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Cardio MT2 > MT2_8_Antiplatelets Pharma > Flashcards

MT2_8_Antiplatelets Pharma Flashcards

1
Q

What happens in primary hemostasis, vs secondary?

A
  • primary: vasoconstriction reduces blood flow, and platelets come together, activate fibrin clot formation
  • secondary: clotting factors form
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2
Q

Steps of thrombus formation?

A
  • adhesion
  • recruitment (via intracellular signaling pathways)
  • aggregation G2b/3a complexes on platelets bind to fibrinogen to make thrombus
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3
Q

What is the MOA of aspirin, a cox 1 inhibitor?

A
  • irreversible inhibition of cox 1 prevents thromboxane A2 from forming platelets
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4
Q

Main indications for aspirin?

A
  • secondary prevention of major coronary events in patients with IHD
  • Afib
  • Stroke
  • Peripheral vascular disease
  • analgesic
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5
Q

Dosing of aspirin?

A

81 mg, equally effective as higher doses

higher doses 325, pt at higher risk for a bleed

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6
Q

Aspirin S/E

DDIs

A

-bleeding, increased risk with antithrombotic agents

  • NSAID (ibuprofen, naproxen)
  • increased risk of bleeding
  • due to competitive inhibition of Cox 1
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7
Q

What drugs fall under phosphodiesterase inhibitors?

A
  • dipyridamole

- cilostazol

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8
Q

MOA of dipyridamole?

High dose?

A
  • PDE5 inhibitor, inhibits platelet aggregation
  • increases adenosine, causing vasodilation
  • vasodilation–>reflex tacky–>myocardial ischemia
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9
Q

Main indications for dipyridamole? IR vs ER

A

IR: prophylaxis of thromboembolism with cardiac valve placement

ER: secondary prevention of stroke + aspirin

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10
Q

For dipyridamole, why is the IR formulation not superior?

A
  • has side effects, dizziness, hypotension, and tachy at high doses
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11
Q

MOA of cilostazol

A
  • PDE3 inhibitor, increases cAMP
  • reversible inhibition platelet aggregation
  • vasodilatation
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12
Q

What is cilostazol indicated for?

A
  • cramping in peripheral artery disease

- used in combo with ASA or clopidogrel improves walking distance in patients with PAD

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13
Q

Cilostazol dosing?

A
  • 100mgBID, w high fat meal
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14
Q

How is cilostazol metabolized?

Caution in…

A
  • cyp2c19/3A4
  • hepatic and renal impairment (CrCl less than 25)
  • if on a 3A4/2C19 inhibitor (zoles) reduce dose to 50 mg BID
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15
Q

SE of cliostazol?

CI?

A
  • skin rash, GI, Headache, hypo,tachy

- heart failure

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16
Q

Name P2Y12 inhibitors with irreversible binding, and reversible binding

A
  • irreversible: ticlopidine (not used, neutropenia), clopidogrel,prasugrel
  • reversible: ticagrelor, cangelor
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17
Q

How do P2Y12 inhibitors work?

All agents need a…

A
  • binds P2Y12 inhibitor
  • prevents ADP from binding
  • prevents GP2b3a activation
  • block platelet aggregation
    (except for ticagrelor, cangrelor, bind directly on receptor)
  • loading dose
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18
Q

How is clopidogrel metabolized?

A
  • 85% active, 15% inactive

- converted into 2 steps via CYP2C19 to active metabolite

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19
Q

Indications for Plavix?

Dose?

A
  • ACS, PCI, CABG
  • Stroke, TIA
  • PAD
  • Stroke prevention w ASA
  • alternative to ASA
  • 600mg or 300mg po x1, then 75 mg po daily
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20
Q

Plavix SE, CI, Hold, BBW

A
  • bleeding
  • active bleeding (ulcers)
  • hold 5 days
  • poor metabolizer for CYP2C19 results in increased CV events
  • omeprazole and esomeprazole inhibits 2C19, decreased efficacy)
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21
Q

Prasugrel vs Clopidogrel

A
  • faster, more predictable anti platelet response (bc of higher absorption and metabolite BA)
  • lack of DDI
  • higher rates of bleeding though
  • rapid on
22
Q

Indications for prasugrel?

A
  • ACS with PCI ONLY

- 60mg x1, 10mg/day, if less than 60kgs, dose of 5 mg ok

23
Q

BBW of prasugrel?

Ci

Hold

A
  • not recommend for older than 75 (increased bleeding)

CI in prior stroke, TIA
and active bleeding ulcer

hold 7 days before surgery

24
Q

MOA of ticagrelor?

A
  • reversible, so it binds directly to the receptor to inhibit G protein activation
25
Q

Ticagrelor vs clopidogrel?

