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Gastritis & Peptic Ulcers for for the American Board of Internal Medicine (ABIM) Exam

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Gastritis and Peptic Ulcers for ABIM Exam
Definition
  • Gastritis: Inflammation of the gastric mucosa, which can be acute or chronic. It often presents with upper gastrointestinal symptoms such as pain, nausea, or vomiting and may lead to complications like ulcers.
    • Acute gastritis: Sudden inflammation due to factors such as NSAIDs, alcohol, or infections.
    • Chronic gastritis: Persistent inflammation often associated with H. pylori infection or autoimmune conditions.
  • Peptic Ulcer Disease (PUD): A break in the mucosal lining of the stomach (gastric ulcer) or duodenum (duodenal ulcer), typically caused by H. pylori infection or NSAID use.
    • Gastric ulcers are more common in older adults, while duodenal ulcers often affect younger patients.
Etiologies
Gastritis
  • Infectious Causes:
    • Helicobacter pylori: The most common cause of chronic gastritis, leading to mucosal inflammation, peptic ulcers, and an increased risk of gastric cancer.
    • Viral infections: Cytomegalovirus (CMV) can cause gastritis in immunocompromised individuals.
  • Non-infectious Causes:
    • NSAIDs: Inhibit prostaglandin synthesis, reducing the protective mucous layer of the stomach, increasing the risk of gastritis and ulcers.
    • Alcohol: Directly irritates the gastric lining, leading to acute gastritis.
    • Autoimmune gastritis: Autoimmune attack on parietal cells, leading to gastric atrophy, vitamin B12 deficiency, and pernicious anemia.
Peptic Ulcers
  • H. pylori infection: The primary cause of duodenal and gastric ulcers, leading to chronic inflammation and increased acid secretion.
  • NSAIDs: Disrupt mucosal protection, increasing susceptibility to ulcers.
  • Other factors:
    • Smoking: Increases the risk of PUD by impairing mucosal healing.
    • Zollinger-Ellison syndrome: A gastrin-secreting tumor (gastrinoma) that causes excessive gastric acid production, leading to refractory ulcers.
Pathophysiology
Gastritis
  • Acute Gastritis: Direct injury to the gastric mucosa by irritants (NSAIDs, alcohol, etc.) leads to local inflammation. Neutrophils infiltrate the mucosa, causing tissue damage and potential ulceration.
  • Chronic Gastritis:
    • H. pylori-induced: Persistent infection leads to chronic inflammation, mucosal atrophy, and increased risk of peptic ulcers and gastric cancer.
    • Autoimmune gastritis: Autoantibodies attack parietal cells, causing a loss of intrinsic factor and hydrochloric acid production, leading to pernicious anemia and risk of gastric carcinoma.
Peptic Ulcer Disease
  • Duodenal Ulcers: H. pylori increases gastrin secretion, leading to elevated acid production, which overwhelms duodenal mucosal defenses.
  • Gastric Ulcers: Result from weakened gastric mucosal defenses due to NSAIDs or H. pylori infection, leading to acid-induced mucosal damage.
  • NSAID-Induced Ulcers: NSAIDs inhibit prostaglandin synthesis, reducing the production of protective gastric mucus and bicarbonate, allowing acid to damage the mucosa.
Clinical Features
Gastritis
  • Acute Gastritis:
    • Epigastric pain: Often worsened by eating.
    • Nausea and vomiting: Common, especially after alcohol or NSAID use.
    • Hematemesis: Vomiting of blood due to mucosal erosion.
    • Melena: Black, tarry stools indicating upper GI bleeding.
  • Chronic Gastritis:
    • Dyspepsia: Chronic epigastric discomfort or indigestion.
    • Weight loss and early satiety: Seen in severe cases with gastric atrophy.
    • B12 deficiency symptoms: In autoimmune gastritis, presents with fatigue, pallor, glossitis, and peripheral neuropathy.
Peptic Ulcers
  • Duodenal Ulcers:
    • Epigastric pain: Typically occurs 2-3 hours after eating and is relieved by food or antacids.
