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Hey guys, I'll give it another few minutes just to let a few more people track a in and probably get going about five past. Yep. Sounds good. All right guys, just for those joining. Um We're gonna leave another few minutes just because there's a few more, a few more joining. Then we'll get started around five past. You all see that. Ok. Yeah. Yeah, thanks very much. Ok. So, um my name is Patty. I'm one of the, one of the F two s currently working in the Belfast trust. Um And yeah, welcome to your first session of foundation for finals. So today I'm gonna cover what I think is everything you could possibly face in your exams for gastro and also for hepatology. So I've separated them. We'll start off with the gastroentero uh gastroenterological conditions and then um in the second half, we'll move on to more liver pathology. Ok. Uh If you do have a question, honestly, just ee either unmute yourself in the uh unmute yourself or, you know, there's a chance to ask questions at the end of the gastro session and at the end of the hip session. So just feel free if you wanna ask as we go along or, or you can wait until the end. Um All right. So, so what we're gonna cover uh so reflux and the consequences of long term reflux, which includes ulcers, um bleeding from the upper tract a bit on IBDA, bit on IBS. And then also just talk about celiac and gi cancers. So, in reflux, um essentially, what happens is your lower esophageal sphincter normally forms tight uh seal to prevent reflux of contents from the stomach into the esophagus. There's various uh various mechanisms. So the diaphragm contributes to the actual muscular musculature of the esophagus itself. Um But uh over time, then if you do end up with reflux, you can um end up with what was formally squamous epithelium over time with uh metaplastic changes will become a columnar in order to withhold the acid. Um and, and, and of course, columnar more er usually lines the stomach. So therefore, if you're getting uh if you begin to develop columnar epithelium, that it itself will secrete some acid um triggers in or, or risk factors for developing reflux if you have a hiatus, hernia. Um and there's various types of hiatal hernias. So, sliding or rolling or a combination of the two. Um obviously, then that if you've got, if, if you have developed a hiatus, hernia, you've got weakness of the lower esophageal sphincter. Anything that weakens that, that uh sphincter mechanism is gonna cause reflux So, herniation um of the top part of the stomach, um excess alcohol and the use of nsaids like naproxen, um excessive caffeine intake, smoking, uh obesity, obesity, of course, putting increased pressure on the thorax. Uh and then other sort of rare conditions like zing or helicin, which is a uh condition in which you have a gastrin secreting tumor. So, if you secret too much gastro and you have uh excessive acid production, um, like I said, you get metaplastic changes as shown on the right there. So this is uh Barrett's esophagus. Um this is metaplasia which comes before dysplasia. So, uh pa patients with known Barrett's will undergo um regular surveillance endoscopies or OGD S just to make sure there's nothing suspicious um symptoms of reflux. Then I, I'm, I'm sure everybody's perhaps uh experienced it, you know, once or twice if you don't have it chronically. So you do get that burning sensation often described as being retrosternal. Um Sometimes if it's significant enough, it will cause an epigastric discomfort. Um And it's also of course, worse, lying flat, uh as you lie flat, it can just sort of it, it's, it's parallel with uh the stomach and the esophagus, it'll just leak back further. Ok. Um You can, patients with the pain will experience some bloating. You can get hoarseness of voice if, if it refluxes far enough to affect the vocal cords. Um And also obviously because it's irritating the firing patients a lot of patients will experience a dry cough. How do we manage this? Then if you focus on the triggers, we've just shown you a lot of it's lifestyle really. So stop smoking, try and reduce your caffeine intake, um cut down on alcohol, lose some weight. Um and also avoidance of certain triggers. So I mentioned caffeine other things like nsaids and other, other medications can, can contribute to it like steroids, uh and SSRI S as well. Um Management pharmacologically would be with an antacid typically over the counter. Um But a lot of patients with reflux, we will um get them started on a PPI usually settles symptoms within a week or two. and they take that long term, so usually daily. Um So PPI S being like omeprazole or lansoprazole or esomeprazole, um if we don't tolerate uh the PPI, we could try something called Famotidine, which is a histamine antagonist. Um Typically, we would avoid uh PPI S if they've got chronic hyponatremia. So PPI S can cause hyponatremia and hypomagnesemia. It can increase your risk of C diff uh and it also just gives you sort of um it doesn't have to necessarily give you c diff diarrhea, but it can cause diarrhea and that can be quite troublesome for some people. So, Famotidine is a good alternative. So it's just taken um once a day as well, uh surgery if it gets significant enough. Um Or if the Barrett's becomes concerning, we can do a fund fundoplication. Um Basically, it's where you've got the esophagus and the stomach is the fundus of the stomach is lifted up and wrapped around to uh sort of solidify and tighten that esophageal sphincter. Um uh And also in these patients um consider H pylori testing. So, uh H pylori contributing to reflux and acid production, you'll, you'll want to uh just check them for that and I'll mention a bit about H pylori shortly. It's just a good few tests that you can do. Um remember just with reflux, red flags are important. Uh I think they do come up quite a bit in examination. So, um, you know, exams might typically say you've got uh 60 year old male. No, you know, tired some difficulty swallowing, uh iron deficiency anemia. These are all sort of um things that can sort of point towards uh or sorry, uh use and exams. And typically if you find red flags, one or two red flags that would warrant um two week, wait O GD just to have a look, make sure there's nothing sinister. So, like I said, here's pylori, he go back to Pylori. It's gram negative arrow. So gram negative because it's in the gut and a um it's sorry, gram negative because the gram negative environment would be, you know, the gut would typically suit that and then an aero. So the there is a good amount of oxygen in the stomach. Um And therefore, it's probably the best or the most tolerable or tolerated place for, for this uh bacteria. So, there's several mechanisms by which it does um increase acid production and, and cause damage. Um It actually with its flagella there. As you can see in the, in the image, the flagella can propel it to, to drive and um invade into in between the gaps between the cells. Um and this widens the gaps between epithelial cells and acid can just leak into there and cause direct uh inflammation and damage. Um The, the, the bacteria itself releases ammonium hydroxide and this will neutralize your acid. And also, um you'll get a release, a direct release of toxins from the bug itself, um which will also harm the epithelial lining. Uh and, and there's various tests. So, um a lot of the time when someone gets a, if, if we're querying an ulcer in the hospital, um and they go for an O GD, they'll get what's done with close testing and that's done during the, during the um otherwise known as alcohol breath test. Uh It's done during the, the scope uh and the results come out quite quickly. Um If they are positive for H pylori, then you want to give eradication therapy. So it's um omeprazole typically and two antibiotics. If they're not panallergic, it's typically amoxicillin and Clarithromycin and you give that for a week, all, all, all three of them. Um And, and you know, a lot of the time the patient would stay on omeprazole long term. So, if uh the reflux is bad enough or it goes untreated for a long time, uh you can develop nasty ulcers. So, ulceration of the mucosa, uh typically it's in the, uh it's in the stomach. So it's a gastric ulcer or in the first part of the duodenum and duodenal ulcers are more common. Uh risk factors as we've talked about very similar to the risk factors for, for reflux. So certain triggers like smoking alcohol, um certain drugs, like we mentioned before, steroids and uh naproxen, uh stress and also increases your chance of developing an ulcer. Um and typically will, will also present quite similar to reflux symptoms. Um So you'll get dyspepsia that sort of discomfort in the tummy. Um This, this pattern here of pain can, can be assessed in exam. So typically gastric ulcers would be worsened by eating. Uh And if you, if you have an undiagnosed duodenal ulcer, the pain is sort of, you know, relieved by eating and then might come back two or three hours later. So what we wanna do is of course, scope them if we suspect an ulcer. And like we said, we do that clo test the alcohol breath test for H pylori. Some, you know, a lot of the time you'll find that ulcers might have a bit of oozing around them or they might have an abnormal or not necessarily a, uh, a nice uniform structure. So what we call suspicious looking ulcers, they would get biopsied. You would just biopsy the, the margins of them, uh, just to make sure it's not, um, rather than being an ulcer, not like a nasty, uh, stomach cancer, um, or duo or, or duodenal cancer as well. Um, bloods, then typically you want to do a full blood count to see if they've dropped their, their hemoglobin iron studies as well. If they've got an iron deficiency uh anemia, that might suggest that they're oozing a bit from that ulcer uh management. Um very much as we've discussed. So, treat H pylori, if you find it on the tests, give them omeprazole or famotidine. Um and of course, stop the offending cause just like the treatment for reflux that, you know, if you find an ulcer as well on endoscopy, typically, they'll have a followup outpatient scope in about eight weeks just to make sure that our assess for res are healing of that ulcer. If it looks like there's been a, you know, it's not necessarily healing. They may, you know, rebiopsy or consider regular scoping. If the ulcer does erode deep enough as you can see from the pictures here, it's, it can get quite messy. So you end up with an upper gi bleed multiple causes. So we've mentioned ulceration. Uh These are two good images on the side here. So we've got esophageal viruses uh typically, which develop after somebody's had portal hypertension from cirrhosis for quite a while. Uh other causes. Um for bleeding, you might have a simple what's called a mallory vice tear. So, just a uh a minor tear in the mucosa of the esophagus that might be from a recent tummy upset where you've been vomiting quite a bit. Um So just all that retching um will can actually just the, the movement of the esophagus with a forceful um moving of the esophagus can cause minor tears. And of course, if they've got like an undiagnosed um esophageal cancer, again, that can ooze. Um And if it, if it's invading deep enough, you can get quite significant bleeds from that presentation as expected. So you're gonna find blood somewhere either passed um uh upper. So in the form of hematemesis or coffee ground vomiting, if it's been altered a bit by the stomach or um or small intestine, uh and also they'll, so it'll pass out the other end. So you'll get it's quite nasty, Melina, um Melina being obviously altered uh or sorry, blood that's altered uh as it moves through the, the gi tract. So has quite a nasty smell, quite a tarry, dark sort of jet black, sticky um appearance to it. If they've lost a significant amount of blood, they're gonna obviously have a bit of vital sign instability. So that'll be probably be quite hypotensive sometimes if they, if they continue to bleed, that might not be responsive to fluids and you wanna