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Exam Prep MCQs > Muscle Relaxant Pharmacology > Flashcards

Muscle Relaxant Pharmacology Flashcards

1
Q

How long would an acquired plasma cholinesterase deficiency last in a patient who has a normal genotype?

A

The prolongation of action in genotypically normal patients, i.e. with acquired deficiencies of the enzyme, is usually no longer than 30 minutes.

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2
Q

What is the commonest genotype for cholinesterase activity?

A

Eu:Eu

commonest genotype and it is present in 96% of the population. These homozygotes have a completely normal recovery from suxemethonium

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3
Q

What are the causes of plasma cholinesterase deficiency?

A
  • pregnancy
  • liver disease
  • renal/cardiac failure
  • thyrotoxicosis
  • cancer
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4
Q

What is a homozygote (re: plasma cholinesterase deficiency)?

A

This means Eu:Eu - they don’t have sux apnoea

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5
Q

What is the dibucaine number for patients who are homozygotes for the fluoride resistant gene? How does this compare to heterozygotes?

A

Their dibucaine number is around 70 (compared with 80 for Eu homozygotes)

Dibucaine is an amide local anaesthetic. The dibucaine number indicates the percentage that it inhibits the various forms of plasma cholinesterase. The normal Eu Eu genotype is most inhibited (80%), Ea Ea and Es Ea genotypes are least inhibited (20%).

The silent gene homozygotes Es Es have no plasma cholinesterase activity to inhibit and so do not have a dibucaine number.

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6
Q

What are the CI to suxamethonium?

A
  • renal failure itself is not one
    • although hyperkalaemia secondary to this would increase risk of arrhythmias
  • burns patients (>10% of body surface) from 24 hrs to 18 months after injury
  • malignant hyperpyrexia
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7
Q

What type of inheritance pattern does MH show?

A

MH is a rare autosomal-dominant condition. Incidence in UK 1 in 200,000.

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8
Q

Which receptor is associated with MH?

A

Is associated with a defect on the ryanodine receptor encoded on chromosome 19

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9
Q

How is MH diagnosed?

A

Diagnosis is based on response of biopsied skeletal muscle to 2% halothane and cafffeine (2mmol/L)

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10
Q

What is the mortality rate of MH without dantrolene?

A

70%

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11
Q

What is the pH of dantrolene when made up?

A

Dantrolene is available as capsules and in vials as an orange powder containing 20 mg dantrolene, 3 g mannitol and sodium hydroxide. Each vial when reconstituted with 60 ml water has a pH of 9.5.

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12
Q

What will prolong the effects of non-depolarising muscle relaxants out of the following: volatiles, hyperthermia, lithium, Ca2+ channel antagonists, hypomagnesaemia?

A
  • volatile anaesthetics
  • hypothermia
  • lithium
  • calcium channel antagonists (reduced calcium influx so reduced ACh release)
  • hypermagnesaemia (due to decrease in ACh release caused by competition with calcium and stabilization of post junctional membrane)
  • aminoglycosides
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13
Q

How many chiral centres and stereoisomers does atracurium have?

A

4 chiral centres

10 stereoisomers

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14
Q

What % of atracurium’s metabolism does Hofmann elimination count for?

A

40%

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15
Q

What effect does acidosis and hypothermia have on atracurium metabolism?

A

Slows Hofmann elimination

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16
Q

What is laudanosine?

A

A product of the metabolism of Atracurium. Both through ester hydrolysis and Hofman degradation.

It is a glycine antagonist.

17
Q

What is cis-atracurium?

A
  • one of the 10 steroisomers of atracurium
  • 3-4 x more potent than atracurium
  • predominantly eliminated by Hofmann elimination and metabolites have no neuromuscular blocking properties
  • can be used safely in renal/hepatic failure
18
Q

What type of neuromuscular blocking agent is turbocurarine?

A

A benzylisoquinolinium

19
Q

How can suxamethonium cause sinus or nodal bradycardia?

A

The initial metabolite of succinylcholine (SCh), succinylmonocholine, produces a tranisent negative chronotropic effect through its stimulation of sinus node muscarinic receptors.

Repeated dosing or infusions of SCh may lead to bradycardia that is appropriately treated with atropine

20
Q

How much can suxamethonium increase IOP by?

A

10mmHg for a matter of minutes following administration

Normal intraocular pressure is 10-15 mmHg making this a 100% rise in intra-ocular pressure which can be significant in the presence of globe perforation.

21
Q

How much does sux raise intragastric pressure by?

A

Raises intragastric pressure by 10 cmH2O

22
Q

Why is vecuronium considered relatively cardiostable?

A

The aminosteroids are not assocciated with the histamine release seen with the benzylisoquinolinium compound

23
Q

How is vecuronium presented?

A

It is unstable in solution and therefore presented as a freeze-dried powder containing mannitol and sodium hydroxide

24
Q

How does the structure of vecuronium differ from pancuronium?

A

By a single methyl group

25
Q
A

Exam Prep MCQs (19 decks)

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