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Fletcher, Christopher D.M.

An atlas of gross pathology.
1. Pathology
I. Title II. McKee, Phillip H.
616.07 RBll1
Project Editor: Michele Campbell
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ISBN: 0-906923-47-6 (Gower)
illustration: Pamela Corfield
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 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
,

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).

•
IV
 Contents
III Ii 1IIIIwing Preface iii

Acknowledgements iv

1 Cardiovascular System 1

2 Respiratory System 13

3 Alimentary System 23

4 Hepatobiliary System 36

5 Breast 45

6 Lymphoreticular System 50

7 Endocrine System 55

8 Urinary System 62

9 Female Reproductive System 72

10 Male Reproductive System 83

11 Nervous System 87

12 Osteoarticular System 94

Index 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.1.5 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 '
Fig.1.3 Coronary artery thrombosis. The left main stem coronary extreme left of the pictu re its tip can be seen IIV' !lIYII II I II "
artery has been opened longitudinally to reveal occlusion of its lumen ventricular flap. Myocardial rupture, which is not III II "II it '
by thrombus (arrowed). Note the presence of atheroma in the occurs within a week of acute infarction,
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 Flg.l.S Left ventricular aneurysm. The d(~ vO IIlI'"1I 11 11 ,
tion, such occlusive aneurysm of the left ventricle is a not uncomllliJlt 111 111 1 III '
thrombosis will be myocardial infarction. It is due to replacemellt (11111 ) I"Y"
detected if the collagenous scar tissue with resultant loss of 0111;, 111 il y 'II
coronary arteries are aneurysms often contain mural thrombus whic:h " Illy I II
examined with suffi­ systemic emboli. The laceration of the anterior' Ili lllllllllY "
cient care. right of the aneurysm occurred during the post 1111111,,,,,
 1 Cardiovascular System

Fig.1.5 Myocardial infarct with mural thrombus and ventricular Fig.1.7 Haemopericardium. The pericardial sac has been opened
rupture. The heart has been opened to expose the septal wall of the (left) to show an extensive haematoma overlying the epicardium. On
left ventricle. A large mural thrombus is adherent to an area of recent the right, the haematoma has been removed to reveal the cause as
myocardial infarction, complicated by rupture of the interventricular being a slil -like ventricular perforation (arrowed) at the site of a recent
septum. The probe has been passed through the rupture and at the myocardial infarct. Haemopericardium may more rarely occur as a
left main stem coronary
extreme left of Ihe picture its tip can be seen overlying the righl complication of dissecting aortic aneurysm or trauma.
occlusion of its lumen
vent ricular flap. Myocardial rupture, which is not uncommon, usually
of atheroma in the
occurs within a week of acute infarction .
. 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 Fig.1.6 Left ventricular aneurysm. The development of an Fig.1.8 Ruptured papillary muscle. The heart has been opened to
tion, such occlusive aneurysm of the left ventricle is a not uncommon late complication of display the posterior aspect of the left ventricle . In the centre of the
thrombosis will be myocardial infarction. It is due to replacement of the myocardium by picture is a portion of the anterior papillary muscle which has been ,
detected if the collagenous scar tissue with resultant loss of elasticity. Such torn and shows obvious necrosis. Rupture of a papillary muscle is a
coronary arteries are aneurysms often contain mural thrombus which may be a source of rare complication of myocardial infarction, which usually occurs
examined with suffi­ systemic emboli . The laceration of the anterior papillary muscle to the within 2 weeks of the primary event: it results in the acute onset of
cient care . right of the aneurysm occurred during the post mortem. 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 .
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.1.13 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

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 Fig.1.12 Mitral stenosis with atrial thrombus. The commonest
High output failure
Paget's disease complication of rheumatic endocarditis is mitral stenosis and , indeed ,
almost all stenotic mitral valves are of rheumatic origin . Fusion of the Marfan's syndrome
A-V malformation valve cusps and fibrosis results in narrowing of the valve orifice. The
-­ -­ -­ - - -­ -­ -­ I
stenosis causes leli atrial dilatation and may be complicated by atrial
Fig.1.10 Causes of left ventricular hypertrophy. fibrillation with consequent thrombus formation , as seen in this case. .Fig.1.14 Causes of mitral incompetence.

3

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 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.
1 Cardiovascular System
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.
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

Rheumatic heart disease bacterial

viral
of congenital bicuspid valve
Infective rickettsial
Calcification
senile
chlamydial

fungal
dome-shaped valve

Rheumatic
I
Congenital supravalvar stenosis
Non-infective thrombotic (agonal)

Libman-Sacks (S.L.E.)
Fig.1.21 Infective endocarditis (normal valve). VIII 11.1 I
subvalvar stenosis

present on all three cusps of th is otherwise nOIIlliII.II 1111< ~

Fig.1 .19 Types of endocarditis. ",Ii ,
Endocarditis affe cting normal valves is usually <111 11 11 < I
disease aHecting immunocompromised patient:; i ll" 1111 111
Hypertrophic cardiomyopathy

the latter group the right side of the heart may lJOIIIVI .lvl" I
- - - -

Fig.1.17 Causes of aortic stenosis.

CAUSES OF AORTIC ~NCOMPETENCE J

Rheumatic heart disease

Syphilitic aortitis

Congenital bicuspid valve

Marfan's syndrome
Fig.1.20 Infective endocarditis (damaged valve). Infection of the
endocardium and valves may be due to a diverse variety of micro­
organisms (Fig .1. 19) and, while it may affect previously normal
Ankylosing spondylitis
tissue, it develops more often in the presence of pre-existing (parti­
cularly rheumatic) valvular disease. Streptococcus viridans is the
I commonest cause of infective endocarditis in previously damaged Flg.1.22 Non-infective thrombotic endocarditis. I I il l . I
Aortic sinus aneurysm valves but Staphylococcus aureus, I)-haemolytic Streptococci and which may aHect the aortic and mitral valves, is 0110[1 1" ,1111
Streptococcus pneumoniae are the most usual aetiological agents in patients dying with disseminated malignant tUIIIOIII" ! I"
cases with no evidence of prior disease. Large friable vegetations vegetations seen on this aortic valve are similar tn. 01111 I III"
Fig.1.18 Causes of aortic incompetence. obscure the underlying fibrosed mitral valve in this case. confused with, those of rheumatic endocarditis .

5
 1 Cardiovascular System

OF E~DOCARDITIS [ TYPES OF CARDIOMYOPATHY-

bacterial Hypertrophic (± obstruction)

viral
alcoholism
!IVII rickettsial
parturition
chlamydial
Congestive ,
fungal may be associated beri-beri
I
with
Friedreich's ataxia
I If I idiv€) thrombotic (agonal)
muscular dystrophies
II Sacks (S.L.E.)
Fig.1.21 Infective endocarditis (normal valve). Vegetations are
present on all three cusps 01 this otherwise normal aortic valve. Restrictive (endomyocardial fibroelastosis)
n'"ndocarditis. Endocarditis affecting normal valves is usually a more fulminant
disease affecting immunocompromised patients and drug addicts: in
the latter group the right side of the heart may be involved . Obliterative (endomyocardial fibrosis)

Loftier's endocarditis
-

Fig.1 .23 Types of cardiomyopathy.

Fig.1.24 Hypertrophic
obstructive cardiomyopathy. A
true cardiomyopathy is, by
definition, any myocardial
disease without an identifiable
cause which appears non­
inflammatory . Hypertrophic
cardiomyopathy is typified by
asymmetrical left ventricular
ndocardltis (damaged valve). Infection of the hyp ertrophy. especially of the
! vlllv'i:. Inny be due to a diverse variety of micro­ septal wall. Most commonly it is
1' 1).11 III. while it may affect previously normal familial, the mode of inheritance
• " 11 '11' , Iitun in the presence of pre-existing (parti­ being autosomal dominant. In
I VIl lvrrloi l tii :.;ease. Streptococcus viridans is the this case the septal hypertrophy
" , " ir IIr ,Ltive endocarditis in previously damaged Fig.1 .22 Non-infective thrombotic endocarditis. This condition, has led to obstruction of the out­
'I ' " , I",reus. j3-haemolytic Streptococci and
/I ' .
which may affect the aortic and mitral valves, is often found in flow tract. Hypertrophic obstruc­
IIIPI"I II.'" i1' O the most usual aetiological agents in patients dying with disseminated malignant tumours. The pink tive cardiomyopathy is a rare but
h'"' 'I ' ,t I ,rr(,l r disease. Large friable vegetations vegetations seen on this aortic valve are similar to, and may be important cause of unexpected
Iy" 'I I I" " 0110(1 mi tral valve in this case. confused with, those of rheumatic endocarditis. sudden death .

6
I Cardiovascu lar Syste m

Fig.1.27 Fibrinous Jlu I ~,

pericarditis. Pericarditis may I rl Gll vn , .
occasiona lly be due to primary I I IPI i
pyogenic infection , but more d l',l ld " It
commonly a fibrinous exudate 11 1 1,111111
occurs as a consequence of a flltt ,",111,
variety of disorders including ,Jt 1I jr ,, ·I\
myocardiat infarction (Fig .13), !l1II1' llIt l
rheumatic le ver , uraemia, III 1"1/1'
connective tissue diseases and ,,,,11,,10 'll
adjacent infecti ve conditions. for 111 11 "" 111' 1
example bacterial pneumonia ' ,II /I II" t
(in which instance the exudate dill ~ Ii tit
may be fibrinopurulent) . In this 11111 II 'It II I

case a generalised septicaemia .dlv .• , "II

has resu lted in a typical 'bread dl' .P d 'fI I
and butter' appearance . 11 111 dl' , II.

Fig .1.25 Congestive cardiomyopathy. Congestive cardio·

myopathy is defined as congestive cardiac failure with no apparent
cause. and re sults in a dilated , flabb y heart. as in this case. This
appear ance may be seen in association with alcohol abuse and
pregnancy .

Fig.1.26 Endo­
myocardial
fibrosis. Endomyo·
cardial fibrosis
occurs most
commonly in tropical
Africans and is mani·
fest as dense
fibrosis of the ve ntri·
cular endocardium .
A popular hypo·
thesis is that the
lesion has a viral
aetiology . Involve·
ment of the papillary
muscles may induce
va lve dysfunction. Fig.1 .30 Left atrial myxoma . The heart 11;1:: 11"",,1 '1",,1
the left atrium and mitral valve. AttacherJ to 11,1 ' III ",1. " 11 11
Fig.1 .28 Tuberculous pericarditis. The adherent parietal and left atrium is a large, pedunculated multiloiJld:! 11111 111111'
visceral pericardial membranes have been separated to disp lay myxomas are rare and clinically may pre sen t w,II" JlIlIi ., II
numerous small white miliary tubercles on the surface of the latter . emboli, or occaSionally, with acute pulmon;IIY 1)0" I. ""., ,I
Note also the pale fibrous thi cke ning of the parietal layer. Tuber· truction of the mitral valve orifice . Their prc!:"'" " "",, . "
culous pericarditis is said to result from lymphatic spread of uncertain since there is argument as to wlloll" 'I II" 'Y 01 '1'
org anisms from adjacent pulmonary or mediastinal foci of infecti on. 'neoplasms or are simply organised thron,1 JI

7
 1 Cardiovascular System

Fig.1.29 Cons­
trictive pericarditis.
This is a very rare
disease in which the
heart becomes
encased by a
densely adherent,
thickened and fibro·
tic pericardium . The
aetiology is often
uncertain. Whi le
some cases may be
due to tuberculous
infection. occasion·
ally a collagen
disease is
implicated .

Fig.1.31 Lambl's excrescence. The occurrence of small fibrin

deposits on the heart valves is not an uncommon finding at post
mortem Occasionally they may acquire tumour·like appearances, as
seen in this case. The aetiology is uncertain.

Fig.1.32 Epi­
cardial secondary
deposits. This heart
was taken from an
elderly male dying
from squamous ce ll
carcinoma of the
bronchus . The epi·
cardium is covered
by small pale
umbilicated
metastases. In
addition there is a
large tumour mass
situated between the
superior vena cava
and the pulmonary
trunk, seen at the top
of the picture
(arrowed). This
Fig.1.30 Left atrial myxoma. The heart has been opened to display resulled in vena
the left atrium and mitral valve. Attached to the posterior wall of the caval obstruction.
left atrium is a large , pedunculated multilobular tumour. Atrial Epicardial or peri·
myxomas are rare and clinically may present with multiple systemic cardial tumour
emboli, or occasionally , with acute pulmonary oedema due to obs· metastases often
truction of the mitral va lve orifice . Their precise nature is , as ye t, induce a fibrinous or
uncertain since there is argument as to whether they represent true fibrinopurulent
neoplasms or are simply organised thromb i. pericarditis .

8
1 Cardiovascular System

Fig.1.35 Fatty
streaks (aorta). This
aorta has been
removed from a
small child and
stained by the Oil
Red 0 technique to
demonstrate lipid .
Small intimal depo·
sits are seen . The
orifices of the inter­
costal arteries are on
the left. Such
juvenile fatty streaks
are found in the
large arteries of (;I UI:l i l VI I
children and h lllll lll' ,I,
adolescents of all nlll I · ,1111 11
Fig.1.33 Brown atrophy. This heart, which was removed from an races and socio· ;1: . ' ''HII ' I
86·year-old woman with senile dementia, is very small and weighed economic groups. It rl! IIY VII
only 180g (normal adult female 250-300g) . Note the brownish dis­ is unlikely that these (I i(l" I I
colouration. This change is an ageing phenomenon, in which lipo­ lesions bear any
fuscin pigment, representing the lipid remnants of effete organelles, pathogenetic rela­
is deposited in many organs in association with atrophic changes, tionship to the future
probably due to a combination of relative ischaemia and disuse . development of
atheromatous
plaques .
Flg.1.34 Myo­
cardial fatty l lii'. /."",
degeneration. Acc· Fig.1.36 Uncomplicated n(1 , III 11111
umulation of lipid atheroma. This section of aorta, 1)1 11 11" ',1 I.
within the myo­ from a middle-aged male, shows II UI'III1II II
cardium may occur numerous raised, irregular tilll H. II " "
in a variety of con­ intimal deposits. Atheroma is the i'l.rll llllt il
ditions including commonest cause of death in p it II 1111 11
severe anaemia, the Western World , largely by oxll " "" VI
alcohol abuse and giving rise to myocardial infarc­ Il l "" 11111 ' I
poisoning. As seen tion and cerebrovascular acci· ,1'1.• 111 11 11 11
in this papillary dents. Known risk factors for its 1'"11 , 'II .11
muscle, it produces a development include increasing 111111111111"
characteristic age, cigarette smoking, hyper· ,'VIUIYII II I
'thrush breast' tension, a diet high in saturated 11 11' h HIIi .,
appearance. fats, hyperlipidaemia and t Ifh ~f '''ifill
diabetes mellitus. Its exact 11 111111 " .,1
pathogenesis is unclear, but 111 :011111111
intra-intimal lipid deposition and t)lll' ,iI "II
incorporation of mural thrombi (I III , III IY
are popular hypotheses. Myo­ JlIII I"II , II
fibroblasts within plaques have
been shown to be monoclonal in
origin, the significance of which
is uncertain.

9
 1 Cardiovascular System

Fig.1.35 Fatty Fig.1.37 Ulcerated Fig.1.39 Syphilitic aortitis.

streaks (aorta). This atheroma. Necrosis The left ventricle and ascending
aorta has been within an atheroma­ aorta have been opened to show
removed from a tous plaque, in the characteristic irregular 'wood
small child and combination with bark' appearance of the aortic
stained by the Oil constant haemo­ intima. The aortic valve cusps
Red 0 technique to dynamic stress may are rolled and thickened and
demonstrate lipid . lead to ulceration, as there is separation of the commi­
Small intimal depo­ seen in this picture . ssures. Syphilitic aortitis is the
sits are seen. The As a consequence, commonest manifestation of ter­
orifices of the inter­ exposure of sub­ tiary infection and usually affects
costal arteries are on endothelial tissues only the intrathoracic portion of
the left. Such may result in the aorta. It results from a florid
juvenile fatty streaks thrombus formation . arteritis of the vasa vasorum with
are found in the This in turn may consequent intimal fibrosis .
large arteries of cause vascular occ­ Common complications of th is
children and lusion of medium condition include aortic incomp­
adolescents of all and small arteries , etence, aneurysm formation and
races and socio­ as seen in the coro­ stenosis of the ostia of the coro­
economic groups. It nary vessels nary arteries.
is unlikely that these (Figs.1.3 and 1.4).
lesions bear any
pathogenetic rela­
tionship to the future
development of
atheromatous Fig.1.38 Compli­
plaques. cated atheroma.
This segment of
Fig.1.36 Uncomplicated aorta has been
atheroma. This section of aorta, opened to show all
from a middle-aged male, shows the major complica­
numerous raised, irregular tions that may occur
intimal deposits . Atheroma is the in atheromatous
commonest cause of death in plaques. There is
the Western World , largely by extensive ulceration,
giving rise to myocard ial infarc­ haemorrhage and
tion and cerebrovascular acci­ dystrophic calcifica­
dents. Known risk fac tors for its tion; scattered small
development include increasing thrombi are present,
age, Cigarette smoking , hyper­ overlying some of
tension, a diet high in saturated the lesions. It is not Fig.1,40 Polyarteritis nodosa. The epicardium has been stripped
fats, hyperlipidaemia and uncommon for frag­ from this heart to demonstrate branches of one of the coronary
diabetes mellitus . Its exact ments of such comp­ arteries, which show fibrosis of the vessel walls and formation of
pathogenesis is unclear, but licated plaques to several small saccular aneurysms. Polyarteritis nodosa is an
intra-intimal lipid deposition and break off and pro­ uncommon disease. thought to be due to immune complex deposi­
incorporation of mural thrombi duce systemic tion and sometimes associated with hepatitis B or systemic lupus
are popular hypotheses Myo- . emboli, the conse­ erythematosus. It affects small arteries and arterioles in any part of
fibrob lasts within plaques have quences of which the bod y and results in inflammation and necrosis of the vessel walls ,
been shown to be monoclonal in will clearly depend commonly with overlying thrombosis. The cl inical effects are largely
origin , the significance of which on the site of the due to ischaemia of the affected organs. Small aneurysms develop
is uncertain . affected artery quite often and may be compl icated by rupture .

10
1 Cardiovascular System

Fig.1.43 Abdominal aortic 1'111 I .

aneurysm. The lower portion of IIf1r 11, n,
the abdominal aorla has been 1III I I ilili

opened to show a saccular dila­ ~ II ' " I II III

tion of the distal end, the lumen I Iy II II II

of which contains a large lamina­ 1111 11 I I Ii I.

ted thrombus . Proximally, the ( ,1111 tv. I II

aorta shows extensive involve· 1111 p lii .

ment by complicated atheroma . II II ; ,I II j

This is the commonest variet y of (l"l i) I

true aortic aneurysm in the till I HI if

Western World and is almost 1\ 111 11 \ d ,·1 1

Ittlrll lll t/tJ
always a consequence of exten­
Fig.1.41 Deep venous thrombosis. The femoral v ein has been sive atheroma, leading to thinn-· tl l!' ll lll'l

exposed in a patient dying of pulmonary embolism (see Fig.2.16). ing or disruption of the aortic Ir . 1l p." ."
11 111 11
The lumen of the vein is vi rtually occluded by thrombus which is media. Older adults, particularly 1 " I

adherent to the endothelial surface. In general terms the pre· (111111 111 I
males, are often affected. Such
disposing faCtors to thrombosis are encompassed in Virchow's triad aneurysms may rupture with I II'I ll i li l \

(1) alteration in the vessel wall , (2) alteration in the blood flow and (3) extensive retroperitoneal haem­ (I I I ,II . U I I
alteration in the blood constituents . Deep ve nous thrombosis is ., IHIIII
orrhage and this may be fatal.
commonest in the calf veins and , as in th is case, may be complicated The formation of large intra­ I. ,I. d, III ,
by pulmonary embolism, although the frequency with whic h this 1\ II ) 111 11 r
luminal thrombi sometimes gi ves
occurs is diffic ult to determine since many venous Ihromboses go rise to aortic occlusion with distal 11 1• 1,11 "
undetecte d. The co mmonest causes include immobility, myocard ial ischaemia or to embolic .,! III' I I

infarction, pregnancy or childbirth, varicose veins or phlebitis and phenomena . , I' I, ttl ;

any severely debilitating disease such as cancer. 'U I ,', 'I I

,II' , ,1 ,11 1
Fig.1.44 Dissec­

-­-I
rI ' I II II I 1
ting aortic
aneurysm. The term
It ""I qi' JI
CLASSIFICATION OF TRUE ANEURYSMS
- -- -
dissecting aneurys m
is a misnomer in that FI{I I III

Atheromatous true dilatation of the IIIU 110111

vessel wall does not muulIV
Syphilitic occur. Rather. the 111 '. 1. 1111 '
IHillll . 1 \ 1
apparent increase in
Infective size is due to the fllJ IlI ltl I
I fi ll II , II It (
presence of
Cirsoid thrombus wilhin the t h 'v , 11 1 iI iI
media of the artery, h . 1i 111 11 11'
A-V fistula as seen here in the I . 1, II idl
I . d' ,\, t'l ' I
arch of the aorta .
Berry (cerebral) Dissecting pl( \III , \1 i

aneurysm is most (1I II IIIIIi ' l

Charcot-Bouchard (cerebral-hypertensive) commonly due to I ldl!!! I'llli
I
IlIlId l d ' ll
mucoid degenera­
Erdheim's medial degeneration (dissecting) tion (Erdheim) of the
media but may also
Marian's disease (dissecting) be seen in Marfan's
J syndrome and in
Fig.1.42 Types of true aneurysm , to be distinguished from a 'false' association with
aneurysm, which represents the site of a walled -off arterial rupture. systemic hype rtension.

11
 1 Cardiovascular System

inal aortic Fig .1.45 Dissecting

vver portion of aortic aneurysm.
'ra has been The process of
saccular dila­ dissec tion is initiated
d. th e lumen by a transverse
a large lamina­ intimal tear
ximally. the (ar rowed) . usually In
sive involve­ the proximal pari of
led atheroma. the ascending aorta
nest va ri ety of (top) . Extens ion of
minthe the process c auses
'd is almost formation of a fa lse
en ce 01 exten­ lumen with in the
ding to thinn-­ media which . on
f the aortic transverse section .
IS. particularly produces a typical
:f1ected Such doub le-barrelled
Ipture with appearance
(bollom) . Dissecting Fig.1.47 Splenic artery aneurysm . The large sac cular aneu rysm
i tonea l haem­
aneurysm is usuall y above the bod y of the pancreas was found in a young woman with no
ay be latai.
fatal either by evidence of atheroma or syphilis. The red probe demonstrates
rge intra­
rupt ure or by retro­ luminal continuit y between the aneurysm and the distal portion o f the
metimes gives
grade Invotvement artery. The lesion probably re presents a rare example of a congen ital
sion with distal
of the co ronary aneurysm due to fibromuscular displasia of th e arterial wall .
boli c
arteries. Ve ry
occasionally the
dissec ting process
44 Dissec­ re-enters the true
o rtic lumen of the aorta .
sm. Th e term
ling aneurysm
i s nomer in that Fig.1.46 Dissect­
i latation of the ing aortic
I wall does not aneurysm . tn thi s
. Rather. the instance th e dissec­
ent increase in tion has resulted in
due to the
rupture of the aortic
nceof
root and the
bus with 'ln the
development of
of the artery ,
haemopericardium
I3n here in th e
External rupt ure may
) f the aorta
atso occur into the
1ing pfeu ral cavity
sm is most (leading to a
o nly due to haemothora x) or
d degenera­ mediastinum . Fig.1.48 Monckeberg's sclerosis. Mbnckeberg' s sclerosis is
rdh eim) of the c haracterised by calci fi catio n of the media 01 the large arteries.
b ut may also particularly in the limbs and pelvis It appears to be part of the normal
",n in Marfan 's ageing process and is commone r in diabetics. The diagnosis is
p meand in usually made radiologically . In th is plain X-ray of a post -mortem
iationwilh specime n of the femoral arteries. the typ ical fine tram-line
nic hypertension. appearance of the c alcific ation is clearly se en .

12
2 Respiratory System

Fig.2.1 Laryngeal squamous Fig.2.3 Lobar pneumonia.

carcinoma. The trachea and
larynx have been opened poster­
iorly to reveal a small fungating
supraglottic tumour arising in the
right aryepiglottic fold .
Squamous carcinoma is the
commonest malignant tumour of
the larynx and arises most often
in the 6th and 7th decades,
affecting males more frequently
than females. Known risk factors
include chropic inflammation
and cigarette smoking. Spread
is largely local or lymphatic and
overall 5-year survival is about
65%.
Uniform red , firm consolidation
of this left upper lobe, with comp­
lete sparing of the lower lobe, is
typical of 'red hepatisation' - the
second stage of lobar
pneumonia. This occurs at about
the 2nd to 4th days in an
untreated patient, being
preceded by engorgement and
succeeded by 'grey hepati­
sation' and resolution at about
the 8th to 10th day . Lobar
pneumonia, particularly in its
cfassical form, is rarely seen
nowadays with the advent of Flg.2.5 Staphylococcal pneumonia. A close ''I' VII ,W " I
modern antibiotic therapy . How­ t:hows numerous characteristic foci of centriloblll; \I ' .111 '1" I
ever, young adults are most which. in the upper centre, have coalesced to fo""., """ II
often affected. over 90% of abscess. Staphylococcal pneumonia most 011 01 1 (; 1JI"l llh ,.
cases being due to Infections or is nosocomial in origin. Suppuratioll lllil l \II Ifl '
Streptococcus pneumoniae. ntion are simitarly seen in Klebsiella pneumonia, wli ll ""II'
Ilospital-acquired infection. Both carry a relalivolv IIIIII! III"
Irlt hose who survive , extensive lung damage IllftV l. tl ll.llI I

Fig.2.4 Lobar
Flg....11
pneumonia. There
pIIOIIII ....
is a fairly uniform
'grey hepatisation' of "I"" , ,111 11
lui" , '.III '\'.
the teft lower lobe
:lI Il ,IIII" 1 I
with five small foci of
(;011' ,\ ,lId /i1
consolidation in the
IIII /l ou t il.11
upper lobe adjacent
(1 11/ 1111"''''
to the oblique 1(11 .Iii,,,,,
I,
fissure. This
mllll ilo It 11 11
appearance is due
1\' ,11 11,11 1, ,, I
to the massive influx
f Jlu lI "'lIlI d
of inflammatory
1I11 1,IIo ,IIe " 1
cells, associated
with relative ""III "," "
ischaemia. Com ­ I" I' " '1 11 '1'11
:: tOll ll il I I
plications of lobar
r,t 1lIIIIli 1111
pneumonia include
L ')l I Tf{ Ii II I
Fig.2.2 Bronchopneumonia. This left lung shows congestion and the development of 11 1< ,,1II ,II,
diffuse multifocal consolidation (left) . A close-up view from a different septicaemia, an
case (right) shows small areas of consolidation and suppuration. WIII I" ""1
empyema, a lung
1111111(11,1.11
largely centrilobular in distribution. Bronchopneumonia is principally abscess or carnifi­
IV" !' tl. IIU I
a disease of the ve ry young and old , but also occurs in immuno­ cation (extensive
suppressed patients. Chronic obstructive airways disease and viral "I ' .Ii ,,11, 1 \
fibrosis ).
respiratory infections are frequent predisposing factors. A very wide '."U" lil ,"
iii. Mlllllhi
variety of causative organisms may be isolated, of which .
Streptococcus pneumoniae, Streptococcus pyogenes and :,V'" """";
Haemophilus influenzae are the most Irequent.

