What is acid reflux relief?
In medically oriented terms, antonyms of the word relief include pain, distress or damage. That links its meaning to both subjective and objective aspects. Subjective, denoting sensations experienced by the sufferer such as pain and objective, meaning physical findings detected by specialists which are either functional distress or organic damage. Actually relief is related to control measures and it quantitatively signifies removal of an unpleasant existence or reduction of its magnitude. The definition of relief, therefore encompasses alleviation of pain, relaxation of distress and healing of damage. Acid reflux on the other hand has two sides; the subjective side (symptoms) which reflects the symptom of heartburn and the objective side (signs) that reflects the functional and/or organic signs of esophageal changes. Acid reflux relief is therefore a broad term that covers all the measures used to control symptoms and signs of acid reflux disease. Normally, the lower esophageal sphincter remains closed except during swallowing. This prevents the passage of food and acid from the stomach into the esophagus. If the lower esophageal sphincter becomes weakened or relaxed, stomach acid may back up into the esophagus. Frequent acid reflux can irritate and inflame the lining of the esophagus, causing symptoms and signs of acid reflux. A better understanding of relief would thus entail knowledge of some aspects of normal structure and function, so that changes in the disease and its control could be easily considered. Actually acid reflux relief involves both preventive and curative measures, and in addition to treatment; orientation with the causes, symptoms and complications of acid reflux are essential for proper management. Acid reflux relief includes: dietary changes,lifestyle modifications, specific medications and surgical operations.Basic knowledge of the underlying causes and progression of acid reflux and answering frequently asked questions about its relief; add to the depth of understanding.
Barrett's esophagus is the metaplastic complication of Acid Reflux Disease.
It is the condition whereby the tubular esophagus is lined with columnar epithelium rather than squamous epithelium was first described by Norman Barrett in 1950. He incorrectly believed it to be congenital in origin. It is now realized that it is an acquired abnormality, occurring in 7% to 10% of patients with GERD, and represents the end stage of the natural history of this disease. It is also understood to be distinctly different from the congenital condition in which islands of mature gastric columnar epithelium are found in the upper half of the esophagus.
The definition of Barrett's esophagus has evolved considerably over the past decade. Traditionally, Barrett's esophagus was identified by the presence of any columnar mucosa extending at least 3 cm into the esophagus. Recent data indicating that specialized intestinal-type epithelium is the only tissue predisposed to malignant degeneration, coupled with the finding of a similar risk of malignancy in segments of intestinal metaplasia less than 3 cm long, have resulted in the diagnosis of Barrett's esophagus, given any length of endoscopically visible tissue that is intestinal metaplasia on histology. Whether to call long segments of columnar mucosa without intestinal metaplasia Barrett's esophagus is unclear. The hallmark of intestinal metaplasia is the presence of goblet cells. Recent studies have identified a high prevalence of biopsy-proved intestinal metaplasia at the cardia, in the absence of endoscopic evidence of a columnar-lined esophagus. The significance and natural history of this finding remains unknown. The term Barrett's esophagus should currently be used in the setting of an endoscopically visible segment of intestinal metaplasia of any length or columnar replacement of the esophagus of 3 cm or more.
Factors predisposing to the development of Barrett's esophagus include early-onset GERD, abnormal LES and esophageal body physiology, and mixed reflux of gastric and duodenal contents into the esophagus. Direct measurement of esophageal bilirubin exposure as a marker for duodenal juice has shown that 58% of the patients with GERD have increased esophageal exposure to duodenal juice and that this exposure is most dramatically related to Barrett's esophagus.
Pathophysiology of Barrett's Metaplasia
Recent studies suggest that the metaplastic process at the GE junction may begin by conversion of distal esophageal squamous mucosa to cardiac-type epithelium, heretofore presumed to be a normal finding. This is likely due to exposure of the distal esophagus to excess acid and gastric contents via prolapse of esophageal squamous mucosa into the gastric environment. This results in inflammatory changes at the GE junction or a metaplastic process, both of which may result in the loss of muscle function and a mechanically defective sphincter allowing free reflux with progressively higher degrees of mucosal injury. Intestinal metaplasia within the sphincter may result, as in Barrett's metaplasia of the esophageal body. This mechanism is supported by the finding that as the severity of GERD progresses, the length of columnar lining above the anatomic GE junction is increased.
What is Barrett's esophagus?
