Rapid Review of Clinical Medicine for MRCP Part 2 (2nd Ed.) teksmedik.com.pdf

8/20/2019 Rapid Review of Clinical Medicine for MRCP Part 2 (2nd Ed.) teksmedik.com.pdf

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Rapid Review of

ClinicalMedicinefor MRCP Part 2

Second Edition

Sanjay SharmaBSc (Hons) MD FRCP (UK) FESC

Professor of Clinical Cardiology Consultant Cardiologist and Physician

St George’s University of London

St George’s Hospital NHS TrustUniversity Hospital Lewisham

London, UK

Rashmi KaushalBSc (Hons) FRCP (UK)

Consultant Physician and Endocrinologist

West Middlesex Hospital

Kingston, UK

MANSONPUBLISHING


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Fourth impression 2010Third impression 2009Second impression 2007

Copyright © 2006 Manson Publishing Ltd

ISBN: 978-1-84076-070-5

All rights reserved. No part of this publication may be reproduced, stored in a retrievalsystem, or transmitted in any form or by any means without the written permission of the copyright holder or in accordance with the provisions of the Copyright Act 1956(as amended), or under the terms of any licence permitting limited copying issued by the Copyright Licensing Agency, 33–34 Alfred Place, London WC1E 7DP.

Any person who does any unauthorized act in relation to this publication may be liableto criminal prosecution and civil claims for damages.

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For full details of all Manson Publishing titles, please write to:Manson Publishing Ltd73 Corringham RoadLondon NW11 7DL, UK Tel: +44 (0)20 8905 5150Fax: +44 (0)20 8201 9233 Website: www.mansonpublishing.com

Printed in Spain

DedicationFor Ravi, Ashna, Anushka, Ishan, Shivani and Milan

Dr L Wilkinson, Ms S Gowrinath, Ms H Derry, Mr P Radomskij, Dr J Waktare, Ms A O’Donoghue, Dr S Rosen,Dr A Mehta, Dr L Shapiro, Professor M E Hodson, Dr G Rai, Dr A Ghuran, Professor C Oakley, Ms F Goulder,Dr J Axford, Dr S Jain, Dr M Stodell, Dr B Harold, Dr D Seigler, Dr C Travill, Dr G Barrison, Dr D Hackett,Dr J Bayliss, Dr R Lancaster, Dr R Foale, Dr W Davies, Professor D Sheridan, Professor W McKenna,Professor G MacGregor, Dr A Belli, Dr Adams, Dr J Joseph, Dr M Impallomeni, Dr D Banerjee, Dr N Essex,Dr S Nussey, Dr S Hyer, Dr A Rodin, Dr M Prentice, Dr N Mir, Mrs K Patel and Dr J Jacomb-Hood.

We are also grateful for the assistance of the Audiovisual Departments at Luton and Dunstable Hospital, St Mary’s(Paddington) Hospital and St George’s Hospital Medical School and the ECG, Echocardiography and Radiology Department at St George’s Hospital Medical School and University Hospital Lewisham.

Acknowledgements We are grateful for the help of several colleagues who helped provide slides for the book:

http://www.mansonpublishing.com/http://www.mansonpublishing.com/


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Contents

Acknowledgements 2

Preface 3Classification of Cases 4

Abbreviations 5

Clinical Cases 7

Data Interpretations Tutorials 415

Calcium Biochemistry 415

Genetics 415

Audiograms 416

Guidelines for the Interpretation of Cardiac Catheter Data 418Respiratory Function Tests 419

Interpretation of Respiratory Flow Loop Curves 420

Echocardiography 421

Acid–base Disturbance 426

Normal Ranges 427

Index 429

3

Passing specialist examinations in internal medicine is adifficult milestone for many doctors, but is a mandatory requirement for career progression. Pass rates in theseexaminations are generally low due to ‘high standards’and ‘stiff competition’. Thorough preparation is essentialand requires a broad knowledge of internal medicine.The pressures of a busy clinical job and nights ‘on call’make it almost impossible for doctors to wade throughheaps of large text books to acquire all the knowledgethat is required to pass the examinations.

The aim of this book is to provide the busy doctor witha comprehensive review of questions featured mostfrequently in the MRCP (II) examination in internalmedicine. The MRCP (II) examination has a best of 5/nfrom many answer format. The vast majority of thequestions in the book follow the same pattern; however, we have chosen to include several scenarios with openended questions to stimulate the medical thought process.The level of difficulty of each question is of the samestandard as MRCP (II) examination. However, some casesare deliberately more difficult for teaching purposes.

A broad range of subjects is covered in over 400questions ranging from metabolic medicine to infectiousdiseases. Precise answers and detailed discussion follow each question. Where appropriate, important differential

diagnoses, diagnostic algorithms and up-to-date medicallists are presented. Many questions comprise illustratedmaterial in the form of radiographic material, electro-cardiograms, echocardiograms, blood films, audiograms,respiratory flow loops, histological material, and slides inophthalmology, dermatology and infectious diseases.Over 200 commonly examined illustrations are included.

Tutorials are included at the end of the book to aidthe interpretation of illustrated material as well as impor-tant, and sometimes difficult, clinical data, such as respir-atory function tests, cardiac catheter data and dynamicendocrine tests.

The book will prove invaluable to all those studyingfor higher examinations in internal medicine, and to theirinstructors.

Sanjay SharmaProfessor of Clinical Cardiology

Consultant Cardiologist and PhysicianLecturer for Medibyte Intensive Courses

for the MRCP Part 2

Rashmi KaushalConsultant Physician and Endocrinologist

Preface


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Cardiology

1, 10, 11, 13, 22, 25, 32, 40, 52, 53, 54, 62, 63, 66, 68,74, 78, 80, 94, 95, 100, 121, 123, 125, 130–132, 138,144, 150, 160, 167, 178, 180, 184, 193, 197, 199, 202,203, 207, 208, 223, 226, 229, 232, 235, 237, 243, 246,259, 266, 270, 285, 287, 291, 296, 301, 305, 307, 309,318, 323, 324, 327, 331, 332, 335, 342, 350, 353, 362,368, 377, 387, 389, 391

Dermatology 116, 154, 173, 316

Endocrinology and diabetes

5, 9, 23, 39, 46, 76, 82, 89, 92, 101, 106, 107, 127,134, 146, 159, 164, 168, 173, 181, 199, 218, 220, 238,242, 254, 260, 261, 273, 281, 328, 334, 372, 373, 379,397, 401

Environmental medicine140

Gastroenterology 3, 6, 19, 24, 33, 64, 72, 75, 104, 127, 133, 143, 148,162, 169, 182, 188, 201, 231, 276, 293, 306, 338, 339,347, 367, 369, 371, 383, 393, 394, 400

Genetics47, 85, 151, 170, 194, 195, 269, 315, 361

Haematology 12, 38, 49, 69, 70, 73, 86, 87, 102, 114, 115, 117, 120,122, 142, 156, 163, 175, 191, 204, 211, 216, 219, 233,258, 263, 265, 295, 297, 299, 308, 313, 336, 346, 351,352, 358, 376, 385, 392, 394

Immunology 15, 155, 374

Infectious diseases16, 18, 26, 41, 51, 83, 88, 93, 110, 128, 142, 143, 149,152, 154, 158, 166, 176, 212, 221, 225, 234, 262, 267,277, 280, 319, 322, 325, 337, 345, 351, 383, 386, 388

Metabolic medicine

9, 29, 34, 38, 50, 71, 74, 81, 82, 84, 90, 129, 134, 136,147, 153, 161, 179, 189, 214, 215, 230, 248, 257, 271,275, 283, 310, 321, 326, 329, 333, 334, 398

Nephrology 4, 17, 24, 29, 44, 53, 59, 60, 85, 92, 118, 119, 126, 135,137, 141, 152, 185, 198, 228, 244, 245, 249, 250, 251,278, 289, 294, 303, 304, 317, 328, 344, 354, 381, 382

Neurology 30, 65, 67, 93, 98, 103, 105, 108, 112, 128, 139, 145,190, 192, 200, 239–241, 247, 253, 255, 256, 268, 274,

288, 290, 292, 307, 314, 330, 345, 365, 390, 395, 399

Obstetric medicine130–132, 190, 193, 348

Oncology 117, 216, 258, 358, 359

Ophthalmology 282, 345

Radiology

2, 18, 64, 88, 97, 99, 124, 183, 187, 222, 227, 252,280, 300, 302, 311, 343, 349, 355, 357, 360, 363

Respiratory medicine8, 14, 21, 35, 36, 37, 43, 45, 55, 56, 58, 61, 72, 79, 91,99, 111, 113, 157, 164, 196, 217, 225, 272, 279, 298,304, 327, 341, 349, 356, 370, 380, 384, 396

Rheumatology 4, 15, 17, 31, 42, 71, 77, 87, 96, 109, 141, 171, 174,177, 196, 198, 200, 210, 236, 264, 320, 324, 340, 364,375, 401, 402

Therapeutics/toxicology 7, 8, 20, 27, 28, 36, 48, 57, 68, 77, 116, 118, 119, 165,172, 175, 186, 205, 206, 209, 213, 224, 251, 284, 286,312, 316, 317, 332, 339, 366, 378

4

Classification of Cases


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5

5-HIAA 5'-hydroxyindole aceticacid

AIIRB angiotensin II receptorblocker

AAFB acid–alcohol fast bacilli ACE angiotensin-converting

enzyme ACTH adrenocorticotrophic

hormone ADH antidiuretic hormone AF atrial fibrillation AIDS acquired immune-

deficiency syndrome AIN acute interstitial nephritis AIP acute intermittent

porphyria ALA aminolaevulinic acid ALT alanine transaminase

(SGPT) AML acute myeloid leukaemia AMP adenosine 5'-

monophosphate ANA antinuclear antibody ANCA antineutrophil cytoplasmic

antibodies ANF antinuclear factor APCKD adult polycystic kidney

disease APTT activated partial

thromboplastin time AR aortic regurgitation ARDS adult respiratory distress

syndrome ARVC arrhythmogenic right

ventricular cardiomyopathy AS aortic stenosis ASD atrial septal defect ASO antistreptolysin AST aspartate transaminase

