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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 Project Editor: Michele Campbell Design: Nigel Duffield ISBN: 0-906923-47-6 (Gower) 0-7131-4557-9 (Arnold)
©Copyrig ht 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.
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 .
•
Acknowledgements ,
•
•
IV
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. 10, 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).
Contents III
Ii 1IIIIwing
Preface
iii
Acknowledgements
iv
1 Cardiovascular System 2 Respiratory System
1
3 Alimentary System 4 Hepatobiliary System 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
13
23
36
45
50
55
62
72
83
87
94
103
.... I
I
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.
1
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 ,I I 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 il y 'II aneurysms often contain mural thrombus whic:h " Illy I II systemic emboli. The laceration of the anterior' Ili lllllllllY " right of the aneurysm occurred during the post 1111111,,,,,
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 vent ricular flap. Myocardial rupture, which is not uncommon, usually occurs within a week of acute infarction .
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.1.6 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.1.8 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 instanc e 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 separatel y after careful dissection, thereby taking into account any degree of associated ventricular dilatation .
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.1.13 Mixed mitral valve disease. Th erl; 1: , II,.lfl" , II , the chordae tend inae wilh fusion and short e"" ,i I 11" , III' process has produced a rigid 'buttonhole' va lv,' 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
CAUSES OF LEFT VENTRICULAR HYPERTROPHY Systemic hypertension
Rheumatic heart disease
Aortic stenosis Aortic incompetence
Papillary muscle rupture or fibrosis
Mitral incompetence coarctation of aorta
Congenital heart disease
Congenital
reversed VSD
Amyloid
Mitral valve prolapse (floppy valvo !,Y'ldJl '" I,
Cardiomyopathy anaemia
Functional dilatation of valve ring
thyrotoxicosis
High output failure
Paget's disease A-V malformation
-
-
-
-
-
-
Fig.1.10 Causes of left ventricular hypertrophy.
3
-
-
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.
Marfan's syndrome I
.Fig.1.14 Causes of mitral incompetence.
1 Cardiovascular System
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
CAUSES OF MITRAL INCOMPETENCE
Fig .1.15 Aortic stenosis. Isolated aortic stenosis may comp licate rheumatic heart disease but more often is associated with mltrat involvement also. The proximal portion of the ascending aorta has been opened to view thi s stenotic valve from above. Aortic stenosis usually gives rise to left ventric ular hype rtrophy and may compromise the coronary blood supply.
I
Rheumatic heart disease Papillary muscle rupture or fibrosis Congenital Mitral valve prolapse (floppy valve syndrome)
Functional dilatation of valve ring
Marfan's syndrome Fig.1.14 Causes of mitral incompetence.
Fig.1.16 Calcific aortic stenosis. Calcification of the aortic val ve 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 coa rse ca lcifi c nodules in the va lve cusps
4
1 Cardiovascular System
r-
CAUSES OF AORTIC STENOSIS
I
TYPES OF ENDOCARDITIS bacterial
Rheumatic heart disease
viral of congenital bicuspid valve Infective
Calcification
rickettsial chlamydial
senile
fungal dome-shaped valve
Rheumatic Congenital
supravalvar stenosis
Non-infective thrombotic (agonal) Libman-Sacks (S.L.E.)
subvalvar stenosis
Fig.1 .19 Types of endocarditis.
Hypertrophic cardiomyopathy
I
Fig.1.21 Infective endocarditis (normal valve). VIII 11.1 I present on all three cusps of th is otherwise nOIIlliII.II 1111< ~ Endocarditis affe cting normal valves is usually 1'1
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2 Respiratory s~eJ
2 Respiratory S) .. Inll
Fig.2.13 Miliary tuberculosis. Throughout the lung parenchyma, and particularly numerous around blood vessels, are small discrete 'tubercles' Miliary spread is due to haematogenous dissemination of Mycobacteria and may complicate either primary infection (in which destructive foci erode into blood vessels) or reactivated post· primary Infection in debilitated, elderly patients.
pUlmonaryl!'P" I
17
Fig.2.14 Tuber culous broncho pneumonia. The right lung shows multiple foci of caseous pneumonia. At the apex of the left lung a small subpleural area of scarring and caseation is apparent (arrowed) Tuberculous bronchopneumonia typically compli cates post-primary (reinfection) disease and results from the intrabronchial spread of the lique fied contents of a caseous cavity.
Fig.2.15 Cavitating tuberculosis. T III ~, I '. an upper 10bectQIIIY specimen whlc ll contains a rag ged, haemorrhagic cRvlly extending just beneath the visco!': II pleura The cavity I:, surrounded by arl area of pale caseolr :. necrosis. Such an appearance may represent pro gressive primary t JI. more common ly, post·primary infection and result:, from liquefaction Il f caseous matenal
Fig.2.16 Pulmonary embolism. The right main pulmonary artery is virtually occluded by a massive laminated thrombus. The lung I', rather pale in appearance Pul monary embolism most of tell complicates deep venous thromboses in the lower limb (see Fig. 141) The commo n()~ 1 predisposing factors are pro longed bed rest, particularly after surgical operations, partull tion, congestive cardiac failure and hypercoagulability. Mas$ lV'" infarction (see Fig. 2.17) or m:ty give rise to pulmonary haemosiderosis.
Ie.
2 Respiratory System Fig.2.17 Pulmonary infarct. At the tip of the lower lobe is a wedge-shaped area of typical, dark-red infarction . Proximally, two branches of the pulmonary artery are occluded by embolic thrombus . Pulmonary infarcts are commonest in late adulthood and are predominantly a comp lication of deep venous throm bosis (see Fig . 1.41). Most pulmonary infarcts are of the 'red' congested type as true ischaemic necrosis is prevented by the dual blood supply from the bronchial artery.
1-_-
Fig.2.19 Coal workers' pneumoconiosis. The lung parenchyma shows patchy dense anthracotic pigmentation, a pattern known as dust reticu lation. Note also the character· istic mild centrilobular 'focal dust' emphysema. In addition a small, black, sil icotic nodule is present (arrowed). Simple dust reticu lation results from long term exposure to coal dust ; the development of nodules is due to co-inhalation of silica . There is no increased risk of lung cancer .
Fig.2.21 SlIIco. l.
I
parenchY"la It l 1111111,,, shows den~;u 111111 11 11' , mentation and 11111111111 culous cavity ill II " , III U hilar nodes ur(l 1.1111 I, I enlarged and tl ll l lll" ,, 1 fissure is SCUll lid ' :,11' seen most olion II I 11 1111 workers in tho '.111111) ,.1 industries. L I III\ I dllll i actually re!';lIit(l lllllllll i of macrOpllO\I'· ( "II, 'j lowing silicCl iltlh .. 111 11 and is morp. 1I:.'iI Illy, Ii ised by nOUlllor 11111, 1111 Fig .2.22). TubUl' 1I1i ,,~ 1 commoncorrll,l" ,111111
CA_USES OF PULMONARY HAEMOSIDEROSIS chronic left ventricular failure
Pulmonary hypertension
mitral valve disease left atrial myxoma
Goodpasture's syndrome Long-standing haemochromatosis Haemosiderosis FIg.2,18 Causes of pulmonary haemoslderosis.
17
Fig.2.20 Progressive massive fibrosis. This coal miner's lung shows, in addition to dust reticulation , large, well demarcated , black fibrous masses and smaller black nodules (top) . Progressive massive fibrosis affects up to 1"10 of coal miners and may also be seen in silicosis. The precise pathogenesis is unknown but it is thought that the degree of dust exposure and the possible coexistence of tuber culosis are important factors . The smaller nodules seen here are probably silicotic in nature , since coal dust often has a high silica content.
Fig.2.22 Haematlte pneumoconiosis. The IUIIU Pi li' " "
shows severe brick-red pigmentation with evictor 11 :11 1,1 111 I diffuse fibrosis and emphysematous change. nlhl !' 1I11 1il . inhalation of iron oxide, is seen most often in irOIl Ill,·,"II1' development of fibrotic lesions is again dependlll it 111 1111 . I existence of silica in the inhaled dust. Well recoqlll' I'H Ii, include tuberculosis and bronchial carcinoma.
2 Respiratory System Fig.2.21 Silicosis. The lung
Flg.2.19 Coal workers' pneumoconiosis. The lung
parenchyma is markedly fibrotic, shows dense anthracotic pig mentation and contains a tuber culous cavity in the apex. The hilar nodes are black and enlarged and the interlobar fissure is scarred . Silicos is is seen most often in miners and workers in the stone and glass industries. Lung damage actually results from the re lease of macrophage cell contents fol lowing silica-i nduced cell death and is more usually character ised by nodular fibrosis (see Fig .2.22) . Tuberculosis is a very common complication .
parenchyma shows patchy dense anthracotic pigmentation, a pattern known as dust reticu lation . Note also the character istic mild centri lobular 'focal dust ' emphysema. In addition a small, black, silicotic nodule is present (arrowed) . Simple dust reticulation results from long term exposure to coal dust; the development of nodules is due to co-inhalation of si lica. There is no increased risk of lung cancer .
