Chronic diarrhea pathophysiology
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Chronic diarrhea Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Omodamola Aje B.Sc, M.D. [2]
Overview
Pathophysiology
The fundamental pathophysiology of all diarrhea is incomplete absorption of water from the lumen either because of a reduced rate of net water absorption (related to impaired electrolyte absorption or excessive electrolyte secretion) or because of osmotic retention of water intraluminally.[1] The causes of chronic diarrhea include inflammatory, osmotic, secretory, iatrogenic, motility, and functional diseases. In general, no single cause of chronic diarrhea is truly unifactorial from a perspective of pathophysiology. For example, cholera is caused by secretion and altered motility[2] whereas pseudomembranous colitis is said to be associated with secretion, inflammation, and motility[3].
Thus, diarrhea is a condition of altered intestinal water and electrolyte transport. The pathophysiologic mechanisms of diarrhea include osmotic, secretory, inflammatory, and altered motility.
- Osmotic diarrhea involves an unabsorbed substance that draws water from the plasma into the intestinal lumen along osmotic gradients.
- Secretory diarrhea results from disordered electrolyte transport and, despite the term, is more commonly caused by decreased absorption rather than net secretion.
- Inflammatory diseases cause diarrhea with exudative, secretory, or osmotic components.
- Altered motility of the intestine or colon may alter fluid absorption by increasing or decreasing the exposure of luminal content to intestinal absorptive surface.
However, from a pathophysiologic perspective, no single cause of diarrhea is truly unifactorial.
Pathogenesis
References
- ↑ Sweetser S (2012). "Evaluating the patient with diarrhea: a case-based approach". Mayo Clin Proc. 87 (6): 596–602. doi:10.1016/j.mayocp.2012.02.015. PMC 3538472. PMID 22677080.
- ↑ Goyal RK, Hirano I (1996). "The enteric nervous system". N Engl J Med. 334 (17): 1106–15. doi:10.1056/NEJM199604253341707. PMID 8598871.
- ↑ Kurose I, Pothoulakis C, LaMont JT, Anderson DC, Paulson JC, Miyasaka M; et al. (1994). "Clostridium difficile toxin A-induced microvascular dysfunction. Role of histamine". J Clin Invest. 94 (5): 1919–26. doi:10.1172/JCI117542. PMC 294602. PMID 7962537.