 Ten years later, her daughter brought her in. She had a piece of clean eggs stuck to that covering it, and the reason the daughter brought her is because it smelled. It was very necrotic. It actually went all the way back through the sinuses. She actually had CSF dripping out. So this is a real housekeeping problem at this point. You can't do a hemi faceectomy. And so this is why you want to treat Morpheus before it gets to this point. All right, let's just go right around here. What do we what do we got here? What would you be concerned about here, especially when you kind of see that orangeish pattern to it? Yes, this is a classic squamous cell. And so squamous cells, when we look at them pathologically, how are they different from basal cells? Right, you see it's all keratin in their keratin purples, and they're pink. They're not blue. So you see the smaller nucleus, you see the pink cytoplasm, you see the keratin worlds, keratin purples, keratin in there. So this is a invasive squamous cell carcinoma. So if you look at lead tumors of the of the anywhere on the lids, 90% are basal cells, probably 6% are squamous cells. And then the others are the less frequently seen tumors. All right, what would you be concerned about here? Nevis versus melanoma. You see, again, loss of lashes, thick irregularity, dark pigment, you'd be concerned more for melanoma than nevis. And when we do the pathology, does this confirm? All right, so you can see that the chromatin, you see the nucleolide, you see the active cells right there. And so malignant melanoma, about 1% of eyelid tumors. But again, you want to, you know, watch for them real carefully because these can metastases, metastasize. What do we see in here? Yeah, it looks like that there is basically just a lot of hemorrhagic changes in the contact area of an ampoule. What's your concern here? Something pretty aggressive, like sebaceous cell carcinoma. Yeah, so sebaceous carcinoma is called the great nemicur. So if it's focal, it can look like a recurrent chelazine. If it's diffused, it can look like this was called blepharoconjunctivitis, was treated by an optometrist for, you know, weeks for blepharoconjunctivitis that wouldn't get better. But if you look, you see it's not only inflamed and red, but you look and you can see the loss of lashes throughout. See thickening of the eyelid, you see that yellow backed up lipid and this indeed turned out to be a sebaceous gland or mybomian gland tumor. And so these are very aggressive tumors. If you just look at it here, you can see a lot of nucleoli, clump chromatin, mycotic figures. These are very aggressive in these can metastasize. So you don't want to miss this. So if you have a recurrent chelazine, if you have a quote blepharoconjunctivitis, I'm quote really be suspicious and look carefully to make sure you don't miss a sebaceous gland carcinoma. All right. So now my tumor. So this is Moe of the three stuches, not Moe of Moe's surgery. Okay, different Moe. All right. So congenitiva. We're going to talk a little bit about the congenitiva. Of course, what are we seeing right here? All right. So this is a teridium and what is the pathology on a teridium? So you see in the substantial appropriate that little squiggly solar elastosis, it looks like a frayed rubber band that's been left in the sun too long. And so that's that. And then you can also get what's called vasophilic degeneration. Now we're looking at a little different one. What's suspicious about this one? The text at the top of the slide makes me suspicious. Yeah, but what kind of tumor? It looks, it looks thickened, really jelly-like, and I'd be worried for ocular squamous surface neoplasia. All right. And so the difference here between this and a teridium is very important because teridium, the pathology is under the epithelium. The epithelium is usually thin. And so you'll see these vessels and fibrotic tissue. When you look at the surface neoplasms, they have this gelatinous look because the pathology is in the epithelium. And so when you see this gelatinous, kind of translucent look, you want to worry about a tumor. All right. So we're looking at the pathology here. So what would we call this lesion? So I think you would be worried about the abnormal cells kind of threw out. So like a CIN and it would be a very severe version. So what's the most important part of the conjunctival epithelium we look at in these lesions? The basement membrane. Exactly. So if you have a strictly intraepithelial lesion, what we call conjunctival intraepithelial neoplasm or CIN, it's very, very atypical, but it's all in the epithelium. So the epithelium, the basement membrane is completely intact. When we divide these, we divide them into mild, moderate, marked. It depending on how much of the epithelium starting at the basal layer is taken up by the dysplastic cells. So if it's the lower third, it's mild. If it's up to two thirds, it's moderate. If it's more