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Human Physiology and Pharmacology > week 12 L3: Skeletal neuromuscular junction > Flashcards

week 12 L3: Skeletal neuromuscular junction Flashcards

1
Q

What 3 drugs interact with nAChR?

A

tubocurarine (curarae), alpha-bungarotoxin, suxamethonium

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2
Q

How can these drugs be analysed?

A

The organ bath = salt solution

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3
Q

How does Organ Bath analysis work?

A

dissect out nerve from muscle (e.g. phrenic nerve hemi-diaphragm preparation)
electrically stimulate nerve, contract, physical change to electrical change
… results on a chart recorder

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4
Q

What effect does Tubocurarine have on muscle?

A

muscle relaxant, skeletal muscle paralysis

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5
Q

How to test tubocurarine effects?

A

Put drug into bath

Blocks size of neurally evoked twitch

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6
Q

What type of drug is Tubocurarine?

A

competitive antagonist

competing with ACh

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7
Q

What can reverse Tubocurarine?

A

neotigmine is an anti-cholinesterase

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8
Q

How do anti-cholinesterase enzymes work?

A

Inhibit acetylcholinesterase enzyme (breaks down ACh to acetate and choline)–> increase ACh levels + time spent in NMJ–> more likely to bind to nAChR.
reverses block on neuromuscular transmission

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9
Q

Is Tubocurarine non or pro depolarising to enplate?

A

non-depolarising neuromuscular blocker

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10
Q

What is Tubocurarine’s effect on epp & mepp?

A

reduce epp & mepp to below threshold–> no contraction on skeletal muscle
Acts on postsynaptic site to block receptors

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11
Q

Where does alpha-bungarotoxin (BTX) come from?

A

venom in Taiwan banded krait

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12
Q

Does the anti-cholinesterase (neotigmine) work with BTX?

A

No, as it binds irreversibly to agonist recognition site on nAChR of skeletal neuromuscular junction

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13
Q

Effect of Bungarotoxin on epp & mepp?

A

decrease epp and mepp as no ACh can bind to post nAChR

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14
Q

What kind of drug is BTX?

A

irreversible antagonist

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15
Q

What kind of drug is Succinylcholine?

A

agonist but still causes skeletal muscle paralysis

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16
Q

What is Succinylcholine used for?

A

rapid tracheal intubation (paralysis)

17
Q

What is Succinylcholine metablised by?

A

Plasma cholinesterase

18
Q

Is Succinylcholine broken down by acetlycholinesteras?

A

NO

19
Q

What happens in the PHASE 1 BLOCK (Succinylcholine)?

A

consistent activation of nAChR,
Prolonged depolarisation,
Inactivation of Na+ channels,
No AP in muscle fibre

20
Q

What happens in the PHASE 2 BLOCK (Succinylcholine)?

A

Desensitisation of nACh,
Re-polarisation of endplate,
Receptor desensitised, maintain blockage

21
Q

Name two types of Cholinesterase enzymes

A
  1. “True” acetylcholinesterase (AChE)

2. Pseudo-cholinesterase

22
Q

Where would you find “True” acetylcholinesterase (AChE)?

A

cholinergenic synapses

bound to postsynaptic membrane

23
Q

Name 2 types of Pseudo-cholinesterase?

A

butyrylcholinesterase & plasma cholinesterase

24
Q

Where would you find Pseudo-cholinesterase?

A

plasma

important in activating and depolarising neurotransmitter blocker, Suxamethonium

25
Q

Effect of neogmine on epp and mepp?

A

increase amplitude of epp & mepp
prolongs their duration
by breaking down AChE to prolong time on R

26
Q

What’s a clinical use of anti-cholinesterases

A

used to reverse non-depolarising skeletal muscle relaxants e.g. tubocurarine

27
Q

what’s a disease that is treated with anti-cholinesterase?

A

Myasthenia Gravis
auto immune disease
loss of nAChR NMJ
muscular weakness paralysis

28
Q

How do you diagnose/treat Myasthenia Gravis?

A

endrophonium

anticholinesterase

29
Q

What effect would endophonium have on Q.C?

A

No change to Q.C
Transmitters not broken down, increase ACh content in synapse
twitch is created and prolonged

30
Q

What is a disease with a decreased expression of a presynaptic terminal?

A

Lambert-Eton Myasthenic Syndrome
produce antibodies that bind to voltage gated Ca+ channels
decrease Ca+ into cell, decrease vesicles released

31
Q

Effect of Q.C with Lamber Eton Myasthenic Syndrome?

A

Decrease epp as fewer vesicles released
mepp not decreased as same number of ACh in vesicles
pre-synaptic deficit

32
Q

How to treat LEMS?

A

Pyridostigmine (AChE inhibitor)

DAP

33
Q

How does DAP work?

A 
blocks K+ channels
prolong action potential
prolonged action of Ca+ channels opening
increase Ca+ influx
increase vesicle release
34
Q

Is Myasthenia Gravis post of presynaptic?

A

post synaptic effects

35
Q

How do you effect the amplitude of mepp?

A

Decrease number of ACh in vesicle or effect number of receptors

Human Physiology and Pharmacology (31 decks)

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