 So everybody ready for OCAPS? That's the norm. What are OCAPS? Like this weekend? Not this weekend. Okay, so still got another week to get nervous. So for those of you who haven't taken it, do interns take that? You guys take it? No you don't. Okay, so you guys will be the first years that are taking it. Okay, so when you take it, when you walk out, you will think that you missed every single question. So don't worry, that's normal. And you'll be in the middle of it, and you'll say, oh my god, you got no questions right. So don't worry, that's normal. So don't panic. If you absolutely don't know a question, just answer it and move on. So don't panic, don't run out of time. But I'm hoping you guys at least will recognize PATH. So our goal today is to go ahead and just show you pictures quickly. And I want you guys to say, okay, what is that? Just as quick as you can. Because I want you to pretend like you're taking an exam and they're showing you pictures. Sometimes they show you pictures, sometimes they ask you questions. But I want you to hopefully remember what we've talked about the last three months. And hopefully some of that will stick when you're doing the OCAPs. Alright, so first of all, what is the art of pathology? The art of pathology is looking at dead tissue and trying to figure out what's going on with it. Alright, so this is just a nice picture of the... What kind of surgery was this? Martial action. Look further. Why would you say that? You see some lid. Yeah, because you see not only lid, but you see muscle and you see orbital fat. So this was actually an exenteration where you removed the entire orbital contents for whatever reason, for tumor or whatever reason that you do it. But the nice thing is, is you get the entire anatomy of the eye on one slide. This is a beautiful slide. It shows you the entire anatomy and the optic nerve in the back and some extractinal muscles and the lids. So we're going to talk about the lids. Alright, so lids have layers, Brad. What's the outer layer of the lid? Are you talking about the eyelid? Yep, the outer layer. The skin? Alright, skin. And what's the skin made of? Non-charitonized squamous epithelium. Alright, and how is the lid skin different from skin like on the face or the forehead? It doesn't have any, like, subcutaneous fat. Right, so it doesn't have like the dermis that you think of when you think of skin elsewhere in the body. So the lid skin, it's thinner, you've got epithelium, you've got some sub-epithelial tissue, but you don't have the fat and the dermis that you have normally in skin elsewhere in the body. What's the second layer? There's four layers now. So you've got the third one, but that doesn't count. What's the second one? Muscle. Alright, and what's the muscle? Alright, so what are the three different parts of the obicularis muscle? Okay, so you think about there's pre-tarsal, you know, in front of the tarsus, closest to the lid margin, there's preceptile in front of the orbital septum, and then there's the orbital part. So it's got three almost consecutive, you know, C-shaped areas of muscle. So that's the obicularis muscle. And then we already said, Teresa, the third layer was the tarsus. What's in the tarsus? The bomean glands. The bomean glands, you can see them nicely right here. What kind of glands are my bomean glands? Subatius. And what class are sebaceous glands in? That was correct, but what class are sebaceous glands in? Well, there are three basic classes of glands, and all three of them are in the lids. Hologram. Alright, so which one does the bomean glands fit into? Hologram. Alright, so the hologram glands are the mybomian or the sebaceous glands. Mike, what's the innermost layer of the lid? It's conge. Conge, and what's the conge made up of? It's verified squamous and non-charitonized epithelium. Very good. Alright, so now what are we looking at right here? Sean, differential diagnosis. What do we see in here? Alright, so what do the basal cells usually look like? Yeah, so this looks like it's more swollen or sticking out. It doesn't really look ulcerated at this point. What kind of lesions can you have in the lid that are like sticking out? So chelazine, ordeolum, or people will call it a sty. Sometimes even cysts will look like this. What's a good way to tell if that's solid or cystic? Yeah, so you put a fan-off head on next to it and you light it up and you trans-aluminate it and see if it's actually hollow, if it's solid. This is what the pathology on that lesion showed. What do we see in here? What cell is this right here? Giant cell. So we've got some granulomidus inflammation. There's a giant cell. There's some lymphocytes. So kind of a chronic inflammation, but also granulomidus inflammation. And then all these little areas, these little white spots in here are dissolved lipids. So what was this lesion? Which one? Chelazine. Exactly. So you know, ordeolums are actually infectious. They're often a staph infection where chelazia are basically insipid, plug lipid. So the lipid backs up and then it causes this granulomidus inflammation. So chelazine. And I get to show you my travel slides. This is not the original Olympics, which were, you know, in 600 BC, but this is the modern original Olympics. So this was the stadium built in 1896 in Athens for the revival of