So, yes, I'm going to talk about IBD and IBS. So these are two similar acronyms but very, very different disease processes. Here's the disclosure slide. So again, we've kind of been going over normal anatomy and physiology of the GI tract and now going through pathology, so we're going to focus on two different disorders that primarily affect the small intestine and the large intestine. So Inflammatory Bowel Disease, or IBD, there are several different forms, but usually we break it down into Crohn's disease and ulcerative colitis. Just to confirm, I didn't ask. Oh. Sorry. That's okay. Let me keep going. So Crohn's disease, so you can see here, you know, these are the normal anatomical images that we've been using, except the areas where it's a little bit—is there a pointer? Okay, yes. Okay. So the area where it's a little bit red here is supposed to represent inflammation. So in Crohn's disease, you can actually have Crohn's disease anywhere from your mouth to your anus, but most commonly in the small intestine and the large intestine, and you can see here that it's kind of patchy. It's kind of all over the place, whereas ulcerative colitis always starts at the rectum and only involves the colon. So at the very most, it can start—so at the very least, it can involve just the rectum here, or it can extend all the way up at the worst to involve the beginning of the colon, but never involves the small intestine or anywhere else in the GI tract. Now there's also a difference in terms of the depth of the inflammation. So these are a picture—or on the left side, you have a picture of a normal intestinal wall, like the small intestine. In Crohn's disease, the inflammation is really severe, and it's deep, or can be severe. So we call it transmural inflammation, and it actually goes all the way down into the walls, and that can lead to cobblestoning. You can also see increased fat involvement around areas that are affected with Crohn's disease, whereas ulcerative colitis, the inflammation is limited to the mucosa, meaning, yes, you can definitely still get severe inflammation, but it's not going all the way—sorry, this pointer is hard to use—it's not going all the way through the wall. So it's only involving the inside lining of the colon. But that inflammation, again, can be severe, can lead to ulcerations, and there'll be some pictures later on in the presentation of that, and pseudopolyps as well, which we also have pictures of. So the symptoms of Crohn's disease and ulcerative colitis can be similar. So it's difficult to distinguish based on symptoms, but—sorry. What we typically teach is that Crohn's disease is more likely to involve abdominal pain, diarrhea, nausea, vomiting, perianal disease, because like I said, Crohn's can involve anywhere from the mouth to the anus. So you can even have inflammation on the outside of the anus and also in the inside of the mouth too, fevers, and weight loss. Now these symptoms are caused by the inflammation caused by the Crohn's itself, but also due to other complications. So you can see here on this top left image, there's a stenosis. So where the arrow's pointing to where it says stenosis is the ileocecal valve. So that's where the end of the small intestine should open up into the colon. That's a common place where you can see stenosis or narrowing, and that can cause obstructive symptoms, similar to what Bill was just describing, where stool chyme is not making it through that stenosed area, and so it can lead to abdominal pain, nausea, vomiting. You have inflammation as well, which can lead to similar symptoms, and you can have fistulas as well. So in particular, where the fistula's pointing to, you can have fistulas, which are basically little connections between anywhere in your GI tract and even outside of your GI tract as well. So here they're demonstrating a fistula or an abnormal connection from the end of the small intestine to the colon. But you can also have fistulas that can connect between parts of the colon and the bladder, which can lead to someone essentially kind of urinating poop. You can have fistula connections between the colon and the vagina, and really anywhere. So because the Crohn's inflammation is so deep and transmural, it can actually extend outside of the GI tract as well. Now diagnosis, like I said, it's difficult to really get the diagnosis itself just from symptoms and just from history, so you need to use your clinical assessment, your physical exam, radiographic, endoscopic, and pathologic findings on biopsy. So on the left here, this is an example of a stricture that you're seeing on a small bowel follow-through. So a small bowel follow-through is, well, we've seen several images today, the black and white barium studies. So this is one where you swallow barium, which is a white, milky liquid that shows up as white on an X-ray. And we've seen images where the barium, you swallow it, and we're looking at the esophagus. This you're swallowing it, but then taking pictures as the barium goes even further through your stomach and into your small intestine. And you can see here that the barium is, there's an area where the barium is not going through. Now in the middle picture here, this is the cobblestoning of the mucosa. This is pretty severe Crohn's disease where you see really deep ulcerations and it kind of looks cobblestoned. And on the right side, this is a granuloma. So that is a type of, a collection of inflammatory cells that usually develops when you have chronic inflammation. And the reason why we pointed out here is that granulomas are