Computer generated transcript

Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.

OK. This is number six. Now, clinical section reasoning um with fish and loss. Um again, it's almost like Pokemon card collections, endless number of possibilities. Lots of ro memorization. My goal is to help you to make it into a system. And that how do you make it in the system? Is you localize, localize, localize because there are four things you can tell where the eye is going wrong by anatomy. Well, there is, those are the four questions. One is, it's the vision loss, are they one eye only or both eye? If it's both eyes, then it's gonna be something more like a stroke or something that is behind the chiasm. So behind there or something that affect the rest of the body system. Because um um whereas if it just affect one eye only, usually the problem is within the eyeball itself. But you know, when you have double vision loss, you check the visual fields and it could be a stroke, but it could also be, you know, pul edema here, you know, it could be caused by having very, very high BP as well. The second thing is, is the vision loss painful or painless. Now, um pain is a good indicator what things are going wrong as I will show you in the next slide. And then also is the pink sun onset a gradual onset. Now, eye is kind of an extension of the brain. So, you know, if you can think about it from neurology, anything that is quick, sudden onset, it's almost always vascular related. So your blood vessels going wrong, you know, either a stroke or ischemia or something. So that's sudden onset. Whereas gradual uh and sudden onset, usually when I'm talking about within minutes to hour, if it's gradual onset, let's say something that takes months to to develop that. It's another story and those are not that many conditions in the gradual onset category, the age and the biological sex of the patient, that one is more minor. Um but it does apply to some conditions. Um and it helps you to clue in very quickly. So the demographics do matter as well. So this is another questions, hopefully not everybody's asleep. I know we are running a little bit over time. Um But uh give it a try on that questions and I think we should be wrapping up very soon. Any ticker of other questions pop that in the message box. Yeah, actually this one is a little harder to tell because it's actually acute angle closure, glaucoma. That's something that you might want to become very familiar with because uh it's an often tested questions. It doesn't happen much in real life as you can see in medical school of often those conditions they test you unfrequently. It does not happen in real life. It's very rare. I mean, even in the ophthalmology department, maybe one or two cases in a week or a month or something like that. But because it's serious, it's vision damaging, they test you on it because they need to, you to know this is important to refer that urgently why this is uh acute angle closure, glaucoma. See you see it's a headache. Ok. So that might lu they you might thought that would be temporal arthritis or migraine or you know, that's ok. But it's associated with nausea, vomiting. If you have a very severe headache around the eyes and it's no associated with nausea and vomiting, you should kind of think about glaucoma because it, the pressure is building up inside the eye is so strong, it just cause you pressing on, you know, the receptors that causes you to vomit, you know, and the uh the other thing is it red right eye and there's a non reactive dilated pupil. Um These are all clues going toward acute angle closure, glaucoma. Now, if it's a regular migraine, you won't have all these eye symptoms, you know. Um maybe if the person is younger and it is a male and have a red eye, you might think, oh, it could be cluster headache you know, but you know, in this case, it's a very, it's a much older woman. Um and it's definitely not migraine in this case with the eye symptoms. Um in terms of the optic neuritis, optic neuritis, it's a much younger population. Again, it's usually in the twenties to forties in the woman. So that also make it unlikely. Now temporal arteritis will fit in terms of the demographic profile. So that's helpful. But why is that not the case? Well, usually temporal arteritis will be happening in somebody with things like scalp tenderness. Um jar claudications or even none of these symptoms might have occurred, but at least it won't cause nausea and vomiting and it won't cause non reactive dilated pupil. And there's a reason why as I go into the glaucoma sections at the end. OK. So another questions here, any people would just pop in answers in the chat box? Mm OK. So in these questions um now this is the part where demographics play a role like I said before, if you are in the twenties to 48 bracket and you will happen to be a woman. Um that fits a lot more with the optic neuritis profile. That's the classic demographics for optic neuritis, which uh if you go into ophthalmology, you know that prob that you know, could be other things could cause optic neuritis. But at your stage, usually that means multiple sclerosis. Um