(BQ) Part 1 book Essentials of Kumar and Clark''s clinical medicine presents the following contents: Ethics and communication, infectious diseases, gastroenterology and nutrition; liver, biliary tract and pancreatic disease; haematological disease, malignant disease, rheumatology, water, electrolytes and acid–base balance.
Medical emergencies Numbers refer to pages in text SYMPTOM BASED Acute chest pain 395 Acute breathlessness 488 Coma 720 Delirium (toxic confusional state) 779 Fever in the returned traveller 22 Headache 695 Shock 552 SYSTEM BASED Infectious diseases and tropical medicine Septicaemia 12 Fever in the returned traveller 22 Malaria 24 Gastroenterology and nutrition Oesophageal perforation 000 Acute upper gastrointestinal bleeding 82 Lower gastrointestinal bleeding 000 Intestinal ischaemia 000 Acute severe colitis 101 The acute abdomen 115 Liver, biliary tract and pancreatic disease Fulminant hepatic failure 144 Bleeding oesophageal varices 150 Acute cholecystitis 000 Acute cholangitis 000 Acute pancreatitis 175 Diseases of the blood and haematological malignancies Fever in the neutropenic patient 196 Sickle cell crisis 204 Warfarin excess 000 Malignant disease 000 Superior vena cava syndrome 000 Acute tumour lysis syndrome 000 Spinal cord compression 764 Fever in the neutropenic patient 196 Hypercalcaemia 633 Rheumatology Septic arthritis 277 Acute monoarthritis 278 Giant cell arteritis 762 Water and electrolytes Hyponatraemia 317 Hypernatraemia 321 Hypokalaemia 322 Hyperkalaemia 324 Hypomagnesaemia 000 Hypermagnesaemia 000 Disorders of acid–base balance 327 Renal disease 000 Renal colic 364 Acute renal failure/kidney injury 369 Cardiovascular disease Acute chest pain 395 Cardiac arrhythmias 408 Cardiac arrest 421 Acute heart failure 432 Acute coronary syndrome 439 ST elevation myocardial infarction 442 Pulmonary embolism 466 Pericardial tamponade 474 Severe hypertension 482 Ruptured abdominal aortic aneurysm 482 Aortic dissection 483 Deep venous thrombosis 000 Respiratory disease Acute breathlessness 000 Massive haemoptysis 489 Inhaled foreign body 496 Acute exacerbation of chronic obstructive airways disease 501 Acute severe asthma 514 Pneumonia 515 Pneumothorax 546 Intensive care medicine Shock 552 Anaphylaxis 552 Sepsis 000 Respiratory failure 563 Poisoning, drug and alcohol abuse Drug overdose 569 Wernicke–Korsakoff syndrome 584 Alcohol withdrawal 585 Delirium tremens 586 Endocrinology Myxoedema coma 612 Thyroid crisis 613 Addisonian crisis 622 Syndrome of inappropriate ADH secretion 629 Hypercalcaemia 633 Hypocalcaemia 636 Hypophosphataemia 000 Hypothermia 644 Hyperthermia 646 Diabetes mellitus and other disorders of metabolism Hypoglycaemia 657 Diabetic ketoacidosis 658 Hyperosmolar hyperglycaemic state 660 The special senses Epistaxis 000 Stridor 687 The red eye 687 Sudden loss of vision 690 Neurology Headache 695 Coma 720 Transient ischaemic attack 000 Stroke 725 Intracranial haemorrhage 733 Status epilepticus 740 Meningitis 750 Encephalitis 000 Giant cell arteritis (temporal arteritis) 762 Spinal cord compression 764 Guillain–Barré syndrome 000 Delirium (toxic confusional state) 779 Dermatology Necrotizing fasciitis 000 Gas gangrene 000 Angio-oedema 000 Bullous disease 000 Essentials of Kumar & Clark’s Clinical Medicine ESSENTIALS Series Editors Professor Parveen Kumar Professor of Clinical Medicine and Education Barts and The London School of Medicine and Dentistry Queen Mary University of London, and Honorary Consultant Physician and Gastroenterologist Barts and the London NHS Trust and Homerton University Hospital NHS Foundation Trust, London, UK and Dr Michael Clark Honorary Senior Lecturer, Barts and The London School of Medicine and Dentistry Queen Mary University of London London, UK Commissioning Editor: Pauline Graham Development Editor: Helen Leng Project Manager: Gopika Sasidharan Designer/Design Direction: Stewart Larking Illustration Manager: Gillian Richards ESSENTIALS OF Kumar & Clark’s CLINICAL Medicine Fifth edition ANNE BALLINGER MD FRCP Consultant Gastroenterologist and General Physician Queen Elizabeth The Queen Mother Hospital East Kent Hospitals University NHS Foundation Trust Kent, UK Edinburgh London New York Oxford Philadelphia St Louis Sydney Toronto 2011 © 2011 Elsevier Ltd/B.V All rights reserved No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the Publisher Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/ permissions