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FRCA Pharmacology > Inhaled Agents > Flashcards

Inhaled Agents Flashcards

1
Q

Normobaric oxygen therapy causes
T/F
Alveolar changes after 6 hours when the FiO2 is 1.0

A

False. In the critically ill patient, oxygen related pulmonary damage may be seen as early as 12 hours. It may take up to 24 hours for similar changed to be seen in a normal subject.

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2
Q

Normobaric oxygen therapy causes
T/F
Alveolar changes after 48 hours when the FiO2 is 0.4

A

False. At a FiO2 of 0.4 oxygen related pulmonary damage is unlikely. This pathological process becomes a clinical problem once oxygen concentrations are above 50%.

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3
Q

Normobaric oxygen therapy causes
T/F
A reduction in functional residual capacity when the FiO2 is 1.0

A

True. When breathing oxygen at 100%, absorption atelectasis is a significant complication resulting in a reduction of both FRC and vital capacity.

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4
Q

Normobaric oxygen therapy causes
T/F
Absorption atelectasis at high concentrations

A

True. Absorption atelectasis occurs at high concentrations.

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5
Q

Normobaric oxygen therapy causes
T/F
Convulsions at high concentrations

A

False. Normobaric oxygen therapy does not typically cause convulsions. This is a complication of hyperbaric oxygen therpay (Bert effect).

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6
Q 
Toxicity from hyperbaric oxygen therapy can cause:
A. Painful joints
B. Pulmonary oedema
C. Acute tubular necrosis
D. Convulsions
E. Bradycardia
A

A. False. This may be a symptom of ‘the bends’, for which hyperbaric oxygen therapy is used to treat.
B. True. The ‘Smith effect’.
C. False. Hyperbaric oxygen therapy is not directly associated with renal dysfunction.
D. True. The ‘Bert effect’.
E. False.

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7
Q

Regarding Oxygen therapy:
T/F
The Bert effect describes the neurological complications caused by normobaric oxygen toxicity

A

False. The Bert effect describes convulsions secondary to hyperbaric oxygen therapy.

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8
Q

Regarding Oxygen therapy:
T/F
The Smith effect describes the pulmonary dysfunction caused by oxygen toxicity

A

True

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9
Q

Regarding Oxygen therapy:
T/F
Retrolental fibroplasia occurs in neonates up to 64 weeks post-conceptual age

A

False. The neonate is at risk of oxygen associated retrolental dysplasia up to 44 weeks post conceptual age.

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10
Q

Regarding Oxygen therapy:
T/F
It is not causative of neonatal bronchopulmonary dysplasia

A

False

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11
Q

Regarding Oxygen therapy:
T/F
Hyperoxia is beneficial post cardiac arrest
The agent is highly soluble in blood

A

False. Recent evidence suggests that hyperoxia post cardiac arrest is related to a worse outcome. This may be related to the negative effects of oxygen free radicals and reduced coronary blood flow. However, adequate oxygenation after cardiac arrest is obviously essential.

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12
Q

A more rapid induction of anaesthesia will occur using inhalational agent if:
T/F

A

False. A high blood partial pressure is reached more quickly if the agent is less soluble in blood with a low blood:gas coefficient.

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13
Q

A more rapid induction of anaesthesia will occur using inhalational agent if:
T/F
The patient has a low cardiac output

A

False. Although a high blood partial pressure is reached more quickly in patients with a low cardiac output, this effect is minimal with modern agents and outweighed by the quicker effect site transit time seen with higher cardiac output states

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14
Q

A more rapid induction of anaesthesia will occur using inhalational agent if:
T/F
The patient has a low FRC

A

True. A low FRC means that there is a lower volume that needs to be filled by inspired anaesthetic agent to produce a high alveolar fractional concentration.

