This Is A Pharmaceutical Tests About Anticoagulants

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This Is A Pharmaceutical Tests About Anticoagulants - Quiz

Anticoagulants are medicines that help prevent blood clots. They're given to people at a high risk of getting clots, to reduce their chances of developing serious conditions such as strokes and heart attacks. A blood clot is a seal created by the blood to stop bleeding from wounds.
This is a pharmaceutical tests about Anticoagulants


Questions and Answers
  • 1. 

    What causes clot formation?

    • A.

      Slowing of blood (atrial fibrillation, congestive heart failure, heart attack, bed rest, paralysis).

    • B.

      Abnormal surfaces in contact with blood (vascular injury, heart valve replacement or disease, atherosclerosis).

    • C.

      Abnormalities in endogenous anti-clotting factors (protein C and S deficiency, antithrombin).

    • D.

      Estrogen therapy.

    • E.

      All of the above.

    Correct Answer
    E. All of the above.
    Explanation
    Estrogen therapy increases the synthesis of clotting factors and can cause ischemic strokes. Protein C and S help keep clot formation in balance.

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  • 2. 

    After tissue injury, place the following events in the correct order. A. von Willebrand factors attracts plateletsB. Platelets secrete ADP - attracts more plateletsC. Collage is exposed, activating plateletsD. Platelets secrete serotonin and thromboxane A2 - vasoconstriction

    • A.

      A, B, C, D

    • B.

      C, A, D, B

    • C.

      C, B, D, A

    • D.

      D, C, A, B

    • E.

      B, D, A, B

    Correct Answer
    B. C, A, D, B
    Explanation
    Collagen is exposed after tissue injury, which activates platelets. von Willebrand factor is then released, attracting platelets to the site of injury. Platelets secrete serotonin and thromboxane A2, causing vasoconstriction. Finally, platelets secrete ADP, which attracts more platelets to the site of injury. Therefore, the correct order is C, A, D, B.

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  • 3. 

    What are the steps in fibrin formation?

    • A.

      "Tissue factor" or thromboplastin is released from endothelial wall.

    • B.

      Contact of blood with collagen.

    • C.

      Clots bind thromboxane A2.

    • D.

      A and B

    • E.

      A, B, and C

    Correct Answer
    D. A and B
    Explanation
    "Tissue factor" or thromboplastin is released from endothelial wall - starts the extrinsic pathway ("tissue factor pathway" - a factor from outside the vascular system is required.
    Contact of blood with collagen starts the intrinsic pathway of blood ("contact activation pathway") - all clotting factors required to start the pathway are present within the vascular system.

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  • 4. 

    Proteins C and S are dependent on which vitamin for synthesis?

    • A.

      Vitamin C

    • B.

      Vitamin B

    • C.

      Vitamin E

    • D.

      Vitamin K

    • E.

      Vitamin A

    Correct Answer
    D. Vitamin K
    Explanation
    Proteins C and S are dependent on Vitamin K for synthesis. Vitamin K is essential for the production of blood clotting proteins, including proteins C and S. These proteins play a crucial role in regulating blood clotting and preventing excessive clot formation. Without sufficient Vitamin K, the synthesis of proteins C and S would be impaired, leading to an increased risk of abnormal blood clotting. Therefore, Vitamin K is necessary for the proper functioning of proteins C and S in the body.

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  • 5. 

    What might cause a deficiency in Prothrombin (factor II) or in Stuart-Prower factor (factor X)?

    • A.

      Liver disease

    • B.

      Renal disease

    • C.

      Vitamin K deficiency

    • D.

      A and B

    • E.

      A and C

    • F.

      A, B, and C

    Correct Answer
    E. A and C
    Explanation
    A deficiency in Prothrombin (factor II) or in Stuart-Prower factor (factor X) can be caused by liver disease and vitamin K deficiency. Liver disease can impair the liver's ability to produce these clotting factors, leading to a deficiency. Vitamin K is essential for the production of these factors, so a deficiency in vitamin K can also result in a deficiency of Prothrombin and Stuart-Prower factor. Therefore, both liver disease and vitamin K deficiency can contribute to a deficiency in these clotting factors.

