In extensive hepatic disease, what change leads to longer PT and PTT?

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Multiple Choice

In extensive hepatic disease, what change leads to longer PT and PTT?

In extensive hepatic disease, the liver’s ability to synthesize coagulation factors is impaired. The liver makes most of the coagulation factors, including II, V, VII, IX, and X; when their production falls, the levels of these factors drop in plasma. This weakens both the extrinsic pathway (which PT mainly reflects) and the intrinsic/common pathway (which PTT reflects), causing longer times to form a clot. Factor VII is particularly short-lived, so PT often lengthens early, while PTT becomes prolonged as other intrinsic pathway factors decrease. Platelet numbers or bilirubin levels aren’t the primary drivers of these test prolongations in this context—the key change is decreased production of clotting factors by the damaged liver.

In extensive hepatic disease, the liver’s ability to synthesize coagulation factors is impaired. The liver makes most of the coagulation factors, including II, V, VII, IX, and X; when their production falls, the levels of these factors drop in plasma. This weakens both the extrinsic pathway (which PT mainly reflects) and the intrinsic/common pathway (which PTT reflects), causing longer times to form a clot. Factor VII is particularly short-lived, so PT often lengthens early, while PTT becomes prolonged as other intrinsic pathway factors decrease. Platelet numbers or bilirubin levels aren’t the primary drivers of these test prolongations in this context—the key change is decreased production of clotting factors by the damaged liver.

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