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Pharmacology Test #4 > Coagulation/Antiplatelet Pharmacology > Flashcards

Coagulation/Antiplatelet Pharmacology Flashcards

1
Q

Hemostasis

A

arrest of bleeding from a damaged blood vessel

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2
Q

Coagulation

A

multi-step process to plus the leaking vessel

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3
Q

Platelets have organelles and secretory granules but no

A

nucleus

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4
Q

The platelet reactions that contact with the ECM initiates

A
  1. adhesion and shape change
  2. secretion reaction
  3. aggregation
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5
Q

First step of platelet activation

A

platelet adhesion and shape change

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6
Q

Platelet adhesion is mediated by

A

GPIa binding to collagen; GP1b binding to von Willebrand factor bridged to collagen; shape change facilitates receptor binding

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7
Q

Intact endothelial cells secret

A

PGI2 (prostacyclin) to inhibit thrombogenesis (inhibits platelet activation and vasodilation)

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8
Q

Second step of platelet activation

A

platelet secretion

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9
Q

Platelet granules release

A

ADP, thromboxane A2 (TXA2), serotonin (5-HT)

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10
Q

ADP, 5-HT, and TXA2 activate and recruit

A

other platelet

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11
Q

TXA2 and 5-HT are

A

potent vasoconstrictors

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12
Q

Third step of platelet activation

A

platelet aggregation

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13
Q

ADP, 5-HT and TXA2 activation induces

A

conformation of GPIIB/IIIa receptors to bind fibrinogen

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14
Q

Platelets are cross-linked by

A

fibrinogen

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15
Q

Cross-linked platelets forms

A

temporary hemostatic plug

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16
Q

Platelets contract to form

A

irreversibly fused mass

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17
Q

What does fibrin do?

A

stabilizes and anchors aggregated platelets and forms surface for clot formation

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18
Q

Antiplatelet drugs

A
  1. COX-1 inhibitors
  2. ADP receptor inhibitors
  3. Blockers of GPIIb/IIIa receptors
  4. Phosphodiesterase-3 inhibitors
  5. Protease-activated receptor inhibitors (in development)
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19
Q

Aspirin is a

A

COX-1 inhibitor

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20
Q

MOA of aspirin

A

irreversibly inhibits platelet COX-1 by acetylation; interferes with platelet aggregation, prolongs bleeding time; prevents arterial thrombi formation

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21
Q

The key to anti-platelet activity of aspirin

A

inhibition of TXA2 synthesis in platelets

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22
Q

Aspirin is maximally effective at doses of

A

50-320 mg per day

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23
Q

Higher doses of aspirin inhibits

A

prostacyclin production

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24
Q

Indications for aspirin

A
  1. prevent coronary thrombosis in unstable angina
  2. adjunct to thrombolytic therapy
  3. reducing recurrence of thrombotic stroke
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25
Q

Clinical actions of aspirin

A

prolongs bleeding time, but no increase in PT time

hemostasis returns to normal 36 hr after last dose

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26
Q

ADP receptor inhibitors

A

P2Y 1 and P2Y 12

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27
Q

P2Y1 is coupled to

A

Gq-PCL-IP3-Ca2+ pathway

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28
Q

P2Y12 is coupled to

A

Gi and inhibition of adenylyl cylase

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29
Q

Action of which pathways is required for platelet activation by ADP

A

both the Gq-PCL-IP2-Ca2+ pathway and the Gi, inhibition of adenylyl cyclase pathway

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30
Q

P2Y12 ADP receptor inhibitors are taken

A

orally to reduce platelet aggregation

31
Q

MOA of P2Y12 ADP receptor inhibitors

A

irreversibly block ADP receptor on platelet and subsequent activation of GPIIb/IIIa complex

32
Q

Difference between Ticlopidine and Clopidogrel

A

Clopidogrel has lower toxicity profile

33
Q

Ticlopidine may induce

A

thrombotic thrombocytopenis purpura (TTP)

34
Q

Uses for P2Y12 ADP receptor inhibitors

A

acute coronary syndrome, recent MI, stroke, established peripheral vascular disease and coronary stent procedures

