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LCRS Pharmacology and Therapeutics > SNS antagonists > Flashcards

SNS antagonists Flashcards

1
Q

What are the main processes that alpha 1 stimulates when bound to?

A

Vasoconstriction and relaxation of the GIT

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2
Q

What are the main processes that alpha 2 stimulates when bound to?

A

Inhibition of transmitter release, contraction of vascular smooth muscle, CNS actions

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3
Q

What are the main processes that beta 1 stimulates when bound to?

A

Increased cardiac rate and force, relaxation of GIT, renin release from the kidney

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4
Q

What are the main processes that beta 2 stimulates when bound to?

A

Bronchodilation, vasodilation, relaxation of visceral smooth muscle, hepatic glycogenolysis

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5
Q

What are the main processes that beta 3 stimulates when bound to?

A

Lipolysis

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6
Q

What adrenoceptors is labetalol an antagonist for?

A

Alpha 1 and Beta 1

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7
Q

What adrenoceptors is phentolamine an antagonist for?

A

Alpha 1 and 2

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8
Q

What adrenoceptors is prazosin an antagonist for?

A

Alpha 1

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9
Q

What adrenoceptors is propanol an antagonist for?

A

Beta 1 and 2

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10
Q

What adrenoceptors is atenolol an antagonist for?

A

Beta 1

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11
Q

What are the main clinical uses of SNS antagonists and false transmitters?

A

Hypertension
Cardiac arrhythmias
Angina
Glaucoma

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12
Q

What is the clinical definition of hypertension?

A

Sustained diastolic blood pressure greater than 90mmHg (NICE guidelines: 140/90 or higher)

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13
Q

What are the three main elements that contribute to hypertension?

A

Blood volume
Cardiac output
Peripheral vascular tone

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14
Q

How does sympathetic innervation control the heart?

A

Via beta 1 receptors

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15
Q

What is the major sympathetic controller of blood pressure?

A

Sympathetic drive to kidneys which stimulates renin release via beta 1- leads to increased production of angiotensin II which is a powerful vasoconstrictor and aldosterone which causes increased blood pressure

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16
Q

What are the targets for anti-hypertensive treatment?

A

Sympathetic nerves that release the vasoconstrictor noradrenaline
Kidneys- regulates blood volume and vasoconstriction
Heart
Arterioles determine peripheral resistance (alpha 1)
CNS- determines bp set point and regulates systems

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17
Q

Blockade of which adrenoceptor causes positive effects in terms of hypertension treatment?

A

Beta 1

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18
Q

How did this information change treatment of hypertension?

A

Instead of non-selective beta antagonists being used, cardioselective beta antagonists were used- beta 1 antagonists

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19
Q

Why is the name caridoselective beta antagonists misleading?

A

They mainly have anti-hypertensive effects in kidney not heart

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20
Q

How do beta 1 antagonists reduce blood pressure?

A

Act on CNS to reduce sympathetic tone
Act on beta 1 receptors in heart to reduce heart rate and cardiac output
Acts on kidneys on beta 1 receptors to reduce renin production

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21
Q

What effect do presynaptic beta 1 receptors have on synthesis and release of neurotransmitter?

A

Positive facilitation effect

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22
Q

How does using a beta 1 antagonist indirectly contribute to an anti-hypertensive effect?

A

It will block the presynaptic beta 1 receptors which will remove the facilitation effect and decrease the amount of noradrenaline coming from the nerve terminal

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23
Q

What is responsible for most of the side effects of beta antagonists?

A

Beta 2 blockade

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24
Q

In what situation would you not give someone a beta blocker?

A

If they have asthma or COPD- life threatening
Cardiac failure- they rely on degree of sympathetic innervation to maintain cardiac output
Diabetics- Block beta 2 mediated breakdown of glycogen

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25
Q

What are the general unwanted effects of beta antagonists?

A

Fatigue- reduced cardiac output and muscle perfusion
Cold extremities- loss of beta mediated vasodilation
Bad dreams

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26
Q

What is propranolol?

A

Non-selective beta antagonist

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27
Q

When is the effect of propranolol seen?

A

When exercising

At rest, propranolol causes very little change in heart rate, cardiac output or arterial pressure

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28
Q

What is the problem with propranolol?

A

All typical adverse effects mainly caused by beta 2 blockade

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29
Q

What is atenolol?

A

Beta-1 selective antagonist

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30
Q

What does atenolol mainly antagonise?

A

Effects of noradrenaline in the heart

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31
Q

What is labetalol?

A

Alpha 1 and beta 1 antagonist (mainly beta 1 - 4:1)

32
Q

How does labetalol reduce blood pressure?

A

Reducing total peripheral resistance

33
Q

What happens to the effect on the heart of beta blockers with prolonged use?

A

Initially it induces a change but the effect wanes with chronic use as the heart resets itself

34
Q

Which adrenoceptor is the main mediator of total peripheral resistance?

A

Alpha-1

35
Q

What is a common problem with alpha antagonist use?

A

When you stand up normally, SNS kicks in to give bp a quick boost to prevent you from fainting and falling over but this is blocked with the use of alpha antagonism= postural hypotension

36
Q

What is phentolamine?

A

Non-selective alpha antagonist

37
Q

What is the desired effect of phentolamine?

A

Causes vasodilation and fall in blood pressure due to blockade of alpha1 adrenoceptors

38
Q

What is the problem with phentolamine and hence why it’s no longer in clinical use?

A

It also blocks presynaptic alpha-2 receptors so removes inhibitory effect on noradrenaline release so there is an increase in noradrenaline which enhances reflex tachycardia, increases GIT motility and causes diarrhoea

39
Q

What is prazosin?