the Olympic Games. So you can still go out there and kind of jog around on the track, you know. Well, if I were jogging, who would be taking a picture of them? I guess you could say that. No, I don't do jog. I do bike, but I don't do jog. Yeah. All right. So we're going to talk a little bit about some lid tumors. It's always important to recognize those. Sneha, what are we seeing here? Loss of lashes. Where do you think that lesion extends to? What I'm saying is, look at, here's the lesion here. So would you just cut it off here? Look right here. Look, here's that lid all the way out to here, all the way out to here. Thicken. Loss of lashes. Alternative in the center. So what would that most commonly be? Basal cells. So where on the lid are basal cells most commonly seen? Upper or lower? Lower lid and medial canthus. Why? That's where the sun hits. So you don't think about it. Your brow shadows it. And basal cells are really sun induced. And so you don't usually see them as much on the upper lid. You see them lower lid, medial canthus. Here's a classic basal cell. Ulcerated center, raised pearly borders. Loss of lashes. Diffusely thickened. And what's the classic sign of basal cell that we see? Classic finding. So you see the nuclei tend to line up. We call it palisading at each of the edges of the nodules. So you've got palisading of the nuclei. And you can see right there, that's the classic nodular type basal cell. Becca, what is this? Right, so that's the type you need to know about. Especially for boards. What else do we call besides sclerosing? Morpheiform. It is indeed. So morpheiform. So this is the kind of basal cell you want to worry about. Because nodular, nodular cystic basal cells, you can see where they are. And you can see the borders. You can see where you're going to cut them out. The problem with the morpheiform is they send little fingers of tumor cells out. Sometimes along the epithelium, sometimes under the epithelium, and then in between them, you get this scurus, this proliferation of connective tissue. So the problem with the morpheiform is you often cannot see where the borders are. What kind of surgery do you usually have to do with these to make sure you've got them all? Modes. So you want to track every one of those little tiny fingers of tumor cells that are spreading underneath the epithelium. So morpheiform is the most aggressive of the basal cells. Don't worry about it because if you let a morpheiform basal cell grow for 10 years, this is what you get. So this is our classic lady from a little ranch in Nevada. She came in with a morpheiform basal cell 10 years prior. And they said, it's morpheiform. We're going to have to do extensive surgery. She said, I'm an old lady. Leave me alone. And went back to the ranch. Her family finally brought her in because this smelled. And so if you let a basal cell grow for 10 years, it can diffusely infiltrate all kinds of tissue. Usually it doesn't metastasize, but you can see it's eating away her cheek, her nose. This is going through the sinuses. And she actually had CSF every month here. So this could be very extensive if you let it go for 10 years. All right. What do we see in here, Chris? There's some lesion on the upper eyelid. It's gray. It's just a matter of roses. And what's the coloration? Orange or yellow. What would you be concerned about here? Exactly. And if you look, you see the extra keratin on the surface. That little crustiness that's on there. So you'd be more concerned about a squamous cell. What are the classic findings, pathologically, on the squamous cell? So you see these nice pearls here made of keratin. Now you see, you know, the basal cells are basophilic. They're big. They're blue. Whereas the squamous cells, the nuclei is in the center of the cell. It's smaller, but the cytoplasm is pink. So you've got this pink cytoplasm around it. So if they just show you a low power and it's out of focus, you're not sure basal versus squamous. You know, the basal will have all those dark blue nuclei, not much cytoplasm. These will have these smaller nuclei, lots of pink cytoplasm. And the tip-off is these little concentric rings of keratin. So you get these keratin worlds keratin pearls on there. Okay. You're a medical student. Student. Okay. Students don't have to answer these. All right. Marshall. Yeah. So I see a pigmented lesion of the upper lid. There's a little bit of variable coloration. The borders are some of the morphis. It's raised. So your concern would be a more melanoma than a nevus, because exactly it's elevated. It's irregular. It's bumpy and it's darker. And so you'd be concerned about a melanoma. Now, I'm sorry, we don't have time to review all the various nevi for this just one hour. We can't cover 14 hours of stuff in one hour. So know your little nevi. What are the cells that look like in a melanoma? You have lanocytes with nucleoli. You have like pleomorphism. Exactly. So what does pleomorphic mean? Different shapes, multiple shapes. Exactly. In sizes. So here you see some cells larger, smaller, clumped chromatin, little nucleoli in there. So very active looking cells. These guys can metastasize. So they can cause problems, disney metastasize, because the baby boom generation were sun worshipers. We got that golden healthy tan. You know, and so you're seeing