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So without further ado, this is gonna be delivering a hepatology, said station. I'm sure you guys enjoy his gastroenterology one last week. Join us for the next station, which is our renal station next Thursday and keep a look out on our Facebook page. If we might put a surprise event on next Tuesday, possibly a crash course of something we still thinking about it, so well, good luck for your finals. Take it away. I see around us. Won't answer. The someone was asking about how slides were sent for last week. Um, the the slides, Firstly, they're they're on metal slide decades. Well, so if when you feel in the feedback from you have immediate access to the slides and the recording, which we'll upload it after a bit of time, obviously, because we need to couldn't get everything in stuff, but, um, moving might be the best person onto this movie. Yeah. So once you feel in the feedback from everyone mentioned you be access will upload it to the what we call the slide deck on metal, where you can just download a pediatrician of defiance. So, um, do you have to create an account on uh huh. I think it's so far it's been everyone's been able to access it. Um, right. Looks like some people haven't received the email also, so check that we'll we'll start it out more. Then they just met. Drop moving a message, and you can try and sort stuff up. Yeah. Okay. Let's get to it. Okay, so Hi, everyone. Um, my name is Michelle. Um, you guys might recognize me from the session I did last week on gastroenterology. Today is a bit of a build up on that session. That's Ah, run off faster and told it's hepatology on Be very interesting specialties. So let's get to it like that. My name's knish. Um, one of the co founders and head of education for our ski easy don't have a lot of lectures as part of the skin. Is he teaching program? And it's only I don't really enjoy And hope and hepatology is, uh, specialty. I have a lot of interest in myself on. Hopefully I can bring in a lot of my passion for the learning this subject and teaching this subject. Ah, into this session today. Yes, Uh, Hepatology is study of the liver. If you guys have any questions throughout the session Ah, please leave it in the chat. What I would say today is that we have a lot of SPS based on the people from last week on the gastro session. I think a lot of people quite enjoyed the, uh, SPS. We did the sort of difficulty and the challenging nature of a lot of the SPS. Uh, this week, I've tried to add in a couple of more SPS tried to switch up the balance to wards, having more SPS and bit less in terms of teaching slides. So hopefully they'll be really useful for your revision and sort of SBA practice as well. What I will say quickly is that some people will spend back that something. SPS were really, really hard. Ah, I haven't changed the difficulty of the escape. Is there gonna be really hard SPS today? But don't Don't worry for getting things wrong. Okay, Take, take getting the wrong answer as a learning experience, okay? These SPF are hard. I've made them hard, but I didn't make them hard just because I mean person, I made them hard because there's, um I wanted to really emphasize, um, important learning points for you guys, and hopefully getting the wrong answer is probably more useful for your original cause. It's going to stick with you better. Okay, so we're going to stop just hep told you that branch of gastroenterology that is rapidly evolving, okay? It's becoming increasingly its own distinct field, and, uh, liver disease and itself is becoming its own interesting, and you need field of research as well. It's a very interesting specialty, and hopefully you guys will get be open to exploring more about this specialty after this session as well. So the liver is a crucial organ that is a place a major role in many life functions. Okay, it's a super hardcore, and it does all of things on. We're gonna touch on something really important things. It does. Disease is affecting the liver are very common throughout the world. Okay, so it's super important as a clinician to have a good understanding off liver disease and in terms of when you're studying hepatology, just like many other specialties underlying the basic principles, it's key to understand the disease. Okay, so to understand what goes on with the liver and dysfunction, we need to first have a good understanding how they look at how the liver is going to function normally. Okay, so today I thought, today it's cover a bit more in terms of anatomy and physiology before we start going into the clinical stuff. But here's our first SPF. One of the team members can let up the pool. Also give you guys a bit more time to answer questions today because I think last time maybe kind of got rushed towards the end of that gave you guys a little less time to answer questions. I'll go and give you guys a much time as you need to answer questions. But I think everyone both of you are getting it here. Pope, Here's the most of you went for C. And that's probably the did considering we're doing a session hepatology. Yeah, it's probably gonna be the right answer, So yeah, so liver. So let's write down this SBA This is ah, bit of a basic SPNS Uh, hopefully a nice, easy one to start off with, but said she would go on a man, a 56 year old man who's presenting palpitations. Uh, what is the rhythm? Once the EKG showing you guys gonna answer in the jut? Well, a half. Very good. Okay, so, uh, it's fasting after Katrina fibrilation with rapid ventricular sponsored, eh, eh? For tachycardia on, Do see if you guys know that atrial fibrilation, you have increased risk off forming from both cysts because of the, um because of the static blood flow in the left atrium. And so the question is asking, basically, which off the organs? If that thrombus amble eyes is that organ, which one is most likely to function? Okay. And the liver out of all these organs delivers most likely to continue to function even if there's an embolic event in that organ. Yeah, tell me, why would the liver continue to function even if there's a you know, if there's an embolus blocking one of the vessels out of all of these are out of all these organs compartmentalized you ever the What's the Yeah, you guys got a job but slight? Excellent. So the liver's got dual. But supplying get supplied through both the proper Patrick Artery and the portal vein. Okay, So in terms of important learning point deliver has do a blood supply from the portal vein. Is Patrick artery proper? Okay, so in terms of clinical relevance of that in the event of an often, um, Bolic, events deliver would could actually continue to function. Okay, that's not to say the liver will always function, but out of all of these other options delivers most likely to continue to function. Okay. In terms of the other options of brain, obviously. You guys know you get strokes. Okay, This is stroke at strokes and atrial fibrilation are very strongly linked together because of embolus spleen. So embolic events are rare in the spleen, but the spleen only receives blood flow from the Spanish guy artery. So, in an embolic event, this mean is very vulnerable. Okay, go by the only received blood from the cystic artery. So it's vulnerable, a swell. And you can get embolic events in the colon and that can present with acute mesenteric ischemia. Okay, so you get embolus blocking the superior mesenteric artery and the inferior mesenteric Terek artery, and you can get mesenteric ischemia. Okay, that question is basically just to introduce, um, physiology and anatomy related to the liver. So we got our beautiful liver here. Okay, so it's a basic concepts about the liver, and that's meats. Liver's look is a huge organ located in the right upper quadrant. Terms of the lobes. You got the right lobe left lobe separated by the false form ligament. And the blood supply is super important to be aware of for the liver. Okay, So here we have, uh, three big structures going into the liver. We have the problematic artery and red behind that. We have a portal vein, and here we have our common bile duct. Okay. And our goal bladder here. Okay, it does the embryology, if you might get us this in finals exams, but embryology in embryologically deliver is derived from the Androderm. Okay, So remember, in your Enbrel embryology, you have your trial. Um, nowadays, you have, um and, um is it, um, and active Them deliver is derived from the endo dumb. And you also have a decent capture, which is the fibers capsule. That and covers deliver. Okay. Ah, Can you guys tell me, what is the clinical relevance off the blues blue since capsule. What condition do you get? Information off the Gleason's Captain. You guys know we'll talk about it later. And what condition can you get? The sense capital information. Yeah. Fits you. Care to syndrome? Very good. This one. There's another one. So fits you, Curtis. That's a complication of B I. D. Help syndrome. Very. Get some about private eye surgery, help syndrome and help syndrome. You can also get liver capsule inflammation. Okay, very good. See if it's you can't doesn't help syndrome. That's why the Gleason's capsules clinically relevant you can get you can get inflamed in certain conditions. Okay, this table some rising. It's sort of the main functions of the liver. Okay, you could do off. There's a you could do it right? The big list, some rising, every single function of the liver. Okay, But in this table, I've tried to summarize the main functions again and try to categorize them into different, different functions. So Liver's involved in detoxification that matter metabolism. It's involved in synthesizing a lot of different things. It stores a lot of different things. It produces very important hormones. It produces bile. Okay, which is important for for fat absorption. And it's also important in the units as well. Okay, now we have all of these different front function's okay, but in terms of what's clinically relevant, can you guys tell me what is the most important marker off the liver function? What's the most important way of measuring the liver's function out of all of these different functions? So you got albumen and clotting? Yes. Oh, yeah. Albert are quoting are definitely the top two options. Okay. In fact, I take clotting is even more important than albumin because albumin can albumin convenient, even acute inflammatory states clotting functions that I am not anything Most important measurements off the liver function. Okay, so if your liver is reducing infection, the clotting is the really important thing you want to be looking at. Okay, so that's very clinically relevant. Never forget that. Okay. Ah, Another quick question. What clotting factors? There's a liver, liver produce. What? Which falling factors. What are the numbers do? 79 and 10 on Do yeah to 79, 10 years. Very good. Okay. And, oh, another quick question. So we have everything in neonaticide off red blood cell production from six weeks until birth. Okay, so the liver is involved in producing red blood cells for the units after six weeks. Um, and certainly when does the bone marrow start taking over red blood cell production. So, obviously in humans in adults Ah, the bone marrow is the main side of red blood cell production. When does the bone marrow start taking over from the liver and producing red blood cells and don't have any idea? 32 weeks. Ah, it's about 18 weeks. I think it's about 18. 