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Gastroesophageal reflux disease (GERD) is one of the most common disorders seen in the general population. Approximately 10% of all people experience heartburn daily, 15% in any given week, and about half the population in any given year.1 The spectrum of disease ranges from occasional postprandial substernal discomfort to the development of peptic stricture or even carcinoma in the setting of Barrett esophagus. It is important for physicians to identify and select appropriate treatments for patients at risk of developing complications. This chapter reviews the etiology, diagnosis, complications, and treatment of GERD.
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Normal Anatomy and Physiology
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The esophagus is lined with a stratified nonkeratinizing squamous epithelium consisting of three layers: superficial, intermediate, and basal. The basal cell layer comprises 15% of the total epithelial thickness and is the only layer that normally contains mitotic figures. The lamina propria, which lies deep to the squamous epithelium, contains glandular structures similar to those found in the gastric cardia. The epithelium is covered by a protective layer of mucin and surface bicarbonates that are produced by salivary glands located in the proximal esophagus and in the region adjacent to the gastroesophageal junction (GEJ). The mucus produced in these glands reaches the intervening sections of the esophagus through peristalsis. Unlike the stomach, the mucus layer that lines the esophagus is rudimentary and provides little protection against prolonged acid exposure.
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The sensations of heartburn or discomfort from reflux are transmitted from the esophagus by the spinal splanchnic afferent nerves. These sensations may be modulated by vagal afferent nerves. A series of high-pressure zones, or sphincters, and zones of complex neural interaction propel the forward movement of food and liquid into the stomach and retard the return or reflux of gastric contents back into the esophagus. The intrinsic lower esophageal sphincter (LES), along with its extrinsic components, is the mechanism chiefly responsible for preventing gastric reflux back into the esophagus (Fig. 37-1). The LES is identified on intraluminal manometry as a 2- to 4-cm-long zone of high pressure at the GEJ. A ringed circular muscle is also present at this junction. The vessel density and amount of connective tissue are greater in LES muscle than in the remainder of the esophagus. This region is also rich in mitochondria and smooth endoplasmic reticulum.
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The LES exerts a resting basal pressure in normal individuals. The tonic muscular contraction that is the hallmark of the LES contributes to the resting tone, distinguishing this region from the esophageal body. Inhibition of LES contraction is mediated largely through nitric oxide, whereas excitation is mediated through acetylcholine. Even with ablation of all neural input, the LES maintains its intrinsic basal smooth muscle tone. This muscular tone is distributed unevenly throughout the ...