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Crohn’s Disease Pathophysiology and Treatment

Crohn’s disease is an inflammatory disorder of the alimentary tract. It can affect almost all parts of the gastrointestinal tract. However, the ileum tends to be more affected than other parts of the alimentary tract. It is characterized by lesions affecting the entire thickness of the intestinal wall. The lesions are not continuous. This paper will discuss the etiology, pathophysiology, signs and symptoms, treatment, and prevention of Crohn’s disease.

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The etiology of Crohn’s disease is not known. However, several risk factors have been identified. Factors that trigger the onset of the disease include smoking, contraceptives (oral), diet, NSAIDs, microorganisms, genetic influence, and immunologic abnormalities. Studies have shown that Jews are the most affected racial group. Asians are the least affected. Children of parents suffering from Crohn’s disease have a greater risk of developing the disease (Orholm, Fonager, Sorensen, 1999). Environmental factors, immunologic factors, and genetic factors have to act together for the disease to develop.

The disorder develops when the body mounts an inappropriate immune response. It happens when the response to food and bacterial antigens is exaggerated. Consequently, excess T helper 1 (Th1) cytokines like interleukin 12 (IL-12) and interferon-gamma are produced. This leads to a loss of balance between inflammatory and counter inflammatory systems. Activation of macrophages and metalloproteinase resulting in mucosal damage follows. In turn, tissue damage leads to an increased risk for infections, absorptive disorders, anemia, and severe pain.

Signs and symptoms of the disorder include severe pain, diarrhea, pallor, anal fissures, weight loss, and abdominal masses. Bleeding may be present. However, bleeding is common in another form of inflammatory bowel disease called ulcerative colitis (Sands, 2004). The inflammatory process damages the absorptive surfaces resulting in diarrhea. Pallor is a sign of anemia, a direct consequence of bleeding. None of the signs and symptoms is specific to Crohn’s disease.

Diagnosis of Crohn’s disease relies on both physical examination and imaging. A thorough history may give enough information to make a diagnosis. Positive family history of the disorder may be used as a starting point. The most commonly used investigative procedure is barium meal swallow. This is an X-ray with a contrast medium. Complete blood count may also be done. Elevated white blood cell count (leukocytosis) is indicative of an inflammatory condition. Other diagnostic techniques include sigmoidoscopy and colonoscopy. They both aid in the visualization of the large intestine.

Drugs used to manage the disorder include immunosuppressive agents, anti-inflammatory agents, antibiotics (broad spectrum), and anti-diarrheal agents. Immunosuppressive agents suppress immune responses. The commonest drug in the class is mercaptopurine. Corticosteroids and infliximab are examples of anti-inflammatory agents (Hanauer & Sandborn, 2001). Loperamide and codeine are the most commonly used anti-diarrheal agents.

Non-pharmacological methods of management include surgery, fluid replacement, and nutritional management. Ulcerated parts of the bowel are surgically removed. Surgery is reserved for cases that are refractory to drugs. Fluid and electrolyte replacement is used to restore fluid chemokinesis. Nutritional therapy is used to hasten the process of healing. In addition, parenteral nutrition may be used during explosive episodes. This allows the alimentary tract to rest. Bulky food and irritating food should be avoided. Complications that may arise include perforation, adhesions, stenosis, and excessive bleeding.

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Crohn’s disease is an inflammatory disorder of the bowel with unknown etiology. Risk factors include smoking, infections, and immunologic abnormalities. It is managed using anti-inflammatory drugs and surgery.


Hanauer, S., Sandborn, W. (2001). Management of Crohn’s disease in adults. Am J Gastroenterology, 96, 635 – 43.

Orholm, M., Fonager, K., Sorensen, H. (1999). Risk of ulcerative colitis and Crohn’s disease among offspring of patients with chronic inflammatory bowel disease. Am J Gastroenterology, 94(11), 3236–8.

Sands, E. (2004). From symptom to diagnosis: clinical distinctions among various forms of intestinal inflammation. Gastroenterology, 126, 1518– 32.

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