CVS S9 - Drugs and the CVS Flashcards

1
Q

What is heart failure and what are its typical features?

A

Chronic failure of the heart to provide sufficient output to meet the body’s requirement

  • Reduced force of contraction
  • Oedema
  • Reduced cardiac output
  • Reduced tissue perfusion
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2
Q

What are the two different lines of drug treatment for heart failure and give examples of each drug type?

A

Positive inotropes which increase cardiac output e.g. Beta 1- adrenoreceptor agonists, Cardiac glycosides

Drugs which reduce preload and afterload e.g. ACE inhibitors

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3
Q

How do cardiac glycosides work?

A

Block the Na+-K+-ATPase which causes rise in intracellular sodium, thereby less calcium ions move out via the NCX and so force of contraction increases

Also increase vagal activity so slow AV conduction and decrease heart rate

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4
Q

How do ACE inhibitors work?

A
  • Inhibit angiotensin converting enzyme
  • No angiotensin I converted to angiotensin II
  • Prevents sodium and water reabsorption and vasoconstriction
  • Decreases blood volume causing decrease in preload
  • Causes vasodilation decreasing afterload
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5
Q

How would angina be treated?

A

Reduce work load of heart via beta blockers, calcium channel blockers or organic nitrates

Improve blood supply to the heart via organic nitrates and calcium channel blockers

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6
Q

How do organic nitrates work?

A
  • React with –thiols to produced -NO2
  • NO2 is reduced to NO (nitric oxide)
  • NO activates guanylate cyclase
  • Increase cGMP production
  • cGMP binds to PKG
  • Causes decrease in intracellular calcium causing vasodilation
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7
Q

How do organic nitrates primarily and secondarily alleviate the symptoms of angina?

A

Primarily- venodilation which decreases preload

Secondarily- dilates collateral arteries

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8
Q

Which heart conditions can increase the risk of thrombus formation?

A

Atrial fibrillation, acute MI, mechanical prosthetic heart valves

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9
Q

What two types of drug can be given to reduce the risk of thrombus?

A

Anti-coagulative e.g. warfarin, heparin

Anti-platelet e.g. aspirin

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10
Q

What is the equation for blood pressure?

A

BP= CO x TPR

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11
Q

What are the two primary causes of hypertension?

A

Increased blood volume or increased peripheral resistance

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12
Q

What are the targets for anti-hypertensive drugs?

A

Lower blood volume, lower cardiac output directly, lower TPR

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13
Q

What are the possible treatments for hypertension and how does each work?

A

Diuretics- decrease blood volume

ACE inhibitors- decrease blood volume and cause vasodilation

Beta blockers- decrease cardiac output

Na+ channel blockers- vasodilation

Alpha 1- adrenoreceptor antagonists- vasodilation

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14
Q

How does ectopic pacemaker activity cause arrhythmia?

A

Damaged area of myocardium becomes depolarised and spontaneously active

Latent pacemaker region activated due to ischaemia and dominates over SA node

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15
Q

What are the two types of after depolarisation that can result in arrhythmia?

A

Delayed- due to high intracellular calcium

Early- due to prolonged action potential seen by longer QT interval

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16
Q

What else, other than delayed and early depolarisation, can cause arrhythmias in the heart and how?

A

Re-entry loop - incomplete conduction damage creates a unidirectional block allowing depolarization to spread through damaged area in the wrong direction and via a longer route

17
Q

How can re-entry loop develop into atrial depolarisation?

A

Several small re-entry loops in the atria

18
Q

Give an example of a Na+ channel blocker, when would it be used and why?

A

Local anaesthetic such as lidocaine

  • Treatment for MI in patients showing signs of ventricular tachycardia
  • Damaged area of myocardium may be depolarised so has more Na+ channels open
  • Lidocaine blocks these open or inactive channels (use-dependent) preventing automatic firing of action potentials
19
Q

Why would beta- adrenoreceptor blockers be given to a patient following an MI?

A

MI causes increased sympathetic activity

Drugs prevent ventricular arrhythmias, reduce oxygen demand so prevent ischaemia and slow conduction in AV node to prevent supraventricular tachycardia

20
Q

How do K+ channel blockers work and what is the disadvantage of their use?

A

Prolong the action potential which lengthens the absolute refractory period

This prevents another action potential firing too soon

However longer action potential means these drugs are often pro-arrhythmic

21
Q

When might a K+ channel blocker be used and what is the name of this drug?

A

Amiodarone used to treat tachycardia

22
Q

What are the main actions of Ca2+ channel blockers?

A
  • Decrease slope of the pacemaker potential in the SA node
  • Decrease AV node conduction
  • Decrease force of contraction
  • Cause coronary and peripheral vasodilation