 Dead tissue. Sorry, I keep getting these these things on you. Alright, so what we're going to do, we're going to go ahead and we're going to start with your lid and we're just going to work our way all the way through to ocular tumors. And so, you know, when we're looking at the eye here, this is an exeneration specimen and it's a good specimen because it's got the lids, it's got the entire globe, it's got the optic nerve, but it's also got extracurricular muscles and fat on it. So it's a good way of looking at things. So we're going to start with the eyelid. Alright now, I don't know who the first Moran is. The first person on here has got the Moran starfish. I don't know who that is. It's me. Alright, just Marshall? Yep. Okay, Marshall, tell me the layers of the eyelid. Outer layer. Marshall, you're muted. You gotta unmute yourself, please. Sorry about that. Outer layer. Skin. Okay, under that. You have subcutaneous fat and some areas and other areas just right to tarsus. Alright, what's in between? There's another layer in between. I don't know. I guess I'm blanking on it. It's the obicularis oculi muscle. Oh, yes. And then you said tarsus. What lives in the tarsus? Got like sebaceous glands. Alright, and what are the sebaceous glands called? Glands of Zeiss. How about the main ones? Mold? Nope, the main ones. All these guys right here. I'm not sure. My bomean. Oh, okay. Yeah. And then the innermost layer? Conge. Conge. Alright, very good. So always keep in mind the layers. So we're going to just go through just looking at pictures and seeing if we can do quick recognition. Catherine, you're next on the list. What are we seeing here? So, yeah, it looks like this elevated kind of red bump in the middle of the eyelid. It doesn't look like there's loss of lashes, but definitely look like there's some kind of focal inflammation. Okay, what's your differential here? So it could be a chelazion. Could also be maybe less likely depending if it's recurrent like a sebaceous cell personoma. Could also be some kind of squamous or basal cell. Okay, so always keep a tumor in the back of your mind, but when you see something like this, it's swollen, it's tender, it's hot, it's angry. Let's say we biopsy it, and this is what the pathology shows. What are we looking at here? So it looks like there's a lot of inflammatory cells, and then kind of to the left, there's a giant cell. All right, so there's a nice giant cell there, and we can see these are, what kind of cell is that right there? Neutrophil? No, wait, wait. Nope, we'll get it closer. A lymphocyte? Well, kind of a lymphocyte. What kind of a lymphocyte? There's another one there, there's another one right here. Is it a macrophage? These are plasma cells. Oh, dang it. So kind of a lymphocyte. Plasma cells, a lymphocyte. So what's the diagnosis here? This is a chelazion. Chelazion, exactly. So chelazion, inspisated lipid from one of the Myromian glands, and then the lipid causes a granulomotor reaction, but also a chronic inflammatory reaction. So when you see giant cells, lymphocytes, plasma cells, this is a chelazion. All right, this is the original, well, not the original, the modern original Olympic Stadium in Athens from 1896. All right, what do we see in here? I guess I'm going down the list, Jordan. I see your name on here. Unmute, tell me what you're seeing here. Yeah, so I'm seeing ulcerated lesion on the lower lid. So like differential for this would, I think primarily be like a squamous cell carcinoma, but there maybe it's like a little bit of like telangiectasia, a little bit of perleborus, so it could also be like a basal cell that has like an ulcerated center. Or it's just kind of like an inflammatory lesion. Like we just talked about like a chelazion or a sty like post rupture. Do you see loss of lashes if you've got a chelazion, post rupture? Oh, no, I didn't notice that. Yes, I do see loss. Yeah, so key thing to look at here, loss of lashes. And here's the lesion here, but if you look, look at the thickening there and there. If you had to guess between a squamous cell and a basal cell and you had no idea, what would the odds tell you? I'd go with squamous cell just based on the ulceration. Okay, so if you're looking at lid tumors and you look at 100 lid tumors, 90 of them are going to be basal cells where maybe five or six of them are going to be squamous cells. So in that sense, your odds are going to be that this is a basal cell. Okay. And so always go by the odds. The odds are it's a basal cell. So we look at the pathology. What does it tell us? Okay, so you kind of, so you kind of have these, I don't know exactly what to like, it's not like an inclusion body, but you kind of have these like worlds of epithelium. It looks like epithelial cells surrounding these like kind of circular clusters of basal skin cells. So if you look at these cells exactly, they've got the appearance of basal cells, but what I'm pointing out here is the cells tend to line up at the periphery of these little nodules and we call this palisading. And so what is this a sign of? I'm actually not entirely