 So, these slides, I don't know, sometimes you do stuff interactive, but I think it's probably more useful for me to just talk in this, but I may ask for audience participation sometimes. We'll see. Retina layers, I feel like it's not high for me to go over this at all, so no. But there they are. I have, I've made a couple little mnemonics, but I feel like those don't always help either when people say them to you, but for the interplexiform layer, you can kind of remember it's in, and for the inner nuclear layer, in the bag, BAG, it has bipolar amachrine and ganglion cells, and then I think also horizontal cells in the interplexiform, and if you can remember what's in the inner, then you don't have to remember what's in the outer, because they, and the only one that they share between the two of them are the bipolar cells, and BAI in that case makes sense, it's like they're in both, so. I don't know. You just did, so many of these questions come up on OCAPS, and on up the questions that you have to find some way to remember it, if you can't just remember little tiny cell layers like me. And the photoreceptor cycle is just something you're going to have to memorize, and it doesn't help for us to go over here, you just have to read it enough times to, but histology sections of the retina are definitely high yield, and that's a little out of the scope of my presentation, hopefully you get it in your path presentation, the way that different, I would say every single year, two or three questions that is just retinal histology, and so I would study it, I would try and look at some common diseases, they like to show diabetic retinas on OCAPS, if you ever have no idea what something is, it's probably a safer bet to go with something more common like diabetic retina, and sometimes they'll pair a diabetic looking changes with an iris, and so they'll either show you neobascularization of the iris, or they may show you lacy-vaculization of the iris, those are things I've seen pop up on OCAPS over the years for sure. Lacy-vaculization is where you have kind of like these lacy, almost cystic changes of the pigmented iris, I don't have a picture of it, but you guys can look at that. Okay, so the fecomatosis always show up, and it's always something obscure, it's never going to be like Lish nodules with NF1, it's always going to be something completely random, I can't necessarily point to it because every year I feel like it's been a different one, but one thing that is high yield is knowing the different names of the different syndromes because you can be totally thrown about what they're talking about, anyone know what Bourneville syndrome is? It's one of the common ones, just another name for it. It's tuberous sclerosis, so they can throw out Bourneville syndrome as one of the options on your test, and there's a classic triad of the adenomus sebacea, mental retardation, and seizures, and they get astrocytic hematomas of the retina, optic disc and brain, peri-ungul fibromas, calf failure spot, chagrin patches, and the ash leaf spot. I've seen at least on off the questions they like to show that. No, I didn't listen today. I'm sorry, that was a fail. I wanted to get the laser pointer, and apparently this is smarter than me. Okay, they'll show you a picture of a face with those very characteristic changes. And then these are some histology. I don't think I've ever seen histology of tuberous sclerosis on one of the tests, but it doesn't mean it can't show up. This is showing the astrocytic hematoma, and this is the adenomus sebacea of the face. I don't think they would show you this path, but they could. Von Recklinghausen disease is the other name for NF1. I think there's 17 letters in Von Recklinghausen disease, and it's on chromosome 17. That's usually how people remember it. There's criteria for diagnosis of the disease. I don't think it's high yield to memorize all the criteria. I think though, you just should be able to put it together if they set you a patient that has some of these features. Caffeolasebots actually freckling nodular neurofibromas, plexiform neurofibroma, and S-shape of the eyelid. You can see that plexiform neurofibroma up there. CNS gliomas, optic nerve gliomas are common, and they get fused to form enlargement of the optic nerve sheath. Meningiomas are less common. Absence of the spinion wing with pulsatile proptosis, that's high yield. I've seen that show up before as well. They get Lyschnodules. Does anyone remember how to differentiate Lyschnodules between brush-field spots and iris mammalations? Iris mammalations are seen the same color as the iris. Brush-field spots are seen in Down syndrome. They are hypopigmented and Lyschnodules are hyper-pigmented, I believe. You'll have to double-check me on that. There's a coloration. Basically, you'll usually not be asked to differentiate between something in Down syndrome. You'll be asked to figure out whether it's iris mammalations or one or the other. Just know the iris mammalations are the same color as the iris. Congenital glaucoma, usually it's unilateral, and it's where the plexiform neurofibroma is. They also get astrocytic hematomas like intubus sclerosis, acoustic schwannomas. They also suffer from pheo and Wilmstimer. Pheo makes its appearance in multiple of these diseases. I have seen path on neurofibromatosis. I would make sure to review that in your path as well. I