 I guess, unless you're, I don't know, even ocular plastics, you know, are going to have to deal with glaucoma to some degree. So it's something that is just, you know, found through all specialties, and no matter what you, I think, almost no matter what you practice. So it is something that we all need to know and know how to deal with. I wish we had some more hands. But so just a few basic things out of the book. And so we talk a little bit about, you know, taking O-caps and taking boards and just kind of the nuts and bolts of some of the things you need to know to do that. I think that O-caps and boards are still the same in that what you need to know is in these basic science series. And so the glaucoma one is a very, you know, manageable book. And so I hope that you read it and study it. And we'll try to do our best to add to that with lectures. But in this first section, some of it is just kind of nuts and bolts of things you probably need to know and things that you'll find on O-caps. So I just wanted to go through a little bit of that with you. So if you just look on, if you have your book or have access to it, no problem. But in terms of the definition of glaucoma, it, right out of the book, it says glaucoma represents a group of diseases defined by a characteristic optic neuropathy that is consistent with excavation and undermining of the neural and connected tissue elements of the optic disc. And by the eventual development of distinctly patterns of visual dysfunction. So that's basically the definition of glaucoma. Glaucoma is an optic nerve disease that is characterized by this very kind of specific kind of optic nerve change, this thing we call cupping, and then thinning of the neural retinal rim. And with an associated visual field defect. And you notice the word pressure is not in the definition of glaucoma. Pressure is the number one risk factor for glaucoma. It's what we treat, it's what we spend all of our time talking about. But yet it's not in the definition itself. So as it says here, elevated intraocular pressure is one of the primary risk factors. It is the most important risk factor, especially the higher that pressure goes. But its presence or absence does not have a role in the definition of the disease. However, we have shown that intraocular pressure plays a pivotal role in the pathophysiology of the disease, no question about that. So in the late 90s, this normal tension glaucoma treatment trial is really the first trial that established pressure as part of the pathophysiology of glaucoma. But it's not part of the definition of the disease. And I think that's really important. We spent so much time talking about it, but it does not define the disease. Does that make sense? So I think the way that the reason that is, we all know that a person can have really even quite severe glaucoma and never have a documentable high pressure. So that's just the definition. The other thing here in this opening part that I think is really, really important is this classification of glaucoma, is this table right here? So just one little recommendation as you're studying for OCAPS and boards, know the tables in these books really, really well. Because oftentimes a lot of questions come from the tables. I remember when I took my board exams many years ago, there were at least two, maybe three questions on this drug called Derenite. I had actually, I was taking my boards. I had actually never heard of that before, Derenite. And I found it, it drove me crazy. So I went and found it in the BCS series after I'd taken the boards. And it was buried in some table. It's an old school, oral, carbotic, and hydrogen-hydronecetazolamide in any way. So these tables are very important. And this table one-on-one about the classification of glaucomas, I think is really an important table in terms of kind of how we think about glaucoma. And I think this table right here not only is it important kind of factually, but I think it's very important in terms of just your clinical orientation to understand these classifications as they are in this table one-one. This table one-two for me is not as helpful like when I'm in the clinic actually thinking about making diagnoses and designing treatments. But this table one-one is very helpful to me. And it's kind of the way I have things organized in my mind as I'm working through diagnoses in the clinic. So if you look at that table, first off about classification of glaucomas, we have open-angle, as you know, we have angle closure, all right? And then we have the childhood glaucomas. And within those categories, the open-angle, you have primary and you have secondary. And then an angle closure, you have primary and you have secondary, all right? So you can kind of see these branching definitions and classifications coming down. So right there in open-angle glaucoma and related diagnosis, primary open-angle glaucoma, P-O-A-G, the one that we see the most and in reality understand the least, I think, of this good old P-O-A-G, what in the world is it? And why do people with this disease have the problems that they do? But P-O-A-G is defined by the angle, right? Looking at it gonioscopically, so we're going to talk about gonioscopy here in a bit. But primary open-angle glaucoma is not associated with any known ocular or systemic disorder that can cause increased resistance to aqueous outflow or damage to the optic nerve, nerve usually associated with elevated IOP. So P-O-A-G, you do gonioscopy and you have a normal appearing angle, all right? And you have no