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Access to Anaesth.

Primary FRC
Pocket Book 3m ·
Physiology and Anatomy
Kirsty Maclennan MBChB, MRCP, FRCA
Specialist Registrar Anaesthesia
North West Region

I
L
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First Published 2007

ISBN: 1905 635 311


ISBN: 978 1905 635 313
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0
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CONTENTS

fo!l'eword

Introduction

Physiology MCQs
Qustioos and an$wers 3.1-3.131
3

Anabny MCQ; ·
~ions and answers 3.132-3.1 so
187
Index
215

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ACKNOWLED.GEMENTS

i would like to thank Dr. Nolan for taking the time to write the foreword; Dr.
vVhitaker for his review; Dr. S. Maguire, Dr. K. Grady and Dr. VV. de Mello for their
advice and encouragement,

u would also like to thank the publishers, PasTest, my family, who have supported
me. And above ail, Ann Maclennan who has been my rock as always!

. il .•.
FOREWORD

The introduction of run-through training 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 Anaes-
thetists [FRCA] examination.
The Primary Multiple Choice Question [MCQ] examination became a
"stand alone" Pass/Fail examination in June 2007. A dose marking
scheme is used where 1 is a poor fail, 1 + is a fail, 2 is a Pass and a 2+
reflects an outstanding performance. The Primary FRCA MCQ examina-
tion consists of 90 questions undertaken in three hours and comprises
three subsections of 30 MCQs examining Pharmacology, Physiology,
Physics and Clinical Measurement. A mark of 2 is required to pass the
MCQ although a candidate who significantly underperforms in one or
more subsection of the MCQ will fail the examination. Negative marking
is applied with one mark being deducted for each incorrect answer.
A candidate may not p.rpceed to the Objectively Structured Clinical
Examination/Structured Oral Examination part· of the Primary without
passing the MCQ. An MCQ pass will be valid for a period of three years
for 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 clinlcal 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 consid-
erable amount of information required to pass the Primary MCQ. Prospec- .l
·~.-~:-~
tive 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 MCQs which cover in detail the
Primary FRCA syllabus. The answer sections are dear and, where appro-
priate, supported by references to recent literature. Trainees commencing
an anaesthesia training programme will 'find these MCQs useful to assess
the depth of knowledge of the basic sciences which will 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 their knowledge and Lnderstanding which may need further
work.

Dr D. Nolan, t .eglonal Advisor for the North West


INTRODUCTION

Having taken both anaesthetic· and medicine postgraduate examinations,


~ .hink that it is alw 3ys difficult to know how best to start revising. U is
important to avoid that unpleasant drowning sensation when you look at
all the information ti-at you have to absorb! i personally find that sitting
and reading a textbook is 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 1, 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 . .I,his enables you to revise a particular
topic or, you can always take 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 or even over lunch!
The examination period is a stressful time, so make best use of all the time
that you have.
Good luck!
Kirsty
.,.-s:

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PHYSIOLOGY MCQs
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3.1 ~(I!;gairdarrng the adult h.mJg$:


/o I A Movement of oxygen into the blood o~eys Fi£~~1aw ,, -
'/, 0
B The blood : gas barrier has a surface area of more than 1-5-0 m2
'f. 0 C There are approximately ro million alveoli in total,
/ ~
-
,1
/,.
D \ - \. ,. ·,
D The main bronchi onitially divide into segmental bronchi
I
.' D E Respiratory bronchioles divide into terminal bronchioles

3.2 Regarding airway physiology:


./o ---
A Through large airways air movement is secondary to bulk flow
D B The main mechanism of ventilation of airways beyond the
terminal bronchioles is by bulk flow ,~
,,·"- D
I C Dust particles settle beyond the terminal bronchioles .
/ D
',/
D N~s~JJ~reat_hi11g_increases the resistance by 50% compared Cit 1

with· mouth breathing , , -=--


·, D E Bronchioles constitute the major resistance in the respiratory
tree -- z.=~ i
Physiology MCQs

3 .1l · Airn§Wteti§~

© A True
© B false
@ C False
l.1) D False
!;) E False
\_Fick's law of diffusion\states that the 1ate 9f_diffusjon acros_~ a
me.mbrane ls p_roportion3l to the con~entration gr!1~t.
2
'The bloocl·~-ias.barrier'has a surface area of 50-100 m •
]}1_<:? lungs contai; ~pp;oxi~ately soo millionialveoli.\
1',The divisions of the airwayS are as follows: the trachea divides to
'form the main bronchi. which form lobar bronchi, which form
segmental bronch': these lead to the'iei-ffi(Oalbronchioles, whicli
are the smallest airways without alveOH; the ijir'rnlrialhr'oochiok>-
then divide into r~s(liratorz brOAchioles; these finally become the
alveoli~. which 'are· Corii[>letel)'liried with alveoli. This area
of the lung contai~ing the alveoli i~ _called the ~:~atory zo~e._.
~,

3.2 Answers:
o A True
o B False
• C False
o D True
E False
Beyond the 1~erm!Q,;l! bronchiol
es\gas movement is dependent
upon ~~~~f@[\as with the larg~ ~irways. .
l ~\settle in the teriniiial b~chiOles because the
velocity of gas
... -
falls rapidly in this- region
~ -, . --------
Most airway resistance is secondary to· e~cuc;tJ!Ley1 l
. ' \ .
.. _J
~om:_~oleS,constitute only 10-20% of a~~ce.
Physiology MCQs

'•

Rega:rdiung the pulmonary drcll.ll~airfon:


A Capillaries have a diam~er ~f approximately 10 ~ around
thg ?lyeoli -- .- - C - •

-·-·---- - -·-.._,.,.
1// D 8 The normalvalue for ~Y~!oqf pulmonary arterypressurs is
approximately 25 mmHg ,c;-=_--:;;:,-----.:.·--~ 1

./ D C \...
_ <.J'
Pressure in the right atrium is greater than that in the left atrium
D D The pulmonary artery vessel wall comprises mostly smooth
muscle ',
1
/. D E Most ~.te ·drop in thefu_~JI'lQ,nary ~fri~]iJi~) occurs just
upstream of the capillary bed ':" \, ,, . " :- .~ -~- .
--·------- - --· ' . )11\ ' ;_) ... , ':; ·'

,.

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e11,
C8 I
Physiology MCQs

33 Ansv1ers: ·
') A Trne
0 B True
.;) C false
~ D False
(l E False
artery
S_y§191,ic Q_l:!lmon~ry pressures are usual !y <;me_:-Jjfth of the
\systemic
~
c}icUlatory~j)i€Ssllr~.
. A normal
----- .. ·-
range 9fJ5=.30 mm Hg
systolic and 0-'8 mmHg diastolic is normally accepted. The
pressure ·in the right atrium is about 2-,SC mm Hg compared with that
of the left atrium, which is approximately 5 mmHg.
The pulmonary artery is very thin compared with the aorta
-
pressure system in comparison.
-
secondary-to7is"relative lack of smooth muscle, as it issuch a low-

Most pressure drop occurs within the capitlary bed as compared


with the ~¥stemic circu1~.tion wnere most pressure drop occurs
just upstream of the capillary bed. Cll 1

Cll 1

i:

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Physiology MCQs

lung volumes: ,
A lnsplratorv reserve volume ORV) is greater than expiratory
reserve volumes (ERV) ~
B Residual volume (RV) is-approximately 1-1.5 litres in a
, 20-year-old person
,/o C Vital capacity (VC) decreases with age
/ 0 D IRV, VC and tidal volume {lV) can all be measured with
spirometry , / .
./ 0 E All
I
measurements are recorded at standard temperature,
pressure dry ,t

Cl r

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Physiology MCQs

3.4 Answell's~
© A True
© B True
® C True
e D True
@ E False

IRV

Litres
ERV
vc FRC.
TLC
RV

where TLC =total lung capacity


VC = vital capacity
RV = residual volume
IRV = inspiratory reserve volume 3 l
TV = tidal volume
ERV = expiratory reserve volume 1 _c) l
FRC = functional residual capacity

figure: Lung volumes


;~V ls approxirn_ately~~compared witth~~hich is
approximately~ :JRY increases with)ge to approximately
3 litres. VC therefore aecreases with age. Only ffi_C, g_v_ and TLC
canl}Qt bC measured with spirometry. All meas\Jremerlts are al
body"femperature and pressure saturated.
----'
Physiology MCQs

3o5 !Regdll'dliil1lg ventilation:


/ D A An inc~e_?lS'? in alveolar ventilation always increases dead
space ventilation -~~:t,.\ 5'-"~ '-"---·- · '
/ I • • -- • • -··•

D B It is true to say::~ _ ~CO2 ~ Pto2. X K where Pco2 partial =


pressure of carbon dioxide; VC02 is volume exhaled of carbon
dioxide per unit time; K = a constant; VA = alveolar ventilation
per unit time· · - - · ·
.// D C Fowler's method of an,atQmkaLdead space analysis is
calculated by e!9.tting nitrogen concentration Y._er~u,--~_ expired
volume ----~ · - · -~-
0 · D \T~~-~~hr_equatiori exactly states' \1). ~- -~- ··-Paco -=-~co : \
2 2
PaC02\
I •

i _ .•••. ·-·
~

• -
I .,..-.--·- ·--· - - - • •• •

D E IPh~iolggi.c~I de_ad
---?-s12a~~
--·-- is a measure of the entire
. lung..!!.ot
eliminating CO2 -

~ i_-,,,-J_
•1 I ''

,__;,
.
:
,

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Physiology MCQs

3.5 J\IJ'n§Welr$~

© A False
® B True
@ C True
e D False
~ E True
Increasing alveolar ventilation by taking a deeper bre~91h does not
inwca_s~ dead space, whe'reas-iiici-easing respiratory §e will. --
Fowler'.?_!:D~!.h.~d cl ra~d nitro·g~~- ~on~~a_!!_QD__?._n_Aly_5-i~ is
plotted on a chart ofllifrogen concentration on the y axis and
volume
r-· --··on the x axis. . --- --------· --------
The:,Bohr_~qyation·') is an equation of\ph_r~~o~<:>s!cal ~~~~__sp~ce 1
w~re: ·
Vo/Vr = (PAC02 - PeC02) + PaC02
§jPAC0 or alveolar partial pressure of carbon dioxide. However,
2
we commonly write PAC02 as it is assumed that arterial CO2 will

.,
be the same as alveolar. Cll 1

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Physiology /viCQs

3.6 Regardnrrng ventilation and diffusion withln the lung:


v-/ 0 A In a lateral position the dependent lung will ventilate best
/0 B The increase in partial pressure of nitrous oxide h1 the blood is
RerfusionlfmHed
.. ~ ·~... ~
= -- - -
i u C The increase in partial pressure of carbon m~mox_itj_e in the
blood is Q~rfusi9_n limited 1 ' · ,_
------ -· --·' -
f D D In fibrotic lung conditions ~~y_g~D is perfusion limited
--·---
/ D E With se~s:!e exercise oxygen may be d~~~:?19~ limited

ca I

i
Physiology MCQs

3J} Ainsw~ir§~

© A True
@ B True
© C False
® D False
e E True
As with .all positions: the lung tissue in the d~endent poi:tton
ventilatesoest~.- - --- - . . - . ·-.
. .-·--- -
Diffusion_i is related to, among other things, the partial pres~ure
difference of the gas. -· --- · - ---
------~ ·- -
There is almost ~q increase in the partial pressure of carbon
monoxide in blood as it diffuses across and therefore it does not
depenlUPon the amount ofblOOd available. Ii i;lherefore said to
? be dlffusion limited.
7 Nitro~ide diffuses across but ~ R_~!"l~aLQ!~ssure builds up in the
blood and therefore the _gradient is lost. This slows transfer and
therefore it is said to be perfusion· limited.
CII - - - -----
1 gxygen can be diffusi_<?n lim_i!_~d with severe exerciseCllespecially
when at altitude. With a rec:!uction in PA02 there is a decrease in
alveolar/arteriaJ_gr~.qient, which means that it diffuses more
slowly· Into-the fast moving circulation. -
--------
-;:.....---

c_p--_..>
(I __ ,, --7

i; I
I

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Physiology MCQs

·3oi Regarding !!~~~fer factor for ~arbon monoxide: _

l/
.,,,,,,,.,.
_,./0 A It is calculated based
-·--· -·
onthe
. ~
assumption that capillary-~airb9n
monoxide tension is zero
.. - ... -- . . . -
--· ·- - . . .
1.

. ,,,-·D B TLCO (carbon monoxide transfer in the lung) differs from DLCO
V (carbon monoxide diffusion within the lung) in that it takes intO
account the chemical combination of carbon monoxide with
haemoglobin as a rate-limiting step
~ D C It is measured using a mixture of ':_~rbon _monoxide and an
insoluble gas
,-- b D The co_¢fi.c;_[ent of gas transfer~Kco))is theGAivided ~
where~is carbon monoxi e transfer i~l~ng an~s
alveolar volume ·
V- D E ~ is measured in~~
, .. \ I
(( ..
I

3.8 Regarding transfer factor for carbon monoxide:


,' D 1-
A ~aemoglobin ~~!1centration does not significantly aff_ect;TLco)
readingsCII r -::.--::".:._

o a 6m1i~ a,comb[na_t[on o~IVe_o_[a,~ volume x efficie,!19' cKCO) \


I specifi.~ 8?..~. ~~~nsfer '\
~ ----. - ·-·-- -·. --- -------
0 C i~s typically measured withjan Fio2 of_o~.?~ \ I l 1,
D D PulmoJ]ary hypertension is associated with decrease{9and
'ecrease
(" .
<2.~~,._. VA'. .d----
j
·
/,... ------- ···-,--·------~
.z , D E \_AsthlTl<I!~ associated with a~e~r~ased nc~J 11'

I
1

\\ - -·-:-- -

~ ,__,__Q_,
. -
I {i
-

' ,/ \ '.- --~- ,


"
()
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'

·~,
·--- ~ - • • ~

' 1·' I. '·1


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,.-.'·•'
1 ~· \
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,.
--
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'------------··-----
Physiology MCQs

3.7
© A Trne
B True
C True
D True
E True
Other countries still measure DLco\(ml/min per mmHg). The
change in concentration of the insoluble gas enables the
calculation of the alveolar volume. --- -- .
\Ga~~-~~-!_,~ng~-~-~p~_c_ity_ CfLCOf ;--alveolar volume (VA) X
efficiency (K,~). A reduction ilJ..iT~f01can occur secondary to a
decrease in~ VAJ>r decrease in ~co_,br a combination of both.

Answers:
~ A False
• B True
• C False
CII i
• D False
• E False ,..--.__,. .
I - ·• - - - • . -·- I I \

\ Haemoglobin concel}Jratj9_n will significantly influence the ~ ..1'


as the chemical binJJi~g of carbon monoxide to haemoglobin is a
r~Je-limiting -~~~p and therefore all readings are corrected to
reference haemoglobin of J 4.5 gldl with a standard equation (1 g
reduction in haemoglobin leads to a 4% fall in TLCO. _:;
~is measured with a mi~ of carbon monoxide/insoluble gas
and typically 18% oxygen, as oxygen competes with carbon
monoxide for haemoglobin-binding sites. - _
I !
I I !Pufrn~~-a.iihrRer!e~~!~n}is a~~9c_l~~~d _with a(decr~in Keo but (-!
a _nQ_~mal VA as is(eulmona~~~oli~m. l
\111
( TLctj may be slightly elevated in asthma and is ~y elevated
I
I\II
in pulmonary haemorrhage secondary to the extravascular
haemoglobin that binds carbon monoxide.
!i
I

1i
,\

l 1 A
Physiology MCQs

3.9 1/hie foH~oWe111Jg are iir1UJe of pulmo!l'Dairy physiology:


/ 0
A The pulmonary~rt_~ries accompany the bronchi as far as the
(1ermi@_6mof+1iol~r~. b~~<i.e_rr1Jn11 sap~ll-'!Q' ~'~ ~-\- ~'-'""'
,'!(,v, ~- c...,..>
to the left atrium q- '
• ..> •, r
B Two large veins drain blood from lungs
__ , _
'f-_ D
C JY\ean pulmonary artery pressure is approximately -:::=- ..
--2n-::fo mmHg 't - ·:- S'"->~
·? ,
'(.f-.---
A"-::)\c A~
"2 - ~~

v' D
D As the lun~QL&.!me increases the extra-alveolar arteries and
veins increase in size
X D E
A ---
rise in pulmonary artery pressure causes a rise in pulmonary
~ /
vascular resistance in the normal lung .

3.10 Pulmonary blood flow:


-./b A Can be measured ~ indicator dilution techniques
_/\ 0 B Can be calculated wi_th knowledge of oxygen_ con~~mption
alone -· ··-·---- -'----·- --
_i, =- '·__)(J _:_ . r- ..,,~ (, ' - .
~~
.
)

IO C Is lower in.'weit i9.ne_3Jthan.in:west z~n~::_t'J


,_..,_ ,-· -~ ' . . ~--·· .
u :~ ,j I

V D D ~eduction by smooth muscle co111r:.ac:tion in small arterio~s


accounts for decrease blood flow in hypoxic areas '
' · /0 E Reduction by hypoxic pulmonary vasoconstriction is chiefly a
result of decreased partial pressure of oxygen in a__!yeoJL
----? \.

.• _:_)
Physiology MCQs

3.9 Alr\l§Wte rsi

® A True
@ B false
© C false
f) D True
fl') E False
fpµr large veins draj_n blood from the lung to the left atrium.
-~~a"n t?l:JJ_monary~_i-te;y press_L!_r~s are within a range between
10 and 15 mmHg.
As the lung exp~.s the extra-alveolar vessels are subjected to th
expanding pull of the parenchyma and therefore increase in size,
As the pulmonary artery pressure rises puim,Jnary vascular
resistance fa_Ui\.vithfn""normal lungs s_econdary to distension 0
and
recru itmeOt Ofcapi llaries. · ,,; ~ i)-)"' •'> > ~

3.10 Answers:
C)<.'> -
-----· --- -

A True
B False
C False
D True
E True
Pulmo~blood flow can be meas_uf.:~9 with haemodilution
techniques or ~a\cula~eQ using Fick_'UJrinciple. Application of
,,
I
- - ·--· --
Fick's principle ·denotes that 0_15yg§.D._cq_n~t, ~----
. 1J!lPJion ---i~
per :-.·,inute
e~l to ~h'.° _arno~~t of~~en taken Uj:) b\' -~,e iung per minute.
locali::ulate Pu!rno.nary _blood •:0w from this principle, ~
consumption,;~rtei :ai oxygen and mixed venous oxygen
conc2n~, anons are needed. The equation reads: -.
1:
l, Q= Vo2 ..;- (Cao2 - Cvo2) . .
\ ; \ii~ where Q _i~'pyl!flon2JY.lili1MIIO
Wi Vo2 ==oxyg~n con~u;,:;ffijpu, >
,I ~
I
i
I'
per minute'.and Cao2 and CV02 are arterial and mixed venous
\/) "'-\- I
oxygen concentr~ions respectively. .
'\K
\ ' '-\
j\,J;'
/
Wesl_?..QD~J has a blood flow.unaffui:_ted by alveolar pressllre as '
--==-- - ~-- ... -· __,
~rterial press.ure is greater than ver,oys. ~sure, Which is greate
·I. I
than a\v~.s,Lar pressure, whereas west zon_e 1 ?lveo\ar pres3ure is
••.. greater than arterlal. so alveolar-----
pre~St. fre-gr'e~.itlfilffects arterial
I u
I ,..
\ - ~ r:--- . ~

I blood flow. ·
Physiology MCQs

Yr Ptidmonary vascular fl'teSn§iarti«:~ (?Vi) ns iirncir~~~~r& byg · · ' ·


D A A decrease in cardiac output :: v- ,(- ) -9 -- -L f"f~ "-->
/,. D B Nitric oxide c__ c-
t../0 c Sympathetic nervous 'system.
vo D Acid<,sis -
/0 E Hypothermia --

- -.h 3.12 Regarding haemoglobin:


·~e. \/// 0 A Each haem binds one Fe2+
• ...!
0
r,_d B Each haemogJQbi.n..m.olecule carries one ~xyge~_f!!oJ~.c;~J~
'-//0 ----··---·- _., __
C Methaem.
3
Q gJ_o bin formation is s_?condary to oxidation of Fe2+
to Fe + - · ~:
I\ 0
D 2,3-Diphosphoglycerate (2,3-DPG) binds the a chains of
haemoglobin .
;l. 0
E 1 "f!ieJ.lres!';nce of methaemoglobin will increase thejHofnerl, _.,
lconstant I
- ---
1- -
q
0 c.'\
• ,
<-· -
, .., ,
1$,•'\t,\W'-"'\
-....._.1
'A·.
s,\;_ llf_~~/ c--,~,1::----t ~

C, ~ \(\A\-. j , ~ \-\ G

.:,
Physio/9gy MCQs

3.11 All'\lsweir§~

® A True
® B false
® C True
(9 D True
© E True
PVR =~P-~ LAP) ~co·,
where PAP= pulmonary artery pressure, LAP= left atrial pressure
and CO = cardiac output
::::(}' A good anaesthetic decreases PVR,~ patient who is calm,
anaesthetised, warm, well oxygenated, normocapnic and with
normal pH. ·

3.12 Answers:
e A True
• B False
0 C True
• D False
0 E False
2
/ Each haemoglobin_.binds on~ Fe +.
/
, Four haem_molecules form o~_b_aemoglobin, which can carry
/ f':?ur o~y~.D_"-1ole,cules.
,., 2,3-DPG binds to the j! chains of deoxyge_nated__haemoglobin, ).

changing protein conformation and decreasi_ng~xygen affinity, so


shifting the oxygen dissociation curve to the right)
gt_
1heri:i"ofner con5!a_!l!]s the volu!,lle (measuredin millilitres)
~~J) r,m:ied b_y_ 1 g hill,..moglobin. ty~r~a_sed ifthe level of
I
l - non-oxygen-binding globin increases,.~g,1with methaemoglobin.

1\:,
"
·1
': ·, '

I
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;-

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II
q
Physiology MCQs

3.13
The oxyhaemoglobin dissociation curve is $linfted to time right
wnilhi: ·
D A An increase in temperature
D B An increase in carbon monoxide
0 C An increase in 2,3-DPG
;

~o D Pregnancy
::l
~ I . 0 E Growth horrnone
./

(._.

/
/

( . ..,
,?'"
<.,
?,/

. ,.
Physiology MCQs

3.13 ATJS'W~l'l'§~

G A True
8 lB F.aise
~ C True
© D True
© E True

50% value = P5o .


75% value = venous blood
97% value = arterial blood
100
97!!--"''-- _

Percentage
Hb 50 I f

sat~ration

oV , , ,
3.5 5.3 -13.3
Po2_kPa

Figure: Oxyhoemoglobiri-dissociation curve

It helps to remember that an(~r~~uscl~ shifts the curve to


f~:' 1
the right. An exercising muscle will be hot, have high CO2 and be ·- ~
acidotic. ~ -===:~.:-;:.~

A shift to the right will decrease the=oxygen affinity of


haemoglobin and thereforep'romotes unloc!_~i~g of ox_ygen in the
tissues, --:--~--
The curve is shifted to the l~ft by methaemoglobinaemia, fetal
haemoglobin and carbon nionoxide poisoning.
Physiology IVICQs

3.14 Regarding gas carriage io11 ~~o~d~


, ,,.- D A Carbon dioxide in venous blood ·is carried predominantly as
,

D B
HC03
-
--·--.
- --- --· - . - ,.
·-· ·-
. ·--·------ - --
. ·---. · ·

Carbon ~i~2(!5Je is~i<1 as solub!~ in blood as oxygen L,U


'!- D C
The Haldane effect refeis·fu the increased oxyg_~n bin_ging
once one oxygen has bound to a haemoglobin molecule
·/ D D Anaemic patients wm have reduced dissolved oxygen ·
I

, compared with patients withnormal haemoglobin :


/DE Qxygen·has.an·affinity for haemoglobin approximately 240
times less-.,. than that of carbon monoxide . ----

'!,·· •.•. t.
• t,,

.~ .) ~· .. ......

~-'!.:

f" --~-

.,
"II/• t -.

$ ,) : ;. j

: ·-

'--~ ·•

. I
Physiology MCQs

3.L
3o14 Ami~weir$~
@ A True
• 1B false
e C faise
• D false
$ E True
- Carbon di~ide is approximately 20 t~s more soluble in blood
. when compared with oxygen. ~--::-::-=:::--
- 1he Haldane effect refers to the in~d aff~~i!Y o!_
~xygeMli<Lha~lobin to cany carbon dioxide. This i§
because reduced ha~~jn is tietter a61~ to bind hydrogen

('\
- , F, ions, so allawing for more transport of carbon dioxide as
d~ssolved in the blood. In ~~ition, the c,pniplex ~ ·
\ · . rogen 10n and reduced haemoglobm as then able to co~1-ne
l'
~ ~rbon d~ide !L~ to f°"'!lca~f11,i!!9~ which
again ancreases ns ·transport- · .
~~tients will have a decreasedc~ carriage ·
r secondary t~reased haemoglobin; however, the di~lved
Q~ !ill ~ reduced. --· .
-Remember: oxygen camage (ml 0]/100 ml blood)= (1.39 x Hb
x saturation) + 0.003 Al<>.z) in mmHg.

. 1

'
\
Physiology MCQs

3,1'5
Regardi111g chest wali moveme11t: -z__\, -1__: ,
't- D 0
A Most of the work of breathing is lo overcome the resistance in
~~M~ ---
I
. "-
8 The internal oblique musdes aid inspiration : .'/ -'-.-: .. ( ., ·,.

C The external intercostal ~uscle°;pull the rib cage upwards and


outwards -

D The internal intercostal muscles aid inspiration


E During exe.!:cise the diaphragm can descend up to 10 cm
-------- ~-- --..>

3.16 Compliance of the lung:


,/
, . D
A In the normal human ~is 200 ml/cmH20 ,, .
/o
' \ B Decreases in old age , ,. '
v-/0
C When specific compliance takes the lung size into account
/0 D Decreases du.ring an acute asthma attack 1 ·l
/. D
E Increases in patients with pulmonary oedema ,_.I,- ,.
\~

CII:

ca,

I
I_ •
Physiology MCQs

Atrnswers~ 3
3.15
0 A False
© B false
e C True
e D false
• E True
;yiost of the work of breathirigJapproximately 65°/o) is to
overcome the elastic_wrk..Qttbe.lungs. This is why expiration in
quiet breathing is passive.
The internal obli~ rnuscles have no role in inspiration but can
assist~
~-- expiration. .
The il}!ernal intercostals aid fgrced expiration and move the rib
cage i~ds and downwards.
----- --- :::.--"'-· --

3.16 Answers:
• A True
@ B False :,,

• C True
• D false
• E False
There are a number of causes of li:i~r,e_~sE:,~_l~ng comr-lianc~
including old ag~ and emphysema, possibly due to the changes
elasticity of the tung. · ·· · · - · --·-
. -
Acute -
asthma increases compliance. The mechanism for this is
nQt clear. - - - -
A d~cr~ase in compliance is seen with pulmonaN fibrosis and
oe~a and with an in~re~se in pulmonary venous pressure.
SQe<;Jfi£_~ompJiao.ce allows the comparison of compliance in
different sized lungs. ~ -

I
I
lI
I:
Physiology MCQs

3.17 Surfactant:
\o A !s synthesised by type lalveolar epithelial cells ; ·
:I
'
0 B
- ·-· - --- --- \_,..;;:.,
Has its main constituent, synthesised from amino acids in the
'

lung
0 C Helps to keep the alveoli dry
''
, ;
;
D D Production is affected by i°m-oking
'/ / D E
Production is partly under the control of the hrn.9, thalamic-
pituitary-adr~nal axis ··
3.n
3.18 Regarding[ ai;;;;y-~~~j .
b ·!.,_ D A It predominan.tly occurs in the segmental bronchi · i ,, ,,

i'< D B During turbulent flow, flow rate is proportional to pressure


·/ D C The use of helium decreases turbulence as it decreases
viscosity of the gas I

,/D D It is calculated by the pressure difference between the alveoli


and-the_!]l_9Uth djyj~ea hy' a flow rate ~ I ' .
1
, D E -[)u~ing quiet respiration the oxygen cost of breathing is
,, f' • I '

approximately)O% · -· ,,

...
t
I_~ f
f
"
Physiology MCQs

3.17 Answers:
;;;, A False
(i) B False
e C True
• D True
E True r··-------· - .... ·--- --------------
Surfactant is synthesised by1!_ypJULalyeol~r_ep_itheJj~l._<;:e!l~~
The main constituent is(cfipalmitoylpfiosphc:tidylcholine,1 which is
synthesised from~ in the lung. It is thought to have its
effect secondarv to the strong repulsion of neighbouring
hydrophilic parts that push each other aw_ay and so splint the
alveoli open (most noticeably when at low volumes).
Production is reduced in areas of 12oor p~_rfu~i9_11. and in h_~a..Y.Y...
smokers. The cells responsible for the production of surfactant
begin to appear at 24 week~ of fetal gestation.
--- -
. .;•-·

3.18 Answers:

• A False
• B False
• C False
• D True
0 E False-· ········-----, .· -·--- -- .
.
Most (airway resistance \js encounte~d at the ~~r_m~ng_l bronchi.:
with ~~lJ.gt.~0_% of resistance occurring b:)'~ airways of less
than .2 , mm
. in diameter. ·
During t~rbulen!Jlow, flow rate is proportional to the square root-
i
' of the pressur,e. ~i
II''

I Aelium decreases the gg_osjt_y not the vLs~i!y°"of gas mixtures. t ., ,


·,
·,...,

\ Remember that during turbulent flow ,decreasfng the d@filt.Y is


:I important compared with d~cre.,gsing the viscosity in laminar flow.
\I.
I.
The Qis¥g~n.c~1 of breathing.!.luring'quiet respiration is 5-10% L.,
i\
- but during exertion this can increase to 30%. .z:-- i '
I

,i
I
---~
----·---
---···-··---
'

I I
!
i'.\i
·'
,./

Physiology ua» r· (
( \

J.19 The ffoUowsng are true of tne


. ·a;entral
. - ..
,.,
~ntrol
..._ -·
of breathing: ~
,/ 0 A Dorsal rnedullary cells are thought to be involved in t_rfggering
respiration
.. .. . . . · -- ·
t.// 0 B Nerves terminating in!h? tractus solitariu_§_affe.ct inspiratory
cells .j GI;·( vS~ /
4
'
; ~ (:::, c,\
) ._,, i ~ ---~-<!~ :, ,--~~ c.;'<~

,/ 0 C -Th;~pper pon_s is thought to regulate inspiratory volume


!/ 0 D The apneustic ~~ntre is si_tuated i~ the I~~~~ pons
-- ~·-
./0
/

E The expiratory, c~lls,of the medulla are inactive during quiet


respiration

3.20 Regarding[chl!moregptOr~ and their function: /'----.. J~ ,. , : , , 'G}


'/ 0 A Central chemoreceptors are situated within the t!!_edulla J . , I l

/
;-
0 B Dissolved carbon dioxide in the cerebrospinal fluid (CSF) acts
I

directly on the central chemoreceP-tQrs to bring about a change


in ventilation
Acidosis is compensated for more quickly in the ~_riaL
circulation when compared with the CSF , ·
Carotid body chemoreceptors respond to co2p2 and pH
changes
0 E Aortic body chemorec~_e!Qrs respond to changes in pH/ ·
------······ .. -··- --·····----·--;::,-·-~

11'
L_ !

