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You're gonna with me, um you're gonna cause an arrhythmia. So you have to give it during depolarization because think of it giving a shock, you're basically telling the ventricles start working. So you just, you're trying to hit it when it's working, but going a bit through over this. So the physiology of the heart, we know that um when blood enters, we have the. So here blood is uh blood. Normally when it first gets from your veins. So from your supra superior vena cava, inferior vena cava goes into the right atrium. What happens is there is passive flow of the blood into the ventricles, um passive flow and then you have your atrioventricular valve. So your mitral valve and your uh tricuspid valve, they shut. Um So they give the last flow, they shut and that when they shut, that's to prevent back flow of blood, your ventricles then eject they cause blood to go all around the body. Um But then yeah, so this here, the ventricular pressure goes up, allows for rejection. So remember when pressure goes up, volume goes down. So that means you're rejecting blood. Um And then we have your aortic valve opening. So your ventricles have ejected, you want your aortic valves to open to allow blood to go out to the rest of the body and then your valve will close. Whereas the rest, the rest of the blood is coming back into the body. So think of it as a system that's continuous. It's not like it's happening, waiting for the whole thing to finish, then again happen. So it's happening all at the same time, sort of thing. But I think what's important to remember that your first heart sound is when your atrioventricular valves close and that's your lab. Your second heart sound is when your um aortic valve and your pulmonary valve close and that's your dub. Then you have other sounds which can be um physiological, but then it's just important to kind of remember what's happening here is atrial depolarization, ventricular depolarization and then you have ventricular repolarization. Um Next question for a cardiac pacemaker, what ion channel is most responsible for the change in membrane potential in the phase outlined by the red bar in the following diagram. So this is a cardiac pacemaker graph and there is different phases that happen. So yeah, what, what's the whatever that is? It's a red line you guys are doing pretty well. Not gonna lie. I thought these were gonna be very, very, very difficult questions, but just give it a go if you know good if you don't know that's why we're learning OK. Five more seconds. OK. We can end up all there. Majority of you got it right. So is the L type calcium channels and we will talk a bit about these graphs. I know these are, I don't know if you guys have been taught these graphs before, but we have two main ones. There are actually many, but two main ones that I want you guys to remember. So you have the um uh electrical to the pacemaker potential or a cardiac pacemaker, um the electrical conductivity. So you have the, these actually have numbers, these diagrams that I put here don't have numbers, but then the red is like a four, the blue is a zero and then the orange is a three. So it's like error 403. And what happens in this thing is you have, so if we start from the red or if we start from the orange, you have a slow influx of sodium that's coming in and that's causing the voltage to become more negative. So it's called starting the depolarization process. So the membrane potential goes up a little bit, goes to 40 minus 40. That that causes the a rapid influx at that level, there's a rapid influx of calcium. Um And obviously, that's positive irons, more positive irons coming in, that means the membrane potential becomes more positive goes all the way up to 20. And then at that point, you have an outflux of potassium. So then more positive is leaving. So your me goes back down again. So minus 40 is the threshold that reach the ion channels open. And then you have this depolarization that continuously occurs. So you guys were right to say the calcium channels were there. So it's, it's good to remember that in here, the influx of calcium is what causes the rapid depolarization. Now, if we think if we look at this one, this is now the cardiomyocytes or your ventricular. Um I don't know what ap is. I put it there but I forgot now. But anyways just let's look at this graph when you see this graph. So this one also has numbers that's 01234. So at this point, you have an influx of sodium channels. Now, the difference between these two is a rapid depolarization here is caused by an influx of sodium channels. So sodium iron, sorry. So sodium irons are gonna come in positive irons cause the membrane uh potential to go up to go up and then when they get to 30 the channels will close. So obviously, if the channels are closing, then you have. So uh calcium channels opening because channels are closed, you're gonna say oh the membrane potential is not coming down slowly. But then because the calcium channels open the it's it's maintained. So even though the sodium is kind of leaving the calcium is still there, so it's still balancing and causes that plateau that you can see. Um And then the calcium channels are also closing. Now. So you're meant to have repolarization because there's no more positive ions coming in. So then starts going down, the membrane potential starts going down. Um And then you have potassium channels closing here completely. So uh actually, this is not a very good diagram. But what's happening at this point is you have an exchange that's causing the plateau between calcium and potassium. But then because the calcium channels close, the potassiums are still leaving, that's what the repolarization. That's why the repolarization happens. And then when potassium channels close again, plateau, I know it's probably not the best explanation, but I think it's just worth remembering that this one is depolarization, rapid influx of calcium depolarization, rapid influx of sodium. I hate physiology. A 68 year old man presents to the ed with central crushing, chest pain, radiating down to his left arm and jaw. You perform an ECG which shows ST elevation in leads one to V one to V four and you diagnose an anterior mi which artery leads to this type of myocardial infarction. Yeah, this is uh it's like an application B um Yeah, we'll do 30 seconds for this one. No, 35 cos I spoke too much. You guys are doing well though. Hopefully, the rest of the slides are not gonna be BCIG. Um OK, we can end the pool there. So the majority of you have voted for a, which is the correct answer. So, it's the lad, um, we'll talk a bit about coronary arteries. So now I know some people think, oh, the aorta, that's, you know, that's the main artery. But then the aorta is supplying the rest of the body from the aorta. There's a little, basically like a little corner, like alleyway. You, you can call it an alleyway if you think of the AORTA as the main highway. But like uh so that little alleyway is where the coronary arteries emerge from. And I think it's called the coronary. No, the coronary sinus is where the veins go in. But anyways, so you have these arteries supply the myocardium, which is the heart muscle itself because again, yes, the heart does work consistently, but it does need blood supply to itself to work. Uh the main one. So you have the left. So you have a left and a right main coronary artery. So they come from two sides, the left art the left coronary artery, you have the left anterior descending artery which branches off it, supplying the right ventricle, left ventricle and your interventricular septum. So it supplies the big guys, you know, the, the the the people who supply the rest of the body. Um then you have the left marginal artery which also helps in supplying the left ventricle. The left ventricle, think of it. It's a very, very thick um chamber of the heart. So it needs a lot of blood supply. Then you have the left circumflex, which also supplies the left ventricle, but also the left atrium. Then the right side, you have the right coronary artery supplying the right atrium, right ventricle. That's quite easy. Just right, right. Right, right, marginal artery supplies the right ventricle and the apex. So obviously, the apex is quite far. So this one comes all the way down if you look at it from the back, um the left circumflex again, we've talked about it, but it just comes all the way and kind of. It's called circumflex because it sort of goes round. Um And then what we can't see on this diagram, what we can see on the other one is the posterior interventricular artery. So sometimes you can get an anterior interventricular artery, but then it's rare. So posterior is more common and it's a branch of the right coronary artery which supplies the right and left ventricles and the intraventricular septum just like the lad um from the back though, then you have the veins. So the marginal arteries accompanied by the small cardiac vein. Your middle cardiac vein usually accompanies the posterior interventricular or the anterior interventricular in some people. Then you have the great cardiac vein which accompanies the left coronary artery. Um Yeah. And the coronary sinus is where all the veins meet and then drain back inside into the right atrium. 70 year old woman brought into the ed shortness of breath. Past medical history of left ventricular systolic dysfunction, ejection fraction of 20% chest X ray confirms acute pulmonary edema treated immediately high dose IV for repeat of oxygen sats levels of 94% on 15 L of oxygen. Heart rate of 124 respirate of 28 and BP of 7450. What management option should be considered? Next? I know you guys are just in here too, but then you also are going to be sitting a PT. So there are some questions that are PT application sort of thing. But also a bit about two. I think with this question, I'm gonna give you a hint. Think ABCD E think of, you know, if you're an, you ask how you're gonna treat this patient? Think airway breathing, circulation, disability exposure. What do you want to fix next? What's, what's important to us here? Is she breathing? Is she fine? Is she, you know, and I can see a variety of answers. ABCDE all of them. It OK. Just, just honestly pick whatever you guys are trying really well doing really well. This is a very hard question. I got this wrong myself when I did it. But um yeah, that's fine. We can end up all there. So majority picked a but the answer is actually D and I will explain. So does it explain here? No, I'll just explain it. So this, this patient has pulmonary edema. Um because the oxygen sites level are fine. I mean, they are a bit low but then 94% is acceptable. Heart rate's tachycardic mm respirate is a bit high but she is breathing, we will, her BP is very low. It's less than 80. So someone who comes in with an ejection fraction of 20% systolic dysfunction. It's telling us cardiogenic shock, pulmonary edema because they have a BP of less than 80 they have a cardiogenic shock, giving fluids not gonna help bisoprolol. Well, that's just gonna lower her heart rate. I think what's important is to admit her, she's, she's very acutely unwell. Um So we need to think about heart failure, we need to think about giving her inotropic support, which is like vasopressors. But um I've put an explanation down as well in the notes for this question. But yeah, cardiac failure. So the heart failure happens when the heart is unable to pump enough blood. Um obviously to meet the body's needs. So there are, there is so many ways that heart failure can occur. This is a little di um just to explain the pathophysiology. But what happens is you can have heart failure during diastole or systole and you can either have really dilated ventricles. You can either have very stiffen ventricles. And what happens is 11 way is blood doesn't fill up during diastole. So you, you don't have enough blood because you don't have enough blood, the blood just goes back or it stays back in the atria, what the ventricles do they want? Because you have less blood, they don't really need to contract as forcefully. So they just don't contract forcefully. And that means you have an increased afterload or a decreased preload as in you have less blood remaining back and you have, you have more blood remaining back, sort of and less blood going around the body. And then you have in cyst in Asyst. So in II wrote Asystole, but it's just systole. So blood not cleared during systole when the ventricles contract now because they're not strong enough to contract, they don't clear all the blood. And that can happen sometimes because you have an increased chamber size or a lot of lots of reasons. But then again, that just that can happen again where because blood's not cleared, it stays back. Ventricles will not contract or they just don't contract with enough force because the heart muscle is not working. Um and eventually you have a reduced ejection fraction, reduced stroke volume and reduced cardiac output. So I think what, what, what I'm trying to explain from all of this is that in cardiac failure, there's lots of reasons why the heart is not going to be ejecting enough blood to meet the body's needs. And next SBA patient in the Coronary care unit has covered with acute heart failure is deteriorating, severe congestion, peripheral tissues look pale. What's which of the following best describe his hemodynamic profile, right? Guys. Come on. Don't pick e now, literally there is no e just give it a go. Yeah. Try and pick any answer. You guys are doing pretty well. To be honest, there's a little competition though. Give it for few more seconds, right? We can end the po there. So many of you went for C and D but then majority were C which is the correct answer. Um I'll explain it now. So in acute heart failure, you can have two things happening. So you can have congestion happening, congestion can happen in the pulmonary or systemic circulation. And what happens is because your left ventricle is unable to empty as we established earlier, you get backflow of blood, you get an increased hydrostatic pressure in your pulmonary vessels. Because so if, if blood cannot leave through the aorta, it's going to try and leave through the pulmonary vein. If it tries to leave through the pulmonary vein, it's gonna end up in the lungs if it ends up in the lungs that causes pulmonary edema. And just that's what you call congestion. So these patients tend to be wet because they have, they have fluid in their lungs um in hyperperfusion because you have reduced cardiac output because well, your ventricles are not shooting blood. You have reduced perfusion of organs and peripheral blo blood vessels because they're at the end, there's not enough blood to go to them, blood's gonna try and you know, stay and go inside the main organs. So then what happens? These patients become pale and unperfused and they're considered cold because they don't have enough blood. So, in our previous patient, she was congested. So she was wet and she was pale. So she's cold. If you, if they're not congested, they don't have pulmonary edema, they don't have pitting edema, then they tend to be dry. And if they're warm as in, they're perfused or you can see that they're not pale, then they tend to be warm. You asked to take a history from Mr John. A patient was presented into A&E a few days ago with an episode of acute heart failure, taking the history established that he has high BP and diabetes. He's had a heart attack a few years ago and he has had surgery for atrial septal defect when he was eight months old. He's currently taking a bunch of medications which of the following is not considered to be a cause of his heart failure. So he has BP. He's had an M I, he's got diabetes. He's had a heart attack, he has atrial septal defect. You know, he could have pericarditis. You never know he's taking a bunch of medications. But what is not considered a cause of heart failure of his heart failure? Mister, did I put his name, Mister John. Yeah. Can I give it 10 more seconds. OK, we can end the ball there. So majority of you went for D um which you know, I understand why you'd think that because he had it when he was really young. Like how would that cause heart failure? But the actual answer is c one, that's the answer because I didn't mention anywhere in the question that he has pericarditis that that can't be the cause of his heart failure. So in this question, I think it was more just about reading the stem um and seeing that he doesn't have pericarditis, but all of them are causes of heart failure. Um Yeah, trick question. Uh Anyways, I wait to remember causes of heart failure is this pneumonic hi vis. So hypertension, one of the most common causes of heart failure, think of it, hypertension is just bad. It causes all the bad things. So, yeah, infection, immune problems. So people who have viral infections, bacterial infections such as carditis, infective endocarditis or autoimmune conditions like sle are more like a more prone to getting heart failure because anything that damages the heart can cause heart well can eventually lead to heart failure. So genetic stuff, you have your ho or your d uh your dilated cardiomyopathies, then your heart attack. So, ischemic heart diseases, uh previous Mr S all of that volume overload. So anything that's causing fluid blood backlog, whatever renal failure, nephrotic syndrome, hepatic failure. So any organ sort of organ failure infiltrate. So, sarcoidosis, amyloidosis hemochromatosis, and these can also cause like restrictive cardiomyopathies. Um then you have structural problems. So your valvular heart disease or your septal defects or ventricular septal defects or a atrial septal defects. But basically anything that can possibly affect the heart can be a cause of heart failure. And next SB 43 female come to the clinic, recent diagnosis of heart failure. Consultant, cardiologist measures her ejection