Flashcards in Anti-platelet Drugs Deck (27)
What is a pearl about the use of antiplatelet agents?
They are used for the prevention and treatment of ARTERIAL thrombosis
Commonly used Anti-platelet agents
-COX inhibitors: ASA
-ADP receptor inhibitors: Clopidogrel*, prasugrel, ticagrelor*, cangrelor
Less commonly used antiplatelets (recognize the name)
-Cilostazol (PDE inhibitor)
-ER Dipyridamole/ASA (Adenosine reuptake inhibitor)
-Vorapaxar (PAR-1 antagonist)
-Eptifibatide (GP IIb/IIIa inhibitor)
-Irreversibly acetylates COX
-Impairing PG, prostacyclin, and thromboxane A2 production
-this leads to decreased platelet aggregation and vasoconstriction
***IRREVERSIBLE platelet effect
Aspirin clinical indications
Falling out of favor for primary prevention due to benefits being offset by bleeding risk
What antiplatelet therapy is indicated in ACS and why?
-Aspirin + clopidogrel or others
-Dual antiplatelet therapy is mandatory b/c coronary lesions & stents behave like unstable plaques as long as they are not fully covered by a cellular layer
How long will you be on ASA + clopidogrel after bare-metal stent placement? What about drug eluding?
-Bare-metal: 1 month
-Drug eluding: minimum 6 months
Pearl about ASA use in cardiac disease
-With few exceptions, pts with CAD, PAD, or a h/o of ischemic CVA are candidates for ASA use
-Take at any time. just be consistent
Do you continue ASA if a pt develops a GI bleed? (Think about their prevention category)
-Primary prevention: D/c for most patients and focus on BP control, statins, smoking cessation
-Secondary prevention: Consider restarting ASA for pts with a CV event history!
What are some pearls about enteric coated ASA related to dyspepsia and GI bleeding?
-Causes decreased dyspepsia but it does NOT decrease GI bleeding
-Monitor for anemia/bleeding periodically (H/H)
-NSAIDs decrease ASA antiplatelet effect**
**Take ASA 1 hour before NSAID, not-enteric coated
Common ASA ADRs
-Bleeding: Daily dose at least doubles GI risk**
What drug can you consider adding on to ASA if the patient is at high risk for GI bleeding?
RF: Hx PUD, chronic NSAIDs, Clopidogrel, anticoagulant use
What are some other dose-dependent ADRs of ASA?
-Aspirin exacerbated respiratory disease (AERD)
Clopidogrel MOA (entire process added for completeness)
-Prodrug that is metabolized twice to get to its active metabolite
-Active metabolite irreversibly blocks P2Y12 component of the ADP receptor
-Prevents activation of GP IIb/IIIa receptor complex
-Prevents fibrinogen binding at that site
-Decreased platelet aggregation/adhesion
-END RESULT IS A IRREVERSIBLE PLATELET EFFECT
What is a pearl about the MOA of Prasugrel?
-It is also a prodrug
-It prevents platelet activation better than clopidogrel
This allele significantly decreases the body's ability to metabolize Clopidogrel into its active metabolite
-Diminished platelet inhibition and higher rate of major adverse CV events
-Genotyping advised for moderate-high risk CV event patients who are treated with clopidogrel
-Clopidogrel: ACS, TIA/CVA, PAD
-Can increase bleeding risk if added with other antiplatelets or NSAIDs
What PPI should you use to avoid interactions in patients taking clopidogrel at high risk of GI bleeding?
Save PPIs for patients with HIGH bleeding risk or multiple risk factors due to the risk of drug interactions
Prasugrel causes bleeding more often than clopidogrel. What patient population is Prasugrel contraindicated in?
-Patients with hx of TIA/CVA
If Clopidogrel is mixed with ASA what is a common side effect?
GI intolerance (N/V, dyspepsia, gastritis)
MOA: Same as clopidogrel but has REVERSIBLE anti-platelet effects (Still hits ADP receptor)
Clinical Indications for Ticagrelor
-ACS (with concomitant low-dose ASA) pts managed medically or with PCI/CABG
-Ticagrelor you need to monitor renal function and uric acid concentration in patients with gout or risk of hyperuricemia