 It's all right, so I'm going to go the other way now, because we don't want it to be personal. Chris, can you tell me a little bit about the trajectory of the measure? We divide it into areas, what do we talk about in the parts of it? You have the ciliary body, you have the iron curve descending on the nose. All right, so when we talk about the ciliary body, there's a couple of different ways you can describe it. You can describe it by what we see anatomically when we look in with the gonioscope mirror. And so gonioscope is that mirror thing that you put other patients on and you try to fill that in and you can see the mesh work, except you can't, it's not like the textbook. When you start doing gonioscopy, all you see is you see about three faint lines and you go shoot, is that what I'm supposed to see is, I hope it isn't closed, you're going to do about 200 gonioscopies to figure out what you're looking at, but when you're looking in with the gonioscope, the first thing that you see that denotes the anterior most point of the trabecular mesh work is Schwabbi's line. What is Schwabbi's line? Some of his line is where the cornea is inserted into the sclera. More specific. The part of the cornea. So the decimates membrane? Decimates membrane, exactly. So where decimates membrane ends and the trabecular mesh work begins, that Schwabbi's line is looking with your goniome mirror that denotes the anterior most edge of the trabecular mesh work. And then when you look in, you see this area here, what is that when you sort of call it? You look in with your goniome mirror. Is that the trabecular mesh work itself? Well, how do we subdivide the trabecular mesh work when the corneas are goniome mirror? Pigment portion. Alright, is the pigment a portion down here or is the pigment a portion up here? Down farther. Exactly. So what do we call this more anterior problem? Nonpigment. Nonpigment. Exactly. So when you see a line that's more than nonpigment and trabecular mesh work, then you see a darker line that's the pigment and trabecular mesh work. What do we see underneath the pigment and trabecular mesh work? You see Schwabbi's line. That was up here. I'm sorry, Schwabbi's line. The sclera's work. The sclera's work, exactly. So here's the sclera's work. The sclera's sticking out. And then finally, what's the last thing that you see? Even below the sclera's work? Scleric body. Scleric body or Irish roof. You can start seeing them. So if you think that the trabecular mesh work is a triangle, its apex is right where Schwabbi's line is, and then its base is denoted by the sclera's work. And the sclera's work is a piece of sclera that comes in and sticks out. And so it actually acts as a shelf where the trabecular mesh work lives. And so it goes around 360 degrees. And it helps support the trabecular regular grain here. Now, Lee, what is this structure I hear? Slum's canal. Slum's canal. What does slum's canal do? Basically, it's the conduit for aqueous humor into the penis system. Exactly. So slum's canal, if you look at it, it's this kind of oval shaped canal. It goes around 360 degrees. You have like a tube. And so the trabecular mesh work, the aqueous goes through the bars of the trabecular mesh work and then into slum's canal and then eventually out of these aqueous veins and then draining out of the eye. So if we look at a close-up right here, other crits, if we look at a close-up right here, what is this area right here called? That is the juxtape cannula flutter. The juxtape cannula, like other salads or areas. So why is that important? Because that's the area of most resistance. Exactly. So this is where you get resistance to aqueous flow. And so when aqueous flows in here, it's not just an open mesh work. It's not like an open sponge, you know, where fluid goes through. You actually do have some cells lining slum's canal, this juxtape cannular area, those. Although they don't have tight junctions, they do have some junctions. So there is some active transporting, in addition to passive transporting, aqueous through these juxtape cannular cells. And so when we look at it, we think this is really where the side of opening of a glaucoma occurs. Something is going on right here. Now when you look at a straight-through mesh work, you really can't tell the difference between a glaucoma and a mesh work. And a non- glaucoma is a mesh work that's aged controlled. So meaning mesh works look different in 20-year-olds than they do in 90-year-olds. But if you take an ideal with glaucoma and an ideal without open glaucoma, they actually look pretty much the same. And here's a close-up of that juxtape cannular tissue right there. All right, what am I showing right here, Karen? So it looks like there's cornea on the top. There's cornea, iris, mesh work. This is the angle. It looks like it is, like, closed off by adhesions or sparks or something. Actually, it's still open. It's a little narrow because there's an Iowa sitting here in the