 before the holidays. So you guys get a two-week reprieve. So this will be your last band blessure until July 8th. Alright, so you guys get to go on my ESCRS trip as always as it's a tradition. This is Vienna. This is the ceiling of the... ...the people that are here. It's spectacular. So basically you go in and everybody walks in and it goes... Oooooh! And that's immediately followed by 500 people going... ...what the thought is. Or they're doing this. Selfies. I was there. Okay, well I don't have a selfie stick. Sorry. I'm not in any of these. You notice there are a number of people in Dr. Manilas' photos? Yeah, because I don't have a selfie stick. No. I mean I don't have a selfie stick. So this is one of the... ...the people... ...the people who's there. This is literally him... ...sitting there in any of these rooms. I don't imagine that there's still any kind of... ...optimic tissue in there that we could evaluate. And this is the altar. I mean up against spectacular... ...spiritacular beauty and carvings and altars. This is still a functioning church. So they've got fires in there and concerts in there. This last time I was in Vienna... ...there was a full blown concert going on when I was there. But I'm not going to put you guys through the video... ...we'll see the concert. And then as you go in it's got the size... ...the passages going up and the ceiling. A lot of natural light. So we're going to talk about the Conjucaiba. So Kela, Conjucaiba, tell me about the main areas... ...of the Conjucaiba. So Bulbar means literally on the globe... ...next to the Bulb. And so the Conjucaiba will actually blend at Olympus... ...with the corneal epithelium... ...and then fornicile here forming the fornices... ...and then palpebro being on the... ...inside surface of the island. So three basic parts to the Conjucaiba. Now, let's go back a little bit... ...to some of the pathology here. First of all, advice. Tell me about the epithelium of the Conjucaiba. It's a stratified, splamous, non-prater. Okay, well I know this is low power... ...with these little white spots on here. It's a goblet cell. Goblet cell. What do goblet cells make? Music. Music. Katherine, why is mucin important? I was talking about the tear film. Okay. So what are the three layers of the tear film? Mucin. Okay. So the mucin layer is the innermost layer of the tear film. It's made by the goblet cells... ...and it makes the surface of the eye wettable. I guess it's a better word. So if you look at the pathology on light microscopy... ...of the surface of the cornea, it looks totally smooth. But if you look at electron microscopy, it's not. There's little microvillies sticking out all the time. And so if you just put water on there on aqueous tears... ...it would just kind of wash off and not spread out equally. And so when you line the inside of the tear film with mucin... ...it covers that. There's a jelly on the surface that allows the aqueous layer... ...to smoothly coat the surface of the eye. And then finally the lipid layer, the outside layer... ...which cells make that? The micromine. The micromine. The micromine. So they keep it from evaporating. So if you'll notice right here, as you get closer to the limbus... ...there are no goblet cells. And so the further away you get from the limbus toward the fornex... ...or toward the medial and lateral canthi... ...the more goblet cells you have. And so this is why if you have a disease... ...a cicatricial disease, a scarring disease... ...where the fornex gets shortened or it gets scarred off... ...you lose that production of the mucin... ...or people get severe dry eyes. So if you go ahead and... ...you'll get some severe dry eyes. Okay. We're going to just talk about some different lesions here. Becca, what do you think this is? It's like a dermoid. Alright, more specific. A limbo dermoid. Okay, so this is even more specific. This is hard because the term dermoid... ...is confusing because you say dermoid. Is that the cyst in the orbit? Is that this little growth at the limbus? So the technical term, it's limbo dermal choristoma. So that's really what the term should be. And this will separate it from the dermoid cyst. What does choristoma mean? It means a proliferation of tissue that's not... ...and it's normal site. Okay, I suppose it's amartoma. Which is... Okay, good. And so choristoma is benign proliferation. It's not a tumor, but it's tissue that normally... ...doesn't belong there. So if you look right here, you see this is a child. And you've got this fleshy white growth right here at the limbus. Alright, we're just going to keep moving down the line. What disease do we often see associated with... ...limbo dermal choristomas in children? Golden heart syndrome. Golden heart syndrome. And what are the other signs and symptoms of golden hearts? They can get like... Yeah, they get these funny kind of skinny teeth with... ...you know, spaces in between. Sometimes some scowl won't always. But the key is if you see a child with these... ...this limbo dermal choristoma, you want to look in front of the ear... ...for these little pre-regular skin tacks. So you can often see that with golden hearts. Alright, so the reason why these are called the choristomas... ...there's