Gastroenterology
Gallbladder
Bile storage organ — and the disease spectrum from gallstones to cholangitis
The gallbladder is a 7-10 cm pear-shaped sac under the right liver lobe that stores and concentrates bile. The liver makes 500-1000 mL of bile daily; gallbladder concentrates it 5-10 fold by absorbing water and electrolytes. Cholecystokinin (CCK) released from duodenal I-cells in response to fat triggers gallbladder contraction and sphincter of Oddi relaxation, releasing bile through the common bile duct into the duodenum to emulsify fats. Bile contains bile acids (cholic, chenodeoxycholic), cholesterol, phospholipids, bilirubin, and electrolytes. Gallstones form when cholesterol or bilirubin precipitate. Disease spectrum — biliary colic (transient obstruction), acute cholecystitis (inflamed gallbladder), choledocholithiasis (stone in CBD), cholangitis (infected bile, Charcot's triad), gallstone pancreatitis. Treatment is laparoscopic cholecystectomy.
- Volume30-50 mL when full
- Bile production500-1000 mL/day from hepatocytes
- Concentration5-10× via water absorption
- TriggerCCK from duodenal I-cells (fat, protein)
- Gallstone prevalence10-15% adults; 80% asymptomatic
- Cholecystectomy volume~700,000/year in US
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Why gallbladder physiology matters
- RUQ pain workup. Most common cause of biliary symptoms.
- Sepsis source. Cholangitis is rapidly fatal without decompression.
- Pancreatitis cause. Gallstone pancreatitis is the leading etiology in many populations.
- Jaundice differential. Obstructive vs hepatocellular vs hemolytic.
- ICU patients. Acalculous cholecystitis in critically ill or burn patients.
- Pregnancy. Stones common; ursodeoxycholic acid for symptomatic cases.
- Sickle cell disease. Pigment stones from chronic hemolysis.
Common errors
- Treating asymptomatic stones. 80% never cause problems; surgery only for symptoms.
- Missing acalculous cholecystitis in ICU. No stones but inflamed gallbladder; mortality high.
- Delaying ERCP in cholangitis. Decompress within 24-48 hours; antibiotics alone insufficient.
- Diagnosing cholecystitis without sonographic Murphy. Stones plus wall thickening have many causes.
- Ignoring porcelain gallbladder. Cancer association warrants discussion of cholecystectomy.
- Calling postcholecystectomy diarrhea IBS. Bile acid malabsorption responds to cholestyramine.
Frequently asked questions
How do gallstones form?
Three types. Cholesterol stones (75%) — supersaturated bile from metabolic syndrome, female, fertile, fat, forty (4 F's), rapid weight loss, OCPs, pregnancy. Pigment stones — black (chronic hemolysis like sickle cell, hereditary spherocytosis) or brown (biliary infection like Clonorchis or stasis). Mixed in many. Three factors — supersaturation (cholesterol or bilirubin), nucleation, gallbladder hypomotility. Most stones are silent; only symptomatic ones need treatment.
What is biliary colic?
Transient stone obstruction of cystic duct after a fatty meal. Right upper quadrant or epigastric pain radiating to right shoulder or back, lasting 30 minutes to 6 hours, then resolves. No fever, normal labs. Ultrasound shows gallstones. Differs from cholecystitis — no inflammation. Treatment — elective laparoscopic cholecystectomy. Pain longer than 6 hours, fever, or leukocytosis suggests cholecystitis or other complication.
How does cholecystitis present?
Persistent RUQ pain >6 hours, fever, nausea, leukocytosis. Murphy's sign — inspiratory arrest with palpation under right costal margin. Ultrasound — gallstones, gallbladder wall >3 mm, pericholecystic fluid, sonographic Murphy. HIDA scan if ultrasound equivocal — non-visualization of gallbladder is diagnostic. Treatment — IV fluids, antibiotics (piperacillin-tazobactam or ceftriaxone+metronidazole), laparoscopic cholecystectomy within 72 hours. Acalculous cholecystitis in critically ill patients — high mortality.
What is cholangitis?
Bacterial infection of bile, usually from CBD obstruction. Charcot's triad — fever, RUQ pain, jaundice (50-70% sensitive). Reynolds pentad adds hypotension and altered mental status — suppurative cholangitis, mortality up to 50% if not decompressed. Causes — choledocholithiasis (most common), strictures, malignancy. Treatment — IV antibiotics, ERCP with stone extraction or stent placement within 24-48 hours. PTC if ERCP fails. Surgery later for stones or definitive management.
When is ERCP indicated?
Therapeutic for biliary or pancreatic disease. Choledocholithiasis with cholangitis or pancreatitis — sphincterotomy and stone removal. Malignant biliary obstruction — stenting. Bile leak post-cholecystectomy — stenting. Diagnostic role mostly replaced by MRCP and EUS. Risks — pancreatitis (3-10%), bleeding, perforation, cholangitis. Indomethacin suppository pre-procedure reduces post-ERCP pancreatitis risk.
What about gallbladder cancer?
Rare but aggressive. Risk factors — porcelain gallbladder (calcified wall — 5-25% cancer risk; controversial), large stones >3 cm, gallbladder polyps >1 cm, female, age >65, chronic typhoid carriage, primary sclerosing cholangitis. Often discovered incidentally during cholecystectomy or late-stage with jaundice and weight loss. Resection if T1b or higher includes liver bed and lymphadenectomy. 5-year survival low for advanced disease.
Life after cholecystectomy?
Most patients tolerate well. Bile flows continuously into duodenum without storage. Some develop postcholecystectomy diarrhea from increased fecal bile acids — treated with cholestyramine. Postcholecystectomy syndrome — persistent biliary symptoms; consider sphincter of Oddi dysfunction, retained stone, biliary stricture, functional dyspepsia. Long-term — slightly increased colon cancer risk in some studies; reflux esophagitis. No dietary restrictions needed.