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Year 2 Pharm > 8 - SNS agonists > Flashcards

8 - SNS agonists Flashcards

1
Q

Where do sympathetic nerve originate from in the spinal chord?

A

in the thoracolumbar region

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2
Q

What is always released from the preganglionic nerve fibre in a ganglion?

A

Acetylcholine

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3
Q

What is released from post ganglionic nerve fibres (in the SNS)?

A

MOST = NORADRENALINE
2 exceptions:
- adrenal medulla = releases adrenaline (80%) and noradrenaline (20%)
- sympathetic post-ganglionic neurones that innervate sweat glands = release acetylcholine

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4
Q

State the difference between directly and indirectly acting sympathomimetics.

A

Directly acting – binds to the adrenoceptor and mimic the action of adrenaline and noradrenaline by stimulating the receptors
Indirectly acting – inhibits the uptake and breakdown systems leading to the accumulation of neurotransmitter in the synaptic cleft

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5
Q

Describe the mechanism of action of the four different types of adrenoceptor.

A

ALL adrenoceptors are G-protein coupled
Alpha 1 = PLC —> IP3 + DAG
Alpha 2 = decrease cAMP
Beta 1 + Beta 2 = increase cAMP

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6
Q

State the main actions of beta-1 receptors.

A

HEART – increase heart rate + increase contractility
KIDNEYS – increase renin release  increase blood pressure
Lipolysis

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7
Q

State the main actions of beta-2 receptors.

A

Bronchodilation
Hepatic glucose output – glycogenolysis + gluconeogenesis
Vasodilation of vessels to skeletal muscle
Relaxation of the uterus (in women)

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8
Q

State some effects that are mediated by both alpha and beta-receptors.

A 
Exocrine secretions (e.g. salivary gland secretions become thick)
GIT motility – decreased muscle motility and tone + contraction of sphincters
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9
Q

What receptors are responsible for the production of aqueous humour by the ciliary body?

A

Beta receptors

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10
Q

State some effects of alpha-1 receptors.

A
  • Mydriasis (contraction of radial muscles of the iris)
  • Vasoconstriction
  • Constriction of trigone and sphincter in the bladder
  • Increased motility and tone of the ureters
  • Stimulates ejaculation (in males)
  • Lacrimation
  • Contraction of pilomotor muscle + increased localised secretion of sweat glands e.g. palm of hands
  • Hepatic glucose output (glycogenolysis and gluconeogenesis)
  • Lipolysis
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11
Q

What is the principle action of beta-blockers?

A

KIDNEYS – it inhibits the beta-1 mediated increase in renin secretion
It also decreases heart rate and contractility but its main action in reducing blood pressure is through the kidneys

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12
Q

Describe the relative selectivity of adrenaline and noradrenaline.

A

Noradrenaline is more selective for ALPHA-receptors

Adrenaline is more selective for BETA-receptors

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13
Q

Briefly describe the metabolism of noradrenaline

What receptors influence NA metabolism?

A
  • tyrosine from diet
  • converted to DOPA by tyrosine hydroxylase
  • DOPA —–> dopamine
  • into vesicles
  • dopamine —–> NA
  • can be uptaken back into the pre-synaptic neurone or extraneuronally
    NOTE: alpha 2 receptors influence the synthesis and release of NA (have a negative effect)
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14
Q

Describe the action of pre-synaptic alpha-2 receptors.

A

Pre-synaptic alpha-2 receptors have a negative influence on noradrenaline synthesis and release

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15
Q

State five directly acting SNS agonists and which adrenoreceptors they act upon ***

A 
Phenylephrine – alpha-1
Clonidine – alpha-2
Isoprenaline – beta 1+ beta 2
Dobutamine – beta-1
Salbutamol – beta-2
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16
Q

Describe the development of hypersensitivity following first exposure.

A

After the first exposure you generate antibodies to the antigen and these circulate around the body and bind to mast cells (in subsequent exposure, the mast cells are primed with the antibody on its surface).
Cross-linking of these antibodies on the surface of mast cells causes massive release of the stored mediators leading to the symptoms of hypersensitivity.

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17
Q

State some symptoms of hypersensitivity.

A

Increase in capillary permeability leads to increased movement of fluid into the tissues. This depletes the circulating fluid volume leading to a drop in blood pressure —–> ANAPHYLACTIC SHOCK (and unconsciousness)
This can also lead to contraction of bronchial smooth muscle and constriction of muscles around the throat causing respiratory distress.
It can also constrict GI smooth muscle causing vomiting and diarrhoea.

18
Q

Why is adrenaline more effective than noradrenaline in dealing with hypersensitivity?

A

During the hypersensitivity reaction, the most important problem to deal with is BREATHING.
Adrenaline is more selective for beta receptors than noradrenaline so is better at causing beta-2 mediated bronchodilation, thus opening up the airways.
Adrenaline also stimulates the heart (tachycardia) via beta-1 to support blood pressure.
Adrenaline also acts on the alpha-1 receptors to cause vasoconstriction and an increase in TPR and blood pressure.
Adrenaline can also slow down the release of histamine from mast cells via beta-2.

19
Q

State two pulmonary obstructive conditions in which adrenaline is used therapeutically and explain why.

A

Asthma
Acute bronchospasm associated with chronic bronchitis or emphysema

causes beta-2 mediated bronchodilation and suppresses mediator release.

