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Okay. Fantastic. Yeah, so I'll just give it a couple more minutes. Um just to allow other people sitting here, that's all of us already. Beef stuff. Okay then. So, good evening everyone. My name is Arthur. I'm an F Y to doctor at Watford General Hospital. Um And today we're going to be talking about ophthalmology conditions, um specifically thinking towards your clinical year examinations. So with the main focus upon multiple choice questions. So this is me, I'm an F fly to Dr West Hartford shirt teaching hospitals Trust graduated from King's College London nearly two years ago. Uh My specialist interest is in ophthalmology and I'm hoping in about a year's time to apply to ophthalmology training. Um I was the runner up in the 2021 Duke Elder National Ophthalmology Prize and today is my second to last day on my F Y to ophthalmology rotation at Watford General Hospital. Um Today's talk, it's going to be about an hour. We might run just over um quick introduction as we're doing now and then I've got 13 multiple choice questions for you and we'll discuss them in some detail. Why the correct answer is the correct answer for those M C Q s. Um And then we'll following each multichoice question, we'll talk through what's going on with the auth um a logical conditions discuss in those questions and some hints and tips for things that might come up in clinical examinations. Based on my experience, we've got plenty of time. So if you've got any questions, just pop them in the chat function for me. Uh If I'm not answering your question, if I've not seen it, then you can probably just pipe up on the microphone and I should be able to answer your question a reasonable time. So the first question, I'll let you guys read that, I'll give you probably 30 seconds a question to read it. Think what the answer is and then we'll talk through each one. So 30 seconds for you. Okay. 5, 10 more seconds. Okay. So question 1, 65 year old lady is referred by her optician with bilateral raised IOP at 25 millimeters of mercury past medical history of asthma. A diagnosis of primary open angle glaucoma is suspected. What's the most appropriate topical ocular treatment for this patient? So, Tim alone prednisoLONE, Latanoprost or brinzolamide. And the correct answer here is option three, which is Latanoprost. Um So three of these options would help with IOP that Timolol, the beta blocker, the town across the Prostaglandin analog and brings on brinzolamide, the carbonic anhydrase inhibitor prednisoLONE as you probably know is a steroid, which can be given in I drop form as an acetate. Um steroids aren't used for raised IOP steroids can actually increase intraocular pressure. So that's why that one's wrong. Um The first line for all patient's, if you're treating them with drops as well, talk through in a second is prostaglandin analog. Um Timolol option one is doubly wrong here because the patient has asthma and beta blockers. A contra indicated in asthma and brinzolamide is a second line option as a carbonic anhydrase inhibitor. So, primary open angle glaucoma, it's usually caused by raised inter ocular pressure. So, ocular hypertension which is typically idiopathic. Now, it's a bit difficult to say we'll probably get into too much detail here. Whether it's a causal relationship between the two, you can get normal tension glaucoma, but there does seem to be a strong link between higher intraocular pressure and open angle glaucoma. And if you reduce the pressures, you stop development of glaucoma or at least slow it down. So the normal range is below 21. When we're speaking of pressures, we don't usually treat until it's over 24 or you get in progressive disease though um risk factors, these are worth knowing. So elderly patient's with the family history, particularly if they've got black skin. And as we just discussed before, steroid use, particularly um topical steroids into the eye, but oral prednisoLONE at decent doses can push the pressure's up as well. Um So glaucoma is a disease. It's progressive irreversible loss of the ganglion cells of the retina at the back of the eye. Uh the ganglion cells are the first neurons going Afrin tely into the central nervous system. So the cells at the back of the eye will then transmit the data down through the optic nerve in the early stages. And this is a difficult thing with glaucoma, patient's will probably a symptomatic. They often lose some peripheral vision first, they might not notice. So they might only present late. This is why it's important to go to opticians for regularly having your pressures checked. So things like glaucoma can be picked up early. Um The right hand image here shows um this shows the kind of scattered omagh's that you can get typically the third one along on the top row. The RQ it scotoma is the first one to present in most patient's a lot of the time you'll hear about tunnel vision with these patient's, as you see in the one below it. This is obviously, this is very advanced disease. The patient will have poor vision. You don't see that in a lot of patient's unless they're known to have quite severe glaucoma and have had it for quite a long time. Um So on examination, they'll have a visual field defect if you objectively measure the visual fields. Um The obvious one that you need to know if your examinations is optic disc upping. So this left hand image, you've got a normal optic nerve on the left hand side and quite advanced glaucoma on the right hand side. So the cup is, if you look at the nerve, there's the paler circle on the inside, that should be less than 30% of the diameter of the total disc. So you can see in that right hand disc, that cup is taking up the majority of the disc. That's probably I'd say 80%. So a 0.8 cup to disc ratio, which indicates that you've lost a lot of the nerves going into the back of the eye. The cup essentially what's going on in the cup. That's an absence of nerves and the bit outside the cup, that's all the nerves dipping down into the optic nerve. So as you've got fewer nerves as the nerves have died off, there's just less of a rim around it because you've literally just got less density of nerves going through there. Um O C T which is a scan where you can have a look at the back of the eye in cross section, you'll see there's a thinning of one of the innermost layers of the eye, which is the retinal nerve fiber layer, which you've got nerves coming in towards the disc. And as you've got fewer nerves, that layer literally gets thinner. So nerve fiber layer thinning on O C T is a good one to know as well. It might be slightly beyond medical student, medical school level. So treatment of open angle glaucoma, um the guidelines have recently changed. Actually, it used to be just put people on drops like prostaglandin analog. However, that's only now considered first line. If the patient doesn't opt for laser, typically, what we'll do as you can see in this right hand image we've got over here is called a selective laser trabecular plastic. So you shine strong laser into the drainage mesh meshwork which I'll discuss in a second in the side of the eye and essentially puts big holes in it. So the pressure inside your eye is controlled by the production of Aquarius humor inside the eye and then the outflow of aqueous humor inside the eye. So this image we've got with the red arrows on it. Um You're a curious humor is produced here in the posterior chamber by the celery body. It then flows round through this cross section. We've got here through the pupil into the anterior chamber of the eye and then into the angle we've got here. So in open angle, glaucoma, we're talking about the angle between the cornea and the iris flows out of the trabecular meshwork mostly. And if we put some holes into the trabecular match work, then we get increased outflow and decreased pressure within the eye. Um So the second line options, if you don't want to do the selective laser trabeculoplasty, uh your eye drops the first line is typically prostaglandin analogs unless these are contrary indicated or, and often these aren't tolerated by the patient's. Um, often they can be quite inflammatory. So people will have uncomfortable gritty, dry eyes with prostaglandin analog, particularly over the other options. Um Some other side effects worth knowing yet long, thick eyelashes known as hypertrichosis iss, you can get hyperpigmentation of the virus and the peri orbital skin. And as we said, lots of ocular irritation, blepharitis, blepharitis describes inflammation of the eyelash base on the eyelids. Um and you often get flaky inflamed eyelids with it as well. Beta blockers such as tim Allal. As I said, these are contra indicated in asthma because they are bronchoconstricted. Um carbonic anhydrase inhibitors. So, if we go back to the question, brinzolamide, anything ending in Olumide tends to be a carbonic anhydrase inhibitor. Um These are contraindicated in sulfonamide energy. So your sulfur containing drugs, for example, sulfaSALAzine. Um they're all, even though they're working to do separate things to things like sulfaSALAzine, um they're all related structures. And if you have an allergy to sulfonamides such as Steven Johnson syndrome type for hypersensitivity, then um you may also get this to carbonic anhydrase inhibitors. Um If these things aren't working, you're still getting progressive disease, then the gold standard treatment is surgical Trabeculectomy, which we can see in this bottom image here, essentially a gap is made near the angle and you essentially create a new pathway up out through the sclera. So through the white of the eye next to the cornea and it drains into a bled between the sclera and the conjunctiva of the eye lowers the pressure a lot. Sometimes it can lower the pressure too much and you get ocular hypertension. But this is the gold standard treatment for very treatment resistant glaucoma, a couple of other types of glaucoma, one of which you probably know is acute angle closure, glaucoma. Now we talked about the angles before and we can see the angles being nice and open in these images here. If the iris presses forward against the cornea, we get closure of that angle and therefore, pressure can build up very, very quickly. This is an ophthalmological emergency. Now, the difference here between open