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15
Q

A more rapid induction of anaesthesia will occur using inhalational agent if:
T/F
The agent has a low blood:gas solubility coefficient

A

True. Low agent solubility means that a high arterial and effect site partial pressure is achieved more rapidly, speeding the onset of anaesthesia.

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16
Q

A more rapid induction of anaesthesia will occur using inhalational agent if:
T/F
There is a carrier gas used in low volumes

A

False. Carrier gases are non-potent and must be used in high volumes.

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17
Q

Regarding the concentration effect:
T/F
It has a greater effect when low volumes of carrier gas are used

A

False. The concentration effect requires high volumes of carrier gas.

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18
Q

Regarding the concentration effect:
T/F
It is not responsible for the second gas effect

A

False. The opposite is true.

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19
Q

Regarding the concentration effect:
T/F
It has no effect upon alveolar ventilation

A

False. The concentration effect increases alveolar ventilation for each tidal breath. It is this process that is involved in ‘concentrating’ the ‘carried’ gases within the alveolus. This is known as ‘augmented ventilation’.

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20
Q

Regarding the concentration effect:
T/F
A potent agent is used to gain its benefits

A

False. A high volume of non-potent carrier gas is used. The low potency of a carrier gas allows it to be used at a high fractional inspired concentration.

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21
Q

Regarding the concentration effect:
T/F
May result in emergence hypoxia

A

True. This is one of the important complications of nitrous oxide and can be prevented by the use of oxygen post emergence.

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22
Q

Regarding GABA receptor
T/F
Its natural ligand is glutamate

A

False. It is GABA.

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23
Q

Regarding GABA receptor
T/F
It consists of 5 subunits, most commonly 2 alpha, 2 beta and 1 echo

A

False. It is 2 alpha: 2 beta: 1 gamma. There are around 18 different subunit types

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24
Q

Regarding GABA receptor
T/F
Its A subtype is metabotropic

A

False. It is ionotropic. GABA receptors are ligand-gated ion channels.

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25
Q

Regarding GABA receptor
T/F
It has over 30 isomers

A

True

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26
Q

Regarding GABA receptor
T/F
When opened it increases the conductance of calcium ions

A

False. Opening of the channel pore increases Cl conductance.

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27
Q

Regarding CNS receptors
T/F
N-Methyl-D-Aspartate receptors are inhibitory in action

A

False. They are stimulatory. Ketamine, xenon and nitrous oxide probably produce their anaesthetic actions by modulating the NMDA receptor.

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28
Q

Regarding CNS receptors
T/F
Benzodiazepines act via positive allosteric modulation

A

True. The binding of benzodiazepines to their GABA site increases the chance of ion pore opening.

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29
Q

Regarding CNS receptors
T/F
Ketamine binds competitively to NMDA receptors

A

False. Ketamine binds in a non-competitive manner.

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30
Q

Regarding CNS receptors
T/F
NMDA receptors are metabotropic

A

False. They are ionotropic. The binding of glutamate increases the conductance of cations such as Ca2+.

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31
Q

Regarding CNS receptors
T/F
Magnesium blocks the central pore of NMDA receptors

A

True. Mg2+ is an NMDA modulator. It binds to the open NMDA pore inhibiting current passage.

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32
Q

Regarding CNS receptors
T/F
Ionotropic receptors are ligand-gated ion channels

A

True

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33
Q

Regarding CNS receptors
T/F
Examples of metabotropic receptors include glutamate and GABAB

A

True. Glutamate is also the ligand for ionotropic receptors such as NMDA and AMPA.

34
Q

Regarding CNS receptors
T/F
GABAA activation promotes Cl- conductance

A

True. GABAA is an ionotropic receptor. The binding of GABA promotes chloride conductance hyperpolarizing the postsynaptic membrane and inhibiting pathway transmission.

35
Q

Regarding CNS receptors
T/F
Alcohol inhibits NMDA function

A

True. Alcohol mediates its effects of tolerance, dependence and withdrawal syndrome via its effects on NMDA receptor numbers and function.

