 So this, surprisingly enough, is a pretty big topic. But Catherine was kind enough to edit my lecture a little bit. But it's objectives. You should be able to differentiate and identify anti-UVIs using definitions and nomenclature. I'm assuming all of you have read the Sun criteria. So the Sun Working Group was a bunch of UVIs nerds who got together and decided what specifically comprises inflammation, how to create inflammation, and to create it in a standardized fashion. There's two reasons you do this. Number one is to make sure that every single patient that you see, if somebody else was to see that patient later, they'd be able to tell you if the patient is less or more inflamed than when you'd seen them before. The second thing is if you've ever done a retrospective chart review and seen that notes are not standardized, it's very, very difficult to conduct retrospective research without some standardization. And the IUSG and the AUS, they came together and they created the Sun criteria. And the vast majority of UVID specialists in the world actually use the Sun criteria. So it's easy to cross-compare across institutions as well. Like to be able to recognize typical signs and symptoms and to UVID us, understand the approach to examination and a little bit about diagnostic modalities and testing, talk about infectious and non-infectious diseases that can be associated with this, and understand treatment and management. So it's the most common cause of UVID us, three to four, about 75% of all cases with an annual incidence of 8 in 100,000. It's the easiest to manage for the most part, but I'll talk about certain complications that make it hard. You can have cataract, glaucoma, CME, band care, top of the endothelial failure. And many pan-UVIS syndromes can actually start as NGUVIS, including VKH. We'll talk about intermediate UVID us on Monday, but there's anti-UVID us generally involves inflammation of the iris and the ciliary body. So you can have an iridus component and a cyclitis component, which is why a lot of patients with iris-cyclitis actually present sometimes with low pressure. People can also present with high pressure in the eye when the trabecular mesh work is involved. Remember, there's no hard barrier between any of these structures, all comprising the UVIA. Therefore, all of these structures can be involved. So question, if there's CME or papillitis, is it still anti-UVID us, Brad? Yes. That's right. So vascular reactivity and leakage, in conjunction with any intraocular inflammation, does not change the kind of inflammation it is. So you can have CME with anti-UVID us, posterior UVID us, intermediate UVID us, and pan-UVID us. Similarly with papillitis as well with severe anti-UVID us, you can have swollen optic nerves. How about retinal vascular sheathing? Can we have retinal vascular sheathing with anterior UVID us? The answer is yes. Absolutely you can. You can have just mild vascular reactivity as well. As long as we're referring. So here's a 17-year-old kid who was followed by optometry and treated with drops for about six months. I refer it in for bilateral anterior UVID us. So is this really anterior UVID us, Catherine? What do you see on the ultrasound? So it is two-scale. It's not that I squished the image. The eye is squished. Looks like there is thickening of the retina. Of the coroid. Coroid. And then there's this white cataract and evidence of old synechia. And this is actually the length of the eye because I was pressing a little with the ultrasound probe. Should that happen now? This patient's pressure was zero. Seven-year-old high school kid treated with anterior UVID, for anterior UVIDs, but never really dilated. So this is, as Eric often mentions, Shagura has a lot of soapboxes. This is one of them. You can't call something anterior UVIDs unless you've dilated the patient because you have no idea. This patient actually had VK age. And it's now the president of the low vision chapter in his college at UC Berkeley. But he does pretty well. He's a trail runner. He's 2400. So you have pain, photophobia. You have to distinguish between photophobia and photosensitivity. Remember, photophobia is kind of a bilateral phenomenon. So if you shine light in the opposite eye, then that which is involved, you'll still have pain in the affected eye. So photophobia has to involve pain. Photosensitivity does not. Certain anterior UVIDs are painless, such as GIA, Fuchs, and Diniu. There's redness. There's reduced vision from the cataract or mediobacity, CME, and pupillary meiosis from posterior scenicia. It'll reduce visual acuity, increase pressure, or decrease pressure, see the reflux. Remember, flair may not always go away. Because flair, what is flair? Chris? Yeah, so basically, it's incompatible blood vessels in the iris as a result of inflammation, resulting