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Pharma2 MCQs > Drugs for Blood Coagulation > Flashcards

Drugs for Blood Coagulation Flashcards

1
Q

Thrombosis is the formation of an unwanted clot within:
a. The brain
b. The liver
c. The blood vessels or the heart
d. The lungs

A

c. The blood vessels or the heart

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2
Q

A clot that adheres to a vessel wall is called:
a. Embolus
b. Thrombus
c. Platelet
d. Fibrin

A

b. Thrombus

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3
Q

Embolus refers to:
a. A clot that adheres to a vessel wall
b. A clot that floats within the blood
c. A clot that forms in the liver
d. A clot that is dissolved

A

b. A clot that floats within the blood

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4
Q

Why are both thrombi and emboli dangerous?
a. They cause hypertension
b. They may occlude blood vessels
c. They increase heart rate
d. They decrease blood pressure

A

b. They may occlude blood vessels

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5
Q

Clot formation requires which of the following processes?
a. Deactivation of platelets
b. Dissolution of thrombin
c. Platelet activation and aggregation, followed by formation of thrombin
d. Reduction in fibrin production

A

c. Platelet activation and aggregation, followed by formation of thrombin

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6
Q

What stabilizes a clot once it is formed?
a. Hemoglobin
b. Cross-linked fibrin
c. Red blood cells
d. White blood cells

A

b. Cross-linked fibrin

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7
Q

Platelets respond to vascular trauma by:
a. Aggregation only
b. Adhesion, release of intracellular granules, and aggregation
c. Release of fibrin
d. Dissolving clots

A

b. Adhesion, release of intracellular granules, and aggregation

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8
Q

The first step in platelet response to vascular trauma is:
a. Release of intracellular granules
b. Adhesion to the site of injury
c. Aggregation of the platelets
d. Activation of thrombin

A

b. Adhesion to the site of injury

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9
Q

During platelet response, what occurs after adhesion to the site of injury?
a. Aggregation of platelets
b. Release of intracellular granules
c. Formation of fibrin
d. Activation of thrombin

A

b. Release of intracellular granules

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10
Q

Which of the following is the final step in platelet response to vascular trauma?
a. Adhesion to the site of injury
b. Release of intracellular granules
c. Aggregation of the platelets
d. Release of serotonin

A

c. Aggregation of the platelets

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11
Q

What chemical mediators are released by platelets during vascular trauma response?
a. Hemoglobin and fibrin
b. Thromboxane A2, ADP, serotonin, PAF
c. Collagen fibers and fibrin
d. Calcium and potassium

A

b. Thromboxane A2, ADP, serotonin, PAF

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12
Q

Platelets are recruited into the platelet plug by:
a. Chemical mediators released by platelets
b. Red blood cells
c. White blood cells
d. Endothelial cells

A

a. Chemical mediators released by platelets

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13
Q

What stimulates the coagulation cascade during fibrin formation?
a. Hemoglobin
b. Red blood cells
c. Factors released from injured tissue and platelets
d. White blood cells

A

c. Factors released from injured tissue and platelets

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14
Q

Prothrombin (factor II) is converted to thrombin by:
a. Factor VIII
b. Factor Xa
c. Factor XII
d. Factor XIII

A

b. Factor Xa

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15
Q

Thrombin catalyzes the conversion of:
a. Prothrombin to fibrinogen
b. Fibrinogen to fibrin
c. Fibrin to prothrombin
d. Plasminogen to plasmin

A

b. Fibrinogen to fibrin

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16
Q

Which factor is responsible for the cross-linking of fibrin strands to stabilize the clot?
a. Factor XIII
b. Factor XI
c. Factor VII
d. Factor IX

A

a. Factor XIII

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17
Q

The role of thrombin in the coagulation cascade is to:
a. Activate platelets
b. Catalyze the conversion of fibrinogen to fibrin
c. Degrade fibrin strands
d. Inhibit coagulation factors

A

b. Catalyze the conversion of fibrinogen to fibrin

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18
Q

Which pathway(s) are involved in the coagulation cascade that leads to fibrin formation?
a. Extrinsic pathway only
b. Intrinsic pathway only
c. Both intrinsic and extrinsic pathways
d. Neither pathway

A

c. Both intrinsic and extrinsic pathways

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19
Q

Factors released from injured tissue primarily affect which part of the coagulation process?
a. Initiation of the coagulation cascade
b. Breakdown of the clot
c. Deactivation of platelets
d. Conversion of plasminogen to plasmin

