 Good morning. This is an OCAP review course. It's condensed from four hours originally, okay, to one hour, okay, so there's a lot to cover in U of I, so I'm trying to hit highlights that I think will be good yield for you guys on your examination. A combination of cases, questions that are clinically relevant, okay, questions that are obscure that you're going to see on your examination and pictures, okay. So we'll start with a 27-year-old white male pain, photophobia, ciliary flush, lower back pain, differential diagnosis, okay, so this is patient presenting with acute anterior uveitis, okay, non-grain along with anterior uveitis, the differential diagnosis, idiopathic number one, the HLA-B27 associated spondyloarthriopathies, herpes, lens-induced basechettes, drug, TINU and postnatal schlossman syndrome, okay, TINU-2-industrial nephritis and uveitis syndrome. The important things to elicit on your history, lower back pain, oral, general ulcers, skin lesions, arthritis, GI symptoms, medication use, and labs, you know, syphilis, serology, and a B-27 would be probably the most important, okay, to get, but CBC and a basic metabolic profile, sacroiliac films are the films to get for patients. It's a board type of question rather than lumbar sacral spine films, which you see here. So the lumbosacral spine films, you know, show angulosus games over by that point in time. Sacroiliatus is a common feature of the B-27 associated disease. So if they ask you what film to order, sacroiliac film, the rheumatologist hardly ever order these films anymore. They go straight to MRI. What is this? Right, and what do you see that with? Formally known as the etiology of which is thought to be, yeah, exactly. So it's an enteric bacteria or thought to actually precipitate this in a genetically predisposed person. What is this? We're on the theme of seronegative spondyloarthropathies. So they may show you a clinical, something like this. This is a patient with psoriasis, okay, so psoriatic arthritis is something you have to think about. What is this in this setting? Okay, so it's a pseudophagic patient, right, with a capsular plaque, okay, and if you're given a history that this patient has a delayed onset of endophthalmitis, you might think that the patient may have actually an indolent bacterial infection with P-acnes or fungi. So capsular plaque, delayed onset, endophthalmitis. Since you just, you know, we can go into way more detail, but just make these associations in your mind. Iris nodules, they may ask you about that. They love to ask you about the difference between kepi and busaca nodules, okay. So this is an example of a patient with sarcoidosis with groinulomus inflammation. Kepi are on the pupillary margin, kepi, you can, with a P and busaca, or where are busaca nodules, right in the stroma, exactly, okay. Herpes, okay. There are usually stigmata of herpatic infection in patients with herpes, not always. You can have herpes sine herpite, but, you know, for bird purposes and clinically, you should always look for stigmata, okay. So in the panel to your left, you have a patient with an immune ring, okay, stromal keratitis on the right, patient with sexual iris atrophy. Truer faults, sexual iris atrophy is pathodinomonic for varicella zoster infection of the eye, faults, okay, right. So you can see them in either one of them. Differential diagnosis of diffusely distributed Kp, herpes, think about herpes, number one, sarcoid can do that, but it also can give you kind of groinulomus inflammation or its triangle. Fuchs will classically give you still called stellate Kp, which this is an example of, and toxoplasmosis. EVIs with elevated intracranial pressure, useful to know in the clinic too, okay. So herpes, number one, number two, number three, okay. Herpes is number one then, of course, the more unusual thing, Pozner-Schlossmann, which is also thought to be herpes, right. It's thought to be due to a CMV. Fuchs heterochromic aerocyclitis is more of an indolent inflammation associated with uveitis, very low-grade uveitis and elevated intracranial pressure sarcoid and toxoplasmosis. So 25-year-old white male presents with the first episode of Sphere 9 groinulomus unilateral hypopion uveitis, what laboratories would be the most appropriate for the initial workout? None? Of course, this is its first episode. ANA and rheumatoid factor, FTA and HLA B-27, PBD, chest radiograph, angiotensic covering enzyme. Anybody? C? C, yeah, right, okay. So B-27 offers prognostic information for the patient. It's not diagnostic, obviously, but it's important to know because if you make this diagnosis, you get them in the hands of rheumatologists, get them on maybe disease modifying medication. You know, he's presenting with severe uveitis. You wouldn't just say, oh, it's your first episode. See ya. Right? Particularly if they come here, they're coming from an opinion, okay? 35-year-old white guy presents with pain-rendous photophobia, poor vision in his right eye. He's got mutin-fat KP, microhyfemia, blood cells, and white cells in his anterior chamber. One plus flair, put your sneakier and high pressure. What are you thinking about in this patient? Yeah, right. Okay, well, amzocyan, yeah, is amzocyan, it's not a microhyfemia, but amzocyan is actually blood in the angle, right? Afroparasintesis, that's that's been described in patients with right, but do you think this is fuxeroprenoviriciclinus? So what gives you this constellation of high pressure? What do you think of high pressure? Herpes. What is that sectoral iris atrophy due to? It's a kind of infarction of the iris, okay? So you can have ischemia, you can have either granulomus or non-granulose KP with herpes, you can do anything, and you can have hyphaemia and bleeding in the eye. So this is the kind of question that I'll ask you on the floor, it's because it makes you, it confuses you a little bit. So the answer would have been the sectoral... What's that? On that question, the answer would have been the sectoral... I'm sorry, yeah, sectoral translimination defects and decreased corneal sensation, sorry. So they're looking for herpes, is it varicella zoster probably. Okay, so in contrast, 12-year-old girl with chronic non-granulose inflammation, white eye, and a cataract, okay, plus the particular arthritis. The differential chronic