Other title in the Aids series

Burt on Aids to Postgrad uate Medicine 6E

Aids to Undergraduate
Burton Aids to Undergraduate MedIcine 6f
Dixon A ids to Pathologv 4E
Habel Aids to Paedi;:u r;C$ 3E
Medicine
Habel Aids to Paediatrics for U ndergraduates 2E
Hayes and MacWaher Aids to Clinical Examination 2E
Mead Aids to General Practice 3E
Mowschen$On Aids to U ndcr ll r "du~w Su rgery.E
Rogers and Spec:t or Aids 10 Clinical Pharmacology and Therapeuti<:s 3E J. L. Burton M D SSe FACP
Ro gers and SpKt or Aids to PharmacologV 3E
Scrat cherd Aids to Phy~iolog V 3E Professor o f Derm at o logy
Si nclai r and Webb Aids to Unool g,,,tJuale Obswlrics and Gv naecology 2E Bristol Royal Infirmary, Bristo l

B. J . L. Burton MA MRCP
Sen io r House Officer
T he N ationa l Hospit al f o r Neu ro logy and Neuros urge ry, Lon d on

SIXTH EDITION

For Churchill Livings/one:

PublislJer: La urence Hunter . / ) ) CHURCH ILL

Projoct Edilor: Barbara Simmons _ LIVINGSTO N E
Copy Editor: Rut h SWll n
Proje<;t Controller: Noncv Arnon ED INBURGH LONDON MADRID MELBOURNE NEW YORK SAN FRANCISCO
DtJsign Direction: Erik Big lan d AND TOKYO 1997
 ,
CHURCHILL LIVINGSTONE
An impri nl 01 Elsevier SCfence Lim ited

C Longman Group Umited 1973

e Longman Group UK Limited 1990 Preface
o Pearson Professionalt 997
C Harcoun Publishers limited 2000
C Elsevier Science Umiled 2002. All rights reserved.

The rights of J, L. Bunon and B. J. L. Bunon to be identified as

authors of this work have been assef1ed by them in aa;ordance
with the Copyright. Designs and Patents Act 1968_

All rights reserved . No pan 01 this pobIiCation may be

reproduced . stored in a re trieval system. or transmitted in any
fOfm Of by any means, electronic. mechan;cal. photocopyHlg.
rllCording or otherwise, without e~hel the prior permission oi
the publ ishers (Pe rmissions Manager. Elseyier &:lence Limited.
Robert Stevenson House, ' -3 Ba~ter"s Place . Leith Walk,
Edinburgh EHI 3AF), or II Hcence perm~ting restri<;ted copying
in the Unitad Kingdom issued by the Copy right Licensing Agency
Ltd , 90 Tollen ham Cour! Road . London WH ~ LP.
First edition 1973
Second edition 1976
Third ed ition 1980
Fourth edition 1984
Fifth ed iti on t 990
Sixth edition 1997
Reprinted 2000
Reprinted 2002
tSBN 0 443 05692 7
Brili sh Library of Cataloguing i n Publication Data
A r-Blalogue record tor this book is available hom the British
Ubrary
LIbrary of Congress Cala loging in Publication Dala
A catalog rtI(;Or(! lor this book is ayailable from the library 01
Congress
Medical knowledge is coostantly changing. As new infomlation
becomes ayailable. changes in treatment. procedules.
equipment and the use of drugs become necessary The author
and publishers have. as far as it is poss i~e , taken ca re to ensure
lhat the information glyen in this le~t Is accu rate and up to date.
Howeyer. readers are strongly advised to coo firm that the
in formation. especially with regard to drug usage. complies
with current leg islatforl tmd standard s ot practice
This book is primarily i nt ended to provide a compac t aid t o
revision f or candidates t aking the fina l MB medicine exam inati on,
though ca nd id ates for other med ical exam inations may also fi nd it
he lpful.
Many medica l educators condemn learning by rote.
Nevertheless, candidates i n m ed ical examinations still find it
necessa ry to reta in a f orm id able numbe r of fact s and we believe
that t he use of 'skeleton' list s as an adj unct t o com prehensive
t ext books can encou rage an o rde rly ap p roach to the su bject as
well as provide a bas is f or expa nsion in answers to exam i nat ion
q uest ions .
It is i mpossible to ach ieve comprehensive cove rage in a book of
th is size, but we have tr ied to select information w h ich is worth
rememberi ng f o r use e ither in the assessment of common clin ica l
sit uations o r i n reply t o some of the more commonly asked
exa m i nation questions. Many of the lists we have included are not
read ily available in the us ual undergraduat e textbooks, and for
some important examinatio n to p ics we have provided lists w h ich
a re more detailed t han those g iven in m ost u ndergraduate
textbooks.
T his sixth edition has been completely upd ated and a new
feat u re is the i ntroductio n of mnemonics. The chapter on
exam ination technique has also been expanded.
Bristol, 1997 J .l. B.
l ondon, 1997 B.J.l.B.

Prirlted in China by RDC Group Limitad

-',
--'"
'"
policy _ 101M

fI" .... ~lortsl'

I
 ,

Contents

1. Hints on the final MB medici ne examination 1

2. Cardiology 13
3 . Electrocardiography 33
4. Chest disease 41
5 . Chest X -rays 55
6. Gastroenterology 63
7 . Haematology 75
8. Neurology 89
9. Endocrinology 11 3
10. Renal disease 129
11 . Rheumatology 141
12. Dermatology 149
13. Normal values 161
Index 165

;
 •

1. Hints on the final MB

-
medicine examination

Examinations are fo rmidable even t o the best prepared, for t he

g reatest foo l may ask more t han the wisest man can answer.
Charles C Colton 1820. Lacon I: 322
T he fi nal MB exam i nation is intend ed t o p revent t he q ual ification
of i ncom petent doct ors, and the exa m iners have t he duty o f
ensu ring that every successful candid at e is safe to be 'licensed to
heal'. T hey requ ire to kn ow t hat:
, . Yo u have a sou nd knowledge of the b asic princip les of
m edici ne and a commo n sense appro ach t o t he subject
2. You have had pract ical ex pe rienc e o n t he wa rds and ca n det ect
and int erp ret physica l signs
3. You can prescribe safely, i.e. yo u know the mode of
adm in ist ration and approximate dosage of important drugs,
and you know thei r ma in actio ns and serious side-effects
4. You can recognize and treat medical em ergencies competent ly
Any ca ndidate who satisfies the exami ners o n these point s is
fa i rly certai n to pass t he exami natio n, b ut bear i n m ind t he
lugubrious co rolla ry t hat if the exam i ners demonst rat e a
deficiency in t hese abilit ies, failure may follow.

REVISION
An im portant f unction o f rev ision is to ident ify and e lim inate 'bli nd
spots' . Nobody can know everyth ing , but you should aim to be
complet ely ignorant about not h ing, and the commoner t he top ic,
t he more you shou ld know about it . A good way to cover t o p ics
w h ich are likely t o occur in t he exam in ation is to see as many
cases on the ward s as possible d uring your training and to 'read
around' t hem. Most good physicians base t heir knowled ge o n
cases they have seen personally, and it is qu ite a good idea as a
st udent to keep a b rief record of t he pat ients you have seen as an
aid to lat er rev ision.
A sou nd kno w ledge o f medic ine is obvi o usly essential, but rapid
reca ll of t hat know ledge in t he exa m is eq ually im port ant. Instead
of read ing part of t he textboo ks in deta il just befo re t he exam, it's
better to ref resh your memory of t he who le f ield, even if o nly i n a
superf icial w ay. This wil l be fac i lit ated if your lect ure notes a re all
kept o n lo o se-leaf paper of a stand ard size so t hat your knowled ge
f rom t he various su bspecialities can be integrated to avoid
confusion and d uplication of efforl.
- Hints o n t he f in a l M B medicine e:ll: amination
ESSAY QUESTIONS
T he p u rpose of an essay q uestio n is t o discover w hether you can
assemble your kn owledge of a su bject, select app ropriate fact s
and o p inions, arrange them in an order ly manner and then
express you rs elf w ith clarity and good style. Yo u sho u ld ask
yourself w hat the e xaminers are trying to test in a particu la r
q uestio n . T hey often have a fai rly rig id m arking code, aw a rding
m arks fo r each of certai n predet erm ined points that are made, and
no extra marks are awarded fo r even the m ost fasci nating
d ig ressio ns. Candidates rarely f ai l fi nal MB on t he essay
q uestions, but those who do are usually fa iled fo r not answeri ng
the questions that we re asked .
An ot her cause f or fa i lu re is m isjudgement o f the ti m e a ll otted to
eac h question . You sho uld apply the 'law of d im inish ing ret u rns'
as it ap plies t o essay q uestio ns - the f irst 40% fo r any qu esti on is
easy, the next 30% is mu ch harder, the next 20% is v irtually
im poss ible and the fina l 10% is i mpo ssib le. Cons istency i n ev ery
quest ion sho uld be y o u r aim . You shou ld not, however, wa ste too
m uc h t ime on a q uestion wh ich you cannot answer. A blan k
sim p ly scores no ma rk s but an effu sion of rubbish w ill prej ud ice
th e exa m i ner aga i nst you.
W he re possible, quest io ns shou ld be answ ered in t erms of
distu rbance of phys io log y. This wi ll dem onst rat e yo ur knowledge
of basic p rinciples and also help you to arra nge yo ur answer in an
o rd erly and r ationa l manne r.
Many cand idates spend hours trying to predict q uestions by
studying o ld papers. The syllabus is too big fo r this to be
profit able in final MS, but it's worth c hecki ng the type of q uestions
you' ll be asked and spend ing time on any to p ics on w hich you are
ignoran!.
MULTIPLE-CHOICE QUESTIONS (MCQs)
You shou ld f ami liar ize y o urself wi th the type of q uestion f avou red
by you r own m ed ical school. Each question consists usually of
five statements w hi ch are either true o r fa lse and you are re qu ired
t o g ive an answer o f tr ue, f alse o r 'do n't know' for each pa rt.
Typ icall y a correct answer sco res p lus one, a w rong an swe r scores
m in us o ne and 'don't kn ow' sco res noth i ng . Exam pa pe rs o ft en
recom me nd answ e rin g on ly the questions you are su re of but if
y ou d id th is y ou wo uld probably end up on ly answering about 5%
of the quest ions and fail ing. It is in the exam iners' int erest that
peo p le don 't g uess beca use the exam will then correctly select out
the poor cand idates; howev er, if all the poo r ca nd idat es guess all
the q uesti o ns, some of t hem w ill pass w ho wouldn't otherwise
have d one so. It fo l lows th at t he re is an adva ntage t o those
ca nd idates who answer m ore q uesti ons tha n othe rs. If you find
this ha rd t o be lieve then t ry answering sa ine practice papers,
Hints o n t he fi n a l MB m e di c ine e xa mi n ation
leaving q uestions o ut that you 3[e unsu re of and the n repeati ng
the paper answ ering all the q uestion s as true o r fa lse. Most
cand idat es wil l improve thei r score by between 1% and 10% . Th e
-
im portant t hing to rem e m ber is tha t you can fa il by answering t oo
few q uestions b ut you ca n't fa il by answering 100 m any, althoug h
you may still fail by being too ignorant. Rem em ber 100 that the
words 'always' and ' never' rarely ap ply to medici ne and re spo nses
w h ich contain them a re u n likely to be true.
A not her problem arises w hen a student has personally seen an
u n usual case which is t he 'exception that p roves the rule' and
therefo re has diffi cu lty in answeri ng an apparently sim ple
q uestio n . Th is is a d ifficu lt d ilem m a, b ut in ge neral it 's p ro bably
best to ignore such personally -w itnessed rarities u nless yo u have
seen t hem m entioned in standa rd textbooks.
Shortage of t ime is rarel y a problem in Mea exa ms and
therefo re answe rs can be checked. In ou r experience however
'second t houghts' in Mea exa m s are rarely an im provement and
we t hi n k it is p ref erable t o w o rk st eadi ly thro ugh th e pape r once
on ly, but noti ng any qu estio n which w ill req u ire later tho ught .
THE CLINICAL EXAMINATION
Exam i ners rightly lay great stress on 'the cl in ica l' whe n assessi ng
a cand idat e and adeq uate p reparation for t h is pa rt of the
exami natio n is vit al. T he major skill requi red is o f course the
abitity to elici t physical signs correctly b ut other factors such as
fluency in case pre sent atio n and cl inical judgem ent in the
i nter pretation of the signs elici ted are also i mportant. The best
way to improve you r style i n 'the cli nical' is t o obtain reg u la r
coac hing from a critical senio r colleague w ho w i ll point out you r
fau lt s. Fa ili ng th is, you s ho u ld make arrangem ents with a fe llow
stud ent f o r each to see the other's cases under exami nat io n
co nditions. To obtain the m aximu m benefit you should of co u rse
'g ril l' each other o n the fi ndi ngs im mediately afterwards. T h is
met hod has the advant age t hat you will lea rn to see things from
the examine r's point of v iew and you will qu ickly come t o
appreciate those bad habits w hich common ly cause an noyance t o
exam iners.
Desp it e cu rrent trends, sa rt o rial and tonso ri al conservat ism is
recommended, as bot h patients and exam iners are likely to be
m idd le-aged if not actu ally sen ile.
THE MAJOR (' LONG') CASE
HI STORY-TA KI NG
A successful hist o ry demands ju st as much skill as t he physical
examinatio n, and w hi le two ex perienced cl i nicians will usually
ag ree o n the physical signs, t he histo ries they obta in may be q uit e
J
- H in t s on t h e fin a l M B medicine exa m in a t io n
different. The examiners realize this and theref ore attach more
importa nce to the objective physica l findi ngs in assessi ng a
ca ndidate. An accurate h istory is important for diagnosis,
however, particu lar ly w ith card io log ica l or neurolog ical patients,
w ho are frequently used as 'long' cases because of thei r st ab le
physical signs. T here is more to t he assessment of a cardio logical
case than merely hear ing and interpreti ng t he m urm u rs, w h ic h,
con trary to popu lar belief, are usually 'loud and clear' i n
exami natio n cases. II is v it ally important to o btai n the fullest
possib le detai ls of previo us ill nesses, especially w ith regard 10 the
du ratio n, symptoms and treatment of any possib le bouts of
rh eumat ic fever, chorea, tonsil litis, S8E, et c., and in fem ale
patients you m ust obta in full detai ls of previo us pregnancies. Ma le
patients can oft en g ive the results of previous m edi cal g rad i ng
p r io r to service in t he armed f o rces, and m any pat ients can g ive
the date and resu lt of p revious chest X- rays. Detai ls of t he
patient's past and p resent exercise tolerance are o f course
essent ial, and you s ho u ld ascerta in from the pati ent exactly how
much p hysica l effo rt h is p resent work ent ails. In ne urology cases
the m o d e of onset (ove r mi nutes, days or weeks), length of hist o ry
and subseq uent course (static, steadi ly pro g ressive or remitting)
w i ll usually suggest the type of patho logica l lesion present (e.g.
vasc u la r, inflamma tory, neoplastic or degenerative). and the
physical sig ns w i ll then confi rm the anat om ical site o f the lesio n.
W hen ta king a h istory in exams it is advisa ble fi rst to list all the
patient's sympt oms br iefly, to d iscover the type of illness and the
syst ems involved. T he symptoms shou ld then be arranged
chronologically a nd full detai ls abo ut each sho u ld be o bt ained .
T h us if the patient complains of pai n you should det erm ine:
1. The site, with the direction a f rad iation
2. It s nature and severity
3. Its duration and period icity
4. Any aggravati ng or relievi ng factors
5. Any associated fea tures
Think abou t the possible d iagnosis fro m the o utset and mod ify
your q uestions acco rd ing ly.
Never accept ter ms such as rheumat ism and vertigo at thei r face
va lue, but ask the patient what he means by t his. You m ay be
su rprised, as was th e GP who g ave severa l prescr ipti ons for
bigger and bette r laxatives fo r an o ld dea r who was 'costive', unti l
he di scove red she thoug ht this was a synonym fo r d iarrhoea.
Cons ide rable persist ence may be needed t o prevent t he patient
dig ress ing. W ith garru lo us patient s t he p revious med ica l and
fam ily histories are particularly d ifficu lt t o obta in. In such cases
stick to essentials and don't hes ita te to as k lead ing q uestions in
o rd er to obta in t he necessary information .
T he hist o ry w ill all ow you to assess the patient's mood, int ellect,
speech and memo ry, and you shou ld of cou rs e observe t he
pat ient closely du r ing the history fo r signs of dyspnoea, t remor,
Hi nts on the fina l M B m e d ic ine examinati o n
etc. It is also a good idea on first meet ing the patient t o ask
you rself 'Could t his be myxoed ema?', as th is d iagnosis is
otherwise easily m issed.
-
Esse ntial paints o f h ist ory-takin g f o r the lo n g case
• Name
• Age
• Occupation
• W hen was the patient last completely well?
• Presen ting complaint and very tho ro ug h h istory of p resent ing
compla int.
~ Ask about d iseases related to the presenting com plaint. For
example if the suspected diagnos is is u lcerative colitis ask
about possible complicatio ns such as e ryt hema nod osu m,
pyode rm a gangrenos um, eye invo lvement, joi nt problem s,
liver involvement, etc.
• Past medical history, particu larly o peratio ns o r previous hospital
adm iss ions .
- As k 'H ave you ever had - high Blood pressu re, hea rt attack
(M I), J aund ice, T ube rc u los is, Rheumatic feve r, A sthma,
D iabet es, Epilepsy, St roke, C lot s (DVT), pept ic ulcer
(D uodena l ulcer )? (M nemon ic = '8 MJ TRADES CD')
- Also ask about sickle cell anaemia i n all b lack patients and
thalassaemia in all M ed iterranean patients.
• Drug history
- Ask w hy patients are on the med ication they ta ke.
~ Always ask about al lergies, particularly to penici llin.
• Famify history
- Remember to ask about sibl ings as well as parent s,
grandparents and ch ild ren. (Autosomal recessive conditions
are un likely to have occurred in p revious generatio ns but
'One of my th ree sisters has cystic fi b rosis' p rovid es a useful
clue if you r patient's p resenti ng comp lai nt is recurrent chest
infections since c h ildhood ).
• Social history
- Ask if the patient has eve r smoked and if so for how lo ng and
w hy did they g ive up? ' I g ave up when they f ound my lung
cance r doc. Oops, I wasn't su p posed to tell you that !'
- Ask abo ut alcohol consum ptio n . Get deta ils of how m uch and
how often ra ther than accepti ng a g l ib answer such as 'on ly
socially'.
- Who is at home and are they able 10 look aft er t he patie nt?
- Does the pati ent have a d istri ct nurse, social worker, mea ls
on wheels, telephone, stairs between h im and the toi let ? Who
gets t he shopp ing, does the housewo rk, and can the patient
w ash h imself ?
- Full occu patio nal history, particu larl y fo r respi ratory cases (,I
spent two years remov ing asbest os from shi ps b ut that w as
40 years ago').
 Hints o n the f ina l M B medicine e llam i nat ion
- 00 y ou hav e pet s (particu larly sick parrots)? W hat are your
hobbies (e.g. pigeon fancie r)?
S y s t e m re vie w
This is im po rtant as it shou ld b ri ng out any important inform ation
that the patient m ay have forgotten to tell you (,Oh, sorry, I
tho ug ht you kn ew about the b lood I' m co ughing up. After all t hat's
the real reason I' m here althoug h as I w as tell ing y ou m y b iggest
p roblem is this terri ble itch I get o n m y head every ti me I p ass
wat er')'
A lways ask about:
• Ap petite.
• Weight loss - how much, over how long ?
• Respiratory syste m . Shortn ess of breath (and when), wheeze,
coug h (p ro ductive?), haemoptysis (how much?), exercise
t olera nce (i n m etres or num ber of stai rs).
.. Cardio vascular sys tem. Chest pain , p alpit atio ns (ca n you t ap out
th e rhyth m ?), postu ral hypot ension , orthopnoea, how m any
pi ll ows do you sleep w it h, d o y ou w ake short of breat h (PND or
asth m a), swelli ng of ankles.
.. A bdominal system. Any dysphagia, refl ux, indigest io n,
vomiti ng, haematem esis, abd omi nal pain ? Bowel hab it and any
recent change? Diarrhoea (if so, h ow often and descr ibe it) ,
constipation, m elaena, blo od m ixed i n w ith stool or only on
pa per.
Genitourinary
- Nocturia or fre quency (consider DM or UTI), incontine nce,
haem at uria, o ffensive sme ll , poor st ream, hesita ncy, post
m ictu rit io n dr ibbli ng.
- Previous p reg nancies, heavy perio d s (consid er anaem ia and
thyroid disorders), interme nstr ua l b leedi ng , rec urrent
abortions (anti p hospholip id syndrom e), premature
menopause (co nsider oth er o rg an-specifi c aut oimmu ne
diseases).
• Nervo us syste m . Fits, faints, visual distu rba nce, severe
headaches, para esthesiae. sen sory loss, weakness, coordination.
• General. Ski n p roblem s, arthritis.
EXAMINATION
The abil ity t o elicit and i nt erpret p hysical sig ns is of course
esse nt ial and consid erable practice on the w ards is req ui red t o
ac hieve this ski l l. A comb inatio n o f speed and tho roug hness is
requi red f or exa m pu rp oses, and t h is applies especiall y to
p u lm o nary percussion , cardiac auscu lt ation and exam i natio n o f
t he e NS. In auscult ation i n particu lar, fi rst impressio ns are o ften
right and p rol o nged listen ing m ay cause confu sion. It's u su ally
more convenient to exam ine a patien t from the head d ownwards,
rather than by system s, and regu lar p ractice w ith an u nvaryi ng
H ints o n t h e f in a l M B m ed ic ine exam i nat io n
routi ne is required if no m ajor points are t o be m issed. We cannot
stress t oo st rongly t hat people fail their long case not th rough
mi ssin g a m inor ab norma l ity, b ut because in their haste they have
-
fa iled to look f or a sign wh ich is in fa ct p resent in a gross fo rm .
Obvious signs such as a la rg e breast m ass, hypert ension, m arked
tracheal sh ift, gross optic atro phy, un ilate ral deafness, seve re
i nten tion t rem or, m assive splenomega ly, etc. , ca n easily be missed
u n less t he appropriate exa m inatio n is perfor med. Suc h sig ns may
not alw ay s be suspect ed to be prese nt from the history, altho ug h
it is o f course advisable t o pay special attention to the system s
w here you expect positive finding s. Thus it wou ld be foolish to
accept the absence o f a m itral m urmu r too readily i n a patient
w ith d yspnoea, haemoptysis, and a ma lar fl ush, or to be sat isfied
w ith perfunct ory palpat ion for splenom egaly in a patient wit h
suspect ed leu kaem ia.
Equivocal fi ndings can usually be safely ign ored un less t hey are
relevant to the sym ptoms or p robab le diagn osis. For exam ple it is
best not to was te m uch tim e ov er m inor d egrees of reflex
inequal ity, slight facial asy m m etry, i mpaired vib ration sense, etc.,
u nless your patient has a neu rological d isord er or a disease w hich
causes a neuropat hy. Other com mon causes of rea l or imag ined
eq uivocation w h ich can often be ignored incl ud e slight b ilateral
pallor or b lu rring of the optic disc, slight tracheal or ap ical
disp lacement, soft m u rmu rs and slight i nequality of breath
sounds. Rem em ber tha t small differences in percussion are easily
i magined and bronch ial b reath ing is u ncommon. If a findi ng is
du bious and it doesn't fit, fo rget it.
For the ma jor case practise working well w ith in th e set t im e
li m it, so t hat you hav e ti me left at the end to rec heck yo ur positive
fi nd ing s and to lo ok aga in for any associat ed signs w hich y ou
m ight expect t o be p resent in t hat particu lar case. Remember tha t
m istakes in the h ist ory m ay occasiona ll y be explain ed away as
being d ue to the pat ient's poor m emo ry, but m istakes in th e
p hysical signs are ent irely the respo nsibility of the ca ndid ate and
can not be condoned.
On completion of the examination you should carefully consid er
the possible diagnoses and then clarify any d oubtful point s in the
h ist ory. You shou ld also amp lify the hist ory regarding any
unexpected p hysica l signs you have discovered.
Quit e apa rt from any h uman it arian considerations it is most
i mpo rtant t o try to est ablish a g ood rap port wi th you r patient.
M any of t he patients used in the exam i nation are ch ron ic cases
w ith more or less st ab le p hYSical sign s. Since such patients are in
freq uent demand f or t eac hi ng pu rpo ses they usually have a long
ex perience of yo ung d octors and thei r diffi cu lti es and they are
oft en w ell aw are wh ich of thei r own phy sical signs are common ly
m issed. Occasionall y such p atient s will spontaneously volunteer
valuable informatio n w ith reg ard t o thei r d iagnosis or p hYSical
signs, b ut i n o ther cases a judiciously w ord ed question at the end
- Hin t s on t h e fi n a l MB m e d ic ine e xa m in a t io n
of your examination such as 'Is there anything e lse you thi nk I
ought to know?' w il l often prove rewarding. Other usefu l cl ues
may be obtained by asking the pat ient to describe the
investigations and treatme nt he has had, and by asking him what
he bel ieves to be the cause of his sym ptoms. Occasionally you'll
h it the jackpot w ith a reply such as 'Well the doctors at Queen
Square said it was Frederick Attacks Yer', You m ust be prepared
fo r misleadi ng answers however. and these shou ld be ig nored if
t hey do not talty with your own assessment of the history and
physical signs. These questions sh o u ld be left until the end as
otherwise the replies will prejudice you r j udgement. Another point
to consider is tha t these questions sometimes provoke in the
patient an u ncooperative attitude of 'That's f or me to know and
you to find out' which can make subsequent h istory-taking
difficu lt.
Before the examiner arrives you shou ld recon sider your
d iagnos is and ask yo urself 'Co uld this be anyth ing else?'
Remember that elderly patients o ften have mu ltip le pathology,
and remember too that althoug h rare diseases occur rarely, thei r
prevalence i n exami nations is g reat ly increased. If the d iag nosis is
uncertain prepare a l ist of d ifferent diagnoses and consider what
investigations you would pe rform, remembe ring 10 mention
simple t est s such as ESA and chest radiograph before more
expensive and possibly dangerous procedu res. In most fina l MB
exams, sim ple u ri ne tests are required as part o f the physical
examination of the patient and this important step shou ld not be
forgotten. If the re i s time, you should consider how you wou ld
answer probable questions reg arding management and prognosis,
and i n appropriate cases you should t ry to anticipate what the
ECG and radiographs might show.
CASE PRE SENTATION
T here is quite an art in presenti ng a case concisely and clearly.
The examiners have no time to waste, and hesitant and long-
w inded presentations are tedious, so you shou ld edit the history,
emphasizing important poi nts, leaving out irrelevant detail and
givi ng negatives only if they are import ant. If the case is
straig htforward the p resentation of the history and exam ination
shou ld f o rm a cohesive account leading to a confide nt diagnosis.
In such cases try to ma ke your assessment as full as you ca n and
say whether the condition in you r patient is acute or chronic, m ild
o r severe, si mp le or w ith complica tions. In more d ifficul t cases
wi th con fli cting evidence or d oubtful signs you wi ll have mo re
reservations, but don't hedge all the time as this ir ritat es
examiners and does noth ing to conceal you r ignorance. Try t o
make up your m ind on the basis of p robabi lities. Doct o rs often
have to act o n the basis of eq uivocal evidence and the examiners
wan t t o see whether you can ta ke a sensible decision.
Hints o n t he fin a l MB m e d ic ine exam ina t ion
W h ile it is important to keep your initial presentation concise, it
is a m ist ake to answer the subsequent questions too curtly. T he
examiner is anxious to see whether you can discuss your patient
-
intell igently and you should try to d isplay your relevant
knowledge as much as possible. If anythi ng about the case puzzles
you, or there is a p roblem relating to d iagnosis o r management.
don't be afraid to acknowledge this. If the line of quest ion ing
seems to be entering one of your fie lds of ignorance, try t o keep
the initiative by talking around the subject. With a bit of luck you
may introduce a fresh topic that interests the examiner. If he
persists in reiterati ng a particular question this is often because he
is trying to establish a very basic point. Examiners can be obtuse
in the way they phrase such questions and p rolonged si lences in
such circumstances can be d isastrous. Try to talk sensibly around
the subject to see what he's ai m i ng at, and with luck a
supplementary quest ion wi ll lead you t o the req ui red answer.
THE MINOR I'SHORT') CASES
Many students regard the minor cases as a l ittle l ig ht rel ief fro m
the more arduous parts of the examination. T his is a serio us
misconception, fo r the exam iners are well aware of the element of
luck wh ich enters into the major case, and they attach
correspondingly greater importance to the candidat e's
perfo r mance while he is under di rect observation. You wil l be
watched as you exami ne t he patient and your style in eliciting
physica l sig ns is importa nt. Make a point of positioning the patient
properly, and a lthough you should preserve the patient's modesty
as far as possib le, remember that you may be penalized if you do
not get the patient adeq uately undressed.
As in the long cases, a reasonable compromise must be reache d
between speed and thoroughness in physical examination, for as
a genera l rule a candidate's score is proportional t o the number o f
cases he has time to examine and diagnose correctl y. It is
obviously better to e rr on the side o f over-caution rather than t o
fa il because of a ma jor error of omission, but remember that few
things ir ritat e an examiner more than the candida te who wastes
time perform ing a t ediously meticulous examinatio n in what
shou ld be a sim p le, rapidly d iagnosed condition. The exami nation
o f the sensory nervous syst em often p rovides cause fo r offence in
th is respect, and cardiologica l auscu ltat ion p rese nts a simi lar
hazard. If you are un sure of the diagnosis in a case with an
'i nt eresting' m urm u r, there is usually no point i n remai ning g l ued
to the patient's praecord iu m in the hope 'of being saved by the
bell, for the examiner w ill certain ly ask you for a diagnosis before
d ismissing you . Far better to th ink quickly, present a sensible
d ifferen tial d iagnosis and move on to the next case.
Another important point i n the m inor cases is to listen carefully
t o the instr ucti ons o f th e exam iner w it h regard to the part or
 Hi nts o n th e f ina l MB m edicine examination
system to be exami ned and obey them implicitly. Before recou nting
you r findings however, you shou ld always pa use and ask yourself
whether fu rther exami nation of more distant parts of the body,
such as regiona l lymph nodes, pe ri pheral pulses, finger nails, etc.,
is required. If you are not clea r wha t the exam ine r wants you to
do, do not be afraid t o as k for clarification , Fo r example, if the
exam iner says 'Exam i ne th is pat ient's heart' it wou ld be
reasonable to ask whet her he wishes you also to fee l the pu lse.
The i mportance of t he recogn it ion of cl i nica l associations i n the
m inor cases canno t be overemphasized. In many cases i nspection
of the patient and h is immediate environment as you approach
the bed may provide a clue to the diagnosis. For example you
may be shown a cu t aneous eruption localized t o the shin in a
p atient wi th exophthalmos (preti bi al myxoedema), or you m ay be
asked to give the likel y diagnosis of an arthritis in a pat ient who
also has a patch of psoriasis, or marked na il p itting. The key to
ma ny minor cases lies in such observat ions and you shou ld
practise looking f o r suc h cl i nica l associat ions until this becomes
habitual.
Having el icited the physical signs correct ly ma ny candidates fai l
to be selective enough in applying the ir knowledge to the
particular patient under discussion. Bl i nd appl ication of ' list s of
causes' oblivious of the patient's age or sex, the asso'c iated
phYsical find ings, etc., are guaran teed to create a poor impression.
The habit of mentioning rare diseases bef ore comm on ones is
another fa iling which is easily eradicated with p ractice.
Hints and tips received from eart ier cand idates in the short
cases are on the whole best ignored. Examine rs have been known
t o change the order of t he patients' beds and they wil l cert ainly
have changed the questions. There is moreover a rea l dange r that
you will j ump to the diag nosis (whic h may in any case be wrong)
w ithout giving adequate co nside ration to the different ial
diagnoses and w it hout elic iti ng the app ropriat e phy sical sig ns.
It is heartening to rea lize that for success in the cli n ica l
examination omn iscience helps, but is by no means essentia l
(indeed a few examiners seem to find it somewhat irritating).
More important are adequate practice in examination techn ique,
quick·w ittedness, thoroughness, clear enunciation, a confident but
m odest bearing, and good luck.
THE ORAL EXAMINATION rVIVA' )
The 'viva' test s the depth as well as the b readth of a candida t e's
know ledge. If he appears to know a topic fai rl y well , t he
examiners w ill switch t o another subject an d if several common
topics are satisfact or ily dealt w ith, they may go on to tes t the
candidate 'in depth'. For this reason, it may be worthwh ile for the
good candidate t o learn about a few unusua l m u ltisystem
condi tions in detail and t o try and introduce them into the
Hints on th e f i nal MB m edicine examination
conversation. For example a student who has spent an elective
period in the U SA m ight choose coccid ioidomycosis as a subject
to revise in det ail, Then if he is asked about pneumon ia,
mening it is, osteomyelitis, tubercu losis, erythema nodos um or
lymphadenopat hy he will, aher discussi ng the commo~er cause,s,
casua lly mention coccidio idomycos is. The exa m iner Will ohen flse
to the bait and say 'Ah yes, now what do you know about that?'
The converse of this p loy is that you should not mention anyth i ng
i n t he v iva un less you' re prepared to t alk about it.
It is vi ta l t o have a good knowledge of the diagnosis and
management of emergencies such as cardiac arrest GI bleeds, M I,
pu lmonary oedema, drug overdoses, ana phylaxis and acute . .
asth ma. Don't wor ry too much about small print as no one Will fa ll
you f or m isd iagnosing p ituitary apoplexy although they might if
you fai l t o shock someone in ventricular fib rillation .
(Recommended re ading: Acute medicine, 2nd edition, by
Spring ings, Chambers and Jeffrey, Blackwell Science. )
Student s are ohen asked fo r th e causes of a cond ition . St ony
silence is not impressive. Even if you have neve r heard of the
con dition you can try the fo llowi ng sieve: TIN M AI DENS, wh ich
stands for T rauma, I nfection, N eoplasia, M etabo lic (or
Mechanical), A lcoho l, Iatrogen ic (or Id iopat hic), D egenerative (or
Drugs), Endocrine, N eu rological, Smoki ng. Infection can be
broken down int o viral, bacter ial, fungal, protozoal and pa rasitic.
Neoplasia shou ld be considered as benign and malignant, p rimary
and secondary, It sound s obvious but if you don't say it the
exami ner won't know that you know it.
It is worth rem embering th at some condi tions such as AIDS,
syphi lis, TB, sa rco idosis, collagen-vascu lar disease and drug sid e-
effects can occasionally cause almost anyt hing.
You may be given a pathology speci men ('pot ') t o descr ibe in
the viva . Examine it ca refully from all sides to try identify the
organ fi rst (not always easy). then descr ibe the patholog ical
lesions you can see, and hazard a diagnosis. If you know the
answer try t o t alk at some length. If you haven't a clue, don't
prevaricate b ut have a guess and go on to the next ·pot' . .'Ti p,?ing it
upside down to look at the label is not recommended as It Will
only make the 'pot' too cloudy to see anything!
If you are shown a radiograph the abnor ma lit y is likely to be
fair ly gross, so stand back and ta ke an overall view befo re looking
at the det ai ls. Remem ber that more than one ab no rma lity may be
present (e.g. an absent breas t shadow w ith pulmonary met astases,
or a bronch ial cancer w ith r ib met ast ases), so exam ine t he whole
fi lm. Assu ming you can spot t he abnorma lity it is best to disc uss
th is from the outset as exam i ne rs get tired of bei ng told tha t the
patient is slight ly rota ted and the film is of POOT qua lity.
Fina lly, have sympathy with y ou r examiner. He cannot be
expected to know everything and if you cross sword s w ith him,
give ground gracefully - aft er all he may be right !
2. Cardiology
-
CYANOSIS
5 9 reduced Hb per 100 ml blood produces cyanosis. (Note t hat
polycyt haemic patie nts can be cyanosed without being hypoxic,
and a naem ic pat ients can be hypoxic w ithout bei ng cyanosed)

