 For those of you that just came in, this is a picture. I want you guys to shout out what you think it is. And then we'll go through the disease very quickly. And for anybody who has taken one of these BFTs before, feel free to chime in with things that are testable questions. OK? And we'll just kind of go through them relatively quickly. And I can provide you guys these slides as well. So you can go over them in your own time. It's a lot to try to cover in an hour. So that's why we're going to go really quickly. And I feel like doing just case-based is probably the easiest way to go. OK? So these are not my views. These are my views and not the views of the Navy or the Department of Defense. There we go. All right. So we'll start off with this one. So somebody just yell out what do you think it is? And if you don't have to be right or wrong, just what does it look like? Yeah, go ahead and turn those off. You can turn them all off. That's fine. They don't need to. Nobody really needs to see me. So if I'm not lit, that's fine. What? Great on action. Great. Nice job. So differential, there's a quick differential of things that you could think about. So it's always concentric to the optic disc or consent or parallel to the auricirata, depending on where it is. So those are things you would do. And there it is. And then the big thing is is choroidal neovacerization through these things. So usually, if it's not involving the phobia, people retain good vision unless they get a CNVM. So what's that? So what is that in the center? What would you call that if you just had to call it something? Cherry red spot. OK. Give me a differential for cherry red spot. What else? Great. Oh, yeah. Sure. This is commotion, which can also look like a cherry red spot, which is OK, because it's the same. You get nerve fiber layer edema, which is the same thing you get in a CRAO, which is why you get a cherry red spot. So that's perfectly fine. This one just happens to be commotion, but it certainly could be a CRAO. And again, usually visual vision recovers, but not always. All right. Great. OK, give me three causes of perjures. Yep. Yeah, long bone fractures, fat embolus, amniotic fluid embolus, and trauma. So what's the pathogenesis? Anyone know? Yeah, it's complement activation. Exactly. So that's something that they may ask. And there we go, fatter, amniotic fluid embolization, crest injury to the chest, pancreatitis, long bone fractures. So we'll skip that one. Yeah, sclopateria. Yeah, I think that's how I pronounce it. I'm not sure, but that's how I pronounce it. So yeah, that's basically a choroidal retinal rupture. OK, and then you get this diffuse scarring. So this is what it looks like in the end. Yep, yeah, it's due to trauma. It's usually a large, mostly blunt, but it can be acute trauma as well. So they give you that and say, great, foreign body. So what are you concerned about for foreign bodies? I mean, other than that, it's an open globe. Sure, yep. And what two types of material? And what else? There's another one then, if you say vegetative. Iron, yeah. So perfect. So remember, no MRIs. That's a question that they will ask. So yeah, you're looking for ciderosis. Chronically, they may ask about ciderosis. They may ask about calcosis. Remember, iron floats, and copper goes, I don't know if you guys have stupid mnemonics, but we did. It was old iron-sized floats, and cops go to the basement. So copper always deposits in basement membranes, which is why you get sunflower cataract, and a Kaiser Fleischer ring, whereas iron floats, it goes to epithelium. So it goes to all the epithelial tissues. And so when you're looking at ciderosis, that's what you're going to see. So and calcosis usually only happens over 85% copper. So if it's less than that, like a BB, which is copper and zinc, you're usually fine. You usually don't get calcosis. Although if it's intraocular, you're probably going to remove it eventually. We'll skip that one because it's retinal detachment. Pretty straightforward. We can go over some of the characteristics. So there's regmetogenous, exudative, and tractional, and don't forget kind of how the difference looks. For an exudative, you should remember some things that are likely to cause exudative detachments like VKH, neoplasms, you know, croital hemangioma, probably being the most common, but not the most serious, and then malignancies as well, obviously. And then tractional attachments. So 10% failure rate of reattachment. What is that? Great. And where's the split? Outer plexiform layer, that's right. And how do you differentiate, how are a couple ways you could differentiate this from retinal detachment? Okay, what are you going to see on visual fields that differentiates the two? Yep. What's one other way? Well, yeah. And what will you see if you laser this? Yeah, it'll take, retinal detachments won't take, but you can usually get a take with these. Because most, because part of the retina is still attached, so you'll actually get a take at the RP junction there. The other thing you can see is you can see little white, little white dots, and sheathing of the retinal vessels, overlying this, which you won't see with, and those are the white dots with a little Mueller cell end plates, and they look like little, almost like little snowflakes. So, and it's almost always infrotemporal, it's mostly bilateral. So you have to figure out whether it's a retinal detachment or not. And then again, it's 5% prevalence. If you look at everybody and really look closely and depress them, 75% are bilateral and it's associated with hyperopia. And it's a split between inner nuclear and