 All right, so this is everything you ever wanted to know about ophthalmic pathology for OCAPs. And so it's going to be just pattern recognition and looking at pictures and trying to figure out what they are. And we'll try to go over as many as we possibly can in the next hour. So this is about two hours worth of slides, but we'll try to do it all in an hour. All right, so first thing, what do pathologists do? They try to figure out what happened to dead tissue. So this is the job of pathologists. So what I want to do today is I want to go just start with the lid, work our way in conch cornea, anterior chamber, lens, serratina, optic nerve, just see what we can do. All right, so first of all, the lid. Okay, what are the layers of the lid? Back up. Out to you. Yeah. Or even less than that. Skin. Skin. All right, skin. First layer, what's the second layer? Well, it's part of the skin. That's not a real layer. Muscle. Opicularis muscle. Third layer. There are all those little yellow things right there. That's the tarsus and what lives in the tarsus. My bohemian lens, exactly. And then finally, the innermost layer, exactly. So people keep forgetting that there's conch lining the inside of the eyelid. So when we look at them pathologically, skin, stratified squamous, keratin, epithelium, epicularis muscle, tarsal, plate with sebaceous glands, and the contric type of lining the inside. So the lid, you've got to remember, the lid has all the glands in it. So it's got equine glands, and you sweat glands, i.e. lacrimal glands, but it's also got the glands that are apocrine glands, which are the glands of maul, which dump into the hair follicles. And then lastly, we've got polocrine glands, which are the sebaceous glands for the mybomine glands, which we have right here. All right, so this is what we do. That's my fellows down in the lab in the pathology. All right, so we're looking right here. Reese, what do we see in here? Okay, so when you're looking at things on boards or O-caps, you want to start thinking of differential diagnoses. So this is a chelazin indeed, but you want to start thinking, what else could this be? It's kind of a swollen red bump of the eyelids. What's your differential diagnosis? I'm going to do something like vasosol potentially, or turbidinus, probably, like a hydrogen soma. Exactly. Or even something infectious, like, you know, proteolums or things like that, chelazin, anything that can cause cysts, and then we look at the inside and we see that there's, it's coming over into the inside here. So that would be more consistent with a chelazin. Exactly. And what is the path of a chelazin? A granulomus. Exactly. So here we see a giant sepsis, granulomus information, but there are also multiple lymphocytes and multiple plasma cells here. So it's a granulomus inflammation. It's due to inspecated lipid. So all these empty spaces here are where lipid was that dissolved as part of a process. This is the original Olympic Stadium in, not the original, but modern original Olympic Stadium in Athens, 1896. All right, so we're looking at lid tumors. Lee, what are you seeing right here? Acrusted lesion, ulcerated basal cell. Well, especially when you see an ulcerated lesion with raised pearly borders, you really want to think basal cell. And then what's the characteristic path findings on a basal cell? So you see lining up, palisading in the nuclei, basal filling staining, nuclei there, and palisading at the edge of them. Now, what's the most common type of basal cell carcinoma? Nodular. Nodular or nodular cystic. And so you can see right here you've got these large nodules. If you look real closely, there is palisading here at the edge, and some of them form a little cyst. What is the one type of basal cell we worry about? Sclerosis or morphiform is the other word that you may want to know about this. And so the problem with these is these tend to not be solid nodules. These tend to send fingers out, or they can spread in a pageatory pattern, meaning they can spread kind of under the epithelium. You see that there's multiple little fingers up to themselves, but surrounded by connective tissue. So we call this morphiform or sclerosis type basal cell carcinoma. And this is what happens if you don't treat a basal cell. They're exposed for 10 years. So even though they're benign and they don't metastasize, they can cause tremendous local damage. All right, what are we seeing right here, Chris? So an orthodontist-raised lesion of the eyelid, and lost myilashes, which could be completely unseized as well, especially with lost myilashes, when you spring the cell around the end of the cell. All right, so when you look at that little, we call it this parchment paper. Kind of that, it looks like little parchment paper, and it's got kind of that orange-ish hue to it, because it's got a lot of keratin in there. This is a squamous cell. And what is this that we see that characterize squamous cell carcinomas? So here are the keratin worlds or keratin pearls. And you see that the squamous cells are not dark basal phylloxidene like the basal cells. They're more eosinophilic-stain. They stay more pink. But the tip off is, is when you start to see these keratin pearls, you think about a squamous cell. Tara, what do we