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They love teaching, they love having students around. Um So if anyone's interested do approach them. Uh And I will give you a bit of a whistle stop tour of ophthalmology. I'm trying to include uh fairly high yield snippets that are written down on the um screens about what's likely to you asked in your after in your exams. It's, it's fairly ophthalmology as a topic is fairly low yield anyway, it's probably only about 5% or so. Um But even before I start, if I forget, let me just direct you to this um this page in the Oxford handbook, which is at the end of the Rheumatology uh section which is ocular signs of systemic disease that will probably uh include a good 40% of the questions you'll get asked, which are some variation of someone comes in with an inflammatory disorder. They've got a red eye is the most likely answer episcleritis or uveitis or something, but give that a read. Um But otherwise I will go through all the rest of the stuff that hopefully has personal points in it. Um I am happy enough if you want to shout out along the way we'll see how that goes. If I find it's throwing off my stride, we'll save them questions to the end. But um do give me a shout if you need to. Uh So can I just confirm everyone can see the slides moving again? Yeah. Yeah, it's perfect. Right. Hospital. That's a good sign. Good. So sixish slides and then we'll get through them. So start, I'm separating ophthalmology into the discipline. So, neuro-ophthalmology, most of it will um will fit around this diagram. And if no one has seen it before, then just Google visual fields pathway, then this is one of the best diagrams that help me understand what's going on. It. Color codes the field of the field of vision that they are seeing in front of them and it color codes the area that it corresponds to that the image will land on the retina. So as you can see just taken in the left eye, left upper quadrant is red and this corresponds to the light from the left, upper quadrant will fall onto your retina in the lower nasal quadrant. So um this is because light, if you draw a single uh a single beam from anywhere that is in your field of view, it passes through the middle, the dead middle of your eye, which is a circular unit and it will then go past it. So once it's passed, once that beam of light is passed through the middle of your circular eye, it's then everything from that plane onwards is gonna be the opposite direction. So if you don't understand that at the moment, that's fine. Just look at this image and try and understand this in your mind. And we all know that the nasal fibers which correspond to the temporal field, they decussate where they cross over in the optic chiasm and then go to the contralateral side. And if you follow uh the colors in this diagram, you can see that the um you can see that the temporal lobe will carry the inferior fibers. And you can see that the um the parietal lobe will carry the superior fibers. And it's when you have uh isolated temporal or parietal lobe uh defects, you have the quadranopia. And this is another helpful diagram. If you use these both together and you just have a little look around it play around and scribble some things down, you will understand it. So rather than me explaining what all the conditions are that cause these, if you understand um these two diagrams, how they work together and how the lesions work together, you're basically one. and I would just say the um the main field defect that you will get is a um bitemporal hemianopia. And that will be because of a um likely a pituitary lesion because it's compressing on the optic chiasm. It's compressing both of the nasal fibers which correspond to the temporal field. And so the person can only see the nasal or inner parts of both eyes. Um and largely, if someone has got a visual field defect, that's totally blind in one eye, then that has to be something anterior to the optic chiasm. So a total injury of the optic nerve such as a demyelinating lesion or a stroke of the nerve itself from the position of the optic chiasm to the eye. Uh and if anything has a hemi field defect, so just the um uh temporal left and nasal right. So just a left or right field defect, that is likely going to be a stroke or a vascular event of the of the optic tract before it gets to this genicular nucleus and splits into the temporal on parietal fibers. Uh So I'd encourage you both to use both of these diagrams, especially the one on the left, which I found really helpful to understand how this works. Uh the pupillary light reflex, this is important as well. Follow the image on the bottom. You shine a light in the uh the left eye. Imagine the patient is looking over to the left hand side of the screen, you shine a light in the left eye, uh it travels through the optic tract. So that's cranial nerve two. So this is in on two, out on three, it goes to the pretectal nuclei, it goes to the er and ves file and then from the pretectal, it has fibers to the ipsilateral and contralateral nuclei and then it's going on the third nerve to the ciliary ganglia. And this will cause constriction of both pupils. This is the direct from the eye you're shining it into and the consensual reflex in the other eye, you will have heard of an rapd. This is relevant relative, afferent pupillary defect. That's when you're shining the light in a, uh, one eye. If you shine it into the damaged eye, it may look like it's ok because it will constrict to some degree, you will switch it swiftly to the good eye and it will constrict markedly and fast and then you shine it quickly back into the bad eye and it will, the first movement is not a constriction, it's almost a little bit of a dilation and then a bit of a constriction. So it still constricts but not as markedly. And that's because the light following the optic tract going, the signals going down the optic tract that, that optic nerve, the cranial nerve two that's been damaged through some sort of neurological or uh insult or neuropathy. And that is a slow um slow signal traveling down to these other nuclear that cause constriction. So it's quick when you shine it in the good eye and then you go back to the bad eye, it gets there finally and causes a constriction, but much slower because the in on two bit has been damaged. Uh So again, when there's a relative afferent pupillary defect in that eye. It's that eye cranial nerve two, almost certainly. Well, definitely after the optic chiasm that's been damaged. Um, and here we've got the nervous supply to the iris. Um, it is on the sympathetic and parasympathetic fibers you'll know from many years ago. Sympathetic is your fight reflex. Your eyes will dilate in order to see as much light and stimuli that it can. And then the parasympathetic fibers cause a constriction of your eyes. And this will become relevant to third nerve and whatnot disorders that we'll discuss later. But if we take this, if we just take this image there on the left, the sympathetic fibers travel along the sympathetic chain. Um and this goes from, it leaves the, the brain uh and it goes down, it goes down the brainstem, not very far just to the initial thoracic ganglia, uh thoracic uh nerve roots, it leaves and then it travels back up uh the the sympathetic trunk uh just next to the nerve next to the spine and then it travels along the vessel and finally reaches the eye. That's why when you have a damage to the sympathetic fibers. So you've got a damage of the fibers that would widen your eye. So you've got unopposed action of the parasympathetic fibers. So you have a constriction of the eye. Uh you are looking for a lesion anywhere along the sympathetic pathway. And that's why we know that a pancreas tumor. Um even as far as down here at the