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Part 2: Five Advanced-Level MCQs

MCQ 1

Question

A 29-year-old patient has had multiple episodes of acute pancreatitis since adolescence. He denies alcohol use, and imaging repeatedly shows no evidence of gallstones or biliary sludge. Genetic testing reveals a gain-of-function mutation in the cationic trypsinogen (PRSS1) gene. Which of the following statements about hereditary pancreatitis is FALSE?

Answer Choices

A. It often presents with recurrent bouts of acute pancreatitis starting in childhood or early adulthood.

B. Gain-of-function mutations in PRSS1 can lead to premature trypsin activation within the pancreas.

C. It is strongly associated with cigarette smoking, although smoking alone rarely contributes to pancreatitis in these patients.

D. Patients with hereditary pancreatitis have an increased lifetime risk of developing pancreatic cancer.

Correct Answer: C. It is strongly associated with cigarette smoking, although smoking alone rarely contributes to pancreatitis in these patients

Explanation

  • Why C is correct (FALSE statement): Cigarette smoking is actually a well-established major aggravating factor for both hereditary and non-hereditary pancreatitis. Describing it as “rarely contributing” is incorrect; smoking significantly worsens the disease course and accelerates progression, including in those with a genetic predisposition.
  • Why A, B, D are true:
    • A: Hereditary pancreatitis often manifests early, with recurrent acute episodes.
    • B: PRSS1 mutations cause premature trypsinogen activation in the pancreas, leading to autodigestion.
    • D: Lifetime risk for pancreatic cancer is notably increased in hereditary pancreatitis.

Key Takeaways

  1. PRSS1 (cationic trypsinogen) mutations are hallmark causes of hereditary pancreatitis.
  2. Patients typically present with recurrent acute episodes early in life, sometimes progressing to chronic disease.
  3. Smoking cessation is crucial, as smoking can exacerbate pancreatic injury in these patients.
  4. Genetic counseling is often recommended because of the higher cancer risk.
  5. Early and accurate diagnosis supports better long-term monitoring and preventive strategies.

Reference

Blumgart's Surgery of the Liver, Biliary Tract and Pancreas, 7th edition, Chapter 55: "Etiology, Pathogenesis, and Diagnostic Assessment of Acute Pancreatitis", Subtopic: "Nonbiliary and Nonalcoholic Acute Pancreatitis" (pp. 787–792)

MCQ 2

Question

You are evaluating a patient with recurrent acute pancreatitis where standard imaging (ultrasound, CT) and initial lab investigations (including triglyceride levels, calcium, liver enzymes) are all normal. Which of the following next-step investigations is most appropriate to identify or rule out an occult biliary or pancreatic ductal anomaly?

Answer Choices

A. Endoscopic Ultrasound (EUS)

B. Magnetic Resonance Cholangiopancreatography (MRCP)

C. Diagnostic peritoneal lavage (DPL)

D. Serum IgG4 level test

Correct Answer: B. Magnetic Resonance Cholangiopancreatography (MRCP)

Explanation

  • Why B is correct: MRCP offers high-resolution imaging of the pancreaticobiliary ducts, helping detect subtle or hidden anomalies (e.g., pancreas divisum, choledochal cysts) that can cause recurrent acute pancreatitis.
  • Why A, C, D are wrong:
    • A: EUS is indeed highly sensitive for certain pathologies (like microlithiasis or small lesions), but MRCP is often the preferred initial noninvasive study to evaluate ductal anatomy in suspected anatomical anomalies.
    • C: DPL is outdated and primarily used in trauma for detecting intra-abdominal bleeding, not for diagnosing ductal anomalies.
    • D: Serum IgG4 is indicated if autoimmune pancreatitis is suspected; however, in a purely “occult duct anomaly” scenario, MRCP is the direct approach.

Key Takeaways

  1. Recurrent “idiopathic” acute pancreatitis requires thorough investigation of less obvious causes.
  2. MRCP is the gold-standard imaging for defining pancreaticobiliary ductal anatomy noninvasively.
  3. EUS can be complementary, especially if MRCP is inconclusive or to evaluate microlithiasis.
  4. Identifying correctable ductal anomalies can reduce the risk of ongoing pancreatic injury.
  5. A structured diagnostic algorithm ensures efficient detection of elusive etiologies.

