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Fluid delivery to the GI tract is 8–10 L/d, including 2 L/d ingested; most is absorbed in small bowel. Colonic absorption is normally 0.05–2 L/d, with capacity for 6 L/d if required. Intestinal water absorption passively follows active transport of Na+, Cl, glucose, and bile salts. Additional transport mechanisms include Cl/HCO3 exchange, Na+/H+ exchange, H+, K+, Cl, and HCO3 secretion, Na+-glucose cotransport, and active Na+ transport across the basolateral membrane by Na+,K+-ATPase.


  1. Proximal small intestine: iron, calcium, folate, fats (after hydrolysis of triglycerides to fatty acids by pancreatic lipase and colipase), proteins (after hydrolysis by pancreatic and intestinal peptidases), carbohydrates (after hydrolysis by amylases and disaccharidases); triglycerides absorbed as micelles after solubilization by bile salts; amino acids and dipeptides absorbed via specific carriers; sugars absorbed by active transport

  2. Distal small intestine: vitamin B12, bile salts, water

  3. Colon: water, electrolytes


Allows propulsion of intestinal contents from stomach to anus and separation of components to facilitate nutrient absorption. Propulsion is controlled by neural, myogenic, and hormonal mechanisms; mediated by migrating motor complex, an organized wave of neuromuscular activity that originates in the distal stomach during fasting and migrates slowly down the small intestine. Colonic motility is mediated by local peristalsis to propel feces. Defecation is effected by relaxation of internal anal sphincter in response to rectal distention, with voluntary control by contraction of external anal sphincter.



Formally defined as fecal output >200 g/d on low-fiber (western) diet; also frequently used to connote loose or watery stools. Mediated by one or more of the following mechanisms:


Nonabsorbed solutes increase intraluminal oncotic pressure, causing outpouring of water; usually ceases with fasting; stool osmolal gap >40 (see below). Causes include disaccharidase (e.g., lactase) deficiencies, pancreatic insufficiency, bacterial overgrowth, lactulose or sorbitol ingestion, polyvalent laxative abuse, celiac or tropical sprue, and short bowel syndrome. Lactase deficiency can be either primary (more prevalent in blacks and Asians, usually presenting in early adulthood) or secondary (from viral, bacterial, or protozoal gastroenteritis, celiac or tropical sprue, or kwashiorkor).


Active ion secretion causes obligatory water loss; diarrhea is usually watery, often profuse, unaffected by fasting; stool Na+ and K+ are elevated with osmolal gap <40. Causes include viral infections (e.g., rotavirus, Norwalk virus), bacterial infections (e.g., cholera, enterotoxigenic Escherichia coli, Staphylococcus aureus), protozoa (e.g., Giardia, Isospora, Cryptosporidium), AIDS-associated disorders (including mycobacterial and HIV-induced), medications (e.g., theophylline, colchicine, prostaglandins, diuretics), ...

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