Antiplatelets Flashcards

1
Q

Indications for Aspirin

A

Atherothrombosis Venous thromboembolism
Colorectal cancer
Cognitive impairment
History of MI
Acute coronary syndromes
Stable or unstable angina
Stroke Transient ischemic attack
Peripheral artery disease

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2
Q

Contraindications for Aspirin

A

True hypersensitivity
Active bleeding
Severe bleeding risk

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3
Q

Side effects of Aspirin

A

Dyspepsia to erosive gastritis or peptic ulcers with bleeding and perforation
Used with NSAIDs increase GI complications 3-4 fold
Increases risk of stroke in men by factor of 1.7, not in women

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4
Q

MOA of Aspirin

A

Blocks synthesis of thromboxane A2 by blocking COX-1 and 2

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5
Q

MOA of Dipyridamole

A

PDEIII inhibitor that increases levels of cAMP in platelets by:

  1. Blocking the reuptake of adenosine
  2. Inhibiting PDE mediated cAMP degradation cAMP reduces Ca levels which inhibits the platelet activation
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6
Q

Indications for Dipyridamole

A

Ischemic stoke or transient ischemic attack
Cardiac imaging - diagnostic IV agent for coronary artery disease (do not use if history of reactive airway disease)

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7
Q

Side effects of Dipyridamole

A

GI complaints
Headache
Facial flushing
Dizziness and hypotension

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8
Q

MOA of Clopidogrel

A

Prodrug that is an ADP receptor inhibitor that ultimately interferes with platelet activation. Metabolized hepatically by CYP2C19 where only 2-15% is active. (Black box warning, some people may be poor metabolizers)

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9
Q

Indication for Clopidogrel

A

Used in combo with aspirin
Acute coronary syndrome
Stent thrombosis after PCI CAD, CVD, or PAD
Minor stroke/TIA

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10
Q

MOA of Prasugrel

A

ADP inhibitor, more potent than clopidogrel and faster onset of action.
Higher concentration of active metabolite, less susceptible to genetic variation and drug interactions. “irreversible”

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11
Q

Contraindications of Prasurgrel

A

Patients smaller than 60kg half dose recommended
Should not be used in patients with Hx of stroke/TIA
Not used in patients greater than 75 years old
Not used in revascularization/PCI
Not to be initiated until coronary anatomy is known and CAPG ruled out

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12
Q

MOA of Ticagrelor

A

Reversible and non-competitively binds outside active site.
Faster onset and more potent platelet inhibition than clopidrogrel.
Starts as an active metabolite.

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13
Q

Adverse effect of Ticagrelor

A

Dyspnea (15%) people get the sensation of dyspnea because of neuronal P2Y12 receptors in neuronal tissues that cause vagal stimulation

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14
Q

MOA of Cangrelor

A

IV only
Also ADP receptor inhibitor
Higher bleeding rates than clopidogrel and can cause dyspnea similar to Ticagrelor

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15
Q

MOA of Cilostazol

A

Phosphodiesterase inhibitor

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16
Q

Indications for Cilostazol

A
17
Q

Contraindications of Cilostazol

A

Heart failure of any severity

18
Q

MOA of Vorapaxar

A

PAR-1 inhibitor (platelet thrombin receptor) Inhibits thrombin induced platelet aggregation

19
Q

Indications of Vorapaxar

A

Post MI patients at risk for secondary atherothrombotic events Initiate in stable patients 2 weeks after an MI on antiplatelet therapy

20
Q

Contraindication of Vorapaxar

A

History of stroke/TIA ICH or active bleeding Used in caution with low body wieght, old age

21
Q

MOA of GP IIb/IIIa inhibitors

A

Inhibit platelet aggregation

22
Q

GP IIb/IIIa contraindications

A

Active bleeding Severe hypertension CVA Major surgery of trauma Thrombocytopenia Bleeding diathesis/warfarin with elevated INR

23
Q

Major adverse effect of GP IIb/IIIa inhibitors

A

Thrombocytopenia

24
Q

Abciximab

A

Short half life, platelet bound for days, use in renal failure patients because not renally cleared

25
Q

Eptifibatide and tirofiban half life

A

Long (2 hours) half life, platelet bound short, renally cleared

26
Q

ADP receptor inhibitors

A
27
Q

ADP receptor inhibitors indications

A
28
Q

ADP receptor inhibitor adverse effects

A
29
Q

Glycoprotein IIb/IIIa inhibitors

A