apex of the lung can be constricting on your sympathetic fibers and cause the syndrome. And what that is is that is that is Horners. So we'll have heard of Horners, it's meiosis. So constricted people because you've got, you've got a blockage of the sympathetic fibers that are giving you a flight response that are giving your dilated eye. So you've got unopposed uh effects of the other way around. So you have constricted pupils, you've got ptosis again. Uh And you have anhydrosis, which is also due to your um uh the, the sympathetic sweating reflux. Uh you have a ptosis because the uh synthetic fibers uh innovate the levator muscle and that is uh that will lose its action and the eye will droop. Uh So that's the distinction uh here and we'll go on to a lesion of the third nerve uh in a, in a short while I won't draw on this too much. Holmes. A these peoples are confusing and I'm a big fan of um of pneumonics. I can't think of one to help you with these. So just read and write a couple of notes like this on Holmes Ad and Argy Robertson people. So Holmes Ad will be unilateral mostly and is mostly postviral. Uh It may, questions to them may say it's preceded by a viral illness or a sore throat or uh uh upper infection two weeks ago and they notice the eye becoming different. Uh it's usually unilateral. Uh it has no light response and is very slow if and may be absent to accommodation. And remember, accommodation is looking at a um a image close to you. This is why it's called tonic pupil because it just doesn't usually move. Um And there's Holmes syndrome, which is usually a young woman, a tonic pupil and an absent knee uh reflex or ankle jerk and can be associated with low BP. And that may be one of these um higher grade questions they may ask you, Argy Robinson is the other one. This is most often associated with neurosyphilis, sometimes diabetic nerve damage. But syphilis is may be the main question ST for this. So rather than on a homes a where you've got a large pupil, it's dilated and fixed. This one is small and not reactive to light as well. The difference is that this is reactive to accommodation. So you follow an object in and the people will constrict to that. There is an old age. If you get it to neurosyphilis, traditionally, these would be um uh sex workers would get syphilis and they are very accommodating to your wishes. And that would be why uh the the old story may you may have heard some people say that it accommodates for that reason. Uh We're looking at um eye movements and this is just some terminology. So if you look at these eyes, the light reflex in the middle of the pupil is called the Hirschberg reflex. You can use this to see if someone's eye is misaligned. You can see on the top there, there's an esotropia. So eso is inside and you can see that the left eye there or the eye on your right hand side is turned in because the light reflex is nearer the temporal side of the iris. And as for the other movements, you can see how the reflex changes. And this is just how by shining a light in the middle of someone's eye. If they've got double vision, you can already take a really good guess at what's wrong with them. So Eso is turning in Xo is turning out hypo is the eye going up, hypo is the eye going down and a tropia is when it's there always and Aphia is there when it is, when it's there occasionally. So the main things of eye movements and palsies you'll need to know is a third nerve palsy here. If I can convince you that this lady has a left eye, third nerve palsy. If you look in the middle of a nine gaze image, the eye is ever so slightly down because you can see this light reflex is at the top of her pupil and is just um brushing the top bit of her iris. And as she looks around, she doesn't have as wide a range of uh looking. Um So you can see on her looking outwards, abduction is full. But as she looks in the other areas, there's not as much uh movement and especially this is most marked when you look at the top image, she, she's looking upwards, but that, that eye is basically not looking up at all. And this is because of the third nerve, you've got your six muscles that I've um that are in that diagram uh on the top, right, third nerve controls them all apart from the lateral rectus, which is 1/6 nerve and the superior oblique, which is the fourth nerve, everything else is third nerve. So if you have a third nerve, palsy, you've got a unopposed action of the muscle which turns the eye out and a muscle which turns the eye down. This is why there's a classic down and out um uh appearance and this may be part of the questions stan 1/4 nerve palsy uh is a bit more tricky to see 1/4 nerve. It the superior oblique um which is um which is far better seen when the eye is looking uh inside. So nasally and downwards, that's how you isolate its movements, all of those on the H test and the logo at the top. This is how you isolate each of those muscles. That's the whole point of the HS. So this gentleman, he has a um he has a right eye. So he ii don't think you can see my cursor. He has a right eye, fourth nerve palsy. So if you're looking in the middle, you can see that it's got um, one of the muscles. So the superior oblique, which brings the muscle down is not working. So you've got unopposed action of the muscle, which brings it up. So you can see his right eye is higher than the left eye. And he's got a very slight slight hip tilt away from that eye. So to the other eye, and this is to accommodate for the double vision. So 1/4 mo palsy is usually after trauma and they'll have an abnormal head tilt to the other side. So to the opposite side to where the lesion is and a sick nerve palsy if you can see here. Um And I've surrounded it, you've got an abduction deficit. So in the middle, it may not be very obvious, but they may have an eye that's going inwards a little bit because you've got unopposed action of the, of um the muscle pulling the eye in and when they look outwards, they can't do it far. Um So incidental. So first of the F BS, I'll just get you to think about it. You can write the uh answer in the chat if you would like. But there's an incidental finding uh of an aneurysm in the posterior communicating artery on CT angiogram of a patient. If this progressed to compress an adjacent structure. What eye position uh would you find? So there's options of down and out, out, up and out and down and in and I'll get you to think about that for a moment. All right. In the meantime, we've just got a question asking what are some causes of a third nerve palsy. So, uh I this will, it will stem, it will come on from this one. So, um I will. So for the for the answer here. So down and out the main thing that we're worried about in the third nerve palsy. Basically, all of these palsies can be microvascular. Um and that is that it's not an overt acute stroke, but it's just microvascular damage in someone that can have diabetes, hypertension, high cholesterol and other risk factors. Any of these lesions can be from a stroke uh to anywhere along the optic nerve path, anywhere along the cranial nerve pathway or for the um or to the nucleus and the brainstem. But this one is the neurosurgical emergency that you have to be aware of is an aneurysm in the posterior communicating artery and this can compress the third nerve along its tract. Um Anything else in the head, uh head injury can cause these um the third nerve is going, we will come across the um cavernous sinus in a moment as well. But it the main thing for you guys uh for third nerve causes as with most things, stroke, microvascular trauma. But what you need to know for the question stem is the um is this the um uh aneurysm of a posterior communicating artery? Uh This is another uh syndrome, this is of the sick nerve. So, on the