angle, glaucoma and closed angle, glaucoma, open angle, glaucoma patient's are often a symptomatic with closed angles. The pressure goes up very quickly to sort of maybe 50 millimeters of mercury. This gives a very painful red eye or get very blurred vision. Um Typically, particularly in questions, they'll say they've got halos around lights and the pupil will become unreactive and you get often a fixed oval pupil. Um these patient's will present being quite unwell. Um they can have nausea and vomiting, they're really uncomfortable with this. I um so you give oral acetaZOLAMIDE, as I said, it's, it's an Olumide. So it's a carbonic anhydrase inhibitor and this can decrease Equus production quite significantly. Um the next thing you want to do is get some pilocarpine eye drops in. These are myotic eye drops. These will constrict the pupil. And if you imagine if you've got a dilated pupil, then your pupils kind of bunched up. So if you constrict the pupil pupil then get stretched out while the iris gets stretched out over a larger area and is therefore thinner. So this might open up the angles a little bit. When you've got the pressure down, you want to make sure this doesn't happen again because you know, this patient is susceptible to getting closed angles. So you do a bilateral yag laser, peripheral iridotomy. You can see in this lower image, there's this little hole in the iris. And essentially what that does is create an alternative pathway for the acquis to flow through near the edge of the iris. So even if the iris pushes forward, there's still a way for that fluid to get through the iris and it prevents a further episode. Um the other types of glaucoma that you might want to know about a secondary glaucomas, these are usually open angle, glaucoma as but rather than being primary where glaucoma is sort of the idiopathic problems starting on its own secondary. Glaucoma is a secondary to another disease grossly, you can fit them into two categories. So you're either getting blockage of the trabecular meshwork in the angles. So a couple of obvious ones of studio exfoliated glaucoma this is where on the lens capsule, you get sort of particularly elderly patient's, you get these fibers that build up and then flake off the lens capsule and literally physically block the trabecular meshwork. And the other one is pigmentary glaucoma patient's can have this thing called pigmentary dispersement syndrome where the iris just gives off bits of its pigment and it slowly leaks them. Or if you've had trauma to the iris, a lot of the pigment can literally just be bashed off the iris. It then floats around in the aqueous humor and eventually reaches the trabecular meshwork and blocks it up. Um The other thing that can be going on is rather than the trabecular meshwork being blocked. You've got increased pressure of the draining vessels further downstream. So if you imagine this is kind of analogous to congestive heart failure where your heart isn't able to pump the fluid away. And therefore you get a Dema in your legs because you've got the pressure build up. Well, if in your eye, you're not able to clear that fluid downstream, you get increased pressure in the eye due to backlog. So Sturge Weber syndrome, um this is where you get a large, large pink inflamed rash on your face that's essentially full of high pressure blood vessels or the other one is cavernous sinus, thrombosis. Um So the blood vessels from the eye then drain back into the cabinet sinus. If this is thrombose, then you're going to get increased pressure in all of those blood vessels and then increased pressure in the acquis and secondary glaucoma. This is a good image of acute angle closure glaucoma. So you've got this red eye, the patient will be very uncomfortable, they might be experiencing nausea and vomiting. Um With the eye of faith, you can sort of see this a slightly irregular pupil. So the iris at the bottom is ever so slightly thicker than the iris at the top. And you will often see a slightly irregular pupil is a difficult sign to pick up, but you can definitely see this pupil is dilated compared to the other pupil. So this left eye that's affected is dilated compared to the right eye. Okay. Question too. I'll give you another 30 seconds to read that and have another think about it. Okay. Um There's a couple of questions from the last one. So the first question from Augusta, can you not give beta blocker and asthma even if it's topical? No, you can't. Um You wouldn't think that much would get into your system and systemically get around the body, but it can be enough to precipitate a asthma attacks. You still don't give beta blockers in asthma at all, even if they're just topical eye drops. Um And the question from Eva is if not managed surgically, does open angle glaucoma require lifelong eye drops. So, if not managed surgically or if not managed with laser then yes, a lot of these patient's are on lifelong eye drops. So, question too. 82 year old lady presents to a and e with painless loss of vision in the left eye. On examination, she has a left rapd swollen, pale optic disc on direct ophthalmoscopy and pain across her shoulder girdle. What is the most likely diagnosis? Is it central retinal artery occlusion, central retinal vein, occlusion, non arthritic anterior ischemic optic neuropathy or artery tick, anterior ischemic optic neuropathy. And the answer here is artery tick, anterior ischemic optic neuropathy. Now, some of the keys in this question, age, pain across the shoulder girdle and the R A P D. So rapd usually indicates unless you've got a massive amount of retina that's affected, that you've got a problem with the optic nerve. So that rules out options one and two. Now, in an elderly lady presenting with painful loss of vision and pain across the shoulder girdle, this is pointing you towards giant cell arteritis. So the pain across the shoulder girdle is saying it's probably polymyalgia, rheumatica, which has a strong link to giant cell arteritis. Um given that it's giant cell arthritis, it's then arthritic anterior ischemic optic neuropathy rather than a non arthritic course, we'll talk through both those options in a second. So G C A, it's inflammation of medium to large size vessels. Typically, the temporal artery is affected. It's a disease of the elderly. It's very rare in patient's under 65 years old and it's got a strong association with polymyalgia. Rhuematica attacks have both often come on at the same time. Um This photograph on the right here shows an elderly gentleman and you can see he's got this very prominent temporal artery. Typically, if he's having an attack of G C A B, very painful to palpate along the temporal artery. And it will also be pulseless because of the inflammation in it. Ocular manifestations are common in giant cell arthritis. Most common of which is our answer here. Arthritic anterior ischemic optic neuropathy. Um and they'll present with your typical findings of G C A. So, headache, jaw claudications. So, pain on chewing, my algia, if they've got the polymyalgia, rheumatic er associated and often constitutional features including Fieger's fevers and fatigue. Um Early treatment is very important because it can spread over to the other eye as well. And if you can't save this, I if it's already too late, you want to make sure this is a good vision and the other other eye and the treatment is high dose or or prednisoLONE. Um to confirm the diagnosis, both ESR and CRP are very useful. Um E S are isn't quite as sensitive. CRP is incredibly sensitive but not as specific erased. ESR with these findings pretty much confirms giant cell arteritis. Um you can do a temporal artery biopsy but again, this you get skipped lesions in the temporal arteries. So your biopsy may be falsely negative and isn't 100% sensitive. So you do need to use a clinical diagnosis rather than using tests to confirm G C A. So, Ontario ischemic optic neuropathy, as we've said, it can be differentiated into our terrific and non artery tick causes. Um It's quite a clinical split that you make there. You don't see any real difference in signs or, or symptoms within the I aside from the pain associated with G C A and the other associated symptoms with D C A, um they'll present with an R A P D. This is very important to know because it affects the optic nerve and decreased visual acuity. Um arthritic, it's almost always G C A, there's a couple of other causes, but as a medical student or you need to know arthritic anterior ischemic optic neuropathy will be associated with G C A in any MCQ question that comes to you guys. Um They'll have a pale swollen optic disc as we can see here. So you got this big optic disc, you can't make out the cup at all. You've got these ill defined boundaries. This is a swollen optic disc. You may get some cotton wool spots and some hemorrhage is nearby. So cotton wool spots, you get sort of pale fluffiness near the disk where the nerve fiber layer has died and some retinal hemorrhages caused by the edema you might see nearby which you just little red flashes near the disc. Um non arthritic tends to be painless loss of vision. And there's a lot of debate in ophthalmology as to why it happens, but it tends to be due to vascular insufficiency to the nerve head. So it could be an embolus thrombosis near the nerve head that specifically is affecting the optic nerve. Um Often these patient's will have had small crowd id optic disks before unlikely to come up in a medical student. Question. Unfortunately, there's no effective treatment for this. So you just have to see how the patient gets on afterwards, keep your eye on them and see what the vision is at the end. So I'll give you guys another 30 seconds to read question three. So Augusta has asked what R A P D is, this is a relative afferent pupillary defect. Um Now we're going to go through RAPD a little bit more in my lecture on Thursday. Um So I don't have to share this with everyone. Now, um, Augusta, if you just pop your email in the chat, I'll be able to send you some good resources to make sure, you know what on R A P D s, it's an examination finding. It's quite important to know for a form, a logical examination. And then if you do attend my talk on Thursday at six o'clock, we'll be able to discuss it in more detail then as well. Um So even in answer to your question, why does the arthritis cause a pale swollen disc? Um So it's all to do with the inflammation that results from the ischemia, from the ischemia to the front of the disk. So, if you've got an ischemic area, if you imagine if my finger became a scheme ick, it would then start to become painful and inflamed later on. And that swelling is all to do with that. Later on, you will see it becomes more pale. So initially, it might just be swollen, it still might have some good color. Afterwards. After the swelling settle down, you'll then left with a hypertrophic disc and it's just a very pale disk. There's a leftover sign of an insufficient disk. So hopefully everyone else has had enough time to read question. 