Complete Revision Notes for Medical and Surgical Finals PDF

Complete Revision Notes for Medical and Surgical Finals This page intentionally left blank Complete Revision Notes for Medical and Surgical Finals Second edition Kinesh Patel ba(hons) mb bs mrcp Specialty Registrar, Gastroenterology St Mark’s Hospital London, UK First published in Great Britain...

Complete Revision Notes for Medical and Surgical Finals This page intentionally left blank Complete Revision Notes for Medical and Surgical Finals Second edition Kinesh Patel ba(hons) mb bs mrcp Specialty Registrar, Gastroenterology St Mark’s Hospital London, UK First published in Great Britain in 2006 by Hodder Arnold This second edition published in 2011 by Hodder Arnold, an imprint of Hodder Education, a division of Hachette UK 338 Euston Road, London NW1 3BH http://www.hodderarnold.com © 2011 Hodder & Stoughton Ltd All rights reserved. Apart from any use permitted under UK copyright law, this publication may only be reproduced, stored or transmitted, in any form, or by any means with prior permission in writing of the publishers or in the case of reprographic production in accordance with the terms of licences issued by the Copyright Licensing Agency. In the United Kingdom such licences are issued by the Copyright Licensing Agency: Saffron House, 6–10 Kirby Street, London EC1N 8TS Hachette UK’s policy is to use papers that are natural, renewable and recyclable products and made from wood grown in sustainable forests. The logging and manufacturing processes are expected to conform to the environmental regulations of the country of origin. Whilst the advice and information in this book are believed to be true and accurate at the date of going to press, neither the author[s] nor the publisher can accept any legal responsibility or liability for any errors or omissions that may be made. In particular (but without limiting the generality of the preceding disclaimer) every effort has been made to check drug dosages; however it is still possible that errors have been missed. Furthermore, dosage schedules are constantly being revised and new side-effects recognized. For these reasons the reader is strongly urged to consult the drug companies’ printed instructions before administering any of the drugs recommended in this book. British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Library of Congress Cataloging-in-Publication Data A catalog record for this book is available from the Library of Congress ISBN-13 978 1 444 120 660 1 2 3 4 5 6 7 8 9 10 Commissioning Editor: Joanna Koster Project Editor: Stephen Clausard Production Controller: Jonathan Williams Cover Design: Amina Dudhia Indexer: Lisa Footitt Cover image © Alfred Pasieka/Science Photo Library Typeset in 10 on 13pt Minion by Phoenix Photosetting, Chatham, Kent Printed and bound in India What do you think about this book? Or any other Hodder Arnold title? Please visit our website: www.hodderarnold.com Contents Contributors vii Preface ix Acknowledgements xi List of icons xiii Abbreviations xv 1 Medicine 1 Nisha Patel, Alexandra Kent and Natasha Patel 2 Surgery 106 Gareth Jones 3 Orthopaedics 162 Gareth Jones and Julian Leong 4 Ear, nose and throat 179 Irfan Syed 5 Urology 186 Simon Bott and Ben Eddy 6 Ophthalmology 196 Jagdeep Singh Gandhi 7 Oncology 204 Kirstin Satherley 8 Public Health 214 Kinesh Patel 9 Paediatrics 220 Sarita Depani 10 Obstetrics and Gynaecology 257 Jane Borley 11 Psychiatry 293 Sophie Atwood and Scott Cherry Index 303 This page intentionally left blank Contributors Sophie Atwood MA MBBS MRCPsych PGCME ST3 Psychiatry Specialty Trainee, Sussex Partnership NHS Foundation Trust, UK Jane Borley BSc MBBS MRCOG Clinical Research Fellow, Imperial College London, UK Simon RJ Bott MD FRCS(Urol) Consultant Urologist, Frimley Park Hospital, Frimley, UK Scott Cherry MBChB MRCPsych PGCME Specialist Registrar, Sussex Partnership NHS Foundation Trust, UK Sarita Depani MBBS BSc(Hons) MRCPCH Specialist Registrar in Paediatrics, South Thames Rotation, London, UK Ben Eddy FRCS(Urol) Consultant Urologist, Kent and Canterbury Hospital, Canterbury, UK Gareth G Jones BSc(Hons) MB BS MRCS (Eng) Specialist Registrar in Trauma and Orthopaedics, Imperial College Healthcare NHS Trust, London, UK Julian JH Leong MA(Oxon) MBBS MRCS(Eng) PhD DIC Specialty Registrar, UCLH rotation, London, UK Alexandra Kent MB ChB MRCP Research Fellow, John Radcliffe Hospital, Oxford, UK Kinesh Patel BA (Hons) MB BS MRCP Specialty Registrar, Gastroenterology, St Mark’s Hospital, London, UK Natasha H Patel BSc(Hons) MB BS MRCP Consultant in Diabetes and AMU, St George’s Hospital, Tooting, London, UK Nisha Patel BSc (Hons) MB BS MRCP St Mary’s Hospital NHS Trust, London, UK viii C o nt r i but or s Kirstin Satherley BSc(Hons) MB BS MRCP Specialist Registrar in Clinical Oncology, The Royal Marsden Hospital, London, UK Jagdeep Singh Gandhi BSc MB ChB MRCS FRCOphth Consultant Ophthalmic Surgeon, Worcester Royal Eye Unit, Worcester, UK Irfan Syed BSc(Hons) MBBS(Lon) MRCS DO-HNS Specialist Registrar ENT Surgery, St George’s Hospital, Tooting, London, UK Preface Finals tend to be a stressful time for medical students, as the requirement to relearn the large volumes of knowledge accumulated over 5 or 6 years is demanding, both physically and emotionally. Often the most difficult part is deciding exactly what level of detail is expected by examiners: the constant fear of not knowing enough inevitably leads students to try to learn too much from complicated texts, and consequently the key points that examiners actually seek are often forgotten. This book is useful as it uniquely contains the entire undergraduate curriculum examined at finals, from medicine to surgery and ENT to oncology. The salient points needed to pass are featured in an easy to read (and remember!) bulleted format. As most examinations are now multiple choice question-based, these bullets provide the essential nuggets of information that are often difficult and time-consuming to extract from a conventional textbook. Particular thought has been given to include facts that are repeatedly tested in finals, although explanations have been kept deliberately brief to act more as an aide-mémoire than to provide comprehensive descriptions of diseases. The content is deliberately broad, but without the unnecessary extensive verbosity that can create real confusion and anxiety in the days running up to exams. The information contained within this book should be sufficient to pass written finals. I wish you every success in your studies. Kinesh Patel This page intentionally left blank Acknowledgements I would like to thank the contributors to the first edition of the book for their hard work. These include Alexandra Kent and Natasha Patel (Medicine), Simon Phillips (Surgery), Julian Leong (Orthopaedics), Alex Charkin (Ear, Nose and Throat) and Ben Eddy (Urology). Finally thanks must go to all the staff at Hodder Arnold for their help, support and encouragement to make this book and its companions a success. The authors of Chapter 11 wish to acknowledge the ICD-10 of the World Health Organization and the NICE guidelines on mental health and behavioural conditions as providing source material for their chapter. This page intentionally left blank List of icons A Aetiology/incidence Cx Complications Ix Investigations P Pathology Px Prognosis Si Signs Sy Symptoms S Signs and symptoms DD Differential diagnosis Rx Treatment This page intentionally left blank Abbreviations AAA abdominal aortic aneurysm AAFB acid- and alcohol-fast bacilli Ab antibody ABC airway, breathing, circulation ABG arterial blood gases ABPI ankle brachial pressure index ACA anticentromere antibody ACE angiotensin-converting enzyme ACS acute coronary syndrome ACTH adrenocorticotrophic hormone AD Alzheimer’s disease ADH antidiuretic hormone ADHD attention-deficit hyperactivity disorder ADLs activities of daily living AE acute endocarditis AF atrial fibrillation AFB acid-fast bacilli AFP a-fetoprotein Ag antigen AGN acute glomerulonephritis AIDS acquired immune deficiency syndrome AIH autoimmune hepatitis AIHA autoimmune haemolytic anaemia AITP autoimmune thrombocytopenic purpura ALL acute lymphoblastic leukaemia ALP alkaline phosphatase ALS amyotrophic lateral sclerosis ALT alanine transaminase AMA