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Chapter 17 - The Gastrointestinal Tract

Chen Liu MD, PhD

James M. Crawford MD, PhD

Esophagus

Normal

The esophagus develops from the cranial portion of the foregut and is recognizable by the third week of gestation. The normal esophagus is a hollow, highly distensible muscular tube that

extends from the epiglottis in the pharynx, at about the level of the C6 vertebra, to the gastroesophageal junction at the level of the T11 or T12 vertebra. Measuring between 10 and 11 cm

in the newborn, it grows to a length of about 25 cm in the adult. For the endoscopist, the esophagus is recorded as the anatomic distance between 15 and 40 cm from the incisor teeth, with

the gastroesophageal junction located at the 40-cm point. Several points of luminal narrowing can be identified along its course—proximally at the cricoid cartilage, midway in its course

alongside the aortic arch and at the anterior crossing of the left main bronchus and left atrium, and distally where it pierces the diaphragm. Although the pressure in the esophageal lumen is

negative compared with the atmosphere, manometric recordings of intraluminal pressures have identified two higher-pressure areas that remain relatively contracted in the resting phase. A

3-cm segment in the proximal esophagus at the level of the cricopharyngeus muscle is referred to as the upper esophageal sphincter (UES). The 2- to 4-cm segment just proximal to the

anatomic gastroesophageal junction, at the level of the diaphragm, is referred to as the lower esophageal sphincter (LES). Both "sphincters" are physiologic, in that there are no anatomic

landmarks that delineate these higher-pressure regions from the intervening esophageal musculature.

The wall of the esophagus consists of a mucosa, submucosa, muscularis propria, and adventitia, reflecting the general structural organization of the gastrointestinal tract.[1] The

mucosa has a smooth, glistening, and pink-tan surface. It has three components: a nonkeratinizing stratified squamous epithelial layer, lamina propria, and muscularis mucosa. The

epithelial layer has mature squamous cells overlying basal cells. The basal cells, constituting 10% to 15 % of the mucosal thickness, are reserve cells with great proliferative potential. A

small number of specialized cell types, such as melanocytes, endocrine cells, dendritic cells, and lymphocytes, are present in the deeper portion of the epithelial layer. The lamina propria is

the nonepithelial portion of the mucosa, above the muscularis mucosae. It consists of areolar connective tissue and contains vascular structures and scattered leukocytes. Finger-like

extensions of the lamina propria, called papillae, extend into the epithelial layer. The muscularis mucosae is a delicate layer of longitudinally oriented smooth-muscle bundles.

The submucosa consists of loose connective tissue containing blood vessels, a rich network of lymphatics, a sprinkling of leukocytes with occasional lymphoid follicles, nerve fibers



(including the ganglia of the Meissner plexus), and submucosal glands. Submucosal glands connected to the lumen by squamous epithelium-lined ducts are scattered along the entire

esophagus but are more concentrated in the upper and lower portions. Their mucin-containing fluid secretions help lubricate the esophagus.

As is true throughout the alimentary tract, the muscularis propria consists of an inner circular and an outer longitudinal coat of smooth muscle with an intervening, well-developed

myenteric plexus (Auerbach plexus). The muscularis propria of the proximal 6 to 8 cm of the esophagus also contains striated muscle fibers from the cricopharyngeus muscle. Besides

creating a unique histologic interplay of smooth muscle and skeletal muscle fibers, this feature explains why skeletal muscle disorders can cause upper esophageal dysfunction.

In sharp contrast to the rest of the gastrointestinal tract, the esophagus is mostly devoid of a serosal coat. Only small segments of the intra-abdominal esophagus are covered by serosa; the

thoracic esophagus is surrounded by fascia that condenses around the esophagus to form a sheathlike structure. In the upper mediastinum, the esophagus is supported by this fascial tissue,

which forms a similar sheath around adjacent structures, the great vessels and the tracheobronchial tree. This intimate anatomic proximity to important thoracic viscera is of significance in

permitting the ready and widespread dissemination of infections and tumors of the esophagus into the posterior mediastinum. The rich network of mucosal and submucosal lymphatics that

runs longitudinally along the esophagus further facilitates spread.

The main functions of the esophagus are to conduct food and fluids from the pharynx to the stomach, to prevent passive diffusion of substances from the food into the blood, and to prevent

reflux of gastric contents into the esophagus. These functions require motor activity coordinated with swallowing, namely a wave of peristaltic contraction, relaxation of the LES in

anticipation of the peristaltic wave, and closure of the LES after the swallowing reflex. The mechanisms governing this motor function are complex, involving both extrinsic and intrinsic

innervation, humoral regulation, and properties of the muscle wall itself.

The control of the lower esophageal sphincter (LES) is critical to esophageal function.[2] Maintenance of sphincter tone is necessary to prevent reflux of gastric contents, which are under

positive pressure relative to the esophagus. During deglutition, both active inhibition of the muscularis propria muscle fibers by inhibitory nonadrenergic/noncholinergic neurons and

cessation of tonic excitation by cholinergic neurons enable the LES to relax. Many chemical agents (e.g., gastrin, acetylcholine, serotonin, prostaglandin F2a , motilin, substance P,

histamine, and pancreatic polypeptide) increase LES tone, while some agents (nitric oxide, vasoactive intestinal peptide) decrease the tone. However, their precise roles in normal

esophageal function remain unclear.

Pathology

Lesions of the esophagus run the gamut from highly lethal cancers to the merely annoying "heartburn" that has affected many a partaker of a large, spicy meal. Esophageal varices, the

result of cirrhosis and portal hypertension, are of major importance, since their rupture is frequently followed by massive hematemesis (vomiting of blood) and even death by

exsanguination. Esophagitis and hiatal hernias are far more frequent and rarely threaten life. Distressing to the physician is that all disorders of the esophagus tend to produce similar

symptoms, namely heartburn, dysphagia, pain, and/or hematemesis.

Heartburn (retrosternal burning pain) usually reflects regurgitation of gastric contents into the lower esophagus. Dysphagia (difficulty in swallowing) is encountered both with deranged

esophageal motor function and with diseases that narrow or obstruct the lumen. Pain and hematemesis are sometimes evoked by esophageal disease, particularly by those lesions associated

with inflammation or ulceration of the esophageal mucosa. The clinical diagnosis of esophageal disorders often requires specialized procedures such as esophagoscopy, radiographic

barium studies, and manometry.


Date: 2016-04-22; view: 779


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