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Ok, great. So it's just coming up to seven. So I've clicked live just to start the recording. Um So welcome everybody to today's talks. We'll be covering, covering respiratory, which is one of the main um general medical topics. Um But before we get started, we've got a message from um the BMA. So D over to you. Thanks, Kirsten. Ok, I'm just gonna put a little message in the chat. Um show my show my screen. I shut up. So yeah, just very quickly from me. Um I was hoping to have a bit of a bigger update for you guys on sort of what's going on. Um Junior wise and the and the talk. Um But yeah, don't necessarily have that today, but possibly um next week. Um So there's a bit of a um a bit of an offer on the screen for anyone who's, who's not a BMA member. This is a bit of an exclusive to today if you join using that link. Um and drop me an email afterwards, you'll get a 10 lb Amazon voucher. So yeah, just use that QR code or link. I'll put in the chat. 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So, yeah, things like things like your contract and your pay. Um, and then locally, uh, so things like when you are sort of next year, uh, in, in your trust, um, it does sort of a collective issue for, you know, an F one, you guys can come to us and, and we'll, we'll sort out any issues, um, and then, yeah, on, on an individual basis. Um, you know, sadly the NHS is not the most perfect place to work in there. There, there will be sort of things that arise throughout your career. Um But yeah, anything nonclinical related, you've got, um, we've got your backs and, and we have people that are on the ground in every, every trust across the country. Um, we usually get answers pretty quickly to, to things and get things pretty sorted. Um, at the moment our memberships at 191,800. Um, so you got to remember that that's just medical students and doctors. So, it's, it's incredible really. Um, the, the backing that everyone's giving each other, um, obviously a, a union only works if you're sort of pulled together and, and everyone's seeing that now with the strength of, of what we're all doing together, um, with the strikes and, and pushing for, for, for better pay. Yeah, like I said, II don't have much of an update. Um, there's been talks for the last few weeks. Um, it's been a bit hush, hush. What's gone on whether they've gone well or not. But, um, yeah, don't be surprised if you sort of hear that we're going back on strike with the juniors. Um, sort of, I don't know if it's the end of next month or sort of January. But, yeah, it's, it's been a bit quiet. So, my, my, um, reckoning is that, is that there may be further strikes soon. Um Yeah, so just a few tools for you to think about in here. And now, I mean, like, I guess you guys have heard all about strikes and what's going on. I hope you'll, you'll keep keeping up with that. Um What's going on with the consultants today? Um But yeah, I just wanted to remind you that there are other things that the BMA does. Um So if you remember um you get access to BMA library, so that's, it's one of the biggest libraries there is. Um everything's moved online now. We used to have all the books at, er BMA house and you do sort of get them posted out to you and post them back. Um Now you can access everything, er, digi, digitally so you can log in bma.org dot UK four slash library. Every book you could, you could ever want is, is right there. So that, that would be helpful in, in front of you. Uh B MJ learning as well. If you've never used it, it's got really good er, vision tools and lots of modules online for you to use. So just have a little play around with that clinical key. I don't know if you've ever used clinical key but if you haven't downloaded the, the app um and you can log in via er, your BMA membership, you may have access to it through the med school as well, but there's no paywalls with the, with the BMA version of the C of clinical key. Um So, yeah, again, you just type in any condition um and it'll bring up every single book journal, um video related to it. So, um really good point of care. Um B MJ. So now you're in your final year, um you can't, you have actually got the right to have the B MJ through the post um every week. So the, the physical copy, um the thing is it's an opt in service. So you just need to give us a call or a quick email and say, look, I'm in. Finally, I'd like to get the, the, the paper version through the post. Um And we'll turn that on. It will be no, it won't be any extra money. So that 3 lbs 75 a month will include um four copies of, of the B MJ. So one every they come every Friday. Um And alternatively, you can obviously switch it off any time as well. Um We have a really good wellbeing service. Um So the unique thing about this is you have the choice of speaking to um a peer, peer support doctor. So someone who's been through um similar situation, oh, sorry. Um Somebody who's been through a similar situation to, to yourselves or, or, or a counselor and, and if you call us more than once, we'll make sure that you speak to the same er, person again, um, s is quite a well used service but it's, it's, it's, that's what's there for. But, yeah, obviously, um, just come to us if, if you, if you feel the need to use it, um, again, completely confidential of the, of, of your med school and of, of the trust, er, er, you'll be working with, um, specialty explorer tool. So this is quite a unique tool. Um, good to sort of do this now, maybe, er, a, a little bit of the way into F one obviously beyond um essentially a psychometric test, takes about 20 minutes to complete. It'll ask all sorts of work life balance questions. And then at the end, it will give you a breakdown of the top suit specialties according to uh the answer you've given. Um So it's good to start to think about specialties now, obviously, I think too seriously, but, but this kind of tool. Um Specialty explorer is a, is a real help for that. So that's it just, just one of a couple of minutes at the start of this to, to sort of remind you that the BMA is more than, than the pay campaigns that are going on. Um, and we can help you. Um, now and again, if you're not already a member, definitely join. This is, this is a pivotal moment in, in uh in the history of, of junior doctors as consultants as well as um SAS doctors. Um So yeah, the more, the more members we have, er, the better we are, um, the stronger we are. I'm gonna stop now because my C has taken over anyway. Um, but yeah, if you're not already, uh, a member join, er, you get that time. 10 Amazon Amazon voucher. If you use that link on the screen, if you go online you don't get that. So, yeah, take advantage of it. Um, and yeah, I'll hand you back to. Hello, thanks so much Daniel and that's really helpful for us all to know about. Um So welcome everybody. Um It's really great to see so many of you tuning in today for today's respiratory talk. Um Just to introduce myself, my name is Kirsten. I'm an fy one doctor on the academic program um on the S FP program at Saint George's Hospital. Um and I'm currently helping co-lead the final year content of mind the Bleep, which includes