AMI- Therapy Flashcards

1
Q

What is included in the spectrum of ACS?

A
  • Unstable angina
  • NSTEMI
  • STEMI
  • Sudden cardiac death
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2
Q

What is the common pathogenesis of ACS?

A
  • Atherosclerotic plaque rupture or erosion
  • Superimposed platelet aggregation and thrombosis
  • Vasospasm and vasoconstriction
  • Subtotal or transient total occlusion of vessel
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3
Q

What is the goal of pharmacotherapy?

A
  • Increase myocardial oxygen supply

- Decrease myocardial oxygen demand

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4
Q

How is myocardial oxygen supply increased through pharmacotherapy?

A

Coronary vasodilation

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5
Q

How is myocardial oxygen demand decreased through pharmacotherapy?

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

Patients with a STEMI have a high likelihood of what?

A

A coronary thrombus occluding the infarct artery

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7
Q

What do STEMIs usually occur as result of/

A

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

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8
Q

When is thrombolysis indicated?

A

If PCI is not available within 2 hours

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9
Q

What are the thrombolytic agents available today?

A

Serine proteases

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10
Q

How do the serine proteases work?

A
  • Convert plasminogen to the natural fibrinolytic agent plasmin
  • Plasmin lyses clot by breaking down the fibrinogen and fibrin contained in a clot
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11
Q

What are the 2 categories of fibrinolytics?

A
  • Fibrin specific agents

- Non-fibrin specific agents

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12
Q

What do all fibrin specific agents do?

A

Catalyse conversion of plasminogen to plasmin in the absence of fibrin

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13
Q

Give 3 examples of fibrin specific agents.

A
  • Alteplase
  • Reteplase
  • Tenecteplase
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14
Q

What are the contraindications for thrombolysis?

A
  • Prior intracranial bleeding
  • Known structural cerebral vascular lesion
  • Known malignant intracranial neoplasm
  • Ischaemic stroke within 3 months
  • Suspected aortic dissection
  • Active bleeding or bleeding diathesis (excluding menses)
  • Significant closed head trauma or facial trauma within 3 months
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15
Q

What are the benefits of timely thrombolysis?

A
  • 23% reduction in mortality

- 39% when used with aspirin

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16
Q

If there is no evidence of a STEMI, what protocol should be followed?

A

ACS medical treatment protocol

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17
Q

What is the ACS medical treatment protocol?

A
  • Aspirin
  • Tigagrelor/clopidogrel
  • Fondaparinux/ LMW heparin
  • IV nitrate
  • Analgesia
  • B-blockers
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18
Q

Other than ACS medical treatment protocol, what other medications should patients be put on?

A
  • Prasugrel
  • Statins
  • Glycoprotein IIb IIIa receptor blockers
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19
Q

What is the management to reduce risk from NSTEMI?

A
  • PCI or CABG
  • Aspirin
  • Clopidogrel, prasugrel, ticagrelor, ticlopidine or cilostazol
  • LMW heparin
  • Fondaparinux
  • GIIb/IIIa receptor blockers
  • Statins
  • B blockers
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20
Q

What is aspirin?

A

Antiplatelet agent

21
Q

What type of aspirin is used in ACS?

A

Low dose aspirin 75-150mg

22
Q

Why is aspirin used in ACS?

A
  • The formation of platelet aggregates are important in the pathogenesis of angina, unstable angina and acute MI
  • Aspirin is a potent inhibitor of platelet thromboxane A2 production
  • Thromboxane stimulates platelet aggregation and vasoconstriction
23
Q

What is the benefit of regular daily us of aspirin in acute MI?

A
  • Reduce mortality by 23%

- In combination with thrombolysis, reduce mortality by 42% and reinfarction by 52%

24
Q

What is the benefit of regular daily use of aspirin in unstable angina?

A

Reduce MI and death by 50%

25
Q

What is the benefit of regular daily use of aspirin as secondary prevention?

A

Reduce reinfarction by 32% and combined vascular events by 25%

26
Q

What is clopidogrel?

A

Pro drug

27
Q

What does clopidogrel do?

A
  • Inhibits ADP receptor activated platelet aggregation
  • Specifically and irreversibly inhibits the P2Y12 ADP receptor which is important in aggregation of platelets and cross-linking by fibrin
28
Q

What does blockade of the P2Y12 ADP receptor result in?

A

-Inhibtion of platelet aggregation by blocking activation of the GP IIb/IIIa pathway.

29
Q

What is the IIb/IIIa complex?

A
  • A receptor for fibrinogen, fibronectin and von WF
  • Activation of this receptor is the ‘final common pathway’ for platelet aggregation and cross-linking of platelets by fibrin
30
Q

What are clopidogrel/ticagrelor always used in combination with?

A

Aspirin

31
Q

What is the relative reduction when clopidogrel/ticagrelor are used in combination with aspirin?

A

21%

32
Q

What is important to not with the combination use of aspirin and clopidogrel/ticagrelor?

A
  • Lower incidence rate of GI bleeding however GI bleeding remain very common
  • Possible interaction with PPI with a reduction in effect
33
Q

Why do some people have resistance to clopidogrel?

A
  • Clopidogrel is active by Cyp2C19

- 14% of the population have low Cyp2C19 levels and demonstrate resistance to clopidogrel

34
Q

What is prasugrel?

A

Member of the thienopyridine class of ADP receptor inhibitors, like clopidogrel

35
Q

How does prasugrel compare to clopidogrel?

A

Prasugrel inihibits ADP-induced platelet aggregation more rapidly and more consistently

36
Q

Give examples of 4 different LMWH products.

A
  • Enoxapirin
  • Dalteparin
  • Tinzparin
  • Fondaparinux
37
Q

What is fondaparinux?

A

A selective inhibitor of factor Xa

38
Q

What are the properties of fondaparinux?

A
  • Single chemical entity
  • Synthetic pentasaccaride
  • Highly selective for antithrombin
  • Once-daily administration
  • No need for platelet monitoring
39
Q

What is GPIIb/IIIa?

A
  • An integrin complex found on platelets

- Receptor for fibrinogen aids in platelet activation

40
Q

What does platelet activation by ADP lead to?

A

A conformational change in platelet GPIIb/IIa receptor that induced binding to fibrinogen

41
Q

Give 2 examples of drugs that target the GPIIb/IIIa receptor.

A
  • Tirofban

- Abciximab

42
Q

How do IV GPIIb/IIIa inhibitors block platelet aggregation?

A

Inihibit fibrinogen binding to a conformationally activated form of the GPIIb/IIIa receptor on 2 adjacent platelets

43
Q

What is the major adverse effect of anti-thrombotic drugs?

A

Bleeding

44
Q

Why are B-blockers used post MI?

A
  • In the treatment of acute MI

- For secondary prevention in the survivors of an acute MI

45
Q

Give 2 examples of B-blockers used post MI.

A
  • Atenolol

- Metoprolol

46
Q

How do B-blockers work/

A

-Competitively inhibit the myocardial effects or circulating catecholamines and reduce myocardial oxygen consumption by lowering hear rate, blood pressure and myocardial contractility

47
Q

Who is at risk of cardiogenic shock?

A
  • Age>70
  • Heart rate>110bpm
  • Systolic BP<120mmHg
48
Q

Who should B-blockers not be given to?

A
  • Patients at risk of cardiogenic shock

- Patients with symptoms possibly related to coronary vasospasm or cocaine use