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Cardiovascular, Renal & Peripheral Nervous System Pharmacology > Peripheral Nervous System Pharmacology > Flashcards

Peripheral Nervous System Pharmacology Flashcards

1
Q

What does the Peripheral Nervous System do?

A

Conveys signals between the CNS and tissues

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2
Q

Describe “afferent” input.

A

Signal from the tissue(s) back to the CNS via somatic afferents (skeletal muscle) and visceral afferents (internal organs)

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3
Q

Describe “efferent” output.

A

Signals from the CNS back to the tissues via somatic motor neuron (mainly muscles and glands) and autonomic neurons (influences internal organs).

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4
Q

What are the three branches of the Autonomic Nervous System?

A

Sympathetic, Parasympathetic and Enteric.

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5
Q

What are the functions of the Autonomic Nervous System?

A
  1. Contraction and relaxation of smooth muscle in Blood Vessels & organs
  2. Regulation of glandular secretion
  3. Control of heart rate
  4. Metabolism
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6
Q

What actions are only governed by the sympathetic branch of the ANS?

A
  1. Sweat glands

2. Dilation or Constriction of blood vessels

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7
Q

What action is only governed by the parasympathetic branch of the ANS?

A

Contraction or relaxation of the ciliary muscle of the eye.

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8
Q

What action is common upon stimulation of both sympathetic and parasympathetic neurons?

A

Salivation.

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9
Q

In a pre-ganglionic fibre, what neurotransmitter is released and where does it act upon?

A

Acetyl Choline, and it acts upon the nicotinic receptor on the post-ganglionic neuron.

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10
Q

How many classes of nicotinic receptors are there and what are they?

A

3, and they are:

  1. Muscle
  2. Neuronal in the CNS
  3. Neuronal in autonomic ganglia
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11
Q

How many subunits make up a nicotinic receptor and state what the autonomic ganglia is compromised of.

A

5 (Pentamer), and autonomic ganglia is compromised of (α3 x 2)+(β4 x 3)

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12
Q

What physiological actions are there as a consequence of nicotinic receptor stimulation in the periphery?

A
  1. Stimulation of voluntary muscle
  2. Stimulation of autonomic ganglia (Parasymp & Symp)
  3. Secretion of ADRENALINE from the Adrenal Medulla
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13
Q

What happens when nicotinic receptor are stimulated in the periphery?

A

Sympathetic stimulation dominates and so blood pressure and heart rate increase

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14
Q

Name three drugs which stimulate autonomic ganglia.

A

Nicotine, Dimethylphenylpiperazinium (DMPP), Acetyl Choline (ACh)

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15
Q

What are the effects of stimulating all peripheral ganglia?

A
  1. Tachycardia
  2. Increase in blood pressure
  3. Increase in secretions such as sweat and salivation
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16
Q

There are many effects of ganglion blocking drugs, but the most significant are the cardiovascular effects. What are they?

A
  1. Fall in blood pressure due to inhibition of sympathetic tone (vasodilation)
  2. Postural Hypotension, loss of sympathetic vasoconstrictor activity upon standing.
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17
Q

Most post-synaptic sympathetic fibres release Noradrenaline (NA). However, there are a few exceptions. What are they?

A
  1. Sweat glands (releases ACh)

2. Renal vessels (releases Dopamine)

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18
Q

Describe the process of heterotropic inhibition using examples.

A

When one presynaptic ganglion inhibits another with a different neurotransmitter. For example, NA will inhibit ACh and vice versa.

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19
Q

Describe the process of homotropic inhibition using examples.

A

When a neurotransmitter will autoinhibit itself at the origin of its release. For example, NA will act on its α2 receptor to provide autoinhibitory feedback.

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20
Q

What is a co-transmitter?

A

A co-transmitter is a substance released at the same neurons as ACh/NA to modulate as a form of modulation.

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21
Q

Most sympathetic post-synaptic fibres release which neurotransmitter?

A

Noradrenaline (NA)

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22
Q

Outline the synthesis of Noradrenaline from the amino acid Tyrosine INCLUDING the enzymes.

