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Summary

The On-Demand session features two guest speakers, Isabel and Callum, medical professionals working at Conquest Hospital who will be discussing respiratory conditions, specifically focusing on asthma, Chronic Obstructive Pulmonary Disease (COPD), and the overlap syndrome between the two. The talk will delve into symptoms, triggers, pathophysiology, and essential components of examination and diagnosis for each condition. The session will also touch on effective medical management, highlighting the differences between treatment for asthma and COPD. There'll also be a section focusing on Asthma COPD Overlap Syndrome (ACOS), a condition which incorporates features of both diseases. The session emerges to be a blend of interactive discussions and detailed analysis of the conditions, making it a must-attend for healthcare professionals seeking comprehensive knowledge in respiratory medicine.

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Description

The fourth talk from Conquer Finals, our near-peer teaching series, will focus on common respiratory presentations for finals! Come join our tutors, Dr Callum Chessell (FY1) and Dr Isobel Mills (FY1) for the next engaging talk of the series!

Learning objectives

  1. Understand the clinical presentation, symptomology, and possible triggers for asthma, COPD, and asthma-COPD overlap syndrome.
  2. Learn to identify signs and symptoms of asthma and COPD exacerbations, including key indicators of disease severity.
  3. Understand the pathophysiology behind asthma and COPD, along with the specific cellular involvement in each condition.
  4. Familiarize themselves with the key diagnostic investigations, including spirometry and ABG interpretations, for asthma and COPD.
  5. Develop a clinical approach to the management of asthma and COPD, including pharmacological and non-pharmacological strategies, and recognize when referral to specialized services might be needed.
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Computer generated transcript

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

Welcome everyone. Um This is I think number four in the Concer final series this week we have um Isabel and Callum two F ones at Conquest Hospital. Um and they're going to cover respiratory conditions. Um It's, it's gonna be a really good talk. So um please put any questions you have in the chat and we'll try our best to answer them. Ok, thank you. Ok. Um So I'm gonna start with some conditions. So asthma COPD and the asthma COPD uh overlap syndrome kind of wanna make this as interactive as possible. So feel free to assume you can like speak as well or put your responses in um the chat. Ok. So as starting with asthma, can anyone shout out uh some symptoms um that they'd expect someone with asthma to have to present with? Let's pretend you're kind of a doctor and GP um Yeah. Wheeze chest tightness, shortness of breath. Nice. Perfect. Yeah. Um Can anyone think of some triggers perhaps? Mhm. Mhm. Pollutants, dust, weather, cold weather exercise. Yeah, perfect. I think you've got all pretty much got all the ones I was thinking of. Um So yeah, when you're taking a history let's say you were in an AK station, not only do you want to say what, what's been affecting them, getting them to kind of start the consultation in an open way. You also then want to be screening for those other symptoms and triggers which kind of shows the examiner you're aware of kind of the condition as a whole. Um I'm not going to go into too much detail because I feel like fifth year now we know all of these things. But uh the highlights of the pathophysiology are kind of you get airway hyperresponsiveness, you get inflammation and bronchoconstriction. Um and you get trigger induced exacerbations and then kind of on a more um molecular level, you get ma cells, um eosinophils and you can get raised IgE and that's why you kind of have the overlap with other atopic conditions such as eczema and allergies. So those are some other things that you're gonna wanna screen for. Um if you have an OS station, but that might come up in like a KT question. Oh, it didn't, I haven't done this slide properly. I will. So this, this is giving you the answers, but um on examination, you'd expect kind of dry cough, um tachypnea, wheeze potentially on auscultation and your investigation. Your mainstay of your investigation is going to be your spirometry, have to have that as part of um diagnosis. Um And you're going to expect uh reduced F EV one to F ec uh ratio. That's because your FEV one will be reduced, your F VC will be normal or near normal. The other part of your diagnosis will be that it improves with bronchodilators. Um And then kind of longer term, you're gonna monitor disease activity through peak flow monitoring. And I think someone earlier said, um you can get a cough particularly at night. We often see like a diurnal variation. So worse in the morning or worse in the evening, um, with asthma. Oh, great. I did it the wrong way around that. Um So these are just some of the drugs that we use. Your Sabr um I CS laser, et cetera. So if you were in A&E, let's say, and you've got someone presenting with an acute asthma attack, what are some drugs that you're gonna consider putting in anybody? Mhm. So we've got salbutamol terbium oxygen for sure. Mhm. We're gonna think about some steroids. Mhm. Great. Cool. So I remembered it using this acronym. Um, and yeah, and uh big one is kind of if you're going down that list of drugs you're