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Thanks for joining. Thanks for joining in this Sunday evening. I'll just share my screen a sunk help dinner, make me coast so I can just share this screen data. Thank you. Okay, so good evening. So it today will be just going over Upper GI I and hepatobiliary disorders. We're gonna cover wide range of topics. So we're just gonna try to list through them and cover the mate basics and the main principles you need to know for the you exams. So my name's Ashwini, and I'm one of the F ones and upper teens. I graduated from glass school. So the topics were going to cover today Our hepatitis, both viral and auto immune, fatty liver disease, alcoholic and non alcoholic liver cirrhosis. A little bit about lft interpretations. And then we'll just quick creek quickly go through primary biliary cholangitis and gilbert syndrome as well. So we'll try and make this a bit interactive. I have a couple cases to be put up, Onda. Um, if you want to undo it yourself and answer questions, feel free to do so. If not, just put them in the chat boxes. Well, so we'll just start with the case. So a 45 year old woman presents with insidious onset of fatigue, malaise, lethargy and Orexigen nausea, abdominal discomfort, Mile per otis. An arthralgia involving the small joints her past medical history includes celiac disease on physical examination reveals a pattern Michaeli and Spider angiomata. So what features in this history stand out to you? Just pop them in the chart box or a neat yourselves? Yeah. Yeah. Anything else? So pure puritis indicating I believe we've been so something wrong with the liver. Anything else? Yep. Her pattern. Medically. Anything else to differentiate this? So if you're thinking that this is a hepatitis picture, um, is there anything that stands out to you that makes it more likely to be one kind of hepatitis to another? Yeah. Oh, to immune condition. Yeah. There we go. Celiac disease. So that was the key word I was looking for. So celiac disease kind of points you towards that. Perhaps this is a not a mean picture. So and yes, no travel history as well. So first topic we're just gonna talk about is autoimmune hepatitis. So it's a Karnik informative disease of the liver of unknown etiology. If which often if left untreated lead service, cirrhosis, liver failure and death. It's more commonly seen in females as your most autoimmune conditions on do It's associated with other autoimmune diseases. Hyper gammaglobulin EMEA actually be 800 or three, and these are a few of the autoimmune conditions that it's associated with. And clinically, it may present what signs of chronic liver disease, um, and signs of acute hepatitis A swell, some being fever and jaundice. And it's also patients. Some patients also developed a man or EOE with autoimmune hepatitis. So what investigations would you do if a patient came and came in to see you with those symptoms? If, you know, just put them in the jump books. Yeah, What immune screen? Anything else I left he is yet. So, So So. Those are the main ones you would want to do. Um, you want to check the LFTs, and you generally see phrase serum Ailton and ST um, And because it's autoimmune breeze serum, IgE a swell and you do the autoimmune screen. And depending on what shows up, whether it's anti nuclear antibody and anti smooth muscle antibody or anti liver and kidney, um, microsomal type one antibodies as well. So the autoimmune hepatitis it's actually grouped into three types, depending on which circulating antibodies found on the blood test. And yes, as someone has mentioned here, you want to, um, you'd also ideally want to do a biopsy. Um, unless the patient has a severe call, morbidity or any contraindications on the typical feature that would be seen on biopsy is interface Hepatitis, um, which means inflammation of the hot pack, two sides at the junction of the portal tract and the Patrick Parent comma. And it's also called piecemeal necrosis or bridge bridging the courses. And so this is generally treated with steroids and, you know, suppression and in in severe circumstances, a liver transplant is indicated. Okay, so we'll just move on to, um, acute and chronic hepatitis now. So two types of kids and chronic anyone knows the difference between chronic. What's the duration that it needs to reach to be considered chronic? More than through, it's the bit longer is more than six months, Um, so there's multiple types on with acute hepatitis. You have the viral hepatitis, um, autoimmune can drug induced with paracetamol and with chronic, um, we'll go over the each of the individual ones. A swell, but we've got happy hep C again. Autoimmune and the metabolic liver disease is so hemochromatosis. Wilson's disease and Alpha one antitrypsin deficiency. Uh, due to time constraint today we won't go over the metabolic liver disease. But we'll go over or the drug induced or paracetamol, but we'll go over the rest. So with viral hepatitis, um, generally patients present with quite known specific symptoms. Oh, Joan, Dismay, lazy fever, headache, nausea, vomiting. And occasionally they come in with the right upper quadrant pain and dark urine. Um, lab results are the standard raised Ailton, S. C and believer been on. You also get a quoting derangement because, um, the liver produces prothrombin, which is required for the question of the vitamin K dependent coagulation factors Onda In order to differentiate between acute and viral, you look at the immunoglobulins produced against the virus where I jam would be acute and I g is produced in chronic situations and in terms of detecting the actual virus, you conduce a PCR or viral nucleic acid detection. So we'll go over hep A, B, C, D and e. Um, just just just generally hep A and