L
CAUSES
O~ HONEYCOMB LUNG_ _ _
---..J
Pneumoconiosis
I I
Extrinsic allergic alveolitis
I
Cryptogenic fibrosing alveolitis (Hamman-Rich syndrome)
I I
Sarcoidosis Drugs/irradiation
I
Rheumatoid disease Systemic sclerosis Extensive pneumoniafTB Pulmonary eosinophilia Fig.2.23 Causes of honeycomb lung. Fig.2.24 Honey comb lung. The
,II\.II •••'lIn mnaalve fibrosis. This coal miner's lun g 1, 11111,1, 1.,1 Ii 11 ,1 II :Ik;ulalion, large, well demarcated, black 11111 "Iu lll' li 1.1lack nodules (top). Progressi ve massive ,I 'I i I'" I· ·.. ( ,I I :')01miners and may also be seen in " 1'1' • I·' plllhll(lollesis is unknown but it is thought that ,I . Ii or,1 '''' IIII~. l lfj I .lnd the possible coexistence of tuber III/ " ,,/ 11,1 101, I, 0/', I lie smalle r nodules seen here are " • III' III '011/, "" . 1,1I":e coal dust often has a high silica
.2.22 Haematlte pneumoconiosis. The lung parenchyma
I",w!: severe brick-red pigmentation with evidence of nodular and
• IIIII I1iU fibrosis and emphysematous change . Th is condition, due to 1I11 1f11HliQn of iron oxide, is seen most often in iron ore miners . The , I, 'V I ,to .oment of fibrotic lesions is again dependent upon the co 1I_I'.l ollce of silica in the inhaled dust. Well recognised complications ,to "I" tubercu losis and bronchia l carcinoma.
I".
apex of the lung contains numerous variably-sized cystic spaces, each having a thick fibrous wall. These cysts represent gross d i latation of bronch ioles and small bronchi in com pensation for destruction and fibrosis of neigh bouring alveoli and respiratory bronch ioles. Th is appearance re presents the end stage of va rious disease processes, the commonest of which are listed in Fig . 2.23 .
l~
2 Respiratory System
LUNG ACINUS
D
o o o
terminal bronchiole respiratory bronchiole alveolar duct alveolus
Fig.2.27 Centriacinar emphysema. In the lung parenchyma, small dilated air spaces surrounded by black anthracotic pigment are visible at the centre of the lung lobules . The surrounding alveoli are spared . These spaces correspond to the respiratory bronchioles and this is the commonest variant of emphysema, seen predominantly in cigarette smokers (especially males) . The upper lobes, particularly the apices, are most often aHected. A similar appearance is seen in coal workers (focal dust emphysema) in which there is usually little fibrosis or destruction .
Fig.2.25 A lung acinus. 3-5 pulmonary acini constitute a lung lobule.
CLASSIFICATION OF EMPHYSEMA Centriacinar Focal dust (in pneumoconiosis) Panacinar Paraseptal (bullous) Irregular Surgical (interstitial) Fig.2 .26 Classification of emphysema. With the exception of surgical emphysema, any lung may commonly show a mixed pattern of involvement.
19
Fig.2.28 Panacinar emphysema. In this lung note the much larger, confluent, dilated air spaces replacing complete lung acini. In places there is also a cent riacinar component. Panacinar emphysema , which is also very . common, affects the air spaces, including alveoli, distal to the terminal bronch ioles. In its classical form it is associated with Ct,-antitrypsin deficiency and previous bronchial obstruction . Most often, the lower lobes, particularly the lung bases, are affected.
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111 11)· ,, 1,,111
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Fig.2.30 Pulmonnry hamartoma .. 1t1(.II IIIIII pleural surfac " 1111111" t. is a very well iI.11 pale tumour. I h(l " ,",,,11 the lung is I1UII 11111 1'11111 hamartomas W' l l lIlt III" developmenl nl l ll llllllllil usually cartil aOH H" ", II , which are only 1111 " Iy 'IV matico They ,UCiIYI III 11 11 pleural in 10c;tll",I. 1111; 1' more than feIl1l,1I ;- ., .1111 entirely beniql1
do""'"
2 Respiratory System
:."Irlllclnar emphysema. In the lung parenchyma , small ' I " I, n· . . "II rounded by black anthracotic pigment are II" \ ' ·,,1,,· ot the lung lobules . The surrounding alveoli are II I, "" .. 'I ql COS correspond to the respiratory bronchioles and i ,ti l" 11( 11 H >f;t variant of emphysema. seen predominantly in II" d·. II ', ( ..'specially males) The upper lobes. particularly , II" "" 1:,1 Ollen affected . A similar appearance is seen in " I (I '" [I I dust emphysema) in which there is usually little I
11
I
4
I. " .1~ ll~ ,I'IC)I I .
Fig.2.28 Pan acinar emphysema. In this lung note the much larger, confluent, dilated air spaces replacing complete lung acini . In places there is also a cent riacinar component. Panacinar emphysema, which is also very . common, affects the air spaces. including alveoli, distal to the terminal bronch ioles. In its classical form it is associated with ai -antitrypsin deficiency and previous bronchial obstruction . Most often, the lower lobes, particularly the lung bases, are affected
Fig.2.29 Paraseptal emphysema. At the apex of this lung is a large emphyse matous bulla with a fibrous wall. The adjacent paren chyma shows mixed centri- and pan acinar change . Paraseptal emphysema predominantly affects the alveoli adjacent to the inter lobular septa or pleural surface . It is usually most pro nouncedinthe upper lobes, often close to an area of previous scarring. This variant is the usual precursor of bullous emphysema and is often seen associated with other variants, as in this case .
Fig.2.30 Pulmonary hamartoma. Just beneath the pleural surface of this lower lobe is a very well demarcated, small . pale tumour. The remainder of the lung is normal. Pulmonary hamartomas are not uncommon developmental anomalies, usually cartilaginous in nature , which are only rarely sympto matic. They are typically sub pleural in location, affect males more than females. and are entirely benign.
Fig.2.31 Bronchial 'adenoma'. In the main bronchus is a smooth . well circumscribed tumour projecting from the epithelial surface . These lesions may be derived either from submucosal glands or neuro endocrine APUD cells and are misnamed since they represent low-grade, malignant tumours which may eventually metastasise . They most often arise in young adults and there is usually extension into the adjacent lung parenchyma. Fig.2.32 Hilar bronchial carcinoma. Arising from the lower lobe bronchus , close to the hilum. is a pale neoplasm which is irregularly infiltrating the parenchyma. Bronchial carcinoma most often originates near the hilum and may be squamous (50%), small cell (oat cell) anaplastic (20%), adeno-(15%) or large cell ana plastiC (10%) in type . It is the commonest cause of death from malig nancy in Great Britain and in many cases is associated with cigarette smoking or industrial exposure to carcinogens. The overall 5-year survival is only between 5 and 10% .
20
2 Respiratory System Fig.2.33 Bronchial carcinoma with distal bronchi ectasis and broncho pneumonia. At the apex of the left lower lobe is a partly necrotic. pale neoplasm which has obliterated the lower lobe bronchus : distally the smaller bronchi are grossly dilated (bn;Jnchi ectasis) and the remaining paren chyma shows consolidation . The adjacent middle lobe shows confluent broncho pneumonia. These are common comp lications of obstruc tive bronchial carcinoma and may also be accom panied by collapse or abscess formation . Fig.2.34 Peripheral lung carcinoma. Just beneath the pleura of the oblique interlobar fissure is an irregular, well demarcated, pale tumour which is situated well away from the main bronchial tree. The majority of peripheral primary pulmonary malignant tumours are adeno carcinomas which compri se about 10-15 % of all lung cancers. These tumours show an equal sex incidence and tend to arise in foci of scarring . An apparently slow growth rate'and frequent operability means that they carry a better prognosis than most bronchial carcinomas.
21
Fig.2.35 Bronchioalveolar carcinoma. The entire lung is diffusely infiltrated by a pale neoplasm which, particularly in the upper lobe, has adopted a nodular appearance. Bronchioalveolar carcinoma comprises about 2% of all primary lung cancers and is a specific variant of adenocarcinoma, which tends to spread extensively within the air passages. Its diffuse nature often prompts mistaken clinical diagnoses of an infective or inter stitial disorder.