3, 82 year old male presents with reduction of visual acuity over the past 18 months and his vision is now 6, 18 fundoscopy shows macula drusen, geographic atrophy past medical history, hypertension and hypermetropia. What's the most likely diagnosis? A central retinal astra inclusion be age related macular degeneration? See, retinal detachment of the optic neuritis. Um The correct answer is to or be age related macular degeneration. Um There's a lot to point you down this way in this particular um in this particular question. Um So macular drusen, a typical of age related macular degeneration and so geographic atrophy is something you get later in age related macular degeneration. Um Another thing this question, hypermetropia Um but you are and just being moved. Uh And you wouldn't really see any of these signs in those other three options. Yeah. Now I noticed I've made a mistake on this slide, so I'll own up early on. That is the wrong picture. That's the picture from one of the previous slides of the pale swollen disc. So please ignore that. But in age related macular degeneration, again, it's another disease of the elderly as the name suggests. And you get a painless, slow onset reduction in visual acuity. Usually it's split into dry and wet A M D. The other thing that people will notice is they've got Metamor fox eah, which is uh change shape of things in your vision. So you can see on this grid here, this is an Amsler grid that people use to monitor progression of their A M D and they'll be seeing squiggly lines like this instead of straight lines as you should usually see in an Amsler grid. So the two types of A M D dry and wet A M D dry AM D, you'll get deposition of these drusen which are little white particles you'll see on fundoscopy in the macular at the back of the retina. Um So these actually sit just behind the retina on Brooks membrane, but you can see them through the retina, just little white dots all over the middle of the macular in the fungus. And then as we said, you can get geographic atrophy where you get large white patches, multiple times the size of an optic disc all over the retina in later dry A M D. Now, at any point, dry AM D can progress to wet A M D. And this means that because you get Kuroyedov neovascularization. So the thick sheet that sits just behind the retina is a highly vascularized layer called the kuroi I'd. Um And if you get in A M D, sometimes you can get some neovascularization that comes through from the kuroi I'd towards the retina and then will leak loads of a Dema into the retina. You get this swollen retina at the back, you'll get a huge increase in your metamor fop CIA and your vision will decrease quite quickly compared to the very insidious progression of dry A M D. Um Unfortunately, you can't treat dry A M D per se, but you can slow down further progression. Two things you can do smoking cessation and there's a series of vitamins you can do that came from a trial called the A R E D s trial and the vitamins and some antioxidants that you can give a vitamin C E zinc copper and then the antioxidants, lutein and zeaxanthin. These can slow down the progression but they can't reverse any changes in dry. Am. Now, if you've got wet A MD, what we can do about once every month to once every three months, depending on response you can give anti veg F injections and these will try and regress that's new blood vessel that you've got. And we'll stop the leaking of fluid into the retina and hopefully dry out the retina. So you can get improvement in vision if you've developed wet A M D. And as we said, this thing here is someone's view of an Amsler grid where they've got metamor fop CIA, we send patient's home with an Amsler grid when they've got A M D. So they can self monitor and come back to us if they notice any significant sudden changes on the Amsler grid. And we think they might be progressing from dry A MD to wet A M D. So it does question for, for you. OK. Quite a quick one, there's a picture around. So the 32 year old female patient presents to the GP diabetic patient with the following lesion has been enlarging over two months. What's the most likely diagnosis collision? Hordeolum squamous cell carcinoma or HPV Papilloma. And the answer is chalasia. So a chalazion, this is a classic Chalasia in and the thing to note with this lump is that it's not on the eyelid margin, it's displaced into the eyelid from the eyelid margin. Now, Hordeolum, many of you will have experienced this is also known as a sty and this is essentially like a spot in the eyelid margin. Uh Squamous cell carcinoma wouldn't present like this. Uh It comes to that in different ways. It's often, often looks more like a scab. You wouldn't get the nice, smooth bit of tissue over the top and an HPV Papilloma. Um As Papilloma suggests you get a fun gated growth. It's like a wart that you can get along the eyelid or on the inside of your eye. So, collision and hordeolum, uh there's a picture of each of them here. So hoarding all of them at the top and collision at the bottom. So Hordeolum or a sty is a staphylococcal infection of one of the glands of the lid margin gets inflamed. It might have a pussy head on it and they're often painful. The advice is not to pop these because that can spread the infection into the eye or further along and lead to more styes. So you treat them with a warm compress until either naturally pop themselves or ideally, it would just regress. Um There's a few types of gland in the eye that are worth knowing about. So there's a few sebaceous glands within the eyelash called Zeiss and mall probably don't need to remember the names of those, but the one sebaceous gland you probably should be aware of is the Mabo me um gland. So if you look at the bottom image here, that's it's in the tassel plate of the eyelid. So the tassel plate is what gives the eyelid its structure. It kind of keeps the eyelid nice and firm and stops it being floppy. And you've got these glands that go deep up into the tassel plate. And what happens in a collision somewhere higher up in this deep Meibomian gland, you'll get a blockage and then you get a sterile swelling from this blockage. A lipo granuloma caused by the obstructive gland. It's essentially full of sterile fluid deeper up into the eyelid in a collision because they're sterile, they're typically painless. And again, ideally, to treat this a bit of gentle massage and some warm compresses will sort out the obstruction and it will eventually drain itself and shrink down over time. Now, if it's persistent for say, six months or so, and you just can't get rid of it or if it's so big that it's pressing the eyelid down over your pupil and it's affecting your vision, they can be incised, but that obviously is a social procedure carries risks of infection, etcetera. So, ideally, it would be treated conservatively with warm compress and gentle massage. Um There's a few risk factors, diabetes. As we saw in this question, Rosacea and blepharitis as well can cause this. So five, I'll give you a few more seconds. Ok. Quite a short stem. This one. So patient's had a stroke which is affected the right optic tract, which of the following is the most likely clinical findings. So, left homonymous hemianopia and left rapd blindness of the right eye with right rapd, left homonymous hemianopia with no Rapd or left homonymous hemianopia and right Rapd. This is quite a hard question. You need to understand what's going on in the optic pathways here to get this one. And the answer is one. So left homonymous hemianopia and left Rapd. So on the next slide, I've got a picture of the optic pathways. First of all, I'll talk through what's going on in this question and why, that's the answer. So just to explain, I think I'm not sure how many of you there are who don't know what an R A P D is. But essentially, if you were to shine a light into one of my eyes. So if you can see me on the camera, if we shine right light into my left eye, both eyes will constrict. And then if we move that light over to my right eye immediately, you would expect the eyes to start to dilate just moving it over and then constrict by the sale amount. Yeah. Now if in this right eye, let's say my optic nerve was completely severed. So I've got no information going to my brain from that. I, we get constriction in this eye and then we move it over and we see both eyes dilate and that's because we've cut off the Afrin pathway in that eye. So we've got an afferent pupillary defect in the right eye. So constriction in both eyes when we shine the light in there and then we move the light over and we get dilatations because we've got the Afrin defect. Now, if you've not severed your optic nerve, but your optic nerve just isn't functioning very well, then you can say, okay, well, if I were to shine light into that, I, and then take the light away and shine the light into that. I, you get some, um, you have some constriction in both eyes. So you can only really detect this if it's relative. So you shine light in one eye and then shine light in the other and then move it back and see if one of them gives a stronger bilateral response than the other. And that's what's going on in an Rapd relative, afferent pupillary defect. Even doctors get very confused with rapd, can't remember what it is. But if you literally just break it down into what it means, then you can, what the individual letters mean, then it's quite easy to remember what's going on here. Anyway, we've digressed. So this question, these, your optic pathways. And we're saying essentially they've got a lesion a 0.4 here. So it was the right optic tract. What do we