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Pharmacology 2 EXAM > Blood Coagulation > Flashcards

Blood Coagulation Flashcards

1
Q

What is thrombosis?

A

The formation of an unwanted clot within blood vessels or the heart.

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2
Q

What is a thrombus?

A

A clot that adheres to a vessel wall.

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3
Q

What is an embolus?

A

A clot that floats within the blood.

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4
Q

Why are thrombi and emboli dangerous?

A

They may occlude blood vessels.

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5
Q

What are the steps required for clot formation?

A

Platelet activation and aggregation, formation of thrombin, production of fibrin, when cross-linked, stabilizes the clot.

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6
Q

How do platelets respond to vascular trauma?

A

By adhesion to the injury site, release of intracellular granules, and aggregation of the platelets.

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7
Q

What initiates the coagulation cascade leading to fibrin formation?

A

Factors released from injured tissue and platelets.

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8
Q

How is thrombin formed?

A

From prothrombin (factor II) by factor Xa.

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9
Q

What does thrombin catalyze?

A

The conversion of fibrinogen to fibrin.

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10
Q

What stabilizes the clot?

A

Cross-linking of fibrin strands.

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11
Q

What do endothelial cells maintain to prevent pathological thrombosis?

A

A nonthrombogenic lining in blood vessels.

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12
Q

How does the maintenance of transmural negative electrical charge help in preventing thrombosis?

A

It prevents the adhesion of circulating platelets.

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13
Q

What activates the fibrinolytic pathway?

A

The release of plasminogen activators.

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14
Q

What degrades coagulation factors in the prevention of thrombosis?

A

The activation of protein C.

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15
Q

What do Heparin-like proteoglycans do in preventing thrombosis?

A

Inhibit coagulation.

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16
Q

What is the role of prostacyclin (PGI2) in thrombosis prevention?

A

It is a potent inhibitor of platelet aggregation.

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17
Q

Name three categories of drugs that affect blood coagulation.

A

Platelet inhibitors, anticoagulants, thrombolytics.

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18
Q

List the platelet inhibitors.

A

Aspirin, ticlopidine, clopidogrel, abciximab, dipyridamole, eptifibatide.

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19
Q

Name the anticoagulants.

A

Heparin,
Low molecular weight heparin: Enoxaparin, tinzaparin.
Bivalirudin, Lepirudin: Not available in Jordan.
dalteparin, rivaroxaban.
Warfarin.
Dabigatran.
Apixaban.

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20
Q

Name the thrombolytics.

A

Alteplase, streptokinase, urokinase.

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21
Q

Name the drugs used in the treatment of bleeding.

A

Aminocaproic acid, protamine sulfate, vitamin K, tranexamic acid, aprotinin.

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22
Q

When should antiplatelet therapy be initiated after an infarction or stroke to obtain significant benefit?

A

Within 2 hours.

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23
Q

Why are antiplatelet drugs administered as adjuncts to thrombolytic therapy along with anticoagulants like heparin?

A

To maintain perfusion and limit the size of myocardial infarction.

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24
Q

What do platelet aggregation inhibitors target to interfere with platelet aggregation signals?

A

Inhibit COX-1, block GPIIb/IIIa, or ADP, or increase cAMP.

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25
Q

What is the goal of therapy with aspirin?

A

To selectively inhibit the synthesis of platelet thromboxane A2 by irreversibly inhibiting cyclooxygenase enzyme, thereby inhibiting platelet aggregation.

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26
Q

What does a small dose of aspirin inhibit?

A

Thromboxane synthesis in platelets (TXA2) but not prostacyclin (PGI2) synthesis in endothelium.

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27
Q

What is the dosage range for low-dose aspirin therapy?

A

81 to 325 mg per day.

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28
Q

What is the mechanism of action of aspirin?

A

Selective inhibition of COX-1 in low dose.

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29
Q

List the therapeutic uses of aspirin.

A

Prophylactic treatment of transient cerebral ischemia, reducing the incidence of recurrent myocardial infarction, decreasing mortality in post-myocardial infarction, and preventing coronary thrombosis in patients with unstable angina.

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30
Q

What are the adverse effects of aspirin?

A

Bleeding and gastrointestinal ulceration.

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31
Q

How do ticlopidine and clopidogrel inhibit platelet activation?

A

By blocking specific receptors for adenosine diphosphate (ADP) on the platelet membrane and inhibiting glycoprotein (GP IIb/IIIa) receptors.

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32
Q

What are the therapeutic uses of ticlopidine and clopidogrel?

A

Alternative prophylactic therapy to aspirin in secondary prevention of stroke, myocardial infarction, and unstable angina.

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33
Q

What is the most serious side effect of ticlopidine?

A

Neutropenia.

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34
Q

What other side effects are associated with ticlopidine?

A

Thrombocytopenia and aplastic anemia.

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35
Q

How is clopidogrel activated and what can diminish its action?

A

Clopidogrel is a prodrug activated by CYP450; hepatic enzyme inhibitors (e.g., omeprazole) can diminish its action.

36
Q

What is abciximab and why is its use limited?

A

A murine monoclonal antibody against GP IIb/IIIa; its use is limited because it is expensive.

37
Q

What is eptifibatide and how is it administered?

A

A GP IIb/IIIa blocker, available only IV because oral is too toxic.

38
Q

How does dipyridamole inhibit platelet aggregation?

A

By inhibiting phosphodiesterase, which increases cAMP in platelets.

39
Q

How is dipyridamole taken and what are its primary uses?

A

Taken orally; primary prophylaxis in patients with prosthetic heart valves (in combination with warfarin) and as prophylactic therapy to treat angina pectoris (in combination with aspirin).

