Gastrointestinal varices pathophysiology: Difference between revisions
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* The major vessels draining blood from the esophagus include, the left gastric (coronary) and less frequently short gastric veins | * The major vessels draining blood from the esophagus include, the left gastric (coronary) and less frequently short gastric veins | ||
'''Porto-caval collaterals in esophagus''' | '''Porto-caval collaterals in esophagus''' | ||
* Portal hypertension develops due to the formation of porto-collateral circulation | |||
* Opening, 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''' | '''Role of hepatic vasodilators''' | ||
Revision as of 19:09, 20 November 2017
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Gastrointestinal varices Microchapters |
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Differentiating Gastrointestinal varices from other Diseases |
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Diagnosis |
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Gastrointestinal varices pathophysiology On the Web |
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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
- Opening, 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
(b) Glucagon
(c) Prostacyclin
Role of hepatic vasoconstrictors
(a) Endothelin
(b) Angiotensin II
(c) Norepinephrine
Role of endothelial dysfunction