(SGOT) ATN acute tubular necrosis AZT zidovudineBCG bacille Calmette–GuérinBIH benign intracranial

hypertensionBP blood pressureBT bleeding timeBTS British Thoracic Society CAH chronic active hepatitisCAP community acquired

pneumoniaCCF congestive cardiac failureCFTR cystic fibrosis

transmembrane regulator(protein)

CML chronic myeloid leukaemiaCMV cytomegalovirusCOPD chronic obstructive

pulmonary diseaseCPAP continuous positive airway

pressureCREST calcinosis, Raynaud’s

syndrome, oesophagealproblems, scleroderma,telangiectasia

CRF chronic renal failureCRP C-reactive proteinCSF cerebrospinal fluidCSS Churg–Strauss syndromeCT computed tomography CVA cerebrovascular accidentCVP central venous pressureCXR chest X-ray DBP diastolic blood pressureDC direct currentDHCC dihydroxy-cholecalciferolDIC disseminated intravascular

coagulationDIDMOAD diabetes insipidus,

diabetes mellitus, opticatrophy and deafness

DM diabetes mellitusDT delerium tremensDVT deep-vein thrombosisEAA extrinsic allergic alveolitisEBV Epstein–Barr virusECG electrocardiogramEEG electroencephalogramELISA enzyme-linked

immunosorbent assay EMF endomyocardial fibrosisEMG electromyogramENT ear, nose and throatEPO erythropoietinERCP endoscopic retrograde

cholangiopancreatogramESR erythrocyte sedimentation

rateFBC full blood countFDP fibrinogen degradation

productFES fat embolism syndromeFEV1 fixed expiration volume in

1 secondFFP fresh-frozen plasmaFNA fine-needle aspirationFSH follicle stimulating

hormoneFTA fluorescent treponemal

antibody

FVC forced vital capacity GBM glomerular basement

membraneGCT giant cell tumourGFR glomerular filtration rateGH growth hormoneGHRH growth hormone releasing

hormoneGI gastrointestinalGP general practitionerGPI glucophosphatidylinositolGT glutamyltransferaseGTN glyceryl trinitrateHb haemoglobinHbSS sickle cell anaemiaHC Hereditary Copro

porphyriaHCC hydroxy-cholecalciferolHCM hypertrophic

cardiomyopathy HCV hepatitis C virusHCG human chorionic

gonadotrophinHELLP haemolysis, elevated liver

enzymes and low plateletsHHT hereditary haemorrhagic

telangiectasiaHIT heparin-induced

thrombocytopeniaHIV human immunodeficiency

virusHONK hypersimilar non-ketotic

diabetic comaHR heart rateHRT hormone replacement

therapy HS hereditary spherocytosisHSMN hereditary sensorimotor

neuropathy HUS haemolytic uraemic

syndromeICD implantable cardioverter

defibrillatorICP intracranial pressureINR International Normalized

RatioIPF idiopathic pulmonary

fibrosisIVP intravenous pyelogramIVU intravenous urogramJVP jugular venous pressureKCO corrected carbon monoxide

transfer factorLBBB left bundle branch block LDH lactate dehydrogenase

Abbreviations


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6

LFT liver function testsLH luteinizing hormoneLHON Leber’s hereditary optic

neuropathy LHRH luteinizing hormone

releasing hormoneLMWH low-molecular weight

heparinLQTS long QT-syndromeLVEDP left ventricular end-diastolic

pressureLVH left ventricular hypertrophy MAHA microangiopathic

haemolytic anaemiaMAOI monoamine oxidase

inhibitorMCH mean cell haemoglobinMCHC mean cell haemoglobin

contentMCV mean cell volumeMELAS mitochondrial

encephalopathy, lacticacidosis, stroke-likesyndrome

MEN multiple endocrineneoplasia

MERRF myoclonic epilepsy and redragged fibres

MGUS monoclonal gammopathy of undeterminedsignificance

MPO myeloperoxidaseMR mitral regurgitationMRA magnetic resonance

angiography MRCP magnetic resonance

cholangiopancreatogramMRI magnetic resonance

imagingMRSA methicillin resistant

Staphylococcus aureus MRV magnetic resonance

venography MSH melanocyte stimulating

hormoneNADPH nicotinamide adenine

dinucleotide phosphate(reduced)

NAPQI N-acetyl-p-benzoquinoneimine

NARP neuropathy, ataxia, retinitispigmentosa

NASH non-alcoholicsteatohepatitis

NIPPV non-invasive positivepressure ventilation

NSAID non-steroidal anti-inflammatory drug

NSTEMInon-ST elevationmyocardial infarction

NYHA New York Heart Association

OSA obstructive sleep apnoeaPAN polyarteritis nodosaPAS periodic acid-Schiff PBC primary biliary cirrhosisPBG porphobilinogenPCOS polycystic ovary syndromePCR polymerase chain reactionPCT porphyria cutanea tardaPCV packed cell volumePCWP pulmonary capillary wedge

pressurePE pulmonary embolismPEFR peak expiratory flow ratePFO patent foramen ovalePKD polycystic kidney diseasePMLE progressive multifocal

leucoencephalopathy PMR polymyalgia rheumaticaPNH paroxysmal nocturnal

haemoglobinuriaPRL prolactinPRV polycythaemia rubra veraPSC primary sclerosing

cholangitisPT prothrombin timePTH parathormone or

parathyroid hormonePVE prosthetic valve

endocarditisRA rheumatoid arthritisRBBB right bundle branch block REM rapid eye movementRMAT rapid macroagglutination

testRTA renal tubular acidosisRV residual volumeSADS sudden adult death

syndromeSAM systolic anterior motion of

the mitral valveSAP serum amyloid proteinSIADH syndrome of inappropriate

antidiuretic hormoneSLE systemic lupus

erythematosusSMA smooth muscle antibody SPECT single photon emission

computed tomography SROS Steele–Richardson–

Olszewski syndromeSTEMI ST elevation myocardial

infarctionSVT supraventricular tachycardiaTB tuberculosis

TCAD tricyclic antidepressantoverdose

TIA transient ischaemic attack TIBC total iron-binding capacity TIPSS transjugular intrahepatic

portosystemic shuntTLC total lung capacity TLCO total lung carbon

monoxide transfer factorTOE transoesophageal

echocardiography TPA tissue plasminogen

activatorTPHA treponema pallidum

haemagglutination testTRH thyrotrophin releasing

hormoneTSAT transferrin saturationTSH thyroid stimulating

hormoneTT thrombin timeTTP thrombotic

thrombocytopenic purpuraU&E urea and electrolytesURTI upper respiratory tract

infectionUS ultrasoundUTI urinary tract infection VDRL Venereal Diseases Research

Laboratory test VF ventricular fibrillation VIP vasointestinal polypeptide VMA vanilyl mandelic acid VP variegate porphyria VR ventricular rate VSD ventricular septal defect VT ventricular tachycardia WCC white cell count WPW Wolff–Parkinson–White

(syndrome)


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A 49-yea r-old ma le presented to the Accident andEmergency Department with a one-hour history of severecentral chest pain. He smoked 30 cigarettes per day.Physical examination was normal. The 12-lead ECGrevealed ST segment elevation in leads V1–V4. There were no contraindications to thrombolysis.

Clinical Cases 7

Question 1

What is the best treatment to improve coronary perfusion?a. IV Streptokinase.b. IV Tenectoplase.

c. IV Alteplase.d. Half-dose tenectoplase and half-dose abciximab.e. Primary coronary angioplasty.

Question 2

A 68-year-old woman presented with pain and tingling inthe left arm when she raised her hands for prolongedperiods. On examination both pulses were palpable in theupper limbs. The chest X-ray was abnormal. Aortography was performed with the arms down (2a) and with thearms up (2b).

What was the abnormality on the chest X-ray?a. Left-sided bronchogenic carcinoma.b. Left cervical rib.

c. Retrosternal thyroid.d. Notching of the ribs.e. Widened mediastinum.

A 28-year-old male presented with a six-month history of weight loss of 8 kg, generalized abdominal discomfortand diarrhoea. On examination he was pale and slim, butthere were no other significant abnormalities.

Investigations are shown.

Question 3

Hb 9 g/dl

WCC 4.6 109 /l

Platelets 200 109 /l

MCV 76 fl

ESR 38 mm/h

Sodium 141 mmol/l

Potassium 4 mmol/l

Urea 3 mmol/l

Creatinine 68 mol/l

Corrected calcium 2.02 mmol/l

phosphate 0.8 mmol/l

Alkaline phosphatase 190 iu/l

Albumin 38 g/l

IgA


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8

Answer 1

Coronary reperfusion may be achieved with thrombolyticagents (which promote fibrinolysis) or by coronary angioplasty. In the UK patients with ST elevationmyocardial infarction are conventionally treated withthrombolytic agents. Early treatment is crucial to salvagemyocardium and reduce the risk of sudden death andsevere left ventricular dysfunction. Current goals for thespeed of treating with a thrombolytic agent include adoor-to-needle time of 20 minutes or a call-to-needletime of 60 minutes.

Thrombolytic agents used commonly includestreptokinase, alteplase, tenectoplase and reteplase.Streptokinase is less favoured compared with the otherthrombolytic agents because it is less effective at restoringcoronary perfusion and is associated with slightly worseoutcomes. The GUSTO I study compared front-loadedalteplase therapy with streptokinase in patients with STEMI. Alteplase was superior to streptokinase in reducingmortality (1% absolute reduction in mortality at 30 days with alteplase) and was associated with greater coronary patency rates. In the GUSTO trial the benefit wasgreatest in patients aged under 75 years and those withanterior myocardial infarction. However, streptokinase isstill used extensively in developing countries and in many hospitals in the UK. Alteplase, tenectoplase and reteplaseappear to be equally effective. Tenectoplase and reteplaseare easier to administer (as a single bolus).

There have been trials evaluating the role of combinedhalf-dose thrombolytic therapy and half-dose plateletglycoprotein IIb/IIIa receptor blockers, e.g. tenectoplaseplus abciximab (ASSENT 3) and reteplase plus abciximab(GUSTO IV). These trials suggest that the combinationmay be associated with slightly higher coronary patency rates and fewer ischaemic events but they have notdemonstrated a mortality benefit. These trials have alsodemonstrated higher rates of intracranial bleeding in theelderly, hence combination therapy is not recommendedat present.

