 All right, perfect. So people forget Leonardo da Vinci was from Milano. So this is where he painted the famous Last Supper. Now it's interesting as the Last Supper was not in a big palace or anything. It was painted on the wall and ceiling of the dining hall of a church where a bunch of monks used to eat. So it's very interesting when you see that. I can't believe they restored it and still kept it up. It's pretty amazing that it's still going after after over 500 years. That's the church next to where the Last Supper is. And now this is not the real Last Supper. They will tackle you and rough you up and steal your camera if you dare take any pictures in that they've got guards that are pretty amazing. And so this is a replica sitting outside of it. But what's interesting is the Last Supper, this is what it looks like here. This is the door where you leave the dining hall to go to the church. And so it's literally painted above the door on the ceiling right here. And so when you go in there, they move you in about 50 people at a time. You have exactly like five minutes to look at it and then they hustle you out. So this is outside of the dining hall. This is where it looks like I couldn't take any real pictures. But it's pretty amazing that it's literally on the paint above the door on the ceiling. And so I'm just stunned that it's still there after all this time. Now we're gonna talk about leads. So let's see, I guess I have a few of the first ones. So what are leads, ogres and onions having common? Layers, all right. So let's talk about the layers of the eyelids starting externally. First layer, skin. Second layer, we'll just go down the line. Orbicularis. Orbicularis. Third layer. Tarsus. Tarsus. So what lives in the tarsus? Bumby and Vines. My bumby and Vines. Fourth layer. Conjure. Conjure. All right, so the palpebo-conjure tops. So now we're looking at this picture. What's different about this picture compared to previous one? It's fucked. Just seeing if you're paying attention. Everyone's in a while on flip ones. Just to see if you guys are waiting. And you said it, what is this stain? Trichrom stain. Trichrom stain. And so what is trichrom stain red? And what is trichrom stain blue? So blue is the connective tissue. And then pink is like epithelium or? Well, pink is epithelium and also mesenchymal tissue. So on a trichrom stain, the muscle, the epithelium will all stain. You said it felt like it felt stained red. But the dead's connective tissue of the tarsus stains blue. And so that's how we can delineate that a little bit. So now we're looking at the skin. We'll just swing around the corner. Tell us about the skin of the lid. So you can see that on the top surface, there is keratin. All right, keratinized epithelium. And then right underneath that would be shrine-fied sphagnum epithelium. And then I think you can see some dermal up into just there. And then right underneath that, there's no dermisophagous right into muscle. All right, so what's different about lid skin, compared to skin elsewhere in the body outside the lid, is there's no true dermis, no true organized dermis. But also there's not fat, except now some of those older vets, you can see they've got a lot of fatty infiltrate underneath, but most of the time there's no fat underneath there. And the other thing is there's not the reedy ridges in pegs that you have in normal skin elsewhere outside the eyelid. So you don't have that epithelium anchored as tightly down to the tissue. If you've seen someone who's got either an allergic reaction or a hit in the eye, you can get a tremendous amount of swelling under that epithelium. What's the layer underneath the epithelium? Muscle. What muscle? All right, obituary muscle. So remember, the obituary muscle has three main parts. All right, what's one part of the obituary muscle? Tarsal. All right, so we call it the pre-tarsal in front of the tarsus. Second part? Presepial. So in front of the orbital septum, the third part. Yeah, they just call it orbital. So it's like concentric Cs. And so it comes in, and again, there's that little gap near the medial canthus. And so in front of the tarsus, and then in front of the septum, and then peripheral to that. And so you can see that. That's what it looks like over there. And remember, the obicularis runs this way. It doesn't run sideways across it. So the obicularis helps you to close the lid. It helps to keep the lid up against the cornean, up against the surface of the eye. All right, now we're going more inward. What's the third? Who's that back there? Is that actually good? All right, who's the, what's the third layer in? The tarsus. Now, in a primate, what is the tarsus comprised of? So very, very dense connective tissue. The reason I said primate, if you're ever working with rats or rabbits or anything like that in research, they have cartilage in the tarsus. But primates do not. So we have dense connective tissue, but we do not have cartilage in our tarsus. Okay, what glands live in the tarsus? Myobomian glands. All right, so now we can look at it right here. You can see that you've got the tarsus right here. You've got the myobomian glands. Now, what I like to do to remember this is think of grape vines. Have you ever seen grape vines? There's