than two thirds, it's marked. So this is full thickness. This is carcinoma in situ. This is CIN. All right. Now we're looking at the substantiate appropriate. Would this be more concerning? I think so. So this would be more along the lines of maybe like a superficial invasive squamous cell. What is that we're looking at here? So those are those somomobodies or some, isn't it? Well, somomobodies look like that, but somomobodies are actually in the meninges. So what are those made of? It's actually keratin. And so you don't think that conchitiva makes keratin, but when it's stimulated enough to become a tumor, it can actually make keratin. So just like squamous cell carcinoma of the lid, you'll see these keratin pearls, keratin worlds. And this has gone beyond the basement membrane in the substantial probe. It's so superficially invasive. And bonus question. How do these spread when they spread? If they've gone, what do you worry about when they start to spread from the lid inward? So metastatic disease. I don't actually know if they spread hematogensically or lithetically. Actually, they spread directly. And when they spread, they go along the nerves. So you really worry, you want to check and make sure there's no areas of anesthesia around the eye. And these can go back along the nerves and go all the way back even into the brain. And so these are the ones you want to treat before they get to this point. All right. What are we seeing right here? We have, again, an external picture of the eye. And what we see in the eye is that there are spots of hyperpigmentation that would be possible, something that's just related to rays like pan. Right. So when you look at this, it's not thick. It's brown. It's flat. It's not irregular. It's not variable pigmentation. And so this is what we call PAM, primary carotonellinosis. But this could also be racial pigment. So you can often see pigment like this in the limbis in people of color. And so this is racial pigment, also same thing. When we look at the pathology, what do we see? Well, basically just pigment that is in the cells. All right. So melanocytes. When there's pigment, there are melanocytes, but they're along the basilar layer and they're not extending up into the epithelium. And so this is PAM and we subdivide PAM into without atypia or with atypia. And so PAM without atypia is like racial pigmentation. It's along the basilar layer with melanocytes benign, not extending into the epithelium, not showing atypical features. Now you may be a little bit more concerned about this lesion. What's concerning here? Here it's much larger. It's diffused. There's some areas of like really dense pigmentation. And there are also some what looks like finger vessels connecting to it. Okay. So you look at the pathology on this one and what do we see in here? Here the melanocytes are kind of spread out about lining up a little bit. It's been memory. You can see some coming up towards like the top of the slide. So I'll be more concerned that it could be like preapolitanic or something. Exactly. So this is now PAM with atypia. And so it's still in the epithelium. It's still kind of an intrepithelium malignancy, but you see that the cells are extending from the basilar layer up into the epithelium and they are atypical. So this is PAM with atypia. The reason that that's important is PAM with atypia is the most common cause of this lesion. And what would this lesion be? Melanoma. Lignant melanoma. So if you see a lesion like this, that's one you're not going to, you know, fudge around with. That's a true malignant melanoma. But malignant melanomas, when you look at them and you see how they arose, about 80% of malignant melanomas arise from preexisting PAM. About 15% from preexisting nevi. So much less from nevi. So PAM is the actor, PAM with atypia that can give rise to malignant melanoma. When we look at the pathology, you see these cells again are definitely malignant. Chromatin, neclioliping, morphism, and some malignant melanoma. You want to remember that it arises from PAM with atypia. All right. And so this is the parthenon on top of the acropolis. They've been rebuilding this now for, you know, 50 years, but they're working on it. The next step that they have to get one whole face, all the marbles is actually in the British Museum, you know, they're called the Elgin marbles. Elgins save them, you know, from those, you know, the Athens where they can't take care of stuff. And so some day the Greek government will sue the British government to get those back and put them on there. All right, cornea. So cornea has layers. What are the layers of the cornea? So there's the epithelium, the fomens layer, the stroma, decimates, and the endothelium. Right, very good. And then just so you're paying attention. And so it could be that. It really is true. So the beginning of the lacy commercials are always blurry. And then at the end when they say the Eye Institute of