outer nuclear, or excuse me, outer plexiform. So difficult to see here, but there we go. There's kind of this thing kind of right here. This is, I'll tell you, because this isn't a great picture, I didn't put this picture in, but this is juvenile retina schesis. So it's the difference between juvenile and typical retina schesis. Yep. And I always remembered that by young people playing the NFL. So, whereas old people, unless you're a Peyton man, we do not. So it occurs at the nerve fiber layer. They usually typically will have, or more likely will have poor vision because it affects the phobia most always. And then they can have peripheral schesis as well. Skip that. I just gave you the answer on that. So that looks very similar to the other one. Cherry red spot. So differential, remember, you can get an ophthalmic artery occlusion. And then you'll have no choroidal perfusion either. And usually that's painful. And I'll typically come in with a low pressure as well because again, you're not getting perfused. So metabolic storage diseases, those are the ones that cause, the most common ones that will cause a cherry red spot. Pasex is the most common nemenpick, sandhoff and hurlers. Remember, you can see the box carring of blood flow and then diagnostic testing. You probably want to get at least some basic diagnostic testing. And so if you remember all those, you don't have to do all of them, but they may ask you, which one of these would you do? Remember what they're for. So management, I guess you can do any of these, but none of them work particularly well. There are case reports for all of them, but nothing significant. And remember, you have to follow these people for iris and neovascularization. Just 10% of them, well, this says 20, but what I remember from BCSC is 10. Most of you guys saw that picture before. So valsalvorretinopathy associated with increased intracranial pressure. There's the differential. You have to think about bleeding diathesis, especially if it's spontaneous, leukemic retinopathy, things like that that are rare that you'd want to check for. So, and remember, you want to get vital signs on these patients and bleeding evaluation and low risk of permanent visual issues. So positive arrow sign, pretty difficult to see there. So, anybody, so branch retinal vein, sorry, branch vein occlusion study. What did they look for? These are some of the things. The studies also put in here and make sure that you guys get a copy of this, but what did the BVOS look for? What did it show? That's correct. No, that's, you're right. So yeah, those are kind of the two conclusions there. So what's that? What was that? Yep. So buzzword for that is blood and thunder. So not necessarily, you need for your rhythms, but definitely for your orals. If you say that term, people know you know what you're talking about as long as you're using it correctly. So if you say blood and thunder and it's a perchers, they're gonna push you harder and say, well, they obviously might not know what this is. But if it's an obvious one, if you say that, then typically they'll say, all right, great. And they'll just have you go through a few things and move on. So you can go quicker. So those buzzwords are nice to know. So central retinal vein occlusion. So retinal hemorrhages and dilated tortuous vessels are what you're gonna see. And remember, you wanna get blood pressure and then the medical evaluation. You guys know most of this stuff, so we won't go through it too much. Non-eschemic versus ischemic, greater than 10 disc areas is the cutoff, okay? Unforeseen. So that's how you decide. But you can also mostly tell by visual acuity. It's not a slam dunk always, but usually non-eschemic will have relatively good vision and ischemic will have relatively poor vision. And there's the CVOS, so PRP for any neovascularization, but don't do it before it happens, just like the BVOS. And then focal is not beneficial for improving visual acuity. So they don't recommend focal laser in central retinal vein occlusions. Somebody other than Julia, yell something out. Anybody, it doesn't have to be right. What could this be? Give me two or three things. BRVO. Okay, what else could be? How about CMV retinitis? I mean, it doesn't have to be perfectly classic, but you could always say two or three things. This could be, but this is a BRVO. So again, pan-rental focal regulation for neovascularization and grid laser for macular edema, and that was three to six months was the cutoff because a lot of them do resolve. We don't really necessarily follow that with anti-veg F treatment anymore, but you still can do scatter laser. You just don't wait three months to see if their vision improves, typically. So that is a horrible picture. Not even sure I know what that is. We'll skip that. All right, great. So important things to know about diabetic retinopathy. There's some of the characteristics. So the DCCT was for type one and what was the study for type two that looked at glycemic control? UKPDS, yeah, very good. UK Population Diabetes Study. And they both basically showed that better glucose control is better for diabetic retinopathy progression. So that's really all you really need to know about those two studies. And then what are the other important studies for diabetes? Name one or two of them. DRS, ETDRS. So know a little bit about those studies. You don't have to know inclusion, exclusion criteria, but know what they were looking at and know whether it was positive or negative. Okay. And again, I'll put slides in for each one of the studies pretty much. It's also in your BCSC. You've got like a two page thing on, or