GASTRITIS MIND MAP
PATHO WEEK 8
S. COE RN BSN MITM
PATHOPHYSIOLOGY CONT'D
DISEASE MANAGEMENT
Acute gastritis:
alcohol,
histamine,
digitalis use
metabolic disorders
H.pylori
inflammation
increased or decreased gastric secretions.
Chronic: loss of t-cell
gastric mucosa degredation
decrease of parietal cells and intrinsic factor.
PATHOPHYSIOLOGY
Infection with the bacterium Helicobacter pylori.
Erosive gastritis may be caused by use of nonsteroidal anti-
inflammatory drugs (NSAIDs) such as aspirin and ibuprofen.
20 percent of people who chronically use NSAIDs develop gastric issues.
Drinking alcohol,
using cocaine,
exposure to radiation (erosive gastritis).
Stresses such as trauma,
major surgery,
severe burns,
or a critical illness may cause erosive/stress gastritis
DIAGNOSTIC MEASURES
Physical exam and history,
X-RAY/IMAGING
GI endoscopy
histology of sample tissue
biopsy obtained in endoscopy
Serological tests for H. pylori and breath test
Prednisolone
antacids
histamine 2 (H2) blockers
proton pump inhibitors (PPIs)
D/C NSAIDS
H. pylori, antibiotics may be prescribed for up to fourteen days.
PPIs are also used to treat stress gastritis.
• May be Asymptomatic
• Gnawing
• Burning
• Pain
• Blood in stool
• Nausea
• Vomiting
CLINICAL PRESENTATION
Epidemiology:
H. pylori discovered in childhood,
hygiene,
household density,
cooking habits lead to risks associated for the disorder.
5% autoimmune in origin,
50% of cases tend to be childhood to adolescence.
