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Esophagus & Stomach Disease Active Drills

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Lecture 15 · GI Block · Infectious Esophagitis, GERD, Barrett's, Gastritis, PUD, Gastric Cancers — LOs 1–13
Primary: GI15 Lecture Guide (HoyaDocs)
LOs: GI Block LOs 1–13
Key: H. pylori, PUD, Gastric Cancer
Step 1: First Aid Pathology Ch. 5
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Click a card to flip · 0 cards seenLOs 1–13
LO 1 — Infectious Esophagitis
Name the three major infectious causes of esophagitis and their typical patient populations.
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Answer
HSV esophagitis: CD4 <50 · vesicles → shallow ulcers
CMV esophagitis: CD4 <200 · deeper ulcers · solitary · "apple core"
Candida esophagitis: immunocompromised or prolonged antibiotics · pseudomembranous plaques
LO 1 — Infectious Histology
What are the key histologic findings in HSV and CMV esophagitis?
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Answer
HSV: Cowdry A intranuclear inclusions, multinucleated giant cells, epithelial necrosis
CMV: owl's eye appearance (intranuclear + eosinophilic cytoplasmic inclusions)
LO 2 — GERD Pathophysiology
What are the primary mechanisms of GERD?
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Answer
LES dysfunction: decreased pressure or inappropriate relaxation
Increased gastric pressure: delayed gastric emptying, obesity, pregnancy
Reduced clearance: decreased motility, reduced saliva
LO 2 — GERD Histology
What histologic changes define reflux esophagitis?
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Answer
Changes: basal zone hyperplasia, epithelial necrosis, intraepithelial lymphocytes
Complications: stricture, Barrett's metaplasia, adenocarcinoma
LO 2 — Barrett's Esophagus
Define Barrett's esophagus and its significance.
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Answer
Definition: columnar metaplasia >3 cm above GE junction
Risk: adenocarcinoma 0.2–0.5% per year
Diagnosis: endoscopy with biopsy showing intestinal metaplasia
LO 3 — Esophageal SCC
What are major risk factors for esophageal squamous cell carcinoma?
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Answer
Risk factors: tobacco, alcohol (synergistic), caustic injury, achalasia, HPV
Location: upper/middle third
Prognosis: poor (5-year ~25%) due to late diagnosis
LO 3 — Esophageal Adenocarcinoma
What is the relationship between Barrett's esophagus and adenocarcinoma?
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Answer
Progression: Barrett's → dysplasia (low/high) → invasive cancer
Location: lower third / GE junction
Epidemiology: rising in white males, age 40–70
LO 4 — Acute Gastritis
Define acute gastritis and list major causes.
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Answer
Definition: acute mucosal inflammation (edema + neutrophils, minimal fibrosis)
Causes: H. pylori (most common), NSAIDs, alcohol, stress, aspirin, caustic injury
Presentation: epigastric pain, nausea, hematemesis if erosive
LO 5 — Erosion vs. Ulcer
What is the histologic distinction between erosion and ulcer?
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Answer
Erosion: limited to MUCOSA (epithelium ± lamina propria) · does NOT breach muscularis mucosae
Ulcer: extends PAST muscularis mucosae into submucosa/muscle
Healing: erosions heal without scar · ulcers leave scar
LO 6 — Chronic Gastritis Types
Compare Type A (autoimmune) vs. Type B (H. pylori) chronic gastritis.
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Answer
Type A: body/fundus · anti-parietal cell + anti-IF antibodies · achlorhydria, pernicious anemia
Type B: antrum · H. pylori+ · hypersecretion acid early, then achlorhydria late
Type C: bile reflux/NSAID · antrum + body · minimal inflammation
LO 7 — H. pylori PUD Pathogenesis
How does H. pylori cause peptic ulcer disease?
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Answer
Mechanism: colonizes antrum → antritis → ↑gastrin → ↑acid → ulcer
Duodenal ulcer: >90% H. pylori+
Gastric ulcer: 60–70% H. pylori+
Key: hypersecretion of gastric acid is the driver
LO 7 — NSAID PUD
What is the mechanism of NSAID-induced PUD?
