Drugs for Blood Coagulation Flashcards
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
c. The blood vessels or the heart
A clot that adheres to a vessel wall is called:
a. Embolus
b. Thrombus
c. Platelet
d. Fibrin
b. Thrombus
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
b. A clot that floats within the blood
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
b. They may occlude blood vessels
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
c. Platelet activation and aggregation, followed by formation of thrombin
What stabilizes a clot once it is formed?
a. Hemoglobin
b. Cross-linked fibrin
c. Red blood cells
d. White blood cells
b. Cross-linked fibrin
Platelets respond to vascular trauma by:
a. Aggregation only
b. Adhesion, release of intracellular granules, and aggregation
c. Release of fibrin
d. Dissolving clots
b. Adhesion, release of intracellular granules, and aggregation
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
b. Adhesion to the site of injury
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
b. Release of intracellular granules
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
c. Aggregation of the platelets
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
b. Thromboxane A2, ADP, serotonin, PAF
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. Chemical mediators released by platelets
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
c. Factors released from injured tissue and platelets
Prothrombin (factor II) is converted to thrombin by:
a. Factor VIII
b. Factor Xa
c. Factor XII
d. Factor XIII
b. Factor Xa
Thrombin catalyzes the conversion of:
a. Prothrombin to fibrinogen
b. Fibrinogen to fibrin
c. Fibrin to prothrombin
d. Plasminogen to plasmin
b. Fibrinogen to fibrin
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. Factor XIII
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
b. Catalyze the conversion of fibrinogen to fibrin
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
c. Both intrinsic and extrinsic pathways
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. Initiation of the coagulation cascade
What is the final product that stabilizes the clot in the coagulation cascade?
a. Prothrombin
b. Cross-linked fibrin
c. Thrombin
d. Plasmin
b. Cross-linked fibrin
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
b. Maintaining a transmural negative electrical charge
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
b. Transmural negative electrical charge
The release of plasminogen activators:
a. Inhibits coagulation
b. Activates the fibrinolytic pathway
c. Promotes platelet aggregation
d. Decreases protein C activity
b. Activates the fibrinolytic pathway
Protein C degrades:
a. Plasmin
b. Coagulation factors
c. Fibrinogen
d. Prostacyclin
b. Coagulation factors
The production of heparin-like proteoglycans:
a. Promotes platelet aggregation
b. Activates fibrinogen
c. Inhibits coagulation
d. Degrades fibrin
c. Inhibits coagulation
Prostacyclin (PGI2) is a potent inhibitor of:
a. Fibrin formation
b. Coagulation factors
c. Platelet aggregation
d. Plasmin activity
c. Platelet aggregation
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
c. Maintenance of a nonthrombogenic endothelial lining
The fibrinolytic pathway is activated by:
a. Protein C
b. Prostacyclin
c. Plasminogen activators
d. Plasmin inhibitors
c. Plasminogen activators
Which of the following is a platelet inhibitor?
a. Aspirin
b. Heparin
c. Alteplase
d. Aminocaproic acid
a. Aspirin
Which drug is an anticoagulant?
a. Streptokinase
b. Clopidogrel
c. Warfarin
d. Tranexamic acid
c. Warfarin
Alteplase is classified as a:
a. Thrombolytic
b. Platelet inhibitor
c. Anticoagulant
d. Treatment for bleeding
a. Thrombolytic
Which of the following drugs is used in the treatment of bleeding?
a. Enoxaparin
b. Protamine sulfate
c. Eptifibatide
d. Urokinase
b. Protamine sulfate
Clopidogrel is an example of a:
a. Thrombolytic
b. Anticoagulant
c. Platelet inhibitor
d. Treatment for bleeding
c. Platelet inhibitor
Heparin is categorized under:
a. Thrombolytics
b. Anticoagulants
c. Platelet inhibitors
d. Treatments for bleeding
b. Anticoagulants
Which of the following is a thrombolytic drug?
