Integrated Clinical Science: Cardiology I – Anticlotting Drugs

Question-and-answer flashcards summarizing mechanisms, examples, indications, and adverse effects of anticoagulants, antiplatelets, and thrombolytics discussed in the lecture.

What are the three major classes of anticlotting ("blood-thinner") drugs?

Anticoagulants, antiplatelets, and thrombolytics.

Why are anticlotting drugs widely prescribed?

To prevent or treat clots in cardiovascular disease.

How does unfractionated heparin inhibit coagulation?

It binds antithrombin III, forming a complex that irreversibly inactivates thrombin and factor Xa.

What is the main mechanistic difference between unfractionated heparin and low-molecular-weight heparins (LMWHs)?

LMWHs (e.g., enoxaparin) predominantly inhibit factor Xa and have little direct effect on thrombin.

Name three common LMWH preparations.

Enoxaparin, dalteparin, tinzaparin.

List two major adverse effects of heparin therapy.

Bleeding and heparin-induced thrombocytopenia.

What is the mechanism of action of direct thrombin inhibitors (DTIs)?

They bind directly to the active site of thrombin, blocking its ability to convert fibrinogen to fibrin.

Give four examples of direct thrombin inhibitors.

Lepirudin, desirudin, bivalirudin, argatroban.

What is the primary toxicity shared by all direct thrombin inhibitors?

Increased risk of bleeding.

How do direct oral factor Xa inhibitors work?

They directly and reversibly bind to factor Xa, preventing the conversion of prothrombin to thrombin.

List four direct oral factor Xa inhibitors.

Rivaroxaban, apixaban, edoxaban, betrixaban.

Explain warfarin’s mechanism of action.

It inhibits vitamin K epoxide reductase.

Why is warfarin unsuitable for emergency anticoagulation?

Its onset is slow because pre-existing clotting factors must degrade.

Identify three important adverse effects or cautions with warfarin.

Bleeding, numerous CYP450 drug interactions, and teratogenicity.

Which class of drugs is used when a clot has already formed and must be rapidly lysed?

Thrombolytics.

Describe the mechanism of tissue plasminogen activator (tPA).

tPA converts plasminogen to plasmin.

Name three recombinant tPA drugs.

Alteplase, reteplase, tenecteplase.

How does streptokinase differ from tPA mechanistically?

Streptokinase forms a complex with plasminogen, causing a conformational change.

What immune-related problem can reduce streptokinase efficacy?

Anti-streptokinase antibody formation.

How does aspirin act as an antiplatelet agent?

Irreversibly inhibits COX-1, blocking thromboxane A2 synthesis.

State the mechanism and give two examples of glycoprotein IIb/IIIa inhibitors.

They reversibly block GP IIb/IIIa receptors, preventing platelet cross-linking; examples: abciximab, eptifibatide, tirofiban.

What are common side effects of GP IIb/IIIa receptor inhibitors?

Bleeding and antibody-mediated thrombocytopenia.

How do P2Y12 (ADP) receptor antagonists prevent thrombosis?

They inhibit ADP-mediated activation of P2Y12 receptors on platelets.

Name three P2Y12 receptor antagonists.

Clopidogrel, prasugrel, ticlopidine.

Explain the anticoagulant mechanism of PDE3 inhibitors.

They inhibit phosphodiesterase 3 and adenosine reuptake to raise platelet cAMP.

Which vitamin can be administered to facilitate clotting in deficiency states?

Vitamin K (restores synthesis of vitamin-K–dependent clotting factors).