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We'll still lives on it. Yeah. Well, anyway, I think we'll just introduce ourselves, I guess in the meantime. So I'm Chris. I'm a doctor at Royal Sussex County Hospital in Brighton. And then m is my friend. So we're both friends. I have. Oh, sorry, sorry, I'm hi, I'm Emily. I'm a doctor at Eastbourne Hospital. I work with Vicky and I'm currently on at the moment. Yes, I'm Vicky. You might have seen me in some of the previous sessions. I'm also part of the committee of Med teaching. Um, so, yeah, thanks to Chris and Emily for joining today to teach us some ent in dermatology. So I think in the interest of time, let's get started. Um, and like I said before this session is gonna be recorded and be uploaded our me page, our youtube, our website. So they're not if you have friends that want to attend the session but can't attend at 630. That's ok. We've got it covered. So let's make a start then. Um, so just a little bit of background about the organization. So the overall organization is called Med Teaching. The, the final series is called Thursday 15, but it's not just for final year students, obviously that's the aim. Um, but it's very relevant for other year groups too. As you're gonna cover these topics in all your exams at any stage. Really. Um, the concept is meant to be sort of 10 to 15 minutes of timed MC QS. And in this session we're gonna spread it out throughout the session. So instead of doing them all at the beginning, we're gonna do it er throughout the session and we'll get some data on whether you prefer that or not at the end. But I think it will just make things go a little bit quicker. Um And we'll make sure to cover the answers and give you a bit background knowledge about why the answers were or weren't correct in the MC Qs. Um And then in terms of future sessions, we mainly run them on Thursdays. However, we've got some coming up on the Tuesdays, for example, next Tuesday we've got GI and next Thursday we've got mental health. Um And you can find recordings on these sessions, like I said on me or youtube and our website and we'll provide links for this at the end of the session. So I will hand over to Chris now to make a start on the Dermatology section. Uh So, yeah, take it away and just let me know whenever to change the slides. All right. OK. Thanks so much Vicky for that intro and for hosting this. So if you just, yeah, go to the next one. So this would be our format and um basically what we will cover. Uh So some of these Il Os, we won't cover everything. But we have basically um given you sort of some questions that will kind of, you know, blanket a few more high yield topics, maybe some things that you haven't seen before in dermatology that could come um on your exam. OK. So if we go to the next slide and then the first question, so how we'll run this one is, um, if you, if I'll read the question out to you and then um the options as well and then if you can just sort of write down the answers, I'll put them in the chat box and then we'll go to the answer after each question. So for this first question, um a 25 year old male with suspected tonsillitis presents to the emergency department following treatment of days or so given to him by his GP, he presented the rash on below. I don't, I know he doesn't look 25 in this picture. So just ignore that. But if you go to the next slide, um So basically, we're gonna ask what's the most underlying cause, most likely underlying cause of a rash? So A is an HIV associated maculopapular Exanthem B. Is it due to treatment of Epstein Barr virus with amoxicillin? C? Is it Urticaria is it a for photodermatosis or is it psoriasis? So, if you guys just put your answer in the chart, I'll give you like a minute to answer the question and then let us know and Vicky, it might be best if you go back to the other slide for a sec, I think just because I can't see the picture that. All right. Um We've got one answer in the chat already but we'll give people another few minutes. Oh, sorry, a few seconds to answer. Yeah. So if you remember a was HIV associated macular papi Exanthem B was Epstein Barr. Um I believe C with urticaria. Yeah. D photodermatosis or gutted psoriasis. OK. So I'll keep it on the side of the moment. Let me know if you want me to switch back. That's OK. Uh Thanks. Is everyone happy with, with that answer? So, nausea sad be um if anybody else wants to put their arms in the chat, they can. But if we go to um the next slide, yeah. So the answer was be that is correct. So basically, it's quite a common question. When I was in medical school. We we'd get asked this quite often. So in this case, when you treat somebody with glandular fever with amoxicillin specifically, you usually get a sort of nonspecific drug rash. Um That's benign in nature. So it's not actually gonna be lifethreatening and doesn't require any treatment. The only thing you're gonna offer them usually is an emollient, um like 5050 ointment or, you know, something like s or something. But like there's no, there's no need for steroid or anything like that. It usually self resolves. Um if we have a look at the other ques other other options. Sorry, see urticaria, this doesn't sort of present like an urticarial rash, you usually see wheels um which are basically raised uh macular lesions with um no overlying pigmentary changes, but they usually are erythematous. And the annular an annular basically means that they are shaped sort of like a circle but like squiggly. So if you think of like a squiggly circle, that's usually what an annular lesion is. Um photodermatosis isn't really aligned with the stem. It's usually triggered by um exposure to the sun and then guttate psoriasis. It's sort of that raindrop like pattern all over the body and that usually happens after the infection has resolved. So it usually comes on 1 to 2 weeks following the infection and the pa patient usually feels completely well in themselves. And that's also something that doesn't usually require treatment. Ok. Um If you go to the next slide as well, the key, yeah. So basically, I'll just put same explanation here. IMIL drug eruption that occurs when glandular fever or SCE virus treated with amoxicillin. It's benign and it will self resolve, usually discontinue treatment, amox, you can maybe even get them a spot test, but that would not be something that's absolutely necessary. Ok. Um, if you go to the next slide as well, I just put here sort of some drug reaction differentials. So, drug reactions that are absent of systemic symptoms are usually far more, um, sort of common and, and less worrying in a clinical setting. So you've got drug induced urticaria, which everybody knows is sort of a, quite a bit of a skin rash when I took that medicine, usually just discontinue that medicine and swap to a more suitable medicine. Um A Mobi drug eruption is usually like sort of widespread but doesn't actually cause any systemic symptoms or upset. Um I mean, acne, you can get acne from, from some drugs as well. Uh That evidence for that's kind of shaky and then a fixed drug drug eruption is usually when you get sort of one little spot on your body blister and that can be a fixed drug reaction. It's usually also nonlife threatening. Um When you wanna be concerned about a drug reaction