Peptic Ulcer Disease
A disruption of the gastric or duodenal mucosa primarily caused by H. pylori infection or NSAID use, presenting with dyspepsia and epigastric pain.
Emergency Management: Massive upper GI bleeding requires immediate resuscitation with large-bore IV access, crystalloids, blood transfusion for Hb < 7 g/dL, IV PPI bolus (Pantoprazole 80 mg followed by 8 mg/hr infusion), and urgent therapeutic endoscopy within 24 hours.
Peptic ulcer disease (PUD) is characterized by mucosal defects in the stomach or duodenum that extend through the muscularis mucosae. It represents a disruption of normal mucosal defense and repair mechanisms, leading to acid-peptic injury. The vast majority of cases occur in the gastric antrum or the first portion of the duodenum.
Detailed Overview
PUD is primarily driven by Helicobacter pylori infection and the use of nonsteroidal anti-inflammatory drugs (NSAIDs). The imbalance between protective factors (mucus, bicarbonate, prostaglandins) and aggressive factors (gastric acid, pepsin) leads to tissue necrosis and ulceration. If left untreated, it can lead to severe complications such as hemorrhage, perforation, or gastric outlet obstruction. Proper eradication of H. pylori and cessation of offending agents are central to achieving long-term healing and preventing recurrence.
Epidemiology & Demographics
Global prevalence is estimated at 5-10%. Incidence of duodenal ulcers is higher in younger populations (30-55 years), while gastric ulcers peak in older patients (55-70 years). Males and females are affected equally, though historical data showed a male predominance.
Etiological Mechanism
The two primary etiologic factors are H. pylori infection (responsible for ~90% of duodenal and 70-90% of gastric ulcers) and NSAID use. Zollinger-Ellison syndrome (gastrinoma) is a rare cause.
Primary Causes
H. pylori bacterial colonization, chronic NSAID/aspirin therapy, hypersecretory states (Zollinger-Ellison syndrome), viral infections (CMV, HSV in immunocompromised), and Crohn's disease involving the upper GI tract.
In H. pylori-associated PUD, the bacteria produce urease to survive the acidic environment and cytotoxins (like VacA and CagA) that damage epithelial cells. The resulting chronic active gastritis increases gastrin release (especially in antral-predominant gastritis), leading to hypersecretion of gastric acid. This excess acid overloads duodenal buffering, causing duodenal metaplasia and subsequent ulceration. In NSAID-associated PUD, systemic inhibition of cyclooxygenase-1 (COX-1) drastically reduces the synthesis of mucosal prostaglandins, which normally stimulate mucus and bicarbonate secretion and maintain mucosal blood flow.
Diagnostic Criteria & Guidelines
Diagnosis is definitively established via esophagogastroduodenoscopy (EGD) showing a mucosal break >5 mm in diameter, with biopsy confirmation for H. pylori status and ruling out malignancy in gastric ulcers.
For H. pylori-positive PUD: Bismuth quadruple therapy (Bismuth subcitrate 120-300 mg QID + Metronidazole 250-500 mg QID + Tetracycline 500 mg QID + PPI [e.g., Omeprazole 20 mg BID]) for 14 days. Alternatively, Clarithromycin triple therapy (PPI BID + Clarithromycin 500 mg BID + Amoxicillin 1 g BID) for 14 days if local macrolide resistance is <15%. For NSAID-induced (H. pylori negative): Discontinue NSAID and treat with PPI (e.g., Pantoprazole 40 mg daily) for 4-8 weeks.
Second-Line & Adjunctive Therapy
Levofloxacin-based salvage therapy: PPI BID + Amoxicillin 1 g BID + Levofloxacin 500 mg daily for 10-14 days.
Surgical & Procedural Management
Endoscopic therapy (epinephrine injection + thermal coagulation or clipping) for bleeding ulcers. Surgical interventions like Graham patch closure for perforated ulcers, or highly selective vagotomy for refractory cases.
Patient Counseling & Advice
Inform patients that completing the full 14-day course of H. pylori eradication therapy is critical to prevent resistance and recurrence. Warn about harmless dark stools associated with bismuth therapy.
Follow-Up & Monitoring Schedule
Perform urea breath test or stool antigen test at least 4 weeks after completion of antibiotic therapy and 2 weeks after holding PPI to confirm H. pylori eradication. Repeat EGD in 8-12 weeks for gastric ulcers to document healing and exclude malignancy.
Preventive Strategies
Test and treat H. pylori before starting long-term NSAID therapy. Use a PPI prophylactically in patients at high risk (e.g., history of ulcer, age >65, concurrent corticosteroid or anticoagulant use) who must remain on NSAIDs.
Excellent with successful H. pylori eradication, with recurrence rates dropping from >60% to <5-10%. Mortality in uncomplicated PUD is negligible, but perforated ulcers carry a 5-10% mortality rate.