That's what you uh want to uh know. Um the other thing is um that the eyes are having red col decreased color sensations. So that's what they mean by red b saturation. So the red, rather than looking at like bright red, it looks like pink or dull red. Ok. That's a sign where your optic nerve is being damaged, you know, um painful because you have inflammation in the optic nerve. As the term optic neuritis imply uh you get decreased facial acuity of that has built up over days. That's optic neuritis now. But in the same vein, temporal arthritis won't fit into this uh demographics which supposed to be looking older, usually over the age of 50 cataracts won't develop over days, it will develop over months. Um acute closure, glaucoma, obvious reason. It's not because it's not causing all these very dramatic symptoms like nausea, vomiting, mid dilated pupil, that sort of things retinal detachment. Um retinal detachment actually has a very, very set sequence which I'm gonna go over later on in this presentations. So, um there's like three things that you kind of screen out for. Uh So we'll hold it on that for now. Um in terms of memorizing what causes vision loss, actually, there's not that many things that causes pain. So if they say they have painful vision loss, you know where to kind of look for. Now again, things that will cause pain are usually where the nerve endings are. So, uh and the eyes doesn't have a lot of pain receptors at the back in the retina, but it has a lot of pain receptors to protect you at the front like the cornea. So anything that require the cornea like cornea ulcer, trauma, anterior uveitis, scleritis, um an acute angle closure, glaucoma. These are guys that are gonna cause you pain and vision loss and also inflammation as well. So, optic neuritis, even though it's right at the back of the eye, the optic nerve is behind the eye. But if it's inflamed, well, it will cause pain, orbital cellulitis. Um I'm gonna have a diagram to show you again. It's caused pain too and vision loss, giant cell arteritis. Um that's the vasculitis like the blood vessels being inflamed um that are supplying the eyes uh that causes pain um mostly in the form of a headache. Um and endophthalmitis, that's rare. The one that I just go over it already. So I'm not gonna talk about it again, but it is a form of inflammation. In this case, it's bacterial infections of the eye after medical procedures usually. And if it's painless, most likely the pathology is in the posterior segment, let's say in the retina, in the optic nerve or the brain. So if it is in the case of the uh brain that will be like stroke, right? Optic neuritis. Uh This is a brief profile to allow you to uh kind of spot it, it's very classic. Uh it's usually asked in the SBA quick recognition and also it's in your third year core condition in the form of multiple sclerosis. So you probably do want to know a little bit of the key things here. So I got a picture that's what red desaturation means. See how the vision is blurred and the red doesn't look like that hot Ferrari red anymore. It's just dull. Um It comes with a few things that is very classic for any sort of optic nerve damage. So you got red, saturation R APD because it's only one eye. So you got the other eye that is not affected, that will have normal pupillary response, but the one affected will have R APD. You have reduced visual acuity but not completely, not lost. And also you could have pain on ocular movement. So when you move your eyes, it can hurt too. The thing about uh optic neuritis, you asked about the histories. Usually for these guys who have sporadic recurrence separated in space and time and is strongly related to multiple sclerosis in this classic demographics of 20 to forties, young woman. Now, um in ca in newer literature, there are cases where it doesn't necessarily have to be multiple sclerosis. But for the purpose of this exam, please think multiple sclerosis and optic neuritis orbital cellulitis and bring back that eyelid diagram again, that's the tarsal plate again, our friend. Uh It's a marker. It happens a lot in you know, if it's gonna ever happen, it's usually in the kids area and thankfully not a whole lot, not a whole lot of time. So, preorbital cellulitis before the torso plate, not serious, no pain on eye movement, no double vision, no vision loss. If it's orbital cellulitis is deep, it's here or there to the uh orbital septums, the the to the torso plate. So you got severe pain and pain with eye movement, you can have double visions, diplopia, you can have reduced visual acuity. So you see blurry visions and orbital cellulitis. It's always a medical emergency contact, the ophthalmologist soon. Ok. Now, this is the painless part. Um and you know, like I promised before acute painless vision loss. If it happens within minutes to hour, it almost always have something to do with vascular and vascular. There are a couple, there is the retinal artery occlusions. So that's the fundoscopy picture of cherry red spot that I showed you earlier. There is retinal vein occlusions. That's the flame hemorrhage that I showed you earlier before. So