This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein) First edition 1995 Second edition 2000 Third edition 2003 Fourth edition 2007 Fifth edition 2011 ISBN 9780702035234 International ISBN 9780702035241 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 Notices Knowledge and best practice in this field are constantly changing As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein Printed in China Working together to grow libraries in developing countries www.elsevier.com | www.bookaid.org | www.sabre.org The publisher’s policy is to use paper manufactured from sustainable forests Contents Medical emergencies Series preface Preface Abbreviations Significant websites Inside front cover vii ix xi xv Ethics and communication Infectious diseases 11 Gastroenterology and nutrition 65 Liver, biliary tract and pancreatic disease 139 Haematological disease 193 Malignant disease 251 Rheumatology 271 Water, electrolytes and acid–base balance 323 Renal disease 353 10 Cardiovascular disease 407 11 Respiratory disease 505 12 Intensive care medicine 571 13 Drug therapy, poisoning and alcohol misuse 589 14 Endocrine disease 607 15 Diabetes mellitus and other disorders of metabolism 667 16 The special senses 703 17 Neurology 715 18 Dermatology 803 Dictionary of terms Index Normal values 819 831 Inside back cover This page intentionally left blank Series Preface Medical students and doctors in training are expected to travel to different hospitals and community health centres as part of their education Many books are too large to carry around, but the information they contain is often vital for the basic understanding of disease processes The Essentials series is designed to provide portable, pocket-sized companions for students and junior doctors They are most useful for clinical practice, whether in hospital or the community, and for exam revision The notable success of Essentials of Clinical Medicine over many editions is shown by its presence in the pockets of all healthcare professionals – nurses, pharmacists, physical and occupational therapists, to name a few – not simply medical students and doctors All the books in the series have the same helpful features: � � � � � � Succinct text Simple line drawings Emergency and other boxes Tables that summarize causes and clinical features of disease Exam questions and explanatory answers – now online Dictionary of terms They contain core material for quick revision, easy reference and practical management The modern format makes them easy to read, providing an indispensable ‘pocket essential’ Parveen Kumar and Michael Clark Series Editors This page intentionally left blank 9 392 • Renal disease Anaemia CNS Pallor Lethargy Breathlessness on exercise Confusion, coma, fits (severe uraemia) Platelet abnormality Epistaxis Bruising Skin Pigmentation Pruritus GI tract Anorexia Nausea Vomiting Diarrhoea CVS Uraemic pericarditis Hypertension Peripheral vascular disease Heart failure Renal Nocturia Polyuria Salt and water retention Oedema Renal osteodystrophy Endocrine/gonads Amenorrhoea Erectile dysfunction Infertility Polyneuropathy Osteomalacia Muscle weakness Bone pain Hyperparathyroidism Osteosclerosis Adynamic bone disease Fig 9.6 Symptoms and signs of chronic kidney disease Oedema may be due to a combination of primary renal salt and water retention and heart failure GI, gastrointestinal results in a form of cardiomyopathy with both systolic and diastolic dysfunction Pericarditis and pericardial effusion occurs in severe uraemia Other complications include an increased risk of peptic ulceration, acute pancreatitis, hyperuricaemia, erectile dysfunction and an increased incidence of malignancy Differentiating AKI from CKD Distinction between AKI and CKD depends on the history, duration of symptoms and previous urinalysis or measurement of serum creatinine A Renal disease • 393 1,25-(OH2)D3 ( conversion) Mechanism Serum Bone mineralization 2+ Ca absorption ALP, Ca, PO4 Low bone turnover ( remodelling bone formation) e.g Calcitriol prescribed for low Ca Iatrogenic, e.g steroids, post-transplantation ± Ca Normal ALP High → low bone turnover later Ca PO4 PTH Osteomalacia Disease PTH Adynamic bone disease Osteoporosis Secondary hyperparathyroidism Tertiary hyperparathyroidism (long term) Osteosclerosis Osteopenia Radiological Pseudofractures (Looser’s zones) signs Subperiosteal erosions Pepperpot skull Rugger jersey spine (Adenomas (brown tumours)) Fig 9.7 