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Ok, there we go. Hi, everyone. And um, thank you for joining us today. My name is Jua. Um, I'm part of a, um, and we are a non profit organization and we have set up this series, um particularly to support students um who are sitting the Q and A exams um in, uh, in, in um, in March, March time, February, March time. So, um, um I've got, so today's topic is the respiratory. I've got two very um uh talented, you know, doctors here with me who will be taking you through SBS type questions and then giving you explanations, um, and just helping you, you know, just guiding you through how to answer uh SBS type questions. Um So, yeah, I think this will be recorded and we put up on the middle page and at the end we'll ask you to fill in some feedback for us. So, um I'll put that in the chart later. So please don't go without, um, filling in the feedback for us first. Ok. If you have any questions, just put it in the group chart and I will try and answer, I'll do my best to answer it. And also if there are any issues, um you know, just speak to me in the group chat, I'll be here. Ok? Um Yeah, I think without further ado I'll hand over to uh Jasmine and Sammy and yeah, if any issues just put it in the group chat. Ok. So today we're gonna be discussing um the common topics in respiratory, the kind of high yield progress test in UK MLA. So I'm Doctor Jasmine Limbo. I'm F two in Birmingham. Um sadly, um Doctor Hania, uh she couldn't uh do the presentation today, but she has uh you know, contributed a lot to the slides. Thank you. And then we have doctor Sammy as well who's uh contributed to the slides and we'll be doing the uh second half of the talk. Ok. So if you guys just think about what are some of the common um respiratory, you know, complaining um presenting complaints that patients come with to either hospital or to GP. Um So just have a little think of the kind of symptoms um that you usually uh see patients come with. So these uh might be some of the common things. So, shortness of breath, cough, um sputum. So whether that's, you know, increased sputum production, new sputum production, changing in color or consistency or um or hemoptysis, if there's any coughing up of blood, uh chest tightness, chest pain, um cyanosis, uh fatigue and wheeze. So these are the common uh presenting complaints So, like I mentioned, um So in this talk, we're gonna uh discuss all the sort of high yield topics. So we'll be discussing asthma versus CO PD pneumothorax and tension pneumothorax community acquired pneumonia. Um and then pleuro effusion. So this is our first question just to get things started. So a 35 year old patient presents to GP practice, they feel as though their asthma is not being optimally controlled. Um They're still frequently having to use this salbutamol inhaler and they still feel short of breath and wheezy. Um especially when exercising, uh they're currently on a saber and a low dose I CS. Uh What do you think is the next step in their management um to optimize their asthma control? So if you guys wanna um have a think or put into the chat, what do you think the answer is that would be good? And then I'll let you know what the answer is in. Uh the next slide. Yeah, sorry. Just to add to what um Jasmine already said. Normally we use the pole. Um that's already integrated into the zoom, but unfortunately, it's not working. We're not working on my uh my side. So, um next time we'll try and do a menter. But for now, for today, if you guys don't mind just putting on the group chat. OK. So we'll, you know, don't worry if, if you worry that you might put in wrong or so you're not sure just message, the speaker privately, there is the option of private message um on the group chat. OK. So I'll um move on to the answer. OK. So the answer is that we would add a LTR A. So that's a leukotriene receptor antagonist. So I'll explain in the next couple of slides how we got to that answer. So, asthma um let's talk a bit about that. So asthma is a chronic condition, um causes inflammation of your airways, uh causing narrow uh narrowing of the airways due to muscle spasm. Um And it's because of the airway hyperresponsiveness. Um So people with asthma, uh they can present with a wheeze shortness of breath, um chest tightness, cough, diurnal variation, which means either sort of in the evenings and the nights is worse in the mornings, it can be worse. And usually, um asthma patients have this atopic triad. So they have asthma, they have eczema and they have allergies. So it's all kind of, you know, related to the hyper responsiveness and uh the systems all more triggered with the inflammatory responses. And the other, the other thing to keep a look out for is also occupational asthma. Um So if the patient has these symptoms, but it kind of seems to happen when they're at work, perhaps due to the um environments or chemicals and things at work. Um So if they have occupational asthma, then we'll need to do a specialist, a referral for that. Um So the sort of causes for asthma can be family, uh, history. So, running in the family, um, if they already, um, sort of have a allergies, uh, so lifestyles, um, if they're obese, um, chemicals, uh exposure and environmental exposure as well, um, and then the uh, investigations that we do, uh for asthma is spirometry with a bronchodilator reversibility test, um, feno. And uh we like to do peak flow and peak flow diaries um just uh to monitor asthma and uh also to uh see how well asthma is controlled in a patient. OK. So I just wanna talk a little bit more about spirometry. Um So in the picture there on the left, you can see a patient doing spirometry. Um So F EV one is uh the volume sort of of air exhaled, um force exhaled in one second and then F EC is the total volume um exhaled. So as you can see there on the graph, uh we got normal and then uh what it would be like in an obstructive picture and what would be like in a restrict uh restrictive picture. So in asthma, you get an obstructive picture because the uh airways are narrowed uh because of the spasming uh the bronchospasm. So the F EV one is reduced. Um and then the F EC can be slightly reduced or it can be normal. So overall the ratio will be uh less than 70 with an obstructive spirometry uh value So, um, asthma investigations. Um, so it sort of depending on age. So, um, you know, in Children of less than five, we wanna use our clinical judgment because it's very hard to do these, uh, kind of tests on Children and then between 15 to 16 as well, I guess, you know, you're still kind of using your clinical judgment, but in the more sort of older teenagers, uh, perhaps we can use spirometry, um with Bronchodilator reversibility. Um And then in adults, we'd want to do spirometry with bronchodilator reversibility and um feno. So um I've made a little table there um for what we sort of want to see. So in spirometry, uh we'll see a obstructive picture. Um um in Bronchodilator reversibility test, we would see a response to that. Um And the airways will open up and hopefully there should be a 12% at least um improvement in the F EV one. So that forced one second, um exhale, exhaled uh volume and then F eo um is 40 plus parts per billion. So the level of nitrous oxide is um sort of in correlation to the inflammation. Um So the inflammation of the airways, I move on to the next slide now. So um short acting beta antagonist. So that's what we mean when we say Saba, then we got LABA uh then we got LTR A. So that's the leucotriene uh receptor antagonist. And then we have mas, which is a combined sort