 Last year, the last year for OCAPS, I told Rhys last year, I was like, if my score was a person, it could vote, but it couldn't drink. So how did I? Rhys would ask you. Yeah, of course. Yeah, oh no, he wanted to know exactly where it was. So I studied differently for boards than I did for OCAPS. Whether or not this strategy will be helpful for OCAPS is hard to say, but I strategically read the BCSE. Instead of just reading it, I tried to think, OK, what are the concepts they're going to try and test me? How are they going to try and test me? What are the things they really want me to show mastery of? And then how are they going to trick me? And then I tried to predict what questions they would ask from that. So I sent you guys my little worksheet thing, I would say, for each section of boards, probably 30% to 45% of the stuff that I put on my little review worksheets that I filled out ended up being a question. So you can kind of outsmart the test if you think really strategically. Cue banks are not going to be enough. They're starting the Academy knows that everyone's doing cue banks now, and so they're starting to think. And then for glaucoma, your highest yield stuff is there's always going to be a question or two on medications. And then the treatment, so knowing when LPI is indicated versus SLT, what glaucoma patients you do SLT on versus who doesn't respond to SLT, and then the pathophysiology. And then last, the pathology, which I'll leave to Dr. Maimel since he has all the good slides, and I don't. So the way we'll do this is just like a really quick review of the topics, and then we'll just do, there's questions at the end. Like a review of medications, and then questions about medications, a review of. So probably the highest yield, like biggest bang for your buck because it's a short chapter, but there'll be probably at least two questions on this section. The best things to know are mechanisms and side effects. They'll almost always try and ask you something like that. But your prostaglandin analogs increase uvus glural outflow. We don't know 100% how they work, but possibly increasing the spaces between the muscles and the ciliary body to allow more fluid to flow out. Side effects are almost entirely ocular and cosmetic, iris pigmentation, less in blue-eyed patients, most in the yellow, hazel-eyed yellow patients, periorbital fat, atrophy, hypersychiasis, redness at night. Know that it will exacerbate herpes, keratitis, and also CME, so they'll try and trip you up that way. And then uveitis is an idiosyncratic response of 1% of patients. Beta blockers, aqueous suppressants that work by decreasing cyclic AMP. Know that it's most effective during the day. You can almost know IOP lowering infection from Timolol that's used at night. So that second dose of Timolol really doesn't get you all that much extra. And then a ton of systemic side effects. This is where they'll probably test you on Timolol. If they test you, the bronchospasm, bradycardia, or the easy ones, things like worsening depression, increasing serum lipids, and worsening myosinia will be probably the things they try and trick you on. There was a question about myosinia on my boards. And then also masks hypoglycemia. And just as a side note, I had a lady who was literally getting a pacemaker placed for severe bradycardia. She was in the 40s. I was like, oh, let's just stop at your Timolol. I inherited her, and she was on Timololol, and her heart rate went up 20 points. So we saved her for having to be a speaker. So just keep that in mind. You're alpha agonist, you're bramanidine and aproclanidine. No one ever uses aproclanidine in real life, but it still shows up on tests all the time. Bramanidine is more alpha two selective than aproclanidine. It's an aqueous suppressant that lowers epi-scleryl venous pressure via unknown mechanism. So mostly we don't know how it works. And then the side effects mostly are that blepharodermatitis and follicular venous that you guys see when the patients come in and they've got that crusting scaly rush around their eyes. It's a lot worse with aproclanidine than it is with bramanidine. And then a lot of patients will get dry mouth and lethargy. Where they'll try and test you is this contraindication if the patient's on an MAOI or a TCA. That was also on my boards. So just keep that in mind. And then your carabinic anhydrase inhibitors, rizolamide, brinzolamide, acetylzolamide. Targets, directly targets the carabinic anhydrase in the ciliary body. 90% has to be blocked before you see an ILP lowering effect. I think that's that question on up the questions. Like how much of it has to be blocked before you get in effect. Bitter taste is a side effect. And then worsening of corneal edema in patients with compromised endothelial cell function. So you wouldn't want to give this to your patients with pseudophagic pulous caretopathy or fuchs. And so that's probably where they'll try and test you on this. And then if you're giving oral medications, you have to know about all these other side effects. Abdominal pain, nausea, vomiting, diarrhea, impotence, depression, renal stones. What about classicosis, hypoglymia. And then no diamox is metabolized by the kidney, but methozolamide is by the liver. So if you have a kidney stone patient, you can't give them a pseudazolamide, but you can't give them methozolamide. And then, again, they'll try and trick you. You can't give diamox patients who are on a thiozide or loop diuretic, because you can make them profoundly hypokalamic. Myotics. We don't really use these very much in clinical practice anymore, but they still show up on tests. Mostly we're talking about palcarbine. Basically the mechanism of action is pulling on the longitudinal ciliary muscle and that tightens everything. So you get more outflow through the TM. Ton of side effects, brow