running this revision series. So we really hope that you've been finding it useful so far. There's a couple more talks to go that will lead us into the Christmas and the New Year at the end of the talk, there'll be a chance to give feedback and it'd be really great if you guys could all complete that, it really helps us guide the content to what's most useful for you. Um moving forwards for the rest of the year and as we develop the series and just for those that usually ask the recordings and the slides are usually available on Medal um afterwards is catch up content and will also be recorded and uploaded to youtube as soon as possible. Um So let's get started. If there's any questions um about the content as we go through, please put your um question the chat and I'll try to answer them periodically as we go along. Cool. Can everyone hear and see the slides? OK, and hear me? OK. If you just confirm in the comments before we get started, everyone able to hear me. Yeah. OK, perfect. Mhm. Great. So this is an overview of what we covered today. I thought refer to such a big topic. Uh I'm gonna cover what's most common and most high yield for your examinations. So first of all, we talk about lung function tests and then some of the really common conditions and presentations you'll see in the MC, Qs and Sys and this is the MLA curriculum for Respiratory. A lot of what we'll cover today um will come under this. So hopefully it'll be a useful talk for you all. Great. So let's start off with lung function tests. Um So we talk a lot in respiratory about F EV one and F VC. Um some wanna type in the comments, what they understand what these acronyms mean. What does F EV one mean? What does F VC mean? The times you've come across before? It's all right. If you not? Um, that's ok. Oh, good. Forced expiratory volume. Exactly. So FV, one is the amount of volume that you can produce on a forced expiratory breath in one second. And, yeah, absolutely. FBC is forced vital capacity. So that's your total amount of, um, kind of forced, um, breath outwards. That doesn't have a defined time period. And that's spirometry is a really useful, um, tool in diagnosing lung disease because it helps us classify between obstructive and restrictive diseases. So, with restrictive diseases that if you picture your lung, for example, in fibrosis or in connective tissue diseases, not able to expand as much um as before. Um then your total forced vital capacity is smaller. However, your F EV one, what you can achieve in one second shouldn't be too much affected um because it's the 1st 2nd. So you usually find that your ratio is normal. So this is common and also neuromuscular disease and obesity. Um which makes sense because you don't have the kind of strength from your respiratory muscles, um accessory muscles to generate a larger forced vessel. And then in obstructive diseases, you usually see your F EV one is markedly decreased and that manifests as a ratio of less than 0.7. So if you think about your obstructive diseases, like COPD asthma is reversible. Um airway obstruction, bronchiectasis, and cystic fibrosis. These are all common obstructive. So this is really important and we often use spirometry and say COPD to define that it's an obstructive pathology. So let's move on to talk about asthma. This is one of your most common respiratory presentations. And the key thing to note about asthma is that it's reversible and this is how we diagnose it, which I'll touch on in a minute. So you've got airway airflow limitation in your airways. And this is usually due to a hyper responsiveness of your airways and you get two types one, which is childhood onset where you see a younger age of presentation. And this can be due to kind of allergens that you inhale. Whereas those who have late onset asthma tend to have a of a occupational nature. And what can precipitate this many different things including house dust, mites, dust, vapors and fumes, even infection, cold air exercise and emotion. And a classic MCQ question is what drugs might precipitate asthma. So you're having to think about nsaids, aspirin and beta blockers. That's a really common one. So you wouldn't give beta blockers in someone who's asthmatic, they're contraindicated. So, asthmatic patients tend to have intermittent coughs, shortness of breath, they have a sensation of chest tightness that they report and they can be wheezy either audibly if it's severe or on auscultation. I mean, you usually see an expiratory wheeze and they also have a dry cough that's non productive. So usually if someone does have a productive cough, you want to be thinking more of an infection if it's purulent and asthma gets exacerbated when they're exposed to these precipitants and different triggers, which can be different for each individual and also at nighttime. So you have nocturnal symptoms. These are questions you'd want to ask in a history of an asthmatic patient to help differentiate between other respiratory conditions. Um And you also see asthma in patients that are atopic. So they also suffer from say hay fever or eczema or in patients where there is a strong family history of asthma as there is a hereditary component. So how do we diagnose asthma? So for those who have done their pediatric revision, we know that you can't diagnose asthma in Children under five, we usually known as viral induced wheeze. But for those who are over than five, we turn to spirometry first. And the key part of spirometry is pairing that to bronchodilators to see if asthma patients improve after receiving a bronchodilator. And the test is positive if the fev one improves by 12% or more as well as an increase volume of 200 mL or more. So, that's a kind of really good way of testing that airway reversibility. And then another way to look at asthma is to look at the fractional exhaled nitric oxide. So the pheno and then um different values, sorry, it should say 40 PPV for adults and 35 B for Children. Um So those are your classic M CQ questions. Um One thing to note is that your feno can be elevated in airway inflammation. It's not just asthma. Um So it's a good way to kind of I have asthma, but it's not specific to asthma. So sensitive but not specific. And you know, many people ask what is actually is it, um it's just a way of indicating how much inflammation there is in the lungs. Um So nitric oxide is a biomarker to indicate the level of inflammation. And so you're testing the levels of nitric oxide in your breath. And then if you're uncertain, you can also add in a peak flow to see um how people can keep. Although it's used only if there's kind of diagnostic uncertainty and then lots of people, especially patients always ask this question, what triggers my asthma. Um So you can use skin prick tests after diagnosis to identify the allergen. But in terms of diagnosing it as a condition that wouldn't be your first line. So, spirometry first and then pheno is what we'd recommend and peak flow is a really good way to monitor asthma as well as people improve. Um not just to diagnose. So how do we treat asthma? So there's kind of a stepping stone treatment um as you've come across. So it just depends on first line and then how