3. Divine Intervention Episode 36 – USMLE Ophthalmology

OK, welcome. My name is Divine. I am gets a PGY one at this point. I just graduated from Med school. Welcome to the 36th episode of the Divine Intervention Podcasts. Today we're going to be talking about ophthalmology as relevant to the USMLE. I would say this is definitely higher for people taking like a medicine shelf or pediatric shelf or Step 2 CQ or most likely Step 3 as well. So let's begin. So the first question says we have a 71 year old male with central, not peripheral central scotomas. Straight lines appear WAVY and blurred when he tries to read. So what's the diagnosis? Well, I hope you're thinking about macular degeneration. OK. ARMD age relief it macular generation macular degeneration and there are actually two types of this disease, right? So there's the wet kind and there's the dry kind. And it so happens that the wet kind is the more rapidly progressive kind. Although even if it's more rapidly progressive, we actually have many more treatment options for wet age-related macular degeneration as compared with dry age-related macular degeneration. Now, for you exams, the big risk factors you want to think about, right? I mean, obviously, it's, in fact, it's the most common cause of vision loss in the developed world, right? So like an industrialized country like the US, for example. But the big risk factors you want to keep in mind for exams are people that smoke. OK, smoking is a very big risk factor. And another unusual risk factor that may creep its way into exams is the use of aspirin. Aspirin, like chronic use of aspirin has actually been associated with the development of age-related macular degeneration. And some big things you also want to keep in mind, right? So macular degeneration, people tend to lose their central vision first before they then begin to lose peripheral vision. OK, So central vision is lost first in macular degeneration before peripheral vision because the macular, right, the macular is very helpful with central vision. Contrast that with glaucoma where people tend to lose their peripheral vision 1st and then they lose their central vision in the end. And in general for dry relief, it dry macular degeneration, right, You find like deposits of drowsing in the eye, right. And again, there's not many treatment options for this. You can give like antioxidants like vitamin ACE, you can give like zinc, you can give beta carotene. Those are classic things that show up on exams as treatment for with ARMD. On the other hand, there are certain things you can do, and I will say classically on exams, First things first, actually, right? If you look in the eye, you'll see like the buzzword on exams you're looking for is neo vascularization, right? So you have all these like weird blood vessels that sort of develop in the retina and they leak fluid behind the retina. And that's what causes many of the findings and the presentation in the disease. Classically, for wet ARMD, you go ahead and do like photo coagulation. You can give VEGF inhibitors like bevacizumab. Remember, VEGF is a growth factor that helps with the formation of new blood vessels. So you can give a VEGF inhibitor like bevacizumab or any bezumab. Those can be used to treat wet ARMD. OK, so that's all I think I'm going to say. And again, the most common cause of vision loss in the developed world is actually macular degeneration. Next slide. OK, so 35 year old male was punched in the eye two hours ago. Oops. He is brought to the Ed by a friend with complaints of visual difficulty in his left eye. He has a sensation of items floating in his visual fields along with bright streaks of light. What's the diagnosis? What's the diagnosis? So trauma victim, floaters in the eye, bright shrinks of light. What do you think this is? I hope you're thinking retinal detachment. OK, this is retinal detachment and actually has a pretty classic presentation on exams. So it could be a person that recently had cataract surgery or a person that was punched in the eye like some victim of trauma or whatever. And then the person could see that, oh, they have like the sensation of like floaters in their visual field or like bright streaks of light. Or they can see that there's like this like shadow that's arising from the periphery of their visual fields and coming more towards the middle or like a veil coming down over their eyes. If you see all those things, I really want you to think about a retinal detachment with regards to risk factors, right? So like trauma, cataract surgery, those are like big risk factors you want to keep in mind for exams. And really the path of Physiology here is that that trauma basically disengages the neurosensory retina from the underlying pigmented epithelia. And if the neurosensory retina then becomes ischemic, then you could run into a lot of trouble. So this is actually an ophthalmologic emergency. Call your friendly ophthalmolog, Opthor resident or internal, whatever and try to get them to fix this as quickly as possible actually. And there are certain things you could do like on exams, classically the thing they go after is like a laser photo coagulation. That's probably the buzzword. You want to go ahead and remember laser photo coagulation. There's some other stuff you can do like vitro bubbles, blah, blah, blah, but that's lower yield. Somebody weren't going to go there. OK, next slide. So newborn with a white reflex in his right eye. So this is a unilateral white reflex and we're suspecting an intraocular mass. Well, I hope this gets you thinking about a retinoblastoma, OK? Remember, it arises from an RBG mutation. And for these kids, you want to watch out for bone tumors in the future, right? Most