Access to Anaesthetics

Primary FRCA
Pocket Book 1 :
Pharmacology and Clinical
· MCQs . ·
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Access to Anaesthetics
Primary FRC
ocket Book 1 :
Pharmacology and Clinical
MCQs
Kifsty Maclennan MBCh.B, MRCP, FRCA
Specialist Registrar Anaesthesia
North West Region
 ;t, 2007 PASTEST LTD
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First published 2007

ISBN: 1905 635 29X

ISBN: 978 1905 635 290

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• , reliable sources. However, while every effort has been rnadato ensure its accuracy,
.I
''

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refraining from action as a result of information contained herein can be accepted
by the publishers or author.

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 CONTENTS·

VII
Acknowledgements

VIII
Foreword

X
Introduction

Pharmacology MCQs
3
Questions and answers 1.1-1.129

Clinical MCQs
161
Questions and answers 1 .130- 1 .150

197
Index

V
 ACKNOWLEDGEMENTS

I would like to thank Dr. Nolan for taking the time to write the foreword;
Dr. Whitaker for his review; Dr. S. Maguire, Dr. K. Grady and Dr. W. de Mello for
their advice and sncouragernent.
I would also like to thank the publishers, PasTest, my family, who have supported
me. And above all, Ann Maclennan who has been my rock as always!
 FOREWORD

The introduction of run-throughtraining in Anaesthesia and the need for

the Royal College of Anaesthetists [RCOA] to structure timing and content
of Postgraduate examinations in accordance with the requirements of the
Postgraduate Medical and Education Training Board [PMETB] has led to
recent changes to the Primary Fellowship of the Royal College of
Anaesthetists [FRCA] examination.

The Primary Multiple Choice Question [MCQ] examination became a

"stand alone" Pass/Fail examination in June 2007. A close marking
scheme is used where 1 is a poor fail, 1 + is a fail, 2 is a 1Jass and a 2+
reflects an outstanding performance. The Primary FRCA MCQ
examination consists of 90 questions undertaken in thre.: hours and
comprises .three subsections of 30 MCQs examining Pha ·macology,
Physiology, Physics and Clinical Measurement. A mark of 2 is required to
pass the MCQ although a candidate who significantly u1 _derperforms in
one or more subsection of the MCQ will fail the ex-unination. Negative
marking is applied with one mark being deducted for each incorrect
answer.
8 I CD1

A candidate may not proceed to the Objectively Structured Clinical

Examination/Structured Oral Examination part of the Primary without
passing the MCQ. An MCQ pass will be valid for? period of three years
{or a trainee working full time.

Although there is currently no limit on the number of attempts at this part

of the examination, implicit in run through training is the need for trainees
to achieve clinical competencies and examination milestones in a timely
fashion.

It is generally acknowledged that an MCQ examination is a good test of

core knowledge and there is no short cut to the acquisition of the
considerable amount of information required to pass the Primary MCQ.
Prospective candidates need to commit to an intensive programme of
study of the syllabus supported by considerable practice of the technique
of answering MCQs.

Dr Maclennan has produced a series of MCQ~ which cover in detail the

Primary FRCA syllabus. The answer sections are dear and, where
appropriate, supported by references to recent literature. Trainees

viii
commencing an anaesthesia training programme will find these MCQs
useful to assess the depth of knowledge of the basicsciences which wil_L _
be required of them, and those for whom the examination is imminent
will find this series of books an invaluable means of self assessment and
an indication of aspects of theirknowledge and understanding which n;tijy;:.-.;t
need further work. :n~dl
Dr D. Nolan, Regional
.
Advisor for
'
the North W@" pi:
fl.:, ~; .
•
, . 11fl:,, ~,,g;; .
•• t:.I' , ~--

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iv
 INTRODUCTION

Having taken both anaesthetic and medicine postgraduate examinations,

lthink that it is always difficult to know how best to start revising. It is
important to avoid that unpleasant drowning sensation when you look at
all the information that you have to absorb! I personally find that sitting
and reading a textbook ls time consuming, not particularly memorable
and not especially useful for actually passing the exam. The best way to
find out the gaps in your knowledge is to do as many practice MCQs as
you can. This will stimulate you to read around the topics you are less
familiar with, whilst improving your exam technique.
"These books are different from others on the market as they are subject
based. Many candidates feel that they have a particular area of. weakness.
These books will at worst highlight those weaknesses and at best, allow
you to home in on specific topics, making them your areas of strength.
Each book contains 150 MCQs, covering pharmacology and clinical in
book l, physics, clinical measurement, equipment and statistics in book
2, physiology and anatomy in book 3. Within each book, the questions
are mostly based in subject groups. This enables you to revise a particular
topic or, you can always takl a selection of questions from each book to
make a practice exam paper.
The questions are based on the primary syllabus but will also be useful for
candidates studying for the basic science part of the final examination.
Being pocket sized, there. is now no excuse! Carry one in the pocket of
your theatre blues and do a few questions before the patient arrives in the
anaesthetic room oreven over lunch!
The examination period is a stressful time, so make best use of all the time
that you have.
Good luck!
Kirsty
.. :.
 PHARMACOLOGY MCQs

.
1, 1 The 'fo!~owi:ng are true of cell mernbranes; .,
0 A The lipophilic chains of the phospholipid bilayer of a cell
membrane face outwards , , · _,_,.~ ..•.. c\ )
D B Capillaries have fenestrae
D C Tight junctions exist in the blood-brain barrier, intestinal
mucosa and renal tubules
---·------
0 D Passive diffusion is the commonest method for substances to
cross into a cell membrane
0 E Ion channels may have their permeability changed by ~tu rally
occurring molecules
- .
or drugs
~-

1.2 Regarding absorption of drugs:

~ A The absorption of ~~~jdj across the gut lumen is~.n example
of facilitated
--~·:- diffusion ~.
0 B Vitamin molecules are transported across the cell membrane
":ia_~inocytosis · ~
0 C The ~p~ed of absqr~ti9n is predominantly dependent on lipid .. \
1
SO I U bili
I tty ·· -\- · , ·'"::l '-I· · ,...,.~ r-J " ---; - r, ·
0
- -' •~ - -~

- I
D D lipid solubility affects the pharmacoklnetics of absorption from
a particular site - j ) . ·,. i
0 E S~e hypoalbuminaemia will increase the al_!lOUnt of free ,. [
~rug ~~ailable for a~sorption across a ~ell membrane

-----
'
 Pharmacology MCQs

1.1 Answers:
0 A False
Gt B True
@ C True
e D True
(! E True '
Lipophilic chains face inward~.
Passiv..e_diffusion is the most common form of diffusion and
requires no energy.
Ion channel permeability maybe altered according to other
substances, for example local anaesthetic and fast-acting sodium
channels. ==--c=- -=-

1.2 Answers:
e A True
e B True
~ 9 C False
e D True
0 E False
Pinocytosis is a mechanism of absorption. The cell membrane
invaginates around the target molecule and moves it into the cell.
for large-·_ moleg,les.
It is a commonly utilised transport_.,,.·--.,- ..
The speed_~f 2b~C?.!Ption depends not only on lipid solubility but
als~ on ionisation and protejn_~ncJrng.
fyAc· I co~.ot~bind{~~ ~rugs whereas albumin tends to
net
bi acidic or(n~.:!!ra!__ ?rugs. -
 \
\, h
\).

Pharmacology MCQs

1.3 Bonasatioro:
X
D A The Henderson-Hasselbalch equation states: A
pH= pK. + log(proton do~otori acceptor) 0
/ 0 B
For an acid (AH) the equation would read: _.
pH = pKa + log([A-J + [AH])
t.,/ 0 C
AQis
h • more ionised in an environment that has a pH lower , .;,
. ,. , ,.Y\ ~,-.___
. .' ..- ._.,., l,<..;,._,.
1>i-\ '/ ,·,::o__ , ,=-
1:> \-', ----- \. J\...,_ .,, ---t-:.
I,
,\ 0 D t an rts pK,,
The pKa of blood at body temperature is 6.4 0 , \·
!/o E
The pKa is the pH at which 50% of the solution exists in
ionised and unionised forms
,....._c,~J
---.-.,.;~:.:-
1.4 Protein binding:
A One albumin molecule can bind a number of different drugs
B Albumin can bind to neutral drugs _,
C Globins bind to basic drugs

.·.,,,.- ./'

0 E Copper is bound to a2-globin

-
D Iron is bound to ~1-globin a--
•. .

-
') \>

r..,
 Pharmacology MCQs

..,

1.3 Arilswen:
@ A false
® B True
® C True
·_,;;.~- • D False
• IE True
The Henderson-Hasselbalch equation states:
pH= pKa + log(lproton acceptor] + [proton donorl).
Therefore, for a base (B), the equation would read:
pH = pKa + log{[B] + [BH+l) ...
The pKa of blood at body temperature is 6.1 .·

1.4 Answers:
• A True
• B True ~
• C True
D True
• E True
Albumin binds~neutral and acic::;-__drugs whereas~
bind ~~~it. dr~s. ere are a number of different bindinf; sites on
an albumin molecule. Binding of one site can cause a
conformational change and can alter ability to bind at other sites.

\:
\
I
\1
I'
 Pharmacology MCQs

r.s The a~etyk~oli_!!t t~~-ptox;,,.

:-, 0 A Is made up of fu:_e ~n.its in an adult: ~-~J~ -~ E .
B Requires the binding of two acetykho!ine molecules in order
D
to open the ion channel - 7
D C Once open allows ~j to pass at a rate of 1_9 per second _
0 D Demonstrates selectivity for the passage of sodium ions ~ r °'
D E Is activated following the arrival of an action potential as
approximately 200 000 molecules of acetylcholine are
0
released
-
"J -;;"'L' v i
/ l r , _ :··- ... ·.. f~ ~ /i j,-
,/
.~, ',.-. .,~

f)\•.·
1--..
!
l I
.

1.6 Regarding ~hoiinergk receptors: --- ... ._ I'·. ~ ..... --- '· ,··
· D A They can be divided into nicotinic and muscarinic receptors
__•..•£Z:::-- -
_\ D B Muscarinic receptors are present on the postsynaptic , \ . · ·'. ..
membraneof neuromusculaJ_junctions ·· -
--------
0 C Sweat glands contain muscarinic receptors ~-r-. -'r
D D Saliva')' glands contain muscarinic-receptors t-" ~
' D E They do not form a functioning part of the sympathetic nervous
system

7
 Pharmacology MCQs

1.5 Answer§~
@
A True
B True
@
C True
~ D False
II) IE False
The acetylcholine receptor demonstrates selectivity for the
passage of small cations but is ~t specific for sodium. It allows
the passage of sodium,
membrane. - -~- ROtassium and calcium across the

Approximately ~ million acetylcholine molecules are released per

action potential.
Approximately 20Q_v~sicies, each containing around 10 000
molecules of acetylcholine, are released per acti, 111 potential.
1.6 Answers:
• A True
• B False
• C True
• D True
• E false

Nicotinic r:e.c.eptors are present in somatic muscle and at the

ganglia of parasympathetic and sympathetic nerves, including
sweat glands. They are also responsible for stimulation of the
adrenal medulla.
Muscarinic receptors are found in the postganglionic
para5¥mpathetic nerve endings and in the postganglionic
sympathetic nerve endings of the sweat glands. Po~tganglioni~
12arasymp_a.the.ti.c_fibre~suppJy the parond, maxillary and
sublingual salivary glanasvia muscarinic receptors.
Most ROsJganglionic sy'llQMhetic_eff.e_ ctor function is via
adrenergic receptors.
References: Yentis SM. Anaesthesia and Intensive Care A-Z. 3rd
edn. Butterwoth Heinemann, 2004.
Power and Kam. Principles of Physiology for the Anaesthetist.

8
 Pharmacology MCQs

1.i The following are true of ~om~!E~lar bl«?_c~~fk~sessment;.

/ 0 A Train of four. (TOE). riquires the. application of a suprarnaxirnal
stfmu~~s at a frequency of~· ?-- ---
/' 0 B One twitch on a TOF is equivalent to.80%
,,.,- neuromuscular
,.,.. __,., a
blockade 00'/e --- i> \
, , ~ a -·-- -i> 'l..
i/ D C Seventy percent neuromuscular blockade is eqUt~~lent to three
twitches on a TOF ,0,., , - o~
J\ D D Post-tetanic count is demonstrated by application of a 50-Hz
stimulus for 5 seconds followed by a 3-second pause and then
application 9-f---2: ::Hz stimuli until the twitches disappear \ \--+-:__
' t/'rJ E Testing of neuromuscular blockade by use of orbicularis oculi J\ ·r, r-J-. -:,)
1
can underestimate the degree of neuromuscular blockade ·f,_y_ , , ~ ·

1.8 Suxamethonium:
/o A Is chemically composed of two adjoined acetylcholine
molecules
v" 0 B · Has a longer duration of action compared with acetylchoHne
because its hydrolysing enzyme is~t present at the
neuromuscular junction .,.
l O C At approximately 50°/4 of an administered dose reaches the.
neuromuscular junction
1
, D D Is entirely hydrolysed in the plasma
/, D E At approximatel_X-30°/ois excreted unchanged in the urine \Q
 Pharmacology MCQs

·3.::,;

1.i Answers:
9 A True
!'a B false
© C True
@ D False
© E True
/ The TOF is a sequence of four supramaximal square wave
electrical pulses each lasting 0.2 ms given at 2 Hz.
-:-.:::t, No twitch on a TOF corresponds to 100% blockade.
---0 One twitch corresponds to ~o blockade.
::::5.:) Two twitches correspond to ~o blockade.
-:::-4>Three twitches correspond to -=75% blockade.
/ Post-tetanic count is useful if there-~no palpable/visible
twitches on a TOF. A 5-second,lsO-Hzhetanic stimulus is aprr'ie~
followed by a 3-second pause a~J<en pulse stimulation at,~
,,/ The post-tetanic count is recorded. A count of .!3 twitches is
equivalent to 2 twitches on a TOF. --
/ The orbicularis ocull muscle is Tess sensitive to neuromuscular
blockade when compared with the diaphragm and vocal folds.
_/" The ulnar nerve is more sensitive.

1,8 Answers:
C, A True
ID B True
• C False
@ D False
® E False
Introduced in the 1950s, suxamethonium offered significant
advantages over the ignger-~cthJg tubocurarine used at the time. It
is metabolised by plasma or pseudocholinesterases that are present
in bolh plasma and liver, therefore vmttle of an administered
doseactually reaches the neuromuscular junction (10-20%). It
can exhibit phase 2 block, thought to be secondary to presynaptic
blockade. Very little is excreted in the urine - approximately 10%.
,_
Chemically it is two acetykholine molecules, adjoined via their
I
·\·, acetvl groups.
i
'I
 Pharmacology MCQs

1.9 Suxamethoniurn:
,/ D A Is metabolised to succinic acid and choline \\ '
_x,-r~ ' .
r I •

'A D B Can cause ~~da_l_ bradycardia s~~-0~9~fY to.sympathetic

ablation .:::a.-.:..- -

/DC Can cause rnyalgla, which is iT)OSt cor}'lmQn in young women

, ,/ D D Can cause a rise in intraocular pressure by approximately
100% for a matter of minutes after administration ·
:.-,.,,./ D E Does not cause an increased .-risk
~ of---·reflux
•;..- as ---it. increases
--.:-
the
~--~--~

tone ofthe lower oesophageal sphincter

7
..,_,,. Y----t>
 Pharmacology MCQs

~ G 9 A!11l§Wle1!'$:
..- . ; \
-- ----· --.'?.
® A True
0 B false i I
-l -~ ..r'. ~1\\·c aC1H-·-'
@ C True -- - I L, ,,!
, .. ._. 1 I'
1'1,i ,,,~

@ D True
e E True
Suxamethonium is initially metabolised to succinyl monochollne
and then further metabolised to succinic acid and choline.
It can cause Qp,dal bradycardia secondary to direct nodal
__.~scarinic receptor stim~lc:tion. -~~ ----
Normal intraocular,pressure f10-15 mmHg) is raised by r-..J 100%
following suxamethonium administration, which clearly presents
a problem with penetrating eye injuries. Although it increases
i1J_tragastric pressµre by approximatelv ljl cmH20 it also increas~s
lower oesophageal sphincter tone and therefore does not increase -
the risk of reflux. ~ ;;z-
~ ---- --·.-:--·-

,, \
oc' /
 Pharmacology MCQs

1Q10 Regarding malignant hyperthermia:

'/, D A it exhibits autosomal recessive inheritance
. •. -- -··-
VD B With in~~gJ!ge there is a reduction in tendency to suffer a
reaction
\r/D ( it is associated with a defect on the receP,!tor coded for on
chromosome 19. • • · ,.. • I '

, / -o O Witho~~ntrolene o,o~l-~ty ca_n approachlQ /o

0

. ,... · D E When anaesthetising a susceptible patient, _the anaesthetic

- machine should first be flushed with 199.°/o oxygen for 20-30
minutes

\
,:. ... v

13
 Pharmacology MCQs

1o10 Answers:
© A False
0 B True
© C True
© D True
$ E
__ . . ... , , erthermia (MH) was thought to exhibit autosom~I
c[o'!l~ inheritance: however, it now seems to be more
a5m plex than that and suspected cases should have ..Qtt~ Jesting
to reduce the risk of erroneous diagnosis.
It has been estimated that the UK population prevalence of
genetic susceptibility lies between ~1-=-5000 and 1 : 10.000~ _
It is associated with a defect on the ~.11odine recg_Qtor, which is
encoded for on chromosome ~ and results in an increase in
intracellplaLcal~j
- = ====___:;_.---==
::::
-.
,
There seems to be a reduction in the tendency to have a reaction
with in~..r~_asingage. Interestingly, most patients found to be
susceptible to ~H will have had, OQ average, three previous
uneventful
- - - anaesthetics.
-
With the introduction of dantrolene mortality is less than lo/o.
Dantrolene prevents the release of calcium from sarcoplasmtc
reticulum instriated muscle. It is presented as an orange powder
containing'io mi)dantrolene, ~-& ri,annitol and sodium ·
hy~de. It is made up with 60 ml water, which gives the
solution a pH of~9.5 ..
Dosage is 0.1 mg/kg to a maximum of 10 mg/kg.
,,· Reference: Malignant hyperthermia. British Journal of Anaesthesia
CEPD Reviews 2003; 3(1 ): 5-9.

I
I'

I·
i
11 14
 Pharmacology MCQs

1.11 Regarding suxamethonium apnoea:

/ D A It can be congenital or acquired
b
X D B 99% of the population are homozygous for the normal gene
f.__ 0 C The gene for plasma cholinesterase activity is located on
chromosornet 9 3
---·-- ~ .... ~ ·- . ·-- ·--·-
./ D D The ~ibu~aine numbes\represents the percentage inhibition
that dibucaine (an amide local anaesthetic) causes to the
plasma cholinesterase
. ,,,,,,.,,,,/ D E The ~ibucaine numberjof a homozygous normal genotype
would be.. 80.

1.12 Suxamethonium metabolism;

/0 A There are6 0 different genotypes responsible for
suxamethonium metabolism
0 8 (!=our differerrt\alleles have been identified in relation to
pseudo/plasma cholinesterase activity
t
\ 0 C The homozygous fluoridi;-resistant allele conveys the longest
duration of action of swZamethonium
,,
/
D D Thyrotoxicosis is a cause for acquir_gd suxamethonium apnoea
r• 1_..,,/ D E Metoclopramide can cause acquired suxamethonium apnoea

"'·-· ~

li
 Pharmacology MCQs

1.11 Answers:
,) A True
€) B False
0 C False
© D True
e E True •
The gene encoding cholinesterase activity is on chromosome 3.
Chromosome 19 encodes the ryanodine receptor:which Is _
responsible for the condition malignanl_h_yperthermia.
A total of ~o of the population are homozygous for the normal
gene. Dibucaine inhiQ!ts normal plasma cholinesterase to a
greater degree thenabnormal cholinesterase. Jl)__e dibucaine
number represents this percentage inhibition/~dibuc~~~~~
~ inhibits the abnormal homozygous atypical gene by o~ .
giving a dibucaine number of 20. ·-

1.12 Answers:
Cl!'

e A True
B True
e
~ C False
® D True
19 E True
Ten different geno1Ypes can occur from f_Q!Jr different a~s.
~ .:::=- ~ =-=------
-
The alleles are silent, atypical, fluoride resistant and normal.
,,; Most prolonged suxamethonium duration is seen with
homozygous silent, homozygous atypical and het~rozygous silenL
a~_pic~_!_!ypes. ·---· - •.. i

/ Pathological causes of acquired suxamethonium apnoea i~e

heart failure, renal failure, fiver failure, hyperthyroidism and
cancer.
/ Physiological causes in,c;lude pregnancy and drug-induced causes
secondary to the drug acting as either a substrate or an inhibitor
(metodopramide) to plasma cholinesterase.
 Pharmacology MCQs

1.13 When using non-depolarising muscle relaxants: /, I ,-..- •

. / -':'\ ,
,'I\ D A Concomitant use of lithium shortens the duration of
neuromuscular blockaae - /
,( D B Mivacurium is !g_n~(tfng benzylisoquinolinium ·:. Y\ .::; -r L-
,,,.,.....-:: .. ·- ---~------
/; D C Pancuroniur:i is:,~uaternary\i!1 _na~ure
, _,/ D D · -~~r~_!:1j_~!1]) differs from P-an~ur?_nfum )by a single methyl
group '
,/ D E Rocuronlurn has a(l~-po~ncy)compared with other
aminosteroid muscle relaxants

1.14 Pancuronium:
v D A Is associated with an increase in heart rate secondary to its
blockade of ~_?.!9iac ~-~s~~-~-~ic r~c-~r!<?!~
/_,, D B Has metabolites that are excreted in bile
! Q _ l_f CJ _/,
'<. D C Is more than 50% plasma protein bound
I
I ~,
, / D D Is predominantly excreted unchanged in the urine
·// D E Is used in doses·of0.1 mg/kgtof;cilitate intubation
"i

~ l CuYOn r() vv1,

1-.

1-,
 Pharmacology MCQs

1 .~ 1 Answers:
© A False
@) B False
© C True
~ D True
e E True
Lithium prolongs the action of non-depolarising muscle relaxants
oecause of its sodium channel blockade effect.·
-= - ---
f\.1ivacurium is a short-acting benzylisoquinolinium lasting
approximately 20 minutes.

1.14 Answers:
) A True
B True
C False
e D True
E True
lll,
Pancuronium is· alfuiguaterna!Y} aminosteroid muscle' relaxant. Its
use is associated with an increase in heart rate secondary to
cardiac muscarinicJec_~ptQ_r_blockade and, because of iri~
sympathomimetic ac!,iY.lty, causes inhibition of norepinephrine
reuptake at post-ganglionic nerve endings. It is between 1_0% and
40% protein bound. Around 35% is metabolised in the liver by
- ~

o
deacetyiation. Unchanged drug is excreted in the urine.
.r= -r..,. ~~ ~

I
 Pharmacology MCQs

1.15 Vecuronium: Y''\ =«. 0 f( u ;, L \ I\ ('• • 1/ .., \'. ·, ·.• (. :. \ ~-r· '·
/ '

,,-, ,, D A Is stored as freeze-dried powder containing m"an'nitol and

S<?9!l:'n:!.~Ydr9xide - ·- ·
,,/'/ · D B Has been associated with. rnyopathy
-~w.._.,_
when used as an infusion
·1 __ /.,D C is mor~ lipid soluble than pancuronium
~-,,."
~=- -----
.__./ D D Has a metabolite, 3-hydroxyvecuronium, that has significant
muscle relaxant properties - ---
,. --: -~
-
D E Causes tachycardia

1.16 D .- " :_, ~' ·, ", " \ u;,' .)?, ,. ~ ·

Atracurium:
~D A Has four chiral centres C., . :?\ )

D B Undergoes Hofmann eliminatio:·,, which accounts f~~!~;of

its metabolism ----.
1
l,:
f,, D C Undergoes Hofmann elimination, which is increased by v
· acidosis

.,
/ .
-/ D D Yields laudanosine (a product of its metabolism), which is a
glycine ~'ntagonist
~
• D E Yields la~darrswe as a breakd~wn product of~oth)Hofmann
degradation and ester hydrolysis ·

'. :-..
,·\t'
,t_i

'i
,,•'

1Q
 Pharmacology MCQs
• { .•. ,. t {

,,..-- Y-1\ u< ~ \ ,_ \' -\ . ;',;.. ·~ \.,(,._ \::i .__z_

1.15. Answers: ,·.-. .·\ {-
~ (\,)&.,'--.,
1 ' <:.
\...;:) ~'1
/
~11 ] I'< r. -r·
{"___.'-'..,f-Jj -

A True - ~ \J :
B True ,, CCV'---.._~~ c. ~-\ ,._ \.0 J__ t
C True --+- '\. r. \,', ,,. 9-L
,v \_1__.-

D True / ::.. c... \ •. v---c. ~- -

E False /'---·-~
Vecuronium is a monoguaternary ~inosteroid.\lt is unstable in
solution and therefore is stored as a freeze-dried powqer. It is
!.!!Q!:_e lipid soluble compared with pancuronium and has 8!:e~er
6mary excretion. Unlike pancuronium it is cardiac stable.--=~
__ . =.--:--~-

1.16 Answers:
A True
B False
C False
..
D True
E True o I ,./.

Atracurium is a~zylisoguinolinium (/>resented as a mixture of

10
-· stereoisomers.
- It has four
_::::::
chiral centres.
When used in intubating doses of 0.5 mg/kg it has a moderate
duration of action. ,.---._
Hofmann eli~nation accounts for 4~ its metabolism.
A total of ~0%pf it is metabolised by ~on-specific esterases.
-=---
Both elimination pathways yield laudanosine, a glycine
antagonist, which has no neuromuscular blocking effects and is
renally excreted.
... ------------~ . -
-= .
,.,.. .. --:--

I.
I

I
\ ·

:
II
:I
'
?() I
 Pharmacology MCQs

1.1 i Regarding muscle relaxants.

1 // D A Cisatracurium is predominantly eliminated by Hofmann
- degradation -··----·------~;-
-·--·- _, / . . "\
I D B Cisatracurium is JO times· more potent than atracurium
X,_ 0 C Cisatracurium has active metabolites, ie with neuromuscular
blocking properties ,
l D D Cisatracurium i~ unsafe f~~ ~~e>in patients with end-stage renal
failure
/ D E Gallamine causes a tachycardia
*'f-\(1-nI 'C.,)v\Dl 1v\t
" ' ?_ P:>
0 .I f tv2: ,-c-
.I\ ,__
:..C_'":. C' - - - - ----._
<:::. ~.:.._ .. :.· (-.
.- 1.18
d h • ( ,~ l .r-- I . r . ' . - . - i- r I
E rop omum: \..__\.J(\~ .. • ·.,',. ,,:-:< i J~;,::-:_~ ·,··_), S Vt<.'. .T, ~r
A
o{:}J.f{(lf .
'; +
Cr-)\..'.\JV_--._ ,.,,, · · \ .-, · '"' -
,,./ 0 A Can worsen a cholinergic crisis __ )
I "\ -
·1 D B Forms a true. covalenfbond with acetylcholinesterase
/
·1• • • "·· •
1 ./
· 0 C Crosses the blood-brain barrier
,, D D Is predominantly excreted unchanged in the urine ·;£):S. ,
\' ~ /_pf,,r1
0 E Has a slower onset of action compared with neostigmine / ,
a, a,

I:
!,
c;;

l: ,
 Pharmacology MCQs

1J7 Answers:
e A True
(j} B false
~ C False
• D False
• E True
Cisatracurium, 1 of 1_Q stereoisomers Q!:_~t in atracurium, is
t~to four times more potent when compared with atracurium.
ltJs~redominantly excreted by Hofmann elimination, undergoing
~.9hect plasma esterase hydrolysis. Metabolites are void of any
n euromuscular blocking activity. It can be used safely in both
renal and hepatic failure. · --
Gallamine, the first ~ynth~tic muscle relaxant, does cause
increased heart rate seconaary to cardiac muscarinic receptor
blockade and sympathetic nervous system stimulation, like
Rancuronium.

1.18 Answers: . / 'f feJe,Hr cf) ft)

• A True
~G Cl,L-l1iMSt<'. :.foJS<::._
& B False
• C False
• D True
e E false
Edrophonium is used in the Tensilon test to aid diagnosis of
myasthenia gravis. It inactivates acety c olinesterase by forming
~k electrostatic boi:1gs with it, thereby blocking its active sites.
It has a taster onset of action when compared with neostigmine
and has fewer muscarinic side effects. .
Edropho~m ~ causes an increase in acetylcholine release(S\ ~
/ is a guaternary_gmine (like glycopyrrolate) and therefore does~
cross the blood-brgin
- / \
barrier
-
or the placenta.
-
- l
j
Approximately 65°1<;,As excreted unchanged in urine with the
---=::---
- remainder undergoing glucurooidation in the liver and bilious
,. '

excretion.