silver soles, which doesn't depend beyond that. That's okay. There's nothing pushing forward, but this angle is still open. Why am I showing this picture? What is the interesting about this? This thing right here. It looks like maybe, well, there's been some penetrating, something penetrating the cornea, maybe, like a PK. If you look, it's aligned here. It's an aqueous vein. So that's why I'm showing you this. So how does aqueous get out of the vein? It goes through the trapezoidal mesh work. It goes through the shox canal, and it eventually goes through these veins and then out onto the surface of the epicellarum. So you've got these aqueous veins. And so your mission, when you look at people with this little amp today, is find aqueous veins. And what you do is you put your slip beam just back from the leg and focus through the conch on the epicellarum. And you'll see, they'll look like veins, but then if you look more carefully, you'll see some little box carving of the blood vessels. And there'll be little spurs of aqueous coming in between. So you'll see some box carving when they move in. You never can think about this. And until I get this lecture, I don't even think about this. But if you look this afternoon, you'll be able to find it. It's not hard to find it. That's how the aqueous drains out of the aqueous veins. All right, again, this just shows you an open-angle glaucoma angle. It doesn't look any different than an angle from someone else who's in H-match control. All right, so when we look at open-angle glaucoma, there are primary open-angle glaucoma, which doesn't show anything exciting on path. And then there are secondary open-angle glaucomas. Now, Reese, what am I showing right here? Mid-perforation. What is that usually associated with? Pigment dispersion. So pigment dispersion syndrome. So one time, there was an argument not that long ago that said, you know, how does pigment dispersion happen? What's going on? And, you know, people look at this, and it's one of those things where you look at this, you say, well, it's pretty obvious. Look, those are linear scraping off of pigment posteriorly. And what lines up with the posterior iris in that area to cause this scraping? Zonules. Exactly. So zonular bundles. So if you look at zonules coming off the crystalline lens and attaching here on the ciliary body, where these zonular bundles are, think of a bunch of guitar strings in that area. And if the iris is bowing posteriorly, it'll scrape on the iris. And so it will release pigment from the posterior iris, which then floats into the anterior chamber across the mesh board. So what setting do you usually see pigmentary dispersion in? Hyprocretation. Actually, it's surprising. It's mildly myopic younger people, which is really weird. Not myopic. Mildly myopic, more males and females for some reason. And it usually starts in this pop it up. People are like 20, 30 when it pops up. But for some reason, when you do OCT or ultrasound on the eye, you'll see that the iris bows backwards, which is weird in these people. And so the way you treat it is you do a perfleuridectomy, kind of the same when you do when you have a blockage of the pupil, you know, when you have angrioclosure. But this way you've got posterior bowing, which you do a perfleuridectomy a lot, so it'll come forward a little bit, and it won't release so much pigment. And here's what you're going to get a wedge for. This is where that pigment's been scraped off, and sure enough, there's that pigment in the angle. It's a secondary open-angle glaucoma due to pigment dispersion. In the setting for that slide, someone that just recently exercised and has like blurring a vision. That's where they'll get blurring a vision. They'll get this stream of pigment that's loosened up. And especially if they're out jogging, bouncing around, they'll get this blurring vision and then it goes away into the lens. It's interesting. It's the release pigment. All right, Chris, this angle looks funny. It's open, but something funny is going on. What's going on here? So, is that pigment in the particular mesh work? Well, there's some pigment here. What else is going on here? It looks like melanocytes. Exactly. So, is this a melanoma that has, it's a metastasizer, they're not melanocytes in the angle? Well, it's a melanoma that has invaded the angle. And so, you can get melanomas of the cylinder body, which then secondarily invaded the angle. Look at the iris. It's clear back here. It's not up here. It's back here. So, that angle's been pushed back and it's been invaded by melanocytes. You can get secondary open-angle glaucoma for tumors invading the angle. And the most common tumor, you know, when an adult is a truck of tumors, melanoma. So, this is melanoma arising from the cylinder body invading into the angle causing glaucoma. All right, Shrop, what do we see in here? Exploitative material on the lens. Okay, so this should look familiar because we just looked at this