The portal venous system is very important in that it collects blood from the spleen, the stomach, pancreas, and the small and large intestine. All the veins from the portal venous system will come together to form the portal vein which then carries substrate-rich venous blood to the liver. The blood in the liver will then be drained by the hepatic veins. Portal hypertension is associated with chronic liver diseases and is a result of an increase in blood pressure in the portal vein. There is a pressure gradient between the portal vein and the hepatic vein which is called the hepatic venous pressure gradient (HVPG). A HVPG of more than 5mm Hg defines portal hypertension, an increase in portal pressure can be due to many things such as an increase
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There are two theories that have been given to explain the development of this disease. The first one is the backward flow theory, which states that the increased resistance in portal venous flow within the intrahepatic circulation is what causes the development of portal hypertension. Then there is the forward flow theory which states that portal hypertension develops because of an abundance of vasoactive amines, nitrous oxide which is a vasodilator, and an abundance of vascular endothelial growth factor in both the systemic and collateral circulation. These abundances will lead to increased blood flow in the systemic circulation and eventually to increased portal blood flow. Collateral circulation begins as a consequence of portal hypertension, when the portal pressure goes above 8mm Hg collaterals will begin to form between the veins that contribute to the portal vein and the systemic veins. The portosystemic collaterals provide a way to decompress the hypertensive portal system, but because the vascular resistance in the normal liver is still smaller than the resistance in the collateral circulation, the portosystemic collaterals do not achieve complete decompression of the portal …show more content…
Collaterals developing is the main pathophysiological event that leads to both variceal bleeding and encephalopathy. Almost 95% of the variceal bleeding is from gastro-esophageal varices with the mortality rate being between 10%-20%. The bleeding can be irregular with chances of re-bleeding in the first six weeks. Hepatic encephalopathy is due to the portosystemic collaterals enlarging and also some other liver disease. It happens in more than 50% of the patients who have cirrhosis. Encephalopathy is a neuropsychiatric syndrome and its symptoms can range from small changes such as attention deficits and irritability to more severe forms such as altered consciousness, stupor, and even going into a coma. The most common complication is ascites. Vasodilation in the systemic circulation can lead to under filling of the arteries which will then activate the renin angiotensin pathway, this pathway will in turn stimulate the sympathetic nervous system. All of this will lead to the retention of sodium and water, and together with low levels of albumin levels and increased portal hydrostatic pressure will lead to ascites. The symptoms of ascites include edema of the lower limbs, increased abdominal girth, and impairments in
There are two theories that have been given to explain the development of this disease. The first one is the backward flow theory, which states that the increased resistance in portal venous flow within the intrahepatic circulation is what causes the development of portal hypertension. Then there is the forward flow theory which states that portal hypertension develops because of an abundance of vasoactive amines, nitrous oxide which is a vasodilator, and an abundance of vascular endothelial growth factor in both the systemic and collateral circulation. These abundances will lead to increased blood flow in the systemic circulation and eventually to increased portal blood flow. Collateral circulation begins as a consequence of portal hypertension, when the portal pressure goes above 8mm Hg collaterals will begin to form between the veins that contribute to the portal vein and the systemic veins. The portosystemic collaterals provide a way to decompress the hypertensive portal system, but because the vascular resistance in the normal liver is still smaller than the resistance in the collateral circulation, the portosystemic collaterals do not achieve complete decompression of the portal …show more content…
Collaterals developing is the main pathophysiological event that leads to both variceal bleeding and encephalopathy. Almost 95% of the variceal bleeding is from gastro-esophageal varices with the mortality rate being between 10%-20%. The bleeding can be irregular with chances of re-bleeding in the first six weeks. Hepatic encephalopathy is due to the portosystemic collaterals enlarging and also some other liver disease. It happens in more than 50% of the patients who have cirrhosis. Encephalopathy is a neuropsychiatric syndrome and its symptoms can range from small changes such as attention deficits and irritability to more severe forms such as altered consciousness, stupor, and even going into a coma. The most common complication is ascites. Vasodilation in the systemic circulation can lead to under filling of the arteries which will then activate the renin angiotensin pathway, this pathway will in turn stimulate the sympathetic nervous system. All of this will lead to the retention of sodium and water, and together with low levels of albumin levels and increased portal hydrostatic pressure will lead to ascites. The symptoms of ascites include edema of the lower limbs, increased abdominal girth, and impairments in