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Medsci 204 > ANS > Flashcards

ANS Flashcards

1
Q

What two sub-nervous systems makes up the anatomic nervous system, and which bodily states do they work under?

A

Parasympathic- controls organs in times when the body is at rest.

Sympathetic- controls organs in times of stress.

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2
Q

What is different between the SNS and ANS?

A

SNS- voluntary. Relays information to and from skin and skeletal muscles.

ANS- involuntary. Relays information to internal organs.

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3
Q

What three categories can sum up the differences betweent the parasympathic and sympathetic nervous systems?

A

Anatomical
Functional
Chemical (neurotransmitter)

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4
Q

Describe the basic anatomy of the ANS:

A

The preganglionic neuron lies in the spinal cord and synapses at the ganglion (a peripheral cluster of neuronal cell bodies), where the post-ganglionic neuron lies, and transmits signals to organs.

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5
Q

What is the function of the vertebrae?

A

To protect the spinal cord.

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6
Q

What ANS division has its pre-ganglion clustered in the lumbar region?

How does this differ in the other division?

A

The sympathetic nervous system has its pre-ganglion clustered in the lumbar region.

In the parasympathetic nervous system pre-ganglion cluster at both ends of the spinal cord.

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7
Q

What is the difference in location of cell bodies of the PSNS and SyNS relative to their target organs and spinal cord.

A

The PSNS has its cell bodies closer to the target organ. The SyNS has its cell bodies closer to the spinal cord.

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8
Q

Describe two anatomical characteristics of the parasympathetic nervous system:

A
  1. Pre-ganglionic fibres leave CNS in cranial nerves (III, VII, IX, X) and sacral spinal roots.
  2. Post-ganglionic neurons usually lie close to or within the target organ.
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9
Q

Describe two anatomical characteristics of the sympathetic nervous system:

A
  1. Pre-ganglionic fibres leave the CNS in thoracic and lumbar spinal roots.
  2. Post-ganglionic neurons form two paravertebral chains on either side of the spinal cord, plus midline ganglia.
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10
Q

Do all organs have a sympathetic and parasympathetic division of their ANS?

A

No- blood vessels only have sympathetic input.

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11
Q

What is the function of the parasympathetic NS?

A

To accumulate, store and preserve resources (rest and digest).

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12
Q

What is the function of the sympathetic NS?

A

To prepare the body for strenuous activity and stress emergencies (fight or flight).

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13
Q

List some effects the parasympathetic nervous systems has on the body:

A

Decreases heart rate
Increases GI tract activity
Glands stimulated to secrete (e.g. saliva)
Pupils constrict

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14
Q

List some effects the sympathetic nervous system has on the body:

A 
Increases heart rate
Decreases GI tract activity
Increases blood flow to skeletal muscle
Decreases blood flow to skin and visceral organs
Increases glycogen and lipid breakdown
Pupils dilate
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15
Q

Define a synapse:

A

This is the junction between the axonal ending of a neuron with another neuron, a muscle cell or a glandular cell.

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16
Q

What is synaptic transmission?

A

The process by which neurons signal to the next cell via the release of neurotransmitters.

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17
Q

How are neurotransmitters stored, and how do they act?

A

They are stored (and synthesised) in vesicles on the nerve terminal and then released. Neurotransmitters then bind to cellular receptors before their action can be terminated.

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18
Q

Describe the 10 steps involved in neurotransmission?

A
  1. Precursor is transported into the nerve terminal.
  2. Enzymes convert the precurson to a transmitter.
  3. Transmitter stored in vesicles.
  4. Action potential reaches terminal and depolarises cell.
  5. Voltage-gated ion channels open, leading to Ca2+ influx.
  6. Vesicles fuse with membrane and release transmitter.
  7. Transmitter diffuses into synapse, acts on post-synaptic receptors AND
  8. Acts on pre-synaptic receptors to act as an autoinhibitory feedback loop, hyperpolarising the terminal and preventing further transmitter release.
    Transmitter terminated by two mechanisms:
  9. Enzymic degradation to give recyclable degradation product.
  10. Transmitter transported back into nerve terminal.
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19
Q

How many potential places are there for drugs to act and change normal events of synaptic transmission, and what do these places correspond to?