gonna wanna be thinking of. Ok, actually, this is quite specialist. We need to involve itu or critical care because if we're having to escalate all the way through that ladder of um management, this person's pretty poorly. So we're gonna need them. But, so as you probably know there are different ways to grade asthma moderate severe and life threatening and I feel like that is a classic KT question. I don't know how many past med questions I did, um, trying to figure out which type of, uh, asthma exacerbation it was. Um, but one thing that I think is really important, um, and catches a lot of people out is that, um, if someone's PCO two on an ABG is normal, um, during an acute asthma attack, that is a really bad sign. It's kind of showing that they're fatiguing. Um, and you need to kind of alert it because, um, they're about to kind of go really downhill. That's more concerning than, um, a low, uh, po two. Ok. So that was asthma. Whistle. Top stool. Well, whistle. Whistle, top stool. Mm. Ok. CO PD. Uh, can anyone think of any symptoms we'd associate with? COPD? Got some, yeah, breathlessness, cough, shortness of breath. Wheeze, clear Sputum. Yeah. Sputum production is a big one. And let's say we're again in that osk situation. So we're saying we're screening for these, um, symptoms. What else are we gonna want to gauge in terms of the presentation? Yeah, I don't know if that's just too vague a question or if people are typing away. So if we think of like with other presentations, you maybe use like Socrates as a template to think about questions you're gonna ask maybe some things related to that. Anyone got any ideas about like a time frame, what would we expect if someone's coming into GP, they've got this cough sputum production. What are we gonna want to establish about the time frame of this presentation? Yeah. Smoking history is a good one to also check for. Can you take some time frame? Are we thinking it's gonna be? Yeah, fine. Perfect chronic issue. Yeah, we're gonna think it's not just something that's happened over a course of days or weeks. This is gonna be kind of progressive chronic issue. It's not getting better and it's kind of gradually getting worse. Um, with asthma, you know, we were saying it can kind of be worse in the mornings, worse in the evenings. Asthma you can get kind of obviously, um, days where it's completely fine days where it's really bad. What are we gonna think about the pattern of the symptoms with CO PD? Do you think it's like very variable? Do we think it's gonna be kind of pretty steady? Yeah. Stays, stays the same throughout the day? Yeah. And over time we're gonna not see it kind of fluctuating, kind of on an hour to day rate, like kind of time frame. We're gonna be thinking of like exacerbations, maybe lasting a couple of weeks and then being stable or just downward progression. Perfect. Mhm. So, again, in that osk situation, that's what you're gonna wanna show that you're asking and establishing in order to show your examiner, you're seeing it through respiratory presentation. You're screening for asthma screening for CO PD and, and figuring out which one it is. Um So it's a chronic airway um inflammatory condition and kind of las down the line. You get this alveolar destruction, loss of elasticity and that chronic bronchitis leads to that increased mucus production. Um with uh asthma, we said you get this kind of the ma cells, the eosinophils. Um and the I GE does anyone know what cells we kind of see increased in CO PD? It's fine if you do him, do you think it's the same or different? Asma? Yeah. Ok. I'll give you this one. It's different. We tend to see it's uh, raised neutrophils. So you're examining this person, um, who they've had this cough, increased sputum production. Um, what are some things you're gonna be wanting to, um, assess for in your examination? What are you looking for? Mhm. Temperature. Yeah, we wanna make sure that this, we wanna see if this is a kind of infective, uh picture. Yeah. Crackles and wheeze oxygen sets on it. Yeah, definitely. Yeah. Barrel chest. So we get this kind of increase in the anterior, posterior diameter of the chest. Perfect. We can also get kind of reduced breath sounds when you're, um, listening to their chest. Um, cool and then, yeah, so you've, you've examined them, you've got a strong suspicion, um, that this might be CO PD. What investigations are we gonna send, send them off for? So, Aaron says F ev one F ec risk Yes. So we're gonna want to do spirometry. Um and what do you think we're gonna expect to see on spirometry? Ok. Yeah, we're gonna be expecting a less than 0.7 or less than 70%. And if we give them some bronchodilators, do we think it's gonna improve that or is it gonna not do anything? Yeah. Perfect. Very little reversibility. All right. Uh let's say we send them for a chest X ray as someone um mentioned, what are we gonna, what do you think we're gonna see on a chest X ray? Yeah, hyperinflated lungs and a flattened diaphragm. Those are your kind of classic things. You see a chest X ray and it's really kind of looks like the lungs are really big. You're gonna be thinking um CO PD and you get that because of this um, obstruction, you get air trapping. Um And uh it basically increases the pockets of air in the lungs, it in flakes them up. So, um, flattened diaphragm just means like the diaphragm instead of kind of being nice, kind of um kind of concave, kind of shape. It's very flattened. Ok. So how do we manage CO PD if you lost a chance? Oh, I've given the answers. I've lost the chat. I