Practice 15 MCQs on MCQ: Gastrointestinal Pathology with OmpathStudy. Built for Kenyan medical and health students to revise key concepts and prepare for exams.
Q1. A 45-year-old alcoholic presents with severe epigastric pain, elevated serum lipase, and chalky white deposits on CT. Which mechanism is PRIMARILY responsible for these white deposits?
Answer: Saponification of peripancreatic fat by liberated lipases
Explanation: Free fatty acids released by lipases combine with calcium, forming chalky white calcium soap deposits.
Q2. In acute pancreatitis, which histological finding distinguishes it from chronic pancreatitis?
Answer: Necrotic acini with preservation of ducts
Explanation: Acute pancreatitis shows necrotic acini but ducts are characteristically preserved. Chronic pancreatitis shows fibrosis and protein plugs.
Q3. A patient with chronic pancreatitis develops steatorrhea and weight loss. What is the underlying mechanism?
Answer: Loss of exocrine acinar tissue causing enzyme deficiency
Explanation: Destruction of acinar tissue reduces lipase production, causing fat malabsorption and steatorrhea.
Q4. Which genetic mutation is found in 90% of pancreatic ductal adenocarcinoma cases?
Answer: KRAS
Explanation: Activating KRAS mutations are the hallmark and earliest mutation in the PanIN → PDAC sequence.
Q5. A 65-year-old presents with painless jaundice, a palpable non-tender gallbladder, and weight loss. Where is the tumor MOST likely located?
Answer: Head of pancreas
Explanation: Courvoisier sign + painless jaundice = classic head of pancreas cancer obstructing the common bile duct. 60–70% of PDAC arise here.
Q6. Which precursor lesion leads to invasive pancreatic ductal adenocarcinoma through sequential mutation accumulation?
Answer: Pancreatic intraepithelial neoplasia (PanIN)
Explanation: PanIN is the established precursor. Mutations accumulate: KRAS → CDKN2A → TP53 → SMAD4.
Q7. A patient with pancreatic cancer develops recurrent migratory superficial thrombophlebitis. What is this paraneoplastic phenomenon called?
Answer: Trousseau syndrome
Explanation: Trousseau syndrome is migratory thrombophlebitis due to tumor-associated hypercoagulability, classic for PDAC.
Q8. What is the KEY histological feature distinguishing serous cystadenoma from mucinous cystadenoma?
Answer: Glycogen-rich cuboidal epithelium with no mucin production
Explanation: Serous cystadenoma has clear, glycogen-rich cuboidal cells and produces NO mucin. Mucinous cystadenoma has mucin-producing columnar epithelium.
Q9. Which pancreatic cyst carries significant malignant transformation potential?
Answer: Mucinous cystadenoma
Explanation: Mucinous cystadenomas have significant malignant potential. Serous cystadenomas are almost always benign. Pseudocysts have no malignant potential.
Q10. A pseudocyst differs from a true cyst in which fundamental way?
Answer: Pseudocysts lack an epithelial lining
Explanation: Pseudocysts have NO epithelial lining; they are walled by granulation tissue and fibrosis, arising as complications of pancreatitis.
Q11. In Type 1 Diabetes Mellitus, which HLA haplotypes confer the strongest genetic susceptibility?
Answer: HLA-DR3 and HLA-DR4
Explanation: T1DM has strong association with HLA-DR3 and HLA-DR4, which influence the autoimmune response against beta-cell antigens.
Q12. What is the role of CD8+ T cells in the pathogenesis of Type 1 Diabetes Mellitus?
Answer: Directly killing beta cells via cytotoxic activity
Explanation: CD8+ cytotoxic T cells directly kill pancreatic beta cells. CD4+ T cells assist via inflammatory cytokines (TNF-α, IFN-γ, IL-1β).
Q13. In Type 2 Diabetes Mellitus, what is deposited in the islets of Langerhans, contributing to beta-cell dysfunction?
Answer: Amyloid (islet amyloid polypeptide)
Explanation: Amyloid (IAPP) deposition in islets is a hallmark of T2DM and worsens beta-cell dysfunction alongside glucotoxicity and lipotoxicity.
Q14. Which loss-of-function mutation in PDAC specifically disrupts TGF-β signaling?
Answer: SMAD4
Explanation: SMAD4 loss disrupts TGF-β tumor suppressor signaling. Its loss is relatively specific to PDAC and is used as an IHC marker.
Q15. A patient with chronic calcific pancreatitis develops diabetes mellitus in late stages. What is the mechanism?
Answer: Progressive fibrosis eventually destroying the islets of Langerhans
Explanation: Fibrosis initially spares the islets but in late-stage chronic pancreatitis, progressive destruction of islets leads to endocrine insufficiency and diabetes.