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  • 6. 

    Why can't Heparin be administered orally?

    • A.

      It is large.

    • B.

      It is negatively charged.

    • C.

      It contains too much magnesium.

    • D.

      A and B

    • E.

      All of the above.

    Correct Answer
    D. A and B
    Explanation
    It is large and negatively charged and cannot cross the membrane to be absorbed.

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  • 7. 

    What does heparin inhibit?

    • A.

      The coversion of prothrombin to thrombin.

    • B.

      The conversion of thrombin to prothrombin.

    • C.

      The conversion of fibrinogen to fibrin.

    • D.

      The conversion of fibrin to fibrinogen.

    • E.

      A and C

    • F.

      C and A

    Correct Answer
    E. A and C
    Explanation
    Heparin acts as an anticoagulant by way of antithrombin (a protease inhibitor) - antithrombin inhibits factors Xa, thrombin (IIa), and IXa, XIa, and XIIa. Heparin therefore inhibits conversion of prothrombin to thrombin (via inhibition of Xa) and fibrinogen to fibrin (via inhibition of IIa).

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  • 8. 

    Heparin also has a:

    • A.

      Carbohydrate binding activity.

    • B.

      Vitamin clearing activity.

    • C.

      Lipid clearing activity.

    • D.

      Hepatotoxic effect.

    • E.

      Renal toxic effect.

    Correct Answer
    C. Lipid clearing activity.
    Explanation
    Heparin releases a clearing factor (a lipoprotein lipase) - this lipase hydrolyzes triglycerides in chylomicrons.

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  • 9. 

    How can heparin be administered?

    • A.

      IV

    • B.

      SQ

    • C.

      Orally

    • D.

      IM

    • E.

      A and C

    • F.

      A and B

    Correct Answer
    F. A and B
    Explanation
    Cannot be administered orally - large and negative. Cannot be administered IM - hematoma. Only IV and SQ.

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  • 10. 

    Heparin is metabolized in the:

    • A.

      Liver

    • B.

      Kindeys

    • C.

      Lungs

    • D.

      GI tract

    Correct Answer
    A. Liver
    Explanation
    Heparinase in liver.

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  • 11. 

    Heparin metabolites are excreted in the:

    • A.

      Liver

    • B.

      Kidneys

    • C.

      Lungs

    • D.

      GI tract

    Correct Answer
    B. Kidneys
    Explanation
    Heparin metabolites are excreted in the kidneys. The kidneys play a vital role in the excretion of waste products and metabolites from the body. Heparin, a medication used as an anticoagulant, undergoes metabolism in the liver and is then excreted primarily through the kidneys. The kidneys filter the blood and remove waste products, including heparin metabolites, through urine. Therefore, the correct answer is kidneys.

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  • 12. 

    Is heparin ok in pregnancy?

    • A.

      Yes.

    • B.

      No.

    Correct Answer
    A. Yes.
    Explanation
    Heparin is the drug of choice for pregnant women because it does not cross the placental membrane.

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  • 13. 

    Heparin's adverse effects include:

    • A.

      Hypersensitivity

    • B.

      Osteoporosis

    • C.

      Alopecia

    • D.

      Hemorrhage

    • E.

      Thrombocytopenia

    • F.

      Thromboembolism

    • G.

      All of the above.

    Correct Answer
    G. All of the above.
    Explanation
    Hypersensitivity is due to animal origin. Osteoporosis and alopecia are only seen in long-term use - 2-3 months. Hemorrhage is the major concern. Thrombocytopenia = hepairin induced (HIT) platelet aggregation - heparin antibody develops 7-14 days after start of treatment. Thromboembolism is induced by HIT.

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  • 14. 

    Which drugs is used in the treatment of heparin toxicity?

    • A.

      Warfarin

    • B.

      Niacin

    • C.

      Ezetimbie

    • D.

      Protamine

    • E.