would not be the person to do that for you, though. Here are the Lyschnodules. These are hyper-pigmented. That can be a clue if you can remember it as to what you're looking at and help identify the case. NF2 has another name and I can't remember it right now. It's kind of descriptive. It's like multiple schwannoma. It's a very long name. I didn't put it in here, but I can't remember it. Look up the other name that they can throw out for NF2. They get bilateral acoustic neuromas. Chromosome 22, it's easier to remember because there's a 2 in the name. They get PSE cataracts and Lyschnodules are uncommon. The thing to remember about NF2 is that they get PSE cataracts. They get combined hematoma as well. It can be ducts of papillary or peripheral. It's kind of an elevated gray ridge of tissue in both of them. Combined retinal and retinal pigment epithelial hematoma is the same thing. It involves all layers and ERMs over them are frequent and they can be visually very significant. They can also develop neobascularization. That's what a typical hematoma looks like. There's a picture of it on FA. Retinal angiomatosis is another name for von Hippel Lindau. Chromosome 3. It's autosomal dominant. You can remember it. Von Hippel Lindau has three words. Eye findings, retinal capillary hemangioma. There's a feeder and drainage vessel and they definitely can get serosexudations. They get cerebellar hemangioma. It's also the brain stem and spinal cord. They don't get mental retardation. They have association with pheo and renal cell. The most common cause of death in these patients is rupture of these hemangiomas and renal cell carcinoma treatment with laser cryo. Here are some path photos and other clinical photos of the capillary hemangioma. This is a nice also clinical photo of the same. Encephalofacial angiomatosis is the other name for Sturge Weber syndrome and it's sporadic. They get caroidal hemangioma, typically the diffuse pattern, and it's classically the tomato ketchup fundus. They get glaucoma in 50%. The O-caps like this, or not O-caps, like the question, if they have a newborn with Sturge Weber and glaucoma. The mechanism of glaucoma is most similar to congenital glaucoma. If it's a teenager or young adult with glaucoma in Sturge Weber, it's more similar to outflow mechanism of low flow AB fistula, so it's like an increased episcopal venous pressure in the more adult population, but newborns are like congenital glaucoma. Systemic findings, they get nevus, flamieus, or skin angioma. They have a pretty characteristic look. They get meningial hemangiomas. They have seizures, normal or mental retardation, hemiparesis. I think there's something with the fecal hematosis that the ones that include Ss get seizures is another way to try and remember if you're trying to figure out what's what and you don't know what's going on. You can try and cheat sometimes. Imaging, they get cerebral calcification. Here's an example of the tomato ketchup fundus, although that's not really a great picture. They both look like they have tomato ketchup fundus. Diffused carotidohemangioma. Here's a pathology picture. If they have a circumscribed carotidohemangioma, it is not associated with Sturge Weber, but the diffuse patterns. This is more circumscribed. You can see a more focal kind of reddish orange and there's a F.A. pattern. High internal reflectivity is characteristic on B.Scan. They can be hard to see on pictures. I haven't seen it show up on tests, but you can see it right there. There's the outline of it. Retinal cavernous hemangioma. It gets confusing because you can have carotidohemangiomas and retinal hemangiomas and you can have capillary hemangioma, which we just learned is associated with Bonn-Hippo-Lindau, and you can have cavernous hemangioma, which is right here and it looks like a cluster of grapes. I've definitely had this question on OCAPS and on OPTO questions before. They will throw in one of these vascular tumors of the retinal dome. You can kind of see the pattern you see on F.A. of the two is quite different. It should be easy to differentiate them. It's almost easier to just remember one and not the other. This is like a cluster of grapes. It doesn't leak. It fills partially similar F.A. findings here. Hopefully just once you've seen enough of it, you can kind of recognize the difference between two. Wyburn-Mason syndrome is the other name for racemals angiomatosis. It's retinal and midbrain AVMs on the same side. It's sporadic. They also get seizures. Mental changes, hemiparesis. They get intracranial calcifications. These are pretty characteristic. I've also seen OCAPS questions about this syndrome before and its inheritance. They get rapid filling. They don't typically get leakage. They can get vein inclusions or their vascular events. There's no treatment that's typically necessary unless they become symptomatic. Anyone know what that is? Bloch-Solberg syndrome. Again, it's just another weird name for incontinentia pigmenti, which is a super rare disease. It's X-linked, but female only. When you see a disease that's X-linked and female only, what does it mean? It means it's X-linked dominant. Therefore, it's lethal in males. You won't see it in males. The only way that you can see it in males is Kline-Felter syndrome if they have an XXY. There are very few X-linked dominant diseases that we have to remember, so put them in a little