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Hello, everyone. Welcome to another crash course finals, er teaching series. So this week we've got gastroenterology. Um we'll just get started so rough. Roughly we are. So if your, if it's your first time here, um we're a bunch of fifth year medical students from Aberdeen and we wanted to come up with a sort of teaching series um to help aid with finals revision, just cos we know how difficult it can be. So we've come up with these er quick fire SBA style questions which is meant to be engaging. Uh So do try and get involved as much as you can. Um So today we've got um Mihal who is a GP trainee, I believe uh we met him in throw away on placement and he's very kindly agreed to run the session. So, um in terms of sessions we've done. So we've done, we've done a few sessions by now. We've still got a few sessions coming up. Um So do keep in the loop following us on Facebook, Instagram and sort of your group stuff as well. Ok, cool. So if you're looking to enhance, enhance your portfolio and you wanna be an ambassador for us. It's really easy. All you have to do is just um kind of put some posts up in your, in your university year group chats and batch email some people and that's, that's it and you get certificates for it at the end of the year. Perfect. So that's where to find us on Instagram. And how we run our sessions is we've got six easy, six medium and six difficult questions. Uh and meow will take you through them each um step by step and any questions that you guys have pop in, in the, in the chat and we'll answer them at the end of each round. OK. Cool. So start around one will let me how um just come on and introduce himself. Yeah. Thank you, Ian. My name is uh Miha mcdonald. I am a G PST three up in the Western Isles of Scotland. Uh I'm not a gastroenterologist and I'm not an internal medical trainee, but just, just so you're aware where I'm coming from. Uh ignoring the medical experience you get in foundation prior to GP training. I did some time on acute medicine and then even more time in A&E before then deciding on GP training. So whilst it's definitely not what I would describe, describe as my specialty. It is certainly in my realize a lot of gi patients can be quite sick and often your first interaction with them outside of a GI ward will be in A&E So it's useful to, to have an idea anyway, what we're talking about. And then I know this session in particular is aimed towards your medical school finals. And I do understand these questions have been based on the new UK medical licensing assessment process. And I'll be honest with you, some of these questions are tough. Uh If you're finding them tough, that's probably not going to change. Just know that in your actual medical practice, a lot of these, you will not be needing to know straight away, you'll just need to know who to contact. But by being here at seven o'clock on a Tuesday evening, I am quite confident you'll already be well on your way to do well in the finals anyway and hopefully learn a thing or two gi in the way. So we'll make a start and we'll go to the first question which I'll go through, I believe a pool will then pop up as we go through the answers, you'll have a few seconds to choose your answer and then we can discuss why one is right. And if able, I'll discuss why the other one's probably not fit so well. So the first case is a 65 year old female. She presents to the GP with fatigue, diarrhea, and abdominal discomfort. This is focused in the left iliac fossa. She notices these symptoms worsen after she's eaten pasta or bread on your examination. You find absolutely no physical abnormalities blood tests reveal a microcytic hypochromic anemia and a blood film demonstrates hypersegmented neutrophils. You do serological testing and that reveals positive iga ttg antibodies. So, what is our most likely diagnosis? Is it a Crohn's disease? B, ulcerative colitis C celiac disease or d bacterial gastroenteritis? Perfect. So I think we have 50 responses there with 100% on celiac disease. So I assume we don't have to spend too long on this. The, the giveaway from, from that question was the result. The TTG result being being positive. Um Celiac disease is the result of your body having a response to gluten mounting an immune response which then damages the cell walls in the gut, preventing, you know, really hindering actually your, your absorption of uh a number of nutrients. The T TG is positive in the blood test. If they have been taking gluten in their diet. Recently, if they have already taking gluten out of their, their diet, you're less likely to get a response there. But symptoms which can be quite general really can apply to a lot of gi conditions would be fatigue, diarrhea, abdominal discomfort, left iliac fossa again, doesn't narrow it down too much. And the question, even before they mentioned the T DG, the giveaway for this question would be the fact that it gets worse after having pasta or, or, or bread or other gluten containing foods. Um They develop a an anemia and the blood film will show a hypersegmented neutrophils because they're going to have a deficiency likely in B12. Um We've discussed the testing already. They mentioned that the Gold standard diagnostic test is a biopsy. I don't think I have ever seen that done prior to TD G. We used to test for E MA uh different antibodies and even then, I don't think I saw anybody do this for celiac disease. The, the, the blood tests are pretty, pretty conclusive. And at the bottom, there is largely for your information. This is genetic testing. HLA DQ two antigens. Um It does mention that in 90 to 95% of patients with celiac, these are positive, they're not that useful because in a huge proportion of people, they will be positive for this but not develop celiac. Um It's, it's, it's almost historical, the focus they'll, they'll, they'll do on this. It's not Crohn's disease. Um Again, it's seen as positive T TG. It's not going to be Crohn's. Um it's not ulcerative colitis. They mentioned dia I'd imagine with a question with ulcerative colitis, they'd probably focus on bloody mucousy, diarrhea. Um Again, T TG rules out this one bacterial gastroenteritis. Uh Again, if they're going for the textbook question, they're gonna mention um nausea, potentially vomiting some epigastric pain and diarrhea. So, really