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We're live now. All right. Brilliant. Um, good evening, everyone. Um, I hope you all can hear and see me. Okay, um, if you can just put in the group chat that you can Another group chat. Sorry. The message chat that you can hear me and see me. Okay, um, you should see on the screen, Um, all about the kidneys by myself, Um, in a picture of the kidneys in the background. So if you can see me, if you can hear me, all good. Just pop something in the group chat or in the chat so we can just see OK, Fantastic. And can see a few people um, saying that they can seem so That's brilliant. Um, so yeah. So my name is cotton. I am an ex, um, imperial alumni. Um, So who am I? Yeah. So I graduated from Imperial 2020 in medicine, Done my BSC in bioengineering. Um, and I worked as a doctor in, um, in E b h. Specifically Broomfield hospital. Um, so if anyone is, you know, planning on working in Broomfield Hospital or the chance that area definitely hit me up on LinkedIn, I'll be more than happy to give advice. Um, and I currently work as an educational specialist with Oxford Medical Simulation. Um, so essentially, I look into how we can integrate virtual reality with medical education. Uh, we actually see a bit of that today in, uh, in my session. Um, so hopefully you guys will enjoy that as well. Now, um, today, as you know, we're doing a reading topic that's going to be the focus on today. Um, we're going to be focusing on a few topics. Um, AKI dialysis briefly on dialysis CKD and read a transplant as well. Um, now, the purpose of this talk, Yes, I know it's the finals, and I know that you guys are all gearing to go, but I want the purpose of, um, this session, too. Yes, Address final related topics, um, and knowledge, but also prepare you for, um, the world beyond that, which is when you actually become and start working as doctors. There are few things that, um, works in theory, but not so much in practice. So we'll go through the topic between AKI and dialysis. We'll have an interactive session. Um, where we'll actually go into virtual reality to see a patient. So hopefully you guys will be able to see that all well as well. So AKI So we all know what AKI is. Acute kidney injury. Um, simply put the kidneys art functional. Well, um, they're not working at their best or the optimum. Um, and it's quite a common thing that we see in the hospitals. A large proportion of the patient that you be seen in the hospitals will have, um, kidney related issues. More specifically, AKI as well. Um so it's very important topic for you to be aware of and also know how to manage and in terms of the management is actually quite simple as well. Um, and when you when it comes to a k, a lot of the that the solutions are quite repetitive as well. So once you're able to grasp AKI unable to grasp management plan for AKI, you're able to deal with a lot of patient's as a result. So there are certain factors that you need to be aware of when it comes to dealing with a K I. And the reason why I want to make sure that you're aware of these factors is because um allows you to categorize individuals based on risk. Um, so there are certain individuals that you'll be more keen or act proactively when it comes to AKI because they have a greater risk factors. So one being above the age of 65. This is a massive risk when it comes to a K I. And the reason for that is because they're over the years. As individuals get older, there's progressive a flow sclerosis of the vascular job that supplies and kidneys. So as a result of that individuals as they get older, they're more prone to having AKI as well. Recent surgery There's another big one, especially abdominal surgery, and and the reason for that is because with abdominal surgery they tends to be. It tend to be quite a messy surgery, and therefore you're at risk of, um, infections. Um, and in addition to that, you also are more likely to lose blood, so individuals who follow up from surgery tend to suffer from hypervolemia. Um, so again, this is something that you need to be able to pick apart when it comes to the history of your patient, certain medication use, you guys are all aware of. You know, the common ones, Um, NSAID for instances, loop diuretics, ACE inhibitors and so forth. And these are all medications that can have an effect on the kidneys. So you know whether a patient's medication history has these particular drugs is very important to know, because you'll be able to identify the one they're risk factor and number two, um, that these medications need to be stopped. Um, of course, if you have any questions as we go along, please do pop it in the chat. I have it on my phone on the side, so I'll be able to see um, where you are. Also, a background of some CKD um, chronic kidney disease or previous repeated histories of AKI also makes the kidneys more prone, um, to, uh, impairment. And the reason for that is because we have CKD or repeated episodes of AKI. The overall functionality of the kidneys over time reduces. Um so further insults actually brings down the threshold, um, further down. That makes it more likely for an individual to happen. AKI, um, recent use of contrast again is very, very important, especially with our patient's who, um are doing or having CT Scan's A lot of CT scans nowadays actually use contrast, especially when you're looking at the Abdel pelvis. Um, you usually they're radiologist will go for a contrast because it gives them better clarity of what they've seen, um, in the abdomen and the pelvis. So it's very important to be aware of whatever history they've had, not only outside of the hospital, but also inside the hospital. Now, this is a one that I've put at the bottom because it is something that if you can pick up quite early, um, it will help you quite a lot. Uh, and these are individuals, especially the elderly or those with a disability who have carers who look after them. Um, we do, you know, have, uh, great carers. But sometimes they have multiple patients to look after. Um, it may not necessarily do certain things for the patient's that they're looking after. So being aware that certain individuals with carers may not necessarily have the optimum fluid intake, Um, it's very important because, of course, if you're not drinking enough, you're not hydrating the kidneys. Well, um, and as a result, you can end up with an acute kidney injury. So I've spoken about obviously the simple term of describing AKI, which, being literally a re, uh, the kidneys aren't working well, but there are three main ways in which you determine. Um, if a patient has a k I now this is this works in theory. However, in practice, it is very challenging. Um, so the freeways on which we identify an individual has AKI is one. There's an increase in 26 many modes of creating over 48 hours. Um, there's an increase of 50% or more in creating over the past week. Or there's a reduction in urine output to below no 0.5 mils per kilogram per hour. Um, So, for instance, if you take a 60 kg, um, individuals, they should roughly be passing 30 mils of urine in an hour. Now, the reason why this is a bit challenging when it comes to real life is because a lot of the Times patient's don't have, um, pre existing blood within the last 48 hours unless they've been in hospital repeated times. Um, and again, they don't have bloods within the last week for you to then enact out 0.2. So sometimes it's very difficult for you to determine whether an individual actually has AKI and what we tend to do in practice, um, is that we look at a the average, um, of the patient's blood over the last couple of months or the last, uh, set of Bloods that they've had. Um, and we take that average as they're normal range. A lot of the computers nowadays are able to actually calculate the average when you go in to see the creatinine or any other value, Um, with the patient's bloods so looking at that average and then seeing the if there's any discrepancy between that patient's resting our average and what you currently have for that patient comparing those two and seeing if there's a general in, uh, incline in terms of results, that can act as a way for you to determine AKI. And then again, with the third point, Uh, no patient comes in telling you exactly how many meals of urine that they've passed so again, it's very challenging. Um, it's very challenging for you to be able to determine that as well. So we have a question here, um, is the increase in serum creatinine over 40 hours, calculated as proportion of their body body weight. Know? So that's a general, um, general increase for everyone. We usually don't calculate it in terms of body weight. We just simply say there's an increase in 26 million. Most, um, over 48 hours. You class it as a K and treat accordingly. Um, but of course, with creatinine, you have to be quite cautious because, for instance, if the person has eaten a large amount of red meat in the last 12 hours, that would actually cause you're creating