likely an osteosarcoma. Don't forget the classic association with the somber sign, right? Some somber sign, Cordman's triangle on on radio graphic imaging. So that's just something I want to keep in mind. This will probably be a Pediatrics shelf exam question or Step 2 CK question. OK, next slide now differentiating between amblyopia and strabismus. Differentiating between amblyopia and strabismus. So this thing is something many people tend to mix up on exams. So let me just spend some time and sort of go over this, right? So amblyopia means just, I mean this is generalization, but this this is fine. For example, think of amblyopia as a kind of cortical blindness. OK, these people's eyes are completely normal, but the brain just does not recognize vision from that eye. OK, So amblyopia is when the brain has suppressed vision from one eye. Now, it so happens that there are many things that can cause amblyopia, right? The most common cause of amblyopia, this is very high. You turn. Actually, the most common cause of amblyopia is strabismus, right? So strabismus is just some kind of misalignment of the eye. So if, for example, a baby newborn has a problem where like one eye is like faced in One Direction versus the other eye, the brain could say, OK, you know what, this abnormal eye, let's just go ahead and suppress vision from that eye. That's why this is actually something you want to fix classically. You want to fix it. If it persists for more than three months after a baby is born, you just want to go ahead and just fix it, OK? Because if you wait for the brain to make all its connections, if vision is suppressed in that eye, then it becomes a permanent problem. So it's not something you sort of like fool around with. So I should not have used that word, but it's not something you mess around with. Let's use that instead, OK, So there are many other things that can cause Amlio pia, right? So anything that can basically obstruct light and going through the eye, right? So if a baby has like cataracts, if a baby has like glaucoma, again, all those things can cause a can cause embryopia. But the most common cause is an eye misalignment, which is a strabismus. Now, in general, to make the diagnosis of strabismus, there are many tests you can do. There's like a cover on cover test that you may see on exams. But one classic presentation they may give you on an exam is they may say that, oh, a fundoscopic exam is done and you try to look at for the popularity, right reflex. And you notice that the reflection of the light from the cornea is different. It's like at different locations when you look at both eyes. That's pretty classic for strabismus. So there's a cover and cover test, but there's that cornea reflex test where you're looking in both eyes and the reflection of the light off of the cornea is in different locations in both eyes. It's supposed to be in the same location if you look at both eyes. If it's not, you're really thinking about strabismus. And in general, for strabismus, you want to go ahead and treat with some kind of like they call it like deprivation therapy, if you may, where you penalize the eye that's affected. I mean, I mean, sorry, the eye that is unaffected. See, I almost made that mistake, the pretty common exam mistake for many people. You penalize the eye that is unaffected, right? Because you want to force the brain to use the eye that it's trying to suppress. OK, so penalization therapy, penalize the unaffected eye, make the brain work the affected eye so that things can be corrected. OK, so I think that's all I'm going to say about strabismus and embryopia. And I mean, you can do the penalization like an eye patch, or you can actually do it pharmacologically. You can give like a muscarinic antagonist, right? Remember your muscarini, the parasympathetic system controls a lot of eye movement, right? So you can try to paralyze that eye with the muscarinic antagonist, like atropine, for example. OK next question. 45 year old Asian male has the sudden onset of severe pain in his right eye along with nausea and vomiting. He took a nasal decongestant an hour ago for some annoying nasal symptoms. So what's the diagnosis? Right? So look at the keywords here. This is an Asian male right? So I'm not just putting Asian here because I'm racist or anything like that. No, I'm actually putting this here for a reason right? So Asian male, OK, And this Asian male has the sudden onset of severe eye pain. If I can just add in something here, let's assume this patient has a rock hard eye, right? Hopefully you're thinking about acute angle closure glaucoma. OK, this nasal, the congestant, let's assume it's phenoliphrine, right? Phenoliphrine. Remember, it's an A1 agonist. So because it activates A1 receptors, it causes mydriasis or papillary dilation. That popularity dilation can acutely trigger an acute angle closure glaucoma. So how do you treat this? Basically, you shoot lasers into the eye. You can do like a laser rhodotomy. You can try to reverse that my dry assist by causing meiosis, right? And you could actually cause the meiosis by giving like a muscarinic agonist like pilocarpine, for example. Alternatively, you could give like monitol or acetazolomide to acutely try to lower intraocular pressures, but usually you want to go ahead and do a laser redundant. This is actually an ophthalmologic emergency so that the patient does not become permanently blind. Now, the other type of this disorder, right? This will be the open angle glaucoma, right? That's that one is more insidious, a little more chronic classically presents with loss of peripheral vision, right? And the big demographic you're looking for in exams, especially for the open angle glaucoma, is