 All right, so you guys are sick of seeing Copenhagen, so I thought we'd go to Jackson Hole. So this is, for those of you who haven't been up to the Grand Tetons, it's worth the trip. It's a fantastic, fantastic trip to go in the summertime. So that's the Grand. That's what David and his buddies climb. So you're impressed with looking peak there. And here's the close up. As a testament to global warming, when I used to go climbing around these things 35 years ago, there were summertime glaciers all the time on here now. Another decade, there's going to be no glaciers left on here, just because climate is warming and things are drying out. It's got no more glaciers up on the Grand this summer. So this is the new Wild West, Wild Life Museum they built, which is pretty cool because they basically put Western art into a museum and they got some donors and did it. And this is on the other side. So this is not looking toward the Tetons. This is looking out onto this massive meadow where in the wintertime, like 30,000 elk live. And so if you go up there in the wintertime, you can go see what 30,000 elk look like. So a lot of them. And this is the Ascus Executive Committee Retreat with families. So hanging out at the museum. OK, retina. So when we talk about the retina, we want to talk about several different areas of the retina. So we, since you're at the hot seat there to my left, what are the different areas of the retina when we describe them? So looking at the retina, talk about the nerve, the vessels, talk about the macula. OK. So basically, you know, macula, fovea, everything else. OK. So that's kind of the main areas we really want to look at. And then when we look at the retina, Eileen, what do retinas, ogres, and onions have in common? Layers. Layers. Layers. I hope you guys studied your layers because we're going to beat these layers to death this morning. All right, so Eileen, starting from the inside to the outside. Interlimiting membrane. Interlimiting membrane. All right. Chris, neurofiber layer. Neurofiber layer. Back there. Gangling cell layer. Gangling cell layer. Shrub. Interplexiform layer. Interplexiform layer, OK. Inter-nuclear layer. Inter-nuclear layer. Outer portion. Outer-plexiform layer. Back to you, Eileen. Outer-nuclear layer. Outer-nuclear layer. OK. Eileen. Photoreceptor layer. Yeah, photoreceptor layer, Chris. Arcane. Rental pigment epithelium. Are you there? Ah! You didn't realize it's part of the red, the hot medicine. Well, is that the Choroid? Choroid, more specific. That part of the Choroid. Choro-capillaries. Choro-capillaries. Exactly. So again, I'm going to count on you guys. Don't let your voice go up when you're dancing. When we're dancing. Save with conviction. Courage of X. Even if you're wrong, you still get half credit. I have an objection. Ma'am, we skipped the layer, which we skipped. Brooks memory, exactly. I was going to come back to that. You know my PIP questions. We skipped the layer. We, the Choro-cap, between the RPE and the Courage of Choro-capillaries is Brooks memory. We're going to go into that. All right, so looking at it a little bit closer now, what I want to do, Choro, we're going to start, we're going to trace a photon of light. So it comes through the cornea. The cornea bends two-thirds of it. It comes through the lens. The lens bends the other third of it. And then it goes back and it hits the retina. So what does that photon of light have to do to become seen? And where are the photoreceptors? Close to the RPE. Exactly. So that light, so the retina's built upside down. I mean, if you're going to build a retina, you put those photoreceptors out on the surface where the light wouldn't have to go through. But there's one major problem. Those photoreceptors are incredibly energy-intensive. And so if you put the photoreceptors out here, they're so far away from their nutrients that they wouldn't be able to function well. So the retinas built such that the photoreceptors are down here near their nutrients near the chloride. So the light has to go all the way through that retina and hit the photoreceptors. So what happens? What part of the photoreceptors does that photon of light hit? All right, so where does the rhodopsin live? So it actually lives right on the little membranes here on the surface of these. And if you look at them, they're stacked up like coins with little tubes on the outside of them. When the guys are talking about retina, I'm sure they're talking to you about the physiology at Nazion, but that photon of light hits a rhodopsin molecule, it goes from cis to trans, and you get a hyperpolarization. So that hyperpolarization starts here in the photoreceptors, it goes through to its cell body here in the outer nuclear layer. Where does it go from there, Ashley? To the... Not yet. To the inner nuclear layer? All right, where in the inner nuclear layer? The bipolar cells. And so it hits, it synapses here in the outer plexiform layer and it synapses with a bipolar cell, so that bipolar cell is a relay cell. So then the bipolar cell sends its axon out here where it synapses to what? I mean, ultimately a ganglion cell. All right, so now that hyperpolarization has gone to the ganglion cell, leave, once it leaves that ganglion cell, where does it go next? So once it leaves the ganglion cell, the axons are then transported along the nerve fiber layer towards the optic nerve. Okay, and where does that axon finally synapse? It finally synapses at the lateral geniculate nucleus. Exactly, so that's a really long axon. So that axon from that ganglion cell goes all the way along the nerve fiber layer through the optic nerve, through the chiasm into the radiations, all the way to the lateral geniculate body. So anything that interrupts that axon, anywhere along that pathway, can eventually lead to death of these ganglion cells here. So a really, really long axon. All right, Eileen, now we