Volatile Anaesthetics and Sedatives Flashcards

1
Q
  1. Propofol
  • a. Accumulates.
  • b. Can produce abnormal muscle movements
  • c. Has minimal effect on the cardiovascular system
A

b. Can produce abnormal muscle movements

  • “Although the drug leads to a general suppression of CNS activity, excitatory effects such as twitching or spontaneous movement are occasionally observed during induction of anesthesia. These effects may resemble seizure activity; however, most studies sup- port an anticonvulsant effect of propofol, and the drug may be safely administered to patients with seizure disorders.”*
  • “The context-sensitive half-time of propofol is brief, even after a prolonged infusion, and recovery remains relatively prompt”*
  • -* ie does not seem to accumulate
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2
Q
  1. Propofol:
  • a. Is less painful when injected than thiopentone
  • b. Causes less hypotension than thiopentone
  • c. Is less likely to cause post operative vomiting than thiopentone
  • d. Causes cumulative effects when given as a continuous infusion.
  • e. Is useful in long term sedation in ICU for periods of 1-2 weeks
A

c. Is less likely to cause post operative vomiting than thiopentone

  • Well known to be antiemetic and cause marked hypotension, and is painful when injected.*
  • Cannot use long-term due to risk of ‘propofol syndrome’*
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3
Q
  1. Propofol:
  • a. Is mainly excreted unchanged in urine.
  • b. Has minimal effects on blood pressure during induction
  • c. Has a recovery rate from anaesthesia similar to the barbiturates.
  • d. Has antiemetic properties
  • e. Hypersensitivity reactions are due to the intralipid component.
A

d. Has antiemetic properties

  • a. Is mainly metabolised in liver and lungs, then water soluble metabolites are excreted in urine
  • b. Well-known to cause hypotension during induction due to vasodilation (compounded by initiating PPV)
  • c. Has a recovery rate from anaesthesia quicker than the barbiturates due to extra-hepatic clearance
  • e. Hypersensitivity reactions are due to the intralipid component.
    • Also true, due to egg protein in the emulsion.
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4
Q
  1. Regarding adverse effects of propofol:
  • a. Post-operative vomiting is common
  • b. Hypertension is a complication
  • c. Severe acidosis can occur with its use in paediatric respiratory infection
  • d. It is positively inotropic
  • e. Tremors are a common side effect
A

c. Severe acidosis can occur with its use in paediatric respiratory infection

  • Propofol infusion syndrome presents with bradycardia and severe metabolic acidosis, typically in unwell paediatric patients receiving high doses for > 24 hours.*
  • Myotonic jerks are a common side effect, and dystonia, though rare, can occur. So e) could also be correct.*
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5
Q
  1. All of the following are anaesthetic agents EXCEPT:
  • a. Midazolam
  • b. Glycopyrrolate
  • c. Propofol
  • d. Fentanyl
  • e. Etomidate
A

b. Glycopyrrolate

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6
Q
  1. Regarding intravenous anaesthetics:
  • a. Ketamine is a cardiovascular depressant
  • b. Respiratory depression is rare following use of midazolam
  • c. Delayed recovery is expected following prolonged infusion of propofol
  • d. Barbiturate anaesthetics have a rapid onset of action due to high lipid solubility.
  • e. Intravenous opioids aid chest wall relaxation
A

d. Barbiturate anaesthetics have a rapid onset of action due to high lipid solubility.

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7
Q
  1. Ketamine is closely chemically related to
  • a. Phencyclidine
  • b. LSD
  • c. Propofol
  • d. Thiopentone
  • e. Enflurane
A

a. Phencyclidine

aka PCP or Angel Dust

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8
Q
  1. Ketamine:
  • a. Is useful as an induction agent in head injured patients.
  • b. Decreases salivation
  • c. Decreases heart rate and may cause bronchoconstriction
  • d. Must be given intramuscularly
  • e. May cause unpleasant dreams in children
A

e. May cause unpleasant dreams in children

Note current evidence supports the use of ketamine in headinjury but it is still theoretical risk, and not 100% adopted.

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9
Q
  1. Regarding inhaled anesthetics, which is NOT true?
  • a. The depth of anesthesia is related to the alveolar concentration of the gas
  • b. The potency of these agents is directly proportional to their fat solubility
  • c. The alveolar concentration is influenced by cardiac output
  • d. Nitrous oxide when administered alone cannot produce surgical anaesthesia
  • e. More than 95% of halothane is excreted by the lungs
A

e. More than 95% of halothane is excreted by the lungs

  • Halothane is an exception to the general rule of inhalational anaesthetic being elimited by the lungs - 40% is metabolised by the liver and these products are excreted by the kidney*
  • NO has a MAC >100% because it can never achieve surgical anaesthesia*
  • I have altered the question: c) originally stated that alveolar concentration is NOT influenced by CO. However increasing CO decreases MAC (due to increased uptake and redistribution to the non CNS tissues), thereby reducing effect. So I’m fairly certain that CO alters AC.*
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10
Q
  1. The MAC (minimum alveolar concentration) is greatest for:
  • a. Nitrous oxide
  • b. Halothane
  • c. Isoflurane
  • d. Methoxyflurane
  • e. Ketamine
A

a. Nitrous oxide

  • MAC > 100% (as it can never achieve full surgical anaesthesia)*
  • Desflurane second highest at 7%, halothane lowest at 0.75%*
  • MAC is the alveolar concentration required to produce deep enough sedation in 50% of subjects that they do not react to a surgical incision.*
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11
Q
  1. Benzodiazepines
  • a. Cross the placental barrier during pregnancy
  • b. Are metabolized in the kidney.
  • c. All have active metabolites.
  • d. Act on nuclear receptors.
  • e. Circulate unbound to plasma
A

