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Ok. Hi. Can anyone hear me? Um, on my mind? Just popping a uh, a message in the chat just to check? Perfect. Thanks very much. Right. So it's just gone six o'clock. I think we'll make a start there. So, to everyone who's just arrived, thanks very much for coming. Um, I'm Dan. I'm one of the F ones in the Northwest region in Liverpool. Today. We're going to be running our series on H PB as part of the mind the Bleep final year series. So hopefully we'll get some good revision in. Uh I'm gonna be presenting this one but my colleague Sara also made a few of the slides, um and just that recording as well. If that's right, we've got some SBA S questions coming up as well. So we'll get some polls going for that. So let's get started. So, aims of this session cover some of the common H PB presentations and conditions based off the UK MLA curriculum. I've got some SBA S as I've just said to try and aid your revision, um, recognition. So presentations, initial exam, investigations, management of these conditions and your role as an F one and I'm actually on a gen surge placement right now. So it's worked out quite well. It's quite convenient. Um, ok. So based off the UK MLA content map here are some of the things we're going to cover. So all the gallstones and the cholecystitis, the biliary pathology, pancreatitis, a couple of the cancers as well. And then the presentation. So things like abdominal pain, jaundice change in stool, color, nausea and vomiting. Right. So we'll start with the first question. Then 40 year old woman called Gabby Alston comes into the emergency department with the sharp right upper quadrant pain nausea. And it came on after eating her Christmas dinner on examination, she has a large body habitus. She's afebrile and the pain settles quickly with analgesia. So, what's the most likely to be raised on blood tests? And if I just start the poll there, I'll give you probably about 2030 seconds just to answer. And, um, by the way, if, if anyone has any questions, just feel free to pop a message in the chart, I can, I can see it as well. So, uh, not a problem at all. All right. So about 55, 10 more seconds if you don't know, just, just have a guess it doesn't really matter. Um All right. So, um, if the thinly veiled pun of her name didn't give it away, this is a typical presentation for gallstones. So simple Biliary colic. Um, so Gabby Alston Galston, um, So, if we go to the next slide, you can see the answers. Ap. Um And so why is the gallstones? Well, it's the typical kind of demographic. It's a forties, lady, large body habitus. It's got none of the features of cholecystitis or cholangitis. So, it's, she's afebrile, most likely the inflammatory markers will be normal. Um, and it's exacerbated by having a fatty meal, a, a, the Christmas dinner and it settles quite quickly with analgesia. So why is ap raise? Well, usually with, um with biliary colic and biliary biliary pathology, you get a cholecystic or cholestatic picture on the LFT S. So the T and the AP will typically shoot up. You only really get raised a LT when, when it involves the liver and the actual hepatocytes. And that's a bit more concerning. Um but usually in just normal biliary colic, you know, your at will most likely be normal um in terms of bilirubin. So that's related to jaundice, you usually get that if something's actually physically blocking the passage of bile through the bile ducts. So you might see that if there's a stone in the common bile duct, but not necessarily, if you just have gallstones in the gallbladder, amylases related to pancreatitis, we'll come on to that in a bit. Um And albumin is probably be normal, to be honest. But if, if, if, you know, in acute inflammation or malnutrition, it's lowered. So it wouldn't be raised really. Ok. So let's get on to gallstones. So, gallstones are very common, especially in western society, about 10 to 15% of, of Westerners have gallstones and most of the time they're asymptomatic. So, in the vast majority, the people won't have symptoms with them. And that's great because then you don't need to investigate them or treat them only between one and 4% actually get symptoms. So, what are they made of? Well, most of the time they're made from either cholesterol or mixed cholesterol and pigment. Ok. And that's related to the whole large body habitus fatty foods kind of picture. In terms of pigment stones, you see those with um you, you see those with conditions like hemolysis or hemolytic anemia. So when the red red blood cells get broken down because then the hemoglobin gets turned into bilirubin and those can form uh bile bile pigment stones if you have too much of that. So the key risk factors, the five fs female fat, 40 fertile, uh not to be confused with the five fs of abdominal distension, fat, fluid, flatus feces and fetus. Um also hormonal causes or risk factors. So the pill C OCP pregnancy bowel malabsorption can also increase your risk of pigment stones. So, if you have Crohn's, for example, it's inflammation of the terminal ilium. So the end of the ilium is one of the key places where you actually absorb, absorb bile salts. So if it's inflamed or you have a terminal resection, you won't absorb bile salts as well and that can also predispose you to pigment stones. Uh And as we've talked about hemolytic anemia, so the breakdown of the red blood cells, um so more, more hemoglobin gets broken down to bilirubin and bile pigments increases your chance of getting stones. Um Then here just in this little box on the top, right, we've got a few of the, the key terms and definitions. Sometimes people can get confused between, uh I think probably the main ones, cholelithiasis and choledocholithiasis. So just to clarify choledocholithiasis specifically refers to stones in the, the common bile duct or the CBD rather than in the gallbladder, which is cholelithiasis. And then another one's a cholecystotomy, um which is insertion of a drain into the gallbladder which you might see in someone with a gallbladder, empyema. So, a collection of pus in the gallbladder or in someone who's not necessarily fit for a full cholecystectomy. Um and gallstones, as we can see in this sort of diagram can cause biliary colic. They can cause cholecystitis, cholangitis, and pancreatitis and what will come on to all of those. But it's a problematic little thing. The humble gallstone. So clinical features while you have the classic sharp colicky, right, upper quadrant pain related to fatty food. Um Does anyone know why fatty foods causes that classic colicky pain? If you know it just, just pop it in the chart. Oh, just take a guess Um, so it's related to, um, cholecystokinin. Yeah, that's right. Yeah. Um, so I hope I pronounced that right. So, yeah, fatty acids from fatty foods stimulate release of cholecystokinin from