right hand side, you see the root of the sick nerve, uh coming from the brainstem, it passes over the petrous bone and uh an infection of the inner inner ear and um spreading uh osteomyelitis and infection of the petrous bone can cause a sick nerve palsy. And the patient may present with hearing loss, systemically, unwell fever may be red, maybe um painful ear. And so that is what this syndrome is. If you get that in the questions stem as well. This again is the main, the main take homes for the causes of these nerves for you guys at your stage. So third nerve be concerned about an aneurysm, fourth nerve. It is the longest course and it's of any nerve in the head. So it's, it can be congenital, but it's most likely to be injured in a trauma. If you're going to get a cranial nerve pathology and trauma, it's likely the fourth nerve and the sick nerve. It's usually what's called a false localizing sign because if there's a high intracranial pressure, um this is one of the first nerves to get knocked out as a result of that. So if someone presents with a sick nerve palsy and other head, uh you know, neurological symptoms. You'd be concerned of a tumor or idiopathic intracranial hypertension. The cavernous sinus here it shows, um, some of the nerves which pass through it. So, you've got, you've got the artery, you've got also cranial ner five, you've got cranial 46 and three. So, a cavernous sinus thrombosis or any cavernous sinus pathology can knock out any one of these nerves. So, this is another differential of your causes of a third nerve palsy is a cavernous venous sinus thrombosis. But you'd expect that you probably have other um uh other cranial nerve pathology as well or maybe a completely fixed eye or you might have a, a swollen disc as well and more systemically unwell. So eyelids nothing too much more profound. Apart from on the right hand side, an entropium is when it turns in and tropium is when it turns out. So this question is 42 year old man presents with the history of episodic diplopia. So, episodic double vision which is not present today on review, his family member note that this eyelid occasionally looks very droopy. There's normal examination today. What is a single best investigation that should be performed here? So I'm not labeled them ABCD, but um to have a little think about that. So the answer here is anti acetylcholine receptor antibody. Now, the condition here with transient and episodic and possibly not constant diplopia or ptosis is myasthenia gravis and a test for this would be to, this is why we get them to look up and hold it for a minute or so. And then the eye, if they have it, the eyelid fatigues with the use of the neurotransmitter and the eyelids become more droopy and to. So that would be the answer here. This is found in 90% of people with myasthenia gravis calcium channel is in Lamba Eaton. So that's incorrect. Aquaporin is for neuromyelitis optica, which will come on to and is a form of it. A differential of swollen discs. And um it may be the other antibody for myasthenia is anti muk and this is present in a percentage of people with mg. But when they don't have acetylcholine receptor. So for the sclera and conjunctiva, episcleritis is something which arises in a in a question, a fair bit. People have a mild uh irritation, they localized redness, it's not red everywhere. Um Usually you treat it with lubricant eye drops and it goes away. Sometimes they may need some steroid eye drops and this is associated with uh autoimmune conditions such as rheumatoid arthritis, Crohn's and ulcerative colitis. Um Scleritis is a diffuse very red eye, almost violaceous. It may be described as because it almost looks a bit purple. The pain is extraordinary, pressing on the eye is painful. Uh and yeah, it may have a blue tinge if it's thinning the sclera and it becomes um uh nec necrotizing. This is treated with oral anti inflammatories. And this is associated again with rheumatoid arthritis less so with Crohn's and ulcerative colitis, but it still is associated with them. But your question stem is mainly likely to give you a history of rheumatoid arthritis or systemic vasculitis, including granulomatosis, polyangiitis. So the sea anchor vasculitis. Now, conjunctivitis can be bilateral, it can be unilateral, it can be simple bacteria. The most common organism is staph ais um and this is treated with chlorin fenicol. Like most things with ophthalmology to be fair. Chinos does everything um viral, uh likely to be bilateral is likely to be one eye, then a sequential uh to bilateral. So one eye symptoms and then within a couple of days, the other symptom is watery, a little bit of white discharge sometimes and usually preceded by a viral illness. And the question is done allergic if they are associated with atopic disease such as eczema asthma hay fever and they are occurring in a spring or summer month and the eyes are red and mildly irritated. They are likely to be allergic and neonatal. We are very concerned about the first two days of life having bad conjunctivitis because it could be gonococcal and this can cause corneal melt and um terrible systemic illness to the baby and blinding condition if not treated. Um if it's associated with a systemic disease or increasingly now, chemotherapy and other cancer treatments are causing conjunctivitis. They mostly just cause a diffuse red, irritated form of it. So another question for you. A 21 year old turns red watery eyes. There's some mild white discharge in the mornings, progressively worsening over the last three days on examination. Submandibular lymph node is palpable. What's the most likely diagnosis here? And have a think about that. And again, if there's any questions, um uh manage to let me know ii appreciate this. I appreciate this is quite, um, quite fast, but it's a, it's a big topic for a small time and a small amount of questions. But um if you are jotting down any of the points I'm saying, then hopefully there are the things that we'll repeat in the exam. Um Good. So the answer to this is viral conjunctivitis. So if a lymph node is present uh on examination and it's mild uh watery eyes, especially if it's bilateral, it's likely to be viral. Um Bacterial will be perent chlamydial will be unilateral and they'll have a lymph node but not usually submandibular submental. They will have a large preauricular either chlamydia or gonorrhea. Uh uh conjunctivitis will have a preauricular node on the same side. And at your stage, they will certainly give some questions to them of um sti recently and uveitis is going to be quite painful, very rare, photophobic. Another question stem two day old baby on the postnatal ward develops uh bilateral perent discharge, needing wiping, frequently, both eyes are red. What's the most important step in the management here have a little think, have a little think of what diagnosis do you think it is and what's the most important thing you should do? So the answer here is cefotaxime uh intramuscularly. So the diagnosis here until proven otherwise, a bilateral terrible perent discharging conjunctivitis with red eyes in a baby is gonococcal conjunctivitis unless proven otherwise. So, cefotaxime iron for the overall health of the baby cefuroxime. Um and then going from the top chlorophenol drops, that's what you'd use for normal bacterial conjunctivitis. Not in this question, stan you treat it as if it's severe. Um and the most, the more dangerous organism, cephuroxime eye drops is correct, but it's not the most important step. Sometimes the questions, try and trick you like this. Um You would definitely give it at the same time but for safety for overall systemic health, the eye and treatment and assess for congenital nasolacrimal duct obstruction. This is a common cause of um gunky eyes in