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Neuropharmacology & Neuroscience > Autonomic Pharmacology > Flashcards

Autonomic Pharmacology Flashcards

1
Q

The first neuron in efferent autonomic pathways uses which receptor?

A

nACh

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2
Q

Which sympathetic pathway only has 1 neuron instead of 2?

A

The chain to the adrenal medulla

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3
Q

Which spinal segments do parasympathetic nerves arise from?

A

Cranial and sacral

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4
Q

Which spinal segments to sympathetic nerves arise from?

A

Thoracic and lumbar

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5
Q

Where are the sympathetic ganglia found?

A

In the sympathetic chain close to the spine

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6
Q

Where are the parasympathetic ganglia found?

A

Close to the target organ rather than the spinal cord

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7
Q

When are the sympathetic and parasympathetic NS not working in opposition?

A

1) When only one of them innervates a tissue
2) They induce complimentary effects such as ejaculation and erection
3) They have a similar effect, only to different extents

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8
Q

What type of receptors are nicotinic?

A

ionotropic

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9
Q

Are nicotinic receptors the same everywhere?

A

No, there are different variations at the neuromuscular junction (Nm) and in nerves (Nn)

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10
Q

What type of receptors is muscarinic?

A

Metabotropic

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11
Q

Where are only M1 subtype receptors found?

A

Autonomic ganglia

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12
Q

Where are only M2 subtype receptors found?

A

Heart

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13
Q

Where are only M3 subtype receptors found?

A

Smooth muscle and secretory glands

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14
Q

Where are M1,2,3,4 and 5 subtype receptors found?

A

In the CNS

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15
Q

Which second messenger do M1,3 and 5 use?

A

Gq GPCR which activates PLC which activates IP3 and DAG

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16
Q

Which second messenger do M2 and 4 use?

A

Gi GPCR which inhibits Adenylyl cyclase

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17
Q

What is the pathway from Tyrosine to Adrenaline?

A

Tyrosine> DOPA> Dopamine> Noradrenaline> Adrenaline

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18
Q

What effect does DOPA have on tyrosine?

A

Inhibitory effect as a part of the negative feedback loop

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19
Q

What is the rate-limiting step in adrenaline synthesis?

A

Tyrosine concentration

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20
Q

Which enzyme catalyses tyrosine to DOPA?

A

Tyrosine hydroxylase

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21
Q

Which enzyme catalyses DOPA to dopamine?

A

DOPA decarboxylase

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22
Q

Which enzyme catalyses dopamine to noradrenaline?

A

Dopamine beta-hydroxylase

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23
Q

Which enzyme catalyses noradrenaline to adrenaline?

A

Phenylethanolamine N-methyltransferase (PNMT)

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24
Q

In order for a cell to produce only noradrenaline and not adrenaline what must it do?

A

Not express PNMT

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25
Q

Where is PNMT expressed?

A

In the adrenal medulla

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26
Q

Where is PNMT NOT expressed?

A

Adrenergic neurons

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27
Q

What is the first method of noradrenaline uptake?

A

Uptake 1- Presynaptic uptake

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28
Q

What are the characteristics of presynaptic uptake of NA

A

Monoamine oxidase has a HIGH affinity but a low maximal rate of reabsorption

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29
Q

What is the second method of noradrenaline uptake?

A

Uptake 2- Postsynaptic uptake

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30
Q

What are the characteristics of postsynaptic uptake?

A

COMT has a LOW affinity but a HIGH maximal rate of reabsorption

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31
Q

With regards to NA uptake, what are good drug targets?

A

COMT and MOA

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32
Q

Where are beta 1 receptors found?

A

The heart

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33
Q

Where are beta 2 receptors found?

A

Smooth muscle

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34
Q

Which second messenger are beta receptors linked to?

A

Gs GPCR linked meaning they activate adenylyl cyclase

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35
Q

Which side of the synapse are alpha-1 receptors found?

A

Post junctional

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36
Q

Which second messenger do alpha-1 receptors use?

A

Gq GPCR which activates PLC

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37
Q

Which side of the synapse are alpha-2 receptors found?

A

Pre and post junctionally

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38
Q

Which second messenger do alpha-2 receptors use?

A

Gi GPCR which inhibits adenylyl cyclase

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39
Q

NA is stored presynaptically in vesicles. What else is stored in these vesicles with NA?

A

Chromogranin and ATP

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40
Q

What is the function of chromogranin?

A

Stabilises noradrenaline and prevents it from leaking out of the vesicles

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41
Q

What is the function of ATP in the vesicles?