two weeks ago. And indeed, you see the classic pattern where you've got the little ring in the center, ring in the periphery, and that's from the people acting as a windshield wiper scraping that material off. Exploitation. And there's a close-up of that exploitive material. Again, we just saw these when we talked about the lens. And when we look at it pathologically, what is the classic term used to describe this? Iron filings. Iron filings. You see now, is this the anterior or the posterior lens capsule? Posterioris. Actually, to the detriment of my coronary artery, posterior is thinner. You have to ultrasound it. I think it's that capsule. I need a aerobic workout. So actually, the anterior capsule sticker, what else is there that the anterior capsule has that the posterior capsule normally doesn't have? So the lens of pthiose cells are normally not along the posterior capsule there. And the anterior capsule, so here's the anterior capsule, lens of pthiose cells, they could have a posterior capsule. There you see the exploitive material deposited on there, almost like little iron filings on the surface of the magnet. And here's a trigger measure to determine if there's this stuff clogging it up. So you can get a secondary opening of glaucoma due to exploitive material. This is glaucoma that, when it begins to occur, it actually can progress quite rapidly because it might not break. So you've got to watch these exploitive people very carefully so they don't get in trouble. I believe we see an error. This is an external photo of the left eye. It looks like it's a very bloody eye, so most likely a trauma related injury. So it looks like it might have some kind of angle recession for iris dialysis. Well that's a thought, but you can't really say that by looking through here what's going on with that cornea. It's very opaque. It's opaque, yes. This isn't a bad picture. This is a general-paked cornea. Can I just really grab a word? If I tell you it's precious, fifty, five-zero, there's no history of trauma. I would have asked it, er, five-zero. Five-zero. This could be related to this. Did he have surgery or something? No, no surgery. Poor vision for a long time. Well, it's corneal edema, certainly from the high pressure. This is what is entered in our angle. Okay. So this would be fake-alytic. Exactly. It's called fake-alytic. I don't know why they call it lytic because it's not like the lens capsule is light, but these are people who have a hyper-mature cataract where proteins is actually leaking out of the capsule bag after an intact capsule into the entire chamber and this protein itself will clog the mesh load as will these macrophages which are stuffed with this protein that's leaking out clogged it up so they get a pretty acute outcome to it. You know, moving that crystal lens and washing out the anterior chamber is curing it so you can rid of that. And this just shows this was just aspiration. There weren't children going on so aspirator, you spit it on a slide, you watch your macrophages, stuff with this stuff. Alright, so this is just to kind of remind us of ways the angle can be different. So when you look in with your Goni-O you're going to look this is a normal angle. This is the angle closed and this is a recessed angle. So you always want to be careful when you look with the Goni-O and say, okay, there's an open angle. Is it too open? Is it not open enough? And that's tricky to do so you've got to keep good at doing it. So what are we seeing in your other person? So you have an external photograph. Right eye is injected with a mid-dilated pupil so concerning like an angle closure. Exactly. So you see that classic mid-dilated pupil? Or I guess a horners on the left. And yeah, right there. Did you see how it's injected? It's kind of painful. The pressure in that eye is going to be high. And the pupil's mid-dilated. And what do we see here on the slip hand? So kind of iris bomb base. Exactly. So bomb bay from the Greek. No. French. You let me run into it. French still was the part we had to do even still for the day. The French were living in caves in the Greeks but, you know, doing literature itself. But from the French bomb bay, V-O-N-B-E with an axon. On the E. Right. So iris bomb A. It's a forward bowing to the iris. So you look at this that beam here. And then you look at the beam against the iris. You can actually see it curving up and almost touching the periphery. So when you look at these, this looked like you could literally see them bowing up. So this would be a narrow angle at which your risk is you can go into angle closure and so on. You can see an angle that you can get a secondary narrow angle to walk on. So primary narrow angle to walk on, how does that happen? So it's usually due to kind of a shallow AC with some kind of bowing forward to the iris. Yeah. So you can get, you know, like a high-high probe. Is it risk? Small eye, is it risk? People with a big lens pushing forward is it