 So if you ever think your hobbies are boring, not as boring as that. We know anterior-intermediate posterior and pan-uvidus, so it's where the predominant side of inflammation is. So you're allowed to have a few cells floating around in the anterior vitreous and it's still anterior-uvidus, as long as most of the inflammation's in the anterior chamber. Intermediate-uvidus, you can have vitreous cells, a few anterior cells, you can have optic nerve swelling, you can have macular edema, and even those are findings in the posterior pole that does not count as being a posterior-uvidus. So that's, I think, the most misused term, is calling intermediate-uvidus with CME and optic nerve edema a pan-uvidus. We get a lot of referrals in for pan-uvidus and it's just an intermediate-uvidus. So posterior-uvidus has to have a focal inflammatory lesion in the coreroid or retina to be considered posterior, and then pan-uvidus is when you have that in addition to anterior and intermediate-uvidus. And I heard they've tested this before, like if you see 10 cells in the anterior chamber, what level of inflammation that is. So a good rule is 10 is 1 plus, 20 is 2 plus, 30 is 3 plus, and then it just gets a little fuzzy right after that because technically up to 50 is still 3 plus, but if you have a hypopium it's like automatically 4 plus because it means there's that many cells that are layering out. And you know, you use the slip beam at an angle with as bright as you can, magnified in a 1 by 1 millimeter box, and that's how to look for anterior chamber cell and flare. And then for flare it's just grading the amount of detail that's obscured from how well you can see the iris and lens, so these are pretty subjective. Hazy, hazy, very hazy. And then vitreous, oh that says add because that was like a slide that I did this morning, not minus the add. Vitreous haze grading is done with the 20 diapher, so you have the patient laying back and you're looking with an indirect and a 20 diapher lens, that's how you officially grade vitreous haze. So if you see us in clinic and we're scribing, you know, we're telling our scribes, they know that like I say anterior chamber cell and flare and I may say, oh there's two plus vitreous cell, but I never say the haze score until I'm with the indirect. So, and it's just based on how well you can make out the nerve, so one is kind of hazy. Once you get to three plus you're really having trouble making out the details of the nerve and then four plus you can't see the nerve. So this review is going to be uveotic syndromes and there's like a billion of them and I'll spend some time going through them today, but there are certain ones that just I'll be like, this is just memorize this and I'll skip a few slides so you have the slides later that you can just go back and look over. And then immunosuppression, I remember being tested on that like every year, like what's the toxicity of methotrexate, drug induced uveitis, I know for a fact I missed a question on that on the real, on the OCAPs, which really bothered me, and then HLA classes, so starting with anterior uveitis, HLA D27 automatically comes to mind ankylosing spondylitis, but there's four syndromes that are associated with uveitis and HLA B27, so writers or reactive arthritis, inflammatory bowel disease, IBD, not IBS, and then psoriatic arthritis. So we're familiar with this, this fusing of the sacroiliac joints, bamboo spine, we see patients like this walk into our clinic, so it's ankylosing spondylitis. R-A-N-G-A-U, anyone know what that stands for? Yep, yep. So a lot of times we'll just say N-G-I-U, non-granium lumbus anterior uveitis, but if you hear recurrent alternating non-granium, it's anterior uveitis, it's B27, like 99% of the time. And the things that can kill you is the aortitis or valvular insufficiency pulmonary fibrosis, it's rare, but no that's part of it. Inflammatory pattern, so you know everyone has some back pain, but if you ask them is it worse in the morning or does it wake you up from sleep and then it gets better throughout the day, that's inflammatory arthritis. Anyone know what this is? The term for this? This is part of the writers, so can't see, can't pee, can't climb a tree, that was the initial teaching. The confusing part of it is the most common eye manifestation is conjunctivitis, not uveitis, but uveitis can be a part of it, so they get heel spur formation and the skin lesion, which is that like crusting and peeling of their heels called carotidur or blenarachicum, and they're often B27 related, so this will be after, oh I had food poisoning a month ago, now I have uveitis, so and I've actually, I've definitely seen this, like people come in and they don't know they're B27 positive, maybe we haven't even checked for it, but they're like, I had like food poisoning a few months ago, really bad diarrheal illness, and then two months later they get uveitis, and I think that's on the spectrum of writers, so. Oh really? Ooh. Didn't get uveitis, luckily. I had this. Arthritis and all that. Arthritis, so the bugs associated with it, cussie, see you SSY, because you'd be cussing