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E-lfh FRCA Primary: Pharmacology Exam Prep Questions > RCOA Guide to the FRCA Examination The Primary (fourth edition) - Pharmacology > Flashcards

RCOA Guide to the FRCA Examination The Primary (fourth edition) - Pharmacology Flashcards

1
Q

Cisatracurium:

is one of two stereoisomers in atracurium

A

False. Cisatracurium is one of the ten stereoisomers present in atracurium.

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2
Q

Cisatracurium:

is of equal potency to atracurium

A

False. It is three to four times more potent than atracurium.

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3
Q

Cisatracurium:

undergoes direct hydrolysis by plasma-esterases

A

False. It does not undergo direct hydrolysis by plasma esterases, but is predominantly eliminated by Hofmann elimination to laudanosine and a monoquaternary acrylate.
This is then hydrolysed by non-specific plasma esterases to a monoquaternary alcohol and acrylic acid.

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4
Q

Cisatracurium:

has no active metabolites

A

True. None of the metabolites of cisatracurium have neuromuscular blocking properties

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5
Q

Cisatracurium:

is more dependent than atracurium on renal function for excretion

A

False. The elimination of both atracurium or cisatracurium is independent of renal function.

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6
Q

Propofol:

Is a water soluble phenol compound

A

False. Propofol is insoluble in water but highly soluble in fat and requires preparation as a lipid emulsion.

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7
Q

Propofol:

Has an elimination half-life of less than one hour

A

False. It has a terminal elimination half-life of five to twelve hours.

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8
Q

Propofol:

Glucuronidation occurs through the hydroxyl group at position 1

A

True.

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9
Q

Propofol:

Acts only on the ß subunit of the GABA receptor

A

False. As well as acting on the B subunit of the GABA receptor it also enhances the effect of glycine which is the major inhibitory. transmitter in the brainstem and spinal cord. It also inhibits neurotransmission at excitatory central nicotinic acetylcholine receptors.

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10
Q

Propofol:

Has anti-emetic effects which may be due to dopamine
antagonism

A

True. Antagonism of the D2 receptor is a possible mechanism for its anti-emetic

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11
Q

The following are true of local anaesthetic drugs:

Lidocaine and tetracaine (amethocaine) are both amides

A

False. Tetracaine (amethocaine) is an ester local anaesthetic.

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12
Q

The following are true of local anaesthetic drugs:

Potency is related to lipid solubility

A

True. Potency is closely related to lipid solubility in vitro.

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13
Q

The following are true of local anaesthetic drugs:

Rate of onset of action is independent of dose administered

A

False. Rate of onset of action is closely related to pKa.
Increasing the dose will increase the absolute amount of unionised drug present and hence increase the speed of onset.

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14
Q

The following are true of local anaesthetic drugs:

Ester local anaesthetic drugs are all poorly bound to plasma proteins

A

False. Cocaine is 95% plasma protein bound.

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15
Q

The following are true of local anaesthetic drugs:

Ropivacaine is more potent than lidocaine

A

True. Ropivacaine is four times more potent than lidocaine, reflecting its greater lipid solubility.

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16
Q

Phase I depolarisation blockade:

Shows ‘fade’ during tetanic stimulation

A

False. Fade is a feature of partial non-depolarising blockade.
Pre-junctional nicotinic receptors normally provide positive feedback to maintain transmitter release during periods of high neuromuscular activity; fade may be caused by non-depolarising neuromuscular blocking drugs acting at pre-junctional receptors. No fade is seen during tetanic stimulation in the presence of partial depolarisation blockade.

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17
Q

Phase I depolarisation blockade:

May be potentiated by anticholinesterases

A

True

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18
Q

Phase I depolarisation blockade:

Shows post-tetanic facilitation

A

False. Post-tetanic facilitation is a feature of non-depolarising blockade.