Children, but Children don't start crying until two weeks of age. So that's incorrect at this time. Reactive arthritis is a good little um uh combination of symptoms which may well come up and it can, it's usually associated with uh um a recent uh dodgy Chinese or dodgy indian takeaway food in the questions done. And also uh chlamydia if they've got, if they've got a urethral discharge, uh it's usually associated with HLA B 27 and for the eyes at your stage. I think that's the only one that you need to know of. There are some others for different conditions, but I don't remember them, the undergrad level. Um I don't remember them coming up at undergrad level. Conjunctivitis, urethritis. So dysuria discharge, um and arthritis. So random. The questions then may say, uh, they've got a knee which uh, flares up and comes swollen and red occasionally as well. So we've, we're 40 slides left. Um And that is in the SBA. So it's not quite true, but we're, we're going ok at the moment. So, cornea, as you can see here, there is a beautiful cornea transplant. Um Part of ophthalmology, cornea is a whole specialty apart from doing laser refractive surgery. If someone's got terrible cornea, you chop it out and put a new one on and uh some really nice surgery that you can do just as an aside. Um So what are these two things called on the left there? You've got a level of blood in the antennary chamber. This is a um hyphema and this can be associated with uh trauma or um severe proliferative diabetes or ischemic eye um diseases. On the right hand side, you have a hypopen, that's a level level of pus and that will be seen in bacterial or fungal infections of the eye and also in a sterile inflammation of the eye. Severe uveitis can also cause a hypopen. And again, going back here, reactive arthritis or juvenile idiopathic arthritis, they may give you a question to them with a child. They have a hypopyon, they've got a bit worse vision and they've got these other symptoms and this will be pointing you in this direction, uh bacterial keratitis. So usually associated with contact lens wear, um when people sleep in them, shower in them or swimming them. Um and pseudomonas is a bug. Uh that's more associated with a contact lens if the pain is extraordinary. And especially if the patient has been treated for some time and it's not going, it's acanthamoeba, which is a um an organism that again is fairly pathognomic for contact lens, overuse and swimming in contaminated water, incredibly rare. But if someone's not got a contact lens and maybe they get a damage to the eye, like they scratch it with a plant and it doesn't heal and they get an ulcer, it's going to be staph aureus, but usually think bacterial ulcer, think contact lens, think pseudomonas. And if it's um severe pain, say acanthamoeba and this just brings me onto on the side, there are three things in medicine. There's a couple more but like three main things that cause masses of pain out of proportion for any of these systems. So, one is ischemic bowel. Um So ischemic enterocolitis, one of them is necrotizing fasciitis and one of them is a can amoeba keratitis. So just as an aside for the rest of your exams pain out of proportion of blood tests or examination findings is likely to be one of these things. HSV herpes simplex virus, keratitis. Um You see what is going to be sold as a dendritic ulcer and usually not a contact lens wearer and usually has a history of genital herpes or cold sores and may have had a recent flare. Um You treat this um with acyclovir and I don't think I realized that um I had the dose up there. So hopefully you didn't read it. Um This first SB is um patient turns to the red eye watering for five days has recently had a flare of cold sores from what I've just discussed. It's no surprise that the answer here is uh herpes simplex. Um varicella zoster would be associated with shingles or um chickenpox and something you need to be aware of is if someone has a Hutchinson sign, which is VZV lesion on the tip of the nose or in the ear canal, that can be a sign of orbital involvement. So they need referral to an ophthalmologist. CMV does not cause this kind of keratitis adenovirus. Doesn't either other question. Patient attends midway through chemotherapy with a red eye water in for five days recently, had a flare of cold sores has previously been diagnosed with herpes simplex keratitis. You can start on acyclovir, what's the dose? And it's either 400 or 800 mg. It's either twice a day or five times a day, it's either 10 or seven days and this is just to incorporate some other knowledge that you need throughout your exam. Bear in mind this patient is immunocompromised. So the doses are different. And remember this for your um psa if you've not done it already, the prescribing exam and just all throughout your um exams, because the 400 M GS is usually a cutaneous dose or a prophylactic dose. We need to treat with 800 M GS, but twice a day is not the dose we use for the eyes. Five times a day is what we use for uh for acute infection. If immunocompetent, it's seven days and if immunocompromised, it is 10 days. So bear in mind the question stem of an immunocompromised patient, they likely need a longer course um than whatever you're thinking of as a basic course. Um Iris. So only one real snippet here, there's an elderly gentleman. Uh there's a gloved finger and tamsulosin. I, when I was looking at these slides, I can't remember if this appears in undergraduate exams, but it's a useful little tip to know if someone is on tamsulosin or doxazosin. So an alpha blocker, the risk in the operation of a cataract operation is intraoperative floppy iris syndrome or a poorly dilating iris. We don't really know why this is. But if anyone has had it, even if they are not currently on it, they, the Iris doesn't um uh dilate as well and the iris can come into your wounds and be uh, hemorrhagic can cause some problems. So this may be a question to, it might say which of these drugs is relevant for pounding an operation, but it may not, but that's just one little snippet. So 30 slides halfway through we're doing well. The lens, this patient has a cataract. The cataract is a bread and butter of ophthalmology. Uh It is an opacification of the crystalline lens in the eye and the only way to fix it is an operation, uh age and sunlight are kind of risk factors. But also it's just age really that we, we think congenital cataracts is important for um when you see a white reflex of a child. Um we don't tell people to wear a sunglasses to prevent cataracts forming. Um So that's that what we've got here. We've got different uh types of cataracts. So looking on the right hand side, it looks very brown on examination through the eye. Um So that's a nuclear sclerotic form. This is a cortical form. So like shards or feathers coming from the outside, like spokes and this is a posterior subcapsular cataract. I don't actually think um that uh level of separation would be in your exam. But if someone has a cataract operation and the vision becomes cloudy afterwards, it they can get something called a posterior capsule opacification down the bottom in image A and we do a laser procedure called a capsulotomy and we laser a hole in the middle and then they can see clearly again through it. The Americans call this a post cataract. Um It happens in a good decent number of people that have had it, but they don't happen automatically in everyone. Good. Uh This is an image of the C A lens being held in place by zonule. Uh and the zonule hold the lens to the um ci body. And uh if anyone can think of a condition that has a deficiency of fibrillin, uh they may be thinking of Marfan Syndrome uh which is correct uh because this can cause um a number of eye problems but mainly um dislocation of the