 Alright, so we're going to be pretty quick about this because I have an hour, you have an hour, and I need to get to clinic and so do you guys, but I'm going to give you if there are any questions if there are any pictures and stuff that I want you guys to interpret, then I'll give you about three seconds before I take over. So the purpose of this lecture is not to not to make you guys struggle. So I want this work. So it's the first few things that they do ask and the hookups is about the basic immunology of the eye. Just remember a few things that there are two blood ocular barriers, there's the tight junctions in the blood vessels in the anterior chamber and also in the retina, but there's also tight junctions in the arc between the RPE cells and those are the those comprised of blood ocular barrier. Remember, there's a concept of immune privilege, which is partially mediated by the fact that there is a blood ocular barrier but also mediated by the fact that there are suppressor T cells, such as D h 17 cells, which mediate this immune privilege or so called immune privilege. One common question for some reason is, where is antigen in the anterior chamber process by macrophages this is a concept that stems back to experimental UV it is in in mice antigen is processed by macrophages in the iris that leave the, the eye through the tobacco to mesh work and present to the reticular endosclerial system. And do you get is what is the most common cause of vision loss remember that that is macular edema. What are the causes of reversible vision loss. The most common is cataract. Abigail what's going on here. And so I think we're looking at x-ray of a heel, and there's a fracture there. That's like anterior to the calcaneus I think that there's actually if you can see my mouse is fusion of the of the calcaneal joint here and there's a calcaneal spur. And there is kind of this, like anification of the posterior aspect of the calcaneus, you see this spur over here. This is actually a process, something called anthocytus. And axial arthritis that you see in each of the B 27 associated UVA is so first they like to give you a little twist, so rather than showing you a spine, they can show you a heel. And just remember that the heel and the Achilles tendon insertion and the the calcaneus can, they can all be inflamed in HLAB 27 disease. So remember that overall worldwide less than 5% of the population is HLAB 27 positive 7 to 11% of Caucasians 18 to 32% of all anterior uveitis in Western countries, less so elsewhere. 50% of patients with non-granulometous anterior uveitis HLAB 27 positives or recurrent disease you're talking about. It's associated with seronegative spondyloarthropathies. 50% of patients with acute non-granulometous anterior uveitis will develop seronegative spondylopathy. On the reverse 25% of patients who are HLAB 27 positive and have seronegative spondyloarthropathy will develop non-granulometous anterior uveitis. So those numbers are important. Four syndromes to know when it comes to HLAB 27 positivity. No and closing spondylitis. No writers now known as inflammatory arthritis. Certain aspects of inflammatory bowel disease can in fact have HLAB 27 positive anterior uveitis. Know that uveitis in an isolated fashion with inflammatory bowel disease is likely to be HLAB 27 positive but scleritis anterior uveitis anterior scleritis and scleritis are not associated with HLAB 27 positivity in the setting of inflammatory bowel disease. Does that make sense? And then of course the psoriatic arthritis which tends to be HLAB 27 positive. So this is kind of the more conventional picture that they'll show for spondyloarthropathies. Specifically there's no ankylosis per se but focus here, does everybody see my mouse here? But can you guys see this sclerosis along the sacroiliac joint? See how there's kind of this radio opacity along the joint line and also narrowing of the joint space. So this is sacroiliitis which is something that you can see most commonly in HLAB 27 disease. But more of course you know and this is from your BCSE textbook but kind of more unmanaged. You see less and less of this now but more unmanaged and closing spondylitis. You can see sclerosis along the joint lines, complete fusion of the vertebra, complete fusion of the sacroiliac joint and this stooped posture which you don't tend to see anymore, at least in the developed world because it's treated. There is sclerosis and narrowing of the joint spaces, 90% of patients with AS are HLAB 27 positive. My guess is that a lot of these negative HLAB 27 negative patients are actually false negatives but there's your statistic. 