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951 Block 3 > 4. Antiplatelet Drugs > Flashcards

4. Antiplatelet Drugs Flashcards

1
Q

Platelets do not have a nucleus. (T/F)

A

True

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2
Q

Where do platelets originate?

A

megakaryocytes from the bone marrow

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3
Q

What is the life span of a platelet?

A

~ 10 days

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4
Q

What is a normal platelet count?

A

150,000 – 450,000 / μL

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5
Q

What are the 4 main mechanisms that activate platelets?

A
  • underlying disease
  • endothelial injury
  • collagen
  • von Willebrand factor
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6
Q

Agonists bind to platelet receptors that initiate a signaling cascade that results in:

A
  • platelet shape change
  • granule release
  • thromboxane A2 generation
  • GP IIb/IIIa receptor activation
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7
Q

What are the platelet receptors that initiate activation?

A

glycoprotein IIb/IIIa

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8
Q

What are potent platelet activation agonists?

A
  • binding to collagen after vascular damage

- thrombin

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9
Q

What are weak platelet activation agonists?

A
  • ADP
  • TxA2
  • Epinephrine
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10
Q

Platelets are activated by what G proteins?

A
  • q and i

- G (12/13) families

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11
Q

Platelets are inhibited by what G proteins?

A

s

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12
Q

Platelet granule release occurs after ______.

A

adhesion

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13
Q

What are the 3 types of granules?

A
  • alpha
  • dense
  • lysosomal
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14
Q

What is platelet adhesion?

A

Platelets bind to damaged area via GP Ib and GP VI

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15
Q

What is platelet aggregation?

A

fibrinogen binds to activated GP IIb/IIIa receptors

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16
Q

Platelets meshed in fibrin is called what?

A

hemostatic plug

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17
Q

What is a hemostatic plug made up of?

A

platelets and fibrin mesh

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18
Q

What are the indications for antiplatelet agents?

A
  • cerebrovascular disease
  • ACS/ unstable angina
  • PAD
  • CABG or PCI
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19
Q

What are the antiplatelet agents?

A
  • ASA
  • thienopyridines
  • GP IIb/IIIa antagonists
  • Phosphodiesterase inhibitors
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20
Q

What are the thienopyridine agents?

A
  • clopidogrel (Plavix)

- prasugrel (Effient)

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21
Q

What are the GP IIb/IIIa inhibitors?

A
  • abciximab (Reopro)
  • eptifibatide (Integrilin)
  • tirofiban (Aggrastat)
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22
Q

What is the MOA of ASA?

A

Acetylation at Ser529 results in irreversible inhibition of COX-1 for the life of the platelet.

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23
Q

High doses of ASA inhibit what?

A

both COX-1 and COX-2

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24
Q

Why are lower doses of ASA effective for antiplatelet response?

A
  • inhibition of platelet COX-1 occurs at lower doses than inhibition of COX-2 in the vessel wall
  • platelets have no nucleus
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25
Q

What is the onset of action for platelet inhibition with ASA?

A

~ 5 minutes

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26
Q

What is the duration of antiplatelet action with ASA?

A

7-10 days

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27
Q

What are the ADRs with ASA?

A
  • GI upset

- bleeding

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28
Q

ASA therapy in combination with _______ can inhibit the site of action for ASA and reduce its antiplatelet effects.

A

other NSAIDs

29
Q

What is the MOA of thienopyridines?

A
  • irreversible antagonist of platelet P2Y12 ADP receptors

- the P2Y12 receptor couples to Gi to inhibit adenylyl cyclase

30
Q

What is the route of administration of clopidogrel?

A

oral

31
Q

Maximal platelet inhibition occurs within _______ of oral administration of clopidogrel.

A

5-7 days

32
Q

Antiplatelet effects of clopidogrel persist for _______ after discontinuing.

