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This set of flashcards covers essential concepts and mechanisms related to platelets and anti-platelet agents, facilitating review for the exam.
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What are the key molecular events in platelet activation?
Key events include change in platelet shape, activation of cell surface integrins (GpIIb/IIIa), granule secretion, and 'flip/flop' of plasma membrane.
What role do platelets play in arterial thrombosis?
Platelets prevent excessive blood loss at sites of injury and contribute to the formation of arterial clots that are rich in aggregated platelets.
What is the mechanism of action of Aspirin as an anti-platelet agent?
Aspirin irreversibly inhibits platelet Cyclooxygenase (COX), thereby reducing the synthesis of thromboxane A2 (TXA2) which promotes platelet activation.
What are the potential side effects of Aspirin?
Side effects include excessive bleeding due to reduced platelet function and gastrointestinal symptoms due to COX inhibition in gastric mucosa.
How do Clopidogrel and Prasugrel function as anti-platelet agents?
They are non-competitive antagonists of ADP receptors on platelets, preventing ADP from recruiting more platelets.
What is the role of GpIIb/IIIa in platelet aggregation?
GpIIb/IIIa is a receptor that binds fibrinogen and von Willebrand factor, promoting platelet aggregation.
What is the mechanism of action of Dipyridamole as an anti-platelet agent?
Dipyridamole is a phosphodiesterase (PDE) inhibitor that elevates cAMP levels in platelets, inhibiting platelet activation.
What is the function of PGI2 (Prostacyclin) in platelet activation?
PGI2 inhibits platelet activation by binding to its receptor on platelets to produce cAMP, which opposes platelet aggregation.
What is the significance of GPIIb/IIIa deficiency in patients?
Patients with GPIIb/IIIa deficiency (such as Glanzmann’s thrombasthenia) cannot accumulate platelet plugs at injury sites, leading to bleeding disorders.
How does Abciximab function as a GpIIb/IIIa inhibitor?
Abciximab is a monoclonal antibody that inhibits platelet aggregation by blocking the fibrinogen binding site on GpIIb/IIIa.