A 32-year-old man with a 10-year history of Crohn disease undergoes surgical resection of a 40 cm segment of terminal ileum due to stricture and perforation. Two weeks postoperatively, he develops watery diarrhea (6–8 stools daily) and steatorrhea. The structure marked **C** in the diagram is responsible for the normal enterohepatic circulation of bile acids. Which of the following best explains the mechanism of diarrhea in this patient?

Explanation

## Why "Unabsorbed bile acids entering the colon stimulate water and electrolyte secretion, causing chologenic diarrhea" is right The terminal ileum (marked **C**) is the site of active reabsorption of bile acids via the apical sodium-dependent bile acid transporter (ASBT). When the terminal ileum is resected, this active reabsorption mechanism is lost. Bile acids that would normally be reabsorbed instead pass into the colon, where they act as secretagogues—stimulating colonic epithelial cells to secrete water and electrolytes, resulting in watery diarrhea (chologenic or cholerheic diarrhea). This is the primary mechanism of diarrhea immediately postoperatively. Harper 32e Ch 26 and Robbins 10e Ch 17 both emphasize that bile acid-induced diarrhea is the direct consequence of ileal loss and is the basis for cholestyramine therapy (a bile acid binding resin). ## Why each distractor is wrong - **Impaired micelle formation due to depleted bile acid pool leading to osmotic diarrhea**: While bile acid depletion does impair micelle formation and cause steatorrhea and fat malabsorption, this is a secondary consequence. The osmotic effect of fat in the colon contributes to diarrhea, but the primary mechanism of watery diarrhea in the immediate postoperative period is the direct secretory effect of unabsorbed bile acids on the colonic mucosa, not osmotic diarrhea from malabsorbed fat. - **Increased colonic pH from bacterial overgrowth reducing water reabsorption**: Bacterial overgrowth and pH changes are not the primary mechanism of bile acid–induced diarrhea. The diarrhea occurs because bile acids themselves are secretagogues; pH changes are incidental and not the driving pathophysiology. - **Loss of absorptive surface area causing reduced nutrient-dependent water uptake**: While ileal resection does reduce absorptive surface area, this explains malabsorption of nutrients and vitamin B12 deficiency (terminal ileum is also the site of intrinsic factor–B12 complex absorption), not the acute secretory diarrhea caused by unabsorbed bile acids. **High-Yield:** Terminal ileum resection → loss of ASBT-mediated bile acid reabsorption → bile acids reach colon → secretory diarrhea (chologenic diarrhea); treat with cholestyramine (bile acid sequestrant). [cite: Harper 32e Ch 26; Robbins 10e Ch 17]