risk? And what you do there is you get a relative pupillary block, meaning that you start to get the aqueous blocked right at the pupil and then as it builds up behind the iris, the iris goes forward and eventually blocks off the angle. So how do you treat that? So that's a PI. Or kind of surgery. About the aqueous to, you know, come around that that relative pupillary block. But sometimes you get a secondary angle closure, secondary narrow angle, and tear out. What are we seeing right here? What's different about this picture? Here's the angle back here. So it looks like maybe even an inflammation or some type of scar you have to close off the angle. Yeah. So you can get the angle closing off here. What do we call that when the angle closes off like that? P-A-S. And what does that stand for? Peripheral anterior synechia. Exactly. So peripheral anterior synechia, closure of the angle for the scarring. And here you can see a secondary angle closure with the direct dimensional effect here. And the angle stuck to it. And then what is a cause of secondary narrow angle glaucoma? What's a common reason for that to happen? We're seeing it right here. Exactly. Exactly. You should see it right now. Neobascular. Exactly. Look at the surface of the IRS. And there's all of these little tiny blood vessels on the surface. And eventually those will broaden the angle and then contract. So you can get a secondary angle closure due to neobascularization. What causes neobascularization? Aside from a gastrointestinal deficiency. So like any type of ischemia. So diabetics you get it or like exactly. So chronic ischemia. So anything that would give you ischemia of the eye can give you secondary neobascularization of the iris which leads to the vascular angle closure. Here's the iris. And there's little tiny blood vessels there on the surface. And so neobascularization of the iris can give you secondary angle closure. Becca, what do we see in here? This looks like a, you know, T-Rex or a chomp down So what part of the eye are we looking at here? So I don't know the angle. Look closer. First of all what tissue is this back down here? It looks like the lens. The lens and this is not the angle but the opposite part of the iris. This is the pupil order. And the way we can tell when we look at the anatomy of this is the sphincter muscle. So not the sphincter that just tightened in you right now but the different sphincter. Okay? But so sphincter is the muscle that closes the pupils. That's how we know where the people are in order. What's going on here? What's happening here? All these pigment themselves are stuck to the lens. And look they came off right here. So what do we call that when the iris of the pupil was sphincter. So you can get a secondary angle closure from people that are blocked due to sphincter but the posterior sphincter closes the edge of the pupil to the iris and this is coming to the lens and this one has been broken. So people broke it and died in it but look at the pigment you can even get an inflammatory membrane growing all the way across the pupil so you get what's called a pupillary occlusion. Now if you get a 360 degree posterior synecii that sticks that whole pupil down they call it pupillary seclusion you know seclusion and this is a membrane all the way across pupillary occlusion. So any kind of cry UBI is crying So I think that it's probably going to come that often but with the noxious ring like from trauma does that is that like it's not nearly as much pigment but you can't get pigment either the pupil you see this little ring of pigment it's almost like you printed on him from trauma I agree this is a little bit of a different view why is this different than the others so we're looking oh it's starting to scar off right there there's an aqueous vein so what is this angle recession angle recession so when you look at it people will often say recession of the iris you know angle recession but if you look at it truly that tear occurs even into the face of the ciliary body so what causes this usually trauma trauma so these are the people who come in they've got trauma and then eventually after the hythema clears up you want to bring them back again you know in 30 days and you want to go any of them because you need to know if someone who's had a blunt trauma has a recessed angle or not and so someone is going to get you know a recessed angle and then they get glaucoma secondary or a recessed angle how long after the trauma does that occur it's like 17 years yeah exactly so you got it this is where you got these are 19 year olds you know 19 year old idiots get hit with paintballs or fists or two dudes or something so you really got it imprinted on them and this is where you use the B word now I never say blind to a patient I say I'll say vision I say lower energy something like that but these are the ones you say you could get glaucoma from this and it'll occur 10 years from now and you could go blind blind is a