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Ophthalmology Lecture



Join us for an interactive and informative on-demand teaching session designed for medical professionals. Our instructor will cover a range of topics relating to ophthalmology and common ocular diseases. Given the brevity of questions concerning ophthalmology in standard MLA and AKT exams, this session will provide you detailed information to prepare for such questions effectively. The session also aims to serve as a refresher course on essential topics typically forgotten post their teaching in third and fourth years. Patient cases will be presented to create an engaging learning environment. Some of the topics covered include diabetic retinopathy, hypertensive retinopathy, and age-related macular degeneration, complete with their pathophysiology, clinical findings, grading, and treatment. We encourage interactive participation and welcome questions. A feedback form will be provided at the end, and post-session questions can be directed via email. Don't miss this opportunity to update your knowledge and skill in this critical medical domain.
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Learning objectives

1. At the end of this teaching session, learners should be able to explain the pathophysiology and signs of diabetic retinopathy and how it affects the eye. 2. Participants should be able to identify the correlates between increasing hyperglycemia (HbA1C levels) and increasing risk of retinopathy, thereby understanding the importance of effective glucose control. 3. Learners should be able to discuss the differences between non-proliferative and proliferative retinopathy, including their management strategies. 4. By the end of this training, participants are expected to be able to describe the characteristics of hypertensive retinopathy, its grading system, and the mainstay of treatment. 5. Learners should be able to differentiate between dry and wet age-related macular degeneration (AMD), understand the implications for life style modification and be able to describe appropriate medical management for both conditions.
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Computer generated transcript

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

Right. I think we'll get going if that's OK with you guys couldn't sge um let me know if you can see the slides. Mhm. Yeah, we can see them. Oh, thank you. Is it in presenting Roger? C? Yes, I think so. Yeah, that's great. That's great. Uh OK, cool. So I think I'm on my own today. I usually there's another pe person here to just help through um but it's being recorded. Um So yeah, I'm gonna run through the ophthalmology peer share talk today with you guys. Um So if you have any questions, whack them in the chat, um I'll have a look if that's uh something you want answered. Now, otherwise there's my email and I'll whack it in the chat as well and you can um email me afterwards. Um and I'll be happy to answer any opthalmology questions or any sort of finals questions. So, um yeah, just go ahead with that and there's a feedback form in the chat as well, which if you complete that at the end, that would be really, really helpful. So, uh yeah, just a few things we'll do today. Uh So we're gonna cover just a bit of the content. I tried to look at the MLA and how many questions you got on ophthalmology and I couldn't find a specific figure, but um I know we had approximately eight questions uh in our MLA er in our A KT. Um and it's quite a lot of content really to cover uh for, for quite small number of questions. But uh hopefully I'll cover sort of the most of the core content today uh over sort of M CQ land and then also uh a bit of ay tips as well at the end. So, yeah, I understand why everyone's staying and often you get teaching in third year, which is great, but then forget about a lot of stuff by the end of fourth year or um even at the end of third year as well and definitely by, by fifth year. So um hopefully, this is a good refresher for some of you. So yeah, I'm gonna do a few questions along the way. Uh If you just could whack in the chat like an answer uh and then I'll run through the answers afterwards and then we'll go over a topic at time. So we'll start question one. So 77 year old female with type two diabetes attends her annual diabetic eye screening appointment. She has previously been diagnosed with non proliferative mild di diabetic retinopathy when, where microaneurysms were noted on visualization of her re examination identifies the additional presence of cotton wall spots in both eyes. What is the pathophysiology of this new finding? So I'll just give you 30 seconds or so. And if you could whack in the chat a few of your answers, that would be really good. You can give it a go. It doesn't matter if you get it wrong. That's fine. No. Ok. Well, first one's a bit hard maybe. Um but the answer is here, uh precapillary artery occlusion. So, basically, in diabetic retinopathy, co wall sports represent areas of retinal infarction, er or ischemic nerve cells. So this patient is playing with new co sports um in sort of presenting with advancement of her M PDR. So other answers settle central retinal rate occlusion, not being correct. This is a cause of acute blindness and commonly occurs due to thrombo embolism or vasculitis lipid deposition. Uh This presents sort of hard exudate or dr and thickening of the of the walls of the retinal arterioles. This is uh silver wiring