don't know where it's gone. Here we go. Fine. Cool. Um So, yeah. Ok. Nice. We're gonna think about um your kind of pharmacological therapies. So that will be our bronchodilators. Um We're going to think of more non pharmacological, like someone said, smoking cessation um also gonna like pulmonary rehab can be a really great tool to use in patients. Um Long term oxygen therapy, it might be required in certain patients. Um An important thing to note though is unlike asthma, um inhaled corticosteroids on a mainstay of CO PD treatment. Um Historically, they have been um but there's been like a fair bit of research now that shows that actually the inhaled glucosteroid don't significantly change kind of the progression of COPD. Um But there are a subgroup of patients um who can benefit from them. So, um patients that have a high eosinophil count um often uh benefit from them. Um There actually has been some studies which have showed that long term use of um I CS can increase the risk of pneumonia. Um So, yeah, just to, just to note that one. Um So this is on the MLA content map now. Um and it wasn't something that I was particularly um familiar um with is the asthma CO PD overlap. Um There's not really a particularly kind of um agreed upon definition of this. Uh It's a, as it, like the name suggests, it's where people have got features of asthma. They've also got features of CO PD. So, um it's characterized by persistent airflow limitation and features of both asthma and CO PD. Um And again, so if we can think about our asthma presentation and our COPD presentation, we're basically gonna have a mixture of the two so persisted, persistent dyspnea, wheezing a history of asthma or a strong family, history of asthma or a personal history of ATP. Um, and then, uh, smoking or COPD risk factors as well. Um, and there's, again, there's not a huge amount on kind of the pathophysiology of it, but, um, it's thought to be an inflammatory component of both asthma and COPD. So you get ra sys and raised neutrophils. Um Yeah, they think it's probably something between the two like phenotype. So, um you're gonna get reduced breath, sounds and examination. Wheeze and some of those signs of chronic lung disease like a bar or chest on your spirometry, you're going to see a slight increase in your um F EV one after bronchodilator therapy. Um So not quite enough to be diagnostic of asthma. Um but not nothing like we would or very little like we would expect with COPD again. So it's like this weird in between. Yeah. So if we go through these um different things, so imagine these as you're gonna be screening for all of this in your os when you're taking your history. Um Can anyone think what kind of age of onset we're gonna be expecting with asthma versus CO PD? Yeah, sorry, I've missed so much in the chat. Just me answering some questions. Don't worry. Thank you. Yeah. So asthma is definitely kind of beginning of life. Um, and CO PD we're expecting kind of older in life. Um, so asthma, I've said before, kind of 20 years and COPD were generally thinking about 40 years or above in terms of pattern of symptoms. We've, we've touched on this. But what are you gonna be screening for? With asthma versus COPD? Yeah, I think everyone's getting quite a lot of those. So with asthma we're gonna have variation in of symptoms over kind of minutes, hours days, it can be really kind of quickly changing. You can get change morning versus kind of the middle of the day versus the evening. And you're gonna have obvious triggers, um, such as allergens, such as, uh, exercise. Um, whereas with CO PD, we're gonna have kind of good days, bad days, good weeks, for example. But you're always gonna have this kind of persistent exertional dyspnea. Uh, well, that shortness of breath on exertion. Um, and it's never gonna kind of fully resolve. Whereas with asthma you can get, like, near to like resolution of, of symptoms. Um, with treatment, if we think about our spirometry, what is that main difference we're looking in between the two. Yeah, exactly. We're gonna expect reversibility in asthma. Um, what do you think if you've got someone that comes and they've got kind of a history of a ZP them, let's say, under 10 years old, maybe around 10 years old, they've got the classic kind of got this cough in the morning they can't stop coughing, they can't stop coughing when they're going to bed. They're getting wheezy when they do exercise or go in the cold. But when you go to do spirometry, completely normal, do you think it's still asthma? Yeah, there are other types. Yeah. But the point I'm trying to make is because you can have kind of improvement of your symptoms. You can have improvement of, um, your results kind of if you aren't being triggered and stuff, you can have normal um lung function between disease activity. Whereas in COPD, you're never gonna like get resolution of your um like complete resolution of your symptoms. Um And then a family history, it's obvious we're gonna be looking for kind of asthma A to P um CO PD, we're gonna be thinking of have they kind of previously been diagnosed? That's a giveaway um or exposure to risk factors. Um And then time course with asthma, we're thinking, ok, can vary seasonally. You can have good patches, bad patches, it can get better over time whereas CO PD is kind of like downward trend is gonna be progressive. Um What do we think a chest X ray of asthma is gonna show someone with asthma is gonna show? Mm. Oh Anyone nice. Yeah, it's normal. Your chest X ray is gonna be normal and we've already said with