PERIPHERAL CVANOS IS
Due to poor periphera l c ircu lation

C a u ses
1. Vasocons triction, e.g. due t o low ambient t empe ratu re or
Reynaud's disease
2. Arterial obst ruction, e.g. atheroma
3. Low card iac output. e.g. f ailure, aortic stenosis

CENTRAL CVANOS IS
Due to low arter ial oxygen saturation

C a u ses
1. Hypovenl i lation
2. Parenchymal lu ng d isease
3. R to l card iac shUn!
4. Dec reased P0 2 of i nspi red gas
May be si m ulated by methaemoglobinaemia and
sul phaemog lobinaem ia

JUGULAR VENOUS PULSE IJVP)

Height of JV P is measu red with re ference t o sterna l an g le with
s.ubject at 45° t o hor izonta l
No rmally less than 4 cm (vertica l height )

CAUS ES OF ELE VATED JVP

1. R ventricular fa ilure, esp. cor pu lmona le, pu l mona ry embolus
2. Fl uid overload (esp. Lv. inf usion)
3. Tricuspid stenosis or i ncompetence
4. Perica rdial effusion or constrictive pericarditis
_ I Ca rdi o lo g y C a rd iolo gy I
5. Very slow heart ra t e, esp. complete heart block 4. BISFERIE NS
6. Obstruction of superio r vena cava (non -pu lsati le)
Combined aortic stenosis and incompe tence
Kuss m aul's sign
JVP rises on inspiration. Seen i n cons trictive pericard itis, 5. ANACROTIC ISLOW-RISING)
pericardia I eHusion. restrictive cardiomyopathy. Aortic st enosis

Nor mal jugular venou s p u lse wa ve in relatio n t o ECG pattern 6. DICROTIC

a Fevers

a " atrial systole

Pulse
, c " effect of tricuspid
valve closure
7. PULSUS ALTER NANS - A lt ern ate stro ng an d w eak
wave beats
y x == lowering of righ t atrial
R
, pressure as tricuspid
ring moves down
Left ventricu lar f ailure

during ventricu lar

contraction 8. PULSUS PARADOXU S - Blood press ure dec reases on
insp irat ion by m o re tha n 10 mm Hg
II '" venous filling
p
T~~./-U~_ _ _ _~ (not ventricular (i) Pericardial effusio n
ECG contraction) (ii) Co nstricti ve pericarditis
(iii) Seve re asthma
y follows opening
01 AV valves
ARTERIAL PULSE RATE
CAUSES OF TAC HYCARDIA
1. Sinus tachycard ia (q.v.J
2. Su p raventricular (atrial or nod al) tachycard ia
TYPES OF ARTERIAL PULSE WAVE
3. Atrial fl uner (usually around 150/m inl
1. NORMAL -- -Tl ---- 4. Atrial fi b rillation
__~l_ L_ __ 5.
6.
Ventricu lar tachyca rd ia (inc. torsade de poi ntes)
Ventricu lar fl uner

2. CO LLAPSI NG IALSO CALLE D WATER- CA USES OF SI NUS TACHYCA RDIA (ove r 100 beats per
HAM MER OR CO RR IGAN PU LSE) min ute )
(i) Aortic incompetence --1'1- ---. 1. Hyperdyna m ic ci rcu latio n (q.v.1
I ii) Hy perdynam ic c irculatio n (see p . 15)
(i ii) Patent ductus a rterios us
(iv) Peri phera l AV m alf o rma tio ns
J __ L __ 2.
3.
4.
Congestiv e card iac fa ilu re
Hypo v o laem ic shock (acut e haemorrhage. etc.)
Const ricti ve perica rdi tis
5. Dr ugs, e.g. ad re na line, at rop ine, sa lb ut amol
6. Pu lm ona ry embo lism, asthma
3. SM ALL VO LU M E
(i) 'Shock' CA USES OF HYPERDYNAM IC CIR CULATION
(ij) Aortic stenosis 1. Exerci se or emotion (anx iety, frigh t. etc.)
(iii) Pericardia l effusion 2. Pregn ancy
1_ I Car diology
Cardiolo gy I
H EART BLOCK (a l l deg r ees)
3. Anaemia
4 . Pyrexia 1. Myocardi al ischaem ia
5 . Thyrotoxicosis 2. Digit al is
6. AV fistulae 3. Ch ronic heart disease, especially aortic stenosis and con genital
lesions
4. Rheu m atic fever
CAUSES O F SIN U S BR ADYCAR D IA (le ss t h an 6 0 bea ts p er
m in u t e) CLIN ICAL D IAGNOSIS OF AN ARRHYTHMIA
1. Extreme physica l fi tness
1. SINUS ARR HYTHMIA
2. Convalescence f rom fever
3. Soon after myocard ial i nfa rction Rate increases w ith inspi ration
4. Hypothyroid ism
5. Hypotherm ia 2 . EXT RASYST O LE S (ect opic beats)
6. Raised intracran ial pressure (wit h hype rtension)
7. Drugs, e.g. dig it al is, beta-blocke rs Atrial, noda l or ventr icu lar
8 . Sinoatrial di so rde r ('sick si nus syndro me') (i) A prem ature beat wi t h a compensato ry pa use fo llowed by
a st rong er beat
I ii ) Usually r uns of no rma l beat s occu r, but extrasy st oles m ay
CA USES OF A N IRREG ULAR PU LSE alt ernat e w it h norma l beats (pu lsus bigemi nus)
(ii i) May disa p pear during exe rcise
1. Extrasyst oles
2. At rial fib rillation
3. Marked sin us arrhythmia 3. AT R IA L FIBR ILLAT IO N
(i) Completely irregu lar i n time and f orce
(ii ) Worse on exercise
COMMON CAUSES OF SOME ARRHYTHM IAS (iii) Carotid compression h as no effect
EXTRASYSTOLES (iv) J VP 'a' waves absent
1. Idiopathic
2. Fatigue, excessive sm oking, alcohol or caffeine i ngestion 4. AT RIA L FL U TTE R
3. Myocard ial ischaemia (i) Regu lar ra dia l pulse ra te, classically 150/m i n in 2:1 b lock
4. Dig italis (b ut can be i rregular if there is fl uctua ti ng heart b lock)
5. Hyperthyroidism (ii) AV block occu rs, so that the JVP 'a' waves greatly exceed
6. Heart diseases w ith atrial en largement (e.g. mitral stenosis) t he p ulse rat e
(i ii) Carotid com p ression slows the rate w hi le pressu re is
m aintai ned
PAROXYSMAL TAC HYCAR DIA
1. Myocardial ischaem ia 5. PAROXYSM AL TAC HYCARDIA
2. Dig it alis, especially after pot assium d ep let ion
Atr ial, nod al or ventricu lar
(i ) M ay be history of p revious attacks w ith sudde n onset and
ATR IAL FIBR ILLAT ION cessation
(ii) Ca roti d com p ress ion may d ec rease t he ra te even after
1. Rheumat ic heart d isease, espec ially m it ral stenosis p ressu re is relaxed
2. Myoca rdial ischaem ia
3. Hype rthyroid ism
4. Idiopath ic 'lone fi b r illation' 6. HE ART BLOCK
5. M it ra l prolapse Com plete (3r d d e gree)
6. Sick si nus syndrome Heart rate of 36-44/min which does not increase wi t h exercise
7. Hypertension
 Ca rd io lo g y Ca rdiolo g y I
2nd d e g ree AV bloc k 2. Pulmonary closure is delayed by inspi ration (due to increased
May be dropped beats (Wenckebach) or 2: 1, 3:1 or 4:1 b lock. venous retu rn caused by decreased in trathoracic pressure)
Instabi lity of rhythm is common The normal split t herefore increases on inspi ration
1 5t d egre e block
FIRST SO UND
Detected on ly on ECG (PR > 0.2 second )
Lo ud in
1. M itral st enosis
APEX BEAT - THE LOWEST AND OUTERMOST 2. Hyperdynamic circul ation
POINT OF DEFINITE CARDIAC PULSATION 3. Tachycardia
Heart is en larged or disp laced if apex beat is:
1. Lateral to midclavicu lar line, or S o ft in
2. Below 5th i nt ercostal space 1. M itral incompe tence
The character o f the apex beat may be: 2. Rheumatic carditis
a. Heav i n g (pressure overl oad) in aortic stenosis or syst emic 3. Severe heart fail ure
hypertension (apex usua lly not displaced)
b. Thrust ing (vo lume ove rl oad) i n ao rtic regu rgitat ion or mitra l
SECO ND SDU ND IN AORTIC AREA
regurg it ation (apex usua lly displaced)
c. Tapping ('pal pable first hea rt sound' ) in m it ral stenosis Lo ud in systemic hypert ension
A left parasterna l heave ind icates RV hypertrophy Soft in aortic stenosis

FAILURE TO LOCATE THE APEX BEAT ON PALPATION SECDN D SDUND IN PU LMONARY AREA
Consider the f ollowi ng possibi lities: Loud in pu lmonary hypertension (e.g. chronic pulmonary d isease)
1. Excessively fa t or muscular chest wall Soft i n p ul monary st enosis
2. Left pneumothorax, p leural effusion o r em physema
3. Large pericardia I effusion
4. Dextroca rdia or ma rked mediastina l sh ift
TH IRD HEART SOUN D

,I
5. Massive LV hypertrophy. (Remembe r to fee l as far round as t he Hea rd at apex ea rl y in
m id -axill ary li ne ) diastole, due to vent ricu lar
di st ens ion
THRILLS (palpable murmurs)
A lways ind icate an organic defect. The area local izes the defect
'II 'I Easi ly con fused w ith
opening snap of mitra l
st enosis wh ich is maxi mal
media l to the apex
HEART SOUNDS C au se s
1. Normal i n young peop le and du ring p regnancy
2. Ventricu lar fail ure (a useful sign)
3. M itral or tricuspid i ncompetence
4. Constr ictive pericarditiS

'/I
,I
FO URT H HEART SOUN D
Hea rd at lowe r end of stern u m

N.B.
Tricuspid and
mitral valve closu re
Aortic and
pulmonary valve closu re
'I _ 'II late in diast ole, due to atrial
contraction (and theref ore not
present in atrial fi bri ll ation)
Always abnormal, indicat es resistance t o LV filling because of
1. Aortic norm ally closes bef ore pulmonary _ i ncreased ven tricular wa ll stiffness
.. Car d iology

C a u ses If no mu rmu r is hea rd and the patient gives a hist ory o f

C. rdio logy

rh e um at ic f ever, you shoul d exercise t he pat ient an d list en aga i n,

I

1. Hype rtension
2. Heart block partic ularly fo r mu r murs of MS or A I.
3. Myocard ial infarct ion
Triple rhythm is due t o a 3rd o r 4th heart sound, or summation
of both Different ia l diagnosis of murm urs
Gal/op rhythm is a f ast t r iple rhythm, and ind icates act ual o r TIming Maximal inrensiry Likely causes
i ncip ient heart fa il u re
Dogmatic p rono uncements on t he state of the second so und EIec1ion systo li<: Aortic /Irea Aort ic stenosis
Aortic scleros is
and the presence or absence of th e th ird and fou rt h sou nds a re 1st 2nd
so und sou nd Coa rctation
not nor ma lly expected of unde rgrad uates
I I Pulmonary al ea Innocent
Pulmonary ste nosi s
CARDIAC MURMURS Atrial septal defect
, 1, 'lIIll lm
n.. 1 Pulmonary
When auscultating, concentrate separately o n the heart rhythm. hyper1ens ion
sounds and murmu rs. T he murmurs most commonly m issed in
exams are t hose o f aortic i ncompet ence and m itral stenosis. A"" Innocent
Ao rt ic stenosis
Aortic i ncom pet ence is m issed eithe r beca use auscu ltat ion was Aort ic sc leros is
not perform ed all d own t he L st e rna l edge w it h t he pat ient sitting
up at t he end of expiratio n, o r becau se t he cand id ate fai led t o Pansy-stolic M itra l incompetence
'IU ne in' to t he h ig h-p it ched m u rm ur. Mit ral stenosis is missed Ventricular septa l
defect
e ither beca use the patient was not auscultated lying on his left
Fallot's tetralogy
side, o r because t he candidate listened t o o n ly o ne site in t he
apica l area . Tr icuspid
incompetence
T he exam ination o f pe ripheral sig ns will g ive you an idea of
w hat y ou m ight fi nd on auscu lt ation . Fo r exam ple if t he patient is l ower sternal border Vent ricula r seplal
in at r ial f ibri ll at io n con sider m it ral va lve disease; th en if t he apex defect
is disp laced t here is likely t o be m itral regurg ita t ion, o the rw ise a
lo ud f irst hea rt sou nd and an u nd isplaced apex beat favou r mit ra l
M id-diast o li c A"" M itra l sto nosis
Opening l ower sternal bo rder Tricuspid stenosis
stenosis. snap {ra.e)

'I 1111I ,~••fl

If t he pat ient is in sinus rhyth m t hen t he p ulse charact er is
useful, a slow rising pu lse indicati ng aortic st enosis, a collapsi ng
pu lse i ndicati ng aortic regu rgitatio n . Sim i larly if t he apex is
d isplaced th en ao rtic reg ur g it at ion is much mo re likely t han ao rtic
Diast olic Anywh ere along Ao rtic incompetence
stenosis. If t he mu r m u r rad iates to t he caro ti ds aort ic steno sis is Pulm onary
sternal border
m o re like ly than m itra l reg urg it at ion, b ut t he converse does not
~II!I! '"
incompetence
fo llow as t he mu rmur o f ao rt ic sclerosis w ill not rad iate to t he
carotid s.
dl
If there is a m id l ine sternoto my scar there may be a p rosthet ic
Continuous Cardiac basc Patent duetus
valve o r two, in which case a systolic m u rm ur may be no rmal.
arteriosus
However most m idline sternot o m ies a re done fo r bypass grafting,
Simultaneous AS
not for valve rep lacement . None o f t hese rules is absolute but t hey and AI
are usef ul.
Above clav icl e Vanous ·hum·
If several murmurs are p re sent, t ry t o decide w hic h lesion is
domina nt by conside ration of associa ted cl in ical feat ures, e.g. in RemBmber the possibility of extracardiac sounds such as a pericardial rub in
sim u lt aneous AS and AI t he pu lse m ay be either 'plateau ' or pericarditis
'collapsing', and in si multaneous MS and M I the presence o f a 3rd
heart sound w ith a soft 1st sound suggest s the incompetence is In any patient i n whom you suspect rh eumatic heart d isease you
dominant. sh ou ld obtain det ai ls of the symptoms, d u ratio n and t rea tment of
_ ! Ca rd io logy '-____________________________________________c_,_,_d_'o__
'oc·cv_1 IIIIIIII
any previous bouts of possible rheumat ic fever, chorea, to n si llitis N.B. Increased severity of st enosis is indicated by increased
or bacter ia l end oca rdi tis. d uration of mu rm ur (not it s loud ness).

CHARACTERISTICS OF INNOCENT SYSTOLIC MURMURS COMPLICATIONS

IN CHILDHOOD 1. T h rombi in L atrium, and system ic embol iza tion
1. No other abnormality d et ect ed (no cardiac enlargement) 2. Pul monary emboli
2. No thrill or added sound 3. Subacut e bact erial endocarditis (u ncommon w ith atrial
3. Never diastolic o r pansystolic, except f or t he continuous fibrillat io n)
mur mur of a veno us hum, w hich is reduced on lying down
4. Inte nsity often va ries with a change i n posture
ELECTROCAR DI OGRAM
1. M ay be broad not ched P wave (L atrial hypertrophy)
MITRAL STENOSIS 2. M ay be atr ial fibrillation
Nea rly always due to rheumatic heart d isease, but rarely may be 3. R ax is deviatio n o r A ventricu lar hype rtrophy
co ngen ita l 4. Usua lly d ig it ali s effects

SYMPTOMS M ITRAL INCOMPETENCE

1. Prog ressive exertional dyspnoea CAUSES
2. Other symptoms o f pu l monary congestion:
(i) Orthopnoea 1. Mitral valve pro lapse (usually myxoid degeneration)
(ii) Paroxysmal nocturnal dyspnoea 2. Rheu m atic fever (probably arou nd 20% o f cases in UK)
(iii) Cough 3. Ischaemia, especia lly posterior infarct, w ith papillary muscle
damage
(iv) Haemoptvsis
3. Acute p ulmonary oedema, usually precip it ated by exertion, 4. Su bac ute bacter ial endocarditis (may be cause or complication)
5. Functional M I due to stretched AV ring i n LVF
p regnancy or onset of AF
4. Recurrent bron chitis
5. In later stages, symptoms of RV fa ilu re (p . 21)
6. Pa lp itations in paroxysmal AF SYMPTOMS
1. Palp it atio ns and exertiona l dyspnoea occu r ear ly
2. Fatigue and weakness
SIGN S 3. Orthopnoea due to pu l monary oed ema
1. T hin fa ce w ith pu rpl e cheeks ('mit ral fa cies' )
2. Pulse may be sma ll vol ume. May be atrial fi brillation
3. BP sh ows low pu lse pressure SIGNS
4. May be 'tapp ing' apex beat and L parasterna l heave 1. L ventricu lar di latation
May be d iasto lic t hrill 2. 1st heart sou nd is soft and muffted
5. 1st heart sou nd is lo ud an d 'slapp ing' 3rd heart sou nd is usual
2nd heart so und is lo ud if pu lmonary hypertension is present 3. Lou d pansyst olic mu rmu r, maximal at apex and propagated t o
M ay be 'o pening snap' (indicates mobite v alve) in ear ly d iasto le
axi lla
6. Roug h, rumbling , low-pitched d iast o lic m ur mu r, local ized to the
Often obscu res 2nd heart sound
apica l area and accentuated by exercise . May be presystolic 4. May be LV fa ilure
crescendo if fib ri ll at io n absent
1. Pu lm o nary c rac kl es N.B. Increased severit y is indica ted by 3 rd heart sou nd, LVF and
8. In lat er stages, signs of RV f ai lu re a displaced apex
_ I C a r d io logy '-~~~~~~~~C-"d-;O--
'09Y I ~
2. Pa lp itations a nd dizziness
AORTIC STENOSIS
3. Sympto ms of l v entricu lar fa ilu re (p . 27)
CAUSES 4. Ang ina
1. Congen it al, pa rticu larly bic uspid v a lve (p resent s at age 40-60)
2. Rheumatic fever SIGNS
3. Sen ile calcifi cation o f an otherwise no rmal valve (p resents over
1. Co llapsing (Corrigan) pulse. M ay be visib le carotid p ulsation o r
60)
'head -no dd i ng' (de Musset's sign ) o r n ail bed pulsatio n
4. Severe hyperc ho lest erolaem ia
(Qu incke's sig n)
2. BP s hows wid e pu lse p ressu re
SYMPTOMS 3. L vent ricular hypertro phy and d ilatatio n
,. May be no ne fo r years 4. Murm u rs:
2. Sym pt o m s o f L ven tricular fa ilu re (p. 26) (i) Soft hig h-pitched b lowi ng d iasto li c m u rm u r d own l
3. Syncope o n effo rt st ern al edge
4. A ng ina (d espite no rma l coro n ary arte ries) (ii) M ay be a systol ic ao rti c m u rm u r due to increased b lood
f low
SIGNS (i ii) May be a diast o lic apical m urmu r (Aust in Fli nt) w h ic h
sim ulates m itral st enos is
1. Sma ll vo lum e, slow -ri si ng p ulse (iv) M ay be ' pistol-shot' no ise ov er fe m o rals synch ro no u s w ith
2. L vent ricular hypertro phy pu lse (Trau be's s ign)
M ay be syst o lic t h ri ll (best felt w it h patient sitting forward at (v) M ay be d iast o lic m u rmu r over fem o rals o n slight
end of expiratio n ) compression w it h stethosco pe be ll (Duroziez's sign )
3. 2nd so u nd i n aorti c area is soft 5. M ay be LV fa il ure
4. Ha rsh sy sto lic 'eject io n' murm ur maxim al at ao rtic a rea and
rad iating to the neck N.B. Increased seve rity is indicated by decreased d u ratio n of
5. Ma y be LV fail ure m u r mu r, LVF and a d isplaced apex
N. B. Increased severity is ind icated b y a slow-r isi ng pu lse, an
inaudib le second h eart so und and a lo w BP. TRICUSPID INCOMPETENCE
Aortic sclerosis m u rmu r is identical, but is distinguished by
n o rm al pu lse w ave and absence of a th rill
CAUSES
1. Infectiv e endocarditis (esp . in drug addicts)
AORTIC INCOMPETENCE 2. Pu lm o nary hypertensio n
3. Rheum atic fever
CAUSES 4. Fu nctional TI d ue to stretc hed AV ri ng in RVF
Cli nica l m an ifest ations usual ly d eterm i ned by coexisti ng an d
A . V a lv a r
p red o m i nat ing m itral st enosis
1. Rheumatic fever
2. Su bacute bact er ia l endocard itis
3. Bicuspid va lve SY MPTOM S
4 . Rheum ato id d isease
1. Exe rtional dy spnoea is commo n, but o rth o pnoea and
paroxy sm al noctu rn al dyspnoea are unco mmo n du e to
B. Ao rtic root disea se
d im i n ished R v ent ric u la r o utp ut int o lungs
1. Type A ao rt ic d issection
2. Gast ro intestinal u pset s due t o ven o us congestio n of GI t ra ct
2. Syph ilis
3. Marian's
4. Sero neg ative arth rit is (p. 143) SIGNS
1. Elevated J VP wi t h large v w aves
SYMPTOMS 2. Pu lsati le hepatic en large m ent
3. Asci t es. which is bo th ch ro nic and rec u rrent
1. M ay be none fo r m any yea rs
- Cardiology

4. Periphe ral oed em a, p leu ral effu sio ns

5. Pa nsyst ol ic mu rmu r, m axim al near low er sternum , and
becom ing louder du ring d eep insp i ration
Symptoms
1. Exertional d y spnoea
2. Ortho pnoea
Cardio logy

3. Pa roxysmal nocturna l dysp noea, often w ith coug hing or

I _

w heezi ng
CLASSIFICATION OF CONGENITAL HEART D ISEASES 4. Pu lmonary oedema (anx iety, d yspnoea, cough and pink fro thy
CYANOTIC II.E. R TO L SHUNT) sput um)

1. Fa ll ofs tetralog y Signs

( i) Pulmona ry stenosis 1. Tachycardia. May be pu lsus altern ans
(i i) Ventricular se ptal d efect 2 . Enlarged heart
(ii i) Over-rid ing ao rta 3. Gallop rhythm
(iv) Rig ht ve ntr ic ular hy pe rtro phy 4. May be f unctional m it ra l incompete nce d ue t o stretched AV
2. Tran spos itio n o f g reat v essel s and tricuspid atresia a re usually ring
fat al in infancy unless co rrected 5. Fine crackles at lung bases . May be w heezes
3. Eise nmeng er's syn d rome (reversa l of a L to R shunt foll ow ing
t he dev elo pm ent of pu lm o na ry hypertensio n)
LEFT VENTRICULAR HYPERTROPH Y
Causes
ACYANOTIC 1. Hypertension
1 . With L to R shunt 2. M it ral incompetence
(i) Ventricu lar se ptal defect 3. Aortic st enosis andlo r inco mpet ence
( ii) At rial septa l d ef ect - usually secundum but rare ly 4. High out put states, e.g. anaem ia, po lycythaem ia, t hyrotoxicosis
se ptum p ri m um 5. Aortic coarctation
(i ii) Persist ent ductus arte ri o sus 6. Hypertrop hic cardio m yo pathy
These pat ients m ay become cy anosed due to card iac fai lure,
pul monary infectio n , severe exerci se o r shunt reversal Signs
1. Fo rcefu l apex beat, left ventricu lar heave
2 . With no shunt 2. loud aortic 2nd sound
(j) Coarcta tio n o f aort a 3. Signs of any und e rlying condition
(ii) Pu lm o nary ste nosis - o ccasio nally cy ano sed
(iii) Congenit al ao rtic stenosis
RIGHT VENTRICULAR FAILURE
(iv) Dextrocard ia
(v) Bicusp id aortic valves Common causes
1. Secondary to l v entricular fa ilure
2. Mitra l stenosis
HEART FAILURE 3. Cor pu lmona le (inc luding pu lm onary embo l ism )
Defi nitio n: a stat e in w hi ch the heart fai ls to meet the met a bo lic 4. Congenital heart d isease
and o xygen need s o f th e body under va rying cond itions,
assum i ng the ve no us ret urn is adequate Symptoms
1. Ti redness, weakness, ano rexia
2. Oedema
3. Gastroi ntestin al upset. May be hepatic pai n
LEFT VENTR ICU LAR FAILURE
Common c a use s Signs
1. Myocard ial ischaem ia 1. Depen dent oedema
2. Hypertensio n 2. Elevated JVP
3. A o rtic stenosis o r incompetence 3. May be functiona l t ricuspid inco mpetence d ue t o stretched AV
4. M itral i ncom pete nce ri ng
_ [ c ardiOlOgy Cardio logy

4. Large tender liver. May be mi ld jau nd ice CAUSES OF SEVERE CHEST PAIN
5. O ligu ria by day and noct ur ia. Uri ne is concent rated and
a lbu m i nuria is common 1. Myocard ial ischaem ia
(i) Co ronary at he roma, t h rom b us o r vasospasm
6. Peri pheral cyanosis o r ascit es in severe cases
Remember that Rand L sided heart fai lu re often appear almost (i i) Ao rtic va lve d isease or ao rt itis
(i i i) Seve re anaemia
sim u lt aneously
(iv) Paroxysma l tachyca rd ia
2. Pe ricardit is
3. Pleurisy
SYSTEMIC HYPERTENSION
4. Pu lmona ry embolism
Defi nit ions vary b ut 140/90 mmHg for a yo ung ad ult and 160/95 5. Oesophagea l pa in (ac id ref l ux, spasm, ca rcinoma )
mmHg fo r a m iddle-ag ed person wou ld be reasonable upper 6. Expand ing aortic aneurysm
lim its 7. Chest wall lesions
(i ) Rib fracture
(ii ) Metastat ic depos it s i n ribs o r fractures
CAUSES (iii) Mya lg ia (e.g . Bornholm disease)
(iv) Herpes zoster
1. Essentia l (v) Id io pat h ic cost ochondrit is (Tietze's syndrome)
2. Rena l d isease (especiall y renal ischaem ia)
8 . Gastric o r d uodena l u lcer
3. Dr ugs, e.g . cycl ospori n. o ral contrace pt ives, g lucocort icoids 9 . Gallblad der col ic or pancreat it is
4. A lcohol ism an d/or sleep apnoea 10. Pain referred from t horac ic o r cervical spi ne
5. Endocrine
(i) Cushi ng's d isease
(ii) Phaeoc hromocytoma
COM M ON RISK FACTORS FOR M YOCAR DI A L INFARCTION
(iii) Pr imary aldost eron ism (Conn's)
6. Coa rct at ion (but BP norma l in legs) 1. Smoking
7. Toxaem ia of p regnancy 2. Hypertens ion
3. Hypercho lest ero laem ia
4. Diabetes mell it us
COR PULMONALE 5. Fami ly history of atheroma
6. Increasing age
Ca rd iac d isease seconda ry to ch ron ic d isease of lu ngs or
7. Male sex
p ulmonary vessels

COMPLICATIONS OF MYOCARDIAL INFARCTION

CAUSES
EAR LY (IN FIRST 48 HI
1. Emphysema and c hro nic bronch it is
2. Pu lmona ry fi bros is 1. Card iac arrhyt hm ia
3. M ultip le pu lmo nary embo li (i) Sin us o r noda l bra dycard ia
I ii ) Supravent ricu lar t achycar dia, at rial f lutter, at rial
4. Severe ky phoscoliosis
5. Id iopat hic p u lmonary hypertens ion fi b rill ation
(iii ) Ven t ricu la r ect opic beat s, tachycard ia, f lutter o r f ib ri llation
(Iv) Heart block
(v) Ca rdiac asyst o le
SIGNS OF COR PU LM ONALE
1. Warm cya n osed extrem iti es w ith bou nd ing pu lse
2. Ra ised JVP, hepatomega ly and oedema
3 . Trip le rhyt hm and lo ud P2 d ue t o p ul mo nary hyperte nsion (but
I 2. Ven t ricu lar fa ilu re
3. Hypot ension or 'shock'
4. Perica rdit is
5. Ruptured papilla ry muscl e o r chordae ten di neae
overl y ing emphysema may ca use soft hea rt sounds) 6. Ventricu lar septa l def ect
4. Funct iona l t r icusp id i ncompet ence in seve re cases 7. Iatrogen ic (pacing, etc.)
_ I Ca rdio log y Cardiolog V I _
MEDIUM (AFTER 48 HI CONTRA-INDICATIONS TO THROMBOLYTIC
,. DVT, pul monary embolism
THERAPY
2. Mural t h ro m bos is, systemic em bol ism 1. Recent haemo rr hage. trauma o r surgery
3 . Card iac r upture (often after several w eeks) 2. Bleedi ng d iathesis
3. Aortic dissect ion
4. Severe hypertension
LATE IAFTER SEVERAL WEE KS)
5. Recent cerebra-vascu lar event (CVA)
1. Cardiac aneurysm 6. Peptic u lcer
2. Dress ler's syndrome due to card iac autoantibod ies (fever, chest 7. Heavy vagi nal bl eedi ng
pa in, pericarditis o r pleu risy) 8. Acute pancreatit is
3. Psychological, incl udi ng 'L chest pa in' 9. Severe liver disease, esp . oesophagea l va ri ces
4. Frozen shoulder and 'sho uld er h and' syndrome 10. Pu l mo nary d isease with cavi t ation
Streptoki nase o r anistreplase should not be g iven agai n w it hi n
12 m onths of a p revious dose, or if t here was an all ergic
CLINICAL ' SHOCK'
reaction
Defin ition : a synd ro m e in w h ich inadeq uat e blood supply and
el iminat ion of t issue metabolites lead t o functional and/or
struct u ral d isturbances in the essent ial o rg ans
RHEUMATIC FEVER
Diagnosed by t he revised Jones' criteria,
CAUSES i.e. evid ence of previous streptococcal infectio n pl us either 2
1, Hypovo laem ia - haem o rrha g e, t rauma, dehydration, b u rns, majo r cr iteria or 1 ma jor and 2 m i no r c riter ia fro m the followi ng
post su rge ry l ist:
2. Ca rdi ac f ailu re .
( i) Pump fa i lu re, e.g. myoca rdial i nfa rct
(ii) Arrhyt hm ia
MAJOR
(i ii) Obstruct ion, e.g. p ulmonary embo lism
3. Sepsis Sydenham 's cho rea
4. Anaphylaxis P olya rthr it is (m ig ratory)
Erythema margi natum
C arditis
PERICARDITIS S ubcutaneo us nodu les (pai nless)
CAUSES Mnemonic - SPECS
1. Myocard ial i nfarct
2. Vi ral (Coxsackie, Echo, et c.)
3. Rheumat ic feve r
MINOR
4. Pyogen ic (pn eumon ia or septica em ia) Pyrexia
5. Tuberculous ECG shows p rolonged PR interval
6. Cancer invad i ng the pericardi um (bronchus or b reast) Arth ralgia
7. Severe uraemia C reactive protein (or ESR) raised

I
8. SLE, rheumatoid disease H istory of previous rheum atic fever
9. Dressler's syn d rome Mnemonic - PEACH
3. Electrocardiography
-
THE NORM AL ELECTROCAROIOGRAM

T
p u
Q
s
PR shou ld be < 0.20 seconds
QRS shou ld be < 0.12 seconds
1 large square (5 mm) on ECG, pape r == 0.2 seconds
300
: . Vent ricular rate/ m i nute ==
No . of large squares
between ad jacent R peaks

STANDARD LEADS
ECG int e rp ret atio n is fac il itated by imag ining th at the standard
leads 'look at' t he electrica l act iv ity of t he heart fr om t he f ollowing
viewpoint s in a coronal plane:

.VR
I Left chest wall
II Left hip
III Right h ip
aVR Right shou lder
aVL Left shoulde r
aVF Pe rineum

T he ca rdi ac axis ca n be worke d out from leads I and aVF,

remembe ring that R waves re p resent the di rection of the vector

j
 Electrocard iograp hy Ele ctrocardiography I _
(l eft ventr icu lar d epolarization ) and S w aves represen t the ARRHYTHMIAS
opposite direction.
Summate Rand S for each of these 2 leads. 1. PREMATURE BEATS
Then height of R min us depth of S for lead I represents the Ar ise from ect opic focus in atrium, AV node or ventricle.
vec tor i n the horizon tal direction, and heig ht of R m inus d epth o f Usually follow ed by 'com pensatory pa use'
S fo r lead aVF represents the vec tor i n the v ertical d irection. A
simple scale d rawing of these two v ectors then gives the cardi ac Suprave nt ricular extrasystole
ax is: P is premature and may be b izarre

Nodal extrasystole
Essent ial ly no rmal GAS but n o p receding P
Lead aVF
Ventricular extrasystole
Biza rre GAS w ith no p receding P
Angle X = Cardiac axis

The nor m al axis is betwee n - 30" and +90° (lead aVL is at _30",
lead I is at 0, and lea d aVF is at +90°)
A n axis of less than _3~'' i nd icat es L ax is dev iation
A n axis of m ore t han +90 0 i nd icates A axis deviation

CHEST LEADS
These lead s 'look at' the heart i n a horizontal plane from the right 2. PARDXYSMAL ATR IAL TACHYCARDIA (PAT)
o f the sternum (V1 ) t o the axi llary line (V6) Norm al QAS, but T w aves altered by fus ion w ith P w aves

PAT with block (usually i nduced by digitalis)

V6 Aapid regu lar P w aves wi th slower GAS waves
V5
V4
V3
V1
V2
Clockw ise or anticlockw ise rot ation is thus d etected by these leads p p p p /
V V
3. PARDXYSMAL VE NTRICULAR TACHYCARDIA
GAS complexes are sl urred and wide b ut f airly regular. P
waves often obscured

~f
_ I Electroca rd iograp hy Electroca rd iography I _
4. ATRIA L FIBRILLATION Mnemonic - V\I1LLlAM MORRO W
V1 V5
Absent P waves an d GRS com plexes irreg ul arl y i rregu lar
W - L- M = LBBB
M - R- W= RBBB

T T
FIRST DEGREE BLOCK
PR interva l exceeds 0.20 second s but rhyt hm is norm al

5. ATR IA L FLUTTE R
P waves in 'sawt ooth' patte rn at 25G-350/m in and GRS
complexes afte r every 2nd, 3 rd or 4t h P. The b lock m ay
fl uctuate rapid ly, causing GRS t o appea r irreg ular
SECOND DEGREE BLOCK
GRS occu rs on ly after every 2nd, 3rd or 4th P wave
P waves reg ular, b ut some o bscu red by T or GRS com p lexes