non-grams, anti-Uvietis, JAA, okay, in a child, most common systemic association, Fuchs, Sargot syphilis TB, you can pretty much do anything, but it would be very unusual to have TB, right? Herpes and immune constitution, Uvietis. Workup as before CBC, basic metabolic profile, and ANA, this is a situation in which an ANA is actually useful, okay, in a child because ANA positivity in a post-articular kid with non-granulose anti-Uvietis is, you know, a risk factor, okay, for Uvietis. Lyme disease in an endemic area, I would order it, okay, if I were to live in New York City or Long Island, okay, Lyme disease is prevalent in that area. I would order it if you had something else, you know, there was tipping you over, okay, so I wouldn't order it here. Okay, Dr. Bell, you know, I think you had this consult actually, or something, I think it was this five-year-old kid with, you know, a discriminating rash on their fingertips, kind of a strawberry kind of tongue, and lips that are erythematous, so diagnosis of Kawasaki's disease. Okay, they love to ask stuff like this, okay, so it's, you know, we've seen two cases in the last three years. Okay, so muco-cutaneous lymph node syndrome, usually children under the age of 10. They have this erythematous discriminative, a rash in their extremities in the oral mucosa, as you saw, fever, painless, cervical adenopathy. The thing that is important to know about this entity is that they can get myocarditis and coronary arthritis, so that's important. They need to be, the diagnosis needs to be made, and usually they're treated with a high dose of steroids. Occurally they can get a bilateral contractivitis, which spares the limbis, and some can get anteroid, you guys, very early in the course of their disease. So just to tribute to my buddy here, okay, so what disease are we going to be talking about in a minute? Everybody knows who the guy on the left is, right? It's David Bowie, he passed away last week, or two weeks ago, and he had iris heterochromia, but not due to fuchs, but due to trauma. So we're going to, this is fuchs heterochromic irdocyclitis, or fuchs uveitis syndrome. There's iris heterochromia classically, usually the lighter iris color is in the brown eyes and darker in blue. There are classically stellate precipitates findings that are very common are cataract and elevated intraocular pressure, okay. The other thing is that they typically will have a very low grade iridus, let one plus cell or less, that's usually not very responsive to corticosteroids, and the absence of posterior sneakia, okay. So low grade inflammation, no posterior sneakia, high pressure cataract. Iris heterochromia does not necessarily have to be present, but it can be. And glaucoma, okay. It's usually unilateral. The other thing about it is that frequently they will have cells in their anterior vitreous, okay, so they can have kind of an anterior, intermediate type of uveitis, so frequently patients with fuchs will complain of flurs. The thing that you need also to know about about fuchs is that there's very good evidence that rubella virus is pathoideological in this disease, okay, by both PCR and Goldman-Wittmer Cooperation of Patients with this Disease. So what's the next therapeutic step in a five-year-old with J, so it's an iris cyclitis with oligotartic disease that is unresponsive to topical corticosteroids with progressive visual loss. So this is a patient that comes into my clinic. This is a typical kind of patient. Yeah, okay, exactly. Why would it not be methotrexate alone? Yeah, exactly. So it takes time. You have to put the fire out with something, okay, and you have to, in most cases, we bridge anti-metabolites with corticosteroids and systemic corticosteroids are less apt to produce, you know, ocaroside effects in the top of which the patients are usually on for a long time when they come in. Okay, a 19-year-old female, age is important, 19-year-old female with bilateral edgier, IUBIS, vitreous cells after a bout of fevers, arthritis, increase in creatinine, and eosinophiluria, okay. Anybody know what the diagnosis is? Just based on that history, TINU, right? So there's a bimodal distribution in this disease, usually in young girls and then in older adolescents or older women, usually around the age of 30, bilateral non-grain alumnus, anti-UUBIS. Think about it. And there is a good screening test for this. Anybody know what that is? Urinary, beta-2-microplotin, exactly, right? And there are criteria for the diagnosis, okay, and the ultimate diagnosis is really made on renal biopsy, but, you know, we... Does it have to be bilateral? Yes, it usually does. And most of them respond to topical corticosteroids, though I have a couple of cases, I have one patient who's on immunosuppressive medications, so in a large series about, I don't know, 11% of patients will require heavy-duty treatment. Okay, 20-year-old white female floaters, decreased vision, snowballs, episodic parasthegias. This is a patient with intermediate uveitis, okay, so the designation intermediate uveitis until proven otherwise, until proven, you know, idiopathic, intermediate uveitis can be associated with systemic conditions, and it is, in terms of nomenclature, referred to as intermediate uveitis associated with X, okay, Y, Z, okay. If it is not associated with that, it is an idiopathic condition known as porous plenitis, right? So here you have classic findings on intermediate uveitis. You have vascular cuffing, macular edema, and staining peripheral renal vessels. So the differential diagnosis are idiopathic diseases I mentioned, porous plenitis, and then MS is associated with intermediate uveitis, sarcoid syphilis TB Lyme, and then uncommon diseases. One question I'd like to ask is, in a young woman who is HLA DR2 positive, okay, what is the chance, what is the likelihood, or the risk of multiple sclerosis associated with that disease? It's about 15% five years. So what you need to know is that porous plenitis in a young woman with symptoms may be associated with development of MS. So in terms of the workup, you want to exclude syphilis, sarcoid, and TB, Lyme serology, where appropriate, and then consider a neurologic workup for MS. For me, I think that I would consider a neurologic workup. We see a lot of patients with porous plenitis that don't have MS, but if there is something