antimitochondrial antibody AML acute myelogenous leukaemia ANA antinuclear antibodies ANCA antineutrophil cytoplasmic antibodies AP anteroposterior APH antepartum haemorrhage x vi A bb r e v i at i ons APKD adult polycystic kidney disease APTT activated partial thromboplastin time APUD amine precursor uptake and decarboxylation ARDS acute respiratory distress syndrome ARF acute renal failure 5-ASA 5-aminosalicylic acid ASD atrial septal defect ASIS anterior superior iliac spine ASO antistreptolysin O AST aspartate transaminase ATLS advanced trauma life support ATN acute tubular necrosis AV atrioventricular (node) AVB atrioventricular block AVSD atrioventricular septal defect AXR abdominal X-ray BaFT barium follow-through BAL broncho-alveolar lavage BCC basal cell carcinoma BCG Bacille Calmette-Guérin BE base excess BMI body mass index BP blood pressure BPH benign prostatic hyperplasia BSO bilateral salpingo-oophectomy BT breath test BZD benzodiazepine CBD common bile duct CBT cognitive behavioural therapy CCF congestive cardiac failure CCP cyclic citrullinated peptide CFA cryptogenic fibrosing alveolitis CFM cerebral function monitor CFTR cystic fibrosis transmembrane regulating (gene) CFU colony-forming units CIN cervical intra-epithelial neoplasia CJD Creutzfeldt–Jakob disease CK creatine kinase CMC carpo-metacarpal CML chronic myeloid leukaemia CMV cytomegalovirus CNS central nervous system COCP combined oral contraceptive pill COMT catechol O-methyltransferase COPD chronic obstructive pulmonary disease CPAP continuous positive airway pressure CPN common peroneal nerve  Abbreviations xvii CrCl creatinine clearance CRF chronic renal failure CRL crown rump length CRP C-reactive protein CRT capillary refill time CSF cerebrospinal fluid CT computed tomography CTG cardiotocograph CTPA CT pulmonary angiography CTR cardiothoracic ratio CVA cerebrovascular accident CVD cardiovascular disease CVP central venous pressure CVS cardiovascular system CXR chest X-ray DCIS ductal carcinoma in situ DDH developmental dysplasia of the hip DEXA dual-energy X-ray absorptiometry DI diabetes insipidus DIB difficulty in breathing DIC disseminated intravascular coagulation DIOS distal intestinal obstruction syndrome DIP distal interphalangeal joint DKA diabetic ketoacidosis DLB Lewy body dementia DM diabetes mellitus DMARD disease-modifying antirheumatic drugs DOT directly observed therapy DSH deliberate self-harm DVT deep vein thrombosis EAA extrinsic allergic alveolitis EBV Epstein–Barr virus ECF extracellular fluid ECG electrocardiogram ECT electroconvulsive therapy EEG electroencephalogram EMDR eye movement desensitization and reprocessing EMG electromyogram ENT ear, nose and throat EPS extrapyramidal symptoms ERCP endoscopic retrograde cholangiopancreatography/evacuation of retained products of conception ESR erythrocyte sedimentation rate ESRF end-stage renal failure ESWL extracorporeal shockwave lithotripsy EUA examination under anaesthesia FAP familial adenomatous polyposis coli syndrome x vii i A bbr e v i at i ons FB foreign body FBC full blood count FDP fibrin degradation products FEV1 forced expiratory volume in 1 s FFP fresh-frozen plasma FH family history FHH familial hypocalciuric hypercalcaemia FNA fine needle aspiration FSGS focal segmental glomerulosclerosis FSH follicle-stimulating hormone 5-FU 5-fluorouracil FVC forced vital capacity GA general anaesthetic GAD generalized anxiety disorder GBM glomerular basement membrane GBS Group B Streptococcus GCS Glasgow Coma Score G-CSF granulocyte colony-stimulating factor GFR glomerular filtration rate GGT gamma glutamyl transferase GH growth hormone GI gastrointestinal GM-CSF granulocyte monocyte colony-stimulating factor GN glomerulonephritis GnRH gonadotrophin-releasing hormone GOJ gastro-oesophageal junction GORD gastro-oesophageal reflux disease GP general practitioner G6PD glucose-6-phosphate dehydrogenase GTN glyceryl trinitrate HAART highly active antiretroviral treatment HAV hepatitis A virus Hb haemoglobin HbA1c haemoglobin A1c HBV hepatitis B virus HBcAb hepatitis B core antibody HBcAg hepatitis B core antigen HBeAb hepatitis B e antibody HBeAg hepatitis B e antigen HBsAb hepatitis B surface antibody HBsAg hepatitis B surface antigen HCC hepatocellular carcinoma hCG human chorionic gonadotrophin HCV hepatitis C virus HD Huntingdon’s disease HDV hepatitis D virus HEV hepatitis E virus  Abbreviations xix HF heart failure HHC hereditary haemochromatosis 5-HIAA 5-hydroxyindoleacetic acid HiB Haemophilus influenzae B HIV human immunodeficiency virus HLA human leucocyte antigen HMSN hereditary motor and sensory neuropathy HNPCC hereditary non-polyposis colon cancer HOCM hypertrophic obstructive cardiomyopathy HONK hyperosmolar non-ketotic coma HPA hypothalamo-pituitary-adrenal (axis)) HPV human papilloma virus HR heart rate HRCT high-resolution CT HRT hormone replacement therapy HSP Henoch–Schönlein purpura HSV herpes simplex virus 5-HT 5-hydroxytryptamine HTLV-1 human T-cell lymphotropic virus type 1 HTN hypertension HUS haemolytic uraemic syndrome HVS high vaginal swab HZV Herpes zoster virus IBD inflammatory bowel disease IBS irritable bowel syndrome ICF intracellular fluid ICP intracranial pressure ICSI intracytoplasmic sperm injection IF intrinsic factor IFG impaired fasting glycaemia IGF insulin-like growth factor IgG immunoglobulin G IgM immunoglobulin M IGT impaired glucose tolerance IHD ischaemic heart disease i.m. intramuscular INR international normalized ratio IOL induction of labour IPF idiopathic pulmonary fibrosis ITP idiopathic thrombocytopenic purpura ITU intensive therapy unit IUD intrauterine death/intrauterine device IUGR intrauterine growth restriction IUGS intrauterine gestation sac IUS intrauterine system i.v. intravenous IVC inferior vena cava xx A bb r ev i at i ons IVDU intravenous drug use IVF in-vitro fertilization IVU intravenous urogram JVP jugular venous pressure KUB kidneys, ureter and bladder LA left atrium/local anaesthetic LDH lactate dehydrogenase LDL low-density lipoprotein LFT liver function test LH luteinizing hormone LIF left iliac fossa LKM liver, kidney, microsomal antibody LLETZ large loop excision of the transformation zone LMWH low molecular weight heparin LOC loss of consciousness LOS lower oesophageal sphincter LP lumbar puncture LRTI lower respiratory tract infection LSE left sternal edge LUQ left upper quadrant LV left ventricle/ventricular MAC Mycobacterium avium complex MC&S microscopy, culture and sensitivity MCUG micturating cystourethrogram MCV mean corpuscular volume MDR-TB multi-drug-resistant TB MDT multidisciplinary team MEN multiple endocrine neoplasia MI myocardial infarction MIBG metaiodobenzylguanidine MLF medial longitudinal fasciculus MMR measles, mumps and rubella MMSE mini-mental state examination MR mitral regurgitation MRA magnetic resonance angiography MRCP MR cholangiopancreatography MRI magnetic resonance imaging MRSA methicillin-resistant Staphylococcus aureus MS multiple sclerosis MSU mid-stream urine MTP metatarsophalangeal joint NA noradrenaline NaSSA noradrenaline-serotonin specific antidepressant NASH non-alcoholic steatohepatitis NBM nil by mouth NCS nerve conduction studies NF1 neurofibromatosis type 1  Abbreviations xxi NGT nasogastric tube NHL non-Hodgkin’s lymphoma NICE National Institute for Health and Clinical Excellence NIPPV non-invasive positive pressure ventilation NNRTI non-nucleoside reverse transcriptase inhibitors NNT number needed to treat NPV negative predictive value NRTI nucleoside reverse transcriptase inhibitor NSAID non-steroidal anti-inflammatory drug NSTEMI non-ST-elevation myocardial infarction NTD neural tube defect OA osteoarthritis OCP oral contraceptive pill OGD oesophagogastroduodenoscopy OGT oro-gastric tube OGTT oral glucose tolerance test OI opportunistic infection ORIF open reduction and internal fixation ORT oral rehydration therapy OT occupational therapy PAPP-A pregnancy-associated plasma protein-A PBC primary biliary cirrhosis PCO2 partial pressure of carbon dioxide PCOS polycystic ovarian syndrome PCP Pneumocystis carinii pneumonia PCR polymerase chain reaction PD Parkinson’s disease PDA patent ductus arteriosus PE pulmonary embolism PEFR peak expiratory flow rate PET positron emission tomography/pre-eclampsia toxaemia PGE2 prostaglandin PH pulmonary