5% will get recurred anterior non-granulometous anterior uveitis. So remember that that is the majority of patients with HLAB 27 disease of course in the minority you can get chronic disease about 3% of patients with HLAB 27 positive anterior uveitis actually get chronic anterior uveitis and those patients are more likely to get intermediate uveitis. Remember also this is another question that I'll ask you on your board, 5% will get erotitis and valvular insufficiency or pulmonary fibrosis. So remember that they can't ask you about cardiac manifestations and manifestations of disease that can kill you. Remember also what inflammatory pattern back pain is the stiffness off the back that lasts for at least 45 minutes after the cessation of sleep after waking up. But of course it can also apply to patients who go on long car rides etc. Who can tell me what the top picture is? It's a foot, it's two feet. It's a carotidermoblenoragium. I can't pronounce it correctly. So this is a carotidermoblenoragium and this is you can see a calcaneal spur in conjunction with enthesitis which can manifest as calcification of the achilles tendon but more commonly just carosis along the insertion of the achilles tendon with the spur. What disease do you think this might be? Reactive arthritis. That's right, so reactive arthritis. Just remember the can't see, can't be, can't have a tree. So arthritis, uveitis and or conjunctivitis and urethritis. Knees, ankles, feet and hands, calcaneal spur formation. Just remember this one, this buzzword carotidermoblenoragium which is a desquimiting rash of the souls which can also be seen in syphilis. Exactly. It's not called the same but it looks very similar. Most common eye manifestation is actually not uveitis, it's conjunctivitis so remember that. 90% of patients with writers are HLAB 27 positive, mostly male. And this is another thing they love to ask is which bacteria can be associated with chlamydia, salmonella, shigella, ureoplasma, urolyticum and eusinia. Not Pestis but enter colitica. So basically just think of some of the sexually transmitted diseases but most commonly actually it's these bowel pathogens. What is this lesion? Tony. Wake up Tony. Never mind. Anybody. Actually I'm not sure. Pyoderma. It's gangrenosome. That's right. So, pyoderma gangrenosome. Is this painful? Looks painful. Generally not. So this is a painless, very, very geographic bunched out through the dermis skin lesion usually in the extensor surfaces of the arm or the leg. This is seen in inflammatory bowel disease. 5 to 10% Crohn's disease 2% to ask about GIS symptoms if you see that. Remember that Crohn's disease affects the entire GI tract so it can affect the mouth, the entire mucosa from, you know, from the lips all the way down to rectum and anus. You get skin lesions, pyoderma gangrenosome, aftus ulcers which are also painless, IBD, and anterior uveitis as I mentioned before. HLAB 27 positive but if there's inflammatory bowel disease and scleroid uveitis or anterior scleritis it's generally not HLAB 27 disease of course there is a spectrum. What do you see here? Name the disease. Sausage fingers. Yes. The dactylitis. And you also see nail pitting and destruction of the nails, the dactylitis. Exactly. This is a patient with psoriatic arthritis. Remember that psoriatic arthritis but not psoriasis per se are related to anterior uveitis so you have to have the arthritis component. So it's a symmetrical polyarthritis. There is asymmetric oligoarthritis, this DIP joint involvement. There is resorption of the phalanges. So you have shortening of the fingers and lysis of the nails as axial arthritis as well so you can see neck and thoracic spine and lumbar spine. And ankle arthritis is unequalysis, nail pitting, and the sausage disease, the dactylitis and anthocytus as well, which is once again information of the insertion of Achilles tendon. And these are just some findings, you can see the dactylitis here, the nail pitting, the sausage digits, and the unequalysis. These are, let's see. Tyler, what do you see here? So it looks like we have some, I don't know if that's Dan carrying out the earplug information on my sound. So there is band. So I would think about GIA. That's right, so GIA specifically. I'm not exactly right Tyler, but if you look at the conjunctiva, most people you see on call who have anterior uveitis have red painful eyes. This is a quiet anterior uveitis. So then the conjunctiva is white and quiet, but you see evidence of a lot of information. So there's cataract and synechia and band care top and then you'd think this I would be explicitly painful but it's not. Exactly, this is GIA. It's the most common cause of childhood uveitis. Chronic area cyclitis occurs in 10 to 20% of all patients with GIA. It's chronic bilateral smoldering and asymptomatic until complications occur. So once you do get angle closure or, you know, synecule glaucoma. Of course, it does hurt or band starts to erode or the eye starts to get ticycle and hurts. But before then, in its earlier phases, not painful. Loss of vision due to band care top of the posterior synechia CME hypoteny is a very common and unfortunately quite devastating complication and cataract. Cataract can be more serious here than in other uveities, because it occurs in an amylogenic age group. So just remember the highest risk of uveitis is female bossy articular, so oligo articular and a positive but I would advise you guys to go back and read basically risk stratification in GIA and screening guidelines I haven't gone through it here