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A2. Respiratory system > ACS and AMI - Therapy (Clinical Pharmacology) > Flashcards

ACS and AMI - Therapy (Clinical Pharmacology) Flashcards

1
Q

What comprises acute coronary syndromes?

A

•Increase myocardial oxygen supply

–through coronary vasodilation.

•Decrease myocardial oxygen demand

–Decrease in heart rate,

–Decrease blood pressure,

–Decrease preload or myocardial contractility

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2
Q

Common pathogenesis of ACS?

A

•Common pathogenesis

–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

–through coronary vasodilation.

•Decrease myocardial oxygen demand

–Decrease in heart rate,

–Decrease blood pressure,

–Decrease preload or myocardial contractility

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4
Q

What is the likelihood of coronary thrombus occlusion of the infarct artery in STEMI?

A

Highe likelihood, •Angiographic evidence of coronary thrombus formation is seen in more than 90% of patients with STEMI

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5
Q

Where does the thrombus which occludes a coronary artery in STEMI lie?

A

Overlies an atheromatous plaque

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6
Q

When is thrombolysis indicated?

A

If no PCI within 2 hours

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7
Q

How is thrombolysis by serine proteases achieved?

A

Work by converting plasminogen to the fibrinolytic agent plasmin.

Plasmin lyses clot by breaking down the fibrinogen and fibrin contained in a clot

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8
Q

What are the two categories of fibrinolytics?

A

Fibrin-specific agents

Non–fibrin-specific agents

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9
Q

Give examples of fibrin specific agents

A
  • alteplase,
  • reteplase,
  • tenecteplase

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

(assuming these agents are therefore inhibited by fibrin)

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10
Q

Give examples of non fibrin specific agents

A

streptokinase,

which catalyses systemic fibrinolysis

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11
Q

What are the contraindications for 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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12
Q

What are the benefits of thrombolysis?

A
  • 23% reduction in mortality
  • 39% when used with aspirin
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13
Q

What is the acute coronary syndrome medical treatment protocol if there is no evidence of STEMI?

A
  • Aspirin
  • Tigagrelor/Clopidogrel (ADP receptor blockers)
  • Fondaparinux/LMW heparin
  • Intravenous nitrate
  • Analgesia
  • Beta Blockers

Other Medicines:

  • prasugrel
  • GIIbIIIa receptor blockers
  • Statins
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14
Q

What is the effect of an ADP receptor blocker?

A

Stops binding of ADP to ADP receptors (P2Y12) Therefore no activation of platelets.

(In normal circumstances an activated platelet produces, thromboxane A2, ADP, Fibrinogen and VWF. Thromboxane activates GP2b/3a receptors which now bind to fibrinogen and cause platelet aggregation - platelet plug and clot)

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15
Q

What is management to reduce risk from NSTEMI?

A
  • PCI or CABG
  • Aspirin
  • Clopidogrel, prasugrel, ticagrelor, ticlopidine or cilostazol
  • Heparin (LMWH)
  • Fondaparinux
  • GIIb/IIIa receptor blockers
  • Statins
  • B blockers
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16
Q

Platelet aggregation is important in the pathogenesis of what diseases?

A

•angina, unstable angina and acute MI

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17
Q

What is the effect of aspirin on thromboxane A2 production?

A

•Aspirin is a potent inhibitor of platelet thromboxane A2 production

18
Q

What is the effect of thromboxane?

A

Stimulates platelet aggregation and vasoconstriction

19
Q

What is the effect of daily use of aspirin on acute MI?

A

–reduce mortality by 23%

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

20
Q

What is the effect of daily use of aspirin on unstable angina?

A

–reduce MI and death by 50%

21
Q

What is the effect of daily use of aspirin on secondary prevention?

A

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

22
Q

Is there a significant difference in the effectiveness of higher dose aspirin versus lower dose aspirin?

A

No - therefore always a good idea to use low dose aspirin

23
Q

How does clopidogrel work?

A
  • Clopidogrel is a prodrug
  • 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
24
Q

What is the effect of ADP on platelet gpIIb/IIIa receptors?

A

Changes platelet gpIIb/IIIa receptors to induce binding to fibrinogen

25
Q

What is the effect of ADP receptor blockers on the GP IIb/IIIa pathway?

A

•The IIb/IIIa complex is a receptor for fibrinogen, fibronectin and von WF. Activation of this receptor complex is the “final common pathway” for platelet aggregation and cross-linking of platelets by fibrin. However if ADP is blocked there is no activation of the 2b/3a complex and so no platelet aggregation

26
Q

What is clopidogrel used with?

A
  • Always used in combination with aspirin
  • Relative risk reduction of 21% when used together with aspirin.
27
Q

Why do some of the population have clopidogrel resistance?

A

Clopidogrel is a prodrug, activated by Cyp 2c19

•14% of population have low CYP2C19 levels and demonstrate resistance to clopidogrel

28
Q

What is the effect of prasugrel?

A

ADP receptor inhibitor like clopidogrel

Compared to clopidogrel prasugrel inhibits ADP–induced platelet aggregation more rapidly, more consistently,

29
Q

What type of heparin is used as an integral part of the acute coronary syndrome protocol?

A

Low molecular weight heparin

30
Q

What are the different examples of low molecular weight heparin?

A
  • Enoxaparin
  • Dalteparin
  • Tinzeparin
  • Fondaparinux
31
Q

What is heparin?

A

A compound occurring in the liver and other tissues which inhibits blood coagulation. A sulphur-containing polysaccharide, it is used as an anticoagulant in the treatment of thrombosis.

32
Q

What is the benefit of fondaparinux over enoxaparin?

A

Reduces Death/MI/RI/Major Bleeding more significantly

33
Q

Can you name GP2b/3a receptor inhibitor?

A

•abciximab, tirofiban

34
Q

What is the effect of a glycoprotein receptor inhibitor?

A

Prevents the conformational change in platelet GP2b/3a inhibitor which would normally cause binding with fibrinogen - no aid of platelet aggregation

35
Q

What is the major adverse effect of glycoprotein 2b/3a?

A

Bleeding

–major bleeding occurrs in 1.4 % of patients

–minor bleeding in 10.5 %.

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

Thrombocytopenia (Thrombocytopenia is a condition in which you have a low blood platelet count) was more often with tirofiban + heparin (1.5 %) than with heparin (0.8 %)

36
Q

What are beta blockers used for post MI?

A

In the treatment of acute MI

For secondary prevention in the survivors of an acute MI.

37
Q

Give two examples of beta blockers

A

I.V.atenolol or metoprolol

38
Q

When is oral beta blockade startes?

A

Started weeks or months post MI reduce cardiac death by 22% and second MI by 26%

39
Q

What is the effect of beta blockers?

A

•Beta-blockers competitively inhibit the myocardial effects of circulating catecholamines and reduce myocardial oxygen consumption by lowering heart rate, blood pressure and myocardial contractility.

Any of a class of aromatic amines which includes a number of neurotransmitters such as adrenaline and dopamine.

40
Q

When is it a bad idea to give patients beta blockers?

A

Patients at risk of developing cardiogenic shock (i.e. age >70 years, heart rate >110 beats/min, systolic blood pressure < 120 mmHg)

Cardiogenic shock is a condition in which your heart suddenly can’t pump enough blood to meet your body’s needs.

Avoid in these and patients with symptoms possibly related to coronary vasospasm or cocaine use.

41
Q
A

A2. Respiratory system (77 decks)

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