other associated secondary findings that will go over in a bit. And there's no other systemic relevance. They're not on steroids, blah, blah, blah, blah, you know, you just make this list of exclusions. It's primary open-angle glaucoma, this fundamental disease. And usually people with P-O-A-G kind of, again, as it stated here, have elevated intraocular pressure, all right? For reasons that we don't entirely understand, their trabecular mesh work is broken down. So P-O-A-G, then you have this other category of normal tension glaucoma. And I like the way they define it here. I think this is the most common way to think of it nowadays. It says it's considered a continuum of P-O-A-G. And I would recommend that you think of normal tension glaucoma as that. It's a continuation of P-O-A-G. If you look at the Baltimore Eye Study, one of the most famous studies done in ophthalmology, published in 1991, the Baltimore Eye Study showed the prevalence of glaucoma as it related intraocular pressure, okay? And so the higher that pressure goes, especially when it gets above 30, the prevalence of glaucoma really starts to take off. But relative to this, the interesting thing is that as you come down that curve of the Baltimore Eye Study, right, you've got prevalence of glaucoma here and intraocular pressure here. Intraocular pressure is 30, you've got a really high prevalence, right? But as you start coming down into other pressures, you still have glaucoma. And as you get down into the lower pressures, it's just this smooth curve of prevalence. There's not another spike down there that might indicate that normal tension glaucoma is some separate disease, it's some separate entity. It's just along the continuum of that curve that associated glaucoma, prevalence of glaucoma, with pressure. And so that's the way I think we ought to think of normal tension glaucoma. It's just a continuum of POEG. But again, normal angle, normal everything else, no secondary cause. It's just that the pressure is kind of on the lower end. Those people don't have documentable high pressures. That makes sense. So POEG, normal tension glaucoma. And then again, within this group of kind of normal open-angle people, you have another category of juvenile glaucoma, and they are defined by age. They tend to have, on set of their disease, say between age 4 or 5, up to maybe age 30, okay? And they fall in this juvenile category. So, and the thing about the juvenile category, that group, they can have very aggressive disease. And also, they're the ones that are found to have the glaucoma GLC1A, the myosiline gene, as 90% of juvenile glaucoma is caused by that gene, okay? So there are your primary open-angle group. You have POEG, usually high pressure, normal tension, same thing, but just lower pressure, and then the juvenile group. Now within the open-angle group, there's this whole secondary category. So these people, you're going to look at their angle, and it's open, but oftentimes you're going to find something wrong with them. That's where the pigmentaries come in, the exfoliation disease come in. Their angle's open, but there's an identifiable secondary cause to their glaucoma. And the two that I just mentioned, pigmentary exfoliation, are by far the most common of that group, right? But you're going to look at their angle, and it's going to be open. So I think that's just a good way to not only understand the information, but a good way to have it in your mind when you're in the clinic, kind of dividing those up. Then we have the next category, which is the angle closure group. And this is, I really like this table. It's a really good way to divide up these angle closure patients. Again, same kind of nomenclature. You have the primary angle closure glaucoma with pupillary block, right? So what is that group? What's the angle going to look like in primary angle closure glaucoma with pupillary block? How's the angle going to look? Closed. Excellent. And what are you going to differentiate that group from, say, the chronic angle closures? What's their angle's closed, but what can you do to that angle? You can open it up like with that indentation or compression goniostomy, right? You're going to open that up and then you're going to almost always see the angle structures. And do you see PAS? No. Okay, that group, in the strictest definition, the angle's closed, but it's because of pupillary block, right? You've got that bowing forward of the iris, but you don't have PAS forming yet, okay? So it says movement of aqueous humor from posterior chamber to anterior chamber restricted, at the point of irritable and ticular contact resulting in anterior iris bowing and contact with trabecular mesh work. That's the classic primary angle closure glaucoma group with pupillary block, okay? Now another category, you have the acute angle closure glaucoma. Those are the ones that you as residents, you know that group, right? Because they're the ones that come to you in the middle of the night. And they have got angle closure. They have actually, you know, they've got pupillary block, angle closure, acute, and the pressure's 60, they're throwing up, and that's when they've gone into this acute angle closure glaucoma attack. There's the subacute angle closure group, which is those are having intermittent spiking, okay? And that's a tough group to diagnose sometimes. It's mostly a historical diagnosis and then, of course, on your gonioscopy, all right? So I think those are kind of the pupillary block group. You've got, you know, just angle closure where