but just know that if you have a female young age of onset with three or less joints involved and in a positive then you have to see her every two to three months in screening. And then of course your risk stratification does dictate your screening. So do things that you need to know about in uveitis when it comes to screening read up GIA screening and read up HIV screening which patients with HIV do you screen and how often. I won't make you guys suffer through this but this is inflammatory. It's a vasculitis. You can see kind of a mixed arterial and venous vasculitis and you can see over here that there's an occlusive vasculitis where there's an area of non perfusion before the, you know after the front of vasculitis. This is actually the chest disease now there are two big manifestations in the eye of the chest disease one is an anti uveitis which is a high, high-po-peon uveitis. But secondly, don't forget that it also causes kind of disseminated systemic occlusive vasculitis not just in the eye but also the brain and the bowel. 25% of patients with just disease of CNS involvement. Do remember also that ischemic necrosis of the bowel is not uncommon patients may also have occlusive retinal vasculitis ban uveitis and ischemic optic neuropathy as a CNS manifestation remember that the Asian variant but not so much the European variant. Sorry, the other way around the European variant but not so much the Asian variant of this disease will have HLAB 51 and HLAB 5 association. And of course there is the benzene reaction of pathogy that they can also ask you about in your boards. And you can see here this is an example of pathogy where 30 gauge needle was was used to make these this linear pattern of punctures and 24 hours later you have these basic this vesicular eruption at the site of off the puncture and this is this is a phenomenon on this pathogy where you get these vesicular eruptions at the site of any skin trauma and this is a hallmark of the chest disease. Sarcoidosis. It's another disease that I could question you about 30 to 60% of patients have eye involvement. What is the most common eye involvement in sarcoidosis abigale sleep. So, most common involvement of the eyes of sarcoidosis is actually lacrimal gland or dry eye. And the UVA is the second most common. Sorry, this was an error in my part. Sorry, this was not supposed to be a trick question. And it's the most common cause of intermediate UVA. It's the most common females, African American origin and Scandinavians. And in Utah most of the patients sarcoidosis you see will have Scandinavian origin. This is another slide that they like to show. These are two non-caseating granulomas within tissue and also a lot of little lymphocytes everywhere. So, very different from the tuberculosis granulomas because they don't have a clear or caseous center. Clinical science suggestive of sarcoidosis. Do remember the mutton fat carotid precipitates. Cappy nodules. You can also get inferior, inferiorly kind of situated carotid precipitates that are not granulometers, although these are less suggestive. You can also see granules or nodules on the anterior surface of the iris known as basacas nodules. Cappy nodules as you can see can evolve into synechium. Other signs of sarcoidosis you can have macroaneurysms associated with inflammation along the blood vessels, optic nerve head granuloma, as you can see here. These little punched out coroidal, retinocoroidal lesions and also coroidal lesions along the retinal vasculature. Classically the vasculitis is very vanilla. So you see kind of this candle wax dripping or touch the bougie. Very vascular infiltrates denoting very phlebitis in sarcoid. 30% of patients will have lacrimal gland enlargement and 30% will have increased gallium optic in the lacrimal gland. So it does most commonly affect the lacrimal gland, even in asymptomatic patients. Okay, anybody? Abigail? You there? I would think, sorry, Maya. I would think fuchs. Yes, right. So heterochromia, these little periodic precipitates and what's going on here? It's really hard to see on my small screen. I think that's the T. So that's the T. You can see these bridging vessels in fuchs disease. And so, you know, commonly when you depressurize the anterior chamber during cataract surgery, one of the things complications of cataract surgery during fuchs, in a patient with fuchs is getting high fema. And because of the rupture of these bridging blood vessels. Remember, 10% of fuchs heterochromic iracyclitis are bilateral, in which case, of course, they do not have heterochromia. There's iris atrophy, there's fine stellate, periodic precipitates with these little connecting legs, minimal cell and flare. It's an achia, almost never formed. That's an important distinction. Cataract and glaucoma are common. And remember that there are fine vessels that cross the TM on gonioscopy, which makes cataract surgery complicated and can increase your risk. It's often difficult to treat. So you often have to just tolerate a little bit of cell. And that it makes sense then that it's there's a possible association