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The human hepatic portal system delivers about three-fourths of the blood going to the liver.The final common pathway for transport of venous blood from spleen, pancreas, gallbladder and the abdominal portion of the gastrointestinal tract [2] (with the exception of the inferior part of the anal canal and sigmoid colon) is through the hepatic portal vein.
Portal hypertension is a condition in which the blood pressure of the portal venous system is too high. It is often the result of cirrhosis of the liver. Liver cirrhosis can lead to increased intrahepatic vascular resistance and vasodilation of portal system arteries, both of which increase pressure in the portal vein. [4]
The portal vein is not a true vein, because it conducts blood to capillary beds in the liver and not directly to the heart. It is a major component of the hepatic portal system , one of three portal venous systems in the human body; the others being the hypophyseal and renal portal systems.
Portal hypertension is defined as increased portal venous pressure, with a hepatic venous pressure gradient greater than 5 mmHg. [3] [4] Normal portal pressure is 1–4 mmHg; clinically insignificant portal hypertension is present at portal pressures 5–9 mmHg; clinically significant portal hypertension is present at portal pressures greater than 10 mmHg. [5]
Portal vein thrombosis, incidental PM finding. Portal vein thrombosis (PVT) is a vascular disease of the liver that occurs when a blood clot occurs in the hepatic portal vein, which can lead to increased pressure in the portal vein system and reduced blood supply to the liver. The mortality rate is approximately 1 in 10. [1]
Portal venous pressure is the blood pressure in the hepatic portal vein, and is normally between 5-10 mmHg. [1] Raised portal venous pressure is termed portal hypertension , [ 2 ] and has numerous sequelae such as ascites and hepatic encephalopathy .
In humans, the only significant example is the hepatic portal vein which combines from capillaries around the gastrointestinal tract where the blood absorbs the various products of digestion; rather than leading directly back to the heart, the hepatic portal vein branches into a second capillary system in the liver.
The first is the use of beta-blockers, which reduce portal pressures. Non-selective beta blockers (such as propranolol and nadolol) have been used to decrease the pressure of the portal vein in patients with esophageal varices, and have been shown to regress portal hypertensive gastropathy that has been worsened by medical treatment of varices. [5]
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