fraction. Turns out to be 45%. How would her heart failure be classified according to her left ventricular ejection fraction? Mm, quick answers. I like this. Continue, continue guys with the quick, the quicker you answer the polls, the quicker we get through this very, very long thing. Oh While the polls going, someone's asked me if he was already treated for his ASD, why is that still a risk factor? So even when you treat, when you treat something for someone, it never goes back to being new. That's my logic. I'm, I'm not giving you a re a particular reason as to why? That's the answer. But what I'm thinking is if someone's already had a defect, they have probably gone undergone surgery for their heart that already puts them at a higher risk of getting heart conditions because you've made the heart undergo surgery. Um, again with ASD entirely, it'll depend how it was treated, whether it completely closed, whether it wasn't, there wasn't that much detail in the um in the stem. I think it was just sort of identifying that it still is a risk factor if you've had these conditions before. Because even with hypertension, he could be on Ramipril and his hypertension and he could, his BP could be 123/70 which is like the same BP as me. But then because he has hypertension, still a risk factor anyways. Uh And the pies majority of you went for C which is the correct answer. Oh, sorry. Um So it's heart failure, cardiac failure can be um categorized as, and that's just the definition of cardiac failure. But anyways, you can either have diastolic heart failure. Oh yeah. So diastolic heart failure, you're not relaxing enough or systolic heart failure where you're um not contracting enough. And then you have this mid a gray area between the two. That's the new, it's newly quite. So I don't know if you guys have learned about it or not. But um yeah. So in diastolic heart failure, you have heart failure with preserved ejection fraction. So because they're not, if the problem is not really the contracting, they can still eject blood, they're just not filling up enough. It's greater than 50. Then systolic heart failure, heart failure with reduced ejection fraction. So they're not contracting enough. So it's less than 40 then between 5040. So 4149 you have this midrange ejection fraction. So here's the previous question was 45. Um So systolic heart failure, we're gonna talk about the main two. Anyways, systolic heart failure, what happens? You have weak contraction, reduced ejection fraction. You can't overcome afterload resistance um because you're not, you're not contracting all of it. So you've got this resistance going on because you're trying to, but you can't and you have reduced blood flow and perfusion. This can be caused by a number of causes. But again, heart failure can be caused by a number of things. Anyways mo more in this one, more or less, these are like mainly what you would see like someone who has ischemic heart disease. Previous Mr S, they tend to have reduced ejection fraction. They tend to have systolic heart failure, people who have hypertension, diabetes, renal disease. But on ultrasound, when you do an echo, you will see dilated ventricles, thin walls, reduced contractile force. So you will actually see that the heart is not very strongly and that's an indication that it's systolic heart failure. You have diastolic heart failure. This is more progressive. It's usually age related. You get stiffening of the ventricles, reduced elasticity and compliance. So they're stretching but they might not come back or they're not coming back and basically not relaxing enough, like stretching, not relaxing enough to allow filling of blood. Um What happens? You have reduced filling. Um You can have backlog of blood. Um I don't know why I put that there but I mean, I guess, yeah, in both of them, you can have backlog of blood and pulmonary edema. But anyways, this can also be caused by ischemic heart disease. I would say I just put these there, but they're not something that you particularly need to like, what are the causes of diastolic heart failure need to know um, important again what you see on ultrasound. So you'll see a normal sized heart and they'll have thick and stiff walls. That's why you have the reduced elasticity and compliance. Then you have an increased filling pressure. However, your contractile force is normal. So it's not reduced because they can still contract. They're just not filling. Well, seven year old male history of progressive shortness of breath exertion over a period of four months. No chest pain has a medical history of diabetes which we, which is controlled and hypertension for which she takes amLODIPine 10 mg. She reports feeling breathless when lying in bed. She has or apnea and on examination, she has mild hepatomegaly and crackles can be heard when auscultating the lungs. What important blood test should the GP request next? Just try guys. Just pick anything. She's got a bunch of symptoms and oh, it's not 70 year old. It's 70 year old. So sorry. It's definitely not a child. My bad. I'll fix that before posting the side. There's a lot of spelling mistakes that I didn't notice. Sorry. But um, you get the gist of the question, we can end up all there. So majority of you have gone for C which is the correct answer. So this obviously she is coming in with a lot of symptoms of heart failure. She has a lot of risk factors. As we said, hypertension, diabetes, shortness of breath is progressive, probably has some pulmonary edema. Um She has orthopnea, she has crackles. So you're gonna request A B type just to see if she has heart failure. So in skating or diagnosing heart failure, so if someone's gonna come in, first thing is obviously a clinical suspicion through history and exam. So your history and examination, very important. You'd probably do a cardiovascular slash respiratory examination, check their legs for any pitting edema. Um blah, blah, blah, then blood test, you do all your bloods. Normally, I think even in GP they request full blood count, use the these, you know, want to check the, the electrolytes, whatever, but you'd also add on an anti pro BNP uh B type peptide thing which is first line and normally someone who has a value of greater than 2000 is considered high, high risk for having heart failure. Normal values are less than um 400. So it's quite a big difference. Then you can do your TTE just your echocardiography. That's just going to tell us whether they're in systolic heart failure, diastolic heart failure is gonna show us what how their heart is functioning. And then we'll do a 12 lead ECG. There are some things you can look for on an ECG. So you like, you can see people mole p mitrale, which can be a sign of hypertrophy and can be a sign of heart failure. And then chest X ray, there are some signs that we can see on chest X ray that indicate heart failure, which I'll talk about and you can do a cardiac MRI which is kind of, you know, now it's used a lot more actually to see what the heart's looking like. Then symptoms of symptoms and signs again, remember symptoms of what the patient is experiencing signs, what you will see on examination. So they're gonna have breathlessness, orthopnea, paroxysmal wheeze chest pain, fatigue, nocturia, anorexia. Uh some of them can be vague, but some of them are very common. Then signs when you do examination, raise JVP wheeze tachypnea S3 rhythm, I say S3 can be physiological, it's normal sometimes in Children. But this one, you know, in someone who's expecting heart failure here and S3 is giving ascites cyanosis, palpitations, tachycardia, rapid weak pulse, pulmonary edema. So the ones with one star are more likely to be seen in right-sided heart failure. The ones in two with two stars are more likely to be seen in left sided heart failure. But um but yeah, sometimes you can get mix of both. Um Sometimes you can get some symptoms, not all it's just identifying that some of them were doing clinical examination. 78 year old woman is admitted to a ward following a three day history of shortness of breath productive cough and white frothy sputum auscultation, bi basal crackles patient is presenting with congest congestive cardiac failure. Again, remember the symptoms, shortness of breath, cough, crackles, giving heart failure, chest X ray, which of the following signs is typically not seen on a chest X ray. You will not be asked negative questions, but I just put that there. Yeah. Yeah. Try and just try and give it a go pick an answer. I might be going too fast. I'm sorry, I just have too many slides. So B BNP, someone's asking what is BNP? So B NPI think what when cardiac muscle is broken down. So when you have ischemia or when uh how do I explain this? Yeah. So when muscle is not, when, when you have ischemia, that muscle is not receiving blood supply. So it breaks down, it dies when it does, it releases B and P. So when someone's having heart failure, they basically the heart's failing. It's not working well. The mu muscle is sort of dying. It's sort of bad. It releases a lot of B and P. That's why the levels are high. That's my, that's what I think. But I will have to confirm that. Um And I'll have a look later, but we need to finish this presentation. That's why it's B NPA. And P is probably a sign of something else. I think it's just a fact. BNP heart failure. But anyways, majority of you have picked the right answer, we can end the po there. Um So it is low lo diversion. So in heart failure, when you look at chest X ray, there's a lot to look at and you guys need to learn how to interpret chest X rays actually because probably will be part of your ische maybe sometimes. Um Anyways, so ABCDE is a good way to remember a alveolar edema, alveolar edema. You'll just see like they look whiter and thicker. You can tell they have fluid in them because air is black, curly bee lines. Now, every time they're like, oh curly bee lines, but no one actually tells you what they are. But curly bee lines are these horizontal lines that go all the way to the end of the thing. And I'm not too sure what they're a sign of but, but I think when you have pulmonary edema, the lung tissue, you guys have done anatomy. So what happens is it's kind of soaks up that fluid sort of thing and becomes spongy. So a sign of the lungs being spongy is clearly b that's like the nicest way I can explain it. But then what you look for in the X ray is, I wish I could draw, I can't see the annotate button. But um oh no, wait, come back sorry, that one came back. But anyways, it's these horizontal lines that go all the way to the end, those are curly bee lines, then you have cardiomegaly. So just a big heart dilated upper lobe vessels. The reason why it's upper lobe vessels are dilated is because think of it as you have your ventilation perfusion situation uh because they have fluid at the bottom. They, when, when they try and perfuse there because there's no air going there. Technically, those vessels are not gonna, they're not gonna go there. So it's gonna shunt away from there and go up. That's why you have the upper lobes um dilated because there's more ventilation going on on the top of the lung because the fluid sits on the bottom. So then the vessels become bigger to allow more perfusion as well and more oxygenation and then pleural effusion. So this is not very good arrow but pleural effusion normally is this side is better. You don't see a good costophrenic angle. So if you see a costophrenic angle, then it's probably not pleural effusion. But if this is gone, it's probably a pleural effusion. Next question. So GP placement, you accompany the GP to do a home visit for a patient named Bet, diagnosed with heart failure. Recently, bedbound symptoms of heart failure at rest. As soon as he tries to move, he strikes in discomfort. GP decides to test your knowledge and asks you how would his heart failure be classified according to the New York Heart Association criteria. Just give it a go guys. It's honestly, it's one of them. All right, we can end the poll there. So majority of you have picked the correct answer which is four. so New York Heart Association classes of heart failure, class 1234 plus one. I think of that. I think of it as us. So you have no limitation of physical activity. You can do everything you older physical activity doesn't cause you fatigue palpitation or dyspnea like you're, you're ok. Class two, you get slight limitation, you're comfortable at rest and ordinary physical activity causes some fatigue palpitations or dyspnea. So ordinary physical activity would be like going one flight of stairs or like um cooking or something. Class three, you have marked limitation, you're still comfortable at rest, but then less than ordinary activity causes fatigue palpitations or dyspnea. So like wearing clothes, I mean, that is ordinary but like it's just something that you wouldn't really think would cause you fatigue or palpitations, um, or like standing up or sitting down or something like that. Class four is the worst one. So there are no, it's not five classes, it's only four and this one, you're unable to carry out any physical activity, you're basically bed bound, you get symptoms of heart failure at rest and if you do anything you feel very uncomfortable. Um So Matthew Denbigh has recently been diagnosed with heart failure, describing his new drug regimen to his family, offering to support him. He tells them of a drug which has which the doctor said it improves his ejection fraction by increasing the vagal stimulation of his AVN. Thus increasing the amount of calcium ions in the cardiomyocytes causing increased inotropy. I know that's a lot of words, but that's the moa of that drug. He's unable to remember the name, his daughter list them to you. The medical student who is listening to this conversation. Now, which of the following drugs is matty describing. Just give it a guess if you don't know, it's fine. Um You don't have to know the m of all drugs usually just the common ones. But then yeah, it's just just try and guess. So what this one does increases vagal stimulation of the atrial ventricular node. Um the AVN will allow more calcium in the ca ca the cardiomyocytes. So increase inotropy because you have more calcium. That means you can contract quicker and a lot more. So it increases contraction. Basically, we can end up all there. Majority of you got it right anyways, it is the second. Um So it's digoxin. Now, in acute management of acute heart failure will vary depending on which health board you're in. But then this is the general rule you try and give patients an ace inhibitor and a beta blocker. Now, there are new drugs such as Sacubitril, Valsartan, which is a combination of an ace inhibitor and an ab sacubitril being the ace Valsartan being the A B that you can give it a very good drug. Um Then you have bisoprolol or carvedilol, your beta blockers, then you have spironolactone, which is your aldosterone antagonist or potassium sparing diuretic. Then you have your SGLT two inhibitors, which previously, I mean, it's used as a diabetic drug, but then it's shown a lot of positive cardiovascular benefits. So it's used in acute heart failure like dapagliflozin. These however, are not the only drugs and these are not like think I'm not saying like these must be given to every patient. I think the basic concept is just knowing new heart failure diagnosis. Ace inhibitor beta blocker. Think about the others depending on how the patient's presenting. We will go through all the drugs though. Another Ace B before that 64 year old man presents to his GP worsening chest pain on exertion, increased use of his GTN medications. Atenolol, aspirin, simvastatin. What medication should be added to this patient's treatment? I'm gonna be nice and give you the um M so Atenolol is a beta blocker. Aspirin is an antiplatelet and simvastatin is a statin. So what else do you think we should give him? Mm Variety variety. II forgot the answer myself, but it's fine. Just, just give it a go. It's fine if, if it's worsening pain, remember it's worsening pain on exertion as well. Gonna give you 10 more seconds guys. Oh, I'm, I'm so sorry, Jamie. I think I'm gonna take up a bit more of your time. But, ok, can we end up all there? So majority of you have gone for D, which is not the correct answer, unfortunately. So it was either E or D. So A and D are both calcium channel blockers, but one of them. So, amLODIPine is a dihydro calcium channel blocker and if someone is, has worsening chest pain and they're already on a beta blocker, you can give them a dihydro a calcium channel blocker to help you don't give verapamil because it's a non hydrodine. Um And if you wanna look up the difference, please do so. 52 year old female is still in the heart failure clinic. She has a history of worsening, exertional dyspnea, leg swelling orthopnea over the last few months, an echo demonstrated heart failure, mid-range ejection fractions of 48% with no significant valve abnormalities. She's asymptomatic at rest, clear lungs and auscultation. Medical history includes hypertension which is already managed with Enalapril. What medications should be added to manage this patient? Think of what this patient has. She's seen in the heart failure clinic. It's getting worse. So she has worsening heart failure. She's symp, she's now asymptomatic, but then she only has one drug. She has an ace inhibitor. She's on an ace inhibitor. So what else do we want to give her? Um She, she has clear lungs. She doesn't have any edema. Um But yeah, she has some leg swelling. But yeah, uh we can end up all there. So there's a split between B and A. But the correct answer is bi know you guys are thinking leg swelling, pitting edema. You want to give her a diuretic, but that would be furosemide if they were thinking of giving her a diuretic. Um general rule, acute heart failure, think of giving a beta blocker alongside an ace inhibitor for um heart failure. So it's carvedilol, then