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Master YLL Pharmacology > CVS - Drugs Affecting Platelets and Coagulation > Flashcards

CVS - Drugs Affecting Platelets and Coagulation Flashcards

1
Q

What are the stages of haemostasis?

A

Vasoconstriction, platelet adhesion, activation, aggregation, and fibrin formation.

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2
Q

What are the classifications of anticlotting drugs?

A

Antiplatelet drugs, anticoagulants, and thrombolytics.

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3
Q

What is the mechanism of action of NSAIDs like Aspirin as antiplatelet drugs?

A

Inhibition of cyclooxygenase, reducing thromboxane A2 and inhibiting platelet aggregation.

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4
Q

How do GP IIB/IIIA receptor blockers function?

A

They prevent fibrinogen binding, inhibiting platelet aggregation.

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5
Q

What are examples of ADP receptor blockers?

A

Ticlopidine and Clopidogrel.

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6
Q

What is the action of PDE inhibitors like Dipyridamole in antiplatelet therapy?

A

They inhibit platelet aggregation by increasing cAMP levels.

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7
Q

What are the clinical uses of Aspirin as an antiplatelet agent?

A

Prevention of myocardial infarction, stroke, and other thromboembolic disorders.

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8
Q

What are common adverse effects of Aspirin?

A

Gastrointestinal bleeding, tinnitus, and Reye’s syndrome.

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9
Q

How does Abciximab function as a GP IIB/IIIA receptor blocker?

A

It is a monoclonal antibody that binds to the GP IIB/IIIA receptor.

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10
Q

What is the pharmacokinetic profile of Heparin?

A

Rapid onset of action, administered intravenously or subcutaneously.

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11
Q

What is the mechanism of action of Warfarin?

A

Inhibition of vitamin K-dependent clotting factors (II, VII, IX, X).

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12
Q

How does Lepirudin work as an anticoagulant?

A

It directly inhibits thrombin.

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13
Q

What is the function of Antithrombin III in anticoagulation?

A

It enhances the inactivation of thrombin and other coagulation enzymes.

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14
Q

What is the therapeutic use of tissue plasminogen activator (t-PA)?

A

To dissolve blood clots in conditions like myocardial infarction and stroke.

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15
Q

How does Urokinase function as a thrombolytic agent?

A

It directly converts plasminogen to plasmin, leading to clot breakdown.

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16
Q

What is the role of streptokinase in thrombolysis?

A

It forms a complex with plasminogen, converting it to plasmin.

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17
Q

What are the adverse effects of thrombolytic agents?

A

Hemorrhage, including intracranial bleeding.

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18
Q

What is the action of Ticlopidine and Clopidogrel?

A

They irreversibly block ADP receptors on platelets, inhibiting activation.

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19
Q

How is Eptifibatide used in antiplatelet therapy?

A

As a short-term intravenous agent during percutaneous coronary interventions.

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20
Q

What is the risk associated with GP IIB/IIIA receptor blockers?

A

They may cause thrombocytopenia and bleeding complications.

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21
Q

What is the indication for using Dipyridamole?

A

Often used in combination with other agents like aspirin to prevent stroke.

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22
Q

How is Aspirin metabolized?

A

Rapidly absorbed and metabolized in the liver to salicylic acid.

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23
Q

What is the impact of NSAIDs on renal function?

A

They can impair renal function and increase blood pressure.

24
Q

What monitoring is required for patients on Warfarin?

A

Regular INR monitoring to adjust dosing and avoid bleeding.

25
Q

What is the advantage of low molecular weight heparins (LMWHs) over standard heparin?

A

They have a more predictable anticoagulant response and lower risk of bleeding.

26
Q

How does Hirudin differ from other anticoagulants?

A

It is a direct thrombin inhibitor derived from leech saliva.

27
Q

What are the indications for using thrombolytic agents?

A

Acute myocardial infarction, ischemic stroke, and pulmonary embolism.

28
Q

How is thrombolytic therapy administered?

