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OK. Thanks for letting us know guys. Uh I think it's because we forgot to press start broadcasting. Can you guys? Um So if you maybe just try and reupload the slides now, Elaine and then we can see if they can see you again. Can you see now? Ok, sorry about this guys. OK. So maybe let's go back to the question, although you can see the answer. Ok, let's just talk through it and the next one will be better. So, um from the, I'll, I'll break down the relevant parts of the question. So this is a young man, um who's presenting with abdominal pain and diarrhea. I have a two day history and watery stools. So watery stools when you see this in a question, usually you can start start thinking about diarrhea caused by amoeba and then bloody diarrhea. Um whenever there's blood in the stool, that means that the colon is involved usually. So this is a colitis and, and actually when there's bloody diarrhea, um that's usually that's usually caused by um entamoeba, histolytica or shigella. Um When there's blood in the stool, we call it bloody diarrhea, we call it dysentery. Um and then there's a travel history which, which kind of points us further towards an infectious cause of diarrhea rather than, um for example, an inflammatory cause. Um And there's risk factors that about contracting amoebiasis, which are um eating food and swimming in um contaminated waters. Um When you s when you see this man, he's pale and clammy and his BP has dropped to 9090 99/64 and he's a bit tachycardic. Um This can be caused by dysentery, um especially there's significant blood loss in the stool. Um And again, there's a temperature which points us further towards an infectious cause rather than an inflammatory cause. Um So over the next slide, um we'll talk about different causes of diarrhea. Hopefully you can read that, but I'll send the slides out anyway. So when you have a question about diarrhea, you wanna think about whether it might be an infectious cause of diarrhea. So, in the previous question, we had a typical example of an infectious diarrhea, which was from a travel history positive. Maybe a young patient with a fever who's had risk factors such as eating contaminated food. Maybe you'll hear in the question or in the case that um they, they also have contacts who have the same symptoms. Um An infectious diarrhea could be bacterial or it can be viral like no norovirus and rotavirus or it can be anemic amoebic. And then I have another slide coming up about how to identify which one of these, it might be, um, alternative causes of diarrhea might be inflammatory such as IBD inflammatory bowel disease. That can be Crohn's or ulcerative colitis. Um, again, tends to, you can find them in questions as a young patients with, um, new or worsening diarrhea in, you're more likely to see blood in the stool. Um, they can come in with a temperature and similar clinically. So hypotensive to the previous example, but there probably wouldn't be a travel history. Although sometimes it's difficult to, to actually distinguish between inflammatory and infectious causes, autoimmune causes of diarrhea would be something like celiac disease. Um, malabsorptive causes will be pancreatitis where the, um, digestive enzymes are not produced effectively. So, you get something called tiaa, um, stools are difficult to flush and foul smelling typically in exam questions and then you can get malabsorption, diarrhea caused by bowel resection where the absorptive, um, part of the bowel no longer. Um, well, has been resected. So there's a large amount of watery stool. Um, it depends what exactly what, what part of this co, the bowel has been resected as to the symptoms. Exactly. But, um, mm, post surgery you can get diarrhea. That's common. Um, a malignant diarrhea. So, if you have a new malignancy that can cause a change in bowel habit and then functional. So, people who actually have something like inflammatory bowel, uh, sorry, um, not inflammatory, um, irritable bowel syndrome, they may describe their symptoms as diarrhea, but in, instead of actually it being, um, large amounts of loose stool pa being passed frequently, they may be passing a small amount of stool frequently or they might be. On the other hand, more constipated. Um, and when these symptoms don't have an organic cause that we can identify, we cause them, we call them functional. Um, that's quite common in GB and in gastroenterology clinics. Um When you have a patient with diarrhea, how would you investigate them? So, as per any unwell patient, you'd use an at E approach. You do observations, you tend off bloods and you'd um correct any um abnormalities in the at E assessment. So for example, if they were hypotensive, you'd uh give them a bonus of fluids, um et cetera. And then if they have a travel history or an acute onset, you would send their stool for culture and microscopy, you'd be looking there for um you, you can look for ova parasites, you can do ac diff um culture from the stool, you can do a PCR for viruses. Um all sorts of things you can look for in a stool. Um And then, whereas if it's a chronic history, so you're not thinking about an infection just cause but more maybe an inflammatory and autoimmune cause. You can do a fecal calprotectin which would be positive in inflammatory bowel disease. You could do a serology for celiac disease. So you're looking for antibodies in the blood. I've got some more information about that. You could do thyroid