visceral word it's a word that goes right to the enigma right to those centers that hopefully will work because you got to put the fear of doubting these guys because these guys have to come back yearly for like 10 years to make sure they don't develop glaucoma secondary recessed angles so for the home cast it's like tearing between the longitudinal circular so it's actually within the face of the you don't get glaucoma as often with those as you do for these recessed angles and this to show you kind of the difference compare and contrast here's the normal on the bottom there's the mesh work there's the iris here's the ciliary body the sclerot sperm and here's recess here's the rectangular mesh work there's the sclerot sperm look it's actually torn into the face of the ciliary body and what happens secondarily is for some reason I don't know why this is but the mesh work actually closes off and it takes years for that to happen here you see the mesh work it just gets almost scleronic so here's a classic trauma so let's see Chris short term memory from two weeks ago what is this right here is that a I'm blanking on the name but it's the leftover cortical material that something rings summer injury summer injury very good so this traumatic rupture of the lens capsule we've got this summer injury I'm going to tell you that look here's the mesh work up here here's the mesh work up here so it's traumatic angular recession look what's happening back here so if you look at that you've measured that cup to disc ratio that would not only be 0.99 that would be like more than one because it's actually even excavated so here you see an end stage glaucoma from previous trauma with angular recession alright so trauma we're looking at optic cups what would you say the cup to disc ratio here is hard to tell because it's a little mild it's a little bit tilted sorry 0.99 or not quite that bad but here's the rim right here so you see the large cupping from high pressure of whatever reason the end stage the damages the eye is cupping loss of nerve fiber later and loss of those axons and then eventually increase cupping and then of course this is now 0.85 maybe big cupping of the optic nerve and then this is you know what this nerve is dead from untreated buccal so it's a totally cupped optic nerve and when you look right here this patient had trauma there's a penetrating wound with a here in the coma a white scar there here to the cornea and again somewhere in the brain and there you see cupping now it's interesting when you look at the cupping is you could actually see an excavation where it actually shaped like a bean pocket so if you look right here here's a temporal look there's not even a fiber there it's gone and then nasally if you look right here when you look at these with your 90 die after you look you'll actually see a vessel going around the nasal edge of that compliment will just disappear for a minute and that's because it goes around the corner and it excavates you see posterior bowing of the laminar crebroso so our whole intent of 3D glaucoma is to prevent that from happening that's our goal right there you can see on the close-up there again totally excavated optic cut temporal nasal look at the close-up there I mean it looks like one of those things paper will climb up you know under the ledge and then hang there and then pull yourself up so with your fingertips I guess that but so there are some other weird glaucomas that you have to just memorize and there are some weird glaucomas and this is a patient who had a sudden pressure rise and so they had sudden pressure rise be it acute angle closure or whatever but their pressure shot way up in a short period of time well look at the optic nerve what do we see in here when you look at this optic you look at this optic nerve here you see these areas here where it almost looks like the optic nuances so it's not so much glauosis it's that these these fibers have been damaged to you but it's in a sector of damage so this is just one you have to memorize this is Schnabel's cavernous atrophy you just have to remember that because we're both putting this on boards this is damaged vocally secondary to an acute pressure rise so you get this acute pressure to go up and it'll actually cause focal damaging what's weird is you do a mucin stain and you see mucin in between these fibers in the anterior portion of the optic nerve so the way I like to think about it is the pressure's so high it just forces vitreous into that optic nerve head because that's where the mucin comes from so I'm not sure exactly the mechanism if it leaks in there it's pushed in there but the way I remember it is the pressure's so high it just pushes this mucinous stuff into the optic nerve head so this is Schnabel's cavernous atrophy that's what they ask on boards do they still have high pressures by the time they get to they may not because how would you differentiate this from like a Naio N I mean I guess you