eye cells in the duodenum which then causes contraction of the gallbladder. And if you have a stone impacting at the neck, you know, blocking it off, it's contracting against a blockage and which causes that classic colicky pain. You might also see nausea and vomiting and the key difference from cholecystitis is the lack of an inflammatory response. So, systemically, these patients are, well, they are inflammatory markers are the white cells. CRP is normal, they won't have a fever. The pain will be intermittent rather than constant. It will settle with analgesia related to fatty food as I've talked about. Um and cholest cholecystitis, you'll see the Murphy sign, which will also come on to in a little bit. So the key investigations, um it's always good, especially if you're in an ay situation to try and structure things like investigations to stratify into bedside blood imaging. You know, more specialized investigations. I always start with the simple things like bedside tests, pregnancy tests, good tests in any acute abdominal pain in a woman to rule out a pregnancy urinalysis as well. So, checking for uti blood, you know, you're simple full blood count using these CRP LFT S. Again, we've talked about you might get a, a cholestatic picture. Um but they can also be normal I've seen a patient this week with gallstones who've had completely normal bloods. So sometimes it's normal um imaging. So first port of call is usually an ultrasound. It's very accessible. It's easy to do uh doesn't have radiation, it's cheap. Um And depending on that, then you might get some more detailed imaging with an M RCP. And usually, so you won't do that on everyone. It's quite selective. It's a very good image, it's very detailed, but it takes a while. It has to get vetted by a consultant at least where I'm working. But it gives you a much more detailed image and reasons why you might want that is if you, for example, on the ultrasound, if you see the, the common bile ducts dilated, so then you, you want, you want better imaging to look to see if there's a stone in the common bile duct, which isn't always so easy to see on ultrasound. Um Or if the LFT S are really deranged, you might want a better look with the M RCP. So that's a bit further down the line. Sometimes you might also get act, you might see people ordering CT S if you're not really sure of the cause. It's just a good kind of, it's like a surgeon's best friend. Really. They love ordering CT S as just a starting line because it gives you so much information. Um Probably less often you might see an E US which is an endoscopic ultrasound. So you put a scope down the esophagus stomach and the duodenum with an ultrasound probe, which can give you some pretty good information. I think it's probably used a bit less these days because M RCP is noninvasive obviously and it provides really detailed imaging um but good to bear in mind. Um So I've got a note here. So according to nice guidelines, consider M RCP if the ultrasound is uh has detected common bile duct stones, but the duct is dilated. So that's more than six millimeters in diameter, although it can also increase a bit with age. Um And if the liver function tests are abnormal, ok. Management is basically conservative in, in the acute phase of just treating the pain, simple things like IV, fluids, analgesia, antiemetics and giving them some lifestyle advice. So, avoiding fatty foods. Um and that's another good tip in oss as well. If you asked about the management stratify things in terms of conservative and supportive treatments first and then some more definitive treatments. So the definitive treatment will be an elective laparoscopic cholecystectomy. So taking it out, removing the cores that will typically be done a few weeks down the line. Um And if you find any bile duct stones on investigations or during the operation, it's a good idea to clear those as well. Okie Dokey. Um Let's move on to the next slide. So, next question, then, um 32 year old man Colin citti presents with uh constant right upper quadrant pain, fever, nausea, and vomiting. He has a history of gallstones but has not had surgery yet. He has raised inflammatory markers. He's not jaundiced, but if Murphy's positive on examination. So, what's the most appropriate first line imaging um in this patient? And I'll just put the pole up the. So again, I'll, I'll give you between 2020 30 seconds. Um And yeah, I II probably gave away the answer in the last couple of slides. But um yeah, the poll is also just completely anonymous. So don't worry about getting the answer on it. I can't really see anyway, like who, who is? OK. So answer is ultrasound abdomen. It's just, you know, if you get a question that's asking for the first line investigation, um you know, imaging wise a lot of the time it's ultrasound. It's just, it's a good one. Uh So uh again, another thinly veiled um terrible pardon? Citti. So this is cholecystitis. Um Why is it cholecystis as opposed to bia colic? Um So the pain is constant or upper quadrant pain is constant. His murphy's positive he has a fever. Uh He has raised inflammatory markers, he's not jaundiced. So we're not thinking of cholangitis just, just yet as the most likely thing. Um So as I explained earlier, ultrasound abdomen's are really good first investigation because it, it'll let you see the gallbladder, any stones in the gallbladder. Um and you know, especially if that's your main differential, it doesn't have radiation simple, easy to do. Um Again, you might consider Mr CPA bit further down the line if you need to look in more detail. And E RCP is not an imaging a modality, it's an intervention. Ok. So, acute cholecystitis, then um it's inflammation of the gallbladder. So presents similarly to biliary colic. But as we've discussed with the question, you get those features of being systemically unwell. So the fever, the raised inflammatory markers. So the raised white cells and crp um the constant rather than the intermittent colicky, right, upper quadrant pain and also just watch out for the features of sepsis. So sometimes in rare cases, they might have a perforated gallbladder um which can cause more um you know, a worse infection. So look out for the hemodynamic instability. So the low BP and the tachycardia signs of peripheral shutdown um on examination, you'll see the right upper quadrant tenderness. You might see some gardening as well as a tensing of their abdomen. If someone's frankly peritonitic, they'll have that classic hard wooden board abdomen. Um or they might have some localized peritonism. So hardening tensing of the muscles just in the right upper quadrant and the Murphy sign. So, does anyone know what exactly the Murphy sign is? If you, if you just wanna quickly pop it in the chart? Ok. So the um what you want to do is you know, uh So pain on inspiration. Yeah. So, yeah, that's