that, if there's another symptom that's associated with it, then I would send them to neurology and consider getting an MRI scan, because as you know, early treatment is effective in MS. In regards to the TB part of that, we've had a couple of patients over the last year, so we've had an intermediate EVI on this, and a quantifying goal has come back positive, and we decided it was late in TB, but they needed to be treated for that. Do you need to see something like a granuloma or a supragenoid reaction to really say this is truly due to the TB? I think so, because I think that intermediate EVI is so, it would be really uncommon to produce only intermediate EVIs. I think that may be a finding, particularly in a white person in a low endemic area, so the likelihood of the positive predictive value of a positive quantifying goal in this place is very, very, very low. The patient's immigrant, if they have pulmonary findings, they say that then it's a different story. So there are people that have exposure to TB and then they develop intermediate EVIs. I can't tell you with certainty that they're not necessarily related, but I think that in most cases, the question is not so much do you need to treat them, but what do you need to treat them with? So that patient may just require INH and revamping for six months, whereas a person with a tuberculoma requires for drug therapy. Does that make sense? So I mean, we were going to get to that a little bit later, but so there's a whole class of drugs that can promote demyelination. Anybody knows what they know what they are. Because they're TNF inhibitors. So TNF inhibitors would be contraindicated in a patient with a family history or with a suspicion of MS, and it can also promote demyelination patients with underlying MS. So it's a little tricky in young women that you may want to put on a TNF inhibitor. I would get an MRI scan on those patients. Sarcoidosis can produce any type of uveitis. 25% of sarcoidos patients may have uveitis. The lung's affected, the lung's skin reticulate endothelial system and the eye. Acin and lysozyme, you know, are useful in patients with active disease, but they're not diagnostic, as they are not specifically to be elevated. Other entities such as TB leprosy, osteoarthritis. ACE is also physiologically elevated in children, and decreased in patients on ACE inhibitors. These are a board type of questions. You know, ACE is not really diagnostically helpful, but it helps you put it in the ballpark. It's one of the laboratory tests that the workshop on the diagnosis of sarcoidosis suggested that would be possibly suggestive of that diagnosis, as we'll see in the next slide. Abnormal liver enzyme tests are actually helpful. So the liver is not uncommonly affected. So if I had to get LFTs or ACE and lysozyme, I'd get LFTs. The best screening test is really a chest x-ray, because 90% of patients with active disease will have an abnormal chest x-ray. In patients in whom you suspect having granulomus intraocular inflammation may have sarcoidosis and have a normal chest x-ray, I would get a thin-cut CT scan, because there has been studies to see just that a CT scan may be more sensitive than a chest x-ray and reveal pulmonary pathology that otherwise be seen on a normal plane film. Diagnosis is tissue biopsy. Definitive diagnosis, definite sarcoidosis requires tissue. Obviously the lungs are a good place to go, but you know, if you can biopsy a place that's not in the lungs, you know, that's not invasive, it is preferable. So it's always behooves you to look, you know, on the contactive of a firm nodule to the parotid gland, lacrimal glands, and the skin. So the skin is also a good place. Lupus pernio is a finding that you see particularly in African-American patients around the nasolabial folds that can give you the diagnosis. Just to show you some of the ocular findings in sarcoidosis, you know, there are categories definitive, presumed, probable, and possible. Definitive is biopsy. Positive, presumed, compatible uveitis with hyaluradnopathy, but no biopsy. Then probable, you know, compatible uveitis, no hyaluradnopathy and no biopsy, but three signs and two laboratory investigations. So here we're getting into this murky area of probable disease. 60% of these people will probably have sarcoidosis if they're biopsy. And the findings that you see are these tent-like PAS in the upper left and the upper right, granulomas in the back of the eye with optic nerve involvement, candle wax drippings to the right, snowballs, so-called snowballs, their inflammatory precipitates, the inferior retina, and these punte areas of quarter-retinal involvement in the periphery are classically seen in patients with sarcoid, making sarcoid an important differential in the diagnosis of what white dots are burgeoned. So they can look similar. So I always think about sarcoidosis in patients that are that are presented, that are referred in with sarcoid. What's this? I'm from Long Island, I write it was. What is the name of this rash? It's diagnostic of this condition, erythema migraines. This is the rash associated with Lyme disease. You can see that it has its targetoid appearance. Okay, this in the context of exposure in endemic area is diagnostic. So Lyme disease, tick-borne disease, borealob, or dwarfary, northeast mid-Atlantic states, bimodal distribution of kids and older people. Okay, because there's the people that are out hiking and stuff. There are systemic stages just as there are in syphilis because it's a spirochetal disease. So early in the disease you have erythema migraines, then there's a disseminated hematitis spread of the disease with fever, meningitis, Bell's palsy, arrhythmia and arthritis. Bell's palsy is something to always think about in a patient from an endemic area. It's very common finding patients with Lyme disease. And then in the persistent disease, which is really difficult to treat, is arthritis and neurologic symptoms. There are many acute manifestations that depend on the stage of the disease, very early disease, conjunctivitis, and anterovitis. But in the disseminated disease, you see mostly intermediate erythema migraines. But a posterior erythema migraines can evolve in this disease. It is a clinical diagnosis with supportive serology. PCR has been done on acute fluids and on skin lesions. The