the giveaway for this question was the uh the T TG, this information will be on the slide. You can access this yourself at the end. This is just a lining, how it changes the lining of your, your, your bowel wall and prevent your, your absorption. So next question and I believe we will stop at the end of, of each round if you do have any other questions to, to add in. So the second question is uh 2022 year old medical student, she's brought into A&E after having multiple episodes of vomiting blood. After a night out of heavy drinking, the vomit was initially yellowish in color. But after the first few episodes, it started to become streaked with blood. Soon after he reports two episodes of vomiting that contained streaks of frank blood and he also complains of acute epigastric pain. So, from this stem, what is the most likely diagnosis? Is it a Boer have syndrome? B Mallory Weiss syndrome. C ruptured esophageal varices, da perforated gastric ulcer. There we go. I think we've had 6060 odd responses. Um I II could see why people would choose any of the above. Really? It is B it's a Mallory Vice Syndrome. Um There's a few giveaways in this, in this question that I'll, I'll discuss once I've, I've read through this this bit for you. Um, really Mary Vice tear, these are small to medium size tears that can occur usually after some pretty severe, heavy or continuous um, vomiting, uh generally, and I'd say this is true in practice partly, but it is almost 100% true when it comes to medical school finals questions. It'll be related to alcohol intake, um, gastroenteritis or um, hyperemesis. Typical presentation. They'd be binge drinking. They'd initially start vomiting. They then vomit. What's the yellow vomiting application for? Please? Uh, the initial color yellow. Is it that, that would be a a that they're empty? They've emptied to their stomach. They're following vomiting their yellow bile, stomach acid. There's nothing else to clear, they're not trying to clear anything else. They're purely vomiting, um, retching, they've caused this tear which then develops the, the blood. If that continues, that blood can become more profuse and you start getting Frank blood vomit. It's written here at the bottom. It's, it's characterized in acute upper g upper gastrointestinal bleeding. It's not gonna be anywhere else. Um And I'll discuss in a wee minute why it might differ from, from the other ones if we were talking about a perforated gastric ulcer. The question may give you a hint towards the past medical history of epigastric pain. Previous ulcers, you'd expect potentially Frank bleeding. But a big giveaway would be discussing epigastric pain and Melina. Um If you were discussing ruptured varices, that's not a diagnosis you're gonna make on this story alone. This patient could have varices, but the stem would be giving you more of a of a hint an in an indication, potentially suggesting some decompensated liver disease or, or or chronic liver disease and Boer have syndrome. The patient would be a lot more unwell. Typically, they'd be discussing severe um kind of upper chest pain and you can have clinic clinical signs of air escape, which is discussed on the next slide, which I'll give you an idea between the two. So Mai Syndrome, it's, it's a tear in the wall. It's not a complete tear, it's not a rupture. You bleed as a result of the pressure and the stress you put in your, your esophageal walls through. Um But then the boer halves is when you have a complete rupture. So not only might you have bleeding into the stomach, you can also have air out of the stomach that can fill the mediastinum. When you're listening to the chest, you, you could hear extensive air. You may even get some surgical emphysema. You can have neck pain, you can have swelling. Obviously, none of these are particularly minor conditions, but of the two the boer have is the the major emergency. So the third case, the a 49 year old gentleman, he presents with jaundice, he's feeling generally unwell and he's got vague abdominal discomfort. The patient notes that he has recently had abnormal stools which are pale and they're difficult to flush away. His past medical history includes several episodes of acute pancreatitis likely due to alcohol misuse. The blood results show a relatively elevated bilirubin, decently elevated ast A L TA LP and a low albumin. So, from this presentation, what is the most likely origin of his symptoms. Is it a, a posthepatic jaundice? Bi have to get the order here. Second. What was ba cholestatic jaundice? C an hepatic jaundice or da pre prehepatic jaundice? We have 18 responses as far as I can see. And I don't know if it's emphasized, but II believe the responses are anonymous here anyway. So have a, have a pump. There we go. We've got, we've got 5050 responses here and I can see between B and C and I can completely understand the focus on, on, on the two there going purely on the content of the the question stem. We would have to state that this would be an hepatic jaundice. I'll discuss the the various reasons for it here and we can compare it to the cholestatic jaundice. So if you think of your, your, your causes of jaundice, um Right. Sorry, I I'm reading the, the comments here as we go along. Um the causes of jaundice can be before the liver and the liver function is absolutely fine. So your bilirubin er which would be unconjugated uh for some reason is being produced at a higher rate than it should. Your liver is trying its best to conjugate it so that it can be um disposed of uh via the bile into your um bowels, but it can't keep up and that is a rate limiting step there. There, there's only a certain rate your liver, your liver can do it, there's an intrahepatic jaundice where your liver itself is now struggling to do the conjugation because of damage to your liver. And then there's a post hepatic jaundice, which would present with a cholestatic picture, which will give you two of the options here where something is stopping the, um the flow of conjugated bilirubin out of your liver, uh causing that kind of essentially a backflow back pressure that prevents your liver from, from keeping up. Um In this picture, you've got your transaminases, they're raised. If you ever see raised transaminases, you should be starting to think that it's, it's uh an intrahepatic picture. If you do have a posthepatic