this is definitely the highest yield of all of the vasculitis it doesn't matter if it's large medium or small this is the most high yield so this is intimal thickening and fragmentation of the lamina and the super super high yield symptoms that you should be aware of are the four things you see here so an elevated esr jaw claudication and temporal headaches its association with polymyalgia rheumatica and some visual problems due to involvement of the ophthalmic artery so giant cell arteritis classically on exams will be someone usually over the age of 50 is chewing their food and they start to get a headache on the side of their face kind of like around their temple area that's jaw claudication occasionally they'll have double vision or trouble seeing that's the visual problems due to involvement of the ophthalmic artery so these are all large uh vessels that are going to be affected here which leads to these symptoms so the other super high yield thing to know besides the associations is that you have to give the patient high dose corticosteroids before you do a biopsy so literally this is very very high yield for step one and step two and i'm going to kind of tie in both here for step two you should know that the first thing you do like what is the most appropriate initial action is give high-dose corticosteroids second action is take a biopsy you have to do this because if you don't give them high-dose corticosteroids and suppress the inflammation in that temporal artery you can cause the patient to go blind and that is irreversible once that happens so you have to give the corticosteroids right off the bat once the patient's covered with corticosteroids then you get the biopsy of the artery to see okay is this in fact intimal thickening and blah blah all that pathophysiology stuff that's low yield for step two but high yield for step one so step one give excuse me first thing you do give high-dose corticosteroids second thing you do take biopsy know that for usm release step two and complex level two for usmle step one and complex level one you should know that this is due to intimal thickening and you'll see that elevated esr jaw claudication temporal headaches association with pmr and visual problems so that's giant cell arteritis so the way that i remember this is for giant cell arteritis i say gca which reminds me to give corticosteroids immediately and i also remember that jaw claudication always happens and jaw is spelled with a g here and immediately is spelled with an a so gca you know that mnemonic might help you but this is definitely one of the more straightforward uh vasculities and it is definitely the most high yield so that is giant cell arteritis takayasu arteritis is another large cell or excuse me large vessel vasculitis that is transm transmural fibers thickening of the aortic branches and this classically occurs in japanese women under the age of 40. now this is sort of easy to remember because takayasu is a japanese name and this occurs in japanese women so it shouldn't be too hard to remember that association but what's extremely high yield is that this is called pulseless disease so because there's transmural fiber thickening of branches off the aorta those are the branches that supply the upper extremities so you know subclavian artery degeneration is exactly what we see here and in this picture you're seeing um some degeneration of the subclavian arteries which are branches off the aorta and because of this you can have things like a decrease or uneven blood pressure in the upper extremities so one of the high yield things that boards love to test you on is they'll give you an uneven blood pressure or a decreased blood pressure in one or both of the extremities and ask you what disease process this is so you have to ask yourself you know are we talking about something like vasculitis are we talking about some congenital congenital cardiac deformity it depends on the other factors in the clinical vignette so in takayasu arteritis in addition to the uneven or decreased blood pressure in the upper extremities they might give you something like an elevated esr which should point you in the direction of takayasu arteritis especially if we're talking about a japanese woman as our patient so remember the degeneration and transmural fibers thickening of the branches off the aorta look for paresthesias decreased blood pressure or uneven blood pressure in the upper extremities that's takayasu arteritis so the way that i remember takuyasu arteritis is i go back to our original mnemonic for remembering all of the large vessel vasculitis and i just think of a samurai getting his arm cut off which reminds me that there are blood pressure problems and perfusion problems to the upper extremities because of the transmural fibers thickening of these branches so that is takayasu arteritis so that's the only things that you need to know for large vessels so pretty straightforward very high yield again for giant cell arteritis now let's talk about the medium vessel vasculitis so the first one and personally my favorite vasculitis is kawasaki disease kawasaki disease is a necrotizing vasculitis that involves coronary arteries usually in children and the reason that this is so high yield for boards is because this is really one of the only disease processes where children actually can have heart attacks so you're going to see mis in children because the coronary arteries in children are going to be involved here a very very high yield point is that you give the patient two things you give iv immunoglobulin and you give them aspirin and this is really really unique because usually you should know that we don't give children aspirin for fear of causing rise syndrome