 All right, well, thanks for sounding out guys. We'll try to cover some, hopefully how you'll retina stuff. A lot of these slides are actually from Becca Genture. So you should all text her, thank you. But we can get into it here. Try to have it interactive and have just a lot of pictures and naming things, but sometimes that's hard in the morning, I get it. All right. All right, so we'll start with some posterior segment trauma stuff that they often like to ask about. So young patient, blunt trauma, you see whitening another retina. I'll start with this one, because I think it's pretty easy. So this is commercial retina. It's also been called Berlin's edema. I don't think they would ask that though. It's transient, although can leave some visual deficit in the area that's affected, especially if it's in the macula. One thing they do like to ask about it is kind of where is the damage? And it's in the outer retina, it's disruption of the outer segments and then can result in some atrophy down the road. Here's another type of trauma that's actually pretty common. Anyone recognize this one? Brutal rupture. Yeah, exactly. So this is gonna be blunt trauma. And then what's the most common cause of secondary vision loss after coronal rupture? Which is the exact same view? Yep, definitely. And I think most likely they'll ask you to recognize the coronal rupture and then you'll have to answer something about CNV. Yeah, all right. This one has been on OCAPS as well. This is optic nerve evolution. This is gonna be a bad injury, of course, NLP. How about a history of head trauma or intracranial hemorrhage? And then you see this. Turcans. Turcans. Yeah. Starting out on the East, it's good. This is dialysis. This is most commonly gonna be in kids and blunt trauma. They often like to ask about dialysis presenting late. So this kid will have a distant history of trauma and then they'll come in with the big RD. You may have to recognize that it's due to a dialysis. This is due to an evulsion of the aura at the vitreous base. Again, almost always gonna be associated with trauma, especially on OCAPS. And more likely they'll ask you where this will most likely happen. This is kind of one of the things where there's actually not very great data on but OCAPS really likes to ask you about it. And so the answer is the infertemporal quadrant. And then super nasal is the second most likely. And kind of the theory of that is that there's less protection of the globe in the infertemporal quadrant with the orbital bones and everything. All right, how about this injury will usually be associated with a bullet that does not result in a ruptured globe? Cool, bacteria, something I remember, perhaps. Yeah, scope area, yep. These patients are really high risk for secondary retinal detachments and primary PVR. So kind of by definition, they don't have scleral rupture but they will often have chloride rupture and retinal rupture and just a bad looking eye. How about this one? Oh, wait, Joe for scope? Yeah, yeah. Sculpt area, is that just due to, like it's almost like a more, since there wasn't direct injury from the bullet, is it just like kind of a more intense commotion or what's the? Kind of, it's from like the shock wave. So this is high velocity projectiles. So this is almost always like a bullet from like a real gun. In my mind, commotion is kind of blunt trauma, counter-coup, thing like on the opposite side of the eye. So I guess in some ways similar that they're trauma but one is always going to be blunt trauma. One is always going to be penetrating bullet trauma and certainly scope area is a lot more destructive. Gotcha. How about this one? Perchers. Perchers, yeah. And kind of a defining feature is these pertur fleckin. They look like little cotton wool spots but they're almost geometric and they have like little lines of clearing between them which defines them as pertur fleckin. And so obviously this is associated with a lot of things if you group, people have split it into perchers or perchers like retinopathy. It looks the same. I don't think that that is really a important differentiation but head and trunk injuries is probably the most common one and most likely what you'll see it associated with on a test but also things that cause like embolic processes can cause this a long bone fractures where there's fat emboli is at least the proposed theory. Pancreatitis and then eclampsia in the study of childbirth have also all been linked to this perchers retinopathy. Pretty much always gonna be bilateral and it's usually pretty symmetric looking too but obviously this is one that you need to be thinking about other things that cause whitening and the retina, infectious, CMD, porn, iron stuff like that too. Okay, moving on from trauma just have a couple of slides on AMD. I think you guys probably have a really good handle on this already but just a couple of facts that I think they've asked about before. So kind of population-based only about 10 to 20% people have wet AMD. Druzen are markers of kind of unhealthy RPE but you do see Druzen in normal retinas so occasional small Druzen does not count as AMD. That's just kind of regular aging. Usually they're between RP and Brooks membrane but we have other things like pseudo-articular Druzen. I doubt they would ask about that. Kind of the higher risk types of Druzen or the larger soft Druzen and then pigmentary changes are both kind of the highest risk factors for developing CMD in the future. They definitely like to ask about size of Druzen and kind of how that contributes to stages of AMD. Anyone to remember the cutoff for either intermediate or large Druzen? Like 64. Yeah. And probably the most important one is distinguishing a large Druzen. What's the cutoff size for that one? 125. 