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X Pharmacological Treatment Of Disease > Angina > Flashcards

Angina Flashcards

1
Q

What is the treatment for angina?

A

Vasodilator drugs

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2
Q

What are the characteristics of angina?

A

Episodes of pain/pressure in anterior chest

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3
Q

What is the most common cause of angina?

A

Coronary artery blockages by atheromatous plaques

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4
Q

What are the risk factors for angina?

A 
Smoking
Obesity
Diabetes
Lack of exercise
Hyperlipidaemia
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5
Q

During ischaemic conditions, what is released?

A

Mediators

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6
Q

What accumulates in ischaemic conditions?

A

Metabolic waste products

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7
Q

What do metabolic waste products do?

A

Metabolites stimulate nerve endings in the muscle and outermost layer of coronary arteries

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8
Q

What metabolites stimulate the nerve endings?

A

Potassium
Kinins
Prostaglandins
Adenosine

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9
Q

What are the 3 types of angina?

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

What is stable angina?

A

3-5 mins on exertion
When greater than usual demand on heart
Most common

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11
Q

What is unstable angina?

A

More dangerous
Still manageable
Risk of MI

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12
Q

What is variant angina?

A

Rare
Occurs at rest
Same time everyday
Very painful - no blockage - artery spasm

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13
Q

Why is unstable angina dangerous?

A

Sustained ischaemia -> necrosis -> more unpredictable

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14
Q

How does unstable angina occur?

A

Plaque with fibrous cap
Cap ruptures
Blood clot forms around the rupture -> blocks artery

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15
Q

What are the treatment aims?

A

Treat pain
Treat blockage - intervene in coronary arteries
Reduce demand - reduce heart rate/ workload OR dilate blood vessels to increase delivery
Improve exercise tolerance
Reduce risk of MI
Deal with plaques and stop them advancing
Correct imbalance between oxygen demand/supply
Increase coronary flow
Decrease cardiac workload

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16
Q

What do vasodilators do?

A

Mainly act on venous side of arterioles (some coronary, but not focused here), peripheral blood vessels

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17
Q

What are the aims of treatment affected by?

A
  1. Preload- increased preload = increased workload
  2. Afterload- increased afterload = increased workload
  3. Contractility- increased contractility = increased workload
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18
Q

What is preload?

A

Extent of muscle stretch before contracting. More stretch = more contraction

starling’s law

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19
Q

What is starlings law?

A

Force of contraction is proportional to resting length of muscle fibres. The most the heart is filled, the greater the degree of fibres are stretched. Greater force of contraction - increase volume of blood ejected (stroke volume)

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20
Q

What is afterload?

A

Resistance against which blood is ejected from the heart

Increased resistance = smaller vessels = greater work = increased oxygen consumption

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21
Q

How do you reduce afterload?

A

Dilate arterioles

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22
Q

How do you reduce preload?

A

Venodilation

OR

Depress myocardial contractility (venal/arterial dilation)/heart rate

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23
Q

What are organic nitrates?

Venous side

A

Dilate peripheral veins and arterioles

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24
Q

What are the aims of organic nitrates?

A

Reduce oxygen demand by reducing work of heart muscle

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25
Q

What is an example of an organic nitrate?

A

Glyceral trinitrate

Aka

Nitroglycerine

26
Q

What is the molecular structure of glyceral trinitrate?

A 
CH2 - ONO2
    |
CH2 - ONO2
    |
CH2 - ONO2
27
Q

How does glyceral trinitrate work?

A

Cause relaxation of smooth muscle
Arterial and venous (mainly) dilation
Reduction in cardiac workload (from reduction in preload/afterload)(from increasing coronary/myocardial perfusion)

28
Q

How does Isosorbide dinitrate reach the blood vessel?

A

Oral (isosorbide dinitrate)
Converted to isosorbide mononitrate in the liver
Acts on blood vessel

29
Q

What happens if you take glyceral trinitrate orally?

A

Inactivated in the liver

30
Q

What happens if you take glyceral trinitrate sublingually?

A

Reaches the blood vessel!

31
Q

By which route of administration should you take GTN/GTN spray

A

Sublingually

32
Q

By which route of administration should you take isosorbide mononitrate and isosorbide dinitrate?

A

Orally

33
Q

By which route of administration should you take GTN patches and GTN ointment?

A

Transcutaneous

34
Q

By which route of administration should you take isosorbide nitrate and GTN?