a. Dipyridamole
b. Streptokinase
c. Rivaroxaban
d. Vitamin K
b. Streptokinase
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
c. Treats bleeding
Which anticoagulant is a direct thrombin inhibitor?
a. Aspirin
b. Bivalirudin
c. Alteplase
d. Protamine sulfate
b. Bivalirudin
Abciximab is classified as a:
a. Platelet inhibitor
b. Thrombolytic
c. Anticoagulant
d. Treatment for bleeding
a. Platelet inhibitor
Which drug among the following is a low molecular weight heparin?
a. Warfarin
b. Eptifibatide
c. Enoxaparin
d. Tranexamic acid
c. Enoxaparin
A drug that inhibits platelet aggregation by blocking the glycoprotein IIb/IIIa receptor is:
a. Eptifibatide
b. Dalteparin
c. Alteplase
d. Vitamin K
a. Eptifibatide
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
b. 2 hours
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. Thrombolytic therapy
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
b. Inhibiting COX-1, blocking GPIIb/IIIa, or ADP, or increasing cAMP
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
c. Release of platelet granules, activation of thromboxane A2 synthesis, and activation of GP IIb/IIIa receptors
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. Release of platelet granules and activation of GP IIb/IIIa receptors
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
b. Interferes in the signals that promote platelet aggregation
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
c. GP IIb/IIIa receptors
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
b. Anticoagulants (e.g., heparin)
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
d. Promoting thromboxane A2 synthesis
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
c. Thromboxane A2
The goal of therapy with aspirin is to selectively inhibit the synthesis of:
a. Thromboxane A2
b. Prostacyclin (PGI2)
c. Fibrinogen
d. ADP
a. Thromboxane A2
Aspirin irreversibly inhibits which enzyme to inhibit platelet aggregation?
a. Thrombin
b. Cyclooxygenase enzyme (COX1)
c. Phospholipase
d. Protease
b. Cyclooxygenase enzyme (COX1)
At low doses, aspirin inhibits the synthesis of which substance in platelets?
a. Thromboxane A2 (TXA2)
b. Prostacyclin (PGI2)
c. Fibrinogen
d. ADP
a. Thromboxane A2 (TXA2)
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. 81 to 325 mg per day
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
d. Treatment of acute deep vein thrombosis
Aspirin is useful for preventing coronary thrombosis in patients with:
a. Stable angina
b. Unstable angina
c. Chronic heart failure
d. Peripheral artery disease
b. Unstable angina
One of the adverse effects of aspirin is:
a. Bleeding
b. Hypertension
c. Tachycardia
d. Bradycardia
a. Bleeding
An adverse effect of aspirin is:
a. Nephrotoxicity
b. Gastrointestinal ulceration
c. Hepatotoxicity
d. Hyperkalemia
b. Gastrointestinal ulceration
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. Reduced thromboxane A2 synthesis
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. COX1
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
b. Blocking specific receptors for adenosine diphosphate (ADP) on the platelet membrane
Ticlopidine and Clopidogrel inhibit which glycoprotein receptors?
a. GP IIa/IIb
b. GP Ib/IX
c. GP IIb/IIIa
d. GP IV
c. GP IIb/IIIa
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
b. Alternative prophylactic therapy to aspirin in secondary prevention of stroke and myocardial infarction
Which adverse effect is most serious with Ticlopidine use?
a. Thrombocytopenia
b. Neutropenia
c. Gastrointestinal ulceration
d. Hypertension
b. Neutropenia
Other side effects of Ticlopidine include:
a. Hypertension and bradycardia
b. Thrombocytopenia and aplastic anemia
c. Hyperkalemia and hepatotoxicity
d. Nephrotoxicity and tachycardia
b. Thrombocytopenia and aplastic anemia
Clopidogrel is classified as a:
a. Prodrug
b. Direct-acting drug
c. Anticoagulant
d. Thrombolytic
a. Prodrug
Clopidogrel is activated by which enzyme?