of maintenance and reliever. Um So that has um I CS and um laba. And then with the ma you can uh have low one with low dose I CS, medium dose I CS and high dose um I CS. So if I go to the um sort of flow diagram there on the left hand side, so initially, um so giving a reliever inhaler, so that's your saber. Uh and then you get your Saba and uh low dose I CS. Um And then if that's not uh well controlled and the patient is still struggling, you can add a um LTR A. And then after that, if it's really still struggling, then we will add a laba with uh the potential of still keeping the LTR A there or, or taking it out. So that's uh that, and then after that, we'll think about um using MS um and using the maintenance reliever therapy. Um And then we again have the option to keep the LTR A there or not. Uh And then after that, if it's still struggling. So after you've done, you know, low dose, medium dose, high dose I CS in the MARS, then that at that stage, uh we would need the specialist to um uh sort of help to help, better, to manage a patient's asthma and the other things to think about asthma management that's um not just inhalers, is thinking about immunizations. Um And then the patient education making sure they have good inhaler technique. So, you know, if they are using these inhalers and they're saying, you know, still not controlled, then it's like, you know, are they using it properly? Are they actually getting that dose that, you know, uh we want administered? Um And then pregnant women would want to continue the management. Uh It's really important that, you know, pregnant women still have uh well controlled asthma. Um And then for people with asthma, we want to do their annual follow up. So, you know, in the community, for example, if you a GP would want to um review these patients annually do that asthma review, making sure things is controlled, uh then move on to the next side. OK. So this is the uh nice definition for um what you know, what they define as controlled asthma. Um So it would be uh no daytime symptoms, no nighttime waking, so no waking up in the night. Um you know, short of breath or coughing. Um no need for rescue medication. Um no asthma attacks um that their asthma doesn't limit their exercise uh that they have normal lung function and that there's minimal side effects uh to their medication. So here's like a nice picture for the visual learners out there just to describe or, you know, put into a visual perspective about asthma. So, you know, the, we see the um the airways constricting that hyper responsiveness, um the inflammation going on in the airways. Um And then a little bit of picture of about um what could happen if someone has asthma, you know, when they, they will use the inhalers, maybe it might not help them, maybe they may need them to go to the hospital and the ambulance, they may need nebulizers, which is what we see in the um top right hand corner in the hospital, they may need ABG done and in some worst case scenarios, they may need to be uh ad uh admitted to ITU. OK. So here's a question. Um So a 20 year old patient presents to the ed with shortness of breath. They have a background of asthma. So they're taking Saber ma and LTR A to manage, um they're promptly diagnosed with severe asthma exacerbation. Uh which of the following would be a feature of severe asthma. Um So like I said, um just put it in the chat or have a little think about what you think the answer might be. OK. So I'll move on to the answer now. Yeah. So, um what we see in severe asthma would be a peak expiratory flow rate of 33 to 50% of best predicted. Um So the rest I put on there, um the other values are for life threatening asthma. So I will explain a little bit more about these criterias in the next following slides. Um So I made a little table there um to dis uh sort of help us remember, sort of the moderate, severe life threatening. Um, so moderate p fr 50 to 70% of best and predicted, uh, severe 33 to 50% and life threatening will be less than 33%. So, in moderate we kind of, you know, the patient, they're not having a particular high respirate, they're not having a particularly high heart rate either. And they can still have a normal speech, but they will say, you know, I'm feeling a bit more breathless than usual, a bit more wheezy than usual. And my um peak expiratory flow is only about, you know, it is much reduced, uh you know, 50 to 70% reduced than the usual. Um And then in severe, that's when they also, you know, sort of start having a high respiratory rate, higher heart rate. Um but their oxygen stats are still 92% plus, but they may have a inability to complete um their sentences in one breath and they may be using a little bit more of accessory muscles to help force in that the air when they're breathing through the constricted airways and then in life threatening. Um That's when you start having your oxygen saturations, you know, going less than 92%. Uh In some cases, in worse cases, the um the carbon dioxide in the blood class might be normal. Uh They may have uh confusion, altered consciousness, exhaustion. In some cases, arrhythmia, uh drop in BP, cyano, um silent, chest, poor respiratory effort. So, uh when you uh come across these cases, so with life threatening, severe, uh you definitely wanna admit them to hospital. Um but with moderate, um let's just say you're out in the community, uh they come in with moderate um asthma exacerbation uh signs and then you, you know, give them salbutamol perhaps with a, a nebulizer. And if that hasn't helped, it's still positioning, then you would want to admit those patients or um if those moderate uh patients come in and um you know, they're a bit more lower threshold for admission. So this means if they have other comorbidities, if in the past, perhaps they've had, you know, severe um asthma exacerbation or if they live alone and, you know, um you'd want them admitted uh for the better management of the asthma exacerbation. So, while awaiting admission, uh let's just say you're out in the community for your GP, things like that. What you'd want to do is you can give them some oxygen, uh give them some salbutamol perhaps through some nebulizers. Uh Yeah, and then um tropium bromide as well in some cases. And you wanna give them their first dose of prednisoLONE and you'd want to uh monitor their peak flow as well. Um But once they get into hospital, obviously, all these managements uh will be continued, for example, albuterol nebulizers tropium. And uh we want to continue giving them other inhalers, uh, as well. And then, um, in some cases in worse cases, uh, potentially you can start thinking about, um, IV magnesium sulfate, uh IV aminophylline. And, um, if a patient is really not responding and, um, then in some cases, we'll have to, uh, think about, uh, admitting the patient to itu for intubation and ventilation. Um, so that's what would happen sort of in hospital and then you, once they start getting better, you'll start thinking about uh discharging the patient. And that's when it's really important that they uh fit the discharge criteria. So the patient needs to be stable on their discharge medications for about 12 to 24 hours. The peak expiratory flow uh has to be um 75% plus the best predicted. And then the patient also needs to be educated on um sort of inhaler use as well as asthma exacerbation and be the better management of the asthma. So this is a nice um sort of pneumonic to help you remember, life threatening um asthma uh signs. So we got, you know, the 33 of the predicted 92 less than 92% stats cynos hypertension, exhaustion, silent