125. Yeah. And who knows why or why they picked that number or I guess rather what else in the retina is that size that you're supposed to compare it to? And? Yeah. And it's a vein at the like optic nerve crossing. Perfect. So yeah. Early AMD is multiple small Druzen or a few intermediate. Intermediate AMD is extensive intermediate Druzen or one large Druzen or GA not involving the fovea. So just because they have GA doesn't mean it's advanced dry AMD. It has to be GA in the fovea. So that's also important when you're thinking about who should be on ARIDs, which they like to ask about just because they have geographic attribute does not mean that they don't qualify for ARIDs. And if it's not under the fovea, they probably should be on ARIDs. And then of course advanced is either wet or GA under the fovea. All right. Original ARIDs formula, decrease the risk of progression to advance AMD from intermediate AMD by about 25%. This is the formulation for the original ARIDs, but of course that's generally not what we use anymore. They switched beta-carotene for lutein and zeozanthine and they almost for sure ask you this, but why did they make that switch? Lung cancer. Yeah, specifically in smokers. There was a slight increased risk that when they looked back at the data there. Perfect. Okay. Some basics about little detachments. So what type of detachment do you think this is? Just based on first impressions. Very metogenous. Good guess. Do you see a break? Exited. Perfect. So remember that the OCAPs, they're not gonna give you all the information out there, but they're supposed to give you enough information to make a decision. So they could show you a picture like this and then you kind of have to assume that if you're not seeing a break or they're telling you that on exam there's no break, even though it's not showing you all the retina, sometimes you have to make assumptions, which is probably the most frustrating part of OCAPs. But so Exited have already defined by kind of no break, this bolus smooth elevation of the retina. We'll see how that looks different in metogenous. I think this one's tricky because it's superior, which is where we usually see regemetogenous. You also get the shifting fluid, which I think is not the best descriptor because you can also see that in regemetogenous, but that might be kind of a buzzword that they use can be associated with lots of things, tumors, hypertension, especially eclampsia, childbirth types of stuff, any inflammation in the eye, especially in the forms of posterior uveitis. And then like anatomical defects in the eye kind of cause exited RDS to so optic pits, nanophthalmos, morning glory syndrome, those things that can for some reason allow fluid under the retina or kind of like nanophthalmos will increase the outflow resistance and therefore kind of be a contributing factor of why fluid can build up under the retina. So regemetogenous looks different. Usually it has this corrugated kind of wrinkly appearance and then of course you're gonna find a break. Sometimes they ask you about these Linckoff rules. There's four and they're all designed to help you find the break or nowhere to look to find the break. I don't really like these rules because I think it can be simpler if you kind of just summarize it. It's just that the break is at the most superior part of the detachment. So I think that kind of covers, definitely rules one through three. So you just kind of look at all the clock hours that are involved in the detachment and then the break is most likely to be in the one or one and a half clock hours that are most superior of the detachment. The kind of the tricky one is rule three. So if it's inferior, you figure out which side of the detachment is highest and then it's gonna be on that side. Rule four is that you can have this little kind of strange configuration where it's bolus inferior and there's kind of the sinus of shallow subretinal fluid coming from a superior break. Joe corrugated means wrinkly. Corrugated means wrinkly, yes. Yeah. I think Catherine knows that better than anyone here now. Okay, treatment, these are just the principles of treatment of retinal detachment. You have to find the breaks, treat the breaks, plug the breaks. So all the ways we fix detachment do these three things. A buckle is just another way to plug the break and that just allows time for the cryo or a laser to help. The buckle really doesn't do much down the road once you have good adhesion from the treatment besides kind of help save you if there's new breaks that develop but really the gas, the oil, the buckle, those are all just, we use those just because they temporarily close the break as the cryo or the laser helps seal the break which is the long-term solution to the retinal detachment. They're generally not gonna ask you like details about like vitrectomy, surgery, repair or really detailed like buckling questions on OCAPs. But they will ask you obscure things like this. So chronic RDS are usually gonna present with low pressure clinically but they're more likely to ask you about ways they can present with high pressure. So one, of course, just kind of for chronic RDS it's a lot of ischemic retina, they can get NV and NVG or there's this kind of theoretical shorts, Matzoo syndrome where detached retinas allow outdoor segments to shed and break off and they're not getting eaten up by RPE cells like they usually do. And then they float kind of to the angle and plug up the angle and cause glaucoma. I don't know if that's like ever really been documented but they like to sometimes ask about that. All right. Which one of these are not associated with detachment or tears? With arrow. Yes, great. Oh yeah, and what is