DIP Episode 651 - USMLE Step 2/3 Rapid Review Series 136

All right, welcome. My name is Devine. This is episode 651 of the Divine Intervention Podcast. To this podcast, we're going to be continuing the Rapid Review Series for step two and step three. Okay, so today we're going to be continuing the Rapid Review Series for step two and step three. Again, a lot of very important things out to be discussed today. All right, so let's jump right into it. So what if they give you a question about, and I'm going to be making quite a number of kind of strange integrations today. So I'd keep this in mind. So I want to focus on a lot of, you know, you'll see what I mean. I'll say go. So what if they give you a question about an old guy, right? And he has like very severe abdominal pain, right? He's a smoker and they tell you that you feel a positive or abdominal mass, right? What should you be thinking about? Well, I'd really hope you're saying that, oh, divine. This sounds a lot like a ruptured triple A, right? This sounds an awful lot like a ruptured triple A, right? So this person has a ruptured abdominal leotic aneurysm, right? And remember, triple A is typically, typically they're going to arise below the renal arteries, right? I think that's one of those kind of high old things you want to make sure you know for your exams, right? They typically arise below the renal arteries. They typically arise below the renal arteries, right? And again, what's the biggest risk factor for an abdominal aneurysm?

Well, the biggest risk factor is going to be smoking, right? Smoking is the biggest risk factor for abdominal leotic aneurysm, right? And one thing you notice on the USMLE exams and this is something you should certainly look up is that sometimes when a person has a triple A that is ruptured, about ruptured, let me show you something called the dripte-yother sign on imaging, right? The dripte-yother sign on imaging, right? So what does that mean? Well, the thing is typically when a person has the dripte-yother sign, it's something you see typically on a CT scan, right? But you'll notice that that the posterior wall of the order, right? The posterior wall of the order, like the margins are very indistinct, right? Very indistinct, right? It's almost like the aorta, the posterior aorta, is draping over the walls of the vertebra because remember the red vertebra come behind or they're very closely associated with the aorta, right? So that's something that's really known for exams if I review, right? So the dripte-yother sign is one of these stains, it's old-timer old-school but it's pretty high to know for your exams, right? And remember, people that have a ruptured triple A, they're going to be hemodamically unstable, they're going to have flank pain, they're going to have back pain, right? Because again, remember the triple A, the abdominal aorta is retroperitoneal, right?

Now, the thing is sometimes our friends at the MBM Es, again, especially they know that these days we live in an Anky and an AI generation, right? So one thing they love to do is instead of just asking about a classic association, they will ask you about the underlying mechanism or the underlying path of physiology. Do not be afraid to pick an answer that talks about elastin and collagen degradation on your test, you're like, wait, what? Yes, I mean exactly what I just said, right? Elastin and collagen degradation in the media, right? From increased matrix metalo-proteinase activity, right? I'm going to say that again. So the thing is when people have a ruptured triple A or when people have an abdominal euric aneurysm, right? The mechanism there is they have increased matrix metalo-proteinase activity, increased matrix metalo-proteinase activity, right? When you have an increase in the activity of matrix metalo-proteinase, that is going to lead to the degradation of elastin and collagen in the media, in the media of your abdominal euror and that can cause problems, right? And the thing is, is actually kind of high you to know that statins decrease the activity of matrix metalo-proteinase, statins decrease the activity of matrix metalo-proteinase, but smoking increases the activity of matrix metalo-proteinase, right? Proteinase again, something that breaks down proteins, right? Think about it for pressing a COPD, right?

