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MD2002 > Pharmacology of the Neuromuscular Junction > Flashcards

Pharmacology of the Neuromuscular Junction Flashcards

1
Q

What are the 3 ways to block neuromuscular transmission?

A

+ Presynaptically, by inhibiting ACh synthesis (rate-limiting step in choline uptake)

+ Presynaptically, by inhibiting Ach release

+ Postsynaptically (by interfering with the actions of ACh on the receptor)

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2
Q

What can inhibit ACh release?

A

+ Local anaesthetics
+ General inhalation anaesthetics
+ Inhibitors/competitors of calcium
+ Neurotoxins

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3
Q

What are examples of inhibitors/competitors of calcium?

A

+ Magnesium ions

+ Some antibiotics

  • aminoglycosides (gentamicin)
  • tetracycline
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4
Q

What are some examples of neurotoxins that inhibit ACh release presynaptically?

A

+ Botulinum toxin (clostridium botulinum)

+ β-Bungarotoxin (Taiwanese banded krait)

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5
Q

What are some clinical uses of neuromuscular-blocking drugs?

A

+ Endotracheal intubation

+ During surgical procedures: ↓ concentration of general anaesthetic needed

+ In intensive care: during mechanical ventilation at extremes of hypoxia

+ During electroconvulsive therapy

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6
Q

what are examples of nicotinic Ach receptor agonists?

A

+ nicotine

+ suxamethonium

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7
Q

what are examples of nicotinic Ach receptor antagonists?

A

+ tubocurarine

+ atracurium

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8
Q

what are non-depolarising blockers?

A

competitive ANTAGONISTS of nicotinic Ach receptors at the NMJ

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9
Q

how do non-depolarising blockeres/competitive antagonists work?

A
  1. prevent Ach binding to receptor by occupying site
  2. decreases motor end plate potential (EPP)
  3. decreases depolarisation of motor end plate region
  4. no activation of the muscle action potential
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10
Q

what are depolarising blockers?

A

AGONISTS of nicotinic Ach receptors at NMJ

- not metabolised by Ach esterase

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11
Q

how do depolarising blockers/agonists work?

A
  1. persistent depolarisation of motor end plate
  2. prolonged EPP
  3. prolonged depolarisation of muscle membrane
  4. membrane potenial above the threshold for resetting of voltage-gated sodium channels
  5. sodium channels remain refractory
  6. no more muscle action potentials generated
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12
Q

how many phases does a depolarising block occur in?

A

2 phases

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13
Q

what is phase 1 of a depolarising block?

A

+ muscle fasciculations observed, then blocked

+ repolarisation inhibited
- K+ leaks from cells (hyperkalemia)

+ voltage-gated Na+ channels kept inactivated

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14
Q

what is phase 2 of a depolarising block?

A

+ prolonged/increased exposure to drug

+ “desensitisation blockade”
- depolarisation cannot occur, even in absence of drug

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15
Q

which neuromuscular blocking drug is unchanged in bile/urine?

A

rocuronium

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16
Q

which neuromuscular blocking drug is affected by hepatic metabolism?

A
  • pancuronium

- vecuronium

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17
Q

which neuromuscular blocking drug is affected by plasma cholinesterases?

A
  • mivacurium

- suxamethonium

18
Q

which neuromuscular blocking drug is affected by ester hydrolysis and hofmann elimination?

A

atracurium

19
Q

what type of onset does suxamethonium have?

A

fast

20
Q

what type of duration does suxamethonium have?

A

short

21
Q

which neuromuscular blocking drugs have a medium onset?

A
  • pancuronium
  • vecuronium
  • atracurium
22
Q

which neuromuscular blocking drugs have a fast onset?

A
  • rocuronium
  • mivacurium
  • suxamethonium
23
Q

which neuromuscular blocking drugs have a long duration?

A

pancuronium

24
Q

which neuromuscular blocking drugs have a medium duration?

A
  • vecuronium
  • rocuronium
  • atracurium
25
Q

which neuromuscular blocking drugs have a short duration?

A
  • mivacurium

suxamethonium

26
Q

what are the main side effects of suxamethonium?

A
  • bradycardia
    (muscarinic agonist effect)
  • cardiac dysrhymias
    (increased plasma K+ concentration)
  • raised intraocular pressure
    (nicotinic agonist effect)
  • postoperative myalgia
    (muscle fasciculations)
  • malignant hyperthermia
    (ryanodine receptor related)
27
Q

what are features of acetylcholinesterase (Ach.E)?

A
  • true cholinesterase, specific for hydrolysis of ACh
  • present in cinducting tissue and red blood cells
  • bound to basement membrane in synaptic cleft
28
Q

what are features of plasma cholinesterase?

A
  • pseudocholinesterase, broad spectrum of substrates
  • widespread distribution
  • soluble in plasma
29
Q

what is the main role of anticholinesterase drugs?

A

inhibit cholinesterase

30
Q

what is the effect of inhibiting cholinesterase enzymes?

A
  • ↑ availability of ACh at NMJ by ↓ degradation
  • increases duration of activity of ACh at NMJ
  • more ACh to compete with non-depolarising blockers
31
Q

what are some anticholinesterase drugs?

A
  • neostigmine
  • pyridostigmine
  • dyflos
  • parathion
32
Q

what is the mechanism of action employed by anticholinesterase drugs, neostigmine and pyridostigmine?

A

formation of carbamylated enzyme complex

33
Q

what is the mechanism of action employed by anticholinesterase drugs, dyflos and parathion?

A

irreversible inhibition (by phosphorylation)

34
Q

what is the effect of carbamylation?

A

slows rate of hydrolysis

35
Q

what are the effects of anticholinesterases on the central nervous system?

A
  • initial excitation with convulsions

- unconscious and respiratory failure

36
Q

what are the effects of anticholinesterases on the autonomic nervous system?

A
  • Salivation
  • Lacrimation
  • Urination
  • Defecation
  • Gastrointestinal upset
  • Emesis
  • Bradycardia
  • Bronchoconstriction
  • Hypotension
  • Pupillary constriction (miosis)
37
Q

what are some clinical uses of anticholinesterases?

A
  • in anaesthesia
  • myasthenia gravis
  • glaucoma
  • alzheimer’s disease
38
Q

what is the effect of anticholinesterases in anaesthesia?

A
  • reverse non-depolarising muscle blockade

- given with atropine or glycopyrrolate to counteract parasympathetic effects

39
Q

what is the effect of anticholinesterases in myasthenia gravis?

A

increase neuromuscular transmission

40
Q

what is the effect of anticholinesterases in glaucoma?

A

decrease intraocular pressure

41
Q

what is the effect of anticholinesterases in alzheimer’s disease?

A

enhance cholinergic transmission in CNS

42
Q

what is sugammadex?

A

selective relaxant binding agent (SRBA)

- reverses effects of rocuronium and vecuronium (very specific)

MD2002 (85 decks)

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