involve your senior quite early if you're suspecting a significant bleed, how do you assess patients? Sort of doesn't really matter if it's, if you think it's a non severe or severe, you wanna do an ABCD just to make sure you're not missing anything. ABCD, obviously standing for airway, breathing, circulation, disability and exposure. Um, so I, you know, uh, you know, if it's a severe enough bleed that can lose their airway, particularly if they're bleeding from esophageal viruses. These things as you saw in that last image, these things will hose blood when they rupture. So, um occasionally if it's si significant enough and they're continuously bringing up large volume of hematemesis, you wanna get anesthetics involved early just to protect uh that airway. A lot of the times these patients are too unstable to have an uh an O GD and endoscopy and they may need tubed and taken to theater to, to pass that scope just in order to protect the airway. Um Glasgow Blatchford score is a very useful tool for endoscopist. So this is uh assesses their, their acute mortality and and um from an upper gi bleed. And therefore, uh it's used quite often to assess whether or not the patient needs an urgent inpatient scope or um if they could probably wait and have AAA sort of red flag scope done as an outpatient. So if you've sort of got a score of one or two, you might want to consider, you know, holding off. But as soon as it goes above two, typically, patients will get um will get scoped as an inpatient. It, it takes into account um your comorbidities. So, liver function, cardiac function, uh hemoglobin, systolic BP, tachycardia, just the real important parameters to assess for whether and when you're considering scoping somebody um urgently or, or le or less acutely, um your bloods in, you wanna do an upper gi bleed, you're gonna send off uh a routine set of bloods. So you're probably gonna see typically and this does get tests and exams, typically in an upper gi bleed, you're gonna see a hemoglobin drop because of course, the bleeding. So acute blood loss, but also they'll get an isolated urea rise. So you compare the urea to the creatinine, the creatinine might be totally normal, but you'll find that the urea shot up by a good few, by a good few points. So this is just because the urea as the blood cells are passed, um as they form Melina are passed down the, down the, down the gut, um the blood cells are broken down and the urea gets uh that's released from the blood cells, it's reabsorbed just along the gi tract. So it might look like they might, they have, they're dry or they have an AK. But if they've got totally normal creatinine, you need to really be suspecting um an upper gi bleed, uh, management. Understandably, if, if they're hosing plenty of blood, you're gonna probably want to activate the major hemorrhage protocol. Um, if it's not as severe, but the hemoglobin is on the lower side, you don't want to transfuse blood. Um O GD, depending on the Glasgow, Glasgow Blatchford score. Um, PPI um, a lot of, you know, studies have looked into whether or not it's, it's indicated or whether or not it should wait until after someone's been scoped. But if they have a severe enough, um if they have a severe enough bleed, you want to probably start IV proton pump inhibitor. Um And then if uh there's a couple of extra steps in the management for viruses. So, um if they are having a suspected variceal bleed, you want to add in terlipressin which will uh vasoconstrict those, it diverts blood away from the uh from those vessels. Um And also tazocin because these patients just with the, if the esophagus being in line with a lot of bacteria, they're at, at risk. If they're hosing blood from there, they're at risk of a lot of those bacteria getting into the bloodstream. So that's upper gi bleeding and reflux and um sort of peptic ulcers move on now to lower down. So, um IBD. So there's, there are quite a few um types of IBD. Um There's microscopic colitis and things, but for your exams, it's really all about Crohn's or C patients for both will typically the patient will come in with crampy or occasionally, quite severe pain. They'll be having a lot of loose stools more so. And, and you see, you typically see, and, you know, they're losing a lot of because it's in the colon, they're losing a lot of water with the di, uh, as part of the diarrhea. And typically, you know, you're more likely to see bloody mucousy stools in, in as well. Um, And a lot of patients, uh particularly for their first presentation when they don't know what they've actually gotten IVD. Um, they'll come to you and you notice quite a bit of weight loss. So whenever we compare and contrast Crohn's disease and these are the defining features and they do tend to come up with a good bit in exams. So, Crohn's affects the whole tract mouth to anus, um is limited to the colon and the rectum. Um And therefore because it's limited to the colon and rectum, it's curative by removing both of those structures called a panproctocolectomy, um You get what you can get what's called skip lesions in Crohn's. So you might have the terminal ilium affected, you might have and then there'll be an area where it's totally fine and then another area higher up or lower down, you'll have an area of disease. Uh Typically when you see it's continuous, a lot of the time you'll notice that it's gone up from the rectum. Um, and it starts to extend into sort of sigmoid descending. Um, but it doesn't typically have, are present with those skip lesions. Um, how, how far across the bowel wall it invades. Um, is also very, it varies as well. So you get what's called transmural, so whole thickness, um, inflammation, whereas you, it's typically just superficial. So it's only the mucosa that's involved. Um, there's often some now very, sometimes you will get some blood or mucus, I've said no blood or mucus. And in rare cases, you will get a bit of blood and mucus and um and very bad Crohn's disease. But, um, you know, that's more so of uh a feature of C um and I think everyone's are well aware that this whole thing was smoking. So typically, you know, there's patients with so often smoking is protective and they find that they have less flares, but smoking would typically exacerbate a Crohn's patient. And then you also get uh stricturing some narrowing of the bowel. Uh And you can get the development of fistula as well. Um Whether that be colon to bladder or colon to vagina. Um You can get the, yeah, fistulas forming or, and particularly around the, the perineal area as well. Uh So with IBD, you do, it's not just limited to the bile you get um and not just the bile, the, the whole Gi tract in terms of Crohn's, you do get what we call extra uh intestinal manifestations. So this is um a wee bit of uh in interactivity. Does anybody want to tell me what they see top left? How are you not sure or not keen on, on sharing? Has anybody seen this before or come across it in um in their revision top left? Just that calf erythema nodosum? Yeah. Spot on. So uh very much um an excellent manifestation. You get this sort of information of the, of the um of the trying to think of my uh subcutaneous uh layer. Um Very good. Yeah. And then next on from that. So sort of top middle. Has anybody seen one of these before? It's OK if you haven't. So um this is what's called a pyoderma gangrenosum. So um sort of superficial, so affecting the skin, superficial ulceration, it can get quite nasty and occasionally get infected and typically, um we do see these in, in IBD patients. Uh and then we've got 22 sets of joints le the left one being normal and on the right, we've got quite a bit of inflammation. So, and I think you're all very aware of what that would be. So we've got what we call an enteropathic arthritis or IBD induced arthritis. Um Bottom, right. Has anybody seen this before? And this is particularly associated with UC primary sclerosing cholangitis. Absolutely. Yeah. So psa your primary sclerosing cholangitis see this in about uh or about it. It's about 70% of patients who with PSA will also have, um, but yeah, it's, uh, it is a very common link and it does get tested at exams, the link between pe and we'll talk, we'll talk a little bit about ps um towards the end of the talk. And then finally, so uh eye manifestations, there's a few but you don't need to tell me exactly what this is. But, um, if anyone can, can tell me what this is. That's, that's impressive. Sometimes it's hard to distinguish from its similar looking condition. Eit close. So apparently this is scleritis. I think a scleritis, uh whilst also a manifestation of IBD, it would have le less of a bloodshot appearance, but, you know, it's always great without the specific test, it's quite hard to tell the difference. Um But yeah, so patients might experience um episcleritis scleritis or um anterior uveitis. So, when we're investigating this, we do bloods, um F BP just to check for anemia, whether that's an anemia of chronic disease or, you know, in the setting of an acute flare, they might be losing quite a bit of blood. Um C RP. And uh actually see, we do see it quite a lot, a lot of patients, although they've got really active nasty inflammatory disease that have plumb, normal CRP S and it is bizarre. I'm not really sure why. But, um, you know, they, they may have a raised C RP, but actually a lot of, a lot of time or in a lot of patients, it will be normal. Um if they've losing quite a lot of fluid, uh quite a lot of fluid loss in the form of diarrhea, they may have a prerenal AKI and then also they are typically uh they'll, they'll be hypoalbuminemic. Um This is both from the fact that it's a negative acute phase reactant. So we say there's certainly, you know, there's many acute phase reactants that there would be a positive acute phase reactant that get tested in exams like ferritin would typically go up in infections or inflammation. But we notice in, in quite active inflam inflammatory disease albumin will drop. Um And well, that's in, in, in terms of IBD, it's usually because quite a bit of it is lost from the bile. Um So yeah, uh an additional test then. So not necessarily bloods, you want to do what's called an CP or fecal calprotectin. So this is um it's a protein that's sort of uh again released from the gut and inflammation. Um It's sensitive for inflammation in the gut but not actually specific to IBD. It is, it is quite a good test to do our initial screening test when you suspect it. Um but it just note that it can also be up in other sort of inflammatory bowel conditions. So, uh gastroenteritis, if they've had a nasty tummy upset recently, and also uh colorectal cancers can put it up as well. Um With, with all these with all IBD, um, patients, even if they've had IBD for a long time or they frequent flaer. You wanna do stool cultures just so you're not missing a, a possible c difficile or um, like a Campylobacter or salmonella. The diagnosis you want to do um, a colonoscopy or, you know, if it, if it sounds more like a proctitis you want to do maybe just a, a flexible sigmoidoscopy. Um, a lot of the time you don't want to be jumping straight in with the scope. Um, somebody is having a really nasty flare, the bowel becomes very friable and quite fragile. So, if you, if you, if you do go in with a scope, you know, it's so inflamed, you're, you're at risk of perforating it. So typically you'll hold off, you would hold off on doing a colonoscopy. Um, and a lot of patients in the acute phase might just have a, a flexible sigmoidoscopy done. Um, so it doesn't go in as far only in, as far as the rectum. Um, and it's just to either get biopsies or have a good look to see how, how active, um, the flare is a lot of the time, you'll find that they come in, they've been on something that's worked for them quite well for a long time and then they'll come in and, you know, they've had a really nasty flare and maybe it's been the third flare of the year and you're gonna have to, you're gonna want to escalate their treatment from um whatever they'd been on that was working for