13
 2 Respiratory System

Fig.2.3 Lobar pneumonia. Fig.2.7 Lipid

Uniform red, firm consolidation pneumonia. This
of thi s left upper lobe, with comp­ lung shows uniform
lete sparin g of the lower lobe, is pale, rather waxy,
typical of 'red hepatisation' - the consolidation . Note
second stage of lobar also the pre-existent
pneumonia. This occu rs at about bronchiectasis and
the 2nd to 4th days in an centriacinar
untreated patient , being emphysema . Lipid
preceded by engorgement and pneumonia may
succeeded by 'grey hepati­ either be
sation' and resolution at about exogenous,due to
the 8th to 10th day. Lobar inhalation of
pneumonia, particularly in its ingested or regurgi­
classical form, is rarely seen tated oils taken in
nowadays with the advent of F1g.2.5 Staphylococcal pneumonia. A close·up view of this lung medication or food ,
modern an tibiotic therapy. How­ ·;hows numerous characteristic foci of centrilobular suppuration or may be endo­
ever, young ad ults are most wh ich. in the upper centre, have coalesced to form a small pulmonary genous, occurring
often affected, over 90% of nbscess. Staphylococcal pneumonia most often complicate s vira l most oft en distal to
cases being due to IIllection s or is nosocomial in ori gin. Suppuration and abscess form­ an obstructing
Streptococcus pneumoniae. It ion are similarly seen in Klebsie lla pneumonia, which may also be a bronchial carcinoma
Ilospital-acquired infection. Both carry a relatively high mortalily and , and result ing from
II I those who sUNive, extensive lung damage may remain.
excessive
Fig.2.4 Lobar accummulation of
pneumonia. There Fig.2.6 Aspiration surfactant .
is a fairl y uniform pneumonia. The
'g re y hepatisation' of apex of this lower
the left lower lobe lobe shows multiple
with five small foci of small foci of pale
conso lidation in the consolidation with
upper lobe adjacent microabscess form­
to the oblique ation principall y
fissure. Thi s locali sed around the
appearance is due small er airways.
to the massive in flu x Aspiration
of inflammatory pneumonia follows
inhalation of material
cells, associated
with relative from the oropharynx,
ischaemia. Com ­ oesophagus or
plications of lobar stomach and is
pneumonia include commonest in un­
the development of conscious patients,
septicaemia, an alcoholics and those Fig.2.8 Lung abscess. This lung has been hemisected to show a
with an upper large necrotic abscess cavity in the upper lobe. Note also the marked
empyema, a lung
abscess or ca rnifi­ alimen tary obstruct­ congestion and pre-existent bronchiectasis. Lung abscess is most
cation (extensive ive lesion . Aspiration often due to infection by Staph ylococci, Klebsie lla or Pneumococcus
fibrosis). of sterile gastric Type 3. It may develop after inhalation of foreign material or result
secretions is known from a septic embolus . Such abscesses are commonest in the upper
as Mendelson's lobes and may be complicated by rupture into a bronchus or the
syndrome . pleural cav ity, pleurisy or extensive lung scarring . Alternative ly , they
may become wa lled-off and resolve .

14
2 Respiratory System

CAUSES OF BRONCHIECTASIS

Mucoviscidosis
CONGENITAL
Bronchial malformation

unresolved
bronchitis or
Pulmonary pneumonia
infection
viral lung
infections

Flg.2.13 Miliary tuberculosis. Throughout ti,,' II"" I I i,Ii

ACQUIRED tumour ,'"\nd particularly numerous around blood ve s~,d' " "I" ',1"
'tubercles' Mitiary spread is due to haemato<j" i!III1· , . I, " ,
Mycobacteria and may complicate either prlln:IIY 1111", III
hilar lymph Fig.2.11 Primary tuberculosis. Just beneath the pleural surface estructive foci erode into blood vessels) or i'('< I(.II Vdtl li I I
Bronchial nodes (lel1) is a small, pale nodule (Ghon focus) . the hilar lymph nodes show I1l lection in debilitated, elderly patients.
obstruction (especially TB) fibrosis and calcification The combination of these two lesions is
known as a primary complex, which in this case is resol ving . Primary
pulmonary tuberculosis remains endemic in underdeveloped rill ·;> 1'1
countries and is almost always caused by Mycobacterium Glll o"" I,
foreign body plleu ..n, .
tuberculosis. Children or young adults are most often affected . Most
1111111 hll "
lesions heal spontaneously, but progressive infection with abscess
1IIIIIIq 11 11 j
Fig.2.9 Causes of bronchiectasis. formation, bronchopneumonia or miliary spread may occur.
j .I' , c 1' l1 f

Fig.2.10 Bronchiectasis. Fig.2.12 Post-primary I'"I" 'II" "

. 11 11" ,til
There is marked dilatation of tuberculosis. In the apex of this ., ' ,I 'Ll I!
most of the bronchial tree. Many lower lobe, there is an irregular ,lf e ', l i '[
of the bronChi contain purulent cavity, containing caseous 1.I"" , illi
material and extensive broncho­ material, which has ruptured into
pneumonia is present. Bronchi­ a bronchus resulting in intra­
.'''I I, II' II
lid !l HI i I
ectasis is defined as irreversible pulmonary bronchopneumonic IHI.' P J!,.
dilatation of the bronchi associ­ spread . Post-primary tuber­
lVI''' .III
ated with chronic suppurative culosis is far more often due to t .11- I' I II
infection . The lower lobes are exogenous reinfection than ( rl 'i fII 1 11 !
most often affected and areas of reactivation of previous endo­ ,llld 11 ' 11
dilatation may assume a fusiform genous infection. The lobar 11111. II III "
or saccular appearance . Comp­ apices are typicall y affected and . ,111 1'1 Ii I I
lications include lung abscess, other complications of cavitation 111111 ( , Ji ll
empyema, lung damage include spread to the upper res­ ( , 1'. 1 q il l
(leading to 'cor pulmonale'), piratory or alimentary tracts.
infective endocarditis, mycotic Secondary amytoidosis may
aneurysms and secondary develop in long-standing cases .
amyloidosis .

15
2 Respiratory s~eJ 2 Respiratory S) .. Inll

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:,
Fig.2.13 Miliary tuberculosis. Throughout the lung parenchyma, from liquefaction Il f
and particularly numerous around blood vessels, are small discrete caseous matenal
'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.

Fig.2.14 Tuber­ Fig.2.16 Pulmonary

culous broncho­ embolism. The right main
pneumonia. The pulmonary artery is virtually
right lung shows occluded by a massive
multiple foci of laminated thrombus. The lung I',
caseous rather pale in appearance Pul
pneumonia. At the monary embolism most of tell
apex of the left lung complicates deep venous
a small subpleural thromboses in the lower limb
pUlmonaryl!'P" area of scarring and (see Fig. 141) The commo n()~ 1
I caseation is predisposing factors are pro­
apparent (arrowed) longed bed rest, particularly
Tuberculous after surgical operations, partull
bronchopneumonia tion, congestive cardiac failure
typically compli­ and hypercoagulability. Mas$ lV<'
cates post-primary emboli, such as the one showli
(reinfection) disease here, prevent the passage of
and results from the blood into the pulmonary cirelll ;1
intrabronchial tion and result in sudden d ea tll
spread of the lique­ Smaller emboli, which lodge III
fied contents of a more distal vessels , may havt, III '
caseous cavity. effect, or may result in pul·
monary hypertension and call>'"
infarction (see Fig. 2.17) or m:ty
give rise to pulmonary
haemosiderosis.

17 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-_- CA_USES OF PULMONARY HAEMOSIDEROSIS
chronic left
ventricular failure
mitral valve
Pulmonary hypertension
disease
left atrial
myxoma
Goodpasture's syndrome
Long-standing haemochromatosis
Haemosiderosis
FIg.2,18 Causes of pulmonary haemoslderosis.
17
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.2.20 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.2.21 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
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

Flg.2.19 Coal workers'

pneumoconiosis. The lung
parenchyma shows patchy
Fig.2.21 Silicosis. The lung
parenchyma is markedly fibrotic,
shows dense anthracotic pig­
mentation and contains a tuber­
L CAUSES O~ HONEYCOMB LUNG_ _ _ ---..J

dense anthracotic pigmentation,

a pattern known as dust reticu­ culous cavity in the apex. The Pneumoconiosis I
lation . Note also the character­ hilar nodes are black and I
enlarged and the interlobar Extrinsic allergic alveolitis
istic mild centri lobular 'focal I
dust ' emphysema. In addition a fissure is scarred . Silicos is is
small, black, silicotic nodule is seen most often in miners and Cryptogenic fibrosing alveolitis
I
present (arrowed) . Simple dust workers in the stone and glass (Hamman-Rich syndrome)
reticulation results from long industries. Lung damage I

term exposure to coal dust; the actually results from the re lease
of macrophage cell contents fol­ Sarcoidosis
development of nodules is due
to co-inhalation of si lica. There is lowing silica-i nduced cell death
and is more usually character­ Drugs/irradiation I
no increased risk of lung cancer .
ised by nodular fibrosis (see
Fig .2.22) . Tuberculosis is a very Rheumatoid disease
common complication .
Systemic sclerosis

Extensive pneumoniafTB

Pulmonary eosinophilia

Fig.2.23 Causes of honeycomb lung.

Fig.2.24 Honey­
comb lung. The
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
,II\.II •••'lIn mnaalve fibrosis. This coal miner's lun g respiratory bronch­
1, 11111,1, 1.,1 Ii 11 ,1 II :Ik;ulalion, large, well demarcated, black ioles. Th is
11111 "Iu lll' li 1.1lack nodules (top). Progressi ve massive .2.22 Haematlte pneumoconiosis. The lung parenchyma
appearance re­
,I 'I i I'" I· ·.. ( ,I I :')01miners and may also be seen in I",w!: severe brick-red pigmentation with evidence of nodular and
presents the end ­
" 1'1' • I·' plllhll(lollesis is unknown but it is thought that • IIIII I1iU fibrosis and emphysematous change . Th is condition, due to stage of va rious
,I . Ii or,1 '''' IIII~. l lfj I .lnd the possible coexistence of tuber­ 1I11 1f11HliQn of iron oxide, is seen most often in iron ore miners . The disease processes,
III/ " ,,/ 11,1 101, I, 0/', I lie smalle r nodules seen here are , I, 'V I ,to .oment of fibrotic lesions is again dependent upon the co­ the commonest of
" • III' III '011/, "" . 1,1I":e coal dust often has a high silica 1I_I'.l ollce of silica in the inhaled dust. Well recognised complications which are listed in
I". ,to "I" tubercu losis and bronchia l carcinoma. Fig . 2.23 .

l~
2 Respiratory System

LUNG ACINUS

D terminal bronchiole

o respiratory bronchiole
o alveolar duct
o 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
n l)l lI', 4 fllll l
this is the commonest variant of emphysema, seen predominantly in
cigarette smokers (especially males) . The upper lobes, particularly 111 11)· ,, 1,,111
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 .
11:.lInll H Ili I
buill/Ill. ,", '
Fig.2.28 Panacinar Wl1I I: .I ,I!l iI
Fig.2.25 A lung acinus. 3-5 pulmonary acini constitute a lung emphysema. In this
lobule. lung note the much
larger, confluent, tt 11 ~. ( , I I'., ~
dilated air spaces
replacing complete
CLASSIFICATION OF EMPHYSEMA lung acini. In places
there is also a cent­ Fig.2.30 Pulmonnry
riacinar component. hamartoma .. 1t1(.II IIIIII
Centriacinar Panacinar pleural surfac " 1111111" t.
emphysema , which is a very well do""'" iI.11
Focal dust (in pneumoconiosis) is also very . pale tumour. I h(l " ,",,,11
common, affects the the lung is I1UII 11111 1'11111
air spaces, including hamartomas W' l l lIlt III"
Panacinar alveoli, distal to the developmenl nl l ll llllllllil
terminal bronch­ usually cartil aOH H" ", II ,
Paraseptal (bullous) ioles. In its classical which are only 1111 " Iy 'IV
form it is associated matico They ,UCiIYI III 11 11
with Ct,-antitrypsin pleural in 10c;tll",I. 1111; 1'
Irregular deficiency and more than feIl1l,1I ;- ., .1111
previous bronchial entirely beniql1
Surgical (interstitial) obstruction . Most
often, the lower
lobes, particularly
Fig.2 .26 Classification of emphysema. With the exception of the lung bases, are
surgical emphysema, any lung may commonly show a mixed pattern affected.
of involvement.

19
 2 Respiratory System

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 Fig.2.31 Bronchial 'adenoma'. In the main bronchus is a smooth .
affects the alveoli well circumscribed tumour projecting from the epithelial surface .
:."Irlllclnar emphysema. In the lung parenchyma , small
I adjacent to the inter­ These lesions may be derived either from submucosal glands or
11 ' I " I, n· . . "II rounded by black anthracotic pigment are lobular septa or neuro endocrine APUD cells and are misnamed since they represent
II" \ ' ·,,1,,· ot the lung lobules . The surrounding alveoli are pleural surface . It is low-grade, malignant tumours which may eventually metastasise .
II I, "" .. 'I ql COS correspond to the respiratory bronchioles and usually most pro­ They most often arise in young adults and there is usually extension
i ,ti l" 11( 11 H>f;t variant of emphysema. seen predominantly in nouncedinthe into the adjacent lung parenchyma.
II" d·. II ', ( ..'specially males) The upper lobes. particularly upper lobes, often
, II" "" 1:,1 Ollen affected . A similar appearance is seen in close to an area of Fig.2.32 Hilar
" I (I '" [I I dust emphysema) in which there is usually little previous scarring.
bronchial
I I. " .1~ ll~ ,I'IC)I I . This variant is the
4
carcinoma. Arising
usual precursor of
from the lower lobe
bullous emphysema
Fig.2.28 Pan acinar bronchus , close to
and is often seen
emphysema. In this the hilum. is a pale
associated with neoplasm which is
lung note the much
other variants, as in irregularly infiltrating
larger, confluent,
this case . the parenchyma.
dilated air spaces
replacing complete Bronchial carcinoma
lung acini . In places most often originates
there is also a cent­ Fig.2.30 Pulmonary near the hilum and
riacinar component. hamartoma. Just beneath the may be squamous
Panacinar pleural surface of this lower lobe (50%), small cell
emphysema, which is a very well demarcated, small . (oat cell) anaplastic
is also very . pale tumour. The remainder of (20%), adeno-(15%)
common, affects the the lung is normal. Pulmonary or large cell ana­
air spaces. including hamartomas are not uncommon plastiC (10%) in
alveoli, distal to the developmental anomalies, type . It is the
terminal bronch­ usually cartilaginous in nature , commonest cause of
ioles. In its classical which are only rarely sympto­ death from malig­
form it is associated matic. They are typically sub­ nancy in Great
with ai -antitrypsin pleural in location, affect males Britain and in many
deficiency and more than females. and are cases is associated
previous bronchial entirely benign. with cigarette
obstruction . Most smoking or industrial
often, the lower exposure to
lobes, particularly carcinogens. The
the lung bases, are overall 5-year
affected survival is only
between 5 and 10% .

20
2 Respiratory System

Fig.2.33 Bronchial Fig.2.35

carcinoma with Bronchioalveolar
distal bronchi­ carcinoma. The
ectasis and entire lung is C! Il lqtt t. 1I I
broncho­ diffusely infiltrated willi " " ,
pneumonia. At the by a pale neoplasm nhl ll",1 " I
apex of the left lower which, particularly in dill II II ,if
lobe is a partly the upper lobe, has It lUlttt .I. ,! li
necrotic. pale adopted a nodular ili lI l lltllj '
neoplasm which has appearance. [q ll ll H lI dl
obliterated the lower Bronchioalveolar ~ III 11 III III 11
lobe bronchus : carcinoma
distally the smaller comprises about 2%
bronchi are grossly of all primary lung
dilated (bn;Jnchi­ cancers and is a
ectasis) and the specific variant of illly .,· ,' ., ..
remaining paren­ adenocarcinoma, ••!'l lOlO ll It,
chyma shows which tends to ru If lllih II
consolidation . The spread extensively 11;·,1,. OIl",
adjacent middle within the air
lobe shows passages. Its diffuse
confluent broncho­ nature often prompts
pneumonia. These mistaken clinical
are common comp­ diagnoses of an
lications of obstruc ­ infective or inter­
tive bronchial stitial disorder.
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 Fig.2.36 Multiple pulmonary metastases. Beneath the pleura and
arise in foci of scarring . An in the lung parenchyma are innumerabte pale, umbilicated nodules of
apparently slow growth rate'and tumour. Up to a third of patients dying of malignant disease have Ig.2.38 Pulmonary lymphangitis carcinomato.n I I ,.
frequent operability means that pulmonary metastases, the commonest sources of which are ',lIdace of this lung shows innumerable small spl ,,,"',tl "'
they carry a better prognosis carcinoma of the breast, colon, stomach and lung itself. The I iI 'posits of pale tumour. This represents extell:.;iv" II ,ldl" i
than most bronchial carcinomas. presence of an extensive vascular and lymphatic system in the lungs I" ilrnonary lymphatic channels, which are fillec1I,y '''1,1, I"
is responsible for the predilection that metastases show for this site. . IIHI may be caused by either primary or seconda,y "" 'tl \

21
 2 Respiratory System

Fig.2.35 Fig.2.37 'Cannon

Bronchioalveolar ball' pulmonary
carcinoma. The metastases. In thi s
entire lung is congested lung. fo ur
diffusely infiltrated well circumscribed ,
by a pale neoplasm almost spherical,
which, particularly in deposits of pale
the upper lobe, has metastat ic tumour
adopted a nodular are present. This
appearance. appearance of a
Bronchioalveolar small number of
carcinoma large secondary
compr ises about 2% depos~s i nthelung.
of all primary lung while not entirely
cancers and is a specific , is classic­
specific variant of ally associated with
adenocarcinoma, spread from renal
which tends to adenocarcinomas or
spread extensively testicular tumours. Fig.2.39 Pleural hyaline plaques. On the parietal pleura of the
within the air posterior thoracic wal l are several foci of yellowish hyaline thickening .
This appearance is most otten seen in individuals who have suffered
passages. Its diffuse
nature otten prompts prolonged exposure to asbestos, usual ly in the course of their
mistaken clinical occupation. Such patients also commonly develop macroscopically
diagnoses of an non-specific pulmonary fibrosis , collapse or bronchiectasis of the
infective or inter­ lower lobes. Crocidolite is pathogenetically the most dangerous type
stitial disorder . 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
\ " .. , II I IYI II.I nro innumerable pale , umbilicated nodules of
III ,11 11111 I>~ pat lonts dying of malignant disease have Ig.2.38 Pulmonary lymphangitis carclnomatosa. The pleural

, \I Id',h","· .. tho commonest sources of which are , " Ir1 t i.l of this lung shows innumerable small spherical and li near

.111 11 I )11,01·,1. colon , stomach and lung itself. The .'''111 i' ,il S of pale tumour This represents extensive infiltration of the

•., " ' \\ 'I" ;IV" vascular and lymphatic system in the lungs I" 11""" IGry lymphatic channels, which are filled by neopl astic ce ll s,

I, ., II,, · I ,,( '(hlnClion that metastases show for th is site. ., " "" IIY be caused by either primary or secondary lung tumours.

22
 f j j d ,tit __ ! dII d
3 Alimentary System

Fig. 3.1 Oral leukoplakia. This Fig. 3.5 O••oP'''' ''

clinical photograph shows ex­ dldlasls.IIII1I1III I11I·1
tensive smooth white patches oesophO\JlIiI iI.11I11 11I
over most of the tongue . Leuko­ immunOCCllllpl' " lli· d
plakia is purely a clinical des­ whether Ihoy II" '1 " 1'I
cription of any white plaque and tated (parlrcilli rrly I I ~ I
is not a pathological diagnosis . disease), rUt;tJIVil " 1' 1
In many cases, oral leukoplakia chemothcrrlPY I" I U ri
is benign, representing hyper­ a primary il1l1l1l II I"" II 'I

keratosis, the commonest order. Th e :,Ilvllllly "

causes of whic h are chronic tion is deprH" 1,·, I( 111"
irritation or smoking. Only cases degree of tJ"hlllly , .,, '
which also show epithelial dys­ appearancI1 ", II ''' I'Ii
plasia can be regarded as pre­ may rango 11 (111 I 1111 ' ~ I
malignant. Other causes of white plaque s Witl, llli"'"I,. i
lesions in the oral cavity include mation to UI OYI· II" III,
lichen planus and candidiasis . lesions with fllII l1II II III
forma tion niH t ,," ,1111>
Fig.3.3 Mixed salivary tumour (pleomorphic adenoma). Thi s is mation, (1:': ::111111 11111 '
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. 3.4
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
Fig.3.2 Squamous carcinoma of tongue. This clinical photograph pharyngeal con­
shows an irregular, raised pale lesion on th e inferior surface of the stri ctor muscles.
patient's tongue. Most malignant tumours of the oral cavity are Elderly males are
squamous carcinomas and postulated aetiological factors include predominantly III J.6 Oesophagus - peptic (Barrett's) ulcer. II "' I,Iq
tobacco smoking, syphi lis and drinking strong spirits. They most affected and ve ry [,I Ir tlil icer with a haemorrhagic base is presollt III "," " 'I
commonly present in late adulthood , aHecting predominantly males. occasionally post­ II" ' Io;:,ophagus . Barrett's ulcer occurs as a cOIII"Ii, <l thll,
The clinical course is very variable but carcinoma of the tongue cricoid carcinoma I ) " Ille metaplaSia or heterotopia with in the dist; 11 111 1'111, ,1,
generally carr ies a worse prognosis than tumours si tuated elsewhere may develop in sucll "lll llmest cause is chronic reflux oesophagiti:;, "li lli' I, I
in the mouth. a pouch . ,II I" 11iotus hernia.

23

..


...1I ••lIvory tumour (pleomorphic adenoma). Th is is
,. I , " 11 '1 )111' ,111 of salivary glands, the parotid being the
' 1I 1V 1111nl.llld site, This section shows a fairly well
" HI, I""Ilill(')(\u lar tumour; the cut surface has a myxoid
Ii 'I ,, '," , II Ice and there are small foci of cystic change
illdlf " 11 1()ne tumours are prone to local recurrence,
II , ' I 1I11' .'lquence of spread through the capsule, which
, ," '1,1, ,t, I curg ical excision. Malignant transformation is
, IIIH
Fig. 3.4
Pharyngeal pouch.
The pharynx has
been opened
posteriorly to show a
diverticulum extend­
ing laterally. A
pharyngeal pouch is
a pulsion diver­
ticulum which
occurs at Killian's
dehiscence, due to
neuromuscular in­
coordination of the
pharyngeal con­
strictor muscles.
Elderly males are
predominantly
ticularly common in
affected and very
alcoholics.
occasionally post­
cricoid carcinoma 'i
may develop in such
a pouch .
3 Alimentary System
Fig. 3.5 Oesophageal can­ Fig. 3.7
didiasis. Fungal infection of the Oesophageal
oesophagus is not uncommon in stricture. The
immunocompromised patients, posterior aspect of
whether they be generally debili­ the oesophagus has
tated (particularly by malignant been displayed to
disease), receiving cytotoxic show a zone of
chemotherapy or suffering from stricture formation
a primary immunological dis­ complicated by the
order. The severity of the infec­ development of a
tion is dependent upon the small acute ulcer.
degree of debility, and the Note the gross di­
appearance in the oesophagus latation of the
may range from flat white proximal (upper)
plaques with minimal inflam­ oesophagus .
mation to greyish, ulcerated Oesophageal stric ­
lesions with pseudomembrane tures may be
formation and florid inflam­ caused by a variety
mation , as seen here. of conditions includ­
ing reflux oesoph­
a(Jitis, peptic
ulceration, ingestion
of corrosives,
scleroderma or
trauma. Clearly, it is
essential to distin­
guish such benign
lesions from a
stenosing carcinoma.
Fig, 3.8 Mallory­
Weiss tear. The
Mallory-Weiss
syndrome is an
uncommon cause of
haematemesis, in
which, most often,
violent or prolonged
vomiting results in
tearing of the
oesophageal or
fundal mucosa with
damage to the
underlying blood
vessels. It is par­
1tllllll,hagu8 - peptic (Barrett's) ulcer. A sharply demar­
, II" ' I I,IIul norrh agic base is present in the lower third of
I! 1\ I' '10 11111' il lI' ~ ulce r occurs as a complication of either
, Ii ,I "11 , ' 11 lililorotopia within the distal oesophagus. The
I "","I', I
I 11101 "" Icllux oesophagitis, often in association
24
3 Alimentary System

Fig.3.9 Oesophageal varices.

These are dilated veins, situated
predominantly in the lower
oesophagus, which develop as a
complication of chronic portal
hypertension, most often due to
cirrhosis of the liver . They are
prone to rupture with resultant
haematemesis . The oesophagus
has been opened long itudinally
to displ ay numerous tortuous,
dilated vei ns and. in the lower
half of the picture, a mass of Fig.3.11 Carcinoma of the oesophagus. The oesophagus has
blood clot is present in the been opened longitudinally to show an exophytic. largely ulcerated
stomach . carcinoma in the middle third . Squamous carG:inoma is the
commonest malignant tumour of the oesophagus and most often
affects older adults. predominantly males. Smoking and a high
alcohol intake are thought 10 be causally related . Tumours in the Fig. 3.13 Acute gastritis. Th is stomach has be,," III ""
upper third may rarely occur in association with the Plummer-Vinson normal rugal pattern with marked mucosal congO! ;I" "' " , "
syndrome which is almosl exclusively seen in females, Tumours in hand side (ef the pyloric antrum on the left) Acull' 11' 1' ,11
the distal third of the oesophagus are most often adenocarcinomas defined as transient mucosal inflammation, Ihe CUll "''' '"I
which arise either in area s of gastric metaplasia or heterotopia. or whiCh are salicylates, excess alcohol intake. cyl'"II '~1I III
represent infiltration by an adjacent gastriC primary tumour . hypotensive shock (of whatever cause), Added illl"IIII'"
oedema and haemorrhage may lead to the devo" "I" ", "~ I
Fig. 3.10 mucosal erosions,
Achalasia. The
oesophagus and
gastric fundus have
been opened to dis·
play gross dilatation
of the oesophageal
lumen. The
oesophago·gastric
junction . not visible
in this pi cture , wa s
very narrow . In the
posterior wall of the
distal oesophagus
are two pulsion
dive rt icula.
Achalasia is an id io­
palhic disorder of
neuromuscular co ­
ordination affecting I" Acute gastric ufcer. The stom Gtcl1l"", I""", , 'I
the autonomic Fig.3.12 Congenital pyloric stenosis. This infant's stomach has 1'.1" 'flow, ,,'Inched-out haemorrhaO 'G III, HI w,II, • , I
plexus in the distal been opened to show marked hypertrophy of the muscle coat at the I' fI ' III" 1)( :pl ,e ulcers represelll all nXI"Il !iH " ' , " II' ,
oesophagus; the pylorus with obstruction and proximal dilatation . This condition is , 1" , " 1/ "." "'S ano as sue r, have larqllly II,,· ' .,11 ,,(1 , I
oesophago-ga'stric idiopathic but usually presents in the neonatal period with projectile , I,ll,,,,,, 11':11, :(1 from an erosion I) y ""'11 lI'v, ,l vII"" ,
junction fails to relax vomiting , It occurs in approximately 1 in 500 live births . is common ly " ,', ,'.,', w,'lI:ls 111C mucosa. At.I,II : 'II""" .I , ""I ~ ,
during swallowing familial and affects males more than females . The mode of inherit­ 1,1~ ! j j 1 1t,.·.{ ;(Jri1lnOn {1~S OClil l( ~dr:;II I ~ ,(, : ,"t l ll ll ll l r

resulting in proximal ance appears to be multifactorial. If untreated. the patient may , I fll, ',,)II" ;"ll:IlIill IIljlllY Hnrf ''''"111',11' '1(1'\1(( "
dilatation . develo p pro found metabolic alkalosis.

