 This is, I think, a better format for the morning. If you guys are ready, I'm going to give you a light stand-up. So let's start with number one. I'm going to give you guys a routine. I'm going to get you to go home already. So, anybody? Because I haven't done that yet. So that makes it a little challenging. Because some of this stuff, I will tell you, you're going to see pretty much almost every time you go home, we'll describe a book on that rotation. We'll include this here at Primaries. There are a lot of weird syndromeic stuff. And a lot of the actual problems are on patients as well. So, let's do number one. We're going to split it up. What do you guys want to name your team? We're playing for Pride here. What's your team? Team one. Team one. Okay. What's your team? Pride. Pride. Okay. Going out strong. So, a number between one and ten. Chris. Seven. Seven. Three. Three. They get to go first. Okay. So, you guys get to... I'm going to start off the question. And then you guys get to the answer. There's a decent amount of time if you can. Then we'll switch over to the other team. Okay. Which of the following is not a classic feature of congenital glaucoma? D. D is in dog-conjunctival injection. That is correct. So, in March 20th, you guys remember that. Now, this goes into another question that we're going to talk about later, I believe. Maybe not. How long... How much time is there? Or what age is... What age range do you see corn and larchin? Like, when is corn and larchin stopped? You've got high pressure in the eye. And, you know, you're probably thinking, is every single case of congenital glaucoma going to present whether they're in March 20th? What's kind of your age now? As you remember. When the corn stops stretching. So, usually around... Okay. So, between zero and three, corn is still very... There's a lot of plasticity in the corn here. So, you can see a lot of stretching if the congenital glaucoma occurs at any time. Okay. Now, if it occurs after that, how do we distinguish? Like, there are different types. Congenital would imply that it happens around what age range? Depending on that range. Or probably more likely in the first year. Okay. But you're going to see that in March. It can happen even, let's say, in 2015 months. That would still be kind of considered congenital glaucoma glaucoma. And then after that, we start calling things infantile. Okay. So, infantile is probably... You know, I think if I were... Let me back up on that definition. It's quite better to say that if something presents after a year, it would be considered infantile. But the ICD-10 code is actually the same. It's very similar. So, what do you call a congenital or infantile? I think it just suggests when the patient presented to you. But in that zero to three range, you're going to see those plastic symptoms. And so, let's go through the other symptoms. Topstria. Do you guys remember topstria? What is that? Obstria. Ornate. Obstria or breaks and decimates membrane. Can I do the usual? Are they vertical or horizontal? They're usually horizontal. Sometimes they can be circumferential. Yeah. So, we've had a few cases on service recently that have this very significant slope. Normal circumferential. It's just going to spiral out. Concentrate surface around. That's not a good point. So, if you guys see that test question, it happens almost every other year. You can see a test question about topstria. Or they'll tell you about stria on the cornea and these breaks on the cornea. And they'll describe to you that they're either vertical or horizontal. And they're trying to get you to see if they need to go home or not. And the direction is important because usually it's a force that's injury. It's vertical. So, remember that for your O-caps exams. Vertical stria are usually implied for such injury. Okay. Hip for up. Water in the eyes, photophobia and blood for spasm. Those are probably, but that's the classic triad. Okay. Hip for up, photophobia and blood for spasm. Okay. Now, this one is open up for anybody. So, we're raising a hand first. Which of the following age ranges portends a better prognosis for patients with PCG? Sorry. So, again. B. B. Correct. So, this is very important when you're counseling patients. There are minority cases. I think if your book says 25 or less than 25% of cases will present as newborns immediately when you're near the birth. As soon as the baby comes out, obviously the cornea is cloudy. They have massive blue felmas. But most of the cases are going to present in that window between birth and the year. So, you can tell parents that the prognosis is usually better if they're between 3 and 12 months. Okay. All right. Next question. Which of the following are not disdain machine features in the accident of all three years? Chris. You said B and C. B and C. So, that is partially correct. Sorry. Sorry. You are correct. There's one more. Sorry. All right. And we want to go for it. Okay. So, the answers are which of the following are not disdain machine features? Chris, you got two out of the three. Autosomal recessive. That is true. That's most