Cholinergic system Flashcards

1
Q

what are the harmful effects of cholinergic?

A
  1. insecticides - organophosphate - target the cholinergic signalling -> increase Ach
  2. bioweapons - sarin - a nerve agent
  3. disease: AD, myasthenia gravies, sympathetic and parasympathetic modulation
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2
Q

where do you find these Ach receptors in the brain?

  1. muscarinic
  2. nicotinic
  3. muscarinic + nicotinic
A
  1. muscarinic - midbrain, medulla, pons
  2. nicotinic - substantia nigra, locus corelrulus, septum
  3. muscarinic + nicotinic - cerebral cortex, corpus striatum, thalamus, hypothalamus, hippocampus, cerebellum
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3
Q

where does the Ach acts in the somatic and autonomic nervous system?

A

somatic - skeletal muscle

autonomic - sympathetic + parasympathetic - smooth muscle (blood vessel), glands, cardiac muscle

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4
Q

what is the main function of sympathetic and parasympathetic?

A
  • sympathetic: fight, flight and fright (freeze)

- parasympathetic- feed and breed, rest and digest

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5
Q

what is the difference between nicotinic and muscarinic receptors?

  1. agonist
  2. antagonist
  3. receptor type
  4. ion channel feature
  5. targets
  6. signal type
  7. mode of action at synapse
A
1. agonist -
N - nicotine 
M - muscarine 
2. antagonist 
N - competitive - curare
M - inverse - atropine
3. receptor type 
N - inotropic 
M - metabotropic 
4. ion channel feature
N - fast, brief, ms
M - slow prolonged, s
5. targets 
N - NMJ, autonomic ganglia, some CNS
M - myocardial and some smooth muscle (inhibitory), CNS
6. signal type 
N - excitation 
M - excitation + inhibition 
7. mode of action at synapse 
N - post-synaptic but now pre-synaptic in CNS
M - pre and post-synaptic
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6
Q

why is the function of Ach in skeletal muscle?

A
  • somatic MN release ACh at NMJ

- net entry of Na+ through ACh receptors channel initiates a muscle AP

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7
Q

what is Ach synthesised from and what degrades them?

A

synthesised from - choline acetyl transferase enzyme (ChAT)

degraded by - choline esterase (AchE) at the synapse

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8
Q

what is myasthenia gravis and what causes it?

A
  • autoimmune disorder
  • increased muscle weakness upon activity
  • auto antibodies against Ach at the post synapse of nAchR
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9
Q

what is common b/w organophosphates, novichok and AD?

A
  • AchE activity blocked

- therefore, acculumuation of Ach at synapse -> chronic depolarisation

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10
Q

name an antidote and how is its mode of action different for nerve agents and in ageing

A

pralidoxime,
nerve agents - couples with it and displaces the nerve agent from the binding site
ageing - permanent binding

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11
Q

What symptoms would be expected from AchE inhibitors?

A

SLUDGEM
salivation, lacrimation, urination, defecation, gastrointestinal upset, emesis (vomiting), miosis (excess constriction of pupil)
MUDDLES
miosis, urination, diarrhea, diaphoresis (unusual excess sweating as symptom or drug side effect), lacrimation, excitation, and salivation

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12
Q

what are the drugs used for OP poisoning?

A
  1. atropine
  2. diazepam - reduces Ach release from synapse, anticonvulsant drug
  3. pralidoxime
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13
Q

how is AchE inhibitor used in MG?

A

Use to prolong Ach in NMJ to improve neuromuscular transmission

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14
Q

how is AchE inhibitor used in AD?

A
  • Cholinergic deficit in forebrain in AD.
  • AchE inhibitors potentiate Ach synapse levels, thus potentiate cholinergic action.
  • Donepezil (Aricept®), rivastigmine (Exelon®), and
    galantamine (Razadyne®).
  • Reversible and selective inhibitors of AchE.
  • Show temporary benefit 12-24 months.
  • Do not alter the course of the disease
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