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Atala Gee and cardiology. So this is our first SBA. If I could get someone to watch the pole for May. So a blood coagulation test of an individual produces the following results. A PTT is prolonged. PT is prolonged on the fibrinogen. Essay is normal where in the coagulation pathway is the most likely defect. So which factors most likely affected give you 5 to 10 more seconds to get your answers in? Don't worry. If you don't know, just give it a guess and we'll explain it. Brilliant. So in the poll there. So it's quite a mix of answers, and that's okay because it's quite a difficult question. So the answer to this question is a factors 10, 5 and two. So let's go through why that's the right answer. So this question basically it required you to have a knowledge of the quick relation cascade. It's pathways and where those pathways overlap with each other. So let's just start off by going through the different pathways. So if I get a can you see my mouse back? A. Yeah, I can see your mouth. Okay, Brilliant. So we'll start off, um, with the intrinsic pathway so this is this one here. So this involves a lot of different factors. So it starts off with factor 12 being activated, which them for back to Bates Factor number 11, which activates factor nine, which then activates factor eight and then activates back to 10 Onda. That gets us into our common pathway, which will go through in a second. Now, this is probably the hardest, but the coagulation cascade to remember. So the way I like to remember it is the start of when you write out the names off the different factors as numbers when you write them out. The first letter of the last letter of the, um of the factor is the first letter of the next one. So I'll explain that. So our first factor is 12. So when you write out the number 12, it ends in a So then your next doctor is 11, which begins a day 11 end in n, which means the our next factor is nine, which begins with then and then nine ends in a, which means on X factor is eight and eight ends in t, which it means on X factor is 10. So I heard that makes sense, and that's generally how I like to remember the intrinsic pathway. Then we have the extras it pathway, So the extra pathway occurs when Factor seven um, is activated when it combines with tissue. Factor on tissue factor is released when there's trauma to cells external to the blood vessels. So when those two combined that activates factor seven and then that goes on to activate factors five and 10, which start our common pathway. So I've talked a bit about this common pathway. So in the common pathway, Factor 10 is activated. Factor five is activated and together those two combined and activate factor, too. On that fact, two goes on to activate Factor one, which is also known as fibrogen and turns fibrinog and into fibrin. So, as you can see from this slide, we have different tests that measure the length of time required for different parts of this cascade to occur. So the a PTT or the activated partial from the plastic in time measures the length of the intrinsic pathways. That's all the way from factor 12 all the way to, um, figure information be the prothrombin time. While the PT is the same. But instead of measuring the entire length of the X in the intrinsic parfait, sorry it measures the entire length of the extra six pathway. And finally, the Fibrinogen essay, which was mentioned in this question. What that does is that measures the length of time it takes the fibrinogen to be combated into fiber. It's it's just measuring that last step, basically, Um, so the way I like to remember this is a PTT. It's longer. There's four letters to it, so it measures the longer pathway, which in this case, is the intrinsic on. I like to remember the PT measures the extra music just because the extremes it contains tissue factor on, um, tissue factor is released to say when it's warmer outside of the blood vessels. And that's how I remember that the tissue fact pathway is the extrinsic pathway on. Because PT is shorter is measuring the short pathway. So going back to this question of what it was asking, um, if only the A PTT was prolonged, but the PT on the fibrinogen assay were normal. That tells you that the defect is somewhere within the factors that are involved in the intrinsic pathway, only so not the ones found in the common pathway or the expense it pathway, but just the intrinsic pathway that's quite common. For example, in a condition known as he matures hemophilia a lot. Some of these factors here in the intrinsic pathway can be affected. On the flip side of that, if the PT was prolonged on the A, PTT and the five pertinent Fibrinogen essay were normal, that suggests that there's a defect in either the tissue factor or factor seven. They're only found in the extrinsic pathway. If the fibrinogen say was prolonged on a PTT and the PT were normal. And that told you that there must be a defect with food religion because only that, I say, is being prolonged. And in this question we have both the a PTT and the PT being prolonged. But the fibrinogen, I say, coming back as normal. So what that tells us is that the the factors that are affected must be within the common pathway before we get to fibrinogen, so that involves factors. 