in kind of this exudation of protein into the anterior chamber. And flair, regardless of how much you treat it, will may not go away, which is why sun does not use it as a measure of inflammation. Assess the quality of the cell. It's pigmented, duskier, fractal, fine versus coarse, fibrin, and plasmoidequoise. So what is plasmoidequoise? If you sit there with a sit-damp and watch cells go by, not that much fun. But you'll see that there's a particular circulation within the anterior chamber. And if it doesn't flow, if the cell's static, it's one of two things. Either you have silicone oil in the anterior chamber, or you have a plasmoidequoise, which means that it's a thick, proteinaceous fluid. And I've actually done anterior chamber daps on these patients, and it comes out, and it's like oil. So if you see fibrin or that, then that's a bad prognostic sign. That means it's a lot of inflammation. It's kind of a prehypopion. So what features do you look for in geriatric precipitates, Marshall? How are the characters? They can be fatty or fine. These modern fatty ones, the granulometous KPs, where you can have fine stellate ones, which you'd see in herbedic disease or CMV distribution. So it's important to know where they are. So remember the normal circulation within the anterior chamber. So you have fluid that comes down and then goes around like this and then kind of circulates that way. If you read anterior chamber dynamics, surprisingly, people have written vipers on that bit using nanodots. That's what is responsible for what's called Arl's Triangle. Arl's Triangle is, everybody likes to name something after themselves, right? But Arl, I don't know who he was, but there's a triangle where you most commonly find the greatest distribution of geriatric precipitates. Now, if you have most conventional ureodities, we'll have kind of a lower distribution of herbedic precipitates. But what if it's distributed all over? Then what are you thinking of? So there's certain diseases that cause kind of an even distribution of herbedic precipitates. Most of them are the herbedic diseases, such as CMB, BZB, and HSV, fuchs, heterogromic hydrocyclicis, which is actually just rubella. You have this kind of floor-to-ceiling distribution of geriatric precipitates. And you can see that with some other diseases as well. So Arianna, name the, what kind of precipitates are these? So first, the distribution is mostly inferior predominant. Yeah, and they're big. They look like bacon grease. Actually, they should call it bacon grease. But this is what they call macrophatic precipitates. And they're kind of these greasy, stuck-on precipitates. And this implies granulomatous disease. And so you'd see this in sarcoidosis. This was actually one of my patients with sarcoid. This is also kind of greasy, stuck-on, so granulomatous. And you'd think sarcoid or TB or something. But no, this is actually vericillus austere. So vericillus austere can also give you these macrophatic greasy kind of precipitates. Then you have these fine stellate ones. This is a patient with HSV. And this is a patient with HLAV27 and TUV8. Notice how it very nicely respects the triangle, right? Whereas these ones, you don't get a good book, but this one actually didn't. This one doesn't as much just because of severity of the information. So Rachel, when can you see a hypopion in anterior uveitis? Which particular diseases are you thinking about? Absolutely. That's probably the most common. What other diseases? Even if it's not anterior uveitis, you can see a hypopion. What must you think of immediately when you see a hypopia? Yes, absolutely. So never doubt that sometimes patients can have kind of an endothemitis without having ever had surgery. Endogenous endothemitis. Eastern mic clinic is actually fairly common. Globally, it's not. But you can see a hypopion in other diseases as well, where there's severe enough information. Even when mismanaged or unmanaged, you can see it with hermetic disease. But conventionally, for the purpose of your boards, the hypopion can be seen in the chest disease, HLAV27, associated anterior uveitis, rifabutant toxicity, which is a drug that they used a lot in early for prophylaxis in patients with HIV. Infectious endothemitis, endogenous exogenous. That's the first thing you should ever rule out. So if a young person who's healthy and not an IV drug because it comes in with an endogenous endothemitis, give them a chance with topical steroids first. But if an older person with, say, an indwelling catheter or who's diabetic or has some form of immunosuppression or likes to shoot up IV meth every once in a while, those patients you should probably tap. So iris nodules are monocytes, an inflammatory degree. So kepi nodules and vasachin nodules, both of them, actually, are granulomas. They're iris