ACS + AMI Therapy Flashcards

1
Q

what is on the spectrum of acute coronary syndrome?

A

> unstable angina
non-ST elevated myocardial angina
ST-elevated myocardial angina
sudden cardiac death

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2
Q

what is the gaol of therapy?

A

> increase myocardial oxygen supply

> decrease myocardial oxygen demand

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3
Q

how is the myocardial oxygen supply increased?

A

through coronary vasodilation

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4
Q

by what mechanisms is myocardial oxygen demand decreased?

A

> decrease in heart rate
decrease in blood pressure
decrease in preload or myocardial contractility

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5
Q

how do thrombolytic agents work?

A

they are serine proteases that convert plasminogen to the natural fibrinolytic agent plasmin that lyses the clot by breaking down the fibrogen and fibrin .

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6
Q

what two categories can fibrinolytics be divided into?

A

> fibrin specific agents

> non-fibrin specific agents

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7
Q

name some fibrin specific agents

A

> alteplase
reteplase
tenecteplase

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8
Q

name a non-fibrin specific agent and what does it catalyse?

A

streptokinase

systemic fibrinolysis

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9
Q

give some contraindications for fibrinolysis

A

> prior intercranial haemorrhage
known structural cerebral vascular lesion
known malignant intracranial neoplasm
ischaemic stroke within 3 months
suspected aortic dissection
active bleeding/bleeding diathesis
significant closed-head trauma or facial trauma within three months

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10
Q

what is the medical treatment protocol if there is no evidence of a STEMI?

A
> aspirin
> tigagrelor/clopidogrel
> fondaprinux/ light molecular weight heparin
> intravenous nitrate
> analgesia
> beta blocker
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11
Q

what is the affect of statins on the athermatous plaque?

A

they stabilise it

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12
Q

how does aspirin help reduce angina and MI?

A

it is a potent inhibitor of platelet thromboxane A2 production. thromboxane stimulates platelet aggregation and vasoconstriction. platelet aggregation is important to the development of angina and MI.

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13
Q

what benefits can regular aspirin use have in acute MI?

A

> reduction of mortality by 23%

> in combination with thrombolysis reduce mortality by 42% and re-infarction by 52%

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14
Q

what benefits can daily aspirin use have in unstable angina?

A

reduction in MI and death by 50%

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15
Q

what are the secondary prevention effects of daily aspirin use?

A

reduction of re-infarction by 32% and combined vascular events by 25%

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16
Q

what does clopidogrel inhibit?

A

> ADP receptor activated platelet aggregation

> irreversibly inhibits P2Y12 ADP receptor that is important in aggregation of platelets and cross-linking by fibrin

17
Q

what pathway does clopidogrel block?

A

the GP llb/llla pathway

18
Q

what is the llb/lla complex?

A

it is a receptor for fibrogen, fibronectin and von WF.

19
Q

what is the final common pathway for platelet aggregation and cross linkiung by fibrin?

A

activation of the llb/llla receptor complex

20
Q

what is clopidogrel used in combination with?

A

aspirin

21
Q

why are some people resistant to clopidogrel?

A

clopidogrel is activated by Cyp2C19. 14% of the population has low levels of Cyp2C19

22
Q

what does prasugrel inhibit?

A

ADP-induced platelet aggregation

23
Q

name four low molecular weight heparin drugs

A

> enoxaparin
dalteparin
tenzeparin
fondaparinux

24
Q

what is GPllb/llla?

A

it is an integrin complex found on platelets that is a receptor for fibrogen aids in platelet activation.

25
Q

what does platelet activation of gpllb/llla by ADP cause?

A

a conformational change in the receptor that induces the binding of fibrinogen.

26
Q

what is the major advesre affect of gllb/llla receptor blockers?

A

bleeding (minor and major). blood transfusion is required to terminate the bleeding and improve anaemia

27
Q

when are beta blocker used?

A

> treatment for acute MI

> secondary prevention in survivors of acute MI

28
Q

how do beta blockers reduce the myocardial oxygen consumption?

A

they competitively inhibit the myocardial effects of circulating catecholamine’s. this reduces the heart rate, blood pressure and myocardial contractility.