A

There are 10 places, which correspond to the 10 steps involved in neurotransmission.

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20
Q

What neurotransmitter is involved in parasympathetic neurotransmission, and what receptors does it bind to?

A

Acetylcholoine (ACh) in both pre and post neurons.

ACh binds to nicotinic (Nn and Nm) and muscarinic (M1-M3) receptors.

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21
Q

What neurotransmitter is involved in sympathetic neurotransmission for the pre-ganglion neuron, and what receptor does it bind to?

A

ACh.

It binds to nicotinic receptors (Nn).

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22
Q

What neurotransmitter is involved in sympathetic neurotransmission for the post-ganglion neuron, and what receptor does it bind to?

A

Noradrenaline (NA).

It binds to receptors alpha1, alpha2, beta1 and beta2.

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23
Q

Describe a situation where the post-ganglionic receptor for sympathetic neurotransmission is not NA:

A

In sweat glands post-ganglionic neurotransmitter is ACh, and binds to muscarinic receptors.

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24
Q

What does neuromodulation describe?

A

The effects of other chemical mediators on synaptic transmission.

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25
Q

How do mediators act?

A

To increase or decrease the efficacy of synaptic transmission, without participating directly as a transmitter.

This generally involves slower processes (seconds to days) than neurotransmission, and occurs both pre and post synaptically.

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26
Q

Describe the two types of pre-synaptic modulation:

A

Homotropic inhibition- transmitter acts on a presynaptic receptor to inhibit further transmitter release (autoinhibition).

Heterotropic inhibition- transmitter acts on presynaptic receptor to inhibit the release of a second neurotransmitter.

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27
Q

How can presynaptic and postsynaptic receptors in the ACh and NA system be distinguised?

A

By using specific agonists and antagonists:

E.g. blocking presynaptic alpha-2-adrenergic receptors (blocking autoinhibition) results in a 10-fold increase in NA release in response to stimultion.

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28
Q

Name some chemical mediators which influence noradrenergic signalling:

A

Histamine inhibits NA release and adrenaline stimulates NA release.

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29
Q

Describe post-synaptic modulation and provide an example of this:

A

Chemical mediators can influence post-synaptic receptors to alter excitability or cell firing.

Example: NA or sympathetic nerve stimulation causes vasoconstriction of a rabbit ear artery. Addition of neuropeptide Y (NPY) enhances this response.

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30
Q

Drugs that block the responses to ACh and NA signalling do not completely block autonomic neurotransmission. What does this suggest?

A

That there are other transmitters (non-adrenergic, non-cholinergic (NANC)).

These could be non-peptides such as ATP, NO, or peptides such as NPY, vasoactive internal peptide (VIP).

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31
Q

Describe co-transmission:

A

Nerve terminal can store and release more than one neurotransmitter (e.g. NA and ATP). This allows for eliciation of differences in tissue response.

For example, ACh and ATP produce a rapid response from the parasympathetic and sympathetic nervous systems respectively.

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32
Q

What releases ACh, and what does it stimulate?

A

ACh is released by all pre-ganglionic neurons and post-ganglionic neurons in the PSNS.

ACh stimulates secretion of adrenaline from the adrenal medulla (no ganglion).

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33
Q

In relation to ACh, what is the difference in presynaptic muscarinic receptors and nicotinic receptors?

A

M receptors inhibit further release of ACh.

N receptors facilitate ACh release.

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34
Q

How does ACh concentration differ in vesicles, the synapse and the bloodstream?

A

100mM in vesicles.
1mM in synapse.
10mM in bloodstream.

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35
Q

What is the function of ChAT (choline acetyltransferase)?

A

Conversts choline and acetyl CoA into ACh and HSCoA in the pre-synaptic neuron.

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36
Q

How is ACh formed, and from what precursor?