chest tachycardia. And in the um case of the normal carbon dioxide on ABG, that's a sign of exhaustion. So that person is no longer sort of blowing off um their uh CO2. So initially, they might have that high respirate, they're blowing out their CO2 and then it's, uh, the CO2 is, um, uh, sort of dropping, but then, you know, they become more, uh, exhausted. And, um, so that's a sign that things are getting more severe and that things are lifethreatening. Ok. So here's a question. Um, and again, uh, I'll just read it out and I'll let you guys, uh, put your answers in the chat. But a 25 year old man presents to the ed with a pleuritic chest pain and shortness of breath that began two hours ago on examination that D is central and there is hyperresonance on percussion of the left side of the chest. Um A chest X ray shows a left uh pneumothorax about two centimeters. Uh The patient expressed uh that they would like a quick management for his symptoms. Uh Which of the following is the most appropriate management for this patient. OK. So I'm gonna review the answer now. Yup. Yeah. So it would be needle aspiration. So the next topic I would talk about is pneumothorax, intention pneumothorax. And then um I'll explain how we got to this answer. So, pneumothorax. So um I'll just put up some X rays here that I uh sort of got from uh radio pia just to show you some examples of pneumothorax. So, the best way that I like to kind of see on um chest X rays is I go from the app side and in and see if I get that line that shows where the lump is. Um which means that there's that ebb in between. So I kind of like using that kind of method to easily identify, especially um if there's any chest x rays or questions. Ok. So pneumothorax was a pneumothorax. So, pneumothorax is air between the parietal and visceral pleura. Um So that air is there and then um this causes people to have um short of breath, ple chest pain. So that's pain when uh which is worse on inspiration, uh reduced air entry and breath sounds when you're auscultating the chest uh and hyperresonant percussions. So, if you just imagine a drum, uh you know, there's the skin of the drum and there's all that air in between. So when you tap it, it, you know, it makes a hyperresonant um noise on percussion. So that's like a nice, easy way of remembering um what you would find on percussion. Um So with pneumothorax, you can split it in um two ways. So you've got the simple and spontaneous and then you have traumatic. So with the simple and spontaneous, there's primary and secondary. So primary um spontaneous pneumothorax would be if a person is a healthy individual, they don't really have any underlying lung disease, but they somehow got this pneumothorax. Um So, yeah, that usually happens to sort of tall uh skinny males, young males that you kind of standard um sort of question stems. Um And then in secondary um spontaneous you have an individual who has uh underlying lung disease. Um And then with traumatic, it's uh due to trauma or there's uh iatrogenic. So it's sort of like medical procedure complications or sometimes mechanical ventilation as well. Um can cause people to have pneumothorax. So, as you can see from the picture there on the left, um so that air really just squishes or that force of that um pressure of that squeezes down the lungs. Um which means it can't really expand much uh when you're breathing. And then that's why you kind of get that shortness of breath. Uh The best kind of way to find out what's happening is just get the chest X ray in and you can identify the pneumothorax. OK. So management of tension pneumothorax, I've split uh the flow chart from the British Thoracic Society um into two. So they uh kind of put this out, I think in 2023. Um So from when I was in med school and in fifth year, um they kind of changed the way um pneumothorax is are managed. Um So the first thing we need to think is is the person symptomatic. So if your answer is no, um and the person, you know, has got no pain, no shortness of breath and there's no um physiological compromise. So there's no hemodynamic instability, regardless of the size of the pneumothorax, we're going to manage the patient conservatively. Um So if it's spontaneous. Um So if you know, there's no underlying lung disease there, so spontaneous, uh then we would um review them in uh 2 to 4 days and then do a follow up in a few weeks afterwards. And then, or uh if it's, you know, they have underlying lung disease, then we would want to um monitor them inpatient and then again, follow them up in um 2 to 4 weeks afterwards as well. And then the next question, so the question you're thinking, OK, is the patient symptomatic? Yes or no. So, yes, they're symptomatic. So then the, then we need to start thinking, um are they high risk or is there no high risk? So high risk would be, you know, hemodynamically unstable hypoxia, maybe they have bilateral pneumothorax. Um They're 50 plus years old and they're a smoker or there's a hemothorax, there's blood there. Um So that, that's how we kind of identify high risk, no, high risk. And then the next sort of question you have to think about is, is it safe to intervene or no? So, um they s they say, you know, about two centimeters laterally or apically on chest X ray or it's just a size that radiology would, you know, would say it's um it's decent size enough for intervention. So, essentially, that's um what we need to think about those questions after that. So let's just say they have symptoms, high risk features safe to intervene, then chest X ray, uh not chest X ray, chest drain. And then so let's just say again. So, oh, I'm sorry. And then let's just say again, symptomatic no high risk features safe to intervene, then got a little bit more options. So I'm gonna go to the next side uh to discuss those. Ok. So that's when we start thinking, what do the patient really want from this. So if a patient is, you know, symptomatic, no high risk features, but they're like, oh doctor, you know, I actually really just don't like having these things done. I'd rather just, you know, see what happens and then, yeah, conservative management. Uh So what I mentioned earlier, if you see that blue box there right there on the left. Um So uh that's when we start looking at like, you know, if it was um primary, then, you know, outpatient review, 2 to 4 days and then uh outpatient review again, 2 to 4 weeks, follow up and then um if it was secondary, um then we wanna keep an inpatient review and then follow up in um 2 to 4 weeks as outpatient. But um let's just say they're like, no, I kind of do want some symptom relief um if they want um then they have a few options. So we have the ambulatory device, um we have needle aspiration and then we have chest drains. So, you know, those are the options there and then standard 2 to 4 weeks outpatient follow up afterwards. So that's pneumothorax in a nutshell there. Um So this flow chart diagram, if you guys want to look at it in your own time, um It's from the British Thoracic Society. Uh So just try and memorize the flow charts and then moving on to tension pneumothorax. So this is a little bit different um from your um standard uh pneumothorax. So, um what's happened is that the pressure um in that pleural cavity is more than the atmosphere. Um So again, it's sort of really uh with much more force compressing on the lungs, it's now compressing on the heart, blood vessels, other structures in the chest. Um you know, all that force causes the trachea to be pushed away as well. Uh And this is life threatening and you would need to act