DIP Episode 384 - IBDs and The USMLEs (Step 1-3)

Okay, welcome. My name is Divine. This is episode 384 of the Divine Intervention Podcast. And to this podcast, we'll be looking at the inflammatory bowel disease and the USMELIS. Inflammatory bowel disease and the USMELIS. As a reminder, if you're taking the USMELIS tip-to-seqos, tip-3 exams, I do have some courses coming up that might interest you. On the 22nd of this month, I have an MBME Testic and Strategy course. It's from 5 to 7 30 PM, Pacific Standard Time. Again, tons of people have taken this course as they've done extremely well on the exams as a result. And then I also have a 20-hour review course. It's going to be 10 hours on two Saturdays. I decided to do it that way so it works better with people's schedules, but basically it's going to be on the 23rd on the 30th of this month. It's going to be 10 hours each day. And we're going to be covering a lot of internal medicine, surgery, OB-GYN, PEED, psych, Neural, Ethics, Bio Statistics, we'll also be covering the multi-systems processes and disorders. So again, if that's something you're interested in, shoot me an email through the website and I'll give you some more information. Now, another thing I want to say is I have a disk school. I call it the USMELIS.2 CT-STEP-3 school. Really, all these courses apply to STEP-2, STEP-3, Complex Level 2 and 3. And basically, the way the school is is going to be 75 hours. There's a limited number of people that can attend.

There's definitely cups made a very extensive podcast on that. But basically in the school, it's going to be 75 hours. We're going to use many different approaches to review a material. And really, like the material we're reviewing is something that has come from years of research and just putting stuff together. But it's something it's a school where if you attend it, you're going to learn so much. And I'm going to try to give as much attention to the people that attend as is possible. That's why I'm going to make the, that's why the school is much smaller. I'm going to make it small so I can give people more more attention. But you're going to learn a ton. It's going to be a very in-depth, very comprehensive review. You'll see the same material from many different angles. It's going to be taking place in the first two weeks of May. There's a limited number of spots available. So if you're interested, shoot me an email through the website. And all these courses will be held via Zoom. I suspect that people that attend the step to CK school will probably be walking away with about 500 to 600 pages worth of notes from the school. Okay. So let's just jump right into the inflammatory bowel disease. Right. So what if you give the give your question about a 33-year-old female, they tell you that she comes to the emergency room or comes to a primary care physician. No, let me say comes to the emergency room because for the last 12 hours she's been having a lot of flank pain, right?

Radiating to the growing. And then they see something along the lines of that, you know, she gets a helical CT, right? Basically like a non-contrast CT of the abdomen and, you know, an opacity scene. Right. And in detail, that this female has a history of chronic diarrhea. If you see all those things, or should we be thinking about? Well, I would really hope you're saying, hmm, divine. This sounds an awful lot like Crohn's disease, right? Crohn's disease. So why does this person have this flank pain, radiating to the growing? Well, she has nephrolithiasis. And the Crohn's disease typically affects the terminal elium. So since he messes up the terminal elium, you're going to have increased absorption of oxalate. So that causes those people to be predisposed to forming oxalate crystals. They have an oxalate nephrolithiasis, right? So what are some high yield things you want to keep at the back of your mind with Crohn's disease? Well, just a few things here and there, right? So I just said that Crohn's disease, the terminal elium is pretty much always involved, right? So they have small bowel involvement, right? Typically the first place Crohn's start is in the small intestine, right? And Crohn's, the thing about Crohn's disease, it can affect, I'll see him pretty much any mucus or surface, right? It can go the way from the mouth all the way to the ines. Most times, right? The manifestations tend to be in the intestines, right?

Especially in the terminal elium and then some parts of the colon, right? Now remember, though, unlike all radiophilithic colitis, Crohn's disease does not go after a person's rectum. It doesn't really affect the rectum. And for the most part, it could affect the ines, right? But again, the rectum is something that is just more commonly affected in UC, than UC affected in Crohn's. Now, it's very high yield to remember that in Crohn's disease, these people tend to have a lot of granulomas in the GI tract, right? So again, if for whatever bizarre reason, our friends at the MBM is, sure you like a small intestinal biopsy, and you see all these epithelioid macrophages, they're pretty much telling you that the person has Crohn's, right? They're pretty much telling you that the person has Crohn's. Now remember, Crohn's, that inflammation, you know, you inflame the entire wall of the of the intestines, right? So you have a transmural inflammation. So if you think about it, it would make sense that if you're inflaming the entire section of the wall of the bowel, you know, it makes sense that you can begin to form fistulas, right? So whenever you see a person that has inflammatory bowel disease and you see fistulas, you always want to think about Crohn's disease, right? Those fistulas are pretty common, right? So they can have fistulas to the skin, they can have like an interocutinious fistula, they can have fistulas to the bladder, right?