10 factors five in fact, is two, which is why he was the correct answer, right? That makes sense we'll move on to our next question. So you're in placement in the cardiology board? And I asked her auscultate the tricuspid valve on a patient. Where would you place your stethoscope? But in those people get in their own season? That's great. Keep on coming. I'll give you 10 more seconds. Okay. 32, one that we get on the pole there, Ondo. Brilliant. Most of you got this right. That's really well done. Eso the correct answer here is See, So it's the fourth intercostal space left sternal border. So the auscultation sites of the heart sounds are very important. It's something that you need to know for your exams. And it's also something you need to know when you get a replacement sending when you go into clinical environments because it's just something that's used day in. Day out is really important to know, So I'll go over the four that you really need to remember. So your aortic valve is your second intercostal space, right? Sternal border. Your palm tree valve is the second intercostal space left sternal border. The tricuspid valve is the fourth intercostal space left. Stay low border on the mitral valve is the fifth intercostal spaces make particular line on the midclavicular line is just what it says on the 10 is if you had to look at the length of the clavicle. If you split it in half and joy vertical line down from that, that's where it is on. It tends to be when you're when you're auscultated on a patient, that tends to be just below the nipple generally. So the way I like to remember this is, um, Courtney. She is. If you look at aortic bicuspid much your bowels, it forms sort of a straight line. I can probably convince you that's a straight line. Onda. I like to remember. This is a T. M. So bit like an ATM. When you get money from a bank, um, that forms one line, and then your primary valve is just above it. So ATM in one line and Paul me just above it. What's important to note, though, is that these auscultation sites don't correspond to the er atomical types of where the valves are, so the valves aren't sitting necessarily just below where these points all on these sites are basically the best places to hear the sound off the heart valves on. That's taking into account the direction in which the heart sets on direction, in which these valve shut and push push blood flow as they shot. So it's not where they are in Atomic Lee, but it's where it's best to hear the heart sounds when you're examining a patient. So our last question for cardiology and hematology so patient is diagnosed with having aortic valve stenosis? What's physiological impact is this disease have on the heart's ability to pump blood pretty in Cuba, Zones is coming in looking ready. Good, safe. I'll keep out guys even done really well going so long Tonight I get E 10 more seconds. 32, one. Brilliant. So once again, well done. The majority of you got that question, right? So the answer in this case was D, which was an increased after load. It's a great job. So let me let me explain a little bit more about after load preload on some other factors that affect cardiac output, because I know it's sometimes difficult topic to wrap your head around. So let's go back to basics what is cardiac out? But while cardiac output is your stroke volume, which is the volume of blood ejected per heartbeat or per ventricular contraction multiplied by your heart rate. So the number of beats you have in a minute when you multiply those together that ultimately gives you your cardiac output, which is the volume of blood ejected from your heart in one minute. Um, as you can see from this diagram, there's many three factors which affect your cardiac output, which are your pre load, your after load and your myocardial contractility. So let's talk through all of those in turn, so your pre loads of pre load is basically the amount of myocardial stretch that your heart has before it goes to contract. So your heart's filled up with blood. How stretched is it before it? Then go squeeze and pushes that blood out. So if we think about it, if you're pre load is high to start with, then it suggests that your heart chamber before it contracts is going to have a lot more blood in it. So therefore, it intuitively makes sense. If there's more blood in that chamber when it contracts, more blood is gonna be ejected, which is going to increase your stroke volume because more blood is coming out the heart and therefore your cardiac output will go up. This is true. Up until the point you may have heard of starlings Law. Starlings law basically describes the fact that basically the more myocardial stretch there is up into a point, um, the great the myocardial contractility on therefore, the greater the stroke volume and therefore the great to the cardiac output. Um, the reason why that's only occurs to a point is because if you can imagine going back to your basic physiology, have you acting in your moisten filaments that are overlapping each other as you're stretching the myocardium, these these filaments getting further and further apart. Um, and this is fine because it's a said with starlings, although will contract even more as they stretch further Teo, increase the amount of