if you got this, so that's how I remembered it, Chlamydia, ureoplasma, SS, and then Y, that's how I remember it. Oh, that looks disgusting. So in the future, if you're looking at these pictures, I have the picture first, and then the syndrome after it, so it's confusing if you're just looking through the slides, like which picture goes with it, and like 90% of the time I have the photo before I have the slide that talks about it, so this photo is of the skin lesions in inflammatory bowel disease, pyoderma gingernosa, so inflammatory bowel disease, it's most often with ulcerative colitis, but I've also seen anterior uveitis with Crohn's disease, always asked about GI symptoms, and then which of the four syndromes is this one related to? Surionic arthritis. Surionic arthritis, so you get these nail changes, pitting, it says resorption of the phalanges, that just makes me go like, like it's literally like resorbing the bones because your arthritis is like erosive, and the uveitis only happens with arthritis, not patients with only psoriasis, so you have to ask about the arthritis changes. Okay, Guy walks in and he has red, painful eye, and you see anterior chamber cell and all this corneal swelling, and he's 60 and he's unilateral. What do you think of first? Okay, but if there's like a lot of inflammation in the eye, and maybe the pressure is only like 24, could be fecalitic, and what's like our number one anterior uveitis, unilateral with corneal changes and high pressure, and some kind of viral uveitis, so hey Docs, how's that? Then you know what it is, so zoster can be any kind of corneal changes, so you know we look for dendrites or pseudodendrites, but any can be endothelitis. If I see anterior uveitis and pretty much any corneal swelling of any type does my membrane folds, I think either zoster or HSD, and that's the segmental irisatrophy, high IOP, decreased corneal sensation, the KPs can really vary. Workup, nothing, right? He has that rash, you know what it is, caveat. If you have zoster and he's 25, check each IV. So you must dilate every patient with uveitis, and we know management, I don't think they ask you doses on the test, so steroids are okay with herpetic diseases as long as they're being covered with antiviral. If they have a dendrite, maybe start with antivirals first. And then this was a great quote from our Dr. Vitalian foster book. It's widely believed that uveitis associated with involvement of any corneal layer is a manifestation of herpetic disease until proven otherwise. And some patients need just a little bit, so this is an argument test you on this, forget this part, that's all very practical stuff that they're not going to test you on. Okay, little girl, funny joints, white stuff on the front of her cornea, band, cure top of the AJA, exactly. So JAA typically is asymptomatic, they don't get red eyes, pain, photobobia, it's often bilateral, chronic smoldering, goes undiagnosed for a long time because kids don't know the complainable revision, they lose vision from the structural complications like CME, cataracts, glaucoma, and it's the highest risk in young females with ANA and Posseo-articular. And Posseo-articular is the same as oligo-articular, I don't know why there's two names for it, I've always driven me nuts, that's the same thing. Immunosuppress, early to prevent structural complications, there's a good study that showed JAA patients that referred early on to a tertiary center that does immunosuppression had decreased visual loss over many years and decreased structural complications, so we do encourage our community private providers for JAA just referred to here. Last question, a little off-topic, do you use zircan and kids? Do I use what? Zircan and kids who have... Not typically, but I also don't use a lot of topical antivirals in general, I think it was really cool. They love this screening chart, I don't know, I remember being asked this, I had literally have a mental block against this chart, you guys provider, and I have a mental block against this chart, so the thing to remember is the only ones that's three months is like young girl nuance at A&A, right, so she was diagnosed early, you haven't followed her for a long time, actually doesn't include girl, but that's more high risk, and then most everything else is six months until you've been following them for long enough, and then it's 12 months, and then systemic disease, even though it sounds worse, doesn't have as much uveitis, so that stills disease, which is like more systemic fever, chills, all that stuff, but do you want us a better way to remember it, let me know. Well, we're talking about this when we're studying one time, and I just memorized the columns, so it's like it's like three criteria, essentially, because only girls write as part of their story, you know, and then systemic disease, you know, so they have all three, then it's three months, if they have two, it's six months, except if they've had really long follow-up grade in seven years, then it's just one, there's just like columns as I memorized, like you said. I don't understand that one word, it's page