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Neuropharmacology > Lecture 5 > Flashcards

Lecture 5 Flashcards

1
Q

What precursors are used to synthesise ACh?

A
  • choline - acetyl coenzyme A
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2
Q

What enzyme synthesise ACh?

A

Choline acetyltransferase (ChAT)

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3
Q

What have amyloid proteins been implicated with?

A

Inhibiting ChAT in patients with Alzheimer’s disease

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4
Q

What is choline uptake blocked by?

A

Hemicholinium 3 (HC-3)

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5
Q

Is hemicholinum 3 competitive or non-competitive

A

Competitive

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6
Q

What is uptake and storage blocked up?

A

Vesamicol

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7
Q

How does tetrodotoxin work?

A
  • blocks voltage gated Na+ channels - inhibits action potentials - no ACh release
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8
Q

How do conatoxins work?

A
  • blocks P/Q and N type voltage gated Na+ channels - inhibits Ca2+ influx - no ACh release
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9
Q

How do dendrotoxins work?

A
  • block voltage-gated K+ channels - prolongs Ca2+ influx - increased ACh release
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10
Q

How does ziconotide work?

A
  • selective N-type voltage-gated Ca2+ channel blocker - given via intrathecal route to manage severe pain
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11
Q

Mechanisms of botulinum toxin action

A

-blocks vesicular release of ACh causing flaccid paralysis - binds to exposed synaptotagmin (Ca2+ sensor) - light chain (a protease) cleaves from heavy chain and attacks SNARE proteins (SNAP-25, syntaxin or synaptobrevin) at a neuromuscular junction - preventing vesicles from anchoring to the membrane to release ACh

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12
Q

What are the effects of botulinum toxin?

A
  • treats dystonias= muscular spasms e.g. belpharospasm (eye muscules) - treats muscle spasticity, tremor - treats sialorrhea (drroling), hyperhidrosis (sweating - cosmetic uses
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13
Q

what do miniature end-plate potentials (MEPP) represent?

A

The release of a single quanta of vesicular content at the NMJ

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14
Q

What does 𝛼-latrotoxin do?

A
  • initial excess ACh release= muscle spasms - afterwards distends nerve terminals - depletion of vesicle pool, desensitisation and inhibition of endocytosis= paralysis
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15
Q

Is the release between synaptic vesicles and quantum of chemical transmitter equivalent or not?

A

Equivalent

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16
Q

How does 𝛼-latrotoxin work?

A
  • dimers= promotes and enhances Ca2+ release - tetramers= embeds itself into channel and is Ca2+ permeable
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17
Q

what do miniature end-plate potentials (MEPP) become?

A

End plate potential (EPP)

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18
Q

What happens if an (EPP) is large enough?

A

Initiate an action potential causing muscular contraction

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19
Q

What enzyme terminates ACh at the NMJ?

A

Acetylcholinesterases (AChE)

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20
Q

What are anticholinesterases?

A

Drugs that inhibit AChE

21
Q

What do anticholinesterases do?

A
  • increase concentration and effects of ACh - can cause muscle spasms
22
Q

What is an example of a competitive non-depolarising blocker?

A

Tubocurarine

23
Q

What happens when you use a competitive blocker with an anticholinesterase?

A
  • anticholinesterase increases the concentration of agonists - regular muscle response returns
24
Q

Is this the action of a competitive or irreversible blocker?

A

Competitive non-depolarising blocker

25
Q

What is an example of an irreversible non-depolarising blocker?

A

𝛼-bungarotoxin

26
Q

What happens when you use a irreversible blocker with an anticholinesterase?

A
  • no effect - even increasing the agonist concentration cannot outcompete the irreversible blocker
27
Q

Is this the action of a competitive or irreversible blocker?

A

Irreversible non-depolarising blocker

28
Q

Names examples of competitive non-depolarising blockers

A
  • tubocurarine - vecuronium - rocuronium
29
Q

What are the side effects of tubocurarine?

A
  • decreased BP due to ganglion block - resultant vasodilation - respiratory paralysis
30
Q

Why would you use vecuronium and rocuronium over tubocurarine?

A
  • fewer side effects - rocuronium is rapid in onset
31
Q

What are competitive blockers reversed by?

A

Anticholinesterases e.g. neostigmine

32
Q

What are the two stages that occur from depolarising blockers ?

A
  • Phase I block - Phase II block
33
Q

What happens in Phase I block?

A
  • persistent activation of endplate nAChRs - prolonged desensitisation of endplate - inactivation of voltage-gated Na+ channels
34
Q

What happens in Phase II block?

A
  • desensitisation of endplate nAChRs - repolarisation of endplate - receptor desesnitisation maintains blockade
35
Q

What is an example of a depolarising blocker?

A

Suxamethonium

36
Q

Why would you use suxamethonium clinically?

A
  • rapid onset of paralysis - short duration (broken down by plasmacholinesterases) - tracheal intubation - electroconvulsive therapy
37
Q

What are the side effects of suxamethonium?

A
  • bradycardia= M2 mAChR activation - K+ release in trauma (e.g. burns)= cardiac dysrythmias and arrest - prolonged paralysis (1:3500 people)
38
Q

What are the subtypes of ganglionic nicotinic receptors?

A
  • 𝛼 (primarily 𝛼3) - β (primarily β4)
39
Q

What are the effects of ganglionic blockers?

A

Reduced actions of both the sympathetic and parasympthetic nervous systems

40
Q

What are examples of irreversible ganglionic antagonists?

A
  • 𝜅-bungarotoxin - hexamethonium - tubocurarine
41
Q

What are examples of competitive ganglionic antagonists?

A

Trimethaphan

42
Q

Why would you use trimethaphan?

A

Occasionally used in surgery for controlled hypotension and hypertensive crises

43
Q

How does hexamthonium and tubocurarine work at the ganglion?

A

Drug sits in channel like plug in a bottle

44
Q

What would you use hexamthonium for?

A

Hypertension

45
Q

What are the side effects of hexamethonium?

A
  • dry mouth and skin - blurred vision - constipation - urinary retention - postural hypotension
46
Q

What are examples of ganglionic agonists?

A
  • nicotine - lobeline
47
Q

How do nicotine and lobeline work at the ganglion?

A
  • repeatedly stimulate receptors - inactivate voltage-gated Na+ channels - desensitise nAChRs
48
Q

Would suxamethonium generate an effect at ganglionic nAChR?

A

No

Neuropharmacology (15 decks)

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