and hypertensive retinopathy and then thinning of the neuroretinal rim. Uh this would be seen in in glaucoma er optic disc cupping. So, moving on to diabetic retinopathy. So, um hyperglycemia leads to sort of blood vessels uh damage uh sort of sort of increase uh retinal blood flow causes abnormal metabolism within the retinal vessels, damaging the endothelium. Uh This leads to sort of an increase in vascular permeability and then leads to the characteristic exudates, you know retinal on fundoscopy. So uh damage to nerve fibers leads to co spots as we've just spoken about in the previous question. Um and then there's various other uh things that we would see. So importantly in neovascularization, this is in proliferative diuretic retinopathy. So, uh in result uh in response to sort of ischemia in the er retina, you have production of VEGF which is vas vascular endothelial growth factor. And then this stimu stimulates newer proliferation of er retinal vessels. And um we can use this uh well, you can use anti vegf at a later date to sort of combat this uh complications alongside this would be vous hemorrhage, retinal detachment um along others alongside other things as well. So, here are some uh just examples of hemorrhages, microaneurysms. And it's important to note that you wouldn't have diabetic retinopathy unless there are microaneurysms on uh fundoscopy. It's gotta have this to get a diagnosis. So, uh management of non proliferative. So we've spoken a little bit about proliferative. Uh so non nonproliferative be before we've got um new blood vessel formation. So the most important thing is really just managing the risk factors for the progression. Um As you can see here on the right, like in er increase in the HP A1C, uh correlates with an increased risk of retinopathy. So, really managing those risk factors, managing high blood sugars and BP. So, making sure um controlling glucose, well, uh and uh controlling other things like obesity, smoking, uh lack of exercise, um poor nutrition and um also importantly making sure people go to their annual eye exam. So a silent disease and isn't picked up until you've had the screening. So um regular uh regular screening is really, really important. So, proliferative, spoken a little bit about it. Um the treatment is gonna be P RP laser. So this is gonna sort of burn the blood vessels and prevent further growth of them and then also anti vegf injections. So these are gonna combat the uh vegf er proliferation of new vessels. And then if there's sort of uh uh quite serious or vitreous hemorrhage, then vitreous surgery is indicated. And yeah, just a mention on maculopathy. Uh So myedema is, is is there when this extra dates on examination and this can be seen on sort of fundoscopy but also oct exam er and then er management for that is gonna be individual anti vegf as well. So now moving on to a hypertensive retinopathy. Uh So there's a couple of versions, there's uh obviously essential then secondary due to endocrine or other uh kidney heart disease and then there's malignant as well. So that's like very high BP with potentially life or sight threatening signs. So some findings we'll see on the fundus um silver wiring, a nipping got more spots again, hard exudates, uh retinal hemorrhages. Um We can grade this with the key Wagner Bark classification. You obviously don't need to know everything of those findings are good just to know a few just to lift off in Aussies. Even if you don't particularly know what everyone means or what everyone looks like. You know, just saying, I don't see a nipping, I don't see coal spots. All these things are good and make you sound like quite slick when you're talking through an examination, um a fundoscopy examination. Um But yeah, so this classification, there's grade 1 to 4 and uh probably the most important thing really is remembering grade four is papilledema. So that's disc swelling uh as a result of raised ICP. Um And then yeah, mainstay of treatment is really gonna be reducing BP. Um And uh yeah, just making sure if they do have malignant hypertension, we wouldn't be one reducing that too quickly. Uh as there's sort of a risk of having organ hypoperfusion. So that's gonna be done over sort of 24 to 48 hours. So now question two and if you wanna have a go that'd be great. Um So a 72 year old woman presents to the eye casualty department reporting bilateral worsening vision over the last 10 years. The patient says that this is affecting her ability to read books on examination, essential visual uh central visual impairment is detected. Metamorphopsia has also demonstrated using a small yellow deposits of visualizing the macular on fundoscopy based on the most likely diagnosis. What was the most appropriate medical management for this patient. Is it monthly individual anti omega three bo modification, photodynamic therapy or V supplementation. So, got a few coming in along the right lines but not the right answer. Yeah. So it's E one guys. So here we go. Um vitamin supplementation is correct. So some of you put monthly individual anti veg. That's a good idea. But um it this patient has dry macular degeneration. So this is highlighted by the poor central vision security, which is good and metamorphosis. So this is distortion uh where straight line car this is gonna be in your central and it's differentiated from wet age uh due to the long time course and the lack of neovascularization. So um yeah, vitamin supplementation is the right answer but