of onset, oh, onset, okay, is less than six, but they've had it for seven years. Okay, Tin Yu, think of this, if you have a kid with bilateral anterior uveitis that is symptomatic, right, that's not your JIA patient, B-27 in young kids can be the exception to that rule, but so if you have, and it can be even a young adult that comes in and they have simultaneous onset of symptomatic anterior uveitis, then continue, and so if you just check your standard labs and you do even like a UA and a creatinine, you can miss it, all those labs can be totally normal, and then you can check a beta-2 microglobulin in the urine, not the serum, and it can be like 10,000 times the upper limit of normal, but you would have missed the diagnosis if you hadn't checked the rest of the labs, and then, visual diagnosis of kidney biopsy, but there's criterias of like probable and things like that that doesn't require the biopsy, and they actually tend to do well once you have a lot of immune suppression, so this is a good practical case I took from another one of my lectures about intermediate uveitis, I'm not gonna like waste all the time going over it, but there's a few slides I'll point out, so floaters, non-painful, kind of any age range, but a lot of time, young otherwise healthy adults, that's intermediate uveitis, so vitreous cell, and they can even have the nerve swelling, vascular sheathing on exam, exudates, NCME, and it's not pan-uveitis, it's intermediate uveitis, so differential diagnosis, number one idiopathic, number two sarcoid, number three MS, remember those idiopathic sarcoid MS, and then a whole bunch of infectious ones, which, you know, take a history, make sure there's no choreoretinal lesions, that's what pushes me more towards it being infectious, but you can have intermediate uveitis just with syphilis and Bartonella, this is the FAA, the circle showing like what we used to see with just, without the wide field, so that could look fairly normal, and then when you expand you see a lot of peripheral vaginal vascular leakage in that fern-like pattern, that's really classic for intermediate uveitis. Ask about review systems, this is a relative workup to do, classic findings, you know, this is some interesting facts, do you know smoking is associated with CME, intermediate uveitis independent than anything else, so another reason not to smoke. The connection between MS and intermediate uveitis is real, but we don't just do MRIs for everyone with intermediate uveitis, we ask about neurologic symptoms, but they're both autoimmune diseases, autoimmune diseases run together, so it's a much higher prevalence over the general population. Management, just topical steroids is the wrong answer. Not every vitreous cell needs to go away, anterior chamber cells, we'd like them all to go away. Vitreous cells we can live with, because they can float around the vitreous for a long time, they don't cause problems necessarily, they don't cause structural issues, sometimes they just trapped in young vitreous that's sticky, so you don't have to go to like zero vitreous cells. We like zero haze or trace haze or less, so when we think of active intermediate uveitis, we're really basing it on what we look with 20 and how much haze there is, and CME, you know, structural changes. Okay, new pictures. So if you're looking at the blood vessels in the top here, it like stops abruptly, I don't see any blood vessels in this area, there's a bunch of dot hemorrhages on FA, it corresponds to a lack of blood flow or non-profusion in this area, so it's a retinal vasculitis that has occlusion and non-profusion beyond it, so this is a occlusive retinal vasculitis, think of the scary systemic things like lupus, vichettes, and that's what this one is. So generalized occlusive vasculitis can be associated with hypopian uveitis, and then its mouth in general ulcers, much more common in Mediterranean, Middle Eastern descent, and then the good differential diagnosis for a hypopian, always think of in real life when we see hypopian, it's almost never vichettes because we live in Utah, it's more often HLV 27 in the United States in general, but worldwide hypopian, non-infectious, is vichettes, and ultlamitis, always think of it in a patient that doesn't have recent surgery, if they're like an IB drug user or have systemic illness, it can be endogenous and ultlamitis, and then tumor can be a pseudo-hypopian, so retinal vasculoma, things that can layer out lymphoma, leukemia, and look like hypopian, that's really not, and then another pseudo-hypopian is the lens induced uveitis, and then steroid, why is steroid can be look like a hypopian? Does anyone know that one? If you inject like intramural triacens or you inject steroid and it ends up in the wrong part of the eye, looks like a hypopian. Okay, this is still for vichettes, 25% have CNS involvement, that's why I can kill you, HLA B51, it's a clinical diagnosis, so the HLA testing I think is confirmatory, but we don't screen patients with UPIs with B51 testing, and then the pathogen test, do you guys know what this is? So you like stick a needle, tiny little needle