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Claude Flashcards > Drugs for Blood Coagulation > Flashcards

Drugs for Blood Coagulation Flashcards

1
Q

What is thrombosis?

A

Unwanted clot formation. A thrombus adheres to the vessel wall, while an embolus floats within the blood. Both can occlude blood vessels.

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2
Q

What are the three main steps of clot formation?

A
  1. Platelet activation & aggregation.
  2. Thrombin formation.
  3. Fibrin production & cross-linking + stabilization of the clot.
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3
Q

List the steps of platelet aggregation.

A
  1. Adhesion to the site of injury.
  2. Release of intracellular granules.
  3. Aggregation of the platelets.
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4
Q

What substance released by platelets is a potent platelet aggregator?

A

Thromboxane A2.

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5
Q

What is the role of ADP in platelet function?

A

ADP is a platelet activator and aggregator.

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6
Q

What is the function of serotonin in platelet aggregation?

A

Serotonin enhances platelet aggregation.

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7
Q

What does PAF stand for and what is its function?

A

PAF stands for Platelet Activating Factor. It activates platelets.

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8
Q

What enzyme converts prothrombin to thrombin in the coagulation cascade?

A

Factor Xa.

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9
Q

What is the substrate and product of thrombin in fibrin formation?

A
  • Substrate: Fibrinogen.
  • Product: Fibrin.
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10
Q

What is the final step in stabilizing a blood clot?

A

Cross-linking of fibrin strands.

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11
Q

Name three natural mechanisms that prevent excessive clotting.

A
  1. Endothelial cells maintaining a non-clotting surface.
  2. Negative electrical charge preventing platelet adhesion.
  3. Release of plasminogen activators to break down clots.
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12
Q

What is the function of protein C in preventing excessive clotting?

A

Protein C degrades coagulation factors when activated.

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13
Q

How does prostacyclin (PGI2) help prevent excessive clotting?

A

Prostacyclin (PGI2) inhibits platelet aggregation.

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14
Q

When should anti-platelet therapy be initiated after infarction/stroke?

A

Within 2 hours.

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15
Q

What are the two main goals of anti-platelet therapy?

A
  1. Maintain blood flow.
  2. Limit infarction size.
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16
Q

What other therapies are often used alongside anti-platelet drugs?

A

Thrombolytic therapy and anticoagulants.

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17
Q

What is the primary mechanism of action of aspirin as an anti-platelet drug?

A

Selective COX-1 inhibition.

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18
Q

How does aspirin’s COX-1 inhibition affect platelet function?

A

It blocks thromboxane A2 synthesis in platelets.

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19
Q

What is the typical daily dose range of aspirin for anti-platelet therapy?

A

81-325 mg/day.

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20
Q

Name two uses of aspirin in cardiovascular disease prevention.

A
  1. Transient cerebral ischemia prophylaxis.
  2. Reduce myocardial infarction.
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21
Q

How does aspirin affect post-myocardial infarction mortality?

A

It lowers post-myocardial infarction mortality.

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22
Q

In which cardiac condition is aspirin used to prevent coronary thrombosis?

A

Unstable angina.

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23
Q

What are the two main side effects of aspirin when used as an anti-platelet agent?

A
  1. Bleeding.
  2. Gastrointestinal ulceration.
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24
Q

Why is a low dose of aspirin used for anti-platelet therapy?

A

For selective inhibition of COX-1.

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25
Q

Which anti-platelet drug works by selectively inhibiting COX-1?

A

Aspirin.

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26
Q

What is the mechanism of action of ADP Pathway Inhibitors like Ticlopidine and Clopidogrel?

A

They block ADP receptors on the platelet membrane.

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27
Q

How do ADP Pathway Inhibitors affect platelet function?

A

They inhibit ADP-mediated platelet activation and GP IIb/IIIa receptors.

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28
Q

Name two examples of ADP Pathway Inhibitors.

A

Ticlopidine and Clopidogrel.

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29
Q

In what situations are ADP Pathway Inhibitors used as an alternative to aspirin?

A

For secondary prevention of stroke, myocardial infarction, and unstable angina.

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30
Q

What are three potential side effects of ADP Pathway Inhibitors?

A
  1. Neutropenia.
  2. Thrombocytopenia.
  3. Aplastic anemia.
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31
Q

Which ADP Pathway Inhibitor is particularly associated with a risk of aplastic anemia?

A

Ticlopidine.

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32
Q

What is unique about Clopidogrel’s pharmacology?

A

Clopidogrel is a prodrug that must be activated by liver enzymes.

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33
Q

Which anti-platelet drugs work by blocking ADP receptors on platelet membranes?

A

ADP Pathway Inhibitors (e.g., Ticlopidine, Clopidogrel).

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34
Q

How do ADP Pathway Inhibitors differ from Aspirin in their mechanism of action?

A

ADP Pathway Inhibitors block ADP receptors, while Aspirin inhibits COX-1 enzyme.

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35
Q

Why might a doctor choose an ADP Pathway Inhibitor over Aspirin for a patient?