cases. I'm sorry. That's false. That's right. Mostly are autosomal. And actually, Chris, I'm sorry. You threw me off there. C is not the correct answer because there are some cases that are sporadic. Okay. So, and then the last one would be D. Okay. Those are all not disdain machine features. It is autosomal. It can occasionally be sporadic. So, the answers are actually B and D. I'm sorry. I'm throwing myself off. These not questions are meant to kind of probe you to make sure you guys know the information. So, let me go over this again. Accent-filled regress. It is bilateral. It's usually autosomal dominant. Occasionally, it is sporadic. And the rule of thumb for most of these syndromic problems for the general public is about a 50% risk. So, if you almost always, it's going to be around 50% risk. If it's associated with some sort of syndrome. So, posterior vertebrate toxin. Do you guys remember what posterior vertebrate toxin is? Anybody? That's the name. So, everybody. Interdisplacement of the Schwalbe's line. Interdisplacement of the Schwalbe's line. So, you have to look for it at the peripheral point. Can you see it in normal patients? You can. Yeah. Can you see it in normal patients? Okay. And then the last three, F, G and H. That's a part of what syndrome? It's all lumped together now. Accent-filled recurs. But these last three, magistrate, epiplasia, epispidias, and the posterior teratrial abnormalities have to do with the recurs. Okay. But now it's just all lumped together. But I know that a reverse anomaly could be associated with pituitary abnormalities. Yeah. I mean, it's not something you think about a lot because we're kind of focused on more of the classic ones, the magistrate, epiplasia, things that are obvious in your book. All right. Moving on. Number four. Which of the following are not distinction features of Peter's anomaly? Chris, you said E. E, that's correct. So, Lecoma. Do you guys remember what Lecoma is? I don't know if you guys have seen Peter's. There's a lot of Peter's floating around. Have you seen a lot on service, Renee? Yeah. Yeah. Peter's on Pete's. Yeah. There's a large population of Peter's population here. So, Lecoma. Does everyone mention what Lecoma looks like? Oh, is it like kind of like a corneal? Yeah. Remember, Lecoma is white. It's just basically a white spot on the cornea. And what does that white spot do, too? Come on, guys. The first years. Come on. You know this. Chris. It's a malformation of the cornea. Almost. No, it is. It is. It's a malformation. But the answers are given in the question here. What happens? You're seeing what processes. What's attached to what? Not just the white spot on the cornea. It's usually a white spot on the cornea. It's just the tip of the iceberg, so to speak. What's underneath it. You'll see variations. You'll see some that are very mild. And some that are extremely severe. So it's here at a corneal adhesions, or even at the particular corneal adhesions. And what the white spot you're seeing is the loss of the endothelium that's made since some of the posterior stroma. Yeah, so remember that when you see a Peter's anomaly, you see that white spot. Remember, that's the tip of the iceberg. You have to look further. In often cases, we have to put these kids to sleep because we have to look and see exactly if they have a viscous significant cataract. These are complete abnormalities in the anterior cycle. If you have a virus that's just attacked up to the cornea, and even worse is if you've got a lens that basically is drawn up and it's attached to the cornea. So those are very complex cases. You probably want to know that before going into the cataract circle. So, good idea to put these kids to sleep, examine. Might need ultrasound. UPM may be helpful to be able to look at the entire anterior segment and see exactly where the attachments occur. So now, remember what I told you that for most of these anomalies and syndromes, what's the risk for polygoma? 50%. 50%. So F is not the right answer. The answer to this question is E, but F would be 50%. So the answers are actually E and F, right? I think, Terry, you just said E, right? So the answer to this is actually E and F, because it's about 50% risk for polygoma. Okay, number five. A parent with a one-year-old, an aerated child presents to your office asking about the long term risk of polygoma. Which statements are not true in really a polygoma? Nobody wants to go for it. So we're just going to do these one by one. So less than 50% risk of polygoma. Is that true? It's about 50%. So 50 to 75%. It's about 50%. So I'm trying to basically create some generalizations for polygoma, because you're going to see these patients clinic and the patients are going to ask you before they ask you for polygoma. So it's okay for you guys to head to say approximately 50% and the polygoma kind of takes away the better, okay? Most of these problems are about 50% risk of polygoma. D, if polygoma is not present at birth, there's no long-term risk of polygoma. Is that true? No. That's false. There is always a long-term risk of polygoma in the patients