or a cholestatic jaundice, that's severe enough that it, it's causing damage. I could see um why that might look like an intrahepatic picture. The, the thing that would be the, the giveaway in this stem is that they haven't given you a gamma GT, which II do not like the way that these questions might be worded that you're having to, to take them purely on, on how the uh the results are. But uh you, you would need a Gamma GT to suggest that you, you've got cholestatic picture and that would suggest an obstruction. The other thing on the question is they have mentioned that alcohol induced pancreatitis would point you away from any potential um stone or cholelithiasis uh based uh pancreatitis. So raise bilirubin transaminases are off and they haven't given you any specific guide in the question to having stones in the past and there's no GAMMA GD suggesting a uh a cholestatic picture. So LFT S, they're tough. You'll always have to think twice about them. But transaminases up, raise bilirubin, assume hepatic. That question. The other slight giveaway was two of the options were essentially the same cholestatic and posthepatic. So question four, a 52 year old lady with a past medical history of rheumatoid arthritis, pre presents to the GP with general tiredness. She is investigated with blood tests that show a macrocytic anemia. Her G EP suspects pernicious anemia. So it's a very, very forward thinking GP who decides that they're wanting to do their next investigation to be the investigation, that would absolutely confirm the diagnosis. So of these four options, which of these would confirm the diagnosis of pernicious anemia. A Vitamin B ba blood film C anti intrinsic antibodies or D an esoph esophagogastroduodenal endoscopy. Good. So we've got about 50 responses there. Uh I would agree with the 34% if the question was, what will your next investigation be? Um, be a brave GP to go straight for the investigations of the antibodies without doing hematinics if they've got themselves a macrocytic anemia. Um And if you did your hematinics, you would expect to find uh a low B12 in this situation. But looking at the wording the question, another one of these frustrating ones asking which investigation would confirm the diagnosis, you would do your hematinics, you would find they were low, but it doesn't tell you why they're low and this one would be anti intrinsic antibodies if they're suspecting pernicious anemia. So, what pernicious anemia is? It's yet another autoimmune um process. Your body has developed antibodies uh against intrinsic factors which are pretty well. They're integral to um absorption of vitamin B12 which will lead to uh vitamin B12 deficiency, which causes your um uh your macrocytic anemia. So, from these ones, the b12, yes, that will be low. So I'm gonna confirm the diagnosis. A blood film probably gonna show you large uh large cells. You're probably gonna get uh hypersegmented neutrophils. Again, uh again, it doesn't tell you what's the underlying cause of it. And then the endoscopy not only would be uh hugely invasive, that isn't part of the question. Uh At this point, you would be specifically looking at the um esophagus, the, the stomach and then to the upper gi tract, you'd have a good chance of not actually biopsying or seeing the area that you want, want to have a look at. So the answer for this one would be the anti intrinsic antibodies. So the fifth one, so a known depressive patient um and you can take from that phrasing what you will, I would probably phrase that a wee bit differently, but a known depressive patient presents to A&E after ingestion of 60 paracetamol tablets 16 hours ago in an attempt to take his own life, he complains of abdominal pain, vomiting and nausea. So what is the most appropriate management from these four options? A? You can start your N Aysal cyst N acetylcysteine your neck. B, you give the patient activated charcoal. C you go for a gastric lavage or D you go for a liver transplant. Good. So I think we're about 5055 responses there. Uh overwhelmingly going for a again, I believe, depending on the guidelines you look at, I can see why you might have seen gastric lavage or the activated charcoal written. But the giveaway in this question is the time towards the overdose. So discussing how paracetamol causes harm, it's not the paracetamol itself. Your body will break down the paracetamol and it's one of its metabolites. This N ADP Q I um which causes damage that causes the damage um to your cells, to your body, to your liver and your body will start breaking that, that paracetamol down in, into that. You then give NAC N gets broken down in your, in your body. And one of its metabolites counteracts the metabolite from the paracetamol and reduces its ongoing damage. The trick is though, if it's ingested within the hour, you ha you assume you make the assumption that that paracetamol, a good chunk of it is still in the, the stomach. So you go activate the charcoal cause that reduces the amount that's absorbed. I don't know where, where you work and I don't know how many people present with intentional overdoses within the hour. I, I've seen it once, I've seen it once most people are much longer than that. So, so I II can't comment from my own experience how well the activated charcoal works. If the ingestion is longer than an hour, it says here 4 to 15. But if it's longer than an hour, you'd be taking a paracetamol level. And if you're able to get the paracetamol levels back, which we're not out of hours, you then follow your guidelines. You should have very good clear guidelines. Anyone who's in Glasgow, they've got very, very clear guidelines. A good, a good system called the snap protocol. You map your levels up against that protocol and you treat giving NAC based on that, the difficulty comes in the patients who had staggered overdoses. So if there's even a suspicion that they've taken multiple doses of paracetamol over the course of the day or even the course of, of, of a few hours, your body will have started breaking down that paracetamol and it's breaking it down to the harmful metabolite. So when you take a paracetamol level, it could be reassuring, falsely, reassuringly low because the metabolites already been broken down and, and it's building up building up in the body. So for those patients, you treat, you treat them with NAC