granulomas. They're exactly what you'd see in a lung. For instance, with sarcoidosis or tuberculosis, except that they're non-casiating. Kepi nodules kind of peek out from the side, from the iris rim. The sarcoid nodules are on the face of the iris. And you can see them in sarcoid syphilis DV leprosy. Actually have a patient with leprosy. Hansen's disease, no relation to him. If anybody can think of a syphilis sign, and then we'll name it after Eric. Eric is dead. So sarcoid syphilis DV leprosy, iris nodules and skin finding, as well, think of sarcoidosis. What is the classic rash of sarcoidosis? Arid. You can see that with sarcoidosis. You can see that with sarcoidosis. You can see that with sarcoidosis. You know Alex, that's a granuloma and neurofibromatosis. All of these can give you these iris nodules, which aren't actually granulometous. You can have peripheral anterior senicae where you have, start with these little nodules in the trabecular mesh work. This is a patient with sarcoidosis. What's this nodule called? That's right. It's a Berlin's nodule. So Berlin's nodules precede the tent-shaped BAS that you see in sarcoidosis. This is a patient with multiple iris nodules, BAS, and posterior senicae, also with sarcoidosis. This kind of tent-shaped BAS, you see. This is a precursor to that. Then you see these. This is kind of characteristic of sarcoidosis. It comes up like that, like a beak. And then your posterior senicae can result in people's occlusion, et cetera. If you have increased IOP, think about HSP and BZB. First up, think about fuchs. I hate the fact that it's called fuchs. It's actually just rubella-associated anterior gliatis. Names should imply etiology. Look for heterochromium. But remember with fuchs, what percentage of fuchs is bilateral? 15%. So it's not always fuchs heterochromic aerosectitis. You can have heterochromic aerosectas without heterochromium in about 15%. Sarcoidosis, toxoplasma, and VKH can all cause increased IOP. And interestingly, all of these diseases can also give you floor-to-ceiling keratic precipitates. So remember, all the diseases that cause floor-to-ceiling keratic precipitates can also cause increased IOP. Why is that? I don't know. All right, so you guys have read about the classification, but let's talk about a few little things. Catherine provided me with these very advanced animations. So here's the first patient. First occurrence of sudden onset. I write this. Inflammation resolves after the course of topical steroids. What is this? Is it acute, chronic, recurrent? Acute. Nice. Why did you pick salmon? I don't know. It matches the border. Yeah, it's the theme color. I mean, I'm impressed with the aesthetic, but anyway. So yeah, the first ever episode comes in, acute aerosectitis. How do you treat this? You treat this with topical steroids. And if it's really bad, then you think about oral steroids and you think about injectable steroids. What do you do before you ever inject or give people oral steroids? That's right. Good job. Which is more than a certain doctor in a certain place, a certain distance north from here. But we'll talk about that at M&M. So box number two. Okay, so she later presents four months later, not three, four months later with a similar episode and has been without symptoms in the interim. You just throw her into the bus. No, I'm not throwing her into the bus. I can hear the wheel. That was wrong. You were wrong, guys. So this is recurrent. Recurrent, why? Four months. Exactly, one in three months. So her husband shows up and you're treated being referred by an optometrist in Roxbury, Wyoming, in high-grade redness, photophobia, foggy vision for six months despite frequent use of lysine, which works for everything. You initiate appropriate therapy on follow-up. He's quiet. He's quiet. His eye, not him. Although he's... I'll say one word as to him. He's also quiet and quiet. But two months later, he has another therapy and he has chronic... Chronic. Well, when will you know it's chronic? Two months. Right? So he has to have recurrent episodes or episodes that are controlled with medication that are controlled or not controlled that span greater than three months. Technically, he's still in the acute phase but if that, it would have to last beyond two months then it would be chronic. But for purposes of this lecture, chronic. Oh, yeah. Which disease is always recurrent and alternating? Almost always recurrent and alternating. Each of them... Which, I write as syndromes are most commonly chronic. Little child. Joint pain. So, JIA or sarcoidosis is most commonly chronic. So by defining whether a disease is chronic or recurrent, you can actually have a hint as to what kind of disease it is. So JIA will never be symptomatic. JIA will never be acute. Except for a few exceptions. Whereas HLV 27 UVI, this is usually