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 coagulation factor is also known as the Leiden variant when mutated, leading to activated protein C resistance?
Answer: Factor V
Factor V Leiden is a mutated form of Factor V where arginine 506 is replaced by glutamine, making it resistant to cleavage and inactivation by activated protein C. This is the most common inherited thrombophilia.
The PT (prothrombin time) primarily evaluates which coagulation pathway?
Answer: Extrinsic pathway
PT evaluates the extrinsic and common pathways, testing factors VII, X, V, II, and fibrinogen. It is initiated by tissue factor (thromboplastin) added in the reagent.
Which laboratory test is most specific for monitoring unfractionated heparin therapy?
Answer: aPTT
The aPTT (activated partial thromboplastin time) is the standard monitoring test for unfractionated heparin (UFH). Therapeutic range is typically 1.5–2.5 times baseline (60–100 seconds).
D-dimer is a fibrin degradation product that indicates:
Answer: Clot formation AND fibrinolysis
D-dimer is formed when plasmin degrades cross-linked fibrin. Its elevation indicates both thrombus formation (cross-linked fibrin was made) and fibrinolysis (that fibrin is being broken down).
In disseminated intravascular coagulation (DIC), which set of laboratory findings is most characteristic?
Answer: High PT, low platelets, low fibrinogen, high D-dimer
DIC is characterized by simultaneous clotting and fibrinolysis: PT and aPTT are prolonged (factor consumption), platelets are low (consumed), fibrinogen is low (consumed), and D-dimer is elevated (fibrinolysis).
Which von Willebrand disease (vWD) subtype is characterized by the absence of high-molecular-weight multimers and is inherited in an autosomal dominant pattern?
Answer: Type 2A vWD
Type 2A vWD shows absence of high- and intermediate-molecular-weight multimers, resulting in decreased platelet adhesion. It is autosomal dominant and represents a qualitative defect in vWF.