a. COX-1
b. GP IIb/IIIa
c. CYP450
d. Plasminogen
c. CYP450
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. Hepatic enzyme inhibitors (e.g., omeprazole)
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
b. Treatment of acute myocardial infarction
Ticlopidine and Clopidogrel work by:
a. Enhancing platelet aggregation
b. Inhibiting platelet activation
c. Activating thromboxane A2
d. Blocking fibrinogen synthesis
b. Inhibiting platelet activation
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. Murine monoclonal antibody against the GP IIb/IIIa receptor
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
b. It is expensive
Eptifibatide is available only in which form due to its toxicity when taken orally?
a. Oral
b. Intravenous (IV)
c. Subcutaneous
d. Intramuscular
b. Intravenous (IV)
Eptifibatide is a blocker of which receptor?
a. COX-1
b. ADP
c. GP IIb/IIIa
d. Thromboxane A2
c. GP IIb/IIIa
Dipyridamole works by inhibiting which enzyme?
a. COX-1
b. Phosphodiesterase
c. ADP receptor
d. GP IIb/IIIa receptor
b. Phosphodiesterase
Inhibition of phosphodiesterase by Dipyridamole results in an increase in:
a. Calcium levels
b. cAMP in platelets
c. Thromboxane A2 synthesis
d. Fibrinogen levels
b. cAMP in platelets
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. Prosthetic heart valves (in combination with warfarin)
Dipyridamole is used as prophylactic therapy to treat angina pectoris in combination with:
a. Warfarin
b. Aspirin
c. Clopidogrel
d. Heparin
b. Aspirin
A disadvantage of Dipyridamole is:
a. Headache
b. Gastrointestinal bleeding
c. Neutropenia
d. Hypertension
a. Headache
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. No excess risk of bleeding
The older type of heparin is known as:
a. Standard heparin
b. Low-molecular-weight heparin (LMWH)
c. Synthetic heparin
d. Unfractionated heparin
a. Standard heparin
Low-molecular-weight heparin (LMWH) is derived from:
a. Animal extract
b. Standard heparin
c. Synthetic sources
d. Plant extract
b. Standard heparin
LMWH has greater _______ than standard heparin.
a. Bioavailability
b. Toxicity
c. Cost
d. Molecular weight
a. Bioavailability
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
b. Longer-lasting effect
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
b. Preventing and treating venous thromboembolism
How is LMWH administered?
a. Orally
b. Subcutaneously
c. Intravenously
d. Intramuscularly
b. Subcutaneously
Which of the following is an example of LMWH?
a. Warfarin
b. Aspirin
c. Enoxaparin
d. Clopidogrel
c. Enoxaparin
LMWH requires less _______ than standard heparin.
a. Dosage
b. Monitoring
c. Efficacy
d. Bioavailability
b. Monitoring
Heparin binds to which protein to exert its anticoagulant effect?
a. Fibrinogen
b. Thrombin
c. Antithrombin III
d. Plasminogen
c. Antithrombin III
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. Thrombin and factor Xa
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
b. Accelerated inhibition of coagulation factors
Which of the following is a therapeutic use of heparin?
a. Deep vein thrombosis
b. Hypertension
c. Diabetes mellitus
d. Hyperlipidemia
a. Deep vein thrombosis
Heparin is the anticoagulant of choice for treating pregnant women with:
a. Myocardial infarction
b. Venous thromboembolism
c. Pulmonary hypertension
d. Arterial thrombosis
b. Venous thromboembolism
How must heparin be administered?
a. Parenterally either subcutaneously or intravenously
b. Orally
c. Intramuscularly
d. Topically
a. Parenterally either subcutaneously or intravenously
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
b. It can cause hematoma formation
Maximal anticoagulant effect of heparin occurs within minutes after:
a. Oral administration
b. IV heparin injection
c. Subcutaneous injection
d. Intramuscular injection
b. IV heparin injection
Heparin is prescribed on which basis?