African Americans for closed angle glaucoma, right? So the acute closed angle glaucoma, you want to think more about Asians on exams and the big risk factors for glaucoma, right? So diabetes is a super, super big risk factor. Being African American is a big risk factor. Let's see what else. If you're taking steroids, steroids are also very big risk factors for glaucoma, although the biggest risk factor, right? So you, for those of you that are taking Step 2 CK, you know, the have this love for risk factors. The biggest risk factor for glaucoma is actually an increase in intraocular pressure. I know it kind of makes sense, but just one of those things you just sort of keep in mind for exams and how is the diagnosis of glaucoma made right? So you can meet the diagnosis with optometry to try to measure intraocular pressures, right? You may also see like this buzzword on exams, gonioscopy. That's also fine. But classically on exams, the right answer is to perform optometry to measure intraocular pressures and on diagnostic testing, right? So if you do like a vondoscopic exam, you'll find an increased optic cop to disc ratio, right? So sort of think of it as the as a doughnut. So think of the this ratio as a doughnut and sort of think of eating the doughnut from the inside. As you're destroying the optic nerve, the, the circle inside the doughnut gets bigger and bigger, right? So the uptake up to this ratio is getting bigger. That's pretty classic for for glaucoma. Now, how do you treat glaucoma? The thing is, there's many drugs that used to treat glaucoma and it's pretty difficult for people to keep it straight. So there are certain ways I try to remember this right? And I feel the best way to remember it is just to be organized. So what do I mean by that? The thing is, how does glaucoma arises? Because we have like aqueous humor problems, right? We have increased intraocular pressures. So The thing is, if you make too much aqueous humor, you could get glaucoma. Or if you have some kind of blockade where the aqueous humor you're making is not leaving the eye, then you could also have symptoms of glaucoma. And The thing is the structures that make aqueous humor in the eye are is the ciliary epithelium. And it so happens that the ciliary epithelium is driven by the sympathetic nervous system. OK. So the ciliary epithelium is activated, if you may, by the sympathetic nervous system classically through beta receptors. Beta receptors. So, and we also said that so you make this aqueous humor from the ciliary epithelium. It goes from the anterior Chamber of the eye, right? Flows into so sorry, starts from the posterior Chamber of the eye, flows into the anterior chamber, and then from the anterior chamber. He drains through the canals of Schlemm, OK. He drains through those angles, the angle between the iris and the cornea drains beyond that through the canals of Schlemm. Think of the canals of Schlemm as being blood vessels, so they are vasoactive so they can respond to vasoactive regions. And then that aqueous humor is drink. So if you basically understand that if that's how everything works, you can basically just go step by step logically and predict the drugs that I used to drink glaucoma. So the first drug class, right, I mentioned that ciliary epithelium makes aqueous humor is driven by beta receptors. So it should make sense that if you give a beta blocker like nidolol or timolol, right, you could potentially treat glaucoma because by blocking those receptors, you decrease the synthesis of aqueous humor. Another thing you could do is you would say, OK, well, norepinephrine is an agonist at beta receptors. So let me just reduce the production of the substrate for beta receptors like norepinephrine, right? So if you give a drug that's an A2 agonist, remember A2 receptors are GI couple, so they inhibit adenylate cyclist, they are found presynaptically. So you release less catecholamines like norepinephrine for example. So if you give an A2 agonist like apoclonidine or bramonidine, those are actually used to treat the glaucoma because they decrease the synthesis of norepinephrine. So there's less sulfate for the activation of beta receptors on cilia epithelium. It also so happens that bicarb, right? Remember, bicarb is osmotically active. It's very good at draining water and increasing the water content of aqueous humor. And we know that bicarb can be made by carbonic anhydrates, right? So if you inhibited carbonic anhydrates with drugs like acetazolamide and dorzolamide, you could also potentially decrease the synthesis of aqueous humor and relieve the symptoms of glaucoma. Now, so we've dealt with the synthesis, right? So we said that. Now let's deal with drainage, right? So a drainage problem. So we know that the angle that can close in glaucoma is the angle between the iris and the cornea. That angle is widened. I mean, I mean, that angle closes when you have mitryasis, but it opens when you have meiosis. So obviously you want it to open, right? So you want to give something that causes meiosis. And we know that that's under the purview of the parasympathetic nervous system. So if you give a drug like pilocarpine, which is a most chronic agonist, you can actually use that to treat glaucoma. And then I also mentioned that the canals of schlemma blood vessels, OK, So those blood vessels, they respond to vasodilators. And we know that prostaglandins are very good vasodilators. So if you give a prostaglandin analogue like a latanoprost or travel Prost, right, those could also be used to treat glaucoma because they dilute the canals of Schlemme. Although remember those drugs can cause like hyperpigmentation of the of the iris or lashes or something like that. It's