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And that my slides don't work. Ok. Very good. Right. Hello, everyone. My name's uh Emelia or Milly to both. Um I am currently an IMT one doctor at the Royal Bo uh to give you a bit of background and I have, I want to do gastroenterology. So I'm doing IMT and then I will hopefully special, specialize in hepatology. Uh a bit of a caveat though. Um I am not a imperial student, so I have not sat the Imperial Paces. Uh I went to Cardiff University uh where we also do an O paces um in final year. So I've based a bit of my um of today's talk on kind of what I would expect to come up in the paces. Um But I've also been speaking to imperial students next imperious students to make sure it's more relevant for you guys. Um So I've got an interest in liver um and I did a liver JCF job last year at the three, which is a liver transplant unit. So, um that's where I've got most of my knowledge from uh this evening. Um Upper G is a huge topic. So I thought I'd split it up into two very common kind of case scenarios that you would come across in, in cases. Um The first one being dysphasia, um which I believe is on, on your list of, of things you should know about by the time you leave Imperial Med school and then we're gonna do a liver case. Um We're also going to intersperse these with spot spot diagnosis. Um I believe in your case is you have spot diagnoses. So we offer you some pictures um and some guessing would be great mental seems to be working. I've got some um uh I got some uh responses on that. So that's really great. I'll be using that as we go through. So case one, John is a 56 year old male presenting to his GP with difficulty in swallowing. So this is a dysphasia case. I think it's really important, the difficulty in swallowing. It also known as dysphagia in uh um in med me medical lingo, it's really important that you can intersperse like you know what medical lingo is, but also know how to describe it in layman's terms. So, difficulty in swallow, swallowing um is dysphagia, Adena um is painful, swallowing, uh dyspepsia, those are your more reflux type symptoms. So your heartburn um remember to know the differences between these because you might get caught out on exam if the examiner turns around and goes. What what? But yeah, but what is dyspepsia? So our case one is gonna be about dysphasia. So how first of all, how do you approach a patient with dysphagia with all cases? You need to think about the urgent considerations and then we need to think is that, is this an oro uh pharyngeal dysphasia or an esophageal? We then think about the history examination and investigations. So I'm gonna go through all of these and then we're gonna see our case and then you can see how thinking about your approach to a patient helps before then going in and seeing a case. Uh because then you can uh think about it logically in your head. So the history is the most important bit, we need to split it in two or a pharyngeal or esophageal. And the most important thing is when you're taking a history, you might be asked to take a history in cases is um identifying red flag symptoms. So when you're asking questions, start off broad and then before the end of your history, you need to be making sure that you've gone through really, really important red flag symptoms. So, within um dysphasia, important red flag symptoms are below. So, weight loss, uh Aden aphagia. So that's pain when uh when swallowing, uh has there been any gastrointestinal bleeding? So, this may be Hemmes or may be indicated by melena um uh and potentially related with dysphagia. So, regurgitation is important, um and this might be of undigested food or liquid and this may signify an obstructive or motility disorder, aspiration. So, when food or fluids are inhaled in the air of your lungs, um it's important to know because that can lead to pneumonia. Um, accompanying neurological symptoms is important uh to explore as a lot of neurological conditions can also lead to dysphasia, uh and previous head and neck cancers. Uh as we don't just think what's in the esophagus causing obstruction or in the airways, there's also head and neck cancers outside can compress um, from externally. So we're gonna go on tea differentials of oropharyngeal dysphasia. I'm gonna give you guys 30 seconds to go on m to her and give me some common differentials which I'm sure you're aware of. Ok. Mm. Ok. I don't seem to have any responses so far. Oh, there we go. Fantastic. They will come through. Fantastic. Ok. Yeah, good. You guys are thinking so, oral pharyngeal mouth and the pharynx. So that's the top half. Find it easier to split it into two. So common causes of oropharyngeal dysphasia, stroke, pharyngitis and postoperative cervical spine s um, cervical spine surgery. Although postop uh, cervical spine surgery is not common. It's a common complication of cervical spine surgery. And then thinking about the uncommon causes. A foreign body and caustic injury. It's really, really important to identify because this, um, may be an emergency. There may be burns causing, uh, dysphagia. There may, uh, or maybe a foreign object sat in the airway, epiglottitis and lots of you have uh mentioned malignancy. So, or in pharyngeal carcinoma, um also more uncommon causes like thyromegaly. So that causes uh an external compression. Um And then Wilson's disease, this is in um in late stage Wilson's uh where you get deposition of the copper in the brain, you get neurological symptoms such as um uh oropharynx, dysfunction and dysphasia from that. Uh and then with myasthenia gravis as well because of the reduced um uh reduced muscle con contraction because of the uh autoimmune um action on the ac uh a uh receptors. The list does go on though. So the this is not an exhaustive list, but it's go good to have a couple of differentials in your head going into these uh stations so that you are thinking about what's uh what's gonna come up. So, differentials of esophageal dysphasia you guys are able to think of. So further down in the esophagus, what might be causing. Uh some of you guys have mentioned on the, on the previous one, but if you could anyone else think of other causes of esophageal dysphasia. Yeah, good. Someone said malignancy, we've got achalasia. It's been said a couple of times. Fantastic strictures, wonderful esophageal web. Cosmic. You guys know your esophageal