• Peptic ulcer disease (PUD) is characterized by mucosal damage secondary to pepsin and gastric acid secretion
• It is the principal cause of upper gastrointestinal (UGI) hemorrhage
• Most commonly occurs in the stomach and proximal duodenum; infrequently, in the lower esophagus, distal duodenum or jejunum
• Giant ulcer with size of 3 cm is an atypical type of PUD that is now rarely encountered
• Dyspepsia is a nonspecific term indicating discomfort in the upper abdomen
• Refractory PUD is considered in patents with ulcer that failed to heal after 8-12 weeks of therapy

• Epigastric pain is the most common symptom of PUD but occurs only in minority of patients
  • Pain of duodenal ulcer usually occurs 2-3 hours after a meal, improves with food or antacid, and sometimes awakens patient at night
  • Pain of gastric ulcer is more commonly worsened by food intake and occurs shortly after meals
    
    • May be associated with weight loss due to fear of food intake

• Other symptoms include indigestion, vomiting, loss of appetite, inability to tolerate fatty foods, heartburn
  
  • Nausea and vomiting are commonly experienced by patients with prepyloric or pyloric channel ulcers

Alarm Symptoms

• Hematemesis, melena, or anemia may suggest bleeding
• Vomiting and early satiety may be due to obstruction
• Anorexia or weight loss may suggest cancer
• Upper abdominal pain radiating to the back that persists may be due to penetration
• Spreading upper abdominal pain that is severe may suggest perforation

• In 70% of cases, 25- to 64-year old patients are affected
• 48% and 50% of cases are secondary to Helicobacter pylori infection and nonsteroidal anti-inflammatory drugs (NSAIDs) respectively
  • Some evidence states that H pylori infection may be food or water borne and may spread from person to person
  • In patients with a bleeding ulcer, it is recommended to test for and treat H pylori
  • NSAIDs inhibit the formation of prostaglandins and their protective effect on the gastric mucosa (ie stimulates mucus and bicarbonate secretion, epithelial cell proliferation, and increase of mucosal blood flow)
    • Patients who are on long-term NSAIDs have an annual risk of life-threatening ulcer-related complication of 1-4%
  • H pylori plus NSAID use increases the risk and intensity of NSAID-related mucosal damage

• Other causes may include use of steroids, bisphosphonates, potassium chloride or chemotherapeutic agents, presence of acid-hypersecretory states (eg Zollinger-Ellison syndrome), cancer or stress [eg multiorgan failure, ventilator support, extensive burns (Curling’s ulcer) or head injury (Cushing’s ulcer)], lifestyle factors, genetic factors
• In patients with NSAID-related GI complications, additional contributing factors include history of complicated GI event, age, concomitant use of anticoagulants, corticosteroids, other NSAIDs including low-dose Aspirin, high-dose therapy, chronic debilitating disorders