. I
• I I
 . .

f.JJ1c1rmacology MCQs

1 .19 Neostigmine: _j
• .. , . ·-
--- --·--·- .-·------·- .• - -
/-CJ A Forms a,carbamy_!_dt~-~ ei:,2v_!:1~E:_'.-~g_mp~_:~_\with
acetylcholinesterase
B May prolong the action of rnivacurium
I ; ' I ) '
C Crosses the blood-brain barrier
lJ Is 50°/4> excreted unchanged in the urine
E May precipitate bronchospasm in people with asthma
•o
1.20 The following are true of anticholinesterase:
~/ D A Edrophonium may be ct more appropriate reversal agent for
./ mivacurium than neosti_gmirie ,
/ D B Physostigmine is well absorbed from the gut \ ,::=,;ov-
" · r _ - e. . ~-"~''"'~c...
~ 0 C ~rganophos~horus compound_s p~osphorylatr thee site
o1 acetylcholmesterase, rendering 1t useless · .
[J D Acetylcholinesterase inbibirors can be used in the treatment of
Alzhcrrner's disease "f>=- V\.Q..- ··,).:.-1.-3 L-•
•
_ / I i F Organophosphorus t ornpounds can be used to treat narrow-
. _ _ ,111gle glaucumc1
,. 1~.·,;r,.v,) .__, le:.
"-~ \:T- ~~,\.p--.\'-

"I:
'jv\
--- .
c:'. \ \
\·

•·"' \ a'"·'"(r-. \._J. • • ', •• .,,..._,.

 Pharmacology MCQs \ (
·--~~/

:::. '\.,·::_;
\ ,.,,~" C
\ \c, l- 1.-v'-.Y-- --i-
\.(A.,.r"L~•- ~

1o19 Answers:
e A True
e B True vv- (\( \_·
;" 'f ---
e C False I

® D True
e E True
Neostigmine is used as a reversal of neuromusc.ular blockade
secondary to its action on acet-rlcholinesterase. It forms a
~-~rb~ylated enzym_e coll).e!_~x with a£etykholinesterase,
thereby preventing the hydrolysis of acetylcholine.
Neostigmine is a quaternary compound and therefore does not
~ :::::: ==;::::- --
cross the blood-brain barrier. It also inhibjts plasma ==--
---

cholinesterase and can therefore le!!Slfienthe block of

suxamethonium and mivacurium. ~

1.20 Answers:

• A True
• B True
• C False
• D True
• E True
__ t0ivacurium is metabolised by ~asma cholinesterase, which
neostigmine inhibits. Edrophonium, which increases
acetylch~line rele~e and decreases acetylcholine hydrolysis,
would therefore be a more suitable aid to neuromuscular
blockade reversal.
. _Physostigm!!le is a _!~!].i[}~ amine and therefore crosses the blood-
brain barrier and placenta. 0!,_ganq_pj:!Q_s.p_ho.rus-comoounds
irreversibly phosphorylate esteratic sites, rendering
acet lcholin~sterase useless.-·
Aricept (donepezil) is a reversible inhibitor of
acetylcholinesterase, used in a once daily dose for the treatment
of Alzheimer's dise_ase.(Ecothiopate Jis an example of an
organophosphorus compound used for the treatment of narrow-
angle glaucoma.

....•
 1.21 Regarding y .. aminebutyric add (~ABA} receptors:
0 A GABA-A receptors are largel~-~ynap;ic. f '0 s-=-;
' D B GABA-B receptors are ~d~a_red ~~~--~-b-~~:nels 0\ · f. r, ·._:_

0 C Activated GABA-B receptors increase <:h loriq~ conductance Y ·'-,-

• I
•

/ 0 D A
Benzodiazepines increase chloride conductance at the GABA-;
receptor-- -. - - - . ~----· -~
--. ,____,
/
/ 0 E E!~mi~te binds to the fl subunit of GABA-~
---- ~
-·-·-

-- .,
• + ~~-

1.22 Midazolam:
/o A At(~) it !:~_~s.ts in an ionised form
; D B Has a pKa(?: 7 .4] -~ >
l'-
: ; D C Causes pain on injection L
. 7'-
.( t' - • r
·.:;

/o
(

D Has effects that can ~e prolonged with concomitant

administration of alfentanil
E Has an ~ral bioavailability of approximately 70% U\-0
)(. D
, ..
b,oc½

{~/
P'
L,..;

25
 Pharmacology MCQs
~ {\t:i f \ - P.1
1 ..
1.21 A~

• A False
I

0 B False ~ . t, :
C---l'_.: • C. "1,)'\_ _.,-)
., \ \ ,.·-•,\ . . ..
•
,,,. M ' • (

C False
. ·,

__.o ½f--r ~c:f \~\'Le,,_+,~---.. .tt,~ tf'-'O...vr-('o-- '---- rv'\.~""~""s··=

• D True
• E True - .
GABA-A receQtors are \ligand gatecf\and largely P2~tsynae!ic. They
potentiate chlQ!ide concfuctance~ ... ·
GbBA-B receptgrs are meta_!?Etropic{~acting via G-proteins, and
are associated with increased potassium conductance. ·
J1:_oth GABA-A and -B receptors c~_use hyperpolarisation of the
n~ronal membrane. =""=··--=,,.

1.22 Answers
• A True
e B False
• C False
• D True
o E False
Midazalam is~\ when adPH\3.5 or less~ring structure is
open and it exists as an ion~olecule. At pH> 3.5, it: ring
~es and it is un~sed.Therefore, it exhibits
tautomerism .::::;:::,
3
It has a~of 6.5,Q9t a pH _7.4 (plasma pH) it will exist
predominantly in a unionised form (89% unionised) and is
as
therefore lipid soluble. It is used a water-soluble solution and it
does not cause pain on injection.
Midazolam has an oral bioavailability of approximately 40%. I,.
j!:==. L_
I'
'I
; I
L.
I

I..
I

.I,
\;t\
l p!
i
1}
I! ~l
I \1:
\ ~ tl
 -- Pharmacology MCQs

1.23 Re5a!_!li~nzodiazepines: .(\_.,,/ ~... ,

D A D · azepam} is '!!Q@ highly protein bound than any of the other
b~~Q~epmes --~ -
.---
,/o 1
)
B pia~epaaj)has a long eli.oination half-life compared with 1 •• , 1
• 1 ~ f

loraz~)pam} 1. "·
1
-~
/-:----.______

/ D C ,.~~f ,diaze~a~)s g'.7'3~er th<ln _that o(forazepa~

, D D'--- L2.raze~has active metabolites ,_, ":>\ <A."2>-<>

/, D E (Lorazepam )has the highest ~~,~~e-of distribution.ris ... " '-11.-11~~

., /
. /'
,..,.:.· -1

..:,

. . --- <"!· t>

:,,,-?
F
1l. /
/
. t,,
~>\
l.,.-
1/'
\ ~
,., C':.. \}
'"\,
..--
(,.,I<

iP
,i
-- I

.,
•.... ~

· l)7....,
7

I
l:_

'17
 Pharmacology MCQs

1.23 All1lSW<etr$:

@ A False
e B True
• C False
0 D false ,..._
!
e E False
Diazepam, lorazepam and midazolam are all atJproximately 95%
protein bound. --'--
Midazolam has the fastest elimination half-life followed by
lorazepam then diazepam (1-4 hours, 10-20 hours and 20-45
hours, respectively). ·
The volume of distribution of diazepam and midazolam are
approximately equal at 1-1.5 I/kg compared with 0.75-1.3 I/kg
for lorazepam.
Clearance of midazolam is greater than that of lorazepam, which
is greater than that of diazepam.
·~ - an~ave active m~~abolites.

-
\ f.1 .Pi-'C'.:
/2 ~-
. _,(' .. ( ~~··· --i. ~--·

r ,
~--'

!'
 -P\ '(- '. :-----. : i '
l

~ , •
\

.
~

·-·
•.

•
- .

I
-~.
i.
\
Pharmacology MCQs

1.24 Tricydic antidepressants: .

;,( D A Take effect as soon as the concentration of neurotransmi.tter in
' · the synapse increases
,_,<·,,b B Cause a-adrenoceptor blockade
/, D C Have a low volume of distribution I
vo D Are highly protein bound ,·
Vo E In overdose may present with _y.,i~en]!}g of the QRS complex
on ECG - .

/
 Pharmacology MCQs

\'\'\ \},'--- C c, •. \ _ •, ·r-, '

Answell'S~
A false ''t'- .•.r ••.. -., ~

• B True
C False
D True
e E True
The effect of tricyclic antidepressants does~ mirror the increase
in neurotransmitter at the synapse but occursup to ~~s after
administration. -- -----··- -=
Other effects \!]dud$ a-adrenoceptor, muscarinic and A.
histaminergic blockaQ.e. They have ~ volume of distr 'bution r
and gjnd plasma proteins.
_: EC~ changes ~ncl@~ sinu~_!c!fb_~a_rdia, y~_ntricular arrhythmias,
right bundle-branch block and prolo_ng~d QJ. _
Following overdose, most life-threatening problems occur within
the fi~t&Jwu!?~ A greater risk of a__!"rhythrri_i9_s and seizu~ is
observed with the following electrocardiograph (ECC-) changes:
CII '
widening of the QRS complex, increased QT interval and right
axis deviation. - -
_ 0-J\
. I; . Reference: Cardiac arrest in special circumstances. Advanced Life
(\ r-,r- \ ~ <,,,,vrJ
1 ~--support. Resuscitation Council (UK). 5th edn. 122-3.

-\
I
 Pharmacology MCQs
\ l').-~
~--- ( \ ?;
1 .25
, Regarding antidepressants: .
D A Fluoxetine ~~-l~~rLy~Jy blocks 5-HT neuronal reuptake
D B Venlafaxine-bi;ck;·S-HT and norepinephrine reuptake
1" D C Monoamin~ase A~pr;fe·;~ntially deaminates tyramine and (
phenyletharnine
'/ ~ 0 D Monoamme oxidasej3 .preferentially deaminates 5-HT and f· ·
catecholamines
/"/ D E New generation monoamine oxidase lnhihitnrs are selective
and reversible . ac..\~
A \ ~ , 1 [t:. ~ l ,.- ('::,_
r fl'
L LL O' L.

11 Y1.-1·1 \..CV1. AJ v .::; ~t,\J· '::, .0 I¾ CV\°"'~~ 't- >-r:::,

1.26 Phenytoin: -f: - - Co-- G ~A ~-"\
'{ 0 A Should be diluted with 5% dextrose
/
D B IDhibits cytochrome P450 enzymes I•

·.•... . .- ; ,re,
D C Initially undergoes zero-order kinetics - ,,
I

0 D Has an oral bloavailabillty of approximately 50%

\
D E Has major metapolites that are excreted in bile ('J {'· I \ ,' .1,\
I • v
 Pharmacology MCQs

1.25 Answers:
® A True
@ B True
® C false
@! D False
® E True
Monoaniine oxidase A deaminates 5-HT and catecholamines
--------- ==="'--
preferentially. Monoamine oxidase ~ deaminaJes tyramine and
P-henyJethamine. ~ew generation rnonoamine oxidase inhibitors,
@moclobe~de, cause less potentiation of tyramine so the
11- patients do ~need dietary restrictions. 001:1<?a~ine oxi~-?se

LnhibJ.!Q_rs have interactions that are important to anaesthesia.

_ Indirectly acting sympathomJ_metics __should be avoided, as these
are reliant on rnonoarnine oxidase for their metabolism. g_i~ectly_
acting SYJ:llpathqmJrnetics are also metabolised by catechol-0-
methyltran~ras~ and may therefore be used safely.

1.26 Ans~~rs: ,.•.

,_
Qi;

• A False
• B False
0 C False
• D False
• E False
Phenytoin is a widely used antiepileptic. It is also an anti-
= ----=--
~rrhythmic, neuroanalgesic and pot~nt enzyme inducer. It
--
i~~t~es sodium channels and may decrease calcium entry into
neurons and E:_nhAD_ce y-aminobutyric acid (GABA) action. Atl!,o,¥i,]
QQ~S it undergoes first-order kinetics. Upon saturation of the --
enzyme system it undergoes zero-order metabolism. It has 90%
oral bioavailability and major metabolites are excreted Lenall.y.
Diluting with 5% dextrose is contraindicated as it is incompatible,
I -·
becoming gelatinous. -
- ~
~-
----·· ...
-
·-----~
I
r-~-

Ii \'
I
l
I
(I
!!'
,1: J!
! I
' I
i; I
'I
1! \ 32
- !
 G -- -i-,
l
\ Pharmacology
_/
MCQs

• 1 ;1,7 The following are true of antacids:

v/o A Th.~_eff~ of sodium citrate wear o~~1~b}_Q 30 minutes
~D B Clmetidine
-------1
------------.
'
has an irnidazole structure
--· ----- -----
D c, --Cimetidi~is
I"'
--·. ~ - ----- --- --
anHj-receptor antagonist
~~
r
.,,
,~' ·
V - \ /

/ D D _fj_~""'~tL~Jis a hepatic microsomal enzyme inducer ' - ,·~,

,/,, 0

0 E (1.....Ranitidine
. . ..
i~ a hepatic microsomal enzyme inhibitor ,, --
__;
t-.r\
'
i-

1.28 Regardi~tacids: /~
(_. ,.
0 A Ranitidi~_e should be avoided in (eorphyria \
0 B Ranitidi~·can cause thrombocytopenia
- ~ D C\.Ranitidin~ has a high oral bioavailability
I . .__ -----· ~--
I
I~
0 D Famotidine is a proton pump inhibitor
y-~ 0 E Omeprazole achieves complete achlorhydria

33
 Pharmacology MCQs

1 .. 27 Answers:
e A True
e B True
* C False
G D False
® E False
\ Sodium citr~!~/is a non-particul~te antactdtused extensively in
· obstetric anaesthesia. Cimetidine is an Hi-receptor antagonist. It
increases gut pH and decreases volume of secretion. It is a
cytochrome P450 enzyme_ inhibitor and-5,0% is excreted
unchanged in urine. Ranitidioe does lf.l@;!,tlhibit hepatic enzymes;
however, it can cause reversr61e derangement of liver function
tests (LFTs).

1.28 Answers:
e A True
B True
C False
• D False
E Tuue ,
As with many drugs, ranitidine is n~afe in porphx.pa. It may also
cause thrombocytopenia and neut~Ren~a, aq!}~r'!.l~J live[
function tests (LFTs) and anaphylaxis. Oral bioavailability is 50%,
as··coulcfoe expected when comparing intravenous and oral drug
dosages. Famotidir:1e is a new H2-receptor antagonist.

I
I

('.

34 _ ·;·
 Pharmacology MCQs

·1.29 Drugs affecting the gastrointestinal tract: ~----

'J
D A Domperidone crosses the blood-brain barrier~~
,. I
D B Dompe~~~~-e is readily available in intravenous preparations
C Metoclopramide can cause acute hypertension in patients
s~fteri ngwith -phaeochromocytoma
_,,,,,.--0 D Cisapride has no antiemetic effect
-" D E High plasma levels of cisapride can precipitate serious
~ -, arrhythmi~s, including torsades de pointes
LaCd-1 e::1J"c9,-e s-rt:[cJ,cs 9; ~ -

v:-o
1.30

/ D
Regarding local anaesthetics:
A They are presented as hydrochloride_salts
B Their ~otency_is attributed to_ionisation. L
, . ,,
1
(> '
I
,
/'\ I ' •
I
I
,._,

1
./\ 0 C Their speed ofacticn is attributed to lipjd-solaoilJ!Y '' ,-. , ''
,... .. -- -------
_,,,./ D D Their duration of action is attributed to protein binding 0 c.
·./ D E In general, local anaesthetics cause vasodilatatlon in high
concentrations · · •, /
 Pharmacology MCQs

1.29 Answers:
e A False
© B False
(D C True
0 D True
® E True I;

Qom~one doesQc:ross the blood-brain barrier and as such

is less likely to pro~;xtrapyramidal side effects compared
with ~9s:lo~ide. Domperidgne (a dopamine antagonist) was
previously given intravenouslybu"fwas deemed ~e secondary
to serious arrhythmias, so now it is available only as oral or rectal
preparations. --- _, ~ =-

1.30 Answers:
c., A True
~ B False
9 C False
• D True
• E False
Local anaesthetics are presented as hydrochloride salts, which
leaves them water soluble. P2tency is related to-llpia solubility,
Sf>eed of onset to pKa (ie ionisation) and duration of action to
protein binding. ~ow concentrations of local anaesthetics tend to
ca!-'se_yasodi!atati?n whereas high concentrations tend to cause
vasoconstriction_._

L'. {\_}~L- I'\

!I

36
 Pharmacology MCQs

1.:n local anaesthetics:

0 A Dibucaine is an/ester t>, · , · r! -'-

.,. D B Systemic absorption is higher with a brachial plexus block c·

· compared with a caudal one ·-- ----::-·::--:- ~~::-:.:-0
./,, D C Esters are less protein bo~nd when compared with amides
--=-- / .· . -=---~·-
)'
D D p-Ami nobenzoate is an '!-:mide metabolite ·· ~~~"=::-- / ,

/ D E Esters do not cross the placenta in significant amounts

/
I =-·."··. ;:j~_::.z.;.. . ':; ::. :., • :. •
''
} 432 : ·P)l~~macologic~.1 Pf~:pe~t_i~s ;of a,~ide local an~esthet~~~; i, ,'.)
1" 0, A The µKa of bupivacain~ is_ g~e~_ter than the pK~_ of procaine _. ,
1

'/( D' B 'Atphysiological,pH·m_ore.Jhin,.,4Q6/4,<?f liqo~~:fr~e,i_s.u·nJonised ·i ·-:, Ii

/o',, c·. . 13'upivaca:ineand ropivacalne.have . ~i~jla. .r-p.~tf~~tag~:P:.i~tein . sS

"
:~;~:~a:~;;·~orelip~·:1::i::~;~~!::~~~~·'., " ,;-~
, . S 'if; ---,-,--~ ~ ~ .A ~. . .. · 1
v.: 5 Q-.1\o,

/o D.
/
ropivacaine
---- -:::.=
~ - ., •..•. · .,,
,., ~-:-:-,.,~,.-,,
.i· r ,,.,, .....•.
r .
~, // D E Amides are extensively protein bound to al--acid:,s,.i~~i_r<:>~~~!1: ~-
~ -;{:~~{ _.;~.J,,:tii - -,
.,; ~·-.,~ ~z

,,
.
_ ,.;./:J-.,..,_
.. f. :. • ·:.' ;1 ;,. ': o-. /
,. :.
; , , ' ...~ '
: ~I
• I I,, < ~ }- .,,. : i
:· : ~-\. .,.·1.~; itj:_:~::,~ :f:;·.'.;-· t,k
'.
.,·1,.
·' " ~;
·',i-r-~: :.:i .,/~

,:t:.i/:;': , ;(;~
::~~,\_:·,

. , '"!'
',: ·,": O ; ':: '.:
.. ~ ,; -~-- .
,.,, •i.:1 ,, ,.,.·; 'l;!'r.;..,"j,'!i/.·,;:- ·f·:;;
·<~~ - - /.' Y~\ .. ; ;}~~ !:..t

.37
 Pharmacoiogy MCQs

1.31 Answen:
\
---. -~ \- ' \
@ · A False 'v~-1 ~::,\ - I f\ "\;,. I
I--'

9 B False '· 1
• C True
D False __,i
E True
Dibucaine (used in the diagnosis of plasma cholinesterase
deficiency) is an amide local anaesthetic. The highest systemic
absorption is associated with intercostal blockade, then caudal,
eP-idural and brachial plexus, and finally the lowest abso!P-tion _
with subcutaneous infiltration. p-Aminobenzoate is the_~i~r_
metabolite that infers its hypersensitivity trait. Est~rs. are rapfclfy_ -
metabolised by plasma esterases so insignificant amounts cross
the placenta. :J

1.32_, AMWers:
• A false·
• B false
• · C True
• D True
• E 1):u
~ •
The' oKa f bugivacaine: is 8.1 compared with 8.9 for procaine. At
phys,o ogical pH lidocaine is 25°{0 unionised and ~ protein
bound to a1-acid glycoprotein. ~h bupivacaine_and ropivacaine
are 95% protein bound. Amides are basic drugs and are therefore
exaensively bound to a1-acid gly.coprotein. B'!f)ivacaine is
appr<>xirnately three times more lipid soluble when compared
with ~ivacaine.

I
,I
I
.1
! j
1
!1·

1\.\··
lV
1i 38
I\
 Pharmacology MCQs

1.33 Regar.ding commonly used t_opical local anaesthetics:

1
:_/ D A EMlA (cream) is an oil at room temperature , :. ,1 , ,: t- ·
... D
1B EMLA cream i$ a 50 : 50 mix of lidocaine and procalne - I

/o C EMLA must be allowed 60 minutes to work

. / D D Amethocaine 4% cream applled topically has a duration of
action of up to 6._hours
"-, D E Am~aane should be avoided in patients with
methaemoglobinaemia

1.34 Regarding local anaesthetics: _r 0

: ,, D A Lidocaine exhibits clas~i-arrhythmic properties
, · D B Only approximately 1 % of an epidurally administered dose of
' bup~ine Cr~ the ~enla ·. . · • \; ~-\-
1 D C The 8 isomer of ropavacame has less desarable S" ~u--A-J- ,r
pharmacological characteristics compared w_ith the s isomer
0 D Cocaine is hepaticaUy ~isectto i!!'ctiw ~
'b E local anaesthetics are mixed with alkaline agent5to increase
. their unionised f'}_dion --
~ ,
. . •. \ e::v--
~ ')_.-?
0-
,o J---
o---t ,r'- I
--0--~ . \._1
d'~
/
-
t'>,..."7Q'
\" ~
,v>-- \..7
O' ~
J.. '"",L.
-
_,
. '.7'
\~ c\
c.,"
o ,

0 ~"
J'

°'-o-\..,_
,i)-..C-..,)
-_,_-+-.
- \.~
-
u- "-J
A,_

. >(_~
~
'v
d'.
"{'
cc,
_,.r'\

q,
~-..['
') --
'Oc; -~--- '<:I" ..r-
~ ~ l<"", b ,'<:5""
./
. f'
. ~
~-'
, -tot)
/ ,<' \.-
.r'

II'./\.~

o,l ,§v..~ .:. .

fv"LL~
yV\.~b
 Pharm~co(o~y MCQs ... ·

1.33 A!l1l§Wfil'§: ; ~ .,,. 1

i ...

0 A True . _: •\.

@ B False ..
. . ,l, _: '
...
;
© C' True ··,: · .. .: ·.. ····
s D _True ·.,
e E ·False
EMLA is an example of a eutectic mixture. It is composed ·of a
50: 50 max of 2.5°a lidocaine and i.5% prilocaine. Prilocairte is.
metabolised to toluidine, which causes methaemoglobinaemia.-"
EMLA cream requires, our to provide effective analgesia,
whereas amethocaine requires only 30)ninutes and also i· •.

produces vasodilatation, which aids with cannulation .

. . ;5--:. ·. ~- .••_--··r-t·-:-,. . . . ,, ,. ....• !'. ~ ·f ..

\.

• A False·
.• , ···.:,. ·- ., , ,
_,, •- ,, ; , 1 • • • • • , • ·
~, r .,
,_",,; ',:,,,,• 'lj..' . •· ....
· >' • •

. ,·. B~·:·]i· . ,:'C. .;·"!': ;~·.· ··;·: .. ·' ·.··, .·· _·. ·· .•.. : . . . : " ' ' .. • I ;'

•. . ... ru~ . . . . . . . .
I (. • ";. ' . , ,, !\..
.
,-.,;,'
- · - . ·· ·
I • ..; ,", • • , ' I " •
.. - - · ., - ·.'
I ',• ,I• ' I

• c···trt: 1e~·t, , .. ,_ - . - · ,.
-:.~· .. ··.-t,·:....;,.·;.:,: ' -~-: . ·;~ ..• ~· •..•.
-u.i, .
, ... .,. • .
,
,i
..
',•• ' • : • .,!_ •• ~ ,:',.- : ',! ~ ~- -~ ·1
• ,D ~ ffrue-~ ·· ' .~ .· :~ · . ·. . . . .. . .. ' .. ,
·:~. ;.c-·E·:,.,ru€·; ·-.i._ .;:; ::i~/·. ··;·:'i ,': _.. :, ~ ~ •. ,·_. .. ~f
i
. ~'\ .·,
• • •·.
... •
.! ;,.. : .• -

.- • • • '··~ .-. •
·- ~;.

•• t
·,.

• ;
••

Lidocaine exhibits class ~nti-arrhythmic properties that are

used to treat ventricular arrhythmia. A total of 95% of a delivered
dose of bupivacaine is protein bound and therefu~e unable to
cross lipid membranes. Of the remaining ~,only 15% is
unionised and therefore able to pass across the placenta, ie
approximately 0.75% of delivered dose. Ropivacaine exists in two
forms - S and R e nantiomers. The R enantiomer is less QOtent and
mor~xic, so a pure S enantiomer form exists. As local

-
anaesthetics are basic by increasing the pH, the drug exists more
in its unionised form and is therefore able to cross nerve
membranes.
I
I

I
I
j·
jtl
I

,\ ,
,1
I 40 I
 I '

-\- 1r,-'. ,\.. ; -!.\r.-j· .. ,>..).

Pharmacology MCQs

1.35 The fo~iowing agents are bacteriostatic rather than bactericidal:

_/ D A Sulphonamides
0 - B Quinolones
0 C Clindamycin
D D Co-trlmoxazole
./ .,,0 E Macrolides

Regarding penicillins:
A Phenoxymethylpenicillin (penicillin VJ is unstable in acid ~ 1• s".--9-. ~
conditions ·- l?-.,_ ~~---b<-R '

0 B Flucloxacillin _is unaffected by ~-lactamases

D C Clavulanic acid is an irreversible inhibitor of ~-lactamases
.// D D Tazocin contains tazobactarn (a ~-lactamase inhibitor)
/·o E Amlnoglycosides act synergistically with penicillins

I
/

i
I.
i .11
 Pharmacology MCQs

1.35 Answers:
@ A True
6) B False
4' C True
0 D False
@ E True

Bacteriostatic Bactericidal

- Macrolides Penicillin
\Tetracycline - - ) Cepha lospori ns
l Sulphonarnide T'<, Ami noglycosides
\ Chlorarnphenicol-' Co-trimoxazole _./"'
,..___ Clindamycin lsoniazid
· -Lincomycin Va neomycin
Metronidazole
Qui nolones->

.,
1.36 Answers:
• A Fabe
• B True
• C True
• D True
• E True
Phenoxymethylpenicillin· must be stable in acid as it is given as an
oral preparation. Tazocin is a combination of piperaclllin and
taz~_tam. Penicillins have their effect by binding
transpeptidase, which is then unable to cross-link bacterial cell
wall peptidoglycans.

l'l I

l•!i
l'
I
 Pharmacology MCQs

1.37 Cephalosporlns;
D A Contain a ~-lactam ring structure
/ D B Of third-generation type (eg ceftriaxone) have a reduced
Gram-nepat'ive action when compared with second-generation
cephalosporins (eg oefuroxime)
,t .• , \
1
D C Undergo enhanced renal elimination with probenecid "" ., "\. ·-- .
. /-0 D Are bactericidal ,
/0 E Of second-generation type have good activity against Neisseria
,,, gonorrhoeae

1.38 The following are. the correct methods of action of antibiotics:

/ D A Tetracyclines inhibit bacterial protein synthesis by binding the
,,-,5-0-S ribosome subunit -~·,c-. . 1- f-N f.)
·>,.,
·, D B Aminoglycosides inhibit bacterial protein synthesis by binding
the -5if-S ribosome subunit 3 ,7 ·
1
C --,J /'
, D C Ciprofloxacin inhibits transpeptidase
(!I
action on peptidoglycans
i

' D D Me_!!:9r:tidazole inhibits RNA gyrase

? .
D E Vanco~ycin binds tra~sprfidase, inhibiting cell wall S·; ,, -;~:"'__u! ,. · <---

ri·· synthesis ,,,,,--. ·/

'
f1·
f
1:
~

I
"t '
It
I
[
LJ
=· t
\
 Pharma·cology MCQs

1.37 Answers:
·11 A True
® B False
e C False
9 D True
0 E True
Cephalosporins are also bacterr.I c_elLw.filUY-nthesis inhibitors.
Their ~-lactam ring renders them less susceptible to p-lactamases
when compared with penicihins. There are three generations of
cephalosporins. The second generation is particularly effective
against Haemophilus influenzae and Neisseria gonorrhoeae. The
third generation has improved Gram-negative but less Gram-
positive cover when compared with second generation. As with
penicillins, probenecid prevents elimination by preventing its
renal secretion.

1.38

•
Answers:
A False
., :i·

• B False
• C False
• D False
• E False
Tetracyclines inhibit bacterial protein synthesis by binding to the
30-S ribosome and inhibiting tRNA. MM;ro1ides bind to the 50-S
ribosome, inhibiting bacterial translocation. Cipro~cin (a
quinolone) is a DNA gyrase inhibitor. Metronidazole releases
agents that interfere with DNA synthesis and function.
Van~~-mx_cin acts in a similar way to pe~n~~ by inhibiting cell
wall synthesis but inactivates the enzyme glycoprotein~ynt~etase ; _[·,,;
not transpeptidasei Aminoglycosides cause misreading of mR~A '.: 'J
(~ ,,, , , -~ , \;: . ,, , }."d bi~d to 3~~ ri'?°50~,<~i~hibiting tRNA. I
l \.. 'I o<; (\ -t::> .

