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LCRS Pharmacology and Therapeutics > SNS agonists > Flashcards

SNS agonists Flashcards

1
Q

Where do sympathetic nerves originate?

A

Thoracolumbar region

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2
Q

What is the neurotransmitter at sympathetic preganglionic nerve fibres?

A

Acetylcholine

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3
Q

What do most sympathetic postganglionic neurones release?

A

Noradrenaline

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4
Q

What are the two exceptions for sympathetic postganglionic neurones?

A

A preganglionic sympathetic neurone drives release of adrenaline (80%) and noradrenaline (20%) from the adrenal medulla
Sympathetic postganglionic neurone that innervates sweat glands releases acetylcholine

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5
Q

What are directly acting sympathomimetics?

A

They mimic the actions of NA/A by binding to and stimulating adrenoceptors (GPCRs)

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6
Q

Due to the actions on where are sympathomimetics mainly used for?

A

CVS, eyes and lungs

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7
Q

What sort of receptor are all adrenoceptors?

A

G protein coupled

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8
Q

What are the 4 types of adrenoceptor?

A

Alpha 1
Alpha 2
Beta 1
Beta 2

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9
Q

What is the mechanism of action of alpha 1?

A

PLC -> IP3 + DAG

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10
Q

What is the mechanism of action of alpha 2?

A

Decrease cAMP

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11
Q

What is the mechanism of action of beta 1 + 2?

A

Increase cAMP

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12
Q

Where are alpha 1 adrenoceptors found?

A 
Iris radial muscle
Lacrimal glands (tears)
Salivary glands
Liver (glycogenolysis/gluconeogenesis)
Adipose- lipolysis
Ureter (motility and tone)
Genitalia- male (stimulates ejaculation)
Skin- generalised sweating
Blood vessels- skin, mucus membranes, splanchnic area, abdominal viscera, salivary glands constriction
GIT- decreased stomach motility and tone
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13
Q

Where are beta 1 receptors found?

A 
Eye- aqueous humour production
Adipose- lipolysis
Kidney- increased renin secretion
Salivary glands
GIT- decreased stomach motility and tone
Heart- increased rate and contractility
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14
Q

Where are beta 2 receptors found?

A

Trachea and bronchioles- dilate
Urinary bladder- relaxes detrusor
Genitalia-female relaxation of uterus
Blood vessels- skeletal muscle blood vessels dilation

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15
Q

What are the principal actions of beta blockers when controlling blood pressure?

A

It is through the kidneys - beta 1 stimulation in kidneys increases renin release which leads to peripheral vasoconstriction and increase in blood pressure
The heart is mainly controlled by beta 1- increases contractility and increases heart rate
Beta blockers inhibit both of these functions

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16
Q

What can all adrenoceptors be activated by?

A

Noradrenaline and adrenaline

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17
Q

What type of receptor is noradrenaline more selective for?

A

Alpha

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18
Q

What type of receptor is adrenaline more selective for?

A

Beta

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19
Q

How is noradrenaline formed?

A

Tyrosine from the diet is converted to DOPA by tyrosine hydroxylase (rate limiting enzyme) which is then converted to dopamine which is taken up by vesicles and converted to noradrenaline

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20
Q

How is noradrenaline deactivated?

A

It is via reuptake into the nerve terminal itself or extra neuronal tissue

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21
Q

Which receptors have an influence on synthesis and release of noradrenaline and what influence do they have?

A

Presynaptic alpha 2 receptors- they have a negative effect (environmental monitoring system within the synapse- high conc of NA will stimulate presynaptic alpha 2 receptors which will decrease synthesis and release

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22
Q

Name an SNS agonist that is selective for Alpha 1?

A

Phenyleprine

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23
Q

Name an SNS agonist that is selective for Alpha 2?

A

Clonidine

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24
Q

Name an SNS agonist that is selective for Beta 1?

A

Dobutamine

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25
Q

Name an SNS agonist that is selective for Beta 2?

A

Salbutamol

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26
Q

What does the selectivity of the drugs depend on?

A

Concentration- low conc high selectivity but high conc lower selectivity

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27
Q

What happens in hypersensitivity reactions after first exposure?