clusters of grapes, and then they're on a central vine and in a trunk. And so basically these clusters of these grapes, the myobomian glands, dump into this central duct, which then comes out just along the posterior surface of the lid and dumps out. And so this is where the myobomian glands, they dump their sebum component into it, okay? Now, while we're here, the myobomian glands dump one of the components of the tear film. What are the three layers of the tear film? Okay? And then the aqueous and then the oil. All right, so what is made by the myobomian glands? The oil. The oily layer. So the myobomian glands make the oil layer that coats the surface of the tears. That's thought to kind of keep the tears from evaporating. So even if you have normal aqueous production and you've got myobomian gland disease, you get what's called evaporative dry eyes. The aqueous will evaporate because you don't have that secretion of the mucin that's coming from these myobomian glands dumping into the surface of the tear film. All right, so what are, what is this? Why would I be showing you this? Plants probably related to the myobomian glands. All right, now look more closely at those glands. Exactly. So are myobomian glands, aqueous glands? Shake your head, no. No. No. No. All right, so when we think of glands and people just take glands, but there's really three major groupings of glands. And the first is the so-called aqueous glands. And these are glands that have an assener pattern. They form a circle of glands and they secrete their material into the center of the lumen. And so these are lacrimal glands. These are also sweat glands which are now doing profusely right now. Acrimal glands are working beautifully at this point. And so lacrimal glands in the lids are what are an example of the acrimal glands. And so they stay completely intact. They secrete into the lumen. Now the other thing is they have these little flattened myobothelial cells that live between the acinia, the lacrimal, of the, you know, the acrimal glands. And so it's thought that these tend to squeeze if you think about it. So they kind of squeeze that secretion out. That's the way to remember it. Okay, now the lid margin is a target. Oh, yes. So is that the, like the kind of sweat glands and all three of the lacrimal, like the cross movement and lacrimal glands? You just took my next PIMP question after this slide but that's okay. The answer is yes. All right, so the answer is yes. You do get credit for that. All right, so now the lid margin, as they say in top-down, is the target-rich environment for asking questions. So a lot going on here on the lid margin. One thing I want to point out that we forget about is that stratified squamous epithelium on the surface of the lid doesn't end, end to your margin of the lid. It ends almost at the posterior margin of the lid. And so if you're not, this is all keratinized. So keratin is incredibly irritating to the surface of the eye. So if you have ectromion, the eyelid is turning in, even without lashes scraping, just that keratinized epithelium will scrape. So that could really make a difference. But there's a lot going on right here. You can see here are the eyelashes. And what's interesting is you can see some of the lash follicles are really deep. So someone's got trichitis, they've got lashes turning in. You want to just pluck them out. They just grow right back. But if you want to kill the follicle, you can't just zap the edge of the lid. You have to go all the way down to the base of that follicle, which is sometimes at the top of the tarsus here. So here you've got a lot of these eyelashes here. You've got some glands associated with them. And then finally, posteriorly here, this is where the mybomian glands don't get into the mybomian wall. This is way on the posterior surface. All right, so we are looking at, this is an eyelash. Okay, so we've got a specific type of gland that can be associated with the eyelash. And we're going to look, in fact, at two of the glands that are associated with the eyelash. Now, we're looking at this gland. What's going on with this gland? I don't see anything. All right, see these apical projections. So what kind of gland is this? It's an apricot gland. An apricot gland. So that's the second kind of gland that you have in the body. So apricot glands are thought to be a scent gland. And so we've got humans with a lot of apricot glands in our axilla and our groin. But even if you in the eyelid, and it's thought to be a remnant of an old scenting mechanism. So some animals, like, I don't know if you've been out watching deer. When deer are marking their territory, aside from urine and other things, they'll often rub the inside of their eyelid on a branch and they'll leave some of that apricot secretion to mark it. And so these are characterized by this apricot projection. I was interesting about these glands is when they secrete, they actually push off that portion of the apricot apex coming out. So they not only secrete a sebum-like material, but they also, you can see it pinches off the top of the apricot projection. Well, how's the, what is the little, you know, mnemonic we use to remember what the apricot glands are called? Anybody? Mole. All right. So what kind of