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Questions and Answers
What is the primary purpose of antiplatelets?
What is the primary purpose of antiplatelets?
Venous thrombosis is caused by atherosclerosis.
Venous thrombosis is caused by atherosclerosis.
False (B)
What are the two main types of pathologic clots?
What are the two main types of pathologic clots?
Venous thrombosis and arterial thrombosis
A condition where a blood clot travels to the lungs is called a __________.
A condition where a blood clot travels to the lungs is called a __________.
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Match the following types of clots with their descriptions:
Match the following types of clots with their descriptions:
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What typically starts arterial thrombosis?
What typically starts arterial thrombosis?
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Hemostasis refers to the process of inducing excessive bleeding.
Hemostasis refers to the process of inducing excessive bleeding.
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What is the term used for blood clots that impair blood flow?
What is the term used for blood clots that impair blood flow?
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Which of the following is NOT an antiplatelet medication?
Which of the following is NOT an antiplatelet medication?
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Glycoprotein IIb/IIIa is also known as Integrin αIIbβ3.
Glycoprotein IIb/IIIa is also known as Integrin αIIbβ3.
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What is the primary function of glycoprotein IIb/IIIa in platelets?
What is the primary function of glycoprotein IIb/IIIa in platelets?
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Aspirin inhibits the synthesis of __________ to prevent platelet aggregation.
Aspirin inhibits the synthesis of __________ to prevent platelet aggregation.
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Match the glycoprotein IIb/IIIa inhibitors with their types.
Match the glycoprotein IIb/IIIa inhibitors with their types.
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How many copies of αIIbβ3 are typically present on the surface of one platelet?
How many copies of αIIbβ3 are typically present on the surface of one platelet?
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PDE inhibitors function by promoting platelet aggregation.
PDE inhibitors function by promoting platelet aggregation.
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Purinergic receptor inhibitors target the __________ receptor to inhibit platelet activation.
Purinergic receptor inhibitors target the __________ receptor to inhibit platelet activation.
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Which drug acts by irreversibly modifying the platelet ADP receptor?
Which drug acts by irreversibly modifying the platelet ADP receptor?
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Prasugrel is activated by carboxyesterase CES1 followed by CYP2C19.
Prasugrel is activated by carboxyesterase CES1 followed by CYP2C19.
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What is the expected lifespan of platelets exposed to clopidogrel?
What is the expected lifespan of platelets exposed to clopidogrel?
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The black box warning for clopidogrel relates to ______% of the US population with low CYP2C19 activity.
The black box warning for clopidogrel relates to ______% of the US population with low CYP2C19 activity.
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Match the following drugs with their activation pathways:
Match the following drugs with their activation pathways:
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Which of the following statements is true about clopidogrel and prasugrel?
Which of the following statements is true about clopidogrel and prasugrel?
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Concomitant use of omeprazole or esomeprazole is advised with clopidogrel.
Concomitant use of omeprazole or esomeprazole is advised with clopidogrel.
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Which enzyme leads to more active drug formation for prasugrel?
Which enzyme leads to more active drug formation for prasugrel?
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Which enzyme primarily metabolizes prasugrel to its active form?
Which enzyme primarily metabolizes prasugrel to its active form?
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Ticagrelor requires hepatic activation to become effective.
Ticagrelor requires hepatic activation to become effective.
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What type of antagonism do prasugrel, clopidogrel, ticagrelor, and cangrelor exert at the P2Y12 receptor?
What type of antagonism do prasugrel, clopidogrel, ticagrelor, and cangrelor exert at the P2Y12 receptor?
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Cangrelor is administered via __________ injection.
Cangrelor is administered via __________ injection.
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Match the following drugs with their characteristics:
Match the following drugs with their characteristics:
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Which of the following statements about prasugrel and ticagrelor is true?
Which of the following statements about prasugrel and ticagrelor is true?
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Cilostazol is classified as a COX inhibitor.
Cilostazol is classified as a COX inhibitor.
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What is the FDA approval year for ticagrelor?
What is the FDA approval year for ticagrelor?
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What effect does aspirin have on platelet aggregation?
What effect does aspirin have on platelet aggregation?
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Aspirin is the only NSAID that inhibits platelet aggregation.
Aspirin is the only NSAID that inhibits platelet aggregation.
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Which receptor do clopidogrel and ticlopidine bind to?
Which receptor do clopidogrel and ticlopidine bind to?
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The therapeutic effect of glycoprotein IIb/IIIa antagonists is to inhibit __________ which prevents platelet aggregation.
The therapeutic effect of glycoprotein IIb/IIIa antagonists is to inhibit __________ which prevents platelet aggregation.
