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 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.  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.  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.  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.  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?  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.  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?   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.  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?  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.  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.  Although kind of the inflammatory glaucomas are a fair game and they'll like to compare and contrast them.  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 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.  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.  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.  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.  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?  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.


Welcome to another episode of Talking Baseball. The Cardinals forgot to get hits again. They lose game two. The Yankees stunned the Astros in game one. What's going on, everybody? Welcome to Talking Baseball. My name is John Boy. I got my co-host Jake with me a little later in the day-to-day, had a crazy airport run, so I apologize if you are waiting. The people that aren't waiting are the people that are listening live as I talk. They don't have to wait until we're done recording. And then I edit it because they are Patreon supporters. They're in the chat. They're watching live. They get it right away. And our most recent Patreon supporters are Kevin Barry. Kevin Barry, like that. Kevin B, baby. Leonard. Jake, you got an MLB player with the first name Leonard. Jim, I've got some huge news for you. OK, excited. There's been a couple of Leonard's first name and last name in MLB history. There's a gentleman. Where can I send you this link? Because you're going to throw up on yourself. I'm already on it. I'm on it. On what? Leonard? Leonard. Read those career stats. There's a player that's name is just Leonard. No last name. He's played in 1892. He played one game. One played appearance, one walk, one stolen base. And that's his stats. Leonard. Congrats to Leonard. Why put this guy in the system if you're baseball reference? Like, can you confirm that this actually happened in 1892? When they were doing like, I guess we'll put this fucker in here, just Leonard. One inning of right field. Yeah, they used the 1,691st MLB player in history, Leonard. Leonard, well, thank you for being a proud Patreon supporter. And coming up third is Vin Scully. How about that? Yeah, huge. Thank you, Vin. We appreciate that. Appreciate that. All right, yesterday, Jake, we had two games. We got two games to recap today. We had the National League CS. The American League CS game two, game one. We had the Nationals with Scherzer on the bump, Scherzer versus Wainow. Scherzer silences the cards bats who maybe forget they're allowed to make noise. It just seems like bad times over there in St. Louis. Do you have a burn of this game? Do we want to get into that right away? How are you doing? Do we need some small talk? I do have a burn of this game. I don't know if their shots fired at the St. Louis crowd. They haven't had anything to cheer for. Over the course of 16 innings, they had two hits. Yeah, it's rough. I mean, how mean is your burn? Not too bad. OK, let's get into the burns. What do we get mean in the burns? Well, I don't know. There's not nice things to say to Cardinals fans right now. You're the mean guy. I'm a nice, pretty guy. I don't know. You're pretty mean to Granky. No, he's bad. All right, let's burn this Nats game. Nats Cardinals game. I apologize. Burn, Jackie, burn. NLCS game two. Adam and the Cardinals try to wane right the ship after getting one hit in game one. That would be a tough ask as three-time Cy Young Award winner Max Scherzer was on the bump for the Nats. Top three, Taylor, gang. Michael A. Taylor rolls up on Wainow with a solo shot in the third, one-nothing Walgreens. Scherzer turned the Cardinal fans into St. Lunatics. I ain't talking Murphy Lee. One hit through seven innings on a ball Soto could have caught. Two hits through 16 innings, yikes. Top of the eighth, it's still one-nothing. STL could steal this game, change the whole series, but Adam eats them up. Two RBI double, tough ending to a heroic effort by Wainwright. Cards would score in the eighth on a ball. Taylor, gang, looked like he rolled up before he tried to catch it, but that was it. Scherzer to do little to Corbin, to Daddy Hudson. Nats win three to one. Take the 2-0 series lead back to the nation's capital. Do you think there's any truth to the rumors that are being spread like wildfire right now that the nationals outfielders hate no hitters?   We're gonna let some drop.  