an animal has a snout? A mole has a snout. And so we mispronounce these. These are the apricot glands of mole. It's actually spelled mole, M-O-L-L. But you mispronounce it as mole and that's how you remember because moles have snouts, apricot glands have snouts. And then of course we, yep. Okay. And of course, we talked about the third type of gland, which is? Holocran gland. Holocran gland. Now, which is characterized by the sebaceous glands, mygomian glands. Now, holocran glands are different. They don't stay intact when they secrete. In fact, when they secrete into their room and they secrete their entire content, they literally regurgitate it. So think back to your days in college when you're out a little bit too late, you buy up a little bit too much and you're sitting on that cool tile floor in the bathroom hugging that porcelain. God, and you become very religious at that point. Oh God, I'll never drink again if I can get through this. And so they literally regurgitate all their contents into the loom. So those are the secretory glands and glands of mygomian glands and also the glands of cites, which are the glands that dump into the hair follicles. So what kind of stain is this? I guess we'll go back. Oil right on. Oil right on. What is this stain? It stains little bits. Yeah, oil. Exactly. So it's a very descriptive stain. It stains little circles of oil red. And so oil red O. What do we have to do to the tissue in order to get this stain? Gotta get to you. Fresh. Fresh, exactly. Because when we process tissue for normal paraffin fixated embedding, we dissolve out the lipids. So if you're concerned about lipids, say you think maybe it's a mygomian gland carcinoma, then you have to have fresh tissue. So this shows you that fresh stain with the oil red O of the mygomian glands. All right, let's talk about some lip lesions. What do we see in here? You're differential of this particular lesion. All right, so now we look at it. Now this is a similar one, only this time it's a younger person who see a couple of these lesions. So sometimes you can have more than one of these clustering. Sometimes these can be external. Sometimes they can be internal. And what's the common pathologic findings in these lesions? Giant cells. All right, so you can see multi-nucleated giant cells, epithelioid cells, but also you have a lot of lymphocytes in these. So this is called a lipogranuloma decyplomation. And if you get plugging of the mygomian bians, then they back up. And the lipid can then leak out of the bians and lipids, very inflammatory, but it's underneath the epithelium and it's in the tissue. And so once this lipid backs up, then it'll reduce the granuloma decyplomation. And that's what we call common, I don't know, proper pronunciation. I don't have, I don't have our German resident here, so. I don't know if it's Kullasian or Shellasian. Well, that pronunciation is really, yeah. Some people call it Kullasian. And here's a close-up. That's a giant, giant cell. Look at the size of that. Huge multi-nucleated giant cell, lots of lymphocytes in here. Lachogranuloma decyplomation. Shellasian or Kullasian. What are we seeing here? It's sort of photographing the left eye drawn to the upper, the lateral flesh pipe, which is cystic region. It's a normal contoured lipid as well. What can you do in the clinic a simple test to see if a lesion is cystic or solid? Translucent. Exactly, so you take your fan off head on your light, you can put it right next to it. And if it's a cyst, it'll just translate right through. If it's solid, obviously the light won't pass through as much. So when we look at a cyst, the key thing we want to look at is we want to look at the cyst lining. So this particular cyst at low power, can you see anything at this low power that'll help guide you to what the lining of that cyst is? Okay. And then what is this stuff? Bunch of keratin. Keratin, so that's the tip off. So when you have a cyst that is lined by stratum excrements epithelium on the lid, it's often got keratin in the middle. You can call these epithelial cysts or epithelial inclusion cysts. And here's a little bit of a close up. There's that stratified squamous epithelium, but this is all keratin. So these cysts will just get filled with keratin. There's a close up. Stratified squamous epithelium, lots of keratin. So epithelial cysts, epithelial inclusions. Now we're looking at another cyst right here. A little bit different location. Kind of the lateral canthal area. And what do we have on the lining of this cyst? Kind of cyst forms as one to two layers thick cuboidal lining. All right, so you can see one, one to two cell layers thick square cuboidal and no keratin or anything in there. So this is called an ekran hydrosystoma. Hydrosystoma literally water-filled cysts. From which language? From the Greek, of course. So the Greeks invented all of ocular pathology. You know that, right? In fact, all of medicine comes from the Greeks, okay? So, sorry, I don't know if we have anyone here whose roots are from China or from India, but they claim they invented everything too. So, as with the Romans, so I really invented everything. So, all right, so that's an ekran water-filled cyst. Now this is a different one. What do we see in here? The filial