major differential in a child would be JIA. And the treatment is with IV antibiotics at neurologic doses just as you would treat syphilis. You may get a Lyme disease question. Okay, erythema migraines, Bell's palsy. What's up, Brennan? Often, do you see patients that you think have Lyme disease? We're here? I think I've seen two or three cases. Yeah. It's very uncommon here. I've seen Rocky Mountain spotted fever, but not a Lyme disease. But there are people that... It's another story. People get tested for Lyme disease by other physicians all the time. The problem with the diagnosis with Lyme disease, the testing is not very sensitive or specific. In terms of testing, there's a Liza test and there's a Western blot. If you have a positive Liza, it always should be reflexed to a Western blot. You should have at least three or four bands of positivity on the Western blot to make the diagnosis. Plus, arthraleges and history. Not just I'm feeling poorly. The hallmark of the presentation of intermediate uveitis is... What is intermediate uveitis? What's the answer here? C. Right. So it's based in the vitreous in the peripheral retina. The prognostic factor for visual outcome in parcellinitis, a poor prognostic factor would be what? Sorry? D. Well, that's a prognostic factor for the development of MS. But a poor prognostic factor would be earlier age onset. It kind of makes sense. If you have a disease longer, the visual prognosis is worse. Did you say... I said C. Sorry, I can't hear you. Anyway. Well, yeah, because you said D and then I said D. No, I thought you said D, but don't worry. We'll go to the board and have them change your answer. So it's not just a younger age of presentation, but kids seem to have a more severe presentation for the disease. I'm sure Jim has seen patients in our clinic and some kids that present with the intermediate uveitis, man, they got a lot of cells in their vitreous, worse than older kids. So sarcoid uveitis is characterized by, yeah, at all of those things, exactly. So, you know, syphilis and sarcoid cause a protein manifestation of disease. Okay, here we go. 25-year-old white female horse rider from Long Island, bilateral intermediate uveitis with periphylbitis and snowmanx. In addition to study, you know, discussion about MS, what would you order this patient? Intermediate uveitis with risk factors for Lyme disease. Okay, so this is a guy that actually presented to my clinic, a 61-year-old man with a history of rheumatoid arthritis, extensive travel history. He was on NREL and presented with his temporal area of retinal whitening, initially referred in with a branch of vein occlusion. Didn't have a branch of vein occlusion because the next day he evolved into more arthritis and severe presentation. We actually took him to the OR at that time because he had a fairly large differential diagnosis given his travel history and his PCR of his vitreous was positive for varicella zoster. So the diagnosis of this patient was acute retinal necrosis syndrome due to, you know, varicella zoster. So the differential diagnosis of a multifocal retinitis, okay, with vasculitis include the necrotizing herpetic retinopathies, arne, porn syndrome, CMV, toxoplasmosis, syphilis, sarcoate, TB, bartonella, and then, you know, metastatic bacterial infections. It's very important to know whether or not the patient's immunocompetent or not, okay, because that will also influence, you know, your differential diagnosis, okay. So CMV retinitis would be a common retinitis in patients, you know, with AIDS who are immunocompromised, plus a disease like toxoplasmosis in an immunocompromised patient can look completely different than it would in a patient who is immunocompetent. So just a word about arne, you know, presents unilaterally in about a third of patients with acute pain, redness, decreased vision, dry and illness, anterior uveitis, may have elevated that hydraulic pressure, and the fellow I may be involved, you know, within a week or even 20 years down the road, okay, so-called barn or bilateral anterior uveitis. In the acute phase, there are these multiple white yellow lesions in the retinal periphery, which coalesce, and then I centripetally extend to the posterior polymasea, retinal hemorrhages, always see vasculitis, always see vitritis, okay, so it's part of the definition of the disease. Late stage, you have widespread atrophy, pigmentary changes, and a very high instance, sorry, of retinal detachment. It's a clinical diagnosis, okay, so you make the diagnosis by looking at the eye and then obtain, you know, confirmatory anterior chamber of vitreous fluid, depending upon how broad your differential diagnosis is. The sensitivity and specificity for PCR is actually quite good with an anterior chamber tap, if you think that this is the only entity, okay, so if you have other intervening historical factors, patients have been on, he's an IV drug abuser, he's been in the hospital, you know, he's got a history of possible risk factors for endogenous endophthalminus, I would take him to the OR and do a vitreous biopsy, but if patients walking in, otherwise healthy young person with classic history of ARN, you know, I would do an AC tap, inject them with antivirals and put them on an antiviral medication, sorry, so the conventional regimen would be IV acyclovir, okay, followed by PO acyclovir to decrease the risk of the fellow eye involvement. Alternative regimens are oral val acyclovir, famvir or val ganscyclovir, so basically you need to treat them with acyclovir, okay, whether it's IV or oral, okay. Oral doses of valotrex at two grams, three times a day are equivalent to IV dosing. In general, I would, a patient that presents with an acute situation, I'll put them on high doses of oral valtrex and inject them with antiviral medication, usually foscarnit, but sometimes a combination of the two, and put them on an aspirin to decrease the risk of occlusive vasculitis and prednisone, okay, after they've been on a medication for 24 hours, okay, because there's a significant inflammatory component to this disease. So it's, again, the principle of never treating an infectious disease with prednisone monotherapy, okay, and allowing, you know, your eduvaral medication to, you know, at least have a chance to work. Rental detachment's common, the prognosis is good, the prognosis is really variable, okay. This is the literature, but in reality, there's a tremendous variation of prognosis, you know, there really is, and it probably has to with host factors as well as bug factors. 