tissue that's normally not there. We're just going to keep going down the line. So what kind of tissue are we seeing here? Exactly, so you wouldn't expect to see those at the limbus. So there's connective tissue here. But you see, here's a hair follicle. And here's even a sebaceous gland with it. So you see a lot of connective tissue. That's why it's that white bump. But you'll see hair follicles. You'll see hair shafts. And then you can even see this kind of stuff. You know, what is this? Two funny things. Here's one. Here's another. Okay, what kind of gland do you think those could be? They sort of look like they're assenar in shape. So I wouldn't call them a sebaceous gland. Yeah, sebaceous glands, do they have assenar shaped glands? No, so what do you call them? They're sebaceous glands, dude. They're working profusely in you right now. They're sweat glands. Sweat glands, well. And also lacrimal glands. And so these are little lacrimal glands. And then there they are, the assenar shaped lacrimals. What is this stuff? That actually looks like bone. Not quite. I'm sorry. Cartilage. Cartilage. And so that's what's interesting about these corastomers. All kinds of tissue could show up there. And so you can see, associated with this, assenar glands, little almost like sweat glands or lacrimal glands. And then cartilage. There's cartilage that's right here. And here's a close-up of the cartilage. And so actual cartilage. Interesting. All right. Bad picture here. But Chris, what are we looking at here? So we see this kind of raised yellowish lesion right down the congee. Exactly. What do you think that could be? I mean, if this was taken in Utah, that could be a pigwecula. Yeah, exactly. So we live in Utah. So, I mean, on my normal orders I have when the technician just writes up any patient. It says, pigwecula dry eyes. And so that's every person in Utah has pigwecula dry eyes because we have its elevation here. There's lots of UV exposure here. And of course, it's very dry here. So pigwecula are just very common because we've got 300 days of sunshine except when there's inversions. But remember, even UV light penetrates the inversion. So where your sun less is even in inversion when you're outside. And so this is a pigwecula. What is this? It's a teridium. Teridium. What's the difference? So the teridium crosses the limb bisque and grows onto the cornea. Exactly. So it's the same pathology. It's just pigweculas over the carcinoma. Teridium crosses and goes onto the cornea. And when you look at the pathology, what is the pathology? You see a lot of, so, solidastosis, a thinning of that kind of substantial appropriate down there. And then we see this basophilic degeneration and oftentimes the thinning of the epiphyllium as well. All right. So it's a disease of the subepithelial tissue, chronic UV exposure. And you get that little fraying, kind of frayed elastic look to the collagen, the so-called solidastosis. But then you can get kind of a smudgy blue basophilic degeneration of collagen. You can even get this stuff. What's that magenta colored stuff? So like some calcification. Calcium. So you can even get calcium in these. So when you look at the Teridium at the slit lab, you can even get sometimes these little white flecks of calcium. And so you can sometimes get a calcification with these. All right. I don't know you. I'm a medical student. All right. Students get immune from pimping. Maybe though. I don't know if you're going to be here in two weeks. Maybe not. Okay. Let's see. All right. What is this? The upper lids inverted. You can see the cystic white structure. All right. So you see this kind of a cystic structure. And how's a good way to tell in the clinic if it's really a cyst or if it's solid? You can trans-eliminate it. Exactly. So you take your fan off head and put it right next to there. And if it trans-eliminates, you know it's cystic. It doesn't. It's solid. And so this looks pretty cystic to me. And so when we look at this, we want to look at the lining of a cyst. So we look at this lining. What do we see right here? So it's multiple layers of stratified squamous epithelium. And what are these? Those are stratified squamous epithelium with goblet cells. So what kind of cyst do we call this? Epithelium. Exactly. So it's very similar to the lid. So for some reason surface epithelium gets deposited underneath. And then it can just start growing in a lofin form of circular cyst. Now these cysts can grow with time. They can even get filled with mucin. So they've got some mucinous material in them. So it's called an epithelial inclusion cyst. All right. So what are we looking at down here? So this is an external photograph of what looks like to be maybe the left eye. And on the lower palpebral conjunctiva, we have kind of a follicular-like reaction. Okay. How do you tell the difference between follicles and papillae when you look with a slip-out? So papillae tend to have like traditionally like a central vascular core. Whereas the follicular conjunctivitis tends to have like that cobblestone type. So if it's got a cobblestone and the vessels tend to be around the periphery of these instead of in the center also. So what's the differential diagnosis if you're pulling the