they're not having an attack, but you look at their angle and you, boy, that's closed, but you can compress. It opens up. There's no PAS. And then that group can go on to either this acute or subacute angle closure group, okay? Angle looks the same, though. Of course, in the acute angle closures, the cornea is usually cloudy and you can't really tell exactly what's going on. Now that's opposed to the chronic angle closure. The chronic angle closure in my mind, they are defined by PAS, some type of closure of the angle that I cannot open on compression gonioscopy, right? Or maybe it's partially open. I could open part of the angle, but part of the angle is stuck closed with PAS. And that's where you start getting into the chronic angle closures. To me, the reason that's important is because in my mind, they present very differently. You know, the chronic angle closures, they just walk into your clinic and they might have a pressure of 40, but they're not having the pain, et cetera, et cetera, because it's built up just kind of chronically over time. I think that that slow rise in intraocular pressure, and so they're not having all the pain and issues that the acute group has. And then you've got in that chronic angle closure group, then you have the secondaries. And the secondary angle closures with pupillary block, they're the ones that the pupillary block occurs as a result of a mechanism other than iridocornial or excuse me, iridolenticular touch and pupillary block in that way, right? They have something else causing the pupillary block. The classic one being a big lens, okay? So I think these are in some ways kind of, this group, there's a pushing mechanism. There's something in the back that's causing the angle to be closed and that's not just the iridolenticular pupillary block. Big lens is a classic one, a massive posterior segment hemorrhage that's pushed everything forward, you know, those kinds of things, all right? And then you have another, the secondary angle closures without pupillary block. And I think of these as like the polling ones. These are the ones like neovascular glaucoma is the classic one of those, right? So you've got this fibrobascular adhesion from all these abnormal blood vessels that's just pulling the angle closed. So, you know, again, in this angle closure group, you've got the pupillary block group that's just the primaries, those are the ones that have the classic, you know, some kind of abnormal contact between the iris and the lens, traps the aqueous behind, classic one, iris bows forward. And those are the ones, you do a PI, you pretty much fix them, okay? And then they can go into a Q or subacute depending on their presentation. Then you've got the chronic angle closures, which in my mind are just kind of defined by PAS, right? And that PAS can just be caused by constant contact between the iris and the trabecular meshwork and finally it just starts to zipper up, okay? But then you can also have, that's the primary angle closure, excuse me, the chronic angle closures with PAS. And then you can have the pushers, those are like the big lens, the hemorrhage at the back, or you can have the pullers, which are the ones that pull the angle closed and the classic one being the avascular glaucoma. Does that make sense? So, you know, that table, I do think it's very helpful. And then the final one is this plateau iris, okay? The plateau iris is an angle closure glaucoma, okay? Plateau iris is an angle closure glaucoma, but it has this unique mechanism and probably kind of an anteriorly rotated ciliary body that is just kind of pushing that iris up against the trabecular meshwork, all right? So that's kind of its own configuration, its own definition. So there's open angle, there's the closed angle, and then you've got the childhood glaucomas, which are their own category, not only based on age, but kind of their behavior. And you can have primary congenital glaucoma, again, that is just kind of equivalent to POAG except in infants. You look at their angle and it's a, quote, normal appearing infantile angle, meaning it looks open, angle structures are hard to identify sometimes, but, you know, the angle looks open, but yet they have this very high pressure and those ones you usually treat with goniotomy or trabeculotomy, depending on what you're doing. And then also in the childhood glaucomas, you've got this large category that is associated with other abnormalities. So the next thing is the glaucoma associated with congenital anomalies, Sturge Weber, there's a large, you know, big category of those. And then a secondary glaucoma in infants and children, I think of that one as the secondary, so you have the primary infantile glaucoma, the open angle, you have the glaucoma associated with systemic abnormalities, okay, and then you have glaucoma that is secondary to some other ocular abnormality, inflammation, retinoblastoma, you know, they can get Neovascular disease, but it's just in kids, all right. So any questions about those? So I just would encourage you to know that table there, not only for taking OCAPs, but just how to divide things up in your mind in the clinic. I do think it's really helpful. And like I say, more helpful to me than this table. Now this table, you know, it's important to kind of understand, but for me personally, it's not quite as helpful to me in terms of my clinical kind of division of these categories, if that makes sense, but I would know this one. Just moving on, if we talk a little bit about epidemiology. So the magnitude of