blood ejected and increase that cardiac output. But you get to a point where actually the acting and the mice in filaments become too far away from each other on, they aren't able to grab on to each other and interlock so that they can then contract. And at that point, the cardiac output in the amount of blood you can inject from your heart goes down because you're not able to give that strong contraction because your filaments aren't touching each other anymore. So, as I say, pre load is, may need to do with how how stretched your myocardium is before your heart contract. So how much feeling it has? Basically, so this is affected by Venus returns. If there's more venous return, you're gonna have more blood going into the right side of your heart. Um, if there's tricuspid or much was two no cysts or chronic aortic stenosis that can also affect how well the ventricles fill as well, Then we have after those so after load is basically the pressure against which your heart pumps when it contracts. Um, so if you have a high BP is is a higher systemic vascular resistance, then you're going to have an increased after load on the left side of your heart. And if you have pulmonary hypertension, zar, high BP in your vessels within your lungs or the pulmonary vascular resistance, so the resistance against blood further there is in those vessels, then you after load will also increase on the right side of your heart, and it makes sense that as your after load increases, then your cardiac output is going to decrease because there is more pressure against which the bench was must contract. So it's almost something pushing against them in the opposite direction is they try and contract on, therefore, less blood is going to be ejected and therefore your cardiac output, we'll go down. Finally, we have myocardial contractility is This is basically the ability of the myocardial cells to shorten, as I say, to eject that straight volume. And to give you that that called jak output. Um, intuitively, if you increase your contractility once again, you're going to increase that straight volume, and then you're going to increase that cardiac output. And there are lots of different factors which you can see on this side which affect my cardio contractivity. So in this question, it talked a little bit about aortic valve stenosis. So when you have a little valve stenosis, you have, um, you have almost in obstruction your aortic valve, which is leading out to the rest of your body through the aorta. When it's still owes. It's quite stiff. It doesn't want to open a smudge, Um, so you can imagine you've got the left ventricle trying to pump against this really stiff bowel. So it's what it's doing is increasing that pressure against which the ventricle is pumping, and therefore it's going to increase the after the load off your system, reducing that straight volume in reducing that cardiac output. So that's why the correct answer was an increased after load. So we're now going to move on to renal. So our next question the Rennin angiotensin androsterone system, is very important in control. Your BP. It involves the enzyme A six, which converts and your attention one toe and you tense in two, which I organ produces the largest volume of angiotensin converting enzyme or a special. But in you guys, you guys know right system very well. Keep those bones is coming in quite a bit of a split, but split. I'll give you five more seconds. Okay, 21 in the poll there, So we've got a bit of a three way split somewhere between the kidneys. The liver is in the lungs. That's okay, because it's quite a confusing system on all three of those organs are involved, so it suggests you know a little bit about the system, so we'll go over it. So the correct answer here is lungs, which was see so well done to everybody that put that That's really good. So that's go through the rest system. So the Renan Andrew tents in Aldosterone system overrides for sure is basically a hormonal system that within the body that's really important for, as we said, controlling BP and controlling fluid balance in the body, which is ultimately going to affect your BP So we'll talk through it really systematically. So it starts with Renan, which you can see here just by the kidney. So running is released from certain cells in the kidney called granular cells, which have found in the renal drugstore glomerular apparatus, which is a part of the kidney nephron, which is really close. The glomerulus, basically on that part of the kidney, is really important because it detects low BP, and it does this mainly by detecting a low sodium reaching the kidneys. If there's not a lot of sodium, it suggests cause sodium and water tend to follow each other. If there's less sodium. There's probably less water and therefore the BP went down. It does detect it in other ways as well, but that's probably the main one that you guys need to know. So going a little bit backwards on this diagram and you're tense. Synergen is a precursor molecule and you're tense in one which has talked about in this question. And you're 10. Synergen is produced by the liver, so angiotensin one is produced. Went NGO 10 saligen is converted to angiotensin one using Renan. Okay, so angiotensinogens 100 his one by the action of runnin and