aids to undergraduate medicine (6th ed)
TRANSCRIPT
Other title in the Aids series
Burton Aids to Postgraduate Medicine 6E Burton Aids to Undergraduate MedIcine 6f Dixon A ids to Pathologv 4E Habel Aids to Paedi;:u r;C$ 3E Habel Aids to Paediatrics for Undergraduates 2E Hayes and MacWaher Aids to Clinical Examination 2E Mead Aids to General Practice 3E Mowschen$On Aids to Undcr ll r "du~w Surgery.E Rogers and Spec:t or Aids 10 Clinical Pharmacology and Therapeuti<:s 3E Ro gers and SpKtor Aids to PharmacologV 3E Scratcherd Aids to Phy~iologV 3E Sinclai r and Webb Aids to Unool g,,,tJuale Obswlrics and Gvnaecology 2E
For Churchill Livings/one:
PublislJer: Laurence Hunter Projoct Edilor: Barbara Simmons Copy Editor: Ruth SWlln Proje<;t Controller: Noncv Arnon DtJsign Direction: Erik Big land
Aids to Undergraduate Medicine
J. L. Burton MD SSe FACP
Professor o f Dermatology Bristol Royal Inf irmary, Bristo l
B. J . L. Burton MA MRCP
Sen io r House Officer The Nationa l Hospital fo r Neurology and Neurosurge ry, London
SIXTH EDITION
./)) CHURCH ILL _ LIVINGSTO NE
EDINBURGH LONDON MADRID MELBOURNE NEW YORK SAN FRANCISCO AND TOKYO 1997
CHURCHILL LIVINGSTONE An imprinl 01 Elsevier SCfence Limited
C Longman Group Umited 1973 e Longman Group UK Limited 1990 o Pearson Professionalt997 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_
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First edition 1973 Second edition 1976 Third edition 1980 Fourth edition 1984 Fifth editi on t 990 Sixth edition 1997
Reprinted 2000 Reprinted 2002
tSBN 0 443 05692 7
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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 care to ensure lhat the information glyen in this le~t Is accurate 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 legislatforl tmd standards ot practice
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Preface
This book is primarily intended to provide a compact aid to revision for candidates taking the final MB medicine examinati on, though ca ndidates for other med ical examinations may also fi nd it he lpful.
Many medica l educators condemn learning by rote. Nevertheless, candidates in medical examinations st ill f ind it necessary to reta in a form idable number of facts and we believe that t he use of 'skeleton' lists as an adjunct to com prehensive text books can encou rage an orderly approach to the subject as well as provide a bas is for expansion in answers to examinat ion q uest ions .
It is impossible to ach ieve comprehensive cove rage in a book of th is size, but we have tr ied to select information w hich is worth remembering for use either in the assessment of common clin ica l sit uat ions or in reply to some of the more commonly asked examinat ion questions. Many of the lists we have included are not read ily available in the usual undergraduate textbooks, and for some important examination top ics we have provided lists w hich are more detailed t han those given in m ost undergraduate textbooks.
This sixth edition has been completely updated and a new feature is the introduction of mnemonics. The chapter on exam ination technique has also been expanded.
Bristol, 1997 l ondon, 1997
J.l.B. B.J.l.B.
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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
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1. Hints on the final MB medicine examination
Examinations are formidable even to the best prepared, for the greatest fool may ask more than the wisest man can answer.
Charles C Colton 1820. Lacon I: 322 The final MB exam ination is intended to p revent the qual ification of incom petent doctors, and the exam iners have t he duty o f ensu ring that every successful candidate is safe to be 'licensed to heal'. They requ ire to kn ow t hat: , . Yo u have a sound knowledge of the basic princip les of
medicine and a commo n sense appro ach to the subject 2. You have had pract ical experience o n the wa rds and ca n detect
and interp ret physica l signs 3. You can prescribe safely, i.e. yo u know the mode of
admin istration and approximate dosage of important drugs, and you know thei r ma in actions and serious side-effects
4. You can recognize and treat medical em ergencies competent ly Any ca ndidate who satisfies the examiners on these points is
fa i rly certai n to pass the examination, but bear in m ind the lugubrious corolla ry that if the examiners demonst rate a deficiency in t hese abili t ies, failure may follow.
REVISION An im portant function o f rev ision is to ident ify and e lim inate 'blind spots' . Nobody can know everyth ing, but you should aim to be completely ignorant about noth ing, and the commoner t he top ic, the more you shou ld know about it . A good way to cover top ics w h ich are likely to occur in the examination is to see as many cases on the wards as possible during your training and to 'read around' them. Most good physicians base their knowledge on cases they have seen personally, and it is qu ite a good idea as a student to keep a b rief record of the pat ients you have seen as an aid to later rev ision.
A sound know ledge o f medic ine is obvi ously essential, but rapid reca ll of that knowledge in the exam is eq ually important. Instead of read ing part of the textbooks in deta il just before the exam, it's better to refresh your memory of the who le f ield, even if o nly in a superf icial w ay. This wil l be faci litated if your lect ure notes are all kept on loose-leaf paper of a standard size so that your knowledge from the various subspecialities can be integrated to avoid confusion and duplication of efforl.
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- Hints on t he f ina l M B medicine e:ll:amination
ESSAY QUESTIONS
The purpose of an essay quest ion is to discover w hether you can assemble your knowledge of a subject, select appropriate facts and op inions, arrange them in an order ly manner and then express yourself w ith clarity and good sty le. You should ask yourself w hat the examiners are trying to test in a particu la r q uestion. They often have a fai rly rig id m arking code, aw arding m arks for each of certain predeterm ined points that are made, and no extra marks are awarded for even the most fascinating d ig ressions. Candidates rarely fai l final MB on t he essay q uestions, but those who do are usually fa iled for not answeri ng the questions that we re asked .
An ot her cause for fa i lu re is m isjudgement o f the t ime all otted to each question . You should apply the ' law of d im inish ing ret urns' as it applies to essay questions - the f irst 40% for any questi on is easy, the next 30% is much harder, the next 20% is v irtually imposs ible and the f inal 10% is impossib le. Cons istency in every quest ion should be your aim . You shou ld not, however, wa ste too m uch t ime on a q uestion wh ich you cannot answer. A blank simply scores no marks but an effu sion of rubbish w ill prejud ice th e exa miner aga inst you.
W here possible, quest ions shou ld be answ ered in terms of distu rbance of phys io log y. This wi ll dem onst rate yo ur knowledge of basic principles and also help you to arrange yo ur answer in an orderly and rationa l manner.
Many candidates spend hours trying to predict questions by studying old papers. The syllabus is too big for this to be profi table in f inal MS, but it's worth checki ng the type of quest ions you' ll be asked and spending time on any top ics on w hich you are ignoran!.
MULTIPLE-CHOICE QUESTIONS (MCQs)
You shou ld fami liar ize yourself wi th the type of quest ion favou red by you r own med ical school. Each quest ion consists usually of f ive statements w hi ch are either t rue or fa lse and you are requ ired to g ive an answer o f t rue, false or 'do n't know' for each pa rt. Typ ically a correct answer sco res p lus one, a w rong an swer scores m inus one and 'don't kn ow' sco res noth ing . Exam papers o ften recom mend answ erin g on ly the questions you are su re of but if you d id th is you would probably end up on ly answering about 5% of the quest ions and fail ing. It is in the exam iners' interest that peop le don 't guess because the exam will then correct ly select out the poor cand idates; however, if all the poo r ca ndidates guess all the q uesti ons, some of t hem w ill pass w ho wouldn't otherwise have done so. It fo l lows that t here is an advantage to those candidates who answer more questi ons tha n others. If you f ind this ha rd to be lieve then t ry answering saine practice papers,
Hints o n t he fi n a l MB m e dic ine e xa min ation
leaving questions out that you 3[e unsure of and then repeati ng the paper answ ering all the questions as true or fa lse. Most cand idates wil l improve thei r score by between 1% and 10%. The important t hing to remem ber is that you can fail by answering too few q uestions but you ca n't fa il by answering 100 many, although you may still fail by being too ignorant. Rem ember 100 that the words 'always' and ' never' rarely apply to medicine and respo nses w hich contain them are un likely to be true.
A not her problem arises w hen a student has personally seen an unusual case which is t he 'exception that proves the rule' and therefore has difficu lty in answering an apparent ly simple question. Th is is a d ifficu lt d ilemma, but in general it 's pro bably best to ignore such personally-w itnessed rar ities unless yo u have seen t hem mentioned in standa rd textbooks.
Shortage of t ime is rarely a problem in Mea exams and therefore answers can be checked. In our experience however 'second t houghts' in Mea exams are rarely an im provement and we t hink it is preferable to w ork steadi ly through th e pape r once on ly, but noti ng any questio n which w ill requ ire later thought .
THE CLINICAL EXAMINATION
Exam iners right ly lay great stress on 'the cl in ica l' whe n assessing a candidate and adequate preparation for t h is pa rt of the examinat ion is v ital. The major skill requi red is o f course the abitity to elici t physical signs correctly but other factors such as f luency in case presentat ion and cl inical judgement in the interpretation of the signs elici ted are also important. The best way to improve your style in ' the cli nical' is to obtain regu la r coaching from a critical senior colleague w ho w i ll point out your fau lts. Failing th is, you should make arrangements with a fe llow student for each to see the other's cases under examinat io n conditions. To obtain the maximu m benefit you should of course 'g ril l' each other on the fi ndings immediately afterwards. Th is met hod has the advantage t hat you will lea rn to see things from the examine r's point of v iew and you will qu ickly come to appreciate those bad habits w hich common ly cause annoyance to examiners.
Desp ite cu rrent t rends, sa rtorial and tonso ri al conservat ism is recommended, as bot h patients and examiners are likely to be m idd le-aged if not actu ally sen ile.
THE MAJOR (' LONG') CASE
HISTORY-TAKING
A successful history demands just as much skill as t he physical examination, and w hi le two experienced cl inicians will usually ag ree o n the physical signs, t he histo ries they obta in may be q uite
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- Hin t s on t h e fin a l MB medicine exam in a t io n
different. The examiners realize this and therefore attach more importance to the object ive physica l f indings in assessing a candidate. An accurate h istory is important for diagnosis, however, part icu lar ly w ith cardio log ica l or neurolog ical patients, w ho are frequently used as ' long' cases because of thei r stab le physical signs. There is more to t he assessment of a cardio logical case than merely hear ing and interpreting the m urm urs, w h ich, contrary to popular belief, are usually 'loud and clear' in examination cases. II is v itally important to obtai n the fullest possib le detai ls of previous ill nesses, especially w ith regard 10 the duration, symptoms and treatment of any possib le bouts of rheumat ic fever, chorea, tonsil lit is, S8E, etc., and in female patients you m ust obta in full detai ls of previous pregnancies. Ma le patients can often g ive the results of previous medical g rading pr io r to service in t he armed forces, and many pat ients can give the date and resu lt of previous chest X- rays. Detai ls of t he patient's past and present exercise tolerance are o f course essent ial, and you should ascerta in from the pati ent exact ly how much physica l effo rt h is present work entails. In neurology cases the mode of onset (ove r minutes, days or weeks), length of history and subsequent course (static, steadi ly progressive or remitting) w i ll usually suggest the type of patho logica l lesion present (e.g. vasc u lar, inflammatory, neoplast ic or degenerat ive). and the physical sig ns w i ll then confi rm the anatomical site o f the lesion.
W hen ta king a h istory in exams it is advisable fi rst to list all the pat ient's symptoms br ief ly, to d iscover the type of illness and the systems involved. The symptoms should then be arranged chronologically and full detai ls about each should be obtained . Thus if the patient complains of pain you should determ ine: 1. The site, with the direction a f radiat ion 2. Its nature and severi ty 3. Its duration and periodicity 4. Any aggravating or relieving factors 5. Any associated features
Think abou t the possible d iagnosis from the outset and modify your q uestions acco rd ing ly.
Never accept terms such as rheumat ism and vert igo at thei r face va lue, but ask the pat ient what he means by t his. You m ay be su rprised, as was th e GP who gave severa l prescr ipti ons for bigger and bette r laxatives for an old dear who was 'cost ive', unti l he di scove red she thoug ht this was a synonym fo r d iarrhoea.
Cons iderable persistence may be needed to prevent t he patient dig ress ing. W ith garru lous patients t he previous medica l and fam ily histories are part icularly d ifficu lt to obta in. In such cases stick to essent ials and don't hes itate to ask lead ing q uest ions in o rder to obta in t he necessary information.
The history w ill all ow you to assess the pat ient's mood, intellect, speech and memory, and you should of cou rse observe t he pat ient closely dur ing the history for signs of dyspnoea, t remor,
Hints on the fina l M B m edic ine examinatio n
etc. It is also a good idea on f irst meet ing the patient to ask yourself 'Could t his be myxoedema?', as th is d iagnosis is otherwise easily missed.
Essential paints o f h istory-taking f o r the lo ng case • Name • Age • Occupation • W hen was the patient last completely well? • Presenting complaint and very thorough h istory of present 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 complications such as eryt hema nodosum, pyode rma gangrenosum, eye invo lvement, joint problem s, liver involvement, etc.
• Past medical history, part icu larly operations or previous hospital admiss ions . - As k 'H ave you ever had - high Blood pressu re, heart attack
(M I), J aundice, T ubercu los is, Rheumatic fever, A sthma, D iabetes, Epilepsy, St roke, Clots (DVT), pept ic ulcer (D uodena l ulcer )? (Mnemon ic = '8MJ TRADES CD')
- Also ask about sickle cell anaemia in all b lack pat ients and thalassaemia in all Med iterranean patients.
• Drug history - Ask w hy patients are on the med icat ion they ta ke. ~ Always ask about al lergies, particularly to penici llin.
• Famify history - Remember to ask about sibl ings as well as parents,
grandparents and ch ild ren. (Autosomal recessive condit ions are un likely to have occurred in previous generations but 'One of my three sisters has cystic fi b rosis' p rovides a useful clue if you r pat ient's present ing complaint is recurrent chest infections since ch ildhood).
• Social history - Ask if the pat ient has eve r smoked and if so for how lo ng and
w hy did they give up? ' I gave up when they found my lung cancer doc. Oops, I wasn't supposed to tell you that !'
- Ask about alcohol consum ption. Get deta ils of how m uch and how often rather than accepting a g l ib answer such as 'on ly socially'.
- Who is at home and are they able 10 look after t he patient? - Does the pati ent have a district nurse, social worker, mea ls
on wheels, telephone, stairs between h im and the toi let? Who gets t he shopping, does the housework, and can the patient w ash h imself?
- Full occupat ional history, particu larl y for respi ratory cases (,I spent two years remov ing asbestos from ships but that w as 40 years ago').
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Hints on the f ina l M B medicine e llam i nat ion
- 00 you have pets (particu larly sick parrots)? W hat are your hobbies (e.g. pigeon fancier)?
S y s t e m review This is im portant as it shou ld bring out any important information that the patient m ay have forgotten to tell you (,Oh, sorry, I thought you kn ew about the b lood I'm co ughing up. After all t hat's the real reason I'm here although as I w as tell ing you my biggest problem is this terrible itch I get o n m y head every t ime I pass water')' A lways ask about: • Appetite. • Weight loss - how much, over how long? • Respiratory system. Shortness of breath (and when), wheeze,
cough (productive?), haemoptysis (how much?), exercise tolerance (i n m etres or num ber of stai rs).
.. Cardiovascular system. Chest pain, palpitat ions (can you tap out th e rhyth m?), postural hypotension , orthopnoea, how m any pi ll ows do you sleep w it h, do you w ake short of breath (PND or asth ma), swelli ng of ankles.
.. A bdominal system. Any dysphagia, refl ux, indigest io n, vomiti ng, haematemesis, abdominal pain? Bowel habit and any recent change? Diarrhoea (if so, how often and descr ibe it) , constipat ion, m elaena, blood m ixed in w ith stool or only on paper. Genitourinary - Nocturia or frequency (consider DM or UTI), incontinence,
haemat uria, o ffensive sme ll , poor st ream, hesitancy, post m icturit io n dr ibbling.
- Previous preg nancies, heavy periods (consider anaemia and thyroid disorders), intermenstrua l b leeding , recurrent abortions (anti phospholip id syndrome), premature menopause (co nsider oth er o rgan-specific autoimmune diseases).
• Nervous system . Fits, faints, visual disturbance, severe headaches, paraesthesiae. sensory loss, weakness, coordination.
• General. Skin problems, arthrit is.
EXAMINATION
The abil ity to elicit and interpret physical sig ns is of course essent ial and considerable practice on the w ards is req ui red to achieve this ski l l. A combinatio n o f speed and tho roughness is requi red for exam pu rposes, and t h is applies especiall y to pulmo nary percussion, cardiac auscultat ion and examinatio n o f t he e NS. In auscultat ion in particu lar, f i rst impressio ns are o ften right and prolo nged listening may cause confusion. It's usually more convenient to exam ine a pat ien t from the head downwards, rather than by system s, and regular practice w ith an unvarying
H ints on t he f ina l M B m edic ine exam i nat io n
rout ine is required if no major points are to be missed. We cannot stress too st rongly t hat people fail their long case not th rough missin g a m inor abnormal ity, but because in their haste they have fa iled to look for a sign wh ich is in fact present in a gross fo rm . Obvious signs such as a la rge breast m ass, hypertension, marked tracheal sh ift, gross optic atro phy, unilate ral deafness, seve re intent ion t rem or, massive splenomega ly, etc. , ca n easily be missed unless t he appropriate exam ination is performed. Such signs may not alw ays be suspected to be present from the history, altho ug h it is o f course advisable to pay special attention to the systems w here you expect positive findings. Thus it would be foolish to accept the absence of a m itral m urmur too readily in a pat ient w ith dyspnoea, haemoptysis, and a ma lar f lush, or to be sat isf ied w ith perfunctory palpat ion for splenomegaly in a patient wit h suspected leukaemia.
Equivocal fi ndings can usually be safely ignored unless t hey are relevant to the symptoms or probab le diagn osis. For exam ple it is best not to waste m uch t ime over minor degrees of ref lex inequal ity, slight facial asy mmetry, impaired vib ration sense, etc., unless your patient has a neurological d isorder or a disease w hich causes a neuropat hy. Other com mon causes of rea l or imag ined eq uivocation w hich can often be ignored incl ude slight b ilateral pallor or b lurring of the opt ic disc, slight tracheal or apical disp lacement, soft m urmurs and slight inequality of breath sounds. Remem ber that small differences in percussion are easily imagined and bronch ial breath ing is uncommon. If a finding is dubious and it doesn't f it, forget it.
For the major case pract ise working well w ith in th e set t im e lim it, so t hat you have t ime left at the end to recheck yo ur posit ive f ind ings and to look aga in for any associated signs w hich you m ight expect to be present in t hat particu lar case. Remember that m istakes in the h istory m ay occasiona ll y be explain ed away as being d ue to the pat ient's poor memo ry, but m istakes in the physical signs are ent irely the respo nsibility of the ca ndidate and can not be condoned.
On completion of the examination you should carefully consider the possible diagnoses and then clarify any doubtful points in the h istory. You shou ld also amplify the history regarding any unexpected physica l s igns you have discovered.
Quite apa rt from any human itarian considerations it is most important to try to establish a good rapport wi th you r pat ient. Many of t he pat ients used in the examination are ch ron ic cases w ith more or less stable phYSical signs. Since such pat ients are in freq uent demand for teaching pu rposes they usually have a long experience of yo ung doctors and thei r difficu lti es and they are often w ell aw are wh ich of thei r own physical signs are commonly m issed. Occasionall y such patients will spontaneously volunteer valuable informatio n w ith regard to thei r d iagnosis or phYSical signs, but in o ther cases a judic iously w orded question at the end
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- Hint s on t he fi na l MB me dic ine e xam ina t io n
of your examination such as 'Is there anything e lse you think I ought to know?' w il l often prove rewarding. Other usefu l clues may be obtained by asking the pat ient to describe the invest igations and treatme nt he has had, and by asking him what he bel ieves to be the cause of his symptoms. 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 for misleading answers however. and these should be ig nored if t hey do not talty with your own assessment of the history and physical signs. These questions should be left unti l the end as otherwise the replies will prejudice your j udgement. Another point to consider is that these questions sometimes provoke in the patient an uncooperative attitude of 'That's for me to know and you to find out' which can make subsequent h istory-taking difficu lt.
Before the examiner arrives you shou ld reconsider your d iagnos is and ask yo urself 'Could this be anyth ing else?' Remember that elderly patients o ften have mu lt ip le pathology, and remember too that although rare diseases occur rarely, thei r prevalence in examinations is great ly increased. If the diagnosis is uncertain prepare a l ist of d ifferent diagnoses and consider what investigations you would pe rform, remembering 10 mention simple tests such as ESA and chest radiograph before more expensive and possibly dangerous procedures. In most final MB exams, sim ple urine 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 t ime, you should consider how you wou ld answer probable quest ions regarding management and prognosis, and in appropriate cases you should t ry to anticipate what the ECG and radiographs might show.
CASE PRESENTATION
There is quite an art in presenting a case concisely and clearly. The examiners have no t ime to waste, and hesitant and longw inded presentations are tedious, so you shou ld edit the history, emphasizing important points, leaving out irrelevant detail and giving negatives only if they are important. If the case is straightforward the presentation of the history and examination shou ld form a cohesive account leading to a confident diagnosis. In such cases try to make your assessment as full as you ca n and say whether the condition in you r patient is acute or chronic, m ild or severe, simp le or w ith complications. In more difficul t cases wi th confli ct ing evidence or doubtful signs you wi ll have more reservations, but don't hedge all the time as this ir ritates examiners and does noth ing to conceal your ignorance. Try to make up your m ind on the basis of probabi lit ies. Doctors often have to act on the basis of equivocal evidence and the examiners want to see whether you can ta ke a sensible decision.
Hints o n t he fin a l MB med ic ine examinat ion
While it is important to keep your initial presentation concise, it is a m istake to answer the subsequent questions too curtly. The examiner is anxious to see whether you can discuss your pat ient intell igently and you should try to display your relevant knowledge as much as possible. If anything about the case puzzles you, or there is a problem relating to diagnosis or 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 to keep the init iative by talking around the subject. With a bit of luck you may introduce a fresh topic that interests the examiner. If he persists in reiterat ing 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 prolonged si lences in such circumstances can be d isastrous. Try to talk sensibly around the subject to see what he's aiming at, and with luck a supplementary quest ion wi ll lead you to the requi red answer.
THE MINOR I'SHORT') CASES
Many students regard the minor cases as a l itt le l ight rel ief from the more arduous parts of the examination. This is a serious misconception, for the examiners are well aware of the element of luck wh ich enters into the major case, and they attach correspondingly greater importance to the candidate's performance while he is under di rect observation. You wil l be watched as you examine t he pat ient and your style in eliciting physica l signs is important. 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 adequately undressed.
As in the long cases, a reasonable compromise must be reached between speed and thoroughness in physical examinat ion, for as a genera l rule a candidate's score is proportional to the number o f cases he has t ime to examine and diagnose correctly. It is obviously better to err on the side o f over-caution rather than to fa il because of a major error of omission, but remember that few things ir ritate an examiner more than the candidate who wastes t ime perform ing a tediously meticulous examination in what shou ld be a sim ple, rapidly d iagnosed condition. The examinat ion o f the sensory nervous system often provides cause for offence in th is respect, and cardiologica l auscu ltat ion prese nts a simi lar hazard. If you are unsure of the diagnosis in a case with an ' interesting' m urm ur, there is usually no point in remaining glued to the patient's praecord ium 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 ifferent ial d iagnosis and move on to the next case.
Another important point in the m inor cases is to listen carefully to the instructi ons o f th e examiner w it h regard to the part or
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Hints on the f ina l MB m edicine examination
system to be examined and obey them implicitly. Before recounting you r f indings however, you should always pause and ask yourself whether fu rther examination of more distant parts of the body, such as regiona l lymph nodes, pe ripheral pulses, f inger nails, etc., is required. If you are not clea r what the examiner wants you to do, do not be afraid to ask for clarification, Fo r example, if the exam iner says 'Examine th is pat ient's heart' it wou ld be reasonable to ask whet her he wishes you also to fee l the pulse.
The importance of t he recogn it ion of cl inica l associations in the m inor cases cannot be overemphasized. In many cases inspection 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 cutaneous eruption localized to the shin in a patient wi th exophthalmos (pretibi al myxoedema), or you may be asked to give the likely diagnosis of an arthritis in a pat ient who also has a patch of psoriasis, or marked na il p itting. The key to many minor cases lies in such observat ions and you shou ld pract ise looking fo r such cl inica l associat ions until this becomes habitual.
Having el icited the physical signs correct ly many candidates fai l to be selective enough in applying the ir knowledge to the particular patient under discussion. Bl ind appl ication of ' lists of causes' oblivious of the patient's age or sex, the asso'ciated phYsical findings, etc., are guaranteed to create a poor impression. The habit of mentioning rare diseases before common ones is another fa iling which is easily eradicated with practice.
Hints and t ips received from eart ier cand idates in the short cases are on the whole best ignored. Examiners have been known to change the order of t he patients' beds and they wil l certainly have changed the questions. There is moreover a rea l danger that you will j ump to the diagnosis (which may in any case be wrong) w ithout giving adequate co nside rat ion to the different ial diagnoses and w it hout elic iti ng the app ropriate physical signs.
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' tests the depth as well as the breadth of a candidate's knowledge. If he appears to know a topic fai rly well , t he examiners w ill switch to another subject an d if several common topics are satisfactor ily dealt w ith, they may go on to test the candidate 'in depth'. For this reason, it may be worthwh ile for the good candidate to learn about a few unusua l multisystem condit ions in detail and to try and introduce them into the
Hints on the f i nal MB m edicine examination
conversation. For example a student who has spent an elect ive period in the USA m ight choose coccid ioidomycosis as a subject to revise in detail, Then if he is asked about pneumon ia, mening it is, osteomyeli t is, tubercu losis, erythema nodosum or lymphadenopat hy he will, aher discussing the commo~er cause,s, casua lly mention coccidio idomycos is. The examiner 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 ing in t he v iva un less you' re prepared to talk about it.
It is vi ta l to have a good knowledge of the diagnosis and management of emergencies such as cardiac arrest GI bleeds, M I, pulmonary oedema, drug overdoses, anaphylaxis and acute . . asthma. Don't worry too much about small print as no one Will fa ll you for m isd iagnosing p ituitary apoplexy although they might if you fai l to shock someone in ventricular f ibrillation . (Recommended reading: Acute medicine, 2nd edition, by Spring ings, Chambers and Jeffrey, Blackwell Science. )
Students are ohen asked fo r th e causes of a cond ition . Stony silence is not impressive. Even if you have never heard of the con dition you can try the fo llowing sieve: TIN MAI DENS, wh ich stands for T rauma, Infection, Neoplasia, M etabo lic (or Mechanical), A lcoho l, Iatrogen ic (or Id iopat hic), D egenerative (or Drugs), Endocrine, N eu rological, Smoking. Infection can be broken down into viral, bacter ial, fungal, protozoal and pa rasit ic. Neoplasia shou ld be considered as benign and malignant, primary and secondary, It sounds obvious but if you don't say it the examiner won't know that you know it.
It is worth remembering th at some condi t ions such as AIDS, syphi lis, TB, sa rco idosis, collagen-vascular disease and drug sideeffects can occasionally cause almost anyt hing.
You may be given a pathology specimen ('pot ') to 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 to talk at some length. If you haven't a clue, don't prevaricate but 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 abnorma lity is likely to be fair ly gross, so stand back and ta ke an overall view befo re looking at the detai ls. Remem ber that more than one abno rma lity may be present (e.g. an absent breast shadow w ith pulmonary metastases, or a bronchial cancer w ith r ib metastases), so examine t he whole fi lm. Assuming you can spot t he abnorma lity it is best to discuss th is from the outset as examiners get tired of being told that the patient is slight ly rotated and the film is of POOT qua lity.
Fina lly, have sympathy with your examiner. He cannot be expected to know everything and if you cross swords w ith him, give ground gracefully - after all he may be right !
2. Cardiology
CYANOSIS
5 9 reduced Hb per 100 ml blood produces cyanosis. (Note t hat polycyt haemic patients can be cyanosed without being hypoxic, and anaemic pat ients can be hypoxic w ithout being cyanosed)
PERIPHERAL CVANOSIS
Due to poor periphera l c ircu lation
Causes 1. Vasoconstriction, e.g. due to low ambient temperature or
Reynaud's disease 2. Arterial obst ruction, e.g. atheroma 3. Low card iac output. e.g. failure, aortic stenosis
CENTRAL CVANOSIS
Due to low arter ial oxygen saturat ion
Causes 1. Hypovenl i lation 2. Parenchymal lung disease 3. R to l card iac shUn! 4. Dec reased P0 2 of inspi red gas
May be sim ulated by methaemoglobinaemia and sulphaemog lobinaemia
JUGULAR VENOUS PULSE IJVP)
Height of JVP is measured with re ference to sterna l an gle with s.ubject at 45° to hor izonta l
Normally less than 4 cm (vertica l height )
CAUSES OF ELE VATED JVP
1. R ventricular fa ilure, esp. cor pu lmona le, pu lmonary embolus 2. Fluid overload (esp. Lv. inf usion) 3. Tricuspid stenosis or incompetence 4. Pericardial effusion or constrict ive pericarditis
-
_ I Cardio lo g y
5. Very slow heart ra te, esp. complete heart block 6. Obstruction of superior vena cava (non-pu lsati le)
Kussm aul's sign JVP rises on inspiration. Seen in constrict ive pericardit is, pericardia I eHusion. restrictive cardiomyopathy.