um uh it would be wet age for monthly individual anti vegf. Er So it wouldn't be fo that's for cataract surgery. Uh Photodynamic therapy is incorrect and Omega three is for uh dry eyes. So yeah, moving on. So yeah, as you can see, this is dry age here. Um there's bruising around the macular and we'll talk a little bit about this now. So yeah, it's it's the most common cause of blindness in the UK. Uh The risk factors would be age uh smoking, real big one and uh family history along with cardiovascular disease, uh we spoke a little bit about the presentation but it's central vision loss as the macular controls your central vision and the metamorphopsia seen on Aza grid. So, wavy lines right in your central vision and then also difficulties in dark adaption. Uh So there's two types, there's dry and then there's wet. So dry is more common and wet is less common but carries a worse prognosis. Uh and tru and effectively builds up er which is accumulated sort of undigested lipids er between R pe and BRS membrane. And um there's also atrophy of R of the R pe and degeneration of the photoreceptors. Um So then sort of moving on to wet A MD, this is characterized by the neovascularization. So dry MD, you can see here the DRN and then wet A MD, we see like uh bleeding and a new blood vessel formation. And then on the right is the AZA grid uh showing uh the metamorphopsia. So yeah, wet age uh or just yeah, visual generation. So, o on examination, you're gonna see uh reduced facial acuity. Er you're gonna use AZA grid and fundoscopy. Er and then also you can use OT O CT which is gonna help you visualize things a bit better. The management. Uh We've spoken a little bit about as well. So dry uh lifestyle, really, smoking, cessation, uh cardiovascular health BP control. And then the one real treatment that you can do is is the vitamin supplementation. So the vitamins are a Ce and beta Carotene. Um And yeah, it's just quite an easy uh M CQ question for them to do and then wet would be avial and anti VGEF because you've got those um new vessel formations and you wanna combat that. Um And it also just important to know for your patients coming in. Um The macular obviously gives you central vision so it never extends beyond the macular and navigation or vision uh remains. So people can often still drive and uh they don't lose their full sight, which is, which is uh reassuring for the patients. Uh So, moving on to glaucoma, now, uh there are a group of diseases uh causing optic neuropathy. The features would be uh most often raised into ocular pressure. Uh So these can be classified as whether or not uh the peripheral iris is clear uh the trabecular meshwork or which is an open glaucoma or covering the meshwork in closed angle glaucoma. So the level of the intraocular pressure uh as sort of shown in this uh diagram on the right is, is determined by the balance of the production and then also uh the removal of ACS humor. So you can see on the line on the right hand side, it's, it's secreted into the posterior chamber by the ci process and then it passes through the pupil usually and then would leave the eye predominantly by the trabecular meshwork. And it's sort of interference in this which cause uh the lack of uh of outflow. Uh And then uh this pressure can cause mechanical damage to the axons and uh also cause ischemia uh due to reducing blood flow at the nerve head as well. And that's why we get uh nerve damaging glaucoma. So, just a question about it. Now, um a 74 year old male presents to his ophthalmologist for a review. His sister has been diagnosed with primary open angle glaucoma and he's concerned that this may be also the cause of his worsening eyesight. He's got a past medical history of hypertension diabetes and prostate cancer. Which of the following findings would support a diagnosis of this condition, astigmatism, central scotoma, hypertropia, myopia or red saturation, you could just walk in the shot again. That'd be great. Nice. Yeah. So we've got d in the chat, which is correct. So, yeah, primary open glaucoma is characteristically sort of associated with myopia uh which is large eye and um you'd have a near nearsightedness as well. So where far away objects look blood and then converse the angle, acute angle closure. Glaucoma is associated with hypertropia uh astigmatism. That's just your cornea shape, uh central scotoma uh as a point of sort of blurred vision in the central visual field uh seen in MS um optic nerve glioma and then um red saturation that's also seen in optic neuritis. So, open angle glaucoma. So sort of discussed through that uh diagram earlier, but there's an increased distance through the trabecular meshwork um and this can lead to nerve damage. So risk factors for this would be age, family history, Afro Caribbean and also having the myopic eye. So presentation is often asymptomatic and only really picked up on routine screening uh to your optometrist or whatever. And uh you're gonna have this loss of peri peripheral vision and this is gonna be termed like an accurate defect. So in the super temporal areas, you, you lose the vision in those, in those er patients. Er so the diagnosis is through er noncontact on what tree and uh lots of other things. So uh the gold standard would be sort of uh Goldman visual fields as well. Uh Your management is trabeculoplasty. If I PS we over 24 millimeters of mercury and then you've got various drops which are gonna help and then ultimately also you could do a