lens in possibly a 30 or 40 year old without a cataract and without trauma or any very mild trauma. So that may be in the question, stan uh congenital cataracts. You get these in the Trisomy, you get this in muscular Dystrophy, Marfan syndrome, uh congenital infections like the torch infection. So, Toxo rubella syphilis um in Truma Pi syndrome and Cruzen Syndrome. So, they are just a couple of the differentials of uh if someone were to see a white reflex on examination, diagnosed with a cataract and leukocoria. So this is the absence of a red reflex or a white reflex on examination, newborn baby check differentials of these are congenital cataract persistent fetal vasculature where there there was a Hyloid artery which goes from the retina to the lens and this should die off through embryo through um embryological development. And if it doesn't, it just leaves a white uh vessel, remaining retinoblastoma is the main one. You're likely to get. At least one question on retinoblastoma. Uh in terms of a white reflex um or um mother took a picture of someone um and realize that one of them is shining back white um retinopathy of prematurity if they've had lots of laser dysplasia. So, maldevelopment or a particular infection called toxicara uh but the main ones here will be uh to bear in mind is cataract and retinoblastoma for the questions done, vitreoretinal. So you can see here a picture of a retinal detachment. So this is a macular off because if you follow next to the nerve into the middle, the macular is um detached here in this image, the macular is attached because you can see to the right hand side of this disc, a slightly darker area. That's the f and the the detachment has not spread there yet. So the detachment, the preceding symptoms are usually flashes and floaters and this will be from a tear forming. So you see the superior side of this image is a retinal tear. This likely happened within 48 hours. The patient probably noticed a flood of floaters and maybe some flashes on moving the eye. This is why you need to get them reviewed urgently. Um So that you can spot the tear laser around it and not have to deal with the detachment if it develops and it encroaches anywhere just near the arcades of the eyes, they are likely to notice a dark curtain sensation. And as it progresses further, you notice the dark curtain over your eye. Um risk factors for this are trauma, traumatic injury, short sighted. So myopia, so minus prescriptions and previous operations, if it's a macular on operation, it's urgent to repair um within the same day or within 24 hours because you've not detached your middle vision yet. So you you are operating to preserve the vision. Macular off has a bit longer. If it's freshly macular off, you should operate ideally as if it's a macular on. But if it's been off for a couple of days, you should just try and get it done as soon as possible because when the macular is off and detached, the horse has already bolted, you've had your damage of the splitting of your photoreceptors from the rest of your retina. And uh the operation is less urgent then. So you may get a question stone saying someone presents blah, blah, blah, question stone. They have a macular on detachment. When should it be operated on? And even though macular on doesn't sound bad, you need to operate sooner than a macular off to prevent the bad thing from happening. Ok. Vitreous hemorrhage is likely to occur in trauma or most likely uh proliferative diabetic retinopathy. Um and this is when you get to the R three stage, the new blood vessels burst and break and you can get a vitreous hemorrhage in the eye which can be small and resolve or it can be um dense and you need to operate to remove it with a vitrectomy procedure. So, best answer, patient with uh treated proliferative diabetic retinopathy, so treated meaning PRP laser all around notice as ne onset floaters, what's the most likely diagnosis? Is it retinal detachment, uveitis, vitreous hemorrhage, or hemorrhagic posterior vitreous detachment. And that last bit is because the vitreous sits in the eye but it is a globular structure and it's surrounded by a thin membrane. So through life, the vitreous does detach from the eye. The answer here, a retinal detachment is unlikely after laser laser PRP laser for diabetic patients is very protective. It's highly unlikely to cause a retinal detachment because if there is, if there was even a tear, the laser would stop that progressing because the laser, each laser band acts like a a fuse of the retina onto the sclera behind it. Uveitis. It's not, this is not the question stand for uveitis. Uveitis would pa would largely be painful for your point of view. It is going to be a vitreous hemorrhage, even patients that have got treated diabetic retinopathy, even if they've not got active diabetic disease, the neovascularization of diabetes grows from the retina up into the vitreous and when the vitreous is moving around during eye movements or through life, even the blood vessels that are shrunken and not dangerous and not, not actively neovascular can get tugged and pulled and it can cause a vitreous hemorrhage, hemorrhagic PVD. Um I'm just thinking now may be slightly confusing to give you any questions stan, but diabetics usually have quite adherent stuck on vitreous and they don't always have it attached to vitreous. So, vitreous hemorrhage in a patient with proliferative disease is likely the answer medical retina. So this is a picture of diabetic retinopathy. This uh is about severe R one or R two stage. You can see here, the disc is nice. You've got uh the middle of the macular. So the FVE you've got a couple of pinpoint um spot dot hemorrhages about the temporal side of of the macular. You have some exudates, you've got some other dots and small blots, hemorrhages. And you find these in all four quadrants right at the bottom there. You've got a larger hemorrhage and that's probably called a blot hemorrhage almost like you've blotted a, a bit of in on some paper. So take a couple of moments to have a look at um the diabetic eye and the hypertensive eye. So this is diabetic retinopathy. The exudates that you see here are usually not around the disc and not around the middle macular, they're a bit off center and they're a bit maybe oval and see it looks like the focus of these exudates. They're kind of roughly surrounding in a circle somewhere temporarily there. If I go to hypertensive retinopathy, if they show you exudates, they're going to be in like a star fashion around the macular or around the disc. So you see the exudates here, the little white blotches are far more centered in the middle than this image here where they are outside. So that's one of the differentiating features. Also, diabetes can get cotton wall spots. But as you see in these pictures, the white fluffy bits, there are cotton wall spots. They are neuronal damage of the retina and they're not really seeing in these diabetic images as much. So just have a look at them spot the differences. That's all I can say. You just have to look at a few and um take your best guess in the exam, going back here to proliferative disease. If you see new blood vessels growing quite evidently, this is going to be diabetic proliferation. So on the left, that's an extraordinary amount around the disc. On the right, you can see these new vessels practically hanging off the arcade like um tinsel um and that is go going to be diabetes in your questions. ST uh And on the right hand side, this is loads of laser and that's how the proliferative disease is treated and then it shrinks back the blood vessels. Uh This is a a central retinal artery occlusion, the retina will look white and there'll be a cherry red spot in the middle. And that's because of the thinning and of the