levels to be much more, uh, much higher. Um, if the person for instances a body builder again that will cause your creatinine levels to be much higher, Um, if they have less body weight. So, for instance, if they're an M. P t. Um, this can also call you creating to be lower. So if you take it with a pinch of salt, Um, but generally speaking, you have a low threshold when it comes to treating and AKI Um and the reason for that is because the solution to treat an AKI tends to be quite, um, quite simple in terms of, uh, what you do. So even if it's not AKI, it will benefit the patient somewhat. Um, so in terms of the third point, how we tend to do go about this is that one. We tend to insert a capital, um, and by inserting the capital will be able to determine if, uh the patient has passed X amount of urine over a certain number of hours. But again, that only happens after the patient's come in. Prior to that, we go by literally history of how many times have gone to the toilet, Um, and the color of the urine as well. So it won't give you the exact amount for you to determine. You know, whoever they've passed below no 0.5 mils per kilogram per hour. But it will give you a rough understanding of whoever. The urine was concentrated, um, and also the free frequency of the U. N. As well. So that's something to note when it comes to real life. So yes, theory when it comes to finals, yes, those are the three ways in which we determine AKI, but in reality it is much more challenging than that. So always have in the back of your mind other ways in which to determine a K and a lot of the time it comes with the history. Um, so yeah. So, as I said before the beginning of our session, Um, yes. So, yeah, I've already I think I already answered the question for finish. Um, but as I said at beginning of our session, I'm gonna give you information for your finals, but also prepare you for the reality of working in the NHS. So when it comes to categorization of the causes of an AK I we all know this is our bread and butter. We know it to be pre Reno Reno. Uh, and pulse read. Um, okay. And this is Please do not forget this when it comes to actually applying this in real life, we tend to forget, and we tend to treat a lot of our patient's with AKI straight off the bat as pre Reno, make sure that you do a thorough investigation or for a history taken to determine which one of these falls under and then treat accordingly. Don't automatically assume that it is prerenal, although that is quite common with the patient's that would come in. Okay. Now, in order to understand the prerenal causes, you need to understand the diagram that I have on the left hand side will go into that in a short while. But the key thing to remember is that when it comes to promotional, the causes are quite simple. All you have to do is remember a ski mia. Okay, Now, the scheme scheme is a major prerenal course of AKI. Um, and there are a variety of courses as that results in the scheme. So the scheme would basically mean a reduction in blood supply to the kidneys. Now, the diagram on the left hand side, we have free main factors that determine grow Merrill. A filtration. Okay, So glamorous situation. Meaning how much we're able to filter through the glomerulus into the tubule. Now we have going in one direction. That hydrostatic pressure. So this is the the hydrostatic pressure. Is the pressure coming from the Afrin and the reference, uh, materials, Uh, and then we have the colloid, um, automatic pressure and the fluid pressure working in opposite direction, coming from the actual nephrons itself. So when it comes to thinking of the causes of prerenal. Um, you can always refer back to this diagram and think of how these things, how these different factors can affect these three different pressures that we're dealing with. So the first thing that we can talk about is a reduction in blood supply. Okay, Now, as I said before, um, elderly individuals or those with disabilities or with carers are quite at risk of having hypovolemia, which is one of the causes of ischemia. So here what happens is that the hydrostatic pressure, um, that is needed for glamorous job situation is reduced, um, as a result of the reduced blood supply, Um, and as a result, you have an increase in terms of the balance, you have an increase in the colloid osmotic pressure and the fluid pressure out way in that of the hydrostatic pressure. So the overall net direction, um, is not glomerulus association or rather, there's a reduction glomerular filtration. Okay, you can also see a reduction in blood supply when it comes to, um, cardiac and liver dysfunction as well. Now, these two organs are so so important when it comes to the functioning of the kidneys. So we have cardiorenal syndrome. We have hepatorenal syndrome. Um, so the fact that we've given them actual title's really does indicate their importance and how they inter link. So if you have any sort of impairment with the other two sort of. For instance, if you've had a patient who has had a heart attack or who has heart failure, this can actually end up impairing the function of the kidneys and result in the scheme. Because again, if your heart is not pumping well, is not pumping blood to the necessary organs, including the liver. I'm sorry, including the kidneys. Then we have liver dysfunction. So if you have a very scerotic, uh, liver for unfortunately, the back up and the pressure that results from that can also cause a ski mia when it comes to the kidneys. So these are two organs that you need to be very much aware of, So a patient may not necessarily come with a low BP or vomiting or diarrhea. It may simply be that they have a background of heart failure or they have a background of alcohol, liver disease, and as a result, that is impairing the function of the kidneys. Um The other thing that we need to be aware of, which are are in tandem is renal artery stenosis, um, as well as medication. Um, that we certain patient's maybe using, um and the reason why these two things can have an effect and cause schema again going back to the diagram. Certain medications have an effect on the diameter, um, of the Afrin and the efferent arterial. When it comes to, uh, the supply of the blue Marylise okay. And then the same thing with the A renal artery stenosis the narrowing of the renal artery then results in a reduction in the hydrostatic pressure. So again, the arrow moving in this direction as a reduction in that, meaning that there's more of an effect of the colloid asthmatic pressure and more of an effect of the fluid pressure resulting in an overall reduction in the glomerular filtration. Okay, so that's the key thing to remember here. Medication such as A C inhibitors ARB s and said, and even, um Newt diabetics as well all have an effect on the hydrostatic pressure and renal artery stenosis have a physical effect by narrowing the blood vessels that lead up to the kidneys. Now, the great thing about when it comes to a K I is that a lot of these issues are reversible. Okay, so that's why it's so important for you to identify what the cause is straight away. Um, And treat it accordingly because, uh the longer you leave it, the more the kidneys are exposed or having these sorts of impaired function, and eventually it will go on to become irreversible, where you can't really do anything about it. Now we have renal, um, causes. So this is the part that is usually skipped over by a lot of medical students because, um, it opens up into a whole pill A to of things, um, that you need to be aware of. But I have broken down into very simple categories for you to remember. Um, and the way to remember is think of the different parts of the nephron. So one, when it comes to Reno or intrinsic issues that cause a k, I think of one issues with the glamorous, so this can be glomerulonephritis, which is very, very common. You can also have issues with the tubules, which can, which comes from acute tubular necrosis, which is again one of the most common causes, um, of intrinsic or Reno AKI that we have issues within the actual space in between the nephrons or in between the tubules, which is the interstitium. So here you have acute institutions, Interstitial nephritis. Then we have issues to do with the vasculature that supports the nephrons. Um, and here we have vasculitis is TTP Um h us, all right. And of course, we have the various other parts, um, left the toxins which have direct effect on these, um, structures, Um, the ones that we commonly know, as I said before medication. But there are other things such as my a global in, um causing rhabdomyolysis, um, and tumor lysis syndrome, which real releases a lot of electrolytes such as potassium, um as well as nucleic acid, which can impair the function of the kidneys. And again, as we mentioned before, contrast again can have a direct effect on the kidneys itself, not just the prerenal aspect. Now, the reason why you have all of this, why the reason why these things are quite an issue