or sort of obviously cases like anaphylaxis where you get um sort of hemodynamic instability, airway distress. And we all know the management for that is usually uh I am a and then in aggressive fluid resuscitation. Um the guidelines now also recommend that you give them antihistamines and steroids but not in the acute phase. They actually don't help very much in the acute phase. Ok. So the guidelines basically recommend the um repeat adrenaline shots and the, and the fluid recess in the acute phase. Um if you've never heard of dr it basically is sort of a drug reaction with erythema and systemic symptoms. So it's, you know, I mean, names a bit silly, but it basically is a nonspecific drug reaction that causes hemodynamic instability. Um, agep is uh basically acute granuloma granulomatous reaction with. Um so they all just present a little bit differently but they are sort of along this of, of the same family. And then Stevens Johnson syndrome or SJS and 10 involve the sort of sloughing of the epidermis. And those are obviously concerning because hemos homeostasis is affected and temperature regulation is also affected, which can lead to sort of um cardiac instability as well. And ecg changes associated with hypothermia like J waves and things that we don't have to get into it, but you just need to be aware that they can happen. OK. And so in this, this table is just gonna differentiating when something is sort of life-threatening when something is not um life-threatening in terms of drug reactions. All right, if we can go to the next slide as well to the next question. So in this question, we have a 21 year old woman who presents to the emergency department following a burden from a corrosive chemicals is pro in the initial stages following insult to the skin, the patient irrigated the wound with which of the following substances causing worsening of the chemical reaction. So, a potassium chloride solution, B mineral oil, C calcium gluconate gel, D sodium chloride 0.9 solution or e water. And you can see in this photo that the patient basically has had some damage to the um epidermis and the dermis. It looks like they've got a bit of um a hematoma underneath the skin and they've had some death of the top layer of skin. And you can see that on the fingertip that's now dead and will probably fall off soon. OK. So if you guys just put in the chart, what you think it might be? Does anyone want a guess? Maybe just like no answer, a silly answer. Um I'll explain why it is what it is after. So just if anyone wants to g one of them, you're not sure. OK. So you got a anyone else wanna ask before we go through it? OK. Let's um Vicky. Can we go to the next slide? OK. So basically, this is actually a really good one to know. Um I know we don't get taught lots about burns. But if you, so if someone works in sort of a chemical plant and they are interacting with um sort of these solutions that are salts of, of metals, right? So um if you have a salt that's basically in involving a me like lithium magnesium potassium sodium and they're quite reactive to sort of the air and water as well, they are usually were like burns or injuries. Um Are you sustained from them or worsened by irrigation with water? Because it actually um the lower the ph and can sort of um increase the rate of reaction of your me chemistry. So, in this case, water will actually donate its H plus ion. OK. And cause worsening of the reaction. So, what you want to do is sort of snuff it out in a way and prevent it from, from reacting further to mineral. OK. Can we just decide on the question once? Um um did you uh let me just finish explaining this? But first, so in this case, when you, if you get burned by a corrosive substance, that's a salt of a, of a metal like lithium magnesium or potassium. Um You usually actually wanna irrigate it with a mineral oil. OK? Because it stops the oxidative process from continuing. So it's a kind of action. Uh Do you wanna go back to the first slide Vicky for question one? Sorry, we'll give it a few seconds. Yeah. Is that OK? No, and we can, we'll, we'll record the session so you can always head back at the end. Is that OK? Yeah. Brilliant. OK. So let's go back to the burns but because we not finished. OK. So yeah. So in this, in this case as well, it's know about skin burns. Um It's actually quite sort of simple to understand, but in a first degree burn, usually the epidermis is the only layer that's affected. Ok. Um, now that what tends to happen with that is that you get the sort of loss of the top layer of skin and it can be quite painful. Ok? Because you've got lots of nerve endings within the, within the, um, epidermis and dermis. Right. When a skin burn goes down to the dermis, it also painful and that's your urine. Um, when you've got a skin burn that's gone down to the dermis, you may not get full recovery of the epidermis. Um It just depends on sort of your ability to heal some people scar more than others, et cetera. Uh We're all a bit different genetically. When you get a third degree burn, these burns tend to go down all the way to the hypodermis or the subcutaneous tissue. Um When you get a third degree burn, it actually tends to be quite painless cause you've lost that layer of the dermis where most of the nerve endings lie. And when you get a full thickness burn like that, um then there's sort of, you know, a higher risk for infection, et cetera. Um And usually it to be managed in a burns unit, um, you may need things like skin grafting. But another thing to remember for burns is that if you use, um, if you, if you've got a patient with a burn, it covers a lot of their body surface area. Remember that they're gonna require more fluids and things like that when you come to sort of an emergency department setting or if they come in as a trauma. So you're gonna need to use a, the Parkland formula, um, to calculate their fluid requirements because it will be much higher than someone who's got all of their sort of skin intact. Um And if you guys have MD CAL, that's a really good app and it's got all the formulas on it. Essentially, you sort of measure your body's your body's surface area in nines. So it's like nine for the front of the arms, nine for the for the thigh, things like that. But if you have a look, you can see, you know, the percent, the sort of percentages that they used to um divide the total body surface area up into. All right. OK. So it's the next slide. So question three is you got a 42 year old female presents the GP with a 12 week history of discomfort at the base of the nail of her left thumb, an expanding white plaque on the nail of the affected finger. Uh You can see that easily in the photo based on the the following treatment. First line. So we've got Ciclopirox. I think that's how you say it, which is um antifungal nail Lacquer, right? It's a nail polish, basically, uh oral terbinafin. Are we gonna do a medical nail avulsion and remove her entire nail. Are we gonna give no and just say it will resolve on its own or are we gonna give her something like oral ivermectin? Um, ok. Uh Maybe like if you wanna go back to this time and then come back to this just so they can see, keep this on for about 10 seconds and I'll move on to the, um, answer options as well on this question. I think it's important to