Renal osteodystrophy Pathogenesis and radiological features of renal bone disease ALP, alkaline phosphatase normochromic anaemia, small kidneys on ultrasonography and the presence of renal osteodystrophy favour a chronic process Management The aims of treatment are: � Specific therapy directed at the underlying cause of renal disease, e.g immunosuppressive agents for vasculitis and tight metabolic control in diabetes � Slow deterioration of kidney function (renoprotection) Renal disease Chronic kidney disease 9 394 • Renal disease � Reduce cardiovascular risk � Treat the complications, e.g anaemia � Appropriate dose adjustment of prescribed drugs based on guidance in a national formulary Renoprotection The goal of treatment should be to maintain the blood pressure at less than 120/80 mmHg and to maintain a urinary protein concentration of less than 0.3 g/24 hours Good blood pressure control may slow the decline in renal function Patients with CKD and proteinuria >1 g/24 hours should receive: � ACE inhibitor, increasing to maximum dose � Angiotensin receptor antagonist if goals are not achieved; in diabetes mellitus start with angiotensin receptor antagonist � Diuretic to prevent hyperkalaemia and help to control blood pressure � Calcium-channel blocker (verapamil or diltiazem) if goals not achieved Reduce cardiovascular risk � � � � � Optimal control of BP and reduction of proteinuria (as above) Statins to lower cholesterol to 10 mL/min/year in years Higher levels of proteinuria ACR ≥ 70 mg/mmol or PCR ≥ 100 mg/ mmol Proteinuria and haematuria Proteinuria with ≥+1 blood on urine dipstick Poorly controlled hypertension Despite use of four antihypertensive drugs Suspected rare or genetic cause of CKD ACR, albumin:creatinine ratio; PCR, protein:creatinine ratio Renal disease accelerate hypertension and, rarely, lead to encephalopathy with convulsions Acidosis Systemic acidosis accompanies the decline in renal function and may contribute to increased serum potassium levels as well as dyspnoea and lethargy Treatment is with oral sodium bicarbonate (4.8 g or 57 mmol daily) Infections Patients with CKD have an increased risk of infections which may be fatal Influenza and pneumococcal vaccination should be administered 9 396 • Renal disease Dialyser membrane BLOOD DIALYSATE [Na+] 140 mmol [Na+] 140 mmol H2O H2O [K+] 1.0 mmol [K+] 6.0 mmol Urea mmol Urea 40 mmol 2+ [Ca ] 1.2 mmol – [HCO 3] 30 mmol [Ca2+] 1.2 mmol [HCO–3] 15 mmol Fig 9.8 The principle of haemodialysis the semipermeable membrane and dialysis fluid is instilled into the peritoneal cavity Haemodialysis Adequate dialysis requires a blood flow of at least 200 mL/min and the most reliable way of achieving this is by surgical construction of an arteriovenous fistula, usually in the forearm This provides a permanent and easily accessible site for the insertion of needles An adult of average size usually requires 4–5 hours of haemodialysis three times a week, which may be performed in hospital or at home All patients are anticoagulated during treatment (usually with heparin) because contact of blood with foreign surfaces activates the clotting cascade The most common acute complication of haemodialysis is hypotension, caused in part by excessive removal of extracellular fluid Peritoneal dialysis A permanent tube (Tenkoff catheter) is placed into the peritoneal cavity via a subcutaneous tunnel The bags of dialysate are connected to the catheter using a sterile, no-touch technique and the fluid run into the peritoneal cavity Urea, creatinine, phosphate and other uraemic toxins pass into the dialysate down their concentration gradients and the dialysate is then collected With continuous ambulatory peritoneal dialysis (CAPD) 1.5–3 L of dialysate are introduced and exchanged three to five times a day Bacterial peritonitis, often with Staph epidermidis, is the most common serious complication of peritoneal dialysis Treatment is with appropriate antibiotics, often given intraperitoneally Renal disease • 397 200 mL/min Semipermeable membrane Haemofiltrate 1000 mL/h Replacement solution 1000 mL/h Fig 9.9 Principles of haemofiltration Haemofiltration Haemofiltration involves the removal of plasma water and its dissolved constituents (e.g Na+, K+, urea, phosphate) and replacing it with a solution of the desired biochemical composition The procedure employs a highly permeable membrane, which allows large amounts of fluid and solute to be removed from