DIP Episode 444 - The Clutch Thromboses Podcast (for Step 1-3)

Okay, welcome. My name is Divine. This is episode 444 of the Divine Interversion Podcast. In today's podcast, I'm going to be talking about the high-yield thrombosis. The high-yield thrombosis. This is one of those seminal podcasts. You know, you're going to get tons of questions right on this stuff on your exam. So just, I would certainly be attenuant to it. This should be a pretty short podcast, but it should be a pretty high-yield podcast. So, I guess maybe one thing that may be helpful to start off with here is differentiating between a thrombosis and an embolism. A thrombosis typically arises within a blood vessel. Erases for many different reasons, but it arises within a blood vessel. Many times, you know, you have injury to the wall of a blood vessel or you have one of a very coarse triads operating. And that messes over blood vessel. You form a thrombus that occludes flow in that blood vessel. And then, unfortunately, in some situations, some of those thrombi can break off and you can then go elsewhere. Whenever you see something that forms in one place, like a thrombus or whatever, that forms in one place, and it travels elsewhere to cause problems, that's an embolism. An embolism. I think of embolism. I think of embassies. Like, oh, if you want to travel to a different country, you go to the embassy of that country and get a visa. So, basically, a thrombus breaks, if a thrombus breaks off and then goes elsewhere, that's going to form...

That's going to be an embolism. Sometimes you call it a thrombo embolism. That means it's an embolism that formed from a thrombus. Now, you might have heard me say, Verkho's triad. Right? Verkho's triad underlies the formation of many thrombi, many embolines in the body. Right? What's Verkho's triad? Well, you can remember the monic sheet. The S stands for steases. Whenever you have blood steases, you can absolutely form embolines. I just kind of... a thrombi. I always think of it this way. Basically, if things... I just kind of think of it this way. Like, if you have food, that's like lumpy, that's like pasty. If you live here standing for a long time, it's going to congeal. It's going to coagulate, in a sense. So, basically, whenever you have blood, that's kind of static. For many different reasons. So, let's say, for example, a person has had a recent MI. The heart is no contracting well. Blood is going to be static in the heart. Or a person has a fib. And the left knee trim is no contracting well. Blood is going to be static. Or a person has had a very long plane ride. Blood is going to be static. That blood, when you're static, when it's kind of just hanging, hanging, hanging. It can begin to clot. You can form a thrombus or you can form an embolus. Number two, the H in the she stands for hyperquagulability. There are many things that make a person hyperquagulable. Many things that make a person hyperquagulable. OC Ps, cancer. Just many different things.

And then there is endothelial dysfunction. But if we have endothelial dysfunction, let's say you place a line. Let's say you place a central line. Or you place a peripheral line. Or you place an IV. Or you have atherosclerosis. All these things cause endothelial dysfunction. Those cancerlicos are a person to have a PE. Or I mean, have some kind of thrombus or embolus. So I think for the rest of this podcast, I just want to go straight into the classic thrombotic patterns that a lot of traditional exams. So let's start with the simplest one. What if they give you a question about a woman? She's a 30-week gestation. And she tells you that for the last two days, she's having very severe leg pain. And then they see on physical exam, the right lower extremity appears much bigger than the left lower extremity. If you say that, that's a DVT. It's pretty simple and straightforward. That's a DVT. And typically when people have DV Ts, you're going to diagnose it with an ultrasound of the lower extremities. I don't know what you're sound of the lower extremities. Typically, you get this, it's been literally it's got a deep venous thrombus for a reason. It affects a deep vein. Very, very common in women that are pregnant. Very, very common in people that have taken long-playing rights. Why may eat a rice in a person that is pregnant? Well, the reason they are rice is very simple.