lower lid down and you see those follicles in there? I think of like viral or allergic. So those are the two main ones. Viral or allergic. Well, I don't know what's happening. I don't know about you guys' clinic, but I've seen three EKCs in the last two clinics. So, you know, viral conjunctivitis is all over the place. And by the way, it's called EKC. What does that stand for? EKC? Huh. It stands for Epidemic Caridoconjunctivitis because when you get these adenoviruses, it can spread not only through an entire household and family, but it can spread through a clinic. So when these were originally described more than 50 years ago, doctors' offices were spreading these around because they weren't cleaning the equipment, weren't cleaning their hands. So people would come in, you do a tenometry, and then you wouldn't clean the tip and then the next person would get the EKC. And so these can spread through a household. So you've got to warn these people, wash your hands, your own face style, your own washcloth. You know, don't spread this around the house. And so viral, but also allergic, look like this. And when we look at these follicles, you can see they've got this, just almost like a follicle elsewhere in the body. It's a lymphoid tissue. You've got the larger pail lymphocytes in the middle, the smaller purple lymphocytes around it, and then the blood vessels go around the edges. So follicular conjunctivitis. Here's a close-up showing these larger pailer staining, but still benign lymphocytes. All right, what are we looking at right here, Marsha? So this you can see at the central, where the central, at the end of this dots, which suggests the central vascular pele, or central vascular cord of the pele. So these would be more papillae than follicles. And what's the difference again? The central vascular cord. Exactly. So here you see this little central vascular cord sticking up. And so you see these papillae, and you don't have that intense mononuclear inflammatory cell reaction, but this is still reactive. The most common time we see papillae, it would be contact lenses. What do we call that? We call it giant papillary conjunctivitis, another pseudonymeanidino-GPC. So these are, you know, these you can see in people from contact lenses. It can be a reaction to the solutions. It can be a reaction of proteins absorbed on there, a lot of different things. And here we see why we call it that. This is giant papillary conjunctivitis, or GPC. All right, this is, you guys, I don't know if I can pick you guys or not, but if you want to make a stab at it. Extrernal photograph of the hypocea, the whole heart-contract type of superiors. Yeah, so you almost see like little bumps on the limits here. What if this is a teenager? It's a teenager and their eyes are itching intently. Yeah, exactly. So there is a condition called vernal conjunctivitis. Vernal meaning spring. And so you'll often see these in younger people, adolescents, and they're coming with intense itching. And they'll also have papillae inside their lids, but they can get these little bumps at the limbus. And so we call this condition limbo-dermaline. And so this is a young person with limbo, I'm sorry, limbo-vernal. Sorry, limbo-vernals. This is a young person with limbo-vernal. All right, do you want to make a stab at this one? So we have the Lord Pelfi rub conjunctiva with a white appearance. Looks like a little raised, I guess. Kind of raised, almost pedunculated, you know, looking piece of tissue. What would your differential there be? So it could be like large, maybe inclusion cyst. So what if you took a fan off head and shined it, and it turned out it was not... not cystic, it was more solid. It could be more like an internal orelum. All right, so again, think of things like orelums, things like that. Now in this particular case, this is what it looked like. What do we see in here when we look at low power? All right, so we're seeing a really loose connective tissue. Very, very loose, not a lot of fibrous tissue to it. All kinds of capillaries all over the place. And all kinds of little blue dots. I don't know if I said this the very first day, but the first rule of pathology, blue is bad. Okay, so a lot of blue in there. Caleb, what the heck can this be? It could be pyogenic granuloma. All right, so why is it weird that we have to memorize pyogenic granuloma? It's a double misnomer, so you have... It's not pyogenic. It's not pus reducers or it's not p-reducing. It's not granulomidus tissue. Yeah, I agree. So this is one of those double misnomers. It's called the pyogenic granuloma, and that's what it's in the literature. Pyogenic literally means fever inducing. From what language? Greek. From the Greek, of course. So fever inducing, it's not fever inducing. It's not infectious. It's not a granuloma. There's no giant cells. There's no epithelial cells in here. It's an exuberant granulation tissue. And so there's a lot of budding capillaries, loose connective tissue, mixed inflammation. There are a few little PMNs in here, but there's lots of lymphocytes. There's even some plasma cells. So this mixed inflammation, it's kind of a demidas, loose connective tissue, and it's a reaction to something. So it's like an exuberant granulation