um it's kind of that. So while you have them flat on the bed and you, you're doing your abdominal examination, you ask them to inspire so to breathe in. Um And then when you're pressing down just over their gallbladder, it's a Murphy's positive sign if it kind of halts their inspiration because of the pain. So if they're breathing in and you press down and they kind of stop their inspiration. So, um that's Murphy's positive and that leads you towards the diagnosis of cholecystitis. So, investigations as we've talked about, always try and stratify these into bedside, you know, bloods, imaging and then further kind of more invasive tests if you need. Um So bedside, we've talked about those already that, you know, same things, pregnancy test, urinalysis, maybe an ECG if they're tachycardic as well. Um Bloods. Yeah. So same as the last time FBC using these C RP LFT S again, there might be cholestatic. So the raised A LP and GGT um probably want to take an amylase as well to rule out pancreatitis. It's, it's just a common add on to any set of bloods you do with abdominal pain, um imaging, we've already talked about all of these. So next few slides, we're just going to go over a few, we're going to go over these images here in a bit more detail. Got these off radio, which is a really good site if you want to see any radiological scans and they have a really generous policy in letting people use it for educational purposes. Um ok, so this is an ultrasound. So you can see here it's a pear shaped sort of organ. You can see the stones actually inside there near the neck and there's areas of opacity. Um And so what, what kind of things are you looking for on ultrasound? There's stones obviously, but so gallbladder wall thickening, which indicates inflammation or any fluid collections around the gallbladder, any fat stranding, which indicates inflammation as well. One of the things you can do is it's called the sonographic Murphy sign. Um So that's, that's when you can use the ultrasound probe to see that the point of maximal tenderness is directly over the gallbladder when you're pressing down. And it's just the radiological correlate of the clinical Murphy sign. Uh This is act so a Coronal section. Um CT ah And as the report says on the right here, you can see that there's wall thickening, so mural thickening. Um There, there are, there aren't any gallstones, so it's acalculous. Um and there's a, there's an incidental hepatic cyst at the top of the, the liver and then this, this is an M RCP. So MRI of the looking at the liver and the gallbladder, you can see quite nicely those stones there, there's a bunch of stones just outlined there. Um So again, on the report you can see there's thickness, thickness of the wall. So try try and have a look at that in the image. Um mural thickness, some fat strobing as well. And so it indicates inflammation. Um but yeah, that's quite a nice picture. Also, the CBD is dilated on this. Um You can see in the report it says it's 11 millimeters, remember it's usually less than six millimeters in diameter of the CBD. Um But again, it slightly increases with age. So if you see someone who's like 80 with a seven or eight millimeter CBD, it could be normal. So management quite similar to just biliary colic, except you're going to add in antibiotics. Um Typically, you know, it will be like keen Met. So, Keim IV and metroNIDAZOLE orally. So that covers the abdominal infections. Um but again, never forgetting things like analgesia IV, fluids, antiemetics, all the basic things. Um and also lifestyle advice as well. So reduce fatty food intake and then moving on to the definitive treatment. Again, it's surgery. So there's a couple of ways you can do this. There's a, there's a thing called a hot versus a cold like coli and hops when you do it pretty quickly. Immediately nice recommends doing it within a week, within a week of symptom onset or presentation if you're going to do it in the acute phase. But really, it should be probably within a few days. Um And that's because as the inflammation goes on over time, it can distort the anatomy. It can cause adhesions and it can increase the likelihood of complications during the surgery. Um, so if you can't get it in that window or surgeon preference, whatever it is, and you can do a cold one where you treat them conservatively at the beginning in the acute phase, you give them antibiotics and then you bring them back for an elective lap co later on once everything's settled down. So you can do it either way. It's, you know, it kind of depends on local guidelines, surgeon preference, whether you've missed the window of opportunity. Um Alternatively, if they're not fit for surgery, you can do a cholecystotomy. So putting a drain in or if they've got a gallbladder and pyema. So we had a patient on the ward last week who had a gallbladder and pyema. He's been waiting a while to get his cholecystectomy and just end up getting a drain in the end, um, to, to relieve the, um, the pass in his, in his gallbladder. But, uh, you know, eventually, um, those patients will also need a cholecystectomy afterwards. Right. Question three. Moving on to the next 1, 52 year old woman complains of right upper causing abdo pain, radiating to the epigastrium. Also nausea and vomiting. She has scleroticus. She's tachycardic, she's hypotensive and she's got a fever temperature. Uh, she started on antibiotics. So, which of the following is not true. So, sorry. About the negative question. Um But you do, you do see them on exams. So, OK, so uh the the one that's not true is e so um you may know Charcot's triad is right, upper quadrant pain, jaundice and fever. Raynaud's pentad is basically just that those three plus hypertension and confusion. So more features of sepsis really. So the the key thing is hypertension rather than hypotension. Um perhaps a little bit sneaky. um but just going through all of the others. So yeah, just to clarify this is cholangitis because you can use Charcots triad to, to work that out. Um So common bile duct dilatation is often seen on imaging. So it's usually because the most common cause is gallstones C which cause obstruction, blockage dilatation of the common bile duct. Um LFT S do show a cholestatic picture a lot of the time with elevated bilirubin because um because the bile is stuck there, er and it er extravasate into the blood. Um and the infection is often associated with the E coli. So um e coli you you might know can cause UTI S. It's also a common common cause of biliary infections. So, uh it's good to know, you know, no one likes micro questions but that that's probably uh one to remember e coli and biliary infections, right. So, acute cholangitis, ah inflammation or infection of the biliary tract due to obstruction. So that's really the key thing here. The obstructing whatever it may be stone in most