under the skin and you inject like a really, really tiny like 0.1 or 0.01 amount of saline, and then you check 24 to 48 hours later, and like the normal person, it goes away, you can't see it at all, and patients with vichettes develop this little pustule or papule, but this only happens in like a small percentage of patients with vichettes, so it's not, if they don't get this, it means it doesn't mean that they don't have vichettes, but if they do have it, then you can get this. I've never done this, nodules on the iris margin, what are those called? Kept me on the cliff. Buried. That's a nodule, that's a nodule. That is a Kp, what would we call that kind of Kp? What kind of Kp would be, how would you describe that Kp? Yeah, mutton fat or granulomus, so this is granulomus disease, and what's the nodule angle called? Berlin's. So differential likenesses for granulomus inflammation, you know, they always separate this in your textbook, a lot of times there's crossover, but pure granulomus definitely thinks sarcoid TB, and then other things can go back and forth, toxo, syphilis, even herpetic can be, and then VKH, and syphilic is definitely granulomus. So sarcoid, up to, you know, 50% or so can have eye involvement. Antriubitis is the most common, but we also know that sarcoid is the most common known cause of intermediate diabetes, and then there's a whole bunch of different posterior manifestations, so we have a lot of pictures. This is the non-caseating granuloma. So look at the angle, tent-shaped PAS, apparently is very specific for sarcoids, so that's what they're showing here, just like a PAS that's in a little triangle, nodules, that's a Berlin nodule. I think these are supposed to show a little Coriorentinal lesions that are appropriate, and then some exudates, and then there's also candle wax drippings. This is actually what we see a lot in clinic, is that there's these peripheral, almost atropic-appearing yellow little spots in the retina, inferiorly. I see that a lot in sarcoid. Hemorrhages, macroanurisms, so intermediate uveitis with weird posterior changes, and you've ruled out infection, and there's some blood, but there's not retinal whitening that looks like ARN can end up being sarcoid. A lot of them can get treated as ARN initially. By Heiler lymphadenopathy, it can be like evanescent, apparently, and come and go, so you may not catch it on every chest x-ray. If you have a high suspicion, do a chest CT. If you think it could be sarcoid, because they can pick up changes on CT. And then the lacrim-ole gland involvement, I think they ask about this, may show like a path slide. Different things they can have. Conjunctival nodules, I think it's like up to 70% of patients not treated, not currently on steroids for sarcoid, can have these like conge nodules, and that's an easy spot to biopsy. Okay, so lens-associated uveitis, these are the ones I can never get straight in my mind. What's the mechanism of glaucoma in sarcoid patients? Is it the vermin nodules or tenting? Super question. I don't know. I think it's probably a combination of inflammatory, like uveitic, and then there may be something in their optic nerve, like some sarcoid changes in their optic nerve. I actually don't know. It's just because they have uveitis and they were exposed to steroids and they have inflammation, which causes glaucoma. If there's something else in sarcoid that makes them more susceptible, I'm not sure. So UGG syndrome, that's when you get recurrent hyphemias, inflammation, worry about the lens position. It can happen with certain types of lenses in the sulcus. What kind do we not put in sulcus? One base, yeah. Single nosulcus. You can treat you can treat inflammation with steroids, but then it typically recurs, so a lot of times it needs lens repositioning. Facolytic, so I remember it's like facolytic, meaning lens lysing through. These names always confuse me. So that's how I remember. I just think it's real big, fat lens, and it's like so big. It's like breaking through, so that's facolytic. So it's a really hyper mature lens, and it's starting to like literally lyse through an otherwise intact lens capsule. So if you haven't had surgery, you haven't had trauma, but you can get information in what looks like inflammation in the eye. So this is not real inflammation in the eye. There's no KPs. It can look like a pseudo-pipopian, but it's just like the lens proteins leaking through. As opposed to lens particle glaucoma, which are the actual pieces of lens particles that are in the anterior chamber and clogging the triangular mesh work after there's been a disruption of the lens capsule, but there's no KP. As opposed to facoantigenic, which is real inflammation in response to lens pieces. So try to remember what these look like on path, because they'll show you different path slides, and one of them is like the macrophages and all the stuff around a lens particle, and that's what's clogging the triangular mesh work, versus just like a little piece of cortex without the inflammatory cells around it. That's the difference between lens particle and facoantigenic on path