function tests. Patients with hypothyroidism can have diarrhea, whereas hypothyroidism can cause um constipation. Um you can look, you can measure the levels of B12 and folate to look for malabsorption. Um The diagnostic investigation for uh inflammatory and um autoimmune bowel diseases are colonoscopy. So on colonoscopy, you can see exactly what pathology is going on in the bowel and you can take histology samples as required. You do imaging um an X ray or MRI or a CT. It really depends on the presentation and not all patients will require imaging. But um i it really depends on the presentation. But for example, in patients who present with an a flare of inflammatory bowel disease, you would probably do um abdominal x-ray to exclude toxic mydon. For example, if you have a patient with known um you realize that they have ameba hea, you don't need to do an x-ray in that case. So this is my slide that I mentioned with um comparing the different causes of infectious diarrhea, bacterial, viral and amoebic. Just in the interest of time. There's a lot of information there. So I'll let you look at that in your spare time in your free time, but um just like very um characteristic or important differences to pick up. So the most common cause of infectious area is norovirus. Um and it has, it has an incubation period of about half a day to two days. The uh whereas the incubation period for a me buzz is much longer. It's weeks and depending on the bacteria can also be a very acute onset with, for example, staph forus or blo, which is the one that's usually found in undercooked rice. Today's depending, for example, shigella, cholera, exac et cetera. Um So really if this comes up, you kind of need to do pattern recognition to, to determine which is the most likely pathogen involved. But, um, these are just some general pointers as to how to distinguish between different causes of infectious diarrhea. Ok. This is the second question. Oh, no, no, no, no. Sorry. I'm sure you didn't see that. So I'll give you a minute to answer this one as well. So a 23 year old woman with a history of intermittent diarrhea, abdominal bloating, tiredness and gradual weight loss present to her GP. There's no blood in her diarrhea or Melina, her GP arranged some investigations for her which have come back as below. So we've got a hemoglobin, a TSH, an IG a TGA fecal carrot protectant and a stool antigen for her to go back to pylori. Um, and this is one of the questions where when I, if I was in an exam, I'd be like, yes, I know what it is. And then it's a second stage question which is given the most likely diagnosis, what would be the most likely finding on histology? So, would it be a presence of goniomma? Would it be a crypt abscesses? Would it be a bit less atrophy and crypt opia pseudopolyps or ulcers? Yeah. Ok. I think most of you have answered now. So we move on to the answer. But actually, first let's go through these, um, findings in, in her blood tests or her investigations in general. So she's, uh, her hemoglobin is 100. So it's not too bad, but she's anemic, her TSH is normal, which points us away from, for example, um the hypo or hyperthyroid picture her IG at DG are positive. So, um that means that um she has antibodies to tissue transglutaminase. This is a very indicative of celiac disease, fecal carrot protectant is normal and he go back to, to androgen. So that's just ruling out other potential causes. Um And given the most likely diagnosis, ie celiac, the most common um finding on histology would be vous atrophy and hyperplasia as I mentioned by um the majority of you. So welcome. Um This is, this is what we've already said. Um So CD usually is an T cell mediated autoimmune disease of the small bowel. Uh The risk factors include um family history and these HLA types D QD Q two and DQ eight. And there may be a history of other autoimmune diseases such as thyroid disease, hepatitis type one, diabetes, um presents as it did with this patient with fatigue, weight loss change in bowel habit, in Children, they can um have f faltering growth as well. Um You diagnose it with um initially you do a um tissue contaminated antibodies and also total IGA because in some patients, if you don't measure the IGA, you may get a false negative result because they might have low levels of IGA. Um they have IGA deficiency. So you have to compare the level of tissue tissue transaminase antibodies to their baseline level of IGA otherwise you don't get an accurate result. Um So you have to do those paired um pair tests. But the standard diagnostic test is a biopsy of the duodenum where you'd find villous, atrophy and crypto hypoplasia and also some increase intraepithelial lymphocytes. So, what you see here is this is a simplified overseas schematic version, but instead of having these lovely Big Villa, they're atrophied. Um whereas the crypts uh there's hyperplasia of the grips. Um so it all looks flattened out and um the absorption absorptive function of the bowel will be affected. Obviously, um if that is easy enough to manage, you have to have a gluten free diet. Obviously, patients have to stick to it, which isn't necessarily straightforward um complications of ce disease, which would be um osteoporosis, anemia, peripheral neuropathy. Um and they have a functional hyposplenism. So they should receive the pneumococcal vaccine as they're at increase risk of infection. I've just got a side here quickly on I VDI think this is quite well taught at most unis. So I