trabeculectomy. So on the right here, uh these slides are going out to you as well. Um But this is from uh this is from passed and it's just quite an easy question for queens to do or the ma to do, you know uh one of the side effects of the mode of action of the medication, a two step process and like a stem diagnosing it. And then knowing what the side effects of the mode of action is of the drug that they wanna use. So good to maybe try and remember a couple of them. So question four, a 62 year old woman presents to her GP with a painful right eye associated with blurred vision, nausea and vomiting. On examination. The patient's right eye is fixed with a is read with a fixed dilated people. When her left eye is covered, she's unable to read a post on the wall. Even with her glasses on her left eye appears normal. GP refers the patient for immediate ophthalmology assessment. What's a definitive treatment for the most likely diagnosis? Uh So yeah, intravital anti VF uh omy. Um tan prost eye drops, pilocarpine or Trabeculectomy. Direct message. She's correct. Nice. Yeah, good, good coming through. So yeah, the definitive treatment here is part on the stem. Um That's what we're looking at. So yeah, really, the definitive treatment is gonna be laser peripheral omy and that's gonna provide the outflow for the build up of AKS humor. Uh Great. So this is for acute angle closure, glaucoma. So this here we have um on the right picture, an extremely red uncomfortable eye. So it's an ophthalmology emergency iris is gonna bulge forward and then block the trabecular meshwork which allows for the drainage. Uh there's gonna be a sudden increase in IP and they're gonna feel pretty rotten. So, um yeah, well, presentation they're gonna have this acute red eye, blurred vision halos and headache and nausea. Vomiting is pretty common as well. And your risk factors are age female family history, Chinese or or Asian and then having the hypermetropic eye. So the small eye and the way I remembered it was for acute ankle closure, you have a small eye and then it's more likely to block off uh, the, the meshwork and then open angle was just the opposite of that. So, having a large eye, um, just the way I remembered it. And then, uh, on examination, yeah, they're gonna have a red eye and then the sort of pat, pat finding is, you know, this fix it dilated people with hazy cornea. And then it, I mean, if you felt someone with it, you'd feel a really tense eyeball. Um But obviously you do the official pressures on that and then your management would be lie them flat to reduce the pressure and then drops drip and up. Uh So the Pilocarpine, firstly, this is a direct symptom mimetic and this sort of causes contraction of the salary muscle and constriction of people uh opening up the trabecular meshwork and then allowing outflow of that blocked ac humor which is causing all the pressure and then um acetaZOLAMIDE as well that reduces aqueous seres uh secretions through um osmotic gradients. And then uh yeah, that peripheral laser iridotomy, which is your uh definitive treatment to allow the uh outflow of the consumer. Cool. So number five, now, um moving on quickly. So we have a 45 year old woman. She attends eye casualty, complaining of blurry vision and glare and bright lights. She has a history of asthma PMR and gout the ophthalmologist finds a lens, opacity in her left eye that is located just deep to the lens and the visual axis, which of the following is the strongest risk factor for subcapsular cataracts. So it's more, you know, or you don't, but that's fine. Give it a go in the chat. Nice. Yeah. Well, and guys, good. So, yeah, steroids is the right answer. Um, it's a really common risk factor for people with cataracts And then obviously, specifically the cca cataracts, you don't need to know them all. It's good to know a couple but steroids is, is a good one to know. Um OK, so cataracts, these are basically just when the lens becomes cloudy and opaque and occurs to most people just as they age. So risk factors obviously will be age and then smoking diabetes, steroids, as we mentioned and then sun damage as well. And your presentation is just gonna be the elderly patient. Um uh Usually it's happened over gra gradual years of decreased visual security. Um They're gonna have difficulty driving at night and having a blurring of vision and also starbursts around light. And then, uh if it's sort of absent red reflex in a child, it's congenital, sort of often bilateral cataracts as well. Um Your management can be conservative, uh waiting on prolonging it and then eventually you're gonna need an uh intraocular lens implant replacement and this is done by fo ossification. This is the surgery they do for right now, which is minimally invasive and you can be in and out in 10 minutes and um again, quite a common. Uh M CQ question for this is is posterior capsule or pa pacification being a complication. Uh years after the fact, uh and after the, the treatment and uh this can be treated with Yaser. Cool. So, infective endophthalmitis, um it's basically an infection of the vitreous and aqueous, uh the intraocular fluids and it's purulent inflammation are usually due to infection. Uh The causes can be postoperative um and post invitro injection, endogenous chorioretinitis or it can be as a result of trauma. So your symptoms, patients can have blurred vision, pain, pior and then the signs you'd see is this red eye uh hazy media and crucially uh the hypopen. So this is