Step 1 · Gastrointestinal

Biliary & Pancreatic Pathology

Name: Biliary & Pancreatic Pathology
Creator: Veli Bakalov, MD

From the 4 F's of gallstones to Courvoisier's ominous gallbladder

Gastrointestinal·Hepatobiliary & Pancreatic Pathology·4 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

Study materialsNo account needed

Card deckActive-recall cards · quick checks · quiz

High-yield

Cholesterol stones (~90%, usually radiolucent) follow the 4 F's (Female, Fat, Fertile, Forty) plus estrogen/OCPs, rapid weight loss, Native American ethnicity, ileal disease, and fibrates; black pigment stones = hemolysis or cirrhosis; brown pigment stones = biliary infection.
Biliary colic = transient postprandial RUQ pain (<6 h) from intermittent cystic duct obstruction, without fever or leukocytosis; ultrasound is first-line.
Acute cholecystitis = persistent cystic duct obstruction: constant RUQ pain, fever, leukocytosis, Murphy sign; HIDA nonfilling of the gallbladder confirms when ultrasound is equivocal.
Charcot triad (RUQ pain, jaundice, fever) = ascending cholangitis from a CBD stone plus infection (E. coli); Reynolds pentad adds hypotension and confusion; treat with urgent ERCP.
Gallstone ileus: cholecystoenteric fistula → stone lodges at the ileocecal valve; Rigler triad = pneumobilia, small-bowel obstruction, ectopic gallstone.
PBC = middle-aged woman, pruritus, xanthomas, anti-mitochondrial antibody (~95%), high ALP and IgM, ursodiol; PSC = man with ulcerative colitis, p-ANCA, onion-skin fibrosis, beaded ducts, cholangiocarcinoma risk.
Acute pancreatitis: epigastric pain radiating to the back with lipase or amylase >3× ULN (lipase more specific); gallstones and alcohol lead (I GET SMASHED).
Pancreatitis complications: hypocalcemia from fat saponification, pseudocyst (granulation tissue, no epithelium), necrosis, hemorrhage (Grey Turner and Cullen signs), ARDS, DIC; chronic pancreatitis = calcifications, steatorrhea, diabetes.
Pancreatic head adenocarcinoma: painless jaundice with a palpable nontender gallbladder (Courvoisier sign), smoking as top risk, CA 19-9, Trousseau migratory thrombophlebitis.

Gallstones

Formation. Stones precipitate when bile is supersaturated with cholesterol relative to bile salts and phospholipids, or when bilirubin load rises, and gallbladder stasis gives crystals time to grow.

Cholesterol stones. About 90% of gallstones, usually radiolucent. Risk follows the 4 F's (Female, Fat, Fertile, Forty), plus estrogen/OCPs, rapid weight loss, Native American ethnicity, Crohn disease or other ileal disease (bile acid loss), and fibrates (which inhibit bile acid synthesis).

Pigment stones. Black pigment stones (calcium bilirubinate, radiopaque) form with chronic hemolysis or cirrhosis. Brown pigment stones form in the setting of biliary infection, when bacterial enzymes deconjugate bilirubin.

Only about 10–15% of gallstones are radiopaque, so most are invisible on plain film; ultrasound is the imaging test of choice.

Gallstone types

Feature	Cholesterol	Black pigment	Brown pigment
Frequency	~90%	Minority	Minority
X-ray	Usually radiolucent	Radiopaque	Radiolucent
Setting	4 F's, estrogen, rapid weight loss, ileal disease, fibrates	Chronic hemolysis, cirrhosis	Biliary infection

Gallstone syndromes

Biliary colic. After a fatty meal, CCK contracts the gallbladder against a stone that intermittently obstructs the cystic duct. Pain is RUQ or epigastric, transient, and resolves within about 6 hours, with no fever and no leukocytosis. Ultrasound is first-line.

Acute cholecystitis. Persistent cystic duct obstruction inflames the gallbladder: constant RUQ pain (often referred to the right shoulder), fever, leukocytosis, and a positive Murphy sign (inspiratory arrest on RUQ palpation). Ultrasound shows wall thickening, pericholecystic fluid, and distension. When ultrasound is equivocal, a HIDA scan is the most sensitive test: failure of the gallbladder to fill with tracer confirms cystic duct obstruction. Acalculous cholecystitis occurs in critically ill patients.

Choledocholithiasis and cholangitis. A stone in the common bile duct causes obstructive jaundice. Superimposed bacterial infection, most commonly E. coli, produces ascending cholangitis, which requires urgent ERCP to drain the duct.

