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
Porto-caval collaterals in esophagus
- Portal hypertension develops due to the formation of porto-collateral circulation
- Dilatation and hypertrophy of preexisting vascular channels lead to the formation of these collateral channels
- Collaterals develop according to the increased portal pressure, and minimum threshold level of hepatic-venous portal geadient may be 10 mmHg for the development of portosystemic collaterals and esophageal varices
Role of hepatic vasodilators
(a) Nitric Oxide (NO)
- Nitric oxide (NO) acts as an intra-hepatic vasodilator
- The levels of NO are decreased in patients suffering from chronic liver disease
- This leads to an imbalance between the endogenous vasodilators and vasoconstrictors inside the hepatic vascular tree
- Reduced levels of hepatic NO production may contribute to the increased intrahepatic vascular resistance in cirrhosis, thereby worsening portal hypertension
- NO-dependent apoptosis maintains the hepatic sinusoidal homeostasis
- NO also leads to apoptosis of hepatic stellate cell through a signaling mechanism that involves mitochondria, and a decreased level of NO may lead to a disturbance of the intra-hepatic homeostasis
(b) Glucagon
- Glucagon is a hormonal vasodilator which is associated with increased blood flow in the splanchnic bed and portal hypertension
- Plasma glucagon levels are increased in cirrhotic patients due to decreased hepatic clearance of glucagon as well as an increased secretion of glucagon by pancreatic alpha cells
- Hyperglucagonemia may play a part in splanchnic vasodilatation of chronic portal hypertension
(c) Prostacyclin
Role of hepatic vasoconstrictors
(a) Endothelin
(b) Angiotensin II
(c) Norepinephrine
Role of endothelial dysfunction