tissue reaction to something, but it's called a pyogenic granuloma. Again, you've got to memorize it. Double misnomer. What advice would we see in here? So this flip-line photo of the left eye, there's an extensive commosis and an injection of the pyogenic ibis. Yeah, what would your differential here be? Like infectious cause. Okay. So this is kind of more redder than usual. I was trying to take a picture here and didn't do a good job and said, this is what they call salmon color, kind of pink color. So when salmon pops up, what do you start to think of? Lymphomines. Lymphomines, so believe it or not, you can have lymphomas of the conjunctiva. Now, most commonly lymphomas occur in the orbit, but number two is under the conjunctiva. And so sure enough, as we look at the pathology, it's this sheet of lymphocytes. So when you look at a picture of a lymphomine, it looks like someone took a handful of lymphocytes and just smeared them across the slide. And so this is a lymphoma. So remember, lymphoma of the conjunctiva can occur. And if you ever hear someone say salmon patch, because salmon are kind of pink on the inside. So you think of lymphoma. And here we see an immunoperoxidase stain. Most of these are B cell, mantle cell lymphomas. And so they're mostly B cells, not D cells. So here's an immunoperoxidase showing this is a B cell stain. All right, what are we looking at right here? Exactly. Kind of gelatinous, translucent appearance. What would you be concerned about here? Exactly. Some kind of a surface epithelial neoplasia of some kind. Because when you see this, it's not your run-of-the-mill teridium. You know, it's more thickening of the epithelium rather than the subepithelium, which is a teridium. So if you look right here, as the beam hits it, you see this kind of a translucent, thick epithelium here as opposed to subepithelium. And here's just another view that you've got this area. It's kind of a bulimba since the gelatinous thickening of the epithelium. Now, we look at the pathology right here. And what do we see in here at this low power? You see, there's some more cellular atypia, as you get closer to the basement membrane. And you also see some keratin at the top. Yeah, this may even have a little bit of keratin. So it's a little dusky keratin at this region. What's the most important layer we need to look at in a specimen like this? The basement. The basement membrane. So let's say, for argument purposes, that the basement membrane is completely intact. What would we call this? We call it CIN. CIN. And what does CIN stand for? Conjunctival Interepithelial Neoplasia. Exactly. And it's even the same category that there's actually cervical interpithelial neoplasia. But we're not doing cone biopsies here. But it's the same idea. It's a mucus membrane that starts to go rogue. And when it does, you can get it replacing the epithelium itself. And the key difference between CIN and Frank's Quimsilcarcinoma is that the basement membrane is still intact. All right, Becca, when we look at CIN, we subdivide it into three different areas pathologically. How do we subdivide it? So... All right, more specific. First category. And what part of the epithelium is involved when it's mild? So now it's really hard. So it's like everybody knows the answer. And as soon as the spotlight hits them, as Winston Churchill said, an iron curtain descends, you know, across your cerebral cortex. When the spotlight hits, it goes chink and you'll... What's your name? The first... The... Exactly, so it's the lower third. So when you remember, epithelium grows from the basement membrane up. And so when it's mild CIN, it's the lower third. Moderate is up to two thirds. Marked is full thickness. So that's how we grade them. And it's important because the more of the atypia you have, the more chance you have of it going on in Quimsilcarcinoma. And so you look here at this one. Here's the basement membrane. And look at all these nucleoline here, pleomorphism. So how would you categorize this one? So this would be... marked or severe. So mild, moderate, marked or severe for CIN. And here you can see again, it's definitely goes full thickness. Look at that. Here's a huge cell, multiple nucleoline, very active looking. So CIN with marked dysplasia. Kara, what do we see in here? What does leukoplakium mean? Basically, because you remember, leukocytes, blood cells, so white plaque. So this has probably got some keratin in it. So again, our differential here would be versus squamous. So these lesions do tend to arise from the limbis initially, both CIN and squamous cell. And so if we look right here, how is this different from the previous one? It looks like in this photo, the basement membrane is disrupted. Exactly. So here's some abnormal cells sneaking through the basement membrane. So the brave Texans are sitting in the Alamo and they're sitting behind the basement membrane wall. And then, oops, you know, a few thousand soldiers come over the wall and breach the basement membrane, and then you're toast. So basically, once those epithelial cells breach that basement membrane, it becomes a superficially invasive squamous cell carcinoma. Stop that. Yawning is contagious when she starts here. Be careful, did it