I
- \'- \· •
\R,
~, 1. •
\C\ ( -~(.'.)!.,v-....s.,~ -->.. .,. '\
t;>- 'f-i
I
· v re\ c:,~
\
V\ --:..., , 1 '" \ ~ \
\_j
s
I
d
;I., --~
--:-p-r-}- ~ 1' \c,,.., J:,.,,. ___;._y 7/\.."" , Le--;;1"'-
!!ii-·
- ~ Y-.
\AA
 ·-
Pharmacology MCqs

1.39 MAC (minimum alveolar concentration) of a volatile anaesthetic:

_.,/ D A Decreases with concurrent lithium administration
D B Is a measure of potency
,< D C Is increased in neonates
·,_ _,/ D D Of isoflurane with nitrous oxide is approximately 0.8
D E Of nitrous oxide is 105

1.40 Halothane:
sAvl \
~"..;v ~
\t
'I D A Has a molecular weight of 184
D B Shouldnot be administered concomitantly with drugs
decreasing atrioventricular (AV) nodal conduction
D C Can induce halothane hepatitis, with a greater incidence In
children when compared with_adults '-- _ ~; ·
D D Is a safe alternative to sevoflurane when anaesthetising patients
with r----,
head injury ·
K D E Has an --oil : gas .,
.- partition coefficient of 22.4

~!
' 1 "
1J
rl'
I
•
'f
t
l
'
. ~,. 45
t
 Pharmacology MCQs

1.39 Answers:
@ A True
~ B True
o C False
• D True
• E True
There are a range of factors both increasing and decreasing MAC.
Lithium administration, acute alcohol and opioid ingestion,
neonate!! period-1 hypometabolic states and concurrent nitrous
oxide administration decrease MAC.
--=::=r-
MAC is increased by hypermetabolic states, chronic alcohol and
opioid use, and some metabolic derangements including
hypernatraemia. r- \\ -.. L\~ ----·--- ,
\--t~C) \Y\_~ 'v~ . I.

\ ,-. ..•• -·~ --

1.40 Answers: \\~,) "" (l
':l0-1-
• A False (2,0·,~7 po<"~
o,
• B True
MAC
7
.•.
• •, C False '1_. 'i
\o\_ l
~°'-~
• D False o·, ~ ~ Q ~~ 1...1- L\
• E False
Halothane has a molecular weight of 197, boiling point 50.2°C,
MAC 0.75, blood: gas partition coefficient 2.4, oil : gas partition
coefficient 224.
Adult incidence of halothane hepatitis is 1 in 2500-35 000
compared with that of 80 000-200 000 in children. Halothane
significantly increases cerebral blood flow so increasing
intracranial pressure and thereby decreasing cerebral perfusion
pressure, which should be avoided in the head-injured patient.
Halothane also causes an increased incidence of bradycardia ,
secondary to its augmentation of vagal tone and sinoatrial (SA)
and atrioventricular (AV) nodal depression, which can be
exacerbated by concomitant medications.

i
I
~
'•I
'I
i
r·I ,··
 Pharmacology MCQs

1.41 The alveolar partial pressure cf volatile agents increases more

rapidly in patients with:
'< 0 A An increased functional residual capacity
_.._,,-
,. -·o B Eisenrnenger's syndrome ·
I
'1<. 0 C An increased cardiac ~t
/0 D Concomitant nitrous oxide administration
./ o E ~ibrotic lung disease

1.42 Regarding volatile anaesthetics:

.// 0 A lsoflurane is presented as a racemic mixture
1 • ,,.0 B 0.2% of inhaled· isoflurane is metabolised
. /0 C Fluoride ion production secondary to enflurane metabolism is
increased in obese patients .- .-
0 D Abnormal electroencephalograph (EEG) activity is associated
with high concentrations of ~flurane in hypocapnic patients
, D E At levels of 1 lvtAC of isoflurane, cerebral autoregulation is
preserved -
 Pharmacology MCQs

~ .41 Answers:
@ A False
e B True
• C False
• D True
• E True
An increase in functional residual capacity causes a greater
dilution of the volatile agents, so decreasing alveolar partial
pressure. A decreased functional residual capacity is associatea
with fibrotic lung disease and l1as the opposite effect, causing
decreaseir; pilution and therefore increasing partial pressures.
JfsenmeQger's s,¥Drlrome 1a right-to-left intracardiac shunt)
reduces the blood flow to the lungs and so increases the alveolar
partial pressure of volatile agents. Nitrous oxide causes an
increase in volatile par:tjal pressures within the alveolar secondary
to itsfse.coodg_as effect. }\n increased cardiac output improves the
concentration gradient, promoting diffusion, and therefore
111
CII
reduces alveolar partial pressure. ;

1.42 Answers:
• A True
• B True
• C TruP
• D True
• E True
lsoflurane is the structural isomer of enflurane: 0.2% of isoflurane
is metabolised compared with-~ of enflurane, <5%yf
sevoflurane and O:O~o of desflurane. Abnormal 3-Hz spike on an
EEG is associated with high concentrations of e[l~ane in
hypocapnic patients. ·
 Pharmacology MCQs

1.43 Sevoflurane:
A Is achiral
B Has a molecular weightof 200

-
D D Decreases cerebral oxygen requirements -
C Has a saturated vapour pressure at 20°C of 22.7 kPa

' .//
D E Does not
~ . affect splanchnic
- blood flow

1.44 Rr gardung volatile anaesthetics:

'f C
A Desfluranehasab~lingpointof21°C --r.? c. ;
/\./ D B Desflurane is administered by a Tee:?. vaporiser ~
v' D C CompoundA has a molecular weight of 1 79
D D More compound A is formed with baralyme compared with
c•./
soda lime
1/' 0 E Xenon (133Xe) may be used to measure cerebral blood flow
 Pharmac9l2gx MCl(s ~------
\_§_"-"-'<> ~" 'f= ~
\
_ _)

1.43 · Answers: M vJ <Lr-~~~

A True
B True \ -~
,rut: - · · -
• L
D True 6\ I <:J°':s )- (,':;
e

• E True O ,\_ \ °' °'- S 't.1 0

lhe physiochemical properties o~sevoflurc>ne include a boiling
point of 58.5°C, an MAC of 1.8%, blood /~o-Spartition coefficient
of 0.69 and an oil : gas partition coefficient of 80.

1.44 Answers:
• A False
• B False
• C Trve '-::-- ,J ~
• D True 0L.-~0v-)

., • E True
Desflurane (boiling point 23.5°C) is adflOinistered in a Tee 6
vapor~ ~o.\ds 450 ml and heats desflurane to 39°C at
~ at~. Com~ can be rorrned by reaction with both soda
lime ancf baralyme. It is formed ,:n increasing amoun~_wj1hhigb
~i~perature.~. A greater temperature rise is seen withl!?ara1y_me.,-
therefore yielding greater amounts of comf)ound A. The
radioactive isotope 133Xe may be used to determine cerebral and
other organ blood flow.

i
I
I
 .-
Pharmacology MCQs·

1.45 Diuretics, thiazide§: t,~./ ~ ,.J r-

,X D A Exert their main hvpotenslve effects secondary to diuresis
·;l D B Cause bypokalaemia and hypochloraemic a9dosis _,. ._, \\,(_ , ,)_,::,-; ~~
,/ D C Increase bicarbonate excretion ...
r , /, D D Increase plasma cholesterol level
E Can cause thrombocytopenia

I 1.46 The following are true of diuretics: . ._

[·
. ~D A Loop diuretics inhibit sodium and chloride reabsorption solely, ('
in the thick ascending limb of the loop of Henle :----/ .,.;- · /J"-')
. I
'/ I
. D B Loop diureticscauss a decrease in renal blood flow ·7 i '-''
·0· ~~

kA~
r,/o
C Loop diuretics may cause a rise in lithium levels
D Canrenone is a metabolite of spironolactone •
E Aldosterone antagonists are available in intravenous
preparations ,,.
GI!

,,i
"

S.1
 -
Pharmacology MCQs

1.45 Answers:
A False \ .
e ,\ ~ t' _) \)' \ ("

II B False
e C True
• 0 True
• E True
Most diuretics, including thiazides and loop diuretics, exe,t their
an!!!!Y,Eert~nsive effect secondary to a decrease in systemic
vascular resistance. Thiazides inhibit sQdium and chloride
reabsorption predominantly in the early distaLcomIDluted tubule.
The increase in sodium reaching the latter part of the distal tubule
causes rapid sodium reabsorption in exchange for hydrogen and
potassium ions. Therefore, the overall picture is that of
hypokalaemia
. with hypochloraemic alkalosis

r-----
-=- //.---- '
__->
'
).
r

Answers: ~ I /
1.46 I /
• A False
• B False
• C True
• D True
• E True
Loop diuretic'. act mainly in the t~~b of the 1!;!2P
of Henle, although they also have some action in the e~tal
tubuJe. Loop diuretics inhibit sodium and chloride reabsorpt1on
and increase renal blood flow (whereas thiazides decrease renal
blood·flow). An example of intravenous aldosterone antagonists is
potassium canrenoate.
s;;:s~
I \
f,:
;..

'
1·, '

'. ~ -\

( \
 Pharmacology MCQs ·

1,47 Diuretics:
, . ,/ D A Marmitol is a polyhydric alcohol
:___,../ 0 B Mannitol may be harmful in head injury
, / D C Mannitol undergoes no significant metabolism
1 ~(~
>' D D Acetazolamidefompetitively inhibits carbonic anhydrase
: ./ D E Acetazolamide renders urine alkaline
; J I ' I f :'\ _I) ,..._ r- .-- .
f f'----__J \ 11 @ft_':) ·-;:-.:> ~

t 1.48 Sodium nitroprusside:

b - D A Is a prodrug
ti ,· <' D B Causes jn~ctivation of the enzyme guanylyl cyclase
fi / D C Causes increased pulmonary shunt
~/ D D Undergoes an initial metabolic reaction that yields
methaemoglobin
D E Increases thiocyanate, which is then converted back to
cyanide ion by the mitochondrial enzyme rhodanase

,
.-
\

53
 Pharmacology M( ()~

1.47 \ nswe 8'§:

..
~ , , True
~ B True
C True
• D False
• E True
Mannitol may be used in head injury to reduce oeden ,a but 111\ISt
be used with care. If the blood-brain barrier is breached rnannitol'
can enter into the brain tissue and draw fluid into it, so further
increasing intracranial pressu~cetazolamide (a carbonic \
~ _,/,}ompetitive blockade. It
anhydrase inhibitor) provides no~ i
inhibits hydrogen ion and bicarbonate production from water ,~, 1d
carbon dioxide. This causes a decrease in hydrogen excretion ,11,ct
decreased bicarbonate absorption, so ieading to alkaline urine
with anyperchloraemic acidosis. . '

1.48 Answers:
• A Trw·
• B Fals<~
• C True
e D True
~ E False
Sodium nitroprusside is a prodrug. Nitric oxide is the active agent.\
This causes activation of g~anylyl cyclase, causing venodilatation \
and arterial dilatation. It reduces pulmonary hypoxic 1

vasocoristriction, so increasing pulmonar_Y- shl}_!lt. Its metabolism is;

'- complex. The initial metabolic pathway is within the red_ blood
_ .~ \~ell and following reaction with oxyhaemoglobin gives rise to (.·,
· nitric oxide, cyanide ions ( x 5) and methaemoglobi!}. '
1
l.::-..-;-

- r~ •. · 'c~ttiaemoglobin the~ combines with cyani~e ions to form

-f r I ,~I• , C¥,~nometh~moglobm. The remaining cyanide ions are
I
cdnverted to thiocyanate by the mitochondrial enzyme
rhodanase. Other cyanide ions combine with vit~f3, ~' ;o
\
form c::.vanocobalamin. Both thiocyanate
•
.and Cv<-
I
irH)(nbcdarnin
··1. '
q, i ;nr· retnllv excreted.

_,I
 ·1.49 Regarding sodium nitroprusside metabolism: ') 1
··'

~fJ A Ioxrcttv Slr:t· _. ',: Of'-tff_dscyanide levels exceed lS µg/ml

,, [l B Cyanide tU\'i( .r, '!- 111on.~ common in the febrile patient , ' - I ..
-< (] C Sodium thiosulphate increases the production of
cvanomethaemogtobm - , r, ' .,,.

.~/ CJ ri Cyanide ion toxicity increases mixed venous oxygen saturation

)\ L.J f Thioc.yanare is 00f h::rrnfui
ust
toll 1.50 Regarding nitrates;
v/ rJ A Induced hypotension is predominantly seoindarv to
venodilatation

11d'
VD B Tolerance is secondary to depletion of vascular smooth muscle
sulphydryl groups
(' .. 1101 /
·/DC lsosorbide mononitrate has 100% oral bioavailability
/cJD The main effect of isosorbide dinitrate is conferred by its
hepatic metabolites tisosorbide 2--mononit:ra!·r· and isosorbide
5-mogonrtrd.te) -
-
. ,,/ -0 hlitritr'. :-1:·i: :,1.1·... trorn nitrate metabolism o.xidisPs the· iron in
CII

.oxvhaen
. tOL'. .. k>bin ·

~ ')( .-.'. .

'r. -~\~
l, ·,..__ o. · -"

=
od -- --- -----i
I
- ,. ~ !."'· ./ --1 ,j_,
7 I r1 VI J
-<~ . - . - -- '
_) -
/

D \(J --
r .;

/
. I' ,-__
-t ·1-·)
~ .-. , ~ -~ \_ {'-. C:--- r"\ ,--.- i
.. _ ,~-;--
( ) I I \ 0 , . ·- ( \ r_) / ,: • __.io .,._/ ---( .~
'--
m ,,
u
I
'-
C_.

55
 Pharmacology MCQs

1 o!

1.49 Answers:
e A False
8 B False
@I C False
G D True
@ E False
Cyanide ion toxicity occurs at levels over 8 µ.g/ml and is more
common in the h~!bernijf.J]atient. Sodium thiosulphate
increa_ses conversion of cyanide ions to thiocy~te, most of
which is excreted in thE;,J.n:ine, thereforedecreasfng circulating
~,
I
cyanide ions. AlthougK not as harmful as cyanide ions, if allowed
r , 1 r\ V' \ 1
( .J > to accumulate thiocyanat e is harmful and can interfere with
\. thyroid function~Cy'amd-e ion toxicity causes inactivation of
cytochrome oxidase and therefore impairs oxygen utilisation, so
increasing mixed ~enous oxygen sa!_~_ration.

.Answers:
e A True
• B True
t11 C Trur-
0 D True
~ E True
The hypotensive effect of nitrates is predominantly secondary to
relaxation of the venous circulation although the arterial smooth
muscle tone is also affected (to a lesser extent) .
Remember Oil and RIG - Oxidation Is Loss of electrons and
-
Reduction Is-Gain of electrons. Nitrite converts oxyhaemoglobin
2
to methaemoglobin b~f ferrous Fe + to ferric~, ie f
I
loss of electrons. Owing to its lack of first-pass hepatic
metabolism, ~de mononitrate has an oral bioavailability of
100%.

L
I
 h·-.,I
" ,-
Pharmacology MCQs
L

1.51 Drugs ;a111ifcectifl1lg coagulation: . · . '.,

x_ D A Aspirin acts by irreverslble methylation of platelet cycle-
oxygenase
8 Dipyridamols inhibits adenosine uptake into platelets
'/ . D C Dextrans are produced by bacteria - . -
/. D D Dextrans have,, no effect on the function of von Willebrand's
factor
D E Dextrans can impair crossmatching

Unfractionated hepa~in:
A Is basic ?,'~ - (.

B Increases the formation of antithrombin III-thrombin inactive

complex by a 1000-fold
, D C Inhibits factor Xa only at high concentrations
/D D Can affect factor Xlla
I! ._/0 .,
E Does not cross the blood-brain barrier

:, ;
.•.. ; 'i~ •. : '• r

".

f.

; . .
 -----fharmacology MCQs
Q . . \
\21'.'\J\.1'-~
1.51 Answers:
\l \
__ -·-------__,\~
- ·-.J o·1.-~
\/
¢•<:i ')
-
@ A False
B nue
'tS y0~·
. ~-
\\~C\ v,l\...o ~z-
--"i
~~ "
1\,(f
C True . - ----- --- -? \_
·\b
© v,V~ ,' C ''Q-..C~ - •••

D False e-'K_\y c<e".f\ \ -- --,.-~ "''

E True ~~-------_j-
Aspirin irreversibly acetyJates cyclo-oxygenase, so causing a
reduction in thrornboxane production. At low doses the platelet
cyclo-oxygenase is inhibited whereas the vessel wall cyclo-
oxygenase is@ffected and still able to confer its useful
properties of prostaglandin synthesis and dilatation.
Dip~a!!lole is a potent coronary artery .vasodilator. It inhibits
phosp odiesterase and phospholipase activity. This renders the
platelets less prone to aggregation! Dextrans are polysaccharides
produced by the bacterium Leuconostoc mesenteroides; their
anticoagulant activity is secondary-fuaeCTeased platelet 1~
adh~ess and von ~illebrand's factor inh_ibiti~ also
produces a protective coating over vessel linings and red cells-so
aiding flow in the@fcrocircula!io~·- Dextran 70 is known to_ ,
interfere with crossmatching secondary to ~oulea~x formation. \

1.s2 Answers:
• A False
• B True
• C False
• D True ~
• E True --~ (__ \\W0 -~ \ \
Heparin is a large acidic molecuf'J, which increases the formation
of the inactive antithrombin 111-thrombin con'lplexby (l
l

rvl000-fold. At~_dos~~fact~r Xa can be affected. Factors~,

Xia and IXa can be affected at pig1"'_do~es) Due to its large size
and charged nature, it crosses~neith~ bloocl-brajn barrier nor
the placenta. '----

\_. b-
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() '·· ·--~
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 r'tiernu«. olugy A1< ().,
I

1 .5 :l Unfractionated heparin:
~L.J A Is bound to fibrinogen m ·plasma
,X U B Metabolites are excreted hepaticallv (' 11 • __

I,/ i .:! C Decreases plasma turbidity ~..,., :>\~~"',,J._,__ ~

/ i.'_l D Does ric)t affect platelets. even at high doses
t__.-/i~] E Induced thrombocytopenia 1s antibody mediated

1.54 When using low-molecular-weight heparins (LMWHs):

• • • !

Ko A Protarnine administration fully reverses the effect ,- .. \ ··--

v/o B, they ha~e an increased factor Xa-inhibiting effect C()!Y1pe1fed
with unfractionated hepari- .' .. ' .. · . .
'f ' I
D C They have increased affinity for VOt', 'v'Villebrand's factor when I \,"

compared with unfractionareo !·,~parin ..,.....

0 D Monitoring· of ar.ti-1actor Xa levels is recommended

.,
0 E Thev affect activated partial thrombin time (APTT) results , 1 1, r[/(r , , /\

l~ r !
l
 Pharmacology MCQs

1o53 Answers:
e A True
$ B False
• C True
• D False
E True
Heparin is negatively charged. In plasma it binds antithrombin Ill
. (so having its eff~t), al~n, pr~ase and fi~gen. lt1s
metabolised by hepatic heparinases and its metabolites are
excreted in urine. At low doses it inhibits factor Xa. At high doses
it effects platelet aggregation and factors '5_!!a, X~ and l~a. Plasma
turbidity is decreased secondary to the reduction in tr'@'yceri~e LYV?
levels. Heparin-induced thrombocyt.qpenia (HIT) is an antibody-
mediated condition occurring in 3% of patients approximately
5 1_Q_days after initiation of therapy.Platelets are bound and
6
removed from circulation, rendering the patient.
thrombocytopenic. · ·
'I
Gil

1.54 Answers:
$ A False
Q B True
~ C False
@ D False
el E False
Protamine, which reverses heparin fully at doses of 1_ ~g/J_QQJ!,J
heparin, does~ully reverse the effects of L_M_WH although it is
still advocated in bleeding. LMWH has an increasea affinity for
factor Xa (which confers its main effect) but decreased affini!y_ for
von Willebrand's factor. ~onitoring anti-factor Xa levels is~o!)
recommended, as it does n~predict the risk of bleeding ancfis
not therefore helpful. APTT is unaltered.
,.__ -- _,J
I'
• I

I
 Pharmacology MCQs

1.55 Regarding anticoagulation:

I/ D A Fondaparinux produces· its antithrombotic effect through factor
Xa inhibition ·
X D B Patients on single daily .dose LMWH should have their epidur~}
catheters removed no sooner than 6 hours ·after the last dose '
vtJ C Subsequent LMWH dosing should occur a minimum of
2 hours after catheter removal in patients on single daily dose ·
·LMWH
.,, O · o··,Ne·u-roaxial blockade is thought to be.safe to perform if the INR
· ·.·/ · (international malised ratio) ir< 1.5 j -=-
L/"v D. E . Clopidogrel should ideally be stopped 7 days before epidural
•. insertion . , , . _\ ~ . . . (1r,' O tY? ,9~
~'C\~1J._v--Q..' z::> \ L-\ V\ ~ • I
~ I.a. Cst.~<\ vv--"'-b
1
-b ~ ci\ ~ t'1,' i~~----~-1_ ~ ~ \,vv-)
1.56 Protamine: . T\ "'"' ~'lo ...,..._Q___ _./ ~

X D A Is prepared from fish ~ggs . :__. ,. -. - ·,.

0 B Is a mixture of basic low-molecular-weight proteins ....t
·/ c Is used in some insulin preparations •, ,~~ (\Go(.."'
,,- \,J-{!.r>\'""-
l/ D
'/ D D In individual doses should not exceed 1000 mg ~

I
f.
/D E With previo us vasectomy may predispose to allergic reaction

,,

.;Jt'

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l:Qr !

61
 / .,• ' ...

Pharmacology MCQs · __!"";- · ~ j,,- · · /

' 11 v/ ~ -- \ ·cf' t - !, -; {..i
-, ..
I' I ')
·~
1.55 Answers: '--~~- - I-~ ,f,~ .. -
e A True
e B false
• C True
• D True
e E True
Patients on LMWH delivered as a single daily dose should have
their first postoperative dose given at 6-8 hours with their second
postoperative dose no earlier than 24 hours after surgery. An
e_Qidur~ should be removed no earlier than 10- 12 hours
after the last dose of LMWH. Once the catheter has been removed
the LMWH dose can be given no earlier than i'hours later.
Reference: Anticoagulants and the perioperative period.
Continuing Education in Anaesthesia, Critical Care ctnd Pain.
British Journal of Anaesthetic s 2006; 6(4):

1.5 6 Answers:
A False
0 B True
• C True
•
•
D False
E True -
,,.___,, ,J').',")
c._ \ -

Protamine is prepared from fish (including salmon) sperm and

/ ironically enough previous vasectomy predisposes to allergic ..
• reaction - as does chronic diabetes and alle~ to (ish! It is~!5)
and as such binds to the acidic heparin, forming a stable inactive
s~lt. _It is present _i~nsulin p!::parations. The recomm~ed
maximum dose 1s ~mg.\ --

'I
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1° I
I

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t. 62
 Pharmacology MCQs
' '

1.57 Warfarin: X
Vo I
A Is acidic
'- A
D
/"
B Binds to cx1 -acid glycoprotein preferentially
~-//0 C Inhibits the synthesis of factor II ..-
! _.,/ D D Inhibits the synthesis of factor V~II · ~ . ~ ,. -Yi·
./o
, E Prevents the oxidation of vitamin K ~~ ~ \'( , j
::l: "~ \, b
W.d"'-u;
~ --~- c,x,'c)..,_\-
-c:><' --N'.. ---0
1.58 Warfarin:
/
., /o A Is more than 95% protein bound
D B Is teratogenic, particularly in the s~-encftrimester ~..- s\ i i\c:,. L '-"~~ \ ""~Y<l.
l.///0 C
Metabolites are pre~minantly excreted in urine o-v-(~..._ •.\ -\--"" ,'½<....'v. ',
/ D D Effects are antagonised by erythromycin
I
A"\..c:.CJ""~'-1 \ ~ ... . ,.J;,")_
0\': ..~
p,_,...I\: ~kl, - \"AR.'\-"'c1

I
/ D E
I ' Effects are. potentiated by barbiturates , ~ c:.""1 (;--{le,
a:,..,.c,\o.,_..,. ,. •.. u.(?~
~· ~
, c:?', v'\t~.,,...,·Jt..

t
t

l ..
 Pha~macq_lpgy MCQs _
K

• A True
& B false
C True
o D false
• E True
Warfarin is an acid that preferentially bind~!2,.Y.!!!J~ It inhibits
the synthesis of vitamin K-dependent clotting factors, ie factors Ii,
~, I~ and~ To activate these clotting factors they undergo i'·
-
carb~lation of their glutamic acid residues; for this to occur
reducedvitamin K is oxidised. Warfarin prevents the return of
vitamin K to its reduced
.. ---=-form
;::- .

1.58 Answers:
e A True
• B False
• C True
• D False I·

• E False
Warfarin is tera~ic in the first trimester. During the third .
~ __ ··--------· trimester, itcrossejJ!f~QJac;;en.ta and may result in fetal A-161_,_---
: ,•J
, ,I, .,.. . paemorrh~ge. Dr~~s that compete for plas_ma_-b_in_ding sites.(~
i,~~L-. J non-steroidal ant1-mflammatory drugs) or inhibit its metabolism
u·\ Q_ r) potentiate the effect of warfarin. The following drugs in~
1' C.» t> --c. metabolism of warfarin: alcohol, allopurinol, erythromycin,
A \\t,rv-J\.;" .JL ciprofloxaciri, metronfdazole and tricyclic antidepressants. The
___.. J:) . following drugs increase the metabolism of warfarin: barbiturates,
t:.--, ,(\ \f\"tJv.~-----rifampicin and carbamazepine. ~-,:I
i 1
,..:.:

~ '\ds f~ '" ~~~ ~-=] L- 1

-- ( ,_ L: r'.. '\. b;
/\ . -1 ,. , v,~. r.~ '- . - ~- -
It-,,,,,,
• l

-
- ' /' ' f_.j '- ,-~----
\
 Ph?rmacology MCQs

1.59 Aprotinin:
l-~_.,.--0 A Is derived from bovine lung_
D B Inhibits plasmin
D C May be useful for the treatment of haemorrhage secondary to
hyperplasminaemia
X D D Increases the risk of deep vein thrombosis
D E Is a proteolytic enzyme inhibitor
'

'
!:..
1.60 Tranexamic acid: ·
)( D A Directly inhibits plasmin -r:- --
/.

~ '/ D B Is more than 50% metabolised in the liver \_).,_ ,_... , \.".:".,-A,~.'A.f'\ <..,:\_
,.....-:-:7 __:-- -j
~D c Can be usedin"menorrhagia
v/D D Dosage needs altering with renal impairment ; '
\},·, ~ \· ,-, . ~·\< <

/ -I
?\ D E ls~usedfn thromboembolic disease c___~~--,_ ;:t--~. t , "'- •. il-~ r":i) _. .l

'
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 Pharmacology MCQs
~~ '( '\~· -~·· '~

f)
\
';) \<',.\ (
'" . '·, ' ,.,-
1.59 Answer§: \ '---
.1 V \\. I •

© A True ,,, \:._... - '\' ( l, \ \ \ f: '< ~ \ \.-.

9 B True
@ C True
(i) D False
~ E True
Aprotinin is a proteolytic enzyme inhibitor. It acts on trypsin,
plasmin (at low doses) and tissue kallikrein (at high doses). It may
also preserve platelet membrane-binding recepto,·s. It is used as a
blood conserver during open-heart surgery and liver
transplantation. It may also be helpful in cases of haem9_rtl!age
'-(· ,.,- ·.f ;--.., due to hyperplasminaemia, eg during disse~o~""m-~Jignant
n, ,, I•,' ~

tumours, -in acute prom__yelocytic therapy and following

tnrombotic therapy.-
_; -
Reference: British National Formulary 52. September 2006.

Cl I
1.60 Answers:
- Q \\-:-\._~ 'N\. \ 'f'... •:,~\/", , .,J-\.__ ' }'A.t:_
~ A False
~ B False
0 C True
~ D True
fj E False
Tranexamic acid inhibits plasrTlinogen activation,~~ plasm in
, directly. It is ~-5~/.excreted uncnanged in urine. It fs used in
• •;· _,.\. ~,~ .
1
V,.,,_,, \ . --. . me~r,rbagia (initially when menstruation has started), hereditary
· '- angioneurotic oedema and eristaxis. It is used in bleeding
: ,, o '(J' \.0 ~c
r\Q_•.1-1\J) conditions in the_Q_r_ej_ence Qf excess fi~~lysis. As it prevents
1
Ye,(! f~~~in!)lysis, ~t i~prothrombo~ and therefore contraindicated in
r _, - ) '
\, _ t\ t---,
0 1
I 'f:?romboembohc di~~-
I
1
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,, '
I
I,'\(\
l y__,
M,
Vv • .A)
r1 C: "\
,)
r
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 Pharmacology MCQs

1.61 Recombinant factor VIia (rFVlla):

,·, D A Its main method of action is replacement of deficient factor VII .
D B Causes a generalised systemic procoagulant effect _\ .- -,?_ ,, f\
~ ' i'

D C Has a half-life of 39 minutesIn normal controls ··;

/ ,-.. r
I.