the fluid level seen here. Uh basically a build up of inflammatory cells uh in the er anterior chamber. So, treatment is gonna be a tap of the vitreous or a consumer for the Grand Stain microscopy and culture and then giving the relevant er intravitreous antibiotics. Um So yeah, moving on to conjunctivitis, uh this is inflammation of the conjunctiva. So this is a thin layer covering the insides of the lids and the scar. So, redness should include the tarsal platelets and these are basically uh the area beneath your eyelids. So, if it is localized just to the episclera, so around the limbus, around the iris uh and not sort of underneath the eyelids, then you need to consider an alternative diagnosis like keratitis uveitis or uh maybe um like acute glaucoma. So, uh yeah, presentation is gonna be unilateral or bilateral red eye gritty sensation and discharge. Uh So the discharge can be purulent, more likely to be bacterial and then, uh if it's viral, it's more likely to be clear and the, the discomfort is typically worse in the morning. So your management is, is rule out the other causes too. Pardon me? Uh Yeah, so management is gonna rule out other causes of red eye. Um And if there is pain, it probably signifies something maybe more serious. Um If it's viral, it's usually self limiting and resolves in 1 to 2 weeks. And uh if it's a bacterial, then likely they're gonna need some antibiotics. So, chloramphenicol uh or fusidic acid eye drops and then counseling the patients, uh especially viral is extremely contagious. So even if you've got it in one eye, you're probably then gonna get it in the other, but you'll give it to your partner or whoever you're sharing towels or hand towels with. So don't share towels, good hand hygiene, washing pillowcases, and then also giving sort of symptomatic relief um by asking people to do um sort of cold compress and, and things like that. And then if they're at the age of one month, urge an ophthalmology review as this is potentially gonococcal infection and that, and that's uh side threatening. So, moving on to uveitis, uh this is inflammation of the uvea tract. So the iris sil body and choroid and this is tongue uveitis. And we had a question our finals uh which in the stem, it was basically a person who had uveitis um and then and a hyperion as well. So the, the answers, one of them was endophthalmitis. One was iritis and a few people got caught out, just saw hypopen and then didn't know that iritis was uveitis. So having like just a little bit of anatomical knowledge in ophthalmology really standing gets dead and they don't overcomplicate the questions generally. So, um yeah, it's just worth having a little bit of an knowledge basically. Uh So yeah, inflammation of the iris and ciliary body is anterior uveitis and then inflammation of the choroid or retina. Uh It's posterior uveitis. So, features are gonna be acute onset ocular discomfort and pain and the people may be small or regular uh due to something called posterior sinus where um people gets affected and uh adheres to the adjacent structures. And then there's also uh potentially photophobia, blurred vision and you're gonna get the red eye as well. And yeah, as I mentioned, the hyperion potentially in some cases. So, uh visual acuity is initially normal but then can become impaired. The word association uh is to do with autoimmune conditions. And then this is usually gonna be in the stem um of the question and uh there's other causes as well. So, infectious can be CMV, fungal toxoplasmosis, uh which is um posterior and then a uh herpes zoster herpes simplex or syphilis. And then your management is the cycloplegics uh which dilate the pupil which help relieve the pain and photophobia and then other drops and uh steroid drops to treat the underlying inflammation. And obviously, if, if they do have an associated condition, then treating that associated condition is going to prevent this from coming back again. Correct. So just a picture here, this is CMV, retinitis on the left and then um posterior sini, which is the sort of uh odd shaped pupil here on the right hand side and then the hypo. So the fluid level cool. Um So question six, a 27 year old woman presents the eye casualty complaining of a gritty sensation in her left eye. She describes blurred vision in the eye. She admits to poor contact lens hygiene on holiday two days ago, on an examination of the left eye, there's excessive lacrimation and conjunctival uh injection, but no eyelid swelling. Given the most likely diagnosis. What is the most appropriate next step in management to prevent complication? Is it artificial tears or antibiotics, paracetamol, topical, antibiotics or cycloplegics? Yeah, that one then cool, we'll move on. Um Yeah. So the patient's symptoms suggest a coronary abrasion and this is likely due to the contact lens or poor contact lens hygiene. Uh Treatment is gonna be top antibiotics and this is gonna be, um, to prevent the complications as asked the question. So it's gonna prevent secondary bacterial infection. You could use oral antibiotics, but this is sort of suboptimal second line to topical antibiotics and um, the others aren't gonna give any, er, so, or aren't gonna prevent any complications. So, question 7, 64 year old woman presents the emergency department with several facial lesions. The lesion suddenly appeared 48 hours ago and tender to touch. Last week, she had an absolute burning pain over her forehead. On examination. She's apyrexial. She