you're tensing. One is then converted toe and you're tense and toe but angiotensin converting enzyme, Which makes sense because it's the enzyme which converts the one type of angiotensin to another. On this conversion maybe occurs in the lungs, which is also where this enzyme called ace, is made and it's mainly produced by the end of CD of cells in the blood vessels within the blood vessels in the lungs know angiotensin two has many effects on BP, so it increases sympathetic activity. So you think five from flight, so it's gonna cause vasoconstriction to increase your heart rate, which all going to raise your BP. It's also going to increase the reabsorption off electrolytes within the kidney within the p C. T. In the collecting ducts said, for example, keeping your sodium not letting that be excreted into year ends. Same of chloride retaining water. Israel. That's really important for raising BP. Um, and just remember that wherever wherever sodium goes or whether salt goes water is going to follow it. So if we retain water, if we retain sodium, we're going to retain water. And if we retain water, we're going to increase our blood volume on because there is more volume of liquid within a close base of our blood vessels off BP will rise it, also under intense and to binds onto his receptors, which leads to aldosterone secretion now are just runs really important for raising BP is well, it has many different effects, but it mainly has a similar effect to the direct effects of angiotensin two of increasing sodium reabsorption within the kidney. As I said before, it raises, um, BP by constricting or what arteries in our body, which will then, as you can imagine, it's decrease in the volume of the blood vessels. So if you decrease the volume, put pressure on that fluid is going to raise the BP on finally as well. It's going to cause 88 secretion from the posterior pituitary. Um, and we know that 88 is a hormone that increases. Read a water reabsorption sorry in the collecting ducts of the kidney. And so what that's doing is that's bringing back water back from the urine filtrate back into the blood vessels, which once again grazes that blood volume raises that BP. And once that BP has risen, there is a negative feedback loop, and that will decrease the amount of rain in released from the kidney. What's also important to know is running. The amount of running can also be affected by a M P, which is a natural pick. Peptide, which is basically a M. P. Is released by the stretch of the atria. So you can imagine as your BP rises. Um, you're like we spoke about before. Your BP and the volume of blood will rise so that venous return back into your atria will rise and the myocardium will be stretched when that myocardium structures that releases the A M. P. And that tells the kidneys. Hang on. We've got quite a lot of blood volume here. We've got high high BP. We don't need to be releasing all this run in to then cause of these effects to raise up BP. We can stop there, and we don't need to do anymore. So in this question, it was saying about this eight enzyme. It's one of the key enzymes in this pathway. And just remember these three main sites angiotensinogens liver, Brennan kidneys and eighths lungs. So our next question in a 67 year old man has been admitted with drowsiness and has recently been having a chest infection. He is diagnosed with COPD, and he's treated for respiratory acidosis. This is when blood acid it increases because the lung struggled to remove the CIA to in the blood. What would the kidneys due to compensate for this Acidosis? No, it's the Po. Thank you. But in in the poll best. So the majority of you got this question right? Really? Really Well, don't graze. So the answer is be so the answer is to re absorb more by carpet, and I'll explain why that happens. So this is quite a busy slide. Um, but what we're gonna do is if you break it down. So in this case, it's detected that the there's an increase in carbon dioxide a Z patients retaining. See? Okay, Now, what's really important to remember is that oh two is an acidic guess, so it could make it. There's too much of it. The blood can become acidic. Um, on bicarbonate is more of an alkaline substance, so it does the opposite. So if there's too much so to what the kidney will want to do is increase the amount of by common reabsorbed in into the blood in order to prevent that acidosis from occurring. And this occurs in the proximal convoluted tubular, the p C t. So I'm going to talk through this diagram slowly because I appreciate that it's quite a complicated diagram ast how we get bicarbonate from PCT so in the urine filtrate back into the blood. So first of all, what happens is within the cells of the P. C. T. Um, hydrogen irons are pumped out into the Lumen, where the urine is in the P C. T. Via sodium hydrogen exchanger, so sodium is coming into these cells. Hydrogen is leaving into the urine filtrate. This then combined with any bicarbonate, which is in the P. C. T. Lumen, where the urine is to form called carbonic acid, which is hate to see Oh, three that you can see here. Um, and that's capitalized. That then isn't around very low, and it is converted to water and carbon dioxide, and that's catalyzed by the enzyme carbonic anhydrase. This water and go to