a ton of these. These have really exploded in the last 20 years. And so you'll see more and more of those in your career. What do we see in here? So we have a really angry red eye with looks to be like some pretty severe iboglant dysfunction and injection and chemosis, all within the upper lower lip and in the conch. This is your classic. They call this pleforoconjunctivitis. Is there anything there that makes you more nervous? Yeah. The materosis. Look, there's a lash there, a couple there, none here. Look how thick that lid margin is. What would your concern be here? This would be a concern for a sebaceous cell. Exactly. So always worry, sebaceous cells called the great mimicar. And so if you see a chelazion that keeps recurring in the same place, send it for a path. Worry about a possible sebaceous gland. If you see a quote, pleforoconjunctivitis, you know, that's been treated with antibiotics, couple of different antibiotics, antibiotics, steroids, not getting better. Always have a high index of suspicion because these are called the great mimickers. So you don't want to miss my Bohmian gland carcinoma. And, you know, this is the path here. I know it's out of focus. I think one of the fellows took this because it must be out of focus. So what is this thing right here? Not a very good picture. Essentially a mitotic figure. So I know it's a bad-looking mitotic figure. But even at this blurry focus, the next time we get on my Bohmian gland, we'll have to take a better picture of it. Look at these nucleoli. Look at the clumped chromatin. Very aggressive-looking tumor. Indeed, behaves very aggressively. So, again, these can metastasize. You don't want to miss one of these. And I'll often do a picture of one and try to lead you down a path of a chronic pleforoconjunctivitis or just a chelazion. All right, so here we have... Sorry, I love the three Stooges. I know I'm a very sophisticated attending, but there's just something about Stooges' slapstick that hits the spot. All right, congenitiva. What's this lesion called? Finally something that an intern can recognize. Looks like a teridium. Teridium, all right. So you see kind of that triangular or elevated lesion growing out on the cornea. What's the difference between a teridium and a pinguecula? Trigiums and crostalimbas, right? Exactly. So they're the same pathology. It's just pingueculas over the sclera. Trigiums, crostalimbas gone onto the cauldron. What do we see pathologically? What's the hallmark of a teridium? Aestosis. Yes. So see this little kind of a squiggly, frayed rubber band look? The solar aestosis. Here you get some darker blue we call basophilic degeneration. So those are the classic. It's UV-induced. It's been within the palpable fissures, sun-exposed tissue. Does this concern you at all, Allie? It looks more gelatinous and raised in the epithelium. Because remember, teridium now, the pathology of a teridium, the epithelium is either normal or thin. So the pathology is underneath it. It's in the substantial property. If you look here, that gelatinous look to it means that the epithelium here is thickened. So the pathology here is in the epithelium and also maybe underneath it. So your concern would be if it is indeed intraepithelial, you would call this, Cianna, what does that stand for? Not cervical, but same idea. Dental. Exactly. So congenitival or corneal, intra-epithelial neoplasia. And so by definition, it is in the epithelium, the basement membrane is completely intact. When we grade these, we grade it as, how much of the epithelium can get up by atypical squamous cells. So if it's the lower third, we call it mild or grade one. If it's the middle two-thirds, we call it moderate or grade two. If it's more than two-thirds, we call it severe. So this is severe atypical. And those are even wisps of keratin. So this can even start to make keratin. So it'll start to look even dusky and white, kind of a local play kick when you look at it if it becomes a Cian or even a squamous cell. And this is what it looks like if it invades, you know, beyond the basement membrane. So it's gone from a Cian to a true squamous cell. This looks like squamous cell of the lid. It even makes keratin. Here's keratin pearls, keratin worlds, nuclei, clump chromatin. These are all in the substantial propane now. So this has now become invasive squamous cell. Bonus question for anybody. Squamous cell from either the lid or the conge, if it does invade back from the eye, where does it usually track along? Exactly. Perineurals. So that's important. So when they spread, they can often spread along the nerves and go back even back behind the eye, go back into the cavernous sinus, go back toward the brain. So these can invade if you leave them there long enough. What do we see in here, Trisa? There's two pigmented lesions on the conch that are one in the limbis and one on the left side. So this would be, you notice it's flat. It's not irregular. It's not thickened. And so what does Pam stand for? I got her. You're going to have to go, get six feet away from everybody, okay? Sorry, I'm sorry. You have to quarantine you for 14 days. You know, I shouldn't say that's really not a joke now. I mean, this is not being funny. So you look at it and when you look at this, what do you see pathologically if you've got just run-of-the-mill