Despite its decrease in incidence in recent decades, the peptic ulcer disease remains as the most common cause of acute upper GI bleed.

Helicobacter pylori infections remain as the most common cause of peptic ulcer disease despite its declining prevalence in the Western world due to improved hygiene.

Helicobacter pylori serology testing has been replaced by breath testing and fecal antigen testing.

Fecal antigen testing 7 or more days after the completion of eradication therapy has identified patients with persistent infection in about 95% of cases.

Helicobacter pylori test and treat strategies are still appropriate in younger dyspeptic patients without alarm symptoms.

Infection with H. pylori is an important risk factor for the development of distal gastric cancer and also is associated with gastric MALT lymphoma, which is a low-grade, B-cell subtype of non-Hodgkin lymphoma of the stomach.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are the second most common cause of ulcer disease.

NSAIDs, via alteration of prostaglandin synthesis pathway, diminish the potency of the protective mechanism of the gastric lining, resulting in increased susceptibility of gastric lining to acid-induced injury.

The development of PUD from NSAIDs is dose and duration dependent. The frequent use of NSAIDs is associated with reported 1% to 4% risk of developing PUD per annum.

Zollinger-Ellison (ZE) syndrome, which results in multiple gastric and duodenal ulcers from acid hypersecretion state, accounts for 0.1% of PUD patients.

ZE syndrome should be suspected in patients with recurrent peptic ulcer disease in the absence of H. pylori infection or NSAID consumption and up to 50% of patients may have diarrhea.

Dyspepsia (epigastric discomfort) is the most common symptom reported by patients with PUD. However, less than 20% of patients with chronic dyspepsia are found to have evidence of active or previous PUD.

Patients with PUD from NSAIDs use are often asymptomatic

It is recommended that patients with a prior history of PUD or its complications should be tested for H. pylori and treated, if necessary, before long-term NSAID therapy is commenced.

Empiric trial of antacid medication such as H2 receptor antagonist or Proton pump inhibitors (PPIs) in patients with suspected uncomplicated PUD is justified and should be implemented prior to invasive testing in the absence of worrisome clinical features/signs in younger patients.

Upper endoscopy (EGD) is indicated in patients with worrisome signs/symptoms such as melena, hematemesis, weight loss, older population with chronic dyspepsia, or those who fail to achieve clinical response with PPI trial.

Peptic ulcer disease accounts up to 40% of the etiology for the acute overt upper GI bleed.

Because most rebleeding from PUD occurs within 3 days of initial presentation, patients with active bleeding or stigmata of hemorrhage, such as pigmented spots in an ulcer crater or clot, can typically be discharged within 3 days if they are stable. In patients with clean-based ulcers, discharge within 24 hours of presentation is reasonable.

Proton pump inhibitors (PPIs) are the most effective agents for healing ulcers by reducing acid secretion in three discrete pathways.

The standard of care for patients with bleeding peptic ulcers now consists of high-dose PPI therapy (the equivalent of omeprazole 40 mg two times a day) as soon as oral medications are permitted or with parenteral PPI therapy for 3 days, followed by conventional-dose PPI therapy for ulcer healing.

Malignancy accounts for approximately 50% of cases of gastric outlet obstruction and should be excluded with adequate biopsy and cytology samples.