dysphagia. So that's really good. So the most common being gastroesophageal reflux um that can patients can pre present with um difficulty swallowing, hiatus, hernias, a very, very common um cause of it as well. Um and that's where you get um, herniation of the uh stomach into uh a above the diaphragm, esophageal candidiasis. This is mostly seen in patients with an immune deficiency. So, such as HIV, it's actually an age defining illness. Um So if someone presents with esophageal candidiasis, you should be thinking uh more naturally actually. Why is why is their immune system not functioning that well, that well, diffuse esophageal spasm um and esophagitis. So, and then the actually more uncommon ones, loads of you guys have mentioned, um Carcinoma, achalasia, scleroderma can also cause um cause dysphagia. So, um scleroderma being um uh tightening of most, most commonly seen the tightening of, of the skin on the fingers and around the mouth. Uh but they can present with uh dysphagia as well. Ok. So moving on to an examination, not actually likely to find um that much because it's possibly or uh internal, but it's always good to remember um to not just looking at the person but to is there anything around the bed? Uh So they might be have a stick with them uh which would suggest that their mobility is not as great uh general appearance with the patient. Are they cachectic cachexia um be suggested more. Have they had any weight loss? Um aso associated with, is there an underlying cancer pallor? Are they anemic? Um tremor actually have they got an underlying neurological condition such as Parkinson's, their hands? Is their Raynauds, which would be associated with scleroderma, lymph nodes. Um are important for um, head and neck cancers. Are there any other neck mas masses? Um, like thyro uh uh thyroid goiter? Um or are there any scars because we mentioned postoperative, um, cervical spine common. Um uh commonly they can deve develop dysphasia uh on the face. Also looking for conjunctival, pallor, oral candidiasis as well, may suggest they've got esophageal candidiasis. And are there any kinds of flesher rings? So, moving on to investigations, I like to split my investigations. I'm sorry? Right. Ok. I like to split my investigations into four whenever I approach it. So I go in if someone asks me. Ok, what investigations are you gonna do? First of all, start with the easy ones, your bedside investigations. So that's your full set of ops, your point of care test. What can I do at the, at the bedside? That doesn't just have to be a full set of ops, but that's your blood sugars. Um, and your, um, other things I can't think off the top of my head but you can do it. But, uh, then we've got bloods and it's all important in exams to not just go, oh, I'm, I'm gonna do F PC and LFs. Why are you doing each of them? You have to do a blood test and then explain why you're doing it, um, imaging and then any other investigation. So, staging it out in those four is is, is really useful. So, if a patient came in with dysphasia, what investigations would you do? Can answer on many for me gonna give you a 15 or 30 seconds to do that? Ok. Yeah. So someone's gone in with the, any other investigations probably, uh, F PC tftslfts. Good. Fantastic. Lovely. Yeah, you've done a re really good job there. So, bedside investigations, uh, full set of s always good to do and then standard bedside swallow test. As someone's mentioned this on the men, it's really important to remember that you can do that at the bedside. Um And this gives you a good um so often done uh by our nursing colleagues or the speech and language therapist. Um gives us a good assessment of someone's swallow very, very easily and quickly by the bedside blood. Same someone has mentioned F BC which is fantastic. We got in uh which cause we're looking for any anemia which might be suggestive. Um Do they have an iron deficiency anemia? Would we be concerned? Therefore about a G I malignancy inflammatory markers? Is there some underlying infection? Uh TFTs is really good. Someone's mentioned that uh looking for any thyroid disease, LFTs and, and Plasmin, we're thinking about Wilson's. So as you can see, I'm not just mentioning a blood test and going yes, we're gonna do that. I'm mentioning a blood test and backing it up with one of those differential diagnoses that I've got on my list imaging. So um imaging the gold standard um for diagnosing most structural abnormalities of the esophagus and the stomach is the OGD. Um This is really good for kind of diagnostic. You can also take biopsies while you're doing it. So it's not just a picture you're taking biopsies and also allows for therapeutic intervention at the same time. So that's why it's, it's so valuable. It's also easily uh accessible in, in, in in all hospitals across the UK. So a couple of people have mentioned barium swallow as well. So bari and swallow and time esophagram exactly the same thing. Uh they're going a bit out of vogue uh but they're still really useful at diagnosing achalasia, which is when the esophageal sphincter fails um to relax. And so uh you get food boluses and, and often regurgitation of liquids and severe achalasia uh because it cannot get through the esophageal uh sphincter into the stomach. Um with the barium swallow, you get three films. So one is taken at one minute after you swallowed the opaque dye at two minutes and five minutes. So they're x-rays where you take a um a contrast medium. Um And it allows you to see the barium uh which is the contrast medium traveling through the esophagus. Um And then any other investigations, someone's already said it which is brilliant uh esophageal manometry. Um and this is to measure the intraluminal pressure and coordination um of the esophagus. So it's useful when you're suspecting kind of diffuse esophageal spasm um or other motility issues of the esophagus. So our case one, John Doe reports experiencing difficulty swallowing for the past six months, he describes the sensation of food getting stuck in his chest. He notes that he has trouble swallowing both solids and uh foods and liquids. The difficulty swallowing has progressively worsened over time and is now interfering with his ability to eat comfortably. He reports some weight loss. His past medical history is hypertension type two diabetes and dyslipidemia. This might be the blurb that is on the wall outside of