Hypertension or high blood pressure is a highly life-threatening disease that affects thousands of Americans daily. The disease is generally detected/diagnosed during regular checkups with your primary physician. Many people are at risk simply because they live unhealthy lifestyles. Today I will talk about an uncommon type of high blood pressure that irritates the veins called "portal hypertension."
The portal vein is responsible for delivering blood to the liver from the digestive organs. When there is an increase in the pressure inside this vein, a condition called portal hypertension occurs. A severe blockage of the blood flow traveling through the liver causes such pressure. More so, the overwhelming stress in the portal vein induces large veins to develop across the esophagus and stomach. The large veins or varices are used to bypass the blockage.
Although there are limited causes for this condition, the symptoms and complications are vast. Most often, portal hypertension is caused by a disease called cirrhosis (scarring of the liver). Cirrhosis occurs as the result of other complications and injuries of the liver such as hepatitis or alcohol abuse. The cirrhosis causes scar tissue that actually blocks the flow of the blood through the liver; thereby slowing down its normal functioning. Yet, another potential cause for portal hypertension is thrombosis or clotting in the portal vein.
The chances of developing portal hypertension are extremely high, especially if you are a previous victim of cirrhosis or thrombosis. In some instances, however, additional symptoms may be detected, yet they are not a direct indication of portal hypertension.
Some symptoms and complications include gastrointestinal bleeding, an accumulation of fluid in the abdomen, confusion or forgetfulness, or reduced platelet levels. At any rate, modifying your lifestyle is necessary for managing or even alleviating these complications. The liver is a major organ of the body. Without proper functioning, it is potentially life-threatening.
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Published On: August 03, 2008