category and just try to remember that you won't see them in males, but they're still X-linked. They get hyperpigmented macules and a splash paint distribution on the trunk. They get seizures, mental retardation, dental abnormalities. They get a very ROP-like peripheral vasculopathy, and then they also can have microaphthalmos, cataract, glaucomastrobismus, and isagmus. These are some of the findings that you'll see in IP, and you can see that the fundus looks very, very sick. There's like tractional tissue there already and scar tissue. This is just showing more vascular and kind of tractional issues. This is a nice little summary slide. Okay, retinoschesis. What layer does this put out? They love this question. I don't know if they're questions. I can't remember seeing it on OCAPS a lot, but just a juvenile splits at the NFL, and then adults, well, I think they should cover it too. The maculose involved, and they have microcystinal radiating folds. It's not projecting super well, but you can see the little kind of radiations coming off of that area that's very classic for what it looks like on the exam. It's non-leaking CME. They get vitreous hemorrhage from vitreous bales, and they can have a normal A wave and attenuated B wave on ERG. It goes into your, there's a set of five or six diseases that can cause negative ERG, so this falls in with that. An adult retinoschesis splits at OPL, which I remember by it's like old people layer or something whenever I think of this disease, but they differentiated into typical and reticular, and reticular is like juvenile, so juvenile splits that inner fiber layer and typical splits at the old people layer, so common location is infertemporal, scatoma, they have an absolute, and you get a relative scatoma with RD. The reason why that happens is because in a schesis, you are missing the connections between the photoreceptors and the ganglion cells reaching the inner fiber layer, ganglion cell layer being able to transmit the information. In a retinal detachment, you have all of the layers up, but they're still together, so they're able to transmit at least something, which also should make sense then for why you get laser uptake in retinoschesis and why you don't get laser uptake in a retinal, in a retinal detachment, because you still have some retinal tissue down in schesis to be able to uptake laser. So if you think, if you can remember those two things, then you don't have to get yourself confused when you're trying to remember this for the test. These are more pictures of juvenile x-linked retinoschesis, and this is a nice path picture. Bullseye maculopathy, differential, stargarts, cone dystrophy, chloroquine toxicity, which is treatment for malaria and RA, AMD, chronic macular hole. I mean, I would also include hydroxychloroquine on there. Most common primary intraocular malignancy in children, retinoblastoma. This is just something you have to memorize or kind of have the breakdown of retinoblastoma. Usually less than three years old with leukocoria or strabismus are the most common presentations. Chromosome 13 is the inherited autosomal recessive version for the tumor suppressor gene of RB. One-third are bilateral, two-thirds are unilateral, and one-third are hereditary and two-thirds are sporadic. And calcium is seen on ultrasound or CT. Trilateral retinoblastoma would include a bilateral intraocular tumor with a pineal gland involvement as well. The tumor grows around blood vessels, and you get flexner wintersteiner rosettes, and they're specific for retinoblastoma, and they're giving retinal differentiation. You can see the flexner wintersteiner rosettes here. And then homerite rosettes are seen in neuroblastoma as well, so they're not specific for RB. So that's just a little minutiae you have to remember, but they look a little different. They're still kind of in that ring pattern. And then florets have photoreceptor differentiation. Pognosis is good with early treatment. Enucleation, radiation, chemo, typically now it's intraarterial chemotherapy. Chryolazor, spontaneous regression is rare, and they often get secondary malignancies. They like to ask about what those common malignancies are. So osteosarcoma, basically sarcoma, is going to be a common secondary malignancy. And they also get melanoma. So there's an opto question where they ask you basically to differentiate between what are the most common malignancies in the field of radiation from retinoblastoma and out of the field of radiation. And so the sarcomas are overall the most common within the radiation field, and the overall most common total is going to be sarcoma plus or osteosarcoma plus melanoma. So I would just try and remember melanoma sneaks in there because it's common and not inside the field of radiation. Yeah, I think so. Coase disease, eyes with active, at massive sub-retinal exudates. And usually it's one eye involvement, males are much more common, often presenting less than 10 years, but there can be a bimodal presentation. They get retinobascular abnormalities, massive exudation, posterior pulse, it definitely looks like RB in some cases, so you differentiate those two based on B scan. Looking for calcification. If you see calcification, it's RB. You can consider coats. FA is pretty characteristic in coats. You see these little like bulbaric, telendectasia, little bulbs, venous beading, non-perfusion. On the