one of your paces stations. This is all the information you get. Um, and then at the bottom it'll, it'll give you um what they want you to do. So it's really important to read these carefully and read the bottom. Please do an abdominal examination really, really carefully. You get normally a couple of minutes outside the station to read it, read it a couple of times, make sure you've taken the history down, um, and make sure you know, and understand what they want from you when, when you go in. So sorry, excuse me. Uh I'm not gonna run through with you how to do an abdominal exam, uh examination. You can go on gi medics watch the video um and practice on your, your friends family and any willing patient on the wards. Um It's pretty straightforward. You just got to learn the motions. Um So we're instead gonna go through those steps that happen after you've done your examination. So you've gone in, you introduce yourself, wash your hands, you wear appropriate P pe. Um You explain to Mister Doe that you want to do an abdominal examination, explain what that entails, gain consent and then go ahead and gaining consent might be. Is that ok? And he will say yes. So on examination, you're looking generally he appears well nourished and in no acute distress, it's always important to know on his hands. You don't know anything, no note anything moving up to the head and neck. There's no thyromegaly, no masses and no lymphaden lymphadenopathy on general abdominal um examination. It's soft, nontender, nondescended and there's no palpable masses. So all in all a pretty unremarkable examination, you come to the end of your examination having gone through all the steps that you'll see on ki medics and summarize that to your examiner. So today I have uh examined Mister do who's a 56 year old gentleman who's uh been reporting experiencing difficulty in swallowing. I did a full abdo examination and on examination, I found no peripheral stigmata of any um of any liver disease or any the um any um concerning features of um of, of disease that may have may be causing his dysphasia. His abdomen was soft and nontender and non distended and there were no palpable masses. So just kind of repeating what you've seen those, those positive negatives, um, to the examiner, the examiner might go. Ok. That's lovely. What investigations would you like to do? So, it's really important here to think. Ok. So what am I looking for and put it out into your, your, um, bedside? Um, your bloods, your, um, your images and your, any other investigations? So you ask for, um, a full set of observations and the bloods that you have listed, The examiner turns around and says to you, oh, here, here are the observations and here are some bloods, take a moment to have a read of those. And now we would like you to go to men and think what are your differentials for John? Yeah. OK. Good. So good. You guys have mentioned um some of the differential we've been talking about. So running through these bloods, you need to be able to recognize those are completely normal ops. Uh They may not give you ranges for observations. You shouldn't need ranges for observations. They're normal, the, the blood, they will always give you ranges. So you'll be able to see what is abnormal and what's not. So here the F PC John is anemic and he's got a low M CV. So he's got a microcytic anemia. If in the exam, you, you look at the bloods, it might be a good idea to verbalize that. So the examiner can see that you are, oh how your brain is working and how you're going through. So you said John has a microcytic anemia. This means that I'm concerned that he is lo losing blood somewhere. Um as this and his, as he has presented with dysphasia, uh the differentials that I would want to, the uncommon but important differential that I would want to rule out is an esophageal carcinoma. You may then go on to say, however, there are more common differentials such as reflux causing esophagitis um or say a hiatus hernia that might be causing um Jo uh John's symptoms, but it's important that you rule out the esophageal carcinoma. So what investigation if these are your differentials now? So esophageal carcinoma being your top differential, what investigation would you do? Go to M meter? Let's make sure all I've dr this in enough? Fantastic, brilliant. OK. As I said, and we've all got it 100% of you said OGD. So gold standard for this would be an OGD and you would consent them for plus or minus a biopsy as well. Um Ct thorax might not be a, a bad, a bad thing to do at present because it would be good to then stage the disease. But gold standard, your first thing to do would be an A GD. So, so we're gonna do some spot diagnoses now. Um So this will all be on someone, tell me what this is. We're not going to spend too long on these good. Ok. Yeah. Esophageal carcinoma. Fantastic. What is this one? Yeah. Fantastic. This is a hiatus hernia. So, this air bubble here, this is a ginormous hiatus hernia um is uh a gastric bubble of gas that is well above the diaphragm. That's a smaller hiatus hernia. And you can see the fluid level here in this, in the gastric bubble that's, that's above. So that's not, this is the heart outline here. This is the hiatus hernia bulging upwards. So three A, does anyone know what that is? Yeah. Good. Fantastic. So, Achalasia, that is a a barium swallow and that is wonderful, which no one has put anything else but Achalasia. Um And that is your classic be uh bird neck pinching at the bottom of the esophagus um as the esophageal sphincter um is, is not relaxing. And b and that's also a barium swallow. Yeah. OK. Good. Uh That's diffuse esophageal spasm. So you get that classical uh corkscrewing um of the esophagus. Uh uh case two something, I'm a, a lot more happy with, right? So case two, this might be on the outside of your next station. So you finish with, with John, you walk out, say thank you to the examiner and leave it be behind. Move on, forget about it. W what happens in that room happens in that room and you need to then move on to the next next station. So on outside the next station, it says John Smith, a 68 year old man who has, has presented to ambulatory care with fatigue, jaundice and abdominal discomfort. Mister Smith reports progressive fatigue. Over several months, he noticed yellowing of his eyes and skin. Over the past two weeks, there has been no significant weight change