hypertension PICA posterior inferior cerebellar artery PID pelvic inflammatory disease PMS premenstrual syndrome PO2 partial pressure of oxygen POC products of conception POP plaster of Paris/progestogen only contraception PPH primary pulmonary hypertension/postpartum haemorrhage PPHN persistent pulmonary hypertension of the newborn PPI proton pump inhibitor PPV positive predictive value PR per rectum prn pro re nata PRV polycythaemia rubra vera PSA prostate-specific antigen x xii A bb r e v i at i ons PSC primary sclerosing cholangitis PT prothrombin time PTCA percutaneous transluminal coronary angioplasty PTH parathyroid hormone PTHrP PTH-related peptide PUJ pelvic–ureteric junction PUVA psoralen plus ultraviolet A PV per vaginam RA right atrium/rheumatoid arthritis RAST radioallergosorbent test RBBB right bundle branch block RBC red blood cell RCC renal cell carcinoma RDS respiratory distress syndrome Rh rhesus RhF rheumatoid factor RIF right iliac fossa RPOC retained products of conception RR respiration rate RSV respiratory syncytial virus RT radiotherapy RUQ right upper quadrant RV right ventricle SAH subarachnoid haemorrhage SALT speech and language therapy SBE subacute bacterial endocarditis SCC squamous cell carcinoma SCID severe combined immunodeficiency SCLC small cell lung carcinoma SeHCAT selenium-75-homocholic acid taurine SFH symphysis–fundal height SGA small for gestational age SIADH syndrome of inappropriate antidiuretic hormone SLE systemic lupus erythematosus SMR standardised mortality ratio SOB shortness of breath SPECT single photon emission computed tomography SSRI selective serotonin reuptake inhibitor STD sexually transmitted disease STEMI ST-elevation myocardial infarction STI sexually transmitted infection SVC superior vena cava T3 tri-iodothyronine T4 thyroxine TAH total abdominal hysterectomy TB tuberculosis TCC transitional cell carcinoma  Abbreviations xxiii TED thromboembolic deterrent TFT thyroid function tests TIA transient ischaemic attack TIBC total iron binding capacity TIPS transjugular intrahepatic portosystemic shunt TJ transjugular TNF-a tissue necrosis factor-a TNM tumour, node, metastasis TOP termination of pregnancy TPHA Treponema pallidum haemagglutination assay TPN total parenteral nutrition TSH thyroid-stimulating hormone TT thrombin time tTG tissue transglutaminase TURP trans-urethral resection of the prostate TVUSS transvaginal ultrasound scan UDCA ursodeoxycholic acid U&E urea and electrolytes URTI upper respiratory tract infection USS ultrasound scan UTI urinary tract infection UVB ultraviolet B VATS video-assisted thoracic surgery VDRL venereal diseases research laboratory VF ventricular fibrillation VIP vasoactive intestinal peptide V /Q ventilation–perfusion VRE vancomycin-resistant enterococcus VSD ventricular septal defect VT ventricular tachycardia VTE venous thromboembolism VUJ vesico–ureteric junction VZV varicella zoster virus vWF von Willebrand factor WBC white blood cell WCC white cell count WLE wide local excision WPW Wolff–Parkinson–White syndrome This page intentionally left blank  C H A P T E R 1 Medicine Nisha Patel, Alexandra Kent and Natasha Patel Cardiology 1 Endocrinology 63 Respiratory 14 Rheumatology 73 Gastroenterology 29 Haematology 84 Hepatology 35 Infectious diseases 94 Neurology 45 Dermatology 99 Nephrology 57 CARDIOLOGY CARDIAC INVESTIGATIONS ECG (electrocardiography): records cardiac electrical activity Echocardiography (echo): ultrasound imaging of the heart which provides an impression of cardiac chambers, valvular heart disease, the pericardium, great vessels and masses. Transthoracic echo is quick and easy to perform, but trans-oesophageal echo gives more detailed images, particularly of the posterior structures Doppler echocardiography: Doppler studies measure the velocity and direction of red blood flow, and are useful for assessing flow across valves, through the great vessels and through cardiac chambers Stress echocardiography: echo is done at baseline, then immediately after exercise or dobutamine infusion (which increases myocardial oxygen demand); systolic function and regional wall motion abnormalities are recorded to assess for myocardial ischaemia Nuclear imaging: thallium or technetium-labelled compounds can be used to assess ventricular function and myocardial ischaemia; at rest and during stress; SPECT (single photon emission computed tomography) and PET (positron emission tomography) are being increasingly used MRI (magnetic resonance imaging)/CT (computed tomography): used to define anatomy; useful in congenital heart disease, tumours, pericardial disease; MRA (MR angiography) can be used to assess the aorta, large vessels and myocardial perfusion, CT calcium Cardiac catheterization: involves passage of a catheter from a peripheral artery into the heart for pressure measurements or injection of a contrast agent; angiography can assess the left ventricle, coronary arteries and aorta; allows for balloon angioplasty or stent insertion 2 M e di c i ne HEART FAILURE (HF) P Occurs when the heart is unable to pump blood at a rate required by metabolizing tissues A Ischaemic, valvular, hypertensive or congenital heart disease, cardiomyopathy, myocarditis, endocarditis, pulmonary embolism (PE) Precipitating factors: myocardial infarction, infection, arrhythmia, anaemia, thyrotoxicosis, electrolyte disturbance, PE, pregnancy, vitamin deficiencies such as beriberi. S Left-sided heart failure (HF): dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, fatigue, lung crepitations, pleural effusions, cyanosis Right-sided HF: peripheral oedema, abdominal distension/ascites, tender pulsatile hepatomegaly, ≠ jugular venous pressure (JVP), hepatojugular reflux Severe HF: reduced pulse pressure, hypotension, cool peripheries, 3rd ± 4th heart sounds, gallop rhythm Ix Full blood count (FBC), urea and electrolytes (U&E), liver function tests (LFT), lipid profile, thyroid function tests (TFT), glucose, cardiac enzymes, ECG, chest X-ray (CXR), echo with colour Doppler studies Rx Treat any risk factor (cholesterol reduction, glycaemic control, weight loss, smoking cessation etc.); remove any precipitant Diuretics, angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers, b-blockers, digoxin, glyceryl trinitrate (GTN) infusion ISCHAEMIC HEART DISEASE P Ischaemia occurs whenever there is an imbalance between oxygen delivery and oxygen demand; the commonest lesion is the atherosclerotic plaque Ischaemia can also occur when coronary blood flow is limited – rupture of the atherosclerotic plaque, coronary spasm, emboli, aortic stenosis with left ventricular (LV) hypertrophy It can be precipitated by severe anaemia (due to Ø oxygen-carrying capacity of the blood) and fluid overload A Obesity, smoking, insulin resistance/Type 2 diabetes mellitus, high-fat diet, hypertension, high cholesterol/low-density lipoprotein (LDL) Ischaemic heart disease (IHD) is the most common cause of death in the developed world ACUTE CORONARY SYNDROME (ACS) This encompasses angina, unstable angina and non-ST-elevation myocardial infarction (NSTEMI) S Central crushing chest pain, ± radiation to neck and left arm, sweating, dyspnoea, pallor, palpitations Ix FBC, U&E, glucose, lipids, cardiac enzymes (troponin, creatinine kinase), CXR, ECG (T wave inversion, ST depression), exercise testing, stress echo/nuclear imaging if patient unable to exercise, ± coronary angiography Rx Acute presentation: oxygen, GTN spray, aspirin, clopidogrel, morphine sulphate, low molecular weight heparin (LMWH), ± GTN infusion, glycoprotein IIb/IIIa inhibitors (e.g. tirofiban)  Ca r d i o l o g y 3 Long term treatment: nitrates, b-blockers, calcium channel antagonists, aspirin, clopidogrel (for up to 1 year following non-ST elevation myocardial infarction [MI]), nicorandil; coronary revascularization Box 1.1 GRADING OF ANGINA I angina on strenuous or prolonged exertion II slight limitation of ordinary activity; angina on moderate activity III marked limitation of ordinary activity; angina on mild activity IV unable to carry out activities without angina; may occur at rest Source: Campeau L. Grading of angina pectoris [letter]. Circulation 1976;54:522–3 (reproduced with kind permission by the Canadian Cardiovascular Society) ST-ELEVATION MYOCARDIAL INFARCTION (STEMI) P Usually