talked about the bipolar cells in this inner nuclear layer. What other three cells live in there? Horizontal, amicron and fielder cells. Exactly, so the horizontal and the amicron cells, they're kind of the mediators of that signal. So if you look at EMs of them, they almost look like octopi, where they've got little tentacles going all over the place. And so what's interesting is that tells us that signal modulation is already going on right there. So if you think about it, you know, these guys at USC and other places, they're putting these electrode arrays in there. You know, there's like 32 little electrode arrays and they're stimulating it and firing it off, but there's really no processing going on there. And so at best, if you look at the pictures, I mean, I think it's wonderful the work they're doing and it's gonna get better, but you look at those pictures when they're checking these people who've had these, there's like an E as tall as I lean. You know, E for I lean. So can you see that? Oh yeah, that's a E, whoa, that's great, that's an E. But there's, without that processing, you know, the ret has a lot more complicated. So you've got horizontal and amicron cells putting little tentacles all over the place to process that signal. Chris, what does a Mueller cell do? A Mueller cell. So it's basically like the easiest way I can think of it is like a scavenger cell basically the red one. It is, it's like a microbial cell. It's a scavenger cell and it's interesting because it sends its little processes all the way out here to the area where these cell bodies and the rods and cones go. It's got a little, and then it actually sends its little tiny pieces up here that internal limiting membrane. So it's kind of like a scavenger, like a microbial cell in the brain. All right, back up, what's different about this picture from the one I showed you previously? I think there's some disruption in the ganglia cell layer. Okay, there's something going on in the ganglia cell layer. That's a little bit of a pathologist with that picture. That's a little bit of a pathologist with that picture. There's something going on in that ganglia cell layer. What's going on? Maybe, it looks like maybe blood vessel or something. Oh, there's only little blood vessel in the ganglia cell layer, absolutely. How many cell layers thick is the ganglia cell layer in much of the retina? Normally just a few cell layers. Yeah, or one, even. All right, how many ganglia cells are... Thicker than usual. All right, so where do you think we are now? Probably closer to the phobia. Yeah, it's actually in the macula. So when you talk with retina people, you know, macula to them is the areas in the arcades. When you talk to a pathologist, retina is the area where there's more than one ganglia cell layer thick. And so by definition, this is in the macula. And so there's more than one ganglia cell layer. The other way you can tell you're in the macula, well, Shroud, this is a, in this picture, there's one other way we can tell or we're close to the phobia, but in the macula. This is a tricky one. Anybody? It worries me. It knows up there. It's out of pocket right there. Exactly. Look at these fibers here. So what do we call this layer where these fibers are running obliquely? Henleys layer. So what happens is, is in the center part of the phobia, it's almost all pure combs. And that's where you get your fine vision in. And the way they're linked is one comb goes to one bipolar, goes to one ganglia cell. It's that one-to-one-to-one. And so because of that, there's a whole bunch of combs there and they've got to go to one ganglia cell. So the ganglia cells stack up. So there's a lot of them around there. But because you want that clear zone in the center of the phobia so that that light can come through uninterrupted, those fibers actually go obliquely to hook up to that bipolar to that ganglia cell. That's Henleys layer. The reason that this is important is what disease process do we usually see evolving Henleys layer? Macular or D, my exact. So here's Henleys layer. When you go out to the periphery, as much as 100 rods are linked to one ganglia cell. So you don't have them all stacked up because they don't link in. And the reason for that is summation. So what does your peripheral vision do? It warns you. You know, when you're out on the tundra there's saber-toothed tigers out there to eat you and you can hide from it or run from it. So it picks up movement. It also picks up light. You've been out on a dark night and you see a little flicker and then you look at it and it disappears. It's a weird phenomenon because those 100 rods to one ganglia cell, some of them, wears an aphobia, it's one-to-one-to-one. And here's the phobia. You can see it's almost like I say this is akin to wind blowing through a wheat field. You know, the vibrous part so that that light can come through unimpeded and hit those cones right in there. So here's the phobia. Here's Henleys layer going sideways and here's all those ganglion cells stacked up. All right, and this is just showing you again. Henleys layer stacked up ganglion cells, blood vessels. All right, you know, I didn't ask one other pin question and I should have put this on a picture. See if I can go back and show this here. Oh man, we're not seeing Brooks Mambrane. So Eileen, you mentioned Brooks Mambrane. Brooks Mambrane is between the gloria capillaris and retinal pigment epithelium. How many layers has Brooks Mambrane? Five. Five, and what are the layers? The base of membrane of the RP. Collagenous layer, no, yes, an elastic layer, another collagenous layer, and the base of membrane of the gloria capillaris. Okay, so how do we remember that? It's like a turkey sandwich. Okay, I like the ones upstairs that's measuring the turkey sandwiches upstairs. So the bread on both sides is the base of membrane of the RPE and the gloria capillaris. The