egg, meiosis, retinal detachment, cataract formation, iris, epiphora. I think I remember a question about lacrimal stenosis with use of palcarbine. Increased bleeding during ocular surgery. They could try and ask you a question like that, like this patient on palcarbine. What's the most likely reason for bleeding during surgery? And then it could be like fuchs or blah, blah, blah, blah. Iris neovascularization or palcarbine. And then stomach, all kinds of crappy side effects. And then just know you can induce paradoxical angle closure, because when you're stimulating the ciliary muscles, the lens-iris interface is moving forward. So while really weak palcarbine can be a treatment for people who are already blocked by breaking that mid-dialated configuration of the iris, anything stronger is gonna actually make it worse, which is why in the textbook we'll talk about palcarbine, but no one will ever actually use palcarbine for treatment. And then pregnancy is almost always a topic as well, just because everyone worries about all those pregnant ladies out there with glaucoma, because there's so many of them. Every glaucoma drop is categorically C, except for bromonidine, which is a class B. Prostaglandins can cause early uterine contractions, so that's why it's a contraindication. The best way to remember this is you can think of me being nine months pregnant and telling my glaucoma attending, I'm going to drink this bottle of Latana pros because I can't be pregnant another day. He told me that I wouldn't do any. And then carbonic anhydrase can cause neural tube defects in animals, so it's thought to be a triatogen. Timolol, even though it's category C, is used orally all the time in pregnant ladies, so it's probably fine, but for the purposes of the test, it is a class C. And then in breastfeeding, everything that was safe in pregnancy is not safe in breastfeeding. So bromonidine, due to severe CNS depression, and beta blockers concentrate four times greater in breast milk, and so you shouldn't give them no pregnant or nursing, no nursing woman should be on a beta blocker. Okay, so we'll do our questions. 71 year old female glaucoma suspect is referred to you for evaluation, her pacimen of clotsery, she's got bradycardia and diabetes, she has dry eye, remote HSV keratitis, and some prolonged CME after a cataract surgery. Basically, which of the following would be the best initial treatment for this patient? You want to avoid Latinapros because of the history of HSV keratitis and CME. Timalol, you want to avoid because she's got bradycardia and also diabetes. In real life, we never avoid it because the diabetes put up for the purposes of a test, just like you never give beta blockers diabetics on your steps. And then COSOFT, also because it has Timalol. So SLT would actually be the best initial treatment for this patient. Your 26 year old patient with juvenile glaucoma is pregnant, she's well controlled and Latinapros in COSOFT. She asks about the safety of drops in pregnancy. What do you tell her? Yes, four. So just a review again of everything we talked about. Latinapros deuterine contractions. Carbonic anhydrase is a teratogenic, Timalol class D, but likely safe. Bremonidine can't be used in nursing mothers. You need to stop a few weeks before birth and Timalol is concentrated heavily in breast milk. So answer is Bremonidine, okay. And which of the following patients is Bremonidine contraindicated? Well, obviously you can't get Bremonidine boards. This is like a favorite of theirs because they don't want you to kill babies. So I think the official recommendation is less than four. You can't use Bremonidine due to CNS depression. Amatryptoline is a TCA or an MAOI, I think it's TCA. TCA. So contraindicated. And then obviously you can't use it in a breastfeeding mother. Lung is not a systemic side effect of topical beta blockers, insomnia. So if anything, you would get more like lethargy insomnalins with a beta blocker than insomnia. All the rest of those are known side effect, bradycardia, reduced libido, syncope, mood changes. I have had several male patients be upset by their beta blockers, so it does happen. And we talked about alteration of serum lipids and then worsening of depression. I feel like there's been more and more a push to be aware of the psychiatric effects of glaucoma medications. So you might see something like that on the test. Your blue eye patient is concerned about the cosmetic side effects of prostaglandin analogs. You tell her, don't worry, iris changes in color are rare in patients with blue eyes. Iris pigmentation, when it happens, it's usually associated with a risk of worsening glaucoma. All the cosmetic changes with prostaglandin analogs are reversible when you stop it, or latinoprost has the highest incidence of redness, so we'll use bematoprost or trivoprost instead. So it's pretty rare in blue eyes, less than 8%, but for all other eyes, it's pretty common and it's more likely the longer you're on it. Overall, the rate is 33% of iris pigmentation changes, but you're hazel-eyed. Green-brown I think is 80%, and then your yellow-eyed patients, it's like 85%. And it's the one cosmetic side effect that is not reversible. Your periorvital fat atrophy and your hypertrochitis and the pigmentation changes around the eye are all reversible after you. Oh, it's like a classification of hazel in your BCSC. What's that? You give more yellow in your hazel, right? Yeah, yeah, I just never heard that. Instead of green-brown, it's like brown-yellow. You don't see it often, but... Dude, we shouldn't have to point it out. Which of the following medications lowers IOP by targeting cyclic AMP production? Shout it out, don't be scared. Two. Two. How does latinoprost work? You can see it's a little out. Yes. What about metarsidil? That's repressant. And it probably won't