36
Q

Regarding CNS receptors
T/F
The glycine receptor is found in high concentration with the cerebral cortex

A

False. Glycine receptors are found in the brainstem and spinal cord, where they function as the analogue of GABAA. Inhalation agents may markedly potentiate the effect of glycine within the spinal cord.

37
Q

Isoflurane:

Is a stereoisomer of enflurane

A

False. It is a structural isomer.

38
Q

Isoflurane:

Causes vasodilatation without reflex tachycardia

A

False. A reflex tachycardia suggests that baroreceptor function remains intact with isoflurane use. The main cause of isoflurane induced hypotension is a reduction in systemic vascular resistance. Myocardial function and cardiac output see only a small decrease.

39
Q

Isoflurane:

Has a saturated vapour pressure of 23.3 kPa at 20 degrees Celcius

A

False. This is the SVP of enflurane. The SVP of isoflurane is 32 kPa.

40
Q

Isoflurane:

0.2% of isoflurane undergoes hepatic metabolism

A

True. Hepatic cytochrome P450 metabloizes the C - F bond. Renal toxicity is rare due to the low levels of fluoride ions produced.

41
Q

Isoflurane:

The chloride group is attached to the chiral centre

A

True

42
Q

Factors that increase Minimum Alveolar Concentration:

Alpha-2 agonists

A

False. These decrease MAC.

43
Q

Factors that increase Minimum Alveolar Concentration:

Hypernatraemia

A

True

44
Q

Factors that increase Minimum Alveolar Concentration:

Chronic alcohol intake

A

True

45
Q

Factors that increase Minimum Alveolar Concentration:

Acute alcohol intake

A

False. Acute alcohol intake decreases MAC.

46
Q

Factors that increase Minimum Alveolar Concentration:

The premature neonatal period

A

False. The MAC is low in preterm neonates. For most agents MAC value peaks at 1-6 months.

47
Q

Sevoflurane:

Has a chiral centre

A

False. It is achiral

48
Q

Sevoflurane:

Produces hydrofluoric acid if stored in glass

A

True. This is highly toxic. Lewis acids degrade the ether and halogen bonds if sevoflurane is stored in water at concentrations less than 100ppm. The highly toxic hydrofluoric acid corrodes glass, driving Lewis acid production.

49
Q

Sevoflurane:

Has a blood:gas coefficient of 1.4

A

False. This is the blood:gas coefficient of isoflurane. 0.7 is the correct answer.

50
Q

Sevoflurane:

Causes coronary steal syndrome

A

False. This is a side effect of isoflurane use.

51
Q

Sevoflurane:

Is metabolised by cytochrome isoform CYP3A4

A

False. This cytochrome isoform is responsible for the metabolism of opiates and benzodiazepines. CYP2E1 is responsible for sevoflurane / isoflurane / halothane metabolism.

52
Q

Minimum alveolar concentration:

Is above 6% for desflurane

A

True

53
Q

Minimum alveolar concentration:

Is above normal atmospheric pressure for nitrous oxide

A

True

54
Q

Minimum alveolar concentration:

May be as low as 0.7 for sevoflurane in 70% nitrous oxide

A

True

55
Q

Minimum alveolar concentration:

Is 0.95 for Halothane

A

False. MAC of halothane is 0.75

56
Q

Minimum alveolar concentration:

Is lower for enflurane than it is for isoflurane

A

False. Isoflurane 1.17, Enflurane 1.68

57
Q

Halothane:

Is an halogenated ether

A

False. Halothane is a halogenated hydrocarbon. There is no ether ‘link’.

58
Q

Halothane:

Has a SVP at 20 degrees celcius, similar to isoflurane

A

True. Halothane 32.3 kPa, Isoflurane 33.2 kPa.