you have so drugs. So you have your diuretics, you have your loop diuretics. Furosemide is mostly used. You'll hear that a lot. Um What it, what it acts on the loop of Henley. I'm not gonna talk about the ma because the case, if you want to learn the ma of these drugs in detail, I would recommend doing the case 12 watching the case 12 revision session, but this is just the S B1. So it's quicker. But leena what happens is what, what's it's it's indicated for cardiac failure with associated edema. So, pitting edema, as you the leg swelling, whatever what the side effects are, hypokalemia and tinnitus. So they're autotoxic drugs, thiazide diuretics or thiazide like diuretics. So you have bendroflumethiazide and indapamide. Commonly used indapamide is used also in the of hypertension. They act on the early distal tubule. This can cause hypokalemia, hypercalcemia and gout gout is actually very common with thiazide diuretics. So if the question in PT someone has gout and you see a thiazide in the options, probably that one aldosterone anti antagonist. So spironolactone is mostly used but you have others. Obviously, it's a potassium sparing diuretic, it outcompete aldosterone. Um this can cause hyperkalemia and gynecomastia. Very common, very common PT question. Um then you have your ace inhibitors. So this is first time therapy in cardiac failure with systolic dysfunction, ramipril, Lisinopril, enalapril, anything pril side effects common ones, dry cough, angioedema, which is like lip swelling or you'll just see tongue swelling or something like that. Then you have your angiotensin two receptor blockers. This I put the MRI there, you can read it but then it just stops the um it causes vasodilation and reduced BP and kind of all of that. Uh So these are your Satin Losartan anything tan beta blockers. So they inhibit beta one adrenoreceptor. Again, the ones that work on the heart are beta one Adreno receptors. The one that works on the lung are beta two. Remember two lungs, one heart, um they cause a lot of effects eventually reducing cardiac output. So they basically make the heart relax a little bit, they help the heart a little bit. But these are your all your metoprolol, carvedilol, metoprolol, blah, blah, blah, blah. Um Yeah, then you have your specialist drug. So you have your digoxin. We talked about the M OA. It's an unclear mechanism, but it probably affects the avian node. It's, you previously was used first line in heart failure. But now it's only used for elderly sedentary people. Patients who the other drugs haven't worked, you know, on you. They, they're very toxic drugs. They can cause someone to have digoxin toxicity, which presents with a lot of symptoms. As I put there. Then you have your dual neurohormonal inhibition. This is what I was talking. Combination of ace and AB which increases BNP. Oh, there we go. Someone was asking about the BNP um MA but normally they Nero an enzyme breaks down BNP, they inhibit that and then that causes increase in BNP level which I guess shows that it's a sign of heart failure. But I don't know anyways um then you have your SGLT two inhibitor. So this is used as a diabetic drug. It works on the SGLT two channel. So in the kidneys and what happens is you have increased diuresis but you also have vasodilation and it has cardioprotective features which is why it's using heart failure. Then you have others. So you have ivabradine can be used if someone has a very low ejection fraction, you have vasodilators. So your hydrALAZINE, your nitrate again, they help in congestion and then you can have resynchronization therapy. 60 year old male, increasing shortness of breath on exertion. Third, heart sound is heard. Respiratory examination is unremarkable. What is most consistent with this finding? Oh yeah. Right. This person just has shortness of breath on exertion and the third heart sound. I'm just gonna do 30 seconds on questions. Sorry, I'm going a bit fast. I know it's a odd topic. But um, so someone asked me if the second line treatment for chronic heart failure would be spiral rather than furosemide after ace and beta blocker. He, I mean, I'm not gonna say yes or no to that. It depends on the patient. So furosemide is used for symptomatic control. So if the patient comes in with lots of leg swelling and you maybe they have heart failure, depending on the patient, you could give them spironolactone, but that might not help that much with the leg swelling. Whereas furosemide will probably help a lot more. But then um because they have heart failure, spirolactone is probably better. So it's patient dependent. I'm not, I'm gonna say. So you'd have to look at the stem of the question and pick your answer based on that. So majority of you have picked a, we can end up both there um is the correct answer. So you have your non ischemic cardiomyopathies, we have your outcome. This is the leading cause of death. So in sudden young, well, in young people, sudden death, like someone is just running, then they fall down, then they die or like athletes, they're just running marathon, then they, they just die. It's probably have, they probably have, how come they usually have no symptoms. Sometimes they can have angina dyspnea, etc, it is ultrasal dominance. So, if your dad had it or someone's dad had it, then they would probably test for that genetically on an ECG, you can usually see some things. So an S wave and V two R wave and V five, which add up to 35. So normally you're just gonna see really long lines on the ECG touching each other everywhere. That's probably your S wave and your R wave. And because they're long, they're greater than 35 millimeters, they're touching each other. That's a sign that it is probably. How come you can also do an echo to check wall thickness, valve dysfunction or tissue fibrosis. Um But yeah, in this, if they bring this in a question, it's probably gonna be like young athletes suddenly died. What do they have now? Dilated cardiomyopathy. You have cardiac enlargement which causes reduced systolic function, but they don't really have any significant coronary disease. They just have a large heart. Um This can be caused by many things. So, idiopathic genetic infective c then it's restrictive. So you have a normal cardiac size, but then you have a reduced systolic and diastolic function and this can be because of infiltration. So you have stuff that's in the heart, infiltrate the heart, restricting it from working properly. So, amyloidosis, sarcoidosis. So, deposition of amyloid or hemochromatosis, deposition of iron on the heart. You can do an ultrasound and ECG you get really small curs complexes in all leads in most leads. Then arrhythmogenic right ventricular cardiomyopathy. So your ARVC, this is usually rare. It usually affects the right ventricle. You get this one, you also get infiltration, but you also get ventricular dilatation. Whereas in the other one, you get normal sized heart, remember and you get hypertrabeculation, you can see that on an echo as it shows here, like look that does not look normal to me. So its right ventricle is large, hypertropic regulation and dilatation. ACG you can get some T wave inversion or something called an epsilon wave, which is basically a little M after the QR S complex um is pointed here which you can have a look later. Uh 65 year old woman into palpitations, regular narrow complex tachycardia, heart rate of 178 despite the administration of 6 mg of adenosine via rapid IV bolus her symptoms persist vital signs, uh heart rate, 174 respiratory rate, 28 BP, 8664. What's the most appropriate next step in management? So this person is very, very tachycardic. They haven't, they have a regular narrow complex tachycardia, probably an SVT, you've treated them with adenosine, but they, they still have symptoms and symptoms are not looking good. I'm gonna end the pulse soon for two seconds. Just give it a go guys. It's fine if you don't get this right. That's the point of this whole presentation to teach you guys um we can end up all there. So most of you pick D which is the correct answer. I actually got this wrong. So well done guys. Um The reason why it's D is because she is. So if obviously you need to look at your tachyarrhythmias and Brady arrhythmias treatment um algorithms. So to giving 6 mg adenosine, if she was hemodynamically stable, we'd continue giving her 12 mg, adenosine still not working. She's hemodynamically stable 18 mg, but then she's hemodynamically unstable. And we know that because her BP is less than 90 it's very low. So we will do synchronized DC cardioversion, right. So bradyarrhythmias where you have a heart rate of less than 60 you can either have a narrow QR S on ECG or a wide QR S narrow CRS, you can either have just regular bradycardia or you can have a V node block. So your first degree heart block, very slow, narrow CRS skiing heart block. Um then you have a wide cure. If you have a wide C think of bundle branch block with um a brady arrhythmia, then you have your tachyarrhythmias. So your heart rate is over 100. You can either have a narrow CRS again or a wide C. You'd have to check the ECG for that. If they have a regular rhythm with a narrow QR S and a tachyarrhythmia, they're probably just tachycardic, everything's regular. Remember it's just narrow, it's just going quick or they have an S VT, if they have an irregular rhythm, it's narrow, they're tachycardic. You could have, if it's regularly irregular, it's an atrial flutter. If it's irregularly irregular, it's afib, I don't like this as much because atrial fibrillation, you can also have slow af, so you can have Brady, you can have a narrow Q RSA bradyarrhythmia irregularly irregular. That's still af, it's not on, it's not, it's not really on the table thing, but I think it's worth remembering with af you can either have a tachyarrhythmia or an or a bradyarrhythmia. Um but it's irregularly irregular always, then you have a wide CRS so tachyarrhythmia wide C they're probably in VFIB or they're probably in ventricular tachycardia. But um all of this is, you know, based on ECG, I think it's just worth remembering that there are so many things that can cause change in rate and rhythm. That's kind of the point of these slides, but you don't have to like cram this. So uh next question, 64 year old man brought into Ed after being involved in a road traffic accident, he denies any recent illness takes no regular medication. He's breathless. Has a visibly raised JVP, heart sounds are muffled on auscultation, hypertensive tachycardic bedside ECG is performed, confirms the likely diagnosis. What's the ECG finding? Which ECG findings are you most likely to see, try and find the diagnosis best, then try and find what you can see on ECG um someone asked me what's, what's considered hemodynamically unstable and stable? I would say when someone is unable to perfuse themselves, I can, the, the BP is way too low. That's one of them. Maybe they're really, that's, I think BP is the biggest indicator of whether someone is hemodynamically stable or unstable. But again, thinking about gcs and all of those others, um you can tell whether someone is stable or not, there's a variety of answers, but majority of you have gone for D which is not the correct answer. Unfortunately. Sorry. Can we end the pool there? Yeah. Ok. Uh So the answer is b so this person has a raised JVP um muffled heart sounds. They're tachycardic and breathless and hypertensive and that's a triad. If someone can, can someone put in the chat, what triad? This is they? No Bex triad. Yeah, exactly. So Bex triad is a sign of cardiac tamponade and uh you will see electrical alternans in on a cardiac tamponade E CG. Next question. 62 year old man with a history of type two diabetes, mellitus, heavy feeling in his chest for the past two hours. Ecgs taken. What's the most likely diagnosis? Right? Look at the ECG, the the last few slides are just a few ECG S that I'll rush through because of time. But um yeah, can we and the pool there? So majority have gone for E which is correct. It's an inferior myocardial infarction and that's because we can see ST elevation in leads 23 and aVF. Um Yeah, very simple. Oh, another question that six year old man presented to Ed with chest pain started around two hours ago. Described as severe pain is central. No radiation, not worse on inspiration, smokes 10 a day fit and well dad had an mi age 61 cardio exam, unremarkable BP 1 36 84 P 96 respiratory rate, 14 S are 98. I'm gonna tell you all of that's normal. What can you see on the ECG? Mhm. Um OK. We gonna give you 10 more seconds quickly. We can end up all there. So majority have gone for B but that's not the correct answer. So with, with an anterior Mr you would get ST elevation in V two to V four. But then first of all, according to the history, it's not really, it's a central chest pain with an MRI. It's more likely to go to the left blah, blah, blah. But that, that also doesn't explain why we have some ST elevation in leads, 12 in the other leads. So it wouldn't be a plain anterior M I but in acute pericarditis, you have widespread ST elevation. So you have ST elevation across all the lead. Well, most of the leads, which is what we can see here. And then again, it's, it's just, yeah, this question is not that great because it doesn't, it doesn't say, you know, the classic pericarditis or he feels better when he's leaning forward. But um it's just thinking about the ECG, right ECG. So when you do, when you're given an ECG on an exam, you have to check the name, date of birth date. Calibration. Calibration is just saying paper speed is 25 millimeters per second. Voltage is 10 millimeters. The rate is very important. Yeah. Are they tachycardic? Are they bradycardic? Is it normal? You calculate the heart rate? I've put two ways to calculate the heart rate there. Just read it in your own time, rhythm, sinus rhythm, non sinus rhythm. Is it regular rhythm, irregular rhythm, axis, not important, but you can check that and then morphology, you know, checking your intervals, your ps your QR S your T waves, your segments again, I'm sure you guys know this but then ST elevation in 23 aVF uh correlates to your RC which is your in uh inferior M I. Then you have one aVL V five V six which is your second flex or your lateral M I um then you have V one to V four, which is your L or your anterior M I. Now, atrial fibrillation, irregularly irregular pulse absent P waves. What do you do think about rate control? People with AF tend to be tachycardic. Most of them are tachycardic. So you want to control their rate with a beta blocker. Use mostly use bisoprolol or you can give them calcium channel blocker. Let's say they're asthmatic. Didn't work. Rhythm control. Amiodarone flacon, if the hemodynamically unstable DC cardioversion, so irregularly irregular, no P waves, atrial flutter, you get so too flatter waves, you get a narrow QR S, as we said, just look at these and then you think about rate and rhythm control just like af then you have your SVT S. So this one, you get a narrow QR S um you get hit in P waves. I mean, sometimes you can see them, sometimes you can't, but then it's irregular, it's regular and it's tachycardic and it's just narrow QR S that's very important. Then you treat with valsalva maneuver which is first line or carotid sinus massage, then you can give them adenosine. Then you, you can do radiofrequency ablation. If they don't work. Obviously, then you have your ventricular tachycardia. So the worst one is Torsades de pointe, which is polymorphic, ventricular tachycardia. Polymorphic just means like looking different in all in looking very different. Um You treat that with magnesium sulfur, the ECG kind of looks like that. Um B broad, complex tachycardia. So broad, complex, broad, you have a broad QR S and this one is a monomorphic VT. It means it looks the sort of the same in like a specific lead. But you have a wide QR S, you do see cardio patients who are unstable if they're stable, you can consider giving them antiarrhythmic drugs. Then you have a ventricular fibrillation. So this is when they're in the, in it's, it's an emergency. They, it's chaotic. You can't identify P waves, you can't see anything. It's just like squiggles, you just shock the patient continue. CPR This is when you think about your uh BLS Wolf Parkinson White syndrome. So this one is usually an accessory pathway, you know, normally you have your sa node, node, blah blah blah Parkin fibers. It you know, normal, normal thing. But then this one is just a new pathway that connects the atrial and ventricles making its own little things waves. So you get delta wave on ecg, delta wave is like a sled up stroke. So you should see that and then you can give antiarrhythmic drugs or consider ablation of the pathway stemi ST elevation in your different leads. We've spoken about this earlier, they get chest pain, whatever they can. You can also important to notice you can get reciprocal ST depression in opposite leads. So if someone's having an anterior Mr, you might see ST elevation in leads uh V one to V four, but you might see ST depression in 23 aVF. Yeah. So NSTEMI T wave inversion and you get ST depression, the ECG may be normal. Their troponin levels might be very high and they get symptoms, they can be asymptomatic, but usually most of the times they, they have symptoms, I've put the management of stemi and Antemi from my, this is from past med. I don't know if you guys have past med, but it's really good summary and just go through it uh in your own time. Then you have bundle branch block. Oh Sorry. Um You have QR S uh so you have a wide QR S as we mentioned earlier and you get this William Morrow thing, you don't really see it everywhere. I think the best way to, for me to remember whether it's, it's like, so this is your ECG, you rotate it 90. If the lines are facing the left, it's probably a left bundle branch block. If the lines are facing the right, it's a right bundle branch