Gastroesophageal Reflux Disease (GERD)

Wednesday, March 19th 2014. | Disease

Gastroesophageal Reflux Disease (GERD)

Gastroesophageal reflux refers to the retrograde movement of gastric contents from the stomach into the esophagus. Gastroesophageal reflux disease (GERD) refers to any symptomatic clinical condition or histologic alteration that results from episodes of gastroesophageal reflux. When the esophagus is repeatedly exposed to refluxed material for prolonged periods, inflammation of the esophagus (reflux esophagitis) can occur and in some cases it progresses to erosion of the esophagus (erosive esophagitis).
Pathophysiology of Gastroesophageal Reflux :
  • In many patients with GERD, the problem is not excessive acid production but that the acid produced spends too much time in contact with the esophageal mucosa.
  • Gastroesophageal reflux is often caused by defective lower esophageal sphincter (LES) pressure or function. Patients may have decreased LES pressures related to spontaneous transient LES relaxations, transient increases in intra-abdominal pressure, or an atonic LES. 
  • Problems with other normal mucosal defense mechanisms may also contribute to the development of GERD, including prolonged acid clearance time from the esophagus, delayed gastric emptying, and reduced mucosal resis- tance.
  • Aggressive factors that may promote esophageal damage upon reflux into the esophagus include gastric acid, pepsin, bile acids, and pancreatic enzymes. The composition and volume of the refluxate and the duration of exposure are the most important aggressive factors in determining the consequences of gastroesophageal reflux.
Diagnosis of Gastroesophageal reflux :
  • The most useful tool in the diagnosis of gastroesophageal reflux is the clinical history, including both presenting symptoms and associated risk factors.
  • Endoscopy is the preferred technique for assessing the mucosa for esophagitis and complications such as Barrett’s esophagus. It allows visualization and biopsy of the esophageal mucosa, but the mucosa may appear relatively normal in mild cases of GERD.
  • Barium radiography is less expensive than endoscopy but lacks the sensitivity and specificity needed to accurately determine the presence of mucosal injury or to distinguish Barrett’s esophagus from esophagitis.
  • Twenty-four-hour ambulatory pH monitoring is useful in patients who continue to have symptoms without evidence of esophageal damage, patients who are refractory to standard treatment, and patients who present with atypical symptoms (e.g., chest pain or pulmonary symptoms). The test helps to correlate symptoms with abnormal esophageal acid exposure, documents the percentage of time the intraesophageal pH is low, and determines the frequency and severity of reflux.
Treatment of Gastroesophageal reflux  :
  • Therapeutic modalities are targeted at reversing the pathophysiologic abnormalities. These include decreasing the acidity of the refluxate, decreasing the gastric volume available to be refluxed, improving gastric emptying, increasing LES pressure, enhancing esophageal acid clearance, and protecting the esophageal mucosa 
Treatment is categorized into the following modalities:
  1. Phase I: lifestyle changes and patient-directed therapy with antacids and/or over-the-counter (OTC) H2-receptor antagonists (H2RA) or proton pump inhibitors (PPIs).
  2. Phase II: pharmacologic interventions primarily with standard or high-dose acid-suppressing agents.
  3. Phase III: interventional therapies (antireflux surgery or endoluminal therapies).
  • Lifestyle modifications should be started initially and continued throughout the treatment course 
  • Combination therapy with an acid-suppressing agent and a prokinetic agent or mucosal protectant seems logical, but data supporting such therapy are limited. This approach should be reserved for patients who have esophagitis plus concurrent motor dysfunction or for those who have failed high-dose PPI therapy.
  • Because combination therapy offers only modest improvement over standard doses of H2RAs alone, patients not responding to standard H2RA doses should have the dose increased or be switched to a PPI instead of adding a prokinetic agent.

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