wouldn't have a DEMA well you wouldn't have the positive staining for the mucins okay but like clinically but clinically you could it's very difficult and this is another interesting thing is when you have an acute pressure rise you can get little focal areas of ischemia of those lens epithelial cells and little focal spots what do we call that Chris oh um when I think of the name I just wrote this from the Deutsche yeah it's uh I'm drawing a blank it just sounds cool it's called Glockenflecken yeah Glockenflecken so it's basically Glocken is like I don't know I think of that it sounds like Glockenflecken or little flecks and so little flecks but that perches the percher fleck percher fleck yeah same thing so focal areas here in the not in the nerve in the anterior um underneath the anterior lens capsule here so these will eventually go away too but they're sign of acute pressure Glockenflecken alright so what does Glockenflecken do to the retina terror what part of the retina is affected by Glockenflecken um um the the outer nerve the nerve layer why do you think you do that Glockenflecken why the spotlight hits and I don't even know what it says across the street or over the the outer Glockenflecken um the outer alright so by next week we're doing retina next week you guys are going to know every layer of the retina by heart for next week you're all fuse your eyes with this laser on the base of your macula so what Glockenflecken does is it's actually inner retina inner being toward the vitreous and so it affects the ganglion cells and their axons so the outer layers of the retina are unaffected inner layer that gets so it's the nerve fiber layer ganglion cell layers that get damaged by Glockenflecken and what you see right here is you see up above here this is the macula lots of ganglion cells have a patient with that stage Glockenflecken so you should have all these ganglion cells up here and you look down here you have part of the inlet so macula is spare to the very end in Glockenflecken so you see Glockenflecken patients they'll often have this little temple island or this little central island vision left and the periphery eventually goes away alright this is just to show you what it looks like this is a congenital Glockenflecken that's usually when you look with a kebulins or a gonioma here in the angle you see a fine developing membrane across the angle and so when people first started describing Glockenflecken kids in general Glockenflecken they call this Parkans membrane Parkans which is the guy we saw it but so their theory is that the angles have this membrane blocking it off you just cut that angle then it'll drop back and the pressure will go down well it actually kind of worked the pressure will go down but it's not just that there's an angle that there's a membrane going across the angle that mesh work it's just not well developed in general Glockenflecken so you get this little membrane going across it still isn't normal so you can't just go there with a knife and cut it that really is not a long-term solution it's normal and there's this abnormal little membrane stuff in front of it alright back the heck is this I mean you can describe it if you want it looks like there's some iris that actually yeah so there's iris actually we could hold it in the iris what do we call it this looks like many different pupils from the Greek Pali means many Corian many people that's and so this is a condition where you look at it the iris is just at your feet it looks like it's just being pulled over in this direction there's a big moth and holes in it and so we want to go into an entity that could cause secondary blood going on there's an entity called ice syndrome what does an ice stand there is a syndrome if you're a lumber ice has various different entities under it if you're a splitter you want to look at each of these individual entities and see what causes them but I actually remember three kind of basic subsets of ice first of all ice do you remember or is it unilateral bilateral 50-50 chance say it with convictions bilateral don't get it don't say it so it's actually unilateral it occurs in younger people 20s 30s it starts showing up alright so Reese this is the first and most common variant of ice syndrome what is this called it's called essential it's called essential iris atrophy so that's the first subset of ice it's got this polychloria it's got this eccentric people and the moth looking iris this is the second entity and Chris what do you think now look there's some moth iris here but what's going on here in the cornea so it looks like there's some opacification maybe some edema exactly so what should the sub-entities have edema cornea animation ice syndrome it's called chandeliers chandeliers is the second subset of ice chandeliers it's still got an iris but you've got corneal edema and what's wrong this is the third subset there are no irregularities or growths on the iris like me my iris edema okay