slides. They get KPs in the last one, because this really is an inflammatory response to lens particles. A lot of the treatments are the same. Okay, what's the name for what this guy has? Not the syndrome. Heterochromia. And once a good professional diagnosis for Heterochromia, if we weren't in UVI this lecture. Okay, General Horner's. Fuchs, obviously, because we're in UVS lecture. And then what else is like, could be a potentially scary thing. Then when you see these stellate KPs, so stellate is like small and kind of star-like, and they go floor to ceiling. So instead of just being on the lower third or lower two thirds of the cornea, they're the whole thing, this is a blurry picture of trying to show fine vessels crossing the angle. So that's why they plead, they can plead during cataract surgery. Amzler sign. So fuchs, 10% bilateral. If it's on your test, it's going to be unilateral. Cinecia, I don't form, and that's why you don't have to treat the anterior chamber inflammation. So it's usually mild anterior chamber inflammation that is like hard to treat with prednisolone, but you don't really have to worry. You can leave, this is like the one exception to the rule, you can leave like trace cells or one-plus cells floating around the anterior chamber. It doesn't tend to cause the same problems as the rest of uveotides, so it's not causing CME and posterior synechiae. So some question of association with rubella, and they lose vision from glaucoma. So no cyclopigia, no steroids to treat the IOP. And you can have anterior vitreous cells in this as well, that's a fairly common. At what point during their course do they actually develop the heterochromia? Like would they come in with the heterochromia? So it has to be, if they already have heterochromia, it means it's been there a while, because it's like gets worse with time. So it won't be initially. Like if a agent came in, you would treat it, because you'd think it's still arthritis. And then it's usually like with years you realize, oh hey, now their eye color is changing, and they've never had posterior synechiae, and so then it becomes more obvious. Posomerschlossmann, not sure if this really exists, or if it's just undiagnosed herpetic anterior uveitis possibly. So really high IOP, like intermittent really high IOP with inflammation, think of posomerschlossmann. I also would almost always give them a course of the Paltrex just in case. And then hypertensive uveotides, herpetic, fuchs, syphilis, toxo, add CMV to that list as well. Retinal whitening, hemorrhages, viral necrotizing, retinitis, right? So this is why we dilate every patient. If you just looked in with your Linaidae, saw this nice little macula, looks good, but you could be missing all this in the periphery. And this is like the one disease that changes in 48 hours that you miss the boat if you miss it on your first exam. So, like missing number one. There it is. So, the kind of confusing thing is necrotizing retinitis can happen in totally normal people or in in neocompromised patients, but they have like different forms. So, ARN, which is like the fast scary one, happens to just a normal, healthy individual that has crap luck. And then progressive outer retinal necrosis and CMV retinitis happens in immunocompromised patients. And they have very similar features. If you just looked at a picture, you wouldn't know. Like they show you a picture, you cannot choose between these three. You have to know like the time course, number one, and patients again. High risk of retinal attachment, even with treatment. Treatment is actually very similar for all of them. And then we'll go into... So, I typically do oral valetrex with 2 grams TID, which is equivalent to the acyclovir IB dose, and then intubitrile either Foscarnet or Gansyclovir every few days until absolute improving and at steroids. So, for ARN, this is the ones that happen in normal patients, and it happens really, really quickly. So, if they come in and they say, you know, all six weeks ago, I noticed a little bit of blurriness, and they're still 2020, it's not ARN. So, this is like 48 hours, I woke up with floaters, and now I count fingers. It typically starts in the periphery, white patches that begin to coalesce. There's a lot of atritus. In younger people, it's usually HSV. In older people, it's usually BCV. And the other eye becomes involved. So, this, you know, this is a viral retinitis. I don't know which one, but progressive outer retinal necrosis. This is like ARN in both immunocompromised patients. So, it's fast, it's scary, but it doesn't have the atritus. It's otherwise very, very similar. So, no atritus. So, I'm out of retinal whitening, and there's no atritus. Think HIV, and progressive outer retinal necrosis. In comparison to CMV. So, this is kind of brush fire appearance along the arcade. This could be any of the three, but that appearance along the arcade, and it's starting a little more in the posterior fold compared to the periphery, I would think CMV. But you have to have a time course. This could be like, I didn't know anything was wrong, and you see this on exam. Or, this started