expect? So there's a few things you've got to know here, what's traveling down the optic tract. So what's going on at the optic chiasm here and what's left over at the optic tract and therefore what you will expect. So, the first thing to know is all the information from your left eye travels down the left optic nerve and all the information from your right eye travels down the right optic nerve they meet at the optic chiasm and then just over half the fibers from each side decussate. So cross over to the other side. And that means that the right side of your brain is processing your left visual field from both eyes. Now, your left visual field is projected onto the right side of your retina. As the light comes through in your eye, it gets crossed over at the lens. So you have your left eye's temporal field and your right isa nasal field, sorry your yeah field coming down through this right optic tracks, okay. I hope that makes sense. And therefore, if we cut the opposite tracks at 0.4, then we lose those things. So therefore we get from the left visual field, we lose the temporal side of the vision to the left, sorry from the left eye, we lose the temporal side of the vision. So the left field and from the right eye, we lose the nasal side. So again, the left field, so we get a left homonymous meaning it's the same on both sides, hemianopia. So loss of half your vision. So we get if you look at the two circles for number four, the red is where you can't see. So you've got your left homonymous hemianopia in the optic tracks. Now, you might ask why is there an R A P D because you've lost a bit of vision from the left hand side and a bit of vision from the right hand side. So surely there isn't an rapd. But as I said, a second ago, about 55% of the fibers crossover and only 45% don't cross over and stay on the same side. So you're losing more of the fibers from your left eye, then you are from your right eye in this lesion of your right track. So you will get a subtle rapd because of this if that makes sense. So that answers the question. So I'm gonna talk through each of the things that can come up. So position one is really simple. You cut the optic nerve, you lose vision in your right eye position to and this is an absolute classic for medical school examinations. What happens if you were to transect the optic chiasm? And that means you lose all the decorating fibers. So the fibers from both your temporal fields. So you get a bilateral bitemporal hemianopia. This is one that's really worth knowing actually came up in my fourth year off ski. Um Now position three, I've never seen this co a period exam, but it's worth knowing. So then you lose the non decorating ipsilateral fibers and the non decorating fibers are the fibers of the nasal field. So you'll lose the nasal field of the side of the optic chiasm. That's been damaged. And then your final ones are your optic radiations. So you've gone, your neurons have come down through your optic nerve reached the cars on either deck, a state ID or not, depending on where they are. And then they come down the optic tract and they all coalesce in this thing called the L G M, the lateral geniculate body and then it shoots off some radiation's back into your brain. There's two sets of radiation's. Um firstly, there's one's going through your parietal lobe, the superior ones, and there's some going through your temporal lobe, the inferior ones. So if you have a parietal lobe stroke, you'll lose half of them, which happens to be a quarter of your vision. And if you have a temporal stroke, then you lose again a different quarter. Now, the way I remember, which is, which is your brain likes to cross things over right. So your left hand is controlled by the right side of your brain, your left visual field projects to your right hemisphere of your brain. Now, what's going hit on here again, is this crossing over? So the superior fibers going through your parietal lobe are responsible for that lower quadrant of your vision. And the inferior fiber's going through your temporal lobe are responsible for the superior quadrant of the vision on that side. So therefore, this is how you get these quadrantanopia as if you get the optic radiations damaged rather than the optic tract. So positions five and six um regarding the Afrin neuro anatomy, this is everything you really need to know regarding the second nerve and then where it projects and these obviously then project to your occipital lobe. I think it's zone 17 and then we'll project forward along the brain, but we're not going into that because we're getting into the realms of neurology rather than ophthalmology. We'll go on to the next question for most people. If anyone's got any questions about that, please pop them in the chat. Okay. So question six, a 30 year old male presents to a G P complaining of bilateral red eye describes a two week history of itchy, watery eyes that are crusty in the morning. No past medical history on examination, hyperemia and excess like a cremation of his eyes, visual acuity and pupil reflexes. There's no problems with what's the most likely diagnosis is anterior uveitis, episcleritis, scleritis or conjunctive itis. Hopefully, this is a bit of an easier question for you guys because this is classic conjunct Vitis. Um So we're gonna talk through some of these other conditions in a second, um particularly the crusting in the morning. These are things that you'd expect in conjunctive itis watery eyes. Um importantly, visual acuity, not affected and pupil reflexes are okay. This means it's probably something to do with the anterior structures in the eye. And if it was a corneal problem, then you would expect him to have decreased visual acuity. That's what makes you think it's the conjunctive er the anterior uveitis, you usually get a bit of a decrease in visual acuity. So, conjunctivitis, inflammation of the conjunctiva, which is the most superficial layer over the white bit of the eye, you can see um it's usually infectious or allergic. Um your infection infectious causes, you can split into bacterial or viral. Normally, you'll get a more purulent discharge as we can see in the upper image here in bacterial and a watery discharge in viral. And that's a particularly purulent discharge you've got on that image there. That's probably chlamydia, all conjunctive itis where you get a very thick sticky discharge. Um in allergic conjunctivitis, a lot of that comes from the history. Um Again, that's a watery discharge but they'll have a history of A two P. Maybe it keeps on happening around the same time every year. And you can usually say it's allergic rather than viral conjunctivitis. So painful eyes or itchy eyes, gritty, foreign body sensation and excess discharge, either sticky or watery will point you towards um conjunctivitis and you get this diffuse hyperemia. So, diffuse red eye um treatment conservative, generally in viral, just self resolves like a viral, upper respiratory tract infection would in allergic conjunctivitis. You can give steroids if it's severe just some week, topical steroids or you can give anti histamines will usually help. And if it's bacterial, we give chloramphenicol bacterial also is generally self resolving. Chloramphenicol tends to decrease the course by only about half a day. But in practice, in the eye clinic, we will just give some chloramphenicol ointment because patient's like to have something to walk away with. When they know they've got a bacterial infection very quickly about viral conjunctivitis. It's highly contagious. So it'll usually spread within families. So it's worth asking again in family history. Anyone else struggling with their eyes at the moment, um it often spreads to the other eye as well. So if they've got bilateral conjunctive itis, think about it being viral as we said before, thin watery discharge points towards viral rather than bacterial. And the advice that we give hand hygiene is very important. Don't share towels with anyone or if they still only got it in one, I try and wash your towels regularly to stop it spreading to both of your eyes. Um I'm going to use this opportunity to talk about sclero itis and Epis Claire itis. Um So these are inflammation of inner layers compared to the conjunctiva. Conjunctiva is the most superficial layer. The sclera is the thick white fibrous layer inside that and the Epis Claire, Epis Clara is a very thin layer just lining the sclera, Epis Claire Itis quite often mistaken for conjunctivitis, but you don't typically get watering episcleritis, quite a benign condition. You get very, very red eyes and a mild pain that you can just treat with nsaids, sclero itis is a more serious condition. It's often associated with underlying connective tissue diseases. It's rarely just idiopathic. Unlike Epis Claire itis, the redness because it's a deeper layer, you kind of get this purple hue. The redness is often less prominent. But the thing about it is it's a really, really deep bad pain that you'll get with square itis as opposed to Epis Claire itis is just a sort of mild irritating pain. Um These patient's will need treatment with oral steroids. They may need immuno suppression. Scleritis is a much more serious condition than the benign Epis Claire Itis. Uh question seven here. I'll give you guys another 30 seconds. I've seen the answer there. Hopefully not. Okay. Quite a short question. This 1, 22 year old man has a painful, right? I for one day had similar symptoms a year ago. He's had episodic back pain and stiffness for four years, which is relieved by exercise and Ibuprofen his right eye is red and photophobic. What's the most likely cause of his red? I this is an absolute classical stem for this condition. And the answer for what he's got here is anterior uveitis. So the back pain as well talk through in a second. It sounds very much like he's got a spondyloarthropathy, spondyloarthropathy, probably Ank spond. Um So you've itis is inflammation of the anterior part of the you via. Now, what's the, you via the U V A is three structures that form the sort of middle layer of your eye. So if we think we're talking about anterior uveitis here, but the posterior you via, you can think of the back of your eye in three layers, you've got the retina, you've got the kuroi I'd and you've got the square, the square wraps all the way around