sure. This is a basal cell. And so basal cell carcinomas have these basilar type cells, they have a large nucleus that not, not quite as prominent side of plasma, basal functioning nucleus, and you get lining up of the nuclei around the edges of the nodules. And then now there's a type of basal cell that is important to know about because these behave a little bit differently than the run of the mill basal cells. Chance to save yourself. What are we seeing right here? Okay. So we see, I see keratin kind of layer at the top. I'm honestly not sure either. Right. So if you see this pattern, you see little fingers of tumors here and the fingers of tumors are interspersed with dense connective tissue in between them. So this is still a basal cell, but this is what we call a morphiform basal cell. And the reason that these are important is that these tend to send little fingers out, almost in a little pageatoid pattern into the subcuticular tissue. So it's very difficult to see where these end as opposed to the nodular type basal cells, where you can see where that is. So this is a morphiform type basal cell, difficult to see the margins. These often require Mohs surgery to go ahead and to make sure you remove them all out. This is what happens when you leave a morphiform basal cell alone for 10 years. And you can see even though basal cells don't metastasize, you can get tremendous local tissue growth if you leave it alone for 10 years. All right. I'm going down the list. Abby, what do we see in here? Go ahead and unmute yourself. It's hard to hear you. Well, you can't hear you, Abby. I don't know if you have speakers or I mean, you have a headset or mic or something. All I hear is just a faint echo. Okay. Is this better? Oh, much better. Okay. So upper eyelid nodule that is kind of orange in color. It's hard to say if there are lash loss or not, but it seems like it may be there, but displaced. So similar differentials as before for an eyelid nodule. So it could be sebaceous cell, it could be a chelazion basal cell. Okay. So eyelid tumor now, the orangish tint to it and that little kind of a thickened, really keratinized look on the surface. And we look at the tumor and the tumor has these kind of cells. So what kind of tumor is this? You see those whirls, like the pearls there. So I would say swim missile. Exactly. So these whirls are keratinized epithelium. And the cells here have a large pink cytoplasm as opposed to the basal cell with the smaller cytoplasm. But you see they're active. There's nucleoli here. There's nucleoli all over. The cells are bigger, some are smaller. You get these whirls of keratin. So this is a squamous cell now. Squamous cell carcinoma. All right, Tyler, I'm just going down my list. What do we see in here? So we have a external photograph of a right eye, upper eyelid pigmented vision that looks like you have corresponding loss of lashes. I would be concerned of a malignant melanoma. Okay. So your concern is always just what you said. When you see a lesion that's irregular thickening, it's got variable coloration, some brown, some black, it's got loss of lashes. You really want to be concerned about a malignant melanoma in this case. And we look at the pathology and does that confirm it? Correct. Yes, it does. You have mitotic figures. You have nucleoli. You have the melanosomes or melanocytes, I believe they are kind of interspersed. So not just along the basal layer. Now, don't be put off by the fact that this is not pigmented because oftentimes, when you look at pathology, not all of the cells in a melanoma are heavily pigmented. So this is indeed a malignant melanoma. And we worry about these because these can metastasize. And so very important that you remove these completely from the lid. All right, now let's see we go back. Next is Allie. Allie, go ahead and unmute yourself and tell me what you're looking at here. So we have an external photograph really injected conch, but really also thickened eyelid margins with loss of lashes on superior aspect. I'd be concerned about a spacious cell in this. Exactly. So look at that diffuse thickening of that lid, loss of lashes, that yellowish coloration to it. And oftentimes, these are misdiagnosed as what people will call blepharoconjunctivitis. They'll treat it with antibiotics. They'll treat it with antibiotic steroids. But this is more than that because look at that diffuse thickening. And I mean, this is really a widespread tumor. And you look at this, and I think Sam must have taken this picture because it's out of focus. And so one of my fellows took this. And so the key thing I wanted to show here is look how active these tumors are. So this is a tumor where how the tumor looks on the pathology really portrays how it behaves. And it's very aggressive. And these little spaces here, Allie, what are these little spaces through here? Go ahead and unmute yourself again. Is that lipid? That's lipid. And so remember, lipid dissolves when we process the specimens. And so you leave all these empty spaces. So this has a lot of lipid in it. So this is a trucebaceous