Iii
Physiology MCQs

3.19 Answers:
e A True
~ B True
6) C True
@ D True
e E True
~ -
. . - ----·-
. \
/ ·porsal medu_U?.J:¥- cells' are thought to be mainly associated with
. inspiration.
/ iyentral -~-~g_ulJ~ cells are thought to control expirat~on and are
~ctive during forced expiration. ·· · · - · --·-
~-r-------- _ _,_, __ -·- ~-··· -- -- - ---
The~Q_(~rJ~OnS jhouses the ~!ffil...Q@_?<i~_cen1rm which is thought
. to inhibit inspiration and therefore control tidal volume and
respiratory rate. Th~wer pqrr~houses the apneustic centre,
which in animal studies increase the inspiratory period.
Vagus and glos?~_P.h'l.'.YD-g~nerv~_s_ terminate in the tr~f!IJS.
I ----- - .,
solitarius and affect the inspiratory dorsal _medullary cells,

3.20 Answers:
• A False
• B False
• C False
~ D True
E False
\
I I Central chemorecep,!_or~ a~~ outsid~ the respiratol'.¥.::Centre, b~ow
'
!1I
the ventral surface of the mg_~ulla. They respond directly to
I
!
changes in hydrogen ions because of carbon dioxide dissoci~tion.
\'\- A change in ~Hin the CSF is guicJsly compensated for with
HC0 - tran~P-Qrt across the blood-brain barrier. This-occurs more
3
I quickly than the process of renal co!D_p_~ns.a.tion for arterial
acidosis.
11-
I' '
\ -Carotid body chemoreceptors respond to pH, 02 and CO2. Aortic
\'
I'
I
·2-· body chemoreceptors respond to changes in 02 and CO2 but not
to changes in pH. ~ -

\,
Physiology MCQs

3.21 Whellil studying the control of weirotifatnollil~


0 A The Hering-Breuer reflex i~. activated by a large l!!_spiratory
volume of gr~ater than 1 litre -= -
·/ D B I-receptor stimulation leads to deep inspiration · ~,. ,..,' · ~ ( . ,-

D C Carbon dioxide levels are the main factor in the control of


ventilation
/ .

1// D D The ventilatory response to carbon dioxide is decreased if the·


work of breathing is, increased
./ D E In the absence of peripher~.l_chemoreceptors, hypoxaemia
depresses ventilation -,: , \, J

3.22Regarding the respiratory system !during exer~~~-=)


1"0A Oxygen consumption increases exponentially · .- ~
~D B Respiratory quotient or respiratory exchange ratio decreases . 4,/
• ./'
1

Vo C There is an increase in the diffusing capacity of the lung ..,..


X D D Ventilat!i:dn and cardiac output increase by similar values 4-\~· ~.)
1'0 E There is aJMge-d1fference between inspired and expired - V\·· ,.. •

oxygen concentrations (when compared with non-exercising


values)

r
Physiology MCQs

3.21 Answers:
El) A True
e B False
e C True
D True
• E True
The Hering-Breuer reflex causes an increase in ~piratory tim~
triggered by a larg~Jn~~lrn.tory .volume that is detected by
. pul~v.trgtch receptors.
( J -fc;r juxtacaQill~!:¥! receg_to~are thought to be found in the
alveol~tls. They respond to p_1:-1Jm~n~ry:_S~PJJ.@cy. engorgement
and i~~ma and cause ~h.a!!gwJaw_9A~athing .. (via
non-myelinated vagal fibres). --
Hypoxafilllia is detected only 'by peripheral chemQreceQ!ors and,
without them, the respiratory centre is actually depressed by a
decrease in oxygen.

3.22' Answers:
• A False
• B False
• C True
• D False
e E False
Oxygen consumption increases lmeally until reaching a Rlat~au
at the 0 max. ----· - - ·-
2
-== quotient (normally quoted as 0.8) increases as
Respiratory
carbohydrate becomes the main en~rgy_~ource rather than fu!..
Diffusing capacity of the lungs increases as there is i_!_l~.reased
alveolar capjllary_ interface secondary to recruitment of
capillaries.
Ventilation increases approximately ~
.
four times)hat of cardiac

.
output. · _:::~
The difference between exercising and n9.n:-exercising inspired
and expired oxygen values .is minim_aL ./
Reference: Physiologkal effectsof ·exercise. Continuing Education
in Anaesthesia, Critical Care and Pain 2004; 4(6}: 185-6.
Physiology MCQs

. 3.23 Regarding respiration at altitude:


, /o A Once the. barometric pressure is -~
below 6.3- k~ the inspired
oxygen concentration is zero ·· ·
,,
D B Th; k;y to altitude survival is hyperventilation: .,0-t)·,,; :;,,,::"1'
,
y D C - - - ·-, + • ·- 4. • ...••• -------

~erventil a!~on increases !in~ady during the first 7 days at


altitude -- r - -
./ 0 D
Erythropoietin production means that the oxygen-carrying
capacity of6lood·can.. be above normal
.// D E
At very high altitudes, breathing is aided by decreased density
of gas

3.24 Regarding the respiratory effects of diving: _


(· D A Pressure increases by 1 atmosphere per 100 metres ' :.J
.
,, D B Risk of 'the-:--
/
bends' increases with increasing depth of dive
I D C Helium :· oxygg_~_mJ.x can be used to decrease the incidence of
,,

/ nitroge!l narcosis when diving


,,,,.

L/ 0 D q~yg~'"! toxicltv can lead to c_o_n_~~!_~ions __


/ D E Hydrogen can be used as a gas mix with oxygen for deep dives

;
I

I
/
/
l
I

I r
I/
r '~'
=!
I ,I
\
~ ~ -=-

Physiology MCQs

3.23 A.trn§W€[!'§~

0 A True
@ B True
tv ·C False
e D True
@ E True
The initictl acclimatisation response to high altitude is
h~ aJlon. This is driven by the hypoxic stimulation of
peripheral chemoreceptors. : , f'/ -------
Hyperventilatio_n continues unt'il halted by a decre.ase in carbon
dioxide and respiratory alkalosis (before 7 days), which is
detected by the ~entral_ and p_erigheral chemoreceptors. The .£.~F
pH
- is corrected first then the arterial Qtlis corrected after
::,:..:=---I"'
approximately 2-3 days. Once corrected, hyperventilation
continues. With time, carotid
~ .-,- .
_body sensitivity to hypoxia
decreases. -
Cll 1

3.24 Answers:

• A False
e B True
C True
D True
E True
Pressure increases by 1~ per l_Q_m. The risk of developing 'the
bends' or nitrogen narcosis is greater with l. 9n~r, deeper dives as
this increases the Rartial pressure of l'!lli:Qgen and therefore forces
the insoluble gas into tissues.
Heiium-:0xygen mb< can be used for deep dives as· ocreases
the risk of n_!!rogen narcosis and also decreases the density, so
decreases the work of breathing.
Q5ygen to«.klty can he preceded by ringing in the ears and facial t·

twitching and can occur at partial pressures of oxygen exceeding


1 atm. ~~-- · · --- · -

----
Physiology MCQs

3o25 Hypo¾k pulmon<011ry vasocorn§irrktnoirn (lHl!P'V) n§ ollilhibnte©l tby~


x: D A Hypercapnla ''"),A·
, D B High left atrial pressure
' D C Vasoconstrictors .,,, '-Jt::>
, ./ D D Lung handling at surgery
0 E High pulmonary ~erial Po2 '-~-
Physiology MCQs

1 .,.
j

3.25 A.il1lSWefi"§~

0 A False
(j) B True
® C False
Ii D True
41) E false
HPVoccurs when the smooth
___. ~ muscle around arterioles
-- -·--···-,---s, . . .., contracts,

. so r~~cing blood supply to the alveolar. How iJ pccurs is


unknown but deinne~ted I~ is able to produce.the effect.and
so it is presumed not to be iiiider central g2ntrol.
It is mainly driven by a decrease in alveolar P02 (~~~r_
---------- ial).
-
H_yQOCapnja inhibits hypoxic pulmonary vasoconstriction .
-~-
_____ _
yasoglt~!Qrs inhibit hypoxic pulmonary vasoconstriction.
__.._ _,,.::-.~

t.:;

L
\
(YviI' r
. '
:-l-:-r !-· / - -·-, r
I-~. ~-, I,.-;_
-:-- , Physiology MCQs

J.l10> fRegardfiililg calclum. ·:- , ;,1_


0 A Approximateiy 70°/o of total calcium in blood is protein bound
D B Acidosis increases ionised calcium concentration
·-·-·· -··--·

D C for every gram per litre albumin < 40 g/1 in blood, 0.02 mmol/
I must be added to obtain a true total plasma calcium value
D D Hypercalcaemia causes a prolongation of the QT interval on
an ECG 1 , __ 1• • •

(
D E The main site of calcium regulation in the kidney is in the
proximal tubule -;,(, _, ··
~ .;1,..-lr--'-·-- ·- ••- . ... ·· --

Physiology MCQs

3.2fi A:rnswer§;
€) A false
6)1B True
0 C True
e D False
~ E False
/ Approximately 50~-of total plasma calcium exists in the
biologically active ionised form, with the non-diffusible calcium
bound to albumin (predominantly) and ---~ glob in. A total of '99% of
total body calcium is in bone.
/ A_sidosis increases ionised calcium. H_yperventmtion causes
alkalosis with a decrease in ionised calcium, which presents as
tetany, carpopedal spasm or laryngeal stridor.
/ For each~.1 decrease in pH, ic:i_nised calclurn rises by "1'
approximately 0.05 mmol/l. -=-=-
J,,;, .
\v
~'J-'
/ (~bsorption of calcium occurs predominantly in the ileum.
-~v~bsorption, which is dependent on vitamin D occurs in the
duodenum, ~unum and l_arge intesti~e. _ _
f ,,· A total of(i(so/q)of renally filtered calc1u~bsorbed, 60°/o in
the proxi~ tubule. However, it is the djsjaUubule that controls
a~ ium levels under the influence o(pai;athy.!Qi.d.J
hor_n1-one.
l"t¥RQCpJcaemia prolongs the QT interval. Hypercalca~mia
shortens it. --- ·- --
Reference: Thyroid and parathyroid hormones and calcium
homeostasis. Anaesthesia and Intensive Care Medicine 2005; 6:
333-6.
Fhysiology MCQs

3.27
D

0
-,
D C
v D D

/ D E

3.28 tements regarding thyroid hormones are


correct:
0 -releasing hormone) is a tripeptide secreted by the

D .. -- , -
. , 0 C TSH '"a.·

ccs: ~,c1..,.... _
D
·/ 0
nine (T3) and T4 inhibit the release of TRH
Physiology MCQs \ I ., \~ ,'\ ')
..-e-ltv-:-) r'--. ~.
:J L\D V'
\~ -

3.27 . . L. ·~\!.{~J-,·c.\~ .. )C >- .,,v-e- ~- -\)(<-~~~ --I_"":';:,


\c-c\,,}J._ .-----> -~ ~
' ~ \ \Oc\ l "\(.:., l"'-'2_
c)
© A True \ \- ~ ,, --- y o
(111.,d\c, ec 'v -;'f;...j) ./0----
./
B False , .:-?-~~
.·,i\c ,\c.: -\- c}. \ -
C Fase
I , . ~-
0 True c'-' ~ c.~,. ·--- c-~-""'<> ·L\ ) \~ __-0\·3
8 E __Jrue
r'- 'i
--=·
,R~ ~--
.,V'\,.,,.,v-~J ">~ ~ ,..---._,
(!"SHjincreases iodide (I-) absorption from the gut. fu_dide}is
. actively taken up into the thyroid follicular cells where it is
oxidised to form iodine. A process catalysed by Qeroxidas~ on the
apical membrane of the follicular cells (hydrogen peroxide
accepts the electron). -
Once formed, iodin~ then binds to trrosin~ in thyroglobulin ~o , _
form monoiodcifyrosine and then diiodotyrosin~. \O cf, >·,c, '>

Cond~nsation ~f two di-i~dotyrosi~e fo~ms T4• Condensatio~.o~ ., t:-


monoiodotyroslne and dilodoryroslne yields T3• ?~J(J-, '
Reference: Thyroid and parathyroid hormones and calcium
homeostasis. Anaesthesia and Intensive Care Medicine 2005; 6:
333-6.

3.28 Answers:
• A True
• B False
• C True
• D False
• E True
TRH acts via Eli_ospholipase C)resulting in increased calcium
releas_e. from endoplasmic retiCulum~ actiVatlOn of(protein J
~~ase CJ Thi~uses the release of SH\from the pituitary.
'_.,,)

~SHJacts ·via (~AM}Jstimulating ·~~~(n-kt~j


,__,
®is initially the deiodinated to T3, which then binds to
Iritracellular receptors. This initiates nuclear gene transcription so
increasing messenger RNA., which activates cytoplasmic
ribosomes and increases cellular protein synthesis.
Physiology MCQs

3.29 !Essefl1ltial ~mnR10 adds obtained from the diet include:


Vo A Tyrosine - /~~ \\\.-~s?fV\
~/_,,O B Methionine " 'y~1 / / /1 1
/ ,,

D C leucine .,, c')~-


, D D Glutamine ·
D E Aminobutyric acid

3.30 Hepatic physiology: ~Q"" o


D A The portal triad contains the hepatic vein
_ ----- o B The periportal hepatocytes receive the most oxygenated blood
supply v.
/lcf" ••.• ,.,,,., -;, j-1'-

__ ./-[J C The centrilobular hepatocytes are the main site of drug


biotransformation
/ D D Hepatocytes outnumber Kupffer cells · · "- '
?"- D E In an adult, Kupffer cells have haematopoetic function \~"\ "'-\
fl'..:>-d~.;)q v,

L
Physiology MCQs \-
L- \ v ,--,
r .
i.-:e: .• ' ~- r ,, •• __.-.

- \' ,,. ';·\,-. _?

if:) A True c:; \._


iB True _ ' · -r,.~ ::. . ~·
C True . (---. 1 '---, , ...•
D False - - -~ · --~.._
E fa I se
Essential amino acids obtained from diet inc ude valineL
£ · - ·
:\ - \
,._ ~'( -c.,.?
I I ,.

y,
/ (_..,(

,,;,_..c...

. isoleucine, methionine, phenylalanine, tyrosine, lysin~ leucine


and threonine:i"hese are all ess~ntial for life.
Ar~nin<:_ a.~d histidine are essential for growth no~fe.
!--A_very
I -· --~------· ·- . , ~- ., - -~----·- '

simp~_~_pneu~~nic may .fi~_!p-you remefr!ber,;..~ 3


- -- · ' )

Very!mportant little things. o:> _ 1 ~ ( ____-::;- \ lr ..> }- _)


V from very . -~ ----· '->

IMPT in important ., \' J:\ \ - _..,; \J_ ~ ~ ,rf\


(I LL in little -:-\'f?)) \"'1 \ ' (QI \
~ . h. /
<t er
. •.....•'\,;
T1n.t mgs. ----
-<._..J. Reference: Power I, Kam P. Principles of Physiology for the
,« .,
Anaesthetist., p. 318, Hodder Arnold, 2001.
~~-

3.30 Answers:
• A False
e B True
o C True
• D True
• E False
The portal triad consists of the portal vein, hepatic artery and bile
duct. · -
The e,~orta_l__ 2-_one surrounds the heggil_c...~fil!:()le and is highest
in oxygen content and has the highest metabolic rate. This zone is
mostly involved with pJotein sy~tbesi~~ --
Kupffer celJs are macrophages. They only have significant
haematopoetic function in the fetus.
Physiology MCQs

JoJ 1 /Regiotl!'dJH!rng carbohydrate metabol o§m~ I ~ ,:_;, .>

\ D A Healthy adult livers contain approximateiy~1fg glyc~gen


?'- D !l Gluconeogenesis in the liver is facjlitated by .insulin J i ,
' D C Insulin secretion is stim_olated by a decreased portal blood J ,i,,
sugar / '

D D Thirty-eight ATP molecules are produced by the aerobic


metabolism of glucose
D E Glycogen formation in the liver is under the control of two
enzymes: glycogen synthetase and glycogen phosphorylase

3.32 Regarding lipid _metabolism:


D A 50% of t_ctglxcerides from diet are ~>-'<lli>ly.sed to glycerol and
fatty acids
0 B Short-chai!:I· fany acids are transported directly to the live~ by
the portal vein -
D C Chylomic;:JQ_ns consist-of lpng-ch~in_fa!_ty_acjd_s that have been
re-esterified and covered in phospholipids and protein layer
. ., /D D 1_:_n,,e)atty ac_ids are produced by the effect of lipoprotein lipase
on c_~.Y!9.!!Ji~ro_ris
. _ D E Acetyl-CoA is formed by the metabolism off~~~d~
Physiology MCQs

3. 1 ~- Ai1ilsWefl'§~

0 A fa\se
@ B False
e C Fa\se
e D True
o E True
Healthy liver conta_ins approximately 1-QQ$.glycogen.
Two ~TP molecules are yielded from lheb~~akdown of glucose to
pyr"Uvate and a further J6 A!!' molecules are produced from the
breakdown of pyruvate"ir1 the tricarboxylic
-==--"'"
acid
~
cycle.
-
G\uconeoge_~~ is facilitated by g\~c~on, which increases
a~anine transport into the _hepa!9cytes and py_r\jva~e into the
mitochondria. ·
\~ulin _secretion is stimulated by l}jgh portal blood sugar. It causes
inhibfilon of glycogen~ysis and glUConeogenesis but stimulates
pyruvate dehydrogenase and glucose phosphorylation to form
tlycogeri: -- - ·· ·· · - -- -------- •,
-------··,..
3.32 Answers:
• A True
• B True
o C True
• D True
• E True
Approximately 40-50% of dietary triglycerides are partially
hydrolysed to monoglyClcrides. ·· - ';t···;
\,Q!lg-chain fa'!}' aci~are over 12 carbon atoms long. They are re-
esterified after absorption, then covered with phospholipids and a
protein layer to form chylomicrons.
_bi!!Qim>tcin.lipase hydrolyses the chylomicrons to produce free
I ,
fatty acids.
The continued oxidation of acetyl-CoA yields ketone bodies.
------·
Physiology MCQs

J.JJ itegatLrrdli~g !the physfofogy of bile:


D A Approximately the same amounts of bile and saliva are

D B
produced per day .
-
~ile salts are made in the liver from fatty acids
-
D C Unconjugated bilirubin is water soluble '' ,
D D Urobilinogen is formed from unconjugated bilirubin__::, .
D E Stercobilinogen is formed in 1he liver,,, ,,-,----,j v_k.
3.34 Protein metabolism:
y D
A Serum albumin has a half-life of !.Q d<!c~.
D B
Raised lasma luca on levels stimulate the catabolism of
amino acids in the Ii~ , · -----..;;..:,.;·--~. ,
D C
AhTP molecu 1es are produce~en c0_and il_"!'!J~a ~t~r
1
t e urea eye 1 e '-----" ,
D D
The l!rea cycle occurs in liver and "!,IJscl!!s _,
,,,.,- ,, /0 E
Deaminafed alanine can enter~e &!.ucone_ogenic;...e,athwa}'. as
py~~va~:. *o ~~~ (;;\#~
Physiology MCQs

3.33 Answers:
•-, ... ~
.,--. \ ' -. -
@ A True - .. -· .
_'f., ;,-.

:" - \

B False . -(:-~.;.1 ·:'


/
, :r ~1-~
®

C False '"'7;]
e ~ ,i
'r--, 1.,, ; . .,1-r "- . . ..
I '

(t D False --·
• E False
Approximately I litr~ of bile is produced per day.
· Bile -~s are produced from c_~oLe_s_ten~_I in the liver. Once these
b~_ai;_i_ds have been acted on in the gut they form secondgry bile
acids. When coniug~!~9 with tau_~~ or glyci~e, ~ile salts are
formed. ------- -- --~ -
-~--_, Haemog!Q!?in is converted first to biliverdin tlien to bilirubin,
which is bound to_aj]:>_µmin and transported to the liver. lnllie liver
,-:.C7 it is conjugates! with glucuronides {now it is water soluble.) It is

excreted in bile. - - -
-~ Q~ia cause the formation of ilil!}:obilio.ogen {passed out in
"""' stool} and urobilin_ggen, which passes into'the portal circulation

--·
and is excreted in the urine. - -

3.34 Answers:

• A False
• B True
• C False
• D False
• E True
~~lbur;nin has a half-life of ~9 qa¥s.
Breakdown of a_:r:ninp_;1i::ids is via oxidative de~~n. Initially t~
amino groups are removed and eventually form glutamate and I

aspilri:ate. Glutamate forms ammonia under the influence of


glutamate dehy~_na~e.
t:,spartate, ammonia and CO2{+ 2 ATP_molecules} enter the urea
cycle to torm··urea~-The uieacycle canno~take place in muscle, so
the transaminated amino acids pass to fl{e liver in the form of
alanine. Deaminated alanine is m:rJJ}';!!e, which can therefore
enter the glucon~og
--·
en·i~-pathwayto
-------~ --- - -
•.
become glucose.
-- .... --
Physiology MCQs

3.35 tltega11rdlnITT1g the systemic CDll'C(Ul~dltHOlll:


--,, ,
D A At rest two-thirds of the capillaries are patent
I,,- D ! -:_ ·- (

B The velocity of blood through veins is greater than through the


capillaries I

-../
/' -=7-:- .
D C In a supine patient blood is divided equally between systemic
and pulmonary circulations , ..
y_
D D The Windkessel effect refers to the prevention of retrogra@ .

,,,D
flow by the venous circulation · ·1, - · -· : ".,. ·._\ -\ \ >' · · ~-
E Resting cardiac output is approximately 5-6 I/min

3.36 The following are correct approximate values for blood flow to
organs:
·:< D A The brain receives 500 ml/min
\/ D B The coronary circulation receives 250 ml/min ,- ..
;?( D '
C The kidneys receive 750 ml/min (total) \\ 0 '-.:>
;< D r>' Skeletal muscle at rest receives 250 ml/min
;< D
E Abdominal organs receive 1 I/min I t.J ~-j ~
Physiology MCQs

3t35 Allil$Wfli§:

~ A false
It) B True
G C false
@> D false
e E True
At rest only a quarter of the systemic capillaries are patent.
· Relative velocities are as follows:
• aorta 2 0 cm/s.
• capillaries 0.5 mm/s.
• vena cava 1 2 cm/s.
In a supine patient 75% of blood volume is in the systemic
circulation compared with 16% in the pulmonary circulation and
8% in-the heart.
The Windkessel effect refers to the conversion of the intermittent
ventricular output of blQ_od i~~ a contfnuolls puisatile_arterial
flow. It results from the stored potential energy in the elastic walls
of the aorta.

3.36 Answers:
0 A False
• B True
C False

• D False
• E False
Approximate blood flow (ml/min)
Organ
750
Brain 250.
Coronary circulation --- .,_ I

I 1100
- --
Kidneys 14QO
Abdominal organs 500
\ Skin 1200
Skeletal muscle (at rest)

I
i
i.
Skeletal muscle (active)
20000
------------------------------· --------------
Physiology MCQs

3.37 Cardiac mu§de fibres:


D A Between right and left atria are continuous
I

D B Have no striations
'o C Form a true syncytium s-00~~ G.\\. \
\

D D Are shorter and thicker than skeletal muscle fibres


D E Form networks with intercalated discs between fibres
containing gap junctions

3.38 Regarding myocardial tissue physiology:


D A Myocardial oxygen consumption is 8-1 O ml/min per 100 g
tissue

D 8 Myocardial oxygen consumption is greater than brain oxygen


consumption
D C Approximate coronary venous blood oxygen content is
5 ml/100 ml blood
r=-R
1 X" D D Carbohydrate and lactate make up the F.aain energy substrate
· of the heart
, I .
,\ D E Oxygen extraction by cardiac muscle increases significantly
=-' during exercise
Physiology MCQs

3o37 Anlswen~
® A True
e B False
9 C False
o D True
~ E True
Continuous muscle fibres between the right and left atria enable
them to contract simultaneously. (There are also continuous
muscle fibres between the right and left ventricles.)
Cardiac muscle is striated similar to skeletal muscle but it does, ~~t
form a true syncytium as each myocardial c~ll has its own n~cTeus
within its b'wn7l'le-mbrane (rather than a mast9W~~(!Plasm with
many nuclei forming one cell). -- -
However, due to the connections between adjacent cells, cardiac
muscle acts as a fu~ctional syncytium.

3.38 Answers:
~ A True
• B True
• C True
• D False
~ E False
Brain uses 3-:_?_!!ll Q2/min pe~-~90 g tissue.
The predominant cardiac substrate of metabolism is esterified and
non-esterified fatty acids at 60% compared with carbohydrate at
40%.
Myocardial oxygen extraction at rest is almost§~, the only
practical way to increase oxygen delivery to theneart is to
increase the blood flow.

_ '. I
Physiology MCQs

3.39 !R(E?gawdJn!l'Bg Ve!l'!Jiil'B«:l!l~alfl" muscle action [!})(O)!<e!l1lia~~§~


·/
,/, D A Phase O is the result of calcium channel opening
I D B Phase 1 is the result of calcium channel opening
'
\
, D C Phase 4 has a resting potential of -70 mV
D D Phase 2 is the plateau phase
,.,. D E Phase 3 sees a return to normal permeability of potassium,
calcium and sodium
Physiology MCQs
\._ \
--: r

3,3«J Answers:
© A false ., ,
B False ...... : -•,~·· \I
e
© C False c-
.....__

• D True <. .~
® E True > C I I
I
"K½
../ V
) ('
~ 1 ' ... (J
',
+20 "'
I ,_ 2 '
\

\
Membrane 0
potential
(mV) 4
-90
.,
300 Time (ms)

Figure: Cardiac action potential

Resting membrane potential is -90 mV during phase 4 secondary


to _potassiumpermeability. h J / -.
' .

Phase o se~s an increase in permeability to sodium as fa~


channels open. Potassium conductanee decreases.
Phase 1 is partial repolarisation as SQdiuf!ll?ermeability decreases. l,l
Phase 2 is the plateau as calcium')ermeability rises on the tf
background of a decrease in sodium permeability.
Phase 3 sees a return to normal permeability as in option E. ~~:t.s L-sJ
' "7. -.\ ( • ---, ( ""- -J
Vt / ... - 1.j I "' , ·. f o "°"' ' " ,
\J. L,1 ~

I
\ I
Physiology MCQs

3 .40 Action
\
potential of the SA/AV node:
I D A Phase O sodium enters the cell C°'-
, D B Phase 4 calcium enters via I-type channels -~
D C Phase 3 potassium flows out of the cell --
D D Parasympathetic nervous supply increases potassium
./
/
permeability
_,/ D E The rate of depolarisation in phase 4 is slower in the
atrioventricular (AV) compared with the sinoatrial (SA) node
Physiology MCQs

3.40 Answers~

Ii' A false
~ B false
• C True
@ D True
• E True

. Membrane
potential
(mV)

-50

-100 I I
300
• I Time (ms)

Figure: Sinootriol node action potential

Phase 4 is secondary to a decrease in potassium permeability and


an increase in calcium influx via T-type channels.
The threshold potential is reached at -50 mV, leading to phase O
depolarisation via L-type calcium channels.
Phase 3 is repolarisation and is secondary to potassium efflux.
Parasympathetic innovation increases potassium permeability,
inhibiting cardiac activity. Sympathetic innovation increases
calcium channel opening.