exclusive and comes in with the tomato eye and all that stuff. So, unilateral and unilateral, bilateral. Think about infectious entities such as HSP or VCV if it's unilateral, especially if the patient is older. Bilateral, most likely is systemic disease. Bilateral HSP can be seen in... People with adopect dermatitis. So people with adopect dermatitis because adopect dermatitis and eczema, they're all D-cell dysregulatory diseases, right? So those diseases, you can see bilateral HSP. So the patient with Down syndrome comes in. First thing you look for is the suspicion of eczema. Because Down's and eczema are very highly related. And if it does, then bilateral disease, which is drastic for the HSP, can be bilateral HSP, right? HSP iridism. If it's alternating, if it goes from one eye to another or if it's explosive, then think about it. Check for the HIV 27 haplotype. So which diseases may present with granulometous KPs? Shout them out. Sorry, sorry. TB. VCV. VCV, HSP as well. And then there's other ones as well. So you can have necrotide, necrobiotica, xanthogranilomet... xanthogranilometous necrobiotica. That's a very rare disease. There's only three cases. But non-granulobrosclerotic precipitates. Fuchs. Basically everything, right? Fuchs, CMV, HSP, VCV, et cetera. So think about DBS sarcoid, but also think about VZV and syphilis. Syphilis can also present with granulometous disease. We talked about this. We talked about this. Fluorocetanin-creatic precipitates. This was actually one of my patients with CMV, anterior vitis. And if you look really closely, you can see that some of these little KPs, they're arenas in these little rosettes almost. And that's kind of classic for... You see better on the computer. But this is kind of classic for the CMV. And this is CMV, not in an immunocompromised patient. This is CMV in an immunocompetent post-unilateral, often hypertensive, resulting in corneal endothelial failure. And this is kind of this indolent course that doesn't respond well to steroids. What do you treat these guys with? Which antiviral do you use? You could, but that's a lot of SIV, right? So you use valgancyclovir. So you can use valcyclovir. What's the problem with valcyclovir? So 15% of CMV develops resistance in the septic liver. That's good. But the other thing is also that gancyclovir can cause aplastic anemia and kidney failure, which is bad. So you can actually... There's other agents you can use as well now. Cromovir is one that's a non-FDA approved for peripheral CMV, but not organ-specific CMV. That's a good drug. And then there's CMV-specific IgG, cytokam. So look at whenever you see a patient that you suspect of, you know, a viral, you check the cornea. Before you let anybody put drops in, check the corneal sensation. Most patients with HSV or VCV, or even CMV will have relative corneal anesthesia. And there's also infiltrate. So if you see any corneal infiltrate, think about viral etiology. Think about associated anti-HMB findings, iris or the angle. We talked about PAS, Berlin's nodules, Bussaker, capion nodules, iris thinning. All these trends illuminate your iris. Think about sectoral or diffuse iris transillumination defects seen in HSV and VCV. Spectatively, although a lot of patients with HSV can have diffuse irisctrophy as well. Think about the onset. Is it explosive? If it's explosive, think about HLAB 27, the chest disease endogenous endothermitis. If it's indolent, think about JAA, fugue, CMV, iridus, endotheliitis, DINU. If it's acute and recurrent, think about HLAB 27. The chest, herpetic and vesiclecal endothermitis or plebitis can wax and wane. DINU, sarcoidosis, trauma of foreign bodies ask if the patient's been grinding metal on metal, but sometimes you can have little copper foreign bodies in the end of your chamber. I actually had a patient who had a pet tarantula who would walk over his face at night when he slept. It was a very loving relationship. And we found in this guy's anterior chamber tarantula spines' hairs that had migrated through his cornea into and you can't take them all up. Yeah. He just keeps it in a tarantula. Why does he do that? It's to cuddle. I'm on his face. How else do you cuddle with a tarantula? He is lonely at night. Is he from Wyoming? No, California. Oh, yeah, of course. No. Let's just do this. Grohnick anterior urethritis, DAF, fuchs, sarcoidosis, DINU, herpetic, infectious, length-induced. So sometimes if you have patients come in, the cataracts are here, the little tiny chip of a nucleus sitting in the angle. It happened recently from Zog's patient. He said it was AMD. I said, no, go back and look at the angle. I tried to be nice, but... Blast syndrome and idiopathic. Blast syndrome is a granulometous disease associated with not two mutations in children. So it's basically a juvenile sarcoidosis with kidney