won't go into it too much. But I like to make tables as you've seen to compare um key features of different conditions. Um You see your ulcerative colitis affects the codon only and it can cause colitis and in um colitis, as we've said, you can get blood in the stool. So it's more likely to present with pr bleeding. Whereas Crohn's is less likely to present with pr bleeding, but it's a mouth to anus distribution. So it can present with mouth ulcers. Um, and, um, they can get ulcers in the anus which can be very painful. Um, and Crohn's, I always think is a, is a little bit worse. Um, obviously c is also not, uh, it's, it's an awful condition to have, but I always think Crohn's is a little bit worse because you can get fistulas and strictures. You're more likely to need surgery. And if you do have surgery, it's, it's more difficult surgery because it's a more distributed, um, area, um, as opposed to, and you see where the colon only is affected. So you can just do a panproctocolectomy or just a colectomy to remove the affected colon and the rest of the bowel will be absolutely fine. Um, ok. So this is next, next question is about the next topic. So just to summarize just diarrhea, um, we have a lot of patients who come in on the general surgery, um, with pr bleeding change in bowel habit. Um, most patients who come in under surgeons tend to get act pretty early on and there's a nonspecific finding of, uh, bowel, uh, wall thickening. So it can be be colitis or it can be small bowel, uh, wall thickening or a sigmoid bowel colon, uh sigmoid, um, colon thickening. Um, and then at, and that, at that point is when you have, OK, your undifferentiated diarrhea, colitis picture, what is it gonna be? Is it an infectious cause? Is it an inflammatory cause? And ultimately, you do a lot of investigations while they're an inpatient, but the diagnostic investigation that would be a colonoscopy. Um And with celiac disease, you don't usually see patients who come into hospital with that because, um, i it's more of a chronic kind of growing um, disease. Um But you might see that more commonly in GPS or in pediatric, in pediatrics with Children. Ok. So the next topic is about um, this page. Um, so uh, difficulty or pain in swallowing. So, in this question, we have a 41 year old male presenting to his GP with an eight month history of difficulty swallowing both fluids and solids. He also describes um, the regurgitation of undigested food, particularly when lying flat and he has some occasional chest pain centrally. He has lost 3 kg of weight over this period. Um His past medical history includes um uh hypertension and he takes amLODIPine. So again, this is one of those two-step questions. So, if you know the, if you know the diagnosis, that's great. But what is the most appropriate next step? Would you do a full blood count for this man? Would you refer him for an upper g endoscopy within four weeks or within two weeks? Or would you do for a barium swallow or would you do a CT test? So I'll give you a few more seconds to get some more answers. Sure. Ok. Um Most of you have got that. Absolutely right. So if we break down this question, um this patient has difficulty swallowing both fluids and solids. So this is quite a typical symptom of achy lesion and he also has regurgitation or lying flat. However, so, yeah, this is a key symptoms of achalasia. Um whereas esophageal cancer, for example, would cause a dysphagia but it would cause dysphagia that's progressive. So because of an obstruction to the lumen that gets bigger over time, it can either be from the outside or from the inside, um You initially start struggling to uh swallow solids and then over time you progress to not being able to swallow liquids either. Um So because you can't exclude esophageal cancer clinically, in this way, this would this this man would be that um sorry would be referred via a two week wait pathway for an oag endoscopy. So he gets an endoscopy to rule out malignancy. And then once you've ruled out the most serious cause you'd investigate for, um, something like Achalasia, which is less serious. So, we've got causes of dysphagia, inflammatory causes. So, if you look, um, all the way from the mouth down to the esophagus, you can get obviously tonsillitis and pharyngitis can cause painful swallowing. Um, esophagitis can be caused by loads of different things including GERD candida, different medications. Um, and that can cause painful, swallowing and also ulcers. Um mechanical causes of dysphasia would be something like a foreign body. Obviously, that's um in disrupting the lumen of the bowel. Um If you've got a stricture, um such as a malignant or benign stricture that would cause obstruction, obviously. Um And then you can get compression from the outside extraluminal, um such as uh lung cancer. A rolling hi is hernia, enlarged lymph nodes, et cetera. And then achalasia fits under the motility disorder causes of dysplasia. So, locally, there is an issue with um with the um passage of food from the esophagus into the stomach, um uh caused by achalasia. And whereas with um systemic mentality disorders such as myasthenia or motor neurone diseases, they can also cause dysphagia, but they would also cause other neuro uh neurological symptoms in other parts of the body. So, what is achalasia? So it's an inability of the lower esophageal sphincter to relax. Um and it also has reduced esophageal peristalsis. Um It's a nervous system issue. Um it characteristically presents