well they tolerate that or how well it controls their symptoms. And in the community, we aim to for asthmatics to be completely symptomless. Um So those that have new um a new diagnosis of asthma, we typically start them on a short acting beta agist. So this will be like salbutamol for those with newly diagnosed asthma. Um New guidelines can also say you can start on a um corticosteroid inhaler. So, inhaled corticosteroids instead of just sa and then you can again review and then review the response. It's important to give um kind of time, treatment, time to see how people respond. And then if not, you can also add in kind of a long acting agonist. So like an LTR A. So and examples of LTR A S would be like Montelukast. So these are leukotriene receptor antagonists. So you've got your salbutamol, then you've got your inhaled steroids like beclomethasone and then your L TRS like Montelukast. And then if that's not doing great, great, then you can add in las these are more your more long acting be agonists. So for example, salmeterol for um there's lots of different names. But if you try to remember the acronyms of the mechanism, that's a really important um to distinguish. And then if you're really struggling on top of that, you can do what's called maintenance and relief therapy. So ma so ma consists of an I CS and a fast acting Laer in a single inhaler and that is used both daily and for maintenance and symptom relief. So that's a really good way. And then you can step up the strength of your um inhaled corticosteroid inhaler based on how well you're responding to the ma treatment. And then if on a medium dose um inhaled corticosteroid, um you're still not even in control, then you can probably seek specialist advice at this point. So a lot of this can be managed in a GP community setting, but you wanna seek more specialist respiratory input if you find yourself here. So um acute asthma. So when a patient with asthma finds themselves very breathless and this is a medical emergency situation, it's really important to risk stratify um between this. So this is a medical emergency and this is when an asthma is not responding to salbutamol, there's worsening shortness of breath cough and a wheeze and it's often an infection that might trigger this all, something that's really important to consider as an ABG because that will help guide you um in terms of their oxygen and CO2, because when someone has an asthma attack, they often get tired of breathing really heavily and that becomes really dangerous when they get exhausted. So when someone has a normal PA CO2 on their blood gas, that starts to become worrying and life threatening. And then for example, if they, they start to retain CO2, that means they're not blowing off carbon dioxide and they're getting even more tired. Um So that's near fatal and that's where you want to escalate as soon as possible. So, yeah, I pretty much put a table summary of all these different values that are really important to learn from an M CQ question. Um You can look at their peak expiratory flow rates, their respiratory rates, their heart rates. It's really important to get accurate observations on your acute asthmatic patients. Um And then on examination, what might you see for an acute asthmatic patient? You see reduced chest expansion, a prolonged expiratory phase and bilateral expiratory polyphonic wheeze, it's really typical in asthma. So yeah, always do an ABG as a first line assessment for asthma. And initially, you'll see respiratory alkalosis as you hyperventilate and blow off C OT. And then as you become acidotic, that becomes more concerning because you're retaining that CO2 as I mentioned. Um So these are patients that tend to need need admitting. And a classic M CQ is when to admit these patients. So if someone's got features of life threatening asthma or after initial treatment, they still have severe asthma or they've previously had a near fatal asthma attack or they're pregnant. Those four criteria of reasons to admit patients into the overnight into a medical team for acute asthma and then how we go about treating acute asthma. So you start off with salbutamol inhaler um and oral prednisoLONE initially, four puffs and then two puffs every minute. And then if that doesn't work, you can consider, consider driving the salbutamol with a nebulizer with oxygen pushing it in. Um And also if they've got an oxygen requirement. Always start acutely on our patients on 15 L of oxygen and then titrate down. You can also consider ipratropium. So nebulizers as well. And then at that stage, you'd want to escalate to a senior if there's still poor response. Um with your ipratropium and salbutamol nebs can consider things like magnesium um and theophylline as well or escalating to it. So it's really important with asthma is it's a life threatening emergency to escalate as soon as possible. Great. So I've got a um M CQ question for you guys to practice. So to pop your answers in the chat. So you're sitting in on a respiratory clinic and you've been asked to review your patient's spirometry result. Sheila is a 52 year old woman who was referred by her GP for spirometry due to symptoms of worsening, breathlessness and exertion and a chronic cough, productive of white sputum. She has a 60 pack year smoking history and her daughter has told her she thinks she has lost weight but she hasn't noticed herself. Her spirometry results show an F EV one of 1.9 predicted 2.94 and an FBC of 3.48 predicted 3.52. What is the most likely diagnosis? So pop your answers in the chat? Cool, getting a lot of bees. So that's really good. And can someone comment why they think it might be bee? I, why have we gone for CO PD smoking history. Absolutely. Significant smoking history. Low se B1. Yeah. Good. So, those are your two main clues is that this is an obstructive picture and someone has a heavy smoking history. And if you also look at that age 52 you're less likely to come across lung cancer for the first time or less likely to come across asthma for the first time if there's no occupational risk factors and good well done. Um So yeah, let's move on to talk about CO PD. So CO PD is chronic obstructive Pulmonary disease and it's umbrella term for two features. So there's chronic bronchitis and emphysema. And that's another classic question and really important to know is how do we go about diagnosing someone with CO PD? It has to be obstructive in nature and you have to have these elements and the most common cause of um COPD is smoking and in younger patients or those without a smoking history can be alpha one antitrypsin deficiency but can really be any kind of respiratory exposure. So for example, chemicals, fumes, dust pollution, they all can contribute to AC APD like picture symptoms of people with COPD is they have chronic shortness of breath that gets worse and worse and they often have cough, it's productive, wheeze and are more liable to recurrent chest infections. And if it's severe, you can often see purse lip bruising as people try generate positive pressure in their airways with purse lips and poor chest expansion investigations. As we said, we diagnose this with spirometry and on chest X ray, you