Inflammatory bowel disease: Pathology review

Alex is a 21 year old college student who has a 2 month history of frequent episodes of abdominal pain and bloody diarrhea. Chris is also a 21 year old college student with painful ulcers in the mouth, intermittent abdominal pain, and non-bloody diarrhea that’s been going on for years. In addition, Chris has a history of recurrent kidney stones.

After careful examination, colonoscopy is ordered in both cases. In Alex’s case, there’s circumferential inflammation that’s continuous throughout an entire section of the rectum and colon. On the other hand, in Chris’ case, there are linear patches of damaged colon with normal mucosa in between, and the rectum is not involved.

Alex and Chris both have inflammatory bowel disease or IBD, which is characterized by chronic gastrointestinal tract inflammation due to autoimmune reactions, as well as systemic symptoms like fatigue, fever and unintentional weight loss. IBD typically has its onset before the age of 30. The exact cause is unknown, but there’s definitely a genetic component because it runs in families. Now, there are two types of IBD - Crohn’s disease and ulcerative colitis.

Okay, now let’s look at each specific disease, starting with Crohn’s disease, which is mostly caused by an abnormal Th1 cellular response, and a known risk factor is smoking. In Crohn’s disease, the inflammation can pop up anywhere in the GI tract, from the mouth to the anus, but the rectum is often spared. It tends to be most severe at the terminal ileum.

Gastrointestinal symptoms include crampy abdominal pain, watery diarrhea that may or may not be bloody, and sometimes malabsorption symptoms like malnutrition, steatorrhea, or B12 deficiency. A very frequent finding to keep in mind are aphthous ulcers in the mouth. Some individuals may also present esophageal involvement, with odynophagia and dysphagia.

Extraintestinal symptoms include arthritis, uveitis and episcleritis, and skin lesions like pyoderma gangrenosum and erythema nodosum. In addition, a high yield fact is that Crohn’s disease leads to a higher risk of kidney stones and gallstones. That’s because damage to the terminal ileum decreases absorption of fats and bile salts in the intestine. The fats bind to calcium, which prevents the calcium from binding to oxalates. Free oxalates are absorbed in the intestine and eventually lead to calcium oxalate stones in the kidneys. On the other hand, the bile salts normally bind to cholesterol to make it water soluble. If there’s a decreased absorption of bile salts, cholesterol can collect and form stones in the gallbladder.