I'm not gonna go through that again. But essentially what that means is just the central retinal circulation is compromised, blood is not going in and the cells are starving of oxygen with the case, the central retinal artery occlusions, you treat it as a stroke because the only reason why you have CR O is because you have um embolus. So, clots that are from other parts of the body traveling up to that central retinal artery. So that's high risk on somebody with arrhythmia like atrial fibrillations or anybody with blood thinner. You know, those are problems because people on blood thinners are likely to clot. That's why we give them blood thinner to prevent them from clotting. So they're, these guys are at high risk of clotting and they're kind of a high risk group with CR O and there's, if that does ever happen, there's no treatment for it, but you need to work up as a stroke case to pre to, to, to prevent them from developing an actual stroke somewhere else that is worse than just losing vision itself. Retinal vein occlusions. That one you treat it um as if some sort of uh blood vessels problem like atherosclerosis. So you do things to reduce the cardiovascular risk, but it's uh nothing you can treat as well. The blindness happened happens. Um And when that happens, it happens like as if the curtain falls on the eye. So it's painless and it's sudden and it's a curtain just coming down on the eyes and you just can't see anymore. Anterior ischemic optic neuropathy. Well, that's a big term. What that means is that your blood vessels, so not the central retinal circulations that I just talked about. But this one is the short posterior ciliary arteries, the SPCA that's affected. Um Well, it can be in the minority case, basically GCA, that's N AO N or the non arteritic versions of it. And that's again, it's basically kinda like uh atherosclerosis, sort of like a cardiovascular problem. You need to treat the risk risk reduction. Um Yeah, sorry, Abby, thank you for hanging out for me so long. Uh I'll be wrapping up soon. Uh Yes, I will get the slides out to attendees. Please make sure you fill out the feedback though. Um The vitreous hemorrhage, it happens. So this is the picture of vitreous hemorrhage. What happens is you have a lot of blood vessels that are newly created. You see blood vessels, um you get the ones when you were born and those are stable and well formed and good. But once you have things like diabetic retinopathies and stuff like that, you get poorly and crappy made blood vessels and those crappy blood vessels will leak and they, when they break, they leak all these blood into the vitreous and blocking your site. And that's why you have vitreous hemorrhage, vitreous hemorrhage will clear out at some point. Otherwise you can do a surgery to do it. But what happened is you have just loss of vision is completely obstructed by the blood. You can't see through it. And some patients would describe it as having a red hue. So if they can see just small amount, just like lights, not like as in detail, they will see a bunch of red, a very red view. Uh the other acute painless onsets. This one takes longer because they're not vascular. One is retinal detachment. The other is red, age macular age related macular degeneration. So the other other questions, I sorry. Um Any answer, sorry, I know it's late guys, guys. OK. We got D right. OK. It is d now um why, you know why I want to tell you this? Because um you know, you hear a lot more about retinal detachment than central retinal artery occlusion, which is right because Cr Ao does not happen very often. Both Cr AO and retinal detachment share this whole curtain thing coming down. But what separates them is the descriptions happening beforehand. So with retina detachment, before they have this curtain coming down on them, they have all these little light flashes. So it's kind of like um but um when American professor explained to me, he says it's like July the fourth firework, but since we uh don't like the whole Independence Day thing, so I've used Sky Fox Day instead. So hopefully, people are not offended in Britain. Um So you've got light flashes. That's because when your fits is tugging on the retina tearing it apart. So you got this light flashes coming on and off and then you got like explosions of floaters. Floaters are basically just like protein or whatever junk that is inside your eye and it just pour right out like an explosion of it. The floaters are black, the co webs are white. So I think there's some co webs here and then after those two signs you get curtain and that's the late stage when you actually got those permanent vision loss unless you go to surgery quick enough, uh hopefully they will repair it. So with retina detachment, really, you need to know about it for your multiple choice. As in uh something that like a key giveaway is those three things. Light flashes in black BB in, in both black floaters explosion of floaters. And then after those two things, you got curtain. So light flash explosion of floaters curtain coming down retina detachment and happens in usually one eye. The other one that's important to know