18. I think it's 18 weeks until both. Okay, that's what I've read. Um, yeah, that's the main function of the liver. So now we're gonna talk about some gonna go into a lot of the hardcore clinical stuff, okay? And we go, just go straight in and I will go. This SBA zooms ask you measure which calling test studio measure PT for clotting. Okay, Okay. I'll call it that. Okay. Uh, yeah, Most of you got it. So most of you were gone for a and the correct answer here is a Okay, So spider Angiomata Okay, so this question is basically testing your knowledge off the stigmata of chronic liver disease. Okay, so we got a man who has a history of alcohol abuse and hepatitis C. Okay, so this patient, likely it's fish has risk factors for for chronic liver disease, and he has lose a different stigmata off chronic liver disease. Okay, correct liver disease. You get a lot of different complications again. All those different complications can lead to different stigmata. And we'll talk about that. Questions asking which of these complications. Which of these stick mater has the same pathogenesis as the as kind of a mass Tia? Okay, So kind of a mass. Yeah, because in chronic liver disease, because off high estrogen. Okay, so in liver, you get a high estrogen state. And out of all of these options, spider angiomata are the ones that occur also in high eastern states. Okay, so the key learning point is that spike spider angiomata often appear in high eastern states. Okay, so that's why they can also appear in pregnancy. Okay, because pregnancy is a high eastern state as well. Um, it's almost on the other options before that. How many spider and spider angiomata is, would you say is normal in a patient? When would you say it's clinically significant to Ah, have if I have chronic liver disease suspended and you monitor yet five. Okay. So, yeah, you have more than five. That's clinically significant. Okay, So less than five, it's still think about it. Okay, but more than five is clinically significant off on currently disease. Okay. In terms of the other options or splenomegaly, that's going to develop because off portal hypertension violated periumbilical vein So, what is dilated Perry on the like a veins Referring to What is that? What is the sign called Compute Medusa. Very good. Okay. Ankle edema and s okay, but Medusa developed because off portal hypertension as well Ankle edema. So ankle edema develops because off hypoalbuminemic in case you get reduced on contact pressure and all the ultimate goal status. So we'll talk about this, but altered mental status in a patient with chronic liver disease. You'd be worried about them developing Compatic and kept locked. Okay. And that's to do more with liver not being able to detoxify metabolize certain toxic compounds. Okay, so before we go into the next couple of SPS, I wanted to spend a little time just teaching some basic concepts in liver disease and particularly Cornick liver disease. Okay, because it's really a lot of understanding that you need to do in order to properly just get it. Okay. If you understand the basic principles, answering the SPS will be a lot easier. Okay, so everything about the causes of chronic liver disease does loads of different causes. Okay? Always say in the western world, all cause a really common course. Okay, on increasingly metabolic causes, particularly fatty liver that's becoming an increasingly recognized causes. Well, but essentially, there's loads of different causes off liver disease. Okay? And we're gonna talk through some of the important ones throughout the session. But we have all these different things that can cause damage to the liver. And damage could happen in mainly in three different ways to deliver. Okay, you can get hepatitis. Okay, So, inflammation off the liver. Okay, get steatosis. So fat deposits in the liver. I guess the a ptosis means fat accumulation. So get damaged through hepatitis. You get damaged through steatotosis. You can also get fibrosis. Okay. So, fibrosis that you guys know this fibrosis and scar tissue, it's collagen on. So these are the three ways that all of these different things condo's damage to the liver okay on it. Essentially, chronic liver disease is referring Teo patients having a combination of these things or just one of those just one of these things. But essentially, it's all these causes all of these different causes needing to damage the liver in some way. And that's what's leading to the stick martyr and the complications off chronic liver disease Okay. Now, chronic liver disease is not the same as liver cirrhosis. Okay, this is a very important point to remember. Okay? Don't Don't Just assume chronic liver disease and cirrhosis are the same thing because they're technically not okay. Heart, liver disease can become cirrhosis. Okay, So can you guys tell me what is the difference between chronic liver disease and liver cirrhosis? How do you How would you define the difference? Reversibility. Excellent. Okay. Yes, that's that's Dustin. It That's the main thing. Reversibility. Okay, so if you plus five is a patient having cirrhosis, that means you're defining that the liver damage is irreversible. Okay, so this is a cirrhotic liver can look like. Okay, so you have loads of nodules, and the key thing is that this That is irreversible. Okay, So when a patient has gone on to develop cirrhosis, it's an irreversible process. Okay? They've developed irreversible remodeling off the liver, okay? And they got fibrosis. Okay, that's the key definition off cirrhosis. Okay, It's It's the reversible step. That's important. Because even if patients have chronic liver disease, you can keep you can. If you correct some of these causes, you could potentially help delay the progression to cirrhosis or even potentially reverse it. Okay. That's why it's really important to not assume patient with chronic liver disease have cirrhosis. Okay, goes it. If you say they're having cirrhosis, you're labeling them as having irreversible liver disease. Okay, Now, also, another important note here is that some patient with cirrhosis can go on to develop liver cancer. Okay, now, emphasis on the some. Okay, no or very. It's very rare for patient with cirrhosis to actually go on to develop liver cancer. Okay, liver cancer is no, not a common. Okay, but if it does happen, it's gonna happen from cirrhosis. Okay? Actually, can you guys tell me what is the most common malignant lesion affecting the liver? What is if you and unless we if you saw a CT scan with loads off malignant lesions on the liver What? What would you think about? Yeah, Mets. Okay, So remember, most common malignant lesion in the liver is in testis cyst. Okay? Liver metastasis, particularly from gas gastric cancer. Okay, particularly from gastric cancer and colon cancer. Okay, No primary about so carcinoma is not that common. Okay. Very important point. So, again, Here's ah reminder of the definition. Okay? Just commit this to memory, okay? It's very useful to remember for exams when you're on the ward when you're talking to consultants, cirrhosis is irreversible. Remodeling of the liver due to fibrosis. Okay, very important. Okay, so go talk about bit more about chronic liver disease. Okay, So when we think about chronic liver disease, you generally think about it. They have compensated disease or decompensated disease. Okay, So, patients, most patients who see we'll probably have compensated disease. Okay, So essentially compensated means that the liver is damaged, but the liver is still continue to function. Okay, The liver has still got function on, so because the liver is continuing to function, the patient's will typically be asymptomatic. Okay, if they got decompensated liver disease, that means that delivers no longer able to meet the body demands on. That's when they start getting complications. Okay. And that we'll talk about these complications. Okay, so and this this is important. Okay, So if if the liver's continue to function, that means that they're clotting will be most likely. Okay? Okay. The main really important clinical distinction. Do you think about in terms of function is the clotting function. Okay, that's an important distinguish it in distinguishing factor between compensated disease and be compensated disease as well. Okay. And also importantly, both these types of currently disease, they can have stigmata. Okay, so even if they have compensated disease, they can still have the stick martyr off chronic lung disease, which we'll talk about. Okay. Ah, yeah, that's it. So I'm gonna ask you what are the different causes of decompensation? What can cause a patient with compensated liver disease too? Decompensate. What would you be thinking about in terms of causes off a compensation in a patient with liver disease? Infection. Very good. Okay. Infection is one of those common ones. Where? What else? What else can cause decompensation? Alcohol? You? Yes, the infection. I'll call you as a main one. So let's ah, bit of a list here of the common ones. So I'd say the really important ones, remember Infection. Constipation. Okay. Constipation is very important. One particularly in patients who are in hospital. Okay, if there an inpatient and hospital, you bet you you you want to make sure that they're not constipated. Okay, Um, so you lost inside find a lot of patients in, in hepatology words on laxatives and things and nurses constantly checking their stool charts. Okay, because you want to make sure that these patients don't get constipated. Okay? Alcohol G I bleeds is well again. There's some other causes. Well, okay, so here's all the potential causes off