when it comes to the renal problem is they are they perpetuate Um and the reason for that is let's take, for instance, glomerulonephritis, which is inflammation of the glomerulus. Um, what it does is that it really release it results in an increase leakage of the blue Marylise, which end up results in, um a passing through of substances that should normally not pass through, um, and one of these structures being the red blood cells. Now, once the red blood cells enter the tubule that then go on to form red blood cells or red red blood cells costs which you can actually see on your analysis. So again, it should be alarm bells or red flags when you see red cell cars on urine analysis or your N N C. S. Um, because it goes on to show that there is inflammation going on as well. Now, with tubular necrosis acute tubular necrosis, it commonly follows on from pre renewal causes of AKI. So if you have prolonged AKI, it can actually result in acute tubular necrosis following from their scheme, and that happens now. What happens with as a result of that is that the epithelium cells, because they die off, they actually detach from the basement membrane and then form clumps themselves. Okay, um, and we call this epithelial cost. Okay, so we have red cell cost, which we mentioned before. Um, and we have a a fellow cost. Now, once this epithelio cost has been formed a lot, it's the immune system, which then brings in inflammatory processes including, um, getting the white cell count and white cells, which when they were in the tube, you then go on to form white cell cost. And this is a perpetuating process. So it's very difficult and challenging to deal with renal causes of, um, an a k I. And it's very important for you at that point to involve the nephrologist or the renal, uh, the renal doctors, because they'll be able to take it further than you would as a your doctor. Um, so it's very important to remember these issues. Um, now, the reason why we go on to hold off a lot of medications when it comes to, um, renal AKI is because the tubules are actually quite prone. Um, two vessel constriction. So what happens in Reno? AKI is that because of the ongoing inflammatory process, the ongoing, um, immune process, there's actually a release of peptides, which causes vasoconstriction of the Afrin and, uh, effort or material. And as a result of that, if you then had, um this particular individual taking, uh, Neffa toxins or certain medication their threshold for them actually having further insults will be very low because already have the peptides that are swimming around the tubules and the nephrons, um, causing vessel constriction. So that's the reason why we stopped or hold off. Nephrotoxic is when we are dealing with a renal AKI. Let's just check if there's any questions at the moment. No. Okay, so post Reno now post Reno is one of the simple groups when it comes to the causes of, um, an an a k I, uh, And here you need to be close friends with the urologist because they are going to be very helpful when it comes to dealing with a lot of the, uh, post renal causes of AKI. Now I think of it. An easy way to remember is that it's pipe work. Um, so if you think of, uh, the renal tract, literally, anywhere outside the renal pelvis can be a site for post renal causes and all you need is an obstruction. Okay, so you can start from the top and have renal cancers. And if they're causing an impairment to the flow of urine, this can also result in an AKI. We have renal stones, okay, which can also cause impairments to the flow of urine. We have Reno bladder cancers. We have cervical cancers, prostate cancers as well, and prostate enlargement. So even simple things such as BP h, which is very common, um, common as men get older and also very common in the Africa Caribbean, uh, community as well. The this will then impair the flow of, uh, urine outside of the body and as a result, can lead to a backflow of urine which causes pressure on the kidneys and then impairs its function. So with post, you know, actually ends up resulting in premium. So it's not Actually, the obstruction itself is causing the the AKI is rather the backflow or the impaired flow which results in renal related um, issues. Okay, so remember when it comes to post, you know, very simple, always feeling covid as pipe work and think. Think that n any structure along the way can cause a post renal, uh, AKI and I've put a uti again, technically, not an obstruction. However, if you have a UTI that tracks up to the kidneys formula, for instance, a palan arthritis, uh, this can also result in post renal AKI. Now, investigations are very common for you to carry out. Um, and it's very good if you're in the E D department as part of your rotation. Um, the medics will be very much happy for the information as much information as you can provide them. Um, so the common things, the bedside things that you can easily do urine dip gives you a lot of information in terms of protein. If there's any blood, and then if you're dealing with with an infection again, it will help you rule in or rule out certain, uh, causes. Then we have your in M. C. N s again infection, but we also give you information on the cost. Whether there's red cell cost, there's white cell cost. Um, and there's epithelial cost as well. You have urine PCR RNA, see, are we no longer do PCR because it takes quite some time and you choose over 24 hours. So we usually now do a spot test, which is the a c R. Which gives you all the necessary information that you need. Um, and it's very important to have when it comes to, uh, glomerulonephritis as well as, um, ckd. Okay, then we have input and output monitoring again. This is very key when you are thinking that this patient has a prerenal cause of, um, an AKI because here you're able to see how much a patient is passing in and taking in and how much the patient is actually passing out. They also give you an indication of whoever there's an obstruction because if you can see that the patient is passing, taking in a lot drinking, you know, liters and liters of water, however, isn't passing out a lot. Then it may give you may start to signal that this patient may have some sort of obstructive picture. And of course, blood's using these, especially because you need to be able to determine whether you're dealing with an A k I, as well as the severity of the 80 I because certain, uh, certain levels you need to start, including the renal doctors for them to take over. Then we have blood. Scan this. I would really advise a lot of people to do that. If you're thinking of obstructive causes, especially when the patient first comes in because you were able to identify that one. Is it truly an obstruction? Because it was truly an obstruction. You should be able to see some sort of retention, um, in the bladder. Um, and also, if there isn't any retention, but we're still thinking obstruction, then it may be that the actual obstruction is above the bladder as well. So the bladder scan gives you a lot of information as to the state of that patient, then renal ultrasound. Um, usually we reserve this for when we don't know what the heck is going on. We need more information. We we can't think of anything from the history. Um, but we think that there may be an obstructive picture, or we think there may be a renal cause, so we usually reserve a renal ultrasound for that. Then we have C T k U B, which again is quite useful when it comes to obstruction. It helps light things up. Um, so you're able to see exactly where the issue is as well. So these are the common investigations that you carry out. However, when you speak to um, when you speak to nephrologist, we're going to speak to a urologist. They may ask you to do specific tests that is relevant to their department. So when it comes to um, management of AKI, it is pretty much supportive therapy. Um, and it involves a good combination of fluids and stop in certain medication. Okay, now, fluids. You have to be quite careful with how much fluid you give a man over what period of time. Um, and the reason for that is because we've impaired kidney function. One of the functions of the kidneys is to actually secrete waste, So if there is impaired function, it may not necessarily be able to do that effectively. So if you're pumping the patient with a lot of fluids, it may that end up worse in the AKI. So you always have to. There's a There's a middle ground essentially when it comes to, uh, managing AKI with fluids. But the key thing to remember is do not give loop directed, directed specifically to boost urine output There are certain situations where you would give loop direct explore, for instance, if the patient is fluid overloaded. But if there isn't any fluid overload, um, and your solar using loop direct Ickes to, you know, increase the urine output. This will be doing so artificially, so make sure that you don't do that. Make sure that you also don't use dopamine to increase renal profusion. Um, there's not something that is