Utah, you see these pictures of these beautiful mountains in sharp focus. So that's what happens when you have a lacy. All right, so corneal infections. What kind of an infection are we seeing here? Right, so see the dendrite, it's standing in the center where the epithelium is denuded. We put fluorescein dye in and you see it's got these little bulbous outcroppings and that's where the infectious cells are. So this is your classic herpes simplex dendrite. And when you look at the pathology, you see again, it's ulcerated, you've got this lymphocytic infiltrate. But remember, you can sometimes get infiltration deeper too. You can get stromal herpes and you can get almost no more immune reactions. So you need to know that for boards too. What are we seeing here? Very red, angry eye. What would you be concerned about here? Okay, so this turned out to be pseudomonas, particularly nasty bug growing in this guy's contact lens case. So this is a real ophthalmic emergency because these can perforate in 24 to 48 hours, not only from the bacteria which could put out collagenases and proteanases, but the body's immune reaction when those PMNs come in here, they put out material that melts corneas and scars corneas. And so you've got to hit these really hard, really early. Here you can see what happened to this patient's cornea. Perforated, so they're on the other side there. You see where it actually perforated and you see an intense acute inflammatory cell infiltrate. So these are more PMNs and this is the bacterial. So now we're seeing this picture. What's different about this one? Okay, and you see that little halo of infiltrate around it? That's important. So let's say this has been here for three weeks. All right, so we did a scraping on this and what did we find? All right, so this would be consistent with a... Fungal. Fungal, sir. And so usually these patients are more indolent. They'll have some kind of exposure to vegetation. They're farmers, they're out in the yard, they're cutting trees, they're doing something, and they get something in the eye. And so these are a little bit more indolent and these are the fungal keratitis. All right, what do we see in here? What would your worry here be? All right, so you can see that chronic epithelial, you know, denuded area of epithelium, and then that ring infiltrate. So this is a classic picture for Acanthamoeba. And for bonus points, what's the stain we use for Acanthamoeba? Gridley. So gridley stains the cornea green. So gridley green and you see the Acanthamoeba cyst and trophozoides on here. All right, so sorry, with corneas, we have to do our contact lens jokes here. All right, what are we looking at here? This looks like the angle. All right, and what is in the angle? The trabecular mesh work. Trabecular mesh work. So we're going to talk just a little bit about glaucoma here. And so remember, when you look at the angle with your goniomere, you can have a normal angle, open angle, you can have an angle narrowed or closed, you can have an angle recessed or, you know, deformed. And you want to be careful. So what do we see in right here? What's going on with this patient? Yep. So what do you worry about here? I hear about angle closure. Angle closure. So here's a nice slit lamp picture. You see the beam on the cornea and then the beam on the iris. You can see the iris coming forward. So you get a relative pupillary block. The iris bows forward because it had iris bombay. And then it can come forward. It can almost occlude the angle completely here. So this is angle closure. And here we see this is kind of the ultimate angle closure. If we don't take care of it soon enough, what's happened here? Um, iris is touching the cornea. Not only touching, but it's stuck right there, blocking our things. So what do we call that? So when it actually gets stuck beyond touch, it's actually stuck. Three letters. I'm not sure. This is a PAS, peripheral anterior synechia. So synechia means stuck. And so it's a peripheral anterior synechia. So if you don't take care of angle closure right away, you can actually get that iris stuck to the peripheral cornea. So peripheral anterior synechia. All right, so glaucoma. This is what a glaucoma cup looks like. That's hopefully we all wouldn't miss that. That's a big, it's a mild. So it's hard to see the edge of that cup. That's a big 0.9 cup right there. When you look at it, we want to prevent it from getting to this point. And this is the ultimate cup. It's like a Boston bean pot. So you see that the posterior excavation and posterior bowing of the laminar crebrosa. And in fact, it actually excavates a little bit. So those vessels go around the edge and then they disappear when you look at them with your hands. All right, this is on the top of the acropolis. These are the famous five maidens. Unfortunately, the British were a little right about the Greeks because the original statues there have been eaten away by 100 years