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GI Pathology Lab — Answer Key
Built from GI Lecture 22 (LOs 1–4). Close notes. Fill from memory. Reveal only after a genuine attempt.
📖 Use alongside: GI Lecture 22 — GI Pathology Lab (HoyaDocs)
Focus on: Histology by organ (esophagus/stomach/SI/colon) + Pathogenesis of GERD/Barrett's/gastritis/peptic ulcer/H. pylori/IBD + Crohn's vs UC comparison + GI tumors (esophageal SCC/adenoCA, gastric CA, GIST, carcinoid, colorectal CA, FAP).
GI Histology Essentials
Esophageal Pathology
Gastric & SI Pathology
IBD & Colonic Disorders
GI Tumors & Neoplasia
Practice Qs
LO 1
ON EXAM — Stratified squamous vs columnar epithelium, villi/crypts, parietal/chief/G cells, goblet cells, Brunner's vs Peyer's patches
Epithelial Lining by Organ (LO1)
Organ
Epithelium Type
Unique Feature/Finding
Esophagus
Non-keratinized stratified squamous epithelium
No serosa, mucous glands in submucosa for lubrication
CEA (carcinoembryonic antigen); monitor recurrence
Lynch Syndrome (HNPCC) (LO4)
MLH1, MSH2, MSH6, PMS2
Microsatellite instability (MSI-high)
Right-sided colon
Mucinous adenocarcinoma
Better prognosis
Colonoscopy every 1-2 years from age 20-25
Colorectal cancer screening (average risk): Start at age 45 (updated from 50); repeat q10yr if normal. FAP: start age 10-12. Lynch: age 20-25.
Q1 (LO1 — Histology). A medical student examines a gastric biopsy showing tall, bright pink pyramidal cells in the fundic glands, each with an abundance of eosinophilic cytoplasm. What is the primary secretory product of these cells?
A. Pepsinogen B. Hydrochloric acid + Intrinsic factor C. Gastrin D. Mucus
B — Parietal (oxyntic) cells These bright pink eosinophilic cells are parietal cells, found primarily in the fundus and body. They secrete both HCl (via H+/K+ ATPase) and intrinsic factor (required for B12 absorption in terminal ileum).
Q2 (LO1 — Histology). A 5-year-old presents with severe diarrhea. A small bowel biopsy shows flattened villi, increased intraepithelial lymphocytes, crypt hyperplasia, and absence of a brush border. Which histologic finding is MOST specific for celiac disease?
A. Crypt hyperplasia B. Villous atrophy C. Plasma cell infiltration of lamina propria + villous atrophy D. Increased intraepithelial lymphocytes alone
C — Villous atrophy + immune infiltration While villous atrophy can occur in other conditions (tropical sprue, Whipple's), the combination of villous atrophy with significant plasma cell infiltration of the lamina propria (B cells sensitized to gliadin) is characteristic of celiac disease. Serology (anti-tTG IgA) confirms diagnosis.
Q3 (LO2 — Pathogenesis). A 55-year-old with a 20-year history of daily heartburn presents with dysphagia. Endoscopy shows a segment of dark/erythematous mucosa in the distal esophagus, distinct from pale squamous epithelium above. A biopsy reveals columnar epithelium with goblet cells. What is the MOST serious long-term complication of this condition?
A. Esophageal perforation B. Esophageal stricture C. Esophageal adenocarcinoma (30-40× increased risk) D. Acute esophageal variceal bleeding
C — Esophageal adenocarcinoma This patient has Barrett's esophagus (metaplasia: squamous → columnar with goblet cells). The defining histologic feature is goblet cells. While stricture and ulceration are complications of GERD alone, the 30-40× increased risk of adenocarcinoma is the most serious long-term sequela. Regular surveillance is needed.
Q4 (LO2 — Pathogenesis). A 28-year-old man presents with epigastric pain relieved by eating, and a biopsy shows chronic inflammation with small curved spiral rods visible on methylene blue staining. The organism produces urease. What is the pathogenic mechanism by which this organism causes mucosal damage?