carcinoma. Again, these can metastasize. These can be very difficult to treat. All right, so this is Moe the stooge, not Moe the surgeon, by the way. All right, so now we're going to talk about congenitiva. Sam, unmute yourself. What are the major parts of the congenitiva here? So this is starting from the limbis. We have the bulbaric congenitiva in the forenex, and then the palpebral congenitiva. All right, so we've got bulbar on the bulb, the forenex, and the palpebral. So what's the most common lesion we see in the path lab of congenitiva? Turidium. Turidium. All right, and you can see the elevated triangular vascularized lesion growing onto the cornea. And what is the pathology of a turidium? So we usually see most commonly solar elastosis and then basophilic degeneration as well. All right, so this is sun induced solar elastosis, basophilic degeneration, epithelium, usually thicker, thin in these lesions. Yeah, usually thin. Thin. All right, good. All right, what are we looking at here? Whoever's the next Moran star that doesn't have a name on it? Dr. Mamelis, could you point out what's the difference between basophilic degeneration and solar elastosis? Basophilic degeneration is this much mushy, smudgy, blue-gray stuff here where the solar elastosis is the squiggly, frayed rubber band look. Gotcha. Well, you see these little squiggly frays here, whereas here you have this smudgy, darker staining stuff. That's the basophilic degeneration. Gotcha, thank you. All right, so I want to look at this picture now. Who's the next Moran star? I don't have a name under it, above Jordan's. Is that still Marshall? I think it's just me. Okay. Yeah, so here you see a gelatinous lesion emanating from the conjectiva that extends onto the cornea. So I worry about some kind of like CIN or a conjectival scrimmous carcinoma. Now, all right, so the important thing, and I apologize for some reason, yours bumped up a couple I haven't pimped yet, so I'll come back. You'll get credit for this. So when you look right here, you can see that the gelatinous look to this, where it's not a pteridium, where you've got subepithelial thickening and you've got blood vessels and fibrous tissue. Here you've got this gelatinous look to the epithelium, and it's growing out onto the surface of the cornea. So here would be concerned about more a tumor involving the, involving the epithelium on the surface. And we look at it right here, what do we see in here? Still Marshall, sorry, because you'll get credit for this though. Looks like you've got epithelium that's really thickened and disorganized. Okay, so if you look real carefully here, you see, again, nucleoli through here, you've got different sizes and shapes, pleomorphism. What's the most important layer to look at when you see a lesion like this? The basal layer. All right, so if you're looking at the basal layer and you look at it right here, what do you see when you're looking here? So it looks to me like they're atypical cells extending throughout the entire epithelium into the basal layer, and you can see some cells that have nucleoli right at the right at the basement membrane. So this is pretty much full thickness from the basement membrane all the way to the top, but the basement membrane is still intact. So what would we call this lesion? CIN. CIN, and how do we grade CIN? I forget if it's like mile, it's like one, two, or three ends based on how like what, like if it's one, third, two, third, or full thickness. Exactly. So you start at the basal layer, 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. But by definition, CIN is intraepithelial, so you don't have extension beyond the epithelium. All right, now this shows what it looks like right here. You see almost like squamous cell of the skin. This is now an invasive squamous cell. It's beyond the basement membrane, large cells, distinct nuclei, keratin pearls, and so this is a CIN that's gone on to form a frank invasive squamous cell carcinoma of the congenitiva. All right, so Sally, I'd skipped you previously. Sally, go ahead and unmute and tell me what this is. Thank you. I'm seeing on the congenitiva some like pigmented both nasolian and temporally. Anything alarming with that pigmentation? Kind of. I'm seeing like the color seems pretty regular. The border is not though. It doesn't really have, it's pretty flat. So I'm not quite sure. All right, so this doesn't have alarming features in that. It looks flat. There's just that little tan dusting on there, just that little tan dusting that's on there. So let me go ahead and we go to the next one. Right, I'm sorry. My screen is frozen here. Let me see. There it goes. Okay. What do we see here on the pathology? So this is showing some pigmented melanocytes at the bottom layer of the epidillium. Okay, so what would we call this? What would we call this lesion? I think this is sister like racial melanosis. Well, that's racial melanotion fits under this category, but what is the category? This is a PAM. What does that stand for? Primary acquired melanosis. Okay, and how do we categorize that? With or without