with an infectious agent. And this hasn't been identified in certain PCR studies to be rubella. Remember, there are many differential diagnoses of heterochromia. Fuchs is one of them, but then you have to think about neoplastic disease, ciderosis, herpetic disease can often cause a heterochromia. And that can be CMV, HSV and various other astro virus. And of course, congenital horners. Okay. What's going on here? So Asian kid with strawberry tongue. And yeah, so Kawasaki's disease. So. Why did the cycle? That's weird. Oh, there you go. So it's mucus detenus. The blood syndrome. Remember mortality is related to coronary artery aneurysm and thrombosis. Avoid steroids. That's one question that they'll ask because that can increase your risk. Coronary death. Two thirds have uveitis, 97% bilateral, five days of fever. Conjunctivitis. It spares the limbis. So there's no discharge as well. Strawberry tongue or oral mucosal involvement as a rash of the palms and soles. And there's generalized lymph adenopathy. This is one. Complex that they like to test you for. Was the Schlossman syndrome, which I don't think really exists, but they'll test you in your boards. So it's bilateral glaucoma. It's a unilateral glaucoma, cyclitis crisis. It's a diagnosis of exclusion. Always think HSV, VZV and CNP first. Now, actually the thing, having done that, having done that, taking HSV, VZV and CNP first now, actually the think having done the CR, patients with so-called Bosner Schlossman syndrome, the founders actually, in many cases associated with CMV, my guess is that it's often associated with any of the her rico welding viruses. It's associated with a very high IOB cornial edema fine. KP very. Scanned cell. and flare and you treat with steroids and glaucoma medicines. Often in fact, if the pressure is not too high, if you just treat day one with steroids, only the pressure will come down because it's purely due to trabeculitis. The differential diagnosis of hypertensive uveitis is herpetic, so HSB, VZV, CMV, fuchs, sarcoid, syphilis, and toxoplasma. Lebanese friend of mine says his grandmother used to admonish him by saying psst and SKT. I don't know if this helps anybody, for some reason it helped me, but think about fuchs, syphilis, sarcoid, carotero-uveitis, and toxoplasma. All of these can cause a hypertensive anterior uveitis, but most commonly it's herpetic. Think Lebanese grandmas. Necrotizing retinitis, acute retinal necrosis, progressive outer retinal necrosis, and CMV retinitis. These are things that you need to know about. Viral retinitis may occur in immunocompromised or immunocompromising patients. Retinal detachment occurs in up to 75% of patients and there has been more than one-third involvement of the retina. There are, you'll often have multiple breaks and early, early proliferative vitro retinopathy. You always need oil and the retina tries to crunch even once you have it completely attached. It's a horrible disease. You treat with IV or oral antivirals and intravitrials. You cannot treat with intravitrials in isolation. And in fact, the role of intravitrials and antivirals is controversial, except perhaps in porn. You can treat with oral valve acyclovir to obtain IV level, IV levels of acyclovir in the blood you treat with two grams, three times a day rather than two grams. The usual one gram, three times a day, we can do that for up to a week and it's safe. You can use IV acyclovir, which would be 10 milligrams per kilogram, three times a day, so every eight hours. You can get intravitrials acyclovir in Europe. You do not get intravitrials acyclovir in the United States. You can use FAMCYCLAVIR, IV or oral, although it's harder to reach the appropriate plasma levels with this drug. You can inject GANCYCLAVIR, you can do IV, Intravitral Orbitricert, which is no longer available, but it was manufactured by Bausch & Lohm. I think I implanted the very last one because it was expired by six months and then we had no more. This was in San Francisco. FOSCARNET can be IV or Intravitrally. The good thing about FOSCARNET is that you use it in the same concentration as what you get in the vial, which is 2,400 milligrams in 0.1 milliliters, so you don't have to re-compound it. Of course, the only oral treatment for... If you want to use something for CMV and if you want to get GANCYCLAVIR in an oral formulation, you have to use VALGANCYCLAVIR. Now, of course, there are three other new antiviral agents that are active against CMV and take an orally. One of them is the DOMOVIR, which is approved for peripheral CMV, but not approved for organ-specific CMV, but we have used it and it has got a much better side effect profile. Remember also that CMV can get resistance to GANCYCLAVIR and by extension to VALGANCYCLAVIR, there is a specific viral mutation that you can actually sequence for, which I forgot. Look it up. Steroids may be added, laser is controversial for necrocritizing retinitis. This is a... Oh, wait a minute, I aren't very critical. So yeah, this is ARN, so you can see GANCYCLAVIR is a rapidly progressive peripheral retinitis, usually multiple