would see hyperinflation. So you see flattening of the diaphragm and you see an increase in the number of ribs seen on chest X ray that would suggest hyperinflation. And then you'd also want to send off sputum cultures for patients with COPD. As we'll touch on later, they're more likely to get recurrent chest infections and grow kind of more weird and wonderful bugs than a patient who doesn't have respiratory disease. And that will help guide antibiotic management. So your follow up question is you have calculated Sheila's F EV one to be 65% of predicted and an F EV one to FBC ratio is NT 0.55. What is the severity of SC APD based on this, this question a little bit harder, but we'll talk through the answer moderate, good. So Bayer's gone for moderate. Um So this is how we classify CO PD. It's based basically on F EV one F EC ratio. Um and then on the right hand column, I've put in some symptoms that you might expect to see. So you, as you can see as your F EV one gets smaller and smaller um of the predictive value, you get increasing breathlessness and it can be even at rest in people with very severe COPD. So this is a really important staging criteria to remember. Um it's all based on FE B1 and then also on the condition that the ratio is less than naught 0.7 cos that proves an obstructive picture. Um So yeah, this is just a classic M CQ question. It was worth remembering. So I put the table in for you for revision. So how do we manage CO PD? So given that most people get CO PD from smoking, the first thing we would do is advise smoking cessation. And does anyone want to put in the chat methods that they know I could aid patients with smoking cessation? Mhm. So this is something we do day in and day out on a respiratory ward, we have a lot of patients with smoke histories. Um Exactly. So nicotine patches are kind of our mainstay to help people kind of quit smoking in an acute setting as long as well as say like nicotine inhalators or nicotine lozenges, they can be really effective too. Um So initially, what we would do is start with a saber. So a short acting beat agonist or a saber. So short acting Muscarinic antagonist like ipratropium. Um and then if you have persistent symptoms or exacerbations, you can add in a long acting vasa agonist and a long acting muscarinic agonist. And then the thing to remember is if AC O PD, patient presents of asthmatic features or they are either ahi or they respond to steroids, you can also consider adding an inhaled corticosteroid that we use in asthma patients. Um and then for patients to prevent cop DS will prevent infective exacerbation. CO PS we can think about rescue packs of antibiotics at home. A pneumococcal vaccine, the annual influenza vaccine. These will all help prevent and can also think about with patients with frequent exacerbations using azithromycin as prophylaxis. And then another thing is you can offer pulmonary rehabilitation for everyone who feels affected by CO PD, feels that their breathlessness is hard to manage. That's really effective. And for those really struggling, you can think about long term oxygen therapy. Um So these patients will have oxygen cylinders at home and can administer themselves oxygen to relieve their symptoms. And this can be indicated if they have a PA O2 of less than 7.3 or if they have a PA O2 of less than eight. And they have either one of these features on top. So secondary polycythemia peripheral edema or pulmonary hypertension. So, these are all really useful tools for someone to manage their C APD in a community setting. Um Obviously long term oxygen therapy is contraindicated in people who still smoke. Um But it's something worth thinking about for severe COPD patients and you would use a APG blood tests to help guide whether they qualify for lo treatment, say long term oxygen therapy. So, a really common presentation in an acute hospital setting is acute exacerbation of CO PD and this is often a bacterial or superimposed viral infection. In a patient with CAD, the most common bacterias you'll see would be Hemophilus influenza and also strep pneumonia and human rhinovirus as a viral cause. Your patient will come in with increased shortness of breath present with a cough, sputum wheeze and be hypoxic and have low saturations and they also might have acute confusion um in the context of acute illness and the complications would be respiratory failure. How do we manage this? First of all, we wanna get a chest X ray to look for other respiratory causes. Look for any consolidation that might be um from the infection. And we'd also do an ABG to help guide us if they're in respiratory failure or if they're struggling to oxygenate. If they're hypoxic, we use oxygen. Don't forget the cop TCO PD patients if they are retaining CO2 on their blood gas, that shows they're a chronic carbon dioxide retainer. And we like to aim lower in our saturations in these patients because the hypoxia is actually a drive for these patients to ventilate. And so we want to aim 88 to 92 deliberately. Um and you can start off with 15 L. But if it's C A BD patient with chronic hypercapnia, you can use venturia masks as well to help adjust the oxygen delivery. And then in terms of treating the exacerbation, you can go for Sabol and Ipratropium nebulizers. It is really common and they also add in oral prednisoLONE for five days. And then if you feel they are infective, depends on your micro guide at each local trust, but we'd go for Doxycycline as a bro. Um broad enough antibiotic cover and other useful tools to treat. Um infective exacerbations are chest physiotherapy to encourage the expectoration of sputum. And also bipap can be considered for patients with worsening respiratory distress. So, with a respirate of over 30 or if they find themselves in respiratory acidosis on their blood gas. So they have a ph of less than 7.35. Um and they've failed to respond to optimal medical treatment. Now, we can think about aiding ventilation or non invasive ventilation. Cool. I hope that all makes sense so far. I've got another M CQ for you guys. So 663 year old woman presented A&E with confusion after a fall, she has a productive cough and is short of breath. Her respiratory rate is 32 and her temperature is 37.8. Her heart rate is 90. Her BP is 85/65 and sat is 94% on air chest. X ray reveals right lower zone consolidation and blood results come back with a urea of eight. What is this patient's curb 65 score? Again, another classic um M CQ question. You just pop your answers in the chat. Cool. They've got a few different answers here. Some threes, some fours has to be a few more people to put their answers in. Again, all three of four people change their mind. OK. Cool. So the answer is C is four. So let's have a look at the breakdown of the criteria of C A. So CB 65 is um super useful helps um kind of aid how we treat patients, whether they should be treated in the community or they should come to the hospital and helps tell us the severity of their infection. Um So this is for pneumonia patients, very classic chest infection. So they present with shortness of breath, they might be febrile, have a productive cough and have some pain from all the