with liquids and solids, um, not being able to be swallowed at the same time and it can also cause regurgitation and weight loss. Um, chronic ankylo increases the risk of a patient developing, um, squamous cell carcinoma. You know, in terms of investigations, um, if a patient, anyone presenting with dysphagia, you would, um, send by a two-week wait pathway for endoscopy. Um, then you would do a barium swallow which would show a dilated bird's beak esophagus. So instead of the esophagus being nice and um uh kind of um even throughout its course, it dilates at the bottom. Um because the sphincter is not relaxed. So the the passenger food from the lower esophagus to the stomach is impaired. And then this would be um the diagno the diagnostic um investigations manometry where you measure the pressure in the lower esophagus and in the stomach. And there's an a higher pressure gradient from the esophagus to the stomach due to this impaired um relaxation of the lower esophageal sphincter. So in terms of management, you can always think about medical and surgical management. So medical management would be calcium channel blockers or nitrates. Um whereas surgical management would be something like Heller's cardiomyotomy. Ok. Another question, I think this might be one of the last questions in my gastro section and then we can have a little bit um, 52 year old male presents to GP complaining of retrosternal pain that has been going on for around a year but has been getting worse lately. He says it's usually better after meals and he's been drinking plenty of Gaviscon, which has stopped helping. Now, he hasn't had any weight loss and he doesn't have any dysphagia. His past medical history is only notable for back pain for which he takes Ibuprofen on examination. He looks pale but he is otherwise stable. So, um, from that history, can you identify which symptoms are red flag symptoms? Oh, thanks. Thank you for that. I'm just selecting random ones to muddy the waters. I think you all answered that pretty quickly. So we'll move on. Um, the majority of you have got the absolutely the correct answer. So, it's the pale appearance. Um, that's a red flag symptom. And the reason for that is that pale appearance is um, a month. Uh a symptom of anemia and anemia is one of the alarm symptoms which, um, when you have new Dyspepsia in over 55 years old or when you have any of these alarm symptoms. And then you need to um refer patient with dyspepsia for endoscopy again. So, dyspepsia um is a general term, um which can be some, which can uh describe sensations of, for example, indigestion, um uh abdominal pain after eating, it can be quite nonspecific. But if you have some of these sym any of these symptoms, it's like anemia, weight loss, anorexia, plus or minus abdominal pain. Um, a recent onset of symptoms. So in the question, I asked you whether the one year course of symptoms was concerning, but actually, if it's more of a recent onset, it's more concerning. And obviously, if someone's presenting with Melena or hematemesis, that is concerning Melina, um being uh passage of blood in the stool and hematomas, being passage of blood in vomitus. Just so everyone's on the same page. Uh if those are present, that's suggestive of an upper gi bleed. So, obviously, that's a very concerning symptoms. Um, causes of dyspepsia are various. You can get functional dyspepsia, which is common where you have patients coming and complaining of this dyspepsia symptom. But, um, they might be really, really, um, troubled by it and they might go to see the GP many times about it. But actually, when you go to do an endoscopy, it's completely normal. Um, gastritis or esophagitis, um, can be caused by H pylori commonly or alcohol use. Um, gas. Oh, sorry. Um, gasses age reflux disease, um, can be worsened by hiatus hernia and it can be caused by a lax esophageal sphincter ulcers in the stomach or the duodenum can cause dyspepsia, malignancies, achalasia and medications. So, the causes are various and varying. Um, when a patient presenting with Dyspepsia, you usually look at their medication list. For example, in this case, this, this gentleman takes ibuprofen. So if he's taking something that can obviously be a cause of dyspepsia like an NSAID then you would, um, as address whether the patient still needs to be on it, whether they can be switched to anything else or whether they need to put on a protein pump inhibitor to decrease your risk of, um, an ulcer, a peptic ulcer. Um, and so you look at their medications and then you check for these alarm symptoms and refer as appropriate. So this is a, just a slide on peptic ulcer disease, which is very common. Um So you can get ulcers in the duodenum or in the stomach and they can have different causes and different presentations. A duodenal ulcer is generally caused by h pylori and it tends to present uh before meals or so, like the pain is worse when someone is hungry. Um Whereas uh when they eat, it gets better. So this is what was happening in our patient where um this guy, um he says it is usually better after meals. That's classic of the duodenal ulcer. Um, whereas a gastric ulcer is, tends to be worse on eating and I always struggle to remember which way around those go. But um, maybe you can think that um uh that when you eat the uh stomach fills up first, so the gastric ulcer would hurt more. That's how I remember it. Um So once you, um once you treat people for peptic ulcer disease, um you for, with um hp eradicate