CBD stoneCholedocholithiasis
ObstructionBile stasis, rising duct pressure
Bacterial infectionE. coli ascends
Ascending cholangitisCharcot triad: RUQ pain, jaundice, fever

Common bile duct stone to cholangitis

Distinguishing the gallstone syndromes

Syndrome	Stone location	Pain	Fever / WBC	Jaundice
Biliary colic	Cystic duct, intermittent	Transient (<6 h)	No	No
Acute cholecystitis	Cystic duct, persistent	Constant; Murphy sign	Yes	Usually no
Choledocholithiasis	Common bile duct	RUQ pain	No	Yes (obstructive)
Ascending cholangitis	CBD plus infection	RUQ pain	Yes	Yes: Charcot triad

Reynolds pentad = Charcot triad + hypotension + altered mental status: suppurative cholangitis, an emergency.

Gallstone ileus. Chronic cholecystitis can erode a cholecystoenteric fistula, letting a large stone enter the bowel and lodge at the ileocecal valve. Rigler triad: pneumobilia (air in the biliary tree), small-bowel obstruction, and an ectopic gallstone. A porcelain (calcified) gallbladder raises the risk of gallbladder adenocarcinoma.

Primary biliary vs primary sclerosing cholangitis

Primary biliary cholangitis (PBC). Autoimmune, granulomatous destruction of small intrahepatic bile ducts (the "florid duct lesion"). The classic patient is a middle-aged woman with pruritus, fatigue, and xanthomas. Anti-mitochondrial antibody is positive in about 95%, with high alkaline phosphatase and high IgM. It travels with other autoimmune diseases and is treated with ursodiol.

Primary sclerosing cholangitis (PSC). Concentric "onion-skin" fibrosis of intra- and extrahepatic bile ducts produces alternating strictures and dilations, a beaded appearance on MRCP or ERCP. Think of a young man with ulcerative colitis and a rising alkaline phosphatase; p-ANCA is often positive. PSC carries a major risk of cholangiocarcinoma.

PBC vs PSC

Feature	PBC	PSC
Patient	Middle-aged woman	Man with ulcerative colitis
Ducts	Small intrahepatic	Intra- and extrahepatic
Lesion	Florid duct lesion (lymphocytes, granulomas)	Onion-skin fibrosis; beaded ducts
Serology	Anti-mitochondrial antibody; high IgM	p-ANCA
Key association	Other autoimmune disease; xanthomas	Cholangiocarcinoma

Pancreatitis

Acute pancreatitis. Prematurely activated pancreatic enzymes autodigest the gland, causing severe epigastric pain radiating to the back. Lipase or amylase rises above 3 times the upper limit of normal; lipase is more specific and stays elevated longer. Gallstones and alcohol are the two most common causes.

3× ULNLipase or amylase rise diagnostic of acute pancreatitis

Causes, I GET SMASHED: Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion sting, Hypercalcemia/Hypertriglyceridemia, ERCP, Drugs.

Complications. Peripancreatic fat necrosis saponifies calcium, causing hypocalcemia. Local complications are necrosis, abscess, hemorrhage, and pseudocyst, a collection walled by granulation tissue with no epithelial lining that forms weeks later. Systemic complications are ARDS and DIC. Grey Turner sign (flank bruising) and Cullen sign (periumbilical bruising) signal hemorrhagic pancreatitis.

Chronic pancreatitis. Caused by recurrent alcohol use in adults and cystic fibrosis in children. Findings are pancreatic calcifications, steatorrhea with fat-soluble vitamin (A, D, E, K) malabsorption, and late diabetes from islet loss. Amylase and lipase may be normal because little functional tissue remains. It raises the risk of pancreatic adenocarcinoma.

Pancreatic adenocarcinoma

Presentation. Pancreatic ductal adenocarcinoma most often arises in the head, where it compresses the distal common bile duct and causes painless obstructive jaundice with a palpable, nontender gallbladder (Courvoisier sign). Stones do not produce this sign, because chronic inflammation scars the gallbladder so it cannot distend. Weight loss and back pain are common.

Risks and markers. Smoking is the top risk factor; chronic pancreatitis, age, and diabetes also contribute. CA 19-9 is the tumor marker. Trousseau syndrome, migratory superficial thrombophlebitis, is a paraneoplastic clue to pancreatic and other adenocarcinomas.

Read the labs to localize: high alkaline phosphatase and GGT with conjugated bilirubin = cholestasis or obstruction; high lipase = pancreatitis; CA 19-9 = pancreatic cancer; anti-mitochondrial antibody = PBC; p-ANCA with beaded ducts = PSC.