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19
Q

Phase I depolarisation blockade:

Is prolonged by prior administration of a small dose of a non-depolarising relaxant

A

False. Small doses of non-depolarising neuromuscular blockers were previously given in an attempt to decrease muscle pains after succinylcholine but have no effect on phase 1 block itself. Phase 1 block may be potentiated by volatile agents, anticholinesterases, magnesium and lithium.

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20
Q

Phase I depolarisation blockade:

Is antagonised by dantrolene

A

False. Dantrolene prevents release of calcium from the sarcoplasmic reticulum and may cause skeletal muscle weakness.

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21
Q

Adverse effects of heparin include:

Thrombocytopenia

A

True. Immune mediated heparin-induced thrombocytopaenia is serious and often associated with thrombotic complications. A non-immune thrombocytopaenia also occurs but is rarely of clinical significance.

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22
Q

Adverse effects of heparin include:

Hyperkalaemia

A

True. This is caused by inhibition of aldosterone secretion.

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23
Q

Adverse effects of heparin include:

Hypersensitivity reactions

A

True

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24
Q

Adverse effects of heparin include:

Intra-uterine fetal haemorrhage

A

False. Heparin has low lipid solubility and does not cross the placenta.

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25
Q

Adverse effects of heparin include:

Osteoporosis

A

True. This is caused by complexing of heparin with mineral substances from bone.

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26
Q

The rapid intravenous administration of 2 g/kg of mannitol will induce:

A decrease in serum sodium

A

True. Mannitol is a polyhydric alcohol prepared in water as a 10 or 20% solution. The initial increase in circulating volume associated with its administration will reduce the serum sodium concentration by dilution.

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27
Q

The rapid intravenous administration of 2 g/kg of mannitol will induce:

Low osmolality of the plasma

A

False. Mannitol increases serum osmolality.

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28
Q

The rapid intravenous administration of 2 g/kg of mannitol will induce:

Hypervolaemia

A

True. The initial increase in circulating volume produces an increased preload and cardiac output.

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29
Q

The rapid intravenous administration of 2 g/kg of mannitol will induce:

A decrease in intracellular osmolality

A

False. An increase in extracellular osmolality will draw water out of cells.

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30
Q

The rapid intravenous administration of 2 g/kg of mannitol will induce:

Reduction in the volume of the brain

A

True. Mannitol is unable to cross the intact blood brain barrier and by virtue of the increased plasma osmolality it draws extracellular brain water into the plasma.

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31
Q

The following are true of diuretics:

Large doses of mannitol increase extracellular osmolarity

A

True. Mannitol is an osmotic diuretic. It is freely filtered at the glomerulus but not reabsorbed in the tubules.

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32
Q

The following are true of diuretics:

Acetazolamide decreases urinary pH

A

False. Acetazolamide inhibits carbonic anhydrase. H+ excretion is inhibited and HCO- is not reabsorbed, giving alkaline urine.

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33
Q

The following are true of diuretics:

Thiazide drugs inhibit sodium reabsorption in the distal
tubule

A

True. Thiazides act mainly on the early portion of the distal tubule inhibiting Na+ and Cl- reabsorption.

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34
Q

The following are true of diuretics:

Furosemide decreases the ototoxicity of aminoglycoside antibiotics

A

False. Furosemide potentiates aminoglycoside ototoxicity.

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35
Q

The following are true of diuretics:

Bumetanide inhibits electrolyte reabsorption in the ascending Loop of Henle

A

True. Bumetanide is a loop diuretic.

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36
Q

The following drug may potentiate warfarin:

Rifampicin

A

False. Rifampicin induces hepatic enzymes and antagonises the effect of warfarin.

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37
Q

The following drug may potentiate warfarin:

Aspirin

A

True. Aspirin impairs platelet function, which will potentiate the effects of warfarin. It also competes for plasma binding sites.

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38
Q

The following drug may potentiate warfarin:

Paracetamol

A

False. There are no interactions between warfarin and therapeutic doses of paracetamol.