They can have like an interversical fistula, right? They can form fistulas in wet, weird places, right? I mean, in fact, they can even give you a question about a person that has Crohn's disease. And you see the person over like two, three days, they are vomiting, they are throwing up, they have abdominal pain, right? And they have like a long history of Crohn's. Then our friends at the MBM is essentially trying to tell you that, hmm, these people have strictures, right? Remember, this is like a concept on the MBM's and just clinical concept. Whenever you have chronic inflammation of a macosophage, that inflammation can heal with the formation of structures. For example, in Crohn's disease, they have chronic, chronic, chronic inflammation that can lead to a structure formation. In people that have peptic ulcer disease, that chronic inflammation of either the, you know, blood numb, blood numb, your ulcer, gastric macosa can lead to a structure formation that can cause a small bowel or gastric outlet obstruction, right? People that have a gird, again, that chronic inflammation of the distal of the soft and gas that can lead to structure formation that can cause this phage. If you see this phage in a person that has a long history of gird, one of the things you should strongly be considering is a structure, right?

If you look at a woman that has had recurrent dilutions and curitashes, you know, for abortions and stuff, or for recurrent PID, again, all that scratching, scratching, scratching, scratching, the wall of the uterus, that inflammation can heal with structure formation. That's essentially what causes Ashaman syndrome, that's essentially what causes Ashaman syndrome. So this whole concept of structures, it's a concept, right? But you can see how it ties across multiple disciplines, right? I remember people that have a chronic disease, right? Most times, these people would tend to have diarrhea, right? Can they have bloodied diarrhea? Yes, but it's highly unlikely on your exams. Most times when you see a chronic disease question on the test, it's going to be a person that has watery diarrhea, right? Many times they're going to have watery diarrhea. And remember, curus disease for the most part does not really have much in the way of biliary problems that come with it, right? Remember that's usually more under the purview of Australian colitis. But curus disease for the most part, it causes many more problems is like, why should I throw in a biliary issue on top of that, right? So most times when people have curus disease, they don't have biliary problems on like Australian colitis, where those people can have like primary sclerosis or colonitis, right? And again, remember I said, yeah, people that have curus disease affect anywhere from the mouth to the inus, right?

Well, it's not a continuous problem, right? Usually these things called skip lesions, right? So you see like patchy areas of involvement all through the all through the intestines, right? So that's something that's very high up to no for for exams, right? That's something that's very high up to no for for exams, right? So for the most part, in terms of diagnosing curals, really, any kind of inflammatory bowel disease, how you're going to diagnose it? One thing that's kind of high up to no is obviously a person is going to have the characteristic symptoms, right? Gonna have the characteristic symptoms, but typically, you know, one thing that I think is very helpful in making the diagnosis, right? Because remember, many times in medicine, I like to do a screening test first, then after we screen it, we like to confirm what we're just screened for. So one thing that you can pick as a good screening test is to check the fetal, the fecal, not fetal, whoops, fecal, calprotectin, right? Fecal, calprotectin. Many times in the question, they will tell you that, oh, fetal, fecal, what do I keep saying fetal? Fecal, calprotectin is positive. When you tell you that, pretty much telling you that, hmm, this person has inflammatory bowel disease. So what's this deal with this fecal, calprotectin?

Well, the thing about fecal, calprotectin is that it's positive whenever you have neutrophils in your GI tract, whenever you have inflammation in your GI tract, your fecal, calprotectin will be positive, right? And so it's very sensitive for IBD, right? Of any sort, BDUC, BD Crohn's, right? Your fecal, calprotectin is very sensitive, but obviously it's not very specific because there are many other things that cause inflammation in the GI tract, you know, like microscopic colitis, celiac disease, tropical spur, all those things, right? To cause an elevated fecal, calprotectin. But if a person comes in with what looks like signs and symptoms of inflammatory bowel disease, B Crohn's or UC, you notice that the fecal, calprotectin is negative. Those people essentially do not have any of those problems, right? So remember, tests that is very sensitive, right? When negative rules out disease, right? You probably learned of this not nomadic, right? Sensitive tests when it comes out negative means you don't have disease, right? And kind of think about it like D-dimer, right? For a person, D-dimer is negative, it's highly unlikely that they have a PE, right? Highly, highly unlikely that they have a PE, right? So the fecal calprotectin will be positive, right? So again, where does this calprotectin come from? It actually comes from the neutrophil.