A

4-8 days

33
Q

Clopidogrel is a prodrug. (T/F)

A

True

34
Q

Clopidogrel is a preferred agent because it has very little variation among patients. (T/F)

A

False: variability is an issue with clopidogrel

35
Q

Prasugrel is a prodrug. (T/F)

A

True

36
Q

What is the route of administration of prasugrel?

A

oral

37
Q

Prasugrel requires hepatic conversion to an active metabolite. (T/F)

A

True

38
Q

Which thienopyridine has the quickest onset of action?

A

prasugrel

39
Q

Clopidogrel is considered more efficacious for ACS than Ticagrelor. (T/F)

A

False: ticagrelor is considered more efficacious

40
Q

Ticagrelor requires hepatic conversion to an active metabolite. (T/F)

A

False: no required metabolic activation

41
Q

What is the route of administration of ticagrelor?

A

oral

42
Q

Ticagrelor is not a thienopyridine. (T/F)

A

True

43
Q

Ticagrelor irreversibly binds to the platelet P2Y12 receptor. (T/F)

A

False: reversibly

44
Q

Cangrelor is a reversible P2Y12 receptor antagonist. (T/F)

A

True

45
Q

What is the route of administration of cangrelor?

A

IV

46
Q

Cangrelor is not a thienopyridine. (T/F)

A

True

47
Q

Cangrelor requires hepatic activation. (T/F)

A

False

48
Q

The antiplatelet effects of cangrelor are reversed ________(slowly/quickly) after stopping infusion.

A

quickly

49
Q

What is cangrelor FDA approved for?

A

Adjunct during PCI to reduce thrombosis

50
Q

What is the MOA of GP IIb/IIIa antagonists?

A

Inhibits binding of fibrinogen to the activated GP IIb/IIIa receptor to prevent platelet aggregation.

51
Q

Monoclonal antibody that binds GP IIb/IIIa receptor

A

abciximab

52
Q

reversible RGD-mimetic peptide that binds GP IIb/IIIa receptor

A

eptifibatide

53
Q

reversible non peptide RGD-mimetic that binds GP IIb/IIIa receptor

A

tirofiban

54
Q

What is the route of administration for GP IIb/IIIa inhibitors?

A

IV

55
Q

What is the onset of action for GP IIb/IIIa inhibitors?

A

minutes

56
Q

What is the duration of action for GP IIb/IIIa inhibitors?

A

abciximab: up to 72 hours

eptifibatide and tirofiban 4-6 hours

57
Q

GP IIb/IIIa inhibitors are often used in combination with _______ during PCI.

A

clopidogrel

58
Q

What is the main ADR of GP IIb/IIIa inhibitors?

A

bleeding

59
Q

GP IIb/IIIa inhibitors are available as oral formulation. (T/F)

A

False

60
Q

What are the anticoagulant phosphodiesterase inhibitor agents?

A
  • Aggrenox
  • Persantine
  • Cilostazol
61
Q

What are the components of Aggrenox?

A
  • aspirin 25 mg

- dipyridamole ER 200 mg

62
Q

What is Aggrenox indicated for?

A

ischemic stroke and TIA

63
Q

What are the components of Persantine?

A

dipyridamole only: not effective antiplatelet

64
Q

What is Cilostazol approved for?

A

intermittent claudication

65
Q

What is the MOA for Vorapaxar?

A

protease-activated receptor-1 (PAR-1) antagonist

66
Q

What is Vorapaxar approved for?

A

reduce trombosis in patients with previous MI or PAD

67
Q

What is the route of administration of Vorapaxar?

A

oral

68
Q

Why is Vorapaxar considered to have irreversible effects?

A

While the antagonism is reversible, the half-life is so long (8 days) that it is considered to be irreversible because the life span of a platelet is 8-9 days.

69
Q

What are the contraindications for Vorapaxar?

A
  • history of stroke or TIA
  • intracranial hemorrhage
  • current active bleeding

951 Block 3 (10 decks)

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