ACS + AMI Therapy Flashcards
what is on the spectrum of acute coronary syndrome?
> unstable angina
non-ST elevated myocardial angina
ST-elevated myocardial angina
sudden cardiac death
what is the gaol of therapy?
> increase myocardial oxygen supply
> decrease myocardial oxygen demand
how is the myocardial oxygen supply increased?
through coronary vasodilation
by what mechanisms is myocardial oxygen demand decreased?
> decrease in heart rate
decrease in blood pressure
decrease in preload or myocardial contractility
how do thrombolytic agents work?
they are serine proteases that convert plasminogen to the natural fibrinolytic agent plasmin that lyses the clot by breaking down the fibrogen and fibrin .
what two categories can fibrinolytics be divided into?
> fibrin specific agents
> non-fibrin specific agents
name some fibrin specific agents
> alteplase
reteplase
tenecteplase
name a non-fibrin specific agent and what does it catalyse?
streptokinase
systemic fibrinolysis
give some contraindications for fibrinolysis
> 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
what is the medical treatment protocol if there is no evidence of a STEMI?
> aspirin > tigagrelor/clopidogrel > fondaprinux/ light molecular weight heparin > intravenous nitrate > analgesia > beta blocker
what is the affect of statins on the athermatous plaque?
they stabilise it
how does aspirin help reduce angina and MI?
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.
what benefits can regular aspirin use have in acute MI?
> reduction of mortality by 23%
> in combination with thrombolysis reduce mortality by 42% and re-infarction by 52%
what benefits can daily aspirin use have in unstable angina?
reduction in MI and death by 50%
what are the secondary prevention effects of daily aspirin use?
reduction of re-infarction by 32% and combined vascular events by 25%
what does clopidogrel inhibit?
> ADP receptor activated platelet aggregation
> irreversibly inhibits P2Y12 ADP receptor that is important in aggregation of platelets and cross-linking by fibrin
what pathway does clopidogrel block?
the GP llb/llla pathway
what is the llb/lla complex?
it is a receptor for fibrogen, fibronectin and von WF.
what is the final common pathway for platelet aggregation and cross linkiung by fibrin?
activation of the llb/llla receptor complex
what is clopidogrel used in combination with?
aspirin
why are some people resistant to clopidogrel?
clopidogrel is activated by Cyp2C19. 14% of the population has low levels of Cyp2C19
what does prasugrel inhibit?
ADP-induced platelet aggregation
name four low molecular weight heparin drugs
> enoxaparin
dalteparin
tenzeparin
fondaparinux
what is GPllb/llla?
it is an integrin complex found on platelets that is a receptor for fibrogen aids in platelet activation.
what does platelet activation of gpllb/llla by ADP cause?
a conformational change in the receptor that induces the binding of fibrinogen.
what is the major advesre affect of gllb/llla receptor blockers?
bleeding (minor and major). blood transfusion is required to terminate the bleeding and improve anaemia
when are beta blocker used?
> treatment for acute MI
> secondary prevention in survivors of acute MI
how do beta blockers reduce the myocardial oxygen consumption?
they competitively inhibit the myocardial effects of circulating catecholamine’s. this reduces the heart rate, blood pressure and myocardial contractility.
