L11 Peripheral Nervous System Flashcards

1
Q

What does the nervous system allow the organism to do?

A
  • to sense information about its enviroment
  • to respond rapidly and accordingly
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2
Q

What are the steps between the input stimulus and the output response?

A

Detected sensory neurones (PNS and afferent) -> integrated & processed interneurons(CNS) -> effect muscles/glands (PNS and efferent)

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3
Q

What are PNS efferent systems?

A

The autonomic nervous system which controls the smooth muscle and glands
- heart rate, respiratory rate, GI secretions (outside the influence of voluntary control)
- divided into sympathetic and parasympathetic

Somatic nervous system which controls the motor innervation of skeletal muscles
- voluntary control

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4
Q

List the characteristics of the sympathetic system

A

Pupils dilate
Lens of eye adjusts for vision
Airways in lungs dilate
Respiratory rate increases
Heart rate increases
Blood vessels to limb muscles dilate
Blood vessels to visceral organs constrict
Salivary secretions reduced
Brain activity general altertness

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5
Q

List the characteristics of the parasympathetic system

A

Pupils constrict
Lens of eye readjust for closer vision
Airways in lungs constrict
Respiratory rate decrease
Heart rate decrease
Blood vessels to limb muscles constrict
Blood vessels to visceral organs more dilated
Salivary secretions normalise

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6
Q

Which neurotransmitters are involved in the sympathetic system?

A

The preganglionic fibre and the postganglionic fibre join at the synapse
Preganglionic = Ach
Postganglionic = NA

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7
Q

Which neurotransmitters are involved in the parasympathetic system?

A

Preganglionic = Ach
Postganglionic = Ach

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8
Q

Which neurotransmitters are involved in the somatic system?

A

Ach is released onto the neuromuscular junction which is a specialised synapse
Controls the skeletal muscle

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9
Q

What are the exceptions in the sympathetic nervous system?

A

Sweat glands
Both fibres contain Ach

Adrenaline is released from the adrenal glands
- activation of the sympathetic system results in activation of adrenal medulla by Ach which releases adrenaline into the bloodstream

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10
Q

What is the precursor choline converted into?

A

Acetylcholine by cholineacetyl transferase

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11
Q

What are the benefits of Ach being stored in vesicles?

A
  • protects it from cytosolic enzymes that can break it down
  • available for exocytotic release
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12
Q

How is the Ach terminated in the synapse?

A

Terminated by an enzyme in the synapse = acetylcholinesterase
Ach -> choline + acetate

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13
Q

What are the classes of acetylcholine receptors?

A

1) Muscarinic
2) Nicotinic

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14
Q

Outline muscarinic receptors

A
  • located at postganglionic parasympathetic synapses
  • 3 main subtypes : M1, 2 and 3
  • G-protein coupled recepor
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15
Q

Outline nicotinic receptors

A

2 main receptor subtypes:
Neuronal type - brain and autonomic ganglia (sympathetic and parasympathetic so excitatory)
Muscle type - neuromuscular junction (excitatory)

They have ligand gated ion channels

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16
Q

What is the function and structure of G-protein coupled receptors?

A

S : 7-transmembrane spanning receptors
F : coupled to Intracellular effector systems via a G-protein
Action is slow - seconds

17
Q

What is the function and structure of ligand gated ion channels?

A

S : made up of 4 or 5 subunits structure
F : coupled directly to an ion channel
Action is very fast - milliseconds

18
Q

Outline muscarinic receptors

A

M1, 2 and 3
G-protein coupled
Slow response
Mainly located on effector tissues

19
Q

Outline nicotinic receptors

A

Nic muscle, nic neurone
Ligand gated ion channels
Fast response
Located in ganglia and on NMJ

20
Q

List the effects of muscarinic agonists

A

Increased pupil constriction
Decreased focal length of the lens
Bronchoconstriction
Decreased cardiac output
Increased GI motility
Increased exocrine gland secretion

They are known as parasympathomimetics as they have similar effects to the activation of the parasympathetic NS

21
Q

What are muscarinic antagonists also known as?

A

Parasympatholytics as they have opposite effects to the parasympathetic NS

22
Q

What are the clinical uses of muscarinic receptor agonists?

A

Used to treat glaucoma
- local application causes ciliary muscle contraction
- focuses on near vision and allows increased drainage of aqueous humour
- contraction of sphincter muscle causes pupil constriction

Treatment of dry mouth/reduced saliva secretions
- can result from radiation, antineoplastic drugs, side effects of drugs
- the treatment stimulates saliva secretions and is taken systematically
- side effects include muscarinic-sweating, nausea and minimal cardiovascular side effects

23
Q

What are the clinical uses of muscarinic receptor antagonists?

A

Pupil dilation in eye surgery
- relaxation of constrictor pupillary muscle

Increased heart rate due to resuscitation in bradycardia

Decrease oral/respiratory secretions before oral procedures and as an adjunct to anaesthesia

Treatment of asthma which relieves bronchodilation

Treats motion sickness
- orally is decreases gastric motility

24
Q

Outline neuronal type nicotinic receptors

A

located on both sympathetic and parasympathetic ganglia
agonists activate both systems
- sympathetic : vasoconstriction, tachycardia, hypertension
- parasympathetic : bradycardia, hypotension, increased secretions

25
Why are neuronal nicotinic agonists not useful?
Their effect is autonomic confusion
26
What are the characteristics of neuronal type nicotinic receptor antagonists?
Loss of sympathetic and parasympathetic reflexes, especially cardiac
27
Outline muscle type nicotinic receptors
Located at the NMJ Stimulation of these receptors by Ach causes depolarisation and contraction of the skeletal muscle fibres - in muscle fibres the depolarisation is known as end plate potential (EPP)
28
What is the effect of a nicotinic agonist on the NMJ?
Initial depolarisation and muscle fibre contraction - because the synthetic agonist is not metabolised rapidly by acetylcholinesterase - the fibre is persistently depolarised resulting in loss of further electrical excitability -> depolarising block - can be used for paralysis/muscle relaxation for surgery
29
What is the effect of nicotinic antagonists at the NMJ?
Hyperpolarisation Inhibition of EPPs Muscle fibre relaxation Paralysis for surgery Non-depolarising blocker
30
How can drugs affect the synthesis in cholinergic transmission?
Hemicholinium blocks the choline uptake, inhibits synthesis and blocks Ach transmission
31
How can drugs affect the release during cholinergic transmission?
Ach release is inhibited by botulinum toxin and bungarotoxin - causes parasympathetic and motor paralysis if injected Botulinum toxin injected locally is used to treat muscle spams and in plastic surgery (BOTOX)
32
What can inhibit acetylcholinesterase?
Anticholinesterases which increases the transmission of Ach
33
What are the effects of anticholinesterase on the autonomic NS?
Increased transmission at parasympathetic postganglionic synapses - increased secretions - bradycardia - hypotension - pupil constriction
34
What are the effects of anticholinesterase on NMJ?
Increased muscle tension and twitching, at large doses can cause a depolarising block Used to treat myasthenia gravis