DIP Episode 232 - Vasculitis and The USMLE

Okay, welcome. My name is Divine, I'm a resident. This is episode 232 I believe of the Divine Intervention Podcast. And in this podcast I'll be talking about a topic that I consider to be very high yield for the US Emily exams. And in this case I'm going to be talking about vasculitis. Okay, the vasculidities, if you may. The vasculidities, they're very high yield. They attested very frequently on the US Emily's. And first off, my apologies for not making a podcast in a while. I've just been extremely busy. There's tons of podcasts I have at the back of my head that I'd like to make. So I just figured at least today things are actually super busy for me today. But I figured let me just go ahead and make a high-out podcast because this stuff is kind of high out for the exams, especially for people that are having pre-metric centers open up for them. I just wanted you to be able to kind of get this in before you take a test. And hopefully in the coming days I'll also be able to make a ton of other podcasts. So vasculitis, right? So this is vasculitis, it's kind of like a nebulous subject for many people and it doesn't really have to be. It's actually pretty straightforward. If you actually really think through it. A lot of what constitutes vasculitis is pretty simple. It just follows again very rational pathology.

And the thing is basically if you listen to an understand what I talk about in this podcast, it should be able to answer pretty much any vasculitis question for step one, step two, second, step three. So, I mean what's vasculitis? Let's maybe start there. Well vasculitis, right? So it means a vasculitis, right? It's a vasculitis. So that means you essentially have some kind of inflammation of a vessel of some sort, right? Like for example, you can inflame like the large vessels, right? There's, and for the most part, those are like elastic arteries. So like the other and it's major branches, right? Like your subclavian artery, and all that stuff. Those are large vessels, right? Those are your elastic arteries. Or you can have inflammation of your medium sized vessels, right? So like your muscular arteries, right? So for example, like your mesenteric arteries, who fall under the purview of those muscular arteries, those medium sized vessels. And then your small vessels, your small vessels actually include things like your capillaries, your arterios, your veniots. Those are all kind of tiny, right? So when you have inflammation of any of those things, right? Those are blood vessels. You are infliming them for many different reasons that's called a vasculitis, right? So the thing is, well, how do vasculities arise? Maybe let me try to give you like some kind of basis so that it doesn't seem like you're just learning associations.

I'll definitely talk about the high-yield associations, but I think you know maybe having some good understanding may be helpful, right? So for example, right? One thing that can cause a vasculitis is if you literally just make antibodies, right, against the blood vessel, right? Because think about what we'll be here for a second, right? The thing is, for example, in the glomerulus, right? The glomerulus, you know, has like glomerular capillaries, right? So there are examples of blood vessels. It's a capillary. If you make auto-antibodies against the glomerular basement membrane, right? That's essentially what we'll give rise to a condition known as good-pastor syndrome. Remember the linear immunofluorescence on the linear immunofluorescence pattern? And remember that in good-pastor syndrome, you'll make auto-antibodies against type 4 collagen, right? So the thing is when those antibodies bind to type 4 collagen, remember the constant region of antibodies has a section, especially IgG and IgM, has a section that complements can bind to. Now when complements binds to those things, they cause destruction, right? And the thing is when the complements binds and you trigger a complement cascade from that constant region, right? One of the complement proteins is C5 A. C5 A, and that's actually, this is actually high-youtinous, is a chemotactic factor for neutrophils.

Remember, ILEAT and LTB4 at the other chemotactic factors, you will attract neutrophils and then those neutrophils will come and cause even more damage, right? So for example, again, in good-pastors, like a type 2 hypersensitivity reaction can give rise to, give rise toovascularities. Another classic one is like a Hienoxion line-prepure, right? Hienoxion line-prepure, again, it's another example of a small vasculitis, right? And pretty much the thing that happens is IgA, you form Ig antibodies against IgA, right? So it's like an antigenantibody complex thing, right? Again, if you form Ig antibodies against IgA, again, that IgA, right? It's constant region has a lot of stuff that can ultimately lead to the activation of your immune system, like your neutrophils, and they will come and, you know, cause some damage to like the kidneys or like vessels in the skin and all that stuff, right? And then the person will be said to have a vasculitis, right? So that's like a type 3 hypersensitivity reaction in that case, right? Another classic one is if a person has like, you know, you've probably heard of all these incas, right? Like, oh, C-Anca, P-Anca. The thing is C-Anca, right? That's your anti-sidoplastic, so anti-neutral philocyteplastic antibody, that's C-Anca. And then P-Anca is the, is also an anti-neutral, neutrophilic cytoplasmic antibody, but the antigen, right? Because again, this is an antigenantibody complex thing, right?