the third picture? It's kind of hard to tell. Is that a meridian fold? Yeah, perfect. So OCAPs will also give you blurry pictures but so left to right, so this is lattice. This is kind of paving stone which is not associated with tears. The third one, I'm pretty sure is a meridian fold which you'll only see if you're looking at the aura. See, and these are often nasally where you have kind of more of those dentate processes which are normal. A lot of people have meridian folds too but you can develop a little hole or tear at the posterior tip of it. So technically they can be associated with detachments. The final one I think is kind of a vituretinal tuft which again also can progress to a tear. Retinoschesis, so most commonly this is infertemporal. So same as dialysis. It's bilateral and most people, they can be associated with pretty nasty detachments but in order for that to happen anatomically you have to have an inner hole and an outer hole. I think that makes sense. Those detachments also associated with a high rate of PDR. That's something that it would maybe ask about. Lots of ways to differentiate schesis from detachments. Schesis will have absolute scatoma. So you can test that I guess with a visual field test but also with your indirect lens and like cotton tip or depressor you just kind of put it above the lens and they can see it moving around on their retina. The schesis reacts to laser because to get laser uptake you need retina touching RPE. So in a detachment you don't have that schesis you do. And then kind of a little more subtle and probably less likely to be on OCAPs but more clinically useful is when you depress it. Fluid doesn't come out of a break. It kind of just stays bolus and elevated and then ultimately ultrasound and OCT if you can get it are super helpful too. All right, this is attraction of detachment. Of course from diabetes, from PDR. If they ask about PDR they'll probably ask you in the setting that it's the most common cause of recurrent RD. And then they may ask you about this gradient system which is also not super health, not super clinically helpful but grade A is kind of just some little vitreous clumps or cells in the vitreous. B is more rolled edges especially on break. So they'll show you a picture of a horseshoe break that looks kind of chronic and rolled up. And then C is pre-retinal membranes or sub-retinal membranes. And then it's kind of relevant whether it's anterior or posterior to the equator and kind of how much of the retina is involved. You guys remember indications for pneumatics, I'm sure. It's pretty simple. No PVR, the break has to be relatively superior. So kind of the superior 240 degrees and all breaks have to be within one clock hour because you're treating them with a small gas bubble. Again, the macula on and off doesn't matter and the distribution of the tet detachment doesn't matter. You're just treating the break, the sub-retinal fluid will resolve. So the indications only have to do with where the breaks are, okay, drug toxicities. So I'm not gonna go over all of them. You kind of just have to stare at a table and remember these, but how about this one? This is probably the one we see most often or at least look for most often. Black window. Black window, yeah. And of course, they're not actually just gonna ask what drug causes this. They'll ask what is this patient being treated for? Something like that. So you have to know what the drug is for. So rheumatoid arthritis, lupus, kind of different autoimmune diseases for black window. How about this one? So pigmentary retinopathy, there's kind of one drug they like to ask about for that, even though there are lots of different things could cause this picture. Like some of the phenothiazines. Yeah, so this is gonna be someone who has like a underlying psychiatric disorder. So yeah, phenothiazine is the drug family and then thyroidazine is the specific drug that's most commonly seen with this. Obviously we don't see this much anymore but they definitely still like to ask about it. How about this one? Like what's the defining feature in that fundus photo that you should recognize? It's not the most typical picture. And the picture does not go with the OCT. Crystals. Crystals, yeah. So this is tamoxifen. That's gonna be the most common drug. It's gonna be associated with the crystalline retinopathy that they'll ask about. So of course breast cancer in the first picture shows kind of pretty extensive crystalline retinopathy but you can also get this just little focal foveal excavation there, which can look a little bit like mactel too but if they have breast cancer then you gotta blame it on the tamoxifen. It was talk too, right? Yeah, so talk can cause crystals. Generally they're gonna be inside the arterials because that's an involunt process. They're mixing talk with their injectable drug of choice. But yes. I've also had the mask like they're already on plaquinil and then what drug puts them at higher risk for toxicity and it's using tamoxifen. Also tamoxifen, yeah. Oh, that's a good question. So other like risk factors for developing plaquinil toxicity. So of course time and dose are probably the biggest ones but I think it's also renal dysfunction, tamoxifen or any underlying maculopathy. That's probably just cause we can't differentiate underlying other maculopathies from plaquinil but those are all reasons that you need to screen them earlier. All right. Rifabutin is not something we see anymore either but it's something that causes a hypopion, a sterile hypopion. It's used for patients with HIV for prophylaxis for Mac. So something that could be confused with endophthalmitis and something that they still occasionally ask about. All right, some pediatric