      Tetracycline

    Correct Answer
    D. Protamine
    Explanation
    Protamine is a small, positively charged molecule that binds with heparin. Dosages is based on the level of heparin - must be dosed to titrate 1:1 with heparin, taking into account the different half lives of the drugs. Adverse effects of protamine are anticoagulation (acts as an anticoagulant if administered without heparin) and anaphylactic shock (derived from fish sperm).

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  • 15. 

    Low molecular weight heparins include which of the following:

    • A.

      Enoxaparin (Lovenox)

    • B.

      Warfarin

    • C.

      Coumadin

    • D.

      Dalteparin (Fragmin)

    • E.

      Tinzaparin (Innohep)

    • F.

      A, D, and E.

    • G.

      A, C, and B.

    Correct Answer
    F. A, D, and E.
    Explanation
    The correct answer is A, D, and E. Low molecular weight heparins (LMWHs) are a type of anticoagulant medication. Enoxaparin (Lovenox), dalteparin (Fragmin), and tinzaparin (Innohep) are all examples of LMWHs. Warfarin and coumadin, on the other hand, are not LMWHs.

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  • 16. 

    What is the mechanism of action of LMWH and why is it different than heparin?

    • A.

      It inactivates IIa via antithrombin but has little effect at Xa because it is too short for thrombin binding.

    • B.

      It inactivates Xa but has little inactivation at IIa (thrombin) via antithrombin because chains are too short for thrombin binding.

    • C.

      It has the same mechanism of action of heparin.

    Correct Answer
    B. It inactivates Xa but has little inactivation at IIa (thrombin) via antithrombin because chains are too short for thrombin binding.
    Explanation
    LMWH (Low Molecular Weight Heparin) inactivates Xa (Factor Xa) but has little inactivation at IIa (thrombin) via antithrombin because the chains of LMWH are shorter compared to heparin. Thrombin has a higher molecular weight and requires longer chains to bind effectively. Therefore, LMWH primarily targets and inhibits Xa, which is involved in the formation of blood clots, while having minimal effect on thrombin. This is different from heparin, which can inhibit both Xa and IIa.

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  • 17. 

    What are the benefits of LMWHs?

    • A.

      Longer half-lives.

    • B.

      High bioavailability.

    • C.

      Less liver clearance and binding to macrophages.

    • D.

      Less non-specific binding with tissues.

    • E.

      All of the above.

    Correct Answer
    E. All of the above.
    Explanation
    LMWHs are cleared renally. Less interactions with platelets means less risk of HIT! (Still can't use in patients who have had HIT.) Additional benefits include little monitoring (don't have to be in the hospital), self-administration SQ.

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  • 18. 

    Which of the following is a synthetic pentasaccharide identical to the antithrombin binding region of heparin?

    • A.

      Enoxaparin

    • B.

      Dalteparin

    • C.

      Tinzaparin

    • D.

      Fondaparinux

    Correct Answer
    D. Fondaparinux
    Explanation
    Fondaparinux (Arixtra) is a LMW Heparin Derivative that does not originate from unfractionated heparin. It is a synthetic pentasaccharide identical to the antithrombin binding region of heparin.

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  • 19. 

    What factor is inhibited by Fondaparinux (Arixtra) in conjunction with antithrombin?

    • A.

      IIa

    • B.

      VI

    • C.

      III

    • D.

      Xa

    • E.

      Xb

    Correct Answer
    D. Xa
    Explanation
    Fondaparinux (Arixtra) inhibits factor Xa in conjunction with antithrombin. Factor Xa is a key enzyme in the coagulation cascade that plays a crucial role in the formation of blood clots. By inhibiting factor Xa, Fondaparinux prevents the formation of blood clots and reduces the risk of thromboembolic events.

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  • 20. 

    Which drug is an irreversible direct thrombin inhibitor that is used in place of heparin when HIT is an issue?

    • A.

      Argatroban (Acova)

    • B.

      Bivalirudin (Angiomax)

    • C.

      Lepirudin (Refludan)

    • D.

      Desirudin (Iparavask)

    Correct Answer
    C. Lepirudin (Refludan)
    Explanation
    Dosing by IV and is expensive - renal elimination so use caustion in renally compromised patients.

