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Pharmacology > NMJ and Cholinergic Pharmacology > Flashcards

NMJ and Cholinergic Pharmacology Flashcards

1
Q

what is a cholinergic nerve?

A

one that uses ACh as a NT

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2
Q

what nerves are cholinergic?

A

para (pre and post), sympathetic (pre), somatic, CNS and enteric

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3
Q

where does choline come from and how is it up taken?

A

from diet, then stored in the liver / transported in the blood
taken up by nerve endings which have a high affinity Na+ dependant carrier

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4
Q

How can choline uptake be inhibited?

A

Hemicholinium - competitive inhibitor of the choline carrier, activity dependant as depleted choline appears after activation and no reuptake, has no clinical use as its effects are widespread

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5
Q

how is Ach formed, what enzymes, what substrates?

A
  • Choline acetyltransferase (ChAT) catalysis’s the formation of acetylcholine by combining choline with acetyl CoA this results In the formation of Ach and CoA
    • This reaction occurs in the nerve cytoplasm
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6
Q

how is the production of Ach inhibited?

A

Triethyl choline is also a substrate for ChAT and results in the formation of acetyltriethylcholine, inhibiting the production of Ach, - not used clinically

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7
Q

how is Ach transported into the vesicle?

A

energy dependant, vesicular Ach Transporter

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8
Q

what inhibts transport of Ach into vesicle?

A

vesamicol

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9
Q

explain the poison of black widow spiders

A

α-latrotoxin causes a massive Ach vesicle release and hence depletion of stores

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10
Q

what is the action of botulinum toxin

A

cleaves proteins needed for exocytosis

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11
Q

what are the uses of botulinum toxin?

A

used to treat achalasia, salivary drooling, axillary hyperhidrosis ( excessive armpit sweating) can be used for cosmetic appearance ( smooth skin), however can also be used in biological warfare - muscle failure, respiratory failure - death

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12
Q

what is the action and uses of sarin?

A

inhibits acetylcholinesterase, blocks skeletal neuromuscular junction transmission, initial contraction and then paralysis and augments parasympathetic effects
used in biological warfare (nerve agent)

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13
Q

what are the 2 main receptors types for Ach and where are they located?

A

nicotinic receptors (mainly peripheral ganglia) and muscarinic receptors (mainly on outside of organs)

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14
Q

how does nicotine effect nicotinic receptors?

A

agonist for these receptors, transiently stimulate ganglia / motor end plates, however after a few seconds receptors can be desensitised, blocking transmission, reducing neuron action

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15
Q

what is the structure of a nicotinic receptor?

A

Nicotinic receptors are ligand gated sodium channels made of 5 subunits

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16
Q

why is Hexamethonium a poor drug?

A

also blocked parasympathetic activity and other essential neurons leading to dry mouth, constipation
also poorly absorbed from the gut so had to be injected

17
Q

what is the action of Galantamine?

A

acts on nicotinic receptors to increase their activity, positive allosteric modulation, can be used to treat Alzheimer’s disease e.g. increases alternes, it is also an acetylcholinesterase inhibitors

18
Q

what is the structure of muscarinic receptors?

A

G protein coupled receptors

19
Q

what are the used of antimuscarinic drugs?

A

inhibit parasympathetic drugs, promote sympathetic modes of action

20
Q

what are parasympathomimetic?

A

muscarinic agonists

21
Q

give 2 examples of an antimuscarinic drug

A

atropine to treat bradycardia
ipratropium, for asthma, promotes vasodilation, inhibits vasoconstriction

22
Q

what effect does binding of Ach to prejunctional nAchR have?

A

increase Ach release, positive feedback

23
Q

explain the structure of botulinum toxin

A

2 subunits, the first subunit binds to the presynaptic membrane, and the second cleaves proteins involved in exocytosis

24
Q

where does botulinum toxin come from?

A

clostridium botulinum which is an anaerobic bacteria that can grow in preserved food

25
Q

what are the 2 treatments for botulinum toxin poisoning?

A

4-aminopyridine, this is a blocker of voltage gated K+ channels meaning that the repolarisation phase is delayed, this means more Ca2+ influxes for a longer period resulting in more drive for Ach release to overcome the effects of botulinum
antitoxin that binds to botulinum which prevents its entry into the nerve terminal

26
Q

what are the 2 categories of post synaptic NMJ blockers?

A

non-depolarising blockers (antagonist) and depolarising blocker (agonist)

27
Q

give 2 examples of non depolarising NMJ blockers

A

pancuronium and vecuronium
(competitive antagonists of nAchR)

28
Q

what was the original NMJ blocker used by Amazonian tribes in blow dart poison?

A

D-tubocurarine

29
Q

how are non depolarising blockers administered and how long do they last?

A

IV administration and can have effects varying from 15mins - 2 hours depending on the individual

30
Q

how are the effects of non depolarising blockers stopped?

A

metabolism or excretion

31
Q

what is the mechanism of suxamethonium?

A

depolarising blocker, it consists of 2ACh linked by acetyl groups
binds to nAChR and cause depolarisation, however due to it not coming from a nerve terminal it binds randomly resulting in fasciculations (uncoordinated fine contractions)
remain and cause prolonged depolarisation, this inactivates the voltage gated Na channels leading to paralysis, this phase is known as the phase 1 block

32
Q

how is the action of suxamethonium stopped?

A

broken down by plasma cholinesterase

33
Q

when is suxamethonium used?

A

brief procedures such as intubation

34
Q

what are the unwanted side effects of suxamethonium?

A

bradycardia (slow HR due to Ach receptors in the heart), it can lead to excess K+ release due to prolonged depolarisation, this can increase risk of cardiac arrest
increase in intraocular pressure due to contraction of extraocular muscles

35
Q

why should suxamethonium not be used to treat burn victims?

A

may express excess nAChR due to denervation super sensitivity resulting in lots of K+ leaking into the blood

36
Q

what are the uses / mechanisms of acetylcholine esterase inhibitors?

A

reverse the effects of non-depolarising blockers after surgery, increase Ach levels, which competes with the antagonist, leading to an increase in end plate potential

37
Q

what type of blocker can acetylcholinesterase not be used on?

A

make the effects of a depolarising blocker such as suxamethonium worse

38
Q

What is myasthenia gravis?

A

autoimmune condition that causes destruction of nAChR at the NMJ, it is a progressive disorder than can lead to paralysis and death if not treated

39
Q

how is myasthenia gravis treated?

A
  • Examples of Acetylcholinesterase inhibitors used to treat MG include Edrophonium – short duration; Diagnostic test of drug efficacy, Neostigmine – medium duration; muscarinic side effects, Pyridostigmine – Better oral absorption; long duration; less powerful

Pharmacology (7 decks)

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