of air pollution. And so these are actually copies of the original statues. They weren't in good enough shape to put out there. So air pollution can do really bad things to the beautiful, beautiful sandstone. All right, crystalline lens. So this is the crystalline lens. Tell me a little bit about the lens. What are these? You can't see them on there. What holds the lens in place? And then what holds the capsule? Still everybody. Okay, so I always say that this is when the spotlight goes on you, your brain just stops. And so Churchill talked about an iron curtain descending across Europe. We see an iron curtain descending on your cerebral cortex. So when the, when the spotlight hits, it's like chum. And so don't worry, that's normal. So the zonules hold this in place. The capsule surrounds it. Central nucleus cortex around it. All right, so I'm going to talk a little bit about cataracts. What kind of cataract would this one be? Looks like there is like at least a cortical component, but probably nuclear component also. All right, so this is what you'll call an intumescent cortical cataract. And so a white cortical cataract really advanced cortical cataract. This is an advanced nuclear cataract. And so this is what we call a bernessent or brown light nucleus. And so this is a really significant nucleus. This is what you see in the developing world. You don't see it. So, well, we do see it here in parts of Wyoming and Southern Utah, but you do see them here. And so this is a bernessent. This is the end stage of a nucleus. So again, it takes a minute to think about it. Always remember when you're in the OR, it is local anesthesia. So don't talk about the jazz game last night or how you went skiing when the patient is in the room because they hear everything. And when we talk, we always have even voices. We don't get excited. We don't say, don't do that. You know, everything calm because the patient hears all. All right, this is the acropolis at night. Now you're only allowed to go up there one night a year at night. So this is a picture I bought. So I wasn't there that night, but they light up the acropolis at night. It's very pretty. So you see the parthenon on top. Okay, so retina. So again, here we go. Layers. All right, let's start with the first layer on the top closest to the vitreous. The inner fiber layer. You go before that. Internal living memory, then? The inner fiber layer. Yanglein cell layer. Inner plexiform layer. Inner nuclear layer. Outer plexiform. Outer plexiform layer. Outer nuclear layer. And then beyond the outer nuclear layer. Oh, that's an obligatory feeling. All right, so RPE, rods and cones, and then RPE. All right, so layers. Always know the layers. What are we looking at here? I think the macular, the phobia. All right, so even the center of the macular, the phobia. So you see that there's the phobia of depression that allows light to come through without having to go through the entire retina. And what's important here is you see that all of those ganglion cells that link up with those cones in the phobia have to stack up on the side. And so those fibers come obliquely. And that's called what layer? The inner fiber layer. I mean, what's the obliquely layer called specifically? The Henleys layer. Henleys layer. Exactly, Henleys layer. Okay, so retinal vascular disease. What's the most common retinal vascular disease? Heritance of retinopathy. It's usually more common than that in our practice. Dynetic. Dynetic. All right, and they can look very similar. So hypertensive retinopathy, diabetic retinopathy, can look very, very similar. So you can see right here, we've got not heme that's deeper in the retina. We've got flame-shaped heme, which is more superficial in the retina. We've got exudate, which is lipid-rich exudative material leaking out. Okay, what's going on right here? All right, so microannuosomes. The most common thing you see with diabetes What are these? Little cotton wool spots. So cotton wool, because they look like little fluffy pieces of cotton. Because what layer are they in? The nerve fiber layer. All right, so they're in the nerve fiber layer. So they tend to block the retina behind them. When we look at them, they're actually micro-eschemic areas. So you get ischemia of the blood supply to the nerve fiber layer. The gangline cells in that area, then they swell up. And so you get the cotton wool spots. All right, what do we see in here? All right, so this is neovascularization of the disc or NVD. You can have NVE, neovascularization elsewhere. And this looks like medusa. Remember the, from mythology, the snakes come out of the lady's head? So this is neovascularization on the disc. And we need to treat that before this happens. What's happened here? Oh, that's right. It's like a boat-shaped hemorrhage. All right, so why is it boat-shaped? Because it's pre-retinal. Exactly. So it bleeds between the retina and the vitreous, and then it sinks down so