just have a look um at where the actual lesion is. Um that will sort of de determine which management is best fine. And I'm just gonna move on to the answer options now. Yeah. There we go. Let me know if you want to switch back. Anybody have any ideas what they might, she, I'll quickly go back to sleep. You've got b so we've got um yeah, one for b anybody else. OK. Why don't we just go to the um A so Vicky is fine? OK. Yeah. So actually these is correct, fairly good job. Um In this case, the proximal nail folds involved, as you can see, and that's gonna affect the nail matrix with the nail matrix is basically where the nail grows from, right? So the nail grows in the nail fold, Atrix. So in this patient, um you're gonna wanna treat them with oral therapy because this is unlikely to resolve with something like nail lacca just because you can see as well with the fact that it's, it's raised, means that it's already in. So, um, sort of far in that's probably causing a little bit of inflammation and antifungals don't really work very well topically, unless there's sort of constant clipping of the nail. So, what they even tell you to do when you have a fungal nail problem when you're using something like a nail locker is you've got to rough on the surface of the nail to try and increase penetrance of the actual um drug like topical drug, topical solution. Um Don't tend to work very well. And then you usually have to treat that nail for up to three months, ok. So it may be a viable option and those with Onychomycosis that I put there. Um But if it only if it affects the distal nail plate and you have to apply, apply it at least a few times per week, usually it quite a lot of time. So it at night and then it's usually, it's usually used for a really long time like three months. So you'll be battling that fungal nail infection for, you know, a while. Um In this case, I would give this patient an oral medicine for at least two weeks or so, see if it helps and then you might give it for a further two weeks until they infect until, until you are sure that the infection it OK? Go to the next slide, please. Right. So this is just a dis uh nail disorders, right in patients in dermatology patients. So it's really, really simple to remember, but just have nail pits or depression, sort of markings on the nails. They usually signs of an autoimmune process going on. So in that second box left, you can see nail pits or depressions usually are a sign of psoriasis, alopecia or a connective tissue disease. So you'd wanna be concerned about something else if you find your patients as I've got loads of pits in my nails, they grow at odd rates or they tend to just fall off on their own and things like that. Um Adding more suspicious of an autoimmune cause uh horizontal wedging can be a sign of zinc deficiency, oh diabetes as well. Um and yellowing of the nail too, that diabetes uh usually because the blood supply is poor to the sort of distal bit of the nail and then it starts to turn yellow just from oxidi oxidization like with the air and because the blood supply is poor, right? So it can and both sign of fungus, but it's not a sign of having a fungal nail infection. Um having brittle nails may also signal pal nutrition, um low, you know, low Vitamin A or Vitamin C, things like scurvy and stuff like that, um or thyroid disease. Ok. So those are just something that you should. So, so some things that you should be aware of um having a dark mark in the nail could be a Melanonychia, which can be completely benign or if it extends definitely from the actual base of the nail, you'd wanna, um, suspect Melanoma. Melanoma are usually in atrial means that they occur on these parties of the fingertips and things like the, um, and they are usually sort of the ones that are most easily missed and they are more common in people of certain tones. Ok. All right. So if you move on to the next slide, so for this question, you've got a 66 year old male who presents a DERM clinic for follow up on his preexisting chronic condition, bullous pemphigoid. He currently takes a step therapy in the form of oral prednisoLONE which add in as adjunctive therapies in order to allow adequate steroid taper. So if you remember the uh sort of pathophysiology of the pemphigoid, it's a chronic condition, tense blisters and it usually occurs in the older age group. Ok. Um It can be quite resistant to treatment at times and it can sort of vary in its degree of severity. So some patients have few lesions are very tolerable and some patients have lots of lesions, lots of itching, very intolerable, very difficult to treat. In this case, we've got a as an option, oral doxycycline and topical clobetasol, butyrate. Uh B coal preparation, C, oral Erythromycin and Dapsone D riTUXimab or E methylprednisolone infusion. Now, when you're thinking about the answer for this question too, it's really important to sort of read the stem. So we're thinking about a steroid taper. So we won't necessarily want to um increase the current amount of steroids that he's on. And then when you guys are ready, you can just put the answer in the chart. Also, guys, just one thing I wanna say sorry that should be clobetasol, propionate, not butyrate. So if anybody knows um apologies for that, but it is clobetasol, not clobetasone. Does anyone know which um might be correct? No. Ok. So basically, um in this case, if we just go to the uh next slide, yeah. So sorry, there should be oral doxycycline and topical clobetasol, clobetasol propionate. Um that's Dermovate cream. So topical, you know, very strong topical corticosteroid. Um in this case, so doxycycline is a great agent. That's, you know, a tetracycline antibiotic that's used for prolonged periods in dermatology, in particular for antiinflammatory effects, um especially in some autoimmune conditions. All right. Um And then topical steroids such as clobetasol, allow the patient to sort of reduce the amount of systemic steroid therapy they might be taking. And if you remember the uh effects of stomach steroid therapies, you've got mood changes, weight gain, you get um cushing weight on. So increased dorsal cervical fat pad, um you can get increased. Um what do you call it? Abdominal stria? Um easy bruising, muscle wasting, things like that. So, uh skin thinning. So, if you got to think of sort of uh effects of, of steroids. Long term, just think of sort of somebody with a Cushingoid Syndrome and then you remember them. Uh Yeah, if we can go to the next slide Vicky. So just to go through some blistering disorders and some of the most common ones you'll come across probably in your exams. So we've got bullous pemphigoid, which is something that they always ask you about. Um, as I said before, it's common in older people and it rarely ever involves mucous membranes, usually involves a forearm, the legs, the abdomen, but it does not usually involve the mouth, the eyes, the genitalia, anything like that. Ok. Whereas something like pemphigus, vulgaris, which is also an autoimmune blistering disorder. But with flaccid blisters that are more easily um popped occurs in a sort of a younger population and it does usually involve the mucous membrane. Um If you think about the type of blistering that occurs, it has to do with autoantibodies against the uh junctional proteins within