the problem, these are just, you know, these are just fun facts that you need to know. The estimated prevalence of POEG in the United States in individuals older than 40 is 1.86 percent, and based on a meta-analysis of population studies. So that would put, according to the 2000 census data, about 2.2 million Americans affected. I swear that number's wrong, or a million of them live in Utah. Okay? So there are so many patients with glaucoma. I just, it just seems like there's so many more than 2.2 million in this country, because every glaucoma doctor I know in this country is just bursting at the seams with patients. So I think we're at least more down to, I mean, it is 2018, right? With the rapidly aging U.S. population, the number of POEG patients is estimated to increase by 50 percent to 3.36 million in 2020. So I know we're pushing that, but I think what, so those are numbers just to have in your mind, right? That prevalence is around 2 percent. However, that is looking at people older than 40. But I think right now what we're seeing, and I think we'll be proven true as these numbers are studied over the next few years, is that we have this aging population in the United States. So if you look down under prevalence, and you look at the various studies, but you look at, as they get older, that prevalence goes up. And it's very different among different ethnic groups, okay? So if you look at the Baltimore Ice Study again, when you look at Caucasian Americans at age 80, their prevalence is still between about 2 and 3 percent. If you look at African Americans over the age of 80, their prevalence is 11 percent, you know, four times what it is amongst Caucasian Americans. And so as we have an aging population and a changing kind of demographic population, and you can put Latinos in that same kind of category, that their prevalence with age is three to four times what it is in Caucasian Americans. So I think the changing demographics and the aging population is really going to push those numbers, I think, significantly higher. And I think that's what we're seeing in the clinic is that kind of change in numbers. Age and different ethnic demographics pushing those numbers higher. So bottom line, there's a lot of glaucoma in this country, a lot of glaucoma. And I really mean that because you look at the Eastern European immigration into this country, which has been quite large to Utah. You know, a lot of Bosnian refugees, a lot of Russian and Ukrainian refugees, like you can't say all, so many of them have exfoliation. It's incredible. And so that just brings a lot of glaucoma with it, and it really is making a difference. So those are the prevalence numbers and the magnitude of the problem. And when you look at risk factors, and all these things are very important, of all the studies, everything you ever read, the number one risk factor just looking at the population demographics is increasing age, I mean increasing age. The older you get, the more prevalent it gets no matter what ethnic demographic you're in. African ancestry, and then you look at some of the others like visual field severity. These are risk factors for progression. Visual field severity, a type of diagnosis. The more severe they are when you first diagnose them, the more likely they are to progress for sure. And certainly elevated intraclular pressure, cup to disk ratio, those kinds of things. But increasing age is just really such an important risk factor for progression of glaucoma. Any questions about any of this? And those are the, that's the open angle glaucomas. If you look at the primary angle closure glaucomas, race, it's incredible the variability within race. So you look at race, and these are really amazing statistics to me. The, in the white populations of the United States and Europe it is estimated at only 0.1%. But you look to the highest known population which are these Inuit Indians, it's 40 times higher than that. It's an incredible variation between an ethnic population. 0.1% to, you know, 40 times that. And then of course, we all know if you look just down, you know, China, Japan, Singapore, that whole kind of Pacific rim, the amount of angle closure glaucoma there is way, way more than we see in the United States. And because those are such densely populated areas, worldwide angle closure glaucoma is a much more significant health problem than open angle glaucoma. Even though here in the United States it would be just the opposite of that. Where the blue-eyed numbers today differentiate the African-Americans into like Caribbean Islanders and that such? It's all seems to be the same. If you look at the whole kind of that African continent ancestry and the Afro-Caribbeans would be a part of that. That it's just, you know, significantly higher. But it's not, it's not that much like, for example, one of the big eye studies is the Barbados eye study and most of those folks obviously would be a, you know, kind of African descent and their numbers match those of the African continent. And not only is the, that's an important thing. I'm from New York City and we go a lot of Islanders over there and they always seem to have very scary glaucoma. I'm just going to say that not only is the glaucoma more prevalent in those, in the people of that ancestry, but it seems to be almost a different disease. If you look at, just looking at these one numbers here, but, you know, like if you look at, yeah, so if you look at persons aged 40, 60, 65, the likelihood of blindness from POAG is 15 times higher among blacks than it