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Drugs and Disease > Drug Treatment of Angina Pectoris > Flashcards

Drug Treatment of Angina Pectoris Flashcards

1
Q

What angina pectoris?

A

Chest pain due to myocardial ischaemia
Build up of metabolites (adenosine, CO2, lactate, K+ ions) activates sensory nerves
Not a disease itself

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2
Q

What is the ischaemia due to?

A

Increase myocardial O2 demand which is not met

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3
Q

What are the 3 types of angina?

A 
Stable angina (most common)
Unstable angina
Variant angina (least common)
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4
Q

What is stable angina?

A

Attacks predictable, e.g. exercise, stress
Myocardial O2 demand not met
Involvement of chronic occlusive coronary artery disease, i.e. atherosclerosis (use of cholesterol-lowering drugs-stains)

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5
Q

What is unstable angina?

A

Attacks unpredictable

Coronary artery occlusion due to platelet adhesion to ruptured atherosclerotic plaque (use of anti-platelet drugs)

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6
Q

What is variant angina?

A

Attacks unpredictable

Coronary artery occlusion by vasospasm

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7
Q

What is dangerous in stable and unstable angina?

A

May cause coronary steal (where dilation can occur, this sends more blood to already well perfused areas, but where dilatation cannot occur, less blood is delivered because of the fall in input pressure)

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8
Q

What is the difference in stable and variant angina?

A

Stable- occulusion

Variant- spasm

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9
Q

What occurs in all forms of angina?

A

Decreased myocardial O2

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10
Q

How can you reduce myocardial O2 demand?

A

By drugs acting directly on the heart

E.g. B1-adrenoceptor blockers

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11
Q

What are B1-adrenoceptor blockers?

A

Competitive reversible antagonists of adrenaline and noradrenaline at cardiac beta1-adrenoceptor

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12
Q

What do B1-adrenoceptors do?

A

Decreases heart rate and force→ decreases myocardial work

Decrease myocardial O2 demand

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13
Q

What types of angina are B1-adrenoceptors used?

A

All form

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14
Q

What are the adverse effects of beta-adrenoceptor blockers in angina?

A

Exacerbate asthma (block of beta2-adrenoceptors in bronchi- avoid by use of alternative drug class)
Intolerance to exercise
Hyoglycaemia
Blockade of beta-adrenoceptors may uncover alpha1-mediated constriction in coronaries

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15
Q

What does Ivabradine do?

A

Blocks If (Na+) current that contributes to SA node depolarisation towards threshold
Sinoatrial node (where heart beat begins)
Decreases heart rate but not force
Decreases myocardial O2 demand

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16
Q

What are vasodilator drugs aiming to do to reduce myocardial O2 demand?

A

Dilatation of arteries
Dilatation of veins
Venous dilatation

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17
Q

How do vasodilator drugs dilate arteries?

A

Decreases after-load (force against which left ventricle contracts)
Decreases myocardial work
Decreases myocardial O2 demand

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18
Q

How do vasodilator drugs dilate veins?

A

Decreases pre-load (diastolic pressure that distends the relaxed left ventricle)

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19
Q

How do vasodilator drugs cause venous dilatation?

A 
Decreases venous return
Decreases pre-load
Decreases stretch of ventricle and atria
Decreases strength of contraction
Decreases myocardial work
Decreases myocardial O2 demand
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20
Q

What is the Starling mechanism?

A

More blood, more contraction

Stretch heart further stronger contraction

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21
Q

What is the Bainbridge (atrial) reflex?

A

A sympathetic reflex initiated by increased blood in the atria

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22
Q

What does the bainbridge reflex cause stimulation of?

A

SA node

Stimulates baroreceptors in the atria causing increases SNS stimulation

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23
Q

What are nitrovasodilators?

A

Most commonly used anti-anginals

E.g. GTN, amyl nitrite, isosobide dinitrate, isosobide mononitrate

24
Q

What is GTN (nitroglycerine, 10% in inert lactose base)?

A

Taken as sub-lingual tablet or spray

Not orally active (destroyed by first-pass metabolism)

25
Q

How is Amyl nitrate (volatile liquid) taken?