ATP. Exactly. So what would this one be? This one. There's some, I see some, well words are escaping me today, the chromosome in the epidillial cells. Well, let's pretend that this is only along the basilar layer for purposes of teaching. Okay. So that would be then without ATP. Exactly. So you can get PAM without ATP, which is like racial melanosis. You can get PAM with ATP where you get atypical cells extending up into the epithelium. And the reason why we worry about PAM with ATP is it can sometimes extend into something a little bit more worrisome. So, Sean, I see you've joined us here. Good evening. Go ahead and unmute. Tell me what you're seeing here. Yeah. So here I see, you know, external photo. There is some pigmentation of the conjunctiva, but it also looks like it is extending into the corneal stroma. And it also looks like there's a prominent vessel feeding into it. So it's actually, this is still superficial, but if you look at it, it's thick. Some of it's black, some of it's brown, it's irregular. What would your concern here be? A concern again would be for malignant melanoma. Exactly. So your concern would be malignant melanoma. Or if the base membrane is still intact, what would this, like if you look at the path here, let's say that in this lesion, the base membrane is still completely intact. What would you call this lesion? It would be melanoma inside, too. And what do we call that? Oh, I've forgotten the short term memory. Something with a B, a... Actually, this is PAM, primary coronary melanosis. PAM. P.A., it was P.A., asking about someone's name. With marked dysplasia. So you see these dysplastic cells go full thickness. So again, base membrane is still intact, kind of a melanoma in situ, if you will. All right. And then sometimes it goes to this, and hopefully nobody's going to miss this. This is a Frank malignant melanoma, and you can see the melanoma cells there. All right. This is the top of the acropolis. This is the parthenon that they've been rebuilding for like 100 years. All right. We're going to go to some corneal lesions. Boy, Tyler, you get an easy one here. Tyler, tell me the layers of the cornea. So from outside to in epithelium, bulmans, stroma, decimates, and then endothelium. All right. Very good. So I just want to put some of these in just to see if anybody's paying attention. All right. Very good. So now we want to talk about corneal infection. So we're going to pop back up again. Katherine, what do we see in here? Yeah, it looks like there is... It's a silt lamb photograph, but there is fluorescein, and there is a dendritic lesion. So it looks like HSV keratitis. Exactly. So you see this dendritic lesion, you see the staining in the center where the epithelium is denuded, and then these thick edges of the bulb. So if you're going to culture one of these, don't culture it where the epithelium is gone. There's nothing there. Culture it here at the edges where these little bulbous dendrites are sticking out. And this is classic for HSV herpes simplex. When you look at it here, what is the inflammation in the cornea characterized by? There's... Well, it looks like there's a lot of thinning, and then there's even... It looks like there's an ulceration. And what's the cellular reaction in a herpes? Acute or chronic? It is acute. Actually, it's more chronic. It's more lymphocytic than it is PMNs. And so these are more lymphocytes than PMNs. Okay. Jordan, what are we looking at here? Go ahead and unmute. Oh, sorry. Is this like a band keratopathy? I'm not entirely sure. Does band keratopathy have redness and swelling of the conjunctiva and infiltrating the cornea associated with it? No, I guess not. I was just thinking like I don't know exactly where the calcium is. I was just seeing the white part. So when you're looking at a specimen and you're looking at a picture, you're looking at a specimen, you have no idea what it is. Just describe it. And sometimes as you're describing it, going through the process of describing what you're seeing, it will help you try to figure out what it is. So here we've got infiltrates in the cornea, we've got diffuse infiltrates all around the cornea, we've got increased vascularity, you got swelling and chemosis of the conjunctiva. What would your concern here be? Definitely for something infectious. Something infectious. So when we look at it at low power, what happened to this? First of all, what happened to this cornea? Why did we get the specimen? Well, I mean, it looks extremely edematous and inflamed. So it's inflamed and edematous. What happened right here? Looks like you had a rupture. Yeah, you had a perforation. So this cornea actually perforated. And so this pale is just necrotic stroma. And then you've got this intense inflammatory cell infiltrate. These are acute inflammatory cells. So this is a bacterial corneal ulcer, a bacterial corneal ulcer. All right, let's see. Abby, what do we see on this picture? So again, it looks like the conjunctiva is very edematous and inflamed. There is this focus centrally and inferiorly of stromal haze and surrounding infiltrate. I