six months ago, and it looks like this. So, different changes, retinal whitening, you know, little patches that coalesce. And so, immunocompromised patients, the C, this is how I was taught, the C stands for chronic. So, CMV is slow. 250 microns a week. That means it moves a half of this diameter in like a month, three weeks. That's really, really slow. So, this is the one you have time to think about it, right? Like, you treat it as R, and then you can think about it. If it's CMV, it ends up being CMV. You have time. Two different kinds. You guys learn about like the pizza pie fundus, and a lot of like blood, and yellow, and like hemorrhage, and white. But that's the fulminant kind. I've more often seen the indolent granular kind, which can be like this. It's just a big swath of retina that's like kind of depigmented, and pigment changes. To me, this looks inactive, but there was like a white border here. He could just still have really slow indolent CMV retinitis. That's the kind that's like missed a lot, and treated as anti-Rubitis for six months. And then you're like, oh, you're immunosuppressed from whatever. Moving on. Cotton will spots, hemorrhages, radiation retinopathy. It could be diabetic retinopathy. It could be HIV retinopathy. And it's not infectious. It goes away once their CD4 counts improve. Buzzwords. Retinal whitening adjacent to a big-minutes guard. Toxic osmosis. This one should have vitritis. This is like a clear vitro, which is kind of confusing. Usually it's associated with vitritis. Sometimes it's a clear view, and there's just like a little clump of vitritis right over that patient. That's pretty typical. And it's a focal retinitis. So the inflammation in the retina is here, but like way out here on the side, there may be vascular sheathing and like peri-perivenular sheathing and vascularitis. That's pretty common for toxin. So uncooked meat, soil, cat poop. It occurs at the edge of an old scar. If they have HIV, they check the brain. Classic treatment. Pyramethamine, sulfidizing, full linic acid, not fullic acid. And then I think when they say triple therapy, they actually mean prednisone with those three. And then there's like a million other things that work. A stalk. A picture of a stalk. A kid. There's a stalk from the nerve. Those are like buzzwords for a toxic cara. Young people, I think in your... But there's just being like a blur of similar syndromes when I was studying about it. And now I'm like, I don't, they're like not that similar at all. But try to remember certain things about them to like delineate them. So older person, nyctalopia. That's a bad picture. But multiple ovoid cream colored lesions scattered throughout the posterior pole. And they have floaters. Bird shot. Okay. ICG. They're showing you an ICG. For the love of God, I just hope it's bird shot. They're showing you an ICG for it. So these hypofluorescent lesions on ICG. More on ICG than exam or FA or already. So it's usually older people. Floaters. HLA A29.2. I think they asked me that on one of the tests. And it's just to be picky. They all need immunosuppression. And we follow them with fields and ERGs. Snake-like appearance. Maybe originated from the optic nerve. Surrogates. Older people. It tends to be really bad. Candidate alkylating agents. Those are strong medications. Block early stain late. Those are kind of buzzwords for ampy and serpiginous. So it's dark early and gets bright later. That's all that means. Mutes. If you have to remember one thing about mutes, it's unilateral. Just remember that. And they're small little spots. So that's like they're young. You're kind of myopic. They had a narrow program. Could be ampy. Unilateral. Small dots. Mutes. Ampy. Bigger dots. Pylitol. So, tiny little dots. The fohial granularity is supposed to be like pathenomonic. Which is insane because so many things have fohial granularity. But we're testing purposes. And then ampy. I always thought this is like the stock photo from, I swear, what they use on the test. And it looks like someone took like cotton balls and dipped them in yellow dye and threw them onto the picture. Right? Like little cotton ball spots. Which is totally different than the pictures they use for anything else. Like this is the ampy picture. Viral prodrome. Young adults. Block early stain late. That's a good picture of block early stain late. So it's dark and that's bright. Most do well. I'm kind of between the size of mutes spots and ampy spots. They're kind of small. But they're bilateral. So pick or multifocal. Little spots everywhere. So pick and multifocal. Probably on a spectrum. Technically pick has no vitritus and only involves a posterior foal. And multifocal has vitritus and goes into the periphery. I've seen some that lie in between. And they both can have CNBMs. As we know it can do anything. A masquerader can happen in any stage of syphilis. It can look like anything. That's why we always test for it. And then EVitis we treat it as neuro syphilis. Even if the LP is negative. But you still get the LP because it can be helpful to follow response to treatment over time. Lyme disease. I've