 Tina, what's the variant of basal cell that we are concerned about? So that's not your typical nodular type. So you notice in multiple small fingers of basal cells surrounded by fabrovascular connective tissue in between. This is a morphia form. And the reason why you have to remember this is if basal cells are going to spread locally, it's usually the morphia form that does it because these send little fingers out so you can't normally see them and remove them all. The nodular type, which is most common or nodular cystic, you can see the edges. You can cut it out, you know, usually. But the morphia form type sends these little fingers out and it's often difficult to find the exact margins. So the morphia form type is the one that's more difficult to remove because you may be leaving remnants of tumor behind. And this is what happens when you let a basal cell grow for 10 years. So this is a basal cell that was left alone for 10 years. This is a rancher or lady from Nevada. She had a morphia form basal cell 10 years ago. They said, we're going to have to do more surgery, remove that. She said, I'm an old lady. Leave me alone. Went home. And then 10 years later, her daughter brought her back because she had a little piece of Kleenex stuck to it and it smelled. And it was actually CSF tripping out. So if you let basal cells grow for 10 years, they can cause really bad things. All right, what do we see in right here? A little orange kind of crackly parchment paper looked to the surface. What would you be concerned about here? That's what it's hard to say. So moving in a squamous cell. All right, so you'd be concerned about a squamous cell. Does this confirm the diagnosis? So what do we see on the path of a squamous cell? So there's keratin pearls. There's cells with higher NC ratios, promenucleol, and they're just like diving through the tissue. Okay, so you can see here these nice squamous pearls, squamous worlds in here. That's a real tip off for a squamous cell. Extra bonus points. If a squamous cell spreads from the lid back, how does it spread? Perineurals. Perineurals. That's important. You really want to watch them because they can spread perineurally. All right, what do we see in right here? What would you be concerned about? There's enough here to tell you the difference between the two. If you had a 50-50 shot here, what would you guess? Oh, 50-50 chance. Let's go melanoma. Okay, so basically when you look at that, you see loss of lashes. You see it's thickened and irregular. You see variable coloration. So whenever you see that constellation of findings, you really worry about melanoma. And so the melanoma is not common in the eye. It's becoming more common. And so as the sun worshipers of the baby boom generation get older, melanomas are sadly popping up more frequently. And here we look at the melanoma cells. They may not necessarily be heavily pigmented when you look at it, but you can see there's nucleoli. There's clumped chromatin. There's pleomorphism. There's different sizes and shapes of the cells. So that's malignant melanoma. These can not only spread locally, but can metastasize. All right, what do we see in right here, Chris? If you can see any sort of photo of the eye, there's an injection on the contactive end. The whole, like this lid martyr just seemed really small. This would make me think, indifferential-wise, maybe like a sebaceous cell carcinoma could look something like this. All right, so sebaceous cell carcinoma is the great mimicry. You got to remember that. So don't be fooled. So this was called blepharoconjunctivitis, you know, treated with antibiotics. And so what you look at, if you look at that upper lid, look at the loss of lashes, look how thick it is. You can even see the yellow from the mybomian secretions that are there. And so this can look like a chronic chelazion. If it's locally, if it's diffuse, it can look like blepharoconjunctivitis. And so this is the great mimicry. You want to be very careful not to miss these, because, again, these can metastasize. And when you look at them, these can be very aggressive looking and they behave very aggressively. They've got mitotic figures. They've got nucleoli. There's still occasionally little dots of lipid in them. But these can be a very bad actor and these can spread also. So you want to not miss a mybomian carcinoma. All right, so here we have, this is not Mo the surgeon. This is Mo the stooge. Come on. You study better when you're not so tense. So chill. All right, congenitiva. So softball here, Brad. What are the three parts of the congenitiva? So you have the non-charitonized strata. Oh, the three areas of the congenitiva. Oh, areas. Sorry. Okay, so you have the bulbar, the palpibral, and you have the fornix. Exactly. So it starts lining the, you know, from the limbus, lining the bulb, the bulbar, and then the fornix, and then lines the lid, the palpibral. And then, so what are the different layers now of the congenitiva? So we have the non-charitonized strata, squamous epithelia. We have the... Yeah, we call that the substantia propria. Substantia propria. What are all those little dots down there in the fornix? So those are probably goblet cells. Exactly. And what do they make? Mucin. Mucin. All right, very good. So mucin, the