Fl utte r w ith 5:1 b loc k Wenkebach phenomenon (M obit z type I)

PR inte rva l prog ressive ly increases u nt i l a QRS is drop ped , afte r
6. VENTR ICULAR FIBR ILLATION w h ich PR shortens and t he cycle is repeated

p p p p p
p p

Rapid biza rr e ven tricula r patterns

Mobitz type II
PR i nterva l is const ant but an occasiona l P wave is not fo ll owed by
HEART BLOCK a QRS com plex
BUNDLE -BRANCH BLOCK IBBBI
Third d egree b lock (com p let e heart b lock)
QRS exceeds 0.12 seconds w it h a not ch ed com p lex P waves and QRS com plexes occu r complete!y inde pendent ly of
each other. Vent r icu lar rate is 25-50/m i n

LBB B
V5 M -shaped wave i n L chest leads T
T
W -s haped wave in R chest leads p P P p p P p

RBBB VENTRICULAR HYPERTROPHY

V1
M-shaped w ave i n R chest lea ds
W -s haped wave in L chest leads
LVH
1. Tall R waves in left ch est leads w it h dee p S waves i n rig ht chest
lea ds
Su m of S in V1 and R in V5 exceeds 37 mm
_ I Electro c a r diogr a phy Electrocardi og ra p hy I
2. May be LV 'st ra in' 1ST depressio n and T inversion) Anterior infarct
3. l eft axis deviation Usually d ue to occlusion of the d escending l coronary artery. T he
4. QRS may be slightly pro longed infarct faces leads I, aVl and t he chest leads

Inferior (diaphragma tic) infa rc t

Due t o occlusion of R coronary o r circum fl ex artery. Faces lead s II,
III and aVE Persistence of the acute i nfa rct ion pau ern fo r more
t han 6 months sug gests ventricular aneurysm

MYOCARDIAL ISCHAEMIA W IT HOUT INFARCTION

LV hypertrophy a nd
s train 5T depression and symmetri ca l T w ave inversion

VI V5
DIG ITALIS
RVH Also causes 5T dep ression and T i nversion but in a 'reversed t ick'
pattern
1. Tall A waves in r ight c hest leads wi th S waves in left c hest
leads Digit ali s also causes:
2. R axis deviation , . Bradyca rdia
2. Pro longed PR
3. Shortened OT
4. Any a rrhyth m ia, especially
bigem ini o r heart block
RV hype rtro phy
and strai n
HYPOKALAEMIA
Prolongatio n of OT int erval, ST depression and T wave fl atten ing
or i nversion . Prominent U waves, w hich may fu se w it h t he
VI V5 succeed i ng P

OTHER CAUSES OF ECG CHANGES

MYOCARDIAL INFARCTION U P

Characteristic changes are:

T
, . Tran sie nt ST elevation and persistent T wave i nve rsion in leads
fac i ng t he infarct
2. Transient ST de p ression in lead s di am et rica ll y oppos it e t he HYPERKALAEMIA
infa rct Sma ll P waves w ith ta ll peaked T waves
3. App earance of 0 wa ves exceeding 0.04 seconds an d 2 mm ORS com plex w idens, and ventricu lar f ib rillation may follow
deep. T hese occur lat er and pe rsist

Recent myocardia l infa rct

_ I Electro ca rd iog rap hy

PER ICARD IT IS
4 . Chest disease
Acut e
Mexica n sadd le-shaped ST elevation in all the standard leads
except aVR, and in most of t he chest leads

LU NG VOLUMES
II II I ___ M.~ j mum i nspi ration

Chronic Tota l
5T becomes isoelectric and the T wave f lattens and may invert l ung
capacity

AC UTE PU LMONARY EMBO LI SM (classica lly 'S1, Q3, T3' )

1. S wave i n lead I Funct ional re s id ua l
~ Maximum exp iration
2. T wave inversion and Q wave in leads II I and Vl - V3 Resid ual vo lume capacity
3. Transient RBBB
4. Right axis dev iation
T he resting expirat ory leve l is t he most consta nt refere nce point
COR PULMONALE on th e spi romet er t rac ing

1. l arge pointed P waves

2. Changes of RV hypertrophy M INUTE VENTILATION
Product of t idal vo lume and num ber of respi rations per minut e
HOW TO READ AN ECG
1. Identify t he r hyt h m a nd ra te VITAL CAPAC ITY
2. A re normal P waves p resent and what is t he PR interval? Largest vol ume a subject can expi re after a single maxi mal
3. Is the ca rd iac ax is n o rm a!? i nspirat ion . Norma l val ues increase w ith s ize of subj ect and
4. Is t he GRS complex abnormally broad? decrease w ith age (about 4'h lit res i n young ad ult ma le) . Can be
{L BBB is always patho log ica l and makes furt her i nter pret at ion reduced in practica ll y any lu ng or chest wall d isease
impossib le)
5. Are t he Q waves pa t ho log ica l?
6. Is the ST segment ra ised o r depressed? FO RCED VITA L CAPAC ITY (FVCI
7. Are the T waves norma l or inverted? T he vita l capacity when the expi rat ion is perf ormed as rapid ly as
Further read ing: The ECG made easy, J R Hampton, Church ill poss ible
Livingst one, Edi nburgh
FEV ,
(Forced exp iratory vo lume i n one second) - vol ume ex pi red
du ring fi rst second of FVC
FEV 1
Ratio - - shou ld be 0.75 o r more
FVe
The rat io is reduce d in obstructive airway d iseases (ast hma,
emphysema, bronchitis)
II I Ch est diseasa
PEAK EXPIRATORY FLOW RATE IPEFR )
Maximum expi ratory flow rate ach ieved during a fo rced
exp iration. A conven ient way to detect a reduction i n ventilatory
function. A lso useful for serial measurements i n the same patient
and for assessi ng response to bronchodilators
RE SIDUAL VOLUME
Obt ained by su btracting expiratory reserve vol ume from
functional re sidua l ca pacity. Residua l volume is norma lly 20-25%
of total lung capacity but i ncreases in elder ly, and in over~ i n flation
of the lungs (emphysema, asthma)
A NATOM ICAL DEAD SPACE
The vo lum e o f ai r in the mo ut h, pharynx, t rachea an d bronch i up
t o t he t erm inal b ronchioles (about 150 m l). In d isease t he
physiological dead space may greatly exceed the anat omica l dead
space due to the disorders of the ven tilation/perfus ion ra tio, but in
health t he two are identica l
DIFFUSION DEFECTS
Carbon dioxide is about 20 times more diffusib le than oxygen. In
d iffusion defects the arterial Po 2 is normal or slightly red uced at
rest, but decreases markedly after exercise due t o increased tissue
uptake of O2 , Arter ial Ft0 2 is norma l or ev en reduced at rest (due
t o hyperventilation) and tends to fall on exercise
DLeO is the transfer factor measured by carbon monoxide
inhalat ion
VA is the alveolar vol ume measured by heli um di lution
KeD, the gas transf er coefficient. '" -=="-
DLeO
VA
CAUSES OF REDUCED DIFFUS ING CAPAC ITY IT RANSFER
FACTOR)
1. A lveo lo-capiliary block
(i) Pu l monary oedema
(i i) Pul monary fib rosis
(iii) Infi ltrat ive lesions, e.g. sarcoidosis
2. Red uction in area ava ilable fo r diffusion
(i) Emphysema
(ii) Mu ltip le pulmona ry embo li
3. Haemorrhage into the alveo li (an artefact rather tha n a true
redu ction )
Chest d is e ase ! _
LUNG COM PLIA NCE
A measure of l ung elasticit y. Compl iance is reduced w hen the
l ungs are abnormally stiff due to pulmonary venous congestion or
i nfi ltrative or fib rotic lesions of the lungs
BLOOD-GAS ANALYSIS
These values must be relat ed t o the norm al levels expected fo r t he
subject, e.g. baby, old man, p regnant wom an
HYPOX IA
Oxygen deficiency at a specified site
HYPOXA EM IA
Oxygen deficiency in the blood. In arterial blood of norma l resting
adult:
Fto z is about 40 mmHg (4 to 6 kPa)
Po 2 is about 90 t o lOa mm Hg (12 t o 15 kPa)
Cause s of hypoxaemia
1. Cardia-respiratory disorders
(i) Hypoventi lation
(ii ) Abnormal ity of ventilat ion/perfusion (Via) ratio
(iii) Impaired diffusion
(iv) Venous to arterial shunt
2. Decreased P0 2 o f i nspi red gas, e.g. high altitude
3. Reduction in active haemoglobin, e.g. car bon monoxide
Type 7 respiratory failurB, with Pao l < 8 kPa and PaC02 < 6.5 kPa,
occurs in asthma, LVF and pu lm onary embolism
Type 2 respiratory failure, w ith Pa0 2 < 8 kPa and Pa C02 > 6.5 kPa,
occu rs i n chronic bronchitis, CNS disease and impaired chest wall
movement
HYPOVENT ILATION
Reduction in l ung vent ilation suffic ient to ca use hypercapnia
Causes of hypoventilation
1. Resp iratory centre depression, e.g. drugs, anoxia, central sleep
apnoea
2. Neuro lo gi cal di sease, e.g. pol io, motor neurone disease
3. Respiratory muscle disease, e.g. de rmat omyositis, Duc henne's
muscu lar dystrophy
4. lim ited chest movement, e.g. kyphosco liosis, thoracop lasty for
TB
5. lim it ed lu ng movement, e.g . p leural effusion, pneumothorax
_ I Chest d iseDs e
6, l ung disease, e.g . collapse, pneumo nia
7. Upper airway obstruction, e.g. obstructive s leep a pnoea
DYSPNOEA
Su bjective awareness of t he need for an inc reased respi ratory
aHort
K U SS MA U~ S BR EAT HING l AIR HUNGERI
Occu rs in acid osis (u raemia, diabetes mel lit us) due to sti mulatio n
of respi ratory centre
CH EYNE- STO KES BREATHI NG
A mp lit ude of resp i ration p rog ressive ly deepe ns t o a maxim um ,
t hen decreases to a per io d of ap noea. Due t o dim in is hed
sensit ivity of respirato ry ce ntre to CO 2 , Occurs in left v ent ric ular
fail ure, ce nt ral respirat ory dep ression and in no rm al i nfant s
OXYGEN THERAPY
In ch ron ic hy poxia d ue to hypo vent ilatio n (e.g. chronic bronch it is)
t he art er ia l Pe0 2 is raised and co rre ction of t he hypo x ia by oxygen
in high co ncentrat ion may release t he respi ratory ce nt re fro m its
'anoxic d rive' and p roduce COz n arco sis. l ow-concent rat io n (24% )
oxygen masks such as t he Vent imask shou ld be used , w it h serial
b lood gas analyses. If CO 2 cont inues to rise, respi rat ory st im u lants
o r m echanica l vent ilation may be needed .
In hypox ia d ue to i mpaired gas exchange (e.g . pneumonia,
p u lmonary oedem a) high concent rat io n masks deliveri ng 35-60%
oxyge n are req u ired
DEFINITIONS OF COMMON PULMONARY DISEASE
CHR ONIC BRON CHIT IS
Chro n ic o r rec urre nt i ncrease in t he volume of m ucoid bronc hial
secretio n suffic ie nt t o cause ex pect orat ion (usua ll y da ily co ug h
w ith sputu m fo r 3 months each year f o r at least 2 co nsec ut ive
y ears ). T here is an obstructive e lement w h ic h is only partially
reve rsib le
EMP HYSE M A (defin e d h istologica l ly)
Is c haracter ized by en larg ement of t he ai r spaces dista l to the
terminal bronch io les, wi t h d estruct io n of the alveolar wal ls
Chest dis e ase
CHRON IC OB STRUCTIVE AIRWAYS DISEASE ICOADI
T his comprises ch ron ic bronch it is and em phy sema, w hich are
o ften present simultaneously. Bronch iecta sis is ofte n
m isd iagnosed as bro nch iti s
ASTHM A
Is chara ct erized by va riable, often paroxysmal, dy spno ea due to
w idespread narrowing of the bronchio les. PEFR or FEV , is
decreased , but at least 20% o f t he decrease m ust be rev ersi b le
over a few m inutes o r days
Feature s of a seve re asthma a ttac k in an adult
, . Can't com plet e sente nces in one bre at h
2. Respi rat o ry rate excee ds 24/mi n
3 . Pulse ex ceeds 110/m i n
.4 . PEFR less t han 50% of p red ict ed o r previous best
Features of a Iife.threatening a sthma attack
,. PEFR less t han 33% of p redict ed o r previous best
2. Si le nt c hest, cyanosis or feeb le respiratory effort
3. Brady ca rd ia or hypotension
4 . Exhaust ion, confus ion or coma
If any of t he above are present, measu re the b lood gases
Blood g as m a rke rs of a life -threatening attack
1. No rmal o r h ig h PacOz
2. Sev ere hypoxia, Pa0 2 less t han 8 kPa d espite oxygen t hera py
3. l ow p H
HARMFUL EFFECTS OF CIGARETTE SMOKING
1. PHARMACOLOG ICAL EF FECTS OF NI COT INE
Rise i n BP, t achycard ia, increased p lat elet st icki ness, etc.
2. PHARYNGEAL A ND BR ONC HIAL IRRITATION
Bronc hit is, post -op. pne umo nia, etc.
3. CARCINOM A RISK IN CREASED
Bronch us, oesop hag us, prostate, b lad der
4. CARD IOVASCULAR DISEAS E
Myocardi al ischaemia, Buerge r's d isease, 'strokes'
II I Chest d isease Chest d isease I

5. OSTEOPO ROS IS RISK INCREASED 3. Idiopath ic p ul monary haemosiderosis

4. Bleed i ng d iathes is
6. PASSIVE SMOKING EFFECTS 5. M ycoses, e.g. aspe rg il losis
6. Fo reign body
(i) Effect on f etus d ue t o smoking in pregnancy: restricted
7. Hereditary haem orrhag ic telang iectas ia
growth, increased per inatal morta lity
8. Wegener's granu lomatos is
(ii) Effect on non-smokers : cough, asthma , angina 9. Goodpastu re's synd rome
Exclude sp urious haemoptys is (nasa l b leeding, etc. )
COM MON CAUSES OF CLUBBING
RESPIRATORY In many patients w ith a sma ll haemoptysis and negative
p hysica l fi nd ings, no cause is ever fo u nd despite fo ll ow-up w it h
1. Bronchia l ca rci noma serial chest X -rays
2. Ch ronic pu lmona ry suppuration, e.g. bronch iectasis, cystic fibrosis
PNEUMONIA
CARD IOVASC ULAR
Primary pneumonias are usually acqu ired i n the commun ity
1. Bact erial endocard itis Secondary pneumonias occur w hen the l ungs are alread y
2. CyanotiC congen ita l heart d isease diseased

LESS CO M MON CAUSES INCLUDE, AETIOLOG ICAL CLASS IFICATION

1. Asbest osis, especially w ith mesothe lioma 1. Infective
2. Fi brosing alveo lit is (] ) Bacterial
3. U lcerative col it is & Crohn's a. Strep . pneumon iae
4. Ma labsor ption b. Mycoplasma p neumon iae
5. Cirrhos is c. Haemophil us influenzae
6. Graves' d isease d. Legionella pneumophila
7. Brach ial arteriovenous fistu la (u ni lat e ral ) e. Ch lamyd ia psittaci
8. Fam i lial f. Staph . au reus (may be abscesses)
g. Klebsiell a p neumon iae (may cavitate)
h. Mycobact er ia (e.g. TB)
HAEMOPTVSIS
Pneumon ia may also be a feature of general ized bacte rial
COMMON CAUSES inf ect ions, e.g. b rucellosis, typhoid fever, plag ue
(ii) Viral
Re spiratory
a. Respira t ory syncytial
1. Bronch ia l carc inoma
b . Inf luenza (usua lly secondary bact erial infection)
2 . Pulmona ry tube rcu losis
c. Mumps (usually secondary bacterial infection )
3 . Bronch it is
4. Bronch iectas is d. Cyt omegalovirus
e. U RT v iruses (adenovirus, rhi novirus, parainfl uenza )
5. Lung abscess
(iii ) Rickettsial
a. Typh us
Cardiovascular b. Q f eve r
1. Pu lm onary infa rct (iv) Yeasts and fungi
2. M itral st enosis a. Candida
3. Acute left ventricu lar fa i lure b. Hist oplasma
(v) Protozoa and parasites
Less common causes include : a. Pneumocystis ca ri n ii
1. Pneumon ia, especially pneumococcal b. To xo plasma
2. Collagen~vascu l a r disease, espec ia lly po lyarteritis nodosa c. Amoebae
II I Che s t d isease Chest disease I

2. Allergic CAUSES OF PULMONARY COLLAPSE

Collagen- vascular d isease (esp . po lyarter itis nodosa)
St evens- Johnso n syndrome (eryt hema mult ifo rme) 1. ABSORPTION COLLAPSE
Due t o complet e bronch ial obst ruction
3. Chemical agents (I ) Int ra lum ina l, e.g. fo reign body, mucus or clot
(I ) Irr it ant gases: NH 3 , S02. C12, oxides of nit rogen (ii) Mu ral, e.g . bronch ial carcinoma o r adenoma
(ii ) Irr it ant liqu ids: vom itus, lipoid pneumon ia (iii) Extramu ral, e.g. peribronch ial lymphadenopathy or aortic
aneurysm
4. Physical agents - irradia t ion
In discussing causes of pneumon ia remem be r the possib ility of 2. PNEUMOTHORA X OR PLEURAL EFFUS ION
1. Opportunistic o rganisms in immune deficiency, especia lly AIDS
2. Pre-existi ng lung d isease . e.g. bronchi al ca rci noma and Remembe r that in abso rption collapse t he mediast in u m sh ifts
b ronchiectasis. especially if the pneumonia is recu rren t o r to the affected side. but in co ll apse due t o air o r fl uid in t he
un responsive pleura l space the mediast inum may sh ift to t he oppos ite side
3. Inhalation pneu mon ia
(i ) Oral an d ph aryngeal sepsis and sinus it is
(i i) Oesophagea l obstr uction and pharyngea l pouch CAUSES OF PLEURAL EFFUSION
(I ii) A lcoho lic debauch, drown ing o r anaesthesia TRANSUDATE
(iv) l a ryngea l cancer
(v) Tracheo-oesophagea l fistu la (less than 30 g p rotei n/lit re. Im p lies a syste m ic cause)
(vi) Inadeq uat e gag reflex 1. Card iac fai l ure
4 . Predisposi ng syst emic disease suc h as diabet es, cirrhos is. 2. Nephrot ic syndrome
alcoholism or agranu locytosis 3. Hepatic fa ilure
5. Fo reign body not seen. on X -ray (e.g . peanut)

EX UDATE
COM PLI CATIONS OF PNEUMOCOCCAL LOBAR
PNEUMON IA (More than 30 g protei n/li tre. Im p lies a loca l ca use)
1. Pu lmonary embo li
1. Pleu risy w ith effusion, o r serous pericarditis 2. Rheumatoid d isease
2. Empyema o r pe rica rdial s uppuration 3. I nfections (pneumon ia, T8 )
3. End oca rd it is, men ing it is (not to be con fused w it h men i ngismus, 4 . SLE and othe r collagen- vascu lar d iseases
in wh ich CSF is no rma l) or cereb ral abscess
5. M alignancy (b ronchial Ca, secondary Ca, Hod g kin 's,
4. Delayed reso lution mesothe lioma )
5. Nonspecific complications 6. S ubph ren ic abscess
(i ) Herpes labia lis
Mnemonic: PRISMS
(ii ) Septicaemia (may be 'shock')
(I ii) Ca rd iac f a ilure
(iv) Ca rd iac arrhyt hmia
(v) Deep ve in thrombosis
CAUSES OF PNEUMOTHORAX
1. Traumat ic
2. Iatrogen ic, e.g. t ho racentesis or surgery
CAUSES OF EMPYEMA 3. Spont aneous
1. Pneumonia, especia ll y lobar, or seconda ry to bronch ial Ca (i) Subpleu ral bulla
2. Lung abscess {iiI Emphysema
3. Subph ren ic abscess (iii) Ast hma
4. Med iastina l sepsis (iv ) T8
5. Chest wound or su rgery (v ) Lung abscess
6. T8 (vi) Pneumocon iosis
I Chest disease Chest d isease I
CAUSES OF ACUTE PULM ONARY OEDEMA CLIN ICAL FEATUR ES
1. Left heart fa i lure 1. Class ical symptom - cough with copious p uru lent sp utu m,
(i) Atrial, e.g. mitral stenosis especia lly on chang ing postu re
{iii Ventricu lar, e.g. hypertension o r myoca rd ia l infa rct 2. Class ical sign - loca lized persistent coa rse crepitatio ns
2. Ov erload of Lv. fl uid 3. May be asym pto matic
3. Inha latio n of i rritan t gas, e.g. chlo rine, dense smoke 4. Mala ise, interm ittent fever, hal it o sis
4. Fu lminat ing viral o r bact erial pneumon ia 5. Weight loss or 'fa ilu re to thrive'
5. Fat embol i 6. Dyspnoea, cyanosis o r cl u bbing
6. Neuroge nic (rare) 7. Haemopt ysis
e.g. Head in j ury or cerebro-vascular accident
TYPES OF CA BRONCHUS
CAUSES OF INTERSTITIAL LUNG DISEASE 1. Squamous (35%)
1. Cryptogen ic fi b rosi ng alveolit is 2. O at ce ll (small cell ) (25%)
2. Sa rcoidosis 3. L arge cell (20%)
3. Extri nsic all erg ic alveolit is 4. A denocarci noma (20%)
4. Asbestosis, pneumocon iosis or sili cosis Mnemonic: SOLA
5. Drugs o r irrad iation
6. Pu lmonary eosi noph il ia COMPLICATIONS OF CA BRONCHUS
7. Collagen- vascu lar d isease
LOCA L EFFECTS
1. Bronchial obstruction: collapse, conso lidation, abscess
BRONCHIECTASIS 2. Mal ign ant pleura l effusion
Per manent di latation of t he bronchi, usually accompanied by 3. Erosion of large vessel
rec u rrent bronch ial su p puration 4. Superior vena cava l obstructio n
5. Di rect spread t o chest wa ll, brachial p lexus (pancoast's)
6. H orner's syndrome from cervica l sympathetic co mpression
PATHOGENES IS H oarseness from recurrent laryngeal nerve compression
An i mal experiments suggest tha t p roxi ma l narrowing of the H ig h d iaphragm from p hren ic nerve involvement
airways and dist al infection are both im portant
M ETASTASES
Especially hilar nodes, l iver, brain, bone, adrenals
CAUS ES
1. Infection
NON-METASTATIC EXTRA-PULMONARY EFFECTS
(i) Bronch iol it is of i nfancy
{i ii Measles o r pertussis in ch ildren 1. Cachexia and anaem ia
(i ii ) Post broncho-pneumo nic collapse in adults 2. Clubb ing (hypertroph ic pu lmonary osteoa rth ropathy)
(iv) Common ly in post -primary TB 3. Endocri ne
2. Bronchial stenosis or occlusion (i ) Gynaecomastia
(i) Adenoma or carcinoma {iii Inappropriate AD H ---> hyponatraemia (often small celt)
(i i) Foreign bo dy o r asthma casts (ii i) Inappropriate PTH ---> hyperca lcaemia (often squamous)
(i ii) Lymphadenopathy (iv) Inappropriate ACTH ~ . pigmentation, hypokalaem ia,
3. Pu l monary asperg i llosis alka los is (often smal l cell )
4. Cystic fib rosis 4. Dermatolog ical
5. Hypogammag lob ul i naem ia Pigmentation, prurit us, etc. (see page 156)
6. Cil iary dysfunction (e.g. Kartagener's synd rome) 5. Neuropathy or myopathy (incl. de rmatomyosit is and Eaton-
7 . Many cases are idiopath ic Lambert syndrome)
_ I Che s t di sease Che s t d isease I _
TUBERCULOSIS 10. T B tracheitis, laryng itis o r st o matit is d ue to expecto ratio n of
myco bacte ria
PRIMARYTB 11. Swallowed sputum may cause i nt estina l T B (usually i n
Occurs i n su bjects never p reviously exposed to T B lymph o id patches)
'Pri mary com p lex ' == Ghon focus + reg io na l lymphadenopathy 12. Amylo id osis
Ab d om inal pri m ary T B and t ube rcu lo us ce rv ical lymphaden itis are
now u ncom m on in the U n ited King dom, except in t he im m ig rant
populat ion CO MMO N PR ESENTATIONS OF PULMON A RY TB
1. Asym pt o m atic (sc reen ing CXR)
PULM ONARY PR IM A RY TB 2. Persiste nt cough
Usually hea ls spontaneously 3. Ti red ness, ma laise, recu rrent coryza, weig ht loss o r fever
4. Pneumonia
Comp lications 5. Hae moptysis
1. Loca l spre ad in lung 6. Dyspepsia
2. Cavitation Note incre ased incidence in imm ig rant s, el derly,
3. Pleu ral effusion (m ay develop before po sitive Mantoux) imm unosu ppressed, d iabet ic and after gast rect omy fo r pept ic
4. Ru ptu re of caseou s node int o bronch us causing w idesp read ulce r
broncho pneu m o nia
5. Segmenta l co ll apse due t o b ro nch ia l co m pressio n by no des
6. ' M iddle lo be syndrome', i.e. bro nch iectasis i n later lif e due to
SARCOIDOSIS
b ro nch ial comp ress io n by nod es
7. Haem atogenous metastasis Defi n itio n: a multisystem g ranulom ato us d isease (of un known
(i) Bone o ri g in ), in w hic h the g ranu lomas consist of w ell-form ed, sharp ly
(ii) Kidney demarca t ed collectio ns o f ep ithel io id cells, wi th linle o r no
(iii) Epid idym is o r Fa llo pian tu bes caseatio n, and little ce llu lar reactio n a rou nd them
l iv) Meninges
8. M il iary T B
CLI NICA L FEATU RES OF SARCOIDOS IS
POST-PRIMARY T B 1. Pulmo nary:
Rein f ect ion o r recrudescence o f pri mary lesion. Usuall y Bilat e ra l hilar lym p had enopathy (SHU
pu lmonary, b ut may be m il iary o r atypical in t he o ld o r 1
immunosuppressed BHl + pre·fi b rot ic pu l mona ry infi lt ra tion
1
Either re solutio n o r pul monary fib rosis
PULM ONARY TB 2. Constitutional sympt oms, feb rile arth ra lg ia
Complications 3. Su perfi cial lym p hade nopathy
1. Caseatio n ('cold abscess' ) 4. Ski n lesio ns - e rythema nodosum, l up us pernio, infi ltrated
2. Bronchog en ic sp read i n lungs plaq ues, nodu les, infi ltra tes in sca rs
3. Pleu risy 5. Oc ula r lesio ns - uve itis, con ju nctiv al i nfi ltrates, etc.
4. Effusion o r T B em pyema 6. Parot id, lacr imal g land lesio ns
5. Haemopty sis, m ay be m ass ive 7. Neuro log ical lesions
6. Tension ca vit y d ue to va lvu lar o bstr uct ion (i) Neu ro p at hy, especially f acial nerve
7. Tube rcu loma of lu ngs (ii) M en ingea l infiltration and local CN S depos it s
8. Haemat og eno us metast asi s o r m il ia ry T B 8. liv er, spleen o r cardiac infiltra tion
9. Ch ronic pu l m o na ry fib ro sis and com pensatory emphysema 9. Bone involvem ent, especi ally phala ng ea l cyst s
(especially i n m iners) 10. Hypercalcaemia ± nephrocalcinosis and calcu li
PHYSICAL SIGNS IN LUNG DISEASE
I
n
~
Ch ••, wall
movement
Mediastinum
and trac h ea
Ta ctile vo.:.'
f . em itu s
Percu•• ion
not.
Br•• th
lounda
Adde d
sounds
•••
~.

Large pleural effu . lo n Decreased on

affected side
Shift 10 opposite
side
Absent Stony dull Absent. May be
bronchial
(:t wh ispering
Absent. May
be pleural
rub above
"••••
pec1oriloquyl "uid
above fluid level

Contla lidation Decreased on Ce nt, al Increased Dull Bronchial Fine Or

affected side medium
cradles
Ma•• ive collep •• Decreased on Shift to affected Absent DLlII Decreased Absf!nt
affected side side

Fibrosi l LQca lli a tt ening Shift to affected Increa sed Dull Bronchia l May be
with decreased side coarse
movement crep itations

La rge pn. umotho ... Decreased on Sh ift to opp osite Decreased In creased Decreased Ab sent
affected sid e side unless bowe l
sounds 8rft
transmitted

EmphVIBma Decrease d Centra l (except Decreased Increased Oec reased Absent

bilateral in unilatera l
('barre l chest') em physema)

Bronchl!11 Decreased Central Normal or Increased Oecll!ased Wheezes and

bilate, alty decreued crackles
t'barrel chesn
5. Chest X-rays

HOW TO LOOK AT A CHEST X·RAY

1. Name, age o f pat ient. date of X-ray
2. Is it a PA fi l m (usual) o r an AP fi lm ? (im p ly ing the pat ient was
too ill t o st and up fo r the fi lm, and t h us prevent i ng assessment
of hea rt size)
3 . Is the f i lm well orientated and correct ly penet rated?
4. The lungs a nd hila '
Cou nt the v isib le R ibs t o assess the size of t he lungs
Look at t he lung fi.e lds fo r any A symmet ry
Is t he T ra chea d isp laced?
A re there any abn orma liti es in t he lung Fields?
A re t he A pices clear? (check for T8 or smal l p neumot horax)
A re the C osto-phren ic angles b lunted?
Are the hila Enla rged ?
M nemonic: RATFACE
5. The hea rt
Is it enlarged and is its outli ne nor mal?
6. The ribs and spine
Look fo r fra ctu res, metastases, rib not ches, etc.
7. Any other shadows1
Tracheostomy, cent ral li ne, prost het ic hea rt valves, ECG
mon ito r w ires, jewe ll ery, pyjama buttons, etc.
B. Any gas o utside the chest1
Surg ical emp hyse m a, gas under A d iaph ragm, et c.

CAUSES OF W HOLE LUN G OPACITY

1 . Consolidation of L lung 2. Massive L ple ura l e ffu s io n

Mediast i num cen t ral Mediastinum and t rachea m ove t o R

_ I Ch est X -rays C hest X-rays I _
3 . Collaps e of e ntire l lu n g Fe atures
1. Dense wedge in heart shadow and diaph rag m beh ind l sid e of
heart obscured
2. L hilar vessels pul led down and w idely spaced
3. L upper lobe hypertranslucenl

R PLEURAL EFFU SION

Fea t ure s
1. Trachea pulled to L
2. A hea rt bo rder not seen
3. l diap hragm obscu red
4. A l ung hypertranslucent
Not e fl u id in horizont al fissu re
COLLAPSE OF R UPPER LO BE
SMALL L PNEUM OTHORAX R HYDROPNE UMOTHORAX

Fe ature s
1. De nse wedge against superior med iasti num Usually traumat ic
2. R h ilar vessels d rawn u p, and w idely spaced (i ncluding pleural asp iratio n)
3. A lower and m idd le lobes hypertransl ucent
4. Tra chea and aortic knob pul led to R PULMONARY OEDE MA

CO LLAPSE OF L LOWER LOBE

Features
1. 'Bat s-wing' shadows - ill defi ned and confluent, spread ing out
from h ila
_ I Ches t X-rays Chest X-rays I •
2. Generalized lower-zone haze MU LT IPLE CI RC ULAR SHADOWS
3. Upper lobe diversion of blood
4. Kerley B lines
5. Enlarged hea rt

EMPHYSEMA

Causes
1. M et astatic ma lignancy
2. Hydatid cysts
3. Caplan's syndrome (rheumat oid arth r itis with pneumoconiosis)
Features 4. Multiple l ung abscesses
1. Hypertranslucent l ung fie lds 5. Wegener's gran ulomatosis
2. Main pu lmonary vessels are large, but peripheral vesse ls are
t h in
3. T h in vertica l heart WIDESPREAD SHADOWIN G
4. Horizontal ribs w ith low flat dia phragm

SINGLE LARGE OVA L SHADOW

Causes include
1. Mi lia ry TB
2. Pu lmo nary oedema
Common causes 3. Bronchopneumon ia
1. Bronchial cancer 4. Pneumocon iosis or haemosiderosis
2. Met ast atic deposit. e.g. breast ca ncer, hypernephroma 5. Sarcoidosis
6. Syst em ic sclerosis
Less common causes 7. Fib rosi ng alveol itis and rheumat oid lung
3. T B (may be ca lcifi ed) 8. Hypersensitiv ity, e.g. allergi c alveo 1it is ('farme r's lu ng', etc .)
4. Abscess 9. Neoplasm:
5. Encysted p leu ral effusion Miliary Ca metast ases
6. Cyst, e.g. hydatid Lym phangitis ca rcinomat osa
7. Adenoma , fi broma or hamartoma Alveo lar cel1 ca rci noma
8. AV aneu rysm 10. Post-v iral pneumon ia w it h mi liary calc ifica t ion (esp. va rice l1a )
- Che lt X-rays

BILATERAL HILAR LYM PHADENO PATHY SYSTEM IC HYPERTENSION

Chest X -r ay s I _

C a uses inc lude

1. Sa rco idosis
2. Lym phocytic leukaemia Features
3. Lym phoma 1. Aortic unf olding
4. Ca rcinom a m etastases 2. LV hyp ertrophy
5. Pri m ary t uberculosis 3. Ker ley B li nes (horizont a l lines in cas t o ph ren ic ang les due t o
6. A c ute i nfect ions, e.g . infecti ous mon onucleosis o r wh oo pi ng- d ilated subpleu ra l lympha ti cs) if LV fa ilu re develops
cou g h
If un ilat era l, exam ine lung f ields carefu lly fo r bronc hia l
carcino m a o r G ho n f ocus M IT RAL STENOSIS

NORMAL CARD IAC SHADOW IN PA X-RAY

Aortic arch
Aortic arch .....
.... .....
" .... __ Pulmonary artery

A. atrium .................. .. ____ ___L atrial appendage

....... .. L ventricle

Features
, . Stra ig ht L hea rt bo rder and convex R bo rde r
2. Increased pu lmona ry va sc ul ar shadow s
Transve rsa d iameter of heart does not norma lly exceed 50% of
3 . Kerley B lines
chest w idth
_ I Chest X-rays

COARCTATION OF AORTA
6. Gastroenterology
-
CAUSES OF ATROPHIC GLOSSITIS (SMOOTH REO
TONGUE)
1. Antibiotics
2. Anaemia d ue t o d eficiency of Fe, 8'2 o r fo late
3. Vitam in def iciency (r iboflavi n o r nicot in ic acid )
Features
1. LV hypert rophy
2. Small ao rtic arch CAUSES OF DYSPHAGIA
3. Rib notch ing
1. LE SIO NS OF MOUTH OR PHARYNX
PERICARD IAL EFFUSION (i) Stomatitis or g lossiti s
(i i ) Tonsill itis
(i ii) Qu insy, retrop haryng ea l abscess
(iv) Lymphoma of tonsil