59
Q

Halothane:

May be given safely with adrenaline infiltration at doses of 100 micrograms per minute

A

False. This dose of adrenaline should be administered over a 10 minute period. Halothane sensitises the heart to catecholamines, which may lead to arrhythmias - particularly ventricular tachycardias and bradyarrhythmias.

60
Q

Halothane:

Its C-Br bonds are metabolised with greater ease than its C-F bonds

A

True. C-F bonds are the most stable carbon-halogen bond.

61
Q

Halothane:

Is metabolised under hypoxic conditions to produce trifluoroacetyl chloride which is implicated in halothane hepatitis

A

False. This metabolite is produced under oxidative conditions. In a hypoxic state reduced metabolites are produced e.g. inorganic fluoride.

62
Q

Desflurane:

Has a boiling point of 39 degrees celcius

A

False. Its boiling point is 23.5 degrees celcius.

63
Q

Desflurane:Is administered via the Tec 5 vaporiser

A

False. Is administered via the Tec 6. This heats the volatile to 39 degrees celcius under a pressure of 2 atmospheres.

64
Q

Desflurane:

Induces tachycardia and hypertensions at MAC values greater than 1

A

True

65
Q

Desflurane:

Produces carbon monoxide on contact with soda lime

A

True. Volatile agents that contain a -CHF2 molecule (isoflurane, enflurane, desflurane) may produce carbon monoxide upon reaction with dry soda lime.

66
Q

Desflurane:

Has a blood gas coefficient higher than nitrous oxide

A

False. Blood gas coefficient of desflurane is 0.42; nitrous oxide 0.47

67
Q

Nitrous Oxide

Has a critical pressure of 72 bar

A

True. In addition to this, the critical temperature is 36.5 degrees celcius.

68
Q

Nitrous Oxide

Is stored in cylinders with a pin index configuration of 2 and 5

A

False. This is the pin index of oxygen. The configuration for nitrous oxide is 3 and 5.

69
Q

Nitrous Oxide

Increases cerebral blood flow

A

True. It may also increase intracranial pressure.

70
Q

Nitrous Oxide

Inhibits methionine synthetase by reducing the cobalt ion in vitamin B12

A

False. It oxidises this cobalt ion. It may also inhibit methionine synthetase directly. Nitrous oxide therefore inhibits methionine, thymidine, tetrahydrofolate and DNA synthesis.

71
Q

Nitrous Oxide

Reduces that MAC of isoflurane to 0.5 when used at 70%

A

True

72
Q

Halothane:

Increases cerebral blood flow less than enflurane

A

False. In descending order; halothane, enflurane, nitrous oxide, isoflurane

73
Q

Halothane:

Has a sweet odour

A

True

74
Q

Halothane:

Has two bromide atoms

A

False. 1 bromide, 1 chloride and 3 fluoride ions.

75
Q

Halothane:

Is prepared with 0.01% thymol to prevent combustion

A

False. It is prepared with 0.01% thymol to prevent decomposition by light.

76
Q

Halothane:

Causes vagal stimulation

A

True. It may also cause bradycardia by inhibiting atrioventricular conduction / activity.

77
Q

In reference to inhaled anaesthetic agents:

Isoflurane does not increase cerebral blood flow at concentrations below 1 MAC

A

True

78
Q

In reference to inhaled anaesthetic agents:

Xenon is hepatically metabolised

A

False. All clearance is by lung elimination.

79
Q

In reference to inhaled anaesthetic agents:

Oxygen has a critical pressure of 50 bar

A

True

80
Q

In reference to inhaled anaesthetic agents:

Entonox seperates into its constituent parts below 7 degrees celcius

A

False. This is likely to occur at temperatures below -7 degrees celcius (pseudo-critical temperature) at pressures of 117 bar.

81
Q

In reference to inhaled anaesthetic agents:

0.1% of nitrous oxide is metabolised

A

False. Less than 0.01% of nitours oxide undergoes metabolism.

FRCA Pharmacology (13 decks)

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