Fig.2.36 Multiple pulmonary metastases. Beneath the pleura and in the lung parenchyma are innumerabte pale, umbilicated nodules of tumour. Up to a third of patients dying of malignant disease have pulmonary metastases, the commonest sources of which are carcinoma of the breast, colon, stomach and lung itself. The presence of an extensive vascular and lymphatic system in the lungs is responsible for the predilection that metastases show for this site.
C! Il lqtt t. 1I I
willi " " , nhl ll",1 " I dill II II ,if It lUlttt .I. ,! li
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Ig.2.38 Pulmonary lymphangitis carcinomato.n I I ,. ',lIdace of this lung shows innumerable small spl ,,,"',tl "' I iI 'posits of pale tumour. This represents extell:.;iv" II ,ldl" i I" ilrnonary lymphatic channels, which are fillec1I,y '''1,1, . IIHI may be caused by either primary or seconda,y "" 'tl \
I"
2 Respiratory System Fig.2.35 Bronchioalveolar carcinoma. The entire lung is diffusely infiltrated by a pale neoplasm which, particularly in the upper lobe, has adopted a nodular appearance. Bronchioalveolar carcinoma compr ises about 2% of all primary lung cancers and is a specific variant of adenocarcinoma, which tends to spread extensively within the air passages. Its diffuse nature otten prompts mistaken clinical diagnoses of an infective or inter stitial disorder .
Fig.2.37 'Cannon ball' pulmonary metastases. In thi s congested lung. fo ur well circumscribed , almost spherical, deposits of pale metastat ic tumour are present. This appearance of a small number of large secondary depos~s i nthelung.
while not entirely specific , is classic ally associated with spread from renal adenocarcinomas or testicular tumours.
Fig.2.39 Pleural hyaline plaques. On the parietal pleura of the posterior thoracic wal l are several foci of yellowish hyaline thickening . This appearance is most otten seen in individuals who have suffered prolonged exposure to asbestos, usual ly in the course of their occupation. Such patients also commonly develop macroscopically non-specific pulmonary fibrosis , collapse or bronchiectasis of the lower lobes. Crocidolite is pathogenetically the most dangerous type of asbestos and occasiona lly only very brief exposure is sufficient to induce pulmonary disease . Fig.2.40 Mesothelioma. Th is apical portion of the lung is encased in pale, infiltrative tumour arising from the pleura. Involvement of the soft tissues at the apex is also apparent. Malignant mesothelioma is uncommon and may arise from the parietal or visceral pleura . The vast proportion of cases arise in patients exposed to asbestos, usually occupation ally, and such individuals or their families are entitled to indust rial compensation . The prognosis is uniformly appalling .
1111"1(,, "ulmonary metastases. Beneath the pleura and
I IYI II.I nro innumerable pale , umbilicated nodules of ,11 11111 I>~ pat lonts dying of malignant disease have , \I Id',h","· .. tho commonest sources of which are .111 11 I )11,01·,1. colon , stomach and lung itself. The •., " ' \\ 'I" ;IV" vascular and lymphatic system in the lungs I, ., II,, · I ,,( '(hlnClion that metastases show for th is site.
\ " .. , II III
Ig.2.38 Pulmonary lymphangitis carclnomatosa. The pleural
, " Ir1 t i.l of this lung shows innumerable small spherical and li near
.'''111 i' ,il S of pale tumour This represents extensive infiltration of the
I" 11""" IGry lymphatic channels, which are filled by neopl astic ce ll s,
., " "" IIY be caused by either primary or secondary lung tumours.
22
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3 Alimentary System Fig. 3.1 Oral leukoplakia. This clinical photograph shows ex tensive smooth white patches over most of the tongue . Leuko plakia is purely a clinical des cription of any white plaque and is not a pathological diagnosis . In many cases, oral leukoplakia is benign, representing hyper keratosis, the commonest causes of whic h are chronic irritation or smoking. Only cases which also show epithelial dys plasia can be regarded as pre malignant. Other causes of white lesions in the oral cavity include lichen planus and candidiasis .
'I
'Ii
Fig.3.3 Mixed salivary tumour (pleomorphic adenoma). Thi s is the commonest neoplasm of salivary gland s, the parotid being the most frequently aHected site. Th is section shows a fairl y well circumscribed, multinodular tumour; the cut surface has a myxoid cartilaginous appearance and there are small foci of cystic change and haemorrhage . These tumours are prone to local rec urrence , mos t often as a consequence of spread th rough the capsule, which results in incomplete surgical excision . Malignant transformation is exceed ingly rare .
Fig.3.2 Squamous carcinoma of tongue. This clinical photograph shows an irregular, raised pale lesion on th e inferior surface of the patient's tongue. Most malignant tumours of the oral cavity are squamous carcinomas and postulated aetiological factors include tobacco smoking, syphi lis and drinking strong spirits. They most commonly present in late adulthood , aHecting predominantly males. The clinical course is very variable but carcinoma of the tongue generally carr ies a worse prognosis than tumours si tuated elsewhere in the mouth.
23
..
Fig. 3.5 O••oP'''' '' dldlasls.IIII1I1III I11I·1 oesophO\JlIiI iI.11I11 11I immunOCCllllpl' " lli· d whether Ihoy II" '1 " 1'I tated (parlrcilli rrly I I ~ I disease), rUt;tJIVil " 1' 1 chemothcrrlPY I" I U ri a primary il1l1l1l II I"" II order. Th e :,Ilvllllly " tion is deprH" 1,·, I( 111" degree of tJ"hlllly , .,, ' appearancI1 ", II ''' I may rango 11 (111 I 1111 ' ~ I plaque s Witl, llli"'"I,. i mation to UI OYI· II" III, lesions with fllII l1II II III forma tion niH t ,," ,1111> mation, (1:': ::111111 11111 '
Fig. 3.4 Pharyngeal pouch. The pharynx has been opened posteriorly to show a diverticulum extend ing laterally. A pharyngeal pouch is a pu lsion diver ticulum which occurs at Killian 's dehiscence, due to neuromuscular in coordination of the pharyngeal con stri ctor muscles. Elderly males are predominantly affected and ve ry occasionally post cricoid carcinoma may develop in sucll a pouch .
III J.6 Oesophagus - peptic (Barrett's) ulcer. II "' I,Iq [,I Ir tlil icer with a haemorrhagic base is presollt III "," " 'I II" ' Io;:,ophagus . Barrett's ulcer occurs as a cOIII"Ii, erostridium difficile (a Gram-positive anaerobe) and the elaboration of its potent exotoxin to occur.
CLASSIFICATION OF-LARGE
Fig.:!.
B~WEL PO~~
adcn lll ~
eX; If"I'''] ,'IV of the hepatic vein are occluded by thromULJ!: II IlId'I'I I (bottom) occupies the lumen of the inferim VO l I;, , ~ ; 'V" primary leiomyosarcoma . This rare syndrorrll ! I!, tlr'" II, the prinCipal hepatic veins or inferior vena L. , IV i I, , I'" I II i endophlebitis, obstruction by tumour eith(;l f II "", II V (II secondary or adjacent, or associated willI I II ,lye.yIl I' '' '11
4 Hepatobiliary System
[
CAUSES OF HEPATIC FATTY CHANGE
Alcohol abuse Starvation/malnutrition
Diabetes mellitus
Glycogen storage diseases
Galactosaemia infarct . In this clo se·up v iew. an approx· area of subca psu lar parenchyma shows a with slight concavi ty of the overlyi ng appearance which results from throm radicle. usually as a consequence of a sm all by tumour The hepatic arterial supply in such cases. but parenchymal atrophy and
acute idiopathic fatty change Pregnancy fatty change with hyperemesis
Severe systemic infection
Pathological obesity
1
Cystic fibrosis
,
,
thrombosis. A large branch of the portal vei n is thrombus. Note that the li ver parenchyma shows Cirrhosis. Portal vein thrombosis is most often local venous obstruction by a neoplasm, or recent abdomin al surgery. While passive romrnon ly ensues, true hepatic infarction does blood supply from the hepatic artery is also
Drugs, especially tetracycline
Flg.4.9 Budd-Chiarl syndrome. The liver parenchyma (top) shows 0111 :lrlllll). I varying size, each separated by dense fibrous 1,111" II' macronodular pattern is a feature of post-viral (11' :lIlI lI v cirrhosis and Wilson's disease. Note, however, 111111' " ' livers show a mixed pattern, irrespective of aetiolnl IV
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'base of the skull are known as glomus
, ," 1\ v,,"nl')le number behave In a malignant fashion .
Fi,.8.1 Fetal renal fobulation. These are kidneys from a stillborn infwl : note the marked cortical lobulation . This appearance is enlirely nOmal but is usually no longer apparent by one year of age How e~r, lobulation. if only partia l. sometimes persists into adult life and it is rnportant to recognise that such a finding is of no pathological iiTl)ortance.