Although thrombolytic treatment is associated with asignificant reduction in mortality from myocardialinfarction, it does have important limitations. Firstly,greatest benefit from thrombolysis is achieved in patientstreated within 4 hours of the onset of symptoms. Even withthrombolysis normalization of blood flow is seen in only 50–60% of cases. Recurrent ischaemia occurs in 30% of cases and frank thrombotic coronary occlusion in 5–15%.Re-infarction occurs in up to 5% of cases while in hospital. Also major bleeding is recognized in 2–3% of cases. Forthese reasons several trials were set up comparing primary angioplasty with thrombolysis in STEMI.

Primary angioplasty is superior to thrombolysis. It isassociated with lower mortality and lower re-infarctionrates. The likelihood of a pre-discharge positive exercisetest is also reduced by primary angioplasty. In hospitals where facilities for primary angioplasty are available,primary angioplasty should be considered overthrombolysis. Best results occur when the door-to-balloon time is less than 2 hours.

e. Primary coronary angioplasty.

There is mechanical occlusion of the left subclavian artery on raising the left arm due to a left cervical rib. Cervical

ribs are common in the normal population and areusually asymptomatic. In rare circumstances a cervical ribmay cause pressure on the subclavian vessels and thebrachial plexus causing transient vascular insufficiency orparaesthesiae in the upper limb.

Answer 2

b. Left cervical rib.

Diarrhoea, weight loss, abdominal discomfort andisolated IgA deficiency are highly suggestive of coeliacdisease. Anti-endomyosial antibodies are highly sensitiveand specific for the diagnosis of coeliac disease. Anti-

endomyosial antibodies are IgA antibodies, thereforethey will not be detected in patients with low IgA antibody levels. Since coeliac disease is also associated with IgA deficiency it is important to be aware of serumIgA levels before interpreting anti-endomyosialantibodies in patients with malabsorption. (See Question276.)

Answer 3

c. Coeliac disease.


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Clinical Cases 9

Question 4

A 53-year-old male was admitted to hospital with a two- week history of coughing and breathlessness. Apart froma longstanding history of mild asthma he had beenrelatively well with respect to the respiratory tract. Hehad been on a skiing trip six weeks previously, withoutany respiratory problems.

He had a past history of depression, for which he took lithium five years ago, and suffered from occasionaltension headaches, for which he took simple analgesia.

On examination he appeared pale and unwell. Hisheart rate was 90 beats/min and regular. His bloodpressure measured 160/94 mmHg. The JVP was notraised. Both heart sounds were normal and the chest wasclear. Abdominal examination did not reveal any abnormality. Urinalysis demonstrated blood ++ andprotein ++.

Investigations performed in hospital are shown.

Hb 7 g/dl

WCC 11 109 /1

(neutrophils 8 109 /l,

lymphocytes 2 109 /l,eosinophils 1 109 /l)

ESR 38 mm/h

Sodium 134 mmol/l

Potassium 4.6 mmol/l

Urea 48 mmol/l

Creatinine 798 mmol /l

Renal ultrasound

Both kidneys measured 12 cm: there was no

evidence of ureteric obstruction.

Question 5

A 52-year-old male presented with impotence. He had afour-year history of insulin-dependent diabetes mellitus.There was no history of headaches or vomiting. Thepatient was a non-smoker and did not consume alcohol. Apart from insulin he took simple analgesia for jointpains.


FBC Normal

Sodium 135 mmol/l

Potassium 4 mmol/l

Urea 6 mmol/l

Creatinine 100 mmol/l

Bilirubin 12 mmol/l

AST 200 iu/l

ALT 220 iu/l

Alkaline phosphatase 128 iu/lAlbumin 8 g/l

Thyroxine 100 nmol/l

TSH 2.6 mu/l

Testosterone 7 nmol/l (NR 10–35 nmol/l)

LH 1.5 iu/l (NR 1–10 iu/l)

FSH 1 iu/l NR 1–7 iu/l)

LHRH test: 20 min: 60 min:

LH 3 iu/l 2 iu/l

FSH 2 iu/l 2 iu/l

What is the most likely diagnosis?a. Rapidly progressive glomerulonephritis.b. Analgesic nephropathy.c. Renal amyloidosis.d. Churg–Strauss syndrome.e. IgA nephritis.

What test would you perform to confirm thediagnosis?

a. MRI scan of the brain.b. Serum prolactin level.c. Serum ferritin.d. Dynamic pituitary function tests.e. Liver ultrasound.


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The clinical features and the data are consistent with thediagnosis of idiopathic haemochromatosis. The insulin-dependent diabetes mellitus suggests pancreatic

involvement, and abnormal liver function is consistent with hepatic infiltration.

The patient has a low testosterone level with aninappropriately low gonadotrophin response indicatingsecondary hypogonadism due to excessive iron depositionin the pituitary. Secondary hypogonadism is the most

The patient has a past history of asthma, eosinophilia andrapidly progressive glomerulonephritis. The most probablediagnosis is Churg–Strauss syndrome. The assumption thathe probably has rapidly progressive glomerulonephritis isbased on the fact that he was well enough to ski six weeksago, which would be highly unlikely in a patient with end-stage renal disease. The identification of normal-sizedkidneys during renal ultrasonography supports acute ratherthan chronic renal failure (Table A ).

Churg–Strauss syndrome is a small-vessel multi-system vasculitis characterized by cutaneous vasculitic lesions,eosinophilia (usually


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common endocrine deficiency in hereditary haemo-chromatosis. Primary hypogonadism due to testiculariron deposition may occur with this disorder but is muchless common than secondary hypogonadism.

In the context of the question, a serum ferritin level>500 mg/l would be diagnostic of primary haemo-chromatosis. Alcohol-related liver disease, chronic viralhepatitis, non-alcoholic steatohepatitis and porphyriacutanea tarda also cause liver disease and increased serum

ferritin concentrations even in the absence of iron overload.Hepatic iron overload in haemochromatosis is associated

with an increased risk of hepatocellular carcinoma. Patients with haemochromatosis are also at increased risk of hypothyroidism and are susceptible to certain infectionsfrom siderophoric (iron-loving) organisms such as Listeria spp., Yersinia enterocolitica and Vibrio vulnificus , which arepicked up from eating uncooked seafood.

Clinical Cases 11

A 38-year-old English male was investigated after he wasfound to have an abnormal liver function test during ahealth insurance medical check. He worked in aninformation technology firm. Apart from occasionalfatigue he was well. He consumed less than 20 units of alcohol per week. The patient had only travelled out of Europe twice and on both occasions he had been toNorth America. He took very infrequent paracetamol foraches and pains in his ankles and knees. There was nohistory of hepatitis or transfusion or blood products. Hehad been married for 5 years. Systemic enquiry revealedinfrequent episodes of loose stool for almost 4 years.

On examination he appeared well. There were nostigmata of chronic liver disease. Abdominal examinationrevealed a palpable liver edge 3 cm below the costalmargin. There were no other masses. Examination of thecentral nervous system was normal.

Investigations were as shown.

Hb 12.6 g/dlWCC 8 109 /lPlatelets 210 109 /lMCV 90 fl

Sodium 136 mmol/lPotassium 4.1 mmol/lUrea 6 mmol/lCreatinine 100 mmol/lAST 60 iu/l (NR 10–40 iu/l)ALT 78 iu/l (NR 5–30 iu/l)Alkaline phosphatase 350 iu/l (NR 25–100 iu/l)Bilirubin 22 mmol/l (NR 2–17 µmol/l)Albumin 38 g/l (NR 34–48 g/l)Total cholesterol 5.2 mmol/lTriglyceride 3.1 mmol/lBlood glucose 6 mmol/lFerritin 256 mg/l (NR 15–250 mg/l)

Serum Fe 28 mmol/l(NR 14–32 mmol/l)

TIBC 50 mmol/l(NR 40–80 mmol/l)

Serum Slightly reducedcaeruloplasmin

24-hr urine copper Slightly elevatedIgG 19 g/l (NR 7–18 g/l)IgA 4.2 g/l (NR 0.8–4.0 g/l)IgM 5.0 g/l (NR 0.4–2.5 g/l)Anti-nuclear Positive 1/32

antibodiesSmooth muscle Not detected

antibodiesAntimitochondrial Not detectedantibodies

Hep B sAg Not detectedHep C virus Not detected

antibodiesAbdominal ultrasound Normal

What is the most probable diagnosis?a. Autoimmune hepatitis.b. Primary sclerosing cholangitis.c. Primary biliary cirrhosis.d. Haemochromatosis.e. Wilson’s disease.

Question 6

Question 7

A 17-year-old girl presented with jaundice three daysafter having taken a paracetamol and alcohol overdoseduring an argument with her boyfriend.

What is the best marker of prognosis?a. Serum aspartase transaminase.b. Serum alkaline phosphatase.c. Serum bilirubin.d. Prothrombin time.e. Paracetamol level.


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This is a relatively difficult question. The history of loosestool is crucial in making the diagnosis in this particularcase in the absence of data from the ERCP. Diarrhoeaand biochemical evidence of cholestasis (alkalinephosphatase greater than transaminases) should lead tothe clinical suspicion of primary sclerosing cholangitis(PSC). The aetiology of PSC is unknown butimmunological destruction of intra- and extra-hepaticbile ducts is the main pathological feature. 90% of PSC isassociated with inflammatory bowel disease, particularly ulcerative colitis, and hence the importance of theintermittent diarrhoea. Ulcerative colitis is the mostfrequent association with primary sclerosing cholangitis. A raised alkaline phosphatase level in a patient withulcerative colitis (in the absence of bone disease) shouldraise the possibility of PSC. The frequency of PSC isinversely proportional to the severity of ulcerative colitis.Other associations of PSC include coeliac disease.

Patients with PSC may be asymptomatic at pre-sentation but can present with advanced liver disease.Fatigue and pruritus are common complaints as with theother cholestatic disorders. Approximately one-fifth of the patients also complain of right upper quadrant pain.