that are in the baby, and even in other types of polygoma. The most common mechanism of polygoma is maldevelopment of the ankle. Is that true? No. So what you should have is basically... Well, the iris stump rotates forward to block the ankle. Block the ankle, okay? That's one of the common things that you see. Now, I will tell you that we still consider doing ankle surgery for some of these patients. I think it just depends on what they present. And sometimes you can get away with ankle surgery, because ankle surgery is thought to be helpful if what is maldevelopment. What are you doing in ankle surgery? As an example, what we're typically doing, either in a goniotomy or trapeziolobium situation, what is it that we're cleaning? Are we cleaning the trapeziolobium canal? Are we cleaning the collector channels? In a goniotomy? Yeah. Yeah, you're going through... Yeah, you're going through... Well, I know that trapeziolobium you're cutting this lung canal, right? Aren't you going through the trapeziolobium canal and then stripping it? So, let me be a little more precise here. So, think about the normal pathway in the Achle South Pole. And we typically think of what site as the area of highest resistance for the lung. TM, Schlumpz canal, collector channels, or downstream. Where is the site of... where we think there is a motion resistance? It's the juxtapotent molecular. Which is part of the... TM. TM. So, when we're doing ankle surgery, our thought process is, there's something wrong with the mesh one. Because we're not actually cutting through Schlumpz canal. We're cutting into Schlumpz canal. But if you cut the back wall of Schlumpz canal, you're now into what structure? It's also light. It's lighter. Yeah. Okay? So, we don't make the cut so deep that we're going into splatter, creaking, spiral legs. All we're doing is we're cutting the mesh work. And that basically starts to break down the area of highest resistance in the world. Go through the mesh work, through that cut that we create, and now accesses to the Schlumpz canal into the collector channels. Does that make sense? So, in aniridase, we do do ankle surgery. And that's because there is some thought process that in some cases, depending on when you present, that the mesh work may actually be dysfunctional. So, cutting the mesh work early on may be helpful in a patient with aniridic glaucoma. But later, the stump may rotate into the mesh work. And unless you remove the stump, you'll apply an acronym to effectively treat glaucoma. Does that make sense? So, just think, PDF for glaucoma is, you've got all these weird syndromes and things to tuck away. But the surgery is quite simple in terms of what we're talking about. In terms of angles. All right. The most common mechanism of glaucoma is senitial angle closure. That's true. Based on what Chris you said, the iris stump is causing senitia rotating into the mesh work. So, that means, for that question, question five, the ones that are not true would be A and B. So, I've got a question about that. When you use that term, just for semantics, senitia, I always think of a senitia being like PAS, like from long-term closure, you have PAS kind of forming. Sure. But all PAS comes from what? What eventually is pulled into the mesh work? To the iris. Okay. Whether it's uvidic glaucoma, whether it's aniridia, and the stump is just pulling in. It's rudimentary for mature iris tissue. The inflammation causes some contractile issues and pulls the iris up into the mesh work. I keep thinking of different mechanisms here. I keep thinking that the iris stump actually closing it off versus PAS actually forming. And I thought that this meant PAS forming. So, let me back up. I will, in this question, in general, when I use the term PAS, whether the mechanism be aniridia or inflammation or neobascular glaucoma, I'm saying that the iris is the clogged mesh work. It's either being pushed in or pulled in. So, like the neobascular glaucoma, you have that abnormal membrane that's laid down early on. And that membrane has to contract off forces and it will actually pull the iris up into the mesh work. Does that make sense? So, you know, when we think about neobascular glaucoma, we have these abnormal, low blood vessels that clog the traumatic glaucoma mesh work. That's not ultimately what causes the damage, right? Because if you give them anti-bed jet, you get rid of all those growth vessels. Long term, one of these patients have terrible glaucoma. It's because of this abnormal membrane that pulls things in and then they just zip up their angle of iris. The iris just gets pulled up into the angle and zips up the entire angle and you can't see the mesh work at all. Okay? So, that's like a severe form of neobascular glaucoma. But I'm using the term as a reference to synepia, PS, those terms to be are some anomalies. So, whatever the underlying mechanism is, the iris is being drawn into it. And we're saying that C is also correct, like, not a right answer, but actually it's about the angle of iris. Yes, I'm sorry. So, A, B and C. The answer is reply or A, B and C. Now, by sitting, knowing