I I
Fi\.8.2 Horseshoe kidney. The kidneys are fused at their lower pees and bOlh renal hila lie anteriorly. The isthmus of renal tissue wt.c h joins the Iwo kidneys layover the aorta in vivo. Renal fusion OO;urs in at least 1 in 250 individuals and results from partial failure of enbryological ascent of nephrogenic tissue, followed by malrotation. Cr.existent anomalies of the ureters or renal vessels are often also se,n and may predispose to urinary infection or obstruction.
Fig.8.3 'Infantile' polycystic disease. The renal parenChyma of this adolescent's kidney is completely replaced by thin wa lled cysts Infantile polyc ystic disea se ma y take a va riety of forms . Classically , it has an autosomal recessive Inheritance and take s a fatal course in infancy. In such cases the kidneys appear normal exter nally but show numerous small. radially arranged cysts on sectioning. There IS always associated congenital hepatic fibrosis ; in some cases (as here) the renal appearances and clinical duration may be ve ry va riable Fig.8.4 Adult polycystic disease. This kidney has been bisected th rough the hilum to show extensive parenchymal replacement by cysts of varying size, into some of which haemorrhage has occured. Adult poly cystic d isease is an autosomal dominant inherited condition ; patients typically presenl in middle age and chronic renal failure usually supervenes there after. Associated hepatiC or pan creatic cysts and cerebral berry aneurysms may also be found.
62
8 Urinary System Fig.a.S Medullary sponge kidney. The cut surface of this kidney shows multiple, smooth walled cysts which are confined to the renal papillae. This condition, thought to be due to develop mentally anomalous collecting ducts, affects males more than females and is usually detected in the 5th or 61h decades. Calculi often develop within the cysts and, in combination with recurrent urinary infection, may lead to impaired renal function .
Fig.a.6 Renal dysplasia. Much, but not all , of this kidney is rep laced by coarse, irregular cysts separated by broad bands of fibrous tissue. Renal dysplasia, which represents failure of nephrogenic dif ferentiation, may affect one or both kidneys and may involve either the whole, or only part, of the kidney. Often other developmental anomalies, usually obstructive in nature , are present elsewhere in the urinary tract.
63
Fig.a.7 Simple renal cyst. Arising from the cortex of the lower pole of this kidney is a large, thin-walled cyst. Simple ,enal cysts are extremely common, particularly with advancing age, and are thought to represent the local effect of previous ischaemia or obs truction. They are usually solitary, are typically located in the cortex and are most often only about 1 cm in diameter, the exam ple here being unusually large.
Fig.a.a Acute pyelonephritis. This hemisected kidney shows intense con gestion and in numerable , radially arranged yellow areas of suppuration and abscess forma tion, especially in the medulla. Acute pyelonephritis is not uncommon and is usually a con sequence of ascending Gram negative infection. Common predis posing causes include urinary obs truction, diabetes mellitus and preg nancy . In general, females are most often affected , probably as a con sequence of peri urethral contami nation by faecal organisms.
Fig.a.g Renal tuberculosis. The parenchYI' "" d 'III kidney shows numerous confluent foci of CW,IICiIl' , ' ,, ' , also marked calyceal invotvement with dllllt.liI"" , ' /'VII called 'pyonephrosis' (despite the absellc(.! ,,11 111' 1) I culosis is often bilateral, is commonest in a dilli I fllIl! due to haematogenous spread from prima,y II d, ,' III " While remaining endemic in some part s 0 11111' Wi "I i I now uncommon in Caucasians. I III
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8 Urinary System
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Fig,B,9 Renal tuberculosis, The parenchyma of this bisected kidney shows numerous confluent foci of caseous necrosis; there is also marked calyceal involvement with dilatation, giving rise to so called 'pyonephrosis' (despite the absence of pus). Renal tuber culosis is often bilateral, is commonest in adult males and is usually due to haematogenous spread from primary infection elsewhere. While remaining endemic in some parts of the world, this infection is now uncommon in Caucasians.
te i ~is_
This lidney e con
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Fig,B.10 Chronic interstitial nephritis. The capsular surface of this kidney shows coarse , irregular scarring and the whole organ is rather shrunken. Chronic interstitial nepl1ritis is the term used to describe chron ic parenchymal inflammation and atrophy , which may be a consequence of various conditions including chronic suppurative pyelonephritis , long standing ischaemia or obstruction and analgesic nephropathy.
lOW
·)uration forma lly in the Ite s is not ndis
ram ction . dis
s Iyobs tes
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Fig,B,11 Renal calculus, Lying within the renal pelvis is an irregular, ovoid stone . Surprisingly , there is no evidence of hydronephrosis. Calculi in the urinary tract are common, are seen most frequently in the kidney and usually present in adult hood . Predisposing causes include urinary obstruction, an elevated urinary concentration of the relevant constituent or altered urinary pH facilitating crystal precipitation .
Fig,B,12 Staghorn renal calculus. This stone has a branched appea rance (resembling the antlers of a stag) and formed an accurate cast of the pelvicalyceal system and upper ureter from which it was removed. Staghorn calculi are typically composed of calcium phosphate (the commonest constituent of renal stones) but may also be made up of 'triple' phosphate or cystine . Compli cations of urinary lithiasis include obs truction, infection and haematuria.
64
8 Urinary System
rllI .1I I
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11 Nervous System
Ij
Fig.11.S Adult bacterial meningitis. The superior surface of the brain is intensely congested and covered in a purulent exudate , particularly over the frontal lobes (left) . Suppurative meningitis may complicate endocarditis, middle ear, sinus or pulmonary infections or trauma. Direct spread of organisms may also occur from the nasopharynx . Important pathogenic organisms include Neissena meningllidiS (in young chitdren and young adulls) , Haemophilus influenzae in young children and Streptococcus pneumoniae in the very young or old . Almost any organism , including fungi . may be responsible in the immunocompromised patient
Fig.11 .6 Neonatal bacterial meningitis. The surface of this neonate's brain shows conges tion and supp uration, especially over the inferior aspect of the right temporal lobe. Neonatal meningitis is seen most often after a prolonged or traumatic delivery and is more common in premature infants. The cu lpable organism is always derived from the maternal genital tract at birth, most often being Streptococcus pyogenes or a coliform, parti c ularly E. coli.
Fig.11.7 Tuberculous meningitis. Over the parietal lobe there is a dense inflammatory exudate associated with numerous adjacent 'tubercles' . Tuberculous meningitis is usuall y seen as a complication of primary Infection in young individuals and is most often due to miliary spread. It may also result from rupture of a localised intra cerebral tuberculous (Rich) focus into the subarachnoid space The base of the brain and upper cerebe llum are most often affected . Fig .11.8 Cerebral abscess. Within this left cerebral hemi· sphere is an irregular abscess cavity which is parlly walled off . There is surrounding con gestion Predi sposing causes are much the same as those for suppura· ..... ~~ tive meningitis (see Fig.11.5) in cluding haematogenous spread of any sys tem ic Infec tion. The latter typically leads to abscesses localised in the distribution of the middle cerebral artery.
88
11 Nervous System
Fig.11.9 General paresis of the insane. This coronal section of brain shows marked cortical atrophy , flattening of the gyral pattern and compensatory hydrocephalus . General paresis is a late (quaternary) manifestatioll of syphilis . Other macroscopical features include leptomeningeal thickening and granular ependymitis. The resultant neuronal loss may be associated with dementia, epilepsy, motor dysfunction and the Argyll Robertson pupil. Cord involvement in quaternary syphilis gives rise to tabes dorsalis .
Fig.11.10 Raised intracranial pressure. This coronal section of brain shows marked compression and asymmetry of the left lateral ventricle and, just above, herniation of the cingulate gyrus. Raised intracranial pressure is most often seen in association with intra- or extracerebral haemorrhage, a tumour or extensive infarction . The cardinal macroscopic features, other than those shown here, are tentorial or tonsillar herniation (cerebellar coning) and uncal grooving ,
89
Fig.11.11 Cerebral fat embolism. This section of brain shows numerous small petechial haemorrhages, most notably in the white matter. Fat embolism most commonly results from damage to a major bone , particularly a fracture, in which medullary fat enters the venous system. This may pass unnoticed or may result in impaired cerebral, pulmonary and renal function, Other causes of such haemorrhages include malaria, leukaemia and thrombocytopenic purpura.
Fig.11.12 Acute subdural haemorrhage. The specimen consists of dura (right), blood clot and the left cerebral hemisphere. An extensive depression is visible in the left temporoparietal region. Subdural haemorrhage is usually traumatic in origin and results from tearing of thin-walled veins as they enter the dural sinuses. Acute lesions may be rapidly fatal if not surgically evacuated, while undetected haemor rhage may result in gradual, chronic cerebral damage.
