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Ok, great. So I think everybody can finally hear me, so we can finally start the session. I'm really, really sorry about all the delays, but let's get cracking. Um So just to introduce myself, I'm Akansha. I am an F one at the Royal Free Hospital in London and today's session is about hepatology. Um and essentially study of the liver. It's a crash course on how to, how we can. All the common conditions are affecting the liver and some high yield information. If you've got any questions at all, just send us a message on the chat and I'm happy to feel all the questions. I've got my colleague here here, colleague and best friend PABA on the chat who's mo very kindly moderating. So she'll let me know if we've got a question, but I should be able to see. All right. Ok. Anyways, anyways, let's make a start. Um Yeah. Ok. So the first thing we're gonna do about in the study of the liver is learn how to interpret liver function tests. Because if you can't interpret liver function tests, you essentially can't do anything in terms of the liver. So let's just talk about the different components of about a liver function test. So the things in the liver function test is uh album. The thing, the parameters that we look at in the liver function test is the ast, the alt uh the bilirubin gamma GT ALP and albumin. So these are essentially the markers of liver function that we look at. The biggest markers are the AST and the alt and the ALP. So let's start talking about the AST. So the AST and the alt are things that the liver produces, they're hepatocellular enzymes. So the cells in the liver produce ast and alt. As you can see, the biliary tree goes into the liver and the, and the biliary tree produces AP and even bones produce ap. So this is the most important thing to know. The liver produces AST and alt, the biliary tree and bones produce AP gamma GT is produced both by the liver and the biliary tree, bilirubin is primarily produced by um the liver inr, which is basically a INR is not really a chemical itself. It's just is the amount of time it takes for your blood to clot. Um The reason we measure Inr when it comes to liver is because the liver is the one that produces our clotting factors. So that's why we look at inr in terms of the liver function and albumin is produced by the liver, is that all clear? So if you've got a raised Ast and a raised alt, we can safely say that there is something going on in the liver in the actual liver itself. So, probably not in the biliary tree, not in the bones. So something in the liver is going on that's causing a raised alt and a raised ast. So things that cause a raised ast and alt is hepatocellular damage. And there's many things that can cause hepatocellular damage. This includes ischemia or death of liver cells, cirrhosis of liver cells, which we'll come to later, but is essentially chronic inflammation of the liver cells, drug induced liver injury. So, when drugs destroy the liver and malignancy, so tumors and cancers that affect the liver, just a handy trick is if the AST is greater than two times the at it probably it's an indicator of alcoholic liver disease. But as long as you know that if the only the AST and the alt is right is increased that and it's a liver problem, that's all is ok. The next one is ALP, if only the ALP is rising, rising and the gamma GT is normal, it's probably coming from the bone. So it means there must be like a bone destruction process going on. That can be either a fracture or a malignancy. But it's not as relevant in liver disease. If there's only an AP rise without a gamma GT AST or a TRS. If there's both an AP and a gamma GT rise, we know it's a post hepatic disease. So something is happening in the biliary tree which is causing both the AP and the gamma GT to go up and things that can cause an increase in. So if you see a patient with an increased ALP and an increased gamma GT, you know, there's something blocking this tree or there's inflammation around the hepatic intrahepatic ducts and the extrahepatic ducts. Um then let's talk about bilirubin. So just a quick uh lesson on bilirubin. Essentially, bilirubin is the product of breakdown of red blood cells. When red blood cells break down, they produce unconjugated bilirubin. Um unconjugated bilirubin is processed in the liver and it becomes conjugated bilirubin. So it's really important, you know, the difference between unconjugated and conjugated bilirubin. So the way I remember it is, I suppose it's quite obvious unconjugated means it's, it's not been processed. So it's un un means no. So it's before the liver. Uh this is a really silly way of remembering it and then conjugated, it doesn't have an un. So it's, it's been processed. So it's, that's that happens in the liver. So it's conjugated bilirubin. So let's talk about the difference. So we can test for serum bilirubin levels. So that adds both the conjugated and the unconjugated bilirubin and gives you a total amount of bilirubin in the body. But if you just focus solely on unconjugated bilirubin. If there's a lot of unconjugated bilirubin, it's probably not related to the liver. So there's probably something going on in the blood itself that is causing a lot of unconjugated bilirubin. So it may, so those things could be Gilbert syndrome that happens in infants about 14 to 21 days after they're born. And the other one is hemolytic anemia. So when the red blood cells get, start destroying them, uh start getting destroyed whether that be through malignancy and autoimmune process. So you'll get an increase in unconjugated bilirubin. The more relevant thing in liver disease is an increased conjugated bilirubin. So, if there's too much of conjugated bilirubin, we know there's something in the cells that's causing damage to the liver cells and causing an increase in bilirubin. So these can include things like malignancy, drug induced liver injury, ischemia, inflammation, biliary obstruction. Essentially, anything in the liver can cause an increase in conjugated bilirubin. To be honest, if you just punched me in the liver right now, you'd probably get an increase in bilirubin um and an increase in the liver markers. So, they're quite sensitive. I would say they're sensitive but not specific to liver injury. So, um but jaundice is only truly classified when the bilirubin is above 50. So bilirubin of 30 even though it's high, we'd say that it's not yet jaundice and you get high inr in patients with liver disease because the liver is not synth synthesizing the clotting factors. So your blood's not clotting. Um So you would get more it, your blood takes more time to clot essentially. And a low albumin because the liver produces albumin and if there's injury, albumin won't be produced. So these are the synthetic markers of liver function, sorry markers of synthetic liver function. So, synthesis means uh producing, creating. So that's this. Uh So inr and albumin means that the liver is not working because it's not creating these things. So hopefully that helps with the liver function test. Let's do some questions now. So we can test our knowledge. Ok. All right. So, um these are our normal liver functions, but don't worry about them. You always have them in an exam. So you don't have to worry about memorizing them. Ok. So if you guys just put option 12345 in the chat, um it would be really helpful. Um And then we can talk through this. So a 43 year old lady attends A&E at 8 p.m. with some right upper quadrant pain, nausea and vomiting on examination. You know, she has a BMI of 33 yellowing of the sclera and she states that the pain is worse after eating, given the likely diagnosis, what pattern would you expect to see on her blood tests? So, what, what sort of diagnosis are you think? I'll just give you two minutes to answer. So, over here, the diagnosis is we're thinking about is um probably acute cholecystitis given the, given the right upper quadrant pain nausea, vomiting, the risk factors of obesity, jaundice and pain worse after eating. So we know that this is a post hepatic cause. So something that's happening with the biliary tree. So we probably see a high amount of conjugated bilirubin because it's affecting the liver. So we've got high conjugated bili. So low normal unconjugated bilirubin because it's got nothing to do with the blood, high conjugated bilirubin and a and a low