the patient (Fig 9.9) It is used mostly in the intensive care setting in the management of AKI Complications of all long-term dialysis Cardiovascular disease (as a result of atheroma) and sepsis are the leading causes of death in long-term dialysis patients Causes of fatal sepsis include peritonitis complicating peritoneal dialysis and Staph aureus infection (including endocarditis) complicating the use of indwelling access devices for haemodialysis Amyloidosis is the result of the accumulation and polymerization of β2-microglobulin This molecule (a component of human leucocyte antigen [HLA] proteins on most cell membranes) is normally excreted by the kidneys, but is not removed by dialysis membranes Deposition results in the carpal tunnel syndrome and joint pains, particularly of the shoulders Transplantation Successful renal transplantation offers the potential for complete rehabilitation in, and is the treatment of choice for most patients with, end-stage renal failure In the best centres graft survival is 80% at 10 years Kidneys are obtained from cadavers or, less frequently, a living donor, e.g a close relative The donor must be ABO compatible, and good HLA matching increases the chances of successful transplantation The donor kidney is placed in the Renal disease Blood inflow Blood return 9 398 • Renal disease iliac fossa and anastomosed to the iliac vessels of the recipient; the donor ureter is placed into the recipient’s bladder Long-term immunosuppressive treatment is necessary (unless the donor is an identical twin, i.e genetically identical) to reduce the incidence of graft rejection This treatment comprises corticosteroids, azathioprine or mycophenolate mofetil and ciclosporin or tacrolimus Monoclonal and polyclonal antibodies such as antilymphocyte and anti-thymocyte globulin or basiliximab and daclizumab are potent immunosuppressives and are used in selected patients The complications of renal transplantation and immunosuppression include opportunistic infection (e.g with Pneumocystis jiroveci), hypertension, development of tumours (skin malignancies and lymphomas) and, occasionally, recurrence of the renal disease (e.g Goodpasture’s syndrome) CYSTIC RENAL DISEASE Solitary and multiple renal cysts Renal cysts are common, particularly with advancing age They are usually asymptomatic and discovered incidentally on ultrasonography performed for some other reason Occasionally they may cause pain and/or haematuria Autosomal-dominant polycystic kidney disease Autosomal-dominant polycystic kidney disease (ADPKD) is a common (1 : 1000) autosomal dominantly inherited condition in which multiple cysts develop throughout both kidneys Cysts increase in size with advancing age and lead to renal enlargement and the progressive destruction of normal kidney tissue, with gradual loss of renal function Most cases are due to a mutation in the PKD1 gene (short arm of chromosome 16), which encodes for a protein, polycystin 1, an integral membrane protein which regulates tubular and vascular development in kidneys and other organs A second gene, PKD2, on chromosome accounts for the remaining cases Clinical features The disease presents at any age after the second decade Clinical features include: � Acute loin pain due to cyst haemorrhage or infection, or urinary tract stone formation (uric acid calculi occur more commonly) � Abdominal discomfort caused by renal enlargement � Hypertension � Progressive renal impairment End-stage renal failure develops in about 50% of patients by 50–60 years of age � Liver cysts (usually clinically insignificant) Rarely cysts in the pancreas, spleen, ovary and other organs Renal disease • 399 Diagnosis Clinical examination commonly reveals large irregular kidneys, hypertension and possibly hepatomegaly A definitive diagnosis is established by ultrasonography In adults with a family history, criteria for diagnosis are at least two renal cysts in patients aged 60 years Management No treatment has definitely been shown to slow disease progression or decrease cyst size Blood pressure should be carefully controlled and disease progression monitored by serial measurements of serum creatinine Many patients will eventually require renal replacement by dialysis and/or transplantation Children and siblings of patients with the disease should be offered screening by renal ultrasonography in their 20s Medullary sponge kidney Medullary sponge kidney is an uncommon condition