2. FOREIGN BODY IN PHARYNX OR OESOPHAGUS

3. INTRINS IC DISEASE OF PHARYNX OR OESOPHAG US

(i) Pl ummer- Vinson synd ro me - i ron deficiency, glossit is,
pharyngeal web and koilo nychia
(ii) Pharyn g eal pouch
(ii i) In flam m ation, strictu re or neop lasm of oesophagus
(iv ) Systemic sclerosis
Fe ature s Iv) Oesophageal achalasia
1. La rge rou nded heart shadow
2. Note sharp cardio -ph renic ang les
Distinction from di lated heart may be ve ry d ifficu lt 4. EXTRINSIC COMPRESS ION
(i ) Tumo urs in neck
(ii ) Medi ast ina l tumour, e.g. retrosternal goit re, ly m ph nodes
(iii ) Bronchia l cancer
(iv) Aortic aneu rysm

5. eNS LES IONS

(i) Bu lba r o r pseud o-b ul bar palsy
(ii) Myasthenia g ra vis
(ii i ) Congenita l muscular incoordina t ion
_ I Gastroe nte ro lo gy Gastroenterology I

COMMON CAUSES OF SEVERE UPPER GI BLEEDING sick le-cell cri sis, lead poisoni ng, hered ita ry ang io-oedema,
Henoch- Sch6n lei n purp ura, etc .
1. Duodenal ulce r
2. Oesophagea l varices
3. Erosive gastrit is (e.g . d ue to aspi rin or NSAID) PEPTIC ULCERS
4. Gast ri c u lce r (may be ma lignant)
DIFFERENCE S BElWEE N GASTRIC AND DUODE NAL
5. Eros ive oesop hag it is (e.g . hiatus hernia)
ULCERS

G astri c Duodenal
COMMON CAUSES OF SEVERE LOWER GI BLEEDING
S ite Usu all v m iddle 2/3 of Usually du od enal bu lb
1. Colon ic d ivert icu lar disease lesser curve
2. Ca rcinoma o f rectum or colon
Ga stri c acid Low o r nor ma l Hvperchl or hvd ria
3. Benig n rectal po lyps
4. Haemorr ho id s o r ana l f issu re Pa i n After mea ls Re lieved by mea ls
5. Colon ic ang iodysp lasia Mav occ ur at about 2 a.m .
6. Ulcerative col itis or Croh n's disease V o miting Commo n U ncom mo n
7. Recta l trauma, i nclud i ng biopsy
8. Hookw orm (in t ropics ) Soc ia l c lass Commo ner in low er Equa l prev alence
soc ial cl ass es
N.B. Hiat us hern ia, co lon ic d iv ertic ulosis and hae morr hoids are
Patho l ogy Ma v be be nign or Virtu all y never mal ignant
common . Massiv e b lood loss sho u ld not be attributed to t hem
m al ignant
un less the sou rce of bleed i ng can be see n, or more ser ious
pathology can be excluded He l icob acter pylo ri ,,% ""%

MEDICAL CAUSES OF ACUTE ABDOMINAL PAIN FACTORS SUGGESTING A GASTRIC ULCER IS

MALIGNANT
,. Food po ison ing or diet ary i nd isc retio n
2. Peptic ulcer, gast ritis, oesoph ag itis Symptoms
3. Biliary col ic or c ho lecystit is 1. Anore x ia and weigh t loss
4. Pa ncreatitis 2. Epigast ric pain not related to food
5. Hepatic congestion (hepat it is, card iac fa i lure) 3. Dysphagia
6. Renal col ic, pye loneph ri t is, cystit is, acute urina ry retention
7. Divert icu litis, ulcerat ive col itis, Cro h n's d isease N.B. The pa in of both beni g n and mal ignant u lcers may be
8. Mese nt eric adenitis (chi ldren) rel ieved by Hrblo cke rs
9. Const ipat ion
10. Mesenteric ischaem ia (atheroma, em bo l ism , po lyarterit is Signs
nod osa i 1. Ep igastric mass
11. Aort ic dissect ion 2. Metastases. look especiall y fo r
12. Gynaeco log ica l, e.g . (i ) l arge irregu lar liver
M ittelschmerz (ovulation) (ii) Supraclavicu lar nodes (Virch ow's)
Dysm enorrh oea (i ii) Deep vein t h rombosis of leg
(IV) Ascites
Salp ing it is
T hrea t ened abortion (v ) Kru kenberg tumou r of ovary (f elt PRJ
13. Pa in referred from sp ine o r c hest (e.g . myocard ial infa rct )
Barium m e al
N.B. Pai n in the abdomen w h ich last s f o r more than 6 hours 1. Fi ll in g defect and fa ilu re of perista lsis in a sit e ot her t han
wi t hout remissio n is likely to be surg ica l m iddle 2/3 of lesser cu rve
Rarer causes of acut e abd om i na l pa in incl ude: ac ute i ntermittent 2. Very large ulcer anywhere in t he st omach
porphyria, he rpes zos te r, d iabetes mell itus (gastric di lat ation ), 3 . Leather-bottle stomach
_ I G a stroenterologv Gastroenterology I
If in doubt gastrosco py (with b iopsy) and gastric cytology CLINICAL FEATURES OF COELIAC DISEASE IN ADU LT
should be performed
1. Loose sto ols w hich mayor m ay not be bulky. pa le and f o u l-
smelling
2. We ight loss (fat and p rot ein deficiency)
COMPLI CAT IONS OF PEPTI C ULCER 3. Oedema (prote in d eficiency )
4. Flatu lence w ith d istend ed abdomen (impai red disaccha ride
1. Bleedi ng hydro lys is)
2. Penetration , e.g . i nto pancreas, l iv er o r retrope rit o n ea l space 5. Hypochromic anae m ia (Fe defi ciency)
3. Pe rfo ration 6. Macrocytic a naemia (fo late o r 8 12 defi ciency )
4. Obstructio n 7 . Perip heral neuritis (S-co m plex defi c iency)
(i) Oedema and spasm - reversib le 8. Glo ssitis and stomatitis (S-com p lex d eficiency)
Iii) Cicatricial st enosis - ir reversi ble 9. Osteomalacia (Ca and vitamin 0 defi ciency)
5. 'M ilk- atkali sy ndrome' - alka losis and calcinosis, due to 10. Pa raesthesiae. t etany (Ca o r Mg defic iency)
excessive i ng estion of m i lk, alkali and ca lcium salts 11. Haemorrh age (vit am in K deficiency)
12. Muscle fla ccidi t y. arrhyth m ias (pot ass ium d eficiency)
13. Weakness and hy pote nsio n (water and elect ro lyte deficiency)
MALABSORPTION 14. Clu b bing
15. De rmat itis herpet if o rm is is strong ly associated
CAUSES
1. Inadequate digestion AIDS AND THE GI TRACT
m Gastr ic o r intestinal resectio n
(ii ) Hepat ic o r bi liary tract o b structio n 1. INFECTI ONS AS SOCIATEO WITH ANAL INTERCOU RSE
(i ii) Pancreati c i nsuffi ciency (especially cys tic fibrosis) e.g. ana l w arts, her pes si m p lex. hepatitis A and S, etc.

2 . Parasites or change in intestinal flora

(i) Tapeworm s o r Giard iasis
2. OPPORTUN IST IC INFECTIONS
(ii) Bli nd-l oop syndromes e.g. candida , c ry ptospo ridiosis, cyto mega lovi ru s, m yco bacteria

3. Tropical sprue 3. KAPOS I' S SA RCOMA

4. Intestinal hurry or fistu l ae
4. LYMPHOMA
5 . Coeliac disease May invo lve CNS, m arrow o r gut
A IDS and erythroderma can also cause partial villo u s atro p hy
5. PARTIAL VILLOU S ATROPHY W ITH MALABSORPTION
6 . Intestinal infil tration
0) TB
(ii) Lympho ma o r leu kaemia CAUSES OF ASCITES
(ii i) System ic scle rosis
(iv) Intesti nal lipodystro phy (W hipple's d isease ) 1. Carci noma, especi ally ovaria n o r aliment ary w it h pe ri t o neal
met astases
7 . Enzyme defects 2. Cirrhos is
(I) Lact ase d efi c iency 3. Hypoal bum in aem ia, e.g . nephrot ic synd rom e
(il) Hartnup d isease 4. Co nstrictive per icard it is, co ngest ive heart fai lure
5. Thrombosis o r obstr uction o f inferior vena cava
8 . Chronic intestina l ischaemia, e.g. mesent eric athe ro m a 6. Tu be rcu lous per it onitis
7. Peritonit is in late st ag es
N. B. The fat-sol ub le vitamins are 0 A K E 8. Chylous ascites due t o lymphatic obstr uction
I Gastro enterology Gast ro ente ro lo g y I _
CAUSES OF OBSTRUCTION OF THE SMALL COMPLICATIONS
INTESTINE 1. Obstructio n due to strictu re
The commonest ca uses are adhesions secondary to operation and 2. Perforation
bowel i ncarceration in an int ern al o r ext erna l hern ia 3. Abscess
4. Fistu la into b ladde r o r vagina
MECHANICA L
BAR IUM ENEMA
1. Compress ion from w itho ut:
(i) A d hesions 1. Diverticu la mayor may not be seen
(i i) Fibrous bands 2. Segmenta l spasm and irri t abil ity of the affected co lon (usually
(i ii) Tu mours, especially of f ema le pelv ic organs sigmoi d )
(i v ) Hernia 3. Chron ic f ibrotic deform ity
2. Com pression from w ithin the bowel wall :
(i) Congen ita l atresia
ULCERATIVE COLITIS
(ii) Acqu i red :
Infl ammatory CLI NICAL FEATUR ES
Neoplast ic
1. Common ly p resent s in 3rd or 4t h decade
Traumatic
2. Ma laise, weakness, weight loss, pyrexia
3. Obstr uction i nsid e t he l umen :
3. Chron ic d iarrhoea, w it h blood and mucus, w hich is often severe
(i) Gallstones
4 . Pa in in L il iac fossa, and recta l tenesmus
(i i) Faeca l i mpaction
(iii) Meco n ium ileus
(iv) Foreign bodies COM PLI CATIONS
(v ) Wo rms
1. Perf o ration
4. Vo lv ulus
2. Per ianal abscess
5. Intussusception 3. Acute 'toxic di latation'
4. Severe haemorr hage
PARA LYTIC ILEUS (no colicky pa i n or bowel sou nds) 5. Hypokalaem ia, hypoprot einaem ia, dehydration
6. Skin lesions:
1. Abdom i nal su rgery
(i) Pyode rma ga ngrenosum
2. Perit on itis
I ii) Aphthous ulcers
3. Acu t e syst emic illness, e.g. pneu mon ia
(iii) Erythema nod osum
4. Pa infu l l umbar conditions, e.g.
(iv) Clubbi ng
rena l co lic
7. Diffuse liver disease and sclerosing cho langitis
retroperitonea l haemat oma
8. Arthrit is and uve itis
·5. Mesenteric ischaem ia
9. Amyloidosis after ch ron ic abscesses
6. Drugs, e.g . gang l ion-blockers
10. Ca rcinoma of co lon
7. Hypokalaem ia
8. Hypot hyroid ism
BAR IUM ENEMA
DIVERTICULITIS ,. Loss of ha ustration
CLI NICAL FEATU RES 2. St raight , narrow, i nelastic co lon
3. May be 'spicu les' due to ti ny ulcer c raters
1. Usua lly m idd le-aged o r elderly 4. M ay be fi ll ing defects d ue to 'pseudopolyps'
2. Recurrent bouts of co licky abdomina l pai n
3. Nausea and vom it ing N.B. Abnorma lit ies are usuall y continuo us (no 'skip' lesions),
4. May be either constipatio n or d iarrhoea and start at the rect um, affecting a variable length of the la rge
5. Tenderness i n L iliac fossa, sometimes w ith a mass bowe l
_ I Gastroente ro logv Gastroentero logy I
CROHN ' S D I SEASE (REGIONAL ILEITISI 2. Neoplasm
(i) Metast ases
CLI NI CAL FEATURES (i i) Lymphoma
1, Usua ll y youn g adults (i i i) Hepatoma
2. Mala ise, weakness, weight loss, py rexia 3. Myelop ro l ife rative d isease, e.g. leukae m ia, myelofi brosis
3. Interm itte nt col icky pain in R il iac f ossa 4. Infective
4. M ild or m oderat e diarrhoea (i) Vi ral, e.g. hepatitis (Q .v.)
5. Tenderness in R iliac fo ssa, someti mes w ith a fix ed mass I ii ) Bacter ial, e.g. Weil's disease
(ii i) Prot ozoa l, e.g. amoebic abscess
(iv) Parasit ic, e.g. hydatid cyst
COM PLI CAT IONS 5. Bil iary o bstr uction, e.g. Ca pancreas
1. Obstruction due t o stri cture 6. Fatty infiltration or earl y ci rrhosis
2. Pe rforation 7. Storage disorders, e.g . amylo idosis, Gaucher's
3. Abscess
4. Fistula i nt o anus, b ladder o r abdom i nal wall
5. F issu re~ i n-ano
6. Mala bso rpt ion (especia ll y Bd
CAUS ES OF A HARD KNOBB LY LIVER
7. Proct oco lit is
,. 1. Ca ncer met astases
8. Erythema nodos um 2. Cirrhosis w ith hepatoma
9. Clubbing 3. Polycystic live r
4. Hydatid cyst s
BA STUDIES (may need both m eal an d enema)
1. l uminal narrowing of ileum (Kantor's 'si ring sign')
2. Distort ed mucosal pattern CA USES OF HEPATO·SPLENOMEGALY
3. 'Ski p' lesions 1. Infectio n, e.g. infectious mononucleosis
2. Myeloproliferative disease
The correlation between rad iolog ical appearance and d isease
3. Lymphoma
activity is oft en poo r
4. Storage d iseases, e.g. amylo idos is, Gaucher's

FEATURES DISTINGUISHING CROHN' S AND

ULCERAT IVE COLITIS CIRRHOSIS
Ci rrhosis is c haracter ized by hepatic pa renchymal d amage w ith
Cro hn '. Ulce ratly" co lhls fibro sis and nodu lar regenera tion througho ut the liver,
G ranulOtna. Present Absent accompanied by d istortio n of the no rmal lobular pattern
In flammation Transmu ral Confined to mucosa
Goblat 0;:.11, Normal number Decreased
Crypt abso;:.sses Unusual Common
Fi ' tulae Common Uncommon
CA USES OF CIRRH OS IS
Sk ip I.,ion , Presen t Absent 1. Cryptogenic (idi o path ic)
T. rmlnat il eum Usua lly inVOl ved Rarely Invo lve d 2. A lco hol ism
Rao;:t al In v o lvema nt U nusual Almost invariable
3. Viral hepatit is (espec ially hepatitis B o r C)
4. 'Autoimm une' live r d isease
(i) Primary bi liary cirrhosis (antim itochond rial Ab in 95% )
CAUSES OF HEPATOMEGALY (ii ) Ch ron ic active hepatiti s (smooth m uscle Ab in 66% )
1. Hepatic con gestion, e.g. card iac f ailure, hepatic vei n 5. Haemochromatosis (primary o r secondary)
th rom bosis. T he liver is pulsatile in severe tricuspid 6. Hepat o-Ienticu lar degeneration (Wilson's)
regu rgita tion 7. Hepatotoxins, e.g. m ethotrexate, carbon tetrachloride
_ I G astroe nterology Gast roenterology

CLIN ICAL FEATURES OF CIRRHOS IS Hepatic

(a) Impa ired conjugation
Features of he patic failure (i) Hepatitis (vira l o r drug-induced)
,. Fi rm hepatom ega ly i n t he early st ages (ii) G ilbert's syndrome
2. Low grade fever (b) Impaired excretion
3. Skin changes: ( i) Hepatitis
(i) J au ndice in late r stages (ii) Met hylte stosterone Id ose-related)
(ii) ' Spiders' (i ii ) Ch lorpromazi ne (hypersensitivi ty)
(i i i) Pa lma r erythema (c) Intra-hepatic o bst r uct ion
(iv) Leuconych ia (wh it e nail s) (i ) Hepatit is
4. Bleedi ng t endency (dec re ased coagu lation fa ctors) (i i ) Cirrhosis
5. Fatigue, weight loss, dyspepsia (ii i) Tumour
6. Foetor hepaticus
7. Encephalopathy: Post-hepatic
(i) lethargy (i) Stone in common bile d uct (CBO)
(ii) Slow, slurred speech (ii) Carcinoma of head of panc reas o r b iliary t ract
(i i i ) Flapping tremo r (i ii) Pressure on CBD fr om lymph nodes
(iv) Dem entia l iv) St ricture of CBD (post -operative or post-inf la mmat o ry)
(v ) Precama progress ing t o d eli rium and com a (v) DeveLo pmenta l anoma l ies (rare)
8. Water retention :
(i) Oedema SUMMARY OF BLOOD CHANGES
Oi) Hy ponat raemia
Obst~uC1 ive Hepe (ocell u la~ Haemolytic
Features of porta l hyperte nsion fa ilure with no
1. Splenomegaly, ofte n with pancytopenia (hypersplen ism ) oba1ructio n
2 . G I bleed ing f rom oeso p hageal va rices Hyperbilirubinae m ia Co niugated Unco niugated Unconiuga te d
3. Ascites (low p las ma album in is also necessary)
Alk e li ne p hosp hatale Marked increase Norma l or in creased Slig htly
increased
Ot her features
1. Cl ubb ing Aaperte t e tren sa mlnase Normal or slight Increased Normal
2. Hyperkinetic ci rcu latio n increase
3. Sexual c hanges:
Females: errat ic menstruation and b reast atrophy
Ma les: gynaecomastia, t esticu lar at ro phy and scanty body hai r
SUMMARY OF URINARY AND FAECAL BILE PIGMENT
4. Parotid en largement l. I .
CHANGES
5. Dupuyt ren's co nt ra ct u re J In a co hohcs
Obs tructive He pa t oce llul a r Haemo lytic
6. Suscepti bil ity t o infections fa il ure wi th no
obatruction
J AUNDICE Urina ry b ilirubin Increased Normal or increased
Jaundice (ict erus) is due to hyperbilirubi naemia . It i nvolves the Ur inary urobilinogen Dec reased Normal or increased Inc reased
sclerae, unl ike the yellow pigmentation due t o mepac rin e or
Feec,,1 s te rcob ili n oge n Oec re ased Norma l Inc raased
caroten aemia

V IRAL HEPATITIS
CAUSES
CAUSES
Pre-h epa tic
1. Haemolysis 1. Hepatitis A - an ent erovir us spread by t he oral-faecal rout e.
2. Ineffective eryth ro po iesis Does not cau se chronic he patiti s
I Ga stroenterology
2. Hepatitis B (Au stralia Ag ) - spread by blood or sexual
intercourse. Worse prog nosis if superinfected w ith hepatiti s D 7. Haematology
3. Hepatitis C - spread by blood or sexua l intercourse
4. Hepatitis E - spread by the oral- faeca l rout e. Dangerou s in
p regnancy
5. Cytomegalovir us
6. Infectious m o nonucleosis

COMPLICATIONS OF GALLSTONES
ANAEMIA (HB < 13 .5 GJDL IN MALES. < 11.5 GJDL IN
COMMON FEMALES)
1. Bi liary coli c CAUSES OF ANAEM IA
2. Cho lecy stitis or cholangitis
3. Ob struct ed neck of gallbladder De fi c ie nt RBe p roduction
4. Pancreatitis 1. Def iciency of:
(i ) Fe
(ii ) 8' 2 or fo lic acid
RA RE (iii ) Vitam in C
1. Ga llstone ileus (iv ) Prot ein
2. Ga ll bladder perforati on 2. Aplast ic anaemia (po 79)
3. Ga ll bladder ca ncer 3. Ma rrow infiltratio n:
(i) Leukaemia
Ii i) Lymphoma, e.g. Ho dgki n's
CAUSES OF ACUTE PANCREATITIS (i ii) Myeloma
1. Bil iary tract disease, including gallstones (iv) Myelosclerosis
2. Alcohol (v) Metastatic carci no m a
3. Idiopathic 4. 'Sympt omatic' (anaem ia of chron ic disease)
4. Met abolic. e.g . hyperp arath yroidism. hyperca lcaem ia (i) Ch ron ic infect ion
5. Trauma. includ ing surgery (i i) U raemia
6. Vi ral. e.g. m u m ps (iii ) Liver disease
(iv) Hypothy roidism
(v) Hypopituitar ism
CAUSES OF CHRONIC PANCREATITIS (vi) Malignancy
1. A lcohol ism (vii) Col lagen-vascu lar d isease, e.g. Sl E. r heu matoid disease
2. Mal nutrition Loss or destruc t ion o f RBCs
3. Cystic fi brosis
1. Haemorrhage
4. Fami lial
2. Haemolysis (p. 77)
3. Hype rsplen ism

SOME RBC ABNORMALITIES SEEN IN A BLOOD FILM

SIZE
Anis ocytosis
Va riation i n size, due t o anaemia

Macrocytosis
Seen in a f ilm as increased diam eter of RBCs, b ut defi ned as an
increase in mea n corpuscu lar volume
_ I HHem at o l o gy Haematology I
Microcytosis CAUSES OF HAEMOLYTIC ANAEMIA
Defi ned as a d ecrease i n mean corpu scular volume
CONGEN ITAL
1 . Spherocytosi s ('acho l uric jaundice')
SHAPE
2. Haemogl obinopathy:
Poikilocytosis
(i) S ickle-cel l anaemia
Variation in shape, due to anaem ia which is usually severe
(ii) Tha lassaem ia syndromes
Sphe rocyto s i s
Spheroidal cells seen i n heredit ary sphe rocytosis and in acqu ired 3 . M etabol ic defec t (enzyme def ects. e.g. G6PD deficiency)
haemolyt ic anaem ia

Elliptocytos is ACOU IRED

Ell iptica l cell s. Hereditary. Haemoly tic anaemia mayor may not 1. Autoimmune hae molysi n s:
occur (i) Id iopath ic warm or cold antibodies
(ii ) Viral or mycop lasmal i nfection
S ickling
Crescentic ce ll s seen whe n red ucing agent s act o n Hb-S. 2 . Secondary (symptomatic):
He red ita ry. 0) Chron ic lymphocyt ic leukaem ia
( ii) Ma lign ant lym p homa
Biza rre s h ap es (iii) SlE
Seen in severe u raem ia and ca rcin o m atosis (iv) M alaria
(v) Uncommon ly:
STAINING Rena l d isease
Liver d isease
Hypoc hro m ia Carcinom a
Decreased i nt ensity of stain, due to Fe deficiency Rheumatoid disease
TB or syphi lis
Polychromasia
Diffuse basophil ia. Indica tes active b lood regeneration, j ust as 3 . Drugs and c h e micals, e.g. lead, met hyld opa, dapsone
ret icu locytosis does
4 . Haemolytic disease of the n ewborn , transfu s ion
Punc t a t e basoph ili a r e ac tions
St ippled appea rance seen in severe a naemia or lead poisoning
5. Mechanical , e.g. cardiac bypass surgery
Target cells (Mexica n h at c ells )
Occur in: 6. Microangiopathic:
(i) Fe deficiency (i) Thrombotic throm bocyt open ic purp ura
(ii) Liver disease (ii ) Haem o lyti c u raem ic synd rome
(iii) After splenect omy (iii) Dissem i nated i nt ravascular coag ulation
(iv) Inherited Hb defect, e.g . tha lassa emia m ajo r
7 . Paroxysmal nocturnal h aemog l obinuria
CAUS ES OF MICROCYTIC HYPOCHR OM IC ANAEM IA
8 . March haemoglobinuria
1. Iron deficiency
2. T ha lassaem ia
3. lead poisoni ng
4. Some sideroblastic anaemias
MACROCYTIC ANAEMIA
5. Some anaemias of ch ronic d isease Folate comes from Fol iage O r L iver
_ I Haem atolo9Y H aematology I
CAUSES OF FOLIC ACI D DEFICIENCY LEUKOPENIA
1. Diet ary deficiency or malabsor ption CAUS ES OF PANCYTOPENIA
2. Pregn ancy
3. Increased cel l turnover, e.g. leukaem ia or lymphoma 1. A plastic anaemia (q.v.)
4. Anti-folate drugs, e.g. a nticonvulsants, methotrexate 2. Acute leukaem ia (in subleukaem ic phase) and some
m yelodysplasias
8 12 is produced by B act eria in ani mals 3. Marrow infi lt ration:
(i) Ma lignant lymphoma
OJ) Metastat ic carcinoma
CAUSES OF VITAMIN B12 DEFICIE NCY (iii) Myelomatosis
(iv) Myelosclerosis (in late stages)
1. Pern icious anaem ia or gastrectomy 4. Hypersplen ism
2. Changed intestina l f lo ra. e.g. bl ind-loop syndrome 5. Pern icious anaem ia
3. Ilea l disease, e.g. Crohn's 6. SLE
4. Fish t ape-worm (Di phylloboth ri um latum) uti lizes avai lable B12 7. Rarely, disseminat ed TB
5. Vegan di et

CAUSES OF NE UTRO PENIA SEVERE ENO UGH TO CAUSE

OT HER CAUSES OF MAC ROCYTOS IS SYMPTOMS (AGRAN ULOCYTOS IS)
,. Alco holism 1. Aplast ic anaem ia
2. Liver disease (i) Idiopat hic
3. Myxoedema (ii) Drugs, e.g.
4. Post-haemor rhage (reti cu locytes are la rge) cytotoxic drugs
5. Mye lodyspl asia p henylbutazone
6. Aplast ic anaem ia ch loramphenicol
7. Cytotox ic d rugs, esp. hyd roxy urea (ii i) Chemica ls, e.g. benzene
8. Pregnancy (iv ) Rad iation
2. Selective drug-induced neutropenia (norm al Hb and p latelets)
e.g. thio uraci l
3. Acute leukaemia (in subleukaemic phase)
CLINICAL FEATURES OF ADDISONIAN PERNICIOUS
4. Hypersplen ism
ANAEMIA
5. Id iopathic (rare)
1. Usually over 30, may have blue eyes, fai r hair, prematu re
greying
2. Anaem ia of ins idious o nset LEUKOCYTOSIS
3. Glossitis, often intermittent CAUSES OF NEUT ROPHI L LEUKOCYTOSIS
4. GI symptoms, e.g. dyspepsia, diarrhoea
5. Subac ut e combined d egene rat ion of sp inal cord 1. Bacteria l inf ecti ons
0) Periphe ral neu ropat hy 2. Myeloprolif erative disease:
I ii) Dorso-Iat era l co lum n involvemen t Myelo id leu kaemia
(iii) Mental changes ('mega lob lastic mad ness') Mye loscle rosis
(iv) Rare ly o ptic atrophy, nystagm us, im potence. etc. Po lycyt haem ia vera
3. Haemo rrhage, especially interna l
N.B. May be mixed uppe r m o tor neurone and lower motor 4. Tissue damage:
neu ro ne signs Trauma (inclu d ing surgery)
6. M ild pyrexia Bu rns
7. Slig ht hepatosp le nomegaly Myocard ial infa rction
8. Ret ina l haemorrhage 5. Ma ligna ncy, especially necrotic tumours and hepat ic
9. Increased incidence of Ca st omac h met ast ases
_ I Haem at o lo g y Hilematol09Y I
6. Drugs, especially steroids CLINICAL FEATURES OF PO LYCYTHAEM IA RU BRA VERA
7 . Collagen vascula r d isease, e.g. Still's juveni le ch ro n ic arthritis
1. Headache, d izzi ness and lassitude
2. Plethoric ap pea rance; engorged conjuncti val and retinal
CAUSES OF EOSINOPHILIA vessels
3. Hypert ensio n
1 . Alle rg y 4. Splenomega ly
Hypersensitivity to food or drug s 5. Genera lized pru ritus
6. Dyspepsia d ue t o GI vessel enlargem ent, or associated peptic
2 . Pa rasites u lcer
e.g. trichin iasis, hydatid, hookworm 7. T h rom bosis, e.g. cerebral. corona ry or mesenteric
8. Haemo rrhag ic tendency
3 . Skin disease 9. Periphe ral isch aemia due to slow ci rculation o r th rombosis
0) Scabies 10 . Gout
Oi) Atopy (eczema, u rticaria, hay feve r, asthma )
(iii) Dermatit is herpetiform is
SPLENOMEGALY
4 . M a ligna ncy
Especia lly Hodgkin's disease CAUSES OF MA SSIVE SPLE NOM EGALY
1. M ye lofib ros is
5. Hypereosi n ophi lic syndromes (pu lmon ary eosinoph il ia) 2. I diopath ic t ro pica l splenomegal y
A range of disease charact erized by radiographic pu lmonary 3. C h ron ic mye loid leu kaemia
infiltrates, eosinoph il ia, and va ry ing deg rees of asth ma and 4. K ala-aza r
vascu litis. e.g. Loeff ler's d isease and the pul monary form of 5. Schistosomias is
polyarteritis nodosa Mnemonic: M ICKS

POLYCYTHAEMIA
CAUSES OF MODERATE SPLENOMEGALY
CAUSES
All the causes o f massive splenomegaly p lus:
Prima ry 1. B lood d yscrasias, e.g. leukaemia, haem o lysis, polycythsem ia
Po tycythaemia rubra vera r ub rs vera
2. Lym p homa
S econda ry 3. I nfections, especially infectious mononucleosis, septicaemia,
1. Hypoxia bact erial endoca rd itis and malari a
Ii) High altitude 4. P o rta l hypert ension
(ii) Cya notic heart disease 5. Storage diseases, e.g. Gaucher's
(iii) Pu lmonary disease Mnemonic: BU PS
(iv) Obesit y
2. Conge nita l abnormalities of haemog lobi n w ith an abno rma l
affi nity for o xygen
CAU SES OF M ILD SPLENO M EGALY
3. Inc reased erYthropoieti n
(i) Heavy cigarette smo king All t he above pl us:
(ii ) Kidney cyst, neoplasm or hy d ro neph ro sis C o ll ag en- vasc ular d isease
(iii ) liver carci noma Hy pe rthyroidis m (rarely)
(iv ) Cerebel lar haemangiob last oma A my loidosis
(v ) Massive uterine fib roma Rheumatoid d isease
4. Ae lat ive polycythaemia M any system ic inf ect ions, TB, br ucellosis, etc.
(i) Dehy drat ion Sa rcoidos is
(ii) Stress Mnemonic: CHARMS
_ I Haem ato logy Ha em atology I
LYMPHADENOPATHY CLINICAL FEAT URES OF THE 3 COMMON
LEUKAEM IAS
CAUSES
Anaemia, constit utiona l symptoms (feve r, ma laise, weig ht loss)
1 . Infect ions and bleed ing (includ ing pu rp ura ) occu r i n all 3 ty pes but are more
(i) Foca l infect ion with regiona l lymphadenopathy, e.g.
severe in acute leu kaem ia and less severe in chron ic lymphocyt ic
sepsis, T8, p rimary chancre
leukaemi a
(i i) HIV, e .g . pe rs istent genera lized lymphadenopa t hy
(iii) Inf ect ious mo nonucleosis
(iv) Ru bella ACUTE MYELOID LEUKAEMIA
(v) Secondary syphilis
1. Occurs at any age
(vi) Toxoplasmosis
2. Onset may be abrupt o r insid ious
(vii) Tropica l inf estation, e.g . filariasis
3. Stomat it is and pharyngit is
4. Suscept i bility to infections, especia lly of upper resp iratory tract
2 . Lymphoma 5. Slig ht lymphadenopathy (but more common i n Al l)
(i) Hodgkin's
6. Slight or moderate liver and spleen ~n l argement
(iil Non-Hodgkin's
7. Bone and joint pa i n, w it h sternal t enderness
8. Gum hypertro phy
3. Leukaemia
Usua ll y lym p hocytic (e l l or ALl)
CHR ON IC MYELOID LE UKAE MIA (a ssoc iated w it h
4 . M a lignancy Philade lphia c h romosome)
(i) Metastases 1. Occu rs in middle age
(ii) Reactive changes
2. Insidious onset
3. Massive splenomegaly
5 . M iscella neous 4. Slight lymphadenopathy
ti l Sarcoidosis 5. Moderate hepatomegaly
(ii) Langerhans cell h ist iocytosis (f ormerty cal led
histiocytosis Xl
(i ii) Ch ron ic inflammatory skin disease CHRONIC LYMPHOCYTIC LEUKAEM IA
(iv) Collagen- vascu lar d isease, e.g. RA, SlE
,. Occu rs i n lat e m idd le age, mo re often in males
(v) Anticonvu lsant drugs
2. Insid ious onset often fo und acc identa lly
3. Moderate or marked lymphadenopathy, usually symmetrical
CLINICAL FEATURES OF HODGKIN'S DISEASE 4. Recurrent ch ronic inf ect io ns
5. Moderate liver and spleen enlargement
1,
Weight loss, malaise, lassitude, n ight sweats
6. May be haemolytic anaem ia
Fever (the period ic Pel- Ebstein pattern is uncommon)
2.
7. Ski n lesions:
3.
l arge, discret e, rubbery, asymmetrical superficia l lymph nodes
(i) Pr uritus
Med iast ina l or ret roperitoneal node involvement
4.
(ii) Herpes zoster
5.
Hepatosplenomegaly
(ii i) Nodula r inf i lt rates
Pulmonary o r pleu ral infilt ration
6. (iv) Eryt hroderma (I'homme rouge)
7.
Pain o r pa ralysis due to p ressure on nerves or spina l cord
8.
Ma rrow i nfi lt ration wit h pain o r pat holog ica l fra ctu re
9.
Skin: CLINICAL FEATURES OF MULTIPLE MYELOMA
Pruritus
Pigmentat ion 1. Progressive anaemia
Herpes zoster 2. Bone pai n:
Nod ular i nf ilt rates til Ost eoly t iC lesions
10 . Infect ions due to decreased cell mediated immunity (ii) Pat ho log ical fraclU res
11 . A lcohol-i nduced pain (i ii) Ost eomalacia (due to renal phosp hate leak)
- Ha ematology

3. Bleed ing, due t o thrombocyto penia

4. Fever
5. Renal inv olve m ent:
3. Anticoag ulant d rugs
Haematology

4. Dissem inated int ravasc ular coagu lat ion (consumptio n

coagulo pathy)
I

0) acute o r chron ic uraem ia 5. Massive transfu sio n o f st o red blood

(ii) Fancon i syndro m e
6. Hepat omegal y, occasio nally w ith jaundice
7 . Hyperca lcaem ia w ith no rma l alka line phosphat ase
8. Hyperu ricaem ia
9. Am y lo id os is
10. Neu ropath y, w ith rai sed CS F prot ei n _ ..
11, S uscepti bil ity to infections, due to d e fective antibodies
12. Hyperviscos it y syndrome (occasio nally)
6. Ci rcu lat ing inh i bit o rs of coa g ulatio n
DISSEMINATED INTRAVASCULAR COAGULATION
T his is cha racterized by excessive formu latio n of fib rino gen
d er iva tives, usually due to increa sed p ro teolysis. T here may be
b leed i ng o r thrombosis of any sev erity