your eye, the white bit and the middle layer there is the kuroi that we mentioned before. This highly vascularized layer coming further forward into the I we've got the intermediate you via which is your celery processes. So this is where we said that the aqueous humor is made and this is where the lens on mules attached and then coming forward to the anterior uvea, that's your iris. So, anterior uveitis is also known as iritis inflammation of the virus. Um Essentially what happens here, your iris gets inflamed and you can see immune cells floating around in your anterior chamber in the aqueous humor. There's a few different reasons you can get it. The main one that's most likely to come up in your questions is autoimmune. So either idiopathic or autoimmune, anyone can have one episode of you Vitis. But if they've had recurrent uveitis like in this stem, you're thinking autoimmune and it's got a strong association with the gene HLA B 27 which is associated with your seronegative spondyloarthropathies. Ank spond is your classic. So if they've got this back pain that improves on exercise. Um, inflammatory bowel disease is reactive arthritis and juvenile idiopathic arthritis are other options that are related to HLA B 27 gene. Um, presentation one sided, painful red eye with photophobia. The reason you get photophobia if your irises inflamed and then you're trying to move the iris. So you look at the bright light and you're Irish tries to constrict. It's like if you've got a damaged muscle and you're trying to use that muscle that's going to hurt. So light hurts because moving the iris around when it's inflamed is painful because the irises inflamed, your pupil isn't functioning very well. So when you're doing your pupil reflexes, your pupil won't constrict very well or dilate very well. You've often got a mid dilated and I don't know if you can see in this bottom image, but the pupil isn't quite round, it's a bit flattened at the top. So you might get an irregular pupil. Um a more severe disease, you get something called posterior Sinek e so these are adhesions of the iris which is inflamed and therefore, I don't have sticky and it adheres to the lens capsule behind it. And therefore, when it's stuck onto the lens capsule, then you'll get a very irregularly shaped iris. So when your iris tries to dilate or constrict, it can't because it's literally stuck on. Um And in this bottom image, if you look just at the bottom of the iris, you've literally, you've got a fluid level and you've got some puffs with some inflammatory cells sitting in the bottom because there's been so much inflammation going on inside that interior chamber. It's literally a level of puss, which is called a hypo pion um management. There's two things you want to give topical steroids, oral steroids if it's very severe. But topical steroids will usually do the job and then a cycloplegic mydriatic such as um uh cyclopentolate eye drops. So cyclops plegic stops the lens from moving. So that stops you being able to accommodate. And my dramatics, this is the opposite of a myotic eye drops, the dilate the pupil. The only reason you, well, there's two reasons you want to give these first of all to stop the lens from being able to get thicker when you accommodate and it therefore might touch the iris and get stuck. So it stops the lens coming forward and being able to touch the iris. Be pull the iris out of the way of the lens again, stopping you're getting posterior sonic e and see if you paralyze this eye open. So you paralyze the pupil nice and wide open. It therefore, isn't constricting, isn't dilating, it's just stuck dilated. So this will help with your symptoms while your eye is improving on the steroids. Um As I said, anyone can have one episode. So if you have one episode, treat it, don't investigate further if they've had a recurrence or bilateral symptoms or it's associated with IBD or back pain. May want to taste, may want to test for HLA B 27. This gene with the blood test. But again, it's not really going to change the course of your treatment is just going to be known to have recurrent uveitis and this is the cause of it. Just the next question. Another 30 seconds. Okay. So the 72 year old diabetic lady is presented to a and E with a painful red left eye and reduce visual acuity four days following uncomplicated cataract surgery on examination, she has a hyper pilot corneal Hayes, victorious capacities. Her visual acuity is perception of light only what's the most likely diagnosis and the answer is end off. That might iss so you could have been tricked into thinking this is anterior uveitis, what we've with what we've discussed about before, specially post surgery. The key here is so we're four days post cataract surgery. So this is your peak time friend of thumb itis. And we've got victorious capacities. The vitreous is in your posterior segment. So it doesn't really fit with anterior uveitis here. So end of thermite iss very serious inflammation of the inter ocular fluids typically due to infection. It's typically POSTOP or after you've had an injection into the eye. Um the most common one acute postop endophthalmitis is caused by staff, epidermal piss off the lids usually or the lashes. Um It's very aggressive, the eye looks really bad, very painful, lots of discharged from the i poor vision because you get this clouding of the cornea and the thing that differentiates it from maybe uveitis is your Vitry itis. So if you're looking at this, I hear the pupils white and that's because in this eye, the victorious is so inflamed, you just got the victory of sitting behind the pupil is just completely clouded over classical of severe end of thumb itis. Um um The other type which is caused by P Acnes bacteria. It's a lot less aggressive and it only takes, but it takes about six weeks for the patient's to present maybe painless because it's so unaggressive and they might not have the hypo P in like you can see on this eye here. Um Either way, both of the treating very seriously. So you will take a needle and get a sample of both the anterior and posterior chambers. So you want some Acquis fluid and some victorious sampling and send both those for M C N s and start them on high dose intravitreal antibiotics. For example, Vancomycin, you might start on oral antibiotics as well to give them the double hit. Um But this is something you want to treat very seriously, can be seriously site threatening this um this infection. The key from the question is that it's four days post surgery. So if you see that in your finals, think endophthalmitis unless proven otherwise. Next question 72 year old gentleman complains a sudden loss of vision in his right eye. Past medical history, hypertension and a half diabetes on examination. He's got a Pale Fund us with a classical cherry red spot. What's the most likely diagnosis? So, I'll give you guys 10 seconds to think what the answer is to that one. There's four questions left after this one will probably run over a little but hopefully not too long. And the answer here, which is given away by cherry red spot is a central retinal artery occlusion. So what's going on with the central retinal artery occlusion is essentially a stroke in the retinal vessels is what you can think of it as. But instead of the embolus going up into the brain, it's come down the thermic artery and got lodged there. Um You can get branch retinal artery occlusions if instead of stopping in the central retinal artery coming up along next to the optic nerve, your embolus is a bit smaller and it gets further along, it can stop anywhere in one of the branches. But your classical finding which you can't miss on fundoscopy is your fund issue that looks like this middle image here. Very pale fund assists with this cherry red spot. The reason for that cherry red spot is because of your fovea, your retina is thinner. So you can see the Kuroyedov shining through from behind if that makes sense. So you're Kuroi I'd is still well perfused behind. It's just the retina itself that's poorly perfused and white. Um sudden painless loss of vision is what will occur here. Now, you do need to rule out are terrific causes. For example, giant cell arthritis because they can giants arthritis can cause occlusion of vessels. Generally, you'll have pain associated because they'll have the headache, scalp tenderness, the jaw claudications um as with a stroke, cardio cardiovascular risk factors and also carotid artery stenosis are very strongly associated with this. This patient past medical history, hypertension, af diabetes, stroke waiting to happen. Basically, um, management is a difficult one. Ocular massages recommended just to try and dislodge this thrombus a little bit, it's not very effective. Um So what we tend to go for is IOP lowering treatment. So you can give oral acetaZOLAMIDE again. If you lower the IOP, you might just be able to dislodge this little clot because there's an increased pressure gradient between behind the clot where your normal blood is. And now in front of the clot where you've lowered the pressure in the eye, it's difficult. Neither of them really work. And um, thrombolysis generally isn't performed anymore the risks because you can get systemic risks. You can have a bleed, a big bleed with thrombolysis. It is quite risky and this isn't life threatening. It's just site threatening in one eye. At this point, they don't tend to recommend thrombolysis to try and break down the clot and re perfuse. Um So you just kind of have to see how they get on. Unfortunately, they'll need a referral to the stroke team because essentially a stroke in the eye and they'll need management of the underlying risk factors um because they're at risk of having a large stroke or the same again in the other eye. Um Now in central retinal, in central retinal artery occlusion, um one in five will actually retain their central vision. So sometimes there's a collateral vessel called the cilia retinal artery that comes from the Kuroi I'd and comes through and just supplies the middle portion of your vision. Um So the fever is still perfused and therefore, they still retain central vision, they just lose their peripheral vision. Um just to show you on the bottom right image, you've got a branch retinal artery occlusion. It's not as obvious as that other image, but you can just