25
 3 Alimentary System

"' 1111 '"11' 01 the oesophagus. The oesophagus has

I I, ,,,, 111 111 III',,II,V I( i :·,ll0Wan exophytic , largely ulcerated
, II" . I il li h II" II III cI ~qua mous car€inoma is the
"" ti l> 11 "1 11 1\lIIIUIH 0 1 the oesophagus and most ollen
I, IIIIi'. Iii'" II IlIlWICl illly males, Smoking and a high
, I" " II h.. " 1111 I!I 1)0 causall y related, Tumours in the
' i IY ' IIl'ly 111.(;11 1 In association with the Plummer·Vinson
I", 1"" ,,111,11' ;1 i 'xctlJslvely seen in females Tumours in
,d , 011111" II ",Iii diOguS are most ollen adenocarcinomas
111,( " IL l, II", 11 , 0 1 gastric metaplasia or heterotopia, or
1,11, , \I " Ililly, ,, \ (Klpqcent gastric primary tumour.
Fig.3.13 Acute gastritiS. This stomach has been opened to show a
normal rugal pattern with marked mucosal congestion on Ihe right
hand side (eI. Ihe p yloric antrum on the lett) . Acute gastrilis is
defined as transient mucosal inflammation, the commonest causes of
which are salicylates, excess alcohol intake, cytotoxic drugs or
hypotensive shock (of whatever cause), Added intramucosal
oe dema and haemorrhage may lead to the development of small
muc osal erosions ,
Fig.3.15 Chronic gastric (peptic) ulcer. The stomach has been
opened to show a sharply demarcated ulcer with straight edges,
which has penetrated the muscular layer of the gastriC wall; its base
is composed of smooth but irregularly heaped-up granulation and
scar tissue , Chronic gastric ulcers affect males more than females,
usually in middle life and are more common in patients with blood
group 0, Most patients are usually hypochlorhydric and it is thought
that relative mucosal ischaemia, an impaired mucosal mucous
barrier, altered gastric emptying rate or reflux of bile acids from the
duodenum may be important pathogenelic faclors , These ulcers are
usually solitary and the vast proportion arise at the border zone
between acid-secreting and non-acid-secreting mucosa, particularly
on the lesser curve,

Fig.3.16 Bleeding gastric

ulcer. Chronic peptic ulcers
commonly damage small
arteries or veins as Ihey erode
the stomach wall, Haemorrhage
is Iherelore the most Irequenl
complication : this may either
occur in small amounts over a
long period 01 lime, resulting in
melaena and iron-deficiency
anaemia , or a larger vessel may
bleed acutely and heavily, giving
rise to haematemesis , There is
Acute gastric ulcer. The stomach has been opened to
clotted blood in the Iloor of this
I 11,1111 IW, punched·out haemorrhagic ulcer with smooth
""IIQIVIHI pyloric stenosis. This infant's stomach has ulcer and blood in Ihe stomach,
1\1 "1,, poptlC ulcers represent an extension of acute gastrilis
, li d ',IIIW11I.III,I·d 11Vpertrophy of the muscle coat at the Nole also Ihe smaller peptic
I I I" , "" I' ,1!lII'" ;~nd as such have largely the same causes, They
" ,1 1',111 ' 1I"Ii ,Hid pI<Jxi mal dilatation, This condition is ulcer jusl above Ihe main lesion,
II I " , Iilil ,I' 'I 11r; Ilc'd from an erosion by their involvement of the
11 11" ',Il,,'iy I'" " ,.,"t', HllIlC~ neonatal period with projectile
,111111." '" I d ' , WI 'II ,j ,; IIle mucosa , Acute ulcers rarely exceed 1 cm
, ', ; , " ~ " " I " ," "' IIII:llr'ly 1 In 500 live births, is commonly
i J~ (l i " I. I I, ",', I Ilfllfllon associated causes include severe burns
I ,11" , 1'.",..1, .', 111""' 1I1,,"I(~lnal es, The mode of inherit·
" • I, , 1'1",,,11,1.;, II If I, II 1IIIIIIreated , the patient may
tI' (
Ililfi. i "I " q) I'll 'I)ral injury and neurosurgery (Cushing's
'I
, ,II " "1\ I '" lldl 'I !II , itlll' ,1(,' ,I',

26
3 Alimentary System
Fig.3.17 Perforated gastric ulcer. Perforation of chroni c peptic
ulcers. i.e. disruption of the full thickness of the stomach wall, occurs
in up to 5% of cases. This is a life-threatening complication which
results in peritonitis . In this specimen, while a small area of granu­
lation tissue remains at the superior border of the ulcer, perforation
has oc curred and part of the left lobe of the liver is visible through the
floor of the lesion.
Fig.3.18 Chronic atrophic gastritis. This'stomach shows extreme
atrophy and pallor with loss of the mucosal folds and marked attenua­
tion of the gastric wall, such that it is almost translucent. This re­
presents the end-stage of chronic autoimmune gastritis, which i's the
commonest cause of pernicious anaemia. Autoantibodies to intrinsic
factor and gastric parietal cells are found in such patients, who
develop a marked deficiency of vitamin 8'2' Up to 10% of patients
with atrophic gastritis may subsequently develop gastric carcinoma.
27
Fig.3.19 Gastric adenoma. At the edge of the greater curve is a
small, rounded, raised lesion projec ting from the mucosal surface
(arrowed) . There is no evidence of ulceration or adjac ent infiltration .
Gastric adenomas, more accurately known as neoplastic polyps,
may be classified like those in the large bowel (see Figs .3.45 and
3.46) although they are only rarely pedunculated. They have exactly
the same malignant potential and are often seen in association with
chronic atrophic gastritis.
Fig.3.20 Gastric adenocarcinoma. In the fundus of the stomach is
an ulcerated neoplasm with irregular rolled edges . Adenocarcinoma
of the stomach is one of the most common causes of death due to
malignancy in Britain, occurring most often in elderly men. There is a
familial incidence and patients with blood group A are at increased
risk. Geographically, the disease is most common in Japan and
Scandinavia. Currentl y fa voured aetiologic al agents are nitros­
amines, derived from ingested nitrates which are used in preserva­
tives and crop fertilisers. Known predisposing conditions include
chronic atrophic gastritis and uncommonly, gastric adenomata.
Macroscopically, ulcerating tumours are far more common than the
fungating or polypoid forms.
Fig. 3.21 Linitis plastica ('leather-bottle' stomaoh),
has been dissected to show diffuse infiltration of II JlII I "
curve by pale, rigid tumour, resulting in shrinka( JI' 01" "
lumen . This macroscopic variant of adenocarcill('" Ii1 " I
represents widespread infiltration by poorly diflol,\l lI lIlt.
an associated dense fibrous (desmoplastic) stl'on ll l ~ " r
tumours only rarely impinge on the gastric lumerl, "'"Y '
present at an advanced stage and the prognosi:; n, V'" ,
Ig.3.22 Gastric leiomyoma. The stoma cl) Ilw: I li")i1
III 'w I ' smooth, rounded and well circurn scrIhud III" " ,i I
Itil I" 01its apex. The cut surface (right) revealn IIt.11 "" I I
, " V, 111)( 1 by a layer of attenuated, normal OpilhlJllIII" I , II,
I I' II II Ilr:ornmon benign gastric tumours, whiCI I ,"" , ,11 ,,"
''''' i; II " rhey arise within the muscular coal (111111 1' ,II 1111
'1< '" 11I[)loc ting into the gastric lumen, am VllIY 1"')111111
,.1> i '1.'lh ,n. Their malignant counterparl, loiolllY, I'"", 111 11
I'"I' I/ lly I,II U
 3 Alimentary System

'I
It IlliuJ1om a. Al lhe edge of the greater cu rve is a
I ,,11.,,11 1It " 11011 rrojecting from the mucosal su rface
' Ii I' '"', 'VI( lonce of ulceration or adjacent infiltration .
'I I" I II" 11" .lccurately known as neoplastic polyps,
lilt '1 1111,,, litora, in the large bowel (see Figs .3.45 and
I, \1 11 ,.,. .11 '" 'Illy rarely pedunculated. Th ey have exactly
1I I' " " II 1"111 illi llil and are often seen in associalion with
I II, 'I'" 11111 '.
Fig. 3.21 Linitis plastica ('leather-bottle' stomach). The stomach
has been dissected to show diffuse infiltration of muc h of the greater
curve by pale, rigid tu mour, resultin g in shrinkage of the gastriC
lumen . This macroscopic variant of adenocarcinoma of the stomach
represents widespread infi ltration by poorly differentiated tumour with
an associated dense fibrous (desmoplastic) stroma. Since these
tumours only rarely impinge on the gastric lumen, they common ly
present at an advanced stage and the prognosis is very poor
Fig.3.23 Chronic duodenal ulcer. The stomach and proximal
duodenum have been opened to show a well circumscribed , deep
ulcer with smooth edges in the first part of the duodenum . Duodenal
peptic ulcers are much commoner than their gastric counte rpart s
and are seen most frequently in males between the ages of 20 and
40. In contrast to gastric ulce rs, these lesions are associated with
marked hyperacidity, the precise cause of which is uncerta in. They
occur most often in the first pari, particularly on the anteri or wall and
produce similar complications to ulcers in the stomach .

hll ndl)nocarcinoma. In the fundus of the stomac h is

II , ' llilll'dil willi Irregu lar rolled edges. Adenocarcinoma
1I II "11111111110 most common causes of death due to
3.22 Gastric leiomyoma. The stomach has been opened to Fig.3.24 Periampullary carcinoma. Thi s segment of duodenum
I. I 1111, "11 , "''1 111 ring most often in elderly men . Th ere is a
,IIIIW .' ~mooth, rounded and well circumscr ibed tumour , with a small has been opened to show a fungating, focally ulcerated tumour
, ' " .. ,11 1<\ " ,11 ;\\1115 with blood group A are at inc reased
Pi< I I dill:.; apex. The cut surface (right) reveals that the tumou r is arising around the ampulla of Vate r. The pyloric canal is apparent on
(I" .
, .1,1, :,dl y, IIl!Jouse is most common in Japan and
"" ' " 11( IIJY a layer of attenuated , normal epithelium . Leiomyomas are the right. Periampullary carcinoma ari ses from the distal end of the
! 1II" ,"l1y Il lv()lIred aetiological agents are nitros­
,,, ,11 11" 1IIIIIYlOn benign gastric tu mours, whic h are often asymp- common bile duct and occurs most often in older adults. It is usually
, " li lt 11 11 " il l" ',h lc! nitrates which are used in preserva­
I, ,". III' Ihoy arise within the musc ular coat of the stomach and, slow-growing and carries a relatively good prognosis. It is very
'1, lf"I IIi ,.III'1 1\l IOWIl predisposing conditions include
III II I '" '1 1lt:ling into the gastric lumen , are very prone to superficial
important to distinguish such cases from carcinoma 01 the head of
1,111' 1/11' 11111' . IIlId IIlIc ommonly , gastric adenomata .
II, , I ""111 litei r malig nant counterpart, leiomyosarcoma, is ex-
the pancreas , which pre sents very similarly, since surgical interven­
IlIv "I, ,II , Ii II 10 111I11I"lr$ are far more common than the Itt· ; 111 dy /.1/1 I tion is undoubtedly worthwhile in periampullary tumours
, " ,1 " 1" ,1.1 1111" II.

28
) Al imentary Syste m

Fig.3.25 Meckel 's diverticulum. This opened segment of iteum Fig . 3.27 Crohn 's d isease. This opened segment of large bowel
shows a wide diverticutum . about 2 cm in diameter. lined by rather shows two quite separate 'skip ' lesions, characterised by florid
smooth mucosa. Meckel's di verticutum is a congenital malformation mucosat ulceration . The tesion on the teft has induced marked
luminal stenosis with obviou s proximat dilatation . Up to 15 % of Fig. 3.29 Intestinal tuberculosis. In contrast tn I III I
representing a remnant of the vitello-intestinat duct. Usually found
ulceration, while still originating in Peyer 's patcil t!t. . ,,, 10
about 60 cm from the ileocaecat valve, it affects about 2% of the patients with Crohn 's disease show large bowel involvement, with or
without small intestinat d isease . There is a definite increased risk of versely around the bowel wall following the lines oltV" '1 I
poputation. White it may become inflamed or obstructed, ectopic
colonic adenocarcinoma, but th is is much less marked than in ulcera­ age . Intestinal tuberculosis may be primary, ret.llilll lIll "
gastr ic mucosa is present in some ca ses, which may tead to peptic
tive cotitis . of unpasteurised milk, or secondary, as a con soq ll'" rr ,
ulc eration . Other ectop ic epithelia whi ch are often found include
ing infected sputum from pulmonary d isease . I\UI.II 111 ,1 I
pancreatic , duodenal and cotonic types.
nodes are usually involved and may later undeIOP I IY'.II'
calcification . Peritoneal involvement may lead to 11',( Ilf"
Fig. 3.28 Typhoid ulceration .
These segments of small intes­
tine have been opened to show
several ovoid ulcers lying
parallel to the bowel wall (cf . Fig .
329) The ulceration has
oc curred al the site of necrosis
of Peyer's patches. Typhoid
fe ver remains endemi c in some
parts of the world, especi ally
As ia and the Far East. It is due to
Fig.3.26 Crohn's disease. This opened length of small bowel ingestion of food or drink con­
shows the typical 'cobbtestone' appearance of the mucosa, each taminated with Salmonella typhi,
nodule being separated by ulcerated fissures . Crahn's disease is an usually from an asymptomatic
idiopathic granulomatous condition which may affecl any site in the carner. Important local com­ III 3.30 Small intestinal ischaemia. This 1001J I II 1!l IW
alimentary tract but shows a predilection for the terminat iteum . It plications include perforation 11111 1IIIIrkedly congested This is the apreArli1 II " ",I Uti li'
presents most often in the 2nd to 4th decades. Postulated aetio­ and haemorrhage. Following IIIIW," wall, but lesser degrees of ischacllliu III, IY I' " ,ri ll I
logical agents include various micro-organisms and fine particutate invasion of the bloodstream , ""11 i J' ,dl llice ration . It most commonly resllil :, III " " .111 ",I'
matter, which have induced an abnormal immunotogical respon se. excretion of Salmonellae in bile 1i1 ,.oIly ,,,Irrhac in origin, occluding il hmlJl:hlll II,,, '''II''
Multifocal invotvement , giving rise to 'skip' lesions , is characterist ic may tead to chronic gallbladder I III ,OII"IV Olher ca uses include Severn hy""I"I II,JI II' II,
and inflammation of the full thi ckness of the bowel wall causes deep infection (whence the c arrier II I 1i1" "I' III 1;,touS vessel, retrograci e IIlfarc' tllll J<i. II . II I III'
fissuring , fistula formation and fibros is. state) . "" "I'. 11 11111 I Ibosls or digitalis thcrO'l l'Y

29
 3 Alimentary System

Fig. 3.31 Mesenteric embolism. The superior mesenteric artery is

totally occluded by thrombus which has emboli sed from the lett
atrium in this patient with atrial fibrillation. Proximal occlusion. such as
IIhll' . tll.OBBe. This opened segment of large bowel
thi s, results in infarction of almost the entire small bowel and is
HI' I ,1'1" 11.IItJ '!;ikip' lesions. characterised by florid
invariably fatal
I 11 11 11 1 II,,· I U I~ l on on the lett has induced marked
Fig.3.29 Intestinal tuberculosis. In contrast to Fig . 3.28. this
, 1', wil l, " l lVl""S proximal dilatation Up to 15% of ulceration. while still originating in Peye r's patches. extends trans­
I "itll" '. I it!••;;lse show large bowel involvement. with or versely around the bowel wall following the li nes of lymphatic drain­
IIl dl ll !lI",I , iI·,ease. There is a definite increased risk of
age . Intestinal tuberculosis may be primary. re sulti ng from ingestion
" I I'. 11 11 illl.,. ljllt this is much less marked than in ulcera­
of unpasteurised milk. or secondary. as a consequence of swallow­
ing infected spu tum from pulmonary disease. Adjacent lymph
nodes are usually involved and may later undergo dystrophic
· ~ Icification . Peritoneal involvement may lead to ascites.
Fig.3.28 Typhoid ulceration.
These segments of small intes­
tine have been opened to show
several ovoid ulcers lying
parallel to the bowel wall (cf. Fig .
329) . The ulceration has
occurred at the site of necrosis
of Peyer's patches Typhoid
fever remains endemic in some
parts of the world. especially
Asia and the Far East. It is due to
ingestion of food or drink con­
taminated with Salmonella typhi. Fig.3.32 Carcinoid tumour. The terminal ileum and caecum are
usually from an asymptomatic shown here. Originating in the ileocaecal valve is a well
carrier. Important loca l com­ 3.30 Small Intestinal ischaemia. This loop of bowel is dilated circumscribed, yellow tumour in the submucosa. In the adjacent
plications include perforation 1I 11 111 11 111\C 'llly congested. This is the appearance of infarction of the mesenteric fat, a lymph node containing metastatic tumour can be
and haemorrhage. Following I " ,w,,1 w.t ll, ill II lesser degrees of ischaemia may result only in seen (arrowed) . Carcinoid tumours arise from neuroendocrine APUD
invasion of the bloodstream. II! II ''' lI ilIIIi .lllAlion. II most commonly results from an embolus.
cells and are usually found in the appendix or small intestine. Tumours
excretion of Salmonellae in bile I,' I, Ill y •."Ii h.ll; III o ri ~ lin , occluding a branch of the superior mesent-
in the appendix tend to be solitary and affect young adults, while
may lead to ch ronic gallbladder I I, 11 1. 111/ I HI II !I Ciluses include severe hypotension. thrombosis in
those in the small bowel may be multiple and usually present in old
infection (whence Ihe carrier III 11111 ' I'"l"h ll l( . v,,~~ se l , retrograde infarction due to mesenteric
people . The appendiceat neoplasms almost neve r metastasise, but
slate) " . •11 ' II I II 'II Ii J(/~ i l: i c)r diqltali s therapy .
small bowel tumours frequently spread to lymph nodes and the liver.

30
3 Alimentary System

":":;"68~ -...-,. . ' t:.(,~.~~

\.1.,'.
....~t~',·I " .. .~. . .
'1 J'" }!~,
tl.~;; ,'.""'~~;
.. ~ .~;''''
, ~\,,",
, , .• . "
"• ot " to- ,,:\"" , , '.,! ; , '.' '
.':,',.
~" ~. '.~.'Ioor." ' . • ',,11\'" ,~
,;J,' .•

~~. '.,.;-,
,I :)-
,,, ,t _ , #"
. '.' «'
" : ):t ~!i{,.,.;. ~".)~ <aL' ,.; " •
." ;, (~ ~.~.~ 'l..r~~~ W; f .,.~~ ,:.;,.s.
":'~'( .''','f.r,!
:~,~~ , "', ,,..'~ t.': ~~:::- . '.,
t.,... ~'\~\·'·
' ~ , .4 ", f ..... ,' . - "
~ ~ ..... , l(\'~'''''''~'
~}. '
{" ",
.
,~"
.,,j6, ' . i:'
I, ,, ' • •

,.... ". ',:\0' 1 i". ',,:

:J~' •." 'I \ ~. .

Fig.3.35 Acute appendicitis. This appendix has been sectionea Fig.3.37 Pseudo-polyps in ulcerative colitis. rlli" 14,
transversely to show copious intraluminal and intramural purulent large bowel shows intense mucosal congestion ;II,d, II I
material associated with congestion and haemorrhage in the wall and mucosa is 'thrown up' into innumerable irregulal I" ,IYI'"
Fig.3.33 Intestinal lymphoma. This segment of bowel shows a adjacent mesenteric fal. trusions . These are not true polyps but simply repl'''."",
solitary, ulcerated turmour Macroscopically, primary gastro· adjacent ulceration, undermining the mucosa will, ; II " "
intestinal lymphoma may be indistinguishabte from a carcinoma . lormation . Even when the disease is in remissioll, II lilt"
Involvement by disseminated lymphoma usually gives rise to multiple Fig. 3.36
Ulcerative colitis. persist as elevated areas between the healeej alli ll ,I,i< I
lesions and may therefore be more easily recognised . Gastro­ nreviously ulcerated mucosa .
The distal portion of
intestinal lymphomas are nearly all non-Hodgkin's in type . There is an
this rectum has a
increased incidence associated with coeliac disease and Ct heavy
granular, almost
chain disease .
velvety, appearance
with haemorrhage
and innumerable
shallow ulcers. The
proximal margin
(above) appears
normal. Ulcerative
colitis is an idio­
pathic disease, pre­
dominantly of young
adults, which always
involves the rectum
and affects the
proximal large bowel
in continuity. It is a
chronic relapsing
Fig. 3.34 Acute appendicitis. The appendix below shows marked condition primarily 11.1 I III OlvortlculaJ disease. r hi:~ :l lHl rl iMI I " II II, I" l
serosal congestion while the one above is covered in a fibrino­ affecting the " 1""'"11 111 '. IIIIW IWll il irnO!l1 pHItI IIOI IIIW:. "I " 'Vlll i h Iltlll
purulent exudate, indicative of more advanced infection . The aetio­ mucosa. It is assoc ry, ,II ,,, W. " I, I, d,vf) 1III :lIln l di f)I)(Ull ' 01 tI,,, 1.1 ,II " I '" 11. 11 ~
logy of acute appen dicitis is still debated but it is thought that luminal iated with HLA R '? 7 , "'"'" 111, 1,," 111 1I1111 1y with lI r1vIIIICII'IIII!I" "" "/1111'1 III It
OIISIIIIClion, usually hy faecal malerial, probably leads to mucosa l and may Il() corn ",' 'j I , , I, ,.ilil " ,"11111111',11 I ,II J'i' II II Ii , :1111. 1')( I'" ,,,1 \I I Ill" "," I'

Illcornliol1lollnwoei hy I'llllt~ l r:llin l l ()f tilt! I1IJwei wall hy:l wHioly of p l,c al ori l}y to ,xi.: I, " '"" I , " " lli lill<l I" IIi 0 PIII II IIIII " II" \l1 'l! It! III "1 ",, ,1. 111
11 '01;1\10101111,:",,(; (), : UI!lH 11 1111 I'll :rlili m; : ;\11 1II, ;t;i H In drflJlly III VIl! Y II l1 l ll l ll:01(1I1.1'01 " 'll ,,11111', '" " i" tilllllllw 11,111,1 11 II,,, , "III II iii II. II II I V '
Yljlll l\l p" I" 11 11 ', wi", I II w<lh)f I pnJfIll./ IIOIl JIll' I I II " 111111,1 1:.. nlh, " , 1/1 " 10 1.(1 iOI1 nllel 1111' I" " I" II I , II 111' 1 !JI I 111 11' "' ill II, '"11111, 111"', I " II I, ,, l ilh ,;
. 11 ~,'t I 'l 'j" II, I II, u I fI ~.I U " .,"II I' t " "" l / IH"lh "~ IJlll.lt llij I II!
(1111 ,)1 11111' , lilt II,d ll llll\ Ih'vIlII ,) 'fll, ,' ii, ,I , III ! II/IIIV"UIII ) JI 1l1I1I :e1l lu'I, ' (,I rl IIV"r. 111"1111 II "I
.,,1,,111111 111'"1111111 II II I !" i l HI IIII II I H I
rI 11' .II II"" 1111
 3 Alimentary System

lin nl,pondlcltls. This appendix has been sectionea Fig.3.37 Pseudo-polyps in ulcerative colitis. Th is segment of
I I IIIW, til 11(1\1:; intraluminal and intramural purulent large bowel shows intense mucosal congestion and , in addition, the Fig.3.39 Diverticulitis. This sigmoid colon has been opened to
I II.. , I w, ll, (~"ngestion and haemorrhage in the wall and mucosa is 'thrown up' into innumerable irregular polypoid pro­ show mucosal congestion associated with a florid, serosal, fibrino­
j r II i ~ I H I. II trusions. These are not true polyps but simply represent the effects of purulent exudate . In th e lumen, the ostia of severa l diverticula are
adjacent ulceration, undermining the mucosa with granulation tissue vi sible . Inflammation complicating dive rt icular disease results from
Fig. 3.36 formation . Even when the disease is in remission , these tags may mucosal ulceration due Ie inspissation of faecal material within diver­
Ulcerative colitis. persist as elevated areas between the healed atrophic foci of ticula . Diverticulitis can be either acute or chronic and may give rise
The distal portion of previously ulcerated mucosa . to fibrosis or perforation .
this rectum has a
granular, almost
velvety, appearance
with haemorrhage
and innumerable
shallow ulcers. The
proximal margin
(above) appears
normal. Ulcerative
colitis is an idio­
pathic disease, pre­
dominantly of young
adults, which always
involves the rectum
and aHects the
proximal large bowel
in continuity. It is a
ch ronic relapsing
condition primarily Ig. 3.38 Diverticular ijlsease. This sigmoid colon has been Fig. 3.40 Chronic ischaemic colitis. This large bowel has been
affecting the "PllnClcl to show two almost parallel rows of diverticular ostia. In the opened from behind to show an area of mucosal congestion assoc­
mucosa . It is assoc­ w, ,',lorn World, diverticular disease of the colon is extremely iated with fibrous thi ckening of the bowel wall and stricture formation.
, ""IIItJn, particularly with advancing age. It results from the eHects of The appearance is typical of long-standing relative isc haemia which
iated with HLA B-27
III' '" .II.od intraluminal pressure consequent upon the peristaltic con­ usually results from mesenteric arterial disease without complete
and may be com­
1' <11 110 111 ' : roquired to propel the more viscid or solid faecal material , occlusion (cf. Fig .3.30) . Commonly, ischaemic colitis is complicated
plicated by toxic
, hi li <I I IIlII:1Iic of a diet low in fibre . The condition may be complicated by bacterial infection and progressive fibrosis: as a consequence ,
megacolon, per­
I IV 1111 111 1\1 , "I acule or chroni c inflammation, perforation or haemor­ the macroscopical appearances can be confused with those of
foration and the
development of 111 111 ,11 I IIvl) rtioular disease does not predispose to colonic inflammatory bowel disease or malignancy.
adenocarcinoma. Ii II" ,,,, .0 1\ II IU m a .

32
3 Alimentary System

Fig.:!.­
B~WEL PO~~
Fig. 3.41 Pseudo­
membranous colitis. This CLASSIFICATION OF-LARGE adcn lll ~
close· up view of large bowel eX; If"I''']
mucosa shows numerous small , <:l< jt ' l u fll
I
raised , yellowish plaques The Anomalous mucosal fold fru, II II"
appearance is virtually diag· tile IlII'f'
nostic of pseudomembranous 'Metaplastic' (hyperplastic) (UPI' ''' )
colitis and is usually found in the sp,', ,",,)
left side of the colon . The con· Inflammatory pseudo-polyp hl1!, II.., 1
dition occurs most often follow· to:,IH 'w !
ing a course of antibiotics, Lymphoid 101 ,1 ,101 1. '1
which, in altering the natural flora ap i II '.1 101
and suscep tibility of the colon to juvenile SIlJ.,III II
bacterial colonisation , allows Hamartomatous pl:" ,I " I
infection wi tt> erostridium difficile Peutz-Jeghers lalll,'1 1i1
(a Gram-positive anaerobe) and (;(lll ' " " "
the elaboration of its potent tubular ~()(: I! i I V

exotoxin to occur. Neoplastic wlH,llll II

tubulo-villous 'lill', IIII'

(adenoma)
V;III,II II '1
villous pl"',III I '
"''''' Illy I.
Fig. 3.43 Classification of large bowel pOlyps. 3<; 11111 1 1
11 ,I.Ov il "
f1,"I1'I ,II
Fig. 3.44 'Meta­
plastic' polyp. Th is P'I' Il h" l!

close-up view of
large bowel mucosa
shows a very small,
pale, polyp oid
nodule situated on
the crest of one of
the mucosal folds .
'Metaplastic' polyps
are, in fact, hyper­
plasti c lesions show­
ing an increased cell
lurnover. They occur
in the large bowel
and may be found at
any age, but are
Fig.3.42 Amoebic dysentery. The colon shows irregular foci of espe cially common Flg.3.46 Villous adenoma. This example btl'l 1)11"" I ,Ii,
mucosal congestion and swelling with adjacent areas of ulceration. from the 5th decade ' III race to show that it is a large, broad-bassrl :1,'" ', 01,, 1"', 1
Amoebic dysentery results from infection with the protozoon onward s. Th ey are whi c h numerous irregular papillary frond s projoCi N, II .. "
Entamoeba histolytica, which is endemic in the tropics After inges­ usually mul tiple, Iflarq ins of this polyp are ill-defined , This vari~1f '1< ,1' 1111 'l 'iI
tion, the organisms invade the bowel wall and cause submucosill small, flat or sessi le '"<)st com mon in the rectum , It tend s to be larfl'" ,lI il l' ,111
necrosis, which results in 'flask-shaped' ulcers with sparing of the and arise most often "' Jv()re dysplasia than the tubular adenoma 111\(1, ,", ','" ,I ,
overlying mucosa in the early stages . Compl ications include chronic in the rectu m. They , 11I ' 1I1'1()nly progresses to adenocarcinoma V,II,.",'"" h""
infection, with fibrosis or exuberant formation of granulation tissue have no malignant ",' :tllm may somelimes secrele large amOllnl ' , 01I" ,I ", ,I
(the 'amoeboma'), and infection of the portal venous system (see potential. ,01 1"" n,n, giving rise to symptoms of hypokflli 1( 1" 11,' , II I'VI '
FigAA). 1IIIII'"';tcm,a .