Pam? The melanocytes are on the bottom of the border if they're pigmented or they don't like it anywhere and there's no atypical... Exactly. So this is Pam without atypical. And this is what racial pigmentation looks like also. But nine melanocytes along the basilar layer of the epithelium, no atypical features, no extension into the epithelium. And would this be more concerning? Yeah, it's a little more concerning. It's more regular pigmentation. So your concern here would possibly be Pam with atypical versus melanoma. Versus melanoma, exactly. And so now this is now... Which one? Pam with atypia. So the basomembrane is still intact. Look at these cells. They're bizarre. They're pleomorphic. There's nucleoli. They extend almost full sickness. This is almost like a melanoma in situ. And so this is now Pam with atypical. Why is Pam with atypical important? It can. And so if you look at 100 cases of melanoma of the conge, 80 of them would arise from preexisting Pam. And so that's why it's critical. Now not, you know, 80% of PAMs go to melanoma. But if you have a melanoma, about 80% of them arise from preexisting Pam. So that's a really important thing that you want to follow very, very, very closely. Do you know what the stat is for the other way around? Like what percentage of PAMs will become melanoma? Don't know that stat. I'm sorry. Because the hard thing is you don't know what the denominator would be. And so that's the hard part because you don't know how many PAMs are just out there that haven't been biopsied. But if you truly have a biopsied proven melanoma and you look at the tissue next to it and see where it tried to arise from, 80% of them will be preexisting Pam with atypia. And then is it, so does it de novo? Is the other one, what's the less? They can arise from Nevi. So about 10 to 15% can arise from Nevi. Very few, maybe 5% arise didn't go both. So you guys know about the three percentages that you have to memorize for boards. You know these 15, 45, and 80. So if you think something is rare and you have no idea what the answer is, you say 15. If you say 10, they think you're guessing. So you say 15%. If you think, well, it's moderate, you say 45 because that can cover like from, you know, 35 to 65. And then if you think it's common, you say 80. So if you have no clue, those are the three percentages you have to know. Okay. These are pearls I'm telling you. These are pearls here, okay. All right. So would you be more concerned about this one, Sean? Yeah, that's what you'd be more concerned about. All right. So it's very, very thickened. It's very dark. It's very elevated. And indeed, these cells have now invaded beyond the basement membrane. They are now invading in the sub epithelial, substantial propria. This is now a malignant melanoma of the conch. All right. So this is on top of the Acropolis. This is the Parthenon. And they're slowly rebuilding. And every time I go to Greece every four or five years or so, they've got a new little chunk of it built. The Greek government is now suing the British Museum to try to get the Elgin marbles back. So Elgin was a British guy at the turn of the century. And, you know, the Greeks were, couldn't take care of this stuff. It was all decaying. So he saved it. So he took one entire wall of the top of the Parthenon and took it to the British Museum. So if you want to see the one wall, you go to the British Museum, and so they're trying to sue to get it back. So see if Brexit allows the Greeks to get back the Parthenon here. All right. Cornea. Tell us about the pathology of the cornea, Sneha. Yep. Top layer. All right. Second layer. Middle. And then the feeling. Okay. Which of these layers is PIS positive? Decimase. Decimase. Remember, bowman's is not a basement membrane. Bowman's is just condensed stroma. So bowman's, if you get a ulceration or bowman's gets damaged, it does not regrow. Decimase is a basement membrane. So if decimase breaks or ruptures, and the other cells can slide over and start laying down new decimase. So did you ever notice that? Think about it. It's really true. There are some commercials for Lasik, and they're all kind of blurry. What are you blurry? Do I need a Lasik? All right. So corneal infections. Becco, what do we see in here? It's like an end rate. Yes. You see the staining in the center of fluorescein, the raised bulbous ones. And so what's the most common cause of this? Exactly. So the answer to every question that a cornea person asks, he said, well, could be herpes. And so they say, which one? Well, likely simplex, but could be zoster. So most commonly simplex will give you the classic, you know, bulbous ends on there. But zoster can sometimes give you dendrites also. So remember that can be there too, but they'll have other findings, you know, the skin and the lids and all. When we look at it, you see the classic ulceration. That's where the fluorescein stains and then the kind of raised edges here. Now, if you were to do a swap to try to get it this way, where would you swap it? Exactly. So the middle where all that fluorescein staining is, that's where you've lost the epithelium. And so you've already sloughed it up there. So you want to go next to that when you want to get a swap to try to get a positive culture for herpes. All right. What do we see in here, Chris? It