that we talked about C, don't remember that there is some thought process early on. There can be some non-revelment in the angle and primarily, we think of synepia closure as the main mechanism. Okay? All right. Question number six. An infant with Sturge presents with congenital glaucoma. Which of the following is not correct? It is not correct. And we said C. C is not correct. So, let me, let's read the question one more time because I put some clues in there. Patient with Sturge wedge presents with congenital glaucoma. So, let's go through these. Elevated at the scolovidus pressure is the likely mechanism of glaucoma as Sturge patient presents with congenital glaucoma. Is that true? So, remember that the clue is congenital. Yeah. So, that's not true. It's not true. It's not true. Okay? So, we classically think of Sturge wedge as the elevated at the scolovidus pressure at the helpline stage, etc. But the key here is that this patient presents with congenital glaucoma. So, another generalization, very broad generalization, if you guys see a patient with congenital glaucoma no matter what the cause is, let's say it's primary congenital glaucoma, it's aniridia, it's Sturge Weber, it's Axanfel Regers, it's an anterior segment, it's Genesis. What is the underlying mechanism practically all of these congenital glaucomas? Maldevelopment in the angle. So, just Genesis. So, just tuck that away as a generalization, because I want you to be able to simplify congenital glaucoma. There's a lot of syndromes out there. If they present early on, that's why we're doing angle surgery, because we think there's just Genesis in the angle. Okay? It's a very simple generalization, but it applies just about to every case. So, A is not true. Glaucoma is more common in the nevus when this involves the upper eyelid. Is that true? That is true. Irodo trapezoidal disgenesis is the lightning mechanism in glaucoma? Yes. That is true. Glaucoma drainage device is preferred over an angle surgery. Is that true? No. Why? Because of E. There's a high risk of corral fusions and corral hemorrhage strain surgery. Okay? So, the answers, again, are A, that is not true, and D, is not true. We would still prefer to do angle surgery in the Sturge-Weberation presented with general glaucoma. Now, this question is different. Let's say I said the patient with Sturge-Weber, an eight-year-old presented with glaucoma and high pressure. This would be different. Our mechanism would be elevated episcoviness pressure. Probably, angle surgery is not likely to be helpful. Okay? It's because of elevated episcoviness pressure. So, do we currently have a way to bypass episcoviness pressure, or... I mean, if you do a goniotomy, the patient with Sturge-Weber with glaucoma six years old or eight years old, if you cut the trabecular mesh work, does that really get to the root of the problem? No. It's further downstream. Does that make sense? So, when you cut the trabecular mesh work, that's something that's more proximal to not a downstream mechanism. So, in order to get around this, you can do a bypass. So, you can do a trabeculectomy, or you can do a glaucoma drainage device. I will tell you just by personal preference, to do a glaucoma drainage in kids is very difficult. Those of you who manage one of our post-ops at the Veterans know that's a challenge already. Okay? Is managing patients, adult patients with a fist showing. Now, let alone a kid, you can imagine how difficult that is. You can't put somebody to sleep every week to manage a trap. Okay? It's just not practical. And just, their exposure to general seizure will just be horrific. Every week, having to go through E-ways, we can manipulate the web. It's just, now, well, does this happen around the world? Yes. Do they manipulate the web? No. What they're hoping to do is tie the sutures just a little bit loose. This is where kind of the arc of glaucoma comes in. But it's a risky, it's a very, it's something that has not a lot of control to it. So, you're either going to get patients that do well, or you're going to have patients with flat chambers the next day, you have to go back in and refill them. So, for me personally, I don't do trabeculectomy to these kids. It's just too difficult to manage. So, most of these kids aren't going to get a true shot of what I can do with my hospital. Okay? But this does happen around the world. Why? Primarily, it has to do with economics, and it also has to do with supply chain. Okay? Most parts of the world don't have access to oral immigration devices. They're expensive. Although, Aravind has made this a lot cheaper. They've created a mock-up of the Aravind tube. It's mainly just for adults who don't know how to use it in kids. It's essentially a device that they've gotten down just below $100 maybe. $50 or $75 for a knockoff at the very least. Okay, seven. Which of the following is true regarding a fakia after congenital cataract surgery? Okay, let's start with A. 15 to 50 percent of more development of glaucoma. Is that true? I'm going to go with true. True. Okay? Again, that 50 percent that's thrown in there. Again, this