r-e-y-e-s rise syndrome so you usually don't give kids aspirin but in this case you say screw it it's worth it because if we can prevent them from having an mi we'll take rey's syndrome so you know don't worry about the rye syndrome if we can prevent the heart attack so you're gonna see mi in children and you're gonna see three other things adenopathy oropharyngeal signs and a discomating rash so the way that i remember this is the cow that mood m-o-o-d m for mi o for adenopathy o for oropharyngeal signs and d for desquimation so the cow for kawasaki that mood mood so really really high yield findings giving the patient iv immunoglobulin and aspirin oropharyngeal signs which you see here as a strawberry tongue very high yield because they love to make you differentiate between this and strep because strep can also cause a strawberry tongue so if you see you know a children with like chest pain oropharyngeal signs like a strawberry tongue and a rash you're giving them aspirin but if you see someone with classic infectious signs of strep then it's not kawasaki disease so that's kawasaki disease very very high yield because of the treatment mi in children and differentiating the strawberry tongue rash so that is kawasaki disease let's talk about thromboangiitis obliterans so thromboangiitis obliterans aka burger disease this is really really simple really really straightforward there's one thing you need to know this causes a distal digital thrombosis usually in men between the ages of 30 and 50 who are like chronic chain smokers their hands are going to look like this whenever they smoke cigarettes their hands are going to black and you'll have like sort of an element of reynaud phenomenon here but just know that this is in men 30 to 50ish years old who are smokers they have degeneration of their medium vessels as a result of smoking and because of that their fingers will actually become necrotic if this is not if they don't stop smoking so treatment is uh stop smoking that's thromboangiitis obliterans now let's talk about polyarteritis nodosa so this is our final medium vessel vasculitis so polyarteritis nedosa is transmural arteritis with fibrinoid necrosis and and actually that description of the pathophys is very very high yield and i'll explain why in just a moment this is going to involve renal coronary and mesenteric arteries the reason that the transmural arteritis with fibrinoid necrosis is really really high yield is because when you do a biopsy you're going to see something called the string of pearl's appearance and basically what this is is that along the artery you have alternating sections of fibronoid necrosis then fibrosis fibrinoid necrosis then fibrosis and so on and so forth and basically what this does is in the necrotic area the artery shrinks and in the fibrotic area the artery is trying to repair itself so it sort of bulges out a little bit and when you alternate these patterns you get what's called the string of pearl's appearance so it literally looks like a pearl necklace where you have like a little string then a bead a little string then a bead so that's the string of pearl's appearance the other super high old thing to know about polyarteritis nedosa is that roughly 30 or so of these patients will be positive for the hepatitis b surface antigen and that will be chronically um coming up on their lab results so how do we remember the string of pearl's appearance and the hep b surface antigen for polyarteritis nodosis so i want to set a scene for you in your mind because this is my pneumonic i want you to imagine that you're buying your wife or your husband if you're female but that you're buying your wife an anniversary gift it's your anniversary you get home from work and you totally forgot to get her flowers you totally forgot to make a dinner reservation so what do you do you go to plan b and you give pearls i think of plan b or pan b for polyarteritis nedosa plan b you give the pearls so the pearls reminds me of the string of pearl's appearance and plan or pan for polyarteries and dosa and b for hepatitis b so it's your anniversary you've totally forgot that it was your anniversary so you quickly go to the jewelry store and you buy pearls you give a pearl necklace pearl necklace that's the string of pearls appearance plan b or pan b for polyurethane dosa and hepatitis b surface antigen so that's it for medium vessel vasculitis we are flying you are learning high yields you are not wasting too much brain space let's get into the last category and arguably the most difficult but i'll simplify it all for you so we're going to talk about small vessel vasculitis and the way that we're going to start is by differentiating cryoglobulinemic vasculitis from henoch online purpura because these are very very similar disease processes so these are our first two small vessel vasculitis now i'm going to start by telling you everything that these have in common first hinok shine line papura is also known as iga vasculitis and cryoglobulinemic vasculitis i call personally this is my nickname for it hep c vasculitis now these both have hematuria palpable purpura and arthralgias so you just know it but like there's no different differentiating between the two they have all three of those findings henoch shineline purpura is due to iga deposition in the artery cryoglobulinemic vasculitis is due to an underlying hepatitis c infection so these are both due to something and that's what you need to know about them now let's talk about the differences between these two the first big one is that in iga vasculitis aka henoch shine line purpura you have gi pain but in cryoglobulinemic vasculitis there's no gastrointestinal pain so that's the first thing again i