decompensation. Okay? So little bit of a spot diagnosis here. Okay? And we'll talk about this more osteo serious, but I'm gonna put up some pictures, and you guys are gonna tell me what the signs are. So what is this sign referring to What is this? What is this? A stigmata? Representing? Yeah. Leukonychia. Okay, look in a k a sign of hypoalbuminemia. What about this one? I'm everything. Very good. What we got here? Spite any by. Excellent. What you got here is some rapid fire questions you could put Medusa. Excellent. What we got here? Yep. Gynie going to go. So some gynecomastia Ah, what we got here? Duper trains. Very good. Okay. These are all signs of liver disease. Uh, it's a little bit harder. Okay. What? I will say that being ripped is not is not part of the stigma of chronic liver disease. What? What is this picture representing? What do you think I'm trying to get with this picture as a sign of liver disease. Steroids know that. They look like the what we think about the chest. Just not could get hair loss. Very good. Okay. Lack of Chester. Okay. Lack of chest is a very subtle but subtle sign off. Chronic liver disease. Okay, that's Ah, Probably the hardest one there. And finally one. Is this from the most obvious one. Was this one representing a society is very good. Okay, But in an Oscar, he How would we describe the societies? How how would we discussed if you saw this patient? And, uh, how would you describe this all ski? How would you describe the societies? Uh, 10 CIA. Um, what else could you describe in us I'm thinking about is a low volume, high volume high bowling. Okay, so I'd say this is high volume ascites. Okay, this is grossly distended abdomen. I describe it as a high volume ascites. Okay, so it's the table summarizing chronic liver disease. Okay, Pretty much everything you need to remember in terms of the signs. Okay, so we've talked about a lot of these stick motor again. We've seen some pictures. So these are all stigmata that you can get in compensated on decompensated disease. Signs of decompensation. So this is really important. Okay, So signs of decompensation are ascites. Okay, so if they develop portal hypertension, they get ascites joined us because liver's not able to process bilirubin properly. And careful, opathy. Okay, so hold on. Mental status. Because liver's not able to metabolize and detoxify certain you're a toxic metabolites, particularly on ammonia. Get coagulopathy. Okay, so remember, coagulopathy is one of the main indicators off reducing liver function. Okay, so that should make sense. Why? Patient would get coagulopathy and G. I bleeds. Okay, So be patients with both of hypertension get viruses on. If they decompensated liver disease, those viruses can rupture, and you can get bleeds. Okay. Particularly esophageal viruses. Didn't get very heavy. Upper gi bleeds. Okay. And you have other complications. Well, so remember, liver is involved with loads of different things in the body. Okay, so if you get liver failure, it's a multi system disease. Okay? You can get loads of different complications from it. Okay. On quickly. Just wanted to touch. There's a scoring system you can use to determine the severity of decompensated cirrhosis. Okay. And that's the child Pugh school. Okay, so this helps characterize the severity off, be decompensated cirrhosis. And essentially, it helps to determine that prognosis and is useful for helping to determine who needs a liver transplant sooner than another patient, for example. Okay. Okay. So covered some basic principles, and I was just gonna fly through loads of different species. So that's why you get high estrogen someone dancer. So you got high estrogen? Yeah, Like the person said, living usually metabolizes history. And so you have liver failure. It can accumulate. Okay, I'll call it that. Okay. You might. You might be thinking these SPS are easy, but wait till later on. If you got I got some proper spicy SBA is coming up, but yeah, most of you went for a I'll call the AIDS on service and yeah, let's break down this SP. Okay, So we got a patient who's got jaundice and some evidence off. Um, some stigmata of liver disease you've got. Do the trends contraction? Palmer erythema. Okay, So we talked about them that both stigmata off chronic liver disease. Eso Can you guys tell me so? Obviously. Basically likely cause of the jaundice. We're going to think this patient is a long time, alcoholic. Okay? Can you tell me, um what in this SBA suggests that the patient is an alcoholic? What? One of the different features that suggests alcohol in this patient. Very good. Macrocytic anemia. Okay, a ST greater than 80. Excellent. Okay. And high GGT get awesome. Very good. Okay, so if you break down So in terms of the important learning points So this patient has alcoholic hepatitis. Okay, so And why? Because this this patient has features off access alcohol, okay. And he's got jaundice. Okay, so this is got evidence off. Long term alcohol use at and sort of, um, peaches off liver failure as well. Okay. In terms of why alcohol. So he's got a C 2 80 the ratio is greater than two. Okay. And that both elevated, um, increased GGT. Okay, We'll talk about allergies later, but increased GGT with a normal LP. Ah, That suggests recent alcohol use jaundice. So he's got hepatitis okay, and a macrocytic anemia is one of the one actually a really good sign off. Recent alcohol use is a macrocytosis. Okay, so these old features off alcoholic hepatitis. And that's why the correct answer his refer them to call the is on service to try and get them to reduce the alcohol intake. Okay. And support deliver. Okay, So we're going to briefly talk about alcoholic liver disease. Okay? And again, I'll call it Liver disease is a spectrum. Okay, you can get. I'll call the hepatitis, you get fatty liver on. You get cirrhosis. Okay. Like we said, chronic liver disease is not the same as cirrhosis. If you have a combination of hepatitis and fatty liver, that's you you referred to. The patient is having chronic liver disease. But again, I'm gonna keep emphasizing if they get irreversible remodeling off the liver due to fibrosis, they've developed cirrhosis. Okay, but these are This is sort of spectrum of liver disease and alcoholic patients briefly on alcoholic hepatitis. So patients get symptomatic hepatitis because they're drinking so much key features on again. You get jaundice because liver is not processing Billy Rubin on you get a fever and a wreck, see a weight loss, and that immediately as well. You talk about some of the features of alcohol. Okay. One of the really important ones is is thie ST to a little ratio. Okay, So, typically, and alcohol, you'd be the ST will increase much more than the 80. Okay, the A C generally goes up much more than the 80. You get increasing duty, and yet you some other findings as well. Let's go into the next year. Ah, this is ah, very hardest. Be as well. I says, Well, this part of the first really hard SPF. Yeah. Knish someone, August Um, what is Theo? Why do you get do patrons contracture from chronic liver disease? Be honest. Do that. The difference. Contractions due to thickening off the palm of fascia in the get beginning of the palm of fashion that can lead to that sort of fixed election deformity that you get into do patrons. Why you get thickening off the palm of fascia? I'm not sure it's completely understood. If anyone one sounds bad and it shot can. But I don't think the actual pathogenesis off the palm of your passion thickening is completely understood. Yeah, it's not completely understood that I was going to see it. Okay, I'll leave it up. Okay? Yes. Uh, this is a very hard escape. Ah, yeah. So most of you went for D. Okay, Andre, you got a bit of a split on the other ones. The least amount of people went for a even though he's the correct answer here. Okay, this is a very hard SPF. That's probably the hardest SP I've put in today, okay? I mean, I say that you guys might keep me for the other S p s, but that's right down this SBA. So got a patient with ascites. Okay, this is a patient with ascites he's got He's got abdominal distention and evidence of shifting build this. Okay. Shifting dullness with abdominal distention. That suggests ascites Okay on he's got non. He's got bilateral non pitting edema on it. We've got values for a cytic albumin and serum albumin on. We've got milk out acidic fluid elevated triglyceride in the ascites fluid. And you've got a white cell on the ascites as well. Okay, There's so there's a lot of information in this SP a Okay, I appreciate that. And it's in Ah, actually examined. I probably I probably have given you more time, but this is very is a lot to break down in this SP. Okay, so does that. Can you tell me just quickly? Why is the answer intraabdominal lymphoma? If anyone knows just quick statement. Why? Why is the answer intraabdominal informer here yet? We got high triglyceride. Okay, What else suggests in trapped? Don't know. Lymphoma? Yeah, I can see ever gets here is not really specific. Okay, but you can see Yeah. Hi. Yeah, milky lymph. Okay. Lymphocytic predominance. Definitely. What else? So this is something else that suggest, uh, why's that? Intraabdominal lymphoma rather than liver cirrhosis. What suggests that other than the color? What else? What? What? What is it? Why is the answer dropped on the lymphoma? Yeah, Soggy. Okay, this patient has a high sock. Okay, so it's a low suck. Okay, so we'll talk about starting a bit, but side is the difference in the serum albumin and the acidic albumin. So the difference in 3.6 and 2.7. So that's, um, no 0.9. Okay, So a soggy, less than 1.1. That's that's low. Okay. And, uh, losartan makes unlikely that the ascites is due to liver cirrhosis and potentially could mean that this ascites due to due to something like lymphoma. Okay, things that point towards this being intraabdominal lymphoma is a low saga. Um, he's got milky, acidic fluid and elevated triglyceride. Okay, So elevated triglyceride is because essentially, what's happening here is the lymphoma is compressing the lymphatic. Really be lymphatic vessels. Okay. And you're getting leakage off, but really lipid rich, limp into the ascites. Okay? And so that's why you're getting loads of triglyceride is in the ascites. Okay on. But he's got long pitting a demon, both ankles. Okay, so someone's asked what is the pathogenesis off nonpitting edema. Okay. Can you tell me what is the A demon non pitting here. What is the How do you describe this patient's Dema? What is the edema here? How would you