cases, um blocking the, the common bile duct. So, um, there's a nice sort of diagram here on, on the right showing the different, um, bit of the anatomy of the bile ducts. So at the top, you've got, you've got the hepatic ducts coming from the liver. So the left and right hepatic ducts, um, and they come together to form the common hepatic duct. And then we've got the cystic duct coming from the gallbladder which joins the common hepatic duct to form the common bile duct to the CBD. Um And it's in the CBD where the blockage usually occurs. So, what's the pathophysiology of it? Um So you get a bile outflow obstruction and stasis. So, let's say a gallstone has dropped from the gallbladder into the CBD and it's got lodged there. So the bile is obstructed and there's stasis and then you get bacterial seeding and contamination. And I think that's theorized to come from the portal vein, um which comes from the gut and it runs in the, you know, with the portal triad, you have the, the bile duct, the portal vein and the hepatic artery, they're all close to each other. So you can get bacterial translocation into the common bile duct from the portal vein. Uh She's got a question here how to differentiate between cholangitis and cholecystitis. So, the main, the main thing really is the jaundice. So, cholecystitis will have the right upper quadrant pain, fever, inflammatory markers. Uh clinically, the main differentiator is the, the jaundice and the raised bilirubin on bloods. Um And that will further be confirmed on imaging if you see a dilated common bile duct because that means, you know, something's probably obstructing there. Ok. Um So you've got, you've got the blocked, the blocked tube, you've got the, the bowel sitting there, it forms a sludge, the pressure increases and then eventually you get extravasation of, of, of the bacteria growing there causing sepsis. Um So, one of the causes, while gallstones we've mentioned is the most common. So that's intraluminal. You can have malignant causes cholangiocarcinoma or further further down, you know, um pancreatic cancer, particularly around the ampulla in the pancreatic head. Sometimes it can be due to instrumentation. So E RCP or surgery um other slightly less common causes primary sclerosing cholangitis or PSC can cause stricturing fibrosis, scarring, which can narrow the duct again, leading to obstruction, sometimes pancreatitis as well and rarely parasites, but I'd say gallstones, malignancy are probably the most likely ones. And so clinical features as, as I've mentioned, jaundice is the the main differentiator from cholecystitis. Er And you get, you get that Charcots tried. So, if you, if you see those three and the question stem, it's probably going to be cholangitis. Um Plus hypertension confusions, Raynaud's pentad. Um And so uh we get the, the dark urine and the pale stool. Uh does anyone want to quickly hazard a guess at how that, how that comes about. Um, so, um, yeah, so, so, um, the pigment, so bile bile and bile shots cause pigment in your stool and your urine. So, um, if you have a blockage in the bile ducts, then the bile can't get into the gut anymore. Can't drain into the duodenum. So you don't get, you don't get the stercobilinogen right in your stools coloring it brown. So it, it goes pale, it goes white. Um And because the um because because it's conjugated bilirubin because it's after it's been conjugated in the liver, it's water soluble. So it goes into your urine and colors it dark and it's not just like dark yellow, it's properly like Coca Cola dark. So key things to ask if you see someone with jaundice and you're worried about, you know, post hepatic jaundice um is to ask them about, you know, have they got dark urine? Have they got pale stools? Um We actually had a guy a couple of weeks ago who he, he did have jaundice and he did have dark urine. Um but he also had dark stools, but we, we think that was because he drank like 20 pints of Guinness the night before. So, um it, yeah, it's there, there are confounding factors. But uh it's a good question to ask. Um And yeah, eventually, of course, it can lead to features of sepsis when you get the disseminated infection. So again, investigations don't forget the bedside ones, ecg pregnancy test, urinalysis among others bloods, all the usual ones you probably want to get a clotting and a group and save as well. Um Why? Because in cholangitis, one of the main interventions is the RCP, which is a slightly invasive procedure. So you're going to want to get a clotting screen before that as well. Um Perhaps a group can save, especially if they're anemic um to start off with going to get some blood cultures as well. So a key thing is to invest early on in that microbiological diagnosis, ideally before you've given them the antibiotics, but of course, if they're really ill, just he's given the antibiotics. Um but, you know, try and get the cultures first, um blood gas as well. You can look at lactate, you know, do the whole sepsis, six. Uh imaging ABDO ultrasound is a good one. It can show again as we've talked about CBD dilatation. So if you, if you're suspecting some kind of obstructive jaundice and cholangitis, um then it, it can confirm it can, you know, confirm that with CBD dilatation. Um And again, you know, similar further investigations, you might consider where your seniors might consider M RCP. If there's diagnostic doubt or to plan E RCP, you can maybe do an M RCP to have a better look at the anatomy um or to better see the common bile duct and where exactly the obstruction is where the stone is or whether the malignancy or lesion or whatever is. So, we've just got a couple of pictures here on the right of the E RCP, which is, I guess it slightly on the wrong slide because it should be in management. But you can see they go through the stomach around the first part of the duodenum and part way down the second part of the duodenum, they uh they go into the, the major propeller. So through the sphincteral body into the common hepatic duct and you know, they can remove stones. Um So it's, it's both a, a diagnostic and a therapeutic intervention. E RCP. Um Speaking of, so management, um it, the, the, the definitive management is the RCA P but um again, not forgetting the conservative um the conservative management to start off with. So you're going to do the sepsis six, probably because, you know, they, they have an infection going. Um So you're going to take those blood cultures, take any other cultures, you want to get, take the bloods, lactate, catheterize them, get the urine output and the fluid input output balance going, you're going to give them those antibiotics. If they need oxygen, you give them oxygen, probably going to give them some IV fluids as well. Algesia and antiemetics. Um And the reason the reason why E RCP is the definition of management