There's all these proteases in the lungs that have increased activity with, smoking, right? So I want you to kind of link those activities together. Proteinase, protease, right? They're kind of similar. Proteinase, protease, protease, breakdown proteins, proteinase, breakdown proteins, right? It's kind of the same idea. All right, so this is part of the reason why when people have atherosclerotic cardiovascular disease, we tend to put them on statins on high intensity statins, why? Because again, we want to decrease matrix metalo-proteinase activity in those vessels, right? So that they don't, you know, have like a plaque rupture or whatever, right? Again, guys, please, today's podcast has a lot of strange things, but they are very high you things to know for your exams, right? And again, you know, again, sometimes on the exams, concerning the triple-ledic and ask you like, what's the mechanism behind these people having back pain? Well, again, typically for the ruptures, it's going to rupture into the left retroperitoneum, right? It's going to ruptum, I'm not saying always, right? But it can typically rupture into the left retro-neum, right? So they can have back pain, just kind of like you have with acupunctitis, which is also, you know, your pancreas, especially certain parts are retroperitoneum, right? And again, what is the most common location of a triple-lay, of a triple-lay, of the rupture and whatnot? It's typically going to be below the renal arteries, right?

And it's going to be above the aortic bifurcation, right? Again, the USML disease these days has become an exam of surrogate, right? It has become an exam of surrogate. They won't typically test you on something direct, they will ask you about something that surrounds the concept, a surrounding concept, right? So it can be a triple-lay question, right? It can be painfully obvious that, oh, yeah, of course, it's a triple-lay question. But then they ask something that you're not expecting, right? So the most common location is going to be below the renal arteries and above the aortic bifurcation, right? And again, remember, when people have aortic aneurysms, right? Typically, we're going to monitor, you know, we monitor these people, right? We monitor these people like every year, or they're about, right? And we're going to intervene if the aneurysm grows by more than half a centimeter in six months, or a centimeter in a year, right? We're going to fix it. And all this situation where we would also fix a triple-lay is if it's more than five and a half centimeters on initial screening, right? Or you have symptoms, right? You're like very symptomatic, you have in CBS symptoms, we're going to go ahead and fix it, right? Or if imaging shows something very concerning, like this drip the other sign, you know, even if it has no rupture, we're still going to fix it as well, right?

Now, what if they give you a question about a patient and they tell you that all this patient just came in for a triple-lay repair, right? And then they ask the tell you that all the patient passes away, you know, like 24 hours after repair. And then they ask you what is the most likely cause of mortality around the repair of this person's triple-lay? I would really hope that you're going to pick the answer that talks about a myocardial infarction. I would really, really hope that you pick the answer that talks about a myocardial infarction. The USMLE is the like to ask these questions that talk about the most likely cause of mortality, the most likely prognosis, right? These are things that I address in many of my podcasts and also address pretty heavily in my classes, right? But the most likely cause of mortality around the triple-lay repair, right? A person that is had their triple-lay repaired, right, is a myocardial infarction, right? And the thing is sometimes on you exams, they can ask that, oh, which of the following provides the best outcomes between endovascular aneurysm repair and open repair? The thing is that they likely have similar, it's not likely they largely have similar survival outcomes, right? And then what if they give you a question about a patient? And this patient has had his abdominal leotic aneurysm repaired, right? And then they tell you that all prior to the patient departed from the hospital, they do a CT angiogram of the abdomen, right?

And they notice fluid extravacating into the excluded aneurysm, they notice fluid extravacating into the excluded aneurysm. When you exams, you want to think of the answer that talks about an endolique, think of, think of the answer that talks about an endolique. An endolique is actually more common with an endovascular aneurysm repair, with an open repair, right? But make sure you know that concept of an endolique, right? So that endovascular procedure you did, things are still leaking a little bit into the excluded aneurysm, right? Now, what if they give you a question about a patient that has had, I'm trying to make this rapid review like a thematic review. And by the way, this is rapid review series 136. I want to kind of make it a thematic in a sense, right? So what if they tell you give you a question and detail you that, oh, this person, you know, has had his abdominal leotic aneurysm, you know, the patient was admitted to the hospital 24 hours ago as had the aneurysm repaired. And then this patient has bloodied diarrhea, has very severe abdominal pain, has lucositis, right? When you see something like this, I want you to consider ischemic colitis, ischemic colitis, right? Ischemic colitis. Again, the thing is repairs of triple laser and not necessarily low risk surgery, right? There's certainly not low risk surgery, right? So one thing that can happen is that you can have ischemia to parts of the, you know, to branches off of the yoder, right?