A

Highly selective alpha-1 antagonist

40
Q

What is the problem with prazosin?

A

Postural hypotension

41
Q

What is a positive effect of prazosin (alpha-1 antagonists) unlike all other anti-hypertensives and a reason that they are becoming popular again?

A

Alpha-1 antagonists cause a decrease in LDL and increase in HDL cholesterol

42
Q

What is methyldopa?

A

A false transmitter

43
Q

What is methyldopa used as?

A

An anti-hypertensive

44
Q

Methyldopa isn’t originally a false transmitter, how is the false transmitter formed?

A

Methyldopa is taken up by noradrenergic neurones, it is then decarboxylated and hydroxylated to form alpha-methyl noradrenaline

45
Q

Why does alpha-methyl noradrenaline tend to accumulate in larger quantities than noradrenaline?

A

It isn’t deaminated within the neurone by MAO

46
Q

How does alpha-methyl NA work as an anti-hypertensive?

A

It displaces noradrenaline from synaptic vesicles and is released in the same way, it is less active than noradrenaline on alpha-1 receptors so is less effective at causing vasoconstriction and is more active on presynaptic alpha 2 receptors so noradrenaline release is inhibited.
Also has CNS effects and stimulates vasopressor system in brainstem to inhibit sympathetic outflow

47
Q

What are some other benefits of methyldopa?

A

Renal and CNS blood flow is well maintained so it’s widely used in patients with renal insufficiency or cerebrovascular disease
It is also the recommended anti-hypertensive in pregnant women because it has no adverse effects on foetus

48
Q

What are the adverse effects of methyldopa?

A 
Dry mouth
Sedation
Orthostatic hypotension
Male sexual dysfunction
(it is rarely used)
49
Q

What is an arrhythmia?

A

Abnormal or irregular heart beat

50
Q

What is the main cause of arrhythmia?

A

Myocardial ischaemia

51
Q

How does myocardial ischaemia cause arrhythmia?

A

Damage to the muscle can result in re-entry of impulses that messes up the rhythm

52
Q

What increases the chance of arrhythmia?

A

Exercise

53
Q

Why are beta blockers a good way of controlling arrhythmias in patients?

A

The sympathetic drive controls the pacemaker current of the heart

54
Q

How can sympathetic drive cause arrhythmia problems?

A

An increase in sympathetic drive to the heart via beta-1 can precipitate or aggravate arrhythmias- particularly after MI because there is increased sympathetic tone

55
Q

What effect do beta antagonists have to prevent arrhythmias?

A

They increase the refractory period of the AV node which interfere with AV conduction in atrial tachycardia and slows down ventricular rate so even if you have a strange re-entry type electrical activity in the damaged tissue it won’t stimulate another beat

56
Q

Which beta blocker is particularly good at treating arrhythmias that occur during exercise or due to mental stress?

A

Propranolol

57
Q

What is angina?

A

Pain that occurs when the oxygen supply to the myocardium is insufficient for its needs

58
Q

Where is the pain in angina distributed?

A

Chest, arm and neck

59
Q

What tends to bring on angina?

A

Exertion or excitement

60
Q

What are the three types of angina?

A

Stable
Unstable
Variable

61
Q

When is pain felt in stable angina?

A

On exertion

62
Q

Why is there pain in stable angina?

A

Due to fixed narrowing of the coronary vessels e.g. atheroma leading to increased demand on the heart

63
Q

When is pain felt in unstable angina?

A

With less and less exertion and culminates with pain at rest

64
Q

Why is the angina unstable?

A

An atheromatous plaque is starting to rupture- you get a platelet-fibrin thrombus but without complete occlusion of the vessels and there is high risk of infarction

65
Q

When is pain felt in variable angina?

A

At rest

66
Q

Why does pain occur in variable angina?

A

Coronary artery spasm- associated with atheromatous disease

67
Q

How do beta adrenoceptor antagonists treat angina?

A

They reduce myocardial oxygen demand by:
Decrease heart rate
Decrease systolic blood pressure
Decrease cardiac contractile activity

68
Q

Which type of beta adrenoceptor antagonists are preferred to treat angina and why?

A

Beta-1 selective antagonists (metoprolol) at low doses reduce heart rate and muscle contractile activity without affecting bronchial smooth muscle

69
Q

What are the adverse effects of beta blockers?

A 
Fatigue
Insomnia
Dizziness
Sexual dysfunction
Bronchospasm
Bradycardia
Heart block
Hypotension
Decreased myocardial contractility
70
Q

In what patients would you not use a beta blocker?

A

Bradycardia
Bronchospasm
Hypotension
AV block or severe congestive heart failure

71
Q

Where and how is aqueous humour in the eye produced?

A

It is produced by blood vessels in the ciliary body via the actions of carbonic anhydrase

72
Q

What is the amount of aqueous humour produced directly related to?

A

Blood flow in the ciliary body

73
Q

What effect can adrenaline have on glaucoma?

A

It can act on alpha-1 receptors to cause vasoconstriction and reduce blood flow through the ciliary body

74
Q

How can beta antagonists be used to treat glaucoma?

A

They affect the action of carbonic anhydrase so reduce the rate of aqueous humour formation by blocking the receptors on the ciliary body

75
Q

What else are beta antagonist used to treat?

A

Anxiety states- controls somatic symptoms with sympathetic over reactivity
Migraine prophylaxis- maintains good blood supply within CNS so reduces risk of migraine
Benign essential tumours

LCRS Pharmacology and Therapeutics (33 decks)

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