levels aren't gonna help you on their initial presentation and then therefore, you don't want information was just some of the things you look out for to decide whether liver transplant is something you're gonna have to consider. Consider in this patient. That'll be bread and butter. Anyone who does A&E you'll be knowing that one inside out. So question six, a nine year old boy who presents to the GP with bloody diarrhea, fever and abdominal pain. He also feels unwell and has been eating less. His bloods reveal low platelets, an acute kidney injury and a hemolytic anemia. So, from these four options, what is the most likely cause of his sys sys his symptoms? Is it a schistosomiasis? B Norovirus CC diff or de Coli? We go, we have a we oh they go 5056 responses. Yeah, mostly saying, saying E coli uh discuss discussing this one. This is uh kind of another textbook medical school question. Um Looking for your hemolytic IC syndrome, which is a result of the toxin produced by the E COLI. Um Generally you get this from undercooked meats or, or similar. Um This question had a couple of giveaways that it was the E coli often in these questions, they will mentioned that they've recently been to a, a picnic or a barbecue or something, something like that. But the low platelets, the hemolytic anemia and the acute kidney injury are all the textbook presentations for your E coli toxin um poisoning. The schistosomiasis doesn't fit this question. Uh it hasn't mentioned anything about any skin cysts, uh, symptoms or anything like that hasn't suggested any travel, hasn't given you a prolonged period of presentation. The novi the, the vomiting bug. This kid is mo isn't vomiting. C diff c diff. Yeah, you could get your, your, your diarrhea, you would get your diarrhea with the C diff. The question would often say they've had a course of antibiotics or something similar to, to pri you and you wouldn't expect low platelets with the C diff if anything, you, you, you'd expect increased platelets um with the C diff as a, as a, as an inflammatory response. And you wouldn't be expecting your, your A KS unless they were getting profound diarrhea leading to dehydration and AK I um or your, your hemolytic anemia. There we go. So that was, that was the end of round two and I, or the end of round one. And I think, is this where we would stop for a wee bit if there's any questions of those, those first few cases? Yes. So if there's any questions, pop them in the chat, otherwise we'll move on to the second round. Ok. Ok. Seems like there are no questions. Let's move on. Yeah, we'll carry on. And if you type them up as we go along, I can, I can try to address them in between. So again, they, they've, they've, uh, labeled as easy, medium hard. Um I II don't know if maybe low and high yields, might, might, might be a better way of putting it. But, um, this, this one's, he's a 3030 year old man. He arrives to clinic and he's got an extensive history of gastric ulcers. He's got abdominal pain and diarrhea. So, you're suspecting a diagnosis of Zollinger Ellison syndrome. So, from these four hormones, which is the most likely cause of ulceration in this patient with your suspected Zollinger lysin. So there's a, a motilin B, Gastrin C somatostatin or D your ghrelin. Mhm. There we go. About 54 and, and brilliant. There's, there's absolutely no way I'd have been getting this one in uh in fourth or fifth year. Um So yeah, the, the, the answer is Gastrin. So what Zollinger Ellison syndrome is, it's a, a neuroendocrine tumor and it produces gastrin. So your gastrin level is too high. And what gastrin does is it promotes um release of your gastric acid. So you increase your or you lower your, your ph in the, in the stomach and then this can lead to ulceration and prolonged exposure to these conditions actually increases your risk of, of cancer. So you can do a gastrin level. I might suggest it's raised uh good. What is good, good question. I, I'll, I'll get to that one. I, in, in a minute, you can raise your, your, you can check your gastro level and look for it to be raised. The gastro levels will not be the same person to person. So you need to do much like many of your endocrine presentations is you need to do some kind of a stimulation slash suppression test. So you can do what's called a secretin stimulation test and secreting the imaginatively named secretin er promotes the secretion of of a few things from your pancreas, including bicarb or bicarb type products that are designed to reduce the acidity from the content of your stomach to make it a wee bit more alkali, raise the ph so that it's more easily and more safely digested in the duodenum darts. But what it also does is it works in a feedback loop to reduce your gastro reduced production in Kron. But secretion will not or should not have an effect on your neuroendocrine tumor that's reducing uh producing the gastrin. So you would give the patient, you would take a gastro level, you would give the patient secretion. You would then do serial gastrin levels. If it drops less likely Solder Anderson, if it stays the same or if it rises, you're like, you go, you, you're consumer. The treatment then is to resect that tumor they mentioned here about somatostatin, um somatostatin uh scintigraphy I II Okot scan. So, octreotide is a uh an analog of somatostatin. Um All of your neuro endocrine system would essentially uptake um octreotide, you can radio label it, it's a wee bit like a spect scan. Uh Give the patient this radiolabeled octreotide, do the scan. It'll show you where the biggest uptake is a wee bit like um pet scans of some of these things and all of these neuroendocrine tumors, they're gonna be associated with one of their tumor syndromes. The, the men, I'll tell you now. But the other three options fatima asked about or ghrelin is motilin in the name should be affecting your, your acid as such. It promotes the motility through your, through your stomach. Soma somatostatin. It, it you can think of it as kind of one of the anti growth hormone type um endo uh endocrine which would slow things down. So actually, you probably expect a wee bit of a reduction in, in, in your gastro and maybe even a a reduction in your pancreatic secretion as well. And ghrelin, that's one of the hunger ones, the, the hunger hormone that makes you feel hungry, let you know how to eat. I cannot