coughing. So, pleuritic chest pain or also kind of pain in their lower zones. If the consolidation, an infection is in one of the lower lobes, on examination, you would expect reduced air entry, um, crackles on auscultation and also reduced expansion of their chest. And then there's different ways you can classify pneumonia. So it can be community acquired versus hospital acquired which um is the onset of a pneumonia 48 hours after hospital admission. And there's other types of pneumonia too. So you can think about um aspiration pneumonia. So if someone developed a pneumonia after kind of choking on food from an unsafe swallow or aspirating on their own saliva, or is it atypical? And that refers to the bugs and the organisms that have caused it. So, for community acquired pneumonia, pneumonia, you would turn to curb 65. So confusion gets you one point. It's also important to establish the patient's baseline confusion because in lots of patients, they have some background level of confusion already. Um blood. So using these will tell you the urea so greater than seven gives you another point. Um and then ob so respiratory rate over 30. So if they're tachypneic, that'll give you another point. And then um B is for BP. So if their systolic is less than 90 or their diastolic is less than 60 they're hypertensive, that will give you another point. And then age increased, age also puts you at risk. So if they're over 65 that'll give you another point. Um So yeah, our patient was four out of five on the curb scale cos they had a, they were 63. So they had one less point from 65 but they had um respirate of 32 and they had BP s uh systolic of 85. Um and they also had a urea of eight and they also presented confusion after a four. So that's why we've got a score of four. And then this little table is something really useful to learn in terms of MC QS about common organisms in pneumonia. So for a typical cap, you see, strep pneumonia is your most common bug. Um And then in CBC O PD patients, it's worth thinking about Hemophilus. Um and you might also get a superimposed influenza viral infection over a bacterial component. And the other atypicals include mycoplasma that you can look for in the blood and also legionella, which you wanna look for in the urine. Um, in those with immunosuppressed um, patients, you want to think more when wonderful bugs. So like Pneumocystis, aspergillus, pseudomonas and cytomegalovirus are more common. And then when you go into a hospital acquired pneumonia, staph aureus, klebsiella and pseudomonas are all your more common bugs. And then you can think about your enteric enteric gram negative bacteria too. And then if the MC stem has some occasional risk factors, think about chlamydia, setacea contact with BS and Coxiella burnetti is contact with farm animals. So one to remember. So for cap, how do we investigate um pneumonia? So, thinking about chest x rays, um just going to look for consolidation in someone with pneumonia and then you want to do blood. So you're looking for your infected markers like white cells and CRP and then your urea and electrolytes and then also send off blood cultures. And it's really important to do this before you start antibiotics. Um so that you have accurate blood results, you do an ABG if you feel there's background as approach disease ready or if they have low saturations, they might have trouble oxygenating. Um We want to do your atypical screen, as I said. So mycoplasma antibodies, urine legionella and also pneumococcal antigen um and send off sputum culture again ideally before antibiotics and then you want to do a flu swab. So respiratory viral panel and of course COVID and influenza swab just to rule out um superimposed viral infection and management really just depends on the guidelines. And so at my hospital with C 0 to 1 can start with oral doxycycline or amoxicillin. Um curb 2 to 5, you want to go in something a bit stronger. So IV Benzylpenicillin and oral doxycycline doxycycline helps cover your atypicals. Um And then if they present with sepsis and you're not 100% sure on the source cos it's hard to be in an acute medical setting. You can start off with IV Comox aab and gentamicin and that will be um a really broad cover for chest sepsis. Great. That's everything about caps. Um very, very common example and that you will see in the hospital and in your exam questions as well. So let's move on to talk about pleural effusions and so pleural effusions is an excessive amount of fluid in the pleural face. So if I just swap to the next slide, this is an example of a chest X ray that you will see a pleural effusion. Um normal pleural fluid volume is around 30 mL, but to be able to see on a chest X ray like this um is around 300 mL of fluid and to be detected clinically. So, if someone's symptomatic of it. It's usually 500 mL and there's lots of different causes of effusions that will go through if someone's having a massive effusion, um they're most commonly malignant in origin. So, how do pleuro diffusion patients present? So, if you just think about how would you feel if you have lots of fluid in your lungs if you'd be short of breath and you have a dry cough and chest pain And on examination, on the side, you've got fluid effusion. So they can be unilateral. Um you'd have reduced expansion, stony dullness on percussion because of the fluid, um reduced breath sounds and reduced vocal resonance. Um And to investigate is chest X ray, you see the meniscus sign and the blunting of costophrenic angles um as you can see here. Um and you see this dense homogeneous shadowing that looks like fluid and you can actually see the fluid level quite well on the right. And then you can see um the meniscus sign as well on the left and then you can actually see fluid in the fissures. So, in between the different lobes, you can see fluid as horizontal lines in the right in the middle zone of the right lung. And then to investigate pleural effusions, um doing a tap. So you're taking some pleural fluid assisted by ultrasound is diagnostic. So you want to look at the appearance and then send it off for protein. Um LDH. So lactose dehydrogenase glucose, ph and cytology for um malignant concern and microbiology for infective concern. So, that's really helpful in diagnosing the course. And that also helps us classify by looking at the protein, whether pleural effusion is transudate or exudate. So if it's less than 25 g, a liter of protein that's transudate. And if it's over 35 then it's exudate. Um and the pathophysiology is transudate means that the higher Dota forces are pushing out fluid into the pleura. So it's usually bilateral. Whereas exudate means there's a damage in the pleura causing fluid and protein to come out. So it's usually unilateral, which makes sense. If it's in the middle, we use what's called lights criteria to try and differentiate. Um So if your fusion protein to serum protein ratio is over naught 0.5 that suggests exudate um or effusion LDH to serum LDH is over naught 0.6 or effusion LDH is greater than two thirds of the upper reference limit of the normal serum LDH. And we'll also suggest X. So these are just kind of ratings you need to learn and they're very