hemoglobin or a normal hemoglobin. So I would say it's probably option. It's option two is the answer for this normal unconjugated bilirubin because um there's nothing to do with the bloodstream, high conjugated bilirubin because it's a hepatic slash post hepatic cause and normal hemoglobin because it's not a pre it's not nothing to do with the bloodstream. OK. Let's do the next question. OK. The following LFT S indicate a problem in which area of the body you've got a normal alt, a normal ast, high ALP and a normal GGT. So alt and ast we know are things that happen in the liver. So those are normal. So we don't think it's going to be a liver problem, high alp. So we know ALP comes from bones and the biliary tree and we know that G TT, the gamma GT comes from both the bones and the from just the biliary tree and the liver. So in the presence of normal GGT, normal ast normal alt, we can say that a high alt is likely because of bone issues. So the answer is option number four. OK. Next question, the following LFT S indicate a problem in which area of the body a high ast high at very high ap very high gamma GT and a normal PT. So we can, so there is both liver dysfunction and but there's even worse post hepatic dysfunction. So the be something really wrong is happening in the biliary tree and is having backup effects in the liver. So it's probably the biliary tree. So the correct answer for this is option five and then uh just two more questions. So the following A FT S would most likely indicate a problem in which area of the body very raised at raised ast, slightly raised. A LP, slightly raised bilirubin, slightly raised GGT prolonged PT. So essentially everything that can go wrong has gone wrong in this poor person. Um We know that if it's a very raised alt, we know that the alt to if the alt is twice the twice the ast, we know that it might be alcoholic liver disease. So it's probably a hepatocellular problem. So the answer is option two. And our last question is you're asked to see a one year old boy with jaundice. He was born by vaginal delivery at 39 weeks to Maria. She's had three pregnancies and two Children. The father is unknown. Maria did not attend any antenatal problems would say the pregnancy was uneventful on examination. You note that the patient has an enlarged liver and significant yellow of the sclera, yellowing of the sclera and the skin. You run some tests to confirm the diagnosis. Consi considering the likely cause of his jaundice, which of the following patterns would most likely be true on the blood test. So, we know that this is a newly born infant and so it's unlikely he's got uh liver disease. Um So it's probably he's got, it's either Gilbert syndrome or autoimmune hemolytic anemia type of picture. So, because it's hemolytic anemia, it's going to be high unconjugated bilirubin. You can get high conjugated bilirubin as well just because there's so much of unconjugated bilirubin going through the liver. So you'll get high conjugated bilirubin and low hemoglobin because the red blood cells are getting destroyed. So it's option number four. So now we know that now we know how to um interpret liver function tests. Uh Let's now talk about liver cirrhosis. Um Liver cirrhosis is essentially the only thing you know, need to know about liver disease. Um So let me just share my presentation about liver cirrhosis. Ok. So OK, what is, so what is liver cirrhosis? So, liver cirrhosis is basically what happens when there's long term inflammation of the liver. So, if you can imagine if you put any, let's say you've got a cut in your skin and you come and it's trying to heal, but then you manage to hurt yourself and the skin over there again. So again, the healing process is restarted and then, let's say by like great bad luck, you've managed to burn yourself where you've cut yourself. So now the tissue is even more damaged. And then again, you manage to cut yourself in the same tissue. So there's like constant inflammation on your skin. Imagine if your skin is like constantly inflamed and it's just not healing, what's gonna happen to it. It's going to become really scarry. It's going to the tissue is just going to be really of really bad quality. There's going to be really scarred, it's going to be um really heavy, it's going to be really fibrosed. So that's essentially what liver cirrhosis is. It's when the tissue in the liver is subject to like chronic inflammation. Um And it essentially because it's subject to chronic inflammation, it bec it becomes like scar tissue, it becomes really fibrotic and essentially, and then we say that livers become cirrhotic. So, um so essentially what happens in a cirrhotic liver is this, the tissue gets really, really inflamed and cells start dying when the cells start dying. The, when the hepatocytes start dying, the body is like, hold on, we can't let up the liver die. So they, they start a process called nodular regeneration. So, as you can see over here is basically sca scar tissue. You can see that circled over here in the Histological s uh slide it's scar tissue that's really inflamed and they have characteristic bands of protein that we call fibrosis. So, essentially the liver isn't healthy. It's really full of scar tissue, full of nodular tissue and it looks really bad. Um I've got a picture of a cirrhotic liver that I really want to show that I don't really want to show you, but it would be quite good actually to see. So this, this is basically the stages of liver disease and this is what a cirrhotic liver looks like. It just looks really horrible. You can see all these nodules over here. It's really full of scar tissue and nodules and it and it becomes, it becomes really small as compared to a nice healthy liver. So this is essentially what you what you want to avoid in liver disease. So going back to cirrhotic cirrhotic liver, I'm gonna show my presentation again. Mm. Mhm. Right. Ok. So let's just talk about what happens at a microscopic level. So what is a hepato uh what is a, what happens at a cellular level in a, in the liver? So this is basically a unit in the liver and the liver is made out of millions of units like this. So it's made of the bile duct, it's made of the hepatocytes, it's made of these stellate cells. And then this is what you call a sinusoid. So you've got the portal vein and the hepatic artery running through the sinusoid and they go all join the central vein. And we know that from, let's say when you eat a meal, like when you eat breakfast, the food needs to be digested. So all the, all the blood that comes from the stomach, the duodenal, it all goes through the liver, it goes through the portal vein uh where it's processed in the liver. The toxins are taken away. It's enriched. Bilirubin is processed, blah, blah, blah. All of that happens in the liver. So we know that the nutrition, the nice nutrient rich blood is coming through the portal portal vein, the hepatic arteries supplying the blood to the liver. You've got a bile duct, you've got the hepatocytes that essentially help um process the toxins in our body, help um process bilirubin, process food. And the, you've got stellate cells, stellate cells are something that they store Vitamin A. But normally they sort of use this, they just sort of store Vitamin A. But there's something that we call Q scent, which means that they're quiet. They don't really do much and they're just chilling over there. But then what happens when there's a lot of inflammation there. When there's a lot of inflammation in the liver, the stellate cells get really angry. They lose their Vitamin A and they start proliferating, they multiply and then they produce something called tissue growth factor. Beta tissue growth factor, which increases collagen, collagen is basically what you have in scar tissue So that increases fibrosis in scar tissue. So then this is putting a lot of pressure on the portal venous system and the hepatic artery and the hepatocytes. So everything basically just starts shrinking. There's so much of pressure on the liver unit. So it starts shrinking gets really scarry, really fibrose, really tissued, it's just not healthy tissue. So as you can see the portal vein and the hepatic artery will start getting squeezed and there's a lot of pressure on these veins. So what we basically say, there's a lot of pressure on the portal veins and that's what we call portal vein