GERD is defined as chronic symptoms of heartburn, acid regurgitation, or both, or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus.1 Reflux esophagitis occurs in a subgroup of GERD patients with histopathologically demonstrated characteristic changes in the esophageal mucosa. Nonerosive reflux disease, also known as endoscopy-negative reflux disease, occurs in patients who have typical GERD symptoms caused by intraesophageal acid but who do not have visible mucosal injury at endoscopy.
Functional heartburn is defined as episodic retrosternal burning without evidence of increased esophageal acid exposure or other structural esophageal abnormalities.
Peptic ulcers (gastric and duodenal) are defects in the GI mucosa, the lining of the Gastrointestinal tract that extend through the muscularis mucosa.
Peptic ulcer disease is the end result of an imbalance between aggressive and defensive factors in the gastroduodenal mucosa. H. pylori infection, NSAIDs, and acid secretory abnormalities are the major factors that disrupt this equilibrium. Although acid peptic injury is necessary for ulcers to form, acid secretion is normal in almost all patients with gastric ulcers and increased in only one third of patients with duodenal ulcers. A defect in bicarbonate production and, in turn, acid neutralization in the duodenal bulb is also seen in patients with duodenal ulcer disease.
This abnormality resolves with eradication of H. pylori infection when it is present. However, a small percentage of ulcers is not related to H. pylori infection or NSAID use. These are classified as idiopathic and may be related to defective mucosal defense mechanisms, tobacco use, genetics, rapid gastric emptying, or psychological stress.