characterized by dilatation of the collecting ducts in the papillae, sometimes with cystic change In severe cases the medullary area has a sponge-like appearance Small calculi form within the cysts and patients present with renal colic or haematuria In 20% of patients there is hypercalciuria or renal tubular acidosis (see p 346) Renal function is usually well preserved The diagnosis is made by excretion urography TUMOURS OF THE KIDNEY AND GENITOURINARY TRACT Renal cell carcinoma Renal cell carcinomas are the most common renal tumours in adults Average age at presentation is 55 years with a male : female ratio of 2 : 1 They arise from the proximal tubular epithelium and may be solitary, multiple and occasionally bilateral Clinical features Haematuria, loin pain and a mass in the flank are the most common presenting features Other features include malaise, weight loss and fever Left-sided scrotal varicoceles occur if the renal tumour obstructs the gonadal vein where Renal disease � Subarachnoid haemorrhage – intracranial aneurysms are more common in APKD patients � Mitral valve prolapse in 20% 9 400 • Renal disease it enters the renal vein Twenty-five per cent have metastases at presentation to bone, liver and the lung Anaemia or polycythaemia and hypercalcaemia are other findings Investigations � Ultrasonography will distinguish a simple benign cyst from a more complex cyst or solid tumour � CT scanning is more sensitive that ultrasound for detecting a renal mass and will show involvement of the renal vein or inferior vena cava MRI is better than CT for tumour staging A presumptive diagnosis of renal carcinoma is made on imaging studies in patients with isolated solid renal masses and they will usually go straight to surgery (which provides tissue diagnosis and definitive treatment) without further investigation Management Localized disease Radical nephrectomy is the preferred treatment Partial nephrectomy is used if there is bilateral involvement or the contralateral kidney functions poorly Ablative techniques (cryoablation or radiofrequency ablation) are used in patients with significant comorbid disease who would not tolerate surgery Metastatic or locally advanced disease Interleukin-2 and interferon produce a remission in 20% of cases Targeted therapies which block the vascular endothelial growth factor (sunitinib, sorafenib, bevacizumab) or mTOR (temsirolimus) pathway are used in patients who cannot tolerate or not respond to this treatment Prognosis The 5-year survival rate is 60–70% with tumours confined to the renal parenchyma, but less than 5% in those with distant metastases Urothelial tumours The calyces, renal pelvis, ureter, bladder and urethra are lined by transitional cell epithelium Bladder tumours are the most common form of transitional cell malignancy They occur most commonly after the age of 40 years and are four times more common in males Predisposing factors for bladder cancer include: � � � � Cigarette smoking Exposure to industrial chemicals, e.g β-naphthylamine, benzidine Exposure to drugs, e.g phenacetin, cyclophosphamide Chronic inflammation, e.g schistosomiasis Renal disease • 401 Patients with bladder cancer usually present with painless haematuria (either visible or non-visible) or sometimes symptoms suggestive of a UTI (frequency, urgency, dysuria) in the absence of bacteriuria Pain is usually due to locally advanced or metastatic disease but may sometimes occur from clot retention Transitional cell cancers of the kidney and ureters present with haematuria and flank pain Investigations Presentation is usually with haematuria and any patient over 40 years of age with haematuria should be assumed to have a urothelial tumour until proven otherwise (Fig 9.3) Management Pelvic and ureteric tumours are treated with nephroureterectomy Treatment of bladder tumours depends on the stage, but options include local diathermy or cystoscopic resection, bladder resection, radiotherapy, and local and systemic chemotherapy DISEASES OF THE PROSTATE GLAND The common diseases of the prostate gland are benign enlargement, carcinoma and prostatitis Prostate-specific antigen (PSA) is a glycoprotein that is expressed by normal and neoplastic prostate tissue and secreted into the bloodstream Serum concentrations can be increased in any of these conditions and also after perineal trauma and mechanical manipulation of the prostate (cystoscopy, prostate biopsy or surgery) Serum PSA