eradication therapy if they're positive or high dose, PPI um, then you need to do a surveillance O GD to ensure that the it's resolved, um, complications of peptic ulcer disease. Um, include upper gi bleeding, iron deficiency anemia and perforation. Ok. Final gastro question. Um, it's a 45 year old man who presents to the emergency department after vomiting blood that looks like coffee grounds, he appears pale and sweaty and is still vomiting profusely blood into a bulb. Um, he has a history of alcoholic liver disease. Um These are his observations um which of these symptoms from the Glasgow from the history? Sorry would score a point on the Glasgow batch for bleeding scale. Um Is it the coffee ground vomiting? Is it the history of liver disease? Is it the systolic BP of 100 and five or is it the heart rate of 95? Um I'll give you a few minutes on that one. They're always difficult when they ask you to remember exact um figures for these um scoring systems. I always find that difficult. Yeah. Ok, let's move on. So the answer to this one is a history of uh liver disease. So this is a Glasgow Ratchford bleeding score. It's a very useful system uh to decide which patients can be discharged. So, um we had an interesting teaching session recently by gastroenterology. You can start to know about this. So Glasgow Ratchford is a is not a very specific score because um it you can get points from it. If you have lots of different um presentations, for example, you get a point just from having a, a heart rate over 100. Um you can get that heart rate over 100 for a multitude of reasons. So it's not specific, but it's very sensitive in that. Um it will pick up patients who are even a little bit concerning for um uh for worsening and for complications. So if a patient is scoring zero, then they can probably be safe discharge because it means that they're not tachycardic, their BP is holding and their hemoglobin is fine. Um And they don't have any history that predisposes them to complication of um uh upper jaw bleeds. So it's again, it's just, it's a um a very sensitive but not very specific tool. So I like this diagram because it can show, it shows all the different causes of gi bleeding, actually not just upper but also lower. So, um you know, I'm sure, you know, all of these already, but um common causes of upper gi bleeding is are bleeding, viruses, esophageal viruses usually caused uh by which are present in patients with cirrhosis, liver cirrhosis. Um You can get gastritis, which um can be hemorrhagic, you can get manner tear in patients who've been vomiting profusely. And then they, they, the classic history with that would be if someone's been vomiting, for example, after a binge drink, um they start vomiting, the vomiting is initially normal, maybe be watery. And then after a few vomits, they start also seeing blood in the vomit. So that's quite a classic history of mono vice tear because they vomited so much they've torn part of their esophagus. Um, then ulcers in the stomach or in the venom can bleed and then moving down, um, into the small bowel, you can get bleeding from ischemic bowel disease, um, which can be usually in patients with peripheral vascular disease or a history of stroke history of um mis um uh acute Coronary symptom syndrome, et cetera. You can get it from intususception or meckel diverticulum and then moving on to the uh large bowel, you can bleed from uh cancers in the colon, um and then more from inflammatory bowel disease such as UC. Um and then distally from things like an anal ship fissure, very, very pa painful condition and hemorrhoids can cause, um, usually you get bleeding when you wipe with your um, tissue paper rather than bleeding, mixing with a stool. So in terms of management of people with upper ja bleeds, you'd start off with an at E assessment. Um And then you address all the abnormalities that you identify in your at E assessment. Um, you would do apr exam as was done in this case to see if there is truly blood mixed in the stool or maybe um there is blood um um just in the anus itself from a fissure or in, maybe you'll be able to see hemorrhoids on your examination. Um Then you do blood tests, obviously, you do things like a group unsafe, which um identify the patient's blood group. So, if they ever need a transfusion, you can do that um, clotting to see if they have the range clotting. Um When you are, if you were worried about, for example, a perforated peptic ulcer, you could do a chest X ray where you can see uh under the diaphragm, which suggested there's a perforated lumen of the bowel. Um It's a very, very bad time. Um You can transfuse them if they're hemodynamically unstable. Um You usually people give PPIs um and then there's specific management for um, variceal bleed where you give um broad spectrum antibiotics and terlipressin. Um So from the recent teaching, um we've had about upper G bleeds. Usually most of them actually resolve without the need for any management. Um And then they can get an O GD as an outpatient and um which is better tolerated and it can see um pathology better if it's not active bleeding. Obviously, if they're unstable, then you do need to take them for an O GD sooner. Um But in general, most are need to preserve by themselves with no intervention. Ok. So that was the first part of the talk which was on gastroenterology. So I'll give you um two minutes break. That's not very long break, maybe three minutes. Um So we restart at quarter to two and in the