is among whites, okay? So I mean, that's a huge discrepancy there. So, yeah, it's more prevalent and it almost seems like a different disease in people with African ancestry. And then the last thing I'd like to talk about here, just kind of going through the book, is about the genetics. So, again, if you can't, you have to say about the genetics of glaucoma that it's so far been really disappointing. So I was a resident at Iowa in 1993 when the Iowa group, you know, Ed Stone and Leal were in that group, published the first found glaucoma gene, this GLC1A, you know, GLC1A. It is the first glaucoma gene, this myosilin, the gene that was found to be, you know, 90% of the cause of juvenile glaucoma and about 3% of POAG, okay? So of these patients that come into your clinic and we define them as POAG because they're a little older, 3% of them that'll be due to this myosilin gene. And who knew that at the time, you know, in 1993, it's 25 years ago that, 25 years later, that 3% POA gene would still be the most important POA gene that we have, really. And that's, you know, unlike macular degeneration where, what, like, you know, you guys help me out. Like 75% of all AMD is explainable by two genes and they've got them and they're working on them and, you know, working on gene-directed drug therapy for those kinds of, those genetically induced AMD. We have nothing like that in glaucoma. There's a few genes, so there's that tiger myosilin. There's the optineurin gene, which came out, you know, a little while later. You know, it represents a very small portion of opening glaucoma, maybe a slightly higher degree of the normal tension glaucoma. But there isn't kind of that slam dunk. This gene represents 30 or 40% of all the POA gene. That gene hasn't been found. And there are many who have been working at this for 25 years who feel like it's not going to be found. And I don't know what that means genetically, but they just say it's not there. So who knows what it is that's going to be found. Maybe some, you know, you think of the AMD, maybe it's like this is some compliment factor gene that's, you know, found this way upstream kind of gene. But we don't have that in glaucoma. I sure wish we did. So this first gene found, the GLC1A, is still really probably the most important. Now if you go down this list, and these are some things you need to know, there are some genes that, you know, for the syndromic, like the rigors, you know, exfoliation, now this is loxylone. You know, there's some of those that are more important. But if you just look at run-of-the-mill, you see the GG not much, which is really too bad. But that's kind of where we're at. So those are just some basic facts. I just encourage you to know those. And again, that table one one in terms of having in your own mind a classification scheme that you can work with in the clinic. And so one of the things I wanted to talk about here today, because we don't have an official lecture on it, but when you look at this topic that we're talking about today, it's so dependent on gonioscopy that I wanted to talk a little bit about gonioscopy. And so gonioscopy is based on, the reason we need to do it is this very simple thing about total internal reflection, right? That the light coming from the angle of the eye strikes the cornea at just the right angle and that all of it is reflected back. So total internal reflection is the issue we're trying to overcome. That's why we can't see the angle. And so we have to come up with a way to do that. And we do that by placing a lens on the cornea, which changes that refractive index right there and allows that light to come through. And on the left, we just have an example of a direct gonioscopy lens where you're looking right at it, the classic one being the kepe lens. You all have probably never even seen a kepe lens before, but that was back in the day, just prior to when I started in ophthalmology, gonioscopy was done by going into this separate room where you had this big thing hanging from the ceiling and it had this special light source and you put on a headlamp and you put on a kepe lens and you would directly look at the angle with this kepe lens. But almost all that we do now is to the right and that is this indirect viewing where we have a mirror which shows us a reflected image of the opposite angle. And this is an example of this kepe lens system. You can see this handheld kind of, almost like a portable slit lamp and you have a light source in your left hand and you're looking directly at the angle that you're looking at rather than a reflected image. But most of what we do is all indirect gonioscopy and this is just some examples of indirect gonioscopy lenses, the classic three mirror on the upper left, a susman lens. My favorite gonioscopy lens by far is this Zeiss in the lower right corner. The optics are fantastic. The handle is excellent. I personally, my arms are kind of short and so one with a handle works better for me than the susman here. And if you're going to do ophthalmology, of course I'm biased, but I think you have to invest in gonioscopy lens. I know they're expensive. I think that Zeiss would cost like 450 bucks or something. They are not cheap. The Posner, which is up there, the upper right, is also a good lens. I don't think it's as good as this Zeiss, but it's way less expensive. I just have my own gonioscopy lenses, of course. I just carry with me that little kit of lenses that I have. It's right in my pocket because you're just taking it out all the time. But you just can't