16-year-old white male with a unilateral of focus of retinitis vitreous vitritus and vitritus over this lesion. So the differential is toxo, okay, and these other entities, the labs I would order are listed here. His toxotiders were extremely positive, okay, clinical diagnosis of toxoplasmosis is made in this patient, okay, just the classic, this is how he evolved, okay, on anti-toxoplasmic therapy with triple classic therapy with pure methamphetamine, sulfidiazene that full in a gas, and steroids, because he had a lot of vitritus, okay, you know, usually after it, and usually the vitritus is not that bad, sorry, periocular steroids are contraindicated, okay. The reason for this is that if you put a depot in there, you can't get it out, you've got infectious disease that may just explode the eye. Same would be true for intravitrile injections of steroids. There are lots of case reports of toxo and syphilis and ARN that in which the eyes just explode with intravitrile patients that in which the differential wasn't considered, and, you know, they've been given intravitrile steroid injection. So this is always, you know, who do you treat, the toxoplasmosis, I usually treat everybody, okay, that comes in, although I think a small, you know, active, very tiny peripheral lesion could probably be observed, okay, sometimes I might do that, but usually they come in with some symptoms, okay, with vitritus, so if they have vitritus and an active disease, I think they may treat me, but it's recommended that if you have any kind of lesion that's vision threatening, which most of them seem to be, okay, in the macular optic nerve or popular macular bundle, visually significant vitritus, or certainly an immunocompromised patient, they require treatment. How do you treat them? I must have missed a slide here, guys, I'm sorry. There's the classic treatment with, like this other patient with triple therapy with, you know, sulfa, dariparum, and fulinic acid. There are some alternative treatments that are helpful. Clinomycin and sulfadizing can be added, you need to be aware of pseudomembers, kind of colitis with clinomycin. Many practitioners will use Bactrum, okay, so in a patient with a peripheral lesion that's not threatening vision, I think that's a really good choice because it's cheap, it's effective, and useful for the patient. In a patient with a lesion that's threatening their optic nerve or their macula, I'll try to put them on triple therapy, although it's really hard to obtain the drugs, as you know, you know, it's dariparum, it's ridiculously expensive, or used it was, okay, and it's hard to obtain, it's hard for the patients to actually take, you know, all those medications. So there are alternatives that have actually been shown to be pretty effective. So if I can get it, Atovacone is actually very helpful, 753 times a day, and azithromycin plus pyrimathemine, maybe plus or minus pyrimathemine are useful medications. In patients that do not tolerate systemic therapy, intravitual clinomycin with or without dexamethasone may be actually very useful, and use that as well in pregnant patients and patients that just can't take systemic medicine. So a couple of questions about toxo, so I just want to show you a couple of pictures. Up in the top left, classic toxo, okay, so scar and satellite lesion with the tritis, okay. To the right is a patient with AIDS, okay, with toxoplasmosis, don't know what's going on in this patient, okay, it's an necrotizing retinitis that can be bilateral, may simulate CMV retinitis. Always scan AIDS patients with toxoplasmosis because about 15% of the time they'll have ring enhancing lesions in their brain that are due to toxoplasmosis, okay. The lesion on the right is in a patient with acquired toxoplasmosis, so it can happen just with and it's usually unilateral, usually without a without a satellite lesion, okay. IGA is usually helpful in that. So these are board type of questions. Most octotoxoplasmosis is congenital disease, true or false? It's false, okay. Recent studies have suggested that actually and due to epidemiologic studies in Brazil and due to recent epidemics that acquired postnatal disease probably represents about two-thirds of the cases, okay. So the classic teaching was that it's a congenital disease with reactivation later on in life. The current thinking is probably it is a more often acquired disease postnatally, okay. So requires treatment paradigms for not only pregnant women but also preventing kids from getting the disease. Acquired disease comes from eating undercooked beef or exposure to cats. Mostly false, okay. So you know this is a little bit of nitpicking stuff but I think that if you had it contaminated ground beef, okay, litter boxes, not cats themselves, all right. And water actually is probably an extremely important contaminant, okay. So contaminating water from feral cats, doing their thing in the reservoir. Octotoxoplasmosis is a clinical diagnosis, laboratory testing is supportive only, true or false? Mostly, okay, true mostly. I agree with that, okay. So there would be certain exceptions in which like the CMV retinitis patient you would want to get some laboratories. When is laboratory testing, when does it really help you? When it's negative, right. If it's negative, patient doesn't have toxoplasmosis, right. So mostly true except when you have an atypical presentation, okay, like an immunocompromised host you might want to actually obtain PCR of your aqueous through the vitreous or get serological testing. And then a negative test can be helpful because it excludes the diagnosis, okay. What is this? Neuroretinitis, right, okay. It involves the optic nerve and this patient with an incomplete macular star. So the most common cause of neuroretinitis is probably bartonella, okay, bartonella, hence they are quintana. Again, mostly a childhood illness. They will present with systemic disease with an erythymus papule at the site of their inoculation with a fluid-like illness and regional adenopathy. So that history is actually important, okay, to elicit that history in your kid. It can bartone, aqueous disease