Fig.11.13 Subarachnoid haemorrhage. Ruplill" 1.1 .1I " aneurysm of the left posterior cerebral artery 1I1I:; 1/1 '.1 III. I' I subarachnoid haemorrhage around the base 0111 11 ' 11111 111 tensive rupture of berry aneurysms (see Fig .1! ! ~l) I'. II " source of subarachnoid bleeding but other imiJl >Iii" II , •I' trauma and extension of an intracerebral haem(1I II 1,," 11 prognosis is generally poor .
Fig.11.14 Cerebral artery aneurysms. On Il u' II ,II, 11 11 have been separated to display a berry aneuIY:lIl l (11111 '1 at the junction of the left anterior cerebral and :1111 11111 II' , cating arteries . On the right, an atheromatous ~.j\\ ! qlill (see Chapter 1) is seen in the left posterior C()11l1 II III ," II Berry aneurysms usually result from degenornll vl' 1Ii,1I1 of a congenital defect in the arterial wall. They frill Y I." II are sometimes associated with polycystic r91l; 11dlllllll'" subarachnoid haemorrhage, they may alsOhi', Gi ll ""III cerebral haemorrhage or infa,rction.
I I Nervous System
. ....c
"" Fig.11.17 Recent cerebral infarct. There is an extensive area of haemorrhagic infarction with a hyperaemic border in the parietal region. Note also the adjacent marked cerebral oedema. Cerebral infarction is the commonest cause of a 'stroke' (CVA) and is most often due to thrombosis in an atheromatous vessel. It may also be embolic in origin (e .g . from the lett atrium in atrial fibrillation) or associated with hypercoagulability or the contraceptive pill. Fig.11.18 Old cerebral infarct. This coronal section of brain shows a massive previous right -sided inlarct which has resulted in loss 01 cortical tissue, cysl ic degeneration and compensatory hydrocephalus. Multiple (usually small) inlarcts over a variable period 01 time may lead to numerous loci 01 cerebral softening (status spongiosus) and Ihe clinical syndrome'ol mull, inlarct dementia.
91
Fig.11.19 Multiple sclerosis. tn the periventricular white matter and adjacent internal capsule (left) there are three well -defined grey plaques (arrowed) indicati ve of foci of demyelination and gliosis . Multiple sclerosis typically affects young adults, particularly females and is a chronic. relapsing and debilitating disease . Aetiologically, a slow viral infection is thought (but nOI proven) to be responsible , perhaps in combination with genetic factors. Fig.11.20 Alzheimer's disease. The meninges have been stripped from the left side of this brain to show marked cerebral atrophy , manifest by sulcal widening and diminution of the gyri. Alzheimer's disease is a chronic form of pre-senile dementia, is commonest in the 5th and 6th decades and may also be seen in Down's syndrome. The aetiology is entirely unknown.
Fig.11.21 Meningioma. A circumscribed nOIIlII;1I tlill II III I from the meninges (left) has been 'shelled out' nll ll(1 " ' 11 1' leaving a deep spherical depression . MeningiC') lnlUl , d. ,,,11' arachnoid villi, most often arise in relation to 111 0 lI1.'i, 1I \I",,' sinuses. They are slow-growing, almost invanailly 1"!I l1 lJ,1 but may occasionally invade the adjacent skllil . 111I 'V"1 , I I dominantly in the 5th and 6th decades and SYflli>I ()1I 1~.. II ' upon the site of the tumour.
Fig.11.22 Glioma. This coronal section of b, Llil •. .1 II I....,. " neoplasm, with foci of haemorrhage and necro::i·. III It lll I, sphere . There is adjacent oedema and distortioll ()III ~I .I' system. Gliomas may be divided, in order of froql I, "ILV II blastoma multiforme (see Fig 11.23), astrocyl \lIl .fI, 11111t1 ., I glioma, ependymoma and choroid plexus pal)illol lIit M I not uncommon . Gliomas do not give rise to Sy ~tl1JJ1I1 Iq, ·1 may 'seed' throughout the CNS and cause de:lll. hy Ih, II effects.
11 Nervous System
matter and grey gliosis larly females Irolog ically, a ponsible,
Fig, 11,21 Meningioma, A circumscribed nodular tumour arising from the meninges (left) has been 'shelled out' of the left parietal lobe, leavi ng a deep spherical depression. Meningiomas, derived from the arachnoid villi, most often arise in relation to the major venous sinuses. They are slow-growing, almosl invariably benign, tumours but may occasionally invade the adjacent skull. They occur pre dominantly in the 5th and 6th decades and symptoms, if any, depend upon the site of the tumour.
Fig.11.23 Glioblastoma multiforme. These coronal sections of brain show a massive haemorrhagic tumour arising in Ihe basal ganglia and dislorting the lateral ventricles . Glio blastoma multiforme is an un differentiated glial tumour, most often of aslrocytic derivatio n, and occurs predominantly in the 4th and 51h decades. It is the commonest variant of glioma, arises mosl often in the frontal lobes, septum pellucidum and basal ganglia and carries a very poor prognosis .
.
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.
.
,
Fig.11.22 Glioma. This coronal section of brain shows an ill-defined neoplasm. with foci of haemorrhage and necrosis in the left hemi sphere. There is adjacent oedema and distortion of the ventricular system. Gliomas may be divided, in order of frequency, into glio blastoma multiforme (see Fig 11.23), astrocytoma, oligodendro glioma, ependymoma and choroid plexus papilloma. Mixed types are not uncommon. Gliomas do not give rise to systemic metastases but may 'seed' Ihroughout the eNS and cause death by their local effects.
Fig.11.24 Ependymoma. Arising in the 4th ventricle and compress ing the cerebellum posteriorly is a large, multUobulated, while tumour. Ependymomas are one of the least frequent forms of glioma but are the commonest to arise in the spinal cord. They are derived from the ependymal cells that line the ventricular system and cord canal. While typically slow-growing , their location often renders Ihem in operable and the prognosis is poor.
92
II
11 Nervous System
Fig.11 .25 Acoustic neuroma. Situated on the left cerebello· pontine angle is a well circumscribed neoplasm arising from the eighth cranial nerve . This is a benign Schwann cell tumour which is sometimes bilateral and may be associated with neurofibromatosis . Clinical features include tinnitus, vertigo and nerve deafness . Compli cations include compression of other cranial nerves or of Ihe brainstem.
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Fig.11.27 Benign schwannoma (neurilemmoma). This is a well circumscribed, encapSUlated, small tumour which has a yellowish cut surface and shows small foci of haemorrhage. Benign schwannoma is a common tumour of peripheral nerves and arises from the nerve sheath. It is usually solitary, arises especially in the 3rd to 5th decades and is most often asymptomatic Occasionally, multiple lesions may be seen in neurofibromatosis but in the latter condition multiple neurofibromas are far more common.
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Fig.11.26 Cerebral metastasis. This coronal section of brain shows a solitary, large deposit of focally necrotic and haemorrhagic meta static tumour , which is situated in the region of the left basal ganglia and is compressing the lateral ventricle . Cerebral metastases, which are usually multiple, are most often situated at the junction of the grey and white matter and are typically well circumscribed (cf. glial tumours). The most frequent primary sites are bronchus, breast, kidney and cutaneous malignant melanoma .
93
Fig.11.28 Plexiform neurofibroma. This is a major pelvic nerve trunk from a patient with neurofibromatosis and shows gross thicken ing and expansion by a diffuse tumour. Neurofibromas are benign tumours of nerve sheath origin . They are often seen in von Reckling hausen's neurofibromatosis, an inherited condition which is charac terised by cafe au lait spots, multiple peripheral nerve tumours and is associated with CNS tumours, phaeochromocytoma and an increased risk of developing neurofibrosarcoma .
12 Osteoarticular System Fig.12.1 Bone fracture. Above, the proximal femur shows an obvious recent subcapital fracture. Part of a rib (below). adjacent to the costochondral junction, shows a transverse fracture, on either side of which is exuberant callus formation. Simple fractures heal by the produc tion of periosteal and then medullary callus. which is followed by new cartilage and bone formation with sub sequent re modelling. The majority of fractures are traumatic in origin but a minority occur through a pre exislent pathological lesion (e.g. a metastasis) Complications include deep ver,ous thrombosis, fat embolism and damage to adjacent tissues (e.g. muscle, tendon, vessels), the latter sometimes leading to Volkmann's cont ractu re.
Fig.12.2 Malunion. This macerated segment of a long bone shows clear evidence of a previous fracture but. malunion has occurred with de formity resulting from overlap of the bony ends. Malunion follows failure to reduce a displaced fracture. This appearance may also be seen, in a less extreme form, after fracture through an epiphyseal plate (prior to completion of ossification) which results in an abnormal growth pattern.