(Selective beta-2 agonists are preferable, though adrenaline is useful in a hypotensive crisis.)

20
Q

Which receptors are involved in the generation of aqueous humour in the eye?

A

Alpha-1 involved in vasoconstriction of the vessels in the ciliary body
Beta-receptors control the enzyme that makes the aqueous humour

21
Q

Why is adrenaline used as a treatment for glaucoma?

A

Adrenaline can stimulate the alpha-1 receptors to cause vasoconstriction of the vessels in the ciliary body thus reducing the blood flow within the ciliary body -> reduced production of aqueous humour

22
Q

State and explain three other clinical uses of adrenaline.

A 
Cardiogenic Shock (the sudden inability of the heart to pump sufficient oxygenated blood) 
•	Beta-1 stimulation has a positive inotropic effect

Spinal Anaesthesia
• Anaesthetising through the spine can take away the sympathetic output to the peripheral resistance vessels
• This leads to relaxation of the peripheral vasculature so the patient can’t maintain their blood pressure
• Giving a little adrenaline with the anaesthetic can constrict the blood vessels to maintain blood pressure

Local Anaesthesia
• Giving adrenaline with the LA causes local vasoconstriction, which reduces the rate of clearance of the anaesthetic from that area (anaesthetic will last longer)
• This is due to alpha-1 mediated vasoconstriction

23
Q

State some unwanted actions of adrenaline.

A

Secretions are reduced and thick
CVS (MAIN SIDE EFFECTS) – tachycardia, palpitations, arrhythmias, cold extremities, hypertension
skeletal muscle - tremor
GIT - minimal

Overdose of adrenaline can lead to: cerebral haemorrhage, pulmonary embolism

24
Q

What receptor is phenylephrine most selective for?

A

alpha 1

25
Q

Compare phenylephrine to adrenaline and describe the resistance to degradation of phenylephrine.

A

Chemically related to adrenaline
(but slight structural change means that ) phenylephrine is MORE resistant to COMT degradation than adrenaline but it is NOT resistant to MAO degradation

26
Q

State some clinical uses of phenylephrine.

A

Mydriatic
Nasal decongestant
It causes vasoconstriction

27
Q

What receptor is clonidine most selective for?

A

alpha 2

28
Q

What receptors foe clonidine act upon? What effect does this have?

A

alpha-2 receptors so has a negative effect on NA synthesis and release.

29
Q

Describe and explain the effects of clonidine (what are the 2 routes of action?)

A
  • binds alpha 2 adrenoreceptors—> less NA produced
  • Clonidine has a central action on the brainstem – acts on baroreceptors and reduces sympathetic drive
  • —-> reduces TPR
  • —-> reduces the amount of NA released at the nerve terminals, thus reducing TPR further

(- Alpha-2 mediated reduction in NA release in the kidneys will also reduce renin release and hence reduce angiotensin II. )

30
Q

State some clinical uses of clonidine

A

It is used to treat hypertension and migraine.

31
Q

Which adenoreceptors is isoprenaline selective for?

A

Beta (more than alpha)

doesn’t discriminate between beta receptors

32
Q

Describe the susceptibility to breakdown of isoprenaline compared to adrenaline.

A

Isoprenaline is less susceptible to uptake 1 and MAO breakdown

33
Q

State three clinical uses of isoprenaline.

A

(used predominantly for cardiac effects)
Cardiogenic Shock
Myocardial Infarction
Acute Heart Failure

34
Q

What is a big problem with isoprenaline with regards to its action on beta 2 receptors?

A

Isoprenaline brings about positive effects via Beta-1 stimulation
However, stimulation of Beta-2 leads to vasodilation of blood vessels in the muscles —–> pooling of blood within the muscles —–> reduced venous return
Via the baroreceptors, you get a reflex tachycardia

So the beta-1 effects are good for patients with heart failure but the beta-2 effects are not

35
Q

Which adenoreceptors is dobutamine selective for?

A

Beta 1

36
Q

State a clinical use of dobutamine. Why is it preferred to isoprenaline?

A

Cardiogenic shock

It lacks isoprenaline’s reflex tachycardia effect

37
Q

How is dobutamine administered?

A

Administration via IV infusion (half-life = 2 mins)

38
Q

Which adenoreceptors is salbutamol selective for?

A

beta 2

39
Q

Describe the relative resistance of salbutamol to degradation.

A

Relative resistance to MAO and COMT

40
Q

State and explain two clinical uses of salbutamol.

A

Asthma
• Beta-2 mediated relaxation of bronchial smooth muscle (bronchodilation)
• Inhibition of release of bronchoconstrictor molecules from mast cells

Threatened premature labour
• Beta-2 mediated relaxation of uterine smooth muscle
• This will prevent abortion

41
Q

State some side effects of salbutamol.

A

Reflex tachycardia
Tremor
Blood glucose dysregulation

42
Q

Where are the adrenoreceptors found?

A

All adrenoreceptor will be found on the post-junctional membrane.

The exception is α2 adrenoreceptors - it is a pre-junctional receptor – it is generally found on the neurone itself. It works as a negative feedback receptor – it DIMINISHES sympathetic effects (decreases NA release into synapse) - α2 impairs sympathetic function.

Year 2 Pharm (9 decks)

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