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The process of hemostasis consists of three phases: vascular, platelet, and coagulation (Figure 14–1). The fibrinolytic phase that follows prevents the clotting process from spreading out of control beyond the site of injury. It may be helpful at this point to review the hemostatic mechanisms in your physiology textbook.


Hemostasis consists of three phases: vascular, platelet, and coagulation. The end result of these phases is the formation of fibrin.

Platelets respond to tissue injury by adhering to the site of injury; they then release granules containing chemical mediators that promote aggregation. Factors released by platelets and the injured tissue cause activation of the coagulation cascade. This results in the formation of thrombin, which in turn converts fibrinogen to fibrin. The subsequent cross-linking of the fibrin strands stabilizes the clot.

Drugs are available that interfere with the platelet and coagulation phases of the initial response to tissue injury. As we review the drugs that prevent clots and those that lyse clots, the drugs that can function as antidotes will be mentioned. Finally, we’ll consider drugs used to treat anemia.


Platelet aggregation inhibitors decrease the formation of chemical signals that promote platelet aggregation. Drugs that inhibit platelet function are administered for the relatively specific prophylaxis of arterial thrombosis and during management of heart attacks (myocardial infarction).

Nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin, inhibit platelet aggregation and prolong bleeding time.

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Antiplatelet Drugs

NSAIDs, including aspirin


P2Y12 ADP receptor blockers





IIB/IIIA receptor antagonists





NSAIDs will be considered in more detail in Chapter 43. These agents inhibit cyclooxygenase. In platelets, this inhibits the formation of TXA2 (a thromboxane). TXA2 is a potent inducer of platelet aggregation. Aspirin acetylates cyclooxygenase-1 (COX-1) effectively inhibiting platelet aggregation for 5 to 7 days.

Dipyridamole decreases platelet adhesion to damaged endothelium, but it does not alter bleeding time. Dipyridamole inhibits platelet uptake of adenosine. It is usually used in combination with aspirin or warfarin.

Ticlopidine, prasugrel, clopidogrel, and ticagrelor inhibit platelet aggregation and prolong bleeding time. They work by inactivating the platelet P2Y12 (ADP) receptor, thus having a prolonged action. This receptor plays a central role in amplification and stabilization of platelet aggregation (i.e., clot formation).

Platelet glycoprotein IIb/IIIa receptor antagonists prevent platelet aggregation by blocking the binding of fibrinogen and von Willebrand factor to the glycoprotein IIb/IIIa receptor on the surface of the platelet.

The glycoprotein receptor, known as the IIb/IIIa receptor, is critical for platelet aggregation. Fibrinogen molecules bind to these receptors and form bridges between adjacent platelets, allowing them to aggregate. ...

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