Normal jugular venous pu lse wave in relation to ECG pattern
Pulse wave
R
a
, y
,
a " atrial systole
c " effect of tricuspid valve closure
x == lowering of right atrial pressure as tricuspid ring moves down during ventricular contraction
p II '" venous fill ing T~~./-U~ ____ ~ (not ventricular
contraction) ECG
TYPES OF ARTERIAL PULSE WAVE
1. NORMAL
2. COLLAPSI NG IALSO CALLED WATER-HAM MER OR CORR IGAN PULSE)
(i) Aortic incompetence I ii) Hy perdynam ic c irculat ion (see p. 15) (i ii ) Patent ductus arterios us (iv) Peri phera l AV malformat ions
3. SMALL VOLU M E
(i) 'Shock' (ij) Aortic stenosis
(iii) Pericardia l effusion
y follows opening 01 AV valves
-- -Tl ---__ ~l_ L_ __
--1'1- ---. J __ L __
Ca rdiolo gy I
4. BISFERIENS
Combined aortic stenosis and incompetence
5. ANACROTIC ISLOW-RISING)
Aortic stenosis
6. DICROTIC
Fevers
7. PULSUS ALTERNANS - Altern ate strong and w eak beats
Left ventricu lar failure
8. PULSUS PARADOXUS - Blood pressure decreases on inspirat ion by more than 10 mmHg
(i) Pericardial effusion (ii) Constrictive pericarditis
(iii) Severe asthma
ARTERIAL PULSE RATE
CAUSES OF TACHYCARDIA
1. Sinus tachycardia (q.v.J 2. Supraventricular (atrial or nodal) tachycard ia 3. Atrial fl uner (usually around 150/m inl 4. Atrial fi b rillation 5. Ventricu lar tachyca rd ia (inc. torsade de pointes) 6. Ventricu lar fl uner
CA USES OF SINUS TACHYCARDIA (over 100 beats per minute)
1. Hyperdynam ic ci rcu lation (q.v.1 2. Congestive cardiac fa ilu re 3. Hypovolaemic shock (acute haemorrhage. etc.) 4. Const ricti ve perica rdi t is 5. Drugs, e.g. ad rena line, at rop ine, sa lbutamol 6. Pu lm ona ry embo lism, asthma
CA USES OF HYPERDYNAMIC CIRCULATION
1. Exercise or emotion (anx iety, fright. etc.) 2. Pregn ancy
1_ I Cardiology
3. Anaemia 4 . Pyrexia 5 . Thyrotoxicosis 6. AV f istulae
CAUSES O F SIN U S BR ADYCARDIA (less t han 60 beats per m inute)
1. Extreme physica l fi tness 2. Convalescence f rom fever 3. Soon after myocard ial infa rct ion 4. Hypothyroid ism 5. Hypothermia 6. Raised intracran ial pressure (with hype rtension) 7. Drugs, e.g. dig ital is, beta-blocke rs 8 . Sinoatrial di so rder ('sick sinus syndro me')
CAUSES OF A N IRREG ULAR PU LSE
1. Extrasystoles 2. At rial f ibrillation 3. Marked sinus arrhythmia
COMMON CAUSES OF SOME ARRHYTHMIAS
EXTRASYSTOLES
1. Idiopathic 2. Fatigue, excessive sm oking, alcohol or caffeine ingest ion 3. Myocard ial ischaemia 4. Dig italis 5. Hyperthyroidism 6. Heart diseases w ith atrial en largement (e.g. mitral stenosis)
PAROXYSMAL TACHYCARDIA
1. Myocardial ischaemia 2. Dig italis, especially after potassium deplet ion
ATRIAL FIBRILLATION
1. Rheumat ic heart d isease, espec ially m it ral stenosis 2. Myocardial ischaemia 3. Hyperthyroid ism 4. Idiopath ic ' lone fi br illation' 5. M it ra l prolapse 6. Sick si nus syndrome 7. Hypertension
Cardiology I
HEART BLOCK (a l l degrees)
1. Myocardial ischaemia 2. Digital is 3. Chronic heart disease, especially aortic stenosis and congenital
lesions 4. Rheum atic fever
CLINICAL DIAGNOSIS OF AN ARRHYTHMIA
1. SINUS ARRHYTHMIA
Rate increases w ith inspi ration
2 . EXT RASYST O LE S (ectopic beats)
Atrial, noda l or ventr icu lar (i) A premature beat wi t h a compensato ry pause fo llowed by
a st ronger beat I ii ) Usually runs of norma l beats occur, but extrasystoles may
alternate w it h norma l beats (pu lsus bigeminus) (ii i) May disappear during exe rcise
3. AT RIA L FIBRILLAT IO N
(i) Completely irregu lar in time and force (i i ) Worse on exercise (iii) Carotid compression has no effect (iv) JVP 'a' waves absent
4. AT RIA L FLUTTER
(i) Regular radia l pulse rate, classically 150/min in 2:1 block (but can be i rregular if there is fl uctuating heart b lock)
(ii) AV block occurs, so that the JVP 'a' waves great ly exceed t he pulse rate
(i ii) Carotid com pression slows the rate w hi le pressu re is maintained
5. PAROXYSMAL TACHYCARDIA
Atr ial, nodal or ventricu lar (i ) May be history of previous attacks w ith sudden onset and
cessation (ii) Ca roti d compress ion may dec rease t he rate even after
pressu re is relaxed
6. HEART BLOCK
Com plete (3rd degree) Heart rate of 36-44/min which does not increase wi t h exercise
Ca rd io lo g y
2nd d eg ree AV bloc k May be dropped beats (Wenckebach) or 2:1, 3:1 or 4:1 block. Instabi lity of rhythm is common
15t d egree block Detected on ly on ECG (PR > 0.2 second )
APEX BEAT - THE LOWEST AND OUTERMOST POINT OF DEFINITE CARDIAC PULSATION
Heart is enlarged or disp laced if apex beat is: 1. Lateral to midclavicu lar line, or 2. Below 5th intercostal space The character o f the apex beat may be: a. Heav i ng (pressure overload) in aortic stenosis or systemic
hypertension (apex usua lly not displaced) b. Thrust ing (vo lume ove rload) in ao rt ic regu rgitat ion or mitra l
regurg itat ion (apex usua lly displaced) c. Tapping ('palpable first hea rt sound' ) in mit ral stenosis
A left parasterna l heave ind icates RV hypertrophy
FAILURE TO LOCATE THE APEX BEAT ON PALPATION
Consider the following possibi li t ies: 1. Excessively fa t or muscular chest wall 2. Left pneumothorax, p leural effusion o r emphysema 3. Large pericardia I effusion 4. Dextroca rdia or marked mediastina l sh ift 5. Massive LV hypertrophy. (Remember to feel as far round as t he
m id-axill ary li ne )
THRILLS (palpable murmurs)
A lways ind icate an organic defect. The area local izes the defect
HEART SOUNDS
'/I Tricuspid and Aortic and mitral valve closu re pulmonary valve closu re
N.B. 1. Aortic normally closes before pulmonary
Cardiolo g y I 2. Pulmonary closure is delayed by inspi ration (due to increased
venous return caused by decreased in trathoracic pressure) The normal split t herefore increases on inspi ration
FIRST SOUND
Lo ud in 1. M itral stenosis 2. Hyperdynamic circulation 3. Tachycardia
So ft in 1. Mitral incompetence 2. Rheumatic cardit is 3. Severe heart fa ilure
SECO ND SDU ND IN AORTIC AREA
Loud in systemic hypertension Soft in aort ic stenosis
SECDND SDUND IN PULMONARY AREA
Loud in pulmonary hypertension (e.g. chronic pulmonary d isease) Soft in pulmonary stenosis
THIRD HEART SOUND
, I Cau ses
'II 'I
Heard at apex ea rl y in diastole, due to vent ricu lar di stens ion Easi ly confused w ith opening snap of mitra l stenosis wh ich is maximal media l to the apex
1. Normal in young people and during pregnancy 2. Ventricu lar failure (a useful sign) 3. Mitral or tricuspid incompetence 4. Constr ictive pericardit iS
FOURTH HEART SOUND , I 'I _ 'II
Heard at lowe r end of sternum late in diastole, due to atrial contraction (and therefore not present in atrial fibri ll ation)
Always abnormal, indicates resistance to LV filling because of _ increased ventricular wa ll stiffness
.. Car d iology
Causes 1. Hypertension 2. Heart block 3. Myocard ial infarct ion
Triple rhythm is due to a 3rd or 4th heart sound, or summation of both
Gal/op rhythm is a fast t r iple rhythm, and ind icates actual or incip ient heart fa il u re
Dogmatic pronouncements on t he state of the second sound and the presence or absence of the th ird and fou rt h sounds are not norma lly expected of undergrad uates
CARDIAC MURMURS
When auscultat ing, concentrate separately on the heart rhythm. sounds and murmurs. The murmurs most commonly m issed in exams are t hose o f aortic incompetence and mitral stenosis. Aortic incompetence is m issed either because auscu ltat ion was not perform ed all down the L sterna l edge w it h the pat ient sitt ing up at t he end of expiration, or because t he candidate fai led to 'IUne in' to the h ig h-p itched murm ur. Mit ral stenosis is missed e ither because the patient was not auscultated lying on his left side, or because the candidate listened to on ly one site in the apica l area .
The exam ination o f pe ripheral signs will g ive you an idea of w hat you m ight fi nd on auscu ltation. Fo r example if the patient is in atr ial f ibri ll at ion con sider m it ral va lve disease; th en if t he apex is disp laced there is likely to be m itral regurg itat ion, o therw ise a loud f irst hea rt sound and an und isplaced apex beat favour mit ra l stenosis.
If the pat ient is in sinus rhythm then the pulse character is useful, a slow rising pu lse indicati ng aortic stenosis, a collapsi ng pu lse indicating aortic regu rgitation. Sim i larly if the apex is d isplaced th en aort ic regurg itat ion is much more likely t han ao rt ic stenosis. If the murm ur rad iates to t he caroti ds aort ic steno sis is mo re like ly than m itra l regurg itat ion, but the converse does not follow as t he murmur o f aort ic sclerosis w ill not rad iate to the carotids.
If there is a m id l ine sternotomy scar there may be a p rosthet ic valve or two, in which case a systolic m urm ur may be normal. However most m idline sternotom ies are done for bypass grafting, not for valve rep lacement . None o f these rules is absolute but t hey are usef ul.
If several murmurs are p resent, t ry to decide w hich lesion is dominant by consideration of associated cl in ical features, e.g. in simu ltaneous AS and AI the pu lse m ay be either 'plateau ' or 'collapsing', and in simultaneous MS and M I the presence o f a 3rd heart sound w ith a soft 1st sound suggests the incompetence is dominant.
C. rdiology I
If no murmur is hea rd and the patient gives a history o f rheumat ic fever, you should exercise t he pat ient an d listen aga in, particularly fo r murmurs of MS or A I.
Different ia l diagnosis of murmurs
TIming
EIec1ion systo li<:
1st 2nd sound sound
I I
, 1, 'lIIllllmn .. 1
Pansy-stolic
M id-diasto lic
Opening snap
'I 1111II ,~ •• fl Diastolic
dl ~II!I!!'" Continuous
Maximal inrensiry
Aortic /Irea
Pulmonary al ea
A""
l ower sternal border
A"" l ower sternal border
Anywhere along sternal border
Cardiac basc
Above clav icle
Likely causes
Aort ic stenosis Aortic scleros is Coa rctation
Innocent Pulmonary stenosis Atrial septal defect Pulmonary hyper1ens ion
Innocent Aort ic stenosis Aort ic sc leros is
M itra l incompetence Ventricular septa l defect Fallot's tetralogy
Tr icuspid incompetence
Vent ricula r seplal defect
M itra l stonosis
Tricuspid stenosis {ra.e)
Aortic incompetence Pulmonary incompetence
Patent duetus arteriosus Simultaneous AS and AI
Vanous ·hum·
RemBmber the possibility of extracardiac sounds such as a pericardial rub in pericarditis
In any patient in whom you suspect rheumatic heart d isease you shou ld obtain detai ls of the symptoms, duration and t reatment of
_ ! Ca rd io logy
any previous bouts of possible rheumat ic fever, chorea, tonsi llitis or bacter ia l endoca rdi t is.
CHARACTERISTICS OF INNOCENT SYSTOLIC MURMURS IN CHILDHOOD
1. No other abnormality detected (no cardiac enlargement) 2. No thrill or added sound 3. Never diastolic or pansystolic, except for t he continuous
murmur of a veno us hum, w hich is reduced on lying down 4. Intensity often va ries with a change in posture
MITRAL STENOSIS
Nearly always due to rheumatic heart d isease, but rarely may be co ngenita l
SYMPTOMS
1. Progressive exertional dyspnoea 2. Other symptoms o f pu lmonary congestion:
(i) Orthopnoea (i i) Paroxysmal nocturnal dyspnoea
(iii) Cough (iv) Haemoptvsis
3. Acute pulmonary oedema, usually precip itated by exert ion, pregnancy or onset of AF
4. Recurrent bronchit is 5. In later stages, symptoms of RV failu re (p. 21) 6. Pa lp itations in paroxysmal AF
SIGNS
1. Thin face w ith pu rpl e cheeks ('mit ral facies' ) 2. Pulse may be sma ll volume. May be atrial fi brillation 3. BP shows low pu lse pressure 4. May be 'tapp ing' apex beat and L parasterna l heave
May be diasto lic t hrill 5. 1st heart sound is lo ud an d 'slapp ing'
2nd heart sound is loud if pu lmonary hypertension is present M ay be 'opening snap' (indicates mobite valve) in ear ly d iasto le
6. Rough, rumbling , low-pitched diasto lic m urmur, local ized to the apica l area and accentuated by exercise . May be presystolic crescendo if fibri ll at ion absent
1. Pu lmo nary crackles 8. In later stages, signs of RV fai lu re
'-____________________________________________ c_,_,_d_' o __ 'oc·cv_1 IIIIIIII N.B. Increased severity of stenosis is indicated by increased
durat ion of murm ur (not its loudness).
COMPLICATIONS
1. Thrombi in L atrium, and system ic embol ization 2. Pulmonary emboli 3. Subacute bacterial endocarditis (uncommon w ith atrial
fibrillat io n)
ELECTROCAR DIOGRAM
1. May be broad notched P wave (L atrial hypertrophy) 2. May be atr ial f ibrillation 3. R ax is deviation or A ventricu lar hype rtrophy 4. Usua lly d ig itali s effects
M ITRAL INCOMPETENCE
CAUSES
1. Mitral valve pro lapse (usually myxoid degeneration) 2. Rheu matic fever (probably around 20% o f cases in UK) 3. Ischaemia, especia lly posterior infarct, w ith papillary muscle
damage 4. Subacute bacter ial endocardit is (may be cause or complicat ion) 5. Functional M I due to stretched AV ring in LVF
SYMPTOMS
1. Palp itat ions and exertiona l dyspnoea occu r ear ly 2. Fatigue and weakness 3. Orthopnoea due to pu lmonary oedema
SIGNS
1. L ventricu lar di latation 2. 1st heart sound is soft and muffted
3rd heart sound is usual 3. Lou d pansystolic murmur, maximal at apex and propagated to
axi lla Often obscures 2nd heart sound
4. May be LV fa ilure
N.B. Increased severi ty is indicated by 3rd heart sound, LVF and a displaced apex
_ I Ca r d iology
AORTIC STENOSIS
CAUSES 1. Congenital, part icu larly bicuspid valve (presents at age 40-60) 2. Rheumatic fever 3. Senile calcificat ion o f an otherwise normal valve (presents over
60) 4. Severe hypercho lesterolaemia
SYMPTOMS
, . May be none for years 2. Symptoms o f L ventricular fa ilu re (p. 26) 3. Syncope on effo rt 4. A ngina (despite norma l coronary arte ries)
SIGNS
1. Sma ll vo lume, slow -ri si ng pulse 2. L vent ricular hypertrophy
M ay be systo lic th ri ll (best felt w ith patient sitt ing forward at end of expirat ion)
3. 2nd sound in aorti c area is soft 4. Harsh systo lic 'eject ion' murm ur maximal at ao rt ic area and
rad iating to the neck 5. May be LV failure
N. B. Increased severity is ind icated by a slow-r ising pu lse, an inaudib le second heart sound and a low BP.
Aortic sclerosis m urmur is ident ical, but is dist inguished by normal pu lse w ave and absence of a th rill
AORTIC INCOMPETENCE
CAUSES
A . Valv ar 1. Rheumatic fever 2. Subacute bacter ia l endocardit is 3. Bicuspid va lve 4 . Rheumato id d isease
B. Ao rtic root disease 1. Type A ao rt ic d issect ion 2. Syph ilis 3. Marian's 4. Sero neg at ive arth rit is (p. 143)
SYMPTOMS
1. May be none for many yea rs
'-~~~~~~~~C-"d-;O--'09Y I ~ 2. Pa lp itations and dizziness 3. Sympto ms of l ventricu lar fa ilu re (p. 27) 4. Ang ina
SIGNS
1. Co llapsing (Corrigan) pulse. May be visib le carotid pulsat ion or 'head-nodding' (de Musset's sign ) or nail bed pulsation (Quincke's sig n)
2. BP shows wide pu lse pressu re 3. L vent ricular hypertrophy and dilatat ion 4. Murm urs:
(i) Soft high-pitched b lowing diasto li c m urmur down l sternal edge
(ii) M ay be a systol ic ao rti c murmur due to increased b lood f low
(i ii) May be a diast o lic apical m urmu r (Aust in Flint) w h ich sim ulates m itral stenos is
(iv) M ay be ' pistol-shot' noise over fe mo rals synch ronous w ith pu lse (Trau be's s ign)
(v) May be diasto lic m urmur over fem orals on slight compression w it h stethoscope bell (Duroziez's sign )
5. M ay be LV failure
N.B. Increased severity is indicated by decreased durat ion of murmur, LVF and a displaced apex
TRICUSPID INCOMPETENCE
CAUSES
1. Infect ive endocarditis (esp. in drug addicts) 2. Pu lm onary hypertension 3. Rheum atic fever 4. Funct ional TI due to stretched AV ring in RVF
Clinical manifestat ions usual ly determ ined by coexist ing an d predom inat ing m itral stenosis
SYMPTOMS
1. Exe rt ional dyspnoea is common, but orthopnoea and paroxysmal nocturn al dyspnoea are uncommon due to d im in ished R vent ricu lar outp ut into lungs
2. Gast ro intest inal upsets due to ven ous congestion of GI t ract
SIGNS
1. Elevated JVP wi t h large v w aves 2. Pu lsati le hepat ic en largement 3. Asci tes. which is bo th chronic and recurrent
- Cardiology
4. Peripheral oedem a, p leural effu sio ns 5. Pansystol ic murmu r, maxim al near lower sternum, and
becom ing louder during deep insp i rat ion
CLASSIFICATION OF CONGENITAL HEART D ISEASES
CYANOTIC II.E. R TO L SHUNT)
1. Fa ll ofs tetralogy ( i ) Pulmonary stenosis
(i i ) Ventricular septal defect (ii i) Over-rid ing ao rta (iv) Right ve ntr icular hypertro phy
2. Tran spos ition o f g reat vessel s and tr icuspid atresia are usually fatal in infancy unless co rrected
3. Eisenmenger's synd rome (reversa l of a L to R shunt foll ow ing t he developm ent of pu lmonary hypertension)
ACYANOTIC
1 . With L to R shunt (i) Ventricu lar septal defect
( i i ) At rial septa l defect - usually secundum but rare ly septum prim um
(i ii) Persistent ductus arteriosus These pat ients m ay become cyanosed due to card iac fai lure,
pulmonary infection, severe exercise or shunt reversal
2 . With no shunt (j) Coarctat ion o f aorta
(i i) Pu lmo nary stenosis - occasionally cyanosed (i ii) Congenital ao rt ic stenosis (iv) Dextrocard ia (v) Bicusp id aort ic valves
HEART FAILURE
Defi nition: a state in w hi ch the heart fai ls to meet the metabo lic and oxygen need s o f th e body under va rying cond it ions, assuming the ve nous ret urn is adequate
LEFT VENTRICU LAR FAILURE
Common ca uses 1. Myocard ial ischaem ia 2. Hypertension 3. Ao rt ic stenosis or incompetence 4. M itral incom petence
Cardio logy I _
Symptoms 1. Exertional dyspnoea 2. Orthopnoea 3. Paroxysmal nocturna l dyspnoea, often w ith coughing or
w heezi ng 4. Pu lmonary oedema (anx iety, dyspnoea, cough and pink fro thy
sput um)
Signs 1. Tachycardia. May be pu lsus alternans 2 . Enlarged heart 3. Gallop rhythm 4. May be f unctional m it ra l incompetence due to stretched AV
ring 5. Fine crackles at lung bases . May be w heezes
LEFT VENTRICULAR HYPERTROPH Y
Causes 1. Hypertension 2. M it ral incompetence 3. Aortic stenosis andlo r incompetence 4. High out put states, e.g. anaem ia, polycythaem ia, t hyrotoxicosis 5. Aortic coarctation 6. Hypertrophic cardiom yo pathy
Signs 1. Forcefu l apex beat, left ventricu lar heave 2. loud aortic 2nd sound 3. Signs of any underly ing condition
RIGHT VENTRICULAR FAILURE
Common causes 1. Secondary to l ventricular fa ilure 2. Mitra l stenosis 3. Cor pu lmona le (inc luding pu lm onary embol ism ) 4. Congenital heart d isease
Symptoms 1. Ti redness, weakness, ano rexia 2. Oedema 3. Gastrointestin al upset. May be hepatic pain
Signs 1. Depen dent oedema 2. Elevated JVP 3. May be functiona l t ricuspid incompetence due to stretched AV
ring
_ [ c ardiOlOgy
4. Large tender liver. May be mi ld jaund ice 5. O ligu ria by day and noct ur ia. Urine is concent rated and
a lbum inuria is common 6. Peripheral cyanosis o r ascites in severe cases
Remember that Rand L sided heart fai lu re often appear almost sim u ltaneously
SYSTEMIC HYPERTENSION
Defi nit ions vary b ut 140/90 mmHg for a young ad ult and 160/95 mmHg for a m iddle-ag ed person wou ld be reasonable upper lim its
CAUSES
1. Essentia l 2. Rena l d isease (especiall y renal ischaem ia) 3 . Drugs, e.g . cycl osporin. o ral contrace pt ives, g lucocort icoids 4. A lcohol ism an d/or sleep apnoea 5. Endocrine
( i) Cushing's d isease (ii) Phaeochromocytoma (i ii) Pr imary aldosteron ism (Conn's)
6. Coa rctat ion (but BP norma l in legs) 7. Toxaemia of p regnancy
COR PULMONALE
Ca rd iac d isease seconda ry to ch ron ic d isease of lungs or pulmonary vessels
CAUSES
1. Emphysema and chro nic bronch it is 2. Pu lmona ry fi bros is 3. M ultip le pu lmonary embo li 4. Severe ky phoscoliosis 5. Id iopathic pu lmonary hypertens ion
SIGNS OF COR PULMONALE
1. Warm cya nosed extrem iti es w ith bound ing pu lse 2. Ra ised JVP, hepatomega ly and oedema 3. Trip le rhythm and loud P2 due to pulmonary hypertension (but
overly ing emphysema may ca use soft hea rt sounds) 4. Funct iona l t r icusp id incompetence in seve re cases
I
CAUSES OF SEVERE CHEST PAIN
1. Myocard ial ischaem ia (i) Co ronary athe roma, th rombus o r vasospasm
(i i) Ao rt ic va lve d isease or ao rt itis (i i i) Seve re anaemia (iv) Paroxysma l tachyca rd ia
2. Pe ricardit is 3. Pleurisy 4. Pu lmonary embolism 5. Oesophagea l pa in (ac id ref lux, spasm, ca rcinoma) 6. Expand ing aortic aneurysm 7. Chest wall lesions
(i ) Rib fracture (ii ) Metastat ic depos its in ribs o r fractures
(iii) Mya lg ia (e.g . Bornholm disease) (iv) Herpes zoster (v) Id iopath ic costochondrit is (Tietze's syndrome)
8 . Gastric o r duodena l u lcer 9 . Gallbladder col ic or pancreat it is
10. Pain referred from thorac ic o r cervical spi ne
Cardio logy
COM MON RISK FACTORS FOR MYOCARDI AL INFARCTION
1. Smoking 2. Hypertens ion 3. Hypercho lestero laem ia 4. Diabetes mell it us 5. Fami ly history of atheroma 6. Increasing age 7. Male sex
COMPLICATIONS OF MYOCARDIAL INFARCTION
EARLY (IN FIRST 48 HI
1. Card iac arrhythmia (i) Sinus or noda l bra dycard ia
I ii ) Supravent ricu lar tachycardia, at rial f lutter, at rial fi b rill ation
(iii ) Ventricu la r ectopic beats, tachycard ia, f lutter o r f ib ri llation (Iv) Heart block (v) Ca rdiac asysto le
2. Vent ricu lar fa ilu re 3. Hypotension or 'shock' 4. Perica rdit is 5. Ruptured papilla ry muscl e o r chordae ten dineae 6. Ventr icu lar septa l defect 7. Iatrogen ic (pacing, etc.)
_ I Cardio logy
MEDIUM (AFTER 48 HI
,. DVT, pulmonary embolism 2. Mural t h rom bos is, systemic em bol ism 3. Card iac rupture (often after several w eeks)
LATE IAFTER SEVERAL WEEKS)
1. Cardiac aneurysm 2. Dress ler's syndrome due to card iac autoant ibod ies (fever, chest
pa in, pericardit is or pleurisy) 3. Psychological, including 'L chest pa in' 4. Frozen shoulder and 'shoulder hand' syndrome
CLINICAL ' SHOCK'
Defin ition: a synd rom e in w h ich inadequate blood supply and el iminat ion of t issue metabolites lead to functional and/or structu ral d isturbances in the essent ial organs
CAUSES
1, Hypovolaem ia - haemorrhage, t rauma, dehydration, burns, post su rgery
2. Ca rdi ac failu re . ( i ) Pump fa i lu re, e.g. myocardial infa rct
( i i) Arrhythmia (i i i) Obstruct ion, e.g. pulmonary embolism
3. Sepsis 4. Anaphylaxis
PERICARDITIS
CAUSES
1. Myocard ial infarct 2. Vi ral (Coxsackie, Echo, etc.) 3. Rheumat ic feve r 4. Pyogen ic (pneumon ia or septica emia) 5. Tuberculous 6. Cancer invading the pericardi um (bronchus or breast) 7. Severe uraemia 8. SLE, rheumatoid disease 9. Dressler's syn drome I
CONTRA-INDICATIONS TO THROMBOLYTIC THERAPY
1. Recent haemorrhage. t rauma or surgery 2. Bleeding diathesis 3. Aortic dissect ion 4. Severe hypertension 5. Recent cerebra-vascu lar event (CVA) 6. Peptic u lcer 7. Heavy vagi nal bl eeding 8. Acute pancreatit is 9. Severe liver disease, esp . oesophagea l va ri ces
10. Pu lmonary disease with cavi tation
CardiologV I _
Streptokinase o r anistreplase should not be given again w it hin 12 m onths of a previous dose, or if t here was an all ergic reaction
RHEUMATIC FEVER
Diagnosed by t he revised Jones' criteria, i.e. evidence of previous streptococcal infection plus either 2 majo r cr iteria or 1 major and 2 mino r criter ia fro m the followi ng l ist:
MAJOR
Sydenham's cho rea Polya rthr it is (migratory) Erythema marginatum Carditis S ubcutaneo us nodu les (painless) Mnemonic - SPECS
MINOR
Pyrexia ECG shows prolonged PR interval Arth ralgia C reactive protein (or ESR) raised H istory of previous rheumatic fever Mnemonic - PEACH
3. Electrocardiography
THE NORM AL ELECTROCAROIOGRAM
R
p
Q s
PR shou ld be < 0.20 seconds QRS shou ld be < 0.12 seconds
T u
1 large square (5 mm) on ECG, paper == 0.2 seconds
: . Vent ricular rate/m inute ==
STANDARD LEADS
300 No. of large squares
between ad jacent R peaks
ECG inte rp retation 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 from the following viewpoints 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
The ca rdiac axis ca n be worked out from leads I and aVF, remembe ring that R waves re p resent the di rection of the vector
-
j
Electrocardiography
(l eft ventr icu lar depolarization) and S w aves represent the opposite direct ion.
Summate Rand S for each of these 2 leads. Then height of R minus depth of S for lead I represents the
vector in the horizon tal direction, and heig ht of R m inus depth o f S for lead aVF represents the vector in the vertical d irect ion. A simple scale d rawing of these two vectors then gives the cardiac ax is:
Lead aVF
Angle X = Cardiac axis
The normal 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~'' ind icates L ax is dev iation A n axis of more t han +90 0 ind icates A axis deviation
CHEST LEADS
These leads ' look at' the heart in a horizontal plane from the right o f the sternum (V1 ) to the axi llary line (V6)
V1 V2 V3
V4 V5
V6
Clockw ise or ant iclockw ise rotat ion is thus detected by these leads
~f
Electrocardiography I _
ARRHYTHMIAS
1. PREMATURE BEATS
Ar ise from ectopic focus in atrium, AV node or ventricle. Usually follow ed by 'com pensatory pause'
Suprave nt ricular extrasystole P is premature and may be b izarre
Nodal extrasystole Essent ial ly no rmal GAS but no preceding P
Ventricular extrasystole Biza rre GAS w ith no preceding P
2. PARDXYSMAL ATRIAL TACHYCARDIA (PAT)
Normal QAS, but T w aves altered by fusion w ith P w aves
PAT with block (usually induced by digitalis) Aapid regu lar P w aves with slower GAS waves
p p p p /
V V
3. PARDXYSMAL VENTRICULAR TACHYCARDIA
GAS complexes are slurred and wide but fairly regular. P waves often obscured
_ I Electrocard iography
4. ATRIA L FIBRILLATION
Absent P waves an d GRS com plexes irregularly i rregu lar
T T
5. ATR IA L FLUTTE R
P waves in 'sawtooth' 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 to appea r irregular
Flutte r w ith 5:1 b loc k
6. VENTR ICULAR FIBRILLATION
Rapid biza rre ventricula r patterns
HEART BLOCK
BUNDLE-BRANCH BLOCK IBBBI
QRS exceeds 0.12 seconds w it h a notch ed com p lex
LBBB V5
RBBB V1
M -shaped wave in L chest leads W-shaped wave in R chest leads
M-shaped w ave in R chest lea ds W-shaped wave in L chest leads
Electrocardiography I _
Mnemonic - V\I1LLlAM MORRO W V1 V5 W - L - M = LBBB M - R - W= RBBB
FIRST DEGREE BLOCK
PR interva l exceeds 0.20 seconds but rhyt hm is normal
SECOND DEGREE BLOCK
GRS occu rs on ly after every 2nd, 3rd or 4th P wave P waves reg ular, but some obscu red by T or GRS com p lexes
Wenkebach phenomenon (M obitz type I) PR inte rva l prog ressive ly increases unt i l a QRS is dropped, afte r w h ich PR shortens and the cycle is repeated
p p p p p p
Mobitz type II
p
PR interva l is constant but an occasiona l P wave is not fo ll owed by a QRS com plex
Third d egree b lock (com p lete heart b lock) P waves and QRS com plexes occu r complete!y independent ly of each other. Ventr icu lar rate is 25-50/m in
T p P P p p
T P p
VENTRICULAR HYPERTROPHY
LVH
1. Tall R waves in left ch est leads w it h deep S waves in right chest lea ds Sum of S in V1 and R in V5 exceeds 37 mm
_ I Electrocardiography
2. May be LV 'st ra in' 1ST depression and T inversion) 3. l eft axis deviation 4. QRS may be slightly prolonged
LV hypertrophy a nd s train
VI V5
RVH
1. Tall A waves in r ight chest leads with S waves in left chest leads
2. R axis deviation
VI V5
OTHER CAUSES OF ECG CHANGES
MYOCARDIAL INFARCTION
Characteristic changes are:
RV hype rtro phy and strain
, . Tran sient ST elevation and persistent T wave inve rsion in leads facing the infarct
2. Transient ST depression in leads di amet rica ll y oppos ite t he infa rct
3. Appearance of 0 wa ves exceeding 0.04 seconds an d 2 mm deep. These occur later and pe rsist
Recent myocardia l infa rct
Electrocardiography I
Anterior infarct Usually d ue to occlusion of the descending l coronary artery. The infarct faces leads I, aVl and the chest leads
Inferior (diaphragma tic) infa rc t Due to occlusion of R coronary or circumflex artery. Faces leads II, III and aVE Persistence of the acute infarct ion pauern for more than 6 months suggests ventricular aneurysm
MYOCARDIAL ISCHAEMIA WITHOUT INFARCTION
5T depression and symmetrica l T w ave inversion
DIG ITALIS
Also causes 5T depression and T inversion but in a 'reversed t ick' pattern
HYPOKALAEMIA
Digitali s also causes: , . Bradyca rdia 2. Pro longed PR 3. Shortened OT 4. Any arrhyth mia, especially
bigemini or heart block
Prolongation of OT interval, ST depression and T wave flatten ing or inversion . Prominent U waves, w hich may fuse w ith the succeeding P
U P
T
HYPERKALAEMIA
Sma ll P waves w ith ta ll peaked T waves ORS com plex w idens, and ventricu lar f ib rillation may follow
_ I Electrocardiography
PERICARDITIS
Acute Mexica n sadd le-shaped ST elevation in all the standard leads except aVR, and in most of the chest leads
II II I
Chronic 5T becomes isoelectric and the T wave f lattens and may invert
ACUTE PU LMONARY EMBOLISM (classica lly 'S1, Q3, T3')
1. S wave i n lead I 2. T wave inversion and Q wave in leads II I and Vl - V3 3. Transient RBBB 4. Right axis dev iation
COR PULMONALE
1. l arge pointed P waves 2. Changes of RV hypertrophy
HOW TO READ AN ECG
1. Identify the rhyth m a nd ra te 2. A re normal P waves p resent and what is the PR interval? 3. Is the ca rd iac ax is n orma!? 4. Is t he GRS complex abnormally broad?