If you're pregnant, especially like, as you go later in pregnancy, that gravity universe is going to be squeezing on the IVC. So everything that drains into the IVC, aka most of your body, is going to start back and open them, especially in your lower extremities. As that blood kind of backs up, as you have that stasis of blood, that's going to cause you to have a DVT. You're literally activating one of the components of a very good striat. It tends to affect the deep veins of the lower extremities like your femoral vein, for example. Like femoral vein IV, for example. Again, you're going to notice these people that are going to have like leg swelling, they're going to have pain, they're going to have a redness of that extremity. And typically, when a person has a DVT again, like I said, you're going to get an ultrasound of the lower extremities to make the diagnosis. And those people need to be placed on anti-coagulation. In this pregnant woman, we're going to give it a head print. It won't make sense to give her a warframe. Because if we did, warframe is a terrible thing, not a smart idea. So in that case, we're going to give that person a head print. Because again, we don't want that DVT to progress to a PE. Because if it does, that's a huge problem. Right? So PE is an symbolic complication of a DVT. PE is an symbolic complication of a DVT. In fact, they can give you an exam question, what is the biggest risk factor for PE?

The biggest risk factor for PE, live it or not, is a DVT. Because most P Es start off as a person having a DVT. And then that DVT, that thrombus, kind of breaks off, and then moves, travels, and goes to the person's heart. Okay, so let's go ahead and continue. Now, what if they give you a question about a 25-year-old male? They tell you that it's a bodybuilder or you own a gym. And that for the last day, he has been having like very severe pain in his right arm. Has very severe pain in his right arm. And you know, they tell you that he has been training a lot for a weak lift in tournament or whatever. And he has severe pain in his right arm. Again, they say on physical exam, this person has a very, very dilated, very distended right arm. If you see something like this, don't you think of Pajeche-roder disease? Pajeche-roder disease. This is basically a DVT, but in the arm. Typically, it's gonna be a problem with the axillary vein or the subclavian vein. So what's the path of this? Again, you can always, you can almost always trace any thrombotic or embolic phenomenon to having one of vehicle's triads. Well, think about it. If you're a bodybuilder, your gym owner, they're very ripped, very buff. All those muscles, remember, many people forget this. Veins are compressible, but odors are not. I mean, you can compress an odore, but you're gonna take a lot of extreme strength, which is not very common. But veins are certainly very compressible.

So if you're a person that's like very jacked, very ripped, all those muscle hypertrophy you get, especially when you've been working out your muscles a lot, they get very hypertrophy. Those hypertrophy muscles can literally squish the veins in your arm. Well, remind me again, one of the veins in the arm, or the acillary vein is a big one, the subclavian vein is a big one. I mean, it's pretty much the same vein, just changes name based on where it gets to. So when you compress those veins, you're gonna have stasis of blood in those veins. When you have stasis of blood in those veins, the thing that's gonna happen is, you're gonna develop a DVD, right? Your literally, it's basically a DVD of the upper extremities. We call it Paje, shorter disease. Paje is spelled PHET, shorter is SCH. RSCHROEWTER, okay? Paje is shorter disease. Paje is shorter disease. Paje is shorter disease, okay? That's probably about as much as you need to know. Typically, again, because of DVD, you're gonna put that person on anti-coagulation. Then put that person on anti-coagulation. Okay, now what if they give you a question about a patient? You know, they tell you that this guy has a hematocard of 75%. And this guy, you know, has this already appearance, whenever it takes a hot shower, he eats a lot. And then they tell you that, ooh, this person for the last 12 hours, he's been having very severe, significant red or percordion pain.

And they tell you that his abdominal cavity has increased dramatically in size. And you know, that his liver, you know, the liver spine is very increased. So when you see this, you'll be saying, oh divine, this person has BOTKIRRI syndrome. BOTKIRRI syndrome. BOTKIRRI syndrome is thrombosis of ward vein. It's gonna be thrombosis of the hepatic vein. It's gonna be thrombosis of the hepatic vein. Typically, it arises in people that have one of two disorders. It's gonna be PNH, paroxysmone, oxygenolhemocluidinuria, one example, or it's gonna be polycythemia vera, as is the case with this person. Remember, P-Vera is that jacked to mutation. They're gonna have a lot of red blood cells. But they're gonna have low Epo, cause of negative feedback. Low Epo is one of those causes of polycythemia that has a low Epo, right? So again, maybe like divine, why would a person with P-Vera develop this thrombosis? Will it make sense? It makes sense. It makes sense. Think about it. When you have polycythemia vera, your hemal creatives is ridiculous. You have a very high hemal creat. So your blood is super, super viscous. Or blood that's viscous, think about it. What's true of the vascular resistance? The vascular resistance is gonna be really high. Remember from P-Vera cells, one of the factors that control total peripheral resistance is viscosity. When you have polycythemia, your blood is super viscous. So that's super viscous blood. It's blood that doesn't flow very well.

It's like sludge, it's like slurry. That's like prime, prime, prime, prime, prime candidate for thrombosis. Right? So these people can have hepatic vein thrombosis. That's what we call balkyri syndrome. Remember, P-Vera cells, more or more like a merubinuria is also another cause of balkyri syndrome. This is the two classic things that cause balkyri syndrome on exams. Right? Again, you're gonna see the triad of severe abdominal pain, usually on the right upper quadrant. You're gonna see these rapid assidies. Long gradual assidies, rapid assidies. You're gonna see that their liver is huge. When you see that, especially in the person that has these risk factors, think of balkyri syndrome. Okay. Now, what if they give you a question about a person? They tell you that, ooh, that this person for the last two days, a person has been having very severe abdominal core vein, and they tell you that the person has developed some kind of assidies. But then they tell you that this person, you know, he's a victim alcoholic, or this person has a he's show of cirrhosis. And you know, the person had like pancreatitis like two, three days ago. They came in two, three days ago, they had a gastric vein going to the back. They got opioids, they metin PO, and they got better and went home. But now, they have this pain that has recurred. Very severe abdominal core vein, this crazy, crazy assidies that develops. Whenever you see this thing of podo vein thrombosis, think of podo vein thrombosis.

Remember, I said balkyri syndrome is a paddy vein thrombosis. The paddy vein drains the liver. The podo vein feeds the liver. Big difference. I'll say that again. The paddy vein drains the liver. The podo vein feeds the liver. Okay. The paddy vein drains the liver. The podo vein feeds the liver. That's a podo system. Remember, there are two venospodal systems in the body. There's the one in the liver. And then there's the one in the brain, that hypothelamic, hypophysial podo system. If you're looking at arterial podo systems where an organ is fed by an artery and drained by an artery, then you're gonna be thinking about the kidneys, right? Because the alpha and arterial feeds the glomerular capillaries. That's a capillary network. And then the glomerular capillaries are drained by the efferent arterial. The thing is, you put podo systems in place when you want to regulate stuff. When you want to have like very heavy relation of inflow and offload of an organ, you're kind of slowing the podo system there. But again, that's a topic for another day. So again, podo vein thrombosis, think about it with people that have, that have recently had a hypogrititis, who would have cirrhosis? Because cirrhosis is gonna mess up, cirrhosis is gonna mess up the fluid dynamics within your liver. Right? So you're gonna have blood steases. Because again, that blood is not flowing well. There's all this fibrosis, all this craziness in your liver. That's gonna cause problems.

And also, we would have like certain bilirium allignances, like oligio-corsinoma. These are people that have a very high risk of podo vein thrombosis, like your podo vein thrombosis. Again, you may be like, well, divine. Podo vein thrombosis presents very similar to what carousine is known. Yes, the presentation is very, very similar. The presentation is very, very similar. So sometimes they almost end distinguishable without you doing some kind of study, some kind of a geography. But just something you kind of wanna keep at the back of your mind, for example. But again, if you see a PNH or a P-Vera association, probably wanna go on a BODCHI-R-E syndrome versus podo vein thrombosis. But podo vein thrombosis, if you see like a histro-pancretitis, or you see a presence that has a histro-cerosis, or you see a presence that has a histro-colangio-corsinoma, think about podo vein thrombosis. Really, again, the presentation is almost identical to BODCHI-R-E syndrome. But is the associated disorder, it's gonna lead you in one direction versus the other again, P-Vera PNH, think of BODCHI-R-E syndrome. Recent pancretitis, cirrhosis, colangio-corsinoma, think about podo vein thrombosis. Okay, now what if they give you a question about a person? It's a guy, you know, has a three year histro-inferotic syndrome. And he has been on ACE inhibitors for his symptoms and you know, he'll get your teeth steroids.