33
 3 Alimentary System

Fig.3.45 Tubular
adenoma. A typical
.:,lf ICATION OF LARGE BOWEL POLYPS example of a tubular
adenoma projecting
I,d, 1I1 ~1 mucosal fold from the mucosa of
the large bowel
pI. I; ,IIC' (hyperplastic) (upper) . A separate
specimen (lower)
II II.(lur y pseudo-polyp has been bisected
to show its smooth,
1111111 1 lobulated
appearance and
juvenile sm all pedi cle Neo­
Ill lITlrltous plastic polyps of the
Peut:;:-Jeghers large bowel are very
common in We stern
tubular society, particularly'
with increasing age. Fig.3.47 Familial pofyposis coli . This segm ent of large bowel is
I,,·,II< : This most frequent
tubulo-villous covered in numerous tubular adenomas of va rying size . Pol yposis
1111 1l d) variant of a neo­ coli is a rare autosomal dominant inherited condition in which patients
villous plastic polyp is develop hundreds of large bowel adenomas, usually in the 2nd and
usually less than 3rd decades. Close sc reening of all famil y members is Obligatory
3cm in diameter. since, if these patients are left untreated, all will develop one or more
Ilflcation of large bowel pOlypS.
They are often adenocarcinomas over a period of 10-20 years . Despite such efforts.
multiple and are all up to 40% of cases have a colonic carcinoma at presentation.
Fig. 3.44 'Meta­ pre-malignant.
plastic' polyp. This
close-up view of
large bowel mucosa
shows a very small.
pale. polypoid
nodule situated on
the crest of one of
the mucosal folds .
'Metaplastic' polyps
are, in fact. hyper·
plastic lesions show­
ing an increased cell
turnover They oc cur
in the large bowel
and may be found at
Fig.3.48 Ulcerating rectal carcinoma. The distal end of this
any age. but are
'H . 3.46 Villous adenoma. This example has been photographed opened rectum (left) shows an ulcerated tumour with irregular rolled
especially common
"/ 11, ,,; 0 to show th at it is a large . broad-based sessile lesion from edges. A similar tumour (right) has been sectioned to show penetra­
from the 5th decade
N illi II III ,rne rous irregular papillary fronds project. Note that the tion of the muscle coat and a lymph node containing metastatic
onwards. They are
I""/ filII " of this polyp are ill-defined. This variant of neoplastiC polyp is tumour is visible in the mesenteric fat. Adenocarcinoma of the large
usually multiple,
,, " 1'.1 , III limon in the rectum. It tends to be larger and show more bowel is the second commonest ca use 01 death from malignancy in
small . flat or sessile
, lV l ' ''' dv~>p lasia than the tubular adenoma and, as such , more Britain, even though up to 45% of patient s are cured . It arises most
and arise most often
, " 11111" II ilv f)rogresses to adenocarcinoma. Villous adenomas of the often in the left side of the bowel. There is a familial tenden cy and
in the rectum. They
1" 1 IIIIIIIII ; IV sometimes secrete large amounts of potassium or postulated aetiological factors inctude a low fibre diet, a high fat diet
have no malignant

III il II I 111 1. I living rise to symptoms of hypokalaemia or hypoa l­ and a dietary alteration in bile salt metabolism. Prognosis is directly
potential.
1,1111 ii I H II ',lll1i,1 , related to staging (see Fig . 3.52)

34
3 Alimentary System

Fig. 3.49
Fungating rectal
carcinoma. This is
an abdomino­
perineal resection
specimen showing a
'cauliflower' fungat­
ing tumour, in the
distal rectum, which
has been bisected
to emphasise its
polypoid mode of
growth . Th is macro­
scopical variant of
large bowel adeno­
carcinoma is com­
paratively
uncommon and is Fig.4.1 Polycystic liver. The anterior surface 011111 , II v.
usually histologically Fig. 3.51 Caecal carcinoma. The terminal ileum and caecum have numerous, multiloculated subcapsular cysts, prodOI l1 I11,
well diHerentiated . been dissected to show three separate lesions arising in the proximal lobe , On the right, a separate case shows the c ui ~ .1111. Ii I
caecal mucosa. The largest (left) is an ulcerated adenocarcinoma ance, Polycystic disease of the liver is an inherit o( I ,II '" "
while the other two are neoplastic polyps . Adenocarcinoma of the dominant condition, frequently associated with :1( lIliI",,'
caecum is commoner in females and , owing to the distensibility 01 the disease. In general it does not impair live r funcllOl1 1\ ' ,II
caecum , g ives rise to symptoms less often. Insidious blood loss, usually less marked, appearance may be seen in i ;Olll I'
possibly with melaena, may lead to presentation as iron-deficiency fibrosis .
anaemia. Th is specimen demonstrates the frequency with wh ich
neoplastic polyps and carcinoma are found in the same specimen .

DUKES' STAGING OF COLORECTAL ADENOCARCINOMA

Stage A B C

Extent of Confined to Invasion through Lymph node

tumour bowel wall bowel wall metastases

5 - year
90% 65% 20%
survival

mucosa
muscularis
mucosae
muscularis
Fig.3.50 Annular stenosing rectal carcinoma. This is another propria IIU, 4,2 Massive hepatic necrosis. Til e liVl)1 I:. I ""I_11111 1
abd omino-perineal resection specimen. The tumour can be seen to serosa 111 "111,1111 , Ihe capsule has a wrinklcri, I a lil t'l l 1. )( 1'.11 111'1 " till
encircle the entire lumen of the bowel and shows central ulceration . fat ~ I, j'.I"\I' · tr" polic necros is is unCO lTl1l10ll PUI r: : " '11 ' ,1 I,. " III,;
Circumferential spread may be faci litated by extension of the tumour lymph nodes I. .1II ' " 1111 1 wllh lulmillanl viraIIIOp<r llli!: (1I ~. udl ly I II 1 1 III III "~ I
through submucosal lymphatics. This macroscopical variant is par­ I" " 1 I I). II 11 Il ly ;t1~C) be Cl'lIl: .ori by "II IIJI IrUPIIII>loXII ,."" " I!
ticularly likely to give rise to large bowel.obstruction with prox imal Fig.3.52 Dukes' staging , conceived by Cuthberl Dukes, St. Mark'!"; I!, 111111111' , d:,Ir" lolllflll(!, "IOlllyld"pl ldlld '''UIlI.1 /1I 1 III' \ !
dilatation, ste rcoral ulceration and possibl e perforation. Hospital , London . iii ." II ' 11I y J II It II [ II It! ; In II,; Il clllll lf(~ lillli II I 1 Ulpll lIy ',11111 11 \111111

35
 4 Hepatobiliary System

carcinoma. The terminal ileum and caecum have
show three separate lesions arising in the proximal
largesl (left) is an ulcerated adenocarcinoma
neoplastic polyps. Adenocarcinoma of the
er in females and, owing to the distensibility of the
to symploms less often. Insidious blood loss,
may lead to presentation as iron-deficiency
\ecimen demonstrates the frequency with which
Ii and carcinoma are found in the same specimen .
Fig.4.1 Polycystic liver. The anterior surface of Ihe liver (left) shows
numerous, multiloculated subcapsular cysts , predominanlly in the left
lobe. On the right, a separate case shows the cut-surface appear­
ance. Polycystic disease of the liver is an inherited autosomal
dominanl condition , frequently associated with adult polycystic renal
disease . In general it does not impair liver function. A similar, though
usually less marked, appearance may be seen in congenital hepatic
fibrosis .
Fig.4.3 Hepatic abscess. Within the liver parenchyma is a large
abscess cavity, lined by purulent material, and showing central
necrosis. There is also an adjacent smaller lesion. Hepatic
abscesses most often complicate suppurative cholangitis or portal
pyaemia, as may be seen in diverticulitis or appendicitis. Such
abscesses are commonly multiple and are usually due to infection by
gut flora such as Gram-negative or anaerobic bacteria.

GING OF COLORECTAL ADENOCARCINOMA

A B C

Confinecito Invasion through Lymph node

bowel wall bowel wall metastases

90°/, 65% 20%

iU,4.2 Massive hepatic necrosis. The liver is pink and mildly
I q ' " 11\; \1 1: the capsule has a wrinkled, rather loose appearance.
, .. IV" Ilfl patic necrosis is uncommon but is most frequently
11 '" loIllld wllh fulminant viral hepatitis (usually hepatitis B or non-A
, '" ,I I 11\. 1IIIIOy also be caused by other hepatotoxic agents including
I" " ,1 1111 11, n.s halothane, methyldopa and isoniazid. The prognosis is
~ ' staging, conceived by Cuthbert Dukes, St. Mark's i"
I' I ,II V IIUOI and acute hepatic failure rapidly supervenes.
I,
Fig.4.4 Hepatic amoebic 'abscess'. In the posterior aspect of the
right lobe is a large necrotic cavity showing surrounding fibrosis. The
contents of the cavity are said to bear some resemblance to anchovy
sauce. Hepatic involvement by Entamoeba histolytica occurs via the
portal venous system (see Fig .3.42) and may be seen in up to 30%
of cases of amoebiasis. Necrosis, as seen here, is caused by the
protozoa and is the commonest manifestation but it should be noted
that no true suppuration occurs.

36
4 Hepatobiliary System

Fig.4.5 Hepatic hydatid cyst. A transverse section through this liver
shows a well circumscribed loculated fibrous cyst. Hydatid d isease
is due to infestation by the tapeworm Echinococcus granulosus. and
is seen most often in sheep-farming communities . Spread to the liver
occurs via the portal system from the duodenum and affecls at least
50% of cases. Such cysts are usually solitary, are found most often in
the right lobe and contain many daughter cysts with brood capsules
and scolices. The case here appears to be 'burnt-out'.
Fig.4.7 Hepatic Zahn infarct. In this close-up view, an approx­
imately wedge-shaped area of subcapsular parenchyma shows a
congested pseudo-infarct with slight concavity of the overlying
capsule. This is the typicat appearance which results from throm­
bosis of a portal vein radicle, usually as a consequence of a small
embolus or compression by tumour. The hepatic arterial supply
prevents true infarction in such cases, but parenchymal atrophy and
sinusoidal congestion occur .

Fig.4.6 Passive hepatic venous congestion. The cut surface of the
liver has a variegated appearance, reminiscent of a nutmeg , with
small multi focal areas of congestion surrounded by a rim of pale
tissue. This appearance is the result of chronic congestive cardiac
failure with centrilobular venous congestion and atrophy, or
occasionally fatty change, of the adjacent parenchyma. In some
cases there may be associated fibrosis, but the development of true
cirrhosis is an extremely rare complication .
Fig.4.8 Portal vein thrombosis. A large branch of the portal vein is
totally occluded by thrombus. Note that the liver parenchyma shows
florid macronodular cirrhosis. Portal vein thrombosis is most often
associated with either local venous obstruction by a neoplasm,
intra-abdominal sepsis or recent abdominal surgery , While passive
splenic congestion commonly ensues, true hepatic infarction does
not occur unless the blood supply from the hepatic artery is also
compromised.
Fig.4.9 Budd-Chiari syndrome. The liver pur I '11, I,v' "
an exaggerated 'nutmeg' pattern (see Fig A ,(;) .1 1111 >,'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

37

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
, ,
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
4 Hepatobiliary System
[ CAUSES OF HEPATIC FATTY CHANGE
Alcohol abuse
Starvation/malnutrition
Diabetes mellitus
Glycogen storage diseases
Galactosaemia
acute idiopathic fatty change
Pregnancy
fatty change with hyperemesis
Severe systemic infection
Pathological obesity 1
Cystic fibrosis
Drugs, especially tetracycline
Flg.4.9 Budd-Chiarl syndrome. The liver parenchyma (top) shows Chemical toxins, such as carbon tetrachloride
0111 <)xaggera ted 'nutmeg' pattern (see Fig.4.6) and several tributaries
I1ltllu hepatic vein are occlu ded by throm bus. A mass of tumour
(11I)1I 0m) occupies the lumen of the in ferio r vena cava. This was a
I "III li lly leiom yosarcoma. Thi s rare syndrome is due to throm bosis of Reye's syndrome
II,,· I'l'Inc ipal hepat ic ve ins or inferior ve na cava, and may be due to
' " " lill liliobilis, obstruction by tumour either primary (as in thi s case ),
. ,' II , l/ Iti llry or adjacent , or associated with polycythaemia rubra ve ra . Fig.4.10 Causes of hepatic fatty change ,
38
 4 Hepatobiliary System

CAUSES OF CIRRHOSIS
-

Alcohol abuse
Post-viral (hepatitis B/non-A, non-B/o agent)
f
Biliary (primary or secondary)

Haemochromatosis
Fig.4.11 Hepatic fatty change. On the left, the liver parenchyma is Wilson's disease
diHusely yellowish and, on the right, a portion of a similar liver has
been stained with Scharlach R which stains the fat orange-red . Fatty Q1 - antitrypsin deficiency
change represents excessive cytoplasmic accumulation of neutral
lipid and triglyceride and, as a consequence of its important meta­
Indian childhood
bolic role, the liver is particularly liable to be aHected. Alcohol abuse
is the commonest cause in the Western World but, on a global scale, Fig.4.15 Macronodular cirrhosis. This close-lip Vi"
Metabolic storage disorders surface of the liver to be composed of large (>:lrlllll). I
malnutrition is probably the single most important factor.
varying size, each separated by dense fibrous 1,111" II'
Drugs (methyldopa, isoniazid.) macronodular pattern is a feature of post-viral (11' :lIlI lI v
- - -­ - --­ _ ._ - ­
cirrhosis and Wilson's disease. Note, however, 111111' " '
Fig.4.13 Causes of cirrhosis. 10-15% of cases remain idiopathic . livers show a mixed pattern, irrespective of aetiolnl IV

.- . : ....

_':' ?,:;(;,~,~ib{~~::~'
,,~...
f:;·
&,,, . . :~.., ,, ..
.,,<~:~~:,:;"'J"
__ ",..~......!__.~~1<·/~'<'.l-,:,t~. ; /,!!~" "'!' >~ .. "
A".·¥- . ';' . ,",.
/~~~ .. ~

.~..;:~~~l~'~-
~\~.~
l¥,'"~.:~'."'(:-''.~- . 'lt,;';~;i~l
"""!l\•. 4''''·';·'-··;':''

/'< '",,'h.';': .
.... ,~: ),_.~,:
.;;.:.;,;,~<"e;~:~L;,
. .I'••

'.11; •.. ~';;'.

.'..... . ,r.~."
' .-' ~""6,
. d'c·...
&i"A.;;...,•. .' ~,_:""~'" ',""", ',"-.~
'r',

Fig.4.12 Hepatic amyloid deposition. The liver parenchyma,
originally rather waxy in appearance, has been stained with Congo
Red to show extensive deposition of amyloid, particularly in the
mid-zone of the lobules. Hepatic amyloidosis is most often secondary
in type, being composed of serum amyloid A protein. Common'
causes of secondary amyloidosis include chronic infection or
chronic inflammatory disorders such as rheumatoid arthritis. While
the liver may become enlarged and firm , functional impairment is rare
despite a degree of parenchymal atrophy.
'A,' . ~
'-, ~ ..~!I;..... ~"'. , " ....'-"'"1!::':'''''
;... ~...,.. "",.
"""_.~iF.~.'~ ':<'i:1i.'':'P';;~ ..'>''.'·:'·~''':::-··'/·~~.1·-:>'\ :i:';':~:;~''''::'
<~ .'.:Ii.'"
~'. .•..' ".v,"- ,'k"""'"
,., .,a ' ,,",'
"~
.,.
'<' , •..".'.,. ,'_",'"
." . ..' .;,J:",,"'"'."''''',
~"'~li;::'~:'.!~" ,
Fig.4.14 Micronodular cirrhosis. The liver is small and the cut Flg.4.16 Biliary cirrhosis. The cut surface flf 1I1I'.ItV' i
surface shows multiple small, pale nodules which are rather uniform tnicronodular pattern, associated with markor l \1" "II I I •
in appearance. Micronodular cirrhosis (nodules < 3mm in diameter) Ililiary cirrhosis, which is uncommon, is most ull< IIII" III
is classically seen in alcohol abuse and haemochromatosis. World­ I his is an idiopathic condition which usually cilluch II ill
wide, alcohol is by far the most common cause of cirrhosis and the Inmales, is associated with anti-mitrochond l inl rllllil" I' J
incidence is increasing . Complications include portal hypertension, I ,c; autoimmune in origin. Very rarely, a simil w . 'PI " 1/ 11 ' I
splenomegaly, ascites, encephalopathy and clotting abnormalities. !loc n secondary to long-standing, extra-hAp"t,, ' "I '1.llt l
,tlllCoviscidosis.

39

.....

 4 Hepatobiliary System

Fig.4.17 Haemochromatosls.
OF CIRRHOSIS The pancreas (right) and, to a
lesser extent, the cut surface of
the liver show deep brown pig­
mentation, due largely to
excessive deposition of
(hepatitis SInon-A. non-B /o agent) haemosiderin. Idiopathic
haemochromatosis is an auto­
somal dominantly-inherited
condition, characterised by
defective iron metabolism, which
results in massive iron de­
position, particularly in the live r,
pancreas , heart , adrenals and
skin . Males are most often
affected and typica lly present in
middle age. Complications
Fig.4.15 Macronodular cirrhosis. This close-up view shows the cut include the development of
cirrhosis, hepatocellular
surface of the liver to be composed of large (>3mm), pale nodules of
varying size, each separated by dense fibrous bands. Typically, a carcinoma, diabetes mellitus,
cardiac failure and Addison's
macronodular pattern is a feature of post-viral (usually Hepatitis B)
cirrhosis and Wilson's disease. Note, however, that many cirrhotic disease.
livers show a mixed pattern, irrespective of aetiology.

cirrhosis. The liver is small and the cut
"I~ small. pale nodules which are rather uniform
lar cirrhosis (nodules < 3mm in diameter)
I abuse and haemochromatosis . World­
most common cause of cirrhosis and the
Compflcations include portal hypertension,
encephalopathy and clotting abnormalities.
Flg.4.16 Biliary cirrhosis. The cut surface of this liver shows a
IIliCronodular pattern, associated with marked green bile-staining.
I Iiliary cirrhosis, which is uncommon, is most often primary in type.
1111:; is an idiopathic condition which usually aHects middle-aged
1III110les, is associated with anti-mitrochondrial antibodies and may
I II) IllJtoimm une in origin. Very rarely, a similar appearance may be
'It .un secondary to long-standing, extra-hepatic obstruction or
"IIII .oviscidosis.
Fig.4.18 Hepatoma with micronodular cirrhosis. The live r is
diffusely nodular but, in addition, two irregular areas of pale , neo­
plastic tissue are apparent. The larger, central portion of tumour has
invaded the main hepatic vei n. Hepatoma, (primary hepatocellular
carcinoma) is not uncommon and is seen most often in Africa and the
Far East. A high proportion of'cases are associated with pre-existent
cirrhosis, particularly alcoholic, viral and that associated with
haemochromatosis. Other known causes include aflatoxins (from
mould y grain) and various alkaloids e.g . from herbal teas.

40
 4 Hepatobiliary System
Fig.4.19 Multinodular hepatoma. The liver parenchyma is diffusely
replaced by numerous greenish nodules of tumour. Between these
nodules , the uninvolved hepatic tissue shows a micronodular
cirrhosis . It is unknown whether this pattern of hepatocellular
carcinoma represents multifocality of origin or intrahepatic meta­
stasis. Occasionally hepatomas may display a diffuse micronodular
infiltrative appearance wh'lch may be difficult to distinguish macro­
scopically from cirrhosis . The aetiological factors and proqnosis of
hepatoma are identical , irrespective of the gross appearance.
Fig_4_20 Angiosarcoma of liver. The hepatic parenchyma is largely
replaced by a diffuse haemorrhagic neoplasm in which multiple small
vascular channels are visible. Hepatic angiosarcoma is rare and may
arise either in infants or, more usually, in adults. Adult cases may be
associated with previous exposure to the contrast medium , Thoro­
trast, or to vinyl chloride monomer in the plastics industry. In general
the prognosis is extremely poor.
41
......... -­
Fig_4.21 Hepatic metastases. Multiple irregular nodules of pale
secondary tumour are randomly distributed in the parenchyma of this
otherwise normal liver. Metastatic involvement of the liver is extremely
common and occurs most often in association with primary tumours
drained by the portat venous system , particularly gastro-intestinal
adenocarcinomas. The liver is also a very common site of secondary
spread from carcinomas of the bronchus and breast and malignant
melanoma. Metastases are very uncommon in cirrhotic tivers,
probably as a consequence of alterations in hepatic blood flow.
Fig.4.22 Hepatic involvement by lymphoma. Throughout the liver
parenchyma there is diffuse infiltration by innumerable, small,pale
deposits of lymphomatous tissue . This is the typical appearance of
disseminated lymphoma, the liver being involved in up to 50% of
cases of either the Hodgkin's or non-Hodgkin's type . Very rarely a
lymphoma may arise primarily in the liver .
Fig_4.23 Acute cholecystitis. This gallbladder 11. 1'.1 11
show intense congestion and ulceration of the $IIJI.I< " '
The serosal surface is also congested and the rUII1IIII1 "
purulent exudate are visible. Acute cholecystiti s I: . 1.111".
association with gallstones (see Fig.4 .2S), partic ul.lliv II
duct is obstructed. Occasional cases may occur I"IYI"
septicaemia Possible complications include pr:rle", ,Ie, II
itis.
Flg.4.24 Chronic cholecystitis. The gallbl;J1 Ie I, 'I II, V' i'
I)nel its wall is thickened and fibrotic . The mur,nt.cl i '.II,l.e.
co ngested and there are several small,ntrahrllllr ll ,l 1/,,11 ,
I'I.ppearances represent the effects of prol oril !elli . eI· " " ,I!
;1tIocks of acute cholecystitis. As such, thp. GI)e'XI'.I, 11 e' •I,
Il' extremely common .

metastases. Multiple irregular nodules of pale
are randomly distributed in the parenchyma of this
liver. Metastatic involvement of the liver is extremely
Irs most often in association with primary tumours
rtal venous system , particularly gastrO-intestinal
, The liver is also a very common site of secondary
",m."S of the bronchus and breast and malignant
are very uncommon in cirrhotic livers,
ence of alterations in hepatic blood flow .
involvement by lymphoma. Throughout the liver
! 'e; diffuse infiltration by innumerable, small,pale
I(Jl n910us tissue. This is the typical appearance of
IIp''()ma, the liver being involved in up to 50% of
t I, lctg kin's or non-Hodgkin 's type. Very rarely a
ml!' primarily in the liver .
Fig-4-23 Acute cholecystitis. This gallbladder has been opened to
show intense congestion and ulceration of the surface epithelium
The serosal surface is also congested and the remnants of a fibrino­
purulent exudate are visible. Acute cholecystitis is seen most often in
association with gallstones (see Fig.4 .25), particularly if the cystic
duct is obstructed . Occasional cases may occur in typhoid fever or
septicaemia . Possible complications include perforation and periton­
itis.
Fig.4.24 Chronic cholecystitis. The gallbladder is very shrunken
[lnd its wall is thickened and fibrotic. The mucosal surface is
~ongested and there are several small intraluminal gallstones. These
appearances represent the effects of prolonged , usually intermittent ,
:'Ittacks of acute cholecystitis As such, the coexistence of gallstones
it extremely common.
4 Hepatobiliary System
Fig.4.25 Cholelithiasis. This opened gallbladder contains two large
mixed gallstones . Note the marked thickening of the gallbladder wall
and the stigmata of acute inflammation of the mucosa. Gallstones are
extremel y common and may be of cholesterol, bile pigment or mixed
type Adults , particularly women, are most often affected . Alterations
in the bile content are probably the most important aetiological
factors . Complications include cholecystitis, biliary obstruction,
cholangitis, and stricture of the common bile duct.
Fig.4.26 Gallstones in the common bile duct. Multiple mixed
gallstones are visible within both the gallbladder (below) and the
grossly dilated cystic and common bile ducts . The passage of such
stones into the bile ducts may result in biliary colic or obstructive
jaundice, sometimes complicated by ascending infection. Damage
to the duct wall can lead to stricture formation or, occasionally,
utceration into the duodenum which may later be succeeded by
gallstone ileus.
42
4 Hepatobiliary System

Fig.4.27 Fig.4.29 Cholangiocarcinoma.

Cholesterolosis. Arising at the confluence of the
The mucosa of the right and left main hepatic ducts
gallbladder is rather is a pale, locally infiltrative
congested and is tumour. Each of the ducts is
studded with markedly dilated , Cholangio­
multiple small, carcinoma (primary bile duct
yellow flecks; th is carcinoma) is more commonlY
appearance is extrahepatic than intrahepatic in
known as the'straw­ origin This tumour typically
berry' gallbladder. arises in late adult life , in either
Cholesterolosis is a sex, and shows no association
very common con­ with cholelithiasis (ct . carcinoma
dition characterised of the gallbladder). In some
by deposition of lipid Orientals, biliary infestation with
beneath the the fluke Clonorchis sinensis is a
mucosa. It rarely predisposing factor.
causes symptoms Fig.4.31 Chronic pancreatitis. The pancreatic li:;,;rll' ',1"
apd is thought to be irregular scarring; the pancreatic duct (right) is dil;rl. ,II -III.
due to a localised pale calculus Chronic pancreatitis may take two" lilli' , 11"
abnormality of type due to repeated acute attacks and the de nUV( I I IlIl lIl
cholesterol Both are sign ificantly related to alcohol abuse althulIlI" 110
metabolism or coexistent duct obstruction or dysfunction . It is unclr ll il wi
absorption. formation predisposes to , or is a consequence of. (;llIlIl1lo
pancreatitis ,
Flg.4.30 Acute
pancreatitis.
Between the porta
hepatis (above) and
an adjacent loop of
small bowel there is
extensive necrosis
of mesenteric fat , the
greyish areas re­
presenting necrotic
pancreati c tissue.
Acute pancreatitis is
relatively common
and is most often
associated with
alcohol abuse or
biliary tract disease, Fig.4.32 Congenital pancreatic cyst. Projectinq fl. "" III
such as choleli­ surface of this otherwise normal pancreas is a small, 'H I li II
Fig.4.28 Carcinoma of gallbladder. This dilated gallbladder has thiasis. Middle-aged loculated cyst. Pancreatic cysts may be congenit al (. 111'11 1
been opened to show a fungating, partly papillary tumour arising in adults are typically with renal polycystic disease or cerebral angioma!":), , II '1"
the fundus. In the body are three small pigment stones'. Adeno­ affected and the pancreatic duct obstruction (retention cyst), neopla;,tll (I,
carcinoma of the gallbladder is uncommon and occurs most often in pathological features a cystadenoma or cystadenocarcinoma) or false ill "-11111' .
old age, predominantly in females . In the majority of cases there is a are attribut able to necrotic areas complicating acute pancreatitis · IJ';( Hldl II
long-standing history of preceding cholelithiasis and cholecystitis . extensive destruction
Invasion of the adjacent liver is an early feature, often resulting in by released
inoperability and a poor prognosis. pancreatic enzymes.

43
 4 Hepatobiliary System

Fig.4.33 Carcinoma of the

head of the pancreas. In the
concavity of this loop of
duodenum, the head of the
pancreas is enlarged and totally
replaced by a pale mass of
tumour , just above which the
grossly dilated (opened)
common bile duct is evident. Up
to 70% of exocrine pancreatic
adenocarcinomas arise in the
head of the gland; males are
most often affected , usually in
the 6th and 7th decades.
Hepatobiliary failure with
j"lUndice, due to bile duct ob·
struction , inoperability and the
Fig.4.31 Chronic pancreatitis. The pancreatic tissue shows marked complications of radical surgery
irregular scarring; the pancreatic duct (right) is dilated and contains a result in a very poor prognosis,
pale calculus. Chronic pancreatitis may take two forms: the relapsing although metastases may be
type due to repeated acute attacks and the de novo chronic type . absent or minimal.
Both are significantly related to alcohol abuse although there may be
coexistent duct obstruction or dysfunction. It is unclear whether stone
formation predisposes to, or is a consequence of . chronic
pancreatitis

Fig.4.32 Congenital pancreatic cyst. Projecting from the superior
surface of this otherwise normal pancreas is a small, smooth multi·
loculated cyst. Pancreatic cysts may be congenital (often assocjated
with renal polycystic disease or cerebral angiomas), acquired due to
pancreatic duct obstruction (retention cyst), neoplastic (being either
a cystadenoma or cystadenocarcinoma) or false in nature (walled·off
necrotic areas complicating acute pancreatitis - pseudocyst).
Fig.4.34 Malignant islet cell tumour. This pancreas contains
multiple, irregular pale masses of tumour, the largest of which is in the
tail of the gland. The majority of islet cell tumours are, in fact , benign,
the commonest being an adenoma of rl cells giving rise to hyper­
insulinism. Other adenomas may secrete glucagon (0. cells),
somatostatin (8 cells), gastrin (perhaps from 8 cells), pancreatic
polypeptide or vasoactive intestinal polypeptide . Islet cell tumours
may form part of the Type I Multiple Endocrine Neoplasia Syndrome.
Up to 60% of gastrin-secreting.tumours are malignant. In this case
the re has been extensive intrapancreatic spread .

44
5 Breast

Fig.5.1

Mammillary fistula.

This section through

areolar skin and
adjacent breast
tissue shows an in­
flamed fistulous
tract, communicat­
ing with a small
abscess cavity (left).
Such a fistula most
often occurs as a
complication of re­
current pyogenic
mastitis and may be
associated with duct
obstruction or duct
ectasia. Lactation is
a common predis­ Fig.5.3 Fibroadenoma. The specimen consists of a well­ Fig.5.5 Giant fibroadenoma (Phyllodes tumour). Wil l
posing factor . circumscribed, pale, lobulated tumour which has been 'shelled out'
tissue is a large, lobulated mass showing myxoirl. 11111 'I '"
from the adjacent breast tissue at operation. Fibroadenomas are cystic loci. These tumours are relatively uncomlllOII, III r
extremely common benign neoplasms, which may be multiple and nantly in the 5th and 6th decades and may attaill il l l lO lli l
typically arise between the menarche and the age of 30. They are
are probably unrelated to the more common fibrnf "I, ,'I, I
mobile and rubbery, whence the term 'breast mouse' , and are not
page 45), Despite their obsolete name, cystOS8 n, Olllu I'"
related to the development of breast cancer.
about 5% behave in a malignant fashion,

Fig.5.6 Duct papillomata. A transverse secti()11 /1 11111111 '

Fig.5.2 Fibrocystic disease. This breast tissue has been sectioned tissue shows a collection of cystic ally dilated dIICI· ., il l " I
Fig.5.4 Fibroadenoma. This is a rather larger example than Fig.5 .3
to show diffuse fibrosis and multiple cysts of variable size . Thi s the lumen is obstructed by soft, brownish, papill:IlY Ii '.' ilil
and demonstrates particularly well the characteristic lobulation that
condition is extremely common, is often bilateral and usually affects represent multiple duct papillomata which typi ca lly, 11 1'11
these tumours often show. The lobules are clearly demarcated by
females in the 4th and 5th decades. It is probably due to a disordered lactiferous duct. near the nipple, Duct papiliomAI!1.11" , I"
pale bands of fibrous tissue. It is worth noting that the historical
or imbalanced re sponse to endogenous sex hormones. Only in those usually solitary. arise in middle-aged women 81 11 I . 11 1' 1" "
division of fibroadenomas into intracanalicular and pericanalicular
cases showing marked epithelial hyperplasia (epitheliosis) is there benign lesions. They frequently give rise to a blo( HI ',/., 11 1
subtypes is probably spurious , since on histological grounds the two
thought to be an increased risk of breast carcinoma. charge. causing clinical confusion with carcinonili
patterns almost invariably coexist.

