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R-Cradio-illness > Acute Coronary Syndrome and Acute Myocardial Infarction Therapy > Flashcards

Acute Coronary Syndrome and Acute Myocardial Infarction Therapy Flashcards

1
Q

What is the basic spectrum of acute coronary syndromes?

A

Unstable angina
Non-ST elevation MI
ST elevation MI
Sudden cardiac death

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2
Q

What is the goal of pharmacotherapy in acute coronary syndrome?

A

Increase myocardial oxygen supply through coronary vasodilation
Decrease myocardial oxygen demand through decreasing HR, BP and preload/contractility

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3
Q

What is there a risk of in patients with STEMI?

A

High likelihood fo coronary thrombus occluding the infarcted artery

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4
Q

Angiographic evidence of a coronary thrombus formation is seen in what percentage of patients with STEMI?

A

More than 90%

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5
Q

What is a STEMI usually the result of?

A

Coronary artery occlusion due to the formation of thrombus overlying an atheromatous plaque

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6
Q

When is thrombolysis indicated?

A

If there can be no access to the cath lab within 2 ours

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7
Q

What are the thrombolytic agents available today? How do they work?

A

Serine proteases that work by converting plasminogen to plasmin
Plasmin lyses the clot by breaking down the fibrin and fibrinogen contained within it

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8
Q

Fibrinolytics are divided into two categories, what are these? Give an example of each

A

Fibrin specific agents e.g. alteplase, reteplase, tenecteplase
Produce limited plasminogen conversion in the absence of fibrin

Non-fibrin specific agents e.g. streptokinase
Catalyse systemic fibrinolysis

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9
Q

Why can antibody-generating agents not be used more than once?

A

They will cause an anaphylactic response on subsequent exposure

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10
Q

What are the contraindications to thrombolysis?

A

Previous intracranial haemorrhage
Known structural cerebral vascular lesion
Known malignant intracranial neoplasm
Ischaemic stroke within 3 months
Suspected aortic dissection
Active bleeding or bleeding diathesis (excluding menstruation)
Significant closed-head trauma or facial trauma within 3 months

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11
Q

What are the benefits of thrombolysis?

A

Timely thrombolysis associated with 23% reduction in mortality, or 39% reduction when used with aspirin
Immediate reduction in death rate shown to continue throughout life, morbidity and mortality are significantly reduced over time

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12
Q

What is the dose of aspirin used in treatment of MI?

A

300mg loading dose then 75-150mg daily

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13
Q

How can aspirin be used to treat MI?

A

Formation of platelet aggregates is important in the pathogenesis of MI
Thromboxane stimulates platelet aggregation and vasoconstriction
Aspirin is a potent inhibitor of platelet thromboxane production

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14
Q

What effect can the regular daily use of aspirin have on mortality in acute MI?

A

Can reduce mortality by 23%

In combination with thrombolysis it can reduce mortality by 42% and reinfarction by 52%

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15
Q

What effect can the regular daily use of aspirin have in unstable angina?

A

Reduce MI and death by 50%

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16
Q

What effect can the regular daily use of aspirin have in secondary prevention?

A

Reduce re-infarction by 32% and combined vascular events by 25%

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17
Q

What is the standard dose of clopidogrel used in treatment of MI?

A

300mg loading dose then 75mg once daily

18
Q

How does clopidogrel work?

A

Inhibits ADP receptor-activated platelet aggregation
Specifically and irreversibly inhibits the P2Y12 ADP receptor which inhibits platelet aggregation by blocking activation of the GP IIb/IIIa pathway

19
Q

What is the IIb/IIIa complex a receptor for?

A

Fibrinogen, fibronectin and vWF

20
Q

What is the activation of IIb/IIIa complex the final common pathway for?

A

Platelet aggregation and the cross-linking of platelets by fibrin

21
Q

What drug is clopidogrel used in combination with?

A

Aspirin

22
Q

What is the relative risk reduction when clopidogrel is used in combination with aspirin?

A

21%

23
Q

What percentage of the population will demonstrate resistance to clopidogrel?

A

14% due to low CYP 2C19 levels

24
Q

What class of drug is prasugrel?

A

Member of the thienopyridine class of ADP receptor inhibitors

25
Q

What is the difference between prasugrel and clopidogrel?

A

Prasugrel inhibits ADP-induced platelet aggregation more rapidly and more consistently, and doesn’t rely on metabolism in the liver

26
Q

What are the products of low molecular weight heparin?

A

Enoxaparin
Dalteparin
Tinzeparin
Fondaparinux

27
Q

Why is fondaparinux recommended?

A

Single chemical entity
Highly selective for its target
Once daily administration
No need for platelet monitoring

28
Q

What is glycoprotein IIb/IIIa?

A

Integrin complex found on platelets

Receptor for fibrinogen aids in platelet activation

29
Q

What does platelet aggregation by ADP lead to in platelet glycoprotein IIb/IIIa receptors?

A

Conformational change that induces binding to fibrinogen

30
Q

What do drugs such as abciximab and tirofiqan reduce at 30 days of treatment?

A

Composite end point of death, re-infarction and need for urgent revascularisation by 46% at 30 days, and by 20% at 6 months

31
Q

Give an example of a glycoprotein IIb/IIIa receptor inhibitor

A

Abciximab

Tirofiban

32
Q

What is the major adverse effect of glycoprotein IIb/IIIa receptor inhibitors?

A

Bleeding

Major bleeding in 1.4% of patients
Minor bleeding in 10.5%
Blood transfusion required to terminate bleeding and improve bleeding-related anaemia in 4% of all patients

33
Q

What is the reduction in mortality following an MI produced by IV atenolol or metoprolol?

A

10-15%

34
Q

Oral beta blockade started weeks or months post-MI can reduce cardiac death and second MI by what?

A

Reduce cardiac death by 22%

Reduce second MI by 26%

35
Q

What are the common complications following an MI?

A 
Arrhythmia
Cardiogenic shock
Myocardial rupture
Valve dysfunction
Papillary muscle dysfunction/rupture
Acute ventricular septal defect
36
Q

What are the long-term complications of MI?

A

Higher risk of bleeding due to anti-platelet medication
Increased risk of further MI/death
Cardiac failure

37
Q

What is necessary before discharging a patient from hospital following an MI?

A

Check that they are on the correct medications
Address risk factors
Cardiac rehabilitation
Follow up plans

38
Q

Why are anti-platelets needed in patients who have a coronary stent?

A

Takes some time for the stent to become endothelialised (embedded into coronary artery wall)
During this time the metal stent is exposed to the blood and can cause thrombosis and block off the stent, unless patient is on anti platelet therapy

39
Q

What is the typical medical treatment protocol of acute coronary syndrome if there is no evidence of STEMI?

A

Aspirin 300mg loading dose then 75mg once daily
Clopidogrel 300mg loading dose then 75mg once daily
Fondaparinux 2.5mg once daily subcutaneous or LMWH
Intravenous nitrate
Analgesia
Beta blockers 2.5mg once daily
ACEI 1.25mg twice daily

Other medications;
Prasugrel
Ticagrelor
Glycoprotein IIb/IIIa receptor blockers
Statins
40
Q

What can be used in management of ACS to reduce the risk from NSTEMI?

A 
PCI or CABG
Aspirin
Clopidogrel, prasugrel, ticagrelor, ticlopidine or cilostazol
LMWH
Fondaparinux
Glycoprotein IIb/IIIa receptor blockers
Beta blockers

R-Cradio-illness (27 decks)

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