fast with a tension pneumothorax and then the patient may be hypertensive, they will hypoxic and then tachycardia. Um So for this, it's immediate needle decompression usually will happen in like Ed and, you know, straight away. Um so second, intercostal space, midclavicular line or fifth intercostal space uh midaxillary. So, in that triangle of safety, um and then hopefully, um the patient will feel a lot better once that air and pressure is all uh released. So that's that. And then um I will let Sammy uh continue on from this point. So, I've, you know, I've talked about asthma, talked about um uh pneumothorax and tension pneumothorax and I'll let him um continue on with the rest of the topics. Let's do it, let's do it. Thank you so much, Jasmine for a wonderful uh presentation. Um Guys, uh Welcome for those of you joined late. My name is Sammy. I'm in Fy two at Luton. First of all, can everyone hear me? OK. Give me a thumbs up. Yes. No. Can you hear me? OK. Good. Very good. All right. So let's delve into this question. Um, I'll read out a little bit of the stem. So there's a 72 year old man who presents with several days of dyspnea cough and wheeze cough is productive with green sputum and he has frequent episodes like this, especially over the winter. He's got a background of COPD osteoarthritis and takes regular inhalers. All right. His audible wheeze upon auscultation and he's Dyne on examination sweet samples for culture. And he started on doxy and prednisoLONE. What organism is most likely to be detected? Now, I want someone to turn their mic on please and, and walk me through the question. Um, no answers in the chat for me. Can someone be brave and just walk me through this question? What they're suspecting the diagnosis is what the, and what the organism is? Simple, simple stuff. There's quite a few of you otherwise I might just pick someone, got you. Ok. Uh, let's pick, let's pick full stop. Uh, there's a, there's a person with the name. Full stop in that dot Can you uh enlighten us or no? I see the chat. Ok. So um Hannah Ali says a uh that's good. Uh Oh no, did I say a sorry? Yeah, Rimsha says C ipad says D OK, fine. If we move on to the next slide, we'll re reveal the onset. This is something that's very uh common exam question. This is easy marks. It's Hemophilus influenza. OK. And what we're suspecting is an infective exacerbation of CO PD classic stuff. This is a gentleman who's got a background of CO PD. He's come with infective symptoms. Most common organism that causes this is Hemophilus influenza, burn that into your brain. Guys. Let's move on. So I think um with that said, let's focus on CO PD now and what that, what that entails. So CO PD essentially is an umbrella term which focuses on two things. Number one, chronic bronchitis, which we often known as blue blue bloaters. Um And that essentially is when there's excessive mucus obstructing our airways. Ok. And then on the other side, there's emphysema which is also known as pink puffers. Ok. And what happens is due to years and years and years of smoking, um The alveoli in our lungs are absolutely destroyed. There's a reduced surface area for gas exchange and that in turn obviously causes these symptoms. So both of these two things are under this umbrella called COPD. And as you might already know presenting complaint will include uh include something like shortness of breath, wheezing recurrent infections, um weight loss and fatigue, you'll often see in questions. Um Someone saying the patient is cachectic, uh cachectic cachexia, um and also chronic productive cough and just moving on to the examination, you'll see very similar symptoms that you see in a lot of different respiratory conditions, including wheezing crackles. But some things that are different in COPD include accessory muscle use. They'll be using their diaphragm to try and get as much air in as possible. They'll be using this pli breathing. So almost like they're breathing through a tiny straw. Ok? And you'll, you'll see some cardiac symptoms as well including RAS JVP and some possible edema as well that links onto a complication that COPD causes in late stages, which we can focus on as well a little bit later. And um as risk factor goes, I think um the main, the most common risk factor, the easiest risk factor in the history of medical conditions. Smoking. Ok. Smoking for COPD. This link should be established in your brains if it's not, um, then establish it. Now, please. Um Other risk factors could obviously include um occupational risk factors. So you'll see, uh you might see there's not, it's not a smoker in the, in the question title. It might be someone who works in a, um I don't know Silicon Factory or, or has been a coal miner or something like that. Ok. And something that is a little bit different is alpha antitrypsin deficiency. Ok. So you, you might see a young patient. He's come in. He's got in the question stem. There's a young patient, 24 year old male, he's come in. He's got no smoking history. Um, but all the signs are pointing towards COPD. And the question might ask, you know, what deficiency does this, does this, uh does this patient have the answer? Is alpha antitrypsin deficiency? Ok. It's a genetic factor that can predispose you to having COPD. OK. Uh We can move on to the, to the next slide. So again, this is a very lovely visual representation of what COPD entails. So we focused on alveolar destruction. Of course, we also focused on our airways getting blocked with this mucus hypersecretion to in, in, in a way it's our body's response to sort of protect the airways from, from bad as you can see in the top right hand corner, um the main perpetrator um and in the bottom right hand corner, you can see a classic uh CC O PD chest X ray. Can someone please turn on their mics and tell me the classic signs of the CO PD chest X ray. Otherwise I'll pick on someone. Amanda. Amanda, Amanda. Are you there, Amanda? OK. Not Amanda. Um Ashna, Ashna. Are you there, Ashna? Can you hear me? No on, can you hear me? Are you able to go through this chest X ray. I think people have just turned on the left of the left. Fine, fine hyperinflation. Oh, very nice. Hi. Hi. Thank you for, thank you for saving me the trouble. Exactly. So hyperinflation, that's very good. That's, that's, that's one of the signs. Um Can you see anything else or you know about anything else? Um That is a classic, you know, signs on CO PD uh on like a chest X ray with CO PD. Um, is it like the trophic angle gets blunted? I'm not sure. I think no, you're on a very good line of thought. Absolutely. So it is something to do with the diaphragms. Um, it's, it's a little bit different to what you said. So usually costophrenic angle blunting could be, uh, in something like a pneumonia or something like pleural diffusion. Um, but in CO PD, you'll see the flattening of the hemidiaphragms. Ok. So you can see this big, big, big, big airspace. Ok. So you see this long sort of torso and you see the diaphragms nice and flat. Ok. Um, so this is a classic COPD chest x-ray. Thank you for, thank you for, um, saving my ba in the room show. I appreciate that. Um, we can move on to the next slide, please. So, um, as all investigations or as all conditions go, sorry, you need to investigate them. Ok. So, um, number one thing we'll, we'll do is a spirometry test. Ok. And like asthma very similar to asthma COPD will show you this obstructive picture as well and as Jasmine so nicely put it. Um what, what exactly is your FE one FBC? She very nicely explained it. So um essentially your F B1, I'll just go over it again. Fe one is your