them quite well. For some time, you do find that a lot of patients will present with treatment failure. Um And here, here's just an example of sort of this is, this isn't too bad. Um But it is, again, it is something, you know, quite a bit of mucosal inflammation here. And you see that you would want to, this is on flexible sigmoidoscopy. This is where you would want to be considering escalating the treatment um to the next step up. So we'll just talk briefly because there is some differences in the management between UC and Crohn's just depending on where it is obviously, as you know, see um a lot of it is colon and rectum. So the the rectal option for treatment is there. So we can give um sort of mesalazine suppository. Uh either oral if we feel that the UC is, you know, more towards the, the caecum or ascending area or ascending colon. Um But a lot of the time patients do quite well with, with either the, the rectal um steroids or mesalazine. Um A lot of the time patients can take a mesalazine and that might just be it for their um for their maintenance, that would just be for sort of like a, like a low grade proctitis, um which is confirmed as you see on their biopsies. Um But typically you want to give them, um, some oral predniSONE if they're flaring a little bit, but you don't think they require admission to hospital if they've got quite nasty symptoms. Um, and you're a bit concerned about them, you, you, you'd want to admit them to hospital and it's typically, first thing you do is get them on to IV hydrocortisone. Uh four times a day, we would con consider something uh in, in certain cases called rescue Infliximab. So a lot, a lot of I uh a lot of patients are going on to what's called infliximab. Um This monoclonal antibody, it's really good for inflammation. It's used quite a bit in um dermatology and ra or not radiology in rheumatology. Um So it's really good. It's a really good anti-inflammatory, it's uh TNF inhibitor. Um And a lot of times if someone's acutely flaring and you might think that they would, you know, would need surgeons involved. Um You want to, you could give what's called a rescue Infliximab. So rather than waiting for the information to settle a little bit, you would, you would start the infliximab whilst they're an inpatient in hospital. Um And again, like, like I've just said, so if you think this flare is, if you think the bile is savable, um or getting to that point, you want to involve the surgeons quite early to come and review and consider a pan protic colectomy. Um Once the, once the initial flare is under control, then it's all about maintaining remission. So this is typically in the form of, like I said, a lot of patients go or have been going on to Infliximab recently. So you would load them um so that we get uh a dose um or their first dose, their first loading dose. Then at two weeks, then at four weeks and then it will comes eight weeks. So every eight weeks you would get um this maintenance infusion. It does work, it does work really well for a lot of patients. Um Other, other options, like I said, if it's sort of mild or moderate disease, you could maintain a remission on mesalazine. Um And also you might consider, if the infliximab isn't working, you might consider um purine synthesis inhibition with azaTHIOprine or mercapurin just to talk very briefly about the surgery. Um So panproctocolectomy, once, once you've removed the bile, they've got two options. Essentially, you're either going to uh bring the, bring the, the terminal ilium out as an ileostomy. Um or you might want to form what's called AJ pouch. This is where the terminal ilium is sort of twisted around on itself and uh shaped into what's called, shaped into a make or made into a makeshift rectum. So that's, that's what before the, the feces would reach the, it's the last part of the bile. Now acting as a rectum would be the terminal and it's just called AJ pouch based on the shape. So you can just see there um in the middle image, there sort of AJ shape. So typically the most common pouch is AJ pouch. So with Crohn's um steroids is the mainstay in an acute flare, whether that's oral or IV. Typically, if they're in hospital and you think they're gonna need escalation of the treatment, you'll start them on IV and just the same as you see. So it'll be typically IV steroids, IV, hydrocortisone four times a day. Uh Again, you want to consider TNF inhibitors, usually Infliximab or another one which is um rather than infusions, it's called Adalimumab, another TNF inhibitor and this is delivered by the patient himself in the form of injections at home. Um uh If TNF inhibitor is not gonna work, then you can consider, like I said, purine synthesis inhibit inhibition uh or methotrexate would be another one. Other, there's other advanced medications used in both these conditions. II don't think they're necessary for exams, but it's purely for interest. It's all, it's all about uh um anti-inflammatory drugs. So there's what we call, you know, Jak um Jak inhibitors or Janus Kinase inhibitors such as the, the cins IPA tofacitinib and Filgotinib, uh Risankizumab and Vidali Zum. These are other um and antiinflammatory medications, but don't be worrying too much about those. I just highlighted at the bottom of this slide that the mainstay is all about manage the acute flare, optimize their medical management. And if that's going to fail, then you would want to consider surgery. Ok. Um, IBS in irritable bowel syndrome. Um, so this is a functional disease. Um, there's no underlying organic issue with the bowels, but they are, of course, patients are still getting symptoms, but there's nothing organic, physically wrong with the bile. It's one of these conditions, uh, that falls into the category of what, what's called D GP or disorder or dysfunction or dysregulation of gut brain interaction. Um So it's just, it's the way that the, the flexi in the bile interact with, with the brain. There's some sort of disorder and it's not, it's not fully understood. Um But we can obviously get on top of the symptoms. So, um there are certain triggers like um certain foods, certain medications, uh stress levels, alcohol can trigger it for a lot of people and it can be linked to. Um so psychiatric conditions, depression and anxiety. Um This can also, like I said, because of a disorder of gut brain interaction, you're gonna, you will have, you know, disease of the mind can cause these physical symptoms. Um It's a diagnosis of what we call a diagnosis of exclusion. So it's really important if somebody's come in with, you know, abdominal pain or perhaps weight loss because they've been off their food or um or they, and they're having, they've had a change in B that, but you really want to really quite sinister things out like I BD and cancer. Um A lot of the time patients will get their anti T CG level checked, um, as part of a celiac screen. Um So yeah, the diagnosis of exclusion, therefore, exclude everything else. Once you're pretty sure it's not cancer, it's not an inflammatory process, it's not celiac disease. Then you can say this is probably an irritable bowel syndrome. Um Typically there's, we would say there's three types, there's constipation, predominant, diarrhea, predominant, or a lot of patients also experience mixed symptoms. Um, and based on the sort of dominance of their symptoms, whether it's constipation or diarrhea, we can give certain medications. Um, as you can see on the right here, it's constipation type, give laxatives if it's diarrheal type and you're sure it's not an infection. Give antidiarrheals like your, um, antispasmodic, uh, medications like mebeverine, uh, and, um, Buscopan, Highosin Butyl bromide. These are all good just to sort of relieve the, the, the spasmodic type pains and then the lifestyle modifications and so adjust your fiber intake accordingly. So, more fiber, if you're, if you're constipated or less fiber, if you're having diarrhea symptoms, uh, increase your fluid intake cause if it's, if it's diarrheal type, um, and also, you know, increase in fluid will also help sort of hydrate the bowel a bit if you've got constipation, um, regular exercise, particularly to get the bowels moving if you're suffering more with constipation, um, and limit your alcohol and your caffeine intake. Again, these, the, you know, the, these management steps all vary based on what type of IBS you're experiencing. Um um typically we, we, we would uh recommend what's called a low FODMAP diet. So, FODMAP is just a specific um type of carbohydrates. So it, it's uh or sorry, a a group of carbohydrates would be high in FODMAP, things like greens and breads, low fat mop is, is more sort of your carbohydrates you get from uh natural foods like like vegetables and things. So, celiac disease um very common and quite underdiagnosed, particularly in the western world. It's an autoimmune condition. So you might find that um if somebody has had Hashimotos or, or has um type one diabetes, they might um typically they should all, you know, anybody with an autoimmune condition, new diagnosis of an autoimmune condition should have celiac serology as well. Um Even because a lot of patients with celiac will be asymptomatic and therefore, it's, you know, really it's going to go undiagnosed. Um the pathophysiology, of course, auto auto antibodies are created in response to gluten er being present along the microvilli of the, of the judgment. Um You'll get just with local in or localized inflammation, you'll get f flattening of the microvilli and you get um malabsorption over time and this sort of not only the malabsorption, but the um crypt hypertrophy, as you can see in that right image lower down. Um you can see when you compare the crypts, they're much, they're much bigger and you get crypto hypertrophy micro flattening over time. This, the, these structural changes can increase your risk of, of uh hemato hematological malignancy. Um And we'll talk about that shortly um features then. So somebody come, you know, coming to you with, uh and you want to do celiac serology that might be asma or asymptomatic. Um And you might be testing them for another reason. Um It might be, you know, typically these patients will be fatigued because they're, they're malnourished. Uh they might have experienced quite a bit of weight loss again through the malnourishment. Um They might get these physical symptoms of, of bloating and diarrhea. Um some patients, um not too many, but some will experience mouth ulcers. Um And there's a, there's a skin manifestation fairly specific to celiac disease, um called dermatitis, herpetiformis. And that's shown there on the right. Um This can just be an itchy sort of irritating rash that patients will get. Um you can be uh anemic, whether it's a microcytic or a macrocytic in the form of iron or B12. Um And also you very rarely, I've never seen it, but some patients might present with um you know, seizures. So even with an epilepsy, uh or it might present with like a ce cerebellar ataxia, cerebellar cerebellar symptoms. Um But again, that's very rare, never seen that before. Um There are several autoantibodies to be aware of um I would really only focus on the first two. so anti TTG, most common one typically would be tested in exams. Uh, and another antibody that you might test for if anti TG is negative, but you still suspect it. Uh, still suspect celiac might be an, an antiendometrial um, treatment. Of course, would be a lifelong gluten free diet in a lot of supermarkets and, and, um, and chains and things are very good at adopting their menus and things around gluten free because the prevalence of it has gone up quite a bit. Um But yes, in, in, in order to diagnose it, patients need to keep eating gluten for a while. Um If you stop, if you think you've got celiac disease, but you know, somebody wants to confirm that and you stop eating gluten, your symptoms will improve. But we're not, we're not able to actually tell because those celiac antibodies will fall. Um If you're, if you are actually managing it yourself with, with gluten free diets, um