And that can cause problems, right? Like this person having ischemic colitis. Many times you can try conservative treatment for this, but if there are signs of necrosis, you need to go ahead and resection to go ahead and resect, right? Or they give you a question about a patient and the tell you that the patient is like completely paralyzed in the bilateral low extremities after triple repair. Then the thing is certainly want to think about is a person having an anterior court syndrome, right? Where they've pretty much infarcted the order of a damn cowards, right? Which supplies the anterior to the third of the spinal cord. You'll notice that those people they are completely paralyzed, you know? They're completely paralyzed. The only thing that will be intact spinal cord wise will be fine touch, vibration and perperceptive sense, right? Because remember the Dorsal Columns and the Buster third of the spinal cord, right? And then what if they give you a question about a patient and they tell you that this patient, you know, had a triple repair two years ago and just returns for a full-up exam. And this patient has a hemoglobin of 7.5 and you're told that, you know, test of his stool for blood is positive, right? That he has hemocort positive stool. If you see something like this, you really, really want to think about a person having something called an aeodotentoric festiola, an aeodotentoric festiola, right?

So basically these people are from the festiola, from the aeodot, right? From the aeodotism that was excluded to their GI tract. So they're literally bleeding into their GI tract, right? These people are going to need vascular imaging of the GI tract pretty quickly, like a CT and geogram or something like that. And you need to fix that problem. If not one day, they're going to have a catastrophic bleed and then they're they're almost certainly going to die. All right. Now, what if they give you a question about a patient, right? That presents with a ruptured triple A, right? Or it looks like a ruptured triple A and they're hemodynamically stable on initial presentation. What kind of diagnostic testing do you want to do? Well, again, I'm hoping you're picking the answer that talks about a CT and geogram, but if they're unstable, right? And they have direct physical exam findings, you know, like they have a pulsed out mask, for example, pick the answer that just digs them straight to your pretty room. Okay? Pick the answer that takes them straight to the operating room. But if they're unstable and they have no direct physical exam findings, get an abdominal ultrasound going. All right. So let's talk through these treatment decisions, right? All these diagnostic workup decisions. For patients are ruptured triple A and on initial presentation, they're hemodynamically stable, pick a CT and geogram, right?

If they're unstable and they have direct physical exam findings, like a pulsed out mask, dig them to the operating room. But if they're unstable and they have no direct physical exam findings of a ruptured triple A, go ahead and do an abdominal ultrasound, right? Now, what if they give you a question about a patient that has very severe gastric pain, right? And they tell you that this person has a history of osteoarthritis and the person has been on chronic pharmacotherapy. Well, I'd really, really hope that you're thinking about a person having like some kind of GI ulcer, right? Like a gastric ulcer or a blood no ulcer, right? Now, the thing is, I tried to be kind here with my initial presentation. A person has the HIKF STS 30th and again, chronic pharmacotherapy, right? They know that all of you have memorized that. Let's do a more difficult vignette. What if they give you a question about a patient, right? And by the way, this person that I just give the easy vignette for, right, has an end-set induced apeptic ulcer disease, right? What if they give you a question about a patient and this person has a history of like severe asthma and the person has been on chronic pharmacotherapy, right? And then the person presents with a cure on set, very severe gastric pain. Then I'd really hope you're seeing that, ooh, divine. This person has a steroid induced ulcer. Whoa. Yeah. Right? You know, I tell people this in many of my classes, right?

Many people always flip out about a USMLE pool changes, right? Let me tell you this. The USMLE is when they do a pool change, right? It's not like they just manufacture like tons and tons and tons of new topics that nobody has ever seen before, right? Don't get me wrong, many cities and ever-expanding science, but it does not expand so much that they can generate completely new topics every single time. No, that'll be ridiculous because they still need to test the basics that people need to understand. But what do they do? What's a pool change? A pool change is the same concept tested differently in many cases, the same concept tested differently in many cases. Right? So just keep that in mind as you prepare for your, for your exams, right? So this person, you know, because they know that many of you have memorizes in probably every on-key deck known to mankind, right? Or you've probably seen a bunch of Q-Bank questions on this, you know, pressing chronically taking in sets for whatever reason, and then they have like sodium-on-set CVAP gastric pain, they probably have like a ruptured ulcer, right? Sorry, I preferated ulcer, right? But you know, one of the things that cause ulcers and the person can have a Q-doncet CVAP gastric pain, it can be a person that chronically takes steroids, right? Well, the person can even have just chronic AP gastric pain, right? That steroids have caused ulcers, right?