do glaucoma. You can't make the diagnosis without doing gonioscopy. I can't tell you how many times I've been either surprised at, wow, this is a closed angle. Just looking at this at the slit lap, I would have never guessed that this angle was closed. Or you do gonioscopy and you realize this is all burned out pigmentary because of all the pigmentation in the limb, but I didn't see it in the cornea or the transnumination, defection. It's just got to be done. You need to have a way to do that, so I would encourage you to invest in a gonioscopy lens and just have it with you as much as you can. So this is just some examples of doing gonioscopy, positioning them at the slit lamp. This is kind of an old three-marrow style here versus the other thing. Of course, it's so nice about these newer ones you don't have to have any gel interface or anything like that. You just go right on the cornea and it's just a great way to do it. These lenses make it as easy as possible now. It's so different from what it used to be. I just got to say, it's interesting to me, it really dates me to how old I am. These pictures were taken when I was a resident in Iowa, and that young girl right there in the slit lamp is Lee Alward, who's the big Iowa glaucoma guy. That's his daughter, and that daughter is now a glaucoma specialist and is just taking Lee Alward's place, just joined her dad back at Iowa, which is kind of a cool thing. When I was reviewing these slides, I was reminded of Lee's young daughter, who is now a glaucoma specialist. These drawings are some of the most famous ankle drawings in the world. They're done by Lee Allen. Are you familiar with gonioscopy.org that Iowa does? It's a fantastic website for all things gonioscopy, and I would encourage you to spend some time there. What this is trying to show here is this idea of the corneal wedge. Can you see that right there? This corneal wedge, the corneal wedge is really valuable, and it's really important to learn how to find that corneal wedge. The way that I find it is, if you have your light beam kind of straight on, you get a narrow beam, and then take it one click to either side. You know what I'm saying about this? Just take it one click, so you've got it on a one click angle, and you can look at that corneal wedge, and what that identifies is Schwalbe's line, correct? Because that's the end of the endothelium and the cornea, and that's where that wedge points you. That is a very, very important thing to learn how to do, because you will sometimes be fooled by an angle that you think might be open, and actually what you're looking at is a sample aces line, which is pigment that's actually anterior to the true pigmented TM. And that's something that just over the years, as residents and fellows have done corneoscopy, and then I've gone in, they've said it's open, and I've gone in, that angle's actually closed, and what you're looking at there is a sample aces line. That's probably the number one kind of diagnostic mistake that I see young, you know, corneoscopists make is confusing the sample aces line with the pigment of TM. And the way you get around that is you are able to find the corneal wedge in that one. It's like the North Star, right? It always points you to where Schwalbe's line is, and that's where you know is your starting point. And, you know, you have that sample aces line sometimes, and then you try to find that corneal wedge, and you realize that those two beams are not meeting. Meeting Schwalbe's line is actually behind that iris, and that angle's actually closed. That's really a common thing. So again, this is just showing the angle anatomy. You can see the corneal wedge that tells you where Schwalbe's line is. See what I'm talking about that corneal wedge? Those two, you know, the external and internal corneal reflections coming together in the Schwalbe's line where the endothelium starts, and then you have the open-angle structures there. Now show some actual clinical pictures here in a bit. Again, this is just a wide-open angle with all of the structures. You see the corneal wedge, that's Schwalbe's line. Then you have the trapezoid meshwork. You have kind of a yellowish scleral spur. So those are your main landmarks, and then you have the ciliary body face, and then, of course, the iris. So the real things you're looking to identify, you're looking at all the structures, but scleral spur, can you see the scleral spur? If you can see the scleral spur, you have an open-angle, right, kind of by definition. If you can see the scleral spur. So recognizing that scleral spur is really an important thing. The meshwork, of course, and Schwalbe's line are all just important landmarks. Again, just another depiction, the little less pigmented. And, you know, sometimes these angles are tricky. If the pigment isn't just right or there's too little or sometimes too much, it's hard to pick it out sometimes. So you just got to do a lot of practice. So here's one, kind of a classic thing where you've got a lot of pigment in the trapezoid meshwork. And so you look at that, and, you know, that's a beautiful angle that you can really zero in on all your landmarks. So here's just, you know, a good old kind of, you know, angle that we can look at. And we're going to call this primary open-angle glaucoma So what do you describe to me some of the structures that you see right there? You see them all? That's right. So you've got... So this is the pigmented TM right here, right? Scleral spur. There's a nice looking scleral spur. So you do have some