retinal diseases. First just a little bit of anatomy which they definitely ask about as well. So one of the trickier things is kind of what is the vitreous doing while the eye develops and kind of this primary secondary tertiary vitreous. So that's something I think kind of just got no cold that they'll quiz you on. So the high load artery kind of fills this embryonic fissure in the second month and then it regresses in the fourth month and then kind of that high load system completely disappears in the eighth month. We'll see in a second what we get when that doesn't happen and kind of that tertiary vitreous that's, or sorry, so the primary vitreous is that high load system. I wanna make sure I'm saying that correctly which completely disappears. The secondary vitreous is the vitreous that we know in the adult and then the tertiary. The only thing that it forms in the adult eye is the lens zonules. So this is persistent fetal vascular sure. So that high load system can stay around and completely connect the nerve to the lens. It's also the most common cause of unilateral cataracts in infants. It can look a little, it can look a lot like retinoblastoma when you first see it. One clue is that these eyes or microbes are small whereas retinoblastoma eyes are sometimes big because of the high pressure and other things. And then they also have persistent fetal vascular eyes elongated ciliary body processes which is something that has been asked before that probably has to do with because those are also, like we talked about kind of related or at least attached to the zonules and therefore a type of vitreous at least during development. You got to worry about glaucoma in these patients and we treat them generally surgically to remove their cataract and then treating their underlying amblyopia is something that OCAPS likes you to not forget about. You can have this to a smaller extent. So this is really the same process that forms a Midendorf dark dot or the Bergmeister papillae. I think you guys know about these anatomically and they're due to the same process of not having complete regression of that primary vitreous or hyeloid or artery. All right, this is ROP over a little bit. Some of the confusing things are things that I find confusing about ROP. So sometimes they may show you just a picture and ask you what this is. You're noticing that there's no vasculature peripherally past that demarcation line and there seems to be a little bit of a ridge at that. So this is probably like stage two. There's not really new vasculation on that ridge as far as we can tell in this picture. So important to know kind of the risk factors or who you need to screen. So these are babies that are 1500 grams or less than 32 weeks of age or if they use supplemental oxygen for a long period of time and this is why ROP has the highest rates in kind of developing nations where they're still relying on a lot of high oxygen which we do less of in the U.S. now. So we... Is it 32 or 30 weeks? I'm sorry? Is it 32 or 30 weeks? I think it's 30. Is it 30? I could definitely be fact checked there. Thanks for catching on. You can double 15 for 1500 and that's your second one. That's a good memory tool. Perfect. I'll have to update that. All right. So we grade these within zones, stages and plus disease. So these are the zones. Zone three doesn't... Your zone two goes all the way to the nasal retina and then zone three is kind of that crescent of temporal retina. And then the radius of zone one is double the distance from the disc to the fovea. And that radius is about the diameter of the 28-diopter lens when you're looking in the eye. And then we also do stage. We're kind of... Stage one is just that demarcation line. Stage two is a ridge. Stage three is new vascularization growing from the ridge into the vitreous. And then four is a partial detachment and five is a total funnel detachment. And then plus disease is just torturous vessels, which is a pretty subjective thing. And people are trying to develop more analytical diagnoses based on imaging and AI now, but plus disease is something that we still use a lot clinically. So I think the most confusing thing for me was treatment of ROP because you learn like kind of this threshold cutoff, but then you also learn kind of the stage one and stage two ROP. And it was always really confusing if those were like related or different or whatnot. So to try to clarify that, so this threshold disease cutoff came first. So they initially just had this threshold disease cutoff to help define which eyes, which babies had a 50% risk or higher of having a bad outcome, meaning like total retinal detachment. So this is what gives us this definition of either five continuous clock hours or eight non-continuous clock hours of essentially stage three. So new vascularization and the in zones one or two. So this came first and defined kind of the worst eyes before they go on to have an RD. So in this study also said that all of these eyes that means that the special should get treated, of course. But then a little later, they said, well, maybe we should be treating eyes with less severe disease. And so that's kind of where this pre-threshold or type one and type two eyes or criteria came in. So when you hear type one or type two, that's all referring to pre-threshold or eyes that do not meet that initial threshold criteria. And so kind of in the e-drop study or early treatment of a ROP study, they looked at treating eyes that met some of these earlier criteria and showed that treatment of type one ROP, which again is less severe than threshold disease was still a good idea, meaning it prevented bad outcomes. So again, type one, again, all of these do not meet threshold criteria. This is