the skin. So like if you look at the table here, it says intraepidermal blistering. So that means that within the actual epidermis, there's fluid leak. And then you get these sort of really flaccid blisters forming on the top layer of the skin. Whereas the junctional protein dysfunction and bullous pemphigoid is within the lower layers, deep layers. So the fluid leak of a comes from below and then the top layer of skin is intact So you get these tense and firm blisters, right? And then if you look at Nikolski sign, Nikolski sign is basically, can the blisters be ruptured with horizontal tangential? So if I have a blister like this, can I push across and pop them? And in Phi var, which is a more serious condition, bullous pemphigoid that usually happens, right? So you usually get quite a lot of abraded and broken skin, easy um sites for opportunistic infection. Um things like staph bacteria. Ok. Whereas in bullous pemphigoid, you'll often get that. Um So what they might say as a sort of positive is that in BP where you can pop the blisters and drain them, but like leave the top layer of skin intact. Um Whereas, you know, disease like pemphigus vulgaris, they may pop on their own from simply um laying back or sort of, you know, doing activities of daily life. And then you get like an opportunistic infection that way. Um And pemphigus vulgaris has a higher mortality rate, higher it, admission rate, things like that. Um That's how they differ in general. So if you didn't know about them, it's a good sort of just quick overview. Uh And I think that's all you really need to know for your final exams anyway, we can move on to the next question. Uh Yeah, question so, question five. We've got a two year old male who presents to the ed regarding strange blistering lesions on the on the plantar surface of the left foot, it has been slowly becoming larger over the past three days. What's the most likely condition? Does anybody know what this is? You got a gold star if you know what it is? But I think if you look at the actual image, you'll see that it's on a frictional surface. So, so he's only got blister on the side of his feet. Ok. Um Vicky, if you move to the next slide, this is the options. So, is it bullous pemphigoid? Is it hand foot mouth disease? Is it epidermolysis, bullosa, sa epidermolysis, bullosa or my senior office? I'll quickly go back to the stem as well just in case. Yeah. So two year old male presents to d strange blisters on the, on the side of his feet. They're slowly becoming larger. Anyone. OK. So if anyone wants to put what they think it might be in the chart, even if it's a guess it's OK. So you got be 100 mouth disease. Anyone else wanna say anything? No? OK. So if we go on to the answer. So in this case, this is actually um a blistering disorder that's not usually discussed in medical school. I know dermatology can be a bit remote for um a lot of us just because we don't get much exposure to it. But in this case, a really common um not common but sort of, you know, if you had a had a look at a kid and Peds Ed and, and you saw this, you might think, ok, this could be, you know, one of my top differentials, basically, it's a, it's all sort of genetic inherited condition, it's caused by the ill functioning in of the junctional. Um So it's quite similar to sort of the other blistering disorders and that's how they all come about. There's this dysfunction of the junctional proteins which allows the interstitial fluid to leak into the skin, right? And this causes blisters at the sites of friction. So, palms and soles are most commonly affected. So if you think that you see a toddler with, you know, the sort of blisters, palms, forearms, soles of their feet, things like that, you know, places that they're sort of using their body to lean and press and um you know, aid in mobility as they learn to walk and things like that. It might be worth thinking. Could this be epidermolysis bullosa? Um It can be quite a debilitating condition. Um But basically, you know, you refer them on to secondary care, they seek specialist advice and then get the help that they need. It can also occur in adults and that's called epidermolysis, bullosa, acquisita. Um So if you look at the name in LA and it basically just means the same thing, but acquisita hasn't acquired. So it's not present at birth, but it appears later on and it's an autoimmune disease and it's sort of similar in its, in its um etiology and pathophysiology. OK. Um So let's move on to the next slide if that's all right. Yeah. So it's just a quick osmosis stolen from osmosis uh summary, but it basically is a skin breakdown that causes blisters. If you look at the name, they break it down there. So, epidermal skin lysis Sequels breakdown below the blisters, right? It's a rare condition, but it's an inherited group of disorders that causes erosions after minor trauma. That that's because of um fragile epithelial tissue and it can affect mucous membranes and nails as well, right? So you get mutations in the keratin desmosomes, junctional proteins, things and things like that. And obviously the um sort of genetic inheritance pattern will determine the severity of disease. All right. Ok. So can we move on to the next slide? Ok. So question six, you've got, this is a question about acne. So two failed treatment cycles. So, two times, three months, right? Two bouts of three months. Um each uh with oral tetracycline in a cystic acne vulgaris patient, which of the following options is the next best step in management of her condition. So, are we gonna refer them to secondary care for commencement of ISOtretinoin therapy? Are we gonna prescribe topical clindamycin and benzoyl peroxide? Are we going to give them a topical retinoid only? Are we gonna advise them phototherapy or are we gonna give them something like topical Azoic acid with topical spironolactone. And I'll explain after what each of these, uh, treatments might be useful for. So, if you look at the nice acne guidelines, it should be pretty, uh, simple to figure out anybody wanna give a guess in the chart. So, if you think about this question, um, which therapies II would, what I would do is narrow it down by which therapies they likely have already tried and which therapy they might be suitable for next and then you get the answer. Um Does anybody wanna guess? Ok, Vicky, do you mind going on to the next slide? Ok. So in this case, um if you look at the guidelines for acne treatment, basically when someone presents with acne and it's noncomplicated. So it's not cystic acne or something like acne fulminans, which um is common in uh people who use steroids. So if you think, you know gem goa using anabolic steroids could be something like a cystic um acne disease like acne fulminans, right? It's just of acnes, you know, normal, typical acne, you start off with a topical antibiotic like Clindamycin and benzoyl peroxide. If that doesn't usually work, usually recommend um a topical retinoid. So you'd add an Adapalene tretinoin tazarotene, something like that plus a topical antibiotic, right? Um Or it'll be a topical retinoid plus benzoyl peroxide like whichever that's um uh they commonly known uh topical treatment called Epiduo that one's adapalene plus benzyl peroxide. Um You got a lot of others, you've got different gel, things