path, you'll see lasavascular endothelium and parasites. And genetics I don't think is completely, I don't think you'll be asked about genetics for coats. If the retina is attached, laser and continual laser, continual laser, continual laser, also will do cryo sometimes in coats. And if they're detached, pretty typical posterior segment surgeries. There's a nice picture of the little kind of tiny sacular aneurysms in coats. And then the massive exudation that you get. And you can definitely have exudative RD. We saw a patient in clinic who looked very similar like this picture with a massive white-ish thing with vessels behind their lens. It ended up being RB. So coats versus RB is definitely a real thing that you have to differentiate. And the treatment is obviously quite different if they look like this. There's the terminal bulbs that you see on FA. Those are really good FA examples. Medulo epitheliuma is one of my favorite tumors because it can form cartilage. And I think anything that can form cartilage is cool. It's also called diktioma. And so remember that weird name. It's a congenital. You can get it later. So I don't know that I would call it congenital always. But ciliary body epithelium. But it can also form on the retina and optic nerve. And you get ribbon-like cells. You can also see rosettes. So you can see right there that these are kind of similar appearing to the rosettes that you see in retinoblastoma. And they secrete mucin and primary vitreous. They can form multiple different kinds of tissue like I was mentioning before. Treatment is in nucleation. You don't want to go into these eyes. You can cause further spread of the tumor. And they may need radiation in chemo. Most common intracular tumor in adult is or malignant tumor in adult isn't met. Most commonly from in women it's going to be breast. In men long they usually get a dome growth pattern as opposed to the color button or mushroom shape in melanoma. And carotomelanoma is next. Wrist factors, ocular melanosis and nebisoboda. I think the risk for carotomelanoma, they ask this ad nauseam is 1 in 400 and then the risk for glaucoma in the melanosis. Oculomelanosis is 10%. It's higher? 80? No. Then don't call me. Maybe it's 40%. I don't know. They like to ask it. 1 in 400 for carotomelanoma. So they have to be screened annually lifetime when they have ocular melanosis. And then the difference between ocular melanosis and nebisoboda is skin involvement. Skin involvement happens in nebisoboda where they have the bluish discoloration of their skin and the slate gray bluish discoloration of the scler. And there can be a sentinel vessel in carotomelanoma and that can be a sign of ciliary body melanoma but you won't see a sentinel vessel in every case of ocular melanoma. Size, extra ocular extension and cell type are factors predicting survival. There's spindle cell, spindle A and spindle cell has the best prognosis and 25% 15-year mortality. And epithelioid melanoma has the worst prognosis. They have these epithelioid cells and it's 75% 15-year mortality. And then you can have a mixed picture between both of them so they may show you a path. They may give you something like say that we have a specimen of a tumor in an eye that stains positive for HMB 45 which is the typical stain that they'll throw out for melanoma. And then they'll show you four different path pictures and say which one of these has the best prognosis. Look for the one that's forming this spindle, the spindle formation as opposed to the epithelioid. There's enough spindle you know associated pathology that hopefully you can pick out the one and just remember spindle and hopefully pick out the one that has the spindles on. You're right, 10%. 10% okay. So 40, 1 in 410% and they love to ask that that shows up on off the questions like a million times which is sad that I can't remember. So when it breaks through Brooks it makes that mushroom that classic mushroom formation and you can have if you're gonna you can get glaucoma from multiple mechanisms but the most common way is direct invasion from liberation of melanin so or direct tumor invasion basically. And ultrasound actually shows low to medium internal reflectivity and it metastasizes to the liver and they love to differentiate between the metastatic pattern of intraocular lymphoma versus congenital lymphoma which goes to the lymph nodes and like head and neck. So this goes to liver just don't get tripped up on that. Inside the eye goes to liver and then on the periocular surface goes to lymph nodes. Melanoma and monosomy 3 is I'm not actually sure to be honest with you about that. Melanosythoma is jet black it's of the optic nerve or retina they can or have visual field loss in the area. Path shows large polyhedral cells small nuclei and set up positive filled with melanin granules. This is a carotid osteoma they can mimic a a melanotic carotid melanoma. They are peripapillary or macula you want to get a B-scan and they have on B-scan you see this highly reflective lesion with loss of the normal orbital echoes behind the lesion and you'll notice it's not like a massive dome shape or because what else gives you a really high internal reflectivity on a B-scan is going to be a carotid hemangioma. So those are going to be more of a mass then they use these are typically more flat and you lose the ultrasound waves behind it. Very common to develop CNV subretinal