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OK. Amazing. Can everyone see? OK. Yeah, we can see that. All right, great, perfect. OK. So today, I'm kind of mainly going to talk about some conditions that you need to be familiar yet. There's a few things I won't cover and I'll put it at the end. Um And then you can obviously look it up in your own time. So the important conditions are asthma, co PD, bronchiectasis, lung cancer, pe and interstitial lung disease. So, first of all, asthma. So asthma is obviously a chronic inflammatory disorder of the airways and the main features of asthma are airway hyperresponsiveness and airflow limitation that's partly reversible. So the key triggers obviously are allergens, irritants, exercise, sometimes respiratory infections and the main features of asthma. I'm sure you're all aware are wheezing, shortness of breath, chest tightness, and importantly, diurnal variation, which means that symptoms can change throughout the day and especially if it's uncontrolled, they can get night symptoms. So the pathophysiology involves inflammation of the bronchi. Um the tubes obviously lead to the lungs causing bronchoconstriction and also increased mucus production. So I'll talk a bit about asthma diagnosis. So, a bit about spirometry, which is the main way we can diagnose asthma. So the graph on the right shows a normal um spirometry result, an obstructive ABT strongly result and a restrictive which we'll talk about later. So an ask me to get an obstructive pattern which is a reduced F EP one divided by F VC ratio. So the F VC is a measure of how much air someone can expel from their lungs after taking a full inhalation in one second. And the F VC which stands for forced vital capacity is the total amount of air that can be forcibly exhaled, exhaled after one deep inhalation. So, the main kind of differential um would be CO PD with an obstructive pattern. And the way that you can tell the difference between asthma and COPD is that um asthma responds usually to bronchodilator. So, um like a salbutamol inhaler and the diagnosis depends on the F EV being about greater than 12% and at least 200 mL difference after giving the bronchio deleter. Another way it can measure asthma is the peak expiratory flow rate, but this is not used in isolation. Um but it is very useful for home monitoring and also chest X rays. But again, they don't really show any specific features and it's more just to rule out other diagnosis such as pneumonia or pneumothorax. So this is a very complicated slide. So I'm not gonna go over in detail. But um I've put all the links at the end, but I'll just go over kind of some of the changes with the guidelines in 2024. So last year, so the BT S nice and sign actually made a combined guideline. Um And the main difference is you should never um just prescribe a Salma. So the short acting beta, so a salbutamol alone anymore for asthma and instead you um prescribe something called a therapy which is a low dose, inhaled corticosteroid and for metal combination inhaler and fetal is a long acting bronchial dilator. Um So a long acting version of a saba, but the reason that it can be used um is because it has a dual action. So it's has a rapid onset of action, meaning it can open the airways faster, but also it has a prolonging effect as well. So that means it can be used both as a reliever and as a maintenance therapy. So that's kind of the main difference. So you'd use that as a first line and then also we can consider a mark regime, which is the same inhaler. So the combined low dose I CS and fetal and you can use this twice a day. But also if someone's getting more short of breath and have an exacerbation, you can use this as a reliever on top. So that's the kind of main differences that these guidelines have shown. So now CO PD. So CO PD is again a chronic progressive disease um categorized by airflow limitation due to chronic bronchitis and emphysema. So, what is chronic bronchitis? It's defined as a persistent inflammation of the bronchia. So the large airways with excessive mucus production leading to your chronic cough and sputum production for at least three months and two consecutive years. And emphysema is a condition characterized by destruction of the alveolar walls and this obviously leads to impairment in gas exchange. So, as you're aware, smoking is the primary cause, but also we have occupational exposures and this is very important to ask about in the social history with patients. Um things like mining or construction industry and additionally, some genetic conditions like alpha one antitrypsin. So ask about family history. Um So I'll just talk a tiny bit about CORAI which is when conditions of the respiratory system affect the right side of the heart. Um and some features of that is signs of right sided heart failure. So a raised JVP, peripheral edema and also some changes in heart sounds. So you can get a loud second heart sound as well. So