MCQ: Gastrointestinal Pathology – 15 MCQs | Kenya MBChB

15 Year 3: Gastrointestinal Pathology exam questions on MCQ: Gastrointestinal Pathology for medical students. Includes MCQs, answers, explanations and written q

This MCQ set contains 15 questions on MCQ: Gastrointestinal Pathology in the Year 3: Gastrointestinal Pathology unit. Each question includes the correct answer and a detailed explanation for active recall and exam preparation.

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?

  1. A. Calcification of necrotic ducts
  2. B. Saponification of peripancreatic fat by liberated lipases
  3. C. Precipitation of bile salts
  4. D. Dystrophic calcification of islets

Correct answer: B – Saponification of peripancreatic fat by liberated lipases

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?

  1. A. Presence of fibrosis
  2. B. Necrotic acini with preservation of ducts
  3. C. Atrophy of islets of Langerhans
  4. D. Protein plugs in ducts

Correct answer: B – Necrotic acini with preservation of ducts

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?

  1. A. Destruction of islets of Langerhans
  2. B. Loss of exocrine acinar tissue causing enzyme deficiency
  3. C. Obstruction of the common bile duct
  4. D. Autoimmune destruction of mucosal cells

Correct answer: B – Loss of exocrine acinar tissue causing enzyme deficiency

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?

  1. A. TP53
  2. B. SMAD4
  3. C. KRAS
  4. D. BRCA2

Correct answer: C – KRAS

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?

  1. A. Tail of pancreas
  2. B. Body of pancreas
  3. C. Head of pancreas
  4. D. Ampulla of Vater only

Correct answer: C – Head of pancreas

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?

  1. A. Mucinous cystic neoplasm
  2. B. Serous cystadenoma
  3. C. Pancreatic intraepithelial neoplasia (PanIN)
  4. D. Intraductal papillary mucinous neoplasm

Correct answer: C – Pancreatic intraepithelial neoplasia (PanIN)

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?

  1. A. Virchow's triad
  2. B. Courvoisier sign
  3. C. Trousseau syndrome
  4. D. Sister Mary Joseph nodule

Correct answer: C – Trousseau syndrome

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?

  1. A. Presence of calcifications
  2. B. Glycogen-rich cuboidal epithelium with no mucin production
  3. C. Desmoplastic stroma
  4. D. Multilocular cysts with thick fluid

Correct answer: B – Glycogen-rich cuboidal epithelium with no mucin production

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?

  1. A. Serous cystadenoma
  2. B. Pseudocyst
  3. C. Mucinous cystadenoma
  4. D. All carry equal risk

Correct answer: C – Mucinous cystadenoma

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?

  1. A. Pseudocysts contain mucin
  2. B. Pseudocysts lack an epithelial lining
  3. C. Pseudocysts are lined by glycogen-rich cells
  4. D. Pseudocysts arise from VHL gene mutations

Correct answer: B – Pseudocysts lack an epithelial lining

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?

  1. A. HLA-B27 and HLA-DR2
  2. B. HLA-DR3 and HLA-DR4
  3. C. HLA-A1 and HLA-B8
  4. D. HLA-DQ2 and HLA-DQ6

Correct answer: B – HLA-DR3 and HLA-DR4

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?

  1. A. Producing autoantibodies against insulin
  2. B. Directly killing beta cells via cytotoxic activity
  3. C. Stimulating beta-cell hyperplasia
  4. D. Promoting insulin resistance in peripheral tissues

Correct answer: B – Directly killing beta cells via cytotoxic activity

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?

  1. A. Fibrin
  2. B. Amyloid (islet amyloid polypeptide)
  3. C. Calcium oxalate
  4. D. Lipofuscin

Correct answer: B – Amyloid (islet amyloid polypeptide)

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?

  1. A. KRAS
  2. B. TP53
  3. C. CDKN2A
  4. D. SMAD4

Correct answer: D – SMAD4

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?

  1. A. Autoimmune destruction of beta cells
  2. B. Progressive fibrosis eventually destroying the islets of Langerhans
  3. C. Increased glucagon secretion from alpha cells
  4. D. Insulin receptor downregulation

Correct answer: B – Progressive fibrosis eventually destroying the islets of Langerhans

Fibrosis initially spares the islets but in late-stage chronic pancreatitis, progressive destruction of islets leads to endocrine insufficiency and diabetes.

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