But in the theory that this person has a sudden decrease in liver function, I mean, in a renal function, that this person's creatinine has bumped up significantly over the last two days. And the person has like very severe flange pain, very severe flange pain. Whenever you see something like this, what do you wanna think about? You wanna think about renal vein thrombosis, renal vein thrombosis. I'll tell you this right now, the biggest risk factor for renal vein thrombosis is nephrodite syndrome. I'm gonna say it again. The biggest risk factor for renal vein thrombosis is nephrodite syndrome. Okay, is nephrodite syndrome. So why do people that have nephrodite syndrome develop renal vein thrombosis or think about it? In a phrodite syndrome, you're gonna pierce out a lot of stuff. The stuff you pierce out is not only going to be albuming. One of the thing you pierce out is antithronome. The antithronome being three is an anticoagulant protein. How does he do that? Well, literally, inhibits factor two and factor 10. In fact, that's how heparin works. How does heparin work? Heparin is a stimulator. It increases the activity of antithronome being three about 1,000 foot, about 1,000 foot, about 1,000 foot. So that he can more effectively inhibit factor two and factor 10. That's literally how heparin works. So the thing is, people that have nephrodite syndrome do also reneed antithronome being three.

If you reneed antithronome being three, then factor two and factor 10 are gonna run a mark where you're gonna land in in some hot water. So if you see, again, sodding onset flunk being a person that has nephrodite syndrome, I noticed that man, this person's renal function is decreases precipitously. You notice that they go from creating of like 1.5, to creating of like four, in a very short time frame, think about renal being thibalosis. It is very, very, very common in nephrodite syndrome. Okay, it's a very common complication of nephrodite syndrome. It's a very, very common complication of nephrodite syndrome. And then, they give you a question about a person that you know, they tell you that, oh, this person has some kind of facial infection. You know, they've had like a nose infection or cellulitis or a cellulose on the face. And in detail to that man, this person, over the last two days or whatever, or last few hours, the person has developed a very severe headache, very, very severe headache. And then, this person, they're telling you that, ooh, this person's extracurricular muscles are not working as well as they shoot. They're not working as well as they shoot. If you see something like this, think of cover nose sinus thrombosis. Think of cover nose sinus thrombosis. The thing is many of these thrombotic issues, you can know exactly which is which, by just looking at the presentation.

That's why if you notice, I'm trying to give you classic presentations of these things. You're gonna see a person that has some kind of facial infection, infection in the face, infection in the nose, infection in some kind of sinus. And then, these later, they develop headache and see cranial nerve deficits. More specifically, it's muscle cranial nerve deficits, especially cranial nerve six. Cranial nerve six is the most commonly impacted vessel in a cover nose sinus thrombosis, because literally passes through the middle of the cover nose sinus. If you see that presentation, think of cover nose sinus thrombosis. Typically, staff warriors is the most commonly implicated bug that instigates a person to develop cover nose sinus thrombosis. So again, basically, if you have an infection in the face, it can spread through those facial, those veins in your face, and spread into the cover nose sinus. And why is cranial nerve six the most commonly affected again? Because cranial nerve six literally runs through the middle. So it's almost like the person that gets everything from every side. So because it's in the middle of the cover nose sinus, you almost always, if you have an extracurricular muscle cranial nerve that's not working, it's gonna be a lot of rectus cranial six with cover nose sinus thrombosis. So again, very, very high yield to know and understand the stuff.

So now that we're done with the venous thrombosis, there are others, but again, these are the classically tested ones on exams. Let's go through the arterial thrombosis. Real quick, I'll put a plug in if you're a taking. Step one, two, step three. I have two classes on actually an extra Monday and Tuesday, then you find to be very, very helpful for your exams. I have a four-hour biostatistics class and a five-hour social sciences and ethics class. The social sciences class covers quality improvement, healthcare systems, professionalism, communication. Just many different things. Like those grab bags of topics that fall on the social sciences and ethics, right? Many people, they're like, wow, divine, 10 to 15% of my exam is the stuff these days. And that is no joke. That is no joke. Like literally one out of every eight or nine questions on any USL exam these days is an ethics, social sciences, healthcare systems, QI, communication, professionalism question. It's a five-hour class, very high yield. Again, I've had people attend the class and be like, wow, divine, I took my exam and I could answer every single bio-stats, every single ethics question, every single social sciences question that I saw. Also, for step one to three, also have a bio- an NV Me test taking strategies class, that's gonna be next month on the 17th of March.