foci that starts to come together and move centripetally. It's very fast, it moves about a disc diameter or two disc diameters per day. Notice also that when you look at the blood vessels and in ARN, there is some very vascular apparent clearing. This is not really clearing, it's just kind of an absence of necrosis because washed away through the capillaries around the major blood vessels. So you'll see clearing, although it's not actually clearing, it's just the appearance of very vascular clearing of disease. This is... The difference between this and the previous picture is simply that you have a better view, you have a clearer picture, and that means that there is less necritis. This is as rapidly progressive, if not more, and it's actually harder to treat. This is progressive outer retinone necrosis, which what is the difference between ARN and foreign? ARN is generally seen in immunocompetent patients and foreign is seen exclusively in immunocompromised patients. That does not always mean HIV, that you can see it in organ transplant patients, bone marrow transplant patients, or even patients that you've locally immunosuppressed that have actually been reports of patients who get progressive outer retinal necrosis after an ozioidex injection or a subtenone scandal. So local immunosuppression, obviously can have the same effect as systemic immunosuppression. Foreign needs to be treated more aggressively, is treated with high dose plus garnet and gans like covariant alternating fashion, and treated with IV or very, very high dose. Valtrex in this situation, I prefer IV. So you most commonly, it's very little zoster, as I said, rapid and relentless progression. It involves immaculate early, and there is no too little bit right. Anybody, what's going on here? It's more like CMV retinitis. Right, so this is pretty classic CMV retinitis. So you see kind of this progression along the arcade. How fast does CMV retinitis progress? Not very fast, about this diameter per week. So even if you saw this, you don't have to panic. Obviously, this one is very close to the macular, so maybe you should panic. And you should treat this with integrals, but if you see peripheral CMV retinitis, you don't have to treat with integrals or go to IVs immediately. In the HIV era, you would often treat peripheral CMV with careful observation and just trying to get patients under control with antivirals and treat the immune suppression first. And then start treating the eye with intrabitural gun cycle where once it starts to show evidence of progression, that's how slow it is. But equally devastating, because it's hard to stop. It's not as devastating now that we have good treatments for HIV. But with CMV, you can see peripheral vascular occlusion and occlusive vascularitis is actually very common in these patients. I have patients with armed to artery time of about a minute with CMV retinitis. So immunocompromised patients, not just HIV, CD4 counts of less than 50, retinitis with hemorrhage, all the layers of the retina tend to be affected in a granular fashion in the periphery. Usually starts along the arcades, but can occur anywhere. And there's a segmental vascularitis that's occlusive. What's this? This is HIV retinopathy. You can see multiple cotton wool spots. It looks a lot like diabetic retinopathy. Kind of a hybrid of diabetic and hypertensive retinopathy. This is a microvascular disease that's induced by immune complex disease in patients with HIV. It is not an infectious retinitis. Remember that it does not, it just means that the patient has uncontrolled or poorly controlled HIV. So it's a microvascular retinopathy along the arcades, not infectious as cotton wool spots and hemorrhages. It resembles very much interferon retinopathy. That's an entity that you will see less and less off because we're using less and less interferon in the treatment of hepatitis. But it does resolve with heart. What's this? Toxin. Yeah, exactly. So you have retinocoriditis adjacent to a scar. With, usually there's overlaying with arthritis, which it's unusual to see such a clear picture, but this is toxoplasma. Remember that it's an obligate intracellular parasite. The cat is the definitive host. I don't know if anybody read the Nature article, but it actually makes mice less afraid of cats as an evolutionary adaptation where a toxoplasma infected mouse will be unafraid of a cat and then go up to the cat, get eaten and perpetuate the life cycle of toxoplasma, which I thought was pretty cool. You can also get it and most commonly you get it from undercooked meat, soil and cat poop. As you can see is number three. In Brazil, the most common, which is the place with the highest incidence of toxoplasma, the main culprit is undercooked meat. Remember that the bradyzoid is the latent system, the tachyzoid is the phase of the organism that causes retinocoriditis. Remember that there's a white yellow lesion with retritis, overlying it. Active lesions occur at the edge of old scars. Inutrious infection is as common as acquired infection. And if you have a patient with de novo