and no change of bowel habit. He has a past medical history of hy hypertension. Please do an exam, ex do an abdominal examination. So while you're waiting there reading through the blurb twice, at least uh trying to memorize the patient's name before you go in. Uh You're gonna be thinking of, OK. What are my differentials of jaundice? Um Going into this into this scenario. Can you go on men mein and give me some differentials for jaundice? OK. Good. Is that anymore? Good? OK. Fantastic. Um So wonderful. You're all thinking, well, when I see a jaundice patient, I like to think. OK, so jaundice can be prehepatic hepatic and posthepatic, the pre hepatic, your hemolytic anemias where you get um uh high levels of um unconjugated uh bilirubin uh due to the excess breakdown of red blood cells and your liver is just not able to conjugate it fast enough. So it's un unconjugated uh you're hepatic. So that's when everything goes wrong with the liver itself and, and then you get jaundice and then you post hepatic. So that's your uh gallbladder and your biliary issues thinking of the diff. So I like to think of it though. So I can think of ones from each decompensated liver cirrhosis of any cause might be I there's lots of causes of which alco alcohol related liver disease. Um, the, the newly named metabolic associated tic liver disease. So, it used to be called a nonalcoholic fatty liver disease. But if you want to come across that you're keeping up to date. Um, in, in June, it was actually, uh, the easel, which is the European Association for the study of liver uh changed the nomenclature for um liver diseases and now it's called Mazz old. So, metabolic associated. And then you get a MET A LRD, which is a metabolic plus alcohol associated related liver disease. So, if you just want, sound like you're keeping up um with the current research, use mail instead of naff um choledocholithiasis. So use gallstones, all your viral Hepati disease. So B and C commonly also in immunocompromised. Uh patients with pregnant ladies, hep E can cause jaundice um as well as less likely see it in HEP A um drug induced liver injuries. Co amox is your biggest culprit for a drug induced liver injury. Um But there are uh lots of others like TB medications um commonly can cause a transaminitis and li and liver disease. Uh and then your cancers mainly in your biliary tract. So your biliary, um your cholangiocarcinoma and your and your pancreatic um cancers, just because if you think about it, the tubes coming out the liver and then um the cancer sits in the way. So it means that the bile can't drain properly out the liver. It then either goes back up into the liver causing disease in the liver or goes out into your bloodstream causing um uh causing jaundice, hyperbilirubinemia. Uh But HC C can in, if it's placed in the right place or in severe disease, also, it called jaundice. And then as mentioned, your hemolytic anemias, it's always good to know some um uncommon um causes as well. So, Gilbert, uh although uncommon loves to pop up in exams, so that is an isolated rise in conjugated bilirubin um which worsens under stress and that's not just taking exam stress but also infection, uh the body stresses. So, um it causes a rise clinically of no significance, doesn't cause any harm to the patient. IgG four disease is a rare um autoimmune um im immunoglobulin disease um causing a cholangiography. Um It is often confused with primary closing and cholangitis as well. They're very closely linked. Uh PS C is linked is the one that's linked to IBD. So it's an autoimmune um uh cholangiography, primary biliary cirrhosis, that's an al also another autoimmune condition that uh often your patient is middle age and female. Um and it's, that's to do with intrahepatic um bile ducts, inflammation and then results in cirrhosis Wilson's disease, which is the inappropriate deposition of copper in the liver, but also in the brain, as mentioned before. Um hereditary hemochromatosis of high iron. Um because of uh of inappropriate uptake of iron from the G I tract and it gets deposited in the liver, uh causing inflammation and cirrhosis and then alpha one an trypsin for some reason in 15% of patients uh with uh alpha 1 90 trypsin deficiency, they also develop a cirrhosis. Uh I'm not quite sure I understand the. So um examination a prehepatic jaundice patient, what are you expecting to find? You're expecting them to be jaundice or, or have icterus? So, it's important to differentiate. I icterus is just the yellowing of the sclera. It's not your skin being you can't say someone's icteric when they've only got um yellow eyes, uh normal uh serum bilirubin is approximately 3 to 20 micromoles per liter. And jaundice is not really noticeable until it's above 35. 40 most people eye 40. If you've got a good liver doctor, they tend to notice some jaundice a bit earlier in a, a prehepatic jaundice. So, from a hemolytic anemia, as usual, you would also expect to see a splenomegaly. And that's because um the breakdown of uh the hemoglobin occurs in the, in the spleen causing the splenomegaly. Um So, or it's due to them kind of filtering out all the, all the breakdown product, products of the hemoglobin. So it causes splenomegaly. So, um examination of chronic liver disease, what are you expecting to find you jump on men and give me some ideas of where you're standing. Yeah. So I asked um an A I picture generator on Google to make me a picture of a chronic liver disease patient to put on these slides. This is what it came up with. So I hope you guys can identify chronic liver disease, but better than A I can generate a picture of it. So we're expecting to see sarcopenia. Sarcopenia is muscle wasting slightly different from cachexia. Um So sarcopenia is low muscle mass. We expect to see bruising which has popped up on mente, someone's thinking of that and that's because of in chronic liver disease, you're expected to see to see low platelets due to portal hypertension. And so they are um they're more likely to bruise easily. Also, if the liver is damaged, you don't create all um the uh factors needed in clotting. So it's not just the low platelets but also all the the clotting factors. Um the majority of them are produced in the liver. So therefore, uh they are very um bleedy and bruise very easily. They've got very fragile skin, hand and nail features. So some of you mentioned these, the lechia, that's