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
Stomach
Small Intestine
Colon
Stomach Cell Types (LO1)
Small Intestine Key Features (LO1)
High-yield: "Brunner's Duodenum, Peyer's Ileum" — each confined to ONE segment. Villi = SI only. Straight crypts + abundant goblet cells = colon.
ON EXAM — Acute gastritis causes/histology, stress ulcers (Curling vs Cushing), peptic ulcer depth (through muscularis mucosae), H. pylori urease+, celiac villous atrophy
Acute Gastritis & Stress Ulcers (LO2)
Peptic Ulcer Disease (LO2)
H. pylori Infection (LO2)
Celiac Disease (LO2)
Meckel Diverticulum (LO2)
LO 3
ON EXAM — Crohn's vs UC location/pattern/depth, transmural vs mucosal, skip lesions, crypt abscess, extraintestinal manifestations, complications
Crohn's vs Ulcerative Colitis Comparison (LO3)
Feature
Crohn's Disease
Ulcerative Colitis
Location
Pattern
Depth of inflammation
Cobblestone mucosa
Fistulas
Pseudopolyps
Crypt abscess
Cancer risk
Crohn's Disease Features (LO3)
Ulcerative Colitis Features (LO3)
Extraintestinal Manifestations of IBD (LO3)
LO 4
ON EXAM — Esophageal SCC vs adenoCA location, Barrett's adenoCA risk, gastric adenoCA H. pylori, GIST c-KIT mutation, carcinoid 5-HT, colorectal adenoCA sequence (APC/KRAS/TP53), FAP APC gene
Esophageal Tumors (LO4)
Type
Location in Esophagus
Risk Factors
Histology
Squamous Cell Carcinoma (SCC)
Adenocarcinoma
Gastric Tumors (LO4)
Gastrointestinal Stromal Tumor (GIST) (LO4)
Carcinoid Tumor (Neuroendocrine) (LO4)
Colonic Polyps & Colorectal Cancer (LO4)
Feature
Tubular Adenoma
Villous Adenoma
Architecture
Malignancy risk
Secretory function
Size >2 cm significance
Familial Adenomatous Polyposis (FAP) (LO4)
Colorectal Adenocarcinoma (LO4)
Lynch Syndrome (HNPCC) (LO4)
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?
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?
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?
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?
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⁻?
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?
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?
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?
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).