Drug action at Neuromuscular junction

Question 1

Explain process of neuromuscular synapse

Answer 1

1. Acetylcholine is stored in vesicles at the pre-synaptic terminal
2. Action potential fuses vesicles and cell membrane causing release of acetylcholine
3. Acetylcholine binds with nicotinic receptors at synapse at post-synaptic cell
4. Activation occurs:
   influx of sodium ions
   depolarisation
   contraction

Question 2

What is tubocurarine

Answer 2

Used for prolonged muscle relaxation
Slow to recover
has adverse effects

Question 3

What is atracurium

Answer 3

Short-acting (15-3-mins)
Can be given by infusion for longer term effects

Question 4

What is pancuronium

Answer 4

Longer duration
Used for longer-term action in intensive care

Question 5

What is rocuronium

Answer 5

Faster onset (2 mins)
Intermediate duration (30-40 mins)

Question 6

What is acetylcholinesterase

Answer 6

enzyme that breaks down acetylcholine into choline + acetate

Question 7

What is neostigmine

Answer 7

Type of acetylcholinesterase inhibitor
slowly reversible
slow to leave the active site
Inhibits acetylcholine binding leading to catalysis

Question 8

What is Sarin

Answer 8

Type of acetylcholinesterase inhibitor
Irreversible
Forms covalent bond with enzyme
Permanent inactivation = no acetylcholine binding at all

Question 9

Why does Sarin gas kill you

Answer 9

Usually after contraction, Acetylcholinesterase would break down into acetylcholine. Due to the presence of Sarin, this is inhibited. This leads to an increase in acetylcholine in the synapse, leading to more activation of nicotinic receptors = more contraction.
E.g patient is paralysed and can’t relax muscles due to too much contraction happening

Question 10

What is pyridostigmine/neostigmine

Answer 10

Antidotes for curare posioning
help reduce muscle control