a. Milligram
b. Unit
c. Volume
d. Percentage
b. Unit
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. Both in vitro and in vivo
One of the adverse effects of heparin is:
a. Bleeding
b. Hypertension
c. Tachycardia
d. Hyperkalemia
a. Bleeding
Another adverse effect of heparin is:
a. Neutropenia
b. Hepatotoxicity
c. Thrombocytopenia
d. Nephrotoxicity
c. Thrombocytopenia
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
c. Recent surgery, liver or renal disease, severe hypertension, and thrombocytopenia
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
c. II, VII, IX, X
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
c. Treatment of venous thrombosis and pulmonary emboli
Which of the following is a significant adverse effect of Warfarin?
a. Nausea
b. Rash
c. Bleeding
d. Drowsiness
c. Bleeding
How is Warfarin administered?
a. Intravenously
b. Subcutaneously
c. Orally
d. Topically
c. Orally
Unlike heparin, Warfarin induces hypocoagulability only in:
a. In vitro
b. In silico
c. In vivo
d. In situ
c. In vivo
Which of the following is NOT a contraindication for Warfarin use?
a. Asthma
b. Pregnancy
c. Gastrointestinal ulceration
d. Severe hypertension
a. Asthma
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
b. Rapid lysis of already formed clots
Which enzyme’s activation initiates fibrinolysis?
a. Thrombin
b. Factor X
c. Plasminogen
d. Fibrinogen
c. Plasminogen
Older first-generation thrombolytic drugs are characterized by:
a. Higher specificity
b. Lack of selectivity
c. Lower efficacy
d. Longer duration of action
b. Lack of selectivity
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
c. Myocardial infarction, pulmonary embolism, and acute ischemic stroke
What is a significant adverse effect of Alteplase (tPA)?
a. Hypertension
b. Bleeding including gastrointestinal and cerebral hemorrhages
c. Renal failure
d. Arrhythmia
b. Bleeding including gastrointestinal and cerebral hemorrhages
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
b. Severe pulmonary emboli and deep vein thrombosis
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
c. 3 hours
What are the adverse effects of Streptokinase?
a. Hypertension and nausea
b. Arrhythmia and renal failure
c. Bleeding and hypersensitivity
d. Drowsiness and rash
c. Bleeding and hypersensitivity
What is a significant adverse effect of Urokinase?
a. Hypertension
b. Bleeding
c. Renal failure
d. Arrhythmia
b. Bleeding
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
c. Plasminogen activator inhibitor
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. Acute pulmonary embolism, venous and arterial thrombosis, and acute myocardial infarction
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
c. Third generation thrombolytic drugs
Which generation do Streptokinase and Urokinase belong to?
a. First generation
b. Second generation
c. Third generation
d. Fourth generation
a. First generation
Anistreplase is a preformed complex of:
a. Urokinase and plasminogen
b. Streptokinase and plasminogen
c. Alteplase and plasminogen
d. Tenecteplase and plasminogen
b. Streptokinase and plasminogen
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
b. Pregnancy, metastatic cancers, and history of cerebrovascular accidents
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
b. Alteplase, streptokinase, and urokinase
What is a significant adverse effect of aminocaproic acid and tranexamic acid?
a. Intravenous thrombosis
b. Hypertension
c. Bradycardia
d. Hypotension
a. Intravenous thrombosis
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. To treat bleeding (to reverse the effect of heparin)
What are the adverse effects of protamine sulfate?
a. Hypertension and tachycardia
b. Bradycardia, hypotension, and flushing
c. Intravenous thrombosis
d. Nausea and vomiting
b. Bradycardia, hypotension, and flushing
Vitamin K is used to treat bleeding caused by which anticoagulant?
a. Heparin
b. Warfarin
c. Streptokinase
d. Urokinase
b. Warfarin
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
c. 24 hours
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
c. Increasing renal elimination of aspirin
Which drug inhibits streptokinase bleeding?
a. Protamine sulfate
b. Aprotinin
c. Sodium bicarbonate
d. Vitamin K
b. Aprotinin