A

As an alternative when Aspirin is not suitable or effective for secondary prevention of stroke, myocardial infarction, or unstable angina.

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36
Q

What are two examples of Glycoprotein IIb/IIIa Receptor Inhibitors?

A

Abciximab (a monoclonal antibody) and Eptifibatide.

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37
Q

What is the mechanism of action of Glycoprotein IIb/IIIa Receptor Inhibitors?

A

They directly block GP IIb/IIIa receptors on platelets.

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38
Q

What are two limitations of Glycoprotein IIb/IIIa Receptor Inhibitors?

A
  1. They are expensive.
  2. They are available only as IV formulations (e.g., Eptifibatide).
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39
Q

What class of drugs does Dipyridamole belong to?

A

Phosphodiesterase Inhibitors.

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40
Q

What is the mechanism of action of Phosphodiesterase Inhibitors like Dipyridamole?

A

They increase cAMP levels in platelets.

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41
Q

How do Phosphodiesterase Inhibitors affect platelet function?

A

They inhibit platelet aggregation.

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42
Q

In what clinical scenario is Dipyridamole used with Warfarin?

A

For prophylaxis in patients with prosthetic heart valves.

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43
Q

How is Dipyridamole used in combination with Aspirin?

A

For treatment of angina pectoris.

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44
Q

What is the main side effect of Dipyridamole?

A

Headache.

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45
Q

Does Dipyridamole increase the risk of bleeding?

A

No, there is no excess risk of bleeding.

46
Q

Which antiplatelet drug works by increasing cAMP in platelets?

A

Dipyridamole.

47
Q

How do Glycoprotein IIb/IIIa Receptor Inhibitors differ from ADP Pathway Inhibitors in their mechanism?

A

Glycoprotein IIb/IIIa Receptor Inhibitors directly block GP IIb/IIIa receptors, while ADP Pathway Inhibitors block ADP receptors, indirectly affecting GP IIb/IIIa activation.

48
Q

What are the two main types of Heparin?

A

Standard heparin and Low Molecular Weight Heparin (LMWH).

49
Q

Name two advantages of LMWH over standard heparin.

A
  1. Better bioavailability.
  2. Longer-lasting effect.
50
Q

What is the primary mechanism of action of Heparin?

A

It binds to antithrombin III and accelerates its interaction with coagulation factors.

51
Q

How does Heparin affect thrombin and Factor Xa?

A

It catalyzes their inhibition by heparin cofactor II and antithrombin III.

52
Q

List three therapeutic uses of Heparin.

A
  1. Deep vein thrombosis.
  2. Pulmonary embolism.
  3. Myocardial infarction.
53
Q

Why is Heparin preferred for pregnant women with venous thromboembolism?

A

It doesn’t cross the placenta, making it safer for the fetus.

54
Q

What are the two routes of administration for Heparin?

A

Subcutaneous (SC) and Intravenous (IV).

55
Q

How quickly does IV Heparin achieve maximal anti-coagulation effects?

A

Within minutes after injection.

56
Q

How is Heparin dosage prescribed?

A

On a unit basis rather than milligram basis.

57
Q

What are the two main adverse effects of Heparin?

A

Bleeding and thrombocytopenia.

58
Q

List three conditions in which Heparin is contraindicated.

A
  1. Recent surgery.
  2. Severe hypertension.
  3. Thrombocytopenia.
59
Q

What advantage does LMWH have in terms of monitoring?

A

It requires less monitoring than standard heparin.

60
Q

Name two examples of LMWH.

A

Dalteparin and Enoxaparin

61
Q

How does Heparin affect blood clotting in vitro and in vivo?

A

Heparin inhibits blood clotting both in vitro and in vivo.

62
Q

What is the primary mechanism of action of Warfarin?

A

It acts as a Vitamin K antagonist.

63
Q

How does Warfarin affect clotting factors?

A

It interferes with the production of vitamin K-dependent clotting factors (II, VII, IX, X).

64
Q

What is the result of Warfarin’s effect on clotting factors?

A

It causes the formation of incomplete clotting factors.

65
Q

How is Warfarin administered?

A

Orally.

66
Q

How does Warfarin differ from Heparin in terms of in vitro and in vivo effectiveness?

A

Warfarin is only effective in vivo, while Heparin works both in vitro and in vivo.

67
Q

What are two main clinical uses of Warfarin?

A
  1. Venous thrombosis.
  2. Pulmonary embolism.
68
Q

What is the primary side effect of Warfarin?

A

Bleeding.

69
Q

Why is Warfarin contraindicated during pregnancy?

A

It can cross the placenta and cause fetal abnormalities or bleeding.

70
Q

List three contraindications for Warfarin use.

A
  1. Active or past gastrointestinal ulceration.
  2. Thrombocytopenia.
  3. Liver or kidney disease.
71
Q

How does recent surgery affect the use of Warfarin?

A

Recent surgery is a contraindication for Warfarin use due to increased bleeding risk.

72
Q

Why is severe hypertension a contraindication for Warfarin?

A

Severe hypertension increases the risk of bleeding complications with Warfarin.