inner layer of the tear film. All right, what do we see here? Right here. You're not graduated yet, so what do we... What do we see in here? What do we see in here? The teridium. The teridium. And so what's the difference between a teridium and a pinguakila? Teridium crosses the limba margin. Exactly. So pathologically, they're exactly the same. It's just that the teridium crosses the limbas onto the cornea. What do we find pathologically? Solar elastosis. All right, so that's that. Squiggly solar elastosis of the collagen and substantia propria. What else do we find more anteriorly? It kind of stains blue, so we call it basophilic degeneration. So they're both solar elastosis, basophilic degeneration, UV induced degeneration of the tissue underneath. Solar elastosis is the breakdown of the collagen tissue. It gives it elastic characters and like a frayed elastic look. And then elastoid degeneration. Same thing. Yeah, same thing. Sometimes I feel like the pinguakila. Well, teridia can sometimes become more fibrotic with time. So as they grow more, they can become more fibrotic. And that's what you're saying, I think, is more fibrosis underneath. So when they're first starting, they are a little bit more translucent and seem a little bit more cystic. What do we see in here? Let's give you a concern. The question is why? Not because it says tumor up there. You know, that's not a hint or anything. Now, remember now, when you look at a teridium, the epithelium is actually thin rather than thicken. And the meat of the tissue is underneath it in the substantia propria. If you look at this, the epithelium is thick in gelatinous. You know, so the epithelium is the thick in part. It's really gelatinous. And so what would this be concerned for? Yeah, this would be concerned for CIN or even squamous cell carcinoma, depending. So when you see this gelatinous thickened epithelium, you have real concern about that. And we look and we see this picture. So does this help our diagnosis? So if you look right there, you can see loss of normal concentration. You see nucleoli. You can see different sizes and shapes. And so this is what we call CIN, Conjuctival Interim Thelogneoplasm. And we grade it mild, moderate, severe, depending on how much of the thickness from the base up is involved. So lower third, mild, up to two-thirds, moderate, more than two-thirds, severe. So this would be severe. It's full thickness. But by definition, the basement membrane is still intact. And so if it goes beyond the basement membrane, that's when we say squamous cell carcinoma, as long as the basement membrane is intact, we say CIN. You guys have to read whatever the latest literature says. We call this, you know, ocular surface, O-S-S-N. So, you know, and again, just because you memorize something, about every 10 years they change it all. So you have to re-memorize it all. And I think it makes it more confusing rather than less. But in any event, you know what's in the BCSC, and that's how you do the nomenclature. That's my last question. Yes. What exactly is Bowman's disease? I know it's like squamous cell, like in situ. Yeah, Bowman's disease really is an old, old term, and I don't think you're going to have it pop up anywhere. Hopefully not in your readings. All right, so what are we seeing right here? Becca. It's organized. There's some keratin whirls in there. And these are actually in the connective tissue under the conch. So this has now become, more technically, squamous cell carcinoma. So this is actually a superficially invasive squamous cell. It looks like the squamous cell of the lid, and it's got keratin whirls, keratin pearls, and cleoline, pleomorphism, and so this is an invasive squamous cell carcinoma of the lid. What are we seeing right here, Tina? So there's localized areas of pigmentation on either side just next to the limbis and the palpiparulospes, sort of racial pigment, and the other would be PAM. What does PAM stand for? Primary acquired melanosis. And how do we break down PAM? What are the two ways we describe it? So within and without utopia. All right, so what would this be? Looking at those cells, trying to see, there's a couple of nuclei, but it's not looking like it's kind of full thickness. If you look, these melanocytes are mostly here in the basilar layer. No other squamous cells above it, but they're mostly in the basilar layer. And so when you have PAM without utopia, the melanocytes are along the basilar layer and they don't show atypical features. And even racial pigmentation will look like this. So you can often see people who are African-American or Asian who will have pigment around the limbus. And this is PAM, it looks exactly like this. PAM without atypical or even racial pigmentation. Does this give you more concern? Why? It looks like it has, like the conch vessels look like they're coming in and spreading out, like feeding the lesion. Another thing you can see, this isn't just that nice superficial brown dusting. There's some areas of younger pigmentation. There's some areas of lighter pigmentation. There's some thickening. So this would be a bit more concerning. And when we look at this now, what would we call this? Or again, this we could still technically say PAM with atypia. Exactly. So these atypical melanocytes