45
5 Bre~t
5 Brea.st

Fig.5.7 Intraduct carcinoma. On the cut surface of this breast

Fig.5.5 Giant fibroadenoma (Phyllodes tumour). Within the breast
tissue is a large, lobulated mass showing myxoid, haemorrhagic and
cystic foci. These tumours are relatively uncommon, occur predomi­
nantly in the 5th and 6th decades and may attain a great size . They
are probably unrelated to the more common fibroadenomas (see
page 45). Despite their obsolete name, cystosarcoma phyllodes, only
about 5% behave in a malignant fashion .
tissue multiple small ducts, obstructed by pale tumour, are visible.
The tumour appears to ooze out, rather like toothpaste - an
appearance also known as comedo carcinoma . lntraduct carcinoma
represents the pre-invasive stage of breast cancer of duct origin:
there is also an intralobular equivalent which may be bilateral in up to
40% of patients. Excision at this stage, in the absence of histological
invasion, is curative.
TOPOGRAPHICAL DISTRIBUTION
OF FEMALE BREAST CANCER

axillary tail
o areola and
nipple

upper lateral
upper medial
quadrant
quadrant

Fig.5.6 Duct papillomata. A transverse section through this breast lower lateral
10%
tissue shows a collection of cystically dilated ducts, in many of which quadrant

the lumen is obstructed by soft, brownish, papillary tissue. These

represent multiple duct papillomata which typically arise in a major
lactiferous duct, near the nipple . Duct papillomata are, however,
usually solitary, arise in middle-aged women and are uncommon
benign lesions. They frequently give rise to a blood-stained dis­
charge, causing clinical confusion with carcinoma. Fig.5.S Topographical distribution of female breast carcinoma.

46
5 Breast

Fig.5.9 Scirrhous adeno­

carcinoma. A cross· section
through the breast shows an
irregular, pale, stippled mass
beneath the retracted nipple.
Note the claw·like extensions of
tumour and fibrous tissue in the
adjacent fat. This is the
commonest macroscopical
variant of breast cancer, which
occurs in about 6% of females ,
usually in the 5th/6th decades,
and is by far the commonest
malignancy in women . The aetio·
logy is uncertain but lack of
previous lactation, geographical
factors and epitheliosis seem to
be important: 90% are of duct Fig.5.11 Ulcerated adenocarcinoma. Above the nipple, the skin of
origin and 10% lobular. Lymph this mastectomy specimen is raised and ulcerated by an underlying
node involvement is the most carcinoma. Local invasion of the skin by breast cancer is common Fig.5.13 Paget's disease of the nipple. Th e Ilil '1 111' P I i i i
important prognostic factor. 5· and may confer a worse prognosis. Cutaneous in vol vement, tocally or shows an eczematous rash which extends to invl1lvll 1111 1.
year·survival is only 30%, largely at a distant site, may also occur due to lymphatic or haematogenous Mammary Paget's disease represents infiltratioll 0 111 111 '11 ,
due to failure in early diagnosis. spread . underlying ductal adenocarcinoma, which is prlj!lOIlI III ,
(even if impalpable) . This is a feature of only abolll I 'L, (II
cancers. Skin biopsy is mandatory in all adult CA ~OI , ( ,1 ,11
nipple since mistaken treatment for dermatitis will d iliro v I I
surgery and may impair the prognosis.

Fig.5.10 Encephaloid adenocarcinoma. Much of this breast is
replaced by a large , fairly well circumscribed, lobulated tumour
showing focal cystic and haemorrhagic change. The cut surface.
resembles cerebral tissue . This macroscopical variant of breast
cancer accounts for about 8 % of cases and most often represents
the medullary or colloid histological subtypes. Both these types carry
a better than average prognosis.
Fig.5.12 Carcinoma with nipple retraction. The breast is severely
distorted by a large underlying carcinoma , with resulting ulceration
Fig.5.14 Peau d'orange. The skin of this bred::1 I', III' 'I II I
and local inflammation. Above the tumour , the nipple is totally
dimpled and pitted , bearing a superficial resemL,llI111 I ' 1' 1
retracted within the areola (arrowed). Recent onset of nipple retrac­
This appearance is seen in advanced breast Calli f" 11111 1
tion may be a very useful clinical sign in the diagnosis of breast
lymphoedema, resulting from lymphatic obstru ~: III )J I I 'v if I
cancer, particularly if the underlying tumour is small or impalpable.
tumour cells. Pitting occurs because mammary " hili \'. " ,II
innumerable sweat glands.

47
 '5 B n..I ~t

lYMPHATIC SPREAD OF BREAST CANCER

supracl avicular
nodes

axillary cfavicfe
nodes

mediastinal
~ p l e,Ihe skin of nodes
an underlying
'ff is common Fig.5,13 Paget's disease of the nipple. The nipple is eroded and
menl, locally or shows an eczematous rash which extends to involve the areola.
'3emal ogenous Mammary Pagel's disease represents infiltrat ion of the skin by an
underlying ductal adenocarcinoma, which is present in every case
(even if impalpable). This is a feature of only about 1 % of breast
cancers. Skin biopsy is mandatory in all adult cases of eczema of the
nipple since mistaken treatmenl for dermal itis wi ll delay definitive
surgery and may impair Ihe p rognosis.

internal
thoracic
chain

:'~st is severely
; ~~g ulceralion
;~ tolally Fig.5,14 Peau d'orange, The skin of this breasl is irregularly
~\iPple relrac­ dimpled and pitted, bearing a superficial resemblance to orange peel .
~ of breasl This appearance is seen in advanced breasl canc er and is due 10 local Fig.5,15 lymphatic spread of breast cancer. Lymph node
~I mpalpable .
lymphoedema, resulting from lymphatic obstruction by invasive metaslases are present at Ihe time of diagnosis in up to 60% of
tumour cells. Pitting occurs because mammary skin is lethered by cases. Local retrograde spread wi thin superficial lymphatics may
innumerable sweat glands . give rise 10 peau d'orange (see Fig.5 14) or carcinoma-en-cui rasse.

48
5 Breast 6 Lymphoreticular System

Fig.S.18 Male
breast carcinoma.
A section through
I CAUSES OF SPLENOMEGALY

this male breasl Congestive cardi;l(: 1,IIh'i

shows diffuse VASCULAR
replacement by pale CONGESTION Portal hypertenSioll
tumour with tether­
ing of the overlying 11111 I,"
nipple, (centre left) . Pyogenic
!'lClflih
The pectoral muscle
(right) is not INFECTIVE III . VII
involved . Male Non-pyogenic 111111 1111.
breast cancer is
(lIIal.l'
about 100 times less
common than its
female counterpart Abnormal RBC's
and tends to affect HAEMATOLOGICAL (haemolytic anaulIlI,I")
rather older patients .
Fig.S.16 Non-Hodgkin's lymphoma. The breast is largely replaced Histologically, the Extramedullary halllll!!1 .,
by a pale, focally haemorrhagic mass which is well circumscribed same types are seen
in both groups but Lipid storage disOi': ,"!'
and not dissimilar to an encephaloid carcinoma in appearance .
the prognosis in men METABOLIC
Primary Hodgkin's or non-Hodgkin's lymphoma of the breast is un · Glycogen storaga ( 11 ',11, 1
common but well recognised and is often succeeded by systemic is even worse,
dissemination. The breast may also be secondarily involved by a probably because Primary 11111 lin .
primary neoplasm arising in lymphoid tissue . extensive local
invasion occurs at lyllll'l ,
an earlier stage due NEOPLASTIC
Secondary lo"koll
to the small size of
the male breast. (;, lIdli

AmyloidosiS
MISCELLANEOUS
Sarcoidosis

SPLENOMEGALY CLASSIFIED BY WEIGHT

MILD < 500g Acute infection (li (; ' " 11 II

Chronic infectioll 0 1 , III '
MODERATE Haematological (;:\11 1,"'.
500-1000g
Amyloidosis
Fig.S.17 Gynaecomastia. The se are bilateral subcutaneous
mastectomy specimens from a young man: each shows ve ry marked Lymphoma, l~lIk : I<'"I1,'
hypertrophy of fibrofatty breast tissue . Gynaecomastia (enlargement
. of the male breast) may be physiological, as sometimes occurs at
MASSIVE
>1 000g
or myeloprolih~ lililV Il "i
puberty or in old age, or pathological. Causes of the latter include Storage disease:,
endoc rine disturbances, a va riety of drugs.(e.g. cimetidine).
Klinefelter's syndrome and testicular or adrenal tumours . This con­
dition is unrelated to the development of male breast cancer. Fig.6.1 Causes of splenomegaly.

49

6 Lymphoreticular System

Fig.6.2 Passive venous

I CAUSES OF SPLENOMEGALY congestion. This enlarged
spleen, weighing 740g, is very
firm (retaining its shape despite
VASCULAR Congestive cardiac failure being sliced) and is rather
CONGESTION rounded in appearance (being
Portal hypertension known as a 'cricket ball spleen').
Passive venous congestion is
bacterial
Pyogenic the commonest cause 01 splen­
septicaemia omegaly: there is usually only
INFECTIVE mild enlargement (most often as
TB, viral, a consequence of congestive
Non-pyogenic fungal, parasitic cardiac failure) but greater
(malaria) expansion (as here) may be
seen in chronic portal hyper­
Abnormal RBC's tension (e.g. due to hepatic
(haemolytic anaemias) cirrhosis).
HAEMATOLOG ICAl
Extramedullary haemopoiesis
lipid storage diseases
METABOLIC
Glycogen storage diseases
Primary haemangioma
lymphoma
NEOPLASTIC
Secondary leukaemia
carcinoma
Amyloidosis
MISCEllANEOUS
Sarcoidosis
~

I SPLENOMEGALY CLASSIFIED BY WEIGHT I Fig.6.3 Splenic infarction. Fig.6.4 Chronic perisplenitis.

Almost the entire spleen shows The splenic capsule is covered
MilD <500g Acute infection or congestion dull reddish infarction, only those in dense, irregular, hyalinised,
Chronic infection or congestion areas with a granular cut surface fibrous tissue. This appearance,
being spared. Thrombus is known as 'sugar-icing' spleen,
MODERATE
Haematological causes clearly visible occluding the may be seen in any case of long­
500-1000g splenic artery. Splenic infarction standing splenomegaly or
Amyloidosis may be embolic in origin, or due associated with chronic pleural
to local thrombosis (e.g. compli­ inflammation. Acute peris­
lymphoma, leukaemia cating atheroma, sickle cell plenitiS, characterised by a
MASSIVE or myeloproliferative disorder anaemia or polyarteritis) or due serosal fibrinous exudate , may
>1000g to torsion. Small infarcts are also occur in cases of septicaemia or
Storage diseases commonly seen in almost any overlying a splenic infarct.
case of moderate or massive
Fig.6.1 Causes of splenomegaly. splenomegaly.

50
6 Lymphore ticular System

Fig.6.S Miliary tuberculosis. Scattered throughou t the splenic

parenchyma are multiple, tiny, pale nodules resem bling millet seed
(hence the name). Miliary tubercu losis represents haematogenous Fig.6.9 Chronic lymphatic leukaemia. Thi s SI'I" .. " ,', "
spread of infec tion, most often from a primary focus in the lung (see Fig.6.7 Amyloidosis. The splenic cut surfac e has a diffuse pale, enlarged and rather paler than normal. SmootillYI I'I ,I III,i.
Chapter 2). Th is vascular dissemination results from encroachment waxy appearance . The spleen is more often involved in secondary. also visible at the hilum. Chronic lymphatic leuknll" " ,I"
and ulceration of the infective process through a vessel wall: this rather than primary, amyloidosis as may be seen in any long-standing common and affects mainly the elderly with a prud! II"Ii'. 1
leads to intrapulmonary spread, in addition to involvement of other infective or inflammatory con dition. Moderate splenomegaly There is usually a massive circulating lymphocyl<l: a: .. ,,"
organs such as the liver. bone marrow and kidneys. commonly results . lymphadenopathy Splenomegaly, as in chronic IlIyllll ", J
may be massive and the long-term prognosis is 11111 1111 1111
although in the elderly life expectancy may not 1)1: ,11 1. " I
Fig.6.8
Myelofibrosis. This
spleen is massively
enlarged, weighing
3,175g, and is
uniformly deep red
in colour . The
myeloproliferative
disorders and
chronic leukaemias
are the commonest
causes of massive
splenomegaly. In the
myeloproliferative
cases this enlarge­
ment is due to the
development of
extramedullary
haemopoiesi s (an
Fig.6.6 Sarcoidosis. Scattered throughout the splenic parenchyma integral part of the Fig.6.10 Hodgkin's disease. The white pulp i ~, 0)'1 hili'
are coarse pale nod ules, arising mainly in the white pulp . Sarcoidosis disease process, not replaced by innumerable , irregular, pale depo:;II:, 1111"11
is an idiopathic, granulomatous. chronic inflammatory disorder, whic h secondary to the classical appearance of so· called 'salami' :;pl""1I 1i 1
is commonest in young adults. LymphOid tissue throughout the body marrow destruction), disease, although almost any macroscopical chil li II Ii " I'
is predominantly aHected. al though palpable splenomegaly is seen while in the
Hodgkin 's lymphoma) may be seen . Splenic illvolv<'" ,, "
in only about 20% of cases . Typically. the lungs are also involved and leukaemias, there is
up to 50% of cases of Hodgkin's disease and is "" " .1 . ,1
patients often present with respiratory symptoms ; pulmonary inter­ extensive infiltration
at staging laparotomy.
stitial fibrosis is an occasional complica!ion . by neoplastic cells.

51

Fig.6.9 Chronic lymphatic leukaemia. This spleen is uniformly
enlarged and rather paler than normal. Smooth lymphadenopathy is
also visible at the hilum. Chronic lymphatic leukaemia is not un·
a
common and affects mainly the elderly with predominance in men .
There is usually a massive circulating lymphocytosis and generalised
lymphadenopathy. Splenomegaly, as in chronic myeloid leukaemia ,
may be massive and the long· term prognosis is generally poor,
although in the elderly life expectancy may not be affected.
Fig.6.l0 Hodgkin's disease. The white pulp is expanded and
replaced by innumerable, irregular, pale deposits of tumour . This is
the classical appearance of so·called 'salami' spleen in Hodgkin's
disease, although almost any macroscopical distribution (as in non·
Hodgkin's lymphoma) may be seen . Splenic involvement occurs in
up to 50% of cases of Hodgkin's disease and is most often detected
at staging laparotomy.
6 Lymphore ticular System
Fig.6.ll Non-Hodgkin's lymphoma. This greatly en larged spleen
is diffusely replaced by coarse nodular deposits of pale tumour .
Splenic involvement is very common in any non-Hodgkin's lymphoma
but particularly in the foll icular (Lukes and Collins) subtypes . Two
points are worth remembering in any patient with lymphoma (1) the
resultant splenomegaly may cause destruction of red cells, white
cells or plalelets (hypersplenism) of itself , and (2) splenomegaly may
be due to recu rrent or chronic coexistent infection.
Fig.6.l2 Burkitt's lymphoma. Both kidneys and the liver are
extensively replaced by mu ltiple large lymphomatous deposits .
Burkitt's lymphoma, a specific sub type of non-Hodgkin's lymphoma,
is typicall y a disease of children, most often seen in equatorial Africa.
It is caused by Epstein·Barr virus and endemic malaria acts as a
co·factor . It has a peculiar tendency to arise in the jaw, ovary, adrenal
or kidney.
52
6 Lympho retic ular System

Fig.6.13
Secondary
carcinoma. Within
the spleen are
multiple, pale, um­
bilicated meta­
slases. Splenic
metastases ,
surprisingly, are
relatively un­
common, being
macroscopically
evident in only about
5% of cases of
disseminated
cancer examined at
posl mortem. The
most frequently Fig.6.17 Non-Hodgkin's lymphoma. This IYII11.II '" III.
responsible primary Fig.6.15 Sarcoidosis. This mediastinal lymph node shows smooth, enlarged and has a nodular, and in places almonl l, ,II" ! I
sites are the lung, yellowish enlargement. Small amounts of anthracotic pigment are surface . Non-Hodgkin's lymphoma is more COI11I"l" , 11111
breast, cutaneous visible on the right. While sarcoidosis is the commonest cause of disease and is particularly prevalent in the elduilv III.'"
malignant bilateral pulmonary hilar lymphadenopathy, lymph nodes at any site preceding autoimmune disease or iatrogenic 1111111111 11.· ,I
melanoma and may be affected . Other organs that are commonly involved include some cases . There are several complex system: : "I l il t I
ovary. skin (lupus pernio) , liver, muscle, eyes or bone . classification, which are a source of confusion tl) ",, '"V,
or Rappaport are probably the most used ,

Fig.6.14 Tuberculous lymphadenopathy. These lymph nodes are
densely adherent to one another and their cut surfaces show diffuse,
irregular, caseous necrosis . Tuberculous infection in lymph nodes is
usually seen in the regional nodes which drain the primary site,of
infection, for example in the mediastinum, mesentery or neck.
Atypical Mycobacteria may produce a similar picture . Healing often
leads to dystrophic calcification, which may be an incidental radio­
logical finding .
Fig.6.16 Hodgkin 's disease. This group of lymph nodes each show
rubbery, smooth enlargement but have remained discrete (cl. tuber­
culosis) . The cut surface is uniform and yellowish-white . Hodgkin's
disease, a lymphoma of uncertain histogenesis, shows a predilection
for males and has a peak incidence in the 2nd/3rd and 6th/7th
decades . The Rye histological classification and Ann Arbor staging
system correlate well with prognosis. There is epidemiological
evidence (case-clustering) of an infective aetiology.
Fig.6.18 Secondary carcinoma. These Iympll l it" I" ~
closely apposed to one another, are diffusely ropll l( I"
expanded by pale , rather granular tumour. Metn:,I. ,II'
the commonest source of neoplastic lymphadel1( I\ldli i
particularly from carcinomas rather than sarCOII ll ll1, wi
to haematogenous spread . Lymph node meta:itm,"', I
worse prognosiS than if the tumour is confined tll II ', I II

53
 6 Lymphoreticular Sy~t (" 111

Fig.6.17 Non-Hodgkin's lymphoma. This lymph node is smoothly

enlarged and has a nodular, and in places almost follicular, cut Fig.6.19 Metastatic malignant melanoma. This lymph node
surface . Non-Hodgkin's lymphoma is more common than Hodgkin's contains a large, well circumscribed deposit of deeply-plgmented,
disease and is particularly prevalent in the elderly . There may be focally necroti c tumour. A rim of uninvolved nodal tissue is visible on
preceding autoimmune disease or iatrogenic immunosuppression in the right. Malignant melanoma is particularly prone to lymphatic
some cases . There are several comple x systems of histological invasion and lymph node involvement is a common finding at
classification , which are a source of confusion to many ; those of Kiel presentation .
or Rappaport are probably the most used .
Fig.6.20 Thymoma.
The thymus is
greatly enlarged and
is replaced by an
encapsulated,
multitobulated
pinkish mass . The
tumour lobules are
separated by bands
of fibrous tissue.
Thymomas are un­
common, 8.rise most
often in middle age
and are slow­
growing, radio­
sensitive tumours
with a generally
good prognosis. Up
to a third of cases
Fig.6.18 Secondary carcinoma. These lymph nodes, which are may be associated
closely apposed to one another, are diffusely replaced and with another
expanded by pale, rather granular tumour. Metastatic tumour is by far systemic illness, in
the commonest source of neoplastic lymphadenopathy, most particular
particularly from carcinomas rather than sarcomas , which tend more myaesthenia gravis
to haematogenous spread . Lymph node metastases usually imply a or systemic lupus
worse prognosis than if the tumour is confined to its primary site. erythematosus .

54
7 Endocrine System

Fig.7.1 Pituitary adenoma. Arising in the pituitary fossa is a well
circumscribed, rather haemorrhagic tumour. Small, non· functioning
pit uitary adenomas are not uncommon. Symptomatic neoplasms,
Wl'lich are less frequent, are most often composed 01 chromophobe
cells (60%) or acidophils (30%): basophil adenomas are very rare.
Such tumours may arise at any age and produce either local
pre ssure effects (e.g. bitemporal hemianopia) or endocrine effects,
Inost commonly due to the excessive secretion of prolactin or growth
I~ ormone. Pituitary adenomas may also be seen in Type I Multiple
endocrine Neoplasia Syndrome (Werner).
Fig.7.3 Thyroglossal cyst. This smooth, multilocular cyst contains
clear, yellowish fluid and measures about 4 cm in maximum
diameter. Such cysts represent vestigial remnants of the thyroglossal
duct, along which the thyroid migrates in utero from the base of the
tongue to its normal position. They may present at any age and are
usually found in the midline of the neck, adjacent to the hyoid bone.
CLASSIFICATION OF THYROID ENLARGEMENT
Graves' disease
Fig.7.S Multinodular goitre. The thyroid is distort l\l II IV III
nodules of varying size, some of which contain collr'll l Wi lli,
have undergone calcification and cystic chang e. I ri ll ' " " " I'
apparent, particularly in the left upper pole. Multlr1n<i11111l II
which are quite common, represent the end sta ge 111,1 ! 1111, I
non-toxic goitre: the latter may be endemic, due to II" II I" " i
or sporadic, due to environmental or genetic facto", 1'lIlilll
multinodular goitre are usually euthyroid but may su"".III, );
autonomous toxic nodules.

~ HYPERTHYROID
Multinodular gOitre
with toxic nodule
Fig.7.6 Colloid goll..
thyroid is ma ssiVl 'lv ," ,I,
multiple diffuse I\nd lllllil
Early Hashimoto's disease which are 'menly' 'I 1. 11 11
r Multinodular goitre while others aPI" '.11 , V',
colloid-l illed. WI,I"'II"
Endemic colloid gOitre appearance rn: Iy 11'1,, ,"
Adenoma early stages of :.'1 111111 1' ,1
toxic goitre due III ,,, IV '
Dyshormonogenesis
prior to the devul(){l" II JI '
EUTHYROID
primary volutional or c! eCjll""1. 01 1
Carcinoma changes), diffLlsl ' I' ,II, i,i
secondary are most oft en 01l ilol lIll
Lymphoma iodine deficiency (I hil i "
Fig.7.2 Craniopharyngioma. Arising in the region of the pituitary is the drinking watql ) II II'.
De Quervain's thyroiditis commonest in 11111111 rI .ri ll
a large, well circumscribed, tumour, with a variegated cut surface,
whic h is compressing the optic chiasma anteriorly and the third End-stage multinodular goitre areas (e.g. th8 1\11'" I II
ventricle superiorly. Craniopharyngiomas are traditionally held to Himalayas) alld W; II. " I,
HYPOTHYROID Chronic Hashimoto's disease a problem alon!) 1111' I " I>
nri se from Rathke's pouch and are usually suprasellar in location.
r hey are slow-growing lesions which present most often in childhood, Endemic cretinism this country (, 001I,v' II 1>1'
llsually due to pressure on the pituitary or optic tracts. They very
commonly undergo cystic change or calcification. Fig.7.4 Classification of thyroid enlargement.

55
 7 Endocrint: Syslt'11

IOssal cyst. This smooth, multilocular cyst contains

1IIIIIrI nnd measures about 4 cm in ma xim um
i I V'JIt1 represenl vestig ial remnanl s of lhe thyroglossal
I ' I1111 0 Ihyroid migrates in utero from the base of the
"." .1 position . They may presenl at any age and are
III " , •'lIdline of the neck. adjacenl to the hyoid bone .
ATION OF THYROID ENLARGEMENT
Graves' disease
Fig.7.S Multinodular goitre. The thyroid is distorted by multiple
nodules of varying size, some of which contain colloid while others
have undergone ca lcification and cys tic c hange . Fibrosi s is also
apparent, particularly in the left upper pole. Multinodular goitres,
wh ich are quite common, represent the end stage of a diHuse
non-toxic goitre the latter may be endemic, due to iodine deficiency,
or sporadic, due to environmental or genetic factors. Patients with
multinodular goitre are usually euthyroid but may sometimes develop
autonomous toxic nodules .
Fig.7.7 Graves' disease. The thyroid is diffusely and smoothly
enlarged; the cut surface ha s a 'beefy' appearance. Graves' disease
(diffuse toxic goitre) is commonest in young women and is an auto­
immune disease, the most important autoantibodies found being
those thai mimic the actic;1 01 TSH. Affected individuals are thyrotoxic
and may show associated ophthalmopathy, pretibial myxoedema
and enlargement of lymphoid tissues. Thi s condition is c losely relate d
to Hashimoto's disease and , if treated surgically, some pa tient s may
develop hypothyroidism.

Multinodular goitre Fig.7.6 Colloid goitre. The

ItY HOID
with toxic nodule thyroid is maSSively enlarged by
mulliple diffuse nodules, some of
Early Hashimoto's disease which are 'meaty' in appearance
Multinodular goitre while others appear cystic or
colloid -filled . While this
Endemic colloid goitre
appearance may represent the
Adenoma early stages of a diffuse non­
toxic goi tre due to any cause (i e
Dyshormonogenesis
U II ) prior to the development of in­
primary volu tional or degenerat ive
Carcinoma chang es), diffuse colloid goitres
secondary are most often endemic due to
Lymphoma iodine deficiency (particularly in
the drinking water). This is
De Quervain's thyroiditis commonest in mountainous Fig.7.S Hashimoto's disease. This thy roid is also diffusely and
areas (e.g. the Alps or smoothly enlarged but the cu t surface has a pale appearance
End-stage multinodular goitre
Himalayas) and was at one time (likened to normal pancreas) . Hashimoto's disease is another au to­
I Ifjln Chronic Hashimoto's disease a problem along the Pennines in immune disease which shows a very marked predilection for young
this country ('Derbyshire neck') adult females, and results in autoantibody-mediated destruction of
Endemic cretinism follicular cells. Patient s may also have coexistent perniciOUS
anaemia, Sjog ren' s syndrome or Addison's disease . At teast50%
11(''111,1011 of thyroid enlargement. eventually become hypothyroid .

56

7 Endocrine System

Fig.7.9 Primary myxoedema . Fig.7.11 Follicular

This thyroid , shown in situ with carcinoma. Within
the trachea, is markedly this lobe of the
shrunken , pale and fibrotic . thyroid , distorted by
Primary hypothyroidism in adults a multinodular
is usually due to chronic auto· goitre, a pale infil·
immune thyroidit is and probably trative neoplasm is
represent s end·stage visible in the lower
Hashimoto's disease . As such , pole . Follicul ar car­
middle·aged females, some· cinoma (25% of
times with ot her autoimmune thyroid malig ­
conditions, are pred ominantly nancies) is rather
affected. Other causes of clinical commone r in
hypolhyroidism include an end · females and tends to
stage goitre , previous thyroidec· occur in middle age
tomy or irradiation and , rarely , Occasionally, it can Fig.7.13 Medullary carcinoma. The cut suil:u :" "III,.
dyshormonogene sis. be distingu·,shed serial sec tions through the right lobe of thi s lilY" III I · ,I" '.
from a follicular reasonably circumscribed tumours of va rying : 01/ " MH. I
adenoma only by cinoma, which is derived from parafollicular c: ill ,I I " il!'
microscopic cells, accounts for about 10 % of thy roid cance r', 1111 10 ,
evidence of vascular (usually in middle age ) or familial (affecting yCII IIIII' 'I "" I
invasion . This often multifoca l), forming part of the Typ e II MI ilt'jlll ' I II I
tumour lend s to local Neoplasia Syndrome (Sipple) , 5-year·survivall:. il t I( 11 " •
infiltra tion and
vascular spread (in
contrast to the
lymphatic sp read of
papillary ca rcinoma)
with a 5-year­
surviva l of about
60% .