This is why if people are going to be on steroids for a long period of time, you tend to, you tend to put them on PPI's, right? Or you see a person having like very CVAP gastric pain, after they've been in the hospital for like a, a virus, you know, bleed that was treated, again, they have an ulcer, right? Remember, if you have a lot of blood loss, that can cause this Schemia to your GI mucosa, and that can cause ulceration of your GI mucosa, right? Or they can give you the exact same question in a person that has, that has suffered a severe burn, right? And the person has had a stable course in the hospital, and then the solely staff complete of CVAP gastric pain, right? You see free air under the diaphragm, right? They have an ulcer that has ruptured, right? That's like a curling ulcer, right? So remember, we can see these things in both with burns, people with the Schemia, people with increasing chocretino pressures, and things like that. All right. Now, what if they give you a question about a person, right? That, you know, has a history of high blood pressure, right? Again, this is going to be an easy video coming in coming through here, right? Tearing chest being redid into the back, I know some of you are like, you divine, eortic dissection. Yes, it's a eortic dissection, right? Remember, typically on imaging, you're going to see a white in the medium, right?

And again, sometimes on your exams, instead of putting eortic dissection as an answer, they'll put vascular intimaltir as an answer. Again, they'll put a surrogate for what they know that you know, right? It's a vascular intimaltir that de-sex through into the media, right? Creates that false lumen. All right. Now, what if they give you a question about a person that is a 45-year-old female and a BMI is 42, right? And she has like very significant upper abdominal pain, right? On your exams, significant upper abdominal and back pain. If you see this on your exams, what should we think about? I really hope you're saying that divine, this sounds an awful lot like acute pancreatitis, right? So again, remember, it's not always people that are alcoholic that will get acute pancreatitis. People that are also obese can get acute pancreatitis. People on GLP1, Agonis can also get acute pancreatitis. People on Valparicacic can also get acute pancreatitis. People on Stavgidin and Dydanosin can also get acute pancreatitis. There are many of the HIV drugs that cause acute pancreatitis, right? So keep that in mind on your exams, right? Now, what if they give you a question about a patient and they show you an EKG and they tell you that this patient for the last three, four hours has been having very severe upper abdominal pain, right? Severe upper abdominal pain or they can see severe left upper quadrant pain, right?

When you see something like this and they show you an EKG, you notice that, well, the curious complexes are on our robot, the spaces between the curious complexes are diminished, right? Or they show you a subtle pattern on an EKG. When you see something like this, I want you to think of acute mesenteric is Schemia. Acute mesenteric is Schemia, right? So the thing is that first EKG I described is a person that has a fib, right? The second EKG I described is a person that has a flotter, a troflotter, right? Believe it or not, it's not only people that have a fib that can get this problem that this person has of acute and mesenteric is Schemia, right? If you have any other rhythmia that causes an uncoordinated contraction of the heart, right? So say, for example, a person has a fib or a person has a troflotter, the person can have acute mesenteric is Schemia that way. And also, don't forget, if you've had a recent MI cardiac muscle as died, so your cardiac muscles are not contracting a unison, they're not contracting in a coordinated fashion, that can also cause acute mesenteric is Schemia, right? And this person that has the left upper quadrant hurting probably has an occlusion of the superior mesenteric artery. That's probably one of the more common arteries that are occluded in acute mesenteric is Schemia on the USMLE exams, right?

