Gastric Ulcers and GERD: The New "Plagues" of the 21st Century Update for the Clinical Nurse Specialist

Patricia O'Malley PhD, RN, CCRN, CNS

In This Article

Pathophysiology of GERD and Ulcer Disease

Acid production is a continuous and complex activity as a result of neural, tissue, and endocrine factors. Hydrogen ions secreted by parietal cells of the stomach, secretion responses to gastrin levels, and vagal outflow in response to the sight, smell, taste, and thought of food are primary factors governing the acid environment of the stomach. The stomach, normally protected by tight intracellular junctions and a mucin layer over epithelial cells, obtains further protection via the presence of prostaglandins present in the gastric mucosa that inhibit gastric secretion, stimulate bicarbonate ion secretion, and enhance blood flow.[5]

GERD is associated with failure of the lower esophageal sphincter (LES) to close properly. The result is reflux of acid into the unprotected lining of the esophagus. Signs and symptoms are the result of exposure of unprotected esophageal tissue to acid.[5] Occasional heartburn does not indicate a diagnosis of GERD and the absence of heartburn does not rule out GERD. While the primary signs and symptoms of GERD are persistent heartburn and reflux, GERD may also manifest as chest pain, trouble swallowing, a tight throat, hoarseness in the morning hours, a dry persistent cough, or bad breath.[6] Anyone can have GERD, including infants, children, and pregnant women. A long-term consequence for untreated GERD is the potential development of Barrett's metaplasia (cancer of esophageal gland cells) that increases the risk for adenocarcinoma and stricture formation. Esophageal cancer is rare in that of the estimated 10 million persons with weekly heartburn, only 3900 may develop adenocarcinoma of the esophagus, which is quite low considering the number of persons without GERD who develop esophageal cancer. Therefore, signs and symptoms of GERD are not strongly predictive of an individual developing cancer.[2]

An imbalance between mucosal defenses, low bicarbonate secretion, and elevated acid as well as pepsin levels in the stomach are primary mechanisms of peptic ulcer disease. The finding that Helicobacter pylori infection may be associated with 80% to 90% of gastric ulcers was a milestone discovery in medicine.[5] H. Pylori is not associated with the development of GERD but is linked to gastritis, gastric and duodenal ulcers, and gastric cancers.[7,8] Treatment of this infection nearly eliminates the risk of ulcer recurrence provided the patient is not taking non-steroidal inflammatory agents (NSAIDs).[5] Among NSAID users, H. pylori infection and male sex independently increased the risk for duodenal ulceration, and patients with advanced age as well as rheumatoid arthritis have a higher risk for gastric ulcers.[9] Generally, single antibiotic regimens for H. pylori fail and can lead to the development of resistant strains and clinical trials continue to discover the best drug combination as well as timeline for therapy.[5,10]

Chronic use of NSAIDs is also associated with the development of peptic ulcers. The role of NSAIDs in mediating peptic ulcer disease is complex since topical injury related to oral dosing appears to play only a minor role in the development of injury. It appears NSAIDs injury is mediated systemically since outcomes with parenteral dosing appear similar to oral dosing. NSAIDs result in prostaglandin inhibition, which results in reduced stimulation of mucosal circulation.[5,9]