is because you need to relieve that obstruction, that's what's causing the picture here, the obstruction and the bile ducts. Um So yeah, that's why, but it's not risk free. E RCP is associated with a number of pretty serious complications. So, pancreatitis, for example, which we'll come on to repeated cholangitis, strictures to any instrumentation can cause stricturing um bleeding and even perforation, which is quite serious. Obviously, I might need surgery. So it's not risk free. It's definitely something you don't want to take it too lightly, you know. Um But if, if the RCP is not suitable for whatever reason, percutaneous transhepatic cholangiography is another thing that you can consider. So you go through the skin, so you go through the the skin to cannulate the bile ducts um through the intrahepatic bile ducts in the kidney itself. Um You probably don't need to know too much about that, but just so it's a second line. Um if the RCP is not suitable. Um And sorry. Yeah, they'll probably need an elective cholecystectomy eventually as well if gallstones is the cause. Um Yeah. OK. So question four, let's just put the pole up first and then I'll read it. So 62 year old man presents with a two month history of progressive jaundice reports, feeling fatigued, itching, dark urine, past medical history of alcohol abuse and obesity denies any recent travel or sick contact and has no history of abdominal pain, nausea, vomiting or fever, which of the following conditions is most likely to be associated with conjugated hyperbilirubinemia. So, it's one of those ones where you sort of don't need the stem. You can just go to the question, isn't it? Um, yeah, I'll give you, uh, about 1520 seconds. So, yeah, I think most, most of you got that right. It's, uh, obstructive jaundice. Um, I think, yeah, I also probably gave that away in one of the previous slides, but, um, conjugation happens in the liver. Right. It, um, it's the, what is it, it becomes glucuronyl or something which makes it water soluble. So, obstructive jaundice is posthepatic. It happens after it's been conjugated in the liver. So, such as by a pancreatic carcinoma. Um So as you can probably guess we're moving on to jaundice now. So, uh it might look like a pretty busy slide. But I think the main, the main thing with jaundice is just probably to understand the um the principles of it rather than learning every single cause. So, you know, the prehepatic intrahepatic or hepatic and extrahepatic or posthepatic. So, prehepatic generally to do with hemolysis, um hematological disorders, spherocytosis, sickle cell, hemolytic anemia, anything where the red blood cells are, you know, being damaged or they're, you know, not great. Um And it causes an unconjugated bilirubin. Ok. Because that's um this is before the bilirubin has been conjugated in the liver. Um So again, things like Gilbert's spherocytosis, sickle cell G six PD, you know, those are some of the P ES ones aren't they or um, um, yeah. So any, any, anything to do with hemolysis, crippling a jaw syndrome as well? That, that's, um, that's a, that's a disease where you can't conjugate um, bilirubin properly uh in the liver due to an enzyme deficiency, um intrahepatic. So, it's basically anything that directly damages the liver and the hepatocytes. Um, and it leads to both an increase in unconjugated, unconjugated bilirubin. Um because if you damage the hepatocytes, it reduces their ability to conjugate bilirubin. But you can also get structural structural damage to the liver that can impair bile flow, um causing obstruction, leading to some conjugated hyperb as well. So things like hepatitis viral, hepatitis, autoimmune, hepatitis drugs, alcohol, liver disease, not food. Um PBC and PSC can also cause uh posthepatic or obstructive. But eventually, you know, they can also cause cirrhosis and that can cause um you know, he hepatocyte damage as well and also hepatocellular carcinoma, extrahepatic. So, anything that obstructs the bile if you cannot conjugate Billy R. So just a question here from Zain. If you cannot conjugate bilirubin in cri in a jar, would that not make intrahepatic? Um It's, I guess that's a good question. Um I think it's, it's mainly classed as a prehepatic because um you get, you get a purely sort of unconjugated hyperbilirubinemia. So, in an intrahepatic, you'd expect a kind of mixed picture of both conjugated and unconjugated hyper bilirubinemia. But um with crile in a jaw, you're getting that pure uh unconjugated hyperbilirubinemia. So, I guess, you know, anatomically, it might be intrahepatic. But the, the kind of picture you see on the blood test with the bilirubin um is uh is, is pretty hepatic and then extrahepatic obstruction of bile leads to conjugated hyperbilirubinemia. Ah, it can be due to intraluminal causes like gallstones, as we've discussed, probably the most common cause mural. So, within the wall itself, cholangiocarcinoma strictures or extramural. So, pancreatic cancer pushing down on the bile duct, um or sometimes inflamed lymph nodes. So, um for example, I think in gastric cancer, you can get invasion of the lymph nodes around the porter hepatis. So the um you know, around the bile duct as it exits the liver, which can obstruct bile duct, which can obstruct the bile duct. Ok. So, clinical features are going to be yellow, look like home Simpson. Um in cholangitis, they'll also have fever, raise inflammatory markers, pruritus because of those bowel salts, they can cause itchiness. Um abdominal pain. It you know, it depends on the cause of the jaundice. What symptoms you're going to get, doesn't it? So, if you have cancers, if you have cholangitis, cholecystitis, you'll get that abdominal pain. Um If you have obstructive post hepatic jaundice, you, you're probably gonna have the pale stool and the dark urine. So, looking out for those. Um So basically, it it depends on the underlying cause and some of the investigations. So, again, um splitting it into bedside tests here. We've just gone straight for the bloods. Um, so there's a, there's quite a lot in those bloods, but in some trusts in mine, for example, there's an option when you're requesting bloods just to do a, a liver screen, like a bloods, liver screen and it just automatically puts all of those on. So, you know, you don't need to think about it too much. But, um, maybe just for your learning, we'll probably go through a few some of those. So, um um in some clotting studies is important because, you know, the liver produces um a lot of your clotting factors and Vitamin K you obviously going to do a viral hepatitis screen. I want to rule out some metabolic causes like Wilson's and hemochromatosis. Look at the immunoglobulins, um and also autoantibodies in case of autoimmune hepatitis. Um and then also an antimitochondrial as well because of um um you know, things like PPP BCI