classic M CQ questions on how to um classify trans date versus exudate. And that will also help us point us into direction of the cause of the effusion. So, transudates are usually caused by, I always think of it as heart failure or liver failure or kidney failure. So, nephrotic syndrome. So low albumin or heart failure and also hyperthyroid and um meg syndrome, which is an ovarian fibroma, um can also cause pleural effusions, something to bear in mind. And then for exudate, it's usually caused by lung cancer, pneumonia. Some rheumatological conditions, tuberculosis and different drugs can also cause it. So, methotrexate, amiodarone, phenytoin and nitrofurantoin are the ones to remember. And if it's um transudate, then we obviously have to treat the underlying disease that's causing it because that these, these things like heart failure and liver failure won't self resolve. Um Whereas with exudate treatments, um treatment is often draining and the fluid off in the hope that you, for example, can treat the pneumonia or the tuberculosis as well. And the effusion will resolve. Ok. If anyone's got any questions as we go along to put them in the chat, but let's move on to talk about pneumothorax is so again, really common. Hopefully, you guys can see the chest X ray here. A pneumothorax is basically just defined as air in the pleural space. So on a chest X ray, you can see that there's a gap between the ribs on the edge of the lung field, which we shouldn't see essentially and that leads to a either a complete or a partial collapse of the lung. Um And chest X ray is the best way to diagnose a pneumothorax unless it's a tension, then you should never see a chest X ray of a tension pneumothorax because you should have treated it before waiting for imaging, you can classify these into primary and secondary. So, primary is also known as spontaneous and that usually occurs. Um So typically in young men, tall, thin young men is your typical osteo patient um as a result of a pleural blood. So you just develop a pneumothorax um or in secondary, just reverse to the fact there is some kind of underlying lung disease and we can also classify it into small or large, small being less than two centimeters at the hilum. And we can also classify it into simple versus tension. So, intention, the, the tear in the pleura acts as a one way valve. So you just get increasing amounts of intrapleural pressure and that can lead to cardiorespiratory arrest because there's just air coming in continuously. Um And that's why you need to treat it urgently because it's life threatening. Um Cool. So how do we know if someone has tension pneumothorax is that they'll have tracheal deviations. It's really important to examine the trachea in a respiratory exam, not just to auscultate the lungs, they have a mediastinal shift. So you might find that the apex of the heart has shifted. Um you have tachycardia and you're hypotensive. So you're, you're hemodynamically unstable. Um So how do we manage tension pneumothorax is? Oh, we'll come on to that. So let's talk about how we manage simple pneumothorax first. So if there's no symptoms and it's a small pneumothorax, you can do no treatment and follow up in 2 to 4 weeks time. They're symptomatic with shortness of breath or it's a large pneumothorax. And what you do is a needle aspiration. And you can also consider a chest strain or if they're unstable or bilateral, you can just jump straight to a chest strain. So this um diagram is a really useful schematic of remembering your managing management of spontaneous pneumothorax. So, is it primary or secondary? Um and then look at the size and then you can aspirate it and then discharge if that's successful in a primary or a secondary. Um If it's small, you can aspirate, you wouldn't just leave it and monitor in the secondary, you'd always treat. And then if it's large, you can go straight in with a chest drain. Um But yeah, these patients often need close monitoring because you can get recurrent pneumothorax easily. So you've got uh another M CQ here. So a bubble wrap like texture is palpated under the skin of the neck during the examination of a patient with a chest trauma, which is diagnosed as subcutaneous emphysema, which of the following signs would further support the diagnosis of tetra pneumothorax. They think first of all, which way your trachea will deviate and they will appear on their obs, would they be stable? What would it affect good? So, lots of answers saying de great. So tracheal deviation away absolutely to away from the affected lung because there's collapse. Um And there's also hypertension and hypoxia. So they're hemodynamically unstable and they're struggling to oxygenate and breathe. So, absolutely hypoxia. Great. So how do we treat attention? Pneumothorax. Um You wanna into the triangle of safety with um urgent needle, thoracocentesis and intercostal tube drainage. Um So you'd go into, you put the chest drain into this triangle of safety. So that's between the lateral edge of the peck major, the fifth intercostal space and the lateral edge of the lettuce, Miss Dorsey. And we call this the triangle safety because it's the safest place to insert a drain. And it also gives you good access um to the pneumothorax. Um So yeah, hopefully you do a chest X ray after you drain to check the resolution of the pneumothorax. But yeah, people always say tension pneumothorax is a chest X ray. You should never see because if you have clinical suspicion of a tension pneumothorax, you treat straight away. You don't organize imaging or you don't wait for imaging to confirm your diagnosis. Well done. Um So the next M CQ is this a 77 year old female patient presents to her GP with shortness of breath that has developed over the past few hours with a stabbing chest pain. She was discharged from hospital eight days ago, eight days ago with antibiotics following an episode of diverticulitis on examination, she is tachycardic 104 tachypneic respirator of 27. And in addition, her right leg is swollen and her cough is tender on palpation. The GV arranges for the patient to be admitted. What single intervention will confirm the most likely cause of her acute breathlessness. ABG, chest, X ray C TPA, CG or D dimer good C TPA. So lots of these are very valid and one could say you'd wanna do all these things um in someone on that you're suspecting a pe um but you would want the single investigation that will confirm the most likely cause. So C TPA is diagnostic um and that will reveal the pulmonary embolism essay. Well done. Um OK. So pulmonary embolus is usually a clot in the pulp. So we just had a question but we just thought I'd answer it quickly going back to the um tension pneumothorax and someone's asking, they got taught to um aspirate from the second intercostal space in the midclavicular line. So you'd use that for kind of needle aspiration or needle thoracocentesis. If you're putting a chest drain in, you want to go into the triangle of safety, which is in your fifth intercostal space, mid axillary line triangle of safety. So needles go into the second intercostal space, midclavicular line drains. It's like tubes go into the fifth intercostal space, hope that