see in here? Okay, so there's lots of lashes. You see it's irregular. It's got different shades of pigment, brown and black. What would you be concerned about here? Melanoma. All right. You'd be concerned about melanoma. And indeed, this is a melanoma now. They may show you pictures of Nevi. And so, you know, when you see that distinct nesting pattern, and you think more Nevi, but when you see cells that have those nucleoli and chromatin, then you start thinking of melanoma. Ashley, what are we seeing here? The eye loge. So, I'm thinking infectious causes. Also, sebaceous carcinoma. Okay. So, they call sebaceous the great mimicar. And so, you know, I just want to keep that in the back of your mind. If you see a, what's called a blepharoconjunctivitis, that's not going the way, or not getting better. And you look carefully, you see that the margin is thickened. And these little yellow areas showing you, there's lots of lashes. So, this isn't just a blepharoconjunctivitis. This is indeed a sebaceous carcinoma. And so, if you've got recurrent chelasia, that's the other ones. You've got chelasia. It keeps recurring in the same place. You want to look at the pathology because you worry about sebaceous carcinoma. And when you look at the pathology of sebaceous carcinoma, they tend to be very active looking. So, these can be nasty tumors. These could metastasize. And if you look at them, they look nasty. All right. So, then we've got our, just to keep you guys awake. All right. Conjunctiva. So, Becca, what are the three kind of parts of the conjunctiva? We talked about one. Papibrol. So, that's part that lines the eyelid. Okay. Bulbar. Bulbar. And then what's in between? The fornic. So, the fornicial conjunctiva. And if you look right here, you'd see it's got that stratified squamous epithelium, just like skin, but it's not keratinized. And so, it's a mucous membrane. And these little dots you're seeing in here are all little goblet cells. They're the ones that make mucous. So, the further you get from the limbus, either toward the fornix or toward the carumpel, the more goblet cells that you see. All right, Reese. What do we see in here? So, elevated. Are there other Reese's? No. I don't know. I don't know. I don't know. I don't know. I don't know. I don't know. So, it's going to like a sail-shaped area of elevation on those. So, what do you think that is? Trigium. Yeah. Or, in this case, it's not quite crossed the limbus or... Pinguicula. Exactly. And so, the difference between a trigium and a piguicula? Exactly. So, the same pathology is just the trigium has crossed the limbus and gone on to the surface of the cornea. What's the classic path that we see? You get the name of the congenit... of the epithelium, basophilic degeneration of solar processes. So, this is that smudgy blue basophilic degeneration. You get that squiggly solar elastosis. So, it's a UV-induced degeneration of the subepithelial tissues. You can even get little flecks of calcium forming in here. This is that classic basophilic degeneration collagen that you see in a trigium. All right. Lee, what do you see in here that doesn't quite look like a trigium? No. There's this gelatinous open growth that's one of So, what would you be concerned about here? Okay. And then, in this particular case, we look at the pathology. And indeed, there's all this plastic epithelium, lots of maturation, some wists with keratin on the surface, but this membrane still looks intact. So, what do you call this? CIN. CIN. Conjuctival Interepithelial Neoplasia. So, when we grade CIN, how do we grade it? Exactly. When we start at the basilar layer, so if it involves kind of the lower third, we call it mild, middle third, we call it moderate, greater than middle third, we call it severe. But it's still intrepithelial, and that's the key thing. It has not gone beyond the epithelial basement membrane. Okay. What do we see in right here, Chris? So, it looks like an inflamed congenitiva, temporal congenitiva. Sorry. So, what does the look of the intergenital congenitiva look like? It just looks a lot more inflamed than the middle congenitiva. What about some of the neoplasia as well here? What is this white stuff here? I'm not sure. Is this for exudate or just for... I'm not sure. It's actually part of the lesion. It's not exudate. Is that keratin? It's keratin. So, what do we call this when it's just white keratin as lesion? Keratinized neoplasia. No, no. It comes from the Greek, of course. We call it leucoplakia. Plack. Plack. Plack. Leucoplakia. So, this is a tip-off that you've got keratin on here. When you've got a big plaque of keratin, you know, your differential is always, is it cian, is it squamous cell. When you look, it's actually invaded below the basement membrane, in the substantia propria. And again, you see these pearls and pearls and it can form keratin even though the conjunctile epithelium is not keratinized. So, this is squamous cell carcinoma of the conge now. All right, we're looking right here. Tara. Anything more is some there? Oh. Okay. So, nothing more is some. What does PAM stand for? Exactly. So, this is indeed primary acquired melanosis. And when we look at primary acquired melanosis, we subdivide it into PAM. Without aegypia and PAM with