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Pharmacology and therapeutics > Introduction to the ANS > Flashcards

Introduction to the ANS Flashcards

1
Q

What is meant by pharmacodynamics

A

What drugs do to the body- their effects

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2
Q

What is meant by pharmacokinetics

A

How the body responds to the drugs (metabolism, excretion)

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3
Q

Describe the basic function of the ANS

A

Peripheral functions- not conscious

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4
Q

What are the 3 outputs (branches) of the CNS

A

§ There are 3 branches to the CNS; the ANS, the somatic nervous system and the neuroendocrine syste

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5
Q

What does the ANS act on

A 
exocrine glands
smooth muscle
cardiac muscle
metabolism
host defence
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6
Q

What does the somatic nervous system act on

A

skeletal muscle,

including the diaphragm and respiratory muscle

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7
Q

What does the neuroendocrine system act on

A

growth, metabolism, reproduction, development,
salt & water balance,
host defence

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8
Q

List some examples of the ANS in action

A

§ Some targets of the ANS include:
o Pupillary constriction – constriction mediated by the PNS via the oculomotor nerve (CNIII).
o Cephalic and gastric phases of digestion – vagal nerve PNS mediation.
o Basal heart rate – PNS is dominant at rest (as the intrinsic rate is 100-110bpm which isn’t normal at rest) however as baroreceptors stretch less as BP drops, less inhibition of SNS leading to increased heart rate.

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9
Q

Describe the effect of reduced baroreceptor firing

A

Loss of fluid (e.g excessive sweating)- BP decreases- decreased rate of firing of arterial baroreceptors- therefore less inhibition of sympathetic neurones- the sympathetic neurone (split into two branches) can then act to increase heart rate, increase BP (vasodilation) and increased force of contraction of the heart

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10
Q

Do all targets have PNS and SNS innervation

A

Note that most targets in the body receive BOTH PNS and SNS innervation BUT some targets only receive one type branch of the ANS – examples include the blood vessels (only the SNS innervates).
2 opposing effects in blood vessels - NA constricts, histamine dilates
Lungs only receive PNS- dilation is by adrenaline in fight or flight response

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11
Q

Effects of ANS on the eye

A

Dilatation (Pupil) - symp
Constriction (Pupil)- para
Contraction (Ciliary Muscle)- para

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12
Q

Effects of ANS on trachea and bronchioles

A

Dilates (Ad)

Constriction- para

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13
Q

Effects of ANS on liver

A

Glycogenolysis
Gluconeogenesis

Both symp

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14
Q

Effects of ANS on adipose

A

Lipolysis- symp

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15
Q

Effects of ANS on kidney

A

Increased renin secretion- symp

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16
Q

Effects of ANS on bladder and ureters

A

Relaxes detrusor; constriction of trigone and sphincter (symp)

Contraction of detrusor; relaxation of trigone and sphincter (para)

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17
Q

Effects of ANS on salivary glands

A

Thick, viscious secretion- sympathetic

Copious, watery secretion - para

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18
Q

Effects of ANS on skin

A 
Piloerection - symp 
Increased sweating (C)- symp (cholinergic)
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19
Q

Effect of ANS on heart

A

Increased rate and contractility- symp

Decreased rate and contractility- para

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20
Q

Effect of ANS on G.I system

A

decreased motility and tone, sphincter contraction- symp

increased motility and tone, increased secretions- para

21
Q

Effect of ANS on blood vessels

A

to skeletal muscle- dilatation- symp

to skin, mucous membranes and splanchnic area)- constrition- symp

22
Q

Summarise the characteristics of the PNS

A

o Has LONG pre-ganglionic fibres and SHORT post.
o ALL transmitters are ACh.
o Is DISCRETE – 1:1 pre- vs. post-.

23
Q

Summarise the characteristics of the SNS

A

o Has SHORT pre-ganglionic fibres and LONG post.
o Releases mainly A and NA.
o Is DIVERGENT (mass discharge) – 1:20 pre- vs. post

24
Q

Describe the exemptions of the SNS

A

ADRENAL GLAND- beaves like post-ganglionic fibre- only peripheral tissue to function like an autonomic nerve- 80% A and 20% NA

Sweat gland- Post ganglionic fibre releases Ach

25
Q

Explain the exemption of the sweat gland

A

PSNS is involved in secretions- sweat is a secretion- but sweat needs to be SNS- so Ach was retained in evolution- despite being a SNS response

26
Q

Why is it important that many pre ganglionic sympathetic fibres can have an effect on many post ganglionic fibres

A

SNS is involved in stress response- 1 pre ganglionic : many post ganglionic- multiple effects required

increase sweat with increased HR, BP and blood flow, whilst decreasing gut secretions

27
Q

Summarise the enteric nervous system

A

network of neurones responding to the gut environment- can communicate and determine response- local signals- no need for brain - but ANS can influence ENS

28
Q

Describe the enteric sensory neurones in action

A

Sensory neurone connected to mucosal chemoreceptors and stretch receptors detect chemical substances in the gut lumen or tension in the gut wall caused by food.
Information relayed to submucosal and myenteric plexus via interneurons.