Fig.12.3 Non-union with false joint. Following a fracture of this humerus the bony ends have not been apposed. This has resulted in fibrous union, succeeded by cartilaginous metaplasia and the formation of a pseudarthrosis. Causes of non-union include delayed union (most often due to ischaemia, excessive mobility, local infection or malnutrition), the presence of extraneous tissue between the bone ends or failed treatment of an extensive or widely displaced fracture.
94
12 Osteoarticular System Fig.12.4 Chronic osteomyelitis. The shaft of this macerated femur shows extensive necrosis (the sequestrum) and is surrounded by a dense outer shell of periosteal new bone (the in vOlucrum) . Chronic osteomyelitis most often follows an untreated acute episode this latter is commonest in children and is usually the result of a bacter aemia (often staphylococcal, streptococcal or pneumo coccal). Salmonellae may be responsible in patients with sickle cell anaemia. Infect ion commences in the highly vascular metaphysis. most often of a long bone, and is followed by subperiosteal and intra medullary spread. Fig.12.5 Spinal tuberculosis (Pott's disease). This portion of the thoracic spine shows caseous necrosis of two adjacent vertebral bodies with destruc tion of the inter vertebral disc . Tuberculous osteomyelitis, although commonest in long bones, shows a predilec tion for the spine. It is most often a result of spread from primary pulmonary infection and may be complicated by vertebral collapse, a paravertebral 'cold' abscess or cord compression .
...
Fig.12.6 Syphilitic periostitis. This is a macerated segment of femur showing a thick layer of sub periosteal new bone. Congenital syphilis classically gives rise to both a florid periostitis (with reactive new bone formation), as in this example , or an osteochondritis (granulomatous inflammation at the ends of long bones). Similar appearances may be seen in tertiary acquired syphilis . in which coexistent gummata may also be present.
Fig.12.8 Ric k.,. throuqlrllr,' I, 'WI'I 10 uppel 111".1, ,1 , , 1'110 , markeclllll( 1" '"1110 1' plat es ,'"1 I .r ' .1' 11111" endochl,,"I/ ,11 1 II, I Rick ets FII II I ! ,'.1, ,, 'It I both c h; II 111 1"1 11 " " I I bon e rnllll :I. II,· .. 011 1" is a dis8;'1,.I' ,'I I 1111 1II compl Clloll l ll'lif llN l l latter IS ~;l'O II III . II II ,II comrTlo r)(,H " I
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Fig.12.9 Tophlll .,' This SO 'l1111'III, ,II " " covere1 1 rntfltl"I.· Ii "." '"' , 110 1 ri!::ik of I II -V I ,I, 'I 111111 i sarCOl1 1.1 t
12 Osteoarticular System
Fig.12.23 Cartilage-capped exostosis. This lesion. which projected from the surface of a femur, shows a pale outer rim of cartilage ove rlying a nodule of cortical bone . These exostoses (also known as osteochondromas or ecchondromas) are thought to be developmental lesions , derived from laterally aberrant epiphyseal ca rtitage, which then undergoes endochondral ossification . They present most often in the lower femur or upper tibia of children or young adults. Rarely, they may be multiple (an inherited condition known as diaphyseal aclasis). in which circumstance there is about a 20% risk of developing chondrosarcoma. Fig.12.24 Enchondromatosis. This coronal section through the lower end of the femur shows multiple blue-grey nodules of cartilage in the epiphysis, meta physis and diaphysis. Enchon dromas are benign tumours, which may be solitary (typically arising in the long bones of young adults) or multiple . The presence of multiple lesions (known as Oilier's disease) is not thought to be hereditary and may be associated with soft tissue haemangiomas (Maffuci's syndrome). Any patient with multiple lesions has a significant risk of developing chondro sarcoma.
!t'0-o::;,t'!5'
Fig.12.25 Aneurysmal bone cyst. This lesion, removed from the femur, is composed of a well circumscribed haemorrhagic mass within which are numerous vascular spaces. Aneurysmal bone cysts are benign tumours, probably of vascular origin, which typically ari se in the long bones or the spine of adolescents and young adults. They are often painful and tend to local recurrence if in adequately excised . Their occasional coexistence with other adjacent benign tumours of bone further confuses their -.L!l uncertain histogenesis .
Fig.12.26 Osteoclastoma (giant cell tumour of bone). Arising in the epiphysis of this femur and extending into the metaphysis is a reasonably circumscribed. haemorrhagic mass. Giant cell tumours of bone are uncommon lesions which tYP ically present in young adults and tend to arise in the epiphysis 01 long bones (particularly in the leg) . Their histogenesis is uncertain and they must be dis tingUished from other giant cell lesions such as chondroblastoma . chondromyxoid fibroma or hyperparathyroidism . Up to 25% behave in a malignant fashion .
100
12 Osteoarticular System
Fig.12.27 Osteosarcoma. Arising in the metaphysis of this femur is an ill·defined, pale and focally haemorrhagic tumour which has elevated the periosteum and eroded into adjacent soft tissue. Osteo sarcoma. in the majority of cases, presents in the first two decades, shows a predilection for males and classically arises in the metaphysis of a long bone (particularly the femur or tibia). A small proportion of cases are seen in the elderly, secondary to Paget's disease (see Figs. 12.16 and 12.17). They tend to extensive local invasion and early haematogenous spread. the overall 5-year-survival being about 20%
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Fig.12.28 Chondrosarcoma. Arising from the pelvis, adjacent to the acetabulum. is a widely invasive tumour, largely composed of irregularly lobulated, blue-grey carti laginous tissue. In contrast to osteo sarcoma. chondro sarcoma typically presents in the 6th and 7th decades and arises most often in the pelvis (although proximal long bone involve ment is not uncommon). It tends to be slow-growing. often attaining a considerable size.. and 5-year-survival is about 75%
101
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Fig.12.29 Multiple myeloma. This portion of skull (top) shows multiple punched-out lesions containing haemorrhagic tumour. Below, a segment of the spine demonstrates ill demarcated, haemorrhagic, osteolytic lesions in the lower cervical vertebral bodies. Multiple myeloma typically presents in late adulthood and is characterised by a neoplastic proliferation of plasma cells, which classically gives rise to osteolytic lesions in the marrow of the axial skeleton. Excessive immunoglobulin production by the tumour cells allows detection of the light chain Bence-Jones protein in the urine. a useful diagnostic aid. Complications include a predisposition to infection. renal damage and amyloidosis The prognosis is very variable.
12 Osteoarticular System Fig.12.30 Meta static breast carcinoma. Within the vertebral bodies are scattered, pale, soft necrotic nodules of metastatic tumour. Metastases are the commonest tumour to be found in bone and are most often osteolytic in character. While any disseminated malignancy may involve bone, the commonest primary sources responsible are carcinoma of the breast, lung, prostate, kidney and thyroid .
Fig .12.31 Meta static prostatic carcinoma. The vertebral bodies at the base of this spine are largely replaced by whitish , firm, ill-defined metastatic tumour. Secondary prostatic carcinoma in bone classically stimulates local new bone formation thus giving rise to an osteosclerotic appearance. Breast carcinoma may sometimes have a similar effect.