is wet, macular related macular degeneration. See the there is something called ems grid that's supposed to be a nice regular straight bit. So it's kind of like this, you know, the whole paper here supposed to all look like this. But for somebody with we age related macular degeneration, what happened is underneath the retina, you got all these inflammations going on, you know, um and you've got all these new blood vessels that destroying the macular and macular is the primary estate, right? That's where we get to see high, the high resolutions uh HD you know, vision, right? So when it's getting damaged, your vision starts to get distorted, not just blurry but distorted. So what's supposed to be straight like this turn into a curvy line and it looked like a black hole here. And basically, that's what it is a black hole for vision. And also you can get bruising, which is like a bunch of, you know, junk that is basically pumped out by these uh inflammations and leak blood vessels and memor force. Yeah, is just the wavy lines that you're seeing curvy, the distortion that is here and that's whole paper is supposed to be straight and nice and straight like the rest of the paper here. And that paper is called ABS OK. Onset of gradual painless vision. There is not that many actually, but they are the bread and butter for ophthalmology. So the top five is the most common cause of vision loss that is painless, that's gradual. Probably a lot of us have it is refractive error. So, nearsightedness, Proia, farsightedness, fix it with glasses, not a big problem. The second one is cataract. Third one is dry, age related macular degeneration. So the dry age related macular degeneration is pretty much the same as the wet A MDI talked about previously. The difference is the wet one happens very quick. We talk about month, weeks to months where the vision are lost. Like you can't see if you don't do anything about it. You will totally lose all visions within weeks to months, very quick progression. Whereas the dry one and also the wet related age related macular degeneration is something that you can fix with medications that involve getting a needle injected into your eyes. Now, the dry one, on the other hand, there's no drug for it, but it's a very, very slow progression. We're talking about years before any vision loss is happening. The primary open angle glaucoma, that's something I'm gonna talk about in the final sections. And then the last one is diabetic and hypertensive retinopathy, which are two separate conditions. But the reason why it's listed is because those two things often happen together in the same eye. So it's kinda hard to tell the difference between the two. What kind of appointments? Dry age, regular regeneration, I touched talk about it. I'm not gonna repeat myself. But the cataract key thing for you to know in S VA is is loss of red reflex and some people will have, some people with cataract will have myopic shift. They actually become short sighted. So they have change in glass prescriptions. But the key thing is loss of red reflex and glare from bright light. So when they see in the dark, when they see bright lights, it give them glare, it's very blurry and uncomfortable sensation and see this eye here with cataract, very advanced, the red reflex is completely gone. It's just all white. Now, most of the other conditions that will give you loss of red reflex tumor inside the eyes, which is very rare diabetic retinopathy. That's basically very quick summary of what happens. What happened is the cells are wrapping the blood vessels inside your retina got damaged. So once that damage, the blood retinal barrier is completely pooped and it happened and it causes a lot of bad things like capillary being occluded, you lose blood supply and when you lose blood supply, the retina will try to preserve itself, right. So we try to get blood toward them. What they do is they pump out a signal called vascular endothelial growth factor. And that's a key step. That's the, that's the way that retina call for help. They want to get blood supply to there. So they pump all these factors to increase blood vessel growth. Unfortunately, the blood vessels they generate are all very poorly made. They're all very crappy. And when you have crappy blood vessels, it breaks, as soon as they build up, they start breaking and when they break, they leak, leak and leak everywhere and it's horrible. It's like a plumber sitting in the kitchen that is flooded with water and you can't do anything to fix it. That's sort of what diabetic retinopathy is about. So, but the funny thing is when your retina is completely burning in hell, your pa the patients often asymptomatic, they don't see that why? That is the case because the damage often are done outside the macular, like I said, the patient, all you can see is what macular gives you, the macular is the center for HD resolutions vision. So if that area is not affected yet. You can still see pretty darn well, you might not notice the restriction but you still pretty breath. Um Well, so usually it's not until too late where things got really bad where you start having