;.
Physiology MCQs

3.41 Cair[lluovascular pilhysnofoigy:. ~; ~ ,, . __ 2-


X D A The absolute refractory period of myocardial fibres is )S{)ms..,

/ 0 B Catecholamine action on the heart is mediated by Gq-coupled


phospholipase C
,___.....,-·o C Digoxin increases intracellular sodium
, / D D The natural SA node discharge rate is 100 beats/min
"<_ D E Bachmann's bundle is within the bundle of His ;f1

3.42 With reference to the ECG:


D A The normal QT interval is 0.45-0.55 s J-s s -
D B lead 1 records between the right arm and left leg
-/ D C The normal second heart sound is heard at the beginning of
the R wave 1 -- , - - -

·_,/· .- D D lsovolumetric contraction coincides with the R wave


.,
>,,. D E Aortic pressure is at its highest immediately before the Twave
.,
Physiology MCQs

3.4

A false
B False
C True
• D True
E false
The absolute refractory period is 4.Q9,.,ms. The relative refractory
. period is,~ ms.
1 -=-
Catecholamines act via ~1-receptors, ie Gs-coupled adenylyl
cyclase to increase calcium channel opening. They also
phosphorylate rnyosin and phospholarnban (iesponsible for
calcium, reuptake)and so increase both contraction and
relaxation.
Digoxin inhibits the Na+K+-ATPase pump, thereby increasing -=
r1 //s°'--~ intracellular sodium and so indirectly increases intracellular
calcium, leading to an increase in force of contraction.
' t..\' I,-- '
' ,....••..
"i
,,.\
Bachmann's bundle transmits the action potential from the SA to
\
the left atrium. lt then travels to the AV node via internodal
pathways.

3.42 Answers:
• A False
• B False
• C False
• D True
• E True C:
A normal QT interval is 0.35-0.43 s. ,_
I •

lead 1 records between the right arm and left arm.


Lead 2 records between the right arm and left leg.
lead 3 records between the left arm and left leg. (This can be I .
remembered by the number of ls in the recording limbs, eg lead 3
~
has 3 ls - left arm and left leg.)
. ./ .••...•

an ECG.
--
The second heart sound is auscultated at the end of th~ T yvave on
~
Physiology M.CQs

3o43 Regardang cardiac physiology:


: D A Atrial contraction accounts for 40% of the end-diastolic
ventricular volume
./
D B Normal stroke volume i~ approximately 70 ml
-J D C The aortic valve closes after the pulmonary valve

- // D D An increased resting length of the papillary muscle increases


the sensitivity of troponin to calcium #
/DE Qyerstretched cardiac muscle produces a weak isometric
contraction
Physiology MCQs

3 .43 .All1lSWelr§~

G;I A False
0 B True
e C False
@ D True
0 E True
Atrial contraction accounts for 1 ~]Jt1/o of the end-diastolic
volume. -
The aortic valve doses before the pulmonary valve.
Option D is correct, it also increas~s the concentration of free
calcium within the cell and therefore increases the force of
contraction.
Overstretched fibres have a high resting tension but are unable to
produce a forceful contraction.
Physiology MCQs

-- -·-
------ - - -- . -
· '.L44 Regairdirng ili(e wentrkular unessuire-voh.ame..cll.llrve r<e~atfo>i!u§hap~
D A The pressure-volume loop for the right ventricle is almost
triangular
D B The area enclosed by the pressure-volume curve reflects the
stroke work done by the left ventricle
.
~"
/
D C An increase in preload significantly increases the area
enclosed by the pressure-volume curve of the left ventricle
D D During ischaemia the pressure-volume loop appears to lean
leftwards i .

/
/ D E The gradient of the end-systolic pressure-vo·iume line provides
an index of contractility
Physiology MCQs

3 .44 Answers~
ID A True
" B True
@ C True
® D False
e E True

'

' lsovolumetric
tsovolumetric contraction
relaxation

Pressure
i II i

\
Diastolic '
,v ,0

filling \.

End- Volume
End- diastolic
systolic volume
volume

figure: Leh ventricular pressure-volume loop


During isi:_haemia the pressure-volume curve leans rightwards.
lhis is as the fibres1 lengthen (rather than shorten) during
isovolumetric contraction because they bulge outwards and the
fibres shorten during isovolumetric relaxation. lhis shortening
may ~ active or recoil, related to the c~ ischaemic
ventricle. -~ ·1
Physiology MCQs

3.45 Regzurdln!l1lg the left ventricular pressl!.llre-voh.nme loop


/ oliilft~wp[l'~iats(OJ[li)~

- '--/,,,- ,,.0 A Compliance is reflected by the slope of the diastolic pressure-


volume curve
0 B Ejection fraction is a poor marker of systolic function v

,_ · D C The cardiac pump is ~e~ e~ergy efficient


0 D The triangle enclosed by the e~d-sys!Qlic pres~~re-volum_e
line, the end-diastolic pressure-volume line and the line
representing isovolumetric relaxation represents the amount of
potential energy_available during contraction
·o
~-·-·....
and -~~-~t generated
--- --
E The pressur~y_oJume area represents total mechanicalwork

/
3.46 Regarding the characteristics of blood and blood flow:
fD A Blood is a newtonian fluid
·/D .,
B In small blood vessels, the red cells occupy the central fast-
flowing stream rather than being adjacent to the lumen wall
ca,

0 C Plasma has a relative viscosity when compared with water


of (};g' , ? ·
';(, D D Capi I Iaries create the greatest resistance to blood flow
../ D E In small diameter vessels the apparent viscosity of bl~od
reduces, so reducing the pressure required to perfuse the
/ microcirculation

/
)
~;~ ... ~ ~,i~_:...- . =~L-

Physiology MCQs

3.45 Answers:
flD A True
~ B false
6) C False
• D True
(,I) E True
Com_plian1=e reflects ~olume change per unit change in pressure.
, · Ejection fraction = (end-diastolic vo~me [~I -:c end-systolic
vol~e [§Y]) + end-diastolic volume (EQV).
Ejection fraction is a ~-~o~ marker (?f ~ystoli~_funct~on. 0
lhe cardia~ump is nBJ:'. ef!!:!gy eff,icient: approximately 2_2, ~1
~st. E_ne~g~ 1,Qst Uat.
-----
lhe pressure-volume area is a summation of the ~~~cen,ergy
area and the e~ternal w91k_-~r~..a. ·

~~46 Answers:

• A False
• B True
• C False
• D False
• E True
N~wtonia_n fluid is a hoSQQg~neQ.l.!0lgig witb a viscosity
unaffected~ its flqw rate. Blood is non-newtonian.
Plasma is dearly more viscous than water second?ry to its
composition and therefore its relative.viscosity mustbe_bigher
-- D~.7).~
than that of water
Larger arterioles present the greatest resistance toJ!.ow. This is
- - -=
because there are fewer vessels in parallel and a gr~er
pro11ortion in series, leading to greater .summation ol resistance.
~ - -------
The decreased viscosity-of blood in small vessels is because the \
'--
red cells occupy the sll(ial, c~nt_ral, fa_§!:i:noving stream ~llo~ing
)
plasrna.to.Ilow slowly near the walls. I.
--- .. , - '

!· -1
Physiology MCQs

3.47 The following statements are correct relating to cardiac


,, physiology:
~. D A Mean arterial blood pressure (MABP) is calculated as diastolic
I
blood pressure+½ (systolic pressure - diastolic pressure)
'{__
D B Arterial pulse pressure = ½ (systolic pressure - diastolic
pressure)
/
,
\/ D C Following ventricular contraction only ,one-third of ejected ~
blood flows directly to the tissue; the remainder rem~ins in the
aorta
,-
j D D Arteries contain 40% of the circulating blood volume
/",,,- D E Pulmonary capillary wedge pressure (PCWIP~ is. needed to
' calculate left ventricular stroke work

-
·v-

I
Physiology MCQs

3.47 AITTJSW~il"$~

© A False
e B False
e C True
G D False
0 E True
Arterial puls~q;ire~sure is_systolic !,lood psessure - diastolic blood
· pressure.
MABP is diastolic+½ (systolic pressure -__diastolic pressure).
Upon ventricular contraction only a small proportion of blood is
propelled into the arteries/tissues; the remainder remains within
the aorta and acts to distend their elastic walls. This is because of
high impedance to flow but is important as it produces continuing
flow. of blood (the Windkessel effect, see Question 3,5).
Arteri~~ contain~ of circulating blood volume.
left ventricular stroke work= SV x (MABP - mean PCWP) x
O.Of36 - - •'
-----~--
where SV - stroke volume.

,.
I'
Physiology MCQs

· I JAB •
aurdill'ag the control of ~nerrfoiar §mooth muscle. tone:
~eg.
"/ 0 A A rising pressure causes relaxation of the muscular wail
\/,,,- D 18 local metabolic control may be responsible for the
hyperaemia seen after blood flow to an organ is temporarily
stopped ·
D
--~
\v·

muscle -
C Kallikreins indirectly cause
.
relaxation of vascular smooth

'" 0 D Thromboxane A is a vasodilator


2 • I ·, . ~-' ' ~·. ,·l
D E •••• J

Epinephrine causes predominantly vasoconstriction in al!


organs ,,-,
~
r
\
- ~
----

.,_

'--·
Physiology MCQs

3.48 AITT§W(E!!'§~

@ A false
~ B True
C, C True
i!) D False
f) E False
Smooth muscle in the arterioles sporitafleously contracts in
response to an increase in pressure wiThin the vessel.
The increase in blood flow tQJ!D organ after a decrease in -
perfusion is known as\reactive hyflerae!Tlla.)Actj~ hyperaemia ls
that observed with increasing tissue activLty. -- .
-----A is a powerful vasoconstrictor and platelet
,Jhr9mboxane
-~ 2 - ~ ..
aggregator. ·
Epinephrin~ acts o~ceQ_tQ!_S causing vasoconstriction and on
~~septo"rs causing vasod:Hatation. The balance of receptor
.,
sttrn-cilation determines the overall
...._response.
-
Kallikrein is responsible for ~c;tivation of ioactiveJdolns to active
forms that cause smooth muscle relaxation.

,--
1
I__.

t_,.
Physiology MCQs

3.49 R~gawdninig fetal dircu.datio!i1l: .


v,, D A The Fl;0 value for fetal haemoglobin is less than 3.6 kPa ·-- '.L '1

/' D B The partial pressure of oxygen in the umbilical vein is ~~:._


approximately 8 kPa · , , , 's 5 ~ 1-,,-,
A tissue flap known as the eustachian valve directs highly
oxygenated blood across the foramen ovale into the left atrium·
0 D
50% of the right ventricular ejectate enters the pulmonary , ·'
circulation .--
J O E ,
I The left ventricle receives approximately 65% of the venous --:. ·
return ;-0 __..

3.50 The effects of posture on the venous system include:


)( D A A decrease in hydrostatic venous pressure in the leg on
standing

'o B A reduction in the arterial and venous pressureJn.the.brain by


approximately 50 mm~g on st_a~~_i-ng •,
" D C Tue collapse of cerebral venous sinuses on standing
D The' rhythmic contraction of skeletal muscle in Jhe_ le~ to
reduce venous blood volume while standing
V D E The bi-directional flow of blood through the venous valves in .. · -
the lower limbs while standing
Physiology MCQs

3.49 Ainsw<ers:
® A True
@ B false
@ C True
c D False
@ E False
The Pso of adult haemoglobin is higher than that of fetal blood.
lherefore, fetal blood is able to obfuin oxygen from maternal
blood (see diagram in Answer 3.13). lhe umbilical vein transports
blood from the placenta to the fetus. lhe partial pressure of
oxygen in the umbilical vein is approximately 4.7 kPa (~80%
saturated). · · -
lhe pulmonary vascular resistance is high and therefore only
approximately 12 % of the right ventricle" output enters the
pulmonary circulation. lhe_ left ventricle receives only
approximately 35°/o of total venous return-
.,
Reference: lhe fetal circulation. Continuing Education in
Anaesthesia, Critical Care and Pain 2005; 5(4): 107-12.

3.50 Answers:
A False
• B True
• C false

• D True
l
• E False I
Standing obviously increases venous hydrostatic pressure of.the
leg secondary to gravitational forces. On standing the CSF .,, 1
pressure also falls, so maintaining a relatively constant "cerebral
venous transmural pressure. The cerebral.Yci.1tsiQUSE!S are also
held open by extravascular tissue even when the intravascular
pressure falls, heOC:e the high risk for air embolus in sitting - i
1.
L:,
position for cranial surgery.
Unidirectional valves ensure that venous leg drainage returns to
the heart. L.

!I:
Physiology MCQs

3e51 Valsalva's manoeuvre:


. '

D A Is performed by forced expiration against a dosed glottis to a


pressure of 40 c_mH2O for 1 0 seconds 'IV',._,_
1
· \ ~

D 1B Phase 1 causes an increase in heart rate


, /,,,, D C Phase 2 results in an increase in heart rate
,,. 0 D Phase 3 results from a sudden fall in intrathoracic pressure
D E A square-wave response may be seen in hypovolaemla

I
'LI
r1
'I ,
L
I
i I

~,
I
f
I .


I

'I

·1
Physiology MCQs

3.51 Answers:
® A False
© B False
11) C True
IO D True
8 E False
Valsalva's manoeuvre is a common physiological phenomenon
on which to be questioned.
There are four phases resulting from changes in intrathoracic
pressure.
The inltial force is~ot cmH20.
~~ase 1 results from an increase in intr_?th_QLacic pre__ssur:e causing
a brief rise in blood pressure, with an accompanying fall in heart
i rate.
. ({ Phase 2 results from increase in intrathoracic pressure causing
decrease venous return. To maintain cardiac output the heart rate
•:
_, increases.
. ,:2 \ With a sudden fall in intrathoracic pressure, having released the
- J ) \·
,. ·. r ' ••• .,- ._·, '~ pressure in phase 3~. there is a transient fall in blood pressure with
,~~•'\. """'
a rise in heartrate. -_;.
'1
Phase 4 results in overshoot as compensatory mechanisms
continue to operate despite restoration of venous return.
As square wave is seen in cardiac failure, cQ.!l_str.ictive pericarditis
or tamponade. -
0-- \ \j C ()
- -..
An exaggeration in fall in blood pressure is observed with
hypovolaemia. 7 7 I
I
i

I 2 l
'
I
1·) ..

~ Ii
~
'
L_
\
-..)
I I

. . rt:.""'~-'~, . "·
~-
rv- \·.
Physiology MCQs
_ ... ·.

Regarding cardiovascular r.esponses to exercise:


p A The initial rise in heart rate is secondary to a reduction in vagal

tone
' D B Blood flow to the brain .increases . . .
D C There is a linear increase in stroke volume as exercise \;· . : :' : ::
} . . '

increases -i
D D When exercise stops there is an abrupt decrease in cardiac t:~ .
, ..

output L.:::·
I . :.:·.
D E Diastolic blood pressure may fall during exercise )_.,··.· =:
..,. '

r
Physiology MCQs

3.52 Airnsweirs;

@ A True
(1) B False
.. : ... ·· ; o C False
.
....
. .
'
' ..
·. 9 D True
.
. ~.:·· . ...... ·1·: 9 E True
·~
I Initially a reduction in ;vagal to~ leads to an increase in heart
.· · ,
. \ · rate. latterly the tachyC:ardia is driven by ~mpa~~et~,: re~ponse.
.. l
: • I Blood flow to the brain is constant no matter what the level of
exercise.
..
'-Ji I
) There is a linear increase in heart rate to a maximum but the
. 1
f increase in stroke value is'----
non-linear.]
- -""-,..,.._
There is a maximum
1 increase in stroke volume occurring with light-to-moderate
I
f exercise and only_:a
exercise; ," small further increment with strenuous
t

The sudden fall in cardiac output at the cessatf_on of~cise is


secondary to the loss of the muscle pump causing a decre_~e in
venous return, along with a loss of motor--mrtical and sensory
nerve activity associated with movement.
.\
I
Diastolic blood pressure rises only slightly during exercise and
may even fall. Systolic blood pressure rises in a ~;!!.nJar
fashion.
Physiology MCQs

J.SJ !Rega11rding caurdn~wa§c!!.llfaur B"~§jpOll'Dse to haemoirrlhiage:


f- D A With a· 1 Oo/o blood loss the pulse pressure is normal v' ·

, , ,, D B Compensatory mechanisms become inadequate to maintain


cardiac output once 20% of blood loss has occurred
D C Sympathetic stimulation is maximal within 30 seconds of
haemorrhage
_,
0 D lactic acidosis caused by hypovolaemia causes an increase in
peripheral vascular responses to catecholamines
,Z D E Decrease in stretch of the right atrium causes an increase in /. ~, / I

atrial natriuretic factor

3.54 Regarding venous admixture:


0
A There are no normal sources of anatomical shunts
vo B The effect of shunt is greater on the arterial partial p~~~eof
oxygen than on the arterial oxygen content ·
--- -
/ D C Shunt greatly affects artel'ial partial pressure of CO
2
. _/' 0 D The shunt equation read~: (}SIQT = (Gf!2._2 - ~02) +
(Cco2 - Cvo2) ~- --' · ·- -
·f.. 0 E Cco2 is measured from blood samples ,,.., "I

<e°"" ", •..,_ n.:\ ' ("' ..


\ ..,.~

r,_
c-:;;"f""'
._j

\It c? \.
t.\tJ.
\
,;., . \l"".~'t")
Physiology MCQs

3.53 Airnsw~ll'§~

e A False
Ill B True
e C True
G D False
e E False
With a 10% blood loss the pulse pressure is r~d~~d but the mean
arterial pressure may be normal.
Lactic acidosis causes myocardial depression and reduces the
peripheral vascular responses to catecholamines.
Decrease in stretch of the right atrium leads to a decrease in atrial
natriuretic factor release, which leads to an increase in ---,~
antidiuretic hormone.

3.54 Answers:
• A False
• B True
• C False
• D True
• E False
Thebesian veins draining the walls of the left ventricle and the
veins draining bronchial circulation are both anatomical shunts.
.=--~
Owing to the shape of the haemoglobin-oxygen dissociation I
i
curve there is relatively little reduction in oxygen content of
blood, unlike that of dissolved oxygen, I
Arterial partial pressure of carbon dioxide is not greatly affected I --1
by the shunt secondary to the steeper carbon dioxide-
haemoglobin dissociation curve and the ventilatory responses
I
secondary to an increase in carbon dioxide. \
• I

When using the shunt equation, Cco2 or oxygen concentration of I I

end-capillary blood, is calculated using the alveolar gas equation II t ·'


..
(to calculate alveolar partial pressure of oxygen) and the oxygen
. .
dissoclation curve.
. ---..... !
\
~-

j
~ .. ;
i -. 11 •i
:-. ..

I
Physiology MCQs
----------·-~---~

3.55 !RegaurdnITTJg the ~§molar t


g-gp aITTJd osmoiarity:
/ D A Osmolar gap is a measure of significant cations minus
significant anions

18 Osmolarity is calculated by 2 x _Na+ +glucose+ urea (in


milliosmoles per litre) -
D C The normal value for the osrnolar gap is less than 1 O mOsrn/1
D D Decreased serum water causes an increase in the osrnolar gap
0 E Ethanol increases the osmolar gap

3.56 The following are true regarding acid-base:


, / D A In metabolic acidosis the predicted Paco2 in mr:t1Hg is
approximately calculated using the formula
0.7[HCO3-J + 20(±2) mmHg
~/, 0 B Uraemia is not a cause of a high anion gap
0 C Type A lactic acidosis by definition occurs in the presence of
tissue hypoxia •,
0 D Type B lactic acidosis can occur because of defects in the
tricarboxylate cycle.
0 E
Peripheral venous bicarbonate is usually within 2-4 mmol/1 of •
arterial bicarbonate

'
~\
Physiology MCQs

3e55 Answers;
~ A false
@ B True
@ C True
® D True
• E True
The osmolar gap is the difference between measured-and
. calculated osmolarity, which is normally is less thari,J_() mgsm~I.
Causes of an increased osmolar gap include laboratory error,
'-.._1 \' decreased serum w~t~ontent, eg high lipids and high proteins,
and additional low-molecular-weight substances in serum,
eg methanol, glycine, ethanol or isoniazid.

3.56 Answers:
• A True
• B False
~ C True ca1

• D True
• E True
. A high anion gap can be secondary to lactic acidosis,
\ ·, -l; _. · :J ·~ -:. · : ketoa£k!gsis, uraemJ? or t~e~e of ~~er organic acids,
\ • ·• 1' eg salicylates, methanol, etnyl g!ycol poisoning.
l , ·· · · . · , r~lactiYci~ccurs in tissue hypoxia, althouglitty~B_\
,. · · :. l lactic aci~osis ~curs with normal tissue oxygenation but
aonormarla'ctate utilisation, eg systemic disorders, drugs and
heredity metabolic disorders. Any condition causing
accumulation of pyr~vate, including errors in the tric~box~l~te
CS-or the electron transport ~a~n, can cause a typ~~ffetic
acidosis. ~::. , -~ .
Per~~ral ven~us bicarbonate is usually slightlyhjg~than the
arterial one. '
rr 1 •.

Reference: Lactate physiology in health and disease. Continuing


Education in Anaesthesia, Critical Care and Pain 2006; 6(3):
128-32.
Physiology MCQs

3.57 Whelf'S «:ompauring a peruphetra!_yenous blood sample watlh an


arteria] !b,fo(Q)(d] $~1lil'ilfp;~(e (tal~emi frrcm the same patairii at tine same
frBll'!liHe)~ ---
0 A Po2 is similar an both samples , _ ; ,-..:. 1-

0 B Pc.o2 is very different in the venous comparedwith the arterial


sample ·
I

0 C pH is similar in both samples , .~ v}'


0 D HC03 - concentration is very different in the venous compared
with the arterial sample -15-~~ ._1.:'
""""~'.:) ~
D E Measured potassium will not vary between the samples -- .,-J"~r .. ~:
/ --::>", oO u
\ ,\'
\~c...,7;;,.
. b Q..,;,.c>-" -
Causes of a n,,Q_rmal ani(!Qgap metabolic acidosis include: ~ ~~ ~~, '--
~ - "--------0\r': ~' tJ
A Vomiting
.:,_, ~
- \ '---
B Distal renal tubuf ar acidosis
0 C Proximal renal tubular acidosis
D D Salicylate poisoning
D E Type B lactic acidosis secondary to heredity ~etabolic
disorders
Physiology MCQs ·

3.!
3.57 Answers:
A False
B False
C True
D False
e E True
Peripheral venous pH compares favourably with arterial pH.
· Venous CO2 also compares favourably with arterial CO2,
although it is on average 0.8 kPa higher than the arterial one.
Peripheral venous bicarbonate is usually within 2-4 mmol/1 of the
arterial concentration.

3.58 Answers:
• A True
• B True
(9.
• C True
• D False
• E False
Normal anion gap metabolic acidosis is secondary to:
, o loss of bicarbonate, eg vomiting, gastrointestinal or renal
causes
- o failure to exc~ete hydrogen ions, eg distal renal tubular
acidosis
_, G) administration of hydrogen ions. eg total parenteral nutrition.
S~ylate poisoning gives a wide anion gap metabolic acidosis
wit a respiratory alkalosis and lactic acidosis gives ahigh anion
gap. -~
To calculate anion gap:
({Na+] + [K+J) - ([CI-J + [HC03 -n -::: J
Physiology MCQs

3.5y Whell1l !l.B§orug a nerve simulator for peripheral nerve focala§atnoll'll:


-- ·- -
\/0 A The rheobase refers to the smallest currentlbat
. i~ requtrsd
. to
stimulate a nerve · -

B The chronaxyJs the len_gth~of the C«::!_rtfill! sti_9).UWSJ~uired to


/
stimulate
·- cl. nerve at twice its
.. rheobase
. .
-
\/0 C With a longer duration of nerve stimulation there is an
·, /
increased
- .=::.~
.
likelihood
.
ofrstimulatingJ2ain fibres
.A
I
D D Aa-fibre stimulation is associated with pain
•, /

1( D F C-fibres are stimulated ~efore c>-fibres with lengthening nerve


stimulation
Physiology MCQs

3o59 Answerri:
8 A True
• 8 True
e C True
9 D False
e E False

Fibre Chronaxy (ms)


0.05-0.1 ?"''""' \
Aa
Ab 0.15
-----
c 0.4

As can be seen with increasing chronaxy there is an increasing


likelihood of painful stimulation.
Pulse duration of 0.3 ms enables selective stimulation of motor
1

fibres with minimal pain ·stimulus. •


Reference: Electrical nerve locators. Continuing Education in
Anaesthesia, Critical Care and Pain 2006; 6(1 ): 32-6.
Physiology MCQs

3,60 Regarding nerve stimulator settings for peripheral nerve


blockade:
>< D A A frequency of JO Hz enables fast-·~-localisation
---
of the nerve -
---
A /
DB A twitch with current amplitude of less than 0.2 mA is desired
, /0 C The needle should ideally be connected to the cathode
' ,.. . ----
D D Higher amplitude settings are required for twitch visualisation
in paralysed patients
,, D E The nerve stimulator should be equipped with a patient
indicator to illustrate deJjyered current
Physiology MCQs

3
3.60 Answers:
© A False
~ B False
@ C True
• D False
• E True
A frequency of 1-2 Hz, ie 1-2 beats per. second, is used to
enable direction of the nerve-blockade needle.
,,,----
Tw§h.with a current amplitude less tha~'°-i~ =--9lay indicate _ .. _,
that the needle is mtraneural. However, twitch loss befor~Q..:s.~m~~-)
may mean that the needle tip is outside the nerve she~th. --
Le~s current is required to stimulate.~ ne~e when t~e c.~~~~~)is__
adjacent to the nerve and the anode.ls distal, A pat1~~t mc:hcator 1s
an important safety feature. If current ~s not being delivered it will
prevent potential trauma to the nerve .. -
If a patient is paralysed a twitch will not be seen.
-------
Cll 1

r' I

I.
Physiology MCQs .

3.61 !F!l.Brrodaons of the kidney indude:


t ./.0 A Ql~~neo~enesis
, 0 B Production of cholecalciferol
·' . / 0 C Renin production
1
· D D Angiotensj_nogen production I
(

_,.
//0 E Long-term regulation of blood volume

3.62 When assessing body fluid distribution:


A Interstitial
- water
r::..- is .·.-.
less than
. half intracellular
, water
3
B Tritium ( ~) can be used t9 estimate total body water
C Markers used to determine extracellular fluid must cross
- ~~ - - --~
capi I laries but n~I _!!lembranes
', - .
i-~D D Thiosulphate is used to measure total body wa,ter
;( D E Intracellular volume can be measured
Physiplogy MCQs

3.61 Answers:
© A True
@ B False
@ C True
e D False
4D E True
Vitamin D is derived from cholecalciferol (vitamin 03) and is
produced in the skin from 7-dehydrocholesterol in UV light. It is
hydroxylated in the liver to form 25-hydroxycholecalciferol,
which is then converted in the kidneys to the active form, 3
1,25-dihydroxycholecalciferol.
In starvation the kidneys are able to produce g!uc~e from amino
acids. - ==
::::""' .
Renin -- is-· synthesised in the - granula~
- cells of the juxtaglomerular
= ----· ...
apear~tus. -- --~
A~~e-;;sinogen
-
·-
., is a protein
- .. --= ---
produced
- •.
in. the liver,
--==-- '-
,.>
)')
,.

3.62 Answers:

• A True
• B True
• C True
• D False
@ E False
In ~ 70 ~g m_~nl 4-LI is_t_be estlrnated total body water content, of .
which.3 I is intravascular,
.... .. -
·"; ..
11
.-... .:-
.
I interstitial•.. and 28
...•.•.
I intracellular.
To estimate intravascular volume, markers that remam within the t 1___

vessel must be used, eg albumin. To determine e~lar fluid 1


see option D; inulin and thiosulphate are used. l
Interstitial fluid volume cannot be directly measured. It is
calculated by subtraction of plasma volume from extracellular
volume. Intracellular volume must be derived.
\ .