never seen this because we live in Utah. But they'll test you on it. Most of the EVitis and keratitis happens in the stage two. Can be intermediate EVitis. The targetoid lesions and treat with tetracycline. Sympathetic ophthalmia. This is brain alumnus inflammation in essentially in trauma can be of attractomy. For OCAPS purposes it spares the coreocapularis and VKH doesn't. I don't know if that's really true. But if you see neurosensory detachment and inflammation, think of this disease. Dallon flukes, flukes nodules are in collections of like epithelioid cells between RP and fruits membrane. And those are good olma and fat KB right there. And then these like multiple punctate staining on FA. And that's the that collection. This is a good pass line. That would be a good question. So you see this, a pass line, and then they give you a history of inflammation. And that's the Dallon flukes nodule and sympathetic. VKH very, very similar. But no previous trauma. They all need immunomodulatory therapy and they like the the systemic symptoms that get with it. So like the ringing in the ears, they get like meningitis tinnitus and the poliosis, they can have like a flop like a piece of white hair or a section of their eyelashes that are white or patches that are skin that turn white. And this is pinpoint leakage on FA and then it pools in the areas of neurosensory detachments. And this could be like 2400 and you give them six to oral predicate come back two days later in their 2030 lymphoma. Always think of lymphoma. If you see intermediate uveitis in like a 65 year old, or you're like, Oh, this is your first bout of intermediate uveitis and you're 75. So I think it's trying to show is an IOL with forgot an IOL with like particulate on it like debris stuck on an IOL. So that's chronic endophthalmitis like piaquines. Yeah, it's so hard to tell what layer they're talking about. Chronic endophthalmitis. So recurrent inflammation years after can get better with steroids and then keeps coming back. And I was surgery always think of chronic endophthalmitis and treated like endophthalmitis tap and inject and often needs lens removal. Okay, red eye and it doesn't hurt. It's probably just like conjunctivitis. But if it's tender to touch, it's painful. They're not saying like itchy and watery, I think episcleritis or scleritis, and there may be a little nodule. So 50% of scleritis, we can find an etiology about 30% we don't. But some of the etiologies are pretty scary. So rheumatoid arthritis is the most common. Infectious is, you know, only one out of 10. And most common is herpetic. So it's still not like they need biopsies or anything like that. And for anterior scleritis, we have diffuse and nodular. And we treat them very similarly. And then for necrotizing scleritis, there's the white, quiet, non painful kind, which is called scleromilatial perforants. And then there can be necrotizing scleritis that's in the setting of like a red painful eye like this. And I've seen this with with wet nurse and it definitely happened with RA as well. So this is a very grainy picture of a macular star. So someone has nerve swelling, and exudates in their macula, especially if it's in both eyes. You want to move loud if you see like nervous sensory attachments and nerve swelling in some exudates. What do you want to make sure he doesn't kill the patient? Not you guys. I live in hypertension. So always think of that when you see like exudates and nerve swelling, and your like brain goes down to you via this pathway. Think first check their blood pressure. But unilateral 20 year old probably Bartonella cat scratch. We typically treat with doxycycline or steroids, but there's apparently no evidence that it changes the course of the disease, like they tend to get better anyways, if it's cat scratch. But there is a subset of just idiopathic recurrent that needs immunosuppression. Bonus round if you think it's like unilateral RP think of these other things first. Old syphilis actually even old CMV retinitis is inactive and all that granular changes in the periphery could be look like RP and it could be old CMV retinitis. Syphilis can have that granular appearance or this entity called Duzin, which is diffuse unilateral subcuter retinitis. It's literally worm crawling around your retina. It's really disgusting. We've had one recently. And then I think they like to test on the things that cause it. I think in North America, the raccoon one, that's not his fellow raccoon. Try to burn the worm, but they're like, the worms are photosensitive guys. So it's hard because you turn on the light and then the worm runs away. But if you get it, you blast the worm with photo-calculation. Otherwise, I'll bend us all in steroids. Okay, immunosuppression. This is just like step back. I mean, if you're all these different immunosuppressive, think of the categories, right? Because it can help you with the side effects because you just put it into that category. And it helps you with like how we actually use them. We don't use two from the same category, right? So anti metabolites, there's three, methotrexate, cell septase, ethyl