low albumin, that's a sign of low albumin, which is a feature of chronic liver disease because albumin is produced in the liver. So, if your liver's not working, don't produce um albumin hypoalbuminemia and then you can develop leukonychia, palmar, erythema is an, is an indication of uh it tends to be alcohol related liver disease. Um However, you can get palmar erythema, which is not associated with alcohol. So, um, don't just say, oh, they're definitely an alcoholic if they've got p uh erythema spider and Nevi are the central filling, um, small red marks and if you squish on them and release, they should go pale and then they fill centrally and then out into their little spider legs. Uh up to five is normal, greater than five, there is some uh pathology going on. Um And you may see needle track marks um on the arm. So it's always good to make sure you're looking in the villa before you move on. Um As this might be a, a sign that there may be uh an IV drug user or ex IV drug user less likely to be seen in places. But when you're in the real world, it's important things to look out for because people might not be as honest with you. Uh facial features. Uh So telangiectasia, it's commonly seen uh icterus. So that's the yellowing of the eyes. Um and conjunctival pala due to um the anemia gynecomastia. Um interesting cirrhotic patients are more likely to develop gynecomastia. Um This is because they think that there's increased e estrogen production. But also if you've got decompensated liver disease and you have ascites, um the diuretic of choice is spironolactone and spironolactone causes gynecomastia. So you've got the double double reason why they might might get that and then abdominal features, there might be hepatosplenomegaly, but there might, might just be splenomegaly um, early on in chronic liver disease. If someone has developed a, a naled certain uh or Mazz, a stoic liver, it might not be cirrhotic at that point. It's all a spectrum. Um, they, their liver might be very, very large. And so you would feel a nice, soft, uh smooth uh liver edge and you would count how many fingers down from the rib cage. Um Do you feel that uh feel that live up? However, as they become more cirrhotic and scarred the liver shrinks. And so you may not actually be able to feel anything, doesn't mean they have liver disease, of course. Um and collaterals such as cap medusa, which are due to coral hypertension. So stiff, liver blood flowing through the liver is reduced. So you get collaterals that go out um externally on the abdominal wall called cap medusa. Um and then you get varices um internally might be esophageal gastric, but you can also get rectal varices. Um So you can get pr bleeding from rectal varices, um and other collaterals within the uh abdominal uh abdominal cavity, which can have a tendency to bleed. So it's uh good to remember. Um varices aren't just in the esophagus and stomach. So those are the are where what you're looking for kind of in a compensated pa uh chronic liver disease patient. Uh but there's also the de things that indicate that this patient is decompensated, which a lot of you uh have said here. So jaundice is um is shows that they are decompensated. If you're compensated, you don't, you shouldn't be jaundice. Um abdominal distension with ascites, this can behi exhibited as uh shifting dullness, peripheral edema. This is due to the increased portal hypertension and causing slow um and more backflow of um of the venous blood, but also because of low albumin. So they tend to be just more leaky their vessels and therefore they develop peripheral edema. So it's important to have a look at the feet encephalopathy. And that's exhibited with a flap, also called asterixis where someone's um uh identified on men. It's great uh hematemesis. So unlikely something that you would see in a piece. But actually, uh they can be really cheeky and pop a bowl on the side which has got some something that looks like blood in it. Um So remember to kind of check around the bed and there's something that comes up in exams and people get very old. You'll definitely see there's hepatic fetal uh which is a, a sweet and putrid smell of the breath in a decompensated cirrhotic patient. And this is to do with kind of secondary portosystemic shunting. I've never come across it. You never really wanna get that close to a patient anyway, to smell their breath. So, but people love mentioning it. So it might be something you want to, to just keep in the back for. Ok. So uh and an examination of a posthepatic patient. So acute post heath patients. So if they've got um something like gallstones, they might acutely become jaundice, you're unlikely to see anything like this in your paces because they're sick and in pain, we're not gonna put these patients in front of you, but chronic causes of a post hepatic jaundice, something like PS C. Um if a if advanced, you can develop chronic liver disease from PSE. So you're, you're gonna see the same um same examinations findings um as kind of your chronic liver disease patients. So, John, this is our John uh John Smith from our case earlier. So our gentleman, um you've been asked to do an abdominal examination on he's yellow jaundice. He's, he's got the lack of body hair. And that's thought to be because of the increased estrogen that happens when um est estrogen production and blocking of testosterone, when you're cirrhotic. Uh the gynecomastia, the muscle wasting sarcopenia. He's got palmar erythema. He just looks like he's in a, in a bit of a pickle. So you've done your, your lovely examination. You've summarized to the examiner. Um, and they've asked you what investigations, um, what investigations would, are you, are you going to do do next? So, bedside investigations, you wanna do a full set of ops and a capillary blood glucose. It's really important to remember the cap blood glucose, uh especially if you're concerned about liver failure. Uh If you think about it, the liver is where a gluconeogenesis occurs. So, if you've had a failing liver, you can't replace the glucose um in uh in the blood. And so they can become hypoglycemic so severely that it can become comma, it's always, always important to ask for um a cap blood glucose bloods. Sorry, we want to identify the cause uh the cause of the cirrhosis. So cirrhosis just means liver scarring. That doesn't tell us what actually caused it. So