A

Precursor glucose produces pyruvate, producing acetyl CoA which is converted into ACh by ChAT.

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37
Q

What is the function of AChE (acetylcholinesterase)?

A

Converts ACh in the synapse into choline and acetate, where choline is taken up through a transporter and back into the pre-synaptic neuron.

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38
Q

What is the rate limiting step in reuptake of choline?

A

The transport through the transporter on the pre-synaptic membrane.

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39
Q

How can hemicholinium influence cholinergic synapse transmission?

A

It can prevent the synthesis of ACh (so prevents choline uptake).

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40
Q

How can vesamicol influence cholinergic synapse transmission?

A

It can prevent vesicular storage of ACh.

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41
Q

How can 4-aminopyridine influence cholinergic synapse transmission?

A

It enhances the release of ACh.

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42
Q

How can botox (botulinum toxin) influence cholinergic synapse transmission?

A

It prevents the release of ACh.

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43
Q

How does neostigmine influence cholinergic synapse transmission?
How is this used clinically?
Give some examples of other drugs with similar actions.

A

It can prevent the breakdown of ACh by inhibiting AChE, which extends the half-life of ACh (indirect agonist).

This is used for treating myasthenia gravis.

Sarin, soman (nerve gases) and maldison (insecticide) are AChE blockers.

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44
Q

Describe direct actions at ACh receptors which may alter the synapse:

A

Agonists or antagonists may mimic or block action of ACh respectively, such as pilocarpine and atropine.

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45
Q

How can effects of muscarinic receptors be produced, and where are these found?

A

Effects that can be produced by muscarine, poison from Amanita muscarine.
These are found at the target organ,

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46
Q

How can effects of nicotinic receptors be produced, and where are thes found?

A

Effects that can be produced by nicotine, found at ganglia, motor endplate (skeletal muscle) and adrenal medulla.

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47
Q

What type of receptors are muscarinic receptors, and what are the functions of their subtypes?

A

They are G-protein coupled receptors (M1-M5).
M1, M3, M5- coupled with Gq to activate the iositol phosphate pathway.
M2,M4- coupled to Gi to inhibit adenylate cyclase, reducinf cAMP levels.

48
Q

What type of receptors are nicotinic receptors, and what are the functions of their subtypes?

A

They are ligand gated ion channels (ionotropic receptors) formed from 5 different subunits (a1-9, B1-4, y, S, E).
Nm-muscle- found at neuromuscular junction.
Nn-neuronal- found in the brain.
Ganglionic- found in autonomic ganglia.

49
Q

What is a consequence of nicotinic receptor binding?

A

Ion channel activation, leading to Na+ and K+ ion influx leading to depolarisation of the post-synaptic membrane and a fast excitatory postsynaptic potential.

50
Q

What type of receptor is the best drug target and why?

A

Muscarinic, because nicotinic receptors have a widespread distribution througout ANS, so most nicotinic receptor agonists affect both ganglion and neuromuscular receptors.

51
Q

How do agonists act at cholinergic receptors?

A

They mimic the effects of ACh.

They have affinity for muscarinic and nicotinic receptors but are fairly non-selective.

52
Q

How do antagonists act at cholinergic muscarinic receptors?

A

They have widespread application.
Inhibit bronchial and gastric secretion.
Relax smooth muscles (bronchii, pupil).
Increase heart rate.

53
Q

How do antagonists act at cholinergic nicotinic receptors?

A

Ganglion specific blockers- no clinical applications.

Neuromuscular blockers- muscle relaxants.

54
Q

How do agonists act on the heart?

A

They slow down the heart rate, resulting in a decrease in CO due to a decrease in contractive force in the atria.
Vasodilation occurs via NO mediation.

55
Q

What receptors are found selectively in the heart?

A

M2 receptors (parasympathetic)

56
Q

How do antagonists act on the heart?

A

Increase the heart rate (modest- 80-90 bpm).

Atropine- used for bradycardia treatment (slow heart beat).

57
Q

How do agonists act on smooth muscle? Other than vasculature.

