drugs and the nervous system L10

Question 1

What does the nervous system allow

Answer 1

A system which allows an organism :
to sense information about its environment (internal & external)
to respond rapidly and accordingly.

Question 2

whats the difference between efferent and afferent peripheral nervous system

Answer 2

afferent is nerves going to the brain and spinal cord, efferent are those going away

Question 3

what is the autonomic nervous system

Answer 3

controls the smooth muscle and glands
autonomic responses which are outside the influence of voluntary control

Question 4

what is the autonomic nervous system split into

Answer 4

Divided into sympathetic (increase) and parasympathetic (return to normal level)

Question 5

what is the somatic nervous system

Answer 5

motor innervation of skeletal muscles.
Voluntary control

Question 6

describe the organisation of sympathetic autonomic nervous system

Answer 6

short preganglionic fibre that terminates onto autonomic ganglion
long post ganglionic fibre that terminates on to target tissue

Question 7

what neuro transmitter is released from pre and post ganglionic neuron in sympathetic autonomic nervous system

Answer 7

pre: acetylcholine
post: noradrenaline

Question 8

what neuro transmitter is released from pre and post ganglionic neuron in parasympathetic autonomic nervous system

Answer 8

both release acetylcholine

Question 9

what are the exceptions to Sympathetic system

Answer 9

1. sweat glands
   - both post and pre release ACH
2. Adrenaline release from adrenal glands

Question 10

give the name of a efferent somatic nervous system, describe its structure and what neurotransmitter does it release

Answer 10

neuromuscular junctions
one long fibre - no autonomic ganglion
releases acetylcholine

Question 11

what are the fundamentals of neurotransmission

Answer 11

Synthesis
Storage
Release
Receptor interaction
Termination.

Question 12

describe Synthesis, Storage, Release , Receptor interaction
and Termination of ACH.

Answer 12

1. ACH is made from choline and AcCoA and catalysed by cholineacetyl transferase
2. ACH is stored in vesicles
3. calcium comes in causing vesicles to fuse with membrane causing release of ACH into synaptic cleft - exocytotic
4. ACH binds to nicotinic or muscarinic receptors
5. acetylcholinesterase breaks down ACH in to choline and acetate
   - choline is recycled

Question 13

what are the two types of cholinergic receptors that ACH binds to

Answer 13

Muscarinic receptors and Nicotinic receptors

Question 14

Muscarinic receptors
how many types are there
where are they found
what type of receptors are they

Answer 14

there are 3 subtypes M1,2 and 3
Located at postganglionic parasympathetic synapses
G-protein coupled receptor - slow receptor

Question 15

Nicotinic receptors
how many types are there
where are they found
what type of receptors are they

Answer 15

2 subtypes: neuronal and muscle
neuronal- brain and autonomic ganglia (both sympathetic and parasympathetic (excitatory)
muscle- neuromuscular junction (NMJ) (excitatory)
Ligand gated ion channels (or ionotropic receptor)
- 4 or 5 subunits structure
- coupled directly to a ion channel
- fast

Question 16

what do Muscarinic receptors mainly effect

Answer 16

parasympathetic effects

Question 17

what are the effects of muscarinic agonists

Answer 17

1. increase pupil constriction (contraction of constrictor pupillary muscle)
2. decrease focal length of the lens (contraction of ciliary muscle)
3. Bronchoconstriction
4. decrease cardiac output, (rate & force
5. increase GI motility
6. increase exocrine gland secretion (sweating salivation, bronchiol secretion)

Question 18

what are muscarinic agonists known as

Answer 18

parasympathomimetics

Question 19

what are the Effect of muscarinic antagonist

Answer 19

1. pupil dilate (relaxation of constrictor pupillary muscle) (blurred vision)
2. increase focal length of the lens (relaxation of ciliary muscle)
3. Bronchodilation
4. increase cardiac output, rate & force
5. decrease GI motility
6. decrease exocrine gland secretion (dry mouth decreased sweating)

Question 20

what are muscarinic antagonists known as

Answer 20

parasympatholytics

Question 21

what muscarinic agonist cause increased pupil constriction and decreased focal length of lens

