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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.

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  1. Which anticoagulant mechanism does antithrombin (AT) primarily use?

    Answer: Serine protease inhibition potentiated by heparin

    Antithrombin is a serine protease inhibitor (serpin) that irreversibly inhibits thrombin (IIa), Factor Xa, IXa, XIa, and XIIa. Heparin binding induces a conformational change in AT that accelerates its inhibitory activity approximately 1000-fold.

  2. A mixing study showing 'no correction' (aPTT remains prolonged after mixing with normal plasma) is consistent with:

    Answer: Factor VIII inhibitor

    Factor deficiencies correct on mixing because normal plasma provides the missing factor. Inhibitors (antibodies against clotting factors) do not correct because the antibody neutralizes the factor provided by normal plasma.

  3. Platelet function analyzer (PFA-100) closure time is prolonged in all of the following EXCEPT:

    Answer: Hemophilia A (Factor VIII deficiency)

    PFA-100 tests primary hemostasis (platelet plug formation under shear stress). Hemophilia A is a secondary hemostasis (coagulation cascade) defect — the platelet plug forms normally, so PFA-100 closure time is normal.

  4. Rivaroxaban (Xarelto) is a direct oral anticoagulant (DOAC) that specifically targets:

    Answer: Factor Xa

    Rivaroxaban is a direct Factor Xa inhibitor. It binds the active site of Factor Xa without requiring antithrombin as a cofactor, blocking conversion of prothrombin to thrombin.

  5. A neonate presents with purpura fulminans and severely low protein C levels. This presentation is caused by:

    Answer: Homozygous or compound heterozygous protein C deficiency

    Neonatal purpura fulminans is caused by homozygous or compound heterozygous protein C deficiency (protein C activity below 1%), resulting in uncontrolled microvascular thrombosis affecting skin, brain, and eyes immediately after birth.

  6. In platelet aggregation testing, which reagent tests the thromboxane A2 pathway and is abnormal in aspirin-treated patients?

    Answer: Arachidonic acid

    Arachidonic acid (AA) is metabolized by COX-1 to TXA2, a potent platelet activator. Aspirin irreversibly acetylates COX-1, blocking TXA2 synthesis. Platelet aggregation with AA is absent or markedly reduced in aspirin-treated patients.