A

They stimulate contraction of smooth muscle in bronchi, gall bladder, bile duct and bladder (via M3 receptors).
Stimulate peristaltic activity in the GI tract.

58
Q

How do antagonists act on smooth muscle? Other than vasculature.

A

Produce relaxation of smooth muscles.

Ipratoprium is a bronchodilator for asthma.

59
Q

How do agonists act on exocrine glands?

A

Stimulate secretion from sweat, salivary, mucous and lacrimal glands. Gastric, intestinal and pancreatic secretions are also increased via M3 receptors.

60
Q

How do antagonists act on exocrine glands?

A

Inhibit salviary, lacrimal, bronchial and sweat gland secretions.
Atropine- used as an adjunct for anaesthesia reduces secretions and is a bronchodilator.
Pirenzepine (via M1 receptors)- used to inhibit gastric acid production as a treatment for peptic ulcers.

61
Q

How do agonists act on the GI tract?

A

Relaxes sphincters in the GI, biliary and urinary tracts.

Bethanechol used clinically to assist bladder emptying.

62
Q

How do antagonists act on the GI tract?

A

GI tract motility is inhibited.

Atropine- treating gastic hypermotility.

63
Q

How do agonists act on the eye?

A

Stimulates contraction of the circular muscles of the iris and muscles of accommodation (pupil constricts, lens accommodated to near vision) via M3 receptors.
Pilocarpine is used to treat glaucoma.

64
Q

How do antagonists act on the eye?

A

Dilates pupils which become unresponsive to light-intraocular pressure may rise.
Tropicamide- opthalmic use, short-acting dilation of pupils to allow examination of retina and lens.

65
Q

How do agonists act as neuromuscular blockers?

A

Depolarising blockers, trigger the sustained depolarisation of the neuromuscular endplate so no new action potential can be generated.
Effects cannot be reversed by increasing ACh concentration.
Suxamethonium- used as a muscle relaxant for anaesthesia.

66
Q

How do competitive antagonists act as neuromuscular blockers?

A

Non depolarising blockers, compete with ACh for binding to the nicotinic receptors. Prevent depolarisaion of the endplate.
Effects can be reversed by increasing ACh concentrations (e.g. via AChE inhibitors).
Pancuronium- used in lethal injection (together with barbituate and KCl), Tubocurarine.

67
Q

How are NA storage vesicles maintained?

A

By vesicular monoamine transporter (VMAT).

68
Q

What is the rate limiting step in NA production?

A

Tyrosine to DOPA conversion by tyrosine hydroxylase.

69
Q

How is DOPA converted into NA?

A

DOPA decarboxylase converts DOPA to dopamine, and dopamine-B-hydroxylase converts this into NA.

70
Q

How is co-transmission occuring in NA?

A

NA and ATP (which is carried in vesicles alongside NA at 1NA:4ATP).

71
Q

What receptors does NA act on, and how does this differ with ATP?

A

NA acts on presynaptic and postsynaptic receptors, and ATP acts on P2 purinergic receptors.

72
Q

Describe adrenoreceptors in terms of distribution and their system type:

A

Adrenoreceptors are widely distributed. They are G-protein coupled and each have a specific second messenger system. There are two main subtypes: alpha (1,2) and beta (1,2,3).

73
Q

Name the enzyme involved with a1 receptors and describe the effects they produce:

A

Phospholipase C

Smooth muscle contraction.

74
Q

Name the enzyme involved with a2 receptors and describe the effects they produce:

A

Directly affect calcium to inhibit neurotransmitter release.

Adenylate cyclase
Smooth muscle contraction.

75
Q

Name the enzyme involved with B receptors and describe the effects they produce:

A

Heart muscle contraction (B1), smooth muscle relaxation (B2) and glycogenolysis (B2).

76
Q

Why can NA not be degraded in the synapse?

A

They is no synaptic enzyme to degrade NA.

77
Q

How is NA action terminated (2 pathways)?

