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Pharm > chapter 52: Anticoagulant, Antiplatelet, and thrombolytic Drugs > Flashcards

chapter 52: Anticoagulant, Antiplatelet, and thrombolytic Drugs Flashcards

1
Q

What are the 2 mechanisms of hemostasis?

A

Platelet plug
coagulation

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2
Q

What are the 3 major groups of drugs that are used for thromboembolic disorder?

A
  1. anticoagulants
  2. antiplatlet
  3. thrombolytics
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3
Q

What suppresses the productioin of fibrin?

A

Anticoagulants

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4
Q

What inhibits platelet aggregation?

A

Antiplatelet

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5
Q

What promotes lysis of fibrin?

A

Thrombolytic

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6
Q

True or false?
Most thrombolytic agents are non-specific and can dissolve any clot found in the body

A

True

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7
Q

True or false?
Warfarin is considered a Vitamin K agonist.

A

False, it is considered a Vitamin K antagonist

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8
Q

What is usually given in combination with warfarin until warfarin reaches therapeutic levels and why?

A

Heparin, warfarins effects do not occur for 3-5 days after it is begun

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9
Q

What drug does not activate antithrombin?

A

Warfarin

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10
Q

warfarin inhibits the synthesis of what?

A

Vitamin-k dependent clotting factors

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11
Q

What are the 4 vitamin-K clotting factors?

A

-Vll
-lX
-X
-ll (prothrombin)

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12
Q

Warfarin does not have an effect on what?

A

already circulating clotting factors

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13
Q

What does heparin enhance the activity of?

A

antithrombin

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14
Q

what are the 2 major clotting factors does antithrombin inhibit?

A
  • thrombin
    -factor xa
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15
Q

What does the enhancing of antithrombin lead to?

A

The production of fibrin to be reduced

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16
Q

What must heparin bind to to inactivate thrombin?

A

-antithrombin
-thrombin

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17
Q

What must heparin bind with to inactivate factor Xa?

A

-antithrombin

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18
Q

Which drug has a more rapid onset of action and shorter half-life.
warfarin or heparin?

A

Heparin

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19
Q

What is the antidote for heparin overdose?

A

protamine sulfate

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20
Q

What pathway does heparin use?

A

intrinsic pathway

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21
Q

What pathway warfarin use?

A

extrinsic pathway of the coagulation cascade

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22
Q

What routes can heparin be administered?

A

-IV
-SQ

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23
Q

What is the preferred anticoagulant in pregnant women and why?

A

Heparin; it does not cross the placenta

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24
Q

What happens when heparin is given oral or IM?

A

It is rapidly inactivated

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25
Q

Bleeding is the principle complication in what type of treatment?

A

Anticoagulant

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26
Q

What can a patient develop from heparin use?

A

thrombocytopenia
(DISCONTINUE IF THIS OCCURS)

27
Q

A pt was given 100 units of heparin, how much protamine will inactive this dose of heparin?

A

1 mg

28
Q

How long should aPTT levels be measured?

A

every 4-6 hours until therapeutic levels have been sustained

29
Q

Normal value for aPTT?

A

40 seconds

30
Q

Therapeutic levels of heparin should increase the aPTT by a factor of 1.5-2.0, what would this make the aPTT?

A

60-80 seconds

31
Q

When should aPTT not be monitered?

A

When giving low-dose SQ heparin

32
Q

What drug is determined by the persons weight?

A

Enoxaparin

33
Q

What does enoxaprin have a greater inhibitor effect on?

A

Factor Xa> thrombin

34
Q

Which class has a longer duration of action and a more predictable plasma level?

A

LMW Heparins

35
Q

How is fondaparinux administered?

A

SQ

36
Q

What drug binds selectively to factor Xa?

A

fondaparinux

37
Q

What is the suffix for the LMW Heparins?

A

“parin”

38
Q

What effect does fondaprinux have on thrombin?

A

Reduces the production (not activity) of thrombin

39
Q

What is an example of a direct thrombin inhibitor?

A

Dabigatran

40
Q

What type of thombin does dabigatran act on?

A

-clot-bound
-circulating thrombin

41
Q

Why is dabigatran administered PO?

A

prevent the conversion of fibrinogen to fibrin

42
Q

Warfarin inhibits the enzyme needed to to convert what?

A

Vitamin K to its’ active form

43
Q

What type of food should remain consistent when taking warfarin?

A

Vitamin K foods (green, leafy vegetables)

44
Q

What receptors are the most effective antiplatelet drugs available.

A

GP llb/llla receptor antagonist

45
Q

What drugs are also called “super aspirins”?

A

GP llb/llla receptor antagonist

46
Q

How is the dose of warfarin determined?

A

INR (less variability than the Prothrombin time (PT)

47
Q

Target INR for warfarin?

A

2.0-3.0

48
Q

What is the antidote for warfarin?

A

Vitamin K1

49
Q

Vitamin K1 is administered how?

A

-PO
-IV

50
Q

What are the 3 main categories of drug interactions that occur with warfarin?

A

-Drugs that increase effects of warfarin
-drugs that promote bleeding
-drugs that decrease effects of warfarin

51
Q

What are the 3 main categories of antiplatelet drugs?

A

-aspirin (ASA)
-ADP receptor blockers
-GP llb/llla receptor antagonist

52
Q

Aspirin blocks COX-1 which leads to the blockage of what?

A

thromboxane A2

53
Q

The blockage of thromboxane A2 causes what two actions to occur that promote hemostasis?

A
  1. platelet activation
  2. vasoconstriction
54
Q

Aspirin is the only NSAID that provides protection from what?

A

-MI
-CVA

55
Q

Clopidogrel irreverisbly inhibits platelet aggregation by doing what?

A

preventing P2Y12 ADP-induced binding between platelets and fibrinogen

56
Q

What is another name for thrombolytics that dissolve/destroy thromi that have already fotmed?

A

fibronlytics

57
Q

Most serious concern r/t bleeding is…

A

Intracranial hemorrhage

58
Q

The GP llb/llla receptor antagonists cause revirsable blockade of platelet Gp llb/llla receptors.When activated, these receptors change change their structure so they can bind to__________.

A

Fibrinogen

59
Q

Alteplase first binds to plasminogen forming a drug complex. This complex does what?

A

-Catalyzes the conversion of plasminogen molecules into plasmin.

60
Q

Plasmin does what?

A

-digests the fibrin meshwork of clots
-degrades fibrinogen and other clotting factors

61
Q

Why is bleeding the major complication of thrombolytics?

A

Ty can destroy preexisting clots of recently healed injuries and can disrupt coagulation by interfering with new clot formation

62
Q

How soon should you begin therapy after onset of symptoms from an acute MI

A

6 hours

63
Q

How long should you being therapy relating to a thrombotic stroke?

A

3 hours

Pharm (11 decks)

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