Pharmacology of Anticoag Part 1 Flashcards
Causes of DVT
THROMBOSIS Trauma Hormones (OCPs) Road Traffic Accidents Operations Malignancy Blood disorder (polycythemia) Orthopedic surgery, old age Serious illness Immobilization Splenectomy
Heparin
Endogenous, normally released by mast cells
Fast acting
Safer pharmacokinetic profiles, lower risk of thrombocytopenia
Potentiates antithrombin III (inactivates thrombin and factors 10, 9, 11, and 12)
Warfarin
Vitamin K antagonist
Safe and cheap
Frequent monitoring, variability, slow acting
Prevents coagulation by inhibiting vitamin K reductase (accumulate inactive vitamin K)
What does vitamin K do?
Involved in the maturation of many proenzymes (especially prothrombin)
Less active intrinsic and extrinsic pathway without it
Dabigatran
Thrombin inhibitor
No monitoring
Fast acting
Rivaroxaban
Factor 10a inhibitor
No monitoring
PCI/PTCA
Percutaneous coronary intervention/percutaneous transluminal coronary angioplasty
Going in and opening the vessel
Minimally invasive but causes restenosis
It is manageable with antiplatelet agents
Diabetics have a much higher rate of chronic complications
Thrombocytopenia
Low platelets
P2Y12 ADP receptor inhibitors
Blocks platelet activation Reduction in thrombosis Reduction in restenosis Used in PCI, high risk MI, PAD Ex: clopidogrel, ticagrelor
DAPT
Dual antiplatelet therapy
P2Y12 ADP receptor inhibitors + aspirin
Aspirin
Inhibits COX and PLT thromboxane A2 production
Vorapaxar
Thrombin receptor antagonist
Stops the activation of PAR-1 so that you inhibit platelet aggregation/activation
For MI and PAD
Patients with high ischemic risk with low bleeding risk
Thrombolytic/fibrinolytic therapy
MI, strokes, VTE
Recombinant TPA
A few hours after initial event
Part of mechanical thrombolysis (controversial)
TPA activates plasminogen into plasmin and degrades fibrin/fibrinogen
