STEPTRACKERGASTROINTESTINAL | PATHOLOGY + PHYSIOLOGY | HIGH-YIELD REVIEW

Pancreatitis

The pancreas digesting itself — acute attacks, their systemic complications, and the chronic burnt-out gland.

FOCUS ON
Acute pancreatitis: gallstones and alcohol first, then hypertriglyceridemia, hypercalcemia, ERCP, drugs. Two of three: epigastric pain to the back, lipase > 3× normal, imaging. Watch for hypocalcemia, ARDS, shock, pseudocyst. Chronic: calcifications, steatorrhea, diabetes; alcohol in adults, CF in children.
TOPIC
MECHANISM · CAUSES
FINDINGS
CLUE
Acute pancreatitis — causes
Gallstones (block ampulla), alcohol, triglycerides > 1000, hypercalcemia, post-ERCP, trauma, mumps, scorpion sting, autoimmune, CF
"I GET SMASHED": Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion, Hypercalcemia/Hypertriglyceridemia, ERCP, Drugs
Gallstone cause → ↑ ALT
Drug causes
Direct toxicity or hypersensitivity
Azathioprine, valproate, didanosine, GLP-1 agonists, loop and thiazide diuretics, sulfonamides, protease inhibitors, estrogen (↑ TG)
Stop the drug
Acute pancreatitis — presentation
Activated enzymes digest pancreas and fat
Severe epigastric pain radiating to the back, nausea, vomiting; better leaning forward
Lipase > 3× normal (more specific than amylase)
Hemorrhagic pancreatitis
Enzymes digest vessels → retroperitoneal bleeding
Cullen sign (periumbilical) · Grey Turner sign (flank) bruising
Severe disease
Systemic complications
Cytokine release, capillary leak; lipase-driven fat necrosis binds calcium (saponification)
Hypocalcemia, hyperglycemia, ARDS (phospholipase A₂ destroys surfactant), DIC, shock, AKI
Aggressive IV fluids
Pancreatic pseudocyst
Collection of enzyme-rich fluid walled by granulation / fibrous tissue (no epithelium); ≥ 4 weeks after attack
Persistent pain, early satiety, palpable mass, persistent ↑ lipase
Rupture, infection, hemorrhage
Necrotizing pancreatitis
Nonviable parenchyma, may become infected
Gas in necrosis on CT → infected
Antibiotics (carbapenem) ± debridement
Chronic pancreatitis
Repeated inflammation → fibrosis, duct strictures, acinar loss; alcohol (adults), CF (children), genetic (PRSS1, SPINK1)
Chronic epigastric pain, steatorrhea, weight loss, diabetes; ADEK deficiency
Calcifications on CT; "chain of lakes" duct; lipase may be normal
Autoimmune pancreatitis
IgG4-related disease; lymphoplasmacytic infiltrate, storiform fibrosis
"Sausage-shaped" pancreas, painless jaundice — mimics cancer
Responds to steroids
Hereditary pancreatitis
Gain-of-function PRSS1 (trypsinogen) or loss of SPINK1 (trypsin inhibitor)
Recurrent attacks from childhood
↑ pancreatic cancer risk

Mechanism — premature trypsin activation

InjuryDuct obstruction, alcohol, Ca²⁺
→
Trypsinogen → trypsinInside acinar cells
→
Activates other enzymesElastase, lipase, phospholipase A₂
→
AutodigestionFat necrosis, hemorrhage
→
SIRSARDS, shock, DIC

Fat necrosis releases fatty acids that bind calcium (saponification) — chalky white deposits and hypocalcemia.

Acute vs chronic pancreatitis

FEATURE
ACUTE
CHRONIC
Top causes
Gallstones, alcohol
Alcohol, CF, genetic
Lipase
↑↑ (> 3×)
Often normal
Pathology
Edema, fat necrosis, hemorrhage
Fibrosis, duct dilation, calcification
Function
Transient
Exocrine (steatorrhea) + endocrine (DM) loss
Complications
Pseudocyst, ARDS, shock
Pseudocyst, cancer, malnutrition

How it's tested

COMMON CONFUSIONA pseudocyst has no epithelial lining — that is what makes it "pseudo." A true cystic neoplasm has epithelium and often mucin.
THE TRAPIn chronic pancreatitis lipase and amylase are often normal because the gland is burnt out. Diagnose with imaging (calcifications) and fecal elastase.
YOUR APPROACHPain + lipase → find the cause (gallstone: ↑ ALT and ultrasound; triglycerides; calcium; drugs) → watch calcium, oxygen, kidneys → look for late pseudocyst.

If you see… think…

Epigastric pain to the back after a binge, lipase 6× normal → acute alcoholic pancreatitis
Pancreatitis + ALT 3× normal → gallstone pancreatitis
Milky serum with pancreatitis → hypertriglyceridemia
Pancreatitis in a patient with parathyroid adenoma → hypercalcemia
Periumbilical and flank bruising → hemorrhagic pancreatitis
Tetany and low Ca²⁺ during pancreatitis → saponification
Hypoxemia and bilateral infiltrates on day 2 → ARDS
Epigastric mass and early satiety 6 weeks after attack → pseudocyst
Alcoholic with steatorrhea, diabetes, calcified pancreas → chronic pancreatitis
Sausage-shaped pancreas + high IgG4 → autoimmune pancreatitis — steroids