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Cardio > Acute coronary syndromes pharmacology > Flashcards

Acute coronary syndromes pharmacology Flashcards

1
Q

Ischaemia is caused when there is an imbalance between supply and demand of oxygenated blood

How is this corrected by drugs?

A

Increase supply through vasodilation

Decrease demand by decreasing heart rate, decreasing blood pressure and decreasing preload or myocardial contractility

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2
Q

What is typically the state of the coronary arteries of someone with a STEMI

A

High likelihood (>90%) of a coronary thrombus occluding the infarct artery. This is usually overlying an atheromatous plaque.

To correct the supply/demand imbalance that causes ischaemia and infarction, the thrombus must be removed

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3
Q

What are the ways that thrombi in coronary arteries are removed?

A

Primary PCI

Thrombolysis

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4
Q

What are the indications for primary PCI?

A

First line for removal of a thrombus provided it can be done quickly (door - balloon in less than 90 mins)

Also better if:

  • High bleeding risk
  • Heart failure / cardiogenic shock
  • Diagnosis is uncertain
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5
Q

What are the indications for thrombolysis?

A

Alternative to primary PCI angioplasty if time before surgery is too long (door - balloon > 90 mins)

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6
Q

How do thrombolytic agents work?

A

Serine proteases that work by converting plasminogen to the natural fibrinolytic agent plasmin

Plasmin breaks down the fibrin and fibrinogen that is in clots

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7
Q

What are the types of thrombolytic (fibrinolytic) agents?

A

Fibrin specific agents

Non fibrin specific agents

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8
Q

Give some examples of fibrin specific agents and explain how they work

A

Alteplase
Reteplase
Tenecteplase

These catalyse conversion to plasminogen to plasmin, only in places where there is fibrin

So basically, plasmin is only produced at the site of the clot

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9
Q

Give an example of a non-fibrin specific agent and explain how it works

A

Streptokinase

These convert plasminogen to plasmin all over the body, so there is a systemic catalysis of fibronolysis

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10
Q

What are the contraindications to thrombolysis?

A

Prior intracranial hemorrhage (ICH)

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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11
Q

What other agent is typically given with thrombolytics?

A

Aspirin

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12
Q

What is the benefit of thrombolysis

A

23% reduction in mortality

39% reduction in mortality when given with aspirin

(However, Primary PCI is better than thrombolysis so is first line)

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13
Q

What is the ACS treatment protocol?

A

If no evidence of STEMI:

Aspirin
Tigagrelor / Clopidogrel
Fondaparinux / LMW heparin
IV nitrate
Analgesia
Beta Blockers
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14
Q

Summarise the agents used to reduce the risk from NSTEMI

A 
PCI or CABG
Aspirin
Clopidogrel, prasugrel or ticagrelor
Heparin (LMWH)
Fondaparinux
GIIb/IIIa receptor blockers
Statins
B blockers
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15
Q

Describe the mechanism of Aspirin and why it is used for management of ACS

A

Aspirin is a potent inhibitor of platelet thromboxane A2 production

Platelet thromboxane A2 stimulates platelet aggregation and vasoconstriction

Low dose Aspirin (75-150mg)

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16
Q

What are the benefits of regular daily use of Aspirin if someone has an acute MI?

A

reduce mortality by 23%

in combination with thrombolysis: reduce mortality by 42% and reinfarction by 52%

17
Q

Why is regular Aspirin good for someone who has an episode of unstable angina?

A

reduce likelihood of MI and death by 50%

18
Q

Why should Aspirin be given to a patient, post acute coronary event?

A

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

19
Q

How long post ACS event should Aspirin be prescribed?

A

Up to 2 years

Reduce risk of reinfarction, combined vascular events

20
Q

Describe the mechanism of Clopidogrel and why it is used for treatment of ACS

A

Clopidogrel is a prodrug that specifically and irreversibly inhibits the P2Y12 ADP receptor

Stops ADP receptor activated platelet aggregation and cross-linking by fibrin

21
Q

What important clotting enzyme pathway thing does clopidogrel block?

A

Blocks activation of the GP IIb/IIIa pathway

The GP IIb/IIIa receptor is found on platelets and binds to fibrinogen once the platelet is activated by ADP

22
Q

What system in the body can be damaged by clopidogrel?

A

Clopidogrel can cause GI bleeding

Although it has a claimed lower risk than previously used agents

23
Q

A small proportion of the population are resistant to Clopidogrel

Why?

A

Clopidogrel activated by Cyp 2C19

14% of population have low CYP2C19 levels

24
Q

What is an alternative to Clopidogrel if it doesnt work?

A

Prasugrel

25
Q

How is the mechanism of Prasugrel different to clopidogrel?

A

Both are in the thienopyridine class of ADP receptor inhibitors

However, Prasugrel inhibits ADP–induced platelet aggregation more rapidly, more consistently

Prasugrel also has lower risks & mortality

26
Q

Give some examples of Low molecular weight Heparin agents

A

Fondaparinux
Dalteparin

Enoxaparin
Tinzeparin

27
Q

How does Fondaparinux work?

A

LMWH

Works by inhibiting Factor Xa which is part of the thrombin fucking clot pathway

It’s better than Enoxaparin

28
Q

How often is Fondaparinux administered to an ACS protocol patient?

A

Once per day

29
Q

What are examples of Glycoprotein IIb/IIIa receptor blockers?

A

abciximab (not a typo)

tirofiban

30
Q

What is a risk associated with GP IIb/IIIa receptor blockers?

A

Bleeding
Thrombocytopenia

Blood transfusion required to terminate bleeding and to improve bleeding-related anaemia in 4.0% of all patients.

31
Q

Why are beta blockers used for ACSs?

A

Used both in the treatment of acute MI

And in secondary prevention of reinfarction for someone who survives an MI

32
Q

What beta blockers are used in treating an Acute MI?

A

IV atenolol (or metoprolol)

33
Q

What beta blockers are used to prevent reinfarction and all that shite

A

Oral beta blockade started weeks/months post MI

34
Q

How to beta blockers work

A

Competitively inhibit the myocardial effects of circulating catecholamines

(hormones like noradrenaline, adrenaline etc which your adrenal gland pumps out during physical stress eg an ACS)

Reduce myocardial oxygen consumption by lowering heart rate, blood pressure and myocardial contractility

35
Q

Beta blockers are really good at lowering the risk of patients dying from cardiogenic shock

What patients are most at risk of cardiogenic shock?

A

age >70 years

heart rate >110 beats/min

systolic blood pressure < 120 mmHg

36
Q

When should Beta blockers be avoided?

A

patients with symptoms possibly related to coronary vasospasm or cocaine use

Cardio (41 decks)

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