A

You generate antibodies to the antigen and these circulate around the body and bind to mast cells

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28
Q

What happens in hypersensitivity reactions after subsequent exposure?

A

The mast cells are already primed with antibody on their surface so the antigen cross links these antibodies on the surface of the mast cells and you get a massive release of mediators

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29
Q

What are the symptoms of hypersensitivity?

A

Fall in blood pressure
Anaphylactic shock- unconsciousness
Respiratory distress
D and V

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30
Q

Why is there a fall in blood pressure during hypersensitivity?

A

Endothelial cells within membranes of blood vessels move apart so you get a lot of fluid moving into tissues which leads to a fall in circulating fluid volume and hence a fall in blood pressure

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31
Q

Why is adrenaline more effective as a treatment than noradrenaline for hypersensitivity?

A

Noradrenaline, like adrenaline, binds to alpha receptors and will cause vasoconstriction and increase blood pressure
But key thing is breathing- you need the patient to get breathing first and adrenaline acts more on the beta receptors the noradrenaline and this stimulates bronchodilation and relaxation of throat muscles
Adrenaline will also stimulate heart to cause tachycardia and slow down release of histamine from mast cells

32
Q

What common conditions is adrenaline used as a treatment for?

A

Pulmonary obstructive conditions-
Asthma
Acute bronchospasm- chronic bronchitis or emphysema

33
Q

What treatments are preferable to adrenaline for these conditions?

A

Selective beta-2 agonists but adrenaline is useful in hypotensive crisis

34
Q

Where are adrenoceptors are in the eye?

A

Alpha receptors on blood vessels in the ciliary body

Beta receptors that control the enzyme that makes the aqueous humour in the eye

35
Q

Why is adrenaline used as a treatment for glaucoma?

A

It stimulates the alpha receptors in the vessels within the ciliary body causing vasoconstriction of these vessels- less blood will be delivered to the ciliary body and production of aqueous humour is reduced

36
Q

What is cardiogenic shock?

A

Sudden inability of the heart to pump sufficient oxygen-rich blood (heart attack/MI or cardiac arrest)- mainly happens via beta 1 receptor

37
Q

Why is adrenaline given during spinal anaesthesia?

A

As you are anaesthetising the spine you are taking away the sympathetic output to peripheral resistance vessels so they relax and patient won’t be able to maintain blood pressure but with a little bit of adrenaline at same time this will constrict blood vessels and maintain blood pressure

38
Q

Why is adrenaline also given during local anaesthesia?

A

Causes constriction of blood vessels so prevents clearance of anaesthetic from the area

39
Q

What are the unwanted actions of adrenaline?

A

Secretions- reduced and thick
CVS effects- tachycardia, palpitations, cold extremities, hypertension
Overdose- cerebral haemorrhage and pulmonary embolism
GIT- minimal
Skeletal muscle- tremor

40
Q

What adrenoceptors is phenylephrine more selective for?

A

Alpha 1 > Alpha 2 > Beta

41
Q

Phenylephrine is chemically related to adrenaline but has a slight change in structure, why?

A

Makes it more resistant to COMT degradation

42
Q

What is phenylephrine used for clinically?

A

Vasoconstriction (slight hypertension)
Mydriatic
Nasal decongestant

43
Q

What adrenoceptors is clonidine more selective for?

A

Alpha 2 > Alpha 1 > Beta

44
Q

What is the effect of clonidine on noradrenaline?

A

It will stimulate presynaptic alpha 2 receptors which has a negative effect on synthesis and release of noradrenaline

45
Q

What will be the effect of reduced noradrenaline?

A

Less stimulation at effector organ so less vasoconstriction and fall in TPR and blood pressure

46
Q

What is the effect of clonidine on the brainstem?

A

Works on baroreceptors in this pathway and reduces sympathetic drive from brain which reduces TPR and reduces amount of noradrenaline

47
Q

What is clonidine used to treat?

A

Hypertension and migraine

48
Q

Why did clonidine fall out of favour?

A

It was very effective at reducing hypertension but patients got persistent colds and felt generally under the weather

49
Q

What adrenoceptors is isoprenaline more selective for?