happy are transmitted through the fecal oral route. Onda Happy CD or blood born right. So hepatitis A is typically a benign, self limiting disease, with a serious outcome being very rare. It's an orange A virus on it's transmitted via the fecal oral route. The incubation period is generally between 2 to 4 weeks, and patients come in with the clinical features of fever and orexin. Uh, nausea, vomiting, jaundice, right upper quadrant pain has mentioned before, and this is The symptoms are typically similar across the various viral hepatitis, and the severity of the infection is generally dependent on the age, those that are less than five years of age or generally asymptomatic because they've got amateur immune system. So when the virus is introduced to the immune system because the immune system has not mature, they make very little response to the virus on they don't develop in acute illness that you would see with adults. Um, those less than five years of age generally have a short episode of the virus. The illness, they clear it off and they're immune for life. Where's those that developed the infection at annulled er, age we create quite a vigorous response to the infection where they become very unwell. That coming yellow jaundiced. Um, so with hep A, you're most likely to clear the infection and survive. So, um, how was it diagnosed? You can do a blood sample and check the i G or IgM levels in the serum. What? The enzyme in, you know, assay, onda, Um, IgM again, this scene in an acute infection and then I, uh, hepatitis a virus G seen in serum would indicate a previous infection. So it's usually self limiting on the treatment is generally supportive where you want to maintain your hydration, avoiding alcohol, anything to trigger the liver. Um, and it's got a very low mortality, though it does exist in the elderly. So just quickly go over this picture. So if you if you do those that do get the virus um, The hell the Altes the red red line represents the lt so practically response. You get liver cell injury. Um, in the short term, you develop I GM antibodies against the virus, and in the long term, you'll this is, uh, I g antibodies against the virus. And, um, with hep a um, there's no chronic hepatitis or no predisposition to have about two cellular carcinoma. It's generally travel of related on. Do you can get immunized to the virus so ineffective vaccine is available? Um, there's two types. There's an inactivated virus and there's a port in, you know, globulin. Um, and those who get the virus are generally, um, if you're gonna get Prius exposed to the virus. So generally travelers, um, IV drug users, those with chronic liver disease and also, um, homosexual men. And you also get immunized if, if there's an outbreak control so post exposure to the virus so we'll just move on. Um, we'll just move on to hep B. Does anyone have any quick questions about hep A. So far, if you have any questions at any point, just pop them in the chart. So with hep, a happy Happy is different to have a in the sense that it's more severe and you do get a chronic infection. So unlike hep A, which was our in a happy is Danny, it's very common, and it's vaccine preventable eso. The HPV vaccination is included in the immunization schedule in babies. Um, it has also spread. It's transmit to differently, as happy was fecal oral route Happy has spread through infected blood or voted lee fluids, including a vertical transmission from um, other toe. A child on the incubation period is also bit longer. It is 6 to 20 weeks. Patients present with fever, jaundice and elevated transaminases um, in the blood on, and the clinical course is generally it's it's It's more. It's more severe, um, so complications of acute hepatitis B virus infection. You can progress to a full minute infection ongoing to fulminant liver failure where it progresses from the onset of symptoms. Deliver failure in 2 to 3 weeks. Most people go into chronic well, you can also recover from it, and the rest go into chronic infection. Um, where in Children like as we discussed before. Um, it's known progressive because the immune system hasn't matured. Where's those with adults? It can progress to cirrhosis or have about two cellular carcinoma. Um, so 25% will develop a chronic hepatitis C virus and go into cirrhosis. Dick, um, liver decompensation on malignancy. Um, so we'll just quickly go through the structure of the hep B virus. Um, it's got a surface antigen, which, if if detected in the blood is a marker of infection, you've got the E antigen, which is a marker of high infectivity. So this would be in those with an acute infection. The hep C E antigen would be high only for a neck you period. Where has those with the chronic infection, which would last about six months or so. The antigen would be present for the whole six months. Um, the core antigen. Um, that's something that's a marker of a current previous infection. So if it's detected, it means that you've either fought the infection in the past. You have, or you have it just now. And you can also detect the D N e um, in the serum to measure treatment response when someone's infected with the virus. So, um, have these diagnosis the surface antigen on the DNA? So this on the any are detectable and the chronic. The treatment for hep B is is it's not, is basically to suppress the viral replication and to prevent further damage, Um, and this can be done with the interferon awful or other anti virals Onda happy is prevented by just education at educating people vaccination. All Children in the U. K run are vaccinated as a part of the routine immunization schedule, and they're given the vaccinations at 23 and four months of age on those that are at risk groups. A swell such as healthcare Workers