are now spreading out through the epithelium itself and they're becoming more atypical to themselves. They're not just Medine melanocytes. And so PAM will go through a phase where you get PAM with atypia. And it's important to recognize that because PAM with atypia can go on to malignant melanoma. PAM without does not. So this is technically a pre-malignant lesion. So PAM with atypia. And is this concern? So even an intern can recognize this. What would your concern here be? Exactly. So this is melanoma. Unfortunately, another patient at the VA kind of ignores it as long as he can until he comes in. This turned out to be an actual malignant melanoma of the contractiva. So if you don't, you got to watch the PAM with atypia very carefully because if you look at malignant melanomas, about 80% of them arise from pre-existing PAM with atypia. Now it doesn't mean 80% of PAMs go on to melanoma. It means if you have melanoma, 80% of those arise from pre-existing PAM. So it's important to watch them real carefully. You could get a malignant melanoma. You know, oftentimes it can be yours. And these will often flare and then subside and flare them subside. So you'll see these people, there'll be areas, you'll remove them, you'll clean them, and then they'll come back a year or two later and they'll have another one pop up somewhere else. And so you really want to be careful. So this is the parthenon on top of the acropolis. They've been rebuilding this for a long, long time. It's nice though, every few years when I go back, they've got another, you know, part of the wall out of the ceiling. So the Greek government's trying to get the so-called Elgin marbles now. One entire face of the top of the parthenon is in the British Museum. And, you know, Elgin was the guy who rescued them, you know, because those Greeks couldn't take care of their antiquities. And so Elgin rescued them and took them to London where they're safe there. So hopefully someday they'll get them back and finish rebuilding this. All right, cornea. We're going to talk about the cornea. What are the layers of the cornea, Chris? So we have the epithelium. Okay. Tell me the difference between bonemons and decimais. So decimais is the true base of the membrane. Bonemons is not. Exactly. So what stain could you do to tell the difference? Yes. All right. So bonemons is just a condensed area of the anterior stroma. Bonemons does not regenerate. So if you have an ulcer, you have an abrasion, you have a cut there, it's a good historical marker because it doesn't regenerate decimais because it is a basement membrane. Decimais grows thicker throughout life. You know, if you scrape it off, you know, and more endothelial cells can come over and they can lay down new decimais membrane. Now, the epithelial basement membrane is not bonemons. It's a separate little basement membrane in front of bonemons. So think about this one. I think this is true. Think about it. All right. So corneal infections. What do we see in right here, Brad? What is this a classic picture of? So this is, we have some fluorescein uptake in the pattern of the denturidic lesion, which is a classic for HSV keratitis. All right. So this is HSV keratitis. You've got the dendri. You've got the little swollen projections. Now, if you were going to take a culture of that, where would you culture it? On a swab. I mean, where on the lesion? Oh, cool. Wait. I got to worry about you. You're way too left brain, so yes. Way too literal. You would do the bulbs. Exactly. So remember now, where the stain is all taken up in the center, that's where the epithelium is denuded already. So if you're going to do a little scraping for a culture, you want to do it kind of at the edge, where the thick epithelium is at the edge of the bulbs, because that's where the active viruses are going to be. And here you can see an area. There's the ulceration. And then you want to do it right next to that. And that's where the active viruses will be. And you don't have time to go into it now, but realize that there's more than just simple dendritic keratitis. You've got variations of stromal keratitis, recurrent herpes. You really need to know that for when you get to the corneas section of the boards. All right, what are we seeing right here? There's ulceration with infiltrate. What would you be concerned about here? Depending on if they're not feeling a ton of pain and considering we're in the higher section I consider like a neurotrophic keratitis, but the ulcer could be considered like a bacterial ulcer as well, like pseudomonas or something. Exactly. This is someone who actually didn't take care of their contacts. And so this is a pseudomonas ulcer. And you really worry about a pseudomonas ulcer because a pseudomonas ulcer in 48 hours can actually cause a corneal perforation. Because not only do the bacteria put out collagenases and proteases and help melt down the corneas, but the body's immune system that comes in there can help melt down the corneas. So you really got to treat these as an emergency. This is a cornea that has become completely necrotic and is perforated. So that's what you really worry about with the bacterial ulcer. What's that? Oh, it is already. Yeah, this is a pseudomonas. This is really thinning. And this actually