• I
'I
I
:I
I
II
Physiology MCQs

3,63 The proximal tulbH!.ll~e of the kudl.l!1ley~


--
D A Reabsorbs ')AO-o/o of the filtrate
. r1 )

D B Reabsorbs glucose
D C Secretes ammonium
D D Secretes bicarbonate '
D E Absorbs filtered protein

3.64 Regarding renal blood flow:


D A It accounts for 20% of cardiac _.2utput
D B A rise in perfusion pressure in the kidney leads to a fall in
afferent arterial tone
' D C It is increased by an increase in sympathetic nerve activity
D D Renal sympathetic activity increases glomerular capillary
hydrostatic pressure . -· ,;
vf'\, D · E Noradrenergic activity
•i decreases afferent arteriole tone '\1 l
0

!..--\ r
\-

I r,, (\ \
/
,
\ i \ I •,, •

·-..J

"\
( · / . ·- J
~./.

I -~
::,j)
I {

-
I
\

83
j
Physiology MCQs ·, 7 . I•
' . \ I '
j, I I \._: .:\
'

Answers:
A False
r-·f'. tf-1 {" --:-
i\ \_Q__.
B True {- I (_ 0
I
-1

• C True
/,-

• D False L.- f'v


c.-,\ l -
E True
The proximal tubule reabsorbs approxima'tely 60°/~ of its filtrate
. including water, sodium, chl~ide, potasgum, bicarbonate,
calcium, glucose, urea, phospbate and filtered P~<?teins. It secretes
(into the lumen-from blood) hydrogen ions, ammonium ions, urate
and organic anions and cations.

3.64 Answers:

• A True
• B False
C False

• .p True
E False 1·
/ As perfusion pressure in_the kidn~)IJ"ises, it~ increased
t
str~tching of the afferent arteri9le seQ:!Ddary to. an increase in
transmural pressure; this causes a contra~tion of the afferent
arteriole-the myogenic mechanism.
/ r-!()radren':'rgic stimulation of a-receptors causes constriction of
both afferent and efferent arterioles. This causes a reduction in
renal blood flow. .
,- lhe syrnp--<1t.Jwti£.,.~yg_em a~ctsj;lomeru~tration in two ways, It
' causes an increase in glomerular c~pilla!Y_hyg_~.Qressure,
which favours filtration. However, it causes a decrease in renal
blood flow, which iQ_~rease.sJhe glomerular capillary o!Jcotic . -~
pressure and therefore. overall, ~igh_tl~~~glomerular ,j,- \ rs
filtrati_gp:_ · ~~ - -- ~_


I
I

i
84
Phys;a/ogy MCQs

· 3,~5 Regarding the tuli.!alo~II@! apparatus: .


; D A The macula densa lies m the walls of the afferent-artenole
\_
D B Adenosine released from the macula
-~ densa causes afferent
arteriole
~
vasoconstriction
- '="

i O C An increase in sodium and chloride content is detected by the


granular cells \"-·'\ ,. , . JJ .. · -

D D Direct ~1 effect_causes renin secre!l9!l fromtbe


juxtaglomerul~r apparatus - --
. ~
D E Me~~~g~aL£_ells are ca~~~le of g_bagocytosis~
., 3.66 Renin:
,/
vD ,,/
A Is produced by the_gra~~l~.r cells \. ,J
\,,-· D B Is a proteolytic enzyme \
·--'

~ C Splits angiotensinogen to form angiotensin I


D Production increases secQ.odary to a decrease ln sodium
delivery~ the macula densa ---
E Is the rate-limiting enzyme in the conversion of
angiotensinogen to angiotensin II

(
. 'hysiology MCQs

3 Ji,5 Answers,
® A false
o B True
e C False
{) D True
© E True
/ The juxtaglomerular arearatus compriseu)i~~~ular cells~ren in
production) found in the walls of the afffil"eOt arteriole·.- - -
/ The macula densaJs.a thickened porti_on~a!I of the
ascet)9in_g__ lilJE_ of the lo.9R_ of Hen~e. it is j,nvolved in the control
of reQin proauction and renal blood flow;This area senses an
increase in.sodium and ~hlorideywhich leads to more adenosine
release and sq~ductio~m]lomerular filtration rate (GFR). I!
releasesrnore ?-den~sine if renal perfQsion pressure rises--L
./ The mesangial cells are located between cap_illaries. They are
' modified smooth muscle cells . with contractile
~- - properties, and so
.

they are able_to_Q._ifi bloodJJ.IDY--Legula!iQn a~ they are continuous


Cl; with the vascular smooth muscle cells. They 'can also produce a
variety of cytqkines ~nd are capable of phagoc~osis.
' ~ ' ~

3.66 Answers:
$ A True
0 B True
• C True
0 D True
• E True f"c~
Renin causes splitting of angiotensinogen (found mainly in the l :;:1
.::·1
G
liver) to angiotensin I, which is alO-amino acid peptide.
--
/ An increase in renin produc!!_on is ~ed by a_decrease in body '
~' --~ decrease -- in .circulating
- blood
-- volume,
- ---:=-- increase
. - in-~ -
symp3the!i~~tivity and a decre.'.'se _in~~~~;1_,t,arteriole ~essure. f
j.
I.
T
.I
I

Physiology MCQs

3.67 Anglot ~lnlsin ll: -


D A Cons' ~icts afferent and efferent arterioles
0 18 Causes -1 reduction on filtration coefficient of the renal
corpuscle
1
· D C Has no di: set effect on renal tubules l .
I "r
D D lndirectlyr::iffects the hypothalamus
D E Stimulates~DH secretion

3.68 The following are true of the physioiogy of the cyclo-oxygenase


enzymes:
,A] A Phospholipase A2 catalyses the release of arachidonic acid
from phosph61ipids in cell membranes
\ D B COX-1 is expressed only on specialist cells, including platelets I ' /

' and renal tubule cells


PGE2 increases gastric acid secretion ,/ J

PGl2 has a role in the maintenance of normal renaljilood flow


I

. I
in patients with renal dysfunction

--
·' · D E COX-1 is a major source of vascular PGli biosynthesis
-:z_..
')
Physiology MCQs

JJ}i J\l!'il§Weirz~

~ A True
© B True
® C False
8 D false
@ E True
/ Constriction of afferent and effere nt arterioles causes a decrease
in renal blood flow.
[&iiotenslijJfdirectly affects be th tubules (causing fluid
/ reabsorption) and the hypothalamus, increasing thirst and ADH
secretion. ~~--- ·
,,,:,, It also increases aldosterone production, Is a vasoconstrictor and
increases sympathetic nervoussystem activity, so leading to an
increase in peripheral resistance and cardiac output.

3.68 Answers: !

• A True
• B false \
'f !· .:
• CD True
False t


E False
•/ COX-1 1
is expressed in most cells, not just specialised ·cells, but it
7
is especially predominant in endothelial, pla!elet and renal
tubular cells. 1
I PGE and -121'&1uce gastric acid secretion. vasajpate mucosa!
2
vessels and increase mucus producti~~
/ COX-2 is a major source of vascular fgz. biosynthesis.

·.·•.
\. . ~ .
;,,.,•_

l .
i

i
!
Physiology MCQs

3.69 Reg~irding COX errazymes:

0 A Long-term inhibition of COX-2 is not associated with renal


/
toxicity --:·--
D B COX-2 is important for reproduction
,,,0 C
' / Long-term use of COX-1 inhibitors causes more
gastrointestinal (GI) problems than does long-term COX-2
inhibition - \ .
· ./ D D _s. ow
!'eripheral
. COX-1 mediates nociception in "rapidly developing
pam
_ _,,
D E
COX-1 is needed for the platelet production of thromboxane

, 3.70 Atrial natriuretic· factor (ANF): 1,~L\


\' 0 A 1.s produced where there is l~~~f stretch of the atria
D B Increases the glomerular hydrostatic pressure
>~ D C Is a powerful vasoconstrictor vo
· · D D Cau~es afferent arteriole constriction "C) I
__/L] E Inhibits aldosterone release from the adrenal cortex

.)t,
Physiology MCQs

A Faise
B True
C True
D False
E True
COX-1 and COX-2 inhibitors are associated with renal toxicity in
s~sce~Ji!?le individuals when used for long periods. ---
'
ReripherJl,COX;J-inediates
-- nociception in slowly developing
pain, whereas spinai;cox-1 mediates nociception involved in
rapidly developin(pain. ·
/ COX-1 and COX-2 are important for fertility) COX-2 is expressed
in cells of the reproductive tract and is ·needed for pregnancy.
COX-1 is required for prostaglandin production, whicnITlaintains •I
a healthy ·pregnancy. """ - --- t
-- .
\
e.10 Answers:

• A False
• B True
• C false
D false
0 E True
ANF is released by atrial ce'is in response to stretching. It causes
afferent arteriole dilatatior and efferent arteriole constricti »n, so
increasing glomerular hydrostatic pressure and increasing L
glome~es. The overall result is di~sis. It also
directly inhibits renin and aldosterone release ancloecreases
sodium reabsorption in the collecting ducts.
( .
I
t ~-
\
t
l
;
l
.I

Physiology MCQs

!Regall'dlu!ril,g ilhre loop of Henle:


A The descending limb of the loop of Henle is impermeable to
water
/

k./0 B
/The descending limb is impermeable to sodium and chloride
, // 0 C The thick ascending limb is impermeable to water .
<
1 0 D Active transport of sodium and chloride into the interstitial
' fluid increases the tubular osmolality in the ascending limb
·/ 0 E ADH affects water reabsorption in the thick ascending limb

J.721
The following are true of the countercurrent exchanger:
- O A It is an active process
0 B The blood flow in the vasa recta is fast flowing
- ' / 0 C The osmolality
. at the base of the vasa recta is low
, / 0 D
Water leaves the descending vasa recta and enters the
/
ascending vasa recta
..//t] · E The descending vasa recta is permeable to urea
Physiology MCQs

3.71 Answer§:
@ A false
0 B True
e C True
(D D False
@ E False
The descending limb is permeable to w~r but impermeable to
sodium and chloride.
Sodium and chloride are actively transported out of the thick
ascending limb, causing a reduction in tubular osmolality and
increase in interstitial osmolality. This draws water out of the
descending limb. The overall effect is to cause fluid in the
descending limb and the interstitial fluid to increase in osmolality.
ADH affects water uptake from the collecting ~ucts.
-~:::

3.72 Answers:
'
• A. False
• B False
• C False
• D True
• E True
The countercur~_m_e~cha~g~ is formed by a n~!_~ork of_blood
vessels, the vasa recta, which supply the loop of Henle and the t
i,. ·-
colleCting ducts. As the blood vessels descend into the medulla
water is lost, which enters the ascending limb. Solutes are t[J
; -,,H
l .·· ·:·,

absorbed into the descending limb of the vasa recta from the
ascending vasa recta. This ensures that the concentration gradient r -
I.
in the interstitial medulla is not washed away.
/ ' L..'
i
The osmolality at the top of the vasa recta is approximately I'
i i
~ mosmol/kg H 0 compared with that al the-bottom, which is
2 l..

approximately 1200 mosmol/kg H2O. lt is a passive_~s


resulting from,!~vement of water and sol~ehNCCri' the
limbs of the s\ow:::.flowing b\oo<l in the vasa recta.
•...••.. .: ~
Physiology MCQs

3.iJ i~garding urea and urine productioll1l:


/_,,/0
A Urea is partly responsible for the high medullary osmolality ~ '(
D B The distal convoluted tubule is impermeable to urea \.t~ ~~
! /

D C ADH stimulates absorption of urea into the medullary ~" ~ ~


interstitium

D D At times of water excess the collecting ducts are relatively


impermeable to water -.
·/ D E In extreme conditions, urine can be as concentrated as
2000 mosmol/kg H20
,.
:---
\ \.-\~"

3.74 Acid-base control in the kidney:


/0 A Under normal circumstances all of the bicarbonate in the
glomerular filtrate is absorbed
/o B Most bicarbonate is absorbed in the proximal tubule ?_/-)
;< D C Bicarbonate is actively absorbed from the tubules in exchange
for ch Jori-de ions • I r~
D D The minimum urine pH is 6.1 :.-\ _ 1--\
0 E Filtered phosphate ions enable hydrogen ions to be excreted in
the urine
Physiology MCQs

3oi3 . fa\rra§'W(eR'§~
t A True
® B True
@ C True
e D True
e E False
Urea is essential for..JJQJD.J.?.1 r_enaLfunction. The loop of Henle,
distal convoluted tubule, collecti~ and outer medullary
· collecting ducts are irii°permea61e _t.9 ureal This results in a higher
urea concentration within the inner medullary collecting ducts. In
times of water deprivation ADH stimulates urea reabsorption into
the interstitial fluid. This promotes a concentrated osmolality
favouring water reabsorption. It also increases water permeability
of the collecting ducts, again facilitating water absorption.
The obligatory urine loss requires a urine osmolality of
,/·,, 1-1.QQ.J!lOSmol/kg H20. - -. -
-- ·----
3.74 Answers: ':
C.

• A True
• B True
8 C False
• D False
E True _"'
QI
.

A total of 85% of bicarbonate ions are reabsorbed in the pr_oximal


tubule. Mc5st of the remaining bicarbonate is absorbed by tile-=--
~--
thick ascending limb of the loop of Henle. ~\G
I
The absorption of bicarbonate is n~ - via active chloride exchange.
--~ l
Hydrogen ions are secreted actively into the tubule whereupon II..w ·1.
I' <l
··.J
they combine with filtered bicarbonate ions forming carbonic !

acid. This breaks down to form carbon dioxide and water, which
then readily diffuse into the lumiriarceHs.-Once inside the cell,
carbonic anhydrase catalyses the reaction of carbon dioxide with
water to form bicarbonate ions (which are reabsorbed into the
peritubular capillaries) and hydrogen ions (which can once again
be secreted into the tubular.lumen).
The minimal urinary pH is 4A, 'below which the elevated
hydrogen ions prevent any further hydrogen ion active transport. .'
I'
f

! •;__..:_:
·!Physiology MCQs

i1eg~trirllff rrog the lie!l'ila~ tre$p@!nl$(e ft©> distua-~edl add-base:


A In metabolic acidosis, ammonia combines with hydrogen ions
withBn the lumen to enable renal hydrogen ion loss
D B At urinary pH 4.4 further hiidrogen ions can be lost by
combination with ammonia in the lumen
D C In metabolic acidosis the amount of filtered bicarbonate is
reduced
s' ·, j() \.\,::-~- \_~
0 D
low extracellular hydrogen ion concentration decreases
tubular secretion of ammonia ions
D E
During metabolic acidosis there is increased hydrogen
secretion from tubule cells into the lumen
Physiology MCQs

A Trrue
B True
C True
D Trrue
E True
Deamination of glutamine in the proximal tubule, the thick
ascending limb of the loop of Henle and the distal tubules causes
the formation of two ammonium ions, NH4 + and two bicarbonate
ions, HC01-. Ammonium ions are actively secreted into the
lumen in exchange for sodium ions. The bicarbonate is absorbed
into the blood, therefore dec~sing the metabolic acidosis.
Further along the nephron, ammonia (NH3), which is lipid
soluble, diffuses from the interstitial fluid into the collecting duct
cells and then into the collecting duct tubule lumen. Here it I
I

combines with hydrogen ions to form NH;t, which is ionised t

-
//X'H\-\
and therefore trapped and SQ excreted. This reacticr- can even
occur in the most acidic urine, thereb increasing hydrogen ion
excretion in extreme metaboli: acidosis.
\ 0
u In metabolic acidosis there is a decrease in blood bicarbonate, so
' less is filtered. Low extracellular hydrogen ions occur in all<alotic
;---
\J.... ,f',.;Sl

states where there would be no benefit in increasing hydrogen ion


excretion. Therefore, there would be no benefit in causing an
increase in tubular ammonium ion secretion.
i: I
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L., , Physiology MCQs
l ·,.
I I
- ..

3.76 e{egardling acute haemolytic transfusion reactions:


,,/'[] A Signs may occur aft~r lransfusion of only 5 ml of incq_mpatiblc
blood
It can occur secor darv io_anti-RhE in the recipient's blood .. -
It can occur secor dary to Kel_l) antibodies in the recipient's
/
blood · - ,___ -
D Jk {Kidd) antigens can be causative, which are difficult to
detect in pre-transfusion sa_~ies - --;-
E It is likely to occur if a rhesus-positive AB recipient receives
rhesus-negative A blood

-~
i
I

Physiology MCQs

3.76 .All1l§W!E!l"§~

0 A True
0 B True
@ C True
© D True
9 E False
Acute haemolytic transfusion reactions can occur after transfusion
of only 5-10 ml of incompatible blood. Other than ABO
incompatibility, there are a number of other red blood cell
antibodies in the recipient's blood that can cause such a reaction
lo::-:.
including anti-RhD, -E and -C and Kell's antibodies. Reactions to f -\

these are usually less severe than the ABO reaction as


complement is IJ9>1activated. However, reactions to J~ (Kidd) and
Fy (Duffy) antigens do activate cofllpkment and can cause severe
transfusion reactions. leading to rE:Qif and cardiac failure.
AB blood group has neither A nor B antibodies and is said to be a t
t
l
universal acceptor, ,_ i
r(
Refere~ McClelland B. Handbook of fransfusion Medicine. i

2nd edn. Blood Transfusion Services of the United Kingdom, t
1996, t

- r·
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l UI II

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Physiology MCQs

s.rr !Regaurdfo'ilg_ bkl)occLgroUj)s:


0 A In the white population the AB blood group is the most
lfufreguent ] .
D B The naturally occurring antibodies, eg anti-A in a blood group
B patient, are mostly I~
D C The persistent immune-antibodies developing on exposure to
foreign red cells are lgG .
D lgM antibodies pass transplacentally : 1 (\
,/ 0 E Small amounts of group A and B antigens can enter the body
-
in food and bacteria
- -

3.78Regarding granulocytes: ~
~-D A Neutrophils are attracted to inflamed areas by chemicals
released by damaged tissues
/

:,/ D . B Opsonisation occurs when foreign particles are labelled with


immunoglobulin or complement L _ o\l-~
•, 'z; ---0 ~
~YV'~ '
0 C Eosinophils circulate in the peripheral circulation for most of
their life span
'. D D Eosinophils are not phagocytic
E Eosinophils release enzymes that inhibit mass cell products
Physiology MCQs

3a77 AinlSWe[('§~
€) A True
® B True
Ii C True
~ D False
c, E True
In the white population the following percentages of blood group
are seen:

• A group 45%
~ 8 group 9%
• AB group 3%
• 0 group 43%.
Naturally occurring antibodies are reactive at 3 7°C but optimally
reactive at 4°C, unlike immune antibodies, which are optimally
reactive at 3 7°C. -= _
The immune antibodies are,~antibodies but~~Jntibodies
may also develop in the ear~hase of the reaction.
e111 Only 1;c)mtibodies pass transplacentally. ,. '
, ___,,...#

3.78 Answers:
• A True
B True
e C False
• D False
• E True
Neutrophils and m2nocytes a1 e also attracted to areasby
co-~ ent or feu~o-~r-tes.ohesion m_gj_ecule interaction with
damag~~ue. They are also attracted towards bacteria ..:
Fe and do receptors on monocytes and neutropHKensure
re~gnit!On and subse9uent J~J~oc_x_tosis of opsonised material.
Eosinophils circulate for upto BJ.ours before entering into the
tissues (predominantly epithelial lining). Their life span is
:approximately_~ days compared-with 4-5 days for
neutrophils. ~hey phag_~ytose a~931-antibody comEle~s.
· They also have a role in reducing spread of inflammation by
destr~~mplex'es:- -==
1
Physiology MCQs

3.79 /
Regarding white blood cells: .
. // D A Basophils are involved in allergic reactions
' D B Basophils are predominantly found circulating in blood
D C Basophils have predominantly ~gG attachment sites
"' 0 D Monocytes, on entering tissues, mature into mast cells
.,./D E Macrophages release tumour necrosis factor (TNF)

3.80 Regarding lymphocytes: f- - ,


\ D A Most circulating lymphocytes are B lymphocytes
/ D B CD3 (part of the T-cell receptor) is present on all T cells \

/ D C T-helper lymphocytes possess a surface glycoprotein CD4


/·o D CD4-surface glycoprotein binds to MHC class II molecules on
antigen-presenting cells
;_. / 0 E Helper T cells aid in the promotion of B-cell maturation
,.
Physiology MCQs

A True
1B False
C False
e D False
E True
Basophils have cytqpt~~mic granules and contain active
.substances including hlstamine, serotonin, hyalu~ acid !Q.d
he,Rgtin. They are occasionally present in blood but are .· .
predominantly tissue bound as in_mast cells. They have~
attac~i:nent sites and are important in allergc and ~rasitl't iI

conditions. 'I

Monocyte~maJure to macrophages i~ssues, where they can


continue· to function for Y,ears. They are ph]-&8£U
Y c and have · -
l
receptors for lgG, compr e'ment and various other lymphokines. As l
well ~tl<
.,
ey c~n also produce _i!i,}~~)~~~-1 (ll-10),
prostag andms and mterferon. ~
·
l
t
f!
3.80 Answers:

• A False l
B True f
• C True
• D True
E True
\
• ~
t
T cells account for 80% of circulating lymphocytes.

---~
CD4 is present on the surface of T-h_elper ~lls and m9Qocytes ~r: t<f/t
I(
-
Approximately 65% of the lymphocytes are T-~elQer lymphocytes.
They promote antibody production and secretefnterleukins,
which cause _B-lymphocyte proliferation and actlvatioo. They are
inhibited by ·1~d interferon. --
Reference: Kalra P. Lymphocytes. Essential Revision Notes for
tt I,•.. . I
t
MRCP. 2nd edn. PasTest Ltd., 2004.

I.
l :•
Physiology MCQs

3.81 Regarding Immunity:


,//0 A Plasma cells are non-circulating 1B lymphocytes
/

0 B The majority of B lymphocytes express MHC class I antigens


D C Suppressor or cytotoxic T cells express CD4 surface
glycoproteins
/, D D All B lymphocytes can secrete antibody J ! -<~

/ D E Plasma cells produce antibodies

s
.,
Physiology MCQs

3.81 AraswteB'S~
@ A True
@ B False
C false
@ D False
• E True
Plasma cells are non-circulating B lymphocytes in QQDe marrow,
lvrnphnodes and gut. Plasma cells produce antlbodies. Immature
B lymphocytes are unable to secrete antib_ody. The~majority of !i
J_y_mphocytes_express ~_ class ILa-ntigeQS. _ -
Suppressor or cytotoxic T cells express ~ surface glycoproteins
that interact with Mtj.C class I molecules expressed on cells. This
is important for destroying virally infected cells.
Cytotoxic T cells secrete cytokine in~rleukins (IL-2), interferon-a
and tumour ~crosis factor. They induce B lY.!!!e.hocytes and
recruit activated immune cells to the area. -
lmmunoglobulins are.n,,ade up of two fragments: the ~b fragment
with anti~inding capacities and the Fc_fragment with the
effector function. =-e:-

I
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'
Physiology MCQs

3.82 iega1rding allergy:


.
)( D A Anaphylactoid reactions are a result of iglE-mediated
hypersensitivity ,-..~.,,. ._ """' ~ \~~\"""
·/ D B Most anaesthetic drug reactions are because of ~usde
relaxation
D C Anaphylactoid reactions require a prior sensitisation
, I
},
' '\
D D Mast cell tryptase reaches its peak after approximately. 6 hours \ I' (

0 E Serum for mast cell tryptase should be frozen before analysis


/\.__,.( r
I p \ \ '
...- •

.•.
•• 1-iw.~~ ••• - - -

Physiology MCQs

&i A false
e B True
e C False
~ D False
• E False
AnaphylaQ-eactions are non-i nmune. They are _n_Q!)gE
· mediated and require ~rior exposure to the allergen. They are
mediated by direct histamine~ release from mast cells or
complement activation. .
Anaphyl®reactions require prior sensitisation and result in
potential catastrophic lgE-mediated hyp~rsens itivity.
Mast cell tryptase reaches its peak afterj)hour and sho~_lg_,Qe i
refrig_!rated but noJ fro~n before analysis, which should be
ideally done within 48 hours. t
BaSQBhil ce.lLsur_fgc~ markers may also help with anaphylaxis \ I

dlagnosis. Al~ough they have a high specificity, their sensitivity t


may be as low ~s 50%. l ..
Also, remember that crossreactivity may occur. Patients with no
previous anaesthetic exposure can be sensitive to agents
secondary to other agents, eg cosmetics or over-the-counter
medication and even cleaning products.
Reference: Anaphylaxis. Continuing Education in Anaesthesia,
Critical Care and Pain 2004; 4(4): 111-13. r

,~ ~ " r \.)1 "c.-.\- ~, ~ 1"--·" 9 I t


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Physiology MCQs

3.33 The fonowill1lg are true, regaur«llnll'Dg life-threatening allergic


reactions during anaesthesia:
D A Antibiotics are the second most common cause
v,,,-. .. D
B Gelatins are the commonest cause for colloid allergy
/ D C Reactions to etomidate are more common than reactions to
'
propofol
\,',, D D Radiocontrast allergy does not typically present at the time of
I
administration
./
i~,,,-- D E Benzodiazepines are more likely to cause allergy than opioids
•..

Physiology MCQs

3o83 Allilswers~
e A False
o B True
© C False
~ · D False
0 E True
Reactions to etomidate
~
are r~
---
Common reactions to
~------===--
. radiocontrast media include flushing, nausea and .varmth.
Hypersensitivity reactions can occur in ~%.: -pf patients and occur
at the time of admi~ration. Having suffered a reaction, the risk .
of allergy to subsequent exposure is markedly increased. \
The table represents the spread of anaesthetic agents causing life- 1·

threatening allergic reactions.


l

f
Agent Percentage

r<:feuromuscular blocking agent 70

I
\
12.6
'l- Latex
', Colloids 4.7 •
_.,
3.6 I
Lf-- Induction agents

-
r
~ Antibiotics
-1 Others
( Benzodiazepi nes
2.6
2.5
2
I
Opioids 1.7
b

Reference: Anaphylaxis. Continuing Education in Anaesthesia,


Critical Care and Pain 2004; 4(4): 111-13.

. -.
----~
\ .i
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Physiology MCQs

3.84 !Pan!rd physfo!ogy~


/ D A Ao-fibres conduct impulses at 5-10 mis
,··' D - ,-
B A&-fibres synapse at laminae II and Ill /

L •

~D C Dull pain travels in· myelinated fibres


v/0 D Fast pain fibres.ascend to the posterior thalamic nuclei
:,/o E Some C'fibres are silent unless stimulated by inflammatory
conditions
Physiology MCQs

3.84 Answers:
*' A false {,

• B False r

o C False ~
l -
e D True [
t
E True r
\
Ao-fibres (fast fibres) conduct impulses at 12-30 mis. They are l
l
I
. myelinated fibres that enter the dorsal horn of the spinal cord and 'f
l
synapse at laminae I, V and X. Conduction continues in the Ir
secondary afferent fibres via the neospinothalamic tract to the
---
pQs!erior_tha@mic nuclei. ,
C-fibres transmit dul.l.gain or slo~ain. The fibres conduct
.

I
impulses at O.~~m/s via unmyelinated fibres that synapse at
laminae II and Ill (substantia gelatinosa) of the dorsal horn.
A total of ~S¾iof C-fibres present in the skin and viscera are silent
or do~~antalfd become a,:_~ivat~dQ:i~~ing Inflammatory . '.
conditions. \'
0 '':) > ".:':>" c..() '- 1 l.. ~ Y-' (' ~- . , o,..r u '-·- •. ~ ..... ''. ,_

Reference: Anatomy, physiology and pharmacology of pain.


Anaesthesia and Intensive Care Medicine 2005; 6: 7-10.

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Physiology MCQs

Pain fibres:
A Fast pain is transmitted from the lamina to the thalamus via a
monosynaptic pathway
/ D B Having synapsed in the laminae, the pain pathway for slow _
pain follows a monosynaptic pathway to the thalamus l ~
I
\
/,D C Fast pain pathways are responsible for circulatory reflex
responses to pain
/D D Visceral nociceptors are very dense compared with somatic
nociceptors
D E Visceral pain exhibits spatial su~_mation . . .~ -'i p,...
--
0 S. \c..-..'vV .:,.r- h-h ~ . ...,- '~ \ ~J'--, ~~{>
r
q",-,,,J. ' 0
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'\
e A True
@ B False
e, C False
6-' D False
e E True
Dull or slow pain travels in C-fibres to laminae II .md Ill where
they synapse with second-order neurons that tran srnit information
via a polysyna2t1f system to multiple regions, incuding the
midbrain, pon?, medulla and hypothalamus. This slow pain
<--- ~ ~ --~.
pafnway is respor.sible for reflex response to pain (including
respiratory, circulatory and endocrine responses):
~ Visceral nociceptors are much less densely placed than somatic
/ nociceptors, which leads to poorly local'ised, diffuse and often
midline pain. -- -
/ Visceral pain exhibits spat~ation. __~_Jarg1~ area .~s ·
stim_ulated the pain threshold ~lo;'!:r_:9 ~res,:~t incutaneous
nociceptors). .:...:.:.-- ··
Reference: Anatomy, physiology and pharmacolugy of pain.
Anaesthesia and Intensive Care Medicine 2005; (.: 7-10.