102
l[f[[I[lrr[[[[lf[II[[[II[[--lf[llr[[I~rrr[ Index Achalasia , 25 Acoustic neuroma, 93 Adenocarcinoma breast, 46-49
duodenum, 28
gallbladder, 43
kidney, 68
large bowel , 34-35
lung , 20-21
ovary , 74-75
pancreas , 44
prostate, 85
stomach,27-28
uterUS , 80
Addison 's disease, 59 , 60 Adenomyoma, 79 Adenomyosis , 79 Adrenal gland Addison 's disease, 59 haemorrhage, 59 nodular hyperplasia, 60 tumours, 60-61 Alzheimer'sdisease , 91 Amyloidosis renal,68 spleen, 51 Aneurysmal bone cyst , 100 Aneurysms aortic , 11-12 berry, 90 cerebral artery, 90 dissecting , 11-12 left ventricular, 2 splenic artery, 12 true, classification of, 11 Ankylosing spondylitis, 98 Aorta aneurysms, 11-12 atheroma, 9-1 0 fatty streaks ,9 syphilis, 10 Aortic valve incompetence , causes , 5 infective endocarditis , 5-6 non-infective endocarditis, 6
103
stenosis , 4-5 Aortitis, syphilitic, 5, 10 Appendicitis, acute , 31 Appendix , carcinoid tumour, 30 Asbestos and lung disease , 22 Atheroma, 1, 9 complicated , 10
risk factors , 9
ulcerated , 10
Atrium , left, myxoma of, 8 Barrett's ulcer, 24 Bileducts carcinoma, 43 gallstones in , 42 Bladder diverticulum , 71 transitional cell carcinoma, 71 Bones fibrous dysplasia, 99 necrosis, 96 tumours, 99-102 see a/so Fractures and specific disorders of bones Bowel, large amoebic dysentery, 33 chronic ischaemic colitis, 32 Crohn 's disease , 29 diverticular disease, 32 diverticulitis , 32 pseudomembranous colitis , 33 tumours, 33-35 ulcerative colitis , 31-32 Bowel , small Crohn's disease , 29 infarction, 30 ischaemia, 30 tuberculosis, 30 tumours, 30 typhoid infection, 29 ulcers, 29 Bowen 'sdisease, vulval, 82 Brain abscess , 88 atrophy, 91
fat embolism , 89
general paresis, 89
haemorrhages, 89-90
hydrocephalus, 87
infarction , 91
meningitis, 88
raised intracranial pressure, 89
tumours, 92-93
Breast carcinoma, 46-49 duct papillomata, 46 fibroadenoma, 45-46 fibrocystic disease, 45 gynaecomastia,49 male, 49 mammillary fistula, 45 non-Hodgkin 's lymphoma , 49 peau d'orange , 48 Brenner tumour, 75 Bronchi , tumours, 20-21 Bronchiectasis , 15,21 causes , 15 Bronchopneumonia , 13, 15 with bronchial carcinoma, 21 tuberculous , 16 Budd-Chiari syndrome, 38 Burkitt's lymphoma, 52 Caecum, carcinoma of, 35 Calculi bile duct, 42 gallbladder, 42 , 43 renal , 64 stag horn , 64 Candidiasis , oesophageal , 24 Carcinoma see sites of carcinoma Cardiomyopathy congestive, 7 hypertrophic obstructive , 6 types of, 6 Cerebral see Brain Cerebral artery , aneurysms , 90 Cerebrospinal fluid , normal circulation, 87 CerebrovaSCular accident, causes, 90, 91
Charcot's joint, 98 Chemodectoma, 61 Cholangiocarcinoma,43 Cholecystitis acute, 42 chronic, 42 Cholelithiasis, 42, "3 Cholesterolosis , 43 Chondrosarcoma, 100, 101 Choriocarcinoma testis , 84 uterus , 81 Cirrhosis, 39-40 Coalminers, lung diseases, 17-18 , 1!) Colon/Colitis see Bowel, large Conn's syndrome, 60 Coronary artery thrombosis, 1 Corpora albicantia, 72 Corpus luteum , 72 Craniopharyngioma , 55 Crohn 's disease, 29 Cushing 's syndrome , 60 Cystadenocarcinoma (ovary) mucinous, 75 serous, 74 Cystadenoma (ovary) mucinous , 74 serous, 73 Duke's staging of large bowel tumOllr~: . : 1'1 Duodenum periampullary carcinoma, 28 ulcers , 28 Dysentery, amoebic, 33 Dysgerminoma, 76
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Chemodectoma, 61
Cholangiocarcinoma,43
Cholecystitis
acute, 42
chronic, 42
Cholelithiasis, 42, .13
CholesterolosiS,43
Chondrosarcoma, 100,101
Choriocarcinoma
testis, 84
uterus, 81
Cirrhosis, 39-40
Coalminers, lung diseases, 17-18, 19
Colon/Colitissee Bowel, large
Conn'ssyndrome, 60
Coronary artery thrombosis, 1
Corpora albicantia, 72
Corpus luteum, 72
Craniopharyngioma, 55
Crohn's disease, 29
Cushing's syndrome, 60
Cystadenocarcinoma (ovary)
mucinous, 75
serous, 74
Cystadenoma (ovary)
mucinous, 74
serous, 73
Duke's staging of large bowel tumours, 35
Duodenum
periampullary carcinoma, 28
ulcers, 28
Dysentery, amoebic, 33
Dysgerminoma, 76
Ecchondromas, 100 ,
Ectopic pregnancy, 77
Emphysema
centriacinar, 19
classification, 19
focal dust, 19
panacinar,19
paraseptal,20
Enchondromatosis, 100
Endoci Irdill•. aculOdl(Jlll llllli. , I ·1 infe(;tivu, ~ , non-lf1feCliv" II". ",il lI/ Iii: , () types or , ~ , Endocrine NI '''II IiI'd, I : 'Y 'IIII' l1Tl O , Multiple see Mulli plt l I 11I 1"l lil l' I N' H!plasia Synd"""" Endometri0111c: ovarian, 7: \ Endometriulll
adenocar,:11 11 1111(1.1\( I
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polyp, 79
Endomyoca rdl lllll, 1,1,14 1'11:1 , /
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Epicardium, tllulll(\llIlil ' dUpOSltS, 8
Epididymitis
abscess,8!)
chronic, 85
tuberculous, 8
Exostosis, carlil ago cappeu, 100
Fallopian tubes
abscess,72
cysts, 77
ectopic pregnancy, 77
hydrosalpinx, 78
inflammation, 72, 78
pyosalpinx, 78
Fatty change
heart, 9
liver, 38-39
Fibroids,79 Fractures, 94
malunion, 94
non-union with false joint, 94
osteoporosis and, 95
Gallbladder
carcinoma, 43
cholecystitis, 42
cholesterolosiS,43
stones, 42
Gastritis
acute, 26
chronic atrophic, 27
Ghon focus, 15
Glioblastoma multiforme, 92
Gliomas, 92
Glomerulonephritis
acute proliferative, 66
chronic, 67
membranous, 66
Glomus jugulare tumours, 61
Goitre
colloid, 56
diffuse toxic, 56
multinodular, 56, 57
Gout, tophaceous, 96
Granulosa cell tumour, 75
Graves' disease, 56
Grawitztumour, 68
Gynaecomastia,49
Haemochromatosis, 39, 40
Haemopericardium, 2,12
Haemorrhages
intracerebral,90
pontine, 90
subarachnoid, 90
subdural, 89
Haemosiderosis, pulmonary, causes, 17
Hamartoma, pulmonary, 20
Hashimoto'sdisease, 56, 57
Heart
brown atrophy, 9
see a/so specific parts and diseases of
heart
Hodgkin's disease
breast, 49
hepatic involvement, 41
lymph nodes, 53
spleen in, 52
Honeycomb lung, 18
Hydatid cyst, hepatic, 37
Hydatidiform mole, 81
Hydrocephalus, 87, 89
causes, 87
Hydronephrosis, 68, 69, 70, 71
104
Hydrosalpinx, 78 Hyperaldosteronism, 60 Hyperostosis frontalis interna, 99 Hyperparathyroidism, 58, 96 Hypothyroidism, 56, 57 Infarct bone,96 cerebral,91 hepatic, 37 intestinal , 30 myocardial, 1, 2 pulmonary, 17 renal,65 testicular, 83 Intestines see Bowel Islet cell tumours, 44 Joints, 96, 97, 98 Kidney acute pyelonephritis , 63 amyloidosis, 68 chronic interstitial nephritis , 64 cortical lobulation, 62 cortical necrosis , 65 cyst, simple, 63 dysplasia, 63 essential hypertension, 66 glomerulonephritis, 66-67 horseshoe, 62 hydronephrosis, 68, 69 , 70, 71 infarction , 65 lobulation , 62 medullary sponge, 63 nephrotic syndrome, causes of, 67 papillary necrosis, 68 polycystic, 62 renal vein thrombosis, 65 stones, 64 transplant rejection, 65-66 tuberculosis, 64 tumours, 68-69 Krukenberg tumour, 77
105
