Anticoagulants, Antithrombotics, Thrombolytic Drugs Flashcards
know steps of localized coagulation
damage; collagen or vWF; plt activation to release ADP, TXA2, 5-HT; fibrinogen to fibrin via thrombin & coagulation cascade
What keeps coagulation localized?
Prostacyclin prevents systemic coagulation.
What is the intrinsic pathway of the coagulation cascade?
factor IX activated by contact system; factor X activated by factor IX; factor II (prothrombin) activated to thrombin by factor X (involves factor V); fibrinogen converted to fibrin via enzyme thrombin (IIa)
What is the extrinsic pathway of the coagulation cascade?
factor X activated by factor VII and tissue factor; factor IX can also be activated by factor VII
How does the body get rid of a fibrin clot?
precursor plasminogen forms enzyme plasmin via streptokinase, urokinase, & tissue plasminogen activator (tPA); degrades fibrin to end the cascade
What are proteins C and S?
anticoagulation factors; inhibit intrinsic pathway and antithrombin (negative feedback)
What is the significance of anti-thrombin?
inhibits factor X and IIa from forming fibrin; activity catalyzed by heparins
What is the INR test?
international normalized ratio; allows you to compare PT values b/n hospitals; changes sensitivity and accounts for changes in tissue factor
What is the PT test?
prothrombin time; tests for extrinsic pathway; has tissue factor and factor VII; sensitive to warfarin action
What is the PTT test?
partial prothrombin time; tests for intrinsic pathway; doesn’t have tissue factor or factor VII; used to monitor heparin
What is HIT?
heparin-induced thrombocytopenia; systemic hypercoagulable state that occurs after autoimmune response to tx with UFH for min of 7 days
Why isn’t HIT a risk with low molecular weight heparin?
LMWHs bind to ATIII, not plts; they have higher affinity
Why does UFH require freq. monitoring?
not as specific, different preps
What decides which direct thrombin inhibitor is chosen for use?
condition of clearing organ
mechanism of action of warfarin
inhibits vit K metabolism which disrupts gamma-carboxylation of several glutamate residues in factors II, VII, IX, X, C & S; partially inhibits synthesis, not degradation; effect on coagulation is dependent on factor half-life
