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Y1S2 > Pharmacology of the NMJ > Flashcards

Pharmacology of the NMJ Flashcards

1
Q

what are the three ways to block neuromuscular transmission

A

presynaptically, by inhibiting ACh synthesis
-rate-limiting step is choline uptake
presynpatically, by inhibiting ACh release
Postsynaptically
- by interfering with the actions of ACh on the receptor

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2
Q

What are the ways of blocking ACh release

A

Local anaesthetics
General inhalation anaesthetics
Inhibitors/competitors of calcium
- magnesium ions (compete with calcium)
- some antibiotics (bind to ca2+)(ahminoglycosides (gentamicin) and tetracycline)
Neurotoxins
- botulinum toxin (clostridium botulinum)
- beta bungarotoxin (botox, stops the triggering of ACh)

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3
Q

Name some clinical uses of neuromuscular blocking drugs

A

endotracheal intubation
During surgical procedures
- to allow surgical access to abdominal cavity
- to ensure immobility
- allow relaxation to reduce displaced fracture or dislocation
- decrease in concentration of general anaesthetic needed
Infrequently used in intensive care
- mechanical ventilation at extremes of hypoxia
During electroconvulsive therapy

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4
Q

what is the structure of the nicotinic acetylcholine receptor

A

found in the NMJ but also in the brain and autonomic nervous system.
has a central pore of 0.7nm in diameter
two alpha helices forming the gate
two ACh receptors

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5
Q

nicotinic acetylcholine receptor agonist

A

this causes ACh to bind and causes a conformational change but then eventually leads to loss of control

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6
Q

nicotinic acetylcholine receptor antagonist

A

This channel is simply closed

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7
Q

what is the action of non-depolarising blockers = competitive antagonists of Nicotinic ACh receptors at the NMJ
TUBOCURARINE

A

prevents ACh binding to receptor by occupying site
Decreases the motor end plate potential (EPP)
decreases depolarisation of the motor end plate region
No activation of the muscle potential

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8
Q

What is the action of depolarising blockers = agonists of nicotinic acetylcholine receptor at the NMJJ = NOT METABALISED BY ACETYLCHOLINE ESTERASE
SUXAMETHONIUM

A

This initially causes a twitch due to a small AP which immediately goes away so does cause an initial conformational change.
Persistent depolarisation of the motor endplate
prolonged EPP
Prolonged depolarisation of the muscle membrane
Membrane potential above the threshold for the resting of the voltage-gated sodium channels
sodium channels remain refractory
no more muscle action potentials generated

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9
Q

Phase 1, in a depolarising block

A

Phase 1:
muscle fasciculations observed, then blocked
depolarisation inhibited (K+ leaks from the cells as sodium enters (hyperkalemia)
voltage gated na+ channels kept inactivated

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10
Q

Phase 2, in a depolarising block

A

prolonged/increased exposure to drug
‘desensitisation blockade’ - tissue desensitisation due to prolonged exposure -depolarisation cannot occur, even in the absence of the drug

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11
Q

the side effects of non-depolarising blockers

A

normally result in tachycardia responses and hypotension (AM) which leads to bronchospasm due to histamine release

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12
Q

the side effects of depolarising blockers include

A 
brachycardia 
cardiac dysrhythmias 
raised intraocular pressure
postoperative myalgia - feeling of flu or space
malignant hyperthermia
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13
Q

What blocker can be used for ester hydrolysis and Hofmann elimination

A

atracurium

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14
Q

what blockers can be used for plasma cholinesterases

A

these provide a prolonged block

  • mivacurium
  • suxamethonium
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15
Q

what blockers can be used for hepatic metabolism

A

pancuronium

vecuronium

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16
Q

what blocker is unchanged in bile and urine

A

recuronium

17
Q

what is the action of ACh regulated by

A

hydrolysis

18
Q

acetylcholinesterase (synaptic cleft NMJ and is readily available)

A

true cholinesterase, specific for hydrolysis of ACh
present in conducting tissue and red blood cells
bound to basement membrane in the synaptic cleft

19
Q

plasma cholinesterase

A

pseudocholinesterase, broad spectrum of substrates
widespread distribution
soluble in plasma
(prevents breakdown of ACh)

20
Q

tell me more about anticholinesterases

A

they are all inhibitors of cholinesterases which result in:

  • increase in availability of ACh at NMJ
  • increases duration of activity of ACh at NMJ
  • More ACh to compete with non-depolarising blockers
21
Q

pancuronium

A

medium onset and long duration, non depolarising so tachycardia

22
Q

vecuronium

A

medium onset and medium duration non depolarising with few side effects

23
Q

rocuronium

A

fast onset and medium duration non-depolarising with tachycardia side effects

24
Q

atracurium

A

medium onset with medium duration, non-depolarising with hypotension/bronchospasm side effects

25
Q

mivacurium

A

fast onset with short duration, non-depolarising with hypotension/bronchospasm side effects

26
Q

neostigmine and pyridostigmine

A

medium duration, anticholinesterase, formation of carbamylated enzyme complex

27
Q

dyflos and marathon

A

long onset and act by irreversible inhibition

28
Q

what slows the rate of hydrolysis

A

carbamylation

29
Q

phosphorylation by dyflos/parathion irreversibly changes the enzyme unless

A

coaxed out by pralidoxime so there can be synthesis of a new enzyme

30
Q

Effects of anticholinesterases on the CNS

A

Initial excitation with convulsions

unconsciousness and respiratory failure

31
Q

Effects of anticholinesterases on the ANS

A 
SLUDGE 
SALIVATION
LACRIMATION 
URINATION 
DEFACATION
GASTROINTESTINAL UPSET 
EMESIS (vomit)
32
Q

what are the clinical uses of anticholinesterases

A

In anaesthesia
– Reverse non-depolarising muscle blockade
– Given with atropine or glycopyrrolate to counteract
parasympathetic effects
Myasthenia Gravis
– Increase neuromuscular transmission
Glaucoma
– Decrease intraocular pressure
Alzheimer’s disease
– Enhance the cholinergic transmission in the CNS

33
Q

Myasthenia gravis

A

autoantibodies may be produced against the acetylcholine receptor blocking the interaction of the acetylcholine receptor with its ligand (acetylcholine) and leading to increased muscle weakness and death.

34
Q

Sugammadex

A

Selective relaxant binding agent (SRBA)

• Reverses effects of rocuronium and vecuronium

Y1S2 (73 decks)

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