has tenderness over the right side of her forehead. Several vesicles around 4 to 6 millimeters are noted on the right hand side. Hutchinson's sign is positive. What feature of her presentation warrants an urgent ophthalmological assessment lesions above the eyebrow lesions on the tip of the nose lesions on the top of the eyelid pain over the affected areas or tender lesions. Oh, yeah. Well, and guys think Children got that nice. So, ok, those slides aren't really. Yeah. So yeah, this patient has herpes zoster because which I slightly touched on earlier. Um but it's caused by essentially just reactivation of herpes zoster in the ophthalmic branch of the trigeminal nerve and the lesions on the tip of the nose are really typical of ocular involvement and this is known as Hutchinson's sign. Um and this is gonna warrant uh urgent ophthalmol ophthalmology involvement, ophthalmology review. So, uh, patients can have management with antivirals, uh acyclovir and they can have topical steroids as well. Um, but any of the other answers aren't as important as Hutchinson's sign, which is the tip of the nose. So, keratitis, this is basically just inflammation of the cornea and is potentially sight threatening. So, there's different causes bacterial, which can be staph aureus, uh pseudomonas. This is typically contact lens whereas, um, most commonly, er, viral acanthoic. So your vignette might be someone swimming in a lake, uh wearing contact lenses and then, er, presents with a red eye, er, and then parasitic, uh your features are gonna be painful, red eye, photophobia, foreign body or gritty sensation and then they might also have a hyperion as well and your management uh depends what type of bacterial. It's an emergency. So, same I felt off and then it's great for microscopy and give topical antibiotics, uh herpes keratitis. So, again, classic M CQ. Um it's the most common diagnosed with fluorescein. And you get this uh dendritic ulcer on slit lamp examination and that's treated with topical ACY of it. And again, you know, don't use topical stars as like a contraindication to keratitis. And uh they love asking that question as well. So, um yeah, here's a photo, this is Hutchinson's sign just on the tip of this lady's nose and a herpes orthalicus as you can see all the Beatles and then on the right, that's the dendritic ulcer cool. So, um episcleritis, scleritis. Um so these are inflammation of the area just below the conjunctiva. So, um they can present quite similarly, but epis scleritis is pretty self limiting and not as dangerous. And scleritis is very, very serious and can cause um uh a lot of damage. So, a sclerisis is usually idiopathic but it is rarely associated with IVD or RA. Um then symptoms, you can have acute onset more discomfort, um red eye and then on examination, the way differentiate is uh the vessels mobile when you, when you use AQ tip and then it will blanch with phenol efferent. And then the management is just sort of give it time, it's self limiting and then you can use steroids in refractory cases. Whereas scleritis um almost always has sort of an autoimmune uh aspect to it as well. Um And the sym uh symptoms is gonna be a more subacute onset with real deep pain or movement and there'll be photophobia maybe as well and reduce f security. And then your examination, the vessels will not be mobile, they'll be adherent and uh they don't blanch and uh they might have like associated rash or joint pain or whatever the autoimmune issue is. Uh So, yeah, the management is authorized a referral, systemic steroids, nsaids and then again, treating the underlying condition uh to prevent reoccurrence. So now moving on to retinal attachment, uh this is where the retina separates from a chord underneath and it's an emergency as uh they can lose sight. So there's two types of tears really as a rheogenic. And this is just a tear where it allows vitreous to gain entry into the subretinal space. And then a tractional which is where um sort of contracting um fibrous tissue from retinopathy of diabetes uh pulls the retina off. So it's a start during emergency, as you said, and your risk factors are gonna be vitreous detachment, Ds AEN uh can be trauma and then age as well. And your presentation is flashes and floaters and um that's sort of your prerequisite towards it. And then um when it happens is the shadow coming across your vision. So um management laser therapy to prevent progression and then if it's more serious reattaching the retina with a vitrectomy scar buckling or pneumatic retina plexi. So question eight, a 72 year old Moko presents to his GP with concerns about a sudden onset of complete vision loss in his right eye that began with the previous day. He reports no ocular pain or recent trauma and he has a history of hypertension and one on examination, neither eye appears red, fundoscopy, repe reveals a small red opacification on an edematous retina. Shining light into the left eye induces greater constriction of the right pupil than when the light is shine directly into the right eye. The response of this left people is normal. What is the most likely diagnosis? An uveitis, central rectal artery occlusion, central rest vein occlusion, rectal detachment or vitreous hemorrhage. Great nice one. Yeah. So it's, it's b it's central retinal artery occlusion. Uh So this is describing that cherry red spot, which is patho for central retinal artery occlusion. And it also mentions the R APD. So this indicates that there's