the bloods you're doing are to find out what has caused the cirrhosis in the first place. And then you want to be doing bloods on um things that might be causing a decompensation. So, can people tell me? So when we ask for bloods, when a patient has cirrhosis, we ask for a noninvasive liver screen, can people tell me what bloods are included in a noninvasive liver screen? And this is all M tea OK. Apple. Amazing, brilliant. Doing really well. This, this was actually a question um I had on my IMT interview this year was um what blood I was, I had a liver case and they asked me about a noninvasive liver screening. So you were writing all the right things already, which is brilliant. So obviously, we're gonna first start off with LFTs. How severe is the hepatitis um and a clotting screen uh as the prothrombin is really, really important in the identification of the severity of the liver disease, uh prothrombin time as well as inr in acute liver failure. They really, um those are really, really important as they're an indication of prognosis. Um And so in that parasal overdose patients, um you want to know their inr and their PT before you're speaking to speaking to transplant centers, if you think they're, they're getting worse because that's, that's what they're gonna be asking you. You're then gonna do all the viral hepatitis bloods. So HEP BC HIV also and CMV. Um he HEP BC and HIV are done at the door for most hospitals now. So that's a really great initiative that's been started um over the past year. Uh And actually we've been picking up loads of patients with um viral hepatic disease. Um Someone said autoantibodies, that's fantastic. And then to be more specific. So they're tissue autoantibodies A N A. Um and smooth muscle antibodies are the um what you're looking for for autoimmune hepatitis. Um And then it anti mitochondrial antibodies or what you're looking for for um P BC. So it's good to know that immunoglobulins. Um These are useful because IGA A is often raised in um in alcoholic related liver disease. Um So a for alcohol, it's always a good one. I always store that one in my head. Um Then we got HB A one c someone else has said and said that uh type two diabetes and other metabolic conditions are associated with metabolic associated tic liver disease says in the name copper, um and Carlo plasmin further down, um hematinic. It's important to look at ferritin that often. Um So looking at whether they have high ferritin, um but also they may be anemic as well. So we're looking at both alpha one antitrypsin, as mentioned, your cancer, uh, tumor markers are a FP for H uh HCC S and uh ca 99 is for um Pan or Cholangio as well. Carcinoma rise. Your ca 19 9, it's not that specific. And then they may, you may ask uh for a conjugated bilirubin if they've got um a high bilirubin because this allows you to um to differentiate, is it pre pre hepatic or is it a hepatic cause? Um And then you can also say F PC news and need crptfs. Um as these are things that will be important to work out why a patient has decompensated. So you're looking at inflammatory markers, have they got an infection on board? Um use knees um as often patients with liver disease can develop a KIS. Um And um this is because of hypo um hypovolemia, it mainly um but then they can then go on um to develop more um more difficult to treat a KIS and it can then become HEPA syndrome. Um and TFT S. So, hyperthyroidism is a common cause of decompensated. Um cirrhosis in chronic liver disease patients um and blood cultures are um, are really important to do on patients um who are jaundice because actually infection is a big driver um of jaundice, um and decompensation. So you're looking for a bacteremia, the liver really important in your immune response. So, chronic liver disease patients are much more susceptible to infections and um, the rate of bacteremia is much, much higher. Uh, so it's always important to get blood cultures off. So, investigations, um important investigations to do for uh patients with chronic liver disease. Uh ultrasound liver is your top easy to get and gives you good idea of of what's going on. You can see is there fat in the liver? Is the liver cirrhotic, is there a lesion that I should be suspicious of is are the pancreatic ducts. Um And the biliary ducts dilated, uh which could mean there is a downstream stream obstruction or there's gallstones. Um So ultrasounds are really good fibroscan. This is a measurement of the um uh of how stiff the liver is. Um, a fiber, um, a fibrous score, a fiber score of greater than 11 is suggested of fibrosis. Um However, things can artificially increase your um liver stiffness such as having a meal just before you have um the fiber scram done. Um So they're not perfect and also very operative dependent, but it's a good along with um an ultrasound liver to decide actually. Does this patient have cirrhosis ct of the pelvis may be useful to request. Um Always with contrast, there's really very little point in in doing a CT ABDO uh uh A CT P without contrast because everything just looks a bit mushy on the inside when there's no contrast in there. Um But it, this can allow you to look uh for stones, uh portal vein thrombus, which can lead to uh cirrhosis or Bud chiari, which is um a thrombus in the hepatic vein to the other side of the liver. And then an MRI liver is really good to looking at the liver more closely. Um looking at um whether there's any looking at lesions more closely. Um and uh being able to characterize those lesions. So then any other investigations, uh you may ask for a liver biopsy. Liver biopsy is uh really good. If you haven't got a definite diagnosis of cirrhosis, it allows you to look more closely at the cells, um, assess the level of, of fibrosis and scarring. Um And also the etiology. Uh uh if that is otherwise you're unable to, um, to assess that there's two ways you can do it, you can do it through the neck or percutaneously. Um So, percutaneous biopsy is the most easy to get, however, shouldn't be done if there's a high risk as a high risk of bleeding. Um And if they got a really high bilirubin as the, the rate of complications is much greater. So, um a transjugular uh liver biopsy is much better if the patient's really sick, old frail, um, or otherwise you may ask for an, er, CP. So, um, that's the one where they go down with, um, the endoscope all the way to the biliary, uh, to