just be careful. This does get tested and exams. So um both anti T TG and anti uh endometrial antibodies, they are ig derived. Um So a lot of patients might be I gi deficient. Um and therefore, uh whenever you test for these, these antibodies, autoantibodies, anti TG and E MA, they might be low, but you still have quite a high suspicion of celiac. So what you want to do is check the total IGA antibody level, if it's, if it's raised, um, sorry, if it's normal and anti T TG and anti E MA are low, then you can be pretty sure it's not celiac disease. But um, if, if, if total IGA is low and anti T TG and E MA are both low, then you can't say for sure that it's not celiac. Um So at that point, you'd want to um, typically arrange an O GD to get a biopsy. That's the most definitive way of diagnosing this. Uh You'll see the changes that we saw there on biopsy. Obviously, these are just fake. The these are fake, but very much would look like that you get flattening of the crypt or uh increase in size of the crypts and also flattening of the Microvilli. So, um if it's un undiagnosed, not correctly managed, you can run into complications. So you get anemia, like we said, a lot of patients would experience osteoporosis. You can get what's called a functional hypersplenism. So the spleen stops working as well. Um And then these patients are typically at risk of uh small bowel cancer. So, uh lymphoma, what, what we call an enteropathy associated T cell lymphoma, which is a form of non hodgkin's. So, don't, don't be put off by this big scary slide. I've just left this in here. Um Don't really want to talk about it too much. I've left it in here because the, the talk is gonna be recorded. It's just uh an overview of, of the cancers. Typically. Typically, this would be covered in the, in the surgical rotation. But um more so on the medical side, you know, you, you'd find that the esophageal might be covered or stomach might be covered a bit more than pancreatic cancers and colorectal cancers in particular would be covered in your surgical rotations. But that's just to make you aware, um the risk factors for a lot of them are quite, quite similar. Uh Certain specific risk factors might come up. Um For certain ones, for example, the genetic causes of, of bowel cancer like F ap and Lynch syndrome. Um and treatment can vary as well. Some, some of these cancers are much more aggressive than others. Um But yeah, I just wanted to leave that up there. Um Just for the cholangiocarcinomas uh as well there, the fourth column. Um I wanted to talk a little bit about because I see II I've mentioned the term PTC there. Um That's an IR procedure. Um So it's a, it's a procedure whereby if the, as you can see in the, in the lower right here, if somebody's got a likely cholangiocarcinoma or um if you're, you're highly suspicious of it. Uh But you can't actually access the ducts through E RCP. Uh The interventional radiology team can go in and do what's called a PTC or percutaneous transhepatic cholangiogram whereby they use imaging to pass um to go in through the skin into the bile ducts, through the liver and then they can access the tumor from above, essentially. Uh, they can get brushings and things like that. And for cytology just to confirm that it's, uh, uh, you know, like a cholangiocarcinoma. Um Also this, you know, by accessing it this way, if, if we're unable to put a stent in to drain, um, the, to drain the bile, if they've got a nasty sort of obstructing cholangiocarcinoma, a drain can be put in um via that, that, that entry site. So it comes out through the skin. That would be an external PTCA lot of the times if, if, if the mainstay of treatment for these cholangio patients is, is palliation, then typically they would go back to IR and have the drain internalized. So once enough bile has been drained off, um, the, the, the drain is then what we call internalized. So as you can see, it then comes out through the um of that and then it'll just drain as normal and that'll stay in there um for sort of the, for the rest of their time. So I appreciate. That's a whistle stop. That is the gi side. Does anybody have any questions at this point? All? Ok. Again, just if there is any questions don't, I don't, don't be worried about, um, don't be afraid just to unmute yourself and, and ask away. So we'll move on to the Hepatology. Side. Um, pretty sure I don't want to keep you for too long. So, um, a few conditions just to rattle through. Um, we're gonna talk a bit about LFT S, uh, and debunking the sort of different types of patterns in LFT S. Um So we'll, we'll look at the hepatitic LFT S and compare that to the cholestatic pattern. Um We'll talk a bit about alcohol related liver disease. Um And what was formerly nonalcoholic fatty liver disease is now called mail or a metabolic dysfunction associated steatotic. Uh We'll talk a bit about viral hepatitis and autoimmune. Uh a bit about PBC and PSC and then talk a little about cirrhosis and transplants. So, um don't wanna dwell too long on this because you have all done your preclinical um years. Well aware of what the, what the liver does. It's big functions in terms of synthesizing proteins, particularly your clotting factors and albumin. Whilst we get a lot of uh of albumin through our diet, a lot of it is also synthesized by the liver. Um metabolisms was involved in the metabolism of glucose amino acids, fatty acids and also a lot of drugs as well and production of bile which is then stored in the gallbladder. Um And it also has storage functions in the form of vitamins. It has iron stores as well and it stores glucose in the form of glycogen. It does also have immune functioning. Um and that is within the cup for cells or specialized cells. So um a little bit more of another interactive question then guys. So can anybody tell me what here in this list of things we might test or we're concerned about a liver issue, which is actually an indicator of synthetic function. Prothrombin. Yeah, absolutely. Like we just said, clotting factors. So, very good prothrombin time. Anything else? No, that's OK. So like we've also said albumin, so quite a bit synth or quite a lot of Albumin synthesized in the liver and also Billy. So your typical patterns and these, these aren't, it's not just tests and exams. This is very much really useful tool. Uh a really useful way to distinguish between um whether it's an obstructive pattern or an inflamed liver. So your hepatitic or your cholestatic pattern. So, the hepatitic enzymes or the enzymes that go up in a hepatitic picture are at and ast in cholestatic, you get AP and GGT. So there's quite a lot of causes of the hepatitic picture. Anything that's gonna cause an acute injury to the liver itself and not necessarily the bile ducts or anything around it. So, anything that causes a hepatitis, whether it's alcohol, whether it's um not uh mash cirrhosis, whether it's a virus autoimmune, um if you get a drug induced liver injury in the form of perhaps a paracetamol overdose or um if you get an ischemic hit to the, to the um to the liver as well and there's other uh other rare conditions like uh hereditary hemochromatosis and Wilson's um just for the exams. Again, another wee, another wee tip for the exams, what we call a massive transaminitis. Uh This is whenever your, your hepatitic enzymes go way up into the thousands, not too many conditions will cause this. So, um basically, if you, if you get a massive transaminitis, it's probably, there's probably been an ischemic hit or, or a paracetamol overdose. Uh And then there's certain patterns we look out for. So, um if the AST is, you know, twice the, the value of the at this would suggest it's quite specific for alcoholic hepatitis. Um And if the A LT is much greater than the AST, it suggests like a nonalcoholic fatty liver. Um So, cholestatic, it's either going to be intrahepatic or extrahepatic and we'll talk about the different causes. Um But in terms of intrahepatic, it's typically uh PBC, um PSC would also be extrahepatic. So that should be in both. Um but also drug induced causes. So, particularly things like flucloxacillin or statins can cause cholestasis. Um And then the extrahepatic causes, you may have a gallstone there, um or they might have a mass such as a cholangio, um anything that might cause stricturing, whether that's benign or malignant, perhaps related to cholangiocarcinoma and anything that's causing compression of the bile ducts from an outside source. So, whether it's a head of pancreas tumor or maybe a quite a significant but small bile obstruction, um timing then. So it'll be an acute liver issue if it's less than six months, anything greater than that is gonna be chronic liver disease. And here we have the stages. So, and this, this is a typical pattern for pretty much all of the, you know, most, if not all of the um chronic uh conditions. So things like alcohol induced injury, uh nonalcoholic fatty liver, um and your other conditions like sort of P BCPs E and, and some of the hepatitis. Uh um so you start off with a nice normal liver uh injury over time leads to fatty infiltrates and then the fatty infiltrates become inflamed in the form of alcoholic hepatitis or, or, or mash. Um in fact that so the inflammation and repair there can cause fibrosis, which leads to nodular scarring in the form of cirrhosis. And then over time, if you're unlucky enough to have had cirrhosis for, for, for a significant amount of time, you can develop uh hepatocellular carcinoma, focusing on alcohol induced uh injury. So it varies. Some patients have a genetic predisposition in that, you know, if you take 11 patient that has a heavy alcohol intake versus another, they, they might uh be unfortunate enough to have a certain gene that predisposes them to an alcohol induced injury, uh that would, that would onset quicker than the other. Um But the stages of injury, as I've just shown you are quite similar here. So you'll get a, you'll get with excess alcohol, you'll get uh fatty infiltrates that build up over time. This becomes inflamed in the form of an alcoholic hepatitis. Um, as, as you can see there in the lower part of that diagram, there's various means by which a patient can, can deteriorate far enough to the point of death and whether that is a really nasty alcoholic hepatitis or from cirrhosis or from cancer. Um But yes, I it follows the same uh stage of uh the of progression. Um The department of Health would recommend not exceeding 14 units a week and this is now as of a few years ago. Um males, um male is equal to female in terms of the, the recommended units. It used to be that they'd recommend males could, could um could have a little bit more, something like 16 or 18 units, but it's not equal. Um And they recommend spreading this out. Um There's many complications as you can see. So they might, you know, acutely uh have e experience a Wernicke's picture of Wernicke's encephalopathy might develop an acute pancreatitis secondary to their alcohol. Um And then sort of more chronic things might be like a cirrhosis or a cardiomyopathy bloods. Then, so with heavy alcohol intake over time, you'll, you, the patient can become B12 and folate deficient. Um and you get uh macrocytic anemia, uh you might have a transaminitis um as we said before, there's a specific ratio that you can look out for in exam. So AST will often be double the amount of at and LCP. Um gamma TT can go up acutely. But, and um remember a ap being more obstructive rather than hepatitic, it would, it could potentially go up later in disease as the patient uh progresses towards cirrhosis. And they might have a low albumin whether that's really related to the fact that they're, you know, dependent on alcohol and therefore malnourished by not taking in enough protein themselves or whether it's se secondary to the actual liver injury. Um and again, liver injury will cause an increased PT. Um and you might have a du du and a very significant alcoholic hepatitis. Um, patients might experience um uh had a renal syndrome. It really, which carries a really poor prognosis