did perf later. And so it is thinning. It did perf. What do we see in here? This is a little bit different. What would your concern here be? A little bit more indolent in history. It's been here for about 10 days. Farmer. Exactly. This is a fungal ulcer. And so you see the little kind of halo of white around it and you get kind of that halo of white around it. It's more indolent and it's slower growing. And you get that exposure to the crop when you're out there. And sure enough, we do a special stain. What stain do we use for looking at fungi? GMM. So this is Gamori methenamine silver. And so the little yeasty beasties will stain a black silver color. So this is your fungal ulcer. All right. What are we seeing right here? You don't see yeasty beasties on warlords. All right. Becca. All right. So it has kind of a ring shaped infiltrate. And you can see that epithelium is disrupted. Yeah. Big chronic epithelial defect. This has been treated for herpes for three weeks. Yeah. So I'd be worried about a neurotrophic ulcer in this case. But if it was... Let's say it's really painful. Exactly. So when you see a chronic non-healing ulcer and you see this ring of infiltrate around it and it's painful, you often think about Acanthamoeba. And sure enough, we stained it. And boy, triple bonus points if you know the stain we use for Acanthamoeba. Gridley. Gridley. The gridley stain. And so you see, here's the Acanthamoeba cysts. And these are really tough to treat because they tend to insist. And so it's tough to get the medication into the cyst. But don't forget people with Acanthamoeba. I've seen it in contaminated contact lens cases. You can get it from soil. You can get it from hot tubs. So don't put your face in a hot tub. If you're hot tubbing it and chilling out, keep your chin above it. Don't put your face in a hot tub. The gridley stain only works if you have an actual cordial specimen. Correct. You have to have a biopsy. It doesn't work on a swab. You have to have a biopsy in order to do it. So speaking of contacts, all right. Now we're going to talk about the anterior chamber angles. We can talk about glaucoma a little bit. So Tina, we're starting, we're looking in with agonium here. And we're looking at the angle, starting at the top. What's the first thing you see? Starting opposite direction. Starting anterior, I guess, rather than posterior. See, like Schwabbi's line? Schwabbi's line. And then what are the ways we describe the trabecular measure when you're looking with agonium? So basically the angle of insertion of the iris. You describe what layers you can actually see within the angle. Yeah, but what are the layers? You said the first one was Schwabbi's line. Oh, oh, yes. Okay. So Schwabbi's line is first. And then we see trabecular mesh work. So pigmented, non-pigmented. And then on the other side of that would be your sclerospora. Okay. And there's your sclerospora. And then lastly it would be ciliary body or where iris inserts. All right. Now this is just, you know, just for students if I'm ever talking to students and so, you know, we kind of describe an angle in either open angle, narrow or closed angle, and then recessed or contusion angle. All right. What do we see in here? Right. So if you really look, even though this patient's got the chronic dry eyes of every Utah, the right eye is definitely redder than the left eye. The right pupil's bigger than the left eye. And the right eye is more painful than the left eye. All right. So you'd be concerned about angle closure here. So mid-dilated pupil, red angry eye, painful eye. Sure enough we put the slip beam on it and we see. All right. So here's iris bombae. The iris is bowing forward. You put agonio in there. You'd see that the angle would be blocked off. So this is angle closure. And now you can get angle closure sometimes from just an eye that's narrow with a big lens or that's hyperopic or that's small. But sometimes you can get some abnormal blood vessels growing along the surface of the iris. What do we call that? Yes. So you can get neovascular glaucoma that can eventually lead to an angle closure. Remember what the causes of neovascular glaucoma are? Chronic ischemia. So you could have a central retinal vein occlusion. You could have a diabetic. You could have an ischemic eye in general. And then you can get abnormal blood vessels growing and then you eventually get an angle closure with that. Okay. So we want to talk a little bit about glaucoma. And this is always the hardest thing for me. As you look at an eye and you see a myopic eye and you see that myopic crescent and you try to say, okay, where is that disc end? And where's the myopic crescent? This is definitely a cupped out disc. This is glaucoma cupped out disc that we've got here. And this is the ultimate end stage. You don't want it to get to this. We want to stop glaucoma before it gets to this point. So this is, it almost looks like a Boston bean pot. So this is excavated here. It's got a little disc, a little vessel going along the edge and then it will disappear. Posterior bowing of the lamina crebrosa. This is end stage glaucoma. We don't want to see this. We want to stop glaucoma before it gets to this. All right. So this is also on the top of the acropolis. This is one of the famous