\ ... / D D Has pH as the key indicator of the likelihood of success of

treatment
l /D
i

l
E Can activate factor X

l
a !
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I
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~
'-·-
 Pharmacology MCQs

1.61 Answer§:
• A False
B False
• C false
e D True
s E True
rFVlla is formed using recombinant DNA technology. It has a half-
lifeof l:]__hours in both normal controls and patients suffering
with haemoe,Wlia. This may be shorter in the bleeding patient.
Although it does provide additional factor VII, this is not)ts main
method of action. It causes activation of co9-gulation with
thrombin generation (by tissue factor-aepenaent and ! .

-independe~hways) and factor X activation.

o.dJo
It is thought cause a generalised systemic procoagulant
effect; instead the action is localised to the site of vessel damage.
Although pH is the main determinant of treatment success (with
acidotic conditions inhibiting its action), currently there is no
evidence that reversal of. acidosis
~
before treatment impro~es
outcome. It is probably a marker of the extreme physiological
state of the p.itient.
Reference: A critical appraisal of the use of recombinant factor
Vila in acquired bleeding conditions. British Journal of
Haematology 2006; 133: 355-63.
 Pharmacology MCQs

1.62 Regarding the drugs used for postoperative nausea and vomiting:
< D A Drugs acting on the chernosensitive trigger zone (CTZ) must
first cross the blood-brain barrier
:/·,,-,·D B Metoclopramide exerts its prokinetic effect by acting as an
agonist at the 5-HT4 receptor
V D C Muscarinic antagonists act on receptors located in the
hindbrain medulla
:~D D Histamine (H1 )-receptor antagonists have an effect on the
vestibular nucleus
,\__/.,-"'[] E Ondansetron antagonises gut and brain 5-HT3 receptors
l'

liQ
 Pharmacology MCQs

1.62 Answers:
@ A false
~ B True
@ C True
• D True
<I E True
The CTZ is situated outside the blood-brain barrier.
Metoclopramide exerts a prokinetic effect on the stomach and
upper gastrointestinal tract by acting as an agonist at S-HT4
receptors. At higher doses it also manifests 5-HT
-~
3 antagonist
function. H1 -receptors and muscarinic receptors are in the
vomiting centre and the vestibular nucleus.
Reference: Physiology and pharmacology of nausea and vomiting.
Anaesthesia and Intensive Care Medicine 2003; 4: 349-52.

.--··---

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Pharmacology MCQs

1.63 Thiopental:
( '")
'I D A Is 50% protein bound
I

l ·-'
K D B is more potent than methohexital
r ' ,-
./
'!- •. D C Forms an acidic solution when dissolved in water - •
I
• I

.,,-0 D Is stored under nitrogen (not air) to prevent acidification by

/
atmospheric ~arbon dioxide
,.. D E Is stored with sodium carbonate to reduce its acidification )_·
,/ _.. .,

1.64 Thiopental:
D A Has an incidence of anaphylaxis of l per .1000 exposures
/ D B Is· ~latively contraindicated in porphyria
/ D C Has a volume of distribution greater than that ~f propofol. :_J, (J"
X D D Has a pKa of l 0.5 -:..;Jj
v" D E In solution is bacteriostatic

I
.. •' .

. ~ ...
I .
 Pharmacology MCQs

i .63 Answer§~
e A False
o B False
• C False
• D True
• E True
Thiopental is 80% protein bound and less poter.t than
methohexital. In water it forms an alkaline solution with pH 1 (0.
~~date~ acid is insoluble so, to prevent its formation,
· -~_carbonate 6°~ ~ ~dded to prevent hydrogen ion build-up
and it is s~d under\_llitrog_en~ .

1.64 Answers:

• A False
• B False
• C False
• D Fa~se
• E True
Anaphylaxis is seen in 1 : 20 000 exposures. Porphrric crisis can
h_!.precipitated by thiopental and therefore it is an~sc[utii)
lc~n, particularly as other intravenous induction
agents are !>afe,including propofol.
It is presented as a sodium salt with a pKa of~nce dissolved
in water it forms an alkaline solution with pH'l 0.5. Remember
that all salts of weak acids are alkaline in solution. It is stable and
as it ii!>act~tatig it can be sto~ for a few days.
It has i°volume of distribution of 2.5 I/kg compared with 4.0 I/kg r-

for propofol. lfl

I
I
I
i

I
l I

- 1·,f ,i
'
i
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I

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i
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 Pharmacology MCQs

1.65 Thiopentai:
x O A In low doses is analgesic · ·"·
·--' D 1B Causes decrease in antidiuretic hormone (ADH) ·"I' \"'

l/ D C Causes decrease in central nervous system (CNS) carbon

dioxide production
/ D D Forms insoluble crystals when injected intra-arterially
. D E Acidotic patients need less thiopental for the same effect
/

2,6-Diisopropylphenol:
A Is a weak acid
~ Has a pKa of 7 .6 J
C Has a greater clearance (ml/kg/min) when compared with
thiopental .
)( D D Has an elimination half-life similar to that of etomidate I
/-,:- ,· ,

/\ D E Has
- ·--·- protein
--· - bind .. 'b c;:irnibr
- hinrfincr
··- .. ., •.•.•••.. . , tn
L'U'
la: .bmina
., •••• u.,111111'-- I ,_
/.-;, . '.
, (

ea ,

rl

I·
I
 Pharmacology MCQs

1.65 Answers:
1:1 A False
'1 B False
@ C True
e D True
e E True
At very low doses thiopental is actually antanalg~c. It causes an
increase in ADH release secondary to its depressive effects on the
cardiovascular system. A decrease in cardiac output also leads to
a decrease in urine output. Thiopental reduces brain activity and
therefore decreases oxygen consumption and CO2 production.
Insoluble crystals form in both venous and arterial systems;
however, the collateral venous supply dilutes these crystals.
Crystal formation in the arterial system can lead to distal
infarction. Thiopental is a weak acid; with a decrease in pH there
isan increase in free unionised drug and therefore it has a greater
response.
CII
•1
1.66 Answers:
• A True
• B False
• C True
• D False
• E False
Propofol (2,6-diisopropylphenol) is a weak acid with a pKa of 11
and almost entirely unionised at physiological pH. It has a
clearance of 30-60 ml/kg per min compared with 3_.5 ml/kg per
min for thiopental. It has an elimination half-life of 5_::.U_hours
compared with etomidate 1-4 hours. Around-~~ of ketamine is
protein bound compared with almost 1..RQ?/o of propofol.

f r , \ ·-l~ ·~ \,)
· 'r .: _,,, \- ,_ ,J -~,
1
I
0

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I

r .
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··, ·- I I,(

I
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1: I --
! -- 74
 Pharmacology MCQs

1.67 The following intravenous induction agents have active

metabolltes:
// D A Thiopental
< D B Propofol
I
,. D C Etom idate
..~ / D D Ketamine
he /0 E Methohexital
I
i)

d
1.68 Propofol:
y D A Can be associated with CNS excitatory effects in 10% of
patients
, ~ ,,,,,.,,,.
~ D B Reduces myocardial contractility
,.,- _,,D C May turn urine green· ,,,.
l D D Is predominantly protein bound to a1-acid glycbprotein ('
I

D E Has glucuronide as its main metabolite "1 . , ,

Cl I

·s
IS
 '.
Pharmacology MC_Qs

1.67 Answers:
@ A True
- - -n~\ ,-, r ( ·-, :.\ -·,
··\ ' ·.".:::) --
Y--

0 B False / ' ;- ,;:__,, ,' ,_, I_:;,___),{._ \ I\ ... ·"_,-

_/
-
.•...

0 C False .,, '-r .r-\ .. _,.,_ , -. ___,,~...•.•.... '-'"\:. ,._,...,.lf.'

, L___. G.c. I~ ~ · ·
~ D True
~ E True
~ ,~,~~?~· ~.;:, "-- --- -:> :)~""'(;" ('11•\..U. q .•. ;l _'
Methohexital has minimally active metabolites. Norketamine (the
active metabolite of ketamine) is thought to be 30% as potent as
ketamine.

1.68 Answers:
e A True
• B True
• C True
• D False \ :·", ,.) .
• E Fa I se r- - ' . ( -
As a weak acid, propofol is predominantly-bound to ~~bumm_. The I
l
main metabolites are a quinol (approximately 60%) and a
glucur<?~~~_(approximately ~0%).
The decrease in cardiac output may be due to a decrease in
contractility, a reduction in systemic vascular resistance or a
combination of the two (dependent upon \Y~id,L~ook you read!).

~ \ ,sco yfCJ"~
----,b

~\. \'-'__.\-
;. . ---2)

0\ j~C_= ----D

ex. '1..--- ~ h CP -------0

, I

76 f _; -·~
,·.
 Phar!Jiacology MCQs .

1.69 Ketamlne:
\·_ 0 A R enantiomer is the more potent when compared with the S
enantiomer
/[] B Can be given intramuscularly for purposes of induction
,,,,.- 0 C Acts at many receptors including N-methyl-o-aspartic acid
(NMDA) receptors
,,,,,,.- D D Is a sympathetic stimulant
b E Can be given rectally for sedation

1.70 Ketamine:
· /0 A Is helpful in managing bronchoconstriction
·-,,_,· D B When given intravenously becomes-effective after one arm-
brain circulation time ">_ ~)
.// D C Alters the a-wave on an EEG
D D Acts on G~BA receptors
( D E 1;1as a significant antiepileptic effect

.•. '
( '
' t. ..,
--
 Pharmacology MCQs
;-
' C '-.,-·\' ,:- \...'\..-....:.
.-
1.69 Answers:
e · A False··
® B True
• , C True.
D True
o E True
Ketamine is present,g as a racemic mixture of two enantiomers.
s+ and/?" of which'2}s three tofour times more potent. It forms
an acidic solution in water with pH 3.5-5.5. It can be
administered orally, rectally, intrave-nously, intramuscularly,
intrathecally or epidurally (if ~r~~ervative free). It increases
circulating levels of norepinephrine and epinephrine and
therefore increases cardiac output, heart rate, blood pressure and
myocardial oxygen requirement.

1.70 Answers:
'S -\-1· 7-
• A True
• B False
• C True·
• D False
• E False
Ketamine is a ~YJ!lP-,iheti;_stimulantland therefore produces
bronchodilatation along with other cardiovascular effects. The
intravenously administered preparation takes approximately 90
seconds to have an effect. It ca_!Js~~-~.D ingeas~J.n cerebral oxygen
consumption and blood flow.ia-Waves are re2@ced.by ~ jln~
waves. It does not affect the GABA receptor.Jt is thought to act on
NMQA," 5:tQ!nd opls,id receptors. It has n~}~_tie~tic effect
but no!, .is it epileptogenic.
"s,:-_;./ -- -
I·,·.
·:;

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 Pharmacology MCQs

. 1,71 With regard to etomidatee ·

,v b A Its initial effect is terminated by rapid redistribution into tissues
:vo B Both etornidate and cimetidine are derived from similar
I _,,/'O
structural groups . - · 1

C It has an increased incidence of nausea and vomiting ":'hen

compared with propofol_
_. ...
<. .
'/ D D It is safe to use in patients with porphyria .
_.) < ' - , ....c:._
)

\/0 E It is more than 50% protein bound

I
~ r.--, · '1 '.,.,. .1 r
~ 1- \ U) \...·· ·,.
~___,> ,.., .~---~,
"2. __.
! 1.72 Morphine:
~D A Strictly speaking is an opiate
'=-d (Y O B ls routinely used for intrathecal analgesia in the UK
D C Has its peak effect within 5 minutes of intravenous bolus
D D Reduces the cerebral sensitivity to hypoxia more than it
reduces cerebral sensitivity to hypercapnia ,
\,.,(,0 E Causes pruritus that.is most marked following intrathecal or
epidural administration

n
~ct
[

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 Pharmacology MCQs

Answers: .. ,
1.71 ,,.,,. \.~) ,.._ /( ('

A True · /> \ J'\~'-- t-~ • (.

( ,.
,h~\i''(,' •! .. l)
.\
·l • "- \'r·

® B True
\-J,,
. -
r- r- '.1;
C True -·- '-~ __ _c:. :., ~ ..,
D False (~ _, -._l . -- --· '·. ~- __,

E True
Etomidate is an imidazole derivative (like-cimetidine) !l 1s
commonly used as an intravenous induction agent when
cardiovascular stability is of importance. Its initial actions are
terminated secondary to distribution into tissues. It •1·--~ i_~ m~t~bolised
-·J_-·- ·. -

by hepatic esterases and plasma cholinesterase, and then rennlly ·

excreted. Around 75% is grotein bound·td albumin. It, like ·
thiopental, is contraindicated in porphyria. Propofol may have
antiemetic properties,
..
particularly- when
.. .
given-wit.-------=--
bo.ut opioids,

1.72 Answers:

• A True
• B False
• C True
• D False
• E Trut
An opiate is a naturally occurring substance- Codeine, morphine
and papaverine are all opiates as they are constituents of raw
opium. Opioid is the broad term for substances both naturally
oc_gmjng and synfu~tic, with affinity for the opioid receptor.
Morphine is-119frout1nely used for intrathecal analgesia· (in the
UK) as it can cause delayed respiratory depression secondary to
its low lipid solubility. It affects the cerebral response to both
hypoxia and hypercapnia but the latter is most markedly affected. i

on
 Pharmacology MCQs

1.73 Morphine: N--K"'- '" ~

--f D A Given orally is absorbed in the stomach

vO B Of all the opioids it is the least extensively protein bound
V'O C !s the least lipid soluble of all the commonly used opioids
/: D D Has a pKa of 7.6 1 -~\,,,, ~-fJ~"'- '"--

/C D E 6-Glucuronide is as potent as morphine \<.l \,""'.t.)

1.7 4 Diamorphine: I . i" \, ,

X D A Is an opiate \ '· · · , ; ·
L/ · D B Has a plasma half-life of approximately 5 minutes
,,,, ~LI~·, . ~. I
· / D C lnitiat~,ff_fergoes conjugation to become its active products
D D Is p,9- orly absorbed orally _
D E Is ~e protein bound than remifentanil ·I )

r
hi•-"•
 Pharmaculog)· MCl)~

1.73 Answers:
.,, (', ~ C ,. \
9 A False - '--' r , ., ~,i\J O \) j,.<,_J\, -. ) 'j"'~

:.) I.. \ /

~ B True
el C True
Ii) D False
,-
e t False
Morphine (a weak base) is absorbed in its tlnionised form 1n the
small intestine {in an alkaline environment). However, only 2 S01.,
will reach the systemic circulation secondary to extensive fi,...,,
pass metabolism. It has a pKa of 8 compared-with that of -;
diamorphine at 7.6 .. /Vh..,,phine has two major metabolites ...
morphine 3-glucuronide (accounting for ,___,70°;~) and morphine 6,.
glucuronide. The latter is over 10 ~
times as...
potent as morphine.

- \b '( ' ---~ \ I\.- \. '-'·

_,\
1.74 Answers: r ·-, '--J r·)
C
V' t I
I. ''_1--.• t-1\''"'
~j,!
• A False ~ ' I
-..._;
• B True ~.
a ( False
• D False
• E False
Diamorphine is not a naturally occurring opiate and is "' pro1irn
It has no .ffect on opioid receptors unti' it has undergone lr ~prd)
/estern vctroiysis to 6-monoacetylmorphine and then liver
meta o ism to morphine. Its oral absorption is good owing to ib
good lipid solubility. However, it ~ndergoes_extensive first-past
metabolism. It is 40% protein bound compared with 70°;<;-Tor
rem1"fentarn·1 . -- ~ <-

i·
'!

I
I
i
I
lu, \
. ,fi?
\'.'
I ,·
 Pharmacology MCQs

1.75 Methadone: '~

1
--
i X D A Has high first-pass metabolism
\
/
f !.,.,,/0 B May prolong the _Q_ T interval in susc~e~ible_ patients
I
I
t
j D C Is approximately 5=0°(o excreted unchanged i~rine
D D Undergoes.-- rnetabolism
- ,
,
to predominantly inactive metabolites
-

0 E Excretion is enhanced by acidification of urine

~! I 1.76
\

Pethidine:
~ ~

!//0 A Has an epileptogenic metabolite M {\ r-- ~ \_

;( D B May be administered in an unlimited fashion by midwifery
staff t~-• C
, ..,.__
f\ D C Is less lipid soluble than norpethidine
D D ls-safe in renal failure 1_,.,5 ,,,,,~c__ _

-i
,, D E Is nef safe to take in combination with lofepramine
/ -~-- ?JA_ ~ ,_ · c / .
-u . )..__ r r-J.1.
Cll 1

.,

83
 1.75
e A False
B True
C True
D True
E True -
Methadone is a synth~pioid which when taken'orally is well
. absorbed, has a low first-pass metabolism and as such has a JJigh
oral biogyailabfilty. It is less sedating and acts for longer periods
than morphine. With prolonged use maximum twice-daily
administration avoids accumulation. It can prolong the QT
interval and monitoring is recommended for patients with !w-e__g!if
or cardiac dis_ease, electrolyte abnormalities, or concomitant
treatment with QT-prolonging Rrepar-at~ons..-M~itoring is also '
1.·

recommended for patients takiri~ >100 mg/day.\

Reference: British National Formulary 52. September 200(.
. \, .
_., .Q_-s\~ ~~ ,c::,_ 'ej~ \ ~
..

Ot f f
1.76 Answers: (
_\Jc\,,.,~
• A True
r
• B False I

• c False
• D False
$ E false
Pethidine is metabolised both by ester ~drolysis (yielding
pethidinic acid) and by N-demethylatiorTTyielding norpethidine).
Norpethidine is less 11Pid soluble tha n pethidine. It accumulates in
renal failure and is associated with hallucinations and grand~ mal
seizures. Pethidine can be administered by (!lidwives, a maximum
of two doses, following which a doctor's prescription is needed
(this policy may vary slightly in different units). Pethidine should t
I
· not--- be administered with monoamine
- -----==---oxidase inhibitors;
- --· -
however, it can be administered with tricyrlic antidepressants
(eg loteprarnine). -- ~

. I
I :
 Pharmacology MCQs ,._ \ .
I ( .A- \-v-f, ~ r-wl \
\ ,' ..!'"-· \.. \ ''1,. J._ (_ -\--flr-0\ )
',,·c. ,rr-f•( , •••..•.• f'-'.
. 0--C' -3 t,-
1.77 Pet h'd'
I me:
~~
o/~ ""- --- , ,, ·1I o - , ;J ' 1
vD A Accumulates in the fetus secondary to ion trapping
,__,,,./o B Reaches peak fetal levels approximately 4 hours after maternal
intramuscular administration
l./ D C Has a lower plasma protein binding when compared with
alfentanil
/ D D Has a higher unionised fraction at physiological pH when
compared with morphine
D E Has a 30 times higher lipid solubility than morphine

Alfentanil:
A Has a pKa of 7.2
B Has significantly lower lipid solubility than f:ntanyl b
C Has a half-life that is increased with concomitant midazolam
administration
' I
X D D Undergoes acetylation to form its metabolites 'N c-:\ ~ ,., • ~,,· '., \. -
._ / D E Metabolites"are renally excreted

n
 Pharmacology MCQ~

~ \,..---..._ - I <e •
~ '") ...,...• _
1.77 Answers:
\:;I A True
€) B True
@ C True
• D false
~ C True
As pethidine is a base, in a more acidic environment it becomes
ionised and therefo~e- becom~~_!rapp_eg_ in_ the fetus. Pethidine is
approximately ~0% plasma protein boJJDQ_ when compared with
the 9Q~/o plasma protein binding of alfentanil. At physiological pH
1 pethidine is only "'5°/4) unionised compared with .-v20% of
I • ___.;. !Ir - ---: -
morphine. ,. _
.::;,,\'-. , ,· n·_-r;
.,/ 'I
1.78 Answers: / \..e...s.: Q_ .' . r,i:-
'
• A .False
B True _-.,-,- ·s v--., ~'-v\ ~ c-\
• C True ..,.- \.e ~ S ~,-::'. :, \_r v·--1'--
• • D False
• E True ----- "'-,-..~, -\Cs-~ -.·.. :':>
ca
\c,_, . ..,.._
• .......••
Alfentanil has a pKa of 6.5. Fenlanyl is approximately six times
more lipid soluble than alfentar ii. It is metabolised in the live, W:_
demetb}'J<!tion)
~
by CYP3A3/4 e, .zyrnes, as is m;dazolam,
.
and -
therefore its elimination can be reduced with concomitant
administration. Metabolites are conjugated and excreted renally.

.!
I
I.

86
 Pharmacology MCQs

1.79 Alfentanu
, f D A Has an ~limination half-life greater than fentanyl
' ' .

:v/t] B Has lip,~1 solubility gr~-n remifentanil

j/ D C Has a vuf~me of distribution less than fentanyl
I /0 D Has a uilfonised fraction at physiological pH that exceeds that
v ./
of remifentanil
VD E Has a clearance less than morphine
 Pharmacology MCQ.'-
/-\_ \;_ I
1.
1.79 Answers:
A False
B True
G C True
@ D True
• E True
Alfentanil has an elimination half-life of 100 min, a clearance of
6 ml/kg per min, a volume of distribution of 0.6 I/kg and a pKa of
6.5. (Remember all the 6s.) At physiological pH~%
unionised compared with _remifentanil, which is 68% unionised.
Alfentanil has a rapid speed of action; this is owing to its rel~t!yely
low pKa, which renders it ,...,,90% unionised at physiological pH.
Fentanyl has an elimination half-life of 190 min, a clearance of
13 ml/kg per min, a volume of distribution of 4 I/kg and a pKa
of 8.4.

L
I
\-.
:;,,IJ\
--- --
-l\ /4 !_
I r;-. ,- I·,.. ..._ ,, .,..- ••. .•

i.:
. ,j -\

,..
F
I

...•• :·1
'.
 Pharmacology MCQs
;.

1.ao Regarding opioids:

t 'f. O A Fentanyl is the most rapidly_cleared of all the opioids used in·
I common practice
l { D B Fentanyl carries no risk of respiratory depression when used to
augment neuroaxial blockade c1,o
., I

1,. 0 C A 25-µg fentanyl patch is the equivalent of 40 mg morphine

, salt daily
1, D D 20 mg Oramorph ;s -oughly equivalent to 20 mg oxycodone
(orally)
~d _ :/0 E 3 mg diam_orph;ne intramuscularly is roughly equivalent to 10
1
· · mg morphine orally

l
<...!

- 89
 Pharmacology MCQs

1.80 Answerrs:
II A False
• B False
@ C False
~ D False
© E True
Fentanyl can cause respiratory depression when used with
neuroaxial blockade as cu, diamorphine, but to a lesser degree
than morphine, which has low lipid solubility and therefore
produces a higher incidence of delayed respiratory depression. Of
all the opioids, remifentanil has the most rapid clearance at
40 ml/kg per min,
Equivalent conversions for fentanyi patch from morphine are as
follows:

Morphine salt - m.[ daily Fentanyi ;1atch µcg - (micrograms)'

GI i equivalent
-----------'---------
-
90
180
270
25
--=--
50

360

Equivalent single doses (which is an approximate guide offered by·

the British National Formulary (BNF)):
~ morphine salt (po) 10 mg
• diamorphine (im) 3 mg
e oxycodone (po) 5 mg
Reference: British National Formulary 52. September 2006
I -,
II
\._~,

II 90
I
I
 Pharmacology ·MCQs

1.81 Regarding isomers:

~D A They are molecules with the same atomic formulas
X D B Structural isomers have identical bonds between atoms
/D C Morphine demonstrates. tautomerism
i-/0 D Prednisolone and aldosterone are structural isomers
>/ D E At physiological pH midazolam exists in an open' < ·-= -,. , __.)
configuration

1. Of

I-

.,

by
 Pharmacology MCQs

1.s:
1.81 Answers:
e A True
• B False
@)
C True
~ D True
@ E False r •
I

Although isomers have the sam__e atomic formulas, they have

different structural forms. Structural isomers have different bonds
between molecules. These different bonds can confer very
dissimilar pharmacological properties, eg dihydro~od~e and
dobutamine! f A...e_c,J;'/'\,"5..:-:/, rlAQ ~ \~ 1 :--.S\..P. A :''.A.._..>-
- --_::---? Tautornerlsrn is a phenomenon whereby a molecule takes on
different structural forms depending on, for example, their
physical environment. This is well illustrated by midazolam. In
acid conditions, it is. ionised but when at physiological pH its ring
structure closes and it becomes a li12_ophiJic, unionised molec;:ule.
f
l

t
I
i
! t:,.:·
i:-::
i ' ,_.
r .'
l .

f'
I

l,

92
 Pharmacology MCQs.

1.82 The following are true of the pharmacology of old age: l .) ( ,

X D A lipophilic drugs have a ~ shorter elimination half-life in elderly
people
/o B Metaraminol may be a more effective hypertensive agent when
compared with ephedrine ·
>( D C Elderly people need increased doses of non-depolarising
muscle relaxants for effective paralysis
/
/[] D Elderly people have an increased number of extra-junctional
cholinergic receptors
,/
D E lnhalational induction is less rapid in elderly people

93
 Pharmacology MCQs

1.~
s A False
@ B True
o C False
e D True
e E True
,"";·,r,.,...,_With age, comes an increase in body ligid content. This increases
_. ,J the volume of distribution of lipophilic drugs and, when
compounded by the reduction in organ-based elimination, it
increases their elimination half-life and duration of action.
-
/ ,,,,/ ~-receptors are not as sensitive in elderly people and, as such, 1
atropine and_ephedrine may not be as effective. a-receptors on
arteries and veins are still sensitive and so metaraminol is still _as
effective. Elderly people have more extra-jun.ctional receptors but
they have a decreased metabolism of drugs and therefore the
u~ dose of non-dep9lasisiQg muscle relaxant can be given
provided that more time is allowed for the drug to work. Due to
increased ventilation-perfusion mismatching and dosing
capacity, achievement of tid~m inhalational induction
./ 7
takes longer.
Reference: Perioperative care of the elderly. Continuing Education
\ ' in Anaesthesia, Critical Care and Pain 2004; 4: 193-6.

I
l--c)
/ i /
_j __
- \ / \ -~.
\ -~ ; 1.1\ '.
·1 '--
\
.
..RJ,.::::;, t./'----':.. - ::;:; /,
,j I __ _,
J,_}
j
r-,
." . - .,1~
' .. I , ,
,
I'S~ : {-
, I
,-
., /
[__

!'-

94
 Pharmacology MCQs

1,83 Regarding local anaesthetics for spinal anaesthesia:

/

D A A hyperbaric solution has a baricity > 1 .0010

D B A hypobaric solution has a baricity < 0.9990
>( D C Addition of alcohol to a solution will render it hyperbaric
i/ D D Dropping the temperature of plain bupivacalne to 5°C makes it
behave like a hyperbaric solution in the cerebrospinal fluid
(CSF)
D E Glucose solutions as low as 2% are considered hyperbaric

1.84 Regarding intrathecal anaesthesia:

)< D A Solutions containin vasoconstrictors have significantly
reduced mea prea compared with those without '. r ( /
, . -·· r
··./ D B Alkalisation of solutions increases speed _of onset_
~
'!
D C Posture
.. . --, influences speed of isobaric
-- _........ solutions
-
in the CSF
;/ D D A 20;head-do'!'Vfl tiltwill cause a_ significant increase in the
mean&\o~erbaric solution .,
/o E It is thought that intrathecal local anaesthetic appears_ to stop

;~
on
Iv spreading approximately 20-25'minutes after injection

l
[~

I
f, ..•
-
 Pharmacology MCQs

1.83 i\ \ C.-_ .~'s_~\\_

\ )
I ,

fa bcv\A c_
® A True "......st-., _,
B True
C False
D True
0 E True I.·.
'
Alcohol and strychnine were used in intrathecal anaesthesia to
render solutions hypobaric; however, neurotoxicity affected their
continued use. Normal glucose solutions of 5% are used in
intrathecal anaesthesia for its hyperbaric effect. Evidence shows
that glucose levels as low as 0.8% produce a solution that
behaves in a hyperbaric fashion.
Reference: lntrathecal drug spread. British Journal of Anaesthesia
2004; 93(4): 568-78.
,.
I

1.84 Answers: I

I I
• A F~l.se
• B False
• C False
• D False
• E True
Solutions with and without vasoconstrictors have the same spread
although the duration of action is altered. inisation of the
local anaesthetic again has no effect on spee ut_ may affect
duration of block. sobaric solution spread is(p_f>tjnfloen
.e_n~~d by
position. Studies s ow that even a 3.0° cephalad tilt~~
minimally affects the mean spread of a hyperbaric solution;
however, it does increase variability. Although spread appears to
stop 20-25 minutes post injection, marked changes in a patient's
position up to 2 hours after injection can lead to significant
changes in extent of the block. This is thought te-be.independent
!_"'
of the baricity and is likely to be secondary to.bulk movement of
CSF that still contains a high concentration of loc~naesthetic.
i.
Reference: lntrathecal drug spread. British Journal of Anaesthesia
2004; 93(4): 568-78.