To be honest with you, if you look at the side of a neutrophil, about 60% of the protein, of the soluble proteins in the side of a neutrophil, it's actually calprotectin. So if there are a lot of neutrophils around, again, neutrophils, they don't live forever. They live for like 24 hours and then they kind of hip-hop dose, you know, as they die and they release their cells soup into the surroundings, right? Part of their cell soup is the calprotectin, right? So the calprotectin will be positive. The presence that's got Crohn's disease, that's very high, you know, for example. And then if you notice that the fecal calprotectin is positive, right? Then you have to do a colonoscopy, right? There is no, really there's no blood test that can help you differentiate you see from Crohn's. So you've got to do a colonoscopy and you'll see some of these characteristics findings, right? That I say for Crohn's like granulomas, scape lesions, you know, you see all these things. But for Australia for colitis, right? So I guess maybe less, maybe do a compare and contrast with all Australia for colitis. Australia for colitis is a little different. Australia for colitis is a little different in the sense that you usually will not find granulomas in the GI tract, right? That's important. Remember you find granulomas in Crohn's. And I said that in Crohn's, you have transmural inflammation. So the entire intestinal wall is involved, not so for Crohn's, for UC.

Most times people that have UC, right? It's kind of high out to know that they have like shallow ulcers, right? They have shallow ulcers. But usually the lesions are not scape lesions. It's usually like a continuous lesion. And one thing I'll just tell you pretty much for purposes of NBM exams, people that have UC is going to be, the rectum is going to be involved, right? Just like I said, the terminal ilium is pretty much always involved in Crohn's. The rectum is pretty much always involved in people that have an ulcerative colitis, right? And remember if they give you an ulcerative colitis question where you see the person having jaundice, parietas, young male, blah, blah, blah, blah. That's going to be primary sclerosis in colangitis, right? That's going to be PSC, primary sclerosis in colangitis. Remember in PSC, many times those people have a pianca that's positive, right? And in PSC, it's typically the intra and extra hepatic bowel docks that are affected, right? So that's how those people essentially get into trouble, right? And really also dial which helps in PBC does not do deadly squat in people that have PSC, right? So in PSC, drugs really don't help. You know, one thing you can try to do is you can do an ERCP and excise whatever strictures that exist. Again, see those strictures come up again, chronic inflammation, they can have strictures in the ability to attract, right? That causes all these problems, right?

So you can endoscopically excise those strictures, it doesn't really do anything. Really the way you're going to cure primary sclerosis in colangitis is by putting out the person's liver and putting a fresh one, right? So you do a liver transplant, that's how you can really treat that. Now it's very high you to remember for PBC has UC and they have a primary sclerosis in colangitis. Eight years after that PSC diagnosis is made, those people need regular screening for colon cancer, right? So eight years after the initial diagnosis of PSC is made, they need colonoscopies, surveillance colonoscopies for colorectal cancer. Because again, if you think about it, if you have this chronic, chronic, chronic inflammation of the GI tract, right? That's going to predispose you to getting a colorectal cancer. Really, Crohn's UC, those will both have elevated risk of colorectal cancer, right? And again, it's pretty high you to remember that when people have ulcerative colitis, many times on in-beaming exams, they're going to have a lot of bloody diarrhea, right? You're going to have a lot of bloody diarrhea. But most times those people tend to not lose weight. That's a pretty high you to know. Most people that have ulcerative colitis, they have bloody diarrhea, a lot of tenesmas, tenesmas just means that you don't feel like your, you don't feel like your, your GI tract is, you don't feel like you've emptied properly. You feel like you've just pooped.