findings and really, really difficult urethritis. So base your history on your symptom complex. So recurrent anterior non-granulometous anterior urethritis ask about back pain. And not just any back pain. Don't say, oh, the patient has back pain after he deadlifts 300 pounds. No, think about specifically inflammatory back pain. So inflammatory back pain is how long should it last after you get up in the morning, greater than 30 minutes. Should it also be present after you've been in a car for a long time? Yes. So if you wake up with back stiffness and you have to work it out until about 45 minutes after, that's kind of this inflammatory pattern back pain. And usually it's not associated with ridiculitis. So ask about, if you have a hypopion, ask about back pain, mouth and genital source. What are you thinking about? The chest. The chest. The chest. The chest. The chest. No, no. The ATM machine. My top. That's Brad said ATM machine. That was really pissed me off. It's an automatic machine. It's like pin number. Like pin number. Non red or chai tea or jackass. Chai tea. So exposure to infectious diseases, HIV, TB, risk factors. Like pet tarantulas. I had a patient with sub-retinal track marks and this thing that was moving around, he had a pet raccoon. And pet raccoons can carry dog tape for him. So that's the dances. So encyclistoma. And so we found this little worm crawling around behind his eyes. So if you have a pet raccoon, don't. And then travel. So travel. I've had patients, missionaries who've come back with interstitial carotiditis and adjuvitis. Think about oncocerca. So river blindness can actually cause adjuvitis in some patients. Other patients with tuberculosis. I have a patient who's a nurse and she travels back to the Philippines every year to work in a TB clinic for two months. So she has TB. And I have another patient who travels back to Indonesia every year and she has adjuvitis, interstitial carotiditis, thickened corneal nerves. What do you think she has? It's an unfair question. She has a lot of procedure. So Hanson's disease. Hanson's disease. Yeah. That's right. So always remember that. Just think of her. Think of her. Ask about lower back pain and the overall general ulcers which you would see in the jets. Skin lesions which you'd see in many things. What we'll talk about them. Arthritis, gastrointestinal symptoms, medication use. What's the latest one? We love to treat patients with walking pneumonia with this. Avalox. So Avalox and moxifloxacin can actually cause a bilateral, very herpetic looking anterior uveitis with irisography. So great information for reasons that previously mentioned. Look at the cornea check sensation. Look at the conjunctiva. If you have sarcoid with conjunctival nodules and if you biopsy those nodules, you have a chance of about 60% of finding nodules. If you just do a blind conjunctival biopsy then you have about 30% chance if it is sarcoid. Iris lesions, lens plaques or precipitates think of a chronic endothemitis. Enter your vitreous cells and dilate all patients. Never should I ever hear from any of you that you didn't dilate your patients. Oh, it's very good. So help me. OCT, fluorescent angiography, rule out any posterior uveitis. Fundus autofluorescence. I've had a lot of patients with syphilis who presented with an anterior uveitis but you did a fundus autofluorescence with black or immaculate changes. So what is that? That's AA? So yes, tertiary syphilis but what kind of uveitis is it? It's supposed to be uveitis. It happens to have antigen for cell. ICG as well. So I generally start with CBC, CFP, FDA, VAS, RPR. So do a direct and indirect tereponeumal test. TV testing can be indicated although there's a really interesting article by Jim Rosenbaum in 1986 talking about a kind of a Bayesian approach to TV testing in uveitis. It turns out that if you do it in an endemic area, sure it's useful, but if you do it in a non-endemic area, you may end up with more false positives than true positives. JustXray is useful for TV and sarproidosis. ACE, lysozyme, and volumetric just CT only if the features are suggestive of sarproidosis. So would you do ACE in a child? No. Why? Kids have high ACE. They always have high ACE. Would you do ACE in a 60 year old hypertensive? What would you ask for first? So all ACE testing is based on ACE activity. So if you have somebody who is on lycinoprol, then the ACE is going to be low. So don't check ACE. And even if you do in the presence of a low suspicion check ACE, well, if it's positive it means nothing. If it's negative it means nothing. It's only got a 60% sensitivity and specificity and a positive predictive value in the 50s. So not a great test. It's like a coin toss. HIV, if you have risk factors, I don't test all patients for HIV. And pre-immunosuppressive testing. So if you're going