whereby the kidneys are typically starved of oxygen because of the, this is in cirrhosis. Uh the kidneys are starved of oxygen or not oxygen, sorry, starved of uh of, of blood flow because uh there's reduced flow to the, to the, to the kidneys because so much of it has been third space in the form of ascites and peripheral edema and it carries a really nasty, really nasty prognosis. Um There's a, a rake of scans that could be done. Um I'm investigating patients and a lot of these scans, you'll find uh this will be quite repetitive. You'll hear me saying ultrasound and fibro scan over and over for the next sort of 20 minutes. Um on an ultrasound. Uh If they've got fatty infiltrates, it'll, it'll, it'll be reported as increased echogenicity. Um And a and, and, you know, if, if we find it or we think that somebody's got a fatty liver, um, or significant fatty infiltrates in their liver, we would refer them for um what's called a fiber scan or, or transient elastography. This essentially just assesses how elastic based uh based on the, the firing of the, of the, what's the, the, the, the wavelength uh from the scanner, how, how elastic the actual liver is. And this gives us an idea of how cirrhotic that, that liver is as well. Um You might want to do an or you probably want to do an O GD if you think they've been alcohol dependent for a while and they're getting features suggestive of the cirrhosis. You want to, you want to scope them just to um rule or just to assess and rule out any sort of early or or significant size viruses. Um Typically, patient will develop viruses if they've had cirrhosis long enough to develop portal hypertension. A CT or MRI might get done. Um Just to assess other um manifestations of cirrhosis such as ascites, any changes to the vasculature, uh or if they've got a big spleen as secondary to portal hypertension as well. Um And you know, not, doesn't necessarily get done all the time. But if somebody's got quite a nasty alcoholic hepatitis, um that's not responsive to steroids, then you might want to do a biopsy. So, uh in terms of the management, of course, you want to, to refer them for, to, to get help, to stop drinking. Um this can be quite difficult for a lot of patients. Um It's quite a tricky thing to wean them off. Um A lot of patients can benefit from psychological interventions like CBT. Um And then the, the vitamin supplementation is really important for these patients. Um particularly if they continue, if they continue to drink a lot of the time, you don't really need to worry about thiamine. But in those that are very likely to continue to drink, you know, on discharge from hospital, you want to make sure they're on things like Forval, which is a multivitamin. Uh thiamine three times a day is quite important for them as well to prevent uh wernickes and courses of coughs. Um high protein diet is important. Uh they lose, you know, they lose quite a bit from, from drinking, but also uh the low albumin from the liver injury as well. Um Steroids is, you know, if they've come in and they've got what's features in keeping with an alcoholic Hepatitis steroids is the mainstay of treatment there. Typically they'll come in and I'll have seven, at least seven days and on day, seven of steroids. Um you know, if you, you, you'll, you'll, you'll be able to predict it based on their liver function tests. But, uh, you know, if, if they, if they still got quite a bit of pain, um, quite jaundiced, uh, in the acute setting of alcoholic hepatitis, she'll calculate what's called a little score. I'll give you an idea of, of whether continuing steroids is worthwhile if they're gonna actually have a response to the steroids. Um, and then if they, if they've got an alcohol related injury that's either led to or they've also, you know, got longstanding cirrhosis, you want to manage these complications and a lot of patients, if they get to the point of cirrhosis, they would be considered for transplant if they're fit for it. Um But a, a really important, obviously, understandably a really important criteria is that they must be abstinent from alcohol. It's just a very brief uh slide on, on sort of what to do if you're working on acute medicine or if you're, if you're on the uh on the medical, take an E and, and a patient comes in acutely or with acute intoxication. Um Or if they've sort of, they, they've come in and they're uh they've got things that, you know, acute withdrawal. Um There's a bit of a timeline that's worth remembering. So, uh within 6 to 12 hours, you get a bit jittery, sweating, adrenergic, overdrive. Um So you get a bit of a tremor, you can feel a bit anxious. Um then the 12 to 24 hour mark, they can maybe experience some hallucinations a lot of the time it can be tactile. And so the 12 to 48 hour point uh if they've not, if they've not received what's called Librium as, as mentioned below, they can see. So it's really important um in patients with a high enough uh Glasgow modified alcohol withdrawal score. Um if they've got a high enough score and, and they really need to be on that. Uh Benzodiazepine called Librium in order to prevent them from seizing. Um And then uh quite a nasty thing is uh if you get, you know, if you leave it long enough and they haven't really, uh if they, you know, if, if, if they continue to deteriorate, they can experience what's called delirium t tremors where they get over their, their um nervous system is overexcited because of a lot a downregulation of uh of Gaba with an up regulation of glutamate receptors and Gaba responsible for um uh neur neural suppression or nervous system suppression or um relaxation. And then ga glutamates is, is sort of neurotransmitter excitatory. Um So they get, you know, a, a quite a hyperactive delirium. Um As I said, you know, you wanna monitor the G OS with, with Librium and with time and being off alcohol, this will come down. So typically they get a, a reducing course of, of this chlordiazePOXIDE or Librium. Um typically patients coming in with acute withdrawal or, or acute intoxication after they've been off alcohol for a, a period of time, they'll go on, uh, what's called IV, PAX, an IV vitamin ABA B of vitamins. Um, and like I mentioned before, it's really important if you suspect they continue to drink, make sure they get discharged on some thiamine regularly T DS. So that's the alcohol side of, of liver injury. Then we move on to um the, the metabolic side, the name recently changed just because there's, there was sort of stig stigma associated with, with using the word alcoholic. So we now call it metabolic dysfunction associated steatotic liver disease or mass rather than NAFLD. Um This is rather than alcohol, this is uh excessive fat buildup because uh of your sort of essentially your lifestyle. So a lot of the time patients with type two diabetes, um poorly controlled type two diabetes, poorly controlled hypertension and obesity, poor diet exercise. And, and anything that makes you quite unhealthy uh can cause quite a significant buildup of, of, of fat deposits in the liver. And again, over time, as you can see below that, that sort of typical stage and pattern is quite similar. You get fatty infiltrates which get inflamed, which cause fibrosis cause cirrhosis. And then when you're cirrhotic, you're at increased risk of liver cancer, it's quite common. A lot of people will be asymptomatic of it. So if you took 25% of, of the random population, they would pro and scan their, scan their liver with an ultrasound. They'd probably have that increased echogenicity. Um, obviously you're gonna have a higher number. And, uh, if you've got more patients with diabetes or hypertension or more that smoke, but, um, it is quite common. Um, here you're gonna, like we mentioned before, that pattern that might get tests and exams if their alt is way up compared to the ast, it suggests fatty infiltrates. Um And then that this repetitive sort of investigative panel of ultrasound, then uh a fiber scan. Before typically here, the liver, liver team would, would do what's called a fib four scan. And this looks at things like uh platelets albumin. Um And it sort of assesses their overall, the overall severity of their, of their liver injury. And then based on the fib four scan will that typically will, um that will help us determine how quickly they need a fibro scan. Um So, you know, if you, if you've got a high enough fib four score, you wanna refer them to hepatology for a fibro scan and they'll decide how quickly they want to do that scan. Um You know, sometimes as well if required, they'll do a liver biopsy if they're not sure that it's definitely um like a muscle type picture. Um Management of course, is gonna be getting on top of their lifestyle. So, um encouraging weight loss, improving their diet tell them that they should stop smoking. Um, optimize glycemic control if they're diabetic and also if they're hypertensive, optimize their BP control as well. Uh, the viral sort of a viral picture then viral hepatitis. So, you've got ABCD and E, we'll not talk too much about D because, um, you know, it's very unlikely you, you never come a really, never, never really come across it very, very, um, uncommon in the UK. Um And HEP D can only uh survive or exist if it's mounted on the surface antigen of HEP B. And so I've left that out. It, it, it shouldn't get tested but then HEP A and HEP A, they both follow a similar sort of pattern and picture. So they're both RNA both spread via infected food and water sources. So f fecal oral roots, um you might sort of exam it, you might find that if they talk about hep uh or infected pork or, or something to the pork. Hep B is very strongly associated with, with off or, or filed pork here in the UK. Um Treatment for both of these is supportive. So there's um there's, there's no, no treatments given, it's largely supportive and they, they will pretty much everybody makes a, a full recovery. Um HEP, a vaccine can be given to people who are going on uh on, on holiday or traveling somewhere far away and where it's where there's a higher prevalence of it. Um Hep B then uh on the next slide I'll focus on the, I'll, I'll talk to you a bit about the serology that might come up in exams. But he HEP B is different. It's the only, only one of the Hepatitis viruses that is DNA virus. Um, like HEP C, it's bloodborne or, or, um, or it's passed on in uh by mixing bodily fluids. Um, it can also be passed on from mother to infant at, at birth as well. Um A, you know, majority of patients will recover. Um you know, a lot of time they get uh antivirals and they'll recover and they'll never, you know, have really have an issue with it again. But there are a small number of, or a small number of patients that develop HEP B that will, will go on to, you know, be asymptomatic of it but will have it chronically. Um They'll have quite a low viral load but, you know, it, it'll not be, they'll not have it uh eradicated um treatment, as I said, antivirals and then, you know, sort of monitoring and assessing for complications. If the, if the, if the hepatitis is so severe that it's, you know, it's causing acute liver failure, you'll want to transplant them quite urgently and we'll talk a wee bit about how quickly patients will get transplanted. And at the end, um it's really important with HEP B that you, that you arrange contact tracing. Um It's all you know, and also just educate the patient on, you know, best means to reduce, transmitted to other patients and just sort of the importance of, of them informing other part for, for example, sexual partners and stuff that they, you know, educating on the and the importance of, of, of informing. Um and yeah, contact tracing is important as well. Um The vaccine is, is given to pretty much uh it's given to everyone as part of the six and one. So it's in the UK vaccine schedule, the HEP C. Um like I said, it's similar enough to, to, to HEP B in that it's, it's a bloodborne virus and also um transferred and bodily fluids, but it is an RNA virus rather than DNA. Um for HEP B treatment is U you know, it's