A

a. Initiation of the coagulation cascade

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20
Q

What is the final product that stabilizes the clot in the coagulation cascade?
a. Prothrombin
b. Cross-linked fibrin
c. Thrombin
d. Plasmin

A

b. Cross-linked fibrin

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21
Q

Endothelial cells maintain a nonthrombogenic lining in blood vessels by:
a. Increasing platelet adhesion
b. Maintaining a transmural negative electrical charge
c. Decreasing fibrinolytic activity
d. Promoting coagulation factors

A

b. Maintaining a transmural negative electrical charge

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22
Q

Which of the following is important in preventing the adhesion of circulating platelets?
a. Activation of protein C
b. Transmural negative electrical charge
c. Production of prostacyclin
d. Release of fibrinogen

A

b. Transmural negative electrical charge

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23
Q

The release of plasminogen activators:
a. Inhibits coagulation
b. Activates the fibrinolytic pathway
c. Promotes platelet aggregation
d. Decreases protein C activity

A

b. Activates the fibrinolytic pathway

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24
Q

Protein C degrades:
a. Plasmin
b. Coagulation factors
c. Fibrinogen
d. Prostacyclin

A

b. Coagulation factors

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25
Q

The production of heparin-like proteoglycans:
a. Promotes platelet aggregation
b. Activates fibrinogen
c. Inhibits coagulation
d. Degrades fibrin

A

c. Inhibits coagulation

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26
Q

Prostacyclin (PGI2) is a potent inhibitor of:
a. Fibrin formation
b. Coagulation factors
c. Platelet aggregation
d. Plasmin activity

A

c. Platelet aggregation

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27
Q

Which of the following mechanisms helps to prevent pathological thrombosis?
a. Activation of fibrinogen
b. Inhibition of plasminogen activators
c. Maintenance of a nonthrombogenic endothelial lining
d. Reduction of heparin production

A

c. Maintenance of a nonthrombogenic endothelial lining

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28
Q

The fibrinolytic pathway is activated by:
a. Protein C
b. Prostacyclin
c. Plasminogen activators
d. Plasmin inhibitors

A

c. Plasminogen activators

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29
Q

Which of the following is a platelet inhibitor?
a. Aspirin
b. Heparin
c. Alteplase
d. Aminocaproic acid

A

a. Aspirin

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30
Q

Which drug is an anticoagulant?
a. Streptokinase
b. Clopidogrel
c. Warfarin
d. Tranexamic acid

A

c. Warfarin

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31
Q

Alteplase is classified as a:
a. Thrombolytic
b. Platelet inhibitor
c. Anticoagulant
d. Treatment for bleeding

A

a. Thrombolytic

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32
Q

Which of the following drugs is used in the treatment of bleeding?
a. Enoxaparin
b. Protamine sulfate
c. Eptifibatide
d. Urokinase

A

b. Protamine sulfate

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33
Q

Clopidogrel is an example of a:
a. Thrombolytic
b. Anticoagulant
c. Platelet inhibitor
d. Treatment for bleeding

A

c. Platelet inhibitor

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34
Q

Heparin is categorized under:
a. Thrombolytics
b. Anticoagulants
c. Platelet inhibitors
d. Treatments for bleeding

A

b. Anticoagulants

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35
Q

Which of the following is a thrombolytic drug?
a. Dipyridamole
b. Streptokinase
c. Rivaroxaban
d. Vitamin K

A

b. Streptokinase

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36
Q

What is the function of Vitamin K in relation to blood coagulation?
a. Acts as a platelet inhibitor
b. Serves as an anticoagulant
c. Treats bleeding
d. Functions as a thrombolytic

A

c. Treats bleeding

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37
Q

Which anticoagulant is a direct thrombin inhibitor?
a. Aspirin
b. Bivalirudin
c. Alteplase
d. Protamine sulfate

A

b. Bivalirudin

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38
Q

Abciximab is classified as a:
a. Platelet inhibitor
b. Thrombolytic
c. Anticoagulant
d. Treatment for bleeding

A

a. Platelet inhibitor

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39
Q

Which drug among the following is a low molecular weight heparin?
a. Warfarin
b. Eptifibatide
c. Enoxaparin
d. Tranexamic acid