either zone one with any stage of ROP and plus disease, zone two, stage three, with or without plus disease. Same with plus disease is kind of repetitive because that was already covered in the first one or zone, in zone two, this is probably the most relevant one. Zone two, stage two or three, so that's any type of ridge with plus disease. So seeing all of those when they're not meeting threshold disease criteria should still be treated. Zone type two, which is kind of anything but type one can be observed until they meet either type one or threshold disease. Any questions about that? Cause that really didn't click for me to be honest, like until fellowship. You guys got it perfect. Since stage four and fives of course, of course those eyes are going to surgery. Some people don't operate on stage fives because it's really hard and they usually have bad outcomes anyways. Okay. How about this? If this is not ROP, what do you think this one is? Toxo. Toxo, could be toxo, especially if it's fever. Yeah. So this one's fever. Toxo is gonna have some inflammation, vitritis and then this kind of stock is gonna be going to a peripheral granuloma. So this, the most common gene is FCD4. You get exactly this kind of, this draging of the retina. This is a pretty kind of extreme picture of what we can see with fevers. A lot of times it's more subtle but they can develop new vascularization, vitreous hemorrhage. Ocaps likes to know what a positive kappa angle is and this is due to, because there's temporal draging of the fovea, they can look like they have strabismus, but they're actually, if you do cross-cover test, they don't shift. So it's not true strabismus. They call it a positive ankle kappa. And then distinguishing this from ROP, it's gonna be a full-term baby. There's gonna be family history typically of fever. How about if you see fever like disease with detachments, it's really bad. It's in both eyes and it's a male. What does that make you think of? Coats. Coats, so coats will cover that too. Coats will almost always be unilateral but it's definitely, pretty much always in males too. This is kind of a little more obscure one but something they will sometimes ask about. So this is- Nori? Yeah, exactly. So this is nori disease, it's X-linked. And in my mind, it's just really, really bad fever. These people get bad detachments and proliferative stuff and it's bilateral. It's really rare, but again, Ocapsule Center likes to ask about that rare stuff, especially when we know the gene. So this is a coloboma. They're most likely to ask kind of like what causes a coloboma anatomically? And it's incomplete closure of an embryonic fissure. That happens at week five. That's why colobomas are generally kind of inferior or more specifically, infranasal. In the, so you can have this, this is of course a coriorentinal coloboma but you can get them in the iris, in the lens. Sometimes for the lens, it's just your missing zonules in that area and most commonly, infranasal. And a lot of times they're bilateral. So this is Coates disease. So there's lots of kind of things to recognize like the Talaeontic Tatic vessels, kind of the light bulb vessels, which especially you see on FA. Again, this is almost, this is mostly in boys. It's almost always unilateral. They like to contrast it, especially to retinoblastoma. So kind of thinking about how you can differentiate that kind of family history with the retinoblastoma, genetic testing, ultrasound is going to be key. You'll have calcification for the retinoblastoma. You generally won't for Coates disease. And really the light bulb aneurysms is kind of their biggest buzzword for this. How about rapidly progressive vision loss, nice stagmas in a six year old, bad ERGs and Ocaps is absolutely, yeah, exactly. So Ocaps wants to ask about stuff that causes permanent vision loss and death. So they're going to favor stuff like that. Oh, I'm sorry. I said yes to labors. And this is Batten's disease. It could have totally been labors too based on the I presentation. And so this is recessive for Batten's. They sometimes want you to know the gene. It's CLM3 and it's important because it's lethal and because they usually present to ophthalmologists first. So their vision symptoms start like kind of age six, usually they'll have profound vision loss and then the thing is caused by profound vision loss like nice stagmas for business, a bad ERG and then they'll develop seizures, cognitive decline and then it's fatal by at least the early 20s. Okay, moving on to some tumors. Are we doing time? Okay, I'm going to speed up a little bit. Okay, so cordial tumors, let's go through these. So this is a melanoma. You can see it kind of breaking through Brooks there causing that mushroom appearance. This is also a melanoma. Sometimes they can have portions which are not pigmented. I think you guys know this pneumonic for things that are suggestive of melanomas especially when you're trying to decide if it's melanoma or just a nevus. So I think the most important ones are thickness based on B scan and then fluid is probably kind of the things that most likely suggest that it's malignant and then of course growth is really the biggest thing that you'll see over time. They can get big, they can break through Brooks and cause that mushroom appearance on B scan. This can look like a melanoma, but this is a melanocytoma. It's always going to be right on the optic nerve and it's super darkly pigmented. It generally does not have malignant potential. This is just another one. Cordal mets will look yellowish. They'll be multifocal. They'll often be in both eyes. They're kind of lumpy bumpy, is a buzzword. And they importantly have high internal reflectivity whereas melanoma has low internal