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  • 21. 

    Which drug is a direct reversible thrombin inhibitor used to treat thrombosis in HIT?

    • A.

      Argatroban (Acova)

    • B.

      Lepirudin (Refludan)

    • C.

      Bivalirudin (Angiomax)

    • D.

      Desirudin (Iparavask)

    Correct Answer
    A. Argatroban (Acova)
    Explanation
    Synthetic drivative of arginine - direct reversible thrombin inhibitor by blocking the catalytic site - treats thrombosis in HIT - IV administration - metabolized by the LIVER so don't have to worry about renally compromised patients.

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  • 22. 

    Which drug is a direct thrombin reversible inhibitor given in combination with aspirin to prevent clot formation with unstable angina undergoing coronary angioplasty?

    • A.

      Argatroban (Acova)

    • B.

      Lepirudin (Refludan)

    • C.

      Desirudin (Iparavask)

    • D.

      Bivalirudin (Angiomax)

    Correct Answer
    D. Bivalirudin (Angiomax)
    Explanation
    Synthetic derivative - IV administration - renal elimination so must use caution in renally compromised patients.

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  • 23. 

    Which drug is a direct thrombin almost irreversible inhibitor used for DVT prevention in hip replacements?

    • A.

      Desirudin (Iparavask)

    • B.

      Bivalirudin (Angiomax)

    • C.

      Argatroban (Acova)

    • D.

      Lepirudin (Refludan)

    Correct Answer
    A. Desirudin (Iparavask)
    Explanation
    Newest of the group - direct thrombin almost irreversible inhibitor - can be used in HIT patients - SQ so more useful - renal elimination, use caution.

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  • 24. 

    Which drug acts by competitive inhibition of vitamin K reductase?

    • A.

      Desirudin (Iparavask)

    • B.

      Warfarin

    • C.

      Heparin

    • D.

      Ezetimibe

    • E.

      Niacin

    Correct Answer
    B. Warfarin
    Explanation
    Warfarin acts thru competitive inhibition of vitamin K reductase - blocks the synthesis of factors II, VII, IX, X, and protein C and S - results in lack of gamma carboxylation of the factors (gamma carboxylation allows calcium to bind, which is necessary for activation and platelet binding).

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  • 25. 

    How much time is required for peak anticoagulant effect of Warfarin?

    • A.

      3 hours

    • B.

      1 day

    • C.

      1 week

    • D.

      3 days

    Correct Answer
    D. 3 days
    Explanation
    Warfarin takes out the synthesis of inactivated factors but you need to wait for the body to get rid of the activated factors before seeing the effects of warfarin. Activated IIa has the longest half life, at 60 hours.

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  • 26. 

    Does Warfarin or Heparin have a longer half-life?

    • A.

      Warfarin

    • B.

      Heparin

    Correct Answer
    A. Warfarin
    Explanation
    Warfarin has a 35 hour half-life! It is well absorbed by the oral route and is 99% bound to plasma proteins (albumin).

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  • 27. 

    What adverse effect can be seen in the fetus when the mother takes Warfarin, especially in the first trimest?

    • A.

      Neural tube defect.

    • B.

      Abnormal heart valves.

    • C.

      Missing eyelashes.

    • D.

      Bone defects.

    Correct Answer
    D. Bone defects.
    Explanation
    Fetal bone defects are due to lack of gamma carboxylation of osteocalcein.

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  • 28. 

    Which drugs act as synergists for Warfarin?

    • A.

      Acetylsalicylic acid

    • B.

      Heparin

    • C.

      Acetaminophen

    • D.

      Antibiotics

    • E.

      A, B, and C

    • F.

      A, C, and D

    Correct Answer
    F. A, C, and D
    Explanation
    Acetylsalicylic acid - platelets - reduce platelet aggregation - displacement of warfarin from albumin (get more unbound, active aspirin and more free warfarin too). Acetaminophen - high dose and long term - inhibits warfarin degradation - competition for CYP1A2 and 3A4. Antibiotics - (broad spectrum) gut flora - bacteria in the stomach synthesize vitamin K - reducing the amount of vitamin K produced means there is less for warfarin to compete with so it is able to work better. Antibiotics - sulfonamides - compete in plasma albumin binding.