A

c. Enoxaparin

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40
Q

A drug that inhibits platelet aggregation by blocking the glycoprotein IIb/IIIa receptor is:
a. Eptifibatide
b. Dalteparin
c. Alteplase
d. Vitamin K

A

a. Eptifibatide

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41
Q

Antiplatelet therapy must be initiated within how many hours after an infarction or stroke to obtain significant benefit?
a. 1 hour
b. 2 hours
c. 3 hours
d. 4 hours

A

b. 2 hours

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42
Q

Antiplatelet drugs are administered as adjuncts to which type of therapy to maintain perfusion and limit the size of myocardial infarction?
a. Thrombolytic therapy
b. Anticoagulant therapy alone
c. Platelet aggregation inhibitors alone
d. Anti-inflammatory therapy

A

a. Thrombolytic therapy

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43
Q

Platelet aggregation inhibitors work by:
a. Activating COX-1
b. Inhibiting COX-1, blocking GPIIb/IIIa, or ADP, or increasing cAMP
c. Enhancing platelet aggregation signals
d. Reducing cAMP levels

A

b. Inhibiting COX-1, blocking GPIIb/IIIa, or ADP, or increasing cAMP

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44
Q

What does elevated calcium (Ca2+) cause in the context of platelet aggregation?
a. Reduction in platelet granule release
b. Decrease in thromboxane A2 synthesis
c. Release of platelet granules, activation of thromboxane A2 synthesis, and activation of GP IIb/IIIa receptors
d. Inhibition of GP IIb/IIIa receptors

A

c. Release of platelet granules, activation of thromboxane A2 synthesis, and activation of GP IIb/IIIa receptors

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45
Q

What are the primary actions of thromboxane A2 in platelet aggregation?
a. Release of platelet granules and activation of GP IIb/IIIa receptors
b. Inhibition of platelet granules
c. Activation of plasminogen activators
d. Degradation of fibrinogen

A

a. Release of platelet granules and activation of GP IIb/IIIa receptors

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46
Q

What role does cAMP play in platelet aggregation inhibition?
a. Decreases platelet aggregation
b. Interferes in the signals that promote platelet aggregation
c. Enhances COX-1 activity
d. Promotes thromboxane A2 synthesis

A

b. Interferes in the signals that promote platelet aggregation

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47
Q

Which receptors are activated as part of the platelet aggregation process?
a. COX-1 receptors
b. ADP receptors
c. GP IIb/IIIa receptors
d. cAMP receptors

A

c. GP IIb/IIIa receptors

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48
Q

After an infarction or stroke, antiplatelet drugs are used alongside which other type of drug to prevent blood clots?
a. Thrombolytic agents only
b. Anticoagulants (e.g., heparin)
c. Anti-inflammatory drugs
d. Beta-blockers

A

b. Anticoagulants (e.g., heparin)

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49
Q

Which of the following is NOT a mechanism by which platelet aggregation inhibitors function?
a. Inhibiting COX-1
b. Blocking GPIIb/IIIa receptors
c. Increasing cAMP
d. Promoting thromboxane A2 synthesis

A

d. Promoting thromboxane A2 synthesis

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50
Q

Which of the following substances is directly involved in the activation of GP IIb/IIIa receptors?
a. cAMP
b. COX-1
c. Thromboxane A2
d. ADP

A

c. Thromboxane A2

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51
Q

The goal of therapy with aspirin is to selectively inhibit the synthesis of:
a. Thromboxane A2
b. Prostacyclin (PGI2)
c. Fibrinogen
d. ADP

A

a. Thromboxane A2

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52
Q

Aspirin irreversibly inhibits which enzyme to inhibit platelet aggregation?
a. Thrombin
b. Cyclooxygenase enzyme (COX1)
c. Phospholipase
d. Protease

A

b. Cyclooxygenase enzyme (COX1)

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53
Q

At low doses, aspirin inhibits the synthesis of which substance in platelets?
a. Thromboxane A2 (TXA2)
b. Prostacyclin (PGI2)
c. Fibrinogen
d. ADP

A

a. Thromboxane A2 (TXA2)

54
Q

What is the range of low doses of aspirin used to inhibit COX1?
a. 81 to 325 mg per day
b. 10 to 50 mg per day
c. 400 to 800 mg per day
d. 500 to 1000 mg per day