29
Q

Describe the enteric motor neurones in action

A

Motor neurones release acetylcholine or substance P to contract smooth muscle or vasoactive intestinal peptide or nitric oxide to relax smooth muscle.

30
Q

Summarise the somatic nervous system

A

§ Very simple – just long neurones with eventual ACh release.

31
Q

What are the Ach receptors

A

membrane bound- muscarinic or nicotinic

32
Q

Summarise nicotinic receptors

A

At all autonomic ganglia
Stimulated by nicotine/acetylcholine
c) Type 1 - Ionotropic

33
Q

Why is it important that nicotinic receptors are type 1- ionotropic

A

Swift signal- impoartant fasted method
ganglia linking pre to post
ligand binds (Ach leading to Ca2+ or Na+ influx in post ganglionic fibre)

34
Q

Summarise the muscarinic receptor

A

At all effector organs innervated by
post ganglionic parasympathetic fibres and cholinergic sympathetic (sweat glands)
b) Stimulated by muscarine/acetylcholine
c) Type 2 – G-protein coupled

35
Q

Summarise GPCRs

A

7-TM receptor

associated G-protein activated- starting I.C machinery (second messenger)- activation of cell signalling

36
Q

Which of the following effects would be observed after blockade
of nicotinic acetylcholine receptors in an individual at rest?

A

Constipation- due to blockage of PNS- can’t act on effectors

37
Q

What effect would blockade of nicotinic acetylcholine
receptors have on heart rate;

At rest
During exercise

A

At rest- PNS is dominant- so HR will increase if PNS is blocked

During exercise- SNS is dominant during exercise- less of an increase (nicotinc receptor at pre-ganglionic sympathetic neurone blocked)

38
Q

List the su-types of muscarinic cholioceptors

A

M1 – Neural (Forebrain – learning & memory)

M2 – Cardiac (Brain – inhibitory autoreceptors)

M3 – Exocrine & smooth muscle (Hypothalamus – food intake)

M4 – Periphery: prejunctional nerve endings (inhibitory)

M5 – Striatal dopamine release

39
Q

Summarise adrenoreceptors

A

§ Found at all effector organs innervated by post-ganglionic SNS fibres (not sweat glands).
§ Stimulated by noradrenaline/adrenaline.
§ Type 2 – G-protein coupled.

40
Q

Describe the location of the different adrenoreceptors

A

alpha 1- smooth muscle in blood vessels and bronchi, dilator pupillae- contraction
alpha 2- smooth muscle in blood vessels, presynaptically on adrenergic synapses- reduced NT release
beta 1- heart muscle, presynaptically on adrenergic symapses- increased HR and force of contraction, increased NT release
beta 2- smooth muscle in blood vessels and bronchi- relaxation

41
Q

What do we need to consider for all drugs

A

What is the drug target?
e.g M3 muscarinic receptors

  1. Where is the drug target?
    e. g gastric S.M, Paneth cells, endocrine cels
  2. What is the end result
    of the interaction?
    contraction, increased acid production, increased gastrin secretions
42
Q

What happens when the NT binds to its receptor

A

it activates it and then it unbinds

43
Q

Why do we have mechanisms to remove the NT

A

Don’t want permanent activation
Want effect to be short lived
rapid activation with quick deactivation

44
Q

Describe the biosynthesis of Ach

A

Acetyl coA (from mitochondria) + choline — Ach + CoA ( Choline acetyltransferase)

Ach is packaged into vesicles – action potential leads to Ca2+ influx- binds to vesicles- transported to pre-synaptic membrane- Ach released

45
Q

Describe the metabolism of Ach

A

Ach can bind to post-synaptic receptor or to acetylcholinesterase (lots of this enzyme- eventually they will all bind to it) Ach converted to choline and acetate
choline taken back up by the nerve terminal- to make more Ach

46
Q

Describe the biosynthesis of NA

A

Tyrosine is the precursor (delivered to nerve terminal by blood)
converted to DOPA ( Tyrosine hydroxylase)
DOPA — Dopamine ( DOPA decarboxylase)

Dopamine is packaged into a vesicles

Dopamine — NA (Dopamine B hydroxylase)

Release as normal

47
Q

Describe the metabolism of NA

A

No enzyme in the synapse of sympathetic neurones- longer lasting effect

Uptake 1 protein- takes NA back into the pre-synaptic neurone- where it is then metabolised
converted to metabolites in the mitochondria by Monoamine oxidase A- MAO-A

Uptake 2- NA taken into the post synaptic neuron- degraded by COMT (Catechol-O-methyltransferase)

48
Q

Consequence of blocking enzymes that metabolise NA

A

Increase NA in pre and post-synaptic neurone (reducing conc gradient)- more NA in synapse- less moves back in by transporter

Pharmacology and therapeutics (30 decks)

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