turkey is the collagen layer, that really stringy turkey that got upstairs, and then the middle layer is an elastic layer, the cheese that's elastic. And so that's Brooks Mambrane. Now, we're looking at one, Lee, I skipped you. Lee, back to you. I skipped a lot of you. Well, we'll start over. Lee, what are we looking at here? What's going on in this retina? A lot of pathology. Yeah, what kind of pathology? There's retinal hemorrhages. Right, hemorrhages? What layers of the retina are the hemorrhages in? It looks like it's in a nerve fiber layer. All right, and what do nerve fiber layer hemorrhages look like? Flame shape. All right, so these little flame shape hemorrhages are in that nerve fiber layer, because remember when the ganglion cell layer sends out its axons, they turn the corner and they run perpendicular to the rest of the retina. So if you have hemorrhages superficially, they look like flames. What do we call them when the hemorrhages are deeper? Dot and blot. Dot and blot. So they're down where the fibers are running now, perpendicular to the surface instead of parallel. So there's dot block hemorrhages. What else is going on in here? There's hard-action dates. Hard-action dates, and where are they located? So they're typically in the outer plectiform layer? Well, what part of the retina in this particular picture? That's in the macula. It's in the macula, exactly. So it's in this layer. And then also, you see here, quite hard to tell, but I don't know if there's a little swelling around the edge of that right there. What do you see when you look at the vessels? Tortures. All right, so especially the venials or tortures. Look at the arterials, though. What do you see in the arterials? Silver wire. Silver wiring. So normally, there's no muscle or layer around the arterials that lining is clear. But if you have a hardening of the arterial sclerosis, what you get is you get this silver wiring. And look, what happens when the artery crosses that vein? You get a sausage in, right? That little vein gets sausage. So what could cause this? Yeah, this is hypertensive retinopathy now. The severe diabetic can look like this, too, but this is the one. Don't forget that thing that's hanging somewhere in the clinic. I don't even know where it is in my clinic that you put her out of a person's arm and you pump it up and what's the less of the difficult. So you can make sure that I'm one of the techs. They know how to do that. But severe hypertensive retinopathy can give you a look like this, where you have hemorrhages in all layers of the retina. You get vascular congestion. Usually it's in the setting of severe arterial sclerosis. And in the long term, you can even get this exudate in the maculans. It's star-shaped. And this, again, corresponds to the exudate out here in Henley's Lake. So you get this star-shaped exudate. You get these hemorrhages. And look at that fuzzy disc. Now, this was someone I saw when I was first here. This is a young child. She was like nine or 10, and I looked and said, what the heck? And we did find a pressure cuff when we measured her. And she's like 200 over 100. Turns out she had a problem with the valves in the ureter, and the urine was backing up into her kidneys and burning out her kidneys. Now, I just saw a patient the other day. I looked in, and I said, man, that can't be hypertensive. It's something else weird going on. I sent her to a hot bar. He said, man, that can't be hypertensive. Something else going on. And then, I don't know why, but fortuitously, he checked the blood pressure, and the patient was like, again, 200 over 100. So you've got to watch for this once in a while. I just missed it a month ago. And here's severe hypertensive retinopathy. Remember, they will grade hypertensive retinopathy. Depending on the scale you look at, 1 through 4, 1 through 5. But the last grade, you actually get papillodema. So you get swelling of the nerve fiber layer, swelling of the disc, hemorrhages are out there. So in severe hypertensive retinopathy, you can even get papillodema. All right, let's see, Chris. OK, so kind of diffuse whitening of the retina with a cherry red spot. So what would this be? Central retina artery occlusion. All right, so this is a central retinal artery occlusion. Why do you get a cherry red spot? From the edema around the actual phobia. So why does it stay red? Because it's so thin, and then you're seeing the capillary, I mean the cordiocapillaris. Exactly, so remember that picture we showed of the phobia where the retina overlying it thins out. So when you get a central retinal artery occlusion, all of the retina inside gets ischemic. But right here, you're seeing a window into the cord. So in the central phobia, you can still see that normal cordial blood flow. And so you see that so-called cherry red spot. And you see that the retina is ischemic. Because of the ischemia, it turns white and it gets swollen. All right. How is this different, Beckham? Oh, so you don't have the same level of diffuse whitening. In fact, there's kind of a more focal area of diffuse whitening. Yeah. So what do we call this? Branch artery occlusion. A branch artery occlusion. And if you look, you can see that you've got this area right here. So this is not the main central retinal artery. But one of the branches now is central retinal and branch retinal artery occlusion thrombotic or embolic. It's usually embolic, exactly. So if you see the central retinal artery or branch retinal artery occlusion, you've got to look somewhere. Because it's usually either a blood clot or a piece of cholesterol or something that's broken off, carotids, aorta, heart valve, somewhere that causes this to be occluded. And so you see this is a branch artery occlusion. And what are we looking at right here, Shravan? What the heck is this? It's like a blood vessel. Yeah, look at that blood vessel. It's got all this fat from the