see there's a sort of whitish area. So the area that's supposed to be perfused by that one vessel is white it out and the rest of the retina still looks healthy. I'm not sure if you can see. But the lower down long arrow actually points to the clot itself. You can see the embolus in the little vessel, but it is quite difficult to see. So we talked about retinal artery occlusions and I'll talk about retinal vein occlusions. Um again, classified into branch or central and then classified again into whether there ischemic or non ischemic. Now, and retinal vein occlusions, essentially what's going on is actually the pathology is in the arteries. If you've got atherosclerosis in your arteries, this can then press down onto the lower pressure veins and occlude the vein because the veins tend to run along quite close to the arteries. If you can see in, in this diagram in the top corner, the veins and arteries crossover quite a bit and it can literally just be occluded by a very stiff artery that's sitting on top of the vein. Um scheme is worse than non ischemic. You might not be surprised to hear. Um And they'll have again, a sudden painless loss of vision. However, on examination, it will look very different. Your veins blocked, you're blocking the drainage, you therefore getting high pressure upstream of this vein. So you'll get a lot of hemorrhage into the retina. The top image we've got is a branch retinal vein occlusion. And the lower two images you've got a non ischemic and then a really bad looking ischemic insult um particularly in exams, this lower option is described as a stormy sunset. So if you ever see that in the exam question, you know, straight away, you might as well stop reading the question. The answer is going to be retinal vein occlusion. Um So management again, optimize you vascular risk factors to stop this from happening again. But there's a few complications of this that we can actually treat um so macular edema. So, like we said with or currently what we're describing before, but because of this increased pressure, you can get in your macula leaking out of fluid into the retina, which we can then treat with anti veg f intravitreal injections, which will hopefully try and reduce that and dry out the retina. And the other thing is we can get retinal neovascularization. So we've got this ischemic retina that's giving out a load of ischemic cytokines and things like that. And the retina tries to make new vessels to try and fix this. Sometimes these new vessels are very weak vessels, very prone to breakage is and you can get a large hemorrhage into the vitreous, completely obscuring your view of the retina and therefore stopping like getting through patient can't see very well. You don't want this. So if you have retinal neovascularization, then what you actually do is panretinal photo coagulation with a laser and you will just shoot aside from the macular, you spare the macula and across the whole peripheral retina, you basically just kill loads of that retina off, stops that retina being able to produce these factors and therefore stops the new blood vessels being formed. Now, you don't get this in a central retinal artery occlusion. You can get it in a branch retinal artery occlusion but not in a central retinal artery occlusion. Why? Because the whole retina is dead, it's not just a bit of ischemic, it's dead and therefore, it can't produce any of these factors. And therefore you don't get neovascularization because there's no sells left to try and produce it. You've literally just killed off the whole retina. If that makes sense. Next question is four questions left. So I'll give you guys 20 seconds to read this one just to ask, to answer ours question, dislodging the thrombus. So thrombus is going to end somewhere in this tree. Yes, but it's not gonna cause another stroke per se. But what it can do is turn a central retinal artery occlusion into a branch retinal artery occlusion, which is better if you can save some vision. If you can dislodge the thrombus and push it further down the tree into a smaller branch of the arteries, then you're just blocking a smaller amount if that makes sense. So 24 year old male patient tens a and a complaining a visual loss in his right eye after hitting his head and a night out reports seeing bright flashing lights and a curtain in his right visual field. Visual acuity is markedly reduced. He wears glasses with a strong negative prescription in both of his eyes. What's the likely diagnosis? And the answer is a retinal detachment so well done for those of you who answered in the chat. Um He's had some trauma and he is a strong myope high myope with a very big I hi. My hopes are at increased risk of retinal detachment. The way I think of it is, I don't think this is actually what's going on, but essentially you're trying to stretch a retina over an eye that's too big. So it's more likely to just pull off the inside. That's why I remember it's high. My ops rather than the hype in the tropes that are increased risk of retinal detachment. Um Ocular migraine doesn't sound like a migraine, especially because he's still got the curtain over his visual field, not killer migraine will sort itself out quite quickly post area circulation stroke unlikely. And someone this age posterior vitreous hemorrhage, you might get someone with neovascularization, but there's no history of any eye problems and acute angle closure, glaucoma unlikely to present with flashing lights and a curtain over the visual field and that would be painful. So, retinal detachment, essentially, what's happened is your retina has pulled away off the material behind the retina and it's now floating around near the vitreous we can see in this image we've got this pulled away bit of retina in focus groups. And the reason everything else is blurry is because that's further back and that's not in focus. It's like a nice picture on you SLR camera. Um They'll see a curtain defect as this retina slowly starts to pull away, starts to lose some of its blood supply from the Kuroi I'd. So the attached retina can still see nicely the unattached retina can't see very well and it's also, there's no light focusing nicely onto the retina because it's floating around too far forward rather than off the focusing plane. Um On examination, you'll see exactly this. Um Now, in older patient's might have proceeded by a posterior vitreous detachment, part of the natural aging process, your vitreous shrinks and at some point in your life will pull off your retina, it may pull the retina with it. Um As we said, your risk factors are high. My, oh, so short sighted with a large I any I trauma or head trauma that might bang it and therefore potentially knock the retina off. Family history or personal history of having had one before any recent eye surgery, particularly injections into the back of the eye that again might just provide a lip for it to come off on and diabetes increases your risk as well. Um Three types. So if you've got a tear in your retina, then your fluid can just sort of flick in the back and it's, it provides a lip that can start to pull off. So that's a red Mattea Jenness retinal detachment, tractional due to pulling forces. So that's maybe a posterior vic detachment or if you've got any other scarring in there that's shrinking and pulling on the retina and then exudative retinal detachment. This is what you're getting diabetes. You can get fluid that builds up behind the retina and then balloons the retina up off the basement membrane, your management. First of all, you take them to the victory retinal surgeons, they will remove the vitreous and usually with silicone rather than gas. Now they'll then try and tamponade basically fill up the vitreous which then will stick the retina back on. So you're literally just pumping that posterior segment full of silicon and it will tamponade the retina back on. It might not be in the perfect place, but it's better than it is when it's just left out there ballooned on its own question. 11. Give you guys 30 seconds for this one. Okay. So 55 year old man refers to ophthalmology because his pupils aren't the same size left pupil larger than the right, right. I constricts the light, but the left does not both eyes constrict and converge to light upon testing of accommodation reflex. It's noticed that the left eye remains smaller than the right for the following few minutes. What's the most appropriate next step for this patient is quite a lot going on here. A lot to interpret and you need to know about your different types of pupil problems. What we've got is a near like dissociation here. The answer is reassuring discharge and that's because this patient has an 80 tonic pupil which will talk to you through in a second. So your options, installation of cocaine eye drops, um cocaine eye drops, you can't get any more. Um But it's good for exam purposes, but you'll never use them in real life. Um, cocaine eye drops would dilate the pupils because they're sympathomimetic and what they're used for is to see if you've got a Horner syndrome. So if you're sympathetic nerves aren't working, then you can't get the no adrenaline to be released by the sympathetic nerves. So cocaine, eye drops won't work if you've got Horner's syndrome, that's not what's going on in this problem. IV Ben Pen. Um that would be if you've got Argel Robertson pupil, which is associated with tertiary syphilis, that will be useful for that. We'll talk about what that is in a second as well. Again, CT aortogram, you can get aortic changes in tertiary syphilis as well. So that might be useful if you're, if you're worried about in Argyll Robertson pupil and CT Chess might be useful for a diagnosis of, of Horner's Syndrome because you can get a pickle lung tumours that can cause a Horner's syndrome because that's where the sympathetic nervous past nearby talk about that in a second as well. So 80 tonic pupil, we've got a near light association. So a pupil that doesn't work well when light is shined upon it for the consensual or direct response, but it does accommodate, it seems a bit strange, but this is actually completely benign phenomenon. Uh it can heal sometimes on its own. Sometimes your I just stays like that. So the 80 tonic pupil as opposed to the Argel Robertson pupil, which is another near like dissociation. The 