Reference

Blumgart's Surgery of the Liver, Biliary Tract and Pancreas, 7th edition, Chapter 55: "Etiology, Pathogenesis, and Diagnostic Assessment of Acute Pancreatitis", Subtopic: "Nonbiliary and Nonalcoholic Acute Pancreatitis" (pp. 787–792)

MCQ 3

Question

“All of the following statements about post-ERCP pancreatitis (PEP) risk factors are correct EXCEPT:”

Answer Choices

A. Difficult cannulation and multiple attempts at cannulation increase the likelihood of PEP.

B. Pre-existing hypercalcemia is a major independent risk factor for PEP.

C. Sphincter of Oddi dysfunction studies are associated with a significantly higher risk of PEP.

D. Female gender has been observed as a patient-related risk factor for PEP.

Correct Answer: B. Pre-existing hypercalcemia is a major independent risk factor for PEP

Explanation

  • Why B is correct (FALSE statement): Although hypercalcemia itself can be a cause of pancreatitis, it is not a well-established patient- or procedure-related risk factor specific to post-ERCP pancreatitis. Key PEP risk factors include difficult cannulation, Sphincter of Oddi dysfunction, and certain patient demographics like female gender.
  • Why A, C, D are true:
    • A: Repeated cannulation attempts can injure the ductal epithelium, increasing PEP risk.
    • C: Sphincter of Oddi manometry or therapies significantly elevate the likelihood of PEP.
    • D: Multiple studies note a higher incidence of PEP in female patients.

Key Takeaways

  1. Post-ERCP pancreatitis is a prevalent and sometimes severe complication of endoscopic procedures.
  2. High-risk scenarios include therapeutic ERCP with repeated pancreatic duct instrumentation.
  3. Sphincter of Oddi dysfunction is a particularly notorious contributor to PEP.
  4. Rectal NSAIDs and prophylactic pancreatic stents are strategies shown to reduce PEP risk.
  5. Recognizing patient and procedure-specific risk factors helps guide informed consent and prophylactic interventions.

Reference

Blumgart's Surgery of the Liver, Biliary Tract and Pancreas, 7th edition, Chapter 55: "Etiology, Pathogenesis, and Diagnostic Assessment of Acute Pancreatitis", Subtopic: "Nonbiliary and Nonalcoholic Acute Pancreatitis" (pp. 787–792)

MCQ 4

Question

In autoimmune pancreatitis (AIP), which of the following findings best differentiates Type 1 from Type 2 AIP?

Answer Choices

A. Presence of abundant IgG4-positive plasma cells in the pancreas

B. Presence of neutrophilic infiltration in the pancreatic ducts

C. Frequent association with inflammatory bowel disease (IBD)

D. Lack of extrapancreatic organ involvement

Correct Answer: A. Presence of abundant IgG4-positive plasma cells in the pancreas

Explanation

  • Why A is correct: Type 1 AIP (lymphoplasmacytic sclerosing pancreatitis) is classically characterized by a dense infiltration of IgG4-positive plasma cells, often as part of a systemic IgG4-related disease.
  • Why B, C, D are wrong:
    • B: Granulocytic epithelial lesions (neutrophilic infiltration) align more with Type 2 AIP.
    • C: Type 2 AIP has stronger associations with IBD (particularly ulcerative colitis).
    • D: Type 1 AIP commonly involves extrapancreatic organs (e.g., biliary tree, salivary glands), so a “lack of extrapancreatic organ involvement” is more consistent with Type 2.

Key Takeaways

  1. Autoimmune pancreatitis is categorized as Type 1 (IgG4-related) or Type 2 (idiopathic duct-centric).
  2. Type 1 typically involves elevated IgG4 levels and systemic organ involvement.
  3. Type 2 features granulocytic lesions and is more frequently linked with IBD.
  4. Both types respond to steroids, but differentiating them is important for long-term management.
  5. Elevated serum IgG4 alone doesn’t confirm Type 1 but is highly suggestive in the appropriate clinical context.