one of those weird things you want to keep in mind. OK, So and you can also give manitol, remember it's an osmotic thingy. So you can basically acutely reduce intraocular pressures. That's used primarily for acute closed angle glaucoma. OK, so I know we spend time on this slide, but that from ecology is very high yield, shows up a lot on exams. So I'll encourage you to sort of maybe like rewind that and just listen to it again. So that's all I'm going to see with that. So let's move on to the next slide. OK, so we have a 23 year old male presents with a 2D history of severe right eye pain and blurry vision. He has been taking Benadryl for a sinus problem. So let's assume he has sinusitis that began 5 days ago. HEENT exam is notable for pain with right eye movement and 20 / 200 vision. That's really bad, right? So 20 / 200 vision means what a normal person will see at 20 feet, you can only see at 200. I mean, no, what a normal person would see at 200 feet, you can only see at 20 feet. I believe that's what that's what's meant by that. So, so this so this person pain with eye movement and they had like sinusitis that started a few days ago, right? Let me add in this information. Let's assume they have like problems moving the extracolar muscles. So what do you think this is? I really hope you're thinking about orbital Cellulitis. OK, Usually for this you actually want to go ahead and do, I mean you can diagnose it clinically, but many people prefer to get like some kind of ocular imaging, like a CT scan to meet the definitive diagnosis because this is actually an ocular is actually an ocular emergency. It's not something you want to mess around with basically orbital Cellulitis, you have like inflammation of the eye, especially like the fat around the eye or the extra ocular muscles. And it's usually caused by like many bugs at the same time, right? So it's classically polymicrobial, although Staph aureus, right? And like Strep species can also cause a 'cause this problem, but most commonly it's a polymicrobial kind of infection. And again, you meet the diagnosis with an like an Oculus CT scan. Remember, you want to be able to differentiate this from preorbital or preceptor Cellulitis. Although in preceptor Cellulitis, the big thing I want to remember is that usually these people don't have any pain with eye movement. And they do not have like involvement of the intracular muscles. Those are two key things that will help you differentiate preorbital Cellulitis from orbital Cellulitis. And again, you confirm the diagnosis of orbital Cellulitis with an ocular CT scan. Now, how do you treat orbital Cellulitis? Right. So I said that. And again, like all these antibiotic regimens, it's really hard to memorize, but there are just certain logical ways to think about this, right? So I just said that these infections are classically caused by like it's usually pulling microbial, right? But it could be caused by Staph aureus or strep species, right? So you already know right off the bat that you want to cover Staph aureus, right? So usually give like a drug cocktail for orbital Cellulitis, right? So you know, OK, I really want to cover Staph aureus, right? So you should make sense that a drug like Clindamycin or Bactrim, right? Trimethoprim sulfa, methhoxazole could be used to treat orbital Cellulitis, but there are also strip species that could cause this problem, right? And strip species are not covered very nicely by Clinda, right? So you usually want to add on something, you want to add on some kind of penicillin, right? You may add like amoxicillin or amoxicillin plus clavolinic acid or like a third generation Cephalosporin, right? Like a like ceptrioxone, for example, IV ceptrioxone, you can use that for for orbital Cellulitis. OK, so let's see, is there any other thing I want to say here? I don't think so. So I'm going to going to keep going. But remember sinusitis is probably like a big risk factor. You want to sort of keep in mind, for example, with orbit ulcerolitis. OK, now next question. A 23 year old female presents with a 2 day history of severe left eye pain. She can barely see anything out of the left eye. That's not good. Now here's the kicker. The patient mentions that the visual difficulty gets worse after she takes a hot shower. So first of what does this patient have neurologic symptoms that get worse in warmer temperatures? That's something known as U tops phenomenon. It's pretty classic in multiple sclerosis, right? So this patient with miss that has visual difficulty obviously has optic neuritis. OK, this patient has optic neuritis. Usually you make the diagnosis clinically. If a person has like a history of miss present on eye pain, you almost pretty certainly have a optic neuritis. Although if the diagnosis is like called into question and they are trying to get you to pick an imaging test on exams, go for an go for Mr. imaging. This can be identified pretty well on an MRI and the classic disease association. Again, multiple sclerosis, like if you see multiple sclerosis and eye problems, the first thing you should have a basically you should have a very good reason to not pick optic neuritis on exams. And really the pathophase involves like an inflammation, like demyelinating inflammation, if you may, of the optic nerve, that's cranial nerve too. So if you have that inflammation, it can present as an Afrin papillary defect. So these people tend to have like visual difficulty. They say like, oh, they're not seen out of this eye. They have pain in that eye, pain with eye movement, blah, blah, blah. And usually it resolves overtime, like over like a two to three month period. The vision usually comes back at least for the most part. Although this is