would be concerned about a corneal ulcer again. I guess what I'm trying to decide is there a ring or not, if that sterile infiltrate would be. Yeah, kind of hard to tell on this picture, because it's advanced, but you might even see a little ring of infiltrate here. What would that raise suspicion of? That would make me think of a canthamoeba. A canthamoeba, or even a little bit, well still infrequent, but a little bit more frequent than a canthamoeba would be like a fungal infection. So this is fungal. So what's the stain we use to look at a fungal infection on a cornea? Is it GMS? GMS stains. So Gomori methenamine silver. So it stains the little yeasty beasties, kind of this silvery black stain. And so this is a fungal ulcer, and you can see that. All right, let me make sure I'm not like skipping people here. Now I guess we're going to just start right over again. So I guess we kind of went, well, I'm just going to go, I'm just going to go down. I still haven't grabbed Abby a second time around. So Abby, let's grab you here. I just went, but I can go again. Sorry, Ali, I apologize, Ali. All right, so we have a photograph. There is congenjection, but my attention is drawn towards the white opacification in the ring and some kind of epic defect in the center as well. All right, what would that be a concern for? This looks like acanthamoeba. Exactly. So that's the classic picture of acanthamoeba, chronic non-healing surface epithelial defect with a ring ulcer. And what sustain we use for acanthamoeba? Gridley. Gridley. And the way we remember it is gridley green. So it stains the stroma green, but you see these nice cysts, these nice cysts of the acanthamoeba here throughout the green staining stroma. All right, so once again, pathology is pretty unexciting. So we try to leaven it up a little bit. Okay, Sam, back up to you. What tissue are we looking at right here? So this looks like the iridocornial angle. Okay, so we're looking at the angle now. And this is just a pretty crude schematic, but remember that you can have normal angle, you can have closed or narrow angle, you can have contusion or recessed angle when you look at these pathologically. So what are we looking at here on this picture? So it looks like the right eye is kind of mid-dialated and injected. All right, what would your concern be? So it's a race concern for an acute angle closure glaucoma. Exactly. And so we look at the slit lamp. Does this confirm it? Yes, you've got iris bombae, and I noticed a wall in the cell lamp. All right, so you have what we call an effective pupillary block here, and then the aqueous builds up behind the iris. You can see it bowing forward, touching the cornea and the periphery. So this is an acute angle closure, angle closure glaucoma. All right, what are we looking at right here, Sally? So we're still looking at like the cornea and the angle. Okay. And you can see that it's closed down with the iris synechia. All right, so what kind of synechia do we call that? Not sure. All right, so this is what we call a PAS peripheral anterior synechia, as opposed to the synechia at the border, which is the posterior synechia at the iris borders. This is a peripheral anterior synechia. So this can be a result of chronic angle closure, or it can be a result of neovascularization. All right, so we're going to go ahead and look at what glaucoma does to the optic nerve in the eye. And I see that Marshall's back. So Marshall, we'll start up at the top again. Marshall, what do we see in here? Well, we see an optic nerve and the big letters of glaucoma. So we can suggest that's like some kind of excavation glaucoma. It's like 100% copped. Yeah, if you look real carefully, boy, that cup goes all the way to the temporal edges. This is a 0.999 cup and that vessel goes in, it disappears under the cup and then it comes back in here. So this is a myopic disc, because that sometimes makes it hard to read, but look at that. That's totally copped. So glaucoma does to the optic nerve, you get massive cupping. And this is what we call the beanpot look. So it's got that vessel coming around the edge, and then it even gets excavated and digs out underneath and tremendous excavation. So this is a end stage optic cupping from glaucoma. So that's what glaucoma does to the optic nerve. All right, this is the top of the acropolis. These are the five maidens. Unfortunately, years of pollution have completely rotted that out. So those are just copies that were put in there, because unfortunately that just they didn't last through all the centuries here. So we're going to go here. And again, I'm trying to think you guys, as you guys come on and off here, it ends up reshuffling. So I think Catherine, you're going to be next here. I'll go ahead and jump to you. And we're going to talk about lens. And we can see here's the pathology of the lens. All right, I want to talk about cataracts. So what kind of cataract do you think this is right here? This looks like it could either be a white nuclear cataract or a really dense like anterior subcapsular cataract or cortical cataract. It's