And so to let that ball drop, Michael Taylor lets the ball go over his head. It's just so bored. They can't chatter in the outfield. They're lonely. They're bored. Do you think there's any credence to that wild rumor I'm seeing all over the place? It's a classic case of fat and happy. You don't want the pitchers getting comfortable now. I mean, this isn't the job. Like, yeah, good game, but we still got a few more to go. So yeah, you gotta keep the pitchers on their toes. If Scherzer were to throw a no hitter, it'd only be down from there. And then his confidence would be shocked. So yeah, it's a lot of game planning by the Nationals. And it's a lot of bad times for the Cardinals. Cuts to someone on YouTube, because I'm a young kid on YouTube commenting that not understanding we're joking.   So they get mad on YouTube. No, but for real, they were sabotaging their picture. Boredoms, everyone's biggest fear. And loneliness, it's a killer. For real. Yeah, boredom doesn't worry me too much. But yeah, A, Max Scherzer, seven innings pitch, one hit, two walks, 11 Ks, 101 pitches. He turned it on even more late. He was incredible. Wayne Wright, the old warrior still battling. He had 11 punches.  The crowd still gave him a huge applause as he deserved. He was incredible. He basically went toe to toe with Scherzer. And yeah, if you're the Cardinals, what's really killing you? Michael A. Taylor was hit in eighth again. The eighth hole hitters have essentially been what have done the Cardinals in when you look outside of their lineup doing nothing at all. But that's brutal. Yeah.  Are there historical numbers behind this? Is this like, could this be the worst offensive performance in the first two games of ALCS history? Because it wouldn't shock me if it was. They let the other team no hit them for the first six innings, both games.  It's gotta be historically bad. Yes, it's involved in being historically bad. Four hits through two games. They get the one run in this game. I'm sure back in the dead ball era, there was a couple NLCS shutouts or something like that, but yeah. No NLCS back then. And there was the two of the Nationals hits in this game. Soto couldn't see it too well and he played it safe and let it hop to give up the no hitter. And then Michael A. Taylor, line drive to center, he comes in on it and he loses it.  I mean, there's a world where we're talking about St. Louis having three hits through two games. And it's just not acceptable. The Soto play, I think if there's not a no hitter, everyone's saying good play in a one nothing game. Oh yeah. Like smart, don't let that ball get by you and give them a triple in a one nothing game. But because the no hitters online, you'd like to see him dive out for it because of history. But even then, I think because it's the playoffs and it's a one nothing game, I still think you can say that's not that bad of a. I disagree fully and wholeheartedly and not sarcastically because what if Scherzer, we talked about the end of a no hitter effect when we talked about Anibal Sanchez's game. This was a one run game. If Juan Soto doesn't catch that ball, the St. Louis stadium came to life for the first time. Scherzer gives up a two run Yabo.  I think I'd rather, I'd rather he dives. And by the way, he could have made the catch. He might not have even had to dive. He, I think the Sun in the stadium was messing with them a little bit. He did play it safe, which well, he's 20. Okay. But yeah, no, I hated it and I still hate it at the time. I would have rather you dive to try to save the no hitter. And actually, and I think a big factor in this is I think he just makes a play then if he did dive and it rolled for a triple, I think that's better. Yeah. I think that's fine. I think it's fine to have both different thoughts. I think they give rules for a triple in a one run game. Now, now an outscores the tying run. Better to keep that guy first, but we'll agree to disagree on that one. The Taylor play is Carlos Martinez, who's probably the most fun guy in baseball. He's up there. I enjoy him a lot. He just throws it. How do you enter on Martinez? Huh? The Cardinals closer? Oh, no, no. Jose Martinez. Yes. Yeah. Ron Martinez, my bad. Same team, same last name.  Jose Martinez is fun. He's a fun dude. Like he's always being silly. He reminds me of the tall criminal and home alone, Marv. Oh, okay. Well, Latin Marv, I like that. Latin Marv. Yeah, electric shock. Anyway, he broke up the no hitter in game one and he gets another hit here, but again, he just throws his bat at it. He's just kind of like doing what he needs to do. I mean, it should have been caught, but Taylor completely read it wrong. Anyway, I felt bad for Doolittle is the point I was trying to make. Doolittle is coming after Scherzer, who no hit him basically. One hit him or whatever, you know? And in the close game, and it's like, oh shit, I can't like let the floodgates open now. And then the run scores because of that play and you can see Doolittle's reaction.  