something you definitely want to treat right because it's pretty painful, it's pretty debilitating. So usually you start with like a topical steroid actually, whoops, sorry, usually start with an IV steroid, IV steroid. That's why I actually put a sorry, I'm seeing many of these things from memory, but usually start with an IV steroid are not oral. So that's why actually put this unique treatment business here on exams, if they give you 2 options and four steroid is one option and oral steroid is another option, go ahead and pick 4 steroid. No one really knows why. But in general, oral steroids increase the risk of recurrence of optic neuritis. So usually when you start treatment, you start first with four steroids and then if you want to like taper the patient, you can then switch to oral steroid. But usually very high. You to know this actually you start with four steroids and again, the most likely sequel of diseases that it will resolve overtime to resolve overtime. OK, so I think that's what I'm going to say here. So let's jump up to the next slide. So a 76 year old female comes to her PCP for a routine annual exam. She complaints of a six month history. So this is the classic we will give you this question on exams. So you probably want to pay attention here. So 76 year old female comes to a PCP for a routine annual exam. She complaints of a six month history of difficulty driving at night and reading Rd. signs. Difficulty driving at night, reading Rd. signs. If you see this, the first and only thing you should think about on any USMLE exam or MBME test is cataracts. OK, you definitely, definitely, definitely want to think about cataracts and really the path of phase here is that you have something that will pacifies the lens. OK, So you don't see as well. So classically these patients they see oh, they have trouble reading small print or they cannot read Rd. signs or they cannot Dr. comfortably at night. If you see all those things, think about cataracts, OK, And the big metabolic risk factor, right, is diabetes. Remember diabetes, you have a very high level of glucose alcohol. Let's see, what is that enzyme known as? Let's see all those reductis, all those reductis, sorry, I had to put on my step one hand there for a second, but all those reductis converts the glucose to sorbitol and that's sorbitol, right? Usually the lens of the eye does not have a sorbitol dehydrogenase, so you cannot convert the sorbitol to fructose. So that sorbitol accumulates in the lens. You can have a pacification of the lens and then you have cataracts, OK, The drug associated risk factor, definitely, definitely think of steroids. Steroids cause many eye problems. They cause glaucoma, they cause cataracts and the big infectious risk factors, right? So these are more congenital infections, right? So like a like congenital syphilis or congenital CMV, right? Those can both definitely both present even congenital toxin or congenital toxoplasmosis. Those can definitely represent as a, as a like their infectious causes of cataracts. And then if you see like a newborn with bilateral cataracts, the first thing you definitely want to think about is classic galactosemia, right? So hopefully remember this from step one, although trust me, this is certainly not low yield for Step 2 CK or pediatric shelf, especially if you see bilateral cataracts in a newborn, you really, really want to think about classic galactosemia, right? Remember the pathophase involves a deficiency of the enzyme galactose 1 phosphate radial transferase or Gault. So we can present as bilateral or cataracts because that galactose is converted to galactitol and it accumulates in the lens and opacifies it. And I just put this here as a as an aside. It's just one of these things that almost everyone gets wrong on exams, but hopefully you won't be one of them because you listen to this podcast. But E coli sepsis is the most common cause of death in patients with classic galactosemia, E coli sepsis. No one really knows why, but it's a bizarre association you want to lock into your mind for the future. OK, next question. So the most common cause of conjunctivitis in the 1st 24 hours of life, right? So hopefully you know this to be a chemical conjunctivitis. Classically it's from like silver nitrate. Generally pediatricians don't do this stuff anymore to kids. They usually, they used to use silver nitrate back in the day to treat prophylaxis against conjunctivitis, but they don't do that do that anymore 'cause it causes a chemical, a chemical, a kind of conjunctivitis. So 1st 24 hours of life, the answer 100% of the time on exams is a chemical conjunctivitis. Now if you have a five day old newborn with super purulent conjunctivitis, I really hope you're thinking about a bacterial conjunctivitis. And actually the bug I'm going for here is a gonococcal conjunctivitis. So this baby basically acquired it from mom's vagina. And for this you generally want to go ahead and treat with like a third generation Cephalosporin. And classically on exams I would say to go with cephotoxin IV. Cephotoxin, ceftriaxone is is an OK option. That's fine, but ceftriaxone can cause lycolaesthesis in newborns and it could also cause chronic ters. So that's classically avoided. So baby self traction is essentially sephotoxin. So that's probably a safer exam answer to go with. And for gonococcal conjunctivitis, the way you prophylaxis is actually with a topical macrolate, like a topical erythromycin. They love to do this play on. They love to mess with people's heads with this stuff. You'll see what I mean when I go to the next presentation. But again, let me review this. The bug for this presentation is gonna caucus right. So like purulent conjunctivitis