35
Q

How long does the action of Ticlodipine and Clopidogrel last

A

lasts for several days after the last dose

36
Q

ADAMTS13

A

protease that cleaves circulating vWF

37
Q

How often is Ticlopidine (Ticlid) used

A

isn’t used much anymore

38
Q

Prasugrel

A

irreversible P2Y12 ADP receptor inhibitor

39
Q

Prasugrel is approved for the treatment of

A

acute coronary syndrome, percutaneous coronary intervention

40
Q

Prasugrel requires

A

metabolism to an active metabolite (prodrug)

41
Q

Faster onset of action and increased potency of Prasugrel is due to

A

rapid metabolism by liver CYP450

42
Q

Ticagrelor (Brilinta) used in

A

acute coronary syndrome; PCI - taken orally

43
Q

MOA of Ticargrelor (Brilinta)

A

binds to an allosteric site, binding is reversible (plaletlet function comes back more quickly)

44
Q

Ticagrelor compared to Clopidogrel

A

Ticagrelor does not require bioactivation by metabolic enzymes and has a faster onset of action compared to clopidogrel

45
Q

Clopidogrel is activated by

A

CYP2C19 (enzyme very variable between populations)

46
Q

Prasugrel is activated by

A

Hydrolases/CYP3A4/CYP2B6

47
Q

Eptifibatide is a

A

Glycoprotein IIb/IIIa receptor inhibitor

48
Q

MOA of Eptifibatide

A

inhibits fibrinogen binding to decrease platelet aggretion

49
Q

Eptifibatide is derived from

A

cyclic heptapeptide derived from rattlesnake venom

50
Q

How is Eptifibatide administered

A

administered by IV bolus, followed by infusion up to 72 hours

51
Q

Duration of action of Eptifibatide

A

short duration of action; 6-12 hours

52
Q

Tirofiban (Aggrastat)

A

Glycoprotein IIb/IIIa receptor inhibitor

53
Q

MOA of Tirofiban

A

reversible inhibitor of fibrinogen binding to the GPIIb/IIIa receptor

54
Q

How is Tirofiban adminsitered

A

adminstered IV in dilute solution

55
Q

Tirofiban combined with heparin is used to treat

A

Acute coronary syndrome

56
Q

Abciximab (ReoPro)

A

Fab fragment of chimeric human-murine monoclonal Ab; binds to GP IIb/IIIa receptor to inhibit platelet aggregation

57
Q

Administration and duration of action of Abciximab

A

administered IV bolus, followed by infusion; long duration of action - increased risk of bleeding

58
Q

Use of Abciximab (ReoPro)

A

prevent thromboembolism in coronary angioplasty

59
Q

Abciximab and t-PA is combined for the treatment of

A

early treatment of acute MI

60
Q

What do PDE3 inhibitors do

A

inhibit platelet aggregation

61
Q

Action of PDE3 inhibitors is related to

A

related to cAMP PDE inhibition (opposing P2Y12 action) and inhibition of adenosine uptake

62
Q

PDE inhibitors

A

Dipyridamole (Persantine) and Cilostazol (Pletal)

63
Q

Use of Dipyridamole (PDEi)

A

combined with warfarin to prevent embolization from prosthetic heart valves; used with aspirin to prevent cerebrovascular ischemia

64
Q

Use of Cilostazol (PDEi)

A

intermittent claudication

65
Q

Protease activated receptor (PAR) inhibitors

A

Vorapaxar and Atopaxar

66
Q

MOA for protease activated receptor inhibitors

A

proteolytic cleavage of PAR-1 receptors on platelet surface

67
Q

PARs are

A

GPCRs coupled to release of Ca2+ from stores

68
Q

Thrombin activates

A

platelets at nanomolar concentrations

69
Q

Vorapaxar

A

reversible PAR-1 receptor antagonist; prophylactic to prevent thrombosis in patients with a previous MI or peripheral arterial disease

70
Q

Vorapaxar is used with

A

aspirin or clopidogrel

71
Q

Contraindications for Vorapaxar

A

history of stroke, TIAs, or intracranial hemorrhage

72
Q

Half life of Vorapaxar

A

half life of 3-4 days; antiplatelet effect persists for days after discontinuation

73
Q

Vorapaxar is metabolized by

A

CYP3A4

74
Q

Avoid use of Vorapaxar with

A

strong 3A4 inhibitors or inducers

Pharmacology Test #4 (9 decks)

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