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FRCA Pharmacology > IV Agents and neuromuscular blockers > Flashcards

IV Agents and neuromuscular blockers Flashcards

1
Q

Plasma cholinesterase:

Acquired deficiencies of the enzyme in genotypically normal patients prolongs suxamethonium activity for several hours

A

False. 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

Plasma cholinesterase:

The commonest genotype for cholinesterase activity is Eu:Eu

A

True. Eu:Eu is the 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

Plasma cholinesterase:

Deficiency occurs in pregnancy

A

True. Pregancy is an acquired factor associated with reduced plasma cholinesterase deficiency. Other causes are Liver disease, Renal and Cardiac Failure, Thyrotoxicosis, Cancer and a number of drugs.

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4
Q

Plasma cholinesterase:

Homozygotes always experience a prolonged suxamethonium block

A

False. Eu:Eu is a homozygote.

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5
Q

Plasma cholinesterase:

Patients who are homozygotes for the fluoride resistant gene have a near normal dibucaine number

A

True. 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

Contraindications to suxemethonium include:

The presence of renal failure

A

False. Renal failure does not itself cause a hyperkalaemic response to suxemethonium, however hyperkalaemia secondary to acute renal failure would increase the risk of arrhythmias.

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7
Q

Contraindications to suxemethonium include:

48 hours following major burns

A

True. Burns patients (>10% of body surface) are at greatest risk of suxemethonium induced hyperkalaemia from 24 hours after the injury until around 18 months.

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8
Q

Contraindications to suxemethonium include:

Malignant hyperpyrexia

A

True. Along with all the volatile inhalational agents.

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9
Q

Contraindications to suxemethonium include:

Pregnancy

A

False. Though it’s action may be slightly prolonged.

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10
Q

Contraindications to suxemethonium include:

Day case anaesthesia

A

False

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11
Q

Malignant hyperthermia:

Exhibits autosomal recessive inheritance

A

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

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12
Q

Malignant hyperthermia:

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

A

True

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13
Q

Malignant hyperthermia:

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

A

True

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14
Q

Malignant hyperthermia:

Without dantrolene the mortality can be as high as 70%

A

True

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15
Q

Malignant hyperthermia:

Each vial of dantrolene reconstituted with 60ml water produces a solution of pH 8.0

A

False. 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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16
Q

The effects of non-depolarising musle relaxants are prolonged by:
Volatile anaesthetics

A

True

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17
Q

The effects of non-depolarising musle relaxants are prolonged by:
Hyperthermia

A

False. Action is prolonged by hypothermia.

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18
Q

The effects of non-depolarising musle relaxants are prolonged by:
Lithium

A

True

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19
Q

The effects of non-depolarising musle relaxants are prolonged by:
Calcium channel antagonists

A

True. There is a reduced calcium influx resulting in reduced ACh release.

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20
Q

The effects of non-depolarising musle relaxants are prolonged by:
Hypomagnesaemia

A

False. Effects are prolonged by hypermagnesaemia due to the decrease in ACh release caused by competition with calcium and by stabilization of the post juntional membrane.

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21
Q

Atracurium:

Has 4 chiral centres and 10 stereoisomers

A

True

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22
Q

Atracurium:

Undergoes Hofmann elimination accounting for 60% of its metabolism

A

False. Hofmann elimination only accounts for 40% of atracurium’s metabolism.

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23
Q

Atracurium:

Hofmann elimination is potentiated by acidosis and hypothermia

A

False. Acidosis and hypothermia will slow down the process of Hofmann elimination.

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24
Q

Atracurium:

A product of its metabolism is laudanosine, a glycine antagonist

A

True

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25
Q

Atracurium:

Laudanosine is a breakdown product of both ester hydrolysis and Hofmann degradation.

A

True

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26
Q

Cis-atracurium:

Is one of the 10 stereoisomers present in atracurium

A

True

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27
Q

Cis-atracurium:

Is 10 times more potent than atracurium

A

False. It is approximately 3 to 4 times more potent than atracurium.

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28
Q

Cis-atracurium:

Is predominantly eliminated by ester hydrolysis

A

False. It is predominantly eliminated by Hofmann elimination and its metabolites have no neuromuscular blocking properties.

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29
Q

Cis-atracurium:

Is safe for use in patients with renal failure

A

True. It can be used safely in both renal and hepatic failure.

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30
Q

Cis-atracurium:

Has metabolites with neuromuscular blocking properties

A

False. It is predominantly eliminated by Hofmann elimination and its metabolites have no neuromuscular blocking properties.

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31
Q

The following are benzylisoquinolinium compounds:

Atracurium

A

True.

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32
Q

The following are benzylisoquinolinium compounds:

Midazolam

A

False. Midazolam is a benzodiazepine.

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33
Q

The following are benzylisoquinolinium compounds:

Pancuronium

A

False. Pancuronium is an aminosteroidal compound.

