Hepatobiliary System

Gallbladder

Gross Anatomy · Microscopic · Biliary Tract · Bile · Embryology · Clinical

Gross Anatomy

Pear-shaped sac (~7-10 cm, 30-50 mL capacity) on inferior surface of right hepatic lobe.

Parts

  • Fundus — blind-ended tip; palpable in cholecystitis
  • Body — main portion on hepatic surface
  • Neck — joins cystic duct; spiral valve of Heister
  • Hartmann's pouch — outpouching at neck; stones can lodge here

Blood Supply

  • Cystic artery — branch of right hepatic artery; runs through Calot's triangle
  • Calot's triangle — bordered by liver, CHD, cystic duct; key surgical landmark
🩺 Clinical

Murphy's sign: inspiratory arrest with RUQ palpation — classic for acute cholecystitis.

Microscopic Anatomy

Wall Layers

  • Mucosa — simple columnar epithelium; highly folded (rugae); NO muscularis mucosae or submucosa
  • Muscularis — smooth muscle; contracts with CCK
  • Serosa — covers free surface; absent on hepatic surface (adventitia instead)
⭐ Boards Pearl

Rokitansky-Aschoff sinuses — mucosa invaginates through the muscularis wall. Prominent in chronic cholecystitis. "Strawberry gallbladder" = cholesterol deposits on mucosa.

Biliary Tract

StructureDescriptionClinical Note
R+L hepatic ductsDrain liver lobesJoin at porta hepatis
Common hepatic ductR+L joinAbove cystic duct
Cystic ductGB neck to CHDSpiral valve of Heister
Common bile ductCHD + cystic ductPasses behind duodenum
Ampulla of VaterCBD + pancreatic ductOpens into D2 of duodenum
Sphincter of OddiSmooth muscle valveRegulates flow; relaxes with CCK
🩺 Clinical

Charcot's triad (RUQ pain + fever + jaundice) = cholangitis. Reynolds' pentad adds AMS + septic shock. Choledocholithiasis → ↑direct bilirubin, ↑ALP, ↑GGT.

Bile

Composition

  • Bile salts — cholate, chenodeoxycholate; conjugated with glycine/taurine; emulsify fats
  • Phospholipids (lecithin) — solubilize cholesterol
  • Cholesterol — must stay in solution via bile salt/lecithin micelles
  • Conjugated bilirubin — yellow-green color

GB concentrates bile 5-10x by absorbing Na+, Cl-, and water. CCK (I-cells of duodenum) → GB contraction + sphincter of Oddi relaxation.

⭐ Boards Pearl

Gallstone types: Cholesterol (80%) — radiolucent; 5 F's: Female, Fat, Forty, Fertile, Fair. Pigment — black (hemolysis/cirrhosis) vs brown (infection/stasis).

🧠 Mnemonic

5 F's for gallstones: Female, Fat, Forty, Fertile, Fair. Also: OCPs, rapid weight loss, Crohn disease (impaired bile salt reabsorption).

Embryology

GB and extrahepatic bile ducts develop from the hepatic diverticulum (pars cystica, caudal portion) of foregut endoderm at ~4 weeks.

  • Pars cystica → gallbladder + cystic duct
  • Failure of recanalization → biliary atresia
🩺 Clinical

Biliary atresia: progressive jaundice after 2 weeks, acholic stools, ↑conjugated bilirubin. Kasai portoenterostomy before 60 days is essential; untreated → cirrhosis by age 2.

Clinical Pearls

ConditionMechanismKey Features
Biliary colicTransient cystic duct obstructionEpisodic RUQ pain after fatty meals; no fever
Acute cholecystitisSustained obstruction + inflammationFever, Murphy's sign, ↑WBC
CholedocholithiasisStone in CBDObstructive jaundice, ↑ALP, ↑GGT
CholangitisBiliary obstruction + infectionCharcot's triad; Reynolds' pentad if severe
PSCAutoimmune; UC-associatedp-ANCA; beaded ducts on MRCP; ↑ALP; cholangiocarcinoma risk
⭐ Boards Pearl

Porcelain gallbladder = calcification of GB wall from chronic cholecystitis. Associated with increased GB carcinoma risk (debated). Visible on plain X-ray or CT as calcified outline.