the ampulla vata, pop up the wire into the biliary, uh, tract, flash, flush, dye up and take lots of photos. And that allows you to see the entire biliary uh tract. It comes with risk though there's a high risk of pancreatitis, especially if they manipulate the pancreatic duct. Um And it's, it's a very difficult procedure. And so it's only offered in certain places, but it's very, very good at helping diagnose PS C. Um And uh IgG four disease as well, um which is more specific when you're looking at cholangiography, it's really um important to do. It also can be used um therapeutically for gallstone retrieval um where they literally can like trawl out gallstones. Um And then OGD uh would help you if you're looking for um if you're looking for portal evidence of portal hypertension. So that would be esophageal or uh gastric varices. So we're going back to spot diagnoses now. So a bit more fun for you but guys than just listening to my voice. So spot diagnosis, one, someone has mentioned this before um on things to look out for on examination. Yeah. Uh two contractures. Good. And what about B palm erythema? Fantastic. So dup contractures. So a the um as I mentioned, drinking lots of al um alco. So I haven't actually mentioned this one juvenile can be caused by alcohol, um, smoking, but it can also, people can just have a family history of it. Um, and diabetes and epilepsy strangely are, are also um predispositions to developing it. It's a thickening of the tendons in the hand, um resulting in contractures in the fingers. Bill nai has bilateral dupage contractures. So that's why he's always doing this. Um It's rectified with surgery. So, ligation of the tendon um is the only real kind of proper solution for it. Um Palm erythema, this has been mentioned. Um So causes are are portal hypertension, chronic liver disease, but more associated with alcohol related liver disease. People you can develop it though in pregnancy. Um and thyrotoxicosis, rheumatoid arthritis, other kind of um more, more weirder ways of developing it. Jones. Ok. So nail the nail signs here. What do we have a good? Fantastic. So, Koilonychia chronic iron deficiency. So you get spooning of the nails and then B Leukonychia. Fantastic. So hypo alb albumin, um low albumin um spot diagnosis. Three brilliant. This is ankylo stomatitis. Um This is associated with iron deficiency anemia. So it's a good one to remember. Um Couple of you guys have got that as well. Brilliant. I know one that they love in exams. I think I've seen it once. Yeah. Fantastic. Kaiser Fly. It rings. So this is deposition of copper um, around the iris. So management of chronic liver disease. So you're, you're in, you're in your, um, even you're with your examiner, you've done the examination, gone through the investigations that you would send off and you explained your differentials of um, of what you, what you think is going on with John. They now might turn to you and go. Ok. So how do you manage chronic liver disease? I like to split it into three things. Treatment of the underlying uh liver disease, monitoring for the complications. And then thinking about what's ahead. So, liver transplant or supportive and or I should have written supportive and palliative care. So, treatment of the underlying disease, the liver is amazing because actually, if you stop whatever is insulting the liver, I it can improve itself drastically. So this may be if it's a viral he um a viral cause, treating the virus. So if someone has HEP B, um you cannot eradicate Hep B easily but you can control it and reducing their viral load um can result in their um in their co compensation of the HEP B cirrhosis or if they're not yet developed cirrhosis, they don't go on to do to develop cirrhosis if you keep their viral load low. Um And you would do that 1st, 1st line um antiviral is Tenofovir for HEP B. Uh If they are um alcohol related liver disease, stopping drinking alcohol is all they need to do to, to recover, then a lot of the function of their liver, um muzzled, uh losing weight, uh doing more activity. You can see where I'm going, stopping whatever is insulting the liver is, is kind of top of what you want to do be because you really, really want to, if, if this patient is cirrhotic, you really, really want to avoid them decompensating a compensating cirrhotic has a median survival of about 9 to 12 years. Whereas a decompensated cirrhotic has a medium survival of two years. So that's a 50% mortality in, in one year time. That's huge, massive difference. Um So treating the underlying disease. So stopping them decompensating um is really important or so, stopping them from developing the cirrhosis in the first place, monitoring for complications. So, in a cirrhotic patient, you want to be looking for evidence of portal hypertension and that may be as I mentioned by doing an OGD. So you're looking for varices or in a ct of the pelvis. With contrast, you'll be able to look for collaterals. If there's evidence of portal hypertension, there is. So there is a fair amount of evidence to show that giving a nonselective beta blocker such as carvedilol reduces the risk of um of bleeding because it reduces the pressure within the um the splanchnic venous system. Um you need to do regular ultrasounds to monitor for HCC if you're cirrhotic. Yeah, there's a high risk of developing um uh HCC So you do an ultrasound scan every six months. Ascites can develop because of your portal hypertension. And if you have ACY and your low albumin, so you get fluid, leak protein rich fluid leaking into your abdominal per, into your peritoneum. You can reduce society's production by having a reduced salt diet. We don't say a no salt diet, that's basically impossible. Um So a reduced salt diet. So cutting out crisps and adding salt to things. Um and a diuretic of choice would be spironolactone um which is more effective uh for ascites alongside furosemide if necessary. Um But you start spironolactone first improving nutrition. So, um as mentioned as an examination, finding you'd expect to see sarcopenia. So, muscle wasting, the liver's really hungry organ and when it's going wrong, your calorie consumption is so much higher. Patients really struggle getting the calories in um on a daily basis. So, um providing them with uh supplementation. Um specialist dietitian input is really important. They also go into a ketotic state very quickly and