A
  1. Tyrosine –> L-DOPA (catalysed by Tyrosine Hydroxylase)
  2. L-DOPA –> Dopamine (catalysed by DOPA Decarboxylase)
  3. Dopamine –> Noradrenaline (catalysed by Dopamine β-Hydroxylase)
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23
Q

Which drug can inhibit the initial enzyme in the synthesis of Noradrenaline?

A

α-methyl-p-tyrosine

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24
Q

Which drug inhibits the enzyme DOPA Decarboxylase (the second stage enzyme in the synthesis of Noradrenaline)?

A

Carbidopa

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25
Q

How are NA vesicles released?

A

Depolarised nerve endings opens VGCCs (Voltage Gated Calcium Channels) which leads to exocytosis.

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26
Q

What is the name of the false precursor used to inhibit the synthesis of Noradrenaline?

A

Methyldopa (is also an α2 agonist which encourages autoinhibition)

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27
Q

Respectively, what are the enzymes which breakdown NA in the neuron cytoplasm and take up NA into vesicles?

A

Monoamine Oxidase (MAO) and Vesicular Monoamine Transporter (VMAT)

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28
Q

How is released Noradrenaline taken up into the pre-synaptic fibre?

A

Neuronal Epinephrine Transporter (NET) (otherwise known as UPTAKE1)

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29
Q

How is released Noradrenaline taken up into the post-synaptic fibre?

A

Extraneuronal Monoamine Transporter (EMT) (otherwise known as UPTAKE2)

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30
Q

How does the drug Guanethidine work?

A

Substrate for both NET and VMAT, so it blocks depolarisation at the nerve terminal and displaces NA slowly

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31
Q

How does Reserpine work?

A

It inhibits VMAT, therefore causing NA to be left in the neuronal cytoplasm, thus, being metabolised by MAO.

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32
Q

Noradrenaline transmission is terminated by two enzymes. What are they?

A 
Monoamine Oxidase (MAO)
Catechol-O-Methyl Transferase (COMT)
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33
Q

List the different adrenoceptors and their respective functions.

A

α1 - constricts MOST smooth muscles (except the GI tract, where it relaxes)
α2 - presynaptic inhibition of neurotransmitter release (AUTOINHIBITION)
β1 - increases heart rate and force of contraction
β2 - dilates/relaxes smooth muscle
β3 - thermogenesis in skeletal muscle

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34
Q

Adrenaline is slightly more potent at which adrenoceptors?

A

α2 and β2

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35
Q

α2 and the β adrenoceptors undergo which secondary messenger process?

A

Adenylyl Cyclase, ultimately phosphorylating a protein causing a cell response.

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36
Q

α1 undergoes which secondary messenger process?

A

Phospholipase C, catalysing PIP2 to IP3 causing calcium release and thus a cell response

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37
Q

Adrenaline (as a drug) can be used for what?

A

Cardiac Arrest

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38
Q

Dobutamine agonises at which receptor and what is its indication?

A

β1 and cardiogenic shock

39
Q

Salbutamol, Salmetarol, Formoterol and Terbutaline act at which receptor and for what indication?

A

β2 and asthma

40
Q

Phenylephrine acts at α1 receptors, but what is it used for?

A

Nasal Congestion

41
Q

Tyramine does what?

A

Releases NA

42
Q

Amphetamine is a sympathomimetic. What is its mechanism of action?

A

It releases NA from its vesicles and also inhibits the MAO enzyme.

43
Q

How does the drug of abuse, Cocaine, work?

A

Blocks the Neuronal Epinephrine Transporter (NET) thus increasing synaptic NA

44
Q

What do α1 antagonists cause?

A

Vasodilation, fall in arterial blood pressure.
Also, relaxes bladder smooth muscle and prostate capsule which is used in the treatment of urinary retention associated prostatic hypertrophy

45
Q

Yohimbine antagonises which adrenoceptor?

A

α2

46
Q

Phenoxybenzamine is used for which indication?

A

Phaeocytochromocytoma (catecholamine secreting tumour)

47
Q

Prazosin is used in the treatment of hypertension. Which receptor does it antagonise?

A

α1 (clue is ‘azosin’ in the drug name)

48
Q

Labetolol and Carvediol are mixed α/β antagonists. What are their respective indications?

A

Hypertension in pregnancy

Heart Failure

49
Q

What are the main effects of β-blockers?

