Gastroesophageal reflux disease pathophysiology

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Gastroesophageal reflux disease Microchapters


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]


Pathophysiology of GERD depends on several mechanisms that lead to the retrograde movement of the acidic content of the stomach to the esophagus. These mechanisms include transient lower esophageal sphincter relaxation, hypotensive lower esophageal sphincter, hiatal hernia, and prolonged esophageal acid clearance.


Normal physiology of the food motility through the esophagus

Source by:BruceBlaus - Own work, CC BY-SA 4.0,


Transient lower esophageal sphincter relaxations

  • Transient lower esophageal sphincter relaxations is considered the main mechanism of GERD development in most of the patients. It occurs alongside a normal LES and more common with obesity. [4]
  • Distension of the stomach worsens the case of transient lower esophageal sphincter relaxation. The diaphragm is also affected by the sphincter relaxation leading to diaphragm inhibition. [5]

Hiatal hernia

Impaired mucosal resistance

  • The esophagus has pre-epithelial and epithelial defensive mechanisms against the acidic components that can lead to esophageal injury. However, these defensive mechanisms are limited and weak to stand against injury in case of excessive acid exposure.
  • In case of an excessive increase of the noxious agents more than the ability of the mucosal defensive mechanism to eliminate them, mucosal injury occurs and GERD develops.
  • The gastric acid leads to erosion of the esophageal mucosa and destruction of the intercellular junctions which leads to increase cellular permeability. The increase in the cellular permeability is proved by the dilation of the intercellular spaces and explains the typical symptoms (e.g, heartburn) of GERD.

Associated Conditions

The most important conditions and diseases associated with GERD include the following: [7][8]

Gross pathology

Findings in gross pathology of GERD include the following:

Microscopic pathology

Biopsies can be performed during gastroscopy and these may show:

Source: Nephron - Own work, CC BY-SA 3.0,


  1. Stein HJ, DeMeester TR (1992). "Outpatient physiologic testing and surgical management of foregut motility disorders". Curr Probl Surg. 29 (7): 413–555. PMID 1606845.
  2. Storr M, Meining A, Allescher HD (2000). "Pathophysiology and pharmacological treatment of gastroesophageal reflux disease". Dig Dis. 18 (2): 93–102. doi:10.1159/000016970. PMID 11060472.
  3. De Giorgi F, Palmiero M, Esposito I, Mosca F, Cuomo R (2006). "Pathophysiology of gastro-oesophageal reflux disease". Acta Otorhinolaryngol Ital. 26 (5): 241–6. PMC 2639970. PMID 17345925.
  4. Fisher BL, Pennathur A, Mutnick JL, Little AG (1999). "Obesity correlates with gastroesophageal reflux". Dig Dis Sci. 44 (11): 2290–4. PMID 10573376.
  5. Kahrilas PJ, Shi G, Manka M, Joehl RJ (2000). "Increased frequency of transient lower esophageal sphincter relaxation induced by gastric distention in reflux patients with hiatal hernia". Gastroenterology. 118 (4): 688–95. PMID 10734020.
  6. Richter J (1999). "Do we know the cause of reflux disease?". Eur J Gastroenterol Hepatol. 11 Suppl 1: S3–9. PMID 10443906.
  7. Morse CA, Quan SF, Mays MZ, Green C, Stephen G, Fass R (2004). "Is there a relationship between obstructive sleep apnea and gastroesophageal reflux disease?". Clin. Gastroenterol. Hepatol. 2 (9): 761–8. PMID 15354276.
  8. Kasasbeh A, Kasasbeh E, Krishnaswamy G (2007). "Potential mechanisms connecting asthma, esophageal reflux, and obesity/sleep apnea complex--a hypothetical review". Sleep Med Rev. 11 (1): 47–58. doi:10.1016/j.smrv.2006.05.001. PMID 17198758.

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