Platelet Aggregation Inhibitors and Aspirin

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Questions and Answers

What is the primary mechanism by which aspirin functions as an antiplatelet agent?

Inhibits the synthesis of thromboxane A2 (correct)

Increases platelet aggregation

Blocks glycoprotein receptors

Reduces calcium levels in platelets

Which receptor does vorapaxar primarily antagonize to inhibit platelet aggregation?

GP-1b

P2Y12

PAR-1 (correct)

GP-2b/3a

What effect does clopidogrel have in the context of platelet aggregation?

Enhances thromboxane A2 synthesis

Blocks the purine P2Y12 receptor (correct)

Increases adenosine levels

Inhibits cyclooxygenase activity

Which of the following does not contribute to increased platelet aggregation?

Prostacyclin Signup and view all the answers

What is the role of dipyridamole in platelet aggregation?

Increases levels of adenosine A2 receptors Signup and view all the answers

What is the primary mechanism of action of cilostazol?

Inhibition of type 3 phosphodiesterase Signup and view all the answers

Which of the following side effects is most commonly associated with cilostazol?

Headache Signup and view all the answers

Which statement about prasugrel compared to clopidogrel is accurate?

Prasugrel is an irreversible P2Y12 antagonist Signup and view all the answers

What is the main therapeutic use of abciximab?

To prevent platelet aggregation during percutaneous coronary interventions Signup and view all the answers

Which of the following antiplatelet agents does not require activation to exert its effect?

Ticagrelor Signup and view all the answers

What potential adverse effect is specifically associated with ticagrelor?

Dyspnea Signup and view all the answers

How quickly does peak platelet inhibition occur after the administration of abciximab?

Within 30 minutes Signup and view all the answers

What effect does low-dose aspirin have on TXA2 synthesis?

It selectively inhibits TXA2 synthesis. Signup and view all the answers

Why does aspirin have a prolonged effect on platelet aggregation?

It irreversibly inhibits cyclooxygenase. Signup and view all the answers

What is the primary role of dipyridamole in treatment?

It serves as a coronary vasodilator. Signup and view all the answers

What adverse effect is commonly associated with aspirin use?

Bleeding, particularly in the gastrointestinal tract. Signup and view all the answers

What is Aggrenox composed of?

Dipyridamole and aspirin. Signup and view all the answers

In which situation is aspirin contraindicated?

Pregnancy, particularly in the 3rd trimester. Signup and view all the answers

How does dipyridamole increase cAMP levels in platelets?

By blocking platelet uptake of adenosine. Signup and view all the answers

What is the major limitation of dipyridamole in thromboembolic disorder treatment?

It has a limited role and is a relatively weak antiplatelet drug. Signup and view all the answers

Study Notes

Platelet Aggregation Inhibitors

Platelets adhere to damaged endothelium via GP-1a and GP-1b receptors, leading to synthesis and release of aggregation mediators like TXA2, ADP, and 5-HT.
These mediators increase GP receptor expression, promoting platelet aggregation via fibrinogen binding to GP2b/3a receptors.
Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit thromboxane A2 synthesis by blocking cyclooxygenase (COX).
Clopidogrel, prasugrel, and ticagrelor block ADP receptors (P2Y12).
Agents like eptifibatide, tirofiban, and abciximab bind to GP2b/3a proteins, inhibiting fibrinogen cross-linking.
Vorapaxar is an antagonist at PAR-1 receptors, targeting thrombin.
Dipyridamole inhibits adenosine reuptake, increasing cAMP, decreasing calcium and platelet aggregation.
Cilostazol inhibits PDE3, elevating cAMP levels.

Aspirin

Aspirin is a non-steroidal anti-inflammatory drug (NSAID) with analgesic, antipyretic, and anti-inflammatory effects.
It inhibits prostaglandin synthesis, notably thromboxane A2 (TXA2) synthesis more than prostacyclin (PGI2) synthesis at low doses.
Aspirin irreversibly inhibits cyclooxygenase, the enzyme responsible for TXA2 synthesis, thus reducing platelet aggregation for the lifespan of the platelet.
It is used to prevent arterial thrombosis in patients with ischemic heart disease and stroke.
Adverse effects include bleeding, particularly gastrointestinal bleeding due to reduced bicarbonate secretion.
Pregnancy, especially in the third trimester, and hypersensitivity are contraindications.

Dipyridamole

Dipyridamole is a coronary vasodilator and relatively weak antiplatelet drug.
It inhibits platelet aggregation by blocking adenosine uptake, leading to increased cAMP levels and reduced calcium release.
Lowers platelet aggregation.
It is used in combination with aspirin, potentially improving stroke prevention.

Cilostazol

Cilostazol is a vasodilator and antiplatelet drug that inhibits type 3 phosphodiesterase (PDE3).
Increases cAMP levels in platelets and blood vessels, reducing platelet aggregation
Often indicated for intermittent claudication, a peripheral vascular disease.

Adenosine Diphosphate Inhibitors (ADP)

Clopidogrel, prasugrel, cangrelor, and ticagrelor inhibit ADP binding to its platelet receptors, hindering GPIIb/IIIa activation and subsequent fibrinogen binding.
Clopidogrel and prasugrel are irreversible inhibitors.
Cangrelor and ticagrelor are reversible inhibitors, used in situations like surgery.

Glycoprotein IIb/IIIa Antagonists

Abciximab is a monoclonal antibody that blocks GP IIb/IIIa receptors, preventing platelet aggregation by hindering fibrinogen binding. Its IV management achieves peak inhibition rapidly but is short-lived.

Vorapaxar

Vorapaxar is a protease-activated receptor-1 (PAR-1) antagonist, preventing platelet aggregation via thrombin's influence on platelets.
Approved for patients with MI history or peripheral arterial disease.

Thrombolytic Drugs

Thrombolytic drugs convert plasminogen to plasmin, which breaks down fibrin and fibrinogen in blood clots.
First-generation includes streptokinase and urokinase.
Second-generation includes reteplase and alteplase ,which are fibrin-selective.
Used to treat acute myocardial infarction, pulmonary embolism, deep vein thrombosis, and acute ischemic stroke.
Hemorrhage is a major side effect due to their non-discriminating action on fibrin.

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Description

Explore the mechanisms and effects of platelet aggregation inhibitors, including the role of various mediators and specific drugs like aspirin and clopidogrel. This quiz covers important pharmacological aspects and interactions relevant to thrombus formation and prevention.