{L BBB is always patho log ica l and makes further interpretat ion impossib le)
5. Are t he Q waves patho log ica l? 6. Is the ST segment ra ised o r depressed? 7. Are the T waves norma l or inverted?
Further read ing: The ECG made easy, J R Hampton, Church ill Livingstone, Edinburgh
4 . Chest disease
LUNG VOLUMES
Tota l lung capacity
___ M.~jmum inspiration
~ Maximum exp iration
Residual vo lume
Funct ional re s id ua l capacity
The resting expiratory leve l is t he most consta nt refere nce point on the spi rometer t rac ing
MINUTE VENTILATION
Product of t idal vo lume and number of respi rat ions per minute
VITAL CAPACITY
Largest volume a subject can expi re after a single maximal inspirat ion . Normal values increase w ith s ize of subject and decrease w ith age (about 4'h lit res in young adult ma le) . Can be reduced in practica ll y any lung or chest wall d isease
FORCED VITAL CAPACITY (FVCI
The vita l capacity when the expi rat ion is performed as rapid ly as poss ible
FEV,
(Forced exp iratory vo lume in one second) - volume expi red during fi rst second of FVC
FEV 1 Ratio -- shou ld be 0.75 o r more
FVe The rat io is reduced in obstructive airway d iseases (asthma,
emphysema, bronchitis)
II I Chest diseasa
PEAK EXPIRATORY FLOW RATE IPEFR)
Maximum expiratory flow rate ach ieved during a forced expirat ion. A convenient way to detect a reduct ion in venti latory funct ion. A lso useful for serial measurements in the same patient and for assessing response to bronchodilators
RESIDUAL VOLUME
Obtained by subtracting expiratory reserve vol ume from funct ional residua l ca pacity. Residua l volume is norma lly 20-25% of total lung capacity but increases in elder ly, and in over~ i n flation of the lungs (emphysema, asthma)
A NATOM ICAL DEAD SPACE
The vo lume of ai r in the mout h, pharynx, t rachea an d bronch i up t o t he term inal bronchioles (about 150 m l). In d isease t he physiological dead space may greatly exceed the anatomica l dead space due to the disorders of the ventilation/perfus ion rat io, 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 Po2 is normal or slightly red uced at rest, but decreases markedly after exercise due to increased t issue uptake of O2, Arter ial Ft02 is normal or even reduced at rest (due to hyperventi lat ion) 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 helium di lution DLeO
KeD, the gas transfer coefficient. '" -=="-VA
CAUSES OF REDUCED DIFFUSING CAPACITY ITRANSFER FACTOR)
1. A lveo lo-capiliary block (i) Pu lmonary oedema (i i) Pulmonary fib rosis (iii) Inf i ltrat ive lesions, e.g. sarcoidosis
2. Red uction in area ava ilable for diffusion (i) Emphysema (ii) Mult ip le pulmonary embo li
3. Haemorrhage into the alveo li (an artefact rather tha n a true reduction )
Chest d isease ! _
LUNG COMPLIANCE
A measure of lung elasticity. Compl iance is reduced w hen the lungs are abnormally sti ff due to pulmonary venous congestion or infi lt rative or f ibrot ic lesions of the lungs
BLOOD-GAS ANALYSIS
These values must be related to the norm al levels expected for t he subject, e.g. baby, old man, pregnant wom an
HYPOXIA
Oxygen deficiency at a specified site
HYPOXAEMIA
Oxygen deficiency in the blood. In arterial blood of norma l resting adult: Fto z is about 40 mmHg (4 to 6 kPa) Po2 is about 90 to lOa mmHg (12 to 15 kPa)
Causes of hypoxaemia 1. Cardia-respiratory disorders
(i) Hypoventi lation (ii ) Abnormal ity of ventilat ion/perfusion (Via) rat io
(iii) Impaired diffusion (iv) Venous to arterial shunt
2. Decreased P02 of inspi red gas, e.g. high altitude 3. Reduction in active haemoglobin, e.g. carbon monoxide
Type 7 respiratory failurB, with Paol < 8 kPa and PaC02 < 6.5 kPa, occurs in asthma, LVF and pu lm onary embolism
Type 2 respiratory failure, w ith Pa02 < 8 kPa and PaC02 > 6.5 kPa, occu rs in chronic bronchit is, CNS disease and impaired chest wall movement
HYPOVENTILATION
Reduction in lung vent ilation suffic ient to ca use hypercapnia
Causes of hypoventilation 1. Respiratory centre depression, e.g. drugs, anoxia, central s leep
apnoea 2. Neuro logi cal di sease, e.g. pol io, motor neurone disease 3. Respiratory muscle disease, e.g. de rmatomyositis, Duchenne's
muscu lar dystrophy 4. limited chest movement, e.g. kyphosco liosis, thoracoplasty for
TB 5. lim ited lung movement, e.g . p leural effusion, pneumothorax
_ I Chest d iseDse
6, l ung disease, e.g . collapse, pneumo nia 7. Upper airway obstruction, e.g. obstructive s leep apnoea
DYSPNOEA
Subjective awareness of the need for an increased respi ratory aHort
KUSSMAU~S BREATHING l AIR HUNGERI
Occurs in acidosis (u raemia, diabetes mel litus) due to stimulation of respi ratory centre
CHEYNE- STOKES BREATHI NG
A mplitude of resp i ration p rog ressive ly deepens to a maximum, t hen decreases to a per iod of apnoea. Due to dimin ished sensit ivity of respiratory ce ntre to CO2, Occurs in left vent ricular fail ure, ce nt ral respiratory depression and in no rmal infants
OXYGEN THERAPY
In chron ic hypoxia d ue to hypovent ilation (e.g. chronic bronch it is) the arter ia l Pe02 is raised and correction of the hypoxia by oxygen in high co ncentrat ion may release the respi ratory cent re from its 'anoxic d rive' and produce COz narcosis. l ow-concentrat ion (24%) oxygen masks such as the Vent imask shou ld be used, w ith serial b lood gas analyses. If CO2 cont inues to rise, respi ratory st im u lants or m echanica l vent ilation may be needed.
In hypoxia d ue to impaired gas exchange (e.g . pneumonia, pu lmonary oedema) high concent rat ion masks delivering 35-60% oxygen are requ ired
DEFINITIONS OF COMMON PULMONARY DISEASE
CHRONIC BRONCHITIS
Chron ic or rec urrent increase in the volume of m ucoid bronchial secretion suffic ient to cause expectorat ion (usua ll y da ily co ugh w ith sputum for 3 months each year for at least 2 co nsecut ive years ). There is an obstructive e lement w h ich is only partially reve rsib le
EMPHYSEMA (defined h istologica l ly)
Is character ized by en largement of the ai r spaces dista l to the terminal bronch io les, wi t h destruct ion of the alveolar wal ls
Chest dise ase
CHRONIC OBSTRUCTIVE AIRWAYS DISEASE ICOADI
This comprises chron ic bronch it is and em physema, w hich are o ften present simultaneously. Bronch iectasis is often m isd iagnosed as bronch itis
ASTHMA
Is characterized by va riable, often paroxysmal, dyspnoea due to w idespread narrowing of the bronchio les. PEFR or FEV, is decreased, but at least 20% o f the decrease m ust be reversi b le over a few m inutes or days
Feature s of a seve re asthma a ttac k in an adult , . Can't com plete sentences in one breath 2. Respi rat ory rate exceeds 24/mi n 3 . Pulse exceeds 110/m in .4 . PEFR less than 50% of p red icted o r previous best
Features of a Iife.threatening asthma attack ,. PEFR less than 33% of p redicted o r previous best 2. Si lent chest, cyanosis or feeb le respiratory effort 3. Bradyca rd ia or hypotension 4 . Exhaust ion, confusion 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. Normal or h igh PacOz 2. Severe hypoxia, Pa02 less than 8 kPa despite oxygen therapy 3. l ow pH
HARMFUL EFFECTS OF CIGARETTE SMOKING
1. PHARMACOLOGICAL EFFECTS OF NICOTINE
Rise in BP, tachycard ia, increased p latelet st ickiness, etc.
2. PHARYNGEAL A ND BRONCHIAL IRRITATION
Bronchit is, post -op. pneumonia, etc.
3. CARCINOMA RISK IN CREASED
Bronchus, oesophagus, prostate, b ladder
4. CARDIOVASCULAR DISEASE
Myocardial ischaemia, Buerge r's d isease, 'strokes'
II I Chest d isease
5. OSTEOPOROSIS RISK INCREASED
6. PASSIVE SMOKING EFFECTS
(i) Effect on fetus due to smoking in pregnancy: restricted growth, increased per inatal morta lity
(ii) Effect on non-smokers : cough, asthma, angina
COM MON CAUSES OF CLUBBING
RESPIRATORY
1. Bronchia l ca rcinoma 2. Chronic pu lmonary suppurat ion, e.g. bronch iectasis, cystic f ibrosis
CARDIOVASCULAR
1. Bacterial endocard it is 2. Cyanot iC congen ita l heart d isease
LESS COM MON CAUSES INCLUDE,
1. Asbestosis, especially w ith mesothelioma 2. Fibrosing alveo lit is 3. Ulcerative col it is & Crohn's 4. Malabsorption 5. Cirrhos is 6. Graves' d isease 7. Brach ial arteriovenous f istu la (uni lateral ) 8. Fami lial
HAEMOPTVSIS
COMMON CAUSES
Respiratory 1. Bronchia l carc inoma 2 . Pulmonary tube rcu losis 3 . Bronch it is 4. Bronch iectas is 5. Lung abscess
Cardiovascular 1. Pu lmonary infa rct 2. Mitral stenosis 3. Acute left ventricu lar fa i lure
Less common causes include : 1. Pneumonia, especially pneumococcal 2. Collagen~vascu l a r disease, espec ia lly po lyarteritis nodosa
Chest d isease I
3. Idiopath ic pulmonary haemosiderosis 4. Bleed ing diathes is 5. Mycoses, e.g. aspe rgil losis 6. Foreign body 7. Hereditary haemorrhag ic telang iectas ia 8. Wegener's granu lomatos is 9. Goodpasture's synd rome
Exclude spurious haemoptys is (nasa l b leeding, etc. )
In many patients w ith a sma ll haemoptysis and negative physica l f ind ings, no cause is ever found despite foll ow-up w it h serial chest X-rays
PNEUMONIA
Primary pneumonias are usually acqu ired in the commun ity Secondary pneumonias occur w hen the lungs are already
diseased
AETIOLOG ICAL CLASSIFICATION
1. Infective (] ) Bacterial
a. Strep . pneumon iae b. Mycoplasma pneumoniae c. Haemophilus influenzae d. Legionella pneumophila e. Ch lamyd ia psittaci f. Staph. au reus (may be abscesses) g. Klebsiell a pneumoniae (may cavitate) h. Mycobacter ia (e.g. TB) Pneumon ia may also be a feature of general ized bacte rial infect ions, e.g. brucellosis, typhoid fever, plague
(ii) Viral a. Respira tory syncytial b. Inf luenza (usua lly secondary bacterial infection) c. Mumps (usually secondary bacterial infection ) d. Cytomegalovirus e. URT v iruses (adenovirus, rhinovirus, parainf luenza)
(iii ) Rickettsial a. Typhus b. Q feve r
(iv) Yeasts and fungi a. Candida b. Histoplasma
(v) Protozoa and parasites a. Pneumocystis ca rin ii b. Toxo plasma c. Amoebae
II I Che s t d isease
2. Allergic Collagen- vascular d isease (esp . polyarter itis nodosa) Stevens- Johnson syndrome (eryt hema mult ifo rme)
3. Chemical agents (I ) Irr itant gases: NH3 , S02. C12, oxides of nit rogen
(ii ) Irr itant liqu ids: vom itus, lipoid pneumon ia
4. Physical agents - irradiat ion
In discussing causes of pneumon ia remem ber the possib ility of 1. Opportunistic organisms in immune deficiency, especia lly AIDS 2. Pre-exist ing lung disease . e.g. bronchi al ca rcinoma and
bronchiectasis. especially if the pneumonia is recu rrent or un responsive
3. Inhalation pneumon ia (i ) Oral an d pharyngeal sepsis and sinus it is
(i i) Oesophagea l obstruction and pharyngea l pouch (I ii) A lcoho lic debauch, drowning o r anaesthesia (iv) l aryngea l cancer (v) Tracheo-oesophagea l fistu la
(vi) Inadequate gag ref lex 4 . Predisposing systemic disease such as diabetes, cirrhos is.
alcoholism or agranu locytosis 5. Foreign body not seen. on X-ray (e.g . peanut)
COMPLICATIONS OF PNEUMOCOCCAL LOBAR PNEUMON IA
1. Pleurisy w ith effusion, or serous pericardit is 2. Empyema or pe rica rdial suppurat ion 3. Endoca rdit is, men ing it is (not to be confused w it h men ingismus,
in wh ich CSF is no rma l) or cereb ral abscess 4. Delayed reso lution 5. Nonspecific complications
(i ) Herpes labia lis (ii ) Septicaemia (may be 'shock')
(I ii) Ca rd iac fa ilure (iv) Ca rd iac arrhyt hmia (v) Deep ve in thrombosis
CAUSES OF EMPYEMA
1. Pneumonia, especia ll y lobar, or seconda ry to bronch ial Ca 2. Lung abscess 3 . Subphren ic abscess 4. Med iastina l sepsis 5. Chest wound or su rgery 6. T8
CAUSES OF PULMONARY COLLAPSE
1. ABSORPTION COLLAPSE
Due to complete bronchial obst ruction
Chest disease I
(I ) Int ra lum ina l, e.g. foreign body, mucus or clot (ii) Mural, e.g . bronch ial carcinoma or adenoma
(iii) Extramural, e.g. peribronch ial lymphadenopathy or aortic aneurysm
2. PNEUMOTHORAX OR PLEURAL EFFUS ION
Remembe r that in abso rption collapse t he mediast inum sh ifts to the affected side. but in co ll apse due to air or fl uid in t he pleura l space the mediast inum may sh ift to t he oppos ite side
CAUSES OF PLEURAL EFFUSION
TRANSUDATE
(less than 30 g protein/ lit re. Im plies a system ic cause) 1. Card iac fai lure 2. Nephrot ic syndrome 3. Hepatic fa ilure
EXUDATE
(More than 30 g protein/li tre. Im plies a loca l ca use) 1. Pulmonary embo li 2. Rheumatoid d isease 3. Infections (pneumon ia, T8 ) 4 . SLE and othe r collagen- vascu lar d iseases 5. M alignancy (bronchial Ca, secondary Ca, Hodgkin 's,
mesothe lioma) 6. Subph ren ic abscess
Mnemonic: PRISMS
CAUSES OF PNEUMOTHORAX
1. Traumat ic 2. Iatrogenic, e.g. t ho racentesis or surgery 3. Spontaneous
(i) Subpleu ral bulla {iiI Emphysema
(iii) Ast hma (iv) T8 (v) Lung abscess
(vi) Pneumocon iosis
I Chest disease
CAUSES OF ACUTE PULM ONARY OEDEMA
1. Left heart fa i lure ( i) Atrial, e.g. mitral stenosis {iii Ventricu lar, e.g. hypertension or myocard ia l infa rct
2. Overload of Lv. f luid 3. Inha lat ion of i rritant gas, e.g. chlo rine, dense smoke 4. Fu lminat ing viral or bacterial pneumon ia 5. Fat embol i 6. Neurogenic (rare)
e.g. Head in j ury or cerebro-vascular accident
CAUSES OF INTERSTITIAL LUNG DISEASE
1. Cryptogen ic fi b rosing alveolit is 2. Sa rcoidosis 3. Extrinsic all erg ic alveolit is 4. Asbestosis, pneumocon iosis or sili cosis 5. Drugs or irrad iation 6. Pu lmonary eosinoph il ia 7. Collagen- vascu lar d isease
BRONCHIECTASIS
Permanent di latation of t he bronchi, usually accompanied by rec urrent bronch ial suppuration
PATHOGENESIS
An imal experiments suggest that proxima l narrowing of the airways and dist al infect ion are both important
CAUSES
1. Infection (i) Bronch iol it is of infancy {i ii Measles o r pertussis in ch ildren
(i ii ) Post broncho-pneumonic collapse in adults (iv) Common ly in post-primary TB
2. Bronchial stenosis or occlusion (i) Adenoma or carcinoma
(i i) Foreign body or asthma casts (i ii) Lymphadenopathy
3. Pu lmonary asperg i llosis 4. Cyst ic fibrosis 5. Hypogammaglobul inaemia 6. Cil iary dysfunction (e.g. Kartagener's synd rome) 7. Many cases are idiopath ic
Chest d isease I
CLINICAL FEATURES
1. Class ical symptom - cough with copious puru lent sputu m, especia lly on chang ing posture
2. Class ical sign - loca lized persistent coa rse crepitations 3. May be asympto matic 4. Mala ise, interm ittent fever, hal itosis 5. Weight loss or 'fa ilu re to thrive' 6. Dyspnoea, cyanosis or cl ubbing 7. Haemoptysis
TYPES OF CA BRONCHUS
1. Squamous (35%) 2. Oat ce ll (small cell ) (25%) 3. Large cell (20%) 4. A denocarcinoma (20%)
Mnemonic: SOLA
COMPLICATIONS OF CA BRONCHUS
LOCAL EFFECTS
1. Bronchial obstruction: collapse, conso lidation, abscess 2. Mal ignant pleura l effusion 3. Erosion of large vessel 4. Superior vena cava l obstruction 5. Di rect spread to chest wa ll, brachial p lexus (pancoast's) 6. Horner's syndrome from cervica l sympathetic compression
Hoarseness from recurrent laryngeal nerve compression H igh diaphragm from phren ic nerve involvement
M ETASTASES
Especially hilar nodes, l iver, brain, bone, adrenals
NON-METASTATIC EXTRA-PULMONARY EFFECTS
1. Cachexia and anaemia 2. Clubb ing (hypertroph ic pu lmonary osteoa rth ropathy) 3. Endocrine
(i ) Gynaecomastia {iii Inappropriate AD H ---> hyponatraemia (often small celt)
(ii i) Inappropriate PTH ---> hyperca lcaemia (often squamous) (iv) Inappropriate ACTH ~ . pigmentation, hypokalaem ia,
alka los is (often smal l cell ) 4. Dermatolog ical
Pigmentation, prurit us, etc. (see page 156) 5. Neuropathy or myopathy (incl. de rmatomyosit is and Eaton
Lambert syndrome)
_ I Che s t disease
TUBERCULOSIS
PRIMARYTB
Occurs in subjects never previously exposed to TB 'Primary com plex' == Ghon focus + reg iona l lymphadenopathy Abdominal primary TB and t ubercu lous ce rv ical lymphaden itis are now uncom m on in the United Kingdom, except in t he im m igrant populat ion
PULMONARY PRIMARY TB
Usually hea ls spontaneously
Complications 1. Loca l spread in lung 2. Cavitat ion 3. Pleural effusion (may develop before posit ive Mantoux) 4. Ru pture of caseou s node into bronchus causing w idespread
bronchopneumo nia 5. Segmental co ll apse due to bronch ia l co m pression by nodes 6. 'M iddle lobe syndrome', i.e. bronch iectasis in later life due to
bronch ial comp ress ion by nodes 7. Haematogenous metastasis
( i) Bone (ii) Kidney
(iii) Epid idymis or Fallo pian tubes l iv) Meninges
8. M il iary TB
POST-PRIMARY TB
Reinfect ion or recrudescence o f primary lesion. Usuall y pu lmonary, but may be m il iary or atypical in t he o ld or immunosuppressed
PULMONARY TB
Complications 1. Caseat ion ('cold abscess' ) 2. Bronchogenic spread in lungs 3. Pleurisy 4. Effusion or TB em pyema 5. Haemoptysis, m ay be mass ive 6. Tension cavity d ue to valvu lar obstruct ion 7. Tube rcu loma of lungs 8. Haematogenous metastasi s or m il iary TB 9. Chronic pu lmonary fibrosis and com pensatory emphysema
(especially in m iners)
Ches t d isease I _
10. TB tracheit is, laryngitis or stomatit is due to expectorat ion of mycobacteria
11. Swallowed sputum may cause intestina l TB (usually in lymphoid patches)
12. Amylo idosis
COMMON PRESENTATIONS OF PULMONARY TB
1. Asym ptomatic (screening CXR) 2. Persistent cough 3. Ti redness, ma laise, recurrent coryza, weight loss or fever 4. Pneumonia 5. Haemoptysis 6. Dyspepsia
Note increased incidence in immigrants, el derly, immunosuppressed, d iabet ic and after gast rectomy fo r pept ic ulce r
SARCOIDOSIS
Defi n itio n: a mult isystem g ranulomato us disease (of unknown orig in ), in w hich the granu lomas consist of w ell-formed, sharp ly demarcated collections o f ep ithel io id cells, wi th linle or no caseatio n, and litt le cellu lar reaction around them
CLI NICAL FEATU RES OF SARCOIDOSIS
1. Pulmonary: Bilatera l hilar lym phadenopathy (SHU
1 BHl + pre·fi b rot ic pu lmonary infi lt ra t ion
1 Either resolut ion or pulmonary f ib rosis
2. Const itutional symptoms, febrile arthra lg ia 3. Superficial lym phadenopathy 4. Skin lesions - erythema nodosum, lupus pernio, infi lt rated
plaq ues, nodu les, infi lt ra tes in sca rs 5. Ocular lesions - uve it is, con junctival inf i ltrates, etc. 6. Parot id, lacr imal g land lesions 7. Neuro log ical lesions
(i) Neu ropat hy, especially facial nerve (ii) Meningea l inf ilt ration and local CNS depos its
8. liver, spleen or cardiac infiltra tion 9. Bone involvem ent, especially phalangea l cysts
10. Hypercalcaemia ± nephrocalcinosis and calcu li
I PHYSICAL SIGNS IN LUNG DISEASE n
Ch •• , wall Mediastinum Tactile vo.:.' Percu •• ion Br •• th Added ~ •
movement and trachea f . emitus not. lounda sounds • • ~.
Large pleural effu . lo n Decreased on Shift 10 opposite Absent Stony dull Absent. May be Absent. May " affected side side bronchial be pleural • • (:t whispering rub above • • pec1oriloquyl "uid above fluid level
Contla lidation Decreased on Cent, 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 Increased Dull Bronchia l May be with decreased side coarse movement crep itations
Large pn. umotho ... Decreased on Sh ift to opposite Decreased Increased Decreased Absent affected side side unless bowel
sounds 8rft transmitted
EmphVIBma Decreased Centra l (except Decreased Increased Oecreased Absent bilateral in unilatera l ('barre l chest') emphysema)
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 lm (usual) or an AP fi lm ? (im p ly ing the pat ient was
too ill to stand up for the fi lm, and thus prevent ing assessment of hea rt size)
3. Is the f i lm well orientated and correct ly penet rated? 4. The lungs a nd hila '
Count the v isib le R ibs to assess the size of the lungs Look at the lung fi.e lds for any A symmet ry Is the T rachea d isp laced? Are there any abnorma liti es in the lung Fields? Are the A pices clear? (check for T8 or smal l pneumot horax) Are the Costo-phren ic angles b lunted? Are the hila Enla rged? M nemonic: RATFACE
5. The hea rt Is it enlarged and is its outline normal?
6. The ribs and spine Look for fractu res, metastases, rib notches, etc.
7. Any other shadows1 Tracheostomy, cent ral line, prosthet 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 emphysem a, gas under A d iaph ragm, etc.
CAUSES OF WHOLE LUNG OPACITY
1 . Consolidation of L lung 2. Massive L ple ura l e ffus io n
Mediast inum central Mediastinum and t rachea m ove to R
_ I Chest X -rays
3 . Collapse of e ntire l lu n g
Fea t ure s 1. Trachea pulled to L 2. A heart bo rder not seen 3. l diap hragm obscu red 4. A lung hypertranslucent
COLLAPSE OF R UPPER LOBE
Fe ature s 1. Dense wedge against superior med iast inum 2. R h ilar vessels d rawn up, and w idely spaced 3. A lower and m idd le lobes hypertranslucent 4. Trachea and aortic knob pul led to R
COLLAPSE OF L LOWER LOBE
Chest X-rays I _
Fe atures 1. Dense wedge in heart shadow and diaph rag m beh ind l side of
heart obscured 2. L hilar vessels pul led down and w idely spaced 3. L upper lobe hypertranslucenl
R PLEURAL EFFUSION
Note fl u id in horizontal fissu re
SMALL L PNEUMOTHORAX R HYDROPNE UMOTHORAX
Usually traumat ic (including pleural asp irat io n)
PULMONARY OEDEMA
Features 1. 'Bats-wing' shadows - ill defined and confluent, spread ing out
from h ila
_ I Ches t X-rays
2. Generalized lower-zone haze 3. Upper lobe diversion of blood 4. Kerley B lines 5. Enlarged hea rt
EMPHYSEMA
Features 1. Hypertranslucent lung fie lds 2. Main pulmonary vessels are large, but peripheral vesse ls are
th in 3. Th in vertica l heart 4. Horizontal ribs w ith low flat dia phragm
SINGLE LARGE OVAL SHADOW
Common causes 1. Bronchial cancer 2. Metastat ic deposit. e.g. breast ca ncer, hypernephroma
Less common causes 3. TB (may be ca lcifi ed) 4. Abscess 5. Encysted p leu ral effusion 6. Cyst, e.g. hydatid 7. Adenoma, fi broma or hamartoma 8. AV aneu rysm
Chest X-rays I •
MU LTIPLE CI RCULAR SHADOWS
Causes 1. M etastatic ma lignancy 2. Hydatid cysts 3. Caplan's syndrome (rheumatoid arth r itis with pneumoconiosis) 4. Multiple lung abscesses 5. Wegener's granulomatosis
WIDESPREAD SHADOWIN G
Causes include 1. Mi lia ry TB 2. Pu lmonary oedema 3. Bronchopneumon ia 4. Pneumocon iosis or haemosiderosis 5. Sarcoidosis 6. Systemic sclerosis 7. Fibrosing alveol it is and rheumatoid lung 8. Hypersensitiv ity, e.g. allergi c alveo 1it is ('farmer's lung', etc .) 9. Neoplasm:
Miliary Ca metastases Lymphangitis ca rcinomatosa Alveo lar cel1 ca rcinoma
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 PHADENOPATHY
Causes include 1. Sa rco idosis 2. Lymphocytic leukaemia 3. Lymphoma 4. Ca rcinom a m etastases 5. Prim ary t uberculosis 6. Acute infect ions, e.g . infecti ous mononucleosis o r wh ooping
coug h
If un ilatera l, examine lung f ields carefu lly fo r bronchia l carcinom a or Gho n focus
NORMAL CARDIAC SHADOW IN PA X-RAY
Aortic arch
Aortic arch ..... .... .....
" .... __ Pulmonary artery
A. atrium .................. .. ____ ___ L atrial appendage
....... .. L ventricle
Transve rsa d iameter of heart does not norma lly exceed 50% of chest w idth
Chest X -r ays I _
SYSTEM IC HYPERTENSION
Features 1. Aort ic unfolding 2. LV hypertrophy 3. Ker ley B lines (horizonta l lines in casto ph ren ic ang les due to
d ilated subpleu ra l lymphatics) if LV fa ilu re develops
M ITRAL STENOSIS
Features , . Stra ight L hea rt bo rder and convex R borde r 2. Increased pu lmonary vasc ul ar shadow s 3. Kerley B lines
_ I Chest X-rays
COARCTATION OF AORTA
Features 1. LV hypert rophy 2. Small ao rt ic arch 3. Rib notch ing
PERICARDIAL EFFUSION
Fe ature s 1. La rge rounded heart shadow 2. Note sharp cardio-phrenic ang les
Distinction from di lated heart may be ve ry d ifficu lt
6. Gastroenterology
CAUSES OF ATROPHIC GLOSSITIS (SMOOTH REO TONGUE)
1. Antibiotics 2. Anaemia due to deficiency of Fe, 8'2 or fo late 3. Vitamin def iciency (r iboflavin or nicot in ic acid )
CAUSES OF DYSPHAGIA
1. LESIONS OF MOUTH OR PHARYNX
(i) Stomatitis or g lossiti s (i i ) Tonsill itis
(i ii) Qu insy, retropharyngea l abscess (iv) Lymphoma of tonsil
2. FOREIGN BODY IN PHARYNX OR OESOPHAGUS
3. INTRINSIC DISEASE OF PHARYNX OR OESOPHAGUS
(i ) Plummer- Vinson synd rome - i ron deficiency, glossit is, pharyngeal web and koilonychia
(ii) Pharyngeal pouch (ii i) In flamm ation, strictu re or neop lasm of oesophagus (iv ) Systemic sclerosis Iv) Oesophageal achalasia
4. EXTRINSIC COMPRESSION
(i ) Tumo urs in neck (ii ) Mediast ina l tumour, e.g. retrosternal goit re, lym ph nodes
(iii ) Bronchia l cancer (iv) Aortic aneurysm
5. eNS LESIONS
(i) Bu lba r o r pseudo-bulbar palsy (ii) Myasthenia g ravis
(ii i ) Congenita l muscular incoordinat ion
-
_ I Gastroe nte ro logy
COMMON CAUSES OF SEVERE UPPER GI BLEEDING
1. Duodenal ulce r 2. Oesophagea l varices 3. Erosive gastri t is (e.g . due to aspi rin or NSAID) 4. Gast ric u lce r (may be ma lignant) 5. Eros ive oesophag it is (e.g. hiatus hernia)
COMMON CAUSES OF SEVERE LOWER GI BLEEDING
1. Colon ic d ivert icu lar disease 2. Ca rcinoma o f rectum or colon 3. Benign rectal po lyps 4. Haemorrho ids or ana l f issu re 5. Colon ic ang iodysp lasia 6. Ulcerative col itis or Crohn's disease 7. Recta l trauma, includ ing biopsy 8. Hookw orm (in t ropics)
N.B. Hiatus hern ia, co lon ic d ivert iculosis and haemorrhoids are common. Massive b lood loss shou ld not be attributed to t hem un less the sou rce of bleeding can be seen, or more ser ious pathology can be excluded
MEDICAL CAUSES OF ACUTE ABDOMINAL PAIN
, . Food po ison ing or dietary ind isc retion 2. Peptic ulcer, gast ritis, oesophag itis 3. Biliary col ic or cholecystit is 4. Pa ncreatitis 5. Hepatic congestion (hepat it is, card iac fa i lure) 6. Renal col ic, pye loneph ri t is, cystit is, acute urinary retention 7. Divert icu litis, ulcerat ive col itis, Crohn's d isease 8. Mesenteric adenitis (chi ldren) 9. Const ipat ion
10. Mesenteric ischaem ia (atheroma, embol ism, po lyarterit is nodosa i
11. Aort ic dissect ion 12. Gynaecolog ica l, e.g.
M ittelschmerz (ovulation) Dysm enorrhoea Salp ing it is Threatened abort ion
13. Pa in referred from sp ine or chest (e.g. myocard ial infa rct)
N.B. Pain in the abdomen w h ich lasts for more than 6 hours wi t hout remissio n is likely to be surg ica l
Rarer causes of acute abd om ina l pa in incl ude: acute intermittent porphyria, he rpes zoste r, d iabetes mell itus (gastric di latation ),
Gastroenterology I
sick le-cell crisis, lead poisoning, hered ita ry angio-oedema, Henoch- Sch6n lei n purpura, etc.
PEPTIC ULCERS
DIFFERENCES BElWEE N GASTRIC AND DUODENAL ULCERS
G astri c Duodenal
Site Usuallv m iddle 2/3 of Usually duodenal bu lb lesser curve
Gastri c acid Low o r normal Hvperchlorhvd ria
Pa in After meals Re lieved by meals Mav occur at about 2 a.m .