one page thing on each study. And go through those because, again, at least for the summaries of here's what's important to know because those are highly testable things. And they'll say, oh, what's the DRS say about, you know, what's finding in the DRS? And they'll have something from the UKPDS. They'll have something from DCCT. And they'll have something from ETDRS. And then one of them will be from DRS. And you have to pick the correct one that came from that study. So it's important, especially for diabetes, since there are a decent number of those studies and they all kind of seem to have similar looks. So is that, what? Yeah, NVD, exactly, Proliferative Diabetic Retinopathy. So high risk versus low risk is 7A. Photograph 7A from the ETDRS study, but it's basically one third of the disc. Or less than one third of the disc if you have hemorrhage or NVE with hemorrhage. Okay, those are the three categories that they said were high risk and that recommended PRP. The DRS just looked at treating patients with PDR and showed a decrease in severe visual loss if you treat them. And then ETDRS was looking at, if you treated people earlier, did you get an improved response? That's where they came up with high risk and low risk. Okay. So this is something that looks like diabetic retinopathy, but it's not. I'll tell you that, I think. I remember this is the right one. So what looks like diabetic retinopathy? What? Sure. Oh, this is CSME, sorry. This one looked like the radiation slide. So CSME was from which study? Which study determined what CSME was and criteria for it? Yes, and what are the three criteria? Cause that's the thing they're gonna ask you for on CSME. So it's swelling within 500 microns of the foveal center, greater than one disc area of swelling that's within one disc area of the center or exudates with an area of swelling that's within one disc area of the fovea. Or excuse me, with 500. The exudates are the 500 microns as well. But then that's associated with thickening. So if the thickening's not within 500, but if the exudates are, that's considered CSME. And so those are treatment. And that's from the ETDRF and showed 50% reduction in moderate visual loss if you treat these eyes with CSME. What's that? Great. And what is that called? What? This is salmon patch hemorrhage. This is a C-fan, yeah. And then you can get other things like black sunbursts and what you're similar to what you see in hypertensive retinopathy. So these are all the things you can see. I remember that you can see anduid streaks in someone who has that. And we'll go through anduid streaks in a bit. Yeah. So like if we're seeing some... Yep. Yep. If they have sickle. Because like... Yeah. Yeah, you know, it really just changes the management if they have high pressure in terms of what you would do and then whether or not you can put them on dimox or, you know, or any CAI. Other than that, it doesn't change the management too much. If they have high pressure and they have sickle, then you tend to take them to wash out earlier. But other than that, if you can get their pressure, you know, if their pressure's controlled, then, you know, all the other stuff is like 100% oxygen and all that stuff is less relevant in the acute setting. So, but I would, there's not much you can do. I mean, really you get a sickle dex. If they don't have any family, if they don't have any history of sickling, they don't have a sickle crisis and you look in the back and they have no sickle retinopathy, it doesn't mean they don't have it, but you know, you do the best you can till the test comes back, pretty much. Because you're not gonna get a sickle dex sooner than a day or two. So, but I would order one and then figure it out. So again, you avoid carbonic anhydrous inhibitors. And SC is the most common, followed by S-sal, followed by SS, for getting sickle. So you're actually more likely if you're not heterozygous, if you have the SC variant. So, remember that, because that's an easily testable question that they'll ask you guys. So what do you think that is? Very good. What's this most commonly associated with? Systemic hypertension, fantastic. What do you do for it? Well, yeah, hopefully watch it. What else could you do? Yep. But you risk having it burst if it hasn't already burst. So, you gotta be a little careful with that, but you definitely can. Okay, what is that? Radiation written up, they call. You knew it was coming up. So usually it's gotta be at least 30 gray and it delayed six months to a year out. And you can get it all over the fundus even if you have a plaque that's not in the fovea, but it's more common over the area. And it'll look almost just like diabetic retinopathy. You'll usually have a little more atrophy, but you'll get micro-aneurysms, you'll get hemorrhages, you can get neovastorization, so. Good job. So, mid peripheral retinal hemorrhages is the big thing that you'll see. And then you guys know they asked a question on one of my tests in the past that I may not name to about ophthalmodynometry. So, for what that's worth. I didn't, I don't know if I got it right. I can't remember for sure. But they did ask that question and they also asked about fluoroscopy for this, which I, again, not sure if I got it right, but. It's, you use fluorescein dye and then you watch it and you'll get seepage into the anterior chamber slower. You get delayed, so. Fluorophotometry. So, same thing. Five year mortality is 40 to 50%, so that's a big one to know. And they obviously don't die from this, but they die from, because they are crazy vascular paths. It could be. It certainly could be. More retinal hemorrhages