IV drug users, Um, should all be given the vaccination as well. Oh ah, Forman in hepatitis that That just means that they go into a liver failure very, very quickly. So we'll go back to that slide and it's Yeah, it just basically means that they go into liver failure from the onset of symptoms, deliver failure in about 2 to 3 weeks. So I don't care. So we'll run to I'll just quickly go over the serological course. So this is for acute, and this is for chronic. So if you look at the red line as the anti itch in, so that's when the virus is present in the virus is present in the blood. Um, foreign acute period of time. So less than six months. That's the surface antigen. When the surface antigen is positive, Um, you condone I A goes the happy infection. Um, when the antigen is positive. It means that they're currently infective, um, during which the immune system. So the yellow line is the I. G. I am antibody, the acute antibody against the virus that is produced, um, and and this blue one is the I G long term one that is, uh, antibody that is produced, um, and with the with the chronic with the chronic infection. So you have the surface antigen in present after for greater than six months. So it's present and you get the acute acute antibody response fades and the chronic antibody response remains, so we'll just move on to help. See so hepatitis C is an or any flabby virus, and it's a really big problem. It affects 170 million people worldwide. It's mainly transmitted in IV drug users, but it's also transmitted through blood transfusions, transplants sexually and vertically and through a little needle stick injury. Though the statistics show that the risk of transmission during the needle sick and jury is about 2% vertical transmission is about 6%. Onda um during sexual intercourse is about just 5%. It's mainly transmitted in IV drug users and through the blood transfusion um with hep C. There is no vaccine, um, no immunity to the virus. So even if you're infected to the virus, you generally don't develop a protective antibody response. The incubation period is about 6 to 7 weeks. Onda with hep C There's a high rate of progression to chronic disease. Um, so somebody, I mean, most of the time it moves into chronic disease rather than resolving, which can progress to cirrhosis, which then later can present progress. Uh, about two cellular carcinoma, um, and and death. And this is generally the rate of progression is generally related to the gender. It's it's it's greater, and males those of increasing age and those that take, um, have Hying alcohol intake. A swell, yeah, So the clinical features for hepatitis C. It's usually it's mostly Isam Timoptic. Only 30% of patients will actually develop jaundiced so on have transient rise in the serum amino transfer eases or present with fatigue and arthralgia. So with investigations like like the other hepatitis viruses, you generally want to a PCR um, look for the antigen, but look for a current infection. And if you do an enzyme immunoassay on, look for the antibodies. If it's I g. You know that it's a chronic infection that's been cleared. IgM means it's an acute infection. So the good thing about Hep C is that it's very treatable. And there's a cure rate of about 95% and only kept the where the aim of the treatment was not to treat the infection, but to suppress the valve application in hep C. The name of the treatment is to treat the infection with during direct acting antivirals but dependent on the viral genotype. So we'll move on to hep D. So hepatitis D is is it's a single stranded RNA virus, um, again transmitted, similar to have hep B Um, and it's a defective virus, So it's easy to remember Hep C dif rejected effective. It only replicates in the presence of hepatitis B. Um, and you can get two types of infections With hepatitis D, You can either get what's called a co infection where you get the hepatitis B and hepatitis C infection at the same time. Or you can get super infection of hepatitis B. Um, where you get where a patient that is currently, um, having hepatitis B infection subsequently develops a hepatitis C infection on top of that, with the co infection when they both come in at the same time. Uh, you have a severe acute disease onda a low risk of chronic infection. However, if you develop a super infected hepatitis D, um, you have a higher risk of severe chronic liver disease. Ah, fulminant hepatitis and cirrhosis, and it can present with an acute picture, and this is generally treated with an interferon. So the last one of the law hepatitis C E. So this is a new one. A virus? Um, it's common in central and South East Asia and also in North and West Africa and in Mexico, and it causes similar disease to hepatitis A. But it, um, where it's transmitted fecal orally on disassociated with large waterborne outbreaks. The incubation period is about 3 to 8 weeks on. In the UK, hepatitis is more common than hepatitis A. On similar to help a the treatment of supportive, mainly hydration with IV fluids on, there's no vaccine. So, um, this congenitally be prevented by avoiding drinking, um, clean water when you're traveling to locations where where the hepatitis C is known on be making sure that you're not eating undercooked foods. Grayer Lee Hepatitis C E can have neurological manifestations off again. Bari syndrome Careful itis a taxi, our myopathy, Um, but it's quite rare. Onda. And usually there's no chronic, and generally there's no chronic infection. And you're not a carrier of the disease disease. Once you fought thing, infection gets cleared completely unless you're immuno suppressed, then chronic chronic for maybe seen. But most of the time, most infections are asymptomatic and mild. Um, a scene in this picture. Um, the infection