Vomiting Common Uncom mo n
Soc ia l c lass Commoner in lower Equal prevalence soc ial classes
Pathology Mav be benign or Virtually never mal ignant m al ignant
He l icob acter pylori ,,% ""%
FACTORS SUGGESTING A GASTRIC ULCER IS MALIGNANT
Symptoms 1. Anorexia and weight loss 2. Epigastric pain not related to food 3. Dysphagia
N.B. The pa in of both beni gn and mal ignant u lcers may be rel ieved by Hrblocke rs
Signs 1. Ep igastric mass 2. Metastases. look especiall y for
(i ) l arge irregu lar liver (ii) Supraclavicu lar nodes (Virch ow's)
(i ii) Deep vein t h rombosis of leg (IV) Ascites (v) Kru kenberg tumou r of ovary (felt PRJ
Barium m eal 1. Fi ll ing defect and fa ilu re of perista lsis in a site other t han
m iddle 2/3 of lesser curve 2. Very large ulcer anywhere in t he stomach 3. Leather-bottle stomach
_ I Gastroenterologv
If in doubt gastroscopy (with b iopsy) and gastric cytology should be performed
COMPLICATIONS OF PEPTIC ULCER
1. Bleeding 2. Penetrat ion , e.g . into pancreas, l iver o r retrope ritonea l space 3. Perfo ration 4. Obstruction
(i) Oedema and spasm - reversib le Iii) Cicatricial stenosis - ir reversible
5. 'M ilk- atkali sy ndrome' - alkalosis and calcinosis, due to excessive ingestion of mi lk, alkali and ca lcium salts
MALABSORPTION
CAUSES
1. Inadequate digestion m Gastr ic or intestinal resect io n
(ii ) Hepat ic or bi liary tract obstruction (i ii) Pancreatic insufficiency (especially cystic fibrosis)
2 . Parasites or change in intestinal flora (i) Tapeworms or Giardiasis
(ii) Blind-l oop syndromes
3. Tropical sprue
4. Intestinal hurry or fistulae
5 . Coeliac disease A IDS and erythroderma can also cause partial v illous atrophy
6 . Intestinal infil tration 0) TB
(ii) Lymphoma or leukaemia (ii i) System ic scle rosis (iv) Intestinal lipodystrophy (W hipple's d isease )
7 . Enzyme defects (I) Lactase defic iency
(il) Hartnup d isease
8 . Chronic intestinal ischaemia, e.g. mesenteric atherom a
N. B. The fat-solub le vitamins are 0 A K E
Gastroenterology I
CLINICAL FEATURES OF COELIAC DISEASE IN ADULT
1. Loose stools w hich mayor m ay not be bulky. pa le and fou l-smelling
2. We ight loss (fat and protein def iciency) 3. Oedema (prote in deficiency) 4. Flatu lence w ith d istended abdomen (impai red disaccharide
hydro lys is) 5. Hypochromic anaem ia (Fe deficiency) 6. Macrocytic anaemia (fo late o r 8 12 deficiency) 7. Peripheral neuritis (S-com plex defic iency) 8. Glossit is and stomatitis (S-com plex def iciency) 9. Osteomalacia (Ca and vitamin 0 deficiency)
10. Paraesthesiae. tetany (Ca or Mg defic iency) 11. Haemorrhage (vitam in K deficiency) 12. Muscle flaccidi ty. arrhythmias (potass ium deficiency) 13. Weakness and hy potension (water and elect ro lyte deficiency) 14. Clubbing 15. De rmat it is herpet iform is is strong ly associated
AIDS AND THE GI TRACT
1. INFECTIONS ASSOCIATEO WITH ANAL INTERCOURSE
e.g. ana l w arts, herpes simplex. hepat it is A and S, etc.
2. OPPORTUNISTIC INFECTIONS
e.g. candida , cry ptosporidiosis, cytomega lovi ru s, myco bacteria
3. KAPOSI'S SA RCOMA
4. LYMPHOMA
May involve CNS, m arrow o r gut
5. PARTIAL VILLOUS ATROPHY WITH MALABSORPTION
CAUSES OF ASCITES
1. Carci noma, especi ally ovarian or alimentary w it h peri toneal metastases
2. Cirrhos is 3. Hypoalbuminaem ia, e.g . nephrot ic synd rom e 4. Constrict ive per icardit is, co ngest ive heart fai lure 5. Thrombosis or obstruction o f inferior vena cava 6. Tu bercu lous per itonitis 7. Peritonit is in late stages 8. Chylous ascites due to lymphat ic obstruct ion
I Gastro enterology
CAUSES OF OBSTRUCTION OF THE SMALL INTESTINE
The commonest ca uses are adhesions secondary to operat ion and bowel incarceration in an intern al or externa l hern ia
MECHANICAL
1. Compress ion from w itho ut: (i) Adhesions
(i i) Fibrous bands (i ii) Tumours, especially of fema le pelv ic organs (iv ) Hernia
2. Com pression from w ithin the bowel wall : (i) Congen ita l atresia
(ii) Acqu i red : Infl ammatory Neoplast ic Traumatic
3. Obstruction inside t he lumen: (i) Gallstones
(i i) Faeca l impaction (ii i) Meconium ileus (iv) Foreign bodies (v ) Wo rms
4. Vo lv ulus 5. Intussusception
PARALYTIC ILEUS (no colicky pa in or bowel sounds)
1. Abdom inal su rgery 2. Peri ton itis 3. Acute systemic illness, e.g. pneumon ia 4. Pa infu l lumbar conditions, e.g.
rena l co lic retroperitonea l haematoma
·5. Mesenteric ischaemia 6. Drugs, e.g . gang l ion-blockers 7. Hypokalaemia 8. Hypot hyroid ism
DIVERTICULITIS
CLI NICAL FEATU RES
1. Usua lly m idd le-aged o r elderly 2. Recurrent bouts of co licky abdomina l pain 3. Nausea and vom it ing 4. May be either constipation or d iarrhoea 5. Tenderness in L iliac fossa, sometimes w ith a mass
Gast ro ente rolo g y I _
COMPLICATIONS
1. Obstruction due to strictu re 2. Perforation 3. Abscess 4. Fistu la into b ladde r o r vagina
BAR IUM ENEMA
1. Divert icu la mayor may not be seen 2. Segmenta l spasm and irri tabil ity of the affected co lon (usually
sigmoid) 3. Chron ic f ibrotic deformity
ULCERATIVE COLITIS
CLI NICAL FEATURES
1. Common ly present s in 3rd or 4t h decade 2. Malaise, weakness, weight loss, pyrexia 3. Chron ic d iarrhoea, w it h blood and mucus, w hich is often severe 4 . Pa in in L il iac fossa, and recta l tenesmus
COM PLICATIONS
1. Perforation 2. Per ianal abscess 3. Acute 'toxic di latation' 4. Severe haemorrhage 5. Hypokalaem ia, hypoproteinaemia, dehydration 6. Skin lesions:
(i) Pyode rma gangrenosum I ii) Aphthous ulcers (iii) Erythema nodosum (iv) Clubbing
7. Diffuse liver disease and sclerosing cho langitis 8. Arthrit is and uve it is 9. Amyloidosis after chron ic abscesses
10. Ca rcinoma of co lon
BARIUM ENEMA
, . Loss of haustration 2. St raight , narrow, inelastic co lon 3. May be 'spicu les' due to t iny ulcer craters 4. May be f i ll ing defects due to 'pseudopolyps'
N.B. Abnorma lit ies are usuall y continuous (no 'skip' lesions), and start at the rect um, affecting a variable length of the large bowe l
_ I Gastroentero logv
CROHN' S DISEASE (REGIONAL ILEITISI
CLI NICAL FEATURES
1, Usua ll y youn g adults 2. Mala ise, weakness, weight loss, py rexia 3. Interm itte nt col icky pain in R il iac fossa 4. M ild or moderate diarrhoea 5. Tenderness in R iliac fossa, someti mes w ith a fixed mass
COMPLICATIONS
1. Obstruct ion due to stricture 2. Pe rforation 3. Abscess 4. Fistula into anus, b ladder or abdominal wall 5. F issu re~ i n-ano
6. Malabso rpt ion (especia ll y Bd 7. Proctoco lit is 8. Erythema nodosum 9. Clubbing
BA STUDIES (may need both meal and enema)
1. l uminal narrowing of ileum (Kantor's 'si ring sign') 2. Distorted mucosal pattern 3. 'Skip' lesions
The correlation between rad iolog ical appearance and d isease act ivity is often poo r
FEATURES DISTINGUISHING CROHN' S AND ULCERATIVE COLITIS
Cro hn'. Ulceratly" colhls
GranulOtna. Present Absent In flammation Transmural Confined to mucosa Goblat 0;:.11, Normal number Decreased Crypt abso;:.sses Unusual Common Fi ' tulae Common Uncommon Skip I.,ion , Present Absent T. rmlnat il eum Usually inVOlved Rarely Invo lved Rao;:t al In vo lvemant Unusual Almost invariable
CAUSES OF HEPATOMEGALY
1. Hepatic congest ion, e.g. card iac failure, hepatic vein throm bosis. The liver is pulsat ile in severe tricuspid regurgitat ion
,.
2. Neoplasm (i) Metastases
(i i) Lymphoma (i i i) Hepatoma
Gastroenterology I
3. Myelop rol ife rat ive disease, e.g. leukaem ia, myelofibrosis 4. Infective
(i) Vi ral, e.g. hepat it is (Q .v.) I ii ) Bacter ial, e.g. Weil's disease (ii i) Protozoa l, e.g. amoebic abscess (iv) Parasit ic, e.g. hydatid cyst
5. Bil iary obstruction, e.g. Ca pancreas 6. Fatty inf iltration or early ci rrhosis 7. Storage disorders, e.g . amyloidosis, Gaucher's
CAUSES OF A HARD KNOBBLY LIVER
1. Cancer metastases 2. Cirrhosis w ith hepatoma 3. Polycystic live r 4. Hydatid cysts
CAUSES OF HEPATO·SPLENOMEGALY
1. Infection, e.g. infectious mononucleosis 2. Myeloproliferative disease 3. Lymphoma 4. Storage d iseases, e.g. amyloidos is, Gaucher's
CIRRHOSIS
Ci rrhosis is character ized by hepat ic pa renchymal damage w ith fibrosis and nodular regenerat ion throughout the liver, accompanied by distortion of the normal lobular pattern
CAUSES OF CIRRHOSIS
1. Cryptogenic (idi opath ic) 2. A lco hol ism 3. Viral hepat it is (espec ially hepatitis B o r C) 4. 'Autoimmune' live r d isease
(i) Primary bi liary cirrhosis (antim itochondrial Ab in 95%) (i i ) Ch ron ic active hepat iti s (smooth m uscle Ab in 66%)
5. Haemochromatosis (primary or secondary) 6. Hepato-Ienticu lar degeneration (Wilson's) 7. Hepatotoxins, e.g. methotrexate, carbon tetrachloride
_ I Gastroenterology
CLIN ICAL FEATURES OF CIRRHOSIS
Features of he patic failure ,. Fi rm hepatomega ly in the early stages 2. Low grade fever 3. Skin changes:
(i) Jaundice in later stages ( i i) ' Spiders'
(i i i) Pa lmar erythema (iv) Leuconych ia (wh ite nail s)
4. Bleeding tendency (decreased coagu lation factors) 5. Fatigue, weight loss, dyspepsia 6. Foetor hepaticus 7. Encephalopathy:
(i) lethargy (ii) Slow, slurred speech
(i i i ) Flapping tremo r (iv) Dem entia (v ) Precama progress ing to deli rium and coma
8. Water retention : (i) Oedema
Oi) Hyponatraemia
Features of porta l hyperte nsion 1. Splenomegaly, often with pancytopenia (hypersplen ism) 2. GI bleeding f rom oesophageal va rices 3. Ascites (low p lasma albumin is also necessary)
Ot her features 1. Clubb ing 2. Hyperkinetic ci rcu lation 3. Sexual changes:
Females: errat ic menstruation and breast atrophy Ma les: gynaecomastia, testicu lar at ro phy and scanty body hai r
4. Parotid en largement l. I . 5. Dupuyt ren's co nt ractu re J In a co hohcs 6. Suscepti bil ity to infections
J AUNDICE
Jaundice (icterus) is due to hyperbilirubinaemia . It involves the sclerae, unl ike the yellow pigmentation due to mepac rine or caroten aemia
CAUSES
Pre-h epa tic 1. Haemolysis 2. Ineffective eryth ropoiesis
Gastroenterology
Hepatic (a) Impa ired conjugation
(i) Hepatitis (vira l or drug-induced) (ii) G ilbert's syndrome
(b) Impaired excretion ( i) Hepatitis
(ii) Methyltestosterone Idose-related) (i ii ) Ch lorpromazine (hypersensitivi ty)
(c) Intra-hepatic obstruct ion (i ) Hepatit is
(i i ) Cirrhosis (ii i) Tumour
Post-hepatic (i) Stone in common bile duct (CBO)
(ii) Carcinoma of head of panc reas or b iliary t ract (i ii) Pressure on CBD from lymph nodes l iv) St ricture of CBD (post -operative or post-inf lammatory) (v) DeveLopmenta l anoma l ies (rare)
SUMMARY OF BLOOD CHANGES
Obst~uC1ive Hepe(ocell u la~ Haemolytic fa ilure with no oba1ruction
Hyperbilirubinae m ia Coniugated Unconiugated Unconiuga te d
Alke line phosp hatale Marked increase Normal or increased Slig htly increased
Aaperte t e trensamlnase Normal or slight Increased Normal increase
SUMMARY OF URINARY AND FAECAL BILE PIGMENT CHANGES
Obs tructive He pa t ocellula r
Urina ry b ilirubin Increased
Ur inary urobilinogen Decreased
Feec,,1 s te rcobilinoge n Oecreased
VIRAL HEPATITIS
CAUSES
fa ilure wi th no obatruction
Normal or increased
Normal or increased
Norma l
Haemolytic
Inc reased
Inc raased
1. Hepatitis A - an enterovirus spread by the oral-faecal route. Does not cau se chronic hepatiti s
I Gastroenterology
2. Hepatitis B (Australia Ag ) - spread by blood or sexual intercourse. Worse prog nosis if superinfected w ith hepatiti s D
3. Hepatit is C - spread by blood or sexua l intercourse 4. Hepatit is E - spread by the oral- faeca l route. Dangerous in
pregnancy 5. Cytomegalovirus 6. Infect ious mo nonucleosis
COMPLICATIONS OF GALLSTONES
COMMON
1. Bi liary coli c 2. Cho lecyst it is or cholangit is 3. Obstructed neck of gallbladder 4. Pancreat it is
RA RE
1. Ga llstone ileus 2. Ga llbladder perforati on 3. Ga llbladder ca ncer
CAUSES OF ACUTE PANCREATITIS
1. Bil iary tract disease, including gallstones 2. Alcohol 3. Idiopathic 4. Metabolic. e.g . hyperparathyroidism. hyperca lcaem ia 5. Trauma. includ ing surgery 6. Vi ral. e.g. m um ps
CAUSES OF CHRONIC PANCREATITIS
1. A lcohol ism 2. Malnutrit ion 3. Cystic fibrosis 4. Fami lial
7. Haematology
ANAEMIA (HB < 13 .5 GJDL IN MALES. < 11.5 GJDL IN FEMALES)
CAUSES OF ANAEM IA
Defic ie nt RBe production 1. Def iciency of:
(i ) Fe (ii ) 8'2 or fo lic acid
(iii ) Vitam in C (iv ) Protein
2. Aplast ic anaemia (po 79) 3. Marrow infiltratio n:
(i) Leukaemia Ii i) Lymphoma, e.g. Hodgkin's (i ii) Myeloma (iv) Myelosclerosis (v) Metastatic carci no ma
4. 'Symptomatic' (anaemia of chronic disease) (i) Chronic infect ion (i i) Uraemia
(iii ) Liver disease (iv) Hypothy roidism (v) Hypopituitar ism (vi) Malignancy (vii) Col lagen-vascular d isease, e.g. Sl E. rheumatoid disease
Loss or destruc t ion of RBCs 1. Haemorrhage 2. Haemolysis (p. 77) 3. Hype rsplen ism
SOME RBC ABNORMALITIES SEEN IN A BLOOD FILM
SIZE
Anisocytosis Va riation in size, due to anaemia
Macrocytosis Seen in a f ilm as increased diameter of RBCs, but defi ned as an increase in mean corpuscular volume
_ I HHem at o logy
Microcytosis Defi ned as a decrease in mean corpuscular volume
SHAPE
Poikilocytosis Variat ion in shape, due to anaemia which is usually severe
Sphe rocytosis Spheroidal cells seen in hereditary sphe rocytosis and in acqu ired haemolyt ic anaemia
Elliptocytos is Ell iptica l cell s. Hereditary. Haemoly tic anaemia mayor may not occur
S ickling Crescentic ce ll s seen whe n red ucing agents act on Hb-S. Hered ita ry.
Bizarre shap es Seen in severe uraemia and ca rcinom atosis
STAINING
Hypoc hro m ia Decreased intensity of stain, due to Fe deficiency
Polychromasia Diffuse basophil ia. Indicates active b lood regeneration, j ust as ret icu locytosis does
Punc t a t e basoph ili a St ippled appea rance seen in severe anaemia or lead poisoning
Target cells (Mexican h at c ells) Occur in:
(i) Fe deficiency (ii) Liver disease
(iii) After splenectomy (iv) Inherited Hb defect, e.g . thalassa emia m ajor
CAUSES OF MICROCYTIC HYPOCHROM IC ANAEMIA
1. Iron deficiency 2. Tha lassaemia 3. lead poisoning 4. Some sideroblastic anaemias 5. Some anaemias of ch ronic d isease
CAUSES OF HAEMOLYTIC ANAEMIA
CONGENITAL
1. Spherocytosi s ('acholuric jaundice')
2. Haemoglobinopathy: (i) S ickle-cel l anaemia
(ii) Tha lassaemia syndromes
Haematology I
3 . M etabol ic defec t (enzyme defects. e.g. G6PD deficiency)
ACOU IRED
1. Autoimmune haemolysin s: (i) Id iopath ic warm or cold antibodies
(ii ) Viral or mycop lasmal infection
2 . Secondary (symptomatic): 0) Chron ic lymphocyt ic leukaemia
( ii) Malignant lymphoma (iii) SlE (iv) Malaria (v) Uncommon ly:
Rena l d isease Liver d isease Carcinom a Rheumatoid disease TB or syphi lis
3 . Drugs and c hemicals, e.g. lead, methyldopa, dapsone
4 . Haemolytic disease of the newborn , transfusion reac tions
5. Mechanical , e.g. cardiac bypass surgery
6. Microangiopathic: (i) Thrombotic thrombocytopen ic purpura
(ii ) Haemolyti c uraemic synd rome (iii) Disseminated int ravascular coag ulation
7 . Paroxysmal nocturnal haemog lobinuria
8 . March haemoglobinuria
MACROCYTIC ANAEMIA
Folate comes from Fol iage O r L iver
_ I Haem atolo9Y
CAUSES OF FOLIC ACID DEFICIENCY
1. Dietary deficiency or malabsorption 2. Pregnancy 3. Increased cel l turnover, e.g. leukaem ia or lymphoma 4. Anti-folate drugs, e.g. anticonvulsants, methotrexate
8 12 is produced by Bacteria in animals
CAUSES OF VITAMIN B12 DEFICIE NCY
1. Pern icious anaemia or gastrectomy 2. Changed intestina l f lo ra. e.g. bl ind-loop syndrome 3. Ilea l disease, e.g. Crohn's 4. Fish tape-worm (Diphylloboth rium latum) uti lizes avai lable B12 5. Vegan di et
OTHER CAUSES OF MACROCYTOSIS
, . Alcohol ism 2. Liver disease 3. Myxoedema 4. Post-haemorrhage (reticu locytes are large) 5. Mye lodysplasia 6. Aplast ic anaemia 7. Cytotox ic d rugs, esp. hydroxyurea 8. Pregnancy
CLINICAL FEATURES OF ADDISONIAN PERNICIOUS ANAEMIA
1. Usually over 30, may have blue eyes, fai r hair, prematu re greying
2. Anaem ia of ins idious onset 3. Glossitis, often intermittent 4. GI symptoms, e.g. dyspepsia, diarrhoea 5. Subacute combined degene rat ion of sp inal cord
0) Peripheral neuropathy I ii) Dorso-Iatera l co lum n involvement (iii) Mental changes ('mega lob lastic madness') (iv) Rare ly optic atrophy, nystagmus, im potence. etc.
N.B. May be mixed uppe r motor neurone and lower motor neurone signs
6. M ild pyrexia 7. Slight hepatosp lenomegaly 8. Ret ina l haemorrhage 9. Increased incidence of Ca stomach
Haematology I
LEUKOPENIA
CAUSES OF PANCYTOPENIA
1. A plastic anaemia (q.v.) 2. Acute leukaemia (in subleukaem ic phase) and some
m yelodysplasias 3. Marrow infi lt ration:
(i) Ma lignant lymphoma OJ) Metastat ic carcinoma
(iii) Myelomatosis (iv) Myelosclerosis (in late stages)
4. Hypersplen ism 5. Pern icious anaem ia 6. SLE 7. Rarely, disseminated TB
CAUSES OF NEUTROPENIA SEVERE ENOUGH TO CAUSE SYMPTOMS (AGRANULOCYTOSIS)
1. Aplast ic anaemia (i) Idiopat hic
(ii) Drugs, e.g. cytotoxic drugs phenylbutazone ch loramphenicol
(ii i) Chemica ls, e.g. benzene (iv) Rad iation
2. Selective drug-induced neutropenia (norm al Hb and p latelets) e.g. thiouraci l
3. Acute leukaemia (in subleukaemic phase) 4. Hypersplen ism 5. Id iopathic (rare)
LEUKOCYTOSIS
CAUSES OF NEUTROPHI L LEUKOCYTOSIS
1. Bacteria l infecti ons 2. Myeloproli ferative disease:
Myelo id leukaemia Mye loscle rosis Po lycythaemia vera
3. Haemorrhage, especially interna l 4. Tissue damage:
Trauma (includ ing surgery) Burns Myocard ial infa rction
5. Ma lignancy, especially necrotic tumours and hepat ic metastases
_ I Haem at o logy
6. Drugs, especially steroids 7. Collagen vascula r d isease, e.g. Still's juveni le ch ron ic arthritis
CAUSES OF EOSINOPHILIA
1 . Alle rg y Hypersensit iv ity to food or drugs
2 . Pa rasites e.g. trichin iasis, hydatid, hookworm
3 . Skin disease 0) Scabies
Oi) Atopy (eczema, urt icaria, hay feve r, asthma) (iii) Dermatit is herpetiform is
4 . Ma ligna ncy Especia lly Hodgkin's disease
5. Hypereosin ophi lic syndromes (pu lmonary eosinophil ia) A range of disease characterized by radiographic pu lmonary inf iltrates, eosinoph il ia, and va ry ing degrees of asthma and vascu litis. e.g. Loeff ler's d isease and the pulmonary form of polyarteritis nodosa
POLYCYTHAEMIA
CAUSES
Prima ry Potycythaemia rubra vera
Secondary 1. Hypoxia
Ii) High alt itude (ii) Cyanot ic heart disease
(i ii) Pu lmonary disease (iv) Obesity
2. Congenita l abnormalit ies of haemog lobin w ith an abnorma l affinity for oxygen
3. Inc reased erYthropoiet in (i) Heavy cigarette smoking
(ii ) Kidney cyst, neoplasm or hy dronephrosis (iii ) liver carci noma (iv ) Cerebel lar haemangiob lastoma (v ) Massive uterine fib roma
4. Aelat ive polycythaemia (i) Dehydrat ion
(ii) Stress
Hilematol09Y I
CLINICAL FEATURES OF POLYCYTHAEM IA RU BRA VERA
1. Headache, d izziness and lassitude 2. Plethoric appea rance; engorged conjunctival and ret inal
vessels 3. Hypertension 4. Splenomega ly 5. Genera lized pru ritus 6. Dyspepsia due to GI vessel enlargem ent, or associated pept ic
u lcer 7. Throm bosis, e.g. cerebral. coronary or mesenteric 8. Haemorrhag ic tendency 9. Periphe ral isch aemia due to slow ci rculation or th rombosis
10. Gout
SPLENOMEGALY
CAUSES OF MASSIVE SPLE NOM EGALY
1. M ye lofibros is 2. I diopath ic t ro pica l splenomegal y 3. Chron ic mye loid leukaemia 4. Kala-aza r 5. Schistosomias is
Mnemonic: M ICKS
CAUSES OF MODERATE SPLENOMEGALY
All the causes o f massive splenomegaly p lus: 1. Blood dyscrasias, e.g. leukaemia, haem olysis, polycythsemia
rubrs vera 2. Lym phoma 3. Infections, especially infect ious mononucleosis, septicaemia,
bacterial endoca rdit is and malaria 4. Porta l hypertension 5. Storage diseases, e.g. Gaucher's
Mnemonic: BUPS
CAUSES OF M ILD SPLENOM EGALY
All t he above plus: Coll agen- vascular d isease Hy perthyroidism (rarely) A my loidosis Rheumatoid d isease M any system ic infect ions, TB, brucellosis, etc. Sarcoidos is Mnemonic: CHARMS
_ I Haem ato logy
LYMPHADENOPATHY
CAUSES
1 . Infect ions (i) Foca l infect ion with regiona l lymphadenopathy, e.g.
sepsis, T8, p rimary chancre (i i) HIV, e .g. pe rs istent genera lized lymphadenopat hy
(iii) Infect ious mononucleosis (iv) Rubella (v) Secondary syphilis
(vi) Toxoplasmosis (vii) Tropica l infestation, e.g . filariasis
2 . Lymphoma (i) Hodgkin's
(iil Non-Hodgkin's
3. Leukaemia Usua ll y lym phocytic (e l l or ALl)
4 . M alignancy (i) Metastases
(ii) Reactive changes
5 . M iscellaneous ti l Sarcoidosis
(ii) Langerhans cell h ist iocytosis (formerty cal led histiocytosis Xl
(i i i) Ch ron ic inflammatory skin disease (iv) Collagen- vascu lar d isease, e.g. RA, SlE (v) Anticonvu lsant drugs
CLINICAL FEATURES OF HODGKIN'S DISEASE
1, Weight loss, malaise, lassitude, n ight sweats 2. Fever (the period ic Pel- Ebstein pattern is uncommon) 3. l arge, discrete, rubbery, asymmetrical superficia l lymph nodes 4. Mediast ina l or ret roperitoneal node involvement 5. Hepatosplenomegaly 6. Pulmonary or pleu ral infilt ration 7. Pain or pa ralysis due to p ressure on nerves or spina l cord 8. Marrow infi lt ration wit h pain or patholog ica l fractu re 9. Skin:
Pruritus Pigmentat ion Herpes zoster Nodular inf ilt rates
10. Infect ions due to decreased cell mediated immunity 11 . Alcohol-i nduced pain
CLINICAL FEATURES OF THE 3 COMMON LEUKAEMIAS
Ha ematology I
Anaemia, constit utiona l symptoms (feve r, ma laise, weig ht loss) and bleed ing (includ ing purpura ) occu r in all 3 ty pes but are more severe in acute leukaemia and less severe in chron ic lymphocyt ic leukaemi a
ACUTE MYELOID LEUKAEMIA
1. Occurs at any age 2. Onset may be abrupt or insid ious 3. Stomatit is and pharyngit is 4. Suscept ibility to infections, especia lly of upper resp iratory tract 5. Slight lymphadenopathy (but more common in Al l) 6. Slight or moderate liver and spleen ~n largement 7. Bone and joint pa in, w ith sternal tenderness 8. Gum hypertrophy
CHRON IC MYELOID LEUKAEMIA (assoc iated w it h Philade lphia ch romosome)
1. Occu rs in middle age 2. Insidious onset 3. Massive splenomegaly 4. Slight lymphadenopathy 5. Moderate hepatomegaly
CHRONIC LYMPHOCYTIC LEUKAEM IA
, . Occurs in late m idd le age, more often in males 2. Insid ious onset often fo und acc identa lly 3. Moderate or marked lymphadenopathy, usually symmetrical 4. Recurrent ch ronic infect ions 5. Moderate liver and spleen enlargement 6. May be haemolytic anaemia 7. Skin lesions:
(i) Pruritus (ii) Herpes zoster
(ii i) Nodula r inf i lt rates (iv) Eryt hroderma (I'homme rouge)
CLINICAL FEATURES OF MULTIPLE MYELOMA
1. Progressive anaemia 2. Bone pain:
ti l Osteoly t iC lesions (i i) Patho log ical fraclUres
(i ii) Osteomalacia (due to renal phosphate leak)
- Haematology
3. Bleeding, due to thrombocytopenia 4. Fever 5. Renal inv olvement:
0) acute o r chron ic uraemia (ii) Fancon i syndrom e
6. Hepatomegal y, occasionally w ith jaundice 7. Hyperca lcaem ia w ith norma l alka line phosphatase 8. Hyperuricaemia 9. Amylo idos is
10. Neuropathy, w ith raised CSF protein _ .. 11, S usceptibil ity to infections, due to de fective antibodies 12. Hyperviscosity syndrome (occasio nally)
BLEEDING May be due to defects o f p latelets, coagulat ion or vessels
PLATELETS CAUSES OF THROM BOCYTOPEN IA
1. Idio pat hic t hrombocytopenic purpura (autoim mune) 2. Causes of pancytopenia (p. 79 ) 3. Drugs, e .g . salicylates. he pa rin 4. Incom patible or m assive blood transfusions 5. Disseminated intravascular coag ulation 6. Massive haemorrhage
N.B. In th rombocytopen ia, bl eeding t ime and ca pi llary fragi lity are increased, but coagul ati on t ime is normal
COAGULATION Vitamin K def iciency affects coagulat ion factors II, VII , IX and X.