A

Lowers the oxygen demand of the heart;
In heart disease, it has an antidysrhythmic effect;
Antihypertensive effect;
Prevents tremor (in skeletal muscle)
Reduces Renin release in juxtaglomerular apparatus (granular cells in the kidney)

50
Q

What are the unwanted effects of β-blockers?

A

Bronchoconstriction (β2)
Cardiac Failure
Bradycardia
Hypoglycaemia

51
Q

What is the clinical use of Propanolol?

A

Angina, Hypertension, Cardiac Dysrhythmia, Tremor, Glaucoma

52
Q

What do the Muscarinic Receptors: M1, M3 & M5 have in common?

A

They are Gq-coupled (PLC –> IP3 etc)

53
Q

What do the Muscarinic Receptors: M2 & M4 have in common?

A

They are Gi-coupled (AC -x-> cAMP etc)

54
Q

‘Muscarine Poisoning’ can be diagnosed with what symptoms?

A 
SLUDGE or DUMBBELS
S= Salivation
L= Lacrimation (tears)
U= Urination
D= Diarrhoea 
G= Gastric Upset
E= Emesis (vomiting)
D= Diarrhoea
U= Urination
M= Miosis (pinpoint pupils)
B= Bradycardia
B=Bronchoconstriction 
E= Emesis
L= Lacrimation
S= Salivation
55
Q

What are the symptoms of muscarinic antagonists?

A 
Inhibitions of secretions
Tachycardia
Mydriasis (widened pupils)
Inhibition of GI motility 
Smooth muscle relaxation 
CNS excitation 
Bronchodilation
56
Q

Atropine, the non-selective muscarinic antagonist, has multiple side effects. What are they?

A

Urinary retention
Dry Mouth
Blurred Mouth
Constipation

57
Q

Scopolamine (Hyoscine) is clinically used as what?

A

An anti-emetic (for motion sickness)

58
Q

In what way is Ipratropium an inappropriate drug in terms of its activities on a receptor level?

A

The ipratropium blocks the M3 receptor - good
Ipratropium also blocks the M2 receptor which is the autoinhibitory receptor, therefore, more ACh is released in the synapse meaning that Ipratropium is only partially antagonising.

59
Q

How do Tiotropium and Ipratropium differ?

A

Ipratropium is non-selective and Tiotropium is M3 selective meaning that Tiotropium completely antagonises.

60
Q

What are the smooth muscles in the eye, and what are their respective functions?

A

Iris - regulates pupil size with sphincteric and radial muscles
Ciliary Muscle - Changes refractive index on lens and accommodates the eye

61
Q

How does parasympathetic innervation affect the iris?

A

Constricts the pupil by the CONTRACTION of the sphincteric constrictor smooth muscle causing MIOSIS (pinpoint pupils)

62
Q

How does sympathetic innervation affect the iris?

A

Pupil dilation by the CONTRACTION of the radial dilator smooth muscle causing MYDRIASIS (widened pupils)

63
Q

At “rest” (no stimulation), what shape is the lens in the eye?

A

Ellipse shape and the focus is distant.

64
Q

During parasympathetic innervation, what happens to the eye to give it a near-focus?

A

The ciliary muscle CONTRACTS and the suspensory ligaments SLACKEN, hence changing the shape of the lens to a sphere granting near focus.

65
Q

Glaucoma is usually as a cause of what?

A

Raised Intraocular Pressure

66
Q

Where is Aqueous Humour formed?

A

In the ciliary body epithelium.

67
Q

Describe the flow of the aqueous humour around the eye.

A

The Aqueous Humour is formed in the Ciliary Body. It then travels through the posterior chamber, through the iris, into the anterior chamber where it passes the trabecular network and then drained through one of two ways: Venous Drainage (90%), or Uveoscleral Outflow (10%)

68
Q

What FIRST LINE drug do we use to improve the uveoscleral outflow?

A

Prostaglandin Analogue - Latanoprost PGF2α

69
Q

Why do β-blockers inhibit aqueous humour formation?

A

Prevents adrenaline from binding to β-adrenoceptors. This prevents cAMP formation, which therefore prevents Aqueous Humour formation.

70
Q

Why do α1 agonists inhibit the formation of Aqueous Humour?