only seen in Crohn's disease and not ulcerative colitis. And you can have granulomas in other types of diseases as well, particularly other autoimmune disorders. But that is one thing where if you're having a tough time distinguishing between ulcerative colitis and Crohn's disease, which we often do, seeing granulomas is, you know, a pathomonic for Crohn's disease. So treatments. So the goals are to improve quality of life always. As you can imagine, these symptoms can be very, very debilitating. And we assess for that by looking for clinical and endoscopic remission. So that essentially means that, so the pictures that you saw before, that's someone coming in, they clearly have a lot of inflammation. They are not in remission. They're not in remission clinically in the sense that they're still having symptoms. And endoscopically, it still looks inflamed. So the idea is that you want to get someone into remission, which is terminology that most people are more familiar with when it comes to cancer care. But in IBD, we use it to mean that clinically remission, the patient is feeling better. And endoscopic remission is when the patient's endoscopic findings are also improved. And then once you get them into remission, you want to maintain remission. So most people need to be on some sort of therapy lifelong. And then histologic healing, there's a question mark here because we've been kind of moving, you know, initially when IBD started to be really treated with these biologic medications, we were really happy just to get patients into clinical remission feeling better. But then we realized that even if you're feeling better, but your colonoscopy still looks bad, you're at risk for having flares of disease. So then we were, our goal was basically to get endoscopic remission as well. And now we've realized that even better than just looking normal, if you take biopsies and the histology has actually gone completely back to normal, those patients do even better. So that's the goal. We call it histologic remission or histologic normalization. So treatment options. So historically, we've used more antibiotics, not as much these days unless there's some sort of a complication like stricturing, fistulizing disease, but antibiotics sometimes. Aminosalicylates, those were kind of the first medication that we used to treat IBD. Still used occasionally, not so much for Crohn's disease, more for ulcerative colitis. Then corticosteroids, things like prednisone, budesonide, we'll talk a little bit more about later. Immunomodulators, these are usually oral drugs, things like azathioprine, methotrexate, biologics. Anti-TNFs were the first class that started with Remicade or Infliximab that came out in the 90s, initially developed for rheumatoid arthritis. And as you know, many of these biologic drugs, they can be developed for one condition, but they're also helpful in other conditions, as you're aware of with Dupixent. And so after Infliximab was seen to be so successful for rheumatoid arthritis, we did start using it for IBD, and patients have done quite well. Then there's anti-integrins, anti-IL-12s, 23s. These are newer drugs that I'm sure you see advertised on TV all the time. And also small molecules. So these are medications that are often oral, that rather than being monoclonal antibodies or affecting actual molecules themselves, rather than antibodies, so working on much smaller targets, and can be easier to tolerate because they're being given orally. Now unfortunately, some of our patients still do need surgical management, including resections, fistulactomies, seton placements, and abscess drainage. Now ulcerative colitis is the other kind of half of IBD. It's also a chronic relapsing inflammatory disease. However, as I mentioned, ulcerative colitis is only limited to the colon, and it's contiguous or continuous, meaning it starts in the rectum and goes all the way up or stops at a certain point. And it always, always involves the rectum. Now ulcerative colitis symptoms can include bloody diarrhea, pus, and mucus, and bowel movements, and all of these other symptoms that we also described for Crohn's disease. And also tenesmus, which is kind of just the sensation that you have to have a bowel movement because it's so inflamed down there in your rectum. It just kind of always feels like you have to have a bowel movement. Now all of these symptoms can be seen in Crohn's disease as well. This is kind of the textbook, but really you can't determine just from symptoms alone what someone has. Now in terms of diagnosis, again, we usually make it endoscopically. So on colonoscopy on the left side here, you can see a patient with very severe ulcerative colitis with very deep ulcers. Those are the white parts. And pseudopolis, which are kind of inflammatory growths in the intervening mucosa. And then this on the right side is kind of a less severe ulcerative colitis, but still moderate probably with red, friable. That means just everything, it bleeds really easily when you touch it, and loss of vascular pattern. There's basically no vascular pattern. And so treatment. So this is the pyramid of treatment for IBD that I was kind of taught in medical school. There's definitely some controversy within the IBD field these days, where essentially you would start with kind of the medications that have the least side effects, things like aminosalicylates and steroids. And then you would go up to immunomodulators and corticosteroids, and then if necessary, biologics. And so that's the framework that we used to use. Now there is a lot. Now