Lambl's excrescence , 8 Larynx, carcinoma, 13 Leiomyoma gastric, 28 uterine , 79 Leiomyosarcoma, uterine , 80 Leukaemias , spleen and , 51-52 Leukoplakia, oral , 23 Linitis plastica, 28 Lipids, cardiovascular deposition, 9 Liver abscesses, 36 amoebiasis, 36 amyloidosis, 39 Budd-Chiari syndrome, 38 cirrhosis, 39-40 fatty change , 38-39 hydatid disease , 37 necrosis, 36 polycystic, 36 portal vein thrombosis, 37 tumours, 38, 40-41 venous congestion , 37 Zahn infarct, 37 Lobar pneumonia, 13 Lung abscesses, 14 acini,19 emphysema, 19-20 occupational disease , 17-18,19, 22 sarcoidosis, 51 tuberculosis, 15-16, 18 tumours, 20-22 Lymph node Hodgkin 's disease, 53 malignant melanoma, 54 non-Hodgkin 's lymphoma, 54 sarcoidosis, 53 secondary carcinoma, 54 tuberculosis, 53 Lymphoma adrenal gland, 61 breast, 49 Burkitt 's, 52
hepatic involvement, 41 intestinal , 31 lymph nodes , 53-54 thyroid gland, 58 see also Hodgkin 's disease ; Non Hodgkin 's lymphoma Maffucci syndrome, 100 Malignant melanoma, lymph nodes, 54 Mallory- Weiss tear, 24 Meckel 's diverticulum , 29 Mendelson's syndrome, 14 Meningioma, 92 Meningitis bacterial,88 tuberculous , 88 Mesenteric artery, embolism , 30 Mesothelioma, 22 Metastatic carcinoma adrenal , 60 bone , 102 brain , 93 heart, 8 liver, 41 lung , 21 , 22 ovary, 77 spleen , 53 Miners, lung disease , 17-18, 19 Mitral valve incompetence , causes of, 4 infective endocarditis, 5 mixed disease , 4 non-infective endocarditis, 6 in rheumatic endocarditis, 3 stenosis, 3 Mbnckeberg 's sclerosis, 12 Mouth leukoplakia, 23 squamous carcinoma, 23 Mullerian tumour, malignant mixed , 80 Multiple Endocrine Neoplasia Syndrome, 58 typel,55 type II, 58, 61
Multiple sclerosis, 9 1 Myeloma , multiple, 10 1 Myocardial infarct, 1, 2 causes , 1 complications, 2 Myocardial rupture , 2 Myocardium brown atrophy, 9 fatty degeneration , 9 Myxoedema, 57 Myxoma, left atrial , 8 Nabothian cysts, 79 Nephritis , chronic interstitial , 64 Nephroblastoma,69 Nephrotic syndrome , causes of, 67 Neurilemmoma, 93 Neuroblastoma, 61 Neurofibroma, plexiform , 93 Neuroma, acoustic, 93 Nipple Paget's disease, 48 retraction , 47 Non-Hodgkin 's lymphoma adrenal gland, 61 breast, 49 Burkitt's, 52 hepatic involvement, 41 , 52 intestines , 31 lymph nodes , 54 spleen , 52 thyroid gland , 58 Oesophagus achalasia , 25 candidiasis , 24 carcinoma, 25 Mallory- Weiss tear, 24 peptic ulcer, 24 stricture, 24 varices, 25 Oilier's, disease, 100 Oophoritis, pyogenic, 72 Osteitis
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Multiple sclerosis , 91
Myeloma, multiple, 101
Myocardial infarct, 1, 2
causes, 1
complications, 2
Myocardial rupture, 2
Myocardium
brown atrophy, 9
fatty degeneration , 9
Myxoedema,57
Myxoma , left atrial, 8
Nabothian cysts, 79
Nephritis, chronic interstitial, 64
Nephroblastoma,69
Nephrotic syndrome, causes of, 67
Neurilemmoma, 93
Neuroblastoma, 61
Neurofibroma, plexiform , 93
Neuroma, acoustic, 93
Nipple
Paget's disease , 48
retraction , 47
Non-Hodgkin 's lymphoma
adrenal gland, 61
breast, 49
Burkitt 's, 52
hepatic involvement, 41 , 52
intestines, 31
lymph nodes, 54
spleen , 52
thyroid gland , 58
Oesophagus
achalasia , 25
candidiasis, 24
carcinoma, 25
Mallory-Weiss tear, 24
peptic ulcer, 24
stricture, 24
varices, 25
Oilier's, disease, 100
Oophoritis , pyogenic , 72
Osteitis
deformans, 98
fibrosa cystica, 96
Osteoarthrosis,97
Osteochondritis , syphilitic , 95
Osteochondromas, 100
Osteoma
ivory , 99
osteoid , 99
Osteomalacia, 96
Osteomyelitis
chronic, 95
tuberculous, 95
Osteoporosis, 95
Osteosarcoma , 101
Ostoclastoma, 100
Ovary
abscess , 72
corpora albicantia , 72
corpus luteum, 72
cystic follicles , 72
endometriosis, 73
torsion , 77
tumours, 73-77
Paget 's disease
ofbone,98
of nipple, 48
Pancreas
cysts, 44
tumours, 44
Pancreatitis
acute, 43
chronic, 44
Papillary muscle, rupture of, 2, 4
Parathyroid glands
hyperplasia, 58
tumours, 58
Pelvi-ureteric junction obstruction, 70
Pelvis, renal, transitional cell carcinoma,
69
Penis, carcinoma , 86
Pericarditis
constrictive, 8
fibrinous, 1, 7,8
tuberculous, 7
Periostitis, syphilitic, 95
Perisplenitis, chronic, 50
Phaeochromocytoma , 61
Pharyngeal pouch , 23
Phyllodes tumour, 46
Pituitary tumours, 55
Pleomorphic adenoma, parotid , 23
Pleura
hyaline plaques, 22
mesothelioma , 22
Plummer-Vinson syndrome , 25
Pneumoconiosis, 17
Pneumonia
aspiration , 14
broncho- , 13, 15, 16, 21
Klebsiella, 14
lipid , 14
10':>ar,13
staphylococcal , 14
Polyarteritis nodosa, 10
Polycystic disease
kidney, 62
liver, 36
Polyposis coli, familial, 34
Polyps
breast, 46
cervix, 81
endometrium, 79
large bowel, 33-34
stomach,27
Portal vein, thrombosis, 37
Polt's disease , 95
Pregnancy, ectopic, 77
Prostate gland
benign hypertrophy, 86
carcinoma, 85
Pulmonary
embolism , 16
haemosiderosis, 17
infarct, 17
Pyelonephritis, acute, 63
Pylorus , congenital stenosis, 25
Pyonephrosis, 64
106
Pyosalpinx, 78 Rectum
tumours, 34-35
ulcerative colitis, 31
Renal vein thrombosis , 65
Rheumatic heart disease , 3-5
Rheumatoid arthritis , 97
Rickets, 96
Salivary glands, mixed tumour, 23
Salpingitis
acute, 72, 78
chronic, 78
Sarcoidosis
lymph nodes, 53
spleen , 51
Schwannoma , benign, 93
Seminoma, 84
Silicosis, 18
Spermatic cord, torsion, 83
Spinal cord, ependymoma, 92
Spine, tuberculosis, 95
Spleen
amyloidosis, 51
'cricket ball', 50
enlargement, 50, 51 , 52
Hodgkin's disease, 52
infarction , 50
leukaemias and, 51-52
myelofibrosis, 51
non-Hodgkin 's lymphoma, 52
passive venous congestion, 50
sarcoidosis , 51
secondary carcinoma, 53
'sugar-icing ', 50
tuberculosis, 51
Splenic artery aneurysm, 12
Squamous carcinoma
cervix , 82
larynx, 13
lung,20
oesophagus, 25
penis, 86
vagina, 82
107
vulva, 82 Stomach
gastritis, 26, 27
'leather-bottle ', 28
pyloric stenosis , 25
tumours, 27-28
ulcers, 26-27
Stroke , causes, 90 , 91
Struma ovarii , 76
Syphilis
and aortitis, 5, 10
and general paresis, 89
and periostitis, 95
Syringomyelia, 87
Teratoma
differentiated,84
malignant intermediate (MTI), 84
malignant trophoblastic (MTT) , 84
mature cystic, 76
ovarian, 76
testicular, 84
Testis
atrophy, 83, 85
torsion , 83 , 84
tumours, 83-84
Thecoma, 76
Thrombosis
coronary artery, 1
deep venous, 11
portal vein , 37
Thrombus, mural, 1,2
Thymoma, 54
Thyroglossal cyst, 55
Thyroid gland
carcinoma, 57-58
enlargement, classification, 55
gOitre, 56
Graves' disease, 56
Hashimoto's disease, 56
lymphoma, ?8
myxoedema,57
Tongue, carcinoma, 23
Tuberculosis
adrenal gland , 59
epididymis , 85
heart, 7, 8
intestinal , 30
lymph nodes, 53
and meningitis , 88
miliary, 16, 51
pulmonary , 15-16, 18
renal,64
spinal,95
spleen, 51
Tumours see sites and specific types of
tumour
Typhoid, small intestine, 29
Ulcerative colitis, 31-32
Ureter
duplication of, 69
transitional cell carcinoma, 70
ureteritis cystica , 70
Urethral valve , 71
Uterus
bicornuate, 79
cervical carcinoma, 82
cervical 'erosion ', 81
endocervical polyp , 81
tumours , 79-81
see also Endometrium
Vagina, carcinoma, 82
Ventricle,lef1
aneurysms, 2
hypertrophy, 3, 4, 6
Vulva
Bowen'sdisease, 82
carcinoma, 82
Waterhouse--Friderichsen syndrome, 59
Wilm's tumour, 69