Malabsorption pathophysiology: Difference between revisions
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==Overview== | |||
== Pathophysiology== | == Pathophysiology== | ||
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Latest revision as of 13:59, 12 July 2016
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Malabsorption |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
The main purpose of the GI tract is to digest and absorb nutrients (fat, carbohydrate, and protein), micronutrients (vitamins and trace minerals), water, and electrolytes. Digestion involves both mechanical and enzymatic breakdown of food. Mechanical processes include chewing, gastric churning, and the to-and-fro mixing in the small intestine. Enzymatic hydrolysis is initiated by intraluminal processes requiring gastric, pancreatic, and biliary secretions. The final products of digestion are absorbed through the intestinal epithelial cells.
Malabsorption constitutes the pathological interference with the normal physiological sequence of digestion (intraluminal process), absorption (mucosal process) and transport (postmucosal events) of nutrients.[1]
Intestinal malabsorption can be due to:[2]
- Mucosal damage (enteropathy)
- Congenital or acquired reduction in absorptive surface
- Defects of specific hydrolysis
- Defects of ion transport
- Pancreatic insufficiency
- Impaired enterohepatic circulation
References
- ↑ Bai J (1998). "Malabsorption syndromes". Digestion. 59 (5): 530–46. PMID 9705537.
- ↑ Walker-Smith J, Barnard J, Bhutta Z, Heubi J, Reeves Z, Schmitz J (2002). "Chronic diarrhea and malabsorption (including short gut syndrome): Working Group Report of the First World Congress of Pediatric Gastroenterology, Hepatology, and Nutrition". J. Pediatr. Gastroenterol. Nutr. 35 Suppl 2: S98–105. PMID 12192177.