BLEEDING CA USES
May be due t o defect s o f p lat elet s, coagulatio n o r vessels 1. 'Shock', esp. G ram-neg . septicaem ia and anaphy laxis
2. Other i nf ections, e.g. T8, vira l and funga l
3. Obst etric
PLATELETS Prematu re p lacental separatio n
CAUSES OF TH RO M BOCYTOPEN IA Ret enti on of d ead f etus
Amn iotic embo li sm
1. Idio pat hic t hrombocyto penic purpu ra (autoim mune) Fetal death du e t o Rh i ncompati bil ity
2. Causes of pancytopenia (p. 79 ) 4. Major surgery, especially w ith extra -co r po real shu nt s
3. Drugs, e .g . salicylates. he pa rin 5. Incom patible blood transfusi o n
4. Incom patible or m assive blood transfusio ns 6. M iscellaneous
5. Dissem i nated i ntravascular coag ulatio n Leukaemia o r carcinom atosis
6. M assiv e haemorr hag e Liver, renal o r p rostatic disease
N.B. In th rombocytopen ia, bl eedi ng ti me and ca pi lla ry fr agi lity Pu lm o na ry em bo lism
a re i nc reased, but coagul ati o n ti me is no rmal
CAUSES OF BLEEDING DUE TO SMALL VESSEL
COAGULATION DEFECTS
Vi t amin K deficie ncy affect s coagulatio n factors II, VII , IX and X. CO NGENITAL
1. Heredit ary haem o r r hag ic telangiect asia (Osler- Weber- Rendu )
COAGULATION DISORDERS 2. Pseud o-xanthoma elasticum
CONGE NITAL 3. Eh le rs- Danlos d isease
Haemophi l ias
1. Haem o phi lia A (V III deficiency) ACQUIRED
2. Haemo p hili a B (IX defi ciency, Christm as d isease)
3. vo n Wille b ra nd 's d isease 1 . Infec tio n
(i ) Septicaem ia, especially meni ng ococcal
Other cong enita l d e fi c i e n cies (i i ) Bacte rial endoca rd itis
Fact o rs I, II, V, VII , X, XI, XII o r Xlii
2 . Drugs, e.g . co rticost ero ids
ACQUI RED 3 . Secondary to systemic disease ('symptom atic' )
1. Vitam in K d eficiency (i) Cushing's
2. liver d isease (ii) Scu rvy
_ I HS8matoio gy Haematology I
4 . Vas culitis COMPLICATIONS OF BLOOD TRANSFUSION
(i) Henoch-Schonlei n purpura
(ii) Cutaneous vasculitis 1 . Fe brile rea c tions
(iii) Polyarterit is nodosa (i) Pyrogens
(i i) Leukocyte or p latelet iso-agg lutinins
(iii) Hypersensitivity t o p lasma
2 . Alle rgic rea ctions
5. Mi s ce lla neous 3 . C irc ulatory overload
(i) Simple easy bru ising 4 . Haemolysis. Red cells of either donor or recipient may be
( ii) Seni le purpura affected
(i i i ) De rmatoses, e.g. eczema (i) Blood g rou p incompat ibi lity
(iv) Fat embol ism (iii Improper o r over long storage of donor blood
5 . Re action due to infe c t ed store d blood
6 . Dise a se t ransmiss ion
(i) Vi ral hepatitis, HIV (A IDS vi r us!, cytomegalovir us,
SCREENING TESTS FOR A BLEEOING DISORDER Epstein- Barr virus
(ii) Syp hil is
1. Bloo d count a nd film (i ii) Ma lari a, t oxoplasmosis
To det ect leukaem ia and assess p late let n um be r, size and shape
(iv) Brucellosis
2. Bleeding time (w ith Duke's m ethod, norma l < 7 m ini 7 . Thrombophlebitis
Usefu l in diagnosis of vo n W ille brand 's d isease
8 . Air embolism
Also prolonged by asp irin 9 . Imm u nological sensitization by previous tra nsfus ion,
3 . He ss t est , w it h sphygmomanometer cuff at c. 100 mmHg for 5 especia ll y Rhesus sensit ization
min (N < 5 petechiae in a ci rc le of 3 em d iameter) 10. Transfusion side rosi s
4. Prothro m bin time IN 12- 15 sec) 11 . Complications of massive tra nsfus ion
Tests the extri nsic system (i) Collapse d ue to cold blood
Prolonged by warfari n (i i) Excess cit rate (exaggera tes bleeding tendency)
5 . A c tivat e d p a rtial throm boplastin time (APIT) IN 30-45 sec) (iii) Excess ammonia fro m stored blood (exaggerates
Tests the intrinsic system (especially VIII and IX) precoma in ci rrhotics)
Prolonged by h epari n (iv) Excess potassium (exag gerates hyperkalaem ia in
6 . Thrombin time (N 10-20 sec) uraemic patient s)
Pro longed i n (v) Th rombocytopenia
iii Fib rino g en d eficiency
(ii) Presence o f some inhib ito rs, e.g. heparin
7 . Ass ays for c o a gulat i on factor deficiency (e.g. fa ct o r VII) CONDITIONS PREDISPOSING TO VENOUS
8 . Fibri n d e gradation produc ts THROMBOSIS
Increased in fib ri nolysis (e.g. d issem i nated intravascu lar A. LOCALIZED
coagu lation)
1. Stasis (tight bandages, sen ility, imm o b ility, etc.)
2. Damaged vesse l wall
(i) Infecti on
Clinica l f eat u res of b l eeding disorders (ii) Atheroma
C l ini ca l f eetu re Coag ul ati o n d i sorde r P latel et d isord er (i ii) Trau m a (i nc. fractu re an d pelvic s urge ry)
Purpura Rare Commo n
Bru l .e. Sing le, deop Multiple, superficial B. GE NERALIZED
Bleedi ng .ite. Joints, muscles Mucous mem branes
S upe rf icial c u te Blc-cding stops Bleed ing prolonged 1. Thrombocyt os is and po lycythaemia
D ....p c ute Bleeding con t inues Bl eed ing stops w ith 2. Prolonged bed rest
despite pressure pressu re 3. Pregnancy and puerperium
Hea ling of c u t . DelaVod Norma l 4. Ora l contracept ives
_ I Hae ma t ology
5. Hyperviscosity o f blood (dysprotei naemia o r polycythaem ia)
6. l ow levels o f anti th ro mbin II I, p rotei n C o r protein S
8. Neurology
7. Cardio li pin anti body (lu pus anticoagulant )
8. Facto r V (l e ide n)
9. Sickle-cell d isorders
10. Malig na ncy
11. Nephrotic syndrome
12. Dehydration
THE SENSORY SYSTEM

A
c •

M idline

(AI Pro prioception, vi bratio n a nd h a lf o f t ouch fibre s t rave l

v ia posterior nerve roots up the poste rior co lumn w it hout relaying
in th e cord. They re lay in the medu lla (nuc lei gracilis and cuneatus)
and cross the m id l ine to continue as the media l lem niscus to the
tha lamus. Tertia ry f ib res t ravel v ia the posterior lim b of the
internal capsu le t o the sensory cortex (post-centra l gyrus)
- N e u r o l og y

Mnemonic: PROVOST
PRO priocept io n , V ibration and S oft T ouch in the POSTerior
column
N e uro l ogy

IA ) In the lower medu ll a the majority of f ibres decussate and

descend in t he lateral corticospi nallcrossed pyramida l) t racts
(8) Some f ib res do not decussate, b ut descend in t he anterior
I_

IB} P ai n a nd t e mpe ra ture fibres rela y in the cord, cross the
m id line imm ediatelv a nd t ravel in the lateral s pinot halamic Iract to
the tha lamus
Mnemonic: PATE L
PAin and TEm p in the Late ral spi nothalamic t ra ct
le i Rem a inde r of t o u c h fibres relay and cross t h e midl ine in
t he cord and t ravel i n t he anterior spinothalamic t ract t o the
t ha lam us
Mnemonic: TOAST
TOuch in the A nterior Spinothalamic Tract
THE MOTOR SYSTEM
corticospinal t ract, and then c ross in the anterio r commissu re of
t he cord to sup ply muscles i n t he neck
Ie) A f ew fibres d escend d irectl y in t he lateral corticospinal
t ract w it h t he crossed f ibres f rom the contralateral corte x
Most f ibres relay w it h internuncial cells in t he cord, and the
anterior horn cells and t heir f ib res t hen f o rm t he ' f ina l common
pathw ay' to the m otor end-plates in the muscle. The o rgan iza t ion
o f movement is much more complex t han t his diagram suggests,
since impu lses are mod ified by t he cerebellum, the extrapyra m idal
system and p roprioceptive and other sensatio ns
Mnemonic: MO LAC
M Otor i n Late ral, A nter ior an d C ont ralate ral tracts

SIGNS OF A LOWER M OTOR NEU RONE LESION

1. Wea kness an d was t ing
2. Hypoton icity
3. Decreased reflexes
4. Fascicu latio n

SIGNS OF AN UPPER MOTOR NEURON E LES ION

1. Weakness
2. Spasticity
3. Increased tendon reflexes, somet imes w it h clo nus
4. Extensor planta r response
\ .f---- .....,. N.B. In py ram ida llUM N) lesions, t he extensors are weake r than
t he f lexors in the ar ms, but t he reverse is t rue in the legs, t hus
account ing for the 'spastic' postu re

CRANIAL NERVE SUPPLY

1 . Olfactory_ Smell
2. Optic . Vision
3. Oc ulomotor
(i) All ocu lar muscles, except supe rio r ob lique and lateral
rectus
(ii) Ci liary muscle
(iii) Sph incter pupi ll ae
•
motor unit
(iv) Levator p al pebrae supe rioris
4. Troc h l ear. Superior oblique mu sc le
N.B. Tested by aski ng patient to loo k down and inwards
Fib res pass downwards from the mot or cortex (p re-centra l gyru s) 5 . Trig eminal
into the posterior limb o f the intern al capsu le. In t he pons the (i ) Sensory for fa ce, cornea, sin uses, nasa l mucosa, teeth ,
fi bres are scat tered , but the y regrou p on the upper medulla t o tympa nic membrane and anterior two-thirds o f t o ng ue
f o rm protubera nces called the pyramids (ii) Mot o r t o m u scles of mastication
,--- -

IIIIIIIIIII LI_N_._U_'_O_'O_gcV~__________________________________________--, Neurol ogy I _

6 . Abduc ens. lateral rect us muscte 1 , Conc entric diminuti on I' tunne l visi o n')
7 . Facia l
(i) Motor t o scal p and facial muscl es of ex p ressio n

o
L R
( ii) Tast e in anterio r two-th irds of tongue (v ia cho rda
tympani)
(i ii) Nerve t o stapedi us muscle
8 . Auditory. A uditory and vesti bu lar component s
9 . Glos sopharyngeal Ch ron ic g laucoma, reti nit is pigmentosa
( i) Sensory fo r poster io r o ne-t h ird of t o ng ue, pha rynx an d Chron ic papi ll oedema can occasional ly cause i rregu lar loss of
m iddle ea r peripheral visual f ield s
(ii) Taste f ibres fo r poster io r o ne-t hird of t o ngue In acute pap illoed ema t here is usually no field defect, t ho ugh
(i ii) Motor 10 m idd le constrictor of pharynx and t he bli nd spot may be en larged.
stylopharyngeus 2 _ Central scoto m a
10. Vagal
0) Mot or to soft palate, larynx and pha rynx (from nuc leus
am b ig uus)
(i i ) Senso ry and mot o r f o r hea rt, respiratory passages an d
abdomi nal visce ra (from dorsal nu cleus) Reti na l d isease involv ing mac ula, ret robul ba r neuritis
11 . Spina l a c ces s ory 3 . Co mplete fi e ld l o ss i n o ne eye
(i)Moto r t o st ernomasto id and t rapezi us
Accessory f ib res to vagus
(i i)
12 . Hypo glossal . Motor 10 l o ng ue and hyoid bone de pressors

CRAN IAL NERVE NUCLE I Optic nerve lesio n (i.e. anter ior to chi asma)
4 . Bitemporal h e mia n o p i a
M id -brain 3,4
Pons 5,6,7,8
Medu lla 9, 10, 11. 12

OPTIC PATHWAY AND PATTERNS OF VISUAL FIELD Pit u ita ry tumour (i.e. al the chiasma)
LOSS 5 . Homonymous h e m ian o pia

Tract lesions posterior to ch iasma

Oplio::: nerve 3 6 . Oua drantie h e mia n o pia
______ 0pIic chiasma 4

- - - Optic tract 5

Tempo ral lobe t umours for supe rio r q uad rant

Lateral Parieta l lobe tumours for inferior quadra nt
genicu late body
7 . Homonymous h e m ianopia with m acula r sparin g
Optjc radiations
7

Occipital pole l esio ns of t he v isual cort ex

_ 1 N eu r o logv L-____________________________________________N
_._ U
_ '_O
_'_o__
g ,~1 IIIIIIII
CAUSES OF OPTIC ATROPHY SQUINTS
, . G lau c oma CONCOM ITANT SQUINT
2. Re t ina l lesions Due to a defect i n the sensory component of the reflex arc (such
Cho ro ido-retin itis
as poor v ision) or a cen tral d isturbance. T he angle of devi ation
Intra-ocu lar ha emo rrhage, etc.
between the eyes rema ins co nstant when looking i n d iffe rent
3. Optic n e uritis (ret robulbar neu ri t is) (q .v.l
directio ns. Th is occurs in all neonat es and often i n chi ldh ood
4 . Ch ro n ic p a pilloed e m a
f ollowing i ll ness
5 . Press ure on optic n e rve
Tumou r Features
Aneurysm 1. Both eyes have fu ll movement if tested separate ly
Paget's disease 2. No d i plopia
6. D iv ision o f optic ne rve
Su rgery
Trauma PA RALYTIC SQUINT
Due to lesio ns of 3rd, 4th o r 6th cranial ne rves. Usua lly causes
d i plopia
CAUSES OF OPTIC NEURITIS
Features
1 . Isch ae mia 1. 'False' image is alw ays peripheral
8.g. temporal arter itis 2. 'False' imag e is seen by affected eye
2. Demye linating d isease 3. Separat ion o f images is maximal w hen looki ng in d i rection of
e .g. mu ltiple scle rosis
action of affected m uscle
3 . Infective
e.g. ret in itis, men ing iti S
4. To x in s 3RD CRAN IA L NERVE (OCULOMOTO R) PA LSY
e.g. methyl alcoho l 1. Marked ptosis
5 . M e t abolic 2. Eye abducted and depressed ('down and out')
e.g. diabetes m ellitus, B12 deficiency 3. Pupil dilated and co mpletely non-reactive
More often partial than co mplet e, especi ally with lesio ns near
FEATURES OF DIABETIC RETINOPATHY the nucleus

1. Bac k g ro und re tino p a thy Causes o f o culomo tor p alsy

M icroa neu rysms leak, producing 'd ot and b lot' h aemorr hages 1. Aneurysm o f posterior communica ting artery
and, some years later, hard exudates 2. Tumou rs
2. Pre -p roliferative re tinopathy 3. Brai n-stem eVA
Soft ex udat es (cotton-wool spots ) appea r. These are deep
reti na l infarcts. Venous dilatati o n an d bleeding occurs CERVICAL SYMPATHETIC PARALYS IS (HORNER'S)
3 . Pro l i f erative r e tino p athy
Extensive new vessel form ation w hich can lead t o vi treous 1. M ild pt osis
haemo rrh age, reti nal detachment, neov ascu lar glaucoma, etc. 2. Pupil c onstrict e d w ith no reaction to shad ing
3. Red uced sweati ng o n ipsi lateral ha lf of head and nec k
4. Abo lit ion of cil iospina l reflex
FEATURES OF HYPERTENSIVE RETINOPATHY
N.B. Everyth ing gets 'sma ll er'
Grade 1. Silv er-w i ring of arteries
Grade 2. Arteriovenous ni pping Ca u ses of Horne r 's syndrome
Grade 3. Fla me-shaped haemorr hages, exudat es and cotton-wool 1. Carcinoma of ap ical bronchus (Pancoast's tumou r)
spots 2. Cervical sym pathect omy
Grade 4. As Grade 3, but w ith pa p ill oedem a 3. Ao rtic aneurysm
_ I N e u ro logy Neuro logy I_
4. Syr ingobulbia or syringomyel ia CAUSES OF FACIAL PARALYSIS
5. Brachial plexu s lesions (e.g . Klumpke 's paralysis)
1. SU PRAN UCLEAR LESIONS
CAUSES OF PTOSIS e.g. cerebrovascular accident affect ing i nternal capsule

1. Congenital
2. Ocu lomoto r palsy 2. N UCLEAR LESIONS
3. Cervical sym pathetic lesion
4. Myasthenia g ravis e.g. pontine neoplasm , polio
5. Myopathy (e.g. dyst rophia myot on ica)

3. INFRANU CLEA R LE SIONS

PAPILLOEDEMA
(i) Ce rebell a-pont ine ang le and internal aud itory cana l, e.g .
SIGNS OF PAPILLOEDEMA aco ust ic neu roma, men ing ioma
1. Engorged ret inal ve ins (ii) Facial cana l, e.g. Bell's pa lsy, trauma, sarcoidosis
2. Pi nk d isc w it h blu rred ma rg in (i ii) Ext ra-cranial, e.g. t ra u ma, parot id neop lasm
3 . Loss of 'c up pi ng'
In uppe r mot o r neurone f acia l palsy t he fo rehead move m ents
4. Cribrosa not v isible are reta ined (due t o b ilateral co rt ica l rep resent ation )
5. Flame-shaped haemo rrhages

CO M MO N CAUSES OF PAPILLOEDEMA
DEAFNESS
1. Accelerated phase hypertension
2. Raised intracran ial press ure (q.v.l CAUS ES OF DEAFNESS
3. Re t inal venous o bst r uctio n A . Con duc tion deafn ess
Papill itis (ret robu lbar neurit is) is usually d ue to d isseminated " Wax o r foreign body
2. Eust achian obst ru ct ion (esp. 'g lue ear')
sclerosis. It is d ist inguished by t he ear ly severe loss o f v isual
ac u ity. There may be no fu ndal abnorm ality (Le. 'pal ient sees 3. Ot it is media
4. Otosclerosis
not hi ng, d oct o r sees not h ing')
5. Paget's d isease
Ca u ses o f rai s e d intra c ra n ial pressu re
1. Int rac ranial mass o r i nfect ion B. Nerve d e a fn ess
2. Obstr ucted CSF fl ow 1. Trau matic:
3. Hypertensive encephalo pathy m Chronic exposu re 10 loud noise
4. Hypercapnia (C0 2 retention) (ii) Fract u re of pelrous temporal bone
5. Ben ig n i ntrac ran ial hypertension (pse udo-t umou r cerebri ) 2. Infect ive:
(i) Th rom bos is of intracran ial venous sinuses (i) Con genit al syphi l is
(ii) Many rare causes, e.g. o ral contrace pt ives, retino ids o r I ii) Rubell a synd rome
vitam in A poison i ng (i ii ) MU m ps, infl uenza
3. Toxic:
(i) Aspi rin . qu inine
CAUSES OF SUDDEN BLINDNESS
(i i) A nt ibiot ics e .g . strept omycin. neomyci n
1. Ret ina l det achment (ii i) To bacco, alcoho l
2. Acu t e g laucoma 4. Degene rat ive :
3. Vitreous haemorrhage (esp. di abetes) Presbyacusis
4. Te m po ral arterit is 5. Tumou r, e.g. acoust ic ne u roma
5. Ret inal artery or vein occlusion 6. Brain-stem lesions (ra rely)
6. M ig raine (t ransient) 7. Ra re fam ilia l syndromes
_ I N e urology N e u ro logy I
RINNE' S TEST Acoustic ne uro ma
Pit u it ary t umou r
The abi lity to hea r a t u ni ng f o rk t hro u g h air and th rou g h t he
m ast o id p rocess are compared . In normal people and in n erve
d eaf ness t he ai r cond ucted sound is loud er, whereas in CLIN ICAL FEATURES OF INTRACRAN IAL NEOPLASM
cond uction d eafness it is softer 1. Raised int racranial pressu re
(i ) Headac he, worse o n st raini ng and on w aki ng
WEB ER' S TE ST (ii ) Drowsi ness
(i i i) Bradycardia and hy pertensio n
T he base o f th e fo rk is placed o n t he ce nt re of t he fo rehead; in (iv) Vomi t ing
nerve deafn ess the note is hea rd in t he normal ear, whe reas in (v) Papill oedema
conduction deafness it is heard in the d eaf ear 2. Pro g ressive loss of neuro log ical fu nction o r f ocal neurological
sig ns (q.v.)
MULTIPLE SCLEROSIS 3. Epilepsy
4. M ental sym pt o ms, e.g. personality ch ange, apathy, dem ent ia
Cha ract erized by mu lt ip le e NS lesions scattered i n t ime and p lace 5. Con ing may occu r, w it h d i lat ed pu pi l an d re spiratory
Lower m otor neu ra nes are not affect ed d ire ct ly depression (may follow bleed i nt o tumou r)

CLI NICAL FEAT URES LOCALIZAT ION OF CORTICA L LES IONS BY FOCAL
1. Spast ic weakness, usual ly st arti ng in legs NEUROLOGICAL SIGNS
2. Re t rob ulbar neurit is: Frontal
M isty vision 1. M e ntal d isturbance
Pai nf u l eye movements (i) Dementia
Slight ly swollen o ptic d isc (ii) Apath y
Cent ral scot o ma (i ii) Inapp rop riate emot ion
(Opt ic atro phy may d evelo p) 2. Epilepsy
3. Nu m bness and para esthesiae 3. G rasp reflex
4. Di plo pia (atax ic nystagm us is ch aracte ristic) 4. U nilate ral anosmia
5. Vertigo
6. Cerebel lar sig ns: Pre·c e ntral
' Scan ni ng' speech 1. J ackson ian ep ile psy
Intentio n t remo r 2. Co nt ralat eral spasti c hem ipleg ia
Nystag m us (may be w o rse in t he abduct ing ey e)
7. Sph incter d ist u rbance and impot ence Pa ri etal
8. Eupho ria o r other m ent al change 1. Sensory d istu rbance, e.g. lack of 2 point discrimi nat ion
9. Painfu l fl exor spasms 2. Visual aphasia
3. Ho m o ny mous hemia nopia or q uad ra ntanop ia (lower)
INTRACRANIAL DISORDERS 4. Apra x ia
5. A stereog nosis
COMMON INTRACRA NIAL NEOPLASMS
Children Temporal
Medu lloblastoma 1. An te rior lesion s - moto r aphasia
Ast rocyt o m a Post er ior lesions - audito ry aphasia
2. Hom onymous hem ianopia or q uadrantanopia (uppe r)
Adults 3. Psychomot or ep ilep sy
Meta stat ic ca ncer
Gl iom a Occipital
Mening ioma Visua l field defects
,

11IIIIIIII 1
L_N
_._u_'_O_'O
_ g_ V
_______________________________________________ N e uro logy I _
SIGNS OF A CEREBELLAR LES ION 2. Lesions of recurrent laryngea l nerve (Ca bronchus, aortic
aneurysm )
1. Intention tremor
3, Vocal cord lesion (infection, tumour, etc.)
2. 'Scanning'speech
3. Nystagmus worse o n looking to the side of the lesion
4. li mb ataxia w ith characte ristic b road-based gait CAUSES OF CEREBRAL INFARCTION
5. Hypotonia and pendular reflexes 1. Atheroma of intra- o r extracranial arteries
2. Cerebral emboli:
(i) Atrial fib rillat ion
CAUSES OF CEREBELLAR DYSF U NCT ION (ii) Myocardial infa rct
1. Mu ltiple sclerosis (iii) Bacterial endoca rd itis
2. Neoplasms (iv) Fat em bo lism
(i) In the cerebell um , e.g . medulloblast oma 3. Cerebral ischaemia d ue to seve re hypot ension
(i i) Para neoplastic neuropathy, e.g . due to bronchia l cance r 4. Cerebral arterial spas m, e.g. mig raine or fo llowi ng
3. Ce rebellar abscess (often seconda ry to otitis media) subarachnoid haemorrhage
4. Vertebrobasi lar i nsufficiency 5. Hypoxia, e.g.
5. Drugs, e.g. alcohol (i ) Ca rd iac arrest
6. Id iopath ic dege ne ration, e.g. p rima ry cerebe ll ar at ro phy (i i ) Ca rb on monox ide po isoni ng
7. Ra re hereditary and fam il ial ataxias, e.g. Fried reich's {iii) Pu lmona ry embo li
6. Arte ritis, e.g. collagen- v ascu lar disease
7. Ce reb ral th ro mbosis, e.g. d ue t o polycythaemia
CLASSIFICATION OF SPEECH DEFECTS 8. Dissecti ng ao rtic aneu rysm invo lving the ca rotid artery
1. Dys phasia (disorde r in use of symbo ls f o r communication 9. Ligatio n of carotid artery fo r intracranial aneurysm
whether spoken, heard, written o r read)
2. Dysarth r ia (d isorde r of articu lation) SUBARACHNOID HAEMORRHAGE
3. Dysphonia (di sord er o f vocalization) (SubARachnoid is ARterial)
4. Dementia (intel lectual deterioration )
COMMON CAUSES
CAUSES OF DYSPHASIA 1. Rupt ured 'ber ry' aneurysm (70%)
1. Exp ressive - due to lesion o f B roca's area (Inferior Frontal 2. Arter iovenous malform ation (10% )
gyrus of domi nant cortex)
Mnemonic: BIF and BROca BROadcasts CLIN ICA L FEATURE S
2. Receptive - due to lesion of WE rnicke's area (S u per ior
1. Often occu rs in m iddle life
T empo ral areas of domi nant cortex)
2. Sudden onset of ca tast rop hic headache, usually occipit al. Often
Mnem onic: WEST
p reci p itated by strai ning . Often 'wa rn ing' headaches in
p revious weeks
CAUSES OF DYSARTHRIA 3. Sma ll leakages - delirium or confusion b ut no loss of
consciousness
1. Bul bar or pseUdo-b ulbar pa lsy Bigger bleeds - vom it ing, convu lsio ns and coma
2. Basa l gangl ia les ions 4. Men ingism
3. Cerebellar lesions 5. Plant ar responses are usually extenso r
4. Weakness o r pa raly sis of facia l m uscles 6. May be slow pu lse, o r hypertension
5. O ra l lesions i nclud ing loose dentures 7. Occasiona lly squint, pap illoedema, ret inal haemo rrh age and
small sluggish pupils . The characteristic subhya lo id
hae morrhage spreads o ut from the edg e of th e disc
CAUSES OF DYS PHONIA
8. May be pa in in back due t o blood in spinal theca
1. Functiona l (hysteria) 9. May be pyrexia
_ I Neuro lo g v N e u rolo gy I _
CHRONIC SUBDURAL HAEMATOMA (i) Hypoglycae m ia
(Ii) Dia betic ketoacidaemia
CAUSE (iii ) Hepatic, renal or adrenal fa ilure
Ruptu re of cortical v eins as they cross th e su bdu ra l space. May be (iv) Myxoedema
tra umati c o r spontaneo us (v) El ect ro lyt e im balance
8. Acu t e CNS infection , e.g. men ing iti s. encephal itis
9. Acu te systemic infection, e.g . se pt icaemia
CLIN ICAL FEATURE S 10. Hysteria, hypnosis
1. Ohen elde rl y pat ie nts, after a trivi al head i nju ry. A lso in infa nts 11. Hypo - o r hyperthermia
o r alcoholics
2. Latent period o f days o r m o nt hs occurs befo re sym p to m s
develop SYNCOPE rBLACK-OUT')
3. Gradual onset of headaches, memory loss, dement ia,
A t ransient loss o f conscio usness caused by cerebral anoxia,
confusio n, d rowsiness and eventual coma. Sympt oms f luct uate
us ually d ue to i nadequate blood f low
from day to day, w ith l ucid inte rva ls
4. May be sig ns of an int racrania l space-occupyi ng lesion, w ith
local izing signs CAUS ES
1. Vasovagal
EXTRADURAL HAEMATOMA (i) Emot ion, heat or standing still
(ExTRAdu ral is ARTerial) (ii) Loss of b lood or p lasma
(ii i) Post ura l hypotension, e.g . drugs or p rolonged
recumbency
CAUSE (iv) Carotid sinu s hypersensiti vity
Fract ure of squam ous t emporal bone w it h rupture of a b ranch of
the m iddle men ingeal artery 2 . Cardiac
(i ) Stokes-Adams (heart block)
(i i) Ventricula r tachyca rd ia or f ibri llation
CLIN ICAL FEATURE S (i ii) Aortic stenosis
1. Any age, b ut oft en you ng adults wi th scal p oedema above the (iv) Cya notic congen it al heart disease (f all i n Po 2 )
.Be (v) Coug h syncope (obst ructed venous return to hea rt )
2. Concussion m ay be followed by recovery of consciousness fo r
mi nutes o r hou rs befo re th e onset o f drowsi ness and 3 . Arte rial occlusion
deepening coma (i) A t heroma or em bo lism (carotid or vertebrobasi lar)
3. Signs of intracran ial compression (p. 99) (i i) Cervical spo ndy lOSis
4. Ipsilateral 3rd nerve palsy due to cerebral herniat ion (ii i) St rangu lation
5. Progressive cont ralateral hemiplegia (iv) 'Subclavian steal syndrom e'
T he signs develo p rapidly and immediate operat ion t o relieve
the p ressu re is mandatory 4 . Anoxaemia
(i) High alt it ude
(ii) Anaemia
CAUSES OF COMA
1. Syncope (q .v.)
2. Head inj ury EPILEPSY
3. Epilepsy Partial seizures (with a sing le cort ica l f ocus) may be eithe r:
4. Drugs or tox ins (especially alcohol or 'overdose') Simple (unim pai red consciousness) or
5. CVA (thrombosis, embolism o r haemorrhage) Complex (i mpaired consciousness)
6. Raised int ra cranial pressure (p. 96)
7. Metabol ic Partial seizu res may progress to become gener ali zed
IIIIIIII IL _N_e_"_'_O_'D
_O_Y
____________________________________________--' Neuro lo gy I
CAUSES OF EPILEPSY B. Extra-crania l
1. Metabol ic (anoxia, hypoglycaemia, liver failure, renal fai lure)
1. IDIDPATHIC 2. Hypo thyroidism
2. FOCAL CEREBRAL LES IONS 3. Vitami n d eficiency (especially B 12 )
4. Drugs (especially barbiturates)
(i) Birt h i njury o r cerebral malformation
5. Toxins, especially alcohol, lead and al umi nium
(ii) Tumou r
(i ii) Tra uma, scar, irradiation, atrophy Depression may cause pseudodementia
(iv) Vascu lar
eVA NEUROLOGICAL MANIFESTATIONS OF AIDS
Hypertensio n
Vasculitis. e.g. SLE 1. FUNCTIONAL
Vascular malformation (e.g. Stu rge-Webe rl
Anxiety, depression, etc., which may lead to suic ide
(v) Infection
Encephali tis or mening itis
Abscess or tuberculoma 2. FO CAL INFECTIO N DR M ENINGITIS
Syphi lis (GPI or gumma) Espec ially w ith opportun istic o rgan ism s:
Hydatid cys ts, cyst ice rcosis or toxop lasmosis (i ) Cry ptococcus (meningitiS)
(iv) Degenerative d isease, e.g. p reseni le dementia (ii) Toxoplasmos is (abscess o r encepha litis)
(iii) Cytomeg alovi rus (encepha litis)
(iv) Progressive mu lt if oca l leucoencepha lopathy (now thou g ht
3. METABDLIC to be due to a vi rus)
(i) Pyrexia in ch ildren
(ii) Anoxia, hypoglycaemia or hypoca lcaem ia 3. PRIMARY HIV IN FECTION
(iii) Electro lyte imba lance, e.g. wate r intox ication
(iv) Uraem ia (i) Acute encephalopathy at tim e of ser oconversion:
(v) Hepat ic coma May be EEG changes and epi lepsy
(ii ) AIDS-dementia complex with parapa resis and
(vi) Drugs and toxi ns
Lead poisoning i ncontinence
Withdrawal of alcohol or barbiturates (iii) Myelopathy due to HIV
'Overdose' (e.g. antidepressant s)
4. OTHER
Cerebral lymphoma, cranial or peripheral neu ropathy, o r
CAUSES OF DEMENTIA
myopathy
PRIM A RY PRE SENILE OR SENILE DE M ENTIA
Id iopathic cerebral atrophy, A lzheimer's, Huntington 's, etc. CAUSES OF PARKINSONISM
1. Idiopath ic (espec ially over 50)
SECONDARY 2. Cereb ral atheroma
3. Drugs (e.g. phenoth iazi nes)
A . Intra · cran ia l 4. Toxins, e.g . manganese, copper, ca rbon mo noxid e, kern ict erus
1. Tumour, especia lly fronta l 5. Traum a (e.g. boxing)
2. Subdu ra l haematoma 6. Post-ence phal itic (encep halitis lethargica outbrea ks occu rred
3. Vascu la r, especially atheroma o r multiple small emboli 19 17- 1925)
4. Infections, e.g. AIDS , encephal itis, neurosyphi lis, 7. Ra re syndromes: Shy-D rager, Wilso n's, Stee le-Rich ardso n
Creutzfe ldt-Jakob
5. Trauma (i nclud ing concuss ion in boxers)
6. M u ltip le sclerosis
CLINICA L FEATURES OF PARK INSONISM
7. Normal pressure hydroce phalus Cha racteristic tremor, rig idity and bradykinesia
__ ILN_._U_'_O_"O~9~YL__________ ______ _ ____---' Neuro logy I _
1. Slowness and poverty o f spo ntaneous movement 9. Involuntary move m e nts
2. Coarse t rem o r (' pili-roi ling') w ith cogwheel rig id it y (j) Choreifo rm - je rky m ovement s of short du ration ,
3. Expressionless. unblinking f ace affecting limbs and face
4. Sh uffling g a it !festinatio n late r) w ith lack of arm -swi nging (ii) Athetoid - slow w ri thing of arm s and leg s w ith flexed
5. Slu rred, m o n otonous speech and sma ll hand w riting fingers, th um b and w ri st
6. Increased sa liv atio n and dribbli ng (ii i) Dystonia muscu/orum (torsion spasm) - intense
7. Oculog yric c ri ses (forced upward d eviatio n of ey es) in drug- susta ined spasm of proxima l and trunk muscles may
induced and post-encephal itic types cause bizarre stepp ing o r bow ing of the I run k
(iv) Hemiballism us - un ilateral forceful throwi ng mov eme nt s
ABNORMAL GAITS w h ich are almost cont inuous

N. B. Most cases are due t o lesions of bone, j o int o r s ki n

SYRINGOMYELIA AND SYRINGOBU LBIA
'NEUROLOGICAL: GAITS SYR INGOMYELI A
1. Uppe r motor n e uro ne h e m iple gia Usua lly starts i n base of posterior ho rn o r cerv ical re g io n
Arm addu ct ed a nd int erna ll y rotated
El bow fl exed and pro nat ed
Finge rs flexed Clinical features
Foot plantar-fl exed, w ith leg sw ung in a lateral arc Insid ious onset of
1, Weakn ess and w asting of sma ll musc les of han d
2. Spa stic p a ra p le gia 2. Dissociated sensory loss in hand (pa in and temperature o nly )
St iff jerky 'sc isso rs' gait, w ith complicated assisti ng 3. Trophic changes:
m ovem ent s of upper limbs (i) Cya nosis of fi ng ers
(i i) Ulce ratio n and scarring
3 . Parkinsoni s m (iii ) Sw ollen f ingers d ue to su bcutaneous hype rtr ophy
Small shu ffling hurried ste ps 4. Lo ss of tend on reflexes
Flexion o f neck, el bows, w r ists and M P jo ints w ith th u m bs 5. Pa infu l arm
adducted 6. Spastic paraplegia
7. Charcot joints (neck and shoulders)
4 . Ce re b e ll ar le sion
'Oru nken' gait o n a broad b ase. Feet raised exce ssiv ely and
p laced ca reful ly. w ith patient looking ahead. Tends to fall t o
SYR INGOBULBIA
side of lesion Medu lla may be in itial sit e, o r m ay be involved by upwa rd
ext ensio n from cord
5 . P o s t e rio r colu mn lesio n
Patient w al ks o n a b road base but bangs feet down cl umsily
and tends t o look at feet. Ro mbergism is p resent Clinical feature s
1. Facial pai n o r senso ry lo ss (C r. 5)
6. High ste pping g a it 2. Vertigo and nystagmus (Cr. 8)
Oue to foot d rop 3. Facia l, palata l o r la ryng eal palsy (Cr. 7, 9, l a, ' 1)
4. Wast ed tong ue (Cr. 12)
7 . Proxim a l m yopathy 5. Horne r's syn d rome (sym path etic)
Wadd li ng ga it wi th broad base, lo rdosis and ma rke d body
sw ing. Th is g a it occurs also in congenit al h ip d islocatio n and
p reg na ncy BULBAR PALSY
Bi lat era l lo w er mot o r neurone lesions of the bu lbar nuclei (9, l a,
8. Hyste rica l '1 and 12 w it h low ermo st part of 7)
Usually b iza rre and inco nsist ent, and the patient rarely fa ll s M nem onic: Bu L ba r = B ila!. Lower
- Neu ro logv