toxoplasma as not associated with the scar, think about HIV. And if a patient is HIV positive and has toxoplasma in the eye, always obtain a CT off the brain because you'll see these ring-enhancing lesions. Treatment options do include triple therapy, pyromethymine, subpoenomy, pyromethymine, is that's from isentrovercone and prednisone after 24 hours. This is an example of toxocara, which is an intestinal parasite. So remember if they ask you what it is, it's a nematode. So this is a larval form, insisted larval form of a nematode. Children and young adults, usually, you know, lateral, it is one cause of glucocorrhea, but when the cyst does erupt, there is the endothelitis phase. It's usually peripheral granuloma. You can treat with albendazol and the steroid. You can actually resect the cyst as well, but do that with caution. White dot syndromes, this is something they love to ask about. Here's a 67-year-old with nictalopia and vitritis. This is birdshot. You can see some of these bicep form lesions, which you can actually enumerate better with ICG and geography. More than patients tend to be greater than 40 years of age. Median age is 57. There's blurring of vision, loss of color vision, nictalopia, contrast, sensitivity problems. Vitritis, vascular attenuation, late discadema is actually a fairly common presentation, CME and significant risk of CNBM. Not as high as PICC or multifocal corridors, but still exists between 50 and 30%. Multiple cream-colored radially-oriented lesions in the post-ecritorial fundus. And then remember, of course, the HLA-A29 association, which is actually one of two HLA associations that I ever looked for in my clinic, because if a patient is HLA-A29 negative, I rethink my diagnosis of birdshot. What is this? Mr. Ali here. Serpigenous. That's right. So Ali and I were seeing a patient that we were suspicious for serpigenous and it was actually just AMD. But this is a patient with true serpigenous. And you can see that there's it's blurring of this area here over the fovea and then the macular is obliterated in this situation. And it's usually older patients over 40 geographic pattern. It used to be called helicoid cororectal atrophy. It's most commonly peripapillary, but it can in about 10% start in the macular. And then it can also start in a multifocal fashion, in which case it's called Ampigenous or Lentus Blackoid. Block early stain late, like most inflammatory couridopathies, there's a transmission defect. It's progressive with multiple crops of recurrence and it can often result in CNBM up to 40%. It often needs treatment with alkylating agents, although I'm more likely to go to Rituximab now before I do an alkylating agent. And geography. This is actually a really good distinguishing test, but number, if you look on the left side of the slide, you can see that there's this early blockage with late staining. So this was the area that I was pointing out to you that stains late and it's central macular progression. And then on the other side, you don't see so much of this early blockage in this staining because it's less active, but one way to differentiate this from other geographic forms of retinal, or geographic retinal disease such as GA and AMD is in the mid and late phases of the angiogram. You see this kind of brush fire type staining at the edge of the lesion. This does not imply involved, actually this does not imply activity. Mudes. Another disease I'd like to ask about young to middle age, women 90%, 90% unilateral, but remember it can also be 10% bilateral. You see granular or puncture changes in the macular if you look really closely. The spots are small about 100 to 200 microns about the size of, between the size of an artery and a vein leaving the upper nerve. There's reeds like staining and this has always confused me. Is it the whole thing? Is it the entire distribution of the spots that are reeds or is it the spots themselves that are reeds? Turns out that the reeds like staining is actually those little spots in themselves that have this little reeds like pattern. You'll see in a large blind spot. And if you do a multifocal ERG or in the peripapillary zone, you'll see why there's an enlarge blind spot you see of the iteration of ERG aptitudes along in the peripapillary zone. So, and geographically you can see these little reeds like spots, these little dots kind of arranged in these little reeds. ICG will show you more numerous lesions, but once again, you can see punctured hyper fluorescence and staining late of these lesions and of the optic nerve. Sometimes you get a little bit of vitritus and a little bit of dyskidema as well. The rate of recurrence of mutes is 10%. Just remember that. This is a case of very classic ampy. So apmopopy, acute placoid multifocal pigment, apitheliopathy. Posterior pigment apitheliopathy. Acute posterior multifocal placoid pigment apitheliopathy, yeah. So this is, has a viral prodrome most common days. Usually young adults, cream colored plaques, approximately one disc diameter is much larger, much, much larger than what you see in mutes. They disappear over