comes once it's gone. It, um, your auntie. Your immune immune system fights it off completely. So that's us with the viral. Hepatitis will move on to fatty liver disease just now, So we'll go through, um, alcoholic liver disease and nonalcoholic fatty liver disease. They both have a similar progression of the disease, where it starts off with a macro vest. Micro vesicular steatosis, um, progresses onto stare to hepatitis on, which then further progresses onto pericellular fibrosis. But we'll go into this more into depth for their own. So just another case, um, 38 year old man presents to the Emergency department for severe alcohol abuse with nausea and vomiting. He has a significant medical history of chronic heavy alcohol consumption off about one bowl of wine each day for about five years until one year ago. Since then, he has had severe intermittent binge alcohol intake reports. No other significant medical problems. Patients confused, Lethargic has a pattern. Megaly um, low be in my, um, and lab values Show ST Elevation lt. Elevation Normal prothrombin. An eye on our high serum alcohol intake on ultrasound of the abdomen shows fatty infiltration of the liver. So this is a typical picture of someone with alcohol. Hepatitis, um, with the history of chronic alcohol consumption and the blood Zahra also consistent with alcohol. Hepatitis. But we'll go through that together. So alcoholic liver disease comes in three stages. UM, starts off with the fatty liver. Stay a Tosis progressive zone to hepatitis, so inflammation across this and then progresses onto it. Reversible changes with cirrhosis. Alcohol. Liver disease is a growing problem, especially in the UK. Accounts for about three million deaths annually worldwide. Um, mean cause, as is in the name is chronic heavy alcohol ingestion, um, bit different for meal and female. So the clinical spectrum they present with. They come in with features of chronic liver disease. Um, Molise nausea had to make a li fever, John dis. And as as it progresses and gets worse to cirrhosis, um, they come in with signs of decompensated liver disease. So Subsys and careful up the Masai it ease and have a high mortality. So And I showed you that picture. But what investigations would you like to do with someone for someone that comes in with you with that kind of history? Yeah. And do you know what in the lft is would be would be specific to alcohol. Liver disease? Uh huh. Anything else? Yeah. So is ST generally greater than yeah? Yeah. Okay, so we're all heading towards. That's so you have a raised GGT raised sc raised Ailton on the thing. That specific toe alcoholic liver disease is that the ST T A L T aviation was generally greater than two. Um, if it's greater than three, it's strongly suggestive of acute alcohol. Hepatitis? Um, you also get raise your be, uh, a race prothrombin ratio, and I and our raise Billy Rubin race white cell count. Um, those that have alcoholic liver disease. If they progress to cirrhosis that can progress the portal hypertension. We'll talk about that further down, but those with portal hypertension if they develop portosystemic and ask them OSIs and have a sofa, Jill Varis is or developed hemorrhoids are more prone to bleeding. Um, which is where you get a raise Urea when you've got, um, leading in the chair, attract race Pro Thurman ratio is well, if the liver is effective, affected to the point that it cannot produce the prothrombin, um, you'll still get raised. Believer Been, um, with the which can be contributed by the bleeding that happens as a result on de decrease uptake off. Um, believe we've been to the liver if it's not working properly and raised white cell count, which comes in with the inflammation that happens in hepatitis S T A N A L T. R um also released by the liver. So when you have problems, So Ailton is generally greater than ST in a nonalcoholic fatty liver disease and other conditions. But what specific two alcoholic liver disease. Just notice for your exams. It's generally S C is greater than a little bit, but usually 1.5 to 2. Um, and this is just clinically relevant. Alcoholic hepatitis. What you'd see typically, Um, what one? A patient comes in his race believer been if they've gotten to the point that that their septic or they have signs features of GI bleeding and so you know there's a slight discrepancy, but it's usually greater than 1.5 or two s. C. Two l t racial on some characteristic features. Air have to Michaeli fever leucocytosis, and if you also take them, you can generally hear a bruit. Ideally, with all patients, you'd like to image the muscle well with the ultrasound and, um, liver biopsy is diagnostic, but it's not indicated. But of course it's diagnostic and all patients, so any damage to the liver can be arrested at the pre cirrhotic stage. Um, if, if so, we'll move on to management with alcohol. Liver disease, um, mean management issue. Abstain from drinking alcohol and those that do so. If if alcohol is abstained, deliver can return to its normal architecture. Um, as an as what's described in these photos. However, if there's continuous exposure to alcohol and there's repeated attacks to the liver it progresses to the ever versatile stage known as cirrhosis. And when the liver undergo scerosis fibrosis and it becomes irreversible, there's disruption to the liver popular and the normal architecture of the blood flow. And that's when you develop portal hypertension on. Lots of complications arise at this stage, but pre cirrhotic stages. Um, if alcoholism is, is if if they don't take alcohol, um, you can reverse the damage to the liver. And in acute situations, someone patients come in with alcoholic liver disease. They're treated with generally steroids and prednisolone, and you can do periodic