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34
Q

The following are benzylisoquinolinium compounds:

Tubocurarine

A

True

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35
Q

The following are benzylisoquinolinium compounds:

Mivacurium

A

True

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36
Q

Other effects of suxemethonium:

Sinus or nodal bradycardia secondary to sympathetic ablation

A

False. Sinus or nodal bradycardia is caused via stimulation of muscarinic receptors in the sinus node.

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37
Q

Other effects of suxemethonium:

Myalgia, particularly in young women

A

True. Muscle pains are commonest in young females mobilizing rapidly in the post operative period.

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38
Q

Other effects of suxemethonium:

Patients with severe burns or neuromuscular disorders are susceptible to sudden, massive release of potassium

A

True. May be large enough to provoke cardiac arrest.

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39
Q

Other effects of suxemethonium:

Can cause a rise in intra-occular pressure by about 10mmHg for a matter of minutes following administration

A

True. 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.

40
Q

Other effects of suxemethonium:

Raises intragastric pressure by 10 cmH2O

A

True. Though suxemethonium simultaneously increases lower oesophageal sphincter tone so there is no increased risk of reflux.

41
Q

Vecuronium:

Is relatively cardio-stable

A

True. The aminosteroids are not assocciated with the histamine release seen with the benzylisoquinolinium compounds.

42
Q

Vecuronium:

Is presented as a powder containing mannitol and sodium hydroxide.

A

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

43
Q

Vecuronium:

May cause critical illness myopathy

A

True. As can all muscle relaxants if used long term.

44
Q

Vecuronium:

Precipitates histamine release

A

False

45
Q

Vecuronium:

Its chemical structure differs from pancuronium by a single methyl group

A

True

46
Q

Propofol

Is highly protein bound

A

True. 97% protein bound.

47
Q

Propofol

Produces vasodilatation by nitric oxide production

A

True. Propofol causes hypotension (reduction in sytsemic vascular resistance and cardiac output) without tachycardia. Bradycardia is common, especially with opiate co-administration.

48
Q

Propofol

Is only partly unionized at physiological pH

A

False. The pka of propofol is 11, therefore at pH 7.4 it is almost entirely unionized.

49
Q

Propofol

Has a hydroxyl group situated on its 4th carbon

A

False. The hydroxyl group is situated on the 1st carbon. Phase 1 metabolism into a quinol derivative involves hydroxylation of the 4th carbon.

50
Q

Propofol

Undergoes both phase 1 and phase 2 metabolism

A

True. Glucuronidation is the predominant metabolic pathway, hydroxylation by cytochrome P450 to a quinol derivative prior to conjugation is also an important pathway. The relative importance of each pathway varies amongst patients.

51
Q

Propofol

Is used at a dose of around 4 mg/kg for IV paediatric induction

A

True. Approx double the typical adult dose.

52
Q

Propofol

Causes a reduction in cardiac output solely by reducing heart rate

A

False. Propofol also reduces myocardial contractility and sympathetic tone.

53
Q

Propofol

Clearance is by hepatic metabolism alone

A

False. Extra-hepatic metabolism is significant, suggested by the fact that clearance is higher than hepatic bolod flow. Sites for extra-hepatic metabolism include the kidneys (responsible for about a third of extra-hepatic metabolism) and lungs (to 2, 6 - diisopropyl - 1, 4 - quinol).

54
Q

Propofol
Acts as an anti-emetic by competitive antagonism of central serotonin receptors situated in the chemoreceptor trigger zone

A

False. The anti-emetic effect of propofol is probably mediated through dopamine receptor antagonism.

55
Q

Propofol

Is a cause of hypertrigylcerideaemia

A

True. This may be a part of the metabolic syndrome seen in children after prologed infusion. Propofol infusions have been linked to organ fatty infiltration with severe bradycardias, metabolic acidosis and increased mortality.

56
Q

With regards to IV induction agents:

Propofol has the same volume of distribution as ketamine

A

False. Propofol 4 L/kg. Ketamine 3 L/kg. Etomidate 3 L/kg. Thiopentone 2.5 L/kg.

57
Q

With regards to IV induction agents:

Propofol has the highest clearance rate

A

True. 30-60 ml/kg/min.

58
Q

With regards to IV induction agents:

The clearance rate of etomidate is 5 ml/kg/min

A

False. Etomidate 10-20 ml/kg/min, Ketamine 17 ml/kg/min, Thiopentone 3.5 ml/kg/min

59
Q

With regards to IV induction agents:

Thiopentone has a higher percentage of protein binding that methohexitone

A

True. Thiopentone 80%. Methohexitone 60%.

60
Q

With regards to IV induction agents:

Thiopentone has a pKa of 10.6

A

False. pKa of thiopentone is 7.6

61
Q

Midazolam:

Is 68% protein bound

A

False. 98% protein bound.

62
Q

Midazolam:

Is 40% unionized at physiological pH

A

False. Midazolam is a tautomeric molecule consisting of benzene and diazepine rings. In a pH > 4 the diazepine ring closes producing a lipid soluble unionized molecule. With a pKa of 6.5 around 89% of molecules are unionized at physiological pH.

63
Q

Midazolam:

Has inactive metabolites

A

False. The phase 1 metabolite 1-alpha-hydroxy-midazolam is active. This may then be conjugated (glucuronidation) prior to excretion.