practice, um, as well. So make sure that you don't do these two things and, of course, treat the underlying cause if there's an infection. Antibiotics. If there's a renal stone, you remove it. Um, usually get the urologist involved. Uh, if there's an obstructive capita, flush it, um, and change the cavity are you may need a freeway capita as well to ensure that there is any further obstruction. Um, but the key thing to understand is know when your remit is done. You know when you what you've done is reached this limit, Okay, so if you're dealing with a patient that is has quite severe AKI, I wouldn't expect you to try and remedy it all in one goal. Do all of the necessary things that you're supposed to do as a junior doctor. Then hand it over to the nephrologist, who then give you further input. Um, if you don't know what the AKI is again, go back to basics prerenal Riedel pulse renal. If you go through all of that and you still can't figure out exactly what's causing the AKI, then definitely get the nephrologist involved. And as I said before, obstruction can also result, uh, can rose the results as a cause of AKI. And in those cases, get the urologist involved and they'll be able to, uh, have an input on them now. As I said before, um, as well as given fluids, there are certain medications that you need to be aware of. Um, there are medications that you need to outrightly stop because they can cause a worsen AKI. And there are certain medication. You stop because, um, they they increase toxic levels in the blood or in the body because the main way in which you Claire, uh, these particular jobs is via the kidney. Um, so those medications include metformin, lithium and digoxin. Um, these are three things that you free medication. You need to be aware of If the patient is on, uh, has AKI So you need to stop them because there's an increase of, you know, toxicity as they build up, because the kidney no longer can function and therefore it can't get rid of, um, these free three medications, Of course, the medication that you should definitely stop because they were worse in the renal function, As I said, NSAID. But of course, aspirin is the cardiac dose for aspirin, 75 mg. Don't worry, that won't cause harm in a in a ks, or the patient can continue that I mean, no glycosides as well ace inhibitors, um, a R B s and diuretics in general. And then we have on the left hand side the medication that you can continue. Uh, I know that there won't be an issue when it comes to dealing with the a. K I. All right. And then one of the things that you need to definitely be aware of is, uh, potassium. Now to a tip for you to always be able to identify. The patient has high potassium Duavee B g. When the patient comes in, uh, yes. To do your bloods but the blood. You should take two hours approximately to get back to you. Um, but if you do a V b g will give you straightaway. How? Well, a snapshot of how well the patient is doing will give you key information on the user knees. But we'll also give you information on the lactate, which will give you a determined a determinant of how dehydrated that patient is. Um um and also give you an understanding of what the Ph is, which will be a reason for you to be able to, uh, involve dialysis or not. Um, but of course, if you have high potassium, um, you need to be very much aware of what you need to do. Um, so one making sure that you're doing the E. C. G or cardiac monitoring to see if there's any changes in the e. C. G. And if there are making sure that you're giving calcium gluconate. So when there is a change in the c g, those are the only times in which would involve gas calcium gluconate. And be aware the nurses are won't give the calcium gluconate. Well, majority of nurses won't, um, it would involve. It would require you to actually give the calcium gluconate and a lot of the time you have to stand there and literally press the syringe at a slow a slow rate. Uh, so be aware of that. When you do prescribe calcium gluconate, you may have a nurse come to you and say, Oh, can you give it because I'm not qualified and so forth? Um, we all know the insulin and dextrose infusion. Um, it defer. It may differ in different hospitals and different Dean Aries in terms of their guidelines. But one thing that is not commonly used is nebulized albuterol. Um, now you have to be slightly careful because we're salbutamol. One of the side effects is of that is tachycardia. Um, so if a patient has an ongoing tachycardia, probably best to hold off on giving them the last albuterol. Although it will cause a shift in, uh, in potassium from extracellular to intracellular. Uh, but it will worsen that patient's tachycardia. So just be aware of that. Uh, then we have, of course, other things that would probably only be initiated by, uh, the renal specialist. So calcium rizzo knee um uh, loot direct ticks and dialysis. Now, what I'm gonna do now is I'm going to stop this particular, um, this particular screen and we're going to actually go jump into a scenario with a patient. Um um and you're going to essentially tell me through the chat what it is that you are seeing, um, and what it is that you want to do, So this is gonna be very interactive. Um, and I'm hoping that you guys will be able to engage with me as well. So I'm gonna just change my screen. It, um So we have a 80 year old patient attending the E d. With vomiting and diarrhea. Um, so just bear in mind this is the case that we're going to be dealing with today. So this is virtual reality. Um, that you be able to actually point practice what we've learned. So it's a bit different to maybe what your other, um, uh, lectures have been doing. However, I have access to as part of my job. So for will be a good idea for us to utilize this as well. So I'm gonna play it, and hopefully you guys will be able to, um here. It's okay. Um let me see if I couldn't go back in. Can you get Can you guys hear me? Okay. I'm really worried about this new patient, Maria. She's eight years old and has just survived in the department, complaining of feeling sick and palpitations. I haven't had a chance to find out any more information, but I think she could should serve you. Can you come and see her pants? Hi, Valeria. I'm your doctor. Escape, Please leave. Fine was coming so quick. I feel dreadful. Can you guys hear that? Okay, So what I'm gonna do is I'm just gonna We're gonna go through the scenario and then hopefully be able to read the caption, cause I don't think Meadow is allowing me to essentially play both on this side. Um, so, yeah, I would just read. Let me just change the to hide the text so you guys can see the screen. OK, um, so we have a patient, 80 year old patient who is coming with some diarrhea and vomiting. Um, so we're just gonna go ahead and find out a bit more as to what's going on. So we have a lady who has come in vomiting and diarrhea. Is there anything that you want to do right now? If you're a doctor, Um, obviously looking after this patient. What information On what things you would you want to do? I want to see you guys put it in the chat. Um, and then we can take it from there. So you guys will go direct me what I need to do. And as you know, there is a time on the back. Um, so hopefully you guys will be able to give me, um, give me some response soon. Yeah, Look at her BP, and that is correct. So her BP is quite low. Um, what would you guys wanna do for that? I'm hovering over it. So be so. You'll be able to see it. Um, so I really want to give her some fluids. But how much would you want to give? Given this patient's age of 80 years old? I just poured the whilst We wait for that. You have fluids. Good. How much we want to give in terms of fluids. 