liver enzyme tests just to monitor the owned going damage. So they mentioned before, um, some complications of cirrhosis, which will move further own, too. Um, are signs off Portales, the stomach anastomosis, where you get a soft ajeel and gastric variceal bleeding can get ascites coagulopathy hepatic and careful up with the on it can progress. The malignancy is well, so about two cellular carcinoma and alcoholic liver disease is associated with a high. Mortality is high as 60% in the short term, so we'll move on to another case on D. I'll just highlight the key words for you purge it here. Oh, man. Referred to the liver clinic with a mild elevation, and Aminotransferase is for several years. He has a medical history of obesity. Hypertension? Hypercholesterolemia does not smoke or drink alcohol. No high risk behavior has a family history of cardiac disease. Um, taking a direct IgG and has elevated liver tests was recommended to discontinue statins other than that complains of mild fatigue feels and, well, freeze via my trunk. Obesity on a part of my ugly. So, yeah, So these are all pointing towards a nonalcoholic picture of fatty liver disease. No alcohol, but deranged lefties. So nonalcoholic fatty liver disease, um, is thought to represent the hepatic manifestation of the metabolic syndrome, Um, and hence insulin resistance of that, she thought to be the key mechanism leading Teo Steatosis. It's the commonest cause of liver disease in the developed world on it's associated with obesity, Tector, diabetes, hyperlipidemia, metabolic syndrome, and hypertension. So it describes a spectrum of diseases from state Tosis to non alcoholic set a pattern site hepatitis and progresses down to cirrhosis. So So this is stay a Tosis. You can see, um, lipid vacuums filling the patent site cytoplasm and it's generally known Peress it. If further damage is done, it progresses to a national. You get, um, so non alcoholic stay at two. Hepatitis is the term used to describe liver changes, um, similar to those seen and the alcoholic hepatitis. But in the absence of any alcoholic abuse, so you get lobular inflammation. Um, and you get ballooning degeneration, which is a form of, um, hepatocyte death. It's a it's a it's a form of liver parent kind of cell death. Participate, uh, and this progresses own to cirrhosis. So the clinical features of nonalcoholic fatty liver disease, or generally it's generally a symptomatic, Um, but when you do the investigations in this scenario, the ST to the Lt ratios journalism lessens your 0.8. Um, and lt's greater than ST um, you Also. This is also diagnose up saquinavir. A what? Diabetes being present on hep a cholesterol anemia, raised triglyceride, low HDL cholesterol and raised HB a one c um, like, like with any condition? Um, imaging is very useful on ultrasound. Imaging usually shows um, increased echogenicity and asymptomatic liver fatty changes on D. Um liver biopsy is always the goal standard, though it's not indicated in most patients and the management for enough. Aled is primarily weight loss and lifestyle modification with diet and exercise. And studies have actually found that weight reduction was associated with remission of the disease in a dose dependent manner. In both patients with the baseline of a bm I less than 25 um, and those with the B m I've greater than 25. So we've just got a table. Just, uh, um, help you distinguish alcoholic liver disease versus nonalcoholic fatty liver disease. So the weight is generally raised in the non alcoholic with raised, um, plasma glucose or HBA one c alcohol and take his race Two alcoholic liver disease. Both have raised Ailton, whereas with alcoholic liver disease, you have a, uh, great rise in the ST with a nasty to a little ratio of greater than 1.5, where, as this is generally lessons or 0.8 and non alcoholic, um, and triglyceride Zerhouni, I, um, in on a colicky as well. So, um, we'll move on to the next case, which I'm sure you can, um, have a guess that what it is through this picture. So how about the main points. A 56 year old man with the remote history of intravenous drug use presents to a knish. Aleve. Is it complaining of increased abdominal girth, but denies jaundice. Um, drinks about 2 to 4 glasses of wine. Um, had abnormal liver enzymes. Physical examination reveals spider in IV I palpable firm liver splenomegaly shifting dullness. Onda ascites liver function is deranged. Elevated S t a L T on. The patient has hep C eso. Can anyone tell me what this history is pointing towards? Yeah. So cirrhosis. So as we mentioned before, any damage of the liver can be arrested at the pre cirrhotic stage. But once there is disruption to the normal liver architecture, you developed the irreversible complications. Um, and cirrhosis is a pathologist, kel, and stage of any chronic liver disease. Yet progressive destruction of the patch of sites on replacement by fibrous tissue. You get complete loss of the liver, a lobular architecture their money causes to it. But the three main causes are happy. Helps see, um, alcohol and nonalcoholic fatty liver disease. So hepatitis and fatty liver disease. And it's a progressive form of fibrosis that because it just disrupts the liver lobular architecture. It destruct. Disrupts the portal. Blood flow on because this portal hypertension and once a patient with psoriasis develops signs of decompensation. Um, survivalist significantly impaired. So this is just a picture with, um, the means clinical features. You see what cirrhosis, Um, there many side effects. A lot of the card. The a lot of the systems. But the main clinical features you see are you see the spider knee by, um, you see you you can smell feature hepatic. It's so, um, in their breath, um, they become in careful of pathic