aegypia. So, this would be PAM without aegypia. So, you see that there are benign melanocytes just in the basilar layer of the epithelium. And so, this is the PAM without aegypia. This is what racial pigment looks like also. But sometimes you can get a lesion that looks like this. Is this more suspicious? Exactly. So, feeder vessels and it's thickened and it's darkened. And so, this has now become PAM with aegypia. But remember, PAM is intraepithelial just like CIN. And so, by definition, the basement membrane is still intact. But, look at these bizarre melanocytes. They're invading up into the epithelium. They've got nucleolide. They've got chromatin. So, this is PAM with aegypia. And this is important because this is a precursor to... to what? To melanoma. Melanoma. Exactly. So, that's what can happen if you don't take care of PAM is it can become malignant melanoma. So, PAM is the most common precursor to malignant melanoma. So, you look at malignant melanoma, 80% of them arise from pre-existing PAM. So, it's important that you remember that. All right. So, there's the parthenon on top of the acropolis. They've been rebuilding for about 100 years, but they're... they're getting there. They keep getting money from the Germans. They'll eventually finish it. So, let me show you a path photo of like Hopefully, they will show you either melanocytes in there or they'll show you a clinical picture because these just look like big malignant cells. You can't tell whether they're melanocytes or not. That's what makes it tough because sometimes they start to lose their pigment. Right. And you don't see them. You expect melanocytes to have lots of pigment but sometimes not. All right. So, we're going to talk about the cornea here. Actually, what are the layers of the cornea? So, we'll give Becca a break from naming layers here. Okay. All right. Very good. And so, when we're looking right here, it's important to remember Bowmans is not the basement membrane of the epithelium. So, you've got a basement membrane right here. That's a base of membrane. Bowmans is some condensed stroma. And so, Bowmans is important because it does not regenerate. So, if you get an injury or an ulcer or something in that area, Bowmans won't regenerate. Now, posteriorly, how do we tell what's a stain we can do to tell decimates from Bowmans? PAS. PAS? Why? What kind of tissue? Basement membranes. Yeah. So, PAS stains basement membranes. And remember, decimates is a basement membrane of the endothelium where Bowmans is not a basement membrane. So, here's something we never see in the path lab. That's called an endothelium. So, that's what endothelium should look like. So, you guys never see that because we always get damaged tissue. All right? So, this is what I love when I'm sitting there on Sunday morning eating my little bowl of Wheaties, watching the I-Institute commercials. All right. So, corneal infections. Becca, what is this? Yeah. It's right here. A dendroid. What kind of stain have we used to show this? Fluorescene. Fluorescene. So, what classically gives you a dendrite up there? What kind of herpes? Simplex. But, you know, the butt could be zoster, but usually it's more herpes, but it could be zoster. So, this is simplex. Classic epithelial dendrite. So, you get lots of epithelium in that area. You get some denuded epithelium here. And you get an inflammatory cell reaction. Okay. What are we seeing right here? Reeds. So, there's an injection in a type of white, and it's white, and it looks like all these have been in the corneal sort of in the ulcer. All right. So, at this point, you look at it, and this is the path you see. Yeah. So, it might be appropriate, but there's just a erratic number in front of your cell. Corneal serum, and then loss of corneal. All right. So, this is more consistent with a bacterial corneal ulcer. On the last slide, so it was, I wanted to ask, so, what's the pseudo-dendrite? What's the other one that gives you a pseudo-dendrite? The metabolic disorders? The systemosis? No idea. Sorry. One of the metabolic disorders can be pseudo-dendrites? That's information I've completely purged from my neurons. So, unfortunately, your neurons don't keep growing when you get older, and you can't add memory, so you just have to start on purging. Don't think stuff you don't need. So, if you ask me about the sphingomylinoses, look it up. Because I'm a grandfather. I don't have to take boards at any points. I don't have to know that. So, lean. We're looking at this leaching. This is kind of similar to the previous one, but there's some subtle differences. So, again, it looks like there's a point. You kind of see that diffuse haze around it in this little numular area. What would you be concerned about here? More than interstitial perioditis. What infectious could cause this? So, HSD can cause that. But also, syphilis can cause that. How about this? That can cause that, too. All right. So, what are these? Those are the focus. Exactly. So, as we call them usedy-beasties, now let's say that on boards again. Board exam is going to go, wow. So, this is a stain that stains for fungi. So, remember, fungal ulcers can be more indolent. They can add that little halo of the infiltrator around them. And what's the stain we use for fungal