Skip to content
Study aid only. Verify against current guidelines before clinical use.
Step 2 CK · Internal Medicine · Gastroenterology

Pancreatic & Biliary Disease

Stones and enzymes: from biliary colic to Reynolds pentad

Gastroenterology·Pancreatic & Biliary Disease·5 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy
Study materialsNo account needed
Card deckActive-recall cards · quick checks · quiz

Acute pancreatitis: diagnosis and causes

Two of three. Acute pancreatitis needs 2 of 3 criteria: epigastric pain radiating to the back, lipase or amylase more than 3 times the upper limit of normal, or characteristic findings on cross-sectional imaging. Lipase is more sensitive and specific than amylase, rising higher and staying elevated longer. Enzyme levels do not track severity. Vomiting and relief on leaning forward are typical; periumbilical (Cullen) or flank (Grey Turner) ecchymoses signal retroperitoneal hemorrhage. When two criteria are met, CT adds nothing to the diagnosis; contrast CT is for diagnostic doubt or a patient not improving after 48–72 hours.

>3× ULNlipase or amylase for diagnosis
>1000 mg/dLtriglycerides that can trigger pancreatitis
≥4 weeksbefore a walled collection is a pseudocyst

Causes. Gallstones and alcohol cause most cases. The mnemonic I GET SMASHED lists the rest: Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion sting, Hypertriglyceridemia (over 1000 mg/dL) or Hypercalcemia, post-ERCP, and Drugs (such as azathioprine, valproate, didanosine, and thiazides). Order a right-upper-quadrant ultrasound and a triglyceride level in every case, plus calcium; an early ALT above about 150 IU/L favors a gallstone cause.

Acute pancreatitis: management and complications

Supportive care. Early isotonic crystalloid, with lactated Ringer preferred, plus analgesia and early enteral feeding is the mainstay. Fluids have traditionally been described as aggressive; recent trial data favor moderate, goal-directed volumes, because very large volumes cause fluid overload without benefit. Feed by mouth as soon as tolerated; in severe disease, nasogastric or nasojejunal feeding beats TPN because it preserves the gut barrier. Prophylactic antibiotics are not given for sterile inflammation or sterile necrosis.

Severity. Score with Ranson criteria, APACHE II, or BISAP (BUN over 25, impaired mental status, SIRS, age over 60, pleural effusion). A rising BUN and hematocrit signal ongoing third-spacing and worse outcomes. Persistent organ failure (beyond 48 hours) defines severe disease.

  1. At admissionAge, WBC, glucose, AST, LDH.
  2. Within 48 hHematocrit drop, BUN rise, low calcium, base deficit, fluid sequestration.
  3. InterpretationThe more criteria met, the higher the mortality.
Ranson criteria timing
Complications of acute pancreatitis
ComplicationClueManagement
Necrotizing pancreatitisNonenhancing gland on contrast CTSupportive care; no routine antibiotics while sterile
Infected necrosisNew fever or sepsis, often in week 2 or later; gas in the collectionAntibiotics (a carbapenem) plus drainage or debridement, delayed when possible
PseudocystFibrous-walled fluid collection (no epithelial lining) forming after 4 or more weeksDrain only if symptomatic or infected
ARDSHypoxemia with bilateral infiltratesVentilatory support
HypocalcemiaFat saponification binds calciumReplace calcium
Splenic vein thrombosis is another late complication and causes isolated gastric varices.

Gallstone pancreatitis. Urgent ERCP is indicated only with concurrent cholangitis or persistent bile duct obstruction. Otherwise, perform cholecystectomy during the same admission once inflammation settles, to prevent recurrence.

Chronic pancreatitis and pancreatic cancer

Chronic pancreatitis. Usually from alcohol (smoking accelerates it; cystic fibrosis is a cause in the young). Expect chronic epigastric pain, pancreatic calcifications on imaging, steatorrhea from exocrine insufficiency (low fecal elastase, fat-soluble vitamin deficiency), and diabetes from endocrine loss. Lipase is often normal in a burned-out gland. Treat with pancreatic enzyme replacement, pain control, and alcohol cessation. It raises the risk of pancreatic adenocarcinoma.

Pancreatic adenocarcinoma. Ductal adenocarcinoma, usually of the head, presents with painless obstructive jaundice, weight loss, and a palpable, nontender, distended gallbladder (Courvoisier sign), which points to malignant obstruction rather than stones. Body and tail tumors present later with pain boring to the back. Trousseau migratory thrombophlebitis, new diabetes in an older adult, and a rising CA 19-9 are classic. Smoking is the key risk factor.

Workup and treatment. Pancreatic-protocol CT is the best initial test; endoscopic ultrasound with fine-needle aspiration obtains tissue. CA 19-9 follows treatment response rather than screening. Resectable head tumors are removed by a Whipple procedure (pancreaticoduodenectomy), but most tumors are unresectable at diagnosis.

The gallstone spectrum

Who forms stones. Cholesterol gallstones favor the fat, female, forty, fertile patient; pregnancy, estrogen, rapid weight loss, and TPN also predispose, and chronic hemolysis produces black pigment stones. Asymptomatic stones do not need surgery. A stone lodged at the ampulla causes gallstone pancreatitis.

From colic to cholangitis
FeatureBiliary colicAcute cholecystitisCholedocholithiasisAscending cholangitis
MechanismStone transiently blocks cystic ductSustained cystic duct obstruction with inflammationStone in common bile ductInfection of an obstructed duct
ClinicalRUQ pain after fatty meals that resolves; no feverPersistent RUQ pain, fever, Murphy signJaundice, with or without painCharcot triad; Reynolds pentad if septic
LabsNormal; no leukocytosisLeukocytosis; bilirubin usually near normalHigh bilirubin and alkaline phosphataseLeukocytosis, high bilirubin and ALP
Key testUltrasoundUltrasound; HIDA if equivocalDilated duct on ultrasound; MRCPUltrasound, blood cultures
TreatmentElective cholecystectomyAntibiotics and cholecystectomyERCP stone extraction, then cholecystectomyIV antibiotics and urgent ERCP

Cholecystitis imaging. Ultrasound shows a thickened wall, pericholecystic fluid, and stones. When it is equivocal, a HIDA scan in which the gallbladder never fills (nonvisualization) confirms cystic duct obstruction. Surgery is best done early in the admission; percutaneous cholecystostomy is the bridge for patients too sick to operate.

Choledocholithiasis. MRCP images the duct noninvasively, while ERCP both diagnoses and removes the stone. An untreated duct stone can progress to cholangitis or gallstone pancreatitis.

Cholangitis. Charcot triad is fever, jaundice, and RUQ pain; the Reynolds pentad adds hypotension and altered mental status and signals suppurative cholangitis. Gram-negative enterics dominate. This life-threatening emergency needs IV antibiotics and urgent biliary decompression by ERCP, or percutaneous transhepatic drainage if ERCP fails.

Fever, jaundice, RUQ pain, hypotension, and confusion mean suppurative cholangitis: decompress the duct emergently; antibiotics alone are not enough.

Special gallbladder situations

  • Porcelain gallbladder: a calcified wall raises gallbladder cancer risk and prompts cholecystectomy.
  • Gallstone ileus: a stone erodes through a cholecystoenteric fistula and obstructs the small bowel, typically at the terminal ileum in an older woman. Rigler triad is pneumobilia, small-bowel obstruction, and an ectopic gallstone; treat with surgical stone removal.
  • Acalculous cholecystitis: gallbladder stasis and ischemia in critically ill ICU patients (burns, trauma, sepsis, prolonged TPN); treat with antibiotics and percutaneous cholecystostomy if surgery is too risky.