They come in very confused on this, um, and they're they also have a malnutrition. Um, does anyone know what the blood results would show in cirrhosis? Besides, besides looking at the besides the past and the lt, what other abnormalities would you see in cirrhosis? Yeah. Abnormal clotting. Yep. Yeah. Braised ammonia in and careful with e. Anything else and yeah, and albumin. Nice. So you get low albumin and clotting factors for long preferment time and bleeding A swell. So you get happened anemia. We'll go through that when we talk about, uh, just liver function tests, but the liver produces albumin. So if, um, deliver is not functioning properly, you get low albumin produced. So, um, the end results of certain cirrhosis causes race portal pressure as we discussed you to the disruption in the blood flow and you get increased resistance to the portal blood flow. So as a result from the portal hypertension, you get a raised portal pressure and you get 42 systemic shunting and hyper spleen is, um So here's an image of a cirrhotic liver and, um, with the increased with the increased portal pressure, you get all these problems that arise. Um, so you get vasal dilation, vice visit dilation. Entering the systemic circulation, you get a reduced, effective circulating volume which results in the splanchnic. They so Tyler patients. So but flow that's flowing towards the cut and the liver are now flowing into the portal system. Um, you get reduced, effective circulating volume. So you get you end up getting a hyper dynamic circulation which results in, uh, compensate tree vasopressin. So the renal undertones, um, out aldosterone system catacholamines they're all released. You got sodium retention, assuage Well, which causes ascites, um, and renal vasoconstriction, which can cause the pattern of Innocence syndrome. Um, and you also get, um, hyper spleen is, um, due to the, um, the back flow to this spleen, Um, which, which causes a splenomegaly and thrombocyte to penia. Yeah. Um, so So basically, with the hyper dynamic circulation, I'll put a slide at the end, which nicely, um, explains all of it. So, um, mainly for the exams. Um, they'll ask how you diagnose cirrhosis. Well, Onda, traditionally a liver biopsy. Why do you get hepatorenal syndrome? Because, um so when you have, uh, it causes changes in the chemo dynamic circulation and causes, um, it causes a vasopressin ear's. It activates savino undertones. Um, and out of staring system ah catacholamines to be produced on. Do we know these? Those construction happens. As a result, it's a whole cascade. I'll put up a picture at the end, which links the whole cascade, which ends up causing hepatorenal syndrome and hyper dynamic circulation. Um, but cirrhosis is diagnose. Generally it traditionally liver biopsy was used, but it was associated with adverse effects such as bleeding and pain. So no imaging using a fiber scan is used. It's kind of like a ultrasound scan. It's called a fiber skin, and it measures the stiffness of deliver. And you can also do a blood based assessment of liver fibrosis. Um, with an inhance liver fibrosis test. And and they're these scores that are done a pre and fight for you don't need to know too much about to just know that it exists. These air just blood basis essence of the fibrosis. So the management of cirrhosis, um, it's the management is generally to treat the underlying liver disease, um, and to avoid superimposed injury to manage complications. And last case scenario is a liver transplant, which is the only curative option for patients with decompensated cirrhosis. Um, further investigations. So having a cirrhotic liver puts you at an increased risk of developing a a part of cellular carcinoma. So those that are those that are diagnosed with liver cirrhosis generally have a liver ultrasound done every six months plus minus and off a feature alpha fetoprotein, which assess for um, about two cellular carcinoma and because those with cirrhosis have a high risk of developing a sofa. Jill Varis is with the portosystemic anastomosis. Um on endoscopy is generally done on patients with new diagnosis. Um, complications of cirrhosis. Um, some of which are spontaneous bacterial peritonitis, Patrick. And careful up with e cerebral edema, renal failure with the battery nose syndrome, um, Subsys metabolic disorder and coagulopathy. So, with a spontaneous bacterial peritonitis, cirrhosis puts you at a higher risk of infection. With the, um, portosystemic anastomosis, you have got a decrease in the compliment level. Decrease in the neutrophil adherence. Onda just put your greater risk of infection. So, yeah, you want to see the slides for? Is this aside for the investigations of cirrhosis? Okay, I'll just little gone. Right. So one of the, um when you have decompensated liver disease as well in cirrhosis, one of the complications are ascites and assess ascites. You generally do a diagnostic top. Um, and the main things you're looking for are the cell count on the albumin. Um so spontaneous spectral peritonitis is quite a n'importe topic. Um, I graduated from Glasko and every year in the, uh, ski, um, when we had the g i station, they give us investigations. Looking at a diagnostic top. It was It was a past paper. It was there, and it was repeated in every year, including mine and the diagnosis was to diagnose SPB um, which can be diagnosed with seen, uh, these values greater than 250 neutrophils percent better? Um, it's it's got a higher mortality unless treated appropriately. And it's generally treated with IV antibiotics on albumin. US. You'll get the sides of the end, Um, in the cell count for ascites. Um, in inflammatory conditions, you see raised white cells. And if, um in those with TB or peritoneal carcinoma, you got a