Answer 21

Pilocarpine, Carbachol

Question 22

what is the clinical use of Pilocarpine
and other muscarinic agonist

Answer 22

1. used to treat Glaucoma
   - Local application causes ciliary muscle contraction –
   focus on near vision + also allows increase drainage of aqueous humour
   - Contraction of sphincter muscle causes pupil constriction
2. Treatment of xerostomia: Dry mouth/reduced saliva secretions
   - Pilocarpine stimulates saliva secretions
   - Taken systemically
   - Side effects: muscarinic-sweating, nausea, minimal cardiovascascular side effect (due to low dose)

Question 23

what is the clinical use of muscarinic antagonists such as Atropine like drugs

Answer 23

1. Pupil dilation in eye surgery (causes pupil dilation)
   - Tropicamide
2. Decrease oral/respiratory secretions before oral procedures and as an adjunct to anaesthesia,
   - Atropine (belladonna, deadly nightshade)
   - Glycopyrronium
3. Resuscitation in bradycardia (causes increase heart rate)
   - Atropine
4. Asthma (causes bronchodilation)
   - Ipratropium
5. Motion sickness- Orally it decreases gastric motility - Hyoscine

Question 24

what are the 2 subtypes of nicotinic receptors and where are they found

Answer 24

neuronal type- brain and autonomic ganglia (excitatory)
- Located on both sympathetic and parasympathetic ganglia
muscle-type: neuromuscular junction (NMJ) (excitatory)
- located at NMJ

Question 25

what do agonists to neuronal nicotinic receptors do

Answer 25

Agonists (nicotine) activates both systems
- sympathetic: vasoconstriction, tachycardia, hypertension
- parasympathetic: bradycardia, hypotension, increase GIT motility, increase secretions

Question 26

what is the effect of having neuronal nicotinic receptors activating both pathways

Answer 26

autonomic confusion
- one pathway tries to increase, the other tries to decrease rate
- not of clinical use

Question 27

what do antagonists to neuronal nicotinic receptors do

Answer 27

hexamethonium
- loss of sympathetic & parasympathetic reflexes, especially cardiac

Question 28

what happens when muscarinic nicotinic receptors cause

Answer 28

Stimulation of these receptors by ACh causes depolarisation (in muscle fibre this is known as an end plate potential (EPP)) and contraction of the skeletal muscle fibre

Question 29

what is the Effect of nicotinic agonists at neuromuscular junction

Answer 29

Agonist (suxemethonium)
- Initial depolarisation/EPP and muscle fibre contraction (muscle twitch)
- Because the synthetic agonist is not metabolised rapidly by acetylcholinesterase, the fibre is persistently depolarised resulting in loss of further electrical excitability-known as depolarising block
- after a muscle twitch, paralysis happens
- Induce paralysis for surgery

Question 30

what is the Effect of nicotinic antagonist at neuromuscular junction

Answer 30

tubocurarine
- Hyperpolarisation, inhibition of EPPs
Muscle fibre relaxation
- Paralysis (for surgery)
- Non-depolarising blocker
- Induce paralysis for surgery

Question 31

describe Drugs affecting synthesis of ACH

Answer 31

Hemicholinium
- blocks the choline uptake, inhibits synthesis and blocks ACh transmission.
- no clinical use

Question 32

describe Drugs affecting release of ACH

Answer 32

botulinum toxin, & bungarotoxin
- inhibit ACh release
- Causes parasympathetic, and motor paralysis if ingested.

Question 33

how can break down of ACH be inhibited

Answer 33

anticholinesterases inhibits Acetylcholinesterase
- This will increase ACh transmission

Question 34

give examples of anticholinesterase and their effects on autonomic NS and NMJ

Answer 34

neostigmine, organophosphates

Effects on autonomic nervous system:
- Reflect increased transmission at parasympathetic postganglionic synapses- increase secretions, bradycardia, hypotension, pupil constriction

Effects on neuromuscular junctions:
- Increased muscle tension and twitching, at large doses can cause a depolarising block.
Neostigmine used to treat myasthenia gravis (autoimmune disease, circulating antibodies against muscle nicotinic receptors)