Anti-Thrombotic Medication Names

Aspirin (acetyl salicylic acid) mode of action.

Antiplatelet agent that irreversibly inhibits COX-1, reducing thromboxane A2 (TxA2), preventing platelet aggregation; also has anti-pyretic and anti-inflammatory effects.

Dipyridamole mode of action.

Antiplatelet agent that reversibly inhibits adenosine and phosphodiesterase-3, increasing cAMP and cGMP, which reduces intra-celullar calcium and therefore platelet aggregation.

Clopidogrel mode of action.

Antiplatelet agent that irreversibly inhibits P2Y12 receptor, inhibiting ADP-induced platelet activation, which subsequently affects the GP IIb/IIIa complex expression and prevents platelet aggregation.

Prasugrel mode of action.

Antiplatelet agent that irreversibly inhibits P2Y12 receptor, inhibiting ADP-induced platelet activation, which subsequently affects the GP IIb/IIIa complex expression and prevents platelet aggregation.

Ticagrelor mode of action.

Antiplatelet agent that irreversibly inhibits P2Y12 receptor, inhibiting ADP-induced platelet activation, which subsequently affects the GP IIb/IIIa complex expression and prevents platelet aggregation.

Name the 3 antiplatelet medications that work by antagonising the P2Y12 receptor on platelets.

Clopidogrel, Prasugrel, Ticagrelor

Eptifibatide mode of action.

An antiplatelet agent that functions as a Glycoprotein IIb/IIIa inhibitor, that blocks fibrinogen binding to platelets, thus inhibiting platelet aggregation. It is used in acute cases such as acute coronary syndromes and during percutaneous coronary interventions.

Tirofiban mode of action.

An antiplatelet agent that acts as a Glycoprotein IIb/IIIa inhibitor, blocking fibrinogen binding to platelets, thereby preventing platelet aggregation.

List the 2 GP IIb/IIIa inhibitors.

Eptifibatide, Tirofiban.

Name major types of antiplatelet medications.

1. COX-1 inhibitors (aspirin),

2. Adenosine and phosphodiesterase-3 inhibitors (dipyridamole),

3. P2Y12 inhibitors (clopidogrel, prasugrel, ticagrelor),

4. Glycoprotein IIb/IIIa inhibitors (epitifidamide, tirofiban).

Name the 3 major classes of heparin.

1. Unfractionated heparin,

2. Low molecular weight heparin,

3. Fondaparinux.

   These major classes of heparin differ in their molecular weight and mechanisms of action.

What is the mode of action of heparin.

Heparin works by activating antithrombin III, which inhibits thrombin (factor II) and factor Xa, preventing the formation of fibrin clots. It enhances the efficiency of antithrombin, leading to a faster anticoagulation effect.

Which class of heparin works more on factor IIa (thrombin).

Unfractionated heparin, as it has a greater ability to inhibit thrombin compared to low molecular weight heparin and fondaparinux.

Which class of heparin works more on factor Xa.

Low molecular weight heparin and synthetic heparin, as it primarily inhibits factor Xa more than thrombin.

Name some brands of low molecular weight heparin.

Enoxaparin, Dalteparin, Tinzaparin, Nadroparin, Danaparoid, Clexane, Fragmin.

Name the agent that can reverse the effects of low molecular weight heparins.

Protamine sulfate.

Name the brand of synthetic heparin.

Fondaparinux.

Name the reversal agent for unfractionated heparin.

The reversal agent for unfractionated heparin is protamine sulfate, which neutralizes its anticoagulant effects.

Name all the major types of anticoagulant agents.

1. Vitamin K antagonists (warfarin),

2. Direct thrombin inhibitors (dabigatran),

3. Direct factor Xa inhibitors (apixaban, rivaroxaban),

4. Heparins (LMWH, synthetic heparin, unfractionated heparin).

Warfarin mode of action.

An anticoagulant agent that inhibits vitamin K epoxide reductase, reducing the synthesis of vitamin K-dependent clotting factors, factors 2, 7, 9, 10, protein C, protein S.

Name the brand names for warfarin.

Coumadin, Mareyan, Jantoven.

Name the agent that reverses the effects of warfarin.

The reversal agent for warfarin is vitamin K, which promotes the synthesis of clotting factors that warfarin inhibits.

Dabigatran mode of action.

An anticoagulant agent that is a direct thrombin (factor IIa) inhibitor preventing the conversion of fibrinogen to fibrin, thereby inhibiting thrombus formation.

Rivaroxaban mode of action.