remember off the top of my head. There was a good genetic study in mice with, with, with the ghrelin uh to, to help them identify this as one of the hunger hormones should be affecting your sore. So 28 year old lady, she's got a history of UC. She prevents presents to the uh A&E with bloody diarrhea. She's normally on oral mesalazine and topical mesalazine which between mesalazine enema to control the B UC, she's been feeling unwell for a couple of days and she's now opening her bowels over eight times a day. So an examination, her ABDO is soft but it's tender in the left leg closer. She's got a raised temperature and the A&E doctor suspects she's got a flare up of her UC. So this is discussing management of flares. So what is the most appropriate management from these four options? Discharge the patient with steroids, admit the patient and start high dose anti-inflammatories by which they'd mean steroids and other similar anti-inflammatory drugs admit and start infliximab biologic antiinflammatory or d reassure and discharge grand. So we've got 30 odd with this one and I can understand my more might not want, want to want to have a guess. B is absolutely right. Um I say absolutely right. It entirely depends on, on where you work. But generally, if you're following the guidelines, this person has had their home treatment of antiinflammatory medication, the mesalazine and yet they've still got their flare up. If you've got a severe flare up or you see, this can be very quickly become a, a medical emergency. So IV steroids, if there's no improvement with them, you can consider increasing your, your a anti-inflammatory, start your cycloSPORINE or you may even need to start considering emergency surgery. Uh, what happens with severe UC is the walls of the vessel, the, the bowel becomes so inflamed, so angry, it stops working, develops a bit of an ili nothing, nothing passes through naturally. And that can actually start building up increase in size. You can form this toxic megacolon. This has got a huge risk of um perforation rupture. You like to have to do a surgical intervention here. So this is even though these patients can seem relatively stable, no one you see worsening flare up, you need to treat, you need to treat infliximab may end up being in this person's treatment at some point. But the initial appropriate emergency management IV anti-inflammatories. So first year medical student attends an occupational health appointment to ensure that their vaccination record is up to date. Uh He had his Hepatitis B vaccine as a child and he's never been exposed as far as he knows to hepatitis B. So which of the following serology results would be expected for the vaccinated patient. So A that you've got your Hep B surface antigen positive, your antibodies to the HEP B surface antigen positive your antibodies for the Hepatitis core positive B your I don't know if you remember all these as I'm just reading them out but your surface antigen negative the antibodies to the surface antigen positive, the antibodies to the core antigen negative, your surface antigen negative your antibodies to the surface antigen positive and your antibodies to the core positive and then d surface antigen positive antibodies to the surface antigen negative and antibodies to the core positive. This would be a rubbish question for you to get but, and I won't hang around too long on it cos it's mostly reading and trying to get your head around these. Ah, there you go. 24 overall. 82%. Honestly, you, you, you're, you're doing great compared to how I would do there. Um, as a medical student. So, yeah, that, that's right. It's b I'll briefly run through why it is. So, the surface antigen is what's in the vaccine you get given the vaccine, your body forms the antibodies to that surface antigen. So when you're testing to see if you've got your um immunity to it, you're testing for the antibodies your body has produced to that surface antigen. You shouldn't have the surface antigen. Unless you've got an active infection, you shouldn't have any core antibodies based on the vaccination because there's no core antigen in the vaccination. If you've had an infection and you've developed your own antibodies to it, or if you're currently infected, then you could well be positive if, if, if you've had an exposure before and then the, this, this, this protein, this, this um hep B protein that, that's, that's put in here, that that's a, a protein that is, there's active viral replication going on. So you've got an active infection, you've got a virus that would be, if that's positive, it suggests you do have an active um infection. So a 78 year old woman presents to a and age, she's got a two day history of feeling generally unwell she complains about abdo pain and temperatures on examination. She's pyrexial jaundiced, her abdomen is soft but tender in the right upper quadrant. And I know the first thing you'll all be thinking is this is obviously an ascending cholangitis. So what would be the definitive management? So the definitive management of ascending cholangitis? A an er CPB an MRC PCI V antibiotics or D ultrasound. Good, good. We'll go with that 1st 3030 responses in you said E RCP. The trick to this question is what is the definitive management? So what is going to cure the underlying issue here? This person's got ascending cholangitis. You have to assume there's an obstruction somewhere in the the tree. Absolutely. You would do an ultrasound of the abdomen. Look for stones. Absolutely. You would give them IV antibiotics to your feet and your cholangitis almost certainly depending where you are. You would do the M RCP to visualize the um the, the bilary tree um and then an E RCP to clear any, any blockage uh dementia Charcot's triad here. This is the Charcot, the neurologist with multiple autonomous neurology um conditions. But uh he's managed to put his name to somebody having a temperature being jaundiced and having right upper quadrant pain and then Reynolds came along to add his name to an extra two to it. But upper quadrant pain and unwell, you have to assume cholangitis. 