Platelet Aggregation Inhibitors and Aspirin

<p>Prostacyclin (A)</p> Signup and view all the answers

<p>Increases levels of adenosine A2 receptors (B)</p> Signup and view all the answers

<p>Inhibition of type 3 phosphodiesterase (D)</p> Signup and view all the answers

<p>Headache (C)</p> Signup and view all the answers

<p>Prasugrel is an irreversible P2Y12 antagonist (C)</p> Signup and view all the answers

<p>To prevent platelet aggregation during percutaneous coronary interventions (C)</p> Signup and view all the answers

<p>Ticagrelor (D)</p> Signup and view all the answers

<p>Dyspnea (A)</p> Signup and view all the answers

<p>Within 30 minutes (C)</p> Signup and view all the answers

<p>It selectively inhibits TXA2 synthesis. (A)</p> Signup and view all the answers

<p>It irreversibly inhibits cyclooxygenase. (C)</p> Signup and view all the answers

<p>It serves as a coronary vasodilator. (A)</p> Signup and view all the answers

<p>Bleeding, particularly in the gastrointestinal tract. (D)</p> Signup and view all the answers

<p>Dipyridamole and aspirin. (B)</p> Signup and view all the answers

<p>Pregnancy, particularly in the 3rd trimester. (A)</p> Signup and view all the answers

<p>By blocking platelet uptake of adenosine. (C)</p> Signup and view all the answers

<p>It has a limited role and is a relatively weak antiplatelet drug. (C)</p> Signup and view all the answers

Platelet aggregation inhibitors are medications that reduce the tendency of platelets to clump together and form clots.

Platelets stick to damaged endothelium via glycoprotein receptors, leading to the release of clotting factors like thromboxane A2, ADP, and serotonin.

Aspirin inhibits the enzyme cyclooxygenase (COX), thereby preventing the synthesis of thromboxane A2, a potent platelet activator.

Aspirin and other NSAIDs inhibit the production of prostaglandins, which are involved in inflammation and platelet aggregation.

Prostacyclin, produced by endothelial cells, inhibits platelet aggregation. Thromboxane A2, produced by platelets, promotes platelet aggregation.

A substance that prevents blood clots from forming by inhibiting platelet aggregation.

A type of antiplatelet drug that inhibits the synthesis of thromboxane A2 (TXA2), a potent platelet aggregator.

Aspirin irreversibly inhibits cyclooxygenase (COX), an enzyme involved in the synthesis of TXA2.

Lower doses of aspirin specifically target TXA2, while higher doses inhibit both TXA2 and prostacyclin.

Prostacyclin, a substance produced by blood vessel walls, prevents platelet aggregation and thrombosis.

Thromboxane A2 (TXA2) promotes platelet aggregation and thrombosis.

Dipyridamole inhibits platelet aggregation by blocking platelet uptake of adenosine, leading to increased cAMP levels.

A combination of dipyridamole and aspirin, shown to be more effective for stroke prevention than either drug alone, but with greater risk of bleeding.

Cilostazol is a drug that helps improve blood flow in the legs by stopping a chemical called PDE3 from breaking down another chemical called cAMP. More cAMP leads to less blood vessel constriction and improved blood flow.

Clopidogrel, Prasugrel, Cangrelor, and Ticagrelor are drugs that prevent platelets from sticking together by blocking a receptor on the platelet called P2Y12.

Clopidogrel and Prasugrel are irreversible P2Y12 antagonists, meaning they block P2Y12 for the entire lifespan of the platelet.

Cangrelor and Ticagrelor are reversible P2Y12 antagonists, meaning their blocking effect is temporary and can be reversed.

Abciximab is a drug that prevents platelets from sticking together by binding to a receptor called GPIIb/IIIa on the platelet.

Vorapaxar is a new drug that prevents platelet aggregation by a different mechanism than other antiplatelet drugs.