(
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t._

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Physiology MCQs

3.86 Cerebrosplnal flti.!ladl <dleli1lsify~ /


, D A Has a mean of 1 .1 000 g/1
D B is greater in women compared with men
\_.,/· D C ls lower in preg~ant compared with non-pregnant women
, , " 0 D Is lower in premenopausal compared with postmenopausal
women
/.D ~ Affects spread of intrathecal solutions
~-._,.,_ __ _ _..,. ,,.,..s,,_.

Physiology MCQs

31.®i& Aml§W(e!f'§~

@ A False
tt> B False
e C True
® D True
® E True
Mean CSF density is 1.0003 g/1 with normal physiological range
of -~_22_06 ± 2 SD g/1. \
CSF density is greater in men compared with women and in non- t
pregnant
--
compared with pregnant women, . II
Baricity of injected intrathecal preparations, ie the ratio of density \
of injectate to the density of CSF, has a marked effect on spread.
Hypobaric solutions will cause a rise and hyperbaric solutions a
fall.
Reference: lntrathecal drug spread. British Journal of Anaesthesia
· 2004; 93(4): 568-78.
Cl

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Physiology MCQs

J.8i li!hi~ f((i)~fowfo11g are ftU1micia((i)ll1l§ (Of the vagus nerve:


f vr D A Sensation to the epiglottis
~,o B Bronchial mucus production
[ ~// D C Sensation to the dura
/0 D Sensation to the external auditory rneatus
[ ~D E Bronchoconstriction in the lungs
....•. ,. ~-» ,$t,,+- ·- .:::· ,c..,.;:. •• ~ ••

Physiology MCQs

3.!87 Answers:

a A True
«> B True
e C True
@ D True
@ E True
The vagus nerve is motor, sensory and secretomotor. It has three
· nuclei: the do§g) nucleus that is mixed, the nucleus ambiguus,
which is motmand the nucleus of tractus solitarius, whichserves
sensory functions including taste. It p;~idesinotor innervation to
the larynx, via the recurrentla~Qg~I and to the bronchial and
upper GI muscles up to the splenic flexure. It has alarge-sensory
role including dura, exter.Dal auditorr_rneatus, respiratory tract, GI
tract to the ascen9ing colon, myocardium and eP-iglQ_ttis. Its
secretomotor function includes bronchial mucus and alimentary
tract.
---
Reference: Urquhart J, Blunt M. and Pinnock C. The Anaesthesia 11

Viva 1. C:reenwich Medical Media, 1996. '

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Physiology MCQs

3.88 The foHowoll1lg are true wegta11rtdlon1g classes (Of nerve fibres:
'f---- D A AP-fibres are the largest A
f-- D B B-fibres are efferent
(' 0 C Spindle afferent fibres have the slowest velocity
/o D Dull pain fibres are the smallest
/o E Motor fibres are the fastest
Physiology AACQs f' -
I

3,8.
I ,
3088 Arro$W~tr$~
@ A False
@ B false
C False
s D True
© E True
Aa-fibres are the largest at 12-20 mm with a velocity of
70-120 mis and they supply somatif=-motor.
A~-fibres are 5-12 mm in diameter with a velocity of 30-70 m/s
and serve touch, pressure and proprioception.
Ay-fibres are 3-6 mm diameter with a velocity of 15-30 mis and
supply spindle affE:rent fibres.
_--· Af>-fibres are 2-5 mm with a velocity of 12-30 m/s and supply
sharp·E2-in and temp!;@.!ure.
B-fibres are <3 mm diameter with a velocity of 3- 15 mis and
supply preganglionic autonomic fibres.
~ c:1, C-fibres are 0.4-1.2 mm with a velocity of 0.5-2 mis-and give

rise to d~in.
Reference: Urquhart J, Blunt M. and Pinnock C. The Anaesthesia
Viva 1. Greenwich Medical Media, 1996.
Physiology /VlCQs

fR:egaur«llsUug obstructive sleep apnoea:


A it is referred to as sleep apnoea syndrome when the patient
suffers with excess daytime somnolence
B In the absence of abnormal .anatorny it occurs because of
relaxation of the pharyngeal constrictor muscles while
sleeping :__ ..
\, D C By definition the oxygen saturation must fall by 10% to meet
the diagnostic criteria
/
/ D D Nasal CPAP (continuous positive airway pressure) is the gold
standard of treatment
··' D E Morbid obesity alone is a predictor of difficult intubation

The following are expected clinical signs for a fit young adult
who has lost 20% intravascular blood volume:
A Heart rate > 140 beats/min
B Urine output is <1 ml/kg per hour

C Cool shutdown of peripheries
.X D D Restlessness and irritation
,,0 E Normal blood pressure when supine
Physiology MCQs

· 3.89 Answers:
!21 A True
• 8 True
ii C False
• D True
e E False
Obstructive sleep apnoea affects up to 5% of the UK population,
80% of whom are male. It is the repetitive obstruction of the
upper airway during sleep, which leads to a decrease in arterial
oxygen saturation. The diagnostic criteria quote a saturation
reducfion of at least 4%0,
with obstructive episodes lasting for ~ 1 0
s. Obesity alone i~~j~a predictor-or difficulty of intubation; .. ~
however, when combined with other scoring measures, eg Wilson
scoring, it increases the predictive.value. ~
R~~nce: Obstructive sleep apnoea and anaesthesia.
Anaesthesia and Intensive Care Medicine 2005; 6: 225.

3. 90 Answers:
• A False
• B True
* C True
e D False
• E True
With 20% intravascular blood loss expected, clinical signs in a fit
young adult include heart rate 100-120,.Jcirthostatic hypotension,
reduced urine output <1 ml/kg per h, cool shutdown of
peripheries and normal CNS.
Reference: Assessment of gastrointestinal problems. Anaesthesia
.and Intensive Care Medicine 2003; 4: 38-41.

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Physiology MCQs

.
J.911 The fo~~OWB[l'l)g ~!1'e ftir!!.Ile iregairdniiilg tliute hf»irlMOlll'il~~ changes of
!Pii'Q .gnancy:

A Growth hormone production is reduced


/ D B Both free and total plasma cortisol increase
\/ D C Aldosterone increases lecause of the natriuretic effect of
progesterone
v'
I D D ~,,,,hig~--plasma concentration of free thyroxine is expected
0 D E There is a reduction in prostaglandins during the first trimester

3.92 Regarding maternal physiology during pregnancy: ·


/o A The basal metabolic rate increases by 20% at 36 weeks
,,· 0 8 Significant cardiovascular changes start to occur in the second
'·.
trimester
'
D
'/
C Colloid oncotic pressure in~!.eases during pregnancy
I
~/
'- /
. V

/D D Stroke volume increases by 20%


~/ D E Downregulatibn of a-receptors contributes to the decrease in
peripheral resistance
Physiology MCQs

ft;~
) r ,J . I fj, ~t '

3o91 AlJ1l§W(elJ'§~

® A True I --
® B True ,:-·, \ r"'' n > 'f-· ·- --·
@ C True
·!
...,,. rt.:,
e D False
E False I ~'v--r.? ,. · ,:_ _ , i:, ,.,.L _
J " .
«ro- ' ·.1 b L---J
Growth hormone produc on iSreduced. This is thought to
happen because of an increase in the production of h~man
placental lactogen from the placenta. Along with a rise in cortisol
and alao~terone, renin and angiotensin concentrations also rise.
Although there is a rise in thyroxine production, there is also a rise
in the thyroid-binding globutinsuchthat the free thyroxine
concentration is unchanged. Prost~glandin@)increases threefold
during the firsttrimester, which results in systemic vasodilatation.
Prostaglandi~-£ Increases significantly during the third trimester.

3.92 ,\nswers:

• A True
• B False
• C False
• D True
e E True
A quick revision tip is that most physiological parameters increase
by approximately 20% or 40% during pregnancy!
Basal metabolic rate and oxygen consumption Increase by 20%.
Significant cardiovascular changes occur ~ly in the first
trimester, with a JE/o increase in heart rate occurring by week 12.
Heart rate peaks in the middle of the third trimester~% above
baseline. Stroke volume increases by\20% and this occurs
predominantly by the end of the first trimester. Peripheral
resistance decreases by_J0-35%J1rhis is because of progesterone,
prostagjandins and downregulatio_
--- - o of a-receptors. Cardiacoutput
-~ ,,
increases by 50% oyweeks 32-36.)
.

_/
Physiology MCQs

3.93 Mat:erna~ changes during pregnancy 01n1dl!ll<dle:


1'>\ D A An increase in renal blood flow of 20o/:
,~' )
/ 0 B Aortocaval compression occuring during the first trimester
C An increase in blood volume of approximately 1.5 I
,, '
D D A marked reduction of diaphragmatic contraction at term
D E A reduction in vital capacity of 30°/~/at term

.~.,,
I
~~--- ..

Physiology MCQs

A False
B False
C True
D False
E false
Renal blood increase@by the first trimester. Aortocaval
compression becomes significant at approximatel~eeks.
Although the diaphragm is displaced outwards, the contraction is
/9aff_~ed. The lower ribs flare out, so increasing both the
anteriOr-posterior (AP) and transverse diameters of the thorax. This I
~e of a reduction in ligamentous tone secondary to \'
1
rela~11~;.

::iratory parameter Effect of pregnancy


Decreases (35) .
(%) I I

Airway resistance Decreases (20) _,


ERV •:
Decreases (2 O,)
RV Decreases (20)
FRC ...----;
Increases (30) r=

w .,
Increases (10)
e __ JC -E)e-creasesl20)
) EC Decreases (5)
t TLC
~ Unchanged
/r VC Unchanged
\__J-ung compliance Decreases (20)
Total respiratory compliance
~ Increases (45)
Anatomical dead space
Increases (50) .
MV Increases (10)
RR
I
/I...:.,, TV
-
Increases (40}
Physiology MCQs

The following i§ true regarding the physiologlcal changes ·


occurrlng during I~
A Each uterine contraction delivers approximately 3~1 of
/ blood back to the maternal circulation =-
'
Cardiac output increases by 4~~ during the e~sive phase
Maternal diastolic pressure can be expected to increase by
20 mmHg during uterine contraction
D D Uterine contractions increase the oxygen consumption by
2-0%
/

1
/ D E The epidural pressure can increase by ~mH20 during the
' second stage.

'l

,/

_J

J
Physiology MCQs

A True
B True
C True
D False
© E True
The combination of auto-transfusion and the re( )\.1:.;.t.'\<:·,.1 ·_,_: - !--~ (:··, ,_,.;.: .
· ?f
the ut~rus on ~he inferio~ vena ~ava results i~ .t,. ~-~.;~:~:~:::,,-;,:~,- . l
mcrease m card tac output immediately followir ·::ir •;Jii1\1t\ir-ltf~t:i I
60-80% greater than pre-labour values). Both s Y?ii}~~,,J:ii·<-~·; .. i
-----
diastolic pressures increase by 10-20 mm Hg di 1~i~~lti\('_, 2tt;,:,ti,~.{.,;1~;:~·-r2, l
Uterine contractions increase ox'ygen consump tl,~f.r.k.1t6!.1t,,:_.iJ~·H·,:
'

CSF pressure is unchanged during pregnancy. Eti<~tf'.i\U~irt~,.;,;t; :-ic,:


pregnancy is slightly elevated at 1 cmH2O, but .ii_=:·~"l~}:,+.:f;t;i,t,q~\t1_:;'~1., .
during a contraction.
Physiology MCQs

3.95 The follo~g results are withnirn normal limits for pregnancy:
~0 A Paco2 3 .46 kPa at 12 weeks' ·pregnancy
'-_/
I D 8 Plasma bicarbonate --,
28 at term I •\
·1
-,
6 - ·- c:)
/ 0 C Base excess -6 at term · ~

D D Haematocrit 45% at term -


. D E \!Vhite cell count (WCC) 20 at term
' I
~-,
J
Physiology MCQs

3-
3o~5 Asil§Wter§:

e A True
~ 18 False
~ C False
@ D False
© t False
His important to realise that the normal ranges for some tests alter '
·during pregnancy. However, do not assume that an abnormal test l
f
must be pregnancy related. As early as the eighth to_tenib_~s,
progesterone has stimulated the respiratory centre to produce
maximal hyperventilation. This change causes a respiratory
I
ai_~?~is with a Paco2 normal range of 3.~q-:-4,_26 kPa. Renal
compensation decreases plasma bicarbonate to a normal range of-
\
18-20 mmol/l and a base deficit of --::,..
-2'--.to- --3:
~ '
Red cell mass increases by 20%. Plasma volume increases by up
to 50%, so haemajocrit decreases to rv33~35%. Hb
concentration at term· is usually rv 1 ~. ~1,atelet count remains
the same or decreases slightly by haemodilution. WCC much 1
·

above 9 x 103 /mm3 is not thought to be normal (Note: think of ;, fu


f
infection or steroid therapy). Cl_otting factors increase throughout I .
pregnancy, and fibrinolysis anclfibrin formation increase as the
pregnancy reaches term. ~
Physiology MCQs

3.96 Regarding fetal changes occurring ~t birth~


7o A Clamping the umbilical cord i~creases systemic vascular
resistance
, < D B When right atrial pressure exceeds left atrial pressure the
foramen ovale closes .,_,_ ,: __ j '

'/, D C Physiological closure of the ductus arteriosus occurs at the


' same time as closure of the foramen ovale , JV
0/
f D D The initial decrease in the pulmonary vascular resistance is \ -·
\
because of abolition of hypoxic: pulmonary vasoconstriction
'/ D E lncr~asfrig levels of prostaglandins E1 and E2 cause closure of
the ductus arteriosus - 7~ ~

., .,
r

Physiology MCQs

3.96 Answers:
@, A True
€) B false
@ C False
@ D False
® E False
Clamping the u..m!?l!ical cord prevents flow of blood to the low
resistance placenta andtheref0re the systemic vascular resistance
(SVR) increases. This also causes
,:c_
an increase.
-
in left ventricular
end-diastolic pressure. A reduction in flow to the inferior vena
c~ reduces the right atrial pre§~ure. On taking the first breath,
the lungs expand causing a huge decrease in pulmonali vascular
resistance (PVR); this reduces right ventricular end-diastolic
pressure.
~-">PVR is further reduced by incre~__art~rifil~gen
7 concentration and decreasing car~on dioxide concentration.
Increased blood flow through the lungs causes an increase in left
-atrlal pressure. When this pressure exceeds right atrial€esae,
the foramen ova le closes. Permanent closure occurs a 4-6
weeks. The ductus arteriosus closes in response to increased
arterial ox.~~ concentration and decre~rosta laooins E1
and_E2• Physiological closure occurs at to-is. hours and 2
.::::-

per manent closure normally occurs at 2~ \.:Yieks. The ductus


venosus closes within\ hours',of birth. -
---·
, ' -- D
_.._ I '--·~
. ' ) ,·
o·.Jl'L ~-~~·'--
t :, /I l < .• ·,
1

-~\ J ._ . ( •••••
1-~t '-- IO-\<; y\r
,.-·

, L;·
, I./ .•

'-.\. . ,., C,; .)


. >
,J ; ,I
r- ; - ~/ \ \ \V~-~ I

I...--

C
,/
-\\. '· •. ,·\ ' ' I'-

I
Physiology MCQs

1, !Regarrding thermoreguiation~
/
0 A The anterior hypothalamus is predominantly responsible for
receiving afferent inputs about temperature
D B The hypothalamus doe~n6thave actual thermoreceptors
' D C The posterior hypothalamus is responsible for the coordination
of reflex responses to heat ~- ,'- \ r,.
D Non-shivering thermogenesis can increase heat production in
infants by 200% ,
D E fever caused by pyogens is because of peripheral mechanism
responses
' that are unable to match the hypothalamic -~-=--·
set p~!nt
Physiology MCQs

3.97 Afnl§W(ell'§~

~ A True
© B !False
@I C False
€} D True I
e E False
I
I
Normal core body temperature ranges from 36 to 37.5°C. Afferent
receptors from the skin, dee tissue and spinal cord pass via the
brain stern to th J?reo ti~~ucleus f the anterior hye~thalarnus.
The anterior hypothalamus also contains heat-sensitive neurons
and receives additional thermal afferents from other areas of the
brain. The po~ior hypothalamus is responsible for coordination
of responses to cold, ie vasoconstriction and shivering. The
anterior hypothalamus is responsible for response to h~~t, ie
vasodilatation and sweating. Non-shivering thermogenesis is the
increase in cellular metabolism in brow,0_ce_LJs,_ occurring in
response to beta-sy_n_:ipathetic stimulation of circulating
~nolam~~~~Adults lack brown fat and so this mechanism is m,
responsible for at most a 15% increase in the rate of heat
production. Infants, however, have significant brown fat and are
able to increase their rate of heat production by up to 200%.
Pyogens alter the set point of the hypothalamus, which then
causes peripheral mechanism activation for heat production.

, __, . \- ;

:'----9_ ~'- __\_:

- t ~-- _)
·. \ ~!_~\ /•. '. ~\c\

:· I
Physiology MCQs

3.~ Hypothermia:
/DA May be more extreme with a regional anaesthetic technique
/
(RA) compared
-....V
with·~ a general

anaesthetic
-
(GA)
~DB Causes decreased activation of the coagulation cascade
/0 C Of 28°( is associated with a reduction in cerebral metabolic
rate by 50%
)<
0 D Has no effect on the triggering of malignant hyperthermia
~D E Causing shivering is caused by bothperipheraland central
mechanisms· . c--- -
Physiology /ViCQs

3.98 All1l§W~lr§~

~ A True
o B True
@ C True
o D False
0 E True
During a GA tonic vasoconstriction is attenuated; this results in
. the early decrease in core temperature: with the loss of the core-
peripheral gradient. Gradually heat loss reduces as a balance is
reached between heat loss and heat production. Should the
patient become sufficiently hypothermic, the-attenuated
vasoconstrictive response will activate. Shivering is rare as the
vasoconstriction normally maintains core temperature. During
RA, the initial heat loss because pf attenuation of tonic
vasoconstriction is reduced as ~nly the blo_s:~a is affected.
However, the patient remains unable to vasoconstrict in the -
blocked area. This may-cause heat loss such that shivering is
triggered. Even then, only the unblocked areas are able to
generate heat. The combination of GA and RA is the worst for
heat loss. Coagulation is also affected, as platelet function is
impaired. H_y~9tl}~rr:Jll~ g~J~xs_th~trigg~r_2[rnalignant
~~rmia. Shivering is involuntary muscle contraction,
consisting of rapid~ tremors under peripheral control •
and slow.L_-
synchronous waves under central control. Interestingly, for each
~ lit~~sed at ambient temperature, the mean core body
,,/, temperature will fall by .-v0.25=...:::~
°C. -
Reference: Stoelting RK, Hillier SC. Pharmacology and Physiology
in Anesthetic Practice. 4th edn. Lippincott, Williams & Wilkins,
2005.
Physiology M(._.Qs.

3.99 The physa«»iogy of old age, In elderly people; ~;- 1 0

+.o A Atrial contraction contributes less to ventricular filling


00
' !~\;... ,~ .
/

D B A normal ejection fraction as diagnosed on echocardiography


excludes the diagnosis of diastolic dysfunction r ,,_, ·r}, 1. - -

' D C Diastolic pressure increases more than systolic pressure, '7- ·':'

/o D There is a reduction in the release of endothelial nitric oxide ,


Y D E Circulating norepinephrine concentrations are~crea~ /;,·f: ·
~\?'-?=\._\r>~
Physiology MCQs

J.99 Answers:
~ A, False
~ B false
® C False
© D True
© E False
Atrial contraction accounts or rv30% of ventricular filling
compared to 10% in young people, this is because of impaired
relaxation of dm:liac fibres as a result of diastolic dysfunction. A
/"- -
normal ejection fraction gives~indication of diastolic function.
Thickening of the intima and media within the vessels leads to
/ enhanced pulse wave propagation in elderly people. A higher
systolic pressure is seen as a result. Diastqpc pres-sure increase.s.,to
a lesser extent. In young people the cush-ioniugeffect of the walls
of the vessels delays therefurn of the pulse wave, gi~ng a lower
systolic and a higher diastolic pressure. Nitric oxide is a
vasodilator. Its release in all vascular beds is reduced in elderly

-
people. Circulating norepinephrine iacreases with age. There is
decreased reuptake at nerve endings, reduction in sensitivity at
the receptors and reduction in contractile response.
References: Physiology of ageing. Anaesthesia and Intensive Care
Medicine2003; 4: 337-8.
Perioperative care of the elderly. Continuing Education in
Anaesthesia, Critical Care and Pain 2004; 4(6): 193-6.

I
Physiology MCQs

JJ({pQ ~!lil eMer~y fi)leO!P)~1E:


/2
, ~/. D A The decline in heart rate response to exercise is because of
receptor downregulatlon .
. \
~ D B Orthostatic hypotension rarely coexists with hypertensi~1h·~,
/
ck
.

D C A restrictive respiratory pattern is seen with decreasing cnest J •

wall mobility
D D Functional reserve capacity (FRC) increases by 3-~(o per decade
;< D E Hepatic enzyme function reduces I •· _.,,
/
.
I
p
# J', t,... ' ./ -"';__..? 1
Physiology MCQs

3.100 Answers:
;; A True
s B False
@ C True
• D True
• E False
Downr~ulation of ~-receptors causes the reduction in maximum
· heart_~ Impaired baroreceptor function and perie_!leral ·
vasoconstrictor responses are responsible fowostural
hy,Eotension. This can be even more marked i~ ~be hyp~rtensive
patient ta~ing salt-wasting pharmacological agents such as
f diuretics. less_ comeliant chest wall with decreased
"f

GOstochondral mobility is seen. The lu.Dg~tissu_e lacks elastici!Y and


changes si~~ar to those seen i~hysem~ develop. There is
also an increase in...th~g_Y-Qlume, with reduced alveolar
surface area, alveolar wall thickening, V/Q mismatching and
marked reduction in gas exchange.' Expected Pao2 can be
calculated according to the-equation: 13.f>. ~ (0.044 x age) kpa.
~-!~~~d FRC)reduce and ~~~V and ~V;i~~~e. Hepatic blood
f1oWreduces but enzyme function is pre$ervec:I.
~ ~
References: Pharmacology and Physiology in Anesthetic Practice.
Fourth Edition. K. Stoelting.
Physiology of ageing. Anaesthesia and Intensive Care Medicine
2003; 4: 337-8.

\ :. ' (:) - _") . ,J L/ L( X :\'!~-(?_-


\\
Physiology uco,

J. il 01 ~egawdlilfllg lymphatics: .
..., D A They are absent from CNS tissues .
D B Their main function is to remove protein from interstitial fluid
. :---
'I D C They are valve!~ vessels·
D D They normally have a protein concentration of -,1,8 g/dl
D E From the right lymphatic duct they can drain into the
innominate veins
Physiology MCQs

® A True
B True
C False
@ D True
• E True
B~e, cartilage, epith~ium and C~ tissues hav~ymphatic
· vessels. Tne lymphatic ve~ have one-way valv~s that al low
flow of fluid and protein ~way from the inferstitium. The left-
sided thoracic duct drains into the venous system at the junction
between the left_interr.ltljugular and the left subdaviari vein. The
right lymphatic duct sometimes is ri.?!)ven present. It is formed
from three lymphatic vessels, which· can drain separately into the
right internal jugular, subdavian vein and innominate veins.
=--

,_, '- ,,
,--._:, ,'\
\ \ 'I ~ r,

I ' --

·-- --· "· \_; .. ~c' "·J '-- ~-:,.._,.-..... . ,. ~, .•..~ -


\ -·- \I.
\
-
't-,._ ,, ,_,, -- .\., \
' .) -
Physiology MCQs

J.1(())2
llhie fo~!owafl1lg are true off hypothala.mk and pitll.8itary plhysnir.D~ogy:
.· D -·- ·------
A The hypothalamus can be stimulated only by substances that
cross the blood-brain
,, barrier.
l-. -
D B The posterior pituitary is the site of synthesis of oxytocin
/
1_.,.,,, D C
Anxiety and stress of anaesthesia stimulate the release of
growth hormone
D D Growth hormone increases the utilisation of glucose by ,~\.
muscles
· _,/ D E Prolactin is a potent inhibitor of ovarian function

(
Physiology MCQs

3.103
3.102 AlIB$wers~ O'
i
fl) A False I

e B False I
I o'
Ill> C True
• D false I C
E True
The hyeQ!_~~us is located outside the blood-brain barrier and
·therefore is able to respond to cir culating stimulants including
sodium and cortisol. The pituitary gland is also situated outside
u
C"
the blood-brain barrier. lhe ~st'IBQr pituiia~J and~
oxytocin and ADH, but these are synthesised in t e hypothalamus
(in th~e_~raventricular and supraoptic nuclei respectively). 3.10,.
( Growth hormone sec~~~~~ is stimulated by ~~~p, [J
hypoglycaemia, f~sti~_g, a agonists, oestrogen, amino acid [
-G. /\ · -· - - --· ---
increase and tree fatty aclef decrease:----
-- - . - 0
The actions of growth hormone include increased protein
synthesis and mobilisation of free fatty acids. It also promotes
lipoTysis and gluconeogenesis in muscles. Prolag_J.n production is
increased during pregnancy and breast-feedmg and reduced by
dopamine.
Reference: Hypothalamic and pituitary function. Anaesthesia and
Intensive Care Medicine 2005; 6: 324-5.


Physiology MCQs

~egamdlnrrng end~crine plhiys~oiogy: ,rz_ 0 .-- '0


A When testing random cortisol levels, a normal result in the
evening may be one-quarter cithe normal morning level
--=-
B in the absence of adrenocorticotrophlc hormone (ACTH), the
zona glomerulosa of the adrenals is most affected
C Exogenous steroids are administered to steroid-dependent
patients perioperatively, as they have functional atrophy of
their hypothalamic-pituitary axis
D Pain is a stimulus for ADH release
E Oxytocin has no antidiuretic properties

Regarding adrenal physiology:


A Cholesterol is the precursor of all corticost~?.-~~s
B The zona glornerulosa secretes glucocortlcolds ·t· -
----··-·----- - . --····· .

C Aldosterone pr_~y~nts excess sodium secretion in sweat


D Serum potassiuQ1~concentration is the most important stimulus
for aldosterone release _ \'\/\ ~->')
E The zona glomerulosa-lacks- ~-i~-hydroxyla-;; C6""\\\ol c;-:::,y)
Physiology MCQs

3.103 Answers
"' A True
~ B False
• C True
• D True
• E False
Normal morning levels of cortisol are ""2Q µg!dl. Evening levels
fall to ""5 µg/dl. The adrenal glands atrophy ~lthQ!J! ACTH
stimulation but the zona glomerulosa is leastaffecfed and
continues to secrete aldosterone and maintain electrolyte
balance. The concern with steroid-dependent-patients is that the.
may suffer a hypotensive event during this stressful period.@!:!
release is increased by increased osmolality, hypovolaemia,
hypotension, pain, hyperthermia and stress. The normal role of
oxytocin is that of uterine contraction and contraction of breast
tissue to release milk. It has some antidiuretic activity but only at

aa,
most 1 % that of ADH.
.,
3.104 Answers: ,P
c.,,r:, Y°'. <' •..•.. - -5 \~ ""'--<'-..J'w~-~<, c->;.,. \'"\'\ "· ,., ,.··. o-\) <-.
~I

• A True f'
J ('I '"--0.. --; ~., ~ (_.:.~ r . ~\0,
" _ . ') ''·,... ' ''·
• B False
- \ . (' . ,, -- -
• C True -... ,-. I' (' \I'-' '. ',) ,- .•· ~'--·\ ,,. ,.._ \,... '-_
-
("• . . (
. /

• D True ,- \ •.

