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Peptic ulcer disease

Peptic ulcer disease (PUD) represents a spectrum of ulcerative lesions in the stomach or duodenum. Predominant causes include Helicobacter pylori infection, chronic NSAID usage, hypersecretory states, and stress-related factors. While epigastric pain is a common symptom, PUD can be asymptomatic in many cases. Management typically involves a test-and-treat approach for H. pylori in patients under 60, or empirical acid suppression therapy. In older patients or those with high-risk features, esophagogastroduodenoscopy (EGD) with biopsies is crucial for diagnosis and to exclude serious differentials like gastric cancer. Primary treatment focuses on symptom alleviation through acid-lowering medication, eradication of H. pylori, and discontinuation of causative agents. Proton-pump inhibitors are often prescribed for 4–8 weeks post-eradication and may extend as maintenance therapy in recurrent cases. Surgical options are reserved for exceptional circumstances. Endoscopic surveillance is advisable in persistent symptomatology or if malignancy is suspected.

Last updated: December 3, 2024 251 views

  • Peptic Ulcer:
    • A lesion in the gastric or duodenal mucosa.
    • Diameter: At least 0.5 cm.
    • Depth: Penetrates through the muscularis mucosae.
  • Gastric Ulcer:
    • A type of peptic ulcer located in the stomach's mucosa.
    • Typically found along the lesser curvature.
    • Located in the transitional area between the corpus and antrum of the stomach.
  • Duodenal Ulcer:
    • A type of peptic ulcer occurring in the duodenal mucosa.
    • Commonly located on the anterior or posterior wall of the duodenal bulb.

 

Note  
Erosions are more superficial than ulcers. Ulcers involve damage to the gastric mucosa extending beyond the muscularis mucosa layer into the submucosa. ملاحظة

  • Common Causes of PUD:
    • H. pylori Infection:
      • Accounts for 40–70% of duodenal ulcers and 25–50% of gastric ulcers.
      • The prevalence of H. pylori infection and related PUD is decreasing.
    • Chronic NSAID Use:
      • Increases PUD risk fourfold.
      • Heightens risk for PUD complications (refer to “Complications of peptic ulcer disease”).
      • Acid suppression medication recommended for ulcer prevention in chronic NSAID users.
  • Associated Risk Factors:
    • H. pylori infection or NSAID use alone rarely causes ulcers; typically combined with other risk factors:
      • Shared risk factors with PUD, GERD, and gastritis (smoking, heavy alcohol use, glucocorticoids, caffeine).
      • Diet.
      • Psychological factors (anxiety, stress, PTSD).
      • Genetic predisposition.
  • Rare Causes of PUD:
    • Acid Hypersecretory States:
      • Zollinger-Ellison syndrome (gastrinoma).
      • Systemic mastocytosis.
      • Hyperparathyroidism.
    • Non-NSAID Medications:
      • Acetaminophen, bisphosphonates, sirolimus, mycophenolate, SSRIs, chemotherapeutics (e.g., 5-FU).
    • Infections:
      • CMV, HSV-1, EBV, Helicobacter heilmannii.
    • Others:
      • Radiation, illicit drug use (e.g., cocaine, methamphetamine).
      • Systemic inflammatory diseases (e.g., Crohn's disease, sarcoidosis).
      • Mechanical causes (foreign body, GI tract obstruction, postsurgical anatomy).

  • Overview of Peptic Ulcer Disease Pathophysiology:
    • Ulcers occur when protective mechanisms of the gastric mucosa are disrupted and/or excessive gastric acid or pepsin is secreted.
    • Normal physiology involves balance between gastric juice secretion and protective measures.
  • Physiological Gastric Secretions:
    • Parietal Cells: Secrete hydrochloric acid (HCl) and intrinsic factor. Stimulated by acetylcholine, histamine, gastrin; inhibited by prostaglandins, somatostatin.
    • Mucosal Cells: Secrete protective mucus, stimulated by acetylcholine, prostaglandins (also inhibit HCl secretion), secretin.
    • Chief Cells: Secrete pepsinogen, stimulated by acetylcholine, gastrin, secretin, VIP.
  • Mechanisms of Physiological Disruption:
    • H. pylori in Gastric Ulcers:
      • Secretes urease, converting urea to NH3 for survival in acidic environment.
      • Colonizes and attaches to epithelial cells, releases cytotoxins (e.g., cagA toxin), disrupting mucosal barrier.
    • H. pylori in Duodenal Ulcers:
      • Inhibits somatostatin secretion, increases gastrin and H+ secretion.
      • Spreads to duodenum, inhibits HCO3- secretion, leading to acidification.
    • NSAIDs:
      • Inhibit COX-1 and COX-2, reducing prostaglandin production, eroding gastric mucosa.
      • Decrease mucosal blood flow and inhibit mucosal cell proliferation.
    • Acid Hypersecretion (e.g., Zollinger-Ellison Syndrome):
      • Increased acid secretion and parietal cell mass, delivering excessive acid to the duodenum.