clears up um cool. So moving on to pulmonary embolism. So it's a clot in your pulmonary arteries and that impairs your blood flow. Um These clots usually arise from thrombi in your DV So basically your dvts in the iliofemoral veins. So small embolus can kind of affect your peripheral pulmonary vessels. And it actually can be silent if it's small. Unless it causes a pulmonary infarction, then you get symptomatic, so shortness of breath and then you get this VQ mismatch in P ES because of impaired gas exchange. And then in very large P ES, you obstruct your right ventricular outflow and this increases the resistance in your pulmonary. So, in your lung vessels, and then you can actually get right sided heart strain and acute right heart failure. In this picture, symptoms can be really vague and not every patient presents the same but things to look out for shortness of breath, cough, hemoptysis, and pleuritic chest pain. Um and if it's a massive pe they might be hemodynamically stable as unstable as well. Um risk factors. So our patient in the MCQ had risk factors because they had a recent operation. So recent surgery puts you at risk of pe and after the surgery, I imagine they would be more immobile than usual. So that also puts you at risk factor. Um Other things are long haul flights, pregnancy estrogen. So thinking about people on hormonal treatment or the contraceptive pill, people with malignancies, um polycythemia, um lupus and thrombophilia are all important risk factors to remember. Um an investigation. So ECG was mentioned as one of the options. Very few people actually have this classic S one Q three T three finding. So having S waves in lead one Q waves just before your complex in lead three and inverted T waves in lead three. So it's not great. You'd do a chest X ray just to exclude other pathology that would contribute to your shortness of breath and chest pain. Um But usually in someone with a pe, their chest X ray will be completely normal. You can use D dimer. Um it's got high sensitivity. So almost everyone with a PE will have a high D dimer, but not everyone with a high D dimer will have a pe. So D dimer is raised in a lot of different settings. Um So it's got poor specificity. It's something good to guide treatment um to rule out the pe, but it's not good because it can be elevated in pregnancy malignancy, post operatively, it's not great. But the best thing to do is a CTPA. So you give a bolus of contrast in your veins and then you can capture the flow through pulmonary arteries or you can still miss small um embolus with CT P and then in patients who can't have a CTP. So for example, they've got kidney failure and contrast um needs to be cleared by the kidneys or they're pregnant. Then you can do a nuclear medicine, um ventilation perfusion scan to look at the mismatch between ventilation and perfusion. And an important thing for deciding on clinical management for P ES is have a look at a well score. So if someone has a well score of more than four, then you go for a C TPA straight off the bat or if they have a well score less than four, then you do DD first and if that's positive, then arrange a C TPA. So do they have signs of a DVT? Is pe your top differential? Are they tachycardic? Do they have this immobility or surgery risk factor? Do they have previous personal history of clots? Did they have hem sis? And do they have a background of malignancy? So how do you manage um peas? So if they're hypoxic, give them oxygen and give them analgesia to manage their pleuritic chest pain and then once you suspect it don't wait for CT P treatment, just start um treatment straight away. So in a hospital setting, we would start someone on treatment based Darin. So a higher um dose of Darin, the low molecular weight heparin. Um because there's no point in waiting. If you already think if you've got clinical suspicion, then you should just go for it and then you can change it back to a prophylactic dose afterwards. Um because often things like TTP is in a hospital depending on what hospital you're in, can take quite a long time to organize. So just start them on high dose of melo heparin. And then when we discharge them, we usually commin them on a doac cos that's a lot easier. They're oral tablets and take them once or once or twice a day. So, Pix or Riv the most common ones, you can also give Warfarin just depends on the patient's background and preferences. It depends how long you treat someone. Um, if it's provoked and you've got an identified risk factor, then just three months or if it's unprovoked, then you want to treat them for longer because you don't know what the cause was, say, six months and including if it's active cancer because the um risk factor of having a pe will kind of remain in the background. So, with cancer patients, it's all really dependent on their treatment plan. If they're having active treatment or it's palliative or what the kind of risk benefit ratio is of carrying on antico treatment can be lifelong if patients do come back with recurrent clots. Um And in patients who have an unprovoked pe, um you might want to consider screening for malignancy. Um So for example, doing a cta pelvis to look for cau causes of a pe, they might have the undiagnosed malignancy. And then another treatment option is if you do have a massive pe angle hemodynamically compromised, you'll solve that clot quickly. And the best way to do that is thrombolysis with intravenous PLS first A bolus and then an infusion. Great. Well, so I think this is the last section of the talk. Um So one last M CQ So, Paul is a 64 year old man. He presents to the medical admission unit with increasing breathlessness over the past year when asked he states he smoked socially back in the day and he was the reports that in the past six months, he has lost a stone and a half. So he lost half a stone. He last traveled abroad in 2021 to visit his daughter in Australia on examination. He has thin crackles and fine crackles. By what is the most likely diagnosis? Is it CO PD? Lung cancer, sarcoidosis, idiopathic pulmonary fibrosis or heart failure. What do you guys think? Great, well done everyone. So lots of people have gone through d idiopathic pulmonary fibrosis. So I wanna talk about I LD I LD is an umbrella. I'm describing lots of different kinds of lung diseases. That the key thing is that um there's bilateral diffuse lung changes that leads to lung fibrosis. It's a fibrotic picture and the looks like in terms of a clinical picture. Three C. So I always think cough clubbing and cough crackles is how an I LD patient would look like. Um So these patients usually have poor prognosis um because fibrotic is not really a reversible um condition. So there's different ways to classify different groups of interstitial lung disease. So you've got your idiopathic pulmonary fibrosis, you've got rheumatological conditions. So, if they've got rheumatoid arthritis, lupus, anx Bon, um Sjogren's polymyositis, they can all present with I LD as well. It can be drug induced. So important ones to remember, phenytoin amiodarone, methotrexate, nitro can be occupational asbestosis and silicosis hypersensitivity, pneumonitis. So, thinking about