An anticoagulant agent, that is a direct factor Xa inhibitor, preventing the conversion of prothrombin (factor II) to thrombin (factor IIa), thus inhibiting the formation of fibrin and thrombus.

Apixaban mode of action.

An anticoagulant agent that is a direct factor Xa inhibitor, preventing the conversion of prothrombin to thrombin and thereby inhibiting fibrin formation and thrombus development.

Name the reversal agent for dabigatran.

Idarucizumab, a monoclonal antibody that binds to dabigatran, reversing its anticoagulant effects.

Name the reversal agent for rivaroxaban.

Andexanet alfa, a recombinant factor Xa decoy that binds to rivaroxaban, reversing its anticoagulant effects.

Name the reversal agent for apixaban.

Andexanet alfa, a recombinant factor Xa decoy that binds to apixaban, reversing its anticoagulant effects.

What is the brand name of dabigatran.

Pradaxa, an oral anticoagulant used to reduce the risk of stroke and blood clots.

What is the brand name of rivaroxaban.

Xarelto, an oral anticoagulant used to prevent blood clots and reduce the risk of stroke.

What is the brand name of apixaban.

Eliquis, an oral anticoagulant used to reduce the risk of stroke and blood clots.

Name complementary medicines with antiplatelet effects.

Garlic, Gingko Biloba, Dong Quai, ginger, ginseng, fish oil, turmeric, glucosamine, evening primrose.

Name non-steroidal anti-inflammatory agents with antiplatelet effects.

Aspirin, ibuprofen, naproxen, diclofenac, ketorolac, indomethacin, naproxen, mefenamic acid, meloxicam, piroxicam.

Name the NSAID that preferentially inhibitos COX-2.

Celecoxib, meloxicam.

Name the NSAID that selectively inhibits COX-1.

Aspirin.

Aspirin pharmacokinetics (absorption, distribution, metabolism, excretion).

Aspirin is rapidly absorbed in the gastrointestinal tract, metabolized to salicylic acid, with peak plasma concentrations reareached in 1-2 hours. It has a half-life of approximately 15-20 minutes.

Clopidogrel pharmacokinetics.

Clopidogrel is absorbed in the gastrointestinal tract, with peak plasma levels occurring 2 hours after ingestion. It has a half-life of about 6-8 hours and is metabolized in the liver to an active thiol metabolite.

Prasugrel pharmacokinetics.

Prasugrel is quickly absorbed and reaches its peak concentration approximately 30-60 minutes after ingestion. It has a half-life of around 7 hours and requires conversion to an active metabolite by hepatic enzymes.

Ticagrelor pharmacokinetics.

Ticagrelor is absorbed within 30 minutes, with peak plasma concentrations in 1-3 hours. It has a half-life of about 7-12 hours and does not require metabolic activation.

Dipyridamole pharmacokinetics.

Dipyridamole is rapidly absorbed and has peak plasma concentrations 1 hour after oral administration. Its half-life ranges from 10-12 hours, and it is extensively metabolized in the liver.

Eptifibatide pharmacokinetics.

Eptifibatide is administered intravenously and has a half-life of approximately 2.5 hours. It is primarily eliminated through renal excretion.

Tirofiban pharmacokinetics.

Tirofiban is administered intravenously and has a half-life of about 2 hours. It is primarily cleared from the body through renal excretion.

Warfarin pharmacokinetics.

Warfarin is administered orally and is absorbed in the gastrointestinal tract, reaching peak plasma concentrations in 1-4 hours. It has a half-life of approximately 20-60 hours. It is extensively metabolized in the liver and is affected by various factors including diet and drug interactions.

Dabigatran pharmacokinetics.

Dabigatran is administered orally and is rapidly absorbed, reaching peak plasma concentrations within 1-2 hours. It has a half-life of approximately 12-17 hours and is primarily eliminated through renal excretion.

Rivaroxaban pharmacokinetics.

Rivaroxaban is administered orally and is rapidly absorbed, achieving peak plasma concentrations in 2-4 hours. It has a half-life of approximately 5-13 hours and is primarily eliminated through hepatic metabolism and renal excretion.

Heparin pharmacokinetics.

Heparin is administered via subcutaneous or intravenous routes and has a rapid onset of action. It is primarily cleared by the reticuloendothelial system and has a half-life of approximately 1-2 hours.

Synthetic heparin pharmacokinetics.

Synthetic heparin is administered via subcutaneous or intravenous routes, offering a more predictable anticoagulant response. It has a half-life of approximately 3-6 hours and is primarily eliminated through renal excretion.