Distributed in all countries exceptJapan by: Edward Arnold (Publishers) Ltd 41 Bedford Square London WC1B 3DQ, UK Edward Arnold 3 East Read Street Baltimore, MD 21202 Distributed inJapan by: Nankodo Company Limited 42-6 Hongo 3-chome Bunkyo, Tokyo 113 Japan British Library Cataloguing in Publication Data: Fletcher, Christopher D.M. An atlas of gross pathology. 1. Pathology I. Title II. McKee, Phillip H. 616.07 RBll1 ISBN: 0-906923-47-6 (Gower) 0-7131-4557-9 (Arnold) ©Copyright 1987 by Gower Medical Publishing Limited. Middlesex House. 34-42 Cleveland Street, London W1 P 5FB, UK. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system or transmitted in any form or by any means electronic, mechanical, photocopying, recording or otherwise, without the prior written permission of the publisher. Project Editor: Michele Campbell Design: Nigel Duffield illustration: Pamela Corfield Set in Garamond and Helvetica by: Informat Computer Communications Ltd. Originated in Hong Kong by: Imago Publishing Ltd. Printed in Singapore by: Imago Productions (FE) PTE Limited. • • • Preface The aim of this atlas is to provide an introduction to the macroscopical appearances of the most common pathological conditions for undergraduate medical students and nurses in training. It will also, hopefully, be of value to postgraduates undertaking the FRCS examinations, for whom a working knowledge of gross pathology is vital . Only important or frequently encountered disease processes are covered. Each illustration is accompanied by a concise legend outlining basic, relevant clinicopathological and pathogenetic details. In collecting material for this atlas, we are deeply indebted to Professor J.R. Tighe of the Histopathology Department at St. Thomas's Hospital for allowing us access to the departmental collection of colour transparencies. Weare also particularly grateful to Dr H. Pambakian, Museum Curator at St. Thomas's Hospital Medical School and Professors H. Spencer and M.S.R. Hutt. Most of all, this book would not have been possible without the consistent generosity and thoughtfulness of all the pathologists in our department, who unselfishly offered us many of their specimens, obtained either surgically or at post mortem, for photography. . • COM Fletcher & PH McKee London . .. 111 . • • IV Acknowledgements , The authors would like to thank the following colleagues for providing illustrative material: Professor P.G. Bullough, Cornell University Medical College, New York (Figs.7.16 , 12.1 bottom, 12.4, 12.7-12.10,12.13-12.15,12.17,12.18, 12.20-22, 12.24, 12.25 & 12.29 top); Dr D.W. Day, Dept. of Pathology, University of Liverpool Medical School, Liverpool (Fig.3.23 ); DrC.W. Elston, Dept. of Pathology, City Hospital, Nottingham (Fig.9.35); Profossor P.L. lantos, Dept. of Neuropathology, Institute of Psychiatry, London (Figs. 11. 1 0, 11.20 & 11.24); Dr].C. Macartney, Dept. of Histopathology, St Thomas's Hospital Medical School, London (Figs.4.26, 4.29, 7.8 & 12.26); Professor F.V. O'Brien, School of Dentistry, Queen's University, Belfast (Figs.3.1 & 3.2); Dr C. Parkinson,"Institute of Urology, London (Figs. 10.7 & 10.13); DrD.E. Sharvill, William Harvey Hospital, Ashford, Kent (Fig. 5.13 ); Dr ].M. Sloan, Senior Lecturer/Consultant Pathologist, Royal Victoria Hospital, Belfast (Figs.2.3, 2.4,2.14,8.24 & 8.30); The Wellcome Museum, Royal College of Surgeons of England, London (Figs.8.20 & 9.28). • III Ii 1IIIIwing Contents Preface Acknowledgements 1 Cardiovascular System 2 Respiratory System 3 Alimentary System 4 HepatobiliarySystem 5 Breast 6 Lymphoreticular System 7 Endocrine System 8 Urinary System 9 Female Reproductive System 10 Male Reproductive System 11 Nervous System 12 Osteoarticular System Index iii iv 1 13 23 36 45 50 55 62 72 83 87 94 .... I I 103 v ' 1 Cardiovascular System Fig.1.1 Recent myocardial infarct. A transverse section through both right and left ventricles, viewed from below. The anterior wall of the left ventricle shows an extensive area of recent infarction, charac­ terised by an almost full-thickness zone of yellow necrotic myo­ cardium, surrounded by a hyperaemic rim . The latter consists of granulation tissue (capillaries and fibroblasts) and represents the early phase of healing. This infarct is of approximately