can then go back into the cells in the P. C. T. And the reaction can basically be reversed this time so that water and go to those back into our carbonic acid, which can then decide. Oh, she ate back into hydrogen islands on bicarbonate. It's. It forms a little loop here with sodium, allowing the hydrogen islands to move into the Lumen of the P C. T. Where the urine is so this once This is DC dissociated, the hydrogen irons can go back into the Luminal PCT on that forms. That cycle on this bicarbonate could be pumped into the blood using a sodium dependent bicarbonate exchanger here. So the sodium that's was in the Lumen then goes into the cells lining the PCT on then that could be pumped in the same directions by carbon it into the blood. So as a summary summary, because the commandant side is acidic, we want to neutralize that in the blood. And so the kidney will increase absorption reabsorption back into the blood of bicarbonate, using this mechanism in order to reduce that acidity. So I hope will those renal questions made sense. We're going to go on to respect you now. So the degrees of ventilation profusion within the lungs different at different levels within the lungs. Which of the following best describes the pattern of ventilation and profusion within the healthy lungs? And this is when someone is sitting upright. Brilliant. I'll give you five more seconds. Get those answers in. Okay, three, 21. Brilliant. Thank you so much So it's a bit of a split. I think the most popular answer seems to be, um, but sadly, that's incorrect. While done to everyone that put D that is the correct answer. So the ventilation in the profusion are both greatest belong bases Um, I appreciate this is a hard topic to grass, so let's talk for it. So this is my diagram of the lung. So we have our two lungs on. We have our appear on bronchial supplying them, So let's quickly talk through some definitions. So ventilation I like to think of as the change in volume of gas or air within the lung tissue. So it's if something is well ventilated, it means that the alveolitis changing volume a lot. So if it just increased a little bit, that's not very well ventilated with the Alvesco like changing in size a lot, that's a sign of really good ventilation. And profusion is basically the total volume of blood reaching the palm very capillaries in a given time period. So within a minute, for example, that's basically the amount of blood reaching the lungs to allow for Gap Gas exchange. So the reason why I've ventilation is greatest at the base of the lungs hasn't found out from this question is because pleural pressure. So the pressure within the pleural space that Becky spoke about earlier so between the two layers of the pleura is more negative at the base of the lungs, and you can imagine that negative pressure is back, it was explaining. Pulls the lungs out with it as the chest wall expands on. If that pressure is more negative at the basis than what it's gonna do is it's gonna have a greater grip on those alveolitis pull them out words towards the chest wall that's gonna pull the hour, pull the alveoli like acts more on. They're going to expand more. That's gonna increase their ventilation. As we said, there's gonna be a bigger change in volume in the valve your life. Another factor that effects. Why those increasing ventilation at the bottom of the lungs is because of gravity. Know if you can imagine the lungs themselves quite heavy, so the when you're sitting upright, the alveolar alvie, a light at the bottom of the lungs, have the mass or the weight of all of the lungs above it, sitting on top of them so they can end up being quite squished. Whereas the albuterol like the top of the lungs, there's no as much lung tissue sitting about them, so they're not necessarily a squished. They're less less kind of contracted together. They're a bit more. They're bit more open if you like. So when we breathe and we ventilator lungs, there is a bigger change in volume in those alveolar like the base of the lungs, then at the top. Because as that air rushes in those alveolar at the Boston that were really, really squished and didn't have much volume to begin with, well, then expand on. They have a lot of expansion rose, the ones at the top. When that air comes in, they are already slightly expanded anyway because they're not a squished so that change in volume, their ventilation will be lower. That's why there's increased ventilation at the base of the lungs. Profusion is for a similar reason in terms of gravity's, and profusion is also greatest at the base lungs because of gravity. Because if you can imagine blood, it has a mass eso. Gravity is going to pull it down words more towards the base of the lungs rather than putting in the extra effort, let's say to pump that blood up to the top of the lungs. So we move on to our next question, which is slightly related. A 29 year old female presents, the any was sudden onset shortness of breath. On examination, she has found to be tachycardia acts or high heart rate and is coughing up small volumes of fresh red blood off. After performing a CT Palmer angiogram, which is basically a scan which looks at the blood vessels within your lungs, a pulmonary embolus is found in her right middle lobe. What would be