you get a flat top and a round bottom. So this is a pre-retinal hemorrhage, boat-shaped. All right, so there's a lot of lacy-cumor in here. Sometimes you watch ball games and you want to just do that right now. Wait a minute, can you see? All right, what's happening here? Gosh, that looks very bloody. Reminds of a big storm, like thunder. I love the names. This is a blood and thunder of fundus, and so what is this? The area. All right, this is central retinal vein occlusion, so backup of blood all over. And when you look at this, you can get, unfortunately, loss and atrophy of the inner two-thirds of the retina. So you can see the outer third of the retina is still intact. Why? Exactly. So when the backup of the retinal of the vein causes damage to about the inner two-thirds, but the outer third stays intact. What are we looking at right here? This looks different. Yeah, so it looks like you have retinal whitening as well as a cherry red spot. All right, what causes that cherry red spot? So the whitening is from axoplasmic edema, and the cherry red spot is the cordial capillaries, your coid. Exactly, so remember the picture we showed of the fovea, the retina pretty much parts in the fovea. So you're seeing a window into the coroidal blood supply, which is still okay. And you're seeing all of the edema of the inner retina from the ischemia caused by the central retinal artery occlusion. It's almost like more like fluffy either cotton wool spot. Yeah, you get the idea. Sometimes the ischemia will almost give you a look of cotton wool on top of it. All right. Yeah, so it actually does look like inferiorly there to the disc because that little fluffy cotton wool look. Okay. Why would I show you this picture? What the heck is this? This is retina artery and vein. Vain? And then there are arteriosclerosis, and this can cause the previously short condition. So you can see all of the lipid built up in that. So that's all those moochies, you know, cheese steaks and crown burgers, all that good stuff we love to eat. And you see that the lumen is getting narrow or narrow or narrow, so it doesn't take much to occlude that. Just a little tiny blood clot or a little piece of cholesterol from your carotid or your aortic arch or somewhere to occlude that. But also the central retinal vein next to it shares a common adventitial sheath when they come into the eye from the optic nerve. And so if you have arteriosclerosis and that big thick artery can push on the vein next to it causing stasis. So really the most common cause of a central retinal vein occlusion is arteriosclerosis because it will push on that vein next to it causing stasis, causing the central vein occlusion. All right, this is what happens when you get a central artery occlusion. You see that the inner two-thirds of the retina are wiped out because you cut off the blood supply but the outer third which gets its blood supply from the coroid is still intact. All right, so this is the Greek parliament. This is the tomb of the unknown soldier. These guys are phenomenal. I stood there for half an hour and I swear this guy didn't blink. So I don't know if he puts contact lenses with fluid reservoirs in them or what, but this guy did not move, not even twitch for a half an hour while he sat there. And when they change guard, it's silent. There's no count, there's no anything. They silently, one guy will march in, two guys will march in and the other two guys will march out. So if you're ever in Athens, watch the changing of the guard. It's pretty cool. You need to get them free for a pair of canons. They must, they must. I think because these guys, I swear, he didn't even blink it. Tourists get right up in their face and take pictures and you guys don't even move. All right, we're going to look at the central part of the macula, age-related macular degeneration. And so you know that, so I'm not going to ask you. So what do we got? Let's see, who did the last one? All right, I think we're, I think we're maybe, Catherine, no it's okay. Close enough. Oh wait, we have her again. With a K. So you see, Drew's in, it looks like yellow, kind of soft. It looks like we're here. So intermediate soft Drew's in, a macular degeneration. Here's the pathology where Drew's in located. Under the RPE. Under the RPE, but in what layer? Technically they're in Brooks because they're under the basement membrane and so technically if you want to really, they want to push it with minutiae. It's kind of intra Brooks, but it's under the RPE. And what happens if we go further along and macular degeneration gets worse? All right, so this is interesting because if you see the center, it's more of a deep red. So that's sub-retinal. If you see around it, it's almost kind of a greenish grayish tint. That's sub-RPE. So it's broken through the RPE and it's sub-retinal, but also sub-RPE. I always wanted the laser to have that sound like Star Wars, you know? So you say, okay, look at