than I would expect with tursons, because mostly tursons tends to be subhyloid, vitreous hemorrhage, but it could look like this. But this one will be, this one is leukemic retinopathy. And so, we saw one patient with this in my residency who had not been diagnosed and we diagnosed him with leukemia, so. It does happen, but most commonly, you'll see it in your leukemics who have a low platelet count and. So, you heard the optic question. Yeah. Did you hurt your radiation on college? Yeah, yeah, and you can get optic nerve involvement from leukemia. ROP, great. I'm not gonna go through that because Peds goes through that. Nice. So, coats is unilateral or bilateral? Oh, yeah, always unilateral. Remember your differential for leukocorea, all the things, because they love that. And always remember the ones that could kill you and the rest are important, but less so, because they'll always ask the ones that kill you. So, it's always retinoblastoma. That's always retinoblastoma until they say it isn't. You laser to the areas of non-perfusion and you can also laser directly over the abnormal vessels and in coats to try to get the exudates to go away. The light bulb aneurysms is kind of the catch phrase or buzzword and if you see an F-A and you see these little out pouchings that look like light bulbs and then everything just leaks, that's its coats. So, it's non-hereditary. Remember that's differentiate it from a lot of the other things that you'll see, 90% unilateral. And, okay, what's this? So, you've got some pigmentary changes right there. You've got this venule and this, that's an arterial. So, that venule right there. So, you've got pigmentary changes out here and then you've got some leakage temporal lofovia. What's that? Mac-tel. Mac-tel, yeah, or juxtaphovial telangiectasia. That's a synonym. So, you'll get right angle vessels, temporal lofovia. You get macular edema and you get pigmentation and it leaks usually a little bit. You can do laser photo coagulation to areas of leakage and you monitor for CNVM but you don't do a lot for these patients usually. These are the three types. I think type one is a coats variant. Type two is bilateral and this is the most common Mac-tel and this is what Dr. Bernstein is. And then you can have a later onset and bilateral that's type three. I don't think they'll ask you anything on that, but if they do, just remember that type one is unilateral and the other two are bilateral because the other two are pretty similar. Great. How often does this smokestack pattern happen? 10%. 10% is what the BCSC says, but it's low. Low percentage. Remember, what's the most common? Expense. Expense out. Perfect. You guys are all over this. So stress, steroid use, especially steroid creams and joint injections, things that sometimes people don't think about, they may ask you about. And remember that posterior scleritis, choroidal tumors can cause agglidative retinal attachments that can look similar. So you have to think about those when you see that but with a smokestack like that or even an expensile dot, that's not caused by choroidal tumors or posterior scleritis. So that's sometimes what they might ask you that question. You have an agglidative central attachment and they might say, well, what would you do to evaluate what this is? And FAA is you're gonna be your response. So focal dot, window defects, smokestack, laser after four to six months. And usually PDT is the laser of choice, but you can do photo coagulation as well. Never fit, great. You guys are gonna go through that with probably Peds and Neuro, I don't know. But you get a central detachment. So that's why it's in posterior segment and retina. Perfect. And what do you see on visual field? Anything? With that patient, what would you see on visual field? Fantastic. Yeah, you get a decreased sensitivity in that area because the light doesn't pass through the myelanus, nerve fiber well. So that's the differential is important here, especially for retinal astrocytoma. Come on, come on. All right. That was a gimme. All right, so remember Areds. Now Areds too, I haven't updated this, so I apologize. But now Areds too is what you would probably recommend. And then you still will see these laser things come up. So you do have to know them if they're in the current BCSC. And I'm not sure if they are, but they certainly were when I was going through. And it takes years for this stuff to get out and for all the anti-vegF stuff to get in. So yeah. Okay, great. All right, so is the MPS still in there? Macular photo coagulation study. It's what showed that laser was beneficial. And then the Visudine therapy, the PDT is still in there. The MPS was what originally gave us classic versus a cult neovascularization and decided when laser was appropriate and when it wasn't a percent risk. There was a question one time on OCAPS for smoking. That's what would you tell this patient? And one of the, they had like the big, long history. You read through it and then it said, you know, this patient has this, what would you tell them to, you know, what would you tell them about, you know, changing their lifestyle or eating? And one of the things was stop smoking. And that was the correct answer. This is not an easy one to figure out. I didn't know this until I saw it. So we'll just go on. It's high myopia. So you can get lacquer cracks. Those were small staphalomas. And it gets... They can be anywhere? They can be anywhere, yes. They're most common in the posterior pole, either with the nerve or just even right over the fovea, like those were. Yeah. Yeah, you get it. It's usually just the posterior pole. And a lot of