Now, what if they give you a question about a patient, you know, that has, you know, you have this 68-year-old male and they tell you that he has a histro of like blood in his stool, right? And then for the last two days, he has been having very severe pain on the left side of his abdomen, right? And the, you know, give you a temperature, you know, left side of his abdomen, you know, they'll be intentionally vague, if they want to be nice, they'll give you left lower quadrant pain, but sometimes they can be intentionally vague and say, you know, left side of the abdomen, right? And this patient has a fever. If you see something like that, you really want to think about that particularitis, right? That particularitis, right? So this person has a histro of painless, you know, bloody bowel movements, right? That's going to be diverticulosis, right? Now this person has fever, this person has left lower quadrant pain, a thing called diverticulitis, right? I remember when a person has diverticulitis, you want to diagnose it with a CT scan and do not do a colonoscopy, do not do a colonoscopy, right? So you don't rupture the person's bowel, you don't rupture the person's bowel. Keep that at the back of your mind as you prep for your, prep for your exams, right? And then, let's just run through a few risk factors real quick, right? So what's the biggest risk factor for a triple A? You know, at least that's going to talk about some of these topics we've talked about, right?

Remember it's going to be smoking, right? What was the biggest risk factor for your redisection? Remember it's going to be high blood pressure, high pretension. What is the biggest risk factor for a stroke? Or remember it's going to be high blood pressure, right? And there was the biggest risk factor for coronary artery disease. It's going to be smoking, it's going to be smoking, smoking, smoking, right? It's going to be smoking, smoking, smoking. You know, there's one confusion that many people kind of pop up with these days on the exams and I see this all the time already and I'm like, what are these people doing, right? See guys, the fact that something is a modifiable risk factor does not make it the biggest risk factor for a problem. It just means that oh, you can modify it basically like, who you can maybe stop doing that thing and you won't get that bad outcome. But the fact that something is a modifiable risk factor does not necessarily make it the biggest risk factor for a problem. Just keep that in mind, right? And then another basic we want to know about triple lesions. We've said so much about triple les today. Remember the screening guideline, right? If you have any smoking history, right? I have between the ages of 65 to 75 and you're a male, we're going to screen you with an ultrasound, right? And also if you're a first degree relative, you should also screen first degree relatives, right?

So if you have a first degree relative that has like a triple leo, he's from a triple leo, you should get screened for a triple leo if you're a man, right? If you're a man, if you're a man. So keep that in mind on your exams, right? And what's the no more diameter of the other, below the renal otters? It's typically two, right? But also it becomes more than one, you know, it becomes 1.5 times or more that amount, right? So like three centimeters or more, then that tells us that okay, you have an abdominal, a uric aneurysm, right? So remember again, if it grows by more than half a centimeter and six months or a centimeter in a year, it's like, we're going to fix it, right? If it's more than 5.5 centimeters on initial presentation, ooh, we're going to fix it. If you're symptomatic, ooh, we're going to fix it, right? So keep that in mind for your, for your exams, right? Now, what if they give you a question about a patient that has, um, sodium onset severe leg pain, right? And they have like no pulses in the legs, they have like just very severe pain, a lot of paresthesia, a lot of power, right? They have like power, they tell you that they have like unilateral lower extremity power. Then you want to think about acute limb is skinny. Think about acute limb is skinny. Today, I'm trying to introduce concepts with simple, I want to kind of kind of get you thinking like the NV Mes.

I want to introduce the concept with a simple vignette and then start going into the more difficult directions that they love to exploit, right? So you're like, okay, divine, yeah, pain in the low extremities, sodium onset, no pulses, paresthesia, power of the extremities. Of course, divine dots are cute limb is skinny, all right? Good, right? And the easy peasy one is you're going to find that in people that have a history of a recent MI or people that have a history of a feb, right? Think of acute limb is skinny, no big deal, right? No harm, no foul. Okay. Now, let's go in some strange directions that you may see on your exams, right? So first thing is obviously, right, these people found an embolite in their heart, right? The person probably has like a feb or a recent MI from the nimble line embolos in their heart, and then they flick the length and occluded a low extremity vessel, right? Now, sometimes on the USML exams, they want to kind of trick you with between this and compartment syndrome, right? So be careful, right? The thing is people that have compartment syndrome typically, they're going to have pain with just any kind of movement of the extremity, right? Pain with literally any kind of passive motion of the extremity that's compartment syndrome. That's not going to be acute limb is skinny, right? So just keep that at the back of your mind for your exams.