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Answer
Mechanism: inhibit COX → ↓prostaglandins → loss of mucosal protection, ↓mucus, ↓HCO3-
Location: usually gastric ulcers (antrum)
Risk factors: age >60, H. pylori co-infection, high-dose NSAIDs
LO 8 — PUD Complications
What are the major complications of peptic ulcer disease?
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Answer
Hemorrhage: erosion into artery → hematemesis/melena
Perforation: free air under diaphragm → peritonitis
Penetration: erosion into pancreas → pancreatitis
Obstruction: scarring at pylorus → vomiting, weight loss
LO 8 — PUD Treatment
What are the main approaches to PUD treatment?
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Answer
H. pylori: triple therapy (PPI + clarithromycin + amoxicillin) × 10–14 days
NSAID ulcers: stop NSAID, PPI or H2-blocker
Acid suppression: PPIs (most effective), H2-blockers
Surgery: for complications (uncontrolled bleed, perforation, obstruction)
LO 9 — Precancerous Gastric Lesions
What precancerous lesions predispose to gastric carcinoma?
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Answer
Sequence: chronic gastritis → atrophic gastritis → intestinal metaplasia → dysplasia → adenocarcinoma (Correa cascade)
Key drivers: H. pylori (most important), pernicious anemia (type A)
LO 10 — Lauren Classification
Describe the Lauren classification of gastric adenocarcinoma.
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Answer
Intestinal type: organized glandular structure · associated with H. pylori, metaplasia · better prognosis
Diffuse type: poorly cohesive cells, signet-ring morphology · worse prognosis, young patients · often CDH1 mutation
LO 11 — GIST
What is a GIST and what is its key genetic driver?
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Answer
GIST: arises from Cajal cells (pacemaker cells) · mesenchymal, not epithelial
Genetics: KIT gene mutation (c-KIT tyrosine kinase) · responds to imatinib
Prognosis: depends on mitotic rate and size
LO 12 — MALT Lymphoma
Describe MALT lymphoma and its association with H. pylori.
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Answer
MALT lymphoma: indolent B-cell lymphoma from mucosa-associated lymphoid tissue
H. pylori: ~90% of gastric MALT lymphomas are H. pylori+
Treatment: H. pylori eradication alone for early stages · chemotherapy for advanced
LO 13 — H. pylori Associations
What diseases are associated with H. pylori infection?
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Answer
Upper GI: antral gastritis, duodenal ulcer (>90%), gastric ulcer (60–70%), gastric cancer (>80%)
Extra-GI: MALT lymphoma, ITP, IDA
Mechanism: chronic inflammation, hypersecretion (duodenal) vs. hypochlorhydria (gastric)
1. HSV Threshold
HSV esophagitis typically occurs in severely immunocompromised patients with CD4 counts below ______ cells/μL.
Very low threshold for HSV reactivation
2. Barrett's Metaplasia
Barrett's esophagus is defined as ______ metaplasia extending >3 cm above the GE junction.
Type of epithelium replacing squamous cells
3. Tobacco & Alcohol
Tobacco and alcohol have a ______ effect on esophageal SCC risk.
Together they increase risk more than additive
4. Most Common Cause
The most common cause of acute gastritis worldwide is ______.
A bacterium that colonizes the antrum
5. Erosion Limit
A gastric ulcer breaches the ______, whereas an erosion is limited to the mucosa.
Muscular layer separating epithelium from submucosa
6. H. pylori Hormone
H. pylori causes antritis leading to increased ______ secretion.
Hormone that increases gastric acid
7. NSAID Mechanism
NSAIDs inhibit ______ enzymes, decreasing prostaglandins and mucosal protection.
Cyclooxygenase isoforms
8. Correa Cascade
The Correa cascade: chronic gastritis → atrophic gastritis → ______ → dysplasia → cancer.
Adaptive change in response to chronic injury
9. Diffuse Gastric Cancer
The ______ type of gastric adenocarcinoma has poorly cohesive cells and signet-ring morphology.
Not the organized glandular type
10. GIST Gene
GISTs arise from mutations in the ______ gene, which encodes a tyrosine kinase.
Receptor targeted by imatinib
Drag items into the correct order, or click Reveal Answer to see the sequence. Click Check to verify your answer.
1. GERD Pathogenesis Sequence
Arrange the pathophysiologic steps leading to GERD symptoms.