Everyone blames the bullpen already. That's a hit in the book. It's like my line looks bad. I don't know if he's the person I think about his line, but his line looks bad now. And then he gets the next out. And did you see the shot of him like saying like, okay, calm down. Yeah, we're good. We're good. It's okay. I really liked the inner monologue that was probably going on and Doolittle's head throughout that whole thing. Cause it's fair. Like, fuck, everyone blames the bullpen already, Taylor. Like, come on, should be out of this. And Jim, can I read to you, I think something you'll be interested in and we're finding solutions for St. Louis. Jose Martinez's last four game locks. So yesterday, one at bat, one hit. Game day before that, one at bat, one hit. Atlanta, October 6th. One at bat, one hit. Atlanta, October 4th. One at bat, one hit. His last four games played, he's had one at bat and gotten a hit. You think they should start him? Game three? And Jose Martinez's last four at bats, he has as many as the whole Cardinals team does in the first two games. Ho, ho, ho, ho, ho! Yeah. Put, someone put that on a quote so we can retweet it. Someone put that on a shirt that has a quote on it that has another shirt on the shirt with those words. Shirt on a shirt. And then delete it, scrap it, scrap it, you went too far. Just do the tweet, just do the tweet. Yeah, go back to the original. In Carlos Martinez's last four at bats, he has double, he has the same amount of hits as the Cardinals do in the last two games. Yes. And technically, he's a part of that. So he has two of the four hits, so he has more than the rest of his teammates. He has double the amount of his teammates in his four. Yes. Yeah, maybe start him. Could be something. Have to, and I mean, I think what other people would be saying is, well, you know, Michael A. Taylor should have caught that ball and it shouldn't have been a hit. Yeah, but you need something. You need anything. And maybe it's luck, maybe he's doing something right. It was a hard hit ball. But yeah, get Jaymart in there. The hits are sad, man. Goldy's got a hit and it's that misplay. Yeah. DeYoung has a hit. I don't forget what it was. I think it's a real hit. The rest is bad. Who's been, so Ozuna is 0 for 8 with no walk. Carpenter 0 for 6, no walk. Damn. The second half of their lineup is only getting three at bats because they're basically getting no hit. Ozuna, Carpenter, and Edmund have a 0 on base percentage in the first two games. Yeah. Everyone else at least got on base once. Fowler walked. Goldy has that hit.  He doesn't have a hit or a walk. What could that be? Hit by pitch. Yeah, maybe hit by pitch or. Yeah. Yeah. Oh, yeah, he did get hit on a ball, right? Hit him. Yeah. I mean, Yachty is batting sixth, I believe. 1, 2, 3, 4, 5th. Yachty's been batting fifth, and he has five at bats this series.  All right. Sorry, Cardinals fans. This is not what you want to hear. Yeah. What do Cardinals feel? What are Cardinals fans telling themselves? They're telling themselves that Jack Flaherty's on the mound for game three, and that Talkin' Jake said that the road game would win the first three games of this series. So they're feeling confident about that. I mean, it's Strasburg coming up, and we'll talk about some of the Tanaka numbers. Him and Strasburger in a fun little race right now for postseason dominance. You're saying we got Flaherty, and the hitting can't get worse, question mark? Unless it does, so it's Strasburg. I mean, Strasburg's prime for a perfect game. And maybe that's what you're looking for. Strasburg has those expectations. I have a fun game for you. Got to get a hit in the first inning of the next game. That's my game for you. What's the breaking point where they quit on the series basically? If Strasburg no hits them through two, through three, through four, when do you think fans, and even like seeps into Cardinals players are like, OK, I guess this isn't happening for us? Like, I think it's four. I think if Strasburg goes through four innings and they don't have a hit, it's like full panic. Like, full, I mean, they're already probably panicking. But full, like, hope is lost. Yeah, they, it's tough. I was going to say the second time through the lineup, which is what you kind of said. They need runs on the board. You need a run on the board before the fifth inning. You need to think you have another chance to score a run. And man, I don't even know. I think I've been on before the start. When the Nats won the wild card game and they did it in magical fashion, it's like, OK. Soto Rindoner locked in. The starting pitching is studs. I was half rooting, half believed in the fall of the Dodger dynasty.  I think Flaherty's going to shove. I think he's a special dude. But I mean, they need anything from the offense.  