ACS & AMI - Therapy Flashcards

1
Q

What are the aims of drug therapy for ACS and AMI?

2

A
  • increase myocardial O2 supply (vasodilation)

- decrease myocardial O2 demand (HR, BP, contractility, preload/afterload)

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2
Q

In patients with STEMI, what would be the indicated treatment if they are unable to get to a cath lab in <2hrs?

A

thrombolysis

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3
Q

Briefly outline the mechanism behind thrombolytic agents.

A

plasminogen is converted to plasmin which lyses fibrinogen and fibrin contained in clot

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4
Q

Outline the main fibrin-specific thrombolytic agents.

How do these agents work?

(3)

A

alteplase
tenecteplase
reteplase

catalyse conversion of plasminogen to plasmin

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5
Q

Name a thrombolytic agent which is non-fibrin-specific.

How does this agent work?

A

streptokinase - catalyses systemic fibrinolysis

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6
Q

What is a complication associated with streptokinase?

A

anaphylaxis

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7
Q

What are some contraindications to thrombolysis?

4

A
  • prior intercranial haemorrhage (ICH)
  • known cerebral aneurysm
  • mets in the brain
  • stroke < 3m
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8
Q

If there is no evidence of STEMI, what would be the medical treatment for acute ACS/NSTEMI?

A

BATMANS

Beta-blocker
Aspirin
Ticagrelor (dual antiplatelet)
Morphine (analgesia)
Anticoagulant (e.g. LMWH, fondaparinux)
Nitrate (e.g. IV GTN)
Statin
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9
Q

What drug is usually prescribed only to patients going for a PCI?

How does this drug compare to clopidogrel?

A

prasugrel

inhibits ADP receptor more rapidly.

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10
Q

What secondary measures are taken to prevent future risk from NSTEMI/ACS?

A

7 A’s

  • Aspirin
  • another antiplatelet (e.g. clopidogrel)
  • atenolol (b-blocker)
  • ACE inhibitor (e.g. ramipril)
  • Anticoagulant (e.g. heparin, fondaparinux)
  • atorvastatin (statin)
  • aldosterone inhibitor (e.g. epleranone)
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11
Q

What is the daily dose of aspirin often prescribed to patients at risk of further AMI/ACS?

A

75mg

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12
Q

Aspirin is a potent inhibitor of platelet ____________ production.

A

thromboxane A2

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13
Q

Thromboxane stimulates platelet _________ and ____________.

A

aggregation

vasoconstriction

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14
Q

What is the difference between low and higher doses of aspirin?

(2)

A
  • they have similar therapeutic effects.

- higher dose comes with higher risk of bleed.

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15
Q

What type of drug is clopidogrel?

2

A
  • antiplatelet

- prodrug

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16
Q

Clopidogrel and __________ both inhibit ___________ activated platelet aggregation.

A

ticagrelor

ADP receptor

17
Q

Which pathway is blocked by blockage of the ADP receptor?

A

GP2b3a

18
Q

What is clopidogrel always used in combination with?

A

aspirin

19
Q

Patients with low _________ demonstrate resistance to clopidogrel.

A

CYP 2C19

20
Q

What type of drug is a low molecular weight heparin?

A

anticoagulant

21
Q

Give examples of LMWH’s.

(4)

What is the other class of heparin? Give an example.

A

Enoxaparin
Dalteparin
Tinzeparin
Fondaparinux

unfractioned heparin (UFH) e.g. warfarin

22
Q

Which ‘LMWH’ is not technically a LMWH?

A

fondaparinux - it is synthetic

23
Q

What is the advantage of fondaparinux over, say, enoxaparin?

2

A
  • less risk of bleed

- less overall harm

24
Q
  • an integrin complex found on platelets receptor for fibrinogen, aids in platelet activation.
  • platelet activation by ADP (blocked by __________) leads to a conformational change in platelet _________ receptor that induces binding to fibrinogen.
A

clopidogrel (antiplatelet)

GPIIb/IIIa

25
Q

Give example of GP2b3a receptor inhibitors.

What are the contraindications to this drug type?

A

tirofiban

  • minor bleed
  • major bleed (less common)
26
Q

When are beta blockers used when treating ACS/MI?

What are the contraindications to beta blockers?

A
  • acute MI (although limited)
  • post MI (secondary prevention)
  • unstable angina
  • MI following sudden cessation
  • bradycardia
  • patients at high risk of cardiogenic shock