A. Direct secretion of HCl into the lumen B. Urease → NH₃ neutralizes gastric acid, allowing bacterial colonization + CagA/VacA toxins trigger inflammation C. Competition with parietal cells for absorbing B12 D. Inhibition of prostaglandin synthesis
B — Urease → NH₃ + toxins H. pylori uses urease to convert urea → ammonia, neutralizing the acidic environment and allowing survival in gastric mucus. The organism then secretes CagA protein and vacuolating toxin (VacA), triggering chronic inflammatory cascade. This causes chronic gastritis, ulceration, and increased risk of gastric cancer (Group 1 carcinogen).
Q5 (LO2 — Pathogenesis). A 32-year-old woman with long-standing GERD is found to have a duodenal ulcer. Which of the following best explains why duodenal ulcers are 10× more common than gastric ulcers despite the duodenum being protected by pancreatic HCO₃⁻?
A. The duodenum lacks protective mucus B. H. pylori preferentially infects the duodenum, and >95% of duodenal ulcers are H. pylori-associated C. Duodenal enterocytes cannot secrete HCO₃⁻ D. NSAIDs are more absorbed in the duodenum
B — H. pylori association (>95% of DU) 95% of duodenal ulcers are H. pylori-associated (vs 70-80% of gastric ulcers). The gastric antral location of H. pylori leads to increased gastrin release → increased acid secretion → duodenal mucosal damage. Even though the duodenum has HCO₃⁻ protection, chronic hypersecretion overwhelms this defense.
Q6 (LO3 — IBD). A 24-year-old male with inflammatory bowel disease presents with right lower quadrant pain, fever, and bloody diarrhea. CT shows a dilated loop of terminal ileum with mesenteric fat stranding. Colonoscopy reveals skip lesions with a cobblestone appearance and deep fissuring ulcers. Biopsy shows transmural inflammation with granulomas. Which extraintestinal manifestation is MOST likely in this patient?
A. Primary sclerosing cholangitis (PSC) B. Ankylosing spondylitis (HLA-B27+ arthropathy) or peripheral arthritis C. Erythema nodosum + pyoderma gangrenosum D. Uveitis + episcleritis
B — HLA-B27+ or HLA-B27− arthritis This patient has Crohn's disease (skip lesions, transmural, ileocecal location, granulomas). While PSC is more common in UC, arthritis (both HLA-B27+ ankylosing spondylitis/sacroiliitis and HLA-B27− peripheral arthritis) is common in BOTH Crohn's and UC. Erythema nodosum and ocular manifestations also occur, but arthritis is most common.
Q7 (LO3 — IBD). A 31-year-old woman with ulcerative colitis spanning the entire colon develops toxic megacolon. Which of the following best explains why total colectomy would be curative for her inflammatory bowel disease?
A. Removal of the colon eliminates the primary source of inflammatory cytokine production B. UC is confined to the colon — removing the diseased organ removes the source of disease (mucosal/submucosal only, NOT transmural) C. The colon's role in water reabsorption is unnecessary for life D. Post-colectomy ileostomy normalizes intestinal pH
B — UC is confined to colon; mucosal disease only Ulcerative colitis, by definition, is confined to the colon with MUCOSAL and SUBMUCOSAL inflammation only (NOT transmural like Crohn's). Removing the entire colon eliminates the diseased tissue and cures the disease. In contrast, Crohn's can recur even after surgery (transmural disease can affect any GI segment). Total colectomy is curative for UC.
Q8 (LO4 — Tumors). A 58-year-old man presents with painless massive hematemesis. Endoscopy reveals dark blue linear dilated veins in the lower 1/3 of the esophagus. CT shows cirrhosis and portal vein enlargement. What is the PRIMARY mechanism by which portal hypertension causes esophageal varices?
A. Direct invasion of esophageal wall by hepatic cancer cells B. Increased pressure in the portal system → blood diverted through portosystemic anastomoses (left gastric ↔ esophageal veins) → submucosal venous dilation C. Splenomegaly compressing the esophageal veins directly D. Hepatic failure → decreased clotting factors → spontaneous esophageal bleeding
B — Portal HTN diverts blood through anastomoses Portal hypertension (from cirrhosis, thrombosis, etc.) increases pressure in the portal system. Blood is diverted through portosystemic anastomoses, including the left gastric vein ↔ esophageal veins. This causes submucosal esophageal veins to dilate (varices). Varices are painless until they rupture (massive hemorrhage).