COAGULATION DISORDERS
CONGENITAL
Haemophi l ias 1. Haemophi lia A (V III deficiency) 2. Haemophili a B (IX deficiency, Christm as disease) 3. vo n Wille bra nd 's d isease
Other cong enita l defic iencies Factors I, II, V, VII , X, XI, XII or Xlii
ACQUIRED
1. Vitam in K deficiency 2. liver d isease
Haematology I 3. Ant icoagulant drugs 4. Disseminated int ravascular coagu lat ion (consumption
coagulopathy) 5. Massive transfu sio n o f stored blood 6. Ci rcu lat ing inh ibit ors of coa gulat ion
DISSEMINATED INTRAVASCULAR COAGULATION
This is cha racterized by excessive formu lat ion of f ib rinogen der ivatives, usually due to increased pro teolysis. There may be b leeding or thrombosis of any severity
CA USES
1. 'Shock', esp. Gram-neg . septicaemia and anaphylaxis 2. Other infections, e.g. T8, v ira l and funga l 3. Obstetric
Premature p lacental separation Retenti on of dead fetus Amn iotic emboli sm Fetal death due to Rh incompatibil ity
4. Major surgery, especially w ith extra-corpo real shunts 5. Incom patible blood transfusion 6. M iscellaneous
Leukaemia o r carcinom atosis Liver, renal or prostatic disease Pulmonary embolism
CAUSES OF BLEEDING DUE TO SMALL VESSEL DEFECTS
CONGENITAL
1. Hereditary haem orrhagic telangiectasia (Osler- Weber- Rendu) 2. Pseudo-xanthoma elast icum 3. Eh lers- Danlos disease
ACQUIRED
1 . Infectio n (i ) Sept icaemia, especially meningococcal
(i i ) Bacte rial endoca rdit is
2 . Drugs, e.g . co rt icosteroids
3 . Secondary to systemic disease ('symptom atic' ) (i) Cushing's
( i i) Scurvy
_ I HS8matoio gy
4 . Vas culitis (i) Henoch-Schonlein purpura
(ii) Cutaneous vasculitis (ii i) Polyarter it is nodosa
5. Misce lla neous (i) Simple easy bru ising
( ii) Seni le purpura (i i i ) Dermatoses, e.g. eczema (iv) Fat embol ism
SCREENING TESTS FOR A BLEEOING DISORDER
1. Bloo d count a nd film To detect leukaemia and assess p late let num ber, size and shape
2. Bleeding time (w ith Duke's m ethod, norma l < 7 m ini Usefu l in diagnosis of vo n W ille brand 's d isease Also prolonged by asp irin
3 . Hess t est , w it h sphygmomanometer cuff at c. 100 mmHg for 5 min (N < 5 petechiae in a ci rc le of 3 em diameter)
4. Prothro m bin time IN 12- 15 sec) Tests the extri nsic system Prolonged by warfarin
5 . Ac tivat e d p a rtial thromboplastin time (APIT) IN 30-45 sec) Tests the intrinsic system (especially VIII and IX) Prolonged by heparin
6 . Thrombin time (N 10-20 sec) Prolonged in
iii Fibrinogen deficiency (ii) Presence o f some inhib itors, e.g. heparin
7 . Assays for c oagulat ion factor deficiency (e.g. factor VII) 8 . Fibri n d egradation products
Increased in fibrinolysis (e.g. d issem inated intravascu lar coagu lat ion)
Clinica l f eat u res of b leeding disorders
Cl ini ca l f eeture Coagulatio n d i sorde r P latel et d isorder
Purpura Rare Common
Brul.e. Single, deop Multiple, superficial
Bleeding .ite. Joints, muscles Mucous mem branes
Superf icial cu te Blc-cding stops Bleeding prolonged
D .... p cute Bleeding con t inues Bleeding stops w ith despite pressure pressu re
Healing of cu t . DelaVod Norma l
Haematology I
COMPLICATIONS OF BLOOD TRANSFUSION
1. Febrile reactions (i) Pyrogens
(i i) Leukocyte or p latelet iso-agg lut inins (iii) Hypersensit iv ity to p lasma
2 . Allergic reactions 3 . Circ ulatory overload 4 . Haemolysis. Red cells of either donor or recipient may be
affected (i) Blood g rou p incompat ibi lity
(iii Improper or over long storage of donor blood 5 . Reaction due to infec t ed stored blood 6 . Disease t ransmission
(i) Vi ral hepati t is, HIV (A IDS vi rus!, cytomegalovirus, Epstein- Barr v irus
(ii) Syphil is (i ii) Ma lari a, toxoplasmosis (iv) Brucellosis
7 . Thrombophlebitis 8 . Air embolism 9 . Immunological sensitization by previous transfus ion,
especia ll y Rhesus sensit izat ion 10. Transfusion side rosis 11 . Complications of massive transfusion
(i) Collapse due to cold blood (i i) Excess cit rate (exaggerates bleeding tendency)
(iii) Excess ammonia from stored blood (exaggerates precoma in ci rrhotics)
(iv) Excess potassium (exaggerates hyperkalaem ia in uraemic patients)
(v) Thrombocytopenia
CONDITIONS PREDISPOSING TO VENOUS THROMBOSIS
A. LOCALIZED
1. Stasis (t ight bandages, sen ili ty, immobility, etc.) 2. Damaged vesse l wall
(i) Infecti on (ii) Atheroma
(i ii) Trau ma (i nc. fractu re an d pelvic surge ry)
B. GE NERALIZED
1. Thrombocytos is and polycythaemia 2. Prolonged bed rest 3. Pregnancy and puerperium 4. Ora l contracept ives
_ I Haemat ology
5. Hyperviscosity o f blood (dysproteinaemia or polycythaemia) 6. l ow levels o f anti th rombin II I, p rotei n C or protein S 7. Cardio lipin ant ibody (lupus anticoagulant) 8. Facto r V (l e iden) 9. Sickle-cell d isorders
10. Malignancy 11. Nephrotic syndrome 12. Dehydration
8. Neurology
THE SENSORY SYSTEM
A
c •
Midline
(AI Pro prioception, vibratio n a nd h a lf o f t ouch fibre s t rave l v ia posterior nerve roots up the posterior 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 idl ine to continue as the media l lemniscus to the tha lamus. Tertia ry f ib res t ravel v ia the posterior limb of the internal capsu le to the sensory cortex (post-centra l gyrus)
- N e u ro logy
Mnemonic: PROVOST PROpriocept ion, V ibration and Soft Touch in the POSTerior
column IB} Pain a nd t e mpe ra ture fibres rela y in the cord, cross the m id line immediatelv a nd t ravel in the lateral s pinot halamic Iract to the tha lamus
Mnemonic: PATEL PAin and TEm p in the Lateral spinothalamic t ract
le i Rem ainde r of t o uc h fibres relay and cross the midl ine in t he cord and t ravel in the anterior spinothalamic t ract to the tha lamus
Mnemonic: TOAST TOuch in the A nterior Spinothalamic Tract
THE MOTOR SYSTEM
\ .f---- ..... ,.
• motor unit
Fibres pass downwards from the motor cortex (p re-centra l gyru s) into the posterior limb o f the internal capsu le. In the pons the fi bres are scat tered, but they regrou p on the upper medulla to form protuberances called the pyramids
N euro logy I _ IA ) In the lower medu ll a the majority of f ibres decussate and
descend in the lateral corticospinallcrossed pyramida l) t racts (8) Some f ib res do not decussate, but descend in the anterior
corticospinal t ract, and then cross in the anterior commissu re of the cord to supply muscles in the neck
Ie) A few fibres descend d irectly in the lateral cort icospinal t ract w ith the crossed f ibres f rom the contralateral cortex
Most f ibres relay w ith internuncial cells in the cord, and the anterior horn cells and their f ib res then form the ' f ina l common pathw ay' to the m otor end-plates in the muscle. The organ izat ion o f movement is much more complex than this diagram suggests, since impu lses are modified by the cerebellum, the extrapyra m idal system and proprioceptive and other sensations
Mnemonic: MOLAC M Otor in Late ral, A nter ior an d Cont ralate ral tracts
SIGNS OF A LOWER MOTOR NEU RONE LESION
1. Wea kness an d wast ing 2. Hypoton icity 3. Decreased reflexes 4. Fascicu lation
SIGNS OF AN UPPER MOTOR NEURONE LESION
1. Weakness 2. Spasticity 3. Increased tendon reflexes, somet imes w ith clonus 4. Extensor planta r response
N.B. In pyram ida llUMN) lesions, the extensors are weaker than the f lexors in the arms, but the reverse is t rue in the legs, thus 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 rior ob lique and lateral rectus
(ii) Ci liary muscle (iii) Sph incter pupi ll ae (iv) Levator palpebrae supe rioris
4. Troc h lear. Superior oblique musc le N.B. Tested by asking patient to look down and inwards
5 . Trig eminal (i ) Sensory for face, cornea, sinuses, nasa l mucosa, teeth ,
tympa nic membrane and anterior two-thirds o f tong ue (ii) Motor to m uscles of mastication
,--- -
IIIIIIIIIII LI_N_._U_'_O_' O_gcV~ __________________________________________ --,
6 . Abduc ens. lateral rect us muscte 7 . Facia l
(i) Motor to scalp and facial muscl es of exp ression ( i i ) Taste in anterior two-th irds of tongue (v ia cho rda
tympani) (i ii) Nerve to stapedius muscle
8 . Auditory. Auditory and vestibu lar components 9 . Glossopharyngeal
( i ) Sensory fo r poster io r o ne-t h ird of tongue, pha rynx an d m iddle ea r
(ii) Taste f ibres for poster io r one-third of tongue (i ii) Motor 10 m idd le constrictor of pharynx and
stylopharyngeus 10. Vagal
0) Motor to soft palate, larynx and pha rynx (from nuc leus amb iguus)
(i i ) Senso ry and motor for heart, respiratory passages an d abdomi nal v isce ra (from dorsal nucleus)
11 . Spina l a cces sory (i) Motor to sternomasto id and t rapezius
(i i) Accessory f ib res to vagus 12 . Hypoglossal . Motor 10 l o ng ue and hyoid bone depressors
CRANIAL NERVE NUCLEI
M id -brain Pons Medu lla
3,4 5,6,7,8 9, 10, 11. 12
OPTIC PATHWAY AND PATTERNS OF VISUAL FIELD LOSS
Oplio::: nerve 3
______ 0pIic chiasma 4
--- Optic tract 5
Lateral geniculate body
Optjc radiations
Occipital pole
, -------------------------------------------------------------
Neurology I _
1, Concentric diminution I' tunne l visio n')
L R
o Chron ic g laucoma, reti nit is pigmentosa Chron ic papi ll oedema can occasional ly cause i rregu lar loss of peripheral visual f ields In acute pap illoedema there is usually no field defect, tho ugh the blind spot may be en larged.
2 _ Central scoto m a
Reti na l d isease involv ing macula, ret robulba r neuritis 3 . Co mplete fie ld lo ss in o ne eye
Optic nerve lesion (i.e. anter ior to chiasma) 4 . Bitemporal he mianop ia
Pitu ita ry tumour (i.e. al the chiasma) 5 . Homonymous h em iano pia
Tract lesions posterior to ch iasma 6 . Ouadrantie hemiano pia
Temporal lobe tumours for superio r q uadrant Parieta l lobe tumours for inferior quadrant
7 . Homonymous he m ianopia with m acular sparing
7
l esions of the v isual cortex
_ 1 N eur o logv
CAUSES OF OPTIC ATROPHY
, . G lau c oma 2. Re t ina l lesions
Choroido-retin it is Intra-ocu lar haemorrhage, etc.
3. Optic n euritis (retrobulbar neuri t is) (q .v.l 4 . Ch ron ic p a pilloed e m a 5 . Pressure on optic n e rve
Tumour Aneurysm Paget's disease
6. D iv ision o f optic ne rve Surgery Trauma
CAUSES OF OPTIC NEURITIS
1 . Ischae mia 8.g. temporal arter it is
2. Demye linating d isease e .g. mu ltiple scle rosis
3 . Infective e.g. ret in it is, meningiti S
4. To x in s e.g. methyl alcohol
5 . Me tabolic e.g. diabetes melli tus, B12 deficiency
FEATURES OF DIABETIC RETINOPATHY
1. Back g ro und re tino p a thy M icroaneurysms leak, producing 'dot and b lot' haemorrhages and, some years later, hard exudates
2. Pre -p roliferative re tinopathy Soft exudates (cotton-wool spots ) appea r. These are deep ret ina l infarcts. Venous dilatati on an d bleeding occurs
3 . Pro l i f erative retinop athy Extensive new vessel form ation w hich can lead to vi t reous haemo rrhage, reti nal detachment, neovascu lar glaucoma, etc.
FEATURES OF HYPERTENSIVE RETINOPATHY
Grade 1. Silver-w i ring of arteries Grade 2. Arteriovenous nipping Grade 3. Flame-shaped haemorrhages, exudates and cotton-wool spots Grade 4. As Grade 3, but w ith pap ill oedema
L-____________________________________________ N_._U_'_O_'_og __ ,~1 IIIIIIII SQUINTS
CONCOMITANT SQUINT
Due to a defect in the sensory component of the reflex arc (such as poor v ision) or a central d isturbance. The angle of deviation between the eyes rema ins co nstant when looking in d ifferent directions. Th is occurs in all neonates and often in chi ldhood following i ll ness
Features 1. Both eyes have fu ll movement if tested separate ly 2. No diplopia
PARALYTIC SQUINT
Due to lesions of 3rd, 4th or 6th cranial nerves. Usua lly causes diplopia
Features 1. 'False' image is alw ays peripheral 2. 'False' image is seen by affected eye 3. Separat ion o f images is maximal w hen looking in d i rection of
action of affected m uscle
3RD CRANIA L NERVE (OCULOMOTOR) PALSY
1. Marked ptosis 2. Eye abducted and depressed ('down and out') 3. Pupil dilated and completely non-react ive
More often partial than complete, especi ally with lesions near the nucleus
Causes o f o culomo tor p alsy 1. Aneurysm o f posterior communicat ing artery 2. Tumours 3. Brain-stem eVA
CERVICAL SYMPATHETIC PARALYSIS (HORNER'S)
1. M ild ptosis 2. Pupil c onstrict ed w ith no react ion to shading 3. Red uced sweat ing on ipsi lateral ha lf of head and neck 4. Abo lit ion of cil iospina l reflex
N.B. Everyth ing gets 'sma ll er'
Cau ses of Horner 's syndrome 1. Carcinoma of ap ical bronchus (Pancoast's tumour) 2. Cervical sym pathectomy 3. Ao rtic aneurysm
_ I N eurology
4. Syr ingobulbia or syringomyel ia 5. Brachial plexus lesions (e.g . Klumpke 's paralysis)
CAUSES OF PTOSIS
1. Congenital 2. Ocu lomotor palsy 3. Cervical sympathetic lesion 4. Myasthenia gravis 5. Myopathy (e.g. dyst rophia myoton ica)
PAPILLOEDEMA
SIGNS OF PAPILLOEDEMA
1. Engorged ret inal ve ins 2. Pink d isc w it h blu rred marg in 3. Loss of 'cupping' 4. Cribrosa not v isible 5. Flame-shaped haemorrhages
COM MO N CAUSES OF PAPILLOEDEMA
1. Accelerated phase hypertension 2. Raised intracran ial press ure (q.v.l 3. Ret inal venous o bstruction
Papill itis (retrobu lbar neurit is) is usually d ue to d isseminated sclerosis. It is d ist inguished by the ear ly severe loss o f v isual acu ity. There may be no fundal abnorm ality (Le. 'pal ient sees not hing, doctor sees noth ing')
Ca u ses o f rai s e d intrac ra nial pressure 1. Intrac ranial mass or infect ion 2. Obstructed CSF flow 3. Hypertensive encephalopathy 4. Hypercapnia (C02 retention) 5. Ben ign intrac ran ial hypertension (pseudo-t umour cerebri )
(i) Thrombos is of intracran ial venous sinuses (ii) Many rare causes, e.g. oral contracept ives, retino ids or
vitam in A poison ing
CAUSES OF SUDDEN BLINDNESS
1. Ret ina l detachment 2. Acute g laucoma 3. Vitreous haemorrhage (esp. di abetes) 4. Tem po ral arteri t is 5. Ret inal artery or vein occlusion 6. M igraine (t ransient)
CAUSES OF FACIAL PARALYSIS
1. SUPRANUCLEAR LESIONS
Neuro logy I _
e.g. cerebrovascular accident affect ing internal capsule
2. NUCLEAR LESIONS
e.g. pontine neoplasm , polio
3. INFRANUCLEA R LESIONS
(i) Ce rebell a-pont ine ang le and internal aud itory canal, e.g . acoust ic neuroma, men ing ioma
(ii) Facial cana l, e.g. Bell's pa lsy, trauma, sarcoidosis (i ii) Ext ra-cranial, e.g. t ra uma, parot id neop lasm
In upper motor neurone facia l palsy t he fo rehead movements are reta ined (due to b ilateral co rt ica l representation)
DEAFNESS
CAUSES OF DEAFNESS
A . Con duc tion deafness " Wax o r foreign body 2. Eustachian obstruct ion (esp. 'g lue ear') 3. Ot it is media 4. Otosclerosis 5. Paget's d isease
B. Nerve de afness 1. Traumatic:
m Chronic exposure 10 loud noise (ii) Fractu re of pelrous temporal bone
2. Infect ive: (i) Con genital syphi l is
I ii) Rubell a synd rome (i ii ) MUm ps, infl uenza
3. Toxic: (i) Aspi rin . qu inine
(i i) A nt ibiot ics e.g . streptomycin. neomycin (ii i) Tobacco, alcoho l
4. Degenerat ive : Presbyacusis
5. Tumour, e.g. acoust ic neuroma 6. Brain-stem lesions (ra rely) 7. Ra re fam ilia l syndromes
_ I N eurology
RINNE'S TEST
The abi lity to hea r a tuning fork t hrough air and th rou gh the m asto id p rocess are compared . In normal people and in nerve deafness the ai r conducted sound is louder, whereas in cond uction deafness it is softer
WEBER'S TEST
The base o f th e fo rk is placed on the ce nt re of t he fo rehead; in nerve deafn ess the note is hea rd in the normal ear, whe reas in conduction deafness it is heard in the deaf ear
MULTIPLE SCLEROSIS
Characterized by mu lt ip le e NS lesions scattered in t ime and p lace Lower m otor neuranes are not affected d irect ly
CLI NICAL FEATURES
1. Spast ic weakness, usual ly starting in legs 2. Retrobulbar neurit is:
M isty vision Painfu l eye movements Slight ly swollen optic d isc Central scotoma (Opt ic atro phy may develop)
3. Num bness and paraesthesiae 4. Diplopia (ataxic nystagmus is characte ristic) 5. Vertigo 6. Cerebel lar signs:
' Scanning' speech Intention t remo r Nystagm us (may be w orse in the abduct ing eye)
7. Sph incter d istu rbance and impotence 8. Euphoria or other mental change 9. Painfu l fl exor spasms
INTRACRANIAL DISORDERS
COMMON INTRACRANIAL NEOPLASMS
Children Medulloblastoma Ast rocytoma
Adults Metastat ic ca ncer Gl ioma Mening ioma
Acoustic neuro ma Pitu itary t umour
Neuro logy I
CLINICAL FEATURES OF INTRACRANIAL NEOPLASM
1. Raised intracranial pressure (i ) Headache, worse on straining and on w aking
(i i ) Drowsiness (i i i) Bradycardia and hy pertension (iv) Vomit ing (v) Papill oedema
2. Progressive loss of neuro log ical fu nction or focal neurological signs (q.v.)
3. Epilepsy 4. Mental symptoms, e.g. personality change, apathy, dem ent ia 5. Con ing may occu r, w ith d i lated pupi l and respiratory
depression (may follow bleed into tumou r)
LOCALIZATION OF CORTICAL LESIONS BY FOCAL NEUROLOGICAL SIGNS
Frontal 1. Mental d isturbance
(i) Dementia (ii) Apathy
(i ii) Inappropriate emot ion 2. Epilepsy 3. Grasp reflex 4. Unilate ral anosmia
Pre·central 1. Jackson ian ep ilepsy 2. Cont ralateral spasti c hemipleg ia
Parietal 1. Sensory d istu rbance, e.g. lack of 2 point discriminat ion 2. Visual aphasia 3. Hom onymous hemianopia or quadrantanop ia (lower) 4. Apraxia 5. Astereognosis
Temporal 1. Anterior lesion s - motor aphasia
Poster ior lesions - auditory aphasia 2. Homonymous hemianopia or quadrantanopia (upper) 3. Psychomotor ep ilepsy
Occipital Visua l field defects
,
11IIIIIIII 1 L_N_._u_'_O_'O_g_V ____________________________________________ ___
SIGNS OF A CEREBELLAR LESION
1. Intention tremor 2. 'Scanning'speech 3. Nystagmus worse on looking to the side of the lesion 4. li mb ataxia w ith characte ristic b road-based gait 5. Hypotonia and pendular reflexes
CAUSES OF CEREBELLAR DYSFUNCTION
1. Mult iple sclerosis 2. Neoplasms
(i) In the cerebell um, e.g . medulloblastoma (i i) Para neoplast ic neuropathy, e.g . due to bronchia l cance r
3. Ce rebellar abscess (often seconda ry to oti t is media) 4. Vertebrobasi lar insufficiency 5. Drugs, e.g. alcohol 6. Id iopath ic degenerat ion, e.g. primary cerebe ll ar at ro phy 7. Ra re hereditary and fam il ial ataxias, e.g. Fried reich's
CLASSIFICATION OF SPEECH DEFECTS
1. Dysphasia (disorde r in use of symbo ls for communication whether spoken, heard, written or read)
2. Dysarth r ia (d isorde r of articu lation) 3. Dysphonia (di sorder o f vocalizat ion) 4. Dementia (intel lectual deterioration )
CAUSES OF DYSPHASIA
1. Expressive - due to lesion o f Broca's area (Inferior Frontal gyrus of dominant cortex) Mnemonic: BIF and BROca BROadcasts
2. Receptive - due to lesion of WE rnicke's area (S uper ior T emporal areas of dominant cortex) Mnemonic: WEST
CAUSES OF DYSARTHRIA
1. Bulbar or pseUdo-bulbar pa lsy 2. Basa l gangl ia les ions 3. Cerebellar lesions 4. Weakness o r paralysis of facia l m uscles 5. Ora l lesions includ ing loose dentures
CAUSES OF DYSPHONIA
1. Functiona l (hysteria)
Neurology I _
2. Lesions of recurrent laryngea l nerve (Ca bronchus, aortic aneurysm)
3, Vocal cord lesion (infection, tumour, etc.)
CAUSES OF CEREBRAL INFARCTION
1. Atheroma of intra- or extracranial arteries 2. Cerebral emboli:
(i) Atr ial f ib rillat ion (ii) Myocardial infa rct
(iii) Bacterial endoca rditis (iv) Fat embolism
3. Cerebral ischaemia due to seve re hypotension 4. Cerebral arterial spasm, e.g. mig raine or fo llowing
subarachnoid haemorrhage 5. Hypoxia, e.g.
(i ) Ca rdiac arrest (i i ) Ca rbon monox ide po isoning
{iii) Pu lmonary embo li 6. Arte rit is, e.g. collagen- vascu lar disease 7. Ce rebral th rombosis, e.g. due to polycythaemia 8. Dissecti ng ao rt ic aneu rysm invo lving the ca rotid artery 9. Ligation of carotid artery for intracranial aneurysm
SUBARACHNOID HAEMORRHAGE
(SubARachnoid is ARterial)
COMMON CAUSES
1. Rupt ured 'berry' aneurysm (70%) 2. Arter iovenous malform ation (10%)
CLIN ICAL FEATURES
1. Often occurs in m iddle life 2. Sudden onset of catast rophic headache, usually occipi tal. Often
preci p itated by straining. Often 'warn ing' headaches in previous weeks
3. Sma ll leakages - delirium or confusion but no loss of consciousness Bigger bleeds - vom it ing, convu lsions and coma
4. Men ingism 5. Plantar responses are usually extenso r 6. May be slow pu lse, o r hypertension 7. Occasiona lly squint, pap illoedema, ret inal haemorrhage and
small sluggish pupils . The characterist ic subhya loid haemorrhage spreads out from the edge of th e disc
8. May be pa in in back due to blood in spinal theca 9. May be pyrexia
_ I Neuro logv
CHRONIC SUBDURAL HAEMATOMA
CAUSE
Rupture of cortical veins as they cross th e subdura l space. May be tra umati c or spontaneous
CLIN ICAL FEATURES
1. Ohen elde rly pat ients, after a trivi al head inju ry. A lso in infants or alcoholics
2. Latent period o f days or months occurs before sym p tom s develop
3. Gradual onset of headaches, memory loss, dement ia, confusion, drowsiness and eventual coma. Symptoms f luctuate from day to day, w ith lucid interva ls
4. May be signs of an int racrania l space-occupying lesion, w ith local izing signs
EXTRADURAL HAEMATOMA
(ExTRAdural is ARTerial)
CAUSE
Fracture of squam ous temporal bone w ith rupture of a b ranch of the m iddle men ingeal artery
CLINICAL FEATURES
1. Any age, but often young adults wi th scalp oedema above the .Be
2. Concussion m ay be followed by recovery of consciousness for minutes or hours before th e onset o f drowsiness and deepening coma
3. Signs of intracran ial compression (p. 99) 4. Ipsilateral 3rd nerve palsy due to cerebral herniat ion 5. Progressive cont ralateral hemiplegia
The signs develop rapidly and immediate operat ion to relieve the p ressu re is mandatory
CAUSES OF COMA
1. Syncope (q .v.) 2. Head injury 3. Epilepsy 4. Drugs or toxins (especially alcohol or 'overdose') 5. CVA (thrombosis, embolism or haemorrhage) 6. Raised intracranial pressure (p. 96) 7. Metabol ic
(i) Hypoglycaem ia (Ii) Diabetic ketoacidaemia
(iii ) Hepatic, renal or adrenal fa ilure (iv) Myxoedema (v) El ectro lyte imbalance
8. Acute CNS infection, e.g. men ing iti s. encephal itis 9. Acute systemic infection, e.g . sept icaemia
10. Hysteria, hypnosis 11. Hypo- or hyperthermia
SYNCOPE rBLACK-OUT')
N eurolo gy I _
A transient loss o f consciousness caused by cerebral anoxia, usually due to inadequate blood f low
CAUSES
1. Vasovagal (i) Emot ion, heat or standing still
(ii) Loss of b lood or p lasma (ii i) Post ura l hypotension, e.g. drugs or p rolonged
recumbency (iv) Carotid sinus hypersensitivity
2 . Cardiac (i ) Stokes-Adams (heart block)
(i i) Ventricula r tachyca rd ia or f ibri llation (i ii) Aort ic stenosis (iv) Cyanotic congen ital heart disease (fall in Po2)
(v) Cough syncope (obst ructed venous return to hea rt )
3 . Arterial occlusion (i) A theroma or embo lism (carotid or vertebrobasi lar)
(i i) Cervical spo ndy lOSis (ii i) Strangu lation (iv) 'Subclavian steal syndrome'
4 . Anoxaemia (i) High al t it ude
(ii) Anaemia
EPILEPSY
Partial seizures (with a sing le cort ica l focus) may be eithe r: Simple (unimpai red consciousness) or Complex (impaired consciousness)
Partial seizu res may progress to become generali zed
IIIIIIII LI _N_e_"_'_O_'D_O_Y ____________________________________________ --'
CAUSES OF EPILEPSY
1. IDIDPATHIC
2. FOCAL CEREBRAL LESIONS
(i) Birt h injury or cerebral malformation (ii) Tumour
(i ii) Trauma, scar, irradiation, atrophy (iv) Vascu lar
eVA Hypertension Vasculi t is. e.g. SLE Vascular malformation (e.g. Stu rge-Weberl
(v) Infection Encephali t is or mening itis Abscess or tuberculoma Syphi lis (GPI or gumma) Hydatid cysts, cyst ice rcosis or toxop lasmosis
(iv) Degenerat ive disease, e.g. preseni le dementia
3. METABDLIC
(i) Pyrexia in ch ildren ( i i) Anoxia, hypoglycaemia or hypoca lcaem ia
( i ii) Electro lyte imba lance, e.g. water intox ication (iv) Uraemia (v) Hepat ic coma
(vi) Drugs and toxins Lead poisoning Withdrawal of alcohol or barbiturates 'Overdose' (e.g. antidepressants)
CAUSES OF DEMENTIA
PRIMARY PRESENILE OR SENILE DEM ENTIA
Idiopathic cerebral atrophy, A lzheimer's, Huntington 's, etc.
