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Gastritis & Peptic Ulcers for the USMLE Step 1 Exam

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Gastritis and Peptic Ulcers for USMLE Step 1
Definition
  • Gastritis: Inflammation of the gastric mucosa that may be acute or chronic.
    • Acute gastritis: Sudden onset of inflammation, often triggered by NSAIDs, alcohol, or infections.
    • Chronic gastritis: Long-term inflammation caused by H. pylori infection or autoimmune disorders.
  • Peptic Ulcer Disease (PUD): A break in the gastric or duodenal mucosa due to acid and pepsin. Ulcers extend into the submucosa, with gastric ulcers found in the stomach and duodenal ulcers in the proximal duodenum.
Etiology
Gastritis
  • Infectious Causes:
    • Helicobacter pylori (H. pylori): The most common cause of chronic gastritis. Leads to inflammation, peptic ulcers, and an increased risk of gastric cancer.
    • Viral gastritis: Seen in immunocompromised patients (e.g., CMV).
  • Non-infectious Causes:
    • NSAIDs: Inhibit prostaglandin production, reducing mucosal protection.
    • Alcohol: Direct irritant that damages the gastric mucosa.
    • Autoimmune gastritis: Autoimmune destruction of parietal cells, leading to vitamin B12 deficiency (pernicious anemia).
Peptic Ulcers
  • H. pylori infection: Major cause of both duodenal and gastric ulcers.
  • NSAIDs: Reduce prostaglandin synthesis, impairing mucosal defense and promoting ulcer formation.
  • Zollinger-Ellison syndrome: Gastrin-secreting tumors cause hypersecretion of acid and lead to multiple peptic ulcers.
Pathophysiology
Gastritis
  • Acute Gastritis: Exposure to irritants (e.g., alcohol, NSAIDs) causes mucosal damage, leading to acute inflammation with neutrophil infiltration.
  • Chronic Gastritis:
    • H. pylori infection: Chronic inflammation, leading to atrophic gastritis, intestinal metaplasia, and an increased risk of gastric adenocarcinoma.
    • Autoimmune gastritis: Loss of parietal cells results in hypochlorhydria, hypergastrinemia, and vitamin B12 deficiency.
Peptic Ulcer Disease
  • Duodenal Ulcers: Linked to increased acid secretion due to H. pylori-induced gastrin release. Duodenal ulcers are more common and typically cause pain relieved by eating.
  • Gastric Ulcers: Associated with weakened mucosal defenses (e.g., from NSAID use). Pain is worsened by eating.
Clinical Features
Gastritis
  • Acute Gastritis:
    • Epigastric pain: Common, often with nausea or vomiting.
    • Hematemesis or melena: May indicate more severe erosive gastritis.
  • Chronic Gastritis:
    • Dyspepsia: Vague epigastric discomfort.
    • B12 deficiency: In autoimmune gastritis, patients may present with fatigue, pallor, and neurological symptoms (e.g., peripheral neuropathy).
Peptic Ulcers
  • Duodenal Ulcers:
    • Epigastric pain: Occurs 2-3 hours after eating, relieved by food or antacids.
    • Nocturnal pain: Often wakes patients from sleep.
  • Gastric Ulcers:
    • Pain worsened by eating: Leading to weight loss.
    • Nausea, vomiting, and anorexia: Common in gastric ulcers.
Diagnosis
  • H. pylori testing:
    • Urea breath test: Non-invasive test for active infection.
    • Stool antigen test: Detects current infection.
    • Endoscopy with biopsy: Confirms H. pylori infection and rules out malignancy in chronic gastritis or ulcers.
  • Endoscopy:
    • Necessary for patients with alarm symptoms (e.g., bleeding, weight loss).
    • Allows direct visualization of ulcers or erosions and biopsy to exclude cancer.
  • Laboratory tests:
    • CBC: May show anemia from chronic bleeding or B12 deficiency in autoimmune gastritis.
Treatment
Gastritis
  • Discontinue NSAIDs and reduce alcohol consumption.
  • H. pylori eradication: Triple therapy with a proton pump inhibitor (PPI), clarithromycin, and amoxicillin (or metronidazole for penicillin allergy) for 14 days.
  • Vitamin B12 supplementation: For patients with autoimmune gastritis.
Peptic Ulcers
  • Proton pump inhibitors (PPIs): Reduce acid secretion and promote healing of gastric and duodenal ulcers.
  • H. pylori eradication: As above, for ulcers associated with infection.
  • Avoid NSAIDs: Use COX-2 inhibitors or PPIs for protection if NSAID use is necessary.
Complications
  • Gastritis:
    • Peptic ulcer disease: Progression of chronic gastritis, especially with H. pylori infection or NSAID use.
    • Gastric carcinoma: Chronic H. pylori infection increases the risk of gastric adenocarcinoma.
    • Pernicious anemia: Vitamin B12 deficiency from autoimmune gastritis.
  • Peptic Ulcers:
    • Hemorrhage: Upper GI bleeding presents with hematemesis or melena.
    • Perforation: Ulcer erodes through the gastric or duodenal wall, causing peritonitis.
    • Gastric outlet obstruction: Scarring from chronic ulcers leads to vomiting and gastric distension.
Prevention
  • H. pylori screening: In at-risk populations to prevent ulcers and gastric cancer.
  • Limit NSAID use: In patients at risk for ulcers, use PPIs or H2 blockers for gastric protection.
Key Points
  • Gastritis involves inflammation of the gastric mucosa, while peptic ulcer disease involves mucosal ulceration due to H. pylori or NSAID use.
  • H. pylori is the leading cause of both chronic gastritis and peptic ulcers.
  • Gastric ulcers cause pain worsened by eating, while duodenal ulcers are relieved by food.
  • Diagnosis relies on clinical history, H. pylori testing, and endoscopy.
  • Treatment involves acid suppression (PPIs), H. pylori eradication, and discontinuing NSAIDs when possible.
  • Complications include bleeding, perforation, and gastric outlet obstruction in peptic ulcers, and gastric cancer in chronic gastritis.

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