citrus hemorrhage or you start having retinal detachment because the blood vessels leak so much, it causes scar and when those scar contract, it dragged the retina away from the rest of the eyeball and you stop seeing, that's when you really notice the problem, when it's too late or when the macular is swollen up. So these leaky blood vessels can sometimes form even in the macular, even the macular cannot get the blood supplies, then they start pumping this vegf the vegf and it causes central vision problem. And those problems are similar to those problems. When you see any time when you have a macular degenerate ma macular vision problem, you get metamorphosis where the wavy lines happen. And then this is just a nice diagram. Talk about all the signs that you can see in the diabetic retinopathy. I know it's time getting late. So I'm gonna give you the answers and the A is heart exudate. So these are just proteins that are, you know, leaked out from those poorly made blood well from from broken blood vessels dot hemorrhage. See these little dot red dots here, these are just bleeding. See is venous dilation. So the ve veins get become dilated because some areas occluded, it's blocked is a traffic jam. B is Ir Ma just a fancy term for saying new blood, sorry. Just fancy terms of saying new blood vessels that are still not leaking yet. And cotton wool spots are just these like white spin. And what they happen is because you have ischemia. So you don't have enough oxygen and blood supplies to the nerve endings. So the nerve ending just swells up and give up and uh all the junks inside the white stuff you see it there. Hypertensive retinopathy is a different process of disease. What happen is your blood vessels are being damaged by all these high BP. So the BP pushes a lot of junk inside the vessel wall and causes, you know, the bus vessel walls basically become really stiff and broken and just damaged. So you got bleeding again, hemorrhage, you got caught in more spot where the blood is blood vessels being occluded. Um And the nerve ending just started to die out and become white and you got exudates. These are heart proteins that are like, you know, just leaking out and then you got copper wiring, whereas the blood vessels will become thick and eventually become occluded because there's all these junk and stuff that is stuck inside the wall itself and the classic papilledema. Whereas the BP just force the blood, the the optic disc to swells up and that's the final section for the glaucoma I promise this is the end now. Um, so the basics is this, um, your body makes, um, the ciliary body makes these aqueous, which is liquid. The reason why they make this liquid is because the cornea doesn't get blood supply, as you can see, in order to keep it clear, you have to have, you'd have to feed it with clear fluids because the cornea is still a living tissues. They just don't have blood vessels. How do they get their nutrients? They get their nutrients, the sugars and all the things they need from the aqueous. So, s body makes doing a very important job making these aqueous to nurture the cornea. So what it does once it's made, it goes through the posterior chamber, which is here, this arrow just beneath the iris and then it goes through the hole between the iris and the lens. It goes through the pupil, it flows into the anterior chamber. And once into the anterior chamber, it goes to most of the majority of them goes through a hole called trabecular mass work mass work, which is just at the angle between the cornea and the iris. And from there it goes back to the vein and then to the rest of the body, the blood circulation system. So glaucoma happens is because the top the a the body that's producing all these aqueous, the water is not drained sufficiently well by the trabecular mass work here. So you got more water than, um, than the clot can. The, the, the, the drain can, can take away. Now, problem is with the sink, it can overflow with the ice. There's no overflow, there's nowhere else to go. It just keeps flowing up and up and up and causing this pressure called in ocular pressure. So, pressure inside the eye and that eventually presses on the nerve and kills and damage the nerve and that's why you can't see very well. And that's why you get glaucoma. That's the back end story of the of, of the um disease itself. And that hopefully will a answer the learning objective there for you. Um So I just kind of said it here. What they want you to do is also to prescribe the pathway. So I list it out very helpfully the pathway. So make bicill body go through the posterior chamber, goes through the pupil, go through the anterior chamber, go to the tri master, go through a whole called can of that is not show very well here it here and then goes into the episcleral vein. And from that episcleral ve vein, which is a very small vein and uh above the, the sclera, it goes back into the rest of the body's systemic circulations. Glaucoma is a triad. Uh First it start with raise intraocular pressure and that raise on intraocular pressure, presses on the optic nerve and it kills them. And so you got the hollowing