CO PD, we're gonna expect um hyperinflation, aren't we? Ok. Right. I feel like I've been talking further. So um a couple of scenarios now, um a 65 year old man has presented with a six month history of uh shortness of breath and we get a chest x ray of them. What do we think? I know you can do your like whole thing, your ABCD. But uh if you sh shout out or try the, the big Yeah. So hyperinflated lungs. So when we say hyperinflated lungs, um what actually are we, how can we objectively tell that? So, yeah, someone said there are so many visible ribs. How many ribs are we talking here? You said it's seven. So is that um so yeah, more than seven of your anterior ribs. So your anterior ribs are the ones that are kind of slightly harder to see. These are the ones which are a bit more like curved looking here. So that's 123, 78 do. And your posterior ribs are the ones which are a bit more kind of like obvious and flatter these ones. Oh, you probably you can't see my mouse, can you? Of course not. Um They're the ones which are kind of like you can see flatter, apologies. I don't know if there's a little tool to show. Yeah. Does e do you, does everyone understand what I mean by the anterior and posterior ribs without me getting a little pointer? Ok. So the ones that you can kind of see like flat, your posterior ones, I mean you can Google it. Um They'll, I'm sure there's going to be like a picture that shows they get narrowed to the anterior and posterior ones. Um Right. So yeah, this was a multiple choice but ii was mean to you guys didn't give you the options. So yeah, lung hyperinflation was the uh answer there. Um And obviously we're gonna expect that with CO PD rather than any of those other ones. Um So which other investigation do you think in this man would be useful? Mhm. Yeah. Lung function tests for sure. Um Nice. Generally speaking, um like uh imaging evidence can be helpful and supportive of a diagnosis, but it's not kind of always needed. Um If you can have lung function tests and you've got a good history that like clinically can, can diagnose it. Ok. We have got now a 30 year old woman who is admitted with an exacerbation of her asthma. Um She normally takes salbutamol and steroid inhalers. Um Which aspect of her history is most suggestive that it's a severe exacerbation. Would it be productive? Cough, deterioration over several days? Recent travel history. She just spent an evening with friends who smoke or she is unable to complete short sentences. I feel like these questions are too nice. Ok. Yeah. Unable to complete your sentences. Um Does anyone know? Yeah. No, that's a severe exacerbation. Yeah. Sorry. Ignore me. Ok. Which uh one of these would be kind of the most concern was the most concern for you. When you, when you've examined her would be BP of 100 and 11/70. Would it be raised? Heart rate? Widespread? Wheeze, quiet breath sounds or an increased rest rate? So, we've got d but not sure. Fine. Ok. So, uh, the answer is d quiet breath sounds. Does anyone know kind of why? That is? Ok. Yeah. Someone said exhaustion. So, yeah, one of the reasons could be because, um, you know, they're, they're getting tired. Um, what we were talking about earlier with the normalization of the um P CO2. So they're getting tired. Um, and they might be heading towards respiratory arrest can also be kind of, they blocked off large areas of their lung. So you literally can't hear that kind of um, gas uh like that air moving through and which of the following would cause you the most immediate concern. Consolidation on chest X ray, the PCO two of 5.8 A po two of 9.2 ACR P of 85 or a white blood cell count of 14. Yeah. Ok. Yeah, nice. I shouldn't have mentioned it the last slide. Should I so? Perfect. Ok. Um, you've decided to add some more medications to her. So we knew she was on a SABA and an I CS before. Um, which of the following. So two of the following uh have been shown to reduce the risk of future exacerbations. By more than 30%. Yeah. Anything else? So all of these have their place in kind of asthma treatment. If you think back to the slide we did with the kind of oh shit me. But this is talking about rather than like acutely what can we add to for her? Like maintenance therapy? What's been shown to reduce the number of future exacerbations? So the answer is C and D um they've been shown to actually between 30 to a half reduce. Um the rate of ex well, yeah, rate of exacerbations, um doubling the dose of I CS can be done, but it doesn't significantly reduce the rate of exacerbations. Um and theophylline and uh anticholinergics um aren't typically used in like maintenance therapy. So you wanna kind of counsel your patient, let's say we start him on an I CS. Um What are some risks that we should warn them about with um long term oral steroids? Three, we're saying three, three of these. So the answer here is cataract, cataracts, weight gain, candida. Um ah, that was a bit a bit mean options for me. So, difference. So a lot, I think a lot of people said be just remembering there's a difference between osteoporosis and osteomalacia. We'd expect osteoporosis with um, oh, have I frozen? Ok. Um, ok. I think some people can hear me. I hope you can hear me. Um ok, fine. Ok, perfect. Um So yeah, osteoporosis. We're thinking kind of uh, inhibition of our osteoblasts. Uh, osteomalacia is more kind of like Vitamin D phosphate. Um, so that was an ea mean trick answer. Um, and then again, the diabetes and syphilis, we would expect diabetes, mellitus, um, increased risk, but obviously that's different to