neovascularization and they can slowly enlarge in years and if the macula is involved the vision will be decreased but these are pretty hard to treat. This is another carotid osteoma and there's path so in ophthalmitis EVS is pretty high yield for life and for the test but EVS is an old study so people often wish that we had a newer version of EVS. 420 patients after cataract surgery initial vision of hand motion or better no difference between tap and inject or vitrectomy and injection initial vision of LP or NLP when we're proven to have a benefit to go straight to vitrectomy and they achieved basically better vision loss or better vision outcomes as I meant to say. You have to have a clear cornea to go. Sometimes people think people say that blood associated in ophthalmitis is kind of in its own category and responds better to vitrectomy. I don't actually know what the board answer is that they want for blood associated I would personally answer early vitrectomy so and I would just read there's always I feel like there's always a question there are always multiple questions about an ophthalmitis on OCAPS so I would read this study and maybe it's abstract once over before the test not not the full study just read it's abstract it's fine or it's main findings um they've heard I've seen them ask at least on ophthalmitis questions about the antibiotics that were used I don't want to state it wrong but I think it was vancomycin and a cephalosporin but I'm not don't quote me on that right now we can look it up later all right and they also love to ask about the most common organisms in an ophthalmitis I think that might be in this presentation later um ERG EOG and VEP it was usually not too many questions on this topic on OCAPS and maybe I've seen one each year mainly usually about an ERG and it's more just involving interpreting an ERG within a picture of a patient but um an ERG measures uh mass retina uh the A-wave is photoreceptors B-wave is Mueller and bipolar cells and C is RPE amplitude is the entire retina response oscillatory potential is the interplexiform layer and ganguine cells are not measured pattern ERG measures ganguine cells and ERG is an indirect measure of voltage between the inner and outer retina um and uh if you have a normal EOG you know you have a normal RP and sensory retina but it's it doesn't honestly ERG is not very useful outside of ruling inner and out best disease I don't really see it used otherwise um visual boat potentials are uh anywhere defect anywhere in the visual system and use best in preverbal infants and it can be used to give an estimation of visual duty and a preverbal infant but they have to be able to they have to be able to pay attention uh so you can't do it to a severe do it be in a severely like a mentally disabled uh a preverbal infant so um if if you have a normal EOG normal ERG and abnormal EOG um it can be basically chloroquine toxicity pattern dystrophy or best disease in its carriers and you would see those in very different patient populations and then in best disease you have the Arden ratio which I think is greater than 1.6 is normal and best disease is less than 1.4 and that's just a random number that has nothing to do with anything but you have to be able to at least recognize have it somewhere in the back of your mind the Arden ratio is uh that that is the result of the ERG um and an abnormal ERG but normal EOG you might see in congenital stationary night blindness or x-link retinopsis um angioid streaks the mnemonic pepsi pageants alers danlos pseudosanthoma elasticum sickle cell idiopathic that gives you your pepsi um differential for vitreous opacities um asteroid hyalosis which are calcium soaps synchesis synth lands which are uh cholesterol crystals after vitreous hemorrhage I always think that one's really hard to remember um because you would think it's just de-hemoglobinized team but it's actually cholesterol crystals so um amyloid and that's going to be associated with um other systemic disease and I would also include lymphoma on there uh and posterior bit uh ubeitis but um intraocular heme turson syndrome um which gives you a subarachnoid and subdural hemorrhage and then pertures retinopathy which is mostly peripopulary and uh you can have it in trauma or a compressive trunk injury but um you can also have pertures like retinopathy from many other conditions like acute pancreatitis lupus ambiotic amyotic fluid embolism fat embolism renal failure and retrobalboranesthesia I try and like I those two syndromes are confusing to me to remember so I try and remember pertures sounds like pushing so you use like crush injury or chest compressions um and then tursons I always remember is the other one uh but they both can kind of present in the acute trauma setting so tursons is going to be from your brain bleeds shaking baby syndrome um 85 percent have retinal hemorrhages most in posterior pole vitreous hemorrhage retina schesis um retinal folds and birth trauma heme really persists more than one month if you're given a question about a newborn who has that fundus or a mild retinal hemorrhage fundus appearance it's most likely related to the trauma of birth and maybe platelet abnormalities at birth rather than shaking baby syndrome but um so you know it's always difficult to say but they if they give you a shaking baby case on elcaps they will give you some history so um