Cardiovascular System

Anticoagulants, Antiplatelets & Thrombolytics: Drug Targets


Drugs that act on blood clotting confuse students only because they all sound similar. The cure is one diagram: place each drug on the clotting cascade, and anticoagulants, antiplatelets and thrombolytics separate cleanly by exactly where they act.

Clotting factors II · VII · IX · X (vitamin K) Factor Xa Thrombin (IIa) Fibrinogen → Fibrin clot Warfarin — vitamin K antagonist ↓ synthesis of II, VII, IX, X (monitor INR) Heparin / LMWH → antithrombin Direct Xa inhibitors: rivaroxaban, apixaban Direct thrombin inhibitor: dabigatran (heparin also inactivates thrombin) Thrombolytics: alteplase, streptokinase dissolve formed fibrin (lyse the clot) Platelet plug — Antiplatelets Aspirin (COX/TXA₂) · clopidogrel, ticagrelor (P2Y12) · abciximab (GpIIb/IIIa)
Anticoagulants act on the clotting cascade, antiplatelets on the platelet plug, and thrombolytics dissolve fibrin once a clot has formed.

Anticoagulants — slow the cascade

  • Heparin (unfractionated) — activates antithrombin to inhibit thrombin (IIa) and Xa. IV, rapid, monitored by aPTT; reversed with protamine. Risk: bleeding, heparin-induced thrombocytopenia (HIT).
  • LMWH (enoxaparin) — mainly anti-Xa, subcutaneous, predictable, usually no monitoring.
  • Warfarin — blocks vitamin-K-dependent synthesis of factors II, VII, IX, X. Oral, slow onset, monitored by INR, many interactions; reversed with vitamin K / FFP / PCC. Teratogenic.
  • DOACsdirect Xa inhibitors (rivaroxaban, apixaban) and direct thrombin inhibitor (dabigatran). Oral, fixed-dose, no routine monitoring; reversal agents: idarucizumab (dabigatran), andexanet alfa (Xa inhibitors).

Antiplatelets — block the platelet plug

  • Aspirin — irreversibly inhibits COX-1 → less thromboxane A₂.
  • P2Y12 inhibitors (clopidogrel, ticagrelor, prasugrel) — block ADP-driven activation.
  • GpIIb/IIIa inhibitors (abciximab, tirofiban) — IV, block the final aggregation step.

Used in arterial disease — acute coronary syndrome, stroke, after stenting.

Thrombolytics — dissolve the formed clot

Alteplase (tPA) and streptokinase convert plasminogen to plasmin, breaking down fibrin. Used in acute ischaemic stroke, massive PE, and STEMI where primary PCI isn’t available. Main danger: haemorrhage.

Arterial vs venous — the key clinical split

  • Arterial clots are platelet-rich (“white”) → antiplatelets.
  • Venous clots are fibrin-rich (“red”) → anticoagulants.
Exam tip: link each drug to its monitoring and reversal — heparin → aPTT → protamine; warfarin → INR → vitamin K; dabigatran → idarucizumab. And remember the split: antiplatelets for arteries, anticoagulants for veins.

One cascade, three drug families, each at its own step. Draw the diagram from memory and you can place any clotting drug — with its monitoring, reversal and indication — exactly where it belongs.

Share

Cardiovascular System
← All articles