The diagnosis is confirmed with ERCP that showsstrictures within biliary ducts. Complications are those of chronic cholestasis, notably statorrhoea, fat-soluble vitamin malabsorption, large biliary strictures, cholangitis,cholangiocarcinoma and colonic carcinoma. There are noeffective pharmacological agents that greatly retard the

progression of the disorder. Patients are treated withcholestyramine to reduce pruritus. Fat-soluble vitaminsupplementation is necessary owing to steatorrhoea. Antibiotic prophylaxis during instrumentation of thebiliary tree is mandatory to reduce the risk of bacterialcholangitis. Ciprofloxacin is the prophylactic antibioticdrug of choice prior to ERCP. Biliary stenting may improve biochemistry and symptoms; however, thedefinitive treatment for PSC is hepatic transplantation.

Although a cholestatic picture is also recognized inprimary biliary cirrhosis, alcohol abuse and viral hepatitisthere is nothing in the history or investigations to indicatethese conditions as the cause of his illness. Primary biliary cirrhosis affects mainly females in the fifth decadeonwards. Furthermore, the absence of anti-mitochondrialantibodies is against the diagnosis. The ferritin is modestly raised but not high enough to suggest hereditary haemochromatosis. High ferritin levels are also a featureof chronic viral hepatitis, alcohol-related hepatitis andnon-alcoholic steato-hepatitis. Hypergammaglobulinaemiaand raised autoantibody titres are features of primary sclerosing cholangitis but also occur in otherimmunological liver disorders such as chronic active viralhepatitis, auto-immune hepatitis and biliary cirrhosis.

Patients with cholestasis also have lowish caerulo-plasmin levels and increased blood and urine copperlevels. The abnormal copper metabolism in this caseshould not lead to the candidate diagnosing Wilson’sdisease, since there are many features above to indicatePSC. Furthermore, patients with Wilson’s disease usually have a hepatitic biochemistry picture and often have co-existing neuro-psychiatric disease.

b. Primary sclerosing cholangitis.

Answer 6

12

Important risk markers for severe hepatic injury afterparacetamol overdose include a PT >20 seconds 24 hafter ingestion, pH 300 mol/l.(See Questions 27 and 206.)

Answer 7

d. Prothrombin time.


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A 40-year-old woman with dilated cardiomyopathy isseen in the heart failure clinic complaining of a persistentdry cough. Her exercise capacity is 1 mile while walkingon the flat. She can climb two flights of stairs withoutdifficulty. Her medication consists of ramipril 10 mgdaily, aspirin 75 mg daily, carvedilol 6.25 mg twice daily and frusemide 40 mg daily. On examination her heartrate is 70 beats/min and her blood pressure is100/60 mmHg. Both heart sounds are normal and thechest is clear.

A 16-year-old girl presented with an 18-month history of progressive breathlessness on exertion. On admission she was breathless at rest. She had a past history of acutemyeloid leukaemia, for which she had been treated withsix courses of chemotherapy, followed by bone marrow transplantation supplemented with radiotherapy andcyclophosphamide treatment five years ago. She wasregularly followed up in the haematology clinic. Lungfunction tests three years ago revealed an FEV1/FVCratio of 80%. On examination she was breathless at rest,and cyanosed. There was no evidence of clubbing. Auscultation of the lung fields revealed fine inspiratory

crackles in the mid and lower zones. Repeat lungfunction tests revealed an FEV1/FVC ratio of 86% and atransfer factor of 60% predicted.

Clinical Cases 13

Question 8

What is the cause of her symptoms?a. Previous radiotherapy.b. CMV pneumonitis.c. Pneumocystis carinii pneumonia.d. Cyclophosphamide-induced lung fibrosis.e. Severe anaemia.

A 21-year-old man was admitted to the intensive careunit after a road traffic accident during which he suffered

a severe head injury. He required ventilation.Investigations are shown.

Sodium 128 mmol/l

Potassium 3.6 mmol/lCreatinine 81 mmol/lUrea 4 mmol/l

Thyroxine 30 nmol/lTSH 2 mu/lSerum cortisol 1000 nmol/l

(NR 170–700 nmol/l)

Question 9

Question 10

How would you alter her treatment?a. Add spironolactone.b. Substitute ramipril with losartan.c. Reduce carvedilol to 3.125 mg twice daily.

d. Double the dose of furosemide.e. Add digoxin.

What is the cause of the hyponatraemia?a. Hypopituitarism.b. Addison’s disease.c. Syndrome of inappropriate ADH secretion.d. Hypothyroidism.

e. Cushing’s syndrome.


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The patient has a low sodium concentration in thecontext of a head injury. The thyroid function testssuggest the possibility of a secondary hypothyroidism, i.e.a low TSH and a low thyroxine concentration, and hencethe possibility of damage to the pituitary. However, the very high cortisol level indicates that pituitary function isprobably normal (high ACTH production secondary tostress) and therefore the abnormal thyroid function testsrepresent sick euthyroid syndrome. Low T4, T3 and TSHlevels are recognized in critically ill patients with non-thyroid illnesses. Originally such patients were thought to

be euthyroid, therefore the term sick euthyroid syndrome was used to describe these biochemical abnormalities.There is evidence now that these abnormalities representgenuine acquired transient central hypothyroidism.Treatment with thyroxine in these situations is nothelpful and may be harmful. It is thought that thesechanges in thyroid function during severe illness may beprotective by preventing excessive tissue catabolism.Thyroid function tests should be repeated after at least six weeks following recovery.

Critical illness may also reduce T4 by reducing thyroidbinding globulin levels, and T3 is rapidly reduced owingto inhibition of peripheral de-iodination of T4.

The patient presents with progressive symptomsassociated with a restrictive lung defect and a lowtransfer factor. The findings are most consistent withcyclophosphamide-induced pulmonary fibrosis.

Cyclophosphamide-induced lung fibrosis is rare and ismost likely to occur in patients who have had concomitantpulmonary radiation therapy or have taken other drugsassociated with pulmonary toxicity. The disorder usually occurs in patients who have been taking low doses forrelatively prolonged periods (over six months) andpresents several years after cessation of the drug andhence the deterioration of symptoms with time. Thedisorder has a relentless progression and inevitably resultsin terminal respiratory failure. It is minimally responsiveto corticosteroids. Fine end-inspiratory crackles andclubbing do not usually form part of the clinicalspectrum.

The diagnosis is clinical. Chest X-ray reveals reticulo-nodular shadowing of the upper zones. Lung functiontests demonstrate a restrictive lung defect. Lung biopsy isnot helpful.

Cyclophosphamide per se is not toxic to the lungs;however, it is metabolized in the liver to toxicmetabolites such as hydroxycyclophosphamide, acroleinand phosphoramide mustard, which are responsible forpulmonary damage. Genetic factors may play a role indetermining which individuals develop pulmonary fibrosis after exposure to the drug.

Cyclophosphamide therapy can also result in an acutepneumonitis during treatment with the drug that causescough, dyspnoea, hypoxia and bilateral nodular opacitiesin the upper zones of the lung. Acute cyclophosphamide-induced pneumonitis responds to cessation of the drugand corticosteroid therapy.

The differential diagnosis in this case is radiation-induced fibrosis. Radiotherapy to the pulmonary areausually causes a pneumonitis that presents with cough,dyspnoea, a restrictive lung defect and low transfer factor.It is more common in patients also taking cyclo -phosphamide or bleomycin. Unlike cyclophosphamide-induced pulmonary fibrosis the condition is notassociated with an inexorable decline. Indeed many patients show improvement in symptoms and objectivepulmonary function testing within 18 months of stopping radiotherapy.

14

Answer 8

d. Cyclophosphamide-induced lung fibrosis.

Causes of drug-induced pulmonary fibrosis

• Cyclophosphamide• Busulphan• Methysergide• Methotrexate• Amiodarone• Nitrofurantoin• Minocycline

• Ethambutol• Penicillamine

Answer 9

c. Syndrome of inappropriate ADH secretion.


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A 60-year-old male was admitted to the coronary care unit with central chest pain. Physical examination was normal.The blood pressure measured 110/68 mmHg. The 12-lead ECG was normal and the troponin T level was notraised. The blood sugar was normal. The cholesterol levelon admission was 6.3 mmol/l. The patient underwent anexercise stress test that was positive. A subsequentcoronary angiogram revealed an 80% stenosis in theproximal aspect of the left anterior descending artery that was successfully treated with a coronary artery stent.Echocardiography revealed a normal-sized left ventricle with good systolic function. The patient was dischargedhome on aspirin 75 mg daily, clopidogrel 75 mg daily andsimvastatin 40 mg daily. He had been completely pain free

after the procedure, and an exercise stress test performedfour weeks after the procedure was negative formyocardial ischaemia for 10 minutes.

The patient is in NYHA functional class II with respect toher symptoms. She is on the correct dose of ramipril andis appropriately being treated with a beta-blocker. Thedry cough that the patient is experiencing is almostcertainly the side-effect of ramipril. Angiotensin-converting enzyme inhibitors are associated with a dry cough in 15–20% of patients owing to increases incirculating bradykinin levels. In such patients the ACEinhibitor should be stopped and substituted with anangiotensin receptor blocker such as losartan. Theefficacy of losartan compared with an ACE inhibitor(captopril) was fully evaluated in the ELITE II study.

The study revealed similar mortality rates and similarrates of progression of heart failure when comparingpatients on losartan 50 mg daily with those prescribedcaptopril 50 mg three times daily. The study suggeststhat losartan is as effective as ACE inhibitors in themanagement of heart failure. However, the use of losartan in heart failure is still currently reserved forpatients who develop side-effects to ACE inhibitors. A recent study evaluating the role of angiotensin receptorblockers (CHARM study; evaluated candesartan) inpatients with heart failure showed reduced hospitalizationrates and mortality in heart failure patients who were oncandesartan instead of an ACE inhibitor, or candesartanas additional therapy to an ACE inhibitor.

Clinical Cases 15

Answer 10

b. Substitute ramipril with losartan.

Question 11

What other medication should the patient receive toimprove his cardiovascular prognosis?

a. Atenolol.b. Ramipril.c. Candesartan.d. No further treatment required.e. Isosorbide dinitrate.

