Peptic Ulcer Disease

Introduction

Peptic ulcer disease (PUD) refers to a group of ulcerative disorders of the upper gastrointestinal (GI) tract that require acid and pepsin for their formation. Pathogenesis of duodenal and gastric ulcers involves pathophysiologic abnormalities and environmental and genetic factors.

• Most peptic ulcers occur in presence of acid and pepsin when Helicobacter pylori (HP), nonsteroidal anti-inflammatory drugs (NSAIDs), or other factors disrupt normal mucosal defense and healing mechanisms. Increased gastric acid secretion may occur with duodenal ulcers, but patients with gastric ulcers usually have normal or reduced rates of acid secretion.
• Normal mucosal defense and repair mechanisms include mucus and bicarbonate secretion, intrinsic epithelial cell defense, and mucosal blood flow. Maintenance of mucosal integrity and repair is mediated by endogenous prostaglandin production.

CLINICAL PRESENTATION

Abdominal pain is the most frequent PUD symptom. Pain is often epigastric and described as burning but can present as vague discomfort, abdominal fullness, or cramping. Nocturnal pain may awaken patients from sleep, especially between 12 am and 3 am.

• Pain from duodenal ulcers often occurs 1 to 3 hours after meals and is usually relieved by food, whereas food may precipitate or accentuate ulcer pain in gastric ulcers. Antacids provide rapid pain relief in most ulcer patients.
• Heartburn, belching, and bloating often accompany pain. Nausea, vomiting, and anorexia are more common in gastric than duodenal ulcers.
• Severity of symptoms varies among patients and may be seasonal, occurring more frequently in spring or fall.
• Presence or absence of epigastric pain does not define an ulcer. Ulcer healing does not necessarily render the patient asymptomatic. Conversely, absence of pain does not preclude an ulcer diagnosis, especially in the elderly who may present with a “silent” ulcer complication.
• Ulcer complications include upper GI bleeding, perforation into the peritoneal cavity, penetration into an adjacent structure (eg, pancreas, biliary tract, or liver), and gastric outlet obstruction. Bleeding may be occult or present as melena or hematemesis. Perforation is associated with sudden, sharp, severe pain, beginning first in the epigastrium but quickly spreading over the entire abdomen. Symptoms of gastric outlet obstruction typically occur over several months and include early satiety, bloating, anorexia, nausea, vomiting, and weight loss.

DIAGNOSIS

Physical examination may reveal epigastric tenderness between the umbilicus and the xiphoid process that less commonly radiates to the back.

• Routine laboratory tests are not helpful in establishing a diagnosis of PUD. Hematocrit, hemoglobin, and stool guaiac tests are used to detect bleeding.
• Diagnosis of HP infection can be made using endoscopic or nonendoscopic (urea breath test [UBT], serologic antibody detection, and stool antigen) tests. Testing for HP is recommended only if eradication therapy is planned. If endoscopy is not planned, serologic antibody testing is reasonable to determine HP status. The UBT is the preferred nonendoscopic method to verify HP eradication but must be delayed at least 4 weeks after completion of treatment to avoid confusing bacterial suppression with eradication.
• Diagnosis of PUD depends on visualizing the ulcer crater either by upper GI radiography or endoscopy. Endoscopy has largely replaced radiography because it provides a more accurate diagnosis and permits direct visualization of the ulcer.

TREATMENT

• Goals of Treatment: Relieve ulcer pain, heal the ulcer, prevent ulcer recurrence, and reduce ulcer-related complications. In HP-positive patients with an active ulcer, previously documented ulcer, or history of an ulcer-related complication, goals are to eradicate the organism, heal the ulcer, and cure the disease with a cost-effective drug regimen.

NONPHARMACOLOGIC TREATMENT

• Patients with PUD should eliminate or reduce psychological stress, cigarette smoking, and use of NSAIDs (including aspirin). If possible, alternative agents such as acetaminophen or a nonacetylated salicylate (eg, salsalate) should be used for pain relief.
• Although there is no need for a special diet, patients should avoid foods and beverages that cause dyspepsia or exacerbate ulcer symptoms (eg, spicy foods, caffeine, and alcohol).
• Elective surgery is rarely performed because of highly effective medical management. Emergency surgery may be required for bleeding, perforation, or obstruction.

Drug Regimens to Eradicate Helicobacter pylori

Proton pump inhibitor–based triple therapy, PPI once or twice daily Clarithromycin 500 mg twice daily Amoxicillin 1 g twice daily or metronidazole 500 mg twice daily.

Cap Esomeprazole (Esso) 40mg PO OD

Tab Clarithromycin (Claritek) 500mg BD PO

Amoxiccillin (Amoxil) 1 g BD PO

Metronidazole (Flagyl) 500mg BD PO