The thing is you make antibodies against a protein is 3. That's the antigen, protein is 3 is the antigen, you make antibodies against it in the C-Anca vasculidities. And really, the only one you need to know about is wagners. Remember wagners, the name has changed to GPA, right? Granolomatosis or polyangitis. And then if you make antibodies against myeloperoxidase, right? So anti-MP-O-Anca, right? That's what causes the P-Anca mediated vasculidities. So things like chryxthrow, things like microscopic polyangitis, and some variants of, of, was the name of this thing associated with the Australia colitis. Primary sclerosis in colangitis, that has an association with P-Anca, right? But again, remember microscopic polyangitis, chryxthrow, chryxthrow, is now E-G-P-A. That's eosynophilic granolomatosis with polyangitis. Those are all examples of P-Anca stala vasculidities, right? And in some cases, even you can have like bugs that can actually cause vasculidities. Like for example, right? Like if they give you a question about a patient from like North Carolina, has very high fevers, has like a rash on the palms and soles that's migrating inward, like going inward towards the trunk, right? That's Rocky Mountain spotted fever. That is actually an example of a vasculitis. Many people think that, oh, the lesions on the palms and soles are rashes. It's a rash, but if you actually dig deep into the pathophysiology, believe it or not, it's actually a vasculitis, right?

Essentially, the thing that happens is the bog, right? Remember Rocky Mountain spotted fever is, I would hope you know this at this point, is caused by rickets here, rickets, right? I remember that it's carried by the, by the dock tick, right? Like the dermiscentor species, right? They carry like, like in the silvery glands of those bogs, like those are ticks. They carry our rickets here, rickets side, right? And basically, the thing is those, those bogs can invade endothelial cells. Remember endothelial cells, they make up like the innermost lining of the blood vessel, right? That tunica intima layer, right? So they will invade those endothelial cells and by attacking those endothelial cells, your body will generate an inflammatory response against them. That inflammatory response is what presents as the rash that starts on the palms and soles and migrates inwards, right? You can remember those rash patterns, right? If it starts on the periphery and comes inwards, right? That's working mountain spotted fever, right? So again, that inflammation is what ultimately gives rise to the vasculolidates. And I guess maybe as a dovetail here, you probably remember for working mountain spotted fever, everyone gets doxycycline. There's no age limit here because usually if you're less than eight years old, you, you don't get doxycycline, you don't get any tetracycline because you know the toothed scoloration and the, and the, all the badness, like photosensitivity, right?

But working mountain spotted fever, the mortality is almost 100%. If it's not appropriately treated, so you don't mess around with this. You go ahead and give the person doxycycline to fix the problem. The only exception to that, everyone gets doxycycline rule for working mountain spotted fever is pregnant women, pregnant women get per-infini-com. For working mountain spotted fever, that's the drug of choice for working mountain spotted fever in pregnant women, right? But again, it's a kind of a vasculitis, right? Or if you see like people, you know, like you're probably used to seeing like this, a nice sermon in jitter-diss, where most times, most times on MBM Es, if a person has like a nice sermon in jitter-diss and all that stuff, like sepsis or whatever, they, those people tend to have like a, again, like, prepare on the skin and all that badness. And I'll actually explain the mechanism behind what a proper constitutes in a second. But basically, right, like all those lesions, like those perplish reddish lesions, you'll find on the skin of a person that has a meningococomy meningitis. That's actually an example of vasculitis. Basically, the bog, again, can trigger an inflammatory response in the philial cells or blood vessels. And then, those are capillaries and all that stuff, they become very leaky, right? And then you begin to see those palpable proper and all that badness on the skin, right?

And again, remember, they can give you an easily-giver meningitis question where the patient suddenly becomes comatose, profoundly hypotensive, has hyponitremia, has hyperkalemia, has metabolic acidosis. If you see that, I hope you're thinking about what a house Friedrichsend syndrome, right? What a house Friedrichsend syndrome. I'm essentially right. You've had like a hemorrhagic infarction of the adgeneral glands. Secondary to a nice, seramine angiitis, right? So for those people, I'm, you know, give them the acetriaxone and, you know, kind of hope for the best. And also replace the things that are missing, right? You know, give them like philodricortisone, give them hydrochordisone, you know, all that stuff. Replace the mineralocorticoids that are gone with philodricortisone, replace the blocochordicoids that are gone with like prednisone or hydrochordisone, right? Or dexamethasone. Again, those are all high yield things you want to keep at the back of your mind, for example. So those are examples of like bugs, like physical bugs, causing a vasculities, right? So the thing with these are vasculities, right? So again, we've kind of like mentioned some, you know, just high yield, like pathophysiology. And personally, to be honest with you, like again, some of the findings that do you know, they kind of seem like completely random, but they're really not, they're really not, right? Because the thing is think about it, right?