And typically, compartment syndrome tends to be associated with trauma as against acute limb is skinny, that tends to be associated more with, you know, like recent MI or a feb and things, things like that, right? And then, if they give you a question, again, let's do some simple things and then let's start hitting some strange things, right? So if they give you a question about a person that, you know, is a big time smoker, right? And the person has pain with walking, that improves with rest, right? Think of peripheral atrial disease, right? Sometimes on your exams, instead of using the term peripheral atrial disease, they'll use the alternate name chronic limb ischemia, okay? So there's acute limb ischemia and then there's chronic limb ischemia, chronic limb ischemia is literally another name for a peripheral atrial disease. Again, remember the USML Es, they may use alternate names on your exams, right? And then remember, if a person has chronic limb ischemia and you notice that these, they study having paralysis, that may be an indication that those people need some kind of a probably they need amputation or they need immediate vascular intervention, right? And then remember, the most common cause of arterial embolized going to be a fifth, the most common cause of arterial embolized going to be a fifth, right? Okay, now what if they try to give you an anatomy question with a person that has acute limb ischemia, right?

And they tell you that, you know, the person has like unilateral food and calf pain, right? And the person has barely palpable or very indistinct femoral pulses and no pulses in the no, you know, pital pulses are absent and whatnot. Where's the problem? Where's the occlusion? Well, the occlusion is going to be at the common femoral artery or the superficial femoral artery, right? But if they give you a question about a person that has like unilateral food pain and they have intact femoral pulses, but they have absent pital pulses, absent pital pulses, they want to think about this person having occlusion of the publictile artery, occlusion of the publictile artery, right? Now, our friends at the MBM is they can literally give you an acute limb ischemia question and ask you like, what's the most likely mechanism behind this patient's presentation? And you'll put an answer that talks about embolic phenomena, you'll put an answer that talks about thrombotic phenomena, you'll put an answer that talks about a vasculine interruption or something like that. What answer should you pick? Let me let you think about that for a second. What answer should you pick? What answer should you pick? Well, please pick the answer that talks about thrombotic phenomena. Whoa, divine. Have you always thought that I can't leave the ischemia and well secondary trombolic phenomena? No, it's not. No, it's not. The most common cause actually believe in an all these thrombotic phenomena, right?

So you have an atherosclerotic plaque in a vessel, especially people that have a histroperephilateural disease. It ruptures, right? And then goes and occludes a distal vessel or whatever, right? Kind of like an M.I. It's almost like an M.I of your lower extremities, like an anorexramity artery, right? So remember, the most common cause of acute limb ischemia is a thrombotic phenomenon, kind of like an M.I. Not necessarily embolic. I know many resources, even I have, you know, talk about aphab, recent M.I. A. flotter, from an embolus in the heart, flicks of goals or clues, a lower extremity artery. Yes, yes, yes, yes, yes, yes, yes, but the most common cause is thrombotic, right? The USM is they love to throw these epidemiologic questions. They love to throw these epidemiologic questions, right? You can see that if you've not heard this from this podcast, I can almost promise you you probably get the stuff wrong on an exam, right? And again, remember how do we treat acute limb ischemia, right? Pretty straightforward, right? Go ahead and give them heparin, right? Give them some kind of anti-conculation, right? Heparin, right? And in do of, do a CT and diagram of the lower extremities, right? And again, if you notice that they have like an irregular rhythm on a quotation, you should probably go ahead and get a TTE trans-thoracic echohodogram to maybe screen them for like some kind of clot in the lefty trill appendage, right?

