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Drugs and Disease > Treatment of Angina > Flashcards

Treatment of Angina Flashcards

1
Q

What is myocardial ischemia?

A

Chest pain

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2
Q

Why do you get chest pain?

A

Because the hearts myocardial oxygen demand is not being met

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3
Q

What happens if the myocardial oxygen demand is not met?

A

It cannot satisfy its own metabolic need

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4
Q

Why is myocardial ischemia usually regional?

A

Due to a build up of metabolites in a region

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5
Q

What metabolites build up in a region to cause myocardial ischemia

A
  1. Adenosines (broken down ATP)
  2. Carbon dioxide
  3. Lactate
  4. K+ ions
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6
Q

Why do K+ ions build up?

A

Because ATP is being depleted and it is needed to transport them

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7
Q

Why does lactate build up

A

Because you arent exercising the muscle

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8
Q

Is myocardial ischemia and disease?

A

No it is caused by other cardiovascular diseases

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9
Q

What are the three types of angina?

A
  1. Stable
  2. Unstable
  3. Variant
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10
Q

Which is the most common type of angina?

A

Stable

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11
Q

Why is stable angina known as stable?

A

Because you are able to tell when an attack will come on e.g. if you are sitting you will be fine

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12
Q

What is involved in stable angina that means the myocardial oxygen demand is not met and myocardial ischemia occurs?

A

A chronic occlusive coronary artery disease

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13
Q

What is an example of a chronic occlusive coronary artery disease seen in stable angina?

A

Atherosclerosis

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14
Q

What happens to the coronary artery in diseases like atherosclerosis?

A

The diameter is reduced due to deposition of lipids (atheroscelerotic plaque)

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15
Q

What are the attacks like in unstable angina?

A

Unpredictable

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16
Q

What happens to the plaque that makes unstable angina worse than stable?

A

The plaque ruptures which causes platelets to adhere to it which blocks the artery even more

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17
Q

What is the least common type of angina?

A

Variant angina

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18
Q

What is involved in variant angina?

A

Smooth muscle cells of the coronary artery going into spasm

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19
Q

What lines the atherscelerotic plaque in order to keep it from rupturing?

A

Endothelial cells

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20
Q

Why can you not just dilate the blood vessels to help stable and unstable angina?

A

Because you cannot decide which blood vessels to dilate you will end up dilating non-diseased ones which causes more blood to be delivered to areas that already had a lot of it - this means that even less blood will go to the coronary artery which needs it (coronary steal) and so the pain gets more intense

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21
Q

Could you dilate blood vessels in variant angina?

A

Yes it could be useful to dilate the vessel that is in spasm

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22
Q

What is the main method of treating all three kinds of angina?

A

Reduce the myocardial oxygen demand

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23
Q

Which drugs could you use that would act directly on the heart and what transmitter would they block?

A

B1-adrenoceptor antagonists would block the action of adrenaline and noradrenaline

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24
Q

What would a B1 adrenoceptor anatagonist do and how would this reduce myocardial oxygen demand?

A

Reduces force of contraction and heart rate so the heart is doing less work so needs less oxygen to satisfy its myocardial oxygen demand

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25
Q

Name a B2 selective antagonist that is used to treat angina?

A

Antenolol

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26
Q

Name a non-selective B-adrenoceptor agonist used to treat angina?

A

Propanolol

27
Q

Who would you not be able to give propanolol to and why?

A

Asthmatics as it also blocks the B1 receptors too meaning that respiration is affected

28
Q

What is important about giving drugs that will reduce heart rate and respiration?

A

You have to get the dose right or they cant exrcise

29
Q

What is a non-cardiorespiratory side affect of using b-adrenoceptor antagonist to treat angina

A

B-adrenoceptors are involved in the breakdown of glycogen to glucose so blocking this could lead to hypoglycemia

30
Q

What channel does Ivabradine act on?

A

The If sodium channel of the sino-atrial node

31
Q

What does the If sodium channel normally do?

A

Contributes to depolarisation of the sino-atrial node towards threshold known as pre-potential

32
Q

What does ivabradine do by blocking this channel and why is it an advantage?

