PRIMARY MECHANISM DEFECT STOOL EXAMINATION EXAMPLES COMMENT Secretory Decreased absorption, increased secretion, electrolyte transport Watery, normal osmolality with ion gap <100 mOsm /kg Cholera, toxigenic Escherichia coli; carcinoid, VIP, neuroblastoma, congenital chloride diarrhea, Clostridium difficile, cryptosporidiosis (AIDS) Persists during fasting; bile salt malabsorption can also increase intestinal water secretion; no stool leukocytes Osmotic Maldigestion , transport defects ingestion of unabsorbable substances Watery, acidic, and reducing substances; increased osmolality with ion gap >100 mOsm /kg Lactase deficiency, glucose- galactose malabsorption, lactulose, laxative abuse Stops with fasting; increased breath hydrogen with carbohydrate malabsorption; no stool leukocytes Increased motility Decreased transit time Loose to normal-appearing stool, stimulated by gastrocolic reflex Irritable bowel syndrome, thyrotoxicosis , postvagotomy dumping syndrome Infection can also contribute to increased motility Decreased motility Defect in neuromuscular unit(s) stasis (bacterial overgrowth) Loose to normal-appearing stool Pseudo-obstruction, blind loop Possible bacterial overgrowth Decreased surface area (osmotic, motility) Decreased functional capacity Watery Short bowel syndrome, celiac disease, rotavirus enteritis Might require elemental diet plus parenteral alimentation Mucosal invasion Inflammation, decreased colonic reabsorption, increased motility Blood and increased WBCs in stool Salmonella, Shigella, infection; amebiasis ; Yersinia, Campylobacter infections Dysentery evident in blood, mucus, and WBCs MECHANISMS OF DIARRHEA 5/2/2023