Chronic Pancreatitis, Pancreatic Cysts, and Pancreatic Neoplasms

• 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 26.1: Etiology (TIGAR-O) and severity grading (M-ANNHEIM)

  Chronic pancreatitis is defined mechanistically as a pathologic fibroinflammatory syndrome of the pancreas in patients with genetic, environmental, or other risk factors who develop a persistent pathologic response to parenchymal injury or stress.

• Section 26.2: Genetic chronic pancreatitis

  PRSS1 (cationic trypsinogen, common pathogenic variants p.R122H and p.N29I) causes hereditary pancreatitis through a gain-of-function mechanism in which the mutated trypsinogen escapes inactivation and produces excessive intrapancreatic trypsin activity, driving recurrent autodigestion.

• Section 26.3: Diagnostic ladder

  Diagnosis integrates clinical symptoms, structural imaging, and functional testing because no single biomarker is accurate and histology is rarely available.

• Section 26.4: Pain management and ESCAPE

  Pain in chronic pancreatitis is multifactorial.

• Section 26.5: PERT and exocrine insufficiency

  Steatorrhea, weight loss, and fat-soluble vitamin A, D, E, and K deficiency appear only after exocrine reserve drops below approximately 10 percent of normal because the pancreas has substantial functional reserve; modest gland injury produces measurable function tests but no clinical malabsorption, while clinically apparent exocrine insufficiency implies advanced parenchymal loss.

• Section 26.6: Type 3c diabetes

  The American Diabetes Association recognizes type 3c diabetes as distinct from type 2.

• Section 26.7: Autoimmune pancreatitis types 1 and 2

  Type 1 autoimmune pancreatitis is lymphoplasmacytic sclerosing pancreatitis, the pancreatic manifestation of IgG4-related disease (cross-link Ch 20 for IgG4-related disease beyond the pancreas, including IgG4-associated cholangitis).

• Section 26.8: Chronic pancreatitis complications

  Pseudocyst occurs in approximately 25 percent of chronic pancreatitis patients (most often alcoholic chronic pancreatitis) as a mature peripancreatic fluid collection with non-epithelialized fibrous wall, formed at least 4 weeks after an acute episode or arising from ductal disruption in established disease.

• Section 26.9: Pancreatic cyst classification

  The five entities to distinguish on cross-sectional imaging plus EUS are IPMN, MCN, SCA, SPEN, and pseudocyst.

• Section 26.10: Cyst fluid analysis

  Cyst fluid CEA greater than 192 ng per mL favors mucinous origin (sensitivity approximately 73 percent, specificity 84 percent) because mucinous epithelium secretes CEA; CEA below 5 ng per mL has 85 percent specificity for excluding mucinous origin.

• Section 26.11: IPMN Fukuoka and Kyoto guidelines

  The Fukuoka 2017 international consensus and the updated Kyoto 2024 evidence-based guidelines define worrisome features and high-risk stigmata that drive management of branch-duct IPMN.

• Section 26.12: IPMN surveillance intervals

  Branch-duct IPMN without worrisome features is surveilled by size, with intervals reflecting the size-stratified malignancy risk.

• Section 26.13: Pancreatic adenocarcinoma diagnosis and management

  Pancreatic ductal adenocarcinoma is the fourth leading cause of cancer-related death in the United States and arises in the pancreatic head in 60 to 70 percent of cases, which is why obstructive jaundice (present in approximately 55 percent at diagnosis) is the dominant clinical signature.

• Section 26.14: Pancreatic neuroendocrine tumors

  Pancreatic neuroendocrine tumors (pNETs) arise from islet-derived endocrine cells and are mechanistically distinct from ductal adenocarcinoma.

Podcast episodes

1. 01

   CP Framework Escape

   This episode covers the chronic pancreatitis framework: how it's classified by cause, the genetic forms and where each one breaks trypsin control, how it's diagnosed as the disease advances, and how the pain is managed, including the shift that moved early surgery ahead of endoscopy in dilated-duct disease.

2. 02

   PERT Type3c Complications

   This episode covers chronic pancreatitis management and complications: enzyme replacement for exocrine insufficiency, the pancreatogenic diabetes with its hypoglycemia-prone physiology, and the anatomic complications from pseudocyst to splenic vein thrombosis.

3. 03

   Autoimmune Pancreatitis

   This episode covers autoimmune pancreatitis, types one and two, told apart by their mechanism, demographics, imaging, serology, histology, and steroid response.

4. 04

   Cystic Lesions

   This episode covers the incidentally discovered pancreatic cyst, told apart by fluid markers and imaging, with the surveillance rules for the mucinous ones. The decision here is costly in the opposite direction from the autoimmune mass of last episode: resection of a cyst that was never going to become cancer commits a patient to the morbidity of a major...

5. 05

   PDAC and PNETS

   This episode covers the pancreatic neoplasms: ductal adenocarcinoma, among the leading causes of cancer death in the United States, and the neuroendocrine tumors, told apart by functional syndrome and grade.