Fig.7.12 Anaplastic car­

cinoma. This large, pale and
focally haemorrhagic tumour has
replaced most of the thyroid and
is involving adjacent lymph
nodes and the tracheal wall by
direct extension, There is an
associated florid tracheitis , Ana­
plastic thyroid carcinoma, which
is relatively uncommon , is vi rt­
ually confined to the elderly , It is
Fig.7.10 Papillary carcinoma. Arising in the righ t lobe of an o th er· a rapidly progressive and lethal
tumour, which tends to very Fig.7.14 Lymphoma. Arising within and enl:II \l IIII III"
wise normallhyroid is a pale, irregular neoplasm: a lymph node
the thyroid is a diffuse pale neoplasm ShOWlllP 11111 1111."
infiltrated by metastatic tumour is adherent to the lower pole . Papillary extensive local invasion (otten
with tracheal stenosis) and is Primary lymph oma of the thyroid is uncommOl' ,II" I " . 1
carcinoma accounts for about 60% of malignant thyroid neoplasms .
elderly females, often with evidence of pre ux,,;I, '1111 I.,'
It arises most often in young adults and shows a predilection for usually fatal within a year of
diagnosis. disease . Such tumou rs are usually non-Hod~k u,", II " YI '
females . It is sometimes multicentric in origin and occasionally
any systemica lly dissem inated lymphoma m:ly "'V' .I v" I
presents with an adjacent lymph node metastasis (known previously as
secondarily . In general the prognosis is poor
the ·Iateral aberrant thyroid'). The overaIl5·year-s urvival is about 90% .

57
 7 Endoc rine Sy~ ... n l

Fig.7.13 Medullary carcinoma. The cut surface of the lelt lobe and
serial sections through the right lobe 01 this thyrOid show mu ltiple .
reasonably circumscribed tumours of varying size . Medullary car­
cinoma. which is derived Irom parafollicular calcitonin-secreting
cells. accounts lor about 10 % 01 th yroid cance rs . It may be sporad ic
(usually in middle age) or familial (affec ting younger individuals and
often multifocal). forming part of the Type II Multiple End ocrine
Neoplasia Syndrome (Sipple) 5-year-survival is about 50% .
Fig.7.15 Parathyroid hyperplasia_ Each of these four parathyroid
glands is marked ly. although rather unequally. enlarged; all have a
nodular appearance. Parath yroid hyperplasia is relatively
uncommon. being responsible lor only about 10% of cases of hyp er­
parathyroidism . It may be a primary idiopathic lesion , sometimes
forming part 01 a Multiple Endocrine Neoplasia Synd rome. or it may
be secondary to chronic renal failure. In long-standing cases of the
latter type, autonomous true adenomas sometimes develop .

Fig.7.16 Parathyroid
adenoma. Beneath the lower
pole of the right lobe of the
thyroid. viewed anteriorly, is a
soli tary. large. browni sh
parathyroid tumour. Parathyroid
adenomas are responsible for at
teast 75% of cases of hyper­
parathyroidism and are
commonest in middle age.
alfecting predominantly femates
They are usually solitary and
sometimes arise in long­
standing secondary hyper­
parathyroidism. Elevated levels
Fig_7_1 4 Lymphoma. Arising within and enlarging the left lobe of of parathormone, which more
the thyroid is a diffuse pale neoplasm showing multifocal necrosis . rarely are due to parathyroid
Primary lymphoma of the thyroid is uncommon and is typically seen in carcinoma or ectopic secretion
elderly females . often with evidence of pre-existent Hashimoto'S by a heterotopiC malignancy,
disease . Such tumours are usually non-Hodgkin's in type. although lead to nephrocalcinosis and
any systemically disseminated lymphoma may involve the thyroid osteitis fibrosa cystic a (see
secondarily . In general the prognosis is poor. Chapter 12) .

5t1
7 Endocrine System

Fig.7.17 Fig.7.20 Ad roll"" 1

Waterhouse­ nodular hYPllqlhull
Friderichsen cortex ClIIIII', li d II ,, ' •
syndrome. The which lIiI~; 110"" 1II \,,1
adrenal gland (top) , bisecled, I plll " 'II'. '"
the outline of which brigll t y( )IIClW 11111 1111 1
is just visible, has of which is VI'IIl,I, 1 .01 I
been totally Such no(llIl. " " VI" 'I
destroyed by idiopatllic ,,",1, '. I'" I
extensive haemor· more COil II II{)II 11 ... 11 I
rhage . Below, the adenoma 1111 ' I,"" II
feet of a young boy however,III,c'II I. II"
show the typical nodules ::Ir!' IVl lII ..II'.'
petechial rash, with funclionill!j ; 11 111, I" I ·
Fig.7.18 Primary Addison 's disease. This adrenal gland. seen in
cyanosis and gan· to any elld,)( I li lt· ,I' ll
cross-section. is markedly shrunken and thinned, measuring less
grene. Waterhouse ­ This app orll I 11 11 , ,"
than 2 cm in lenglh. Addi son's disease, or ch roni c adrenocortical
Friderich sen associal od Will, I " ' ii i
insufficiency, is most often due to idiopathic autoimmune destrUClion.
syndrome refers tension , all 1111' " 1,11,11
analagous to primary myxoedema. More Ihan 90% of adrenocortical
solely to the phenomCllC111
tissue has to be lost before the typical symptoms or electrolyte
occurrence of
disturbances result.
adrenal haemor­
rhage associated
with a severe
seplicaemic illness .
It is classically seen
in children or young
adults, most often
with meningococcal
septicaemia The
ad renal haemor­
rhage, which is
usually fatal , is
thought to result
from a combination
of endotoxin­
induced ce ll
damage, 'stress'
and a degree of
disseminated intra­
vascular
coagulation .

Fig.7.19 Addison's disease due to tuberculosis. The cortex and

medulla of this adrenal show ex tensive caseous nec rosis and the
surroundi ng capsule has undergone dystrophic calcification. Prior to
the recognition of autoimmune disease, TB was regarded as Ihe
commonesl identifiable cause of Addison's disease , although this
occurrence is now rare in the Western World . However, it is typica lly a
complication of pre-existent pulmonary infection . Other causes of
Addison's disease include amyloidosis. melastatic carc inoma.
haemochromatosis and histoplasmosis.
Fig.7.21 Adrenocortical adenoma. On Ihe- Iell , I I ' ,11""
circumscribed lumour projects from the COrlic; 11 ,11)( I,,, ,
adrenal. The same gland in cross-seclion (riglll) ',1" 'w'
brownish lesion with marked atrophy of the aCliftt , ' I II , , II I
solitary functioning adenomas. as opposed Iu c( li l li , II",
above) . are relatively uncommon but may re silli '" ( '" !I I
syndrome with consequent pituitary suppresslol' (, I ' . I,d,
hyperaldosteronism (Conn's syndrome) .

S9

 7 Endocrine ~y:-' l llli

Fig.7.20 Adrenocortical
nodular hyperplasia. The
cortex of this adrenal gland.
which has been partially
bisected , contains multiple
bright . yellow nodules, the largest
of which is visible at the apex.
Such nodular hyperplasia is
idiopathic and is probably far
more common than a solitary
adenoma . The true incidence is,
however, uncertain since these
nodules are typically non·
functioning and do not give rise
to any endocrine disturbance. Fig.7.22 Adrenocortical carcinoma. This adrenal gland ,
This appearance is sometimes measuring 20cm in maximum diameter, is massively enlarged by a
associated with benign hyper· multinodular tumour showing extensive cystic change and haemor­
tension. an unexplained rhage. Adrenocortical carcinoma is rare but may occur at any age.
phenomenon These tumours are typically non-functioning and therefore otten attain
a great size prior to presentation The presence of metastases is far
more reliable than the histological appearances in distinguishing
malignant lesions but, in general, these latter tend to rapid and
extensive haematogenous dissemination.

Fig.7.23 Meta­
static carcinoma.
This partially
bisected adrenal
gland is irregularly
distorted by
numerous nodules
of pale secondary
tumour, some of
which show necrosis
or haemorrhage,
While any malignant
tumour may metas­
tasise to the adrenal,
by far the
commonest to do so
is carcinoma of the
bronchus, followed
by breast carcinoma
Fig,7.21 Adrenocortical adenoma. On the left , a smooth, well and malignant
circumscribed tumour projects from the cortical surface of an melanoma . Such
adrenal. The same gland in cross-section (right) shows a solitary spread is usually
brownish lesion with marked atrophy of the adjacent cortex. Such bilateral and may
solitary functioning adenomas , as opposed to cortica l nodules (see occasionally give
above), are relatively uncommon but may result in Cushing's rise to Addison's
syndrome with consequent pituitary suppression (as here) or in disease (see Figs.
hyperaldosteronism (Conn's syndrome) 7.18&7 .19)

60
7 Endocrine System

Fig.7.26 Neuroblastoma.
Re placing the left adrenal (top
right) is a large, multinodular
haemorrh agic mass, Deposits of
metastati c tumour are vis ible in
this child's skull and femur.
Neuroblastomas arise from non­
ch romaffin cells in the adrenal
medulla (or sympathetic chain)
and are seen almost solely in
young c hildren. They are highly
malignant lesions, which
occasionall y secrete catech ola­
min es; modern modes of treat­
ment have led to an im p roved
survival rate. Interestingly,
lesions in the right adrenal
metastasise more ofte n to the
Fig.7.24 Adrenal lymphoma. Th is adrenal gland is totally repl aced liver, in contrast tothe case here.
Fig.8.1 Fetal renal lobulation. These are kit III! 'Y' , II , III 1
by an irregular mass of pale yel lowish -pi nk Jissue. Primary lymphoma
of the adrenal gland , whi ch is usually non-Hodgkin's in type, is infant note the marked corlicallobulation. Ti ll, ', " 1'1" " II , I
normal but is usually no longer apparent by (lI lt' Y",,, , d
extremely rare, Even secondary involvement by any histological type
undergoin g systemic dissemination is very uncommon, ever, lobula ti on, if only partial, sometimes PO",,,,I', 1111".
is important to recog nise that such a finding i:: ," II" I', III
im portance .

Fig.7.25 Phaeochromocytoma. The adrenal medulla is g rossly
expanded and repla ced by a tan-coloured, rather vasc ular tumour
showing foci of haemorrhage, The attenuated cortex is visible as a
yellow rim of tissue. Phaeochromocytomas arise from chromaffin
cel ts, typically in young adults, and ma y be associated wit h neuro­
fibromatosis or Type II Multiple Endocrine Neoplasia Synd rome,
While Ihe vast majority are benign, they secrete excessive amoun ts of
catecholam ines , giving rise to paroxysmal hypertension , They are not
uncommonly bilateral.
Fig.7.27 Chemodectoma . This specimen comprises a we ll
circumscribed , b rowni sh, vasc ular mass showing areas of haemor­
rhage. Chemodectom as are the commones t neuroendocrine
tu mours of the extra·adrenal paraganglionic system and may be
seen at any age They most often arise in th e ca roti d body and are
commo ner in populations living at high altitude (p robabl y as a
co nsequence of prolonged hypoxia) . Similar lesions arising in the
temporal bone or at the base o lthe skull are known as glomus
jugulare tumou rs. A varia b le number behave in a malignant fashion
Fig.8.2 Horseshoe kidney. The kidney s fH(! III""tI ,.111
poles and both renal hila lie anteriorly . Th e d 1111 III; , , " " "
whi ch joins Ihe two kidneys la yover the aorlilill VI V" HI 'I
oc curs in at least 1 in 250 individuals and resllll' , 1/"" , I II
embryological ascent of nephrogenic lissue: , 1(Jlluw", 1I"
Coexistent anomalies of th e ureters or renal VI",',' ,I' , .11,11
seen and may predispose to urinary infeclinll (il "I,',I""

61

Fig.7.26 Neuroblastoma.
Replacing the left adrenal (top
right) is a large. multinodular
haemorrhagic mass. Deposits of
metastatic tumour are visible in
this child's skull and femur .
Neuroblastomas arise from non­
chromaHin cells in the adrenal
medulla (or sympathetic chain)
and are seen almost solely in
young children. They are highly
malignant lesions, which
occasionally secrete catechola­
mines; modern modes of treat­
ment have led to an improved
survival rate . Interestingly.
lesions in the right adrenal
metastasise more often to the
liver, in contrast to the case here .
111odoctoma. This specimen comprises a well
I I n.' 'w n l ~ h. vascular mass showing areas of haemor­
I", h Irn:,s are the commonest neuroendoCrine
! II.' .It/renal paraganglionic system and may be
" I I'I 'Y 11'10s1 often arise in the carotid body and are
Ii 'I (l 1 ~. IN)lIS living at high altitude (probably as a
OO;urs in at least 1 in 250 individuals and results from partial failure of
,11'" ,low led hypoxia) Similar lesions arising in the
enbryological ascent of nephrogenic tissue, followed by malrotation.
. 'I ." 11 11>base of the skull are known as glomus
Cr.existent anomalies of the ureters or renal vessels are often also
, ," 1\ v,,"nl')le number behave In a malignant fashion .
8 Urinary Syste m
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
Fi,.8.1 Fetal renal fobulation. These are kidneys from a stillborn
infwl : note the marked cortical lobulation . This appearance is enlirely
Fig.8.4 Adult
nOmal but is usually no longer apparent by one year of age How­
polycystic disease.
e~r, lobulation. if only partia l. sometimes persists into adult life and it
This kidney has
is rnportant to recognise that such a finding is of no pathological
been bisected
iiTl)ortance.
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
Fi\.8.2 Horseshoe kidney. The kidneys are fused at their lower aneurysms may also
pees and bOlh renal hila lie anteriorly. The isthmus of renal tissue be found.
wt.c h joins the Iwo kidneys layover the aorta in vivo. Renal fusion
se,n and may predispose to urinary infection or obstruction.
62
8 Urinary System

Fig.a.S Medullary Fig.a.7 Simple renal cyst.

sponge kidney. The Arising from the cortex of the
cut surface of this lower pole of this kidney is a
kidney shows large, thin-walled cyst. Simple
multiple, smooth­ ,enal cysts are extremely
walled cysts which common, particularly with
are confined to the advancing age, and are thought
renal papillae. This to represent the local effect of
condition, thought to previous ischaemia or obs­
be due to develop­ truction. They are usually
mentally anomalous solitary, are typically located in
collecting ducts, the cortex and are most often
affects males more only about 1 cm in diameter, the
than females and is exam ple here being unusually
usually detected in large.
the 5th or 61h
decades. Calculi
often develop within
the cysts and, in Fig.a.g Renal tuberculosis. The parenchYI' "" d 'III
combination with kidney shows numerous confluent foci of CW,IICiIl' , ' ,, ' ,
recurrent urinary also marked calyceal invotvement with dllllt.liI"" , ' /'VII
infection, may lead called 'pyonephrosis' (despite the absellc(.! ,,11 111' 1) I
Fig.a.a Acute
to impaired renal culosis is often bilateral, is commonest in a dilli I fllIl!
pyelonephritis. This
function . hemisected kidney due to haematogenous spread from prima,y II d, ,' III "
shows intense con­ While remaining endemic in some part s 0 11111' Wi "I i I
gestion and in­ now uncommon in Caucasians.
Fig.a.6 Renal numerable , radially
dysplasia. Much, arranged yellow I III I
but not all , of this areas of suppuration t"I "~ I
kidney is rep laced and abscess forma­ IIIl1Jh
by coarse, irregular tion, especially in the I "I "il
cysts separated by medulla. Acute II l1 i. 1
broad bands of pyelonephritis is not I IJ . II

fibrous tissue. Renal uncommon and is 'I I , II!

dysplasia, which usually a con­ Will II.

represents failure of sequence of ';l ill II
nephrogenic dif­ ascending Gram­ 11 111 11 '
ferentiation, may negative infection. I h" I,
affect one or both Common predis­ d lllic
kidneys and may posing causes " . 1/ 111
involve either the include urinary obs­ ",11," ,
whole, or only part, truction, diabetes " ' "111
of the kidney. Often mellitus and preg­ I }O I II

other developmental nancy . In general, ,.1 \ll li

anomalies, usually females are most illl !Iii
obstructive in often affected , ' ,l lpl i
nature , are present probably as a con ­ \lYI,I,
elsewhere in the sequence of peri­ ' ,Int It
urinary tract. urethral contami ­ ( )I I II!

nation by faecal .111111.

I II ~ I ,I i
organisms.

63
 8 Urinary System

Fig,B,11 Renal
calculus, Lying
:sa within the renal
,mple pelvis is an irregular,
ovoid stone .
·1 Surprisingly , there is
hought no evidence of
ctof hydronephrosis.
s­ Calculi in the urinary
tract are common,
ted in are seen most
,ften frequently in the
1er, the kidney and usually
~ ually present in adult­
hood . Predisposing
causes include
urinary obstruction,
an elevated urinary
Fig,B,9 Renal tuberculosis, The parenchyma of this bisected concentration of the
kidney shows numerous confluent foci of caseous necrosis; there is relevant constituent
also marked calyceal involvement with dilatation, giving rise to so­ or altered urinary pH
te called 'pyonephrosis' (despite the absence of pus). Renal tuber­ facilitating crystal
i ~is_
This culosis is often bilateral, is commonest in adult males and is usually precipitation .
lidney due to haematogenous spread from primary infection elsewhere.
e con­ While remaining endemic in some parts of the world, this infection is
{l ­
now uncommon in Caucasians. Fig,B,12 Staghorn
pdially renal calculus. This
lOW Fig,B.10 Chronic stone has a
·)uration interstitial branched appea­
forma­ nephritis. The rance (resembling
lly in the capsular surface of the antlers of a stag)
Ite this kidney shows and formed an
s is not coarse , irregular accurate cast of the
ndis scarring and the pelvicalyceal system
whole organ is rather and upper ureter
shrunken. Chronic from which it was
ram­ interstitial nepl1ritis is removed. Staghorn
ction . the term used to calculi are typically
dis­ describe chron ic composed of
s parenchymal calcium phosphate
Iyobs­ inflammation and (the commonest
tes atrophy , which may constituent of renal
be a consequence stones) but may also
of various conditions be made up of
including chronic 'triple' phosphate or
suppurative cystine . Compli­
con­ pyelonephritis , long­ cations of urinary
peri­ standing ischaemia lithiasis include obs­
mi ­ or obstruction and truction, infection
I(.al analgesic and haematuria.
nephropathy.

I
64
8 Urinary System

rllI .1I I

trmll,.,II.
rolll' ,II",
1, "I,,, ,y I
' il I'll !I Ii

.tl lll tilll

'fI'lIp f" ,
( :1Ht 11111

n 11 ~ r Idll

l! ~ I II It I. (

:., ~VI II dI

(lVlllt Vi

'1/,11111 11 1
<-.1'1 1I . 1I .l i

,I' ,y lllill

lli 'V' 01 1'I ii

",11 " ' 1 11\

Fig.8.l5 Renal vein thrombosis. The entire kidney is pale and the fll ll'11 Iii
main renal vein is completely occluded by organised thrombus. .,Y' rill ~ 111
1
While renal vein thrombosis may be acute in neonates (giving rise to III!JllfJliJ

red infarction), in older individuals the onset is usually gradual , I~I \t I tl Ui I

resulting in oedema and tubular atrophy. In the latter group, throm· ,III, 'II , II I
I
Fig.8.l3 Renal infarct. Much of the renat cortex shows marked bosis is usually secondary to chronic glomerulonephritis or
(<11" ' I"

pallor, allhough the lower pole is spared. The margins of the infarct amyloidosis and the outcome is most otten fatal. IIIIt II l lth
l
are hyperaemic. This is an unusually large renal infarct, small wedge·
shaped lesions being more common. Infarc tion of the kidney is nearly
('': 111111 I" n

Fig.8.l6 Acute (..(11111 111

always due to arterial occlusion by embolism or thrombosis. Emboli transplant qh ilili Ul J

I
are usually cardiac in origin and, if derived from the vegetations of rejection . The renal .11 14 I hili ;
bacterial endocarditis, may give rise 10 septic infarcts with abscess cortex is pale,
formation . swollen and shows
small petechial
Fig.8.l4 Renal corticaf haemorrhages. The
necrosis. The entire renal cortex medulla is very '.11I11f11 " 1
is pale and necrotic, while the intensely congested. 1 .. 11 11,1 1110
corticomedullary junction is This is a classical ' .II1,W' . 11I
congested . Renal cortical example of acute :,1 ,""" (1
necrosis is usually a conse­ rejection which ::IIVt " , !I

quence of disseminated intra­ usually occurs within I ,y',I' . II,

vascular coagulation , as may a year of transplan· ~ 'I'dl l! 'I f

occur in antepartum placental tation and is most

I'VI " lI l"1
haemorrhage, septicaemic often due to the
1. 1111" IV "
illnesses or severe trauma. development of ,1I1(1 · 1i" 1
Acute rena l failure rapidly super­ recipient anti-graft I~ ,I 11 . 11 Htl
venes and the prognosis is antibodies . Rejec­ 11 1" 1' I I

generally poor Multifocal tion may also be If ,Ill Y 111 11

cortical necrosis may also be hyperacute, due to II q 10 11 1111
i
seen in the haemolytic·uraemlc pre-existent sensiti­ ,·1

syndrome. sat ion to donor lli 'vl· le" i

antigens, or chronic
(see Fig.B.17).

65


Fig .8.16 Acute
transplant
rejection. The renal
cortex is pale,
swollen and shows
small petechial
haemorrhages. The
medulla is ve ry
intensely congested .
This is a c lassical
example of acute
rejection which
usually occurs within
a yea r o f transplan­
tation and is most
often due to the
development of
recipient anti-graft
antibodies. Rejec­
tion may also be
hyperacute , due to
pre-existent sensiti­
sat ion to donor
antigens, or chronic
(see Fig.B.17).
8 Urinary Sy~l ..: !ll
Fig.8.17 Chronic
transplant
rejection. This
kidney shows a non­
specific, congested
and rather mottled
appearance
Chronic rejection of
a renal transplant
tends to occur
several months, or
even years, after
grafting and is often
characterised by the
asymptomatic
development of
either hypertension
or the nephrotic
syndrome. It is
thought to be due to
chronic low-grade Fig.8.19 Acute proliferative glomerulonephritis_ Thi s bisected
arterial damage kidney is rather swollen and there are petechial haemorrhages in the
(due to deposition of cortex Acute proliferative glomerulonephritis is fairly uncommon,
microthrombi), occurs predominantly in children and usually follow s a group A
combined with streptococcal upper respiratory infection. It is thought to be due to
complex- mediated deposition of circulating immune complexes and often gives rise to
glomerulonephritiS the nephrotic syndrome. In the majorit y of cases spontaneous
and tubular atrophy. recovery occurs.
Fig.8.18 Essential Fig.8.20 Mem­
hypertension. This branous
kidney is slightly glomerulo­
shrunken and the nephritis. This
capsular surface kidney has been
shows fine granular sectioned to show
sca rring . along with extreme cortical
several small si mple pallor, oedema and
cysts . Renal blurring of the
chang es in benign corticomedullary
hypertension are junction . Mem­
largely microscopic bra nous glomerulo­
and are principall y nephritis is an idio­
isc haemic in nature. pathiC cond ition,
There is usually little due to the deposi­
if any impairment of tion of circulating
renal function but up immune comptexes.
to 5% of patients which typicall y
devel op malignant presents in adult­
hypertension with hOOd . Up to 70% of
subsequent renal patients develop
failure. chronic renal failure .
66
8 Urinary System

- - - -- - - - - -- -

CAUSES OF NEPHROTIC SYNDROME

minimal
change

membranous

Glomerulo­ membrano­
nephritis proliferative
PRIMARY
RENAL focal
DISEASE segmental
glomerulo­ Fig.8.24 Renal papillary necrosis. In both "l l ir ,I'Y" III '
sclerosis papillae show greyish necrosis; on the right. :;( >1 111' , dil l'
have sloughed off. Renal papillary necrosis n!(J: ,1 "II, '" ''
Fig.8.22 Chronic glomerulonephritis. Thi s kidney is shrunken and complication of diabetes mellitus , analge SIC CIIIII' .I ' lill I
Alport's shows severe granular scarring of the cort ical surface. Chronic anaemia or urinary obstruc tio n with sup erackl ('( I >I II" , II,
Congenital glomerulonephritis is the non-specific end-stage form of many
va scular damage is thought to be respon Slblt' II, I'" ,. Ii I
syndrome primary glomerular diseases. However, in a proportion of cases , the colic or oliguria may result.
prima ry initi ating episode has passed unnoticed. Chronic renal
Renal vein thrombosis failure always develops and , without dialysis or transpl antation, death
is invariable .

Diabetes mellitus Fig.8.23 Chronic I' , I II I I f ~'~ I

glomerulonephritis wll l ll l hil
Amyloidosis with secondary f ili i" I I
cystic change. In II IPdl lll, i
addition to being 11, 11111 I 'Y
Systemic lupus erythematosus markedly shrunken
Ilyil " ''',
and scarred, the 11 " 11111' I,
renal parenchyma
Drugs penicillamine III Illd l 'II t

SECONDARY contains innumer­ I . III' ,l t' ,

RENAL able small cysts.

hepatitis B This app earance is
DISEASE now well recogn ised
Infections
in patients who have 111 1111 1111
malaria been maintained on II i 'tI ' 11111
I
long-term dialysis for 11, '1, ,, I
chronic renal failure .
lymphoma 11' '.f Il I .l ji
It is thought to be a 11 11 ' ; " II
Malignancy secondary Itlll -, I , It
bronchial phenomenon,
carcinoma perhaps related to
renal tubular
obstruction .
11111 \.IiI I"
,,1,'11 111 j
Fig.8.21 Causes of nephrotic syndrome. 1" 1.11 ,, II

67
 8 Urinary System

Fig.8.26 Renal amyloidosis.

The renal parenchyma shows
waxy pallor with blurring of the
cortico medull ary junc tion The
ki d ney is more often involved in
secondary than primary or
myeloma-associated
amyloidosis . Amyloid is a
fibrillary protein. arranged in 13­
pleated sheets, which is derived
from serum amyl oid A protein in
secondary cases and from
immunog lobulin light chain s in
the primary or mye loma­
associated group. Renal
involvement is bilateral and
usually result s in proteinuria and
Fig.8.24 Renal papillary necrosis. In both kidneys the renal chron ic renal failure.
papillae show greyish necros is; on the right . some of th e papillae
have sloughed off Renal papillary necrosis most often occurs as a
mlc glomerulonephritis. This kidney is shrunken and complica tion of diabetes mellitus , analgesic abuse. sickle cell
If .1l1ular scarring of th e co rtical surface. Chronic anaemia or urinary obstruction with superadde d infec tion. Micro­
11,11', IS the non-specific end-stage form of many vas cula r damage is thought to be responsible in most cases ; renal
jlll.1I diseases . However. in a proportion of cases. the Fig.8.27 Renal
colic or oliguria may result. cortical carcinoma.
11 1 "pisode has passed unnoticed . Chronic renal
Ilw(J lops and. without dialysis or transplantation, deat h Arising in the upper
Fig.8.25 Hydro­ pole of this kidne y is
nephrosis. The a large, lobulated
pelvicalyceal system mass; the cut sur­
Fig.8.23 Chronic is grossly dilated . face has a typically
glomerulonephritis with marked atrophy variegated appea­
with secondary of the cortex and rance. being
cystic change. In medulla. There is yellowish wi th foci of
addition to being florid pyelitis. haemorrhage and
markedl y shrunken Hydronephrosis nec rosis . Renal
and scarred, the result s from distal cortical ca rci noma
renal parenchyma urinary obstruction. (clear cell car­
contains innumer­ causes of which cinoma , hype r­
able small cysts. inc lude pro static nephroma, Grawitz
Thi s appearance is enlargement. pelvic tumour) arises most
now well recognised or ureteric tumours , often in the 6th and
in patients who have ure teric calcu li . 7th decades. affects
been maintained on neuromusc ular predominantly me n
long-term dial ysis for defects and retro­ and is deri ved from
chronic renal failure . peritoneal fibrosis. tubular epilhelium .
It is th ough t to be a Thi s condi tion IS Spread is largely
second ary often complicated haematogenous,
phenomenon, by urin ary infection including direct
perhaps related to but renal function is exten sion within the
renal tubular impaired only if the renal vein. 5-year­
obstruction. obstruction is surviva l is abou t
bilateral. 40 % .

