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Semester 2 > M&R Session 10 > Flashcards

M&R Session 10 Flashcards

1
Q

Is the ANS efferent, afferent or both?

A

Entirely efferent

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2
Q

What type of input regulates the ANS?

A

Afferent inputs

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3
Q

Where do parasympathetic nerves originate from?

A

Lateral horn of medulla and sacral spinal cord

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4
Q

Describe parasympathetic pre-ganglionic neurones.

A

Long

Myelinated

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5
Q

Describe parasympathetic post-ganglionic neurones.

A

Short

Unmyelinated

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6
Q

Where are the ganglia in the parasympathetic division of the ANS?

A

Target tissues

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7
Q

Where do sympathetic nerves originate in the sympathetic nervous system?

A

Lateral horn of lumbar and thoracic spinal cord

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8
Q

Describe sympathetic preganglionic nerves.

A

Short

Myelinated

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9
Q

Describe sympathetic postganglionic nerves.

A

Long

Unmyelinated

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10
Q

Where are sympathetic ganglia found?

A

Paravertebral chain

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11
Q

Which neurotransmitter is used in all preganglionic neurones?

A

ACh

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12
Q

What type of receptors are found on postganglionic neurones in both the sympathetic and parasympathetic nervous systems?

A

Nicotinic AChR

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13
Q

Which neurotransmitter and corresponding receptor do postganglionic parasympathetic neurones use?

A

ACh

mAChR

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14
Q

Which type of neurotransmitter and corresponding receptor do postganglionic sympathetic neurones utilise?

A

NA

Alpha and beta adrenoceptors

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15
Q

How may genes code for adrenoceptors in the human genome?

A

9

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16
Q

Are all sympathetic postganglionic neurones noradrenergic?

A

Nope

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17
Q

Which sympathetic postganglionic neurones are cholinergic?

A

Sweat glands

Piloerector muscles

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18
Q

When can NANC transmitters be released?

A

Coreleased w/NA or ACh

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19
Q

Give four examples of NANC transmitters.

A

ATP
Nitric oxide
5-hydroxytryptamine
Neuropeptide

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20
Q

How is ATP used as a NANC transmitter?

A

Copackaged into vesicles, especially w/NA

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21
Q

What does ATP use as a NANC transmitter regulate?

A

BP

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22
Q

Give two examples of neuropeptides used as NANC transmitters.

A

Vasoactive intestinal peptide

Substance P

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23
Q

What do sympathetic postganglionic neurones in the adrenal glands differentiate to form?

A

Neurosecretory chromaffin cells

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24
Q

What is the function of chromaffin cells?

A

Release adrenaline into blood

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25
Q

What type of receptors are found in chromaffin cells?

A

nAChR

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26
Q

Which area/s of the heart does parasympathetic ACh release act on?

A

Atria - sparse if any input to ventricles

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27
Q

What two effects does activation of M2 receptors by ACh have in the heart?

A

SAN –> bradycardia

AVN –> decrease cardiac conduction velocity

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28
Q

Which receptor subtype is found in the lungs and GI tract and is activated by ACh?

A

M3

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29
Q

What is the affect of ACh release on the lungs and GI tract?

A

Lungs - bronchial contraction

GI - increased mobility and secretion

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30
Q

What are the effects of ACh release on the GU tract?

A

Bladder contraction
Sphincter relaxation
Penile erection (increased bloodflow)

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31
Q

What is the affect of ACh release on the eye?

A

Ciliary muscle and iris sphincter contraction

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32
Q

What causes the increase in bloodflow which causes penile erection?

A

Nitric oxide

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33
Q

Which receptor type is found in glandular tissue which is activated by ACh release?

A

M1/3

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34
Q

What is the affect of M1/3 activation by ACh in glandular tissue?

A

Control level and composition of secretion

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35
Q

Which component of the lungs, GI tract, GU tract and eye is affected by ACh release?

A

Smooth muscle

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36
Q

What does the ANS exist in parallel but separate to?

A

Somatic nervous system

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37
Q

What effects does NA release have on the heart?

A

SAN –> +ve chronotropy

Ventricle –> +ve inotropy

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38
Q

Which receptors are activated in the heart by NA?

A

Beta-1 (mainly)

Beta-2

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39
Q

What does the balance of beta-1 and beta-2 receptors in the heart depend on?