diabetes and syphilis. Um, so, yeah, your classic things would be cataracts, osteoporosis, diabetes, mellitus, um, weight gain, um, an increased risk of infections such as Candida and that can also be with the inhaled corticosteroid. It's important to say the risks are kind of like of steroid therapy with the inhaled ones are lower, but that is um, one to warn your patient about. So make sure they're kind of rinsing their mouth out when um, they're using their, I see. Ok. Final uh scenario for me. Um, you've got a 39 year old, um, who has presented with worsening shortness of breath and a wheeze and you've been diligent and done a chest X ray. Can we see here anyone? Can anyone see it straight away? If not, I can give you some multiple choice answers. Give you like a minute maybe? Ok. Right. I'll give you, I'll give you some options. So I don't know if you can see that large enough now. But do we have a collapse of the left lower lobe? Do we have uh pleural effusion? Do we have some consolidation in the left lung? Do we have some lung fibrosis? Ok. Go on. You've got a 25% chance just have a, have a go nice. Ok. OK. Um So it is collapse of the left lower alone. Um So if we go back to the big picture again, this is annoying that I can't um show you um with arrows, but if you look um at the left lower lobe, so obviously on your right of the screen, you can see that there's like a line down um kind of where the heart border is just kind of within that giving like this weird appearance over the heart. Um I know, I think I actually do have an annotated best of us. So here, um and that is called sale sign. Um And it's basically the left lower lobe has collapsed and you can see that as this triangular area of increased density um behind the left heart. Um It's quite, I think once you know what it is, it's obvious, but I think it's surprisingly hard to, to see and then a bit more nuanced as you can see, actually the rest of the left lung, the markings, the lung markings compared to the right look quite like widespread like that looks like a lot of gaps between them. The markings look kind of larger if that makes sense. And that's because you've got that um upper lobe just filling out the space where the left lobe has collapsed. So you kind of get like the rest of the left lung just kind of expanding to take up the, the gap. Um, so, yeah, that's just, uh, something to look out for right over to Callum now. Hello. So, I, oh, it's come back to the start. Let me flick through this quickly. So I'm gonna talk to you about ps. And so peas, I actually think, sound quite scary whenever I was on my first on call. I got a call from a nurse saying I think my patient's got to pee and I thought, oh no. Um I don't know what to do. Um He's the one that out there. Um What happens a lot as an F one is you have to lift a lot of things up, but you'll once you do that, you know, you learn it and you remember it and it is a learning process. So, so these slides are looking very sturdy for me. So talking about what actually is a pe no PS or clots in the lung? They come from DVTs. But can anyone tell me what the three factors are that cause the hypercoagulability that actually causes a clot? It's known as a triad. If anyone can remember that from probably first or second year, any guesses, if it prompts you, I'm probably pronouncing this terribly wrong, but ver triad, that's it. Exactly. So that is venous stasis trauma and hypercoagulability. And those three things can lead to thrombus formation. And before I move on to the next slide and reveal my answer. Can anyone guess how many DVTs result in P ES just gas? So 30%. Ok. So it's actually fif, well, 51. So it's 5050 chance, um, of the DVT becoming a PE DVTs we're not really worried about, to be honest. It's when they become a pe, that we get worried, but because that 5050 chance it really sets off alarm bells when someone's got a DVT. So in terms of the actual symptoms of a PE, there's usually three key things that I ask a patient when I'm looking for a pe, if they've got signs of a DVT, what do you think those three symptoms might be and don't be afraid to guess and get it wrong because I think if you get something wrong, you remember it and you won't get it wrong in your finals. So shortness of breath and chronic chest pain are two of them. There is one more which I have never seen. Um, but it is a symptom. Oh, there we go. Hemoptysis of the many peas I've seen and treated, I've never seen a case of hemoptysis, but you always ask about cough and coughing up blood. So in terms of actually investigating a pe, so of course, you need to really have symptoms of a DVT for a PE. But what would you do if a patient presented to you with a red, swollen, painful leg? And they told you they had a cough and they had chest pain. What would be the first thing you do? Yeah. So the first thing that I would do is making sure is this patient stable, you know, a set of s and potentially an A to e assessment if they looked on well, because when it comes to management, there's the management of the unstable, unstable pe so what we normally start with if they're stable is we do bloods, particularly the D dimer, we will calculate the well score which you, you'll never remember off the top of your head. You always have to look it up and A C TPA, the ultrasound is very good for looking at um A DVT, but for what tends to happen is you treat these things before you confirm the diagnosis. So for the DVT, if you think someone's got a DVT, and you're worried that if they're stable and you don't think