Like you, if you've, you know, studied for step one or any of these exams, you've probably heard about the, the classic highlights of acute inflammation, right? There's like color, there's tumor, there's rubour, there's dollar, right? I want you to pay a special attention to the word tumor, right? It just means all that posts an inflammatory crap, right? And like dead and decaying organisms, right? They kind of collect with like inside like fluid, right? From inflammation and stuff. That's what's called tumor. The thing is whenever you see a person, right? Whenever they tell you that a person has like poppable proper on their skin, you really want to think about a vasculitis. In fact, to be honest with you, poppable proper is called word for small vasculitis on mbim exams. You know, again, like I said, there's large vasculities and I'll talk about those separately. There's medium vasculities, I'll talk about those separately as well. But the small vasculities, right? Like the classic homework on mbim exams of any sort is the presence of poppable proper, right? Those poppable proper are essentially the tumor component of acute inflammation, right? But again, in this case, it's the tumor component of acute inflammation of blood vessels, right? It's the tumor component of acute inflammation of blood vessels, right? The reason it's poppable is literally because it's a tumor because they actually, there is actually proper that are not poppable, right?

There is actually proper that are not poppable, in fact. If I'm not mistaken, sometimes some people loosely, I'm not saying this is the right thing to do, but some people loosely refer to them as PTI, right? But in general, if you see poppable proper think about small vasculitis, if you see proper that is not poppable, right? Then usually it will be from, you know, like a person having like low platelets for some reason, or it can be from a person having like some problem with like collagen synthesis, right? Where like they are blood vessels and are very sturdy. So those blood vessels are kind of leaky, right? So the skin overlined those like nasty blood vessels kind of looks right, right? That's like non-poppable proper. If you see that thing, more about low platelets, or like I don't know, like vitamin C problems, right? Because remember vitamin C is necessary for collagen synthesis, right? So if you have like scurred of vitamin C, or you have no vitamin C, or you have a vitamin C deficiency, that will obviously cause a proper, but it will be non-poppable. So again, inflammation of the blood vessels overlined skin kind of getting like red and all that stuff, that's essentially what happens in people that have a small vasculitis, right? That's the poppable proper. I mean like think about it. Henoxionline per per rha, right? It's a small vasculitis. That's kind of where the name actually comes from.

So, so again, those are the big things like small vasculitis, those are the major things you should expect. If you're looking at like a medium or a large vasculitis, those things tend to cause like, because remember, inflammation can actually trigger thrombosis, right? Because inflammation is actually one of those things that can trigger the, that can trigger the like primary and secondary hemostasis, right? So if inflammation triggers he more like primary and secondary hemostasis, obviously you can begin to occlude blood vessels, right? So for example, you can occlude like the ophthalmic artery in the large vasculitis that's called a giant cellaritis, or you can occlude like a blood vessel, like a branch of the ural whatever in like tachyastus, right? So again, all that inflammation can trigger thrombosis. That's why you get most of these symptoms. In fact, to be honest with you, the vast majority of the symptoms that people experience when they have a vasculitis is because they've occluded a blood vessel because of the inflammation. They've had thrombosis, they've had all this badness happen, so they've occluded a blood vessel. So essentially, you have like a stroke of the organ, right? Because that organ is not going to be getting adequate amounts of blood. If it's not getting adequate enough amounts of blood, you'll start dysfunctioning and the person will have clinical symptoms.

So that's the pathophysiology behind most of the symptoms that arise in people that have a vasculitis, right? So I think one thing that may be helpful here is to go ahead and talk about the different vasculities and I'll kind of go from large vasovasculitis to medium vasovasculitis to small vasovasculitis, right? So what if they give you a question about like a 35-year-old female? And they tell you that she has hands, like she knows she's a 35-year-old like Korean or Japanese female. They tell you that her hands tend to hurt quite a bit. And they tell you that the notice that you know her blood pressure in like a left arm is like 120 over 80 in the right arm is like 170, right? And you know she tells you that oh that she had this episode like three days ago where like she couldn't see in her right eye, but after like a few hours it kind of got better, right? If you see that, I would really hope you're thinking about Takayasu at right, right? Takayasu is very likely going to be an Asian woman on your test. They'll be less than 50 years old, right? And or I mean it could also be like an Asian kid, right? So as long as they give you the classic presentation, the age doesn't really matter, but the person must be less than 50 though, right? So for the most part, Takayasu at right is it's a large vasovasculitis. For the most part, it affects like the yoder and the branches of the yorick arch. That's a high-o thing to keep in mind.

So you can affect the subclavian artery, it can affect the carotid arteries, right? It can cause some pretty significant problems, right? And sometimes they can even tell you that you see like a string of beads appearance in like aortic branches. If you see that, do not think about polio at a radius nodosa, think about Takayasu at a radius on the those circumstances, especially in an Asian female. That's the classic way it presents on exams, right? And then if the person is over 50, right? So they'll describe a woman, it's probably not going to be a man on your test. It's going to be a woman over the age of 50, right? And they'll tell you that she has problems like when she choose like, oh, whenever she choose, her jaw hurts a lot, right? That's jaw cladication, right? Or they may tell you, oh, that she has like proximal muscle pain, right? Like she has been in a hips, been in a shoulders, right? That's the thing that's known as polio myodromatic, they'll have like a very mildly elevated CpK, like creatinine, phosphokinase, right? Those are all things that have an association with this next diagnosis, right? Which as you probably know already, right? Or do we have like a headache that is on one side, like on the side of the brain, of their skull, right? If you see that, this is pretty classic for giant cell laryxin. Again, it's going to be in a present that's above the age of 50 on MDMA exams, right? So again, don't forget your associations, jaw cladication, right?

