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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
what is the main risk factor for red clots
slow disturbed flow, hyper-coagulable state
26
what is the clinical presentation of white clot
myocardial infarction, cerebrovascular stroke
27
what is the clinical presentation of red clot
venous thromboembolism, cardioembolic stroke (Clot forms in heart and travels to brain)
28
what is the treatment for red clots
anticoagulant drugs
29
what is the treatment for white clots
anti platelet drugs
30
what do you use anti platelet drugs for
white clots
31
what do you use anti coagulant drugs for
red clots
32
what are 2 preventions for thrombosis
anti platelet and anti coagulants
33
what is 1 treatment for thrombosis
thrombolytic drugs, fibrinolytics
34
what are the 5 classes of anti platelet drugs
acetylsalicylic acid, thienopyridines, non-thienopyridine P2Y12 antagonist, dipyridamole, GPIIb/IIIa receptor antagonists
35
what are 3 examples of thienopyridines
ticlopidine, clopidogrel, prasugrel
36
what are 3 examples of GP GPIIb/IIIa receptor antagonists
abciximab, eptifibatide, tirofiban
37
what is 1 example of non-thienopyridine P2Y12 antagonist
ticagrelor
38
what do anti platelet drugs do
prevent platelets from sticking together (aggregating) so then less CV events
39
what does collagen do
its a potent platelet activator
40
what do platelets release once activated
ADP and TXA2
41
what does ADP and TXA2 release from platelets cause
GPIIb/IIIa activation and fibrinogen binding
42
what does GP11b/111a activation and fibrinogen binding cause
aggregation
43
what is the most important receptor on platelets
GPIIb/IIIa
44
what activates GPIIb/IIIa
fibrinogen
45
what kind of blood effects does aspirin have
anti-platelet effects
46
what is the mechanism of aspirin
irreversibly acetylates and inhibits COX-1 thereby preventing TXA2 synthesis
47
what is the role of TXA2
potent platelet aggregation stimulator
48
how long does ASA inhibition last
for life span of platelets, 7-10 days
49
why does it last so long with ASA
because platelets have no nucleus to resynthesizes COX
50
what are unwanted GI effects of ASA
ulcer formation and bleeding
51
what is a bad side effect of all anti platelet drugs
increased bleeding (decreased hemostatic function)
52
what is a syndrome that ASA can cause
Reye's syndrome
53
how does reyes syndrome happen
in children that take ASA with viral infection
54
what happens to some people with asthma and nasal polyps and ASA
they get hypersensitivity allergic reactions
55
what can happen to people with renal disease who take ASA
decreased glomerular filtration
56
what can happen to liver with people who take ASA
mild hepatitis (with high doses)
57
what is the activity of thienopyridines
orally active prodrugs requiring hepatic conversion to active metabolites
58
what is the mechanism of action of thienopyridines
irreversible, non competitive antagonists of ADP binding to P2Y12 receptors on platelet surface
59
which drug class inhibits the TXA2 pathway
ASA
60
which drug class inhibits the ADP pathway
thienopyridines
61
which was the first thienopyridines
ticlopidine
62
what are the unwanted effects of ticlopidine
neutropenia (low neutrophils) and thrombocytopenia (low platelets)
63
what drug replaced ticlopidine
clopidrogrel
64
what is unwanted effects of clopidrogrel
indigestion, rash, diarrhea
65
who usually takes clopidrogrel
ASA intolerant individuals (like people who get bleeding, ulcers)
66
what is the rate of metabolism of clopidrogrel
quick after oral admin, like 5 hours
67
what is a main problem with clopidrogrel
some patients with variant CYP2C19 alleles are poor metabolizers, so it isnt made into the active metabolite
68
which is the newest thienopyridine
prasugrel
69
what is the rate of biotransformation of prasugrel
30mins (almost as fast as ASA)
70
what is the main pro/con of prasugrel
more efficacious=more bleeding
71
what is ticagrelor (class)
non-thienopyridine P2Y12 antagonist
72
what is ticlopidine (class)
thienopyridine
73
what is prasugrel (class)
thienopyridine
74
what is clopidogrel (class)
thienopyridine
75
what is the mechanism of action of ticagrelor
orally active reversible allosteric P2Y12 antagonist
76
what is the activation of ticagrelor
direct action!!!! not a Pro drug
77
what are adverse effects of ticagrelor
dyspnea (shortness of breath), bradyarrythmia
78
which 3 drugs are often combined for dual anti-platelet therapy
ASA with P2Y12 inhibitors (ticagrelor and clopidogrel)
79
when is dual anti-platelet therapy often used
one year following MI and one month following cerebrovascular stroke
80
what is the main mechanism of dipyridamole
cyclic nucleotide phosphodiesterase inhibitor (more cAMP & cGMP so longer signal to prevent platelets from sticking together)
81
what are 2 other mechanisms for dipyridamole
blocks adenosine uptake (weak platelet inhibitor) decrease platelet TXA2 / or increase endothelial PGI2 synthesis
82
what does adenosine do
weak platelet inhibitor
83
is dipyridamole effective alone
no, so its used with ASA
84
when/ how is dipyridamole used
with ASA to prevent transient ischemic attacks and stroke
85
what is the role of fibrinogen
cross links platelets upon aggregation
86
what is GPIIb/IIIa
fibrinogen receptor
87
what is the mechanism of action of GPIIb/IIIa antagonists
block receptor or compete for occupancy with fibrinogen
88
what step does GPIIb/IIIa inhibit
the final common step leading to platelet aggregation (after the ADP and TXA2 steps)
89
what is abciximab
mouse/human chimeric monoclonal Ab vs. GPIIb/IIIa
90
what is eptifibatide
synthetic cyclic heptapeptide
91
what is tirofiban
synthetic non-peptide
92
how does tirofiban and eptifibatide work
they have a similar amino acid sequence to the GPIIb/IIIa ligands, so they can block the receptor
93
how are the GPIIb/IIIa antagonists administered
IV
94
who are GPIIb/IIIa antagonists given to
prevent thrombosis in patients with acute coronary syndromes or undergoing coronary angioplasty
95
what are 2 unwanted effects of GPIIb/IIIa antagonists
bleeding and thrombocytopenia (low platelet counts)
96
is ASA a potent anticoagulant
no
97
is ASA reversible
no

PMCOL 344 (27 decks)

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