You're like, man, I don't feel like I've completely emptied my GI tract. That's something that you find a lot in inflammatory bowel disease, right? But again, it's a lot more common in ulcerative colitis. They just feel like they've never completely emptied themselves, right? Almost like it's not a real stool in continents, but they just feel like they've never completely emptied themselves, right? And again, they tend to have more just bloody diarrhea, right? They tend to have just more bloody diarrhea. And all these things, I say, with fistulas for Crohn's disease, like enterocutaneous, enterovysical fistulas, entero-inophistulas, those are not things you really find in ulcerative colitis. Again, if you see those fistulas on exams, think of a problem that's associated with transmural inflammation. That's going to be more along the lines of a Crohn's disease on tests, right? There's usually more along the lines of Crohn's disease on tests. Even these structures that I said we find in Crohn's disease. Again, we pretty much never find them in ulcerative colitis on NV Me exams, okay? On NV Me exams. Now, what are some other just weird things that our friends at the NV Mes will kind of like you to know about these Crohn's disease ulcerative colitis so in terms of treatment, right? So the thing is, most times people that have these problems, you know, it's been diagnosed by colonoscopy with biopsy, right? Typically, if it's ulcerative colitis, these people have mesalazine is great.

It's a great first-line therapy. It's pretty amazing, works for these people pretty well. Although, again, remember, the only way you can truly cure ulcerative colitis is by calling out the presence, if you're doing a procto-collectomy, not a colectomy, a procto-collectomy. So a procto-collectomy means you're resetting the colon and the rectum. If you just reset the colon, or you're kind of living the rectum, it's not pretty, not particularly wise, right? So, again, you see, you're going to cure it by calling out the entire colon. You see, gone, because you see, it does not affect anything beyond the colon. But Crohn's disease, right? Again, most times, surgery in Crohn's disease is when you're resetting structures, resetting fistulas, really doing a colectomy. It doesn't really prevent, it doesn't cure Crohn's. Many times, the Crohn's is going to recur at the point of an asthmosis, right? So, for the most part, again, surgery is not as helpful in Crohn's. Even mesalazine, not as helpful in Crohn's, right? So, most times, these people, if you've tried mesalazine, or you've tried sulfazalazine, and it's not working, you can usually jump up to a TNF inhibitor, a two-minute curses factor inhibitor. Actually, in some people, especially people that have Crohn's antibiotics, that really work pretty well, pretty effective long-term. So, that's just something I want to consider on exams. Sometimes, you may see an antibiotic as the right answer for Crohn's disease.

But most times, these people, they respond pretty well to TNF inhibitors. Obviously, if you have a flare of either of these diseases, you see a Crohn's. The smart thing you're going to be doing is, you're going to be giving those people sterites, right? Sterites have a treatment of choice for flare, fliers, right? You don't use them for maintenance therapy. Please do not use sterites for maintenance therapy in alternative colitis or in Crohn's disease, right? So, one question you may get on an exam is, what is the most common, extreme intestinal manifestation of IBD? Lead Crohn's BDUC? Well, if you see stuff like that, I really, really want you to think about, of course, they're going to put arthritis as an answer. It's going to be wrong. The most common extreme intestinal manifestation of these problems, actually, believe it or not, is anemia, right? Because again, you have that chronic inflammation of the GI tract. You're going to not be reabsorbing iron very well, right? And really, what kind of anemia would you find in a person that has inflammatory bowel disease? Again, a friend that the NBM is, they're smart. They're going to put iron deficiency anemia as an answer. Don't pick that answer. You'll be wrong, right? But if you see the answer that says anemia of chronic disease, that's the one you want to pick. Because think about it, inflammatory bowel disease. The meme is pretty, pretty helpful, right? You have chronic inflammation.

Hepsides is going to be doing its thing. It's going to be locking up iron in your vulnerable micro-fages, right? And it's also going to be, remember, Hepsides in also just literally prevents you from reabsorbing iron, right? So, these people's ferritin will be really, really high. So, the ferritin will be up, right? The ati BC will be down, right? The atransferin saturation will be down, right? And the near-of-cronic disease will be normalcytic, it will be microcytic, right? But again, these people, many times when they have anemia, the way you're going to treat the anemia is by giving them IV iron, parentary iron, not oral iron. Because if you give them oral iron, think about it. Hepsides in is doing its job, right? If Hepsides in is doing its job, it's going to prevent you from reabsorbing iron. Well, if you can reabsorb iron, then giving oral iron is going to be pretty useless, right? So, typically, for poor, they have Australia's collitis or Crohn's, they're just going to give them IV iron, right? Because that essentially bypasses the GI tract that's pretty helpful in these people, right? Pretty helpful. And again, remember, people that have IBD, they can have like these being full tender lesions on their sheds, that's their theme on the dosaum, right? They can also have, you know, all these other problems, right? There's like this, uh, uh, enteropathy associated arthritis, right?