Reference

Blumgart's Surgery of the Liver, Biliary Tract and Pancreas, 7th edition, Chapter 55: "Etiology, Pathogenesis, and Diagnostic Assessment of Acute Pancreatitis", Subtopic: "Nonbiliary and Nonalcoholic Acute Pancreatitis" (pp. 787–792)

MCQ 5

Question

A 52-year-old with acute recurrent “idiopathic” pancreatitis undergoes endoscopic ultrasound (EUS). No microlithiasis or obvious ductal lesion is found, but a small portion of the dorsal pancreatic duct appears to drain separately into the minor papilla. Genetic screening reveals a SPINK1 variant. Which congenital anomaly, often linked with recurrent pancreatitis and sometimes requiring genetic predispositions, is most likely present?

Answer Choices

A. Choledochocele (Type III choledochal cyst)

B. Pancreas divisum

C. Annular pancreas

D. Sphincter of Oddi agenesis

Correct Answer: B. Pancreas divisum

Explanation

  • Why B is correct: Pancreas divisum is a common congenital ductal anomaly, whereby the dorsal and ventral pancreatic ducts fail to fuse properly, leaving most of the gland draining through the minor papilla. When coexisting with genetic abnormalities like SPINK1 or CFTR mutations, recurrent pancreatitis risk increases.
  • Why A, C, D are wrong:
    • A: A choledochocele is a cystic dilatation at the distal common bile duct within the duodenum, unrelated to dorsal duct drainage.
    • C: Annular pancreas causes a ring of pancreatic tissue around the duodenum, often presenting earlier in life with obstructive symptoms.
    • D: Sphincter of Oddi agenesis is extremely rare and not a typical congenital anomaly to explain these findings.

Key Takeaways

  1. Pancreas divisum is the most frequent congenital duct anomaly, found in up to 5%–12% of autopsy/imaging studies.
  2. Alone it may not always cause symptoms, but genetic factors (e.g., SPINK1) can predispose to recurrent pancreatitis in this setting.
  3. The minor papilla often has a narrower orifice, leading to ductal hypertension under high pancreatic secretory load.
  4. EUS and MRCP are crucial in revealing subtle duct anomalies contributing to “idiopathic” pancreatitis.
  5. Therapeutic endoscopic or surgical interventions to improve drainage may help selected symptomatic patients.

Reference

Blumgart's Surgery of the Liver, Biliary Tract and Pancreas, 7th edition, Chapter 55: "Etiology, Pathogenesis, and Diagnostic Assessment of Acute Pancreatitis", Subtopic: "Nonbiliary and Nonalcoholic Acute Pancreatitis" (pp. 787–792)

Key Takeaways for the Entire Topic

  1. Diverse Etiologies: While gallstones and alcohol remain the most common causes of acute pancreatitis, up to 25% of cases can stem from alternative etiologies like hypertriglyceridemia, hypercalcemia, genetic factors, autoimmune mechanisms, and iatrogenic causes (e.g., post-ERCP).
  2. Genetic Insights: Mutations in PRSS1, SPINK1, or CFTR can contribute to recurrent or chronic pancreatitis. Cigarette smoking often exacerbates the disease in genetically predisposed patients.
  3. Imaging & Diagnostics: High-quality imaging—CT, MRCP, EUS—enables identification of ductal anomalies (e.g., pancreas divisum), subtle calculi, and inflammatory changes missed by standard ultrasound or CT alone.
  4. Autoimmune Component: Autoimmune pancreatitis, especially IgG4-related Type 1 AIP, can mimic malignancy but usually responds dramatically to steroids. Distinguishing Type 1 from Type 2 has important management implications.
  5. Tailored Management: Recognizing and addressing the underlying cause—whether metabolic, genetic, or structural—optimizes outcomes. For example, strict metabolic control in hypertriglyceridemia and hypercalcemia, discontinuation of offending drugs, prophylactic strategies for ERCP, and potential endoscopic or surgical drainage for pancreas divisum.