Do you think they come out attacking early? I think you have to. I think you have to just hunt fastballs early in the account your first time through the order for that one big swing. That one big swing can change the whole momentum. And if you take you allowed Strasburg to dice you up. You need a base runner, too. I mean, would you rather, if you're a Cardinals fan, you don't want to see them swinging at three curveballs in the dirt if they could take a walk. Like, they just need traffic. They need to see a ball go over the fence. How about a home run for St. Louis? That's what I'm saying. The best way to do that is to attack Strasburg early in the count. Take that walk to run home. I'd come out swinging. I'd come out swinging. Because that homers can need a homer. Like a little base hit will feel OK, but it's not going to put any. It's not going to do anything for you. They're in a tough spot. Good for the Nats. Their pitching is pretty good. I mean, when Anibal Sanchez sets the stage for Scherzer, that's a good sign. Yeah, I mean, we could look back and say that was the end of the series, because it was Scherzer, Strasburg, Corbin on deck. That was game one. Let's go to game one of the ALCS. First, a quick word from maybe a sponsor, or maybe there's not a sponsor. All right, Jakey, let's burn game one. Now, talking baseball listeners already know that we have another podcast called Talking Yanks. That's where the burns originated from. You do every game during the regular season. It's fantastic. So you're not going to write two different burns. So these Yankee burns may have a little more Yankee bias to them because they're written for a Yankee crowd, correct? Luckily, this game had some Yankee bias, too. I'm just letting them know. But yeah, it's really good burn. I'm excited to hear it again. All right, here we go. On your mark, get set, burn! Game one of the 2019 ALCS rematch of 2017, the New York Yankees and Mass Hero Tanaka versus the Houston Astros and Zach Morris Grinke as he hopes he doesn't need to be saved by the bell from the Yankees offense. Some good defense and some bad luck has a scoreless till top four. I don't know about you. I'm feeling 22. Glaver, Torres, RBI double makes it one, nothing after four. Top six, shake dad healthy butt. Glabe got back into the Crawford Seats. Two, nothing, fight in Glaver's. Junkalo, let the rhythm take you over Junkalo. Solo shot, too deep right. Three, nothing in the seven. Bases hooked, the kid, the Venezuelan victor, Gracia's de Caracas, two RBI single for Glabe, baby. Five, nothing by the way. Tanaka was the Mass Hero this city needed. Like a criminal with a good lawyer, Tank faced the minimum. Astros through six, Yankees get religious with Geo to God going yard late. And sure, Glaver knocks in his fifth ribby of the day. Tank to Otto, to Britain, to Johnny Ells, who hands one out to Houston. Yankees wins seven, nothing final. That criminal line faces the minimum. It's great. It's there. What meal spinning? Tanaka did not no hit the Stros, like Anabaal or Scherzer through the six innings. But he did face the minimum through six. A lot of double plays helped him out. And the Astros never sent four batters to the box in one inning last night versus Tanaka. Pretty impressive. He cardinals them. He gave them the one hit treatment. One hitter. Did the Stros send four in any other inning? Or were they one, two, three, the whole? Audivino gave up the two hits but had the double play ball. Was that technically five? But yeah, Britain had one walk. Tank had one walk. That's it. Yeah, I think the Yankees definitely kind of punched the Astros in the mouth here. They had home field advantage.  And Tank comes out here and does postseason tank stuff and deals. Yeah, in the seventh inning, Jake, they sent four. No, no. In the seventh inning, they sent three to the plate. No, that's got to be, Audivino gave up two hits in the seventh. Yeah, but fly out, single, single, double play. Wait, hold on. Oh, they just word this weird on MLB game long. Yeah, four. So in the seventh inning, they sent four. So they never sent five batters to the plate in an inning, which for the Houston offense, that's pretty wild. Yeah, pretty wild. This was a must win for the Yankees with Grankey pitching game one and then Verlander Cole going 2-3. It was not. And Schmoltz said this on the broadcast and a lot of Yankees fans took offense, but it's dead on accurate. The Astros can kind of flick this off their back or whatever. We have Verlander Cole going 2-3. We could afford to lose game one. The Yankees, they couldn't afford to lose game one. This was a must win, but now it flips. Now game two is a must win for the Astros and the Yankees are kind of playing with house money. We took one on the road. Let's give it our best shot. But the Yankees needed to win this game, and they did, and they looked really good doing it. Yeah, I'm going to disagree with you on must win a little bit. I mean, the 2017 series, all the home games won, so I just think the shtick would have turned into like, all the home teams are back at it. We'll see if we could get something at Verlander and we'll shake Cole at the stadium. But no, this was the weak link in their armor right now is Grankey. Who was solid? I said I didn't think he could have one of these lines. He finishes six innings, pitched three in runs, technically a quality start. He gives up two homers. Yanks hit into some bad luck. So did Houston. There's a lot of the hardest hit balls in this game and the first three innings were caught, and two of them turned into double play balls. But that's kind of baseball, Susan. But yeah, man, the Yankees had an edge, the top three in their lineup. I think we did this last night, I think they got on eight out of 14 times. Yeah, DJ judging the labor. And that's just brutal if you're a pitcher or a reliever. I mean, you're just not going to get through them clean. And if you've got traffic on the bases in the postseason, that's kind of what it's all about.  