A

Intravenously

35
Q

What is the mechanism of action of the administered drugs?

A 
Peripheral dilation (mainly venous)
Blood pools in veins
Venous return is decreased
Ventricular volume/preload is decreased
Force of contraction decreases
Oxygen consumption decreases
Pain, due to metabolite build up, is relived
36
Q

What is the mechanism of vasodilation?

A
  1. Glyceryl trinitrate liberates nitric oxide (NO)
  2. This acts on vascular smooth muscle cells
  3. It stimulates an increase in cGMP concentration in cells
  4. cGMP causes relaxation of vascular muscle
37
Q

How does release of NO cause relaxation?

A

Release of NO
|
Activation of guanylate cyclase
|
GTP ———->——cGMP
|
Relaxation

38
Q

Characteristics of short acting drugs

A

30 mins
Glyceryl trinitrate
Sublingual

39
Q

Characteristics of long acting drugs

A

Hours
Isosorbide-5-mononitrate
Sublingual, oral, transdermal

40
Q

What are the adverse effects from excessive vasodilation?

A 
Hypotension
Fainting
Reflex tachycardia 
Facial flushing
Headache
Tolerance (except sublingual GTN)
41
Q

What are calcium channel blockers and what do they do?

A

Dilate peripheral vessels (arterial side)
Reduce contractility
Treats afterload
E.g. Nifedipine

42
Q

How does nifedipine work?

A

Nifedipine amiodipine -> block ca2+ entry into smooth muscle cells of blood vessels -> peripheral -> reduce cardiac work

43
Q

How can you use nifiedipine in the lab?

A

Krebs, physiological saline contains calcium, NaCl, potassium, magnesium and is OXYGENATED. Buffers for pH.

+drugs -> relaxation/contraction

44
Q

What happens if you block Ca2+?

A

Block Ca2+ -> peripheral vasodilation -> reduce cardiac work (for afterload - same mechanism of action as nitrates, but they affect preload) -> coronary vasodilation

45
Q

What other Calcium channel blockers are there?

A

Nifedipine, diltiazem, amlodipine, felodipine

46
Q

What advantages do calcium channel blockers have over beta blockers?

A

Fewer side effects

Block from the inside - inhibit Ca2+ flux through Ca2+ channels

47
Q

How do calcium channel blockers treat angina?

A

Decrease cardiac work by dilating peripheral blood vessels -> lowers resistance to blood flow -> also dilate coronary blood vessels -> treats angina, especially if coronary spasm involved

48
Q

How does vasodilation treat angina?

A

Vasodilation of blood vessels (especially coronary arteries in spasm) -> force of contraction reduced -> work of heart and afterload reduced -> myocardial oxygen demand reduced -> blood flow to cardiac muscle is increased

49
Q

Is nifedipine short acting or long acting?

A

Short acting

50
Q

Is felodipine short acting or long acting?

A

Long acting

51
Q

Is amlodipine short acting or long acting?

A

Long acting

52
Q

What are verapamil and diltiazem?

A

Rate limiting CCBs

53
Q

What are beta blockers and what is their mechanism of action?

A

Block sympathetic drive to the heart
Reduce heart rate and force of contraction
Acts on beta receptors in the heart
Contractility

54
Q

?????? Adrenaline circulating hormone and noradrenaline neurotransmitter

A

Finish

55
Q

What can beta blockers treat?

A

Hypertension
Angina
Cardiac arrhythmias
Heart failure

56
Q

What is the mechanism of action of beta blockers?

A

Beta-adrenergic antagonists block:
Positive chronotrophic and inotrophic effects of endogenous catecholamines at beta-1 receptors

Decreased heart rate and contractility
Reduction in O2 consumption
Reduction in ischaemia and pain

57
Q

What does chronotrophic mean?

A

Increase rate

58
Q

What does inotrophic mean?

A

Increase contraction

59
Q

What condition would you use long term beta blockers? Which drug would you use?

A

Prophylaxis

Atenolol

60
Q

Which receptor is atenolol selective for?

A

Beta 1 selective

Can affect beta 2 at high doses

61
Q

Which receptor is propanol selective for?

A

Beta 1 and beta 2

62
Q

What is propanolol contraindicated with?

A

Asthmatics taking salbutamol

Beta 2

X Pharmacological Treatment Of Disease (9 decks)

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