A

a. 81 to 325 mg per day

55
Q

Which of the following is NOT a therapeutic use of aspirin?
a. Prophylactic treatment of transient cerebral ischemia
b. Reduction of recurrent myocardial infarction
c. Decrease in post-myocardial infarction mortality
d. Treatment of acute deep vein thrombosis

A

d. Treatment of acute deep vein thrombosis

56
Q

Aspirin is useful for preventing coronary thrombosis in patients with:
a. Stable angina
b. Unstable angina
c. Chronic heart failure
d. Peripheral artery disease

A

b. Unstable angina

57
Q

One of the adverse effects of aspirin is:
a. Bleeding
b. Hypertension
c. Tachycardia
d. Bradycardia

A

a. Bleeding

58
Q

An adverse effect of aspirin is:
a. Nephrotoxicity
b. Gastrointestinal ulceration
c. Hepatotoxicity
d. Hyperkalemia

A

b. Gastrointestinal ulceration

59
Q

The inhibition of COX1 by aspirin results in:
a. Reduced thromboxane A2 synthesis
b. Increased prostacyclin synthesis
c. Decreased platelet production
d. Increased fibrin production

A

a. Reduced thromboxane A2 synthesis

60
Q

Which of the following is selectively inhibited by a low dose of aspirin?
a. COX1
b. COX2
c. ADP receptors
d. GP IIb/IIIa receptors

A

a. COX1

61
Q

The mechanism of action of Ticlopidine and Clopidogrel involves:
a. Inhibiting COX-1
b. Blocking specific receptors for adenosine diphosphate (ADP) on the platelet membrane
c. Activating thromboxane A2
d. Inhibiting plasminogen activators

A

b. Blocking specific receptors for adenosine diphosphate (ADP) on the platelet membrane

62
Q

Ticlopidine and Clopidogrel inhibit which glycoprotein receptors?
a. GP IIa/IIb
b. GP Ib/IX
c. GP IIb/IIIa
d. GP IV

A

c. GP IIb/IIIa

63
Q

What is a therapeutic use of Ticlopidine and Clopidogrel?
a. Primary treatment of myocardial infarction
b. Alternative prophylactic therapy to aspirin in secondary prevention of stroke and myocardial infarction
c. Treatment of chronic heart failure
d. Management of acute deep vein thrombosis

A

b. Alternative prophylactic therapy to aspirin in secondary prevention of stroke and myocardial infarction

64
Q

Which adverse effect is most serious with Ticlopidine use?
a. Thrombocytopenia
b. Neutropenia
c. Gastrointestinal ulceration
d. Hypertension

A

b. Neutropenia

65
Q

Other side effects of Ticlopidine include:
a. Hypertension and bradycardia
b. Thrombocytopenia and aplastic anemia
c. Hyperkalemia and hepatotoxicity
d. Nephrotoxicity and tachycardia

A

b. Thrombocytopenia and aplastic anemia

66
Q

Clopidogrel is classified as a:
a. Prodrug
b. Direct-acting drug
c. Anticoagulant
d. Thrombolytic

A

a. Prodrug

67
Q

Clopidogrel is activated by which enzyme?
a. COX-1
b. GP IIb/IIIa
c. CYP450
d. Plasminogen

A

c. CYP450

68
Q

The action of Clopidogrel can be diminished by:
a. Hepatic enzyme inhibitors (e.g., omeprazole)
b. NSAIDs
c. Beta-blockers
d. Calcium channel blockers

A

a. Hepatic enzyme inhibitors (e.g., omeprazole)

69
Q

Which of the following is NOT a therapeutic use of Clopidogrel?
a. Prevention of stroke
b. Treatment of acute myocardial infarction
c. Secondary prevention of myocardial infarction
d. Management of unstable angina

A

b. Treatment of acute myocardial infarction

70
Q

Ticlopidine and Clopidogrel work by:
a. Enhancing platelet aggregation
b. Inhibiting platelet activation
c. Activating thromboxane A2
d. Blocking fibrinogen synthesis

A

b. Inhibiting platelet activation

71
Q

Abciximab is a:
a. Murine monoclonal antibody against the GP IIb/IIIa receptor
b. Phosphodiesterase inhibitor
c. COX-1 inhibitor
d. Prodrug activated by CYP450

A

a. Murine monoclonal antibody against the GP IIb/IIIa receptor

72
Q

Why is the use of Abciximab limited?
a. It has severe gastrointestinal side effects
b. It is expensive
c. It is only available orally
d. It has a short half-life