especially if they give you like any nucleated eye you know if they give you no history and a nucleated eye you know it's shaking baby syndrome um or you're pretty sure it is if they if it has classic findings um because otherwise their child never would have gone to autopsy so um other things to consider x-linked retina schesis parsplanitis child abuse um blood dyscrasias i would include on there salt and pepper fundus rubella retinopathy leavers congenital amaurosis congenital syphilis um carriers of albinism coridoremia and rp and uh cpeo um which is chronic progressive external ophthalmoplegia and differential for bull's eye maculopathy we already had this sorry cherry red spot differential sphingolipidosis tasax sandhoff nemenpick gauchers favorite uh farbors disease crao definitely ois more rarely trauma mainly commotion is going to be your um you know a major confusion between a crao and uh uh and and uh did they have crao or commotion a oct can help you to differentiate between those two or an fa um and then quinine and methanol toxicity toxicity um and uh sspe does anyone remember what sspe is subacute sclerosis panacephalitis it's seen um years and years after mumps infection and it's uh a terminal condition um and it's associated with a cherry red spot um and usually if they're going to give you that question which i've never seen before um about sspe they'll give you a scenario with an unvaccinated child who is having neurologic changes at an adult age and vision changes and then maybe a cherry red spot so have it in the back of your head okay albinism and there's two i think they they do i have seen questions on this before and i think they test it because they're potentially lethal so they want they they want you to recognize things that are potentially lethal and be able to make the correct referral so chidiak kigashi and which uh they get recurrent infections and hermanski pudlak syndrome they get bleeding diathesis so um and then they also have albinism as well so you have to refer these kids for a full evaluation okay vitro retinal degenerations uh main one that you need to worry about is sticklers they get optically empty vitreous they get optic atrophy um severe myopia increased risk of rd and extremely hard to fix rds glaucoma they have a marfinoid habitus pier robin uh sequence hearing loss metro valve prolapse they get a decreased b wave on erg and it's a defect in type 2 collagen and uh wagner syndrome is autosomal dominant and they don't have a risk of rd um they can have an abnormal erg i wouldn't worry too much about Wagner syndrome it's even hard to find information on a wagner or something like the internet so i don't know why they test they they always ask about it um um i'm like off the questions but don't think it's high yield um and they don't have a risk of rd so um depositions copper um you get into decimus membrane and the lens capsule um if you have so if you think about copper deposition and decimus membrane from systemic disease i don't remember that one yeah wilson's disease and it's called the remember what it's called sorry no sorry oh yeah that's right hepatolenticular degeneration is right but no do you remember what the ring is called yeah and then the lens capsule copper deposition i think you can also see in wilson's but uh you might think of that more clinically from the retina perspective uh and someone who has an intracliform body that's copper so um they they can get in the lens capsule or the endothelium as well um and uh that can help you to know if someone's presenting with a chronic IOFB what it might be containing of iron uh deposits in the epithelium mercury deposits in the lens capsule uh these are just things uh i don't think this is super high yield to go over um right now i think you all probably by now know the 421 rule of um four quadrants of diffuse inter retinal heme and micro aneurysms um two quadrants of venus beating or one quadrant of erma and that is the definition of severe n pdr and then very severe is greater than two um of those uh csm e is cme within 500 microns of the phobia hard exudates within 500 microns of the phobia with adjacent cme or edema one disc area within one disc diameter of phobia i think those are really hard to remember but if you stare at them enough times pdr is a quarter to a third disc area of nvd or any nvd with vitreous hemorrhage or half disc area of nve with vitreous hemorrhage clinically many times always see as the vitreous hemorrhage you can't identify the new so um these are good just like single liners about the diabetes studies i'm i don't think i need to read this out loud but i'll let you guys just kind of digest it for a second if you guys want copies of these slides i'm happy to share them with you because it's these lectures i always felt like were so fast that you just don't really have time to digest too much but and then these are the um diabetes studies i'll be honest i they don't often ask about studies on ocaps i i can very i can remember very few and all the years i've taken ocaps i have not studied and memorized the different studies i think they're more likely to ask maybe something from like a very old classic study that's still relevant today like et dr s and they're more likely to ask you about the like big glaucoma studies and maybe i've had a question about like um a gs or normal tension glaucoma based on one of those