describe this patient? A demon? What would you call the edema here if you're getting blockage off lymphatic vessels and you're getting ah, deem nonpitting edema would How would you say is the patient's a demon here? They don't know. Very good lymphedema. Okay, so this patient got lymphedema. Okay. The lymphedema is the main one of the main major causes off non pitting edema. Okay, this non pitting edema is there's only really two conditions. You can get it in lymphedema, and you can get it in, um, myxedema. Okay, mix it in, men. Diarrhea disease. Okay, so this patient has lymphedema because he's got non pitting edema in both ankles because the lymphoma is compressing the lymphatic vessels. And that's what leading to the edema in case you're getting buildup off lymph inside the, um, inside the lex. Okay. Someone else. Can you repeat the cause of hydrate triglyceride? So you're getting high trick triglyceride because you're getting leakage off lymph lymph into the ascites. Okay, so the ascites is essentially lymphatic fluid. It's called a kind of societies. Okay, so it's full of triglyceride. Okay, I understand that that was a lot to break down, but I'm gonna teach some of these principles from basic concepts. Hopefully, you guys will understand it, but essentially, the key learning points here is that the milky, acidic, fluid, low soggy and elevated triglyceride indicates chylous societies. Okay, so ascites full of lymphatic fluid on non pitting edema here suggests lymphedema. Okay, that that the lymphedema that makes it unlikely that it's TB. Okay, you don't meet TV is in our common cause of lymphedema on the patient. Doesn't have risk factors for TB as well. Uh, Nephrotic syndrome of Nephrotic syndrome would cause pitting a demon, not non pitting edema. And also the patient's albumin is normal as well. Okay, spontaneous. Back to your peritonitis, so we'll talk about it. But with SPP, you get neutrophil. It's not lymphocytes, okay? That's the key thing with SPP. We'll talk about that as well. So you got about societies now, And so why do patients get ascites? So in ascites. So in cirrhosis, you get a combination of both total hypertension as well as salt and water retention as well. Okay. And the combination of both of these things will lead to ascites. Okay, so you get also hypertension because of the scerotic liver, okay. And that leads to fluid leaking out. And because you have a reduction in the effective circulating volume, you get increase the dose from being produced. That's going to lead to a lot of salt and water retention as well. On both. These factors are going to just exacerbate dear societies in patients. Okay, Now, when we asked analyzing acidic fluid, one of the most the most important calculation you do with Ascites is to calculate the saga. Okay, so the serum ascites albumin. Um, Grady, it's okay. So, essentially, the calculation is you're measuring the difference in the albumin and the blood and the albumin in the ASCITES. Okay, so I've made a couple of schematic diagram to try and explain this. So if it's gonna talk about a situation off increased capillary hydrostatic pressure so this would be portal hypertension. Okay, so situations off portal hypertension, where you get increased capillary hydrostatic pressure. If you get increased capillary hydrostatic pressure, what's gonna happen is you lose a lot of water into the peritoneal cavity. Okay? Do you primarily lose water? But you don't lose any albumin, okay? With increased compared your hydrostatic pressure, you mainly just lose water. And so So if we think about the calculation eso again, the calculation is serum albumin minus acidic fluid albumin. If you're primarily only losing water from the blood, what's gonna happen? The serum albumin will increase because it's going to get more concentrated in the blood and the actual out albumin. in the her to know cavity. The acidic fluid is going to decrease because the water's gonna basically dilute out, be out albumin So the actual acidic fluid albumin will reduce. Okay, now, if we think about the calculation So we're getting increased serum albumin and reduced a cytic albumin. This is gonna increase the sock. Okay, so this is going to cause a high sock. Okay, so this is why patients with portal hypertension who get ascites they they have a high sock. Okay, so a sock above 1.1 g per liter. Okay, in terms of the other causes of sight is so these are causes which relate to reduced oncotic pressure or increased capillary permeability. With this type of ascites, you get lost off both water and albumin. Okay, So because with the reduced oncotic pressure, you have a low albumin. Okay, so you're not able to hold on to water and you're losing albumin into the ascites as well on with increased compared to Comey ability. So you're having very leaky blood vessels, and that's allowing throaty like albumin to leak into the ascites. Okay, so we're losing both water and albumin from the blood So if you think about the calculation, Okay, what's gonna happen? You're losing albumin from the blood. So the serum albumin is going to decrease, and the albumin is going into the ascites. So the actual acidic fluid albumin is gonna increase. Okay. And so this is going to cause the sock to reduce. Okay, So this Saad reduces. This is why you get a low sock for these for conditions that cause reduce oncotic pressure or increased capillary permeability. Okay, so hopefully that made sense. This is why I totally hypertension. You get high sock, and for other conditions, you get low suck. Okay, So common causes of the high side would be liver cirrhosis and right sided heart failure. Okay. Where you get portal hypertension conditions, which can cause ascites with a low side would be things like the folic syndrome and created cancer patting malignancy. Okay, interrupt on a billion. See, um, and TB is welcomed or cause ascites where they go suck. Okay, Okay, that makes sense. That was a lot of sort of physiology to understand, but it's very important clinically to understand this calculation. We got a quick SBA here. Okay. Just sort of Uh uh. Just if you know what you know what kind of sp Um, just have a go. Yeah, 11 g. So it's one. It's 1.1 g per deciliter. That that's the value that you're looking at to differentiate High sock and low sub. Okay, someone wants to explain socks, so I can I'll explain. I can explain. Start at the end of the session. If you want it just full time, we'll just keep going on. Yeah, I can explain again at the end of it is quite complicated. Okay, this is just testing if you know, it's it's this is I sort of if you know what you know what kind of question, But I quote that most of you went for a and the second most picked option. Was he correct? Answer here. Is he okay? So this question is basically asking, What is the diagnostic value off? What is the diagnostic reading for spontaneous Back to your peritonitis. Okay. So can use something. What is the What is the actual, um what is the actual point when you diagnose SPP? What is the ah, diagnostic point? What's the numbers? What are the numbers yet? to 50. Okay, So greater than 2. 50. Greater than 2. 50 p. Um, microbiota on. But the actual fluid is predominantly neutrophils. Okay, They're white cells are predominantly neutrals. Those are the two things you're looking for. Okay, So 2 50 eso? Yes, The white cells. More than 2. 50 per cube. Okay, so I think I've got, like, Michael. It's a, you know, use both, but and they're predominantly neutrophils. Okay, so most of you went for a So it's actually 2 50. Okay, on, but predominantly neutrophils. Okay. So quickly. This is basically a summary off acidic fluid analysis. Okay, this table basically summarizes how you interpret acidic fluid. Okay, so you look at the color we talked about white cells. If it's greater than 2. 50 and predominant, you filled starts spp. Okay, So an infection within the societies we talked about, um, protein and saw hgb Okay on there. Some other useful indicators of what the potential cause of the ascites. Is. Okay, So have a read when you get the slides. Um, yeah, and it was a management ascites. So general principles, you don't need to know too much about this as an undergraduate. but general principles is that for any patient with new ascites you want to do a paracentesis. Okay, You want to do a top on a cytic top cause you want to know where the ascites has come from. You want to know what the fluid has come from? So you do an initial person TC president, he says to diagnose the cause of the ascites. But if the site is a very large volume and it's not responding to medications, you can also do the paracentesis of the top to drain a lot of the fluid out as well. Salt and fluid restriction so avoid avoid at the low salt salt diet if they have ascites diarrhetics very important to try and remove some of the fluid and spiral. Spironolactone is the main one is the first line. Okay, remember, not fruit furosemide. Spironolactone for ascites at the main indication to use spironolactone as a diuretic is in ascites. Okay, that's the only situation where spironolactone is his first line as a actual diuretic. Okay. And for refractory ascites, you can do a procedure called tips. Okay, so, essentially, we'll talk about it. But it's a procedure to resolve portal Hypertension. Okay. And that can help for that's obviously going to help for ascites terms of quickly about SPP. So SPP is just going to an infection off the ascites. Okay? And what we mean by a spontaneous, it means that we don't actually know where the bacteria come from, Okay, They just appear suddenly. So you don't know where the source of the infection is? Okay, Most cases are due to hematogenous spread, but you call it SBP cause you don't know where the bacteria are coming from. Okay? Clinical features. So you can sometimes present with sudden peritonitis, Okay, But usually it's you suspect in patients with worsening ascites. Okay, on in patients who developed and careful opti. Okay, so this is a key learning point. Any patient with ascites who develops and careful up a B, you're worried about them having an infection. Okay, you're worried about them having SPP. Okay, We talked about the diagnosis, so it's 2 50. That's the magic number for SPP on predominantly neutrophils. Okay, so another SBA here and this is, uh, on the concept off ascites as well. Yeah, Calico that. Okay, so yet most of you got it So this is what this is Quite a tricky Caspi again. It's important doing point Cesamet Have you went for a give potassium chloride? Okay, so I