times it'll include the nerve, but not always. But yeah, you just get like this kind of, so the characteristics for high myopia are more than six diopters near-sided or 26.5 axial length. And then malignant myopia is nine, I think, and 28.5. So those are easy, easy O-cap questions. That's what it is. That's what this whole test is, is memorize as many little things as you can. But yes, if you can narrow it down to two, you're doing pretty well. So that's why we go through these reviews relatively soon before, is so that you can hopefully say, oh yeah, I remember it was, I don't think it was four, so that's wrong and get rid of a couple and then figure out what it is. So what are these? All right, give me five things that are associated with anjoid streaks. Renee, one. Great. Yep. Great. So, sous-les-entho-, yeah, sous-les-entho-, you're adding it. What re-said? And Ehlers-Danlos, sickle, Padgett's disease, idiopathic. Those are five right there and then you can, there are the ones, Betis Thalassemia is also there and there are a few others. But those are kind of the five that I remember because they're the Pneumonic. So there it is, sous-les-enthoam, Elasticum, Ehlers-Danlos, Padgett's, sickle cell and 50% of these are idiopathic. Remember, if you can remember, a few things about each of these in case they want you to differentiate which one it is, they may give you that picture and say, the patient has hyper-flexible joints. What test would be appropriate to order? And they want you to be a pediatrician and order a cardiac workup. Like those are some of the tertiary kind of, you first have to figure out what it is, then you have to know the disease and then you have to know what test you should order for the manifestations. So those are the fun ones of OCAPs. They're not the, which glaucoma medication is a beta blocker. So those are nice. You do get some of those, they're very nice. So, all right, great. Stage is a macular hole. Obviously one, two, three, four, but what's one? Great, and then there's a one A as a subset, but what's number two? What's stage two? Full thickness hole, less than how many microns? 400. 400. Full thickness less than 400 microns. Stage three is greater than 400 microns and stage four is a full thickness hole with a PVD. So those are the four stages. The Watski Allen test, yeah. So that's where you shine a light, a straight beam of light and they'll say that they miss the center of it. So yeah, there it is, stage one, two, three and four. Fantastic. So 10% prevalence, all right? So it's pretty common in the population if you look. Now most of them aren't visually significant so it's not like we do peals on 10%, but what's that? What's this, just yeah. Sure, yeah, this is definitely a hemorrhage. This one probably a hemorrhage just based on the kind of dark appearance, but maybe an effusion as well. And the giveaway here that it's not something else is one, it's not infrotemporal if it was a schesis. It's dome shaped, so if it's gonna be a retinal detachment, it would have to be exudative, right? It's not likely to be rheumatogenous, but then you've got this lobular appearance here. So the fact that it's not like a continuous single lob and you've got two little lobules, that's consistent with choroid, okay? So those are the things you're kinda looking for when you're saying, what are they trying to show me? Cause this is the best picture you're gonna get in OCAPs. They suck. You guys, Julie and Eileen probably know, unless they've gotten better. They were not very good. So you look and you'll be like, that's an eye. Maybe, I don't know what they're trying to show me. So choroidal detachment. Most common reason for choroidal detachment is post-surgical hypotony. So usually glaucoma surgeries, but not always. You can get inflammation, maybe UVO fusion syndrome, stuff like that is rare. And then typically we observe these unless they're kissing and then we'll take them to surgery for drainage. Hemorrhagic drainage usually wait two weeks. It's so that it can reliquify before you go in. What is this? What is it? Yeah, sure, subhyloid hemorrhage, yeah. Subhyloid vitreous hemorrhage was, and that would just happen to be subhyloid. So I think of all the things that can cause that, we kinda went over that when we did our FAA last week for Valsalva, but these are a lot of the things you can think of for vitreous hemorrhage. These are kind of the most common. Great. With three things here, make you know that it's RP. Perfect, yeah. Yeah, they don't always look like perfect bone spicules and they won't always give you that. And there is also the retinitis pigmentosa sine pigmento, which is retinitis pigmentosa with no pigment. And they'll look just a little bit atrophic, but they'll have crazy atrophic vessels and a waxy pallor and their visual fields will be like zero and they'll have CME in 2400 vision. But they just don't get the pigment, okay? And I think that's like 10% or 5% of retinitis pigmentosa. It's not uncommon. But you need to think of the things that look like it that are treatable, like syphilis, diffuse unilateral sub-retinal neuro-retinitis dozen, which will give you unilateral RP, which is not necessarily a thing. And then vitamin A deficiency, A beta lipoprotonemia, because those are treatable. If you give them high-dose vitamins, you'll slow the progression of the disease. So there it is. You also can get CME and vitreous cells. So that should be on your differential of CME, is RP. Mine is deprive-not, diabetes, E2 prostaglandins, parisplanitis, retinitis pigmentosa, inflammation and idiopathic vein occlusion. E is, let's see, other E. I'll have