an optic nerve issue and retinal artery supplies the optic nerve. Um So the other questions uh patients know with pains, vision loss. So that's atypical for anterior veit uh central retinal vein occlusion. Um The fundoscopy is gonna have like a blood and funder appearance uh which will come to you later and no sy symptoms of rectal detachment in the stem and vitreous hemorrhage. Yeah, it can cause some pain, vision loss similar to what is reported here. But um on fundoscopy, you'd see diffuse bleeding throughout vitreous cavity. So, yeah, the central retinal artery occlusion is rare but it can uh cause sudden unilateral visit loss and then you have the R APD as well. So the positive swimming light test uh indicating some sort of uh optic nerve issue. So the causes are thromboembolism or an arteritis like GCA. Your risk factors would therefore be cardio acid disease, smoking, hypertension dyslipidemia, all of that. And on fundoscopy, you're gonna see this cherry red spot with a power retina. Um If it is GCA. So your symptoms for that is, is gonna be your uh temporal pain and D claudication and your diagnosis, you're gonna work up with a raised E sr and they'll have a temporal icu biopsy for a definitive diagnosis. And you're gonna need high dose steroids. And this is sort of common in elderly patient, but important for everyone to know. And they love asking on GCA. So if there is emboli ocular massage, collagen inhalation or, or uh intra arterial thrombolysis if they presented early. Um So you can do uh the first one in uh in Ed. But uh I think it's quite poor outcomes for these patients. Unfortunately, then retinal vein occlusion. So, yeah, it's a thrombus which forms the retinal vein and then blocks the drainage of the blood from the retina. And you're gonna get a pooling of blood leading to leakage and edema and release of vegf. So all this neovascularization and blood around the retina and your presentation is gonna be a sudden pain, a loss of vision again and your risk factors quite similar. But the fundoscopy is gonna show this uh pizza pie fundus loads of flame hemorrhages, ma edema, blood neovascularization. Um And uh management is treating myedema and prevent neovascularization. So that's P RP, anti VF and individual steroids. So then uh yeah, preseptal versus auto cellulitis again, one's um really dangerous, one's less dangerous and you need to be able to sort of differentiate between the two and that's usually what the questions will be on. Um But yeah, the eyelid skin infections, uh preceptor was in front of the or septum and then orbital is is past the oral septum. Uh you differentiate um orbital cellulitis, it's gonna have symptoms of uh pain or eye movement, reduced eye movements, decreased visual security, abnormal pain reactions, uh or proptosis and preceptor will not have those symptoms. It's just gonna be inflammation and swelling around the eye. Um So your investigation is gonna be ct orbit and your management will be pure antibiotics in preceptor. And then IV if orbital and you're gonna get um ent involvement, uh orbital cellulitis is, is really serious and can cause blindness and spread to the brain and cause an abscess. So it's something you want to rule out uh early. So then eyelid disorders got styes so called external, that's internum outside and inside the eyelid. And it's basically an infection of the sebaceous glands at the base of the eyelashes. And your management is gonna be hot compress analgesia and then if they do have infective symptoms, treat them with an antibiotic. So, blepharitis really common, you're gonna see this everywhere, whatever you work in and people might not present with it, but it gives a lot of irritation. Uh it's inflammation of the eyelid margins and the adnexa and it's gritty, itchy, dry eyes and it's quite intractable and people just can't do much about it. But the hot compress, gentle cleansing, um and cleaning of the debris around the eye, uh lubricating preservative free eye drops are the best and then um occasionally you can give steroids eye drops for refractory cases. But um yeah, so conclusion this is just a block Mi Gland. Uh it's not tender and your management is gonna be a hot compress and then watch and wait. But in some instances if they've got pain or for cosmetic reasons and it hasn't gone down, uh then you can have surgical management as well. So then ion, so this is an inversion of the eyelid where it rubs against the eyeball, the eyelashes. So it's gonna lead to corneal damage, obviously, and then you're gonna get an ulceration, uh, really painful for the patients and often see this on geriatric wards. Um, patients with really, really sore eyes and nothing really being done about it. Um, management is tape, um lubricating eye drops and then in some severe cases, surgery and then respectively, ectropion and so the ear version of the eyelid and you're gonna get, uh, the risk of exposed to keratopathy, which is basically just damage to the cornea occurring primarily from, you know, prolonged exposure of the surface to the outside environment. And that can lead to ulceration and keratitis and uh ultimately, um, perent vision loss, uh from the scarring. So management, conservative lubricating eye drops and if milder men surgery, uh, if more severe. So, last question here, um, 34 year old woman with a history of MS presents to the ophthalmology clinic, complaining of pain in her left eye that worsens with movement, which she has experienced for the past