lymphocytosis is the other aspect of ascites that you look at his albumin. So you want to look at the serum ascites album ingredient, which is the serum albumin minus the ascetic albumin on a portal. Hypertension is diagnosed if the serum ascites album ingredient is greater than 11. So management of ascites is generally a low salt diet. Um, Diarrhetics to get rid of the fluid is generally treated with a spironolactone on aldosterone antagonist plus minus furosemide. Um, which is a look diuretic? Um, other Other ways to manage ascites are paracentesis, where needles inserted into the paratonia will cavity to obtain an acidic fluid or trans jugular Intrahepatic Portosystemic shunt is done in the later stages. those that come in with the society. Is there generally given prophylactic antibiotics to reduce the risk of the spontaneous bacterial peritonitis? Um, which is associated with high mortality and with every liver condition, the only curative treatment is a transplant. Um, bear in mind that when you're treating a societies you want to aim for a weight loss of 0.5 to 1 kg a day, so tips is transgenic. You alert inter intrahepatic portosystemic shunt. Um, it's basically a shunt that connects the portal circulation to the systemic circulation. Because in this case, you get a portal hypertension, which you shouldn't do, which results in the whole cascade of events that lead to the complications of cirrhosis. Huh? Uh, so the paracentesis is, um, it's it's it it it removes the fluid as it's it's a proper procedure where they removed a lot of the fluid. So, um, for cirrhosis for many years, um, that the child classifications was used to classify the severity of the liver cirrhosis. However, in recent years, the model for end stage liver disease is being increasingly used, particularly in patients were on a liver transplant waiting list. Um, but the in order to score. Um, the cirrhosis, the main aspects that are looked at our cuff allopathy ascites, the Billy Rubin levels albumin and the n and R and based on the points that are but the some of the points, um, it's classified into being mild, moderate and severe. So, um, we'll just move on to a liver function test interpretation. So the LFT is our a panel of biochemical tests, often deranged in patients with liver disease, which I'm sure you've all come across. A typical LFT consists of believer been lp GGT s C A, l T. And opium in. And just keep in mind that no single test is a reliable indicator of liver function. Delivers got many different functions in a diverse possibility of diseases. And it should always be interpreted, interpreted in the context of the clinical scenario, um, with an understanding of the degree and develop reliability and the specificity of the test. So, yeah, so the synthetic function of the liver So the liver the liver produces deliver produces, um, ap in men that produces clotting factors. So that's isn't that tick function of the liver in terms of the things that synthesizes and deliver function can be indicated by albumin, Billy Rubin and Prothrombin time um so LFTs air. Generally used for screening, it's a known invested tool. Um, recognize different types of liver diseases, as we saw earlier. Different sheets. Um alcoholic versus nonalcoholic fatty liver disease. The disease is a different sheets, acute for all hepatitis. Call a static disorders as well, and it can assess the severity of diseases and value with the response to therapy. However, some limitations to a lefty's air that black sensitivity, um, where LFTs may be normal in certain liver diseases and Lex specificity. Um believer been a nice, elated race believer. Been may indicate Hummel Asus because, um, the overthrow sides are broken down by the macrophage is in the spleen on the bone marrow. And they release um, he, which is converted toe build. Virdon and Billy Rubin uncontradicted Billy Rubin, which goes to the liver to get conscious to to become conjugated and so on and so forth, which is a physiological process. Um, if you have increased Tamala sis, it doesn't mean that there's something wrong with the liver. It means that there's a it's just that there's more believer been in the blood stream, which is why you get a raise Billy Rubin, brother, than a problem and the liver and up taking the bilirubin. Does that make sense on D um, what the alkaline phosphatase It's found in the liver, but it's also found another tissues, such as the bone but intestine. The placenta, Um, and it's located in the cells lining the biliary ducts in the liver, so it's generally a marker of raised. A little pea is generally a marker of Cholestasis ST, which was raised in alcoholic liver Disease is also present in the heart, muscle, kidney and brain. Um, so it can also be raised in my cartilage for action on a muscle injury. In addition to a patch, a cellular disease and albumin is decreased in chronic liver disease disease. But how Hypoalbuminemia is not specific for liver disease. It also is. It's also seen an nephrotic syndrome, as you know, and in protein malnutrition. But just the main things you need to know are that raised and isolated raised. Billy Rubin is, um, is a sign of hemolysis ST and they'll t are mainly rapist in a patch, a cellular disease where there's damage to the practice sides. Um, on raised ailed P and G t are mainly seen in an obstructive cool static picture. So where you have a damage to the bile doctor or where you have a gallstone? So in so in prehepatic jaundice, you have a raised bolivar been in hepatic jaundice. You'll generally have damage to the hepatocyte. It's see have a raised S e N l t onda. In post hepatic jaundice, you generally have a raised ailed pee and digiti does that make sense? Does anyone have any questions on that? I don't care. So