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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
main indications for vorapaxar
coronary artery diease (MI) and peripheral arterial disease (PAD)
26
main adverse effects of vorapaxar
increased risk of bleeding
27
contraindications to vorapaxar
- history of stroke, TIA or intracranial hemorrhage | - active pathologic bleeding or underlying bleeding risk
28
antiplatelet agents aka
glycoprotein IIb/IIIa inhibitors
29
GP2b3a is a
platelet surface protein | - a receptor for fibrinogen & von Willebrand factor
30
upon activation, GP2b3a
anchors plts to each other via fibrinogen & to the surface of the injured vasculature via von WIllebrand factor
31
thrombin, TX-A2, ADP, collagen, NE, & other factors result in the activation of
GP2b3a-> plt aggregation
32
all GP2b3a inhibitors inhibit
the interaction of GP2b3a with fibrinogen & von willebrand factor-> impair plt AGGREGATION
33
GP2b3a agents
abciximab (reopro) eptifibatide (integrilin) tirofiban (aggrastat)
34
abciximab (Reopro)
- monoclonal antibody | - blcoks the receptors from activation
35
therapeutic use of abciximab
- in combo w/ precutaneous angioplasty for coronary thromboses - in combo with aspirin & heparin to prevent restenosis & recurrent MI
36
main adverse effects of abciximab
- bleeding | - thrombocytapenia
37
eptifibatide (integrilin)
a cyclic peptide inhibitor of GP2b3a
38
tirofiban (Aggrastat)
a non-peptide inhibitor of GP2b3a | - inhibit ACTIVATED plts; shorter half-life
39
therapeutic use of eptifibatide & tirofiban
- UA, ACS, MI | - angioplastic coronary interventions
40
main ADE of eptifibatide & tirofiban
- bleeding | - thrombocytapenia
41
what converts plasminogen to plasmin
tissue plasminogen activator (tPA)
42
activation of plasmin leads to
enhanced fibrinolysis
43
fibrinolytic aka
thrombolytic agents
44
fibrinolytic (thrombolytic) agents
alteplase (activase) reteplase (retavase) tenecteplase (TNKase)
45
alteplase (activase)
- tPA produced by recombinant DNA technology
46
reteplase (retavase) & tenecteplase (TNKase)
- recombinant mutant variants of tPA | - longer T1/2 than alteplase
47
therapeutic use of fibrinolytic agents
acute MI & thromboembolic stroke
48
main adverse effect of fibrinolytic agents
- hemorrhage - lysis of fibrin in physiological thrombi at sites of vascular injury - systemic lytic state in the result of systemic formation of plasmin
49
contraindications for fibrinolytics is the same as
for GP2b3aI
50
main adverse effects of statins
myopathy | hepatoxicity
51
beneficial effects of statins
- lowering LDL, improve endothelial function (pleiotropic effects)
52
efficiency of statins in reducing
fatal & non-fatal CHD events, stroke & total mortality documented in multiple trials
53
main ADE of ACEI
dry cough, hypotension, angioedema
54
ACEI MOA
block angI to angII
55
pure antianginal agents
ranolazine (ranexa)
56
ranolazine (ranexa)
- used for the treatment of chronic angina | - usually in combo with amlodipine, BB or nitrates
57
MOA of ranolazine (ranexa)
- 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
pharmacokinetic properties of ranolazine
- primarily metabolized by CYP3A4 (caution w/ diliazem & verapamil) - is a substrate of P-GP (PGP inhibitors-cyclosporine, incr its circulating conc.)
59
main ADE of ranolazine
``` dizziness HA constipation nausea - prolonged QT interval if overdosed ot combined w/ other drugs affecting it ```
60
precautions in using ranolazine
- in pts w/ pre-existing QT prolongation - history of torsade de pointes - pts w/ hepatic or renal impairment & filaure
61
contraindications to rnolazine
- concomitant use with potent inhibitors or inducers of CYP3A4 - hepatic cirrhosis
62
stroke
disease affecting blood vessels that supply the brain
63
two main types of stroke
hemorrhagic & ischemic
64
hemorrhagic stroke
damage of a vessel & bleeding | - higher death rate
65
ischemic stroke
blockage of a blood vessel by clot or some mass | - 87% of all cases
66
wandering clot
- embolus - formed awy from the brain, blocks the blood flow - usually from heart in the result of Afib
67
therapeutic goals of ischemic & thromboembolic stroke
- reduce ongoing neurological injury - decrease mortality & long-term disability - prevent complications secondary to immobility & dysfunction - prevent stroke recurrence
68
non- pharmacologic ischemic stroke treatment
- carotid endarterectomy | - carotid stenting
69
pharmacologic agents used in ischemic acute stroke
- 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
pharmacologic agents used in secondary prevention of ischemic stroke
- 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
pharmacologic agents used in ischemic stroke to lower BP
- 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
statin use in ischemic stroke
- reduce risk of stroke by 30% in CAD pts & pts with elevated plasma lipids - use in ALL ischemic stroke pts
73
what do you use in all ischemic stroke pts?
STATINS!!!
74
beneficial effects of statins in ischemic stroke are attributed to
- 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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