gastrointestinal disorders
Crohn Disease
Pathophysiology of Crohn Disease
Crohn disease begins with crypt inflammation and abscesses, which progress to tiny focal aphthoid ulcers. These mucosal lesions may develop into deep longitudinal and transverse ulcers with intervening mucosal edema, creating a characteristic cobblestoned appearance to the bowel. Transmural spread of inflammation leads to lymphedema and thickening of the bowel wall and mesentery. Mesenteric fat typically extends onto the serosal surface of the bowel. Mesenteric lymph nodes often enlarge. Extensive inflammation may result in hypertrophy of the muscularis mucosae, fibrosis, and stricture formation, which can lead to bowel obstruction. Intra-Abdominal Abscesses are common, and Noncaseating granulomas can occur in lymph nodes, peritoneum, the liver, and all layers of the bowel wall. Although pathognomonic when present, granulomas are not detected in about half of patients with Crohn disease. The presence of granulomas does not seem to be related to the clinical course. Segments of diseased bowel are sharply demarcated from adjacent normal bowel (called skip areas), hence the name regional enteritis ( Pathophysiology reference ): About 30% of Crohn disease cases involve the ileum alone (ileitis). About 40% involve the ileum and colon (ileocolitis), with a predilection for the right side of the colon. About 30% involve the colon alone (granulomatous colitis), most of which, unlike Ulcerative Colitis , spares the rectum. Occasionally, the small bowel is involved (jejunoileitis). The stomach, duodenum, or esophagus is clinically involved only rarely, although microscopic evidence of disease is often detectable in the gastric antrum, especially in younger patients. In the absence of surgical intervention, the disease almost never extends into areas of small bowel that are not involved at first diagnosis. Crohn disease is categorized into 3 principal patterns: (1) primarily inflammatory, which after several years commonly evolves into (2) primarily stenotic or obstructing or (3) primarily penetrating or fistulizing. These different clinical patterns dictate different therapeutic approaches. Some genetic studies suggest a molecular basis for this classification. There is an increased risk of cancer in affected small-bowel segments. Patients with colonic involvement have a long-term risk of Colorectal Cancer equal to that of ulcerative colitis, given the same extent and duration of disease. Chronic Overview of Malabsorption may cause nutritional deficiencies, particularly of vitamins D and B12. Toxic colitis is a rare complication of colonic Crohn disease. It is a clinical syndrome of ileus accompanied by radiographic evidence of colonic dilation; many cases must be treated aggressively with surgical intervention. 1.Dulai PS, Singh S, Vande Casteele N, et al: Should we divide Crohn's disease into ileum-dominant and isolated colonic diseases?Clin Gastroenterol Hepatol17(13):2634-2643, 2019. doi: 10.1016/j.cgh.2019.04.040 