occurs due to atherosclerotic plaque rupture, leading to thrombosis formation, and coronary artery occlusion Sy Similar to that of ACS, but more severe Ix As for ACS; ECG will show ST segment elevation and Q waves evolve Echo will indicate myocardial damage with abnormal wall motion Rx Acute presentation: oxygen, GTN spray, aspirin, clopidogrel, primary percutaneous transluminal coronary angioplasty (PTCA), fibrinolysis (if PTCA not available) Long term management: b-blockers, ACE inhibitors, aspirin, statins Cx Heart failure, cardiogenic shock, arrhythmias, pericarditis, ventricular septal rupture, recurrent pain, LV aneurysm HYPERTENSION P Defined as blood pressure >140/90 mmHg Box 1.2 CLASSIFICATION OF HYPERTENSION Essential hypertension: arterial hypertension with no specific cause; >90 per cent of cases Secondary hypertension: due to conditions including: – endocrine disorders Cushing’s syndrome phaeochromocytoma acromegaly Conn’s syndrome thyrotoxicosis – renal disease chronic renal failure renal artery stenosis – acute porphyria – coarctation of the aorta – iatrogenic ciclosporin contraceptives steroids 4 M e di c i ne A Obesity, salt intake, alcohol, diabetes mellitus, genetic inheritance Sy Headaches, dizziness, blurred vision, epistaxis, angina, syncope, signs of heart failure ± symptoms related to underlying causes Si LV heave, 4th heart sound ± 3rd heart sound, hypertensive retinopathy, carotid/ renal bruits Ix FBC, U&E, fasting glucose and lipid profile, haemoglobin A1c (HbA1c), urine for sugar/protein/blood/creatinine clearance, ECG (LV hypertrophy ± strain), CXR Other investigations would be to rule out secondary causes, e.g. calcium, TFT, cortisol, dexamethasone suppression test (Cushing’s), 24-h urine for hydroxyindoleacetic acid (HIAA) (carcinoid)/catecholamines (phaeochromocytoma), aldosterone:renin ratio (Conn’s syndrome), renal Doppler flow studies, renal MRA (renal artery stenosis) Rx Lifestyle: weight loss, salt restriction, stop smoking, reduce alcohol intake, optimize glycaemic control Medical: diuretics, ACE inhibitors, angiotensin receptor antagonists, calcium channel blockers, b-blockers Cx Atherosclerosis, heart failure, cerebral infarct, cerebral haemorrhage, renal impairment MALIGNANT HYPERTENSION This is a medical emergency. P Fibrinoid necrosis of small arteries/arterioles and dilatation of cerebral arteries A ♂ >♀; usually in 5th decade S Headache, vomiting, visual disturbance, convulsions, papilloedema Rx Intravenous labetalol/GTN, bring blood pressure (BP) down slowly Cx Microangiopathic haemolytic anaemia, renal failure, cerebral haemorrhage, coma, death ARRHYTHMIAS ATRIAL FIBRILLATION (AF) P Disorganized atrial activity, resulting in an irregular ventricular response A See Box 1.3. Box 1.3 CAUSES OF ATRIAL FIBRILLATION Ischaemic heart disease Hypercapnia Lung disease Alcohol Hypoxia Mitral stenosis Hypertension Atrial septal defect Rheumatic heart disease Metabolic abnormalities Sepsis Thyrotoxicosis Sy Palpitations, dizziness, shortness of breath (SOB) and heart failure Si Irregularly irregular pulse, with or without haemodynamic compromise Ix ECG, investigations into the underlying cause  Ca r d i o l o g y 5 Figure 1.1 Atrial fibrillation: note the absence of P waves and irregularly irregular rhythm Rx Treatment of underlying cause; rate control (digoxin, b-blockers, diltiazem), anti-arrhythmics (amiodarone, flecainide), anticoagulation (warfarin/heparin), DC cardioversion to return to sinus rhythm Cx Systemic embolization, rapid ventricular rate leading to hypotension/angina/heart failure ATRIAL FLUTTER P Atrial re-entry tachycardia, leading to rapid atrial rate (~300 beats/min); usually occurs with slower ventricular rate due to 2:1 or 3:1 block in the atrioventricular (AV) node A Acute cardiac or respiratory problems e.g. pericarditis, pneumonia Sy Palpitations, dizziness and heart failure Si Tachycardia, with or without haemodynamic compromise Ix ECG: usually reveals characteristic saw-tooth pattern with AV block Rx Rate control: anti-arrhythmics, anticoagulation Curative: DC cardioversion, catheter ablation of aberrant pathway Flutter waves Figure 1.2 Atrial flutter: note the characteristic ‘F’ waves WOLFF–PARKINSON–WHITE SYNDROME (WPW) P Atrial re-entry tachycardia, with an accessory excitatory pathway linking the atrium to the ventricle (bundle of Kent) A Idiopathic Sy Palpitations, dizziness and collapse Si Tachycardia Ix ECG: short PR interval, delta wave (slurred upstroke to QRS), wide QRS Rx DC cardioversion, b-blockers, calcium-channel blockers, catheter ablation Cx Rarely may progress to ventricular fibrillation (VF) 6 M e di c i ne Figure 1.3 Wolff–Parkinson–White syndrome: note the short PR interval and slurred upstroke to the QRS complex VENTRICULAR TACHYCARDIA (VT) P Sustained VT is VT that lasts for >30 s or causes haemodynamic compromise A Most commonly due to ischaemic heart disease ± MI; cardiomyopathy, metabolic abnormalities, drug toxicity, long QT syndrome Sy Palpitations, chest pain, syncope Si Tachycardia with hypotension, varying 1st heart sound, occasional cannon waves (giant ‘a’ waves in JVP) Ix ECG (wide complex tachycardia) Rx Anti-arrhythmics (amiodarone, lidocaine), DC cardioversion, implantable cardiac defibrillator to treat recurrence Cx VF Figure 1.4 Ventricular tachycardia VENTRICULAR FIBRILLATION A Ischaemic heart disease, post-infarction, torsades de pointes, prolonged QT interval, severe hypoxia; VT can always degenerate into VF S Syncope, cardiac arrest Ix ECG/heart monitor Rx DC cardioversion, anti-arrhythmics, intravenous magnesium, cardiac pacing, implanted cardiac defibrillator Cx Death Figure 1.5 Ventricular fibrillation  Ca r d i o l o g y 7 ATRIOVENTRICULAR BLOCK (AVB) P Due to damage to the atrial node, AV node or His/Purkinje system A Myocardial infarction, drugs (digitalis, calcium channel blockers, b-blockers), myocarditis, acute rheumatic fever, sarcoid, infections (e.g. Lyme disease) Box 1.4 CLASSIFICATION OF AV BLOCK 1st degree AVB: PR interval >0.20 s (five small squares on ECG) 2nd degree AVB: some atrial impulses fail to conduct to the ventricles – Mobitz Type I (Wenckebach): the PR interval gradually increases in length until there is a ‘missed beat’ – Mobitz Type II: occasional dropped QRS complexes are not related to changes in the PR interval 3rd degree AVB: atrial and ventricular impulses are completely dissociated 1st degree heart block (a) Mobitz Type I 2nd degree heart block (b) Mobitz Type II 2nd degree heart block (c) 3rd degree heart block (d) Figure 1.6 (a) 1st degree heart block: prolonged PR interval; (b) Mobitz Type I 2nd degree heart block: progressive PR elongation; (c) Mobitz Type II 2nd degree heart block: fixed PR interval, with occasional P waves not being conducted to the ventricles; (d) 3rd degree AV block, there is no relationship between atrial and ventricular activity. The wide QRS complex is the result of a spontaneous escape rhythm of 35–40 beats/min S Syncope, dyspnoea, heart failure Ix ECG, cardiac monitoring Rx Atropine, isoprenaline (b-agonist); any patients with symptomatic 2nd or 3rd degree heart block should have cardiac pacing 8 M e di c i ne VALVULAR HEART DISEASE AORTIC STENOSIS P A pressure gradient between the LV and aorta >50mmHg or aortic orifice 么; idiopathic, rheumatic heart disease, ischaemic heart disease, cardiomyopathy, connective tissue disorders, e.g. Marfan’s syndrome, Ehlers– Danlos syndrome Sy May be asymptomatic; palpitations, syncope, chest pain, sudden death (rare) Si Arrhythmias, mid-late systolic click, high pitched late-systolic murmur Ix ECG, echo Rx Medical: aimed at symptoms: anti-arrhythmics, antibiotic prophylaxis, b-blockers for chest pain Surgery: Mitral valve repair/replacement if MR is a problem Cx MR, infective endocarditis PULMONARY STENOSIS P Outflow obstruction may be valvular, subvalvular or supravalvular; transvalvular gradient grades the severity: 80 mmHg: severe A Congenital, associated with carcinoid syndrome Sy Asymptomatic; fatigue, dyspnoea, syncope, symptoms associated with heart failure Si a wave in the JVP, soft P2, 4th heart sound, left parasternal heave, thrill and ejection systolic murmur (left upper sternal border), increasing severity leads to a longer murmur, Ix ECG (right axis deviation and RV hypertrophy), CXR (large left atrium), echo Rx Balloon valvuloplasty; valve replacement rarely indicated TRICUSPID REGURGITATION P Usually functional: due to dilatation of the tricuspid annulus following right ventricular dilatation A Functional (pulmonary hypertension, CCF, cardiomyopathy), rheumatic, tricuspid valve endocarditis, carcinoid, trauma, post-infarction, endomyocardial fibrosis Sy Clinical features are due to venous congestion and reduced cardiac output Si ≠ JVP with prominent v waves, pansystolic murmur heard best at left lower sternal edge, pulsatile hepatomegaly, peripheral oedema, ascites, dyspnoea Ix ECG, CXR (enlarged RA and RV), echo Rx Aimed at underlying cause or surgery CONGENITAL HEART DISEASE ATRIAL SEPTAL DEFECT P Ostium primum: septal defect lies adjacent to AV valve Ostium secundum: mid-septum; 70 per cent of cases Sinus venosus: high in septum, near superior vena cava (SVC) A Congenital; 乆 > 么; Down syndrome associated with ostium primum Sy Usually asymptomatic until adulthood; palpitations (arrhythmias), dyspnoea, cyanosis  Ca r d i o l o g y 11 Si Left parasternal heave, wide fixed splitting of 2nd heart sound, mid-systolic murmur at left sternal edge (due to increased flow across the pulmonary valve), cyanosis, clubbing, occasional mid-diastolic murmur Ix ECG (ostium primum: left axis deviation, ostium secundum: right axis deviation, right bundle branch block (RBBB); RV or RA hypertrophy), CXR (large hilar arteries, enlarged RV and RA, increased pulmonary vasculature), echo Rx Small atrial septal defect (ASD) with minimum left-to-right shunts can be left; surgical closure Cx Arrhythmias VENTRICULAR SEPTAL DEFECT P Usually in the membranous portion of the septum A Congenital, post-infarction; commonest congenital anomaly; incidence ~0.2 per cent births; associated with Fallot’s tetralogy Sy Usually develop with reversal of the shunt; dyspnoea, chest pain, syncope, haemoptysis Si Cyanosis, clubbing, loud pansystolic murmur Ix Echo Rx Spontaneous closure occurs in ~50 per cent small ventricular septal defects (VSDs); surgical correction when there is a moderate/large left-to-right shunt Cx Congestive cardiac failure (CCF), pulmonary hypertension and reversal of shunt, RV outflow tract obstruction, aortic regurgitation, infective endocarditis INFECTIVE/INFLAMMATORY CONDITIONS PERICARDITIS P Inflammation of the pericardium A Viral, post-MI, uraemia, tuberculosis, rheumatic fever, connective tissue disorders, malignancy Sy Substernal sharp chest pain, worse on movement and inspiration; relieved by sitting forward and worse on lying flat Si Pericardial friction rub, fever Ix ECG (widespread ST elevation, concave in shape, followed by T wave inversion) Rx Non-steroidal anti-inflammatory drugs (NSAIDs) for pain; treatment of underlying condition (a) (b) Figure 1.8 (a) Pericarditis. Note the concave ST elevation, compared with myocardial infarction (b) 12 M e di c i ne MYOCARDITIS A Infection, drugs, radiation; commonest cause is viruses – Coxsackie Sy Variable; may be asymptomatic, chest pain, heart failure, palpitations, death Si Often normal; occasionally 3rd heart sound, pansystolic murmur (MR) Ix ECG (T wave or ST changes), viral screen (stool samples, throat swab, nasopharyngeal washings etc.), cardiac enzymes, echo Rx Usually self-limiting; treatment aimed at symptoms/complications; patients rarely require intensive therapy unit (ITU)/cardiac transplantation Cx Chronic myocarditis, dilated cardiomyopathy, heart failure INFECTIVE ENDOCARDITIS P Infection of the endothelium; usually involves the valves; vegetations are a mixture of bacteria, fibrin and platelets A Intravenous drug use (IVDU), prosthetic valves, sporadic Bacteria involved: ~10 per cent no causative organism, Staphylococcus aureus (IVDU), Streptococci, Enterococci, Gram-negative bacteria, Candida Sy Separated into acute endocarditis (AE), a rapidly progressive illness, and subacute bacterial endocarditis (SBE), a slowly progressive condition Fever, anorexia, weight loss, myalgia Si See Box 1.6 Box 1.6 DIAGNOSIS OF ENDOCARDITIS Duke Criteria: 2 major, 1 major + 3 minor, or 5 minor for diagnosis Major: – blood culture positive for typical organism or persistently positive – evidence of endocardial involvement Minor: – fever – previous heart condition or IVDU – immunological phenomena (due to immune complex deposition): Osler’s nodes (raised tender nodules on finger pulps), Roth spots (small retinal haemorrhages), glomerulonephritis, clubbing, petechiae, arthralgia – vascular phenomena: mycotic aneurysms, Janeway lesions (painless macules on palm), septic emboli, intracranial haemorrhage, visceral infarct, splinter haemorrhages – positive blood culture with atypical bacteria Ix FBC, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), blood cultures (minimum of 3), rheumatoid factor, immune complex titre, ECG, echo (trans-oesophageal echo is more sensitive) Rx Broad-spectrum intravenous antibiotics until culture results available (check hospital policy, but usually i.v. benzylpenicillin + gentamicin); add flucloxacillin in IVDUs Cx Septic emboli, mycotic aneurysms, meningitis, intracranial haemorrhage, emboli, glomerulonephritis  Ca r d i o l o g y 13 MISCELLANEOUS HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY (HOCM) P Left ventricular hypertrophy, especially involving the septum; varying degrees of myocardial fibrosis A ~50 per cent patients have a +ve family history; multiple mutations have been identified; associated with Friedrich’s ataxia Sy Many are asymptomatic; dyspnoea, fatigue, palpitations, angina, syncope, sudden death Si a wave in the JVP, double apical impulse, ejection systolic murmur at lower left sternal border, pansystolic murmur at the apex, 4th heart sound Ix ECG (LV hypertrophy, Q waves, arrhythmias), CXR (increased cardiothoracic ratio [CTR]), echo (asymmetric septal hypertrophy, systolic anterior motion of the mitral valve, small LV cavity with posterior wall motion, MR) Rx b-blockers/verapamil to improve LV function, amiodarone as anti-arrhythmic, surgery (myotomy/myectomy), ethanol injections into the septum (causes partial infarction of the septum), cardiac pacing; avoidance of any drugs that significantly lower the preload Cx Arrhythmias, ischaemia, sudden death ATRIAL MYXOMA P Benign tumour; gelatinous polypoid structure attached to the atrial septum; usually left atrium A 乆 > 么; 3rd–6th decades; most are sporadic; occasionally familial (autosomal dominant) Sy Fever, dyspnoea, weight loss, arthralgia, syncope; can mimic mitral valve disease (stenosis from the tumour prolapsing into the valve, or regurgitation from related valve trauma) Si Loud 1st heart sound, tumour ‘plop’ (a loud 3rd heart sound), clubbing Ix Echo, FBC (anaemia or polycythaemia), ≠ ESR Rx Surgical resection Cx Peripheral or pulmonary emboli 14 M e di c i ne RESPIRATORY RESPIRATORY INVESTIGATIONS Chest radiography (CXR): be careful to look at the apices, behind the heart and costophrenic angles Computed tomography (CT): better at distinguishing between tissue densities and assessing lesions; high-resolution CT shows subtle parenchymal changes useful in the diagnosis of interstitial lung diseases; CT pulmonary angiography (CTPA) can diagnose pulmonary emboli in the segmental and larger pulmonary arteries Ventilation–perfusion scans: albumin labelled with technetium 99m is administered intravenously to FVC demonstrate blood flow, and FEV1 radiolabelled xenon gas is inhaled to demonstrate ventilation. This shows Volume mismatches in ventilation and perfusion, and is commonly used to diagnose pulmonary embolism. Positron emission tomography (PET): used to identify malignant lesions and stage lung cancer. A radiolabelled 1 second Time glucose analogue is injected and is taken up by metabolically active FET malignant cells. Arterial blood gases: for interpretation Normal see ‘Respiratory failure’ section (p. 15) Restrictive PEFR (peak expiratory flow rate): Volume useful in asthma Spirometry: measures inspired and expired gas volume against time: – FEV1 – forced expiratory volume in 1 second – FVC – forced vital capacity (total Time volume exhaled) FEV1 Normal Volume : FVC Obstructive normal range 0.75–0.80 0.80 = restrictive defect FEV1 Sputum: microscopy, culture, Gram stain, Ziehl-Neelsen stain, cytology and sensitivities. Bronchoscopy: allowing direct 0 1 2 3 4 5 visualization of the bronchial tree. Time (seconds) Samples can be taken by biopsy, brushings or broncho-alveolar lavage (BAL). Figure 1.9 Interpretation of spirometry results Video-assisted thoracic surgery (adapted with kind permission from Dakin J, (VATS): a rigid endoscope is passed into Kourteli E and Winter R, Making Sense of the pleura to allow visualization and biopsy Lung Function Tests A Hands-on Guide, of pleural or parenchymal disease and London: Arnold, 2003) pleurodesis.  