A

b. It is expensive

73
Q

Eptifibatide is available only in which form due to its toxicity when taken orally?
a. Oral
b. Intravenous (IV)
c. Subcutaneous
d. Intramuscular

A

b. Intravenous (IV)

74
Q

Eptifibatide is a blocker of which receptor?
a. COX-1
b. ADP
c. GP IIb/IIIa
d. Thromboxane A2

A

c. GP IIb/IIIa

75
Q

Dipyridamole works by inhibiting which enzyme?
a. COX-1
b. Phosphodiesterase
c. ADP receptor
d. GP IIb/IIIa receptor

A

b. Phosphodiesterase

76
Q

Inhibition of phosphodiesterase by Dipyridamole results in an increase in:
a. Calcium levels
b. cAMP in platelets
c. Thromboxane A2 synthesis
d. Fibrinogen levels

A

b. cAMP in platelets

77
Q

One of the primary prophylactic uses of Dipyridamole is in patients with:
a. Prosthetic heart valves (in combination with warfarin)
b. Chronic kidney disease
c. Diabetes mellitus
d. Hypertension

A

a. Prosthetic heart valves (in combination with warfarin)

78
Q

Dipyridamole is used as prophylactic therapy to treat angina pectoris in combination with:
a. Warfarin
b. Aspirin
c. Clopidogrel
d. Heparin

A

b. Aspirin

79
Q

A disadvantage of Dipyridamole is:
a. Headache
b. Gastrointestinal bleeding
c. Neutropenia
d. Hypertension

A

a. Headache

80
Q

An advantage of Dipyridamole is that it has:
a. No excess risk of bleeding
b. A short half-life
c. No drug interactions
d. Rapid onset of action

A

a. No excess risk of bleeding

81
Q

The older type of heparin is known as:
a. Standard heparin
b. Low-molecular-weight heparin (LMWH)
c. Synthetic heparin
d. Unfractionated heparin

A

a. Standard heparin

82
Q

Low-molecular-weight heparin (LMWH) is derived from:
a. Animal extract
b. Standard heparin
c. Synthetic sources
d. Plant extract

A

b. Standard heparin

83
Q

LMWH has greater _______ than standard heparin.
a. Bioavailability
b. Toxicity
c. Cost
d. Molecular weight

A

a. Bioavailability

84
Q

One of the advantages of LMWH over standard heparin is:
a. Shorter duration of action
b. Longer-lasting effect
c. Higher risk of bleeding
d. Requirement for frequent monitoring

A

b. Longer-lasting effect

85
Q

LMWH is more effective than standard heparin in:
a. Increasing platelet count
b. Preventing and treating venous thromboembolism
c. Treating arterial thrombosis
d. Managing hypertension

A

b. Preventing and treating venous thromboembolism

86
Q

How is LMWH administered?
a. Orally
b. Subcutaneously
c. Intravenously
d. Intramuscularly

A

b. Subcutaneously

87
Q

Which of the following is an example of LMWH?
a. Warfarin
b. Aspirin
c. Enoxaparin
d. Clopidogrel

A

c. Enoxaparin

88
Q

LMWH requires less _______ than standard heparin.
a. Dosage
b. Monitoring
c. Efficacy
d. Bioavailability

A

b. Monitoring

89
Q

Heparin binds to which protein to exert its anticoagulant effect?
a. Fibrinogen
b. Thrombin
c. Antithrombin III
d. Plasminogen

A

c. Antithrombin III

90
Q

The interaction of heparin with antithrombin III accelerates the inhibition of:
a. Thrombin and factor Xa
b. Fibrin and fibrinogen
c. Plasmin and plasminogen
d. Platelets and ADP

A

a. Thrombin and factor Xa

91
Q

The conformational changes induced by heparin in antithrombin III lead to:
a. Increased platelet aggregation
b. Accelerated inhibition of coagulation factors
c. Activation of thromboxane A2
d. Stimulation of fibrin production

A

b. Accelerated inhibition of coagulation factors

92
Q

Which of the following is a therapeutic use of heparin?
a. Deep vein thrombosis
b. Hypertension
c. Diabetes mellitus
d. Hyperlipidemia

A

a. Deep vein thrombosis

93
Q

Heparin is the anticoagulant of choice for treating pregnant women with:
a. Myocardial infarction
b. Venous thromboembolism
c. Pulmonary hypertension
d. Arterial thrombosis