we're trying to move towards staging the patient in terms of the severity of their disease right away, and recognizing there are some patients who really need to start at the top of the pyramid. And so we don't have to do kind of a graded approach. If we diagnose someone and their disease is severe to begin with, that they really just need to start with a biologic. Now complications of ulcerative colitis specifically, you can see toxic megacolon. So this is when the colonic mucosa is severely inflamed, and you basically have a loss of tone, a loss of muscle tone. And so the colon is very lax, and it becomes extremely dilated. You're at high risk for perforation, and this typically requires surgery. Now you can see this in ulcerative colitis. You can also see it in severe osteofiscial infection as well, too. Now microscopic colitis is another form of inflammatory bowel disease, and it's controversial whether people consider it to be IBD, but I do. And it's another inflammatory condition of the colon, and as the name suggests, the inflammation is typically only apparent microscopically, so when you take biopsies. So in theory, a patient will come in with chronic watery diarrhea. They'll have a normal appearing colonoscopy, but when you take the biopsies, you can see changes. Now I say in theory because if you look at, there are certain findings on colonoscopy that can suggest that someone has microscopic colitis, especially in people who see it a lot, but that's how it was originally described. Now there's two forms of microscopic colitis. So on the left side here, we have collagenous colitis. So that's when basically everyone should have a layer of collagen, which is the kind of light pink stuff. Sorry, I'm not good with the pointer. But in these folks, that layer is expanded. And then on the flip side, lymphocytes are basically all of the cells that have kind of round centers and round purple centers that are the nuclei. And in folks who have lymphocytic colitis, there are more of those compared to normal. And both of those conditions have very similar symptoms, so chronic watery diarrhea. Now diagnosis of microscopic colitis, we have to make it on colonoscopy. So you go through, you do your whole colonoscopy, you don't see Crohn's disease, you don't see ulcerative colitis, but you're still suspecting some form of IBD causing their symptoms. You take biopsies, and then you'll see the findings on the previous slide. Now treatment for microscopic colitis, honestly, a lot of patients do respond to antidiarrheals, meaning just like abodium or loperamide, diphenoxylate, which is lamodal, other things like that. Some patients have been treated with five ASAs, but that's kind of fallen out of favor these days. Now first one is budesonide, which is another type of cortical steroid. However, it's ideal because it's not as absorbed into the bloodstream as something like prednisone or methylprednisolone. So most of its infects are on the inside of the GI tract. So there's less systemic effects. Other steroids can be an option. And in very rare cases, there has been work in the literature about using biologics for microscopic colitis. Now on the flip side, irritable bowel syndrome, which is actually what I see most of the time. My clinical focus is in functional bowels. So irritable bowel syndrome is a functional GI condition, or nowadays we're kind of using the phrasing disorders of gut-brain interaction. It's a chronic condition of the lower GI tract that can have either, well, it has to involve abdominal pain or discomfort and a change in bowel habits, which we'll go over the criteria. So epidemiology is incredibly common. Most people know someone who has IBS, even if they don't kind of talk about it. It's about 15% of the US population. It is much more frequent in women, about two times more. And there are several described subtypes, but the main one we'll stick to today are IBS-D, where it's mostly diarrhea, IBS-C, where you have constipation, and IBS-M, where you're kind of a mixed type. Now the ROAM criteria, the ROAM Foundation is basically a group of physicians and scientists who meet together to come up with definitions for various disorders, usually of gut-brain interaction, so that we're all kind of on the same page when we're describing these disorders that often don't have clear kind of endoscopic or radiologic or laboratory data to define them. So the most recent criteria for irritable bowel syndrome are that a patient has to have abdominal pain, and I always emphasize this with students and residents and fellows. Someone who is just having diarrhea or just having constipation without abdominal pain or discomfort technically does not have IBS. So it's really an abdominal pain syndrome first, plus change in bowel habits. Now that abdominal pain should be related to defecation. Usually patients will have improvement in their symptoms after a bowel movement, but not always. It has to be associated with either a change in stool frequency or a change in the stool form or appearance. Now causes, so it's definitely multifactorial. So we know that their psychosocial factors are incredibly important, and I see that in my practice all the time. We also know that infections can put you at risk for IBS, or particularly another subset called post-infectious irritable bowel syndrome. But even an infection in general can affect the gut microbiome, which can lead to symptoms very similar to IBS. There's alterations in gut motility, visceral hypersensitivity, which essentially means that certain individuals are more sensitive