SECONDARY
A . Intra ·cran ia l 1. Tumour, especia lly frontal 2. Subdu ral haematoma 3. Vascu la r, especially atheroma o r multiple small emboli 4. Infections, e.g. AIDS, encephal itis, neurosyphi lis,
Creutzfe ldt-Jakob 5. Trauma (i nclud ing concuss ion in boxers) 6. M ultip le sclerosis 7. Normal pressure hydroce phalus
Neurology I
B. Extra-crania l 1. Metabol ic (anoxia, hypoglycaemia, liver failure, renal fai lure) 2. Hypothyroidism 3. Vitamin def iciency (especially B12)
4. Drugs (especially barbiturates) 5. Toxins, especially alcohol, lead and aluminium
Depression may cause pseudodementia
NEUROLOGICAL MANIFESTATIONS OF AIDS
1. FUNCTIONAL
Anxiety, depression, etc., which may lead to suic ide
2. FOCAL INFECTION DR MENINGITIS
Espec ially w ith opportun ist ic organ isms: (i ) Cry ptococcus (meningit iS)
(ii) Toxoplasmos is (abscess or encepha litis) (iii) Cytomegalovi rus (encepha litis) (iv) Progressive mu lt ifoca l leucoencepha lopathy (now thou ght
to be due to a vi rus)
3. PRIMARY HIV INFECTION
(i) Acute encephalopathy at t ime of seroconversion: May be EEG changes and epi lepsy
(ii ) AIDS-dementia complex with parapa resis and incontinence
(i ii) Myelopathy due to HIV
4. OTHER Cerebral lymphoma, cranial or peripheral neuropathy, or myopathy
CAUSES OF PARKINSONISM
1. Idiopath ic (espec ially over 50) 2. Cerebral atheroma 3. Drugs (e.g. phenoth iazines) 4. Toxins, e.g . manganese, copper, ca rbon monoxide, kern icterus 5. Traum a (e.g. boxing) 6. Post-ence phal it ic (encephalitis lethargica outbreaks occu rred
19 17- 1925) 7. Ra re syndromes: Shy-Drager, Wilso n's, Stee le-Rich ardson
CLINICAL FEATURES OF PARKINSONISM
Characteristic t remor, rig idity and bradykinesia
__ ILN_._U_'_O_"O~9~YL __________ ______ _ ____ ---'
1. Slowness and poverty o f spontaneous movement 2. Coarse t rem or (' pili-roi ling') w ith cogwheel rig id ity 3. Expressionless. unblinking face 4. Shuffling gait !fest inat ion later) w ith lack of arm -swinging 5. Slurred, m onotonous speech and sma ll handw rit ing 6. Increased salivat ion and dribbling 7. Oculogyric crises (forced upward deviat ion of eyes) in drug
induced and post-encephal it ic types
ABNORMAL GAITS
N. B. Most cases are due to lesions of bone, j o int or skin
'NEUROLOGICAL: GAITS
1. Uppe r motor n e uro ne h e m iple gia Arm addu cted and interna ll y rotated Elbow fl exed and pronated Fingers f lexed Foot plantar-fl exed, w ith leg sw ung in a lateral arc
2. Spa stic pa ra p le gia St iff jerky 'sc isso rs' gait, w ith complicated assisting movem ents of upper limbs
3 . Parkinsoni s m Small shu ffling hurried steps Flexion o f neck, elbows, w r ists and M P jo ints w ith thum bs adducted
4 . Ce re be ll ar le sion 'Orunken' gait on a broad base. Feet raised excessively and p laced ca reful ly. w ith patient looking ahead. Tends to fall to side of lesion
5 . Po s t e rio r column lesio n Patient w alks o n a broad base but bangs feet down cl umsily and tends to look at feet. Rombergism is present
6. High stepping g a it Oue to foot drop
7 . Proxim a l m yopathy Wadd ling ga it wi th broad base, lordosis and marked body sw ing. Th is gait occurs also in congenital h ip d islocation and pregnancy
8. Hyste rica l Usually b izarre and inco nsistent, and the patient rarely fa ll s
Neuro logy I _
9. Involuntary move m e nts (j) Choreiform - jerky m ovements of short duration,
affecting limbs and face (ii) Athetoid - slow w ri thing of arm s and legs w ith f lexed
f ingers, thum b and w rist (ii i) Dystonia muscu/orum (torsion spasm) - intense
susta ined spasm of proxima l and trunk muscles may cause bizarre stepp ing or bow ing of the I run k
(iv) Hemiballismus- unilateral forceful throwing movements w hich are almost cont inuous
SYRINGOMYELIA AND SYRINGOBU LBIA
SYRINGOMYELI A
Usua lly starts in base of posterior ho rn or cerv ical regio n
Clinical features Insid ious onset of 1, Weakn ess and w ast ing of sma ll musc les of han d 2. Dissociated sensory loss in hand (pa in and temperature only) 3. Trophic changes:
(i) Cyanosis of fi ngers (i i) Ulceratio n and scarring
(i ii ) Sw ollen f ingers due to subcutaneous hypertrophy 4. Loss of tendon ref lexes 5. Pa inful arm 6. Spast ic paraplegia 7. Charcot joints (neck and shoulders)
SYRINGOBULBIA
Medu lla may be in it ial site, or m ay be involved by upwa rd extensio n from cord
Clinical feature s 1. Facial pain o r sensory loss (C r. 5) 2. Vert igo and nystagmus (Cr. 8) 3. Facia l, palata l or la ryngeal palsy (Cr. 7, 9, l a, ' 1) 4. Wasted tongue (Cr. 12) 5. Horne r's syn drome (sympath et ic)
BULBAR PALSY
Bi latera l lower moto r neurone lesions of the bu lbar nuclei (9, l a, '1 and 12 w it h low ermost part of 7)
M nem onic: BuLba r = B ila!. Lower
- Neuro logv
CLI NICAL FEATURES
1. Dysarthria 2. Dysphagia. especially w ith fl uids 3. Wasted f ibr illat ing long ue 4. Pala ta l paralysis
CAUSES
1. Motor neurone disease 2. Polio 3. Encephalit is 4. Syringobu lbia
PSEUDO-BULBAR PALSY
Bi lateral upper motor neurone lesions of the same nuc le i Mnemonic: PSeudo-bulbar is Super io r
CLINICAL FEATURES
1. Dysarth ria 2. Dysphagia 3. Spastic tongue 4. Exaggerated jaw-jerk (spastic masseters) 5. Em ot ional liability
CAUSES
1. Ischaemia of internal capsule 2. Motor neurone disease 3. Disseminated sclerosis
SPINAL CORD COMPRESSION
SYMPTOMS
1, Root pains occu r early. Often p rec ipi tated by movement or st ra ining
2. Prog ressive wea kness, paraest hesiae and sensory loss 3. Sph incter di sturbances occur at a late stage
SIGNS
, . Lower motor neurone signs at leve l of com pression and spast icity be low
2. Sensory or refl ex 'level' . May be hyperaesthesia at the affected level
3. Loss of abdominal reflexes in t horacic or cervical lesions
Neuro logy I _
CAUSES OF CORO COMPRESSION
1. Vertebra l Ii) Metastat ic cancer (esp. b ronchus, breast, prostale)
( ii) Osteoporot ic collapse (iii ) Pott's d isease (TS) (iv) Spondylosis w ith d isc p ro lapse (v) Trauma (fract ure, dislocation)
2 . Ex tra-dural I i) Abscess
3. Intra-dural (i) Inf ilt rat ion of meninges - lymphoma, leukaemia
(i i) Extra-medu llary tum ou rs - mening ioma, neurof ibroma (ii i) Intra-medu l lary tumours - gl ioma (iv) Inflammation - t ran sverse myel it is
CAUSES OF ROOT LESIONS
, . Disc prot rus ion 2. Spondylosis (osteophyte) 3. Metastatic cancer
CLINICAL FEATURES OF ROOT LESIONS
,. Pain in the appropriate myotome, aggravated by stra in ing 2. Paraest hesiae in the dermatome 3. Spinal muscle spasm, e.g. lumbar scol iosis or restr iction of
neck movement 4 . Weakness, w asting and fascicu lation o f the myotome, w ith
decreased tendon reflex
DERMATOMES AND MYOTOMES
DERMATOMES OF HEAD AND NECK
Trigeminal "~, l
OPh<h"m;,
Maxillary ---'1'-,/ Marldibu!ar - --t--
_ I Neu rology
Oerma1o m e s in the lowe r limb
u " S> ~ 53 ~
S2
L1
" " "
u
12
L1
" "
Dermatomes in t he upper limb
C3 c,-
C' - -'3
" C6 - -
--n ~
MYOTOM ES WORTH REMEMBERING
C6 - Biceps, brachiorad ial is, radial extenso rs of wrist C7 - Triceps, u lnar extensors of wrist, f inger extenso rs C8 - Finger flexors l4 - Quadriceps femoris L5 - Extenso r hallucis longus 5 1 - Planta r f lexors
REFLEXES
An kle je rk 5 1,2 Knee L3, 4 Biceps C5,6 Triceps C7, 8
(Start low and work up)
CAUSES OF PARAPLEGIA
1. Heredi tary spastic parapleg ia 2. Cerebra l bi rth inj ury (cerebra l pa lsy) 3. Trauma 4. Cord compression - int ra- or extramedu llary (p. 109) 5. Mu ltiple sc le rosis 6 . Syringomyelia 7 . Motor neu rone d isease
c,
CI
Neurology I _
8. Po liomyel it is 9. Sub-acute combined degeneration
10. Gu illa in- Barre (acute post·infect ive po lyneurit is)
PERIPHERAL NEUROPATHY
Cha racte rized by symmetrical f laccid weakness and sensory changes of 'g love and stocking' d ist ribut ion
CAUSES OF POLYNEUROPATHY
1. Many cas e s a re idiopathic
2 . Drugs and chemicals Vincristine, am iodarone, mercury Lead causes motor neuropathy Ison iazid (via pyridox ine deficiency) Many organ ic chemica ls
3. M et ab o lic Diabetes melli tus Amylo idosis Acute intermittent porphy ria Uraemia Myxoedema
4 . De fici e ncy states 812 deficiency A lcoholism Beri·beri (thiamine deficiency) Pel lagra (nicotinamide deficiency)
5 . Infections Leprosy Diphtheria Tetanus Botu l ism
6. Misc ellaneous 'Acute infective polyneurit is' of Gu i llain- Barre Collagen- vascu lar disease, esp. polya rteritis and rheumatoid d isease Ma l ignancy Sarco idosis
7. Congenita l Rare hered ita ry ataxias and neuropathies (e.g. Charcot- Marie- Tooth )
I Neurology
CAUSES OF PROXIMAL MYOPATHY
CONGENITA L
Muscu lar dyst rophy
RHEUMATIC
Polymya lgia rheumatica Polymyositis or dermatomyosit is
METABOLIC
Diabetes mell itus Glucocorticoids (Cushing's o r iatrogenic) Osteoma lacia Thyrotoxicosis or myxoedema Carcinomatous neuromyo pathy
9. Endocrinology
THE PITUITARY
PITUITARY HORMONES
Anterior FSH, LH, A CTH, TSH, G rowth hormone, Prolact in Mnemonic: FLAT GP
Post erior AOH Oxytoc in
PITUITARY SPACE-OCCUPYING LESIONS
1. Secret ing adenomas (j) Prolactinoma Oil Cush ing's IACTH)
(iii) Acromega ly IGH) 2. Non-secreting adenomas 3. Cran iopha ryng ioma 4. Metastati c ca rcinoma or lymphoma 5. Granuloma, e.g. sarco id, TB
PRESENTATIO N OF PITUITA RY LESIONS
,. Symptoms due to excess secretion of hormones (i l Prolactin - amenorrhoea, galactorrhoea, hi rsut ism Iii) ACTH - Cushing's d isease (i ii) GH - acromega ly
2. Hypopitu ita rism due to destruction o f normal p itui tary tissue 3. Headache 4. Visual f ield defects, usua ll y bitemporal hemianopia 5. Pituitary apo plexy (rare)
CLINICAL FEATURES OF ACRO MEGALY
Sympt o ms 1. Often insid ious, w ith no symptom s 2. Headaches 3. Paraesthesiae (median nerve com pression) 4. Proximal weakness and jo int pains
- Endoc rinolog v
5. Polyu ria 6. Im potence and loss o f libido in men 7. Hirsut ism and amenorrhoea in women 8. Visual deterioration 9. Ga lactorrhoea
Signs 1. Characterist ic facies, large hands, feet and tongue 2. l eathe ry f urrowed skin. May be seborrhoea, hyperh idros is or
p ig mentation 3. Hoa rse deep voice 4. Non-toxic goitre 5. Gynaecomastia 6. Bitem poral hemianopia, optic atrophy, ocu lar palsies 7. Genera lized organomegaly 8. Cardiac fa i lu re (hypertension and ischaem ia) 9. Signs of di abetes mell itus or its com plicat ions
10. Hypopit uit a rism 11. Progressive kyphos is 12. Arth ro pat hy
HYPOPITUITARISM
CAUSES
1. Tumours: (i) Ch romophobe adenoma
(ii) Eosinophil adenoma (basophi l adenoma is rarely large enough to ca use hypopitui tarism)
(iii) Craniopharyng ioma (iv) Metastat ic can cer
2. Iat rogen ic - hypophysectomy or irradiation 3. Pitui tary necrosis due to ante- or post pa rtum haemorrhage
(Sheehan's syndrome) 4. Granulomatous infi ltration, e.g . sarcoidosis 5. Trauma 6. In fec tion, e.g. T B, m eningit is
CLINICAL FEATURES
Loss o f anterior pit u itary hormones is usually part ia l, in t he fo ll ow ing order of f requency:
1 . Somatotrophin (GH) : (i) Dwarfism in children
(iii Insulin sensit iv ity in adults
2 . Prola ctin: Failure of lactat ion in postpartum patients
3 . Gonado trophins (lH a nd FSH): (i ) Delayed puberty in ch ildren
Endocrino logy I _
(ii) Loss of body hai r, f ine w rinkled skin, impotence, infert i lity and amen orrhoea in adu lts
4 . Thyrotrophin (TSH) : Hypothyroid ism
5 . Corticotrophin (ACTH ): Hypoad renalism (asthenia, nausea, vom iting, hypog lycaem ia, collapse)
6 . Me la noc yte -stim ula t ing hormone (MSH): Skin pallor
THE THYROID
HYPOTHYROIDISM
CAUSES
P rima ry (thyroid gla nd f a ilu re) 1. A utoimmune thyroid itis (Hashimoto's disea se and its atroph ic
variant, myxoedem a). In Hashimoto 's the thyroid is large and may be tender, but in mYKoedema it is im palpable. Ci rculating thyroid ant ibodies occur in bo th
2. Iatrogen ic: (i) Su rgery
(ii) Irrad iat ion (ii i) Ant ithyro id drugs (iv) Li th ium
3. Endemic creti nism (maternal iodine def iciency) 4. Absence or ma ldevelopment of thyroid g land (rare) 5. Dyshormonogenesis (rare co ngenital enlyme defects affect ing
hormone synthesis)
S econdary (TSH d e f icie ncy) 1. Pitu itary lesion 2. Rarely hypothalamic lesion (due to t hy rot rophin releasing
ho rmone deficie ncy)
CLIN ICAL FEATURES
, . Ment al and physica l sluggishness 2. Co ld intolerance 3. Const ipation 4. Weight gain 5. Croaking voice, w ith slow speech 6. Rough, dry yellowish skin
- Endoc rinology
7. 'Myxoedema facies' w ith general ized thickening o f subcutaneous t issue, periorb ital puffiness, b rittle sparse hair and thin eyebrows
8. Bradyca rd ia 9. Delayed relaxation of tendon jerks
l e ss commonly 10. A naemia (may be macrocytic) 11 . Cyanosis, Raynaud's phenomenon or angina 12. Carpal tu nnel syndrome 13. Perceptive deafness 14. Mya lg ia o r arthralgia 15. 'M yxoedema madness' 16. Coma
ORGAN-SPECIFIC AUTOIMMUNE DISEASES
1. Hashimoto's t hyroid it is 2. Adrenal it is (Add ison's) 3. Pern ic ious anaemia 4. Juven ile-onset d iabetes me ll it us 5. Vitiligo 6. ? Alopecia areata
CAUSES OF 'NON-TOXIC' GOITRE
1. 'S imp le' colloid goit re (id iopathi c), common during puberty and pregnancy
2. Diffuse mu lti nodula r goitre (may become toxic) 3. Iodine def ic iency 4. Goitrogens, e.g . antithyro id drugs, excess iodine 5. Auto immune thyroid it is (Hash imoto's)
Possibility of mal ignanc y is sugge sted by: ,. Asymmetr ical enlargement with 'cold area' on scan 2. Very hard t hyroid 3. Pressure effects, e.g. hoarseness 4. Cerv ical lym ph adenopathy
HYPERTHYROIDISM
CAUSES
1. Graves' d isease 2. Toxic mu lt inod ular goitre. Resembles Graves' d isease but
pat ients tend to be o lder, w ith fewer eye signs 3. Toxic adenoma 4. Iatrogenic (excess thyroid hormone)
Endoc rinology I
CLINICAL FEATURES OF GRAVES' DISEASE
Thyroid gland 1. Goit re, usually diffuse (but may be nodular) 2. Increased thyroid vascu larity (th r ill, bru it)
Metabolic 3. Increased heat product ion (warm moist skin, heat into lerance) 4. We ight loss, increased appetite, di arrhoea 5. Tachycardia, exertiona l dyspnoea, hyperdynamic circu lat ion 6. Ti redness, irritabil it y, nervousness 7. Fine t remor, hyperkinesia 8. Proximal muscle weakness with hyperactive reflexes 9. Occasionally, bone pain due to osteoporosis 10. In e lderly patients, alrial f ibrillation or cardiac fai lure
Extra-thyroid m a nifest a t ions (possibly immunological) 11. Eye signs:
Eyel id oedema Conj unctivitis Exophthalmos Lid retract ion or lag Ophtha lmopleg ia (usual ly superio r rect us)
12. Pretib ial myxoedema 13. Thyroid acropachy (clubbing) 14. Vit iligo 15. Splenomegaly
MANAGEM ENT OF THYROTOXICOSIS
1 . Indications for thyroide ctomy (i) Possib le mal ignancy
(ii ) Pressure symptoms (ii i) Retrosterna l go itre (iv) Large goitre (v) Refusal or failure o f medica l t reatment
(vi ) Hypersensit ivity to antithyroid drugs
Patient m ust f irst be made euthyroid to avoid thyro id 'storm'
2. Indications for m e dical treatment (i) Young patients
(ii) Pregnan cy (i ii) Mi ld hyperthyro id ism w ith small goitre (iv) Pat ients unsuitable for surgery
3. Indications for radioiodine therapy (i) Relapse after thyro idectomy
(l j) Patients over age 45 (i ii ) Toxic adenomas
Subsequent hypothyroidism is common (about 40% at 10 years)
_ I En d ocr in o logy
THE PARATHYROIDS
HYPERPARATHYROIDISM
CAUSES
1. Prima ry (i) Adenoma (single or multiple) (85%)
( i i ) Hyperplasia (i i i ) Carcino ma
2 . Seconda ry Hyperplasia d ue to chronic renal failure. osteomalacia or rickets
3 . Te rtia ry A com plicat ion of secondary hyperpa rathyroidism in which autonomous hyperparathyroid ism develops
CLINICAL FEATURES
('Bones, stones, abdom ina l groans and psychic moans')
1 . Due t o hyperca lca emia Ii) Anorexia, nausea and vom it ing
( ii) Constipa tion (iii) Polydipsia a nd polyuria (iv) lethargy and depression, p rog ressing to coma and
convu lsions
2 . Metas t a tic calc ification ( i ) Re na l ca lculi
(i i) Nephrocalcinosis (ii i) Conjunct iva l deposits and keratopathy
3 . Bo ne resorption (i) Pai n and deformity
(ii) Patholog ical f ractures
4 . Rarely Peptic ulcer, pancreatitis, pseudo-gout
HYPOPARATHYROIDISM
CAUSES
1. Postoperative (e.g. t hyroidectomy) 2. Idiopath ic (possib ly autoimmune) 3. Neonatal (transient. but dangerous)
Endocrino logy I
CLINICAL FEATURES
1 . Due to hyp ocalcaemia OJ Tetany (paraesthesiae, stridor, c ramps, hyperref lexia)
Trousseau's and Chvostek's signs are present {iiI Convu lsions (especia ll y in ch i ldren)
(i ii) Cata racts
2 . In idiopathic hypoparathyro idism (i) Mental subno rmality
Iii) Dry skin, sparse hair, poor teeth, na il dystrophy o ften wit h candidosis
(i ii ) Papilloedema and calcif ied basal gangl ia (mimics brai n tumour)
(iv) Other autoimmune d isorders, e.g. hypoadrenalism, pern icious anaemia
THE ADRENAlS
CUSHING'S SYNDROME
CAUSES OF CUSHI NG'S SYNDROME
1. Iat rogenic (prednisolo ne or ACTH) 2. A lcohol ism (pseudo-Cushing 's) 3. Cush ing's d isease (pituitary-dependent adrenal hyperp lasia) 4. Adrenal carcinoma o r adenoma 5. Ectop ic ACTH (e.g. smal l cel l b ronch ia l cancer)
CLINICAL FEATURES
1. Obesity of t runk and face w ith ' buffa lo hump' 2. Hype rtension 3. Skin changes:
(i) Striae (ii ) Bru ising
(ii i) Hirsut ism (iv) Pigmentation
4. Osteoporosis 5. Proximal myopathy 6. Menstrual d isturbances 7. Neurosis or psychosis 8. Facial plet hora due to polycythaemia
LA BORATORY FEATU RES
1. Increased plasma 11-hydroxyco rt icosteroids ('cortisol') Normal values:
9 a.m . 190-690 nmol/l
(7- 25 IJgl100 ml)
12 midnight 80-190 nmolll
(3-7 IJg/ 100 mil
_ I Endocri no log y
Loss of d iurnal rhythm occu rs early in Cushing 's syndrome (i.e. midnight sam ples give increased value)
2. Polycythaemia w ith leukocytosis and eosinophi l decrease 3. Hypokalaemia, w ith sod ium in upper normal range 4. 'Diabetic' glucose tolerance test 5. 24 hou r urinary 'free l 1-hydroxycort icosteroids' increased
Low dosage dexamethasone (0.5 mg q.d.s. fo r 2 days) ca uses litt le suppressio n in Cush ing's syndrome
High dosag e dex amethasone (2 mg q.d.s. for 2 days) causes suppression in ad renal hyperp lasi a, but has little or no effect in adrenal adeno ma or carcinoma, o r ectop ic ACTH secret ion due to extra-adrenal ca rcinoma
HAZARDS OF SYSTEMIC GLUCOCORTICOID THERAPY
1. Growth reta rdat ion in ch ildren 2. Cushingoid facies, buffalo hump 3. Adrenal suppress ion and atroph y 4. Weight gain , sod ium and w ater retention, potassium
depleti on 5. Hype rtension 6. Hyperg lycaemia 7. Hyperli p idaemia 8. Infections, especially v iral, TB and fungal 9. Osteoporosis, aseptic bone necrosis, ruptured Ach il les
tendon 10. Gastroi ntestina l
Dyspepsia PePt ic u lcer and perforation Pancreat it is
11. CNS Euphoria Psychosis Increased intracrania l p ressure Increased tendency to epi lepsy
12. Skin changes Thinning, stri ae and easy bruising Poo r wound heal ing, en largement of venous leg u lce rs Acne Hypert richosis
13. Myopathy or musc le atrophy 14. Cataracts, and ra ised intra-ocu lar pressu re 15. Amenorrhoea or p remature menopause 16. Teratogen icity (fetal cleft palate) 17. 'RebOund' o f disease on reduct ion of dosage
CAUSES OF HYPOADRENALISM
ACUTE
Endocr inology I
1. Stress occur ring in patients w ith chron ic hypoadrenalism 2. Septicaemia, especial ly meningococcal
(Waterhouse-Friedr ichsen) 3. Surg ical adrenalectom y 4. Abrupt w ithdrawal o f stero id therapy 5. Pituitary necrosis (e.g . Sheehan's)
CHRONIC
Primary 1. A uto immune adrenal it is (Ad dison's) 2. TB 3. Metastat ic cance r deposits occu r commonly, but rarely cau se
hypoadrenal ism
Sec ondary (ACTH deficiency) 1. Pituita ry or hypothalam ic d isease 2. Pro longed cort icosteroid therapy
CLI NICAL FEATURES OF CHRONIC HYPOADRENALISM
1. Pigmentat ion, especially in exposed sk in, mouth, areolae, palmar creases, pressure areas and scars (except in hypop ituitarism )
2. Deb ility and tiredness 3. Nausea, vom it ing, weig ht loss, abdominal pain, d iarrhoea 4. Hypotension, wi th low-volume pulse 5. HYPoglycaemia, especially reactive after a meal 6. l oss o f body ha ir in wom en 7. DepreSSio n 8. May be associated auto immune diso rder, e.g. v itil igo
LABORATORY FEATU RES OF HYPOADRENALISM
1. Plasma 11-hydroxycort icosteroids may be norma l or low but fai l to respon d adeq uately to 250 ~g Synact hen i.m . ( sho~ ld rise by more t han 193 nmolll (7 ~ g/ 1 00 m l) at 30 m inutes )
2. l ow plasma sod ium and ch loride, w ith raised potaSSium and urea
3. Low vo ltage ECG w ith f lat T waves 4. Low blood sugar, especiall y after fast ing
_ I Endocrino logy
D IABETES MELLITUS
CAUSES OF DIABETES MELLITUS
1. Id iopath ic ( i ) Insulin·dependent ('juvenile')
(i i ) Non-insu lin-dependent ('m atu r ity onset') 2 . Drug-induced
Glucocort icoids. thiazides, diazoxide 3. Panc reatic disease
Pancreat it is, cancer, haemochromatosis, g lucagonoma, cystic fi b rosis
4. Other metabolic disease Acromega ly, phaeoc hromocytoma, Cush ing's, thyrotoxicosis
5. Genetic syndromes Glycogen sto rage d isease, Down's syndrome, etc.
DIFFERENCES BETWEEN THE 2 MAIN TYPES OF DIABETES MELLITUS
'Juvenile' 1, Thin 2. Young 3. Tendency to ketosis 4. Low insu lin sec retion
5. Sensit ive to insul in 6 . Requi re treatment w ith insu lin
7 . HLA-associated (DR3 and 4) 8. Sib lings rarely affected
'Maturity onset' Obese Midd le-aged o r e lderly Resistant to ketosis Normal or increased in su lin secret ion Insul in resis tant Respond to d iet, and oral hypoglycaemic d rugs No association Siblings often affected
DIFFERENCES BETWEEN 'DIABETIC' AND HYPOGL YCAEM IC COMA
Ketoacidaemic coma 1. Preceded by infection or
insulin underdosage 2. Onset over hours or days 3. Deep rapid b reathing 4. Dehydration 5. Sweating ab sent 6. CNS changes unusua l
7. Urine - usua lly g lycosu ria and ketonuria
Hypoglycaemic coma Preceded by exercise, missed meal or insulin overdosage Onset in m inutes Stertorous breath ing Norma l hydrat ion Sweating m arked CNS changes common, especially Babinski response U rine not helpfu l
COMPLICATIONS OF DIABETES MELLITUS
1 . Ocular (i) Blurred v ision due to f luctuat ions in blood sugar
Endocrino logy I _
(ii) Cataracts (i ii) Retinopathy (see p. 94 ) (iv) Rubeosis ir id is (new blood vessels over i ris)- may cause
g laucoma
2 . Neurologica l (i) Peripheral neuropathy (early sign is loss of ankle jerks
and malleolar v ib ration sense) (i i) Mononeurit is mult ip lex (neu ropathy of several periphera l
or cranial ne rves; ohen asymmetrical) (i ii) Autonomic neuropathy:
a. Diarrhoea b . Postura l hypoten sion c. Im potence d. A bnorma l sweating e. Dependent oedema
3 . Renal (i) Pyel onephri t is, sometimes w ith papilla ry necros is
(ii) Glomerulonephrit is a. Kimmelstiel- W ilso n (eos inoph ilic nodules in
glomeru lar t uft) b. Proliferative, with sc lerosed basement membrane
(iii) At heroscl erosis and hypertensive vasc ular changes
4 . Vascular Occlusion by atheroma (large vessels) o r endarterit is (smal l vessels) may cause ischaem ia of feet, myocardium, b rain or kidneys
5 . Dermatological (i) Fat atrophy or hypertrophy at insu lin injection sites
(ii) U lcers due to neuropathy or ischaem ia (i ii) Infect ions, especially furuncles and cand idosis (iv) Pigmented scars over shins ('d iabet ic dermopathy') (v) Xanthomata
(vi) Necro biosis tipo id ica
6 . Systemic infections Incidence of TB and deep mycoses is increased
CAUSES OF SHORT STATURE
1. 'CON STITUTIONAL'
Rac ial, fam ilial or sporadic
2. NUTRITIONAL
(i) Starvation
_ I Endocrino logy
(ij) Malabsorption (i ii) Prote in loss
3. CHROMOSOMAL DEFECTS
(i) Trisom ies, e.g . Down's (i i ) Turner's
4. SKELETAL DEFECTS
( i ) Rickets (i i ) Achondroplas ia
(ii i) Gargoylism (Hurler's)
5. CHRONIC SYSTEMIC DISEASE
(i) Cyanotic congen ital heart d isease I ii ) Rena l fai lu re
(ii i ) Hepatic fai lure (iv) Pu lmonary d isease (v) Anaem ia (vi) Infecti ons, e.g. TB
(v ii ) Long-term steroid therapy (e .g. for asthma)
6. ENDOCRINE DISEASE
(i) Sexual precocity (i i) Hypopituitarism /iii ) Hypothyroidism (iv) Congenital ad renal hyperplasia
7. M ISCELLANEOUS RARE DISEASES
Diseases of unknown cause, e.g . progeria
CAUSES OF GYNAECOMASTIA
1. Neonatal, or normal puberty 2. Ci rrhosis 3. Ma lignancy 4. Testicular or ad rena l tumours 5. Drugs
(i) Oestrogens (i i) Cyproterone acetate
(iii ) Spirono lactone (iv) Cimetidine (v) Methy ldopa
(vi) Digoxin 6. Klinefelter's syndrome (XXY)
CAUSES OF GALACTORRHOEA
1. Physiological (postpartum or neonatal) 2. Prolactin-secreting pitu itary tumour J. Ectopic prolactin, e.g. bronchial Ca 4. Drugs
(i) Phenothiazines (ii) Ora l contracept ives
(i ii) Methyldopa
Endocrino logy
SIDE·EFFECTS OF ORAL CONTRACEPTIVES
1. SYMPTOMS DUE TO OESTROGENS
Fluid retention, we ight ga in Nausea and vo mit ing Headache Ti redness and i rritabi lity Venous hypertens ion in Jegs Inc reased menstrual loss
2. SYMPTOMS DUE TO PROGESTOGENS
Depression Acne Decreased libido, dry vagina Muscle cramps Breast d iscomfort Reduced menstrual loss
3. GYNAECOLOGICAL
Amenorrhoea on contraceptive withdraw al Cervical erosion Vaginal candidiasis Increase in size o f f ibroids
4. EN DOCRINE AND METABOLIC
Abnormal ca rbohyd rate tolerance Increased plasma t riglycerides and cholestero l Abnorm al liver funct ion tests Plasma prote in chan ges, e.g. increased t ransfe rrin Increased th yrox ine and p lasma cort iso l Ra rely :
Hypertension Ch loasma Ga lactorrhoea Ga llstones
_ I En doc r inolo gy
5. THROMBOEMBOLIC EFFECTS
Increased risk of thrombosis (e.g. coronary, cerebral) or embolism (e.g . pulmonary) due to increased clotting factors and platelet st ickiness
CONTRA-INDICATIONS TO OESTROGENIC ORAL CONTRACEPTIVES
1. Pregnancy 2. Hepatic d isease 3. Breast or cerv ica l ca rcinoma 4. Histo ry of t hrombosis o r embolism 5. Ca re is req uired in pat ients w ith a h isto ry of epilepsy, arter ia l
disease, hypertension, va ricose ve ins, oedema, diabetes mell itus, p rolactinoma, ga llstones, m igra ine or f ibro ids. Women over age 35 are at increased risk of th romboembo lic d isease (esp. smokers)
OSTEOPOROSIS
A reduct ion in bone mass below the normal expected for t he age and sex of the patient. Histo log ically the trabecu lar bone is reduced, and the m inera l- matrix ratio is approximately norma l
COMMON CAUSES
1. Old age 2. Immobilizat ion 3. Glucocorticoid therapy (or Cushing's d isease) 4. Sex hormone def iciency, e.g. prematu re menopause, Turner's
syndrome 5. Cigarette smoking 6. Rheumatoid arth rit is causes loca lized osteoporosis
OSTEOMALACIA
A reduct ion in the m ineral- matrix rat io, although the total bone mass may be norm al, decreased or even increased
CAUSES
, . Deficiency o f cho leca lcife ro l (vitam in OJ
Endocrino logy I (i) Inadequate diet, possibly agg ravated by preg nancy or lack
of UV radiation (i i ) M alabsorption
(i ii) Phenyto in 2. Chronic renal failu re 3. Hepat ic disease (d isturbed v itamin 0 metabolism)
Causes o f hypercalcaemia 1. Hyperpa rathyroidism 2. Mal ignancy wi th or wi t hout metastases 3. Myelomatosis (ra re ly lymphoma or leukaemia) 4. Vit o 0 sensit ivi ty, especially sarcoidosis 5. Vit o 0 excess 6. M ilk-alkali synd rom e
Causes o f hy pocalcaemia ' . Hypoparathyroid ism
(i) PosHhyro idectomy (i i) Id iopath ic (sometimes w ith hypoadrena lism and
can didosis) 2. Def iciency of choleca lcifero l 3. Malabsorption 4. Chronic ren al fa ilure or Fanconi syndrome 5. Hypoa lbuminaemia
PAGET'S DISEASE
CLINICAL FEATURES
1. Often asymptomat ic . Incidence increases wi th age 2. Bone deform ity
Ii) Enlarged sku ll (i i) Sabre t ibia
(ii i) l ong bone fractures 3. Nerve entrapment
(i) Deafness (ii) Basilar invag ination
(ii i) Ce rvical spondy losis 4. High out put card iac failure 5. Increased inci dence of bone sa rcoma
10. Renal disease
CLASSICAL PRESENTATIONS OF REN AL DISEASE
1. Haematuria alone 2. Prote inuria alone 3. Nephrotic syndrome (severe proteinuria, hypoa lbuminaemia,
peripheral oedema and often hyper li p idaemia) 4. Neph rit ic syndrome (haematuria, hypertension and periphera l
oedema) 5. Acute rena l fa ilu re (ol iguria w ith acute uraemia) 6. Ch ronic rena l fa ilu re (po lyuria wi th ins idi ous uraemia)
Renal disease which affects the glomeruli is called g lomerulonephrit is, and t his is classif ied by the pathology shown on rena l biopsy (p. 132) . Many diseases can cause more than one of the above presentat ions. Thus membranous g lomeru lonephritis usua l ly causes the nephrotic syndrome, but it can occasionally present as acute or chronic rena l fa il u re.