A 62-year-old obese male with a known medical history of hypertension presented with generalized headachesand lethargy. He was taking bendroflumethiazide,2.5 mg once daily for hypertension. The only other pastmedical history included a left-sided deep veinthrombosis six months previously. There was no history of alcohol abuse or smoking.

On examination he was obese. His chest was clear andexamination of the abdomen did not reveal any abnormality.


Hb 20 g/dlMCV 88 flWCC 15 109 /lPlatelets 500 109 /lPCV 0.66 l/lSodium 141 mmol/lPotassium 4.2 mmol/lUrea 8 mmol/lCreatinine 110 mol/lUrate 0.44 mmol/l

What is the cause of his symptoms?a. Obstructive sleep apnoea.b. Gaissbock’s syndrome.

c. Polycythaemia rubra vera.d. Renal cell carcinoma.e. Chronic hypoxaemia.

Question 12


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The Heart Outcomes Prevention Evaluation Study (HOPE) evaluated the role of angiotensin-convertingenzyme inhibitors (ramipril) in populations at high risk of cardiovascular events without any evidence of left ventricular dysfunction. The study assessed 9297 high-risk patients, defined as (1) aged >55 years; (2) history of coronary artery disease, stroke or peripheral vasculardisease; or (3) diabetes mellitus and at least one risk factor for coronary artery disease including hypertension,increased total cholesterol, smoking and micro-albuminuria. The patients were randomized to ramipril10 mg daily or placebo. The primary outcome was acombined endpoint of myocardial infarction, stroke orcardiovascular death. The mean follow up was five years.

Patients treated with ramipril had a 14% event rate of the combined morbidity and mortality endpoint whereasplacebo-treated patients had a 17.8% event rate. The 21%decrease in events was seen in all pre-specified groups,indicating that ACE inhibitor therapy with ramiprilsignificantly reduces morbidity and mortality in a high-

risk population with normal left ventricular function.Based on this study all patients with coronary artery disease, cerebrovascular disease, peripheral vasculardisease and diabetes mellitus plus one other risk factor forcoronary artery disease should be prescribed an ACEinhibitor, specifically ramipril.

The patient should remain on aspirin for life and takeclopidogrel for a year following deployment of a stent.The CURE study showed that aspirin and clopidogreltogether were associated with a lower incidence of myocardial infarction and death in patients with unstableangina and non-ST elevation myocardial infarctioncompared with aspirin alone for up to a year.

The patient no longer has subjective or objectiveevidence of myocardial ischaemia, and in the absence of hypertension or left ventricular dysfunction there is noindication for a beta-blocker.

Nitrates do not alter prognosis in coronary artery disease. There is no evidence as yet that angiotensinreceptor blockers improve cardiovascular prognosis inpatients with coronary artery disease in the absence of hypertension or left ventricular dysfunction.

16

Answer 11

b. Ramipril.

The high Hb is suggestive of polycythaemia. There isnothing in the history to indicate a secondary cause, e.g.hypoxia, renal carcinoma, adrenal tumour. Although he was obese, there was nothing else in the history to allow the diagnosis of obstructive sleep apnoea.

The high white cell count and platelet count favourprimary polycythaemia (polycythaemia rubra vera).Headache and lethargy are common symptoms of polycythaemia rubra vera. Polycythaemia rubra veracauses lethargy due to hyperviscosity and raisedinterleukin-6 levels. Other classic features include visualdisturbance, abdominal pain and pruritus.

Many patients with polycythaemia rubra vera havesplenomegaly; however, a palpable spleen is absent inapproximately one third of patients.

Answer 12

c. Polycythaemia rubra vera.

Criteria for the diagnosis of polycythaemia rubra vera

Raised red cell mass and normal pO2 with eithersplenomegaly or two of the following:• WCC >12 109/l• Platelets >400 109/l• Raised B12 binding protein• Low neutrophil alkaline phosphatase

concentration

(See Questions 39, 73 and 211.)


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An 18-year-old male was admitted with sudden sharppain in the left infrascapular area. He was not breathlesson mild exertion. He was usually fit and well. He was anoccasional smoker. There was no history of respiratory problems. On examination there was reduced air entry atthe left lung base. The oxygen saturation on air was 96%.The CXR revealed a left-sided pneumothorax. There wasless than 2 cm rim of air between the edge of the lungand the ribs.

Clinical Cases 17

Question 14

What is the management?a. Admit and observe for 24 hours.b. Attempt aspiration of pneumothorax.c. Prescribe 100% oxygen for a few hours.

d. Insert chest drain.e. Allow home and repeat CXR after a week.

The ECG below was taken from a young boy whoexperienced syncope. On examination he had a systolicmurmur.

Question 13

What is the most probable underlying diagnosis?a. Coarctation of the aorta.b. Dextrocardia.

c. Pulmonary stenosis.d. Wolff–Parkinson–White syndrome.e. Hypertrophic cardiomyopathy.

13


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18

The question tests knowledge of the guidelines for themanagement of pneumothorax set by the BritishThoracic Society.

The patient has a relatively small pneumothorax(2 cm rim of airbetween the lung and the chest wall on the CXR, or haspain or dyspnoea at rest or on minimal exertion thenaspiration is recommended. If aspiration is successful thepatient is allowed home and reviewed with repeat CXR inone week. If aspiration is unsuccessful a second attempt ismade at aspiration. If the lung still remains deflated theninsertion of a chest drain is recommended.

In patients with chronic lung disease the followingcriteria should be used to decide whether aspiration orinsertion of a chest drain is the first procedure of choice.Patients aged 50 years, with symptoms and with largerpneumothoraces (>2 cm air between lung and chest wall)a chest drain is necessary.

Answer 14

e. Allow home and repeat CXR after a week.

The patient has a systolic murmur. The ECG showsright axis deviation, a dominant R wave in V1 andrelatively prominent S waves in V5 and V6. The sum of the R in V1 and in V6 is > 1.25 mV which indicates right

ventricular hypertrophy. The answer that would fit withall the information is pulmonary stenosis. Coarctation of the aorta and hypertophic cardiomyopathy are associated with left ventricular hypertrophy. The absence of a shortPR interval and delta waves are against the diagnosis of WPW syndrome.

Answer 13

c. Pulmonary stenosis.

Spontaneouspneumothorax

< 2cm rim of air on CXR Minimal symptoms

Yes No

Allow homeRepeat CXR in

7–10 days

Aspirate

SuccessfulIf unsuccessful,

repeat aspiration.If still unsuccessful,insert chest drain

Management of pneumothorax


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Clinical Cases 19

A 44-year-old was seen in the rheumatology clinic inDecember complaining of malaise, joint pains andtingling in the hands and feet. She had been diagnosed ashaving Raynaud’s phenomenon several years ago. Thepatient had consulted several doctors for intermittentmalaise and joint pains. There was no history of nightsweats, dyspnoea, or problems with swallowing. Thepatient took paracetamol on a PRN basis for joint pains.

On examination she had palpable purpura on thethighs and arms. There was no obvious evidence of jointswelling. Abdominal examination revealed hepatomegaly palpable 3 cm below the costal margin. Neurologicalexamination revealed decreased sensation in the handsand feet. The blood pressure was 110/80 mmHg.


Hb 10 g/dl

WCC 9 109 /l


ESR 90 mm/h

Sodium 139 mmol/l


Urea 9 mol/l

Creatinine 140 mol/l

Bilirubin 15 mmol/l

AST 90 iu/l


Albumin 33 g/l

Rheumatoid factor IgM Positive (titre 1/640)

C3 0.2 g/l (NR 0.55–1.2 g/l)

C4 0.09 g/l (NR 0.2–0.5 g/l)

Hep C Virus AB Positive

Hep B sAg Negative

Urinalysis Blood +

Protein ++

Question 15

Question 16

A 30-year-old businessman developed sudden onset of fever, sore throat, diarrhoea and myalgia. Over the nextthree days he noticed a widespread rash affecting his face,trunk, palms and soles. He was usually fit and well andhad only consulted his GP once in the past 10 years for atyphoid vaccine before travelling to India. Over the pastfour months he had established business links with acompany in Thailand and had visited the country onthree occasions. His last visit to Thailand was eight weekspreviously. He was married with two young children. He was not taking any medications and had no history of drug allergy.

On examination his temperature was 38.6°C. There was cervical lymphadenopathy. Inspection of the oralcavity revealed several painful ulcers affecting the tongue.The pharynx was oedematous and red with minimaltonsillar exudates. The chest was clear. Abdominalexamination was normal.


What is the best management of the patient’s illness?a. Prednisolone.b. Cyclophosphamide.c. Chlorambucil.d. Pegylated interferon- plus ribavarin.e. Plasmapharesis.

What is the diagnosis?a. Acute HIV infection.b. Secondary syphilis.c. Acute hepatitis infection.d. Infectious mononucleosis.e. Acute CMV infection.

Hb 13 g/dl

WCC 11 109 /l(neutrophils 6 109 /l,

lymphocytes 4 109 /l)


Monspot test Negative

Sodium 135 mmol/l


Urea 6 mmol/l

Creatinine 80 mol/l

Bilirubin 23 mol/l

ALT 45 iu/l

AST 49 iu/l


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20

The main differential diagnosis is between infectiousmononucleosis, CMV infection and acute HIV infection. All three are associated with sore throat, rash, fever andatypical lymphocytes. Mouth ulcers are usually absent in

EBV and CMV infection. Furthermore the rash ininfectious mononucleosis is usually an idiosyncraticreaction to ampicillin whereas it is part of HIV seroconverson. The main clinical features differentiatinginfectious mononucleosis from acute HIV infection aretabulated below. The rash in CMV infection usually sparesthe palms and soles. (See Question 325.)

Answer 16

a. Acute HIV infection.