forced air in one second, the the as much air as you can force out in one second and FVC is your full, so forced vital capacity. So all the air that your lungs can hold and that can, that creates a ratio for us to tell. Ok. Is this an obstructive uh disorder? Is this a restrictive disorder? Ok. So in COPD, our ratio uh is less than 70% between fe one and FBC. So it's an obstructive disorder and like Grisha explained to us as well on the chest X ray, you'll see hyperinflation of lungs, you'll see bully as well and you'll see a flat hemidiaphragm. Very classic on the blood test. You'll see polycythemia. Ok. And, and what do we mean by polycythemia is when there's too many red blood cells? Ok. And the reason that is um your body is constantly in a hypoxic state because there's poor gas exchange because remember we focus on our alveolar destruction in one of the previous slides. So your body has poor gas exchange, your body needs to compensate somehow. So it starts creating more red blood cells to try and carry, carry more and more oxygen around the body. So that's why you get this polycythemia increased red blood cells because of chronic tissue hypoxia. Ok. And ECG changes. Now, in the first slide, we, we spoke a little bit about the effects of the COPD on the heart. Now, usually in respiratory conditions, you wouldn't think about an ECG because you'd be like, you know, it's nothing to do with the heart, you know, it's respiratory. But um in COPD, what essentially happens is because all of this is going on. Um and, and because you're having this chronic tissue hypoxia, you're having this bad gas exchange. What will happen is essentially this will lead to pulmonary hypertension, ok? Your body will try to force more and more blood through um through essentially the gas exchange system in your lungs, try and get more and more oxygen in. It would lead to higher blood pressures. Now, the issue with that is now in the pulmonary circulation that leads to more pressure on the right hand side of the heart. As we can remember, the body returns the blood into the right atrium. It goes into the right ventricle, the right ventricle pumps that deoxygenated blood into the lungs. Ok. So you'll get this backlog almost of pressure and your right heart will try and compensate for it. This is too much pressure for me. It'll pump harder and harder and harder and it will get bigger. So you'll see right ventricular hypertrophy and this will show on an ECG. OK. So we can move on to the next one and just a little bit about the classification, there's uh like with asthma as well as mild, moderate, severe and very severe and it's um uh guided to us by our F EV. So percent predicted. OK. Uh We can move on to the next one please. Now, in terms of the management, uh I think the main point you want to get um again, uh this is a tip for you guys. A lot of the times a question can ask, you know, yada, yada, yada. Um The the patient has CO PD. Uh This patient presents to the GP asking for advice. What is the most important advice you'd give the patient? One option would be, you know, um eat more bananas in your diet. One option would be have this inhaler. One option would be uh stop smoking and that is always always always the right answer in this sort of scenario. OK? Whenever someone has COPD, number one, number one, excuse me, number one piece of management, stop smoking. OK, advise the patient to stop smoking. You also like to offer them annual flu vaccine and a one off pneumococcal vaccine. And if the COPD is quite extensive, you can give them pulmonary rehab, refer them to pulmonary rehab as well if they're functionally disabled by COPD. Ok. There's medical, obviously there's medical um options as well, which we'll focus in on the next slide and there's surgical options as well, which include lung volume reduction surgery. Ok. This is something that is quite, quite, quite end of the line. And let's focus a little bit on the medical treatment. So similarly to, to, to asthma, I think our first step will be when someone's come in with symptoms of COPD or suspecting is COPD in a GP setting, what would you prescribe them? Well, the first option is Saba or Sama. OK. And now oftentimes the questions stem, the patient will already be on a Saba or Sama and they'll ask what next. OK. This is where CO PD is different to asthma. So this if you guys are taking anything away from that, so just make sure you remember this, we need to make sure that we assess for asthmatic features. OK. This will directly uh change our management. So do they have asthmatic features? This includes whether they have a history of asthma, whether they have H pie sort of allergies? Um That AP triangle, if you remember, do they on their blood test have raised eosinophils or do they have diurnal variation in the one or the 400 mils plus variation? OK. Or 20% plus diurnal variation. OK. If they don't, that means they don't have asthmatic features, then you can start them on laba and lama. OK. If they do have asthmatic features, then as we know, we prescribe inhaled corticosteroids, so instead of the lama, we give I CS, if it's still getting worse, then you can combine those two treatments together. Ok. Saba la la s if that's not working specialist, uh respiratory referral for possible consideration of oral theine azithromycin prophylaxis rescue packs for them at home. And so much more including possible long term oxygen therapy as well. And the main criteria for long term oxygen therapy, which is important as well, which could definitely be tested for you is number one, the patient needs to stop smoking. Ok. Think about it this way. If you're smoking near an oxygen tank, it's bound to explode. Ok. So that cannot happen. All right. Um Other things include if their SATS are less than 92% or they're quite sinus. If their fe one is less than 30% ie their lungs are absolutely finished if they have polycythemia, um or if they have pulmonary edema or they have cardiac signs, ok, which shows that this is quite advanced COPD and they need a little bit of extra support. And then as you can see that LTO T machine, now, often times where I falter in exams as well is I'll know my pathways of, you know, saba, sama sabaa, laba I CS, but I actually wouldn't know the names of the inhalers. Ok. Now, in your exam, they'll ask you by the names of the inhalers. So please just take a screenshot of this, burn it in your mind, remember the different sabas, the sabas, the LAMAs, the laba, ok? Because you don't want to lose that mark, it hurts then through it. Ok? And now just like asthma, when you have your exacerbations as well, you have a different set of management. So in exacerbation of COPD, you'll see an acute increase in shortness of breath, coughing, wheezing with also infective signs, uh including worsening uh sputum production. Um And again, like we did in the question, the most common organism that causes that is Hemophilus influenza. Other uh organisms include strep, pneumonia, and Moraxella, catarrhalis. Um What do you mean by bananas and co PD? Uh No, I was just, I was just making uh I was, I was trying to be funny, I failed. Um Sorry about that. It was, it was irrelevant, it was irrelevant. Um Anyway, um So essentially, yeah, hemophilic influenza is the most common um organism that causes COPD exacerbations, infective exacerbations. Obviously, you can have viral exacerbations as well from something like rhinovirus influenza or Coronavirus in the community. You treat it with prednisoLONE 30 mg for five days, you increase their bronchodilator or nebulizer frequency and you also can give them