kind of hard to tell from the when you see it's hard to tell, but you see these little peripheral spokes here. And then it's turning white in the middle. So this is a white cataract, probably cortical in nature. So remember the cataracts, unfortunately, we don't have good cataract path because the path doesn't really show real well. So we've got we can have nuclear, we can have cortical, we can have PSC. What kind of nuclear cataract is this? It's a Brunessan cataract. This is the end stage kind of a blackish brown Brunessan hard cataract, kind of a third world cataract. All right. So always remember your patients are under topical anesthesia. We had one of our surgical nurses yesterday who was really trying to be friendly and talking about the jazz and where it grew up and everything. And I just couldn't stop him from talking. So when you're doing a surgery under topical anesthesia, the patient hears everything. So once that patient's in the room, conversation about the jazz and where you're from stops, and you concentrate on the patient because they can hear everything. Here's the Acropolis, the Parthenon on the top of the Acropolis at night. All right, we're going to talk about retina. So Jordan, tell me about the layers of the retina. Okay. So starting at the vitreous is way up here at the top. So starting at the vitreous, this layer right here. Okay. So starting at the top, you have vitreous and then it's the, isn't it the ganglion cell layer? All right. What's between the vitreous and the ganglion cell layer, this layer right here? The outer nerve fiber layer. Nope. So here's the ganglion cell layer right down here. What comes out of the ganglion cell layer? Okay. We'll go ahead and I'm not going to put you through torture here because we've got a lot more to cover and you're young. So, so, you know, read the home study book between now next year and then you can answer all these questions. Abigail. So you have the RFL first. Okay. Retinal nerve fiber layer. Retinal nerve fiber layer and then the inner. Right. What layer is this right here? I'm sorry, right here. Ganglion cell layer. Okay. Then right here. The inner plexiform. Okay. And after the inner plexiform is the inner nuclear. Okay. And then outer plexiform, the outer nuclear and then you have the photoreceptors. All right. So I'm sorry, we don't have time to go into detail on this, but know those layers because they will always ask you, Tyler, what are we looking at right here? So we're looking at the macula and corresponding fovea. So center of the macula fovea, you see how everything parts so the light rays can come straight into those cones that are in there. All right. We're going to talk about retinal vascular disease. Ali, what's the most common retinal vascular disease we see in the clinic? Diabetes. Diabetes. And what are the findings on this picture that would go along with diabetes? You have exudate with cotton wool spots. You have flame hemorrhages and blot hemorrhages. Okay. So what's the difference between a flame hemorrhage and a blot hemorrhage? Which layer it is in the retina? All right. So where are flame hemorrhages located? Flame hemorrhages are in the RNFL. Exactly. Because remember the RNFL goes kind of parallel to the surface. And so flame hemorrhages spread out parallel there, whereas the deeper hemorrhages look like more round dots. And those are in the deeper layers. And then these are all exudate that's leaked out. And then these are the so-called cotton wool spots there on the surface. Sean, what are cotton wool spots? Hold that thought. What are we looking at here? Sorry, I didn't realize I had put these in. I didn't know I had time to talk about these. What are we seeing here? So this is a very high magnification view of retinal vascular disease. Exactly. So these are the micro-annuals of the transcription digest. All right. Now we're going to look at cotton wool spots. And cotton wool spots, we're going to go next to, looks like we're going to go next to, oh, we've lost my fellows because they're getting a little patient's ready. Boy, this is thinning out and thinning out. All right. So we're going to go back up to Marshall. Marshall, what are cotton wool spots? Cotton wool spots are basically a small infarct of the RNFL. So what you actually see is a swelling, a focal swelling of the RNFL. Exactly. So you're looking right here. Here's the surface of the retina. And these are ischemic swollen, nerve fiber layer, ganglion cells here. So those are the cotton wool spots. All right. What do we see in right here? Let's see. I'm going to have to go back up. Abby, what do we see in right here? It looks like new vascularization around the disc. So NVD, new vascularization of the disc. And what does that cause? That can cause pre-retinal hemorrhages and it looks boat shaped because you see the boat shape. Flat top, round here, new vascularization with hemorrhage there. And this is what you'd like to do when you hear the umpire call a strike that's over the guy's head. Okay. And I'm sorry, I went a little bit of out of order because, you know, people are