Anticoagulants:

Warfarin : Oral vitamin K antagonists

ー Monitoring parameters: PT/INR
ー Half-life : 36–48 hours
ー Reversal agents:
o Vitamin- K(delayed reversal)
o 4-factor prothrombin complex concentrate(PCC; rapid reversal)
o Fresh frozen plasma(FFP; rapid reversal)
Heparins:
ー Heparin (Unfractionated heparin)
o Monitoring parameters: aPTT
o Half-life : 60–90 min
o Reversal agents: Protamine sulfate
ー Low molecular weight heparin:
o Drugs:
 Enoxaparin
 Dalteparin
 Tinzaparin
o Monitoring parameters: Anti-factor-Xa activity level
o Half-life : 3–6 hours
o Reversal agents: Protamine sulfate
ー Synthetic pentasaccharide factor Xa inhibitors; Fondaparinux
o Monitoring parameters: Anti-factor Xa activity level
o Half-life : 17–21 hours
o Reversal agents:
 Activated prothrombin complex concentrate (aPCC)
 Recombinant activated factor VII
Direct oral anticoagulants:
ー Direct thrombin(Factor-IIa) inhibitors
o Drugs:
 Bivalirudin,
 Argatroban,
 Dabigatran ; Reversal of dabigatran: Idarucizumab
ー Direct Xa inhibitors
o Drugs:
 ApiXaban
 EdoXaban
 RivaroXaban
o Reversal agents:
 Andexanet alfa (inactive, recombinant factor Xa)
 Activated prothrombin complex concentrate (aPCC)
Thrombolytics catalyze the formation of endogenous plasmin from plasminogen precursor; plasmin is a
serine protease that degrades clots (thrombi), ↑PT, ↑PTT, no change in platelet count
ー Drugs :
o tPA (alteplase); tPA is clot-specific acts only on fibrin-bound plasminogen
o Reteplase
o Tenecteplase
o Streptokinase
o Urokinase
ー Reversal agents:
o Antifibrinolytics;
 Aminocaproic acid,
 Tranexamic acid

Antiplatelet agent:
ー Aspirin/ Acetylsalicylic acid(Irreversible cyclooxygenase inhibitors)
o MOA:
 Irreversible COX-1 inhibition → inhibition of thromboxane (TXA2) synthesis in platelets
→ inhibition of platelet aggregation (antithrombotic effect)
 Onset of antiplatelet action: within minutes
 Duration of antiplatelet action: 7–10 days
 Irreversible COX-1 and COX-2 inhibition → inhibition of prostacyclin and prostaglandin
synthesis → antipyretic, anti-inflammatory, and analgesic effect
o Effects;
 Low dose (below 300 mg/day): inhibition of platelet aggregation
 Intermediate dose (300-2400 mg/day): antipyretic and analgesic effect
 High dose (2400-4000 mg/day): anti-inflammatory effect
ー P2Y12 receptor antagonists (ADP receptor inhibitors)
o Clopidogrel
o Prasugrel
o Ticagrelor
o Cangrelor
o Ticlopidine
ー Glycoprotein-IIb/IIIa inhibitors
o Abciximab
o Eptifibatide
 o Tirofiban
ー Phosphodiesterase(PDE-3) inhibitors
o Includes:
 Cilostazol,
 Dipyridamole(Also acts as a PDE5 inhibitor)
o MOA: PDE3 inhibition → ↑cAMP
 In platelets:
 ↑ cAMP → inhibited platelet aggregation
 ↓ Adenosine reuptake → ↑Extracellular adenosine concentration →
Vasodilation (Dipyridamole)
o Clinical use:
 Vasodilation and antiplatelet action in Intermittent vascular claudication;
Especially Cilostazol
 Antiplatelet/ Inhibition of platelet aggregation for;
 Antianginal/ angina prophylaxis,
 TIA/stroke prevention, and
 Coronary stent restenosis prophylaxis
 Dipyridamole dilates the coronary arteries and can therefore be used in cardiac stress
testing