the VQ ratio in this part? The lungs. I'm going to give a couple more seconds. Um, well, in the polls, guess so. I think the majority you mainly spit between zero and infinity, which is along the right lines. That's really good. The majority of you went with be for infinity, and that is the correct answer is a very well done. So let's explain this, so we'll go back to this diagram. So the VQ ratio is basically a measure of the difference between the ventilation to a certain area of the lungs, on the perfusion to a certain area of the lungs. Now the ideal VQ ratio would be one if you want to maximize our lung function, and that's because the ventilations the amount of air reaching the blood vessels on the amount off profusion is the amount of blood getting to the alveoli. Life would be the same, so there would be a 1 to 1 ratio between the blood and the air. And therefore it suggests that all the blood says that come along to the lungs are going to receive all of the oxygen that they need on. We're gonna have very good primary lung function. However, as we just spoke about, the ratio of Bentyl a shin profusion on how much there is in different parts of the lungs varies depending on what part, the longer women. So within the apex of the lungs, ventilation tends to exceed profusion. So even though both of them are highest at the base like we said in the previous question, the ratio between the two changes so ventilation is higher than profusion. At the apex, rose profusion is higher than ventilation at the base. So in this question, we are talking about this ratio of Vita Q. So I'm gonna look at it. So here we've got, uh, what would happen if mentally a shin is not occurring on what would happen if profusion is not occurring so If we say that lvot eyes not being ventilated, it's not receiving any air to it. Then if we look at this fraction here, ventilation will be zero. So we put zero on top on a Q would be whatever the fusion is for that. So that part of the lungs So we do zero over any number that always brings out with zero. Um, unless I say that, because when there's blood that's getting to analgesia, all right, but there's no gas to exchange with in this scenario where this lady had it embolus or some people have a clot as well. It's very similar. Blood is coming along to the audio, but it's not able to reach it to do any gas exchange because the profusion is being stopped and it's not occurring because this clock is blocking it basically. So if perfect perfusion was Norco and going back to our ratio, V could be whatever the ventilation is. But the profusion is going to be zero. So if we do any number over zero, it gives us infinity, which is why the answer to the last question was infinity on. This tends to occur in situation such as this where there's an embolism or clot that's blocking the lungs and not allowing it. Alveolitis be venter to be perfused sorry or it also occurs in anatomical dead space within the lungs. So there might be part of the lungs that receiving Aricept was the trachea and the bronchioles. They've got those of air in them. Um, but you're not going to refuse those because you can't do gas exchange over those surfaces on their four that would also have a VQ ratio of infinity. So we're going to go on two g I. So our next question a 45 year old male presents to his GP with indigestion. His BM wise 36 he has a 39 year pack history. His GP suspects gastroesophageal reflux disease or good, and it's that explains, the patient has symptoms that caused my stomach acid, mainly comprised of hard cast it irritating his lower esophagus. Which of the following is not responsible for secreted gastric hormone, which decreases hydrochloric acid secretion? Brilliant lows of answers coming, rushing in. That's great. I'll give you 10 more seconds. 321 pretty and thank you. So the majority of you got this right. Really? Well done, Grace. So the correct answer is be, which is Jesus Hours. So what I've done is I put together a little table for you. I won't go through it all now because it's quite a big table. Basically all the cells that you need to know where they are on the hormones they release and how that effects acid secretion. So, as you can see from just briefly from this table, your enterochromaffin cells they found in the stomach, they release histamine on that causes an increase in heart card acid secretion GI cells also found in the stomach, um, released gastrin and late Well, system you lightheaded cork acid secretion and your vagus nerve. So your vagus nerve is mainly a person pathetic nerve that releases acetylcholine on that stimulates 100 forecasted secretion. Which makes sense because parasympathetic we think of his arrest and digest loves er hydrochloric acid is going to help us digest food. So therefore it's going to stimulate a person. But that nerve is going to stimulate acid secretion so that we can digest our food now seeing or chewing foods, anything in the cephalic faded phases of digestion which you may have heard off. That leads to stimulation of the vagus nerve on the vagus nerve acts on parietal cells, which I've written about in our second table, which actually secrete the hydrochloric acid. GI cells are, um, activated by the vagus nerve on they say release gastrium that goes into the