Portal vein carries blood with nutrients from the intestines to the liver, for further processing. In normal state the pressure in the portal vein is around 9 mm of mercury, about twice the pressure in other veins in the body. This pressure gradient is required to push the blood across the liver tissues, into the heart. However when the liver shrinks from disease, the resistance to blood flow increases several fold. This state is called portal hypertension. This results in accumulation of fluid in the abdomen (ascites) and diversion of blood flow through some narrow bypass vessels, which results in varices. Variceal veins are thin walled and found lining the upper stomach and lower food pipe. When the pressure increases beyond a threshold, the wall can break, resulting in severe bleeding. Hence, ascites, GI bleed, hypersplenism and portal hypertensive gastropathy are the result of portal hypertension. Since resitance to blood flow can only be altered by a liver transplant, certain mechanical and medical strategies are used to avert the problems. Drugs like beta blockers (propronolol) used to reduce PHT. The dosage starts at 20 mg thrice a day and titrated to reduce the heart rate to less than 60. Glue injection and elastic banding (EVL) of variceal veins is another approach to prevent bleeding. In severe bleed, an oesophageal balloon is used to stop bleeding followed by glue injection, band ligation or TIPS procedure. Increased portal pressure also causes enlargement of the spleen, as they are connected to the same venous drainage. The enlarged spleen hyperfunctions, causing a fall in all the cell types in the blood like white and red cells as well as platelets. This state is called hypersplenism. Extreme hyper-splenism is treated by partial embolization of spleen or create a shunt (TIPS) to reduce portal pressure. Removal of spleen in a patient with cirrhosis is not advisable and can be dangerous.