Back
ditki Logo
medical & biological sciences

Gastritis & Peptic Ulcers for the USMLE Step 2 Exam

Start your One-Week Free Trial
Already subscribed? Log in »
Gastritis and Peptic Ulcers for USMLE Step 2
Definition
  • Gastritis: Inflammation of the gastric mucosa, either acute or chronic.
    • Acute gastritis: Sudden inflammation often due to irritants like NSAIDs, alcohol, or infections.
    • Chronic gastritis: Prolonged inflammation, typically from H. pylori infection or autoimmune conditions.
  • Peptic Ulcer Disease (PUD): Mucosal ulcers in the stomach (gastric ulcers) or duodenum (duodenal ulcers), caused by an imbalance between aggressive factors (acid, pepsin) and protective mechanisms (mucus, bicarbonate).
Etiology
Gastritis
  • Infectious causes:
    • Helicobacter pylori (H. pylori): The most common cause of chronic gastritis, leading to peptic ulcers and an increased risk of gastric cancer.
    • Viral gastritis: Occurs in immunocompromised patients (e.g., CMV).
  • Non-infectious causes:
    • NSAIDs: Inhibit prostaglandins, reducing the protective mucus layer of the stomach.
    • Alcohol: Directly damages the gastric mucosa.
    • Autoimmune gastritis: Leads to destruction of parietal cells, resulting in atrophic gastritis and vitamin B12 deficiency (pernicious anemia).
Peptic Ulcers
  • H. pylori infection: Increases acid secretion and reduces mucosal defenses.
  • NSAIDs: Cause mucosal injury by inhibiting prostaglandins, impairing mucosal protection.
  • Zollinger-Ellison syndrome: Gastrin-secreting tumor causes hypersecretion of acid, leading to refractory ulcers.
Pathophysiology
Gastritis
  • Acute gastritis: Irritants (NSAIDs, alcohol) cause direct mucosal injury, leading to inflammation and infiltration by neutrophils.
  • Chronic gastritis:
    • H. pylori-associated: Causes chronic inflammation, mucosal atrophy, intestinal metaplasia, and increased risk of gastric adenocarcinoma.
    • Autoimmune gastritis: Immune-mediated destruction of parietal cells leads to achlorhydria, hypergastrinemia, and vitamin B12 deficiency.
Peptic Ulcer Disease
  • Duodenal ulcers: H. pylori increases gastrin secretion, causing excessive acid production, which overwhelms duodenal defenses.
  • Gastric ulcers: Result from impaired mucosal defenses, typically worsened by NSAIDs and H. pylori infection.
Gastritis & Peptic Ulcer Disease Pathophysiology
Clinical Features
Gastritis
  • Acute gastritis:
    • Epigastric pain: Often associated with nausea or vomiting.
    • Hematemesis: Vomiting of blood in severe cases of mucosal erosion.
  • Chronic gastritis:
    • Dyspepsia: Vague upper abdominal discomfort.
    • B12 deficiency: In autoimmune gastritis, leads to anemia, glossitis, and neurological symptoms like peripheral neuropathy.
Peptic Ulcers
  • Duodenal ulcers:
    • Epigastric pain: Occurs 2-3 hours after eating, often relieved by food or antacids.
    • Nocturnal pain: Common due to increased acid secretion at night.
  • Gastric ulcers:
    • Pain worsened by food: Patients may avoid eating, leading to weight loss.
    • Nausea and vomiting: May accompany gastric ulcer pain.
Diagnosis
  • H. pylori testing:
    • Urea breath test: Non-invasive test for active infection.
    • Stool antigen test: Detects current H. pylori infection.
    • Endoscopy with biopsy: Gold standard for diagnosing H. pylori and assessing for malignancy.
  • Endoscopy:
    • Indicated for patients with alarm symptoms (e.g., weight loss, bleeding) or refractory symptoms.
    • Visualizes mucosal erosions, ulcers, and allows biopsy to rule out cancer.
  • Laboratory tests:
    • Complete blood count (CBC): May reveal anemia from chronic bleeding or vitamin B12 deficiency in autoimmune gastritis.
Treatment
Gastritis
  • Remove offending agents: Discontinue NSAIDs and alcohol if possible.
  • H. pylori eradication:
    • Triple therapy: PPI, clarithromycin, and amoxicillin (or metronidazole for penicillin allergy).
    • Quadruple therapy: PPI, bismuth, tetracycline, and metronidazole in resistant cases.
  • Vitamin B12 supplementation: For autoimmune gastritis with B12 deficiency.
Peptic Ulcers
  • Proton pump inhibitors (PPIs): Reduce acid secretion and promote healing of ulcers.
  • H. pylori eradication: Same regimens as above.
  • Discontinue NSAIDs: Use alternatives or add a PPI for gastric protection.
Complications
  • Gastritis:
    • Peptic ulcer disease: Common complication of chronic gastritis.
    • Gastric cancer: Increased risk with chronic H. pylori infection or autoimmune gastritis.
    • Pernicious anemia: From vitamin B12 deficiency in autoimmune gastritis.
  • Peptic Ulcers:
    • Bleeding: Presents with hematemesis or melena.
    • Perforation: Leads to acute peritonitis and requires urgent surgical intervention.
    • Gastric outlet obstruction: Chronic scarring causes vomiting and distension.
Prevention
  • H. pylori screening: In high-risk populations to prevent ulcers and cancer.
  • Limit NSAIDs: Use PPIs or H2 blockers for protection in high-risk patients.
Key Points
  • Gastritis is the inflammation of the gastric mucosa, while peptic ulcers are mucosal breaks in the stomach or duodenum.
  • H. pylori is the leading cause of chronic gastritis and peptic ulcers.
  • Gastric ulcers are worsened by eating, while duodenal ulcers are relieved by food.
  • Diagnosis relies on clinical history, H. pylori testing, and endoscopy for severe or refractory cases.
  • Treatment includes PPIs, H. pylori eradication, and cessation of NSAIDs.

Related Tutorials