Pathophysiology

Approximately 1500 ml of fluid normally passes into the cecum each day, although only 100 to 200 ml are lost in feces. The maximum colonic absorptive capacity is approximately 4500 ml/day. Diarrhea (increased fecal water loss) occurs when the volume of fluid entering the cecum exceeds the maximum absorptive capacity, if colonic water absorption is impaired, or if there is net loss of fluid into the colon. Colonic water absorption is linked to electrolyte absorption. Energy-dependent active transport of electrolytes across the colonic mucosa draws water through the mucosa into the intercellular space. Unlike the ileum, where absorbed electrolytes are accompanied by isosmotic quantities of water, the colon can transport water against an osmotic gradient of up to 50 mosmol/l. The permeability of the colon decreases from cecum to rectum, with the rate of water absorption being greater in the ascending colon than in the descending colon and rectum.

Mixing contractions, which correspond to the radiological haustra, retard flow and maximize absorptive function. Rapid transport through the proximal colon, for example in patients with carcinoid syndrome, is associated with diarrhea.

Secretory diarrhea, caused by toxins produced by Vibrio cholerae, enterotoxigenic Escherichia coli, Staphylococcus aureus, and Clostridium perfringens, is associated with increased salt and water loss into the small intestine. This is mediated by increased cyclic adenosine monophosphate (cAMP) concentrations generated in enterocytes in response to the bacterial toxins (HaDsen.l.┬žD.d..l.S.kadhauge..l1995). High intracellular cAMP concentrations phosphorylate enterocyte microvillus membrane proteins, including the protein of the chloride channel. This results in increased chloride secretion and inhibition of sodium chloride absorption, with the associated water loss causing diarrhea. Tumors secreting vasoactive intestinal peptide (vipomas) cause secretory diarrhea through the same mechanism. Other enterotoxins are believed to act by increasing enterocyte cytoplasmic free calcium concentrations (e.g. Clostridium difficile) or by depleting colonic mucosal ribosomal RNA, halting protein synthesis and killing the cell (e.g. Shigella).

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