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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
What are the general unwanted effects of beta antagonists?
Fatigue- reduced cardiac output and muscle perfusion Cold extremities- loss of beta mediated vasodilation Bad dreams
26
What is propranolol?
Non-selective beta antagonist
27
When is the effect of propranolol seen?
When exercising | At rest, propranolol causes very little change in heart rate, cardiac output or arterial pressure
28
What is the problem with propranolol?
All typical adverse effects mainly caused by beta 2 blockade
29
What is atenolol?
Beta-1 selective antagonist
30
What does atenolol mainly antagonise?
Effects of noradrenaline in the heart
31
What is labetalol?
Alpha 1 and beta 1 antagonist (mainly beta 1 - 4:1)
32
How does labetalol reduce blood pressure?
Reducing total peripheral resistance
33
What happens to the effect on the heart of beta blockers with prolonged use?
Initially it induces a change but the effect wanes with chronic use as the heart resets itself
34
Which adrenoceptor is the main mediator of total peripheral resistance?
Alpha-1
35
What is a common problem with alpha antagonist use?
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
What is phentolamine?
Non-selective alpha antagonist
37
What is the desired effect of phentolamine?
Causes vasodilation and fall in blood pressure due to blockade of alpha1 adrenoceptors
38
What is the problem with phentolamine and hence why it's no longer in clinical use?
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
What is prazosin?
Highly selective alpha-1 antagonist
40
What is the problem with prazosin?
Postural hypotension
41
What is a positive effect of prazosin (alpha-1 antagonists) unlike all other anti-hypertensives and a reason that they are becoming popular again?
Alpha-1 antagonists cause a decrease in LDL and increase in HDL cholesterol
42
What is methyldopa?
A false transmitter
43
What is methyldopa used as?
An anti-hypertensive
44
Methyldopa isn't originally a false transmitter, how is the false transmitter formed?
Methyldopa is taken up by noradrenergic neurones, it is then decarboxylated and hydroxylated to form alpha-methyl noradrenaline
45
Why does alpha-methyl noradrenaline tend to accumulate in larger quantities than noradrenaline?
It isn't deaminated within the neurone by MAO
46
How does alpha-methyl NA work as an anti-hypertensive?
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
What are some other benefits of methyldopa?
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
What are the adverse effects of methyldopa?
``` Dry mouth Sedation Orthostatic hypotension Male sexual dysfunction (it is rarely used) ```
49
What is an arrhythmia?
Abnormal or irregular heart beat
50
What is the main cause of arrhythmia?
Myocardial ischaemia
51
How does myocardial ischaemia cause arrhythmia?
Damage to the muscle can result in re-entry of impulses that messes up the rhythm
52
What increases the chance of arrhythmia?
Exercise
53
Why are beta blockers a good way of controlling arrhythmias in patients?
The sympathetic drive controls the pacemaker current of the heart
54
How can sympathetic drive cause arrhythmia problems?
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
What effect do beta antagonists have to prevent arrhythmias?
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
Which beta blocker is particularly good at treating arrhythmias that occur during exercise or due to mental stress?
Propranolol
57
What is angina?
Pain that occurs when the oxygen supply to the myocardium is insufficient for its needs
58
Where is the pain in angina distributed?
Chest, arm and neck
59
What tends to bring on angina?
Exertion or excitement
60
What are the three types of angina?
Stable Unstable Variable
61
When is pain felt in stable angina?
On exertion
62
Why is there pain in stable angina?
Due to fixed narrowing of the coronary vessels e.g. atheroma leading to increased demand on the heart
63
When is pain felt in unstable angina?
With less and less exertion and culminates with pain at rest
64
Why is the angina unstable?
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
When is pain felt in variable angina?
At rest
66
Why does pain occur in variable angina?
Coronary artery spasm- associated with atheromatous disease
67
How do beta adrenoceptor antagonists treat angina?
They reduce myocardial oxygen demand by: Decrease heart rate Decrease systolic blood pressure Decrease cardiac contractile activity
68
Which type of beta adrenoceptor antagonists are preferred to treat angina and why?
Beta-1 selective antagonists (metoprolol) at low doses reduce heart rate and muscle contractile activity without affecting bronchial smooth muscle
69
What are the adverse effects of beta blockers?
``` Fatigue Insomnia Dizziness Sexual dysfunction Bronchospasm Bradycardia Heart block Hypotension Decreased myocardial contractility ```
70
In what patients would you not use a beta blocker?
Bradycardia Bronchospasm Hypotension AV block or severe congestive heart failure
71
Where and how is aqueous humour in the eye produced?
It is produced by blood vessels in the ciliary body via the actions of carbonic anhydrase
72
What is the amount of aqueous humour produced directly related to?
Blood flow in the ciliary body
73
What effect can adrenaline have on glaucoma?
It can act on alpha-1 receptors to cause vasoconstriction and reduce blood flow through the ciliary body
74
How can beta antagonists be used to treat glaucoma?
They affect the action of carbonic anhydrase so reduce the rate of aqueous humour formation by blocking the receptors on the ciliary body
75
What else are beta antagonist used to treat?
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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