five maidens. Sadly, maybe the British were right. This is a remake of the statues because the original statues were so eaten up by the pollution in Athens that they degenerated so they couldn't put them back out again. So these are exact copies, but they're not the original ones. All right. We're going to talk a little bit about the crystalline lens. And this is just pathologically where the lens sits. All right. So cataracts. Mike, how do we break up cataracts? How do we describe them? So you're talking about... All right. So posterior capsular, anterior subcapsular cataracts. Remember, there can be various different areas that are affected and that can have some bearing on the prognosis. So if you have posterior subcapsular cataract, what's the etiology for that? Not usually PSC. Polar. Polar. You think of polar now. One of the mild posterior subcapsular. Diabetes, ocular inflammation, and then medications, most commonly steroids. So PSC, people can be on steroids. They can have uveitis can cause them. They can have diabetes can cause them. Nuclear cataracts are usually aging. Cortical cataracts are a mixed bag. All right. So this is the ultimate nuclear cataract. What do we call this? Brunessin cataract. Brunessin. Brown-like Brunessin cataract. So this is what you see in the third world or parts of Wyoming, depending. But it's a supernessin cat. You're allowed to say stuff about your own kind. You're allowed. Don't send a letter to the dean and say, I'm disparaging Wyoming. All right. So I always want to make sure you guys remember that we do surgery with topical anesthesia. Patients hear everything. So one of my favorites. A patient was very astute. I was doing surgery with the second year. And the patient asked me the next day, what is this position one you kept saying? Because you guys keep getting so panicked you come off the pedal. Position one. Position one. Position one. So what is position one? You want to know what that was. The other thing is I have to stop saying stab incision because the patient got really perturbed when I said stab. He said paracentesis. Remember they always hear you whenever you're doing cataract surgery. So don't be talking about the jazz game in the middle of surgery. All right. Here's the acropolis at night looking at the parthenon. You're allowed to go up there one day a year at night and take pictures. They light it up every night, but you're only allowed to go up there one night. All right. We're going to talk about the retina. So when we're talking about the retina in terms of the different parts of the retina, what are the parts of the retina that we can describe anatomically? You're not talking about the layers. No. We'll get to the layers in a minute. Okay. I mean you think about the parts that are in between the arcades. Okay. So in between the superior and inferior arcades you talk about what's temporal to the arcades. What do we call the area within the arcades? The fovea. The macula. Of course the center of the macula is the fovea and anything external to that we consider external. So now we want to talk about the layers. What is the... Let's start with the vitreous sides. We're going to describe vitreous to coreate. What's the first layer? Internal limiting membrane. Internal limiting membrane. Next layer. Nerve fiber layer. Next layer. Ganglion cell layer. Inner plexiform layer. Inner plexiform layer. Inner nuclear layer. Inner nuclear layer. Outer plexiform layer. Outer nuclear layer. And then below that we have the... We have photoreceptors. Okay. I'll pass that. Below the photoreceptors. Yeah, the RPE. RPE. Alright, very good. So know the ramification of the various layers of the retina. Know how they are all interconnected. Alright, now what are we looking at? So this is a cross-section of the fovea. The fovea. And so, what goes on in the ganglion cell layer adjacent to the fovea as opposed to the rest of the retina? It thins out and disappears right above the fovea. Alright, so it disappears. How about adjacent to it? Begins. So the ganglion cell layer, by definition, is more than one cell layer thick in the macula. And that's how the pathologists define the macula. That does happen to be, you know, within the arcades. But that's what the pathologists do. If you look at the fovea, the cells all, you know, branch out so that light rays can come in unimpeded. And so, all those ganglion cells that are linking up with the cones in the fovea pile up adjacent to it. And you go ahead and you get multiple ganglion cells adjacent to the fovea there. Alright, so what do we see in this picture? Alright, exudate, and? Okay, so in addition to exudate, you've also got Doppler hemorrhages. You've also got flame hemorrhages. Boy, right here, that may even be, maybe a little cotton wool spot. Exactly so, enunciate. Project. So, cotton wool spot. So this is a diabetic. And so this has kind of all the findings of not only background retinopathy, but even getting into a little bit of pre-perliferative retinopathy at this point. Alright, so what do we see in here? So those look like some macroaneurysms. Exactly, so the first thing that you get is you get the vessels affected. The parasites drop out. You get weakness. You get macroaneurysms. And then eventually you can go ahead and you can