block. So ECG clockwise 90 and it's, it, you know, the lines are very long. So you, when you turn it, they're gonna be facing one side. That's just a quick way of remembering. But yeah, you can look for William Morrow as well. Sometimes you see it first degree heart block. It's a regular sinus rhythm. You get an increased pr interval. So they, they're asymptomatic. They, it's usually in athletes and you don't treat it. So it's just an increased pr but you can, you have PQ RST, you have everything for second degree heart block. You have two types, type one and type two in type one, you have an increasing pr interval. So it's like this then like this, then like this, then like this. In type two, it's fixed. But in the difference between Mobitz type two and first degree heart block is in Mobitz type two, you will have dropped QR S complexes in first degree heart block. Even though it's a fixed pr it's elongated, it's like increased pr interval. That's the same size. You don't have dropped QR S complexes. Third degree is complete heart block. So you have a very, it's a brady arrhythmia. Less than 40 literally no association between your atri your atriums and your ventricles. You can give atropine pacemaker. Yeah, pericarditis. We've talked about this. You get widespread ST elevation, think of nsaids and colchicine to treat it cardiac tamponade. So bex tried hypertension, raise JVP. You get electrical alter nos and that you treat it with pericardiocentesis. Electrical altern. Nos are basically oh long cures, short cures, long cures. And that's just because of the way the heart is depolarizing and repolarise. But because you have infection, it's going a bit all over the place. Um ECG diagrams, the ones with labels, all of them have come from Doctor Coffey's E learning. I strongly recommend you do that if you want to learn ECG S. But um yeah, two more questions and we're done patient with an increased risk of thromboembolic events is intolerant to warfarin. They are then started on a DOAC which inhibits thrombin s ability to convert fibrinogen into fibrin. Which one of the following drugs has this Mr Oh sorry, send the wrong message. Uh Can we end up all there? Um So all of you have picked the last one, which is the correct answer, put the explanation down, you can look at it last question and we're done. 70 year old man normally fit and well attends GP for annual health review. He's found to have a new diagnosis of AF on his ECG. What which of the following is a tool to determine the risk of ischemic stroke in patients with af sorry, I rushed you guys so much for the ECG S and on, I've put, I've put notes and I've put like um the ECG S are very self explanatory. So if you guys go through the slides later, you should be able to learn a lot more just in the interest of time. Um So we can end up all there. Majority of you have big B which is the correct answer. Well done. So just, just to just last thing, child's VSC is used to determine the risk of having a stroke or bit is to determine the risk of a patient bleeding after you've given them the anticoagulation, like how likely are they to bleed? So, two important ones to think of and thank you. That's all done. Sorry for going over time. F thank you for that. Si Think we can all agree that was um well needed revision on the topics that are quite high yield. Um Normally we would have a break but just in the interest of time, I think everyone would prefer if we just cracked on. So, Jamie, if I could ask you to share your screen. Um Yeah, I was just gonna say, should we give them a couple of minutes just in case they want to grab a drink or anything? Because that teaching was so useful. I'd imagine that I'd probably need a minute or two to decompress after how good that was. Yeah, we shall we come back by quarter past? Yeah, just if that's if people don't want that, put it in the chat and we'll roll straight through. But I also think it's good to take breaks. Yeah, three minutes is good. I'm so sorry. I think I overloaded them with information. It's such a big case. Um for people who don't know, case 12 used to be two separate cases a few years ago and then they combined it into one. Which is why so much. So that was fantastic. See, yeah, someone's just asked me is it has bled or orbit for bleeding after? So both of them were used before. Both of them are for bleeding after anticoagulation. Orbit's a new one. It's which is used more now. So has bloods going out of use basically. So for us, it's orbit basically. Yeah, I think I'll share my screen just so we're ready to start at quarter past. So can you guys see my shared screen. Yeah, we can see. So a couple more seconds then we'll start again. Ok, it's called, hello guys. My name is Jamie. Um, so I'm gonna be teaching you today on um, case 13 which is traumatic head injuries. Um, for those of you who are joining again from last night. Nice to see you all. Um, as you probably know, I'm quite a fast talker, um especially when I'm nervous. So if at any point I'm talking too fast, please just let me know. Um It's also really helpful. If you guys have any questions at all, please put them in the chat. It's a good chance for you guys to ask any questions you do have and also it does make the session a bit more engaging for me. Um So the topics I'm gonna cover today are anatomy stroke, meningitis, some brain injuries, imaging. And then lastly, I'll just go over a little bit of the airway. Um Please don't worry if you guys don't get questions right in this session. Um It's just a chance for you guys to try and pick up some extra um, points. And also just because I do think these topics are high yield, but just because I put them in, my thing doesn't mean they necessarily will come up in the S two. So please don't feel stressed at any point. Ok. So we'll start off with our first SBA. So a 58 year old female sends to A&E when you try to take a history, you find it impossible to understand her. For example, when you ask her name and address she applies with drive, speaks tough. You know, however that her speech is fluent, you suspect an area of her brain has been damaged and is causing this presentation. Where is the damaged area most likely to be located? If we could launch the pulse? That would be great. This one's quite a tricky question. So don't worry if you don't get it, just gonna set a timer on my phone. OK. F really good to see the answers coming in guys just like with yesterday. Pretty much everyone is getting it right. Which is so, so good to see you guys are experts. Um Keep going guys give you a few more seconds to get those answers coming in. Lovely stuff. Another 10 seconds. We can't see who votes for what? So don't worry about getting the answer wrong at all. Fab. Really good. OK. Fab, I think we'll end the poll there if that's OK. So well done guys. So most of you got this question right? So the answer to this one is the left temporal lobe, like I said, it's a bit of a mean question. So it's asking you to comprehend a lot of different key points of information. So the first thing you have to identify is that it's Brocker Aphasia. Um And you then have to know where Broca's aphasia is which is a temporal lobe. And then you also have to know that the majority of people um a left brain dominant and the BRCA area and Vernier's area only found in the dominant hemisphere of the brain are not found on both sides of the brain. So very quickly, we're just gonna go over the kind of main, well the lobes of the brain. So we've got the front our frontal lobe, this is responsible for motor movement, personality, decision making, and then also the speech production. Then we've got our temporal lobe, this is responsible for memory or fractions through smell, hearing and understanding like language. And at the very back, we have our occipital lobe which is responsible for vision. And then above our temporal lobe, we have our parietal lobe which is responsible for sensation calculation and two point discrimination. And what two point discrimination means is that essentially you can feel that if you touch something, you can feel it in two points, you can work out the edges of something that's what two point discrimination is. So going on to what I think is the kind of key areas of the brain. So within our lobes, we don't have these areas. So starting off just as a bit of an anatomical landmark, what divides our frontal lobe from our parietal lobe is our central sulcus in front of our central s sulcus. So anterior to it, we have our motor cortex, this is responsible for all the movement in our body posterior. So behind the central sulcus, we have our somatosensory cortex. This is responsible for our interpretation of sensation of the body. Then the two kind of the areas we were talking about earlier about speech production. So we have Broca's area, this sits at the bottom of our motor cortex. So it's within our frontal lobe. And the way I like to remember that it's in the frontal lobe is because it's below the motor cortex. Broca's area is responsible for speech production. So actually the um ability to talk and that's kind of something motory ish. And if you get damage to Broca's area, you can get something called Broca's aphasia, which is the question we saw Brock's aphasia causes broken speech. So you can remember it with Bro or Brocker br broken. So what this means is that a patient can understand you and they're able to give understandable answers, but their speech is just really um stilted and it's really an issue for them to get those words out. On the flip side, we have Wernicke's area. This is also involved in our language skill, but this time, it's for language comprehension. So our ability to understand language, this one is located within a temporal lobe. And if you get damaged with this, you can get Wernicke's aphasia. And the way I like to remember with Wernickes aphasia is, it's kind of like, what are they saying So they're speaking completely fluently. But the words that they are saying make absolutely no sense. If you ask them what time of day it is, they might reply with like dog, cat chicken, something like that, no relevance. And you can't understand it. And at the very back of the brain, we have our primary visual cortex. This is responsible for our um understanding of the um of our ability to process visual information. So going back to the answer for this question. Oh sorry, I've gone the wrong way because someone's asked me to very quickly. So um I think I said earlier in the answer that I it was Brocker aphasia. I'm really sorry. I meant it was Wernicke's aphasia which is located in our le left temporal lobe. Thank you for picking me up on that. I am really sorry. I meant it was Wernicke's aphasia. This is Wernicke's aphasia which is located in the left temporal lobe. I'm really sorry about that guys. Thank you for picking me up on it though. OK. Then another little bit of brain anatomy, we have our meninges. So the meninges consists of three layers. The outmost layer is our dura mater. It's tough, it's inflexible and it's got a thick layer of dense irregular connective tissue and it also has these folds within the brain. So the way that the gyrus comes together is it kind of sits around the brain and it also has these folds in it like this. And these are really important because they not only divide the brain in between its two hemispheres, they also create little channels for which we can um have what we'll come to talk on later. Our sinuses. So our ability for fluid to flow through the brain. So these dural folds are your falx cerebri, which separates your um two hemispheres of the um cortex. And then your, also your falx cerebelli which separates the cerebellum and then your tentorium cerebelli, which kind of separates the cortex from the brainstem. Below the gator, we have our arachnoid mater and below this, we have what's called our arachnoid um a subarachnoid space and this is a space for CSF to flow and coat that brain and keep it weightless. And then the very last layer we have of our meninges is the PTER. So this is just a very thin layer, which is highly vascularized, which basically just sits on top of the um on top of the brain. And the best way to remember this is with the acronym pad. One thing about me is that I really love an acronym. I think it's the best way to remember things. So you remember Pad Zia Arachnoid Jira? OK. So another SBA for you guys, a 73 year old male presents to A&E complaining of difficulty swallowing. The F one takes a full history. The patient has not experienced any limb weakness or spurred speech on examination the F one noticed that the patient has an absent gag reflex and that the uvula is deviating towards the left side. The F one suspects a cranial nerve has been damaged, which cranial nerve has been damaged. So fav really nice to see the answers coming in so quickly. Really good guys. Really nice. Keep them coming in and I am sorry about getting the Wernick and Brock on, she refused earlier. So if that makes you feel any more reassured about getting into third year, you guys will be able to do it. OK? Nice. Really good. This one is a really tricky question. So don't worry, you guys are doing great. OK? A few more seconds. Get those answers in. OK. Lovely. I think if we end the pole there, that would be great. OK. Fab so still the majority of you guys have got this one right, which is fantastic to see, but it is quite a tricky one. So the correct answer to this one is the right vagus. So I'm gonna go through in a second a bit more in detail of the cranial nerves. But I do have another question on cranial nerves. The reason this is the right vagus is that we've lost our gag reflex and we've got a deviated uvula. Those are the signs of a lesion to the vagus nerve. How you differentiate between right and left is which point the uvula uvula is deviating towards. So the uvula deviates towards the opposite side. So in this case, it's deviating towards the left. So it must be the right vagus. Ok. Um And just how you would tell it between the glossopharyngeal, which is also responsible for um, swallowing is that the glossopharyngeal, if you've got a lesion to that, you wouldn't have a uvula, you wouldn't have that uvular deviation. Ok. Fab. So we'll keep going. Um So 36 female potential to their GP with left sided facial drooping on taking a history. The GP finds out the patient has also been hearing noises louder than usual on examination. The patient is unable to move the left hand side of their face and there is no evidence of forehead sparing. What is the most likely diagnosis? Oh, fantastic guys. Really, really good to see. Wow, guys are so good. Really nice. Keep those questions coming in. Um I just got a question saying, would you say your S two was similar to these types of questions? Um Just keep your answers coming in. I would say that they tend to be a little bit longer and a bit worthier. Um In all honesty, I don't remember much of the Yes two. I've kind of blocked it out. Um But I would say they are similar. Yes, it will often be a clinical lead in with then a question like this. Ok. So we'll end the poll there if that's OK. Please keep your questions coming in guys. Any questions about anything whatsoever? Happy to answer them if I can. Ok, Fab. So you guys got the correct answer. Pretty much everyone. The correct answer to this one is Bell's palsy. So why is this one? The correct answer? Well, we've got that the patient is hearing, lo louder, louder than usual. And we've also got um facial paralysis. So this is pointing towards our cranial nerve seven. The next thing we need to work out is whether this is an upper motor neuron or lower motor neurine lesion for a cranial nerve seven. So the two main differentials for this one would be a Bell's palsy and a stroke. How you differentiate the two is whether there is forehead sparing. What that means is that someone's able to raise their eyebrows or not, if you can't raise your eyebrows, there's no forehead sparing. So Bell's palsy is a lower motor neuron injury to cranial N seven. Whereas a stroke would be an upper motor neuron injury to cranin F seven. The reason that you get this forehead sparing in a stroke is because as you can see in this diagram, the uh the um the sorry, the facial nerve has two branches, one which supplies the forehead and one which supplies, oh, sorry, it's got multiple branches. But the um the feeding for the top one has its own split as well. The one that supplies to the forehead gets upper motion, neurine innervation from both sides of the brain. So if you knock out the upper motor neuron on one side, the other u upper motor neuron is still able to compensate for it. So the forehead is still able to move up and down. On the other side, the lower motor neuron, it doesn't have this kind of um getting the ability from both sides of the brain. For the for the forehead. If you get a lesion in it, you cut all supply to it. So you don't get that forehead sparing because there's no extra supply to the forehead. I hope that makes sense. It's quite a complicated um explanation. It's quite hard for me to explain because I'm not, not the best at this. But basically, if you get forehead sparing and you can move the eyebrows, it's an upper motion neurone lesion of the cranial F seven. So it's a stroke. Otherwise, it, if you can't move your eyebrows, it's a low motion neurine lesion just quickly as to why the other ones were wrong. Multiple sclerosis. This is more for the PT not for us to multiple sclerosis is gonna present um with kind of diplopia. So um diplopia and also optic neuritis, that's gonna be pain on moving the eyes and it's also gonna present with motor and sensory um symptoms in the rest of the body, motor neuron disease. Um Again, we'll talk about this a bit later, only presents really with motor symptoms and it tends to affect more of the body. And myocytic gravis is your one that's gonna um present with kind of ptosis or drooping of the eyelid