meantime, if you can fill in that feedback form, that would be really, really helpful. Um And there's also another chance to give feedback uh at the end of the talk. So I'll just give you, um, three minutes. We restart at 745. Ok. Let's start again. Hopefully most we will be back. Um, um, I have a question in the chat. Can someone remind me what toxic Meuron is pathology for? It's um usually a complication of inflammatory bowel disease, including ulcerative colitis. So, not an embarrassing question at all. Um So it's something that you want to exclude when you see a patient who presents with um inflammatory bowel disease. So, right, moving on to hepatology, very difficult to summarize this, but we've just gone for um key high yield aspects of the topic. So, uh how does liver disease present? Um It can have symptoms such as fatigue, jaundice, bruising or bleeding confusion. Um in terms of signs or what you'd see in the patient, you'd see some ascites. Um So swoll intense abdomen, you could see cap what medusa, which is what's shown this picture on your bottom, right of your side, um dilated veins in the abdomen, secondary to portal hypertension, you might see rectal hemorrhoids, um which is so the rectum and the esophagus are sites of viruses from um which from which are caused by portal hypertension. Um And then you can get signs of hyperestrogenism um such as um these spider Nevi which are um in your top left part of your side. Um Gynecomastia, pulmonary fema, et cetera. And then on an examination, you may also find hepato IV which is an or liver, I'm sure you know. Ok, next question. A 44 year old woman is admitted to the emergency department with reduced G CS. An ambulance was called by a family member as she had not been contactable for a couple of days. We don't know much about her past medical history at present on examination. She has a G CS of eight. Her flare are noted to be jaundiced. Her abdomen is sorry, uh slightly descended and there is withdrawal from pain when palpated in the right upper quadrant and she has blood tests taken which show um the results on the right. So now we have to look at these results and then consider what is the most common cause for the suspected diagnosis. So we're looking at the blood test, um seeing what we um what we think might be going on and then what's the most common cause? So I'll give you a minute or so. Ok. Um Not have many responses for this one. Maybe you're getting a bit tired, but um let's move on anyway. Um, the most common. Ok. So what um do these findings show? Well, um we've got a raised a LT adenine transferase, um A raised ast and a raised bilirubin. Um So what we're looking here at a hepatitis picture and the most common co and this is um a, a patient who's acutely unwell. So it's an acute hepatitis picture. And the most common cause for acute hepatitis is a, a paracetamol overdose. So that's the most common cause. Um And when you think about liver failure, you can uh break it down into acute liver failure, which itself is breaking down into different uh types depending on how long the onset of symptoms is. So, hyperacute, being less than seven days, acute, being 1 to 4 weeks, um and have acute, being up to 12 weeks and then there's also chronic liver failure, um which is kind of caused can be caused by different um pathologies. Um with acute liver failure, there are some investigations you can do for the most common causes. And then here the slide also summarizes the appropriate treatment. So for a paracetamol overdose, you would do a paracetamol level. And then as I'm sure, you know, if the level of paracetamol is above the treatment line, then you would give treatment with NAC. Um if you have something like acute fatty liver of pregnancy or any of the hepatitis caused by pregnancy, the treatment for that is delivery of the fetus, viral hepatitis um is picked up on hepatitis screen. So I'm sure, you know, there's a lot, this comes up in exams a lot. But the um all the different antigens involved in hepatitis B. So the surface antigens, the core antigens, et cetera. And then similarly for the other um hepatitis viruses and um you can treat them with anti uh virals. Wilson's disease is um caused by a buildup of copper in the liver and also in other organs. And you can um uh diagnose that by doing um measuring serum copper, serum cytoplasm, which is a protein that transports copper and a urinary copper as well. And that can be treated with copper chyl or he filtration or plasmapheresis. Um But carry syndrome is when there's a clot in the portal vein um which uh can be diagnosed with an abdominal ultrasound. Um and with a Doppler which shows the um uh blood flow. Um and you can give anticoagulation to treat that and you can do a tips procedure as well. Um autoimmune hepatitis, you can do an autoimmune screen where you look for the antibodies associated with autoimmune hepatitis, usually treated with steroids. And finally, this is also hepatitis B is a type of viral hepatitis. So similarly, there is antivirals to treat that. This is a very quick summary because it's a huge topic, but you can look into all of these different causes of acute liver failure in more detail and identify exactly what you'd, how you'd investigate them and how you manage them. There's a specific slide here on autoimmune hepatitis because it does come up in the exams and it's very difficult to remember. Um So there's three different types of autoimmune hepatitis. They're associated with