40
Q

What is the main disadvantage of dipyridamole?

A

Headache.

41
Q

What is an advantage of dipyridamole compared to other platelet inhibitors?

A

No excess risk of bleeding.

42
Q

What are the two types of heparin used clinically?

A

Standard heparin and low-molecular-weight heparin (LMWH).

43
Q

How is LMWH derived?

A

From standard heparin.

44
Q

What is the advantage of LMWH over standard heparin?

A

Greater bioavailability and longer-lasting effect.

45
Q

Why is LMWH more effective than standard heparin?

A

It is more effective in preventing and treating venous thromboembolism.

46
Q

How is LMWH administered?

A

Subcutaneous administration (e.g., dalteparin, enoxaparin).

47
Q

What is a monitoring advantage of LMWH over standard heparin?

A

LMWH requires less monitoring.

48
Q

How does heparin work?

A

Binds to antithrombin III, inducing conformational changes that accelerate the interaction of antithrombin III with coagulation factors; also catalyzes the inhibition of thrombin by heparin cofactor II and factor Xa.

49
Q

What are the therapeutic uses of heparin?

A

Deep vein thrombosis, pulmonary embolism, myocardial infarction, and treating pregnant women with venous thromboembolism.

50
Q

How must heparin be administered?

A

Parenterally, either subcutaneously or intravenously.

51
Q

Why is intramuscular heparin contraindicated?

A

Because of hematoma formation.

52
Q

How quickly does maximal anticoagulant effect occur after IV heparin injection?

A

Within minutes.

53
Q

How is heparin prescribed?

A

On a unit basis rather than a milligram basis.

54
Q

What does heparin inhibit?

A

Both in-vitro and in-vivo clotting of blood.

55
Q

What are the adverse effects of heparin?

A

Bleeding and thrombocytopenia.

56
Q

In which conditions is heparin contraindicated?

A

Bleeding, recent surgery, liver disease, renal disease, severe hypertension, and thrombocytopenia.

57
Q

What is the mechanism of action of warfarin?

A

Warfarin is a vitamin K antagonist that induces hypocoagulability by forming structurally incomplete clotting factors.

58
Q

What are the therapeutic uses of warfarin?

A

Treatment of venous thrombosis and pulmonary emboli.

59
Q

What is the main adverse effect of warfarin?

A

Bleeding.

60
Q

How is warfarin administered?

A

Orally.

61
Q

How does warfarin differ from heparin in terms of hypocoagulability?

A

Warfarin induces hypocoagulability only in-vivo, unlike heparin.

62
Q

In which conditions is warfarin contraindicated?

A

Pregnancy, gastrointestinal ulceration, thrombocytopenia, hepatic or renal disease, recent surgery, and severe hypertension.

63
Q

What is the purpose of thrombolytic therapy?

A

Rapid lysis of already formed clots.

64
Q

How is fibrinolysis initiated?

A

By activation of the proenzyme plasminogen into plasmin.

65
Q

What does plasmin do in fibrinolysis?

A

Catalyzes the degradation of fibrin.

66
Q

What initiates the conversion of plasminogen to plasmin?

A

Plasminogen activators, tissue-type plasminogen activator, and single chain urokinase type plasminogen activator.

67
Q

How do older first-generation thrombolytic drugs compare to newer drugs?

A

They are not selective.

68
Q

What is alteplase (tPA) and its generation?

A

A second-generation tissue-type plasminogen activator.

69
Q

What are the therapeutic uses of alteplase?

A

Treatment of myocardial infarction, pulmonary embolism, and acute ischemic stroke.

70
Q

Why is alteplase superior to streptokinase and urokinase?

A

It is more effective in dissolving older clots.

71
Q

When should alteplase be administered for an ischemic stroke?

A

Within 3 hours of the ischemic stroke.

72
Q

What are the adverse effects of alteplase?

A

Bleeding, including gastrointestinal and cerebral hemorrhages.

73
Q

What are the therapeutic uses of streptokinase?

A

Acute pulmonary embolism, venous and arterial thrombosis, and acute myocardial infarction.

74
Q

What are the adverse effects of streptokinase?

A

Bleeding and hypersensitivity.

75
Q

What are the therapeutic uses of urokinase?

A

Severe pulmonary emboli and deep vein thrombosis.

76
Q

What is the main adverse effect of urokinase?

A

Bleeding.

77
Q

Name two third-generation thrombolytic drugs.

A

Reteplase and tenecteplase.

78
Q

What is anistreplase?

A

A preformed complex of streptokinase and plasminogen, and it’s a prodrug.

79
Q

In which conditions are thrombolytic drugs contraindicated?

A

Pregnancy, metastatic cancers, and history of cerebrovascular accidents.

80
Q

What are the therapeutic uses of aminocaproic acid and tranexamic acid?

A

To treat bleeding and overcome the effect of alteplase, streptokinase, and urokinase.

81
Q

What is the adverse effect of aminocaproic acid and tranexamic acid?

A

Intravenous thrombosis.

82
Q

What is the therapeutic use of protamine sulfate?

A

To treat bleeding and reverse the effect of heparin.

83
Q

What are the adverse effects of protamine sulfate?

A

Bradycardia, hypotension, and flushing.

84
Q

What is the therapeutic use of vitamin K?

A

To treat bleeding and overcome the effect of warfarin.

85
Q

How long does the response to vitamin K take?

A

24 hours (time required to synthesize new coagulation factors).

86
Q

What is the therapeutic use of sodium bicarbonate?

A

To treat aspirin toxicity by increasing renal elimination of aspirin.

87
Q

What is the therapeutic use of aprotinin?

A

Inhibits streptokinase bleeding.

Pharmacology 2 EXAM (6 decks)

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