So that's been when they're chewing. Basically, the reason that they have the jaw cladication is that as you chew, right? I mean, think about it. You can even try this right now. Take your palm, put it on like your side of your forehead, right? And true, you'll see that that part of your head is moving, right? The thing is, as you chew, especially if you're like a violent truer as some people are, you notice that you kind of stretch the artery that is inflamed, you're stretching, like the ophthalmic arteries, you're stretching the superficial temporal artery. I'll say really, for the most part, the pinaritis because you're stretching the inflamed superficial temporal artery, right? So those people can have a gen cell array, so they can have jaw cladication, they can't pull in my algebra America. And the thing is, classic, for these people on MDMA exams, they are ESR will be elevated. If the ESR is motivated, on MDM As, I'm not saying the real world, but on MDM As, they don't have gen cell arrays, so the ESR will be elevated. And again, just like Takaiasu's, right? You trade with corticosteroids, is just for gen cell arrays, actually very high, you'll know that you don't do any diagnostic testing before you initiate treatment. You need to initiate corticosteroids, high dose corticosteroids immediately. And then, after the person, you know, you have up to three days to go ahead and do a perform a temporal artery biopsy. And if a person has like polymageurromatica, right?

You treat them with low dose, not high dose, low dose corticosteroids, they get significantly better quick. But after you do that, you also need to perform a temporal artery biopsy because they may not be symptomatic from an eye perspective, but down the line, they may actually begin to get into trouble. They may have a concurrent temporal artery that is asymptomatic, right? While they are having the polymageurromatica. So as you are working on polymageurromatica, you do actually have to go ahead and get a temporal artery biopsy. But again, you also need to give those people low dose corticosteroids. So that's it for a gen cell arrays. And then, what if they give you a question about a patient? You know, they tell you that this patient is like a commercial sex worker. And for the last like three weeks, she's been having like pretty high fevers. And she's telling you that she's, complete of like various, she's been having like these severe episodes of abdominal pain and sometimes she has noticed like blood in her stools and all that stuff. If you see that, right? And maybe they'll give you like some labs and you may see that, oh, the hebi-surface antigen is positive and the hebi-surface antibody is negative and the hebi-core antigen, maybe like IgM or IgG is positive. If you see that, this is pretty easy. I should think about polymageurromatica. I just know dose on MBM exams, right?

For the most part, these tends to affect people that, you know, in fact, they may even make this a risk factor question, right? This is actually high-youtuna. What is the biggest risk factor for polyaryllus nodosa on MBM exams? It's having a history of hebi infection, right? So they may put hepsi there, but don't mix it up. He has hepsi can cause pa and for the most part, it's hebi. Hebi is like a much more common cause, right? It's a much more common cause or they can even ask you a question like, which of the following is most likely to be positive in this patient? And it's actually a hebi surface antigen. That's something high-yout to give out the back of your mind for tests, right? So, again, for the most part, people that have polyaryllus nodosa, again, it's a medium vessel. So the only two large vessel vasculatities, you need to know, for example, tachyasus and chian cell, right? But polyaryllus nodosa, it's a medium vessel vasculitis and it tends to affect these people almost always on MBM exams. We'll have a donor thing, it's very high-youtuna. And the way you make the diagnosis, obviously the inflammatory markers will be elevated and, you know, you do like angiography, like CT angiography, you'll see the string of pros appearance, right? And you make the definitive diagnosis by performing a biopsy, right? Of the vessel that is involved.

And again, there is, in people who have abdominal pain, they tend to like infarct the atmospheric vessels, they can have like kidney problems, you can basically, you notice like bleeding from those organs, right? Again, just because of the infarction, right? So they can have like abdominal pain from infarcting, they have mesenteric vessels, they can have like renal failure, right? Sometimes they can even have M Is from all those problems, right? And again, for the most part, you give these people like steroids and cyclophosphamide, it's a pretty bad thing to have, but actually one high-youther thing I will see to know is that these people, they don't have involvement of the lungs. Polyaryllus nodosa does not involve the lungs on MBM exams, it's very, very high-youtuna. Okay, now what if they give you a question about like a four-year-old boy and he tell you that, oh, for the last five days, he has been having like temperatures of like 105, he has like unilateral cervical lymphatic anapathy, has like a red tongue, and has a rush on the palms and souls. This one is pretty easy, right? This is Kawasaki's disease, right? Kawasaki's disease, again, don't forget this, right? Those people have a rush on the palms and souls, right? They can even have like a, they may tell you that they have a dim of your hands and feet, right? Or they may tell you that they have kilosys, where like they're, their hands and feet are kind of like peeling off, right?