to put a patient on immunosuppression check hepatitis B, hepatitis C. So the CDC recommends happy surface antigen, happy versus antibody, and happy core antigen. So those three. And for hepatitis C testing check for that immunohistochemical sorry, ELISA-based test for C. But the definitive test is the looking for basically quantitative PCR. So kind of a screening and confirmatory test. So check those because if you immunosuppress somebody with viral hepatitis you will kill them. They often go full minute. Similarly, check for tuberculosis if you're not going to, if you're going to put somebody with TB on a biologic they'll end up with miliary or disseminated TB or TB meningitis and that's a bad look. So, what would you check if there's recurrent alternating non-granulomatitis? Very good. My anti-machine. So also spine and sacroiliac x-rays in a room console. Useful. What if you have hypertensive UVA so stellate floor to ceiling KPs and a corneal infiltrator. Just really easy. How do you check for that? Is a blood IgG IgM useful? No. No, because everybody's had very little disaster and about 70% of the population is zero positive for HSV. So it makes no sense. It's useful to rule out the disease because if you have a child who's negative for HSV, vis-a-vis then, yeah, sure that means they've never been exposed therefore they don't have hepatic disease. But if you have an HIV positive patient or otherwise immunosuppressed patient you check them for HSV IgG IgM that means nothing because they won't have the antibodies. So granular risk erratic precipitates, what would you check? Yes, you especially emphasize TB in sarcoid testing and in those patients that often you know go straight to a CT scan because if it's a negative chest X-ray only very few patients actually have a Batwing Hyaluridinopathy. More patients are likely to get you know have findings on just CT. Yeah, I'm female, indolent, bilateral. I'm a microglobulin, I think about DINU and a hypopoeia. Consider blood culture, AC type of culture, bacterial fungal BCR. But a chest disease, so there's only the Asian phenotype that is positive for the HLA B51 and B5 haplotypes. So it's actually not a very good test. Other European phenotypes of the chest disease are not positive for those haplotypes. It's not as good as the HLA B27 or HLA A29 for birth chart. So young with joint pain check an A&A, rheumatoid factor HLA B27 and root console, looking for what? Right. History, if you've had Echesia, Melna, chronic or recurrent diarrhea transferred GI for or ulcerative colitis. Yeah. Do they come to your clinic? Do they come to you? Gene Daven, who goes to Great Lens. You come in for RETA and you come out with a colonoscopy. Don't do that. Urethritis and arthritis, what do you think about? Reactive arthritis. Reactive arthritis, previously known as Raita syndrome, Raita was a Nazi. HLA B27. Salmon color, skin plaques, arthritis and fingernail pitting. Soriatic. Soriatic arthritis, right? So, is generally psoriasis does not, in the absence of joint pain does not have iridus, but psoriatic arthritis certainly does. Remember for HLA B27 as well, so these patients often HLA could be twice as positive. Sexual risk factors, history of IV drug abuse, basically the gamut of things. I mean, you could check for anything, but HIV is important. There is no utility in ordering any of the following. ANA, even though the wills manual written by the esteemed doctor, says that you should check ANA for anti-UBI just don't. Unless you're looking for JIA, there's no other reason. And the only reason you look for it in JIA is the food factor, useless. All these SSASSB ones, not useful. HSV, VZV, titers except for when you're trying to rule out disease. Epstein-Barr virus, even if it is positive, who cares? Yeah. Isn't RF negative in JIA? RF can be negative in JIA, but you do have a subset of JIA in males in particular where you have this systemic onset, still disease, kind of, where you have a positive RF. But RF is what? RF is basically anti-IGG, ITG, right? Yeah. Which is why arthritis is an immune complex mediator, for the most part. So a huge recurrent anti-OVS. Go through this really quickly. I know we don't have much time. We have seven younger male, 90% is explosive recurrent, alternating, and dear, the best predictor of which I was going to be involved next, is which I was involved last. Associations with enclosing spondylitis, reactive arthritis, inflammatory bowel disease, psoriagnetic arthritis, and Wippel's disease. HLAB-27 is positive in 7 to 11% of the population, so interpret that with caution. If you're at M&M this next week, then we'll talk about that. Ask about inflammatory patterns of axial arthritis. Think about rheumatology, referrals, or SI joint films. When you have recurrent, alternating non-granulomatous, anti-UVI, just plus