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  • 29. 

    Which drugs act as synergists for Warfarin?

    • A.

      Thyroid.

    • B.

      Miconazole (intravaginal)

    • C.

      Gemfibrozil (fibric acid derivatives)

    • D.

      Niacin

    • E.

      All of the above.

    • F.

      A, B, and C.

    Correct Answer
    F. A, B, and C.
    Explanation
    Thyroid - increased metabolism of clotting factors so there are less clotting factors around. Miconazole - is able to cross the membrane and affect warfarin enzymes - inhibits CYP450 - increased warfarin levels. Gemfibrozil - competes for plasma proteins.

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  • 30. 

    Which of the following are Warfarin antagonists?

    • A.

      Barbiturates.

    • B.

      Rifampin.

    • C.

      Vitamin K.

    • D.

      Estrogens.

    • E.

      Choletyramine.

    • F.

      All of the above.

    Correct Answer
    F. All of the above.
    Explanation
    Barbiturates increase metabolism by inducing degradation enzymes. Rifampin increases metabolism by inducing CYP450 enzymes. Vitamin K competes for binding (role of foods). Estrogens increase factors VII and X which increases the synthesis of coagulation factors. Estrogens also decrease the synthesis of antithrombin. Cholestyramine - binds fat soluble vitamins and so eliminates warfarin if given concurrently

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  • 31. 

    What is the treatment for Warfarin toxicity?

    • A.

      Phytonadione

    • B.

      Transfusion of fresh frozen plasma

    • C.

      Heparin

    • D.

      Fondaparinux

    • E.

      A and B

    • F.

      All of the above.

    Correct Answer
    E. A and B
    Explanation
    Phytonadione (K1) can be given orally, IV, or SC and it competes with warfarin. Transfusion of fresh frozen plasma provides a lot of fresh clotting factors.

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  • 32. 

    Is bound plasmin or circulating plasmin better?

    • A.

      Bound plasmin.

    • B.

      Circulating plasmin.

    Correct Answer
    A. Bound plasmin.
    Explanation
    We want plasmin associated with the clot (bound) - systemic lysis can occur when plasmin is present in circulating plasma - it will destroy clotting factors in addition to clots!

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  • 33. 

    Which drug is a protein from group C, beta hemolytic streptococci that induces a lytic state?

    • A.

      Alteplase (Activase)

    • B.

      Streptokinase

    • C.

      Reteplase (Retavase)

    • D.

      Tenecteplase (Tnkase)

    Correct Answer
    B. Streptokinase
    Explanation
    Streptokinase forms a non-enzymatic complex with circulating plasminogen which catalyzes thrombolytic reactions - used IV and infused directly into coronary arteries *(less than 6 hours for MI)*

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  • 34. 

    Which drug is antigenic?

    • A.

      Alteplase (Activase)

    • B.

      Streptokinase

    • C.

      Reteplase (Retavase)

    • D.

      Tenecteplase (Tnkase)

    Correct Answer
    B. Streptokinase
    Explanation
    If patient has had a previous strep infection or has been given streptokinase before, the patient will have antibodies to streptokinase that will cause an allergic reaction or neutralization of streptokinase).

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  • 35. 

    Which of these drugs is a tissue-type plasminogen activator (t-PA) and is basically the clone of what we produce in our bodies?

    • A.

      Alteplase (Activase)

    • B.

      Streptokinase

    • C.

      Reteplase (Retavase)

    • D.

      Tenecteplase (Tnkase)

    Correct Answer
    A. Alteplase (Activase)
    Explanation
    activates plasminogen bound to platelets and endothelial cells (relatively clot specific) - not very antigenic (unless allergic to E. coli) - inhibited by t-PA inhibitor - short half-life of 5-10 minutes - long infusion of 90 min. infusion - higher intracranial bleeding risk but no hypotension (which can be an issue with streptokinase).

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  • 36. 

    What are the advantages of the new derivatives of alteplase (reteplase and tenecteplase)?