that's all to do with the, the um lack of ability to do gluconeogenesis. So, overnight, starving for six hours or eight hours overnight is like a person with a healthy liver starving for 24 hours and they go into a ketotic state. Um uh and then the uh that causes an muscle breakdown. So to avoid that, you tell patients to have a snack right before they go to bed, um high high carb snack, 10 g of carbs that will last them through the night. Um And then they eat first thing in the morning and that avo uh avoids that muscle breakdown because patients who are um, scope are much more likely um to decompensate and have worse outcomes. And then also you're looking for kind of acute on chronic liver failure. Um So a AC LF is, um, it's kind of not new, but in the past few years has, has taken a lot of um uh a lot of speed wi within the Hepatology world is this new phenomenon. So, um this may be this an extra insult or another insult to the liver that is already fragile because you've got chronic liver, liver disease and then that can red uh result in uh liver failure. Um So that might be um a new virus, ongoing um alcohol consumption um or uh drug induced liver injury, causing an acute on chronic liver failure. And it basically means a rapid deterioration in liver function on the background of, of having chronic liver disease. So you're monitoring for changes in LFTs um has their bilirubin shot up, has their uh A T shot up. And then it's always important to think. Um does this person need a liver transplant and or supportive and palliative care? Because a as mentioned, the mortality rates are really, really poor in liver disease. Um So you need to be having that conversation if, if they can go for liver transplant or supportive and, and palliative care. Ok. So to finish up, we've got a couple more spot diagnoses for you. So let me see if I can play this. Can anyone identify what's going on here? This is in a patient with constipation stolen from Twitter today? Ok. Fantastic. Someone said it increased ammonia and someone else said a asterixis. So asterixis is this, you get the patient to put their arms out, straight, cock their wrist back and they do a, it's a proper flap as opposed to CO2 retention where they've got a fine tremor and then do this. It is a proper distinctive flap within uh when someone has hepatic encephalopathy. Um this patient um has increased ammonia. Um and so this, they would flap so aggressively if you turn their hands over. Um and the reason constipation, so ammonia is a breakdown product from bacteria in your gut. Uh normally filtered out by the liver. When the liver's not working, you get increased ammonia um in the blood stream. The way you deal with this is by ensuring someone opens their bowels 2 to 3 times a day, soft stools. Uh and you would give um a laxative such as laxido being preferential, which is an osmotic, uh laxative brings fluid into the lumen um and uh to soften the stool. Um It is important to avoid constipation because if you, if you're constipated, you're not pooing out the ammonia you're allowing for greater uptake into your bloodstream. Um So that's why we always want um our patients to be putting regularly. Ok. This is a bit of a different one. Ok. That one spot diagnosis you may come. I don't know how, how mean Imperial spot diagnoses. Are anyone? Fantastic. This is an A V fistula. And now you're thinking this woman has been chatting on about liver disease for the past half an hour. Why on earth is she now showing me an A V fistula? Can anyone make the link between a, a patient who is cirrhotic and then having an A V fistula? So this was also shamelessly taken off Ned Twitter this afternoon. Yeah. So this patient is on dialysis. Um So they have CK D. Uh and then if you think so someone's put her hepatic renal syndrome. So that this is what I kind of wanted someone to say. I want to say actually hepatic syndrome, you don't tend to use dialysis. You might use dialysis in the short term, but the outcomes are quite poor. So you'd use ter in your, in your main management and albumin um in treating someone with hepatic renal syndrome. However, this person's got CK D which can't be caused by hepatic renal, it's HEPA syndrome. Um syndrome is an A K I equivalent. So in CKD, um that's when you go on to dialysis causes of CKD, common one type two diabetes and type two diabetes. Is associated with Mazz. So this patient likely has um cirrhotic um Mazz uh metabolic associated death of the liver. Um They've also got uh CKD um and requiring dialysis. A patient like this would be a really good uh patient to have a double um liver kidney transplant, which has been, has been done. I've seen it. Um So yeah, it's quite cool. So to summarize uh when you are standing outside the, the very few takeovers, I'd like you to take from this session when you're doing your session. When you're doing your exam, stand outside of the the booth, read what is in front of you really, really care carefully. The number of people I know that went into the exam having read it and misunderstood and did completely the wrong examination, do what they're asking. Um, if they say please do an abdominal examination, do an abdominal examination, don't go and listen to their chest because that's not what they want to see you doing. They want you to just see doing a boring abdominal examination, think of differentials before you go in. I find that really helps. It might not help with you because it allows you to think about what I should be looking for and then investigations, I like breaking it down to bedside blood imagings and other and that helps you structure from easy stuff. You can get done first to more, more niche things as you go along. Um, practice is summarizing. So um met quite a lot of Imperial students recently and I think a lot of you get quite stressed about summarizing normal findings. A lot of patients that you'll see in um in cases have no signs. So practice summarizing a normal patient as well as ones that have signs. Um and, and identifying those important negatives that you're not seeing. I hope that was useful. I'm sorry, I've ran over by 10 minutes, but I would appreciate if you could fill in this feedback form. Thank you. That was so good. That was really, really helpful. Uh Yeah. Can everyone please fill out the feedback to make sure we can um then release the video. Um So you guys can watch in the in the future.