sprayed down this SP. This is quite a hard spn. So this is a patient who has is the patient has, um, liver disease. And he also has ascites okay as evidence of shifting dollars. So he has ascites. Uh, can you tell me what is the what complication has this patient developed? What is the complication? This patient's developed and get allopathy. Very good. Okay, so this patient developed attic income floppy on. That is evidenced by two things here. Okay, the main thing is, is he's got asterixis. Okay? He's got a the liver flat, which is a sign off. Batic and Keppra Lockley. Okay. And actually, one of the more better indicators of hepatic and care floppy is the sleeping problems. Okay, well, one of the first sign off the Patrick and careful Opti is sleep disturbance. Okay, Interestingly so this patient has increased, um, sleeping habits. Okay. Sleeping more than usual. And that's actually the first sign of Patrick. And careful up the states sleep disturbance. Okay, so and So what else in the essay? So you've been recently started on a Dyazide diuretic, and he's anybody's done. And that showed a metabolic alkalosis with a low potassium. Okay, so remember, one of the complications of diabetes I do is I can cause a metabolic alkalosis and hypokalemia. Okay, So why do we give potassium chloride in this patient? What? Why is it really important to get the test employed in this patient? What's, uh what? What's the reason for correcting Batasan here even though just because it's low? Yeah, low potassium because of written here. But why is it relevant to be? Why is it relevant to the YMCA? Floppy? Yeah, You guys are on good making good points. Protected. Pericardium is already low. But what what's actually happened? Why is he got in? Careful. A pretty are very good. Someone someone's private, messy. So high book hypokalemia is actually it can actually precipitate. And careful apathy. Okay, low potassium is one of the precipitating factors for hepatic encephalopathy. Okay, so that's that's one of the most important reasons why the first step in battle gen care floppy years to correct the cause of the income floppy. Okay, So in this patient, um, the hype hype. Okay, let me, uh and as well as the metabolic alkalosis that's what's precipitated. The That's what precipitated the hepatic and careful. Ah, pretty. Okay. That's why that's why this is the most important step here. Okay, to correct the precipitating factor wise. So if I tell you Lactulose is also the mainstay of treatment in attic and careful, opti wise lactulose wrong here. What if I tell you if I tell you, you should give actually on this patient wise actually is wrong here. Very good to give you Give lactulose orally. Okay. No IV okay. And you give it orally because lactulose knees are act on the bowel. Okay, too. Basically increased the excretion off ammonia, and that's gonna help with the income floppy. Okay, because I'm careful up. He develops because, you know, you know, you have excess accumulation off toxic compounds such as ammonia. Okay, and rifaximin also can help. Okay, but again, you give it orally. Okay, stop spironolactone. So spironolactone. But actually, actually, you wouldn't stop it. Because if you stop it, that might worsen the hypokalemia. Okay, that might worsen. It's potassium. So you wouldn't stop it here and tips is definite. Definitely a no, no. In careful off the because tips if you think about it, tips is a procedure that's going to bypass the liver. So if you have and careful up the means, you already have excess toxic compounds in the liver in the in the blood. Okay, so if you do, if you put in a shunt that's bypassing the liver. I mean, the liver's not going to detoxify any of it, so that's gonna potentially worsen the and careful octopi. Okay, so that's an important learning point. So sleep disturbances is one of the earliest signs off hepatic Been careful about me. Okay. And hypokalemia is one of the key precipitating factors up in couple of the as well, so quickly on and kept allopathy so and careful, Opti, It's ah state off altered mental status. Okay, so it's where the we have liver cirrhosis and then decompensated and they got neurologic symptoms. Okay, because liver's not able to process toxic substances such as ammonia. Okay, we talked about some of these situations. So infections, particularly spontaneous bacterial peritonitis. Okay, so remember patients and the patient. We just discussed you definitely be worried about SPP A swell. Okay, um, so the patient would need to have a paracentesis as well. G I bleeds. Um hypokalemia metabolic alkalosis these role important signs of ammonia off important triggers Off and careful. Opti. Okay, cloak a feature. So earliest sign is sick disturbance. Okay, you get asterixis on that. You can see my beautiful arms. Here, Get this. I couldn't find any non copyright images off asterixes, so I just took a picture of myself. So showing the liver flat and you can see my beautiful tandems here, but yeah. So, essentially, just trying demonstrate the ah asterixis. Okay. Treatment. You want to correct the precipitating factors? Okay. Such as hypokalemia and that patient lactulose is the mainstay, okay. And lactulose were decrease absorption of ammonia and reduced and help with the income property. Yeah. Next question. This is a two part question and it's on Upper gi bleeds. Yeah, Michelle, for this question. Do you mind if I take to minister and on Just talk about something? If you don't mind, It's two minutes. Break off this question. We'll do it this way to about questions. We'll just do the next one is. Well, sure can call it that. Okay, most of you got this. So every mostly went for be so totally press in. And that is the correct answer here. Okay, so this is a patient who has presented with an upper gi bleed. Okay? Hemodynamically unstable on day of what they've been given. So this is a virus you have later. Okay. I've told you, this is a virus. You bleed. So it's ah, ruptured virus Barcia bleed. That's like to a a pretty upbeat okay. And in terms of what he's already being, look, this patient's already being given given fluids has been given blood blood products, and he's also been given antibiotics. Okay. And as part of that initial resuscitation and stabilization off patients with acute variceal bleeding, you should give it to early present as well, in case the total pressing will help reduce portal pressures and also help with reducing the bleeding. Well, okay. Ah, we'll do the next part of the question is well, before you start discussing some of the other things, so yeah, it's a learning point. Early person will reduce portal pressures, and it's given before endoscopy. Okay, so still on the topic off off that patient. Uh, like the pool again. Quickly. Okay, I think most you got this one? Yeah. Call it. Uh, okay, most of you went for a and that is the correct answer here. So propantel. Okay, so this patient has been has had an endoscopy. Is that band ligation again? That is the variceal bleeding has been controlled. So for secondary prophylaxis, you need to give you you give her pannel. Okay, So why is the answer not bisoprolol? Oh, if I tell you, you need to give a beat a Braca. Why do you? Why is this operable? Not be correct. Answer here. Yeah, so you have to give and not you have to give a nonselective beta blocker. Okay. Bit about this. Uploads. Ah, it's ah, selective cardio selective beta blocker. So you give her a panel because it's nonselective. Okay, so nonselective beta blockers such as propinal is given for secondary prophylaxis. Okay, so yes, the nutri to take a break. Yeah, just I want to introduce quickly. So we're trying to evaluate a service on will be really great for your ms releasing a link on to the chat If you can ski despair. Let me take two minutes a few time. We're trying to see whether we can make these sessions or interactive on Ms is also a big part of this project. So he wants to see whether we can improve our sessions. Improved interactivity improved over. You ask questions. And as you can see from this brilliant session, if there's any way we can improve it, even for that, I'll be really good for us. I'm good for you. So it's completely voluntary. Don't feel pressured into doing anything. We're trying to evaluate what this everything doing right now on an improvement we can make. And we really, really great for if you could fill out the form on the check I thought I wanted to say can continuous soon as you want to. Fine. Uh, before we go on, is there any burning questions for anyone right now? How to be two blockers? Help beat box is gonna help just reducing the amount of bleeding. Okay, They're gonna reduce pressures and they reduce their useful long term in secondary prophylaxis that that helps. Okay, we'll keep going on. We have quite a quite a lot of other STDs that so we'll keep going on. We'll talk about upper gi bleed stuff. Okay, so, yeah, you just take the time to fill out that form. We really appreciate it, but I'll keep going on. So upper job lead. So we cover this with gastroenterology last week, Okay, when we were talking about bleeding peptic ulcer, so I'll do it a bit quicker today. Main coaster up job leads are most commonly, it's due to bleeding peptic ulcers. But you can also get variceal bleeding as well. Critical feature. So with Barcia leads you get, you usually get more fresh blood vomit. Okay, You generally get more fresh hematemesis because typically, you get your supper deal Galaxies, and that you saw for your advice is there bit higher up? So when they rupture the blood, the blood generally comes out with a fast transit. Okay. Generally moves very quickly, So generally the blood is quite fresh. Okay, coffee, ground vomit. If the patient has true coffee grande vomit, that would suggest more peptic ulcer. Okay, that's bleeding. Okay, Molina, you could get Mirena because off with opportunity to get Melena because of the hemoglobin getting metabolized and ending up in the stools and getting awesome, oxidized and and darkening the stools. A swell, Remember with upper job. So we didn't have to be on this last week. But one of the key fit findings and upper GI bleeds on blood test is a high urea. Okay? And endoscopy needs to be done to diagnose and treat upper gi guy beats. So we got this is slide. That's the floater that summarizes the management off Barris Ear bleeds. Okay, this is, uh, basically, as summarized, some right. A summary off the guidelines for managing variceal bleeds. Okay, so up a Japanese that they're emergencies. Okay, so you do the