Question: All of the following decompensating events in the natural history of cirrhosis are closely associated with increased sinusoidal pressure and portal hypertension except:
A. variceal bleeding
Answer: Recall Ohm’s law: Pressure = Flow x Resistance. In cirrhosis, resistance inside the liver is high due to the combination of fibrosis and vasoconstriction. Flow is also high due to splanchnic vasodilation and increased inflow. Naturally, then, portal pressures are very high.
As a result, we make note of clinical decompensating events. Of the answer choices above, the first three are all directly attributable to increased sinusoidal (and therefore, portal) pressures. Because of high intrahepatic resistance, collateral vessels form and allow portal blood to bypass the liver. This results in hepatic encephalopathy as well as variceal bleeding. Ascites occurs because of the high hydrostatic forces within the liver sinusoid.
Jaundice, while occurring in the presence of portal hypertension, is not directly due to the sinusoidal pressures. Late in the course of cirrhosis, the hepatocyte itself becomes dysfunctional. Although it can conjugate bilirubin, it is not able to efficiently export it across its membrane into the bile ducts. Congestion and hyperbilirubinemia ensues.