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39
Q

The following drug may potentiate warfarin:

Amiodarone

A

True. Amiodarone inhibits warfarin metabolism.

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40
Q

The following drug may potentiate warfarin:

Tamoxifen

A

True. Tamoxifen inhibits warfarin metabolism.

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41
Q

Ketamine:

Is an antagonist at glutamate receptors

A

True. Ketamine is a non-competitive inhibitor of ion channels associated with NMDA receptors.

42
Q

Ketamine:

Is a butyrophenone derivative

A

False. Ketamine is a phencyclidine derivative.

43
Q

Ketamine:

Is presented as a racemic mixture

A

True. Ketamine has one chiral centre and is presented as a racemic mixture of its two enantiomers, S (+)-ketamine and R (-)-ketamine.

44
Q

Ketamine:

Causes bronchodilatation

A

True

45
Q

Ketamine:

Has a direct positive inotropic effect

A

False. Ketamine causes sympathetic nervous system activation, increases plasma catecholamine concentrations and it thereby produces an indirect positive inotropic effect on the heart. This counteracts the mild direct negatively inotropic effect of ketamine on the heart.

46
Q

The following statements regarding intravenous induction agents are correct:

Etomidate is approximately 2.5 times more potent than thiopental

A

False. Etomidate is ten to twenty times more potent than thiopental.

47
Q

The following statements regarding intravenous induction agents are correct:

Ketamine is metabolised in the liver

A

True. Ketamine is demethylated to the active norketamine by hepatic P450 enzymes and then undergoes further glucuronication.

48
Q

The following statements regarding intravenous induction agents are correct:

Propofol emulsion has a pH of 7

A

True

49
Q

The following statements regarding intravenous induction agents are correct:

Thiopental has a high hepatic extraction ratio

A

False. The hepatic extraction ratio describes the arteriovenous gradient across the liver. It is influenced by liver blood flow, plasma protein binding and hepatic enzyme activity. Drugs with a high extraction ratio such as propofol are readily extracted from blood passing through the liver. Propofol clearance is high and sensitive to changes in liver blood flow. By contrast, thiopental has a low extraction ratio. Clearance is primarily influenced by changes in protein binding and hepatic enzyme activity.

50
Q

The following statements regarding intravenous induction agents are correct:

Etomidate is broken down by ester hydrolysis

A

True.

51
Q

The following statements concerning benzodiazepines are correct:

They act at GABA(a) and GABA(b) receptors

A

False. Benzodiazepines bind to the a-subunit of GABA(a) receptors.

52
Q

The following statements concerning benzodiazepines are correct:

Lorazepam has active metabolites

A

False. Unlike diazepam and midazolam, the metabolites of lorazepam are inactive.

53
Q

The following statements concerning benzodiazepines are correct:

They can cause ataxia and impaired motor co-ordination

A

True.

54
Q

The following statements concerning benzodiazepines are correct:

They cause a decrease in plasma chloride concentration

A

False. Benzodiazepines increase the frequency of opening of the GABA(a) chloride channel but do not affect plasma chloride.

55
Q

The following statements concerning benzodiazepines are correct:

Midazolam can be administered by the rectal and intranasal routes

A

True. At pH >4 the ring structure of midazolam closes, rendering it unionised, lipid soluble and able to cross lipid membranes.

56
Q

True statements about bronchodilating agents include:

Salmeterol has a longer duration of action but a slower onset and should not be used to treat acute asthmatic attacks

A

True. Salmeterol binds to the beta-2 adrenoceptor, giving it a duration of action up to twelve hours.

57
Q

True statements about bronchodilating agents include:

Isoproterenol (isoprenaline) has both beta-1 and beta-2 adrenergic actions

A

True

58
Q

True statements about bronchodilating agents include:

Aminophylline increases cyclic AMP through inhibition of phosphodiesterase

A

True. Aminophylline is a non-selective phosphodiesterase inhibitor.