hypertension. So whenever there's so remember, the cell walls of arteries and veins are porous. So plasma can leak out. So when, whenever there's a lot of pressure on these portal veins, all the fluid starts leaking out of these because there's literally no space and they and things will flow from an area of high oncotic pressure to low oncotic pressure. And because there's so much of pressure in this, the fluid is looking for somewhere to go. So it gets pushed out and it'll go in anywhere where there's low oncotic pressure. So that, that essentially is your peritoneal cavity when it comes to the liver. So when you get a lot of fluid that's getting pushed out of the, out of the portal veins, you get something called ascites. Is that making sense so far? Has anybody got any questions at all? I know it's a bit tricky to get you wrap your head around. But essentially, just imagine you've got a pipe and there's a lot of pressure around the pipe because let's say it's just constantly raining and there's like tree trunks, wrapping around it. So the pipe burst essentially. And there's like lots of fluid that's coming out and polluting the environment. And that's what ascites is. Basically, it's a lot of fluid. Um So all the fluid builds up in the peritoneal cavity. Um This is a terrible drawing, but you can look at the photo and this is actually quite a good photo because you can see some very, very good signs of chronic liver disease in one photo. So the first thing you can see here is obviously the abdomen is really, really distended. So there's lots, it's unnaturally distended. So that means there's lots of fluid in the tummy. And one way to find out whether the ascites is when you tap on it, when you pus, the tummy is quite dull, to dull on percussion because of all the fluid in there. The other sign of liver disease that you might be able to see over here is can you see all these lesions? It's almost like she's been itching. So these are what we call excoriation marks. So because jaundice can make you really bilirubin, makes you really itchy. So if you got high levels of bilirubin, you get really itchy. So clearly this person's really itch themselves into oblivion. And the other thing you can see over here is, I don't know if you can really appreciate these very faint lines of here, but they're really quite obvious blood vessels. This is what we call spi uh spider Nevi. So, basically, because the abdomen is so distended, it's putting a lot of pressure on the um surface blood vessels. So they're coming up to the surface. So they're quite obvious because they're stretching those blood vessels out. So if you can say you can, uh if you see an acetic abdomen, you can really diagnose a pa person with a lot. So, one of the signs of cirrhotic liver is um ascites. Um and as you can imagine, it's not really comfortable to walk around with this much fluid in your tummy. And obviously, it affects people's appearance. Um it affects their mental health because of their appearance and it's really uncomfortable to walk around with 56 L of fluid in your tummy. And because there's so much of fluid in your tummy, it can um push up the diaphragm. So it can cause you, it can make you find, you can start finding it really difficult to breathe. Um People are bed bound because they can't move with the ascites. So how do we manage this ascites? Well, the only sort of cure for as there's no cure for ascites, you can't do anything to stop the ascites. The only cure for ascites is curing the underlying liver disease and cirrhosis is irreversible. Unfortunately, you can't reverse cirrhosis. The only cure for liver cirrhosis is liver transplant. Um So the so we can only simply manage ascites. So things we can manage. Ascites is with spironolactone. It's an aldosterone and ag agonist which helps diurea. So it'll reduce the amount of fluid, a low sodium diet paracentesis which is basically draining the abdomen. So you can insert a drain in the tummy and all the fluid comes out. But it's a temporary solution. You have to keep, you have to keep draining them sometimes on a weekly basis so that they can be comfortable. A trans intrahepatic portosystemic shunt, we will come to that later. And um as like anything in the body, the fluid in the tummy is prone to getting infected again. So, um when the fluid in the tummy, we don't really know why it gets infected, but it can get infected. And that's what we call spontaneous bacterial peritonitis. And the way you diagnose spontaneous bacterial peritonitis is you obtain a sample of the fluid in the tummy and you send it to the lab. If the sample shows more than 250 white cell count, 250 white cells, you diagnose them with spontaneous bacterial peritonitis and it's quite dangerous. So you need to give antibiotics. The two most common causative organisms of SBP are E coli and CPS and pneumonia and then you just treat them with antibiotics. Um It differs according to local trust, but the most common is ciprofloxacin. Um Any questions just checking, no questions. Great. Ok. So now because we know there's so much pressure on the liver, the liver, the fluid is being pushed out. So when we know it goes to the peritoneal cavity, the other thing it does, it can cause something called a shunt. So because the fluid is looking for places to go to where it does low pressure, sometimes what they do is it creates a shunt between the vessels, supplying the liver and the liver itself. And let's imagine all the fluid is being put into the shunt that goes into the heart. There's a lot of pressure on the heart. And if there's a lot of pressure on the heart, there's a lot of pressure on all the other organs of the body. It's mainly the kidneys. So let's say if this, if kidneys are pumping, if um the heart's pumping blood at a really high pressure in the kidneys, the kidneys start deteriorating as well. And that's when you get um so basically fluid build fluid builds up, pressure, builds up on the heart because the heart, heart pressure in the heart builds up the f the vessels in the kidneys will also start constricting and you'll get very little blood flowing through the kidneys. And because you've got little blood flowing through the kidneys, toxins will build up and your kidneys also fail. So that's what we call hepatorenal syndrome. So, basically, because of the pressure build up in the liver, there's pressure build up in the heart and consequently, pressure build up in the kidneys. So when you get both liver dysfunction and kidney dysfunction, ha kidney dysfunctioning happening because of the liver dysfunction, that's what you call hepato renal syndrome. And lastly, you can get splenomegaly cause again, there's just so much of backflow to the spleen, the spleen becomes big. Um So these are the markers of what these are. A couple of the markers of liver cirrhosis. You get si TS, you get hepato renal syndrome and you get splenomegaly. It's really quite, it's one of the most horrible diseases. I think another, another co um consequence of liver cirrhosis is something that you call hepatic encephalopathy. So, hepatic liver, um cephalus is brain. So, cephalops means uh inflammation of the brain. So essentially what happens in hepatic encephalopathy is that the liver's main job is to process toxins. Yes. Um If the liver is damaged, it's not going to be able to pro process any of the toxins and then the toxins in the liver build up and that's what they cause causes hepato hepatic encephalopathy. Um The main toxin that we've identified that causes encephalopathy is something that ammonia. So, ammonia is produced in the gut after um breaking down a food and then ammonia is syn is um absorbed by the liver and synthesized and is uh sorry, not synthesized. Ammonia is absorbed by the liver and processed by the liver. So, if the liver is not working, um the ammonia is not gonna be processed. It builds up in the bloodstream and it builds up in the brain and eventually causes encephalopathy. The signs of encephalopathy are confusion. You get something called a flapping tremor. So if you put your hands out like this and ask the patient to put their hands out like this, you get like a flap like a flap over here and it can be quite subtle, but it can be sometimes it can be really obvious. So that means they're encephalopathic. Um The other things that the liver processes is estrogen. So if you've got liver dysfunction, your estrogen