to think of it again for it. Yeah, for CME. There's another E and then it's niacin, other, and I'll look it up again. All right, but if you know most of them, you'll probably be pretty good. So vitamin A. That's it, that's all we really can do in genetic counseling. There it is, autosomal dominant. Like most things, it's always the best one to have in terms of your prognosis. You know, you're likely to pass it on, but typically things that are autosomal dominant are less severe than recessive, because if they were very severe, then it wouldn't be passed on. So, and then remember, they love this. They love it. It's like their favorite thing about RP. If it's an RP patient, 70% of the time, they're gonna ask about heart block. I'm just telling you, they like things that kill people, so that's the one that they will ask you on if they're gonna give you an RP. They'll give you a picture and then they'll say, what test would you wanna order in this patient? And it's always EKG, so. And what are you gonna see on pathology if you buy, if for some reason decided to buy to see their heart? Ragged red fibers. Nice. Julia's killing it up here. Maybe it's because she's the only one talking, but. Renee, you're shaking your head. Cororimia, boom. So, you get progressive loss of the retinal pigment epithelium. There's the differential. You know, you probably wouldn't think this is retinitis pigmentosa, but you can get a similar appearance in terms of visual fields. It's usually more atrophic, so you're not gonna, you know, if you have a picture, you're not necessarily gonna say it looks exactly like it, but it can be similar in that people have progressively worsening visual fields, night blindness, and so it's excellent. And you can see changes on ERG in these patients as well who are carriers, the female carrier patients. Geridatrophy, yes. So, what are they lacking? And what do you test for? What? Yeah. And so what do you test for and what do you treat them with? Anyone know? So plasma ornithine levels for this. Ornithine and mesotransferase, it's OAT. And what do you treat them with? Anybody remember? Paradoxine and restrict arginine. Vitamin B6. A lot of things to remember, but hopefully if you have seen it once, maybe it'll trigger a memory. Okay, what do we got here? Name some things that could be. What's that? We're in Carolina immaculate. Sure, what else could it be? That's probably unlikely considering North Carolina immaculate dystrophy is pretty uncommon, but what else could it be? That's a possibility. What? Immaculate degeneration. Sure, immaculate degeneration. Plaquenol. Plaquenol toxicity. Cone dystrophy. Really, is that a cone rod? What's that? Cone rod, sure. Star guard. Star guards, fantastic. So yeah, that's a bullseye maculopathy pattern. So again, mine was Bob Chaps, but Chaps are the five most important. So that's cone rod dystrophy, macular hole, AMD, Plaquenol star guards. You can see Biedi crystalline dystrophy as well, which is a vitamin deficiency. They can... It usually doesn't cause this. It kind of causes a more RP-like picture. But this happens to be a cone dystrophy. So people complain mostly of extreme lights, a lot of light sensitivity with this and wash out when they go into bright lights because they don't have cones and so their rods get bleached. And what's that? Looks almost the same as the last one. So you could probably use the same differential. But the FA is striking for two things. So one is this and then one is this stuff, yes. So if you look, you've got this obvious area of hyperfluorescence doesn't really leak. So you wouldn't say it's leakage, but it's definitely early hyperfluorescence at 38 seconds. And those are usually mostly just related to window defect. But then this is the kind of sign that you'll see. And that's dark chloride, okay? And that's kind of a buzzword for stargarde. So if you see an FA and you say dark chloride, everybody says, oh, they're thinking of stargarde. Okay, so again, it's inherited both in autosomal dominant and recessive fashion. If the flecks are all, what? That's the ABCA41, yes. Yeah, the E, whatever it goes for. Yeah, I think they, in the BCSC, they lump that all into stargards. And that, you know, I'll have to read the BCSC over on that to see, but that's what, you know, if you have a question like that, sometimes don't get too much into the weeds because the BCSC typically does not. And so if you're like trying to break it down way too much for this test, you don't want to do that. Be a lumber and not a splitter for the OCAP test, for the OCAP test, for the most part. And then fundus flavimaculatus is, which I always got confused with fundus albipunctotatus, but this one is a stargarde's variant that's just happens to the flecks are all outside the macula. What's that? Best disease, great. What's the gene? Vestrophin gene, very good. All right. And what's, what are, what do you look for on EOG versus ERG? What was that? Great, and what's the abnormality in the EOG? What ratio are you looking for and what's the number that's normal versus not normal? Arden ratio. What? One to four? Like, it's, it's anything less than 1.8. Anything less than 1.8 is considered abnormal, but diagnostic is like 1.4, 1.6. And it just has to do with the EOG whether light versus dark. So, and that's important because most other, most everything else that has an abnormal EOG will also have an abnormal ERG. But this is the exception. So that's why we really only get EOGs for this when we're considering this is cause everywhere else the EOG's gonna be abnormal if the ERG's abnormal. So it's only really helpful in this situation for