diplopia. And again, um will have more areas of sorry, less areas of the face affected, but more areas of the rest of the body affected. OK. Um So let's go on to this table. Please don't be scared by this. I remember finding so many resources on the cranial nerves and it was really hard to see them altogether. So I've created this table which hopefully covers everything you need to know about the cranial nerves. So I've got what the cranial nerve is and you want it to remember them also the exit, they leave the skull by this confused me, but essentially the cranial nerves originate from with inside the skull, but they act on things outside of the skull. So they need a way to get out of the skull and that's what they mean by their exit. I've then got their function and then also what happens if you get evidence of a lesion? I do have this slide repeated again at the end of my session, which I will talk through it properly for those of you who want to kind of stay maybe a bit longer. But in the interest of time, I'm just gonna talk through the important parts of this one first. But if you want to get a more in depth explanation, I will do it again at the end. OK. So first thing that I think is important to know is just a new monitor to try and help you remember the exits. So most of the exits match up to kind of where roughly where the cranial nerve is leaving. So the cranial nerves that are acting on the eye all leave through something that kind of sounds a bit like the eye. So maybe that's the optic come out or orbits, you know, you've got orbits in your eyes. Um So that's a way to remember that one. Then another tip is that all cranial nerves with a two in it. So cranial nerve two and cranial nerve 12 leave through the hypo, leave through something that's called with a canal in it. So that's either the optic canal or the hypoglossal canal. So canal will um if there is a two in it. And then the other thing that confused me is the trigeminal nerve has got three branches to it. V one supplies everything above the eyelid and into the scalp. V two supplies everything from the corner of your eye to the corner of your lip. And then V three does everything below the corner of your lip. And the way to remember the exit is that cranial nerve two, sorry branch, two of the trigeminal leads through the Foramen rotundum. So you can remember that with Foramen rotundum. So it sounds like it's got a two in it and then the cranial nerve three leaves through foramen ovale and then cranial nev one because it's going to supply the area above our eyes. It's gonna leave through something to do with the eyes. Another thing that I think is important to mention is a little bit about the kind of some tips on how to remember the deviation, sorry, the lesions. So cranial nerve 10 where I remember a bit about the uvula is cranial NV 10 is your vagus nerve that's got a V in it. So it's uvula. And then another tip for you guys is that in terms of working out which side of the hypoglossal nerve is damaged. Um So the hypoglossal nerve controls your tongue movements, whichever side, the tongue deviates towards is the affected side. And the way you can remember that is with the tongue never lies. So the tongue always tells the truth. OK. So like I said, I will go through these again um in a second um sorry at the end of the session, but just the interest of timer, we'll move on if that's OK with everyone. So got another question for you guys. A 67 year old female with atrial fibrillation presents to a with left sided facial weakness and slurred speech on examination. There is evidence of forehead sparing. The consultant orders A CT which confirms a diagnosis of an ischemic stroke. The consultant after initial management orders a CT angiogram as the patient is a candidate for thrombectomy. The CT angiogram shows the presence of clot in the left middle cerebral artery. What is the origin of the left middle cerebral artery? So, keep those questions coming in guys, really, really good and also um keep having, having a go at the answers. You're doing great. It'll help you learn and help you remember. Um So just quickly you've got another question. So Bell's palsy is a lower motor neuron in to cranial nerve seven and a stroke is an upper motor neurone lesion to cranial nerve seven. So, uh by that, a cranial nerve, an upper motion lesion, neurine lesion, sorry, will be anything within the brain itself. OK? I hope that answers your question. Yeah. Really good guys. Keep those questions coming in and answer. Sorry. Um I think we'll end the poll there if that's OK. Yeah. Again, pretty much everyone is getting this question right? Which is so good to see you guys are doing fantastic. So we'll talk about the circle of Willis in a second. But just an important thing for you guys to remember. The middle cerebral artery is the most common location for a clot. OK. So the circle of villous. So um I think it's really important with the circle of Willis to pick a starting point when you're drawing it out. So I always used to start with the internal carotid arteries. They come into the middle and they directly continue as the middle cerebral artery. And that is why you're most likely to get a clot in the middle cerebral artery because it's the direct continuation, there's no branches off it, it's just an easy flow. Um So then we get our middle cerebral artery which continues coming off our internal carotid artery. Also get our anterior cerebral artery which comes up here connecting our two anterior cerebral arteries is our um anterior communicating artery. Ok. Then I'd like to work backwards through the um so I've done the front half and now I'm gonna work through the back half. So connecting our middle cerebral artery to our posterior cerebral arteries is our middle, connecting arteries, the posterior cerebral arteries then kind of come together and they form the basilar artery. And just before they do that, they give off the superior cerebellar artery, then our basilar artery continues, it then branches into the anterior inferior cerebellar artery and then it branches into the posterior inferior cerebellar artery and then finally, the vertebral artery. So what this red line demarcates is the areas of the brain or the arteries which come from the internal carotids and the vertebral arteries. I'd say this is probably an important thing to learn from sycophilus because they quite like to ask questions about origins of arteries. You might have noticed that in case six, or in PT S, they ask origins of arteries quite a lot. So it's important to remember that anything above this line is the internal carotid artery and anything below this line is the vertebral artery. Ok. So, moving on, I hope that sounds to, to c for this, I think annoyingly, this is just one of the things that sometimes you just have to sit down and draw and you probably forget it um, when you come back to learn it again, but just try and remember and have an order that you always draw it out with. Ok. So talking a little bit about the areas of the brain that are supplied um er by the um different arteries. So sorry about my awful shading in but the anterior cerebral artery supplies the anterior medial portion of the brain. What that means is it supplies the front of the brain and then also the medial aspect of the brain and by medial they imagine they mean if you put a cut through the middle of your head and you have one half of your brain, the inside portion of it. Ok. So as you can see here where you can see the inside part of our brain, so it's supplying this whole region here. OK. Our middle cerebral artery supplies the majority of the lateral portion of the brain. So you can see here it's how it's applying the majority of the temporal lobe, parietal lobe and frontal lobe. OK. And then our finally, we've got a posterior cerebral artery which supplies to the posterior portion of the brain. So that's gonna be the majority of our posterior lobe and then also a tiny bit of the bottom of our temporal lobe. Now, it's really important to remember that our brain has, has um is mapped out to specific parts of the body. So what you see here is a cross section cut through the brain. And this is an example of what how the somatosensory cortex and the motor cortex. Those areas I was talking about earlier are specifically mapped to the part of the body. A way that you could remember this is that it's like someone's kind of lying this way down on the brain. So they're kind of relaxing. There might be sun sunbathing, something like that. So the inside of our brain. So this bit here is supplied by the anterior part of anterior cerebral artery and this matches up to our legs and our lower limbs as you can then see as the person's lying back, we're then gonna move up towards their trunk, their arms and their face. This part correlates to the outside aspect of our brain here. OK. So you can see that the middle cerebral artery supplies um our trunk, our arms, our um face. This is gonna become important a bit later on when we talk about the different presentations of um damage to the different arteries. But we will keep coming back to this con this um idea about how each part of the brain is matched or each part of the somatosensory and motor cortex is matched to a specific part of the body. Ok. Very quickly flip side to our arterial supply. We have our venous drainage of the brain. So rather than calling them veins, for some reason, we call them the sinuses. That's because remember those gal folds, I was talking about earlier as the dura folds down, it creates those spaces. Those are our sinuses. So running on the top of our brain, we have our superior sagittal sinus in the inside of our brain, we have our great cerebral vein and our inferior sagittal sinus. So our inferior sagittal sinus is this one and our great cerebral vein is this one. These two come together to form a straight sinus, the straight sinus then joins up with the superior sagittal sinus at the conference of the sinuses, they then come together and continue down as the transverse sinus, the sigmoid sinus and then go into the internal jugular vein. OK? I wish I'd made this diagram, but it was actually another a easy person, but I just think it's a really good way to see it. OK. So moving on to my next question, an 85 year old male presents to A&E with sudden onset limb weakness. When questioned further. He said he's struggling to move his left arm and leg and has also lost sensation to these areas. His past medical history includes angina hypertension and he is a long standing smoker on examination. Power in his left leg is MRC two out of five and power on his left arm is MRC four out of five. What is the most likely diagnosis? Again? This is quite a difficult question. So we don't worry if you're not sure, just have a go see if you can try and work it out, but don't worry too much. We will talk through the explanation. Ok. And smart in the chat. Um So while the uvea deviates towards the opposite side, um of the vagus nerve, is this the same as tiny vision damaged hys on. So the hypoglossal nerve, the tongue deviates towards the same side because our tongue muscles push. Um So if you remember how the muscles are always supplied contralaterally, if I lost this side of my, if I this side of my tongue lost its muscles, then my tongue is gonna point that way. And the reason that it's this side would actually correlate to this side of my brain. But because the tongue pushes rather than contracts, it means it deviates towards the same side. The va the uvula I think doesn't have that pushing effect. It's more of a contracting. So it's gonna be the um opposite side of our vagus nerve. I hope that makes sense. I'm sorry, that's, that was my best explanation. But II will try and again to come back to that question at the end. OK. Anyway, sorry guys. Fantastic. We'll end the pole there. So brilliant. Yet again, pretty much everyone is getting this answer right. It's so good to see you guys are fantastic. So why is it not the basilar artery? The basilar artery presents with something called locked in syndrome. And what that means is you can't move any part of your body apart from your eyes. The reason it's the left anterior cerebral artery is wrong is well than if you pick this one for picking up that it was the anterior cerebral artery. The reason it's wrong is because our brain hemispheres corre like to our opposite side of our body. So if I was answering this question, I'm saying it's a problem with the left arms and the left um legs and it's the left side of the body. So instantly I'm gonna, oh sorry, I just realized that I said the right, that um the reason. So as soon as I'm gonna rule out anything that is to do with the left hand side because it's the opposite side. So the reason it's not the middle thre three is because if we look at the um hour in their arms, we're seeing MRC two out of five in their legs and MRC four out of five in their arms. MRC is um a way that we grade movement and strength of muscles. So five is the best number and one is the worst and zero, sorry is the worst number. So five is normal movement. 54 is kind of weakened movement against resistance. Three B is movement um without resistance, two is movements with gravity removed and one is a little flicker of a movement and zero is no movement whatsoever. So what this is basically saying is that the power in our legs is weaker than our, in our arms. And as we were saying earlier, the anterior cerebral artery supplies our legs more than our arms. So if it's a problem with the anterior cerebral artery, our legs are gonna be affected more than our arms. And then lastly, um why it's not the posterior inferior cerebellar artery stroke. I've added this in quickly cos someone asked me about it earlier. So a posterior inferior cerebellar artery stroke, also known as lateral medullary syndrome presents with vertigo diplopia. So that's um blurring of the um blurring of the vision dysphasia. So we can't speak an ipsilateral Horner syndrome, which is a triad of ptosis and hidrosis. And um I can't remember the la and I can't remember and meiosis or mysis, sorry. So the eye um becomes very small and shut. So and then it also presents with ipsi lateral loss of pain and temperature in the face and an contralateral loss of pain and temperature in the body. Our anterior inferior cerebral artery is the same similar presentation. But you also get hearing loss and facial paralysis. If I see hearing loss in a question about a stroke it's probably gonna be the anterior inferior cerebellar artery. I'll leave you guys to have when you get these slides, we recommend having read through these again just to make sure you've got the understanding of them. Um But yeah, so moving on to talk about stroke. So there are multiple different ways we classify stroke. The first way we can do this is by type. So it can either be an ischemic stroke, which is our more common type of stroke. Risk factors include atrial fibrillation. And that's the most important one, hypertension, smoking, any of your cardiovascular risk factors. In terms of how we manage an ischemic stroke. The first thing we have to do is a non contrast CT head. We're gonna do that before anything else because we want to make sure it's not a hemorrhagic stroke. We're then gonna give 300 mg of aspirin and then consider thrombolysis and or thrombectomy. Don't really worry about learning thrombolysis and thrombectomy at your stage. That's way too early. Just have an idea that you need to do a CT head and then anticoagulant. Ok. On the other side, we have a hemorrhagic. This is a less common form of stroke. And in contrast to ischemic, which when you get a clot and lots of blood supply in hemorrhagic, it's more that the blood vessels break. Um So then you get blood leaking out everywhere. Risk factors for this are age, hypertension, atri venous malformations and anticoagulation therapy and there isn't really any management for hemorrhagic stroke, it's supportive casts, you managing any symptoms that come up in terms of stroke by location. I think the most important ones that you need to know are the anterior cerebral artery, the middle cerebral artery and the posterior cerebral artery. So how an anterior cerebral artery presents is it presents as a contralateral loss of sensation. Our brain remembers supplies the opposite side of our body. So it's gonna be contralateral to whatever side of the body that's affected. So it's gonna present with also that same contralateral motor weakness. And importantly, the lower limbs are gonna be affected more than the upper limbs. So you're gonna have weaker lower limbs compared to your upper limbs. You're gonna have more loss of sensation in your lower limbs compared to your upper limbs. On the other side, we have a middle cerebral artery. This is, this also depends with contractual loss of sensation and contralateral motor weakness. But in this side, in this one, instead, the upper limbs are affected more than the lower limbs. So the upper limbs are gonna be weaker, the upper limbs are gonna have less sensation. They also present with those aphasias. We spoke about earlier, the Broca aphasia that broken speech and the wernickes aphasia where you can't understand what they're saying. And it also causes a third nerve, third nerve palsy. So a third nerve palsy means that it's the oculomotor nerve. So it's gonna be a down and out eye. OK. And then the other most important stroke is our posterior cerebral artery. So because it supplies our visual fields, it's gonna present with contralateral homonymous hemianopia, with macular sparing. So what the macular sparing means is that as you can see in my really poor diagram, I I'm sorry is that you have the macular, that center of the eye is spared, but you still get heart the same side, um loss of vision and it also presents with prosopagnosia. If anyone knows how to say that properly, please let me know what prosopagnosia is, is an inability