A

b. Venous thromboembolism

94
Q

How must heparin be administered?
a. Parenterally either subcutaneously or intravenously
b. Orally
c. Intramuscularly
d. Topically

A

a. Parenterally either subcutaneously or intravenously

95
Q

Why is intramuscular heparin contraindicated?
a. It is ineffective
b. It can cause hematoma formation
c. It has a slow onset of action
d. It is poorly absorbed

A

b. It can cause hematoma formation

96
Q

Maximal anticoagulant effect of heparin occurs within minutes after:
a. Oral administration
b. IV heparin injection
c. Subcutaneous injection
d. Intramuscular injection

A

b. IV heparin injection

97
Q

Heparin is prescribed on which basis?
a. Milligram
b. Unit
c. Volume
d. Percentage

A

b. Unit

98
Q

Heparin inhibits clotting of blood:
a. Both in vitro and in vivo
b. Only in vitro
c. Only in vivo
d. Neither in vitro nor in vivo

A

a. Both in vitro and in vivo

99
Q

One of the adverse effects of heparin is:
a. Bleeding
b. Hypertension
c. Tachycardia
d. Hyperkalemia

A

a. Bleeding

100
Q

Another adverse effect of heparin is:
a. Neutropenia
b. Hepatotoxicity
c. Thrombocytopenia
d. Nephrotoxicity

A

c. Thrombocytopenia

101
Q

Heparin is contraindicated in patients with:
a. Diabetes mellitus
b. Chronic obstructive pulmonary disease
c. Recent surgery, liver or renal disease, severe hypertension, and thrombocytopenia
d. Hyperlipidemia

A

c. Recent surgery, liver or renal disease, severe hypertension, and thrombocytopenia

102
Q

Warfarin is a vitamin K antagonist required to catalyze the conversion of which clotting factors?
a. II, VII, IX, XI
b. I, II, V, X
c. II, VII, IX, X
d. III, V, VIII, X

A

c. II, VII, IX, X

103
Q

What is the primary therapeutic use of Warfarin?
a. Treatment of myocardial infarction
b. Treatment of stroke
c. Treatment of venous thrombosis and pulmonary emboli
d. Treatment of hypertension

A

c. Treatment of venous thrombosis and pulmonary emboli

104
Q

Which of the following is a significant adverse effect of Warfarin?
a. Nausea
b. Rash
c. Bleeding
d. Drowsiness

A

c. Bleeding

105
Q

How is Warfarin administered?
a. Intravenously
b. Subcutaneously
c. Orally
d. Topically

A

c. Orally

106
Q

Unlike heparin, Warfarin induces hypocoagulability only in:
a. In vitro
b. In silico
c. In vivo
d. In situ

A

c. In vivo

107
Q

Which of the following is NOT a contraindication for Warfarin use?
a. Asthma
b. Pregnancy
c. Gastrointestinal ulceration
d. Severe hypertension

A

a. Asthma

108
Q

What is the primary purpose of thrombolytic therapy?
a. Prevention of clot formation
b. Rapid lysis of already formed clots
c. Reduction of platelet aggregation
d. Inhibition of thrombin formation

A

b. Rapid lysis of already formed clots

109
Q

Which enzyme’s activation initiates fibrinolysis?
a. Thrombin
b. Factor X
c. Plasminogen
d. Fibrinogen

A

c. Plasminogen

110
Q

Older first-generation thrombolytic drugs are characterized by:
a. Higher specificity
b. Lack of selectivity
c. Lower efficacy
d. Longer duration of action

A

b. Lack of selectivity

110
Q

Alteplase (tPA) is used for the treatment of which conditions?
a. Hypertension and atrial fibrillation
b. Chronic obstructive pulmonary disease
c. Myocardial infarction, pulmonary embolism, and acute ischemic stroke
d. Deep vein thrombosis and varicose veins

A

c. Myocardial infarction, pulmonary embolism, and acute ischemic stroke

110
Q

What is a significant adverse effect of Alteplase (tPA)?
a. Hypertension
b. Bleeding including gastrointestinal and cerebral hemorrhages
c. Renal failure
d. Arrhythmia

A

b. Bleeding including gastrointestinal and cerebral hemorrhages

110
Q

What are the therapeutic uses of Urokinase?
a. Myocardial infarction and stroke
b. Severe pulmonary emboli and deep vein thrombosis
c. Hypertension and atrial fibrillation
d. Chronic obstructive pulmonary disease