250. Most fantastic. So when it comes to elderly patient, um, you always want to start off small. Um, rather than going heavy. Okay. So obviously cannula his name place. So let's get some calendars in place. So we're just gonna put in the cannula. Good. So 250 mils, no 2500.9%. Slowest through okay. You can go one liter over 12 hours. However, I would opt for you to give a bolus first. Um, And once you got the bolus in, once you ate within good range, then you can give something slow over time. So we give 215 mils. So it's usually good for individuals who are quite old or who have a cardiac related background. So let's find out a bit more. So this lady had, um, went to her daughter's over the weekend. Uh, for those who can't see the captions, I'm just gonna read out for you. Um, and she ate a dodgy, um, barbecue, Essentially a dodgy hamburger. And ever since then, she's been sick. She's had bad diarrhea, um, literally coming out of both ends, Um, and also, uh, vomiting and diarrhea. And as a result of that, now, at this. So we're gonna ask her if she has any other symptoms, whether she's been hot or sweaty Now, why do you think we are arcing? That whether she's been hot or sweaty and if there's any blood in the store, if you just put in a group chat? Yep, she has lost a lot of fluid over diarrhea. That's correct. And why would we ask about the hot and cold if you guys can just answer to that hot and cold while? Is that part of the history? Yep, fantastic. So we want to just make sure that there isn't any ongoing infection with this patient as well. So it's very, very important that yes, when you're assessing patient, you keep an open mind, Um, with what they have. So the reason why is because certain patient may come with one issue. But some people may actually come with more than one issue, so it's always important to keep on given over in mind. Now, what are some risk factors that we've identified from the history that we've just taken? Can anyone sport that out? So risk factors for the AKI? So as we mentioned before, I've already gone through it. So what are some of the risk factors that this lady has. That may mean she has an a k I. So just keep it coming through the comment section. Good age over 65. Fantastic. Lots of fluid. Pre, you know, cause of AKI. Fantastic. Anything else? I don't think I think that's all at the moment. All right, let's find out a bit more. Okay, so let's find a medical history. And while we're doing that, we'll get the nurse to also take some bloods as well. And also, take some blood coaches. Okay, Good. Excessive fluid loss, Faridi and be fantastic guys. So she has heart problems. Um, And she also has had, um, Rosa has had a history of she has breast cancer, so she had a heart attack a few years ago. Um, but the pay, um, and she's had she actually has heart failure. So it's good that we started over 2 50 mil, uh, again. Otherwise, that would have worsen her. Her levels, uh, for the heart failure. And the doctor says that she has kidney related issues as well. So the kidneys aren't functioning as well as she should, um, as it should. And she's also on a hormone tablet as well. Okay, All right. Now let's find out if she's on any medication. So she's not taking any prescribed any, um, out over the counter. So any other medication apart from a prescribe medication, So she's taking quite a few. She's taking ramipril this by super low piracy to more aspirin. So can you guys just put in the group chat? Which ones will be a problem for us when it comes to, um, a k I and I'm just gonna give her a bit more fluid because it's, uh uh, Still, on the low side, she also takes a g t m, which is the screen under the tongue, and she takes hormone know tablets for breast cancer. Good. So ramipril fantastic ramipril will be a problem. Okay, Aspirin. Obviously, we don't know the dose, so let's just find out. Let's have a look at the computer. So she's on aspirin. 75 mg. Again. That's cardiac. Protect protective. So again, a small dose. So it won't be much of an issue. The water tablet. Fantastic. Somebody picked that up. Brilliant. G t n. Not the same as, um the johnson. Just a spur underneath the tongue Um, and the Jackson would more likely be for if she had a history of a F or atrial fibrillation. So the main things that we need to be worried about is the ramipril. Uh, the freezer, Meyde. Uh, and that's pretty much here. Everything else we can pretty much continue. Now. Let's just take a V B G as well, just to see what things are due, How things are going right now. You know, we'll see if she has any allergies as well. So she's allergic to penicillin. Uh, it upsets her stomach and also kept Cody makes her feel sick. So unless you just do a quick system review, considering that she's been, you know, passing, she's vomiting and diarrhea that just find out a bit more. So no difficulty when she pees. But she hasn't been paying much. Okay? She can't keep any fluids down. So again, these are all risk factors for us to be aware of. So we've given her some fluids. Um, is now 100. Usually I'll go one extra and give another 2. 50. Usually, if I can get the patient to, like 1 10, um, systolic, then I'm usually quite happy, and then I'll put the patient on maintenance. So let's just update the patient. So they didn't know exactly what's going on to updated our patient. Okay, now the VBG results are here, so, as you can see, so pauses. You can see we have a low ph 7.28. So this patient is currently acidotic. What else is problematic on this particular E c g. If you can just put in the the chat as well. What else can you see? That is problematic in this on this, so no e c g v b g. Yep. Potassium is 5.8. Good. So we're dealing with hyper Kaleem eah. Um, and again, as we mentioned before, this is a common finding when it comes to a K I, um because there's an impaired, uh, secretion or excretion. Sorry of waste products? Um, yep. Low bicarb and high potassium. Good spot. So hyponatremia. Okay, good. Metabolic acidosis. Yep. Brilliant. That's the overarching A feature of this V b g. Uh, Now, the thing to remember is that when it comes to, uh, acidosis, usually what happens is that you're you're respiratory will kick in first before your kidneys, Your kidneys take a lot of many days for it and then correct whatever is going on. So the first one that usually kicks in is your breathing. Okay, so now let's have a look at the blood results. So I'm just going to pause it again. So again, this pretty much confirms what we have going on. But now we can see that there's a creating of 100 and 50. Okay, so we do. Do we have an impaired? And do we have an A k? Would you say we have an a k? Let's see if you can put in the group chat or in the chat. The question is, do we have an ongoing AKI? Uh, so we need to know her baseline. So again, this this is again while saying the issue when it comes to patient's who come in, especially when you don't have any sort of history from the patient. So in this particular case, because we don't have any history, we will take the normal range and base it on that. So the normal range for the upper normal range is 100 and 20 in this case is coming we're creating over 100 and 50. So we would treat it, um, as an AKI because there's an increase in creatinine as right you said, um, by finish, there's an increase in creating it, Um, by more than 26 modes. Uh, Mac, most. So it's very, very important to remember that a lot of the patient that you come to to, uh, come to meet won't have a previous history, um, for you to be able to compare things. But if you look at the normal range, we'll look at you know, any history that you have any blood history that you have and see what the average is of that, then you'll be able to roughly see, um, if there's an A k I or not. We can also confirm that there isn't any infection. Um uh, as well. So we don't need We need to worry about that, but and even given her, you know, lots of fluids. Her lactate is fairly okay, which is quite reassuring as well. And look at her e g f r c e g f. I is 33. We'll touch on e g f r in a in a short minute when it comes to, uh to that. So now obviously we've identified There's hypochelemia on the background of AKI. Now let's find out. Let's treat that hypochelemia. So, as I said before, we need to be able to determine if there's any impaired heart function. So they just asked her if she's had any chest pain. All right, William. So that's reassuring. She hasn't had any chest pain or any palpitations. Yep. So she can't lie flat for long and see for three pillows. Um, and of course, it has been the same over many years. Mean that there hasn't been any drastic change recently. And that goes on to fit in with her heart failure background as well. Um, now, let's have a look at your e c g. So, as you can see with an E C g. Can you guys just put in the group chat? What you can see on this E C G. Yeah, and I know E C. T s are quite challenging, so don't be worried if you don't necessarily get it right. I just want you to see Tell me exactly what you're seeing tend to t wave good and What does tend to t waves indicate hypokalemia Fantastic. So, again, this confirms, um, what we found on on our V b g and our bloods. So again, with the e c g changes, it goes on to indicate that this patient will require, um, calcium gluconate. Okay, because there has been e c g changes. And ideally, we need to put this patient under cardiac monetary as well. So let's go on and give her this patient some calcium gluconate. So again, the dose in may change will be different. Um, to your hospital. So we're giving us some calcium gluconate. Uh, let's actually treat the hypokalemia. So in this case, uh, medications, Um, and then we'll go on to, um sorry. Oops. Let me go back. So here, 10 units soluble incident and 25 g. Um, glucose again, your hospital may do something different, so make sure that you check that now we can give salbutamol. But why would I not give salbutamol? What here would prevent me from giving salbutamol? I want you to just put that in the chat. Good. It's good. So patient is tachycardia. So remember, Fantastic. So remember, tachycardia is a major issue when it comes to, um, salbutamol is one of the major side effects of salbutamol. So it's very important for you to note the heart rate before you decide