antibiotic therapy, something like Clarithromycin or amoxicillin or a tetracycline. For example, Doxycycline, I used to remember it as a cat. So, Crocin amoxicillin, tetracycline, ok. For COPD exacerbations. So, if you wanna take that, that's fine. Now, in the hospital, of course, um you would wanna give them some oxygen uh therapy, some nebulizers, IV, steroid IV thyle and possibly some, um, noninvasive ventilation as well. Um, and why would we admit a patient to the hospital? Uh, if they're showing some, you know, s systemic symptoms that the infection is not, um, you know, uh, doing so well for them. So some symptoms include severe, severe shortness of breath, low sats, uh, visible cyanosis confusion, um, a background of a lot of comorbidities, but they're already on long term oxygen therapy and they're quite advanced COPD. OK. Yeah. Now this is the next question if you have a read of it and I won't, I won't read it. I think you guys are probably, uh, already tired of hearing my voice too much. So I'll be quiet for a second. You pick your options and then we'll go through it. OK? All right. Any ideas, everyone, you can put it in the chat. It's no problem. Any ideas, any ideas, anyone or maybe I haven't stop it. OK. So, uh, b there's a some people think a, some people think b a couple of people think eight. OK. Shall we find out what the answer is? So, it is a very, very good to those who got it. If you didn't, no problem, we'll go through it as well. Now, why is it a, uh, what this question is asking? And why are we thinking a, this question is asking about a patient who has pneumonia? Ok. And how do we assess the management of pneumonia is through the curb 65 score again? Very classic question. Let's go through it. Ok. Now, pneumonia is an inflammatory condition of the lung secondary to infection or sometimes noninfectious agents such as aspiration, aspiration pneumonia. Symptoms include, uh, cough, shortness of breath, fever, fatigue and severe systemic symptoms can happen as well. And quite severe pneumonias which can include hypotension and tachycardia signs on examinations. You can see when you do the chest expansion test, there'll be reduced to chest expansion. It'll be dull to the CS because obviously there's something there that is sort of a, there's some fluid build up or whatever it is. Um, there's something there which is causing a bit of dullness. Ok. Also, you can hear crackles on auscultation, um, increased vocal fres a tactile vocal fremitus. You also can, um, uh, see some bronchial breathing and pleural rub as well. And investigations, of course, with any infection, you'd get blood tests, you see a white cell crp, you get a sputum sample to see what kind of organism is causing this pneumonia. And also, of course, you get a chest X ray as part of your septic screen. Ok. As you can see this chest X ray you can see in the left chest X ray, it's quite a normal looking chest X ray on the right hand side, you can clearly see that there's a lobar pneumonia in the right lobe. Ok. And it's a, it's worth knowing there's a point at the bottom of the slide. Whenever someone has had pneumonia, all cases should have a repeat chest X ray, six weeks after resolution after treatment to exclude underlying abnormalities such as a tumor. Ok. This is the thing about chest x rays. It could, you know, we see a mass. This is why I think in OSC as well, if you, if you still do osk, it's very important to not say that this is um, you know, when they ask you to interpret chest X ray, um don't say, oh, I see a possible pneumonia. You say I see a pacification. It could be likely to be pneumonia because chest X ray doesn't give us that much detail. That thing that, that thing we see it could be pneumonia, it could be something else as well. Ok. But we are suspecting it's pneumonia based on all the symptoms. Ok. And the, and the, yeah, and the presenting complaint. Ok. Common organism, the commonest organism, the easiest answer you'll get is strep pneumonia. It's in the name, most common organism with C AP. Ok. Hemophilus influenza, which is we spoke about is the most common organism that causes CO PD infective exacerbations. OK. And again, guys, these are classic, classic questions. So, so get the slide down. All right, strep pneumonia is the most common in cap Hemophilus influenza in COPD patients, CPSA, most commonly in alcoholics and those with impaired swallowing. Ok. Pseudomonas. Uh commonly in patients with immunocompromised or who have cystic fibrosis. And as you know, with cystic fibrosis, you have excessive mucus hypersecretion. So you, you prevent to get rid of the bacteria. Ok. You have less ciliary, uh ciliary work as well. All right. And staph auris as well. This is a classic question. I literally don't have a question like this a couple of days back. Um it's common in hospital acquired pneumonia if develops 48 of uh, hours after hospital admission, or you'll often see a patient has recently had a bout of flu. 10 days later, they come in with these pneumonia like symptoms, staph aureus, postinfluenza pneumonia, staph auris. All right. And sometimes you'll see these atypical pneumonias. All right. And the reason why they're called atypical is because they don't present quite similarly to our typical pneumonias that we just spoke about. Sometimes in atypical pneumonias, you might have rashes, ok. Sometimes you might have these systemic symptoms which you, you can't explain. Ok. And the conditions that cause these, uh, the organism, sorry, that cause these include mycoplasma pneumonia and legionella, pneumo pneumophilia. Ok. Pne pneumonia, pneumophilia, fine. Um, so mycoplasma affects young adults and produces diffuse infiltrates. It can also, um, sometimes cause, um, rashes. Um, and legionella is something that's associated with common contaminated water sources or air conditioning as well. Ok. Air conditioning units. All right. So if you hear a question about uh, someone returning from Spain, it's often, almost always Spain. They just had a, you know, had a beach holiday in Spain and they were in and out of the room with AC and now they've come down with symptoms of pneumonia was the organism legionella. Ok. Now, as we spoke about in the question that we did earlier. Curb 65 is the main score that we, um, assess the severity of pneumonia. Ok. In the primary care, it will be CRB 65 and in secondary care, second ie or hospital it'll be Curb 65 and these are some of the markers that we assess on. Ok. So each marker gets one point and then we add up the scores and then we refer to our lovely little box there, which the nice recommendations. Ok? Um and you can have a look there. Ok? So I'll I'll pose you guys a question. Um I am a, I am a 65 year old man. I've come in with new onset of cough. Um and you take my BP and it's 100 and 20/80. My respirate is 22 and uh I my my abbreviated mental test score is 10 out of 10. What kind of treatment should be considered for me? Anyone to shout up please. Is ipad still here? No, Ipads, not still here. And you want Rimsha, do you wanna, do you wanna get it again or? Sorry, I forgot what you said in the middle part? That's what? Ok, I'll give you the, I'll give you the scenario. So I'm a 65 year old man. I've come in with um all all symptoms that, that point towards pneumonia. Ok? You take my BP is 1 20/80. My respirate is 22 and my, I'm not confused. My AM MTs is 10 out of 10 according to this nice recommendation. How should I be treat? How should I be treated? Two? I'm gonna say is an admission to hospital? Ok. What makes you say that? Uh I think it's the BP as well as your