earlier, and I want someone to yonze every distance. Stop that. All right, so you can see right here in this one, these cells have gone well beyond the basement membrane. And in fact, what is this stuff right here? Is that a keratin pearl? It's a keratin pearl. And so these can actually make keratin, even though, you know, normal conjunctivitis doesn't make keratin when they're stimulated, you know, whatever it is that makes them displastic. You can actually see here's the displastic cells and they're passive basement membrane, and it's just as appropriate. And you can even see keratin worlds and keratin pearls. And so these can be pretty nasty. This is an exenteration. And here you can see this is actually going into the sclera. And so you see this squamous cell carcinoma actually growing down through and even under the sclera. And so if you can remove these before they spread, you can cure them surgically, but once they start to spread, they can go into the orbit. They can go into the scar. They usually don't eat through the sclera and go into the eye, but they can certainly spread throughout the orbit. And that's Rachel. So if these tumors spread, where do they go? Or how do they get out of the eye sometimes or the orbit sometimes? What the heck is this? It's a structure here with some funny tumor cells involving it. It's a nerve. And so boopy will often stress this. When you've got squamous cell carcinomas, oftentimes they can spread along the nerves if not even inside the nerves and go through the orbit even back to the brain. And so one of the things that you'll really stress when you're concerned about these squamous cells spreading is look for hyposthesias. And so especially if they're going inferiorly and going along, you'll look for some inferior-infra-orbital hyposthesia in some areas where these tumor cells have gone along the nerve because that's how they spread back. So about once every other year we'll show one of these at orbit conference and the anesthesiologists will show how it's spread along the nerves to get back out of the eye. So remember these squamous cells, they can go to the... the ones from the lids will often go to the nodes, but the ones from the... that spread from the conjunctiva can often go along the nerves and then spread. There you can see again, here's a nerve and here's these tumor cells right going along the side of that nerve to spread. Tina, what are we seeing here? So this is a good picture. The reason I show this is look at... here's pigment here, superficial along the limbus. What is that right there? All right, so there's a lot of pigment here, but look at the change in the color. Look, this is that brown pigment on the surface. Where is this located? It's deeper to the sclera. So the reason I like this picture kind of shows the difference between superficial pigment and then deeper, deep to the sclera pigment. So when you see someone like this with this deep pigment, maybe even underneath the sclera, what do you think about? Well, eventually you would, but this is still really early on. Where would you want to look elsewhere in this patient if you see this deeper pigment here? You'd want to look elsewhere around the eye. So this is actually an oculocutaneous melanosis. And so it's not yet melanoma. It could become melanoma, but the difference is it's not surface melanocytes, it's deep melanocytes in the coroid or underneath the sclera. And these people can also have melanosis on the skin and the eyelid and even on that half of the face. So people could get, it's called oculocutaneous melanosis. You can also get what's called the nevus of odor. And so this is melanosis, rather than melanoma, it's a deep pigmentation. All right, Chris, what are we looking at right here? Here we're seeing, it's kind of, it looks a little raised and maybe a little pigmented to me, almost a yellowish-brownish lesion on the conch right there. Just probably medial to the limbis right there. All right, so what would you be concerned about here? So I mean pigment of lesions, we think about, you know, could this be just a nevus, could this be Pam, could this be, in the worst case, melanoma? All right, so if you look, you don't see that superficial, you know, dusting that you normally see with Pam. So this is more just kind of a diffused, lighter-brown color there. Sometimes these can even look red. And so this is a nevus. And the classic story, usually you'll see these, these will be adolescent age. And so oftentimes you'll question mom and mom will say, yeah, it's been there for a few years, it's bigger. And so oftentimes these can even be congenital in nature, but they'll look kind of pink. It won't be that elevated. But as the kids hit the beginning of adolescence and finally into puberty, melanocytes really grow. And so these things will grow when kids start to hit their growth spur, which gets younger and younger every year now. And so my theory is it's all the hormones they give the, you know, cattle that they grow. So when we eat those McDonald's burgers, we get hormones and so on. They're really nutritional. And so people are hitting puberty much earlier now than 100 years ago. I mean, we're talking like two years earlier. So these kids hit puberty, they hit