be on your test yet, but it's the first, the first squelchal medication that works at the level of the travecular mushwork to increase outflow through the TM. It just keeps asking me to sign into the internet, so maybe that's why I keep doing this. Which of the following patients will the latinoprost be the best choice for IOP lowering therapy? This one's kind of tricky, but basically, it's trying to get you to think about all the side effects. Anytime you're only gonna start, um, sorry, number three should say with pigmentary glaucoma in one eye. So anytime you're gonna start a latinoprost in a, like, only on one eye, you have to be really aware of the cosmetic side effects. So the best choice would be the 75-year-old patient with pseudo-exfoliation in both eyes. And then you would obviously avoid an inpatient with TME. It can exacerbate myestinia. It's most effective during the day and hardly effective at all at night. Most formulations are beta-1 receptor selective, except for which one? Tassel. I've never actually seen anybody on the tassel. And it can increase your serum lipids. Acetazolamide is contraindicated in all the following patients, except a patient with reduced liver function, a patient with Astrea of kidney stones, a patient taking hydrochlorothiazide, or a patient with Astrea of anaphylaxis to sulfur. Right. And that's because Acetazolamide is metabolized by the kidneys, so it's okay for pullover of the interpretation. Which of the following is expected with systemic carbonic and hydraise administration? Increase in serum potassium? Decrease in serum glucose? Metabolic alkalosis or metabolic acidosis? Yes, you get a metabolic acidosis. In fact, I just put a guy in the hospital because I gave him a metabolic acidosis from his dimox. But his pressure was down. Which of the following are known side effects of pylocarpine? Yes. Oh my God, that's computer- This'll be your life soon. This is Chris, actually. Share these slides, I'm just gonna go over to surgery. Oh yeah, go, go, go. Awesome. Okay, on to diseases. They generally tend not to ask a lot of questions about just traditional primary open-angle glaucoma because it's hard to trick you guys on it for one. And it's hard to come up with good questions on it or two. It's a pretty straightforward disease and it's a pretty straightforward treatment. So the things to know are the risk factors. Obviously, ocular hypertension is the biggest one and then age closely followed by age. Myopia is a proven risk factor. Family history and race are also, everything else they've looked at has been kind of neither here nor there. And then just know that lowering IOP by 30% reduces the five-year risk of visual field progression from 35% to 12%. The other, I've never actually been, I don't think I've ever seen a test question on a glaucoma study ever. In fact, I don't know that I've ever seen like a question on any study ever. I think there were two on OCAPs last year. Really? Okay, were they glaucoma? No, R&B and something else. But it was like, I felt like it was a wasted effort. It's so much to learn all the studies. It is so much. Like if you just know the concepts behind them, lowering IOP reduces visual field progression, how many of you are surprised by that? I mean, I feel like, again, they just want you to know the concept behind it, but they're not gonna be like, from which landmark glaucoma trial did we learn this? You know, I just don't think that that's really fair or relevant question. They don't care that much. It probably doesn't mean very much, but the AO questions have had about five or six questions on glaucoma trials so far, like very specific ones. Like, which trial was the first one to demonstrate that such and such? Seriously? Yeah, there were some where it was like, I've never even heard of those trials. Those questions are not at all representative of the kind of questions you'll see on OCAP. They're actually varying, for the most part, they're very straightforward, so they can help with the new question bank. Yeah, I've heard about it, but they don't have access to it. But it's not very good. Like, although to be fair, I actually think that OCAP questions are not very good. No, I feel like perhaps maybe the Academy questions, perhaps, are more inclusive of the quality of the OCAP. It's true, I remember the first time taking OCAP, sorry, I know we're digressing. The first time I took OCAPs, I was like, these questions are not at all what I was expecting. They were so, that's all I had done was off the questions, and I was like, what? You expected like a, you know, three paragraph questions. What the heck is going on? And also be prepared for those of you taking it for the first time, the pictures are just god-awful. You'll stare at it for probably a solid 10 minutes and be like, I don't even know what part of the eye. I think I really don't. And you just prepare yourself. No one leaves that test field, and it's okay, we all make it somehow. So, I guess if you find yourself with a lot of free study time, maybe study the glaucoma landmark trials, I put it on the list of things to study on your own if you're so inclined. But I guess there were two questions about it last year. Maybe that probably means there won't be any, that probably means you guys will all study for it this year and there won't be any on it this year. Oh, patient syndrome. You know, they like to ask questions about genetic defects. So the LOX1 gene has been identified for pseudo-exfoliation. The target like distribution of fibular material on the lens. They could show you that pathology picture of all of the little things standing up. Translumination defects at the people are a margin and that moth-eaten people at the margin appearance. If they're showing you translumination defects and they're at the margin, it's almost always gonna be a