    • A.

      Increased half-life

    • B.

      Shorter infusions

    • C.

      All of the above

    Correct Answer
    C. All of the above
    Explanation
    Increased half-life because the plasminogen activator inhibitor doesn't degrade these as quickly. Only specific approved indications.

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  • 37. 

    Which of the following is a derivative of tPA that is only approved for acute MI?

    • A.

      Tenecteplase

    • B.

      Streptokinase

    • C.

      Alteplase

    • D.

      Reteplase

    Correct Answer
    D. Reteplase
    Explanation
    Reteplase is clot specific but less so than alteplase - not very antigenic - 13-16 min. half-life - 2 separate 2 minute IV bolus separated by 30 min. - bleeding risk.

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  • 38. 

    Which drug has the highest fibrin selectivity and only a 5 second IV bolus injection?

    • A.

      Reteplase (Retavase)

    • B.

      Tenecteplase (Tnkase)

    • C.

      Streptokinase

    • D.

      Alteplase (Activase)

    Correct Answer
    B. Tenecteplase (Tnkase)
    Explanation
    Only 3 AAs different from alteplase - 20-24 minute half-life - more resistant to t-PA circulating inhibitors - highest fibrin selectivity - wont have as many issues with extraneous plasminogen formation.

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  • 39. 

    In what order are the following drugs clot specific? (From most clot specific to least.)1. Tenectaplase2. Reteplase3. Alteplase

    • A.

      1, 2, 3

    • B.

      3, 1, 2

    • C.

      1, 3, 2

    Correct Answer
    C. 1, 3, 2
    Explanation
    This is also the order for activating thrombin - tenectaplase the least and reteplase the most.

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  • 40. 

    Which of the following drugs inhibits platelet aggregation?

    • A.

      Tenecteplase

    • B.

      Niacin

    • C.

      Acetylsalicylic acid (Aspirin)

    Correct Answer
    C. Acetylsalicylic acid (Aspirin)
    Explanation
    Mechanim of action: irreversible inhibition of cyclooxygenase (COX-1 and COX-2). COX-1 is ubiquitously present in all cells - inhibiting COX-1 inhibits the synthesis of thromboxanes which inhibits platelet aggregation. COX-2 is not present on platelets.

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  • 41. 

    What disorder(s) can be caused by aspirin?

    • A.

      Metabolic respiratory acidosis

    • B.

      Salicylism

    • C.

      Gout

    • D.

      All of the above

    Correct Answer
    D. All of the above
    Explanation
    Gout - low doses of aspirin increase uric acid levels - competes for excretion of uric acid. Salicylism - aspirin is an acid - use sodium bicarb to treat - excrete in anionic form.

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  • 42. 

    Which adenosine diphosphate receptor antagonist does not work any better than aspirin but is recommended for those patients allergic to aspirin?

    • A.

      Clopidogrel (Plavix)

    • B.

      Prasugrel (Effient)

    • C.

      Abciximab

    • D.

      Tirofiban

    Correct Answer
    A. Clopidogrel (Plavix)
    Explanation
    Clopidogrel (Plavix) is indicated in thrombosis and coronary artery disease - side effects include a low risk of TTP (thrombotic thrombocytopenia purpura), bleeding, hypersensitivity, abdominal pain, constipation - resistance to clopidogrel (Plavix) can be seen if the patient has a defect in CYP450 enzymes - prodrug doesn't get converted to active form.

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  • 43. 

    Which adenosine diphosphate receptor antagonist is similar to clopidogrel but has fewer thrombotic events but increased risk of major bleeding?

    • A.

      Prasugrel (Effient)

    • B.

      Eptifibatide

    • C.

      Clopidogrel (Plavix)

    Correct Answer
    A. Prasugrel (Effient)
    Explanation
    indicated in arterial thromboembolism prophylaxis

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  • 44. 

    Which of the following are Super Aspirins?

    • A.

      Abciximab

    • B.

      Eptifibatide

    • C.

      Tirofiban

    • D.