A

The individual

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40
Q

What affect does NA release have on the smooth muscle of the vasculature?

A

BV contract

Arteriolar relaxation in some vascular beds

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41
Q

What type of receptors constrict visceral BV upon NA release?

A

Alpha-1

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42
Q

What type of receptors dilate BV in exercising tissue?

43
Q

What subtype/s of receptor cause smooth muscle relaxation in the lungs, GI tract and GU tract upon NA release?

A

Beta-2

Beta-3

44
Q

What does the activation of receptors (thought to be beta-3) in the GU by NA cause the bladder sphincter to do?

45
Q

What does alpha-1 activation by NA cause in the eye?

A

Radial muscle contraction

46
Q

What increases viscous secretion in the salivary glands?

A

NA release

47
Q

What causes renin release in the kidney?

A

NA release

48
Q

How is the prostate gland innervated by the ANS?

A

Parasympathetic on epithelial cells controlling generation of secretion
Sympathetic on smooth muscle contraction –> release of secretory products

49
Q

What additional medication were prostate cancer patients with a better prognosis noted to be taking?

A

Beta-blockers

50
Q

What is seen in all prostate cancers irrespective of age of patient that affects the rate of development and metastasis?

A

Neurogenesis

51
Q

What constantly modulates efferent ANS neurone activity?

A

Afferent/sensory ANS inputs

52
Q

What monitors carbon dioxide, oxygen, arterial pressure, GI tract content and chemical composition?

A

Sensory neurones

53
Q

What is sensed by the carotid body/ chemoreceptors at carotid artery bifurcation?

A

Blood oxygen, carbon dioxide and pH

54
Q

How are the inputs to the carotid body/ chemoreceptors at carotid artery bifurcation coordinated?

A

Glossopharyngeal nerve –> CNS

55
Q

What forms the nucleus tractus solitarius (nTS)?

A

Primary sensory neurones acting on second order sensory neurones in medulla oblongata

56
Q

What is the function of area postrema?

A

Detect toxins in blood and CSF
Essential for chemical-induced vomiting
Essential for conditional taste aversion

57
Q

What integrates all visceral afferent information?

A

Nucleus tractus solitarius

58
Q

What are the 12 basic steps in neurotransmission?

A 
Uptake of precursors
Synthesis of transmitter
Vesicular storage of transmitter
Degradation of transmitter
Depolarisation by propagated AP
Depolarisation-dependent influx of calcium ions
Exocytotic release of transmitter
Diffusion to post-synaptic membrane
Interaction w/ post-synaptic receptors
Inactivation of transmitter
Re-uptake of transmitter
Interaction w/pre-synaptic receptors
59
Q

Which steps of neurotransmission can be targeted by drugs?

A 
Degradation of neurotransmitter
Interaction w/post-synaptic receptors
Inactivation of transmitter
Re-uptake of transmitter
Interaction w/pre-synaptic receptors
60
Q

Why is degradation of ACh immediate?

A

Abundance of AChE

61
Q

What can be used to irreversibly inhibit AChE in terrorist attacks?

62
Q

How is ACh formed?

A

Acetyl CoA + choline –> ACh + CoA

Uses choline acetyltransferase (CAT)

63
Q

Where can cholinergic function be manipulated in the ANS?

A

Ganglia

Effector - especially parasympathetic branch

64
Q

What does interfering with the cholinergic function at the ganglia of the ANS effectively do?

A

Switch off ANS

65
Q

Why can nAChR at autonomic ganglia be targeted and the nAChR at the NMJ be unaffected?

A

Different receptor structures

66
Q

What is Trimethapan?

A

Ganglion-blocking drug used in hypertensive emergencies and when hypotension is needed during surgery

67
Q

How many mAChR subtype specific agonists or antagonists are currently available clinically?

A

Only a few

68
Q

What is Tolterodine?

A

mAChR antagonist used to treat an overactive bladder w/limited tissue selectivity

69
Q

How can endogenous ACh release be enhanced?

A

AChE inhibitors

70
Q

Pyridostigmine and Donepezil are AChE inhibitors. What are they used to treat?

A

Pyridostigmine - myasthenia gravis

Donepezil - Alzheimer’s

71
Q

What often has to be given with a mAChR agonist to prevent unwanted side effects caused by low specificity?