A

b. Severe pulmonary emboli and deep vein thrombosis

111
Q

Alteplase is superior to streptokinase and urokinase in dissolving older clots when administered within how many hours of ischemic stroke?
a. 1 hour
b. 2 hours
c. 3 hours
d. 4 hours

A

c. 3 hours

112
Q

What are the adverse effects of Streptokinase?
a. Hypertension and nausea
b. Arrhythmia and renal failure
c. Bleeding and hypersensitivity
d. Drowsiness and rash

A

c. Bleeding and hypersensitivity

112
Q

What is a significant adverse effect of Urokinase?
a. Hypertension
b. Bleeding
c. Renal failure
d. Arrhythmia

A

b. Bleeding

112
Q

What is another name for Alteplase (tPA)?
a. Single chain urokinase-type plasminogen activator
b. Tissue-type plasminogen activator
c. Plasminogen activator inhibitor
d. Prothrombin activator

A

c. Plasminogen activator inhibitor

113
Q

What are the therapeutic uses of Streptokinase?
a. Acute pulmonary embolism, venous and arterial thrombosis, and acute myocardial infarction
b. Hypertension and atrial fibrillation
c. Chronic obstructive pulmonary disease
d. Deep vein thrombosis and varicose veins

A

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

114
Q

What are Retaplase and Tenecteplase classified as?
a. First generation thrombolytic drugs
b. Second generation thrombolytic drugs
c. Third generation thrombolytic drugs
d. Fourth generation thrombolytic drugs

A

c. Third generation thrombolytic drugs

114
Q

Which generation do Streptokinase and Urokinase belong to?
a. First generation
b. Second generation
c. Third generation
d. Fourth generation

A

a. First generation

115
Q

Anistreplase is a preformed complex of:
a. Urokinase and plasminogen
b. Streptokinase and plasminogen
c. Alteplase and plasminogen
d. Tenecteplase and plasminogen

A

b. Streptokinase and plasminogen

116
Q

Thrombolytic drugs are contraindicated in which of the following conditions?
a. Hypertension and diabetes
b. Pregnancy, metastatic cancers, and history of cerebrovascular accidents
c. Asthma and renal failure
d. Heart failure and COPD

A

b. Pregnancy, metastatic cancers, and history of cerebrovascular accidents

117
Q

Aminocaproic acid and tranexamic acid are used to treat bleeding by overcoming the effects of which drugs?
a. Heparin and warfarin
b. Alteplase, streptokinase, and urokinase
c. Aspirin and ibuprofen
d. Clopidogrel and ticlopidine

A

b. Alteplase, streptokinase, and urokinase

118
Q

What is a significant adverse effect of aminocaproic acid and tranexamic acid?
a. Intravenous thrombosis
b. Hypertension
c. Bradycardia
d. Hypotension

A

a. Intravenous thrombosis

119
Q

What is the therapeutic use of protamine sulfate?
a. To treat bleeding (to reverse the effect of heparin)
b. To treat bleeding (to reverse the effect of warfarin)
c. To treat bleeding (to reverse the effect of aspirin)
d. To treat bleeding (to reverse the effect of streptokinase)

A

a. To treat bleeding (to reverse the effect of heparin)

120
Q

What are the adverse effects of protamine sulfate?
a. Hypertension and tachycardia
b. Bradycardia, hypotension, and flushing
c. Intravenous thrombosis
d. Nausea and vomiting

A

b. Bradycardia, hypotension, and flushing

121
Q

Vitamin K is used to treat bleeding caused by which anticoagulant?
a. Heparin
b. Warfarin
c. Streptokinase
d. Urokinase

A

b. Warfarin

122
Q

What is the response time for vitamin K to overcome the effect of warfarin?
a. 12 hours
b. 18 hours
c. 24 hours
d. 48 hours

A

c. 24 hours

123
Q

Sodium bicarbonate is used in the treatment of aspirin toxicity by:
a. Neutralizing stomach acid
b. Binding to aspirin in the blood
c. Increasing renal elimination of aspirin
d. Decreasing aspirin absorption in the intestines

A

c. Increasing renal elimination of aspirin

124
Q

Which drug inhibits streptokinase bleeding?
a. Protamine sulfate
b. Aprotinin
c. Sodium bicarbonate
d. Vitamin K

A

b. Aprotinin

Pharma2 MCQs (6 decks)

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