looks like something infectious, probably an ulcer. All right. To be concerned now, more than a virus, this would be a bacterius. Bacterius. This is a corneal ulcer. And here you see the pathology. What's happened to this cornea? Yeah. So look, here's the spot of perforation. So you can see the problem is, is those bacteria themselves, especially gram-negative bacteria, can elude things that melt proteins and they elude collagenases and proteanases. But also the body's immune system, when these PMNs come in here, they dump all kinds of things in there until the bacteria, which then kills the stroma, too. So that's why these are an emergency. You can melt, a pseudomonas can melt a cornea in 48 hours to the point of perforation. So these are truly ophthalmic emergencies. So you want to not miss a corneal ulcer. All right. What do we see in here, Marshall? So you see the cornea with, what looks like an ulcer in the center, a lot of countertile injection around it. Seems to be some stromal haze. It's a little halo of stromal haze. So what do you think this could be? Another kind of corneal ulcer could be, bacteria could be fungal, depending on. So when you see the haze here around there, often that's a tip off to fungal. And of course the history is important. History, they may say, yeah, this has been here for a week, it's getting worse. What were you doing? Ah, I was chopping down trees in the yard, punting bushes out on the farm, something. So there's usually a vegetative exposure. And what kind of stain do you do to look for this? GMS. GMS. And so what does that stem for? You have mori, smethal, silver. Close, because it's comorium, methenamine, silver. But the reason I want to know that is because silver, it kind of stains the fungi, silvery black. So that's how you remember it. Comorium methenamine silver, it stains them silvery black. So that stains the fungal elements. All right, Brad, what do we see in here? So, see the cornea, once again there's some haze. It looks to be like a ring infiltrate with essential epithelial defect. So, be more concerned here for like acanthamoeba. Exactly. So here's the little beasties. What stain do we use for acanthamoeba? Gridley. Gridley. So here's these acanthamoeba cysts. And a trophozoite there. And so this is acanthamoeba. And what's the classic history with these? It's like a non-healing. It can start off as kind of like this, like chronic non-healing, maybe infection. You treat them for herpes, keratitis. Exactly. So that's the thing. These are often misdiagnosed for herpes. And so people will treat them with herpes. But now remember, herpes, the cornea often gets anesthetic. You know, you don't really feel it as much. Whereas when you get these acanthamoeba, they can do perineural spread. And so they can hurt. So they'll have pain. So you want to get them early. If they've invaded beyond the cornea into the sclera, these are really difficult to eradicate. So you want to recognize these and treat them early. Sorry. Keep something interesting here. All right. What tissue are we looking at right here called? The angolin. What lives in the angle? What is this triangle right here called? Trabecular mesh work. And so this shows you nicely. Trabecular mesh work triangular. The apex is up here in the cornea. The base is down here with the scleral spur coming in and triangular shaped. And so they will often put on boards gonioscopic pictures. So you've really got to know what the anatomy is like. Sometimes they're not blatant. Like you'd hope they would have a totally closed angle or an angle that's way open and you're looking at syllabi, but sometimes there'll be some subtle in-betweens. And so know what your anatomy looks like because if you're looking at it with agonium here. And of course this is a crude schematic, but just to show you the difference between a closed angle and angle recession dramatically. And so when you look in with agonium here, they'll sometimes give you pictures to tell. Allie, what's going on here with this patient? Exactly. So you worry here by angle closure. Here's a normal pupil. This is kind of mid-dilated. It doesn't react really well. It's painful. It's injected. And then you look with your slit lamp mirror and sure enough that's called Iris Bombay, B-O-M-B-E, with an accent, a goo, an accent, a goo, Bombay. So you've got this forward bowing of this. And so what happens is you get a relative pupil area block. The chamber is narrow to begin with so they're predisposed. And then you get this forward bowing of the iris. So you can get angle closure, which can then lead to glaucoma. Now what happens if you don't treat this right away, you can actually get apposition of the peripheral iris to blocking off the angle to the cornea. What do we call that, Teresa? Yes. And that stands for peripheral anterior synechium. What's the other kind of synechia that can happen that can cause iris bombay? Exactly. What do we call that kind of synechium? It's a posterior synechia. So as Winston Churchill said, when you shine the light on you, this iron curtain descends in front of your cerebral cortex. What's your name? Oh, I know it. I know it all. I know my name. It's coming. And so it's just something about a spotlight that makes the brain just stop working at all. So a posterior synechia, where you get