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Questions and Answers
What is the primary role of prostacyclin under normal conditions?
What is the primary role of prostacyclin under normal conditions?
What effect does low-dose aspirin predominantly have on TXA2 and prostacyclin?
What effect does low-dose aspirin predominantly have on TXA2 and prostacyclin?
Why is aspirin considered to inhibit platelet aggregation for the life of the platelet?
Why is aspirin considered to inhibit platelet aggregation for the life of the platelet?
What is the primary mechanism of action of vorapaxar?
What is the primary mechanism of action of vorapaxar?
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Which condition is a contraindication for aspirin usage?
Which condition is a contraindication for aspirin usage?
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Which of the following thrombolytic agents is described as fibrin selective at low doses?
Which of the following thrombolytic agents is described as fibrin selective at low doses?
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How does dipyridamole inhibit platelet aggregation?
How does dipyridamole inhibit platelet aggregation?
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What is the ideal timeframe for administering thrombolytic drugs after symptom onset for maximum benefit?
What is the ideal timeframe for administering thrombolytic drugs after symptom onset for maximum benefit?
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What combination therapy has shown to be more effective for stroke prevention than either dipyridamole or aspirin alone?
What combination therapy has shown to be more effective for stroke prevention than either dipyridamole or aspirin alone?
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What major side effect is associated with aspirin use?
What major side effect is associated with aspirin use?
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Which thrombolytic agent is derived from human kidney cells?
Which thrombolytic agent is derived from human kidney cells?
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In what situation is dipyridamole primarily used?
In what situation is dipyridamole primarily used?
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What is the expected half-life of alteplase?
What is the expected half-life of alteplase?
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In which condition are thrombolytic drugs NOT indicated?
In which condition are thrombolytic drugs NOT indicated?
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How does reteplase differ from alteplase?
How does reteplase differ from alteplase?
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What condition is a contraindication for administering thrombolytics?
What condition is a contraindication for administering thrombolytics?
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What mediators are primarily responsible for promoting platelet aggregation?
What mediators are primarily responsible for promoting platelet aggregation?
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Which receptor is targeted by dipyridamole to decrease platelet aggregation?
Which receptor is targeted by dipyridamole to decrease platelet aggregation?
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What is the primary action of aspirin in relation to platelet aggregation?
What is the primary action of aspirin in relation to platelet aggregation?
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Which of the following statements about aspirin is true?
Which of the following statements about aspirin is true?
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Which class of drugs directly binds to GP-2b/3a proteins to inhibit platelet aggregation?
Which class of drugs directly binds to GP-2b/3a proteins to inhibit platelet aggregation?
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What occurs during platelet activation in the context of platelet aggregation?
What occurs during platelet activation in the context of platelet aggregation?
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Which drug acts as an antagonist at PAR-1 receptors on platelets?
Which drug acts as an antagonist at PAR-1 receptors on platelets?
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Which mechanism does cilostazol employ to inhibit platelet aggregation?
Which mechanism does cilostazol employ to inhibit platelet aggregation?
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What is the primary mechanism through which cilostazol exerts its effect?
What is the primary mechanism through which cilostazol exerts its effect?
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Which of the following is a common side effect of cilostazol?
Which of the following is a common side effect of cilostazol?
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How does prasugrel differ from clopidogrel in terms of its action?
How does prasugrel differ from clopidogrel in terms of its action?
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What advantage do cangrelor and ticagrelor provide in clinical settings?
What advantage do cangrelor and ticagrelor provide in clinical settings?
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Which drugs are classified as glycoprotein IIb/IIIa antagonists?
Which drugs are classified as glycoprotein IIb/IIIa antagonists?
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What is a key characteristic of vorapaxar's mechanism of action?
What is a key characteristic of vorapaxar's mechanism of action?
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During the administration of abciximab, how soon does peak platelet inhibition typically occur?
During the administration of abciximab, how soon does peak platelet inhibition typically occur?
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What is the therapeutic use of abciximab?
What is the therapeutic use of abciximab?
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Study Notes
Platelet Aggregation Inhibitors
- Platelets adhere to damaged endothelium via GP-1a and GP-1b receptors interacting with collagen and vWF.
- Platelet activation leads to mediator release (TXA2, ADP, 5-HT).