different types of antibodies. Um and they tend to present in different subtypes of patient populations. Um So when you are suspecting autoimmune hepatitis, you would send off all these different antibodies. Um how to differentiate from? Sorry, I just saw a question in the side. Um So you, you wouldn't be able to differentiate. Um It's a good question, paracetamol uh overdose to from, from drug toxicity. Um just from the presentation alone, especially in this patient who is um confused. Um and she's with, she's not been contactable. She won't be able to give you a history, she won't be able to tell you what they've uh what she's been taking. But um the question was just about what's the most common cause for the suspected diagnosis and the most common cause for acute hepatitis is um paracetamol overdose. But you're right, it's difficult to distinguish in the history. Absolutely. Um So I'll in the interest of time, I'll leave you to look at the different causes of autoimmune hepatitis in your own time also because it's one of those things that unfortunately me telling you probably won't help. You remember, you have to kind of um read through it, make notes or flashcards or however you revise. Um and then these are different causes of hepatitis. So you alcoholic and nonalcoholic hepatitis. So alcoholic is um so, ok, so this is how I remember it. Um You can measure the AST and the A LT, they'll both be raised in alcoholic and nonalcoholic hepatitis. However, if the AST is higher than the A LT or the ratio of them is mo more than two and the alcoholic liver disease is more likely. And how do you remember that? Well, spirits, which is Ast. So the s sounds spirits is stronger than Lager. So the AST will be higher than the A LT in alcoholic liver disease. That's how I remember anyway. Um Whereas if the ratio is less than one ie there, um the at is higher than the ast, then it is more suggestive of nonalcoholic fatty liver disease, non alco uh nonalcoholic is liver disease is usually caused by fatty liver. So high triglycerides, obesity, these are all the risk factors associated. Um There's all sorts of different um risk factors associated with a viral hepatitis. So A&E are the ones in transmitted by PCA oral root. Whereas um B and C are the ones that are more likely to cause chronic liver disease. Um It's really good to know about the serology of Hepatitis B and how to identify acute um or chronic infection with Hepatitis B that comes up in exams. Um And also you can identify from the serology whether a patient has had a vaccine to Hepatitis B rather than has a previous infection. Um And then there are specific different treatments um for different causes of hepatitis, of course. Um And I'll, I'll leave you to read that in your own time as well. Ok. Another question. Um, a 58 year old woman is seen in Hepatology clinic. She's been referred by her GP with the range liver function tests. She feels completely well in herself and is asymptomatic. Her past medical history includes hypertension hyperlipidemia and type two diabetes. She has a full liver screen which is unremarkable. She denies alcohol intake. Her BM I is 33 and she's referred for an ultrasound of her liver. Um, so we want to know what is the most likely finding on her ultrasound scan? Is it um, normal ultrasound? Is it a thickened gallbladder wall? Is it uh reduced liver eco texture compared to kidneys diffuse hyperechoic Ecco texture or common bowel obstruction? And um, I've been a bit unfair in this case, I haven't given you the normal ranges for the at AST and ALP. Um, um, and I also don't remember them off the top of my head, but let me just, um, just to, to, to, um, help you out, let's just say that the A LT is more raised than the AST and the A LP is raised as well and the bilirubin is raised as well. Obviously, the H ba one T is above normal range as well. Mhm. Ok. Mm. Ok. Well done. The majority of you have got that. Absolutely right. So the correct answer. Is d uh diffuse hyperechoic echotexture. So this is an explanation as to why that's the correct answer. So in the question, we've got a few uh points that um point us towards the diagnosis. So this is a lady with um high BM I hyperlipidemia um type two diabetes who doesn't drink alcohol. So we think that the most likely diagnosis is um a nonalcoholic fatty liver disease and the characteristic finding in this pathology is the, the diffuse hyperechoic eco texture. Um There is there is a bright liver because there's fatty infiltration in it, a thickened gallbladder wall would be more typical in cholecystitis, which is not the kind of pathology that is described in this um SBA um a reduced liver eco texture um is so it will be the opposite. So you see an increased eco in the liver. So that's also caused a hyperechoic cu texture. Um And then the common bile duct obstruction would be um uh would be a cause of higher um more deranged ap and also a very different presentation. So this is a side on common causes of c well, not necessarily common but it uh causes of liver failure or cirrhosis, which you have to know about. Um we've mentioned most of these before. Um you have to know sort of the associated um factors that you need to know about for your exam. So for example, that um alcohol, alcoholic liver disease um is also associated with uh excess alcohol intake and it can cause cirrhosis. Um, but also that you can get um, cirrhosis caused by primary biliary cirrhosis and autoimmune conditions, which is associated