68
8 Urinary System

Fig.8.28 Pelvic
transitional cell
carcinoma (TCC).
Above, a small
papillary tumour is
seen arising in the
renal pelvis; below,
a much larger, more
solid tumour has
filled the renal pelvis
and caused
secondary hydro­
nephrosis. TCC of
the renal pelvis is not
uncommon, arises pi lII'I 1111
most often in the 6th jill ' 11,,11
and 7th decades 1111 1>1 11" ,
and may be l,yllll)I" '1
associated with II I1 ,V I ,, "
similar lesions in the 11i 11
1'1I '"
bladder or ureter. !l UI,.! ·!.1
Workers in the ani­ Fig.8.29 Nephroblastoma. This kidney is largely replaced by a 11/111111 " '1
line dye and rubber large, well circumscribed tumour. The cut surface is pale with cystic, Vllklpll l!
industries, along haemorrhagic and myxoid foci. Nephroblastoma (Wi 1m's tumour) is til IrM 1111 1
with cigarette one of the commonest malignancies in infancy, affects predominantly
smokers, are at males and almost invariably presents by the age of 7 years It may
increased risk. occasionally be bilateral or associated with corporal hemihyper­
Fig.8.32 Urourlll
OveraI15-year­ trophy or aniridia. With modern multimodal therapy, the prognosis is
Projectinq 11<," ,11" , ' I
survival is about extremely good.
face of the 111 1,1, 11 III'
40%, solid tumours small, thi n,wlIlI,,>!. ,' V
carrying a worse Fig.8.30 Ureteric structures, I jllll"l1l1
prognosis than duplication. Ema­ repres en ls <l " ,'!1I11 "I
papillary. The nating from this renal standinq r:III IIII,1 " III
development of pelvis are two of whatever (.. ,111,/1 , "
multi focal neo­ separate ureters. entirely coru plln d ,It i
plasms along the The kidney is other­ cystic a in 1111' hllllil I,
length of the urinary wise normal. are dilated VIJII/lil il I,
tract is now Congenital which ar0. IOL lil"l 11 I '
regarded as a 'field­ anomalies of the growths UII Jl I,IIH,\i IJl
change' effect rather urinary tract are in chroni c iI1IIIU II " " 11 1
than metastatic common and may Occa sion;'llIy 111,'1111 11
'seeding' from a be associated with. may give 11,;" 1,, ,,, .,1.
proximal lesion. genital tract malfor­ obstructi oll
mations. Up to 3% of
the population may
have accessory
ureters, although the
bifurcation is usually
distal to the renal
pelvis.

69
 8 Urinary System

Fig.8.31 Pel vi­ Fig.8.33 Ureteric

ureteric junction transitional cell
obstruction. This carcinoma (TCC).
kidney shows Emanating from the
marked hydrone­ posterior wall of this
phrosis with gross thickened ureter is a
pelvic dilatation In rounded solid
vivo, two aberrant tumour (top); a
arteries (bottom cross-section
right) were com­ through a separate
pressing the lesion demonstrates
proximal end of the well the typical
ureter (bottom left). papillary nature of a
Obstruction at the Tee (bottom). The
pelvi-ureteric pathology of ureteric
junction is an Tee is much the
important cause of same as that in the
hydronephrosis and renal pelvis (see
may be due to idio­ Fig .8.28). Multifocal
pathic neuro­ Tee in the urinary
muscular incoordi ­ tract is common,
nation or a de­ and is thought to
velopmental represent a 'field­
anomaly of the renal change' effect. It is
vessels or ureter. said that the thin­
ness of the ureteric
Fig.8.32 Ureteritis cystica. wall predisposes to
Projecting from the urothelial sur­ early deep invasion
face of the ureter are multiple, of these tumours
small, thin-walled, cystic and hence to rapid
structures. Ureteritis cystica lymphatic spread.
represent s a result of long­ Generally, the
standing chronic inflammation, prognosis of these
of whatever cause, and is tumours is worse
entirely comparable to cystitis than that of their
cystica in the bladder. The cysts counterparts in the
are dilated von Brunn's nests, bladder.
which are localised down­
growths of urothelium often seen
in chronic inflammation.
Occasionally ureteritis cystica
may give rise to ureteric
obstruction.

70
8 Urinary System

Fig.8.34 Bladder
diverticulum. Projecting from
the fundus of the bladder is a
thin-walled diverticular sac
(above); the bladder itself is
trabeculated and markedly
congested. Bladder diverticula
are usually a consequence of
outflow tract obstruction and are
therefore commonest in elderly
males with prostatic hyper­
trophy. Because urine stagnates
within such diverticula,
secondary infection and stone
formation are common. The
development of carcinoma is
also a well recognised
complication . Fig.9.1 Corpus luteum. Within the ovary is d Willi I III "
nodule, measuring 1.5 cm in diameter. Th e 0\111 ,,1111, I' , I
in colour , while centrally it is composed of IOOb!.; II, ,,11 '11 I)
Fig.8.36 Vesical solid transitional cell carcinoma (TCC). This within which is a small cavity. The ovarian foil ic /t , 1' ,11 "I,
bladder has been opened to show gross urothelial distortion by a corpus luteum after ovulation, during the COIIf ~j ' "I wI II,
multi lobulated , predominantly solid, pale neoplasm . A papillary area rhage into the central cavity is invariable . The YI 'lIuw ''''
is visible just above the urethral orifice. Solid vesical TCC is less the luteinised granulosa and theca cell layers , WII Il .11,,, I
common than the papillary variant, although the two patterns may be secrete progesterone and, to a lesser extent, CJ( ",II I "1111
mi xed . Solid lesions, which are usually poorly differentiated histo­ paration for implantation . If fertilisation does 11(11 " I 'I II I
logically, carry a worse prognosis. luteum involutes.

Fig.8.37 Urethral
valve.. A flap of
redundant epith­
elium is visible in the
prostatic urethra
(marked with a
green probe); the
bladder is trabecu­
lated and congested
and there is marked
bilateral hydroureter
and hydronephrosis.
This congenital mal­
formation is virtually
Fig.8.35 Vesical papillary transitional cell carcinoma (TCC). confined to males
Projecting from the urothelial surface is a small papillary tumour and is one of the
composed of innumerable frond-like excrescences. In the urinary commonest causes
tract, the bladder is the commonest site of origin of TCC. In addition of urinary obs­ Fig.9.2 Corpora albicantia. This atrophic OVIllY 1""1 ' 11
to the aetiological factors mentioned in Fig.8.28, other predisposing truction in infancy. woman contains multiple small, yellowish-whito 111 " 1,,1, ,,
causes include schistosomiasis, bladder diverticula and exstrophy. Age at presentation albicantia represent corpora lutea which have 1111< 1' " 1I'"
Multifocality is common and the overall mortality is about 50%, many is dependent upon logical involution, being replaced largely by llynl" 1111111I,
deaths resulting from the complications of obstruction or infection the degree of such, they persist after the menopause when II II ' Y I " II , "
rather than from metastases . obstruction. conspicuous as a consequence of ovarian atr0pliV

71
 9 Female Reproductive System

Fig.9.1 Corpus luteum. Within the ovary is a well circumscribed
nodule, measuring 1.5 cm in diameter. The outer rim is bright yellow
in colour. while centrally it is composed of loose haemorrhagic tissue
within which is a small cavity . The ovarian foll icle transforms into a.
corpus luteum after ovulation , during the course of which haemor­
rhage into the central cavity is invariable. The yellow rim represents
the luteinised granulosa and theca cell layers, which at this stage
secrete progesterone and , to a lesser extent, oestrogen in pre ­
paration for implantation. If fertilisation does not occur, the corpus
luteum involutes.
Fig.9.3 Cystic follicles. This bisected ovary shows several small,
smooth-walled cystic spaces beneath the serosal surface . Such
cysts represent germinal follicles which have undergone partiaf
maturation, but then become atretic and cystic rather than rupturing .
They are a common finding in perimenopausal women, in whom
deteriorating ovarian function may be contributory. Occasionally they
are associated with continued oestrogen secretion and thus may
cause endometrial hyperplasia (see Fig.9 .30). Larger examples may
be described as follicular cysts.

Fig.S.37 Urethral
valve. A flap of
redundant epith­
elium is visible in the
prostatic urethra
(marked with a
green probe); the
bladder is trabecu­
lated and congested
and there is marked
bilateral hydroureter
and hydronephrosis .
This congenital mal­
formation is virtually
confined to males
and is one of the Fig.9.4 Tubo-ovarian abscess. The ovary and adherent fallopian
commonest causes tube (left) show extensive suppuration and haemorrhage. Such
of urinary obs­ Fig.9.2 Corpora albicantia. This atrophic ovary from an elderly pyogenic oophoritis is most often associated with acute salpingitis .
truction in infancy. woman contains multiple small, yellowish-white nodules. Corpora (see Fig.9.22) , but may occasionally result from haematogenous
Age at presentation albic anti a represent corpora lutea which have undergone physio­ spread of infection from elsewhere. An important cause of infective
is dependent upon logical involution, being replaced largely by hyalinised collagen : as oophoritis, although non-pyogenic, is mumps, which may impair
the degree of such, they persist after the menopause when they become unduly fertility. Susprisingly, tuberculous salpingitis only rarely spreads to
obstruction. conspicuous as a consequence of ovarian atrophy. involve the ovary .

72
9 Female Reproductive System

I CLASSIFICATION OF OVARIAN TUMOURS

Serous
cystadenoma/carcinoma

Mucinous
cystadenoma/carcinoma
EPITHELIAL
Endometrioid carcinoma

Mesonephroid
adenofibroma/carcinoma
Fig.9.S Ovarian endometriosis (,chocolate' cyst). The bulk of this
ovary is replaced by a haemorrhagic cystic cavity, filled with blood Brenner tumour
clot. Endometriosis (i.e. ectopic endometrial tissue outside the
uterus) is commonest in the ovary, broad ligament and pouch of Granulosa cell tumour
Douglas but may be seen almost anywhere. The aetiology is un·
certain, but the ectopic endometrium undergoes normal cyclical Thecoma
SEX-CORD
changes, including menstrual bleeding which results in the formation
of a 'chocolate' cyst. Interestingly, this condition is often cured by STROMAL
Hilar cell tumour
pregnancy,
(arrhenoblastoma) I

Teratoma

GERM CELL Dysgerminoma

Choriocarcinoma

Fibroma/sarcoma
STROMAL
Leiomyoma/sarcoma
MESENCHYME
Lipoma/sarcoma

UNCERTAIN
Yolk sac tumour
HISTOGENESIS

Fig.9.S Mucinous cystadenoma. Replacing III" 1111111 V

Fig.9.S Serous cystadenoma. The ovary is replaced by a thin­
walled , fairly large unilocular cyst, over the surface of which the
fallopian tube is stretched (bottom right). Serous cystadenomas are
the commonest benign ovarian neoplasms and are derived from
surface epithelium . They are typically smaller than their mucinous
counterparts, are bilateral in up to 30% of cases and often show
papillary excrescences on the internal surface.
Secondary carcinoma
large, multiloculated , smooth cyst (top) ; the LJ"~IIII" 11111< Ii
in the bottom right-hand corner for size compall','"1 I I, II,
MISCELLANEOUS primary of this cyst 's lining shows multiple , smaliloc ul o~: lill, ill WI!
Lymphoma Mucinous cystadenomas are common benin" Ii 11111 1111'·1, '
secondary ovarian surface epithelium. They arise most ()1I"'i III II "
decades , are bilateral in 10% of cases and ,llllY, 111 ,111 ' <II
Fig.9,7 Classification of ovarian tumours. size. Rupture or leakage may give rise to PSC!I I< I, JI ny " ""

73
 9 Female Reproductive System

Fig.9.9 Serous
IFICATION OF OVARIAN TUMOURS cystadeno­
carcinoma. The
ovary is replaced by
Serous a large unilocular
tumour (top), the
cystadenom a/carcinoma
lining of which
(middle) is
Mucinous composed of solid ,
papillary tumour
cystadenoma/carcinoma
showing haemor­
If IIAL rhage and focal
Endometrioid carcinoma necrosis. Below, in a
different example,
Mesonephroid tumour can be seen
extending through
adenofibroma/carcinoma the serosal surface.
Serous cystadeno­
Brenner tumour carcinoma is the
commonest primary
Granulosa cell tumour ovari an malignancy
and is bilateral in up
onD Thecoma to 40% of cases.
MI\L Women in the 6th
Hilar cell tumour and 7th decades are
(arrhenoblastoma) most often affected
and 5-year-survival
is only of the order of
Teratoma 25%. It is important
to note that a g roup
LL Dysgerminoma of serous and
mucinous tumou rs of
Choriocarcinoma
borderline malig­
nancy can be
Fibroma/sarcoma
defined histo­
~I\I
Leiomyoma/sarcoma logically; these carry
I ~CI IYM E a much better
Lipom a/sarcoma prognosis.

tlAIN
( ,I NESIS Yolk sac tumour

Secondary carcinoma Fig.9.a Mucinous cystadenoma. Replac ing the ovary is a ve ry

large , multiloculated, smooth cyst (top); th e uteri ne fundus is visible
I I I\NEOUS primary in the bottom right-hand corner for size comparison. Below, a portion
Lymphoma of this cyst 's lining shows multiple, smaillocuies filled with glairy fluid .
secondary Mucinous cystadenomas are common benign tumours, derived from
ovarian surface epithelium. They arise most often in the 3rd and 4th
decades, are bilateral in 10% of cases and may attain an enormous
'''cation of ovarian tumours. size. Rupl ure or leakage may give rise to pseudomyxoma peri tonei .

74
9 Female Reproductive System
Fig.9.10 Mucinous cystadenocarcinoma. The ovary is replaced
by a solid, haemorrhagic mass composed of multiple papillae and
locules, containing viscid fluid. Mucinous cystadenocarcinoma is
common, arising largely in the middle-aged or elderly and, like its
benign counterpart, may attain a great size. It is derived from ovarian
surface epithelium, as is its serous equivalent, but carries a better
prognosis, with a 5-year-survival rate of up to 50% .
Fig.9.11 Mesonephroid adenocarcinoma. Arising in the ovary is a
large, predominantly solid, yellowish neoplasm which shows focal
cystic change and necrosis. Mesonephroid (clear cell) adeno­
carcinoma is uncommon and is also derived from ovarian surface
epithelium (despite its mistaken nomenclature). The clinical features
are almost exactly the same as those of serous cystadenocarcinoma
(see Fig. 9.9).
75
Fig.9.12 Brenner tumour. The ovary is replaced by a well
circumscribed, irregular neoplasm, the cut surface of which is
yellowish-white with mucoid and fibrous foci. Brenner tumours are
derived from ovarian surface epithelium but show Wolffian differen­
tiation. They are comparatively uncommon but may arise at any age
and are sometimes bilateral. In the vast majority of cases these
tumours are benign.
Fig.9.13 Granulosa cell tumour. The ovary is replaced by a large,
well circumscribed, yellow tumour , within which are small foci of
cystic change. Granulosa cell tumours, which are sex-cord stromal in
origin, are relatively uncommon but arise most often in the peri­
menopasual years. They should be regarded as malignant (although
often low-grade) and they typically secrete excessi ve oestrogens,
leading to endometrial hyperplasia or carcinoma . Rare cases seen in
young girls usually give rise to precocious pseudopuberty .
Fig .9.14 Thecoma. The cut surface of th is small, 'v' III, II I
predominantly fibrous bul shows a typical area l)1V' .111 'WI
ation , representing accumulated lipid Theco mw, " " ' ' ,.
stromal tumours which most often arise periman!. '1"" ,... Iii
are almost invariabty benign , they commonly S (~' ; II ' I" " ,
oestrogens which may result in the developmc llt I ,1, "1, Ii
hyperplasia or carcinoma
Fig.9.15 Mature cystic teratoma. The ovary I" I' , I,. ·. , i I
show replacement by a mullicystic tumour . wltlllil wl, " I ,
materia l and matted hair are evident. Mature CY'.II' I. 'I, II ,
benign ovarian dermoid ) IS a common germ (:,·11 11111 1/ \1"
most often in the 2nd to 4th decades . It is r arll (,IILIlIV I ' II '
undergoing lorsion (see Fig .9.19). often bell HI II/ ·.III.1i II I
ovarii is an uncommon variant of the same 1111111)'" " '" '1"
dominantly of thyroid tissue. Malignanl ovamlll I· :1011. II " ,
uncommon (eI. testicular tera tomas)

renner tumour. The ovary is replaced by a well
,,,, I. Irreg ular neoplasm, the cut surface of which is
Ifltll with mucoid and fibrous foci. Brenner tumours are
" / Ivnrian surface epithelium but show Wolffian differen­
, !l U comparatively uncommon but may arise at any age
" ,tJ' nes bilateral. In the vast majority of cases these
I Hl nign.
nuloS8 cell tumour. The ovary is replaced by a large,
rII ,ull , yellow tumour, within which are small foci of
I IllInulosa cell tumours, which are sex-cord stromal in
IIIVl!ly uncommon but arise most often in the peri­
ylll II n n 1ey should be regarded as malignant (although
.10 ) I Hid they typically secrete excessive oestrogens,
Ii IJIIOlrJ AI11yperptasia or carcinoma. Rare cases seen in
I II Illy give rise to precocious pseudopuberty.
Fig.9.14 Thecoma. The cut surface of this small ovarian lumour is
predominantly fibrous but shows a Iypical area of ye llowish colour­
ation, representing accumulated lipid . Thecomas are sex-cord
stromal tumours which most often arise perimenopausatly . While they
are almost inva riably benign, they commonly secrete excessive
oestrogens which may result in the development of endometrial
hyperplasia or carcinoma .
Fig.9.15 Mature cystic teratoma. The ovary has been bisected to
show replacement by a mullicystic tumour, wilhin which sebaceous
material and matted hair are evident. Mature cystic teraloma (or
benign ovarian dermOid) is a common germ ceiliumour which arises
mosl often in the 2nd to 4th decades . It IS particularly prone to
undergoing lorslon (see Fig .9.19) , of len being pedunculaled . Struma
ovarii is an uncommon variant of the same tumour , composed pre­
dominantly of thyroid tissue . Malignant ovarian teralomas are very
uncommon (cf leslicular teratomas).
9 Female Reproductive SYMt:!l1
Fig.9.16 Dysgerminoma. Arising in this ovary is a large, uniform .
well circumscribed. whitish tumour. similar in appearance to a
potato . Dysgerminomas are comparatively uncommon germ cell
tumours which show no identifiable differentiation. They are
commonest between 10 and 30 years. are analogou s to the testicular
seminoma (see Fig.1 0.3) and should be regarded as malignant. They
are extremely radiosensitive and the prognosi s is excellent.
Fig.9.17 Fibroma. The ovary is replaced by a pale, lobulated
tumour, the cut surface of which is fibrous and whorled. Ovarian
fibromas are derived from stromal mesenChyme , usually arise in the
5th and 6th decades and are almost invariably benign . They may be
associated with the development of ascites or pleural effusions
(Meigs' syndrome), an entirely unexplained phenomenon .
76
9 Female Reproductive System

Fig.9.22 Acute salpingitis. Serial sections tilrDlllIlIlI lI I

tube show florid luminal suppuration and congcfllll ll' /'I, ,
salpingitis is most otten sexually transmitted : t~I U II ,, ;[.t I" .
organisms responsible are chlamydia, mycopla',IIld I " " ,
The gonococcus is now thought to be only an il lit II 1111 " II ",
Fig.9.18 Metastasis to the ovary. Both ovaries are diffusely predisposing factors include abortion, surgical "",1111111 11,
replaced by pale , rather nodular tumour, in this case of breast origin the use of an intra-uterine contraceptive device .
Note also the follicular cyst (right). The ovary is not infrequently the
site of metastasis, particutarly from primary carcinomas of th e endo­
metrium, gastro-intestinal tract and breast. Bilateral involvement is
common. The term Krukenberg tumour is reserved only for those
metastases , (most often of gastric origin) which histologically show a
signet-ring, mucus-secreting pattern .

Fig.9.20 Tubal ectopic-pregnancy. This fallopian tube is dilated

and the wall is thickened and haemorrhagic; within the lumen lies a
tiny 9 week fetus. Ectopic implantation of the fertilised ovum is
commonest in the fallopian tube, most otten in its ampullary portion.
About 1 in 100 pregnancies are ectopic; possible causes include
previous tubal inflammation or impaired tubal motility. Up to 60% of
tubal ectopics rupture, usually by about the 12th week.

Fig.9.21 Paratubal cyst. This is

a simple, smooth-walled , fluid­
filled cyst which was an inci­
dental finding in the broad
ligament. Such cysts are insig­
Fig.9_19 Torsion of ovarian cyst. This large ovarian cyst has nificant benign structures which
twisted about the fallopian tube and broad ligament (top) resulting in may be derived from the ovarian
tense, haemorrhagic engorgement. Ovarian torsion is not uncommon hilum or from vestiges of the
in association with an ovarian cyst or neoplasm, the size or weight of mesonephric (Wolffian), para­
which results in twisting of the broad ligament or mesovarium. mesonephric (Mullerian) or
Peritonitis or gangrene may rapidly develop. Gartner's ducts.
Fig.9.23 Chronic salpingitis. While the IUlno 11 1,11111' , I
is focally patent (lett), the remainder is distortoli t 'y " t,l l l
focally necrotic mas s. I n such cases, it is un(':Oll" II' "' " ,
infective organism but tubal damage such as till:, I' , h, I '
bilateral and may result in infertility. Macroscnl'il i llly , III
salpingitiS may look very similar.

77
 9 Female Reproductive System

Fig.9.22 Acute salpingitis. Serial sections through this fallopian

tube show florid luminal suppuration and congestion . Acute
salpingitis is most often sexually transmitted: the most frequent
organisms responsible are chlamydia, mycoplasma or anaerobes .
The gonococcus is now thought to be only an initiating factor. Other Fig.9.24 Pyosalpinx. Thi s fallopian tube is grossly dilated and
predisposing factors include abortion , surgical instrumentation and
distorted and the lumen contains yellowish , purulent debris . Note
the use of an intra-uterine contraceptive device.
also the simple paratubal cyst (left). This appearance is another
possible outcome of chronic salpingitis but may also be seen in very
severe acule infection. Bilateral involvement is again common .

•Iblli ectopic-pregnancy. This fallopian tube is dilated

I', 1I IIckened and haemorrhagic; within the lumen lies a
1111,. Ectopic implantation of the fertilised ovum is
111 1110 fallopian tube, most often in its ampullary portion.
'11 11'l ognancies are ectopic; possible causes include
II,,, lliammation or impaired tubal motility. Up to 60% of
II" )Iure , usually by about the 12th week.

Fig.9.21 Paratubal cyst. This is

a simple, smooth-walled , fluid­
filled cyst which was an inci­
dental finding in the broad
ligament. Such cysts are insig­
nificant benign structures which
Fig.9.23 Chronic salpingitis. While the lumen of this fallopian tube Fig.9.25 Hydrosalpinx. This fallopian tube is dilated and rather
may be derived from the ovarian
is focally patent (left), the remainder is distorted by a fibrotic and elongated and the lumen contains milky, clear fluid . Note the dense
hilum or from vestig es of the
focally necrotic mass. In such cases, it is uncommon to isolate the adhesions to paratubal structures. This appearance, which is seer:1 in
mesonephric (Wolffian), para­
infective organism but tubal damage such as this is frequently the ampullary portion of the tube, is most often due to long-standing,
mesonephric (Mullerian) or
bilateral and may result in infertility. Macroscopically, tuberculous low-grade infectio n but may also be associated with idiopathic pelvic
Gartner's ducts.
salpingitis may look very similar. inflammatory disease.

78
9 Female Reproductive System
Fig.9.26 Bicornuate uterus. This specimen shows two apparently
normal uterine cavities which converge on a single cervical ca nal.
This is a congeni tal malformation, representing partial failure 01 Ius ion
01 the Mullerian ducts . Up to 1 in 500 women have developmental
anomalies of varying severity in the genitaltraCl, which may give rise
to menstrual or obstetric problems.
Fig.9.27 Endometrial polyp
and Nabothian cysts. This
coronal section of the uterus
shows a polypoid lesion arising
Irom the endometrium: in
addition there are several
smoo th cystic cavities in the
endocervix. Endometrial polyps
are common, most often peri ­
menopausal, lesions which may
be multiple. Whether they
represent true benign neo­
plasms or a localised reaction to
oestrogen hypersensitivity is
uncertain. Nabothian cysts
represent cystic dilation of
endocervical glands and are of
no known signilicance .
79
Fig.9.28 Localised
adenomyosis, Thi s sagittal
section through a uterus shows a
well circumscribed, whorled
mass in the anterior wall, within
which there are haemorrhagic
and yellowish areas.
Adenomyosis is defined as the
presence of endometrium deep
in the myometrium and is , 1' .' .I)f hil i'
commonest in parous peri­ 'Y' .t " ' hi
menopausal women. It results 1 .,,' II II IIHI)
from downward extension of the I: . I II Itt II , ~
basal endometrium and either fU'> ,II II I PI
involves the uterus diffusely or is IIPI 1 ~ I tI r,
localised, as here , when it may .1I 1IIVIII.,I ,
be known as an 'adenomyoma'. 1I !j 11l 1,11I1 I
The aeti ology is possibly related II r • I ' .' j' ,~
to excessive oeslrogenic (I V,III:lli
stimulation . :.11111 11 .111
I t!' ,10 d, 'Il
;II YI'" ,II
1111" .• IIll d
II II' ""V'.,
. "U I«III Il .1
C, lI c 11 11 11 1
F,i g.9.31 Endollllll, l
carcinoma. AIII,I' II II,
endometrilill "" II" I ,
uterus is a 1;11'1' ' . 1" 11
locally neCl ol" '" ' I 'I '
Endometri;II I..1I 1"",,,
uncommon Hilt 1_" , II
often after 1111 ,,,,,,, 11 '1 '
Proven 3 !;S()( .10I11i ",, I
null iparity , 1I1t. " llId
all of whir.l< ;111'11""" 1
cool actors 01,' " , " '110 1
oestrogen ~~ llIlI lI loI lil li
year -survlvill 1.11"" "
of 70%, dul" ,,,01,,, II "
Fig.9.29 Uterine leiomyomata. The uterus on the lett shows several logica l (Jraclc ' d /lil "t ,
well circumscribed, whorled fibrous neoplasms w',thin the
myometrium; that on the right shows a single, pedunculated sub­
mucosal tumour of a similar nature which is distorting the endometrial
cavity. Uterine leiomyomata ('fibroids') are very common benign
tumours of smooth muscle which develop during the reproductive
yea rs, probably as a result of oestrogen sensitivity. Degenerative
changes, including calcification or infarction , are common.
 9 Female Reproductive System

Fig.9.28 Localised Fig.9.30 Endo­ Fig.9.32 Malignant

adenomyosis. This sagittal metrial hyper­ mixed Mullerian
section through a ulerus shows a plasia. Within the tumour. Ari sing in
well circumscribed, whorled body of the uterus. the uterine fundu s is
mass in the anterior wall, within the endometrial a large, polypoid,
which there are haemorrhagic lining shows haemorrhagic mass.
and yellowish areas. irregular, almost Extensive
Adenomyosis is defined as the polypoid thickening. myometrial invasion
presence of endometrium deep Endometrial hyper­ is apparent.
in the myometrium and is plasia , which is Malignant mixed
commonest in parous peri. associated with Mullerian tumours
menopausal women . II re sults cystic dilatation of are derived from
from downward extension of the endometrial glands, Mullerian
basal endometrium and either is due to unopposed mesenchyme and
invo lves the ulerus diffusely or is oestrogen stimula­ thus contain both
localised, as here, when il may tion as may occur in epithelial and
be known as an 'ad enomyoma'. anovulatory connective tissue
The aetiology is possibly related menstrual cyc les or elements. They arise
to excessive oestrogenic in association with most often in the
stimulation . ovarian sex-cord elderly and car ry a
stromal tumours. poor prognosis .
Histologically Mixed Mullerian
atypical var iants of tumours may some­
this condition may time s have only one
be associaled with malignant com­
the development of ponent , which is
endometrial adeno­ usually
carcinoma. mesenchymal ,
(adenosarcoma) or
Fig.9.31 Endometrial adeno­ be entirely benign
carcinoma. Arising from the (adenofibroma)
endometrium In the body of the
uterus is a large, polypoid . Fig.9.33 Uterine
focall y necrotic neoplasm . leiomyosarcoma. In the
Endometrial carcinoma is nol myometrium of the fundus and
uncommon and occurs most body is an irregular, pale
often after the menopause. neoplasm showing focal
Proven associations include haemorrhage and necrosis .
nulliparity. infertility and obesity, Serosal invasion is apparent
all of which are thought to be (top) . Leiomyosarcoma of the
co-factors of ex ces sive uterus is comparatively rare,
oestrogen stimulation. The 5­ usually occurs in the 5th and 6th
year-survival rate is of the order decades and may be associated
lerlne leiomyomata. The uterus on the left shows several of 70%, dependent upon histo­ with nulliparity . These tumours
I .li l II ,el. whorled fibrous neoplasms within the logical grade and staging. arise de novo and not from
II 111.11 1.) 11 Ihe right shows a single , pedunculated sub­ leiomyomas : the 5-year-survival
'" " " (,I ;) similar nature which is distorting the endometrial is about 30%.
'II' I', il(ilTlyomata ('fibroids') are very common benign
It il ,,,Iii muscle which develop during the reproductive
., Il y , I~' <l result of oestrogen sensitivity. Degenerative
, 1IIIIu I(J calcification or infarction, are common.