pseudo-exfoliation patient compared to your pigmentary patients who have the translumination defects mid-perfury. So that could be, you know, they like to compare and contrast or like they're asking you a question about TIDs or IRIS configurations. Just know all the different glaucoma IRIS appearances and they'll try and trick you that way if that makes sense. And then SLT is really effective in anybody with a densely pigmented angle, but the effects generally don't last as long and they're more likely to get a pressure spike afterwards. So they might ask you that. And then we already talked about pigment dispersion. You get your densely pigmented trabecular mesh work and a sample AC line. The sample AC line is not specific just to pigmentary. You can also get it in pseudo-exfoliation. But you get this mid-peripheral spoke-like IRIS TIDs. And then if they ever mention a concave IRIS on gonio, that is gonna be pigment dispersion. Then the typical age group, your young myopic males and the IOP spike after exercise. SLT, same thing as with pseudo-ex, it's really effective, but the effects don't last as long and they're at higher risk for pressure spikes afterwards. And then they're at higher risk of hypotony with filtering surgery, probably more because of the myopia than just for the mechanism of their condition. But just know that they might try and ask you, like, which of the following patients is at higher risk for hypotony after a trabecula to me and it might be like a young myopic guy with pigment dispersion. The lens-associated glaucomas almost always, there's a question about these because they're easy to mix up when you're not really, like when you're just kind of like giving a cursory glance to them. But if you just know every single one of them has like one easily identifiable feature, then you shouldn't ever mix them up. So your fake-olytic, it's caused by leakage of lens particles by a hyperventure cataract. So if they don't have a cataract, they can't have fake-olytic glaucoma. And it's caused by macrophages in the trabecular mesh work. Macrophages generally don't cause KP, so you're not gonna have KP in this patient. And then lens particle is caused by like a piece of the lens, just like it sounds. So they are your pseudo-fake-ic or your traumatic patients who no longer have lens. You just have pieces of it and the mechanism is actual cortical material blocking the TM. And then your phacoantigenic or phacoanaphylactic depending on how old your BCSE is, but phacoantigenic is the newer term. You're actually sensitized to the lens protein. So this is like a true hypersensitivity, immune reaction, and you will have KP. So that makes sense, right? And also you've been sensitized to your lens proteins because we ground up your lens and released all these lens proteins and taken them out of your eye or you've had trauma. So if you have a cataract, you have phacolytic. If you don't have a cataract, you have lens particle or phacoanagenic, essentially. And then if you put them all in a chart, you can see, oops, go back. Phacolytic, angle, open, inflammation, yes, KP, absent, mature cataract, and then the mechanism. So three of the four have opened. So if your angle's closed, it's fakeomorphic. Your angle's open and you have a dense cataract, it's phacolytic. If your angle's open and you have KP, it's phacoanagenic. Like there are just no, no like the key buzzwords and you'll never mix these up on a test. Does that make sense? Any questions about these? This is almost always on something. Seriously, it makes me connect to the internet every like three seconds and then I can advance the slides. Turn your wifi off. Although kind of the inflammatory glaucomas are a fair game and they'll like to compare and contrast them. So they'll try and trick you between Pawsner-Schlossmann, Fuchs, and then in the closed angle glaucoma, things like ice syndromes. We'll throw all of these together in a question and try and make you pick out which one it is. But just to know Pawsner-Schlossmann and Fuchs, the angle is always open. And then with ice, it's the mechanism of glaucoma's angle closure. So if the angle's open, you're not getting PAS, right? That makes sense. So there's nothing closing the angle off. So just keep that in mind too. If you're talking about PAS, it's not one of these things. Glaucoma, cyclinic crisis, you get low grade inflammation, an IOP spike where the IOP is markedly elevated out of proportion to the amount of inflammation on exam. And they'll then might ask you about treatment, like which of the following is the best means of treatment for this patient with Pawsner-Schlossmann? Just know that steroids don't help. So you never put a Pawsner-Schlossmann patient on steroids. All it would get you is an IOP spike. And then Fuchs heterochromic is iris heterochromia and the affected eye. On gonia, you'll see fine vessels that don't cross the TM, which is different than ice syndrome where they do cross the TM. And the vessels don't lead to PAS formation. So just as we were talking about the angle remains open. And then they might ask you about disease association. So Fuchs is questionably associated with rubella, which you would think then would mean we wouldn't really see it anymore because no one gets rubella. But the Pawsner-Schlossmann and the questionable association with HSV or CMV, elevated effi-scleryl venous pressure. So most common in these diseases, they pretty commonly will put like a fistula on the test. I think I've seen it on OCAPs maybe twice. And then your orbital varix patients can get it. Your Sturge Weber patients, the older Sturge Weber patients, I think there's often questions, question about this where your young Sturge Weber patients, it's more of a disgenesis of the angle structures. And the older patients, yeah. The older patients, it's elevated effi-scleryl