1. Chronic Gastritis and Gastric Cancer
Thomas Rosenzweig, MD

2. Chronic Gastritis H. pylori = most common cause
spiral-shaped or curved bacilli
fecal-oral
Intra-epithelial neutrophils and sub-epithelial plasma cells
Autoimmune gastritis = most common form of chronic gastritis in patients without H. pylori infection
diffuse mucosal damage of the oxyntic (acid-producing) mucosa in the body and fundus
spares the antrum
associated with hypergastrinemia
60 year old women
Symptoms: nausea and upper abdominal pain
Complication: Peptic ulcer disease (PUD)
chronic mucosal ulceration affecting the duodenum or stomach
H. pylori infection, NSAIDs, or cigarette smoking
Most common: H. pylori-induced antral gastritis in gastric antrum or duodenum
↑ gastric acid secretion
↓ decreased duodenal bicarbonate secretion

3. Helicobacter pylori Gastritis
H. pylori infection
antral gastritis
↑ acid production
risk of duodenal peptic ulcer.
Intra-epithelial neutrophils and sub-epithelial plasma cells
May involve the gastric body and fundus
multifocal atrophic gastritis
↓ Decreased acid production
risk of gastric adenocarcinoma
Inverse relationship between duodenal ulcer and gastric adenocarcinoma

4. Helicobacter pylori Gastritis
H. pylori
Flagella (can move in mucus)
Urease (↑ gastric pH)
Adhesins (attach surface foveolar cells)
Toxins (cytotoxin-associated gene A (CagA))
Atrophic mucosa ↓ parietal and chief cells
mucosa-associated lymphoid tissue (MALT)
B-cell lymphoma risk
Treatment
antibiotics
proton pump inhibitors

5. Autoimmune Gastritis intestinal metaplasia
↓ parietal cells (killed by CD4+ T cells)
↓ gastric acid (negative feedback gone)
↑gastrin release (nothing to stop it)
Hypergastrinemia
Hyperplasia of antral gastrin-producing G cells
↓ intrinsic factor
↓ ileal vitamin B12 absorption
pernicious anemia
intestinal metaplasia
Goblet cells
Associated with Oxyntic atrophy
↑ risk of gastric adenocarcinoma
Risk is greatest in autoimmune gastritis

6. Gastritis Comparison Table

7. Key Concepts

8. Gastric Polyps and Tumors

9. 1. Inflammatory (Hyperplastic) Polyps
Most polyps
H. pylori infection
associated with chronic gastritis
irregular, cystically dilated, and elongated foveolar glands
2. Fundic Gland Polyps
occur in the gastric body and fundus
irregular glands lined by flattened parietal and chief cells
sporadically
no cancer risk
individuals with familial adenomatous polyposis (FAP)
Dysplasia and even cancer
More common due to proton pump inhibitor therapy
↓ acid production → ↑ gastrin secretion → ↑ oxyntic gland growth
3. Gastric Adenoma
50 and 60 year old males
In the antrum
Risk of adenocarcinoma in lesions greater than 2 cm in diameter
Pt. likely has chronic gastritis with atrophy and intestinal metaplasia
Risk of cancer is much higher in gastric adenomas than in intestinal adenomas.

10. Gastric Adenocarcinoma ***Most common***
Intestinal type
Bulky masses (glands)
↑ signaling via the Wnt pathway
Diffuse type
Signet ring cells (mucin vacuoles)
↓ CDH1 (↓ E-cadherin)
Familial gastric cancer
Half of sporadic cases
Linitis plastica
(leather bottle appearance)

11. Gastric Adenocarcinoma Morphology
Intestinal Type
Japan, Chile, Costa Rica, and Eastern Europe
develops from precursor lesions
male-to-female ratio is 2 : 1.
Pts. with multifocal mucosal atrophy and intestinal metaplasia
Diffuse Type
is relatively uniform across countries,
no precursor lesions
males and females are equally affected
5-year survival is less than 30%.
involves the gastric antrum and the lesser curvature

12. Key Concepts