won't be produ processed. So that's why men get things like gynecomastia where because there's too much estrogen in the body, they start developing breast tissue bilirubin won't be processed. So you'll get jaundice and then albumin won't be produced. So you'll get low albumin levels and then clotting factors won't be produced as well. So you'll see that patients are a lot more prone to bleeding, they'll get bruised very easily. So, essentially, if you get toxin, build up in the liver, um you can get encephalopathy and it's really dangerous. Um The biggest concern with encephalopathy is that when patients are confused and delirious, you can lose your airway because you're so confused and delirious and there's so much of toxins built up in your body, your brain stops focusing on maintaining an airway. And hence, that's why so many people end up in ICU where they're intubated and ventilated because they're so cephalops teaching liver disease makes me really sad because all I think about is all these poor patients with all these conditions. Um anyways, uh try not to get liver disease. So, um people with liver cirrhotic liver disease um can have intermittent periods of encephalopathy. So like anything that mm, anything that attacks your body physiologically, anything that makes your body lose physiological balance can cause encephalopathy. So things like constipation, essentially what happens in constipation when there's too much of pool build up, there's too much ammonia being produced. Hence, that can make you encephalopathic infection can make you encephalopathic dehydration can make you encephalopathic gi bleeds can make you encephalopathic. Honestly, if you stubbed your toe, you'd probably become encephalopathic if you were cirrhotic liver disease. Um So we try to manage um hepatic encephalopathy by preventing it essentially. And what we do to prevent it is lactulose. That is the biggest thing. Lactulose reduces ammonia production. So it's really good. Rifamycin is an antibiotic. Um that helps reduce am ammonia production as well. And focusing on nutrition is really important in patients with cirrhotic liver disease because obviously the liver is not, is not processing nutrition. So you're gonna lose a lot of weight. So making sure that the patients have like high fat, high protein diets is really good to prevent hepatic encephalopathy. So, these are just some signs of liver disease. Um, palmar erythema, this happens because there's too much of estrogen gynecomastia. This is what we call caput meuse. So essentially, it looks like it's um well, I can't remember the exact physiology behind caput medusa. But it's, if you've got liver disease, you might see caput medusa and it's called medusa because it resembles the hair of medusa. So those are some cool um signs of liver disease. And I'm sure um you practice all of them in when you do an abdominal examination. Um Any questions so far, I can see no questions on the chart. Ok. Fine. Let's continue. So, so far we've caused, we've um we've talked about ascites as a consequence of cirrhotic liver. We've talked about shunting as a consequence of cirrhotic liver, hepato renal syndrome. Um Hepatic encephalopathy. Uh uh So the next one, portal hypertension and varices. So this is really important, I want, this is I think the one of the most important signs of de of liver cirrhosis. Um So let's talk about what portal hypertension is. So, here we can see this is the liver, this is the stomach. As I was saying before, with all of these, all of the veins from the stomach, the gastric veins, they absorb the blood from the stomach and they take it into the liver through the portal vein. When the, there's, when the liver becomes very cirrhotic and scar tissue, it becomes really heavy. So it starts putting up a lot of pressure on the portal vein. So now if there's a lot of pressure on the portal vein, it'll start blo blood will start back flowing. There'll be a lot of back pressure build up over here, over here, over here and all of these veins go into the esophagus, go into the stomach, go into the gi tract. And because there's so much of pressure on one point, there's a lot of pressure on all the other points of the blood vessels as well. And that is essentially what we call portal hypertension. So hypertension in the portal vessels and because there's so much of pressure in the circulatory system, your veins are only this small, right? And when there's a lot of pressure, they start dilating, they start dilating, they start dilating and the venous wall becomes really thin. So that's what we call esophageal. That's what we call varices essentially. Um Let me try and show you a photo of it. And endoscopy actually should have in included that on my slight show. Yeah. OK. Let me see if I can share my screen. OK. I don't know if you can appreciate it, but do you see these raised areas? Um these are basically that the veins are dilated and there's a because so over here, the tissue is really thin and the veins are dilated. So let's, and these are really high risk to bleeding. So you can develop a bleed of these varices any time and that's really dangerous. That's what kills a lot of people with liver cirrhosis. Um Let's see if I can find another picture. So over here, you can see there's a lot of, over here you can see bleeding varices. So there's lots of blood over here. Um What else can I show you? Ok. So hopefully that helps you understand what esoph like viruses are and they don't only happen in the, in your esophagus, they can happen in the rectum, they can happen in the large bowel, they can happen in the stomach. So, um so it's really quite so and those are really prone to bleeding. So that's what. So when patient, when these viruses start bleeding, patients start, can go into hypovolemic shock because they're losing so much of blood volume. Um So the only way you can diagnose varices is via endoscopy. So as I showed you, if you do a camera test, you can see those from what I showed you. The treatment of varices is um basically non uh nonselective beta blockers. So things like propranolol, carvedilol, what they do is they reduce the um reduce the contractility of the heart. So there's less pressure in the blood uh in the venous system and hence less pressure on the viruses. So they're unlikely to bleed as much. And the other thing is variceal band ligation. So that's basically when they go in through the mouth via an endoscope and they put a band around the varices to stop it from bleeding. Um So let's say you're in a ward and you've been called to see a patient who has been admitted with liver disease and the nurse says doctor, he's just started vomiting blood. What are you going to do? So you want to start an A to do an A two E and you might find that the patient is in hemorrhagic is in hypovolemic shock due to the hemorrhage. So you might want to activate a major hemorrhage protocol. So the way you do that is you dial quadruple two. Um The other thing is you should get senior help as soon as possible. So how do you, how do you treat bleeding viruses? The first one is a same stack in Blackmore tube, which is basically a, a tube that looks like this, it's inserted through the uh mouth into the esophagus and into the stomach and it's inflated so that the balloon will hold the tube in place. And what this tube does? It basically tampon out the esophagus of the varices. So they stop bleeding. So they just put pressure on the varices to help stop the bleeding. The other thing is something called a trans ischemic porto hepatic shunt. So it's basically like a shunt that you put in the portal venous system which helps reduce the pressure that's going. So it goes through the inferior vena cava. No, in sorry, it goes through the jugular vein and then they feed it down to the hepatic vein. It's like a shunt. And then when it's in the hepatic, in the portal veins, it'll expand. So it's like um it's like a stent holding the up the portal venous system. So when you've, so let's imagine in portal hypertension, your portal venous system is this narrow. When you put the shunt, I shunt in, it becomes a little bit bigger. So it relieves the pressure a little bit. So, um that's how tips a trans ischemic, portosystemic shunt helps hope that makes sense. Um Any questions? Nope, no questions. Ok. Great. Back. Nope. OK. All right. So we've essentially covered everything about