    • Nocturnal pain: Commonly wakes patients from sleep due to acid secretion during fasting.
    • Weight gain: Some patients eat to relieve pain.
  • Gastric Ulcers:
    • Epigastric pain: Worsened by food, leading to weight loss.
    • Nausea and vomiting: May accompany pain.
    • Anorexia: Reduced appetite due to discomfort with eating.
Diagnosis
  • H. pylori Testing:
    • Urea breath test: Non-invasive test for active H. pylori infection.
    • Stool antigen test: Detects H. pylori antigen in stool.
    • Endoscopic biopsy: Histological examination and rapid urease testing for H. pylori during endoscopy.
  • Endoscopy:
    • Indicated for patients with alarm symptoms (e.g., bleeding, weight loss) or those with refractory symptoms.
    • Can directly visualize gastritis, ulcers, and perform biopsies to rule out malignancy.
  • Laboratory Tests:
    • Complete blood count (CBC): May show anemia in cases of chronic bleeding or B12 deficiency in autoimmune gastritis.
    • Serum gastrin levels: Elevated in Zollinger-Ellison syndrome.
Treatment
Gastritis
  • Remove offending agents:
    • Discontinue NSAIDs: Use alternative pain management such as acetaminophen.
    • Reduce alcohol consumption: To limit gastric irritation.
  • H. pylori Eradication:
    • Triple therapy: Proton pump inhibitor (PPI), clarithromycin, and amoxicillin or metronidazole for 14 days.
    • Quadruple therapy: PPI, bismuth, tetracycline, and metronidazole in cases of resistance or intolerance to standard therapy.
  • Autoimmune Gastritis:
    • Vitamin B12 supplementation: Lifelong treatment with intramuscular B12 for pernicious anemia.
Peptic Ulcers
  • H. pylori Eradication: Same regimens as for H. pylori-induced gastritis.
  • PPIs (Proton Pump Inhibitors):
    • First-line therapy for acid suppression in both gastric and duodenal ulcers.
    • Examples include omeprazole, esomeprazole, and pantoprazole.
  • Discontinue NSAIDs:
    • If necessary, use COX-2 inhibitors (e.g., celecoxib) or add a PPI for gastric protection.
  • Surgical Intervention:
    • Indicated for complications like perforation, refractory ulcers, or uncontrolled bleeding.
Complications
  • Gastritis:
    • Peptic ulcer formation: Chronic gastritis, particularly from H. pylori or NSAIDs, can lead to ulcer development.
    • Gastric cancer: Increased risk in patients with chronic H. pylori infection and autoimmune gastritis.
    • Pernicious anemia: Due to vitamin B12 deficiency in autoimmune gastritis.
  • Peptic Ulcers:
    • Perforation: A life-threatening complication where the ulcer creates a hole in the stomach or duodenal wall, leading to peritonitis.
    • Hemorrhage: Upper GI bleeding presents with hematemesis or melena, requiring urgent management.
    • Gastric outlet obstruction: Chronic scarring and inflammation can narrow the pylorus, causing vomiting and severe gastric distention.
Prevention
  • H. pylori screening: In high-risk populations to prevent chronic gastritis and ulcers.
  • Limiting NSAID use: Avoid long-term NSAID use in at-risk patients or co-prescribe PPIs.
  • Lifestyle modifications:
    • Limit alcohol and smoking, which can exacerbate gastritis and PUD.
    • Avoid spicy foods and other known gastric irritants.
Key Points
  • Gastritis and peptic ulcers are frequently caused by H. pylori infection and NSAID use.
  • Gastritis can be acute or chronic, with chronic forms increasing the risk of ulcers and gastric cancer.
  • Peptic ulcer disease presents with epigastric pain, and the diagnosis relies on clinical history, H. pylori testing, and endoscopy.
  • Treatment includes acid suppression (PPIs), eradication of H. pylori, and discontinuation of offending agents like NSAIDs.
  • Complications include bleeding, perforation, and gastric outlet obstruction. Chronic gastritis may lead to gastric cancer or pernicious anemia.

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