retina, of the natural shape. And you see the underlying blood vessels, but the retina goes white. This is a sudden painless loss of vision. And if they, if the question stem is there and it says someone came to you two hours after painless loss of vision and noticed an artery occlusion, you treat that like a stroke. If it happened hours and hours ago or days ago, you treat it like a tia with a tia referral. But if it's happened acutely within the thrombolysis window, you will treat it as a stroke and you may well thrombo um a branch retinal vein occlusion or central vein occlusion is backing the blood of the vein trying to drain out the retina gets backed up and all the the retina, the blood vessel becomes hemorrhagic and the blood goes everywhere. So you can see that the, the the pattern of hemorrhage here is far more like it's following in the blood vessel uh moving outwards from the disc and it's very, very hemorrhagic. It's much more hemorrhagic than either the hypertensive or the diabetic versions will be. Um So this is a vein occlusion, either branch or central. Uh and the risk factors for these are hypertension diabetes, cholesterol, just like ischemic heart disease, uh no acute treatment as needed here but if they develop macular edema, then we need to give them injections. This is uh CMV, cytomegalovirus. Usually in immunocompromised people, they may either have HIV or be undergoing cancer treatment. It's a viral um retinitis and vasculitis, which may look slightly similar to this in some ways, but it's got largely, the optic nerve will be swollen and the vessels will be surrounded by whitening. Uh and there'll be areas of white retina and necrosis, which there is not here. Toxoplasmosis would be a scar at the posterior pole of the eye. Um It's likely to just be black and burned out, but it could be white and fluffy uh if it's active, but just know this can be one of the uh uh infections you can get in the eye macular degeneration. This is another bit of bread and butter of ophthalmology. You've got the dry form on the right, which can take for on the, on the left of the screen there, which can be driven or geographic atrophy in the middle of the macular. And that can cause worsening vision on the right side of your screen, you've got wet form. The wet form is where a um blood vessel grows from the choroid, the outer layer of the eye and the blood vessel. So just underneath the sclera is the choroid. So a blood vessel will grow from there through the basement membrane just under the retina and it can leak and bleed cause fluid to release and this can cause atrophy of the retina. So, uh we have to treat these with anti vegf injections. There's lots of other type, there are more and more other types of injections. But basically the question stem will uh give you this condition and uh you will need to treat with intravitreal injections of some kind. So, one of the questions, 85 year old gentleman, 30 pack year smoking history type two diabetes, hypertension, osteoarthritis, a tens of metamorphopsia which is a distortion of vision for two weeks. An optician notices a bleed in the macular, the other eye has drn what is the most likely diagnosis? This is wet. A MD in an elderly person of acute, acutely noticed distortion and especially with a bleed at the back, you must suspect wet macular degeneration because nationally we have a guideline, we must treat these people within two weeks of referral. So they must be seen and treatment started because this is within two years without treatment, you will go centrally blind. And we know that for a fact um taking the other options, dry, macular degeneration, drin is a form of dry AMD, but it shouldn't cause you acute distortion and with a bleed, that's unlikely diabetic retinopathy, even if the diabetes caused a bleed. Uh it's unlikely to be the type of bleed which causes distortion. Um So, um and so acutely, it shouldn't really cause that diabetic macular edema. Uh again, it's the acute distortion noticed uh and the age which points towards um this being wet A and D. So what is the biggest? This is the same question, Stan, what's the biggest modifiable risk factor here? Have a little thing. And this is another question where they can, um, catch you out age is by far the significant risk factor of AMD, nothing else that you do is really that significant. Uh But the older you are, the more you get it, but modifiable smoking. Um, and if you stop smoking, then you, um, will reduce your risk of progressing from the dry form into the wet form, uh, and produce, uh, the deposits that cause the atrophy in the first place. You can take vitamin supplements as well. I haven't included that in the, um, answers. Uh, again, that would probably be an even lower modifiable adjustment that you could do than smoking. But ad people at risk, we say stop smoking, diabetes, hypertension aren't shown to be risk factors in ad 15 more sws left. Excellent. So the optic nerve, this optic nerve is swollen. Um, yeah, any que I might just finish this because we're getting on for an hour and then we'll ask some ques, uh, answer some questions at the end. So this optic nerve is swollen. When you're examining patients, you can see here the, you can't see a clear cup. You can't see a clear outline of the disc. It's fuzzy and it's hazy. You can see maybe inferiorly, the vessels are starting to become obscur so blocked by the swelling, but there is no hemorrhages around which you can notice in optic to swelling. But there are no pattern lines around and pattern lines are ruffles of the retina because it's so swollen cupping. So this is a swollen disc and there's a differentiation between uh a swollen disc and papilledema. Papilledema is optic nerve swelling secondary to raised intracranial pressure. A swollen disc from multiple sclerosis is not papilledema because the pressure in the head is not high. Do you get me? So people use them interchangeably, but that's incorrect and it will be incorrect before your exam. So if you, if you see a sign like this in an osk or wherever you comment on it and say it's a swollen nerve, you don't say it's papilledema because you can't prove that unless you find space occupying lesion or raised intracranial pressure. So this is swollen on the left is a normal nerve and on the right is a cup nerve. So glaucoma causes optic nerve cupping. Uh I because it causes individual nerve fiber axon death. So imagine you've got millions of axons going from all around the retina into this cup. So crudely, I'm gonna do this with my panels here. So you've got all these nerve fibers going in the middle and then throughout time because they get damaged, they start dying off and they get, I'm I'm pulling out the pens from the middle of this and then I'm pulling more and more and then what's left, you've got barely any nerve fibers, but your cup is still there. And then that's why you get left with a 0.9 or 0.95 cup because all the nerves that were going into that cup have died off. Um This is different to optic atrophy, which is when the nerves don't work, but they don't individually get killed off. Like with glaucoma, glaucoma just raised pressure causes the nerves to die off. In this way, neurological insults and nerve damage like um um like a stroke to the optic nerve will not cause the cupping like this. It will cause uh just a pallor and a pale nerve. So pale nerve is nerve damage. Cupped nerve is pathogenic for glaucoma and usually glaucomatous nerves are cut and pale. You've got primary open angle, glaucoma. Um One gene that can be associated with that in question stands is a GLCA one, but there are quite a few and it's either a abnormal resistance to outflow or it's an overproduction of the aqueous. And you a visual field can develop as with these visual field