liver cirrhosis. Um And the consequences of liver cirrhosis. Um let's now get back to uh So essentially what I'm what I'm getting at by talking so much of in liver cirrhosis is that all liver disease essentially leads to liver cirrhosis. And um so anything hepatitis malignancy, alcoholic liver disease, fatty liver disease, PSC, PBC Wilson's hemochromatosis. They, they can all lead to liver cirrhosis and liver cirrhosis is the, is complex. It's not curable, it's irreversible and the way it manifests is ascites um encephalopathy uh viruses. Um Yeah. Um Do you guys know the pneumonic ahoy, I didn't put it on my slides, but I think it's really good. So, you've got compensated liver disease and decompensated liver disease. Uh, just bear with me one second. Sorry, I should have actually put this on my slideshow. I just remembered a high pneumonic disease. Ok. No, no. Ok. Um, I'll, I'll make sure that I put a, add it to my slides before I upload it. Basically. I think it stands for, uh, the features of decompensated live liver cirrhosis is ascitis. A for a, a for ahoy hepatic encephalopathy. Oh, is esophageal viruses? And I can't remember what, why is. So if you guys put, if you guys remember what, why is just put on the chat. So essentially the most important thing you need to know about liver disease is cirrhosis and what are the consequences of cirrhosis? Um Right. Ok. Fine. Let us now do some case studies. Ok. Right. So we've done these questions. Ok. So we've got 27 year old Billy who's presented to A&E complaining that he's feeling tired. He's got tummy pain. He's vomiting. His past medical history is none. No, he's not got any past medical history. You fit and well, 27 year old guy, um, you pro, you poke him a little bit more to get a little bit more history. He tells you, he drinks about two beers a week. He occasionally uses marijuana. He is, um, an Emerson. So he has, uh, sexual intercourse with other men and he last had unprotected sex three months ago. He works as a construction site manager and he's originally from Romania and last visited Romania two years ago. Um, you do some bloods on him and it shows an at of 420 an ast of 200 an ap of 120 a bilirubin of 30. What are we given his history? What do you think he might have any, any guesses as to what the diagnosis is? You can just put it in the chat if you can think of something. Mhm. Really good Shruti. You've bang on the money. Hepatitis. Um any guesses as to what, which hepatitis A BCE? ABCD. That is a good guess. Why do you think it's C? OK. So essentially um the answer for this is hepatitis B. So um hepatitis B is a double stranded DNA virus. It's transmitted through bodily fluids. So, but unprotected sex, needle use common use of toothbrushes, razors or that you know, that have been contacted with open cuts and you can get vertical transition transmission from mother to baby. So, um the most important thing with hepatitis B. Well, the only thing that's relevant to your exams is um the serology of hepatitis B. So let me, let me show you my slides on Hepatitis B serology. OK. So, hep B serology. OK. Right. So we all know that antibody, we all have antibodies, our antibodies react to antigens and the antibodies attached to antigens form immune mediated complex and all of the first year immunology stuff happens. I can't remember anything. I'm really sorry. But let's just look at the structure of Hepatitis B molecule. Oh, sorry. Hepatitis B DNA strand. So you've got surface antigen over here, there's three antigens that you really need to know very well. Over here you've got your surface antigen. You've got on the surface of the hepatitis B. You've got HEP E antigen which is between the core and the membrane. So it's in the middle and you've got your core antigen on the core. So what do you need? So all, all your exam questions will essentially be give you like things like this person's HEP B surface antigen. Is this the HEP A surface antigen? Is this antibody? Is this the HEP E antigen? Is this, does this patient have acute infection, chronic infection, past infection, past immunization? And that's what you need to interpret. Um What would be a fun exercise is get your occupational health records out after this and try and interpret what you've had. That's what I did after this. And um it's quite fun actually. So Hepatitis B surface antigen is the antigen that's pre presenting the surface of the virus. So if you test somebody's blood and they've got HEP B surface anti antigen, um it means either they've got an active infection and remember the HEP B vaccinations are basically uh getting are basically HEP B surface antigens. So when we get hep B vaccination. It's HEP B surface antigens. So just remember that if you find HEP B surface antigen, it probably means they've got either a vaccination, they've just been vaccinated or they've got an acute infection. Does that make sense? Ok. Now, let's talk about HEP B core HEP be antigen. So hep be antigen is an antigen that occurs when HEP B virus is replicating. So this is basically what happens. This is what causes replication of the virus. So if you have lots of Hep E antigen in the blood, you know that the virus is actively replicating. So it means that you've, if a virus is actively replicating, you can be pretty sure you've got an active infection of hepatitis E and um the more Hep E antigen you've got, the more infe infectious you are is because you have lots of n new hepatitis molecules being produced in your body. So hep E antigen shows active infection and it shows how infectious you are. So let's say like you've got a really, really high amount of hepatitis E antigen, hepatitis be antigen. It means that you're probably very, very infectious. And then hepatitis core antigen is only relevant in the sense of hepatitis B core antibody. We'll come to that later. So as we said, hepatitis surface antigen is positive in active infection. Hepatitis E antigen, it escapes during infection. So it's positive in the acute phases. And the more Hepatitis B antigen, the more infectious you are. And then we said in vaccinations, hepatitis B surface antigen is infected. So then hp surface antigen is injected in you or there is HB surface antigen, surface antigen surface antibody. Ok. So it's very simple. Remember there's three antigens from hepatitis E surface antigen, hepatitis be antigen and core antigen. So surface is on the surface, E as in it e escapes during infection and then core is that it's in the core. So, hep B surface antigen, if you just use your common sense and think it's on the outside of the virus. So it probably means that I've either had like I've got active infection. So if you've got HEP B surface antibody, it either means you've got past infection or you've got past um immunization. Does that make sense? Hopefully, it makes sense. It's a bit tricky. But if you have any questions, feel free to ask them again. And then Hep B antibody we know is a response to HEP E antigen. So hep E antibody is um if hep E antibody is positive and hep E antigen is positive, that means there, there's active infection. But let's say HEP B antigen is negative and hep be antibody is positive. So it means that once upon a time, there were lots of viruses that were replicating but now they've stopped because there's no HEP be antigen but there's HEP be antibodies. So hep be antigen negative, hep, be antigen, posi antibody positive. It means past infection. OK. Does that make sense? And then lastly, hepatitis B core antibody, it shows us whether the infection is like acute, if it's chronic or if it's passed. OK. So, um whenever you measure Hep B core antibody, you should measure IgG. And IgM, we know that IgM is an acute phase reactant and IgG is a chronic phase reactant. So if they've got positive HEP B core antibody with positive IG IgG, it means they've got an active infection. Um If they've got high IgG gi low IgM and high IgG IgG, it means they've had a past infection. OK. This is all kind of tricky but hopefully it all makes sense. Oh And the last one is HPV DI so it hepatitis B viral uh road. So it just shows you the amount of hepatitis B virus in the blood. So if you've got a large amount of Hepatitis B virus, that probably means you've got an active infection. Um Any questions at all? It's um so remember surface antigen, surface antibody hep E antigen hep E antibody, hep E HEP B co sorry, hep be