ulcers? GMS. GMS. So, the way you remember that is Gamorimithenamine silver. And it stains the fungal element, silvery black. So, that's a fungal stain. And then, Chris, what do we see in here? Looks like another big corneal ulcer, really infiltrated, really just moving through the bones. Well, if you look right here, that's actually not an ulcer. That's just a chronic epithelial defect. You've got a chronic epithelial defect, and there's one more thing on here that can give you a hint as to what this is. That's not my boby like it's home care. God, all these years I've been showing this picture. I've never noticed that there's my boby. That's good. That is absolutely correct and that has nothing to do with my diagnosis, but that is correct. It looks like there's maybe thinning as well in the cornea, but it's hard for me to tell, I'm not sure. What is this right here? It's, I guess, a ring of some sort. Yeah, there's kind of an immune ring. So, this was treated as a chronic herpes and this non-healing epithelial defect, very painful immune ring around it. I know it should all be just, you know, fireworks in my head. Okay, does that help? Yes, that looks like amoebas. Exactly. So, this is a classic acantamoeba picture. Chronic non-healing ulcer, not to be herpes, but not, and then this ring infiltrate and then the pain as these acantamoebas just, trophazoids tend to grow into the nerves and so, this is a classic acantamoeba. So, you know, whenever they give you a little history you ask someone who's in a hot tub or something like that, you know, soil exposure, then you start to think of things like we're in a hot tub, don't put your face in it, because love living in hot tubs and just keep it up to the chat, that's all. All right, so here again, some optometric humor here. Dr. Marbles, I'm good at it, I can't do, what is, I forget the name of this stain that you showed us. Oh, it's a grubly stain, but you can also do, they can do fluorescence through the stuff fluorescence. So, you do a fluorescent microscope and we like to do the grubly stain. All right, so corneal dystrophies, now I don't have time to show them all to you in an hour, but a terror, what's the mnemonic that we need to know for corneal stromal dystrophies? Right? Marilyn Monroe, really, always gets her man in LA County. All right, so if you can memorize that, there's always every year one of the corneal stromal dystrophies, always, remember it. So, Marilyn, M, Ashley, what does M stand for? That's the second M. What's the first M? Macular. Macular, so macular, mucopolysaccharide, what does the R stand for? Recessive. Recessive, so the others are dominant, so macular, mucopolysaccharide, recessive, always, all should blue. Okay, Becca gets, okay, he gets, granular, her, Highland, man, mason's, mason's trichrome, L, A, County, Congoreg. Okay, so if you remember that mnemonic, you'll get at least one question right on George, one. All right, and here's just one of the stains, this is the trichrome stain just showing you that. All right, Chris, kind of a weird retro-lumination of the corneal, what am I trying to show here? So I'm trying to show us the the stroma, probably, you know, hard to tell. Yeah, hard to tell on this, but when you do a retro-lumination that really highlights kind of the posterior corneal, this is kind of a, a view of posterior, what do we see in here? An area that is not quite as translucent as the rest of the surrounding corneal, as soon as there's granular corneal. If you, if you look at the hinge, you see those little bumps all over the place. It looks like someone took a little round hammer, just hammered it, man, man, man, man, man, man, man, man, man, man, man. You look at the path and you see these guys, these guys right here. The generation of those cystic spaces. All right, that's actually normal stroma. We're looking back here, what layer is that? That looks like disemaze. Disemaze, and that is massively thickened. That's like four times normal thickness. What are these guys back here? Ptata. Ptata. So that's what you were seeing on that. So this is fuchs dystrophy. So ptata, fuchs dystrophy. And so what you see is when you look, these are actually little tiny ptata. You can see them well on retro elimination of the cornea. And they're characterized by these excrescences of these affected endothelial cells on disemaze membrane, but then disemaze membrane gets marketed and thickened. Tara, what are we showing right here? Monson sign. And what is this characteristic of? Charitaconis. Charitaconis. So nowadays, it's pretty rare that we see charitaconis this bad. So this is like a 30 year old slide. But if you look right here, you can literally see the cone shape of that cornea. This was before we had topographers. And so you have to kind of look and say, is that cornea thin? Is it butching out? Now with topography, you can tell really well, what is the pathology of charitaconis? That's the end state. That's the end stage. What's the most common pathologic finding? Okay, so the stroma does thin, and S does the epithelium, but the key is right here, in Bowman's layer, you get these vocal discontinuities or breaks or squiggles. And some people would even argue that charitaconis is an anterior, like Bowman's layer or