get Doppler hemorrhages. Exudate right here. You've even got cotton wool spots. What's a cotton wool spot? Exactly, so it's the superficial nerve fiber layer. You get a little infarct there. Eventually that swelling can go down and you'll have a focal defect there, but you don't see anything different. So that's a cotton wool spot. It's on the nerve fiber layer. And so it looks like someone put a piece of cotton on the surface of the retina. Alright, what do we see in right here? The vascularization of the disc. Alright, so this is NVD, the so-called Medusa's head. Remember Medusa from mythology with all the snakes coming out of her head. So you've got NVD, the vascularization of the disc. And you worry because if you don't treat NVD, what do you get? Exactly, so this is how do we describe this hemorrhage? Well, it's specific shape to it. Come on, you're out on Galveston Bay in one of these. It's a boom. So you go on ships. I'm impressed. You have ships that you go out on. Okay, sailing on ships. So it's flat-topped. So you can see it's flat-topped and it's got kind of a round bottom like a boat. So this is actually hemorrhaging pre-retinal. So it hasn't quite broken through to the vitreous, but it's pre-retinal. So it's between the retina and the vitreous. And so if you don't treat neo, you can get hemorrhages like this and then you can even eventually get scarring and get gliosis. You can get retinal detachment. Alright, so this is the latest commercial, you know, for laser vision. Alright, what are we seeing right here? Chris. This looks like a lot of blood. It looks like a blood and thunder retina to me. Alright, so what does blood and thunder retina usually signify? Alright, so this is a central retinal vein occlusion. Backup of blood everywhere. It goes from the optic nerve all the way out to the auraserata and the so-called blood and thunder look. And then here's a picture of the retina that's had a vein occlusion. You can see loss of kind of the inner two-thirds of the retina from that, from the chronic ischemia. What are we seeing right here, Brad? Brad. So we see retinal whitening with what looks to be like a cherry red spot suggested above the CRAO. Alright. So if you were Dr. Yamani, you could cannulate that central artery and inject in there and make that better. I was impressed by that. Cataract surgeon cannulating the central retinal artery, that was pretty impressive, I thought. So this is a classic central retinal artery occlusion, ischemic retina, which is white. Why do you see a cherry red spot? Because of the underlying corroid. Exactly. So it's a window of the normal coroidal flow still showing through and that's why you see the cherry red spot. Alright, what am I showing here? So you see too many crown burgers and that central retinal artery, you see it's massively arterial scarotic and narrowed, but look at the sheath next to it. So remember, the most common cause of central retinal artery occlusion is arterial sclerosis, you've got a narrowed artery, it's susceptible to emboli, but the most common cause of vein occlusion is arterial sclerosis of the central retinal artery which causes stasis next to it because they share a common habitual sheath. And here's an eye that has had a central retinal artery occlusion. The outer third which receives its blood supply from where? Alright, still intact. The inner two thirds is wiped out. Alright, this is the Greek Parliament building. This is the Avzon who guards the Greek Parliament. I sat there and looked at this guy for five straight minutes. He never blinked, so I don't know, I'm totally impressed that he could do that. He never blinked, they don't flinch, they change the guards. If you're in Athens, you've got to see they change the guards silently in perfect step. It's pretty impressive. We're going to talk about some macular diseases here. What are we seeing here? Exactly. I soft drusen all over the place there. And when we look pathologically, where are drusen located? Exactly. So if you think about the base membrane of the RPE in the first layer of the Brooks, technically it's even intra Brooks. But it's certainly underneath the RPE. And then you get overlying degeneration of the RPE under the retina. What are we seeing here, Meg? So you can see the extensive edema around it looks to be sub-retinal. So you see that kind of a yellowish grayish look in the periphery there. That means it's even sub-RPE when it starts. Then as it gets more darker red, it breaks through under the retina. So this is a patient with macular degeneration, sub-retinal neovascularization. So, okay. So this is the temple at Delphi. This is where the oracle lives. And so you would go to the oracle and you would say, please give her an offering, and you'd say, tell me what's going to happen. And the oracle would say things like, I see the destruction of a great empire. You'd say, alright, we're going to kick butt. And so then they would go and invade and they'd get their own butt kicked. And so the oracle was never specific so you have to be careful when you get information from the oracle that it'd be more specific. So this is where I go and I ask how the residents are going to do in surgery. So the answer is sometimes a little cloudy. A little cloudy. Alright, optic nerve. This