      All of the above

    Correct Answer
    D. All of the above
    Explanation
    abciximab (Reopro) = murine-human chimeric antibodies. eptifibatide (Integrelin) = synthetic peptide form. tirofiban (Aggrastat) = synthetic peptide forms.

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  • 45. 

    What type of anticoagulant acts as a platelet glycoprotein IIb/IIIa receptor antagonist?

    • A.

      Heparin

    • B.

      Warfarin

    • C.

      Thrombolytic Agents

    • D.

      Super Aspirins

    Correct Answer
    D. Super Aspirins
    Explanation
    Acts as reversible antagonists of glycoprotein IIb/IIIa - the receptor on the platelet for adhesive proteins such as fibrinogen and von Willebrand factor. Maximally inhibit the final common pathway involved in platelet adhesion, activation, and aggregation.

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  • 46. 

    What are the indications for platelet glycoprotein IIb/IIIa receptor antagonists (Super Aspirins)?

    • A.

      MI

    • B.

      Coronary artery syndrome

    • C.

      Renal failure

    • D.

      Following coronary artery revascularization (angioplasty)

    • E.

      A, B, and D

    • F.

      B and D

    • G.

      All of the above.

    Correct Answer
    F. B and D
    Explanation
    Drugs are infused - rapid acting - and rapidly reversed after stopping infusion - major side effect: bleeding.

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  • 47. 

    Which (2) drug'(s) mechanism of action is proposed interference with platelet function by increasing the cellular concentration of cyclic AMP, by decreasing phosphodiesterase activity, or raising adenosine levels?

    • A.

      Aspirin

    • B.

      Cilostazol (Pletal)

    • C.

      Dipyridamole

    • D.

      Abciximab

    • E.

      A, B, and C

    • F.

      B and C

    Correct Answer
    F. B and C
    Explanation
    Inhibits platelet activation by increasing cellular cyclic AMP by inhibiting a phosphodiesterase that degrades cAMP.

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  • 48. 

    What is the major difference between cilostazol (Pletal) and dipyridamole?

    • A.

      Cilostazol is more potent than dipyridamole.

    • B.

      Cilostazol must be given with aspirin to be effective.

    • C.

      Dipyridamole is toxic in children.

    • D.

      Dipyridamole must be given with aspirin to be effective.

    Correct Answer
    D. Dipyridamole must be given with aspirin to be effective.
    Explanation
    Dipyridamole and aspirin formulation (Aggrenox) is recommended for use with prosthetic heart valves in combination with aspirin. Technically A would be true too but is not the most important difference between the two. More platelet inhibition is seen with cilostazol than with aspirin or dipyridamole.

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  • 49. 

    What disorder is cilostazol strongly contraindicated in?

    • A.

      Renal failure.

    • B.

      Gout.

    • C.

      Alzheimer's.

    • D.

      Congestive heart failure.

    Correct Answer
    D. Congestive heart failure.
    Explanation
    (I'm not sure why, but according to my notes, emphasis was placed on the importance of this point...)

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  • 50. 

    What drug would likely be prescribed for a patient with atherosclerosis in the legs (intermittent claudication) causing pain, cramping, and weakness in calf muscles when walking?

    • A.

      Aspirin

    • B.

      Dipyridamole

    • C.

      Cilostazol

    • D.

      Niacin

    Correct Answer
    C. Cilostazol
    Explanation
    Cilostazol would likely be prescribed for a patient with atherosclerosis in the legs causing intermittent claudication. Cilostazol is a medication that helps improve blood flow by dilating the blood vessels and reducing platelet aggregation. It is specifically indicated for the treatment of intermittent claudication, which is characterized by pain, cramping, and weakness in the calf muscles during physical activity such as walking. Aspirin, Dipyridamole, and Niacin may have other uses, but Cilostazol is the most appropriate choice for this particular condition.

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Our quizzes are rigorously reviewed, monitored and continuously updated by our expert board to maintain accuracy, relevance, and timeliness.

  • Current Version
  • Apr 17, 2024
    Quiz Edited by
    ProProfs Editorial Team
  • Nov 08, 2010
    Quiz Created by
    Krys2001
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