based on one of the studies so but uh i really haven't seen them ask about these uh the diabetic studies amd small drusen classified as less than 64 microns large is greater than 125 um and worse prognosis of their large soft pigmented densely packed with drusen drusen with pd um categories uh category one being very very mild less than five small drusen mild uh one medium drusen pigment changes multiple small drusen intermediate greater than one large drusen non-central ga or extensive medium drusen and uh for being severe ga or wet arm d and uh vision is uh very poor um and i don't think they meant we meant to write 32 sorry a reds uh i would look up the doses every once in a while i think that pops up of the or they the uh i wouldn't sorry not look i've memorized the dose of dosing of each one of those if you can um and then a reds two added 10 milligrams of blue teen zia xanthine and omega three uh they took away beta carotene and they decreased zinc and they basically showed that the new revised version was uh you know equally effective and so they were they showed that that's safe to do so they a reds two is pretty much a standard of care now uh amd studies uh i think are at this point low yield they're just historical and um injection studies the same um i i just have never seen them ask about it i wouldn't spend too much time on it personally if you want a 99 percent go for it um i just i still don't know if it would be high yield for you and then these are some of the um vein occlusion studies um basically just you know kind of taking you through the history justifying first laser and then next identifying the use of anti-veget so um one of the takeaways from um the vein occlusion studies is that you don't do PRP unless they develop neil so i had a couple let me see you had a couple of just like notes of things that i think are high yield um you can see a negative ERG um in CRVO, CRIO, X-linked retinoschisis, melanoma associated retinopathy and CSNB there's a pretty short list of entities that cause a negative ERG and that's where you have a normal A wave and a flat B. chloroquine binds the RPE i think there have been questions about its site in the eye which causes toxicity uh if you have P acne or you suspect it um you want to do a tap and inject and take out it depends uh it depends what clinical scenario they give you typically they're going to give you a patient who has uh had surgery relatively remotely um you know within the last couple months who has ongoing inflammation and has some sort of a capsular opacity they can never be tapered off of steroids they keep flaring um they have a little bit of vitreous cells and you can do a tap and inject but then the definitive treatment if they don't get better with a tap and inject is to take everything the bag the lens and then they you don't re-implant something right away you would wait so uh i included some uveitis stuff in here that i think is how you uh against cyclovir toxicity uh especially when combined with azathioprine is very myelotoxic fosternet has less myelosuppression um you should definitely know how uh the different antibiotics work don't get too far into their mechanism but there have been questions every single year about um what how fluoroquinolones work how aminoglycosides work um and uh just study that it's fast and easy and i think it's high yield um if someone develops anaphylaxis from an f a know the dose of um epi that you give which is uh i think one to one thousand sub q um and then uh be able to recognize optic nerve head drusen on a b scan um and we already looked at a b scan of an osteo one um anyone know what idiopathic sclerochorotal calcification looks like and where it forms it's like a rare thing it's kind of like scleroplax where it just basically age related changes but they can look like tumors and they typically form like in the kind of the like right off the arcade and kind of hypopigmented if you guys have never seen it before just look up a picture or i can just pull one up in the end i'll just do it now because i'll probably forget um and tell me when it's time to leave and i'll stop uh here's a picture of idiopathic sclerochorotal calcification it's pretty striking right these are both good this is a good example you see that and you're like whoa is that like a a melanotic melanoma so you're gonna do your typical work up but if you find nothing then you can call idiopathic sclerochorotal calcification uh okay ghost cell glaucoma you can get it after vitreous hemorrhage um we already talked about the f a of a retinal cavernous hemangioma um j r a and a kid they always ask a question about j r like multiple questions about j r a um so i think it's a high yield topic to study basically i think the way to break it down is every three months visits for posiarticular a and a positive rf negative those are the highest risk girls uh and then everyone else pretty much is every six to 12 month in the standard of care is going to be methotrexate know why you need to give phalanic acid in toxo treatment um most common organism after a trap for end ophthalmitis maybe is h flu so ophthalmation says differently i would know that h flu rather than this is the way i remember this h flu is present in uh in post-trab or b re but liberated end ophthalmitis and it's not a present it's not a common culprit or as common of a culprit in run of the no post op