64
Q

Midazolam:

Is metabolised by the same cytochrome P450 system as alfentanil

A

True. CP450 3A3/4. The action of midazolam may be prolonged by co-administration of alfentanil.

65
Q

Midazolam:

Is given in oral doses of up to 1 mg/kg in paediatric premedication

A

True. 30 minues prior to induction. Monitoring is required if doses >0.5 mg/kg are used.

66
Q

Ketamine:

Is a competitive antagonist of NMDA receptors

A

False. Non-competitive antagonist.

67
Q

Ketamine:

Is prepared as a racemic mixture in which the R- isomer is more potent than the S+

A

False. S+ is 2-3 times more potent than the R- isomer. It may also produce less intense emergence phenomena.

68
Q

Ketamine:

Is used as an oral premedication in doses of 2-5 mg/kg

A

True. 20% bioavailability. Doses of up to 10 mg/kg have be used in extreme cases.

69
Q

Ketamine:

Emergence phenomena is less common in the young and elderly

A

True

70
Q

Ketamine:

Undergoes cytochrome P450 de-methylation to the inactive metabolite norketamine

A

False. Norketamine is active, this then undergoes glucuronidation to an inactive metabolite which is excreted.

71
Q

Ketamine:

Is stored as an aciditc solution

A

True. pH 3.5-5.5. Ampoules can contain 10, 50 or 100 mg/ml.

72
Q

Ketamine:

Induces dissociative anaesthesia with predominant beta activity on EEG

A

False. Theta and delta activity is pre-dominant during ketamine induced dissociative anaesthesia.

73
Q

Ketamine:

Reduces cerebral oxygen consumption

A

False. Cerebral oxygen consumption, blood flow and intracranial pressure are all increased by ketamine.

74
Q

Ketamine:

Is 25-50% protein bound

A

True

75
Q

Ketamine:

Is a direct myocardial depressant

A

True. Ketamine increases sympathetic tone and circulating levels of adrenaline and noradrenaline. This produces the cardiovascular effects seen clinically of tachycardia, increased cardiac output, increased / maintained blood pressure and elevated CVP. However, ketamine also produces a mild direct myocardial depressant effect that is masked, less so for the S+ isomer.

76
Q

Etomidate:

Is prepared with 35% propylene glycol

A

True

77
Q

Etomidate:

Produces pain on injection in 75% of cases

A

False. Produces pain in around only 25%.

78
Q

Etomidate:

Causes nausea and vomiting

A

True

79
Q

Etomidate:

Is given as an IV induction dose of 2-3 mg/kg

A

False. The IV induction dose is 0.2-0.3 mg/kg

80
Q

Etomidate:

Produces excitatory movements with epileptiform activity on EEG

A

True. Etomidate is the most likely IV induction agent to cause myoclonic movements and epileptiform activity on EEG - in around 20% of cases.

81
Q

Etomidate:

Has an ester bond

A

True. Etomidate is an imidazole derivative and an ester.

82
Q

Etomidate:

May be used in patients with porphyria

A

False. Etomidate is known to cause a porphyric crisis.

83
Q

Etomidate:

Is predominanlty protein bound

A

True. Around 75%.

84
Q

Etomidate:

Inhibits adrenal medullary function

A

False. Etomidate has been shown to inhibit 11-beta and 17-alpha hydroxylase function and impair aldosterone and cortisol synthesis for up to 24 hours after administration. Steroidogenesis occur in the adrenal cortex.

85
Q

Etomidate:

Has the same volume of distribution as ketamine

A

True. 3 l/kg

86
Q

Thiopentone:

Is prepared as a hygroscopic yellow powder in 8% sodium carbonate

A

False. 6% sodium carbonate.

87
Q

Thiopentone:

When reconstitued with water produces a 2.5% solution

A

True

88
Q

Thiopentone:

At physiological pH 60% of the drug is unionized in blood

A

True

89
Q

Thiopentone:

Is metabolised to pentobarbitone

A

True. Pentobarbitone is an active metabolite.

90
Q

Thiopentone:

When in solution is found predominantly in its keto form

A

False. It is predominantly in its enol form when in solution. The enol form is soluble. Thiopentone is tautomeric and alkaline conditions promote the switch from keto to enol.

91
Q

Thiopentone:

Has a sulphur group on its 2nd carbon

A

True. There is an oxygen group in this position in oxybarbiturates.

92
Q

Thiopentone:

Is a bronchodilator

A

False. Thiopentone may produce laryngospasm and bronchospasm.

93
Q

Thiopentone:

Stimulates anti-diuretic hormone release

A

True. This is one of the reasons why thiopentone causes a reduction in urine output.

94
Q

Thiopentone:

Is an enzyme inhibitor

A

False. Thiopentone is an enzyme inducer.

95
Q

Thiopentone:

Is more active in alkalotic conditions

A

False. Acidosis and hypoalbuminaemia increases the amount of free unionized drug. A lower dose is often needed in critically ill patients.

FRCA Pharmacology (13 decks)

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