crown burgers, pastrami, that kind of air, that kind of tourists or else that human. It's like this, by the way, I love crown burgers. That human is like this big. It's really easy to food. But what part of the eye are we looking at right here? Give me a hand. Look out here. Believe it or not, this is the optic nerve head. And this is where the central retinal artery and vein share a common advantage. So she does it come into the eye. Why would I be showing you this? Because the most common cause of central retinal vein occlusion is arteriosclerosis in the central retinal artery. So that artery is all fat with cholesterol and with the sandwiches from mucis and all that stuff that we love. And so that is susceptible to emboli forming in there. But if you look at it, it shares a common advantage in the tissue or sheath with the central retinal vein. And so that fat artery can push over on the vein and then cause stasis and actually cause a central retinal vein occlusion. And so arteriosclerosis can cause a vein occlusion in addition. And so when you look at what a retina looks like in a central retinal artery, Ashley, what part of the retina gets affected when there's a central retinal artery occlusion? Actually, no. Oh, oh yeah, inner. How much of the inner? It's like an inner third. Yeah, maybe even the inner are almost two thirds. And so when you look at the blood supply to the retina, it's a dual blood supply. The inner almost two thirds gets its blood supply from the central retinal artery. The outer third gets its blood supply from the coroid. And so when you get a central retinal artery occlusion, that ganglion cell layer is wiped out. Almost all of the inner nuclear layer is wiped out. But that outer nuclear layer and the rods and cones are still intact. They just got no place to connect. And so they get their blood supply from the coroid. But that inner two thirds gets it from the central retinal artery. So it wipes out about two thirds of it. What do we see in right here? This is more like blood and thunder. Yes, this is the so-called blood and thunder retinas. I don't know who names these, but blood and thunder. I don't know what thunder looks like. Blood and thunder just sounds cool. Whoa, blood and thunder. And you want to name it like a defense, you know? Oh, the Patriots' defense, the blood and thunder defense. So what causes this? So this is a central retinal vein occlusion. So as opposed to the artery occlusion, where blood is not getting in and it's a schemic, here blood is not getting out. So it blocks it off. Now it can still cause a schemia, but you see a central retinal vein occlusion. You get blood all over. It's in all layers. It's all over. Now what is this? What's going on right here? This is more of a branch. So this is a branch vein occlusion. Again, like a branch artery occlusion. It's more in one focal area. Usually, at what point do the veins get occluded at arterial crosses? Exactly. So again, when the veins cross those fat arteries that have arterial sclerosis in them, you'll often get pressure and stasis, and you'll get blockage. Right there, one of the veins crosses over where that arterial is. And so this is a branch vein occlusion. And you see not only does blood back up, but you can also get ischemia in these. And these are what you worry about, especially a central retinal vein occlusion. Not only does it affect the retina, but you get ischemia, and you get all kinds of problems down the road. So this is an eye that's been cut in half-sadually. Here's the optic nerve. Here's the aureus erotic. And you see the hemorrhages are just diffuse throughout the entire retina, and in all layers. Here's the RPE. Here's the retina. You see it's swollen. There's exudate here, and there's hemorrhages all over. So that's a central retinal vein occlusion. All right, back to Lee. Kind of almost a similar picture. What are we seeing here? Similar findings. You have the flame-shaped hemorrhages. You have the heart exudates, and you also have congenital spots, congestion of the vasculature. So what could be causing this? Well, a lot of things. Diabetes can cause that. All right, so the most common would be diabetes. And unfortunately, we're just seeing an explosion of diabetes now, again, because of all this darn Crown burgers and reality TV shows that act to make us all obese as Americans. And so in my average clinic now, you guys don't rotate with me, because I just have a general clinic, and that's my registered resident. So I probably see five to 10 diabetics per clinic now. And almost all of them are now type 2 diabetics. And so we're seeing an explosion of type 2 diabetes. And so you guys are going to see this for the rest of your career. And what we see is, in background retinopathy, you see dot blood hemorrhages. You see flame hemorrhages. You see heart exudate. And then as you begin to get ischemia, you even start to see so-called cock and wool spots. All right, let's look closer. So, I mean, what are we showing here? You're showing the retinol capillaries, and those are microangerisms. Exactly. So the first thing that happens in a diabetic retinot is you get dropped out of the little perisites that line up along the vessels. And you start to get microangerisms. So this is a trypsin digest. We've taken a retinopreparation, just digested everything but the vessels. And you see that the little microangerisms are the first thing that you see. And then you start to see this later on. Chris, what is this? It's a laryngeal exudate. All right, so they call it heart exudate. The reason they do that is they used to call cock and wool spots 100 years ago soft exudates, which they're not exudates. And so that's out of the literature, but the term heart exudate has stayed. And so when you get leakage out of the vessels, again, in a diabetic eye, there's the Dopplot hemorrhage is you start to get heart exudate. And if you start