73
Q

Which oral anticoagulant works by antagonizing Vitamin K?

A

Warfarin.

74
Q

Name the four vitamin K-dependent clotting factors affected by Warfarin.

A

Factors II, VII, IX, and X.

75
Q

What is the main purpose of thrombolytic therapy?

A

Rapid lysis of already-formed clots

76
Q

What is the primary mechanism of action of thrombolytic drugs?

A

They activate plasminogen to plasmin.

77
Q

How does plasmin affect blood clots?

A

Plasmin breaks down fibrin in clots.

78
Q

What initiates the thrombolytic process?

A

Plasminogen activators.

79
Q

What are two examples of first-generation (non-selective) thrombolytic drugs?

A

Streptokinase and Urokinase.

80
Q

List three clinical uses of Streptokinase.

A
  1. Acute pulmonary embolism.
  2. Venous & arterial thrombosis.
  3. Acute myocardial infarction.
81
Q

What are the two main side effects of Streptokinase?

A

Bleeding and hypersensitivity reactions.

82
Q

What are two clinical uses of Urokinase?

A
  1. Severe pulmonary emboli.
  2. Deep vein thrombosis.
83
Q

What is the primary side effect of Urokinase?

A

Bleeding.

84
Q

How do thrombolytic drugs differ from anticoagulants in their primary action?

A

Thrombolytics break down existing clots, while anticoagulants prevent new clot formation.

85
Q

Which thrombolytic drug is associated with hypersensitivity reactions?

A

Streptokinase.

86
Q

In the context of thrombolytic therapy, what is the role of plasminogen?

A

Plasminogen is converted to plasmin, which then breaks down fibrin in clots.

87
Q

Why are Streptokinase and Urokinase considered “non-selective” thrombolytics?

A

They activate both circulating and clot-bound plasminogen, potentially increasing bleeding risk.

88
Q

What is the full name of tPA?

A

Tissue-type plasminogen activator (now known as Alteplase).

89
Q

List three clinical uses of Alteplase.

A
  1. Myocardial infarction.
  2. Pulmonary embolism.
  3. Acute ischemic stroke.
90
Q

What advantage does Alteplase have over first-generation thrombolytics?

A

It is more effective on older clots.

91
Q

Within what time frame should Alteplase be administered for acute ischemic stroke?

A

Within 3 hours of stroke onset.

92
Q

What are the main side effects of Alteplase?

A

Bleeding, including gastrointestinal and cerebral hemorrhages.

93
Q

Name two examples of third-generation thrombolytic drugs.

A

Reteplase and Tenecteplase.

94
Q

What is Anistreplase?

A

A preformed complex of streptokinase and plasminogen.

95
Q

How does Anistreplase differ from other thrombolytics in terms of its pharmacology?

A

It acts as a prodrug.

96
Q

Which thrombolytic drug should be administered within 3 hours of an ischemic stroke?

A

Alteplase (tPA).

97
Q

How does Alteplase’s selectivity compare to first-generation thrombolytics?

A

Alteplase is more selective, preferentially activating fibrin-bound plasminogen

98
Q

What is the main risk associated with all thrombolytic drugs, including Alteplase?

A

Bleeding complications.

99
Q

In what way is Anistreplase related to first-generation thrombolytics?

A

It contains streptokinase, which is a first-generation thrombolytic.

100
Q

What are the two main purposes of drugs used to stop bleeding?

A
  1. To counteract the effects of anticoagulants and thrombolytics.
  2. To stop or prevent excessive bleeding.
101
Q

What is the primary use of Aminocaproic acid and Tranexamic acid?

A

To counteract the effects of thrombolytic drugs (e.g., alteplase, streptokinase, urokinase).

102
Q

What is a potential side effect of Aminocaproic acid and Tranexamic acid?

A

Risk of intravenous thrombosis.

103
Q

List three side effects of Protamine sulfate.

A

Bradycardia, hypotension, and flushing.

104
Q

What anticoagulant does Vitamin K counteract?

A

Warfarin.

105
Q

Why does Vitamin K have a slow response in reversing warfarin’s effects?

A

It takes about 24 hours due to the time needed for new coagulation factor synthesis.

106
Q

What is the purpose of using Sodium bicarbonate in the context of bleeding control?

A

To treat aspirin toxicity.

107
Q

How does Sodium bicarbonate work to treat aspirin toxicity?

A

It increases renal elimination of aspirin.

108
Q

What is the primary use of Aprotinin?

A

To inhibit streptokinase-induced bleeding.

109
Q

Which drug is used to reverse the effects of heparin?

A

Protamine sulfate.

110
Q

Which drugs are used to counteract the effects of thrombolytic drugs like alteplase?

A

Aminocaproic acid and Tranexamic acid.

111
Q

Why might there be a delay in the effect of Vitamin K when used to counteract warfarin?

A

Because it takes time for new coagulation factors to be synthesized.

112
Q

What is the main purpose of Protamine sulfate?

A

To reverse the anticoagulant effect of heparin.

Claude Flashcards (6 decks)

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