includes, you know, paranoid's aqueous glandular syndrome and neuroretinitis. Neuroretinitis is, you know, a broad differential diagnosis including infectious entities, syphilis, Lyme, TB, Duzum, Toxotoxicara, sarcoidosis, and then bascopathic entities. As far as bartonella is concerned, there's no, there are no definitive treatment guidelines for neuroreinitis associated with it because the prognosis is usually quite good. 85% of patients will have visual cues in 20 to 25 this or better. However, patients have systemic disease. They need to be treated usually with erythro, well, doxycycline and rifampin. So peripepillary scarring punched out mid peripheral scars, crudely vascularization, absence of vitreous cells. What diagnosis is this? What? Right, ocarohistoplasmosis. This is a lady, a patient of mine, older lady with floaters and a history of glaucoma and allergy to penicillin. And she has these kind of characteristic dots in the back of her eye, okay, with poorer vision, right? She had a mild vitritus, pretty good vision, right? Okay, with these multiple dots. And then imaging, her fluorescein shows some retinal vascularis and some angiographic macrodema. But her fluorescein, her ICG shows characteristic hypofluorescent spots that are probably more numerous than the dots we've seen there. Okay, so her laboratory workup was possible for HLA-829, okay, the diagnosis of bird shrapnel in her cortopathy in this patient. Major differential would be sarcoid, right? If the HLA-829 were negative, you'd think about sarcoid. What other entity might you think about in an older patient that presents with that? Maybe a little more vitritus. Lymphoma. Yeah, lymphoma. Here's a younger person that presents with previous viral progroma, okay, one week history of decreased vision in one eye, okay, and a history of urinary tract infection. Decreased vision with these multiple plaquoid, that's how I describe these lesions, plaquoid lesions in the back of the eye, and myelitis cells in the anterior chamber in vitreous. Her fluorescein angiography shows early hypofluorescence and late staining of these lesions. What white dots do you know is this characteristic of? Campy. Parapapillaries scarring, punched out, mid-fertilous scars, parotidine vascularization. In the presence of vitreous cells, this characteristic of punched out. So, yeah, A, idiopathic multifocal corditis, also known as multifocal corditis and panubiatis, also known as pseudoesteplasmosis. So, multifocal corditis and panubiatis syndrome, that's what it would be called. So, Birchot is characteristically associated with the following clinical feature. Let me, this isn't really a good question, sorry, but what would be the best answer? What's the major, what's the major cause of visual loss in patients with acute visual loss? Cystoid macular edema, okay? So, iris nodules and posterior sneakia, usually you don't see that in Birchot, okay? Vitalago, the skin in the eye are seen in what entity? VKH, right? Punched out corded out lesions. The lesions that are associated with Birchot are creamy in the cororide, radiated from the nerve, okay? So, that's sometimes, it's more like how to take a test question, you know, because you will get bad questions, right? Okay, coronary vascularizations reported in all of these entities except, what? Or is a characteristic complication? A, right, okay? It's an anterior UBI. So, idiopathic multifocal corditis or panubiatis or multifocal corditis panubiatis, PIC, and ocular histoplasma, so the three entities you think of, patients presenting with coronary vascularization, and you've got this, the most common. Serpidinous-like corditis, okay, is, what does it do to, do you think, what is serpidinous-like corditis associated with? Scordia TB, all right? So, it is usually, it can be unilateral, but it can be bilateral. It's frequently complicated by corollary basterum membranes, and it's more commonly seen in patients who are PPG positive. This is an example of a patient with a multifocal corditis, okay? This patient had a history of ocular surgery in the fellow eye, so we're talking about sympathetic ophthalmia. The differences between sympathetic and VKH, they're very, very similar diseases, probably share a similar pathogenesis. In fact, there's a guy that I know that was charged with giving a lecture, you know, at a national symposium on the difference between VKH and sympathetic, and he said, he got up and he said, surgery and walked off, okay? He was kidding, and then he went back on and finished his lecture, but it's pretty much true, okay? So previous ocular surgery or trauma, you see in patients with sympathetic, you may see vitiligo, polios, and alopecia with both entities, okay? It's more characteristic of VKH, but you can see them in both, okay? And then there's a pathologic distinction that may be an artifact of proper, not an artifact of acquisition, okay? But for board purposes, the coriocapolaris is usually spared in patients with sympathetic ophthalmia. Another way to put it, the coriocapolaris is usually involved in patients with VKH, okay? Because you're obtaining the pathologic specimen usually within two weeks, okay, in a patient with sympathetic. So you have thickened uvia, non-necrotizing, granulose inflammation of epithelial cells with pigment, phagocytosis, lymphoid infiltration of the coriocapolaris. This is the kind of question I'd like to ask you on the boards, okay, in sympathetic ophthalmia. You see RPE metaplasia into epithelial cells on Brooks membrane, also known as Dallon Fuchs nodules, again, board question with relative sparing of the retina and coriocapolaris. Again, probably an artifact of acquisition of the pathologic specimen. The treatment classic teaching is to enucleate the traumatized eye within two weeks to prevent the onset of sympathetic ophthalmia in that fellow eye. It may be useful in delayed onset cases, probably diagnostically only, but not therapeutically. And, you know, enucleation is usually is performed much, much less frequently these days because, you know, there's way better micro-surgeable technique and repair of traumatized globes. Plus, we have good immunomodulatory therapy. Treat patients. This is a exudative retinal detachment in a young person with VKH. This woman has vitiligo and poliosis. The classic fluorescein angiographic signs