• E True
Corticosteroi~s -~r to both glucoEorti~oJ.ili and
\J,.}1~7ocorticJ:>ids\ The adrenals are divided into !~ree_ZgQ_~_ S of
different cells. The zona glomerulosa secretes mi~.9locorti,eoids,
the zona fasciculata secretes glucocorticoids and the zona
reticularis secretes cortisol and andrqgens. Aldosterone affects
sweat glands and salivary glands, reducing sodium loss and
increasing potassium secretion. Even small increases in serum
~otassium can hugely increase the release of aldosterone. The
<!?' ,_,._,
renin-angiotensin axis is also a stimulator for its release. The
zona glomerulosa is unable to synthesis cortisol as it lacks
~~~dro~ylase. -=-~---
Physiology MCQs

A Increases gluconeogenesls
,f"
,-- D B increases migration of leukocytes into inflamed areas ~-
I
. /-0 C Decreases the number of circulating eosinophils /'" • l'

./DD Binds to nuclei resulting in production of mRNA


/DE May remain elevated for l,J,. hou~s postoperatively

3.106 Regarding the adrenal medulla:


~--)----:... '·.
'k ~ A lt is supplied by pcstgangltonic cholinergic fibres ~-\

,/D B Most of the norepinephrine formed is converted to epinephrine


/

,/0 C Epinephrine synthesis is stimulated by cortisol


,,o D Upon stimulation, the adrenal medulla releases
catecholamines by exocytosis of vesicles
D E The plasma half-life of epinephrine is longer than that of
noi;.~pinephrine ~L

0
,.r-~~\<'¥u
,__o ( (.;;,
---
-}~:;.
"" I:!.,....,
., ~.
::;;.-- .... ·-,
~
~
Physiology MCQs

3.105 All1§Wflr§:

.7) A True
0 B false
C True
© D True
E True ~1
The actions of cortisol~increasing gl~coneogenesis,.
· protein_~1,abolism, fatty acidJDQbilisation and anti-inflamm~_!ory
effects. These anti-inflammatory effects ind_ude stabilisation of
lysosomal membranes, a reduction in migraffon 9_f le~~cytes into
inflam~~ues, a reduction of circulating e~sin~ghils and
decreased capillarx,permeability. Cortisol att,enygje.S }he
complement system and the f~ation of~f
inflammation from the arc1chidonic _Q~thway (decreases
phosphol.ipase ~rodugjon} b4t does riot.-irectjy~ffect
antibody-a~tige-n_ ~n qr histamine ~e e~.s_e. In response to
surgery, the cortisol level rises because of hypoth~lamic
stimulation f~ injured tissue ~nd-p_.!.oinflaf!!!Tiatory mediators
directly activa~the adrenals. The levels normally retur~ to
normal within~olJJ2; however, can remain ~le~ted for longer
dependi_Qg on the extent of the surgery. --

3.106 Answers:
• A False
• B True
• C True
• D True
E ----
o --- False
. ------,
----- ·- - - - -- . -----
/ ~~!l-~P-~r!~~ is converted to J~girieph~~~lbr---
phenylethanolamine-N-methyl transferase./Cortisol
- - --- ! .::.-=--:----/passes via
i QY,a;ad rentlQ_ort~ 1 vessels to increase the activity of this enzyme,
so increasing the sy~esis and re~se of epinephrine.
Stimulation of the ~I medulla b_y release of ace~lcboline
from preg?nglionic cholinergic fibres causes an increase in
calcium entry; this causes exocytosis of vesicles containing the
catecholamines. The plasma half-life of epinephrine is 10-15
seconds compared to that of norepin~rine
.;:.a
at 20-30 seconds.
'.'.:·,. .:·J~'.:hiJf t:f: J_:-; :;tt_r.p;.;:~G~)ii.,/i .,: ,/#~HL~,;~,,~i}:'~t:,::_~.; 1.:·;+ :,r.:~~~-.~\i,:s ~..fr.¾l~~(~.t;t(
1

{f~j-~~t~~jJ-. -'.

;.; . , ::.~~;:,~'!7-\)~¥;-~J,i~i-~ .: ;r:·,:rfs-,,;/:r .\si;;~}f\i{%.ql., ),, ;. ;;,.;,! ~ ', ,:--_,.;; }i,·"~i--d ,;~xr·-~·:·};, ·,~.
;:. ~~ ~ i~~1f~'{ ~ _; '.~ ·
fhU~~?~J~+:}N?t\{iJ,t!v~t:; f7 iri"~~!·!ti_l~~~¼tr-~;):~~f/~\~:~:j-9·;-L:/fh ~Mi-1~ ~1::~~/(1~~-
.t ~~~fr~)t~~~;~ L_ ~ ~ ·

,:· '!· , l {~t-i\~~µ'f,f :\ (,.,i,,{~,; if~- -~- i ~ ·.:{:\(l ·q\{_.;J !~ _;t:~}\{f-;{t~ ¥~i :;,,j;\ C~i~j J~k. r,}~~~-. i·

r.
-r
i

Physiology MCQs
\' . .t'-
\-\- - ~ ~\~ -) . ._;..,,
p
,:-,-,

3.107 AITT!§Wf[l'§~ <' -. '\


t

@l A False --r I ....• /.'\ ,- ,,.


i) B False J .. \. '-:""' r
----
,_
• C True
@ D False
E True
A total of 35% activity level for factor VIII is the cut-off for the
likellhood of bleeding and, even then, this is unlikely. Sickle cell
anaemia is inherited in an autosomal recessive fashion.
~-Thalassemia major causes reduced synthesis of the ~-globin
chain. This leads to a microcytic, hypochromic anaemia with
reduced HbA. Its inheritance is autosomal recessive. HbBarts
results in death in utero or during the neonatal period. It results
from having no a-globin gene.
Reference: Inherited Haematological Conditions. Education
Forum. Doctors.net.uk.

3 .108 Answers:
• A False
• B True
• C False
e D False
• E ,,True
Only 1-2% of the pancreatic mass is attributed to the islets of
Langerhans. They are made up of rv25% a cells that produce
'\
glucagon, rv75% ~ cells that produce insulin, ""5% f> cells that
,' ~
J
/
I
produce somatostatin -=--
and rv5% F cells that produce pancreatic
0,·// 1·
', polypeptide. ,Glucagon is released in response to hypoglycaemia,
1/
','
~:,.,
"::,(J,/'
r. ;.J
amino acids, se~is, trauma, ~-adrenergic agonists,,...- --=-- --
'1 . giucoc~coids and theophylline. Glucagons act via Gs-erqtcinJ
/
I coupled receptors causin-g'activation of adenylyl cyclase and
producing cAMP. Insulin acts via tyro~nase.
r,·
. \\
) 'J'I,_.:,,
/ . -~ _--\\/ .•. '

..
1. (
Physiology MCQs

3.109 insulin:
1

/o A Is stored in the pancreas complexed with zinc


v/0 B Has a plasma half-life of 5 minutes <,

X D C Release is increased by the hormone somatostatin \...'. _..-1 ...;: •

/D D Release occurs because of voltage-dependent calcium-


1/ channel opening
'///0 E Valine is dependent on insulin for its cellular uptake
<;. _.,,.--,;-. -~-~ ~ ... ::.a.--:::oc.
T
!

Physiology MCQs

J.109 J\U'l1§Wte!l'§~

\t A True
© B True
~ C False
@ D True
E True
Insulin release is increased by carbohydrates, amino acids,
--
. hormones (glucagon, gastric inhibitory peptide, gastrin, secretin,
..,,,...
choleilstokinin) and neural factors. r---.,_,_ -
Insulin is stored in ~ cells complexed with''~ Depolarisation of
the ~-cell membrane, by blocking potassium channels, causes
influx of calcium that causes insuli~sicles to fuse with the
membrane. Certain amino acids are dependent on iD,Sulin for their
cellul~,bgptake, including vay, lel!f_ine, tyr.2,~ine and=-- .
pheQyJ.alanine.

--- ,_ l
\r (-::::, -·

'('\. ' ..••. ,. l

(_,
Physiology MCQs ·

!Effects of insulin include increased;


' ;,_)
1 D A Gluconeogenesis '· I
' _,
f"-0 B Cell membrane permeability to sodium
D C G iycolysis in muscle
r- /0 D lipoprotein lipase activity
/o E Esterificauon of fatty acids
Physiology MCQs

3.110 All'i!$Wle!r§~

<>l A False
1:1 B false
@ C True
D True
E True
lipoprotel!!J.l~~e~?ctivity i!!f!eases; this causes the breakdown of
. triglycerides into fatty acids, so facilitating their storage in fat cells.
Hormone-sensitive lipases are inhibited, reducing_f!iglyceride
breakdown within fat cells.
-
The table demonstrates the effects of insulin.

Substrate Increases ·. Decreases

Carbohydrate G lycogenolysis Glycogen synthesis


Glycolysis Gluconeogenesis
Protein
., Amino acid uptake and oxidation
Protein synthesis
.,
Protein breakdown

Fat Fatty acid and Ketogenesis


a-glycerophosphate synthesis
Lipoprotein lipase Hormone-sensitive
lipase
Triglyceride
breakdown
-,,,..,. ,<
Physiology MCQs
(b\, \

JR.egawdou11g the lower oesophageal sphincter (LOS):


A The mechanism of its action consists of both smooth muscle
and skeletal muscle
~ D B Its neurogenic tone is influenced by vagal innervation
/' D. C LOS pressure minus lntragastric pressure gives a gastric barr~er
pressure
/\. D D LOS pressure is increased by cricoid pressure · '~\·
/

v,,. D E LOS pressure gradually decreases during pregnancy


Physiology MCQs
I
i'
3oil1

3o 111 Answers:
® A True
@ B True
Ii} C True
0 D False
® E True
The LOS is formed by smooth muscle at the lowest 2-4 cm of the
oesophagus. The mechanism for its action also involves skeletal
muscle from the diaphragm. Muscle tone is multifactorial,
neur~genic and myogenic. Normal LOS pressure is
10-30 mmHg. Gastric barrier pressure is LOS Qressure minus
intr~<;!Stric; p_ressure. LOS pressure inay decrease with cricoid J J
pressure secondary to the stimulation of afferent
mechanoreceptors in the pharynx.
/,DP-~------- -,
Decreased LOS tone
Increased LOS tone
•1 Cricoid Rressure
Gastrin
~ Alcohol-
--
Modulin
~Adrenergic stimulation
~drenergic
_/
o~es
stimulation
Metoclopramide
Secretin
HistamTne ~
Anticholinesterase "-. "~-~~~-, __ _:_ Glucagon
Gastric inhibitory peptide
1oc"reased intragastric pressdre
Bilateral vago\Ol;1Y V
Suxarnethon ium
Physiology MCQs

3.112 Durang exercise:


D A ATP stored within the muscle can supply the energy required
for the first 1 minute of vigorous exercise "
V/0 B Approximately one-fifth of the lactate released due to
/ anaerobic metabolism is utilised by the heart
'.// 0 C Anaerobic metabolism in the tissues releases three ATP
molecules per six-carbon unit of carbohydrate-
0 D There is a leftward shift of the oxyhaemoglobin dissociation
curve
) ./ D E Oxygen deficit in muscles occurs as anaerobic metabolism
. .. supports energy demands before enhanced oxygen uptake

\c
T
Physiology MCQs

3J 12 Airnsweir§~
@ A false
e B True
e C True
@ D false
@ E True
The ATP store\within muscle are limited and can supply enough
-energy for~nj! 1~ seconds of vigorous exercise. After this time,
ATP is supplied by aerobic and anaerobic metabolism. Anaerobic
metabolism can produce a rapid energy source but with limited
amounts, whereas aerobic metabolism can produce large
amounts at slowerrates. Most of th~ lactate]is cony_erted to
.,glaen in the lfver, although cardiac muscle uses some.
r,
~ Regari:ling option aer_obic metabolism of a simil<lr CHO
molecule yields 38 ATP molecules. (fwo ~;;;l~cules are
yielded from the hreakdown of glucose to · · ate and a further
36 ATP molecules are produ- ·ed from the rea · own of pyruyate
in theJt~~lic acid c~cle) Wirh iol;reases in H+, CO2 and
temperature, the curve sniffs to .he r~Oxygen debt is paid
back at the end of exercise, ie the oxygen consumption remains
high despite exercise cessation.
Reference: Physiological effects of exercise. Continuing Education
in Anaesthesia, Critical Care and Pain 2004; 4(6): 185-8.

••
Physiology MCQs

3.113 The fo~!cwRinlg are correct regall'dlh11g typgJ. muscle fibres when
compared wWh tyre n ~ mMsde fi!bll"f§~
/ D A They are fast acting · ~ \ --::.
,~ B They have a high mitochondrial content
,/ 0 C They have a high myogtobln content
" D D Their main energy supply is anaerobic
~ D E Their time to peak tension is approximatel}- 1yice as fast _

~ ./F'· --
'---'"

I
Physiology MCQs
I
i
3.1

s A False
@) B True
© C True
Q D False
~ E False
Type I muscle fibres are slow twitc;h fibres. They are more
numerous in the muscles involved in posture and are well suited
for prolonged activities and activities of low intensity. They rely on
aerobic metabolism and contain a high content of both ~
rry_Y-Q&~obin and mitoc~_ondria')Their time ~~-~ion is
r-.11-+9:_,ms compareaw1Th so
~s for type II muscle f16res. Type II
muscle fibres are fast twitch:-They are recruited for fast acting and
forceful exercise. They rely on rapid anaerobic metabolism, and
appear white in colour, containing low numbers of mitochondria
and myoglobin.
Reference: Physiological effects of exercise. Continuing Education
in Anaesthesia, Critical Care and Pain 2004; ~(6): 185-8.

-r.11,·'-<
,... , '.: . ---
..,:-
,

• J.- , .,,.I..•.,,_I
I / ·~-) -.I
I ' ')
., .. -{/ - ,.
'' \.,.
I

/,/
~ ('/,. f-
J/ 1.U_1'.., , . :::,,- '/ /''
v'
,r --r;V.-__-,,_
_
fl

/ I ( 0 :~,, /
,I
Physiology MCQs

3.114 The physiology of exercise:


A Breathing capacity limits oxygen delivery to tissues at
I I·~ D
maximum exertion
l
k,/D B As lactic acid increases P.aco2 decreases to normalise pH
j/DC The initial increase in ventilation can be attributed to the
l . changes in Pao2 and Alco2
-~ D Trained athletes do not have such an increase in heart rate at
maximum exercise when compared with non-trained athletes
D E Blood pressure increases during exercise
~
I

Physiology MCQs

3 .11l 4 A!nl§WIJ2tr§:

A false
@ 1B True
C False
D True
• E True
Breathing capacity doe~limit oxygen delivery in normal
· individuals even during maximum exercise, and haemoglobin
saturation remains unaffected, ie fully saturated. As lactic acid
- ~ metabolism in the tissues, Paco
increases because of anaerobic --:..... 2

decreases to maintain Q_H. There is a rapid increase in ventilation


=--==--
at the start of exercise. This is thought to be because of motor and
proprioceptive input from the exercising muscles and joints.
Peripheral and central chemoreceptors, temperature changes,
braln-stern and resplratory.centre activity all seem to have a part
to play in lncreasingventilatlon. Trained athletes increase their
stroke volume largely to result in a lower heart rate than non-
rrained athletes. Blood pressure increases slightly with a ~i'se in
cardiac output. This rise1s attenuated by the decrease in
peripheral yas~ul-9:! resistance by vasodilatation. -
Reference: Physiological effects of exercise. Continuing Education
in Anaesthesia, Critical Care and Pain 2004; 4(6): 185-8.

ll
Physiology MCQs .

3.115 V02ma?!:
/
.
'/ 0 A Refers to the maximum oxygen delivery l ~ r
··\ ' -
I(\ \' -

,/o 18 Can be reduced when at altitude secondary to pulmonary


/
limitations
D C During maximum exercise is most affected by increased blood
flow
/
· .,/ 0 D Is increased with the use of erythropoietin
0 E Is doubled if mitochondria are doubled
Physiology . ACQs

3.115 Airn§Wf8"§;

0 A False
0 8 True
«> C True
~ D True
~ E False
V02max = cardiac output X (arterial oxygen conten~_:- mixed
. venous oxygen content). - - -· ·
It refers to m__g~imalQ)5.xgen uptake. Normal subjects exercising at
sea level will have Vo2m:X limited by delivery of oxygen to the
muscles. The uptake-=aT oxygen by the muscles is:~ the limiting
3~_t,J. factor. It may be in~itive that doubling the mJto~ondria would
, double the oxygen uptake; however, this ha~ n~J'een shown to
be the l_imiting step. Increasing capillary density increases the
time and volume
. ..••. of blood within the muscle; this increase
__ .,-
oxygen extraction. Arterial oxygen cC>ntent is altered by altitude
and-~soaltering \/02max· ·
Refe~ence4f Phy~iologicai effects of exercise. Continuing Education"
in Anaesthesia,· Critical Care and Pain 2004; 4(6): 185-8.
Physiology MCQs

! 3.116 Regarding the physiology of sleep:


; '/,/o A Rapid eye movement (REM) sleep decreases with age
i \ _,
/D B facts learned just before sleep are poorly remembered when
/
compared with facts learned earlier in the day
'-/ ,, D C REM sleep is associated with limb twitching
D D Hyperpolarisation of a-motor neurons during REM sleep
prevent individuals actlng out their dreams
-o E There is an increase in ADH secretion
Physiology MCQs

3.116 Aii']§Wie ll'§~

G) A True

'i7
B True
C True
D True
0 E True
Neonates experience ,..__,50% REM sleep; tl.is falls to ,..,_,25% in 2
year olds. A normal adult experiences "-' 15-20% REM sleep. As
age increases REM sleep decreases and sleep becomes more
fragmented. REM sleep is characterised by eyeJ!lQYgQl_ents and a
characteristic ..~ of mi~~ncy, lo~~olfage and saw-tootl
"'{_aves. It has two phases: tonic and ph~. Tonic REM sleep is
associated with a reductio'nin muscle activity. Phasic REM sleep
is associated with muscle movement and twitching. Option D
refers to the atonia of REM sleep causing relaxation of skeletal
muscles. Waking 9utiQg this stage of sleep can occur and is
alarming although~harmful. The muscles of respiration and
upper airway tone are f)reserved.
--=-
Reference: Physiology of sleep. British Journal of Anaesthesia
CEPD Reviews 2003; 3(3): 69-74.

- ' .. -.,.. ,,,. )

:-I
j
t
' l Physiology MCQs
I
i

3.11 i The following is correct regarding sleep: '·.,: ;...- ·- ,--< - {

/ D A Thermoregulation is inhibited during sleep


!! ,;'' -/1I ,,,#. /

i /- D B Melatonin secretion occurs usually at dawn


I .,,/
l ·,.,--/'·o C y-Aminobutyric acid (GABA) secretion is associated with slow-
l
wave sleep induction ( ,
D D The first night after anaes hesia, the patient will have more / ·
REM sleep than normal
·__/o E Nights 2-5 postoperative,y are important for recovery of a
normal sleep pattern

3.118 Platelets:
. .

~/o A Take 10 days to be produced in the bone marrow


-~D B Are cell membranes surrounding megakaryocyte cytoplasm
,D C Are nucleated 't

f D D Express HLA antigen but not the ABO antigens \::.)0 ' Ir

,1/° E Have glycoproteins GPllb/GPllla that bind to vtYn Willebrand's ·


factor (vWF)
Physiology MCQs

3 .11 7 Arus-w1<eus~
@ A false
® B False
e C True
o D False
0 E True
Thermoregulation i~ preserved with sleep, although the threshold
for shivering is reduced and core temperature is reduced by some
0.5°C. Melatonin is secreted from the pineal gland in response to 3'
onset of darkn~. Is thought to allow the onset of sleep without
being hypnotic. It is available over the counter in the USA but is
currently available only 'by prescription in-the UK. The first
postoperative night is thought to contain little,orfri?)REM sleep
which may be because of the surgical in~lt or medications.
Nights~ are important for re~~very of this lost sleep.
Reference: Physiology of sleep. British Journal of Anaesthesia
CEPD Reviews 2003; 3(3): 69-74.
.,
3.118 Answers:
• A True.
• B True
o C False
D False
• E True
Bone marr~ cells develop into megakaryocytes, which
undergoftlon-mitotic nuclear replication. Platelets bud off the
surface oftnese enlarged megakaryocytes. This ~cess takes 10
days. Platelets express both ~ and H!Af lass Lantigens.
Platelets lack a nucleus and are unable to manufacture their own
proteins. They havea number of gfycoproteins on their external
coat includj_ng_~~ which binds c,oge~;and Gpllb/GPllla,
which bind vWFand fibronectirt
=-- /

.I
Physiology MCQs

3.11,9 The fo,~~(Q)wnmig increase platelet aggregation;


v /'.D A Thrornboxane A2
f D B Prostacyclin
/o /
C Released ADP
//0 D Fibrinogen
1, • /D IE Von Wi I lebrand's factor

3.120 Regarding coagulation:


Y D A The initial activation of the plasma factor XII is calcium
dependent
> D B In vitro, kallikrein release reduces the activation of factor XU
·· o C Factor XI is found on the surface of platelets .
, I .•

/ 0 D Activation of factor X occurs in the presence of factor-V


·.,..,.-
/ D E In vivo, activated factor VII seems largely to activate factor IX
rather than factor X
Cl I
Physiology MCQs

.# \\"- ·{ '5'-""'---~ C? y:...._, ·I"-----'<-,


3.119 Arn§WeliS~

® A True
B False
--
C True
D True - '-\ '"-J ~
E True
Thromboxane 5ynthetase is released when platelets contact
damaged endothelium. The released thromboxane causes an
increase in ADP levels and platelet aggregation. The ADP binds
and activates the GPllb/GPllla complex. Aggregation leads to
more ADP release, ie positive feedback. Prostacyclin, in the
vascular endothelium, stimulates platelet cAMP production,
which decreases ADP release and reduces aggregation. The
-=::;-

release of fil?_~!Dggen and vWF from a-granules enhances platelet


adhesion and aggregation. ·

., 3.120 Answers:
~ A False
B False
e> C True
• D False
I) E True
Initial activation of factor XII is calcium independent. It is caused
by the interaction of factor Xll with negatively charged surfaces on
collagen or glass in vivo. Kallikrein activates the coagulation
cascade (as used in the thromboelastogram).
Factor XI is found on subendothelial tissue and on g@!filet
surfaces. Plasma concentrations are ,..,,5 µg/ml. Factor X activation
occurs in the presence of activated factor~ factor 'all, ca~
and platelet phospholipids (including phospholipid Pf3).
---
Reference: Haemostasis, blood platelets and coagulation.
Anaesthesia and Intensive Care Medicine 2004; 5: 189-91 ,

i ..•
1 ••
•,
Physiology MCQs

«:(l)mp~eme/J'ilft $}'$lem~
••
Jhe classic pathway is irutiated by antigen-antibody
omplexes
H antibodies are capable of activating complement
ell-bound C3b facilitates T- and 8-cell activation
adiofogical media can activate the alternative complement
athway
he final common pathway results in bacterial cell membrane
sis

.•.
The complement system describes a series of proteins (mostly
hepatically synthesised) that are involved in in~lammation,
autoimmune disorders and host defence. The classic pathway
inv~e acti~tion of Cl by antiSen-antibody complexes.
Only~and t~are able to activate the classic pathway. Once
·/ activated, ~ and C2 are cle~d and activate C3, which in turn
< " activates C5. C3a fragments cause vascular leakage and histamine
release. Damaged cells, pathogens, foreign m~t~rial ?r l~
accelerates the spontaneous cleavage of C3, g1vmg nse to the
alternative pathway. The final common pathway is the _!11~1llg@.fle
attac~thway, producing CSb-9 complex. This causes non:
receptor~mediated cell activation and cyt<!oxici!}'. The
complement system is C<?~plex. This is ~ly<a brief overview.

) \ • ..L
\ t \ '· ,-, .••.• ,-._ ,\..1~---- -
,,-c· •

I
~- ,.,.
\ !"·, . \
\ \ -~· ~ '-

r:_ - \ ~\ ...., .._. \ ,:_


Physiology MCQs

3.122 Th~ fo~~owsil'\lg can be expected ~ll'il an area ;anffo<etedl by complex


regional pain syndrome (CRPS) type 2~
,/o A Nail changes
· · D B Hot skin
- /" D C Abnormal sweating
· ·' D D Osteomalacia
/1] E Actual nerve injury

-~

., Cl I
,-
,.
! .

Physiology MCQs

@ A True
e B False
e C True
e D False
® E True
Complex regional pain syndromes are associated with
. sympathetic dysfunction. ..

Type 1 consists of pain in an extremity that does [l~orrespond to


the distribution of a single peripheral nerve whereas, in type 2, the
pain is normally in the distribution of a damaged nerve (ie there is
a_c~Q'). Sympathetic dysfunction leads to iensory,
'_v__ascul~r, o~dema/sweating and motor/trophic abnorm~
(including n~Lihan_ges and osteo__eoro~is). The area affected

""
~ Vitamin D
--
classically feels c7d and clamm~--
deficiency in
.
adults
'

gives rise to osteomalacia:


-===----
. The reference below includes.the revised diagnostic criteria for
CRPS. I

Reference: Complex regional pain syndrome. Continuing


Education in Anaesthesia, Critical Care and Pain 2007; 7(2):
51-4.
~i
-~['c

_;

.~-/,-:, . \ : l ,d ;__,.,
,-.(

[_ 'V} ." ', .) IJV'.__/-!


. ,, /___...,-

_ ,~) ---.,.

I
_, I. ,,, ,
"l ~ \_, . •- ' _. -
Physiology MCQs

3.1! 23 ~fgardn1rug (!RP§:


i·/ D A Type ii results from peripheral nervous system activity after a
j partial nerve injury
. __/ 0 B Nociceptor activity increases in response to prostaglandin
release ·--
:_//0 C Increased circulating cytokines may be detected in the early
phase ·---
.'/DD The peripheral nervous system is responsible for the long-term
changes seen
to /o E NMDA_ tN- methyl-o-aspartate)'."receptor enhancement rr,dy
l
IS
have a role to play
Physiology MCQs

3o 123 Answers;
@ A True
@ B True
e C True
@ D False
® E True
F The pathogenesis of CRPS is still not certain. ai-Receptors
(Gi-coupled receptors, widespread throughout the nervous
system) become sensitised in the nociceptor C-fibres such that
they are more sensitive to the circulating and local (from
postganglionic sympathetic fibres) noreein;ehrine.
1'. Norepinephrine also induces the release o · ero~.ta. landins that
increases the nociceptor activity. During th initial i flammatory
phase cytokine levels increase. Although the initial response may
be peripherally mediated, the wind-up of the CNS is responsible
for the disabling symptoms.
Reference: Complex regional pain syndrome. Continuing
Education in Anaesthesia, Critical Care and Pain 2007; 7(2):
51-4.

=I
P. vsiology MCQs

3. ~~ 24 Regarding the ascending and descending tracts of the spinal


'!:0 rd;

D A The fasciculus gracilis conveys proprioception sensation from


the upper body
B The lateral splnothalarnic tract transmits pain and temperature
sensation
1"
_\ D C The anterior spinothalarnic tracts cross at the levels of
' innervation
\_,,---_,, D D Lateral corticospinal tracts decussate in the medulla
~D E Proprioception is conveyed to the cerebellum via the
spinocerebellar tracts

~CL\S,j._ ~~~\
Tc,vs.<:.~
\-::b_ \ ~
\/'MS5~
¾w--...p
Physiology MCQs

3o 124 An§W~lr§~

® A False
e B True I .

s C False
D True
c E True
Of the ascending pathways, the posterior column is divided into
. the fas~ilis and cuneatus. These ascend in the dorsal
column to reach their respective nuclTu~~decussate, in the 3
medu_lla. lh~ fasciculus gracilis carrie touch'y\~atio.~nd
, ~oenocept•()r1rom the lower body, wheremlfelasc1culus
cuneatus carries these senses from the upper body. The
*fothalamic tracts enter the cord and decussate to ascend on
l e c<lntralateral side. The lateral spinothalamic tract conveys pain
~mperature whereas the anterior spinothalamic tract conveys
~and pressure. Of the descending pathways, the lateral
· cort1cospinal tracts decussate in the medulla and descend in the
spinal,cord. It conveys motor innervation from the cerebral cortex.
The anterior corticospinal tract does not decussate until reaching
·,\~- ·--me\
' '
