Gastrointestinal varices pathophysiology
|
Gastrointestinal varices Microchapters |
|
Differentiating Gastrointestinal varices from other Diseases |
|---|
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Gastrointestinal varices pathophysiology On the Web |
|
American Roentgen Ray Society Images of Gastrointestinal varices pathophysiology |
|
Risk calculators and risk factors for Gastrointestinal varices pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Pathophysiology
Varices arise from hemodynamic disturbance between the systemic and portal venous system. The majority of venous drainage of the gastrointestinal system occurs via the portal venous system. Whenever there is an interruption of drainage through the portal system (for example due to cirrhosis), the vessels contributing to the porto-caval shunts become more prominent due to increased pressure gradient. The interruption in blood flow leads to the creation collateral vessels that involve veins of the esophagus, stomach, pelvis (hemorrhoids), retroperitoneum, liver, abdominal wall, and other areas.
Esophageal varices
Esophageal varices are a major complication of portal hypertension (increased blood pressure in the portal venous system). In order to understand the mechanism leading to the development of esophageal varices, it is important to understand the normal vascular architecture and venous drainage of the esophagus.
Vascular architecture and venous drainage of esophagus
- Vascular resistance increases against portal blood flow in cirrhosis, noncirrhotic portal fibrosis, idiopathic portal hypertension, extrahepatic portal vein obstruction, Budd-Chiari syndrome, and other portal hypertensive disorders, inducing congestion of blood in the splenic and mesenteric veins that lie upstream of the portal trunk
- The major vessels draining blood from the esophagus include, the left gastric (coronary) and less frequently short gastric veins