to recognize faces. So why do we get these specific presentations? Well, it comes back to what we were talking about earlier in matching up the blood supply to the brain and the area supplied by each artery to what's going on in that area. So, as I was saying about the person lying back because our anterior cerebral artery supplies that middle part of the brain and the top part of the brain, this is what correlates to our legs and our um to our legs and our lower limbs. So that's why you get the um lower limbs affected more than the upper limbs. Similarly, in our middle cerebral artery, it supplies the parts of the body and um the motor cortex provides the mo somatosensory cortex and the motor cortex areas responsible for our hands, our trunk, our face and our mouth. Um It also supplies the lateral side of the brain, which is the parts which contain wernick and Broca's area. And that's why you get the aphasias. And with our posterior cerebral artery, we get the visual, it supplies the visual cortex and also the lower part of our temporal lobe, which is what can the fusiform gyrus and the fusiform gyrus is what allows us to recognize faces and a way to remember that is fusiform starts with F so does um facial recognition. So that's why we match those up. So it's I think it can be quite helpful sometimes to learn. I know it's not, it's not always what you want to do but to learn the kind of underlying um physiology to then be able to apply it to the um actual presentations. So again, please, any questions guys put them in the chat, I will do my best to answer them. So I've got another question for you guys. A 28 45 7 year old female sends to A&E with a three week history of headaches which are worse in the morning and on lying down, they also report feeling nauseous on examination. They have evidence of papilledema. The F two suspects hydrocephalus and orders an MRI the MRI shows a narrowing of the structure connecting the 3rd and 4th ventricles. What is the name of this structure? So if we have the poles launch, that would be great fab. So give it your best shot, guys. Really good. Nice. See all those answers coming in. I'm sorry, I've been talking for a while but really good. Keep them coming in. Fantastic. You guys are doing great if you guys another 10 more seconds for answer this one really good. And don't worry if you don't know the answer, I definitely don't know the answer. Um So fantastic. AK Fab. I think we'll end the poll there really, really well then guys. So as with all of these questions, the majority of you are getting the answer right is really, really well done. And don't worry if you're not. So the correct answer to this one is our cerebral aqueduct. So this question is asking about the flow of CSF within the brain. So how does CSF flow? So it's made within the choroid plexus of our lateral ventricles, which is located here. It then flows through the intraventricular foramen or the foramen of Monro into our third ventricles, which are here. It then flows from our third ventricles through our cerebral aqueduct or the aqueduct of Sylvia into our fourth ventricles from our fourth ventricles. It then has two options as to where to go. It can either go through the Foramen of Madi or the Foramen of Lucca. If it goes through the Framan of Lucca, it's gonna come down into our spinal cord and it's gonna flow around the spinal cord. If it flows in through our frame of ma Madi, it's gonna flow around the brain and into the subarachnoid space. In the subarachnoid space, it then is absorbed into the superior surgical sinus via the arachnoid granulations. So a monitor to try remember this is little infants, try crying for food, sorry, all done. So little infants for lateral ventricle, little for lateral ventricles, infants for interventricular foramen, try for third ventricles, crying for three aqueduct, four for four ventricles. You can remember that four, for four, food is through a foramen. Then s for subarachnoid space. A for um arachnoid, um granulations and D for geral space or a or a sinus. Ok. So why is this important? But it's important for me to think about hydrocephalus. So what is hydrocephalus? It's a build up of fluid within the ventricles, how it's going to present where it's going to present with the headaches which are worse in the morning and worsened by lying down and papilledema. So, papilledema is um swelling of the optic disc. And the reason you get these symptoms is because you're basically getting an increased pressure in your head. So there are different causes of hydrocephalus. It can either be an obstructive or a non communicating cause what this means is that um there is something blocking that flow of C CSF the ventricles and the spaces aren't communicating. So, causes of this are things like tumors, abscesses, cysts, congenital aqueduct stenosis or chiari malformations. So basically anything that could compress and shut. Our ventricles is an obstructive cause on the other side, we have our non obstructive or communicating causes. This isn't where you've got a problem with your flow through the system. It's that you've got too much fluid within the system. So it's gonna be something like an intracranial hemorrhage, an infection, meningitis or posttraumatic, anything where you might have increased fluid in the brain or a bleeding within the brain which can then enter the ventricles. So how do we manage? Um Hidro Aus. Well, it firstly just depends on if someone's unconscious or conscious. If they're unconscious. Brilliant, we're going to do an extraventricular brain drain. Sorry, we're gonna go cut a hole in the brain and we're gonna put a drain in to drain it out of the body if it's an obstructive course. Um then we want to do a va tro peritoneal shunt. I'm so sorry. I realized that those two are the wrong way round. I am really sorry about this. So if it's a non obstructive course, of course, then we want to do a VRE peritoneal shunt. We're gonna take the brain from the ventricles and put it into the peritoneum. If it's an obstructive course, then we want to get rid of that obstruction. We want to make a cut. So we're gonna do a third ventriculostomy. So that's basically a cut within the ventricles. I am really sorry about that. I will make sure this slide is changed before it goes out to you guys. Ok. So any questions, please keep them in the chat and I am sorry for the mistakes I've made. Um But I'm just doing my best. So we've got another question for you guys. A 63 year old male presents their GP with a headache, photophobia, neck stiffness, fever and a widespread non blanching, purpuric rash. GP suspects a diagnosis of meningitis. What is the most likely causative organism? Ok. Really good guys. Another tough question. Don't worry about this one. I'm being really confused about the different types of bacteria but just have it go really good. Keep those answers coming in a nice, a couple more seconds. Just have a guess. Even if you don't know. And again, any questions, please put them in the chat and I will do my best to answer them. Ok. Lovely. I think we're kind of tapering off there. So we'll give you a few more seconds. Oh, ended, don't worry. Ok. So you guys have, as you just managed to get the right answer. The two most popular ones were my Neera meningitis and streptococcus pneumoniae. So, well, if you've got either of them because I can see where you're coming from with picking D So when it comes to picking the organisms for um meningitis, the most important thing to look at is the age of the person. So, what are the bacterial causes of um meningitis? So, in your 0 to 3 month year olds. The causes are group B, streptococcus, streptococcus pneumoniae, listeria monocytogenes and E coli. The most important one I've put and the most common one I've put in bold. Ok. So then in our three months to six years, we get streptococcus pneumoniae Neisseria meningitidis. I'm not quite sure how to pronounce that one. Hemophilus influenza and group B streptococcus. So that's now three months to six years in our six years to 60 years, we get Neisseria meningitis and streptococcus pneumonia. So I think that's kind of why is that? Remembering the age can be difficult sometimes. And then finally, in our over 60 year olds, we get streptococcus pneumoniae cerium meningitides op and friends of B Group B, streptococcus and Listeria monocytogenes. So I came across, I find these really hard to remember, but I came across the most random, um, I came across the most random new monitor to come up with. Um, just in terms of I've had someone saying I thought, um, Listeria was the most common for over sixties. I've based this off the teaching from the slides that we were given from the university because I think that's the most likely thing they're gonna use to make those questions. So some sources may say different ones. These are the ones the university use have chosen to stick with them for this session. So if you were picked different answers because you had another image, don't worry, well done for knowing that I've just gone for the uni ones because that's the most likely ones. So, how to remember the organisms came across a very weird mnemonic. I don't remember where it was a, basically about, I think it's meant to be set in like a, a playground or something with two kids arguing. So how to remember? This is, it's like a conversation between three Children. So first it is Grant. Stop licking Emily. That's your 0 to 3 months, your first sentence. Then it says, sometimes Natalie hates Grant. Ok. Then it's like grants replying saying Natalie sucks. And then finally, you have, sometimes Natalie hates Grant loads. It's a very weird mnemonic but it has always stuck with me and I'd never forget these ones. Sometimes it's really good to come up with a weird mnemonic or to find a weird mnemonic because you won't forget it. There's another rule that you can use to remember the most common causes and the, um, order of them is it's called the, um, the 21 rule. So the second most common organism within the group before it will become the most common organism. So, Streptococcus pneumoniae is, um, the second most common in your, 0 to 3 months. But the most common in three, in your three months to six years. Nicerium meningitides is your most common, um, in, is your second most common in your three months or six years. But then your most common in your 6 to 60 years and then so forth for the last one. So those are just tips and tricks to help you remember them. But maybe try and come up with your own pneumonic or something that helps you remember them. Cos trying to just rote learn them is gonna be really difficult. So having new on it will help you. OK. So another question for you guys. A 61 a 63 year old um male presents to their GP with a headache, photophobia, neck sickness, fever, and a widespread nonblanching purpuric rash. The GP suspects a diagnosis of meningitis. She wants to send the patient to be admitted before he leaves. She wants to prescribe an antibiotic. Which antibiotic should she give the patient? Really good guys. Keep those answers coming in. This one is quite a tricky one and I have been mean with this question. So I am sorry, but really, really well done guys. Keep those answers coming in. Um I'll give the new monitor that I just used again at the end and I'll make sure it goes in the chat so you can use it. OK. Keep those answers coming in. Really well done guys. Nice fab. OK. I think we will end the poll then if that's OK. So well done everyone. You gave this one a really good go. This one was a very mean question but I just thought in your exam, you are probably going to have questions where actually you're not sure what the answer is and you might feel scared and confused. So it's ok to feel that way for this and it will be ok to feel that way in your exam. You don't need to get everything right. So the correct answer for this one was actually b the majority of you put cefTRIAXone and I can completely see why. So that's a really good guess or a really good um knowledge to go for. So why is it Benzylpenicillin? Well, it depends on the setting that people are in for what um antibiotic you give them. So this was a GP. So she's out in the community. So in the community, our first line antibiotic is benzylpenicillin because you don't tend to have IV access and um cefTRIAXone is given through an through IV access. You can't actually give it in the community. So meningitis, what is meningitis? What it is inflammation of the meninges? What are the causes? The most common cause is a virus? So it's coxsackie a or just any virus. Just try and remember that as the most common cause, it can be also caused by bacteria, fungal infections and TB fungal infections are really only seen in people with immunosuppression like HIV or some other kind of immune disorder. What are the clinical features? Well, it's gonna present with fever, neck stiffness, photophobia. So that means that light hurts your eyes and people are shying away from light a non blanching rash. So, rash. So when you press on, press on it, the rash doesn't go away. Headaches and seizures. There's also two clinical signs for meningitis and that's Kernis and BRS. So kni is when you extend someone's knee with meningitis, it's painful or it's limited a way to remember. This is Koenig starts ke so it's gonna be knee extension. Then you have Brzezinski, which when you flex someone's knee, um head with meningitis, it then causes knee flexion. A way to remember. This is knee bin's called and, and it starts with neck and it's also got ak in it. So knee and neck are linked. OK. So going on to diagnosis or diagnosis of meningitis is with a lumbar puncture, that's the only way to diagnose it. How do we treat it? So if it's bacterial with the first thing we need to do is contact tracing anyone who saw the patient within seven days is gonna need ciprofloxacin or rifampicin. Then if it's the person itself, if we're in the community, what you're gonna do is you're gonna give them a dose of benzylpenicillin and immediately send them to hospital. However, if someone came to hospital, then the first line of antibiotics depends on their age. So the first thing we're gonna do is give people dexamethasone and an antibiotic. So if they're less than three months, you're gonna give them cefotaxim and amoxicillin. If they're over 50 years old, you're gonna give them cefotaxim or cefTRIAXone and amoxicillin. And if they're three months to 50 years old, you're gonna give them cefotaxim or cefTRIAXone. This is just your initial antibiotics until you get your cultures and sensitivity back and then you might adjust the antibiotics. Two important notes, dexamethasone and cefTRIAXone can't be given in Children under three, sorry, three months. So that's why the first antibiotic for under three months is cefotaxim and why we don't give them dexamethasone? Ok? I hope that's covered meningitis. Any questions, please let me know, then we're gonna come on to lumbar puncture next. So lumbar puncture can seem scary. The best thing to do is to work out what are the differences and what's gonna lead me towards my answer? So, first of all, your history is gonna help you as well, but also looking at lumbar puncture. So just quickly polymorph and neutrophils. So straight away, we're gonna look at the color of our um lumbar puncture. The most important one to notice is the viral is clear. So if you can see clear fluid, it's likely to be viral, then we're gonna look at our polymer. If we see just raised neutrophils, then it's more likely to be bacterial. So, a good way to spot bacterial is it will be the one that's got raised neutrophils compared to the others which are gonna have your raised lymphocytes. So the next thing that we're gonna look at is our lymphocytes. So, in viral these go up massively, they don't go up that much in bacterial and they also go up quite a lot in TB and fungus. Then it's important to look at protein. So bacteria um in viral, the protein can go up in bacteria, the protein goes up a lot. And in TB, the protein also goes up, then you want to look at glucose. So in bacteria, the glucose goes down in TB, the glucose goes down and also it can go down in fungal infection. So how to spot them. So my ways I look at it, I look for viral is gonna be clear fluid with raised lymphocytes. If I see that. Ok, it's viral. How do I recognize bacterial? Ok. I'm looking for a rise in neutrophils. If I see a rise in neutrophils, it's probably bacterial. Then how about TB in fungal? Those are very similar. The way to tell it apart is the protein TB. You get a rise in protein whereas in as fungal, you don't get a rise in protein. So I think when you're looking at these, it's important to try and work out. OK. What actually do I need to remember? I need to remember the differences so I can spot which one? It is? OK. So moving on, got another question for you guys. A 24 year old unconscious man is rushed into a by paramedics. The paramedics tell you he was in a fight and suffered a blow to the side of his head with a brick. The patient initially lost consciousness when the paramedics arrived at the scene, he had regained consciousness. They tell you he was alert and orientated during the ambulance ride and it was only when they arrived at the A&E that he lost consciousness again. What is the most likely diagnosis? So, really good. That's some answers coming in. Fantastic guys who are doing great, really, really good, lots of answers coming in. Really nice to see you again. Any questions, please pop them in the chat. A five more seconds fab. Ok. I think we'll end the pole there if that's OK. Lovely. So again, the majority of you pick the right answer, which is an exo hematoma. The key to this is that in our history, we've got a low impact injury to the head and then we've also got an initial loss of consciousness, then the person seems fine. Then they lose consciousness. Again, I see that as extra hematoma, it's not a carotid dissection