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PMCOL 344 > Anti-Platelets > Flashcards

Anti-Platelets Flashcards

1
Q

what is hemotasis

A

the arrest of bleeding from damaged vessels

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2
Q

what happens after vascular injury

A

platelet adhesion

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3
Q

what happens after platelet adhesion

A

platelet aggregation

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4
Q

what happens after platelet aggregation

A

fibrin formation (coagulation)

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5
Q

what happens after fibrin formation (coagulation)

A

fibrinolysis

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6
Q

what happens after fibrinolysis

A

vascular repair

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7
Q

what is platelet aggregation

A

Platelets going through will stick to the ones that are already stuck - platelet aggregation, platelet plug formation

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8
Q

what is the role of fibrin

A

it sticks to initial platelet plug and strengthens it (large strands)

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9
Q

what does prothrombin get converted into

A

thrombin

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10
Q

which factor is prothrombin

A

2

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11
Q

which factor is thrombin

A

2a

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12
Q

what does fibrinogen turn into and how

A

fibrin via activation by thrombin

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13
Q

what does plasminogen turn into and how

A

plasmin via activation by tPA

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14
Q

what does plasmin do

A

degrades fibrin clots - fibrinolysis

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15
Q

what activities tPA

A

PA-I turns into it or something

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16
Q

what is thrombosis

A

pathological formation of hemostatic plug, often occurs in the absence of bleeding

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17
Q

what is the difference with thrombosis and hemostasis

A

‘haemostasis’ is to the normal response of the vessel to injury by forming a clot. Thrombosis is pathological clot formation that results when haemostasis is excessively activated in the absence of bleeding

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18
Q

where do white clots occur + description

A

arterial, rapid blood flow, more platelet activation and aggregation (arteries of heart and brain)

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19
Q

where do red clots occur + description

A

venous, relative stasis, not enough fast flow (veins, chambers of heart)

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20
Q

which clots of in the brain

A

white

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21
Q

which clots of in the chambers of the heart

A

red

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22
Q

what is the composition of white clots

A

mainly platelets with some fibrin (platelets are white)

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23
Q

what is the composition of red clots

A

fibrin and erythrocytes, few platelet (fibrin traps RBC)

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24
Q

what is the main risk factor for white clots

A

ruptured atherosclerotic plaque

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25
Q

what is the main risk factor for red clots

A

slow disturbed flow, hyper-coagulable state

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26
Q

what is the clinical presentation of white clot

A

myocardial infarction, cerebrovascular stroke

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27
Q

what is the clinical presentation of red clot

A

venous thromboembolism, cardioembolic stroke (Clot forms in heart and travels to brain)

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28
Q

what is the treatment for red clots

A

anticoagulant drugs

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29
Q

what is the treatment for white clots

A

anti platelet drugs

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30
Q

what do you use anti platelet drugs for

A

white clots

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31
Q

what do you use anti coagulant drugs for

A

red clots

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32
Q

what are 2 preventions for thrombosis

A

anti platelet and anti coagulants

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33
Q

what is 1 treatment for thrombosis

A

thrombolytic drugs, fibrinolytics

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34
Q

what are the 5 classes of anti platelet drugs

A

acetylsalicylic acid, thienopyridines, non-thienopyridine P2Y12 antagonist, dipyridamole, GPIIb/IIIa receptor antagonists

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35
Q

what are 3 examples of thienopyridines

A

ticlopidine, clopidogrel, prasugrel

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36
Q

what are 3 examples of GP GPIIb/IIIa receptor antagonists

A

abciximab, eptifibatide, tirofiban

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37
Q

what is 1 example of non-thienopyridine P2Y12 antagonist

A

ticagrelor

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38
Q

what do anti platelet drugs do

A

prevent platelets from sticking together (aggregating) so then less CV events

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39
Q

what does collagen do

A

its a potent platelet activator

40
Q

what do platelets release once activated

A

ADP and TXA2

41
Q

what does ADP and TXA2 release from platelets cause

A

GPIIb/IIIa activation and fibrinogen binding

42
Q

what does GP11b/111a activation and fibrinogen binding cause

A

aggregation

43
Q

what is the most important receptor on platelets

A

GPIIb/IIIa

44
Q

what activates GPIIb/IIIa

A

fibrinogen

45
Q

what kind of blood effects does aspirin have

A

anti-platelet effects

46
Q

what is the mechanism of aspirin

A

irreversibly acetylates and inhibits COX-1 thereby preventing TXA2 synthesis

47
Q

what is the role of TXA2

A

potent platelet aggregation stimulator

48
Q

how long does ASA inhibition last

A

for life span of platelets, 7-10 days

49
Q

why does it last so long with ASA

A

because platelets have no nucleus to resynthesizes COX

50
Q

what are unwanted GI effects of ASA

A

ulcer formation and bleeding

51
Q

what is a bad side effect of all anti platelet drugs

A

increased bleeding (decreased hemostatic function)