like that, uh retina, stuff like that. So they all, if you look them up, you can, you know, find loads of them online. Um But that's what they usually recommend. First. If that's not controlling the sort of current lesions and preventing new ones from coming up, then we usually add an oral antibiotic. So you're gonna give Lymecycline oxytetracycline, sometimes Doxycycline or Erythromycin and then that's usually prescribed and as a course of three months and what they recommend is two cycles of that. So two times three months equals a total of six months. And then you get basically some relief, hopefully, uh it can sort of mess your gut help up. So it's not necessarily something you wanna continue for a very long time. And then obviously prolonged antibiotic use leads to antibiotic resistance, right. So the bacterial burden of your skin might be something that's contributing to your acne. And then usually those patients respond well to antibiotics if that's not the cause and it might be sort of more due to testosterone, um increased sebum production, things like that, then it doesn't usually work as well. So sometimes you need um oral ISOtretinoin therapy, which is commonly um known as Roacutan or Accutane, uh which people sort of, you know, talk about it on youtube a lot, but it's a dose adjusted lipophilic drug. So it basically is stored in your fat cells cause it's Vitamin A, it's oral Vitamin A high dose and you basically get sort of a drying effect, a reduction in the number of sebaceous glands within the skin. And then that usually if there are less receptors for the testosterone to act on those sebaceous glands cause they've sort of been reduced the number and you got a bit less oil production and reduction in the number of acne lesions are gonna come up. Ok. So, yeah. So basically in this case, this kid has tried topicals. So we've, we've exhausted topicals and then we tried oral antibiotics that haven't worked. So it'd be appropriate now to refer for um, Vaut. Ok. Uh The other options, if you just go back one side, Vicky, sorry, the other options. Um as we discussed the topical therapies that we have. So B and CD phototherapy not usually helpful in acne. I mean, e topical azoic acid with topical spirolactone might be prescribed for sort of a female who has uh hormonal acne or Acne. That's sort of more in line with her sort of menstrual cycle, et cetera. So in this case, you know, you wanna move straight on to uh, referral to secondary care. Ok. Uh Yeah, if we can go two slides ahead, Vicky. Thanks. I think I just put, yes, I just put this really good graphic here which shows how acne treatment might work. Um And they do all these things like a failure at three months So it's actually really helpful to see what, what might be used next, right. And also depends if you've got a patient who's come in has very severe acne and there are loads of nodules. It may cover their, you know, body as well. It might be worth saying, look, I think we should start with an oral therapy first. Um But it's all sort of patient specific. OK, if we move on to the next slide, right? Oh oh no. So I think you guys saw the answer, but hopefully you didn't anyway. So this question, you've got a 65 year old man who presents a DERM clinic with a rapidly expanding lesion on the right side of his abdomen, which of the following parameters is most useful in determining mortality and potential morbidity of this condition. So we've got degree of evolution, we've got Brazil thickness, mitotic indices, the size of the lesion or his own comorbidities as a patient. What do you guys think? Any ideas? Anyone? It's the last question before you move on to Ent with Emily, then you wanna give it again. OK. So in this case, if you look at the arms is actually um they're all sort of important in determining sort of the, you know, I guess how aggressive of a skin cancer this would be. So we do wanna look at the degree of evolution as part of the ABCDE criteria. You basically do wanna look at mitotic indices when they've um sort of looked at the lesion under the, when they biopsied it and looked at it under the slide. And the histopathology lab, um size of the lesion can sort of determine, you know, whether this might be something we should really should worry about or not. And obviously, the patient's own comorbidities would be uh sort of useful in knowing how they might fare with immunotherapy or chemotherapy or radiotherapy. Right. So, in this case, though the most important prognostic factor re thickness and if you go to the next slide, please, thanks Vicky. Um This good, this graphic basically shows how you might um grade a melanoma. So one breath thickness, you know, in dermatology long been the most important prog prognostic factor in determining the mortality and morbidity of a patient with a melanoma. So it measure the vertical depth of the lesion in one plane only. Um and basically lesions with grades of r depth are more likely to metastasize. And the reason that is ok is because the der you can't see the slides. Oh no. Um maybe log in and log log out, log back in. Um If anyone else can't see them, please speak up. But yeah, so basically Brazil thickness um has to do with the depth of the actual lesion. So the f the closer the lesion is to the dermis and obviously, the vasculature, the more. Um so I think Vicky, do you mind just having the shot as slides of different. I'm seeing that. I'm not sure why, cause we're loading it, let me just reload. Is that better? Oh It's next apparently. Yeah, I think it's OK. So I was just gonna say that. So in this case, right. Me Melanoma into the vasculature, it's more likely to metastasize when it's more likely to metastasize. Obviously, you've got a worse prognosis, right? So if you have a lesion that is sort of four millimeters deep, you've sort of, you know, gotten the worst great in terms of, you know, TNM staging, you got basically stage four. So stage four me e it's very deep down for the thickness is, you know, at its maximum. And we're now concerned about um metastasis. You wanna do things like staging CT cap and things like that to have a look at if there are any other lesions, um anywhere else. And Melanoma in particular has one of the highest mortality rate of any cancer because one, it po it responds very poorly to chemotherapy, it responds better to immunotherapies, which we only now have sort of discovered recently and also it metastasizes to places that are difficult to treat, such as the small bowel and the brain. OK. So in this case, if you have a look at the image, you can see that a Melanoma less than 0.8 millimeters is not worrying. It's a Melanoma in situ and then you've got page 23 and four so that basically, um and you can have a look, I basically at the kind of, you know, ranges but it's basically one millimeter to, I think 1.5, you just keep going from there, 1.5 to 22 to 3, et cetera. So it's um pretty self explanatory. Um Any meters is just sort of, you know, put a stage four and con and is highly concerning. All right. Um um I think the next one. Oh yeah, this is the image references. But anyway, thank you guys so much for listening. I do have to go to my shift now. But um yeah, let him take over. Thanks Chris. Um And just a welcome to those who've joined us. I know we've started a bit