is why it's okay. I think if you just kind of tuck that away, if you see patients that are presenting glaucoma, infants, general patients, you can kind of hedge and say roughly 50 percent, but for certain cases there's a range. Okay? But this is where the 50 percent will come in. B, the patient is only at risk for developing glaucoma within the first three years after surgery. Now let me back up and say this is a fakia after congenital cataract surgery. Okay? So the patient presents the congenital cataract, you operate, you're not being faking. Is there a certain risk window? Or are they always at risk of developing glaucoma? Always at risk. Always. Okay? So this is false. It is false. Okay? This is a lifetime risk after they graduate from health and address practice. They come in with the adult practice and we follow these patients for the rest of their life. Okay? So this is false. C, the mechanism of glaucoma is related to irregular dysgenesis. Now think about this. This is a patient that had a normal presenting eye otherwise and normal pressures have just taken general cataract and removed the cataract. No. That's not true. That's not true. Okay? So usually what can happen after a fakia there's thought to be this roll between the lens, the zonules and the cellular processes. When you don't have the lens inside of the eye anymore you don't have as much stretch on the zonules and then likewise you may not have enough stretch on the spur of the spur and that may affect the overall treatment of the patient. So remember you've got two sets of muscles that are attached to the spur of the spur. You have your circumferential muscles. I'm talking about the cellular body muscles okay? And then you've got your tangential fibers, right? There is that relationship. There's an interplay of the tangential muscles. So you remember an angle recession, right? An angle recession you get a splitting of those fibers between the circular fibers and the tangential fibers. Okay? And by splitting that muscle you basically open up the cellular body. Okay? And so it's almost related in that same way but not quite. If you have a patient with traumatic glaucoma an angle recession, right? You get that splitting of the muscle fibers and there's thought to be contraction of the tracheal muscle because those cellular muscles can't maximally pull the cells, right? Okay? So it's almost although we're not splitting muscle fibers in a patient with congenital cataract there is this interplay between the lens on those cellular processes and how we work together. Okay? So next part. So C is true. D removal of all residual cortex and they produce the occurrence of glaucoma. That's true. Yes. That is true. Small portal diameter is a risk factor for development of glaucoma. That would go with true. Yes. Cataract surgery in the first year of life is a risk factor for development of glaucoma. I'm going to say yes. Yes. That's true as well. Okay. Eight. Which of the following surgical techniques is the preferred method of treatment in a one-year-old with PCG parloratogenal glaucoma and cloudy corneas? B. B. Trabeculatomy. Okay. So, Tara, do you remember the difference? Can you explain for the group what the difference between goniotomy versus a trabeculatomy? They essentially do the same thing. The approach is what you need to remember. So, with goniotomy it requires clear cornea because you're like directly viewing the ankle structure and then I think trabeculatomy it's like inter I guess you don't don't doesn't require direct viewing because it's an indirect approach. So, not quite I think both of them you're talking about a view versus a direct view or I guess a direct view versus like trabeculatomy it's like There's a special word is it at internal or at external traditional idea? At external at external okay so the way to remember this very easily so what instrument do you need that's critical to performing goniotomy during surgery it's in the name gonioscope okay so those of you that have seen using a gonioscope or goniotomy prism and surgery you're using a microscope you're tilting the patient's head away from you putting the prism on the eye and directly viewing through the microscope looking directly at the patient okay so thus if you're using something that is allowing you direct view it requires a relatively clear goni if you don't have a clear goni doing a goniotomy is very difficult now this comes this is these are things just for you to tuck away in terms of generalizations if you need a clear goniotomy or trabeculatomy you don't and that's because you're doing the surgery from the outside in you take down the conjunctiva you do your sclerodisection into Schlegz canal and then you pass either a suture or a catheter or a harms trabeculatomis another device that is really no longer used it looks like a pitchfork and basically you slide the device into the angle and then you pull it through the meshfork and clean the meshfork but you're doing that from the outside in approach so it doesn't matter if you're goniotomy they're not any from the outside remember the water as it's