not noticed, and I'm a liquor fan for those people that are wondering. So I will see you later. Have a wonderful rest of your day. I hope to turn out more podcasts within the next couple of hours. So I'll see you next time. God bless you. Thank you.

Unstable angina, NSTEMI, and STEMI.

STEMI (ST-elevation myocardial infarction).

Type A involves the ascending aorta and requires immediate surgery; Type B can be managed medically.

Increasing preload (squatting) makes MR louder; increasing afterload makes MR louder. Correction: Both increased preload and increased afterload make MR louder.

Staphylococcus aureus.

Patent Ductus Arteriosus (PDA) or Aortic Regurgitation.

Blood culture.

AS is heard best at the right upper sternal border; HOCM is heard best at the left lower sternal border.

Increasing preload (e.g., squatting).

Stasis, Hypercoagulability, and Endothelial dysfunction.

Eccentric hypertrophy (addition of sarcomeres in series), leading to Heart Failure with Reduced Ejection Fraction (H FrEF).

AV nodal blocking agents (e.g., beta-blockers, calcium channel blockers).

Streptococcus viridans.

Men over 65 with a history of smoking; or any age group with a family history.

AS is heard best at the right upper sternal border; HOCM is heard best at the left lower sternal border.

Increasing preload (e.g., squatting).

Stasis, Hypercoagulability, and Endothelial dysfunction.

Eccentric hypertrophy (addition of sarcomeres in series), leading to Heart Failure with Reduced Ejection Fraction (H FrEF).

AV nodal blocking agents (e.g., beta-blockers, calcium channel blockers).

Streptococcus viridans.

Men over 65 with a history of smoking; or any age group with a family history.