lining, it's hard to make Let's go with higher power. Oh, look at that. What are those, look at that. I mean, you know, those could be some big snouts. Yeah, those could be big snouts. Yeah, it almost looks like a single, like maybe one or one to two layers thick, lots of snouts, so we're gonna go for all this. It's got me thinking about apricotin. You can actually have an apricran hydrosystoma, lots of snouts. So, you get an ekran hydrosystoma, it's much more commonly, but also you forget, you've got those aprican glands of, who, mole in the eye beds, and so this is an aprican cyst, so you get aprican cysts also. And here you can see it again, look at all those little snouts, sticking out into the room. Aprican hydrosystoma. All right, what do we see in right here? I guess we'll go. All right, what makes you say it's moluscoma. All right, so a hint for oral boards. You guys still take oral boards, I'm sure they're now on Zoom, but when you're showing a picture, first thing you do is you do the thing, well, it's an external photograph of the right upper head, and it features several little lesions that have an raised burly border and a bellicated center. This is consistent with moluscoma. So don't jump right to the diagnosis described first, and then they'll know what you're thinking was, I'm not gonna give you credit for that. But you're thinking was all correct, we just don't know what it was. And so indeed, a cluster of these little lesions, they've got the burly border, they've got this little unbellicated center. This is classic for moluscoma contagiosum. And what does it look like pathologically? All right, so the central crater with the raised edges epithelium markedly thickened, and what else do we see in moluscoma that tells us pathologically that's moluscoma? Exactly, so they call them moluscoma bodies. And so moluscoma is a viral induced disease, and so it tends to take over the cellular machinery like most viruses do. And so it'll take over the cell, and that epithelial cell will suddenly become a virus factory, and then you'll get all these clumped viruses, eosinophilic staining material in the center, and they call this moluscoma bodies. And the thing is, is they all dump out on the surface, which then infects the epithelium adjacent to it. So it's pretty rare to have just a single, molusk, I don't know what a single or molusk is, but you usually have clusters because the virus will spell out, and you'll get multiple clusters of these. What are we looking at right here? I guess that's my bar up back there. Okay, what are we looking at right here? All right, so what would your differential be for a plaque yellowish looking lesion on the skin now? Now we look at the pathology, and this is low power, and I want you to note, shout-out to Grimace Caronite's epithelium, but look at these little kind of foamy, pale staining cytoplasm with the nucleus to the side. Here's a close-up, look at these nucleus here, they're in the center on the side, and it's really ground-glassy, foamy-looking cytoplasm. So what is this consistent with? What is that material that's in there? Exactly, so it's cholesterol, it's lipid, and so these are really foamy macrophages, we call them, if you want to sound intelligent, you say everything with a British accent, so you say macrophages, these are macrophages, and that lesion measured 1.2 centimeters in size, and so it just makes you sound more articulate when you say it that way. You could see these foamy macrophages, and so it's almost like they come in like little pacman, and they gobble up that lipid, and they gobble up, and then they get really fat with lipid, and so you can see these nice foamy, fat macrophages. All right, guess we're back, back here to Abby, what are we seeing right here? Normal lesion, not involved in the margin, no lash loss, it's raised to a regular surface. What would you think this could be? It doesn't look cystic, it could be a, it could be an SK or a papilloma. Yeah, so when you see this kind of raised, bumpy surface, one of the things you think about is a papilloma, and so when you go back here, you can see at low power, indeed, you see that there are these little fingers of epithelium sticking out, and there's hyperkeratosis, a lot of keratin in between, but what I would answer is, look at these little teeny tiny blood vessels coursing in between these little fingers of epithelium sticking out, so the way we remember squamous papilloma is it's like a gloved hand, and so you've got a thick glove, which is the thickened epithelium and the keratin in it, and then the fingers of these little fibrovascular pores in between, so this is a papilloma, classic papilloma. Another view, again, showing these fingers sticking out around the thickened, acanthotic epithelium, and a lot of hyperkeratosis on the surface, and here's a nice close-up that shows it beautifully, so gloved hand, here's the glove, thick epithelium with the keratin, here's the finger, those little fibrovascular pores in between, so this is a papilloma, it can be viral, or it can be just a reaction, and so squamous papilloma, but not, now sometimes you can get a lot of keratin worlds and keratin parolts mixed in here, a lot of these worlds and parolts of keratin, so definitely