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FOUNDATION OVERVIEW

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Inflammatory bowel disease (IBD) is a chronic relapsing and remitting inflammatory condition of the gastrointestinal (GI) tract, and it consists of ulcerative colitis (UC) and Crohn disease (CD). While the underlying pathophysiology of IBD involves an abnormal immune inflammatory response directed against the intestinal tract, the true cause of IBD has not been identified. Genetic and environmental factors have been implicated as contributors to the development of IBD. IBD has been observed to occur more commonly in patients who report a positive family history of IBD. Another leading theory is that the inflammatory response is induced by the local bacterial flora that inhabits the human GI tract. Ultimately, the inflammatory response results in injury to the GI tract that may vary in location, depth, severity, and duration.

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While both UC and CD involve inflammation of the GI tract, there are some key differences between the two. UC is localized to the colon and is characterized by diffuse continuous mucosal inflammation with the absence of granulomatous changes. The rectal area is involved in 95% of patients with UC. In contrast, CD may affect any area of the GI tract, but most frequently involves the ileum or colon. The inflammation in CD is often discontinuous in nature, resulting in “skip lesions,” and often penetrates deeper into the intestinal wall compared to UC. Inflammation confined to the intestinal wall is referred to as luminal CD, and may progress to fibrostenotic disease with development of strictures and luminal obstruction. Likewise, severe inflammation resulting in fistula formation occurs in 20% to 40% of patients with CD, while patients with UC do not develop fistulae.

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Owing to the location and inflammatory nature of the disease, most patients with UC will present with bloody diarrhea, urgency, and tenesmus as their main symptoms. Patients with CD may exhibit similar symptoms, but most commonly present with diarrhea, abdominal pain, weight loss, fever, perianal lesions, and signs of malnutrition. In addition to GI tract involvement, patients with IBD may also develop inflammation in various other organ systems, referred to as extraintestinal symptoms. Examples include arthritis, erythema nodosum, pyoderma gangrenosum, uveitis, episcleritis, and primary sclerosing cholangitis.

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The diagnosis of IBD is based on presenting signs and symptoms, along with radiographic and endoscopic findings. Endoscopy is particularly helpful in characterizing the extent and location of the disease, as well as ruling out other potential causes of intestinal inflammation. Disease location also directly impacts selection of drug therapy. Patients with UC can be classified as having “extensive” disease if inflammation extends proximal to the splenic flexure. The terms “distal” or “left-sided” disease are used if inflammation is distal to the splenic flexure. Last, ulcerative proctitis denotes inflammation localized to the rectum, while proctosigmoiditis involves both the rectum and sigmoid colon. While these terms are used for denoting the subtype of UC based on extent and location of inflammation, the extent and location of CD is ...

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