antigen, hep, be antibody and HEP B core antigen, hep B core antibody is um produced. So how do we test? So if you go into an, if you go into a hospital, everybody gets a Hepatitis B test. I think if you attend the A&E nowadays it's um so if you get hepatitis, so they'll send hepatitis B core antibody and hepatitis B surface antigen when people come in. So if they've got hepatitis B core antibody, which is positive, you know, they've had a, they've got an infection, whether it's a previous infection or past infection. We don't know. So we can check, check hep B surface antigen. So if that's positive, we know that's an active infection. So if those two are positive, we can check HB E antigen which will show us how infectious you are and HBV DNA, which will show you the viral load. And then if they're HB surface antigen positive and HB surface antibody positive, it means they've had a, they've had a previous vaccination or a past infection. Does that all make sense? That was quite a mouthful. Um If you guys are struggling, just let me know and we can, we can go through it again. Let's go back to the normal slides, right? OK. So we went, so the most important thing about hepatitis B, all you need to know is the serology really? Because that's what comes up in exams. Um The management of hepatitis B is like any other infe viral infection really is it's usually self-limiting. You just um so it's, you refer them to a specialist, um you give them symptomatic relief. So, paracetamol, you can actually give paracetamol and Ibuprofen in hepatic disease as long as there is no signs of active hepatic disease. Um you can give weak opioids, metoclopramide cyclizine. Uh contact tracing is really important and um you need to check their hepatitis um serology in a couple in about three months and then six months as well to make sure they're not chronically infected with hepatitis B. Um, then all, all the hepatitis A to E is they're all notifiable diseases. So you need to notify public health England. Um, if a patient of yours has hepatitis. Ok. Um, this is a quick table with all the HEP. You don't need to know much in detail, to be honest, you just need to know how they're spread and what and just have a basic idea of if they've got a vaccination and what the treatment is. Um the most important thing in hepatitis is really the serology. So hepatitis A is fed through the fecal oral route. There's a vaccination for it and the treatment is just fluids, rest analgesia. It's very uncommon in the UK. It's unlikely you'll see it. Hepatitis B is also uncommon in the UK. It spread through blood and bodily fluids. Um So, and as we said, the treatment is supportive or you can give antiviral medication. Hep C is spread through blood. Um So there's no vaccination. So it's, you have to give a direct and a acting antiviral HEP D is a consequence of HEP B. So you won't get HEP D random. You, it's always with HEP uh B that you get it and the treatment is a peg Interferon alpha and HEP E is also very rare in the UK, it's transmitted fecal oral. So things like contaminated food, contaminated water, contaminated surfaces, there's no vaccine and the treatment is supportive. Um So we've covered all the viral hepatitis. Uh Let's now talk about autoimmune hepatitis. So, autoimmune hepatitis is like what it says in the name, it's basically an autoimmune inflammation of the liver. Uh We don't know what causes it really. Um It's people think it's part of the HLA D3 spectrum of autoimmune conditions, but we don't know yet. Um The presentation for autoimmune hepatitis is really nonspecific fever, jaundice, signs of chronic liver disease. Most people will present with signs of decompensated liver disease just because it's really difficult to know whether you've got autoimmune hepatitis and it's usually too late. By the time you figure out you've got autoimmune hepatitis. There's three types of autoimmune hepatitis is type one. You'll be positive for a ana uh antinuclear antibodies and anti smooth muscle antibodies. Type two is you'll be, it happens in both adult and Children. Type two is happens in you get positive antiliver kidney microsomal type one antibodies and it affects Children only and type three is soluble liver, kidney antigen. It affects adults in middle aged. I don't think you'll be tested on autoimmune hepatitis. So um don't worry about the types, I guess it's just helpful to know the treatment of. It doesn't really differ as per what type you have. Um the management is high dose steroids. So like prednisoLONE, um usually or hydrocortisone immunosuppression. So, tacrolimus, thyro azaTHIOprine methotrexate, not methotrexate cause that's toxic to the liver. And finally, liver transplant if you have cirrhotic liver. Um but the problem with liver transplant and autoimmune hepatitis is that it can come back. So it's not really, it's not the most pleasant disease to have. But what you need to do from a medical student perspective is autoimmune disease. Hepatitis is like any other autoimmune condition. It happens randomly. We don't know what causes it. And the treatment is usually high dose steroids, immunosuppression and liver transplant if they've got decompensated liver disease. Um Yeah. Ok. Next one. So liver cirrhosis we covered in great detail. Um Most common liver disease in the developed world, uh nonalcoholic fatty liver disease. But um the nomenclature is changing now because people get upset that when you call it nonalcoholic fatty liver disease cause you're calling them fat. Um So it's now it's called uh metabolic uh nonalcoholic stea stoic liver disease. It's a lot more com but basically meta metabolic liver dis steatotic liver disease, which is basically a fancy way of saying nonalcoholic fatty liver disease. I understand and honestly, I wouldn't want to have a disease that's called nonalcoholic fatty liver disease. It's quite insulting. Um And it's a bit kind to the patients as well. So in your exams just be aware that it might be called NAFLD or Mad um, it's also called mash, which is metabolic nonalcoholic, um, steatohepatitis or NASH, which is nonalcoholic steatohepatitis. Um I'll just put it on the chart. So you don't get confused. Nash, mash. Um, so what is nonalcoholic fatty liver disease? It's very self-explanatory as it is in the name. It's fatty liver. That's not a consequence of alcohol. And it usually happens because of diabetes, hypercholesterolemia, obesity, um, gastric bypass surgery because of and remember, um, it's malnutrition from gastric bypass surgery and sudden weight loss or starvation that can cause um nonalcoholic fatty liver disease. Um, like I the most liver disease, the features are all liver disease. The features are exactly the same. Um jaundice, if it's late liver disease, uh features of decompensated liver disease, ascites, um ascites, uh hepatic encephalopathy, uh viruses um with um tiredness. Um just not feeling generally. Well, all liver disease presents exactly the same. It's in your history and the blood test that you can usually differentiate. Um in fatty liver disease, you will see that alt is typically greater than AST and alt and AST will be higher than the AP. And on ultrasound, you'll see increased echogenicity. The ho how do you diagnose uh fatty liver disease is you do a liver biopsy? It'll show fat infiltration in the liver cells. So, um uh the management is that uh weight loss is the biggest management abstained from alcohol. Um There's something called an elf. It's an elastase fibrosis, blood test. So it just tests for the amount of fibrosis in the liver. And um um yeah, the management is supportive if they've got decompensated liver disease or liver cirrhosis. Um, they need to be referred to a specialist hepatologist or gastroenterologist. Um I just want to make clear. So this is your normal liver, it becomes fatty. Usually at this stage, it's reversible. So if you abstain from alcohol, if you lose weight, you can go back to a normal healthy liver. Even the HEPA hepatitis is reversible to some, to an extent. So, if you've got a patient who's coming and the ultrasound shows fatty liver, um, either in GP or in clinics, it's really important to have a conversation with them about the importance of exercise, good diet, alcohol abstinence because this is reversible and people can live much longer if they don't develop cirrhosis. Ok. All right. Um Next one, another case study. So