A

Typically intravenously, sometimes directly into the clot during procedures.

29
Q

What are the contraindications for thrombolytic therapy?

A

Recent surgery, bleeding disorders, and severe uncontrolled hypertension.

30
Q

Why is Aspirin used in low doses for antiplatelet therapy?

A

To minimize side effects while effectively inhibiting platelet aggregation.

31
Q

What are the risks of combining NSAIDs with anticoagulants?

A

Increased risk of bleeding and gastrointestinal ulcers.

32
Q

How do Tirofiban and Eptifibati0de differ from Abciximab?

A

They are small molecules and non-antibodies, with a shorter half-life.

33
Q

What is the benefit of ADP receptor blockers in IHD patients?

A

Reduction in the risk of atherothrombotic events in patients with IHD.

34
Q

What are the indications for Antithrombin III administration?

A

Used in hereditary antithrombin deficiency and in certain cases of heparin resistance.

35
Q

What is the mechanism of action of t-PA in thrombolysis?

A

It binds to fibrin in a thrombus and converts plasminogen to plasmin.

36
Q

What are the side effects of using Heparin?

A

Bleeding, heparin-induced thrombocytopenia, and osteoporosis with long-term use.

37
Q

What is the role of vitamin K in Warfarin therapy?

A

Vitamin K is necessary for the synthesis of clotting factors inhibited by Warfarin.

38
Q

How is Lepirudin dosed in anticoagulation?

A

It requires dose adjustments in renal impairment.

39
Q

What is the main use of Urokinase in clinical practice?

A

Primarily used in pulmonary embolism and severe deep vein thrombosis.

40
Q

Why is Clopidogrel preferred over Ticlopidine?

A

Due to a better safety profile and less severe side effects.

41
Q

What are the monitoring parameters for antiplatelet therapy?

A

Platelet counts, bleeding times, and signs of bleeding or bruising.

42
Q

What is the mechanism of action of Dipyridamole in combination with aspirin?

A

It enhances the antiplatelet effect of aspirin.

43
Q

What are the main indications for using Beta-blockers

A

43

44
Q

Why are lipid-lowering drugs important in IHD management?

A

They help reduce atherosclerotic plaque progression and risk of myocardial infarction.

45
Q

What is the importance of lifestyle modifications in IHD?

A

They complement drug therapy in reducing the risk and progression of IHD.

46
Q

How do oral antiplatelet agents prevent thrombus formation?

A

They target the adhesion, activation, or aggregation of platelets.

47
Q

What is the mechanism of action of aspirin as an antiplatelet agent?

A

Aspirin inhibits cyclooxygenase-1 (COX-1) to prevent platelet aggregation.

48
Q

What is the onset and duration of clopidogrel’s antiplatelet action?

A

Antiplatelet action within 2 hours, with a slow offset duration of 7-10 days.

49
Q

What is the mechanism of action of ticagrelor?

A

It inhibits P2Y12 through a unique mechanism allowing for quicker offset of action.

50
Q

What are the thrombin receptor antagonists used in antiplatelet therapy?

A

Vorapaxar and atopaxar.

51
Q

How do vitamin K antagonists like warfarin function?

A

They disrupt the formation of vitamin K-dependent clotting factors.

52
Q

What are Nonvitamin K oral anticoagulants (NOACs) and their excretion route?

A

NOACs include dabigatran and factor Xa inhibitors, partially excreted through the kidneys.

53
Q

How are NOACs used in venous thromboembolism treatment?

A

Initial therapy with parenteral heparin or higher-intensity NOACs, followed by usual or lower doses for extended prevention.

54
Q

What is the risk comparison of NOACs to warfarin regarding bleeding?

A

NOACs have reduced intracranial hemorrhage risk but increased gastrointestinal bleeding risk compared to warfarin.

55
Q

Is routine monitoring advised for NOAC agents?

A

No, but qualitative assessment can be made using prothrombin time or activated partial thromboplastin time if necessary.

Master YLL Pharmacology (36 decks)

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