farmer's lung with mold and bird fanciers, looking at the occupational risk factors and it can also be granulomatous. So think about the sarcoid tuberculosis and GPA um vasculitis. So yeah, as I said, cough, shortness of breath, malaise weight loss, crackles. And then in terms of what caused the interstitial lung disease, always try to think of it as anything inhaled, um tends to be upper zone fibrosis. Um So things like TB hypersensitivity, pneumonitis, occupational, the only exception is asbestos and then anything that's caused it from the bloodstream tends to cause lower zone fibrosis. So, idiopathic fibrosis, drugs, rheumatological causes and the only exception is Anxon where you get upper like apical fibrosis. Um So that's another easy way to help differentiate between upper and lower zone fibrosis, how we investigate these people. So we look at blood tests. So we wanna look at autoimmune screens to think, is there anything rheumatological going on or vasculitic? They'll have increased inflammatory markers with SE RP and ABG might show a type one respiratory failure. So, um it's worth doing a gas on acutely unwell respiratory patients, vasomet, as we said before will have a restrictive picture. So, reduced, forced vital capacity and hopefully a preserved ratio. The chest X ray will show bilateral pulmonary infiltrates and what were reticular nodular shadowing. And then on CT, this is your classic sign to remember for M CT S, it looks like honey comb. Um So it's what we call ground glass appearance, which is kind of increase gray matter. And then you also get the honey comb um with the fibrosis. So you can do lung biopsy as well, but it's not often done in practice. And then how do we treat this? Treat the underlying cause? So, if it was a drug withdrawal drug, um avoid the allergens treat the rheumatological disease, but it's often just supportive therapy and there's not a huge amount we can do for patients with this disease. Um For the one thing to say is that if it is hypersensitive fatigue pneumonitis, we control or oral steroids and further down the line immunosuppressants because these do show a response and then the more new class of drugs called dmards disease modifying drugs, um There's no conclusive evidence about it, but you can use it in select patients. So you might have heard of Pirfenidone, it's a novel antifibrotic to try to reverse some of the pathology, although it's not exactly proven. And then also you can think about this um Tyrosine kinase inhibitor called nintedanib to try to reverse some of the pathophysiology. So that's everything I wanted to co cover in this talk today. Again, put your questions in the chat if there's anything I might have missed out. Um And here's a QR code to um put in any feedback. Our next talk will be next month on Thursday. Sorry. So every Monday and Thursday we've got a talk and then we also want to start introducing some ay content. So I'm just gonna share my screen with you again um because I just want to really quickly talk through um how to go for a respiratory exam at the end. And then if you guys could put in the feedback, if you think obviously teaching um virtually. So over meal would be useful for you guys or not. Then let us know. Ok, so for a spiritual examination, as you start with every examination, you wanna inspect your surroundings. So have a look at the table on the ward. Um What medications do they have on the table? How are they sitting? How are they breathing? Look at a patient, are they in respiratory distress? Are they coughing? Do they have audible wheeze or stridor and then always start peripherally. So you're looking at the hands, look for clubbing especially. So five CS are the five causes of clubbing. Um So there are different causes of clubbing. So five C is one of them. So clubbing can be um as we said in the last case from fibrosis, look at the color of the hands, look for any cigarette tar or the yellowing of the fingers, um can be cancer or you can also look for a CO2 retention flap um these are your five CS of cupping. Um And then look at the arms, so have a feel of the radial pulse. What's their heart rate like? And whilst you're having a feel of the radial pulse, um take a look at their respirate, but don't tell the patient you're looking at their respirate because it will um change the way they breathe. So if someone says they're looking at the way you're breathing, you're often either hypo or hyper ventilate. So you want to do it distracted and you wanna look at their face, look for any pallor in their conjunctiva and then you can look for other signs in the eyes, like facial plethora and someone who is a CO2 retainer um and then look in their mouth. Are they clinically dry or they well hydrated? Do they have central sinois? Do they have any kind of um cyanotic mouth or tongue? Look at four things to look at in the neck. So look at feel their pulse lie them back 4 to 5 degrees and look at the J BP that helps with fluid balance. And then as we said before tracheo radiation can be really important and then have a feel for lymph nodes again, looking for any kind of cancers or any reactive lymph nodes from infection and then look at the chest. So first of all, start by having a look, any scars from surgeries, any skin changes, are they hyperinflated? Do they have a barrel chest like AC APD. Are they do they have a particular breathing pattern? Like a see, so breathing pattern and then palpate. So put your hands around the chest and then measure chest expansion. Have a feel for the apex beat. Look for any right ventricular heave for any right heart strain, which is common in lung pathologies, then pus both anteriorly and posteriorly and then um anterior and posteriorly, we always recommend if you're short on time in an A to do just the posterior because you can access the lung feels and hear them a lot better. But it's good practice to do both sides. And then um you can test vocal residents by getting the patient to say 99 and then have a look at their legs. Do they have any pitting edema? Like it's just heart failure? They've got tender calves that suggest DVT can look for skin changes like everything, no dos. And then once you've worked your way around the whole body, it's time to present, present your patient and then to complete your respiratory examination, you want to do some basic tests. So spot X is a really good acronym for respiratory patients. So you want to do a sputum sample and culture that will help guide antibiotics, peak flow that's indicated. For example, asthmatic patient, one to do oximetry to check their saturations, temperature of their febrile. They've got an infection and of course, chest X ray to look for pathology. So I hope that's helpful. Um I'll stick around and keep having me and keep, keep an eye on the um chat questions. So if there's anything people want to clarify, um But otherwise please fill in the feedback. Um I'll put a link to the feedback form in the chat. You should receive it automatically um in you should receive automatically when you kind of come off this talk, it's part of meal. Um But yeah, thank you so much for attending. Um And yeah, I hope to see you at further talks. Thanks guys.