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Cardiology Exam > Antiplatelet & Anticoagulant Meds > Flashcards

Antiplatelet & Anticoagulant Meds Flashcards

1
Q

clopidogrel - MOA

A

*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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2
Q

prasugrel - MOA

A

*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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3
Q

ticagrelor - MOA

A

*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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4
Q

aspirin - MOA

A

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

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5
Q

clopidogrel - uses

A

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

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6
Q

prasugrel - uses

A

*acute coronary syndrome (ACS): PCI/stent

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7
Q

ticagrelor - uses

A

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

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8
Q

aspirin - uses

A

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

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9
Q

clopidogrel - ADEs

A

*bleeding
*RASH
*TTP

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10
Q

prasugrel - ADEs

A

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

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11
Q

ticagrelor - ADEs

A

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

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12
Q

aspirin - ADEs

A

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

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13
Q

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

A

*clopidogrel/prasugrel/ticagrelor > aspirin

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

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14
Q

dipyridamole - MOA

A

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

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15
Q

dipyridamole - ADEs

A

*dizziness
*headache
*GI upset

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16
Q

cilostazol - MOA

A

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

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17
Q

cilostazol - ADEs

A

*dizziness
*headache
*GI upset
*edema
*palpitations

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18
Q

vorapaxar - MOA

A

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

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19
Q

vorapaxar - ADEs

A

*bleeding
*rash

20
Q

abciximab - MOA

A

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

21
Q

eptifibatide - MOA

A

*IV antiplatelet
*glycoprotein IIb/IIIa inhibitor: peptide

22
Q

tirofiban - MOA

A

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

23
Q

abciximab - ADEs

A

*bleeding
*thrombocytopenia

24
Q

eptifibatide - ADEs

A

*bleeding
*thrombocytopenia

25
Q

tirofiban - ADEs

A

*bleeding
*thrombocytopenia

26
Q

cangrelor - MOA

A

*IV antiplatelet
*REVERSIBLE P2Y12 INHIBITOR

27
Q

cangrelor - ADEs

A

*bleeding
*dyspnea

28
Q

unfractionated heparin (UFH) - MOA

A

*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

29
Q

enoxaparin - MOA

A

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

30
Q

fondaparinux - MOA

A

*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

31
Q

heparins - ADEs

A

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

32
Q

direct thrombin inhibitors - bivalirudin, argatroban

A

*MOA: directly inhibits factor IIa (thrombin)
*bind free AND clot-associated thrombin

note - significantly more expensive than IV heparin

33
Q

bivalirudin - drug class/MOA

A

*directly inhibits thrombin (IIa)

monitor serum creatinine

34
Q

argatroban - drug class/MOA

A

*directly inhibits thrombin (IIa)

monitor LFTs

35
Q

protamine sulfate

A

*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

36
Q

heparin-induced thrombocytopenia - types

A

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

37
Q

heparin-induced thrombocytopenia - diagnosis

A

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

38
Q

heparin-induced thrombocytopenia - management

A

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

39
Q

warfarin - MOA

A

*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

40
Q

warfarin - goals of therapy

A

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

41
Q

warfarin - ADEs

A

*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)

42
Q

reversal agents for warfarin

A
  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!
43
Q

direct oral anticoagulants (DOACs) - examples

A
  1. dabigatran (direct thrombin inhibitor)
  2. factor Xa inhibitors: rivaroxaban, apixaban, edoxaban, betrixiban
44
Q

direct oral anticoagulants (DOACs) - advantages over warfarin

A

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

45
Q

direct oral anticoagulants (DOACs) - reversal agents

A
  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

Cardiology Exam (47 decks)

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