venous pressure. Your thyroid eye disease patients, we had one of these at the VA the other day, will have elevated effi-scleryl venous pressure. Things to know, if you see blood in Schlund's canal, that's their way of telling you that this patient has elevated effi-scleryl venous pressure. And if they offer you an SLT, don't do it. Then if you think about the mechanism of how SLT works, you should be able to logically reason out that an SLT isn't gonna work on these patients, but don't SLT them. And then you can imagine that glaucoma surgery is gonna be riskier in these patients. They're more prone to supercoital hemorrhages or effusions after surgery. So keep that in mind too. Complications from surgery is probably gonna be high yield. And then comparing hemolytic to ghost cell, I had questions on this on my first OCAPs. Basically, just know they both happen after vitreous hemorrhages. So they're both from the vitreous coming forward into the anterior chamber. At hemolytic, you've got the macrophages blocking the TM, so that's where you'll get the half slide of the cells with the stuff in them. And you're like, what? Is that supposed to be there? I don't know, I can't tell. And hopefully they'll give you some kind of clue that this patient had a vitreous hemorrhage. And then you'll say, oh, those are macrophages with hemoglobin in them. Yay, this is hemolytic. Yes. I heard a good way to remember, but anything with what? Lytic in it has macrophages. So like, fake-molytic, hemolytic. Oh, that's a good, yeah, that makes sense. It's funny, because I have a mnemonic for almost everything a Sophia can attest to, but not for glaucoma. I realize all my mnemonics are like retina or cornea. And then ghost cell is the actual degenerated red blood cell products in the TM, instead of the macrophages. That's also later, right? Like with the cute, you're not gonna get a ghost cell. You can still get them in that relatively same time period, but yes, the blood products tend to be older in ghost cell versus hemolytic. It's gotta be at least 14 days because that's the life cycle of it. I'm gonna say yes. And then you get like the yellow khaki colored. Pupillary block. So this is the most common mechanism for angle closure. Level of pathologies at the lens iris interface. So you're getting obstruction of flow from the posterior chamber to the anterior chamber because it's blocked the level of the lens iris. So they might ask you about some kind of, what's the underlying mechanism for pupillary block and throw you a bunch of stuff about how the iris is blocking the TM, but the problem starts because fluid can't get around the lens at the iris lens interface. Then you get iris bombay and then everything shifts forward and that closes the angle. You're most likely to get that obstruction when the people is mid dilated. So just know what the treatment recommendations are. Officially you can try a mild cholinergic like pylocarbin to induce meiosis and get rid of that mid peripheral iris configuration. But strong myotics, they might ask you this, why wouldn't you use a strong myotic in angle closure? It increases vascular congestion for one and then rotates the lens iris interface anteriorly so it worsens the obstruction of the angle. Definitive treatment is LPI at least according to my BCSC. So don't do cataract surgery on them as the first line treatment. Yes, I mean in real life, yes, but in BCSC, OCAPs world, LPI is the answer. And then just know again, if they show you an angle closure patient but it's not a pupillary block patient. So it's a neobascular, there's PAS. If there's no component of pupillary block, LPI is not the treatment. That's how they'll try and trick you with that. Chronic angle closure, they might give you, they might tell you a story about a patient with optic nerve damage and kind of chronic migraines and then you look in and their angles closed but it doesn't open appositionally. They'll have like circumferential PAS that is chronic angle closure. Officially the treatment is iridotomy, iridectomy, but if their angle is closed down with PAS, even that's probably not gonna be enough and you have to do something else. But officially, you would still do an LPI to remove any component of pupillary block that's there. And then know for any patients with a narrow angle, they might ask you what medications do you need to counsel this patient to avoid. There are a lot of the allergy and cold medications, anti-depressants and neurological medications. I don't think they'll get this specific but they could try and trick you that way. And then platoiris, this one's a favorite one to ask for the angle closure because it's tricky and there's a lot of exam findings they can show you to try and get you to think of it. But anytime the AC, they describe a patient with a deep AC but a narrow angle, you should be thinking could this be platoiris or they show you a UBM and they're talking about glaucoma and the iris looks kind of funky at the angle, then you should be thinking that this is platoiris. The treatment is always LPI first to remove whatever pupillary block component is but just know that they might tell you oh, this patient had an LPI which did not relieve there. Their narrow angle, what would be your next step? If you think it's pupillary block, the next step would be a myotic to pull the iris away and then if that doesn't work, you can do irritoplasty, which I, and then ice syndrome, like we talked about, they might try and throw this in with your late partner Schlossman and the inflammatory glaucomas but if you see unilateral findings in women ages 20 through 50 with high PAS, you should be thinking ice syndrome and the reason why the PAS are able to grow that high is because if you think about it, the endothelium is dysfunctional, it's diseased and so abnormal tissue that's not