they've got a pe, you can usually wait for an ultrasound scan, but most hospitals will only do that 9 to 5 Monday to Friday. So if they're unstable or you don't think you're gonna get an ultrasound any time soon, we often just start treatment with anticoagulation. So you've got say you've confirmed it. A patient's got a DVT and you think, yeah, I think this person's got, you know, they've got a cough and they've got chest pain. So I think they might have a pe and you do a C TPA. So C TPA. S, you can see very big clots, very small clots. But, and also the issue with the C TPA is it requires contrast. And a lot of people who are at risk of DVTs and P ES tend to have poor renal function and some trusts I think, um depending on their EGFR is between 3030 sometimes it's 50. If it's below that, they say no, we're not giving contrast, you actually can't do the CT and we again, we just tend to treat. So we do see TPA on someone. Can anyone spot the diagnosis on this one? Anyone can guess where they might see something. What if I show you the next slide? So if you look at this slide, which is a normal CT PA apart from, you can see a bit of a shining whiteness that's probably just a bit of metal or artifact. But if you now look at this one, you might be able to spot the diagnosis. So this we call a sidle pea. Yeah, that's it. So this is a pea is the one that can be missed. Thankfully, we have radiologists that look at scans. People always go into the pulmonary arteries and the small arteries looking for clots and they often don't actually look the p the big major vessels. Um This is a very, very big subtle p it usually much more subtle, much, much smaller and you can just see it sat there, but this is a very big one. This is, this is going definitely going to be a very unstable patient, something that we've been very worried about. So we go into management, like I said before, we've got the unstable versus the stable. So in an unstable patient, it can often present peri arrest, it can cause um arrest. Sometimes people have a massive pe and they just drop and their heart stops. So if they're unstable, we use unfractioned, unfractionated heparin, which is an IV infusion because it's got a short half life and we give big doses and it's more easily reversible. And we would give thrombolysis like we do in a stroke as well. But we don't tend to see that very often and it's not very survivable either if someone is very unstable like this. But what you do see very often is a stable pe and there is different options. Some people use low molecular heparin, subcu um enoxaparin or Donax. We tend to use low molecular heparin for peas. And for some reason, we use Dox for DVTs, even though the evidence says they're both as effective as each other. The only very useful thing to do is the Pezzi score, you can find that on MG CALC and that's a mortality score. So usually when people present stable um with a pe, they can often go home. But if you look at the Pezzi score of the risk of mortality, it kind of helps you judge, can this person go home on anticoagulation or do we think actually this person needs to come in because they could, um, they could get worse and get very unwell because if the, if the treatment doesn't work and the, it gets worse and you get a bigger clot, you can go very, very, very quickly. So, I've got a scenario, 58 year old woman comes into Amy short of breath, right sided chest pain, long haul flight from Australia, no cough or fever X ray doesn't show anything. E CDE CD doesn't show anything which is quite a typical presentation. Um What would you do in this sit? And what's the first thing you would do? Great. So what is we do? We get taught about well scorers and what it means often you'll find that actually everyone gets a C TPA. Um um Quite literally everyone they have um we always calculate that, you know, we use a ddimer and we use the well score to indicate they need a C TPA. But actually virt virtually everyone gets a C TPA. Go for help. Um Yes, definitely. If you are ever unsure about managing someone, you're worried about anyone, definitely um ask for help. So the first thing we would do this patient cause we're thinking she's stable. So, you know, her heart rate and her BP were ok. Her respiratory rate's ok a little high, but there's nothing ringing alarm bells that this patient is very, very unwell. So the first thing we do tend to do is bloods. So the reason we do creatinine and egfr, main reason we're doing that is actually for the C TPA. But also it will determine the dose of treatment that you give. Platelets can be helpful and hemoglobin. Um But the big one is AD dimer and one thing that I didn't know when I started was an F one, I actually did not know what the ddimer mean. The lab ranges say greater than 400. But actually that's, that, that doesn't mean anything. Um Does anyone know how you actually interpret what would be classed as a positive ddimer? And I'll be impressed if you get it. Cos to be honest, I had no idea when I started as an F one. Yeah. So low values if it's negative, we definitely think, yeah, this is not, this is not a, a pe um high value. This is our interpretation gets tricky, but we have a very helpful test that we use and it does vary. But in our trust, we use the age adjusted ddimer. Some people will tell you it's, the patient's age is times six other will tell you five. I just go for five because it's a safer option. Um So this patient's quite young. 