you've got a 57 year old man who's attended um ei don't know why I put the, it's just the emergency department after experiencing a seven day history of a productive cough, um, productive cough. Um, so you decide to admit him for IV antibiotics to treat him for a community acquired pneumonia. On day two of his admission, you're bleep by the nurses because he appears a bit funny. You go to view him and he's trembling and he looks unwell. You look at his admission clocking and see he generally drinks about eight cans of cider a day. What is your diagnosis? Any clues you guys, um What do you think might be going on here? You've got a man who you've admitted for IV antibiotics cause he's got a community acquired pneumonia. And you look, and he just, you come to see him and he's trembling, he's shaky, he's a bit sweaty, just doesn't look that great. Um And he tells you he drinks up to eight cans of cider a day. Yeah, very good delirium tremens. That could be a cause. So the answer to this is essentially alcohol withdrawal. So if you take a person who's drinking eight cans of cider a day and put them in hospital and, but they've not got any access to alcohol and they're bed bound, they will develop alcohol withdrawal. So as when you are doctors, it's really important to take a thorough alcohol history because alcohol withdrawal can kill people. So if you don't take and in terms of taking a good alcohol history, you have to poke and pry because people will always underestimate their alcohol usage. If somebody says they're drinking 10 cans of cider a day, they're probably drinking 20 cans of cider a day. So it's really important you take that history and you foresee that need and um make sure you treat them for alcohol withdrawal even before they develop alcohol withdrawal. So the way alcohol withdrawal works is you first in the 1st 6 to 12 hours of alcohol withdrawal. You get premise sweating, headaches, craving of alcohol and anxiety in about 12 to 24 hours, you get hallucinations. So, the most common hallucination with alcohol withdrawal is something that we call delusional parasitosis. Delusional parasitosis. Can I have a glass of water, please? Can I have a glass of water? Hello. Uh delusional parasitosis. So basically they have a feeling where like bugs are crawling up all the way to their body and into their ears. Um It's actually quite scary. And then in the next 24 to 48 hours, they can develop seizures which can be life threatening. And in the last 72 hours they get delirium tres, which is basically them being very tremulous, they're delirious. Uh They don't know what's going on. So just one second. Yeah. Yeah. So alcohol withdrawal is a life threatening condition because what happens with seizures is they can lose their airway, they can go into comas, they can die. So it's really important to anticipate for that in power. So how do you, how do you diagnose alcohol withdrawal? They'll have all of these symptoms and how do you treat alcohol withdrawal through sa scoring? Um So sa scoring. Can you see this? Yeah. So it's basically the nurses do this. It's actually quite good. You don't have to do this but the nurses will see the patients and they'll score the patient. So if they've got, so they score patient on if they've got vomiting, uh tremors, paroxysmal sweating, anx, anxiety, agitation, tactile disturbance, auditory disturbance, visual disturbances, headaches, orientation. Uh like they feel disoriented and the nurses will calculate this. And if let's say they got a score of more than eight, they might, they will require, they will require medication. And the medication you give them. It's um oh no, sorry. It's, it's disappeared. Ok? Can you guys see this? Yeah. So the me uh the medication that you give them is benzodiazepines. So, oxazepam, Chloro chloradiazepoxide or LORazepam, you give them PEX which is basically highly concentrated vitamin b1 thiamine and then you monitor for one a case. Kough uh I've just realized I haven't really told you why alcohol withdrawal happens. So what happens in alcohol withdrawal is essentially um one um alcohol basically causes upregulation of the neurotransmitter glutamate in your bo in your brain. And then when there's upregulation of glutamate, there is upregulation of the, there's more excitation of your glutamate res receptors, which are your Gaba receptors and your NM NMDA receptors. And when your al when there's no alcohol, there's no neurotransmitter being released and your receptors get really confused and hence, that's why you get alcohol withdrawal. Um Does that make sense? Um hopefully, it does make sense, right? Ok. Alcohol withdrawal. Um So then um with alcohol withdrawal, we worry that patients will develop. But so um why do you replace pa patients with pabx and thiamine when they've got alcohol withdrawal, why this particular vitamin essentially, what happens is when patients consume a lot of alcohol, it erodes the stomach lining. And the stomach is where B vitamin B12 and folate is Vitamin B is absorbed. And if you've got no very low Vitamin B you get um both neurological effects and um blood effects. So the neurological effects is basically, your brain depends on vitamin B1 to function and when that doesn't happen, um if you don't have enough Vitamin B your brain start dysfunctioning. And that's why you get Werner case Werner case syndrome. Um So, Wernicke cough cough is when there's alcohol leads to vitamin b1 deficiency. And when there is vitamin b1 deficiency, you get Wernicke encephalopathy. The how Wernicke cephal cephalops presents is ophthalmoplegia, ataxia and confusion. So, ophthalmoplegia basically means abnormal eye movements. So if you can see nystagmus, you can see their eyes rolling, that's ophthalmoplegia. Ataxia means that they have an unsteady gait and they're confused. So that means they've got one, a case encephalopathy, the way you treat it is you give them a lot of pex a lot of vitamin fluids, you monitor them and then one case can then develop into cause a cough where the patients start forgetting. So they get amnesia, it can be both anterograde and retrograde. So they can happen, they can forget things in the past, they can forget things in the present and the confabulation, which means basically they lie, but their lies seem implausible. So, Korsakoff syndrome is often irreversible. And if you don't treat Wernicke's and Korsakoff, they can develop a coma and, and then that, so it's really important. I cannot, I cannot highlight how important it is to identify, to take good alcohol histories and anticipate the need for alcohol withdrawal when you see patients. Ok. Fine. So, alcohol, liver disease, what is alcohol, liver disease? It's hepatic steatosis, which is basically fatty liver. And if there's fat in the liver, there's inflammation of the liver and then you develop liver cirrhosis. The recommendation for um alcohol in the UK is you have to drink less than 14 units a week and you have to avoid binge drinking. Um So how would you see alcoholic liver disease in your bloods? You get a raised mac M CV. So mean raised mean cell volume. Um So macrocytic anemia is really common in alcoholics due to B12 and Folin deficiency. Um your ast and A to alt ratio will be greater than 1.5 or two. And you have a raised gamma GT. The treatment of alcohol, liver disease is complete alcohol abstinence. So they can't even drink like 4% alcohol or like 0% low alcohol percentage or cut down on the alcohol. It has to be complete alcohol abstinence. However, be really, really careful when you're giving patients advice about alcohol abstinence. You should never tell them to quit. You should tell them it try and cut down on your alcohol intake. So if you're having eight cans of cider a day, try 7.5 cans of cider for a week, then cut down to seven. And oftentimes it's good to admit people in hospital for alcohol withdrawal because it can be really dangerous. Remember, alcohol withdrawal kills people. So you have to be very careful. Um So complete alcohol abstinence steroids can be quite helpful because it can reduce the inflammation in the liver, nutritional support. So the thing with alcoholics is that they get a lot of calories from drinking alcohol. So when you drink lots of alcohol, you don't feel hungry because all the calories come from the alcohol, but they're not good calories, they're really bad calories because there's no vitamins