to give salbutamol. So here it is not necessary for us to give the salbutamol. Um, because one, we already have an alternative, which is the insulin and the dextrose. Um, and number two, um, this patient has a high heart rate. Okay, so we've given that. So once you give that normally, what I would do is you'd leave, like, roughly 30 minutes for you to then repeat the V b G just to see if there's any improvement of, uh, the potassium. Okay, so let's go and just speak to our senior and find out what the senior would want to say. So we start some management for hypochelemia, which is good. Um, we want to monitor her as well under a cardiac monitor, or just continue doing e c g. Um, And again, as I said, we need to repeat the gas. Care to see if, uh, potassium is improvement, improving with treatments. And then, of course, you want to withhold an effort toxin. So we found out that she was on remand Peru and Theresa my information that we don't prescribe. Well, if we do prescribe it on, um, on the drug chart, make sure that you put some crosses in place to prevent the nurses from giving those particular medications. Okay, so let's just repeat the V v. G. And then we'll also have a few of her belly when she's done, and then I'll give us some longstanding, uh, fluids as well. And as you can see on the red mark or the red on her skin. And the red wristband indicates that she does have an allergy. So always keep be aware of, you know, the surroundings. Okay, so we're just gonna have a few of the belly. Okay, so she's in a bit of pain, and so she's most likely suffering from some gastroenteritis. Um, as a result of eating that dodgy hamburger as well. Um, so something to be aware of. All right, so let's update, um, And what? Before we do that, let's just doing some urine dick. And then we also put in a urine capital because we want to be able to measure the output, input and output So we have a capital in place, which is draining quite well. Let's have a look at the urine results. So urine result is quite reassuring again. Doesn't indicate any infection. Um, and blood is negative, and protein is only Plus, we usually worried when there's protein free plus two plus and so forth because it goes on to indicate that is usually a renal cause of the patient's AKI. So let's have a look at the second VBG that we've done. Um, so there is a slight improvement in the potassium not think that Great. Um, how there is improvement with the sodium lactate isn't has improved as well. So again, we're heading in the right direction. Not completely there, but we're heading the right direction. So that's that's I'm gonna come out of this scenario. You pretty much don't know that we need what I've come. I've done a put across all that I wanted to get you to see, so we're gonna return back to our session. So just close this, especially one second, Okay? Hopefully, you guys can hear me. Can you guys hear me? Okay. Brilliant. Fantastic. Um, cool. All right. So we've all obviously dealt with a k R. We've gone through a scenario with a patient who had a k i, um, specifically pre renal AKI. And we dealt with one of the complications being high potassium. So again, this is what you would experience when you are, you know, on the ground dealing with these patient's. So always remember that you know, yes, you're having you're dealing with the a K. But also remember the complications that may result from it. And I'm gonna quickly breathe through a few other things because I know that where time is quite short. So dialysis. The key thing for you to remember is that dialysis this comes into play when things aren't going right or when, uh, when you know what you've done is not working. Okay, so the best way to remember dialysis and their indications with dialysis is a e I o u so ab and acidosis or in this particular patient that we dealt with Ph was 7.28. It was less than seven 0.1 then. This will be an indication for dialysis, electrolytes and balance as well. So, again, hypochelemia that we dealt with if the hypokalemia was still raging high even after treatment again. Indications for you to, um, use dialysis intoxication overload. Um, as well. If you can't really get rid of that overload with, um, the necessary diuretics again, indication for dialysis. And lastly, things that people tend to get is you remake pericarditis and your a mc encapsulitis. So you're making careful itis the patient will be there will be a change in the patient's mood and aura. The patient maybe a bit more confused as well complained of headaches, for instance. Um and you you make pericarditis. The patient may have chest pain, which, um, fluctuate, which comes and goes with the patient's breathing. Um, or even with hardly as well. So always bear this in mind. And if this is coupled with a very high urea again, keep that in mind for your a MC pericarditis or your a mc encapsulitis. This is something that can be easily missed. Um, when you are assessing patients' so let's go into CKD. Um, So again, AKI is abrupt decline in each and a g f r c k d. On the other side has happens over a long period of time. Um, so when a patient comes to women Acute deterioration in, um, the each year. Far, we don't say that the patient has CKD. We need to see that there's been a casual trend over time which would indicate that the patient has ckd AKI reversible potentially CKB once you've reached their, unfortunately, it's irreversible. You can't turn back the, uh, turn back time, AKI. We usually the treatment will be targeted to reverse the disease. Or, you know, so whatever the issue is this causing the AKI in CKD, On the other hand, you're literally treating the complications. Okay? You're trying to prevent the complications and trying to prevent the progression of the kidney failure. Okay, so that's the key differences they need to know between AKI and CKD. So, as I said before CKD, your focus is on the complications raveling disease. But in order for you to understand what it is that you're treating in Oh, sorry. What was the Oh, from, um, overload. Okay, So overload. Um fluid wise, Refractory to medication or diuretics. Okay. All right. Brilliant. Um, so yeah, So in order for you to understand what it is that you're managing when it comes to, um CKD. You need to know the other things that the kidney does. So obviously we know that the kidney is involved in secretion or waste for this re absorption of the great stuff and flu balance. But there are other things that the kidneys, uh, responsible for one vitamin D processing and number two area for priority in the hormone production. Okay, these are two other factors that you need to be aware of or two other functions of the kidneys that needs to be aware of. So let's talk about vitamin D. So the kidney is one of the factories for the activation of vitamin D. Okay, kidneys that you can see on the diagram on the right hand side is part of the process for you to successfully activate the vitamin D for it to then go and do its job without the kidneys. You don't have a fully activated vitamin D, and therefore vitamin D can't do its job. Vitamin D is responsible for the re absorption or the absorption of calcium, and it maintains that calcium homeostasis Okay, so, literally, if you have a problem with the kidneys, um, long term CKD you have a problem with vitamin D activation. And if you have a problem with vitamin D activation, you then have an issue with the calcium balances as simple as that. And the issue here is that no matter how much vitamin d you pump that patient with okay, if it's not activated, all right, it's not going to do its job. Now, as a result of this, um, you get a few issues due to this low vitamin D one, you get a high phosphate. Okay, Now, the reason why you get a high phosphate is because the kidneys itself can't pass out the phosphate. Okay, so in general, you get rough. You produce roughly 5600 mg of phosphate in a week. Dialysis can only clear up half of that in a week. So as you can see, there is still some surplus that's leftover. Now, with this hype of phosphate, it can go into cause forever issues. So who? Okay, so why is an ace inhibitor renal protective in ckd nfo texting me? Uh, so is a very interesting question. And the reason for that is because with with ace inhibitors, uh, they are they help with the remodeling um, of the heart, Uh, when it comes to heart related issues or heart related complications, which are which, actually very permanent prominent when it comes to CKD. So usually when you have CKD, you tend to have a lot of cardiovascular related issues. Um, when we give a sin, him bitters, ace inhibitors actually cardioprotective. And by being cardioprotective, they end up also protecting the kidneys as well. That's a result of the those two combinations. However, AKI, um, their effect is that it actually ends up producing glamorama filtration, whereas in CKD that reduction in glamorous filtration actually helps with CKD because the kidney is actually not overloaded with the world that he needs