are punctate areas of hyperfluorescence at the level of the pigment epithelion which increases the intensity and leak and then pool into the subneurosensory space with exudative retinal detachment. This is the sequela of subneurosus in a patient that was inadequately treated initially. So, importance of treatment I can't underscore in treatment aggressively at presentation and continual treatment after you get the exudative retinal detachment under control. So, the American UBI Society criteria for the diagnosis, no history of trauma or surgery, right, and then three of the following at some point in time in their disease, okay, bilateral chronic erosyclitis, which one sees in the late stage of the disease, which is the thing that actually really blinds a lot of patients, okay, cataract and glaucoma, and chronic anterior uveitis that's left untreated. Post-Uveitis with exudative retinal detachment is an acute finding. Sunsyclofundus depigmentation of the RPE is something you see late in the disease, okay, and then neuroallergic signs of inextipitous tinnitus, cranial nerve, were seen as problems. Cutaneous findings include alopecia polyosis and vitiligo. This is kind of useful clinically, I think. Differential diagnosis of exudative retinal detachment and uveitis, syphilis, posterior scleritis, central serous, uveal of fusion syndrome, sympathetic, intraocular lymphoma, sarcoidosis. Not a poor question, really, but who knows, maybe, you know, which of the following produce exudative retinal detachment, right? Differential diagnosis of dandlon-fuchs nodules is definitely a poor question, okay? Sympathetic, always think about VKH, you can also do it in sarcoid and TB. This is a patient with hypopia and uveitis and Bechette's disease, okay? This classic 10% of patients present like this. This is what you read in the textbooks, but very few patients actually present with hypopia and uveitis. It's a classic teaching of Bechette's disease. More commonly, the more blinding complication is a retinal vasculitis, which is an occlusive retinal vasculitis and retinitis. You've seen patients with Bechette's. You can see in this series, this patient has, you know, significant occlusive vasculopathy and staining of both the arteries and veins with larger areas of non-profusion, you know, temples to the macula. Occur findings, occlusive retinal vasculitis, cotton wool spots ocular vagema, neovascularization, vitreous tamarid. Okay, so anything that produces an occlusive vasculitis can produce ocular ischemia, can produce neovascularization. Fluorescine angiography is actually a very useful test in and prognostic. So if you see a large area of ischemia, you know, you know this patient isn't going to do very well, or he might actually consider prophylactic lasering them depending upon, you know, the patient's situation. Systemic findings, oral muca-, oral athelous ulcers, 100% of patients. Okay, erythema nodosum, classically taught, but most of the time patients have more acne-formed rash, thrombophilobitis, not only the legs but of the gut. Okay, arthritis, large vessel occlusion, so-called angiobachette's disease, and CNS disease. So patients can get CNS bachettes, so it's a multi-systemic disease. Here's a picture of an ap- this is not your typical cancer sore, this is a rosa painful apis ulcer. Differential diagnosis of oral ulcers, Dr. Choi, bachettes, reader, writers, or reactive arthritis and sarcoidosis. Switching gears, okay, we know here this is a patient with a vitreous tamarid, okay, neovascularization of periphery, leakage. This is a patient that has- happens to have a diagnosis of IELS disease or idiopathic retinal vascularitis initially described by Henry IELS among young Indian men with epistaxis vitreous haemorrhage and constipation. It's usually bilateral, usually in patients with exposure to tuberculosis, sorry, it's 8 o'clock, floaters decreased vision and neovascularization. This is an example of a patient with tuberculosis, okay. She was- had a positive PPD, as you can see in this picture, she has a multiple- multifocal corridoritis. This is another patient with tuberculosis uveitis, with optic nerve involvement, multifocal corridoritis, and vitritis. This is another example of a patient with tuberculosis uveitis with a tuberculoma, so the answer to your question, I definitely worked this patient up for tuberculosis. This is another example of a patient with probably a tuberculosis uveitis, with tuberculosis serpigenous-like corridoritis. It is you, as we discussed as the fluorescein conference, okay. Usually it is bilateral, usually it is associated with vitritis, and usually it's multifocal as opposed to serpigenous in which the lesion comes off of the optic nerve. You see more areas of multifocality. Well, you know, I know the initial description was unilateral disease, okay, but I think as more evidence is- as more cases have been reported as more bilateral. TB is tough to diagnose, you know, quantiferent- it's a, you know, clinical diagnosis with, you know, confirmatory testing sputum, PCR is actually useful in vitreous. Quantiferent gold assay detects latent, not active disease, that's important to know. Chest x-ray may be normal in 50% of patients, so you can have extra pulmonary TB that presents in the eye. One, one case of TB, I mean, that have been reported in the literature that you always think about in a patient with a necrotizing, non-responsive scleritis who's maybe from, you know, not from here, think about TB. The treatment, as you know, is, you know, with multi-agent chemotherapy. One of these medications needs to be monitored by ophthalmologist, right, ethambiotol for opic nerve, in toxicity. The incidence of uveitis is increased in the United States, true. Quantiferent gold assay is screening test for Lyme disease, no. Confirmatory test for active tuberculosis, no. Okay, screening test for latent disease, important. I think I kind of gave this lecture to you a little bit. I'll give you the bottom line. All these guys have syphilis, okay? Okay, you can do anything. Okay, there are distinct clinical presentations that they may ask you about. Acute, you know, plaque white puts your coriopathy. So you see these large plaque white areas here, and then pan-uveitis with retinal precipitates. Think syphilis. There are pathopneumonic presentations. Okay, you