earlier this session. So we've got a few more people who've come in half with your sessions. We're going to start the ent section now. Um Let me know if there are any issues of size, sorry that if you couldn't see them properly, but hopefully they've, I just reloaded them. So hopefully that's fine. OK. OK, perfect. So yeah, I just gonna go through some ent questions, obviously. Um can't cover the whole syllabus, but I just chose someone's just to get the the hot, the hot topics. Um So yeah, next slide, please be OK, sorry, you can't see them that well because of the purple. But the first question is a 22 year old male um with a five day history of sore throat and poor oral intake due to pain on examination. Um The patient is febrile and speaking with a hot potato voice and has trismus of the jaw. What is the most likely diagnosis? So, A is glandular fever. B is bilateral acute tonsillitis. C is epiglottitis D is Quinsy and E is pharyngitis. Um Yeah. Um Yes, you guys can put your answers in the chat or just do them in your head if you don't mind. Ok, cool. So most of you are thinking it's d um Yeah, so if you go to the next slide, please. Um So yeah, the key um the key parts to this question um kind of distinguish it as being a Quinsy rather than a tonsillitis or just a glandular fever. Um is just, well, one of the key things is like the trismus of the jaw. So that basically just means that like the patient won't be able to open their mouth fully and that's like quite a high um diagnostic indicator that somebody has um a Quinsy. Um just like just having a sore throat and like um uh like inflammation in post in the tonsils doesn't necessarily mean that somebody has a Quinsy. Um next slide, please. Um So yeah, it's a clinical diagnosis. Um and usually it starts with someone just having tonsillitis, they might have like pus on their tonsils, they might have been given um antibiotics by the GP. Um but basically, um pus collects in the um in the peritonsillar space. So from the picture, um you can see like normally you have like the, the pharyngeal arches and they should be symmetrical um with somebody in a Quinsy where you look in their mouth, one pharyngeal arch will be kind of displaced more medially than the other one. That's shown by like the arrow in the picture. So it's not, it's not the tonsils themselves will be enlarged, but it's actually kind of the area around the tonsils. Um That basically that's where the abscess is. Um And the reason that people get trismus is due to the pus um irritates the muscles of mastication. So it's the tero muscle um generally, which is like spasming. Um So that's why they can't open their mouth. Usually they say like kind of three finger thickness. So if you can't like, if you were to kind of measure with your fingers, if you ask someone to open their mouth, um then that's like a very key one. Boys are more likely or males are more likely to get Quinsy. So that's like another risk factor within from the stem of the question. Um And then Hot potato voice is basically just like, it sounds like as if someone's got like, they, their voice will sound quite distinctly like different from normal. It's like not necessarily like when someone has a whispering voice with a sore throat like it's like, it sounds like they've actually got hot, so something hot in their mouth. Um, but yeah, so the main thing with these patients is that they're gonna need to be admitted. Um, so we're gonna admit them gonna start IV antibiotics. Um, uh, usually we give, uh, Benzylpenicillin is the first line. Um, and then they get a stat dose of dexamethasone. Um, and also like analgesia is really important. Um, So like patients generally with the like, especially with the trism aren't able to eat and drink. So that's kind of the main reason for admission. Um And basically the kind of um what's called definitive management is that they need to have be it needs to be aspirated. So that will just involve like sticking a needle into kind of like the most fluctuant point um and kind of trying to drain the pass. Um So yeah, that is, that's, that's a Quinsy next slide, please. Um Let me know if I'm speaking too fast or going too fast. Um But yeah, next question. Um this is a 54 year old lady presenting with sudden onset hearing loss in her left ear. She also has tinnitus in her left ear, no pain or discharge. Um and on examination of her ear, um it's normal in the canal, no uh tenderness of her external ear. Um She's rin's positive and the Weber test lateralizes to the right side. What is the most appropriate immediate management. So A is urgent. MRI head B is pred for two weeks. C is amoxicillin uh for 10 days and D um put them in the Sorry. Oh OK. Cut on these, but I'll just put them in the chart as well. OK. So D is watchful waiting and then e is myringotomy within two weeks. So we had one response before I put the um other options in the chat because he's already answered this one. Ok. Um Yeah, next slide, please. Vicky. Um Yeah, so this question, like the key bit of this question is the fact that it's immediate management. Um And yeah, the correct answer is prednisoLONE. Um If we go to the next slide, I will explain why. Um So this is just about kind of interpreting the um the runny and the Webers test. Oh, shit apologies. I think I might just have a bit of a technical issue there. Um I'm just gonna check in with what is happening. She may or may not have lost her, uh Think she's lost her battery power. So give us two seconds. She's just getting her charger in apologies and we'll get um we'll restart where we were. Yeah, just give her a men. So thanks everyone for bearing with. Yeah, she's back. Hi. Sorry. Am I back now? Sorry, I didn't. Yeah. So just interpreting the R and the Webers test. Um So we're kind of trying to assess for um like sensory neural hearing loss, that's like the key thing. Well, you're trying to differentiate between the two. So in a normal patient and also in somebody with um so air should be louder than, than bone. So that basically, so when with the Rs test, um you hold it, you tap, you tap the tuning fork and you hold it by the ear and then you put it, place it on the bone, on the mastoid bone behind their ear. And in patients um with um sensory neural hearing loss, it will lateralize um to the same, the same side. Um and then er conductive hearing loss, the bone, the bone, the bone, the, the bone will be the, the bone will be louder. Sorry, I just said it the wrong way. Round bone will be bone will be louder than air than air if it someone has conductive hearing loss, whereas it will be air will be louder than bone if it's sensory, your hearing loss. Um So that's just a diagram to explain the runny and Weber's tests next question. Um So with patients that present with um like sudden onset hearing loss, um it's kind of important to um identify like, first of all, you wanna like rule out that they haven't had any like recent head trauma, no recent ear surgery or like if they're systemically unwell cos you might need to rule out meningitis. Um But if you, if you see somebody um that's presenting with this if it's in like a very sudden onset hearing loss. Um The first line management is steroids. Um A lot of people. So on the, the first bit, I've just talked through like um the different causes of sensory