is a normal optic nerve. What stain is this? This is a trichrome stain. Trichrome stains. You see that the connective tissue stains blue, mesecimal tissue stains red. You can see the pia, subarachnoid, the columns. This is an optic nerve seen in cross-section. What do we see? Oh, of course. Sorry, I got to wipe out. Papalodema, that's a good intern question. Papalodema. What are the signs of papalodema though? Do you see paling and you can't see the entry of the vessels to the desk as well. Now, it's not even paling. It actually is often darker staining because the blood vessels get engorged. So you see that the edges are elevated. You don't see a good sharp edge. You have a congestion of the vessels. You have little micro hemorrhages. Now, be careful with the term papalodema. Again, when I took oral boards one of the guys was trying to pit me on this because by definition papalodema is optic nerve swelling, secondary re-increasing, trochanal pressure. They show you a picture of just a single disc like this. You say, this is a swollen optic disc. And then if they say, well, what's the differential? Well, if this were bilateral and had increased pressure, we would call it papalodema. But you want to be careful because they'll always try to nab you on that on boards. Here's the swollen disc seen pathologically. Now, in the movies and TV, you always see the audience place where they can sit and watch a surgery going on. I've never seen that in an operating room I've ever been in in my life except in Russia. They had one when Fyodorov used to operate you could stand up and watch it in the peanut gallery. But on TV, they're always up there looking down on the surgery and discussing it, so never seen it happen. Now, all right, so remember the glaucomodus nerve is the opposite of a papalodema nerve. Glaucomodus nerve is actually excavated and coming down. Hi, Chris, what are we seeing here? So here we're seeing left eye. She has ptosis on the left and that left eye looks a little low as well. A little low and almost a little prominent kind of a little proptotic. And this is what we find on the specimen. So this looks like tumor found in the optic nerves like a half nerve tumor. All right, so glioma is the most common optic nerve tumor in kids. There's astrocytes in the optic nerve. And so this is grade one. It's called a juvenile astrocytic glioma. It's a grade one astrocytoma. It's intrinsic to the nerve itself. It's more common in kids. And what are these called? Little cytoplasmic eosinophilic staining inclusions. Rosenthal fibers. So named after Rosenthal. All right, and here we have this is an older lady. So this is an external photograph in the right eye you can see some injection of the lateral conch. Also a fullness in the lower eyelid looks proptotic with inferior scleral show. You do the scan. What are we seeing here? So we see enlargement of the right optic nerve. So concerned for tumor here. If it's a lady middle aged we're concerned for like an optic nerve meningioma. So if you see this is what we call the tram track sign. You can see the nerve still in the middle and then you see the thickened tumor tissue around it. So that's a sign of a meningioma. So it doesn't grow from the inside of the nerve. It grows around the nerve. And that's called the tram track. Like the two tracks on a tram going up the mountain. Meningioma and for bonus points what do we call these? Sonoma bodies. Sonoma with an M. Not sonoma the part of California. So sonoma bodies. Sonoma with an M. Sonoma bodies. So I know you guys are just about daydreaming there. So I'm going to put electrodes on you real quick here. Retinoblastoma. We just went over this a week ago. So you know just realize the two growth patterns which are endophytic and exophytic. And what do we see classically? Calcification, necrosis. Necrosis, dystrophic calcification or at the growth of the tumor cells. What's the most common pathological? The rosettes. Yeah. And whose names go on that? Flexner Wintersteiner. Flexner Wintersteiner rosettes. So. And when it spreads it spreads how? Through the nerve. Through the optic nerve. So remember when retinoblastoma spread they spread via the nerve. And I know your brain is almost full. You have to sleep with your hats on. So malignant melanoma real quick. What's the most common growth pattern that you see in these types of the coroid? What is the shape? What vegetable is this shaped like? Mushroom shape. So it'll start in the coroid, pop through Brooks membrane, grow into the retina mushroom shape. So what is the classic classification we use to describe these from the 1930s? It's the calendar classification. And so calendar classification this is spindle A. So technically not really a melanoma. You can get spindle B cells and then you can get really nasty epithelial cells. And that's really important prognostically. Becca how do they spread when they spread? But how do they get out of the eye? Through any emissarial channels. So they'll usually go out along the vortex veins and get out but you can go out where any artery is coming in any vein is coming out. So they go out through the emissarial channels through the sclera. Where do they spread when they go? To the liver. And so we say goodbye to Delphi again. And good luck on Ocaps.