RENAL FAILURE
CAUSES OF ACUTE RENAL FAILURE
(A I Pre renal 1. loss of blood, plasma or water and electro lytes 2. Hypotension with normal b lood volume, e.g. myocardial infarct
or septicaemic shock
IBI Re nal 1. Acute-on-chronic fa ilure, precipi tated by renal infect ion or
dehydration 2. Ac ute 'tubu lar necrosis' (or rarely cort ica l necrosis)
(i) Sustained hypotension (ii) Obstet ric causes, e.g. abortion or antepartum
haemorrhage (ii i) Septi caemia (especia ll y Gram-negative) (iv) Free circu lating haemog lob in (v) Extensive tissue damage
(vi) Drugs and toxins, e.g. heavy metals, carbon tetrach loride, NSAID
3. Pr imary renal d isease (i) Acute g lomeru lonephrit is
_ I Re na l dillle.a
(i i ) Fu lminating pyeloneph ritis (i ii) Acute 'collagen- vascular d isease'
4. Hepata-rena' syndromes (includ ing Weil's disease) 5. Vascular
0) Arteria l - thrombosis, em bo lism, trauma (ii) Venous - thrombosis
leI Postre na l Obstruction in urinary tract (p. 137)
CAUSES OF CHRON IC RENAL FAILURE
1. Glom erulonephrit is 2. Pyelonephrit is or T B 3. Hypertension 4. Co ll agen- vascu lar disease, especially SLE and PAN 5. Meta bol ic
( i ) Diabetes me ll itus (i i) Gout
(i i i) Chronic ana lgesic ingest ion (iv ) Amy lo idosis (v) Hyperca lcaem ia
6. Obstruct io n in rs nal l rac! 7 . Myeloma 8. Schistosom iasis (rare in UK) 9. Congenital
iii Po lycystic kid ney (i i) Tubular acidosis
( i i i) Fanconi syndrom e
CLINICAL FEATURES OF SEVERE CHRONIC RENAL FAILURE
1. DERMATOLOGICAL
(i) Pruri tus (iiI Pal lor
(ii i ) Pigmentat ion (iv) Petechiae (v) W hite na ils
(v i) Ra rely ' urea f rost'
2. NE UROLOG ICAL
(i) Mental changes (co nfusion, parano ia, etc.) I ii) Apathy and wea kness (i ii) Muscle tw itc hing and seizures (iv) Coma in term inal cases (v) Peripheral neuropathy in chron ic undialysed cases
Renal disease I
3. CARDIOVASCULAR
(i) Pericarditis (may be tamponade) (ij) Ca rd iac failu re d ue to salt and water overload
(iii ) Hypertension with retinopathy (iv) Arrhythmia (d ue to hyperkalaem ia)
4. GASTROINTESTINAL
(i) Dry m outh, foetor, may be paro t itis Iii) Anorexia, nausea and vom iting
(i i i) Hiccups (iv) GI t ract ulcerat ion and b leeding
5. GEN ITOURI NARY
(i) In acute rena l failu re - ol igu ri a « 300 mll24 h ) (ii) In chron ic renal failu re - po lyuria w ith fixed u ri nary
specif ic grav ity (1.010)
6. RESPIRATORY
(j) Hypervent ilat io n due to ac idosis (ii) Pleu ral effusio n
7. HAEMATOLOGICAL
(i) Anaem ia due to: GI b leeding Haemolysis Dietary restr ictions Eryth ropoiet in deficiency
(i i ) Bleeding tendency due to platelet dysfunct ion (iii) Suscept ib ility to secondary infection
8. DEFECTS IN BONE AND CALCIU M M ETABOLISM
(i) Osteoma lac ia ('rena l rickets' in ch ildren) (ii ) Secondary or tert iary hyperparathy roid ism (osteit is
f ib rosa cyst ica ) (i ii) Patchy osteosclerosis (iv) Occasionally osteoporos is (v) Occas ionally metastat ic calcif icat ion of m uscles, blood
vesse ls and conj unct ivae
FACTORS WHICH MAY PRECIPITATE 'URAEM IA'
1. Flu id and elect rolyte imba lance 2. Infect ion, systemic o r urinary
- Renal d isease
3. Increased protein ingestion 4. Obst ruct ion o f renal t ract 5. Catabolic o r nephrotoxic drugs (e.g. tetracycline) 6. Congest ive card iac fa ilure 7. Gastrointestina l haemorrhage or su rgery
GLOMERULONEPHRITIS
Th is may be: Focal - some g lomeruli are affected or Diffuse - all g lomeru li are affected
Segmental - part of a glomeru lus is affected or Global - all of a g lomeru lus is affected
Thus, in focal segmenta l g lomeru loneph r it is, parts o f some glomeru li are affected
CLASSIFICATION OF GLOMERULONEPHRITIS
1 . M i nimal cha nge No change on l ight m icroscopy but EM show s loss of podocytes Typica lly affects ch ildren but may be due to NSAIDs in adults Produces acute nephrotic syndrome, but good prognosis
2 . IgA disease (Berger's disease) Sim ilar to Henoch- Schon lein purpura,. w ith w hich it may overlap Typical ly causes haematuria in young men 20% develop renal fa i lure over 15 years
3 . Pro l iferative Trad it ionally fo l lows Group A streptococcal infect io n, but now not usually associated in UK. Low C3 during t he acute attack. Good prognosis
4 . Me m bra nous Due to M alaria M alignancy (e.g. b ronchia l ca ncer) Hepat it is B Rheumato id A rthrit is (and penic illamine or gold therapy for RAJ S LE Mnemonic: MeMBRAnouS
Prognos is: 1/3 im prove, 1/3 stay the same, 1/3 progress Commonest form of de novo glomeru lonephrit is in rena l al lografts
5 . M esangiocapillary (types I and II) C3 usually low
Rena l diseas e I
Type II is associated with partial lipoatrophy and with C3 nephr itic factor
6 . Foca l Associated w ith WEgener's g ranulomatosis, SlE, Endoca rd it is, Polyarter itis nodosa, HEnoch- Schonlein purpura Mnemonic: WE SLEEP HEre
7 . Rapidly progressive (crescentic) Assoc iated wi th Wegener's granulomatosis, Henoch- Schon lein purpura, A ntig lomeru lar basement membrane (Goodpastu re's), M icroscopic polyangi it is, Immune com plex disease Mnemonic: WHAM I
8 . Focal segme ntal glome rulos c lero s is Sometimes id iopathic, particu la rly in chi ldren, but in adu lts usually secon dary to other forms o f g lomeru lonephrit is o r other rena l d isease such as pyelonephrit is o r seve re hypertension
CAUSES OF NEPHROTIC SYNDROME
1. Glomeru lonephrit is accounts for 80% (usually membranous in ad ults, m inimal change in ch ildren)
2. Metabolic (i) Diabetes mell it us
(ii) A myloidosis (i iil Myelomatosis
3. SLE 4. Drugs - mercurials, pen ici llam ine, trox idone 5. Renal vei n th rombosis
CAUSES OF LARGE KIDNEY lOR KIDNEYS)
1. Cystic kidneys 2. Hydronephros is or pyonephrosis 3. Hypernephroma 4. Hypert rophy following contralateral nephrectomy or fai lure 5. Nephrotic syndrom e
Also consider the poss ibi lity of per irena l haematoma
TYPES OF RENAL TUBULAR DYSFUNCTION
1. RENAL DISEASE AFFECTING MEDULLA e.g. pyeloneph ritis. Impai rment of urinary co ncentration, ac idification and e lectro lyte reabsorpt ion
_ I Ren al d isease
2. RENAL GLYCOSURIA (ben ign)
3. 'VITAMIN D RESISTANT RICKETS'
Inabi lity to reabsorb phosphate
4. IDIOPATHIC HYPERCALCIURIA
Inabi lity to reabsorb calcium
5. RENAL TUBULAR ACIDOSIS (Type I - distal tubules)
Inabil ity to acidify the urine causes metabolic acidos is. Less ca lcium is bound to protein and ca lcium f iltration is increased, leading to nephroca lcinosis and rena l stones
6. RENAL TUBU LA R ACIDOSIS (Type 2 - prox imal tubules)
Occu rs as part of Fanconi synd rome, wi th defect ive reabsorption of g lucose, am ino adds and phosphate (GAP) Hyperchloraemic acidosis occu rs, but no nephrocalcinosis May also be due to toxins (lead, mercury, outdated tetracyc line), kidney transp lant or cyst inosis
7. CYSTINURIA
Defect in reabsorption of cystine, ornithine, arginine and lysine (COAL) -Cystine stones form
8. NEPHROGENIC DIABETES INSIPIDUS
Impai red response to ADH
ACID-BASE BALANCE
These headings re fl ect changes in ext racellular f luid on ly, e.g. in metabolic alka los is there is an associated intracellu lar acidosis
1. RESPIRAT O RY ACI DOSIS (low p H, h igh CO 2 content )
Any ca use of hypoventi lation (p. 43)
2. RESPIRATORY A LKALOSIS (hig h pH, low CO2 cont ent)
Any cause o f hyperventi lat ion (e.g. asp irin overdose or anxiety)
Renal disease
3. M ETABO LI C ACIDOSIS (low pH, low CO2 content)
Causes
til Ingestion of acidic compounds Ammonium chlor ide, salicylates, etc.
(iii Metabolic overproduction of a cids Ketosis, e.g. starvation, d iabetes mel litus l actic acidosis
(iii) Intestinal loss of base Diarrhoea Fistu lae
(iv) Renal failu re: renal tubula r a c idos is
4. M ETABOLIC A LKALOSIS (h ig h pH, h igh CO2 conten t )
Causes Ingest ion of alkali, e.g . NaHC03• fo r indigest ion Vomit ing, or gastric aspirat ion Hypoka laemia
CAUSES OF HYPOKALAEMIA
1 . Increased renal loss (i) Diuresis
Drugs, e.g. thiazides Diabetes mellitus
(i i) Minerolocorticoid excess, e.g. pr imary aldosteronism (Conn's t umour) and Cushing's d isease
(i i i) Primary renal d isease, e.g. chronic pyelonephrit is
2 . Increased intestinal loss e.g. dia rrhoea, vom it ing Consider purgative abuse
3. Decreased intake Dieta ry lack (especially in alcoholism, or duri ng protein anabol ism in convalescence, or fo ll owing prolonged i.v. fluids) Ma labsorption
CLIN ICAL FEATURES OF POTASSIUM DEPLETION
1. Muscle wea kness 2. Apathy, anorexia and confusion 3. Ileus 4. Increased cardiac excitabi lity and d igitalis toxicity 5. Th i rst and polyuria
Renal disease
CAUSES OF HYPONATRAEM IA
1 . Excessiv e w at e r inta ke Oral (polyd ipsia) or intravenous
2 . Excess iv e w at er r et ention Inappropriate ADH secretion
3 . Inadequat e sodium intak e (rare)
4 . Inadequat e sodium retention Ii) Vomit ing, diarrhoea, ileus, f istu la, drainage of ascites
Iii) Hypoadrenalism (ii i) Rena l loss (iv) Skin loss
a. Excessive sweating b. Cystic fi bros is c. Burns
CAUSES OF POLYURIA
1. Chronic renal fa ilure 2. Diabetes m elli tus 3. Diuretic drugs 4. Compulsive water drinking 5. Diabetes insip idus
Ii) Pitui tary (deficiency of ADH) (ii) Nephrogen ic (no response to ADH)
6. Potassium deplet ion 7. Hypercalcaemia
CAUSES OF PROTEINURIA
1. Conlamination (semen, prostatic or vaginal secretion) 2. Postural (orthostat ic) 3. Renal disease
(i) Glomerulonephritis, especially nephrotic syndrome (ii) Pyelonephritis
(ii i) Obst ruct ive nephropathy (iv) Malignant hypertension (v) Tubercu losis
4. Disease of renal tract, e. g. cystitis 5. May be slight a lbuminuria in fever or congestive heart fai lure 6. Multip le myeloma (Bence Jones protein)
CAUSES OF HAEMATURIA
(A) KIDNEY LESIONS
1. Glomeru loneph ri tis, pyelonephritis, TB 2. Trauma
Re na l d isease I
3. Anticoagulant overdose, bleeding diathesis 4. Hypernephroma 5. Rena l infarct (incl uding polya rteritis nodosa) 6. Polycystic kidney 7. Bacterial endocarditis
(8) RENAL TRACT LESIONS
1. Papillary tumour o f bladder 2. Acute cystitis (including cyclophosphamide toxicity) 3. Calcu li 4. Prostatic lesions:
Hypertrophy Cancer Prostat itis
5. Urethra l inflammation or t rauma 6. T8 (now rare in UK) 7. Sch istosomias is (rare in UK)
CAUSES OF 'STERILE' PYURIA
1. Rena l TB 2. Analgesic nephropathy 3. Rena l calculi 4. Urinary infection treated w ith chemotherapy 5. Non-specific urethrit is
CAUSES OF 'DARK COLOURED' URINE
1. Concentration 2. Bile 3. Blood, haemoglob inuria and myoglobinuria 4. Methaemoglobinuria 5. Porphyria 6. A lkaptonuria 7. Melaninuria 8. Beetroot, dyes in sweets, drugs (e.g. rifampicin), etc.
CAUSES OF URINARY TRACT OBSTRUCTION
1. Stone 2. Strict ure (post-op or inflammatory) 3. Stenos is (congenita l) 4. Neoplasm 5. Clot 6. Neuromuscular incoordinat ion 7. Retroperitoneal fi b rosis 8. Spread of cancer from pelvic o rgans
)
occur t hroughout the urinary tract
} ureter
Re n al disease
9. Prostatic en largement or cancer 10. Retroverted g ravid uterus 11. Trauma of labour 12. Congenital valves 13. Phimosis or paraphimosis
} b ladder neck
} urethra
Common ca uses of acute retention in adults are:
Males 1. Post-operative retention 2. Prostatic lesio ns
3. Urethral str icture
Females 1. Trauma of labo ur 2. Pressu re from uterus (fetus or
f ibroid l 3. Hysteria
Remember that retent ion m ay also be due to antichol inergic drugs Of a neuro log ica l lesion such as multi ple scle rosis o r co rd compress ion
URINARY CALCULI
FACTORS WH ICH PREDISPOSE TO UR INARY CALCU LI
1. Metabol ic abnorma lit ies (q.v.) 2. Urinary tract infections, e.g . Proteus 3. Urinary t ract stasis 4. Foreign bodies in urinary t ract 5. Geograph ica l fac tors (e.g. hot, dry climate, hard water)
M ETABOLIC CAUSES OF URINARY CALCULI
CALCIUM STONES (composed of calcium oxa late, phosphate o r both)
1. Hypercalciur ia (on normal d iet, > 300 mg/24 h in m ale or > 250 mg/24 h in female)
( i) Id iopathic hypercalciuria ( ii) Hyperparathyroid ism
(ii i) Vita m in 0 excess (iv) Sarcoidosis (vi M ilk- alkali syndrome (vi) Rena l tubular acidosis
(vii ) Ma lignancy (vi i i) Immobi lization
(ix) Cush ing's syndrome 2. A lkaline urine 3. Oxa luria
URIC ACID STON ES
Primary or secondary gout Uricosuric dru gs
CYSTINE STONES
Cyst inu ria Fancon i syndrome with cystinosis
XANTHINE STONES
Xanth inuria
RENAL STONES
Radio-op aque Calcium (80%) Mg ammonium phosphate (10%) Cyst ine (2%)
Rena l d isease I _
N o n-o paque U ric acid (5%) Xa nth ine (1 %)
NEUROLOGICAL CONTROL OF BLADDER FUNCTION
Norma l bladder capacity is 300-400 m l and larger vo lumes shou ld st im ulate the des ire to m ictu rate. Afferent fibres trave l v ia parasympathetic nerves to sp ina l 'mict urition centre' (S 2, 3, 4) and b ladder contract ion is in itiated by parasym pathetic efferents. The spina l 'm ict urition ce ntre' is no rmally inhibited by higher motor centres, wh ich bombard it wi th faci litatory impulses w hen m ictu r ition begins, so that the bladder empties completely
TYPES OF DYSFUNCTION
1. LACK OF NORMAL INHIBITION
Frequency with sm all volumes Occurs in anxiety, cold weather, etc.
2. ATONIC BLADDER
Distended bladder w ith overflow, but no desire to m ictu rate Occu rs w ith sensory neu ropathy, e.g. diabetes mell itus, tabes dorsal is
3. AUTOMATIC BLADDER
Bladder empties part ially when vo lume of about 250 ml is reached, but w ithout desi re to micturate Occurs with co rd sect ion above S 2, 3, 4
4. AUTONOMOUS BLADDER
Large residual ur ine volume, w ith wea k uncoord inated b ladder contractions but no desire to mict urate. Occurs wi th LMN cord lesions at S 2, 3, 4 leve l
_ I Renal disease
Unilatera l neu ro log ical lesicns may cause either frequency with smal l vo lumes or a large hypotonic b ladder w ith residual u rine after m ictu rit ion
RENAL CLEA RAN CE
The number o f m l of p lasma w h ich contains the am ount of a substance excreted in the u rine in one minute is the rena l clearance of that substance, i.e. C ", UV/pT m l w here U ", concentration of substance in urine
V = volume of urine collected in time T P = concentration of substance in plasma
Creatinine clearance gives a more accurate measure o f renal funct ion than th e plasma urea
11. Rheumatology
PATTERNS OF POLYARTHROPATHY
PRIMARY OSTEOARTHROSIS
Symmetrical, affecting many jo ints 1. Knees 2. Great toes and th umbs: MP joints 3. Fingers: term inal IP jo ints 4. Acrom ioclavicu lar joints 5. Smal l joints of sp ine
SECONDARY OSTEOARTHROSIS
Asymmet rica l, affecting weight-bea ring joi nts 1. Knees 2. Hip 3. Intervertebra l discs
RHEUMATOID A RTHRITIS
Usual ly symmetr ical, intermin ent and inflam ed 1. Hands: intercarpal jo ints, M P joi nts and proxim al IP joi nts 2. Feet: tarsal and lateral MP jo ints 3. Knees 4. Sma ll jo ints o f cervical spine and subacrom ial bursae
ANKYLOSING SPONDYLITIS
1. Spine and both sacro i liac joints 2. Knees, shou lders, w rists
PSORIASIS
1. Hands, te rm ina l IP j o ints (look fo r nai l pits) 2. Sacroiliac jo ints 3. 'Rheumatoid' pattern 4. Asymmetrica l ol igoarthritis (e.g. knee) 5. Arth rit is mut ilans
REITER'S DISEASE
1. Ankles and all joints o f feet
-
1
_ I Rheumatology
2. Knees 3. Hips, sacroi liac jo ints and spine
X-RAY CHANG ES OF OSTEOARTHROSIS
1, Joint space narrowing 2. Subarticu la r sclerosis 3. Osteophytes 4. Bone cysts
JOINT COMPLICATIONS OF RHEUMATOIO ARTHRITIS
, . Deformity, sub luxation, m isa l ignment. swell ing 2. Infection (sept ic a rth ritis) 3. Tendon rupture 4. Synovial sac p rot rusion and ru ptu re (e.g. Baker's cyst ) 5. J uxta-articu lar osteoporosis 6. Muscle atro phy secon dary to d isuse
EXTRA-ARTICULAR MANIFESTATIONS OF RHEUMATOID DISEASE
1. ANAEM IA .
(i) Fe defic iency (G I blood loss ca used by d rugs) I ii) Defect ive i ron ut i lization (a naemia of ch ron ic d isorders)
( i i i) Marrow depress ion
2. PU LMONARY
(i) Pleu ritis, effusions (i i) Nodu les in lung or p leu ra
( i i i) Fibrosing a lveol itis
3. CARDIAC
Ii) Perica rd it is ( ii ) Nodu les in myocard ium
4. OCULAR
( i) Scler it is, ep iscie ritis (i1) Scleroma lac ia perforans
(iii) Sicca syndrome (Sjog ren's)
5. ARTE RITIS
0 ) Digita l ischaem ia (m ay be Rayn aud's ) (i i) Na il fo ld lesions
(ii i) Leg u lcers (iv ) Mesenteric ischaem ia
Rheumat olo 9V I _
6. PERIPHERA L N EU ROPAT HY (due t o vascu l iti s)
7. ENTRAPMENT N EUROPAT HY, e.g . spinal cord at cervi cal level f rom atlanto-axial subluxatio n, o r ca rpa l tunnel syndrome
8. FELTY'S SYNDROME (RA w ith leu ko pen ia and sp le nomega ly)
9. LYMPHADENOPATHY
10. A MYLOIDOSIS
SERONEGATIVE SPONDYLOARTHRITIS (HLA-B27 ASSOCIATION)
A rth ritis invo lv ing the spine but wit h consistent absence of rheumato id facto rs from serum 1. An ky losing spondyl it is 2. Psoriatic arthrit is 3 . Enteropat hic arthrit is (Crohn's, u lcerat ive colitis, Wh ipp le's,
enteric infection, intest ina l bypass for o besity ) 4. Reite r's d isease
FEATURES OF ANKYLOSING SPONDYLITIS
1. Ankylosis/arthr it is of sp ine (bamboo sp ine) 2. Anterior uveit is 3. A rrhythm ia 4. Aortic regurgitat ion 5. A pical pu lmonary fibros is
(N.B. 5 A s)
CAUSES OF LUMBAR BACKACHE
1. MECHANICAL
(i) Muscu lotendinous and l igament strain (ii ) Prolapsed interve rteb ral d isc
(i ii ) Spondylos is and spondylo l ist hesis (iv) Spinal f ractu re
a. Major trauma b. Crush fract ure in osteopo rosis c. Stress fractu re of t ransverse process due to muscu lar
effort
/
_ I Rhe u matology
2. DEGENERATIVE OR M ETA BOLIC
(i) Osteoa rthrosis ( ii ) Osteoporosis
(ii i ) Osteoma lacia
3. INFLA MMATORY
(i) Infection, e .g. T8, pyog enic ( i i) Seronegative spondyloarthriti s (q.v.)
4. NEOPLASM
( i) Usually metastatic mal ignancy (i i) Primary ma lignancy - Osteosa rcoma
Myeloma Lymphoma
5. REFERRED PA IN
(i ) Posterior duodena l ulcer (i iI Cance r of pa ncreas
( i ii) Rena l colic (iv) Pelvic carcinoma (v) Dysm enorrhoea. labour pains
CAUSES OF A SINGLE HOT RED JOINT
1. Traumat ic, e.g. sprained ankle 2. Septic arthrit is
May be secondary to penetrati ng in j ury, osteomyelitis, septicaemia, rheumatoid arthritis or osteoarth ros is
3. Gout or pseudo-gout (chondrocalci nosis or periart icu lar ca lcif icat ion)
4. Haemophilia 5. Gonococcal arthritis 6. Occasionally rheumatoid arthrit is
CAUSES OF A TRANSIENT ' FLITTING' ARTHRITIS
, . Rheum atic feve r 2. Henoch- Schon le in purpura 3. Serum sickness and drug react ions 4. SLE 5. Systemic infecti ons
( i) Gonococcal or meningococcal sept icaemia (ii) Bacterial endocardit is
(iii) Ru bella
•
Rheumatology I _
(iv) Infectious mononucleosis (v) Infect ive hepat it is
(vi ) Mycoplasma pneum onia 6. Reiter's di sease 7. Occasionally, acute rh eumatoid arth rit is
CAUSES OF HVPERURICAEMIA
1. INCREASED PURINE SYNTHESIS
Pr imary gout (in 25% of cases)
2. DECREASED RENAL EXCRETION
(i) Primary gout (i n 75% of cases) (ii ) Chron ic renal fai lu re
(ii i) Drugs Sa licy lates (in low dosage) Uricosu rics (in low dosage) Thiazide d iuretics A lcohol
3. INCREASED TURNOVER OF PREFORMED PURINES
(i) M yelopro liferat ive disease and lymphoma (esp. after cytotoxic drugs)
(ii ) Chronic haemolysis (ii i) Psoriasis
CLASSIFICATION OF VASCULITIS
No classificat ion is completely satisfactory. since the c lin ical syndromes may overlap, and thei r pathogenesis is imperfect ly ,.nderstood
1. SYSTEMIC NECROTIZING VASCULITIS
(i) Po lya rterit is nodosa (ii ) Churg- St rauss synd rome (with ast hma and eosinophi l ia)
(ii i) Wegener's granulom atosis (upper and lowe r respi ratory t racts and kidneys)
(iv) Beh<;:et's d isease (w ith o rogen ita I apht hous ulcers)
N.B. Ant ineutrophi l ic cytoplasm ic ant ibod ies: cANCA is fairly sensitive for Wegener's pANCA (perinuclear) is found in a broader range of vascul itides,
,,,el ud ing PAN
_ I Rheumatology
2. 'HYPERSENSITIVITY'VASCU LITIS (small vessel disease. often cutaneous with circulat ing im mune comp lexes)
(i) Serum sickness is the classical example, but now rare (ii) Drug al lergy
(iii) Henoch- $chonlein purpura (affects skin, joints, GI t ract and kidneys)
(iv) Infection (classically TB, e.g . Bazin's) (v) Idiopathic cutaneous vascul iti s (often nodu lar, on legs)
(vi) Malignancy, e.g. breast cancer
3. COLLAGEN VASCULAR DISEASE
Rheumatoid, SLE , systemic scle rosis, de rm atomyosit is/polymyOSitis
4. LARGE VESSEL VASCU LITIS
Giant ce ll aorti t is (e .g. Ta kayashu'sl Temporal arte rit is Kawasa ki disease (usually yo ung ch ildren, may be coronary arteri t is)
5. THROMBOANGIITIS OBLITERANS (Buerger's disease. occurs in smokers)
CLINICAL FEATURES OF POLYARTERITIS NODOSA (PAN)
Usually young or m iddle-aged men 1. Fever, ma laise, weight loss 2. Gastro intest inal ischaemia
Central abdominal pain Bleeding
3. Proteinuria and haematuria. Hypertension is common 4. Periphera l neuropathy, often painful
Focal eNS lesions 5. Arth ralg ia and mya lg ia 6. Myocardial ischaemia 7. Skin les ions:
Nod ules Livedo reticu laris Nec rosis and u lcerat ion
CLINICAL FEATURES OF SYSTEMIC LUPUS ERYTHEMATOSUS
Usually young or m idd le-aged women 1. Fever, ma laise, weight loss
Rheumatology I _
2. Arth ralg ia, flitt ing or episodic 3. Skin changes
(i) Photosensit ive rash, classically in butterfly d istribut ion . May be erythematous, urticated or purpur ic
(iil A lopecia (i ii) Di lated nail fo ld capil laries (iv) Raynaud's phenom enon
4 . Proteinuria, g lomerulonephrit is, nephrot ic syndrome or hypertension
5. Lym phadenopathy 6. Myocarditis, endocard it is (Libman-Sacks), or pericard itis 7. Pleurisy with effusion, pneumonit is 8. Hepatomegaly and splenomegaly 9 . Pancytopenia . May be haemolysis
10 . Psychosis, neuropathy or epi lepsy. M ay be retina l exudates 11 . Gastrointest inal upsets (nausea, pai n , d iarrhoea, etc.)
RAYNAUD'S PHENOMENON
Paroxysmal d igita l ischaemia, which usua lly causes a cha racter istic sequence of colou r changes (white, then blue, then red)
CAUSES
1 . Reflex vasoconstriction (i) Raynaud's d isease (idiopathic)
(ii) Vibrat ing machinery
2 . Arterial occlusion (i) Thoracic outlet syndromes
(i i ) A theroma. Buerger's disease
3. Collagen- vascular disease, espec ia lly system ic sclerosis and SLE
4 . Increased blood viscosity (i) Dysproteinaemias (macro- and cryog lobulinaemias)
(i i) Po lycythaemia, leukaemia
5. Neurological disease. especia ll y syringomyel ia or para lysis
12. Dermatology
PSORIASIS
DISTINCTIVE MORPHOLOGICAL TYPES
,. Nummular - d iscoid plaques, w hich may be conf luent. Typica lly on extensor surfaces
2. Guttate - 'showers' of sma ll lesions, o ften post-streptococca l 3. Erythroderm ic - very widespread ery thema, w ith exfo l iat ion 4. General ized pustular psor iasis 5. Pustu la r erupt ions of t he hands and fee t
Atyp ical form s are common, e.g. fo ll icu lar, i ntert rig inous, etc.
'Napkin psoriasis' (pso riasiform les ions in infants) may be related to cand ida infection
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-vesicles w ith erythema and scaling.
M any cases have a mult ifactoria l aetiology
rYPES OF ECZEMA
(AI Exogen o us I Primary irr itant dermati t is, e.g. due to ca ustics, detergents or
solvents "J . Allerg ic contact dermat it is, e.g. due to hypersensit iv ity to
Illeta ls, rubbe r, medicaments, etc. :1 Infect ive dermati t is, e.g. around infected wounds o r ulce rs
(8) Endogenous I. A top ic derm ati t is (infa nti le eczema). Typica lly on f lexor su rfaces
"J Seborrhoe ic dermat it is I Disco id eczem a ~ Pompholyx - vesicles on palms or soles '. Pit y riasis alba - patches of sca ly eczema w hich leave
depigmented areas (~ I\sl oatotic eczema - due to excessive d ry ing ('chapping' )
Gmv itat ional eczema - secondary to venous insufficiency
-
_ I De rmatology
BLISTERING ERUPTIONS
COMMON CAUSES
1. Viral Ii) Herpes simplex
(ii) Herpes zoster - varicella 2. Impetigo 3. Scabies 4. Insect b ites and papula r urticaria 5. Bu llous eczema and pompholyx 6. Drugs, e.g. barbiturate overdose, photosensitiv ity
UNCOMMON CAUSES
7. Eryt hema mult iforme 8. Dermatitis herpet ifo rm is 9. Pemphigoid
10. Porphyria cutan ea tarda '1 . Pemphigus group
) sub-epidermal
intra-epiderma l
Remember pemphiguS is Superf icial and pemph igoiD is Deepe r
RARE CAUSES
12. Congenital (i) Epidermolysis bu llosa
(i i) Ichthyosiform eryth roderma (ii i) Incontinentia pigment i
CAUSES OF PHOTOSENSITIVITY (ENHANCEO RESPONSE TO UV IRRADIATION)
1. Drugs, e.g. t o lbutamide, c h lorpropamide, p henoth iazines, t hiazides, amiodarone, n alidixic ac id Mnemonic: r ep-TAN
2. Contact photosensit izers, e.g. tar, pe rfu mes, soaps, etc. 3. Dermatoses, e.g. porphyr ia , po lymorphic light erupt ion, lupus
erythematosus 4. Decreased me lan in in skin, e.g. albinism, v iti ligo
CAUSES OF LEG ULCERS
t. Venous hypenension (90% ) 2. Ischaemia
(i) Atheroma {i iI Aneritis
3. Neuropathy (i) Diabetes mellit us
{i i i Spina b ifida (iii ) Ta bes dorsalis (iv) leprosy (in endemic areas)
4. Rheumatoid arthritis - u lceration is mult ifactorial
Oonnatology I _
5. Malignancy - usually squamous-cell skin carcinoma 6. Haemolytic anaemia, especially sickle-cel l 7. Syphil it ic gumma 8. Necrob iosis lipoid ica (may be diabetic ) 9. Pyoderma gangrenosum - often due to ulcerat ive colil is
Many leg ulcers have a mu lt ifac torial aet iology, e.g. ischaemia, anaemia, venous hypertension and infection
CAUSES OF ALOPECIA
t . Mal e-pattern ba ldness 2. Id iopath ic diffuse alopecia o f women - usua lly post
menopausal 3. Telogen effluvium' - loss of c lub hairs after febri le illness,
su rgery or partu r ition 4. Alopecia areata 5. Drugs:
(i) Cytotox ic agents (ii) Anticoagu lants
(iii ) Dextran (iv) Oral co nt raceptives
6. Scalp infection : (i ) Fungi
(ii) Pyogenic bacteria 7. System ic d isease:
(il Syph ilis (i i) HypothyrOidism
(i ii) Fe def iciency 8. Trau matic:
(i ) Traction from rol lers (ii ) Scalping inj ury
(i ii ) Burns (iv) Excessive bleach ing, pe rming, etc.
9. De rmatoses: (i) Psoriasis
(i i) Disco id lupus erythematosus (iii) Lichen planus
10. Congen ital- many rare di seases, e.g. mon il ethrix
CAUSES OF HIRSUTISM
1. Id iopathic (incl uding racial and familia l variat ion) l . Ovarian disease
(i ) Polycystic ovaries (common) (i i ) Vi rilizing tumo ur (rare)
_ [ DermatolOgy
3. A drenal hyperplasia or tumour 4. Obesity and hyperinsulinaemia 5. Prolact inoma 6. And rogenic drugs, e.g . methy ltestosterone, anaboli c stero ids.
(Oth er drugs such as m inoxidi l and di8zoxide cause hypertrichosis rather tha n true hi rsut ism)
CAUSES OF OIFFUSE HVPERPIGMENTATION
1. Congen ita l (racial or fam il ial) 2. Irradiation, e s p. ultravio let 3. Post -inflammatory, e.g. after erythroderma 4. Endocr ine causes
( i) Pregnancy, oestrogens (i i) Hypoadrenal ism (due to MSH{beta-l ipot ro ph in )
(ii i) Ac romega ly 5. M iscell aneous system ic di seases
(i) Cachexia (esp. TB or mal ignancy) (ii) Chronic ren al fai lure (ii i) Primary bi liary ci rrh os is (iv) Haemochromatosis (v) Ma labsorption
6. Drugs, e.g. busu lphan, chlorpromazine, ACTH, arsenic
SKIN OISEASES WHICH CAUSE SEVERE ITCHING
1. Pa rasites: scabies, pedicu losis, flea bi tes 2. Eczema 3. U rt icaria 4. lichen p lanus 5. li chen simplex ch ronicus 6. Dermat it is herpet iformi s
SYSTEMIC CAUSES OF GENERALIZEO PRURITUS
1. Obstructive jaundice (especially bil iary cirrhosis) 2. Chro nic renal failure 3. lymphoma (especially Hodgkin's) o r m yelopro liferat ive d isease
(especially polycythaemia veral 4. Carcinoma (especially bronchial) 5. Iron def iciency 6. Hypo- or hyperthyroidi sm 7. Drugs
(i) A ll ergy (ii i Pharmacological. e.g . cocaine, morph ine
N.B. a. Many w omen develop pru ritu s during p regna ncy b. Scabies is easily m issed in hygien iC pat ients - rem em ber
to look for burrows in the fingerwebs, and examine the n ipp les or pen is for typical papules
CAUSES OF GENERALIZED PALLOR
1. Vasoconstriction (cold, emotion, vasovaga l, etc.) 2. Anaem ia (includ ing acute haemorrhage) 3. Diffuse hypomelanosis
0) Protection from UV rad iat ion (ii) A lbin ism
(iii) Phenylketonuria (iv) Hypopitu itari sm (v) W idespread v it iligo
Dermato logy I _
CAUSES OF WHITE PATCHES ON THE SKIN (leu kod e rm a)
1. Congeni ta l (rare), e.g . tuberous sclerosis, partial al bi nism 2. Post-inflammatory, e.g. eczema, burns. d iscoid lupus
erythematosus 3. Infection, e.g. leprosy, p ity riasis vers icolor 4. Immunological. e.g . vit i ligo, halo naevus
ERYTHEMA
CAUSES OF PALMAR ERYTHEMA
1. Dermatoses, e.g. eczem a or psoriasis 2. Increased oeslrogens
(i) Pregnancy (i i ) Alcohol ic ci rrhosis
3. Rheumato id arth rit is 4. Shoulder- hand syndrome 5. Polycythaem ia
CAUSES OF FACIAL FLU SHING
1. Heat and exe rtio n 2. Psycholog ical (b lushing, anger ) 3. Menopause 4. Rosacea 5. Food and drugs
(i) A lcohol; marked in M ongolo id races, and in some d iabetics taking chlorpropamide
(i i) Peppers, chi ll ies (ii i) Nit rites, sod ium m onog lutamate, morphine. etc.