dystrophy. So you get these discontinuities here in Bowman's layer. And then thinning stroma, thinning epithelium, and then thinning stroma, thinning epithelium, and then thinning epithelium, and then thinning epithelium. Notice the endothelium is still pretty good, unless you get a massive break-in dissonance, which is what causes hydrox. All right, what are we looking at right here, Ashley? Okay, so this is a big bow, and what stain is this? Short-term memory? Exactly. That's not PAS. It is a PAS. Now note though, this is why I showed you this. Look, here's the basement membrane of the epithelium, PAS-positive. Here's Bowman's not PAS-positive. So that's what the difference is. I know the iron curtain descends across there. So this is my favorite one, varnish. This is one of the 12 requisites for an oculus in the surgeon. This was in the 16th century. Some of them I love is that he said, not to be greedy for money or hotting, not to be a drunkard, not to be presumptuous or vainglorious. I love that I have to be nimble with the hands, be able to draw to be married. And they have these were all the ones. I love that. And so I love him too because this is what he said, since I could not afford a high school and university education, I had to restrict myself to surgery. I love that comment. Okay, Becca, what part of the eye are we looking at right here? This is the angle. Here's the trabecular mesh work. And what are the different parts of the trabecular mesh work? So if you're looking in with a Goniomir, and you see those little rectangular posts here, I'm going to make you compulsive before you leave here. So starting anteriorly, you're looking in with a Goniomir. Well, anteriorly is actually the end of decimates membrane. It's called Schwabbi's line. And then you see a nonpigmented mesh work. Then you see a pigmented mesh work. Then you see the scleral spur coming underneath it. And you see the iris root. All right, so these are the different kinds of pictures. Now, every once in a while they'll put pictures on OCAPs. And there'll be a series of them. And I hate these because they'll show you like five different pictures. And then there'll be questions relating to each one. And one year they just put in a bunch of Goniopictures. One was a closed angle. One was an open angle. One had some vessels in it. One had no clue what it had. And so they'll often show you these. And on the right there's kind of an injection and a mid-dialed and a bit of a solution. All right, so you look in with the slip beam and you see this. Iris long day. Exactly, that iris bowing forward. So that's a narrow angle relative people are blocking. This is what can lead to angle closure of glaucoma. Now, what's going on here, Lee? This is something a little different. Exactly. What does PAS stand for? The peripheral iris is stuck to the cornea and that can happen from chronic angle closure but also there's some fine little vessels along the surface of the cornea. So this is PAS secondary to neovascularization. Okay, so glaucoma, we're going to look at glaucoma. What are we seeing here, Chris? Very cup disc with periaparacid. Exactly. Some marculi cup. That's like a one disc. In fact, you can even see more than one because these actually excavate like a beanpot. So you look at this, this is an end-stage glaucoma. Posterior bowing of the lamina crebrosa, you can see the vessels dip along the rim there and it actually widens out like a beanpot. So that's end-stage glaucoma. So you want to worry about that. These are the maidens of the temple on top of the acropolis. So we're going to take a look at that. And Tara, what are the different parts of the crystalline lens? Okay. So nucleus, cortex, lens capsule. And remember, there's lens epithelial cells under the anterior capsule. They go to the equator. There should not be any posterior lens. So that's abnormal if there is. Ashley, what are we seeing here? Okay. So what entity do you worry about there? Marfan. And for some reason, marfans, you get superior temple. That doesn't make sense to me because if zonules are weak, you think it would sink down. But in marfans, it goes up and out, almost just an area down and in. You can also get weak zonules in spiro-fakia, but there it's different because there the lens is small and round and then it can dislocate anteriorly. So know your dislocations. All right. So cataracts, various different types of cataracts. And focal types of cataracts. Of course, this is your ultimate nuclear cataract. This is a brinescent or brown-light nucleus. And there's a portable cataract from behind. All right. So this is my plea for you guys when we do surgery. You remember the patient hears everything. So we never say, oops, we don't say, oh shoot. You don't do that. Okay. And there's another cataract. All right. Now, I've got to go to another talk here and blitz through these really quick. Okay. Any questions on the first part so far? When you just were talking about the cordial dish fees, was that macular? Should you show it or what kind of tissue was that? It was actually a lattice. A lattice? Yeah. Because a lattice looks like a little lattice line. And so it's well-named. The retina. So remember different parts of the retina. To a retina person, the macula is the