Gastrointestinal · Topic 8 of 20
Gastritis (Acute & Chronic)
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Gastritis (Acute & Chronic)
Inflammation of the gastric mucosa, often superficial and widespread or patchy, where an ulcer is a deeper, focal crater. The danger is GI bleeding.
What causes it
The main causes: NSAIDs and aspirin, alcohol and H. pylori
What you'll see
Epigastric pain or burning, but many clients have no symptoms
In erosive gastritis, erosions can appear within 12 hours of the insult, and bleeding usually shows within 2 to 5 days.
Labs & diagnostics
EGD with biopsy confirms gastritis; breath or stool tests find H. pylori
H2 blockers do not affect the test. Antibody (serology) tests are not usually used to confirm cure, because antibody levels can stay elevated for months after successful treatment.
Red flags
These signal GI bleeding: report at once
Bismuth can cause harmless, temporary darkening of the stool and tongue; tarry stool with dizziness or tachycardia still needs reporting as possible melena.
Treatment
Acute gastritis usually resolves once the cause is removed
IV fluids and electrolyte replacement as ordered
Then advance the diet as toleratedPPIs and H2 blockers reduce acid
Space antacids from other drugs
Finish every dose, even after symptoms stop
Lifelong parenteral B12
H. pylori regimen and long-term risk
Nursing priorities
Acute or chronic?
Acute comes on suddenly; chronic persists
| Acute | Chronic | |
|---|---|---|
| Course | Comes on suddenly | Persists |
| Outcome | Usually resolves once the cause is removed | Can lead to mucosal atrophy |
| Classic setting | Acute stress gastritis in critical illness | H. pylori is the main cause |
Autoimmune gastritis destroys parietal cells, so intrinsic factor falls and B12 is not absorbed; see the anemia topic for pernicious anemia.
Teach your patient
Avoid NSAIDs, aspirin, alcohol and smoking; acetaminophen for pain unless told otherwise
Diet changes are for symptom relief: diet is not an important cause of most gastritis.
Gastritis is widespread or patchy inflammation of the gastric mucosa; an ulcer is a focal crater. Remove the cause, reduce the acid, and report hematemesis, coffee-ground emesis or melena at once.
Sources · Overview of Gastritis (Merck Manual) · Erosive Gastritis (Merck Manual) · Helicobacter pylori Infection (Merck Manual) · Autoimmune Metaplastic Atrophic Gastritis (Merck Manual) · Drug Treatment of Gastric Acidity (Merck Manual) · Caustic Ingestion (Merck Manual) · Gastritis & Gastropathy (NIDDK) · Gastritis (StatPearls) · Treatment of Helicobacter pylori Infection, Clinical Guideline 2024 (ACG) · Gastritis (Cleveland Clinic) · Bismuth subsalicylate Drug Facts (DailyMed) · Gastritis nursing care (Free-Ed.Net) · Overview of Gastroenteritis (Merck Manual) · Follow your facility's protocol for holding drugs before H. pylori testing.
Gastritis (Acute & Chronic)
Gastritis is inflammation of the gastric mucosa, often superficial and widespread or patchy, whereas an ulcer is a deeper, focal crater in the lining. The main causes are NSAIDs and aspirin, alcohol and H. pylori infection, and H. pylori is the main cause of chronic gastritis. Expect epigastric pain or burning, nausea, vomiting, anorexia and early fullness, though many clients have no symptoms. Hematemesis, coffee-ground emesis, melena, hypotension or tachycardia signal GI bleeding and are reported at once. EGD with biopsy confirms gastritis, and a urea breath or stool antigen test detects H. pylori after PPIs, antibiotics and bismuth are held per protocol. While the client is vomiting, expect NPO status with IV fluids and electrolytes as ordered, then a diet advanced as tolerated; PPIs or H2 blockers reduce acid. The client finishes every dose of the H. pylori course and avoids NSAIDs, aspirin, alcohol and smoking. Autoimmune gastritis destroys parietal cells, so B12 is not absorbed and the client needs lifelong parenteral B12.
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