the most part. So autosomal dominant, probably this is, this is a rare, more rare one. This fund is albipunctatus. So they complain of a lot of night vision problems obviously because it's all peripheral. You have to separate it from retinitis, punctata, albicins, okay? So the reason you have to separate it from retinitis, punctata or it's cause that's a retinitis pigmentosa and it just happens to have a similar looking appearance. So, what's that? This is not, this is, I think it's sporadic. I didn't put it down on here. I'm sorry, I should have. I think it's sporadic. I'll check and I'll update it before I give you guys these slides. What's that? And what's this called? So I'll tell you, this here is normal and this is after they dark adapt for an hour. Yeah, nice. Yeah, so the Oguchi disease is the name and this is called the Mizuho phenomenon. You get this weird kind of iridescent sheen and then when you dark adapt them it goes back and looks normal. And they have a lot of issues. So yellow iridescent sheen, you have to dark adapt them and they will have their color will return to normal. So yeah, so what are a couple retinal changes that you'll find in albinism? Perfect, usually myopia too. So they usually have, they're usually relatively myopic. And you get phobia, hypoplasia and hypopigmented fundus. And then there's the two that they always like to ask. So in the history here, why frequent infections and why bruising in nosebleeds? So the two are, which one? Shediakigashi, which manifests with what? Abnormal T cell function, right? You get abnormal T cell function so you get frequent infections, sinusitis, chronic sinusitis, things like that. And then this one is hermansky pud lack. And we get abnormalities of platelets, platelet function. So again, they love shediakigashi for some reason because you could die from it. So they just love these kind of things. So if you see an albinism, those are the two things to know, to think about with albinism when they ask you a question because a lot of times they wanna lead you to that secondary systemic association that they want you to know. So tyrosinase positive versus negative is not really relevant, but they may ask you. It's a, you know, oculocutaneous versus ocular and then these lethal systemic associations. Oh, sorry, I forgot to mention they also get lymphomas, like most things with immune dysregulation. Hermansky pud lack is almost always Puerto Rican descent. What's that look like? I'm gonna guess that, but they still ask, they still ask questions about that, surprisingly. Even though most people are not on phenithisins anymore. Sorry, now I'm getting to like the end where I didn't up-paid all these. So sometimes I'm not even sure. So that's chloroquine that you'll see and that's similar to plaque mineral toxicity, same thing. So those are the doses that they have in the BCSE. Typically that should be 6.5 milligrams per kilogram per day. Sorry, not milligrams per day. And that's based on ideal body weight and not on actual body weight. So that's the one thing that you'll see a lot with people who do have plaque mineral toxicity is they'll be like 5.3, 2.25. And they'll put them on a dose. You know, they'll put them on 200 milligrams BID, which is what they give everybody. And they'll get toxicity. Almost nonexistent within five years. So that's why the normal recommended schedule is to see them for a baseline when they're first put on and then at five years. You don't need to see them between the first five years. The risk is like 0.17% or something like that. It's very, very rare to see within that first five years. So, and then remember that after you take them off, it continues to progress. So that's why screening and finding it early is important. It's because of the toxic metabolite or the toxic properties build up in the RPE and continue to damage over the next couple of years even after you stop it. What could that be? Nice. Yeah, these, other things, canthazanthine and tamoxifen can also cause that same crystalline type retinopathy. You can also have a look that's similar to that with talc retinopathy, but usually you're gonna see them in the vessels and you're not gonna see this perfect ring, but you can get a lot of these kind of iridescent crystals and they'll be scattered all throughout the fundus. You can also see the limbo crystal deposition and then you'll get blocked for instance in those areas. There's some recessive. Could be a lot of things. That could be adult viteleiform, but this just happens to be a solar retinopathy from a sudden gazer. So, if you see bilateral things in the macula, you always ask about sudden gazing even though I've never actually had anybody say that they do. But, and you can get CNVMs from these, scars, but typically it's non-progressive and you just tell them not to do it anymore. And there are a lot of case reports, not so much anymore after prolonged cataract surgery under high, high light. Not so much a problem because the scopes have gotten better now and the light is lower with still being able to visualize, but I think that we had one person that had it many years ago from an operative from somebody else that I saw in residency and they had used an ENT scope instead. And those are much brighter. Those are like the halogen super bright lights and had a two hour cataract case because it was complicated and needed an iris repair and this, that and the other and ended up having poor vision in that eye. From light toxicity. What's that? Yeah, you just have to be careful because they can be much brighter. So, and like the ENT scopes that they use for ears and stuff like