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Hey, hello everybody and welcome to our 10th episode of our teaching series. Today's episode will be about all things, Gi and Hepata Bili preparing you for your UK MLA. Coming up just a little bit about who teaching frontier are teaching. Frontier is a group of doctors from F one onwards who've gotten together to put together teaching series for you all to help you prepare for the upcoming UK MLA. Today, we'll be going over um a variety of topics. We'll be starting off with inflammatory bowel disease before moving on to our upper and lower gi bleeding. And then um we'll, we'll finish on viral hepatitis um along with some other um hepatic pathologies and then some liver function test interpretation and handing over to our first presenter. OK. So today we're gonna look at uh our first topic which is inflammatory bowel disease um from the UK M standpoint. From the exam point of view, the main things you need to really focus on is the difference between uh Crohn's and Ulcerative colitis. That's the main thing you'll be tested on and it will be a form of a case in which we'll have to uh find the difference. Most likely you get confused between ulcerative colitis and Crohn's and you'd have to pick one. So, um, starting, um, we have, so what is an IBD inflammatory bowel disease or IBD as it's commonly known? Um, it's a chronic immune mediated inflammation of the gi tract. So, as you can see, it's an umbrella term and the main two aspects which are covered in it is Crohn's and ulcerative colitis. And also there is one third uh form of this disease, which is kind of a mix of the both, it's called inte indeterminate and indeterminate colitis. What happens is um it's probably one of the starting stages of the disease which can either become Crohn's or become ulcerative colitis. So it's a bit of a mix of both. But for your exam, remember Crohn's and ulcerative colitis, what going on. So why does it occur? Nobody knows there's a lot of uh research into it. But for the sake of the exam, we need to give some definitive answers and moving on those would be environmental factors sometimes when there's a disregulate immune response and also a genetic predisposition. So how does this all work together? Um We'll just see it in the next slide. So moving on. So I want you to think of the microbes as a stand, as a performer or stand, let's say in our case, like a stand up comedian and then the audience is the immune system like you see the two images on the left hand side of the screen, uh you have the microbes, there's millions of microbes, there's bacteria, fungi, viruses in your gut. And then you have the immune system. Usually it's like the left hand side screen where there's a bit of harmony and there's everything is good. The performer is fine. The audience is also quite receptive and everything is in harmony. Now, if you look to the right hand side of your screen, you would see that there's a lot of disharmony like the it can be the either the former is bad or the audience is not very receptive and they're pretty pissed off. So, moving on to the next slide. So just as how there was disharmony, that would be the chronic inflammation that we see in our gut. Sometimes it's because of the microbe or let's say the performer, when there's dysbiosis, by what I mean by dysbiosis is when there is an increase in good bacteria, sorry, uh increase in the bad bacteria and a decrease in the good bacteria, then you have antibiotic use which destroys the gut microbiome dietary factors like uh a low uh a low fiber diet and uh also very high meat, high fatty diets. And then also when it looks at, look at the audience, it's an over reactive system, the audience is not trained for it. It's an untrained gut. So which means uh this goes back to the hygiene theory where exposure, lack of exposure at a very young age, uh doesn't really train our gut to know which is foreign and which is uh normal microbes. So it just overreacts for everything. And also, like I said, there was a genetic uh component to it and that's something very important. The mutations called a nod two mutation. Hold on. So this is just a summary of what happens. Either it's a microbe issue or it's an overreactive system, either ways microbes come in and there's a big chronic inflammation and that causes the lesions of an inflammatory bowel disease. So, moving on. So who does it affect? We have two peaks of age. Uh We have 15 to 35 and another peak in older adults, 60 to 80. Also to note the 15 to 35 is weight is more seriously affected than the 60 to 80 in any. And when it comes to geography, it's a more of a western uh disease. You see it in the UK, you see it in, in the US and also in Europe. What's happening right now is a lot of people who migrated from eastern eastern hemisphere, who's coming into the western hemisphere. They have also started developing it. So there is an environmental trigger to this and in ethnicity. You have to remember uh mainly Caucasian populations, certain uh Jewish uh Descents and uh also a first relative, uh a first degree relative with uh Id Crohn's. You can find it slightly more in women and ulcerative colitis affects both genders equally moving on. So the main difference between Crohn's and ulcerative colitis, as you all previously would know, it's the pattern of involvement. If you look at colitis on your left hand side, it starts at the rectum and then it proceeds in the reverse fashion. In a retrograde fashion, it starts from the rectum goes to the sigmoid. As you can see, it's going up the ascending colon and into the transverse colon. And there's no skips in between. Coming to Crohn's. As you can see, it can affect any part of the Gi tract. It starts, it can affect from the mouth to the anus. So anywhere is affected. And as you can see, there's a lot of skip lesions, meaning there's a lot of normal mucus, unaffected mucosa in between the affected mucosa moving on. So when you zoom in even closer, this is what you go, what what it looks like you have an ulcerative colitis, it's only the superficial layers that is the mucosa and the submucosa. They are the only ones which are involved. The other layers are fine Crohn's, as you can see, it's a deep ulcer, it is a very uh deep ulcer going through every layer. This is what's classically called as the transmural inflammation. And as you can see, because it's going out of outside the bowel wall, this is what causes fistulation or abnormal connections with rest with other organs and other parts of the bowel. So moving on, this is just a more uh more images for you guys. Um As you can see the ulcerative colitis is what you can see on the left hand side. And Crohn's is on the right hand side, you can see the cross section of that bowel on the right hand side of Crohn's see how thick it is. And whereas it's just a, just a superficial ulceration. And uh if an affected segment in the left hand side, also note how it comes out of the bowel, it goes into the centric nodes. There's a lot of inflammatory uh uh inflamed centric nodes and this Iliosacral junction is the most common site for uh Crohn's disease. So that's why I put mainly this uh photo there. So it can get confused with appendicitis. It can get confused with uh TB it can also be uh uh with the uh confused with typhoid also. So these are kind of some differentials which we need to know and it will present with the right lower quadrant pain moving on. So it's not just the gut. What happens is all the inflammation, which is happening in the gut. All those cells get activated in the gut, but then they go into the circulation and they affect every other part of the body. You have aphthous ulcers, you have nephrolithiasis prescri arthritis and primary sclerosing cholangitis. The main things you need to note here is primary sclerosing cholangitis. It's an inflammation of the entire biliary tract and it's very common in ulcerative colitis. And the, and the other thing you need to remember is arthritis, which is the among all these symptoms, you call them as the extraintestinal manifestations of an IBD and arthritis is the most common one. And it's the one which correlates with the disease severity. If your IBD is severe, your arthritis is also severe, you control the IBD, the arthritis becomes fine. Moving on. So how will we diagnose the patient? Like, like every standard diagnosis you have, you have to take a good history. The main thing we're looking for is a change in bowel habits. And are they having any uh rectal signs? Like, is there blood, is there cramping? Is there an urgency? Do they feel incomplete after passing, uh, after going to the toilet? So, is that like a tennis feeling beyond the gut? We're looking for all those extra in uh manifestations, uh lifestyle and family. We're looking for any genetic component in it. And also a very interesting thing is smoking because smoking actually makes Crohn's disease worse and makes ulcerative colitis better. So probably in your history, they would give you that when I smoke my bowel, my bowel habits are far better. So that's one thing to look for and any, all, all these IBD are all quite protein losing. So you will, there will be a lot of weight loss and in Children, there will be a delay in puberty. So moving on the main blood test, we're looking.