58 5 times 58 290 the D dimer was over 1000. So in this patient, it's positive what we would call a true D dimer is in the thousands. Um, usually greater, much greater than 1000. That's a, yeah, this is, this is a pe, a lot of the time you're finding pretty much most people you do ad dimer in. It will sit in this awkward position between 4, 600. And that really doesn't tell you very much. What do you call that borderline? And that doesn't, that doesn't, um, doesn't make it very helpful. We just tend to, like I said before, we do C TPS in basically everyone. Um So although we do the D dimer, you re you request ad dimmer and at the same time, you request a C TPA sometimes depending on your hospital, but radiology might be like, no, we need ad dammer a well score. We're not accepting the scan, but often I think for us they tend to just scan them anyway. So it is helpful. Um But where a Dunger is very helpful is if you suspect a DVT in someone and the ultrasound scan doesn't show a DVT, so you don't need to treat because the, it's negative, but the, if the D dimer is raised, they have to come back within a week to get another ultrasound scan just to rule out. Um I don't know exactly what a ddimer is actually, to be honest. Um I'm sure someone can help look that up and help us out, but I don't, I don't really know what D number, um, specifically measures. Um, is your test? I wanna lift it up for me. Um So b before I just finish with, um, PS and DVTs, um, I think the really important thing is, is that always be safe in these patients and you will f you will get a lot, a lot, a lot, a lot of query, D VTI see it all the time and it's very rarely DV. TPE. But just, even if you don't think it is a DVT, you just need to make sure um, that you're safe and that you always speak to a senior. Um and they can sort of help you make that decision and to be honest, they're probably gonna scan them anyway. Um And thank you Eric Monomer Release for fiber and breakdown. That is more than I know. So I'm very impressed. So, is there any other questions on PS and DVTs before I move on to talking about pneumonia? I'll just give you a second to type out any questions before I move on? Ok, I'll move on. If there's any questions, I'll go back to the end. So pneumonia is probably one of the most common um, things that you will see presenting the hospital query, uti query cap, probably the most common things you'll see. Um So with pneumonia, it's either a cap or a hap community acquired or hospital acquired. Pneumonia tends to be after 48 to 72 hours. Um Is uh some of being in hospitals when you can label it as a hap. And that's important because it would, the main reason really is the antibiotic you use because the likely organism that you get in a hospital acquired pneumonia will be different from a community, acquired pneumonia. And I'm, I'm sure you all know the curb 65 score and it is very helpful. Um, if you're unsure or if you are, you know, a GP or in the community and use a CRB 65. But in hospital, we tend to not use it so much in terms of treatment, but it's more of a guide of will we send this patient home? We don't usually rely on the curb 65. We usually just clinical judgment. Does this patient look well or unwell? But officially the curb 65 will determine whether or not they stay in hospital or they can be treated in the community. And this is just it here as I'm sure you all know, I can never remember. I always forget one. I really honestly always forget one. and I sometimes do have to look it up. Um but you will become very familiar with it. So the main sort of factors in diagnosing it is your cough with sputum production, shortness of breath, chest pain rigger, night sweats, you just usual signs of a chest infection. And in terms of investigations, virtually everyone coming into A&E gets a chest X ray and E CG. Um I have it has been known for reasons to be put on a chest X ray request as ed patient. Um So basically everyone can get a chest X ray. So the new score and the curb 65 really as high on. Well, this person is in an exam situation, you always ask for an ABG. Oh, we've jumped, we always ask for an ABG, but in reality, you very rarely do an ABG unless they're very unwell and your patient will not thank you for doing an ABG either. So we do your bloods and your blood cultures. If you think they're septic and sputum culture, which again is that classic exam thing. I would like a sputum culture but your patients very rarely provide you with a sputum culture. They never really managed to bring it up, but they always end up throwing it away when you've been begging for days for a Sputum culture. Cos uh microbiology have insisted on getting one. That's just the joys of being an F one. So this is just your typical pneumonia on a chest X ray you can see drawn in here is the consolidation pneumonias like this tend to be quite obvious. And um not a whenever you get asked by a consultant, what, so what's on the chest X ray? They don't usually want you to do the osk scenario of L doing the A to E thing, but definitely learn that for your exams cos it will get you points, but you can be relieved that when you are actually a doctor you would not be expected to do that. Um, and the other thing just to talk about is atypical pneumonias. Um, does anyone know what makes this an atypical pneumonia? Any guesses? So on this x-ray, you can see the eyes on both sides. So 10 atypical, you know, you can't see the low bar consolidation is in one place. So we label that as atypical and atypical is very, is a very broad term. Um, but there's two specific tests that we do and again, I'll be impressed if you get this, but