a. Cross the placental barrier during pregnancy

  • Hepatic metabolism*
  • Lorazepam and oxazepam do not have active metabolites*
  • Act on GABAa receptors which are Cl- channels*
  • Midazolam is highly protein bound*
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12
Q
  1. Diazepam
  • a. Is less lipid soluble than lorazepam
  • b. Binds sparingly to plasma proteins
  • c. Is potentiated by flumazenil.
  • d. Undergoes microsomal oxidation in the kidney
  • e. Is mainly metabolised to desmethyldiazepam
A

e. Is mainly metabolised to desmethyldiazepam

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13
Q
  1. Flumazenil
  • a. Has a half-life of around 10 hours.
  • b. Is cleared renally
  • c. Predictably reverses denzodiazepine induced respiratory depression
  • d. Antagonises CNS effects of opioids
  • e. Can precipitate seizures in mixed overdose
A

e. Can precipitate seizures in mixed overdose

as the anticonvulsant effects may be the only thing stopping toxic seizures

  • a. Has a half-life of 0.7-1.3 hours, l**ess than some benzos, so re-sedation can occur
  • b. Is cleared rapidly via hepatic metabolism
  • c. Unpredictably reverses denzodiazepine induced respiratory depression
    • reverses sedative effects, but effect on resp depression less predictable
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14
Q
  1. Buspirone relieves anxiety without sedation by
  • a. Direct GABA stimulation
  • b. Indirect GABA stimulation
  • c. Direct noradrenaline receptor stimulation
  • d. Indirect noradrenaline stimulation
  • e. None of the above
A

e. None of the above

5-HT agonist

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15
Q
  1. The most potent sedative is
  • a. Diazepam
  • b. Midazolam
  • c. Temazepam
  • d. Phenobarbitone
  • e. Chloral hydrate
A

b. Midazolam

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16
Q
  1. Ethanol is used therapeutically in methanol poisoning because:
  • a. It induces the microsomal ethanol oxidising system (mixed function system) and increases the clearance of methanol
  • b. It induces alcohol dehydrogenase and increases the clearance of methanol
  • c. It has greater binding affinity to alcohol dehydrogenase than methanol and hence prevents the metabolism of methanol by that enzyme
  • d. It increases the NADH/NAD ratio in the liver, thus reducing liver injury
  • e. It inhibits the NMDA subtype of glutamate receptors in brain cells
A

c. It has greater binding affinity to alcohol dehydrogenase than methanol and hence prevents the metabolism of methanol by that enzyme

17
Q
  1. regarding ethyl-alcohol
  • a. excreted unchanged in the lungs
  • b. causes CNS excitation then depression
A

b. causes CNS excitation then depression

  • Absorption rapid from GI tract as water-soluble, peak levels within 30min
  • Distribution rapid (Vd of total body water, about 0.5-0.7L/kg)
  • Metabolism - predominantly liver, zero order kinetics
    • Mainly via alcohol dehydrogenase by microsomal ethanol oxidising system (MEOS)
    • Other zero-order drugs: phenytoin, theophylline, warfarin, salicylates, heparin, paracetamol
  • Excreted via lungs and kidneys
  • Note the accumulation of NADH from excess ethanol metabolism causes
    • Lactic acidosis and hypoglycaemia in acute poisoning
    • Metabolic disorders in chronic alcoholism
18
Q
  1. Regarding ethanol metabolism
  • a. The MEOS system is the main pathway.
  • b. The alcohol dehydrogenase pathway is inducible
  • c. Obeys first order kinetics.
  • d. Most alcohol dehydrogenase is found in the stomach
A

b. The alcohol dehydrogenase pathway is inducible

  • MEOS is a minor pathway*
  • Obeys zero-order kinetics (saturated at low doses)*
  • Most ADH is found in the liver, then stomach*
19
Q
  1. Chronic alcohol consumption:
  • a. Has no significant effect on the lethal dose of alcohol
  • b. Causes tolerance via an increase in its own metabolism
  • c. Causes malnutrition primarily as a result of dietary insufficiency
  • d. Inhibits liver metabolism of other drugs
  • e. None of the above are true
A

c. Causes malnutrition primarily as a result of dietary insufficiency

  • “Malnutrition from dietary deficiency and vitamin deficiencies due to malabsorption are common in alcoholism. Malabsorption of water-soluble vitamins is especially severe.”*
    • Katzungs*
20
Q
  1. Methanol intoxication
  • a. Is partly due to inhibition of aldehyde dehydrogenase
  • b. Is due to formation of oxalic acid
  • c. Is treated in part with activated charcoal
  • d. Produces renal damage due to crystal formation
  • e. Can be treated with 4 methylpyrazole
A

e. Can be treated with 4 methylpyrazole​ (aka fomepizole)

  • *works by competitively inhibiting alcohol dehydrogenase, stopping methanol and ethylene glycol being converted into toxic metabolites.**
  • due to formation of formic acid (ethylene glycol -> oxalic acid)*
  • Treated with ethanol and dialysis, and fomepizole*
  • toxicity occurs due to the metabolism of formaldehyde to formic acid by aldehyde dehydrogenase - I do not think that inhibition causes intoxication (unless they are seperating toxicity and ‘intoxication’)*
  • ethylene glycol causes renal damage due to calcium-oxalate crystals*