CLI NICAL FEATURES

1. Dysarthria
2. Dysphagia. especially w ith fl uids
CAUSES OF COR O COM PRESS ION
1. Ve rte bra l
Neuro logy

Ii) Metastat ic cancer (esp. b ronchus, breast, prostal e)

I _

3. Wasted f ibr illat i ng l ong ue (ii) Ost eoporot ic collapse

4. Pala ta l paralysis (iii ) Pott's d isease (TS)
(iv) Spondylosis w it h d isc p ro lapse
(v) Trauma (fract ure, dislocation)
CAUSES
1. Motor neurone disease 2 . Ex tra-dural
2. Polio I i) Abscess
3. Encephalit is
4. Syringobu lbia 3. Intra-dural
(i) Inf ilt rat ion of meni nges - lymphoma, leukaemia
(i i) Extra-medu llary t u m ou rs - mening ioma, neu rofibroma
PSEUDO-BULBAR PALSY (ii i) Intra-medu l lary tu mou rs - gl ioma
(iv) Inflammation - t ran sverse myel it is
Bi late ral upper motor neu rone lesio ns of the same nuc le i
Mnem onic: PS eudo-b ulbar is S uper io r
CAUSES OF ROOT LES IO NS
CLIN ICAL FEATURES , . Disc p rot rus ion
1. Dysarth ria 2. Spondylosis (osteophyte)
2. Dysphagia 3. Metastatic cancer
3. Spastic tongue
4. Exaggerated jaw-jerk (spastic masseters)
5. Em o t ional liability CLINICAL FEATURES OF ROOT LE SIONS
,. Pai n in the approp riat e myotome, aggravat ed by stra in ing
CAUSES 2. Paraest hesiae in t he d er matome
3. Sp inal muscle spasm, e.g. l umbar scol iosis or restriction of
1. Ischaemia of internal capsule neck moveme nt
2. Mot or neurone d isease 4 . Weakness, w asting and fa scicu lati on o f the myotom e, w it h
3. Disseminated sclerosis decreased t endon refl ex

SPINAL CORD COMPRESSION DERMATOMES AND MYOTOMES

SYMPTOMS DERMATOMES OF HEAD AND NECK
1, Root pains occu r early. Often p rec ipita ted by movement or
st ra ining
2. Prog ressive wea kness, paraest hesiae and se nsory loss
3. Sph inct er di stu r ba nces occu r at a late stage OPh<h"m;,

SIGNS
, . Lower motor neu rone signs at leve l of com pression and
spast icit y be low
2. Sensory or refl ex 'level' . May be hy p eraest hesi a at the affect ed
level
3. Loss of abdomi na l reflexes in t horacic or cervical lesions
Trigeminal
"~,

l
Maxillary - --'1'-,/
Marldibu!ar - --t--
_ I Neu ro lo gy Neurology I _
Oerma 1o m e s i n the Dermatomes in t he 8 . Po liomyel it is
lowe r limb upper limb 9 . Sub-acute combined degeneration
10 . Gu illa in- Barre (acut e post·i nfect ive po lyneurit is)
u C3
c,-
u
~
"S>
53
12
c, PERIPHERAL NEUROPATHY
~ C' - -'3
S2 Cha racte rized by symmetrical f laccid weakness and sensory
changes of 'g love and stocking' d ist ribut ion

L1 L1
"
C6 - - CAUSES OF POLYNEUROPATHY
-- n ~

1. Many cas e s a re idiopathic

" CI

" " 2 . Drugs and chemicals

V incristine, am io d arone, mercu ry
" Lead causes mot o r neuropathy
Ison iazid (via pyridox ine deficiency)
" Many organ ic ch em ica ls

3. M e t ab o lic
Diabetes mellit us
MYOTOM ES WORTH REMEMBERING Amylo idosis
Acut e i ntermittent porphy ria
C6 - Biceps, brachiorad ial is, radial extenso rs of wrist
U raem ia
C7 - Triceps, u lnar extensors of wrist, f inger extenso rs
Myxoede m a
C8 - Finge r flexors
l4 - Quad riceps femor is
4 . De fici e ncy states
L5 - Extenso r hallucis long us
8 12 d eficiency
51- Planta r f lexors
A lcoholism
Be ri·be ri (thiam i ne deficiency)
Pel lagra (nicotinamide deficiency)
REFLEXES
An kle je rk 5 1,2 5 . Infections
Knee L3, 4 Leprosy
Biceps C5,6 Diphtheria
Triceps C7, 8 Tetanus
(St art low and work up) Botu l ism

6. Misc ellaneous
CAUSES OF PARAPLEGIA 'Acut e infective polyneuritis' of Gu i llain- Barre
Collag en- vascu la r disease, esp. polya rt eritis and rheumatoid
1. Heredi tary spastic parapleg ia d isease
2. Cerebra l bi rth i nj ury (cerebra l pa lsy) Ma l ignancy
3. Trauma Sarco idosis
4. Cord compression - int ra - or extramedu llary (p. 109)
5. Mu ltiple sc le rosis 7. Congenita l
6. Syri ngomyelia Rare hered ita ry ataxias and neuropat hies (e.g .
7. Motor neu rone d isease Charcot- Ma rie- Tooth )
I Neurology

CAUSES OF PROXIMAL MYOPATHY

9. Endocrinology
CONG ENITA L
Muscu lar dyst rop hy

RH EUMATIC
Polymya lg ia r heumatica
Po lymyositis o r der m atomyositis
THE PITUITARY
META BOLIC PITU ITARY HORMONES
Diabetes mell itus Anterio r
Glucocorticoids (Cushing's o r iatrogenic) FSH, L H, A CTH, T SH, G rowth hormone, P rolactin
Ost eoma lacia Mnemonic: FLAT GP
T hyrotoxicosis o r m yxoedema
Carcinomat ous neuromyo pat hy Post e rior
AOH
Oxytoc in

PITUITARY SPACE-OCC UPYING LESIONS

1. Secreting adenomas
(j) Prolactin oma
Oil Cush ing's IACTH)
(iii) Acromega ly IG H)
2. Non-secreti ng adenomas
3. Cran iopha ryng ioma
4. Met ast ati c ca rcinoma or lymphoma
5. G ran ulo m a, e.g. sarco id, T B

PRES ENTATIO N OF PIT UITA RY LES IONS

,. Sympt oms due to excess secretio n of ho r mones
(i l Prolactin - amenorrhoea, galacto rr hoea, hi rsu tism
Iii) ACTH - Cush ing's d isease
(i ii) GH - acromega ly
2. Hypopitu ita ri sm d ue to d estruction o f nor mal p itui tary tissue
3. Headache
4. Visual field defect s, usua ll y bitempo ral hemianopia
5. Pituit ary apo plexy (rare)

CLI N ICA L FEATUR ES OF AC RO M EGALY

Sympt o ms
1. Often insid io u s, w ith no sympt o m s
2. Headaches
3. Paraesthesiae (median nerve com pression)
4. Proximal weakness and jo int pains
- Endoc rin olo g v

5.
6.
7.
Po lyu ria
Im pot ence and loss o f li bido i n men
Hirsutism and ameno rrhoea i n women
3 . Gonado trophins (lH a nd FSH):
(i ) Delayed pu berty i n ch ild ren
Endocrino logy

(ii) Loss of bod y hai r, fine w rinkled skin, i mpotence, i nfe rti lity
I_

8. Visual d et erio ration and am en o rr hoea in adu lts

9. Ga lactorrhoea
4 . Thyrotrophin (TSH) :
Signs Hypothyro id ism
1. Characte ristic f acies, large hand s, f eet and t o ng ue
2. l eathe ry f u rrow ed skin. M ay be sebo rrho ea, hype rh idros is o r 5 . Corticotrophin (ACTH ):
p ig ment ation Hypoad renalism (asthenia, nausea, vom iting, hypog lycaem ia,
3. Hoa rs e de ep voice collapse)
4. No n-toxic go itre
5. Gynaecomastia 6 . M e la noc yte -stim u la t in g hormone (MSH):
6. Bitem pora l hemianopia, o ptic atro phy, ocu lar palsies Skin pallo r
7. Ge nera lized o rgano megaly
8. Cardiac fa i lu re (hypertension and ischaem ia)
9. Signs of di abet es m ell itus o r it s co m p licat ions THE THYROID
10. Hypopit uit a rism
11. Pro g ressive kyph os is HYPOTHYROIDISM
12. Arth ro pat hy CAUSES
P rima ry (thyroid gla nd f a ilu re)
HYPOPITUITARISM 1. A uto i mmu ne thyroid itis (Hashi m oto's disea se a nd it s atro ph ic
v ariant, m yxoed em a). In Hash im ot o 's the thy roid is larg e and
CA USES may be tender, but in m YKoed ema it is i m pal pable. Ci rc ulating
1. Tum o u rs: thyroid a ntibo d ies occu r in bo th
(i) Ch romoph o be adeno m a 2. Iatrogen ic:
(ii) Eosi no phil adenoma (basophi l adeno ma is rarely large (i) Su rge ry
enough t o ca use hypo pitui t arism) (ii) Irr ad iatio n
(iii) Cranio p haryng io m a (ii i) An t ithyro id d r ugs
(iv) Met ast at ic can cer (iv) Lith ium
2. Iat rogen ic - hypophysect o my o r irrad iation 3. End em ic creti nism (maternal iodi ne deficiency )
3. Pitui t ary necrosis d ue to ante- o r p ost pa rtum haemorrhage 4. Absence o r ma ldevelo pme nt of thyroid g land (rare)
(Sheehan's syndrome) 5. Dyshormonog enesis (rare co ngenital enlyme defects affecting
4. Gran u lomatous infi ltratio n, e.g . sarco idosis hormone synthesis)
5. Trauma
6. In fec tio n, e.g. T B, m eningitis S e condary (TSH d e f icie ncy)
1. Pitu it ary lesio n
2. Rarely hypothalamic lesio n (due to t hy rot ro p hin releasi ng
CLINICA L FEAT URES ho rmone defi cie ncy)
Loss o f ant erio r pit u it ary hormones is usually part ia l, i n t he
fo ll ow ing o rde r of f requency:
CLIN ICAL FEATURES
1 . Somatotrophin (GH) : ,. Ment al and physica l slug g ishness
(i) Dwarfism in c hild ren 2. Co ld i ntole rance
(iii Insuli n sensit iv ity i n adults 3. Constipation
4. W eight gain
2 . Prola ctin: 5. Croaking voice, w ith slow speech
Failu re of lact atio n in postpartum patients 6. Ro ugh, d ry yellowish skin
- Endoc rino logy

7. 'Myxoedema fa cies' w it h general ized thickening o f

subcutaneous t issue, periorb ital puffiness, b rittle sparse hair
and thin eyebrows
CLI NICA L FEATURES OF GRAVES' DISEAS E
Thyroid gland
1. Goit re, usually diffuse (but may be nodular)
Endoc rinology I

8. Bradyca rd ia
2. Increased thyroid vascu larity (th r ill, bru it)
9. Delayed relaxation of tendon jerks
Metabolic
l e ss commonly 3. Increased heat pro d uct ion (warm moist skin, heat i nto lerance)
10. A naemia (may be macrocytic) 4. We ight loss, increased appetit e, di arr hoea
11 . Cyanosis, Raynaud's phe nomenon or angi na 5. Tachycardia, exertiona l dyspnoea, hyperdynamic circu lat ion
12. Carpal tu nnel syndrome 6. Ti redness, irritabil it y, nervousness
13. Perceptive deafness 7. Fine t remor, hyperkinesia
14. Mya lg ia o r arthralgia 8. Proxi m al muscle weakness with hyperactive refl exes
15. 'M yxoedema madness' 9. Occasionally, bone pai n due t o osteoporosis
16. Coma 10. In e lderly patie nts, alrial fibrillation or cardiac fai lure

Extra-thyroid m a nifest a t ions (possibly immunological)

ORGAN-SPECIFIC AUTO IMMUNE DISEASES 11. Eye signs:
Eyel id oedema
1. Hashimoto's t hyroid it is
Conj unctivitis
2. Adrenal it is (Add ison's)
Exophthal mos
3. Pern ic ious anaem ia
Lid retract ion o r lag
4. J uven ile-onset d iabetes me ll it us
Opht ha lmopleg ia (usual ly superio r rect us)
5. Vitiligo
12. Pretib ial myxoedem a
6. ? Alopecia areata 13. Thyroid acropachy (club bi ng)
14. Vit iligo
CAUSES OF 'NON-TOXIC' GOITRE 15. Splenomegaly

1. 'S imp le' colloid goit re (id io pathi c), common d u ring puberty and
M ANAG EM ENT OF THYROTOX ICOS IS
pregnancy
2. Diffuse mu lti nodula r goitre (may become t oxic) 1 . Indications for thyroid e ctomy
3. Iodine def ic iency (i) Possib le mal ig nancy
4. Goitrogens, e.g . antithyro id d r ugs, excess iodine (ii )Pressure symptoms
5. Auto immune thyroid it is (Hash imoto's) (ii i)Retrosterna l go itre
(iv) Large goitre
Possibility of mal ignanc y is sugge sted by : (v) Ref usal o r failure o f med ica l t reatm ent
,. Asymmet r ical enlargement wit h 'cold area' on scan (vi ) Hypersensit ivity to antith y roid drugs
2. Very hard t hyroid Patient m ust first be made eut hyroid to avoid t hyro id 'storm'
3. Pressure effects, e.g. ho arseness
4. Cerv ical lym ph adenopathy 2. Indications for m e dical treatment
(i) Young patie nts
(ii) Pregnan cy
HYPERTHYROIDISM (i ii) Mi ld hy pert hyro id ism w ith small goitre
(iv) Pat ients unsuit able for su rg ery
CAUSES
3. Indications for radioiodine therapy
1. Graves' d isease
(i) Relapse afte r thyro id ectomy
2. Toxic mu lt inod ular goitre. Resembles Graves' d isease but
(l j) Patients over age 45
pat ients tend to be o lder, w ith fewe r eye signs
(iii ) Toxic adenomas
3. To xic adenoma
4. Iatrogenic (excess t hy roid hormone) Su bsequent hypothyroidism is common (about 40% at 10 y ears)
_ I En d oc r in o logy Endocrino logy I
THE PARATHYROIDS CLINICA L FEATURE S
HYPERPARATHYROIDISM 1 . Due to hyp o cal caemia
CA USES OJ Tetany (paraesthesiae, stridor, c ramps, hyperref lexia)
Trousseau's and Chvost ek's signs are present
1. Prima ry {iiI Conv u lsions (especia ll y in ch i ldren )
(i) A de noma (single or multi ple) (85%) (i ii) Cata racts
( ii ) Hyperplasia
(i ii ) Carcino m a 2 . In idiopathic hypopar athyro idis m
(i) M ental subno rmality
2 . S econda ry Iii) Dry skin, sparse hair, poor teeth, na il dyst rophy o ften wit h
Hy perplasia d ue t o chronic renal f ail ure. osteomalacia or ca ndid osis
rickets (i ii ) Papilloedema and calcif ied basal g angl ia (m imics brai n
t umour)
3 . Te rtia ry (iv) Ot her autoimmune d isorders, e .g . hypoadrenalism,
A com p licat ion of secondary hyper pa rathyroidism in which pern icious anaem ia
autonomous hy perparathyroid ism develops
THE ADRENAlS
CLINICA L FEATURES CUSHING'S SYNDROME
('Bones, st ones, abdom ina l groans and psychic moans') CAU SES OF CU SHI NG'S SYNDROME
1. Iat rogenic (prednisolo ne o r ACTH)
1 . Due t o hyperc a lca emia 2. A lcohol ism (pseudo-Cushing 's)
Ii) Anorexia, nausea and vom it ing 3. Cush ing's d isease (pit uitary-dependent adrenal hyperp lasia)
(ii) Constipa tion 4. Adrenal carcinoma o r adenoma
(iii) Po lydipsia a nd polyuria 5. Ect o p ic ACTH (e.g. smal l cel l b ro nc h ia l cancer)
(iv) letharg y and depression, p rog ressing to coma and
convu lsio ns
CLINICAL FEATUR ES
2 . Me tas t a tic calc ification 1. Obesity of t run k and face w ith ' buffa lo hu mp'
( i) Re na l ca lculi 2. Hype rtension
(i i) Ne phrocalci nosis 3. Skin changes:
(ii i) Co nj unct iva l deposits and keratopathy (i) Striae
(ii ) Bru isi ng
(ii i) Hirsut ism
3 . Bo ne resorption
(iv) Pig ment ation
(i) Pai n a nd def ormity
4. Ost eoporosis
(ii) Patholog ical f ractures
5. Proximal myopathy
6. Menstrual d ist urba nces
4 . Ra r e ly 7. Neurosis or psych osis
Peptic ulcer, pancreatitis, pseudo-gout 8. Facial plet ho ra due to polycythaemia

HYPOPARATHYROIDISM LA BORATORY FEATU RES

1. Increased plasma 11-hydroxyco rticost eroids ('cortisol')
CAUSES Norm al v alues:
1. Postoperativ e (e.g. t hyroidectomy) 9 a.m . 12 midnight
2. Idiopath ic (possib ly autoimmu ne) 190-690 nmol/l 80- 190 nmolll
3. Neonatal (transient. b ut dangero us) (7- 25 IJgl100 ml) (3-7 IJg/ 100 mil
_ I Endocri no log y Endocr inology I
Loss of d iurna l rh yth m occu rs early in Cushing 's syndrome (i.e. CAUSES OF HYPOADRENALISM
midnig ht sam ples give increased v al ue) ACUTE
2. Po lycythaemia w it h leukocyto sis and eosino phi l d ecrease
3. Hypoka laemia, w it h sod i um in u pper norm al ran ge 1. Stress occur ring in patients w ith chro n ic hy poadrenalism
4. 'Dia be tic' glucose tole ra nce test 2. Septicaemia, especial ly m ening ococcal
5. 24 hou r u rinary 'free l 1-hydroxyco rticost ero id s' inc reased (Waterhouse-Fried r ic hsen)
3. Surg ical ad renalecto m y
Low dos age d exame thason e (0.5 m g q .d .s. fo r 2 d ays) ca uses 4. A b rupt w it hdrawal o f stero id t herapy
little suppressio n i n Cush ing's synd rom e 5. Pit uitary necrosis (e.g . Sheehan's)
High dosa g e dex amethasone (2 m g q .d .s. fo r 2 days) causes
suppression in ad renal hy perp lasi a, b ut has little o r no effect in
adrenal adeno m a o r carcinoma, o r ect o p ic ACTH secret io n d ue to
CHRONIC
extra-adrenal ca rcinoma
Primary
1. A uto immu ne adre nal it is (Ad d iso n's)
HAZARDS OF SYSTEM IC GLUCOCORTICOID 2. TB
THERAPY 3. Metastat ic cance r depo sit s occu r comm o n ly, b ut rarely cau se
hypoad renal ism
1. Growth reta rd at io n in ch ild ren
2. Cushi ngoid f acies, buffalo hump
3. A drenal su ppress ion and atroph y Sec ondary (ACTH deficiency)
4. Weig ht g ain , sod iu m and w at er retention, potassi um 1. Pit uita ry or hypothalam ic d isease
depleti o n 2. Pro longed corticosteroid therapy
5. Hype rt ensio n
6. Hy perg lycaemia
7. Hyperli p id aemia
8. Infection s, especially v iral, TB and funga l CLI NICAL FEATURES OF CHRON IC HYPOADRENA LISM
9. Osteoporosis, aseptic bo ne necro sis, rupt ured Ach il les 1. Pigmentat io n, especially in exposed sk in, mout h, areolae,
t end o n pal m ar creases, pressure areas and scars (except i n
10. Gastroi ntes tina l hy po p ituitarism )
Dyspepsia 2. Deb ility and tiredn ess
PePt ic u lcer and perfo ratio n 3. Nausea, vom it ing, weig ht loss, abd omi nal pain, d iarrhoea
Pancreat it is 4. Hypotensio n, wi t h low-vol ume pulse
11. CNS 5. HYPoglycaemia, especially reactive after a meal
Eu phoria 6. l oss o f bod y ha ir in wom en
Psyc hosis 7. Dep reSSi o n
Increased i ntracrania l p ressure 8. May be associated aut o immu ne diso rder, e.g. v itil igo
Increased tendency to epi lepsy
12. Skin chan ges
T hinni ng, stri ae and easy bruisi ng
LABORATORY FEATU RES OF HYPOA DREN A LI SM
Poo r wo und heal ing, en largement of venous leg u lce rs
A cne 1. Plas ma 11-hyd roxy cort icost eroids m ay be no rma l o r low b ut
Hy pert richosis f ai l t o respon d adeq uately to 250 ~ g Sy nact hen i.m . ( s ho~ l d rise
13. Myo pathy o r musc le atrophy by m ore t ha n 193 nmolll (7 ~ g/ 1 00 m l) at 30 m in utes )
14. Cataract s, and ra ised intra-ocu lar pressu re 2. l ow plasma sod ium and ch loride, w it h raised potaSSiu m and
15. A m e no rr hoea or p remat u re menopa use u rea
16. Terat ogen icity (fet al cleft palate) 3. Low v o ltage ECG w ith f lat T waves
17. 'RebOu nd' o f disease o n reduct ion of dosage 4. Low blo od sug ar, especiall y aft er fast ing
_ I Endoc rin o log y Endocrin o logy I _
D IABETES MELLITUS (ii) Cat aract s
CAUSES OF DIABETES MELLITUS (iii) Retinopathy (see p. 94 )
(iv) Ru beosis ir id is (new blood vessels over i ris)- may cause
1. Id iopath ic g laucoma
( i ) Insuli n·dependent ('juvenile')
(i i ) Non-i nsu li n-dependent ('m at u r ity onset') 2 . Neurologica l
2 . Dr ug-i nduced (i) Peri pheral neuropathy (early sign is loss of ankle jerks
Glucocort icoids. thiazides, diazoxide and malleolar v ib ration sense)
3. Panc reatic disease (i i) Mononeu rit is mult ip lex (neu ro pat hy of several peri phera l
Panc reatit is, cancer, haemochromatosis, g lucagonoma, cystic or cranial ne rves; ohen asymmet ric al)
fi b rosis (i ii) Autonomic neuropat hy:
4. Other metabolic di sease a. Diarrhoea
Acromega ly, phaeoc hromocytoma, Cush ing's, thyrotoxicosis b . Postura l hypoten sion
5. Genetic syndromes c. Im pot ence
Glycogen st o rage d isease, Down's syndro me, etc. d. A bnorma l sweating
e. Dependent oedema
DIFFERENCES BETWE EN THE 2 M AIN TYPES OF DIABETES
MELLITUS 3 . Renal
'Juvenile' 'Maturity onset' (i) Pyel o neph ri t is, sometimes w ith papilla ry necros is
1, Thin Obese (ii) Glomerulonephrit is
2. Young Midd le-ag ed o r e lderly a. Kimme lstiel- W ilso n (eos inoph ilic nod ules in
3. Tendency to ketosis Resist ant to ketosis glomeru lar t uft)
4. Low insu lin sec retion No rmal or i ncreased in su lin b. Prolife rative, with sc lerosed basement membrane
secret ion (iii) At heroscl erosis and hypertensive vasc ular changes
5. Sensit ive to insul in Insul in resis tant
6 . Requi re treatment w ith insu lin Respond to d iet, and o r al 4 . Va s cular
hypoglyca emic d ru gs Occlusion by atheroma (large vessels) o r endart erit is (smal l
7 . HLA-associat ed (DR3 and 4) No association v essels) may cause ischaem ia of feet, myocardium, b rain or
8. Sib lings rarely affect ed Siblings often affected kid neys

5 . Dermatological
DIFFE RENCES BETWEEN 'D IABETIC' AND (i) Fat atrophy o r hy pertrophy at i nsu lin injecti on sites
HYPOG LYCAEM IC COMA (ii) U lcers due to neuropathy or isch aem ia
Ketoacidaemic coma Hypoglycaemic coma (i ii) Infect ions, especially f uruncles and cand id osis
1. Preceded by inf ection or Preceded by exercise, missed (iv) Pigmented scars over shi ns ('d iabet ic dermopat hy')
insulin underdosage meal or insuli n overdosage (v) Xanthomata
2. Onset over hours or days Onset in m inutes (vi) Necro biosis tipo id ica
3. Deep rapid b reathing Stertorous breath ing
4. Dehydration Norma l hydrat ion 6 . Systemic infections
5. Sweating ab sent Sweating m arke d Incide nce of TB and deep mycoses is i ncreased
6. CNS changes unusua l CNS changes common,
especially Babins ki response
CAUSES OF SHORT STATURE
7. U rine - usua lly g lycosu ria U rine not hel pfu l
and ketonuria 1. 'C ON STITUTIONA L'
Rac ial, fam ilial or sporadic
CO MPLI CATIONS OF DIABET ES MELLITUS
1 . Ocu la r 2. N UTRITIONAL
(i) Blurred v isio n d ue to f luctu at ions in blood sugar
(i) St arv atio n
_ I Endocrino logy End oc rin o logy

(ij) Malabso rption CAUSES OF GALACTORRHOEA

(i ii) Prote in loss
1. Physiological (post partum o r neonat al)
2. Prolactin-secreting pitu it ary t umour
3. CHROMOSOMAL DEFECTS J. Ect opic prolactin, e.g . bronchial Ca
(i) Tri som ies, e .g . Down's 4. Drugs
(i i ) Turner's (i) Phenothiazines
(ii) Ora l contracept ives
(i ii) Methyldopa
4. SKE LETAL DEFECTS
( i ) Ricke ts
(i i ) Achondroplas ia SIDE· EFFECTS OF ORAL CONTRACEPTIVES
(ii i) Ga rgoylism (Hurle r's)
1. SYMPTOMS DUE TO OESTROGENS
Fluid retention, we ight ga in
5. CHRO NI C SYSTEMIC DISEASE
Nausea and vo mit i ng
(i) Cyanotic congen it al heart d isease Headache
I ii ) Rena l fai lu re Ti redness and i rritabi lity
(ii i ) Hepatic fai lure Venous hypertens ion in Jegs
(iv) Pu lmonary d isease Inc reased menstru al loss
(v) Anaem ia
(vi) Infecti ons, e.g. TB
(v ii ) Long-term st eroid therapy (e .g. for asthma )
2. SYMPTOMS DU E TO PR OG ESTOG EN S
Depression
Acne
6. ENDO CRINE DISEASE
Decreased libido, dry vagina
(i) Sex ual precocity Muscle cramps
(i i) Hypopituitarism Breast d iscomfo rt
/iii ) Hypothyroidism Reduced menstrual loss
(iv ) Congenital ad renal hyper plasia
3. GYNAECOLOGICAL
7. M ISCE LLANEOU S RARE DISEASES
Amenorrhoea on contraceptive withdra w al
Diseases of unknown cause, e.g . progeria Cervical erosion
Vag inal candidiasis
Increase in size o f f ibroids
CAUSES OF GYNAECOMASTIA
1. Neonat al, o r norma l pu berty
2. Ci rrhosis
4. EN DOCRINE AND METABOLIC
3. Ma ligna ncy Abnormal ca rb o hyd rat e tolerance
4. Testicul ar or ad rena l tumours Increased plasma t riglycerides and choles tero l
5. Drugs Abnorm al liver fun ct ion tes ts
(i) Oestrogens Plasma prote in chan ges, e.g . increased t ransfe rrin
(i i) Cyproterone acetate Increased th yrox ine and p lasma cortiso l
(iii) Spirono lactone Ra rely :
(iv) Cimetidine Hy pertension
(v) M eth y ld opa Ch loasma
(vi) Digoxi n Ga lactorr hoea
6. Klinefelter's syndrome (XXY) Ga llstones
_ I E n do c r ino lo gy Endocri no logy I
5. TH ROMBOEMBO LIC EFFECTS (i) Inadequate diet, possi bly agg ravate d by preg nancy or lack
Increased ri sk of thrombosis (e.g. coronary, cerebral) o r of UV radiation
embolism (e.g . pul monary) due t o increased clotting factors (i i ) M alabsorption
and platelet st ickiness (i ii) Phenyto in
2. Chronic renal failu re
3. Hepat ic disease (d ist urbed v itamin 0 metabolism)
CONTRA-INDICATIONS TO OESTROGENIC ORAL
CONTRACEPTIVES
1. Preg nancy Causes o f hype r cal cae mia
2. Hepatic d isease 1. Hyper pa ra t hyroidism
3. Breast or cerv ica l ca rcinoma 2. Mal ignancy wi t h o r wi t ho ut metastases
4. Histo ry of t hrombosis o r embolism 3. Myelomatosis (ra re ly lymphoma or leu kaemia)
5. Ca re is req uired in pat ients w ith a h isto ry of epilepsy, arter ia l 4. Vit o 0 sensit ivi ty, especially sarcoidosis
disease, hypertension, va ricose ve ins, oedema, diabet es 5. Vit o 0 excess
mell itus, p rolactinoma, ga llst ones, m igra ine or f i bro ids. Women 6. M ilk-al kali synd rom e
over age 35 are at increa sed risk of t h ro mboembo lic d isease
(esp. smokers)
Cau ses o f h y p ocalcaemia
' . Hypopa rathyroid ism
OSTEOPOROSIS (i) PosHhyro idectomy
A reduct ion in bone mass below the norma l expected f or t he age (i i) Id iopath ic (someti mes w it h hypoadrena lism and
and sex of t he patient. Histo log ically t he trabecu lar bone is can d id osis)
redu ced, and the m i nera l- matrix ratio is ap proximately n orma l 2. Def iciency of choleca lcifero l
3. M a labsorption
4. Chronic ren al fa ilure or Fanconi syndrome
COMMON CAUSES 5. Hypoa lbum inaem ia
1. Old age
2. Immobilizat ion
3. Gl ucocorticoid therapy (or Cushing's d isease) PAGET'S DISEASE
4. Sex hormone def iciency, e.g. prematu re menopause, Turner's
synd rome CLI NICAL FEATUR ES
5. Cigarette smoking 1. Oft en asymptomat ic . Incidence increases wi t h age
6 . Rheuma toid arth rit is causes loca lized osteoporosis 2. Bone deform ity
Ii) Enlarged sku ll
OSTEOMALACIA (i i) Sa bre t ibia
(ii i) l ong bone fractures
A reduct ion i n t he m ineral- m atrix rat io, although t he t otal bone 3. Nerve ent rapm ent
mass may be no rm al, decreased o r even increased (i) Deaf ness
(ii) Basilar invag ination
CAUSES (ii i) Ce rvical spondy losis
4. Hig h o ut put card iac failure
, . Deficiency o f cho leca lcife ro l (vitam in OJ 5. Increased inci dence of bo ne sa rcoma
10. Renal disease

CLASS ICAL PRESENTATIONS OF REN A L DISEASE

1. Haematuria alone
2. Prote inuria alone
3. Nephrotic syndrome (severe proteinuria, hypoa lbuminaemia,
peripheral oedema and often hyper li p idaem ia)
4. Ne ph rit ic syndrome (haematuria, hypertension and periphera l
oedema )
5. Acute rena l fa ilu re (ol iguria w ith acute uraem ia)
6. Ch ronic rena l fa il u re (po lyuria wi t h ins idi ous uraemia)
Renal disease which affects the glomeruli is called
g lomerulonep hrit is, and t his is classif ied by the patholo gy shown
on rena l biopsy (p. 132) . M any diseases can cause more than one
of the above presen tat ions. T hus membranous g lomeru lo nep hritis
usua l ly causes the neph rotic syndrome, but it can occasionally
present as acute or chronic rena l fa il u re.