And typically, we're going to manage it with an embolectomy, right? We can do a catheter, direct it through thrombolysis, right? Although that tends to be more for malchesis. And then what if they give you a question about a patient that you know, they had a acute limb ischemia, they were successfully re-vascularized. And then they give you an EKG. I noticed that, this person has like a YQRS and they're creating a study, a study rising. He's like, gee, what's going on here? If you see something like this, I want you to think of a reprovision injury, right? Reprovision injury, right? So remember, after you fix a part of a limb that has been ischemic, sometimes that reprovision, you know, the influx of blood and oxygen back, sometimes can cause like some ferroidic odamage. And you start having muscle cells exploding, right? You'll notice that this was creating kinases elevated, right? And they can have like, because muscle cells are exploding, because of the ferroidical injury, they may have myoglobinuria, that's what's causing the creatinine to rise, right? And as those muscle cells are exploding, remember potassium is an intracellular eye. Right? So those people can have hyper-kilimia. This book can have what hyper-kilimia. This book can have what hyper-kilimia, right? Obviously, right? Like if they're having these EKG findings, you want to go ahead and give them calcium, glucone, calcium, glucone, calcium, calcium, glucone, all right? So stabilize that, myocardium.

All right. So thank you for listening to me today. I think I'm going to go ahead and stop here. I think I've made a lot of, not for vascular integrations, right? So please, this podcast is just one of those rapid reviews that kind of sits there on its own, but there is so much higher stuff I talked about today, right? And if you love the way I teach, you're going to love my classes. You know, literally starting next week, Tuesday, I have a 25-hour step one review for step one and for those taking step two, step three, that have a poor or a distant B6 science foundation, right? Tell me that that class is going to be really, really helpful to your to your studies. It's going to be really helpful to your studying, because again, the USML is these days on step two, step three. They have started testing B6 sciences more and more, right? In fact, these days, I think I strongly recommend more and more people take that step one class. And then, you know, after that, so it's a 25-hour class, and then after that, I have a step three CCS framework class, right? So if you're taking step three, I want to think of it as like the pathophysiology of CCS cases, right? I have that class on the 18th. And then I have a testing strategies class that's for step one to three, Biosdats class for step one to three, social sciences, quality improvement, ethics, and a hospital medicine review, also for step one to step three, right?

And then after that, I have a last mini review, just for step two and step three, and a 20-hour step two step three review, right? And then in the month of June next month, I have a very, very clutch 50-hour step two step three review, right? We go through tons of questions that that class is just exceptional, right? Very, very, very limited sports still available. So if you're interested, shoot me an email and I can give you some more information. I remember I also offer one on one tutoring for all the USML and complex exams, and I have this podcast on Apple Google and Spotify, and I have a You Tube channel, Divine Intervention, USML, Podcasts, and videos where I have some really good videos on there and some podcasts as well. And then also, you know, many of you know I'm a Christ follower, I have another website called Divine Intervention Lifelesses.com, Divine Intervention Lifelesses.com. Every week I post one or at least a podcast where from a biblical perspective, I address a life lesson, there's 309, you want episodes on there, right? There's actually an Apple podcast as you're here with that called the Divine Intervention Lifelesses podcast. So thank you for listening to me today. Share this with your friends and your colleagues. Please, this podcast is really high. Yo, there's a reason why you see me emphasize certain things I emphasize in this podcast. But I'll see you in episode 652. Have a wonderful day. God bless you and bye for now. Thank you.

Smoking.

The Dritte-Yother sign.

Degradation of elastin and collagen in the media due to increased matrix metalloproteinase (MMP) activity.

CT angiography (CT Angio).

ALI often follows an embolic/thrombotic event; Compartment syndrome causes pain with any passive movement of the extremity.

Colonoscopy (to prevent perforation).

Thrombotic phenomena (atherosclerotic plaque rupture), rather than embolic.

Proton Pump Inhibitors (PP Is).

Acute mesenteric ischemia.

Complete paralysis in the bilateral lower extremities due to aortic infarct affecting the anterior spinal artery.

Heparin (or other anticoagulant).

Diverticulitis or diverticular bleeding.

Thrombotic phenomena (atherosclerotic plaque rupture), rather than embolic.

Proton Pump Inhibitors (PP Is).

Acute mesenteric ischemia.

Complete paralysis in the bilateral lower extremities due to aortic infarct affecting the anterior spinal artery.

Heparin (or other anticoagulant).

Diverticulitis or diverticular bleeding.