A

Assists in signalling (mechanism uncertain)

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42
Q

What is the purpose of presynaptic alpha-2 receptors?

A

They detect critically high levels of NA and inhibit its release. Gi inhibits AC which prevents cAMP synthesis and subsequent PKC activation. This prevents the activation of Ca2+ pumps on vesicles which release NA

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43
Q

Why do adrenergic neurons express ACh receptors?

A

So that the sympathetic neurons (adrenergic) can be inhibited by parasympathetic neurons (cholinergic)

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44
Q

Why do cholinergic neurons express adrenoceptors?

A

So that the parasympathetic neurons (cholinergic) can be inhibited by sympathetic (adrenergic) neurons

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45
Q

What can muscle prostaglandins (PG) do to adrenergic neurons?

A

Inhibit them

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46
Q

What effect does nitrous oxide have on cholinergic neurons?

A

It can inhibit and activate them

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47
Q

What is pre-synaptic inhibition?

A

When the neuron inhibits itself

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48
Q

What is heterotrophic inhibition?

A

When one neuron inhibits another

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49
Q

What is post-synaptic synergism?

A

When neurotransmitters released from the same presynaptic membrane have a synergistic response (enhance each other’s effects)

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50
Q

What is the purpose of neuromuscular blockers?

A

To prevent signal transmission at the neuromuscular junction

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51
Q

Are depolarising NM blockers agonists or antagonists?

A

Agonists

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52
Q

Are non-depolarising NM blockers agonists or antagonists?

A

Antagonists

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53
Q

What is the naturally occurring example of a non-depolarising NM blocker?

A

Tubocurarine

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54
Q

Name 3 synthetic non-depolarising NM blockers.

A

Gallamine, Pancuronium and Atracurium

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55
Q

What do most synthetic non-depolarising blockers have in common?

A

They have a quarternary ammonium group that mimics that of acetylcholine

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56
Q

Which ACh receptor type does tubocurarine block?

A

nicotinic

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57
Q

How many receptors on a given neuron are required to be inhibited before it is functionally inhibited and what is the purpose of this?

A

> 90% of ACh receptors need to be blocked before the neuron cannot function. This significant redundancy prevents neurons from being easily blocked by a toxin

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58
Q

Typically, with non-depolarising Nm blockers, what are the first and last muscles to be affected?

A

The eyelids first and the respiratory muscles last

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59
Q

Do non-depolarising NM blockers have effects anywhere other than at the motor end plate?

A

Yes. Nicotinic receptors are expressed in autonomic ganglia and, therefore, it can inhibit certain autonomic functions

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60
Q

Typically, do non-depolarising or depolarising NM blockers have a shorter active period?

A

Non-depolarising Nm blockers do not typically display effects for as long as depolarising ones

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61
Q

Name some depolarising NM blockers.

A

Decamethonium, suxamethonium and succinylcholine

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62
Q

How do depolarising NM blockers work?

A

They bind to ACh N receptors at the NMJ and act as ‘hyper’ agonists, inducing receptor activity and depolarisation so much that the receptors cannot return to their ground state; the voltage-sensitive Na+ gates are inactivated. This means that it cannot then fire again.

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63
Q

As a result of the initial depolarisation with depolarising NM blockers, what happens to the muscles of some species?

A

It causes an initial muscle spasm before the paralysis kicks in

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64
Q

What is Phase I of depolarising NM blocker action?

A

The depolarising ‘spasm’ stage

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65
Q

What is Phase II of depolarising NM blocker action?

A

The receptors are desensitised preventing further depolarisation

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66
Q

Why do humans not display the same ‘spasm’ as some other species?

A

Species, such as chickens, have several neurons arriving at the motor end plate for each fibre whereas humans only have 1 neuron per fibre. This means the extent of depolarisation and electrical activity is much greater in chickens than in humans

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67
Q

Due to the increased permeability to ions caused by the depolarising NM blocker, what happens with respect to K+ ions?

A

They increase in concentration in the extracellular fluid and subsequent plasma

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68
Q

Does increased potassium permeability matter?

A

In healthy individuals, this change can easily be compensated by endogenous mechanisms. However, individuals who have a decreased sensitivity to potassium ions due to burns or trauma are at risk.

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69
Q

What does muscle denervation do to ACh receptors?

A

It causes ACh n receptors on muscles to spread at and away from the motor end plate making a larger surface area of the muscle susceptible to suxamethonium. This significantly increases the individuals sensitivity to the drug.

