Portal hypertension associated with cirrhosis of the liver results from:
|A||Thrombosis of the main portal vein|
|B||Large effluent from enlarged spleen|
|C||Intrahepatic shunts between hepatic artery and portal vein branches|
|D||None of the above|
a. In patients with cirrhosis who are being followed chronically, the development of portal hypertension is usually revealed by the presence of thrombocytopenia; the appearance of an enlarged spleen; or the development of ascites, encephalopathy and/or esophageal varices with or without bleeding.
b. Abdominal imaging, either by CT or MRI, can be helpful in demonstrating a nodular liver and in finding changes of portal hypertension with intraabdominal collateral circulation.
c. Interventional radiologic procedures can be performed to determine wedged and free hepatic vein pressures that will allow for the calculation of a wedged-to-free gradient, which is equivalent to the portal pressure.
d. The average normal wedged-to-free gradient is 5 mmHg, and patients with a gradient >12 mmHg are at risk for variceal hemorrhage.
e. As a result, profibrogenic cytokines are produced that initiate and perpetuate stellate cell activation, with the resultant production of excess collagen and extracellular matrix.
f. Connective tissue appears in both periportal and pericentral zones and eventually connects portal triads with central veins forming regenerative nodules.
g. Hepatocyte loss occurs, and with increased collagen production and deposition, together with continuing hepatocyte destruction, the liver contracts and shrinks in size.