96
 Pharmacology MCQs

1.85 Pulmonary vascular resistance (PVR) is lncreased by:

\//D A Norepinephrine ~-..,"~~ 1;, \ ~- )L-t ".:.
11
(·· :.,.":,. ,

,./ D B Histamine
1//D C 5-HT
D D Acetylcholine ~,~ ~a:i
,' o E Prostacyclin ~
1.86 The following are true of drug metabolism by the lungs:
;_,,.,.__.-[] A Prostacyclin (PGl2) is not metabolised by the lungs
~_,.,,,/ 0 B Prostaglandins (eg PGE2) are removed by the lung
K D C leukotrienes .ar~ unaffected by the lung · /_:.·
1_,,,/ 0 D Norepinephrine is partially removed by the lung
-../,. 0 E Bradykinin is largely inactivated by the lung
- -----

l
or

!
L
 Pharmacology MCQs

l \
t
I
- ---- '

1.85 Answe §'§~ l

i

~ A True
i I \
i
I\
@ B True (__
. ) - - \/
@ C True 'J
e D False ) ,~
@ E False \ I·.•
I
A helpful pneumonic to remember agents that decrease PVR is
PIANO: Prostacyclin, lsoprenaline, Acetylcholine, Nitric oxide
and Oxygen.

1.86 Answers:
• A True
• B True
• C False
e D True
e E True
PGE2, PGF2u, l~pkotrienes and 5-HT are almost completely
removed by the lung. PGl2 and PGA2 and PGA1 are unaffected by
the lung. Up to 30% of norepijjephrine is removed by the lung.
Epinephrine, angiotensin II and ADH are not significantly affected
by passage through the lung.
Reference: West, JB. Respiratory Physiology- the Essentials. 7th
edn. Philadelphia: Lippincott Williams and Wilkins, 2004

/ ~11 ; ,. u ~-- ~l t:. _ -~ I

/ .. .,._ ..• '·
_,_;,,
I ,. I
I

, ,:.,. __I,. l
I

F ~ - 1_ if i:-:;j
1··J

0 /
l :"i ' f· < I ,·t .

,. ~· \ I t" I )
\
I' , !e . .,. :"' ,-. t ·'. _ /' l....1

/-r •v-l\
I.
·._::,

,- - - I I
\- . :.J \
I
{-, - ·"'~ •.._} '..,"' -
T

Pharmacology MCQs

1.87 · Regarding drugs affecting calcium homoeostasis: ,

0 A Glucocorticoids inhibit osteoclast activity C..--..\; .,.,:,\,J)' c_
. /~ B They may have an anti-vitamin _p action
;,_,/ 0 C Growth hormone increases calcium urinary excretion A ~.J:,_().'
/o D Thyroid hormone can cause hypocalcaemia
1/ 0 E Insulin increases bone formation ~~\.:i ..Q·,'"'--

1.88 Amiodarone:
V O A Has solely class IV actions (Vaughan-Williams classification)
~-_,,, 0 B Is extensively protein bound J c;
v O C Has metabolites with some anti-arrhythmic action
0 D Has a low oral bioavailability - - ·) __-; )
Y D E Decreases the refractory period of myocardial action potentials fi:,,
 Pharmacology MCQs

1.87 Answen:
@ A True
ci B True
o C True
~ D True
o E True

Glucocorticoids inhibit osteoclast formation and activity; over

. long periods they also cause osteoporosis by decreasing bone
formation and increasing bone resorption. Growth hormone does
increase calcium urinary excretionbut it also causesrncreased
calcium intestinal absorption with a resultant positive calcium
balance. People with untreated diabetes have significant bone
loss as lusuJia_increases bone formation.
Reference: Calcium homeostasis. RCOA Bulletin 2003; 18:
883-6; ~_ ~ c__\,_o. Y\Y\..o_~ \-:~ l,"', _)(-u.
.- ,, 7-
1.88
®
Answers:
A False
~
--
---- '----'
'
'\.)
\
\
- -· -
\
'·
II ,, .
I

0 B True .

f) C True Lc\u--s~ '7. ~

• D False o\. v-V-
><~'
• E False
Amiodarone is a useful anti-arrhythmic for SVT (supraventricular
tachycardia) and ~ VT. Although classified as having class Ill activity
it also demonstrates class I, II and IV activity. Its blocking effect on
the potassium channel causes a prolongation oi_ehase 3
(repolarisation). This lengthens the action potential and the
refractory period. The oral bioavailability is 50-70%. It is 95%
plasma protein bound and is hepatically metabolised to
~sme!hJ'.!arri iodarone, which has some anti-arrhythmic activity.

C'/..._~---

-
\-
( {\ ')
\
I • ;
• I
(1 -\·•'
~\
' .,,. ._;..
'
\
100 -
\
.I
 T

Pharmacology MCQs

1.89 Regarding lidocaine toxicity:

/ tJ A Toxicity occurs with bloodconcentrations over 4 µg/ml
,/ .

/o B CNS toxicity is an early sign of intravenous overdose

, / D C Cardiac arrest precedes respiratory arrest
_,, 0 D The maximum recommended infiltration dose of plain 2%
I lidocaine in a ?~,,!<ft. man is~,~ mt~,.~
0 E It is more likely in- the presence of liver failure

·s 11,90 Regarding the metabolism of sodium nitroprusside:

/o A Reaction in the red blood cell causes release of cN- and
methaemoglobin
f D B CN- combines with vitamin B12 to yield toxic thiocyanate
'/4
p C Rhodanase enzyme is found~in the liver ..-.~ ., ' ' . ,
D D Red blood cells can liberate CN- from thiocyanate via the
enzyme thiocyanate oxidase
.;
10 E Thiocyanate and cN- are equally toxic to cytochrome oxidase
c:_{J / \oo Th,'o '-::)c~~
.,

·-~ -· ~.

101
 Pharmacology MCQs

1.89 An$wers: ,, 1.91

~ A True
e B True
f:D C False
e D False
~ E True
Lidocaine toxicity can be viewed as plasma concentrations:
G >4 µg/ml - circumoral tingling, tinnitus, dizziness, paraesthesia
" 10µg/ml - loss of consciousness, convulsions ·
() 15 µg/ml - coma, stroke, myoca~ d~eression
@ 20 µg/ml - cardiac arr~ythmia, respirato~
$ 25 µg/ml - ventricular ar~ .-..~_ . .
-------
Toxic doses are 3 mg/kg of plain solution or 7 mg/kg of lidocaine
with epinephrine. A 2%_solution contains 20, m~-tnl. Therefore, a
70 kg man should .. receive an .upp~r limit of ~I 2°(o lidocaine.
This is the recommended dose. Lidocaine undergoeshepatic
metabolism and therefore will present increased risk of toxicity in
1
patients with hepatic failure. OJ

Reference: Urquhart, Blunt and Pinnock. The Anaesthesia Viva 1

(Physiology and Pharmacology). 2nd edn.

(
1.90 Answers:
...:J
r- - I,, C, A True
~,/ B False
~

•
~
C False
D True ·
6$~)
• E False
Sodium nitroprusside enters red blood cells and combines with
oxyhaemoglobin to form five cN- ions and methaemoglobin. ·.
CN- and methaemoglobin for~anomethaemoglobin (non-
toxic). CN- ions react with sulphydryl groups in liver an<i!:_enal
tissue secondary to the enzyme action of. rhodanase. Thiocyan~!_e ,
is produced, which is 1 QO times less toxic than <:;N-. Thiocyanate
is excreted renally with an·
elimination half-life ori days. It ca~
also be converted to ~rs_- by thiocyanate oxidase found in red 1'

blood cells. · - -- · ---

102
 Pharmacology MCQs

1.91 Regairda~g th~ ttreatmeimt of sodium nitroprusslde toxicity:

I
. ,,/0 A Plasma CN- > 8 ~g(mJ results in toxicity
D B Dicobalt edetate chelates cN- ions so decreasing toxicity
/ D C Sodium nitrate increases available methaemoglobin so
producing more thiocyanate
D D Vitamin B12 is most effective as a prophylactic agent
'-../

- ---
D E Sodium thiosulphate decreases cN- ions by increasing
-
thiocyanate production

1.92 Phosphoduesterase inhibitor aminophylline:

/
, D A Inhibits all five phosphodiesterase isoenzymes
[,. /

, D B Blocks the adenosine receptor on mast cells, inhibiting

v degra~_ulation
l
Vo C Reduces seizure threshold
1 ~D D Causes fluid retention
1
0 E Elimination is reduced by phenytoin
1 I

103
 Pharmacology MCQs

1.91 Answers.
e A True
Cl, B True
('i C False
@ D True
0 E True
Sodium nitrate and amyl nitrate cause an increase in
methaemoglobin, so providing more substrate for the production
of non-toxic cyanomethaemoglobin. Vitamin B12 combines with
CN- to form cyanocobal~n_,jn which is also ~~Q-t~ic· but of little
.:va-lue in the acutese
tting. .
...-

.- ·.( \ 0 \'\ ~~,.. \s. ~'-",....-l?

1.92 Answers:
• A True - c:--'\;'-\..V\.e ~- '--

• B True
• C True -- f t-f \ ") ' JC\\.:i a-\<. ..,
.,
~<'".1\1<:)\V'\ <:, .

• D False
• E False
Aminophylline is a non-selective phosphodiesterase inhibitor. It
prevents tubular sodium reabsorption and is therefore a (diy_(e!!f f It
is metabolised via the cytochrol'!,1_~ _P450 system. As phenytoin
induces this system it therefore increases elimination.

104
 Pharmacology MCQs

. 1.93 Diazoxide: ,
X D A Is a diuretic ') ,:-,, -,. . , -\ .
,'.) (\ I
,.

__/ D B Causes hyperurlcaemta :.

'I. 0 C Causes hypoglycaemia '
, . /·o o Is used to treat hypertensive crises associated with renal
disease
Effect on blood sugar lasts longer than its effect on blood , \;, ,
pressure . (1\ c? ( 1
l'
./ /r...> \ . (
/ \... ) ·y,I .,,
(brr::, ,
1.94 Regarding anticholinergics: .
vtJ A Hyoscine crosses the blood-brain barrier A_.+.-lb fl '~ ( ~~\,· ~ ~~)
1/0 B Only the L-atropine isomer is active
- c.,,/4] C Glycopyrrolan, is a quaternary amine,
D D Glycopyrrolate is predominantly excreted unchanged in the
unne
v;'D E Atropine may cause transient bradycardia
·"

\
 Pharmacology MCQs
\)
-- Y\.t·1\ t?.
1.93 "1(:::). '. '...\--~ '-J
- vv_
.

A False
• B True
~ C False
e D True
• E True
, /Related to the thiazide diuretics chemically, it may be confusing
_ , >~· , t9 find that it actually causes a reduction in urine output \
~------ · )-,":__,? · secondaryto -~n in_c.!:_:.~s~- i_n renin and ~ldosterone. Diazoxide
~. ,.._,~ ~, - , ~ causes Ere~.QS!llp ?ecr~n1 which canbe-used to t~t
~ ....-..·· / hyp281Ycaeniia. It also causes ~rterial vasodilatatio~(secondary to
' ~-s'·'" ' q_y:tl'- increased cAMP effect in arterioles), which is useful for the
·. · ~"9 treatment of hypertensive crises. While producing arterial
/ ·'\ ~- .-~ ~- vasodilatation, it also increases catecholamine release, causing an
· ' increase in heart rate and cardiac output. Its hypoglycaemic
,/ effects last approximately 8 hours compared with. its effects on
blood pressure, which last 5 hours. Oral bioavailability is 80%
.,
and it is 90% protein bound.

1.94 Answers:
• A True
• B True
• C True
• D True
• E True _
. Hyoscine and atropine are~rtiary am~ and are therefore able
to cross the blood-braj_n barrier,unlilce glycopyrrolate (a
quaternary amine).,~ of glycopyrrolate is excreted unchanged
in the urine. Atropine' may cause a transient bradycardia reflecting
its partial agonist effect at card.ia~muscarinic· receptprs. Although
present in a racemic mixture o~h~-atropine' isomer is active
(as is the case with hyoscine).
~

; I
 Pharmacology MCQs

,..,_

Regardilllg chirallty: 2_;,__, J-.. J\1JI--~_

_,;1 V O ,_.::; - ,__;/ .
1.95
'< 0 A Ster.eots-Qm~rs have the same atomic structure but different
bbnds between molecules
,/ 0 B Enantiomers are chemicals that are mirror images of each other
._/D C -~bupivacaine is an s- enantiomer
.\ c , '-' I ' :· , -·
·t D D The R/5 (rectus or sinister) naming system reflects the direction
of rotation of a plane of polarised light
D E Mivacurium is a geometrical isomer existing predominantly in
the cis-cis configuration - h-,1 :, J .

1.96 Sympathomimetics - epinephrine: .,J I I /J/11/Jr, '"""' ~

X O A Is used in doses of 1 ml/kg of 1 : 10 000 iv during paediatric ,,.,,__'-- ~
an I asystolic arrests
/o B At low doses can cause a fall in peripheral vascular resistance B
,/ 0 C When used with halothane, doses should be kept to within
· 100 µg/10 min to avoid arrhythmias
11/0 D lv\etabolites are excreted in the u;i~e as vanillylmandeli~ add
v/0 E At high doses, inhibits insulin. secretion · -

\,:j"-"'.) -

'./

107
 Pharmacology MCQs

1.95 Answers.
® A False ,-_
\ ~,C)_..
.['~ .•..\
.
.,.\ s""~
e B True
• C True \ ~C)~j~ \ ;.\\yrJ
@. D false
• E False
Option A refers to structural isomers. Stereoisomers have both the
same atomic formulas and bonds but different arrangements
around a chiral centre (or centres).
Option D describes the{dextro'/ev~ing system with
clockwise rotation of the polarised light being dextro (to the right)
and anticlockwise rotation being levo (to the left). The RIS naming
system refers to the orientation of molecules around a chiral
centre, R standing for rectus and S for sinister (the ~atfn for right
and left respectively). There is· no link between the two naming
systems. Levobupivacaine is an ·enantio-pure preparation,
ie containing only one isomer. Most isometric drugs have helpful
therapeutic properties conferred by the siniste,enantiomer. .,
Mivacurium exists predominantly in the tmns-trens form ( •....• 60%).
(€0
1.96 Answers:

• A False
• B Trut.
• C True
• D True
• E True
Paediatric resuscitation doses for epinephrine are 0.1 ml/kg
1 : 10 000. At low doses, ~ effects predominate which decrease
peripheral vascular resistance and increase insulin secretion. At
high doses a eff~ ·predominate, causing vasoconstriction and a
decrease in insulin secretion.

11\A
 Pharmacology MCQs

1.97 Pharmacokinetics - ~ut~ i,'l)k!,m!tte~l.Et!1~Y!B~:

.,,,./0 A Can be precipitated by sulphonamide antibiotics
1
f D B is more common in eastern Europeans , · '1 '
1

XO C Results from a deficiency in porphobilinogen -:~-": "· ·, ·

. _,,,,-0 D Attacks are more common in women than men
[_, 0 E Attacks can present with gastrointestinal symptoms
me I
1.98 Adverse drug reactions - examples of ~~A (or augmented)
reactions to drugs include the following:
-·-----·-
/0 A Tinnitus with aspirin ---
~ng I ._/o B Hypoglycaemia with insulin --
·-<' 0 C Malignant hyperthermia with suxamethonium
·,tt
1. I ;
//o D Ataxia with phenytoin -
, D E Acute intermittent porphyria with barbiturates
1ful
.,
0%).
·-------- (!):l\ ,,) I\l, \
1-ey__-\\ L~ / I-,:- '-J I - _ _.) -l .• -.
\ .) ')
\t
' ,,
, ~
l
J

\.j< j s ·1 ./
11, 1. .,
I
. ' .'
,_, . .._,-'
----- _) '· \ :
'.)

-1 p I\ ,, 1 / ,- :
', , ,;'' _ \I, - { \
,~l
I
1.
 Pharmacology MCQs
I
-
_;p.-·.:D:1,
• • I .
.,.
...
I

Answers; :- · ·: . · ·- · ·- --~ -·. ·---- -- - ·~f·

1.97 1
-~ l !: : ••. ;

A True · · ··:~-~-.
--) -f DP;_ :::: ·.::_, ~·. _t.
B fa I se
/_ __.,_· . ·--;;·- , > -- - · 1
, •
·:c'.._
C fa I se v1!.---.... .. ·, _ ::::1 - ·, ~ .1
-7 \~ ".;,_}) \..J
, . '-'--i·-·- 1
LtA-i'k'A ;·.,,-it ~ ·0,_,;r
1

• D True ,--. :'- ·-i -- , ••• - /

, . ~·r vF°n ,_ -~J-,, 6)__ .. ,
_) ,- '-' V~

-- 1 '
r'\ • ., , (
9 E True I (;'\--, t · -. ...: .., -~ _ .•.. • · -
-· ,-- --1-.-· .. _j'/1 ·
1-· .~ -"

~C.JJJ~lnt~rroittent porphyria is an example of a familial var_W!Qn

in drug response that affects anaesthesia. It can be precipitated by
barbiturate anaesthetics, anticonvulsants, sulphonamide
antibiotics, ranitidine, diclofenac, hyoscine, clonidine and
Ildocaine, to name a few! -- - -
Attacks are more common in women and nort~ern Europeans
(Sweden}. Attacks present_with ~strointestinal symptorl_!s.of pain,
diarrhoea and vomiti_ng, _neurolo_gical symptoms including muscle
weakness, convulsions and tremor. It results from a deficiency of
the enzyme porphobilinoge'!_ deaminase, which leads to the
accumulation of the haem precursors d-aminolaevulinic acid and
.I porphobilinogen, initially in the liver.
Answers: .
~-- •
~ls~- d f!X::\
111

re:d-i. c: V
I

1.98 _.,....____ .., r.. '• -·j

•.. ,.
• A True -.---·· ·- \,
\'j P'L-
° -0/'
/

-- T .. '•e 1....1 , ..,

r
' c _
~ -L..:.,]

•
J .

B True I . ! j
(,\---·
\ .x:;~l ... l.
.J \) \' 1-P ,,
I -~- -~
-•. :·. . .. , ... _ , . .. ,
· ···'

• C False V ) ._ 1 '/ CAi'.·i'--·' ' -.:'·) ,' :-

•• D True
E False
One way to classify ~dverse drug reactions is as .••. type A or
augmented or type B or bizarre. Type A reactions are common
and are often related to the pharmacological effect of the drug.
They are commonly d~ed. They can be a prima!Y- r~c!ction ,.
I

due to an exagger~tea r~pons_e to the drug, ~ hypoglycaemia r:

with insulin or a secondary reaction, hot directly related to the
desired effect, eg ti"!!!tus with aspirin. T,.¥ge_]:'.'~~g!ons are
bizarre, unpredicted and ·~~o,s_e rela~cl. Examples of type B
reactions include suxarnethonium apnoea, malignant
hyperthermia and hepatic porphyria.
Reference: Adverse drugreactions. Anaesthesia and Intensive
Care Medicine 2005; 6: 245-50.
•
lj
 Pharmacology MCQs

1.99 Regarding adverse drug reactions - hypersensitivity

- ·- ·-···-- --
'
reactions:
-

vD A T_ype _1_ h_y~~~nsl~i_vi!y reactions with penicillin are mainly

caused by their degradation pr<:>d~cts
vD B Presentation with bronchospasrn results frornleukotriene
release in the lungs
. . .,---
Vo C They can occur ~econdarr to lgs,.\~~or~gMI activation I\.
,<
D D They are classed a~n the case ofliier,,olytic anaemia. 1:. '
after methyldopa - _
)'( D E They are described a~_~lass,11.when resulting from soluble
antigens combining with circulating antibodies
I -•·-~1·
-i \ 1 !~~-_£__)

\
.\. ~;__. I
)' .
_J_..,. :- \

d .
"'-·-- -~
r

\
f>~-.rfY\·J\ v· ,;:,-.,
----- \J - .

\ ~ J\ \
......, .. ;·::.. /' _l\ \_

•.•\..

1 1 1
 Pharmacology MCQs

1.99 Answers:
~ A True
G B True
e C True
D False
• E False

Type of Cause Example

Reaction

Type I Antigen + protein causes lgE Degradation products

....___
hypersensitivity antibody formation attached to of penicillin, insect
mast cells stings, peanut