HLAB-27, there's 30% chance of AS, or other theronegative spondyloarthroopathies. If you have the arthritis plus HLAB-27 positive plus back stiffness, you have a 60% chance of developing AS. So, you know, it's pretty common. Let's get that. Anti-UVI is in 25% of patients with AS. This is what it used to be before we had biologics, you had this kind of foreshortening of the spine with angiolosis, and this is actually one of my patients who has had AS since the 1960s and they're actually like this, and it turns out it's terrible, but he's also got steroid associated osteoporosis and pathological fractures. We've come a long way. So, you react to arthritis, we already talked about this, it's polyureligoarthritis. You can have UVIs and conjunctivitis. You can't see, you can't be, you can't climb a tree. Just remember that the triad. There's an infectious trigger, it's often Shigelo, you said, you know, compel bacteria, but it can also be certain medications and the methicin can cause reactive arthritis. What's this rash? It's a great word. It's called Charter Derma It's a discriminating slander or a palmar rash associated with which disease? Reactive arthritis. So, but if you saw this and it was scaly and somebody with a high risk of high risk sexual activity or, yeah, so syphilis can also cause this, but the main thing is that you have these kind of blisters here, so that makes it KB. But in syphilis you have this erythematous but radiating with our blisters rash and the palms and the soles. So, I won't go into this, but I'll give you guys the lectures if you want the statistics and stuff. Soriatic arthritis, systemic findings HLAB 27 positivity in 50%. UVA is developed in 25%. So, you have skin and nail petting, you have saucis digits and anchor like lysis where you have like the lysis of the nails. So, this is a patient with psoriatic arthritis that they've started to lose their fingernails that they're spitting of the off the fingernails is this deformity DAB, MCB mostly and also kind of also has this one neck deformity that you see in rheumatoid arthritis. This is psoriatic arthritis and of course you look for these salmon colored skin regions. So, Bob Morty is one of the retina physicians I know who takes pictures of skin. So, inflammatory bowel disease 20% of IVD have secondary. The ITIS 60% are HLAB 27 positive. Iodocyclitis in 12%. You can have UVitis, scleritis, episcleritis, optic neuritis and all of these other things. Then you use most common females it has increased urine beta due microglobulin. You can end up with renal failure which is often asymptomatic. Patients do very well on steroids and very well on anti metabolites and cyclosporine. It's also associated with a high anchor and rheumatoid factor and hypocomplementemia. It's most like the chronic and it's usually young females but young males can get it too. Bosna Schlossmann syndrome is not really Bosna Schlossmann syndrome. The majority of patients with Bosna Schlossmann syndrome actually have CMV positivity in the anterior chamber most likely herpetic and their inflammatory cells in the trabecular mesh work is most likely unilateral. It's better not to name things I don't know Bosna Schlossmann were but it's better to just call them recurrent herpetic hypertensive anterior uveitis therefore you'll treat them with the appropriate things. Herpetic we talked about hypotensibly but remember floor-to-ceiling herpetic precipitates most like the VCD ophthalmicus but you can have HSP keratitis resulting in this 10%. You can have HSP uveitis in the absence of corneal findings as well often hyper-tensive. You can get hereter uveitis where you have corneal infiltrates and end rates with and to your chamber cell. You can still treat these with steroids despite what head says but for your boards if you have epithelial disease don't treat with if you have a dendrite don't treat with steroids but in practice steroids actually work really well decreased corneal sensation and what you see here is the sector iris atrophy if you're transilluminated and you can see and I think Mike we saw a patient together so we won't get into this as uveitis or glaucoma high fema syndrome something else you should read about but often because of empty chamber lenses or you can see it now in sulcus lenses with iris sutured lenses and you have high intracular pressure from trapeculitis and from the accumulation of junk in the DM kind of high eye pressure etc. The definitive treatment is to remove the lens but you can sometimes treat them with chronic steroids there's a whole bunch of drugs that can cause at uveitis but the ones to remember are moxifoxicin and rifabutin for MAI prophylaxis but there's a whole host of others so what is this child but look at the one thing that you should look at is look at the conjunctiva and yet you have all this brain