Gastrointestinal varices pathophysiology
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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.[1][2]
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.[3]
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[4][5][6]
- 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
- Prostacyclin is an endogenous vasodilator
- Prostacyclin levels are inversely related to the size of varices
- Decreased prostacyclin levels are found in cirrhotic patients
Role of hepatic vasoconstrictors
(a) Endothelin
(b) Angiotensin II
(c) Norepinephrine
Role of endothelial dysfunction
Associated Conditions
Genetics
Gross Pathology
Microscopic Pathology
- ↑ "Anatomy - The Gastrointestinal Circulation - NCBI Bookshelf".
- ↑ Mahl TC, Groszmann RJ (1990). "Pathophysiology of portal hypertension and variceal bleeding". Surg. Clin. North Am. 70 (2): 251–66. PMID 2181704.
- ↑ Maruyama H, Yokosuka O (2012). "Pathophysiology of portal hypertension and esophageal varices". Int J Hepatol. 2012: 895787. doi:10.1155/2012/895787. PMC 3362051. PMID 22666604.
- ↑ Moreno AH, Burchell AR, Rousselot LM, Panke WF, Slafsky F, Burke JH (1967). "Portal blood flow in cirrhosis of the liver". J. Clin. Invest. 46 (3): 436–45. doi:10.1172/JCI105545. PMC 297064. PMID 6023778.
- ↑ Ponziani FR, Zocco MA, Campanale C, Rinninella E, Tortora A, Di Maurizio L, Bombardieri G, De Cristofaro R, De Gaetano AM, Landolfi R, Gasbarrini A (2010). "Portal vein thrombosis: insight into physiopathology, diagnosis, and treatment". World J. Gastroenterol. 16 (2): 143–55. PMC 2806552. PMID 20066733.
- ↑ Tanaka M, Wanless IR (1998). "Pathology of the liver in Budd-Chiari syndrome: portal vein thrombosis and the histogenesis of veno-centric cirrhosis, veno-portal cirrhosis, and large regenerative nodules". Hepatology. 27 (2): 488–96. doi:10.1002/hep.510270224. PMID 9462648.