A

Vials opened and inhaled
Not now used clinically but has become drug of abuse (poppers)
Both drugs rapid in onset, but action short-lived

26
Q

What are the uses of nitrovasodilators?

A

Prophylaxis in stable angina (i.e. taken immediately before exercise)
Rapid relief of ongoing angina attack (all forms)

27
Q

How are isosobide dinitrate and isosobide mononitrate taken?

A

Taken orally
Slower in onset and more prolonged in duration than GTN
Used for sustained prophylaxis in all forms of angina

28
Q

What are all nitrovasodilators?

A

Pro drugs

29
Q

What are nitrovasodilators?

A

Lipophilic- readily enter smooth muscle cells and are reduced to nitric oxide

30
Q

What are nitrovasodilators termed?

A

“NO donors”

31
Q

What do nitrovasodilators mimic?

A

Action of endothelium- derived NO

32
Q

What does nitric oxide activate?

A

Soluble guanylate cyclase (sGC)

Cytoplasmic (soluble) enzyme

33
Q

What does the receptor on soluble guanylate cyclase contain?

A

A ferrous (Fe2+) haem moiety (like O2 binding site of haemoglobin)

34
Q

What does NO bind to?

A

Haem receptors

35
Q

What does the binding of NO to haem receptors cause?

A

Enzyme activation
Converts GTP to cGMP
Increased cGMP causes vasodilation

36
Q

What are anti anginal actions of nitrovasodilators?

A

Venous dilatation > arterial dilatation

37
Q

What are the side effects of nitrovasodilators?

A

Headache (dilataton of cerebral arteries)

Tolerance on prolonged use- need drug free “washout” period to restore efficacy

38
Q

When do L-type voltage operated calcium channels open?

A

Upon membrane depolarisation

39
Q

Where does calcium enter in L-type voltage operated calcium channels?

A

Cardiac and vascular smooth muscle

40
Q

What is the mechanism of L-type channel block?

A

Open channel block
Allosteric modulation
Tissue selectivity

41
Q

What drugs use the open channel block mechanism?

A

Verapamil and diltiazem work this way

42
Q

What is allosteric modulation?

A

Bind at allosteric site and reduce channel opening

Nifedipine work this way

43
Q

What is tissue selectivity?

A

Smooth muscle: nifedipine > dilitiazem > verapamil

Cardiac muscle: verapamil > dilitiazem > nifedipine

44
Q

What is the anti-anginal action of L-type blockers?

A 
Dilate arteries (little effect on veins)
Decreases heart rate and decreases force
45
Q

What does the dilation of arteries by L-type blockers cause?

A

Decreases after-load

Decreases myocardial O2 demand

46
Q

What does the decrease in heart rate and force by L-type blockers cause?

A

Decreases myocardial O2 demand

47
Q

What types of angina can L-type blockers be used in?

A

All forms

48
Q

What is dilatation of coronary arteries useful for? And what it is harmful in?

A

Valuable in variant angina (vasospasm)

Dangerous and may cause coronary steel in stable unstable angina

49
Q

What is vasospasm?

A

A condition in which an arterial spasm leads to vasoconstriction. This can lead to tissue ischemia and tissue death (necrosis).

50
Q

What is a coronary steel?

A

Where an alteration of circulation patterns lead to a reduction in the blood directed to the coronary circulation.

51
Q

What does Nifedipine cause?

A

Coronary steal in 10% of patients

52
Q

What are other uses of L-type blockers?

A

Anti-hypertensive agents (decreases TPR; Decreases HR and decreases SV→ decrease in CO
Anti-dysrhythmic agents (Class IV)

53
Q

What are adverse actions of L-type blockers?

A

Coronary steal
Headache
Constipation

54
Q

What can occur in an extreme overdose of L-type blockers?

A

Heart block

Cardiac failure

55
Q

What are the steps following the diagnosis of stable angina?

A
  1. Short-acting nitrovasodilator (GTN) plus Beta blocker or calcium channel blocker plus drugs for secondary prevention (antiplatelet, lipid-lowering, or anti-hypertensive drugs, as appropriate)
  2. Combine beta blockers and calcium channel blockers
  3. Consider adding long-acting nitrovasodilator or ivabradine
  4. Consider surgical intervention: stenting or coronary artery bypass grafting

Drugs and Disease (25 decks)

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