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Ok. Ok, good evening everyone. Um Can someone please just drop us a message in the chat to let us know if you can hear us and then we'll get started in a couple of minutes. Ok, lovely stuff. Thank you, Paul. Ok. All right. So let's get side. So, uh, welcome everyone. Uh My name is Harish and with me, I have uh bart with both fifth year medical students at UCL and today we're gonna be talking about jaundice and liver failure. So just before we get started for those of you who haven't been to teaching things before. Welcome. It's nice to have you. Uh We do weekly tutorials open to all starting at six o'clock every Thursday and we do a various number of topics and we always have our presentations reviewed by doctors to ensure that we're not feeding you rubbish. Um Please do follow us on the teaching things page so that you get notifications for future tutorials and all of these tutorials will be available including the slides after the event if you want to refer back to them. Ok, so let's get started with jaundice. So before we get started, can someone in the chat. If you're willing, tell me what is jaundice um in time if you're gonna say it as a medical term, what is jaundice? Was it caused by? If someone wants to drop a message in the chat, just give it a second. Anyone feeling brave. Ok. So jaundice is hyperbilirubinemia. OK. So this is when you have excess bilirubin in the body resulting in yellow discoloration starting with the eyes, um which is known as sclero ius. And then followed by that, you, you see the yellowing of the skin. So the normal levels of bilirubin in the body is about 3 to 17 micromoles per liter. Um Once it reaches above the 30 level, that's when you start to see jaundice of the eyes. So your first um like the first thing you'll notice when you have jaundice is that clear away to us in your eyes. And then once it reaches above 50 that's when it starts to affect the skin and the rest of your body. OK. And this the the cause of jaundice has various causes and we'll split them up. But it's, it's some result of some either some kind of impaired excretion or increased production of bilirubin, which is then deposited in the eyes and skin because of increased reabsorption. OK. So let's just first quickly go through the normal physiology. Now, this diagram looks very confusing. So I'm gonna talk through it and on this slide, I also have it kind of in a bit more of a worded form. OK. So starting off, we have red blood cells and these go under death or you know, there might be some kind of hemolysis going on. OK. And this gets then split into your two components. So it gets split into your glo globin component and your heme component. Now your globins, they get converted into amino acid. They're is for uh protein synthesis and your heme component gets split into your iron, which is then transported using transferrin. It's converted back into ferritin in the liver. And then again, it's used to reproduce your red blood cells. Now, the other part is biliverdin and this gets converted into bilirubin. Bilirubin then is um transported to the liver. Um And at this point, it's an unconjugated form. Now, what that means is it is insoluble, OK. This insoluble bilirubin gets converted in the liver and this is done by this enzyme called u uridine diphosphate. Glu I I'm not gonna try to say this. It's converted by this really long enzyme name. OK. Um uridine diphosphate, glucuronosyl transferase. Um So this is the enzyme that converts this. Now, this then gets converted into a conjugated form of bilirubin, which is then uh stored in the is is in your bile, it's in your gallbladder and then it goes into the small intestine. And this, at this point, bacteria converts this bilirubin into lin. Now, some of this will get reabsorbed into the body, very, very small amount. And about 10% will get uh excreted by the kidney as urobilin. But the majority is excreted in the feces as stercobilin. Ok. So that's kind of your normal physiology. And again, you'll be able to look at these slides later. So you can kind of go through this um in a bit more detail. So what is causing jaundice? Now, the best way to think about this is your prehepatic hepatic causes and you're post hepatic. Now, post hepatic is almost always some kind of obstructive cholestasis. So something blocking your bile duct from getting rid of that bilirubin and transporting it into the small intestine, which is why we can say post hepatic jaundice is obstructive cholestasis. So let's go through these. So prehepatic jaundice. Now, this is anything that is increasing the breakdown of red blood cells uh resulting in the increased release of unconjugated bilirubin in the blood which causes jaundice. And this is because your body is enable to, is unable to kind of maintain and it doesn't have the capacity to, you know, convert all of this excess extra bilirubin into a conjugated form and excrete it. So you get increased levels of unconjugated bilirubin which then gets absorbed into the the body um and deposited in the eyes and the skin. So there's a number of causes here. So you've got your autoimmune hemolytic anemia, any kind of increased hemolysis, sickle cell disease. G six PD deficiency, um thalassemia major and then you've got these couple syndromes down here. So, Gilbert and uh Craig Nara. So let's talk about a few of these. So autoimmune hemolytic anemia. Now, this can be a bit confusing but so there's two types, there's a warm type and a cold type. Now what this is means and essentially is a warm type is, first of all, it's done by I GG antibodies and this happens at body temperature and this happens at sites such as the spleen, these kind of extravascular sites and this is caused by a number of things. So, autoimmune diseases, any kind of cancer and it can just be idiopathic um and sometimes drugs such as methyldopa can cause this and you treat this using steroids and just treating the underlying disorder, your cold autoimmune hemolytic anemia. On the other hand is I GM antibodies and this only really happens when it's quite cold. So it's about four degrees um temperature and this is mediated more by my, more by complement and it's commonly more intravascular. So just within your blood vessels and these result in things like Raynaud's and they don't really respond well to steroids and again, caused by things like cancers and this also infections. Ok. So, hemolysis and I think this one is kind of self explanatory. If you have acute bleeding and acute hemolysis, um and increased breakdown of red blood cells, you have increased levels of unconjugated bilirubin being produced and like I said before, the body just does not have the capacity to conjugate this. And instead it gets reabsorbed into the blood and gets deposited in the eyes and the skin resulting in jaundice. Now moving on. So sickle cell, um G six PD thalassemia, these are all issues to do with misshaped cells. And this can sometimes cause hemolysis, especially when you have like a sickle cell crisis and you have blocking of er vessels and all of these things which can increase your bilirubin. I'm not gonna go into these too much um other than G six PD. So this is a deficiency of a very key enzyme within the blood cell itself. And this is involving this specific pathway um which when you have a deficiency, it increases your susceptibility to oxidative stress and this can cause jaundice, but more specifically in the neonates because they just can't, they, you know, they're, they're very new, obviously, the they're newborns, they don't have the ability to kind of manage when there's increased um oxidative stress in the body. And it's exacerbated in adults by things like fava beans. So broad beans infections and your sulfur group drugs. So, so your sulfaSALAzine, sulfonylureas and sulfonamides. So this is something that you have to be aware of when you're prescribing um these medications. And then we have Gilbert syndrome. So this is one of our two syndromes. So Gilbert syndrome is a lack of the UDP er enzyme. Um So this is the one that conjugates your bilirubin. So Gilbert syndrome is, you have a reduced amount of this enzyme, which means that you have this isolated rise in conjugated bilirubin. And what this means is when you get, when you come to do your investigations, especially like your LFT S, your LFT S are completely normal, but you just have this isolated rise in bilirubin. Um and it's usually unconjugated, it doesn't present with any other symptoms and it's typically exacerbated by any time when there's increased stress on the body. So that's just, you know, it could just be exercise, it could be fasting, um and it could be some kind of intercurrent illness. So, for example, it's currently the month of Ramadan, some of you may be fasting and those pa those people with um Gilbert syndrome.