Recent data support the likelihood that GERD begins in the stomach. Fundic distention occurs because of overeating and delayed gastric emptying secondary to the high-fat Western diet. The distention causes the sphincter to be taken up by the expanding fundus, exposing the squamous epithelium with the high-pressure zone, which is the distal 3 cm of the esophagus, to gastric juice. Repeated exposure causes inflammation of the squamous epithelium, columnarization, and carditis. This is the initial step and explains why in early disease the esophagitis is mild and commonly limited to the very distal esophagus. The patient compensates by increased swallowing, allowing saliva to bathe the injured mucosa and alleviate the discomfort induced by exposure to gastric acid. Increased swallowing results in aerophagia, bloating, and repetitive belching. The distention induced by aerophagia leads to further exposure and repetitive injury to the terminal squamous epithelium and the development of cardiac-type mucosa. This is an inflammatory process, commonly referred to as carditis and explains the complaint of epigastric pain so often registered by patients with early disease. The process can lead to a fibrotic mucosal ring at the squamocolumnar junction and explains the origin of a Schatzki ring. Extension of the inflammatory process into the muscularis propria causes a progressive loss in the length and pressure of the distal esophageal high-pressure zone associated with an increased esophageal exposure to gastric juice and the symptoms of heartburn and regurgitation. The loss of the barrier occurs in a distal to proximal direction and eventually results in the permanent loss of LES resistance and the explosion of the disease into the esophagus with all the clinical manifestations of severe esophagitis. This accounts for the observation that severe esophageal mucosal injury is almost always associated with a permanently defective sphincter. At any time during this process and under specific luminal conditions or stimuli, such as exposure time to a specific pH range, intestinalization of the cardiac-type mucosa can occur and set the stage for malignant degeneration.
Thursday, February 21, 2008
Wednesday, July 18, 2007
Mechanisms of acid reflux
The central mechanism in acid reflux disease is disturbed acid clearance. Acid is produced in the stomach, and as long as its rate of clearance from the stomach into the small intestine is normal, it will not accumulate in the stomach and reflux into the esophagus. An example of a disorder that hinders clearance of acid from the stomach is obstruction of its outlet resulting in an increased pressure inside the stomach.
At certain circumstances during daily activities some acid may normally regurgitate from the stomach into the esophagus. Again acid clearance back into the stomach is accomplished by gravity and the esophageal propulsive movement towards the stomach. Accordingly any disturbance of esophageal motility would affect its acid clearance mechanism.
Role of the lower esophageal sphincter:
The sphincter is anatomically configured and functionally organized to act like a valve allowing one way movement of swallowed substances from the esophagus into the stomach. anatomical disturbances such as Hiatal Hernia and functional disorders as incompetence or transient relaxation would favor acid reflux.
These are the main primary factors involved in causation and are mostly electromechanical.
Secondary factors actually operate after reflux and are meant to prevent esophagitis. They are mainly chemical and include saliva and the bicarbonate content of the glandular secretions on the inner surface of the esophagus.
All these factors should be well investigated when acid reflux relief is considered.
Related posts:
Constituents of the reflux
Acid production in the stomach
Acid reflux disease in pregnancy
Causes of acid reflux
About heartburn
Esophageal defenses against reflux
Lifestyle changes can prevent reflux
A special advice on fatty meals for acid reflux relief