≡LES becomes incompetent or relaxes inappropriately
≡Gastric contents reflux into distal esophagus
≡Mucosal injury and inflammation (reflux esophagitis)
≡Heartburn, regurgitation, esophageal pain
  1. LES becomes incompetent or relaxes inappropriately
  2. Gastric contents reflux into distal esophagus
  3. Mucosal injury and inflammation (reflux esophagitis)
  4. Heartburn, regurgitation, esophageal pain
2. Barrett's Progression
Arrange the histologic progression from normal to dysplasia.
≡Normal squamous epithelium of esophagus
≡Chronic GERD → intestinal metaplasia (Barrett's)
≡Low-grade dysplasia
≡High-grade dysplasia
≡Invasive adenocarcinoma
  1. Normal squamous epithelium of esophagus
  2. Chronic GERD → intestinal metaplasia (Barrett's)
  3. Low-grade dysplasia
  4. High-grade dysplasia
  5. Invasive adenocarcinoma
3. H. pylori Duodenal Ulcer
Arrange the steps of H. pylori duodenal ulcer pathogenesis.
≡H. pylori colonizes antral mucosa
≡Chronic antritis → increased G-cells and gastrin
≡Increased gastric acid production
≡Acid-peptic injury to duodenum → ulcer
  1. H. pylori colonizes antral mucosa
  2. Chronic antritis → increased G-cells and gastrin
  3. Increased gastric acid production
  4. Acid-peptic injury to duodenum → ulcer
4. Correa Cascade
Arrange the multistep sequence to gastric adenocarcinoma.
≡Chronic inflammation from H. pylori
≡Atrophic gastritis and mucosal atrophy
≡Intestinal metaplasia
≡Low-grade and high-grade dysplasia
≡Invasive gastric adenocarcinoma
  1. Chronic inflammation from H. pylori
  2. Atrophic gastritis and mucosal atrophy
  3. Intestinal metaplasia
  4. Low-grade and high-grade dysplasia
  5. Invasive gastric adenocarcinoma
Match each disease on the left with its key feature on the right. Click an item to select, then click its match.
Infectious Esophagitis Causes
Match pathogen with clinical/histologic finding.
Pathogen
HSV esophagitis
CMV esophagitis
Candida esophagitis
Key Feature
Cowdry A inclusions; shallow vesicular ulcers
Pseudomembranous plaques with whitish exudate
Owl's eye (intranuclear + cytoplasmic inclusions)
0/3 correct
Gastritis Types & Features
Match gastritis type with its location and pathophysiology.
Gastritis Type
Type A (Autoimmune)
Type B (H. pylori)
Type C (Reactive/NSAID)
Location / Feature
Antrum and body; bile reflux or NSAID injury
Antrum; H. pylori+ with hypersecretion initially
Body/fundus; anti-parietal cell antibodies; pernicious anemia
0/3 correct
Gastric Tumors
Match tumor type with key driver or feature.
Tumor Type
GIST
MALT Lymphoma
Gastric Adenocarcinoma (Diffuse)
Key Feature
Poorly cohesive cells, signet-ring; worse prognosis
Arises from c-KIT+ Cajal cells; imatinib responsive
Associated with H. pylori ~90%; responds to eradication
0/3 correct
Read each statement. Is it True or False? Click reveal to understand why.
Trap 1
Barrett's esophagus inevitably progresses to adenocarcinoma in all patients.
FALSE. Barrett's carries increased risk (0.2–0.5%/year) but NOT all progress to cancer. Many remain stable or regress with PPI therapy. High-grade dysplasia = cancer until proven otherwise.
Trap 2
CMV esophagitis typically requires CD4 <200 cells/μL, whereas HSV requires CD4 <50 cells/μL.
TRUE. CMV reactivates at higher CD4 (~200 cells/μL), while HSV requires severe immunosuppression (<50 cells/μL). Key thresholds for board exams.
Trap 3
An erosion and an ulcer are histologically identical; the difference is only clinical severity.
FALSE. Erosions are limited to MUCOSA; ulcers penetrate PAST muscularis mucosae. This is a fundamental histologic distinction. Ulcers heal with scar; erosions do not.
Trap 4
H. pylori causes duodenal ulcers through decreased gastric acid production.
FALSE. H. pylori causes duodenal ulcers through INCREASED acid (not decreased). Antritis → ↑gastrin → ↑acid → ulcer.