80 tonic pupil is classically dilated and basically, you've got rubbish, parasympathetic innovation. So it's not able to constrict very well, but it does constrict to accommodation because the pathway is different. Um The funny thing is with this pupil, when you accommodate, then the eye doesn't go back to its normal size very well. It stays in a bit of spasm. So that was the classic thing to pick up in this question, the eye stays smaller in the 80 tonic pupil and the I was slightly larger before that's exactly what happens in this situation. Um If you want to do more investigation, topical pilocarpine drops to both eyes. So if you imagine the dodgy pupil is bigger to start with and you put pilocarpine drops in both eyes, they are parasympathomimetic drops. So what happens is in both eyes, it will constrict. But because this eye has had poor parasympathetic, parasympathetic innovation, the nerve terminal is very, very sensitive. So therefore you put the Pilocarpine in and you'll get a massive constriction in this one eye and a normal constriction in the other. So the size of the eyes will actually swap over and the affected I will be the most constricted pupil if that makes sense. That's the idea tonic pupil. And you can see that from this diagram here. So let's have a look in dim light, the right eye. So the guy on the left of our image is bigger. And then if we move across the response to near target, so the fourth image, then you can see it constricts well, and then responds to dilute Pilocarpine. I look at it now it's now the smaller pupil rather than the larger pupils. So the patient's right eye to the eyes were looking at it on the left, they've swapped over the pupils and that's the 80 tonic pupil. Argel Robertson pupil happens in tertiary syphilis. It's known as prostitutes pupil, but I don't know if we can say that anymore. Um And as opposed to an idea, tonic pupil, it's a constricted pupil at rest rather than a dilated pupil. Um The neurology behind it's quite complicated and you don't really need to know it as a medical student. I wouldn't imagine. Um Typically it doesn't maintain the increased tone as we saw in this question. So it doesn't have the spasm after accommodation. That's only the ada tonic pupil that has that and it's naturally constricted, slightly, rather naturally dilated. Despite being naturally constricted, it still won't constrict further when you put extra light in. So that's something these two have got in common, the near light dissociation if that makes sense. Um, a little table for you for anisocoria. So if you've got pupils that aren't the same size, they can either be ones dilated or ones constrictors, you got to work out. Which side the problem is it is dilated. So, mydriatic that can be an 80 tonic pupils we've discussed or a surgical third nerve palsy. If it's a medical third nerve palsy, it's just affecting the third nerve um, motor fibers, that one of the ones under conscious control that won't affect the parasympathetic, but a surgical ones or something pressing on the nerve or something that's transected, the nerve will cause this because the fibers go along the outside of the third nerve. Um a myotic pupil, so constricted pupil at rest, as we said in our goal, Robertson pupil and the other one is a Horner's syndrome. I'll talk about third nerve palsy and Horner's syndrome again now. So third nerve palsy, what does the third nerve do? It innovates the elevator, palpably superiorize. So it lifts up the eyelid. It does most of your eye muscles apart from your lateral rectus for adduction, sorry abduction and your um and the trochlear nerve does the, oh I can't remember what it's called, but the nerve that the muscle responsible for in torsion of the eye. Therefore, if you lose the third nerve, you get a complete tosis. So the islands close and the eye is down and out. So it's pointing down and outwards because of the remaining muscles that are working. So you need to know with the third day of policy is their pupil involvement because as we said, it's either surgical or medical and that's how you differentiate between the two and is it painful because that can differentiate your causes of what's going on? Could it be an aneurysm? Which is very worrying? Um So if you've got a man, dramatic pupil is a surgical third nerve palsy, and you're worried about a PCA aneurysm here and this is your most worrying thing. So the third nerve passes just behind your circle of Willis near the posterior communicating artery. Um And this is your most common cause and most worrying cause of a third nerve palsy. If you've got normal pupil, it's likely to be a medical third nerve palsy, like hypertension or diabetes causing some neuropathy. Moving onto Horner's syndrome. You've got disrupted sympathetic pathway to the eye. So you'll have the way I remember what's going on is M A P. So may osis and hydro cious partial tosis. So the way I remember sort of what sympathetic does and what parasympathetic does. If you're out in the wilds, gathering some berries and you see a bear, you get startled and wide eyed and you need to gather in as much light as you can to make decisions to fight off. This bell run away from this bear. So your fight or flight response, you get dilated pupils and your wide eyed and you get this partial tosis because Muller's muscle is again, gives a sort of wide eyed, startled look, is responsible for about 10 to 20% of lifting your eyelids up. So most of it is done by the third nerve, consciously with elevated palpably superiorities. But Muller's muscle is a sympathetic muscle that lifts up your eyelids slightly as well. So you get a partial tosis, but it's very subtle in a unilateral Horner's syndrome. Um, you can use different drops to work out if it's a 3rd, 2nd or first order Horner's syndrome, based on which of the three nerves along the pathway is affected by the Horns Syndrome. But in the interests of that's kind of post grad, I don't think you really need to know that um for medical student Horner's syndrome, but you might need to know the causes of the different ones. So if it's the first nerve coming down from the hypothalamus down the descending sympathetic pathways to the upper thoracic spinal cord. This can be caused by a tumour compressing on it somewhere in the uh somewhere in the ponds or in the medulla or by Wallenberg syndrome, which is a classic one or lateral medullary syndrome as it's also known, which is a posterior inferior cerebellar artery stroke. That's worth knowing that syndrome and a peek. A stroke P I C A stroke causes Wallenberg Syndrome, which can cause a first degree Horner Syndrome. Um Then the next you're on along the pathway, the preganglionic neuron, a pancoast tumor cause this, this is your apical lung tumor. Your apical lung adenocarcinoma can affect this second neuron along the pathway and then your postganglionic, your own. It comes up along this thing called the carotids plexus from the superior sympathetic cervical ganglion. And so internal carotid artery dissection can affect it as it comes along there and then the nerves pass through the cabinet sinus. So if you've got cavernous sinus, thrombosis, anything like that, then this can cause a Horner's syndrome as well. It's worth knowing all of these different reasons. You can get a Horner's syndrome. Don't get too bogged down in the order of them though. Just know what your causes of Horner's Syndrome are because they can come up in questions. Okay. This is the penultimate question. Give you a little bit of time for this one. So a 55 year old male attended annual diabetic eyescreen reports, no visual symptoms, but um it's worse than diabetic control over recent months. Fundoscopy shows dots and blocked hemorrhages and gorged tortuous veins and cotton wool spots. What's the most likely diagnosis? Mild, non, mild, non proliferative diabetic retinopathy, severe, non proliferative diabetic retinopathy, central retinal vein occlusion, diabetic maculopathy or central retinal artery occlusion. And the answer here is diabetic retinopathy and this is quite severe. So, diabetic retinopathy. First of all, you split it up into pre proliferative and proliferative diabetic retinopathy. And then you can grade both of those separately, pre proliferative changes. Sometimes you can have a terrible looking fungus where you've got absolutely no really signs know really uh loss of vision. Sometimes it can have effects on your vision. So first of all, you'll get some little dot and block hemorrhages and some micro aneurysms that can be quite subtle signs to pick up on the fund. Assess. Um cotton wool spots and venus beading have seen in more advanced disease. I've got some pictures coming up in a second. So you can see these cotton wool spots there. This kind of like fluffy white change that you see on the fungus. Um they're caused by a ski mia in the retinal nerve fiber layer. Um that in more advanced disease, you start to get proliferative changes where you get neovascularization as we talked about in some other pathologies earlier on, categorized into N V D N V E N V I, which mean new vessels at the disk, new vessels elsewhere or new vessels on the iris and spain inclusions with pandora. So you laser all of the peripheral retina decrease the factors, decrease the number of living retinal cells that are producing the ischemic factors. Therefore, leading to fewer new vessels because these new vessels can lead to a vitreous hemorrhage, which is rubbish for the patient's maculopathy because at the same time as retinopathy and at the macular. So at the very middle of the vision, um you can see hard exudates, which of these sort of waxy things that I'll show you in a second and diabetic macular edema. So you get leaky vessels in diabetic retinopathy and they lead to a Diemer. A bit like you see in some other conditions and as with other conditions like wet A N D and in retinal vein occlusions, it's treated with intravitreal anti veg F injections every few months. And this will hopefully help dry up the retina and improve the vision. So these are some signs you can see we've got the, this is a little subtle cotton wool spot, a little tiny micro aneurysm. You can see there elsewhere on the retina, not in any of the boxes, but down on the right hand side, you can see some dot and block hemorrhage is just some