Differentiation between infectious mononucleosis and acute HIV infection

Parameter Infections mononucleosis HIV infection Onset of symptoms Over a few days AbruptMouth ulcers Absent usually Often presentRash Usually secondary to ampicillin Part of HIV seroconversionDiarrhoea Unusual CommonTonsillar exudates Prominent Mild White cell count May be elevated Elevated or suppressed Atypical lymphocytes Frequent (90%) and numerous Present in 50%Transaminitis Common Common

Thrombocytopenia Common Common

This is a difficult question; however, the clue lies in thefact that the patient has evidence of current or previousinfection with hepatitis virus and has Raynaud’sphenomenon, palpable purpura (vasculitis), neuropathy and hypocomplementaemia. The diagnosis is consistent

with mixed essential cryoglobulinaemia. Cryoglobulinsare immunoglobulins that precipitate in the cold. They are associated with auto-immune haemolysis, Raynaud’sdisease (in severe cases they can cause acronecrosis), vasculitis, peripheral neuropathy, glomerulonephritis andhepatosplenomegaly. Complement is reduced. HCV isthought to play an aetiological role in the development intype II and type III cryoglobulinaemia.

Answer 15

d. Pegylated interferon- plus ribavarin.

Types of cryoglobulinaemia

Type Immunoglobulins Associated condition(s)I Monoclonal immunoglobulin Multiple myeloma

Waldenstrom’s macroglobulinaemiaII Polyclonal IgG and monoclonal Hepatitis C and hepatitis B

rheumatoid factor IgMIII Mixed IgG and polyclonal Chronic inflammation

rheumatoid factor Hepatitis CLymphoproliferative disease

The diagnosis is based upon history, skin biopsy (if purpura present), hypocomplementaemia and presence of cryoglobulins. Investigation for cryoglobulinaemiashould always include serology for hepatitis C infection.Treatment for acute cryoglobulinaemia causing severerenal impairment or acronecrosis is plasmapharesis,though in less acute situations prednisolone and

cyclophosphamide are effective. Chlorambucil has alsobeen used with success. When cryoglobulinaemia issecondary to HCV infection, the treatment of choiceincludes the combination of pegylated interferon-a andribavarin. Ribavarin should be used with caution inpatients with renal failure.


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Clinical Cases 21

A 69-year-old woman with rheumatoid arthrit ispresented with swollen ankles. She was diagnosed ashaving rheumatoid arthritis over 18 years ago and hadbeen relatively well controlled on non-steroidal anti-inflammatory drugs until six months ago, when her jointpains and swelling required the addition of penicillamineto control her symptoms. The patient had a past history of hypertension, for which she took bendroflumethiazide.

On examination she had symmetrical joint deformitiesconsistent with rheumatoid arthritis. The heart rate was90 beats/min and irregular. Her blood pressuremeasured 140/90 mmHg. The JVP was not raised. Both

heart sounds were normal and the chest was clear. Abdominal examination was normal. Inspection of thelower limbs revealed pitting oedema.


Hb 11 g/dl

WCC 5 109 /l


Sodium 134 mmol/l

Potassium 4.5 mmol/lUrea 6 mmol/l

Creatinine 70 mol/l

Bilirubin 11mol/l


Albumin 26 g/l

Urinalysis Protein

Question 17

What is the management?a. Stop penicillamine.b. Start prednisolone.c. Start ACE inhibitor therapy.d. Arrange renal biopsy.e. Arrange IVU.

A 59-year-old female presented with weakness of bothlegs. An MRI scan of the spine is shown (18).

Question 18

What is the cause of her symptoms?a. Syringomyelia.b. Paravertebral abscess.c. Thoracic disc prolapse.d. Metastatic spinal cord compression.e. Extradural meningioma.

18


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22

The patient has heavy proteinuria and gives a relatively recent history of onset of swollen ankles shortly afterstarting penicillamine. The most likely diagnosis ispenicillamine-induced membranous nephropathy, whichusually occurs within 6–12 months of the initiation of drug therapy. Proteinuria resolves in virtually all casesafter stopping the drug but this may take several months.Other causes of heavy proteinuria secondary tomembranous nephropathy in rheumatoid arthritis includegold therapy.

Renal amyloidosis is a recognized cause of heavy proteinuria complicating chronic rheumatoid arthritis. While it is possible that the patient may have renalamyloidosis, the relationship of the proteinuria to the

initiation of penicillamine points to a drug-inducedmembranous nephropathy.

Other causes of renal disease in rheumatoid arthritisinclude analgesic nephropathy, focal segmentalglomerulonephritis and rheumatoid vasculitis. All arecharacterized by blood in the urine. Analgesicnephropathy is usually secondary to non-steroidal anti-inflammatory drugs and paracetamol. The proteinuria israrely severe enough to cause nephrotic syndrome. Focalsegmental glomerulonephritis is rare and is excluded by the absence of red cells in the urine. Rheumatoid vasculitis has a predilection for skin and the peripheralnervous system but in very rare circumstances may affectthe kidneys. It is more likely in patients with severedisease, nodule formation, high titres of rheumatoidfactor and hypocomplementaemia. (See Question 320.)

Answer 17

a. Stop penicillamine.

Answer 18

This is a T2 weighted image that shows evidence of cordcompression from a collapsed thoracic vertebra. The

vertebra in question is infiltrated by tumour and appears white. The ve rtebra above are al so in fi lt rated wi thtumour (appear white). The vertebra below the collapsed vertebra appear normal (black).

d. Metastatic spinal cord compression.

Interpretation of MRI Scans

Substance T1 weighted T2 weighted

Water/vitreous/CSF black light grey or whiteFat white light grey Muscle grey grey Air black black Fatty bone marrow white light grey Brain white matter light grey grey Brain grey matter grey very light grey

T1 Weighted Imaging

Provides anatomical information

Low signal – Black • Cortical bone• Air• Rapidly flowing blood• CSF

Intermediate signal – Grey

• Grey matter is darker than white matterHigh signal – White• Fat in bone, scalp and orbit

T2 Weighted Imaging

Provides pathological information

Low signal – Black • Cortical bone• Air• Rapidly flowing blood• Haemosiderin

Intermediate signal – Grey

• White matter is darker than grey matterHigh signal – White• CSF or water


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Clinical Cases 23

A 16-year-old girl presented with intermittent episodes of lower colicky abdominal pain for six months. In theinterim she had lost almost 6.4 kg in weight. Herappetite was not impaired. There was no history of diarrhoea, although the patient had complained of intermittent constipation and abdominal bloating. Thepatient was English in origin. She had no family history of note. She had last travelled abroad to Barbados onholiday a year ago. The only other past medical history included a short episode of painful ankles associated withcircular erythematous skin lesions.

On examination she was thin and mildly clubbed. Theheart rate was 90 beats/min and regular. The bloodpressure measured 100/55 mmHg. There was evidence

of a BCG scar on inspection of the left upper arm. Bothheart sounds were normal and the chest was clear. Abdomina l examinat ion revealed vague tendernessaffecting the hypogastrum and right iliac fossa.


Question 19

Hb 10 g/dl

WCC 11 109 /l


ESR 55 mm/h

U&E NormalAST 20 iu/l

ALT 22 iu/l

Bilirubin 12 mol/l

Albumin 33 g/l

Stool culture Negative

Chest X-ray Minor calcification, a few

perihilar nodes

What is the diagnosis?a. Sarcoidosis.b. Intestinal lymphoma.c. Intestinal tuberculosis.d. Crohn’s disease.e. Irritable bowel syndrome.

A 24-year-old patient was admitted to hospital with acuteasthma for the fourth time in the past six years. Theasthma was usually precipitated by a coryzal illness orexposure to allergens. There was no other past medicalhistory of note. The patient usually inhaled ventolin asrequired, salmeterol inhaler twice daily, becotide inhalertwice daily and had recently been prescribedaminophylline 450 mg twice daily.

On admission she had a bilateral wheeze. The PEFR was 200 l/min. The oxygen saturation on air was 86%and on 28% oxygen it was 94%. The chest X-ray revealedhyperinflated lungs. The patient was commenced onnebulized bronchodilators, prednisolone 30 mg daily andamoxycillin. The following day she developed a rashtherefore the amoxycillin was substituted witherythromycin.

The patient improved significantly over the next 48hours but then suffered three successive grand malseizures, which necessitated ventilation.

Question 20

What was the most likely cause of the epilepticseizures?

a. Hypoxia.b. Meningitis.c. Benign intracranial hypertension.d. Theophylline toxicity.e. Herpes encephalitis.


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24

Abdominal cramps, weight loss, erythema nodosum(raised circular skin lesions) and raised inflammatory markers are highly suggestive of inflammatory boweldisease. Tenderness in the right iliac fossa points to thepossibility of terminal ileal disease and hence Crohn’sdisease, although this is a non-specific feature since many conditions may cause right iliac fossa tenderness.Diarrhoea is not always a prominent feature in Crohn’sdisease.

Although ileo-caecal TB may present in a similar fashion,her race and the presence of a BCG scar is against thediagnosis. Sarcoidosis enteropathy has been reported butthis is very rare and usually in association with otherfeatures of this multi-system disorder. Small bowellymphoma may present in a similar fashion; however,diarrhoea is a prominent feature. Raised inflammatory markers are against the diagnosis of irritable boweldisease, which is a functional rather than inflammatory disorder. (See Answers 31, 394.)

Answer 19

d. Crohn’s disease.

The question tests the candidate’s knowledge aboutdrugs interacting with aminophylline and inhibiting itsmetabolism. With respect to the treatment of lowerrespiratory tract infections, both quinolone andmacrolide antibiotics (e.g. ciprofloxacin, erythromycinrespectively) inhibit aminophylline metabolism.

Features of theophylline toxicity include nausea, vomiting, hypotension, cardiac arrhythmias and seizures.Other drugs that inhibit the metabolism of theophyllineinclude cimetidine, propranolol, allopurinol,thiobendazole and the contraceptive pill. In the context

of asthma, hypokalaemia (sometimes a consequence of nebulized salbutamol) is also associated with theophyllinetoxicity.

Symptoms do not usually occur until plasmatheophylline concentrations exceed 20 mg/l. The mostadverse effects of theophylline toxicity, such as cardiacarrhythmias and seizures, generally occur at plasmatheophylline levels >40 mg/l.

The management of theophylline toxicity is usually supportive. In patients who have taken an overdose, theaim is to prevent absorption in the stomach. There arethree main strategies in the management of theophyllinetoxicity (shown below):

Answer 20

d. Theophylline toxicity.

