Biliary Tract Disease

• Audio chapter
  Attending-narrated, listen on the commute.
• ABIM-format MCQs
  5-option vignettes with full wrong-answer teaching.
• Study guide
  Tables, decision trees, primary sources.
• AI tutor
  Chapter-grounded, answers the question you're stuck on.

What this chapter covers

• Section 27.1: Cholelithiasis stone biology and risk factors

  Three stone phenotypes derive from three distinct biochemical environments.

• Section 27.2: Symptomatic cholelithiasis and indications for cholecystectomy

  Roughly 10 percent of US adults harbor stones and 75 percent are asymptomatic.

• Section 27.3: Acute cholecystitis Tokyo grading and treatment

  Persistent cystic duct obstruction by an impacted stone converts simple colic into acute cholecystitis: bile becomes increasingly concentrated, mucosal phospholipase liberates lysolecithin, and bacterial superinfection completes the picture with right-upper-quadrant pain, fever, leukocytosis, and a positive Murphy sign.

• Section 27.4: Acalculous cholecystitis and emphysematous variants

  Acalculous cholecystitis accounts for approximately 5 to 10 percent of acute cholecystitis but carries higher mortality (commonly cited at 30 to 50 percent in critically ill patients) for two mechanistic reasons: it occurs in fasting, often intubated trauma, surgical, burn, or septic patients where the diagnosis is delayed by sedation, paralysis, and competing diagnoses, and the pathogenesis (gallbladder ischemia from low-flow states with prolonged TPN, sepsis, or vasopressor exposure, plus cystic duct functional obstruction from inspissated bile) leads more rapidly to gangrenous wall progression than calculous disease.

• Section 27.5: Mirizzi syndrome and porcelain gallbladder

  Mirizzi syndrome (less than 1 percent of cholelithiasis complications) is extrinsic compression of the common hepatic duct by a stone impacted in the cystic duct or Hartmann's pouch at Calot's triangle, with chronic local inflammation that may progress to a cholecystocholedochal fistula.

• Section 27.6: Gallstone ileus and Bouveret syndrome

  A long-standing impacted gallstone with chronic inflammation can erode through the gallbladder wall into an adjacent hollow viscus, creating a cholecystenteric fistula (most often cholecystoduodenal, sometimes cholecystocolonic, gastric, or jejunal).

• Section 27.7: Gallbladder polyps and adenocarcinoma

  Gallbladder polyps are seen on approximately 5 percent of ultrasounds; 95 percent are benign.

• Section 27.8: Functional gallbladder disorder

  Rome IV criteria define functional gallbladder pain as biliary-type pain (epigastric or RUQ, at least 30 minutes long, severe enough to interrupt activities, not relieved by bowel movement, antacids, or postural change) in the absence of stones, sludge, microlithiasis, or other structural disease, with normal liver chemistries and normal lipase or amylase.

• Section 27.9: Choledocholithiasis and ASGE 2019 risk stratification

  Bile duct stones present with biliary colic plus more pronounced liver enzyme elevation, jaundice when obstruction is complete or prolonged, cholangitis when bacterial infection supervenes, and gallstone pancreatitis when the stone impacts at the ampulla.

• Section 27.10: Acute cholangitis and Tokyo Guidelines

  Cholangitis is ascending bacterial infection of an obstructed biliary tree, most commonly from choledocholithiasis but also from malignancy, anastomotic stricture, or stent occlusion.

• Section 27.11: Choledochal cysts and Caroli disease

  Todani classifies cystic dilations of the bile duct into five types that reflect anatomic location and dictate surgical strategy.

• Section 27.12: Bile leak and post-cholecystectomy stricture

  Bile leaks typically present within 10 days of cholecystectomy with abdominal pain or bile peritonitis, fever, leukocytosis, and elevated liver enzymes; persistent bilious drain output or biliary ascites confirms the diagnosis on imaging.

• Section 27.13: Sphincter of Oddi dysfunction (Rome IV)

  Sphincter of Oddi dysfunction is a non-calculous obstructive disorder at the level of the sphincter of Oddi caused by either passive obstruction from fibrosis or inflammation or active sphincter spasm; the two mechanisms are not mutually exclusive.

Podcast episodes

1. 01

   Gallstones and Cholecystitis

   This episode covers gallstone disease and acute cholecystitis: the stone types and what each one tells you about the biochemistry that made it, when symptomatic stones send a patient to cholecystectomy, how acute cholecystitis is graded and timed, and the acalculous and emphysematous variants that change the host risk and the urgency.

2. 02

   Uncommon Gallbladder

   This episode covers the less common gallbladder presentations: Mirizzi syndrome, porcelain gallbladder, gallstone ileus and Bouveret syndrome, gallbladder polyps, and the functional gallbladder disorder where the main risk is over-treating.

3. 03

   Duct Stones and Cholangitis

   This episode covers the stone in the bile duct: the probability framework that decides who goes straight to ERCP, and acute cholangitis, where the same stone turns septic and the timing of decompression becomes the whole management.

4. 04

   Cysts Leak Stricture SOD

   This episode covers the structural and iatrogenic bile duct: the congenital choledochal cysts and their cancer-driving anatomy, the post- cholecystectomy bile leak and stricture, and sphincter of Oddi dysfunction as it's now classified.