IBD, that's what, you know, IBD associated arthritis, uh, is one of those, uh, some, it's kind of similar in some situations to these, HCILEB27, uh, thropathies, right? Those are all things you can see in people that have these, uh, inflammatory bowel diseases, right? So again, IBD, it's a pretty high-yield topic, it's just one of those things, uh, you know, it doesn't warrant a super long podcast, right? But it's stuff you pretty much want to make sure you know. And to be honest with you, the thing I'll just say at the end here is that, uh, you can give you a question about a person, looks like they have IBD, these people are for sure going to have watery diarrhea, not bloody diarrhea, it's going to be watery. And then they're going to tell you that you do the colonoscopy, and the colonoscopy grossly looks normal, but you know, you take a lot of specimens and then you notice, wow, you look at this person's GI tract and you're like, hmm, man, I see a lot of lymphocytes, right? If all you're seeing is a lot of lymphocytes, then you want to think about something called microscopic colitis. More specifically, you want to think about a subtype called lymphocytic colitis. But if you see a lot of lymphocytes, right? Again, this person has a normal colonoscopy, remember your colonoscopy would not be normal in curs or UC, right?

But this person has a normal colonoscopy, you take a biopsy, and you see a lot of lymphocytes, and you see like a sub epithelial collagen layer, it's very high yield, sub epithelial collagen layer. Then that's something that's called collagenus colitis. Collagenus colitis, it's the second subtype of microscopic colitis, right? So there's lymphocytic colitis, where you see lymphocytes only, there's collagenus colitis, where you see lymphocytes, and a sub epithelial layer of collagen. How do we treat microscopic colitis, give you deconitis? Your deconitis will pretty much take care of their symptoms, although most times when the stop is going to come right back, right? But again, that's just an extracted bit I kind of wanted to throw in for you for exams. So I think I'm going to go ahead and stop here. Again, as I do at the end of every podcast, I do a for one on one tutorial for many exams, step one, step two, CK step three, preclinical med school exams, 30th shelf exams, complex level two and three, I don't tell you to OEMM, but for the most part I tell you to pretty much every every subject. Again, if you want to learn from me, you typically have to book these weeks in advance, just something to keep in mind. And then again, I offer review courses. I even have a step one review course coming up on the 14th of May. It's going to be a 10-hour, very rapid review course. We're going to review a lot of the high-yield information that's routinely tested on the exam.

So again, if you want to sign up for that, shoot me an email through the website. And then I have all these podcasts on Apple podcasts, on Google podcasts, so if you're interested, again, just find it's called the Divine Intervention Podcasts. Although if you want everything from episode one, because these podcasts absolutely let me put the most recent 150, if you want everything from episode one, then go on the website, divineinterventionpodcast.com. If you actually sign up for your Word Press account, if you subscribe to your Word Press accounts, then you get an email notification whenever I make a new podcast. And then I have a You Tube channel called Divine Intervention, USMD Podcasts and Videos. That's where I post the videos that I make. And then I also have a Life Lessons website. It's a Bible-based website. It's called Divine Intervention Life Lessons.com. In fact, there's an associated podcast. It's called the Divine Intervention Life Lessons Podcast. That's an Apple Podcasts. I have about 72 episodes so far. And again, most of it is 5, 10, 15 mini teachings from the Bible that just highlight a common problem that's faced by people in this work. So thank you for listening to me today. I'll see you in the next podcast. Have a wonderful rest of your day. God bless you. Enjoy. Thank you.

Transmural inflammation, skip lesions, granulomas, and fistulas (e.g., enterocutaneous).

The rectum.

Granulomas.

Anemia of Chronic Disease (ACD), due to chronic inflammation sequestering iron.

Colonoscopies for colorectal cancer screening 8 years after the initial PSC diagnosis.

Bloody diarrhea and tenesmus (feeling of incomplete emptying).

Crohn's disease.

Terminal ileum (due to impaired bile salt absorption and increased oxalate).

Lymphocytic only shows lymphocytes; Collagenous adds a subepithelial layer of collagen.

Intravenous (IV) iron.

UC involves mucosal/submucosal layers; Crohn's involves transmural (full thickness) inflammation.

Primary Sclerosing Cholangitis (PSC).

Crohn's disease.

Terminal ileum (due to impaired bile salt absorption and increased oxalate).

Lymphocytic only shows lymphocytes; Collagenous adds a subepithelial layer of collagen.

Intravenous (IV) iron.

UC involves mucosal/submucosal layers; Crohn's involves transmural (full thickness) inflammation.

Primary Sclerosing Cholangitis (PSC).