hematemesis, melena, or
blood in the nasogastric
aspirate
Dyspepsia, N/V
Chronic
Symptoms
Few or None
Dyspepsia, N/V
Causes
NSAIDS
Stress
ETOH
Mechanical
Ventilation
Treat Propholactically
PPI & H2 Blockers
Early Enteral Feeding
Head Trauma
Burn Patient
viral (CMV
Vascular injury or
Trauma
Pathophysiology
Acidic Gastric
erosion of mucosa
Destruction of
Mucosal Defense
Treatment
Endoscopic
Hemostasis
PPI & H2
Blocker
IV Fluids & Blood
Transfusion
Sugery (Fall Back)
Non-Erosive
Pathophysicology
Superficial
Lymphocytes & Plasma cells w/neutrophils
infiltrate inflammatory cells. Superficial, involve
antrum, body or both. Increases with age
Deep
Mononuclear cells & neutrophils infiltrate the
entire mucosa to the level of the muscularis, but
exudate or crypt abscesses seldom result, as
might be expected by such infiltration
atrophy
Type A
Some patients with gastric atrophy have
autoantibodies to parietal cells, usually in
association with corpus (type A) gastritis
and pernicious anemia
Type B
Atrophy of gastric glands in gastritis, most
often long-standing antral (sometimes
referred to as type B) gastritis
Metoplasia
Mucosal Gland
(pseudopyloric metaplasia) occurs in the
setting of severe atrophy of the gastric
glands, which are progressively replaced by
mucous glands (antral mucosa), especially
along the lesser curve.
Intestinal
begins in the antrum in response to chronic mucosal injury & may
extend to the body. Gastric mucosa cells change to Gastric mucosa
cells change to resemble intestinal mucosa—with goblet cells,
endocrine (enterochromaffin or enterochromaffin-like) cells, and
rudimentary villi—and may even assume functional (absorptive)
characteristics.
Cause
Helicobacter pylori infection
Diagnosis
Endoscopy for symptomatic
gastritis patients
Sympoms
Mild dyspepsia vague symptoms
Treatment
H pylori + patients
Eradication of H pylori
Negative H pylori - patients PPI & H2
blockers or antacids