we'll just look at a case. So a 40 year old house wife complains to her GP for generalized severe itching during the previous nine months, No other symptoms. Low alcohol consumption slightly John dissed and Billy Ruben was checked in the urine on these air. The results of the LFTs um, does anyone want to open the chatter box? What is the most likely cause of the jaundice? Anyone? And why is that? It is. And why is that why you all saying be Yeah. So it's a CBD stone because you have raised LP on GGT primarily. Yeah, Okay, um, we'll just go to the next case, um, 52 year old male, um, presenting complaint so there could be right upper quadrant pain. Um, but it's just not in the history. So it was just interpreting it from the blood results. And, uh, you with the raised LP and the rain Streett. It points to, um, CBD Stone. So just the next case, a 52 year old male presenting complaint, tired for a few weeks and then jaundiced, um, drinks 25 units of alcohol a week for many years, has a history of blood transfusion for road traffic accident. And his cousin had his iron in the body. Um, he presents what signs of chronic liver disease disease on ascites. Um, what is the most likely diagnosis looking for from these blood results? Uh huh. Anyone else? So this is a trick question. Um, look specifically at the look Look specifically at the at the individual blood results. Yeah. So this was tricking you to think of hemochromatosis, but if you look specifically at ST T A l t. Um, the sed to the l t. A ratio is is about I'm 221 so it's actually, um, alcoholic liver disease. So they may do that in your exams, because I I this This also caught me out on the the first time I saw it. So we'll just go on to the third question. So this is a 70 year old male with cirrhosis and has a rising alpha fetoprotein and a focal liver lesion on ultrasound scan. What is the probable diagnosis? Just give it a couple of minutes. Yeah, so we didn't go over it over this talk, but, um, off of fetoprotein is a marker of a pack. Two cellular carcinoma, so smack spent. Um, and it's it's been our we'll just quickly was through a primary biliary cholangitis on Gilbert syndrome. So, um, primary biliary cholangitis is an autoimmune disease disease, which is diagnosed with serum anti mitochondrion antibodies and a high I g m. I'm the typical picture you'd get in your exam would be on itching in a middle aged woman. And despite the name, a primary biliary cholangitis is not cirrhotic from the onset, it progresses to fibrosis and then cirrhosis. Over the years, um, the pathophysiology behind it is that the interloper bile ducts become damaged by a chronic inflammatory process, causing progressive, coolest Stasis, which may eventually progress to cirrhosis. So it's generally key Features are, um, anti my to control antibodies female, which and management. Just remember this, that it eases symptoms and slows progression. Onda. Um, like what with any, um, liver pathology at the end stage Is a liver transplant a security? Um, because it's autoimmune. It's associated with other autoimmune diseases, such as a dragon syndrome from Twitter threat issues, stomach sclerosis and thyroid to see disease. Um, complications, um, of primary biliary cholangitis are cirrhosis portal hypertension ascites Barris. I'll hemorrhage on. But, um, it puts patients at a greatly increased risk of a pack. Two cellular carcinoma, um, Gilbert syndrome, um is an autosomal recessive, um, it's an autism all recessive syndrome, which is very common scene in around 8% of the general population. Um, it is, it's It's caused by a deficiency off this, which leads to decrease congregation of uncontradicted Billy Rubin. So generally patients are, but but But they're just a bit more yellow than the average person, but it's asymptomatic. Um, they may have mild jaundice during times of fasting or physiological stress seen during an interferon illness or exercise. Hum. But And and if you do check their blood's, they will have a raised, uncomplicated hyper Billy Rubin, Um, and Fries and Billy Rubin following prolonged, uh, fasting. Um, there is no treatment required. There's no liver injury or progression toe on end stage liver disease. It is very mild, and it's it's quite common. One of my friends has a swell. It just means that your bit more yellows than the average person is, um, so that's that with Gilbert syndrome. Um, I'll add on the side, which shows the pathophysiology with the cascade off. Um, all the events that's cirrhosis causes that leads to the the the hyper dynamic circulation, the part of, you know, syndrome and etcetera. I don't have the side of pure, but I'll put at the end, and we'll send you a lot of slides out. Um, besides that thank you for listening to the presentation that concludes the end of the talk. Does anyone have any questions? And if you could kindly scan this cure code and just fill out the feedback form, um, we'll send you the slides once you've done that. Awesome. Thanks Actually, that's actually really helpful on greedy, useful sorts of questions, finals and things. If everyone could fill out the feedback form, that's really helpful for us to know. And also it's useful. Fashion is I'm portfolio good. I mean, people are asking for a link. Just Sorry. I'll just start. I leave this, uh, Aleve. The just a second. If you just scan this cure quoted should work. Let me see if I can get your over days. See, Let's see if that works. Awesome. So keep be, um um using, going. Just think you will have any questions. Otherwise, once you filled out that form, then you guys are things Go right. It's, um Actually, I've just got message from someone to you Go through the answer to the case, too. Yeah. Let me this one. Yeah, I think that's one. Right. Um so this was