think it's associated with and then imaging ultrasound CT M RCP, kind of, it depends on really, it sort of depends on the cause which you're suspecting there. Um and diagnostic procedures, um E RCP, which can also be therapeutic as we've talked about in, in cases of um bowel obstruction like cholangitis. Um Or if you think it's just to do with the liver, liver problem, you can do a liver biopsy as well. Um You know, for things like if you think it's a cancer or if you think it's an autoimmune problem as well. Histology might be useful there. So, next question, I will just put the pole up. So 45 year old female comes into s au very severe upper abdominal pain, radiating to the back, uh nausea, vomiting, history of alcohol dependence and gallstones. Her serum amylase is more than three times the upper limit of normal. So, what are we thinking? Mhm. Ok. So the, well, the, the vote so far is, is quite split. Um, it, it is acute pancreatitis that, that's the diagnosis. Um, but the, the, the treatment for, for most pancreatitis is uh conservative management. Um You, you know, you probably wouldn't do an emergency laparotomy unless you're thinking they've perforated a viscous or, or their bowel or something. Um, and you, you wouldn't tend to use antibiotics unless uh there's a good reason to. So if they're spiking a lot of temperatures, fevers, um, if they've, if they have an infected necrotic part of the pancreas, um basically there has to be good evidence of a super added infection on top of the pancreatitis to add antibiotics. But most of the time it's just conservative management. So, controlling the pain, giving them fluids and antiemetics. Um and also nutrition and dietetics is really important in pancreatitis as well. So why is it pancreatitis? Severe epigastric pain? That's the classic, which radiates to the back and the serum amylase is virtually diagnostic. Um, when it's really raised. So I've said it's more than three times the upper limit of normal. That's technically the diagnostic, um you know, level. But so the normal, the normal is about 100. So technically, that's above 300. But a lot of the time you'll see it well over 1000 into the thousands. And that's basically virtually diagnostic. So here's just a, a little break for, for your eyes. Just a diagram of the pancreas here, you can see the duodenum curving around the head in that, in that C shape. Um the gallbladder just just laterally. Uh and those blood vessels there just coming under under the pancreas or the superior mesenteric vessels. Um Another picture of a few labels. So the pancreas is divided into 55 different bits from the uncinate process. So that like kind of hook at the bottom to the head. I mean, you can't see it here, but there's the neck as well uh in between the head and the body. And then you've got the body and then the tail and then you got the pancreatic duct, which at the ulla combines with the common bile duct and then enters the second part of the duodenum via the major papilla. And behind it, you can see the, the portal triad and behind the pancreas, you'll also have the AORTA and the, the IV IVC as well. So a little bit of anatomy. So uh moving on to acute pancreatitis um, it's a really good acronym for the, for the causes. I get smashed. So, um, yeah, I'm not going to read all of them out, but probably the main ones, the most common ones to know are the gallstones and the alcohol. Um, by far the most common two causes about 10 10% are idiopathic, I think as well. So you don't really find the cause. And another one to look out for is E RCP causing it. So, we've got a patient on the ward right now over the last week who's had a really, really severe uh necrotizing pancreatitis after she came in for an E RCP. Um So just reiterating earlier, it can have um you know, I II it is associated with pretty serious risks. Um How does the pathophysiology work? So you get overactivation of the pancreatic digestive enzymes, particularly thinking about trypsin. So you get pepsin from the stomach and trypsin from the pancreas that leads to autodigestion. So, as well as trypsin, you get the lipase which causes fat necrosis, get protease. So trips in the protease isn't, it can digest blood vessels leading to hemorrhage. Uh One of the key things about the fat necrosis is that the uh the fatty acids you get combined with the calcium um with combined with the calcium in the blood or um that leaks from the blood to form chalky deposits. Uh and that, that can lead to low levels of calcium cos they're all getting used up uh combining with the fatty acid. So you can get hypocalcemia with pancreatitis. Um Another key thing to remember is that you get quite serious fluid shifting in third spacing of pancreatitis. So, vascular dilatation, permeability. Um So aggressive fluid management is a really important part of management. Um And we'll come on to it a bit later, but it can also progress to multiorgan dysfunction, pancreatic necrosis. So, uh does anyone know what these are signs? Clinical signs? Yeah. Yeah, that's right. Collins and Gray turners. Um So the, yeah, the bottom one's Collins, that's the central kind of periumbilical bruising, um indicating abdominal hemorrhage and the gray turner sign is on the flanks and that specifically indicates retroperitoneal hemorrhage. Um The pancreas is a retroperitoneal organ if you remember the mnemonic sad PCA um or Macron or whatever, uh the, the peas for pancreas. But yeah, you won't see these in every patient with pancreatitis, but it, it indicates it's become hemorrhagic. So, blood vessels are getting digested and whatnot. Um So we've touched upon the clinical features but um severe epigastric pain radiates to the back, nausea and vomiting, um kind of features of shock. It it can be quite severe, it can be quite serious. So you'll get that, that tenderness, you might get some guarding, distension, reduced, bowel sounds colons and gray turners as we've talked about, you might get jaundice if um you know, for example, if, if the cause is gallstones and the gallstones are also obstructing the CBD. You might also get jaundice. Ok. So investigations again stratifying into bedside bloods. So amylase will be high or lipase in some places. But I think in the UK, it's mainly amylase. So that'll be pretty high. Um, key thing about amylase as well is it doesn't correlate with severity how high the amylase is. So the difference between 5000, it doesn't mean it's necessarily a worse pancreatitis in terms of severity. So it is really useful for diagnosis but not for severity stratification. We use this risk scoring on the right here, the Glasgow Emory criteria to do that. Um but just, just touching on some of the other blood tests. So your usual ones um group and save and clotting in case the hemorrhage, you need to give them some blood products, calcium as well. So as we've