to get that exudate building up in the macula, that can be a real problem. And that's really lipid rich. So what happens is lipids and proteins and fluid leak out. You eventually absorb the fluids, but the lipids and proteins are really big and they're hardly reabsorbed. And so they end up getting deposited here. You can imagine what that's going to do to your vision. Here we see what heart exudate looks like. It's this kind of pink on the H&E spade. And so you see exudative material. Here you see a big dilated vessel, a lot of exudative material in the retina. It's a heart exudate. Becker, what are we highlighting right here? Those look like cotton wool spots. Cotton wool spots. What exactly are cotton wool spots? Areas of ischemia. OK. So they're focal areas of ischemia. What layer are they? Layers. Well, they're dot-shaped. They're not flame-shaped. So I'm going to guess that they are deeper in the retina. Actually, they almost are kind of flame-shaped. So if you look at it, it's not. So they're kind of deeper but superficial. So they're actually in the ganglion cell and nerve fiber layer. So they're actually superficial. And the way you can tell that is every once in a while, you get one of these right overlying vessels. You can literally see it inside of the vessel or above the vessel. And so what these are is they're focal ischemia here in the nerve fiber layer in ganglion cells. And so these ganglion cells get ischemic. Now these can come and go because you get focal ischemia. And then the ischemia will go down. But it can kill off little focal areas. And so when you get a lot of these cotton wool spots, although they may eventually go down, it'll leave a little dead area in there. And if you were to truly get a pinpoint of the focal ERG, you'd be able to find where these are. But diffusely, they're not going to cause any changes. And here you can see, again, these are ganglion cells. Spollen they are. These swollen ischemic ganglion cells. And then you get this cotton wool spot right here. Shrava, what are we looking at here? It's the lightning of the retinone. And the pressure looks like it's dark. That's just a bad picture. I'm sorry. That's just a bad picture there. So ignore anything that looks darker. I've been looking here. I wonder for the sinks here in the retinas of the core. Actually, this is still superficial retinone. So there's some cotton wool spots for you. And what's going on in here? There's hand wedges. But even beyond that, yeah, there's neobascularization. So we've gone from background retinopathy to pre-perliferative, where you've got cotton wool spots in ischemia and funny tortuosity. Finally, to this, which is now called or proliferative retinopathy. So neobascularization. Now we divide neobascularization crudely into what two types? And those would be, this is an easement, because it's neobascularization of the disc and neobascularization elsewhere. So basically, the disc is the most serious, but everywhere else counts as elsewhere. So this is now NVE, neobascularization elsewhere. So this is peripheral neobascularization. And then, of course, we can have neobascularization of the disc, NVD. And this looks like, I like to call this, it's like Medusa. Remember in Greek mythology, Medusa, with the snakes coming out of her head? So this is the Medusa look. Look at all those abnormal blood vessels coming out here. And so those could be a real problem, because if you don't treat those, those vessels are very fragile. They don't have perisites around them. And you can get hemorrhaging, you can get scarring. And you can see right here, here's some scarring along the arcades. The reason that's pink is there's hemorrhage here on the vitreous. And this is the classic hemorrhage. Ashley, what's the shape of this hemorrhage? Look, like a boat. It's called boat shape. So it's kind of flat on top, and then rounded at the bottom. Why is it that shape? Because it's under the ILM, so it's just basically just pulling. Exactly. So it kind of pulls between the retina and the internal limiting membrane kind of between the retina and the vitreous. So pre-retinal for that kind of shape. What's that? It's a Greek word for that kind of shape. I don't know. Someone look that up. Scaffoy. Scaffoy. I don't know. Scaffoy is like the scapula. The scapula is boat shape. So, you know, coming from the Greek, of course. So you know, kimono is a Greek word. No, no. So this is actually a hemorrhage from head near vascularization in front of the retina between the retina and the vitreous. And so this is the so-called boat shape hemorrhage. So you want to try to prevent these. So what are some of the other complications that can occur from diabetes? That's neovascularization of the iris. Neovascularization of the iris. What do we call that? VI. Okay, NVI, neovascularization of the iris. Okay. Or some people would call it rubiosis, you know, redness of the iris. We used to call this ropiosis because you know, the vessels are so big you and a student can see them. An intern can see them, so. This is iris neovascularization and it's caused by ischemia. So ischemia in the retina can cause neovascularization in the iris because it makes these magical angiogenic factors be produced. And so our whole treatment now, macular degeneration, is blocking these angiogenic factors. Okay, we didn't know what these were 30 years ago, but now we know. So they're not magic anymore. We actually know what they are. So these humors come forward into the anterior segment and they actually stimulate neovascularization of the iris in addition to neovascularization of the retina. And so we look at it, Lee, what are we looking at here? What part of the iris? The iris. The iris. And what's happening here? It's like a trope in UVA. Exactly. So you see the edge of that pigment epithelium is coming around the corner. So it's as if something has pulled it from the back to