distal anterior horn./ cells. \ · 0t
/
r- ,- . _._:,_I ( t ,---~
• V, \ I \ \\ ' .- \ \ .• , /7 I f ~(\. \_I ~ :;:, \. "\, \..J;__:, \°'\_(',__;, '

'_\-===------·-
\ \'''
. / /·~.,-,;.,?
,_\ ,1/ ?'

'

- .... - - --- --··-


'
~
p';<
. e 'to,>- cl!\
~,, \\"\ (..
\ I ~v' "-.)
I'. '."'.J\. I ,.J
' VJ APJA_
I
1 rr---·
I
•..... --- I I "
v
frof·l,,'rf~\ --------~

\
I

I
/
I r

1,1> \y1·s_J,J~-
l .( \ ~ _)
Ji~ I /\, I .

I# -'.\\ JJ\J- -~" j I\-.·., +- . / ._

I
'I
Physiology-MCQs

3.125

/' D B
,1 D C

~ D D Anal sphincter impairment
1~D E loss of vibration sense in the left foot

' 3.126 Positive pressure ventilation increases:


--
1/o A ADH release C O
'< ~
',/o 8 Dead space ~ 0""C" -\-,_,_\..si.. -
---,.><:. . c-
~or-/' _t_\ <
'f D c left ventricular compliance -\:~/I?~-
n j
/, D D Renin-angiotensin system suepression ~,e.Q\::t
I
AD E Cerebral perfusion pressure 0b
., ,r,/\ Pi-() ~
.,
Physiology" MCQs

3.125 Answers:
.;; A True
@ B false
~ C False
e D False
e E True
Hemisection of the spinal cord, or Brown-Sequard syndrome,
affects both ascending and descending tracts, so knowledge of
both is required: see Question 3.37.
It would result in iesilateral 10s5. of vibration and p~oprioception,
contralateral loss of pain and tem~era~re, and ipsila~I
paralysfs. A brisk knee reflex (L3-4)°would be expected with a
a
Tl 'lesion as it would act as an upper motor neuron lesion.

3.126 Answers:

• A True
B True
• C False
• D False _ JL
• E False _.,_,_-v"'-Y< ., -5 , r ,..,__ , -,:,j,Y:Jy,. ---
Raised intrathoracic pressure caused by positive pressure during
inspiration decreases cardiac output by decreasing venous return,
mild cardiac~iamponade and increased_PVR. left ventricular
compliance reduces secondary to lung expansion and bulging of
the right ventricle against an increased PVR. Dead space
increases with the introduction of tubing and airway devices. The
decreases in cardiac output decre_a~e renal blood flow and
increase activation of the renTn~ngiotensi!l..s~stem. Cerebral
perfusion pressure falls as the mean arterial pressure (MAP) is
lower and the cardiovascular performance (CVP) higher- with
intermittent positive pressure ventilation (IPPV).
Physiology MCQs

3.1 '1.'J Magnesh.11m~

.·/ 0 A Increases end-plate sensitivity to acetylcholine


j

l J//~ B Is a predominantly intracellular ion


/0 C Activates membrane pumps in cells that transport calcium
outside the eel I

1\9
1/ D
D Is an NMDA-receptor agonist ::r ,,,.,

E Deficiency resembles digitalis toxicity on the ECG


:- - ~

3.128 Regarding CNS physiology:


~ A A-waves on an intracranial pressure (ICP) monitoring trace are
associated with raised ICP

/ D B Brain tissue accounts for: 50°/o of the total fixed brain volume.
/ ,, D C A rising ICP initially triggers changes in CSFdistribution
, ,,/ 0 D Cerebral blood flow autoregulation occurs at an MAP range of
50-4ilr50 mm Hg •r
'{. D E Cerebral blood flow starts to rise onl~nce Pa92 falls below
10 kPa 1 _... - ·
Physiology A1CQs

3.127 Answers:
o A True
e i8 True
,z, C True
® D False
@ E True
Magnesium is the second most prevalent intracellular cation after
potassium. Half of all magnesium is present in bone, 20% is in
muscle, 30% is protein bound and only 1 % is extracellular. It is
the natural
~ ..:==
calcium antagonist, increasing its expulsion from cells
and preventing its intracellular access by acting as a competitor
for transmembrane channels. Magnesium is an NMDA-receptor
antagonist and is being investigated for pain therapies.

3.128 Answers:

• A True
• B False
• C True


D
E
True
False I
ICP monitoring demonstrates A-, B- and C-waves. B- and C-waves
are affected by the normal pressuJe~hang~s associated with
variations in respiration and blgoi_pre??ure. A-waves are
associated with raised ICP; they are also known as plateau waves. ~
The skull is a fixed volume containing "-'85% braintissiie, rv10%
cranial CSF and . .. .,5% cerebral blood. With a rising ICP, the first _
compensatory mechanism is the change in distribution of CSF to
the spinal space and an incr~~ in_(:~F reabsorption. Limited
changes in the volume of the other compartments occur. Cerebral
blood flow increases linearly, 2-4% for every 0.13 kPa increas_e in
fa,W2 (between 2.7 and 10.7 kPa). Note that severe hypotension
canabolish arteriole respop~o Paco2• Cerebral blood flow
rises when Pao2 falls below~Pa,

!1
Physiology MCQs .

~egall"crfonig scoring systems:


A An Ashwel I shape chart is a score of waist to height ratio
!
(in centimetres)
l
: ·,\ D B A body mass index (BMi) of Z 7 is described as being normal
l /
i ·/ D C An APACHE II score us~20 physiological measurements in
I the acute physiology score
D The maximum points awardable on an apgar score is 10
.' D E Flexing in response to pain earns two points on a Glasgow
Coma Scale (GCS) score

The following blood tests are within the normal range:


A Ionised calcium 1.2 mmol/I ~ _ \ . 'L. '6
B Magnesium 0.85 mmol/I , 7;· r _ ';,::,;r
~./D C Glycated haemoglobin 5% ,. c;· - Z, ·,r J

{ D D Mean red cell volume 98 fl -. i O r


r ~0 --~· ()
/ D 111E Chi on·d e 8 2 mmo 1/1 r /
'3~ - Iu <,
Physiology MCQs

3~129 Answers:
I& A True
@ B False
fj C False
• D True
• E False
A score of 41-50 on an Ashwell shape chart is desirable, with a
score of 51 -60 caution is recommended and with a score of over
60 action is required.
BMI is weight (kg)/height (m2). A score of 18.5-24.9 is considered
normal, 25-29.9 is overweight and >30 is obese.
APACHE II or acute physiology and chronic health evaluation
version II uses 12 physiological measurements in the acute
physiology score. It also takes into account age and chronic
healthpoints, yielding a maximum score of 71.
Apgar scoring assesses heart rate, respiratory effort, muscle tone,
irritability and colour, glvlng a maximum score of 10. Flexing in
response to pain is awarded a score of three points on the GCS.

3.130 Answers:
• A True
@ B Trrue
• C True
• D false
e E False
The following are the correct ranges:
@ ionised calcium 11 1.0-1 .~5 mmol/1
o magnesium ._. ~ mmol/1
0.75-1.05
@ glycated haemoglobin (HbAlc) 5-8%
o mean red cell volume 7_6--~6 fl
e chloride 95-105 mmol/l.
Reference: Longmore M, Wilkinson 1B et al. Oxford Handbook of
Clinical Medicine. 3rd edn. Oxford Unviersity Press, 2004.
Physiology lvlCQs

! 3.1 J 1 ~eganlHllHg phaeochromocytomas:


}-/o A 1 0% oc_cu r outside the adrenal medu Ila
' /o 18 They are tumours of chromaffin cells
C Up to 50% of in-patient hospital deaths from this condition
occur during anaesthesia
,,
D D Epinephrine secreting tumours present with sustained ... ~-_,,

hypertension f (IJ•j)!- '-'


1

E The most sensitive test for diagnosis is elevated urinary


u
vanillylmandelk acid-(VMA)- . _u,_i',..__ ,,... , ~ _) /~ 1-,..----
Physiology ,V1CQs ,...

( () /~ -C .f-r-\_J\ '\,Ir
c-,;, . rt
,j •• ,.,,
~
· ,

:·<t" -
Answers: Ii.._: ] t 0-/
3.1 J1 n I
I . . -;
I ) ,'1 \ (' I

© A True
,a B True
~ C True
<.I D False
C E False
Phaeochromocytomas are the disorder of 10 per cent: 10% are
extra-adrenal, 10% are bilateral and 10% are metastatic. A total of
25-50% of deaths in hospital occur during anaesthesia; "'80% of
phaeochromocytomas will secrete norepinephrine. The ,
presentation will be that of sustained hypertension, headache and i'
palpitations. Epinephrine-secreting tumours will present with
paroxysmal symptoms including sweating, anxiety and tremor.
Although urinary VMA is tested for, it is a less sensitive diagnostic
tool than testing for elevated
~-
plasma and urinary catecholamines. -.;;:;:::::_

Reference: Recognition and management of ·


phaeochromocytpma. Anaesthesia and Intensive Care Medicine
2005; 6: 336-40.
L ·. _.

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,ANATOMY fv1CQs

'·"dic~rl~ your $]flTJ$W~rt$ wut!hJ in1 lirdk or cross DllTJ i!hre boxes ptr@widkedo
I

Yo
i
Regardirnig vertebrae:
typical cervical vertebra has a bifid spinous process
A A

10 B The body of the first cervical vertebra is small to allow


articulation with C2 t.,. .\\<.Jo-)
'-·'f D C The dens of C2 is held in position by the transverse ligament of
!
the C1
D D The transverse processes of the thoracic vertebrae articulate
with the ribs.
D E The spine consists of 25'true vertebrae /
L
l \
Anatomy J\ACQs

3:U32 Arm§werr§~
• r:
.,31~i
Il . I •

:'.:l A True
""

@ B [false I
l

© C True
l
© D True ( .. .,,
I
el E false i
There are 24 true vertebrae, 7 cervical, 12 thoracic and 5 lumbar.
--~ --
f~e.brae refer to the fused sacral and vestigial coccyx.
Bifid cerrcalspiDD rocesses allow connection of the neck
extensors. Cl, the atlas lacks both body and spine as it articulates
with C2, allowing free movement of the head. The dens of C2 is a
projection from its superior surface that articulates with the
anterior arch of Cl . Both the transverse processes and bodies of
the thoracic verteorae have-facets with which to articulate with
the ribs. ·
Reference: Cervical, thoracic and lumbar vertebrae. Anaesthesia
and Intensive Care Medicine 2003; 3:-434-6.

!
IL.

\\
·11 I!
':\.1,
-:I\
'.'I
Anatomy MCQs·
l
l
l

,3J33 !Regartd!H:rng spinalnerves and dermatomee


xo A Ail cervical spinal nerves leave the cord above their associated
cervical vertebrae
:/0 B The posterior nerve rootcarries sensory fibres from the skin
VD
l
C The anterior nerve roots carry motor fibres to the skeletal
muscle
if O D Cell bodies contributing to the posterior nerve roots lie within
the anterior grey horns of the spinal cord · ;I , , 1

D E The posterior primary rami supply only sensory innervation _,__ ,~/'
' I/ :l_-
_.,,
~ . l YN\/'"/ (')/',
\
,.;

u
Ana?omy 1VJCQs

.A false
© B True
C True
D False
® falseE
There ar@airs of spinal nerves. There are eight cervical
nerves. Cervical nerves l~Vll leave the spinal cord ~heir
respective vertebra via dfelntervertebral foramen. The-eighth
cervical and subsequent spinal nerves leave below their
associated vertebra. The anterior roots are motor and autonomic
JJll&, --- :G'tS"S Ode o,

and have cell bodies within the anterior ~y horns of the spinal
cord. The posterior nerve rQOts are sensory and have their cell
bodies in the posterior.~r:- ganglion, which lies outside th~ cord. u
The anterior and posterior ~ nerve roots fuse.
/ Having fused they then divide into a~or and p~ior primary
1111,
rami The anterior primary rami provide m~r ap~ s~ory
~ation to the limbs and front and sides of the neck, thorax
and abdomen; The posterJor primafY::@mi provide sens~ry and
motor innervation to the back-with a few exceptions,e'g the first
• I • • /' I \ -
cerv_1ca..!.P-ostenor ramus ~r.
Reference: Spinal nerves and dermatomes. Anaesthesia and
Intensive Care Medicine 2004; 5: 150-1.

(\ l. f,..,~--;1
/;-
-; (If ,,, i 7 /-, ; )7 f_
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---

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Anatomy MCQs ·
r'-" ••• --

3.134 The foJifo,wn!l'ilg nerves are correctly matched wot!tn the foremen
I\._
t!hi1r(Q)ij,llglhl w!Mdhi tlhey exit ttlhie ·§k!J.!l~~~
1,-, iJ A The internal acoustic meatus transmits the facial nerve J-~~
'D B The foramen ovale transmits the~1a~;1division of the r~
'
J
trigeminal nerve <"~J.-;~~
l·/o
1I C The superior orbital fissure transmits both the superior and
j inferior branches of the oculomotor nerve
t/
,1/o D D The hypoglossal nerve exits the skull with the vagus nerve

E All the nerves controlling movements of the globe of the eye


exit the skull via the superior orbital fissure

3.135 Regarding interpretation of cervical spine radiographs:


(
X, D A Adequacy of film requires visualisation from the lower clivus -,
to the upper body of C7 vertebra
B The distance between the odontoid and the axis is accepted as
normal if it measures 2 mm .,
C An open-mouth view is used to assess the odontoid process
D The spinal cord lies in the canal between the posterior
vertebral and spinolaminar lines
X D E Above the larynx, acceptable soft tissue thickness is less than
one-half of the vertebral body width
- -,,_,
Anatomy_MCQs F
,.
'
(

!
J.13f:.. ·.
Jo1J4 Answers ~
t' A True Q,
© B False
t.
e C True Q,,
© D False (
© E True -- Q
The~riternal acoustic meatus transmlts the facial and the n·
L~
vestibulocochlear nerves. Theftoramen ovale transmits the
!,-. . '

· mandibular division of the trigeminal nerve. The maxta~ _ .


rd~i~Ofl ls transmitted by the \?ramen_~._;The jugular J 3.1l.,
~oramenjransmits thgglQsso ha ngeal, vagus and accessory
nerve. The u erior or ital fissure ransmits a number of structures
including the following nerves:Tacrimal, frontal, trochlear, _,-_
oculomotor, nasociliary and abducens. It also transmits the
superior ophthalmic vein. r
Reference: Andreas Erdmann. Concise Anatomy for Anaesthetists.
Cambridge University Press, 2001.
3.135 •Answers:
• A False
• B True
• C True
e D True
e E False
_..,..-,Adequacy of film requires visualisation from the base of tb.e_skulL
(clivus) to the upper bod)! of Tl. Open-mouth odontoid views
-== =
=--
enable visualisation of C1 and C2. There are four lines that must
- ---=- .,.--
be assessed for alignment when reviewing a cervical spine
radiograph: the anterior vertebral line, the posterior vertebral line
(which forms the anterior wall of the spinal canal), the facet line
and the spinolaminar line (which forms the posterior wall of the
spinal canal).
Acceptable soft tissue distances are less than one-third of the
vertebral body width above the larynx and not more than one
vertebral body width below the larynx: 2 mm is the normal
odontoid, axis distance but up to 5 mm is accepted.
Reference: Advance life Support Group, Advanced Paediatric Ufe
Support: The Practical Approach. 4th edn, 2004.
l
Anatomy MCQs _
lj
3.136 The stenate-ga1r9gikm:

1
0 A Is the ganglion through which all sympathetic efferents to the
../
head, neck and arm pass
'.AD
B Is present in all patients
./D C lies behind the vertebral artery
L/. 0 D Blockade may help alleviate Raynaud's syndrome
j·f, 0 E Blockade is performed lateral to the carotid sheath
I

3.137 Chest radiograph interpretatoon:


~D A In a posteroanterior (PA) film, the normal heart shadow is
<50% of-the thoracic diameter . · , )
/ D B On a lateral radiograph, the mitral valve lies a~he line O • .;_
from the anterior costophrenic angle to the hilum
/, 0 C The left hilar lies 3~4 cm above the right
VD 1
D The left hemi-di;phragm is usually 2 cm below the right
/ 0 E In left lower lobe coll!pse, the left heart border is ~9st'
Anatomy /vi CQs

3.136 AnsweR'§~
© A True
i
l
j
© B False l
1
C True
©

@ D True
I
® E False
This ganglion represents the fused inferior cervical and first
· thoracic sympathetic ganglion. It is present in 80% Jf patients.
Sympathetic blockade results in vasodilatation~:::.which alleviates
is
Ra~naud's syndrome. To perform the-b):>_sk, the patient usually
supTne, once the transverse process of0is detected; the needle
is inserted medial to the carotid sheath, which is retracted laterally
to avoid injury~ ""'.

3.137 Answers:

• A True
• B False01
• C False
• D True
• E False
Option B descriP.e~ normal position of the a_prtic value; the
mltral valve lies!>e.!9\J this li_!le. The left hllar normally lies
1 -2~ cm higher thanthe right. The left hemi-diapb_ragm is usually
~2 _fffi
lower than the right, the right being hignerbecause of the
liver, Collapse of the l~f!lo~er lobe gives rise to the sail sign with
a triangle of increasedopacity behind the heart. The leffneart
border is preserved. ~'
Reference: Anaesthesia and Intensive Care A-Z. Third edition.
S. Yentls,

\ '
II
:\ 1l t! . I
Anatomy MCQs ·

3.13$ fR(egaurrrllKITTlg cerebral anatomy- '" '


- -.( D A A total o(,80°/~ of the arterial blood supply is supplied by the
intemalcarotid artery -
B The circle of Willis dS the anastomosis of the carotid and
, vertebral arterial supplies ·
,_/ 0 C The posterior cerebral artery supplies the occipital lobe
D D The anterior cerebral artery supplies the lateral part of the
cerebral hemisphere
D E The superior cerebellar artery is most commonly a branch of
the vertebral artery \'

Coronary circulation: ,_ .
A I~_ 90% of individuals the righi coronary artery is dominant
B The left coronary artery carries six-sevenths of the coronary
blood flow
· D C Blood flow to the left ventricle in-the epicardial and sub-
epicardial vessels ceases during systole 1,~J' ',-' --J ,_
D Normal resting coronary blood fr o'w is 250 ml/min·
·.'O E
Most venous blood from the coronary circulation drains into·
the right atrium via the thebesian veins ,- :. 1 ·' ·

~
Anatomy MCQs

'\ \
' \
,,-.;.,
. \

3J38 Answers:
,9 A false -- __,/
--~
© B True
© C True
© D false
e E False
Two-thirds of the cerebral blood supply is from the internal
carotid artery. One-third is supplied by the vertebral arteries.
/ The,2~ri9r-'-q
_ ~rebr9-l_,artery supplies superior and medial parts of
the cerebral hemisphere.
/ The '}'liddle ceJeb_r~l_a~~ supplies most of the lateral side of the 3.1.
hemis phere. .
/ The RosteriQr cerebralartery supplies the occipital lobe and
medial side of the temporal lobe.
/ The s~perior c~~bellar and anterior inferior cere_p_e~lar art~ries are
branches of the basilar artery formed from vertebral and anterior
spinal arteries. •' - 1·

Reference: Yentis SM, Hirsch NP and Smith GB. Anaesthl'sia and


intensive care A-Z. An encyclopaedia of principles and practice.
'3rd edn. Butterworth Heinemann 2004.
3.139 Answers:
0 A false
0 B True
0 C False
@ D True .
C8 E False
The right coronary artery is thought to be dominant in 50% of
patients. -- --- -
ERL.c_?_r:d~l and subepicardiai vessels are largely unaffected by
extravascular systemic pressure: however, su~~O~?rdial vessels
of the left ventricle are compressed ~ sy.ili?,le. I:.
•... ~:
I
~;?-linto the right
,.
/~- r----
/ The th~~sian veins drain venous blood directly into11e!!,:v~nt_ride:
Anatomy MCQs

3.140 Regaiidlotrng coronary nervous nnITTJ<eirvatnorrn:


A Both parasympathetic and sympathetic nervous systems
innervating the heart originate in the medulla
B The right vagus acts mainly on the atrioventricular (AV) node ·1
C The left vagus slows conduction through the AV node
D D The sympathetic fibres synapse in the stellate ganglion
E The effect of the sympathetic nervous system is of slower but
longer duration than the parasympathetic nervous system , \ ,_....,.,_
--~-----;- .., ' ~ ' 0~ \' """-L Q '5
\__\':> '("''-'~ "'''----"' ,,..._ , ..
-3,141 Regarding the cranial nerves: r r ~. J
I I'D A The trigeminal nerve originates solely in the medulla
(:
1 /0 B The trigeminal nerve has four autonomic ganglia
lI ~ID
I\ C The nasocl I iary nerve is a branch of the mafi r'lary nerve ~ \'~ :\ · 1

iVo
I D The optic nerve is purely sensory
. ·1 D
E The mandibular nerve ~xits the skull through U1e foramen
ro~um _) ,_) _, - " .
Anatomy MCQs

.;,,)
30140 Aresw<ew§~ ~ . ;""~
f· -
@ A True \~
"...,..~ J'
/ \-~
~ B false s\> ~-
@ C True ~
;.J ~ / ----- --
~ D True
e E True
Both parasympathetic and sympathetic ner:YQUs.sy~tems originate
in the cardiovascular control centre in the' medulla.
- '<

The ri~us acts mainly on the sinoatrial (SA) node.


5== -=-
The nodes are rich in cholinesterase and so deactivate the vagal
effect quickly. -
N~rE:pinephr~ has a slow onset of action but l~metabolised
so quickly and therefore has a longer duration of action.

3.141 Answers:

• A False
• B True
• C False
0 D True
• E False
The trigeminal nerve is the largest cranial nerve.
The motor nucleus is in the upper pons and the sensory nuclei are
situatedin the midbrain, pons and spinal tract.
The nasociliary nerve is a branch of the ophthalmic nerve, as are
the frontal and lacrimal nerves. -
/ The mandibular nerve exits the skull via the foramen ovale.
~ -~
/ The maJCill~~ ne!:Ve is purely sensory and exits the skull via the
forarnen rotundum ..Jhe ophthalmicnerve exits via the superior
orbital fissure.
1
L
Reference: Andreas Erdmann. Concise Anatomy for Anaesthetists.
, --t? F:mbridge University Press, 209L:- (\, --1 ~ ~--. 1 J l
l ..
l::.••

or/111111rJJ r,1 ( C - -- (7' l_;,•/f· 0 Y0·'/{l_l . b - ./ -


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v', r/., rJ·- ---
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Anatomy MCQs

Jo 1142 !Regardlsng the cranial rnHeu·ves:


, \., 0 A The eighth cranial nerve can· be affected by tumours at the
· oerebellopontine angle
\, D B The glossopharyngeal nerve
/ . leaves the skull via the foramen
1 magnum _, .-.
I . '-- '-
iv 0 C The glossopharyngeal nerve can be damaged during central
venous cannulation of the internal jugular
D The glossopharyngeal nerve supplies the carotid body
receptors
t\
1
D E The vagus nerve gives off the recurrent laryngeal nerve on the
'. right but not on the left ·--=- .1
1
,'..:.( ---
Anatomy MCQs

3L142 Ara§wetr$~ 3.1ft


[
I

€ A True
© B false
@ C True
@) D True
e E False
-1"" The vestibulocochlear (eighth nerve) originates from the
· cerebelloponttne angle and can therefore easily be affected by
lesions in this area.
~ The glossopharyngeal, vagus and accessory nerves leave the skull
via the jugular foramen.
/ Both vagus and glossopharyngeal nerves are in danger of being
damaged during internal cannulation, as they lie between the·
internajjygular vein and the interl')al ca_rotid artery.
= =-•
/ The glossopharyngeal nerve supplies many structures, including
- the carotid sinus and body.
,, The vagus gives off the recurrent laryngeafnerve bilaterally, but
the route that it takes is slightly different on each side.
Reference: Andreas Erdmann. Concise Anatomy for Anaesthetists.
Cambridge University Press, 2001.

t
i ,I
Anatomy MCQs·

3.143 Regarding lhe larynx:


·. ,,/. D. A The hyoid bone is at the level of C3

,. / 0 B The external branch of the superior laryngeal nerve supplies


motor to the cricothyroid muscle
..
I

D C The superior laryngeal nerve is a branch of the recurrent


1
laryngeal nerve --- v ·' J
v-0 y-

-_/ 0 D The laryngeal arterial supply is derived from branches of the


J thyroid arteries
! ,_/ D E Sensation to the airway below the cords is supplied by the
recurrent laryngeal nerve
Anatomy ·M CQs

A True
B True
C false
D True
© E True
The vagus gives off both the sue_el!Qf:L~al and the recurrent_
laryngeal nerve. -·~ 1
I
1
The superior laryngeal nerve gives off two branches: the external \
and internal laryngeal nerve. The external laryngeal nerves supply
motor to the cricothyroid. j
The internal laryngeal nerves supply sensation above the vocal
cords and to the interior surface of the epiglottis.
The recurrent laryngeal nerve supplies all intrinsic motor muscles
of the larynx (with the exception of the cricothyroid) and
sensation below the vocal cords.
-Reference: Andreas Erdmann. Concise Anatomy for Anaesthetists.
Cambridge University Press, 2001.

I
Anatomy MCQs

3o i 44 Regarding the effects of laryngeal nerve damage:


D A Partial recurrent laryngeal nerve palsy affects the adductors
more than the abductors • I

D B Superior laryngeal nerve· damage leads to a slackening of the cf _r


COrdS v"-UA\~ V~,'6-.

D C Complete bilateral recurrent laryngeal nerve damage causes


loss of voice
D D Unilateral complete recurrent laryngeal nerve damage causes
loss of voice L 1 ·". ·:. · :.· ":. ,
0J
,,
'\ )

D E Cords are held midway between the midline and abducted


position in complete laryngeal nerve damage

3.145 Regarding the bronchial tree and lungs:


. /
----\
D A The trachea bifurcates at the level of--T6
, •••• i

/ 0 B The right main bronchus is longer than the left J;ih I' ~

.,
0 C The right lower lobe has six segmental bronchi
D The apex of the lung lies at the level of the clavicles ,\:_,, . ...__
E The horizontal fissure follows the line from the fourth
costochondral
- junction to meet the obliquejissure
. •.. -

\2)o\ 1
~ ~ -D c_3
Cc::/1.u---- ----..:::> \ I-\
p,. 0- 'f.-_ __;t:> L{_ C:»>:
I
I
Anatomy MCQs

3 .144 Answers:
® A False
8 True
C True
D False
E True r:i.
19' A partial recurrent laryngeal nerve damage affects :abductors more
than a,g~i_uctors. This is Semen's law. r-
Complete unilateral recurrent laryngeal nerve damage does not ) i,
cause loss of voice because the contralateral cord may move
1 'l
across and restore the voice.
The following voice changes may be heard: I
.l
~: ~
I
~ Superior laryngeal nerve damage Weak voice
-1 Partial recurrent laryngeal nerve damage Hoarse voice
/ Complete bilateral recurrent laryngeal nerve damage Voice lost

Reference:..Yentis SM, Hirsch NP and Smith GB. Anaesthesia and 0, l


intensive care A-Z. An encyclopaedia of principles and practice.
- 3rd edn. Butterworth Heinemann 2004.
3.145 Answers:
• A False
o B False
o C False
e D False
e E True
The tracheal bifurcation is at the level of T4.
The right main bronchus )s-ShQ[ter than the left, giving off the right
upper bronchus after only 2.5 /cm. (.J
Both l~_ft and right lower lobes have ~~egmental bronchi:
superior, medial basal, lateral basal, anterior basal and posterior
basal.
The apex of the lung lies 4 cm above the clavicle, rendering it