area within the arcades to a pathologist. The macula is the area where the neurofiber layer and the ganglion cell layer is more than one layer thick. So that's the view of the pathologist. Okay. So know your layers. So let's go through the layers real quick from coroid, beckett, innermost layer of the retina. Even in front of that. Oh. Exactly. The inner limiting membrane neurofiber layer reach? Ganglion cell layer. Okay. Lee? Okay. Chris? Outer ganglion layer. That's a new one. It wasn't outer ganglion layer. It was publishing soon. The inner nuclear layer. Exactly. Terra. Outer plexiform layer. Outer nuclear layer. Back up. Look at these right here. Rods and cones. Very good. And then you get your RPE, Brooks membrane. Remember the layers of Brooks, Corey capillaris and Cori. And of course, here's our phobia. It's in the part of the phobia where you get parting of the cells there. What do we call the area orese where the the cells here in the phobia send fibers over here in an oblique direction. Henley's layer. Exactly. This is important because Cystoid macular edema occurs out here in Henley's layer. Look at that. Alright, it's a retinal vascular disease. Lee, what are we seeing right here? Well, you could do both, but name the findings here. Okay. So there parting of the areas. There's cognitive spots. There are plane temperatures. There is retinal vascular disease. Okay. So what could this be? This could be hypertensive or diabetic. Exactly. So this could be preperliferative diabetic retinopathy, but don't forget hypertensive. Hypertensive can look like this, too, and believe it or not, I just missed one last year on one of these. I missed hypertensive. Okay, so when we look at diabetic retinopathy, what's the first thing that happens here, Chris? With diabetic retinopathy. Diabetic, huh? We're trying to get blood vessel weakening from the high glucose load and weakening the blood vessel walls. So what do we call these little outpouchings? Microaneurysms. Microaneurysms. The first thing you get is you get microaneurysms. Tara, what are we seeing here? Exudate. Exactly. So you can get hard exudate, especially in the macula. Here's the Dopplot hemorrhages. Here's the flame hemorrhages, but you can get hard exudate. And here's a picture of this young, kind of that serum, if you will, kind of pro-tenacious, lipid-rich material. Stop that. Again, you're making me do it. What do we see in right here, actually? Cotton wool spots. And what are cotton wool spots? Exactly. So they're superficial, little ischemic infarctions of the nerve fiber layer and ganglion cells. So here you see some swollen ganglion cells, swollen nerve fiber layer. These can come and go. So they're just going to go from background to what we call re-berliferative retinopathy. You're starting to get significant ischemia. Becca, what do we see in here? And where is it located? At the disc. So we've subdivided the investigation into neo of the disc and neo elsewhere. Neo of the disc is important because these can really bleed and they can cause problems. So you've got this classic, we call it medusa, you know, from mythology with the snakes and the nerves. What can happen if we don't treat those? And this is even like we call it pre-retinopathy. So it's kind of under the internal limiting membrane you get this classic boat shape. So that's what we want to prevent is we want to make that neo go away before we get that boat shape hemorrhage. This is what happens if we don't. You get scarring, baleosis, chronic hemorrhage and you can get traction retinal detachments. So this is sort of diabetic retinopathy is something we really need to treat. Now we used to take a laser and blast the whole vertebra. But now people are looking more at doing anti-veg F injections either in addition or in place of it. So that may change your future. But for OCAPS, for all you guys, OCAPS is the knowledge that was in the book three years ago. Okay. All right. Here we go. Again, we always wish to do that and say, oh, you're blind. So there's Dr. Hupp's, you know, doing his lacy there. All right. So other things that can cause findings that almost look like diabetic retinopathy. Reese, what is this? Oh, this is what happens. It's hypertensive and you see there's even a little bit of diabetes, but there's some fuzziness of the disc. In fact, hypertensive retinopathy, you can get elevation fuzziness of the disc. You can get this classic star-shaped exudate. It's almost like Cystoid macular edema with the flower petals, except it's exudate. And so when you get macular hard exudate, you get this star-shaped pattern. And this is a severe hypertensive retinopathy. The damage from hypertensive retinopathy. Lee, what do we see in here? It's a retinal vein occlusion. Yeah, so this is blood and thunder retina. And so this is a central retinal vein occlusion. You see backup of blood everywhere. It goes all the way from the disc out to the oracerata. And so it's like you have a massive retina on the freeway and the whole freeway is backed up. And so this is what it is. And you can get damage mostly to the innermost layers of the retina because remember, the inner two-thirds of the retina gets its blood from the central retinal artery. The outer third gets its blood supply from