can also see optic nerve-heavy involvement. Always good to consider syphilis. Always think about syphilis in your differential diagnosis. Always consider in the differential, always test for HIV in a patient that you think has syphilis, and always treat them with neurological doses. Okay, so give them a shot of penicillin in the butt isn't going to do the job. Okay, they need to be admitted. They need to have IV treatment. They need to have an LP, okay, before and after treatment. This is a lady that has lymphoma. Okay, can you stick around for five minutes? Okay, this is a lady that has lymphoma. Her story is basically she'd been treated with steroids for a year, okay, and didn't get better, and had these subrennial precipitates and vitritus, and she underwent a biopsy, or as they would say in Sopranos, a biopsy, and it was positive for poorly differentiated malignant neoplasm, and she underwent an IgH rearrangement which showed a monoclonal B cell population. Okay, so you're going to get these kinds of questions. 45-year-old white male. It's a little young, okay, for this. Laboratory work is on revealing no neurologic symptoms, so nothing to suggest a neurological involvement. Vitrious biopsy reveals monomorphic lymphocytes with large nuclei, prominent nuclei, and scanty cytoplasm. That's typical description of lymphoma, cytopapology. MRI and LP are negative. Okay, the oncologist and ophthalmologist should recommend, okay, certainly not observation, right? Repeat vitrious biopsy, have the diagnosis, okay. Intervitual methotrexate or rituximab. Yes, I think this is the way to treat them. The systemic and possibly intrathecal chemotherapy controversial, but the evidence suggests that with lymphoma isolated to the eye only, okay, that you treat the eye, okay, because of the morbidity associated with treatment and the fact that it doesn't necessarily prevent disease. It's controversial. A lot of people disagree with that recommendation, but that's what it is, okay. Have you ever seen it in a person? Pardon me? Have you ever seen that in a person? Yeah, I have. It's pretty unusual. So you would think it, so for intraocular lymphoma, you think about it in an older patient population, okay, so over the age of 65. Patients presenting with uveitis that is initially responsive to corticosteroids that recurs, okay, upon discontinuation of corticosteroids. Patients to present with sheets of vitreous cells, okay, that are more prominent or more extensive than you would, than the visual acuity would suggest. So the sheets of cells in the patients have relatively good visual acuity, okay, and sometimes they subepithelial infiltrates. So those are things that go into the diagnosis. The diagnosis needs to be made by obtaining, you know, tissue. The vitreous is the place to go most of the time, although about 15% of the time you can make the diagnosis by doing LP. So part of the workup of a patient with lymphoma is, you know, ophthalmologic workup, but also, you know, a neurologic workup, including an LP and MRI scan, okay. There are certain findings on imaging that are, that are very highly suggestive of this, including a leopard spot angiographic picture, and the infiltrates of the, the sub-retinal and sub-RP infiltrates are frequently between the retina and Brooks memory, so that's also something you frequently see. You can see that actually on, on OCT as Brian actually presented last year. The, and then, you know, the treatment is for just disease isolate to the eye, usually individual injections. The problem is that, you know, that at least in my experience 100% patients end up having CNS disease, dying from that. So their survival is a little bit longer, but the evidence to date suggests that treatment with, with chemotherapy does not extend survival. Just want to go through these last questions, okay, or, and, okay, so the following tests need to be performed on a patient with maintenance services of prednisone, okay. Bone density scan, important, okay. The most common side effect of mycophenolate is gastrointestinal, okay. It's the most common side effect of any of the anti-metabolites, okay. You need to know also that there's an increased risk of non-melanotic skin cancer associated with mycophenolate, not just in, okay. Which immunosuppressive medication is most likely to be associated with secondary neoplasms? Another way, another word to look at this, the site study showed that anti-metabolites are not associated with secondary neoplasms or increased more bit, or increased mortality. Cyclosporine is not associated with increased mortality, but the anti-met, the cytotoxic agents, cyclophosphamide and chloramazole are, okay. It's the most common malignancy you see with cyclophosphamide is, is bladder, okay. So they need to be, you know, caution to drink plenty of fluid, so the metabolites don't expose their bladder, and then of course, secondary hematological malignancies. Hyaline is gone, infliximab therapy causes all of this stuff, okay. So usually congestive heart failure on higher doses, an IV, exacerbation of demyelinating disease, drug induced libous, lymphoma, can't, been reported and all of them, skip that. Okay, just a word on AIDS, can CNP retinitis the most common opportunistic infection in AIDS? This is CNP retinitis, okay. Three presentations of CNP retinitis. This classic pizza pie wedge-shaped retin, multifocal retinitis usually coursing along the, the inner fiber layer, a peripheral retinitis, so-called granular brush fire appearance and a frosted branch angiitis, okay. The incidence of CNP retinitis has plummeted, okay, with the advent of heart. The treatment of patients with CNP retinitis includes not only heart, but oral or systemic gansychovir, systemic valve gansychovir, gansychovir, because it decreases visceral, it decreases the risk of visceral involvement, it decreases the risk of the fellow eye, okay, and it increases mortality. And then Zoster is a, can be a presenting sign of AIDS in patients with CD4 counts are greater than 200, okay. So in the developing world, you know, in Africa, patients presenting with Zoster, think about, think about AIDS, they can get acute retinal lacrosis, okay. They can get porn, which is a variant of paracelal Zoster, which is seen in patients with very, very low CD4 counts. That's it, that's a wrap. I hope that helps.