Respiratory 15 RESPIRATORY FAILURE P Respiration requires the integrated function of the nervous system, airways, alveoli, musculature and vasculature. Failure of any of these can lead to respiratory failure: – Type I respiratory failure: hypoxia with normal partial pressure of carbon dioxide (Pco2) – Type II respiratory failure: hypoxia and hypercapnia A See Fig. 1.10 Hypoxaemia has four causes: – hypoventilation · · – ventilation–perfusion (V/Q) mismatch – shunting – Ø in inspired partial pressure of oxygen (Po2) Rx Management is aimed at the underlying cause: – initial treatment is to administer high-flow oxygen – patients may require assisted ventilation; this can be given as non-invasive posi- tive pressure ventilation (NIPPV) – this can eliminate CO2 (and hence acidosis) – if this fails they will require mechanical ventilation Nervous system sedatives hypothermia brainstem stroke overdoses Airways Vasculature asthma pulmonary COPD embolism tumour pulmonary stricture RESPIRATORY hypertension FAILURE intracardiac shunt Musculature Alveoli sedatives pneumonia myasthenia gravis ARDS Guillain–Barré syndrome pulmonary oedema myopathy pulmonary haemorrhage myositis hypothyroidism Figure 1.10 Respiratory failure ARDS: acute respiratory distress syndrome; COPD: chronic obstructive pulmonary disease 16 M e di c i ne AIRWAYS DISEASE ASTHMA1 P Chronic reversible inflammation of the airways caused by increased sensitivity to various stimuli; leading to variable airway obstruction A Atopy, family history (especially maternal), parental smoking increases the risk of childhood asthma Triggers: dust, emotion, exercise, cold weather, NSAID/b-blockers, etc. Sy None when well Wheeze, cough, dyspnoea, chest tightness, night-time waking Si None when well Tachypnoea, tachycardia, cyanosis, wheeze Diurnal variation Ix FBC (includes eosinophil count), U&E, CRP, PEFR (peak expiratory flow rate) and spirometry: expected >25 per cent variability CXR: if any atypical symptoms or exacerbations (to rule out pneumothorax/infection, etc.) Rx Avoidance of pollutants/allergens/smoking; weight loss in obesity Step 1: short-acting inhaled b-agonist as required Step 2: low-dose steroid inhaler Step 3: long-acting b-agonist and increase to a high-dose steroid inhaler Step 4: increase steroid inhaler further ± leukotriene receptor antagonist/theophyllines Step 5: oral steroids ± immunosuppressants (only under the care of a respiratory physician) Figure 1.11 Management of chronic asthma NB: 1 beware the side-effects of long-term steroids: osteoporosis, diabetes mellitus, hyper- tension, oral candidiasis, easy bruising (see Cushing’s syndrome, p. 66) 2 check inhaler technique – need for a spacer device?  Respiratory 17 Acute asthma This is a medical emergency. Box 1.7 CLASSIFICATION OF ACUTE ASTHMA Moderate exacerbation – PEFR 50–75% predicted/best – Worsening symptoms Severe asthma – PEFR 33–50% predicted/best – Unable to complete sentences in one breath – Exhaustion/poor respiratory effort – Tachycardia (HR >110 beats/min) – Tachypnoea (RR >25 breaths/min) Life-threatening asthma – Silent chest – Po2 2 L for pneumonectomy Radiotherapy (RT): radical RT for inoperable non-SCLC patients Chemotherapy: first-line treatment for SCLC  Gastroenterology 29 Figure 1.20 Pancoast’s tumour at the left apex REFERENCES 1 The British Thoracic Society/Scottish Intercollegiate Guidelines Network British Guideline on the Management of Asthma. Thorax 2003;58(Suppl I). 2 British Thoracic Society Guidelines for the Management of Community Acquired Pneumonia in Adults. Thorax 2001;56(Suppl IV) and 2004 update. 3 British Thoracic Society Guidelines for the Management of Pleural Disease. Thorax 2003;58 (Suppl II). 4 British Thoracic Society and Standards of Care Committee. The diagnosis assessment and treatment of diffuse parenchymal lung disease in adults. Thorax 1999;54:1–28. GASTROENTEROLOGY GASTROINTESTINAL INVESTIGATIONS Iron, folate, calcium: absorbed in proximal small intestine B12: absorbed in the terminal ileum Endoscopy: allows direct visualization of gastrointestinal (GI) tract and therapeutic procedures, OGD (oesophagogastroduodenoscopy)/jejunoscopy/sigmoidoscopy/colonoscopy therapies include variceal banding, injection of bleeding points with sclerosants, dilatation of strictures, stent placement, video capsule endoscopy Contrast studies: (including barium and Gastrografin studies) allow visualization of GI mucosa Urinary d-xylose test: tests carbohydrate absorption; d-xylose is absorbed in proximal small intestine and excreted in the urine, therefore low excretion reflects poor absorption Breath tests (BT): commonly lactose–hydrogen BT (for lactose intolerance) or glucose– hydrogen BT (for bacterial overgrowth) 30 M e di c i ne SeHCAT scan: (selenium-75-homocholic acid taurine) nuclear medicine scan which assesses bile salt malabsorption; radiolabelled bile salts ingested, then scanned at 3 h and 7 days; if 55 years with new-onset dyspepsia, or anyone with alarm symptoms should undergo an OGD and testing for H. pylori; if 40 mmol/L: Hyperbilirubinaemia: Indirect bilirubin is produced as a water-insoluble, albumin- bound form which is conjugated in the liver to form direct bilirubin, a water-soluble form. 36 M e di c i ne Jaundice can be divided into three forms: 1 pre-hepatic: due to haemolysis – LDH:AST ratio >12, no bilirubinuria 2 intrahepatic: hepatocellular damage – LDH:AST ratio 35 30–35 250/mm3), respiratory compromise, hernia, compression of renal vein/IVC (inferior vena cava), hepatorenal syndrome, encephalopathy, electrolyte disturbance Rx Fluid restriction, salt restriction, diuretics, paracentesis, TIPS (transjugular intrahepatic portosystemic shunt, see Information Box, p. 39) VITAMIN DEFICIENCY Typically B vitamins (especially thiamine) COAGULOPATHY IMPAIRED IMMUNE SYSTEM VARICES P Portal hypertension leads to the formation of collateral circulations; occur when portal pressure exceeds 12 mmHg Rx Acute variceal bleed: ABC, fluid resuscitation, endoscopic treatment (sclerosant, band ligation), balloon tamponade (Sengstaken–Blakemore tube), terlipressin, antibiotics Prevention: b-blockers (propranolol), endoscopic screening, TIPS, liver transplantation 38 M e di c i ne HEPATORENAL SYNDROME Renal failure in the presence of severe liver disease, where all other causes have been excluded HEPATOCELLULAR CARCINOMA (HCC) Cirrhosis is found in 65–90 per cent of patients with HCC ALCOHOLISM P Steatosis, fibrosis, cirrhosis A Degree of liver damage dependent on genetic susceptibility and coexisting liver disease; women progress to cirrhosis faster S CAGE questionnaire: – do you feel you should Cut down your alcohol consumption? – do you feel Annoyed when people criticize your drinking? – do you feel Guilty? – do you ever drink first thing in the morning – an Eye-opener? Otherwise, the symptoms/signs depend on the degree of liver damage Ix As for cirrhosis: LFT (≠ GGT), Ø albumin, coagulation, FBC: ≠ MCV (mean corpuscular volume), Ø platelets, U&E, ≠ IgA, ≠ cholesterol; USS; liver biopsy will give the exact degree of damage, but is not required for diagnosis Rx Abstinence, nutrition, vitamin replacement, laxatives, liver transplantation ACUTE ALCOHOLIC HEPATITIS S Fever, nausea, RUQ (right upper quadrant) pain, jaundice, ascites, oedema, encephalopathy Rx All the above measures ± steroids/pentoxifylline Px Mortality rate ~10 per cent HEPATIC FAILURE There are three types of acute liver failure: 1. hyperacute or fulminant liver failure – encephalopathy develops within 1 week 2. acute liver failure – encephalopathy develops within 2–4 weeks 3. subacute liver failure – encephalopathy develops within 4–8 weeks. P Acute necrotizing hepatitis leading to cell destruction A Viral hepatitis, infections (viral, bacterial, parasitic), drugs, toxins, alcohol, ischaemic, complications associated with pregnancy, malignancy Sy Lethargy, weakness, nausea, anorexia, sleep disturbance Si Jaundice, fever, fetor hepaticus, encephalopathy, cerebral oedema leading to bradycardia, hypertension, tachypnoea Ix Liver screen to look for an underlying cause; poor prognostic indicators include: ≠ bilirubin, severe hyponatraemia, rising lactate, acidosis, rapid drop in transaminases, renal failure Cx Renal failure, coagulopathy, respiratory failure, sepsis, circulatory failure, hypoglycaemia, pancreatitis Rx Supportive treatment in an intensive care setting; liver transplantation  Hepatology 39 BUDD–CHIARI SYNDROME P Hepatic venous outflow obstruction; this leads to increased hepatic sinusoidal pressure and portal hypertension A Hypercoagulable states; myeloproliferative disorders are the most common cause S Depends on speed of onset; abdominal pain, hepatomegaly, ascites; varices and splenomegaly can be seen in the chronic form; nausea and jaundice in the acute form Ix ≠≠ ALT/AST, ≠ ALP/bilirubin, Ø albumin, USS with Doppler studies of the hepatic vein, CT/MRI Rx Anticoagulation Ascites is controlled with sodium restriction and diuretics ± paracentesis Thrombolysis, angioplasty, TIPS, liver transplant INFORMATION BOX: TIPS A Transjugular Intrahepatic Portosystemic Shunt is a procedure performed by a radiologist whereby a connection is made between the portal vein and the hepatic vein via a catheter introduced into the jugular vein. This aims to reduce the portal hypertension causing some of the symptoms of liver disease, but can precipitate encephalopathy. VIRAL HEPATITIS HEPATITIS A VIRUS (HAV) P RNA virus; transmitted by faecal-oral route. Does not cause cirrhosis A Poor hygiene correlates with increased risk Sy Nausea, anorexia, vomiting, diarrhoea, weakness, fever, malaise, arthralgia, dark urine Si Jaundice, hepatomegaly, splenomegaly, lymphadenopathy Ix LFT: raised transaminases and bilirubin, HAV IgM (immunoglobulin M) Rx Supportive HEPATITIS B VIRUS (HBV) P DNA virus A Parenteral, sexual, vertical transmission Sy Similar to hepatitis A, but often more severe; often found on antenatal testing Si Jaundice, pruritus, tender hepatomegaly, lymphadenopathy, splenomegaly Ix See Box 1.14 Box 1.14 SEROLOGY IN HEPATITIS B INFECTION HBsAg: first serological marker; usually becomes undetectable at 6 months HBsAb: detectable once HBsAg clears; remains indefinitely HBcAg: not detected routinely HBcAb: detectable 1–2 weeks after HBsAg (IgM initially, then IgG) HBeAg: occurs shortly after HBsAg; correlates with viral replication 40 M e di c i ne HBeAb: correlates with lower viral replication and infectivity HBV DNA by PCR (polymerase chain reaction): quantifies viral replication HBsAg, hepatitis B surface antigen; HBsAb, hepatitis B surface antibody; HBcAg, hepatitis B core antigen; HBcAb, hepatitis B core antibody; HBeAg, hepatitis B e antigen, HBeAb, hepatitis B e antibody Rx alcohol avoidance, antivirals e.g. lamivudine, pegylated interferon, adefovir, tenofovir, entecavir, telbivudine, interferon a Cx >90 per cent patients will clear the virus Carrier state: HBsAg persists for >6 months with no signs of acute hepatitis 10–20 per cent of carriers will develop cirrhosis ≠ risk of hepatocellular carcinoma HBeAg anti-HBe HBV DNA JAUNDICE IgM anti-Hbc HBsAg anti-Hbs 0 1 2 3 4 5 6 12 24 Months after infection Figure 1.23 Changes in hepatitis B enzymes after acute infection HEPATITIS C VIRUS (HCV) P RNA virus; six genotypes A Spread parenterally or sporadically Sy Prodromal symptoms usually mild or absent; fatigue may be pronounced Si Jaundice, hepatomegaly Ix HCV antibody, HCV RNA by PCR Rx Antiviral therapy: usually peginterferon a and ribavirin, although many new treatments in development Cx >80 per cent develop chronic HCV infection ~30 per cent develop cirrhosis ≠ risk of hepatocellular carcinoma  Hepatology 41 HEPATITIS D VIRUS (HDV) P RNA virus, dependent on presence of HBV for infectivity A Corresponds to HBV infection S As for HBV Ix HDAg, HDV RNA by PCR Anti-HDV and RNA are markers of replication; persistent HDV antibody is consistent with chronic HDV Rx Treatment is usually supportive; limited response to antivirals Prevention is only by immunity to HBV; HBV carriers should avoid HDV endemic areas Cx As for HBV HEPATITIS E VIRUS (HEV) P RNA virus, faecal–oral transmission S Very similar to hepatitis A Ix HEV antibody, HEV RNA Rx Supportive, prevention by improvements in sanitation Cx Fulminant hepatic failure: 20 per cent incidence in pregnant women AUTOIMMUNE DISEASE AUTOIMMUNE HEPATITIS (AIH) P Periportal piecemeal necrosis/bridging necrosis; fibrosis A More common in young women Sy Fatigue, abdominal discomfort, decreased appetite, myalgia Si Hepatomegaly, icterus, signs of chronic liver disease/cirrhosis Ix Raised transaminases, ≠ ESR, ANA +ve, smooth muscle antibody +ve, anti-LKM (liver, kidney, microsomal antibodies) +ve, ≠ IgG, liver biopsy Rx Steroids, azathioprine, ursodeoxycholic acid (UDCA), liver transplantation PRIMARY BILIARY CIRRHOSIS (PBC) P Chronic inflammation and destruction of the small and medium bile ducts A 80–90 per cent women; age 30–60 years S Fatigue, pruritus, arthralgia, xanthelasma, hepatomegaly, splenomegaly, jaundice, signs of chronic liver disease, osteoporosis Ix cholestatic LFTs; ≠ IgM, antimitochondrial antibody (AMA) +ve (in ~95 per cent), ANA +ve (in ~40 per cent), liver biopsy Rx Pruritus: colestyramine, UDCA, antihistamines Osteoporosis and hypercholesterolaemia: bisphosphonates, statins Immunosuppression: prednisolone, azathioprine Liver transplantation 42 M e di c i ne PRIMARY SCLEROSING CHOLANGITIS (PSC) P Progressive fibrosis and obliteration of the biliary ducts A 70 per cent men; 3rd–5th decade; associated with inflammatory bowel disease (mainly ulcerative colitis) S Can be asymptomatic; fatigue, weight loss, fever, pruritus, RUQ discomfort, hepatomegaly; may have relapsing cholangitis Ix Cholestatic LFTs; pANCA +ve, ANA +ve, ≠ IgM, MRCP/ERCP (endoscopic retrograde cholangiopancreatography), liver biopsy Rx Medical: UDCA, prednisolone and methotrexate Endoscopy: therapeutic ERCP: sphincterotomy/stent insertion Surgery: liver transplantation METABOLIC DISORDERS NON-ALCOHOLIC STEATOHEPATITIS (NASH) P When liver fat content >12 per cent = fatty liver; this can lead to inflammation and fibrosis A 乆>么 Viral hepatitis and autoimmune conditions must be excluded Multiple other causes – commonest are obesity, diabetes and hyperlipidaemia S Often asymptomatic and found after routine blood tests reveal abnormal LFTs, hepatomegaly, fatigue Ix LFT-raised transaminases, liver screen to rule out other causes of liver disease, lipid screen, HbA1c, USS, liver biopsy is diagnostic Rx No specific treatments; aim at removing any causative factors; alcohol abstinence HEREDITARY HAEMOCHROMATOSIS (HHC) P Autosomal recessive mutations in the HFE gene leading to abnormal absorption of iron A 么:乆 ratio = 5–10:1 Si Iron overload in multiple sites throughout the body, leading to a wide variety of signs: hepatomegaly, stigmata of chronic liver disease, ascites, splenomegaly, fatigue, arthralgia, pigmentation Sy Symptoms of cardiomyopathy, diabetes mellitus, hypothyroidism, hypogonadism, hypoparathyroidism, joint pain Ix ≠ ferritin, iron and transferrin saturation; HFE genotyping and family genotyping; raised transaminases, ≠ IgG, USS/CT/MRI, liver biopsy Rx Venesection, desferrioxamine, low iron diet, alcohol abstinence, liver transplantation, screening for HCC Cx HCC, liver failure WILSON’S DISEASE P Autosomal recessive; abnormal hepatobiliary copper excretion S Related to the degree and sites of copper deposition  Hepatology 43 Liver disease fatty liver Æ acute hepatitis Æ chronic acute hepatitis Æ fulminant hepatitis Æ cirrhosis, with symptoms and signs related to the degree of disease Psychiatric Haematological personality change haemolysis behavioural problems SIGNS OF WILSON’S DISEASE Ophthalmic Neurological Kayser–Fleischer rings (copper ataxia deposition in cornea) seizures tremor dysarthria Figure 1.24 Signs of Wilson’s disease Ix ≠ serum free copper and urinary copper, Ø caeruloplasmin, USS, liver biopsy, penicillamine test To assess other organ involvement: slit lamp eye examination, MRI, ECG, echo, EEG, EMG (electromyogram) Rx