coming through trabeculatomis Schlegz canal the back wall of Schlegz canal if you cut that you now enter the scleron so now you can do that full dissection from the outside in take down the conch cut the scleron get into Schlegz canal pass your suture or your catheter around and then do your cleavage now this has changed because now we have newer techniques some of you guys have seen the gap procedure which allows me to do the surgery I can do a full trabeculatomy now usually for the goniotomy you're treating just the nasal area but now with the trabeculatomy at internal I can do essentially the same surgery that was previously at external and I can do it from the inside as long as I have a reasonably clear point it doesn't have to be exquisitely clear but as long as it's recently clear for me to be able to make the cut in the meshfork and then pass the suture or catheter around the whole 260 degree trabeculatomy now at internal but for your boards for your questions just remember that you need to have a clear point here for goniotomy so you're using gonioprism or gonioscope on your trabeculatomy that's done at external okay nine the parents of a six month old child with PCG wants to know how successful anal surgery will be in their child what is the 70 to 80 percent and what do you guys remember that we already talked about in the previous question what's that magic window where anal surgery seems to be a better prognosis three to twelve three to twelve one okay so if they were sent really really early one month old with congenital prognosis that's not as good of a prognosis versus someone who presents in that three to twelve month window that's kind of a magic window for prognosis success with surgery okay ten which of the following positive medications should be avoided in infants with glaucoma this was discovered by norms of risky here reported case series C C alpha adrenergy that is correct do we use myotics so maybe you guys have rotated their beads not really every well you can but you can but we don't usually so I'll tell you for myotics make the biggest difference it's a wonder drug for a fake glaucoma okay what do myotics do they constrict the pupil what are they doing they're pulling on trapezoid mesh work so it actually increases aqueous outflow right that's the idea so that's why it works so well in a fake glaucoma because remember we took out the lens in a fake glaucoma we don't have that stretch that we normally do okay and so by pharmacologically that stretch in a fake glaucoma myotics may be helpful so you'll see it in a few of our patients but be looking at now when you're in the bead service look for the a fake glaucoma patients that may be on phosphine iodide rarely use it but it is available on hybalcarpene but typically if we're going to put somebody on long term myotics we're using a phosphine iodide in case you ever have to write the prescription it's very rare but it's 0.125% I think the idea alright how about CAIs how about dimox do we use dimox for infants is that safe yes yes I mean if someone's going to be on for a while it's probably a reasonable thing to check electrolytes and their normal things that can be checkable for patients that are on long term CAIs but we use them temporarily now a common thing that you guys may get called on is that they're going to call you from Wyoming or Montana and we'll tell you this classic story of kids tearing without less than 20 years and one thing that you guys can do in conjunction with consulting myself or talking to other trees is place in the patient on dialogues before they get here to our facility or in the UAE why is that helpful so we can see we might have a chance to do angle surfing if you can clear the colony ahead of time okay so the dosage for this is 10 to 15 milligrams per kilogram per day okay so Dr. Hoffman likes to just say 12 he just says those are 12 milligrams per kilogram but the range is 10 to 15 okay so 10 to 15 milligrams per kilogram per day and then divide that tier if you have to start a pediatric child on CAI dialogues 11 you've decided to use a beta blocker in an 8 month old PCG patient cells for the colony times 2 which are the following important considerations you know start from the beginning beta blockers are contraindicated to the children younger than one year old is that true that is not true that is false we still use them B nasal lacrimal duct conclusion can be helpful is that true yes yes it's a good idea to tell your parents to do nasal lacrimal duct destruction when they're using all blocker drops particularly beta blockers because they're going to be a lot of systemic absorption 0.5 percent is a preferred concentration is that true do you guys know what the normal concentration is that we use the adults like the COSOFT or the Timalol straight 0.5 that's the normal dosage so for kids you might want to back off 0.25 percent okay so that's that comment you guys are just used to writing Timalol BID COSOFT BID you forget about percentages you're working with kids if you're going to prescribe straight Timalol in a 0.25 percent concentration so be aware