the chloride. So when you look at a damaged retina from a central vein occlusion, the outer third is still normal, still functional. All right, what do we see in right here? Chris? Exactly. So you see the whitening from ischemia. It's kind of opposite of the red from the vein. So ischemic area, and this one is in one particular area here where the arterial splits. And so this is a branch artery occlusion. What is this? Central artery. Central artery occlusion. Why do we see that cherry red spot in the center? Because the phobia gets itself what's supplied from it. Well, and that's actually almost like it's a window into the correlate. And so remember when we showed you that picture of the phobia, the superficial retina kind of splits off like wind blowing through the wheat field. And so you're actually looking down in that phobia of depression into normal correlated blood supply. So this is where you see diffusoschemia central retinal artery occlusion. Yeah, you see a severe arterial sporadic pack here. So this is all those crown burders and moochies and all that saturated fat building up in here. And it's narrowed the artery so this is very susceptible to tiny embolism. But also this sporadic artery shares a sheath with the central retinal vein as it comes into the eye. And so it'll push over on the vein and cause stasis. And again, here's the central retinal artery occlusion wipes out the inner two thirds. Outer third is still intact. Very sure it will be the central retinal vein occlusion is arterial sporosis. So you see that that fat artery pushes on the vein and causes some stasis. And again, here's the central retinal artery occlusion wipes out the inner two thirds. Outer third is still intact. This is the tumult of the unknown soldier this is the Evzan who guards the unknown soldier and okay I can't make this up there are two criteria well actually three criteria to be an Evzan you have to be male first of all so very discriminatory you have to be over six foot tall and you have to be handsome. So short, ugly, you know women forget it and pump pumps on their shoes so very secure but these guys are amazing I sat there for like five minutes and looked at her this guy did not blink I mean it was amazing they just sit there they freeze and they stand there they don't even blink for like an hour that they sit there okay so what do we see in right here so you see the Jerusalem the yellowish white deposits underlying the retinal pigment epithelium and and this is a Druzen pathologically it's this deposit technically it's intra Brooks because it's under the basement membrane of the RPE so it's under the RPE here's the RPE and you see these focal areas of Druzen what do we see in here actually exactly so this this hemorrhage because it's good that greenish gray color is actually under the RPE and then if it's broken through the RPE to come under the retina it has more of a reddish color so this is what we want to prevent now in macular degeneration is we want to prevent these sub-retinal hemorrhages because if we and here it is on a floracy you can see the leakage there because if we don't prevent them you can actually get sub-retinal gliosis what we call a disco form scar that can really cause loss of central vision all right so retinitis pigmentosa becco what are the classic findings of retinitis pigmentosa there's three hush and they're all right here what do you make of that optic disc well it's hard to see because it's really pale it's white it's got waxy power what do you make of the little arterioles yeah very attenuated that's a second one and what do we see it out here yeah the so-called bony spicule pigment changes and so when you look at a peripheral part of retinitis pigmentosa you get this RPE totally disrupted and you get this bony spicule pattern here and the reason for that is the pigment for some reason as it's liberated from the RPE will settle along the vessels in the retina so the retina degenerates that pigment cells along the vessels and that's what gives you that bony spicule when you see that so you're going to probably have to know the genetics of retinitis pigmentosa which is basically everything you can dominate it can be obsessive it can even be x-linked and so all kinds of retinitis pigmentosa like diseases too that they may throw at you so know those all right so my favorite clinic I love this guy who drives draws these the lady with the white eyes he did the one about the doctor talking about how he cut himself shaving to the same picture so retinal detachment's Reese what are the different kinds of retinal detachment and what does retinotaginus mean exactly there's a break in the retina and it's caused caused by a tear and then the other type you can get actually so here it's hard to tell because you kind of see this I don't know if this is exudative or not but if we look at this this is retinotaginus you see the classic horseshoe tear usually implies there's some kind of traction in the vitreous pulling on it you get that classic horseshoe tear in the retina and so what happens when you get a total retinal detachment what shape is it funnel so you've got attachments at the aura serata attachment of the optic nerve and then you get this total funnel shape detachment retina