Coagulation Flashcards
6 cards from real ASCP practice questions. Tap to flip, then mark Knew It or Still Learning — missed cards come back until you master them.
Read the first 6 Coagulation flashcards as text
Which factor is the first to decrease to critically low levels during warfarin therapy due to its shortest half-life?
Answer: Factor VII
Factor VII has the shortest half-life (approximately 4–6 hours) among vitamin K-dependent factors II, VII, IX, and X. It decreases first during warfarin initiation, explaining the early PT prolongation before full anticoagulation is achieved.
The Bethesda assay is used to quantify:
Answer: Factor VIII inhibitor titer
The Bethesda assay measures Factor VIII inhibitor (neutralizing antibody) titer in Bethesda units (BU). One BU is the amount of inhibitor that neutralizes 50% of Factor VIII activity in a normal plasma mixture.
Lupus anticoagulant (LA) causes what pattern on mixing studies?
Answer: Prolongs the aPTT that does NOT correct on mixing study
Lupus anticoagulant prolongs phospholipid-dependent clotting tests (aPTT, dRVVT) in vitro, but does NOT correct when mixed with normal plasma because the antibody is still present in the diluted mixture — an inhibitor pattern.
Protein C deficiency leads to thrombosis because protein C normally:
Answer: Inactivates Factors Va and VIIIa
Activated protein C (APC), with its cofactor protein S, proteolytically inactivates Factors Va and VIIIa, downregulating thrombin generation. Protein C deficiency removes this brake, causing hypercoagulability.
A prolonged thrombin time (TT) with a normal reptilase time most likely indicates:
Answer: Heparin contamination
Thrombin is inhibited by heparin via antithrombin, prolonging TT. Reptilase (ancrod) is not inhibited by heparin or antithrombin, so reptilase time is normal with heparin. Both TT and reptilase time are prolonged in fibrinogen deficiency and dysfibrinogenemia.
A patient with hemophilia B (Christmas disease) has a deficiency of which factor?
Answer: Factor IX
Hemophilia B (Christmas disease) is caused by deficiency of Factor IX. It is X-linked recessive, clinically identical to hemophilia A, and is treated with Factor IX concentrates or recombinant Factor IX.