the front. So when you look at the iris from the front, you'll see a little dark edge around it. This is ectropion UVA. And what's it, what is it here that's causing that? It's a neobascular membrane in fibromasculin. Exactly. So you see that little neobascular membrane on the surface of the iris as it contracts. It pulls that pigment epithelium around the corner and causes that trope in UVA. What else could it cause, Eileen? Lacy vacuolation of the iris pigment epithelium. Okay, could do that. What am I showing here, though? Sorry. Neobascular elation of the angle. Sorry, I was so excited to get that lacy, though. But I don't really see it here. Actually, there it is right there, so you can tell me. So it can cause lacy vacuolation of the epithelium, but what else does it cause? Neobascular elation of the angle. Exactly, so you see these neobascular membranes grow on the surface of the iris right here now so that regular measurement would clear over here somewhere. So you get closure of the anterior chamber angle with broad peripheral anterior synechia. And then due to ischemia, you get focal lacy vacuolization. All right, Chris, what are we showing here? What part of the iris are we in? Why the heck would I show this? So iris, some periphery then. So see, this is all folded, kind of plight-keeded. Oh yeah, so this is a parse placata, but no, that's not it. Yeah, parse placata, the folded part of the cylinder body. What stain is this and why am I showing it to you? So it's a PAS stain. And what is PAS stain? So it's basically stains and membranes. What membranes? Basement membranes. So if you look right here, you see that the basement membrane of the cylinder of the film is massively thickened. Why that happens in diabetes? I don't know, but it does. So this is a sign of diabetes. The reason I love this picture, I took this when I was a Dave Appel fellow. Dave Appel said, I have to submit a bunch of pictures to the American Board of Ophthalmology for boards. Take some and submit them. So I took a bunch and submitted them. And so when I was a senior, taking no caps, my picture was on there. I took that picture on there. So you get thickening of the basement membrane of the cylinder body. That's what that's showing here on the PAS. How do we treat it? Becca, how do we treat neovascularization? Antibedgef. I should say, how did we treat it? I don't know what the previous treatment is. We would do pan-retinal laser. There you go. And so the analogy of this is, I call it the Vietnam analogy. You guys are too young to remember Vietnam, but they would put these generals up there and say, well, we bombed this village in order to save it. Get those, kill all those Viet Cong. Yeah, but you destroyed the village. So what you would do is, you would do pan-retinal photo coagulation. You would laser the entire periphery of the retina, which then would kill off ischemic retina, decrease the ischemic factors, and the neovascularization would regress. And so you'd kill the peripheral retina to save the central retina. And here's what one of those laser spots looks like. It's absorbed by the RPE. It really destroys the RPE, kind of fuses off the core capillaries, kills off part of the peripheral retina. And in doing that, decreases the ischemic load in order to have the neovascularization go away. All right, Shroff, what is this picture of? Okay, of course you do. Neovascularization? Exactly, there's a big frond of neovascularization, but if you look more peripheral to it, that's not an artifact, that's just black. So there's like no blood vessels beyond that. So you've got this frond of neovascularization, you've got this black vest beyond it. What could cause that? Do you laser? No, no. You know, I guess in a kid, this could be right now through prematurity also. This is an adult. An adult from the Indian subcontinent, which includes Pakistan. This is Eald's disease. And so you can get a disease where you get lockage of the blood vessels. You get dropped out perfectly and then you get this C-fantai neovascularization. Also what can cause this is sickle cell can do this too. Sickle cell, Eald's disease, things like that. Is Eald's, you know how to work by the way? By the way. By the way. So this happens to be a patient with sickle cell. And so if you look right here, you see the sickling out of the vessels there and then you get eventual occlusion and you can get all kinds of problems in the retina from sickle cell disease. All right, what are we looking at right here, Ashley? Oh, it looks like a... All right, so you look at the macula. You've got this macular hole right here. And you wanna try to catch these before it gets to that point because when you have a full thickness macular hole that's about, you know, 500 microns across, by then the game's over. So even if you seal it, the vision still isn't very good. This is a close-up. You'll see you'll often have that cuff of edema around it. Pathologic, oh man. I have a fellow picture here, sorry. So you've got a macular hole here. This is the edge and then you get an edema of the macula around it. It's a macular hole. Boy, this one's a little more subtle, Reese. I mean, there's a little bit of white thing there. What else is going on here? The vessels look a little drag. Exactly, the vessels look a little squiggly and tortuous, it could give you that picture. It could be like something that hadn't run off of the primaturity or fever. This is a 75-year-old distortion of vision. It could be an epiretinal membrane. Exactly, this is a subtle epiretinal membrane. And I'll show you one that's not quite so subtle. So this is a severe epiretinal membrane and you see that it's pulling the little vessels in so you get the tortuosity of the vessels and this epiretinal membrane pulls the man and this is a red-free image kind of showing you that. We don't do many red-free images but you see that little subtle epiretinal