RENAL FAILURE
CA USES OF ACUTE RENAL FAI LURE
(A I Pre r e nal
1. loss of blood, plasma or wat er and elect ro lytes
2. Hypotensio n with normal b lood volume, e.g . myoca rdial i nfarct
or septicaemic shock

I BI Re nal
1. Acu te-on-ch ronic fa ilure, precipit ated by renal infect ion o r
dehyd ration
2. Ac ute 'tubu lar necrosis' (or rarely cortica l necrosis)
(i) Sustai ned hypotension
(ii) Obstet ri c causes, e.g. abortion o r antepartum
haemorrhage
(ii i) Septi caemia (especia ll y Gram-negative)
(iv) Free circu lating ha emog lob in
(v) Ext ensive tissue damage
(vi) Drugs and t oxi ns, e.g . heavy met als, carbon t et rach loride,
NSAID
3. Pr imary renal d isease
(i) Acute g lomeru lonephrit is
_ I Re na l dillle.a Ren al disease I
(i i ) Fu lm i nating py eloneph ritis
3. CARDIOVASCULAR
(i ii) Acute 'collagen- vascular d isease'
4. Hep ata-rena ' syndro m es (includ ing We il's d isease) (i) Pericarditis (may be t ampo nade)
5. Vascular (ij) Ca rd iac f ailu re d ue to salt and wat er overlo ad
0) Arteria l - thro mbosis, em bo lism , trauma (iii ) Hypertension wi t h retino pathy
(ii) Venous - throm bosis (iv) Arrhythmia (d ue to hyperkalaem ia)

leI Pos tre na l 4. GAST RO INTESTINAL

Obstruction in urinary tract (p. 137)
(i) Dry m outh, f oetor, m ay be paro t itis
Iii) Anorexia, nausea and vom iti ng
CAUSE S OF CHR ON IC RENAL FAI LURE (ii i) Hiccups
1. Glo m erulo nep h rit is (iv) GI t ract ulcerat ion a nd b leed ing
2. Pyeloneph ritis or T B
3. Hypert ension 5. GEN ITOURI NARY
4. Co ll agen- vascu lar disease, especially SLE and PA N
5. Meta bol ic (i) In acu t e rena l f ailu re - ol igu ri a « 300 m ll24 h )
( i ) Diabetes me ll itus
(ii) In ch ron ic ren al f ailu re - po ly u ria w it h fix ed u ri nary
(i i) Gout s pecif ic g rav it y (1.0 10)
(iii) Chronic ana lgesic ingest ion
(iv ) Amy lo idosis 6. RES PIRATORY
(v) Hyperca lcaem ia
6. O bstruct io n in rs nal l ra c! (j) Hypervent ilat io n du e to ac idosis
7 . Myeloma (ii) Pleu ral effusio n
8. Sch istosom iasis (rare in UK)
9 . Congen ital 7. HAEM ATOLOG ICAL
iii Po lycystic kid ney
(ii) Tubular acidosi s
(i) Anaem ia due to:
( i ii) Fanconi syndrom e GI b leed i ng
Haemo lysis
Diet ary rest r ictions
CLINICAL FEATURES OF SEVERE CHRONIC RENAL Eryth ropoiet i n d eficiency
FAILURE (ii ) Bleed ing t endency due to platelet dysfu nct io n
(iii) Suscept ib ility to secondary inf ectio n
1. DERMATOLOG ICAL
(i) Pru ri tus 8. DEFECTS IN BON E AND CALCIU M M ETABO LI SM
(iiI Pal lor
(ii i ) Pigme nt at ion (i) Osteo ma lac ia ('rena l rickets' in ch ild ren)
(iv) Pet echiae (ii ) Second ary o r tertiary hy per pa rathy roid ism (ost eit is
(v) W hite na ils f ib ro sa cyst ica )
(v i) Ra rely ' urea f rost' (i ii) Pat chy ost eosclero sis
(iv) Occasionally osteo po ros is
(v) Occas ionally met ast at ic calcif icat ion of m uscles, blood
2. NE UR OLOG ICAL v esse ls and con j unct iv ae
(i) M ent al ch anges (co nf usio n, parano ia, et c.)
I ii) A pat hy a nd wea kn ess
(i ii) Muscle tw itc hi ng and seizu res FACTORS W HICH M AY PREC IPITATE 'U RAEM IA'
(iv) Coma in t erm inal cases 1. Flu id and elect rolyte imba lance
(v) Perip heral neu ropath y in chron ic und ialysed cases 2. Infect io n, sy st emic o r urinary
- Re n a l d isease

3. Increased protein ingestion

4. Obst ruction o f re nal t ra ct
5. Catabolic o r nephrotoxic drugs (e.g. tetracycline)
5 . M e sangioca pilla ry (type s I a nd II)
C3 usually low
Ren a l disea s e

Type II is associated wit h partial lipoat rophy and wit h C3

I

6 . Congest ive card iac fa il ure nephr itic factor

7. Gastrointestina l haemor rhage o r su rgery
GLOMERULONEPHRITIS
T h is may be: Focal - some g lomeruli are affected
o r Diffuse - all g lomeru li are affect ed
Segmental - part of a glomeru lus is affected
or Global - all of a g lomeru lus is affect ed
Th us, in fo cal segmenta l g lomeru lone ph r it is, parts o f some
glomeru li are affected
6 . Foca l
Associat ed w ith WEgener's g ran ulomatosis, SlE, Endoca rd it is,
Polyarter iti s nodosa, HEnoch- Schonlei n p urp ura
Mnemonic: WE SLEEP HEre
7 . Ra pidly progressive (crescentic)
Assoc iated wi t h W egener's gra nulomatosis, Henoch- Schon lein
purpu ra, A ntig lomeru lar basement membrane
(Goodpastu re's), M icroscopic polyangi it is, Imm une com plex
disease
Mnemonic: WHAM I

8 . Focal segme ntal glome rulo s c lero s is

Somet i mes id io pathic, particu la rly in chi ldren, but in adu lts
CLASS IFICATION OF GLOMERULONEPHRITIS usually secon dary to other form s o f g lomeru lo nephrit is o r
1 . M i nima l cha nge other rena l d isease such as pyelonephrit is o r seve re
No change on l ight m icroscopy b ut EM show s loss of hypertension
pod ocytes
Typica lly affects ch ildren b ut may be due to NSAIDs i n adults CAUSES OF NEPHROTIC SYNDROME
Produces acute nephrotic syndrome, but good prognosis
1. Glomeru lonephrit is accounts fo r 80% (usually membranous in
2 . IgA disease (Berger's disease) ad ults, m inimal chan g e in ch ildren )
Si m ilar to Henoch- Scho n lein pu rpura,. w it h w hich it may 2. Metabolic
overlap (i) Diabetes mell it us
Typical ly causes haemat uria in young men (ii) A m yloidosis
20% develop renal fa i lure over 15 years (i iil Myelomat osis
3. SLE
3 . Pro l iferative 4. Drugs - mercurials, pen ici llam i ne, trox idone
Trad it ionally fo l lows Group A streptococcal infect io n, but now 5. Renal vei n th rombosis
not usually associated in UK. Low C3 duri ng t he acut e attack.
Good prognos is CAUSES OF LARGE KIDNEY lOR KIDNEYS)
4 . Me m bra nous 1. Cystic kidneys
Due to 2. Hyd roneph ros is o r pyonephrosis
M ala ria 3. Hypernephroma
M aligna ncy (e.g. b ronchia l ca nce r) 4. Hypert rophy followi ng contralat eral neph rect omy or fai l ure
Hepat it is B 5. Neph roti c syndrom e
Rheumato id A rthritis (and penic illami ne o r gold the rapy fo r RAJ A lso consider t he poss ibi lity of per irena l haematoma
S LE
Mnemonic: MeMBRAnouS TYPES OF RENAL TUBULAR DYSFUNCTION
Prognos is: 1/3 i m prove, 1/3 st ay the same, 1/3 progress 1. RENAL DISEASE AFF ECTING MEDU LLA
Commonest form of de novo glomeru lonephrit is in rena l e.g . pyeloneph ritis. Impai rm ent of urinary co ncen t ration,
al lografts ac idifi cation and e lectro lyte reabsorpt ion
_ I Re n al d ise ase Re n al disease

2. RENAL GLYCOS URIA (ben ign) 3. M ETABO LI C AC IDOSIS (low pH, low CO 2 con ten t)
Causes
3. 'VITAM IN D RESISTANT RICKETS'
til Ingestion of acidic compounds
Inabi lity to reabsor b phosphate Amm o n ium chlor ide, salicylates, etc.

4. IDIOPATHIC HYPE RCALCIU RIA (iii Met abolic overproduction of a cids

Ketosis, e.g. starvation, d iabetes mel litus
Inabi lity to reabsorb calcium l actic acidosis

(iii) Intestinal loss of base

5. RENAL T UBULAR AC IDOSIS (Type I - distal tubules)
Diarrhoea
Inabil ity t o acidify the uri ne causes meta bo lic acidos is. Less Fistu lae
ca lci um is bou nd to protein and ca lcium filtratio n is increased,
leading t o neph roca lcinosis and rena l stones (iv) Renal failu re: renal tubula r a c idos is

6. RENAL TU BU LA R AC IDOS IS (Type 2 - prox ima l 4. M ETABOLIC A LKALOSIS (h ig h pH, h igh CO 2 co nte n t )
tu bules) Causes
Occu rs as part of Fanconi synd rome, wi th defective Ingestio n of alkali, e.g . NaHC0 3 • fo r indigestion
reabsorption of g lucose, am i no adds and phosphate (GAP) Vomi t ing, or gastric aspirat ion
Hyperchloraem ic acidosis occu rs, but no nephrocalcinosis Hypoka laem ia
May also be due to t oxins (lead, mercu ry, out dated
tetracyc line), kidney transp lant or cyst inosis CAUSES OF HYPOKALAEM IA
1 . Increased renal loss
7. CYSTI N URIA (i) Diuresis
Drugs, e.g. thiazides
Defect in reab sorption of cystine, ornithine, arg inine and lysine
Diabetes mellitus
(COAL) -
(i i) Minerolocorticoid excess, e.g. p r imary ald osteronism
Cystine stones fo r m (Conn's t umour) and Cushi ng's d isease
(ii i) Primary re nal d isease, e.g. chronic pyeloneph ritis
8. NEPH ROGEN IC DIABETES INSIPIDUS
2 . Increased intestinal loss
Impai red respon se t o ADH e.g. dia rrhoea, vom iting
Consider pu rgative abuse

ACID-BASE BALANCE 3. Decreased intake

Dieta ry lack (especially in alcoholism, or d uri ng prot ei n
These headi ngs re fl ect changes in ext racell ular fluid on ly, e.g. in ana bol ism in convalescence, o r f o ll owing p rolo nged i.v. fluids )
metabolic alka los is there is an assoc iat ed intracellu lar acidosis Ma labsorption

1. RESPIRAT O RY ACI D OSIS (lo w p H, h igh CO 2 conte nt ) CLIN ICA L FEAT URES OF POTASS IUM DE PLETION
Any ca use of hypoventi lation (p. 43) 1. Muscle wea kness
2. Apathy, anorexia and confusion
3. Ileus
2. RESPIRATORY A L KALOS IS (hi g h pH , low CO 2 con t ent) 4. Inc reased cardiac excit abi lity and d igit alis toxicity
Any cause o f hyperventi lat ion (e.g. asp irin overdose o r anxiety) 5. Th i rst and polyuria
 Re n a l disease Re na l d isease I
CAUSES OF HYPONATRAEM IA 3. Anticoagulant overd ose, bleeding diathesis
4. Hypern ephroma
1 . Excessiv e w at e r i nta ke
5. Rena l infarct (incl uding polya rt eritis nodosa )
Oral (po lyd ipsia) or intravenous
6. Po lycystic kidney
2 . Exce ss iv e w at e r r et ention 7. Bacterial endocarditis
Inappropriate ADH secretion

3 . Inadequa t e sodium inta k e (rare) (8) RENAL TRACT LES IONS

1. Papillary tumour o f bladder
4 . I n adequ at e sodium re tention 2. Acute cystitis (including cyclophosphamide toxicity)
Ii) Vomiting, diarrhoea, ileus, fistu la, drainage of ascites 3. Calcu li
Iii) Hypoad renalism 4. Prost atic lesions:
(ii i) Rena l loss
Hype rtro phy
(iv) Skin loss
Cancer
a. Excessive sweating
Prostatitis
b. Cystic fi bros is
5. Ureth ra l inflammation or trauma
c. Burns 6. T8 (now rare in UK)
7. Sch ist osomias is (rare i n UK)
CAUSES OF POLYURIA
1. Chronic renal fa il ure
CAUSES OF 'STERILE ' PYURIA
2. Diabetes m ellitus
3. Diuretic d rugs 1. Rena l TB
4. Compulsive wa ter drin king 2. Analgesic neph ropathy
5. Diabetes insip id us 3. Rena l calculi
Ii) Pitui tary (deficiency of ADH) 4. U rinary infection treated w ith chemotherapy
(ii) Nephrogen ic (no re sponse to ADH ) 5. Non-specific urethritis
6. Potassium depletion
7. Hypercalcaemia
CAUSES OF ' DARK COLOURED' URINE
CAUSES OF PROTEINURIA 1. Concentration
2. Bile
1. Conlamination (semen, prost atic or vaginal secretio n )
3. Blood, haemoglob in u ria and myoglobinuria
2. Postural (orthosta tic)
4. Methaemog lobinuri a
3. Renal disease 5. Porphyria
(i) Glomerulonep h ritis, especially neph rotic synd rome
6. A lkapto nuria
(ii) Pyelonephritis 7. Melaninuria
(ii i) Obst ruct ive ne phropathy
8. Beetroot, dyes in sweets, drugs (e.g. rifampicin), etc.
(iv) M alignant hypertension
(v) Tubercu losis
4. Disease of renal tract, e. g. cystitis CAUSES OF URINARY TRACT OBSTRUCTION
5. May be slight a lb umin u ria in fever or congestive heart fai l ure
6. Mu ltip le m yeloma (Bence Jones protei n) 1. Sto ne
2. Strict ure (post-o p or i nfl ammatory)
3. Ste nos is (congenita l) occur t hroughout
CAUSES OF HAEMATURIA 4. Neoplasm ) the u rinary tract
(A) KIDNEY LES IO NS 5. Clot
6. Neuromuscular i ncoordinat ion
1. Glomeru loneph ri tis, pyelonephritis, TB 7. Retroperitoneal fi b rosis } u reter
2. Trauma 8. Spread of cancer from pelvic o rg ans
 Re n al disease Rena l d i sease I_
9. Prost atic en largement or cancer CYSTINE STONES
10. Retroverted g ravid uterus } b ladder neck Cysti nu ria
11. Trau ma of labour Fancon i syndrome with cystinosis
12. Congen ital valves
} u rethra
13. Phimosis o r paraphimosis
XANTHI NE STON ES
Common ca uses of acute reten tion in adults are:
Xanth in uri a
Males Females
1. Post-operative retention 1. Trauma of labo ur
2. Prostatic lesio ns 2. Pressu re fro m uterus (fetus o r RENAL STONES
fibroid l Ra dio-op aque N o n -o paq ue
3. Ureth ral str icture 3. Hysteria Calcium (80%) U ric acid (5%)
Mg a mmonium phosphate ( 10%) Xa nth ine (1 %)
Remember that retent ion m ay also be due to antichol inergic
Cyst ine (2%)
drugs Of a neuro log ica l lesion suc h as multi ple scle ro sis o r co rd
co mpress ion
NEUROLOGICAL CONTROL OF BLADDER FUNCTION
URINARY CALCULI No rma l bladder capacity is 300-400 m l a nd larger vo lumes shou ld
st im u late the des ire t o m ictu rate. A fferent fibres trave l via
FACTORS WH ICH PRED ISPOSE TO UR INARY CA LCU LI
parasympathetic nerves t o sp ina l 'mict urition centre' (S 2, 3, 4)
1. Metabol ic abnor ma lit ies (q.v.) and b ladder contrac tion is in itiated by parasym pathetic efferents.
2. Urinary tract infections, e.g . Proteus The spina l 'm ict urition ce ntre' is no rm ally in hibited by higher
3. Urinary t ra ct stasis motor centres, wh ich bomba rd it wi th faci lit atory impulses w hen
4. Fo reign bodies in u rinary t ract m ictu r ition begins, so that the bladder empties completely
5. Geograph ica l fac t ors (e.g. hot, dry climat e, hard wa t er)
TYPES OF DYSFUNCTION
M ETABOLIC CAUSES OF URINARY CALCULI 1. LACK OF NORMAL INHIBITION
CALCIUM STONES (composed of calciu m oxa late, Frequency wi th sm all vol umes
phosphate o r bot h) Occurs in anxiety, cold weather, etc.
1. Hypercalciu r ia (on normal d iet, > 300 mg/2 4 h in m ale o r > 250
mg/24 h i n female) 2. ATON IC BLADDER
( i) Id iopathic hypercalciuria
( ii) Hyperparathyroid ism Distended bladder w ith overflow, but no desire to m ictu rate
(iii) Vita m in 0 excess Occu rs w ith sensory neu ro pathy, e.g. diabetes mell itus, tabes
(iv) Sarcoidosis dorsal is
(vi M ilk- alkali syndrome
(vi) Rena l tubu lar acidosis 3. AUTOMATIC BLADDER
(vii ) Ma lignancy
(vi i i) Immob i lization Bladder empties p artially when vo lume of about 250 ml is
(ix) Cush ing's syndrome reached, but w ithout d esi re to m icturate
2. A lkaline u ri ne Occu rs with co rd section above S 2, 3, 4
3. Oxa luria
4. AUTONOMO US BLADDER
URIC ACID STON ES Large resid ua l ur ine vol ume, w ith wea k uncoord inated b ladde r
Primary o r seconda ry gout contractions but no desire t o mict urate. Occ urs wi th LMN cord
Uricosuric d ru gs lesions at S 2, 3, 4 leve l
_ I Rena l disease

Unilat era l neu ro log ical lesicns may cause either frequ ency
wi th smal l v o l umes o r a large hyp ot o nic b ladder w ith residual
u rine after m ictu rit ion
11. Rheumatology
-
RENAL CLEA RAN CE
T he num ber o f m l of p lasma w h ich con tains t he am ount of a
substance excreted in t he u rine i n one min ute is t he rena l
clearance of that substance, i.e. C ", UV/pT m l
w here U ", concent ration of subst ance in urine PATTERNS OF POLYARTH ROPATHY
V = volume o f urine collected i n time T
P = concentration of su bstance in plasma PRIMARY OSTEOARTHROSIS
Creatinine clearance gives a more accu rat e measu re o f renal Symmet rical, affecting many jo ints
1. Knees
function than th e plasma urea
2. Great t oes and th u mbs: MP joi nts
3. Fi ngers: t erm inal IP jo ints
4. Acrom ioclavicu lar joi nt s
5. Smal l joints of sp ine

SECONDARY OSTEOARTHROSIS
Asymmet rica l, affecting weig ht-bea ring joi nt s
1. Knees
2. Hi p
3. Intervertebra l discs

RHEUMATOI D A RT HRITIS
Usual ly symmetr ical, intermin ent and inflam ed
1. Hands: intercarpal jo i nts, M P joi nts and proxi m al IP joi nts
2. Feet: tarsal and lateral MP jo ints
3. Knees
4. Sma ll jo ints o f cervical spine and sub acro m ial bursae

ANKYLOS ING SPONDYLITI S

1. Spi ne and bot h sacro i liac joi nts
2. Knees, s hou lders, w rists

PSORIAS IS
1. Hand s, te rm i na l IP j o ints (look fo r nai l pits)
2. Sacroiliac jo i nt s
3. 'R he umatoid' pattern
4. Asymm etri ca l ol igoarthritis (e.g. knee)
5. Arth rit is mut ilans

REITER'S DISEASE
1. Ankles and all joint s o f feet

1
_ I Rh eum atol ogy Rheu mat olo 9V I _
2. Knees 6 . PERIP H ERA L N EU ROPAT HY (due t o vascu l iti s)
3. Hi ps, sacroi liac jo ints and spine
7. ENTRAPMENT N EUROPAT H Y, e.g . spi nal cor d at cervi cal
X-RAY CHANG ES OF OSTEOARTHROSIS level f rom atla nto-a xial subluxatio n, o r ca rpa l t u nnel syndrome
1, Joint space narrowi ng
2. Subarticu la r sclerosis 8. FELTY'S SYNDROME ( RA w ith leu ko p en ia and
3. Osteo phytes
sp le n omega ly)
4. Bone cyst s

9. LYMPHADENOPATHY
JOINT COMPLICATIONS OF RHEUMATOIO ARTHRITIS
,. Deformity, su b luxation, m isa l ignment. swell ing 10. A MYLOIDOS IS
2. Infection (sept ic a rth ritis)
3. Tendon rupture
4. Synovial sac p rot r usion and ru ptu re (e.g. Baker's cys t )
5. J uxta-articu lar osteoporosis SERONEGATIVE SPONDYLOARTHRITIS (HLA-B27
6. Muscle atro phy secon dary t o d isuse ASSOCIATION)
A rth ritis invo lv i ng t he spine but wit h consistent absence of
EXTRA-ARTICULAR MANIFESTATIONS OF rheumato id f act o rs fr om serum
RHEUMATOID DISEASE 1. An ky losing s pondyl it is
2. Psoriatic arthrit is
1. ANAEM IA . 3 . Ent eropat hic arthrit is (Crohn's, u lcerat ive colitis, Wh ipp le's,
(i) Fe defic iency (G I blood loss ca used by d rugs) enteric inf ectio n, i ntest ina l bypass for o besity )
I ii) Defect ive i ron ut i lization (a naem ia of ch ron ic d isorders) 4. Re ite r's d isease
( i i i) Marrow de press ion

2. PU LMONARY FEATURES OF ANKY LOS ING SPONDYLITIS

(i) Pleu ritis, effusions 1. Ankylosis/ arthr it is of sp ine (bam boo sp ine)
(ii) Nodu les in lung or p leu ra 2. An t erior uveit is
( i i i) Fibrosi ng a lveol iti s 3. A rrhythm ia
4. Aortic regurgitat ion
3. CARDIAC 5. A pical p u lmona ry fibros is
Ii) Pe ri ca rd it is ( N.B. 5 A s)
( ii ) Nodu les i n myoca rd i um

4. OC ULAR CAUSES OF LUMBAR BACKACHE

( i) Scler it is, ep iscie ritis 1. MECHANI CA L
(i1) Scleroma lac ia perf orans
(iii) Sicca syndrome (Sjog ren's) (i) Muscu lotendino us and l igament strain
(ii ) Prolapsed i nterve rteb ral d isc
(i ii ) Sp ondylos is and spondylo l ist hesis
5. ARTE RI TIS
(iv) Spinal f ractu re
0 ) Digit a l isch aem ia (m ay be Rayn aud's ) a. Ma jor trauma
(i i) Na il f o ld lesions b. Cr ush fract ure in ost eopo rosis
(ii i) Leg u lcers c. Stress fr actu re of t ransverse process due to muscu lar
(iv ) Mese nt e ric ischaem ia effort

/
 •

_ I Rh e u ma tology Rhe umato lo gy I _

2. DE GENERATIVE OR M ETA BOLIC (iv) Infectio us m o no nucleosis
(v) Infect ive hepat it is
(i) Osteoa rt hrosis
(vi ) Mycoplasma pneum onia
(ii ) Osteo porosis
6. Reit er's di sease
(ii i ) Osteoma la cia 7. Occasionally, acu t e rh eumatoid arth rit is

3. INFLA MMATORY
(i) Infe ction, e.g. T8, pyog e nic
CAUSES OF HVPERURICAEMIA
(i i) Seronegative spond y loarthriti s (q.v.) 1. INCREA SED PUR INE SYNTHE SIS
Pr imary gout (in 25% of cases)
4. NEOPLASM
( i) Usually metast atic mal ig nancy
(i i) Primary ma lignancy - Oste os a rcoma 2. DECREA SED RE NAL EXCRETION
Myeloma (i) Primary g out (i n 75% of cases)
Lymphoma (ii ) Ch ron ic ren al fai lu re
(ii i) Drug s
5. RE FERRED PA IN Sa licy lates (in low dosage)
U ricosu rics (in low d osage)
(i ) Posterior d uodena l ulcer T hiazide d iuretics
(iiI Cance r of pa ncreas A lcohol
(iii) Re na l colic
(iv) Pelvic carcin o ma
(v) Dysm enorrhoea. labo u r pai ns 3. INCREA SED TUR NOVER OF PREFORMED PUR INES
(i) M y elopro life rat ive disease and ly mpho m a (esp. afte r
cytot o xic d rug s)
CAUSES OF A SINGLE HOT RED JOINT (ii) Chro nic haem o lysis
1. Traumat ic, e.g . sp rai ned ankle (ii i) Psoriasis
2. Septic arthrit is
May be seco ndary to penetrati ng in j ury, o steomy elitis,
septicaemia, rheu matoid arthritis o r osteoarth ros is CLASSIFICATION OF VASCULITIS
3. Gout o r pseudo-gout (ch ondrocalci nosis o r periarticu lar
ca lcif icat ion) No cla ssificat ion is co mp letely satisfa ctory. since the c lin ic al
4. Haemoph ilia sy ndromes m ay overl ap, and t hei r pat hogenesis is imperfect ly
5. Gonococcal arthritis ,.nd erstood
6. Occasionally rheumatoid arthrit is
1. SYSTEMI C NECROTIZING VASCU LITI S
CAUSES OF A TRANSIENT ' FLITTING' ARTHRITIS (i) Po lya rt erit is no dosa
(ii ) Ch urg- St rauss synd ro me (wi th ast h ma and eosi no p hi l ia)
, . Rheum atic feve r
(ii i) W egener's g ranulom atosis (uppe r and lowe r res pi ratory
2. Henoc h- Schon le in purpura t racts and kidneys)
3. Serum sickn ess and drug re act io ns (iv) Beh<;:et's d isease (w ith o ro gen ita I ap ht hous ulcers)
4. SLE
5. Syste mic infecti ons N.B. Ant ineut rophil ic cyt oplasm ic ant i bod ies:
(i) Go n ococca l o r m e ningococcal sept icaemia cANCA is fairly sensiti ve for Wegener's
(ii) Bact erial endoca rditis pANCA (peri nuclear) is fo u nd in a broad er range of v asc ul itides,
(iii) Ru bella ,,,el ud ing PAN
_ I Rheumatolo g y Rheumatology I _
2. 'HYPERSENSITIVITY'VASCU LITIS 2. Arth ralg ia, flitt ing o r episodic
(sm all vessel di sease. often cut aneous with circulat ing 3. Skin cha nges
im mune comp lexes) (i) Phot osensit ive rash, classically in butterfly d istribut ion .
(i) Serum sickness is the classical example, but now rare
May be erythemat ous, urticated o r p urp ur ic
(ii) Drug allergy (iil A lo pecia
(iii) Henoch- $chonlein purpu ra (affects skin, joints, GI t ra ct (i ii) Di lat ed nail fo ld capil laries
and kidneys) (iv) Raynaud's phenom enon
(iv) Infectio n (classically T B, e.g . Bazi n's) 4. Proteinuria, g lomer ulonep h rit is, nephrotic synd rom e or
(v) Idiopat hic cutaneous vasculiti s (often nodu lar, on legs) hypertension
(vi) Malig nancy, e .g . breast cancer 5. Lym p hadenopat hy
6. Myoca rditis, endoca rd it is (Libman-Sacks), o r pericard itis
3. CO LLAG EN VASC ULAR DISEASE 7. Pleurisy with effusion, pneumonit is
8. Hepatomegaly and splenomegaly
Rheumatoid, SLE , systemic scle rosis, de rm atomyosit is/poly- 9. Pancytopenia . May be haemolysis
myOSitis 10 . Psychosis, neu ro pathy or epi lepsy. M ay be retina l exudates
11 . Gastroint est i nal upsets (na usea, pai n , d iarrhoea, etc.)
4. LARGE VESSE L VASCU LITIS
Giant ce ll aortit is (e .g. Ta kayas hu'sl RAYNAUD'S PHENOMENON
Temporal arte rit is
Kawasa ki disease (usually yo ung ch ildren, may be coronary Paroxysma l d igita l ischaem ia, which usua lly causes a
arteri t is) cha racteristic seq uence of colou r changes (whit e, then blue, then
red)
5. THRO M BOANGIITIS OB LITERANS
(Buerge r's disease. occurs in sm oke rs) CAUSES
1 . Reflex vasoconstriction
CLINICAL FEATURES OF POLYARTERITIS NODOSA (i) Raynaud's d isease (idiopathic)
(PAN) (ii) Vibrat ing machinery

Usually young or m iddle-aged men 2 . Arterial occlusi on

1. Fever, ma laise, weight loss (i) Thoracic outlet syndromes
2. Gast ro intest inal ischaemia (ii ) A t heroma. Buerger's disease
Central abdom inal pain
Bleeding 3. Collagen- vascular disease, espec ia lly syste m ic sclerosis
3. Protei n uria and haematuria. Hypertension is common and SLE
4. Periphera l neuropat hy, oft en painful
Focal eNS lesions 4 . Increased blood viscosity
5. Arth ralg ia and mya lg ia (i) Dysprotein aemias (macro- and cryog lobulinaem ias)
6. Myoca rdial ischaemia (i i) Po ly cythaemia, leukaemia
7. Skin les ions:
Nod ules 5. Neurological disease. especia ll y syringomyel ia or para lysis
Live d o reticu laris
Nec rosis and u lcera t ion

CLIN ICAL FEATURES OF SYSTEMIC LUPUS

ERYTHEMATOSUS
Usually youn g or m idd le-aged women
1. Fever, ma laise, weight loss
12. Dermatology
-
PSORIASIS
DISTINCTIVE MORPHO LOGICAL TYPE S
,. N umm u lar - d iscoid plaques, w hich may be con f luent.
Typica lly o n extensor surfaces
2. Guttate - ' showers' of sma ll lesions, o ften post-strept ococca l
3. Erythro derm ic - very wi despread ery t hema, w it h exf o l iat io n
4. General ized pustular psor iasis
5. Pustu la r er upt ions of t he hands and fee t
Atyp ical fo rm s are common, e.g. fo ll icu lar, i nt ert rig inous, etc.
'Napkin psoriasis' (pso riasif orm les ions i n infants) may be
related to can d ida inf ection

ECZEMA
Eczema is a distinctive inflammatory response of the skin,
cha racterized h isto log ically by spongiosis (epidermal oedema) and
cl in ically by cl ustered papu la-vesi cl es w it h erythema and scali ng.
M any cases have a mult ifactoria l aetiology

rYPES OF ECZEMA
(AI Exogen o us
I Pri mary irr it ant d ermatit is, e.g. d ue to ca ustics, d etergents or
solvents
"J . Allerg ic contact dermat it is, e.g. due t o hypersensit iv ity to
Illeta ls, rubbe r, medicament s, et c.
:1 Infect ive de rmati t is, e.g. around i nfected woun d s o r ulce rs

(8) Endogenous
I. A to p ic derm atit is (infa nti le eczema). Typica lly on f lexor su rf aces
"J Se bo rrhoe ic derma t it is
I Disco id ecz em a
~ Po mpholyx - vesicles on palms or soles
'. Pit y riasis alba - pat ches of sca ly eczema w hich leave
depigmented areas
(~ I\sl oatotic eczema - due to excessive d ry ing ('chapping' )
Gmv itational eczema - second ary to venous insufficiency
_ I De rma tology Oonn atology I _
BLISTERING ERUPTIONS {ii i Spina b ifi d a
(iii ) Ta bes dorsalis
CO MMON CAUSES
(iv) lep rosy (in end emic areas)
1. Viral 4. Rheumat oid arthritis - u lceration is mult ifact orial
Ii) Herpes simplex 5. Malignancy - usually squam o us-cell skin carci noma
(ii) Herpes zos ter - varicella 6. Haemolytic anaemia, especially sickle-cel l
2. Impetigo 7. Syphil it ic g u mma
3. Scabies 8. Necrob iosis li poid ica (may be diabetic )
4. Insect b it es and papula r urticaria 9. Pyoderma gangrenosum - often d ue to ulcerat ive colil is
5. Bu llous eczema and pompholyx
6. Drugs, e.g. barbit urate overdose, photosensiti v ity Many leg ulcers have a mu lt ifac torial aet iology, e.g. ischaemia,
anaemia, venous hypertensio n and infection

UNCOMMON CAUSES CAUSES OF ALOPECIA

7. Eryt hema mu ltiforme t . M al e-pattern ba ldn ess
8. Dermatitis herpet ifo rm is sub-epidermal
9.
10.
Pem p h igoid
Po rphy ria cutan ea t ard a
) 2. Id iopath ic diffuse alopecia o f women - usua lly post -
menopausal
3. Telogen effluvi um' - loss of c lu b hairs after f ebri le illness,
'1 . Pemphigus grou p intra-epiderma l su rge ry or partu r itio n
Remember pemph igu S is S upe rf icial and pem ph igoi D is 4. A lopecia areat a
Deepe r 5. Dr ugs:
(i) Cytot ox ic agents
(ii) Anticoagu lants
RARE CAUSES (iii ) Dextran
12. Congenital (iv) O ral co nt ra ceptives
(i) Epidermolysis bu llosa 6. Scalp infection :
(i i) Ich t hyosifo rm eryth roderm a (i ) Fungi
(ii i) Incontinentia pigment i (ii) Pyogenic bact eria
7. System ic d isease:
(il Syph ilis
CAUSES OF PHOTOSENSITIVITY (ENHANCEO (i i) Hy poth yrOidism
RESPONSE TO UV IRRADIATION) (i ii) Fe deficiency
1. Drugs, e.g. t o lbutamide, c h lorpropam ide, p henoth iazines, 8. Trau m atic:
t hiazides, a miodarone, n alidixic ac id (i ) Tractio n fr om rol lers
Mnemonic: r ep-TAN (ii ) Scal pi ng i nj ury
2. Contact photosensit izers, e.g. tar, pe rfu mes, soa ps, etc. (i ii ) Burns
3. Dermatoses, e.g. porphyr ia , po lymorphic light e rupt ion, lupus (iv) Excessive bleach ing, pe rming, etc.
erythematosus 9. De rmat oses:
4. Decreased me lan i n in ski n, e.g. al bi nism, v iti lig o (i) Psoriasis
(i i) Disco id lu p us erythematosus
(iii) Lichen plan us
CAUSES OF LEG ULCERS 10. Congen it al - many rare di seases, e.g. mon il ethrix
t. Venous hypenension (90% )
2. Ischaem ia CA U SES OF HIRSUTISM
(i) Atheroma 1. Id iopathic (incl uding racial and f amilia l varia t ion)
{i iI Aneritis l . Ovarian disease
3. Neu ropathy (i ) Polycystic ovaries (common)
(i) Diabetes mellit us (ii ) Vi rilizi ng tumo ur (rare)
_ [ DermatolOgy Dermat o logy I _
3. A drenal hy perplasia o r t u m ou r CAUSES OF GENERALIZED PALLOR
4. Obesity and hyperi nsuli nae m ia 1. Vasoconstrictio n (cold , em otion, v asovaga l, etc.)
5. Prol act i noma 2. Anaem ia (includ i ng acute haemorrhage)
6. And rog enic drugs, e.g . m et hy lt estosterone, anabo li c st ero ids.
3. Diffuse hypomelanosis
(Oth er drugs such as m i noxidi l and di8zoxide cause 0) Prot ection fro m UV rad iat io n
hypertrichosis rather tha n true hi rsutism) (ii) A l bin ism
(iii) Phenylketo nuria
CAUSES OF OIFFUSE HVPERPIGMENTATION (iv) Hypopitu itari sm
(v) W idespread v it iligo
1. Congen ita l (racial o r fam il ial)
2. Irradiatio n, e s p. ultravio let
3. Post -i nflammatory, e.g . aft er erythro d erma CA USES OF W HITE PATCHES ON THE SKIN (le u kod e r m a)
4. Endocr ine causes
( i) Pregnancy, oestrog ens 1. Congeni ta l (ra re), e.g . t u bero us sclerosis, partial al bi nism
(i i) Hy poadrenal ism (due to MS H{beta-l ipot ro ph in ) 2. Post-inflamma tor y, e.g. eczema, burns. d iscoid l upus
(ii i) Ac romega ly erythematosus
5. M iscell aneo us system ic di seases 3. Infection, e.g. leprosy, p ity riasis vers icolor
(i) Cachexia (esp. TB or m al ignancy) 4. Immunological. e.g . viti ligo , halo naevus
(ii) Chronic ren al fai lure
(iii) Prima ry bi liary ci rrh os is
ERYTHEMA
(iv) Haemochromat osis
(v) Ma labsorptio n CA USES OF PALMAR ERYTHEMA
6. Drugs, e.g. busu lphan, chlo r promazine, A CTH, arsenic
1. Dermatoses, e .g . eczem a o r psoriasis
2. Inc reased oeslrogens
SKIN OISEASES WHICH CAUSE SEVERE ITCHING (i) Pregnancy
1. Pa rasites: scabies, pedicu losis, flea bit es (ii ) A lcohol ic ci rrhosis
2. Eczema 3. Rheu mat o id arth ritis
3. U rt icaria 4. Shoulder- hand syndrome
4. lic hen p la nus 5. Polycythaem ia
5. li chen simplex ch ronicus
6. Dermat it is herpet iformi s CAUSES OF FACIAL FLU SHING
SYSTEMIC CAUSES OF GENERA LIZEO PRUR ITU S 1. Heat and exe rtio n
2. Psycholog ical (b lushi ng, anger )
1. Obst r ucti ve jau ndice (especially bil iary cirr hosis) 3. M eno pause
2. Chro nic re nal fail ure 4. Rosacea
3 . lympho ma (especially Hodgkin's) o r m yelo p ro liferat ive d isease 5. Food and d rugs
(especially poly cythaem ia veral (i) A lcoho l; m arked i n M o ngolo id races, and in some
4. Carci no ma (especially bro nchi al) d iabetics taki ng c hlo r propam ide
5. Iron def iciency (i i) Pep pers, chi ll ies
6 . Hypo- o r hyperthyroidi sm (ii i) Nit rites, so d iu m m o nog lutamate, morphi ne. et c.
7 . Drugs 6. Carc inoid synd rome
(i) A ll ergy
(ii i Pharmacological. e.g . cocaine, morph ine
SOME CAUSES OF A CIRC U MSC RIBEO PATCH OF RED
N.B. a. Many w omen develo p pr u ritu s duri ng p regna ncy SCA LY RASH
b . Scabies is easily m issed i n hygien iC pat ie nts - rem em ber
to lo ok for b u rrows in the fi ngerwebs, and examine the 1. Psoriasis
n ipp les or pen is for ty pical papules 7. Eczema
_ 1 De rmat o logy Dennatology I _
3. Fixed d r ug er uption CAUSES OF PYODE RMA GANGRENOSUM
4. Fungus
1. Grahn's and other inflammatory bowel d isorders (UC, etc.)
5. Lichen simplex
2. Rheu mat o id and ot her inflammatory joint disorders
6. Bowen's d isease (squamous Ca i n sit u)
3. Id iopathic
7. Discoid lupus erythema tosus
4. Rarely dysprot einaemia o r mye lopro li fera tive d isease (esp.
8. Lupus vulgaris (a form of T 8 )
leukaemia)