reflectivity on B scan. Coral hemangiomas will be kind of orange and red. They can cause exudative detachments kind of most commonly compared to any other tumor. These also have high internal reflectivity. And this is Sturge Weber. It's going to be probably most commonly seen in the setting of Sturge Weber where they can also have these either circumscribed which the first picture showed or these diffuse coroidal hemangiomas which can take up the whole coroid. They can look a little different. They don't have very well-defined borders at all. And when you see these eyes, what they're going to be asking about is probably glaucoma. So these eyes have high risks of high rate of glaucoma. Retinoblastoma. So you're just going to present as leukocorea. They're going to have calcium on the B scan which is key. They might be multifocal like this. We'll talk about the genetics here in a second. So, and then also important to know that these kids have a high rate of secondary malignancies. I think sarcoma I believe is the most common one but they also have pinealomas and melanomas. And the trickiest differential is comparing these to Coates disease which I think we talked a little bit about. They do like you to know these two pathologic findings. So Homer right. I always thought of Homer donut with a jelly donut in the middle. Although that's kind of confusing because the other one looks like a donut too but the Homer right rosettes are less mature. So you can also see them in like embryomas or some types of other tumors. The flexiner winter steiner ones are specific to retinoblastomas. They're more mature photoreceptors. They have central clearing. You know they're more mature because the photoreceptors are functioning. They're making outer segments and that's kind of why you have that central clearing and why you know they're more mature. Genetics of retinoblastoma is tricky. So it's a tumor suppressor gene but it's inherited like an autosomal dominant process which again is not typical but it's because the RB1 gene is so big and so prone to sporadic mutations that if you inherit one mutated copy you're almost, you have a very high rate of developing a second sporadic mutation and therefore getting the disease. Genetic counseling and kind of thinking about the inheritance is also tricky and something they test a lot. So if you're looking at the patient they have multifocal tumors or bilateral disease they're almost for sure have a germline mutation and can therefore pass it on. If you know the parent has bilateral retinoblastoma or therefore you know that the patient has risk of inheriting the RB1 mutation. They're not quite 50% for having the disease because penetrance is only 90% meaning there's a chance that they might not develop it and then those patients will be mostly bilateral if they're inheriting the disease but a 15% will have unilateral disease. And then if the parent has unilateral retinoblastoma then that's a little trickier because you don't know whether they're that 15% that do have, that does have a germline mutation it could therefore pass it on or the higher rate of 45% let's see I think I'm confusing myself. So if it's unilateral disease in the parent you're not sure whether it's a germline mutation or not. So there is a 15% chance that the kid will have retinoblastoma. If they do have, if the kid has retinoblastoma then you automatically know that it is a germline mutation and therefore the second kid kind of just falls into the initial algorithm of that 45% chance of developing it. And if the parent is unaffected then you have kind of just your sporadic risk of developing retinoblastoma which is far less than 1%. Again, most of those are gonna be unilateral but sometimes they can have bilateral disease. So that's a confusing topic probably helpful to sit down and like look at the charts to understand the genetics there. This is a astrocytic hematoma associated with two diseases that we know about which is tuberous sclerosis in neurofibromatosis. If you see this, you gotta think of on Hippolindal syndrome it's a retinal, a capillary hemangioblastoma. Also important to know what you also see in VHL so that's renal cell carcinoma, Pheos and CNS hemangioblastomas. Sometimes they want you to know the mutation is on chromosome three so VHL three letters chromosome three. This is a retinal cavernous hemangioma. You see these fluid levels where there's kind of clotted blood and then fluorescing that flows above it. If you see this you wanna think about hemangiomas in the brain because that's kind of the combination of Wyburn-Mason which is one of these diseases that does not have a gene and is not hereditary. And there's an association with bleeding with dental procedures because they might have hemangiomas under their teeth. We're gonna, this is vasopriliferous tumor. I don't think they're gonna ask you about that. The chirpy have lacunae. Again, this is hypertrophy, not hyperplasia. That's what differentiates it from anivis. So the same number of cells, they're just getting bigger and swollen. This is anivis with drusen which are, if you remember, you're two fine small melanomas. Acronym drusen are a good thing because they are a sign of chronicity. If you see this combination of just lots of pigment on the sclera and in the coroid, you think about ocular melanosis and if they have pigmented skin too, then this is ocular dermal melanosis which is associated with glaucoma and high melanoma risk. B-dump is really uncommon. They will, if they ask you this, I think it'll be in the setting of ovary cancer which is kind of the most classic association but it can be associated with other cancers too. This is bilateral uvial or coroidal thickening and pigment, usually with kind