respirate. Ok? Um So my BP is 1 20/80 ok? So it's satisfy that criteria and my respirate is 22 which is fine as well. I'm not confused my age however, is 65. So what are we thinking? Oh try and refer to the table and then just refer to that box because you're 65. Is it the hospital assessment should be considered? Absolutely bingo. Perfect. That that's exactly right. Exactly. So I'm just trying to get you guys used to uh the curb 65 score, the CRB 65 score and what that means in terms of management. Ok. Thank you so much Rimsha again for, for volunteering. I really appreciate it. Um And exactly. So uh this is the main thing we want to focus on the, the C RB 65 and how it correlates to, to our management. So this is in the community setting if we focus on the second secondary care setting. Now, excuse me, you're in the hospital. Curb 65. We've added this urea more than seven millimoles. Um OK, I'll pose this question again. We've got a uh we've got a 70 year old gentleman. He's come in uh with a new onset of cough and um purulent sputum Um on examination, if you note that his BP is 89/61 his resp rate is 25. Uh and urea is 7.2. He is not confused. How would you manage him in a secondary care setting? You'd consider ICU assessment because he has a kind of 65 score of three. Very good, very good. So where did you get those three points from? So I think you uh it was age for one of them. Urea BP. Very good. Thank you very much for contributing. Absolutely. So, uh three or more IC assessment. So again, we're trying to get you used to um seeing that curb 65 score and um seeing how that will affect our management directly. Ok. Wonderful. Thank you so much for contributing. Um That is the, that is the main point of this C 65. And of course, in terms of management, I think, um primarily we'll focus on uh community acquired pneumonia management. Now, if it's a low severity uh, cap, you can give them a five day course of a mo, ok. That's classic. Um, if it's, uh, if they're pen allergic, they can give them a macrolide or tetracycline. Ok. Toromycin, Erythromycin tetracyclines include Doxycycline. Ok. If they have a moderate or high severity cap, you'd usually give them a longer course of antibiotics and usually it'll be dual antibiotic therapy. Amoxicillin and a macrolide like Erythromycin. Ok. Um, obviously if they're amoxicillin allergic, then you can give them a macrolide and a tetracycline combined. Ok. And number two, if it's, uh, you know, if it's quite, quite high severity, which this is for high severity of pneumonia, you would consider something like Augmentin or coamoxiclav, cefTRIAXone or PTAs. We call it piperacilline with tazobactam. Um And plus a macrolide in high severity uh community acquired pneumonia. Now, from my experience, I think you won't get asked questions like that. I think mostly it would be about low severity and moderate severity in cat especially. Um, but it's, it's worth still knowing that information. Ok. Now, this is a question if you guys can read, um, and if someone wants to turn their mic uh on and read it for us or uh w walk, walk us through what they're thinking or anything, by the way, guys, there's, there's no wrong answers or anything. So, so sorry. II, don't mean to grill you or pick on you guys. I think it's just, you'll learn more in this uh in this environment, I feel that's, that's how it works for me. Otherwise it's quite easy to fall asleep uh behind the screen. OK. So um if you read the questions, start study the answers through, we can have a read and, and figure it out. OK, good. We have some answers coming through. So someone says a good anyone else with any thoughts? All right. So if we can reveal the answer please and full stop as a as well, very good anyone else? Ok. So if you can reveal the answer please, and it is indeed a now, the reason of that we'll focus into in our next slide. Now, I just wanna preface this by saying that pleural effusion was a topic that was um quite ok. But I sometimes struggled with especially in an exam context. So I hope I can do a better job of explaining it as opposed to my own performance on a questions of pro effusion, right? Pleural effusion is accumulation of serous fluid within the pleural space. OK. As we already know uh our pleural space and our, so we have a visceral um lining and our pleural lining. Ok. Think about a balloon within a balloon. Ok. So a balloon within a balloon and when those balloons are touching, that's that, that space. OK. Pleuro fusion is when there's fluid in that space. Ok? Between the balloon and the balloon. If that makes any sense. Now, like every respiratory condition. The symptoms would be dyspnea, which is shortness of breath. You'll get a nonproductive cough because there's no underlying infection that might be causing this. Ok. And you'll get this pruritic chest pain, which um jasmine um quite nicely explained as well. You get this pain, sharp pain on inspiration and signs, examination signs, you'll hear a stony dullness to percussion. So now you, you know that there's a fluid, there's a solid matter, filling up that space, which used to be air. So there will be some dullness to percussion. OK? And because there's obviously reduced um lung lung volume, there'll be reduced lung expansion and investigations, your primary primary investigation will be a chest X ray. OK? If you are aspirating that pleural fluid, you'll do an ultrasound and you, this is something that this is more, more of a management that I'll put, put this there anyway. So when you aspirate a pleural uh a pleural fluid, you can do it with a 21 gauge needle and a 50 mil syringe and you send that off to the labs. OK. Now, this test, you send off to the labs is very important in determining what type of fluid is in that pleural space. OK? Because that directly then affects our management. All right. So this is why it's so important to get a sample of that pro fluid, send it to the lab to see if there's proteins in there. If there's lactate dehydrogenase um uh what's the ph OK. That will all lead to the management. OK. If we move on to the next slide, please. Um So this is lights criteria. OK. Now, light's criteria determines whether the pleural effusion is transudative or exudative. OK. What transudative um pleural effusion is is when there's imbalance of hydrostatic and oncotic pressure in the pulmonary capillaries? Ok. So there's an imbalance of the pressures. What happens is when the fluid is forced through the pulmonary capillaries and it has nowhere to go. But plural space. Ok. Comparatively, excitative effusion is something like an inflammatory disorder which causes increased in capillary, permeability. Ok. That means the holes between the cells of the capillaries are larger. So different things can flow through as opposed to just fluid. So that's why we should get our, our, our, our mind thinking. Ok. So, um I would like to explain it in another way as well. Um Translative fluid, you think about a hosepipe, a garden hose pipe, you get a pin, you poke a hole in it and the uh water will flow out. It's just water, it's clear fluid. Um And it's, it's flowing out into this uh air which will call our, um, which will call our um parietal parietal layer between the viscera and the parietal layer. Ok. Comparatively, our fusion will be something like if you have a bowl of soup which has all these different bits in it and that falls over. Ok. And that will be something like our exudative effusions. Ok? And the main thing is how we tell between the two is the protein and the LDH. So as we spoke, translative, essentially, clear fluid is a clear water