concentration >4.0 ng/mL is abnormal and can be due to benign disease or cancer However, prostate cancer is present in 50% of men with a serum PSA >10 ng/mL Benign enlargement of the prostate gland Benign prostatic enlargement (hypertrophy, BPH) is common particularly after the age of 60 years There is hyperplasia of both glandular and connective tissue elements of the gland The aetiology is not known Clinical features Frequency of micturition, nocturia, delay in initiation of micturition and postvoid dribbling are common symptoms Acute urinary retention or retention with overflow incontinence also occurs An enlarged smooth prostate may be felt on rectal examination Renal disease Clinical features 9 402 • Renal disease Investigations Serum electrolytes and renal ultrasonography are performed to exclude renal damage resulting from obstruction Prostate cancer may present with similar symptoms Serum PSA may be elevated in benign disease but an elevated value is usually an indication for specialist referral and prostate biopsy Management Patients with mild symptoms are managed by ‘watchful waiting’ Selective α1-adrenoceptor antagonists, such as tamsulosin, relax smooth muscle in the bladder neck and prostate producing an increase in urinary flow rate and an improvement in obstructive symptoms The 5α-reductase inhibitor finasteride blocks conversion of testosterone to dihydrotestosterone (the androgen responsible for prostatic growth) and is an alternative to α-antagonists, particularly in men with a significantly enlarged prostate Patients with acute retention of urine or retention with overflow require urethral catheterization or, if this is not possible, suprapubic catheter drainage Further management is then with prostatectomy or a permanent catheter Prostatic carcinoma Prostatic adenocarcinoma is common, accounting for 7% of all cancers in men Malignant change within the prostate is increasingly common with increasing age, being present in 80% of men aged 80 and over In most cases these malignant foci remain dormant Clinical features In developed countries many patients now present as a result of screening for prostate cancer by measurement of serum PSA although this is not widely recommended (see later) Presentation is also with symptoms of bladder outflow obstruction identical to those of benign prostatic hypertrophy Occasionally, presenting symptoms are due to metastases, particularly to bone In some cases malignancy is unsuspected until histological investigation is carried out on the resected specimen after prostatectomy Rectal examination may reveal a hard irregular gland Investigation The diagnosis is made using transrectal ultrasound of the prostate, elevated serum PSA (see above) and transrectal prostate biopsy If metastases are present serum PSA is usually markedly elevated (>16 ng/mL) Endorectal coil MRI is used to locally stage the tumour Renal disease • 403 Microscopic tumour is sometimes managed by watchful waiting Treatment of disease confined to the gland is radical prostatectomy or radiotherapy, both resulting in 80–90% 5-year survival The treatment of metastatic disease depends on removing androgenic drive to the tumour This is achieved by bilateral orchidectomy, synthetic luteinizing hormone-releasing hormone analogues, e.g goserelin, or antiandrogens, e.g cyproterone acetate Screening Screening for prostate cancer by annual measurement of serum PSA and digital rectal examination reduces the mortality from prostate cancer but the benefit is small and there is the potential for overdiagnosis and treatmentrelated complications Most major medical organizations world-wide not recommend screening for prostate cancer TESTICULAR TUMOUR Testicular cancer is the most common cancer in young men More than 96% of testicular tumours arise from germ cells There are two main types: seminomas and teratomas The aetiology is unknown and the risk of malignant change is greater in undescended testes Clinical features Typically the man or his partner finds a painless lump in the testicle Presentation may also be with metastases in the lungs, causing cough and dyspnoea, or para-aortic lymph nodes, causing back pain Investigations � Ultrasound scanning will help to differentiate between masses in the body of the testes and other intrascrotal swellings � Serum concentrations of the tumour markers α-fetoprotein (AFP) and/or the β subunit of human chorionic gonadotrophin (β-hCG) are elevated in