charts there on the right hand side and it's usually superior. So, optic nerve damage like glaucoma or from GCA temporal arteritis when it damages, the nerve is usually an altitudinal or superior or inferior uh defect. Um The, if there is a visual field defect which respects the horizontal and it's either a left or right side, that's usually neurological. So posterior to the chiasm. If you get in your question stem or this in some type of osk a superior or an inferior field defect, that's likely optic nerve head. And therefore, it's likely glaucoma or ischemic damage. So the pressure, as I've said, compresses the nerve at the back, the treatment, there's four types of treatment for this. I don't think you need to know the order of treatment, but it is a Prostaglandin analog first, likely latanoprost. Then it would be a beta blocker called timolol. Then it would be a carbonic anhydrase inhibitor such as dorzolamide. And then it would be something called an alpha agonist called um uh apraclonidine or um similar. And uh oral acetaZOLAMIDE can lower the eye pressure just like it can lower. Yeah, intracranial pressure. Sorry, Manish. Is this going to cut us out in a minute or um, are we able to extend? No, no, it doesn't cut off, don't worry. Ok. Cool Grand. I not got long left. Um, and we started five minutes later, I think. Anyway. So this is the drainage system of the eye. The, I don't think you can see my cursor but the um the fluid gets made at the ciliary body, uh which is behind the iris next to the lens, the fluid flows over the lens through the pupil and it drains through Schlemm S canal. So any pathology. So the two, the two pathologies of um glaucoma, which is nerve death from raised ocular pressure is either overproduction in the salary body part or under under drainage uh of the Schlemm S canal and the drugs that I've mentioned before work on uh either of those things, but I don't think that's necessary for you guys. Um And again, as a bit of a misnomer, people can have raised intraocular pressure. But if you don't have nerve damage or a visual field defect, it's not glaucoma, glaucoma is defined as optic nerve damage um related to raised intraocular pressure. So you can have ocular hypertension without glaucoma, but you, you need raised. Um but then when the nerve gets damaged, if you've got high pressure, it's then uh glaucoma, you can also get normal tension and low tension glaucoma. But that's another ket of fish. The, the the other separate glaucoma that you need to be aware of is an acute painful red eye. Usually, I've come up with this little acronym, uh Withered white women worse at night. So it's usually elderly, it's usually white population, it's usually women and it's usually at night when the, the lens you may have a cataract, um the front of the eye becomes the anterior chamber becomes very small at night. When it's dark, your eye will dilate your pupil will move back and block the schlemm canal outflow will be blocked and your aqueous continues to be produced. And in a closed system, this raises the pressure extremely. So you get extremely red eye, mid fixed dilated pupil, hazy cornea, worse vision and the symptoms they say in the handbooks are seeing halos around objects. So bear this in mind. Elderly person has not had a cataract operation. Um seeing halos, acute painful eye, it's likely to be closed angle glaucoma. As a note, if they've had a cataract operation, they're almost certainly never going to get closed angle glaucoma. So that may be a a question to, to catch you out and to treat this IV acetaZOLAMIDE and uh yag laser iridotomy. Um optic neuritis is inflammation of the of the optic nerve. It usually presents with swelling at the front of the eye. And the main differential for this people may notice a bit worsening vision maybe to 6, 12, 615. Um They may be young women, the color vision may go because color vision is one of the optic nerve functions. Um And you would like to get an MRI on them to see if they've got any demyelinating white matter lesions in the eye in the um in the brain, you would test once you see this for anti mog anti aquaporin. Uh because both of these are severe autoimmune related optic neuropathies which they need intravenous steroids. Uh Technically optic neuritis does not. Um but if the vision is bad and the uh presentation is very acute. It's happened over the course of 24 hours or so, then a lot of people would give them steroids. Um, I think there's something called the, the, um, the optic neuritis treatment trial, which showed that IV steroids wasn't that useful just for normal bound or MS related optic neuritis. So, they are unlikely to ask you, would you give steroids or not? But if the vision is extremely poor and if they had aquaporin or something like that, then you would give steroids. If the vision was a bit down, the nerve is swollen, they've got a bit of pain on eye movement. The question stem is likely going to ask, what investigation would you do? And it would be either the blood tests or the MRI to see if the white matter lesions to diagnose, to investigate for MS. And this is typical optic neuritis, atypical is when it's fast, lots of vision loss. And they might have other neurological symptoms because the anti morgan anti apurin disease can present with other things like transverse myelitis and other systemic problems. Giant cell arteritis. This is you'll always get a question on this pain on the temple. You can't feel the pulse, pain, on brushing, pain, on chewing. Esr will be high CRP. Now is mostly what we go on that will be high. Um You take a temporal artery biopsy uh and uh this is treated with high dose steroids and it can either be IV or or oral. Um if they give you the option IV is likely the answer because it's an emergency. Uh but usually the 60 mg or was fine for most people for ages. And this can present with an altitudinal defect and this can present with a swollen disc. And the main reason you are doing this is to save the other eye and prevent the vasculitis from going there. Uh I explained that I wasn't paying attention here. So a patient at attempts for temporal artery biopsy, um a largest possible length of artery is taken for histology. Why is this? I said this just on this. So uh you take multiple cups uh of as much of a length as you can because they've got skip lesions. So giant cell arteritis causes hypertrophy of the arterial wall because of the inflammation. It's not like a thrombotic event really where it causes um uh of the blood to coagulate in the vein. It's a, it's a um hypertrophy of the muscle from the inflammation causing a blockage that way. Um Idiopathic intracranial hypertension, swollen discs. This is really, this is high intracranial pressure. Usually young women usually high BMI they've got a headache worse in the morning and that's not just diurnal, but that's because they're lying down. The headache is worse when they're lying. Uh because more of the CSF goes towards the brain rather than as if they're standing up. Uh Some of the CSF has drained downwards. The headache is worse when bending over again because more of it goes to the head. The lumbar puncture opening pressure is over 25. They may or may not have visual symptoms. They may or may not have swollen discs. In contrast, there's something called a low pressure headache and you may get a question stem. This may be after transsphenoidal surgery. This may be after neurosurgery, maybe after LP when someone gets a lot of pain, when they're standing up, soon after they wake up in the day, they might within 20 minutes get severe pain. Analgesia doesn't really work and lying down helps that. That's because we've got low pressure headache. You've got not much CSF, the brain sits onto your skull and that causes the pain. And when