A
  1. Noradrenaline transporter (NET): 75% NA recycled (in vesicles) or metabolised. HIGH affinity.
  2. Extraneuronal transporter (EMT): 25% NA taken up by non-neuronal cells (i.e. smooth muscle, cardiac muscle, endothelium). LOW affinity.
78
Q

Name the enzyme responsible for converting NA into metabolites:

A

Monoamine oxidase (MAO)

79
Q

Which branch predominates in NA metabolism, and what products does it give as the main metabolite?

A

The ADH (aldehyde dehydrogenase), gives VMA as the major metabolite.

80
Q

What minor product does ADH give, and where is it found?

A

MHPEG, the brain.

81
Q

Drugs can have a direct action on adrenoreceptors with agonists/antagonists. In addition to effecting NA uptake, name 4 ways drugs can effect NA release:

A
  1. Effects on a-2 receptors (autoinhibitory feedback loop).
  2. Prevent NA release e.g guanethidine.
  3. Increase or decrease available stores of NA e.g. reserpine or MAO inhibitors.
  4. Effects on NA release in the absence of nerve terminal depolarisation (indirectly acting sympathomimetics) e.g. amphetamine.
82
Q

Where do B-adrenoreceptor agonists act, and how may they be used clinically?

A

They act on smooth muscle and may be used for asthma treatment.

83
Q

Where do a- and B-adrenoreceptor antagonists act, and how may they be used clinically?

A

They act on the heart, and may be used in cardiovascular disorder.

84
Q

Name two non-selective agonists:

A
  1. Adrenaline

2. Noradrenaline

85
Q

Name four selective agonists (with examples):

A
  1. a1 agonists (phenylephrine, oxymetazoline)
  2. a2 agonists (clonidine)
  3. B1 agonists (dobutamine)
  4. B2 agonists (salbutamol)
86
Q

Name a non-selective antagonist:

A

Phentolamine

87
Q

Name four selective antagonists (with examples):

A
  1. a1 antagonists (prazosin)
  2. a2 antagonists (yohimbine)
  3. B1 antagonists (atenolol propranolol)
  4. B2 antagonists (butoxamine)
88
Q

When might adrenaline be used?

A

In allergic reactions and cardiac arrest.

89
Q

When might phentolamine be used?

A

Prior to sugery for pheochromocytoma (tumour on adrenal medulla). Blocks a regulated vaso-constriction in the heart and leads to a fall in blood pressure (baroreflex) which increases cardiac output and heart rate.

90
Q

Describe how a1-adrenergic agonists affect vascular smooth muscle:

A

Stimulate contraction of smooth muscle (except for that in GI tract). Main effect is on vascular smooth muscle. This leads to decreased compliance, increased central venous pressure, increased peripheral resistance, increased systolic and diastolic arterial pressure, triggering baroreceptor reflex which induces bradycardia and inhibits respiration.

91
Q

Name an example of an a1-adrenergic agonist which is a nasal-decongestant:

A

Phenylephrine.

92
Q

Describe how a1-adrenergic antagonists affect vasculature smooth muscle:

A

Cause vasodilation, decreased peripheral resistance, decreased blood pressure.

93
Q

Give two examples of a1-adrenergic antagonists, what they are used for clinically and their advantages and adverse effects:

A

Prazocin, doxazocin for hypertension.
Cause less tachycardia than non-selective blockers.
Major side effects are postural hypotension, reflex tachycardia and impotence.

94
Q

Describe how a2-adrenergic agonists affect vasculature smooth muscle:

A

Activate presynaptic receptors in the cardiovascular control centre (brain) and reduce sympathetic nerve activity, decreasing blood pressure.

95
Q

Give an example of an a2-adrenergic agonist:

A

Clonidine-hypertension.

96
Q

Describe how a2-adrenergic antagonists affect vasculature smooth muscle:

A

Block presynaptic a2-receptors and increase NA release (sympathetic nerve activity) and can also block postsynaptic a2 receptors so responses are complex.

