The predominant presenting symptom of reflux is burning chest pain (heartburn) resulting from recurrent mucosal injury, frequently worse at night, when lying supine, or right after consumption of foods or drugs that diminish lower esophageal valve tone. Typical causes of reflux esophagitis are those problems that outcome in persistent or repetitive acid exposure towards the esophageal mucosa.
These consist of disorders that increase the rate of spontaneous transient reduced esophageal sphincter relaxations or impair reflexes that usually adhere to transient lower esophageal sphincter relaxations having a secondary wave of esophageal peristalsis. Problems that increase gastric volume or pressure (eg, partial or total gastric outlet obstruction and problems that improve acid production) also lead.
Occasionally, reflux esophagitis could be caused by alkaline injury (eg, pancreatic juice refluxing through both an incompetent pyloric valve along with a relaxed lower esophageal sphincter). Hiatal hernia, a disorder by which a portion from the proximal abdomen slides into the chest cavity with upward displacement from the lower esophageal valve, can lead towards the development of reflux.
Normally, the tonically contracted lower esophageal sphincter offers an effective barrier to reflux of acid from the stomach back into the esophagus. This really is reinforced by secondary esophageal peristaltic waves in response to transient reduced esophageal sphincter relaxation.
Effectiveness of that barrier could be altered by loss of lower esophageal valve tone (ie, the opposite of achalasia), increased frequency of transient relaxations, reduction of secondary peristalsis right after a transient relaxation, increased stomach volume or stress, or increased manufacturing of acid, all of which can make more likely reflux of acidic stomach contents sufficient to trigger pain or erosion.
Recurrent reflux can damage the mucosa, resulting in inflammation, hence the term “reflux esophagitis.” Recurrent reflux itself predisposes to further reflux simply because the scarring that occurs with healing from the inflamed epithelium renders the lower esophageal valve progressively less competent being a barrier.
Even though typically a consequence of acid reflux, esophagitis can also outcome from reflux of pepsin or bile. In most instances of esophageal reflux disease, a typical pathophysiologic thread could be identified. Recurrent mucosal damage results in infiltration of granulocytes and eosinophils, hyperplasia of basal cells, and at some point the improvement of friable, bleeding ulcers and exudates over the mucosal surface.
These pathologic modifications set the stage for scar formation and valve incompetence, predisposing to recurrent cycles of inflammation. Elevated frequency of transient reduced esophageal valve relaxations might be partly in response to increased gastric distension. Normally, transient lower esophageal sphincter relaxations are accompanied by elevated esophageal peristalsis.
Individuals with defects in excitatory pathways that promote peristalsis might, consequently, be at elevated risk for the development of esophageal reflux. Changes in the kinds of prostaglandins created by the esophagus are already noted in reflux esophagitis, possibly contributing to impairment of healing and predisposing to recurrences.
In contrast to other types of acid-mediated injury, H pylori infection does not appear to lead to the improvement of reflux or esophagitis. Heartburn is the usual symptom of reflux esophagitis, typically worsening on lying prone. With recurrent reflux, a array of problems may produce. Probably the most typical complication may be the development of stricture within the distal esophagus.
Progressive obstruction, initially to solid food and later to liquid, presents as dysphagia. Other problems of recurrent reflux include hemorrhage or perforation; hoarseness, coughing, or wheezing; and pneumonia consequently of aspiration of gastric contents to the lungs, particularly throughout sleep.
Epidemiologic studies recommend that cigarette smoking and alcohol abuse associated with recurrent reflux outcome in a change within the esophageal epithelium from squamous to columnar histology, termed Barrett’s esophagus. In 2-5% of cases, Barrett’s esophagus leads towards the development of adenocarcinoma.