care to offer the posters and you can white cataract and the ship has sailed so any patient with GA needs to be screened it's the most common cause of childhood uveitis and which patient is the most at risk of developing uveitis in GA are negative and positive young female early onset and how many joints the oligarchitis three or less joints so that incidence is the highest so for GA do ANA, RF, ESR, CRP, CBC and an HMV 27 other syndrome sarcoidosis this is a patient with iris nodules periodic precipitates and this is sarcoidosis it's a multi-system inflammatory disease where you can have effects of the lungs, the heart so remember about 15% of the sarcoidosis has cardiac dysrhythmias always get an EKG if you have a patient with sarcoidosis particularly the young you have live involvement kidney involvement eye involvement, CNS involvement you can see granulomotus carotid precipitates and iris nodules there are many signs that are suggestive of sarcoidosis iris nodules trabecular meshwork nodules Berlin's nodules tension be as snowball capacities macroaneurysms associated with periflebitis this is 100% specific but not very sensitive because rare this is an optic nerve granuloma these kind of punched out laser looking spots this candle wax dripping like vascular periflebitis french word phrases tache de bouger you see central rectal vein obstruction in the presence of all this vasculitis think about sarcoidosis this was a bad one what do you see here what do you call it this is the majority of fumes but you can see the granulomotus carotid precipitates if you look at it on my screen you see the legs floor to ceiling you see these with fine intercollecting filaments heterotromia in 85% indolent usually with no symptoms if you do paracentesis on these patients you often get a high femur 750% of bilateral chronic and 90% don't respond well to steroids associated with rubella if a patient has HIV think about infectious it's 34% infectious versus only 5% infectious in the routine population cephalus is very common but also toxo and herpetic the most common cause of vision loss glaucoma always perform corneoscopy there are four main mechanisms of glaucoma and antiretrovirus you can have secretricial where there's synechia occlusive where there's debris there's trabeculitis and lastly you could be causing the glaucoma with steroid response vancuitopathy can be seen in almost all chronic uveitis particularly in J associated uveitis corneal decompensation can happen in herpetic including CMP HSP CME is the most common cause of vision impairment in uveitis 47% of one in one study showed CME remember that what you see with an FAA is the spetuloid leakage into the macula remember that the concordance between FAA and OCT is not perfect there's a 85% concordance so you can have vision with angiographic CME that don't have true CME you still haven't treated them if they have vision loss hypotomy is a dreaded complication it happens with this it's like ciliary body failure once you have this it's usually game over and then you start getting into ocular taxidermy that's what my role are we won't get into this just remember there is all be careful with there is all especially in children about 30 to 40% of patients kids under is all had a 30 point increase in IOP so there is all sounds like a good idea but then they started using it post cataract surgery just be careful with that drug in order for IOP elevation the worst is dexamethasone especially if you use an ointment the only saving grace dexamethasone has is a short half life and there is all is number 2 if there is a family history of glaucoma then yeah there is a higher risk Jen Thorne published a paper in 2000 in ophthalmology where they found that 3 year less drops over a period of 3 years is safe I use 3 years less so you can use that any more than that then you have to think about immunosuppression very oculocortico steroid injections we won't get into that but I'll give you guys this presentation so you can read through it so in general if you have chronic disease and if you keep treating episodically then you end up with cumulative damage every time there is a spike so you have to make sure that you consider either steroid implants or you can use an NGVase such as red asserts and now Iluvian or you can use immunomodulatory therapy with methotrexate and team metabolize d-cell and ubiquisetocyclosporin dachrolymus and biologics the only thing that works in enclosing spondylitis that prevents joint damage and fusion is biologics but if nothing else works you can methotrexate can alleviate the UVitis but it never fixes the ankylosis the only thing that prevents spine deformity is a TNF alpha inhibitor so far there's some evidence that IL-6 inhibitors that is dacillusimab may work but that's untested sorry I went a little over any questions