membrane and you see the vessels being dragged to the center of it. And so when we look at this on OCT, you see that little curve every reprimanded membrane there on the surface. And this shows you're gonna have to update my... I said T, so this is the generation. Sorry. There's a severe epiretinal membrane here on the surface of the retina and so it causes wrinkling and distortion. And the nice thing is these OCTs now basically give you pathology. I mean, they're so good now that you don't have to do pathology anymore. Here you see the wrinkling on the surface of the retina from that epiretinal membrane. So a very common thing that we see. What do we see in here, Leigh? Looks like full of light spots in the macular area. Could be a drusen. All right, so they look like drusen now. How do they characterize drusen? You characterize it based on the size, shape, and how discrete the borders are. Exactly, so we say they can be kind of little small, discrete, hard drusen. They can be larger, softer drusen. What would this be? This looks more confluent and soft. Yeah, so this looks like kind of a soft drusen and they're almost confluent here. When we look at a drusen, where are the drusen, where are the deposits occurring? So they concur basal laminar or basal linear. Basal linear, it's within the Brooks basal laminar is between the RP, our basement membrane. Technically, if you get just a regular, small, hard drusen, it is actually on Brooks, but under the basement membrane of the epithenium. So technically, it's intra Brooks. And so you see right here, they're on Brooks, but they're underneath the RPE, these focal deposits right here, and eventually what they can do is they can cause the RPE to drop out in that area, to be damaged in that area, which eventually damages the retina. This is a larger drusen, so this is a large soft drusen. Here's Brooks' membrane down here, and you see that the RPE and the retina have been completely disrupted, overlying it. So larger, softer drusen. And here you can start to see they become confluent. So you worry when drusen become confluent because not only can they cause more loss of vision, but they can sometimes be a precursor to eventually getting sub-retinal neovascularization. And here's confluent drusen. RPE on here, go right down here, totally disrupted with these large, affluent, softer drusen. All right, what do we see in here, I mean? We see RPE hyperplasia and loss of the folgale reflex and RPE atrophy. Yeah, pretty much the RPE atrophy is all around here. So what do we call this? Geographic atrophy. Exactly, so geographic atrophy, GA, and this is difficult because you can't really treat it with VEGF injections or anything. This is just diffused geographic atrophy and you can get severe loss of vision for macular regeneration with geographic atrophy without going on to sub-retinal neovascularization. And here you see diffused geographic atrophy. RPE totally wiped out some soft drusen here and here. And you just see the retina is pretty much gone. There's some vessels, but the retina's just gone. So diffused geographic atrophy. People are looking at ways to treat that now. We will get some treatments here someday. What do we see in here, Chris? So salmon hemorrhage, so something that's more red. Yeah. But we'll go right here. Yeah, and there's some elevation, a demon of kind of that area there. So I mean, this could be wet and need neovascularization. So when you have sub-retinal neovascularization, especially sub-RPE neovascularization, it almost looks kind of green and straight red. Because it's under the RPE and then it can break through to underneath the retina where it looks red. And so this is a picture I copied out of the book because I'm not lucky enough to get this exact cut. But look, here's the RPE. Here's the cordic capital errors right there. There's a focal break in the RPE. These vessels are growing through and they're growing underneath the RPE. So this is, we call it sub-retinal, but it usually starts off as sub-RPE neovascularization. This is the nice thing about it, this is what we do treat it with the anti-veg F injections nowadays. So sometimes you get a big one. So you see, this is sub-retinal where it's red, sub-RPE where it's kind of dark green. And eventually, if you don't treat these, what do you get? Chris? See, it gets, this is a dis-conformed scar. It's actually a gliotic scarlet conformant. That's that white scar you often see in severe end stage sub-retinal neovascularization. And so I guess that's stained with PAS, basically. No, it wouldn't be PAS because that's not a basement membrane. It's got sphaliosis. It's connected up to a shoe. All right, this is kind of what we're looking right now. So we've got some funny things going on in the macula, but we've got these little peripheral lesions here too. And so I'm sorry, I'm running out of time, so I'm gonna have to go a little quicker. This is presumed ocular histoplasmosis because you've got macular problems and you've got punched out lesions peripherally. We call it presumed because it's not an active histo. It's thought to be results of a histo. So when you do blood tests, you find signs of histo, but you don't really find live histobugs in there. So histoplasmosis, this is one where I'm looking here and boy, what's happening? I'm gonna show up to that folio reflex there. That's pretty light. That's pretty light. There's some funnies going on there in the fovea. We do a fluorescent angiogram. What do we see in here? Exactly, look at the pattern, this flower petal pattern. So this is called cystoid macular edema and it is actually in what layer? Outer plexiform or near the macula here in Henley's leg. So this is cystoid macular edema in Henley's layer and there you see the ganglion cell layer, multiple layers thick. Okay, what is this, Ashley? So it's also lost the folio reflex migraine. This is one of those pattern