- These mediators increase GP receptor expression and promote platelet aggregation (fibrinogen binding to GPIIb/IIIa).
- NSAIDs block COX, inhibiting TXA2 synthesis.
- Clopidogrel, prasugrel, ticagrelor block ADP receptors (P2Y12).
- Eptifibatide, tirofiban, abciximab bind to GPIIb/IIIa, preventing fibrinogen cross-linking.
- Vorapaxar is a PAR-1 receptor antagonist.
- Dipyridamole inhibits adenosine reuptake, increasing cAMP, and decreasing platelet aggregation.
- Cilostazol inhibits PDE3, increasing cAMP levels.
- Platelet aggregation inhibitors reduce platelet-rich clot formation or inhibit chemical signals promoting aggregation.
Aspirin
- Aspirin is a non-steroidal anti-inflammatory drug (NSAID) with analgesic, antipyretic, and anti-inflammatory effects.
- Inhibits prostaglandin synthesis from arachidonic acid.
- Blocks TXA2 synthesis more than prostacyclin synthesis at low doses.
- Irreversibly inhibits COX, permanently inhibiting platelet aggregation for the life of the platelet.
- Often used to prevent arterial thrombosis in patients with ischemic heart disease or stroke.
- Can cause bleeding, especially in the gastrointestinal tract.
Dipyridamole
- A coronary vasodilator and relatively weak antiplatelet drug.
- Inhibits platelet adenosine uptake, increasing cAMP levels, reducing calcium release, and decreasing platelet aggregation.
- Limited role in thromboembolic disorders.
- Combined with aspirin (Aggrenox) more effective for stroke prevention than either drug alone, but with increased major bleeding.
Cilostazol
- A vasodilator and antiplatelet drug inhibiting type 3 phosphodiesterase (PDE3).
- Increases cAMP levels in platelets and blood vessels.
- Indicated for intermittent claudication (peripheral vascular disease).
- Headache is a common side effect
Adenosine Diphosphate Inhibitors (ADP)
- Clopidogrel, prasugrel, cangrelor, and ticagrelor inhibit ADP binding to its receptors on platelets, inhibiting activation of GPIIb/IIIa receptors.
- Clopidogrel and prasugrel are irreversible P2Y12 antagonists.
- Cangrelor and ticagrelor are reversible receptor blockers.
- Clopidogrel and prasugrel are prodrugs, requiring metabolism to active metabolites.
- Ticagrelor doesn't require activation.
Glycoprotein IIb/IIIa Antagonists
- Abciximab is a monoclonal antibody binding to platelet GPIIb/IIIa receptors, preventing aggregation.
- Administered intravenously.
- Peak platelet inhibition within 30 minutes, lasting 24-48 hours after infusion cessation.
- Used with heparin and aspirin during percutaneous coronary interventions (PCI).
Vorapaxar
- A protease-activated receptor-1 (PAR-1) antagonist.
- Prevents platelet aggregation by occupying PAR-1 receptor.
- Reduces thrombotic cardiovascular events and mortality.
- Used for patients with MI or peripheral arterial disease (PAD).
Thrombolytic Drugs
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Convert plasminogen to plasmin, dissolving clots.
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Indicated for patients with acute myocardial infarction where benefit outweighs risk.
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First generation: Streptokinase, Urokinase
- Streptokinase forms a complex with plasminogen altering its structure to facilitate conversion to plasmin.
- Urokinase directly converts plasminogen to plasmin.
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Second generation: Alteplase, Reteplase
- Recombinant human tissue plasminogen activator.
- Catalyze conversion of plasminogen to plasmin.
- Alteplase is fibrin-selective, targeting fibrin bound plasminogen in the thrombus.
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Third generation: Reteplase and Tenecteplase
- Bind to fibrin, activating plasminogen.
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Thrombolytics are administered intravenously.
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Used for severe pulmonary embolism, deep vein thrombosis, and arterial thromboembolism.
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Optimal use is within 6 hours of onset of symptoms.
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Adverse effect is hemorrhage.
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Description
This quiz covers the mechanisms of platelet aggregation inhibitors, including their actions on platelet receptors and the effects of drugs like aspirin and clopidogrel. Understand how these medications prevent clot formation and their role in cardiovascular therapy.