of some of these funny patterns. Coroidal osteoma, the key thing will be that it'll be hyperechoic on ultrasound and have a shadow because there's calcification there. Running through some of the white dots syndrome. So ampy, classically, this is gonna be block early, stain late. Young women, good prognosis. Mutes can look kind of similar but they have that brief like appearance to the fluorescein lesions. It's more commonly unilateral where ampy is usually bilateral. They're gonna complain of photopsias especially on OCAPs associated with mutes and this can come after a viral illness. Birdshot I think is easier for you guys to recognize. I think the important thing here is that vision loss is often from CME in the kind of acute phase and then just kind of a scheming and atrophy in the long phase and that you wanna treat these patients aggressively with kind of immunosuppressive therapy. Multi-focal cortis and panneviatus and PIC are essentially the same disease. Just one has vitritis, one doesn't and here the key for OCAPs is that vision loss is due to secondary CNV. Pose is probably the most, the key thing is that there's no vitritis or pose. Blow syndrome is pretty obscure. It's kind of pediatric sarcoid disease where they have kind of a multifocal corditis type of look to it. Okay, so we got like 13 minutes to run through some random things for retina. So this is blood associated endothelmitis. It can be staff and strep, but in OCAPs it's probably gonna be hemophilus which is unique to blood associated endothelmitis and these eyes do bad. The endothelmitis vitrectomy study is for cataract surgery does not apply to these patients. Usually we try to take these patients to surgery a little earlier, but it's tricky because sometimes the view is horrible. Post-surgical endothelmitis. So blood related is the highest rate cataract surgery. We have the EVS study to guide us. So it's not important to know that if they have light perception vision or worse, they should go straight to vitrectomy. If they have better vision than that they can go to vitrectomy or you can do a tap and inject. Post-traumatic, I think the only thing to know about this is that bacillus is kind of that key one. Kind of like hemophilus is to blood related. Bacillus is to traumatic endothelmitis and having a foreign body in the eyes is a bad risk factor. If you see this and they have no visual complaints this is asteroid. One thing they might ask what asteroid is that if you need to see through the asteroid the asteroid disappears on fluorescein angiogram. So if you have like a diabetic patient you wanna look at that, you can get a fluorescein. I don't think they'll ask you about the pathology of the asteroid. Wait, really? That's so cool. It is pretty cool. And it's something we don't do too much, but yeah, it works. I've seen it work. Cholesterolosis can look like asteroid, I guess. I don't think I've ever seen this before, but apparently you can get it in the anterior chamber which asteroid does not go in the anterior chamber. So I guess if you see this, you wanna like test for systemic chai systemic cholesterol levels. Car and mar. I don't think they'll get into too much details of this but recovering is kind of the first antibody described in car. There's more now. Car is classically cones and rods. Mar is just rods and mar will kind of, we think attacks like the bipolar cells so that therefore has an electronegative ERG. That's you get the first inflection, the A wave from the photoreceptors but then you don't have functional bipolar cells. So you don't get the second, you don't get the B wave. That's what defines a electronegative ERG. They'll probably ask you about this. So if you see just a bunch of random cotton wool spots, you gotta think about all of these things, probably most importantly HIV because that can kill the patient. But of course other things like leukemic retinopathy, sickle cell, interferon retinopathy. So which will be used for viral hepatitis is an important kind of drug effect as well. Lasers, you don't have to know any of this except I think twice for me, they asked what does laser stand for and they gave different fake acronyms. So it's important to know light amplification by stimulated emission of radiation. I think I remember it being kind of like the only one that made sense. So you guys can probably figure that out if they ask you that question. See, this is a horrible acronym. Don't remember the acronym. Lots of things can cause CMV. I think, or I'm sorry, CME. You guys know all these. Niacin is a tricky one that they will ask for. That's used to treat high cholesterol. Niacin is the same as nicotinic acid and it doesn't leak on fluorescent angiogram. Chlorofolds, another horrible acronym. Don't remember that, but it's essentially like low pressure, inflammation or things pressing on the back of the eye can cause chororhenyl folds. Ischemia, so you guys may wanna, I'm sure you'll be able to recognize retinal whitening in a vascular pattern that's gonna help you differentiate it from infectious stuff. So most importantly, you gotta think about emboli. You guys know how to work that up. You see that a lot. Then of course, you can't forget about GCA and patients. This is over than 60. Some say over than 50. And then kind of just other random things that can cause arterial occlusions in the eye. I think you guys know these. This is Android Streaks. You guys know the Pepsi Mnemonic. Probably Pseudocentrum Elasticum is the most, definitely the most common association and probably the most important one because you should get an echo to look at their heart. There's some cardiac things that they have to worry about. And then similar to lots of other things, the most common cause of