Antiplatelet & Anticoagulant Meds Flashcards by Kyra Porter

clopidogrel - MOA

*oral antiplatelet: decreases platelet aggregation via P2Y12 receptor inhibition (irreversible)
*blocks ADP (P2Y12) receptor → decreased ADP-induced expression of GpIIb/IIIa

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prasugrel - MOA

*oral antiplatelet: decreases platelet aggregation via P2Y12 receptor inhibition (irreversible)
*blocks ADP (P2Y12) receptor → decreased ADP-induced expression of GpIIb/IIIa

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ticagrelor - MOA

*oral antiplatelet: decreases platelet aggregation via P2Y12 receptor inhibition (REVERSIBLE)
*blocks ADP (P2Y12) receptor → decreased ADP-induced expression of GpIIb/IIIa

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aspirin - MOA

*oral antiplatelet: decreases platelet aggregation via thromboxane A2 (TXA2) inhibition
*IRREVERSIBLY blocks COX → decreased TXA2 release

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clopidogrel - uses

*acute coronary syndrome (ACS) [med management or PCI/stent]
*peripheral artery disease (PAD)
*thrombotic stroke

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prasugrel - uses

*acute coronary syndrome (ACS): PCI/stent

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ticagrelor - uses

*acute coronary syndrome (ACS): med management or PCI/stent

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aspirin - uses

*acute coronary syndrome (ACS)
*chronic stable angina
*stroke prophylaxis
*peripheral artery disease (PAD)

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clopidogrel - ADEs

*bleeding
*RASH
*TTP

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prasugrel - ADEs

*bleeding
*rash
*AVOID USE in: TIA/STROKE; age > 75; or < 60kg

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ticagrelor - ADEs

*bleeding
*dyspnea
*increased serum creatinine
*increased uric acid

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aspirin - ADEs

*bleeding
*GI upset
*angioedema
*gastric ulcers
*tinnitus
*allergic reactions
*renal injury
*Reye syndrome (in children)

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drug effectiveness in platelet aggregation inhibition: aspirin vs. clopidogrel, prasugrel, ticagrelor

*clopidogrel/prasugrel/ticagrelor > aspirin

*clopidogrel/prasugrel/ticagrelor are MORE EFFECTIVE AT INHIBITING PLATELET AGGREGATION compared to aspirin

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dipyridamole - MOA

*oral anti-platelet: decreases platelet aggregation
*inhibits platelet adenosine deaminases & phosphodiesterases → decreased cAMP hydrolysis and increased cAMP in platelets

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dipyridamole - ADEs

*dizziness
*headache
*GI upset

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cilostazol - MOA

*oral antiplatelet: decreases platelet aggregation
*inhibits platelet phosphodiesterase-III → decreased cAMP hydrolysis and increased cAMP in platelets

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cilostazol - ADEs

*dizziness
*headache
*GI upset
*edema
*palpitations

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vorapaxar - MOA

*oral antiplatelet: decreases platelet aggregation
*inhibits thrombin & thrombin receptor agonist peptide (TRAP) at PAR-1 receptor

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vorapaxar - ADEs

*bleeding
*rash

abciximab - MOA

*IV antiplatelet
*glycoprotein IIb/IIIa inhibitor: monoclonal antibody

eptifibatide - MOA

*IV antiplatelet
*glycoprotein IIb/IIIa inhibitor: peptide

tirofiban - MOA

*IV antiplatelet
*glycoprotein IIb/IIIa inhibitor: non-peptide

abciximab - ADEs

*bleeding
*thrombocytopenia

eptifibatide - ADEs

*bleeding
*thrombocytopenia

tirofiban - ADEs

*bleeding *thrombocytopenia

cangrelor - MOA

*IV antiplatelet *REVERSIBLE P2Y12 INHIBITOR

cangrelor - ADEs

*bleeding *dyspnea

unfractionated heparin (UFH) - MOA

*activates antithrombin III → inhibition of thrombin (IIa), IXa, Xa, XIa, and XIIa *used for immediate ANTICOAGULATION note - does not affect clot-bound thrombin or platelet-bound factor Xa

enoxaparin - MOA

*low-molecular-weight heparin *acts mainly on factor Xa (and a bit on IIa) *long-term anticoagulant of choice in pregnancy!

fondaparinux - MOA

*anticoagulant that inhibits factor Xa only *must bind to antithrombin III to exert pharmacologic activity *black box warning: increased risk of epidural/spinal hematomas with neuraxial anesthesia

heparins - ADEs

*monitor PTT *bleeding *decreased platelets *HIT/HITT

direct thrombin inhibitors - bivalirudin, argatroban

*MOA: directly inhibits factor IIa (thrombin) *bind free AND clot-associated thrombin note - significantly more expensive than IV heparin

bivalirudin - drug class/MOA

*directly inhibits thrombin (IIa) monitor serum creatinine

argatroban - drug class/MOA

*directly inhibits thrombin (IIa) monitor LFTs

protamine sulfate

*REVERSAL AGENT FOR HEPARIN anticoagulants *alkaline protein molecule *binds heparin & reverses anticoagulant activity *partially reverses low-molecular-weight heparin anticoagulant activity note - does not reverse fondaparinux or direct thrombin inhibitors

heparin-induced thrombocytopenia - types

*type 1: mild, transient thrombocytopenia *type 2: autoantibodies against heparin-platelet factor 4 (PF4) complex → thrombosis

heparin-induced thrombocytopenia - diagnosis

*onset 5-10 days after heparin initiation *platelets decrease 50%+ *new thrombosis *(+) platelet factor 4 heparin antibody, serotonin release assay

heparin-induced thrombocytopenia - management

*STOP heparin products *switch to DTI or fondaparinux for anticoagulation *treat at least 4 weeks; if thrombosis, 3 months *note heparin allergy

warfarin - MOA

*anticoagulant: vitamin K epoxide reductase inhibitor *prolongs clotting time by inhibiting synthesis of vitamin K-dependent factors (II, VII, IX, and X) *inhibits proteins C & S note - must bridge warfarin with another anticoagulant b/c of half-life of vitamin-K dependent clotting factors

warfarin - goals of therapy

*anticoagulant effects monitored by INR (PT) *monitoring frequency influenced by many factors (time since last dose change, stability of INR, etc)

warfarin - ADEs

*bleeding *lots of drug interactions (most of which increase the effects of warfarin, leading to increased bleeding risk) *food interactions (foods with high vitamin K content can affect INR)

reversal agents for warfarin

1. vitamin K - promotes synthesis of clotting factors; delayed response 2. fresh frozen plasma (FFP) - contains factors II, VII, IX, X 3. prothrombin complex concentrates - FEIBA or Kcentra; preferred for emergent or life-threatening reversal; must be administered with vitamin K!

direct oral anticoagulants (DOACs) - examples

1. dabigatran (direct thrombin inhibitor) 2. factor Xa inhibitors: rivaroxaban, apixaban, edoxaban, betrixiban

direct oral anticoagulants (DOACs) - advantages over warfarin

*quick onset/offset *fewer drug interactions *minimal food interactions *more predictable dosing *decreased monitoring (CBC, serum creatinine)

direct oral anticoagulants (DOACs) - reversal agents

1. prothrombin complex concentrates - FEIBA and Kcentra 2. idarucizumab - human monoclonal antibody; binds dabigatran; ineffective in binding other direct thrombin inhibitors 3. andexanet alfa - modified human factor Xa molecule; binds direct and indirect factor Xa inhibitors