end ophthalmitis so just remember if you if you're seeing if h flu is on the list for you after a trap from the common organisms for end ophthalmitis i would go with that one they get really tricky and ophthalm questions and they give like two different combinations of um bacteria after uh trap so um if it's you know some of this minutiae is so hard to remember but um but mainly everything else coag coag negative staff um is going to be common and strep is also common after um strep is also common after a trap um if you see someone who has an adult with n l d o and a u r i um they don't always give you all the information so put those things together and link them in your brain for that being uh like white nurse okay uh i don't know why i included this one in here vitamin a get gobbled itself dysfunction i guess i included that because uh sometimes they'll give you a um a scenario where a patient is presenting with night blindness and they have no retinal changes they may have some erg changes and some visual field changes and they may ask you what the sequelae are of this disease and you have to and or they may show you a veto spot um so that i'm just trying to point out some of the minutiae that they like to ask about vitamin a deficiency um gyrate atrophy i always have trouble remembering gyrate atrophy versus coridoremia um so coridoremia is x linked and gyrate atrophy is oat gene and so that history is going to be different between the two of them that you'll get and then gyrate atrophy requires vitamin supplementation um and they and uh you it's also diagnosed with a plasma ornithine level uh if you see somebody who has presents with acute bilateral crvo's you definitely should think of a blood dyscrasia like walden strums macular globinemia would be the classic presentation you could also think of multiple myeloma in the same category if you have somebody presenting with erythema nodosum think about sarcoid and tb this is just one random ubi just one i've seen uh this keratoderma blenoragicum which is uh strange looking foot uh lesions i don't know if you guys have seen it before keratoderma blenoragicum oh yeah it looks just like that it's very characteristic looking they might give you a picture of that and that's associated with reactive arthritis if you see i should have talked a little more about phpv it's just not enough time to cover everything i put it erythema nodosum phpv uh association also with micro ophthalmos and micro cornea so you see a kid in clinic they have uh leukocoria of some sort differential being the same things we talked about coach retinoblastoma phpv is in there um definitely if they're micro ophthalmic and have a micro cornea then think about phpv as well so that these are little ways that can tip you one way or another on a test uh vitreous attachment they um sometimes will ask about what in the vitreous what what part of the vitreous is responsible for the attachment it's the cortical vitreous detaching from the internal limiting membrane uh i kept this in here because pylocarpine increases uvuloscleral flow but it also increases your rate of rd formation and worse than cme and uviatus so uh infliximab uh no just try and know some of the mechanisms of actions of some of the biologic agents the infliximab being tnf i have two agents on here that can cause hypopoeons i would know those cold they like to ask about that uh rifabutin and then i think the other one is sedofavir at the end yeah sedofavir uh i think i'm out of time i'll let you guys go but uh is there anything like super high yield in here commotion on path you'll see photoreceptor dysfunction uh remember task presents 24 hours it looks like end up the minus but it's going to be on post op day one i would definitely know the clock hours uh i would know that the et rop definitions for the test there's always one or two rop questions on every single cap um apparently there was something about fundus fundus albapunctatus um which is a very characteristic looking hereditary there are just ones that i think have been high yield over the years that i've taken notes on to like make a quick note to like study before the test um so this is what fundus albapunctatus looks like it's really it's really odd looking the i think the only thing you could confuse it with is star darts um and they can see the macula looks pretty normal i didn't make a slide on it but look it up at home um i think we're pretty much good and that's uh yeah oh this is another one every year there's going to be something it's like literally every year on the ocaps about which one of these little peripheral retinal lesions makes you have an increased risk for an rd so mainly merdione folds um i think uh enclosed or bay um and uh of course lattice so um but i would just that's like minutiae to look up before the test and it's high yield because there will be a question on oh raffa butan they i think i've seen a question too before where they ask you to differentiate between or to to know um the difference between the risk factors for crvo and brvo and i can never remember it by uh memory but it's like yeah there's obesity diabetes and hypertension or risk factors and crvo has two and brvo has two and they don't overlap it's like one of them was taken out i i don't know why but they've tested on it before um as far as the risk factors for us so i would look that up too you're welcome