initial eight to the assessment. A spot of that initial resuscitation. You give fluids, you give blood products, you give too early, press in, and you also should give antibiotics as well. Okay. To reduce the risk of infection. You can see it. A glass of Blackfoot score for, um, for all upper gi bleeds. And ideally, if they have breast, you're beating. You should organize the endoscopy within 24 hours. Okay. Um yeah. So on the endoscopy. In terms of the definitive management for Barris, you bleeds. It's a bit different, depending on where the virus COPD is for you suffered deal viruses, which are the most common ones. You generally do bond ligation. Okay. Just try to find the virus is together. Gastric viruses. You tend to go rather than by see, with band ligation. You go for what's called Sign. Uh, Accolate. Okay. And some trust might use Trump in a swell. Okay, so it's like differences, depending on the location. Okay. If the bleeding is not controlled by these procedures, then um, you might try it again. And if that's not working, then you can put them on what's called a balloon. Tampa not okay. So you try and stabilize them. You can put them on a balloon, dumping out a balloon. Tamarod is essentially, it's very effective in reducing the bleeding, but it's just a temporary option. Okay, Essentially you. But you put them on balloon. Tampa Not as a means off stabilizing the patient until they can have a procedure called tips. Okay, So tips is the definitive management. Okay, If they're refractory to medical therapy and endoscopic there be, Then you can try tips on them, and tips will usually resolve the beating because it will reduce the little hypertension. Okay. Remember, patient should be started on a nonselective. Beta blocker searches for panel A second reproof Lexus. Okay, this is summary of manual up a jab leads for Barcelona. Bleeds and bleeding. Peptic ulcer is okay. We talked about bleeding peptic ulcers last week s o have a read when you get the slides. Just quickly on tips. So tips. What you're doing is you're creating a shunt between the systemic circulation and the portal. Venous circulation. Okay, so your best, essentially bypassing the liver. And that's going to reduce the portal hypertension. Okay. And there are some contraindications of it, but that's essentially have tips. Works okay, next year. Yeah. Okay. Someday someone someone's told me I should do an integrated BSC and medical education bit late for me. Now I'm doing a B S. C and something else, Missus. A quick question. There's a very interesting question here. Why would you could you briefly explain why I g I bleed and hypokalemia can cause liver clearly decompensation and you corrected infections and medication. So I think that's what everyone We have a question, so, yeah, it's It's a good point Okay. The thing with decompensation so essentially compensated liver disease you have the the concept is that you having damaged to load the liver cells loads of a patch sites But the ones that are remaining are still somehow able to maintain functions to deliver. Okay. And that's why they're remaining compensated. Okay, as soon as you get a big insult to deliver. Okay. Such as an infection, where you having massive, massive, massive increase in body requirements and those remaining apart sites are not able to cope with the demands that constipation your bye. I was not able to flow properly. So your liver is working harder to produce bile on with upper GI bleeds. The well, the the decompensation can cause bleeding and bleeds themselves can actually cause the conversation. Okay, It's sort of a vice versa thing, but leads essentially they there's increased, um, increase Syria and increase increase ammonia and there's increased workload for the liver. So again, the remaining about sites it's the demand for the work has increased too much and they're not able to cope. So that's why they decompensate okay, Essentially the remaining paths eyes are not able to continue maintaining homeostasis and deliver. Okay. Okay, that makes sense. So I call it there. Okay. Mostly the one for be okay. And that is the correct answer. Hepatitis B infection. Okay, so this is a patient. That's this is a classic description off a patient of a history of bio hepatitis. Okay, we got patient. Who has non specific symptoms of fatigue fever after all. Gym okay on. He's also got abnormal. Lft is okay with particular increase in a little and ST Okay, this is classic description for acute viral hepatitis. Okay, Kenya's. So if you break down, why hepatitis B? Because multiple sexual partners is one of the key risk factors for hepatitis B infection. Okay. Can you tell me what is Thesiger difficult off the vasculitic rash? What am I trying to get up here? What? What is the vasculitic rash representing poly arthritis in a dose? A very good. Okay, so with hepatitis B, one of the complications you can get is polyarteritis nodosa. Okay, so it's ah, medium vessel vasculitis. Uh, not gonna go into it, but that's with any type of vasculitis. Where your information of blood vessels, you can get a vasculitic rash. Okay, We'll talk about the basket. Itis in detail during the rheumatology session. Uh, but yeah. So why is the answer not hepatitis C here? What makes the cancer more likely to be hepatitis B compared to hepatitis C? Yeah, but I do see is chronic. Okay, Have to see. It doesn't really cause is subclinical usually okay? You generally acute is not common. Okay? You don't get very symptomatic. Acute hepatitis C. And generally, um um multiple sexual partners are much stronger risk factor for hepatitis B compared to hepatitis C. OK, Haven't I see is rarely transmitted through multiple sexual partners, so keep learning point. Sexual contact is a much stronger risk factor for hepatitis B infection compared to hepatitis C. So this is some rehab status model hepatitis. Okay. Not going to go through any of this, okay? This is purely for your revision, but have a read, and it basically covers the sort of key points you need to know about vial hepatitis. Okay, so this a question. Another question relates to buy a hepatitis. So have ago. Ah, just be aware. Sorry, I keep doing this, but this session will probably be run on about 45 50 but everything's recorded. So please do to stick around If you happy to discussions, testing your knowledge of hepatitis B serology. Okay, I will call it there. Okay, so most of you went for C. Okay. And that is the correct answer. Resolved. Hepatitis B infection. Okay, So in terms of the not going to much into detail serology. But why is this? Why is he on to see here so quickly? If you look at this, we have, ah, patient who has, um, by the record of hepatitis B serology results. Okay, Uh, he's so in terms of keep on tests, she is six ounce, two negative. Okay, So that means that she's not infected, okay? She doesn't, She's know, infected currently with hepatitis B virus. Um, she is positive for surface antibody. Okay. And the key thing is, if you're positive for surface antibody, that means you're cured. Okay? That means you are if you have immunity to hepatitis B infection. Okay. Another thing. Now, in terms of the options that we have the two options that suggests cured immunity to viral hepatitis is resolved. Hepatitis B, infection or vaccination against hepatitis B virus. Okay. And the key thing to remember is that the hepatitis B vaccine only contains the surface antigen. Okay, so if a patient has immunity only from vaccination, they'll only be positive for surface antibody. Okay, But this patient has is also positive for core antibody as well. Okay, so that that suggests that it's not. The immunity is not due to vaccination. The immunity is because they've been previously exposed to hepatitis B. And that's why they have developed antibodies against the corn body as well. Okay, so that's how you differentiate. Uh, these two options, sometimes with the learning points presence off surface antibody, indicates immunity. The vaccine only contains the surface antigen so quickly in terms of keep wants with neurology of just highlight what each of these markers are indicating. So surface antigen is indicating infection. Okay, they posted Pacific's understand. It means they're infected. If they have an increased ent Jen, that means that there's increased rapidly replicate replication. Okay, an increase in Factive itty of the virus. Okay, E antigen is a measure off viral replication and in terms of the antibodies, So if they have a GM call antibodies, that's just an acute infection. If his IgG. It's more of a chronic infection. Okay, if they have antibodies against infection, that means that they're able to respond to the he antigen and reduced replication okay, and reduce infectivity of the virus. And the most important antibody is Theseus office antibody. Okay, Because if they're positive for surface antibody, it means that they're cured. Okay? And they can either be cured because they've had had a resolved infection or they've received a vaccination. Okay, this a table that summarizes all these cereal article profiles for different stages of hepatitis B infection. Okay, so have a read and try and make sense off. Why Certain things are positive and why certain things are negative at different points. Okay, next question. This is ah, got a spicy SBA again. Yeah, Okay. We'll call it. That, uh, is here and the answer. Okay, So most of you going for a here, and so it's a bit of a split between a and see again. Understandable. Slept. I'll go for it. Correct answer here is see a gallstone disease. Okay, just break down this SP. Why does this patient Goldstone disease so patient presented with the right upper quadrant pain. Okay, so there's a lot of differences, All right, Upper quadrant pain. But why is this a Goldstone? Okay, so let's break this time, this patient has had an ileocecal resection. Okay, Onda, uh, this patient's also receiving TPN. Okay, so total parenteral nutrition. So what that means is that that receiving nutrition primarily through a through the circulation. Okay. Intravenously. Okay. They're not taking anything through them through, through or feeds. Okay? And also, the LP and GGT are both elevated. Okay? And this is the key thing here. Elevation in both ap and do duty on liver function tests that suggests coli Stasis. Okay, on what happened? The Goldstone diseases. You get cold, cold Stasis because the Colson is blocking the flow off while Okay, you can also get it with PSC so prime it grows in cholangitis where you get fibrosis. You can also get cold. Is Stasis