kind of jumping in and out of here. Catherine, what do we see in here? Yeah, it looks like there's a lot of basically a lot of diffuse hemorrhage, definitely in kind of like a blood and thunder pattern. No, so this is still called blood and thunder pattern. What does this cause? A central retinal vein occlusion. This is a central vein occlusion. You look at the pathology, you get blood through all layers of the retina and it pretty much wipes out much of the retina, all the layers that are right here. So that's a central retinal vein occlusion. What do we see in here? Let's see, Jordan, what do we see in here? So here you're kind of seeing pallor. It looks like of the kind of of the maculata between the two arcades and then maybe a little bit of hyperemia. The disc of this looks like possibly central retinal occlusion. Okay, so what do we call that little area? That little area of pink amongst all the how? Like a cherry red. It's a cherry red spot. So that's the fovea, caroidal blood supply still intact with the overlying central retinal artery occlusion, blocking that off. So Tyler, what am I showing here? You're showing the central retinal artery and adjacent central retinal vein that share a vascular sheath. So look at all that cholesterol built up in here. I mean that artery, that's all those crown burgers here, building up that cholesterol mark narrowing of the artery. So you can get an embolus here that can cause a central retinal artery occlusion. But right next to it, it pushes on that vein, which can give it stasis in the vein, which can give you a central retinal vein occlusion. And that's the central artery occlusion. It basically wipes out the inner two thirds of the retina, but the outer third is still intact because the coroid is still giving it nutrition. This is the parliament building of the Greek parliament in Athens, and here's the guard who stands there. I don't know if he has hydrated contact lenses or not, but I sat there and looked at him for five minutes. He did not blink once. So very impressive. I don't know how they do that. Okay, we're going to look at macular degeneration. And boy, just by chance, Lydia, good evening. Welcome. Hello. Yeah, this is macular degeneration, a fondest photograph of an eye with a lot of drusen, which is the hallmark of AMD. All right, so what do drusen look like pathologically? Drusen are lipofusen and waste products, so kind of like visual systems by products that are deposited between the RPE and Brooks membrane, so sub-RPE deposits. Exactly. So here's the RPE, here's Brooks membrane. You get this waste material building up in here, and it deposits between Brooks membrane and the RPE, so that's a drusen. All right, what happened to this patient? Let's see, let's go back up. Boy, we're just, we're getting smaller and smaller here. All right, Jordan, what's happening here? Okay, so in the macular, it looks like you have like a few different layer, like blood that's probably in a few different pairs. So you have what looks like potentially sub-retinal, intra-retinal, and maybe even a little bit of pre-retinal. All right, so this is sub-retinal here, this is even sub-RPE, so this is sub-retinal neovascularization in the setting of macular degeneration, and so... Okay, so you could have like a, like potentially curatal neovascular membrane. Yep, that's curatal neovascularization. All right, so that's Delphi. Let's move on. Let's look at the optic nerve. We're going to skip the normal path because we don't have time. All right, obviously this says papillodema, and so that I've given away the diagnosis, and so I'm just going right down the list as it reshuffled here. Abigail, what is papillodema characterized by pathologically? I'm sorry, I don't know why I'm blinking, but... What's kind of the opposite of glaucoma? Where glaucoma, you've got a huge excavation. What do you have in papillodema? It's very edematous, and so it protrudes. So it protrudes into the vitreous. It's swollen. You see that the vessels are engorged. You can even have little hemorrhages on here. So kind of the opposite of the excavation, it pushes out toward the vitreous here. So this is papillodema. You know, remember when you take boards, be aware that papillodema is by definition bilateral optic nerve edema, secondary increase in drug pressure. So if you see a swollen nerve, don't say papillodema, say swollen nerve. All right, so a couple to cover here real quick. Again, this is just showing you how it's different from glaucoma. All right, boy, just going down the list again. Tyler, what are we seeing here? So this is an external photograph, and it looks like the left eye is hypoglobus with some corresponding bluff rotosis. All right, so possibly is proptotic. Yeah, so you get the idea that it's pushing out toward you. It's got some fullness behind here, and this is what it looks like when we look at the pathology. So what do we see here? Yeah, so it looks, you have this obvious enlargement of the optic nerve causing compression on the posterior aspect of the globe. In a child, I'd be concerned for an optic nerve