A

Antagonist

72
Q

How can low specificity mAChR agonists and antagonists be used effectively clinically?

A

Administer locally not systemically

73
Q

How are mAChR agonists pilocarpine and bethanechol used to treat glaucoma and to stimulate bladder emptying respectively?

A

Used w/pharmacodynamics to localise drug effects

74
Q

What are mAChR antagonists ipratrapium and tiotropium used to treat?

A

Asthma

COPD

75
Q

What are Tolterodine, clarifenacin and oxybutynin?

A

mAChR antagonists used to treat an overactive bladder

76
Q

What do postganglionic sympathetic neuron axons form to allow for specialised sites of calcium-dependent NA release?

A

Highly branched atonal network w/numerous varicosities which are regularly arranged
(Beads on a string)

77
Q

What do varicosities allow for?

A

Coordinated responses on a wide field of the effector organ

78
Q

Give the intermediates of noradrenaline synthesis

A

Tyrosine –> DOPA –> dopamine –> noradrenaline

79
Q

Which enzymes are needed for NA synthesis?

A

Tyrosine hydroxylase
DOPA decarboxylase
Dopamine beta-hydroxylase

80
Q

Which stage of NA synthesis takes place in the vesicle?

A

Conversion of dopamine to NA

81
Q

What type of receptor forms the auto-regulatory feedback system in NA release?

82
Q

How does alpha-2 activation prevent further NA release?

A

Beta-gamma subunits inhibit VOCCs

83
Q

How can DOPA be sued to treat Parkinson’s disease?

A

Delivered in pharmacokinetic protected dose

84
Q

How is NA release terminated?

A

Rapidly by Uptake 1
Rest by Uptake 2
Small amount escapes

85
Q

What is Uptake 1?

A

High affinity, sodium dependent NA transporter

86
Q

What percentage of released NA is recaptured by Uptake 1?

87
Q

What is Uptake 2?

A

Lower affinity, non-neuronal NA transporter protein

88
Q

Why can NA metabolism only occur after uptake?

A

Lack of extracellular enzymes

89
Q

What happens to the majority of NA uptaken after release?

A

~90% is repackaged into vesicles

90
Q

What happens to the NA uptake that is not repackaged into vesicles?

A

Metabolised by monoamine oxidase (MAO) or catechol-O-methyltransferase (COMT)

91
Q

What are tyramine, amphetamine and ephedrine examples of?

A

Indirectly acting sympathiomimetic agents

92
Q

How do indirectly acting sympathiomimetic agents intervene in adrenergic transmission?

A

Taken up into vesicles –> allow NA leak from vesicles and into synaptic cleft without influx of calcium ions

93
Q

What are tricyclic antidepressants and selective NA re-uptake inhibitors examples of?

A

Uptake 1 inhibitors

94
Q

Where do Uptake 1 inhibitors exert their major therapeutic action?

95
Q

What must be minimised by drug choice and dosage when using amitryptyline, imipramine or reboxetine for example?

A

Peripheral actions e.g. tachycardia and cardiac dysrhythmia

96
Q

What are salbutamol and salmeterol?

A

Beta-2 selective agonists used to treat asthma

97
Q

What are doxazosin and atenolol, drugs used for CVS disorders incl. hypertension?

A

Doxazosin - alpha-1 antagonist

Atenolol - beta-1 antagonist

98
Q

What are the NICE guidelines for treatment of chronic heart failure?

A

Beta blocker
ACEI
Diuretic

99
Q

What do the NICE guidelines for treatment of chronic heart failure using three classes of drugs cause?

A

Proven mortality and morbidity benefits

100
Q

Give three examples of proven efficacy drugs which are better than other types of beta-blockers for treatment of chronic heart failure.

A

Bisoprolol
Metoprolol
Carvedilol

101
Q

Which adrenoceptors do bisoprolol and metoprolol act on in chronic heart failure?

102
Q

Why is Carvedilol which acts on beta-1, beta-2 and alpha-1 receptors very effective?

A

Causes uniques adaptations to receptors not seen with other drugs

103
Q

How does the paradoxical increase in alpha-adrenoceptor subtypes seen when using Carvedilol to treat chronic heart failure present clinically?

A

Initially patients become very tired but a week later they are much better

104
Q

What percentage of the population is affected by chronic heart failure, which is classified as a disease of old age?

Semester 2 (45 decks)

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