okay? But can you guys tell me why is the answer more likely? Goldstone's here compared to PSC. What's in this patient suggest that he likely has a gallstone. Yes. See more common. And you see it then Crone's. Yeah, that that that is a point. But why? But there's something else in this question. It makes it more likely that ah, goals that this patient, Whatever. Goldstone? Yeah, the ileocecal resection. Okay, so if they remember the physiology, bile salts are generally reabsorbed in the terminal ileum. Okay, but this patient has had an ileocecal resection. Okay, so they're not absorbing bile salts if you know, absorbing bile salts the and you're becoming deficient and about salts. And you're losing a lot of bile salts in your stools. Yeah, it'll cholesterol in the bile is gonna be much more concentrated. Okay? Competitive about salts, which would balance out, balance out the cholesterol. If you're losing bile salts in your stools, the actual cholesterol becomes much more concentrated Onda that can precipitate and cause a goldstone as well. Okay. And also, if you're receiving nutrition, parentally okay and you're taking nothing orally that's going to slow down the flow of bile. Okay, because there's there's nothing going through the GI tract and nothing stimulating the production of bile. All that bile is gonna be moving really slowly in the bile ducts. Okay? And then and so you got cholestasis. And that can increase the risk off Goldstone's. Okay. That's why this patient. Goldstone's here. So that's the key learning point So increasing about a lipid and GGT indicates coli Stasis. Um, enter a Patrick circulation of bile acids. So the way by last, it's get reabsorbed. That's likely impaired here, Okay, because this patient has had a resection off the terminal ileum okay, so quickly on lft. So liver function test. So there's a little cheats cheats like that we made to help everyone understand the key principle. So increase in a little and see that suggests liver damage so apart to sell a damage, increasing more LP and Judy. So I'll be ingenuity that found more in the bile duct. So if they go up that suggest coli Stasis okay or some kind of obstruction in the low file, okay, remember, if both of them go up, that's highly suggestive coli Stasis. But if only the LP goes up and not the GGT not suggest other things, okay, because remember, AARP is also found in bone and percenter. So can you guys tell me what? What what condition would you think about if they have only an increase in LP, but with a normal GGT, What would cause a nice, elated increase in AARP. Paget's very good. Okay, Yeah. Projects. Just anything which is gonna increase bone turnover. Pregnancy. Very good. Okay, you get increased LP in pregnancy physiologically Okay, Very good. Okay. So, yeah, those are key points with regards to the enzymes. Another high yield fact to remember is that if someone has an a little in the thousands, there's only two main conditions that can do it. Okay, It's it's chemo, hepatitis and the paracetamol overdose. Okay, Uh, remember, when these are all sort of the liver enzymes are all signs off damage to the liver. Okay. They don't tell you anything about how the liver is functioning. Okay? They only go up when the liver is damaged. Okay, Like, I emphasize that the start the only true measures of liver function are the clotting. Okay. And some of the other things here, but the most important ones, that most important one the most important marker of function is the clotting. Okay, the iron a prothrombin time. Okay, Okay. Next question thing. We have maybe three more SPS after this, and then we should be done. Yeah, Okay. I'll call it that. Okay, you got a big split a perfect split between a and see. Okay, So correct and tst. Okay, so this is this is something that you learn more when you come on two clinical placement and things and learn more about how disease is Get investigated. But let's go through this. So we got a patient who has it was drawn, Just okay, this is got scleral. Actress means that you got yellow eyes, and that's a sign of jaundice. Okay, so we have yellowing of the eyelids. Ah, this patient also is taking as presented with, like, discolored stools as well as dark urine. Okay. And on the lft is this patient has raised Billy Ruben. Okay, then that's in keeping with the jaundice and also raised a low p and G t. Okay, now, remember, like I just thought you raised LP and digiti that indicates coli Stasis. Okay, That means that there's for some reason by there's not flowing properly and in this patient and most most likely due to some obstruction in the flow of file. Okay, So can you tell me why? Uh, the stools lighter in this patient. What is? What's the cause off the, um, still lightening destructive. John. That's very good. Okay, so this is talking about cause of jaundice now, So this is an obstructive jaundice. Okay, So because there's a way we're not gonna go to the cycle, but because you have an obstruction, the Billy Rubin is not able to flow properly. And essentially, Billy Ruben, normally eventually a metabolized into stroke. Oberlin on Stoker billing would normally give brown pigmentation to stools, but because of the obstruction, the bilirubin is not able to flow properly. So you're not having stroke a bill and being produced. So that's why you having lighter colored stools? Well, okay. And you're also getting darker urine because Billy Rubin is leaking into the blood on day, Um, in this patient, because the obstruction you having conjugated Billy Rubin, which is water soluble, and that's gonna cause darker colored urine. Okay, so this question basically asking how you're gonna investigate obstructive jaundice on the most appropriate initial investigation for anything involving billion obstruction is to do an ultrasound. Okay. Ercp is a very it's an invasive procedure. Okay, so it's well, it's diagnostic and therapeutic, but initially you have to do you should do the ultrasound. Okay, That's good practice. Okay, If you start referring patients for Ercp without an ultrasound gastroenterologist, I'm not going to be very happy with you. Okay? You should get the ultrasound first and evaluates and visualized the liver and the biliary tree. Okay? Yeah. The abdominal understand, Is the first step in evaluating obstruction. Well, another question on join us similar mean, but have ago, this one? Yeah, can call it that. Okay, so we got split between a and he gets that we got split. I expected this place is a split between cholesterol, Goldstone's and chronic analysis. Okay. In fact, the correct answer here is chronic Humala, sis. Okay, so let's break this down. I'm sure a lot of you will be confused by this one. This is quite a trick. ESP again. It's got a sneaky SBA, but essentially, we break down. This is the patient was right. Upper quadrant pain pain worse after eating fatty fruits. Okay, uh, it's got increased lb and digiti on, but he's got a negative urobilinogen okay, on in the urine. So the's are all signs off a goldstone. Okay, There's all signs that suggests Goldstone in the biliary tree, and that's causing obstruction. So you're getting because of the obstruction you're getting increase in LP and GGT because of the obstruction, you get negative. Your ability gyn in urine. Okay, that's a sign of obstructive jaundice. That's a sign of obstruction. Okay, Onda. Yeah. So these are these are all signs off this patient having a goldstone. Okay, but can you guys tell me why is the answer not cholesterol? Goldstone's here. Why is this patient actually got a gallstone? What's the cause of the Goldstone in this patient? What is the cause of the Goldstone? Anyone have any idea? High bio. So there's something in this this question that suggest something else already. Trees, feticide, Spio, hereditary spherocytosis. Okay, so I sneak this in to the SBA, but the history of hereditary spherocytosis. So this is a condition where you get chronic Amal assists. Okay, where you get chronically. You having red blood? Cell break breaking down on red blood cells contained Billy Rubin. So you get Billy Rubin constantly being leaked out of the blood on this. If you have Billy Rubin constantly, big doubt, they can get get processed by the liver and you can get Billy Rubin Goldstone's. Okay, so this patient has Goldstone's, but they're not cholesterol. Goldstone's that Billy Rubin Goldstone's okay, that pigmented Billy Rubin Goldstone's okay, because of the chronic mal assess that this patient has. Okay, difficult question. But it's ah, it's a very It's an important learning 0.7. Um, but some of the leading points of chronic mollusc and lead to patients developing pigmented Billy Rubin Goldstone's This is something a billion pathway. Okay, not gonna go through it, Just have a read. Okay? And these are the different sort of abnormalities that you can get when you have, um, disturbances in that Billy Rubin cycle. So again, just try and follow the pathways and, um, try and understand it, and I'm not gonna go through all this, but this is a table that summarizes jaundice, and this is a summary of jaundice and one table. Okay, so have a read try. Make sense of it. Ah, yeah. We're gonna keep going on. Um, I got too many SPS left. This is another very spicy SGA. Uh, you guys probably young real me with this one, but this is ah, spicy SGA. I'm sorry if I made the escape. Is a bit too hot today, but, uh, probably you guys are learning some stuff from them. I appreciate that. They're very hard SPS I made them purposely hard, but, uh, hopefully thing I do is we want to make these SPS hard so that the SPS in your actual exam will seem a lot more easier when you start approaching them. Uh, yeah, let's call it there. You got a big split here way. Basically got a total split between most of most of the answers yet, but ah, yeah, Let's go. Let's break this Done. So this is a patient who has. This is a middle aged woman who has generalized arthritis on dot So what's the diagnosis if I tell you that the correct answer here is biliary obstruction? What is the actual diagnosis? Said the What is the cause of the practice? Yeah, PBC. Okay. It's a primary biliary cholangitis. Okay, so sp a land. It's the middle aged female with pruritis. That's PBC. Okay, that's the main description off PBC. Okay, so in PVC primary biliary cholangitis, you're getting, um, destruction of bile ducts. So you having obstruction in the flow of bile? Okay, so I've also told you that this patient is having near collisions when she drives at night. Okay, so she's almost crashing into