87 year old man, he presents to A&E he's had abdominal pain for three days. He also reports that he's passing black stool for the past two days associated nausea but he's not vomiting. He's got a past medical history of an ulcer this resolved after PPI on examination, he is alert and oriented. His abdo is soft but he's got epigastric tenderness. His bowel sounds are normal. You do apr it reveals black stool no masses on pr his obs are tachycardic at 100 and four. His temperature is 37. He's hypertensive at 93. Over 60 respirate is 17 and his SATS are slightly low. Fortunately, he's already been given some pain relief and he has access. So what is the next best step? So what's your next step? Best next step in managing this patient given them maybe omeprazole arranging an upper gi scope, arranging a CT Abd Orvis or giving an IV Bolus of Saline. Good, good 3030 odd responses. Um This is another one looking at the wording of the question. They specifically say next best answer. This patient is showing some sign of shock. So he needs some kind of resuscitation fluid um depending on where you work, that may be Saline, that may be harman's this patient. I think we can all work out has likely got a bleeding duodenal ulcer. You would absolutely not be in the wrong to consider a blood transfusion. You would absolutely be giving IV omeprazole, you would absolutely be arranging uh an upper gi scope depending where you work, you may be may be faffing about with act. But the next best step is to treat their shock, give them fluids and then you can start addressing the the underlying ulcer. So, a 45 year old lady, she's got chronic liver disease. It's secondary to an autoimmune hepatitis and she prevents with hematemesis and melena. So scope shows bleeding, esophageal varices, they're banded and she's noted to have portal hypertension on examination. This lady's jaundiced, she's got palmar erythema and she's got a distended abdomen with shifting dullness. So, jumping straight onto what your specialist intervention is going to be. Which of the following is an indication for a transjugular intrahepatic portosystemic shunt, otherwise known as tips. So, encephalopathy, portal hypertensive gastropathy, refractory ascites or severe heart failure. Here we go. 42 responses. And I feel like I'm saying this a lot. I'm not saying condescending, very, very impressed. This was the question that prompted me to ask around and quite a few people thought this one was particularly unfair. So essentially what are, what are tips is, is you're putting a shunt between the hepatic and the portal circulation to try and bypass some of the blood from the liver, try to reduce some of the pressure from the liver. So actually, it would, it would help with hypertensive gastropathy. It, it it it it would mm arguably severe heart failure, encephalopathy, potentially less. So, but the indication for it would be if you've got ascites that keeps reoccurring despite best management, medical or drainage. And then the great thing about these interventions is once it's in, they really shouldn't be requiring any further acidic drains, you bypass the, the hepatic circulation or have partly bypassed it reduced some of the pressure and cut down on the ascites. But that, that was a tough one. So round three, we didn't have any questions after round one, I'll carry on blasting through round three here if anybody, oh, there we go. So what exactly is portal hypertensive gastropathy? So the big one you'll be talking about there would be your varices. So if you can imagine what, what the varices are is you've got an increased portal hypertension, your blood's working against the the pressure there in the liver. You could get these big dilated variceal veins around your, your esophagus into your stomach. And that's your, your concerned. They're the ones that when they rupture, they bleed and they bleed and they bleed. So getting any control you can over the the portal hypertension relieve any of the pressure you get from these vessels. You're getting that under. Well under as best control you can, you will see this in A&E anyone who works in A&E and anyone who works in A&E in Scotland with the alcohol issues we've got here. You will see bleeding vices and they are always horrible and we'll go on to the next one. So 50 year old female. She pre presents to her GP with a two week history of nonbloody diarrhea, bloating and a loss of appetite. She reports feeling extremely fatigued. She's had a weight loss of 4 kg. In the past three weeks. She returned from work in India one month ago. On examination, she's got generalized abdominal pain, abdominal pr vaginal examinations are otherwise normal. So what's the most appropriate investigation to perform next for this lady? A stool over cysts and parasites BCA 125 C fecal calprotectin and D colonoscopy. Great. There we go. See, labeling this as hard was, was, was completely wrong. Completely wrong. Absolutely. This is uh I have to say this. This is one of your, your typical medical school questions. They, they, they mention India and a UK exam. You, you're gonna have to assume that they, they're trying to get some kind of tropical disease. The other giveaways here, if they hadn't mentioned India at all, the giveaway would be the timeframe. The timeframe we're only talking about a few weeks. Few wets are bloating. Ca 125. There you go. You'd be thinking of any ovarian pathology. I would almost always test it with patients. Uh consent informed consents. If they're presenting with some kind of thing, it can happen quickly. But the time frame they're, they're getting that here is, is too quick for that. In your textbook medical school questions. Fecal count protectant. If they mentioned maybe bloody diarrhea, um, mucusy diarrhea. Anything else pointing towards a colitis? Crohn's absolutely colonoscopy. Wouldn't be wanting to do a colonoscopy with ongoing diarrhea unless there was any suggestion that this would be an emergency, needing any kind of intervention you'd be wanting to avoid that. So, what they're trying to get out here is they're trying to talk about giardia waterborne food poisoning. Um, you would test for the stool vessels and parasites and again, depending where you work, you have to be very specific. But that's what you're wanting to, to investigate. Can't just send say cultures or whatever you need to ask that particularly. But time frame and recent travel, that's what they're getting at here. But you all knew that. So 60 year old lady with a past medical history of osteoarthritis, she's a long term naproxen. She presents to the A&E with dizziness