Bile Composition and Function
Bile is produced by hepatocytes (~500-1000 mL/day) and stored/concentrated in the gallbladder (10x concentration via water/electrolyte absorption). Primary function: emulsification of dietary fats to aid lipase digestion.
| Component | Source | Function |
|---|---|---|
| Bile salts | Hepatocytes (from cholesterol) | Emulsify fats; form micelles for fat-soluble vitamin absorption (A,D,E,K) |
| Bilirubin (conjugated) | Hepatocytes (from heme) | Waste product; gives stool brown color |
| Cholesterol | Hepatocytes | Excreted in bile; excess → gallstones |
| Phospholipids (lecithin) | Hepatocytes | Solubilize cholesterol in bile; prevent gallstones |
| Water and electrolytes | Bile ductules | Vehicle; adjusted by secretin and aldosterone |
CCK and Secretin Regulation
| Hormone | Stimulus | Source | Gallbladder Effect |
|---|---|---|---|
| CCK (cholecystokinin) | Fat and protein in duodenum | I cells (duodenum) | Gallbladder contraction + sphincter of Oddi relaxation → bile release |
| Secretin | Acid (H+) in duodenum | S cells (duodenum) | Stimulates bile duct bicarbonate secretion (watery bile); augments CCK effect |
| Somatostatin | Protein, fat, acid | D cells (pancreas, gut) | Inhibits CCK, gastrin, secretin; decreases bile secretion |
⭐ Boards PearlGallbladder contraction requires CCK. Acalculous cholecystitis risk: TPN use (no CCK stimulus → bile stasis → infection). Vagotomy also impairs gallbladder emptying.
Enterohepatic Circulation
Bile salts are reabsorbed in the terminal ileum (95% actively reabsorbed; 5% lost in stool) → portal vein → liver → re-secreted into bile. Total pool circulates 6-8x per day.
🩹 Clinical RelevanceTerminal ileum resection (Crohn's disease) → bile salt malabsorption → steatorrhea (fat malabsorption) + bile salt diarrhea (cholerheic diarrhea). Cholestyramine binds bile salts → used for cholestatic itch and hypercholesterolemia.
🧐 Gallstone TypesCholesterol stones (80%): supersaturated bile + nucleation; risk factors: female, fat, fertile, forty, fair (5 Fs). Pigment stones: black (hemolysis — sickle cell, hereditary spherocytosis); brown (infection — Clonorchis, E. coli).
Clinical Pearls
⭐ Murphy's SignInspiratory arrest on deep palpation of right upper quadrant = Murphy's sign = acute cholecystitis. Sonographic Murphy's sign (tenderness with ultrasound probe) is highly specific. Choledocholithiasis: stone in CBD → obstructive jaundice + elevated ALP and direct bilirubin + acholic stools + dark urine.
⭐ Charcot's Triad vs Reynold's PentadCharcot's triad (ascending cholangitis): RUQ pain + fever/chills + jaundice. Reynold's pentad: + altered mental status + hypotension (septic shock — emergency ERCP needed).