supposed to be there can grow. If you have a healthy endothelium, the PAS won't extend that high. That makes sense. So like an NVE patient, their PAS won't be high PAS because the endothelium, the cornea is normal. Aqueous misdirection is another favorite so they might show you a bunch of different ACs and then ask which patient recently had. Cataract surgery, an aqueous misdirection, you get the uniform flattening of the AC and despite an LPI, so everything is flat. The iris is a snack up against the cornea unlike angle closure where it's iris bombae which is relatively deep centrally and then really shallow peripherally. Treatment, the first step is intense cycloplasm. Well, LPI if you haven't done that already is more diagnostic than therapeutic but you have to have a patent LPI and then intense cycloplegia. So you put them on atropine, yag the anterior highlight phase which almost never works and then you send them to retina. They might ask you like what percentage of these patients resolve without surgery? Technically what the book says is 50%. If you ask anybody upstairs, they'll tell you 0% resolve on their own and they all have to have surgery. All right, so questions. Which of the following is the most appropriate initial treatment of pupillary block in a patient with microspherofakia? Yes, pulls the pupil anterior, it pulls the pupil so the anterior dislocated lens is pulled back. It's the opposite of what amniotic does which is pushes everything even more forward. Dilating, so this is the only case where pupillary block is treated with a dilating drop. Microspherofakia, that anterior lens dislocation. So you're pushing everything backwards. Does that make sense? Which of the following is not a risk factor for acute narrow angle glaucoma? Actually pseudo exfoliation is because of the zonulopathy. So myopia, but the pseudo exfoliation is where we'll try and trip you up. So you can get a severe like zonulopathy in the pseudo exfoliation patients. So those patients are at risk for angle closure. So oftentimes we'll see pseudo ex patients who also have really, really narrow angles and that's just because their zonules are so weak that everything's really pushed up forward. The most likely glomuscopic finding in a patient with elevated IOP and radial men peripheral IRSTIDs would be? Yes, so this is your pigment dispersion patient. You don't always have to have a case spindle in your pigment dispersion patients but you do always have to have that pigmented TM. That's like the first finding that you see usually. Bilateral PAS in an elderly hypo-rope is most likely secondary to ice syndrome is obviously unilateral. The QV it is almost always unilateral, axinfeld anomaly. I mean, you're not gonna be an elderly type of with axinfeld anomaly. You would not expect to see blood in Schlem's canal in which of the following disease processes? SLT would be the most effective in which of the following patients? Four, yeah. So SLT not effective in traumatic glaucoma and not effective in UVA glaucoma can make UVA just worse. Again, juvenile glaucoma tends to be more of a like AC malformation. So SLT not as effective there either. And then thyroid ophthalmopathy is usually more of an episclovenous pressure. So SLT is not effective there. It's the best choice pigmentary. Which of the following is true of laser trapeculoplasty in pseudo-acceleration glaucoma? Less effective than in primary glaucoma. It is very effective and the effects last longer. Due to intense pigmentation of the TM treatment will require more energy. IOP spikes are more common at lower energy settings or none of the above are true. IOP spikes are more common with higher energy settings. So you wanna do your really pigmented patients the lowest possible energy you can and then you get less IOP spikes if you're using lower settings. And it is very effective but the effects last shorter than with your primary glaucoma patients and the treatment usually requires less energy. Which of the following is exam finding correctly matched with the disease? Which of the lens glaucomas do you get Kp? Which exam finding would you expect to see in a patient with known Fuchs heterochromic, heterochromic erotociclitus? Three. They do get Kp but they're pancornial. This is like a really mean way to trick you but I do remember a couple questions like that. So you get pancornial Kp, fine vessels traversing the TM that don't lead to PIS formation and then posterior subcapsular cataracts. So I feel like they like to try and trick you that way too. Like, oh, anterior cataract versus posterior cataract. Which of the following medications should be avoided in patients with hyphema and sickle cell? This is probably a high yield. So you shouldn't give any of these to a patient with sickle cell and hyphema. Dorsolomide and aproclonidine, carbanic anhydrase inhibitors, increased sickling, alpha one agonist cause anterior segment ischemia. So those ones are really specific to topical treatment for sickle cell hyphemas. And then hyperosmotics can induce a global sickle cell crisis. So you don't want to give those. And then never give pylocarpine to anybody with any type of hyphema. So that's true of whether or not they have sickle cell. The difference between hemolytic glaucoma and ghost cell glaucoma is best represented by which of the following statements is a lot of chords, I'm sorry. I'm just looking forward if it were true. I was writing these ones. I was writing these ones during UOS and I was getting bored. Also it's really hard to come up with like realistic fake answers. So they'll often do this to you where they know you'll know the basics of it, but just remembering which one is which and they'll switch them on you. So just make sure you have a way of remembering lytic macrophages is a good way. But just have some kind of way of saying like, okay, this