hyperkeratotic, a lot of worlds and parolts. There's a cross-section, so just so you think you've got your gloved hand here, and you basically just cut the fingertips off right across, and so you see the center, the finger, and then the glove around it, so central fibrovascular pores, thickened, acanthotic epithelium surrounding it. All right, what are we looking at right here? This is a lesion, that's raised, it's pigmented, it's got multiple areas, they're kind of rough. This looks stryas. So what would this most likely be? This looks like a separate keratosis. Exactly, so all that crusty looking material that that is all keratin, so these often look like what we call stuck-on, and so it's almost like you could just get your finger under there and peel this guy off, and sometimes patients do that, try to peel these things off, because there's a lot of keratin on there. And when we look at it pathologically, boy, it kind of looks a lot like a papilloma. The only difference is, is instead of those fingers sticking way out, the fingers go inward. And so this is kind of like a hairy spider and like a tarantula, so instead of the fingers going out, it's like they go in. And so you've got these epithelial cores going in, and then these fibrovascular tissue in between, again, hyperkeratosis, keratin worlds, keratin plugs and seborrheic keratosis. And the other thing is these can often be brown or tan, and so it's not uncommon that you'll have this little layer of benign melanocytes along the basilar layer of the seborrheic keratosis, and that'll often give it its kind of brown or tannish color. All right, we've got kind of a similar lesion right here. External photograph of the left eye, tension drawn to the lower lid, almost at the lid margin. There's a rough, patchy, nodule, probably some sort of keratin on the surface. Okay, so kind of a similar looking thing to seborrheic keratosis. Now, when we look at it, we see that the epithelium, again, very thick, little fibrovestic cores in here. What is all this stuff down here? What is going on down here? Generationally. Okay, exactly. So what causes this? Solar, sun damage. Yeah, so this is what we call basophilic degeneration. So this is a UV, a solar induced damage. And so remember, these lesions are often on sun exposed skin. And so you can see a lot of UV damage underneath here. Now, when we look at the epithelium, I just want to point out it's a little bit more active than we've seen in normal seborrheic keratosis. On low power, you can see that there's a little muclea in here. The cells are just more active. There's a lot of keratin down deep. And this is consistent with what we call an actinic keratosis. So this is kind of a seborrheic keratosis, maybe more down the line. So this is kind of a pre-malignant lesion. So solar damage, a lot of keratin, epithelium, but just a little bit more active. Clialy, clump, chromatin. So kind of similar along the scalates, every keratosis, but now a little bit more active. So it's what we call an actinic keratosis. All right, what are we seeing on this picture? So external fluid, central ulceration. That's cosmic. Lash loss. Yeah, so this is different than what I've shown you before. Here, there's lash loss. And the margin is kind of thick, and then you've got this ulceration here. Is that important? Yeah, it suggests some kind of more malignant process. All right, so whenever you see lash loss, you really want to be concerned of a possibility of a malignant lesion. So you're looking at this. It's on the lower lid. It's got race, borders, ulcerated center. What would be the most common cause of this lesion? Most common would be it. OK, so if you're looking at lid tumors, and you have 100 lid tumors, 90 of them would be basal cell. And so if you're looking at this, probably 90% of all lid tumors are basal cell. 5%, 6% squamous cell, and then maybe 1%, 2% the other tumors. So by far and away, the most common basal cell. Now, it's most common in the lower lid in the medocampal area. Why? Yeah, your brow shades. And so if you think about it, your brow and your eyebrow here and your bomi prominence here kind of shade the upper lid a little bit. So if you're looking at a sun-induced lesion, which basal cell is, it's more inferior and inferior medium, because it's not quite shaded. So that's where you most commonly see these. Now, these can present sometimes differently. Believe it or not, this is a basal cell. Yet, it almost looks like a solid nodule. But again, some nodule, look at the loss of lashes. So again, concern for a basal cell. What does the basal cell look like, pathologically, if we go ahead and put it in order? Yeah, we see palesating nuclei, and then meaning far and far, which is just kind of like the space that we see around the palesating nuclei. All right, so we call it palesating or lining up, like a little picket fence. No, that's bigger than 5%. It contains lots of lashes, if you saw that from it. But you would have to move it. Exactly. So the problem is, is sometimes you don't know exactly where the tumor is and where it is. And so if you've got a nodule here, you may not want to just remove it there and there, because look over here, a little bit of thickening here, a little bit of thickening here. So you probably, when