A

Blocks the heart rate but NOT the force of contraction so you dont have to comprimise contractility

33
Q

Why would using a vasodilator to dilate the systemic arteries be a way of reducing myocardial oxygen demand?

A

Dilating systemic arteries and thus arterioles means the heart is beating against a lower resistance (reduced after load) so the heart is doing less work so does not need as much oxygen

34
Q

Why would using a vasodilator to dilate the systemic veins be a way of reducing myocardial oxygen demand?

A

Leads to a decrease in venous return to the heart and therefore a decrease in preload

35
Q

Why would a decrease in preload lead to less work done by the heart?

A

The more you stretch the ventricles the stronger the force of contraction so if there is less blood coming back the force of contraction is reduced and so the heart is doing less work

36
Q

What are the most common kind of vasodilators used to treat angina?

A

Nitrovasodilators

37
Q

Name the most common nitrovasodilator

A

Nitroglycerin (Glycerl trinitrate)

38
Q

How is nitroglycerin administered?

A

Sub-lingually

39
Q

Why can nitroglycerin not be given orally?

A

Because it is destroyed by first pass metabolism in the liver

40
Q

What is it about nitroglycerin that allows it to be taken sublingually?

A

Very lipophillic so can easily cross mucosa membrane

41
Q

How fast acting in nitroglycerine?

A

Very fast acting takes about 10 seconds to get into systemic circulation so you can use it when you feel an attack is about to come on

42
Q

Is nitroglycerine long or short acting?

A

Short

43
Q

What is an additonal advantage of nitroglycerine for stable angina?

A

Can be taken as a prophylaxis (taken before exercise)

44
Q

Nitrovasodilators are pro-drugs; what does this mean?

A

They are inactive and are metabolised in the body to produce the active form

45
Q

What are nitrovasodilators reduced to in smooth muscle cells?

A

Nitric oxide

46
Q

What does NO normally do?

A

Bind to

47
Q

What are nitrovasodilators reduced to in smooth muscle cells?

A

Nitric oxide

48
Q

What does NO normally do that nitrovasodilators can mimic to increase vasodilation

A

Bind to haemreceptors which activates guanylate cyclase that converts GTP to cGMP which leads to vasodilation

49
Q

As previously described you can treat angina by vasodilation of systemic arteries and of veins; which side of the circulation do nitrovasodilators work on?

A

The venous side

50
Q

What are the side effects of nitrovasodilators?

A

Headache and tolerance

51
Q

Why would nitrovasodilators cause a headache?

A

They dilate the cerebral arteries

52
Q

How do L-type voltage operated calcium channels?

A

Cells depolarise due to an electrical event and open calcium channels which causes calcium to flood into vascular smooth muscle and causes contraction

53
Q

How could L-type voltage operated calcium channels be utilized to help reduce myocardial oxygen demand?

A

Blocking the LTVOCC would reduce the force of contraction and therefore reduce the myocardial oxygen demand

54
Q

What two ways can LTVOCC be blocked?

A
  1. Open channel block

2. Allosteric modulation

55
Q

What is an open channel block?

A

When drugs flow in and block the channel

56
Q

What is allosteric modulation?

A

Binds to an allosteric site on the receptor to reduce the chance of it opening

57
Q

What side of the circulation do LTVOCC blockers work in?

A

The arterial side

58
Q

What do LTVOCC blockers decrease in order to decrease myocardial oxygen demand?

A

After load

59
Q

LTVOCC blockers can be described as having a two pronged attack on force of contraction; what does this mean?

A

They reduce force of contraction by reducing heart beat AND slowing depolarisation

60
Q

In the algorithm of stable angina diagnosis what is step one?

A
  1. Prescribe short acting nitroglycerine
  2. Prescribe LTVOCC blocker
  3. Prescribe anti-platelet
61
Q

What is step 2?

A

Combine a B-adrenoceptor blocker such as antenolol or propanolol plus the LTVOCC blocker

62
Q

What is step 3?

A
  1. Long acting nitrovasodilator

2. Ivabradine

63
Q

What is step 4?

A

Surgery - angiography

Drugs and Disease (15 decks)

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