59
Q

True statements about bronchodilating agents include:

Salbutamol increases the activity of adenylyl cyclase

A

True. Salbutamol stimulates beta receptors which are coupled to Gs proteins and activate adenylyl cyclase.

60
Q

True statements about bronchodilating agents include:

Salbutamol lowers serum potassium concentration

A

True. Salbutamol stimulates Na+/K+ ATPase, transferring K+ from the extracellular to intracellular compartment.

61
Q

Alfentanil:

Is 90% unionised at pH 7.4

A

True

62
Q

Alfentanil:

Has a higher clearance than morphine

A

False. Alfentanil has a lower clearance than morphine, but a shorter half-life due to its smaller volume of distribution.

63
Q

Alfentanil:

Has a smaller volume of distribution than fentanyl

A

True. The shorter half-life of alfentanil in comparison to fentanyl is due to its smaller volume of distribution despite lower clearance.

64
Q

Alfentanil:

Is more potent than fentanyl

A

False. Fentanyl is approximately ten times more potent than alfentanil.

65
Q

Alfentanil:

Is more protein bound than pethidine

A

True. Alfentanil is the most protein bound of the opioids at 90%.

66
Q

Cyclizine:

Has a duration of effect of one hour

A

False. The effects of cyclizine last four to six hours.

67
Q

Cyclizine:

Is a potent inhibitor of gastric acid secretion

A

False. Cyclizine may have some effect on gastric acid secretion through its anti-cholinergic activity but this is not clinically useful.

68
Q

Cyclizine:

80% is excreted unchanged by the kidney

A

False. Cyclizine is metabolised by N-demethylation to the inactive molecule norcyclizine.

69
Q

Cyclizine:

Has an atropine-like effect

A

True. In addition to its antihistamine activity cyclizine also has mild anti-cholinergic activity.

70
Q

Cyclizine:

Is non-sedating

A

False. As with most older antihistamines, sedation is a significant side effect.

71
Q

The following are true of non-steroidal anti-inflammatory drugs (NSAIDs):

NSAIDs are highly bound to albumin in the plasma

A

True. NSAIDs are weak acids that are extensively (up to 99%) protein bound, with a small volume of distribution (0.1 to 0.2 L/kg).
Therefore, they may potentiate other highly protein bound drugs by displacing them from their binding sites.

72
Q

The following are true of non-steroidal anti-inflammatory drugs (NSAIDs):

NSAIDs have a volume of distribution greater than 500 ml per kg

A

False. NSAIDs are weak acids that are extensively (up to 99%) protein bound, with a small volume of distribution (0.1 to 0.2 L/kg).

73
Q

The following are true of non-steroidal anti-inflammatory drugs (NSAIDs):

Parenteral administration of NSAIDs ensures that gastric mucosal damage does not occur

A

False. COX-1 inhibition impairs prostaglandin production in the gastric mucosa regardless of route of administration.

74
Q

The following are true of non-steroidal anti-inflammatory drugs (NSAIDs):

It is safe to use COX-2 inhibitors in the presence of established ischaemic heart disease

A

False. Specific COX-2 inhibitors (and some non-specific NSAIDs) are associated with an increased risk of thrombotic events including MI and stroke.

75
Q

The following are true of non-steroidal anti-inflammatory drugs (NSAIDs):

NSAIDs enhance platelet aggregation

A

False. Reduced thromboxane production inhibits platelet aggregation and adhesion.

76
Q

Sevoflurane:

Has a boiling point of 48°C

A

False. The boiling point of sevoflurane is 58°C, isofturane is 48°C.

77
Q

Sevoflurane:

Has a saturated vapour pressure at 20°C of 21 kPa (160 mmHg)

A

True

78
Q

Sevoflurane:

Is metabolised to a greater extent than desflurane

A

True. Sevoflurane is 3.5% metabolised compared to desflurane

79
Q

Sevoflurane:

Is a respiratory stimulant at low concentrations

A

False. Sevoflurane causes a dose-dependent respiratory depression.