And yeah, I mean, Yankees dominated. The Yankees had 13 hits. Houston had three. Seven runs. Tanaka, his playoff numbers are special now. They're still special, I should say. 36 innings to the tune of a 1-3-2 ERA in seven playoff starts. He's never given up more than two earned runs in a playoff start. Pretty incredible. And yeah, now you're right. I mean, it almost feels like if you're the Yankees, the Rays talked about getting verlandered in their first game. And I'm interested to see what Verlander's got today on full rest, coming off his worst playoff start ever. But if you're the Yankees, you say, hey, we got two shots at Verlander and Cole. If we split them somehow, and one of those games is at the stadium, that's kind of a fun mindset. Or if you could somehow get to Verlander today, if he's not sharp again, I mean, you're doing what the Nationals did. You just went 2-0 and now you're heading back home. And two of those home games would be started by Jose or Keady and Grinke. Yeah, they got to win. They got to win tonight, the Astros do. And they have a really good chance to do so with Verlander on the mound. Jake and I are both always very excited to watch Verlander when he's not facing the Yankees and still kind of in awe of him when he's, because when Verlander's right, it's my favorite pitcher, I think. I think when Verlander is on, like when he no hit the Blue Jays, like, and you watch those highlights, that's my, I think that's my favorite pitcher to watch. It feels like a clinic. It feels like you're at camp watching, learning how people pitch. Yeah, and we, man, they really neutralized. Springer goes 0-4. His postseason is starting to get ugly. Bregman, he has a nice walk. But then he gets doubled off first, a really nice play by Aaron Judge. Basically threw it 89 miles per hour off his back foot. So that's pretty good. And then, yeah, I mean, everyone's talking about Glaver. Glaver goes 3-5, 5 RBIs. They slid him up to the three hole for this game. And he, it worked. Plan worked. Plan worked. Yeah, I didn't realize Springer's having a rough postseason. He's got a 154 on base percentage in the six games and a 274 OPS. That's a tough, some tough stats for Springer there.  I did this on one of the end of the regular season talk in Yang's episode. If he didn't get nicked up this year, he was going to be easy in the 50s with his home run total. And he's the guy that won the World Series MVP for them. George Springer, I think Altuve, Correa, they get a lot of love. And they deserve it, so does Bregman, obviously. But Springer is just as key of a cog. He's the lead-off dude in center field. He's having a tough postseason right now. Yeah, what's Altuve? What did Altuve do yesterday? No hits? They got him. He went one for three. They were making him chase. If you're a Yankees fan, we did a very in-depth, more cocky recap, because we were in our feelings a little bit more right after the game last night. I think Altuve's the head of the snake. I know he doesn't bat lead-off. But I think if you can silence Altuve, I think you silence the whole order. So I think it's important. He got a hit. Dude, Altuve has a hit in every game this postseason. He's a monster, man. Jesus Christ, he's got a 348 batting average or 1.201 OPS in the six games. Move them up to second. Probably just going to play Jose Altuve highlight reel in my kid's crib growing up. It's another guy who I love watching play baseball. Because me copying Albert Pujol's stance didn't work in this body. Didn't work. Did not work. I can't emphasize it enough how much it didn't work. I'd slide Altuve up to the two hole if I was them. They have Brantley ahead of them. Get Altuve at bats. They had Altuve first, the first three games, and they switched it. I think they like the balance of breaking up some of their righties a little bit, because I think their righties are the danger on the team. Jordan Alvarez, obviously young and really good, but he's going to have to prove himself on the postseason stage. Brantley really solid. He did have a hit yesterday. Yeah, no, I think as of right now, there'd be a bigger fear factor for the Yankees if you saw Jose Altuve leading off.  That would almost be, I think that would be viewed as kind of a panic move in Houston. Well, Altuve was batting second in the postseason. Like, it wouldn't be strange. I don't know where they have Brantley. Sir, they had Altuve second in games one, two, and three of the DS. Yeah, it packs in on the bump today. Maybe they can use that as an excuse to slide Altuve up. I don't know. Yeah, I don't know why they slid them down. They made the change going into game four. They slid Brantley up. I think it's maybe like Brantley versus Tanaka. And then I think it was to give Brantley better pitches to hit.  