Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

NUR1125 > Antiplatelet > Flashcards

Antiplatelet Flashcards

1
Q

what is 1 caution over drug-drug interactions for aspirin

A

increase risk of bleeding if taken w other antiplatelet/anticoagulant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how long does it take to replace functional COX2

A

3-4hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is 2 caution when using clopidogrel

A
  1. pt w increase risk of bleeding
  2. variant elles of CYP2C19, which reduced metabolism to active metabolite & diminished drug response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

list examples of drug-drug interactions with clopidogrel that increase the antiplatelet effect and risk of bleeding

A
  1. warfarin/NSAIDS/salicylates increase the risk of bleeding
  2. rifamycin increase drug effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

list examples of significant drug-drug interactions with ticagrelor

A
  1. anticoagulant/fibrinolytics/long term NSAIDS therapy
    - increase risk of bleeding
  2. aspirin >100mg/day
    - reduce drug effect but increase risk of bleeding
  3. CYP3A inducer
    - reduce drug level & effect
  4. CYP3A strong inhibitor
    - increase drug level & risk of a/e
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the pharmacokinetic of ticagrelor

A

onset: 20-30min
peak: 2-3hrs
duration: 2-3 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

list 2 cautions over the use of dipyridamole as an antiplatelet agent

A
  1. hypotension
  2. severe CAD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

list 3 drug-drug interactions of dipyridamole when used as an antiplatelet agent

A
  1. anti-arrythmic effect as drug increase cardiac adenosine level & effect
  2. worsen myasthenia gravis as drug decrease cholinesterase inhibitor
  3. increase risk of bleeding if taken w heparin/antiplatelet/anticoagulant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

list the adverse effects of dipyridamole when used as an antiplatelet agent

A
  1. headache
  2. hypotension
  3. flushing
  4. dizziness
  5. GI disturbance eg. diarrhoea, nausea/vomiting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

why are the antiplatelet effects of aspirin stronger when it is used at a low dose than when it is used at a high dose

A

once COX1 is inhibited, it takes 7-10 days to produce newly functional COX1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

explain how aspirin works as an antiplatelet drug

A

it is a irreversible COX inhibitor (COX1 > COX2), therefore inhibit the production of TXA2, resulting in decrease platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the 7 a/e of clopidogrel

A
  1. haemorrhage/bleeding (including ICH)
  2. easy bruising
  3. dyspnea
  4. dyspepsia(~5%)
  5. rash (~5%)
  6. bronchospasm
  7. hypotension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

name 1 example of an irreversible cyclooxygenase-1 (COX-1) inhibitor used as an antiplatelet drug

A

aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the MOA of clopidogrel

A

it is a pro drug w an active metabolite that binds irreversibly to P2Y12 receptors

drug require the activation of CYP2C19, resulting in
- interindividual variability
- slow onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

list 3 class of antiplatelet drugs

A
  1. adenosine reuptake & PDE3 inhibitor (eg. dipyridamole)
  2. irreversible COX inhibitor (eg. aspirin)
  3. ADP P2Y12 receptor inhibitor (eg. clopidogrel, ticagrelor)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

explain the effect of dipyridamole as a vasodilator

A

it is a vasodilator as it also inhibit adenosine & PDE in VSMC, this result in a dose limiting a/e which limit the efficacy of drug, therefore
- it is use as an adjunct therapy with other antiplatelet/anticoagulant
- can be administered IV as an alternative for myocardial stress perfusion imaging

17
Q

why does pt on aspirin have a high risk of upper GI bleed

A

inhibition of COX1 inhibit the production of protective PG in stomach

18
Q

what is 1 contraindication when using clopidogrel

A

pt w active bleeding

19
Q

what is the pharmacokinetic of clopidogrel

A

onset: 2-4hrs
peak: 6-8hrs
duration: 7-10 days

20
Q

what is the pharmacokinetic of aspirin on once daily dosing

A

onset: 3-4hrs
peak: 2-3 days
duration: 7-10 days

21
Q

what are the processes involving blood cells that occur during primary haemostasis

A

platelet activation & aggregation occur during primary haemostasis

22
Q

list 4 contraindications of ticagrelor

A
  1. breast feeding women
  2. hx of ICH
  3. active pathologic bleeding
  4. severe hepatic impairment
23
Q

list 3 caution when giving ticagrelor

A
  1. pt w risk of bleeding
  2. elderly
  3. moderate hepatic impairment
24
Q

why is dipyridamole often administered in a modified- or extended-release preparation

A

due to drug having a short half life, resulting in a duration of action of 3hrs

therefore given as a modified release to prolong the duration of action

25
Q

list 2 adverse effects of aspirin when used as an antiplatelet agent

A
  1. upper GI bleed
  2. increase risk of bleeding/bruising
26
Q

what is the MOA of dipyridamole

A

it inhibit platelet aggregation & activation by increasing cAMP within the platelets via
- inhibiting adenosine reuptake, which increase plasma adenosine activation of a2 receptors on platelets
- inhibit PDE3, which prevent the degradation of cAMP within platelets

27
Q

what is the MOA of ticagrelor

A

drug w it metabolite bind reversibly to other binding sites (not ADP binding site) on P2Y12 to inhibit G protein activation & signalling

28
Q

what is the major caution over the use of aspirin

A

caution over the use of patient w bleeding/platelet disorder

29
Q

which class of drugs inhibit primary haemostasis

A

antiplatelet

30
Q

what is the pharmacokinetic of dipyridamole

A

onset: 20-30min
peak: 2-2.5hrs
duration: ~3hrs

31
Q

name at least 2 examples of ADP P2Y12 receptor inhibitors used as antiplatelet drugs

A
  • clopidogrel
  • ticagrelor
32
Q

list examples of drug-drug interactions with clopidogrel that decrease the antiplatelet effect

A

macrolides/mod-strong CYP2C19 inhibitor reduce drug effect

33
Q

name 1 example of an adenosine uptake and PDE3 inhibitor antiplatelet agent

A

dipyridamole

34
Q

list 5 a/e of ticagrelor

A
  1. haemorrhage/bleeding (eg. ICH)
  2. dyspnea
  3. easy bruising
  4. cough
  5. bradycardia
35
Q

what is the haemostasis process

A
  • when blood vessel is damage, it vasconstrict to minimize blood loss
  • primary haemostasis - platelet adhere to the site of injury & release ADP & TXA2 to stimulate platelet activation & aggregration
  • secondary haemostasis - thrombin convert fibrinogen → fibrin to form a mesh
  • clot stabilization - thrombin convert XIII → XIIIa in the presence of ca2+, which then crosslink w fibrin to create a more stable clot

NUR1125 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions