A patient with short bowel syndrome after massive ileal resection has diarrhoea due to bile salt malabsorption. The primary mechanism is:
- A Unabsorbed conjugated bile salts reach the colon where bacterial deconjugation produces dihydroxy bile acids (cholic/deoxycholic acid) that stimulate colonic water and electrolyte secretion (cholerrhoeic diarrhoea) ✓
- B Reduced hepatic bile acid synthesis leads to fat malabsorption and osmotic diarrhoea from undigested lipids
- C Loss of terminal ileum reduces GLP-2 secretion, impairing mucosal adaptation and reducing absorptive capacity
- D Reduced ileocaecal valve function allows colonic bacteria to colonise the small bowel, producing bacterial overgrowth diarrhoea
Explanation
The terminal ileum is the exclusive site of active bile salt reabsorption via ASBT (apical sodium bile salt transporter). After ileal resection, conjugated bile salts spill into the colon. Colonic bacteria deconjugate and 7-dehydroxylate primary bile acids to produce secondary dihydroxy bile acids (deoxycholic acid, lithocholic acid), which are potent secretagogues — they stimulate colonic Cl- and water secretion and increase colonic mucosal permeability, causing secretory (cholerrhoeic) diarrhoea. This is treated with bile acid sequestrants (cholestyramine). If resection is large (>100 cm), the bile acid pool depletes, causing steatorrhoea due to fat malabsorption — a different mechanism from smaller resections.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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Written and medically reviewed by the StethoPrep medical team.