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Cardio Exam 2 > lecture 7 > Flashcards

lecture 7 Flashcards

1
Q

aggregated platelets

A

form the initial hemostatic plug at sites of vascular injury & are key played in thrombus formation

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2
Q

antiplatelet agents- ADP receptor blockers aka

A

thienopyridines

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3
Q

ADP is a

A
  • potent initiator of plt aggregation.

- effects are mediated via P2Y12 & P2Y1

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4
Q

what must be stimulated to result in plt activation?

A

BOTH P2Y12 and P2Y1

- inhibition of either receptor is sufficient to block plt activation

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5
Q

thienopyridine (ADP receptor block) drugs

A

prasugrel (effient)

clopidogrel (plavix)

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6
Q

thienopyridines

A
  • prodrugs
  • bind covalently to P2Y12-> permanent blockage
  • short half lives, but long lasting effects
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7
Q

life of a platelet

A

5-7 days

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8
Q

therapeutic use of thienopyridines

A
  • initiated during ACS, particularly with angioplasty & stenting
  • continued for secondary prevention of both MI & atheroembolic stroke
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9
Q

main adverse effects of thienopyridines

A
  • increased risk of bleeding

- thrombotic thrombocytopenic purpura (TTP)

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10
Q

metabolic activation of thienopyridines

A
  • enzymatic formation of the active metabolite PRECEDES covalent binding (S-S) to the P2Y12 receptor on plts
    1. metabolism is required for activity (inhibition of plts)
    2. inhibition is IRREVERSIBLE
    3. nature of metabolizing enzyme is key for efficacy
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11
Q

what enzyme activates clopidogrel

A

CYP2C19

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12
Q

what enzyme activates prasugrel?

A

CYP3A4

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13
Q

what is the REVERSIBLE ADP receptor antagonist?

A

ticagrelor

non-theopyridine

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14
Q

MOA of ticagrelor

A
  • NOT a prodrug- more consistent
  • REVERSIBLE blockage of P2Y12 receptor-> recovery of plt function after stopping the drug is more rapid.
  • less risk of bleeding!
  • BID
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15
Q

what enzymemetabolizes ticagrelor?

A

CYP3A4

- also inhibits it

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16
Q

adverse effects of ticagrelor

A 
bleeding
dyspnea
bradyarrhythmias
increased serum uric acid & Cr
- Prego C
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17
Q

thrombin receptor (protease-activated receptor 1: PAR1) antagonist

A

vorapaxar (Zontivity)

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18
Q

vorapaxar (zontivity) MOA

A

binds PAR1, thrombin can still chop it, but it won’t be activated

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19
Q

thrombin causes

A

plt activation & aggregation through PAR1 & PAR4 receptors

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20
Q

thrombin is considered

A

the most potent endogenous activator of plts

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21
Q

PAR1 is

A

the high-affinity receptor

- responds more sensitively & rapidly to thrombin

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22
Q

what is the first FDA approved thrombin receptor antagonist which prevents actions of thrombin on plts (mediated via PAR1)?

A

vorapaxar

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23
Q

what enzyme metabolizes vorapaxar?

A

CYP3A4

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24
Q

vorapaxar caution

A

not recommended to use with CYP3A4 inhibitors & inducers

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25
Q

main indications for vorapaxar

A

coronary artery diease (MI) and peripheral arterial disease (PAD)

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26
Q

main adverse effects of vorapaxar

A

increased risk of bleeding

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27
Q

contraindications to vorapaxar

A
  • history of stroke, TIA or intracranial hemorrhage

- active pathologic bleeding or underlying bleeding risk

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28
Q

antiplatelet agents aka

A

glycoprotein IIb/IIIa inhibitors

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29
Q

GP2b3a is a

A

platelet surface protein

- a receptor for fibrinogen & von Willebrand factor

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30
Q

upon activation, GP2b3a

A

anchors plts to each other via fibrinogen & to the surface of the injured vasculature via von WIllebrand factor

31
Q

thrombin, TX-A2, ADP, collagen, NE, & other factors result in the activation of

A

GP2b3a-> plt aggregation

32
Q

all GP2b3a inhibitors inhibit

A

the interaction of GP2b3a with fibrinogen & von willebrand factor-> impair plt AGGREGATION

33
Q

GP2b3a agents

A

abciximab (reopro)
eptifibatide (integrilin)
tirofiban (aggrastat)

34
Q

abciximab (Reopro)

A
  • monoclonal antibody

- blcoks the receptors from activation

35
Q

therapeutic use of abciximab

A
  • in combo w/ precutaneous angioplasty for coronary thromboses
  • in combo with aspirin & heparin to prevent restenosis & recurrent MI
36
Q

main adverse effects of abciximab

A
  • bleeding

- thrombocytapenia

37
Q

eptifibatide (integrilin)

A

a cyclic peptide inhibitor of GP2b3a

38
Q

tirofiban (Aggrastat)

A

a non-peptide inhibitor of GP2b3a

- inhibit ACTIVATED plts; shorter half-life

39
Q

therapeutic use of eptifibatide & tirofiban

A
  • UA, ACS, MI

- angioplastic coronary interventions

40
Q

main ADE of eptifibatide & tirofiban

A
  • bleeding

- thrombocytapenia

41
Q

what converts plasminogen to plasmin

A

tissue plasminogen activator (tPA)