out of the optic nerve. And that makes the optic disc with a bigger cup because the cup, it's where the, that's just an empty hole. The, the the rim of the disc is where the nerves are. The inside. The pale part is the cup is the hollow part. And when the optic disc cupping, so that as normal optic nerve die, you start losing sight and you start losing the area that you can see with your eyes. So the visual field got defect and uh open angle. So the open angle is similar to what this diagram is. So you can still see the trabecular master here, but for some whatever reason, there's resistance. So you can't get liquid through that hole. So that's the problem there. Now, with the closed angle, on the other hand, um literally the the the angle is obstructed. So here it's just closed off. So that's the difference between open versus closed and closed angle. Gloma you got six set of symptoms that are very obvious. So you got sudden onset, painful red eye. That's usually just the one side of the eye. Thankfully, uh headache and nausea, vomiting, which is very distinctive, decreased visual acuity. So you see blurry visions. Why? Because your cornea is all messed up, the pressure is so strong and pushes the water into the cornea. So the cornea swells up and when it swells up, it become hazy. It be you, you see halos around the light and then also you get fixed mid dilated pupil. That's because that's what causing it in the first place. And because the intraocular pressure is so high, sometimes when you touch on that eyeball, that is very firm, you can't even press down on it. So you can try it on yourself. You can press your eyeball right now because you don't have angle closure, glaucoma, you can press down quite easily. It's actually quite, just quite soft still. But with those guys, they are so hard, it's like just you can feel it. Um the reason why you get this angle closure is because you what you call pupillary block. So whatever reason the iris just stuck to the lens and the pupil is closed off. So you see the aqueous supposed to flow through the pupil into the anterior chamber, right? But this they can't. So they just keep being made by body, keep building up gradually. And you know, over within minutes to hours, you know, it just push it, push it, push until the rest of the iris just basically stuck to the cornea and completely close off any pathway to the trabecular master. And that's why you get the angle AQ angle closure, glaucoma. OK. This is the last learning objective. Sorry to uh keep you guys for so long. This is the optic disc, a normal optic disc would like this. So all the nerve fiber endings have to converge to exit the eye through the optic nerve that is in the optic canal, right? So this is the optic nerve, uh the disc that contains the nerve on the side, on the rim of the disc. And the inside is pale because there's no optic nerve there, it's just an empty hole. So that's the cup and then there's the disc. Now normal disc should look like clearly demarcated disc. So the disc is very blurry margin, then what you have is papilledema. So you can compare that to back in earlier thing where you know, you can't even make out the border of the disc that's, you know, swelling of the disc, right? Whereas a normal optic disc, you could see the clear border, it's very clearly demarcated the cut to this ratio. There's no set definition, some say 0.5 some say 0.6 but usually it's below 0.5. OK? And when you're trying to measure for glaucoma, progress, usually always measure this as a, you know, as one of the thing that indicates possibility of glaucoma, right? You got pink and orange appearance if it's pink and orange, that means well perfused with blood, these tissues are living in the happy. If it's pale, it's white. That means the optic nerve probably might have dye in that area. You got optic neuropathy already there. So that's a good sign, the optic disc. If it's normal and healthy, you should pink and orange and uniform up neuroretinal rim so the rim should be uniform both all the way through if you start to set thinning, especially on the vertical side, like superior or the inferior end. That is a sign that, you know, some sort of optic nerve dying is dying and you could have glaucoma and this is uh the what glaucoma like a osk script will look like. Uh just give it out to you as uh fy I it's uh you don't have to know this for now. I'm not gonna go over that, but that's the end of the presentation. Thank you for sitting through this really long, 2.5 hour ordeal. Um Thank you. And uh please, if you have any comment, just uh you know, sit, put it on the feedback. Um And uh and uh yeah, and um yeah, hopefully, uh you will uh join us um because uh we have um actually a, a big ay day practice coming up after the break, the Easter break. Um So if you uh uh if you uh to follow us on our Instagram, um you know, you will get more informations about that. And um yeah, and also if you like ophthalmology, I just wrote ABM J article and I think it's about to be published next week as well. So how to get, make the most out of your ophthalmology placement? And um yeah, so thank you so much.