things. Bullseye. Bullseye, so what can cause bullseye maculopathy? They're basically toxicity is. What's the one we worry about? We worry about timoxifen's reminiscence with them. Yeah, I see probably four of these a month now. Platinum. Platinum. So you can see this in chloroquine, you can see it in timoxifen, but this is an end stage bullseye maculopathy. Again, we wanna catch these sooner than that. So we do a central phobia visual field, we do a OCT in the macula. So this is a bullseye maculopathy, usually due to toxicity. Plaquanil is now the number one that we wanna look for. When you do fluorescein angiogram, you see a little bit of staining in that area, but no leakage and you see window defects. So you get this bullseye maculopathy. All right, Thrice, what do we see in here? Those angelic streaks. Exactly, so you see these little things, they look like vessels, but they're not. They are underneath breaks in, what layer? Brooks membrane, so breaks in Brooks, they look like vessels. These are called angioid streaks because they kind of look like blood vessel streaks, angioid streaks. So why am I showing you this ladies' chin? Snack anthoma last year. Exactly, so this is the plucked chicken look they call it. So there's a condition called suposanthoma elastica that can cause Brooks membrane and other connected tissue to be brittle. So you get these angioid streaks, you can also get it in what other diseases besides suposanthoma? Colors, damlos, hash disease. Padgets. There's idiom happening in the ass, what is the ass, what's the symbol? Sickles, exactly, so that's sickle. So know that in mind. Good, all right. What is this leak? All right, what makes you say RP? What are the findings you're gonna tell you? It's an aspingmintosa. So you look at the nerve, it looks, powers, you look at the vessels, they look, are tenuous, you look at the bone spigilization. So that's kind of the triad you look for. You have a pale disc, attenuation of the vessels, and then in the periphery, you get the bony spigial pigment. So for extra bonus points, why do they form that bony spigial pattern? It's let a pleasure, the RP, go along the vasculature. Exactly, so you get the RPE cells, release that pigment, it's either deposited along the vessels, or for some reason grows along the vessels. So you get that bony spigial pattern, but the RPE eventually gets wiped out, as does the retinase, the retinase pigmentosa, many different types, many different inheritances, but they all look the same at the end. Eileen, what do we see in here? We're seeing like a yolk. Yes, this is the sunny side up egg. What disease is this? Best disease. Best, or if you see it in an adult, they call it the teleformed history. And that's not from the Greeks, sorry. So you see these deposits of this material underlying the RPE in the center of the macula, best disease. Doctor, yes. In the book they say it's between the photoreceptor layer and the RPE, is that correct? Why, well you have to say to me, I've always thought it's under the RPE, because usually RPE are here. But you have to go by what's in the book, because that's what you're gonna be tested on. So whether the book is true or not, the book may have some alternative facts. Oh, I didn't say that. So there's some alternative facts in the book. So the book is a Trump-like book, so alternative facts, but whatever the book says is the Bible, so you have to go by the book. All right, what do we see in here, Chris? You've seen some flecks kind of around the macula, maybe Stargardt's disease. Exactly, some people call these piece of form, or fish-like, I don't see it, but they supposedly look like the little goldfish things that you eat, and so this is what Stargardt's? Stargardt's, or phobias, fundus flavii maculottum. But in any event, it's characterized by this lipophucillic periodal that gets deposited in the RPE cells, so Stargardt syndrome. What do we see in here? This is not out of focus, Becca. My guess would be vitreous hemorrhage, but then we can't see it. It's kind of white here, though. And you're seeing the nerve through this. Yeah, there's something hazy in the vitreous. So we see that, and you see this, it's called the so-called headlight in the fog. You can still see the optic nerve barely through all this haze in the vitreous, but there's this white going on right here. This is acute toxoplasmosis. This is active toxo, because you get a vitritus secondary to it. So this is a toxo lesion, and when you look at them afterward, you get these pigmented with these white lacunae in them. So this is a quiescent toxo, but those toxobesties are pretty sturdy. There's still some toxo in here that might be able to reactivate later on. So toxo, it's thought to be congenital when you get it, and then it can activate later on. So this is toxo, and the problem is, is it could have wiped out, again, the retina and the RPE and the choral. So toxoplasmosis. What do we see in here, Sean? People call this kind of the pizza pie or tomato ketchup retina. What infections? Infections? This is CMV. So we had a huge outbreak of this when the HIV was rampant, but now with triple therapy, we just don't see these anymore, which is nice. And so this is CMV, subtle magulovirus. Usually we see these in severely immunocompromised people, HIV, chemotherapy patients, things like that. And you get hemorrhages, but you also get areas of ischemia and whitening, and so these, we call this, as I said, the pizza or the tomato ketchup retina. And when you look, you actually get both intranuclear and intracelloplasmic inclusions in the ganglion cells here from CME, subtle magulovirus. Okay, and as we're floating the snake on a flat part, there's the gray ad popping up logistically. All right, so next week you guys get a week off. Isn't that nice? Because there's a fifth Tuesday and that's, so the first Tuesday in February is optic nerve. Questions? Sorry.