in it, no minerals. So a lot of these people will be malnourished, will be mal there'll be lots of malnutrition. So it's really important to give them vitamin supplementation. So thiamine Vitamin D vitamin A and a high protein diet. And it's, and um if you have alcoholic liver disease that turns into liver cirrhosis and you get decompensated features, then you'll be, then it'll have, you'll have to treat the complications like si ts portal hypertension, hepatic encephalopathy and then eventually liver transplant if they meet the criteria. But I think you have to be abstinent from alcohol for more than a year to meet the criteria for liver transplant. So it's really important to uh achieve abstinence in patients with liver liver disease, alcoholic liver disease. Ok. Just a couple more things. Um, a couple more diseases and then we'll wrap up. So the next liver disease is alpha one antitrypsin deficient disease. Um So what is alpha one, a antitrypsin? It's basically a protease inhibitor. So what happens in alpha one antitrypsin deficiency is there's a gene mutation of this gene called serpena 14 that's found on chromosome 14. Um So when this gene is mutated it, um ok. Sorry. Let me just think. Um So w what is protease protease is an enzyme that essentially breaks down uh connective tissue. So what alpha one antitrypsin is, it's an inhibitor of protease. So it stops excess protease and he and then then helps break, stop breakdown of uh connective tissue. When there's no alpha one antitrypsin, there's too much protease in the body, there's breakdown of connective tissue and mainly there's breakdown of lung tissue. So, if you get breakdown of lung tissue, you'll develop emphysema bronchiectasis, hence difficulty breathing low oxygen saturations. So this is a marker of alpha one antitrypsin deficiency. How does it affect the liver? Now, we know it affects the lungs because it breaks down all the tissue in the lungs. How does it affect the liver? So, the gene that the protein that produces alpha one antitrypsin is in the liver. If the protein isn't producing this liver, it gets uh sorry, the protein and alpha one antitrypsin deficiency is mutated. So it gets trapped in the liver cells and is really toxic and causes the inflammation. So when there's too much of inflammation, like we said before, any inflammation of the liver causes fibrosis and then c cirrhosis. So, hence alpha one antitrypsin deficiency can be really can be both really dangerous for the lungs and the liver. So patients who have alpha one antitrypsin deficiency often have both liver and lung problems. So, um how do you diagnose it? So, it's usually diagnosed in childhood when patient, I think it is part of the newborn screen. Now. Um and patients will re usually present with both liver and lung symptoms. So, difficulty breathing, um cough, longstanding cough, phlegm production, um abdominal pain, jaundice. So, um and so you can measure serum one alpha antitrypsin. You can do genetic testing and liver biopsy and the treatment is largely supportive. So you can replace alpha one antitrypsin. You can, they might be considered for liver transplantation if they've got decompensated cirrhotic disease. Um But essentially all you need to know is what alpha one antitrypsin is and have that as a differential. You usually see it in more younger patients. Ok. Another case study. So we've got a 27 year old female who presents to the ulcerative Colitis clinic. So we know that this woman's got ulcerative colitis and she's coming to clinic for a routine appointment and she's complaining of itching and right upper quadrant pain. She says that her friends say that she looks a little bit more yellow than usual but thinks she's just a bit more tan. She says she hasn't, she's got some pain in her abdomen and just isn't feeling very well. She asked you if she's got some kind of viral infection. What do you think is happening? Do you guys have any differentials? Ok. Um Just pop your differentials into the chart. I'll give you a bit. Mhm. Mhm OK. OK. Good. Right. So the main differential. So, oh, here I think the most important thing for medical students to identify is um number one, she's come to the Ulcerative Colitis clinic. As soon as you see, ulcerative colitis, you need to think of something called primary sclerosing cholangitis. So what is primary sclerosing cholangitis or PS C? It's an autoimmune condition essentially. What happens is um there is inflammation of the ducts of the hepatic ducts of the intrahepatic bile ducts and the post hepatic bile ducts. And because it happens, it's autoimmune. So it just happens. And because there's inflammation of these bile ducts, there's inflammation of the surrounding liver tissue. And as we said before, constant inflammation of the liver tissue, you get um cirrhosis, they very, very strong association with ulcerative colitis. I guarantee you you'll get an exam question that someone's got ulcerative colitis and they've got primary uh and they've now developed jaundice and right, upper quadrant pain. What is the diagnosis. Um So if you don't remember anything about primary sclerosing cholangitis, just remember it's associated with ulcerative colitis. The risk factor usually happens to men. They're aged between 3040. Um they have ulcerative colitis and there's a strong family history. The presentations are like any every other liver disease, abdominal pain, itching, fatigue, jaundice, hepatomegaly, splenomegaly. How do you investigate for PS C? So you get a raised alp because the bile ducts are inflamed. Um you get uh sometimes it can be P ANCA A N A anti smooth muscle antibody positive, but they're not diagnostic. Um and a magnetic M RCP of the liver will show bile duct strictures and you can do a colonoscopy to check the features of. So, the management is basically symptom related. So you can get steroids to help with the autoimmune component. Um If there's stricturing in the bile ducts, you can do ERCP to help widen the strictures and uh keep put stents in place. Um you can give cholestyramine for the itching and you can um cholestyramine is a bile acid ses ses. So basically, it bile binds to bile acid and helps reduce the amount of bile acid in the body and helps reduce itching. Um and you have to provide nutritional support. What are the complications of PSC? So, a lot of the complications comes from the stricturing itself. So the strictures can get inflamed, the strictures can block the bile ducts. So it's important we like get rid of the strictures. You can get infection of the strictures itself, you can get infection of the bile duct, which is called cholangitis. Um and then cholangiocarcinomas are really common in patients with primary sclerosing cholangitis, likely to do with the amount of inflammation in the, in the bile duct. So those are the main complications. The biggest things to remember with PSE is its strong association with UC and cholangiocarcinomas that brings us to the end of the presentation. There's a few more diseases um that we haven't covered today. Hemochromatosis, which is iron, build up in the liver. Co Wilson's disease, which is copper, build up in the liver um and primary biliary cholangitis, which is basically inflammation of the bile ducts. Um So if you guys have any questions, do, let me know, I'll stick around for about five more of the questions. Um The main resources I use was zero to finals, geeky metics and past me osmosis to create the slide show. So if you guys are studying for finals, I think these the osmosis youtube videos are amazing for learning. Um The pathophysiology of these things and past medicine is really good for question BS. Um So if you guys have any questions, pop it in, um you can always go to these resources and look up more information. Um You can always pop in any questions you have on this chat. And I think I've mentioned my email earlier on. So um please feel free to um email me with any questions or any, even any questions about uh being a foundation ear doctor. Um uh this is my email if you'd like to email me and I'll stick around for five more minutes if you guys have any questions. Thank you so much for attending. I really, really appreciate it. Um And uh next week we're going to do a session on how to be an F one. So if any of you guys are in your final year and are going to be a doctor in oh God, three months time, um that will be really helpful.