The pathogenesis of
gastro-oesophageal reflux disease (
GERD) is multifactorial, involving transient lower oesophageal sphincter relaxations (TLESRs) as well as other lower oesophageal sphincter (LES) pressure abnormalities.
GERD is associated with a decrease in LES pressure, which can be provoked by factors such as foods (fat, chocolate, etc.), alcohol, smoking and medications. These factors have also been shown to increase TLESRs. As a result, reflux of
acid, bile,
pepsin and pancreatic
enzymes occurs, leading to oesophageal mucosal injury, which can potentially progress to oesophageal
adenocarcinoma in a minority of patients with Barrett's
metaplasia. In addition, duodenogastric contents can also contribute to oesophageal injury. Other factors contributing to the pathophysiology of
GERD include
hiatal hernia, poor oesophageal clearance, delayed gastric emptying and impaired mucosal defensive factors.
Hiatal hernia has a permissive role in the pathogenesis of reflux oesophagitis by promoting LES dysfunction. Delayed gastric emptying, resulting in gastric distension, can significantly increase the rate of TLESRs, contributing to postprandial GER. The mucosal defensive factors have an important role in
GERD. When excessive
acid causes a breakdown in oesophageal epithelial defenses, epithelial resistance may be reduced. Nocturnal
GERD is associated with prolonged
acid exposure and proximal extent of
acid contact, which elevates the risk for oesophageal damage and
GERD-related complications. In sum,
GERD is a complex problem caused by many factors that are exacerbated when the patient is in the supine position.