D-penicillamine (chelates copper), low copper diet, liver transplantation INFECTIONS LIVER ABSCESS P Bacterial, helminthic, fungal or protozoal Spread via blood, post-traumatic, directly or via the biliary tree S Fever, RUQ pain/tenderness, right-sided pleural effusion, septicaemia, rupture Ix FBC, LFT, CRP, ESR, CXR, USS ± CT, angiography is required to assess arterial anatomy pre-operatively, USS/CT-guided aspiration Rx Intravenous antibiotics, aspiration, percutaneous drainage, surgery 44 M e di c i ne HYDATID DISEASE P Majority due to Echinococcus cysticus, a tapeworm; commonly found in areas of cattle breeding; spread via faecal–oral route Larvae travel to the portal system via the intestine and form fluid-filled cysts (hydatids) in the liver; these can grow up to 1 cm/year Sy RUQ pain once the cyst is large enough Si Hepatomegaly due to hydatid growth Ix Eosinophilia, LFT, serology, USS Rx ~10 per cent spontaneously regress; surgical removal, mebendazole/albendazole Cx Rupture of the hydatid will cause an anaphylactic reaction Figure 1.25 Hydatid cyst: a well-delineated multiloculated cystic mass, with orderly internal septations (daughter cysts), in the right lobe of the liver HEPATIC TUMOURS HEPATIC ADENOMA P Vary in size and number, usually solitary and found in the right lobe A Found in women in their reproductive years; often associated with oral contraceptives S Usually asymptomatic and found by chance; if large, they may be associated with abdominal discomfort; haemorrhage: severe pain Ix LFTs normal; USS, CT, MRI, liver biopsy Rx Embolization, surgery HEPATOCELLULAR CARCINOMA (HCC) A Affects all age groups; slight increased incidence in men (ratio 2–3:1) Liver disease: cirrhosis, HBV, HCV, HDV, haemochromatosis, a1-antitrypsin deficiency, autoimmune hepatitis, PBC Alcohol, smoking; drugs, genetics  Neurology 45 Sy Weight loss, anorexia, abdominal pain Si Cachexia, hepatomegaly, fever, lymphadenopathy Metastases may also add to the symptoms and signs: lungs, bone, lymph nodes Ix Raised transaminases, ≠ alpha-fetoprotein, CRP and ESR may be raised; there may be cholestasis if the tumour affects the intrahepatic bile ducts; USS (microbubble contrast), CT, MRI; liver biopsy (only if diagnosis is in question, as the procedure may cause tumour spread) Rx Resection, liver transplant, chemoembolization, ethanol injection, laser ablation Figure 1.26 Hepatocellular carcinoma: localized poorly marginated mixed density area in the right lobe of the liver NEUROLOGY NEUROLOGY INVESTIGATIONS CT: study of choice in acute trauma and haemorrhage; usually given with contrast to help enhance tumours, infections and infarcts MRI: T1-weighted images enhance acute haemorrhage; T2-weighted images enhance oedema, infarction, demyelination and chronic haemorrhage Angiography can also be performed with or without contrast EEG: electrodes are placed on the scalp and electrical activity of the brain is recorded; particularly important in evaluating epilepsy Evoked potentials: electrical potentials are measured while nerves are repetitively stimulated; the commonest use is in visual evoked potentials to diagnose multiple sclerosis Nerve conduction studies: nerves are stimulated and the electrical activity is measured from different points; conduction velocity can be recorded EMG: electromyography records electrical potentials from needle electrodes in muscle at rest and during contraction; this can differentiate between neuropathic and myopathic disorders Lumbar puncture: cerebrospinal fluid (CSF) is taken via a needle inserted into the spinal column between L3/4 or L4/5 Tensilon test: a short-acting anticholinesterase (edrophonium) is given intravenously to see if there is any improvement in those with suspected myasthenia gravis 46 M e di c i ne ISCHAEMIA CEREBROVASCULAR DISEASE/ISCHAEMIC STROKE P Acute occlusion of an intracranial vessel leading to hypoxia and infarction; if blood flow is restored prior to significant cell death there may be transient symptoms: transient ischaemic attack (TIA) A Diabetes mellitus, hypertension, smoking, hypercholesterolaemia, family history, age, atrial fibrillation, valvular lesions, cardiac congenital defects, hypercoagulable states, vasculitis S Symptoms are variable and dependent on the area and arteries involved; Box 1.15 gives an idea of symptoms related to territories. Box 1.15 SYMPTOMS OF CEREBROVASCULAR DISEASE ACCORDING TO TERRITORIES Anterior cerebral artery occlusion Contralateral hemiplegia Gait apraxia Abulia (severe apathy) Urinary incontinence Lower limb sensory loss Middle cerebral artery occlusion Contralateral hemiplegia Homonymous hemianopia Contralateral sensory loss Dysarthria, dysphasia Non-dominant symptoms include: – Aphasia – Neglect – Constructional apraxia Posterior cerebral artery occlusion Homonymous hemianopia ± macular sparing Contralateral hemiplegia Ataxia/hemiballismus Visual agnosia Cortical blindness Posterior inferior cerebellar artery (PICA) occlusion Syncope Vertigo Hemiplegia Dysarthria Ipsilateral face numbness Contralateral limb numbness Basilar artery occlusion Dizziness Vertigo Diplopia Dysarthria Facial numbness Ipsilateral hemiparesis  Neurology 47 Ix FBC, U&E, lipids, ESR, CRP, fasting glucose CT, MRI with diffusion- weighted imaging (DWI), MR angiography, carotid dopplers, echo, ECG, 24-hour tape Rx Medical: aspirin, clopidogrel, dipyridamole, anticoagulation Thrombolysis is not yet in widespread use Collateral blood flow is blood pressure dependent, therefore BP should not be lowered unless there are signs of malignant hypertension Surgery: carotid endarterectomy Figure 1.27 Large left posterior cerebral artery infarct CEREBELLAR SYNDROME A Vascular lesion, alcohol, demyelination, tumours, paraneoplastic phenomenon, hypothyroidism, phenytoin toxicity, metabolic disorders (e.g. Wilson’s disease) Sy Poor balance, dysphasia Si ‘DANISH’, see Box 1.16 Box 1.16 FEATURES OF CEREBELLAR SYNDROMES Dysdiadochokinesis Ataxia Nystagmus Intention tremor, past pointing Scanning speech, dysarthria Hypotonia, hyporeflexia Ix MRI Rx Treatment aimed at underlying disorder INFECTION MENINGITIS P Infection of the meninges; commonest pathogen is Streptococcus pneumoniae; other bacterial pathogens include Neisseria meningitidis, Haemophilus influenzae, Listeria monocytogenes and Mycobacterium tuberculosis Can also be caused by viruses and fungal infection A Higher risk in immunosuppressed individuals 48 M e di c i ne Sy Headache, photophobia, nausea, vomiting, neck pain Si Fever, neck stiffness, confusion, drowsiness, petechiae, Kernig’s sign (hamstring spasm when attempting to straighten leg) Ix FBC, U&E, LFT, coagulation, blood cultures, CXR, lumbar puncture (LP). NB do not perform LP if patient has a petechial rash, without the results of clotting profile (need to exclude DIC [disseminated intravascular coagulation]); if there are any neurological signs or conscious level is reduced, perform a CT head prior to LP (? brain abscess) CSF samples can also be sent for PCR to identify meningococcus, AFB and viruses Table 1.4 Lumbar puncture results Neutrophils Lymphocytes Protein Glucose (¥106/L) (¥106/L) (g/L) (ratio CSF/ serum) Normal 0 1.0 1.0 left side Triggers include talking, chewing, smiling, brushing teeth, touching the face, or swallowing 52 M e di c i ne Attacks recur at varying intervals (up to hundreds per day) and last for days, weeks, or months at a time, and then remit for months or years Attacks rarely occur during sleep Si Neurological examination is normal Ix No specific investigation required as diagnosis is clinical; if any neurological deficits are present trigeminal neuralgia is unlikely and brain imaging should be performed Rx Anticonvulsants (carbamazepine, gabapentin); neurosurgical treatment may be required if medical treatment fails PUPILLARY ABNORMALITIES HORNER’S SYNDROME/PTOSIS P Interrupted sympathetic innervation to the eye, at any level from a central lesion to the post-ganglionic fibres A Central lesions: basal meningitis, demyelinating disease, cerebrovascular accident (CVA), basal skull tumours, pituitary tumour, intrapontine haemorrhage, neck trauma, syringomyelia Preganglionic lesions: Pancoast’s tumour, cervical rib, aneurysm/dissection of aorta, trauma/surgical injury, lesions of the middle ear, neuroblastoma