,__ \ Type II Drug combines with proteins Methyldopa -

~~~
hypersensitivity in ceHs, inducing formation of haemolytic anaemia
., --
lgG of lgM antibodies
-;:::..-
Carbimazole
--
letJ~penia
-

Type Ill Soluble antigen reacts with Serum sickness

hypersensitivity circulating lgQ antibody ' Rheumatic disease
-=· - - .- -
Type IV Macrophage ingestion+ Tuberculin reaction
hypersensitivity T-lymphocyte activation Contact dermatitis

Reference: Adverse drug reactions. Anaesthesia and Intensive

Care Medicine 2005; 6: 245-50.

112
 Pharmacology MCQs

1.100 Bioavailability:
;/o A
Is defined as the fraction of an oral dose of a drug that reaches
the systemic circulation when compared with a standard route
of administration (usually intravenous) ,
i,D
B Of warfarin is increased't,ii/; concomitant use of barbiturat~'
xo I

C Of aminophylline is increased-in smokers

/
XO D Of a buccally administered drug is decreased secondary to
first-pass metabolism
,1/D E
When plotting plasma ~~11.G. entration vs ti'!!~ of an oral and
intravenous preparation of a drug, the bioavailability is given
by the area under the curve of oral divfded by the intravenous
preparation

,r
i
·i
:1
I
 ::--

Pharmacology MCQs

'·, -!
• >

1.100 · Answers:

© A _True
~ B False
• C False
a D False
0 E True

Key ~ = Intravenous preparation

Plasma &§'§ = Oral preparation
concentration
Bioavailability

Time
•:
•1 Figure: Bioavailability

Enzyme i~~rs increase the breakdown of the drug and

therefore decrease the bioavailability, eg warfarin with
barbiturates and aminophylline in smokers. Enzyme inhibition
reduces drug breakdown therefore increa5ing the bioavailability
of the drug, eg metronidazole with alcohol; intravenous,
intramuscular, subcutaneous, transferral, sublingual, buccal and
nasal drug administration avoid significant first-pass metabolism.

Enzyme inducers Enzyme inhibitors .,

Barbiturates Ecothiophate
Phenytoin Metronidazole
Alcohol Cimetidine
Smoking lsoniazid
Rifa_mpicin Phenelzine

\\ "'"- J .,,:_, ~:\ ,_ ,J•

~ ~

t \'
I' l
I
I

Ii
11 ii
-\~ ( \ ~ - .- ..... !"" -, \r...

'
~ -~-

' \ Lft·
'tI
'
 Pharmacology MCQs

1.101 Drug distrlbution;

0 A Of warfarin is almost entirely confined to the plasma
D B Of monoamines is negligible across the blood-brain barrier
(BBB)
D C Is in general greater across a placenta when compared with a
BBB
· D D Between mother and fetus is affected by the drug's relative
plasma acidity
:, 0 E Of highly protein bound drugs is very low

1.102 Drug metabolism:

/\ D A By sulphation is an example
. ~
of a phase I reaction
. J,.
-~- D B By acetylation occurs solely in .
the liver
\.. . ·:

. D C In liver failure usually affects phase II metabolism.before

I
I
phase I · ··: :.· '.,

Of sevoflurane is by cytochrome P450 (isoform ~~l )·.

Of halothane is predominantly by reduction if the liver
becomes hypoxic ,...

-1

11.

11.5 .
 Pharmacology MCQs

1.101 Answers:
1.11
• A True
• B True
• C True
• D True
• E False
Warfarin is a highly protein-bound drug that is confined to the
plasma as its unbound fraulon is negligible. That is not to say that
all highly protein bound drugs have minimal distribution.
Propofol is 98% protein bound but has extensive distributions
owingto the dynamic nature of the protein binding The passage
of monoamine_ across the BBB is negligible as it contains
monoamine oxidases. The p~~s~_g~9f .drugs across a placenta is
greater than across a BBB asit is less selective. Even moderately,
lipid:-soluble drugs can pass withease. The drug distribution
between mother and fetus can vary according to their plasma pH,
eg pethidine will become more ionised in the lower pH of thf'
fetal plasma, so leadin& to i~ing.
1

1.102 Answers:

• A False
• B False
• C False
• D True
• E True
Phase I reactions include oxidation, reduction and hydrolysis.
They are carried out by the mixed function oxidase system or the
cytochrome P45Usystem within the endoplasmic reticulum,
Other enzymes can also perform phase I metabolism, eg
monoamine oxidases. Phase II reactions include glucuronidation,
sulphation, acetylation, methylation and glycination. Phase II
metabolism increases the water solubility of the drug so allowing
excretion in bile and urine. Acetylation occurs in the liver, luni'
and spleen. Liver failure generally affects phase I reactions f'.~t:

. 116
ta
 Pharmacology MCQs

1.1 OJ Receptor agonlsts and antagonists. The following stems are

correct 31111 relation to the log dose-rrespo~se curve illustrated;
co A Curve c could represent a partial agonist
( 0 B Curve b could represent a drug that is less potent than that
giving rise to curve a
D C Addition of a competitive antagonist to the drug giving curve a
could lead to the dose-response curve c
D D The position of the curve on the abscissa denotes efficacy
D E Curve b could represent the action of phenoxybenzamine at
e "'"'.,,_... ._,.,,.. r,.,:/'i:
t h e a-receptor 17'-. _ --~ •

'7(_. \y... .•, ~) --

a-·
Response

Log dose
Figure: log dose-response curves

')
 Pharmacology MCQs !
I
! .
I
l

1.103 Answers: 1.1

@ A True
@ B True
~ C False
® D False
ti} E False
This sort of question is also easily examined in the viva. When
interpreting these curves, remember, their position on the abscissa
reflects potency, their maximal height reflects the efficacy and
their slope is influenced by the number of receptors that must be
activated to achieve that response. Note that the dictionary
I definition of abscissa: the shortest distance from a point to the
,, I vertical or y axis, measured parallel to the borizontal or x axis, ie
I
{ the closer to they axis, the more potent. The dose-response
'...J i
' j curves a and b represent full agonists, the drug giving curve b
I

j
I
I
being less potent than that giving curve a. The dose-response
i
I
curve b could also represent the addition of a competitive agonist
'3'--· I
J_ i to the drug, giving rise to curve a. The addition of a non- Cl
f

competiti~1agonist to the drugs represented by curves a orb

could lead to a dose-response curved. Non-competitive agonists
affect all aspects of the curve. Phenoxybenzamine is an
insurmountable antagonist at the a-receptor, no amount of agonist
~, will produce t11e full receptor effect.
Reference: Receptors, agonists and antagonists, Anaesthesia and
Intensive Care Medicine 2004; 5: 350-2.
f\

1.1.8
I ·,
'
Pharmacology MCQs

.104 The folio.wing are true of receptors:

1
, _D' A All subunits of a ligand-gated ion channel traverse the
• membrane
ys G-protein coupled make up the
membrane-bound receptors ·
largest proportion of

C Cholera toxin causes persistent activation of the G-protein that

stimulates adenylyl cyclase (Gs)
D Thyroxine exerts its effect via membrane tyrosine kinase
E Activity of a receptor is analogous to affinity

C11 r

CII I

..... . ....

119
 Pharmacolbg v MCQs

1.1 04 Answers:
@ A True
f) B True
• C True
• D False
• E False
Receptors can be divided broadly into:
• Ligand-gated ion channels eg nicotinic, GABA !:.e._ _ceptor
• G-protein linked, eg sympathomimetic receptors
• Direct enzyme linked, eg insulin, atrial naturetic peptide (ANP)
• Intracellular receptors affecting gene transcription, eg steroids,
thy!:Q._xine -
Ligand gated channels are multi-subunit receptors. All these
subunits traverse the membrane. G-protein-coupled receptors are
the largest group 9imemh@pe-bound receptors, (covered in
Question 1 .107). ~inds to an intracellular, nuclear,
., thyroid hormone receptor. Insulin binds to an extracellular
receptor. Binding triggers the phosphorylation of tyrosine, by the
intracellular portion of the receptor. This greatly increases the
activity of tyrosine kinase, which in turn initiates insulin's
intracellular effect. Affinity refers to how well a drug binds to a
receptor, Activity refers to tbe extent.ol .receptor activity caused by
the drug binding.
Reference: Receptors, agonists and antagonists. Anaesthesia and
Intensive Care Medicine 2004; 5: 350-2.

t :

120
 Pharmacology MCQs

1.105 Drug binding:

·/'- D A The stable heparin-antithrombin m complex is an example of
a covalent bond
,., D B Dipole-dipole interactions depend on van der Waals' forces
t,/ D C Covalent bonds form following the transfer of electrons _ j
/\ D D The hydroxyl group of edrophonium is. attracted to the ftnio¼'c -
site of acetylcholinesterase -·
-~ E Albumin binds on5neutral or ~cidic drugs · J< r~

i !>y

nd
 y

Pharmacology MCQs

1.105 Answers: l
I!
• A False I ,
• B True
• C True
• D False
• E False --~
Ionic bonds are readily___reversi9le b~ds between~~mi_se_v .
/ compounds and~d c~c)ites on prot~eparin
contains an~ 'pentasacc~group that is attracted to
·· basi~ arg0ine residues in antithrombin Ill
-bifloie-dipole interactions occur between !!JQ.!ef 1-~at are
/ partial! ositive and others that are partialf¥--Q~~ ativel charged.
The strertgt of the bond depends on the distance between the
molecules. The critical distance that yields the greatest attraction
is called van der Waals' radius.
Hydrogen bonds are another example of dipole-dipole
r interactions. These occur between partially ~ydroge~
atoms in hydroxyl or secondary amine groupmcl etectronegative I
atoms with unshared electrons, eg ox~. Edrophonium forms a 1 ,.
hydrogen bond by its hydroxyl group at the ~steratic site on l
acetylcholinesterase. Covalent bonds involvethe sharing_9f
electrons rather than cor11plete~~r. Stabl~oncls are formed.
Albumin predominantly binds~ and neutral drugs but also
binds some basic drugs. - - -__.1
Reference: Bonding, binding and isomerism. Anaesthesia and
Intensive Care Medicine 2004; 5: 345-8.

.. I

j
!,
\
 Pharmacology MCQs

1.106 The following drugs are over_ 50% protein bound in plasma:
~ D A Ropivacaine
t/ D B Warfarin
X D C Morphine
'/-. D D Atenolol
L/o E Phenytoin

.-.-.~.:~.

1 'l 'l
 T

Pharmacology MCQs

1.106 Answers:
1
( A True
e B True
Iii C False
0 D False
® E True

Drug Percentage protein bound

Ropivacaine 94
Bupivacaine 95
Lidocaine 65
~ _Atracurium <20
Fentanyl 80
Alfentanil 90
___,, Morphine 30
Pethidine 65
Warfar,in 99
Phenytoin 95
_ / Atenolol 5

Reference: Bonding, binding and isomerism. Anaesthesia and

Intensive Care Medicine 2004; 5: 345-7.

;\ .r
\
I

124
 Pharmacology MCQs

1.107 The following are true regarding sympathomimetic Ga(Oll.llp~ed

proteins:
' .,
A a1 -Receptors are Gi coupled
·/0 B P2-Receptors are Gs coupled
D C All dopamine receptors are Gs coupled
D D Activation of Gs-coupled receptors increases cAMP action
1
D E Stimulation of Gq-coupled receptors decreases the activity o(') f
protein kinase C
 Pharmacology MCQs

1.1 Oi Answers:
8 A false
• B True
• C False
• D True
• E false

Receptor G-coupled protein

Gq
Cr:-x-:>-.
a.,
Cl2
Gi
'1 t -H tc_
(3, Gs
~\-

(32 Gs
(33 Gs
D1 Gs
Gi
02
,t
Gs-coupled receptors cause stin:1ul~n o~MP_p_rq_ductian. This
. '" in turn stimulates protein kinase A by binding to one of its sites (R
, . ~'-s- -~·< _ ~ c:.Or regulatory site). This causes its active site (C unit) to_b_e__~
, r<- , ~ 0\ rev,?aled, which _is resp2nsible for its effects, i nCI udi n!\ positivej
:,"J-.~ 0' ~and c~ronotropic)e1!ect in the heart and relaxation o(
sTnooth musde"1rfthe bronchi and vascuiature by ~t - and ~r
rece~o~. M
, Ci-coupled proteins inhibit cAMP_groduction~ ai-Receptors are
::::::==a a=.
___,,(_.,.-;-
•...
an example. They are widespread in the CNS and a decreased
-::.>
\' C'.__.•
cAMP causes sedation and analgesia.
t_j-7-7 ~'3- 0 Gq-coupled protein activation causes lncreased a.c_tio_n_9f
/ phospbollpase C, causing the breakdown of eli_<>sphatidylinositol
-~:J 4,5-bisphosphate (PIP2) to inositol trisphosphate (IP3) arid
diacylglycerol (DAG). IP3 causes calcium release in the
endoplasmic reticulum~and DAG causes ~f pr9J~
-· •..
c~

klnase c;=. This increase in calcium causes its effects including

vasoconstriction in vascular smooth muscle by ~1.:receptor
activation. '
'1
.,, '
I
 Pharmacology MCQs

1.1 08 The following is true regarding pharmacokinetics in the obese .

patient:
.,,/D A Ideal body weight (IBW) is calculated by (height in cm - 100)
for adultmales
:__,,. D B Lean body mass (LBM) is calculated using height, weight and
sex
/o C Below IBW, LBM and total body weight (TBW) are similar
\(". C--)

·; D D Remifentanil shows a significant increase in volume of

i \
distribution in the obese patient
•/0 E If a drug is hydrophilic, its dose should be calculated
according to an obese patient's LBM

:::, lj C o. ,..,._ (J
 r

Pharmacology MCQs

1.108 A nswers:
~ A True
B True
. \...SvV'-;:, ~ ,,.,r B~
G.l

(;)
C True
® D False
~ E True

~
IBW is calculated as
.
shown:
IBW
~
(kg) = height (cm) - x
(where x. =. 100
. for adult men and 105 for adult women).
.

LBM can be calculated as shown:

Male LBM = 1.) (weight) - 128(weight + height)2
or for female LBM = 1 .07(weight) - 148(weight + heig~t)~ _ J '::.
A Highly lipophilic drugs show an increase in volume of distribution
7
in the obese patient. Remifentanil is highly lipophilic; however, it
showsi~ ,ignificant change in distribution in obese patients. As a
result, tne dosage should be calculated based on the~ IBW. The
~
obese patient has an increase in LBM when compared with non-
obese individuals by up to 20-40%. Therefore, when calculating
.. ---
the dosag~ of a b\drop.l)il\ic dru~, it is more accurate to correct the
dose ~o th~ LBM t an the IB_W. 1
.
Reference: Pharmacokinetics in obese patients. Continuing
Education Anaesthesia, Critical Care and Pain 2004; 4(5): 152-5.

i ~ \ \
\)
<
f :_, \
·.\
' \
,,
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128
 Pharmacology MCQs

1.110 Regarding pharmacokinetics.

:v-o A The elimination rate constant (K) is the fraction by which t_he

I concentration of a drug reduces during_~pecified_period

0 B The time constant is the time (measured from a point zero) at
which the elimination ofthe drug would have been complete
if the initial rate of elimination had continued -- - - - -- -
/
,/U C A drug with a volume of distribution at steady state of 0.16 I/kg
'.) is likely to be highly ionised
·\/~ D A unit of measurement for time constant is minutes
·/ D · E The volume of distribution of fentanyl is significantly larger
than propofol ·-~- ', __ 1 r-

as

al of

131
 Pharmacology MCQs
I.·,

1.110 Answers:

• A True
• B True
• C True
• D True
@I E False 1
The elimination rate constant (K) is measured in units of time t- •
The time· constant corresponds to the time taken for the
concentration to fall to 37% of its initial value. It is measured in
the unit time.(iiighly i°-~i~ed drugs do ~t readily cross lipid
membranes and so have a low volu_ID.e-6f__disyibl~_!LQIJ, e_g ,
glycopyrrolate with a \lit_0.16 I/kg. f«;Utany!Jlnd prop2J.ol have
similar volumes of distribution at 4 1/~- - --·

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Pharmacology MCQs

1.111 · Pharmacekinetlcsr
Y D A Absorption of weakly acidic drugs is facilitated by high pH
~ D B Dopamine is metabolis~d in the gut mucosa
i D C After an intravenous drug administration, high cardiac output
causes a higher peak blood concentration (when compared
with a lower cardiac output state)
i/ D D The rapid redistribution of thiopental is known as the a phase
1/ D E At high concentrations aspirin can undergo zero-order
kinetics.
 '":,\, ..

Pharmacology MCQs

1.111 Answers:
• A False
lit B True
It C False
• D True
• E True
Acids become mor

B + H+ --+ BH+.
If an intravenous drug is given to a patient" with a high cardiac
output state, the drug is diluted by the volume of blood; this leads
to a lower plasma concentration. The rapid emergence from
anaestfiesla aft:er an
initial intravenous bolus of thiopental is a
result of the,~)hase. Initially the thiopental is concentrated in the
fat-soluble tjssue ~ith a rich blood supply including the brain.
Howe"'Tr, as the less well-perfused tissues absorb more of the • ,
drug, the plasma concentration drops and therefore the drug ·
leaves the brain and enters the plasma down the concentration
gradient. The fall in brain concentration leads to emergence from
anaesthesia. · · - -==- -
First-order kinetlcs oc~U.!! in n_9..n::'.satut.c1ted-enzyme reactions.
Elimination is dependent.on.the conc;_,mJration of the drug and is
exponential. Zero-order kinetics occur in ~turate..cd enzyme
systems. The amount of drug eliminated J{const~nt per unit tim~
and is limited by the enzyme action. At low concentrations, a
drug can undergo firs!1>rd~1.kinej!g, but as the enzyme system
becomes saturated, the elimination kinetics _can change to ~
order, eg as.g!g!!_, · --
~

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 Pharmacology MCQs

1.112 Aspirin: ._
XD A Absorption is greater in the stomach than in the small intestine
)\ D B Is preferentially excreted ~n acidic urine
l\ D C Has a pKa of 6
i\ D/
D Is predominantly unionised at physiological pH I , ·
I

L,/0 E Is predominantly bound to albumin in the systemic circulation

-- ./' ,,.
,...,...

e
 Pharmacology MCQs

:::::=-
f· r .
f.
- .\

1.112 Answers: ?' , -, r _,,.

e
®
A False
B False -- L ·_. '
r /,
r-.
j'~
'
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r
C False _I /, I
e \
r •. ,J
'- - r
• D False \,.
ID E True
Aspirin is an acid with a pKa of 3. In the acid environment of jhe
stomach, it is in its unionised form, which may lead you to believe
that its absorption would be greater than in the basic environment
of the small intestine. The unionised aspirin, however, b1 , -ornes
ionised and trapped in the gastric mucosal cells preventing
absorption into the systemic circulation. The large surface area of
the small bowel means that the grea~ part of its absorption
occurs here. Alkaline urine promote sits excretion, as more
ionised molecules are excreted in urine. It is predomjpantly
ionised at physiological pH. Remember: -
A- +H+ ~ AH.
c:,lt is 85% protein bound in the plasma, mainly to albumin.
 Pharmacology MCQs

1.113 The volume· of distribution ( Vd):

/ D A Is the plasma concentratlon divided by the initial dose
/D B Of a drug that is confined to the extracellular space is
approximately 14 litres '>'/c-
,/o c Of diazepam exceeds total body~ater \-',St-\\(-~
0 D Divided by the clearance gives the. rate constant f9.rJhe
exponential process of elimination \<- ==- ..S.' ' -
:--_o
I

E Is equal to the time constant divided by the clearance

~
___::::!_-- (_Q._
c.'-..ev---<,rr-
 Pharmacology MCQs

1.113 Answers:
@ A False
@ B True
~ C True
D False
fl E False
The volume of distribution (Vd) of a drug is the dose of drug·
divided by the plasma concentration. A drug with a low VcLthat is
highly protein bound and lo~id solubility will be largely
confined to pl~~a. A lipid-soluble drug that is concentrated in
tissues, eg diazepam, will have a large Vd (1-1.5 I/kg). Some
equations to aid calculation of Vd are shown ~
K =clearance+- Vd
Time constant= 1 +- K = .Vd +- clearance
where K is the rate constant for the exponential process of
elimination of a drug.

138
 Pharmacology MCQs

1.114 Clearance:
vb A Of a drug is given in the units ml/min
~D B Of a drug by the liver is given by the product of hepatic blood
flow and hepatic extraction ratio
\ D C Of a drug by the liver will depend predominantly on enzyme
activity if the hepatic extraction ratio is >O. 7 ~o , -s .
/o D Of a drug by the kidneys that exceeds the glomerular filtration
rate (GFR) is by both sec'lilion and filtration ;
/4 E Of an unionised drug by the kidney is reduced secondary to
tubular reabsorption
 Pharmacology MCQs

1 . 114 Answer§:
e A True
@ B True
C False
e D True
& E True
Hepatic clearance = hepatic blood flow (ml/min) x hepatic
extraction ratio.
Q~ If the drug has a high hepatic extraction ratio >~.7 then an
alteration in hepatic blood flow will be the main determinant of
. clearance. This is termed Rerfusion-deQendent elimination. If the
~ hepatic extraction ratio is small (<0.3)~ then an increase in blood
flow will have minim~ff~g,Jhe_Q1ain determinant of hepatic
clearance being en zyme activity !t1is is termed 'c?pacity- -
1
dependent elimination ._Renal aearance is by botfi filtration and
secretion. If a drug Is unionised then it is able to pass freely into
the renal tubules and therefore its renal clearance is reduced. This
explains why altering thepH of t!rine, and therefore the
percentage of unlonlsed drug free to be absorbed, alter the
a
clearance of drug, eg aspirin and alkaline urine.
Refererce: Modes of drug elimination and pharmacok inetic
analysis. Anaesthesia and Intensive Care Medicine 2005; 6:
277-82.

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 Pharmacology MCQs

1.115 Pharmacokinetle, of inhaled anaesthetics. Thie foUownirng will

increase the alveolar partial pressure ( PA):
~D A High alveolar ventilation
,., 0 B A large functional reserve capacity
\10 1_
/' (ffiC) c~{ '"'~ ~..,"' -t ~'(-L
f, 0 C A high cardiac output

~D D A I~ blood : .gas partition coefficlenr

-,
'D E A high oil: gas partition coefficient &<::)
'

1.116 Context-sensitive half-time: ..

-
~D A Describes the time necessary for the plasma drug · •
I I
1e . · concentration to halve after the-cessation of a continuous
infusion designed to maintain a constant plasma concerurauon
<
D B Bears a constant relationship to the drug elimination half-time
1

-~O C ls~if the conductance ratio is~ · .

)
v·o D Of propofol after 2 hours is of the order of 20 minutes

.,
1
/0 E Of remifentanil is relatively constant /
Cl I
 Ii

1
Pharmacology MCQs / .) .- • , __ )

I I -\ (
K. :· \ ,,_ J, ~... .. . ,. .... i,,.~" .._ ·1 •••

1.115 Answers:
A True
•
•e B False
C False
e D True
• E False
A high inspired concentration leads to a rapid rise in PA, as does
an increase- in alveolar ¥:~tjl~tion. A large FRC will in effect dilute
the inhaled anaesthe~ic agen~ and. lead to a lo_wer PA. A high
cardiac output maintains a constant gradient for diffusion of the
anaesthetic agent and therefore the PA rises more _slo~ly. A high
blood : gas partition coefficient means that the agent has a high --
solubility and therefore diffuses easily, so reducing PA. Th~1oil: gas;
partition. coefficient affects the ~tency and th~efore the ·· =--
minimum alveolar .concentration (MAC) of tile agent.

1.116 Answers:
e A True CID

e B False
• C True
• D True
E True
fl
The context-sensitive half-time of a drug may differ ma~ly from
the elimination half-life. The elimination half-life does n.gt take
into account the ebarma~o-~etics of a multi-compartm£'ntal
m~I. The\c9~ucta(lce ra_tinJ!escribes the effect of_e~natioti·
and distribufiorfon the reduction of drugJrom the c~ntral
c~~' ie @!!~a. A high c~nductance ratio signifies that a
large amount of drug returns from the peripheral compartments
into the plasma- after cessatio_n· of drug, A low conductance ratio
signifies that the redistribution of drug from the peripheral
compartments into plasma is_ slow and so the drug is rapidly
metabolised and. the plaS_ma IeYet is kept low/insignificant.
The context-sensitiv~ hai_!:!itne-Of remifentanil is relatively
constant at approximately -c~ s as it is r~id_!y metabolised
~:!'.,
by pl~nd tis~_µe estera~es.
• - __::a.
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1 Pharmacology MCQs · ' . . .7
?

1.117 The foliowil!llg drugs have a. volume of distribution greater than

41/kg:
..--
:._
0 A Thiopental /
I

D B Atracurium
,.
1~, D C Digoxin
D D Flecainide •
,j

11,te D E Midazolam I - L;

e 1.118 The following are correct statements regarding drug response:

D A Hyperreactivity describes an allergic response to a drug
,/·..,.D 8 Tolerance to a drug that develops acutely is known as
tachyphylaxis
D C Cellular tolerance is the most important factor in the
development of opioid tolerance .
\I
\I D D The combination of two volatile anaesthetic agents would
have a synergistic effect // -. ) )
OI'
,_J~.,--c ·
///0 E Desensitisation can occur secondary to a structural change in
receptor morphology

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{\ \ ~. (\ \ 0 L-<.___)

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 Pharmacology MCQs

1 ..
u .117 Answers:
(.!) A False
© B False
C, C True
e D True
9 E False
Volume of distribution of a drug is altered by plasm~nd tissµe.
protein binding, the distribution of the drug to the tissues (ie lipid
i') (\
solubility and molecular size) and their blood flow. Drugs that
\~\ ro\" ,)\ o ~ have a large volume of distribution, ie >4 I/kg, include proEQ.fQl
--.
\·I .
'''t.
,\
, '•'\ ' . .,..\,
\
,- \,___
fentan~I, fleg.inide and 9igoxin (secondary to its affinity to bind
to cardiac tissue). Thiopental has a Vd of 2.5 1/kg. Atracuriuni has
'\ .'
(
"-,,,\ \~·
,,,· .•
\ C.. ·~
a Vd of 0.1_ 5 I/kg. Midazolam has-a ½Jof r:s I/kg.
-'\ . -~ '( ,,.._,___,,

1.118 Answers:
• A False
• B True
• C True
• D False
• E True
Hyperreactivity is said to occur when unusually small doses of
drug produce the expected pharmacological effect. The
commonest cause of tachyphylaxis is secondary to depletion of
stores, a common example being the decreasing effect seen with
repetitive use of ~~ne as norepinephrine stores are depleted.
Neuronal adaptation or cellular tolerance is seen with opioids,
barfiitillates-and alcohol. This reflects a reduction in sensitivity of
receptors in the CNS because of either reduction in number or
S~!1siti.x_ity. A synergistic effect is seen when two drugs cause a .
greater pharmacological response than that expected by simple
addition of their individual responses. The effect of using two
volatile agents is additive,
- !:a .•.,

/ Desensitisation occurs over a long period because of either

,,,,, receptor loss or structura],change.
Reference: Hysteresis in drug response. Anaesthesia and Intensive
Care Medicine 2005; 6: 286-7.
I
I, .11
-
I.
 Pharmacology MCQs

1.119 The following drugs have active metabolites:

!
0 A Etomidate
:..,.-----/0 B Pancuronium

I
'/ D C Lithium
/0 D Ciprofloxacin
;\ 0 E Gentamicin
11~
ioid 1.120
The following are metabolised by plasma cholinesterases:
1fol, l~D A Suxamethonium
v' D 8 Mivacurium
X D C Cisatracurium
I- 0 D Esmolol
/o E · Remifentanil

of
'1
I Jf
ith
_ed.
ds,
of
ur

~ensive
 Pharmacology MCQs
,t]-r \.\_, - - ---
1.119 Answell'§:
e A False
B • True
C <I False
D • True
• E False
Of the im.@Y_~n~u~i!'du~t_!?n ~gentsr ketamine and thiopental
,., { , ,.. \. _J have_acth,~_!:fletabolites. Propofol and etomidate do not Of the
~,-\-,.,\'A,:~ muscle relax~nts\ pancuronium and vecuronium have active
. ,\ metabolites whereas atracuriurn (metabolite being laudanosine),
· ~ '-
0
°?2·"·,j O ,,\_Q_ cisatracurium, mivacurium and rocuronium (predominantly
·(C\'.-\<= \_,,,., excreted unchanged) do not have active metabolites.
-~ r_,~~ c' \'v-· C_i.e_rofloxaci_!' metabolites are active. A large range of antibiotics,
=---._,.~ f\ . ._;,,· ,; l c:< c-•. c.-- including the aminoglycosides, is excreted unchanged and
\ ,::;. therefore they have no metabolites. Lithium is excreted
unchanged by the kidneys.

1.120 "Answers:
• A True
• B True
• C False
• D false
• E True
Cisatracurium, unlike atracurium, is~irectly metabolised by
pla~a est~r,ases. It undergoes Hofmann degradation. Its
metabolites are then hydrolysed by non-specific plasma esterases.
Esmolol is metabolised by red
~
cell esterases. Remifentanil is
metabolised by non-~,eecific plasma ana tissue cbo~i~~~ase.

j
 Pharmacology MCQs

.121 Tachyphylaxis occurs with the foUowill'

'
ilg drll.llg§:
'" n
--
~ c.,..,-,...
vD A Ephedrine -X ~ 0 ~v..?5 ~~"
)(0 B Morphine
~/ D C Sodium nitroprusside
/o D Trimetaphan
'I- 0 E Esmolol

1.122 The following drugs preferentially act at «radrenoreceptors:

~o A Clonidine ""''.J~.,."'·}~-s\ - -
v·o B Yohimbine vv-A ts

\ 0 C Phenoxybenzamine----
·I' 0 D Metarami no! /
·/ 0 E Prazosin ,/.

s.

!
,.
 Pharmacology MCQs
'

t__\~ \ ~"\_ '--- ·, '-- --'"-

1.121 · Answers:

f3 A True
~ ,.., Y\~\ -~ v·r \.'-~~~
@ B False
\y \ '·" ~ "~ ~Q.._ y
• C True
@ D True
~ E False
Tachyphylaxis is the rapid reduction of effect after short-term
administration of a drug. It is commonly secondary to depletion of
neurotransmitters, eg norepinephrine in the case of ephedrine.

1.122 Answers:

• A True
• B True
• C Fal·se
• D False
• E False
Clonidine is a partial agonist at the a2-receptor (a2 : a1 = 200 : 1 ),
• causing analgesia, sedation and hypotension. Prazosin is a highly
selective postsynaptic a1 -blocker, causing hypntension and
bladder sphincter relaxation. Phenoxybenzamine is a long-acting