because that's gonna present with neck pain and then also stroke symptoms. Um And it's also not a stroke um because we'd also see other symptoms, you know, we'd have loss of sensation and loss of motor and I'll talk about the other hemorrhages in a second. So another question for you guys, sorry, two in a row, we will come to the answers properly. A 77 year old female presents with a headache. Confusion and slight weakness in one of her hands on further questioning her family. Say that over the last few months she's been experiencing problems with her memory that she's become more irritable. They also say that she drinks three bottles of wine a day and has done so for the last 15 years, the regr orders a CT scan. What is the most likely diagnosis? Nice. Really good guys. Keep these answers coming in. You're doing great. Fantastic guys. Lovely. A few more seconds. Keep them coming in. OK. Brilliant. I think we will end the poll there. That's OK. So yet again, majority of you got the answer right? It's really well done guys. You are doing great with your revision. So the correct answer to this one is a subdural hematoma. It's quite hard to see. But if you can see here, I hope you guys can see my mouse on the right on. Well, it's technically the left hand side, but the right hand, the left hand side of the brain. So the right hand side of the image, you can see the slightly darker area which kind of looks a bit like a banana. That's a subdural hematoma. It's a chronic subdural hematoma, which means that it's been going on for a long time. That is also hinted at in the question with the fact that we've got a long history doesn't seem like a very acute um presentation. And we've also got risk factors just quickly when it comes to Iski, when you have given data interpretation, the most important thing they want to see is that you have a systematic method for approaching it. It's not necessarily that you get the right diagnosis. It's just that you approach imaging and blood results and things like that in a systematic way. So a good way to approach a head CT in an Iski is with BBV C as a mnemonic. So first I'm gonna look for any blood. Is there any areas of white? Then you're gonna look for any for the bone. Is there any fractures? Then you're gonna look at the brain itself. Is there anything within the brain? You can see any abscesses masses, et cetera. Then you're gonna look at the ventricles, are they bigger, smaller, compressed? Is there blood within them? And then finally, you'll look at the systems. So we'll talk about what the systems are in a minute, but they are essentially at the bottom of the brain and you're gonna see a subarachnoid hemorrhage just quickly, why the other answers are wrong. So, cranial abscess, that's when I'm done with fever and it's also gonna look different thing on an um imaging frontotemporal dementia, unlikely to be able to see it on a um act and a stroke again would present with slightly different symptoms. Ok. So, keep going on. So we're gonna talk about the main types of bleeding. So the first one, we've got is extradural hematoma. What is it? It's a collection of blood in the extradural space between the skull and the dura. So remember we talked about those layers earlier. So above our dura, is this where this its most common cause is damage to the middle meningeal artery and the middle meningeal artery passes behind your pterion, which is on your temple. So if you get it below here, it can really easily damage it and it's caused by trauma, historic, sorry, traditionally, low impact trauma, how it's gonna present. The classic thing is a lucid interval that losing consciousness, regaining consciousness and being completely alert and then becoming unconscious again. So you're looking for a history of a low impact uh low and then also this unconscious conscious unconscious again. And you can also get third nerve palsies, how it's diagnosed is with a noncontrast ct. And what you'll see is a hyperdense. So what that means is it's bright, it's bright white biconcave. So it's kind of got two concave sides, convex, sorry, two convex sides to it and it doesn't cross the suture lines. People say it looks like a lemon. So the suture lines are about here here and here and you can see that it's confined to just them and it does look a bit like a lemon. How it's managed is with craniotomy. So making a whole um a piece in the skull, getting it out and then pushing a piece of skull back OK. The next one we have is our subdural hematoma. What this is, is a collection of blood in the subdural space. It's caused by rupturing of bridging veins. So the bridging veins I mentioned earlier in they're within our subarachnoid, sorry, our subdural space and there's two types can either be caused and acutely which would be hard impact trauma or shaken baby syndrome or it can be chronic. So that's gonna be brain atrophying. So that's people who drink a lot of alcohol and elderly. Like in the question, we just saw where it was a person who was elderly who was drinking a lot of alcohol, it's more likely to be a chronic thing. So it's gonna happen over time how it presents depends on if it's acute or chronic. So if it's acute, there'll be a history of trauma, a focal neurological defect, focal neurological defect is basically anything that um is like a any nerve palsy, any motor weakness, anything like that. And also the key thing for this one is altered mental state. So it's fluctuating consciousness. So, in comparison to r um uh extradural one where you get unconscious conscious um unconscious. Again, this one you kind of have coming in and out of consciousness and it also might be that they're confused, that can also mean that can also affect um consciousness seizures and a raise intracranial pressure. On the other side. A chronic will be over a week or months will be progressive, worsening of memory loss, anti changes, confusion and reduced consciousness. And then also that um neurological deficits, it's diagnosed again with a non contrast CT and it will show a crescent shape which crosses suture lines. So someone's just asked about the suture lines. So you can see here how it covers the whole side of the brain. That means it must be subdural because a suture will, will be about here ish It does. It kind of depends on each person. But if it covers the whole side of one brain, it's subdural. If it only covers like a quarter or less than, then it's extra dural. If it's acute, it'll be hyper dense, it'll be bright white. So as you can see here, if it's chronic, it'll be hypodense. It'll be dark how we manage this. It depends on if it's acute or chronic. If it's acute, we want to do a decompressive craniectomy that's different to a ran craniotomy craniectomy. You take the piece of skull out, you put it in their stomach and then you, you leave it for a little bit and then you'll come back on the other side, we get a chronic, which is decompression by a burr hole. So you basically drill holes into the brain. Ok, subarachnoid hemorrhages. So what is a subarachnoid hemorrhage? It's a collection of blood in the subarachnoid space. It's caused by damage to the circle of Willis. It can be caused by either traumatic which is the most common cause or spontaneous. So, the um it could be ruptured the bar aneurysms or ATRIO venous malformations. Bar aneurysms are basically like little aneurysms within the vessel which can then rupture and burst. So how it presents the thing for this one is a headache. There'll be thun a thunderclap headache which will be sudden onset and people will describe it as the worst headache of their, you'll also get nausea and vomiting, seizures and it can also cause meningisms. So neck stiffness and photophobia. So it's a good one to rule out between the two diagnosis is a non contrast CT. If the CT is negative, you can do a lumbar puncture which will show xanthochromia. So yellowing of that um cerebrospinal fluid. So you can see it here on the imaging where some people describe it as like a spider. So these are the systems I was talking about at the bottom of the brain and you can see that they're bright white and filled with blood. I don't can't always see the spider how I recognize this one is that the other slices of the brain. The other ones tend to be in a higher slice of the brain, whereas this one's lower down. So you can see that it looks slightly differently. You can't see the ventricles. So it's more likely to be subarachnoid. And this one is managed with niMODipine which prevents vasospasm. And if it was traumatic, you're just gonna monitor someone if it was spontaneous, you're gonna use coiling. So essentially you thread um, metal and it then causes coagulation and um clot formation. Ok. Another question for you guys, a 45 year old female suffers a traumatic head injury. They're feeling nauseous and vomiting, have a headache and they seem confused and drowsy on examination. They have papilledema, um, sick, nerve, palsy and dulls eyes. You suspect they have raised intracranial pressure. Which of the following would you expect them to have as well? Ok. Fantastic. Straight away some answers coming in guys. Really, really good. I am sorry. We are running over a bit. We'll probably finish about half eight. I hope that is ok with everyone. Fantastic. Keep those answers coming in. You guys are doing brilliantly really, really good. I definitely did not know this when I was at your guys stage and I, to be honest, I still don't really know this or I wouldn't remember it. Fantastic guys. Really, really good. Another few more seconds get those answers in if you want to. Ok. Brilliant. I think we'll end the poll there. So well done guys. You've done brilliantly. She um So the correct answer to this one is Cushing's Triad. So Cushing's triad, I'll talk about it in a second is what we see in raising intracranial pressure. Beck's triad was mentioned by CNA and that's um cardiac tamponade. It's not being able to hear heart sounds raised JVP and low BP. Charcot's triad is seen in ascending cholangitis and it's where you get um uh fever jaundice and right upper quadrant pain. Raynaud's pentad is also seen in ascending cholangitis and that's the additional. So Charcot's tried plus um confusion and hypotension and Murphy's triad is seen in appendicitis and that is rightly at left, rightly at fss of pain, um nausea and vomiting. Ok. So, raising cranial pressure. So what happens in it is you get because of the Monro Kelly doctrine, which says that our brain is 80% brain or skull, sorry, it's 80% brain, 10% blood and 10% CSF if you get an increase in any one of these, it will cause compression of the other and decreasing of the other. This is bad because we don't want our brain to compress because that's gonna cause damage. How does it present? Well, symptoms are gonna be headache, vomiting, nausea, confusion, and reduced consciousness. The signs are papilledema. So blurring of the optic disc margins, cranial nerve palsies commonly the ones to do with the eyes. So 34 and six doll's eyes, which is basically when you move someone's head, they, their eyes don't move with it, which in a normal person, if I turn to my head, my eyes move a person with doll's eyes, their heads will stay in the center as you move their head, the eyes that will stay in the center and an affixed lone pupil and there's also a quote called sunset eyes, which is called sunset eyes because basically you can see the flare visible above the pupil. So it looks like the iris. Imagine that the kind of irises of the sun they're setting co they're gone down. It also tens with Cushing's triad. So what this is, is hypertension with widened pulse pressure. So that means the difference between systolic and diastolic BP is bigger bradycardia and irregular respiration. So that's your cushing's triad and that's raising cranial pressure. How do you manage it? Well, you manage it conservatively, you can manage it conservatively with tilting the bed to 30 degrees, hyperventilating someone. So that means they'll blow off CO2 and increased oxygen causes vasoconstriction, which then means that you get less blood flow to the brain. Then medically, we can treat it with hypertonic saline or Mannitol or dexamethasone if it's a a tumor, how do we manage it well? So, um sorry, in terms of how we can manage it surgically, it depends on the course. If it's idiopathic, we don't know where it's come from repeated lumbar punctures if it's, we want definitive management. So we need to stop this. We need to Brexit way. We need to do a decompressive craniectomy just very quickly in the drugs to lower BP, intracranial pressure. There's two main groups got hypertonic saline, um or you can use Mannitol and dexamethasone. So, hypertonic saline and Mannitol, they're osmotic therapeutic agents. So they increase the concentration of blood which basically draws fluid out of the injury to then be weeded out. They're indicated for an acutely raised intracranial pressure and they're given IV. So they're making you wean more. So the adverse drug infections are gonna be diuresis, weaning more hypertension because you've lost more fluid and electrolyte imbalance because you've lost more electrolytes and they're contraindicated if you're anuric. So you're not weaning because you need to be able to weave for them to work. And if there's a breach of blood brain barrier on the other side, we've got dexamethasone, which is a steroid. So it's gonna upregulate anti-inflammatory processes and downregulate low inflammatory ones. It's indicated when there's ra in cranial pressure due to tumors or infection. If you want to give dexamethasone, not the other ones and it's adverse drug reactions. Like all steroids are Cushings syndrome, osteoporosis and immunosuppression. And it's contraindicated if you've got Cushing's or immunocompromised. OK. Another question for you guys, a 23 year old female is on a ward recovering after traumatic head injury, on examination. You notice that uh that they're becoming increasingly drowsy and their respiratory rate has decreased. What is the most likely cause of this deterioration? So, if we can launch the polls, that would be great. Thank you. So keep going guys. You're doing really, really well. Oh, fantastic. Wow. You guys are so good. Brilliant, really, really well done guys. Keep those answers coming in. I know it is late, but you're doing so well. I will be over soon. Don't worry. Really, really well done guys. 10 more seconds. Really nice. Any questions, pop them in the chat, I'll do my best. Ok, fab we end the pole there. Really nice. So again, the majority of you got this one right? So the correct answer is a tonsillar herniation just quickly. Why? It's not an opioid overdose is because if you look at the history, it's saying about how they've got a traumatic head injury. So often history can point um or something that might seem i relevant in history can sometimes point towards the answer. So there's no mention of opioids. So it's not going to be opioids. Ok. So what is brain herniation? Brain herniation is basically when you get a an abnormal movement of the brain, there are five different types. There's cingulate or subfalcine, which is why our cingulate gyrus herniates under the falx cerebra. And it typically causes um compression of our anterior cerebral arteries. So it's going to present with anterior cerebral artery stroke signs, then we have central which is just downwards displacement of the brain. And the most important ones I would say are your cerebellar and your uncle ones. Remember. So the uncle or transtentorial is when the uncus, which is just a part of the temporal lobe, herniates down under the tentorium, cerebelli, which is here. And um you typically get third nerve palsy. So you get a down and out eye. The most dangerous one is our cerebellar, our tonsilla. This is when the cerebellum herniates down through the Foramen magnum, which is the hole in the bottom of our brain, which our spinal cord enters through and causes direct compression of the brainstem. The reason this one's the most dangerous is because it can compress our as ascending reticulate activating system, which is responsible for consciousness and also our brainstem which is responsible for our breathing. Our um heart rate, all the things we need to stay alive. And then finally, we've got transcalvarial which is when part of the brain herniates through a defect in the skull. OK? Another question for you guys. Any questions, please put me in the chat but you are in A&E when where a patient is rushed in following them, falling in a river, you are asked to assess their level of consciousness. So perform a Glasgow coma scale on examination. The patient's eyes do not open even to pain. When you ask them where they are, they do not respond at all. And when you do a trapezia squeeze, you know that their arms and legs extend. What is their G CS? So good to see some answers coming in guys. Well done. Keep them coming. You're doing great fab brilliant, really good guys. Just have a go really nice. Another 10 more seconds. OK? We'll end the pole there. So the correct answer um for this one is four. So just quickly, there is the lowest G CS you can have is three. So if you get a G CSE question and you see anything less than three immediately rule it out, it is wrong. You can't have that. So G CS, like I said, lowest point you can get is three, highest you can get is 15. So if on an SBA, you see any values outside of that range, get rid of them immediately. So it combines four components. The first one is our eyes. So there's four points available for the eyes, but it's got four letters in it. So four points. So four points would be if they open, when you walk in the room, they just open three would be if they open to sound. So when you say their name, two would be if they open to pain and then one is no response terms of speech is available for five points. So if there's, if they, when you ask them a question, if they're orientated, they