with IBD. Um, and also PSC is another um associated with IBD likely autoimmune disorder. Um, you can get drug induced liver failure, um by medications such as methotrexate isoniazid methyl dood and you can get Wilson's disease. Um, and hemochromatosis, which are the build up of hemochromatosis is um the buildup of iron in the liver. And Wilson's is the buildup of um copper. So there, so there's just so many different causes, but it's all good to know about and learn about. So I'll leave the slide for you to look at in your um at your leisure and let's just move on to the last SBA of the dog. Um So you've got a 54 year old man in this case who attends a GP with his wife feeling generally unwell. He has a history of nonalcoholic fatty liver for which he has been lost to follow up from the Hepato Hepatology Clinic. He describes malaise for several months and a feeling of weakness when he exerts himself on examination. He is disorientated with an abbreviated mental test score of six out of 10. Um He has excoriation marks on his arms and torso but no evidence of jaundice. He has some mild discomfort in his right upper quadrant on palpation of his abdomen and he is not too stone since his last clinic appointment. Yeah. So, um, we want to think about the symptoms of advanced liver disease in this case. Um, which ones of these are most concerning, is it weight loss, right? Upper cord and discomfort, weakness, confusion or malaise. Um, I think we might have lost our, um, um, so our room she to do our, um, pulled, so I'm just gonna quickly do one. So I'll get you guys to answer this last question as well as you can. Oh, you had already answered it. Sorry. Um I didn't see that there was already a pull up. Um So most of you had already answered it um previously well done um answering D for the majority of you, which is absolutely correct. So, confusion is in, is a sign of a complication of chronic liver disease, which is hepatic encephalopathy, which is caused by a buildup of ammonia in the blood due to um impaired um breakdown of ammonia by liver. Um So that can cause confusion and it's a very serious complication of chronic liver disease. Other complications of liver disease would be esophageal viruses which can cause an age. I bleed um ascites, which can cause spontaneous bacterial peritonitis, which is a very bad infection, difficult to treat hepatocellular carcinoma can be a complication, encephalopathy we've discussed and coagulopathy. So, the liver synthesizes many of the clotting factors. So, when you have liver disease, sometimes you can get coagulopathy impaired clotting, um, patients are more prone to bleeding. Um And that this can be um serious complication as well. Um And that brings our presentation to a close. So, thank you for listening. Um We've covered um uh the first part of the talk was on gastroenterology and we've covered different causes of diarrhea, um causes of dysphagia and how to investigate them causes of dyspepsia and upper gi bleeding. Um And in the hepatology section of the talk, we covered presentations of liver disease, causes of acute and chronic liver disease and complications of um chronic liver disease. So, thank you for listening again. Here is your feedback form as a QR code. And if you've complete it, you can get a certificate of attendance the next talk. Um by mind, the bleep will be a hematology talk on the sixth of November as far as I understand. Um And if you have any questions, um email this email final year at mind the bleep for um any um questions. Um But I can also see there's two messages in the poll in the um in the chat. Sorry. So got you. So do we do an endoscope for a patient with APIC peptic ulcer disease without any of the red flags and signs for diagnostic purposes. Basically is diagnosis of P EDA clinical diagnosis. Um So it's a, it's a good question. So what you would do is you would initially treat it conservatively. Um If you suspect peptic ulcer disease without any of the alarm symptoms, you would first treat it conservatively with a trial of PPI treatment. Let me find the appropriate slide to go back to. Yeah. So, uh initially you try a high dose of PPI treatment for 6 to 8 weeks. If that doesn't resolve the symptoms, then you would, um, you would uh, that you would send them for an endo for an endoscopy for an O GD to evaluate if there's any other causes of these symptoms. Um Specifically malignancy. Hopefully, that answered your question. Let me know if not, do we get a copy of this presentation? Um If it does resolve, do we still do a GD? No, you wouldn't cause you've treated it clinically. Um And do we get a copy of this presentation? Um I think that you um do if you've complete the feedback form but Rome has gone. So I've lost my guide. I'm sorry, I'm not too sure. Um If not, you can definitely see this, this uh presentation recorded. Um And you'll be able to see the sides from there. Dia sorry, I'm here but II just missed. What was, what was the question? I thought you were gone. Sorry. Um Someone's wondering if they get a copy of the presentation. Um So the, the this whole lectures recorded. So we'll be uploading it onto youtube as well as med all at a later date. So, yeah, you should all be able to access it on there. It might just take a few days slash a week or so to come through. Um But yeah, it should all be available afterwards. Oh, thanks Roel. Great. Ok. If there's no other questions, I'll close this there. Um And yes. Oh, thanks. Take care a minute. Go. Bye.