general bits of red blobs, some good hard excavates here. These waxy looking extra dates with well defined borders and this hemorrhage that's in the box here actually looks like a flame hemorrhage based on the shape which is in the nerve fiber layer. Whereas dot and block hemorrhages are a little bit deeper in the retina, the smaller hemorrhages. Um This next image it's a really bad looking i loads of hemorrhage is in there. But what I've put this in to point out is these, the veins look very strange and this is severe venous beading which you get in more advanced non proliferative diabetic retinopathy. And the next image here, we've got some really severe neovascularization so that these sort of fan shaped blood vessels that you can see, you can see some in the bottom left. You can see loads around the disc there's also some at the very top of the image just by the edge of the image. So there's some N V E and lots of envy d this patient's at really risk of a vitreous hemorrhage and we'll need significant panretinal photo coagulation. Um This is an O C T image. I don't know if you've seen oh CT images before, but this is a cross sectional image of the back of the retina. The top images normal, we're looking through the fovea. So the top left image is a black and white image of the macula just on the very edge of the image. You can see the corner of the optic disc and one of these green lines coming through the middle is the cross section that we're looking along and up to down is depth. So the middle of the fovea is this shallow pit that's completely normal. And in the bottom image, what we can see is some diabetic macular edema. So because of the leaky vessels, you're getting these pouches of fluid, this cystoid macular edema, which is then going to cause worsened vision. And this is what we treat with the intravitreal injections. I'm gonna quickly talk about hypertensive retinopathy. It's pretty easy, just learn these four stages, stages 123 and four and a few of them are quite well highlighted here. So early stages you get silver wiring. This is if you look at the white arrow, can you sort of seeing that large vessel near there, the middle of the vessel looks a little bit white, a little bit shiny and silver. That's what silver wiring is. Next. Four, you'll get a V nipping that's best shown by the blue arrow. So as the artery comes over the vein, the vein is kind of occluded underneath the artery a bit because the artery is under such pressure. Um The next stage which we haven't got any of here, you get some dot And block hemorrhage is like we saw in the diabetic retinopathy. And then stage four, this is actually incorrect. It's not papilledema but you get blurred disc margins. Papilledema is technically only in raised intracranial pressure. But what you'll get is optic disc swelling. It should be described as rather than papilledema. Just learn those four stages because hypertensive retinopathy, it's a really easy question where you don't actually have to learn very much about it. Question 13 is coming up. I'll be really grateful if you could just follow this QR code, give you a couple of minutes to fill in the feedback. Um I'll do it as the same, same time as you guys. So I can see how long it takes you. And then we've got one more question for you where I'll talk through everything and then we're all done. But the feedback is very useful for me to know how I can improve these sessions next time. Um So anything you thought was good. Anything you thought could be improved, please do let me know in the comments. That's, that's great. Uh Fill those out would be great. Yeah, sure. I'll copy it into the chat now. I'll give you guys another 30 seconds for that. If you're not done filling out the feedback, then um, please do come back to it at the end of the session just for those who have got to get away and where it's been an hour and a half, it's been quite a slog for you guys. Um So we'll get on with the next question. So then you can get on with your evenings doing something hopefully more interesting but maybe less. Who knows? Maybe you've loved this. Okay. So question 13, have a quick look at this question. Okay. So question 13, a 26 year old female presents the urgent eye clinic with one week of severe pain and movement of her left eye over the first four days. Her vision was significantly reduced in that eye but somewhat improved over the last three days. Acute optic neuropathy is suspected which of the following signs, sings signs or symptoms is most specific for acute optic neuropathy. Number one, optic disc power to photopsia and floaters. Three reduced issue or a plate score, four redness of the eye or five, an accurate visual field defect and the answer is reduced issue or a plate score. So I just go through these answers now, optic, this pallor, you can see in optic neuropathy, as we mentioned very early on in this talk with the um anterior optic neuropathies. But you see that later on so damaged optic nerve that's then settled down to its new baseline might be pale. But this is specific for acute optic neuropathy in this question. Um Photopsia and floaters, you're more like so photopsias means flashes, flashes and floaters, you're less likely to get an acute optic neuropathy. If you do, they're not very specific. There's a lot of other things that can cause flashes and floaters and posterior victories, detachments, retinal detachments. As we've discussed, redness of the eye, you can get very severe optic neuropathy, you don't typically get a red eye. And again, it's not very specific at all for optic neuropathy, lots of different things can cause a red eye and an arcuate visual field defect. You're more likely to see this as we discussed earlier in glaucoma. So the answer is reduced, Ishihara plate score. Um Ishihara plates, I should say, are your test for color vision? So they're, you've probably seen them before circles with loads of dots in and within the dots in one color, there's a number spelled out and if you've got good color vision, they're really easy. And if you've not, you've got no idea what's going on and you can play tricks on all your color blind friends. Um So optic neuritis, typically rapid onset, you get retro bulb of pain, essentially, the nerve is behind the ice, the pain is behind the eye. And when you move the eye around, it moves the nerve behind, move the nerve around at the back of the eye and therefore, is a little bit painful. And typically pain comes first and then your vision will start to drop a bit. You'll have an R A P D because you're not getting good transmission of signals down the nerve as we discussed earlier and you'll get optic disc swelling, which this time is correctly described as politis. So, because this is inflammatory, it's inflammation of the optic disc. Um you don't always get optic disc swelling because sometimes the only bit of inflamed tissue is further back in the optic nerve and it doesn't affect the optic nerve head at the optic disc. So you can have a normal looking optic disc. But if you're clinically suspicious enough, you can still diagnose or investigate further with imaging for optic neuritis. Um There's a few causes of optic neuritis, um a few obvious ones. So M S is your classic for exam questions and for our skis. So your demyelinating optic neuritis with M S um schema coptic neuropathies as we've discussed with G C A earlier on. Um if it's technically um both with Gjoka, an arthritic and non arthritic deemed um inflammatory. So they are actually in your itis. Um you can have compressive causes. So an optic nerve glioma that I believe is seen in neurofibromatosis type one or metastasis into the globe. Somewhere compressing on the optic nerve can cause optic neuritis, an optic neuropathy and then a couple of other options are nutritional causes. So, B 12 and folate deficiency is classic. This will usually cause a bilateral rather than unilateral optic neuritis. The others are more likely to be unilateral apart from in G C A which would start unilateral and then maybe go bilateral. Um The other thing is if you've got neurotoxicity, um there's a few medications, amiodarone is a common one and exam questions can cause neurotoxicity. So can Ethan Butul and revamp acing for your patient's on TB treatment. They're probably three classics for optic neuritis. Um They call slightly less of a neurotic picture. So you don't quite get the inflammation as much, but you'll have more of the chronic picture where afterwards they'll have the pale optic nerve after the neuritis has settled down and you're just left with your damaged optic nerve long term if that makes sense. Um That's the end of the talk. Thank you for sticking around for an hour and a half. I know there's been quite a lot going on. Um Any questions at all, please do ask that question from our painful eye movements referred to as a Pharma plegia. So a farm, a pleasure plegia refers to poor city of movements. So a Pharma plegia um means reduced eye movements rather than painful, eye movements, painful eye movements. I'm not sure if I know a word for painful eye movements, painful. I is um op Talaja. Um, but I don't know if there's a specific word for pain on movement per se. I'll speak to the guys to see if I can get the slides sent over to you. Um That is absolutely not a problem. Um Would you be right to put the two are co back up and yeah, the slides and recorded should be available online on the medal account. It's kind of thanks. Yeah. Um Once again, I just put the feedback form in the chat and for those that I couldn't scan the QR code. But thank you very much. That was really, really informative talks. Thank you so much. You are all welcome. I'll hang around for a couple more minutes now if you guys have got any more questions, but if there's nothing in a couple of minutes, then enjoy your evenings, everyone. Um, and back on Thursday, same time. Um, so anyone who wants to attend another ophthalmology to talk, we're doing history taking an examination. I've got some very thorough slides for you all on that, that you're more than welcome to join and see if I've got any more pearls of wisdom that might help you with your examination's over the coming years. All right, I'm gonna shoot off. I think, I think that's all the questions I'll see you on Thursday. You're absolutely welcome. See you later.