vision loss in these patients is secondary CNV because Brooks membrane is damaged. These are lacquer cracks. These can look really similar, but they're in high myopes. That's kind of how you're going to differentiate them. Macular hole, I think. Oh, Pijoo. Yes, yes. Real quick for lacquer cracks. Are those also associated with CNV? I always forget or- Yeah, it's tricky because high myopia is associated with CNV. And so these patients are gonna have really high myopia. So they'll have like myopic CNV. Will the CNV come directly through the lacquer cracks? I don't think so because I don't think they're breaks in Brooks membrane. Actually, I don't know anatomically exactly what they are, but you can definitely see CNV in these patients because they're high myopes. Right, okay. Macular hole has this like crazy complicated gradient system which is really stupid. And all you have to know is that once it becomes a full thickness hole, that's when we take them to surgery. That's really, there's all these stages but really it's just kind of, once you hit stage two, then it's full thickness and then you take them to surgery. And surgery has generally a high success rate. This one, oh, who can recognize this one? I make me really happy. It's my favorite diagnosis. Is it retained PFO? No. There's a yellow spot. Popper one. Oh, I like popper that I think- Or is it laser? Yeah, it's laser. So laser or solar you're gonna spray in the phobia. This one, the fondest picture is pretty bad here, isn't it? But you're gonna see generally like a yellow grayish spot in the phobia or if it's laser, you can see, you know, obviously more. They will not show you laser. That's too like modern for them but they can definitely show you solar retinopathy where it's just gonna be a single spot in the phobia. And then they probably won't show you that CT either but if they do, it's gonna be outer retinal, hyper reflectivity, whether it's laser or solar, it's gonna look kind of the same. It's just in laser, it can be more non-central. And then something that they might ask you about is kind of, so drugs that photosensitize you, usually we think about this like for sunburns but can also make your, theoretically, like your retina more sensitive to solar retinopathy. So sometimes it's usually like either someone like on acid or someone who took a lot of like tetracycline in the vignette who's gonna get solar retinopathy. And it's cause like when they're high, they do some sun-staring type stuff, sickle cell. So you can see the C-fan configuration, the top one, these kind of salmon spots which are kind of like, I think they're just kind of like older hemorrhage and then the black sunburst is kind of, is like dead RPE from ischemia, all changes you can see in sickle cell. Probably the one important thing to know is that unlike systemic disease where SS is the worst, SC and S-thal are actually the worst for retinopathy. It's a kind of a weird association there. We treat these patients generally with laser, sometimes with anti-vegeta. How about this finding? I had this on O-cap splints. What disease is this in? Susak. Yes. Susak. Beautiful. They're not Dawson's fingers. Right. Yeah. Dawson's fingers I think is above the corpus callosum, but you guys probably know that better than me. So this is going to be a young woman with confusion, vision loss for multiple BROs, hearing loss, and then these spots in the corpus callosum, they get treated aggressively with IVIG and steroids. They also have these kind of weird gas plaques. They won't ask you about that. They're essentially just things in the retinal arterios that are not at the bifurcation, which is obviously the more common spot for emboli. This is just some foveal anatomy that you guys know about. You guys know about the blood flow. It's kind of, you know, this is what makes some people retain some central vision in a CRAO because they have that cellular retinal artery. I think that's about 20% of people. Couple more minutes, retinal trials. So I think the only ones that are actually important that they'll ask you for are comms. The conclusions are small melanomas are okay to observe. Medium melanomas are okay to plaque. And then large melanomas, you don't need a radiation before you enucleate them. Those are the major outcomes. And then these are the sizes. There are also, these are the thickness sizes. That's the most important one. If you're going to remember any of the size cutoffs. You guys know clinically significant macular edema. Again, this is not based on OCT. This is a clinical exam finding. This, the DRS just showed that PRP works and defined high-risk PDR. So that's any PDR with vitreous hemorrhage or if you have a lot of NVD or if you have NVI. That's who we PRP. Nowadays we PRP really anyone with PDR, but this was by the study answer. EVS where we talked about that. These were kind of some random factoids that after taking OCAPS for many years was seemed relevant and are kind of random. I don't think I have time to read them all, but I think this is being recorded. See, if you want, you can come back and look at these random but high yield facts. Let me show them on the screen. VKH, the recurrent stage is anterior UVIS. The chronic recurrent stage, the last thing where they have exacerbations are anterior UVIS. It's more the acute first presentation that they get the more classic posterior effusions and all that, that can be a high yield fact factoid. This is CSR, you get that expansile dot more common than the smokestack pattern. This is juvenile santhobranium loma they present with hyphemas in young babies. And it's a two ton giants cell on path. Okay, thanks for sticking through it. I know those reviews are tough. Good luck guys, you're gonna crush it.