told you that henoch shineline is due to iga deposition and cryoglobulinemic is due to an underlying hepatitis c infection which causes deposition of cryoglobulins in things like the skin and the joints which is the reason that you get the palpa the palpable purpura and arthralgias the last really really high old thing that you should definitely know and be able to differentiate between these two is that iga vasculitis classically follows a recent uri and if not a recent uri it can follow things like parvovirus or group a strep so if a patient has a recent uri and then all of a sudden you know they're peeing blood there's gi pain arthralgias etc you think iga vasculitis um tests love asking you what's the pathophysiology here and the answer will all be uh like iga ige igg et cetera and you might be really confused because you're like i don't know what they're talking about but you need to remember it's henoch henoch shanlein purpura aka iga vasculitis so the answer is iga for cryoglobulinemic vasculitis you just have to treat the underlying hepatitis c infection and upon doing so the the cryoglobulin deposition should sort of resolve a bit and the symptoms should lessen so that's the difference between the two students get confused all the time because they're both small vessel vasculitis very similar again gi pain in iga no gi pain in the hep c one um know the difference between them and how you treat them and that iga follows a recent uri so if you're looking for some mnemonics here it's one of the ways that i used to remember this was that for hsp the patient has stomach pain and for cgv c gets viral aka hepatitis c gets viral that's the difference between these two small vessel vasculitis now let's talk about church straus syndrome so church straus syndrome i told you this is our first nazi german guy who's no longer his name's no longer included in textbooks but i'm including it here for completeness sake this is also known as eosinophilic granulomatosis with polyangiitis so if you see that name it's the same thing usually on exams i know that sometimes they'll give you both of these names sometimes they won't so memorize both of them but no shark strauss because it still shows up in cubans and and practice tests and what have you so this is a necrotizing eosinophilic granulomatosis infiltration and if you didn't know that it's in the name eosinophilic granulomatosis with polyangiitis so the name literally is telling you what's going on there's eosinophils granulomas and polyangiitis multiple arteries inflamed so this has pianka positive pianka which is a little marker that you should know this classically is in patients who have things like asthma or allergic rhinitis they have nasal polyps which i remember as balls in the nose and i'll explain why i call it balls in the nose when i get to the pneumonic these patients can sometimes have sensory deficits so peripheral neuropathy is a finding that if they give you this on the exam in conjunction with something like pianka or in a patient with asthma or allergic rhinitis you want to think church strauss and then lastly this is due to ige antibodies so the reason that i wrote it out this way p-a-b-s-t is because when i think strauss syndrome i think chug strauss syndrome and what do you chug pabst blue ribbon pabst p-a-b-s-t p for pianka a for asthma and allergic rhinitis b for balls in the nose aka nasal polyps s for sensory deficits aka peripheral neuropathy and t for ige and t bodies that is church straw syndrome aka chug straus syndrome eosinophilic granulomatosis with polyangiitis so our next german name for a small vessel vasculitis is wegner granulomatosis aka granulomatosis with polyangiitis so it's the same thing as turks strauss minus the eosinophilic part so this is not due to eosinophils this is not due to ige but you still have granulomas and you still have polyangiitis so um dr sitar who owns pathoma came up with the best mnemonic for this and i'm going to give him credit here with wegner granulomatosis he found that well you see si anka an involvement of the lungs kidneys and nasopharynx so he focused on that letter c and said wechner instead of wagner wechner the c he would draw over a stick figure and where that c crossed the stick figure is the involvement of the organs so it crosses over the nasopharynx it crosses over the lungs and it crosses over where the kidneys would be the c crosses over all three involved areas and it reminds you of the si anka for wechner aka wegener aka granulomatosis with polyangiitis so really straightforward if you need more information about that i would really encourage you to check out pathoma dr sitar is amazing and i also have another video on renal pathology in the nephritic versus nephrotic lecture where um i go over this more in depth so that's wegner granulomatosis the last small vessel vasculitis that we need to know about is microscopic polyangiitis so this disease process in contrast has p anka so p anchor in microscopic polyangiitis this involves only the lungs and the kidneys there's no nasopharynx involvement here so we're contrasting this to wegener aka wechner um in this situation the difference here being that it's pianka instead of sianka and that it involves the lungs and the kidneys but not the nasal pharynx so just like i did the c in wekner we're going to do the p in microscopy in microscopic polyangiitis and where the p crosses the stick figure is the involved organs so the p crosses the lungs and then the front or right side of the p hits where the kidney would be protruding if this was the patient's true left kidney that's microscopic polyangiitis so guys i got great news for you that's it you learned all of the high yields about the vasculitis