Antiplatelet medications

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Antiplatelet medications

Prerequisite basic sciences

Prerequisite basic sciences

Prerequisite basic sciences


Antiplatelet medications


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Antiplatelet medications

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A 68-year-old woman is brought to the emergency department with sudden onset of epigastric and chest pain accompanied by sweating for the past hour. The patient’s symptoms improved with aspirin and sublingual nitroglycerin administered by the paramedics. An ECG is shown below. Troponin levels are normal. She is started on conventional therapy for unstable angina. Upon re-evaluation, the patient’s chest pain is not improved, and another drug is administered to reduce the risk of coronary thrombosis. At the same time, she is scheduled for percutaneous coronary intervention later today. Which of the following best describes the mechanism of action of this drug?
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Abciximab p. 120

Glycoprotein IIb/IIIa inhibitors p. 445

thrombogenesis and p. 419

Antiplatelet antibodies p. 721

abciximab as p. 120


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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  2. "Rang and Dale's Pharmacology" Elsevier (2019)
  3. "Goodman and Gilman's The Pharmacological Basis of Therapeutics, 13th Edition" McGraw-Hill Education / Medical (2017)
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  7. "Assessment of platelet function in patients receiving tirofiban early after primary coronary intervention" Interventional Medicine and Applied Science (2016)
  8. "The first‐generation phosphodiesterase 5 inhibitors and their pharmacokinetic issue" Andrology (2019)

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