If you see that, think about like the skin of the hands and feet peeling off, think about Kawasaki's disease, right? And again, don't forget the rush on the palms and souls, they'll have like a strawberry tongue, they'll have fevers, if the person doesn't have fevers, it's not Kawasaki's on your test, right? And they'll have a cervical lymphatic anapathy and it's usually unilateral, a unilateral anterior cervical lymphatic anapathy, right? If you see that, think about a Kawasaki's disease and again, it's probably going to be in a Japanese boy, okay? Very common in, very common in kids, Asians, especially in the Japanese. So, and usually it's boys, right? Boys tend to get more than girls even in the real world, right? And we're young kids, right? Pressing that is 30 years old does not have Kawasaki's disease on an MBME, right? Again, look at the timelines, look at the ages of people before you pick certain answers on the exams, right? Like, it's like picking cystic fibrosis in a 60 year old, right? It's kind of a bad spot there, so don't do that on a test, right? So, Kawasaki's disease, again, I've kind of talked about the key findings and remember, these people got high risk of getting like M Is, right? So, give them like aspirin and IVIG, try to not give those people steroids on MBME exams, right? IVIG and aspirin is the big thing I want to give those people.

And one plastic finding, in fact, they may say which of the following is the most likely finding on a CBC, in a patient with Kawasaki's disease, pick the answer that says thrombocytosis, right? These people can have platelet counts more than a million on MBME exams, right? That's something I want to watch out for. And again, in Japanese kids or, you know, just Asian kids in general, sometimes they may tell you that this patient is completely of like severe red-upacadrine pain. You want to think about gallbladder hydrops, they can develop like, like hydropic swelling of the gallbladder, that's actually a very high you'll think to know for example, very common in kids with Kawasaki's disease. And again, don't forget that it's a medium vessel of vasculitis. And then what if they give you a question about a patient and they tell you that, you know, this patient has like Ashkenazi Jewish, Ashkenazi Jewish ancestry, right? And they tell you that all this patient has been having like severe painings by lateral or extremities, and they tell you that he's right, great toe has auto-amputed, and this person smokes like two packs of cigarettes per day. And he has moved for the past 15 years. And you know, this person is like 30 or 40 years old. If you see that, try to want to think about a bird, let me spell it out. And then you pronounce it how you want. It's B-U-E-R-G-E-R disease, okay? Burgers disease or whatever it's called, right?

So basically, right, this is going to be in a guy on your test. It'll be unusually the making of a woman, right? They'll make it in a women can get it, but it's a man that's going to get it on your test. So it's going to be a man, it's going to be relatively young or like approaching middle age, right? Like a young guy, and they'll tell you that he smokes a ton, right? And he'll have like, they can even give you like a clodication style question on this, right? Or they can tell you that the person's fingers, you know, auto-ampute, or they look dark, right? Because of like like ischemia and the Crocs's and all that badness, right? Like gangrene. And if you see that, think about Burgers disease sometimes, on MB Ms, they will try to change the name to mess with your hair, that it's called a thrombone giitis of literants, right? If you see that, you know, again, think about Burgers disease, right? And again, it tends to affect young male smokers, right? Although it also has a predilection for people that have a Ashkenazi or Jewish descent. And for the most part, these people, you know, it tends to affect the extremities, like the outbreak extremities, lower extremities. Essentially, everyone will have the lower extremities involved. The outbreak extremities, you know, it cannot happen, like half the people that have the disease, but everyone that has a Burgers disease, they are lower extremities, they are toes, their feet, their ankles, all those things tend to be involved.

And for the most parts, these people need to stop smoking, very important, they need to stop smoking. Does the only thing that will really improve their symptoms? I mean, you can kind of help them along by giving them like visual dialed letters, like a die hydroperioding calcium channel blocker or an alpha blocker like Prasusin, or you can give them like a Prosteglandin analog. But for the most part, those people just need to, if they stop smoking, the vasculitis will disappear. If they don't stop smoking, then they are lower extremities and upper extremities will disappear instead. So, again, just big thing, you want to keep at the back of your mind, for example. And then there's one dichotomy I think I want to establish. I mean, it's a kind of vasculitis if you really think about it. But people tend to mix this up on MBMI exams. There is something known as Renaud's disease, and there is something known as Renaud's phenomenon. Renaud's disease is where, again, the Prasusin has like the classic symptoms, and it's usually a woman. It's almost never a man on MBMI exams. So, you'll see like a woman, like a young woman, and she tells you that whenever she steps out in the cold, her palms turn white, and then after a while it turned blue, and then after a while it tonared, especially when she walks into our back into our apartment. If you see that, and that's the only thing the Prasin has, think about Renaud's disease, right? Think about Renaud's disease.