adherence of the pupil border to the lens behind it, and then give you a pupil area block, and then it can move forward, too. All right, so glaucoma. Obviously, I wanted to show you a picture of a cup. Sometimes glaucoma is difficult at a patient who's myopic, because we like to do now neurofibrillator OCTs and look for thinning, but myopia screws it up, because myopia can affect the nerve fibers as they go across here. It can affect the visual field also. So always keep in mind, look at this one. Look at those vessels diving in. That's a big glaucoma disk. And this is an end stage. And so we want to prevent it from getting to this. And so you can see the vessels actually diving underneath it, even excavate. So we call this a beam pot. So total, total, total glaucoma optic nerve. All right, this is also on top of the acropolis. These are the five maidens that sit here. Unfortunately, you know, a hundred years of air pollution in Greece has eaten them away. So these are actually copies. So the original ones just got eaten away. So maybe Elgin was right. Maybe it should have taken all the marble away. But these are copies made. These are all maidens here. The acropolis is pretty cool because it's really up high. So you can look all over Athens and see it. All right, lens. A little bit about the lens. And this just shows you again the pathology of the lens. Nucleus, cortex, lens bow, capsule. All right, cataracts. Various different types of cataracts. Mike, what kind of cataract is this? What color are nuclear cataracts usually? Yeah, more like brown, orange, yellow. This is more white. So what are cataracts? Cortical. So this is an advanced cortical. This would be almost an intimesin, an advanced cortical cataract. But you know the most common cataracts we see are nuclear. This is the ultimate nuclear cataract. Sean, what is this? This is brunessen, brown-like. So these can turn brown even almost black in the third world. So this is a dense, you know, brown-black cataract. And so the ultimate cataract is where you have a dense, dense nucleus, the side of, I mean the cortex turns to liquid and then the nucleus sinks down. What kind do we call that? Weird one. Sneha, do you remember? Morgagnon, exactly. So sometimes the ultimate cataract, the cortex will liquefy. The dense nucleus will sink down morgagnon. But this is a dense, brunessen, end-stage nucleus. All right, so remember, patients hear everything when you're in surgery. And so we all have a tendency to say, wow, did you see that jazz game last night? Oh, what do you think of this corona? And the patient's sitting there. They hear all of this. And so it really doesn't engender their confidence if we're bs-ing about something while we're operating on their eyes. So we always don't talk about anything beside their eye when we're in surgery because they hear everything. In fact, I kept hearing one. When you guys are second-years, you have a tendency early on to always come off the pedal. And so you're in a position where it claps. It says, position one, position one, position one. And this patient the next day said, doctor, what is this position one? You know, she's very confused by that. So they hear everything. So be careful what you say. Here's the acropolis at night. You're only allowed up there one night a year. And so I had to borrow this picture, but you can go up one night a year and climb around it. All right, so retina. So again, we've pounded these layers of the retina. Let's get closer to the vitreates. First, IOL internal limiting membrane. Chris, nerve fiber layer. Marshall, ganglion cell layer. Brad, interplexiform layer. Interplexiform layer. Cole, internuclear layer. Alley, outer plexiform layer. Thresa, outer nuclear layer. Mike, photoreceptor. Rods and combs. Rods are the short fat guys. Cones are the long skinning guys. All right, so photon of light goes through the cornea, through the lens, through the vitreous, hits these fibers here, starts an electrical signal. So where do these rods and cones synapse? Who do they synapse to? Right, so the cell bodies are in the outer nuclear layer and then they synapse in this outer plexiform layer. What do they synapse to? Nope, it's one in between. Bipolar cells, so these ganglion, these outer nuclear cells, the rods and cones, they synapse to a bipolar cell here. Sneha, what do the bipolar cells synapse to? The ganglion cell, okay. Becca, the ganglion cell sends that axon out. Where does it synapse? Lateral geniculate body. So it goes all the way through the optic nerve head, the creation, the chiasm, and then back to the lateral geniculate body. So remember that. Chris, what are the other cells in this inner nuclear layer beside the bipolar cell? Amicron? Sorry, since we're doing one on these anyway. Marshall. Wait, save your, save your on that one. Bipolar, there's amicron, there's two more. Maybe some microglial cells. What's the name of the microglial cell? The microglial cell, it's partially correct. It's called a Mueller cell. So there's a Mueller cell. What's the final one? This is in the inner nuclear layer. Bipolar's in there, that's already been said. Amicron, Mueller. Horizontal. Horizontal cells. Becca's back there trying to help you. The other thing is when the spotlight's not on you, you always know the answer. So you always know the answer