What is acid reflux?

GASTROESOPHAGEAL REFLUX DISEASE
GERD is one of the most prevalent gastrointestinal disorders. Population-based studies show that up to 15% of individuals have heartburn at least once a week and about 7% have heartburn daily. Symptoms are caused by back flow of gastric acid and other gastric contents into the esophagus due to incompetent barriers at the gastroesophageal junction.

Pathophysiology: The normal antireflux mechanisms consist of the LES, the crural diaphragm, and the anatomic location of the gastroesophageal junction below the diaphragmatic hiatus. Reflux occurs only when the gradient of pressure between the LES and the stomach is lost. It can be caused by a sustained or transient decrease in LES tone. A sustained hypotension of the LES may be due to muscle weakness that is often without apparent cause. Secondary causes of LES incompetence include scleroderma-like diseases, myopathy associated with chronic intestinal pseudo-obstruction, pregnancy, smoking, anticholinergic drugs, smooth-muscle relaxants [b-adrenergic agents, aminophylline, nitrates, calcium channel blockers, phosphodiesterase inhibitors that increase cyclic AMP or cyclic GMP (including sildenofil)], surgical destruction of the LES, and esophagitis.tLESRwithout associated esophageal contraction is due to a vagal reflex in which LES relaxation is elicited by gastric distention. Increased tLESR is associated with GERD. A similar reflex operates during belching. Apart from incompetent barriers, gastric contents are most likely to reflux (1) when gastric volume is increased (after meals, in pyloric obstruction, in gastric stasis, during acid hypersecretion states), (2) when gastric contents are near the gastroesophageal junction (in recumbency, bending down, hiatus hernia), and (3) when gastric pressure is increased (obesity, pregnancy, ascites, tight clothes). Incompetence of the diaphragmatic crural muscle, which surrounds the esophageal hiatus in the diaphragm and functions as an external LES, also predisposes to GERD.
The total exposure of the esophagus to refluxed acid correlates with potential for mucosal damage. Exposure depends on the amount of refluxed material per episode, frequency of episodes, and rate of clearing the esophagus by gravity and peristaltic contractions. When peristaltic contractions are impaired, esophageal clearance is impaired. Acid refluxed into the esophagus is neutralized by saliva. Thus, impaired salivary secretion also increases esophageal exposure time. If the refluxed material extends to the cervical esophagus and breaches the upper sphincter, it can enter the pharynx, larynx, and trachea, causing chronic cough, bronchoconstriction, pharyngitis, laryngitis, or bronchitis.

Reflux esophagitis is a complication of reflux and develops when mucosal defenses are unable to counteract the damage done by acid, pepsin, and bile. Mild esophagitis involves microscopic changes of mucosal infiltration with granulocytes or eosinophils, hyperplasia of basal cells, and elongation of dermal pegs. Endoscopic appearance may be normal. Erosive esophagitis involves endoscopically apparent mucosal damage, redness, friability, bleeding, superficial, linear ulcers, and exudates. Peptic stricture results from fibrosis that causes lumenal constriction. These strictures occur in ~10% of patients with untreated GERD. Short strictures caused by spontaneous reflux are usually 1 to 3 cm long and are present in the distal esophagus near the squamocolumnar junction. Long, tubular peptic strictures can result from persistent vomiting or prolonged nasogastric intubation. Erosive esophagitis may cause bleeding and heal by intestinal metaplasia (Barrett's esophagus) that is a risk factor for adenocarcinoma.

Clinical Features: Regurgitation of sour material in the mouth and heartburn are the characteristic symptoms of GERD. Heartburn is produced by the contact of refluxed material with the inflamed or sensitized esophageal mucosa. Angina-like or atypical chest pain occurs in some patients, while others experience no heartburn or chest pain. Persistent dysphagia suggests development of a peptic stricture. Most patients with peptic stricture have a history of several years of heartburn preceding dysphagia. However, in one-third of patients, dysphagia is the presenting symptom. Rapidly progressive dysphagia and weight loss may indicate the development of adenocarcinoma in Barrett's esophagus. Bleeding occurs due to mucosal erosions or Barrett's ulcer. Severe reflux may reach the pharynx and mouth and result in laryngitis, morning hoarseness, and pulmonary aspiration. Recurrent pulmonary aspiration can cause aspiration pneumonia, pulmonary fibrosis, or chronic asthma. By contrast, many patients with GERD remain asymptomatic or self-treated and do not seek attention until severe complications occur.