A

Beta 1 + 2 > Alpha 1 + 2

50
Q

Isoprenaline is chemically similar to adrenaline but has a slight change in structure, what does this cause?

A

Less susceptible to uptake 1 and MAO breakdown

51
Q

What does this decrease in susceptibility of isoprenaline mean?

A

It has a much longer plasma half-life (2 hours) than adrenaline so can provide long-term beta stimulation

52
Q

What are the clinical uses of isoprenaline?

A

Cardiogenic shock
Acute heart failure
Myocardial infarction

53
Q

What is a problem with isoprenaline?

A

It drives beta-1 receptors in heart to support heart but will also stimulate beta-2 receptors in VSM which will cause dilation of the blood vessels in the muscles so you get a lot of pooling of blood within the muscles hence you get decreased venous return so via baroreceptors you will get reflex tachycardia

54
Q

What adrenoceptors is dobutamine selective for?

A

Beta 1 > Beta 2 > Alpha

55
Q

Why is dobutamine better as a treatment for cardiogenic shock than isoprenaline?

A

It doesn’t cause reflex tachycardia because it’s selective for beta-1 - it is administered by IV and has a plasma half life of 2 minutes

56
Q

What adrenoceptors is salbutamol selective for?

A

Beta 2 > Beta 1 > Alpha

57
Q

What is salbutamol (ventolin) most commonly used to treat?

A

Asthma

58
Q

How does salbutamol treat asthma?

A

It causes beta-2 mediated relaxation of bronchial smooth muscle and inhibits release of bronchoconstrictor substances from mast cells

59
Q

What effect does using an inhaler have?

A

Provides a localised effect in the lungs

60
Q

What else is salbutamol used to treat?

A

Threatened premature labour

61
Q

How does salbutamol prevent threatened premature labour?

A

Beta 2 mediated relaxation of uterine smooth muscle- prevents abortion of foetus

62
Q

What are the side effects of using salbutamol?

A

Reflex tachycardia
Tremor
Blood sugar dysregulation

63
Q

What are the two main indirectly acting SNS agonists?

A

Cocaine

Tyramine

64
Q

How does cocaine act as an SNS agonist?

A

Inhibits the uptake 1 mechanism for dopamine and noradrenaline

65
Q

Why does cocaine give you a high?

A

In the nucleus accumbent (centrally in brain), dopamine is neurotransmitter and cocaine inhibits reuptake of dopamine at uptake 1 site so you get an accumulation of dopamine at the synapse

66
Q

What are the effects of cocaine on the CNS in low doses?

A

Euphoria, excitement and increased motor activity

67
Q

What are the effects of cocaine on the CNS in high doses?

A

Activation of chemotactic trigger zones (vomiting), CNS depression, respiratory failure, convulsions and death

68
Q

What are the effects of cocaine on the CVS in low doses?

A

Tachycardia, vasoconstriction and raised blood pressure

69
Q

What are the effects of cocaine on the CVS in high doses?

A

Ventricular fibrillation and cardiac arrest

70
Q

What is tyramine and where is it found?

A

Dietary amino acid that is commonly found in cheese, red wine and soy sauce

71
Q

What does tyramine work as?

A

A false neurotransmitter

72
Q

What effect does this have on normal people?

A

None except from stimulating dreams

73
Q

When does a problem occur with tyramine?

A

If a patient is on MAO inhibitors to control depression

74
Q

How does tyramine act as a false neurotransmitter?

A

It acts as a weak agonist at effector organ at which noradrenaline will stimulate receptors
It also piggy backs on the uptake systems and competes with NA for the uptake 1 site so more NA in synapse
Tyramine then gets taken up into vesicles and displaces NA
Normally displaced NA will be broken down by MAO but tyramine competes with NA for MAO binding site- less breakdown of NA which leaks out into cleft and there is build up of NA in synaptic cleft

75
Q

What happens with tyramine in patients on MAO inhibitors?

A

MAO capabilities are completely blocked so NA can’t be broken down and this leads to mass build up of NA and will lead to a hypertensive crisis

LCRS Pharmacology and Therapeutics (33 decks)

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