stuff when she's driving at night time. Can you guys tell me What? What is the relevance of that? What am I trying to get out with the, um, reduce vision during the night? Awesome. Vitamin A deficiency. Okay. Why is this patient deficient in vitamin A? Why would this patient Why? What? Why could this patient develop? It's been a deficiency. Yeah. Which one is one of the fat soluble vitamins? Okay, so if you have biliary obstruction, you're not gonna be able to absorb fats properly. If you can absorb fat. Probably you can't absorb the fat soluble vitamins such as vitamin A. And so you. Because if you get deficient in vitamin A, you can get Mike blindness. Okay, That's one of the complications of vitamin A deficiency. Okay, this is it's ah, it's it's it's got a hard escape, but once you get it, it's quite interesting. Bit of a part of physiology. Okay. Yeah, let's get into it so that the learning points of vitamin is a fat soluble vitamin and in biliary obstruction it could be mild absorbed. Richman, a division see leads to night blindness. Okay, again, it's just thinking through the different physiological steps that happened. And hopefully, that's make that's quickly and your head now. So it says summary of autoimmune liver disease. Okay, I'm not gonna go through. All of this is just a summary table of all the different fax you need to remember about what? Um, your liver disease. It's a spectrum off altered immune, hepatitis primary, biliary cholangitis on primary sclerosing cholangitis. Okay, so have a read when you get some guys. You guys have any questions about it? You can ask me at the end of well, but we will keep going on. Yeah. Yeah, I think I have. Ah, I think I have one this morning. We after this, and then we will be done. Okay. Having most of you have got this one. Ah, tingle. Okay, well, I'll give it 10 more seconds. Okay, good. Okay, So this is the most you've gone for a That is the correct answer in intrahepatic. Cody States is off pregnancy. Okay, so they were basically discussion. We're gonna talk about liver disease and pregnancy. Okay. Slightly overlapping with obstetrics. But the things that makes this diagnosis off intrapelvic really Stasis. The correct answer is that this patient is pruritis. Okay, That's one of the hallmark features off introverted coli Stasis. And she has mild elevation and other things. Okay, She has mild jaundice, mild elevation and AARP. Okay, remember, AARP can be mildly elevated anyway in pregnancy, but things that makes it abnormal is that she has elevated a little and ST Okay, in pregnancy, you shouldn't get elevated LDL or ST. Okay. Lt and ST should be normal pregnancy. So elevation that suggest disease. Okay, so that's why intravesical the states that have the most likely diagnosis here. Okay, It's of the other other things. So PBC, it's not a condition that happens in pregnancy. Okay, Even though you got pruritis, it's not not a pregnancy condition. Acute fatty liver of pregnancy is very rare. Okay, It's where patients get, um, if patient they use happens in the third trimester, patients can get severe complications, like, do you? I see it's not fitting with this clinical picture off the scenario Help syndrome, so help syndrome. It's It's a complication off preeclampsia. So I haven't told you anything about hypertension or protein, Urea or anything Or any evidence off hemolysis? And I've told you that the full blood count is normal. Okay, so that removes out help syndrome Hyper Mrs Gravidarum. So it's Ah, it's where you get pathologic. Um, vomiting. Okay, so it can happen in pregnancy. Ah, with happiness is you can get abnormal liver, liver enzymes, but it's there's no history off excessive vomiting or anything. That's why intraparty cool Stasis is the right answer here. So prices and joined us in the third trimester of pregnancy is suggestive off coli Stasis. Okay, so this is summary of liver disease and pregnancy. Okay, Have a real when you get the slides. Uh, it summarizes the three main ones you need to know. Um, yeah, and this is the last test here. Okay, Just, uh, quick question on paracetamol over those, and then we'll talk about overdose, and then we'll be done so that this is Ah, this is the guidelines. Question what? This is based on the BMJ guidelines for managing paracetamol. Overdose can vary across practices. Eso call it that most of you going for C uh, C is not the right answer here. Correct. Answer is actually be so. Measure party tomorrow in two hours. Okay, so basically this patient presentable Paracetamol overdose. Okay, this isn't a staggered overdosed. This is just this patient's taking paracetamol all that once taken 40 tablets again. Classic symptoms are nausea and vomiting. Okay. Keeping is according to be and a flu shot If patients present with suspected paracetamol overdose between 1 to 4 hours after ingestion, you should wait until you can get an accurate measurements off the paracetamol levels before you give an acetylcysteine. Okay, so because this patient presented two hours after the ingestion, so you should wait another two hours and then measure the privacy tomorrow and then assess if that assess if we need to treat assess if you need to give the anesthesia assistant. But I met by plotting the policy to more level on a normal gram. Okay, so if the level is above the normal gram level, then you can give the other seats are cystine. If it's not, then you don't need to give it. Okay, so you should wait until two hours because before hour mark the four hours after. That's when the paracetamol reaches its highest dose. Okay. And then, you know, if you need to give the and acetylcysteine good activated charcoal is given if they can be given if they present with it. One hour. Okay, one hour off ingestion. Okay. Not when they present all sports. One hour off the ingestion through Mazon. Oh, is given for benzodiazepine overdose on D IV by common. It can be used in aspirin notice. Okay, So this is my correct answer here is be so patient. Present between 1 to 4 hours. Post injection ingestion. Measure the paracetamol levels at four hours. Post injection ingestion. Okay. A sticky learning point. So this is some resupplied on medications that can damage the liver. Okay, Uh, parts of toxic medications, as there's a lot of them. So haven't read when you get the slides quickly on acute liver failure. So the most common cause of acute liver failure in western in west western countries is paracetamol overdose. Okay, worldwide. It's viral hepatitis. If you have. If your liver acutely fails, the main try out of symptoms that will happen is jaundice in capital opathy and coagulopathy. Okay, we keep coming back to this coagulopathy. It's one of the most important things in liver disease. Okay, you get reduced clotting function, and it's an emergency. So 80 assessment and generally the mainstay for acute liver failure is to support the liver again. Because you're acutely having disruption to multiple body systems. They should be managed in a intensive care setting. Onda, you should consider if they need a transplant very early using King's college criteria. Okay, quickly. In terms of pathophysiology what happens in a paracetamol overdoses that, uh, normally and Parsifal is metabolized through salvation and glucagon occasion into non toxic metabolites. Okay, a small proportion can get metabolized through the side to go on pathway. And this is when you get production off this compound called Nap Q. I okay? I'm not going to try and say the full version, it's ah, very long name, but essentially get production of knock You I okay. And normally in the body you have a little tired, which will, um, which will conjugated nap. Try and that will then be excreted into the urine. Okay. So, normally, good surviving will constipate inaccurate I and then it could be excreted into the urine. Okay, Problem is, and an overdose this part for gets overwhelmed. Okay, So this part way of salvation and blue corrugation is overwhelmed Most of the prostate focal, and a person will start going through the cytochrome pathway. Okay, Eventually, what can happen is you get too much napkin by being produced. We just leading to Bluetooth. I own stores being depleted. Okay, so you don't have any glutathione left. And so if you don't have any groups of time left, you're not able to congregate the napkin. Uh, I and that's when you get the symptoms. Okay, So if the napkin why doesn't get conjugated, it can lead to help out a toxicity. Okay, that's what's happening. That's a part of physiology off the overdose. Okay, In terms of the treatment, the mainstay of treatment is to give an issue tell system because it will replenish the stores of fluid if I own. And so it will, um, help conjugated. It will help conjugated all the napkin. Why, that's there into and then get excreted into the urine. Okay, that's that's the basic pathophysiology loss light here. So this is somebody of management of overdose. Okay, so we talked about this. If they present within one hour. You can give Taco okay between 1 to 4 hours. You should measure it up four hours after ingestion. Okay? And if it's elevated, so if it's above the normal gram treatment line, then you can give the acetylcysteine. Okay. If they present after four hours in between eight hours, you should measure it immediately. Okay? And if it's elevated, you give the neck, okay? And for the other situations, you can follow it according to charts. Okay, key point to remember is that if it is a staggered overdose, so if they've taken paracetamol oh, over multiple hours of multiple days, then you give it over the you give the knock immediately. Okay? So if it's a staggered overdose or you're not sure when they've actually ingested all the paracetamol, then you can That you're the NAC is immediately indicated. Okay. On King's college criteria can be used for to assess if a patient needs transplants again. So that's a quick picture of a normal gram. What it looks like. Okay. So, basically, depending on what the paracetamol level is, you plot it on this graph, and if it's above the treatment line so highlighted in red uh, then you can give the knock. Okay, that's what's a normal gram is so that's it for today. I just I put some post lecture notes in for you guys. Have a read. So we have some notes on hemochromatosis Wilson's disease about Chiari syndrome. How to sell a carcinoma. Okay. Know, bit on liver masses. A little cheap table on liver masses on a little cheat table on tumor marker associations. Okay, that's it for me today. Thanks for Junior. That completes our