is really like the first two to five days of life. Think about nicer gonorrhea, okay? Vertical transmission from mum you'll treat with cephotoxin, IV cephotoxin. If that's not an answer choice, we would IV ceptrioxin. But you can prophylax by giving a baby topical erythromycin, OK? That's why every newborn like within the first 48 hours of life, they get erythromycin applied to their eyes, OK, Because you're trying to prophylax against my serial gonorrhea. It is mega high you to know that that topical erythromycin does not prophylax against Chlamydia trachomatis. It only prophylaxis against my Syria gonorrhea. Very high. You ought to know that. Now the next presentation says we have a 12 day old newborn with watery discharge, conjunctivitis and eyelid swelling. So what's the bug? The treatment, prophylactic relationship to presentation to pneumonia presentation down the line, numbilias blah blah blah blah blah. OK, so let's talk about that. So the Bulg I'm referring to here, right, is chlamydia, right? So chlamydia classically causes a conjunctivitis in newborns. It's usually like 5 to 14 days after birth and on exams. If you see purelline discharge, you're thinking of gonorrhea. If you see watery discharge, think more about chlamydia. Think more about chlamydia. And the way you treat chlamydia conjunctivitis is actually with oral, not topical oral erythromycin. Again, not topical oral erythromycin. So you may say like, oh divine wait, you're 3IN erythromycin around so much. Let me make the point clear again. Oral erythromycin is used to treat chlamydia conjunctivitis. Oral Erythromycin is used to treat chlamydia conjunctivitis. However, topical erythromycin does not prophylax against chlamydia conjunctivitis. Typical erythromycin only prophylaxis against gonococcal conjunctivitis. I know you may say I'm being too particular with this, but I promise you this is super, super high yield. For example, Now remember chlamydia, right? It can cause a pneumonia in newborns, and classically, they'll describe a newborn with a staccato cough. If you ever see that buzzword, you want to think about a chlamydia or pneumonia. And if for example, let's assume a kid has chlamydia conjunctivitis as a newborn, they get orally through MYCIN for treatment and resolves and then they tell you that weeks later the kid presents with a non bilious vomiting. I really hope you're thinking about pyloric stenosis, right? Remember pyloric stenosis loves to afflict a first born males. But exposure to a through MYCIN in the first few weeks of life is a very big classic risk factor. OK, so non bilious vomiting, peer shape mass in the abdomen, think about pyloric stenosis. And really of the three conjunctivitis presentations that I present here, basically the gonorrhea 1 is the worst it can cause like a corneal ulceration, it can cause permanent blindness. So you don't mess around, you go ahead and give a IVCF traction within hours to prevent to prevent blindness. OK, good. So next one. So this is 9 B, what is the most likely cause of conjunctivitis? So the first presentation is glutenize in the morning and unilateral, although this may subsequently become bilateral if you may watery discharge and the person has rhinorrhea, right? So they have like a viral program, if you may, right? So hopefully you're thinking about a viral conjunctivitis. And in general for this on exams, they may ask you like, oh, how do you treat this? And I can almost promise you they'll put an answer that says to give like antibiotics and all that crap. Don't do any of those things. Usually the answering exams is like a warm or cold compress of some sort. OK, if that has already been done in the exam question, then you could consider giving like a like an antihistamine eye drop or something like that. But I'll say you'll go to answering exams is like a warm cold complex, blah blah, blah. The high yield bug you probably want to think about is adenovirus. In fact, adenovirus causes this. They classically call it a pharyngal conjunctivitis. Pharyngal conjunctivitis it causes, if you see a person that has pink eye and sore throat, think about adenovirus. And I just want to draw your attention to the fact that adenovirus can actually also cause like a gastroenteritis and it can also cause a hemorrhagic cystitis. Just one of those bizarre things people never think about, but sort of keep it in mind with adenovirus. And actually viral conjunctivitis is the most common kind of conjunctivitis, OK? The most common cause of conjunctivitis, just in general, if you're looking in through the lens of epidemiology, viruses now presentation #2 or glutenize in the morning, that's unilateral. But again, this usually starts unilateral, then becomes bilateral, and then you see like a purulent discharge and no rhinorrhea. Think more about a bacterial conjunctivitis, it's usually caused by like staph or strep species, but the most common cause, so this is higher, the most common cause of bacterial conjunctivitis in human beings is Staphorus is Staphorus. And in general for this you want to go ahead and give like a, an antibiotic ointment or drop, right? So like an erythromycin eye drop, for example. But if the person has these symptoms and in the question you see that the patient is a is a person that uses contact lenses, you probably don't want to use a topic or like a macrolide eye drop. You want to go ahead and use a fluoroquinolone eye drop. OK, like an off oxysing eye drop if you may, but it basically has to be a fluoroquinolone because you're trying to cover Pseudomonas. Pseudomonas is a very common cause of conjunctivitis in contact lens wears. Now the third presentation is a patient with a history of asthma and you have a bilateral itchy