on questioning. She reports passing black Tarry stool for the previous two days on examination. This lady she's hemodynamically stable, but she's got cool pale peripheries and she's mildly pale blood tests show low hemoglobin her M CV 78. So a low M CV provisional diagnosis is made of an upper gi bleed. So you do your bloods. These are all your your standard bloods, which of the following findings is most likely to be found in this lady that would be suggestive of your suspected diagnosis. Is there a a low urea ba high urea c, a low potassium or da high creatinine and apologies. If you can hear the cat going out the door, he's on a bit of a bandage now. Grand, 4046 responses. These are doing well. They keep responding at this stage. So high urea is, is the answer here. And that's because with an upper gi bleed, you are digesting your swallowing, you're breaking down a lot of your, your, your red blood cells and you're actually absorbing them, you're digesting them. So urea comes from the breakdown turnover of your cells, red blood cells. So digesting red blood cells, your urea is gonna be high. So low, urea wouldn't necessarily put you off for this story. I'd still be pretty convinced it was an upper gi bleed, but I wouldn't be suggestive of it. A low potassium unlikely unlikely we are dealing with cell breakdowns here. So if anything, it would be normal to, to high uh and a high creatinine would be suggestive of maybe a long term renal issue or a severe dehydration which could all present with this. But the high creatinine wouldn't be suggestive of the upper upper gi fleet. So I think after this, we've got, yeah, a list of causes of upper gi bleed. There's plenty of causes of upper gi bleed. Um If you've got an upper gi bleed, you, as we discussed before, you need to stabilize them, you need a scope. So a 28 year old lady, she presents to the GP she's had three days of progressive bilateral lower limb weakness. This patient reports that they've recently been unwell with a fever and bloody diarrhea and they deny any recent trauma on examination. They've got abnormal tingling in the lower limbs and you also note they've got absent reflexes in the lower extremities. So you've got a suspected diagnosis, which of the following is the best treatment for that suspected diagnosis. A pyridostigmine and prednisoLONE b plasmapheresis and immunoglobulin c emergency, neurosurgery and D analgesia and tricyclics. Ok. Good work. Good work. Absolutely. I would agree with you on B there's a couple of things they're getting out here that would point towards the um Guillain Barre syndrome, the, the GBS, the fact that they hint towards a recent infection. So that that tends to be the trigger in GBS and any infection can do it. The, the textbook ones would be your CMV EBV S your Campylobacter, which I think is what they're hinting at here in, in the question with a bloody bloody diarrhea. What you look for is symmetrical, ascending weakness, they affect the reflexes. It's a peripheral nerve system issue affects the reflexes and you may or may not identify an infection beforehand. It's a clinical diagnosis. So, if you have a neural, that isn't quite fitting, you also have to wonder whether it's GBS, you can get atypical GBS. But the textbook ones would be symmetrical, ascending weakness, loss of reflexes with a recent infection. If you, if you have it, a lot of these patients can be managed supportive care, manage them through them the plasmapheresis. Um For anybody who's, who's not familiar with it, it's kind of an extracorporeal sieving of your plasma to get rid of the antibodies that your body's creating, that's attacking your, your nerves causing the, the GBS and immunoglobulins. That's, you know, supposedly from healthy individuals replacing your, your own immunoglobulins pigment. I'm guessing they're thinking a myia gravis here doesn't fit emergency surgery. No history of trauma. Whilst you can get bilateral, you'd be thinking more unilateral if you needed any kind of emergency neurosurgery unless they're suggesting spinal issues. But again, no trauma and then the analgesia and amitriptylines. I'm guessing they're just going down to neuropathic pain here, la lack of reflexes. This isn't just neuropathic pain. For a five year old woman. She presents to her GP with complaints of dysphagia to both solids and liquids, regurgitation, chest pain that worsens when she eats. She's experienced these symptoms for the past six months. On further inquiry, she has had weight loss of a of approximately 5 kg of the same time period. You do a physical exam and it's unremarkable. You do arrange your body and swallow. This shows a dilated esophagus with a bird's beak appearance and poor esophageal emptying. So you might have an idea for a diagnosis on this. Well done if you do because the question is for your diagnosis, which of the following is the best management for your suspected diagnosis. Are you gonna refer this patient to oncology? Are you going to arrange pneumatic dilatation? You're gonna get a Haler cardiomyopathy myotomy on an intrasphincteric infect injection. That should be of botulinum toxin. Good. There we go. 43. And I can see the majority have gone for C and then the next majority D and then B then a honestly on that question, well, from tho from those options probably would have gone for the di dilatation as the first line because from that story, what they're telling you about the bird's beak, the um inability to swallow solids and fluids, the regurgitation and the pain when they eat is achalasia. So achalasia, the lower part of the esophagus loses its ability for pedestals. So it becomes narrowed, it doesn't ex expand, it doesn't help uh progress the food and the fluid down. So it's a blockage bird's beak, they're talking about the imaging, but it'll come down and narrow it to a beak point and the food can't get past. So it does say best treatment here. This is what I could argue with you on this one. Exactly. Best treatment. The first line treatment for this would be the dilatation. If the dilatation doesn't work, you can then consider the cardiomyotomy surgical intervention here. If the patient isn't surgically fit, you can then consider injecting Boline and do toxin, relax that down. Let things go through So I would probably agree with you. Wording this question for best treatment is, is