And then if you're taking step one, I have a step one review, it's a 25-hour step one review, that's gonna be taking place next month as well in the month of March. I have an announcement podcast on that. Just check out the website. And then finally, if you're taking step two or step three, have a 20-hour review, that's gonna be taking place next month as well. Again, I made a podcast pretty recently on that. Just listen to that podcast, don't tell you about the dates and the times. If you want more information, just should be an email through the website. And I'll give you some more information on how to register. All these classes are held over Zoom. Again, many people have taken these classes, found them to be tremendously helpful. I've got in emails, even as recently as like last night, to a person that took one of these classes and did extremely well on the exams. You could be one of those people, so just reach out to me through the website and I'll give you some more information. So let's go to the material from both of these. The material from both of these, thankfully, to be honest with you, these ones are actually pretty bad. You know, videos from both of these, they're not ideal. But many times people recover. The material from both of these, you should have some pretty devastating consequences. I mean, like, for example, most strokes are some kind of material from both of these. Most M Is are, I mean, every M Is is a material from both is pretty much right?

If you occlude like your LED or whatever, that's a material from both of these. Well, you see a person that develops a cutely embiskemi, you see a person, typically it's gonna be a person that has a history of e-fib, or a person that has had a recent MI, right? Person that has a history of e-fib or recent MI. And they notice that, hmm, this person, they tell you that they have this solid nonsense if you're depending there in one of the extremities or whatever. Think of a cutely embiskemi, they tell you that you don't feel any pulses. That's a very big difference between a DVT and an acute limbiskemi. And a DVT, the pulses are still gonna be intact. The lower extremity pulses are still gonna be intact. But if you have a cutely embiskemi, the pulses are gone. That's a very nice way to tell, because a cutely embiskemi is an arterial thrombosis. A DVT is a venous thrombosis, very big difference, very, very big difference, right? Although an acute limbiskemi has more from symbolic phenomena, DVT is more from thrombotic phenomena. But again, use that pulse to, use the presence of the absence of pulses to help you differentiate those two things, okay? Very, very important to keep that in mind. Obviously, if a person has a cutely embiskemi, your very first step is you're gonna give those people a pepper. After that, you're gonna do some kind of CT angiogram. And this is a surgical emergency. That person's gonna need an embolectomy very, very quickly, very, very quickly.

Okay, now, this whole concept of people that have a recent MI or have a fib, they can actually get thrombosis of many things. So just be careful, they can get many different kinds of arterial thrombosis. I just used a cutely embiskemi as my model, right? Where you can occlude like the popleytil artery, or the femoral vertebral artery or something. But you can occlude many different arteries. Believe it or not, people that have a history of e-fib or a recent MI, they can actually occlude that e-yoda. Believe it or not, they can occlude the e-yoda. Basically, the place where you have the occlusion tells you how many symptoms you're gonna have. Sometimes people can have like this, almost like bilateral limbiskemia. Because they occlude the e-yoda very high up, right? They can have like an e-yodic embolism that can cause that problem. They can also have, you see them, again, e-fib, a recent MI, they have like very severe sodium-nose-yod abdominal pain. They think about like acute mesenteric ischemia. It basically form a clot somewhere, an embolus in your heart, flicked off and then it went and pretty much occluded one of your mesenteric vessels. Many times it's gonna be the superior mesenteric artery. The person's gonna land in some very big trouble. Now, the very last one I think I wanna talk about is, what if they give you a question about a person, they go to liver transplant within the last few weeks.