one week's duration. In nearly all cases, myocardial infarction is caused by occlusive thrombosis in an atheromatous coronary artery. Rare causes include syphilitic aortitis, polyarteritis nodosa and coronary artery embolism from a variety of cardiac lesions. Fig.1.2 Healed myocardial infarct. The heart has been opened to display the inner aspect of the left ventricle. Marked pale fibrous scarring is seen in the posterior wall and in the papillary muscles. Mural thrombus overlying the scar is also present. Healing, by fibrosis, commences about 3 weeks after acute infarction and is usually complete after 2 months. Fibrous replacement of the myo­ cardium predisposes to aneurysm formation (see Fig .1.6) within 'vhich thrombus may form. Fig.1.3 Coronary artery thrombosis. The left main stem coronary artery has been opened longitudinally to reveal occlusion of its lumen by thrombus (arrowed). Note the presence of atheroma in the ascending aorta and a fibrinous pericarditis. Occlusive coronary thrombosis almost always occurs at the site of an atheromatous stenosis (see Figs.1.36-1 .38) and is thought to be initiated either by ulceration or haemorrhage into a plaque. Fig.l.4 Coronary artery thrombosis. The left anterior descending coron­ ary artery is shown in transverse section. The lumen is mark­ edly diminished by atheroma, and over­ lying thrombus has resulted in total occ­ lusion. In the vast majority of cases of myocardial infarc­ tion, such occlusive thrombosis will be detected if the coronary arteries are examined with suffi­ cient care. Fig.1.5 Myocardial infarct with mural thrombulI '''''' ~ rupture. The heart has been opened to expo:'!!) III" 'jill ,II left ventricle. A large mural thrombus is adhOlull1 Il ' lLI l !Il myocardial infarction, complicated by rupture (111I1I ! illli ll septum. The probe has been passed through II" , It 11110 II ' extreme left of the pictu re its tip can be seen IIV' !lIYII II I II " ventricular flap. Myocardial rupture, which is not III II "II it ' occurs within a week of acute infarction, Flg.l.S Left ventricular aneurysm. The d(~ vO IIlI'"1I 11 11 , aneurysm of the left ventricle is a not uncomllliJlt 111 111 1 III ' myocardial infarction. It is due to replacemellt (11111 ) I"Y" collagenous scar tissue with resultant loss of 0111;,111 ily 'II aneurysms often contain mural thrombus whic:h " Illy I II systemic emboli. The laceration of the anterior' IlilllllllllY " right of the aneurysm occurred during the post 1111111,,,,, 1 1 Cardiovascular System left main stem coronary occlusion of its lumen of atheroma in the . Occlusive coronary of an atheromatous to be initiated either by Fig.1.4 Coronary artery thrombosis. The left anterior descending coron­ ary artery is shown in transverse section. The lumen is mark­ edly diminished by atheroma, and over­ lying thrombus has resulted in total occ­ lusion. In the vast majority of cases of myocardial infarc­ tion, such occlusive thrombosis will be detected if the coronary arteries are examined with suffi­ cient care. Fig.1.5 Myocardial infarct with mural thrombus and ventricular rupture. The heart has been opened to expose the septal wall of the left ventricle. A large mural thrombus is adherent to an area of recent myocardial infarction, complicated by rupture of the interventricular septum. The probe has been passed through the rupture and at the extreme left of Ihe picture its tip can be seen overlying the righl ventricular flap. Myocardial rupture, which is not uncommon, usually occurs within a week of acute infarction . Fig.1.6 Left ventricular aneurysm. The development of an aneurysm of the left ventricle is a not uncommon late complication of myocardial infarction. It is due to replacement of the myocardium by collagenous scar tissue with resultant loss of elasticity. Such aneurysms often contain mural thrombus which may be a source of systemic emboli. The laceration of the anterior papillary muscle to the right of the aneurysm occurred during the post mortem. Fig.1.7 Haemopericardium. The pericardial sac has been opened (left) to show an extensive haematoma overlying the epicardium. On the right, the haematoma has been removed to reveal the cause as being a slil-like ventricular perforation (arrowed) at the site of a recent myocardial infarct. Haemopericardium may more rarely occur as a complication of dissecting aortic aneurysm or trauma. Fig.1.8 Ruptured papillary muscle. The heart has been opened to display the posterior aspect of the left ventricle. In the centre of the picture is a portion of the anterior papillary muscle which has been , torn and shows obvious necrosis. Rupture of a papillary muscle is a rare complication of myocardial infarction, which usually occurs within 2 weeks of the primary event: it results in the acute onset of mitral incompetence and left ventricular failure. 