usually curative. Um it's, it's curative with a specific type of antiviral based on their genotyping. So you test for specific genotypes when you, when you test for HEP C. Uh And then based on that specific genotype of HEP C, you'll get specific, very, very specific antivirals that, that uh will, will cure this uh in, in practically all patients. Um there's no vaccine available but that's, you know, the the the the the intent is to cure. So um very quickly, this is some serology that that can come up on exams quite a bit. Um If somebody has an, has an active infection, they're acutely infected with HEP B, their their surface antigen or, or sa it's gonna go up. Um And depending on how contagious they are, their hip, they enveloped antigen and also at the bottom there, they, they're viral DNA HEP B hep B DNA. Uh both, both will be raised if they're quite contagious in, in, in a high infectivity period um for the core antibody. Now, the core and surface antibody, we can test for um the core antibody. It, it, it can be nonspecific and therefore you have to test for other things. So it might indicate a past a, a chronic uh or, or like an a, an a current acute infection, it's always best to check IgM and IgG core antibody because the IgM core antibody will be up in an acute infection. But if it's a past infection core, I or sorry, core antibody, IgG will be up. Um And if, if, if um if it's a chronic infection, then the, the IG M will also be up but the IgG will not be present because it's not been cleared. Um surface antibody typically, if they've not got an er if they've not got high um surface antigen, but they've got surface antibody, that means they've been vaccinated in the past. And we've talked about uh checking how, how infectious they are by checking both the e antigen and the, the, the actual he DNA viral load very briefly on the auto autoimmune um hepatitis picture. So two types don't, don't be worrying about getting too bogged down on this. Um, there's two types and based on which type you have, um, an, a specific autoantibody tends to flare up or, or be positive. So type one and type two, type one. it more so often it's more common and more often affects, um, sort of middle age women and type two affects younger people. Typically, uh, female patients, younger female patients are affected more than males. And it is, it is quite a acute presentation. And you'll also find that, you know, somebody with an autoimmune hepatitis, they've probably got another auto underlying autoimmune condition. So that might be type one diabetic celiac have, have uh underlying thyroid disease or Addison's or something, something autoimmune in the background. And, but just remember that's quite good for exams as well. If they've got something autoimmune, always suspect another autoimmune condition. Um definitive diagnosis with this, um particularly if they're not really responding to treatment. You want to do a liver biopsy. Um A lot of the time if you've high suspicion of, of autoimmune hepatitis, you might um you would treat maybe not worry too much about the biopsy in the acute phase and you would treat them with quite high dose of prednisoLONE. You obviously don't want to keep them on predniSONE for too long and particularly at a high dose. So this is typically weaned and a lot of patients will go on to a very, very long course, you know, several years, sometimes of the steroid sparing agent is the Thia and just, just for example, as well, always make sure before you start somebody on azaTHIOprine that you've checked their TPMT level, which is their thiopurine s methyltransferase, which is the enzyme responsible for breaking it down. So just make sure you, you check that um before you prescribe azaTHIOprine. So PBC and PSE and sort of differentiating between the two of them. Uh PBC, this uh this affects your intrahepatic ducts only really. Um And it's the smaller, smaller bile ducts intrahepatically that are affected. And a very, very typical patient would be again, quite like that type one autoimmune picture. It's middle aged women, sometimes it can be hard to differentiate between the two. But typically your autoimmune hepatitis will present a bit more acutely than, than a PBC. Um The path of is is that you get autoimmune destruction of or damage to the epithelial cells that line the duct. And then as with anything you get inflammation, chronic inflammation will lead to fibrosis and scarring. And over time, the patients can become cirrhotic. Um because it's uh a cholestatic picture, you're gonna get um this is where all the symptoms will come from because you've got cholestasis. So if you, if you got cholestasis, it means you can't clear or excrete your bile acids or bilirubin or cholesterol all in the form of bile. Um just because these can't be excreted, you'll get a buildup of bile acids which can cause a, quite a nasty itch as well as the bilirubin. Um, and, uh, as well. And also you can get, um, like quite a nasty diarrhea, um, with the, and build up of cholesterol. Of course, you're gonna get deposition in the form of xanthomas and xanthomas, but it also increases your risk of atherosclerotic disease, um, investigations. Then you're, you're gonna have your AP and your gamma GT are gonna be raised compared to the hepatitic uh enzymes. Um The most specific uh autoantibody for PBC is antimitochondrial. Um And in some cases, you'll get antiar positive as well. Again, I'm repeating myself. So you want to do an ultrasound liver typically in any sort of LFT derangement, um especially if you've got right upper quadrant pain as well. Ultrasound liver just to rule out another obstructive cause maybe like a stone. Um And then very occasionally patients might get biopsied. Um The most important treatment for patients in PBC and this will actually slow. The progression of their disease is given a treatment called ursodeoxycholic acid. It is also, it's also a treatment used in cholestasis of pregnancy. So, again, quite similar, you get cholestasis and um it's, it's a, it's a specific type of bile acid that actually reduces the damage from that stagnant bile. So it's really important that this gets started early whenever somebody has, um, suspected or confirmed PBC. Um, cholestyramine is a symptom relief medicine. So it would relieve the itch um immunosuppression sometimes in patients not always considered. But um because these patients will, you know, over time, despite giving Urso um over time, they will progress to endstage disease and you know, that require work up for a transplant. And then when we compare this to PSE because sometimes there's a bit of overlap and a bit of confusion, PSE is, there's a lot more scarring involved tends to name um you get scarring and structuring. Um And there's, of course, there's also cholestasis, hence why your cholestatic liver, liver enzymes go up. Um This uh affects intrahepatic but also more, more more typically the extrahepatic, the larger ducts uh outside the liver. Um you know, it, this is, as we mentioned before, it's got a really strong association with UC. So, II mentioned before, about 70% of P PSE cases will also have um an underlying ulcerative colitis. Um like PBC, it will just, you know, the damage and the inflammation leads to fibrosis, laying down of scar tissue and that nodular cirrhosis um risk factors in this case. So, uh PBC more typically affect um middle aged females. Uh it typically, it tends to be younger males, sort of not adolescent, but that sort of thirties to forties is your typical um male patient who would be affected by PSA. Um If they've got UC, you should always, you know, if you got, if they've got UC with LFT derangement, you'll know to suspect uh to suspect um PSE um investigations, as I said. So gamma, gamma GT and A LP in particular will be up um as markers of cholestasis. Um You want to do an M RCP to have to directly visualize those ducts. Um O on, on the scan, you'll see, you'll, you'll, you'll see the sort of that beating, um beating on a string sort of appearance. Um And uh also you want maybe want to consider a colonoscopy. If you think they might have another line, you see um management here is, is really and you know, and I'll tell the patients at the point where needing transplant, typically, you want to get the bile ducts managed with um an E RCP to, to put stents in or to do a balloon dilatation in order to treat those strictures. And therefore, you know, improve the flow of bile PSC as it affects, you know, extrahepatic ducts, a big risk factor with, with scarring, just like scarring in the liver, causing HCC scarring in the bile ducts can increase the risk of cio carcinoma. Um I appreciate it. I don't wanna keep you too much longer. So just uh mainly to focus on cirrhosis. Now, once all these, once all these conditions have, you know, whilst being treated, you know, ultimately cirrhosis is the, is the end picture really for the majority of these patients with uh uh despite treatment. So it's as we talked about nodularity and irreversible scarring. Uh All those diagrams I showed you before where you saw the progression. It's all just to highlight it's all reversible up until the point where cirrhosis develops, that's irreversible. And um at that point, yeah, there's no no reversibility at all but fatty liver, um even the sort of the uh steatohepatitis, it's all reversible change. Um When you get the, when you, when cirrhosis develops, you're at risk of portal hypertension because there's increased pressures in those vessels to the liver as it's trying to force blood through a very hard firm sclerotic structure. Um And then with portal hypertension, you'll get the effects of portal hypertension itself, most notably viruses um is the most sort of, you know, thing you want to, you'll be tested on or uh want to be most aware about. Um So that's why we, we typically scope these patients who with confirmed portal hypertension. Um But also, you know, patients with cirrhosis with a high suspicion of portal hypertension will get scope to check for viruses and al also to surveil these viruses as well. Um If we're not too sure as to why a patient is presented, you know, some patients will present with cirrhosis. So if we're not too sure why, um or they've got, you know, any sort of liver disease, you'll do an ultrasound, but you'll also do what's called called a noninvasive liver screen. It's a big massive panel of bloods. So it's checking for things like Wilson's checking, uh, autoantibodies as we mentioned before, checking immunoglobulins, um, and just sort of checking things like iron studies, um, alpha one antitrypsin. So it's just sort of, it, it's, it's a really, it's a really good panel for when, when, perhaps when you're not sure but you want to cover all grounds. Um, so we'll do that, those bloods as well as your routines. Um, and with cirrhosis, as we've talked many times, you'll get the, you'll get uh in increased bleeding risk with thrombocytopenia and raised PT. Um if they've got cirrhosis and they've developed portal hypertension, they might have hrs about a renal, which we talked about. Um And again, you know, you know, you'll, you'll typically with a CT or an MRI, you'll know that they've got cirrhosis, but you might want to do a liver biopsy just to, just to absolutely confirm it, make sure they've not got like a, like a quite a nasty focal nodular hyperplasia. Um But a lot of the time it's not necessary. We got some signs of chronic liver disease here. All the major ones that can come up on exam. So again, just a wee bit of interactivity do um if anybody wants to shout out, uh So we start top left should be fairly obvious for you. Scleral. Absolutely. Yeah, that's way more fancy than I put. So I've just said jaundice, but you're absolutely right. The jaundice, not only in the skin but the, you know, particularly in the sclera. Um Next then does anybody know a very specific type of, uh telangiectasia? Lovely. Number three. Yeah. Uh, number four, gynecomastia. Yeah. Lovely. Um, and then bottom left, this isn't very specific, this is just in keeping with the