late adolescence, these start to grow. They become noticeable, noticeable to mom, noticeable to the, to the teenager. And so we can remove these. And when you remove them, this is what we see on this particular lesion. What the heck are these cystic areas? Show you a close-up. There's melanocytes here. And then scattered throughout are these little cystic structures. What kind of cells are these? They look like goblet cells, exactly. So these are actually epithelial-aligned cysts. So when you remove anivis, you know, anivis, and you see epithelial-aligned cysts, that's a good thing. And that means this has been there for a long time, maybe even congenital or certainly since the child was very, very young. And so the way I remember these is which embryologic layer do melanocytes come from? Neurocrest. So the melanocytes come from the neurocrest. They migrate out to the junction, you know, between the epithelium and the substantial property. They start to grow. Eventually they drop off into the sub-epithelial tissue. And while they're doing that, they grab epithelium and pull it with them. Okay, now don't say that on boards. That's not, but that's how you remember it. Okay, so remember this, just don't, when they ask you on boards, how does that happen? Well, it grabs epithelium and pulls them down, so don't do that on oral boards. But that's the way to remember it. So when you see these epithelial-aligned cysts with these benign neva cells, this tells you this has been here for a long time, maybe even congenital. All right, so when we, I can just do, when we subdivide, so Shrava, when we subdivide these, you know, nevi, there's a lot of it depends on where they're located. So what kind of a nevus would this be? So I see some bolognus sites in the epidermal, and that's how nevus? Well, this would be definitely at least a junctional nevus. Now, if you look down here, a lot of these cells are actually plasma cells, lymphocytes, and even macrophages chewing up a little bit of pigment. So technically this one is still right there at that area. So this is called a junctional nevus. And then as those cells drop down, you can get more of a compound nevus. So you get melanocytes, both at the junction and subepithelial. And then lastly, when you completely lose your connection with the junction, this is the equivalent of a dermal nevus in the skin. Obviously there's no dermus in the conch, so we call this a subepithelial nevus. So you can have junctional, you can have junctional and subepithelial, it's called compound, and then you can have just subepithelial nevi. The reason that's important is, once nevi lose their connection to the junction, they lose their malignant potential. So when you have a junctional or compound nevus, still that could become a melanoma. When you have a strictly subepithelial nevus, there's no malignant potential. Alright Brad, what are we seeing right here? So this is an external photograph. When you see around the limbo region, there's an area of pigmentation. And so differential at this time would be, like a nevus or primary acquired melanosis or worst case scenario of melanoma. So when you look at it though, you don't see thickening, you just kind of see superficial dusting, and so this would most likely be a... A PAM. A PAM, what does PAM stand for? Primary acquired melanosis. Melanosis, exactly. Every year I tell this story, but it's a great story. So this lady comes in, you know, on the psychiatric rating system, on an anxiety scale of, you know, one to four, she's a 10. And so she has this lesion on here. She's convinced she's going to die of cancer. She went to the internet. She's convinced she's going to die of melanoma. I told her, don't worry about it. This is, you know, just superficial. It's not a tumor. We're going to take pictures of it. Come back in six months. If it ever grows, we'll take it off. But if you notice any change, give me a call. So that evening, I'm sitting at home. The resident on call calls me. Said, did you see Mrs. Sonso today? Yes, I did. Well, she's calling me now. It's growing. And so we removed it, which is good, because we often don't remove, you know, what, you know, lesions that don't have any atypia. And sure enough, we got this pathology. And so what do we see in here? So we can see that this is stratified squamous epithelium, not a keratinase. So coming from the conge, and along the basal layer there, there looks like to be pigmented cells, which would flow into melanocytes. Exactly. So in PAM, we subdivide it into PAM without atypia and PAM with atypia. So this is PAM without atypia. It's pigmented melanocytes right along the basal layer, no atypia, no spread through the epithelium, no atypical features. And this is what racial pigment looks like. And so, you know, if you see someone who's darker skin and they've got this little pigment around the limbus, that's what this looks like also. So benign melanocytes along the basal layer. Here they are, totally benign, PAM without atypia. What are we seeing right here? So we see a small photograph of the right eye showing hyperpigmentation, a temple to limbus, and there seems to be disruption of the limbus and surrounding tissue. You'd be more concerned about this one, because