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Match the medications to their characteristics:
Match the medications to their characteristics:
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What is the primary action of dipyridamole?
What is the primary action of dipyridamole?
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Cilostazol is a phosphodiesterase 3 (PDE3) inhibitor that decreases platelet aggregation.
Cilostazol is a phosphodiesterase 3 (PDE3) inhibitor that decreases platelet aggregation.
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What does PDE inhibition in relation to cilostazol increase that helps inhibit platelet activation?
What does PDE inhibition in relation to cilostazol increase that helps inhibit platelet activation?
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Dipyridamole also inhibits the reuptake of ________ into platelets, red blood cells, and endothelial cells.
Dipyridamole also inhibits the reuptake of ________ into platelets, red blood cells, and endothelial cells.
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Match the following drugs with their primary mechanism of action:
Match the following drugs with their primary mechanism of action:
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What effect does dipyridamole have when given at high doses over a short time?
What effect does dipyridamole have when given at high doses over a short time?
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Vorapaxar acts as a PDE inhibitor.
Vorapaxar acts as a PDE inhibitor.
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What type of activity does dipyridamole potentiate?
What type of activity does dipyridamole potentiate?
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Study Notes
Hemostasis (Blood Clotting)
- Hemostasis is a delicate balance, preventing blood loss from a disrupted intravascular space but allowing unrestricted flow under normal circumstances
- Four physiological processes occur:
- Vascular constriction (slowing blood flow to the damaged site)
- Platelet plug formation (clot formation)
- Fibrin formation (clot formation)
- Fibrinolysis (clot degradation after the damaged site is healed)
- Endogenous clots need to be degraded after formation
- The processes are connected and occur simultaneously with multiple reinforcements
Inhibitors of Blood Clot Formation
- Antiplatelets prevent the platelet plug
- Antithrombotics prevent the fibrin clot
Enhancers of Blood Clot Degradation
- Thrombolytics will be covered in P3 (acute, hospital use, intravenous)
Hemostasis - Definition
- Hemostasis is the process for maintaining circulatory system integrity following blood vessel damage, maintaining a delicate balance between clotting and bleeding
- Hemostatic clots are localized to the vessel wall and do not greatly impede blood flow
- These are "good" clots and prevent unwanted bleeding
- Pathologic clots impair blood flow and often cause complete vessel occlusion
- Also called thrombosis
- These are "bad" (pathologic) clots
Types of Pathologic Clots
- Two main types of pathologic clots:
- Venous thrombosis:
- A clot blocks a vein
- Carries un-oxygenated blood back to the heart
- Flow is rather slow
- Typically started by endothelial damage and contains mostly fibrin
- Deep Vein Thrombosis (DVT) occurs in deep veins, often in the lower leg, thigh, pelvis, or arms with IV lines
- Pulmonary Embolism (PE) occurs when a DVT clot breaks loose and travels to an artery in the lungs
- DVT and PE together are called Venous Thromboembolism (VTE)
- Arterial thrombosis:
- A clot blocks an artery that carries oxygen-rich blood away from the heart
- Flow is rather fast
- Typically started by atherosclerosis and contains platelets and fibrin
- Coronary thrombosis occurs in an artery in the heart and causes a heart attack (MI) or myocardial infarction or angina
- Stroke occurs when arterial thrombosis happens in an artery in the brain
- Venous thrombosis:
Drugs Altering Blood Clot Formation and Degradation
-
Inhibitors of clot formation:
- Antiplatelets: prevent platelet activation and/or aggregation
- COX inhibitors (irreversible), decreases Thromboxane A₂ synthesis (Aspirin)
- Glycoprotein IIb/IIIa antagonists (abciximab, tirofiban, eptifibatide)
- Purinergic receptor antagonists (ADP-receptor, P2Y12): (clopidogrel, prasugrel, ticagrelor, cangrelor)
- Phosphodiesterase 3 inhibitor (cilostazol)
- Adenosine Reuptake inhibitor and PDE inhibitor (dipyridamole)
- Inhibition of protease-activated receptor-1 (vorapaxar)
- Antiplatelets: prevent platelet activation and/or aggregation
- Anticoagulants: prevent fibrin formation (next slidepack)
###Platelet Activation & Aggregation and Drugs causing antiplatelet effect
- Many mechanisms exist
Additional Information
- Students should watch the videos provided after the lecture to understand the topics
- These videos come from a group sponsored by Bayer Pharmaceutical called ThrombosisAdvisor.com
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Description
Test your knowledge on antiplatelet medications and blood clotting processes with this quiz. It covers key concepts such as thrombosis, hemostasis, and the roles of glycoprotein IIb/IIIa and PDE inhibitors in platelet function. Perfect for students and professionals in the medical field.