symptoms. So, um these are just excoriations because liver itch is one of the most troublesome symptom. You know, one of the most troublesome symptoms for patients is liver itch. So they might have ascites which can make them short of breath. Um and they might have, you know, jaundice or, well, the jaundice is gonna cause the itch but a lot of the time for patients, the itch is the thing that drives them, you know, almost drives them crazy with, with um irritation. Uh the next one then again, should hopefully be quite obvious. Yeah, lovely type specific type of virus you here or vi virus. Do you know what this specific sign is? Cap up? Medusa? Lovely. And then two more so fingernail changes, anyone know in, in particular? No, that's ok. So it's uh it, this is here and then finally, I know this would be more, this would be better if it was in the form of a video. But I think, you know, you probably know what we're trying to check you for here. Liver flap. Absolutely. So liver flap or asterixis management of cirrhosis, we I think we've been through it quite a bit. So we wanna screen people from, for, for complications. We've got scoring systems which I'll briefly talk about um underlying cause is important to get on top of whether it's been a, whether or not it's been an um an alcohol related injury or maybe a mass. You wanna um you wanna, you wanna act on the cause? Um so AAA lot of the time patients are not patients, sorry. So a lot of the time we find that, you know, students or, or juniors like myself are confused by what, what we mean by when somebody's got a cirrhosis that's decompensated. And you know, the best way to, to think about somebody who's in decompensation with a cirrhosis is just to remember four sort of pillars of decompensation which I've listed here. So if somebody's got a, you know, a cirrhotic liver, they can manage fine for a good while. But as soon as they sort of develop one of 123 or four of these, they're, they're deemed to be a decompensated liver cirrhosis. So that'll be ascites hepatic encephalopathy, esophageal viruses or jaundice. And it's just, it's just handy to remember this by the wee acronym. Ahoy. So if you find that somebody's got one of one of four of these, you know, typically would say it's a decompensated picture. Generally, you know, generally patients will have, you know, 23 of these things if they're in a proper decompensated picture. But uh you know, typically you could say it's a decompensated cirrhosis if they have just ascites or, or they're, they're, or they're, they're, they're uh encephalopathic, uh a couple of important scoring systems that can come up in your exams. So, the model for end stage liver disease are mild. This is just a scoring system to calculate mortality at three months in anybody who's got compensated cirrhosis. It is um calculated every six months. It's not, it's not used whenever they're decompensated because at this point, we're prioritizing transplant. Um but it's just a sort of uh every six months in compensated cirrhosis, they'll get a three month score. Um and it's a, it's a percentage score, percentage risk of, of dying within three months. Child Pugh then would be used um a bit more. So uh it's a bit more complicated. So there's three different stages, child QA B or C based on how many points you have and the, the sicker, the patient, the, the more towards the sort of C point they are. So they've got more points. Um Each of the five ABCD ES album and Billy clotting by checking their I nr dilation by whether or not they've got ascites and how much ascites they've got. So, um uh all these things are, are, are, are checked. So if they've got really large following ascites, there'll be a three, if they've got minimal ascites, there'll be a one. The lowest score obviously is being five and the highest being 15. Again, these things are used to stage and, and decide who is, who is really at the point of needing work up for transplant complications. Finally, just as we talked about um ascites and, and, and SBP or spontaneous bacterial predni is a big one to, to be aware of in the exams. Uh if they've got portal hypertension, all the effects of it. So ascites can be secondary to the portal hypertension. But also viruses is an important one. And if somebody's got a massive severe bleed from those viruses, you wanna consider what's called a tips procedure. Um This is a transjugular intrahepatic port, a systemic shunt. So an interventional radiologist goes in through the jugular down into uh down the, the IVC into the, into the hepatic vein and then it's basically into the liver and they, they bypass the liver by creating a shunt between the portal vein and the hepatic vein. So, obviously, there's still be a bit of flow to the liver but a good amount, you know, a good amount of pressure is relieved on the on the portal vein by bypassing a little bit of that or a good bit of that blood into the hepatic vein. Um malnutrition, um again, not just so, you know, not just from the alcohol, but um you'll find that cirrhotic patients will be malnourished, particularly lack of albumin. Um and they can be um we avoid salt with these patients because they're quite hypo hyponatremic from all the fluid retention. Um, so avoiding salt because you can just worsen that, uh, you can actually worsen that hyponatremia. Um, high calorie, of course, being malnourished. Uh, and it's important to encourage regular meals for these patients. Uh Hepato renal syndrome and cirrhosis as we've talked about can, it can carry a very, very poor prognosis. Um Typically patients with hepato renal syndrome, the, the two main stay of treatment are tore and albumin infusions if they can, if the uh if, if you know, they're very lucky if they make a recovery from this in a lot in, in uh in a lot of cases of hepato renal syndrome. Um prognosis is very poor, some patients can pass away. So, you know, within days. Um and then in hepatic encephalopathy, uh of course, you know, this is treated with lactulose to try and um not only reduce ammonia uptake from the bile, uh but also it by, by giving the laxative, you encourage um prevent or reduction in absorption across the bile and by keeping them the, the bowels moving regularly. Um Refax it BB because the main thing in, in, in hepatic encephalopathy is is ammonia, getting into the bloodstream and crossing the blood brain barrier. So these, these two treatments, the mainstay is reducing ammonia, uptake lactulose will flush it out in the bile, but it'll also it a it actually also kind of neutralizes and prevents uh its uptake that way. Uh rifAXIMin will reduce uh bile or sorry sort of small bile, large bile uh growth of bacteria which are typically ammonia producing. Uh So it's all about reducing ammonia absorption with these two treatments. Um And then HC um obviously a AAA big complication to be aware of and it has a different or a very separate transplant criteria. Um OK. Ascites then very briefly you get increased portal pressure, uh portal hypertension will cause leakage of fluid. Uh And this gathers within the, within the um perinatal cavity. It's third spacing. Um So, as men, as we mentioned before, uh if you got quite a big uh quite a big volume of ascites, you're gonna reduce blood flow to the kidneys. This can uh you know, in, in cirrhosis with significant ascites. This can cause, as we mentioned, hepato renal syndrome. But you know, if, if you're not, if it's not that severe, but you know, you've still got a reduction of blood flow to the kidneys and the kidneys will react by activating the ras system and you'll get sodium and therefore water retention and any water retention if it's going to the wrong place is gonna cause it, it's, it's, it's or sorry, any, any water water retention. Um firstly, and through the vessels, if it's going in the wrong places by third spacing, it'll accumulate in the, in the, in the ascites or in the flu or in the legs and then also in the lungs and that can cause uh pulmonary, you know, pulmonary edema and, and, and uh obviously nasty symptoms from that. Um It's important, like I mentioned before, low salt diet because you can worsen that fluid retention and hyponatremia um mineralocorticoid antagonists in the form of Spiro are really good. Um So essentially, you're, you're sort of targeting the ras system. Uh So not only diaries you preventing further a activation of, of the rass that way. And then, you know, if for a lot of patients we managed well on Spiro, you can go up to about 400 mg of Spiro a day. But if this, if their, if their ascites continues to accumulate despite sort of higher maximum doses of spironolactone, and you're gonna want to drain that fluid. Um that's done with an L VP for large volume bio. Uh Somebody's got um like a refractory ascites. So they go have to go for regular drains because it just really accumulates too much. Or if they're not really responding to the spiral, if they're, you know, if they're fit enough for it, you might consider the tips procedure we just talked about again just to reduce portal hypertension, this will reduce ascites over time that way by reducing pressure on the portal vein. Um And if they're a suitable candidate, then you, you would work them up for a liver transplant because as you said, in, in terms of Ahoy ascites is one of the pillars of decompensation. At that point, you wanna work them up for a transplant within the next few months. And because it's a stagnant amount of fluids, it's, it's nutrient rich containing albumin. So it's gonna be um it's gonna be quite uh an albumin and Gluco glucose is gonna be quite uh sort of a breeding ground for bugs. The commonest in SBP would be E coli and CBS more so E coli for exams. Um And uh the, the mainstay is once you've done a diagnostic tap. So it's not the same as a uh a large volume paracentesis. Diagnostic tap involves just putting a small needle into that space. Um And, and particularly with this image, you can see that's quite, you know, quite a large volume of. So you probably don't need an ultrasound machine. They, they that that patient is quite tense in that photo. But if it's sort of moderate, minimal to moderate and you know, they've got ascites, you may want to get IR to get the sample just so you don't perforate the bowel. Um But if they're quite tense, it's good to get a sample at the bedside of that fluid, send it off to the lab and check for uh check level fluid albumin fluid protein um and to be able to calculate the sag. Um but also not only do we do these things in ascites, we also send it for culture and just to see what exactly. We're looking for usually E coli but, um, typically before we, we don't give the IV antibiotics before we do the tap. So do the tap and then get the antibiotics started pretty quickly. Um, uh diagnostic tap is positive for SPP if the nuclear, uh the neutrophil count is greater than 250 within that fluid and then um just very quickly a bit on cancer and transplant. So HCC or hepatocellular carcinoma, this is not metastases, this is a liver cancer itself. So, cancer developing a primary cancer from within the liver. Biggest risk factor worldwide is cirrhosis. Um As we've talked about plenty of this talk. Um and then patients with cirrhosis, um you know, if they're gonna be, usually if they're gonna be a transplant or if they're gonna be a candidate for transplant, they'll go into what's called the HCC surveillance um list. Uh So this is, this involves basically six monthly ultrasounds and also an A FP level, which is the tumor marker that would be raised in a HC. Um Unfortunately, you know, the prognosis with these cancers can be poor because it can present late. And that's why, that's why the HCC surveillance um scheme is set up just so these things are, these cancers are caught early. Um But they will, it will, you know, at the point of presentation, if, if they've not been surveilled, they might have quite nasty pain. If it's big enough, they could have a palpable mass. Um and then everything that comes with sort of decompensation, maybe, maybe jaundice worse than ascites and