bloodstream on get finds its way to the prior to cells, which then causes the hate sale to be released on the and enterochromaffin cells as, say, they release histamine Onda. They release that into the stomach and that histamine binds onto page two receptors on the prior to cells, and that's what causes them to release the hydrochloric acid. Then we have these four other types of cells that are in our question D s incase cells, which released various hormones that you can read here, which all inhibit 100 contrast in secretion. These are other important cells that you might have heard off in your GI I teaching. So chief cells, they secrete pepsinogen, which is a precursor to Patteson, which is a protein that breaks, which is an enzyme that breaks down proteins on do these cells as well. The five your cells basically mucous, and that's really important because it lubricates your food, your food bolus that's gonna move into the duodenum in your small intestine and that mucus also coats the epithelial lining of the stomach on protects those epithelial cells from acidity. So let you guys read the rest of that, um, table in your in time and commit that memory. So our next question a 52 year old female visits her GP for her three monthly B 12 injection. She was diagnosed with a B 12 deficiency for years ago. Where in the digestive tract is B 12 absorbed. Okay, great. Great ounces coming in and I'll give you 10 more seconds. Okay. Free 21 in the whole day. So well done. The majority of you got it right. Don't worry if you didn't know this one. This is one of those things I think sometimes can be missed in teaching. It's it's more of an issue item. Um, so the arteries days, it's the terminal ileum. So I wanted to quickly talk through B 12 because it's very important on gets absorption is also one of the more complex. So to start off with, why do we use B 12 or B 12 is really important in DNA and are on a synthesis, um, blood cell production and also lipids synthesis. So it's important for making the myelin sheets that coats are nerve fibers to make sure that they stay nice and healthy and conduct really well. So I've tried to make this diagram to make it clear. Let's talk through it. So vitamin B 12 is also called about cabal um in. And that's mainly phone in food such as eggs and meat and fish. So that's going to head down to the stomach. Will come back to that in just a second when we digest that. And what you need to know is that saliva grounds to create a protein called Had to corn, which along with this food, travels down to the stomach. Now, as I said, we have, um, Enron, such as pets in that break down the proteins in these food on when they do so they release B 12, and as I said, this happened. Coroner's traveled down to the summit. So now in the stomach, we have this B 12 and we have this hap to corn on in the stomach, where we have a low pH in a very high acidity. Be 12 has a high affinity for haptic or in, and therefore they bind together. On this form is the B 12 hats. Korean complex on this conflict is really important because by binding on to have a core in B 12 is protected from the stomach society and what be broken down at the same time. Within the stomach, a different protein called intrinsic factor is released from the prior to themselves, which you may have seen on my table in the last diagram. For the last question that is also releases they from the prior to cells on heads. With this B 12 have to Korean complex off to the duodenum. So within the Judean, um, as we know, the acidity changes. So it's the stomach is very acidic, the duodenum is less acidic, so a disappoint. The B 12 is released from the hat Corrine due to the halftime being broken down by proteases from the pancreas, which breaks down. This have to call him protein on that, then allows the B 12 to bind onto the intrinsic factor instead. So now we have a B 12 intrinsic factor complex, and this, once again, is for the protection of B 12. But this time against pancreatic enzymes, which, being considered factor protects against. So then this interesting factor. B 12 complex head through all of this moment, test in until it gets to the terminal ileum. On here. The B 12 intrinsic factor complex is absorbed once a day gets into through the cells where it's absorbed. B 12 is then transferred to another molecule called Trans Cobalamin, which allows B 12 to be transported to all the issues throughout the body. So this is quite important part way to know. But for this question, you may need to know where is between absorbed. And that's where the B 12 intrinsic factor complex is absorbed, which is in the terminal terminal ileum. So our last topic of the nights and pharmacology, so activation of different classes of adrenal receptors affect tissues differently. Which type of adrenal receptor causes bronchodilation amazing. You guys are really smashing this question. You know your pharmacology. I'll only give you five more seconds. Brilliant, really well done. We've got overwhelming majority majority. There's the world on everybody. So yes, well done. The correct answer is beast to adrenal receptors on. This is really important clinically, because this is the mechanism of salbutamol. You'll talk to her in that in a second. So adrenal receptors I won't go