Figure 6. Crohn’s Disease (https://howshealth.com/crohs-disease/, 2017)
Crohn’s disease (CD) is a chronic inflammatory bowel disease of unknown origin characterized by periods of remission and exacerbation. It can occur anywhere along the gastrointestinal tract from the mouth to the anus, but most commonly CD affects the distal small intestine and the proximal large colon (McCance & Huether, 2014). Many gene mutations have been identified to be associated with CD, with CARD15/NOD2 having the strongest association (McCance & Huether, 2014). The CARD15/NOD2 genes code for a protein that helps recognize gram-positive and gram-negative bacteria. It is possible that CD is a result of an overactive response to normal flora in the gut of individuals who have a genetic predisposition (McCance & Huether, 2014).
Crohn’s disease begins as inflammation in the intestinal submucosa and crosses the intestinal wall to involve the mucosa and serosa. Type 1 helper T-cells begin the damaging inflammatory response and activate leukocytes and cytokines which cause further injury (McCance & Huether, 2014). Prostaglandins, proteases, reactive oxygen species, leuokotrienes, and nitric oxide are released by leukocytes and continue the inflammatory response and subsequent injury (McCance & Huether, 2014). Aphthoid lesions (shallow ulcers) result after neutrophils invade and destroy the intestinal crypts (McCance & Huether, 2014). The inflammation and lesions can be interspersed with healthy mucosal tissue creating what are known as “skip” lesions (Smith & Harris, 2014). One side of the intestinal wall may be affected while tissue on the other side remains healthy.
Longitudinal and transverse fissures and crevices commonly extend into lymphoid tissue, surrounded by areas of edema in the submucosa which results in granulomas with a cobblestone appearance of the diseased bowel (Smith & Harris, 2014). The intestinal lumen can narrow subsequent to inflammation, edema, and fibrotic strictures. Fistulas can develop between loops of intestine or between the intestine and the bladder, vagina, and perianal area (McCance & Huether, 2014).
Figure 7. Gut-wrenching Characteristics of Crohn Disease (Smith & Harris, 2014)
The most common clinical manifestations of Crohn’s disease are abdominal pain and diarrhea (greater than five stools per day) with the passing of blood and mucus, although symptoms can vary depending on the location and progression of the disease (McCance & Huether, 2014). Many individuals complain of an “irritable bowel” with no other specific symptoms for several years before diagnosis. Weight loss is common and nutritional deficiencies may result from decreased colonic absorption (Smith & Harris, 2014). These deficiencies may lead to anemia, hypoalbuminemia, and bone disease from low folic acid, vitamin B12, vitamin D, and calcium levels (McCance & Huether, 2014). Patients may also experience extraintestinal manifestations including fever, gall stones, mouth ulcers, erythema nodosum, primary sclerosing cholangitis of the liver, uveitis of the eye, and migratory polyarthritis. 30% of individuals experience anal fissures, fistulas, and/or perianal abscess (McCance & Huether, 2014). There is an increased risk of intestinal adenocarcinoma for patients with a long duration of CD (McCance & Huether, 2014).
Figure 8. Ulcerative Colitis and Crohn’s Disease (https://howshealth.com/crohns-disease/, 2017)