Pharmacotherapy of Cardiac Disease Flashcards Preview

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Flashcards in Pharmacotherapy of Cardiac Disease Deck (10)
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1

What are the principles of treatment for acute coronary syndromes?

Increase oxygen supply of the myocardium

  • Increase coronary blood flow
  • Give oxygen

Reduce oxygen demand of myocardium

  • Reduce heart rate and contractility
  • Reduce cardiac afterload
  • Reduce cardiac preload

2

Describe the treatment strategies for chronic heart failure 

Improve contractility:

  • Positive inotropes e.g. sympathomimetics (and modulate with beta blocker)

Reduce oedema:

  • Diuretics

Reduce preload and afterload:

  • ACE-Inhibitors
  • Angiotensin II receptor blocker

3

Why does the use of positive inotropes in heart failure often need to be modulated with a beta blocker?

Inotropes can cause enhanced and sustained cardiac adrenergic drive 

4

What are the principal targets for treatment of heart failure?

Heart:

  • Cardiomyocytes
  • Coronary arteries

Kidney:

  • Renal tubular epithelial cells

Peripheral arteries:

  • Vascular smooth muscle cells

 

5

What classes of drug used for HF act directly on the heart itself?

ACE-inhibitors

Sympathomimetics

Inotropes

Calcium channel blockers

Beta blockers 

Anticholinergics

Angiotensin receptor blockers

Aldosterone antagonists

6

What classes of drugs used for HF target the kidney?

Diuretics

Aldosterone antagonists

ACE-inhibitors

Angiotensin II receptor blockers

7

What classes of drugs used in HF act on the vascular smooth muscle cells?

Calcium channel blockers

ACE-inhibitors

8

Describe the actions of angiotensin II on vascular smooth muscle cells 

  1. Angiotensin II binds to and activates angiotensin II receptor.
  2. Angiotensin II receptor releases IP3 which stimulates Ca2+ release from sarcoplasmic reticulum
  3. Intracellular calcium modulated by calmodulin 
  4. Calcium activates myosin light chain kinase (MLCK)
  5. MLCK phosphorylates myosin light chain to induce contraction. 

 

9

Describe how the stimulation of B1 adrenoceptors in cardiac muscle drives contraction

How does this differ to the activation of B2 adrenergic receptors in smooth muscle of the lung?

  1. Activation of B1 adrenoceptor activates cAMP
  2. cAMP activates protein kinase A 
  3. Protein kinase A releases Ca2+ from intracellular stores
  4. Increased intracellular Ca2+ in the cytoplasm induces muscle contraction 

Opposite effects in smooth muscle- in smooth muscle protein kinase A reduces intracellular Ca2+ by driving it into storage therefore reducing contraction.

 

10

Which 2 classes of drugs can be used to prevent cardiovascular disease without affecting blood pressure?

HMG-CoA Reductase inhibitors (Atorvastatin, Simvastatin)

Antiplatelets (Aspirin, Clopidogrel)