talked about, you can get hypocalcemia um and glucose as well. Again, for the, the the risk scoring imaging probably be act to be honest or an ultrasound. Um And then you can also get a, you know, a chest x-ray if you're worried about perforation, co that's a differential for severe abdominal pain. So the modified Glasgow scale is quite a widely used risk stratification um because you know, pancreatitis can be severe, it can require HD or it input early on. Um So this kind of aids and guides that decision. So quite nicely, you can remember it by the acronym pancreas, uh pancreatitis has all the best acronyms. So p pressure, oxygen age neutrophils by that, I mean white blood cells, uh calcium. So again, low calcium renal. So you can get an AK I as well because of those fluid shifts that we talked about. So a prerenal AK I, so looking at urea uh enzymes LDH and AST you might want to add those onto the blood tests as well, low albumin and then glucose. And um so the reason why the glucose might be high is because obviously the pancreas has an extra cr and also an endocrine function. So you get enough damage, you can damage those islets of Langerhans and the insulin producing uh beta cells. So if you're not able to produce enough insulin, then um it can lead to diabetes, you know, secondary to pancreatitis. And that's especially seen in chronic pancreatitis um which we, we weren't going too much into chronic pancreatitis, but it's, it's caused by recurrent episodes of acute pancreatitis. So management as, as we've touched on in the question, um supportive treatment is the mainstay. So just remember that as, as your default supportive treatment, analgesia fluids, antiemetics, um they might need an NG tube if they're vomiting a lot. Um dietician input is really key as well. It's super important. They might need Creon as well because again, because the pathological process is an autodigestion of the pancreatic tissue. They're not going to be producing as many digestive enzymes, they're not going to be producing as many hormones. So, um so Creon supplementation might be needed uh as well as just, you know, nutritional supplements like ensures and milkshakes, um or parenteral nutrition if they can't have anything orally treating your reversible cause. So, if it's gallstones, you can do an ACP, cystectomy will come into complications in the next bit. Um And then, you know, itu input, get that early on if you need it, um alert them and uh yeah, definitive management afterwards. Um So I'm ju I can just say that it's seven o'clock now. So I um we're, we're actually nearly at the end. But if, if anyone does need to go, I'm just gonna put the feedback form in the chart um just in case, but it, it'll probably only take 10 more minutes to be honest. Um So, complications of acute pancreatitis, um the way I would structure this is splitting it into systemic complications and local complications. So, systemic, um if you kind of think about all of those, um all of the criteria in the pancreas, Glasgow, Emory scoring thing, you can, you can kind of relate it to, to the complications. So if you look at po two right, that's related to the lungs. So um A R DS is a, is a systemic complication, you know, so lung inflammation, effusions there might need ventilatory support in itu um hypocalcemia. We've talked about the calcium reacting with the um the the fatty, the fatty acids turning into a chalky, er, deposit hypoglycemia. Again, we've talked about so not able to release as much insulin because of the damage to the beta cells. You get D IC, you can also get hemorrhage as well. So you might need to give them some blood products. Ileus, so severe inflammation, the, the pancreas is literally right next to the small bowel and the duodenum, as you can see in the diagram at the bottom. So it can cause an ileus AK I as well. So, the prerenal AK I, which is why the urea is part of the pancreas school. Um because of those fluid shifts um and then moving on to local complications. So see with this expertly crafted diagram, you can get pancreatic necrosis. So the tissue just dies and that that can become infected. It also reduces the functional ability of the pancreas abscesses. So that that's an indication for antibiotics. Um You, you probably see them spiking fevers as well if, if that happens. Um and you know, you, you might get some radiology input to drain it as well. Um Pseudocysts. So, pseudocysts are these kind of packages of fluid, sometimes blood, um you know, blood and tissue inside that develop around the pancreas and typically you want to leave those be for a little while for a few weeks because a lot of the time they can resolve by themselves. Um, but if they don't, after, let's say, like 55 weeks or so, then you can drain them again with radiology. Um, what are they called pseudocysts rather than cysts? So that they don't actually have, uh, an epithelial lining and a cyst is technically defined by an epithelial lining. Um, you can also drain them through the stomach actually. Um, so if you, if you do endoscopy and you can poke a hole through the stomach and drain it into the stomach sometimes. Uh and then hemorrhage, as we've talked about the autodigestion of the blood vessels. So, um again, blood products um and this is really just a reference table from ah pulse notes. Um is a pretty good resource. I think if you want to check it out for revision, just thought this table was quite nice, highlighting the differences between uh all of these conditions that we've gone through so far. Um So yeah. OK. So next question just coming on to the last, the last couple of, of things here. Um put the pole up. So a 70 year old woman is referred in by a GP to a gastroenterologist. Um, epigastric discomfort, she's developed jaundice over several months, she denies any pain. Uh She's also noted some weight loss on examination. There is no tenderness or mass uh on serology. She's recently developed diabetes. What's the most likely diagnosis? Ok. Doke. So we call time there. So the answer is pancreatic cancer basically. So the key features, um the key, the key features for pancreatic cancer, you can see that the weight loss, that's probably the first one. developing diabetes as well in the context of weight loss is suspicious for pancreatic cancer as well. For a similar reason to the pancreatitis. You know, if, if, if you're losing the functional capacity of the pancreas to produce insulin because of damage to the beta cells, then you can develop secondary diabetes from that um slightly cheeky that there's no mass felt. Sometimes you don't, you don't have a mass, but also just the the presentation of painless jaundice is um a classic, a classic sign which should make you suspicious for pancreatic malignancy. So, painless jaundice is probably the takeaway from this. So, pancreatic cancer presents generally presents