you're going to try to remove these, you're going to make sure you've got clear margin. So you want to remove a lot more than you think just by looking at the lesion. All right, so palesating, the nuclei in a basal cell, they form these nodules. They line up at the edges. Think of it as a white picket fence surrounding a house. And so it's like a little picket fence surrounding it. And then because these tumor nodules tend to be more solid, they shrink more when we process. This is what we call a meaningful artifact. Meaning it's an artifact, but it's meaningful because basal cells, nodules then shrink more than the tissue around them and you get this little white space around them. So-called meaningful artifact. And here's a close-up. You see the cells themselves, they're large, the space looks like a nucleus, very scant-cytoplasm, but benign in theory. So if you look at these, they really do behave in a more benign way. They'll often be solid or cystic and they don't usually metastasize basal cells. And here's what we call a cystic basal cell or nodulocystic. So big nodule, cyst in the center, but look, you get a low power. Look at the palesating. Look at the little white halo around them where the tissue shrinks more. So nodulocystic basal cell, by far the most common variety. But you can have another variety, let's go behind you there, Anthony, another variety of basal cell. So nodules, these look more like tissues, finger-like, projections, and I think this would be more fiat form. All right, so more fiat form. Is that something that you need to be concerned more about than a nodulocystic basal cell? I think it'd be worse. So the reason is, the morphia form basal cell sent little fingers of basal cell out underneath the tissue and it can even spread under the epithelium and what's called the Pagetoid type spread. So the problem is, you can't see where this is. So nodular type can see the nodule, you can cut it out, morphia form type, these little fingers extend out and it induces a dense, fibrous-connected tissue in between. So they call this a scarce reaction, fibrous tissue reaction. So morphia form, if you're doing a surgery for a morphia form basal cell, you often have to do a particular technique and who's this technique named after? Mo, so now, it's Mo, M-O-H-S, it's not Mo, you know, of the three stooges, you know, not Mo, not Mo. And so if you ever look at those three stooges, it's very bad for kids, they wouldn't allow them on TV now because they're poking each other's eyes out all the time. I got you, look at that, so, different Mo. So this is Mo's, the surgeon. And so Mo's surgery, what you do is you shave off little pieces around the tumor and then you actually have a area right next to the OR where they freeze the tissue and stain it for you and you can look and that way you can make sure you've taken out all of this tissue. And so now this is another type, a little, you know, really obscure variant, I don't even ask anybody about that, but sometimes these basal cells could take on a more glandular element and so they'll even have like a glandular type of basal cell. Now, this is a little bit of a different look in basal cell, now Mo, what are we looking at right here? This is C, top C, top B. Exactly, so we call this a basal squaine. The reason that that's important is the basal squaine is a little bit more aggressive than a simple basal cell. So basal squaine is, of course, and they take on more characteristics of a squamous cell addition to a basal cell. Now, the reason for that is basal cells arise from a pluripotential cell along the basal layer of the epithelium. So they can actually transform into more like squamous cells or more like basal cells, both. Now, you say basal cells are benign lesion. Yeah, that's true. This is a patient that Rick Anderson had seen even before he was here, this is an old picture. This lady is a rancher from Nevada. She came in, we did a biopsy, she had a morphiform basal cell. They said, we've gotta take this out or it can grow. She said, I'm an old lady, leave me alone. And she went back home. This is now 10 years later. Now, her daughter brought her in, and she had a piece of Kleenex stuck over this lesion. We took off the Kleenex, that's what it looks like. Now, the reason that the daughter brought her is because it's melt. And so you can see if you let a basal cell grow for 10 years, believe it or not, that's the sinuses you're looking at. And there was even CSF dripping out. So by now, this is more than just a housekeeping problem. I mean, you have to do a hemifaceectomy to take care of this. And so, you know, morphiforms, get them out while you can. Don't let them grow to this type of lesion. This took 10 years, but it can be quite destructive if you let it grow locally. All right, different kind of lesion. I guess this looks like external photograph of the left eye, on the lateral, central area of the upper eyelid. This is extremely large from hearing of crusty ulceration. And if you can surround it like this, great, this could be a basal as well. All right, so because you've got this kind of parchment look to it, not so much ulceration, but this parchment look to it, you'd be concerned about a epithelial lesion in this case. Of course, the most