2 1 Cardiovascular System Fig.1.9 Left ventricular hypertrophy. Left ventricutar hypertrophy is a not uncommon finding at post mortem owing to the frequency of essential hypertenSion in the population. A list of causes is given in Fig:1.10 In this instance the increased thickness of the left ventricular wall is obvIous (in excess of 20mm) However, a much more accurate method of assessing venlricular hypertrophy involves weighing the chambers separately after careful dissection, thereby taking into account any degree of associated ventricular dilatation. CAUSES OF LEFT VENTRICULAR HYPERTROPHY Systemic hypertension Aortic stenosis Aortic incompetence Mitral incompetence Congenital heart disease coarctation of aorta reversed VSD Amyloid Cardiomyopathy anaemia High output failure thyrotoxicosis Paget's disease A-V malformation -­ -­ -­ - - -­ -­ -­ Fig.1.10 Causes of left ventricular hypertrophy. Fig.1.11 Acute rheumatic endocarditis. Characteristic small pink vegetations (arrowed) are present along the line of closure of this mitral valve cusp. Rheumatic fever, a multisystem autoimmune process, is a rare complication of (3-haemolytic (Group A) strepto­ coccal infections. It results from the development of heterophilic cross·reacting antibodies to the streptococcal M protein and an, as yet unidentified, connective tissue antigen . Manifestations include a pancarditis, joint involvement, skin rashes, subcutaneous nodules and , rarely, Sydenham's chorea . Fig.1.12 Mitral stenosis with atrial thrombus. The commonest complication of rheumatic endocarditis is mitral stenosis and, indeed, almost all stenotic mitral valves are of rheumatic origin. Fusion of the valve cusps and fibrosis results in narrowing of the valve orifice. The stenosis causes leli atrial dilatation and may be complicated by atrial fibrillation with consequent thrombus formation, as seen in this case. Fig.1.13 Mixed mitral valve disease. Therl; 1: , II,.lfl" ,II, the chordae tendinae wilh fusion and shorte"" ,i I 11" , III' process has produced a rigid 'buttonhole' valv,' II" ,jO .j 'I stenotic and incompetent - the latter has resulu)d '" II I'" II of left ventricular hypertrophy. as seen in th e Ix ,II", II ' If I1 I1 corner. CAUSES OF MITRAL INCOMPETENCr Rheumatic heart disease Papillary muscle rupture or fibrosis Congenital Mitral valve prolapse (floppy valvo !,Y'ldJl '" I, Functional dilatation of valve ring Marfan's syndrome .Fig.1.14 Causes of mitral incompetence. 3 I 1 CardiovascularSystem Fig.1.13 Mixed mitral valve disease. There IS marked fibrosIS 01 the chordae tendinae with fusion and shortening. The rheumatic process has produced a rigid 'buttonhole' valve, thereby being both stenotic and incompetent· the latter has resulted in the deve lopment of lelt ventricular hypertrophy, as seen in the bottom right hand corner. I I CAUSES OF MITRAL INCOMPETENCE Rheumatic heart disease Papillary muscle rupture or fibrosis Congenital Mitral valve prolapse (floppy valve syndrome) Functional dilatation of valve ring Marfan's syndrome Fig.1.15 Aortic stenosis. Isolated aortic stenosis may complicate rheumatic heart disease but more often is associated with mltrat involvement also. The proximal portion of the ascending aorta has been opened to view this stenotic valve from above. Aortic stenosis usually gives rise to left ventricular hypertrophy and may compromise the coronary blood supply. Fig.1.16 Calcific aortic stenosis. Calcification of the aortic valve most commonly occurs in a congenital bicuspid valve, but may also arise as a consequence of rheumatic disease and is sometimes a feature of the ageing process. Note the coarse calcific nodules in the valve cusps Fig.1.14 Causes of mitral incompetence. 4