Strategy 1 (if patient is stable)• Gastric lavage followed by oral activated charcoal administration is effective.

Strategy 2• Treat arrhythmias with beta-blockers; unfortunately many patients taking theophylline for therapeutic reasons

have contraindications to beta-blockers. In these patients lignocaine may be used for ventricular arrhythmiasand verapamil for supraventricular arrhythmias including atrial fibrillation.

• Treat seizures with diazepam or barbiturates; phenytoin is not very effective.Strategy 3 (rarely required)• Haemodialysis is very effective in treating life-threatening toxicity, i.e. patients with a plasma theophylline

level of >100 mg/l who have profound hypotension, fatal cardiac arrhythmias and seizures. Age andconcomitant hepatic disease are important factors in relation to prognosis with theophylline toxicity. Patientsaged >60 years with liver disease may be dialysed at theophylline levels of around 60 mg/l.


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Clinical Cases 25

A 64-year-old Asian man presented with a six-week history of dyspnoea and wheeze. For two weeks he hadalso developed a cough productive of yellow sputum andfever. There was no history of night sweats. The patienthad not travelled abroad for over 20 years.


Question 21

Hb 13 g/dl

WCC 11 109 /l

(neutrophils 8 109 /l,

lymphocytes 1 10 9 /l

eosinophils 2 109 /l)


ESR 30 mm/h

Biochemistry NormalChest X-ray Diffuse perihilar infiltrates

Sputum culture Negative

What is the most probable diagnosis?a. Churg–Strauss syndrome.b. Tuberculosis.c. Allergic bronchopulmonary aspergillosis.d. Tropical pulmonary eosinophilia.e. Asthma.

A 78-year-old patient presented with sudden onset of severe breathlessness. He had a history of ischaemic heartdisease and had suffered two myocardial infarctions in thepast three years. He had an 11-year history of hypertension that had been well controlled. He was anon-smoker. His medication consisted of aspirin,ramipril, atenolol, bendroflumethiazide and simvastatin.

On examination he had a heart rate of 146 beats/min.The pulse was irregular. The blood pressure was100/68 mmHg. Both heart sounds were quiet. Auscultation of the lungs revealed widespread inspiratory crackle and expiratory wheeze. The ECG showed atrial

fibrillation with a rapid ventricular rate and q waves in theanterior leads.

Question 22

What is the safest drug for restoring sinus rhythm?a. IV digoxin.b. IV amiodarone.c. IV flecanide.d. IV esmolol.e. IV dofetolide.

Question 23

An 81-year-old man with non-insulin-dependent diabetesmellitus was found unconscious by his carer. Blood testsperformed on admission to hospital are shown.

Sodium 153 mmol/l


Urea 40 mmol/lCreatinine 310 mol/l

Glucose 60 mmol/l

What is the best combination of infusions in themanagement of the patient?

a. IV saline (0.45%), IV insulin and subcutaneousheparin.

b. IV saline (0.9%), IV insulin and subcutaneousheparin.

c. IV sodium bicarbonate, IV insulin andsubcutaneous heparin.

d. IV dextrose saline, IV insulin and subcutaneous

heparin.e. IV dextrose (5%), IV insulin and subcutaneous

heparin.


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26

The history of cough sputum, eosinophilia and perihilarinfiltrates is most consistent with allergic broncho -pulmonary aspergillosis in the context of the history given. There is no drug history to indicate aneosinophilic pneumonitis, nor a history of travel to thetropics to suggest tropical pulmonary eosinophilia.Churg–Strauss syndrome is unlikely in the absence of vasculitis, neuropathy or renal involvement. Asthma doesnot cause pulmonary infiltrates. Tuberculosis does notusually cause eosinophilia.

The diagnosis of allergic bronchopulmonary eosinophilia is made in patients with asthma, proximal

bronchiectasis and parenchymal infiltrates in the perihilararea. The presence of high titres of IgE and IgGantibodies and a positive hypersensitivity skin test to

Aspergil lus fumigatus testing confirm the diagnosis.Treatment is with a prolonged course of itraconazole.

Tropical pulmonary eosinophila is an immune reactionto infection with the human filarial parasites Wucheria bancrofti and Brugia malayi . It is characterized by a non-productive cough, wheeze, fever, weight loss,lymphadenopathy, eosinophilia and patchy infiltrates onthe chest X-ray. The condition occurs in patients infectedin the tropics. The worm is rarely identified but thecondition responds to diethycarbamazine, the drugnormally used to treat filariasis. (See Question 396.)

Answer 21

c. Allergic bronchopulmonary aspergillosis.

The patient has rapid atrial fibrillation in the context of ischaemic heart disease and has evidence of pulmonary oedema. One has to assume that left ventricular functionis impaired to answer this question since it is highly unlikely that a heart rate of 146 beats/min would causeleft ventricular failure in a patient with normal left ven tri cu la r fu nc tion. Amioda rone, do fetoli de andflecainide are capable of restoring sinus rhythm. Of theseamiodarone is the least negatively inotropic.

Flecainide is relatively contraindicated in patients withknown coronary artery disease. Dofetolide is a class III

anti-arrhythmic agent that is effective at restoring sinusrhythm in patients with persistent AF (up to seven days)or more permanent AF. Dofetolide is less negatively inotropic than many other drugs that may be effective inrestoring sinus rhythm such as propafenone (class IC),quinidine, disopyramide (class IA) and sotalol (class III),but experience regarding its use in the UK is relatively limited. Digoxin is effective in controlling ventricular ratein AF but does not restore sinus rhythm. Esmolol is a very short-acting beta-blocker (class II antiarrhythmicagent) that is not useful at restoring sinus rhythm.

Answer 22

b. IV amiodarone.

The patient has a hyperosmolar non-ketotic diabeticcoma (HONK). The fluid of choice is saline. Thestrength of saline used initially is always 0.9% since it iseffective at restoring volume and has a lower risk of causing large drops in plasma osmolality, a risk factor for

the development of cerebral oedema. If despite adequatehydration, the sodium remains >150 mmol/l someauthorities advocate switching to half-strength saline(0.45%). The patient has severe dehydration creating ahyperviscosity state that may predispose him to arterialand venous thromboses. Heparin therapy is mandatory toprevent such complications during the management of HONK. (See Question 84.)

Answer 23

b. IV saline (0.9%), IV insulin and subcutaneousheparin.


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Clinical Cases 27

A 13-year-old girl was admitted with a two-day history of lower abdominal pain and blood-stained diarrhoea. Threedays later, she developed pains in her ankles and rightelbow and felt nauseous. Positive findings onexamination were a purpuric rash affecting the arms andlegs, periorbital oedema and a blood pressure of 150/95 mmHg.


Question 24

Hb 10 g/dl

WCC 12 109 /l


MCV 70 fl

ESR 35 mm/h

PT 13 s (control 13 s)

APTT 34 s (control 36 s)

Sodium 138 mmol/l


Creatinine 130 mol/l

Urinalysis Blood ++

Protein ++

2: List two investigations that would be most usefulin confirming the diagnosis.a. Skin biopsy.b. Renal biopsy.c. Blood cultures.d. TT.e. Serum fibrinogen level.f. Serum IgA level.g. Serum ANF level.h. Serum ANCA.i. Blood film. j. 24-hour urine collection for protein.

Question 25

A 39-year-old African male was referred to the bloodpressure unit with persistent blood pressure readings of 140–150/90–95 mmHg over the past six months. He was a non-smoker and consumed 4 units of alcohol per week. The patient weighed 89 kg and measured 1.7 m.Physical examination was normal with the exception of ablood pressure reading of 150/92 mmHg.


What is the best initial management for the raisedblood pressure?

a. Beta-blocker.b. Angiotensin-converting enzyme inhibitor.c. Low-salt diet, regular exercise.d. Calcium channel antagonist.e. Thiazide diuretic.

Sodium 136 mmol/l

Potassium 4.2 mmol/lUrea 5 mmol/l

Glucose 4.1 mmol/l

Total cholesterol 4.1 mmol/l

Triglycerides 1.2 mmol/l

12-lead ECG Sinus rhythm

Right axis deviation

Urinalysis Protein 0

Blood 0

Cells 0

1: What is the most probable diagnosis?a. Haemolytic–uraemic syndrome.b. IgA nephritis.

c. Henoch–Schönlein purpura.d. Systemic lupus erythematosus.e. Polyarteritis nodosa.


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The combination of lower abdominal pain, bloody diarrhoea, purpuric rash and nephritis in a young girlare highly suggestive of Henoch–Schönlein purpura.The condition is a small-vessel vasculitis that occursmost commonly in children aged 4–15 years. It ischaracterized by gastrointestinal symptoms whichcomprise abdominal pain, diarrhoea, and rectalbleeding, flitting arthralgia affecting large joints, apurpuric rash characteristically affecting the lower limbsand buttocks and an acute nephritis. Complicationsinclude intestinal perforation, haemorrhage andintussusception and acute renal failure.

The diagnosis is usually clinical; however, tissuediagnosis is possible with skin or renal biopsy. Skinbiopsy demonstrates a leucoclastic vasculitis with IgA deposition. Renal biopsy reveals mesangial IgA deposition associated with a glomerulonephritis. Renalhistology is indistinguishable from IgA nephropathy. Inthis case, more marks are given to skin biopsy because itis safer and more practical than renal biopsy. Serum IgA levels are depressed in approximately 50% of cases. Themanagement is usually supportive, although there may be a role for methylprednisolone in cases of acutecrescentic nephritis.

The condition must not be confused with thehaemolytic uraemic syndrome (discussed in Answer152), which is also characterized by diarrhoea and renalfailure.

Answer 24

1: c. Henoch–Schönlein purpura.2: a. Skin biopsy.

b. Renal biopsy.

The patient is young and has mild hypertension onpresentation. He does not have any other risk factors forcardiovascular disease or evidence of secondary end-organ damage as a result of the raised blood pressure.In this particular case the initial management planshould include a low-salt diet, regular exercise and weight loss. The patient should be observed carefully for up to a year and should only be commenced onpharmacological therapy if the blood pressure remainsabove 140/85 mmHg.