stuff. Um They'll probably notice a good bit of weight loss because that tumor will be uh eating up a lot of nutrients. Um You'll want to get more definitive staging scanning done. So, Mr MRI or CT, usually full body ct, chest, abdomen, pelvis for staging. And um typically, uh you want to get a biopsy of this done by the IR team. So CT guided or ultrasound, guided biopsy, um Management of this, you might, you know, if you're gonna get do surgery if it's small enough. And as you can see from that, and obviously, that's quite a big tumor, but if it's resectable, so if it's actually do you know if it's not deeper than the liver, it's sort of close to the liver edges. Yeah, some patients would, would go for a, a surgical resection. And so it's removing a, maybe like a wedge resection or removing a AAA small amount of, of the liver that contains the cancer and good margins. Um If it's, you know, if it's big enough or uh if it's in their best interest, perhaps they've got cirrhosis uh and they meet the criteria, you probably wanna transplant them other treatments if they're maybe not at the point of transplant or if they're not fit for something like that, you can do um what's called radio frequency ablation sort of with, with, with, with the radio waves or you can do another fancy um procedure called a tace. So there's two parts to this tace would be um it again done on, done by the interventional radiologist. So it's chemo embolization is the, is the key part to the name. So you the IR doctor will go in with um will will use this, this technology to, to trace the, the specific artery that's, that's supplying the tumor. They'll go in access that artery and deliver a small amount amount of chemo via that artery specifically. So that, that chemo is only going towards that tumor. And then, you know, at the point of withdrawal, they'll then embolize that vessel so that no further blood flow can go there. So it's sort of a two in one. You're, you're, you're, you're blasting a lot of chemo at it and then you're stopping any further blood flow to prevent um it from growing any further. And so it can be quite a successful treatment for patients with small sort of nodular HCC. Um And then other other, other important things to consider would be radiotherapy, sometimes palliative radiotherapy. Uh and there's certain targeted therapies with, with, with monoclonal antibodies that might be considered as well for this very fine. Then um just to talk a little bit about liver transplant, um either you're either gonna get a transplant or a whole liver transplant from a deceased donor or you can get what's called a living donor transplant, which is a portion of their liver. Obviously, they're gonna need to keep a portion themselves. So it's a, it's a portion of their liver that you would get transplanted. Um And there's specific criteria for the living donor transplant. You need to make sure that they're an appropriate match and that kind of thing. Um When considering transplant, either they need a liver, uh they need a, a liver acutely or if they're a chronic failure, then they go onto a waiting list. So typically patients that present with maybe a very nasty hepatitis from a virus or a paracetamol overdose and these patients are sort of teed up with King's College in London and flown over quite urgently. Um They'll be in 60 over in the royal or they'll be in ICU and then they'll get flown from the roof of the royal over to King's and get transplanted, stay there for a wee while and then come back. Um But patients who are on the waiting list for the, um if they've got chronic liver failure, typically we'd be waiting maybe 4 to 5 months at the moment for, for a, for a liver and again, based on their child p and their male scores. Uh the, the, the waiting waiting times can vary for certain patients and their suitability for it. Um contraindications for a transplant. Then there are, there are a few, that's why the, the criteria, it's such a strict process as to who is suitable and who's not. So, if you've got quite significant comorbidities, you, you're not gonna survive, survive the transplant essentially or the extent of the operation. So, if you've got quite advanced sort of cardiomyopathy, uh, or quite advanced COPD, um, you might, you probably, you know, it wouldn't be fit for the surgery. Um, if you continue to drink alcohol, of course, is a major. No, because it's, you know, essentially deemed as a wasted liver. Um, if you've got an untreated HIV, uh and also if you've got, um, cancer that's outside of the liver. Um, typically these patients would be considered for liver transplant, but there are certain factors that come into play and depending on how aggressive the cancer is uh extrahepatically. Um And finally, just a bit about post transplant care, these patients have to be on lifelong immunosuppression because it is a foreign body, a large foreign body living inside their body. Um, so their immune system is going to be, it needs to be suppressed. Otherwise, there's a high risk of rejection if they're not on adequate immunosuppression. And again, if they're on too much immunosuppression, then they're at risk of overwhelming infections. So a lot of patients might be on um like a, like a long term or lifelong antibiotic, prophylaxis and anti antimicrobials, antifungals and things. Um It's important that they're reviewed by the hepatologist at clinic. Um, they get followed up, um, and monitored for disease recurrence. Um And typically lifestyle implications are also emphasized um sometimes, but, you know, patients do relapse in terms of their alcohol. So they might, um, you know, if they, if they relapse it's, it's, it is unfortunate. So it's all, it's all about, sort of encouraging uh through CBT and, and substance misuse teams, sort of avoiding it. And that's us, apologies. That was, it's, it's quite a beefy talk. II think we're about an hour and 20 minutes here. But um are there any questions at all? There's a couple of we, I can't actually see it. Oh no, there we go. Oh, sorry. People are typing uh grand. Um I have a couple of wee I know I don't wanna keep you much longer. I have a couple of wee questions for you just to make it even more interactive. Um Do you know what? I'll just stop the, I'll stop the. Oh no, I'll just keep it going let Queens do that. So. Um ok. Um Just about, I think it was about four questions I've got for you. So 65 year old man comes to, he's had three episodes of passing dark stool at home and this is associated with feeling a bit lightheaded and dizzy. His past medical history includes COPD, a bit of reflux. He's got cirrhosis confirmed. Uh and he also has type two diabetes. His hemoglobin on admission is 85 and his BP was, he was hypertensive. So 95/60 he received some, you know, adequate IV, fluid resuscitation and, and improved for a period of time. But actually then on the ward suddenly has a large volume, uh vomit containing bright red blood. So what do we think in this case is the most likely cause of the bleeding? He just want to either shout them out or put it in the chat, whatever suits see what people look in the chart date. D Yeah. Spot on. So you have to, you know, sort of take home. I think here is anybody with confirmed cirrhosis and they have an upper gi bleed. You really need to suspect viruses, um, or it's viruses until proven otherwise. Ok. Um And I tried to throw you off there by saying you had reflux and maybe make you think it might be an ulcer. But I think really the mainstay here is if they've got confirmed cirrhosis or if they've got confirmed portal hypertension, but, you know, you're not 100% sure that they have viruses always assume it's a virus. He bleeds because they're more, they're more, they're, they're more likely to exsanguinate quicker on that, you know, that are not usually than an ulcer but yeah, well done. Um, same. So, uh same, um, same stem of the question then, but then which of the following doesn't form part of the initial management plan for this guy? What do you think? Couple seven B. Yeah. Um Absolutely. Yeah. Tranexamic acid is not great. Uh It doesn't actually do, doesn't improve outcomes. There's been a big study um in the past doesn't improve uh outcomes in terms of their um in terms of overall mortality from gi bleeds and actually, uh uh will apparently increase your risk of um thrombo thromboembolic events like a DVT or a PE. So it's avoided in gi bleeds. Um That's the take home there. It's better for gynecological urological tract bleeding but not, not typically used in gi tract bleeding a couple more. Um So a young patient, 23 year old female comes to Ed, she's got abdominal pain, she's passing quite a lot of stools per day. Um and they're bloody as well. She's got a history of, she normally receives infliximab every eight weeks at the clinic which of the following doesn't form part of her initial management plan. Mm We bit tricky, understand. But what do you think? What do you reckon? Just think back by, think back about what I know some people are saying. So we've got CD um C and D. OK. So think back as to what I told you before. Um anybody coming in uh like I said before, anybody coming in with what sounds like a flare, what you want to do first is absolutely make sure that it's not an effective cause. So just hold off on the loperamide temporarily and make sure that you send your fecal O NS and C diff tests or send samples sorry for those tests just to rule out an effective cause. All right. And then last one guys, just a wee bit of hepatology very quickly. So, um this is a 50 or 50 year old lady, um, comes to or attends her GP. She's noticed that she's passing sort of loose, uncomfortable stools. She's also found that they're quite pale. Um, and she's been feeling a bit unwell for a month or so. Uh, she's noticed that her urine is also quite dark but she's been drinking plenty. So she's not too sure why. Um, she has no past medical history of note and the GP does routine bloods and finds the following on her LFT S. So she's got slightly raised, Billy A L PS up. Uh, reasonably A LT and AST are ok. And the Gamma GT is up a bit as well. So, which of the following autoantibodies do you think is gonna most likely be positive in this, in this lady's case? A bit of a harder question. But, um, I don't think they'd be too, I don't think they'd be too harsh and give you a specific anti or autoantibodies. But it's, it is good for the exams to know sort of the barn or autoantibodies for each condition, but not the rarer ones, I guess one of God on for a, just the one. Ok. Uh, yeah, you're spot on it. Is antimitochondrial. Does anybody know for bonus, bonus points, what the condition is? Primary biliary cholangitis? Absolutely. Yeah. BBC. Brilliant. Um, I try again, try to throw it off a wee bit by saying she's not, she's not got any past medical history. You know, sometimes if, if I maybe said she has celiac disease or type one diabetes, she might have thought it might have been an auto autoimmune picture. But, yeah, you're absolutely spot on these sort of vague symptoms of a month. Feeling. Not great. She's noticed or she's, we're picking up on the fact that she's a little bit jaundiced. She's not maybe clinically jaundiced. But uh but, you know, she's, she's or sorry, not clinically. She's not, maybe, you know, she's not, maybe her complexion maybe hasn't changed, but she is sort of heading that way in terms of that slow presentation of PBC. So, yeah, well done. Uh I think that's, that's me. So thanks very much for listening. If you have any questions at all, it doesn't have to be gi or hepatology related, even if it's just about foundation years or whatever you can, I've left my email there. You can get in touch. Um One more thing I'd ask if you just, if you don't mind. So it's important for our portfolios and our training. If you don't mind just filling out a wee feedback form for um foundation for finals just based on the, the talk this evening, that'd be great and yeah, thanks a lot for listening. Hope you took, took something home. Thank you. No problem. Thanks a lot.