detaches completely that's what it looks like pathologically you get this exudate underneath it and then you can even get proliferation of gliotic cells we call this condition Lee what PVR proliferative which you're right now with you this is why most retinal detachment surgeries fail is because you get this PVR going in there that's why they fit so there's Delphi that's where the oracle sat all right so the optic nerve we're going to look just a couple of different lesions of the optic nerve now this is the optic nerve with the trichome stain again showing you the columns with the PL set day in between the subarachnoid and then lastly there's an optic nerve sheath outside of that optic nerve sheath arachnoid subarachnoid Pia central retinal artery in pain all right so papillodema Chris very important what is the definition of papillodema exactly so don't use the term papillodema they'll try to trick you especially if you take oral words they'll say oh you say papillodema they say oh really so if you just see unilateral disc swelling you say disc swelling you don't say papillodema because again papillodema means a specific thing but when you look here you see that the disc margins are irregular the veins or sausage shape there's a little flame hemorrhages and so that's a classic papillodema and here's the swollen nerve surface hemorrhages dilated vessels swelling of the nerve so I love in the movies there's always like this this gallery where people are watching people operate I've never seen one of those I saw one of these in Moscow the Fyodorov Institute has one of these but I've never seen one in the US but on TV they always had to sitting up there discussing you know something and all the cases going on never seen it all right so we're looking at an optic nerve now Tara what are we seeing here yeah so that's the opposite of papillodema this would be end-stage glaucoma exactly so different than papillodema so we're getting close to the lectures that we just had the last couple weeks Ashley what are we seeing here and even proptosis look I feel it's proptotic and there's the scan fusiform enlargement of the nerve and what is that characteristic of glioma the optic nerve and here's that classic fusiform enlargement because it's intrinsic to the nerve itself and what are these Rosenthal fibers so this little eosinophilic stain degenerative you know deposits sitting here in the stroma so remember optic nerve gliomas are low-grade grade 1 astrocytoma very low-grade or people may call these juvenile pylosidic astrocytomas pylosidic when you hear life and so these are the most common optic nerve tumors that you see in kids what are we seeing here back up it's a methodic edema some subconch hemorrhage and we look inside them see this is this little shut vessel so when something is easing on the optic nerve and slowly squeezing the life out of it try to get the blood out of it if once you get these funny shut vessels and then we do an MRI scan and we see this is called the tram track side so you see here's the nerve and here's this thicket tissue around it what kind of tumor is this so it's in the tissue that surrounds that this is a meningioma and so gliomas arise from the astrocytes that live in the nerve meningiomas arise from the little men and geoselves around the nerve when you look at them there's this classic path finding this calcified hyalinized circular structure this is called a somomobody with a p.s. means double aminitis this is classic for an optic nerve meningioma most common optic nerve tumor in adults all right so we're almost there you guys are not ready to go to sleep and I'm hoping that the panic of boards is at least keeping you awake for these so you pay attention all right so we just went over retinoblastoma a week ago short-term memory Reese how do we tell retinoblastoma from other causes of leukocoryl we've got the kid asleep what's a simple test we can do these scans because it's got tons of calcium so here we see here's this viable tumor cells surrounding blood vessels and then they outgrow the blood supply they die they undergo the secondary dystrophic calcification that's classic and what's the finding that we see on a differentiated retinoblastoma what kind exactly so flexor wintersteiner rosette are the most common finding that we see in a differentiated retinoblastoma how do they get out of the eye through the optic nerve all right and this is what happens if you don't treat this is young kid from Nigeria and these can grow explosively and people die from this if you don't treat them okay so you guys cannot be excused even though your brains are full all right malignant melanoma leave what is the classic pattern shape that you see in a malignant melanoma of the cori a mushroom shape as it breaks through Brooks membrane and spreads underneath the retina you get a mushroom shape what is the classification that we use to classify these right there's spindle a and there's spindle be then there's a mix then there's these cells epithelioid and how and this is a mixture now spindle be epithelioid how do they spread when they spread and serial channels and where do they metastasize to the liver so how do we remember that beware the yellow man with the glass side all right good luck on board