the line. You go, meh, meh. I'd love to have them do that. All right, all right. So this is now Delphi. This is where the Oracle was. And so they would, she would sit there and predict the future. And so if she predicted that your city state would do well and win a big battle, then you would come and build a temple in her honor. If she didn't, it didn't matter because you'd be wiped out. So this is where the Oracle sat. All right, optic nerve. Okay, so what stain is this? Great, so you can see there's the optic nerve. It's got columns. You've got the optic nerve sheath, which is equivalent to the dura, the arachnoid subarachnoid, the pia, and then the little columns of axons coming down. And here you see it in cross-section. Again, optic nerve sheath, arachnoid subarachnoid central retinal artery and vein in the middle. All right, so papillodema. Tell me about papillodema. What is that by definition? Okay, that's important because I missed that once when I took words for real because you can't, just because they're swelling doesn't mean it's papillodema. It has to be disc swelling bilateral with secondary two, I should say, increase intracranial pressure. And so when they do oral boards, they'll go, tell me more. And then you go, oh, shoot, got that wrong. So I never say, wrong. They go, oh, tell me more. And then you go, uh-oh. So you guys have that to look forward to. All right, so swollen disc due to increase intracranial pressure. Here you can see the pathology of that. You actually see outward, you know, growth of the nerve or outward swelling of the nerve toward the eye. You see superficial hemorrhages. You can see that the vessels are engorged. And so that's papillodema. So only on television do they have theaters where doctors watch others do surgery. I always love that. I've never seen that in an OR, at least in the U.S. Okay, what do we see in here? It kind of looks like the opposite. Yeah, so these are polar extremes from elevation and swelling to excavation due to severe glaucoma. So kind of opposite extremes. All right, so now we've got a young person here. What do we see in here? Asymmetric red ball. Well, not only is it totting, but you get the idea that there's a fullness there as if that eye is actually being pushed towards you. I realize this has not got depth reception, but you get the idea that something's in there pushing that eye forward. And this is what we found on this child. What is this? Exactly. So that's why I consider it. It can't be the retina back there. So what is this? That would be concerning for like a juvenile astrocytoma, I guess, in kids. Exactly. So they call it an optic nerve glioma, which is really a grade one astrocytoma or juvenile glioma. So you see it's got a fusiform enlargement. It's within the sheath. Slowly enlarge. It's in young people. And when we look at it, what's the classic finding that we see? Rosenthal fiber. This is a synophilic cytoplasmic conclusion that you see in these. So this is a glioma. Children, benign, but can cause damage because it's growing in the optic nerve and grow back even into the optic nerve canal. All right. When we look at this patient, what do we see in here? Yeah. So the right eye, you have some fullness, some subcontractival hemorrhage temporarily. And almost the eye seems to be displaced downwards. Exactly. So you see it looks like it's out and down almost. So again, there's something behind it. And we do the MRI scan. And what do we see here? So the left eye you see posterior to the posterior to the eyeball. It looks like it's, looks like a meningioma to me. Yeah. And what do we call this kind of pattern where you see something around the nerve, not within the nerve? The tram. Just the tram tracks. If you've been up to, you know, snowbird, you're taking the tram up, you know, you'll have the big thing in the middle and you'll have the two cables around it that are going up. And so you'll see the nerve in the center and you'll see this growth around it. So that's the classic appearance of a meningioma, which is the most common optic nerve tumor in adults. And we look at the meningioma, I'll give you a chance to save yourself. What is this? These should have some of them. Somomobodies. Very good. It's a short-term memory. Yeah. All right. So you get these, these concentric calcified areas among the meningothelial cells and they do look like pearls in a squamous cell. They really do. And so these are the somomobodies that are classic for the meningioma, the optic nerve. All right. Now, you guys keep falling asleep. I'm going to put monitors on you. Know that you're falling asleep there. All right. So we just talked about this a week ago. So hopefully your short-term memory is good. Now, we're talking a little bit about retinoblastomas. So what are the two different growth patterns of retinoblastomas? You weren't here last week, so you didn't know. Do you have any? If you don't know, just say don't know. Okay, that's