several weeks. The FA will remain abnormal, usually bilateral most do well, but many end up with a little bit of scarring. I tend to treat with steroids, but as far as your own caps are concerned, you can just say that it's a self-limiting disease. Yeah, and just also remember that a lot of these patients have headache. And if you do have patients with headache, always do at the very least an MRA, M-R-B because about five to 10% in literature patients with MPR do have cerebral vasculitis as well. And I've seen, you know, fleeting cases of cerebral vasculitis in MP, and but I've also seen bilateral pontine in parts in Amphigenus. So it's important to screen for cerebral vasculitis. This is a case of PIC, or punctate inner choridopathy, where you see these little spots, most classically in the macula, but you can have extra macular spots. The difference between PIC and multifocal choriditis is that PIC does not have vitritus. That was the dogma, however, it's more now recognized to be a spectrum between PIC and multifocal choriditis, where you do in fact see a little bit of a difference in a little bit of posterior vitreous cell if you were to do a swap source imaging or OCT of the premacular vitreous. This is a case of multifocal choriditis where you can see more vitritus, discodema, kind of a more blood and thunder type appearance. And more with the pan-UVI, I just can kind of appearance rather than PIC, which is more quiet looking. So remember in multifocal versus PIC, there's vitritus versus no vitritus, the lesions are smaller in PIC, whereas in multifocal choriditis, they're up to 200 microns. The course is chronic in multifocal choriditis and often the majority of patients will need immunomodulatory therapy, whereas in PIC, needing immunomodulatory therapy is the exception of the rule. It's self-limited. And the most common manifestation of PIC is CNBM. Ciflis, this is something we're seeing more and more often in our clinics. You remember there's a difference between congenital and secondary Ciflis. Congenital Ciflis usually presents with, it can present with UVA's, but most commonly presents with interstitial keratitis and peripheral congenital looking retinopathy and deafness and all that stuff. Secondary Ciflis will present with rash and arthritis, iridus, retinitis, choriditis, basically it can do anything. In testing previously, you would do a trapanemial and non-trapanemial test. So you do an FDA and an RPR or you do an MHATP and a BRDL. But now we tend to do something called reverse sequence testing. This is that will not be tested in your OCAPs because it's very new, but in reverse sequence testing, you start with IDG testing in the blood. And if that is positive, then you go on to do your trapanemial and non-trapanemial test. That's a pretty good way of going about it. If the patient has UVIS, you always need to do a lumbar puncture to rule out neurociflis. And despite what some of your ID friends may say, all patients with Ciflitic UVIS need to be treated as if it is neurociflis. So CDC guidelines are to do a lumbar puncture at day zero before treatment and then in six months to check for CSF, VDRL. You can use penicillin G, IV, or IM for two weeks, but you have to make sure that you use IV if there is neurociflis. Lyme is also a spirochete related to, at least morphologically, and in size to Ciflis. They always ask you the name of the tick. It's Ixides or the deer tick. It also has stages very similar to Ciflis, where there's a primary stage one month after infection with erythema chronicum migrans and follicular conjunctivitis. Stage two, one to four months after infection with neurocardiac abnormalities and arthritis. And in this stage, you start to get ocular involvement with iritis, keratitis, and intermediate ubiitis. Stage three, chronic arthritis, meningitis and keratitis. And you treat with tetracycline or Ib-CEF-triaxone if CNS involvement is present. Over here in the West, people laugh about Lyme diagnosis and that's true because your pre-test probability is very, very low because it's not transmitted here. However, we had several cases of Lyme keratitis and Lyme ubiitis in Long Island, New York. So if you end up practicing out East, then doing a test for Lyme is not foolish. But if you're practicing out West, doing a test for Lyme is not particularly a good idea because you get false positives. Sympathetic oftalmia, you get bilateral granulometous banubiitis, remember it is bilateral. So even if you were to take the, of course, you don't really look at the inciting eye because it's often ticycle or there's no view. But if you were to take this eye out and do a pathological examination of this eye, just remember that it is still a bilateral disease. It happens due to 50 weeks or longer after injury to the inciting eye. There's diffuse granulometous coroidal information that's bilateral, exudative RD. Previously, they would say that it spares a coriocapularis. Sympathetic is sympathetic to the coriocapularis. This is not true. This is a histological artifact. It does in fact involve the coriocapularis. But depending on