A
  • rapid onset

- consistant inhibition

26
Q

Ticagrelor indications and Dose

A
  • indicated for ACS w/wo PCI
  • alternative to ASA or P2y12 inhibitor
  • dose: LD 180 mg x1, 90mg BID
27
Q

Ticagrelor DDIs

A
  • substrate and inhibitor of 3A4, so dose simvastatin/lovastatin high like at 40
  • inhibits PGP, can increase digoxin levels
28
Q

Ticagrelor SE, Hold

A
  • dyspnea, bleeding
  • increase in adenosine concentrations due to blocking nucleotide transporter..vasodilation
  • hold 5 days before surgery
29
Q

Ticagrelor BBW?

A

BBW: use only with low dose aspirin less than 100

CI: active bleeding, history of intracranial hemorrhage
severe hepatic impairment

30
Q

Cangrelor …what makes this drug different?

A

MOA is the same as ticragelor….IV

31
Q

Indication for cangrelor?

Dose?

A
  • undergoing PCI, pt does not get P2y12 inhibitor or GP2b3a inhibitor
  • LD 30mcg/kg bolus, then 4 mcg/kg/min
32
Q

How long does platelet function return after dc cangrelor? When to give plavix

A
  • 1 hour

- after to avoid a decrease in activity

33
Q

SE of cangrelor
CI
Place in therapy

A
  • bleeding, renal insufficiency,dyspnea
  • CI inbleeding
  • bridge
34
Q

Example of a thrombin receptor antagonist (PAR1 antagonist)

A
  • vorapaxar
35
Q

MOA of vorapaxar?

A
  • reversible competitive PAR1 receptor antagonist
  • inhibits thrombin platelet aggregation, but does not interfere with coagulation cascade, therefore does not affect PT or aPTT
36
Q

Vorapaxar indication? Dose?

A
  • reduce the risk of major adverse cardiac events in patients with a previous MI or PAD
  • Dose: 2.08mg QD, WITH aspirin/clopidogrel
37
Q

Major DDI with Vorapaxar?

A
  • avoid use w strong 3A4 inhibitors/inducers
38
Q

Vorapaxar SE/CI/BBW?

A

-SE: bleeding, anemia, depression, rask, skin issues

  • CI/BBW: Hx of stroke, TIA, ICH
  • active bleeding
  • severe hepatic impairment
39
Q

Name the G2b3a receptor inhibitors

A
  • abciximab
  • eptifibatide
  • tirofiban

ALL IV

40
Q

How do GP 2b3a receptors work?

A
  • inhibits fibrinogen from binding to GP 2b3a receptor on activated platelets
  • used as an adjunct
41
Q

When are GP2b3a inhibitors used?

A
  • ACS with PCI

- usually given with an anticoagulant (heparin or LMWH) + aspirin

42
Q

CI of GP2B3A inhibitors?

A
  • Intercranial issues (aneurysm, mass)
  • AV malformations
  • HTN
  • hemorrhagic stroke/recent stroke
  • recent surgery/trauma
  • GI bleed
  • thrombocytopenia (platelets less than 100)
43
Q

MOA of abciximab? ReoPro

A
  • noncompetitive irreversible inhibitor of G2b3a

- antibody against GP2b3a receptor, which causes steric hinderance blocking access of fibrinogen

44
Q

When is abciximab indicated?

A
  • PLANNED PCI (STEMI and UNSTEMI if no response)

- Dose is 0.35 mg/kg bolus, then 0.125 mcg/kg/min

45
Q

In what pop is abciximab good for? how long does it take to dissociate from receptors?

A
  • good for renal

- up to 4 hours , therefore duration is a lot longer

46
Q

SE of abciximab?

A
  • bleeding, hypotension, nausea

- antibody development on readmit: anaphylaxis, thrombocytopenia, reduced efficacy

47
Q

MOA of eptifibatide?

A
  • LMW competitive and reversible G2B, 3A antagonist

- has high specificity, low affinity to the GP2B3A inhibitor

48
Q

Eptifibatide indication and dose?

A
  • indicated for ACS, PCI

- Dose is 180mcg/kg IV bolus, then 2 mcg/kg/min

49
Q

CI for eptifibatide?

SE?

A
  • ESRD , half the dose if CrCl is less than 50

- SE- bleeding, hypotension, thrombocytopenia

50
Q

MOA of tirofiban?

A
  • similar to eptifibide, high specificity, high affinity
51
Q

Indication for Tirofiban?

A
  • ACS
  • PCI
  • 25mcg/kg IV bolus, then 0.15 mcg/kg/min
52
Q

Need to renallyadjust for tirofiban?

A
  • yes, if CrCl is less than 60, has the infusion rate

Cardio MT2 (12 decks)

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