PHYSICAL EXAMINATION

LABORATORY STUDIES

DIAGNOSIS

Gastroesophageal reflux disease (GERD)

PATHOPHYSIOLOGY OF KEY SYMPTOMS

The major symptom of GERD is chest pain, often called heartburn. The pain is a result of inflammation of the esophagus caused by the reflux of acidic contents from the stomach. GERD does not normally occur because the lower esophageal sphincter maintains enough tone to prevent the acidic gastric contents from entering the esophagus.

The esophagus is normally isolated from the stomach by both anatomic and physiologic mechanisms. Anatomically, these are the crural diaphragm and location of the gastroesophageal junction below the diaphragmatic hiatus. Physiologically, the isolation is achieved by the contraction of the smooth muscle of the lower esophageal sphincter.

The band of smooth muscle that comprises the lower esophageal sphincter is normally contracted. During the swallowing reflex, the wave of peristalsis descending along the esophagus causes the relaxation of the lower esophageal sphincter. Relaxation is mediated by the enteric nervous system, using nitric oxide and vasoactive intestinal peptide as neurotransmitters.

Food ingestion increases acid production by the parietal cells of the gastric mucosa. There are three separate mechanisms stimulating acid secretion: the cephalic phase mediated by the central nervous system and the vagus nerve, a gastric phase caused by the presence of food within the stomach, and an intestinal phase caused by the entry of moderately acidic chyme into the duodenum (Fig. 54-1). Acid secretion is enhanced by acetylcholine, gastrin, and histamine; and acid secretion is inhibited by somatostatin. The high rate of acid secretion results in gastric contents being much more acidic than the ingested food that originally passed through the esophagus.

FIGURE 54–1 Phases of gastric secretion and their regulation.