going through the hosepipe. So the protein and the LDH in the pleural fluid will be less than the protein in the LDH in the blood comparatively. And an exudate the protein and the LDH, there will be higher levels in the pleural fluid compared to the blood. OK. You've got all that gunk that soup falling over. OK. And there's some examples, there's all the common causes of transudative versus exudative pleural effusions, which is very, very worth remembering because they are very commonly tested. OK. And in terms of management. So, um we've obviously sent, we've sent our sample to the lab if effusion is purulent or uh purulent, sorry or turbid uh slash cloudy. Um You want to insert a chest strain, OK. And especially we should insert a chest strain if the patient is septic and the PH is less than 7.2. If they have recurrent uh pleural effusions, then we'll pleurodesis with TALC to seal the pleural space. Now, what is pleurodesis with TALC? Um Essentially, it's a sort of a medical talcum powder which sticks those two surfaces together. OK. So you put the whack the chest drain in, you take all the gunk out and then you put uh essentially you put a needle in and you inject this talcum powder like situation, I would say into that gap between the two balloons that we spoke about and that allows them to stick together to prevent any fluid from getting through again. Ok. It allows a little uh you would say in a way the surface tension keeps them, keeps them together. Ok? And we can move on to the next slide and we'll end off. Uh ladies and gentlemen. Oh, sorry. Is someone saying, I don't think it does. Me. Uh uh Jasmine, sorry, I just wanted to say, ladies and gentlemen, we'll end off with a couple of questions. Jasmine, if you want to take over, that's absolutely fine. Um uh And we'll let's get some active involvement guys because this is the final time where we can um, ask any questions and, and get really stuck in. Ok? So Jasmine, I'll, I'll let you take over. Thank you everyone for listening. Yeah, we just thought we'll circle back to the earlier topic. So, um we're just gonna do just two questions quickly just to make sure that we haven't forgotten knowledge as all the other slides have come about. Um So if you guys, like I said, wanna give her a read, um put the answer in the chat or anything like that, then yeah, this is the question. So a 27 year old lady reviewed an asthma clinic. Um So she's got uh salbutamol and beclomethasone. Um but, you know, still not quite managed. Um So what do you think would be the next thing? And um the sports Sammy mentioned earlier about, you know, how important it can be sometimes to remember the, the names of the inhalers rather than sort of like Saber and Lama and things like that. Ok, let me check the chart. Um ok. Got beat. Yeah, so that's the answer. Um So I'm glad you guys have started to remember the little flow chart um that we discussed earlier and then move on to the next one. So another sort of inhale like question. So what do you guys think? So we got three and somebody said one, let's have a look. OK. So the reason of um why is obviously you got that smoking history and 72 year old. So we're thinking, you know, more sort of CO PD. Um And then they got that diurnal variation. So that's more asthmatic features. So if you follow that flow chart through the COPD, then that's why uh we want to go and use the ics uh which is the betamethasone um on the dilator. OK. Um And then the OL so uh Q and A questions. So if you either got questions for me or Sammy on any part of the slides, I can happily kind of like flick back to whatever and give more explanations if you guys have anything that you are still not quite clear on or want something a little bit repeated or explained a bit further. I think guys, it could be, to be honest, it could be questions on anything. That's, yeah, the working life. Um Anything. Yeah, high risk features of pneumothorax, please. Ok. So I'll go back um uh probably. Ok. So high risk features. So if you, if I don't know if there's a way I can zoom in is can you guys see that a bit more zoomed in? So that's the uh what they clarify on there. So, hemodynamic compromise, significant hypoxia, there's bilateral pneumothorax, uh underlying lung. So, you know, symptomatic and underlying lung disease, we'll class that as high risk. Um 50 plus years of age with smoking history as well. Um And as well as if they got any bleeding. So, you know, hemo ora, so those kind of things, if you see them, uh we'll put them into more high risk, I think it's worth worth remembering as well whenever you're talking about high risk characteristics, just think about is this going to increase the morbidity and mortality of the patient? Right. So if you now read about this hemodynamic compromise, of course, the patient is not doing very well. So they compromised ok, tension pneumothorax again, you know, it's a it's irreversible, flat air is only going in, it's not coming out. So obviously, it's gonna have trouble, you get midline shift, you can have all sorts of troubles. So all these characteristics keep in mind that you can remember them quite easily by thinking. Hm. Is it gonna fasten that process of morbidity and mortality for the patient? All right. So that might help you remember? Ok. So that one's that. And I think earlier on someone asked me um, on the message, what is s and lti don't know whether I just wrote a shorthand for myself in one of the slides before, but I'll try and see what that was for. Um I think it might have been somewhat earlier on. No, I can't remember where I had written that. Um Yeah, bye. Someone mentioned about bananas and co PDI still can't get over it. Sorry for saying that guys. Sn Lt. OK. What? Yeah. What did I mean by that? I think you must have wrote a shorthand for something but sorry about that. Oh, I don't remember now. What did last or ah severe or long term or persistent? That was it. Yeah. So consider Pitro bromide while awaiting if yes, if it's severe uh lo uh life threatening, sorry or if it's a persistent. Yeah. So I just wanted to create spaces in the slides. I think so. I just created a shorthand. Um But yeah, that was, I hope that addressed to that first question. Any other question guys? We've just, we've got six people in here or five people in here. Any questions, shoot no problems? I see. Great session. Thank you. Thank you. So much for, for contributing and for participating. Um If you guys could do the feedback, that would be lovely. Um OK. Yeah, I agree. Thank you. Thank you both. That was really good. Um Clear slides and also very clear explanations um for each SB um Yeah, so guys, please make sure you fill in the feedback form for our speakers. OK. Um Because they've taken their time um to present tonight so that the feedback form um to make sure that you fill that. Yeah, just, yeah, make sure you fill the feedback. It's just, um, I've just put it in the group chat. Um And yeah, and if you have any other questions that come up later on, uh, feel free to message over Facebook. We've got a Facebook group Facebook page, just message there or, or Instagram and then we'll try and answer. Um Otherwise, yeah. Thank you so much, Jasmine and Sammy. That was excellent. Uh I've got everything recorded, so I'll put that up on the middle page and um and yeah, yeah. Any, uh I if everyone is happy uh for me to end the meeting. Yeah. No, that's OK. Uh Thank you for having us. Um, me and Sam obviously really enjoyed presenting and Yeah. Yeah. Yeah, that was, that was excellent. Thank you both. Thank you. Thank you so much for the opportunity.