But, and they want to get Brantley going. Who knows? But I would, if I was Astros, as a Yankees fan, I don't want to see, I'd like seeing Altuve third. Less at bats, just, I'd rather see him third than second. So they should probably make room second if I was doing the lineup. Springer, Brantley get on first inning today. It might be a different feeling. But Springer's 0 for the postseason, so. Yeah. No, I mean Springer, Springer is definitely the talk when they zoom into the lineup. That's who they're focused on, that he needs to do something or get out of the way. Because he's kind of holding them back right now. Tanaka was special. His pitch mix and everything was just beautiful. Houston was really struggling to line them up. 68 pitches through six innings. He gets pulled. It was a little bit of a conversation. The Yankees want to go to their bullpen. The Yankees want to go to both bullpens. But yeah, they're up 5-0. They go to Adavino, which kind of works out. And there's some logic behind that. I really like the fact that the next time Houston has to see Tanaka, they're still going to be saying, I don't know what to do against this guy, where the top of the order was coming up. If Tanaka goes back in, Springer, Brantley get a couple hits, they're saying, OK, yeah. We got Tanaka now. We figured it out.  Adavino, with all these tough Houston varieties, he can be an X-factor in the series. He comes in, and he doesn't give up a run, two hits. There's kind of a misplay by the Yankees in field. He still gets the double play ball, and he looked pretty solid. The Yankees had three double plays turned in this game, which I mean, that's pretty huge, especially when one's an outfield assist. I mean, they got out of trouble, and judge is good, man. That play was awesome. By the way, Giancarlo Stanton, who's on the Yankees, a lot of people forget this. He hit a home run. He's still really good. He is good.  Let's take a quick break, and then we will talk about game two of the ALCS. All right, only one game to preview today. Game two, Yankees versus Astros. Like I said earlier, I think this is a must win for the Astros. You've got home field advantage, and if you were to lose both games and then go down to play three in a row, Yankee Stadium, that's pretty shitty, especially with Verlander on the mound. I think all odds are on the Astros' favor here. I think Verlander is really good. He scares me. You got Paxton pitching for the Yankees. Paxton made one start against the Astros. This season, he was tipping his pitches, and they lit him up. They were all over his stuff. Hopefully, he's not tipping his pitches again. And I mean, the game is, this game, is Verlander. Verlander is this game, because the Astros bullpen isn't good. Yankees nicked him up a little bit last night. I think the Yankees are licking their chops, hoping that whenever they see that bullpen, and it's all about how good is Verlander and how long can he stay in the game, would you agree that that's kind of what dictates this game, the biggest factor at least? A little bit. I mean, obviously, the starting pitchers, and especially when it's someone as special as Justin Verlander, especially special, said those words a lot. Jim, something that I stumbled into last night when we were talking about it, and I fully believe in. And the example I used is, if you watch an NFL football game, and one of the defenses is super hyped up, the great Baltimore Ravens defenses, and they play another team who's got a solid defense, but that whole week, they're only talking about how good the Ravens defense is. That other team ends up winning, and you hear them saying, yeah, keep talking about that Ravens defense, because we're pretty good, too. The Yankees starting pitching is pretty good. Tanaka is a playoff stud, like bonafide. There's not an argument against it. James Paxton is extremely talented. He's won what? His last 11 starts? 12? I don't know if he did any blip at the end of the year. I don't think so. Yeah, he had a no decision. OK, well, either way. He's either won 12 of his last 13, and then Luis Severino is arguably the most talented guy, and he can absolutely shove and hit triple digits for as long as he can go. So yes, those Houston guys are incredible. Verlander, the Hall of Famer, one of the best pitchers of our generation. Garrett Cole just put together one of the best seasons you'll see this time period. Zach Grinke could also be a Hall of Famer. The Yankees guys are also good, and that's what it felt like Tanaka did yesterday, where it's like, oh yeah, keep talking about how good those guys are. I'll shove for six innings one hit.  And for me, it's the early runs. We did a Sharp Stats episode, and I think Houston's got some unbelievable numbers. They're like 27-0 if they have a two-run lead or something. At home, yeah. Yeah, and if they score first, they're essentially unbeatable is what the numbers say. If the Yankees get on the scoreboard first, and I don't think it's going to be a blow-up inning like the Reyes kind of did to Verlander. If anything, it's Judge Clipsum, or one of the guys pokes a solo shot. But if a couple innings go by and the Yankees have the lead, I mean, it's panic time in Houston. If it's the fourth inning, and George Springer has a second strikeout of the game, and the Yankees are up on the scoreboard, yeah. It's going to be panic o'clock. So it'll be interesting to see there's no reason to not believe in Verlander. In Houston, they will be rowdy. It is