Trap 5
NSAIDs and H. pylori cause PUD in equal proportions (each ~50%).
FALSE. H. pylori is responsible for >90% of duodenal ulcers and 60–70% of gastric ulcers. H. pylori dominates the epidemiology of PUD.
Trap 6
Intestinal-type gastric cancer has better prognosis than diffuse-type because of H. pylori association.
TRUE. Intestinal-type has better prognosis (~40% 5-year) vs. diffuse (<5% 5-year). Intestinal-type arises from H. pylori-induced atrophy/metaplasia.
Trap 7
GIST is an epithelial malignancy arising from gastric glandular cells.
FALSE. GIST is a mesenchymal tumor arising from Cajal cells (pacemaker cells), NOT epithelial cells. Driven by KIT mutations.
Trap 8
MALT lymphoma of the stomach responds to H. pylori eradication in early-stage disease.
TRUE. ~90% of gastric MALT lymphomas are H. pylori+. Eradication alone is sufficient for ~75% of early-stage (stage I) MALT lymphomas.
Infectious Esophagitis Comparison
Pathogen CD4 Threshold Histology Endoscopy Treatment
HSV Less than 50 cells/μL Cowdry A inclusions, multinucleated cells Shallow vesicular ulcers Acyclovir IV
CMV Less than 200 cells/μL Owl's eye (intranuclear + cytoplasmic inclusions) Deep ulcers, often solitary Ganciclovir / Foscarnet IV
Candida Variable (any immunocompromised) Yeast and pseudohyphae, minimal inflammation Whitish plaques, pseudomembrane Fluconazole PO
GERD & Barrett's Esophagus
Condition Pathophysiology Histology / Appearance Complications
Reflux Esophagitis LES dysfunction, delayed gastric emptying Basal hyperplasia, epithelial necrosis, lymphocytes Stricture, Barrett's, adenocarcinoma
Barrett's Esophagus Chronic GERD → intestinal metaplasia >3 cm Columnar mucosa with goblet cells (intestinal metaplasia) Dysplasia, adenocarcinoma (0.2–0.5%/yr)
Gastritis Types & PUD
Type Major Causes Histology Key Location
Acute Gastritis H. pylori, NSAIDs, alcohol, stress Edema + neutrophilic infiltration; minimal fibrosis Fundus / antrum
Type A (Autoimmune) Anti-parietal cell antibodies Atrophy, plasma cell infiltration Body/fundus
Type B (H. pylori) H. pylori infection Lymphocytic infiltration Antrum
H. pylori Duodenal Ulcer H. pylori → ↑gastrin → ↑acid Mucosal/submucosal necrosis with inflammatory base First/second duodenum
NSAID Gastric Ulcer COX inhibition → ↓prostaglandins Mucosal/submucosal ulceration Antrum/lesser curve
Gastric Tumors at a Glance
Tumor Type Origin Genetic Driver Prognosis
Gastric Adenocarcinoma (Intestinal) Epithelial; H. pylori-associated p53, KRAS mutations Better (~40% 5-yr)
Gastric Adenocarcinoma (Diffuse) Poorly cohesive epithelial cells CDH1 (E-cadherin) mutations Worse (<5% 5-yr)
GIST Cajal cells (mesenchymal) KIT (c-KIT) mutations ~95% Variable; imatinib responsive
MALT Lymphoma B-cells (mucosa-associated lymphoid tissue) H. pylori-driven monoclonal proliferation Indolent; responds to eradication early
H. pylori Disease Associations
Disease H. pylori Association Pathophysiology
Antral Gastritis ~95% H. pylori+ Chronic antral inflammation → ↑G-cell density
Duodenal Ulcer Greater than 90% H. pylori+ Antritis → ↑gastrin → ↑acid
Gastric Ulcer 60–70% H. pylori+ Focal damage at metaplastic border
Intestinal Metaplasia Common after chronic H. pylori Chronic atrophic gastritis → adaptation
Gastric Adenocarcinoma Greater than 80% H. pylori+ Chronic inflammation → Correa cascade
MALT Lymphoma ~90% H. pylori+ Chronic antigen stimulation → monoclonal B-cell
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