fine. Two patterns? Endophytic and exophytic. All right. So if it grows into the vitreous, it's called endophytic. If it grows under the retina, it's called exophytic. So what would this one be? It looks endophytic. So it's growing into the vitreous, so it's endophytic. All right. And then what's the classic finding that we see in retinoblastoma? You'd see calcium. All right. So that's magenta-colored areas of calcium. And so the tumor grows very rapidly, outgrows its blood supply, becomes necrotic, dies off, and then secondarily calcifies. And so you see these round clumps of viable tumor cells around the vessels, and then they die off, and you get this secondary dystrophic calcification. So last week, we spent a lot of time talking about the differential diagnosis of leukocorya in kids. And so, no, all of those entities we covered last week. I'm sorry, we just don't have time to cover them today. And so, no, all of the different entities that we talked about last week. All right. And what are these? So they're flexor-vintersteiner rosettes. Exactly, flexor-vintersteiner rosettes. And these are the classic rosettes that you see in a differentiated retinoblastoma. How do retinoblastomas spread? All right. So they spread through the optic nerve head. It's very important you remember that. So when these tumors spread, they go out through the optic nerve. And so when we do any nucleation, we want to get a long piece of nerve to make sure there's no tumor left where we cut that nerve off. Nowadays, with the intrarteriochemotherapy, I mean, we're down from six of these a year to one a year. So it's really cut down the nucleations with intrarteriochemotherapy. All right. So after all this, you're going to have to wear earmuffs because all this knowledge is going to pour out of your brain and out your ears. So wear earmuffs to keep that in there. All right. So melanoma, again, we talked about this last week. We know about the different iris melanomas, all the different classifications that we just talked about. But this is a melanoma of the coroid. And what's the classic configuration? Oh, this one's easy because it looks just like it's a mushroom shape. So when they grow through the coroid, they pop through Brooks membrane. Brooks membrane, very elastic, kind of tethers them. And then they grow out under the retina like a mushroom. This is a mushroom-shaped melanoma. And we need to know calendar's classification for coroidal melanomas. What is this one? Spindle A. So technically, people would say this is a neva. Spindle-shaped nucleus, known as Cliali, indus spincidoplasm, Spindle A. What are these? These look more epithelial. Epithelioin. So large, irregular cells, lots of Nucleol I, clump chromatin. In between, you have the Spindle Bs, again, that we went over last week. And then you have the mix. And how do these spread? Those emissarial channels. The emissarial channels. So it's common to be a vortex vein, but it can also spread through the, where arteries or nerves come in and out. But most commonly, it's where the vortex veins that drain the coroid. So they go out. And where does this metastasize to? The liver. So beware the yellow man with the glass eye. Okay. So we're saying goodbye to Delphi. I always wondered why Greeks loved coming to Utah. And then I went to where Delphi is, and that looks like Storm Mountain in Big Cottonwood Canyon. So it looks exactly like this. And that's why they loved coming here. Now, all right. Quick questions for OCAPs in a couple of minutes here. Yes. What's the most common site for metastatic disease? The sebaceous cell carcinoma. The sebaceous cell carcinoma, usually it's a local before it goes in. So oftentimes they'll invade locally into the orbit. They can even go back from the orbit from there. And then metastasize, I'm sorry, I don't know the answer to that. Good question. So I'll do whatever you're attending. Oh, he says, why don't you look that up and report back to us. That's what people always say when you don't know the answer to something. Good question. All right. Well, good luck when you guys do the OCAPs. Remember, they do multiple part questions. And so they'll show you a picture or something. You'll say, aha, my bomean carcinoma. And then they'll say, what's the most common site of metastases? And you go, damn. They ask two part questions just to see how, you know, how much you know. So when you guys take them for the first time, if you've never taken these before, you will walk out thinking you missed 90%. So don't worry, that's normal. Don't worry, that's normal. You come out, you go, oh my God, what did I study for? And so don't worry, you'll think you missed everything. But they grade you against your peers, not against somebody who's had a couple more years training. So that's a key thing is you just have to do as well as your peers. So good luck. Okay. Thank you. You're welcome. Honestly, it is a group test with Rachel Patel.