red eye, right? This is pretty classic for an allergic conjunctivitis. Usually for this you don't do much. I mean you can give like an antihistaminide drop or a mast cell stabilizing eye drop. I know some names have seen the literature drugs like azelastine or olapatadine blah blah blah. But those are super low. You'll just think of antihistaminide drop or mast cell stabilizing eye drop and that should be fine for for allergic conjunctivitis. And this one starts off bilateral right off the bat and you'll describe a person just has like water secretions from the eye is bilateral. There's a lot of itch. If you see that think about an allergic conjunctivitis. Now next one. So eye pain plus pain worsened with light in a twin 3 year old male with a history of chronic low back pain and a morning stiffness right. So this patient probably has a A history of ankylosing spondylitis. Remember, all right, like young male with low back pain, stiffness in the morning, that's ankylosing spondylitis. Remember it's one of your seronegative spondyloarthropathies which are associated with HLAB 27. So this is so this what does this patient have? So anterior ankylosing spondylitis with visual problems. I really hope you're thinking about anterior uveitis. OK, Until UVIT, it's also associated with like sarcoidosis, right? So African American female bilateral highlightenopathy, like difficulty breathing, think about sarcoidosis until UVIT can be a presentation of sarcoid. If you're going into the realm of pediatric rheumatology, you probably should really think about what is this condition called Posiarticular Gia, although I think now it's called oligo, oligoarticular, if I am not mistaken. But yeah, where you have like involvement of like 4 joints or less, that's actually a pretty common presentation. In fact, one common exam question is to say that like basically describe a kid with JA. And then they say like, so I mean juvenile idiopathic arthritis, excuse me? And then they say that in addition to blah, blah, blah, what is the next best step in management? And the answer may be to do a slit lamp exam. Watch out for that because again, anterior uvit is a very common presentation in oleggo. I think the older term was like posiarticular juvenile idiopathic arthritis. You should probably drink some water. OK, so so how do you diagnose this slit lamp exam? How do you treat this, right? So if it's caused by HSV, right, you may want to go ahead and give like acyclovir, like oral acyclovir. That's usually a Val Acyclovir talked about that in the Micropharma podcast on antivirals. Although in addition to that, you can also add like a topical steroid, OK, If it's caused by an autoimmune phenomenon, you also want to again use a topical cortical steroid like a topical or glucocorticoid. If that's not working out so well, then you can go to the oral stuff. You can switch to an oral steroid, but if it goes by some kind of bacterium, just go ahead and treat the bug. Like if it's caused by Pseudomonas, you want to specifically treat Pseudomonas. OK, Generally for bacterial causes of anterior uveitis, you don't need to use any kind of steroids. So steroids are used primarily for viral, for viral causes and for autoimmune rheumatology causes, if you may. So next question, a 70 year old female with difficulty reading books, she often has to move the book away from her eyes, right? So like holding the book at arm's length to make our words on the page, right? So this is a pretty classic presentation of Prince biopia. OK, Basically as a person gets older, the lens gets less elastic, right? So he cannot adjust to accommodate when a person is trying to read. So they have like loss of lens elasticity. That's the path of Physiology right there. And classically they will say like, oh, if they hold the book close to their faces, they can't see very well. Because they cannot accommodate because the lens is inelastic. So they have to hold the lens at like arm's length to be able to see anything. That's pretty classic for presbyopia. OK, next question, differentiating a central retinal artery occlusion from a central retinal venous occlusion. So this thing is, it's like Florida High yield for exams. So let's talk about it. So on exams, if you're trained to differentiate a central retinal artery occlusion from a central retinal vein occlusion, there are certain big things you need to look out for, right? So for a CRA for retinal artery occlusion, right? So this usually presents on exams as like acute painless monocular vision loss. OK, so remember that buzzword acute. So it's like very quick painless doesn't hurt monocular in one eye, not in both eyes, in one eye. OK, acute painless monocular vision loss. Acute painless monocular vision loss. And they may also say that it may also present as a like a morosis fugacs where for example, the person says like, oh, they felt like a curtain coming down over their visual field. In general, for that, you you can do like a fundoscopic exam, but usually you try to do like some kind of like ocular ultrasound to meet the diagnosis. But on exams, they almost always put what you find in the fundus. They could tell you that you'll find a chariot spot in the retina. OK, but here are the things that would guide you away from a central retinal vein occlusion and say, Oh yeah, this is definitely a central retinal artery occlusion on an exam. They will tell you that there is a, they are thin retinal vessels, right? So the retinal vessels are thin and then they will also tell you that the person has fondal power. So the fondus is like pale and white. If you see that presentation, do not pick central retinal venous occlusion as you answer pink as pick a central retinal artery