common one in the upper lid is a squamous cell. Now, sometimes, look at this patient, a lot of sun damage all over the skin, but it's interesting, they call this a rodent lesion. Now, again, my brain remembers things differently. And so, a rodent lesion, it looks like a rodent took a bite out of it. So that's how I remember a rodent lesion. It looks like a mouse nibble on it. And so, it's got this little erosion here. And that can also be a squamous cell. And how is a squamous cell different than a basal cell? Hapercaritosis, get keratinorols as well. Keratinorols, and the cells are not these big blue nuclei. They're more this pink cytoplasm with a nucleus that's got nucleoli in it and a pink cytoplasm. So a lot different looking. Looks like epithelium, basically. Only it is active at this point. Squamous world, squamous world. So this is a squamous cell, of course, in my mind. Now, what are we looking at right here? I start photographing the right eye. There's thickening, especially in the upper eye, the margin of the eye is very any objective. And, you know, in this context, what's that to do with thickening and lousy clashes? We'll be concerned about sebaceous carcinoma. Okay, so we call sebaceous gland or mybomine gland carcinoma the great mimicar because they'll often present like something else. So this particular patient had a red irritated eye. This has gone on for like a month. And so first thing, what do they do? They go to the dock in the box, you know? So what do you get when you go to a dock in the box? Everybody gets genomycin. So I don't know where in the teaching of medical students now, they trained you to use genomycin, but nobody uses genomycin. You guys have probably never even written a script for genomycin, so you get genomycin. And then the patient comes back two weeks later and they say, oh, it's the irritated eye here. We'll switch you to Neosporin. So then they use Neosporin, it's not any better. Finally, the patient comes in to see you and you see them, you say, wow, look at this. Lin-margin, look how thick that is. And those yellowish areas that they could have a little bit of lousy clashes. So you're concerned here, would not be a crime, you know, for a congenitivitis, but would be in my bone and gland carcinoma. Now, these can sometimes be a little bit more subtle. In fact, this particular patient presented with what was called a recurrent chelazion. So they had a chelazion and then they drew you up with hot packs, bless you. It went away, it came back again, but look at that, it's kind of lumpy, bumpy loss of lashes. And so, again, a great mimicker. And so sometimes my bone and gland carcinoma is gonna present as a recurrent chelazion. And you look at them, you can see this particular one at least, it's got kind of a glandular look to it. You see all those little white spaces, that's the dissolved lipid from when you do the normal processing. So it still at least looks like a gland, but sometimes these can be extremely anti-plastic and they don't even look like glands. And if you look right here, look at how active that looks. Now that's important because remember I showed you basal cells, they look kind of benign, they behave benign. These look really malignant and they can't be malignant. In fact, these can metastasize. So these can be very nasty tumors. And in fact, if we look at a closeup, Ashley, what do we see in right here? Exactly, that's a mitotic figure. So these are very active lesions. They have mitotic figures in them. Now these can be poorly differentiated. That's a nice mitotic lesion. But one of the things that can help, look at these little white areas here, that is dissolved lipid. And so that often helps to differentiate this when you look at it pathologically. And then of course, what kind of stain is this? Oil red oak. So it stains the oil, little round ores of oil. And so this tissue has to be, how do you have to prep the tissue to do this stain? Oh, fresh. Fresh, so remember, you can't put it in formal and this has to be fresh tissue. So this is an oil red oak stain of a mycomaean gland carcinoma. All right, what do we see in right here? See, okay, so what would you be concerned about here? All right, so we see a pigmented lesion. First thing you always want to think about is, boy, you don't want to miss a melanoma. And so you look at it and you say, wow, there's no loss of lashes. It's kind of uniformly elevated. Probably a nevus. And we look at it and what is the show? All right, so they're at the junction, but also they are at, so what would we classify this as? Compound. So if the melanocytes are just at the junction, we call it junctional nevus. If they're at the junction and underneath it combined, we call it a compound nevus. If they are just completely below the epithelium and don't affect the junction, we call this a dermal nevus, exactly. Now remember, in the lid, there's no dermus. It's an incorrect term, but it's there. So we still call it dermal nevus. But take it, I guess, you should call it subepithelial nevus, but it still is a dermal nevus. All right, now we're looking here. Abby, anything alarming in this picture? Yeah, the spread along the margin as well as lash loss. All right, so your concern here would be what? Like a melanoma. Melanoma, exactly. So