when the spotlight's on there again. So also the horizontal cells live in there too. All right, what part are we looking at here called? Fovia. So you look at the fovea, it really parts. And then you have just the outer nuclear layer and almost all cones here in the fovea. Now adjacent to the fovea, you've got all these ganglion cells stacked up here. All this area right here, this layer. Well, I mean the layer here where the axons are starting to go horizontally instead of vertically. Henley's layer, exactly. So how do we tell the macula from the peripheral retina? Multiple. So the ganglion cell layer and the periphery just one cell layer thick. You have 100 rods maybe pumping into that. But in the center of the fovea, one cone goes to one ganglion cell. So all those ganglion cells stack up adjacent to the fovea. So by definition, to a pathologist, the macula is the area where the ganglion cells are more than one cell layer thick. All right, retinal vascular diseases. Teresa, what do you think is going on with this patient? My pretension or both. So what do you see here that tells you that? It exudates cotton wool spots and hemorrhages as well. Exactly. So flame hemorrhages, dot blot hemorrhages, hard exudates, cotton wool spots. So this is a diabetic, pre-proliferative diabetic. So the most common early finding is you get these little microannurisms, which can then lead to macroannurisms, can then lead to edema. And here we have these little cotton wool spots. Mike, what's a cotton wool spot? Exactly. So superficial infarction. Here's the swollen nerve fiber layer. And so when you look at them, they look like little wisps of cotton on top of the retina. So it kind of obscures the tissue underneath it. What's happening here, Sean? All right. So the so-called NVD, neovascularization of the disc, the Medusa's head, all these little snakes in here. So neovascularization of the disc. And what can happen, Sneha, if we don't treat that? Boat shape. So this is pre-retinal, kind of between the retina and the vitreous, flat due to gravity, and then this boat shape underneath it. So you've really got to treat it before it gets to this point. So this is sometime what you wish you could do at a ball game, you know? We used to take glasses in games, you know, when you're in college and the referee's in here. Have these glasses so you can see. All right. What the heck is this, Becca? Blood and thunder. So what causes blood and thunder? All right. So central retinal vein occlusion, CRVO. And here you can see you've got blood backed up. You get some atrophy, especially of the interlayers of the retina. Chris, why is this picture different? So what would this be? Central retinal artery occlusion. How do you get the cherry red spot? Yeah. So remember that picture we showed of how the retina really thins out over the phobia. So this is actually still intact. Corital circulation showing through that. Swollen ischemic white retina. So the cherry red spot. Why would I show this picture, Marshall? Show the vessels are thickened. Sclerotic. Which vessel? The one on the left. Which is that? 50-50 chance here. I guess it's the central retinal. There's the central retinal vein. Right there. What is this? Central retinal artery. Central retinal artery. So remember, when they're coming into the optic nerve head, the artery in the vein share a common adventitial sheet. So here's an artery. All that lipid in here, all those cheeseburgers and moochies and everything in there, narrowed lumen. And so arterial sclerosis can push on the vein next to it and cause stasis. So arterial sclerosis puts you at risk for central retinal artery occlusion but also for vein occlusion because they come into the optic nerve together. And this is a central retinal artery occlusion. It wipes out the inner two-thirds of the retina. The outer third of the retina gets its blood supply from the ciliary artery. Well, from the core, basically. So that's why that stays intact. This is the Greek Parliament building. And that's the honorary guard. And so I always say, I stood there and looked at this guy for five minutes. He never blinked. So I don't know if they put in like bandage contacts or what, but this guy didn't move. He didn't even blink for the whole time I was watching him. All right. So macular degeneration. What is the hallmark here? Druzen. Druzen. So here's the Druzen you see under there. What is a Druzen? It is lipofusion in between the layers of the RPE and Brooks. Exactly. So here's Brooks membrane. It's sub-RPE. And you get this deposition of this waist-like material. There's a lot of lipofusion in it. There can be some pigment in it. A lot of waste material building up. What's happening here, Carl? You see some, looks like sub-retinal fluid as well as components of acidity. So what do you think happened here? The evascularization and then sub-retinal hemorrhage that ended up passed in through. So you can see this is sub-retinal hemorrhage. This is actually sub-RPE hemorrhage still at this point because you see it's kind of gray-green. And then it breaks through under the retina. It's still under the retina here. So this is macular degeneration wet. Sub-retinal meal. I always wanted that. You know that sound effect before you do a laser when you're in the clinic. All right. Now this is Delphi. This