free, like phenylate, the cell sept. Then calcineurin inhibitors, we use cyclosporine more often than tachylimus, which you can use either. And then alkylating agents, I should put the one down here because we kind of go like in this order. Alkylating agents are the ones that have the really scary side effects, may cause cancer, but actually the only ones to show that it induces remission. All the other ones, like don't really induce remission. You get off the drug and if ZZ hasn't finished its course it's going to take, it can come back. And we think cyclosporine can actually induce remission. And then TNF agents, infliximab, that's IV, adelibumab is the humanized monoplonal antibody to TNF, and it's subcutaneous injection, etanercept, full frowny face. Enbril is the only one we don't use in uveitis. Like pretty much every immunosuppression you can think of helps uveitis if they're using it for anything else, with the exception of enbril. We think it is either not helpful or potentially deleterious. So, enbril, no uveitis. It may actually be like worse than placebo. Oh, that's nice. Didn't finish that slide. So tosylibizumab is one of the newer ones that there's a recent good study showing it helps with vitreous haze and CME. So we're going to just pick like one from each category for anti-metabolites, methotrexate, dihydrate, folate, reductase inhibitor. The folic acid can prevent a lot of the side effects. This is how. Just read through this slide. And I think this is kind of the things to know. Milo-suppression, hepatotoxicity, don't get pregnant during alcohol. Cyclosporine, calcineurin inhibitor. We usually don't use cyclosporine alone. Actually, I can say I have never used cyclosporine alone, but we use it as like adjuvant therapy in addition to one of the ones from the previous category, especially in bird shot or VKH. You can add it to methotrexate or cell sept. The big ones to remember is it's nephrotoxic, hypertension, it's like phosphamide. It's the mustard DNA cross-linker that is cytotoxic and bone marrow suppression, hemorrhagic cystitis, which apparently you can prevent by drinking a lot of water and taking mesna and then cancers. There's like several studies that show that it can increase lymphoma, non-melanomous skin cancers, anti-TNF inhibitors, the contraindications, heart failure, hep C, MS, untreated TB. You can use this in latent TB if they're untreatment for it and induce alupus-like syndrome. So the drug-induced uveitis that says infliximab, it's usually in a setting of infliximab inducing like alupus-like syndrome and then they get scleritis-reunivitis. Enbrel may actually like worsen or cause anterior uveitis. That's debated. And so we typically will use low-dose methotrexate in addition to anti-TNF because I think it helps the anti-TNF work better and it prevents the chimeric antibodies that makes it ineffective. So enbrel can make sarcoid angiobiotis worse and then this is a little bonus thing I think they ask you on. TNF inhibitors can make multiple sclerosis worse. So what's the disease that we treat a lot in uveitis that can be associated with MS? Intermediate uveitis, yes. So if you're thinking of starting your intermediate uveitis patient on a TNF inhibitor, like you've already used methotrexate and it's not working, you want to add him here. So we're getting MRI, Ascovignuro history. Okay, drug-induced uveitis. This is the definite systemic categories. Is it off of your rifabutin, bisphosphonates. I missed that one on my test. And sulfonamides. So this treats CMV, MAC, osteoporosis. Remember those. And then this is probable for anti-TNF agents. And then maybe category down here. Something carboxylamin, I can't remember what it treats. Oh, MAC. Topical definite, this is a topical beta blocker that was used to treat glaucoma, but it was at a higher dose of .6 and it apparently definitely called anti-Uveitis and it's no longer in the market. So I don't think all topical beta blockers call cost uveitis, but apparently this one, they had some pretty good evidence that it did with like re-challenging. Bramonidine, there's like a lot of reports of granulomus anti-Uveitis with bramonidine. I haven't personally seen it. And then prostaglandin analogs like latanoprost, they always mention it can cause CME or reactivate HSV keratitis. But it is like more recent studies shown that in patients with uveitis from something else that using prostaglandin analogs does not cause CME and it does not worsen or exacerbate their anti-Uveitis. So we use prostaglandin in patients with known anti-Uveitis. And then topical steroids was on the list of drug-induced uveitis, which really confused me, but they meant withdrawal of the steroids can cause uveitis. Steroids don't cause uveitis. And then reports of individual bedjab injections causing uveitis, there can be like the sterile inflammatory response, things like that. HLA associations E27 and E29 are about seven or eight percent in the general population anyways. So that's like one in thirteen, so we don't just screen for it, right? But if it's the right scenario. And then intermediate uveitis in DR15.