And again, it's actually a kind of medium vasculitis, right? Tends to affect mostly the fingers and toes on MBMI exams. And for the most part, these people tend to be young women, and really the way you treat it is just tell these women to stop going out in the cold, or tell them to wear things that will protect them from the cold like gloves. Or again, you can also use a dihydroperidine calcium chanel blocker, like my phydipina and stuff like that, right? But if a Prasin has like that Renaud's, like you see the observatory notes in that patient, but this patient has some other weird systemic disease like Lupa. So they have crest sluradimer. Don't forget your anti-centrumia antibodies with that, right? If they have that, it's called Renaud's phenomenon. When it's a component of some other systemic problem, think of it as Renaud's phenomenon. That's very important to keep out the back of your mind, right? And yeah, that's the classic presentation. Really the treatment is just again, those dihydroperidina calcium chanel blockers remember they are very nicer viso-diilitres, the blocker L-type calcium channels. And then, what if they give you a question so I've talked about all the large and medium vasculitis, right?

The small vasculitis, what if they give you a question about like like a 40-year old man, and they tell you that, oh that he has been having like episodes of him obtuses, and that he has recently been treated for an ear infection, and he's also noticed a lot of himaturia and scratch, and he's like super, super high, and you find like red blood cell cast and you find like, I don't know, like two grams of protein in 24 hours and he's urine. If you see that, I hope you're thinking about Wagner's. Again, remember, it's known as a GPA, right? Granolomatosis or polyngitis. And the thing is, those people would pretend to have hematuria. It's a triad hematuria. So kidney squibles, essentially they have like a rapidly progressive, or you can call it chrysente, glomerular arthritis, and then they'll have like lower airway problems, right? They will have hematitis. And then they will have like a sinusitis. And again, remember sinusitis can mean many things on end-beam exams. Your friends at the end-beam if you're getting very exotic with this stuff, right? So for example, these people can have like a saddened deformity, they can have sinusitis, they almost never do that on tests anymore, they can have like nasal polyps, they can have ear infections, they can have like strider from tracheal colapse, they can have mastoiditis, they can have a tightest external.

Basically any infection of like your airways and sinuses can count or like your mastoid cells can count as the sinusitis component of Wagner's. And again, don't forget it's associated with C and C, right? So C and C, that is the only C and K pathology that you probably ever see tested on any of the USMLE exams, I insure it with steroids and a cyclophosphamide. And again, it's a small vasovascularitis, right? And then, you know, the two Pianca neighbors, like Trux Straves, you remember Trux Straves is EGPA, you're seeing a Philly Granulomatosis, a Polyanjitis, these people have like a family history of like all these allergies, like skin allergies, X-Yema, asthma, all that badness, right? And then you have like hematuria, right? If you see that again, just think about a EGPA, right? And again, for the most part it's going to be an older person, that's actually one thing I found to be really helpful on tests. It'll be a person that's usually above the age of 50 on NBM exams. And it may be a person that usually recently stopped a corticosteroid, or maybe was recently started on a Lycotrain receptor antagonist, that's like a classic association on NBM exams. If you see that, right? And the person has like, again, a history of like allergic granitis, asthma and all that stuff. And you see that, your synophils are like 10% in the CBC. Think about EGPA, think about Trux Straves on a test. And for the most part you just treat those people with a corticosteroid.

And then microscopic polyangitis, just remember that it's PNK positive, like Trux Straves. There's really no like big, big, big association, right? So they'll literally have to give you like the PNK is positive. And they very likely will not give you that allergic history and all that badness. And then you pick microscopic polyangitis. And actually PNK is very, very, very strongly associated with microscopic polyangitis, right? So there's really nothing super classic about it, right? So if you see a PNK positive pathology, if you see, if you do not see like allergic asthmatic symptoms, and you don't mention those astusions with like, oh, the person recently stopped steroids or recently studied in a Lycotrain receptor antagonist, like Monte Lucas, those are for Lucas. Think about a microscopic polyangitis under those circumstances. And again, don't forget it's PNK positive. And then we'll give you a question about a child. And they tell you that this child has poppable preparations below the buttocks. And this child has like joint pain and abdominal pain, pay attention to the spot abdominal pain. If you see that, you absolutely want to think about what? I hope you're thinking about HSB, right? Henochron line preparer, right? Henochron line preparer is going to be in a kid on your test, okay? And these kids are going to have poppable preparations below the buttocks and abdominal pain.

If the kid does not have abdominal pain, I will encourage you to think long and hard before picking HSB as an answer. In fact, they can make a question like this where they say, what is the most common physical exam finding in these people, right? After like poppable prepare whatever, think about abdominal pain. Like literally, poppable prepare is found in like almost like 98% of people that have HSB. And the abdominal pain is found in almost 90% of people that have HSB, right? So these kids, right again, the class presentation, poppable prepare below the buttocks telling you that it's a small vessel of asculitis, they have abdominal pain, they have joint pain, right? They can even have like some malgi bleeding just from the involvement of the abdomen, like those small vessels that you find in the laminate appropriate of the GI tract, right? So these kids can have like pretty significant problems. And for the most part, you know, you know, it kind of sucks to have, right? But for the most part, these kids will get better without treatment, right? So actually reassurance, right? And you know, just kind of checking their labs and stuff on a routine basis is the right thing to do on MBM Es. You typically do not have to treat these kids, right?