arguable. Best first line treatment will be pneumatic dilatation. And also II wouldn't judge any of you for referring to oncology. Somebody with swallowing difficulties over that kind of period of time, but you probably wanna do a wee bit investigating, investigating. First. I think I've got some images here for you. That, that, that's the bird beak there. The narrowing, I don't have a pointer here, but the narrowing there at the bottom of the esophagus just need to stretch that open. They'll be back. They'll have numerous um scopes and stretching to, to keep that open. So 65 year old female patient presents to the ed with severe abdominal pain, distension and vomiting. She's diagnosed with complete bowel obstruction, upon examination. Her abdomen is tender and she's got reduced bowel signs. Which of the following medications would you be wanting to avoid when you're trying to manage this patient's symptoms? So, Ondansetron, metoclopramide, diphenhydrAMINE and paracetamol. Good. Good. Perfect. So this is gonna go into all the actions of the, the, the medication and how it works. All you need to think of is metoclopramide. It's a prokinetic. You've got an obstruction. If you start giving somebody a prokinetic to the, obviously, it's, it's an antiemetic, it works by trying to empty the contents of the stomach, die, die in the way. If you've got an obstruction, it's gonna work against that it's gonna cause pain, it's gonna worsen things. You wouldn't be a million miles. I'm thinking Ondansetron, Ondansetron, one of the big side effects obviously can be constipation. This patient is obstructed if you worry about constipation, if, if it's constipation causing obstruction, you know, you're already a bit late for that. She needs some help with her, her, her, her sickness, but there could be any number of other things. So, Merom is, when you were thinking here, um C is an antihistamine, there should be no issue with, with using that. Not quite sure why, why, why, why you would before you've got other options and then D is paracetamol. Yeah, you can use that, use that your heart's content. These are the side effects of using the metoclopramide. Essentially, it's centrally acting, mostly antiemetics, centrally acting. You want to avoid them in Parkinson's interestingly there, there's a couple of central acting ones that you can go for, which is my preference but central acting be a bit concerned. Uh six year old male, he's a smoker. He presents to his GP and he's complaining of weight loss and pale stools. He has no abdominal pain on examination. He's jaundiced. You can feel a nontender irregular mass north within the epigastric region. You do some lab tests and he's got elevated bilirubin and an elevated alk phos. So, with your diagnosis here, which of the following investigations would you be wanting to do for your own suspected diagnosis? Oh, I should have gone through them. Shouldn't I read them out? You've got your ultrasound, your CT, your X ray or do a blood test for the C A 19.9? Good. You got 25 responses. Is that the, the 25 you managed to last till eight o'clock? Yeah. B CT is what you'd want to go for. So painless jaundice. In any question, any question you get for painless jaundice, it's gonna be pancreatic cancer as the answer that they're, they're wanting here, the majority of them will present um jaundice by that stage of the quite late stage. Often you will actually, or, or I wouldn't be surprised if you can palpate a mass pretty severe ultrasound. You would be com completely wrong in doing it. You will miss some um pancreatic um masses with, with, with ultrasound. CT. Much more um much more sensitive at picking up um your, your masses painless jaundice. You're gonna request a CT. Um That's, that's it. Really x-ray isn't gonna show you almost anything and do, do your blood test for pancreatic cancers useless for diagnosis. Um You want to do your CT CT ABDO? Oh And that's it. And that's it. So, thanks for listening to me waffle on. I hope there was some use in that if you have any questions whatsoever, type them away. Now, ask them and see if I can help. Thank you very much mi for, for taking time over here. Tuesday to deliver the session. It was very good. It's very useful. I'm sure you get great feedback. Um, regarding feedback. Can we just ask everyone who's, who's on the call to please fill out the feedback? It should be on in the chat, takes you 30 seconds to fill up and it's really useful for Mihal uh and us as well just to find out how we can improve the sessions. Um, you get a certificate at the end of the feedback as well, which is always useful. Uh If you're in Scotland and you're 1/4 or fifth year medical student, um if we'd really appreciate if you fill out this survey that we're doing, um just to compare your experience in rural medicine versus um urban settings just to see what the difference is like. Ok, perfect. So, um if you're not following us already, follow us on Instagram, Facebook at crash course finals. And if you want to get in touch with anything, uh you can email us at crash course finals UK at gmail.com. Next session is undecided yet. It's, it's most likely to be a, a neuros next week. Um But do sort of keep updated by following us on socials and things. Once again, thank you very much Miel for joining us. Um stick around for any questions as well. The last thing I would like to mention as well, um We're gonna send out invites to become members of the crash course finals page on medal and what this membership will give you, it's free, completely free. Uh We just put up sort of useful resources that we found quite useful to have during our finals. So I've put up some things like the Dermatology handbook, which helps describe common derm conditions and how to describe lesions, which is very useful as well as a guide to interpreting chest x rays and some osk cases with mark schemes. So we'll send out an invite for that. So if you just keep your eyes peeled for that, that'd be very good. I was gonna say, I think was it a la was asking to go back to a slide to do these slides get sent out or is it recorded the video slides get sent out? Um Once you complete the feedback. So yes, um essentially you have access to this after you fill up feedback form as well as the access to the recording. OK, perfect. We'll stick around. Thank you very much everyone for joining.