is this versus this is this. Describe the mechanism of angle recession, glaucoma or traumatic glaucomas. So why do you get glaucoma in these patients? There's a tear between the longitudinal and ciliary muscle and the ciliary body restricts aqueous outflow through the TM. The tear between the iris root and the scleral spur results and scarring that will cause PAS formation. The damage to the angle itself is not the cause of elevated IOP, but rather a sign that the TM has sustained injury or a tear between the longitudinal and ciliary muscle. The ciliary body restricts the aqueous outflow through the uveal scleral path. You guys all agreed it was three, right? Because it doesn't make sense if you've got angle recession, why that will cause elevated IOP. You're getting more flow through that area. So what's happening is that you'll initially see probably a lower IOP than that cleft will heal. You might get an acute IOP spike when that cleft heals, but over the long term, they're still at risk and that's not because of any of those angle changes that you can see, it's because the TM has been damaged. You can't see that, but all of that are their findings on gonio or your markers of the damage. Which is the following is true regarding steroid response glaucoma. The risk of steroid response is not dependent on the potency of the steroid. Patients with PoEG are no more likely to experience IOP spike versus someone without pre-existing glaucoma. Only a small percentage of patients treated with steroids experience IOP elevations. A patient is unlikely to experience an IOP spike from steroids if the IOP stays normal for the first two days if therapy all are correct or none are correct. It's actually none are correct. So glaucoma patients are much more likely to get an IOP spike than your average patient. And if patients do get an IOP spike, it should make you think, oh, maybe this patient's at risk for developing glaucoma later. Same with the traumatic glaucoma. They're at risk for glaucoma in their other eye because they just seem more prone to develop glaucoma, if that makes sense. So people who tend to spike their pressures just have a higher baseline risk of developing glaucoma somewhere. We all know that it is dependent on the potency of the steroid. Anybody who gets Dersal is gonna spike their pressure low to max, it's pretty uncommon. So there's a lot of questions and opto questions about ranking the potency of the steroids. And then the BCSC says 30% of patients who are treated with steroids will get a pressure spike at some point while they're on treatment, which is pretty high. But the IOP is usually rarely going to spike within the first two days of treatment. If it's gonna spike, it's almost always after a week at least of therapy. So if someone comes to see you after surgery the next day and their pressure's high, they might ask you, is this a steroid response? And the answer is no, because you don't get a steroid response in the first two days. Does that make sense? Which is the following history regarding people who are black. It occurs when the iris is maximally dilated. It occurs when heaped up iris tissue blocks the flow of fluid out of the angle. It occurs when the flow of fluid from the posterior chamber to anterior chamber is impeded at the level of the linsirer's interface or when chronic angle changes such as PAS or NV and P the flow of fluid out of the angle. Good job. Which is the only types of PAS is frequently seen in chronic angle closure. That's right, you get that creeping angle closure. And that makes sense just to tend to close your angle off inferiorly first and then it kind of slowly creeps around circumferentially. And so that's what that means. 76 year old female, three days after IOL exchange with the iris sutured IOL, her IOP is high and her chamber is shallow. She's underazole and ophoxicin, which the following is the most likely ideology for her condition. Most likely is aqueous, is number one. Aqueous in this direction because her chamber is diffusely shallow. She can theoretically have pupillary block with her iris sutured IOL, but you get more of that traditional pupillary block configuration even though she's pseudophagic you'd still get that iris on the configuration. And then again, if she had high IOP with routine biscoelastic, you would expect a normal chamber and it's too early for a steroid response. This is actually a patient that Tina and I were up with all night during my fellowship had this exact thing. It's not fun. Which of the following would LPI be the treatment of choice? So, vagomorphic because there is an element of pupillary block. So muddy. None of the rest of these have any component of pupillary block in them. Does that make sense? Eist syndrome, it's all PAS formation. Facoantigenic, the angle is open and then secondary angle closure following dense PRP. Does anyone know the mechanism for that? Magnetism for angle closure after PRP? They get dense chordal effusions that can push everything forward. So the treatment for that is just what? They control the pressure while you're waiting. All right, now people should not get to position time. Question about what kind of random tear perforation was like, or it was like four different things and two of them were aromatitis, retinal attachment is definitely not gonna cause angle closure. Seriously? Push, there's nothing there to push the angle forward. It was a really hard question. That sounds, yeah. Definitely make a list of some of these questions and I can just kind of block the test out of my memory. No, I do too. I can only remember the ROP in some studies say that you should start. No, it wasn't the treatment. It was like the theory of edge effin angiogenesis. Oh, geez. I don't even think that's in my current BCSC. But I think that that's, because it barely talks about using