So again, your friends at the MBM they love to kind of mess people up the way where you know, you're putting all these glorious answers and you're like, oh, I got to pick something, I got to pick something, no, you don't need to pick anything on the test. These kids for the most part will do well, right? But you know, let's say that's persistent for a long time, they're not getting better, they have severe symptoms. You can give them like corticosteroids for the most part, right? But another one high you think to maybe think about is if the person is having like massive GI bleeding or their creatinine is rising pretty significantly from the HSP, go ahead and give those people corticosteroid. So if you see severe symptoms, go ahead and give those people a corticosteroids. And again, don't forget that this is actually an example of a type three high-percentive theory action. And these kids actually should not get the rotavirus vaccine in the future, right? Remember, the asserting disorders were given the rotavirus vaccine is contraindicated in MB Ms. If people have this history, history of HSP, history of intusus ception, history of there's one more mechols that are particular. If a person has any of those problems, they should not be getting the rotavirus vaccine at any point in the future. I remember rotavirus is like, so what like a single stranded universe is the most common cause of like blood-diring like kids.

That's probably something you want to keep at the back of your mind, for example. And then what if they give you a question about a patient, right? And they tell you that oh, this patient has a history of like hip C, right? And then this patient has like renaled stile symptoms, right? Renown stile symptoms or the material that the person has even has had a stroke and you know, maybe they move to like a quarter-climate or something. If you see that, I will hope you're thinking about like a mixed cryoglubulinemia, right? Mixed cryoglubulinemia. The classic way will present on examples is you'll be in a female, right? Like 75% of cases of mixed cryoglubulinemia in females, right? And these people almost always have hip C, right? So again, the biggest MDMA exam results factor for mixed cryoglubulinemia is a history of a hip C infection, right? I remember these people can get like two kinds of globalins, right? But for the most part is the cryoglubulinins that we're going to worry about here, right? Remember for the most part, it tends to be IgM, right? And those IgM's, right? They tend to like agglotinate at cold temperatures, right? So those people have like renaled stile symptoms on the test. And again, they may have like bubble prepared on the skin. They'll tell you that if you're better when they go into like a warm room, if you see that again, kind of think about this. And again, it's not just Hep C that is the only association, right?

Like, you know, like if a person has like scleroderma, that can be a so you don't cryoglubulinemia, right? So those are things to keep at the back of your mind. And if they have Hep C, treat the Hep C, right? And you know, sometimes you also give them like immunosuppression, like cyclophosphamide to kind of help them out there. And there are some other things that maybe as you're a Hep C that you should probably keep at the back of your mind, for example, right? So remember Hep C is a sort of like preferred cutinia tarda, right? And remember, it's a sort of like MPG and like membrane or proliferative agglomerate or fritis, right? Those are all like with things that have an association with Hep C on NBMS. So again, to summarize, the large vasculatidides, right? We have just 12 those. We have chancelatoritis and tachyasoiditis. And then the medial vasculitis, we have like P and remember that does not involve the lungs. We have chalasaki's, we have burgers disease, right? And we have like those renolder things, right? Those are also webinars, right? Like EGPA is actually an example of, I mean, sorry, GPA is an example of a medium vessel of vasculitis, but then pretty much everything else. Our link origin is the memory, they each each little bit you want. Just remember the two large vasculatidides, remember the medium vessel vasculatidides, and then everything else is a small vasculatidides, right? So I think I'm going to go ahead and stop there.

This podcast is kind of going on for longer than it should run back to the work I was doing. Thank you for listening. As I do at the end of every podcast, again, I don't for one or one theory for many exams. Step one, step two CK, step two CSTEP three, preclinical medical exams, 30-ish-off exams, alpha booster courses for the USML Es, they're like crash courses essentially where you know, we review the most notes, the high yields for these tests, is 20 hours for step one, two CK, and step three. Again, if you're interested, reach out to me. I've done you many people, there are many people that have worked with that, they're like, oh, after I did this, my next practice test was like so many points higher, right? So again, if you're something you're interested in, if you're free to reach out to me, and then also do like longitudinal tutoring, right? So like, if for example you're studying now first year or second year or third year, I'll tutor you like throughout the year, like I'll meet you maybe like once or twice a week, and then as I'm doing that, I'm also teaching you for your upcoming USMLE exam. Again, most people have done this with the crush like their class or their shelf, whatever exams, and then at the same time they've also done extremely well on their upcoming abort exams, right? And then let's see, we're medicine applying to residency, right?