how your OCAP question is asked, sometimes you do have to give false information. Remember the Dallons-Fupe nodule is a pathological lesion. There was some controversy about whether or not you should inoculate the inciting eye before one to two weeks have evolved. But that becomes for two reasons. Number one, we can treat sympathetic ophthalmia really well with immunomodulation. And secondly, now the number one inciting factor is actually surgery, especially vitroretinal surgery. So you wouldn't be able to think about removing the inciting eye when the inciting event is surgery. So not pretty relevant to do that anymore. That's not an eye, it's an eye. God. So this is an example of sympathetic ophthalmia, granulometers and vanuviitis with an exudative retinal detachment. You can see that this is somewhat multi-lobulated. And if you were to turn the patient to the side, this retinal detachment would shift. So kind of a hallmark of exudative retinitis, or exudative retinal detachment. This is what a Dallons-Fupe nodule looks like under the RPE at the level of the cordial capillaris with overlying elevation of the outer retina. VKH is basically just sympathetic ophthalmia without trauma. That's all it is. It's an histologically indistinguishable disease. However, there are systemic manifestations of chronic diffuse bile for granulometers, uveitis, exudative RD. No prior history of trauma and it's in certain populations such as indigenous American populations, the Inuit and in Japan, but I've seen it in India, Pakistan and Iran as well, and in the Middle Eastern or Saudi populations as well. So remember this vitiligo, poliosis. Poliosis is a whitening of eyelashes. You'll have headache, meningismus, loss of consciousness, paralysis, deafness and tenitis. Those are the main neurological manifestations. Know also that interestingly, you can see these manifestations also in sympathetic. I've had patients with sympathetic with hearing loss and ringing in their ears and whatnot. But here's an example. So you see this multi-lobed neurosensory RG with kind of these corrugations and dyscypremia. The angiogram is very telling this kind of this, this punctate hyperfluorescence that then pools into the sub-retinal space given this initial starry sky pattern followed by this pooling everywhere. You can see a good example of pooling here. This is, I'm moving on. This is, these are examples of intraocular lymphoma where you see atypical vitrious cells in sheets. You see kind of an iris and ciliary body mass in a patient with B-cell lymphoma. See how the mass is pushing the IOL backwards. And then you see this patient who was sent in as Arne, who I looked at and said, this does not look like Arne. This was actually lymphoma as well. One reason you can tell is that there's these different ages of lesions which you don't see so much in Arne. So large B-cell lymphoma is the most common presentation in the eye. It may be primary, ocular or CNS. Bilateral is more likely to be CNS. If you see unusual cells in clumps, think about lymphoma. If it's partially responsive to steroids, think about lymphoma, but even lymphoma can respond partially to steroids because there is some pericellular inflammation, something called Desmoplasia. So treat with intravitral rituximab and methotrexate if ocular only, but if it's bilateral, do consider systemic treatment in fact, a lot of centers do that for bilateral disease without CNS involvement. Coroidal lymphoma is a different animal. Remember small B-cell lymphoma, not large B-cell lymphoma. CNS involvement is almost unheard of. Systemic involvement at presentation is common. So you see this retroperitneal or hiler or mediastinal involvement without CNS involvement. But ongoing screening is not often necessary because if there is no systemic involvement in presentation, that tends not to be a future systemic involvement. This is a patient with, you can see this tiny hypopion and some exudate along the IOL. This is the chronic endophthalmitis. B-acne, but it can also be others. I've seen clostridium. I've seen corinibacterial. I've even seen strep chronic endophthalmitis, which was weird. But you can get inflammation in the eyes up to two years after any kind of surgery. You'll see AC cell, geriatric precipitates in a small hypopion. You see plaques on the intraocular lens, vitritis. And actually sometimes when you see these plaques on the IOL and you do a YAG, you can actually liberate these organisms into the pictures precipitating an attack of B-acne endophthalmitis. So always think of endophthalmitis when the patient has a history of surgery. And also I'm going to give you guys this presentation to look at, but these are all the various HLA associations. And I don't know about you guys right now, but back in my day, the OCAPs would love to ask what HLA associations, which are totally useless, except for HLA B-27 and HLA A-29. That's the only two HLA associations that in practice you know about, but unfortunately for your OCAPs, it's nice to know some of these others just because they love to ask. And that's it. Any questions?