neural hearing loss. Um So obviously there's congenital, but here we're looking at acquired causes and most causes of sensorineural hearing loss are idiopathic. So we don't really know exactly um why that is, but we know that steroids um can um help to reduce the amount of hearing loss that somebody has. Um So yeah, we give prednisoLONE for two weeks. Um So that's like, that's like the immediate management. However, given that one of the other differentials for sudden onset hearing loss is um acoustic neuroma, um you want to refer somebody to the, to ent um and they'll, they'll have audio audiometry and tympanometry and if that is um confirms that they have sensorineural hearing loss, then they, they will need an MRI head. So that was why like MRI head isn't, it is part of the management for sensory neural hearing loss, but it's not the immediate um immediate management. Um So, yeah, acoustic neuroma is quite rare, but it's an important one to rule out. Um And sometimes like people might also present with um like uh facial nerve palsies that's like another thing to be aware of. Um cos sometimes the um as the cos the facial nerve is also er runs in a very close proximity to the um vestibular nerve. Um that's something else to be aware of. Um but yeah, basically high dose steroid and urgent ent referral for somebody. So this could be someone that you see in GP but then it gets referred to to ent. Um yeah, next slide perfect. Um So this is a 67 year old male with a background of hypertension diabetes and knee osteoarthritis. He presents with unilateral foul swelling discharge and a four week history of gnawing ear pain. The pain is worse at night. Um What is the most likely causative organism? Um Yeah, if we go to the next slide, perfect. Um So yeah, the key bits of this question that kind of might lead you to the diagnosis um of necrotizing otitis externa would be the fact that it's a immuno compromised patient. Um So he's got type two diabetes. Um and um kind of like the insidious onset. So the fact that it's kind of a longer history of the air pain. Um And the fact that the air pain is worse at night, um those are the kind of key suggestions that point towards the diagnosis of um necrotizing um otitis externa. Um So if we go to the next slide, so yeah, it's called malignant otitis externa or necrotizing o otitis externa. Um It's not actually a malignancy. Um It's more just the fact that um it's like a, it's a complication of um like classic otitis externa. Um but it occurs in immunocompromised patients, especially older patients. So sometimes people might have already been treated with antibiotics previously and it just hasn't completely resolved, but it's really important to treat it very promptly and they will need admission as it's potentially um as potentially life threatening. Um So first line, um yeah, you want to start the antibiotics very promptly. Um But you're probably gonna send some ear swabs for MC NS um as well as pathology of the. Um you get like granulation tissue inside the, the ear canal. Um and they may need further imaging to see if it's um eroding the bones of the skull. Um So, um they will need extended antibiotics usually for six weeks. Um So you want to kind of do like a septic septic screen as well. So, like full blood count, use these um and like give them, they might need like fluid disci um and like kind of like suctioning out any of the pus and debris inside the air. Um And yeah, the, the com the combination is probably uh something like IV cefTRIAXone. Um that, that would be the first line antibiotic. Um And they, they will need like close, close monitoring. Um and they might need to be discussed at kind of an MDT MDT meeting. Um If there is um like if there's bony, if there's like bony involvement of the, of the bones of the air, um features of that have worse prognosis for somebody with malignant otitis externa. Um They could have hearing loss as well associated. Um So if they have hearing loss, that's a poor prognostic feature. Um And so you might want to get kind of like baseline um hearing tests. Um And um also sometimes people again can present with facial nerve palsies. Um So that's another poor prognostic um poor prognostic feature for um malignant otitis externa. Um So yeah, that is everything for that question. OK. Question four is a 38 year old female who recently underwent total thyroidectomy. Um So during the day and the patient is complaining of fluctuant swelling over the incision site and is short of breath. Um You go to assess her, she has Stridor and um a drop in her s her sats are 92% on air. Um What do we think is the most appropriate management? Cool. Let's go to the next slide, please. OK. So this question is kind of just about like identifying an unwell patient um given that she has Stridor and, and drop in SS um that's quite a severe presentation. Um So this is kind of just like trying to highlight the importance of like the at E assessment. So, in this situation, it sounds, it looks like this patient has their, their airways compromised. Um So if we go to the next slide, um so this, this picture shows like what, what we might see in this in this case. Um So it's kind of like a swelling that, that is, is fluctuant. Um and patients might present with difficulty with breathing stridor. So that's like the upper upper airway um noise if someone has um occlusion of the upper airway, um and these patients can get on well very quickly. Um So if you, if you ever kind of have a nurse call you to see a um a post thyroidectomy patient then, uh or like a POSTOP patient that they're saying that they've got an airway problem, it's really important to go and assess them very quickly. Um, because you probably, you might need to escalate it and they, they might need to go back to theaters, um, with the airway with the airway um, situation. Again, this is another thing to, another thing to consider that you might be considering might be that sometimes people get like a seroma. Um So this, this patient is probably a hematoma given it if, if it happens acutely. Um, and they have an air problem, it's likely to be, um, a hematoma. Whereas if it's kind of the next day or two days, it might be more likely to be a serum which is like the serous fluid leaking out. Um, if we go to the next slide. Um So, yeah, it's really important that if you, if you see a patient that's like, has stride or low starts, then you're gonna need to like probably like press the emergency buzz or get as many people in to come and help you. Um put oxygen on the patient, uh sit the patient upright. Um And basically the, the acronym that they advise as the scoop. So, um you want to have to cut the stitches, open the skin and the muscles um and pack the wound. Um So the reason that the other answers weren't correct was just that they're not the most like immediate management. The patient probably will have to go back to theater. Um But given that they have an a problem, you're going to have to deal with that straight away. Um Yeah, that's all, that's all good. OK. Question five. This is a 92 year old male who takes Apixaban for af um he's had one hour of bleeding from his first, sorry, from his right nostril not stopping with first aid measures. Um Where is the most likely source of bleeding? OK. No, no w out we've got one