So like an ERAS application or a collision applying to Mexico's like an AMCA's application, I'd offer like what I call like coaching or consulting, right? So like rec letters, editing personal statements, editing applications, more interviews, and again, most people have worked with, they've much said their first choices, right? And again, if you have a tricky application, low scores, no research, no experiences, graduated from Mexico a long time ago, oh, you're an IMG and all that stuff, reach out to me again, there are people that have had like pretty strange stories, right? But I've been able to craft the applications and they've matched people like in very dire circumstances. And then you know, if you're a medicine resident or you have a medicine or a pediatrician, buddy, I tutor for those in treating exams and those are respective abort exams. And then you know, if you have like a college buddy that needs to learn for any of the pre-med subjects or the MCAT subjects, I'll tutor for those. So you know, thank you for listening. Please, I guess let me talk about my life lesson for today. So my life lesson for today, as again, I do have the Hindu Vary podcast is making the most of time, right? It's very important, right? Like given there's a part of the Bible that says that a person should redeem the time because these are evil, right? So, you know, you see many people, they kind of have like just like, like for example, this COVID-19 period, right?

It's like, you know, you're at home, right? You know, you can spend your entire day, your entire mandatory vacation, you know, kind of watching Netflix or tentatively one smart thing you can do is maybe like try to learn a new skill. I'm not saying you should all watch Netflix. Again, please don't miss, I'll show what I'm saying. Even I divine, I watch Netflix, I watch Hulu, I watch sports, well, that's kind of dead now with the NBA not going on. I'm a big time leaker's fan. So, you know, obviously with no NBA has nothing I can really do with that on that front. But basically, right, make the most of the time that's presented to you, make the most of every opportunity, right? The thing is, if you make the most of every opportunity, you leave a high old life because regardless of whatever is going on in the world, there is something you can do that can make your life better or make the lives of other people better, right? So, you know, make the most of every opportunity because you never know like you may not have time to do that thing in the future. You may that present time you have maybe the best opportunity you have. And again, if you're setting your hand to do anything, try to do a good job, right? Try to do a good job. The thing is, if you do a good job, you will acquire good reputation. And when you acquire good reputation, when it's time to reward someone or it's time to promote someone, they will call on that person, they know does a good job.

Because think about it, right? Like with this economy crisis that's going on, right? Like, I don't know, maybe people are not, uh, uh, needing a particular service anymore. But you know, for the few people that still need it, they'll look for the best of the best, they'll look for the criminal crap, right? To help them with those things, right? So, let's do something to keep at the back of your mind. Always do your best. Always try to do an excellent job. When you do an excellent job, you'll always have job security, right? A person that does an excellent job always has job security. Job security comes from doing an excellent job. Although maybe in the future, we'll talk about why, um, you know, you should try to like have the mindset of not working for people and actually like having something of your own. Um, but that's a different life lesson, uh, we'll talk about in the future. So thank you for listening to me. Uh, please be, it'll be great if you go subscribe to the You Tube channel. It's called Divine Intervention USMD Podcasts and Videos. Uh, subscribe to my Word Press website, uh, Divine Intervention Podcasts.com. Whenever I post a new episode, you'll find out about it. And if you're a podcast person, again, a bo podcast, Google Play Spotify, I have all these podcasts on them, right? So, you know, just, uh, please subscribe every little bit of help or subscription or whatever helps, right? Definitely, definitely helps.

And again, if they're podcasts you want me to make, just send me an email. I kind of have like a stack of podcasts that I know I'm going to make a soon. I've just like I have all this thing floating around in my mind. I just literally don't have the time to meet them. Um, but again, I think over the next few days, I should be able to crank out a ton of podcasts, uh, to kind of meet, uh, especially like many of the emails people have sent out. So thank you for listening. Uh, please listen to this podcast. It's super high yield to know for all the USMD exams. I'll see you in the next podcast. Thank you. God bless you.

Inflammation of any blood vessel (arteries, arterioles, venules, capillaries).

New-onset headache, jaw claudication, and visual symptoms in patients typically over 50 years old.

Eosinophilic granulomatosis with polyangiitis (EGPA).

Hematuria/glomerulonephritis, sinusitis/upper airway involvement, and lower respiratory tract issues.

Starts on the palms and soles and migrates inward toward the trunk.

Hepatitis C infection (Hep C).

Large elastic arteries, particularly those branching off the aortic arch.

Anti-Myeloperoxidase (MPO)-ANCA.

Henoch-Schönlein Purpura (HSP) / IgA Vasculitis.

Takayasu's arteritis and Giant Cell Arteritis.

Hepatitis B (Hep B).

IVIG and Aspirin.

Raynaud's phenomenon; if it occurs as part of another systemic disease (like Lupus), it is called Raynaud's phenomenon.

Large elastic arteries, particularly those branching off the aortic arch.

Anti-Myeloperoxidase (MPO)-ANCA.

Henoch-Schönlein Purpura (HSP) / IgA Vasculitis.

Takayasu's arteritis and Giant Cell Arteritis.

Hepatitis B (Hep B).

IVIG and Aspirin.

Raynaud's phenomenon; if it occurs as part of another systemic disease (like Lupus), it is called Raynaud's phenomenon.