that are much, much brighter than our scopes are. And they're like a single direct beam that's focused on something whereas they're kind of diffused and we have the angled light and stuff like that now. Okay. What is it most commonly associated with? Great, what chromosome? Nope, three. Von Hippolindo has three words so it's three. So I remember it. Von Hippolindo. So what things do you need to get in a patient that you see that? What systemic testing are you gonna get? Three things that will kill them if you miss them. So what can they get? What can they get and then what would you do the test for? Renal cell carcinoma, great. What else? Mangioblastoma cerebellar typically and what that could kill them. I mean, it's probably not gonna immediately kill them but probably relatively quickly. Pheochromocytoma. So the three tests you're gonna get are MRI of the brain, renal ultrasound and urine VMAs, right? At least, I think there's, so there it is. You get MRI of the brain, CT scan of the abdomen and they said CT scan, that's fine. And urine VMAs are gonna be the three things you're not gonna wanna forget. It's autosomal dominant, it's on chromosome three because there are three words in Von Hippolindo. Cerebellar humaniomas, renal carcinomas, pheos. And then you wanna continue doing those testing. What's that? Sturgeweber, great. And what sort of inheritance pattern? Sporadic, great. The W's are wild. So I remember that. They don't have an inheritance pattern. Sturgeweber and Weiber and Mason both have no inheritance pattern. Everything else is either autosomal dominant or recessive or excellent. So, sorry, I'm just, these are things that I had to use to have to remember. So, remember you can get a diffuse choradal hemangioma with Sturgeweber so they can have the tomato catch-up fundus. And they can get agi-dative retinal detachments from that. So they also get glaucoma very commonly, obviously, right? You wanna look for intracranial hemangiomas. Again, no hereditary pattern. If they have it on the upper eyelid, it increases the chance of glaucoma. If they don't, it does not. Seizures. And if I remember right, this is the one where you get the tram track sign. Railroad track sign on, if you do CT or a, is that incorrect? What? Okay, what's that? Weiber and Mason. Racemos hemangioma. Again, another wild, it's not, and then you get intracranial AV malformations. You can get bleeding with dental procedures. They love that one. Because people have died from getting a dental extraction when they had this. Because they'll have an AV malformation underneath their tooth. They'll pull the tooth and it'll just bleed, no bleeding death. Because they're in a dentist's office and they don't have anything to resuscitate them. So, seizures, mandible, again, and maxilla. What's that? So what is that on the retina? Anyone know? What disease is this? Yeah, tuberculosis. Very good. And so what is that? No, that's a tuber. And the reason they call it tuberous sclerosis is because they used to see these things on X-ray and they look like big potatoes in the kid's brains. So that's why it's called tuberous sclerosis, actually. It's because they look like big tubers on X-ray. Then they get this adenoma sebaceum and then they get these umbil, I can't even remember what they're called, sub-ungle something. And then this is a retinal astrocytoma. Okay, it's kind of whitish, cottage-cheesy appearance almost. Almost looks like a regressed retinal blastoma would look as well. So that would be in your differential. And there it is, differential. So again, adenoma sebaceum, which are little angiofibromas, sub-ungle angiofibromas, ash leaf spots, and then the tubers in the brain. So that's the big thing is if you want to get a CT or MRI of the brain, they can get renal angiomyolipomas and cardiocardoma sarcomas. So Zitz fits in nitwits, is the thing that I remember tuberous sclerosis for. So they get adenoma, they have seizures, and they're mentally handicapped. Nitwits, yeah, don't repeat that, but now it's on camera forever. Now, I mean, that's a way to remember kind of some of the most common things that are associated with these. And most of them are pretty PC, that one's not too bad. So you got ultrasounds and you've even got an A-scan. So what could this be? Sure, it could be a metastatic lesion. What else could it be? Yeah, amelonotic melanoma, sure. Why would it not be amelonotic melanoma? Yeah, pretty high, right? It's at least not low, so that would be less likely. But malignancy would certainly be on the list. What else is second in the commonality after malignancy? Let's say this is a 24-year-old female with no history or risk factors for cancer. I mean, you'd still be concerned about possibly a metastasis, but what else? What's the most? What? What is? It could be a carbine hammer tomol, though usually that's mostly just associated with the RPE. So usually you're not gonna get this caroidal elevation. So this is a caroidal hemangioma with high internal reflectivity and sometimes exudative retinal detachment. Do you guys need to go? I've got like 300 slides. So whenever we're supposed to be done, just tell me. Is it time? Great. Caroidal hemangioma, so high internal reflectivity that can have exudative retinal detachments. And you usually observe these unless there's a serious detachment and then you can treat the caroidal portion with laser to try to get it to stop leaking as much fluid. Great, thanks. All right, great. I'm gonna add, I'll just add on the study. Nice, cool for you. And then you'll email it to me? Yeah, it's too large. That should be fine, it's emailable. Okay, thank you. No problem.