occlusion. Contrast this with and actually for this, I guess I'll just go ahead and talk about it all at once. You can try to show like hyperbaric oxygen if the person is like en route to the hospital, you can do like an ocular massage you when the person gets to the hospital, you can actually go ahead and give ATPA. You try to give it within like 4 hours to prevent the permanent blindness. So contrasting was a central retinal venous occlusion right where they may tell you that oh you see like the cherry red spot on the retina. But there are certain things that will guide you away from a CRO and and instead guide you towards the CRV as your diagnosis right? So if they mention that you see like dilithet retinal vessels right? Think more about CRVL, contrast that with the thin retinal vessels that you find in CRL and then instead of having the fondle power that accompany CRL and CRVL, you tend to have like a blood and Thunder appearance of the retina, right? You see like cotton wool spots, blah, blah, blah. If you see those things, think more about a central retinal venous occlusion. And actually the I said that central retinal outer occlusion, you do a fundoscopic exam and do like an ocular ultrasound for a central retinal venous occlusion. You actually do a fluorescein and geography. OK, not an ultrasound. You do fluorescein and geography and the treatment is also different. You don't do like TP or any of that crap. No, the thing you do here is you, you can give a VEGF inhibitor, you can do a like laser photo coagulation. Those are things you can classically do for a central retinal venous occlusion. That is not what you do in a central retinal artery occlusion. OK. And then step one, throwback to lysosomal steroid diseases. I'm just throwing this in here as a bonus for you. Don't forget that your T Sachs disease, right? So a kid that's losing more milestones has an abnormal startle response and they say he has a cherry red spot on the macular. You really want to think about T Sachs disease, right? That's a hexo so many days, a deficiency. But those kids tend to not have hepatosplenomegaly, right? Contrast that with the analogous close causing disease, Neiman Pick disease where those kids may have like a chair red spot on the on the macular, they have hepatosplenomegaly. So that's I believe from a sphingomyelinase deficiency, OK, from a sphingomyelinase deficiency in T Sachs, it's a hexosemidase E deficiency. So GM2 gangliocyte builds up. So just a throwback there since we're talking about chair red things in the eye, I guess now in diabetic retinopathy, right? The classic findings on an exam, right? You see, you see like dot and blocked hemorrhages. Then you put hard exudates. These are just buzzwords you want to remember. You don't necessarily need to be able to like see those like be able to like see those things on an exam. They usually describe it for you, right? So let me see cuts in wool spots, but on blood hemorrhages, heart exudates. Think about diabetic retinopathy. Diabetic retinopathy actually usually has two types. There's like the proliferative type and the non proliferative type. If you see the buzzword neovascularization on exams, you want to think more about a proliferative diabetic retinopathy. And basically if your person is diagnosed with diabetes, you go ahead and do a fundoscopic exam at the moment where you meet the diagnosis of diabetes and then you go fundoscopic exam every year afterwards. But if you're suspecting diabetic retinopathy, if you want to make a definitive diagnosis, you use fluorescent angiography. You may be seeing that. Wait, divine. Many of the findings for diabetic retinopathy appear to parallel central retinal venous occlusion. Yeah, that is absolutely right. That is why both disorders are diagnosed definitively with fluorescent and geography. And really, how do you treat diabetic retinopathy? Right. So you go ahead and try to control the blood pressure, control the glucose. You can do laser photocoagulation, you can give a VEGF inhibitor just like a central retinal venous occlusion. OK, so hopefully that helps you make a certain parallels with regards to treatment. OK, so the last question, a 19 year old female presents with pain and a foreign body sensation in the eye. She wears contact lenses, right? So you should never get this kind of question wrong on an exam. What is this? I'll let you think about it for a bit. So this is a corneal abrasion. OK, it's a corneal abrasion. Usually you don't see this with a naked eye. So you need to your diagnostic test is usually like you put like that fluorescent dye in people's eyes and do like a like a slit lamp exam. And for this in general for treatment, you can give like a topical inset drop for the eye. You can put on like an eye patch, whatever. But in general, if they give you the buzzword that the patient wears contact lenses, you definitely want to give that patient antibiotics. You may want to use like antibiotic eye drops, right? Especially like a fluoroquinolone eye drop because you're trying to cover pseudomonas. Basically, if you ever see the word contact lens and eye and like an infection or whatever eye problem, think about giving that person some kind of anti pseudomonol eye drop. OK, classically on exams, it's a fluoroquinolone eye drop. So I know this podcast sort of run along, but I can promise you that it will pay off huge on either the pediatric shelf, your medicine shelf, definitely. And on Step 2C can almost certainly on Step 3 as well. So this is something I would definitely listen to over and over again. Take good notes, try to make sure you can keep these things straight. And I will see you in the next podcast. Have a wonderful Sunday and God bless. Thank you.