Locations of anatomic narrowing of the esophagus seen on an esophagram include all of the following EXCEPT:
Three normal areas of esophageal narrowing are evident on the barium esophagogram or during esophagoscopy. The uppermost narrowing is located at the entrance into the esophagus and is caused by the cricopharyngeal muscle. Its luminal diameter is 1.5 cm, and it is the narrowest point of the esophagus. The middle narrowing is due to an indentation of the anterior and left lateral esophageal wall caused by the crossing of the left main stem bronchus and aortic arch. The luminal diameter at this point is 1.6 cm. The lowermost narrowing is at the hiatus of the diaphragm and is caused by the gastroesophageal sphincter mechanism. The luminal diameter at this point varies somewhat, depending on the distention of the esophagus by the passage of food, but has been measured at 1.6 to 1.9 cm. These normal constrictions tend to hold up swallowed foreign objects, and the overlying mucosa is subject to injury by swallowed corrosive liquids because of their slow passage through these areas.
The cervical esophagus receives its blood supply primarily from the:
The cervical portion of the esophagus receives its main blood supply from the inferior thyroid artery. The thoracic portion receives its blood supply from the bronchial arteries, with 75% of individuals having one right-sided and two left-sided branches. Two esophageal branches arise directly from the aorta. The abdominal portion of the esophagus receives its blood supply from the ascending branch of the left gastric artery and from inferior phrenic arteries. On entering the wall of the esophagus, the arteries assume a T-shaped division to form a longitudinal plexus, giving rise to an intramural vascular network in the muscular and submucosal layers. As a consequence, the esophagus can be mobilized from the stomach to the level of the aortic arch without fear of devascularization and ischemic necrosis. Caution should be exercised as to the extent of esophageal mobilization in patients who have had a previous thyroidectomy with ligation of the inferior thyroid arteries proximal to the origin of the esophageal branches.
All of the following cranial nerves are involved in the swallowing mechanism EXCEPT:
Swallowing can be started at will, or it can be reflexively elicited by the stimulation of areas in the mouth and pharynx, among them the anterior and posterior tonsillar pillars or the posterior lateral walls of the hypopharynx. The afferent sensory nerves of the pharynx are the glossopharyngeal nerves and the superior laryngeal branches of the vagus nerves. Once aroused by stimuli entering via these nerves, the swallowing center in the medulla coordinates the complete act of swallowing by discharging impulses through cranial nerves V, VII, X, XI, and XII, as well as the motor neurons of Cl to C3. Discharges through these nerves occur in a rather specific pattern and last for approximately 0.5 second. Little is known about the organization of the swallowing center, except that it can trigger swallowing after a variety of different inputs, but the response is always a rigidly ordered pattern of outflow. Following a cerebrovascular accident, this coordinated outflow may be altered, causing mild to severe abnormalities of swallowing. In more severe injury, swallowing can be grossly disrupted, leading to repetitive aspiration.
All of these are parts of the human antireflux mechanism EXCEPT:
If the pharyngeal swallow does not initiate a peristaltic contraction, then the coincident relaxation of the lower esophageal sphincter (LES) is unguarded and reflux of gastric juice can occur. This may be an explanation for the observation of spontaneous lower esophageal relaxation, thought by some to be a causative factor in gastroesophageal reflux disease (GERD). The power of the worm-drive pump of the esophageal body is insufficient to force open a valve that does not relax. In dogs, a bilateral cervical parasympathetic blockade abolishes the relaxation of the LES that occurs with pharyngeal swallowing or distention of the esophagus. Consequently, vagal function appears to be important in coordinating the relaxation of the LES with esophageal contraction. The antireflux mechanism in human beings is composed of three components: a mechanically effective LES, efficient esophageal clearance, and an adequately functioning gastric reservoir. A defect of any one of these three components can lead to increased esophageal exposure to gastric juice and the development of mucosal injury.
Physiologic reflux happens most commonly when a person is:
On 24-hour esophageal pH monitoring, healthy individuals have occasional episodes of gastroesophageal reflux. This physiologic reflux is more common when awake and in the upright position than during sleep in the supine position. When reflux of gastric juice occurs, normal subjects rapidly clear the acid gastric juice from the esophagus regardless of their position.
There are several explanations for the observation that physiologic reflux in normal subjects is more common when they are awake and in the upright position than during sleep in the supine position. First, reflux episodes occur in healthy volunteers primarily during transient losses of the gastroesophageal barrier, which may be due to a relaxation of the LES or intragastric pressure overcoming sphincter pressure. Gastric juice can also reflux when a swallow-induced relaxation of the LES is not protected by an oncoming peristaltic wave. The average frequency of these "unguarded moments" or of transient losses of the gastroesophageal barrier is far less while asleep and in the supine position than while awake and in the upright position. Consequently, there are fewer opportunities for reflux to occur in the supine position. Second, in the upright position, there is a 12-mm Hg pressure gradient between the resting, positive intra-abdominal pressure measured in the stomach and the most negative intrathoracic pressure measured in the esophagus at midthoracic level. This gradient favors the flow of gastric juice up into the thoracic esophagus when upright. The gradient diminishes in the supine position. Third, the LES pressure in normal subjects is significantly higher in the supine position than in the upright position. This is due to the apposition of the hydrostatic pressure of the abdomen to the abdominal portion of the sphincter when supine. In the upright position, the abdominal pressure surrounding the sphincter is negative compared with atmospheric pressure, and, as expected, the abdominal pressure gradually increases the more caudally it is measured. This pressure gradient tends to move the gastric contents toward the cardia and encourages the occurrence of reflux into the esophagus when the individual is upright. In contrast, in the supine position, the gastroesophageal pressure gradient diminishes, and the abdominal hydrostatic pressure under the diaphragm increases, causing an increase in sphincter pressure and a more competent cardia.
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