97
Q

Describe the effects of B1-adrenegeric agonists on the heart:

A

Increase contractility (postive inotrope) and increase heart rate (positive chronotrope). Increase CO and O2 consumption, but can cause disturbance of cardiac rhythm (ventricular fibrilation).

98
Q

Name two B1-adrenergic agonists and describe their effects on the heart:

A
  1. Dobutamine (cardiogenic shock) has a strong inotropic effcts but little chronotropic effect, leading to increased CO but not much effect on HR.
  2. Adrenaline- intravenous for cardiac arrest.
99
Q

Name two B1-adrenergic antagonists and describe why they are used:

A

Propanolol- B1 and B2.
Atenolol- B1 selective.

Used for cardiac dysrhythmias, myocaridal infarction, heart failure, agina pactoris, hypertension.

100
Q

What do the effects of B1-adrenergic antagonists depend on, and what is an example of this occuring?

A

The effect depends on the degree of sympathetic activity, so has little effect at rest.

At rest, propanolol produces minimal changes in heart rate, cardiac output or blood pressure but causes these to decrease when coupled with exercise or excitement.

101
Q

What is an unexpected effect of B-blockers, and how does this work?

A

An unexpected effect is that the B-blockers lower blood pressure in hypertensive patients. This mechanism involves reduction in CO, reduced sympathetic activity (central actions), reduction in renin release from the kidney.

However, there is no hypotension in normal patients.

102
Q

Describe the effects of B2-adrenergic agonists on bronchial smooth muscle:

A

Stimulate the relaxation of smooth muscle.

103
Q

Give two examples of B2-adrenergic agonists acting on bronchial smooth muscle and their effects:

A
  1. Salbutamol- treatment of asthma (bronchodilator), or used to realx uterine smooth muscle to delay premature labour.
  2. Adrenaline- used in anaphylactic reaction to help breathing, but has cardiac side effects.
104
Q

Describe how B2-adrenergic antagonists act on bronchial smooth muscle:

A

Triggers bronchial constriction (so no clinical application).

105
Q

Describe the effects of B adrenergic agonists on metabolism:

A

Encourage conversion of energy stores (glycogen, fat) to freely available fuels such as glucose and FFAs.

106
Q

What may B3 agonists treat?

A

Obesity

107
Q

What role does Rauwolfia play in NA modulation?

A

It blocks the transport of NA into vesicles so NA accumulates in the cytoplasm (broken down by MAO), causing tissue NA levels to decrease and no neurotransmission occurs.

108
Q

What is an adverse effect of Rauwolfia that prevents it from being used as an anti-hypertensive drug?

A

Depletes 5HT and dopamine levels, so it can induce depression.

109
Q

Name two sympathomimetics which act indirectly to effect NA release:

A

Ampetamine, ephedrine.

110
Q

How do sympathomimetics function?

A

They are transported into the nerve terminals by uptake 1 and displace NA from the vesicle. This NA is then broken down by MAO or diffuses out, causing receptor activation.

111
Q

In addition to acting as a sympathomimetic, what does NA do?

A

Reduces NA reuptake by the transporter, so action of released NA is enhanced.

112
Q

What would happen to NA levels in the synapse if an MAO inhibitor was given alongside a sympathomimetic?

A

They would increase.

113
Q

What would happen to Na levels in the synapse if rauwolfia was given alongside a sympathomimetic?

A

There would be little to no change.

114
Q

What are some peripheral effects of sympathomimetics?

A

Bronchodilation, increased heart rate and force of myocardial contraction, peripheral vasoconstriction, tachycardia, inhibition of gut motility.

115
Q

What are some CNS effects of sympathomimetics?

A

Euphoria, excitement, wakefulness and increased attentiveness, as well as loss of appetite. Unfortunately these are highly addictive.

116
Q

How do inhibitors of NA uptake work?

A

They block the NA uptake nerve terminal such as desipramine (used to treat depression), and cocaine (local anesthetic) which causes tachycardia, increased arterial pressure and CNS effects of (euphoria and excitement).

Medsci 204 (8 decks)

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