there's two particular tests that you do in addition to the ones we've already talked about. If you think someone's got atypical pneumonia, if anyone can guess so. Yeah, urinary legionella antigen is definitely one of them. Again, I've never seen one positive, but we always do one and there is a second organism that we're looking for. It can be tested in different ways but tends to be swab of the cheek or sputum culture. If you can get the sputum, think of your classic atypical pneumonia that would scare you if you saw it on a chest X ray. Yeah, mycoplasm. Exactly. Um, that's another atypical pneumonia. So if we go into our management, of course, your septic patients is your sepsis six and IV antibiotics. Um, but we tend to, although you're sepsis actually think broad spectrum. And a lot of people often try to think of tazocin, but usually people don't present as sort of acutely as it's made out. You, you know, you've got a 10 minute OSC and you think seps a six and you bang out your sepsis six gotta do this straight away. But actually, in the guidelines, it actually says that someone in septic is to give um treatment within one hour. So when someone presents to A&E although they've been there, they might have been there for a while. You do tend to have time to look up and speak to someone and actually get the, the right antibiotic the first time depending on what the guidelines say. So again, this is the curb 65. You'll see it if you use E PM, it asks you to, to also, um categorize although clinically don't often use it to um, judge the antibiotics. But for exam purposes, of course, um, if it's low severity, we often think oral antibiotics at home and we often start with amoxicillin and then if it's more moderate, it's kind of in that borderline of hm. Are we gonna do oral? Are we gonna give IV do they need to be an inpatient outpatient? And we start with amoxicillin again. But sometimes we can also add in Clarithromycin or you can um, give it camox instead which you can see in the high severity if you're quite worried about someone you just jump in with IV. Camox and Clarithromycin. Does anyone know why we avoid IV, Telithromycin? This is something that I've had both nurses and pharmacists. Tell me off for prescribing any guesses. Ok. Yes. So it is just as bioavailable. Um, so if someone's on oral, it has, it's just as effective as IV, but the reason you try to avoid IV as well, especially is because it can irritate the veins and, and irritate. So it can um stop the cannulas can cut off and cause pain to the patient. But also, um, if you need to use it, you need to use it. You know, someone's vomiting or they're too unwell to swallow. Of course, then you need to use it. But often in ward settings when people aren't doing well, have been told off for prescribing IV Kari. So, and a question to finish yourself. So a 62 year old man is at his GP. So his shortness of breath, difficulty breathing got yellow sputum. He's tired, he's got a fever, not really any medical history. And when you examine him, he's alert and orientated, normal respirate heart rate, sat normal BP. You could argue he's a little low but not necessarily in someone who's young. They do have a fever and you can hear by basil crackles. So what do you think in this situation? Are you going to do with this patient? Anyone have any ideas? Yeah. So if you think if you look at his, if you were to calculate a new score for this patient, you probably get a three. I think if I can remember correctly. Um, the BP is sort of the low one. But if we remember this person is in a GP surgery and it's something that very commonly will trip you up in exams is actually the setting that you're in. I made it a bit harder for you because this is a past med question with multiple choice and I've not given you that, but he's in a GP. Um So the first thing you would tend to do is the CRB 65. We don't have Urea available. So that's why we do CRB 65. So he's not confused. His respirate is normal, his BP, it is a bit low, but it doesn't actually meet the curb 65 definition of hypotension. I think it's less than 90 correct me if I'm wrong. But this would actually score C RB 65 of zero, which is tells you that actually this person has a very, very low risk of less than 0.7% chance of mortality. So you can be confident to manage this person in the community. So the GP wouldn't need to refer this patient on to hospital. And of course, in your community, you're only gonna have oral um, medication. So oral amoxicillin is your first line. I didn't mention though if you're penicillin or panallergic that we don't go in with amoxicillin and we can use CFC and Erythromycin. Um, but again, it would probably vary on what hospital you're working in. So you can never really rely on which antibiotic you give, you really should always be looking it up. Um, which is a good point. So that is the end of my slides. Um Has anyone got any questions about both mine and Izzy's part of the presentation? I'm gonna give you guys a few minutes to uh send in any questions you have and of course, please, please please provide feedback. Um One thing as well you'll learn as an F one is that the portfolio never ends. You'll be doing your portfolio for the rest of your life constantly asking people for feedback. Um So we appreciate it very much guys. Um Again, just any questions. Thank you, both of you for a great talk and thank you to the audience for answering all the questions. Otherwise we'd be speaking into the void. Um If you have questions you think of later, um You can message us on.