a baston. It's like, this is still carnivore gel. Oh. There's actually, there's a table. There are only really dates by BCSC. You're gonna have to get new ones so that I can have accurate questions for everyone. In a patient with aqueous misdirection, all the following are acceptable methods for treating elevated IOP except. Not your friend. Almost never will this be like, we just wait this year, it will be a correct answer for something, but Paolo's never the answer. It's never the answer. Don't give it. Okay. Match the exam finding to the underlying pathology. High IOP closed angle flat chamber. What is that? Right, aqueous misdirection. High IOP closed angle iris bombe. A cute angle closure. High IOP closed angle high PAS above Schwalbe's line. What is that? Nice. And then high IOP closed angle and PAS ended at Schwalbe's line. So you guys see how they might try and like use all of these findings to, so just kind of, I would just make a chart or something, watch there won't be any questions about this, but. What are the following mechanisms as thought to be the etiology for glaucoma and anorhagia patients? You have dysgenesis of the angle structures that result in outflow obstruction. You have anterior rotation and eventual adhesion of the iris tissue to the angle. You've elevated episculial venous pressure due to poor iris vascular outflow or chronic subclinical inflammation resulting in creeping PAS and eventual angle closure. Right, your iris stumps get stuck. Yeah, the more iris you have, the less likely you are to have glaucoma for your anorhagia patients. Which of the, let's see. Oh, this is my favorite one. I think I've shown you guys this before. Okay, and then they might ask you about the glaucoma minutia and this stuff that's just hard to study for. A couple of questions in, but I find this like, definitely if you're prioritizing your studying, start with the medications and then like the diseases, but thinking strategically like mechanisms of how they're causing glaucoma and then relating that to treatment. So if you understand the mechanism of the glaucoma, you'll understand what the treatment is where you know, open angle versus closed angle, high PAS, people are blocked versus non-pupillary block, elevated episcleral venous pressure versus not. How does SLT work? And you'll be able to kind of logic through most of those answers. This stuff is just memorizing. So UVO scleral outflow is inversely proportional to intracular pressure measured by fluoro photometry, which we do all the time increased by atropine or responsible for about 10% of total outflow. It's about, well, according to my VCSD, it's 20% of UVO scleral outflow. This is one of the questions from the back of the book. UVO scleral outflow is independent of IOP, so they might just know the equation, what all the variables are, because they might use that to try and do something like this. And if you know the equation, you'd know UVO scleral outflow is independent. Fluoro photometry measures aqueous production, not drainage. The Besco Neolens for distinguishing appositional angle closure from synecule angle closure. I forgot to animate that one, but you have to be able to indent the cornea, so you have to know what lenses indent versus which ones don't. So the answer is the Zeiss form here, and under the breath of those can do compression gonioscopy. The rate of aqueous production, two microliters per minute. Facility of aqueous outflow is best measured by geography. Monometry is FB scleral venous pressure, tonometry is IOP, and fluorophotometry is aqueous formation. All the following statements regarding the Goldman equation are true except... Yes, that's right. I'll send this out to you guys if you want, which is probably an accurate statement regarding IOP. It has a normal distribution when measured in large epitingeliogic studies, varies two to six millimeters mercury in individuals with glaucoma over 24 hours. Transiently increased following alcohol consumption or linearly related to... Right, that's a normal variation. Patients always ask me that. Why is it so different? Yesterday it was 19. Yesterday it was one point lower. It's 18. Which of the following testing strategies may allow earlier detection of glaucoma compared to standard automated perimetry? Standard automated perimetry is just visual fields. They throw that in and you're like, what does this mean? Superthreshold testing, frequency doubling, confocal, laser, ophthalmoscopy, or all of the following are good. Basically, superthreshold testing. It's like testing, like can you see it? Or are you totally blind? Or can you see it? Are you looking through your eyelid? Like, you know, like no, you can't see it or yes, you can't, but it doesn't tell you anything more than that. Frequency doubling is what you'll often get on those like weird, like square, boxy looking visual fields that come from optometry because it's a good screening test, but it doesn't give you any data to follow people over time. And then just to review on your own, more of like the visual field OCT stuff. We don't have time to go over all of that. The childhood glaucomas, not sure how much of that is really all that high yield. Again, just know that childhood glaucoma, it's almost always a surgical treatment because the anterior's, you know, segment isn't made right. If you're born with glaucoma, something went wrong while you were developing. The glaucoma studies, debatable on how low yield that will be, I'm interested to see if you guys can do that. And then the other kind of, they are game stuff is the surgical management of glaucoma. So just knowing the rest of glaucoma surgeries, they'll probably focus on traps and tubes, which is what they usually do. And just knowing who's at risk for like, supercoital hemorrhagin, hypotony are probably the biggest high yield things.