Usually this is something that happens like less than four months after a liver transplant. And then the person just develops very severe abdominal pain. And you notice this profound rise in the AST and the AST. And it's gonna be very sudden. It's gonna be very, very acute. I'll say this again, you see our presence that had a liver transplant weeks ago. This is a classic pattern. This is a classic pattern. So, personally, had a liver transplant weeks ago, weeks, weeks, weeks ago. And they notice that over the last like 12 hours, they are AST, AST just go berserk, just go crazy. And you see them, they develop this very rapid asides and all of this badness. In fact, actually, to be honest with you, these people may not necessarily develop asides. So, asides is not a very common finding in these people. But you're gonna see a person very crazy, crazy rise in AST and ALT, especially AST, the AST goes up a lot. And you see they had a transplant a few weeks ago. When you see something like this, don't you think of hepatic artery thrombosis? When you think of hepatic artery thrombosis. Hepatic artery thrombosis. So, maybe like divine, can't this be rejection? Can't this be like a transplant or a leery infection? It can be. But the suddenness of the symptoms is the thing that tells you that, man, this is hepatic artery thrombosis. Hepatic artery thrombosis is the most common, if I'm not mistaken, but also the most devastating complication of a liver transplant.

Again, it's a very common pattern of thrombosis that can develop after a liver transplant. That's probably about as much as you need to know about hepatic artery thrombosis. So, I think I'm gonna go ahead and stop here. Again, please, I'm begging you, this podcast is extremely high-end. For all the USML exams, step one, step two, step three. I'll be very shocked. You take any USML exam, and you don't see one question that kind of dances around one of these concepts. So, pay attention to it. Super, super high-end. I think again, it's something I'm gonna find you to find to be profoundly helpful. Okay, so, again, as I do at the end of the review, podcast I offer one or one tutoring for all the USML exams. Step one to step three, complex one to three. And then I also offer tutoring for shelf exams, and preclinical medical exam. And then finally, I also have these podcasts on Apple podcasts on Google podcasts on Spotify. Just check those out. I actually have a You Tube channel to run intervention, USML, podcast and videos. That's where I post the videos I make. And I also post some versions of these audio podcasts on that You Tube channel. And then, I also have with applications, eras applications, personal statements, letters of recommendation, mock interviews, things like that. And then I also have, again, review courses for step one, for step two and step three.

And then, you know, for step one, all the way to step three, have the four biostatistics class, the five hour social sciences and ethics class, and the two and a half hour NV Me testing strategies class. And then finally, finally, finally, also have another website called divininterventionallifelessons.com. Many people were like, wow, divine. I love the life lessons you post at the end of your podcast. So I was like, you know what, I might as well just go ahead and make something separate website. And then, you know, you can go to divininterventionallifelessons.com. It actually has an Apple podcast as a shooter with it. It's called the divininterventionallifelessons podcast. Basically, every week I post two podcasts about 10 to 20 minutes long and from a biblical perspective, address a common life problem that people face. We've talked about many things from anxiety, to depression, to exposures, just many different things. Again, it's something that many people have found to be really helpful. So check that out, divininterventionallifelessons.com. Again, it's also an Apple podcast. So joining me today, I will see you in the next podcast, episode 445. We finally did the Lostress episode 4444. So thank you for joining me. Have a wonderful weekend. Bye for now. God bless you.

A thrombus forms within a blood vessel; an embolism is material (like a clot) that has broken off and traveled elsewhere.

Stasis (slow flow), Endothelial Injury, and Hypercoagulability.

Oral Contraceptive Pills (OC Ps) or malignancy/cancer.

Paje-Schroetter Syndrome.

Paroxysmal Nocturnal Hemoglobinuria (PNH) and Polycythemia Vera (PV).

Cranial Nerve VI (Abducens nerve), because it passes through the center of the sinus.

Virchow's Triad: Stasis, Endothelial Injury, and Hypercoagulability.

Mechanical compression of the IVC by the gravid uterus.

Paje-Schroetter Syndrome (or Effort Thrombosis).

Budd-Chiari Syndrome.

Nephrotic Syndrome (due to loss of Antithrombin III).

Cavernous Sinus Thrombosis.

In DVT, peripheral pulses are usually intact; in acute limb ischemia, the pulses are absent.

Virchow's Triad: Stasis, Endothelial Injury, and Hypercoagulability.

Mechanical compression of the IVC by the gravid uterus.

Paje-Schroetter Syndrome (or Effort Thrombosis).

Budd-Chiari Syndrome.

Nephrotic Syndrome (due to loss of Antithrombin III).

Cavernous Sinus Thrombosis.

In DVT, peripheral pulses are usually intact; in acute limb ischemia, the pulses are absent.