to the normal sensations that we get when we eat and digest food. And then there can also be an imbalance in gut neurotransmitters as well. Now diagnosis, IBS is a clinical diagnosis, meaning that, as I was mentioning, there aren't any clear kind of objective findings that we can use to diagnose it. Essentially what we want to do, you know, and historically what I was taught was that it's a diagnosis of exclusion. So you want to make sure that there isn't something serious like Crohn's disease or cancer or celiac disease that's causing their symptoms. Nowadays we're being encouraged to more kind of use a positive diagnosis approach, which essentially means that if the patient meets room for criteria and they don't have any clear alarm symptoms, that you can diagnose them without doing endoscopies and colonoscopies. The alarm symptoms we do worry about are just age, being over 50 or even over 45 now, weight loss, anemia, low blood counts, and GI bleeding. Now treatment for IBS is varied. Now there are definitely certain things that we do know work well for people regardless of the subtype of their IBS. So in particular, fiber can help with global symptoms of IBS, whether you're having diarrhea or constipation, but we usually recommend it for folks who are either on the constipated side or mixed. Dietary modification, particularly the low FODMAP diet, which I go over all the time in my clinic, but it's basically excluding certain carbohydrates, not all carbs, not a low carb diet, but certain carbohydrates that we know are fermented by the GI tract and can cause a lot of bloating and promote looser stools. And then also psychological evaluation. If you're lucky, you have a GI psychologist who works with you. Not everyone does. I have an amazing one and it's a great resource to have. Now in terms of symptoms, that management, that kind of depends on what subtype of IBS you have. Antidiarrheals can help, laxatives, antispasmodics, those are medications that actually reduce muscle spasm and can help with pain. Angiolytics, so anti-anxiety medications, antidepressants. Some people are surprised by how many antidepressants I do prescribe as a GI doctor, but they can definitely help with that gut-brain access. Now receptor drugs or secretogogs, these are newer drugs that are, or sorry, some of them are secretogogs, some of them are just drugs that work on specific receptors. So Losatron is a medication that's useful for IBSD, patients who have really severe diarrhea that doesn't respond well to any other over-the-counter medications. Only approved for use in women, something to keep in mind. Aloxadoline is a kind of opiate analog that's also helpful for folks who have IBS with diarrhea. A main thing to keep in mind there is that you can't use it in folks who have not had, who have had their gallbladder removed. So it raises your risk of pancreatitis. Linacletide, lupiprostone, and fluconetide are all secretogogs, so these are all medications that are basically like laxatives. They increase water and electrolyte secretion into the gut. And then alternatives, hypnotherapy. So if you do have a great GI psychologist, they can also do gut hypnotherapy. Ours does it as a group, and it's basically what it sounds like. You're basically kind of teaching the patients how to almost like go into a state of hypnosis so that they can kind of overcome the overwhelming sense, overwhelming effect that the symptoms are having on their life. Stress management, very important. And holistic medicine as well. So any questions? Sorry, I know I went a bit over. Yeah. I have a question around the goal of treatment for IBD being clinical and histologic. My assumption is then you're doing a lot of repeat colonoscopies? Yes. Okay, so there's some parallels with like EOE, right? So my question is, we see in the community that a lot of times they're not doing repeat and managing just on symptoms. With IBD, do you think community doctors, would that be similar? Are they much more willing or able to do those repeat colonoscopies? I think part of it is that IBD is something that we've been treating for longer and that we're more familiar with the disease state. So even in the community, we're definitely, I think everyone's doing their appropriate kind of surveillance. There's kind of differences between, you know, scoping someone to assess a response to treatment. And then there's also a separate issue of surveillance. So in patients who, I didn't talk about this, but in patients who have IBD that involves the colon, particularly large parts of the colon, that increases your risk of cancer. Because inflammation anywhere in the body increases your risk of cancer. We know that that happens in IBD as well. So in folks who have IBD involving most of their colon, they should be getting colonoscopies. There's controversy on the timing there, but somewhere between one and five years, depending on where you live in the world, what guidelines you follow. So that I think everyone is doing. In terms of assessing response to treatment, the guidelines are a little bit less clear. So there's no guideline that necessarily says you start someone on a biologic and then you scope them exactly six months out. It's kind of just where you trained. And I basically just do what my IBDologist taught me to do as a fellow. And it's a little bit less clear. But I think people are more willing to do it than any other. We need to be better. Thank you. That's very helpful.

Inflammatory Bowel Disease

IBD

Irritable Bowel Syndrome

Crohn's disease

ulcerative colitis

diagnosis of IBD