Gastritis

Epidemiology & Etiology

Gastritis is acute or chronic inflammation or erosion of the gastric mucosa (gastropathy) with multiple causes: Helicobacter pylori, NSAIDs, and alcohol are most common, along with stress (burns, trauma, sepsis, multiorgan failure/uremia) and portal hypertension. Curling ulcer follows severe burns and Cushing ulcer follows CNS injury. Atrophic gastritis is associated with vitamin B12 deficiency and is a risk factor for gastric malignancy.

Pertinent Anatomy

The gastric mucosa is protected by a mucus-bicarbonate barrier, prostaglandin-mediated blood flow, and rapid epithelial turnover. Parietal cells secrete acid and intrinsic factor; chief cells secrete pepsinogen. Breakdown of the protective barrier exposes the epithelium to acid and pepsin, producing inflammation and superficial erosions. Chronic injury (e.g., autoimmune or H. pylori) can destroy gastric glands, causing atrophic gastritis and loss of intrinsic factor.

Pathophysiology

Agents that disrupt the mucosal barrier cause injury: NSAIDs inhibit protective prostaglandins, alcohol directly damages mucosa, and H. pylori induces chronic inflammation. Physiologic stress (burns, sepsis, shock) reduces mucosal perfusion, producing stress-related erosions. Mucosal erosion exposes submucosal vessels, causing bleeding that ranges from occult/coffee-ground to brisk hemorrhage. Autoimmune destruction of parietal cells produces atrophic gastritis with loss of intrinsic factor and B12 malabsorption.

Clinical Manifestations

Gastritis classically presents with GI bleeding without pain, ranging from mild coffee-ground emesis to large-volume hematemesis or melena; severe erosive gastritis can cause epigastric pain. NSAID use or alcoholism in the history is a clue. There are no unique physical findings for gastritis. Coffee-ground emesis or guaiac-positive stool indicates small-volume bleeding, while melena and hematemesis suggest larger volumes.

Diagnosis

Gastritis cannot be diagnosed from history and physical alone. Upper GI endoscopy is the gold standard, visualizing erosions and excluding ulcer or malignancy, and is indicated for upper GI bleeding and alarm features (age over 55, weight loss, anemia, dysphagia, persistent vomiting). Test for H. pylori with stool antigen, urea breath test, or gastric biopsy. A normal CBC rules out chronic but not acute bleeding.

Treatment

Suppress acid with a proton pump inhibitor (or H2 blocker) and remove the cause, stop NSAIDs and alcohol. If H. pylori is present, eradicate it to prevent recurrence with triple therapy for 14 days: a PPI, clarithromycin, and either amoxicillin or metronidazole. Liquid antacids relieve breakthrough pain. Most stable patients are discharged on a PPI with primary care follow-up; patients with bleeding or other complications require consultation and usually admission.

Prognosis

Gastritis generally resolves with acid suppression and removal of the offending cause. Untreated H. pylori predisposes to recurrence and peptic ulcer disease. Chronic atrophic gastritis predisposes to vitamin B12 deficiency and increased gastric cancer risk. Severe stress-related erosive gastritis can cause life-threatening hemorrhage.

Differential Diagnosis