the CO PD diagnosis. So again, spirometry, um and it will confirm the same as asthma and obstructive pattern, but it doesn't change when you give bronchio Gil or there's very little change. And then once we've confirmed that it is um an obstruction pattern, then we can grade it. And the main way to do this is based on the fe one which is how much they can blow out in one second. So as you can see on my screen, it goes from mild to very severe depending on the percentage of the F EV one another way to grade CO PD or another way to kind of um measure um how severe someone's CO PD is using the scale on the left. Um So this is the severity scale of how um far they can walk before becoming breathless. Again, other things such as a chest X ray to rule out other causes and a filled blood count, of course, again, um quite a detailed slide, but you can go back and have a look at this obviously in your own time. Um It's similar to the asthma one except you can a stepwise approach offering a Saba or sama and then adding as needed. And it also depends on whether a patient has some asthmatic features, whether you add in first of all, an inhaled corticosteroid or whether you go for first of all, the long acting musculin antagonist. Um and the asthma features you can see in the bottom um such as uh history of asthma or um history of hay fever allergies, a high il count in the bloods or a variation of the FBC one over time. So bit about acute exacerbation. So, an increase in symptoms is the main way we can tell. So increase in shortness of breath sputum production um and it can be infective or non infective. And I've put some common um pathogens that cause infective COPD that I think you should be aware of for exams and in terms of what we do, so we get a sputum culture is important. An ABG gives them regular nebs and oral prednisoLONE and I won't go into detail about N IV, but I'll just briefly describe what N IV is. So N IV is noninvasive ventilation. Um And for CO PD in people that are retainers retain oxygen, carbon dioxide, we can use bipap um which provides two levels of pressure. Um There's one pressure called the inhalation pressure that helps move um or into and out of the lungs during inspiration. Um And the other is the exhalation pressure which helps keep open the Aveno and prevent them from collapsing and that helps the patient exhale more easily. And I put some of the um indications when we would give N IV. Um but that might be a wee bit a wee bit high for your grade right now. So we won't cover that in detail and then briefly on bronchiectasis. So I talked a bit about bronchi um bronchitis in when I was talking about COPD. So bronchiectasis is slightly different. So it's when there's chronic dilation of these airways and it's usually due to recurrent inflammation or infection and this commonly occurs due to repeated respiratory infections. So people with CO PD can have bronchitis and the kind of key feature on CT scanning is that the bronchi are dilated and there's a lack of what we say, what we call tapering of the bronchi. And that's when, um, the bronchi maintain a widened appearance as they progress to the smaller airways of the lung instead of being large at the top of the lung and then going narrower as it progresses to the bottom of the lungs. And similar to CO PD, we can use antibiotics if they have infections, bronchial chest therapies and sometimes they need long term antibiotics. So a pe um so a bit about a pe um I put up um the well score. So the well score helps determine whether you need to do a DDIMER first or whether a patient can go straight for a CTP. Um I'll let you look through that in your own time, but essentially, it takes some risk factors for uh pa um and looking clinically at the patient and the symptoms of her pa are usually sudden onset chest pain, which is pruritic in nature. Um taking a deep breath in it hurts shortness of breath and um hemoptysis. And of course, the treatment is anticoagulation and in severe cases, thrombolysis. So, in the next slide, I've heard a bit about um if a patient has an acute pa, when would we think about thrombolysis? So, of course, we think about thrombolysis. If a patient is hemodynamically unstable, that is they have a massive pe and their BP is very low, usually less than 90 systolic. Then we can give, uh, thrombolysis treatment to help, um, thin the blood and hopefully help with the breathing when someone has, um, they don't have a low BP and they don't have what we think is a massive pe, then there's some, um, elements that we can go in to determine how risky we think the pe is. And there's some tests here that we can class them either as intimated high risk or low risk. And that depends on whether they have got any element of right sided heart failure on the echo. Again, I think this is a little bit above your grade. So I won't go into massive detail as, but as long as you know, for a massive pe, we usually give thrombolysis and for