to do. So that's that, in a nutshell. But again, I can find you, um, some papers for you to, uh for you to explain that essentially after this, um, lecture as well to make it that but as a as a whistle stop tour into how ckd how ace inhibitors is more useful in CKD, but less so in AKI. Okay, so remember Reno Reno protective cardioprotective okay, usually tend to have cardiac related issues when you have CKD so with ace inhibitors being cardioprotective, um, as well. If they have an effect on the kidneys, Um, And then when it comes to, um, AKI ace inhibitors actually reduce glomerular filtration, whereas in CKD, this effect is actually beneficial. Okay, so hopefully that answers that. But I can I can give you more information if you, uh if you want more. Essentially, um, So yeah, so when it comes to, uh, chronic kidney disease, the low vitamin D there's high phosphates because it's reduced or impaired clearance. Um, or phosphate phosphate also acts as a binder for calcium. Okay, that's one thing that people need to remember. Phosphates access a binder for calcium. So if you have high levels of phosphate in the blood is gonna bind up to three calcium, therefore reducing the amount of calcium okay. And that's a result of that's why you get low calcium with CKD. Okay, another reason why you get low calcium with CKD is obviously due to the lack of it's activated vitamin D. So if you don't have an activated vitamin D, you can't absorb the necessary calcium from the diet and from the food that you eat. Okay, so that's the key thing to remember then we have secondary hyperparathyroidism again is literally a perpetual cycle. So because you have high phosphate, um, and also low vitamin D, you have low calcium and because you have low calcium, the brain and the body kicks in to produce even more or produce more P T h okay. And by producing P th, um, this will respond to the low calcium that is currently present in that patient's body, Um, and also help deal with the high phosphates because I'm very sure that Amir Sam has told you guys the lecture that P. T. H is a phosphate fraction hormone. I'm very sure that you guys have heard that plenty of times during your lectures, but it's very true. P. T. H does do exactly that, and it will help reduce the high phosphate is going on. Um, and also tackle the issue with the low calcium. Any questions on that before I move on? Because it's very, very important for you to be aware of this, and it serves as the foundation for CKD. Okay, I don't see any questions so far. Okay. All right. So, as a result of the this related bone related vitamin D and calcium issues. It also have has an effect on the bone. So by the body trying to replenish the low calcium, it ends up eaten up the bone. Okay, Now, because of that, you can actually end up having a lot of bone related issues. Um, so osteo itis fibrosis cystica, which is a result of over activity of the parathyroid gland, which ends up eating up the bone. Um, so the osteoclasts activity is increased more so than the osteoblasts. Then we have also osteo osteoporosis, osteo sclerosis, osteomalacia, which is basically like crickets, but an older, uh, older individuals. And again, this is due to low vitamin D. So you end up having very, um, um spongy bones rather than having firm solid bones because there's a lack of calcium. Um, and then we have a dynamic bone activity. Um, here there's both. There's a reduction in both the osteoblasts and the osteo class, um, in the bone. And due to this, um, you actually end up having bones that are brittle, um, and don't work as well. Now, can anyone tell me what the um what's that picture on the side is what does that indicate? Yeah. Anyone? Anyone know what that is? Brown tumor. Fantastic. Yes. So that is a brown tumor. Okay, So brown tumor, um, is what you're seeing in that x ray. Um, and again, the reason why you have this so brown tumor tumor is a benign tumor. I mean, it's as a result of osteo class activity in a particular regional bone. Basically, the osteo class has gone crazy and eating up a lot of calcium from that section and the results in brown tumor. So the kidneys, e p o. And anemia. So kidneys are responsible for the production of erythropoietin, so the peritubular or the cells that surround the tubules are responsible for this. So they produce the e p O than the e p o goes and works on the bone marrow to produce more red blood cells. Okay. However, in renal failure, you have, um, issues with this. What happens is that the kidneys themselves, um, don't produce a lot of relief reporting because they're not functioning well. Um, and as a result, there's less activity on the bone marrow to produce red blood cells. But there's also issues with the actual bone can. There can be issues with the bone marrow itself. So if you have high levels of urea, it can actually have a toxic effect on the bone marrow, meaning that even if you have airflow poet in, there's so much that you can get from the bone marrow itself because the bone marrow itself is not working as well. Um, then there's reduced absorption of iron. Can anyone in the group's I'll be very impressed if anyone in the group chat can tell me, um uh, why there is reduced absorption in, um, an iron? I'll be very, very impressive. Anyone can tell me exactly that. And whilst I wait for that will go into the other other things. Um, so anorexia, nausea. So if you have high levels of urea, um, it can actually trigger, um, your chemo receptors, Um, essentially trigger, um, you feeling sick or nauseated? Um, there's also reduced red cell survival, especially with the hemodialysis. Um, that patient's with CKD would tend to have, um, and also there's blood loss because the platelets don't work as well, and the capillaries are as actually quite fragile, so they cause a lot of blood loss to to happen and then if you have CKD or, uh, risk of stress ulceration within the stomach, for instance which can lead to chronic blood loss. Oh, so it's actually due to the reason why you have reduced absorption of iron is because the kidneys actually, uh, the kidneys actually have an effect on hep sudden, um, which is a structure that is important when it comes to the absorption of, um um iron. So hep Sedin actually reduces, uh, the absorption of iron by in, uh, interacting or destroying Farah Farah importing, which are essentially structures, um, in cells that allow iron to go from the gut into the various places that it needs to be. So when you have impaired kidney function, um, you actually end up having high levels of hep students because you're not being cleared away. And because you have high levels of hep Sedin, they attack more of the therapy reporting channels and because they're attacking the fair a protein channels that reduced, um, absorption of iron even when you're eating it. So these patient's can eat a ton of iron from the food. But because the hep student levels are so high, Um it actually affects the absorption of, uh, iron. Okay, so that's the reason why it's always keep in the back of your mind. If you see kidneys and chronic kidney disease and iron, always think of hep sudden. So, management. The key thing here is to always remember that you need to check if the patient actually has the right iron levels. Okay, so the first thing you need to be checking is the ferritin and the transferring levels. Okay, so ferritin above 100 and transparent above 20% is ideal. Okay, So once you have these things set in place, you know that the e p o would then be able to work. There is no point given e p o if the patient doesn't have the iron required to make those red blood cells. So you always want to make sure that the red blood cells and there are enough red blood. Enough iron for the red blood cells are going to be produced. Okay, Now, typically speaking, we normally offer our start off by offering oral iron when we are when we are dealing with low irons in CKD. Um and usually this is reserved for patients who are not on human dialysis or taking, um, any sort of, um, here for Putin, Um, stimulating analogs. Um, And with that, if the patient is taking any of his own, it's on hemodialysis. Then you'd switch it to IV iron. Okay, so that's the prerequisites. So if the patient is not on hemodialysis or I iron, if they are on hemodialysis, then IV iron. But the key thing to remember here is that E p. O also acts as a growth hormone in malignancy. Okay, so remember that, especially in individuals who have a malignancy background such as renal cell carcinoma. Okay, so always remember that E p. O can actually end up having a more detrimental effect if the patient has a background of cancer. And the key thing is, when we're given e. P. O. We want to ensure that there's actually a benefit, and there's going to be an improvement in the quality of life, so it's not gonna have a direct effect on CKD and limits the progression. Rather, E p o would give that patient a bit more energy for them to move on that around increase their quality, quality of life