Antiplatelets Flashcards
Indications for Aspirin
Atherothrombosis Venous thromboembolism
Colorectal cancer
Cognitive impairment
History of MI
Acute coronary syndromes
Stable or unstable angina
Stroke Transient ischemic attack
Peripheral artery disease
Contraindications for Aspirin
True hypersensitivity
Active bleeding
Severe bleeding risk

Side effects of Aspirin
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

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

MOA of Dipyridamole
PDEIII inhibitor that increases levels of cAMP in platelets by:
- Blocking the reuptake of adenosine
- Inhibiting PDE mediated cAMP degradation cAMP reduces Ca levels which inhibits the platelet activation

Indications for Dipyridamole
Ischemic stoke or transient ischemic attack
Cardiac imaging - diagnostic IV agent for coronary artery disease (do not use if history of reactive airway disease)
Side effects of Dipyridamole
GI complaints
Headache
Facial flushing
Dizziness and hypotension

MOA of Clopidogrel
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)

Indication for Clopidogrel
Used in combo with aspirin
Acute coronary syndrome
Stent thrombosis after PCI CAD, CVD, or PAD
Minor stroke/TIA
MOA of Prasugrel
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”

Contraindications of Prasurgrel
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

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

Adverse effect of Ticagrelor
Dyspnea (15%) people get the sensation of dyspnea because of neuronal P2Y12 receptors in neuronal tissues that cause vagal stimulation
MOA of Cangrelor
IV only
Also ADP receptor inhibitor
Higher bleeding rates than clopidogrel and can cause dyspnea similar to Ticagrelor
MOA of Cilostazol

Phosphodiesterase inhibitor

Indications for Cilostazol

Contraindications of Cilostazol
Heart failure of any severity
MOA of Vorapaxar
PAR-1 inhibitor (platelet thrombin receptor) Inhibits thrombin induced platelet aggregation
Indications of Vorapaxar
Post MI patients at risk for secondary atherothrombotic events Initiate in stable patients 2 weeks after an MI on antiplatelet therapy
Contraindication of Vorapaxar
History of stroke/TIA ICH or active bleeding Used in caution with low body wieght, old age
MOA of GP IIb/IIIa inhibitors
Inhibit platelet aggregation
GP IIb/IIIa contraindications
Active bleeding Severe hypertension CVA Major surgery of trauma Thrombocytopenia Bleeding diathesis/warfarin with elevated INR
Major adverse effect of GP IIb/IIIa inhibitors
Thrombocytopenia
Abciximab
Short half life, platelet bound for days, use in renal failure patients because not renally cleared



