UC or CD: What's the Difference?

Marita Kametas, MSN, APN, from the University of Chicago, begins a series on the basics of inflammatory bowel disease, explaining the differences between ulcerative colitis and Crohn's disease.

Click to full screen for maximum clarity of slides. 

TRANSCRIPT:

Hi, my name is Marita Kametas, nurse practitioner and ostomy specialist at University of Chicago Medicine and the Inflammatory Bowel Disease Center. Today we're going to be discussing disease states and inflammatory bowel disease. We're going to talk about the natural history of inflammatory bowel disease.

Inflammatory bowel disease has been mainly found in developed countries, but patterns are shifting as the biology is changing. IBD was traditionally thought of as a disease diagnosed in early adulthood, but very early onset and elderly patients are being seen even more in this bimodal disease distribution. Since the first descriptions of IBD, many major scientific advances in the genetics, immunology, and microbiology have been enhanced, and so our understanding is increased on the behavior and the underlying causes of IBD. These advancements have unlocked many more increasingly effective treatments for our patients.

This is a historical map of the disease distribution of Crohn's disease and ulcerative colitis. And you'll see that there's some countries that are more predominantly affected than others. But what we're seeing over time is that the expanse of Crohn's disease and ulcerative colitis is expanding across the world. And so there's many populations that are being affected that previously were not. And we're working to understand why that is.

I describe to my patients when they come into my office and they say, "I've just been given a diagnosis of Crohn's disease or ulcerative colitis. I don't know why. What did I do?" And often I describe it as a perfect storm.

IBD is a combination of genetics—so a genetic susceptibility, environmental catalysts and triggers, the microbiome, and oftentimes an immune response or catalyst. I often have many patients that come into my office in January and February and they'll say, "Hi, everyone at Thanksgiving got food poisoning and I'm the only one who's still sick." And so we look at what was the catalyst? Did they maybe have a death in the family or did they quit smoking or tobacco use? And that was enough of an immune catalyst to tag into that genetic susceptibility.

This is a nice depiction of the inflammatory cascade. So on the left of your screen, you'll see the normal bowel. There's a thick mucus layer, there's tight junctions in those cells, and you've got antimicrobial benefits that are happening. When you look at a patient with IBD, and you look at patients that are smoking, or they've got diet or medication changes, you'll see that those junctions start to become less tightly locked, and that allows for antagonists to get in and cause an inflammatory response.

You'll often see as well the thin mucus layer. So some of that protective mucus is gone and that again allows some of these bad actors to get in and start the inflammatory action. So looking at the disease distribution of Crohn's disease versus ulcerative colitis.

So you'll see on the left of your screen a depiction of Crohn's disease. Crohn's disease can often spare the rectum. It can happen anywhere from the mouth into the anus. The disease distribution is patchy, so you won't see this continuous inflammation that you see in ulcerative colitis. And oftentimes Crohn's disease can affect the area of the ileocecal valve where the small bowel and the colon join.

When you look at a patient with ulcerative colitis, they will have continuous circumferential inflammation from the rectum leading upwards, and this can involve isolated proctitis, which is just rectal involvement. It can go to the left side of the colon, or eventually the entire colon can become involved. And an important distinguishing feature is that ileitis component. So a patient that has ileitis, it's very important to look at our pathology and converse with our pathology colleagues to ensure is this a backwash ileitis from a severe ulcerative colitis patient, or is this a patient that maybe has a more appropriate diagnosis of Crohn's disease?

One of the other pathology features that can be helpful in identifying Crohn's disease versus ulcerative colitis is the presence of granulomas. Granulomas are present in Crohn's disease; they are not present in ulcerative colitis. Looking as well at fistula formation, so the connection of two things that shouldn't be there. Those can be bowel-to-bowel fistulas. Those can be enterocutaneous fistulas to the skin, rectovaginal fistulas, fistulas to the bladder, and even other surrounding structures. That is a hallmark of Crohn's disease, as well as stricturing or narrowing of the bowel. So when we look at Crohn's disease, not all patients will be affected by all of those things, but they are things that are classic for Crohn's disease.

Looking at disease behavior, so as I said Crohn's disease can affect anywhere in the GI tract. So it's important that we are all-encompassing when we review our patient's symptoms. It's a transmural process, so it affects all layers of the bowel wall. It has the stricturing and penetrating disease that can be present in some patients and those typically are patients that will have a more severe disease phenotype and risk for progression. Perianal disease can be present, so they'll be fistulas from the skin into the rectum and into the bowel. There can be large skin tags on the anus as well as fissures; patchy inflammation of the mucosa, so it's not that circumferential mucosal inflammation that I discussed in all sorts of colitis. And granulomas will be present on histology in some of your patients. But certainly, we don't identify those in all of our pathology samples for these patients.

And one important distinguishing feature, which is a great interview question for your patients, is it's worse with tobacco use. We know that smoking dramatically worsens the course of Crohn's disease. And even when patients are on the most effective therapies, if they continue to smoke, it's going to be a little bit more challenging to get those patients into remission.

Looking at ulcerative colitis, as I mentioned, it is confined to the colon. It's primarily mucosal involvement, though our understanding of transmural properties is evolving. There is no stricturing or penetrating disease present. If you do have a patient with ulcerative colitis, who has a confirmed definitive diagnosis and they have stricturing, that's a patient that's really important to look more closely at to ensure that there's no dysplasia or carcinoma present. There is no perianal disease in these patients. Circumferential inflammation of the mucosa is hallmark for this disease. There are not granulomas present on histology. And it's often worsened by tobacco cessation. And it's often one of the patient presentations that we see most often as a patient will be quite well, they'll quit smoking, they're trying to focus on wellness. And then all of a sudden they have these ulcerative colitis symptoms that kind of rear their head a few weeks to months after quitting smoking or tobacco use.

See part 2 of this series, Severity vs Activity, here.