Chronic Pancreatitis, Pancreatic Cysts, and Pancreatic Neoplasms

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• ABIM-format MCQs
  5-option vignettes with full wrong-answer teaching.
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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

  Autoimmune pancreatitis is the autoimmune category of TIGAR-O, and it matters most because it mimics pancreatic cancer and responds to steroids.

• 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 third 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

   Chronic Pancreatitis and Cysts: Diagnosis and Pain

   Chronic pancreatitis is scar replacing the tissue that secretes and drains, and each decision in this episode follows from that idea. The episode starts with the finding that proves the disease, pancreatic calcification on CT, then classifies the cause with TIGAR-O, weighs alcohol against tobacco, and keeps obstructing cancer in mind. It then covers who needs genetic testing and what PRSS1, SPINK1, and the other genes mean. Next it shows how to make the diagnosis when CT is normal, using secretin MRCP, EUS, and function tests. It closes with pain: medical therapy first, then drainage of an obstructed duct, then total pancreatectomy with islet autotransplantation for a narrow group.

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2. 02

   Chronic Pancreatitis and Cysts: Late Complications

   This episode follows the pancreas after scarring, through what it stops making and the structural trouble it causes. A man with a calcified gland shows that steatorrhea appears only when exocrine function falls below about ten percent, so bone density, vitamins, and B12 are checked, enzymes are given with meals, timing and adherence are fixed before the dose rises, and type three c diabetes is managed cautiously because glucagon is lost. A woman then shows the complications by anatomy: a symptomatic pseudocyst drained endoscopically, a recurrence from a disconnected duct, a fibrotic bile duct stricture, splenic vein thrombosis with gastric varices, high-amylase ascites, and long-term cancer risk.

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3. 03

   Chronic Pancreatitis and Cysts: Autoimmune Types

   Autoimmune pancreatitis imitates pancreatic cancer and melts away with steroids, so the organizing idea is excluding cancer before treating. The episode follows an older man with painless jaundice who has type one disease, then a younger woman with ulcerative colitis who has type two. It covers the clues outside the pancreas, why an IgG4 level cannot settle the diagnosis, how the HISORt and international consensus criteria are applied, histologic differences between the types, prednisone dosing, what no response means, and who relapses and what maintains remission.

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4. 04

   Chronic Pancreatitis and Cysts: Naming the Cyst

   The organizing idea is that every pancreatic cyst is first sorted as mucinous or not, because mucin carries the cancer risk. The episode starts with a woman's incidental tail cyst and the five cyst types, then reads fluid CEA, glucose, and amylase, combines CEA and amylase into a two-by-two, and adds cytology, KRAS, GNAS, and the string sign. A young woman's part-solid mass shows the cyst cured by resection. A man with a branch-duct IPMN then shows MRI surveillance intervals, worrisome features that lead to EUS, high-risk stigmata that lead to surgery, the growth threshold, and when surveillance stops.

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5. 05

   Pancreatic Cysts and Neoplasms: Two Solid Tumors

   This episode covers the two solid tumor families of the pancreas through two patients. A woman with painless jaundice and new diabetes shows adenocarcinoma: ultrasound confirms obstruction, pancreas-protocol CT or MRI stages the tumor, CA 19-9 is read with caution, and EUS core biopsy gives tissue. Vessel contact sets resectable, borderline, or locally advanced disease, and borderline disease gets neoadjuvant modified FOLFIRINOX. Germline testing follows. A woman with fasting hypoglycemia shows insulinoma: prove it with a seventy-two-hour fast, exclude injected insulin with C-peptide, find it with EUS, and check for MEN1. Short cases then cover rarer functioning tumors, incidental tumors, and metastatic treatment.

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Key topics

• ·Definition and pathognomonic calcification
• ·TIGAR-O classification of causes
• ·Alcohol, tobacco, and CLDN2
• ·Excluding obstructing adenocarcinoma
• ·Selective genetic testing and PRSS1 surveillance
• ·CT, secretin MRCP, and EUS Rosemont criteria
• ·Why ERCP is not used for diagnosis
• ·Fecal elastase and secretin function testing
• ·Sources of pain and medical management
• ·Endoscopic versus surgical drainage and pancreatectomy with islet autotransplantation
• ·Late onset of steatorrhea
• ·Baseline bone density, vitamins, and B12
• ·Pancreatic enzyme replacement dosing
• ·Poor response to enzymes
• ·Type three c diabetes
• ·Pseudocyst drainage with LAMS
• ·Disconnected duct syndrome
• ·Distal bile duct stricture
• ·Splenic vein thrombosis and gastric varices
• ·Pancreatic ascites and cancer risk
• ·Autoimmune pancreatitis in TIGAR-O
• ·Type one features and imaging
• ·Other organ involvement in IgG4-related disease
• ·Limits of serum IgG4
• ·HISORt and consensus criteria
• ·Histology of type one and type two
• ·Prednisone induction and taper
• ·Relapse and rituximab maintenance
• ·Type two and ulcerative colitis
• ·Board traps