vulnerable to puncture during central venous cannulation.
Reference: Erdman A.G. Concise Anatomy for Anaesthesia,
Cambridge University Press, 2001.
~-' I
Anatomy MCQs

Regall"dling the autonomic nerve system:


3.146
:j" D A The cranial parasympathetic innervation is via cranial nerves
,,,Al, VII, IX and X '}j_

1
~D B The ninth cranial nerve innervates the otic ganglion
' /

; V D C Sympathetic innervation to pelvic organs is via lumbar nerve


l routes
!~D
l
D The cell bodies of the sympathetic system are found in the
lateral horn of the spinal cord
j ~/ D E
I
~;-~;nglionic sympathetic fibr~s ar~orter than L. I
1 postganglionic parasympathetic fibres I

l
i
l 3.147 Regarding peripheral nerves:
/ v---- -D A The plantar nerve is a branch of the tibial nerve \ ,,\a (.J"--:./
I
4

X D B The sural nerve is a direct branch of the-selatie-nerve


1 --f
.. -: )

f 1( 0 C The sural nerve innervates the medial aspect of the foot


/ D D Posterior cutaneous nerve-of the thigh is formed from S3-4 ,:, -z. 3·
nerve routes
D E The lower lateral cutaneous nerve of the arm is a branch of the
radial nerve. - - .-
Anatomy MCQs

3.146 Answers:
di\
A False
e 13 True
e C True
D True
e E False
Cranial parasympathetic innervation is via cranial nerves Ill, VII,
IX and X .
The sympathetic innervation to the pelvic organs is via the lumbar
routes and the inferior mesenteric ganglion. .
innervation is via sacral routes II-IV.
I Parasympathetic
..... _=:.=---
The postganglionic sympathetic fibres (grey rami communicantes)
ar~~~er_ than the postganglionic parasympathetic as the
sympathetic cell bodies do not lie close to the end organs.
Reference: Andreas Erdmann. Concise Anatomy for Anaesthetists.
Cambridge University Press, 2001.

3.147
.,
Answers:
e A True
• B False
0 C False
0 D False
• E True
The sciatic nerve gives rise to the tibial nerve, which in turn

-
branches to form the sural and plantafnerves.
---- .
The sural nerve travels laterally to innervate the lateral aspect of
the foot.
The posterior cutaneous nerve of the thigh originates from S1, -2
and -3 (predominantly S2-). -
S-
Reference: Erdman A.G. Concise Anetomy for Anaesthesia,
Cambridge University Press, 2001.

\ : .

\ ;-··
Anatomy MCQs

l.148 IR.egairda!lilg the nerves 10f tlh? brachia! plexus:


"f. D A The upper trunk is formed from CS, C6 andC?
B The divisions cross the posterior triangle of the neck ~--, ,- ·, ·- --
C The cords are named according to their position around the
axi I lary artery
X DD The medial cutaneous nerve of the forearm originates from the
posterior cord · r. i, . , ·
1 -
' /
~ VD E The ulnar nerve is formed from the medial cord
~---
! ----- -·- --- - --- ----- -,
;:11 C ~ 4
•i
!, . ' ? \
I' \.. J ) \ (_ \ vJ"-- --r·•~-- l
--- --·- - - ··-· --- - _,,

~ ·,
~.:. ."-i .....•..
\"*-~f\..-'-Q,\'\j._'.J

C''- \~· \-\ ~ I_<.,__:.)

_.. -- - ---

\ ,,J . I
I
!
Anatomy /viCQs

3.7148 Answe rs~ J.1t'r


@ A false
@) B !False r
I
© C True (

@ D False
© E True
The best way to answer questions about the brachial plexus is to
. draw it.

Roots Trunks Cords Branches


Divisions
CS~ pper Lateral Muscu locutaneous
C6 \. 7

C7 Z) Posterior( '>--Median
Radial
~8=:>wei Medial / Uln'ar
T1 ' -,
'------~ yY-, C!_J, -
1
,-j 11 "t' ; I r~
O •. --.----.;..---
Figure: Brachia! plexus •- ·._") _../
J 0 f' . . .fl__ '

-- I

The upper trunk is supplied by CS and C6. The roots lie in the
interscalene groove, the trunks cross over the posterior triangle of
the neck and first rib, and the divisions occur behind the clavicle,
giving rise to the c~ds in the axilla. The branchesarise at different
levels. The medial cutaneous nerve of forearm is a branch of the
medial cord. ----e-
~

1, ,,· -1
r·· \~. Jv-Jo
".- . '.\ \/ __....:,- ...
\l ~
\
.i·\ \ \'•
;
',, ~
_

\ \\
I
/\. '·x j J ·--- C\..
') f ,-)
Anatomy MCQs

J. il 49 !Regarding sacral anatomy:


·,,// 0 A The sacrum is formed from-five fused sacral vertebrae
'~/,,,,0 B The unfused fifth sacral lamina forms the sacral hiatus
\., 0
C The sacral hiatus is covered by the coccygeal membrane
//0
D The sacral canal contains CSF
,.
. .1 D
E Obliteration of the sacral canal would not be a reason for a
failed caudal

')f'IQ
r
Anatomy A-1CQs

3.149 Answers:
It A True
@ B True
~ C False
@ D True
1'11 E False
The sacrum is formed from the five fused sacral vertebra.
Superiorly it articulates with the fifth lumbar vertebra, inferiorly
with the coccyx and laterally with innominate bone. The unfused
fifth sacral vertebra forms the sacral hiatus. This is bound
superiorly by the fused fourth sacral lamina, inferiorly by the
posterior body of S5 and laterally by the unfused fifth lamina. It is
covered by the sacrococc eal Ii ament. The sacral canal
c;ontainsJbe du~~ IJlC u mg CSF) which usually terminates at the
> '7- ~E:,<:o~i.l~craj)yerte~ on a line joining the posterosuperior iliac
spines. It also contains the cauda equina, filum terminale,
meninges, sacral and coccygeal nerves, and epidural vasculature.
There are a number of reasons for a fafled caudal including
obliteration of the sacral canal and calcification of the
sacrococcygealjlgarnent. --
Reference: Sacrum and sacral hiatus. Anaesthesia and Intensive
Care Medicine 2002; 3: 435-6.
I'·I
I

210
Anatomy MCQs ·

R~gardlB!l1lg ·thlf diaphragm;


A Its nerve supply passes po~or to scalenus anterior c '"-,k::_- -
B its movement accounts for ~-9o/o of the total tidal volume of ~ -:,
ventilation
C The opening for the inferior vena cava is at Tl o" '·

D The vagus n~rve P,~~~f,,S .through the diaphragm with the _9Qrta
E All SE:9sifryonnervation to the diaphragm is via C3, c4_and CS
/
Anatomy f.ACQs

3.1150 Arra swe rs:


~ A false
e B False
© C False I
t"
e D false
. Pov
@ E false . f:
l
The motor innervation for the diaphragm is via C3-5, which pass
<i=-~--- Yer:
ant~_to scalenu?3nterior. It also supplies proprioception to the
diaphragm. The peripheral parts of the diaphragm receive their
sensory innervation from the lower thoracic nerves. Movement of
the diaphragm accounts for up to 75% of total tidal volume
ventilation. There are three openings in the diaphragm.

Structure Level
:d
Inferior vena cava TB I
0
Oesophagus ;; ---- T10 )1
V Vagus T10 ~
0
Oesophageal- branches of left gastric vessels T10 ~
/\ Aorta ·--
- - -- - -- - --- - ' __ _,_ - --= 1f2 ~
T Thoracic duct T12?
f' Azygos vein T12P

Reference: Diaphragm. Anaesthesia and Intensive Care Medicine


2005; 6: 301-2.
-----\
,·\ \) ,\J \\ ~

, ('T~ '. 'f---- -- - vC>


co-
--
'.,k Q { "'(.___ C

R,."' \N,-':,
~ -
CORE TEXT REFERENCES

-~,s, Respiratory Physiology. The Essentials. 6th edn. Lippincott,


.-illiams & Wllkins 2001.
·= •. I, Kam P. Principles of Physiology for the Anaesthetist. Hodder
_ nold 2001.
~..u: SM, Hirsch NP and Smith GB. Anaesthesia and Intensive Care A-Z.
1 encyclopaedia of principles and practice. 3rd edn. Butterworth
-leinernann 2004.
'\Y) ,-

, \2.:• ~'?Lr'\.,~ -\-CJ


,.-
() C ')' :,1•1-i-<ct\ \"'-(,:cf\..---.~
.ocato.
iumh\

1bso1r
1cety11
add-p,
kl

acidc-
actio~.
activ=
activ.
acute

acute,
a2-a<..
(

ader
/\DH
(

adrc
adrei
.adu
adve
aer:
'airv
·airw
,alb·
ialb't'
1 altj_~1
aif{
alle
(

'
'At'
I
alt
am
~NDEX

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

~ zero 2.24 amplifiers 2.75, 2.91


.aaoline receptor 1.5 anaesthesia:
e 3.56 and allergic reactions J.82, 3.83
eys and acid-base awareness during 2.106, 2.107
control 3.74, 3.75 concentration of anaesthetic
3.11, 3.23, 3.56, 3.75 agents 2.44
riotential of SNAV node J.40 monitoring depth 2.108, 2.109
;:.r.f charcoal 1 . 12 5 · saturated vapour pressure 2.40
jetabolites · 1.67, 1.119 anaesthetics:
iaernolytlc transfusion amide local anaesthetics 1.32
.ctions 3.76 inhaled 1.115
.• terrnittent porphyria 1.97 intrathecal 1.84
•noreceptors 1 . 122 local 1.30, 1 .31, 1.34
,e 3.65 ca I
pregnancy and 1 .13 7
ecretion 3.67, 3.71, 3.103, regional and general 3. 98
16, 3.126 spinal 1.44
. medulla 3.106 topical local anaesthetics 1 .33
physiology 3.104 volatile 1.33, 1.39, 1.41, 1.42
ff 2.4 anaesthetic machine 2.120, 2.121
~ drug reactions 1 . 98 androgens and oxyhaemoglobln 2.12
metabolism of glucose 3.31 Angiotension II 3.67
.!)hysiology 3.2 · anion gap metabolic acidosis,
esistance 3.18 normal 3.58
1 1.112 antacids 1.27, 1.28
n' J.26 antacid prophylaxis 1.13 7
.one 3.70, 3.104 anti-arrhythmic drugs 1.139
cc)~ 1.78, 1.79 antibiotics 1.38
3.82 anticholinergics 1.94
sthesia and allergic anticholinesterase 1.20
• J reactions 3.82, 3.83 anticoagulation 1.55
· lelines 1. 148 antidepressants 1.24, 1.25
.partial pressure 1 .41 aorta 3.47
adds, essential 3.29 aortic pressure 3.42
one 1.88, 1. 140 apgar score 3. 129
;: l."i p 1.81 aprotinin 1.59
r_.

arteriolar smooth muscle tone, control blood groups 3.77 cardiz


of 3.48 recipient reactions 3.76
drui '
Ashwf'b! shape 3L 129 blood pressure 22.3 car d•..J
kf
asprin 11.112, 11 .129 monitoring 2.4, 1.5, 1.78
OU
blood pressure machine 2.4
asystole 2.17
measuring blood flow 2.82
mr f
atmosphere, pressure of 2.52 · cardia
ATP molecules 3.31, 3.112 blood sample, peripheral venous and
cardic
atracurium 1.16
atrial fibrillation (AF) 1.140, 1.141
arterial compared 3.57
blood volume 3.50 cardf
r
atrial natriuretic factor (ANF) 3.70 loss of 3.90 cardr
auditory evoked potentials 2.73 regulation of volume 3.61 tei.
autonomic nerve system 3.146 blood-brain barrier 1.1 01 to
Avogardro's hypothesis 2.21 Bodak seal 2.121 Carl'.
awareness during anaesthesia 2.106, body fluid distribution, assessing 3.62 cath
2.107 body temperature 2.26 cell r-.
aysystole 2.1 7 Bourdon gauge 2 .12 9 cent
box-and-whisker plot 2.139 cent
bacteriostatic and bactericidal Boyle's law 2.21 cep'
agents 1.35
baricity 2.96
basic life supp~rt (BLS) in
brachial plexus block 1.138
brachia! plexus nerves 3.148 .,
breathing systems, anaesthetic 2.112,
cere;
cerf'l
ce~
adults 1.145 2.113
basic measurement concepts, bronchial tree and lungs 3.145
ch~
statistics 2.150 Broselow tape 1 . 131 cht
benzodiazepines 1.23, 3.83 ChP•
Bernou Iii effect 2. 1 O 1 calcium 3.26, 3.39, 3.109 ch,
nebuliser 2.102 calcium channel blockers 1.139 chi
bile, physiology of 3.33 calcium homoeostasis, drugs
bloavailabillty 1I.100 affecting 1.87 ch,
bioburden 2.103 candela 2.1 chc
biological potentials 2.70, 2.73 capacitors 2.90, impedance of 2.17 ch
bispectral index 2.73 capacity and charge l .85 ch
blood caratoid body chernoreceptors 3.20
blood flow 3.36, 3.46, 3.64 carbohydrate metabolism 3.31
blood flow to organs 3.36 carbon dioxide 2.1241 3.14, 3.21
blood gas analysis 2.98 carbon dioxide analysers 2.32 d-.
blood transfusion 1.143 infrared measurement 2.31 C
blood volume~ . ,2.64
..
measurement 2.30
cerebral 3. o 26 carbon monoxide transfer factor 3.7,
tests, normal range 3.130 3.8
vscostty 2.59 and haemog!obin 3.14
nae arrest in adults 1.146 clearance. drug 11.114
ugs used during 1l .14«f clonidine 1l .122p 1.123
c muscle l.70 CNS physiology 3.128
output 2.95 coagulation 3.120
res 3.37 drugs affecting 1.51
cnac physiology 3.43, 3.47 coanda effect 2.61
[opulrnonary resuscitation combustions 2 .4 9
(CPR) 1.145, 1.147, 1.148,1.150 complement system 3 .121
diovascular physiology 3.41 complex regional pain syndrome
I
iovascular responses: (CRPS) J.122, 3.123
10 exercise 3.52 compressed spectral array 2.73
haemorrhage 3.53 context-sensitive half-time 1.116
ens' tube 2.136 contingency tables 2.143
thode ray tube 2.78 contractility 3.44
membranes 1 .1 coronary circulation 3 . 139
• 1lral control of breathing· 3.19 coronary nervous innervation 3. l 40 ·
ral nervous system (CNS) 2.120 correlation statistic 2.145
alosporins 1.3 7 cortisol 3.105
rebral anatomy 3.138 countercurrent exchanger 3.72
brospinal fluid density 3!'86 COX enzymes 3.69
avical spine radiographs, . cracking pattern and mass
interpretation of 3.135 spectrometry 2.47
_ ating agents 1.126 cranial nerves 3.134, 3.141, 3.142
1emoreceptors 3.20 critical temperature 2.23
t radiograph interpretation 3.137 currents, direct and alternating 2.81
-.~t wall movement 3.15 cylinder connection and anaesthetic
"'dren, calculations machine 2.121
_ involving 1.130, 1.131 cylinder pressures 2.124
hirality 1.95
·-1esterol 3.104 Dalton's law 2.22
, .. :ulinergic receptors 1.6 DC cardioversion 1.141
omatography 2 .44 dead space, anatomical and
lJgas chromatography 2.45 physiological 3.5
defibrillators 2.86 ·
gas chromatography
detectors 2 .46 degree Celsius 2.2
(.,tonaxy 3.59 density 2.96
:~!omicrons 3.32 depth of anaesthesia 2.108, 2.109
'_jrofloxadn 1.119 dermatomes 3.133
:lark's electrode 2.73 desensitisation, drug 1.118
ansing of medical diarnorphine 1.74
equipment 2.103, 2.104 diaphragm 3.150
(-
1

endocrine physiology 3.103


15 stora
diathermy 2.83
1stroir'
diathermy smoke 2.119 entonox 2.127 '
I a-i
sl:rgical 2.117, 2.118 eosinophils 3.78, 3.105
.coupl
diazepam 1.113 ephedrine 1.121
-ilatirt ·'
C"
diazoxide 1.93 epinephrine 1.96, 1.147, 3.106 I 1
diffusion within the lung 3.6, 3.22 erythropoietin 3.23
1omen.
diffusion 2.33, 2.35
diffusion capacity 2.34
digoxin 1.117, 3.41
etomidate 1.71
eustachian valve (fetal
circulation) 3.49
l
i
om~'-
i .
ucor
_lycog{
-
\yco;.
2,6-diisopropylphenol exercise 3.6, 3.15, 3.52, 3.112 j
lycdp
(propofol) 1.66, 1.68, 1.109, cardiovascular response 3.52 I
i-prrt\
1.116 physiology of 3.114
·;rah~-
diuretics 1 .45, 1.46, 1.47, 1.93 and respiratory system 3.22
ranul,
dopamine 1.111 expiratory reserve volume (ERV) 3.4
uan
Doppler effect 2.95
double-lumen tubes 2.136 farad 2.90
1aer;n•
drip counters 2.69 fatty acids 3.32
1ae~
drug metabolism 1.102 esterification 3.110
.aem
binding 1.105 fetal changes at birth 3.96
ialc ',
disft"ibution 1.101 fetal circulation 3.49 •1 I
-lar.... ;
in lungs 1.86 fetal haemoglobin 2.11
HbH
response 1 . 11 8 fibrinogen 3.11 9 ( .•

nea<
drugs, absorption of 1 .2 Fick's law 3.1
heat
filters 2.110
ECG 3.42 fibres filtration 2.111
heL_
!ECG trace 2.87 flecainide 1.117
Herl
edrophonium 1.18 flow meters 2.62, 2.66, 2.68, 2.130,
he.
electrical components 2.84 2.131
hep;
electrical potential generators 2.76 bubble flow meters 2.68
he-
electrical safety 2.15, 2.16, 2.17 thermistor flow meters 2.68
electricity 2.82, 2.87 fluid flow 2.58, 2.60
electrodes 2.74 force 2.50
electroencephalograph (EEG) 2.108, Fowler's method 3 .5
2.109 fresh gas flows (FGFs) 2.112
potentials
2.72 Friedman's test 2.143
electromagnetic spectrum 2.94 fuel cell 2.13
elcctromvograrn (Elv\G)
potentials 2.71 GABA (y-aminobutyric add)
:e~ectron capture detectors 2.46 receptors 1! .21, 3.11 7
r.t.~ "--~ ~4! ....,,,.·=- ...,,.. 4- ~, .
o ,, .•
:.-~~rHi.!,1.J..ftA! ~,:Ht'. constant. t"Jl. .o.
1.110 gas carriage in blood ], 14
~:-rne,·p-~,.)-CV sureerv 2.106 6't"s J. laws
<:':J""S •.. ~? r, "1· :n.
,:;;..;.a.&.; ~-..,._-
L~ ~ ~~ I
age 2.123 . hypersensitivity reactions to
stinal tract, drugs drugs 1.99
·----ting 1l .29 hypothalarnic physiology 3.102
.led protein 1.107 hypothermia 2.59, 2.116, 3.11, 3.98
liergy 3.83 . hypoxic pulmonary vasoconstriction
.ilar filtration rate (GFR) 1.114 (HPV) 3.25
r hydrostatic pressure 3.70
--genesis 3.61, 3.105 ibutilide 1.139
3.31 ideal body weight (IBW) 1.108
3.110 immunity 3.81
/rrolate 2.107 impedance 2.17, 2.90, 2.91
s 1.104 indicator dilution techniques · 3 .10
. __ law 2.35 inspiratory reserve volume (IRV) 3.4
3.78 insulin 3.109
ine 1.138 effects of 3.110
intravenous induction agents 1.67
bin 3.7, 3.12, 3.14 intravenous infusion devices 2.69
v __ binopathies 3.107 iodine 3.27
rrhage 3.53 ionisation 1.3
1.40, 1.,.02. isomers 1 .81 CII I

1n·'s solution 2.37 isosbestic points 2.9


:'rase 3 .1 08 isotopes 2.18
. city, specific 2.27 isovolurnetric contraction 3.42

--
ss 2.26
Its 2.99
rnperature relationship 2.28
joule 2.2

w 2.21, 2.35, 2.41 Kallikrein 3.48


_ .- hysiology 3.30 katharometer 2.45, 2.46

-
tis C 2.103
es 3.30
t'tlreuer reflex 3.21
ketamine 1.69, 1.70
kidney, acid-base control in
kidney, functions of 3.61
3.7 4

. 92 proximal tubule 3.63


_. ow oxygen enrichment renal corpusde 3.67
-iAFOE) devices 2.101 kidneys and drug clearance 1.114
l 19 Korotkoff, fifth phase 2 .4
Jtion and treatment 1.136 Kupffer cells 3.30
l~ation devices 2.8, 2.102
., 2.7 .. labour, physiological changes occurring

r
hrey system 2.112
ions and measurement 2.29
·,,eter, hair and Regnaulrs 2.7
during 3.94
laminar flow 2.54, 2.55
Laplace's law 2.58
laryngeal nerve damage J. o 44 sterilisation2.1 05
laryngoscope l.1 a 4 medulla 3.140, 3:141
larynx 3.143 membrane bound receptors 11.104
esepa
I I

lasers 2.19 mesanglal cells 3.65


safety precautions 2.100 meta-analysis 2.146 ana~
lean body mass (LBW) 1.1 08 methadone 1 .7 5 jstruc~ :
leucine 3.29 methionine 3.29
hm's la
lidocaine toxicity 1.89 methylene blue 2.1 O Uager
linear regression 2.144
phy~)
micro-organisms 2.105
lipid metabolism 3.32 midazolam 1.109, 1.22 . ,.1coti<;:-
, ioidl
lipoprotein lipaes activity 3.110 minimum alveolar concentration
I iver and drug clearance 1.114 (MAC) 1.23, 1.39, 2.43, 2.106
tsonis
liver 3.32
1'd'1n2 • -
mivacurium 1.120
l,ci\k._
loop of Henle 3.71 monoamines 1.101
lower oesophageal sphincter
kcil\01
morphine 1.72, ·1.73
I
(LOS) 3.111 mRNA 3.105
i5mot,
low-molecular-weight heparins muscle fibres, type I and type II 3.113
(LMWHs) 1.54
lung volume 2.62, 3.4
muscle relaxants 1 .1 7
myocardial tissue physiology 3.38
l·smo'·-
-mci ·
lung, compliance of 3.16 myocarditis i r 136 1s mos
lungs, adult 3.1 myoglobinuria · 1.133
Ostvt
I I

lungs, drug metabolism in 1.86 ixyge


'•)Xyf··
lymphatics 3.101 neostigmine 1.19
lymphocytes 3.80 nerve fibres, classes of 3.88
)XYL
nerve simulator 2.76, 3.59, 3.60
magnesium 3.12 7 settings 3.60
oxy
magnetic flux 1.79, 2.80 nerve: biological potential 2.70
oxy~
magnetic resonance (MR) 2.20 nerves and foramen 3.134
magnetism 2.79 neuromuscular blockade
magnets 2. 1 6 assessment 1 . 7
malignant hyperthermia (MH) 1.10, neutrophils 3.78 t
1 _

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 2.14
Mapleson circuits 2.112, 2.113 nitrous oxide 2.35, 2.41, 2.42, 2.123,
mass spectrometry 2.47 2.124, 3.6
McCoy laryngoscope 2.114 and diamagnetism 2.14
mean arterial pressure V-AAP) 2.3 non-depolarising muscle
medical air 2.124, 2.128 relaxants 1.13
medical equipment: non-parametric tests 2.142, 2.148
cleanslng 2.103, 2.104 normal distribution ·2.149
needed to treat (NNT) 2.146 papaverine 11.138
paramagnetism 2.14
tients, drugs and il .108, partition coefficient 2.42
~.109 pasteurisation 2.104
thetics and 2.107 Penaz technique 2.5
e sleep apnoea 3.89 .penicillins 1.36
law 2.89 peripheral nerve localisation 3.59
- 3.100 peripheral nerve blockade 3.60
. ,1'0logy of l. 99 peripheral nerves 3.147
· .... ressure 2.38 pethidine 1.76, 1.77
1.80, 3.83 PGl2 3.68
sation 3.78 phaeochromocytomas 3.131
ata 2.138 phagocytosis 3.65
__ope 2.78 pharmacokinetics 1.108, 1.110,
nometer, von 1.111,1.97
_ klinghausen 2.4 of inhaled anaesthetics 1.115
1lity 2.36, 2.39 pharmacology of old age 1 .82
gap and osmolarity 3.55 phenytoin 1.26, 1.106
__ .ty 2.38 . phosphodiesterase inhibitor
. lj.36 aminophylline 1.92 •,
solubility coefficient 2.42 phospholipase A2 3.68
, and paramagnetism 2.14 physiology of the cyclo-oxygenase
easurement 2. 9 enzymes 3.68
__torage 2.125, plezo-electric effect 2.48
centrators 2.126 pin index 2.122
ension management 2.13 pipeline gas and anaesthetic
n· 2.11,2.124,2.125,3.14, machine 2.120
4 pituitary physiology 3.102
__ ... oglobin and plasma cholinesterases, drugs
oxyhaemoglobin 2.9 metabolised by 1.120
ciation curve 2.12, 3.13 plasma:
.aspirinand 1.112
2.147 fresh frozen plasma (FFP) 1.143
kers 2.76, 2.115, 2.116 oncotic pressure 2.38
~ric resuscitation 1.150 plasma cells 3.81
siology 3.84, 3.103 plasma drug concentration 1 .11 6
rm fibres 3.85, 3.85 proteins bound in 1.106
s 3.109 volume 2.64
tic function 3.108 platelets 2.110, 3.118, 3.120
rronium 1.14,11.119 aggregation, increase of 3.119
drug effects on t .129 radioactive particles 2. ·, 8
pneumotachograph nits:
Raman spectrometry 2.48
c'iaracterisncs 2.67 Raoulrs law 2.39
basic r
poisoning, treatment for 1.125, 1.126 derive
rapid eye movement (REM) J.116 1ai-'io-r
polio blades 2. 114
receptor agon ists and 3,r~-
positive pressure ventilation 3. 12 6
antagonists 1.103 ;1p
' l
postoperative nausea and vomiting, Ja lime
receptor morphology 1. 118 jium v1-t
drugs used 1 .62
receptors 1.104, 1.107 meta~
l
postpneumonectomy 2.34
recombinant factor VIia (rFVlla) 1.61 toxicit
posture · 3.50
red cell fragility test 2.38 µbilit{-
Poynting effect 2.127
released ADP 3.119
prazosin 1 .124 fuldidc
remifentanil 1.116, 1.120 icific o:i
pre-eclampsia 1.134, 1.135
pregnancy 3.13, 3.95
renal blood flow 3.64
renal response to disturbed acid
'.nal.a~.
anaesthesia and pregnancy 1. 13 7 ;r,al car
base 3.75 trar
and drug distribution 1.101
hormonal changes 3.91
renin 3.61, 3.66 left-s.,'
repolarisation 1.139 inal nei
maternal physiology during 3.92,
3.93
residual volume (RV) 3.4
resistance 2.89
tome;·
and oxyhaemoglobin 2.12 ;ndard 1

preoperative fasting 1.142


.r~sistance to current flow 2.90 · cs~·
peripheral resistance 2.3 tisticz..
pressure gauges 2.129
resonance and damping 2.6 1tistical
pressure measurement 2.53
respiration at altitude 3.23 Ilate ;-
procaine 1 .38
respiration 3.19 [late g;
prostacydin 3.119
respiratory effects of diving 3.24 rilisa"
protamine 1.56
respiratory system and exercise 3.22 eq
protein binding 1.4
reverse transcriptase 1.136 iichion
protein metabolism 3.34
Reynolds' number 2.57 rtacta ·:,,
PRST scoring 2.108
ropivacaine 1.106 xarneu
pulmonary artery flotation
rotameters 2.65, 2.66 2.1.
catheter 2.97
pulmonary blood flow 3.1 O sux.
suxar
pulmonary capillary wedge pressure sacral anatomy 3.149 r--,
(PCWP) 3.47 mpai_·:!,::·1·
sarcoidosis 2.34 ,mpa •..,
pulmonary circulation 3.3
saturated vapour pressure 2.40 p~r,
pulmonary physiology 3.9
Schrader socket 2.120 mpaL
pulmonary vascular resistance
scoring system 3.129 stemic
(PVR) 1.85, 3.11
Seebeck effect 2.25 (

pulse oxametry 2.9, 2.1 O !
semi-permeable membranes 2.35 chvp½·
I '
Severinghaus electrode 2.30
radiation 2.18
sevoflurans 1.43, 1 .-i 02
\ . ,/. ,,ngnt
I
uansrrnss1on
' • •
ano '
ventricular pressure-volume curve
U
humidity :2.7 relationship 3.44, 3.45
ventricular tachvcardia.
card.rovernng
,. "J..
"Brc
vacuum insulated evaporators . vertebrae 3.132
viruses 2.104
(VIEs) 2.125
vagus nerve, functions of 3.87 viscosity 2.59
valine · 3.109 vital capacity (VC) 3.4
Valsalva's manoeuvre 3.51 vitalographs 2.62
valves, ·physics of 2.51 . vitamin K-dependent clotting
van der Waals' forces 1.105 factors 1.127
Van Slyke's apparatus 2.1,1 V02max __ 3.115
vaporisers 2.132, 2.133 volume of distribution 1.113, 1.117
vapour_analysis -2.48 von Willebrand's factor (vWF} 3.118,
Vaughan-Williams 3.119 .
'classiflcation 1-.139
vecuronium 1.15 warfarin 1.57, 1.58, 1.101, 1.106
venous admixture 3.54 drugs increasing effectof 1.128
venous P02 2.11 waves and wavelengths 2.92, 2.93
venous system and posture 3.50 webers 2.80
· ventilation 3.5, 3.6
.,. Wheatstone bridge circuit 2.6
control of 3 .21 white blood cells 3.79
ventilators 2.134 Wright respirometers 2.63
servo ventilators 2.135
ventricular fibrillation (VF) 1.146, yohimbine 1.122
1.147, 2.17, 2.83
ventricular muscle action zidovudine 1.136 ,,·.;

zona glomerulosa 1.104 •.··.-.~)-#


potentials 3.39
i
,. measurement 2.25
i,: 2,1 body 2.26
lved l.2, :2.50 TfNS 1..77
to-noise ratio 2.88 fi-thalassemia major 3.107
3.117, physiology of 3.116 theatre shoes, impedance of 2.15
me 2.137 thermocouple 2.25
, nitroprusside 1 .48, 1.121 therrnoregulation 3.97
tabolism of 11.49, 1.90 thiazides 1 .45
icity, treatment of 1.91 thiopental 1.63, 1.64, 1.65
ity 2.41, 2.42 post-injection treatment 1.138
ling classification 2.103 thrombozane A2 3 .119
c gravity 2.96 thyroid hormones 3.28
anaesthesia 1.83 thyroid metabolism 3 .2 7 .
cord: ascending and descending thyroid-r~lea-sing hormone (TRH) 3.28
·acts 3.124 · thyrold-stimulating hormone
:-sided partial transaction 3.125 (TSH) 3.27, ~.28
nerves 3. 1 33 tidal volume (TV}:. 3.4
retry 3.4 time constan(tlrog elimination 1.110
.rd error of the mean tolerance, drug 1 . 11 8
SEM) 2.141 total body weight (TJ3rW) 1.108, 1.109
cal analysis 2.143 total intravenous anaesthesia
cal statements 2.140. (TIVA) 2.106
e ganglion block 1.138 trachea 2.8
e ganglion 3.36 tranexamic acid 1.60
.ation of medical transducer, strain gauge 2.6
squipment 2.105 transformers 2.84
iometric concentrations 2.49 transfusion-related acute lung injury
tant 3.17 (TRALI) 1 . 1 44
iethoniurn 1.8, 1.9, 1.120, tricyclic antidepressants 1.24
!.116 trimetaphan 1.121
xamethonium apnoea 1.11 tubuloglomerular apparatus 3.65
xamethonium metabolism 1.12 turbulent flow in tubes 2.56
ithetic nervous system 3. 11 type A (augmented) drug
athornirnetic G-coupled reactions 1 . 98
oroteins 1.107 types of electrical equipment and
athomimetics 1.96 safety 2.15, 2.16
nic circulation 3.35 tyrosine 3.29

ohylaxis 1 .118, 11.121


erature 2.24 unfractionated heparin 1 .52, 1.53
instant 2 . .21 urea and urine 3.72, 3.73

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