pigment anterior to the traditional pigmented TM, okay? But that's an open-angle. No, you know, there's not any secondary identifying markers are just good old open-angle. You can see all the structures. You know, that picture is obtained without compression or indentation. Gonioscopy, that's just the way the angle looks. So, you know, all the structures are there, open-angle, and that's just, you know, helps you to make the classification. What do you think about this angle? Heavily pigmented, all right? Very much so. And not only is the angle pigmented, but the iris is all pigmented. Do you see that? I mean, there's pigment kind of speckled around on the iris. Heavily pigmented posterior TM, significant amount of pigment anterior to the traditional TM, but a beautiful scleral spur, right? The anterior face of the sclerary body. So, you know, these are really nice structures here. There's the anterior sclerary body face, scleral spur, right? Very heavily pigmented TM that kind of spills on over into the traditional non-pigmented TM. So, what do you think this is? What's that? Pigment dispersion. This pigment, yeah, pigmentary. Pigment dispersion. If they have glaucoma, you can call it pigmentary glaucoma. So, this is secondary, right? This is a secondary open-angle glaucoma. Pigmentary. And there's one of the most important ones. The most important secondary open-angle glaucoma, especially around here by far, the most important secondary one is exfoliation disease, okay? So, exfoliation disease, it is something else, this disease. You know, as I follow this more and more, I have a whole clinic full of exfoliation disease patients. And these eyes are so abnormal. I mean, they are abnormal from front to back. And I think their corneas are more fragile. We know their lens iris diaphragm issues with cataract surgery, et cetera. Their glaucoma is very aggressive. I swear their optic nerve is more susceptible to damage. Exfoliation is nasty. And so, that's a tough diagnosis to give a person. But it is absolutely the most common secondary open-angle glaucoma. So, let's look at an angle of theirs. And this is a classic to me. This is the classic kind of exfoliation kind of angle appearance. It's open, right? But you have this kind of... People describe it in different ways. For me, I just kind of call it junky. You just kind of get this junky-looking angle. It's not the real smooth, heavily pigmented angle that we saw of pigmentary, right? It's much more splotchy than that. You can have pigment kind of going all over the place. It's kind of got that look. And the iris is a little bit kind of scallopy-looking, not entirely regular. You just look in there and it is open, right? You can see all of our structures there, but it just kind of looks like that. That's a classic-looking exfoliation angle to me. And you just look at that and you go, you know, that didn't look very normal. That didn't look like that's going to work very well. And, boy, does it not work very well. So, that's an exfoliation angle. It's a good thing to just kind of have that image in your mind. Okay, what are we getting into here in these two slides? So, you've got a closed angle at the top. Now, one of the most important tricks to know about doing gonioscopy is what I call, not just I, but we all call looking over the hump, right? They can have this hump of iris out there, but actually behind that, the angle is open. Okay? You just got to see over that hump. Now, how do you do that? When you have a mirrored gonioscopy lens, and let's say you're looking, you know, it's opposite, right? So, you're looking in, say, the nasal mirror, but that's giving you the temporal angle, right? And you can't really quite see the structures. How do you have them try to make those structures more visible, this idea of looking over the hump? You have them look toward the mirror that you are looking into, right? So, if you're looking into the nasal mirror, you're looking in a right eye, you're looking into the nasal mirror, you have them look to the left. I just say, okay, just look a little bit to your left. And that kind of rotates that eye, and that's something that you want to always be able to do. If you can't see structures, there's a couple of things you do. If you can't see the structures, the first thing I have them do is look a little to the left or right, depending on what mirror I'm looking into to see if I can see over the hump. And very commonly, that angle is wide open, you just got to get over the hump. If that doesn't work, then you do this. That's kind of the order I go in. You do compression or indentation, and it blows open. So, is this a more primary angle closure or a chronic? There's no PAS, right? I mean, that's a wide open angle. So, that's a classic angle closure with pupillary block kind of appearance, right? You blow it open, you get this beautiful angle, all the structures, easily identifiable. And then, you know, just very gently let that compression off and just watch that iris kind of come back into place. And I think that's a good indicator of how they might respond to a PI, right? You blow it open, boom, wide open looks great, and then you just kind of let off your pressure a little bit and that iris kind of bows right back up and covers it. That's usually an eye that responds well to a PI. Okay? I've got just a couple more here. This is just more of the same. Now, sometimes when you're doing that indentation, you can see here, no angle structures on the left, but you can see them on the right, but sometimes when