answer the question, they get five points if they're confused. So if you ask them, where are you today? And they said, oh, I'm in my living room, then they would get four points. If you asked them a question, they gave inappropriate wisp. So that might be something like you ask them. Where are you today? And they said something along the lines of um my sister's called Julie that's inappropriate. That's not answering my question. Then two points would be incomprehensible sounds and then one point is no sound whatsoever. Then we also have our motor. So this has got six points. So six would be a base command. So if I say put your hands out, they put their hands up six points, um five points as if they move to localize pain. So if you get slapped by someone or for example, you're probably more likely to put your hand up to it and that's and move your hand towards it. Um if someone withdraws from pain, so if they flinch away, that's worth four points, if they do a decorticate posture, so normal flexion, that's three points. Decerebrate is um abnormal extension, that's two points. And if there's no response at all, it's one point. So that, that always confused me was de cerebra and decorticate. So decorticate is um when you get flexion of the elbows and abduction of the arms, so your arms come like this, the way to remember, this is the core, sounds like core and the arms move towards the core and it indicates damage to the cortex, the cortex is the top of our brain and that's why it's three points because damage to the cortex isn't going to affect your consciousness as much as damage to the brainstem. So the decerebrate part of the um body, um the de cerebra, you get head extension and arm and leg extension to oration. So your arms move away from your body and this indicates damage to the brainstem. So just to try that one out again, I've got another G CSE G CS question for you. Don't worry, you're not having to do G CSE S the patient whose G ce you assessed earlier. G CS seems to be improving. So you called them back to review their G CS again, on examination, their eyes open. When you say their name, when you ask if they know where they are, they respond um with mum's car breakdown. When you perform a Trapezia, squeeze their hand, moves up to the shoulder. What is their G CS? So have another go with this one guys. Yeah, I will go through the treatment of meningitis again. It is a bit confusing essentially. If you're in hospital, you're gonna give someone a cephalosporin. If you're in a community, you're gonna give them a penicillin and yeah, the MRC um I will go over that one as well. Um Really good to see your answers coming in guys who are doing great. Um They should also cover that in case 15 as well. I just thought I'd chuck the MRC go in just for now. Ok. Fab Fantastic guys. Keep those answers coming in. We are getting close to the end. I promise nearly there. It's the last little bit. Now, I am sorry that we've run over, but you guys are doing fantastic. OK. Lovely. We'll end the poll there, please. So fantastic. Again, the maturity. Have you got this one? Right? Which is 11. So what are they scoring points for? So they're scoring points for their eyes opening. When you say their names, that's three points. When you ask them if they know where they are and what the date is they respond with. That's inappropriate words. So that's three points again. And when you perform a Trapezia, squeeze in the hand, the hand moves up towards their shoulder. So that's almost a full point for that one. But that's gonna be five points altogether. 11. OK. So last few questions, I think it's three more. What is the name of the structure indicated by the arrow? Really good guys. Keep those answers coming in. You're doing fantastic. A couple more seconds for this one. Really, really good guys. You're doing great. OK. Lovely. I think we'll end up hold that for this one. So I can the majority of you got this answer, right? So the correct answer to this one is the pons. So this, I think is a really important thing to learn. Um because this is actually it's very like to come in your is it came up for me and my mock and I think of my actual is as well. So learning being able to um label MRI S the best thing to do is to try and identify structures which you easy to identify. So your corpus callosum is this big bright white thing here. Then below that, and the dark space is your lateral ventricle. Then you get your midbrain your pons and then your medulla behind the pons is your fourth ventricle and behind your fourth ventricle is your cerebellum. Then this little bright white part here is the pituitary gland and then above it sits the optic chiasm. So if you get a line pointing to something above the Pituitary gland, it's the optic chiasm. And then also this confused me as I got given this question in my iki and I was trying to overcomplicate things. I didn't understand what they meant by just pointing here. What they just meant was gray matter. And so sometimes don't overcomplicate your answers. Just say the the simplest thing cos it might be the answer like it was in this case. OK. I've got another imaging for you guys. So what is the name um of the structure indicated by the ARIC? So give it a go guys. Really, really good. Fantastic. You guys are doing great, especially for so late in the night, please keep the doctors coming in. It's really good to see really well done guys. I think there's one more question after this. So we are at the end you've done brilliantly. OK? I think we'll end the pole there if that's OK. So the correct answer for this one was the cord nucleus which the majority of you got right again. So this is what the brain looks like when you kind of slice through it like this. So again, a good thing to identify is something that you recognize. So the lateral ventricles are always at the back here and they connect to form the third ventricle and either side of your kind of this black midline is your thalamus and working out your thalamus, you get your globus pallidus and then your Putamen. And then if we go up just next to the other um lateral ventricles, we get our pu our cordate nucleus surrounding them and then connecting our two hemispheres is our corpus callosum. OK. Very briefly, I'm just gonna go for airway anatomy. I think with anatomy, there's a lot of content to learn and it's not always the most high yield. So I've tried to pick the most important things. So airway anatomy ha the part that I chose to focus on was um intubation and airway support because that's the most important part of your airway anatomy when you're practicing as clinicians. So what is the order of the airway? So if you were to intubate someone, the first thing you would go through would be the mouth, you'd then go into the pharynx, then to the larynx, then through the vocal cords to the trachea. So that's the process of intubating someone. The gap between your vocal cords is called your rimmer glottidis. OK. Then what are some other important an airway anatomy points, ok, airway muscles. So we've got cricothyroid, what this does is tense his vocal cord. So it gives us pitch. It's, it is the only um airway muscle supplied by the superior laryngeal nerve. So that's an important thing to learn. And what happens is if you get this one knocked out, then your pitch, you can't change the pitch. So people get hoarse voices. So it's gonna be impact for the patients. The other important one and I would say is the most important one is our posterior crico retinoid. What this does is it abducts. So opens our vocal cords and this one is supplied by the recurrent laryngeal. If you get damage to the current laryngeal, you can't open your um vocal cords. So this can then cause problems with your breathing and could lead to death. How do we keep airways open? So there's two airway adjuncts we use, which is a nasopharyngeal airway, which in through the nose and it, we're gonna use that if the patient is conscious, but we're concerned about their airway. So I'm worried that they're not getting enough air, but they're awake on the other side. We've got our oropharyngeal airway. This is known as a gel. This one goes through our mouth and this is if the patient is unconscious, you know this one because if you try to put an oropharyngeal in someone who is conscious, they won't tolerate it, they'll gag, they'll spit it out and the airway adjuncts are used before you intubate and ventilate someone. So when you're trying to keep airways open, cos you're worried about someone, but you've got to um go over but you've not got the, the uh interfacing equipment yet. So last thing as well is our A three approach. This should be covered a bit in case 17. But essentially, it's a structured way of approaching a very unwell patient. So the first thing we look at is airway is the patient is the airway breathing, sorry patent. If it is brilliant, move on to be, are they breathing? What's their respirate? What's their O2 sats, a little mini lung? Then we're gonna go on to cardio, we're gonna put Cannulas in, we're gonna do an EKG BP, heart sounds and refill. Then we're gonna move on to D which is disabilities. So are they alert? Are their pupils reactive to light? Have they got low blood glucose if, have they taken a drug? And then finally, you're gonna expose and examine the patient? So you're gonna look at the full body and I've got a nice little chart here which I thought was really useful that tells you what you're gonna do in each step and what your intervention might be. So, if I didn't see an no way, what am I gonna do if I'm not breathing, what am I gonna do? And then also what the goal is? So as promised I said, I'd just go over the cranial nerves one more time and the key parts of it. But that is everything that is the new content. So if you don't want to listen to the cranial nerves part, please feel free to go. Thank you so much for joining. You guys are going to do absolutely amazing on your S two. The way you are answering the questions tonight, I know you answered last night is just absolutely phenomenal and you know, a lot more than I did and I've somehow made it to the third year. Um Just a couple of questions in the chat mrc grading. So there's five that's um it's a scale of 0 to 55 is normal movement. So normal power four is you can move a little bit against resistance. So I happen to put less resistance to stop them, to allow them to move. Sorry. Um Then you've got um, the MRC grading of three which is if I take resistance away, they can move. Um Then MRC of two, which is, there's these special movements, I don't know them. You're not expected to know them where if you take gravity away, they're able to, um, they're able to move. And then one would be, could you, if you can um, twitch a little bit. Um And then, um if you, if you twitch a little bit, that'll be one and zero is no movement. I will put the mnemonic in the slides because it won't let me message everyone. Um So I will put them in the slides about the different types of meningitis. But you guys are absolutely fantastic. You're gonna be absolutely fine for your S two. Please have the absolute best summer when you're done. Enjoy it as much as you can come back to 30. You feeling relaxed, you don't need to do any work over the summer. You've definitely earned a break so well done, everyone. So very quickly you crane your nerves for those you do want to stay through it. So there's 12 cranial nerves. We've got our olfactory optic oculomotor trochlear, trigeminal obducens, facial vestibular cochlea, glossopharyngeal vagus, spinal and excess spinal accessory hyperlocal. A way to remember. This is 000 to touch and feel very good velvet r heaven. There is some more promiscuous um pneumonics out there. But I think this one is a good one. It covers the bases without being too promiscuous. Um How do they leave the um how do they leave the cra the skull? How do they exit out to do their function? So often, the name of where they exit will relate to where they're going. So the cribiform plate is located near the nose. So olfactory is gonna go through the cribiform plate, optic canal. It's a optic nerve, it's gonna leave through the optic canal. It's also got a two in it. So it's gonna be leaving through a canal cranial nerve three, oculomotor is gonna be leaving through superior orbital fissure. So is our nerve, our trigeminal v one of it is gonna leave through orbital fissure V 23 and rotundum and V 30 Valli and so forth for the rest of them. Um And just so you can see the jugular foramen. The way to remember these ones is these are nerves that are acting on things outside of the head. The Juggler foramen is the big hole in the bottom of our skull, which our our spinal cord comes and leaves through. Um So remember this one is is through, they're the ones that are leaving to go act out, act elsewhere in the body. So in terms of the function, most of them do what they say on the tin. So olfactory nerve is responsible to a false fraction. So smell optic for vision, some important ones to notice are ocular motor. This one is gonna move our eyes up down and also move them in. And it's also responsible for pupil constriction, accommodation and focusing and eyelid opening. So if you get a cranial nerve, um three lesion lesion, you're gonna get a down and out eye, a thick dilated pupil ptosis. So the eye is gonna droop and you're gonna get loss of your consensual um uh corneal reflex trochlear. This one always confused me. Trochlea in Latin means like a pulley the way the chole nerve works and how to remember the way that it works is that it, um, loops back around itself around something called the Trochlea, which is where it gets its name from. And it always confused me that it moves the eye down even though it's the superior one. But basically, if you put your arm like this and attach it to the back of your head as though you've looped around yourself and then you pull on your arm, your head moves down. So that's hard to remember that it acts from moving down. Um Some other important parts as like I said in tram, it's got five branches. V. One is your ophthalmic and supplies everything above the corner of the eye. V two is maxillary supplies the cheek and V and so between the lower eyelid and the upper lip and then mandibular is the lower chin and it also innovates our chewing muscles. Our muscles are mass location. Cranial F seven moves the eyes out. It innervates the lateral rectus muscle and it's called ausin. So it's going to abduct. Um And in seven is facial movement tastes the anterior three thirds of the tongue, salivation, lacrimation snot and innervates to be muscle. So sounds being too lo and in cranial nerve, too late is vestibular coul. So that's kind of the movement and balance. Cranial nerve nine is taste from posterior one third of the tongue of swallowing. Cranial N 10 is speech and swelling and invade the viscera. Um I think so in this guys, we, we leave that there. Um Hopefully you guys should have got um through all of that. But I think if you just have a read through the evidence of the lesion, it basically, if the what the function is, it will have a le it will lose that function. If you get the lesion, could you show all the question with all the triads, please? Yes, of course. Sorry. So, going very quickly back. So triads bex triad is for um uh it's for cardiac tamponade. It's hypotension. Um muffled heart sounds and a raised AVP. Charcot's triad, ascending cholangitis. Um That's gonna be fever, right? Upper quadrant pain and jaundice cushing's triad is are kinds of a raised ICP and that's gonna be um hyperventilation, sorry, regular breathing hypertension and bradycardia. Raynaud's pentad pentad is for um ascending cholangitis and that Charcot's triad plus confusion and hypertension. And murphy's triad is um appendicitis. It's right, fossa, pain and nausea and vomiting. So I hope you guys have enjoyed this session. I'm sorry that we went on a bit today. It is a lot to get through. Um But you guys have all done fantastically. Um And yeah, I just wanna say good luck for you too. Don't panic. You will be fine and I'll stop sharing my screen now. Thanks, Jamie. That was so helpful. And I know in, for the S two, I would have loved something like that. Um Yeah, again. Make sure you get some rest before the S two. It's really important to not burn out before the exam. Oh, I realized I forgot to answer someone's question. Um, very quickly meningitis management. Sorry, someone did ask and I think I, my explanation was a bit confusing. Sorry slides get through. Ok. So uh sorry, my laptop is going crazy. So management of, of um of meningitis if you are in the community, give someone Benzyl penicillin. If you're in hospital, you're gonna give them if they're over three months, IV dexamethasone, plus these antibiotics. If they're less than three months, Cef OTA and amoxicillin. If they're over 50 months, cefotaxim or cefTRIAXone and amoxicillin. And if they're aged between three months and 50 years, either cefotaxime or cefTRIAXone and that's just your initial anti um antibiotics, you then kind of want to get a lumbar puncture back and blood cultures, you then might adjust them or you might not. I hope that's answered the question too for the meningitis. Was that what you wanted it for? And as sex, but again, this will all be slides and they will fix them. So I made as well what it was. So, thank you. Um So you can't give people under the age of three months. CefTRIAXone. They have to get cefotaxim. So that's why you don't have the option of either all. But so if you just wanna learn one, just learn cefotaxim. Well, I think that's all for today. Have you, has anyone got any more questions? Just before we finish? That was really good, Jamie. I was literally learning everything again. I was like, I remember this. I probably got all the sbs wrong myself. Yeah, that's great teaching. I think we can end it, to be honest. So stop the recording and finish it. P.