glioma. Exactly. So in children, we see gliomas, so extra bonus points. What's this intracellular plasma, centrival inclusion called? Rosenthal fibers. Exactly. Rosenthal fibers. So this is a low grade astrocytoma of the optic nerve. It's an optic nerve glioma, more common in children than in adults. All right, we're going to go to Catherine. What do we see in here? So yeah, this looks like external photograph, and then attention is drawn to the right eye where it also does look very full, both the upper and lower lids, and also she also has proptosis and temporal subconch heme. So it definitely looks like, and scleral show as well, so it looks like there is proptosis. All right, so we look at the scan here and it looks like it's, oh, what do we call it where there's a nerve in the center and this stuff around it? Yeah, it looks like tram tracking. Tram tracking. So what is that a sign of? A meningioma. Meningioma. So we look at the meningioma and what do we see here in these meningiomas? Yeah, you have these kind of, these inclusion bodies that are somoma bodies. Exactly. So somoma with a PS, it's OMM, somoma body. And so these are made of calcium. They're these concentric concretions that are in here in between the meningothelial cells of proliferate. So this is meningioma, most common optic nerve tumor in an adult. All right, I know you guys are not paying attention now since we're down to just five of you now. I guess everybody else feels real comfortable taking path on OCAP. So we're down to five of you now. So retinoblastoma. I've cheated here because I told you what this was back up to Jordan at the top again. Jordan, what is the characteristic finding on a retinoblastoma? I'm not entirely sure. All right, so we're looking at it at low power and what happens is at low power, you see these nodules of tumor cells, but in between them, you see all this pink amorphous stuff. What is this stuff? Is it just calcium? Exactly, it's calcium. So these cells grow so rapidly, they outgrow their blood supply, the cells die, and you get dystrophic calcification. So when you put an ultrasound on here, you'll see just really bright spikes corresponding to the calcium. So you see nodules of tumor cells and then necrosis in between and then calcification. So that's a real tip off that this is a retinoblastoma. Okay. And Abigail, what's the classic finding when we look at the cells a little bit higher power? You can see the rosette arrangement. Exactly. So what kind of rosettes are these? I think is it Homer, right? Those are the neuroblastoma. What is your retinoblastoma? I'm sorry, I don't remember. So these are the Flexner wintersteiner rosettes. So these are the classic rosettes you see in a retinoblastoma. Tyler, when retinoblastoma spread from the eye, how do they get out of the eye? They spread via the optic nerve. Okay. And there you see a tumor and there you see it growing into the optic nerve. So when these tumors spread in these kids, they go out via the optic nerve. So it's very important if you're going to do any nucleation, you've got a big tumor, you can't control it with chemo, then you want to get a long piece of nerve posterior because you don't want to leave tumor behind in the remnant optic nerve. All right, we're almost done here, I promise. All right, malignant melanoma, Catherine. What is the classic configuration grossly of a malignant melanoma? It's a mushroom. So you see it growing from the coroid, it breaks through Brooks membrane, and then grows underneath the retina. So it's a mushroom shaped melanoma. All right, let's go over the different cell types that you can have of malignant melanoma. So Catherine, just I'll give you one more question. What is this cell type here? It's a spindle. I'm not sure if it's A or B. I think it's A. I think A is a skinnier one. So it's skinnier, it doesn't have nucleolides and inducing cytoplasm. This is a spindle A pattern. And then right next to it, you can have some of these where they have nucleolide in them, and they're more cigar shaped. So this is a spindle B. All right, Lydia, what's the worst type of cell that you can have in a malignant melanoma? The epithelial epithelioid cells, which are in large bizarre cells. So in large bizarre cells, this is the epithelioid cell. So those are the more nasty and aggressive. And last but not least, how do these tumors spread? Lydia, while you're here, you can, yeah, they spread through the epithelial channels, and most favorably spread to the liver. All right, so they come out via one of these emissarial channels. Channels going through the sclera, those can be vortex veins. They can be where arteries posteriorly go through the sclera. They can be where nerves penetrate the sclera. So they can go out through any one of these. And when they metastasize, they spread to the liver. All right, so we said goodbye to Delphi. Good luck with your O-caps if you have any questions regarding pathology. Please fire me off an email. All right, thanks for your attention this morning. Thank you, Dr. Manlens. Thanks, Dr. Manlens. Thank you, Beth. Thank you. You bet.