of that that when we typically prescribe COSOFT let's say you want to do combined therapy it is 0.5 percent that's a COSOFT or a generic COSOFT so if you're going to be prescribing straight Timalol try to use it 0.25 percent okay D should be avoided in patients with asthma or significant chronic disease that's true okay 12 which of the following is not true regarding Joad Juvenile which of the following is not true C and E C and E that is correct so let's go through each one presents between the ages of 4 and 35 that's correct most are inherited as an autosomal dominant correct that's why family history is important and if you notice in our client next time you guys see patients with Juvenile parents too in many cases you'll see that a parent has Juvenile in the name of local women as well C the angle can appear dysgenic like in PCG is that true that's not true okay remember these kids present later in life right so their angle has been working fine and then after the age of 4 between 4 and 35 they suddenly get glaucoma you should think of that as being just a miniature version of adult local women the mesh work is becoming dysfunctional it's not dysgenic it's dysfunctional so the angle anatomy looks normal when we're operating on kids with PCG the angle looks very, very mouth-developed it looks very mature you can't see landmarks you can't see the mesh work you can't see this girl square very well all you see is a high iris root insertion and then it almost looks like it's just corn that's it so remember for Juvenile they've had time to develop their angle now their angles are going to look normal progressive myopia can continue to develop until 10 years of age it's a little tricky this is true it's not true because throughout their life they actually get myopia they can progress right because the so the answer so you're saying that it is true that they can develop progressive myopia past the age of 10 yes so D is not one of the answers for this question but that statement is true okay book balance and hops are common you see that in Joe Agnes you know these kids look normal there's really nothing wrong with them except if you can notice that they're becoming more myopic then you obviously you check the pressure look at the nerve and it really looks comfortably classic violence true or false the wall of CCT as well established should be at the bulk and it should be routine measured in all children at the bulk home it's false false there's no criteria it's not that's your clue okay not just because it's hard but even when we come into EUAs we don't check the chemistry inside the award last question the normal corneal diameter of a full term full term newborn is switching the following it's a question say the range B B 10 is normal so what about the age of 1 what should you expect the normal corneal diameter between 11 and 12 11 and 12 okay alright some things about EUAs just look quickly and then we run out of time in general when we're doing EUAs we try to check the IOP as soon as we can because general anesthesia can do what to do to the IOP it can lower it so we try to not always I mean the book tells you to try to do it immediately after activation or after reduction try to get the pressure but that doesn't always happen okay what's the normal pressure for a newborn you guys are going to be called to a service and someone's going to tell you this patient has an eye problem you'll be checking the pressure assuming you've gotten a good examination without any squeezing what should be kind of the normal pressure range for a newborn low teens low teens okay and then over their time usually about middle childhood the pressure will kind of go into that normal range that we talked about 10 to 22 newborns should have teens in the low pressure one question I forgot to ask neurofibromatosis you guys remember there's two types of neurofibromatosis there's only one of them that's associated with glaucoma do you know which one an F1 an F1 and an F1 is on which chromosome 17 17 do you know how do you remember that that's why 17 letters 17 letters in the bottom right of the house thanks one more thing about anoremia because this always comes up you guys remember most of the cases are autosomal dominant one third are sporadic this is where you can make a life or death diagnosis what is associated with sporadic with two realms tumor okay it's important to get those patients screened and the sporadic a sporadic form of anoremia they need to get my I don't know what the protocol that usually is like renalgia sounds in the end checking for a room tumor okay alright any question can you run out of time is that helpful that's great thank you Justin hopefully some broad generalizations as you're rotating on service I'll tuck away don't forget the 50% rule don't forget that when kids percent young it's because of irregular disgenesis of any cause at your second disgenesis surge webber PCG the mesh work is dysfunctional and forget the anoremia that you need for goniatomy because you've used the gonioprism you've got to look directly through can't do a gonioprism here thank you