quite advanced, quite late and has a poor prognosis. Um risk factors for developing at age. So the older you get smoking, obesity, family history and also chronic pancreatitis, which can be caused by long term alcohol misuse. Uh and most pancreatic cancers are adenocarcinomas. Um because pancreas is glandular organ and adeno means gland, um I probably wouldn't go into too much detail about the less common subtypes, but uh mo most common ones, adenocarcinoma. So the, the cardinal, the cardinal clinical feature is painless obstructive jaundice. Um and if we go down to the bottom called Voices law, that's another classic um clinical finding. So if you can feel a palpable gallbladder in the presence of jaundice in the context of jaundice. Then that also makes you suspicious for pancreatic cancer and in multiple choice questions, that's probably going to be the answer. So, painless obstructive jaundice cos law and then other things like weight loss. Um You know, that that's your, that's your pancreatic cancer. Sometimes in some cases, you can get abdominal or back pain if it's, you know, become invasive, um or, you know, locally invasive and advanced again, the weight loss. Um, sometimes you can, you can feel a mass but if it, if it's got big enough, sometimes you can't. Um, and the, the new onset of diabetes is, uh, makes you suspicious as well. Um, investigations. So the diagnosis is usually with imaging with a CT scan and confirmed with a biopsy with the histology. Ok. Um, and then after you've made the diagnosis, you need to stage it. So a lot of them will probably be metastatic at um, presentation so that the CT tap CT cap and the pet CT as well. Uh, you're going to do your biochemical work up as well. So the LFT S cancer 99 is a pancreatic cancer marker. It, it's not so useful in actually diagnosing it but um, which is not really sensitive or specific but it can be used to monitor treatment. Um, so it's, it has got use. Um, and then some of some of those other er, investigations further down the line. So the management in a lot of cases, it, it's palliative but, um, uh, in some cases, approximately 10% of cases you can do surgery and, um, it's called a whipple procedure. So you take out the head of the pancreas, the duodenum and the gallbladder and the bile duct. But in, in most, and, you know, you sort of patch everything up together in this weird new anatomy. But in most cases, it will be palliative. And you know, if, if, for example, if they have jaundice, if the pancreas, if the tumor is obstructing the bile duct, a good thing to do is put a stent in. So that'll be a gastro gastro procedure. Um putting a stent in to relieve biliary obstruction. Um You know, they might be itchy, they might be jaundiced, might be causing them pain or infections and nopal chemotherapy and radiotherapy symptom control, antiemetics, painkillers. Last question. Last short slide. Um Put the poll in. Ok, I'm very nearly there. Um And if you do go early ple, please, could you fill out the feedback form? It's really useful. So 58 year old man presents with jaundice worsening over the last three months, denies abdominal pain. His stools look pale urine has been dark, takes sulfaSALAzine for ulcerative colitis. He's recently been on holiday to Thailand. Uh He has Hepatomegaly, he's apyrexic and he's hemodynamically stable. So, what have we got here? Last question. Just have a guess. All right. So cool time there. Um So cholangiocarcinoma. Um why is it? So, I suppose, first of all, looking at the time frame, um, so three months he's had jaundice. So it's a gradual process. It's not, it's probably not pancreatitis if it's, you know, acute pancreatitis, if it's been going on for three months. Uh, he hasn't got abdominal pain again. Probably not pancreatitis then or cholecystitis. He's got features of obstructive jaundice. So pale stools, he's got hepatomegaly and he's got ulcerative colitis. So, um I think the th the Thailand thing was probably a bit of a red herring, but ulcerative colitis is associated with PSC primary sclerosing cholangitis and PSE is associated uh with a chondrocarcinoma. So, first of all, we'll talk about hepatocellular carcinoma. Um, it comes from the hepatocytes cirrhosis is the major risk factor. So, chronic hepatitis NAFLD or alcohol will put you at risk of hepatocellular carcinoma. Ah, presents late. Generally, it's got a poor prognosis. Basically, all the HP HPV cancers are pretty rubbish. Um And you offer screening to patients with liver cirrhosis as well. So you get uh weight loss, anorexia, abdomen, pain, nausea, vomiting, you can get jaundice if it's blocking the bile as well. Pruritus as well. Um, sometimes you can get hepatomegaly and, and abdominal mass investigations. So, liver ultrasound again, it's a really good first line investigation for imaging. A FP is a marker which is associated with hepatocellular carcinoma. Um And then you can do staging with CT and MRI scans biopsy to confirm for histology. Uh management depends on um how advanced it is surgery. If it's early disease, it hasn't metastasized everywhere. Um liver transplants, um radiofrequency ablation drugs. Um It probably depends on how advanced it is and then last slide cholangiocarcinoma. So, the cancer originating not from the liver but from the bile ducts. Majority are adenocarcinomas. Um And there's a type of cholangiocarcinoma called a Klatskin tumor, which is um at the hilum of the bile ducts. So, if you see clot skin tumor in a question, then it's a cholangiocarcinoma. Um So clinical features again, the obstructive jaundice because if it's constricting or obstructing the bile ducts, then it's blocking off the bile, isn't it? So, the pale stools and the dark urine and the pruritis again, weight loss because it's a cancer, you can get some pain, you can get a mass. If it's big enough, you can get hepatomegaly investigations again. So, um, do all that work up with the imaging. Uh, so CT or MRI and then confirm on the biopsy. Um and then, you know, to relieve the obstruction, you can do an E RCP, put a stent in management is either curative surgery or palliative chemotherapy. Um And again, remember, voices law because it can present in, in, you know, in a similar way to pancreatic cancer with the painless jaundice or the palpable gallbladder. Ok. So just a page with all the sources we've used. Yeah, and please, please, please, uh can you fill in the feedback form um, before you go? Um So that, that's the end of the presentation? Thanks for coming along. Um And yeah, just, just be honest in the feedback, if, if there was anything that was, um, that we can improve on you, were the questions pitched at the right level? Um Were the slides too wordy? Were there enough pictures? Was it too long? Um, just any, anything you can think of to improve it and I hope it helped you in your revision? Ok. Mhm.