a low um low or medium risk, we give anticoagulation usually and their scoring systems to know whether we can safely discharge them or whether we need to keep them in hospital and the anticoagulation choice. So the main thing we use now is a doac um So Apixaban, Rivaroxaban, um and sometimes we can use enoxaparin, especially if they um have other risk factors and the duration. So of provoked is a pe that has a known cause such as uh malignancy. Um And this is usually for three months and an unprovoked. It's usually for three months. However, at review, they can consider if um they need long term and a bit about lung cancer. So I'm conscious I'm doing this quite fast, but of course, all these labs will be available. So, lung cancer is the most common, um, and the most essentially deadly, um, cancer in the UK. Um, and it is primarily caused by cigarette smoking. So there's two main types, there's non small cell which makes up the majority of cases. And small cell, a non small cell can be further categorized into different types as well. The key difference. And you should remember this for your exams is that small cell tends to present late and it's usually metastatic. So it's usually surgery is usually not um recommended for small cell. Whereas non small cell, if it presents earlier, surgery can be done. And just a wee bit about what we call paraneoplastic syndromes associated with lung cancer. And again, this could come up in exams quite easily and this is particularly with small cell lung cancer. So some common are Cushing's Syndrome and this is when the cancer secretes ACTH leading to an increase in cortisol. And they can get the signs such as Cushing's also hyponatremia. You can get hypercalcemia. You can also get neurological, such as Lambert Eaton syndrome, which is muscle weakness or you can get clubbing of the fingers. Another thinking gap is something called S VC obstruction. So sup superior vena cava obstruction. And as you can see in this picture, it's essentially compression of the superior vena cava via tumor. And this can lead to the signs in the picture such as swelling of the face and neck distended veins in the neck, headache and very short of breath. And this would be, you know, an emergency situation. They would need scanning to determine, you know, if they've got cancer or if they've got no one cancer. Um, then this needs to be escalated for treatment. And a pancoast tumor is a tumor that sits on the, usually the top of the lung and it can involve the brachial plexus usually. And this can lead to some kind of common um signs. And the main sign that comes of big exams is Horner Syndrome and this is when there's ptosis, um meiosis and, and hidrosis or lack of sweating down one side of the face. The management again, not in detail, but as I said, nonsmall cell surgery, small cell tends to be advanced. So, chemoradiotherapy if or palliative and briefly about I LD, and then we'll go on just to do some questions at the end. So I LD is interstitial lung disease and it's essentially a group of disorders that leads to um inflammation and fibrosis of the lungs. And this causes a progression in pulmonary dysfunction and there's a wide range of cause. Um and for exams, it's important to ask about their social history if you come across a case like this. Um as a lot of environmental exposures can cause this So there's idiopathic, which we don't know the cause. Um there's hypersensitivity or occupational exposure and this is things like asbestos silica and also um the lungs being hypersensitive. So things such as farmers lungs, um bird fanciers lungs, um stuff like that where they're sensitive to a certain thing, sometimes mold and the next would be drug related. Another cause is uh autoimmune such as rheumatoid arthritis or S LA and the clinical features, it's usually a progressive condition. So it's progressive shortness of breath, a dry cough, weight loss and you can get clubbing, especially in idiopathic and on examination. Um it's spine, usually velcro like creps on the lungs. The main way to diagnose this is a high resolution CT and this can show um mm inflammation of the lungs are, are honeycomb signs and the pulmonary function test shows a restrictive pattern. Um As I said, you can go back a slide for COPD um about the um look at the graph to see the difference between the obstruction pattern and the restrictive pattern that might come up in the exam. And additionally, sometimes if we don't know the cause, we can, we can do it bronchoscopy and the management. So it obviously depends on the cause. So the idiopathic um sometimes we can use um pone antifibrotic therapy um but it has a very poor prognosis and usually they um they don't survive past about five years. Um and rarely, they could be eligible for a lung transplant. Um And then depending on the other cause, we can um obviously give treatments for that and what's really important as well is getting palliative care involved early. Um