If treatment is indicated after a year, the drugs of choice are thiazide diuretics or calcium channelblockers. Angiotensin-converting enzyme inhibitors andbeta-blockers are not particular ly effective asmonotherapy because both drugs act by suppressingrenin levels, which are already relatively low in Afro-

Caribbean patients. However, these patients may respond to ACE inhibitors and beta-blockers whenprescribed with drugs that activate the renin–angiotensin–aldosterone system, i.e. thiazide diureticsand calcium channel blockers.

Both lifestyle modification and pharmacologicaltherapy would be indicated if the patient had a bloodpressure ≥160/100 mmHg, or evidence of secondary end-organ damage, or other risk factors for coronary artery disease at presentation.

There is a high prevalence of hypertension inindividuals of Afro-Caribbean origin, with almost 50%of patients over the age of 40 years being affected. Thisparticular group of patients generally develop hyper-tension at a younger age and are at higher risk of hypertensive complications such as stroke, heart failureand renal failure than Caucasian patients. Hypertensionin Afro-Caribbean patients is salt sensitive and responds well to a low-salt diet.

Answer 25

c. Low-salt diet, regular exercise.


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Clinical Cases 29

Question 26

A 41-year-old male was admitted to hospital with acuteconfusion. He had been generally unwell for two days. A worried neighbour looked through his letter box when hefailed to answer the doorbell, and found him lying on thefloor. There was no other history of note.

On examination, he was confused. He had a wide-spread rash (26a). His left eye is shown (26b). The heartrate was 120 beats/min; the blood pressure wasunrecordable. There was no evidence of nuchal rigidity,and Kernig’s sign was negative. There was no focalneurological deficit. Examination of the cardiovascular,respiratory and gastrointestinal tract was normal.

Investigations are shown.Hb 11 g/dlWCC 24 109 /l

Platelets 30 109 /l

Sodium 135 mmol/l

Potassium 5 mmol/l

Creatinine 156 µmol/l

PT 48 s (control 13 s)Fibrinogen degradation >25,000

products

A 36- ye ar -o ld wo man is seen in the Acci dent andEmergency Department after having taken 40 paracetamoltablets with a quarter-bottle of vodka six hours earlier,following an argument with her husband. She wasnauseous, but had not vomited. There was no past medicalhistory of note. A physical examination was normal.


Sodium 138 mmol/l


Urea 5.1 mmol/lBicarbonate 18 mmol/l

PT 15 s (control 15 s)

Serum paracetamol 200 mg/l

level

1. List two immediate management steps from thefollowing list:

a. Gastric lavage.b. IV dextrose 5%.c. Oral activated charcoal.d. Fresh-frozen plasma.e. IV sodium bicarbonate.f. IV N-acetyl cysteine.g. IV flumazenil.

h. IV vitamin K.i. IV saline (0.9%). j. IV prochlorperazine.

2. Which one of the following investigations would you perform the next day to assess her prognosis?

a. Serum potassium.b. Serum magnesium.

c. Arterial pH.d. Serum paracetamol concentration.e. Serum aspartate transaminase.

Question 27

Which single investigation would you perform next?a. Blood cultures.b. CT scan brain.c. CSF for microscopy and culture.

d. Chest X-ray.e. Throat swab for culture.

26a 26b


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The eye demonstrates a conjunctival haemorrhage. Therash is a necrotic purpuric rash, which is typical of meningococcal septicaemia. The patient has septic shock and requires immediate therapy. The recognition that hehas meningococcal septicaemia is important for the choiceof antibiotics that you will use. In medical emergencies, thereader must be familiar with the drugs that are used in thatparticular emergency, but not necessarily the dosage, asthis can be found in the British National Formulary or theequivalent. Although most Neisseria meningitidis strainsare sensitive to benzyl penicillin, it is prudent to cover thepatient with additional cephalosporin or aminoglycosideantibiotic therapy until the sensitivities of the organism areknown. The circulation must be restored to preventhypoperfusion of vital organs, particularly the kidneys. Thepresence of low platelets, high fibrinogen degradationproducts and abnormal clotting is suggestive of DIC, which should be treated with fresh-frozen plasma toprevent haemorrhage.

Neisseria meningitidis , the causal Gram-negativediplococcus, can be cultured from the CSF in over 80% of cases with evidence of neurological involvement. However,

the presence of very low levels of platelets and DIC iscontraindicated because of the dangers of bleeding into thespinal canal, particularly because the yield is just as highfrom nasal swabs. It is also possible to isolate themeningococcal antigen from blood before blood cultureresults are available. This test is particularly useful if antibiotics have been given before the patient is brought tohospital (negative blood cultures).

Meningococcal meningitis and septicaemia are causedby serogroups B and C. Septicaemia is associated with wid esprea d petec hi al haemor rhage. Con ju nc tiv alhaemorrhage may be the first physical manifestation. Shock is common owing to the production of a circulatingendotoxin. DIC is a commonly recognized complicationthat may result in adrenal haemorrhage(Waterhouse–Friderichsen syndrome). Meningitis is oftencharacterized by a myalgia, headache, photophobia, neck stiffness, nausea and vomiting. In the absence of DIC, thediagnosis is made rapidly by performing a Gram stain onthe CSF. Blood cultures are positive in the majority of patients with meningitis. Focal neurological signs are lesscommon than in pneumococcal meningitis.

Note: individuals in contact with affected patients mustreceive rifampicin chemoprophylaxis.

Answer 26

The drug should be given within 8–10 hours of ingestionof the overdose, and continued while the liver function isabnormal. It is useful because it replenishes cellularglutathione stores and reduces oxidative damage causedby the toxic metabolite, NAPQI. An alternative to this ismethionine. Gastric lavage is useful if performed within 1hour of the overdose.

The patient has taken 20 g of paracetamol. Aningestion of 15 g is considered potentially serious in mostpatients. The toxicity of paracetamol is related to theproduction of a toxic metabolite of paracetamol. This isNAPQI, which usually is immediately conjugated withglutathione and excreted. In paracetamol overdose, thetoxic metabolite is produced in excess and depletes

cellular glutathione. The liver is unable to deactivateNAPQI, which is responsible for massive hepatic necrosisand hepatic failure. Patients may have nausea, anorexia or vomiting on the first day. After 72 hours, features of liverand renal failure may ensue.

The three most important prognostic markers inparacetamol overdose are serum creatinine concentration,arterial pH and prothrombin time. A rise in serumcreatinine level due to renal failure is a bad prognosticsign. A level of over 300 mmol/l is associated with over70% mortality. Systemic acidosis (due to the failure of clearance of lactate by the liver) more than 24 hours afterthe overdose is associated with a poor prognosis. A pH of below 7.3 is associated with only a 15% chance of survival.The PT is usually the first liver test to become abnormal. A PT of >20 s at 24 hours after overdose is suggestive of significant hepatic damage, and a peak PT of >180 s isassociated with a 90% mortality.

1. c. Oral activated charcoal.f. IV N-acetyl cysteine.

2. c. Arterial pH.

Answer 27

a. Blood cultures.


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Clinical Cases 31

A 52-year-old female was broughtinto the Accident and Emergency Department after being foundcollapsed outside a public house.There was no one accompanyingher, and there was no informationregarding her next of kin.

On examination, she was very drowsy and had a Glasgow comascore of 6 out of 15. Her pupils were 10 mm each and reacted very sluggishly to light. On attempting toexamine her fundi, she was noted tohave coarse nystagmus, but a clear view of her fu nd i di d no tdemonstrate any abnormalities. The tone in all her limbs was increased and her reflexes were brisk. The plantars were both upgoing. The heart rate was 135 beats/min,and regular. The blood pressure was 105/60 mmHg. Therespiratory rate was 20/min. Examination of theprecordium and lung fields was normal, but examination of the abdomen revealed a firm palpable mass 4 cm above thesymphysis pubis. The patient was catheterized and drainedof 2 litres of urine. Investigations are shown.

Shortly after the lumbar puncture, the patient had ageneralized seizure which lasted 30 s. The attending nurseraised concerns about an arrhythmia on the cardiacmonitor, and a 12-lead ECG was performed (28).

Question 28

Hb 14 g/dlWCC 12 109 /l


MCV 88 fl

Sodium 144 mmol/l


Urea 13 mmol/l

Creatinine 100 µmol/l

Bicarbonate 20 mmol/l

Chloride 108 mmol/l

Calcium 2.4 mmol/l

Phosphate 1.3 mmol/l

Bilirubin 12 µmol/lAST 33 iu/l

Gamma GT 28 iu/l


Plasma osmolality 333 mOsm/l

Urine osmolality 120 mOsm/l

Blood glucose 6 mmol/l

Chest X-ray Normal-sized heart and

clear lung fields

Skull X-ray Normal; no fractures seen

Brain CT scan Normal

Lumbar puncture:

CSF pressure 100 mmH2OCells 3/mm3

Protein 0.35 g/l

Glucose 3 mmol/l

ECG Sinus tachycardia; right

axis deviation

1. Calculate the plasma osmolality.2. Explain the discrepancy between the calculated

plasma osmolality and the measured plasmaosmolality.

3. Give two possible explanations for the low urine

osmolality.4. What is shown on the ECG?5. What diagnosis best fits all the information given

above?6. What three investigations would you perform to

help in this patient’s management?

28


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Arrhythmias usually settle on correction of hypoxia andacidosis. Administration of class I antiarrhythmic agentsmay paradoxically worsen arrhythmias, with the exceptionof phenytoin. Status epilepticus should be corrected withintravenous diazepam.

Epileptic seizures and ventricular arrhythmias in apatient found collapsed should raise the suspicion of tricyclic antidepressant drug overdose. The low urineosmolality suggests that the patient has probably takenthe overdose together with alcohol, and it is possible thatshe may have also taken lithium. The normal CT scan of the brain and normal CSF are against pathology in thecentral nervous system. She has dilated pupils, which isagainst narcotic abuse. Indeed, the combination of dilated pupils, tachycardia and urinary retention are allsuggestive of the anticholinergic side-effects of tricyclicantidepressants. Severe lithium toxicity is associated withseizures, coma and ventricular arrhythmias, but

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