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70
Q

Name one disorder for which depolarising NM are ineffective for

A

Myasthenia Gravis. Antibodies bind to ACh n receptors preventing them from being used for neurotransmission.

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71
Q

Individuals with myasthenia gravis become more or less sensitive to non-depolarising NM blockers

A

Significantly more sensitive as they have a reduced number of functional ACh n receptors and, therefore, do not require as much of the drug to achieve >90% block.

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72
Q

Which reversal agents work for non-depolarising blockers?

A

AChease blockers. This allows ACh concentration to build up and competitively outcompete the non-depolarising NM blocker as the ligand.

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73
Q

What happens with AChease blockers and depolarising NM blockers?

A

They increase ACh concentration which can increase the effectiveness of the depolarising blockers (ACh is a also depolarising agent)

74
Q

What is mutual antagonism?

A

A depolarising agent works as a reversal agent for non-depolarising NMB and non-depolarising NMB work as a reversal agent for depolarising NMB. (They have inverse effects).

75
Q

Suxamethonium and decamethonium are selective for NMJ ACh Nm receptors, which drugs are not?

A

Nicotine and lobeline are agonists to nicotinic receptors in the autonomic ganglia as well as at the NMJ

76
Q

Can AChease degrade synthetic ligands?

A

Yes, but very slowly

77
Q

Does the length of the carbon backbone of a drug affect its selectivity to a receptor?

A

Yes

78
Q

What is the selectivity of a 6-carbon backbone drug (in the context of ACh receptors)?

A

They have a greater affinity for the receptors found in the autonomic ganglia (Nn)

79
Q

What is the selectivity of a > 10-carbon backbone drug (in the context of ACh receptors)?

A

They have a greater affinity for the NMJ receptors (Nm)

80
Q

What does hexamethonium block?

A

It selectively blocks ACh receptor channels.

81
Q

What do trimetaphan and mecamylamine block?

A

They selectively block ACh receptors (antagonist)

82
Q

What happens if you block autonomic ganglia with ACh blockers?

A

1) Decreased heart rate
2) Decreased gut motility
3) Increased bladder emptying

83
Q

If parasympathetic and sympathetic inhibition is in equilibrium, what will change in the body?

A

Nothing largely will change, however, postural reflexes in heart rate will not occur.

84
Q

Do drugs binding to ACh receptors need to ‘look’ like ACh?

A

No, Pilocarpine is structurally very different

85
Q

Where is oxotremorine most effective?

A

The CNS. It is not very effective in the PNS

85
Q

Name two drugs that block choline transport into the nerve terminal

A

Hemicholinium and triethylcholine

86
Q

How does hemicholinium block choline uptake?

A

Competitively inhibits it

87
Q

How does triethylcholine block choline to acetylcholine?

A

It is uptaken, acetylated, stored and released as a false neurotransmission instead of choline

88
Q

Comment on choline transport blocker onset

A

Slow but dependent on frequency of use of neuron

89
Q

Can choline transport blockers be reversed?

A

Yes, easily

90
Q

Which ion affects calcium ion channels in the nerve terminal?

A

Mg2+ competes for and blocks Ca2+ channels

91
Q

Which antibiotic affects calcium ion channels in the nerve terminal?

A

Aminoglycoside

92
Q

Where do calcium channel blockers exert their greatest effect?

A

The heart

93
Q

How does botulinum toxin produce an effect?

A

Deactivates molecules required for vesicles to duse with presynaptic membrane

94
Q

Which toxin works in a similar way to botulinum toxin?

A

Bungarotoxin

95
Q

Are nerve blocks still possible when AChE is inhibited?

A

Yes, a depolarising block is possible with the use of drugs such as suxamethonium

96
Q

Which functional group do all AChE inhibitors share?

A

Quarternary ammonium group

97
Q

The quarternary ammonium group of ACh and AChE inhibitors are attracted to which part of the AChE?

A

The anionic esteratic site

98
Q

What does the esteratic site do

A

Cleaves ACh to acetate and choline

99
Q

What are the three classes of AChE inhibitors?

A

Short-acting, medium-acting and irreversible

100
Q

Name a short-acting AChE inhibitor

A

Edrophonium

101
Q

Which type of bond do short-acting AChE inhibitors have?

A

Ionic

102
Q

When are short-acting AChE inhibitors used clinically?

A

Diagnostically, such as in the diagnosis for myasthenia gravis

103
Q

Name three medium-acting AChE inhibitors

A

Neostigmine, pyridostigmine and physostigmine

104
Q

What do medium-acting AChE inhibitors have instead of acetyl?