So, just briefly about oy, so, um social history is so important in OS. Um it's kind of things that could come up for obviously peak flow um assessment and evaluation, spirometry interpretation, they like they like chest x ray interpretation um and pneumothoraces at the top of the lungs. Um So don't miss the top when you're looking at the lungs. Um and also obviously reviewing patients with um asthma COPD that um become a bit more unstable and you need to decide to isolate their therapy. And this is a bit about chest X ray interpretation. I'll let you read this, but there's a Pneumonic you probably have heard about um doctor doctor's ABCD. E just to help you interpret that. Ok. So now is um time for some questions. So if you want to get involved and unmute your mics, that's fine or I can just talk through them. Um I'll give you a chance. So which of the following investigations is most appropriate to assess the metastatic spread in a patient with suspected advanced lung cancer? So, does anyone want to say what they think? CDC? Yeah. So this is quite, you know, obvious it's act um but obviously CT is the most appropriate scan. Um And sometimes they like to phrase um examination questions that are saying, what is the most appropriate or the next step. Um So, although pet scans are obviously very useful in detecting um meths, um it wouldn't normally be the first line investigation. It's quite a straightforward question. So the next one is about a 70 year old male with a long smoking history presents with a chronic cough and shortness of breath. So, spirometry shows um an FEV one slash F EC ratio of 60% and the fe one is 50% of predicted. So what is the most likely diagnosis? COPD? Yeah. So again, COPD. So spor findings, we know um, the F EP one slash F PC ratio less than 70%. So that's um, you almost diagnosed COPD. So a 60 year old man presents with acute onset shortness of breath, chest pain, hemoptysis after going hip replacement surgery. Um, so he's a swollen tender heart right leg and the observations he's a bit tacky, his BP is fine. Um, his SATS are ok. His respirator rate is a bit up and his temperature is ok. So which one is the most appropriate next step? C TPA. Yeah. And why would you do A C TVA? Not the D dimer cause as well score is high enough, you can go straight to CT P. Yeah, exactly. So again, so make sure that when you're doing questions like this, you, you know, pay attention to what is the most appropriate one. So a 67 year old, famous with uh female with um, moderate CO PD has a persistent cough, shortness of breath, frequent exacerbations, slight treatment with a laba and inhaled I CS. So there's some spirometry investigations. So the F EP one is down. Um, and according to the nice guidelines, what do you think is the next step in management? So I'll go ahead and say so it's to give the llama. So with CO PD, we don't increase the dose of the I CS. Um usually as a first line because this can increase the risk of pneumonia. So you're using the step wise and using night skylines, we should add Alama next before we shouldn't resort to increasing the dose of the ics um that you might consider obviously an asthma. So a 58 year old man with progressive um shortness of breath and a nonproductive cough um for several months. Um He's got a history of smoking, works in the ship building industry. Um examination. He's got fun. Asper crackles cr um CT shows hr ct sr shows honeycombing intra bronchiectasis. So according to the nice guidelines, what do you think is the next step in this um investigation was? So essentially what we do is we'd me, we try to find what is causing the likely ILD before resorting to any treatment or resorting to biopsy. So we could measure the serum markers for an underlying connective tissue disease causing the ILD. Um Before we'd consider treating that. Um because only some forms of ILD will respond to steroids. Um And additionally, um lung biopsy is reserved for cases where we find we need to find a definitive diagnosis and it's not kind of the first line. So kind of not what was not covered. Um I didn't talk much about um pneumonia, um pneumothorax, pleural effusion kind of interpretation of ABG S or a chest X ray um interpretation in detail. And this is just a little bit about feedback. Um, a cure just ask me to put on, um, if you want to, um, give a wee bit of feedback about it, um, or just about these lecture series in general that would be helpful. Um And does anyone have any questions that they want to ask? Hopefully the slides will be useful to kind of go back and look, you know, at the guidelines and everything. Um I know I quickly ran through it. Um But just so you have an idea of kind of what conditions are important and what kind of things come up? Great. I'll just check. Thank you. No worries. Thank you. Just check. There's nothing, no one asked anything in the chat. No. Great. All right. Thank you for coming guys. Thank you so much. No worries.