a passionate fan base, and Verlander with a couple dirty strikeouts could get that crowd going real quick. But yeah, I don't know. I think I'm expecting a good baseball game. I don't think I walk away from this, and I'm like, yeah, Verlander shoved six-one Stroes. Well, yeah, you talk about trying to jump on Verlander early. That is what the Astros have to do against passion. He struggles in the first inning, and he's going to be on the road and a history of tipping his pitches. He did face them twice this year. The first time he was tipping his pitch, got lit up. Second time he went five innings pitched, one earned run against a less-than-stellar Astros lineup. It rounded out with Tyler White, Marisnik, and Miles Straw at the back end, but it was actually White and Marisnik that got the run against Paxton. He has a lot of history, since he was with Seattle for so long. He has a lot of history against this team. A lot of them have more than 20-played appearances. Braggman has 29-played appearances with a 276-on-base percentage. Let's see, Springer has a 278-on-base percentage. It's not that great. The OPS is pretty good. And Altuve has a 429-on-base percentage, Jake, and Carlos Correa in 24-played appearances has a 458-on-base percentage with a 1.OPS. So there's some history there. Some of those numbers come from when he was tipping his pitches and they were smacking him around. Altuve got him for two home runs in that game, I believe, just jumping first pitch fastballs because he knew it was coming. Paxton also changed his pitch mix. He was more of a two-pitch guy when he was tipping, so it might be harder. But yes, it's really, both pitchers can get through the first inning clean. Then I think we settle in for kind of a fun pitcher stall. Yeah, well, the thing we have to ask to risk on that that you've been all over is, I mean, Paxton's only going to get to see each hitter twice. Houston needs Verlander to get through three times. So yeah, I mean, that's an interesting dynamic. If James Paxton runs into trouble in the fourth inning, the Yankees will pull them. They will go to their bullpen. Yeah, they got five innings out there. If Verlander's in trouble in the fourth, there's no safety net. The Yankees have five plus innings, five plus. Up to six innings, they can get out of their bullpen happily. It is not scary to go Chad for one or Chad, Kainley, Otto, Britain, Chapman and have one inning like split where two guys go 1.1, 1.2. That is not a worry. It's like, damn, we have to do this. It's kind of like, OK, let's do it. Cool. And my other notes, I think Chapman has to pitch in this as a Yankee fan. Chapman, he pitched game three versus the twins. I think I got, what, four off days. And then yesterday was off. So he's five off days in a row. We have an off day for the Yankees tomorrow. And Chapman, you don't want them to get rusty. I think no matter the score, up 10, down 10, one run game either way, Chapman has to get an inning in this game. So hopefully it's up 10. And Chapman comes in for the Yankees. But expect to see him, I would guess. Got anything else?  Let me see Verlander stats versus the Yankees. And then we'll get out of here. I got to go have some cake with my dad for his birthday. What's your favorite kind of cake and why is it carrot cake? It's not carrot cake. Carrot cake's a good cake. It just gets lost in the shuffle a little bit. And to say carrot cake's the best cake, that's pretty asinine. It's a good cake. It's my favorite cake. No, no, it's not. That's my whole expectations thing. No, carrot cake's my favorite cake. If you expected carrot cake to be the best cake, then you wouldn't think it's the best cake. If you expect carrot cake to be, it might be OK. I don't know. Let's see what they got. You're like, whoa, this shit's pretty good. When we went to Yankee Stadium and they do the dessert cart and there's every kind of cake you can imagine, I'm grabbing carrot cake. Well, yeah, you've got to end healthy.  You've had a lot of drinks. You have to have a little vegetable to wash it down. I don't know. I really do enjoy an ice cream cake, but I don't even think that counts as a cake. I think that's just ice cream. So I don't know. Does cheesecake count as cheesecake? A pie? We're getting lost. What are Verlander stats? Got a crust on it. It's a pie. Didi has really good stats against Verlander. He has a 400 on base percentage, 7 hits and 22 at bats, a double, a home run. Brett Gardner has better stats than you'd think. A 330 on base percentage in 57 plate appearances. Brett Gardner just needs to grind out at bats. Edwin and Karinassion in 43 plate appearances gets carved up by Verlander. Nothing good there. DJ has five hits and 15 at bats. That's a 333. Aaron Hicks has terrible stats. Aaron Judge has terrible stats. Gary Sanchez has terrible stats. And Glebert Torres has terrible stats. So Verlander has some fun to be had. And Verlander guy is pretty good. He's pretty good. All right. Everyone enjoy the one game. Enjoy your Sundays. Enjoy the football if you like watching football, but this is a baseball show. Have a, we will see you tomorrow I guess and the next day and the next day. Can I get stuck anymore?