is where the oracle lived. So she would predict things. And so I don't know. My prediction is really hazy on how you guys are going to do on OCAP. So please sharpen up that prediction for me. Okay. All right. Optic nerve. And this is a normal nerve. We want to show you the lamina crebrosa, the normal fibers of the optic nerve. Here's the cross-section. Artery vein. All right. Well, obviously you said what this is. So, Allie, how do we tell Papalodema when we look at it? The disc margins are blur elevated. Elevated. Vessels are kind of engorged. Gorge vessels and? Flame hemorrhage there. Even get little flame hemorrhages. Now Papalodema, by definition, what does that mean? It's due to itching. Exactly. So if they ask you a question on boards, not all swollen discs are Papalodema. By definition, Papalodema is swollen disc secondary increase intracranial pressure. So there could be other reasons for Papalodema. Here you see the swollen disc, dilated vessels, hemorrhage on the surface. So I love on television, there's always like a gallery when you're looking at the operating room. I've never been in an OR where there's a gallery in it. But on TV, they always have to have a gallery where you can look at it. All right, so this is an optic nerve, the opposite of Papalodema. This is a severely cupped optic nerve. It's opposite. All right. What's going on with this kiddo? Here, Theresa. Look, there's some anus aquariums and ptosis from the left. And also if you look at it, it's almost like that. Right. Eye is fuller though. That eye is also pushing out at you. It's proptotic. And then we look and sure enough, this was the lesion. What do we worry about in kids that can affect the optic nerve? Which one in kids? Gliomas. This is an optic nerve glioma. It's a grade one or juvenile astrocytic pilocercoma. And this is a, what is the classic path finding? Somomobody. Somomobody. So this isentophyll-extaining body in the cytoplasm. Somomobody. Not somomobody. Perfect. What's it called? Not somomobody. Sorry. You almost got me moving here. Wait. Somomobodies are a meningioma. Yeah. What is this one? The spotlight is so bright today. I know that. Shoot. Anybody? Rosenthal. Rosenthal fibers. Okay. Very good. That's all right. Rosenthal fiber. Elderly person. Proptosis. What would you be concerned about here, Mike? The meningioma. So when you look at the MRI scan, what's the classic finding? Tram tract. So it's not intrinsic to the nerve. It's around the nerve. And so you'll often see thick meninges around the nerve, like a tram tract. And then, of course, we already said, what are these? Somomobodies. And so you can see that the proliferating meningothelia cells often look like squamous cells. Pink cytoplasm, smaller nuclei. But then they get, I like to think of these. They're almost like the world you see of keratin. Except this is more calcified and other materials in it. But somomobodies are classic for meningioma. All right. We are almost there. All right. So I'm going to wire you guys up. So when you're sleeping here, you know, you'll get buzzed. All right. Retinoblastoma. We just talked about this a week ago. So what's the classic pathologic finding here, Sean? Yeah. Necrosis. Calcium. So viable cells surrounding a vessel, then they die off dystrophic calcification, necrosis. And what is this? Lexner wintersteiner rosette. All right. How do they spread, Sneha? Optic nerve extension. So very important that you look at that peripheral optic nerve when you're looking at a potential retinoblastoma. So all right. Now remember, you guys have to wear earplugs after this so that all this information doesn't like pour out of your brain and out your ears. So your brain is getting full now. Okay. Lignant melanoma. What is the classic configuration that you'll see with cordal melanomas? Mushroom shape. So breaks through Brooks' membrane, grows underneath the retin and a mushroom shape. What are the classification here? Who was the one who described the classification we use for malignant melanomas of the cori? Calendar. Calendar. So calendar classification. What is this one? A spindle cell. More specific. No, those are irises. I remember. So this is spindle. There's two spindles. Well, spindle. Spindle A. All right. So spindle. You get spindle A. Spindle-shaped nucleus, no nucleoli, indistinct cytoplasm. You could get spindle B. Cigar shape, brown, single cytoplasm, or single nucleolus. Brad, what is this type? Epithelioid. Epithelioid. So you have spindle A, which maybe is not a melanoma. Spindle B, mixed, and then epithelioid. So this is epithelioid. Large, bizarre cells, multiple cells, multiple nuclei, multiple nucleoli. And how do they spread coal? Or emissarial channels? I mean, vortex veins are the most common, but they can even spread out of channels where arteries or nerves are coming in through the sclera. So that's how they spread. And where do they go when they spread? Liver. Exactly. All right. So here's Delphi again. So again, here's where the oracle used to sit. So, you know, I wondered, Greeks loved to have picnics up in Big Cottonwood Canyon. And then I drove up to Delphi once when I was in Athens, and it looks like Storm Mountain. So now I know why the Greeks love that place. It looks like home. So this is the oracle of Delphi. All right. Enough. Good luck on boards.