this isn't just superficial dusting. So we take off this tissue, and sure enough, what are we seeing here? We see the hyperpigmented melanocytes, but they seem to be all over. There is a big basement membrane there, but this is still not beyond the basement membrane. So this is now PAM with atypia. So when you start to see the melanocytes invading up into the epithelium and showing dysplastic features, it now becomes PAM with atypia. The reason that this is important is PAM with atypia can be a precursor to malignant melanoma. So if you take 100 malignant melanomas of the conch, 80% of them will have pre-existing PAM with atypia. Now it's not the flip side. It's not 80% of PAM with atypia goes to melanoma. It's not, but if you have malignant melanoma, about 80% of them will arise from pre-existing PAM. And so this is something you've got to watch really carefully. It'll pop up in different places. What's interesting about this picture right here is if you look, there's some scarring here. This patient has had previous removal of lesions, and he would just keep popping them up. And so you would take them off, and then a year later he'd come back. There'd be different ones in different places. And they start looking like this. And so your concern is when you get PAM with atypia, you know, sometimes you can see this. Look at all the scarring and the Cymbalepheron. But you see pigment here and here, but look, pigment in the fornix. And so one thing you've got to take away today, pigment of lesions in the fornix is melanoma until proven otherwise. So if you see pigment down here in the fornix, you don't say, wow, it could be PAM. But you can't just take that for granted. You've got to remove it. So pigment in the fornix there is melanoma unless proven otherwise. And as we look right here, I know it's a low power. I'll go to higher power. Here is epithelium. Here are the melanocytes. In the epithelium, in the epithelium, oops, breaking through the base of membrane in the sub-epithelial tissue. So this has now gone from PAM with atypia to malignant melanoma. So you can see, look at these bizarre cells, these big cells, big nucleoli, lots of clump chromatin, bizarre-looking cells. So malignant melanoma arising from pre-existing PAM. And then you can do special stains if you're not sure. Reporting differential to tumors are hard to tell, but this is an immunoperoxidase stain and this is a stain called HMB45, which stains four melanocytes. It doesn't tell you whether the benign or malignant but it tells you they're melanocytes. So you can always do special stains for sure. This is what happens if you don't take care of these. And so these can invade locally, they can invade into the orbit, they can metastasize, they can be very nasty. So don't let them get to this point. This is Mozart. All right, so see, I do put people in here. There's some people in there. I just don't want to make you guys look at pictures of me. And so, all right now, I left like a couple of minutes here for questions. Questions on any conclusions, including malignant lesions. So if you see a new patient and they have like PMS, would you generally take photos of them to track that? Or do you see if they look normal so you don't bother? Yeah, no, I'll take pictures because pictures is very good to document something. I mean, you know, if you're really convulsive, you would draw something and you could draw it in there and you can measure it and all that. And I do measure pigment lesions, but it's always a good idea to take a picture because then when they come back again, in six months you can compare the person directly to the picture. So I'll often photograph them, any of the pigment lesions that are suspicious. Other questions? Yes. Do you have like a lid or skin question? How is a nevus different from like a freckle? And how would we do similar set on pathology? Is there a difference? Freckle is a bad term because freckles are just variations of nevi. I feel this or something. What's that? So the E-P-H-E-L-I-S or there's like a more technical term for it that comes up on questions like on all the questions. That's a term I don't know. I'm sorry, I'm not aware of that term. So what's it again? You be able to tune me and I'll see what it corresponds to. Yes. So in terms of pyogenic granulomas, I find that the hardest one to see on pathology is in terms of identifying it. So what are some like characteristic features of it that we should look for? Hang on, we'll get to it. So one of the key things when you look at low power is it's a very loose connective tissue. It's almost a deminus. So when you look right here, you see it looks white. So instead of being fibrotic, instead of being pink, instead of being collagen all over the place, it looks white. It's got edema. It's got fluid all over it. And it's got all of these little capillary spaces in it. So these little blood vessels, if you look carefully, there's blood vessels everywhere. And most lesions are not that vascularized. Even a papilloma is not that vascularized. And so when you look right here, you see that it's very, very vascularized. It's got loose connective tissue. And then when we look at higher power, it's the cell type. It's a mixture. It's not only lymphocytes