Abstract
Portal hypertension is a common clinical syndrome associated with chronic liver diseases and is characterized by a pathological increase in portal pressure. Increase in portal pressure is because of an increase in vascular resistance and an elevated portal blood flow. The site of increased intrahepatic resistance is variable and is dependent on the disease process. The site of obstruction may be: pre-hepatic, hepatic, and/or post-hepatic. In addition, part of the increased intrahepatic resistance is because of increased vascular tone. Another important factor contributing to increased portal pressure is elevated blood flow. Peripheral vasodilatation initiates the classical profile of decreased systemic resistance, expanded plasma volume, elevated splanchnic blood flow and elevated cardiac index. The elevated portal pressure leads to formation of portosystemic collaterals and oesophageal varices. Pharmacotherapy for portal hypertension is aimed at reducing both intrahepatic vascular tone and elevated splanchnic blood flow.
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