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Risk Factors
Commonly Prescribed Drugs
Treatment and Management
Doctors to Consult

Group of ulcerative disorders of the upper gastrointestinal tract that require acid and pepsin for their formation. Most peptic ulcers occur in the presence of acid and pepsin when Helicobacter pylori, NSAIDs, or other factors disrupt normal mucosal defense and healing mechanisms.


  • Gastric ulcer- forms in the lining of the stomach. Pain may precipitate or accentuated by food.
  • Duodenal ulcer- forms in the upper small intestine. Pain often occurs 1 to 3 hours after meals and is usually relieved by food


  • Helicobacter pylori (H. pylori) associated ulcers
  • Nonsteroidal anti-inflammatory drug (NSAID)induced ulcers
  • Stress ulcers
  • Abdominal pain which is often epigastric and described as burning but can present as vague discomfort, abdominal fullness, or cramping
  • Heartburn, belching, and bloating
  • Nausea, vomiting, and anorexia
  • Complications of ulcers caused by H. pylori and NSAID:
    1. Upper GI bleeding. Bleeding may be occult or present as melena or hematemesis.
    2. Perforation of peritoneal cavity associated with sudden, sharp, severe pain, beginning first in the epigastrium but quickly spreading over the entire abdomen.
    3. Penetration into an adjacent structure (e.g., pancreas, biliary tract, or liver)
    4. Gastric outlet obstruction. Symptoms typically occur over several months and include early satiety, bloating, anorexia, nausea, vomiting, and weight loss.
Risk Factors
  • Cigarette smoking
  • Stressful-life events
  • Coffee, tea, cola beverages, beer, milk, and spices
  • Alcohol ingestion
  • Drug-induced. NSAIDs, and concurrent use with corticosteroids
Commonly Prescribed Drugs
  • Proton-pump inhibitors (PPIs) 

Suppresses gastric acid secretion by inhibiting the gastric H,K-ATPase or the proton pump. Proton pump inhibitors are used to promote healing of gastric and duodenal ulcers and to treat GERD, including erosive esophagitis, which is either complicated or unresponsive to treatment with H2 receptor antagonist. They are also the mainstay in the treatment of pathological hypersecretory conditions, such as the Zollinger-Ellison syndrome. Drugs: Omeprazole, lansoprazole, pantoprazole, esomeprazole, rabeprazole, dexlansoprazole

  • Histamine-2 receptor antagonists

Act selectively on H2 receptors in the stomach, blood vessels, and other sites, but they have no effect on H1 receptors. They are competitive antagonists of histamine and are fully reversible. However, recurrence is common after treatment with H2 antagonists is stopped. Patients with NSAID-induced ulcers are advised to be treated with PPIs, because these agents heal and prevent future ulcers better than H2 antagonists. Drugs: Cimetidine, famotidine, nizatidine, ranitidine

  • Clarithromycin

Bacteriostatic agent that inhibits protein synthesis by binding reversibly to 50s ribosomal subunits of sensitive organisms including H. pylori.

  • Amoxicillin 

Has bactericidal property which action is to interfere with the last step of bacterial cell wall synthesis, resulting in exposure of the osmotically less stable membrane which leads to cell lysis. Penicillins are only effective against rapidly growing organisms that synthesize a peptidoglycan cell wall such as H. pylori. 

  • Metronidazole 

Has antibacterial activity against all anaerobic cocci and both anaerobic gram-negative bacilli and anaerobic spore-forming gram-positive bacilli. It is clinically effective in trichomoniasis, amebiasis, and giardiasis, and in a variety of infections caused by obligate anaerobic bacteria, and microaerophilic bacteria such as Helicobacter and Campylobacter spp.

  • Tetracycline

Inhibit bacterial protein synthesis by binding to the 30S bacterial ribosome and preventing access of aminoacyl-tRNA to the acceptor (A) site on the mRNA-ribosome complex. They enter gram-negative bacteria, such as H. pylori, by passive diffusion through channels formed by porins in the outer cell membrane and by active transport that pumps tetracyclines across the cytoplasmic membrane.

  • Mucosal Protective Agents

Suppresses action of H. pylori by promoting ulcer healing due to inhibition of pepsin activity, increase in mucosal prostaglandin production and mucus and bicarbonate secretion. It is largely unabsorbed and is excreted in feces. In the colon it reacts with hydrogen sulfide and forms bismuth sulfide, which blackens the stools.

a. Bismuth subsalicylate

b. Sucralfate

  • Other drugs: Antacids

Nonabsorbable medication that binds to gastric mucosa and ulcerated tissue. These properties favor healing and provide cytoprotective effects. When exposed to gastric acid the sulfate ions bind to proteins in the damaged gastric tissue of ulcer craters and stimulate angiogenesis, delivery of growth factors and formation of granulation tissue.

Treatment and Management
  • Eliminate or reduce psychological stress.

  • Refrain from cigarette smoking, and use of nonselective NSAIDs. If applicable, alternative agents such as COX-2 selective inhibitor should be used for pain relief.

  • Avoid foods and beverages that cause dyspepsia or exacerbate ulcer symptoms.
Home Remedies
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