42
Q

activation of plasmin leads to

A

enhanced fibrinolysis

43
Q

fibrinolytic aka

A

thrombolytic agents

44
Q

fibrinolytic (thrombolytic) agents

A

alteplase (activase)
reteplase (retavase)
tenecteplase (TNKase)

45
Q

alteplase (activase)

A
  • tPA produced by recombinant DNA technology
46
Q

reteplase (retavase) & tenecteplase (TNKase)

A
  • recombinant mutant variants of tPA

- longer T1/2 than alteplase

47
Q

therapeutic use of fibrinolytic agents

A

acute MI & thromboembolic stroke

48
Q

main adverse effect of fibrinolytic agents

A
  • hemorrhage
  • lysis of fibrin in physiological thrombi at sites of vascular injury
  • systemic lytic state in the result of systemic formation of plasmin
49
Q

contraindications for fibrinolytics is the same as

A

for GP2b3aI

50
Q

main adverse effects of statins

A

myopathy

hepatoxicity

51
Q

beneficial effects of statins

A
  • lowering LDL, improve endothelial function (pleiotropic effects)
52
Q

efficiency of statins in reducing

A

fatal & non-fatal CHD events, stroke & total mortality documented in multiple trials

53
Q

main ADE of ACEI

A

dry cough, hypotension, angioedema

54
Q

ACEI MOA

A

block angI to angII

55
Q

pure antianginal agents

A

ranolazine (ranexa)

56
Q

ranolazine (ranexa)

A
  • used for the treatment of chronic angina

- usually in combo with amlodipine, BB or nitrates

57
Q

MOA of ranolazine (ranexa)

A
  • not well understood
  • antianginal & anti-ischemic effects are NOT bc of reduction in BP, HR, or myocardial workload
  • maybe: inhibition of FA oxidation-> ATP from glu-> improved O2 consumption or inhibition of late Na currents-> dec Ca overload during ischemic attack
58
Q

pharmacokinetic properties of ranolazine

A
  • primarily metabolized by CYP3A4 (caution w/ diliazem & verapamil)
  • is a substrate of P-GP (PGP inhibitors-cyclosporine, incr its circulating conc.)
59
Q

main ADE of ranolazine

A 
dizziness
HA
constipation
nausea
- prolonged QT interval if overdosed ot combined w/ other drugs affecting it
60
Q

precautions in using ranolazine

A
  • in pts w/ pre-existing QT prolongation
  • history of torsade de pointes
  • pts w/ hepatic or renal impairment & filaure
61
Q

contraindications to rnolazine

A
  • concomitant use with potent inhibitors or inducers of CYP3A4
  • hepatic cirrhosis
62
Q

stroke

A

disease affecting blood vessels that supply the brain

63
Q

two main types of stroke

A

hemorrhagic & ischemic

64
Q

hemorrhagic stroke

A

damage of a vessel & bleeding

- higher death rate

65
Q

ischemic stroke

A

blockage of a blood vessel by clot or some mass

- 87% of all cases

66
Q

wandering clot

A
  • embolus
  • formed awy from the brain, blocks the blood flow
  • usually from heart in the result of Afib
67
Q

therapeutic goals of ischemic & thromboembolic stroke

A
  • reduce ongoing neurological injury
  • decrease mortality & long-term disability
  • prevent complications secondary to immobility & dysfunction
  • prevent stroke recurrence
68
Q

non- pharmacologic ischemic stroke treatment

A
  • carotid endarterectomy

- carotid stenting

69
Q

pharmacologic agents used in ischemic acute stroke

A
  • fibrinolytics: help restore perfusion in affected areas; caution- some pts may have CI; must follow strict protocol
  • antiplt (ASA): reduces aggregative activity of plts; caution- incr bleeding with fibrinolytics
70
Q

pharmacologic agents used in secondary prevention of ischemic stroke

A
  • antiplt agents: primary used for atheroembolic stroke where plts are a major component of the thrombus
  • anticoagulants: primarily used for cardio/thromboembolic stroke where clotting factors primarily constitute a thrombus which travels to the brain
71
Q

pharmacologic agents used in ischemic stroke to lower BP

A
  • ACEI: beneficial independent of accompanying HTN; reduce risk of stroke recurrance by 28-43%; not used in the first 7 days of acute stroke (to avoid dec cerebral blood flow)
  • ARBs: alt to ACEI; cross BBB-may have more beneficial effects?
72
Q

statin use in ischemic stroke

A
  • reduce risk of stroke by 30% in CAD pts & pts with elevated plasma lipids
  • use in ALL ischemic stroke pts
73
Q

what do you use in all ischemic stroke pts?

A

STATINS!!!

74
Q

beneficial effects of statins in ischemic stroke are attributed to

A
  • lipid lowering effects (ischemic stroke is an equivalent of CAD)- high levels of LDL is a risk factor for ischemic stroke
  • pleiotropic effects

Cardio Exam 2 (12 decks)

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