SOME CAUSES OF WIDESPREAD PATC HES OF RED SCALY COMMON CAUSES OF A PIGMENTED PAPULE
RASH
1. Basal cell papil loma ('seborrhoeic w art')
1. Psoriasis 2. Melanocytic naevus ('m o le')
2. Eczema 3. Malignant melanoma
3. Pityriasis rosea 4. Pigment ed basal cell carci noma
4. Pity riasis versicolo r 5. Dermatofibroma
5. Secondary syphi lis
6. Liche n planus
7. Fungus FEATU RES SUGGESTING MALIG NA NT CHANGE IN A
MOLE
CAUSES OF ERYTHRODERMA (in f lammat ory skin disease M ajor f eat u r es:
aHecting more than 90% of body surface) 1, Change in size (esp. steady en largement, t hough ben ign moles
often enlarge at puberty and in p regnancy)
1. Eczema of va rious types (esp . atopic) 2. Change in shape (i rregu lar o utline may be important)
2. Psoriasis 3. Change in c%ur (blotch y variation, or spread of pigment
3. Lymphoma o r lympha tic leukaem ia beyond margi n may be i mportant)
4. Drugs, esp. gold or mercury
5. Id io pathic and rare congenital d isorders M inor f eatures:
4. Diameter more than 7 mm
5. Inflammation
CA USES OF ERYTHEMA NODOSUM (tende r nodules on 6. Ulce ration o r bleed ing
legs) 7. Itch (t hough th is is common in ben ign moles)
1. Sarcoidos is
2. Streptococcal infection If diagnosis is uncerta in obta in an expert opinion o r excise for
h istology
3. T8
In malignant melanoma, the best ind icat or of prognosis is the
4. Drugs. e.g. su lphonam ides
Breslow thickness (verti cal th ickness on histology)
5. U lcerative colitis o r Crohn's d isease
6. Other infections, e.g.
0) l eprosy CAUSES OF XANTHOMA
(i i) Systemic mycoses
1. Idiopathic, w ith normal b lood lip ids
(ii i) Toxoplasmosis
(iv) l ymphogranu loma venereum
2. Primary hyperl ipidaem ia, e.g. type 2 (hypercholeste rolaem ia)
3. Secondary hyperlip idaem ia
(i) Diabetes mellitus
CAUSES OF ERYTHEMA MULT IFORM E (ofte n 'ta rgets' on (ii) Hypothyroid ism
pa lms) (ii i) Chronic rena l fa ilu re or nep hrotic synd rome
(iv) Gholestasis (esp. primary b iliary cirrhosis)
1. Infections, esp. herpes simplex, o rf or mycoplasma
2. Drugs (m any, esp. long-acting su lphonamides) Other causes of hyper lip idaem ia, less li ke ly to produce
3. Id iopathic (recurrent forms may be due to occult herpes sim p lex) xanthomas, include obesity, alcoholism, pancreatitis and drugs,
4. Rarely collag en-vascular d isease, pregnancy o r malignancy o.g. isotretinoin
_ I De rm at o logy Derm at o logy I _
SKIN CHANGES ASSOCIATED W ITH SYSTEM IC 3. Bl ue n ails
MALIGNANCY Cy anosis
4. Ye ll ow nai ls
1. GENET IC SYNDROMES PREDISPOSING TO Ye ll ow na il syndrome, wi t h lym phoed ema
MALIG NANCY
8. g. neu rof ibromat os is (may deve lo p g lio ma ), fam i lial tylosis
(palm ar keratoderma) w it h oesophagea l carcinom a CAPILLARY CHA NGES
1. Spli nt er haemo rrhages
(i) Su bacute bacte ri al endocard it is
2. SIGNS OF EX POS URE TO A CARCINOGEN (ii) Vascu lit is, e.g . r he umatoid
e.g .: 2. Nai l-fo ld capill ary d i latati o n
(i) N ico ti ne st ai ning of fi ngers Col lagen-v ascular disease, esp. dermatomyosit is, S l E
(ii ) Pal mar keratoses due to arsenic
N AIL CHANGES DUE TO SKIN DISEASE
3. DIRECT INVOLVEM ENT OF SKIN BY M ALIGNANT CE LLS Psoriasis : p itting, o nycho lysis, ri dg ing '
( i) Direct sp read fr o m und erly ing canc er (espec ially b reast ) Eczema: defo rmed na ils with r id g ing
( i i ) Cutaneous metastases flnea: t h icke ned, d isco lo u red, friab le
(ii i) l e u kae mic o r ly m pho m ato us infi lt rat e M yxo id c yst : single g roove
'Picking ' at matrix: rippled g roov es
M olanoma: b row n o r b lack streak (m ay mimic su b-Iungua l
4. M ISCELLANEO US ENDOCRINE, METABOLIC AN D haemato ma )
IMMU NOLOGICAL EFFECTS I I yfhroderma : shed ding o f nails
(i) Pigment at io n. pallo r o r pru rit us
(ii) Ac ant hosis nig rican s PATTERNS OF DRUG ERUPT IONS
(iii) De rm at o m yositi s
(iv) Clu bb ing I\ IIy d rug can occasi o na lly cause an e ru ption . Any erU Pti o n can
(v ) Widespread v i ra l infect io n (e .g . he rpes) d ue to i m mu ne '" t:ilsiona lly be m i m icked by a drug react ion. The fo ll owi ng list is
defici en cy, etc. I." from com p rehen siv e:
I I xa nth emat a (m o rbill if o rm , etc .), e.g . pen icill i n
I U rt ica ria, e.g . pen icill in
NAIL CHANGES D U E TO SYSTEMIC DISEASE I I Iylhro de rma, e.g. g o ld
,I lIu ilous, incl ud ing erythem a m ult iforme , e.g. su lphona m ides
ABNORMAL MORPHOLOGY
t. I , yt hem a nodosum, e.g . su Jp honamides
1. Cl ubb ing (p o 46) h I'll, pura (d ue to eit her thrombocytopen ia or v ascu lit is)
2. Ko i lo nychia (i ron def iciency) i'lu)IOSensit iv ity, e.g . c hlorprom azine
3. Beau's lines (following ser ious illness) II I\nwform (see below)
4. Onycho lysis (thyrot oxicosis) II " x l~d d r ug erupt io n (interm ittent infl ammatio n fo ll owed by
IlIjll lIc ntati o n, alwa y s at same site), e.g . p he nol pht halei n

ABN ORMAL COLOUR

I tl tiJGS W HICH PROVO KE A N AC NEFORM RASH
1. Pallo r
(i ) Anaemi a I " " " J,id es and iod ides
(ii) Pale w it h d ista l b rown zo ne (rena l f ail u re) I A II III :u ll v u lsa nts
(i ii) Opaque w h ite na ils (hypoalb u m i naemi a) I Rl nrllids (g lucoco rt ico id, ana bo lic and a nd rog enic)
2. Redness ~ .,1.
"' I;IIid
(i) Po lycythaemia Il l ltllll l il l

(ii) CO po ison ing M ' '''III/lIIic: BASil

I D e rm atol og y De rmat o logy I _
CAU SES OF MOUTH ULCERATION TYPES OF PORPHYRIA
1. Aphthous u lcers 1. ACUTE INTERM ITIE NT PORPHYRIA
(i) Mino r
Classica l tr iad of da rk u rine, abdom i nal pain (sometimes w ith
(ii) Majo r
nausea or consti pation) and neu ropsych iatric sym pt oms. No
(iii) Herpetiform
skin invo lvemen t
2. Squamous carc inoma (often m isd iagnosed)
Au t osoma l dominant . Acute attacks provoked by drugs, e.g.
3. Infecti on, e.g . herpes simplex, syphi li s
o ral contraceptives, alcoho l, barbiturates, sul phonam ides,
4. Lichen p lanus
ch lorpropamide
5. Pemph igus or benign mucous membrane pem p higo id
6. Drugs, e.g . methotrexa t e
7. Trauma, e.g . from dent ures 2. PORPHYR IA CUTANEA TARDA
8. Beh eet's, Reite r's or Stevens-Johnson
Photosensiti vity and ski n frag ility. Usually develops in midd le-
aged pat ients w it h hepatic d isease, especially alcohol ic men.
Associated w it h i ncreased iron stores, and treated by
THREE SYSTEMIC DISEASES WHICH CAUSE venesect ion
CONJUNCTIVITIS WITH ULCERS OF THE MOUTH
AND GENITALIA
1. RE ITER'S SYNDROME CONDITIONS PREDISPOSING TO CANDIDIASIS
Clinical feat u res 1. Ski n t rauma and maceration, e.g . dentu res, perleche
(i) Non-specifi c uret hritis, haemat uria, steri le pyuria 2. Infancy, pregnancy, o ld age
(i i) Recu rren t con j unctivitis or uveitis 3. Systemic i ll ness
(ii i) Symmetrica l su bacute arth ritis, tenosynovit is, periost itis of (i ) Cachexia or malignancy
ankle, kn ee and spine (ii ) Imm u nosu ppression, e.g. AIDS
(iv) Circi nate balan it is (iii) Iron defic iency
(v) Buccal ulcers (iv) Endocrine d isorders
(vi ) Keratoderma blenorrhag ica (resem b les pustu lar pso riasis) Diabetes mell itus
Cushing's d isease
Addison's hypoadrena lism
Hypo parathyroi d ism
2. STEVENS-JOHNSON SYNDROME
4. Dr ugs
C lini cal f eatures (i) Broad spectrum anti b iotics
(i) Constitutional symptoms and high fever (ii ) Glucocort icoids
(ii) Con j unctivit is. corneal ulcers, uve itis (iii) Immunosup pressant s
(iii) Oral bu l lae and haemo rr hagic crusting of lips
(iv) Eryt hema mu lt iforme
(v) U rethritis, balan itis, vu lvo-vagini tis HIV AND AIDS
(vi) Bronc hitis, pneumonitis, or renal lesions Grou p 1- patient s are infected with HIV and seroco nvert, often
w ith a glandu lar feve r-like i ll ness and rash or neurologica l
symptoms
3. BEH~ET' S SYN DRO ME
Grou p II - HIV pos itive pat ients who appea r perfect ly well and
Clinical f eatures may remain so for many yea rs
(i) Bucca l and gen ita l aphthous ulce rs w it h a red areola
(ii) Con j unctivitis, uveitis or retinopath y Gro up II I - persistent general ized lymphadenopathy, PG L {i.e.
(i ii) Cuta neous pustules, dermal nodules lymphadenopathy due to reactive hyperplasia involving 2 o r more
(iv) CNS lesions: meningo-encephal itis. bra i n-stem syndromes sites ot her than the inguinal g lands, and pe rsisting for 3 or more
(v) Thromboph lebitis months}
,
_ I Dermat o lo gy

Group IV A - constitutiona l symptoms associated with HIV. CD4

cou nt is g reatly d ecreased. Clinica l featu res include f atigue. night-
sweats, lym phadenopathy, weigh t loss, fever, diarrhoea, etc.
13. Normal values
-
Gro u p IV B, C, D, and E are ro ughly eq uivalent to AIDS. That is the
development o f one or more A IDS indicato r diseases f or which
there is no o ther explanation and evidence of HIV infection such
as positive serology o r a low CD4 coun t. There may be
neuro logical disease (B), secondary infections (e), secondary
ca nce rs (D) or other conditions (E) The International System of Un it s (51 u nits) has now been w idely
introd uced in British laborat o ries i n place of the traditional
OPPORTUN ISTIC INFECTIONS Imperial Units, w hich were empi rical. Submultiples of 5 1 un its use
the fo llowing prefixes:
1. Viral, e.g . cytomega lovirus, d issem inated herpes simplex
2. Bacterial, e.g. atypica l mycobacter ia such as Mycobacteria Name Symbol
Factof
aviurn-i ntracellu la re com p lex
3. Funga l, e.g . systemic candid iasis, crypt ococcus "r' dad
4. Protozoal , e.g. Pneu m ocystis car ini i, toxoplasmosis "r' canl; ,d
,, ~ milli m
". m icro
MA LI GNANCY IN AIDS
, . Kaposi's sarcoma
",
10-"
nano
pico ,""
10-'5 Ic ml a f
2. lymphoma, especially ce rebra l
Even with $ 1 un its, values may vary in different laboratories
SKIN CHANGES ASSOCIATED WITH AIDS
1. Transient rash at ti me o f seroconversion CLINICAL CHEMISTRY
2. Skin infect ions - o hen extensive, exaggerated, or exotic Adu lt ref e r e n ce ranges - b lood
3. Kaposi's sarcoma
4 . Hairy leukoplak ia of tongue Acid phosphatase: to tal 4-11 iull
5. Many other d ermatoses are commoner or more severe than in prostatic < 4 iull
general population, e.g.: A lanine am ino-transferase (All) 5-45 lull
Sebor rhoeic dermatitis A lbumin 35-50 gIl
Psoriasis Alkaline phosp hatase 30-90 iujl
Drug er uptions Amylase < 300 iull
Xeroderma or pruritus Aspartate transaminase (AST ) '0-50 iul l
A lopecia B" ' 00-1000 ngll
Bicarbonate 24-30 mmo l/I
HUMAN MALIGNANCY CAUSED BY A VIRUS (PLUS Bi lir ubi n (total ) 3-17 ~mol/l
Corrected calci u m 2.2- 2.7 mmol/I"
A CO-PROMOTER)
Chloride 95-105 mmoll l
Virus Cho lesterol 3.6-6.7 mmol/I
,. Ca rc inoma cervix Hu man pap illoma v irus (HPV) (T he WHO
2. Hepatocellu lar cancer Hepatitis B recommends an
3. Nasopharyngeal cancer EB virus (in Ch inese) upper li mit of
4. Burkitt's lymphoma EB v irus (in malaria reg io ns of Africa) normal of 5.2
5. Kaposi's sarcoma HIV plus herpes virus 8 mmol/l fo r a
6. T cell lymphoma HTlV-, health ier
popu lation, except
in fema les over 60)
I

_ I N o r mal val u es N o rm a l v a lu es I _
Cortisol: 9 am 140-690 nmolJl M EAN CE LL VO LUME (MCV)
12 midnight 80-190 nmol/l
Adu lt s 80-98 f l(clJ )
C-reactive protei n (CRP) < 10 mg/I
Creatine kinase: tot al < 90 lul l
M B isoenzyme < 6% of t ota l M EAN CELL HA EM OGLOBIN (MCH )
Creatinine 60-120 ~molJl Adults 27- 32 pg
Ferriti n 12- 200 IJg/I
Folate : 3-15 lJg/1
Red cell folate 160-640 1-19/1 MEA N CORPUSCULAR HAEM OGLOBIN CONCENTRATION
Gamma-g lut amyl transpeptidase (gamma-GTI < 60 iull (MCHC)
Gl ucose (f asti ng) 3.6-5.8 mmolJl Ad u lts 31 - 35 g/dl (g.%)
Glycated haemoglobin (Hb A l e) 4.5-8%
Iron: ma le 14-32 IJ mol/l
fema le 10-29 IJmolll LEUKOCYTES
Magnes ium 0.75 ~ 1 . 0 mmolll A d u lts 4- 10 x 109 /1
Osmolality 280-290 mmol/kg Differential : Neutroph ils 2.5- 7.5 x 109/1
Phosp hate 0.8-1. 4 mmol/I (i. e. Lymphocytes 1.5- 3.5 x 109/1
ap prox imately half M onocyte s 0.2-0.8 x 10 9/1
of calcium) Eos inophi ls 0.04-0 .44 x 109/1
Potassium 3.6-5 .1 mmol/I Basoph ils 0- 0. 1 x 109/1
Prot ei n (t o l al ) 60-80 g/I wee
In Black A f rica n ad u lt s, total is 2.5- 9 x 109/1
Sod ium 135--145 mmol/l
T hyroxi ne (T4) : tota l 60-150 nmol(1
free 9-26 pmol/ l PLATELETS
Total iron bind ing capacity (TIBC) 45--72 IJ mol/1 150-400 x 109(1
Triglycerides (fasting) 0.3~1 . 7 mmol/I
Tri-iodothyron ine (T31 1 . 2~3 . 0 nmol/l
Ure a
RETICULOCYTES
2.5-6.6 mmol(1
U r ic acid 0. 1-0.4 mmolfl 0.2-2%

HAEMATOLOGY PLASMA VISCOSITY

HAE M OG LOB IN 1.50-1.72 cp
Men 13.0-18.0 g/dl Parallels ESR b ut is unaffect ed by age, sex or anaemia
Women 11.5-16.5 g/dl
ESR (WESTERGREN)
RED CE LL COUNT (RBC)
Men - upper l imit o f no rm a l = age in years .,. 2
Men 4.5- 6 .5 )( , 0 12/1 Women - up per li mit of norma l = (age in years + 10) .,. 2
Women 3.9-5.6 )( 1012/1
CLOTTING T IMES
HAEMATOCRIT (PCV)
APTT 35- 45 seconds
Men 0.40- 0.54 PT 10- 14 seconds
Women 0.36-0.47 INR 1
• Calcium is bou ... d to albuml ... a ... d it is import a... t to make sure t ha t you have
co rrected the ca lcillm w he ... t he album i ... is abnormal. He ... ce : BLOOD GASES (ARTERIAL )
Corre<:ted ca lcium _ [(40 gIl- albllmi ... IgII)) multiplied by 0.02] + mea sured calcium
Imm olm Oxygen 12- 15 kPa (90-l 00 mmHg)
- No r m a l values

Carbon d ioxide 4.5-6. 1 kPa (3 4- 46 mmHg)

pH 7.35-7 .45
Base excess ± 2 mmol/I
Index
URINE (ASSUMING A NORMAL DIET)
Specific g ravity 1.008-1.030
p H 4.8-7.5
Prot ein tess t han 0.3 g/I
Osmolality 350-1000 mosmol/kg
Abdomina l pa in , 64
Abnorm a l red c e lls, 15
CSF Ac id b a se ba lance. 134
Acne fo r m r as h, 157
Gl ucose, two-th ird s of blood g l ucose v al ue Ac rom ega ly. 11 3
Protei n, up t o 0.4 g/I A IDS
Lymph ocytes, u p to 4 cells/lJ l (i.e. 4 cells/m m3 ) <.lcfinitio n, 159
Open ing p ressure less than 210 mm of CSF gastro· in tc stina l.67
neuro log ica l. 105
sk in , 160
Addison 's di sease , 121
AurJ" ul ocyto s is, 79
A lkalo sis. 135
Alopec ia, 15 1
A"aemi a , 75, 76, 77
Allatomic a l d ea d space, 42
Ang ina , 29
I\n kvlnsing s pon d ylitis, 143
I\ortic incompetence . 2 4
I\"" ic sc lerosis, 24
I\, ,,ric stenos is, 24
Apex heat, 18
Apl.~sl ic a naemia, 79
A" hylhm ia
";' uses, 17
d,nlCal di a9nos is . 17
[CG.35
A' icria l pul se. 14
A,lhfulhl thy, 14 1
A,lInilis. fli tt ing. 144
A·.d l"s. 67
1\·.lh ma. 45
/1 111,,1 fib rill at ion. 16. 17.36
11.111,,1 11.,\Ier. 17,36
/I I< "I' hy. o pl ic. 94
fI"' " im mu n" d isease.
"'! I~n - sp ec i t i c. 116
1\ " ., "e vi~ t i un. 33
II ." b ehe. 143
11,.I' ~c t's syndrome. 158
Ihl" plym ents. 73
" ". I""c ns pulse. 15
111. .. 1.1", dysfunction. 139
-
BIe.. d ing, 84-$
Clinic al fea tur ..s, B6
gUlro-inleStinal. 6.
scr ...." ing lests, 86
Blindness. sudden. 96
Blis ter in g er uptions. 150
Blood-gas a nulysis, .3
Bloon gas . nor ma l va lues , 163
Blood t ra nsfusion. 87
a ra dycll rd ia .16
Brea lh so unds. 54
Bro nchia l ca nce r, 51
Bronc hilK:tlls is. 50
Bronc hit is. 44
Bul ba r palsy. 101
Bundle-bra r.c h block. 36
Calcu li, ' ''" III. 138
Candidiasis, pred isposing
condilions, 159
Ca rci noma 01 bronchus, 5 1
Carcinoma. gaSl riC. 53
Cardiac a~ is, 33
Ca rdiac fll ilur .., 26
CllrdillC murmurs, 20
Cardillc rOllllion. 34
Cardiac shadow. 60
Case presentation, 8
Carabe llar leSion, 100
Cereb ral infarclioll, 101
Ce re bra l-spina l pressure. 96, 164
Chest leads. 34
CheSI moveme nt . 54
Chest pa in. 29
Ches t x-ray. 55
Cheyne- S tokes brea thing. 44
Choles la s is. 73
Ciga r.. tt .. sm oking. 45
Ci rrhosis
ca ulie6. 7 1
clin ical fa atu res. 72
defin ition. 1 1
Clin ical "~lI m i nat ion. 3
Clu bbing, 46
 ..
II1II ______________________________________~
IL'_n_de_X ~________________________
'nd.~
x l ..

COAD.45 p le ura l, 54, 57 Goitre, 116 Ileit is, 70

Coag u lation Electr ocard iog r am IECG ) Graves' disease, 11 6, 11 7 Ileus, 58
delects, 84 arrh yth mias, 35 Gynaecomast ia, 124 Infa rction
dissem in ated intra vascul ar, 85 COr pulmonale, 40 cerebral, 101
f actors, 84 d igita lis e ffects, 39 myocard ial, 29, 38
Coa rction of aorta. 62 heart b lock, 36 Hae m atology, nor m a l va lues, 162 Innocent murm u rs, 22
Coe liac synd rome , 67 h yperkalaemi a, 39 Haem atoma Int erstitia l lun g disease, 50
Co litis, ulce rat ive, 69 h ypokalae m ia, 39 e><tradu r al, 102 Intestina l obstr uct ion, 68
Co ll apse of lung mi tra l ste n os is, 23 su bd u r al. 102 Intracran ia l neop lasms, 98
causes, 49 myocard ia l ischa emia, 38 , 39 Haematuria, 136 Intracran ial pressure
radiograp h, 56 n or m al,33 Haomophi li a, 84 ca u ses, 96
sig ns, 54 p e ricardit is, 40 Haemolysis, 77 cl inica l featu res, 99
Co ll apsing pul se. 14 p ulm on ary embo lism , 40 Haem optysis, 46 Intravascu lar co agul at ion , 85
Coma, 102 r eading, 40 Hard kno b bly live r, 71 Involu ntary movements, 107
Comp liance, 43 ve rltricu lar hyp ertrop hy, 37, 38 Hoart b lock Itch ,152
COrlgenit a l he art disease, 25 Em p h ysema ca uses, 17
COr>junctiv itis, 158 dcfin ition,44 classi f ica tion, 17, 37
Ja un dice, 72
COflso lidation rad iograph, 58 ECG,36
Jug u lar venous pu lse, 13
rad iograph, 55 signs, 54 Hea rt fail u re, 26
s ig ns, 54 Em pyema, 48 Hea<1 soun ds, 18, 19
Hepat ic fa ilu re, 72 Ketoacidaem ic com a, 122
Cor pu lmona le, 28, 40 Eos inop hi lia, 80
Kidrley, large , 133
Cord comp ressio n. 108 Epilepsy, 103, 104 Hepatitis, 73
Ku ss m aul 's sig n , 14
Cortica l loca li.at ion, 99 Erythem a, 153 Hopatom e9a ly, 70
Ku ssmaul's b reath ing, 44
Cra n ia l n e , ves, 91 Erythema mu ltiforme, 154 Hepato· sp lenomega ly,71
Cro hn's disease, 70 Erythema nodosum, 154 Hirsutism, 151
History-taking, 4 l eg ulcer, 150
Cush ing 's syndrom e, 119 Erythoder ma , 154
HIV in fect io n , 159 l e ukaemi as , 83
Cyanosis, 13 Essay question s, 2
Hodgkin 's disease, 82 l eu kocytos is, 79
Examinat ion, 6, 20
Horne r's sy ndrome, 95 l eu koderma, 153
Epirator y f low rate, 42
Dark u r in e, 137 Hot j oint. 144 l eu kopen ia, 79
E><t radura l haem ato m a, 102
Dead space, 42 Hydropn e u mothorax, 57 l iver, enl arged, 70
Ext rasysto les, 16, 17
Dea fness. 97 Hypercalcaem ia, 127 loba r p n eumoni a, 48
Exudate , p leura l, 49
Dement ia. 104 Hyperdyna mic circu lat ion, 15 Loca l ization, neuro logica l, 99
Derm ato mes, 109 Hypereos in oph il ia, 80 'l ong' case, 3-9
Dexamet hasone sup p ression, 120 Fac ial flushin g, 153 l u mbar backach e, 143
Hypc rka laem ia,39
Diabetes mell itus, 122 Facia l pa lsy, 97 lung compl iance, 43
Hype rli p idaemia, 155
Fa ll ors tetralogy, 25 Lu ng disease, sign s, 54
Diabet ic com a. 122 Hype rparath yro idism, 118
Diabetic retinopat hy, 94 Fanconi syn drome, 134 l u ng opacity, 58
Hype rp igm entat io n , 152
Diffu se a irways obstruction, 45 FEV, 41 lUrl9 vol um es, 41
Hype<1en sion
Diff usio n defects. 42 Fibros is of lun g, 54 Lymphaderlopath y
po rta l, 72
'F litting' arthrit is, 144 causes, 82
Digita lis, 39 r adio logy of, 61
Dissem in ated coag u lat io n , 85 Flu shi ng, 153 h ilar,60
syste m ic. 28
Dissem in ated sclerosis, 98 Flutter, 17, 36 p er sistent gen era li zed, 159
Hyperte ns ive ret inopathy, 94
Fo late def iciency, 78 lymphocytic leu kae mia , 83
Diverticulitis, 68 Hypert hyro idis m , 116
Drug eru pt ion s, 157 Forced v ita l capacity, 41
H yperu r icaem ia, 145
Duodena l ul cer, 65 Hypoad rena lis m, 121 Macrocyt ic anaem ia, 69, 77
Dysarthria, 100 Ga its, 106 Hy poc~lcaem i a, 127 Major case, 3-9
Dy sph ag ia, 63 Ga lactorrhoea, 125 Hypog lycaem ic coma, 122 Malabsorpti on , 66
Dysph asia, 100 Hy pokalae mi a,39 Mal igna n cy, skin ch anges, 156
Ga llstones, 74
Dysph onia, 100 Ga llop r hythm, 20 Hyponat raemia, 135 Maligna nt m e lanom a, 155
Dyspn oea, 44 Gast r ic cancer, 65 Hypopa rath yroid ism, 118 M ed iastin a l shi ft, 54
Gastr ic ul cer, 65 Hypopituita rism, 1 14 M icrocytic anaem ia, 76
Ectop ic ven tricul ar bea ts, 17 Gastro-intest inal b lee ding, 64 Hypothyr oidism, 115 M ictu rition, 139
Eczema, 149 Glom erul on eph r it is, 132 Hyp oven ti lation , 43 M in or cases, 9-10
Effu siorl Gloss it is, 63 Hypoxaem ia,43 M inut e ventilat io n , 4 1
pe r icard ia l, 62 Glu cocort ico ids, 120 Hypox ia, 43 Mitral incompetence, 23
_ '---I'n_do'_ _ _ _ _ __ _--'
Mitral stenosis. 22. 6 1
Mo b ill block, 37
Mo le, 155
Molor neurone lesions, 9 1
Motor syste m. 90
M ou th ulcers, 158
Mulliple-choice questions, 2
M uUiple sclerosis. 98
Murmurs
ausc ultation o f. 20
differen tial diagnosis. 21
innocen t, 22
Myelo id leukaemia. 83
Mye lomatosis, 83
M yoca rd ial in farct io n
compl ica tions, 29
elec troca rd iogram, 38
Myoca rd ial ischaemia, 29
Myopathy. 1 12
Myo tomes. log
N a ils
in skin disease, 157
in systemic d isease, ISS
Necro l iling vllscull'is. 145
Neop lasm
j br onch ial. 5 1
gastric. 65
intracran ial. 98
I
Neph rolic syndro me, 133
Neuritis, optic. 94
Neu ro path y. 111
Neutropen ia, 79
I Neutroph ilia, 79
No rmal values, 161- 164
Obstr uct ion of int estine. 68
Obstructive ai rways d isease, 45
Oculomo to r palsy. 95
Oedema, pulmonary, SO, 57
Opac ity in lung, sa
Opport u n is tic in fecti ons, 160
Opt ic a trophy, 9 4
n e uriti s, 94
pa th way, 92
Oral con traceptives, 126
Oral exa m in ation I'vivlI'). 10
Organ-spedfic a uto im m u ne
d isease, 1 16
Os teoarthros is, H I , 142
Ostoomalacia, 126
Ostooporosis, 126
Oxygen t herapy, 44
Paget's dise ase, 127
Pain
abdominal. 64
chest 29
Pa llo r, 153
Palmar erythema, 153
PAN, 146
Pancreatitis, 74
Pancytopenia, 79
Papilloedema, 96
Papillitis, 96
Pa ralytic ileus, 68
Paraple9 ia, 110
Parathy roids, 1 18
Parkin sonism, loti
Paroxysma l t ac h yca rdia, 17
Pea k flow, 42
Pept ic u lcer, 65
Pe rcussion , 54
Per icardia l eff(lsion, 62
Pe ricard it is, 3D, 40
Pe rip he ra l n eu ropathy, 111
Pernicious a n aemi a, 78
Photosensitiv ity, 150
PGl, 159
Pigmenta tion, 152
Pigmented papules, 155
P ituita ry, 113
Plate lets, 8 4
Ple ura l effusio n
c a uses, 49
radio graph, 55
signs, 54
Pne umonia, 47
Pneumococcal p neumo n ia, 48
Pneumothorax, 57
Polya rte ritis nodosa, 146
Polyarthropathy, 141
Po lycythaem ia , 80
Po lyneuropathy, 1 11
Po lyu ria, 135
Porphyria, 159
Portal hyperten sion, 72
Potassi um depletio n , 135
Pre m at ure b e ats, 16, 17
Proteinur ia, 136
Pr ur itus, 152
Pse udo-b u lb a r pa lsy, 108
Psori asis, 149
Ptosis , 96
Pu lmonary collapse , 49, 5 4, 56
Pu lmon a ry embolis m, 40
Pu lm onary e osinop h ili a, 80
Pulmonary oede m a
causes, 50
'----_ _ __
Pulm on ary oedema Conr'd
rad iograph, 57
Pulmon ary TB, 52
Pulse
arterial,1 4
irre9u la r, 17
venous, 13
Pu ls u s paradoxus, 15
Pyoderma gang rerlOSum, 155
Pyuria, 137
Radiolo gy
cardiac shadow, 60
coa rcta tio n, 62
co ll apse, 56
emphysem a, 58
h il a r ly mph aden o p athy, 60
hydropneu m othorax, 57
hype rte n s ion, 61
m il iary dens it ies, 59
mit ral stenos is , 62
mu lt ipl e sh a d ows, 59
perica rd ia l effus ion, 62
p leu ra l effus ion, 55, 57
p ulmona ry oedema , 57
sing le shado w, 58
who le lung opa city, 55
Rash
circumscribed , 153
widesp read, 154
H"ynaud 's phe nomenon, 147
RBC abnorm a lities, 75
nellexes,110
Re g iona l ileitis, 70
Rei ter's d ise ase , 158
Renal
clearance, 140
disease, p rese nta tio n, 129
e n largeme nt, 133
fa il ure, 129, 130
sto nes, 138
tubu lar dysfunct ion, 133
Residu a l volum e, 42
Re tent io n o f u rine, 139
Revision, 1
Rheu ma tic feve r, 31
Rheuma toi d art h riti s, 14 1, 142
Rinne's test , 98
Root lesion s , 109
Rotation of heart , 3 4
Silrco idosis, 53
Sca ly rash es, 153, 15(
Sensory syst em , 89
Seronegative spondyloarthr itis, 1 (J
_ _ _ ___'nd_o, 1 _
S had ow
single large, sa
mu lt iple, 59
w idespread, 59
Shock. 30
'Short' cases, 9-10
S inu s e rr hythmia, 17
b radycardia, 16
tachycardia. 15
S~ i n ,n systemic malignancy, 156
Smo~ i ng , 45
Spee<:h dafocts. 100
Spi rometry, ' 1
Sple n o m egaly, 81
SpondyloaM hr it is , 142
Sq u ints, 95
S tan dard leads, 33
Sta tur e, short, 123
'Ster ile ' pyuria, 137
Sterokl th e rapy, ha 2a rd s of, 120
Ste vens-Jo h n so n s yndrome , 158
S to nes, re nal, 138, 139
S ub araChn o id ha emo rrhage, 10 1
S ubdurul haematoma , 102
Supraventricul a r tnc hycard ia, 15, 35
Syncope, 103
Svring obulbi a, 107
Sy ringomye lia, 107
Svswm review, 6
Systemic IUPU8 eryth ematosus. 146
TachYClirdia, 15, 16, 17, 35
Terget celiS, 76
Thr ills, 18
Thr ombocytopen ia, 8(
Thrombolytic therapy, 3 1
ThrombosiS,
cerebra l, 101
ven o u s. 87
Thyroid carc inoma, 116
Th yroto~icosis, 116, 1 17
Transfer lac tor, 42
Tra n s u date, pleural, 49
Triciisp id incompetence, 25
Tripl e rhyth m, 20
Tuberc ul os is , 52, 53
Tub u lar ac idosis, 134
Tubu lar d ys fu nct io n, 133
Ulcer
leg, 150
mouth,l58
pept ic, 65
Ulcerat ive colitis , 69
_ ] lndeX
L -_ _ _ _ _ _ _ _ _ _ _ _ _ __ __ _ _ _ _ __ _ _ _

~
Uraemia. 130. 131 stra in, 38
Ur in e, dark, 137 ta chycard ia , 35
Urina ry ca lculi, 138 Vesse l defects, 85
Urinary Iract obstructio n, 137 Viral hepatitis. 7J
Vi ral pneumonia, 41
Vascu litis, 145 Visu a l lield d e fects, 92, 93
Venou. Vital capacity, 4 1
pulse, 13 Vitamin Bll deficiency. 78
thrombos is, 87 'Viva' examination, 10
ulcer. 150
Ventr icula r W ebe r's test, 98
ectopies, 17 Wenkcbach phenomenon, 37
fai lure, 26, 27 White skin patches. 10
fibrill ation. 37
h ypertro phy. 27, 37, 38 Xa nt homa , 15 5

I
l