you do indentation, you get those corneal folds. You can get them more or less depending on the patient, and you kind of have to look through those a little bit sometimes when you're doing indentation, but you can still kind of see through and see what you need to see, okay? But just another example of indentation. Intentation corneoscopy or compression corneoscopy. These is? Yeah. So this is a terrible diagnosis to give. NVG, you got the, you got PAS drawn up there, you got blood all over, you got the abnormal vessels. So, you know, it's interesting sometimes that when you're diagnosing NVG, sometimes you can have NVG without NVI. So, you know, when you're, it's just one of those things. You got somebody in your clinic, it's high pressure, you know, you're kind of trying to figure things out. You just got to do corneoscopy. It's amazing sometimes, you know, there was no NVI, there was no, we didn't really suspect NVG, but you do corneoscopy and voila, there it is, you know. And this is a real obvious one. It can sometimes be more subtle. Sometimes you just see, you know, to have a glaucoma, to have high pressure, you don't necessarily need PAS in NVG, and you don't need tons of blood around. Just those blood vessels alone that are crossing up over to the TM, the idea is that those blood vessels are just a marker of this kind of fibrovascular membrane that's kind of growing up over that whole thing. And so, you know, it doesn't, it can be pretty subtle. I mean, you can be looking at a pressure of 45 and do corneoscopy, and the neovascularization can be pretty darn subtle, but you have to really look for it, okay, and make sure that that's not what you're dealing with, because obviously you're going to take them down in a totally different path of treatment. It's NV, okay. Very good. And then I think I've got maybe one more here. Okay, so in contrast to some of the other compressions that we've seen, what do you see here? Some synecail. What's that? There's some synecail. Yeah, so this is, you know, this is hard to get, this is, I think, a really good one. You can see when you, again, this is compression, so we're blowing that open. You can see some kind of, this is what I call low PAS. You have the iris that's just starting to get up to the ciliary body, just starting to fasten up there, but then you have this over here, which is just a PAS that's up over the whole angle structure, okay? So that's kind of my definition of low PAS. You'll see me write that in the chart sometimes, low PAS, that's what you see on the right, but then PAS closure is over here on the left. We're kind of the whole, all the angle structures are covered by PAS. So this is definitely in that kind of chronic angle closure category with PAS. Okay, very good. So I think that does it for what I have this morning. So just a few things about this introduction to glaucoma. Oh, I'm sorry, I was going to say one other thing. So the epidemiology, know the prevalence data, know those kinds of numbers, but they are increasing, I think age and demographics is changing it. Genetics, I wish we were better. The basic definitions, definition doesn't include pressure. It's an optic nerve disease with a corresponding visual field defect, but pressure is definitely part of the path of physiology. Gonioscopy is critical. It's our classification system, so you just got to do a lot of gonioscopy and make sure that you know exactly what you're dealing with. Then the final thing I was going to say, just this introduction, is about examining the optic nerve and about the tools of examining the optic nerve. So glaucoma specialists tend to be big fans of the 90-dopter lens. The 90-dopter lens is the lens I use almost all the time because you can get through a relatively small pupil and you deal with a lot of small pupils. It gives you a stereoscopic view, unlike the direct ophthalmoscope, and it gives you an adequate level of magnification. So the 90-dopter lens, I'd encourage all of you to have one of those if you don't. Now there is like a super pupil or a myotic pupil lens, super pupils, and I had one of those for a period of time, and I was using it several years ago, and it's fantastic for getting through the pupil. And holy cow, it's amazing the view that you can get even through a very small pupil. The optics are remarkable, but in my mind it didn't give me enough magnification of the optic nerve like the 90, and so I left that and went back to the 90-dopter lens. It just wasn't enough magnification. Now the other lens that is really, really good is either a 78 or a super 66. Fantastic for a magnification, but you really need a dilated pupil to use that one very well. So I think a classic set of lenses, if you're going to do a lot of glaucoma, would be to have a 90 and either a 78 or a 66, of course a 20 for your fundus exams, and then a gonioscopy prism. That's kind of the set that I think is best for examining and doing a lot of glaucoma. Those are expensive, I know, but they really do make a difference. I've had lenses, I still have my lenses. In fact, I've had to bring back out my lenses that I had when I was a resident. I still have them. They're still working and still function really well. So you get a case, take care of them, keep them with you. They get lost more than they wear out. But those ones I'd recommend a 90, either a 78 or a 66 or 20, of course, and then a good gonioscopy prism. If you can get this ice, that's the one that I recommend. Any questions or anything? All right, thanks everybody for being here. Appreciate it.