A

Carbamyl

105
Q

What makes medium-acting AChE inhibitors medium-acting?

A

The carbamyl takes longer to be broken down than the acetyl group, although it can be broken down eventually

106
Q

Which common chemical structure is found in irreversible AChE inhibitors?

A

Pentavalent phosphate

107
Q

What is a labile group?

A

A highly reactive and changeable group on a chemical

108
Q

What are examples of labile groups in irreversible AChE inhibitors?

A

Fluoride (Dyflos), parathion and ecothiapane (organic)

109
Q

How are AChE inhibitors usually administered?

A

Topically, to avoid systemic effects

110
Q

What central effects do organophosphates have?

A

Depressive effects

111
Q

What is the effect of organophosphates on the NMJ

A

Convulsive effects

112
Q

What is the general effect of organophosphates on the body?

A

Initial muscular convulsions followed by physical ssytemic depressive effects

113
Q

Can non-polar organophosphates cross the BBB?

A

Yes, this property allows them to be particularly effective in the CNS

114
Q

What longer-term effect do organophosphates have?

A

They can cause demyelination of nerves and the issues associated with that

115
Q

Which two drugs can be used in the treatment of organophosphate poisoning?

A

Atropine and pralidoxime

116
Q

Can atropine and pralidoxime cross the BBB?

A

Atropine can, pralidoxime cannot

117
Q

How does atropine help in organophosphate poisoning?

A

It antagonises the muscarinic receptors, preventing them from being overloaded by acetylcholine

118
Q

How does pralidoxime help in organophosphate poisoning?

A

It binds to the organophosphate residue in the esteratic site, substituting itself in so the AChE can be free

119
Q

Name 3 drugs that inhibit noradrenaline synthesis

A

Carbidopa, alpha-methyltyrosine and 6-hydroxydopamine

120
Q

How does carbidopa inhibit NA synthesis?

A

Blocking DOPA decarboxylase, blocking formation of NA precursor

121
Q

Can carbidopa cross the BBB?

A

no

122
Q

How does α-methyltyrosine inhibit NA synthesis?

A

It inhibits tyrosine hydroxylase from converting tyrosine to DOPA. α-methyltyrosine is converted to α-methyl DOPA then α-methyl NA

123
Q

What happens to α-methyl NA when it is released at the presynaptic membrane instead of NA?

A

It binds to and activates only the presynaptic α-2 receptors, initiating the negative feedback loop that ultimately inhibits NA signal transmission

124
Q

What does 6-hydroxydopamine do to dopaminergic and adrenergic neurons?

A

Gradually destroys the nerves of the sympathetic nervous system

125
Q

What is 6-hydroxydopamine used for?

A

Chemical sympathectomy

126
Q

Name a drug that affects noradrenaline storage

A

Reserpine

127
Q

How does reserpine prevent NA storage?

A

It blocks vesicles from accumulating NA

128
Q

Can reserpine cross the BBB?

A

Yes

129
Q

Comment on the selectivity of reserpine

A

It is highly unselective and can prevent the vesicular uptake of a number of neurotransmitters

130
Q

Name 2 adrenergic neuron blocking drugs

A

Guanethidine and bretyllium

131
Q

How fast do adrenergic neuron blockers act?

A

Slowly, they need to be uptaken to the vesicles and deplete NA stores. This means it is also slow to reverse them

132
Q

How do adrenergic neuron blockers act?

A

Prevent the NA vesicles from fusing with the presynaptic membrane

133
Q

Name 3 indirectly acting sympathomimetic amines (IDAS)

A

Tyramine, amphetamine and ephedrine

134
Q

Are IDAS specific?

A

They are highly unspecific

135
Q

How do IDAS have an effect?

A

They are uptaken by route 1 and replace NA in the storage vesicles.

136
Q

Name drugs which block uptake 1 of NA

A

Cocaine and tri-cyclic anit-depressants

137
Q

Name drugs which reduce uptake 1 of NA

A

Amphetamine, phenoxybenzamine and guanethidine

138
Q

Name drugs that block uptake 2

A

Phenoxybenzamine and corticosteroids

139
Q

What is structure activity function?

A

The concept of the structure of a molecule being used to predict its activity with regards to how it may bind to a receptor

140
Q

On a catecholamine, what is the effect of ‘bulking up’ the nitrogen atom?

A

It will become a β-agonist that is susceptible to MAO but resistant to uptake 1

141
Q

On a catecholamine, what is the effect of adding a methyl group?