and plasma cells, but it's also PMNs and even eosinophils sometimes. And so loose connective tissue edematous, lots of budding capillaries, and a mixed inflammatory cell reaction. PMNs, eosinophils, lymphocytes, plasma cells. But it's not, I mean, it's not an infection, right? No, it's actually a granulation. It's an exuberant healing response. Yeah, I guess I'm kind of, why do you have neutrophils in there? Because when I think of neutrophils, I think of like an acute inflammatory cell. Well, sometimes this can be due to, like, a foreign body irritation. Sometimes this can be due to an old suture fragment and just anything that triggers it will do that. And so whenever you get an exuberant healing response, PMNs are part of the healing response. So it's like a healing response from a muck. It's kind of like a cheloid, only of the congenitiva. But I hate it because it's a double misnomer. So you've got to memorize that, you know, it's not pyrogenic. It's not a granuloma. It's granulation. Other questions? Yes? Oh, you don't, they look the same. It can be either one. They really look the same. It's those little melanocytes along the basilar layer. So we'll often see that in people who are darkly pigmented. You'll see around the limbus, this brown pigment all the way around. And if you were to take the pathology of that, it would look exactly the same as Pam without ATB. Oh, that's not true. Well, it's not necessarily Pam. I call it racial pigmentation. But pathologically it's Pam. But it's racial pigmentation. Pam you usually see in lighter pigmented people. But it's exactly the same pathology. It's benign melanocytes just along the basilar layer. So racial pigmentation looks just like Pam if you were to take path. If it grows, if it's thick, if it's irregular. And so when you look at this, Pam is just strictly flat, almost like somebody just dusted the conch with pigment. Well, Pam with atypia definitely can look irregular. So we're talking about Pam without atypia. That's where you see right here. It's just that little surface dusting. It's almost like the good fairy came and sprinkled, you know, melanocyte dust on there. And so you can see right here it's flat. It's not elevated. It's just that little area of dusting right there. Whereas Pam without atypia, Pam with atypia, is often thickened. It's irregular. You know, you can see right here. It's irregular. It's thickened. It's got fingers going out. It's multi-centric. That is what you really worry about. So that's when you worry about that it's either Pam with atypia, or maybe even going toward melanoma. So you've got to continue to remove this. And atypia, we saw a few years ago, and literally he had a couple of different times these would pop up. You'd take them off. He'd be fine. And then you'd come back, you know, six months a year later. And then boom, you'd have more lesions popping up elsewhere. So something is disordered with his melanocytes or maybe had chronic sun exposure, or whatever that triggers these. Regarding those lesions, have you heard of this new classification system in semen or contractival melanocytic and trapezole myoplasm? Is it just a different way of... You know, we're not good enough with just classifying something so you can memorize it and remember it forever. And so about every 10 years, you have to sit down and reclassify it so you have to learn a whole new thing. In my career, the lymphomas, the lymphocytic lesions have now been reclassified three different times. So you have to drop everything you know and reclassify it. Surface neoplasia of the eyes, you know, including skin and contractiva with the squamous cell, neoplasma, those have all been changed. And you know, all this stuff where I used to talk about, you know, is it carcinoma and situ? Is it, you know, just within the epithem, is it beyond? Now they all lump it together into this ocular surface neoplasia. So for boards, you guys have to remember that. I'm grandfathered. I don't have to take boards anymore and I don't have to waste neuronal space learning new nomenclature for the same thing. But for you guys, you do. So when you look at that, make sure. Because you know, we've got all this nice thing about CIN and all that. Now it's all lumped under the category of ocular surface neoplasia. But it's all part of CIN going to squamous cell. I think it's easier to understand if you think it in terms of CIN and the three levels, and then microinvasive and then invasive. But again, we have to reclassify everything by every 10 years. And so once you guys know them all and you pass boards and you're in practice 10 years later, you're going to be reading a journal and go, what? So don't worry. It'll happen like three times in your career. They'll reclassify everything. You have to re-memorize everything. And for racial pigment, can that eventually change into PMM? It can, but very uncommon. Usually it does not. And so, you know, melanocytic lesions just like melanomas of the skin and elsewhere, very uncommon in pigmenting people. More common in people who are just really white, you know, white white people. Other questions? All right, very good. Have a great Christmas. Thank you for the interview yesterday. Oh, you're welcome. You're welcome.