as well. Okay, so transplant. So we're wrapping up. There are four main transplants that we we should be aware of. One autographs. So autographs are transplants, Um, which come from the same person. So the same person as a donor and recipient. For examples of this being skin grafts, for instance, you take skin from one area of the body, Um, and you place in another part of the body. You may have isograft. Okay, which is when the transplants coming from individuals who are genetically identical, such as the twins, which is the most ideal transplant that we we want. Then we have allographs, which is the most common, which is transplants where, um the donor and recipients are, you know, not genetically identical. However, they come from the same species. So again, not the most ideal. But it's what we commonly get. Okay, and then we have xenograft, which is when there's a donor. Recipients come from different species. So between transport between animals and humans, this is not done so much nowadays. So the question that you may typically get is which one last longer in a nut show? Um, living donor transplants last longer. However, by the amount that they last by is only marginal. So for one year between a graft and living donor transplant, the living donor transplants would would last longer by five more percent. And then over 10 years, we last longer over 10%. So again the difference is not that great. But in terms of overall, which one lasts longer, it is the living donor transplants. Now, to understand why they fail, you need to understand HLA so HLA is essentially the tagging system that your body uses to determine whether something is foreign or not. Now there are two antigens or two class advantages that the h l a have so class, um, one in class too. Class one is A B and C, whereas class too is D P d Q and D are when it comes to transplant. Our aim is to first make sure that we match the patient's by D r, which is the most important anti gin. Then be then a Okay, so these are the three that we tend to match by so d r b, then a Okay, if you're able to match According to this, you increase the likelihood of there being a compatible match between the donor and the recipient. Okay. All right. No questions. So far, so good. So remember that the reason why they fail is because there's an issue with this matching. Now, there are essentially, um, two ways in which, uh, individuals can have a rejection of a transplant. Um, one is direct, and one is indirect. So the indirect way, um, again, remember, as I said, the body has a specific tagging system that uses So when you introduce, uh, an organ from a different individual into that mix, that organ will also have its own particular tags. Um, and that will be recognized by the body as a foreign object. Okay, so remember that that's the foundation of understanding, um, transplant rejection. So the first thing that you want to obviously make sure is that when you are, um, uh, when you are matching patient's up, you make them aware of the the likelihood of rejection. Okay, with the transplant now, what happens here is that when the host receives that don't have transplant. The host antigen presenting cell will recognize that the tag on the donor tissue, um, as foreign and then What will happen is that that antigen presenting cell. So as you can see here on my diagram. So the antigen presenting cell, um, will take, um, will digest a bit of that host that donors tag and then present it to the T helper cells. Okay, so the CD four T helper cells, once it presents to the CD 40 episodes, Basically what the antigen presenting cells saying is like, Hey, look, this I don't think this is one of us. Um, I'm just giving it to you so you can, you know, further assess the CD four T cells will assess, and then it will obviously also know that it's a foreign object. And then it will produce a chemical signals, which will then go on to activate B cells to become plasma cells. Okay. And when they become plasma cells, they reproduce specific antibodies for that antigen that was presented to the T helper cells. Okay, so it's not just going to be any random antibodies that's going to be produced. It's specific to the donor, uh, tissue that was initially ingested. Another thing that the CD four T cells will also do is they may stimulate or activate the complement pathway, which is what you see on the side here. Now, the complement pathway will then kick off a inflammatory process which would then start attacking the tissue. But one thing I want you to remember is that it actually forms what we call, um, membrane attack complexes, which is essentially forms pause in the membranes of that donor tissue, um, and then causes it to break down and be destroyed. Okay, so because of that, you actually end up with damage. And Ophelia well, cells, which then activates cytokines and adhesion molecules. Um, and then that results into further inflammation information. Okay, so it's literally perpetuating cycle, and it all starts from the post body identifying the tissue as a abnormal abnormal thing. Um, so that's the indirect pathway. Now, the direct pathway is when the donor tissue shoots itself in the swap. Um, and what it does is that it uses its own antigen presenting cells and goes to the host T cells and like, Hey, look, I'm I'm a a foreign body, and basically the CD four will take that information and do the same thing and start attacking that body. So that's a direct method. So the direct method, the donor tissue does the harm or basically presents itself to the host as an issue. Whereas the indirect the host itself identifies the donors, um, a foreign body, and it works from them. So we have three main ways in which, um, you can get transplant rejection. We have hyper acute, acute and chronic. So hyperacute will happen within minutes and hours from when the patient has the transplant. So it's something to be aware of when the patient comes in a straight of a transplant in they're feeling unwell. Um, you can see that the the Bloods are worsening. Um, and they're generally quite poor. And the reason why this tends to happen is that one. Um, there is a mismatch when it comes to the blood that was used. Okay, um so ab Oh, incompatibility. And number two, the patient already has an existing antibodies to donor the to the donor antigens. Now, this can happen because one of the patient has had previous transplant or even a simple thing as a blood transfusion in the past can also impair, um uh, this transplant and also cause a hyper acute rejection. So? So the history of the patient gives you a lot of information as to, um, what could be the cause? Um, what's going on? And it's not reversible. As soon as that happens, you need to take that patient back into theater. Um, and essentially get that particular, uh, organ removed. So just checking to make sure that we don't have any questions. Okay, We're all good that we have acute, which happens within six months. Um, so here, the patient will probably be, uh, asymptomatic. Um, uh, that's a type of so it's a symptomatic. And you would see that the bloods or the user needs will start getting worse over time. Um, and this happens because there's a, uh there's small Rachel, a mismatch small HLA a mismatch over time and eventually impairs the function of that particular transplant. Um, and this is why we tend to use immuno suppressants because it's supposed to prevent that from happening. Then we have the chronic, which happens after six months. Here. The body has created, um, antibodies over time, which start to attack that tissue and cause fibrosis, so you won't necessarily see an impairment straight away. But the fibrosis, which happens over time, will impair the activity. Um, And then also one thing that can happen with chronic is that you can actually have re occurrence of the original disease. Um, and what I've put here in brackets is the likelihood of which disease, um, will cause, um, will re occur with judiciary transplants. So m c g n in i g h n f s g s. Okay, So this is the in order of the most common to cause re occurrence. All right, so this I was still presenting. So this is essentially renal kidneys. In the nutshell apologies that I may have taken a bit longer than usual. Um, but I hope you're able to gain some understanding of, um, the kidneys. If you have any further questions, please do not hesitate, um, to, um, let me know or contact me through LinkedIn, for instance. Um, I am on LinkedIn. Um, so, yes, it'll be great for you to, uh, send me any questions that you have. Please do. Give me some feedback. I will be returning. Hopefully next year. Um, it would be good to see what I need to improve for the next set of students. Um and yeah, if you like what you saw the m s as well. You can hit me up and we can get chatting about that. So thank you very much, guys, for spend some, uh, this evening with me. And I hope you've gained some valuable lessons both for finals and for, uh through life. Thank you so much. Quantity. Take care.