6. Carc inoid synd rome
SOME CAUSES OF A CIRCUMSCRIBEO PATCH OF RED SCALY RASH
1. Psoriasis 7. Eczema
_ 1 De rmat o logy
3. Fixed drug erupt ion 4. Fungus 5. Lichen simplex 6. Bowen's d isease (squamous Ca in sit u) 7. Discoid lupus erythematosus 8. Lupus vulgaris (a form of T8 )
SOME CAUSES OF WIDESPREAD PATCHES OF RED SCALY RASH
1. Psoriasis 2. Eczema 3. Pityriasis rosea 4. Pity riasis versicolor 5. Secondary syphi lis 6. Liche n planus 7. Fungus
CAUSES OF ERYTHRODERMA (in f lammatory skin disease aHecting more than 90% of body surface)
1. Eczema of va rious types (esp. atopic) 2. Psoriasis 3. Lymphoma or lymphatic leukaem ia 4. Drugs, esp. gold or mercury 5. Id iopathic and rare congenital d isorders
CAUSES OF ERYTHEMA NODOSUM (tender nodules on legs)
1. Sarcoidos is 2. Streptococcal infection 3. T8 4. Drugs. e.g. su lphonamides 5. U lcerative colitis or Crohn's d isease 6. Other infect ions, e.g.
0) l eprosy (i i) Systemic mycoses
(ii i) Toxoplasmosis (iv) l ymphogranu loma venereum
CAUSES OF ERYTHEMA MULTIFORME (often 'ta rgets' on pa lms) 1. Infections, esp. herpes simplex, orf or mycoplasma 2. Drugs (many, esp. long-act ing su lphonamides) 3. Id iopathic (recurrent forms may be due to occult herpes simplex) 4. Rarely collagen-vascular d isease, pregnancy or malignancy
Dennatology I _
CAUSES OF PYODERMA GANGRENOSUM
1. Grahn's and other inflammatory bowel d isorders (UC, etc.) 2. Rheumatoid and ot her inf lammatory joint disorders 3. Id iopathic 4. Rarely dysproteinaemia or mye loproli fera t ive disease (esp.
leukaemia)
COMMON CAUSES OF A PIGMENTED PAPULE
1. Basal cell papil loma ('seborrhoeic w art') 2. Melanocytic naevus ('mo le') 3. Malignant melanoma 4. Pigmented basal cell carcinoma 5. Dermatofibroma
FEATURES SUGGESTING MALIG NA NT CHANGE IN A MOLE
M ajor f eat ures: 1, Change in size (esp. steady en largement, t hough ben ign moles
often enlarge at puberty and in pregnancy) 2. Change in shape (i rregu lar out line may be important) 3. Change in c%ur (blotchy variation, or spread of pigment
beyond margin may be important)
M inor f eatures: 4. Diameter more than 7 mm 5. Inflammation 6. Ulce ration or bleed ing 7. Itch (t hough th is is common in ben ign moles)
If diagnosis is uncerta in obta in an expert opinion or excise for h istology
In malignant melanoma, the best ind icator of prognosis is the Breslow thickness (vertical th ickness on histology)
CAUSES OF XANTHOMA
1. Idiopathic, w ith normal b lood lip ids 2. Primary hyperl ipidaemia, e.g. type 2 (hypercholeste rolaem ia) 3. Secondary hyperlip idaemia
(i) Diabetes mellitus (ii) Hypothyroid ism
(ii i) Chronic rena l fa ilu re or nephrot ic synd rome (iv) Gholestasis (esp. primary b iliary cirrhosis)
Other causes of hyper lip idaemia, less li ke ly to produce xanthomas, include obesity, alcoholism, pancreatit is and drugs, o.g. isotret inoin
_ I De rmat o logy
SKIN CHANGES ASSOCIATED WITH SYSTEMIC MALIGNANCY
1. GENETIC SYNDROMES PREDISPOSING TO MALIG NANCY
8. g. neu rof ibromatos is (may deve lop g lioma), fam i lial tylosis (palm ar keratoderma) w ith oesophagea l carcinoma
2. SIGNS OF EXPOSURE TO A CARCINOGEN
e.g .: (i) N icotine staining of fi ngers
(ii ) Palmar keratoses due to arsenic
3. DIRECT INVOLVEM ENT OF SKIN BY MALIGNANT CELLS
( i) Direct sp read from underly ing cancer (espec ially b reast ) ( i i ) Cutaneous metastases
(ii i) l e ukae mic o r ly m phom atous infi lt rate
4. M ISCELLANEOUS ENDOCRINE, METABOLIC AND IMMUNOLOGICAL EFFECTS
(i) Pigmentat ion. pallo r o r pru ritus (ii) Acant hosis nig ricans (i ii) Derm atom yositis (iv) Clubb ing (v ) Widespread v i ra l infect ion (e .g . he rpes) due to immune
defici en cy, etc.
NAIL CHANGES D U E TO SYSTEMIC DISEASE
ABNORMAL MORPHOLOGY
1. Clubb ing (p o 46) 2. Ko i lonychia (i ron def iciency) 3. Beau's lines (following ser ious illness) 4. Onycho lysis (thyrotoxicosis)
ABNORMAL COLOUR
1. Pallo r (i ) Anaemi a
(ii) Pale w ith d ista l b rown zo ne (rena l fail u re) (i ii) Opaque w h ite na ils (hypoalbum inaemia)
2. Redness (i) Po lycythaemia
(ii) CO po ison ing
3. Blue nails Cyanosis
4. Ye llow nai ls Ye ll ow na il syndrome, with lym phoedema
CAPILLARY CHA NGES
1. Splinter haemo rrhages (i) Subacute bacterial endocard it is
(ii) Vascu li t is, e.g . rheumatoid 2. Nai l-fo ld capillary d i latation
Derm at o logy I _
Col lagen-vascular disease, esp. dermatomyosit is, Sl E
NAIL CHANGES DUE TO SKIN DISEASE
Psoriasis : p itt ing, o nycho lysis, ri dg ing ' Eczema: defo rmed na ils with r idg ing flnea: th icke ned, d isco lou red, friab le M yxoid c yst : single groove 'Picking ' at matrix: rippled grooves Molanoma: brow n or b lack streak (m ay mimic sub-Iungua l
haematoma) I I yfhroderma : shedding o f nails
PATTERNS OF DRUG ERUPTIONS
I\ IIy d rug can occasi ona lly cause an eru ption . Any erU Ption can '" t:ilsiona lly be m im icked by a drug react ion. The fo ll owing list is I." from com prehen sive: I I xa nthemata (m orbill ifo rm , etc .), e.g . pen icill i n I Urt icaria, e.g . pen icill in I I Iylhroderma, e.g. go ld
,I lIu ilous, incl ud ing erythem a m ult iforme, e.g. su lphona m ides t . I , yt hem a nodosum, e.g . su Jphonamides h I ' ll, pura (due to either thrombocytopen ia or vascu lit is)
i'lu)IOSensit iv ity, e.g . chlorprom azine II I\nwform (see below) II " x l~d drug erupt ion (interm ittent inflammation foll owed by
IlIjll lIcntation, always at same site), e.g . phenolpht halein
I tl tiJGS W HICH PROVOKE A N ACNEFORM RASH
I " " " J,ides and iod ides I A II III :u ll vu lsa nts I Rlnrllids (g lucoco rt ico id, anabo lic and androgenic) ~ .,1. "' I;IIid Il l ltllll l il l
M ' '''III /lIIic: BASil
I D ermatology
CAU SES OF MOUTH ULCERATION
1. Aphthous u lcers (i) Minor
(ii) Major (iii) Herpetiform
2. Squamous carc inoma (often m isd iagnosed) 3. Infection, e.g . herpes simplex, syphi li s 4. Lichen p lanus 5. Pemph igus or benign mucous membrane pemphigo id 6. Drugs, e.g . methotrexate 7. Trauma, e.g . from dent ures 8. Beh eet's, Reite r's or Stevens-Johnson
THREE SYSTEMIC DISEASES WHICH CAUSE CONJUNCTIVITIS WITH ULCERS OF THE MOUTH AND GENITALIA
1. REITER'S SYNDROME
Clinical feat ures (i) Non-specifi c uret hritis, haemat uria, steri le pyuria
(i i) Recu rrent con junctiv itis or uveitis (ii i) Symmetrica l subacute arthritis, tenosynovit is, periost it is of
ankle, knee and spine (iv) Circinate balan it is (v) Buccal ulcers
(v i ) Keratoderma blenorrhag ica (resem bles pustu lar pso riasis)
2. STEVENS-JOHNSON SYNDROME
Clinical features (i) Constitutional symptoms and high fever
(ii) Conjunct ivit is. corneal ulcers, uve it is (iii) Oral bu l lae and haemorrhagic crusting of lips (iv) Eryt hema mu lt iforme (v) Urethri t is, balan it is, vu lvo-vagini t is
(vi) Bronchitis, pneumonitis, or renal lesions
3. BEH~ET'S SYN DRO ME
Clinical features (i) Bucca l and gen ita l aphthous ulce rs w it h a red areola
(ii) Conjunctiv itis, uveit is or ret inopath y (i ii) Cuta neous pustules, dermal nodules (iv) CNS lesions: meningo-encephal itis. bra in-stem syndromes (v) Thromboph lebitis
Dermat o logy I _
TYPES OF PORPHYRIA
1. ACUTE INTERMITIE NT PORPHYRIA
Classica l t r iad of da rk urine, abdominal pain (sometimes w ith nausea or const ipation) and neuropsych iatric symptoms. No skin invo lvement Autosoma l dominant . Acute attacks provoked by drugs, e.g. oral contracept ives, alcohol, barbiturates, sulphonamides, ch lorpropamide
2. PORPHYR IA CUTANEA TARDA
Photosensitiv ity and skin fragility. Usually develops in midd leaged pat ients w it h hepatic d isease, especially alcohol ic men. Associated w it h increased iron stores, and treated by venesect ion
CONDITIONS PREDISPOSING TO CANDIDIASIS
1. Skin t rauma and maceration, e.g . dentu res, perleche 2. Infancy, pregnancy, o ld age 3. Systemic i ll ness
(i ) Cachexia or malignancy (ii ) Immunosuppression, e.g. AIDS
(iii) Iron defic iency (iv) Endocrine disorders
Diabetes mell itus Cushing's d isease Addison's hypoadrena lism Hypoparathyroid ism
4. Drugs (i) Broad spectrum anti b iotics
(ii ) Glucocort icoids (iii) Immunosuppressants
HIV AND AIDS
Group 1- patients are infected with HIV and seroconvert, often w ith a glandu lar fever-like i ll ness and rash or neurologica l symptoms
Group II - HIV pos itive pat ients who appea r perfect ly well and may remain so for many yea rs
Group II I - persistent general ized lymphadenopathy, PGL {i.e. lymphadenopathy due to react ive hyperplasia involving 2 or more sites ot her than the inguinal g lands, and pe rsist ing for 3 or more months}
, _ I Dermato logy
Group IV A - constitutiona l symptoms associated with HIV. CD4 count is greatly decreased. Clinica l features include fatigue. nightsweats, lymphadenopathy, weight loss, fever, diarrhoea, etc.
Group IV B, C, D, and E are roughly equivalent to AIDS. That is the development o f one or more A IDS indicator diseases for which there is no o ther explanation and evidence of HIV infection such as positive serology or a low CD4 count. There may be neuro logical disease (B), secondary infections (e), secondary ca nce rs (D) or other conditions (E)
OPPORTUNISTIC INFECTIONS
1. Viral, e.g . cytomega lovirus, d isseminated herpes simplex 2. Bacterial, e.g. atypica l mycobacter ia such as Mycobacteria
aviurn-intracellu lare com plex 3. Funga l, e.g . systemic candid iasis, cryptococcus 4. Protozoal , e.g. Pneum ocystis car ini i, toxoplasmosis
MALIGNANCY IN AIDS
, . Kaposi's sarcoma 2. lymphoma, especially ce rebra l
SKIN CHANGES ASSOCIATED WITH AIDS
1. Transient rash at t ime o f seroconversion 2. Skin infect ions - ohen extensive, exaggerated, or exotic 3. Kaposi's sarcoma 4 . Hairy leukoplak ia of tongue 5. Many other dermatoses are commoner or more severe than in
general population, e.g.: Seborrhoeic dermatitis Psoriasis Drug eruptions Xeroderma or pruritus A lopecia
HUMAN MALIGNANCY CAUSED BY A VIRUS (PLUS A CO-PROMOTER)
, . Carc inoma cervix 2. Hepatocellu lar cancer 3. Nasopharyngeal cancer 4. Burkitt's lymphoma 5. Kaposi's sarcoma 6. T cell lymphoma
Virus Human pap illoma v irus (HPV) Hepatitis B EB virus (in Ch inese) EB v irus (in malaria reg ions of Africa) HIV plus herpes virus 8 HTlV-,
13. Normal values
The Internat ional System of Un its (51 units) has now been w idely introd uced in Brit ish laboratories in place of the tradit ional Imperial Units, w hich were empi rical. Submultiples of 5 1 un its use the fo llowing prefixes:
Factof Name Symbol
"r' dad d
"r' canl; , ,,~ milli m
". micro " ", nano " 10-" pico , 10-'5 Ic mla f
Even with $ 1 un its, values may vary in different laboratories
CLINICAL CHEMISTRY
Adu lt ref erence ranges - b lood
Acid phosphatase: to tal prostatic
A lanine am ino-transferase (All) A lbumin Alkaline phosphatase Amylase Aspartate transaminase (AST)
B" Bicarbonate Bi lirubin (total ) Corrected calci um Chloride Cho lesterol
4-11 iull < 4 iull 5-45 lull 35-50 gI l 30-90 iujl < 300 iull '0-50 iul l ' 00-1000 ngll 24-30 mmol/I 3-17 ~mol/l 2.2- 2.7 mmol/I" 95-105 mmoll l 3.6-6.7 mmol/I (The WHO recommends an upper limit of normal of 5.2 mmol/l for a health ier popu lation, except in fema les over 60)
-
I
_ I N or mal values
Cort isol: 9 am 12 midnight
C-reactive protein (CRP) Creatine kinase: total
Creatinine Ferriti n Folate :
MB isoenzyme
Red cell fo late Gamma-g lutamyl transpeptidase (gamma-GTI Glucose (fasti ng) Glycated haemoglobin (Hb A l e) Iron: ma le
fema le Magnes ium Osmolality Phosphate
Potassium Protein (to lal ) Sod ium Thyroxine (T4) : tota l
free Total iron bind ing capacity (TIBC) Triglycerides (fasting) Tr i-iodothyron ine (T31 Urea Ur ic acid
HAEMATOLOGY
HAEMOGLOBIN
Men Women
13.0-18.0 g/dl 11.5-16.5 g/dl
RED CELL COUNT (RBC)
Men Women
4.5- 6 .5 )( , 012/1 3.9-5.6 )( 1012/1
HAEMATOCRIT (PCV)
Men Women
0.40- 0.54 0.36-0.47
140-690 nmolJl 80-190 nmol/l < 10 mg/I < 90 lul l < 6% of tota l 60-120 ~molJl 12- 200 IJg/I 3-15 lJg/1 160-640 1-19/1 < 60 iull 3.6-5.8 mmolJl 4.5-8% 14-32 IJ mol/l 10-29 IJmolll 0.75 ~ 1 .0 mmolll 280-290 mmol/kg 0.8-1. 4 mmol/I (i. e. approx imately half of calcium) 3.6-5 .1 mmol/I 60-80 g/I 135--145 mmol/l 60-150 nmol(1 9-26 pmol/ l 45--72 IJ mol/1 0.3~1 .7 mmol/I 1 .2~3 .0 nmol/l 2.5-6.6 mmol(1 0.1-0.4 mmolfl
• Calcium is bou ... d to albuml ... a ... d it is importa ... t to make sure that you have co rrected the ca lcillm w he ... t he albumi ... is abnormal. He ... ce : Corre<:ted ca lcium _ [(40 gIl- albllmi ... IgII)) mult iplied by 0.02] + measured calcium Immolm
M EAN CE LL VOLUME (MCV)
Adu lts 80-98 f l(c lJ )
M EAN CELL HA EMOGLOBIN (MCH)
Adults 27- 32 pg
N ormal va lues I _
MEAN CORPUSCULAR HAEMOGLOBIN CONCENTRATION (MCHC)
Adu lts 31 - 35 g/dl (g.%)
LEUKOCYTES
Adu lts 4- 10 x 109/1 Differential : Neutroph ils 2.5- 7.5 x 109/1
Lymphocytes 1.5- 3.5 x 109/1 M onocytes 0.2-0.8 x 109/1 Eos inophi ls 0.04-0 .44 x 109/1 Basoph ils 0- 0. 1 x 109/1
In Black A frica n ad u lts, total wee is 2.5- 9 x 109/1
PLATELETS
150-400 x 109(1
RETICULOCYTES
0.2-2%
PLASMA VISCOSITY
1.50-1.72 cp Paralle ls ESR but is unaffected by age, sex or anaemia
ESR (WESTERGREN)
Men - upper l imit o f normal = age in years .,. 2 Women - upper limit of norma l = (age in years + 10) .,. 2
CLOTTING T IMES
APTT 35- 45 seconds PT 10- 14 seconds INR 1
BLOOD GASES (ARTERIAL)
Oxygen 12- 15 kPa (90-l 00 mmHg)
- Normal values
Carbon d ioxide 4.5-6. 1 kPa (34- 46 mmHg) pH 7.35-7 .45 Base excess ± 2 mmol/I
URINE (ASSUMING A NORMAL DIET)
Specific gravity 1.008-1.030 pH 4.8-7.5 Protein tess t han 0.3 g/I Osmolality 350-1000 mosmol/kg
CSF
Glucose, two-th irds of blood glucose value Protein, up to 0.4 g/I Lymph ocytes, up to 4 cells/lJ l (i.e. 4 cells/m m3) Open ing pressure less than 210 mm of CSF
Index
Abdominal pa in, 64 Abnorm a l red ce lls, 15 Ac id base ba lance. 134 Acne form rash, 157 Ac romegaly. 11 3 AIDS
<.lcfinitio n, 159 gastro· in tcstina l.67 neuro logica l. 105 sk in, 160
Addison's disease, 121 AurJ" ulocytos is, 79 A lkalosis. 135 Alopec ia, 151 A"aemia , 75, 76, 77 Allatomica l dead space, 42 Ang ina, 29 I\n kvlnsing s pond 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" hylhmia
";' uses, 17 d,nlCal dia9nos is . 17 [CG.35
A' icria l pulse. 14 A,lhfulhl thy, 141 A,lInilis. fli tt ing. 144 A·.d l"s. 67 1\·. lhma. 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 mun" d isease.
"'!I~n -spec i t i c. 116 1\ " ., "e vi~ t i un. 33
II ." b ehe. 143 11,.I'~c t's syndrome. 158 Ihl" plyments. 73 " ".I""cns pulse. 15 111. .. 1.1", dysfunction. 139
BIe .. d ing, 84-$ Clinical fea tur .. s, B6 gUlro-inleStinal. 6. scr .... " ing lests, 86
Blindness. sudden. 96 Blis ter ing eruptions. 150 Blood-gas a nulysis, .3 Bloon gas . nor ma l va lues , 163 Blood t ra nsfusion. 87 a radycll rd ia .16 Brealh sounds. 54 Bro nchia l cance r, 51 BronchilK:tlls is. 50 Bronchit is. 44
Bulba r palsy. 101 Bundle-bra r.c h block. 36
Calcu li, ' ''" III. 138 Candidiasis, predisposing
condilions, 159 Carcinoma 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 Cerebral infarclioll, 101 Cere bra l-spina l pressure. 96, 164 Chest leads. 34 CheSI moveme nt . 54 Chest pa in. 29 Ches t x-ray. 55 Cheyne- Stokes brea thing. 44 Choles las is. 73 Ciga r .. tt .. smoking. 45 Ci rrhosis
ca ulie6. 71 clin ical fa atu res. 72 defin ition. 1 1
Clin ical "~lIm i nat ion. 3 Clu bbing, 46
-
II1II IL'_n_de_X ______________________________________ ~
COAD.45 Coagu lation
delects, 84 disseminated intravascular, 85 f actors, 84
Coarction of aorta. 62 Coe liac synd rome, 67 Colitis, ulce rat ive, 69 Collapse of lung
causes, 49 radiograp h, 56 signs, 54
Collapsing pulse. 14 Coma, 102 Compliance, 43 COrlgenit a l heart disease, 25 COr>junctiv itis, 158 COflso lidation
rad iograph, 55 s ig ns, 54
Cor pu lmona le, 28, 40 Cord compression. 108 Cortica l loca li .at ion, 99 Cran ia l n e ,ves, 91 Crohn's disease, 70 Cushing 's syndrom e, 119 Cyanosis, 13
Dark ur ine, 137 Dead space, 42 Deafness. 97 Dement ia. 104 Derm atomes, 109 Dexamet hasone supp ression, 120 Diabetes mell itus, 122 Diabet ic com a. 122 Diabetic retinopat hy, 94 Diffuse a irways obstruction, 45 Diffusion defects. 42 Digita lis, 39 Disseminated coagulat ion, 85 Disseminated sclerosis, 98 Diverticulitis, 68 Drug erupt ions, 157 Duodenal ulcer, 65 Dysarthria, 100 Dy sphagia, 63 Dysphasia, 100 Dysphonia, 100 Dyspnoea, 44
Ectopic ven tricular bea ts, 17 Eczema, 149 Effusiorl
per icardia l, 62
p leural, 54, 57 Electrocard iogram IECG )
arrhythmias, 35 COr pulmonale, 40 d igita lis e ffects, 39 heart b lock, 36 hyperkalaemia, 39 hypokalaemia, 39 mi tra l stenos is, 23 myocardial ischaemia, 38, 39 norm al,33 pericardit is, 40 pulmonary embolism , 40 reading, 40 verltricu lar hypertrophy, 37, 38
Em physema dcfin ition,44 rad iograph, 58 signs, 54
Em pyema, 48 Eos inophi lia, 80 Epilepsy, 103, 104 Erythem a, 153 Erythema mu ltiforme, 154 Erythema nodosum, 154 Erythoderma, 154 Essay questions, 2 Examinat ion, 6, 20 Epiratory f low rate, 42 E><t radura l haematom a, 102 Ext rasysto les, 16, 17 Exudate, p leura l, 49
Fac ial flushing, 153 Facia l pa lsy, 97 Fa llors tetralogy, 25 Fanconi syndrome, 134 FEV, 41 Fibros is of lung, 54 'F litting' arthrit is, 144 Flushing, 153 Flutter, 17, 36 Folate def iciency, 78 Forced v ita l capacity, 41
Ga its, 106 Ga lactorrhoea, 125 Ga llstones, 74 Ga llop rhythm, 20 Gastr ic cancer, 65 Gastr ic ulcer, 65 Gastro-intest inal b leeding, 64 Glom erulonephr it is, 132 Gloss it is, 63 Glucocort ico ids, 120
.. ~ ________________________ 'nd.~x l ..
Goitre, 116 Graves' disease, 11 6, 11 7 Gynaecomast ia, 124
Haematology, normal va lues, 162 Haem atoma
e><tradural, 102 subdural. 102
Haematuria, 136 Haomophi lia, 84 Haemolysis, 77 Haemoptysis, 46 Hard knobbly liver, 71 Hoart b lock
causes, 17 classi f ica tion, 17, 37 ECG,36
Heart fail ure, 26 Hea<1 sounds, 18, 19 Hepat ic fa ilure, 72 Hepatitis, 73 Hopatom e9aly, 70 Hepato·sp lenomega ly,71 Hirsutism, 151 History-taking, 4 HIV in fect io n, 159 Hodgkin 's disease, 82 Horner's sy ndrome, 95 Hot jo int. 144 Hydropneumothorax, 57 Hypercalcaemia, 127 Hyperdynamic circu lat ion, 15 Hypereosinophil ia, 80 Hypcrka laem ia,39 Hyperlip idaemia, 155 Hyperparathyro idism, 118 Hyperp igm entat ion, 152 Hype<1ension
portal, 72 radio logy of, 61 system ic. 28
Hypertensive ret inopathy, 94 Hyperthyroidism, 116 Hyperur icaem ia, 145 Hypoadrenalism, 121 Hypoc~lcaem i a, 127 Hypog lycaem ic coma, 122 Hypokalaemia,39 Hyponatraemia, 135 Hypopa rathyroid ism, 118 Hypopituitarism, 114 Hypothyroidism, 115 Hypoventi lation, 43 Hypoxaem ia,43 Hypox ia, 43
Ileit is, 70 Ileus, 58 Infa rction
cerebral, 101 myocard ial, 29, 38
Innocent murmurs, 22 Int erstitia l lung disease, 50 Intestinal obstruct ion, 68 Intracran ia l neoplasms, 98 Intracranial pressure
causes, 96 cl inical featu res, 99
Intravascu lar coagulat ion, 85 Involuntary movements, 107 Itch,152
Jaundice, 72 Jugular venous pu lse, 13
Ketoacidaem ic com a, 122 Kidrley, large, 133 Kussm aul 's sign, 14 Kussmaul's breath ing, 44
l eg ulcer, 150 l eukaemias, 83 l eukocytos is, 79 l eukoderma, 153 l eukopenia, 79 l iver, enlarged, 70 lobar pneumonia, 48 Loca l ization, neurologica l, 99 ' l ong' case, 3-9 l umbar backache, 143 lung compl iance, 43 Lung disease, signs, 54 l ung opacity, 58 lUrl9 vol umes, 41 Lymphaderlopathy
causes, 82 h ilar,60 persistent genera li zed, 159
lymphocytic leukaemia, 83
Macrocyt ic anaemia, 69, 77 Major case, 3-9 Malabsorpti on, 66 Mal ignancy, skin changes, 156 Malignant melanom a, 155 Med iastinal shi ft, 54 M icrocytic anaemia, 76 M ictu rition, 139 M inor cases, 9-10 M inut e ventilat ion, 4 1 Mitral incompetence, 23
_ '---I'n_do' ________ --'
j
I I
Mitral stenosis. 22. 61 Mo bill block, 37 Mole, 155 Molor neurone lesions, 9 1 Motor system. 90 M outh ulcers, 158 Mull iple-choice questions, 2 MuUiple sclerosis. 98 Murmurs
auscultation o f. 20 differen tial diagnosis. 21 innocent, 22
Myelo id leukaemia. 83 Myelomatosis, 83 M yocard ial in farct ion
compl ications, 29 elec trocard iogram, 38
Myocard ial ischaemia, 29 Myopathy. 112 Myotomes. log
Nails in skin disease, 157 in systemic d isease, ISS
Necro l iling vllscull'is. 145 Neoplasm
bronchial. 51 gastric. 65 intracranial. 98
Nephrolic syndrome, 133 Neuritis, optic. 94 Neuropathy. 111 Neutropenia, 79 Neutroph ilia, 79 No rmal values, 161- 164
Obstruct ion of intestine. 68 Obstructive ai rways d isease, 45 Oculomo tor palsy. 95 Oedema, pulmonary, SO, 57 Opacity in lung, sa Opport unis tic in fections, 160 Opt ic a trophy, 94
neuriti s, 94 pa th way, 92
Oral con traceptives, 126 Oral exam ination I'vivlI'). 10 Organ-spedfic a uto im m une
d isease, 116 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 Paraple9ia, 110 Parathyroids, 118 Parkinsonism, loti Paroxysmal t achyca rdia, 17 Peak flow, 42 Pept ic u lcer, 65 Pe rcussion, 54 Per icardia l eff(lsion, 62 Pe ricard it is , 3D, 40 Pe riphe ra l neu ropathy, 111 Pernicious a naemia, 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
ca uses, 49 radiograph, 55 signs, 54
Pne umonia, 47 Pneumococcal pneumo nia, 48 Pneumothorax, 57 Polya rte ritis nodosa, 146 Polyarthropathy, 141 Po lycythaemia , 80 Po lyneuropathy, 111 Po lyu ria, 135 Porphyria, 159 Portal hypertension, 72 Potassium depletio n, 135 Pre m at ure beats, 16, 17 Proteinur ia, 136 Pr ur itus, 152 Pseudo-bulba r pa lsy, 108 Psori asis, 149 Ptosis , 96 Pu lmonary collapse, 49, 5 4, 56 Pu lmonary embolis m, 40 Pu lmonary eosinophili a , 80 Pulmonary oede ma
causes, 50
'----_ ___ _ _ _ ___ 'nd_o, 1 _
Pulmonary oedema Conr'd rad iograph, 57
Pulmonary TB, 52 Pulse
arterial,1 4 irre9ula r, 17 venous, 13
Pulsus paradoxus, 15 Pyoderma gangrerlOSum, 155 Pyuria, 137
Radiology cardiac shadow, 60 coarcta tio n, 62 co ll apse, 56 emphysem a, 58 h il a r lymphadeno pathy, 60 hydropneum othorax, 57 hype rte ns ion, 61 m il iary dens it ies, 59 mit ral stenosis , 62 mu lt iple shadows, 59 perica rd ia l effus ion, 62 p leu ra l effus ion, 55, 57 pulmona ry oedema, 57 single shado w, 58 who le lung opacity, 55
Rash circumscribed , 153 widesp read, 154
H"ynaud 's phenomenon, 147 RBC abnorm alities, 75 nellexes,110 Reg iona l ileitis, 70 Rei ter's d isease , 158 Renal
clearance, 140 disease, prese nta tio n, 129 en largement, 133 fa il ure, 129, 130 stones, 138 tubular dysfunct ion, 133
Residual volume, 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 lesions , 109 Rotation of heart , 34
Silrco idosis, 53 Scaly rashes, 153, 15( Sensory system, 89 Seronegative spondyloarthr itis, 1 (J
S hadow single large, sa mult iple, 59 w idespread, 59
Shock. 30 'Short' cases, 9-10 S inus 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 Spleno m egaly, 81 SpondyloaMhr it is , 142 Squints, 95 S tandard leads, 33 Sta tur e, short, 123 'Ster ile ' pyuria, 137 Sterokl th erapy, ha2a rds of, 120 Stevens-Johnson syndrome, 158 S to nes, re nal, 138, 139 S ubaraChno id haemorrhage, 10 1 S ubdurul haematoma, 102 Supraventricul a r tnc hycard ia, 15, 35 Syncope, 103 Svringobulbia, 107 Syringomyelia, 107 Svswm review, 6 Systemic IUPU8 erythematosus. 146
TachYClirdia, 15, 16, 17, 35 Terget celiS, 76 Thr ills, 18 Thrombocytopenia, 8( Thrombolytic therapy, 3 1 ThrombosiS,
cerebral, 101 veno us. 87
Thyroid carc inoma, 116 Thyroto~icosis, 116, 117 Transfer lac tor, 42 Tra nsudate, pleural, 49 Triciisp id incompetence, 25 Triple rhyth m, 20 Tuberculos is , 52, 53 Tub ular ac idosis, 134 Tubu lar dys funct io n, 133
Ulcer leg, 150 mouth,l58 pept ic, 65
Ulcerat ive colitis , 69
_ ] lndeX L-__________________________ ~
I
l
Uraemia. 130. 131 Urine, dark, 137 Urina ry ca lculi, 138 Urinary Iract obstruction, 137
Vascu litis, 145 Venou.
pulse, 13 thrombosis, 87 ulcer. 150
Ventr icular ectopies, 17 fai lure, 26, 27 fibrillation. 37 h ypertro phy. 27, 37, 38
strain, 38 tachycard ia , 35
Vesse l defects, 85 Viral hepatitis. 7J Vi ral pneumonia, 41 Visu a l lield d e fects, 92, 93 Vital capacity, 4 1 Vitamin Bll deficiency. 78 'Viva' examination, 10
Weber's test, 98 Wenkcbach phenomenon, 37 White skin patches. 10
Xa nt homa , 15 5