80
Q

Sevoflurane:

Relaxes bronchial smooth muscle

A

True

81
Q

The MAC value of an inhalational anaesthetic agent may be decreased by:

Clonidine

A

a: True. Stimulation of CNS a2 receptors causes sedation and a reduction in MAC of up to 50%.

82
Q

The MAC value of an inhalational anaesthetic agent may be decreased by:

Neostigmine

A

False. Neostigmine is a quaternary amine and does not cross the blood brain barrier, and therefore has no central effects.

83
Q

The MAC value of an inhalational anaesthetic agent may be decreased by:

Amphetamine use

A

True. Amphetamines are powerful central sympathomimetics, and with acute use act as stimulants and increase MAC. However chronic use leads to a reduced anaesthetic requirement, possibly due to depletion of CNS catecholamines.

84
Q

The MAC value of an inhalational anaesthetic agent may be decreased by:

Methyldopa

A

True. Methyldopa decreases MAC by reducing central and peripheral noradrenaline levels.

85
Q

The MAC value of an inhalational anaesthetic agent may be decreased by:

Digoxin

A

False

86
Q

Drugs whose action is prolonged in patients with acute renal failure include:

Morphine

A

True. Hepatic metabolism of morphine produces active metabolites, including morphine-6-glucuronide, which are subsequently excreted in the urine.

87
Q

Drugs whose action is prolonged in patients with acute renal failure include:

Ranitidine

A

True. Ranitidine is partially metabolised in the liver, however 50% is excreted unchanged in the urine.

88
Q

Drugs whose action is prolonged in patients with acute renal failure include:

Alfentanil

A

False. Alfentanil is metabolised in the liver to inactive compounds.

89
Q

Drugs whose action is prolonged in patients with acute renal failure include:

Propofol

A

False. Propofol is metabolised in the liver to inactive compounds.

90
Q

Drugs whose action is prolonged in patients with acute renal failure include:

Labetalol

A

False. Labetalol is metabolised in the liver to inactive compounds.

91
Q

Hypoglycaemic agents with a rapid onset of action (less than one hour) include:

Soluble insulin

A

True. Soluble insulin acts within 30-60 minutes.

92
Q

Hypoglycaemic agents with a rapid onset of action (less than one hour) include:

Insulin glargine

A

False. Insulin glargine consists of hexameric microcrystals at physiological pH, delaying absorption.

93
Q

Hypoglycaemic agents with a rapid onset of action (less than one hour) include:

Insulin lispro

A

True. Insulin lispro is a fast-acting insulin analogue with an onset within fifteen minutes.

94
Q

Hypoglycaemic agents with a rapid onset of action (less than one hour) include:

Protamine zinc insulin

A

False. Complexing insulin with zinc reduces solubility and delays absorption.

95
Q

Hypoglycaemic agents with a rapid onset of action (less than one hour) include:

Isophane insulin

A

False. Also known as Neutral Protamine Hagedorn (NPH) insulin. The addition of protamine causes the insulin to form a hexameric complex, delaying absorption.

96
Q

Diamorphine:

Is a naturally occurring opioid

A

False. Diamorphine is a synthetic 3,6-diacetyl ester of morphine.

97
Q

Diamorphine:

Is more lipid soluble than morphine

A

True. Unlike morphine, diamorphine is highly lipid soluble.

98
Q

Diamorphine:

Has a higher affinity for opioid receptors than morphine

A

False. Diamorphine is a pro-drug with no affinity for opioid receptors. It is rapidly metabolised in the liver to active 6-monoacetylmorphine and morphine itself.

99
Q

Diamorphine:

Is well absorbed after subcutaneous administration

A

True. High lipid solubility facilitates absorption from subcutaneous tissues.

100
Q

Diamorphine:

Is converted to monoacetylmorphine

A

True. It is rapidly metabolised in the liver to active 6-monoacetylmorphine and morphine.

E-lfh FRCA Primary: Pharmacology Exam Prep Questions (3 decks)

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