two days or examination of visual acuity is measured at 6/20 in the affected eye and 66 in the unaffected eye. What additional finding might be expected on an examination? Given the most likely diagnosis. A anestia central scotoma, dendritic ulcer, home 80 pupil or hyperion. Take us mice. Yeah. So that's the centro scotoma is the correct answer it. So, the patient's history points towards optic neuritis and it's the most common cause in this case. So centro scotoma is a, is a blind spot in the center of the visual field and, and common in uh optic neuritis aoria, that's a discrepancy in people's eyes um between the two eyes and not characteristic of optic neuritis. Uh dendritic ulcer. We, we know now um it's caused by herpes keratitis and then homes pupils just abnormally dilated pupils, sluggish to a light stimuli and hypopyon that's sort of infective. Nothing infect. So, yeah, the palsies, um you can't go through everything but the way I remember it and was taught it er, was LR six. So four and everything else. Third nerve, so lapre to six uh Superb league four and then everything else. Third nerve palsy. Um So yeah, these are the eye movements and you're gonna have the third nerve, the eye down and out and ptosis, mydriasis. So, pupil dilation and uh if you're having a surgical nerve palsy, then um you're gonna have this pupil dilation and this is as a result of the compression of the optic nerve and then also the parasympathetic fibers which run next to it or parallel to it. And they can be affected, therefore, leading to this uh pupil dilation. Whereas if it's just a medical palsy. So this is like from diabetes or hypertension, then the people spared and that's like a a more microvascular um reason um which doesn't affect the localized parasympathetic fibers. It's just the nerve itself. Um So fourth nerve palsy um is the nerve uh eye amen and then second nerve aden's later recta. So that's gonna do your auction and it's most affected by raise ICP coss, it's the longest nerve. Um again, quite a good uh M CQ question. And then, yeah, these are just few done diagram schematics just how you understand. Um And then, yeah, also just uh knowing, knowing about Horners as well. It's not on here but um ptosis, miosis and hidrosis and knowing maybe a a few causes like central then preganglionic. Uh So that's like your pancreas tumor and then postganglionic, which is the carotid aneurysm or dissection. So, just having a few of them uh at the top of your head. Um and then oss now, obviously, any of these things we've been through today that can do histories on, there's obviously a bit of an overlap with neurology and I think we had a bit hemianopia with visual fail examination. And third year we didn't get anything in finals. So that was the only one we ever had. But there's anything from history, acute angle exposure, glaucoma, probably one of the more emergency ones would, would be better. Um But knowing how to examine the eye visual fields, visual security uh using a SN chart properly and uh doing fundoscopy. So yeah, really having a practice looking at youtube and looking at the portal, what Michael Williams wants, like just do it and you'll get the marks. Uh And yeah, I remember one at a time for the pinhole and pupil assessment and then I always forget, but just always inspect and then a few general sort of resources pretty similar to everyone really. But its finals passed ResMed um bang out as many as you can. Some people do it differently. But ii like them both. Um geeky medics uh MCL Clinic examination. That's a really good book. It's just like slightly more detail and especially moving towards finals. It gives you um better understanding around the topics as opposed to just learning and then just practicing early with your friends basically uh is, is the best thing having your study bodies and um you know, really like being critical on each other, but spending lots of time practicing together is, is the best way to learn for almost, I mean OSC but also M CPS as well. Cos you, you quiz each other on things. Uh and then just extras if you are interested in eyes, then there's this GG exam and the deadline to sign up is seventh of May. And you know, Doctor Michael Williams, if you wanna, if you wanna join, and it's good for your portfolio, whether or not you want to do ophthalmology. But if you get in the top 60% then you get a point. And it's basically uh uh you, you'd get it if you were uh applying for ophthalmology or it's just great. If you, if you don't want to do ophthalmology, that's fine. Um And join the KI B Ophthalmology Society with Instagram. I think we'll be doing some teaching in a few weeks time on a weekend, maybe the 20th of April or something like that for um teaching sort of oy. So head down to that and then a few references as well. But yeah, I've got a uh feedback in the, in the shot. I'll put it back in again just in case you haven't seen it and you get a certificate for tonight's attendance. And then also you can have um and also that will give you the slides as well. So if you could do that, that would be really, really great. It helps me out a lot. Um And yeah. All right, I send that directly. I send it to everyone. Oops, cool. Anyway, that's great. Thank you very much. I'll stay out online for a little bit in case anyone's asking questions and feel free to email me if you have any questions on anything else. Um But yeah, thanks for turning up and hopefully you enjoyed that. I found it helpful.