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Systems: Cardiovascular > Acute Coronary Syndrome > Flashcards

Acute Coronary Syndrome Flashcards

1
Q

Describe the spectrum ACS? (4 points )

A
  • Unstable angina
  • Non-ST elevation myocardial infarction
  • ST-elevation myocardial infarction
  • Sudden cardiac death
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2
Q

Common pathogenesis of ACS?

A
  • Atherosclerotic plaque rupture or erosion
  • Superimposed platelet aggregation and thrombosis
  • Vasospasm, and vasoconstriction
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3
Q

What are the two goals of pharmacotherapy?

A
  • Increase myocardial oxygen supply

- Decrease myocardial oxygen demand

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4
Q

How do you increase myocardial oxygen supply?

A

-Through coronary vasodilation

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5
Q

How do you decrease myocardial oxygen demand?

A
  • Decrease in heart rate
  • Decrease blood pressure
  • Decrease preload or myocardial contracility
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6
Q

What do patients with STEMI have a high likelihood of?

A

A Coronary thrombus occulding the infarct artery

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7
Q

How does STEMI usually occur?

A

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

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8
Q

What thrombolytic agents are available today?

A

Serine proteases

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9
Q

How do thrombolytic agents work?

A

converting plasminogen to the natural fibrinolytic agent plasmin

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10
Q

What does plasmin act on?

A

fibrinogen

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11
Q

What are the two categories of thrombolytic agents?

A
  1. Fibrin-specific agents

2. Non-fibrin specific agents

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12
Q

name 3 fibrin specific agents?

A
  • Alteplase
  • Reteplase
  • Tenecteplase
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13
Q

How to fibrin specific drugs work?

A

All catalyse conversion of plasminogen to plasmin in the absence of fibrin

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14
Q

Where are streptokinases taken from?

A

from mycobacterium (causes sensitation so only one dose available)

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15
Q

When would you not give thrombolytic drugs? (7)

A
  • Prior intracranial hemorrhage
  • Known structural cerebral vascular lesion
  • Known malignant intracranial neoplasm
  • Ischaemic stroke within 3 months
  • Suspected aortic dissection
  • Active bleeding/diathesis
  • Significant closed-head trauma or facial trauma within 3 months
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16
Q

What do you do if there is no evidence of a STEMI ACS?

A
  • Aspirin
  • Tigagrelor/clopidogrel-antiplatlete
  • Fondaparinux/LMW heparin
  • IV nitrate
  • Analgesia
  • Beta Blockers
17
Q

What is the dose given of aspirin?

A

low ( 75-100mg)

18
Q

What is aspirin is apotent inhibitor of what?

A

Platelet thromboxane A2 production

19
Q

what can the daily use of aspirin reduce the risk of?

A 
ACute MI (mortality 23%)
Unstable angina (death 50%)
Secondary prevention (reduce reinfarction by 32% and combines vascular events by 25%)
20
Q

What is clopidogrel?

A

a Pro-drug

21
Q

How does clopidogrel work?

A

Inhibits ADP receptor activated platelet aggregation

22
Q

What receptor does clopidogrel act on?

A

P2Y12 ADP

23
Q

What is P2Y12 ADP responsible for?

A

Important in aggregation of platelets and cross linking by fibrin

24
Q

What is Clopidogrel activated by?

A

CYP2C19

25
Q

How much of the population have low levels of CYP2c19?

A

14%

26
Q

What is the IIb/IIIa complex?

A

it is a receptor fibrinogen, fibronectin and von WF

27
Q

What happens when IIb/IIIa complex is activated?

A

“final common pathway” for platelet aggregation and cross-linking of platelets by fibrin

28
Q

What is clopidrogrel always used in combination?

A

aspirin

29
Q

What is more effective than clopidogrel with aspirin?

A

Ticagrelor and aspirin

30
Q

What is more rapid and consistent in than clopidogrel in inhibiting the ADP- platelet aggregation

A

Prasugrel

31
Q

What are clopdiogrel and prasugrel members of?

A

Thienopyridine class of ADP receptor inhibitors

32
Q

Name the four low molecular weight heparin?

A
  • Enoxaparin
  • Dalteparin
  • Tinzeparin
  • Fondaparinux
33
Q

What is the most safe in terms of major bleeds of the low molecular weight heparin?

A

Fondaparinux

34
Q

Why is fondaparinux a good choice?

A
  • Single chemical entity
  • Synthetic pentasaccaride
  • Highly selective for antithrombin
  • Once-daily administration
  • No need for platelet monitoring
35
Q

What are beta blockers used for?

A
  • In treatment of cute MI

- For secondary prevention in the survivors of an acute MI

36
Q

How do beta blockers work?

A

Competitvely inhibit the myocardial effects of circulating catecholamines and reduce myocardial oxygen comsumption by lowering heart rate, blood pressure and myocardial contractility.

37
Q

How much does atenolol or metoprolol reduce mortality by?

A

10-15%

Systems: Cardiovascular (31 decks)

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