most men with teratomas They are used to help make the diagnosis, to assess response to treatment and in following up patients β-hCG is elevated in a minority of men with seminomas, and AFP is not elevated in men with pure seminomas � Tumour staging is assessed by chest X-ray and CT scanning of the chest, abdomen and pelvis Treatment Orchidectomy is performed to permit histological evaluation of the primary tumour and to provide local tumour control Seminomas with metastases Renal disease Management 9 404 • Renal disease below the diaphragm only are treated by radiotherapy More widespread tumours are treated with chemotherapy Teratomas with metastases are also treated with chemotherapy Sperm banking should be offered prior to therapy to men who wish to preserve fertility URINARY INCONTINENCE Normal bladder physiology As the bladder fills with urine, two factors act to ensure continence until it is next emptied: � Intravesical pressure remains low as a result of stretching of the bladder wall and the stability of the bladder muscle (detrusor), which does not contract involuntarily � The sphincter mechanisms of the bladder neck and urethral muscles At the onset of voiding the sphincters relax (mediated by decreased sympathetic activity) and the detrusor muscle contracts (mediated by increased parasympathetic activity) Overall control and coordination of micturition is by higher brain centres, which include the cerebral cortex and the pons Stress incontinence Stress incontinence occurs as a result of sphincter weakness, which may be iatrogenic in men (post-prostatectomy) or the result of childbirth in women There is a small leak of urine when intra-abdominal pressure rises, e.g with coughing, laughing or standing up In young women pelvic floor exercises may help In post-menopausal women the contributing factor of urethral atrophy may be helped by oestrogen creams Urge incontinence In urge incontinence there is a strong desire to void and the patient may be unable to hold his or her urine The usual cause is detrusor instability, which occurs most often in women, and the aetiology is not known Mild cases may respond to bladder retraining (gradually increasing the time interval between voids) More severe cases are treated with anticholinergic agents, e.g oxybutynin, which decrease detrusor excitability Less commonly, urge incontinence is caused by bladder hypersensitivity from local pathology (e.g UTI, bladder stones, tumours) and treatment is then of the underlying cause Overflow incontinence Overflow incontinence is most often seen in men with prostatic hypertrophy causing outflow obstruction There is leakage of small amounts of urine, and on abdominal examination the distended bladder is felt rising out of the pelvis Renal disease • 405 Neurological causes These are usually apparent from the history and examination, which reveal accompanying neurological deficits Brainstem damage, e.g trauma, may lead to incoordination of detrusor muscle activity and sphincter relaxation, so that the two contract together during voiding This results in a high-pressure system with the risk of obstructive uropathy The aim of treatment is to reduce outflow pressure, either with α-adrenergic blockers or by sphincterotomy Autonomic neuropathy, e.g in diabetic individuals, decreases detrusor excitability and results in a distended atonic bladder with a large residual urine which is liable to infection Permanent catheterization may be necessary In elderly people incontinence may be the result of a combination of factors: diuretic treatment, dementia (antisocial incontinence) and difficulty in getting to the toilet because of immobility Renal disease If the obstruction is not relieved with urethral or suprapubic catheterization then renal damage will develop This page intentionally left blank ... 000 Essentials of Kumar & Clark’s Clinical Medicine ESSENTIALS Series Editors Professor Parveen Kumar Professor of Clinical Medicine and Education Barts and The London School of Medicine and. .. 2 71 Water, electrolytes and acid–base balance 323 Renal disease 353 10 Cardiovascular disease 407 11 Respiratory disease 505 12 Intensive care medicine 5 71 13 Drug therapy, poisoning and. .. edition of ‘Pocket’ Essentials of Clinical Medicine and we continue to strive to produce a small medical textbook with anatomy, physiology and pathophysiology as a key part to understanding 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