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X Pharmacological Treatment Of Disease > Angina > Flashcards

Angina Flashcards

(62 cards)

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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
What is an example of an organic nitrate?
Glyceral trinitrate Aka Nitroglycerine
26
What is the molecular structure of glyceral trinitrate?
``` CH2 - ONO2 | CH2 - ONO2 | CH2 - ONO2 ```
27
How does glyceral trinitrate work?
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
How does Isosorbide dinitrate reach the blood vessel?
Oral (isosorbide dinitrate) Converted to isosorbide mononitrate in the liver Acts on blood vessel
29
What happens if you take glyceral trinitrate orally?
Inactivated in the liver
30
What happens if you take glyceral trinitrate sublingually?
Reaches the blood vessel!
31
By which route of administration should you take GTN/GTN spray
Sublingually
32
By which route of administration should you take isosorbide mononitrate and isosorbide dinitrate?
Orally
33
By which route of administration should you take GTN patches and GTN ointment?
Transcutaneous
34
By which route of administration should you take isosorbide nitrate and GTN?
Intravenously
35
What is the mechanism of action of the administered drugs?
``` 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
What is the mechanism of vasodilation?
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
How does release of NO cause relaxation?
Release of NO | Activation of guanylate cyclase | GTP ---------->------cGMP | Relaxation
38
Characteristics of short acting drugs
30 mins Glyceryl trinitrate Sublingual
39
Characteristics of long acting drugs
Hours Isosorbide-5-mononitrate Sublingual, oral, transdermal
40
What are the adverse effects from excessive vasodilation?
``` Hypotension Fainting Reflex tachycardia Facial flushing Headache Tolerance (except sublingual GTN) ```
41
What are calcium channel blockers and what do they do?
Dilate peripheral vessels (arterial side) Reduce contractility Treats afterload E.g. Nifedipine
42
How does nifedipine work?
Nifedipine amiodipine -> block ca2+ entry into smooth muscle cells of blood vessels -> peripheral -> reduce cardiac work
43
How can you use nifiedipine in the lab?
Krebs, physiological saline contains calcium, NaCl, potassium, magnesium and is OXYGENATED. Buffers for pH. +drugs -> relaxation/contraction
44
What happens if you block Ca2+?
Block Ca2+ -> peripheral vasodilation -> reduce cardiac work (for afterload - same mechanism of action as nitrates, but they affect preload) -> coronary vasodilation
45
What other Calcium channel blockers are there?
Nifedipine, diltiazem, amlodipine, felodipine
46
What advantages do calcium channel blockers have over beta blockers?
Fewer side effects | Block from the inside - inhibit Ca2+ flux through Ca2+ channels
47
How do calcium channel blockers treat angina?
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
How does vasodilation treat angina?
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
Is nifedipine short acting or long acting?
Short acting
50
Is felodipine short acting or long acting?
Long acting
51
Is amlodipine short acting or long acting?
Long acting
52
What are verapamil and diltiazem?
Rate limiting CCBs
53
What are beta blockers and what is their mechanism of action?
Block sympathetic drive to the heart Reduce heart rate and force of contraction Acts on beta receptors in the heart Contractility
54
?????? Adrenaline circulating hormone and noradrenaline neurotransmitter
Finish
55
What can beta blockers treat?
Hypertension Angina Cardiac arrhythmias Heart failure
56
What is the mechanism of action of beta blockers?
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
What does chronotrophic mean?
Increase rate
58
What does inotrophic mean?
Increase contraction
59
What condition would you use long term beta blockers? Which drug would you use?
Prophylaxis Atenolol
60
Which receptor is atenolol selective for?
Beta 1 selective Can affect beta 2 at high doses
61
Which receptor is propanol selective for?
Beta 1 and beta 2
62
What is propanolol contraindicated with?
Asthmatics taking salbutamol | Beta 2

X Pharmacological Treatment Of Disease (9 decks)

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