you can see again, sun damaged skin. These lesions don't just pop up out of the blue. They'll often occur in people who have had a lot of sun exposure, a lot of UV exposure. Now, just like my Gobi black arsenomes, these can metastasize and people can die from these. So you wanna not miss these. And when you look at it, you see these nests of melanocytes. They're underneath the epithelium here. But you look at them in close-up. So you see these are active. Now, they don't necessarily have to be black in pigment. They can be just brownish pigment. And then, that's a malignant melanoma. Now, we're looking at a lesion here. This guy did not get punched out. So this isn't, you know, your Saturday night referral from Rock Springs. You can talk about your own hometown. You're allowed to talk about your own. So that's okay. What are we seeing here? My attention is drawn to a very swollen left upper lip. Kind of swollen, push out. It's not cystic. It's very doughy. It's almost infiltrative. And then you look at it and you see these cells. What are these? Like lymphocytes. Exactly. So this is just a sheet of lymphocytes. So don't forget, although lymphomas are most common in the orbit and also projectiva, they can extend sometimes underneath the lid. And so you don't want to miss a lymphoma that either. Now, primary lymphoma rising just under the lid is pretty darn uncommon. It's usually an extension of an orbital lymphoma. But you see this uniform sheet of these lymphocytes. And so this is lymphoma of the lid. And when we get to orbit, we'll talk more about how we're seeing and how we differentiate lymphomas. This is an interesting lesion. What are we seeing right here? So external photograph potentially to the left by the upper lid is a sort of violaceous counter of carrying lesion with erosion of the lid itself, especially with more lateral. All right, so you would be concerned about this. Now, I don't expect you to know what this is because I just want to show you that can be really obscure regions in the island. But the key thing I want you to recognize is it is this big kind of violaceous dome-shaped lesion, loss of lashes. It's really irritating and there's this crustiness around it. And we did a biopsy on this. And this turned out to be a very obscure tumor called a Merkel cell tumor. And these are tumors that again can be very aggressive. Look at that mitotic figure there. Big mitotic figure, these big cells with mitotic figure. So you can get very obscure tumors. This is thought to be a neuroendocrine-derived cell, very obscure tumor, but just remember, you can get weird, rare tumors of the lid also. So I want to show you one more. It's kind of an epithelial-looking cell and then surrounded by all this stuff around. Yeah, I'm not exactly sure what that is. Okay, believe it or not, you can also get tumors that are mucin-producing. So this is an adenocarcinoma. And so I really miss Fred Jacobiak, who was the ophthalmopathologist. He used to be at the AFIP in New York and then he actually ended up in Boston, outside of New York. But he was the best lecturer on ophthalmology. Sadly, passed away a year and a half ago. But he would describe this as islands of epithelial cells surrounded by a sea of mucin. And so think about it, these little islands of these epithelial cells, this is actually adenocarcinoma and this is all mucin. And then we do a mucin stain and you can see the mucin stain's pink here. This is called a mucicarmine, a mucin stain. And you get these islands of epithelial cells surrounded by a sea of mucin. So I just wanted to show you those last two. I hope they don't put something that obscure on boards. You never know, but hopefully they wouldn't. But you can have very strange, very weird tumors occurring in the island, both primary and metastatic, mostly primary but weird ones. And so this is an adenocarcinoma of the lid. And so very obscure tumor. And last but not least, we say goodbye to the Last Supper once again. And this is actually said to door into the church from the dining hall. And there's the Last Supper. No, I wanted to leave just a couple of minutes or we've got like five minutes. Questions? That means you guys know it all. Yes. How's the sebaceous cell? Is there anything unique, like characteristically that causes like the pedagogy of spread through the skip lesions that they talk about? You know, I'm not sure exactly what it is that leads to that. And so sometimes what'll happen is you get that little pageatoid spread, it'll skip around. And it's almost like the basal cell carcinomas, the morphiform basal cells. For some reason these cells will skip areas and go around. I'm not sure what it is. They're not the ones that have that pageatoid type spread. If you look at them, it's not like they're less differentiated because the tumors are poorly differentiated anyway. So I'm not sure what exactly the etiology is. But those amorphiform basal cells, for some reason they're not continuous. So they'll actually skip the spread and the pedagogy doesn't matter. So that makes them, again, amenable to more of a most type surgery than just a direct surgery. Other questions? All right, next week is conge. I believe we're in order again. So next week we'll be conge. All right, thanks.