so it's iris edema and this is where it's coconut reese syndrome and the guys who described it but again iris edema so this is the third subset and you see now what is the unified field theory of what happens to cause all of these lead unified field theory of it's the epithelialization of the endothelial layer so it's just kind of overgrown so the endothelial layer will just grow across the tremendous looking onto the iris with that will come decimates memory so some people will call this gorgeous pictures on my corrupted stick I'll have to figure out what happened to that kind of factor we love those I'm going to be really upset and then when you look this is an actual peripheral endectomy from a patient with the iris edema here is the abnormal decimates memory this is a PIS but this is the anterior surface of the iris decimates memory on the anterior iris and here's the close up there's one of those little nevi-popping food so you've got this velvety PIS positive memory on the anterior surface you've got these nevi-popping food so iris nevi-popping food so you want to remember the central isatrophy big mothy pupils chandeliers is that plus corneal and then iris nevi-popping reese medization anophilic growth of the anterior chandelier so that's the ice syndrome there's a close up of one of those nice little nevi-popping okay other chris there is a second mass of things you have to memorize for possible secondary bacombas this is the first of those are we seeing here or here's this first of all so that's decimates here so it's kind of additional I mean it's posterior embryotoxin exactly so it's called posterior embryotoxin it is a thickening of shawabi's line even moved more to the center and so what is this whole group axon-filled reager exactly so when you look at these these were called the anterior segment dysgenesis syndrome or anterior chamber this is incorrect because the anterior chamber doesn't form by a cleavage of mesodermis actually waves of neural crest performance so this was called wrongly you know 40 years ago now but they call this the anterior chamber cleavage syndrome so you may see that it still sticks but George Waring actually in the mid 70s put together a really nice what he called the stepladder classification of these entities in this that go from that z step e but the first thing you see is the so-called posterior embryotoxin and more centrally displaced thickened shawabi's line and there you see it and then here's here's that posterior embryotoxin but now you're starting to see some thing in the iris and you're starting to see some kind of strands across the pupil terrible business for them so this is the iris strands that are adherent to a strong and slanted what entity is this now the stepladder is this still axon oh is this axon felt reekers they used to call them separate but now we know they're kind of the same so they used to say well axon felt means little strands kind of from posterior embryotoxin across the angles and reekers you get a little more iris attribute but they put this together and call it axon felt reekers basically you get fibers coming across from that posterior embryotoxin from the cornea down across the angle you also get thinning of the iris and it's an anomaly if there's no systemic stuff if the kids got funny looking teeth and funny bones then it becomes a syndrome so axon felt reekers is the next step along and the stepladder classification and then finally Peters Peters anomaly what is Peters anomaly character on the spot exactly so you start to see all those other things plus you get a big opaque area in the center of the cornea and the reason for that is what loss of endothelium in those areas and not only loss of endothelium but loss of of decimates in that area so you get the central gap in decimates endothelium that then leads to central edema when you look you'll see these strands coming down to the iris the angle narrowing so the strands of the asher then you get the central defect and sometimes they'll have a focal anterior subcapsar cataract underneath it so again in my simplistic thinking it's like that lens went up and took a bite out of the posterior cornea and then kept it when it went back so you'll see this defect in the posterior cornea and then you can even see a focal anterior subcapsar cataract so posterior embryo toxin axon felt reekers Peters and it's a stepladder it was a classic paper that said George Warren wrote in the mid-70s sadly just passed away last year when young he was like I don't know 70s but really healthy he comes out here and goes skiing every year although two years ago he came to the Ryan Christmas Party after he'd been stented for his part so his heart gave way sadly last year but he named this and so look that up it's a classic art of wearing that's the kitchen and we still use it and here you can see there's that central cornea there's that light taking out of it no decimage no endophilia cells and that's our fault