52
Q

what is a syndrome that ASA can cause

A

Reye’s syndrome

53
Q

how does reyes syndrome happen

A

in children that take ASA with viral infection

54
Q

what happens to some people with asthma and nasal polyps and ASA

A

they get hypersensitivity allergic reactions

55
Q

what can happen to people with renal disease who take ASA

A

decreased glomerular filtration

56
Q

what can happen to liver with people who take ASA

A

mild hepatitis (with high doses)

57
Q

what is the activity of thienopyridines

A

orally active prodrugs requiring hepatic conversion to active metabolites

58
Q

what is the mechanism of action of thienopyridines

A

irreversible, non competitive antagonists of ADP binding to P2Y12 receptors on platelet surface

59
Q

which drug class inhibits the TXA2 pathway

A

ASA

60
Q

which drug class inhibits the ADP pathway

A

thienopyridines

61
Q

which was the first thienopyridines

A

ticlopidine

62
Q

what are the unwanted effects of ticlopidine

A

neutropenia (low neutrophils) and thrombocytopenia (low platelets)

63
Q

what drug replaced ticlopidine

A

clopidrogrel

64
Q

what is unwanted effects of clopidrogrel

A

indigestion, rash, diarrhea

65
Q

who usually takes clopidrogrel

A

ASA intolerant individuals (like people who get bleeding, ulcers)

66
Q

what is the rate of metabolism of clopidrogrel

A

quick after oral admin, like 5 hours

67
Q

what is a main problem with clopidrogrel

A

some patients with variant CYP2C19 alleles are poor metabolizers, so it isnt made into the active metabolite

68
Q

which is the newest thienopyridine

A

prasugrel

69
Q

what is the rate of biotransformation of prasugrel

A

30mins (almost as fast as ASA)

70
Q

what is the main pro/con of prasugrel

A

more efficacious=more bleeding

71
Q

what is ticagrelor (class)

A

non-thienopyridine P2Y12 antagonist

72
Q

what is ticlopidine (class)

A

thienopyridine

73
Q

what is prasugrel (class)

A

thienopyridine

74
Q

what is clopidogrel (class)

A

thienopyridine

75
Q

what is the mechanism of action of ticagrelor

A

orally active reversible allosteric P2Y12 antagonist

76
Q

what is the activation of ticagrelor

A

direct action!!!! not a Pro drug

77
Q

what are adverse effects of ticagrelor

A

dyspnea (shortness of breath), bradyarrythmia

78
Q

which 3 drugs are often combined for dual anti-platelet therapy

A

ASA with P2Y12 inhibitors (ticagrelor and clopidogrel)

79
Q

when is dual anti-platelet therapy often used

A

one year following MI and one month following cerebrovascular stroke

80
Q

what is the main mechanism of dipyridamole

A

cyclic nucleotide phosphodiesterase inhibitor (more cAMP & cGMP so longer signal to prevent platelets from sticking together)

81
Q

what are 2 other mechanisms for dipyridamole

A

blocks adenosine uptake (weak platelet inhibitor)

decrease platelet TXA2 / or increase endothelial PGI2 synthesis

82
Q

what does adenosine do

A

weak platelet inhibitor

83
Q

is dipyridamole effective alone

A

no, so its used with ASA

84
Q

when/ how is dipyridamole used

A

with ASA to prevent transient ischemic attacks and stroke

85
Q

what is the role of fibrinogen

A

cross links platelets upon aggregation

86
Q

what is GPIIb/IIIa

A

fibrinogen receptor

87
Q

what is the mechanism of action of GPIIb/IIIa antagonists

A

block receptor or compete for occupancy with fibrinogen

88
Q

what step does GPIIb/IIIa inhibit

A

the final common step leading to platelet aggregation (after the ADP and TXA2 steps)

89
Q

what is abciximab

A

mouse/human chimeric monoclonal Ab vs. GPIIb/IIIa

90
Q

what is eptifibatide

A

synthetic cyclic heptapeptide

91
Q

what is tirofiban

A

synthetic non-peptide

92
Q

how does tirofiban and eptifibatide work

A

they have a similar amino acid sequence to the GPIIb/IIIa ligands, so they can block the receptor

93
Q

how are the GPIIb/IIIa antagonists administered

A

IV

94
Q

who are GPIIb/IIIa antagonists given to

A

prevent thrombosis in patients with acute coronary syndromes or undergoing coronary angioplasty

95
Q

what are 2 unwanted effects of GPIIb/IIIa antagonists

A

bleeding and thrombocytopenia (low platelet counts)

96
Q

is ASA a potent anticoagulant

A

no

97
Q

is ASA reversible

A

no

PMCOL 344 (27 decks)

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