non-selective a-blocker with a higher affinity for the a1- th,P1 the
a2-receptor. Metaraminol is a synthetic amine that is an a1 -
agonist with some (3-adrenoceptor activity, Yohirnbine is a
selective a2-blocker that was used in the treatment of impotence.

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 Pharmacology MCQs
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'
,-., ~.,-~. ~ ,,·~ .• •. -- t

... ,...
__ ,.,. 'i7C-'\."-~
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1.'123 Clonidine: -==:-===> ';. . ;. ~

- _., s ,-::.i
0 A Reduces MAC
-f- D B When administered with opioids, it potentiates thelr:
respiratory depressant effect
,v · D C Can be administered to stop shivering
'/ D D Causes a more profound reduction in diastolic compared with
systolic blood pressure
of ,- ./0 E Has an oral bioavailability of nearly 100%

1.124 Regarding prazosin:

Y D A It is a postsynaptic a2-antagonist t~

~/0 B It is used to relieve vasospasm in the Raynaud phenomenon } )

/DC It should be stopped when screening urine for van.ll~yl- _-:, ' I' .
mandelic
- acid
•::.._..,-- .
--
X D D It causes an increase
.//
in renin release
/tJ E It can exaggerate the hypotension seen during epidural
1 ), anaesthesia
siily

..
~·; .- :. :.-:. ·• '; . :,,. ~ · ... .,
• I
...
' ~

'';. f '\
"J. :J. ,:: • ~.. :I

:,,1 .\.:~·.

149
 iI ,
it
Pharmacology MCQs
/ ~.,

1.123 Answers:
8 A True
9 B False
• CD True
False
e
~ E True
Clonidine is a centrally acting partial ai-agonist. Acting centrally
it causes a reduction in sympathetic outflow. MAC appears to be
reduced by up to 50%. Clonidine does oo_!)caus~ or potentiate the
respiratory depressiOrl seen with oeioidS:-lt is used to stOf'
shivering at doses of _75 !lB· 1his may be due to its ability to inhibit
central therm~gy_latory control. ~~iovascular effect is more
profound o(s_yst<]!ic h,.ther than c\i~tolk\,Pressures. It has the
desirable effect of decreasing systemic blood pressure without
paralysis of compensatory homoeostatic mechanisms. It has
excellent oral bioavailability, reaching its maximum plasma level
within 90 minutes. It is minimally protein bound (20%) and has a
volum~_gisJrlbution of 2 I/kg. !a I

l 1
1.124 Answers:
• A ·False
~ B True
@ C True
• D False
_ • E True ,-- .
,c / p razosm. .1s a se l ective
. I postsynapticI . a,-a d renerg1creceptor
.
-. ----------1 --- . ~
antagonist. It causes vasodilatation of 00th art"eri"es and Veins, but
has greater affinity for venous a-receptors. This causes it to have
~-
. \--.).
C
postural hypotensive effects si milar to GTN. It does~t cause
·,-t.. reflex tachycardia or release of renin. This is because a2-receptors
I~-
'~"
, .'
II I _.
. ,.' '
-1 ,,,
), ,· are unaffected and they inhibit the release of renin. Due to the a,·
blockade caused by prazosin, the usual compensatory
I /
vasoconstriction mechanism is lost. Therefore, hypotension with
~o
I •

,. · - epidurals may be exaggerated, as the vessels not affected by the

\ ~ I ; I
epidural are unable to vasoconstrict. Prazosin must be stopped
before screening for urinary catechotami~e metabolites, as it can
yield a f~ls~~pq~si!iye r'2ult.
1/
 J

I· Pharmacology MCQs

1 ,'1 25 Activated charcoal:

, /0 A Is most effective if used within the first hour of ingestion
'/,I D B Has its principal mode' of action, in the lower gastrointestinal
, I

tract
'// D C Before use is activated using oxidising gas
0 D Is effective in chelating lithium ~
0 E Should be used as first-line treatment of early methanol
poisoning

as a

but
,_ive

151
 Pharmacology MCQs

I g,
10125 Answers:

• A True
• B False
• C True
e D False
9 E False
Activated charcoal is a f~e, black, od~ss and tafil®S pow~er
made from wood or other materials that have been exposed to
very high temperatures, in .an airless environment. It is then
activated to increase its ability to adsQ!b various substances, by
reheating with oxidising
~
gas or other chemicals,
- .
so breaking it
into c:,. very fine powder. Activated charcoal is pure carbon
specially processed to make it highly adsorbe,!}1 of particles and
gases. It is most effective when given within the_jirs,t hOYf;Of
ingestion and when Qnly small amounts have been ingested. Its
principal site of action
.
·,(ga strfc)nd in the small intestfr1e:)Dosage
... - -
. - -------
\.

is 50-100 g/i hours or 25-g/2 hours. It is effective for chelating

~aroiturates and tricyclic antidepressants but is ineffectiv&, for
lithium, ethanol and methanol poisoning.
Reference: www.toxbase.org
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 Pharmacology MCQs

1.126 The following are correctly paired woth their ilPP!Opriate

chelating agent:
D A Dicobalt and lead poisoning
·f D B Ferrihaemate and iron poisoning
""/oC Activated charcoal and amitriptyline
. ~
v<O D Thiocyanate and cyani_de
wder l·//o E Dimercaprol and gold
t I
0

. by
t

=nd <

I. Its
""sage
.,
tmg

1~]
 Pharmacology MCQs
I 1
I
1.126 Answers:
© A False
e B False
e C True
It D False
@ E True
A chelating agent binds a toxic substance and prevents tissue
damage. Thioc~anate is formed in the liver and kidneys, when a
~~ ---
cyanide ion combines with a sulphydryl group. Sodium
thiosulphate provides more sulphydryl groups to facilitate the
. conversion of tyanide ions to thiocyanate.\ferriha~ma1_e)s a
nephrotoxic breakdown product of m·yoglobin in acidic
conditions.

Chelating agent Chelates

Iron, aluminium - ----- .1
\ Desferrioxamine
Arsenic, bism_uth;, mE::_cury, gold \
'L. Dimercaprol •'
L~ad, c0_Pper~ radioactive '!'etals ,
~ Sodium calcium edetate
.~r, leadJgold, mercuri,zinc
L\ Penicillamine Cyanide ~-
5 Dicobalt,
 '

Pharmacology MCQs

1.127 The following is true regarding the vitamin K-dependent clotting

/
factors:
'.,,./ D A The half-life of factor II is by far the longest
'/" D B These factors include factor XI
·'// D C Oestrogen increases their production.
I

·~/'tJ D Carbamazepine reduces the effect of warfarin on them

i/,,. D E After receiving warfarin factor VII is the first to become
depleted

1.128 The following may increase the effect of warfarin:

Vo A Amiodarone
\//D B o-Thyroxine
l -· /D C Acute illness
[_./o D Broad-spectrum antibiotics
,_/ D E Cholestyramine

\a

1 r: r:
 Pharmacology MCQs

1.127 Answers:
0 A True
e B false
e C True
© D True
@ E True
Factors II, VII, IX and X are the vitamin K-dependent clotting
. factors. Their half-lives are 60 hours, ~ hours, ~ hours and 40
hours respectively. Therefore, following warfarin treatment factor
Vil, with the shortest half-life, is depleted first. Oestrogens
Increase their production. Carbamazepine redu2'es-tne effect of
warfarin and therefore reduces the oepletion of vitamin K-
dependent clotting factors.
Reference: Anticoagulants and the perioperative period.
Continuing Education in Anaesthesia, Critical Care and Pain
2006; 6(4): 156-9.

Cl:
1.128 Answers:
A True / \-\ vv,; ,.:::, ~ C.V\..... r V'I~

B True / 1--=:, - :t.. · , ,_?(Y -~ -

C True / /\ (· :L;i~ ·J.;_.,,,-~, (

D True ./ ·,. r.' r;_ .- [ , ~- - \ • I
-~·. ? . \
E True / ,,-..r, oG.-si,:-, r-.. - --· _t>

The effects of warfarin can be potentiafed by displacing warfarin

from its protein binding or by decreasing vitamin K absorption.
Arniodarone displaces warfarin from its binding sites and
therefore increases the free fraction and therefore
- effect.. o-
Thyroxine increases the potency-of warfarin by increasing hepatic
receptor sites, as does quinidine. Acute illness reduces vitamin K
absorption. Broad-spectrum antii_)iotics reduce the level of gut
bacteria requTr ecf forvitamin K absorption. Cholestyramlne
decreases vitamin K absorption. ·
Reference: Anticoagulants and the perioperative period.
Continuing Education in Anaesthesia, Critical Care and Pain
2006; 6(4): 156-9.
 Pharmacology MCQs

10129 Drr1U1g effect on platelets:

/o A Aspirin inhibits prostaglandin production

I /" D B Selective cyclo-oxygenase (COX)-2 antagonists cause

l significant platelet dysfunction
/o C Dipyrldarnole inhibits platelet metabolism of adenosine.
>/lo D C!opidogrel blocks the ADP-induced platelet activation
pathway
,/o E Platelet glycoprotein llb/llla antagonists also reduce thrombin
concentration

tic
K
,t

157
 Pharmacology MCQs

1.1129 Answers:
• A True
c B False
• C True
• D True
• E True
Aspirin inhibits both prostaglandin and thromboxane production.
_Selective COX-2 antagonists do not cause significant platelet
dysfunction. Dipyridamole may have a number of mechanisms of
action, including the one in option C. It may also have its effects
via prostacy~~Ji.n. It potentia~ ~_f!:e~t bY. be~~g a = _,.
phosf?~O-~iest~rase inhibitor and also by dir~ctly gj_mulat_Lng the
release_ of prosta£Y-~lin by the endothelium. ·
Reference: Anticoagulants and the perioperative period.
Continuing Education in Anaesthesia, Critical Care and Pain
2006; 6(4): 156-9.
I
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; r,~ri/v--~. . I
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 CLINICAL MCQs

!
. 1.130 Basic calculations in childrem the following are appropriate
doses for children during resuscitation:
l
I/ D A Amiodarone S_µglkg· ··· '-_7: / J< ~
I

'.·//Do B 5 ml/kg _10% dextrose for a l1yQoglycaemic child

·- - l?f ,,f~d-~ojersion of ventricular
- -
C 2 J/k~Joy,J~itial fibrillation
D 0.1 J))g/k~epinephrine for resuscitation of asystole
E 20 ml/kg fluid bolus for hypovolaemia

1.131 The following are true of calculations for children:

·/ D A The Broselow tape relates height to weight
,"· 0 B The estimated weight of a term newborn i~2--kg
.,,,_...,
·:; .- ;
0 C The estimated systolic blood pressure of a child can be derived
from the following-equation ~J
+ (age in years X ffgc ~/-2,
+~
D D The appropriate size cannula for a cricoJhyro!~~to~ in an
infant would be-18 g~uge --· ----
0 E Approximate weight of a child aged_]? 1 Qy~ars can be
calculate by the equation (age-in years+'!) x2

161
 1 .. 130 Answen~
@ A False
• B True
• C False
• D False
e E True
The following doses are correct for rie_~n-Of-a--c-hild:
~ epinephrine 0.1 ml/kg of 1:10 000, which is equivalent to
~
• amiodarone Sdm~kg
• 5 ml/kg 1 0% extrose
• fluid bolus of 20 ml/kg for resuscitation of hypovolaemia
• 4 __J/kg
, -
for DC shock.
--=---
·
Reference: Advance Paediatric Life Support Course Manual.
Fourth edition. (Updated January 2006)

1.131 Answers:
e A True
• B False,
• C False
• D True
• E True
The Broselow tape was designed to estimate body weight, drug
dosage and endotracheal tube size in paediatric emergencies,
based on patient height. A study performed in 2002 (British
Journal of Anaesthesia 2002; 88: 283-5) showed that it provided
accurate estimation of body weight based on measured}?ody _
LeQ&!h but it slightly un-d~~~mfl!gd,bo~....w.ejght in all cases. In
iI, smaller children, <20 kg, this underestimate was negligible but
i was more pronounced in children >29 kg. Tracheal tube size met
clinical needs better than age-based estimates.
The estimated weight of a newborn is 3 .5 kg at term. Systolic
blood pressure can be calculated using 80 + (age X 2). The
cannula sizes recommended by APLS-{Advanced Paediatric Life-.
Support) for cricothyroidotomy are 'l8 ·1,t}
gau~)n an infant and
gauge for a child. -----
Reference: Advance Paediatric l.ife Support course manual - The
practical approach. Fourth edition (Updated January 2006); British
Journal of Anaesthesia 2002; 88(2): 283-5.
 Clinical MCQs

1.132 When diagrmsang malignant hyperthermia (MH):

I/ D A A negative family history precludes the diagnosis
I ·:>' D
B Having identified a MH patient, the family members can be
l reassured that they are not MH susceptible if they have a
-orrnal DNA test
·{ D C A rise in postoperative temperature with no preceding
tachycardia or increased CO2 production could be MH
''{_ D D
It can occur after cessation of the trigger \

D E All patients with central core disease should be suspected of

being potential MH sufferers

(! f'" ' {\.-,,.

. Q <"· Q

met
 Clinical MCQs

l
1. 132 Amiswers~
e A False
@ B False
@ C False
® D False
8 E True
The inheritance of MH was initially thought to be in an autosomal
dominant fashion. This is now known not to be the case. There
i
are to date 15 clinically relevant gene mutations for the ryanodine
receptor protein (RYR)1. There are also several other genetic loci
not associated with RYR1 that have been linked with MH in some
families. In other families, no genetic abnormality has been found.
Once an abnormal gene has been identified in one family
member, other family members can be DNA tested. _If the
abnormal gene isfound they are k_np~ to be MH patients.
However, a normal DNA test does 'Q9iexclude MH susceptibility
(ie false-negative result) and therefore the family member should
go on to have m__µs.,_cler biopsy and contr_acture testing.
The exclusion of MH based on intra.operative events is dependent
of the calibre of the perioperative records. A late rise in
temperature without preceding tachycardi~ and increased CO2
production is not MH. MH cannot commence once the trigger
has been removed. Central cor,e_clise~se'is an inherited disorder
causing peripl!~ ~~ness that i! iis5()!=ia!ed with ~--
Reference: Malignant hyperthermia. British Journa_l (?f Anaesthesia
. .

CEPD Reviews 2003; 3(1 ): 5-9.

,,
I'
i

: .I
 Clinical MCQs

1.133 lRegairding malignant hyperpyrexia:

' D A Vigorous cooling is always beneficial
\
,, D B Dantrolene must be mixed in dextrose :. ~
//o C Myoglobinuria occurs before a rise in creatine kinase (CK)
, /o D Low concentrations of volatile anaesthesia may give rise to a 's;'.

/. more insidious onset

-
---=- \f.V
a1 // D E An alkaline diuresis may reduce post MH renal failure

nd.

,.\. •: ~ I :,, ' :- ~

~! ••,

Id '~ ,. \ .• j. •••

. ·- ·1.:··-:

ent

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 I

Clinice! MCQs
l
i
l·
I

1. 133 Answers:
e A False
@ B False
• C True
@ D True
0 E True
MH is a condition of uncontrolled muscular contraction owing to
/- a defect in intracellular calcium homoeostasis. This leads to
. persistent muscle contraction with its accompanying metabolic
sequelae, including tachycardia, increased
~ CO2 production,
..

acidosis, hyperthermia and rhabdomyolysis.

=--
/ Dantrolene prevents calcium release from the sarcoplasmic
reticulum, so reducing the reaction. It is presented as a powder
with mannitol and sodium hydroxide. It is reconstituted in 60 ml
water per 20 mg vial. . '}I
Myoglobinuria is apparent before CK increases, the peak CK rise
being approximately 24 hours after the insult. One causative
agent of renal failure in rhabdomyolysis is ferrihaemate, a
i;
nephrotoxic breakdown product 'acidic conditions.
Alkalinisation of urine promotes its excretion.
/,,. Vigorous cooling can lead to severe peripher~I vasoconstriqtion
that can actually ca~se a ri~ in c~re temee1ature.
Reference: Malignant hyperthermia: British Journal of Anaesthesia
CEPD Reviews 2003; 3(1 ): 5-9.

!
'.

166
 Clinical MCQs

1.134 Pre-ec lam psi a:

:'/ D A Occurs in the first trimester - _,_. c,;- ·,,.:.:::, v
!~o B Is diagnosed as severe if the patient presents with pulmonary
j oedema
,/0 C Is associated with uric acid concentrations of >360 µmol/1
;<' 0D Is associated with a---·
decrease in thromboxane production
~~
I
'/ D E Associated with HELLP syndrome occurs post partum in _ .50°1' -
I
.)

of cases

.,
 Clinical MCQs r

1.
1.134 An§wers:
~ A False
• BC True
True
•
• D False
False
• EPre-eclampsia can be diagnosed in pregnancy after 20 weeks. It
c\assical\y presents as a triad of hypertension, proteinuria and
oedema. It is defined as mild, moderate or severe. Severe pre-
edampsia is defined as any one of the following: severe
hypertension
~ (SBP > 160 mmHg, DBP > .110 mmHg); proteinuria
--- -
> 5 g/24 h; oliguria < 400 ml/24 h; cerebral irritation; epig~c
or right upperquadrant
- pain; pulmon_
_. .E-Y
-- oedema.
-·

lhe precise aetiology of pre-eclampsia is unknown. Placental

insufficiency causing ischaemia results in the release of
~; " Vasoactive substances that cause a multi-system diSOrder.
·~ '~ Thromboxane production.increases and prostacyclin
concentration decreases, Which cause platelet dysfunction and
vasoconstriction. HELLP syndrome - haemolysis, elevated liver
- enzym and low platelets 7ocwrs with severe pre-eclampsia in
up tr :5.Qo/o f cases. Aroun~/of \ cases occur post partum.
-
Reference:·- Diagnosis and management of pre-eclampsia. British
Journal of Anaesthesia CEPD Reviews 2003; 2(2): 38-42.

\ ~ f(
! i

'-1 C
~- '- 7l,\ iv;~0f\
 Clinical MCQs ·

1.135 Whe1n1 managing severe pre-eclampsia:

I·/ 0 A CV~monitoring is valuable as it gives a good correlation with
i / Jeff atrial pressure ~ 7-__
I
j_. D B Before loading with magnesium, fluid is required for volume
I expansion
I~ D C A mean BP of less than 80 mmHg is ideal \C\¥) - 1~,:)

ll \ t< 0 D The severity of hypertension correlates well with the incidence

of progression to eclampsia
}, D E Magnesium dose is calculated according to serum
concentration
1a
J
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 Clinical MCQs

1.135 Answers:
0 A False
@) B True
~ C False
'II D False
0 E False
Central venous pressure (CVP) monitoring can be used to gauge
fluid requirement; however, it is known to be a poor correlator
with left atrial pressure, particularly in severe pre-eciampsia.
The vasodilatory effect of magnesium is counteracted by cautious
fluid administration. This is particularly important antenatally to
maintain adequate placental perfusion. A profound reduction in
blood pressure should be avoidecl as this compromises placental
circulation. Aim for mean blood pressure of 100-140 mm Hg.
Hypertension severity correlates poQ[ly with development of
eclampsia. MaP-~~?]um levels are .Q_qt ~outinefr titrate~ ~erum
values.. Respiratory rate, tet:1c:lon reflexes and urine output are
closely moffitorea. tv\agnesium IS renally excreted. IfThe patient is
a~c, magnesium therapy is re9u_ced and levels may be useful.
R~ence: Diagnosis and managen rent of pre-eclampsia. British
Journal of Aneestuesie CEPD Reviews 2003; 7(2): 38-42.

170
 Clinical MCQs

1. 136 Regarding HIV infeciaon a~d treatment:

A Zidovudine inhibits the synihesis of ONA by reverse
~
i
transcrlptase
l(o B Non-nucleoside reverse transcriptase inhibitors bind to reverse
transcrlptase and inhibit enzyme activity
D C Protease inhibitors decrease the effect of opiates J. /L
~
I
D D The average risk of transmission of HIV following rnuco-
cutaneous contact is 10 times less than following needle-stick
injury
1s \ J/D E Myocarditis is common in HIV sufferers

n
-,I

IS
.,
JI.

171
 Clinical· MCQs

}'·
1.136 Answers:
A True
. .
B True .,_; .,·· .
,•:-

• C False
D .True
• E True
Treatment for HIV is· broadly split into three groups.'..-~oside
analo ue ~~-~~~i tase inhibitor (NRTls)~ eg zidovudine,
act as a fa se nuc eotide so preventing the production of DNA
from viral RNA. Non-nucleoside reverse transcriptase inhibitors
(NNRTls) bind to reverse transcriptase preventing enzyme activity.
· Protease inhibito~ (Pis) prevent production of active viral
proteins. HAART or h.igh!Y. active anti retro iral therapy consists of
two NRTls and either a Pl or an NNRTI. Pis inhibit the metabolism
- ,_.'! -

of opioids and b~nzru;!iazepines. -- /--------,

The average risk of transmission after a needle stick inju if0.3%''
4
~ compared with mucocutaneous contacc w en it is· 0.03%. L
'llp to 50% of HIV sufferers will have an abnormal~'
Myocarditis i~ common secondary to drugs, lymphoma,
opportunistic infection or the disease .tself.
Reference: Anaesthesia and critical care for patients with HIV
infection. Continuing Education in Anaesthesia, Critics I Cere and
Pain 2005; 5(5): 153-6.

. .,; I) U J.z. .e~·, __ ,_9' . ,.

I' (

\\0 {\ (\'\I ,) V '••"? :~ _., \. v).. ~

-~
V) 1.f't.: L ~) (' /
\\L . \,,,_
" __,. .f\ ~
. .. ·'r\ \~~

172
 Clinical MCQs

Anaesthesia for non-obstetric surgery durlng pregnancy: \ r

, D A Teratogenicity risk to the fetus is greatest during the first 14~

days of gestation
D B Non-steroidal anti-inflammatory drugs are safe to use for pain
relief
C Ideally, surgery should be performed before commencement of
the second trimester
D Antacid prophylaxis is recommended from the beginning of
the second trimester
E MAC (minimum alveolar concentration} is increased in
pregnancy

After intra-aflerial injectien et llliDI tidal, dte feltowing may lte

8'henefit:
A Intra-arterial ·papaverine
B Intravenous guanethidine
C Stellate gangli~n block
D Brachial plexus block
E Intra-arterial procaine

i
•

173
-
 Ciinicai l/iCQs

1~~t3~Y A.0sv11,ers~
t)
. -i-atse
/1....
'

(, B False
0 C False
0 D True ,_J .·r
'2.. vi-- v (:·.-.11
0 E False
Teratogenicity is greatest between days 15 and 56 _ of gestation. If
possible surgery is postponed until the. se_CQf1.f1 trimester to reduce
the risk of teretogenicity and _miscarriage. 1·--lon-steroidal anti-
inflammatory drugs are contrain-dicated in pregnancy secondary
to the risk of closure of the fetai ·ductus arteriosus. MAC decreases
in pregnancy from as early as ~ weeks' gestation. Also, remember-
I
the risk of uterine atony with voGitil~ anaesthesia.
'
Reference: Anaesthesia for non-obstetrical surgery during
pregnancy. Continuing Education in Aneesthesi«, Critical Care
and Pain 2006; 6(2): 83-85.

1.138 Answers:
~ A True
~ B True
Q C True
© D True
® E True
intra- arteria I injection of thiopental causes intense pain. The
thiopental crystallises in arter ioles and capillaries and there is
local release of norepinephrine causing vasospasrn. Treatment is
aimed at pain reduction and counteracting the vasospasrn.
After intra-arterial injection, the cannula should be left in situ;
5 ml 0.5%, r.rocaine (local anaesthetic for analgesia) and
40 mg pa,.e.averine _(vasodilator) should be injected. Other
treatment options include svmpathetic blockade either with a
stellate ganglion or brachia! plexus block or with intravenou_s
gu::rnethidine.· .

174
 Clinical MCQs

·1.139 The fellowing is true of the Va1Uighari-Williams classification qJJf

antomarrhythmic drugs:
.. _,,.D A lbutilide is a class Ill anti-arrhythmic -
~ /
l,/D B All ~-blockers are class II ·anti-arrhythmics
' ,,

v-fJ ·c
I
Calcium channel blockers are class. IV
-~..
~D D Class Ill drugs shorten repolarisation l-:;, r·
- . -
. ...., ,, -
I ,,
~ -· ·\.•
,, . .,__, .
~D E Class IC drugs prolong repolarisation
(

) ~
-=-

ises
er

GI!

•
 Clinical MCQs

10139 Airnswens: : ,_
' ,_

® A True
v B False
@ C True
@ D False
e IE false

Class IA Prolong repolarisation Quinidine, procainamide,

-----·-- .---- ------~s~eY!ami~e
Class IB Shorten repolarisation Lidocaine, mexiletine,
------- Jili~!D1Qi!:}, tocainide
Class IC Little effect on repolarisation Encainide, iTecainide,
propafenone _
Propranolol!--~molol,
Class II (3-Adrenergic blockade acebutolol i-sotalol
-· -
~one---,-1.-e...r--i ium, o- or
·-

Class ill Prolonged reQ_olarisation 1.¥1~ ibutilide, dofetilide

(potassium channel
blockade; other) _ -
Verapamil, diltiazem, bepridil
Class IV Calcium channel blockade

• The (3-blocker sotalol is in both classes II and Ill.

• lbutilide and dofetilide are examples of class Ill drugs that are
recommended for first-line therapy in patients with atrial
fibrillation (AF) of <7 days' duration, as are flecainide and
propafenone.
Reference: ACOAHNESC Guidelines for the management of
patients with atrial fibrillation: executive summary. Circulation '-I
2001; 104: 2118-50.

176
 Clinical MCQs ·

.1.140 Amiodarone in AF: I•

I
.I D_.,,,• A Provides swift rate control secondary to its class 1_11 effect
1\- ·TI B Has a toxicity that is predominantly dose dependent
K
I
DC Can be changed for flecainide as a reasonable alternative in
patients with ischaemic heart disease
i
, x o D Is currently recommended as first choice for pharmacological
cardioversion of less than 7 days' duration lb,A.tY, J :;
..._. J_... D E Can offer additional benefit when given intravenously to
' '
~~ -
1
!; ) ,,_ :) / 0 0
patients who are fully loaded with oral amiodarone therapy J

f\
02.
r
I
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yv\ ,·~) c:a,

-\
-_/

1n'dil . I

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,f
'ition

1 -,-,
 Clinical MCQs

1.140 Answers:
@ A False
,, B True
• C False
• D False
E True
The ~~ft rate control of amiodarone in AF is secondary to its~-
blockade and calcium channel-blocking effect. Its anti-arrhythmic
effects start 8-24 hours later.
# Current guidelines (_ACC/A~NE~C ~ui_deli_nes for the.
· management of patients with atrial f1bnllat1on: executive
summary. Circulation 2001; 104: 2118-50) recommend the use
. .,-~t: of propafenone, flecainide, ibutilide and dofetilide as first-line
-- therapy for AF of less than 7 days' duration.
,,..::( Both intravenous and oral arniodarone may have different
,, _electrophysiological properties and so intravenous preparations
may offer additional benefit to patients already on loaded oral
therapy. -- •'
Reference: Atrial fibrillation. Continuing Education in
Anaesthesia, Critical Care and Pain 6(6): 219-24.

\ .

178
. _ .•
 Clinical MCQs

1,141 Regarding elective DC cardioversion in AF:

D A Success is increased with anteri9~-posterio_L[>.Qs.itioning of
paddles compared with art~i-or-J_aJeraJ posltioning
l XD B Following cardioversion, a rise in cardiac troponins signifies
cardiac damage
C When using a monophasic defibrillator, the initial energy
selected is l.QQ_J--:--- - ---
?_..;;:-·~
' .

-·o
I\
D It should be preceded by anticoagulation if the patient has
been in AF for over _-;:---
2_4 hours LJ.~Z 1r. .--·
;\ 0 E It is contraindicated in patients wit~ ~~rnal defibrillators
iJ'"------.

,
'\. ,,
I .•
':.:
·. ~ "J_; '} ~ (~
:. '.
')- \ ,.
'
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 Clinical MCQs

1.141 All1lswers:

• A True
• B false
• C True
D False
• E false
~ When using monophasic defibrillators, an initial energy of
· 200 J is recommended. With further direct currents set at 200, 300
then 360 J. --
A following cardioversion, a transient ris Jn ST segments and
7
// cardiac troponins can occur even with~ardiac damage.
Anticoagulation should be achieved if the patient has been in AF
for longer than 48 hours and should be continued for 3-4 weeks
following successful cardioversion. Chronic AF is associated with
a 3-7% annual risk of CVA (cerebrovascular accident). DC
cardioversion of AF is not contraindicated by internal
defibrillators or pacemakers; however, they should be
interrogated before arid after cardioversion. The paddle position Ts
placed as far. from the device as possible, preferably anterior-
posterior. -- - --
Reference: Atrial fibrillation. Continuing education in anaesthesia,
critical care and pain. British Journal of Anaesthesia 6(6): 219-24.

180
 , •• ~ I Clinical MCQs

With regard to preoperative fasting:

A Gastric emptying of liquid is an exponential process
' ,,/0 B 95% of ingested clear fluid is emptied from the stomach within
.\...,,..
1 hour

,~
I!
I
. I

0 C Obesity delays gastric emptying

D D Residual gastric volumes are smaller with prolonged fasting
D E Regurgitation is common in the first 6 months of lif~\7

AF
•••••
s
iVith

Ts CII I

1esia,
24.
 r
I•

Clinical MCQs
f .
I..
(7
1 !
1.142 Answers: l
.e A True , ..•
B True L!
C Fa\se
• D Fa\se
CD
E True
• Obesity does not P~lay gastric emptying. It does, however,
increase the ifSk of hiatus hernia and other associated
pathologies. Studies ShOw that longer starvation periods cause an
increase in residual gastric voium~ when compared with shorter

times.--
In the first 6 months of life, the intragastric
.
pressure is high as the
stomach is small and compressed by other intra-abdominal

org·ans.
The accepted guide\ines for starvation:
• 2 hours water and clear fluids 1

., •
•
4 hours
6 hours
breast milk •,
drinks with milk, food and sweets. h
See Royal College of Nursing, Recommendations for Preoperative I
Fasting 2005.
Reference: Pre-operative fasting. Continuing Education in
Anaesthesia, Critical Care and Pain 2 006; 6(6): 215- 18.
r
'~

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 Clinical /\:cqs

1.143 Regarding blood and blood transfusion:

D A A massive blood transfusion is defined as more than 6 units of
blood within 8 hours
_/ D B Fresh frozen plasma (FFP) and platelet additive solutions
contain significant amounts of citrate compared with red blood
cell (RBC) concentrates
D C Hyperkalaemia is common in massive transfusion