A

It will become α-2 selective agonist that is resistant to MAO but susceptible to uptake 1

142
Q

On a catecholamine, what is the effect of removing OH groups?

A

It decreases its adrenergic action and moves it structurally closer to becoming dopamine

143
Q

On a catecholamine, what is the effect of modifying the catechol OH?

A

It will become a β-agonist and resistant to COMT and uptake 1

144
Q

On a catecholamine, what is the effect of adding an alkyl side chain extension, N - atom extensions and a catechol OH extension?

A

It will become a β-agonist

145
Q

On a catecholamine, what is the effect of removing all OH groups?

A

It will have no adrenergic receptor affinity, but it will be susceptible to uptake 1

146
Q

Name two β-agonists

A

Isoprenaline and salbutamol

147
Q

What is isoprenaline selective for
?

A

β-1 and 2

148
Q

What is salbutamol selective for
?

A

β-2 only

149
Q

Why is salbutamol still functional at lower doses?

A

It is resistant to COMT degradation

150
Q

Name three β-antagonists and one partial β-antagonist

A

Propranolol, atenolol and metoprolol
Oxorpenolol is the partial antagonist

151
Q

What is propranolol selective for?

A

β-1 and 2

152
Q

What are atenolol and metoprolol selective for?

A

β-1 only

153
Q

What is another term for β-1 selective antagonists?

A

Cardio selective β blockers

154
Q

When does oxprenolol act as an agonist and antagonist?

A

At rest, it acts as an agonist and during exercise, it acts as an antagonist

155
Q

What are β blockers used to treat?

A

Anxiety, tremor, migraine and angina

156
Q

What are some potential side effects of β blockers?

A

Bradycardia and bronchoconstriction

157
Q

Name two α-1 selective agonists

A

Methoxamine and phenylephrine

158
Q

What do α-1 selective agonists cause?

A

Vasoconstriction

159
Q

Name two α-2 selective agonists.

A

Clonidine and methylnoradrenaline

160
Q

What do α-2 selective agonists cause?

A

Reduce hypertension by reducing NA release

161
Q

What is the secondary mechanism of action of clonidine?

A

It prevents other agonists from binding to α receptors

162
Q

Comment on how structure-activity relationship applies to α antagonists

A

It does not apply as cleanly here, some molecules antagonise receptors despite not being structurally similar to the endogenous ligand

163
Q

What are the 4 heterogeneous classes of α antagonists

A

Ergot alkaloids, halo alkylamines, yohimbines and miscellaneous synthetic chemicals

164
Q

Where are ergot alkaloids naturally found?

A

Fungi

165
Q

What is St. Anthony’s fire?

A

The intense peripheral vasoconstriction caused by ergot alkaloids

166
Q

Name an ergot alkaloid that is an α-antagonist and one that is a partial agonist

A

Dihydroergotamine is an antagonist and ergotamine is a partial agonist

167
Q

What are some functions of ergot alkaloids?

A

They act as adrenaline reversal agents as they suppress the pressor response

168
Q

Name a halo alkylamine α antagonist

A

Phenoxybenzamine

169
Q

What is special about one of the functional groups on PBZ?

A

It has a highly unstable chloroethyl group, which easily covalently binds to substrates

170
Q

Comment on the specificity of halo alkylamines

A

They are not selective antagonists for only α receptors; they show effects at histamine, serotonin and cholinergic receptor sites

171
Q

What systemic effects can halo alkylamines cause?

A

A drop in arterial blood pressure

172
Q

What is yohimbine selective for?

A

It is a selective α-2 antagonist

173
Q

How does it exert its effect?

A

It binds to presynaptic α-2 receptors and thus blocks the mechanism that decreases NA release

174
Q

What is the systemic effect of yohimbine?

A

The increased NA release causes vasodilation

175
Q

Phentolamine is a miscellaneous synthetic α antagonist, comment on its selectivity

A

It is selective for both α- 1 and 2

176
Q

What is phentolamine structurally similar to?

A

PBZ, except it binds reversibly

177
Q

Prazosin and indoramide are also miscellaneous synthetic α antagonists, comment on their specificity

A

They are α-1 selective only

178
Q

Comment on the specificity of labetalol

A

It is a mixed α and β antagonist (blocker)

179
Q

Why are sympathetic blockers not commonly used clinically?

A

They are not particularly effective at reducing B.P and come with the side effect of increasing gut motility (leading to diarrhoea)

Neuropharmacology & Neuroscience (10 decks)

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