So the wild style is a unique superior fire axe which is just too good for you guys to skip Today with this guide, you'll have this thing in no time at all How's it going guys? My name's DPG and if you do enjoy the video I'll leave a like really helps out and if you like what you see and want to see more be sure to subscribe So first things first, I do believe this quest only unlocks upon you complete in the story campaign I might be mistaken here, but it's when I noticed it pop up Okay, so for this quest and to start it you need to head to that ocean Avenue area within the Serling Hotel Safe point within this area right here. You can see on the screen now people across from the bar vendor is Rosa Speak with her to get this quest started Now this quest consists of you going and checking out a military stash within the metro system So that's where you have to go So it's at this point within the metro area that you need to come to Here you have to interact with this laptop and while it works its magic you have to stay alive by defeating tons of zombies Upon this stage being completed, you then progress on to ransacked again supplies This consists of you checking out the highlighted spots which will appear on your map and inspecting certain stashes Be careful of all shotgun trap soul while doing this Once the inspections are over you then have to take out this putrid commuter Once you do this he drops a key for the store. So go ahead and enter it Your next step here guys is to take out the zombie gang. So get that done Once you are done here people enter this room open its crate and the quest is done And you are rewarded this amazing superior weapon and it really is as simple as that Guys if you enjoyed the video leave me a like really helps out if you like what you're seeing one see more Be sure to subscribe and hopefully guys. I will see you on that next one


Yeah, this is all right I'm gonna switch to an SMG Showrunner, I think I'll use a pended mag and a red dot two maos. That's what it's when I like And yeah, we just we just use this we just use this I know I said everyone tells me SMG is a garbage I haven't really given a good drive Whoa this one mounts I melted him then I'm not sure about any range but at close range. Where you going?  There's got to be something they're good for That's what should always we're gonna we're gonna try and find out that oh my I mean like I'll I'll take a night shade any day I'll take a nerd your any day Whoa, it's not bad not bad I actually like it. I like it This one in the other was having this the seam all over the place this one This showing there's a lot more controls. See if that's me anywhere. Yeah, it burns through bullets The allies have your back I'll take that. Thank you.   Oh, there's a few yet I died and he got wasted. We were doing it Whenever there's a heavy Chris is by 100% Heavy ammo comes in Chris is already waiting. I'm being chased. I'm being chased. I need to reload Hey, it's just back out now Back out now You're breaking them Again chance to fight anyone with it. They lost We'll get this point because I'm a team player How it should be And then this in this game points are definitely needed. Are you coming a bit late now kid? Oh, you see he's almost caught and you want to come in and nick a point No, mate, and I got a lot of luck for that. Where was your there? Where was your there kid? Where was you there? I'm a super Zone B lost Now that my super is to do anything to anybody but yeah Just met him and run I'm dead. I love I'm dead Oh, it was a good head. I thought he murdered me from that range and so how did he do that? You're evenly matched. It ain't that bad Oh, I think that may have been a good head. No, she'll have We could have been the sunshot I think it's like a good head. No, she'll Like I'll get one kill with this Where was he?  You can't fight anyone at range But at close range like that they are beastly They are beastly I'm like each weapon should have a set Well a set perk so to speak where It it's better than any other weapon in that kind of category A little bit Scouts should be range Auto rifles all round SMGs close range Hand cannons mid-range Sidearms just I don't even know about sidearms anymore. People even use them What's the point using a sidearm that's a close range weapon? What's the point in using it? When is this some juice? I don't get the need to I've tried that so I don't I mean it just does not work It just does not work.  That took a hundred and two half off. I didn't remove his shield and that's a hunt. That's a one half the gut You captured zone. Inclusion shield. It's gonna be about two Two 20 maybe Three you're two melees and uh Four bullets left for me SMG.  I got the kill, but obviously the cis cancer's killed when you're putting a lot of damage So you lost 30 seconds and counting You captured zone me. You have advantage Don't think so mate. If you can hit to the head with this it absolutely just tears them up But if you hit body shots where they're hitting head shots, it doesn't matter what Get out of here zone a lost sit in this corner Thanks for that six weeks for my um half to recover because I'm on a warlock, you know Ah look at that at the end Yeah smg's all right All right, but uh Oh, excuse me. I'm so tired I mean like I did okay. I got about three kills with my also rifle before that probably a few more I figured it okay For an smg that is anyway Yeah Yeah, but no, I wouldn't recommend it. I would not recommend it


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