you lie down, the CSF floods back into the head and it lubricates it a bit more. So, bear that in mind as well. Low pressure headache. Usually after a surgical procedure, a 32 year old woman, newly diagnosed with ih swollen discs are found on examination, vision is good in both eyes. What's the best disease modifying treatment? Just for a few seconds, read those and the best disease modifying treatment is weight loss is the only disease modified treatment in ih. For migraine, you have lots of a proven ladder of analgesia. You can use them to some degree in this uh such as topiramate, but it doesn't really work. Um acetaZOLAMIDE, people think it treats their headache and their condition, it reduces their CSF volume by reducing production. But this is basically a bridge for them to lose weight. And then the body will respond better and the CSF production and drainage will get in the creps, um balance again and uh systemic steroids. Uh this is not an indication. So, weight loss is the modifiable disease treatment. AcetaZOLAMIDE, you do use acutely if they're bothered by the headaches and that's a bridge until they lose weight and then you can wean them off a bit, the orbit. So orbital trauma can damage any of these structures. So, muscles, optic nerve and the eyeball and you can fracture your bones and an orbital exam. If you get anyone with orbital cellulitis, what you do to assess all of these structures, you test the pupil reflex because that's part of the optic nerve assessment. You test color vision because that's part of optic nerve. You test a visual field and that's part of optic nerve. You test your eye movements up down left, right, because that's part of your uh muscles and you feel the orbital rim and you feel for paresthesia around because that's part of examining the orbit um for any fractures and any damage to any of the nerves that come out of the orbital rim. So orbital trauma, uh panderi will likely be a blowout fracture of the orbital floor as your questions stem. Um And if there's an orbit full of blood. That's called a retrobulbar hemorrhage. That is an emergency. You have to do a lateral canthotomy cantholysis where you cut the canthal ligament to free up the lower eyelid, you provide an additional space for anything in the orbit to decompress outwards and therefore, you are not causing ischemia to your optic nerve. So, retrobulbar hemorrhage, if you ever see that on the question stem is an emergency. It needs a canthotomy, cantholysis, uveitis. The main one that you'll be um asked about is anterior uveitis. Anterior is usually painful red. It may be up to a week of symptoms. Photophobia is the patho economic thing here. Sensitivity to light and it may or may not have a hypopyon. So hypopyon doesn't always mean bacterial infection. It can be uveitis. You have to read the questions to carefully, you can get posterior uveitis, but they're unlikely to comment on that endophthalmitis. It can be endogenous such as um spread from different parts of the body such as Candida or staph infection um from an intravenous drug user or someone with lots of lines who's been in a hospital for a while. They've got indwelling catheters or Cannulas, they may have abscesses in different parts of the body and it may just present itself one day by spreading to the eye and causing an infection. Otherwise you've had exogenous, which would be postoperative or post injection. So that leads on this is a question today. You may well, get patient turns three days after intravitreal injection with the juice division, red eye, hypopyon vitreous inflammation. What's the most likely diagnosis? So, we've just gone through that really. It is not going to be acute anterior uveitis because it's a bit the history of surgery just before. Uh means that you will consider that less. You'll be worried about that. Less exogenous endophthalmitis would be the answer because you've just done a surgical procedure. You've likely brought a bug into the eye from the outside endogenous endophthalmitis. Of course, the bug has got into the body from the outside somehow, but it's likely sitting there in a liver abscess or as an endocarditis lesion and then it spreads. Um And this, if someone has endogenous endophthalmitis, uh it's most likely going to be staph aureus or um candida or yeast. Yeah. And this is not a presentation of vasculitis, POSTOP infective organisms. They may be cheek enough to ask you this between day one and two, pseudomonas, day two and four, staph aureus and later staph epidermis. The treatment is intravitreal sampling and injection of antibiotic. Um The best part of reducing surgical site infection in ophthalmology is iodine in the eye. So iodine on top of the eye when cleaning. So iodine will clean and kill all the bugs from the eyelashes, which is where most of the organisms that cause endophthalmitis live. And for cataract, the single rather than iodine, the single best thing shown to reduce infection is intracameral so into the ac cefTRIAXone. But if that's not an option, then iodine is the best way to prevent infection for any surgery. The end, well done, well done, well done. Uh These are little flow maps that you can find in the Morefield manual of Ophthalmology. Your library probably has one or two copies of it. So you can have a little look at that and I think some other books will have a similar thing here. It just separates it into loss of vision, red, eye, painful, and painless loss of vision and diplopia and gives you a little bit of a flow map. Uh So well done guys. I know that was a lot. Um As I said, it's a big uh it's a big topic in a way, but they don't ask you many questions about it, but hopefully that included enough snippets and keywords and buzzwords that you've found it somewhat useful. Yeah, thank you very much. That was really useful and it was um a good comprehensive guide to ophthalmology in such a short amount of time as well. Um And yeah, like there's a lot of information there that I didn't know before, but I feel a bit clear on now. So thank you very much. Um I'm putting the feedback form a link in the chat, everybody. It's really important um for do do and for me as well that you complete this because um you know, do do has taken time out of this day to do this and it's been, it's been really good. So, thank you. So, any, any questions from anyone at all? There was a question earlier, um which said you mentioned a neonate conjunctivitis complication earlier. Could you repeat it? Oh, yeah, that's um that was corneal corneal uh melt. So when you've got such a bad infection on the front of the eye, even as a late stage, um, late stage corneal ulcer from a contact lens, it can just thin and thin and thin. And you've got a focus of perent bacterial infection that it will exude pus, but then it will be destroying the cornea around it and it can go, it can get so thin that it perforates and then aqueous will fall out of the eye and that's an emergency. You've got to either suture or put a glue patch on top of the eye. So, yeah, like it untreated gonococcal conjunctivitis will cause a corneal keratitis as well where the gonococcal bugs will just cause it to become pus and erode. So that's corneal melt. Corneal melt can also be seen in patients with vasculitis and rheumatoid arthritis and lots of other inflammatory conditions. But that's the questions stan would be a little bit difficult to um understand. But yeah, usually that's with someone with an autoimmune history. Yeah, or late stage un untreated bacterial ulcer. Grand well done guys. Uh Best of luck. I know. This is a bit of a niche topic, but hopefully you had a couple of pointers in there. Thank you. Thank you very much. Thanks for coming guys. Cheers. Thank you. Yeah, thanks Manish. Uh Yeah, the point of that was um it get.