'VD D Naturally occurring anti-A antibody in B blood groups is of
.n I lgM class 1- ~ )
ter I
i --I D E Antibodies resulting from transplacental passage are of lgM
i
I class ·
I
u1€

••
anv

183
 Clinical MCQs

1.143 Answers:

• A false
• B True
C False
• D True
•
• E False
Massive transfusion is defined as the replacement of a patient's
total blood volume in less th~n 24 hours. Hyperkalaem1a after a
massive transfusion is uncommon unless the patient is acidotic
and hypothermic. This is because the RBC membrane's NA+ /K+
pumping mechanism is quickly re-established, which clearslhe
potassium load of the transfused blood. fueocalcaem"§]can
'i occur because of the chelating effect of citrate, which is in higher
concentrations i_!l_ff P and platelets. Transplacentally acquired
antibodies are ~
lgG .....1
Reference: Complications of blood transfusion. Continuing
Education in Anaesthesia, Critical Care and Pain 2006; 6(6):
225-9. Cll1
 Clinical MCQs

1.1144 TRAU (ill"aJ.f/lldllJJSHOlrlHl"elatedl acute

nnjury):
D A -- ~ -
Occurs within 6 hours of a blood transfusion
h.JJ!lilg

.
. D B Is antibody mediated in approximately 90-% of c;~~~s ~ ·: . ~ ,. \ ~ :. :, l

::> -
)'l

,/o /
.
C Is caused by activation of neutrophil granulocyte_cells_ i
~ '."1·' .

~-/0/ D In non-antibody-mediated cases, has a lower mortality

a
~-_/"[] E Is more commonly caused by FFP than RBC products
--, -
+

Cl I
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, 1;,
 Clinical MCQs

11 144 Answers:
o

• A True
B False
• C True
• D True
•
• E True
TRALI causes acute respiratory distress within 6 hours of a blood
t@millsion. There are tl,\lo rn~chanisms: immune (or antibody
mediated in 60% of cases) and non-immune
--=:.==:- mediated. Immune
f!led~ed_IW!is caused by. leuk~te antibod~s in thidonOr
blood reacting with recipient human le~kocyte antigens and
human neutrophil alloantigens. ~.Of'l::i.InimJ_Qe_.mediated T~AU is
not caused by leukocytes but by reactive lipid products relea'sed
from donor blood cell membranes-; The common final pat~way is
the activation of ~~-~tr_ophi_l__S!~!'ulocyt~~ that migrate to the
I I lungs and become trapped. Free radicals and proteolytic enzymes
!
I
I are released causing a capillary leak and pulmonary oedema. FFri
and platelets contain more plasma and therefore
•r are more likely
to cause TR.ALI.
Reference: Complications of blood transfusion. Continuing
Education in Anaesthesia, Critical Care and Pain 2006; 6(6):
225-9.

f <2-"' ,ru -[>½, L

~-re~~4
Ctl\-:.,
 Clinical MCQs

1.145
Basic life support (BlS) Dii11 adults (wpdated guidelanes December
2005):
'. / 0
/"' A On confirmation of cardiac arrest, two effective breaths should
be administered
1.-- 0 B
Chest compression should be commenced at a rate of 100 per
minute
ood
dy \/ D C The chest compression to breath ratio is 30: 2
une l \ _ -0 D
Chest compression-only cardiopulmonary resuscitation ((;PR)
unor is effective for a limited period only . 1
/
D E Transmission of HIV during CPR has occurred
·\LI is
ased ;.·

way is
to the
""" azyrne
.,.,a.
I
FF
likely l
!
 Clinical MCQs

1.145 An§Weir5:
• A
B
false
True·
e

• C True
8 D True
(II E false
Current teaching now enforces immediate administration of chest
compressions before effective breath administration. This is to
reduce the pause. before comjressions. Chest compression-only
CPR has been highlighted asjfiere is a reluctan~e to perform
mouth-to-mouth ventilation. Chest compression-only CPR ls only
effective for approximately ~inutes. There have been no
documented cases of HIV transmission during CPR
I - --

administration,
Reference: Advanced Life Support. 5th edn. Resuscitation Council
(UK) April 2006.

••
 Clinical MCQs

1.146 Regarding cardiac arrest i_n adults:

D A It is the leading cause of death in European adults
~- D B Successful resuscitation is likely if the original ECG _is asystolic
C The delay from collapse to delivery of the first shoc:'k decreases
the chance of survival from ventricular fibrillation (VF) by 10% /~""''"
per minute
D BLS helps maintain a snockable rhythm for deterioration to X _{__
asystole
\/ o E Current guidelines for treatment of VF recommend the delivery
of a single shock, then returning to CPR

1.147 The following is correct regarding the management of VF:

D A After a single shock, CPR is continued for 2 minutes before a
/
rhythm check
ncil 1., _/ ,,,--0 B All monophasic shocks for defibrillation should be at 360 J

_AC Epinephrine should be administered if VFNT persists after the

second defibrillation ai • I}; 1 .P--1L-
D D Amiodarone should be given after two unsuccessful
i.
defibri 11 at ions
L~ D E Fine VF should be defibr'illated immediately ./ /, ~J-/
\
 Clinical MCQs

1 .. 146 As,swers:
• A True
o B False
• C True
• D Jrue
• E True
Asystole or PEA (pulseless electrical acti~i~ is associated with an
· extremely poor survival outcome.
. .
BLS is\not
~definitive treatment
for a shockable rhythm but helps to maintfun a shockable rhythm
I
I until such time as defibrillation is available.
I
--~
Reference: Advanced Life Support. 5th edn. Resuscitation Council
(UK) April 2006. 1
I.

1.147 Answers:
l(i' l
- •
•
•
•
A True
B True
C True
D False
•
• E False
Recommended initial energy for a biphasic defibrillator is 150-
~0 J, with se~d and subs~nt shocks.at 150~360 J. -
/ Amtodarone should be gjyeo if VJ-NT (VT = ventricular
tachycardia) persists after a third shock. The chance of
successfully shgc~lng fine VF lsverv unlikely. G~od quality ,CPR
may improve the amplitude and frequency of VF ancfso improve
the likelihood of success~Jibr~llation. Repeated delivery of
shocks increase_s_!llYogw::llal injury.
- ---·- .-- .
-=
Reference: Advanced Life Support. 5th edn. Resuscitation Council
(UK) April 2006.

I
190 1 :···..
 Clinical MCQs

1 .148 The following are true regarding ALS guidelines:

J
A Precordial thump is delivered over the apex
f"'-D B Single shock protocol comp~th th~ed shocks
\.,/ 0 decreases the CPR-free period and improves chances of
survival · ---=-.:: ~- -=-
\// ,, D C The first shock efficacy of a biphasic waveform is >9Q%
/
?nt I
v "O / D Asystolic rhythm should be reassessed every 2 minutes
/
m I
0 E During defibrillation oxygen masks should be held at least
1· / '/
I 1 metre awci.y from the patient's chest . .
cil u; , .· - ·;. ..

1.149 Drugs used in during cardiac arrest:

iC o A:, Epinephrine ~hould be· ~i~~~~~~i~.1~: . ·_ , '. -. . / .\ .' v\:' / < ~
D B Li~ocaine may ,be given foq:~fractory }!F .at .a. dose of 1 mg7kg-' ./
-~[] C If the rhythm is slow P_EA (<60 beats/min) atropine.B ..mg .~~: i
should be administered
, / 'ca O D Vasopressin is the ne~~op!essor of ciJ._oice m,YF arrest

,
1
b E 10 ml 10% calcium chloride contains less Ca2+ than 10 ml
10% calcium gluconate

ve
, of

.ouncil

1Q1
 Clinical MCQs

1 . 148 Answers:
® A false
® B True
® C True
~ D True
@ E True
A precordial thump should be delivered only aft~ a witnessed
. cardiac· arrest. A sharp _im~ct should be administered to the
lower half of the sternum from a h~ht of approximately 20~cm. It
is much more likely to convert a yr Jo sinus rhythm than VF. In all
reported successful case~--1fieerecordial thum_i ~~ given within
the first 1 -·-
O seconds.
-·- -
.

Reference: Advanced Life Support. 5th edn. Resuscitation Council

(UK) April 2006.

.. 1.149 Ariswers:

• • A False •r
• B False
• C True
• D False
• E False
A dose of 1 mg epinephrine should be administered every 3-5
minYtes, not necessarily every cycle if on the shockable sloe of
the algorithm. If arJOOfl~rone is Qg1:available, lidocaine ~glkg
can be used as an alternative. Vasopressin s_h~ws ~tatistically
significant difference in the rate of death. before. hospital discharge
when compared wii~pinephr1ne; ,-q mL 10% _calcium chloride
contains 6.8 mmol Ca2+ andfo ml 10°/o.calcium glucongte .
contains2 .2 mmol Ca
.,..--- .
2+. ··
Reference: Advanced Lfe Support. 5th edn. Resuscitation Council
(UK) April 2006 .

192
 Clinical MCQs

10150 Paedlafrlc resuschatiom ·

/"0 A An infant is defined as ~year old
, 0 B Standard automated externat defibrillators (AEDs) can be safely
'
used in children <8 years old (. · · .
. /)
;\ 0 C ~pon confirmation of no breat~o rescue breaths should be
given
t i
I
I
,/o D Two-person resuscitation utilises a ratio of 15 : 2 chest
I compressions to breaths
in J
!
vD E Assistance should be sought after 1 minute of unsuccessful
I CPR
l
lcil

'·-
 · Clinical MCQs

1.150 Answers:
@ A True
e '- B False
• C False
D True
e E- True
Infants are defined as <1 year old. A child is between 1 year and
puberty. Standard AEDs can safely be used in children over the
r
age of 8 years. P_U!P.Ji§e-oo_pde paediatric pads or programmes tha\ 1:
attenuate the energy output of an_fiE.P are rec_g_mm~nded for ·-
chilgrefl-undeJ.lLY~ars. Cui-rent' practice supports the '
administration of fiv~scuebreath·s. after confirmation of absent
respiration. Onl/fn ·cases of a child with a witnessed sudden :
·1
collapse should a rescuer not perform l minute CPR before i):·
calling for help. '··
I

Reference: Advanced Paediatric Life Support. 4th edn. (updated il ·

January 2006). ~ 1)·
,(

{i
\ ..
i

t
· .... ,;,,

r
L;
·~

{
I

194
 CORE TEXT REFERENCES

Peck TE, Williams M. and Hill SA. Pharmacology for Anaesthesia and
Intensive Care. 2nd edn: G.M.M. 2003.
Stoelting RK and Hillier SC. Pharmacology and Physiology in Anaesthetic
"r and Practice. 4th edn. Lippincott Williams and Wilkins 2005.
=r the 1 Yentis SM, Hirsch NP and Smith GB. Anaesthesia and Intensive Care A-Z.
rsth~ An encyclopedia of principles and practice. 3rd edn. Butterworth
ior Heinemann 2004.

ated

195
 ,,~,
. I

I' .
i,. _.:)LI
I '
i
!! I I

I11 I

I,
 INDEX

Locators in bold refer to book number, those in normal type refer to question
number.

amplifiers 2.75, 2.91

absolute zero 2.24
. acetylcholine receptor 1.5 anaesthesia:
and allergic reactions 3.82, 3.83
acid-base 3.56 awareness during 2.106, 2.107
kidneys and acid-base
concentration of anaesthetic
control 3.74, 3.75
agents 2.44
, acidosis 3.11, 3.23, 3.56, 3.75
monitoring depth 2.108, 2.109
action potential of SA/AV node 3.40
saturated vapour pressure 2.40
activated charcoal 1.125 ·
, active metabolites 1.67, 1.119 anaesthetics:
amide local anaesthetics · 1.32
acute haemolytic transfusion
reactions 3.76 inhaled- 1.11 S
1
j acute intermittent porphyria 1.97 intrathecal 1.84
local 1.30, 1.31, 1.34
l a2-adenoreceptors 1.122 pregnancy and 1.13 7
I adenosine .;J.65 regional and general 3.98•'
I ADH secretion 3.67, 3.71, 3.103,
spinal 1.44
3.116, 3.126
topical local anaesthetics 1.33
adrenal medulla 3.106
volatile 1.33, 1.39, 1.41, 1.42
adrenal physiology 3.104
1
anaesthetic machine 2.120, 2.121
, adult cuff 2.4 androgens and oxyhaemoglobin 2.12
l adverse drug reactions 1. 98
I Angiotension ll 3.67
I aerobic metabolism of glucose 3.31
1 anion gap metabolic acidosis,
airway physiology 3.2
normal 3.58
airway resistance 3.18
antacids 1.27, 1.28
albumen 1.112 antacid prophylaxis 1.13 7
albumin 3.26
anti-arrhythmic drugs 1.139
aldotestrone 3.70, 3.104
antibiotics 1.38
alfentanil -1.78, 1.79
anticholinergics 1.94
allergy 3.82
anticholinesterase 1.20
anaesthesia and allergic
reactions 3.82, 3.83 anticoagulation 1.55
antidepressants 1.24, 1.25
· ALS guidelines 1.148
alveolar partial pressure 1 .41 aorta 3.47
amino acids, essential 3.29
aortic pressure 3.42
amiodarone 1 .88, 1.140 apgarscore· 3.129 .
aprotinin 1.59
ampere 2.1, 2.81

197
 C~li'dH{.'

arteriolar smooth muscle tone, control blood groups 3.77 dru

of 3.48 recipient reactions 3.76 c;li'<dlof-
Ashwell shape 3. 1 2 9 blood pressure 2.3 oiL
asprir; 1.112,1.129 monitoring 2.4, 2.5, 2.78
flfbg
asystole 2.17 blood pressure machine 2.4 card~~
atmosphere, pressure of 2.52 measuring blood flow 2.82 cardJ3cs
ATP molecules 3:31, 3.112 blood sample, peripheral venous and cardir-,
atracurium 1.16 arterial compared 3.57
atrial fibrillation (AF) 1.140, 1.141 blood volume 3.50 cardioi
tor:
atrial natriuretic factor (ANF) 3.70 loss of 3.90 1
auditory evoked potentials 2.73 regulation of volume 3.61 to n
autonomic nerve system 3.146 blood-brain barrier 1.101 .
Carlen-
Avogardro's hypothesis. 2.21
catho,
Bodak seal 2.121
awareness ·during anaesthesia .. 2.106, cell me
body fluid distribution,. assessing .. 3.:62.
. 2.107 ,. centra'
body temperature 2.26 ..
aysystole 2.17 centra..
Bourdon ga.uge. -~:_129 , . . .:: ..
box-and-whisker plot . 2.13~.
cephah
. . \'._,,
cerebi ··
bacteriostatic and bactericidal. Boyle's law 2.21 _. . , . \ :
agents 1.35 brachia! plexus block l .138 .
cerebrc
baricity 2.96 brachia! plexus nerves . 3.1A8 cervi~r
basic life support (B.LS) in bseathing systems, anaesthetic . 2.112,
....
\.'

adults · 1.145 2.113 chelatir

basic measurement concepts, bronchial tree and lungs 3.14~ chemc.
chest t_
statistics 2.150 Broselow tape 1.131
chestw
benzodiazepines 1.23, 3.83
Bernoulli effect 2.101
childn
calcium 3.26, 3.39, 3~ 109
nebuliser 2.102 calcium channel blockers 1 .. 139
in•
bile, physiology of .3.33 calcium homoeostasis, drugs
chirali''
bioavailability. 1.100 affecting 1.87
choles
bioburden 2.103 choline
candela 2.1
chrom
biological potentials 2.70, 2.73 capacitors 2.90, impedance of 2.17
bispectral index 2.73 capacity and charge 2.85
gas-
blood caratoid body chemoreceptors 3.20 gas(-,
blood flow 3.36, 3.46, 3.64 carbohydrate metabolism 3.31 l1"1.·,
chrona/
blood flow to organs 3.36 carbon dioxide 2.124, 3.14, 3.21
chylorr ·
blood gas analysis 2.98 carbon dioxide analysers 2.32
ciproflL
blood transfusion 1.143 infrared measurement 2.31
blood volume 2.64 measurement 2.30
Clark's t
cerebral 3.128 ·· carbon monoxide transfer-factor 3.7, ·
cl~ans,_I ·
tests, normal range 3.130 3.8 elf
viscosity 2.59 and haemoglobin 3.14

1QA
 cardiac arrest in adults 1.146
drugs used dwing 1.149
cc1irdoac muscle 2.70
output 2.95
fibres 3.37
cardiac physiology 3.43, 3.47
cardiopulmonary resuscitation
(CPR) 1.145, 1.147, 1.148,1.150
cardiovascular physiology 3.41
cardiovascular responses:
to exercise 3.52
to haemorrhage 3.53
Carlens' tube 2.136
cathode ray tube 2.78
cell membranes 1.1
central control of breathing 3.19
central nervous system (CNS) 2.120
1
cephalosporins 1.37
j cerebral anatomy 3.138 ·
1
cerebrospinal fluid density 3.86
i cervical spine radiographs,
interpretation of 3.135
: chelating agents 1.126
i
I
chemoreceptors 3 .20
j chest radiograph interpretation 3.137
1 chest wall movement 3.15
1 children, calculations
; involving 1.130, 1.131
j chirality 1.95
i cholesterol 3.104
cholinergic receptors 1.6
chromatography 2.44
gas chromatography 2.45
gas chromatography
detectors 2.46
chronaxy 3.59
chylomicrons 3.32
ciprofloxacin 1.119
:
1
Clark's electrode 2.73
cleansing of medical.
equipment 2.103, 2.104
ciearance, drug 1.114
donidine 11.122P 1.123
CNS phy!£iology 3.128
<eoagulation l.120
drugs affecting 1.51
. coanda effect 2.61
combustions 2.49
complement system 3.121
complex regional pain syndrome
(CRPS) 3.122, 3.123
compressed spectral array 2.73
context-sensitive half-time 1.116
contingency tables 2.143
contractility 3 .44
coronary circulation 3.139
coronary nervous innervation 3.140
correlation statistic 2.145
cortisol 3.105
countercurrent exchanger 3.72
COX enzymes 3.69
•·
cracking pattern and mass
spectrometry 2.47
cranial nerves 3.134, 3.141, 3.142
critical temperature 2.23
currents, direct and alternating 2.81
cylinder connection and anaesthetic
machine 2.121
cylinder pressures 2.124
Dalton's law 2 .22
DC cardioversion 1.141
dead space, anatomical and
physiological 3.5
defibrillators 2.86
degree Celsius 2.2
density 2.96
·depth of anaesthesia 2.108, 2.109
dermatomes 3.133
desensitisation, drug 1.118
diamorphine 1.74
diaphragm 3.150 ·

199
 endocrine physiolo,gy 3 .103
diathermy 2.83
entonox 2.12 7
diathermy smoke 2.,119
eosinophils 3.78, 3.105
::..1,·gical 2.117, 2.118
ephedrine 1.121
diazepam 1.113 ·- epinephrine 1.96, 1.147, 3.106,
diazoxide 1.93
diffusion within the lung 3 .6, 3:22 erythropoietin, 1.23
etomidate 1.71
diffusion 2.33, 2.35
eustachian valve (fetal
diffusion capacity 2.34 g
circulation) 3.49
digoxin 1.117, 3.41
exercise 3.6, 3.15, 3.52, 3.112
2,6-diisopropylphenoi cardiovascular respo, .. ~ 3.52
(propofol) 1.66, 1.68, 1.109,
physiology of 3.111•
1.116 and respirator; system 3.22
diuretics 1.45, 1.46, 1.47, 1.93 \.
expiratory reserve volume (ERV) 3.4
dopami"ne 1.111
Doppler effect 2.95
double-lumen tubes 2.136 farad 2.90
fatty acids 3.32
drip counters 2.69
esterification 3.110
drug metabolism 1.102
fetal changes at birth 3.96
binding 1.1 OS
fetal circulation 3.49
distribution J 101
1•
fetal haemoglobin 2.11
in lungs 1.86
fibrinogen 3.119
response 1 .11 8
Fick's law 3.1
drugs, absorption of 1.2
filters 2.110
fibres filtration 2.111
ECG 3.42
flecainide 1.117
ECG trace 2.87 flow meters 2.62, 2.66, 2.68, 2. 1 30,
edrophonium 1.18
electrical components 2.84 2.131
bubble flow meters 2.68
electrical potential generators 2.76
thermistor flow meters 2.68
electrical safety 2.15, 2.16, 2.17
fluid flow 2.58, 2.60
electricity 2.82, 2.87
force 2.50
electrodes 2.7 4
electroencephalograph (EEG) 2.108, Fowler's method 3 .5
fresh gas flows (FGFs) 2.112
2.109
,1 Friedman's test 2.143
potentials 2.72
electromagnetic spectrum 2.94 fuel cell 2.13
electromyogram (EMG)
GABA (y-aminobutyric acid)
potentials 2.71 receptors 1.21, 3.117, .
electron capture detectors 2.46
gas carriage in blood 3.14
elimination rate constant 1.110
emergency surgery 2 .106
gas laws 2.22, 2.23
I
.\I
~,
 gas storage 2.123
gastrointestinal tra~ drugs
affecting 1.29
G-coupled protein 1.107
gelatins, allergy 3.83
glomerular filtration rate (GFR) 1.114
glomerular hydrostatic pressure 3.70
gluconeogenesis 3.61, 3.105
glycogen 3.31
glycolysis 3.110
glycopyrrolate 2.107
1 G-proteins 1.104
,.4 Graham's law 2.35
granulocytes · 3.78
guanethidine 1.138
haemoglobin 3.7, 3.12, 3.14
haemoglobinopathies 3.107
haemorrhage 3.53
halothane 1 .40, 1.102
Hartman's solution 2.3 7
HbH disease 3.108
heat capacity, specific 2.27
heat loss 2 .2 6
in adults 2.99
_ heat/temperature relationship 2.28
l Henry's law 2.-21, 2.35, 2.41
- hepatic physiology 3.30
hepatitis C 2.1.03
hepatocytes 3.30
Hering-Breuer reflex 3.21
hertz 2.92
high airflow oxygen enrichment)
(HAFOE) devices 2.101
HIV 2.119
infection and treatment 1.136
humidification devices 2.8, 2.102
humidity 2.7. -
,, Humphrey system 2.11 ~
hydrogen ions andmeasurement 2.29
hygrometer, hair and Regnault's 2.7
hypersensitivity reactions to
drugs 1.99
hypothalamic physiology 3.102
hypothermia 2.59, 2.116, 3.11, 3.98
hypoxic pulmonary vasoconstriction
(HPV) 3.25
ibutilide 1.139
ideal body weight (IBW) 1.108
immunity 3.81
impedance 2.17, 2.90, 2.91
indicator dilution techniques 3.10
inspiratory reserve volume (IRV) 3.4
insulin 3.109
effects of 3.110
intravenous induction agents 1.67
intravenous infusion devices 2.69
iodine 3.27
ionisation 1.3
iso~rs 1.81
isosbestic points 2.9
isotopes 2.18
isovolumetric contraction 3.42
joule 2.2
Kallikrein 3.48
katharometer 2.45, 2.46
ketamine 1.69, 1.70
kidney, acid-base control in 3.74.
kidney, functions of 3.61
proximal tubule. 3.63
renal corpuscle 3.67
kidneys and drug clearance 1.114
Korotkoff, fifth phase . 2 .4
Kupffer cells 3.30
labour, physiological changes occurring -·
during 3.94
laminar flow 2.54, 2.55
Laplace's law 2.58
 r·
I __,
ill
laryngeal nerve damage J.14.4 sterilisation 2.105
laryngoscope 2.114 medulla 3.140, 3.141 I·
~
larynx 3.143 membrane bound receptors 1.104
lasers· 2 .1 9 mesangial cells 3.65 r-
/
safety precautions 2.100 meta-analysis 2.146 (JI_
lean body mass (LBW) 1 .1 08 methadone 1.75
leucine 3.29 methionine 3.29.
lidocaine toxicity 1.89 methylene blue 2.10
linear regression 2.144 micro-organisms 2.105
lipid metabolism 3.32 rnidazolarn 1.109, 1.22
lipoprotein lipaes activity 3.110 minimum alveolar concentration
liver and drug clearance 1 .114 (MAC) 1.23, 1.39, 2.43, 2.106
liver 3.32 mivacurium 1.120
loop of Henle 3.71 monoamines 1.101
lower oesophageal sphincter morphine 1.72, 1.73
(LOS) 3.111 mRNA 3.105
low-molecular-weight heparins muscle fibres, type I and type II 3.113: . OS
C:
(LMWHs) 1 .54 muscle relaxants 1 .1 7 c ...
lung volume 2.62, 3.4 myocardial tissue physiology 3.38 OSI
r -.
lung, compliance of 3.16 myocarditis 1.136 (1
lungs, adult 3.1 myoglobinuria 1.133 t
ox
lungs, drug metabolism in 1.86 c·.
lymphatics 3.101 neostigmine 1.19 (; -
lymphocytes 3.80 nerve fibres, classes of 3.88
nerve simulator 2.76, 3.59, 3.60 C
magnesium 3.127 settings 3.60
magnetic flux 2.79, 2.80 nerve: biological potential 2.70
magnetic resonance (MR) 2.20 nerves and foramen 3.13.4
magnetism 2.79 neuromuscularblockade
magnets 2.16' assessment 1.7
malignant hyperthermia (MH) 1.10, neutrophils 3.78
1.132, 1.133, 2.43 newton 2.2
Manley ventilator 2.113 nitrates 1.50
Mann-Whitney test 2.143 nitric oxide and paramagnetism 2.11
Mapleson circuits 2.112, 2.113 nitrous oxide 2.35, 2.41, 2.42, 2.121
mass spectrometry 2.47 2.124, 3.6 ,
'
McCoy laryngoscope 2 .114 and diamagnetism 2.14
mean arterial pressure (MAP) 2.3 non-depolarising muscle
medical air 2.124, 2.128 relaxants 1.13
medical equipment: non-parametric tests 2.142, 2.148
cleansing 2.103, 2.104 normal distribution 2.149

i!- ')(\')
 numbers needed to treat (NNT)
obese patients, drugs and 1.1 08,
1.109
anaesthetics and 2.107
obstructive sleep apnoea 3.89
Ohm's law 2.89
old age 3.100
physiology of 3. 99
oncotic pressure 2.38
opioids 1.80, 3.83
opsonisation 3.78
ordinal data 2.138
oscilloscope 2.78
osci I lotonometer, van
Recklinghausen 2.4
osmolality 2.36, 2.39
osmolar gap and osmolarity 3.55
38
osmolarity 2.38
osmosis 2.36 .,
Ostwald solubility coefficient 2.42
oxygen and paramagnetism 2.14
oxygen measurement 2. 9
oxygen storage 2.125,
concentrators 2.126
oxygen tension management 2.13
oxygen 2.11, 2.124, 2.125, 3.14,
3.24
oxyhaemoglobin and
deoxyhaemoglobin 2.9
dissociation curve 2.12, 3.13
Pvalues 2.147
pacemakers 2.76, 2.115, 2.116
paediatric resuscitation 1 .150
pain physiology 3.84, 3.103
pain fibres 3.85, 3.85
pancreas 3.109
pancreatic. function, 3.108
pancuronium 1.14, 1.119
148
I-
2.146 papaverine 1.138
paramagnetism 2.14
partition coefficient 2.42
pasteurisation 2.104
Penaz technique 2.5
penicillins 1.36
peripheral nerve localisation 3.59
peripheral nerve blockade 3.60
peripheral nerves 3.147
pethidine 1.76, 1.77
PGl2 3.68
phaeochromocytomas 3.131
phagocytosis 3.65
pharmacokinetics 1.108, 1.110,
1.111, 1.97
of inhaled anaesthetics 1.115
pharmacology of old age 1.82
phenytoin 1.26, 1.106
phosphodiesterase inhibitor
aminophylline 1.92
phospholipase A2 3.68
•,
physiology of the cyclo-oxygenase
enzymes 3.68
piezo-electric effect 2.48
pin index 2.122
pipeline gas and anaesthetic
machine 2.120
pituitary physiology 3.102
plasma cholinesterases, drugs
metabolised by 1.120
plasma:
aspirin and 1.112
fresh frozen plasma (FFP) . T .143
oncotic pressure 2.38
plasma cells 3.81
plasma drug concentration 1. 116
proteins bound in 1.1 06
volume 2.64
platelets 2.110, 3.118, 3.120
aggregation, increase of 3.119
701
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SI units.
ba .
radioactive particles l.18
drug effects on 1.12 9 Raman spectrometry 2.48 d~
pneumotachograph. Raoult's law 2.39 · signal-t
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C'haracteristics 2.67 rapid eye m~':'.ement (RE~) · 3.116 sleep i ·
(
so d a 11;
poiso11ing, treatment for . 1.125, 1.126 receptoJ agoni,_sts and
polio blades 2.114 antagonists 1.103 sod~~-
positive pressure ventilation · 3. 1 2 6 receptor morphology 1 : 118
postoperative nausea and vomiting, receptors 1 .104, 1.107 tox
drugs used 1.62 recombinant factor Vila (rFVlla) 1.61 solub'
postpneumonectomy 2.34 red cell fragility test 2.38 Spau.,
posture 3.50 released ADP 3.119 specif
Poynting effect 2.127 remifentanil 1.116, 1.120 spine
prazosin 1.124 renal blood flow· 3.64 spinai
pre-eclampsia 1.134, 1.135 renal response to disturbed acid •
pregnancy 3.13, 3.95 11
base 3.75
anaesthesia and pregnancy 1. 13 7 spinal
renin 3.61,3.66 1
and drug distribution 1. 101 repolarisation 1.13 9 ;spire:
hormonal changes 3.91 residual volume (RV} 3.4 .stan,...
maternal physiology during .3.92, resistance 2.89
i
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3.93 resistance to current flow 2.90 lstatl

I '
and oxyhaemoglobin 2.12 periph;r'al,resi~tance 2.3 ·· -statist
CJ,
preoperativ~ fasting 1.142· .. resonance and damping 2.6 istellr~·
pressure gauges 2 ..129
pressure measurement 2.53
procaine 1 .38
prostacyclin 3. 119
respiration at altitude 3.23 .
respiration 3.19
respiratory etfects of diving 3.2 4
respiratory system and exercise 3.22
r~ili
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protamine 1.56 surf;\

reverse transcriptase 1.136 1sux
protein binding 1.4 Reynolds' number 2.57
protein metabolism 3.34
PRST scoring 2.108
ropivacaine 1.106
rotameters 2.65, 2.66
1
pulmonary artery flotation . 'I l::.

sym1
catheter 2.97
pulmonary blood flow 3.10
pulmonary capillary wedge pressure
sacral anatomy · 3.149 ~sy~2
sarcoidosis 2.34
(PCWP) 3.47 saturated vapour pressure 2.40 syl!'
pulmonary circulation 3.3 Schrader socket 2.120 sy.
pulmonary physiology 3.9 scoring system 3.129
pulmonary vascular resistance ta(t
Seebeck effect 2.25 .
(PVR) 1.85, 3.11 semi-permeable membranes 2.35 ·te;;
pulse oximetry 2.9, 2.10 Severinghaus electrode 2.30
sevoflurane 1.43, 1.102 1•.
radiation 2.18
 SI units: measurement 2.25
basic 2.1 body 2.26
derived 2.2, 2.50 TENS 2.77
signal-to-noise ratio 2.88 ,8-thalassemia major 3.107
_ sleep 3.117, physiology of 3.116 theatre shoes, impedance of 2.15
; soda lime 2.137 thermocouple 2.25
; sodium nitroprusside 1.48, 1.121 thermoregulation 3.97
metabolism of 1.49, 1.90 thiazides 1.45
toxicity, treatment of 1.91 thiopental 1.63, 1.64, 1.65
solubility 2.41, 2.42 post-injection treatment 1.138
; Spaulding classification 2.103 thrombozane A2 3.119
'specific gravity 2.96 thyroid hormones 3.28
spinal anaesthesia 1.83 thyroid metabolism 3.27
spinal cord: ascending and descending thyroid-releasing hormone (TRH) 3.28
I
tracts 3.124 thyroid-stimulating hormone
1 left-sided partial transaction 3.125 (TSH) 3.27, 3.28
spinal nerves 3.133 tidal volume (TV) 3.4
spirometry 3.4 time constant, drug elimination 1.110
standard error of the mean
(SEM) 2.141
statistical analysis 2.143
tolerance, drug 1.118
.,
total body weight (TBW) 1 .1 08, 1.109
total intravenous anaesthesia
statistical statements 2.140 (TIVA) 2.106
stellate ganglion block 1.138 trachea 2.8
stellate ganglion 3.36 tranexamic acid 1.60
sterilisation of medical transducer, strain gauge 2.6
equipment 2.105 transformers 2.84
stoichiometric concentrations 2.49 transfusion-related acute lung injury
,, surfactant 3.17 (TRALI) 1 .144
suxamethonium 1.8, 1.9, 1.120, tricyclic antidepressants 1.24
1 trimetaphan 1.121
2.116
suxamethonium apnoea 1.11 tubuloglomerular apparatus 3.65
suxamethonium metabolism 1.12 turbulent flow in tubes 2.56
sympathetic nervous system 3.11 type A (augmented) drug
~ sympathomimetic G-coupled reactions 1 . 98
proteins 1.107 types of electrical equipment and
sympathomimetics 1.96 safety 2.15, 2.16
systemic circulation 3.35 tyrosine 3.29

tachyphylaxis 1.118, 1.121

temperature 2.24 unfractionated heparin 1.52, 1.53
constant 2.21 urea and_urine 3.72, 3.73

'lni::
 ventricular pressure-volume curve
UV light transmission and
relationship 3.44, 3.45
humidity 2.7
ventricular tachycardia,
cardioverting 2.86
vacuum insulated evaporators vertebrae 3.132
(VIEs) 2.125 viruses 2.104
vagus nerve, functions of 3.87 viscosity 2.59
vital capacity (VC) 3.4
valine 3.109
Valsalva's manoeuvre 3.51 vitalographs 2.62
vitamin K-dependent clotting
valves, physics of 2.51
factors 1. 127
van der Waals' forces 1.105
Van Slyke's apparatus 2.11 V02max 3.115
volume of distribution 1.113, 1 .11 7
vaporisers 2.132, 2.133
von Willebrand's factor (vWF) 3.118,
vapour analysis 2.48
3.119
Vaughan-Williams
classification 1.139
warfarin 1.57, 1.58, 1.101, 1.106
vecuronium 1.15· drugs increasing effect of 1.128
venous admixture 3.54 .
waves and wavelengths 2.92, 2.93
venous P02 2.11
venous system and posture 3.50 webers 2.80
• Wheatstone bridge circuit · 2.6
ventilation 3.5, 3.6
white blood cells 3.79
control of 3.21
Wright respirometers 2.63
ventilators 2.134
servo ventilators 2.135
ventricular fibrillation (VF) 1.146, yohimbine 1.122
1.14 7, 2 .1 7, 2 .83
zidovudine 1.136
ventricular muscle action
zona glomerulosa 1.104
potentials 3.39

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