through this side for because it's unfortunate just something that you have to kind of commit to memory, but just a son. Summary. The adrenal receptors are basically a class of G protein. Couple of receptors which are targeted by molecules. Hold catacholamines that includes adrenaline or general in think of all are kind of fight or flight reflex related molecules. So we have five main types of angina receptors that you need to know to alpha receptors, one in two on three beaters 12 and three. The main thing that you need to know is there effects which are on this slide on also where they found. So alpha one receptors are found in the smooth muscle of blood vessels that therefore, if you think vital flight, what we want to do, want to. So that's gonna cause peripheral razor construction so that all of our blood is diverted back to our main organs to make sure we survive. Um that's the main effective Alpha one. Adrenoreceptor is the bladder sink to contraction is also another effect that can have mainly focus on the basic constriction. Um, altitude is found in pre selected nerves. That one's less common. Uh, then we have beetle one and B to These are probably the two main ones that you need to know. Subito One adrenal receptors are found in the heart. They increase the corona trippy of the heart, so they increase the heart rate. The drama Tropea, which is basically the conductions speed through the ab note, and they increase the heart. I literally be a swell, which is the force of contraction of the heart, then beats. Two receptors are found in the smooth muscle, mainly in the trachea, which is what was required for this question. On their main effect is bronchodilation. So if you think when you're having a fight or flight response, you're running away from that really scary thing. You need lots of oxygen to make sure that your muscles come work and you can perform that aerobic respiration. So therefore, the best way to get more oxygen in is the bronchodilator, Um, and therefore that's what salbutamol is it's a beat two agonist. So it acts on beach two receptors to activate them and cause that problem dilation, which can be used in an asthma on be 23, is less common for that sound. In fact, tissue and other post. So our last question of the night Well, don't make it this fall Verapamil baby used in the control of arrhythmias, angina and hypertension according to the vomiting is classification. Which class does verapamil belong to? So last question A Z many hours has become on the pole. Even if you don't know if I guess because it's on last question Great answers coming in. I'm going to get 10 more seconds quite hard. One to finish on. If you don't know, Don't worry. But just pop in the guess You never know. You might be right. Okay, 321 also since is okay, So we've got a bit of the split here, mainly between B, c and D. And that's okay because it's a This is quite a hard question. Um, well done total of you that put d d is the correct answer. Which was the majority of you. So very well done. But don't worry if you found this one hold because this is definitely a hard question. So the form Williams constipation off drugs is used to describe different drugs affect the action potentials within nerves, mainly. So each of these drugs basically affects a different part of the ventricular action potential. So our class one drugs are, uh, sodium channel blockers. So in phase zero of a ventricular monocyte action potential, um, we have sodium going in which depolarizing is our Oh, no. So on. Therefore, if we block that, then we're not going to get the action potential. Our class two is over. Here is our beater blockers. So these block those are genetic receptors that we were just talking about. Class three is our potassium doctors, which block this phase three of our action potential and class for calcium channel blockers, which includes verapamil, which was the answer to this question which effects calcium. So it's a calcium channel blocker. In this question, we sneakily put in class five, but classified just know exist. You don't need to worry about cross five. Um, so it's really important that you know these it's sadly another thing. Just have to commit to memory because in questions they might give you the form Williams classifications drugs rather than a drug name or their mechanism of action such as a beet book or calcium General block. And they might just say its class for now, expect me to know. So hopefully this diagram makes sense is their actions And where in the ventricle actually attentional they So that is the end. Well done, everyone from making it this fall. Thank you. So so much for coming. We really hope you enjoyed it. Um, if we can get the feedback formalise that's been released, that's great. Um, if you feel that in, you'll get the pdf to, um, this presentation. We've also added on some extra questions as well for you to go through for other ones that just great last minute revision before your exams. And if any of you have got exams coming up soon, we wish you the best of luck. We hope our sessions last home and today of really helped, um, we recommend it's a joining your main our mailing. This just to make sure you hear about all our pre clinical sessions coming up, we've got one tomorrow at seven o'clock