answer in the chart so far. OK, perfect. If we uh go to the next slide, please. Oh yeah. I um so the correct answer is the anterior inferior septum. So it's like the middle of the, yeah, in, inside the nose, at the, at the front um in the septum. Um So your wrist, if I go to the next side as well, please. Um So yeah, this diagram shows little's area which is basically like the area which is very rich in blood supply. So most bleeding will be from that as that area of the nose. Um, obviously there's lots of patients who are on Apixaban or Warfarin. Um, so they're kind of more high risk patients. Um, often it's just like there isn't necessarily like a, an identifiable cause people just have nose bleeds. Um, but sometimes, er, like nose picking can, can be a, a common one that people are necessarily admit to. Um, so generally they're anterior bleeds. Um but sometimes they can be posterior bleeds. So it's really important. Um So towards the back of the nose, it's really important to look in the patient's mouth. Um just to see if you can see like any um like trickling into the back of the throat. Um And so the first aid measures is to lean the patient forwards and to like pinch the, like soft part of the nose and usually to apply continuous pressure for 30 minutes. So that's like, that's like the first, the first stage and that generally like, can be managed like in A&E or like by the patient. But if that doesn't work and they're still bleeding, um then um either you can, um you can try using like Nasopore, which is basically like some dissolvable, like porous things that you put up the nose. Um But some patients um might need to, you might need to insert a rapid Rhino. I think I put a picture on the next page. Um So yeah, basically, um any patients that you have to put nasal packing in, so that's, that would be the Rapid Rhino, then they would need to be admitted. Um So any patients who are like older and frailer, they'll need admitting um and anybody with nasal packing, so they just need to be monitored for 24 hours. Um before we take the pack out, um generally the the pack for anterior bleeds will stop, but sometimes you might need to use a longer pack. Um that, that reaches kind of up towards posterior bleeds. If someone is still bleeding with the pack in, that might be more suggestive that they have a posterior bleed. Um so that they'll kind of need senior review. Um And if it's not stopping then um or if it is more of a posterior bleed that is stopped by the packing, they might need to go um to be referred um to be seen in clinic for sphenopalatine artery ligation. Um So, yeah, anybody that um has a nose bleed um on discharge after we've removed the packing, um We give them naseptin. Um and it's really important to ask about um peanut allergies because it contains peanut oil. Um So you need to ask about allergies. Um And basically you just apply that twice a day um for seven days afterwards and that just kind of helps to lubricate the area um to like prevent further bleeds um And sometimes we also use uh cauterization. Um So that's just like using the silver nitrate stick. And that's only if there's a kind of identifiable bleeding point, then we, that's when we would do nasal cautery. Um And it's really important to only cauterize one side of the, of the septum. Um If you do both, then you might risk um, perforating the, the septum. Um So yeah, first line is basically like first aid measures, then second line would be the nasal packing. Um And uh you can also kind of put ice on the front of the nose um to um encourage the the blood vessels to um was also dilate to constrict. Um So yeah, that is, that's epistaxis. Um And then we're on to the last question, which is a 56 year old male presenting with a two week history of um reduced sense of smell and facial pain, especially when leaning forwards. Um And what is the first line option? Ok, next slide, please. Um So if we go to the next slide as well. Um So this patient um likely just has um just has like like simple rhinosis, sorry, simple rhinosinusitis. Um so that he's just gonna need um nasal decongestant. So that's something like Xylo Metalazone. But when patients present with, um so normally that can just be like managed by primary care. But if people kind of have like worsening, like worsening symptoms, so, symptoms aren't getting better or symptoms that initially get better and then get worse. It's like a biphasic presentation. Um or who, like I say, they're like systemically unwell or immunocompromised. Um then they're the patients that will need um antibiotics. Um So the four, the main key symptoms of um rhinosinusitis is um like nasal congestion. So like uh nasal discharge, facial pain, like typically like on the forehead and under the eyes is like a common one. and like tenderness when you press over the the sinuses, um the most common bacterial causes would be haemophilus influenza and strep pneumonia. Um But yeah, it's just quite important to differentiate between um acute versus chronic. Um So acute is just kind of like about four weeks, subacute 4 to 12 weeks and then chronic is when someone has symptoms lasting longer than 12, longer than 12 weeks. Um And you can get like acute and chronic as well. Um So if you go to the next the next page, um So for someone that you think need antibiotics, so that would be like kind of longer symptoms, positioning longer than 10 days, uh red flag symptoms like fever, um or very, very severe pain. Um then they'll probably need phenoxymethylpenicillin um and then nasal decongestants. So that was in the question and that's something like Xylo Metalazone, but it's important not to prescribe um the nasal decongestants. Um It's, it's prescribed for a week and then they need to stop after a week because sometimes patient can get rebound symptoms of the rhi rhinosinusitis. Um So it's important to like explain and safety net to the patient just to use it for a week and then just to have a break afterwards. Um So yeah, that is, that is everything. Well, thanks so much Emily and thanks for everyone um who's attended. I am just putting the feedback link in the chat. So um if you could please fill that in whilst Emily's here. If you have any questions about ent, she can answer those. Um, but otherwise, thank you so much for attending. And we will be posting this recording, um, on our youtube and um, website as well and we will have this on our med all as well, so many different ways of accessing this. So, yeah, please fill in the feedback and thanks again. Yeah, we'll hang around for a bit if there's any other questions, but if not feel free to enjoy your evenings. Ok. It looks like there aren't any questions that I can see. Um, but yeah, keep filling in those feedback forms and yeah, this is just a little, um, reminder of, uh, our airways that you can get in touch with us and slash see content. Um, the other things I don't hear is the youtube. So if you, if you type in med teaching on youtube, you should be able to get our youtube as well. All right. Well, if there's nothing else. Um No further questions. We'll probably end the session here then. Uh just keep filling in those feedback forms. You can still fill it in even after we've discontinued the um streaming. But yeah, have a lovely evening, everyone and thanks again. Bye. Thank you.