00:00 / 00:00
Anticoagulants: Direct factor inhibitors
Ribonucleotide reductase inhibitors
Platinum containing medications
DNA alkylating medications
Antimetabolites for cancer treatment
0 / 15 complete
Glycoprotein IIb/IIIa inhibitors p. 445
thrombogenesis and p. 419
abciximab as p. 120
Elizabeth Nixon-Shapiro, MSMI, CMI
Sam Gillespie, BSc
Robyn Hughes, MScBMC
Antiplatelet medications prevent blood clot formation during hemostasis, where hemo means blood, and stasis means to halt or stop.
Hemostasis is divided into primary hemostasis, where circulating cell fragments called platelets form a plug at the site of an injured blood vessel, and secondary hemostasis, which involves multiple coagulation factors working together to form a fibrin mesh to stabilize the platelet plug.
Antiplatelet medications inhibit the steps of primary hemostasis to prevent the platelet plug from forming.
Primary hemostasis can be further divided into five steps: endothelial injury, exposure, adhesion, activation, and aggregation.
Endothelial injury is when the innermost layer of the artery, called the endothelium, gets damaged.
The second step is exposure, where the damaged endothelium exposes the underlying collagen.
The underlying collagen and endothelial cells then release a protein called Von Willebrand's factor, or vWF, that binds to this collagen.
The third step is adhesion where circulating platelets bind to the vWF via a surface protein called GPIB. The fourth step is activation, where platelets become active after binding to vWF.
First, the platelet changes shape and its membrane forms tentacle-like arms allowing it to grab onto other platelets.
Second, platelets release more vWF, as well as serotonin, a tiny molecule that attracts more platelets to the area.
Third, the platelets also release adenosine diphosphate or ADP, and thromboxane A2, or TXA2. These two molecules can activate other platelets that haven’t bound to vWF.
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