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Cardiovascular System > ACS & AMI - Therapy > Flashcards

ACS & AMI - Therapy Flashcards

1
Q

What does ACS stand for?

A

Acute coronary syndrome

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2
Q

What does AMI stand for?

A

Acute myocardial infarction

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3
Q

What is in the spectrum of acute coronary syndrome?

A

1) Unstable angina
2) Non-ST elevated myocardial infarction (NSTEMI)
3) ST elevated myocardial infarction (STEMI)
4) Sudden cardiac death

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4
Q

What does NSTEMI stand for?

A

Non-ST elevated myocardial infarction

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5
Q

What does STEMI stand for?

A

ST elevated myocardial infarction

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6
Q

What are some causes of acute coronary syndrome?

A

Atherosclerosis plaque rupture or erosion

Superimposed platelet aggregation and thrombosis

Vasospasm and vasocontriction

Subtotal or transient total occlusion of vessel

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7
Q

What is the goal of pharmacotherapy for acute coronary syndrome?

A

Increase myocardial oxygen supply

Decrease myocardial oxygen demand

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8
Q

How can myocardial oxygen supply be increased?

A

Vasodilation

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9
Q

How can myocardial oxygen demand be decreased?

A

Decrease heart rate

Decrease blood pressure

Decrease preload or myocardial contractility

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10
Q

What has a high likelihood of being the cause of patients with STEMI?

A

Coronary thrombus occluding the infarct artery

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11
Q

What is coronary thrombus formation usually due to?

A

Formation of thrombus overlying an atheromatous plaque occluding the coronary artery

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12
Q

What is the treatment for coronary thrombus formation?

A

If no percutaenous coronary intervention (PCI) within 2 hours then thrombolysis is indicated

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13
Q

What does PCI stand for?

A

Percutanous coronary intervention

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14
Q

What is percutaneous coronary intervention?

A

Non-surgical procedure that uses a catherter to place a stent to open up blood vessels in the heart that have been narrowed

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15
Q

What is a stent?

A

Thin flexible tube

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16
Q

What is a non-surgical procedure that uses a catheter to place a stant to open up blood vessels in the heart that have been narrowed?

A

Percutaneous coronary intervention

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17
Q

What agents are used for thrombolysis?

A

Serine proteases

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18
Q

How do serine proteases work?

A

Converting plasminogen to the fibrinolytic agent plasmin

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19
Q

How does plasmin destroy clots?

A

Breaks down the fibrinogen and fibrin contained in the clot

20
Q

What are the 2 categories of fibrinolytics?

A

Fibrin specific agents

Non-fibrin specific agents

21
Q

What are examples of fibrin specific agents?

A

Alteplase

Reteplase

Tenecteplase

22
Q

What is an example of a non-fibrin specific agent?

A

Streptokinase systemic fibrinolysis

23
Q

What are some contraindications to thrombolysis?

A

Prior intracranial haemorrhage

Known structural cerebral vascular lesion

Known malignant intracranial neoplasm

Ischaemic stroke within 3 months

Suspected aortic dissection

Active bleeding or bleeding diathesis

Significant closed heart head trauma or facial trauma within 3 months

24
Q

What are the benefits of thrombolysis?

A

23% reduction in mortality

39% when used with aspirin

25
Q

What can thrombolysis be used with to increase the reduction in mortality?

A

Aspirin

26
Q

What does the medical treatment protocol if no evidence of STEMI include?

A

Aspirin

Tigagrelol/clopidogrel

Fondaparinux/low molecular weight heparin

Intravenous nitrate

Analgesia

Beta blockers

27
Q

What does LMW stand for?

A

Low molecular weight

28
Q

What does the management to reduce risk from NSTEMI involve?

A

PCI or CABG

Aspirin

Clopidogrel, prasugrel, ticagrelor, ticlopidine or cilostazol

Heparin

Fondaparinux

GIIb/IIIa receptor blockers

Statins

Beta blockers

29
Q

What are examples of antiplatelet agents?

A

Low dose aspirin

Clopidogrel

Prasugrel

Low molecular weight heparin

Glycoprotein IIb/IIIa receptor inhibitors

30
Q

What is considered to be low dose aspirin?

A

75-150mg

31
Q

What is the formation of platelet aggregates important in the pathogenesis of?

A

Angina

Unstable angina

Acute myocardial infarction

32
Q

How does aspirin work?

A

1) Potent inhibitor of platelet thromboxane A2 production
2) Thromboxane stimulates platelet aggregation and vasocontriction

33
Q

What does thromboxane stimulate?

A

Platelet aggregation and vasocontriction

34
Q

What kind of drug is clopidogrel?

A

Prodrug

35
Q

How does clopidogrel work?

A

1) Irreversible inhibits the P2Y12 ADP receptor which is important in aggregation of platelets and cross linking by fibrin
2) Blockage of this inhibits platelet aggregation by blocking the activation of the GP IIb/IIIa pathway

36
Q

What does clopidogrel combine to?

A

P2Y12 ADP receptor

37
Q

What is the IIb/IIIa complex?

A

Receptor for fibrinogen, fibronectin and von WF, activation of this is the final common pathway for platelet aggregation and cross linking of platelets by fibrin

38
Q

What should clopidogrel always be used in combination with?

A

Aspirin

39
Q

How do some people demonstrate resistance to clopidogrel?

A

Low levels of CYP 2C19 which is used to activate the drug

40
Q

What activates clopidogrel?

A

CYP 2C19

41
Q

How does prasugrel work?

A

Just like clopidogrel, ADP receptor inhibitor

42
Q

What are some different examples of low molecular weight heparin?

A

Enoxaparin

Dalteparin

Tinzeparin

Fondaparinux

43
Q

What is a major adverse effect of most antiplatelet agents?

A

Bleeding

44
Q

What are beta blockers used post myocardial infarction for?

A

Treatment in the acute myocardial infarction

Secondary prevention in the survivors of an acute myocardial infarction

45
Q

How do beta blockers work?

A

Competatively inhibit the myocardial effects of circulating catecholamines and reduce myocardial oxygen consumption by lowering heart rate, blood pressure and myocardial contractility

46
Q

What is an important drug to be given post myocardial infarction?

A

Beta blockers to reduce mortality and second myocardial infarction

Cardiovascular System (41 decks)

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