From poisons to surgery Part 1 Flashcards

1
Q

from what plants do curare alkaloids come from

A

condo-dendron tomentosum plants

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2
Q

What are curare alkaloids?

A

a group of highly effective arrow poisons

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3
Q

What type of poison are curare alkaloids and how does this affect the body

A
  • muscle relaxant poison
  • stops your from being able to move
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4
Q

what type of antagonist is D-tubocurarine at nicotinic acetylcholine receptors

A

It is a reversible competitive antagonist
at nicotinic acetylcholine receptors

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5
Q

what is D-Tubocurarine sometimes called

A
  • a non-depolarising neuromuscular blocking agent
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6
Q

what happens at the synapse between the neuron and muscle (Somatic nervous system)

A
  • acetylcholine is released and combines with nicotinic acetylcholine receptors
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7
Q

how many nanometres is the gap between the presynaptic membrane and acetylcholine receptors?

A

50nm

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8
Q

Explain how neuromuscular synapses work in reference to acetylcholine (ACh) molecules

A
  1. ACh molecules are stored in vesicles in presynaptic terminal
  2. incoming action potential causes vesicles to fuse with the cell membrane and release ACh
  3. ACh molecules bind to nicotinic receptors on post-synaptic cells
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9
Q

what type of ion channels are nicotinic acetylcholine receptors?

A

ligand gated ion channels

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10
Q

Describe the steps for skeletal muscle contraction starting with ACh

A
  1. ACh binds to nicotinic acetylcholine receptors
  2. influx of sodium ions
  3. depolarisation (an increase in membrane potential)
  4. this ultimately leads to muscular contraction
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11
Q

describe the 4 steps for the termination of action potential response

A
  1. ACh is broken down by acetylcholinesterase (AChE)
  2. ACh becomes just acetyl and Choline, terminating the action of acetylcholine
  3. Choline is transported ack into the presynaptic terminal
  4. Choline is combined with Acetyl-CoA to form acetylcholine again inside the presynaptic neurone.
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12
Q

what 2 things does activation of nicotinic receptors lead to?

A
  • Depolarisation of membrane
  • activation/opening of voltage-gated sodium channels
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13
Q

Outline the 2 step effect of an antagonist (eg: curare) on membrane potential

A
  1. motor nerve stimulated with ACh released, leading to short depolarisation
  2. amplitude pf depolarisation would be reduced by curare
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14
Q

what does washing out curare eventually lead to for motor nerve stimulation

A
  • eventually leads to recovery of nerve, so depolarisation can occur again
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15
Q
  • what is the clincal issue with tubocurarine that means it is superseded by other drugs
A
  • slow to recover and has adverse effects
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16
Q

what are the 3 reversible competitive antagonists at nACh receptors?

A
  • Atracurium
  • pancuronium
  • rocuronium
17
Q

what are 2 features of Atracurium

A
  • short-acting (15-30 mins)
  • can be given by infusion for longer term effects
18
Q

what are 2 features of Pancuronium

A
  • longer duration (60-120 mins)
  • used for longer term action in intensive care
19
Q

what are 2 features of rocuronium

A
  • faster onset (within 2 mins)
  • intermediate duration (30-40 mins)
20
Q

What are 3 clincal uses for atracurium, Pancuronium and Rocuronium

A
  • Muscle relaxant
  • due to muscle relaxation, ligher anaethesias can be used
  • relaxs vocal cords for tracheal intubation or mechanical ventilation
21
Q

what 2 things are important to realise when using muscle relaxants clinically

A
  • respiration must be assisted/controlled until patient recovers
  • patient must receive sufficient anaesthetic or sedation to prevent awareness