  • Asymptomatic PUD:
    • Up to 70% of peptic ulcer patients may not experience symptoms.
    • NSAID users are more likely to have asymptomatic ulcers and present with complications.
  • Symptomatic PUD:
    • Abdominal Pain:
      • The most common symptom.
      • Typically located in the epigastrium.
      • Often described as “gnawing” or “burning”.
      • Relationship to meal intake varies with ulcer location.
    • Other Associated Symptoms:
      • Belching.
      • Indigestion.
      • Gastrointestinal reflux.
      • Nausea and/or vomiting.
      • Bloating or abdominal fullness.
  • Clinical Symptoms of Gastric and Duodenal Ulcers:
    • Common to Both:
      • Dyspepsia symptoms: postprandial heaviness, early satiety, epigastric pain.
      • Pain relief with antacids.
      • Potential signs of internal bleeding (anemia, hematemesis, melena).
      • Stool sample positive for occult blood.
    • Gastric Ulcer:
      • Pain increases shortly after eating, potentially leading to weight loss.
      • Less common nocturnal pain.
    • Duodenal Ulcer:
      • Pain relieved by food intake, potentially leading to weight gain.
      • Pain increases 2–5 hours after eating.
      • More common nocturnal pain.

 

Note  
Gastric ulcer is associated with pain after light (weight loss) Gorging. Duodenal ulcer is associated with relief after massive (weight gain) Desserts. ملاحظة

  • Initial Evaluation:
    • All Patients:
      • Screen for common etiologies (e.g., NSAID use).
      • Consider CBC, BMP, fecal occult blood test for occult bleeding.
    • Patients ≤ 60 Years Without Red Flags:
      • Begin with noninvasive H. pylori testing (urea breath test, stool antigen test).
    • Patients > 60 Years or > 45 Years in High Gastric Cancer Prevalence Areas; Patients with Red Flags; Patients Unresponsive to Medical Therapy:
      • Direct referral for Esophagogastroduodenoscopy (EGD) or other diagnostics (e.g., liver chemistries, abdominal ultrasound).
  • Further Evaluation:
    • For Uncertain Etiology:
      • Consider specialized tests (e.g., secretin stimulation test for gastrinoma).
    • Alarm Features Warranting EGD in Younger Patients:
      • Include progressive dysphagia, odynophagia, rapid weight loss, persistent vomiting, suspected GI bleeding, family history of upper GI malignancy.
  • Esophagogastroduodenoscopy (EGD):
    • Most accurate test for confirming diagnosis.
    • Applications include malignancy screening, visualization, biopsy, invasive H. pylori testing, therapeutic measures.
  • Endoscopic Findings:
    • Differentiating between benign and malignant ulcers based on base, edges, surrounding mucosa, and location.
    • Histopathology: Chronic inflammatory changes (benign) vs. dysplasia, deeper layer invasion (malignant).
  • Indications for Biopsy:
    • Gastric Ulcers:
      • Recommended multiple biopsies from ulcer edge and base.
      • Biopsies from various stomach areas for H. pylori testing.
    • Duodenal Ulcers:
      • Biopsy ulcers with malignant features.
      • Usually benign, routine biopsy not required.
  • Specialized Laboratory Studies:
    • Consider if unclear etiology or recurrent ulcers.
    • Tests: Fasting serum gastrin, secretin stimulation test (for Zollinger-Ellison syndrome), serum intact PTH level, testing for systemic inflammatory diseases.

  • General Measures:
    • Nonpharmacological: Avoid NSAIDs, restrict alcohol.
    • Follow-up: Confirm treatment success, consider endoscopic surveillance.
    • H. pylori test-and-treat strategy:
      • Positive: H. pylori eradication therapy (antibiotics + PPI), continue acid suppression for 4–8 weeks.
      • Negative: Trial of acid suppression (PPIs) for 4–8 weeks, followed by reevaluation.
    • Failure of medical treatment: Consider elective surgery.
  • Medical Treatment of PUD:
    • Acid suppression therapy and H. pylori eradication if detected.
    • Complement with antacids for rapid symptom relief.
    • Cytoprotective agents for mucosal protection.
      • Sucralfate: Forms a protective barrier over mucosa, acts as acid buffer.
      • Misoprostol.
    • Antibiotics: Clarithromycin triple therapy (with amoxicillin and PPI).
  • Nonpharmacological Measures:
    • Restrict alcohol, smoking, caffeine; avoid stress.
    • Discontinue or reduce medications worsening PUD (e.g., NSAIDs, corticosteroids).
    • Avoid eating before bedtime.
  • Elective Surgical Treatment:
    • Indications: Refractory symptoms, NSAID continuation, intolerance to medical treatment.
    • Surgical Procedures:
      • Vagotomy: Division of vagal trunks, reduces acid production by ~70%. Possible complications include delayed gastric emptying, diarrhea, hypergastrinemia, dumping syndrome.
      • Combined with drainage procedures:
        • Pyloroplasty.
        • Antrectomy.
        • Subtotal or Partial gastrectomy (Billroth I or II).
        • Total gastrectomy and reconstruction (Roux-en-Y).