A

Vasoconstriction happens and therefore the blood supply the ciliary body is reduced, thus reducing capacity to formulate Aqueous Humour

71
Q

Why do α2 agonists inhibit the formation of Aqueous Humour?

A

AUTOINHIBITION through the inhibition of Adenlyl Cyclase, thus preventing the formation of cAMP and therefore Aqueous Humour

72
Q

What is the carbonic anhydrase inhibitor used for the prevention of glaucoma called?

A

Azetazolamide

73
Q

What is the neuromuscular junction?

A

A highly specialised synpase between the presynaptic motor neuron and the post synaptic muscle membrane

74
Q

Describe the process of Acetyl Choline biosynthesis

A

Acetate + CoEnzyme A (CoA) –> Acetyl CoA (enzyme: AcCoA synthetase) (in the mitochondrion)
Acetyl CoA + Choline (Ch) –> Acetyl Choline (enzyme: Choline Acetyltransferase)
Acetyl Choline –> Choline + Acetate (enzyme: Acetylcholinesterase)

75
Q

How is Acetyl Choline released?

A

An action potential leads to the depolarisation at the presynaptic nerve and causes calcium channels to open, thus leading to the exocytosis of the vesicles containing Acetyl Choline into the synapse

76
Q

Nicotinic receptors on skeletal muscle or what sort of channels?

A

Ligand-gated ion pentamer channel containing the subunits (α1x2), β, δ and γ

77
Q

How does a non-depolarising agent work?

A

Acts by blocking the ACh (competitive antagonist)

78
Q

How does a depolarisation blocking agent work?

A

weak agonists of ACh receptors

79
Q

Tubocurarine is what type of drug?

A

Non-depolarising agent

80
Q

How does α-bungarotoxin work?

A

Irreversibly binds to nicotinicACh receptors at the NMJ.

81
Q

Decamethonium and Suxamethonium are examples of which type of drugs?

A

Depolarising blocking agents. They give initial twitches, but linger at the ACh receptor site, preventing ACh from binding. Thus a response isn’t given.

82
Q

What are the side effects of Non-polarising agent?

A

Hypotension
Histamine release from mast cells
Respiratory failure
Tachycardia

83
Q

What are the side effects of depolarising-blocking agentss?

A

Bradycardia
K+ release
Increased intraocular pressure
Prolonged paralysis

84
Q

How does Hemicholinium work?

A

It acts as a competitive inhibitor of choline uptake into the presynaptic nerve.

85
Q

How does Vesicamol work?

A

It prevents Acetyl Choline transport into their synaptic vesicles.

86
Q

How does Triethylcholine work?

A

Its a false transmitter. It gets transported, acetylated and released, but has no effect.

87
Q

How do Mg++, Streptomycin and Neomycin work?

A

The are calcium channel inhibitors. Influc of Ca++ ions normally induces exocytosis, but inhibition of them coming in would prevent exocytosis, thus the release of ACh into the synapse.

88
Q

How do the Botulinium toxin and the β-bungarotoxin work?

A

They are neurotoxins which prevent the release of the vesicles into the synapse.

89
Q

Highlight the process of hydrolysis of Acetyl Choline with cholinesterase.

A
  1. Acetyl Choline binds to the anionic site of the enzyme via its CHOLINE MOIETY.
  2. The Acetyl group is transferred to the Serine-OH group. Choline is released.
  3. Acetyl-Serine is spontaneously hydrolysed to reveal the enzyme in its resting conformation.
90
Q

Edrophonium is an example of which type of drug, and how does said drug work? (Also, what is the disease it is used for?)

A

Edrophonium is a SHORT-ACTING ANTICHOLINESTERASE which means it forms a REVERSIBLE ionic bond with the anionic site of the cholinesterase. (Used for Myasthenia Gravis)

91
Q

Neostigmine and Physostigmine are what types of drug?

A

Medium-Duration Anticholinesterases, and they act by forming a carbamyl-complex rather than an acetyl-complex, which makes hydrolysis a lot slower.

92
Q

Dyflod and Sarin are what kind of drugs?

A

Irreversible Anticholinesterases. They act by covalently binding to the enzyme

93
Q

What is the antidote for Dyflos/Sarin poisoning?

A

Pralodoxime

Cardiovascular, Renal & Peripheral Nervous System Pharmacology (3 decks)

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