80
9 Female Reproductive System

Fig.9.38 Cervical squamous carcinoma. Ari si! I! I 1,, 11 11 Ii

Fig.9.34 Hydatidiform mole. This specimen consists of a mass of
grape-like hydropic villi which has been removed from the uterine
cavity. Hydatidiform mole arises in about 1 in 1,500 U.K. pregnancies
but is much commoner in the Far East. Such moles are derived from
abnormal trophoblastic proliferation and usually affect females at the
extremes of reproductive life. Up to 3% go on to develop chorio­
carcinoma and therefore careful follow-up by serum r3-HCG
estimations is mandatory.
Fig.9.36 Cervical 'erosion'. Around the external os, the cervical
epithelium appears reddish . This appearance is, in fact, physio­
logical and is not due to epithelial erosion at all. Rather, it is due to
eversion of endocervical mucosa, which occurs with elongation of the
endocervical canal during adolescence, and which then undergoes
squamous metaplasia.
ectocervi x is an irregular, fungating, pale neopIBn", ( "" .
the cervix is common and Increasing in incidenCll , wll,l!! Ii
most frequently in the 5th and 6th decades, yountJi If w',, ,, ,
infrequently affected. It is thought to arise in prO-OXIIII' \f11"
intra-epithelial neoplasia (dysplasia) over a peri'" I " I 1111,
Aetiologically, Herpes simplex type II and human 111 11"II, ii'
types 16 and 18 are thought to be important, witl'l ,)fllly ,II
coitus being the most critical co-factor. Overall !J yonl '"''
about 50%, dependent upon the degree of inva~ i,,, I

Fig.9.35 Choriocarcinoma. This uterus has been opened to show

diffuse replacement of the myometrium by an extensive haemor­
rhagic tumour. Choriocarcinoma is a malignant tumour of tropho­
blast, the incidence of which parallels that of hydatidiform mole, since
50% of cases are preceded by a mole. It may also arise following
spontaneous abortion or a normal pregnancy. Despite a tendency to
extensive vascular invasion, up to 90% of affected patients are cured
by chemotherapy in conjunction with careful follow-up using r3-HCG
estimations.
Fig.9.37 Endocervical polp. A close-up view of the endocervical
canal and vaginal vault shows a small, rather mucoid polyp in the
endocervical canal, surrounded by operative haemorrhage . Endo­
cervical polyps are extremely common, occurring most often in the
4th and 5th decades, and represent focal hyperplasia of the endo­
cervical epithelium Superimposed inflammation is common but
malignant change is excessively rare.

81
 9 Female Reproductive System

Fig.9.40 Vulval Bowen's

disease. This simple vulvectomy
specimen shows a raised, rather
nodular, reddish area around the
inferior margins of the introitus.
Vulval Bowen's disease (intra­
epithelial neoplasia) represents
carcinoma-in-situ and is not
uncommon, particularly with
increasing age. Aetiologically,
the viruses implicated in cervical
carcinoma are thought to be
important (see Fig.9 .38) .
Progression to invasive
carcinoma is not uncommon but
Fi~.9.38 Cervical squamous carcinoma. Arising from the occurs most often in the elderly
eDtocervi x is an irregular, fungating, pale neoplasm. Carcinoma of or immunosuppressed.
th~ cervix is common and Increasing in incidence; while it occurs
m()st frequently in the 5th and 6th decades, younger women are not
infrequently affected. It is thought to arise in pre-existent areas of
Fig.9.41 Vulval
intra-epithelial neoplasia (dysplasia) over a period of 10 to 20 years.
squamous
A~tiologically, Herpes simplex type II and human papillomavirus
carcinoma. The
tY10es 16 and 18 are thought to be important, with early age at first
labia majora of this
COitus being the most critical co-factor. OveraIl5-year-survival is
radical vulvectomy
about 50%, dependent upon the degree of invasion.
specimen are
diffusely infiltrated
Fig.9.39 Vaginal by a raised, nodular
squamous and focally
carcinoma. Arising ulce rated neoplasm .
in the posterior Vulval carcinoma
vaginal wall is a occurs most often in
raised, irregular the 7th and 8th
neoplasm. decades, usually in
Squamous cases with pre­
carcinoma of the existent intra­
vagina is a rare epithelial neoplasia
tumour of the or chronic inflam­
elderly, which is mation.OveraIl5­
probably aetio­ year-survival is
logically similar to about 70%. A rare,
cervical carcinoma. very well differen­
Vaginal adeno­ tiated warty variant, .
carcinoma is also known as verrucous
extremely carcinoma, only very
uncommon but is rarely metastasises
typically a tumour of and has a better
young girls, whose prognosis.
mothers were
treated with di·
ethylstilboestrol
during pregnancy.

82
10 Male Reproductive System

Fig.10.1 Testicular atrophy. A

co ronal section through Ihi s CLASSIFICATION OF TESTICULAR TUMOURS
tes li s shows Ihat it is much
smaller than normal. part ic ularly
whe n compared to the sp ermatic 1i11"lh ,
classical 38%
cord (abov e). We ll re cog nised wtll il I
ca uses of testicular at roph y Seminoma :1(111 11 11
include matdescenl. oestrogen , ~ III II \
the rapy , alcoholism, irradiation, spermatocytic 2%
!t " 41111
Klinelelter's syn drome and 11111 1 \ 1'
hormonal abnormalill es olthe 1 11' 1111 11
hypothalami c-pi tu itary-adrenal differentiated 1% 111 ' 111
axis. Such tes tes typ ica ll y show II IH III
markedly diminished or absent ,11 ,11 1"
sp ermatogenesis. GERM CELL intermediate 20% II "II'"
Teratoma . III ' d ~ Ii
, I~ ".1 I
undifferentiated 10% !l II IV
'1111 ', 1,
/1 '111011,
trophoblastic 1% , IY" I I'
1"1 ' I
: ~. II I Iii

Combined seminoma! teratoma 14% !' . ' " 11

'11", '.11
' ,1/ ' VI'
I! Ii F.I '
Yolk sac tumour 1%

Fig.10.5 0111.-"" ,
NON-GERM
Leydig cell tumour 2% teratoma.'W,lI iII ' II
CELL we ll circlllII'" III" ,
is multicystl' .11" I,
Sertoli cell tumour 1.5% yellowisl-I kl ' /.,111 " "
Differenti;ltl ', 1," '1,1
uncommOIl, ,II i I II
about 2% "I I, " ,,",
primary
teratomas, ;11 II I" I
Lymphoma 7% age from 1," 11 1' "
are comp"',' 'I I ' j ' ,I
secondary
tissue Iron I, "' V' II
OTHER germinal Illyl II' I I II
apparentl y I II '1 11i I'
Leukaemic infiltration <1 % 10% mel a" t. I' ,"II
Fig.10.2 Testicular torsion. The testis, epididymis and distal those OCC'"I11"I "
spermatic co rd show dark haemo rrhagi c infarc tion. This condi tion is,
in fact, due to torsion of the spermati c cord , in whi ch ve nou s obstruc­ Metastases < 1%
tion occurs lirst, resulting in intense distal congestion. It is .
co mmonest in the 2nd decade and is usua lly due to an abnormally
long or malorientated spe rmat ic cord or mesorchium . Early diagnOsi s Fig.10.3 Classification of testicular tumours (mod ifi ed infor·
may allow preservation 01 testicu lar lunc tion and co ntralateral mation from the U.K . Testicu lar Tumour Panel ) Thes e ligu re s
orchidopexy sh ould always be perfo rmed. represent percentag es of the total number of testicular tumours.

83

 10 Male Reproductive System

Fig.10.4 Fig.10.6 Malignant

.::iIFICATION OF TESTICULAR TUMOURS
~ Seminoma. Much
of this testis is
re placed by a well
teratoma inter­
mediate (MTI) Th e
lower pole of the
classical circumscribed, teslls is replaced by
38% lobulated pinkish­ a multinodular.
Seminoma white tumour. rather necroti c
Seminomas are the tumour , above which
spermatocytic 2% commonest p rim ary is an extensive zone
testicular tumour of infarction due to
and are derived from torsion . MTI, which
differentiated 1% germinal cells. They retains some
occur most often in differenti ated foci (in
H~ E LL
the 4th decade and cont rast to MTU) is
intermediate 20% are the most typically a tumour of
Teratoma frequent tumours to young adu lt males. It
arise in an un­ tends to both
undifferentiated 10% descended te stis. haematogenous an d
They are indistin­ lymphatiC sp read
guishable from the and the 5-year ­
trophoblastic 1% female ovarian survival is about
dysgerminoma (s ee 55% (beller th an
Fig.9 .16). MTU or MTT). Note
Combined seminoma! teratoma Seminomas are that any teslicular
14% extreme ly radio­ tumour may predi­
sensitive an d 5-year­ spose to, and
Yolk sac tumour survival is now at occasionally present
1% least 90%. wi th. torSion
t ri M
Leydig cell tumour Fig.10.5 Differentiated
2% teratoma.With in this testis is a
we ll circ umscribed mass wh ich
Sertoli cell tumour is multicystic and contains
1.5% yellowish keratinous debris .
Differentiate d teratomas are
uncommon , accounting for only
primary
about 2 % of testicular
Lymphoma teratomas, an d may arise at an y
7%
age from b irth to 30 years . They
secondary are com posed solely of mature
tissue from any of the three
germinal layers but, despite their
Leukaemic infiltration < 1% apparently ben ign na tu re . up to Fig.10.7 Malignant teratoma trophoblastic (MTT). Th is testis is
10% metastasise, pa rticularly complete ly replaced by a multinodu lar, dark, haemorrhag ic mass
those occurring in young adults. showing paler foci of necrosis. MTT (or choriocarci noma) is the rarest
Metastases < 1% subt ype of teratoma and is typified by the presence of syncytio­
trophoblast and cytotrophobl ast. Characteristicall y this tumour is very
haemorrhagic. The prognosis was previously abysm al, but the use of
.,lftcation of testicular tumours (modified Infor­ both modern multimodal th erapy and p-human chorionic
I,,' U 1< , Testicular Tumour Panel). These figu re s gonadotrophin as a serum marker has led to greatly improved
'IfItiJ £leS of the total number of lesticular tumours. survival.

84
10 Male Reproductive System

Fig.10.8 Chronic Fig.1 0.10 Tuber­

epididymitis. The culous epi­
epididymis and didymitis. The epi­
distat spermatic didymis is totally
cord are markedly replaced by an
thickened and irregular cavity
fibrotic and in containing copious
places , obstructed caseous material.
ducts are visibly The testis is com­
dilated . There is pressed but
secondary testicular completely spared.
atrophy. Tuberculous epi­
Epididymitis is didymitis is most
usually associated often seen in young
with lower urinary adults, usually in
tract infection or association with TB
urethritis and is of the urinary tract: it
commonest in adult­ has become very
hood. The condition uncommon in the
is most often uni­ indigenous Western
lateral and may population Bilateral
spread locally to the infection is frequent
testis or tunica and while the sper­
vaginalis. Recurrent matic cord may be
infection and affected, the testis is
chronicity are not onty rarely involved .
uncommon.

Fig.10.9
Fig.10.11 Prostatic
Epididymal adenocarcinoma. A transverse
abscess. The section through the whole
epididymis appears prostate gland, near the bladder
rather thickened and neck, shows diffuse replacement
scarred but in by pale, irregular and focally
addition, there is a necrotic tumour. Residual
small central nodular areas of benign tissue
abscess cavity with are also present. Prostatic car­
adjacent conges­ cinoma is very common from the
tion . The testis 6th decade onwards but often
shows partial pursues an unaggressive Fig.10.12 Benign prostatic hypertrophy. AlII 'Vi ' 11"
atrophy. This is an course. The aetiology may be bladder of an elderly male are shown. Til e PI UI,I. II I ' I', I,
example of acute­ hormonal. The outer prostatic with a particularly prominent median lobe ul1~: tll" '" " 111 1
on-chronic infection glands are the usual site of neck. The bladder wall is thickened and tr;.\l 1\)(.1II. ", ,, ' I
which , in very severe origin, particularly in the transverse section through a retropubic rred l il l II tlllli V
cases, may be posterior tobe. A raised serum shows marked enlargement, the prostatic tll a,II" I 11111 II I '
complicated by level of tartrate-labile acid muttiple yellowish-white nodules. Benign pn ,' ,1. 1111 II VI "
abscess formation. phosphatase is a useful diag­ (nodular or myoadenomatous hyperplasia) 1', IIIC" ', ,',11"
Gonococci are often nostic marker and metastasis to with advancing age, being almost univers(1i I 'V II I" ' 11 1, ,
isolated from such a bone is a characteristic feature due to an, as yet unclear, imbalance b etwc\ 'I I I, " Ill " ,1, "
lesion. of this tumour. oestrogen. The inner group of prostatic ql;lI lr l' , ,,'" IVI,I,
leading to urinary obstruction . It does not p" "II' .1 P" I,
"

85
 10 Male Reproductive System

Fig.1 0.1 0 Tuber­ Fig,10.13 Penile

culousepi­ squamous
didymitis. The epi ­ carcinoma. Arising
didymis is totally at the base of the
replaced by an glans penis (top) is a
irregular cavity pale , ulcerating
containing copious neoplasm, which is
caseous material. better seen in cross­
The testis is com­ section (bottom) .
pressed but Squamous car­
completely spared. cinoma ot Ihe penis
Tuberculous epi­ is relatively un­
didymitis is most common in the
often seen in young Western World, but
adults, usually in tends 10 arise in
association with TB elderly uncir­
of the urinary tract it cumcised men . In
... has become very some cases there
uncommon in the may be pre-existent
indigenous Western Bowen's disease.
population. Bilateral The majority of these
infection is frequent tumours develop
and while the sper­ from the glans peniS
matic cord may be or the prepuce
affected, the testis is While this tumour
only rarely involved. lends to exophytic or
locally invasive
growth , metastasis
Fig.10.11 Prostatic is usually a late
adenocarcinoma. A transverse phenomenon. How­
section through the whole ever, presentation is
prostate gland, near the bladder often delayed by the
neck, shows diffuse replacement patient's shyness or
by pale, irregular and focally mistaken belief that
necrotic tumour. Residual he has a venereal
nodular areas of benign tissue disease.
are also present. Prostatic car­
cinoma is very common from the
6th decade onwards but often
pursues an unaggressive Fig.10.12 Benign prostatic hypertrophy. Above , the prostate and
course. The aetiology may be bladder of an elderly male are shown . The prostate is hypertrophied
hormonal. The outer prostatic with a particularly prominent median lobe obstructing the bladder
glands are the usual site of neck. The bladder wall is thickened and trabeculated. Below, a
origin, particularly in the transverse section through a retropubic prostatectomy specimen
posterior lobe. A raised serum shows marked enlargement, the prostatic tissue being composed of
level of tartrate-labile acid multiple yellowish-white nodules. Benign prostatic hypertrophy
phosphatase is a useful diag­ (nodular or myoadenomatous hyperplasia) is increasingly common
nostic marker and metastasis to with advancing age, being almosl universal by the 9th decade. It is
bone is a characteristic feature due to an, as yet unclear, imbalance between testosterone and
of this tumour. oestrogen. The inner group of prostatic glands are typically affected,
leading to urinary obstruction . It does not predispose to carcinoma.

86
11 Nervous System

[ CAUSES OF ~Y~~~C~P~A~U~ --- - - - - ]

r I
Arnold-Chiari malformation

Bifid aqueduct

Atresia of 4th ventricular foramina

CONGENITAL
(Dandy-Walker syndrome)

toxoplasmosis
Intra-uterine
infection
Fig.11.1 Hydrocephalus. This coronal seclion of brain shows gross syphilis
Fig.11.5 Adult bacterial meningitis. The SUP ' , II<l1 ",,,I ,,,
dilation of the lateral ventricles , due to obstruction of the cerebral
brain IS intensely congested and covered in a plill iii" II ,
aqueduct by a glioma . Hydrocephalus may be classified into 4 types
Posterior fossa tumours particularly over the frontal tobes (left) . SUPP\.II:III VI ' 111i ' 1 III
Non·communicatmg (internal) due to obstruction of the aqueduct or
complicate endocarditis, middle ear, sinus or I" lill i' "I , II V I
foramina of the fourth ventricle; Communicating due to obstruction at
trauma. Direct spread of organismS may al sO ocr I II III" " ,
the subarachnoid cisterns; External due to impaired reabsorption of
ACQUIRED Post·meningitic nasopharynx Important pathogenic organism, ', II H II II II ' /Ii
CSF; and Compensatory, associated with cerebral atrophy. 1
meningilidis (in young children and young adl lll ;,). II, 11'/ 1
influenzae in young child ren and StreptocOC(;II.', 1'1" 'I /1 Jr' I,
Compensatory very you ng or old. Almosl any organism, inclu( III It I I,,, 1\ I' I
FLOW OF CEREBROSPINAL FLUID responsible in the immunocompromised patH' 111

pineal choroid lateral Interventricular

Fig.11.3 Causes of hydrocephalus.
palhol
cereb rospinal fluid gland plexus ventricle foramen
[J
D
arac',nOld mater

ependyma
-t-...2
~f :"\
anterior
horn
~)
~. "­ -- third
ventricle
Inferior
horn
pituitary
gland
{'ft JJ lateral
aperture

cerebello­ ::-=-s - pons

medullary ...... pontine Fig.11.6 Neonatal bacterial meningitis. 1111' '.1 II I,II " '
cistern
Fig.11.4 Syringomyelia. This segment of cervical spinal cord
cistern contains a dilated, cystic cavity (syrinx), which has compressed the neonate's brain shows congestion and SUPI "II"III \II , " 'I I
median ifF medulla central canal anteriorly to a barely discernible slit. Possible associa· the inferior aspect of the right temporallot,r. NOI,,,,,I, ,I ,
aperture seen most often after a prolonged or traurn;III' . ' 1" ItV' '''''
tions include four1h ventricle out flow obstruction, resu lting in
hydromyelia, and neurofibroma tosis (see Fig . 11.28) Typica l clinical common in premalure infants. The culpabllo) nIC Ii III" ,II I I'
1
Fig.11.2 Simplified representation of flow of cerebrospinal fluid, features include impaired pain and temperature sensations and the derived Irom the maternal genital tract at 1' 1111>, 1110'.11 11
seen In the left hemisphere (medial vi ew) . 'claw-hand' deformity, due to nerve tract compression Streptococcus pyogenes or a coliform, pallll:tll.llly f •

87
 11 Nervous System

Ij

Fig.11.S Adult bacterial meningitis. The superior surface of the Fig.11.7 Tuberculous meningitis. Over the parietal lobe there is a
brain is intensely congested and covered in a purulent exudate , dense inflammatory exudate associated with numerous adjacent
particularly over the frontal lobes (left) . Suppurative meningitis may 'tubercles' . Tuberculous meningitis is usuall y seen as a complication
complicate endocarditis, middle ear, sinus or pulmonary infections or of primary Infection in young individuals and is most often due to
trauma. Direct spread of organisms may also occur from the miliary spread. It may also result from rupture of a localised intra­
nasopharynx . Important pathogenic organisms include Neissena cerebral tuberculous (Rich) focus into the subarachnoid space The
meningllidiS (in young chitdren and young adulls) , Haemophilus base of the brain and upper cerebe llum are most often affected .
influenzae in young children and Streptococcus pneumoniae in the
very young or old . Almost any organism , including fungi . may be Fig .11.8 Cerebral
responsible in the immunocompromised patient 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
Fig.11 .6 Neonatal bacterial meningitis. The surface of this to abscesses
neonate's brain shows conges tion and supp uration, especially over localised in the
the inferior aspect of the right temporal lobe. Neonatal meningitis is distribution of the
seen most often after a prolonged or traumatic delivery and is more middle cerebral
common in premature infants. The cu lpable organism is always artery.
derived from the maternal genital tract at birth, most often being
Streptococcus pyogenes or a coliform, parti c ularly E. coli.

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.11.21 Meningioma. A circumscribed nOIIlII;1I tlill II III I

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.11.19 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.
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.11.18 Old Fig.11.20

cerebral infarct. Alzheimer's
This coronal section disease. The
of brain shows a meninges have
massive previous been stripped from
right -sided inlarct the left side of this
which has resulted brain to show
in loss 01 cortical marked cerebral
tissue, cysl ic atrophy , manifest by
degeneration and sulcal widening and
compensatory diminution of the
hydrocephalus. gyri. Alzheimer's
Multiple (usually disease is a chronic
small) inlarcts over a form of pre-senile
variable period 01 dementia, is
time may lead to commonest in the Fig.11.22 Glioma. This coronal section of b, Llil •. .1 II I....,. "
numerous loci 01 5th and 6th decades neoplasm, with foci of haemorrhage and necro::i·. III It lll I,
cerebral softening and may also be sphere . There is adjacent oedema and distortioll ()III ~I .I'
(status spongiosus) seen in Down's system. Gliomas may be divided, in order of froql I, "ILV II
and Ihe clinical syndrome. The blastoma multiforme (see Fig 11.23), astrocyl \lIl .fI, 11111t1 ., I
syndrome'ol mull,­ aetiology is entirely glioma, ependymoma and choroid plexus pal)illol lIit M I
inlarct dementia. unknown. 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.

91
 11 Nervous System

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 .
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
II
matter and arachnoid villi, most often arise in relation to the major venous
grey sinuses. They are slow-growing, almosl invariably benign, tumours
gliosis
but may occasionally invade the adjacent skull. They occur pre­
larly females
dominantly in the 5th and 6th decades and symptoms, if any, depend
Irolog ically, a upon the site of the tumour.
ponsible,

.
"Y
.
/~; ~ ~.
' y.

. ,

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
11 Nervous System

Fig.11 .25 Acoustic

neuroma. Situated
on the left cerebello·
pontine angle is a " tll'W'dl l t
I n, I tl d - I II
well circumscribed
neoplasm arising 11 , 1, 11 11' I

from the eighth (I ,,,lr'W I

cranial nerve . This is 1111 ' 1 I" II"

1111 11 lit I I i

a benign Schwann
cell tumour which is II. II I 'IV I "

(, I \ , qlli o l
sometimes bilateral
and may be willi I I I •
I,rilr, · 1, ,"
associated with
~ ;111 11 Ii 11 II

neurofibromatosis .
Clinical features III '.rl I IV II "
111 111" , , 11 I
include tinnitus,
1111 11 11111 1, 11
vertigo and nerve
deafness . Compli­ I .ril,,' Wi
,
cations include Fig.11.27 Benign schwannoma (neurilemmoma). This is a well " IIiI1WII I I I
compression of circumscribed, encapSUlated, small tumour which has a yellowish cut ( ,lIllh \ ~ Ii

other cranial nerves surface and shows small foci of haemorrhage. Benign schwannoma 111I11I +ll tl u 1

or of Ihe brainstem. is a common tumour of peripheral nerves and arises from the nerve '.or II '''111 I
sheath. It is usually solitary, arises especially in the 3rd to 5th 11 If )~ I, \1111 I'

decades and is most often asymptomatic Occasionally, multiple 11 \. qt lill y I

lesions may be seen in neurofibromatosis but in the latter condition ,11 1" ', 11111

multiple neurofibromas are far more common. I" 11111 ' I" I

I ii \1 111111 1
I \ ~ I ' ,II \I dI

Ii " \11111 I' ,

I III Il . .. ·I>! '
\
\ ~C,lI l II 11'11 I

II II 1111 " ~ , I
VI '11i II I' II

1, 11 111 11 111 11
11. 111 1,11 1' 1
11',' ,111" I'
Ie I/lf l. II I , V
1.111 1" ',1111
1,' , 1' hili, Ii
V' III'I,,,lli l
C O II II I I I II

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 .
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 .

93
 12 Osteoarticular System

Fig.12.1 Bone Fig.12.2 Malunion.

fracture. Above, the This macerated
proximal femur segment of a long
shows an obvious bone shows clear
recent subcapital evidence of a
fracture. Part of a rib previous fracture but.
(below). adjacent to malunion has
the costochondral occurred with de­
junction, shows a formity resulting
transverse fracture, from overlap of the
on either side of bony ends. Malunion
which is exuberant follows failure to
callus formation. reduce a displaced
Simple fractures fracture. This
heal by the produc­ appearance may
tion of periosteal and also be seen, in a
then medullary less extreme form,
callus. which is after fracture
followed by new through an
cartilage and bone epiphyseal plate
formation with sub­ (prior to completion
sequent re­ of ossification) which
modelling. The results in an
majority of fractures abnormal growth
are traumatic in pattern.
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.12.3 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 .
95
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.12.7 Osteoporosis. Thi s
macerated section of the lower
thoracic and lumbar vertebrae
shows a very marked reduction
in the amount of cancellous bone
associated with a crush fracture .
Osteoporosis, defined simply as
a decrease in volume of other­
wise normal bone, is pre­
dominantly a disease of the
elderly (particularly females) .
Causes , other than ageing or the
menopause. include prolonged
immobility, disuse, Cushing 's
disease or thyrotoxicosis , but
most cases remain idiopathic .
The spine and pelvis are most
often affected and the principal
complication is a fracture.
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 , III' II ,
serum Vll dll lllil ' WII
due to (lilll.II Y t ll ·,11o "
suffic icill '.1111 "" I '"
sorption. 1;111 11, ,11 ,.
or ch roili c " V"I, Ii '"
plicaliol"; "" 11,11" I ii
deforrTlilll': .. IIl1III01'
Fig.12.9 Tophlll .,'
This SO 'l1111'III, ,II " "
covere<.ll lYI ,·!I" III '
excrescc," ,". (I, 'I,l l
compo:;" " ,,1111. 11, ,
Goul rn i:lY I II ' 1'1111 Ii II
idiopalllil il l'., "d", ,
metab u ll~ ·,rr1 . ~Ir ' .. ,~ r I I
either to 1;111111, ·, ,111 1'
excretrur 1 (ll ,' )I i 1 ,1 , ~ I
of nUCI I,; II~ ;II Il l'. i .. ' i
nantejl som,I 'l1l 1 vii'
theraflY) 11 ,1 '" ",I,
hyperUIl CIII 'IIII.I " ",,
deposllloll 111' 111 " " ,.
crystal:; II' 11'"11 '. 1""
SUbClJt (:II!1 ~ IHI·.II' .· Iii
cation s 1111 10 1(1,· II" , I,
urate Sl(llll". II' 111, ' "
and I1le ,I"I" J'"I" 'I' i ,
cryst al:; 11111,, · " '"lil
sometllnl".I,·."I IIII ,1
failure .


Fig.12.6 Syphilitic
periostitis. This is a
macerated segment
of femur showing a
thick layer of sub­
periosteal new bone.
Congenital syphilis
classically gi ves rise
to both a florid
periostitis (with
reactive new bone
formalion). as in this
example, or an
osteochondrilis
(granulomatous
inflammation at the
ends of long bones).
Similar appearances
ma y be seen in
tertiary acquired
syphilis. in which
coexistent gummata
may also be present.
,
1­
Fig.12.7 Osteoporosis. This
macerated section of the lower
thoracic and lumbar vertebrae
shows a very marked reduction
in the amount of cancellous bone
associated with a crush fracture.
Osleoporosis, defined simply as
a decrease in volume of other­
wise normal bone, is pre­
dominantly a disease of the
elderl y (particularl y females) .
Causes, other than ageing or the
menopause. include prolonged
immobility, disuse. Cushing's
disease or thyrotoxicosis, but
most cases remain idiopathic
The spine and pelvis are most
often affected and the principal
complication is a fracture.
Fig.12.8 Rickets. Thi s section
through the lower femur and
upper tibia of a child shows
marked thickening of the growth
plates and a significant failure of
endochondral calcif ication.
Rickets and osteomalacia are
both characterised by failure of
bone mineralisation ; the former
is a disease of children (prior to
completion of growth) . while the
latter is seen in adults . The
commonest cause is diminished
serum vitamin D which may be
due to dietary deficiency. in­
sufficient sun exposure, malab­
sorption. chronic renal disease
or chronic liver disease . Com­
plications include bony
deformities and fractures.
Fig.12.9 Tophaceous gout.
This segment of tendon IS
covered by pale. Irregular
excrescences (tophi) ,
composed of urate crystals.
Gout may be primary, due to an
Idiopathic disorder of purine
metabolism . or secondary, due
either to failure of renal urate
excretion or excessive turnover
of nucleic acids (e.g . in malig­
nant disease'or cytotoxic
therapy). The consequent
hyperuricaemia results In
deposition of monosodium urate
crystals in jOints, periarticular or
subcutaneous tissues. Compli­
cations include the formation of
urate stones in the urinary tract
and the deposition of urate
crystals in the renal tubules,
sometimes leading to renal
failure .
12 Osteoarticular System
Fig.12.10 Hyper­
parathyroidism (Osteitis
fibrosa cystica). A coronat
section through the symphysis
pubis shows irregular resorption
of the para'articular cortical
bone and adjacent hyperaemia.
Hyperparathyroidism may be
primary, secondary or tertiary
(see Chapter 7) Up to 25% of
affected patients develop bony
changes . characterised by
Increased bone resorption .
medullary fibrosis and the
formation of 'brown tumours'.
whi ch are haemorrhagic foci of
fibrosi s with cyst formation. In
cases secondary to chronic
renal failure the features may be
modified by coexistent
osteomalacia.
Fig.12.11 Avascufar
necrosis. This
irregular femoral
head shows a large.
poorl y'circumscribed
area of yellowish
necrosis, associated
with bony collapse
Avascular necrosis
(osseous infarction),
which occurs pre­
dominantly in the
femoral head, most
often follows a sub·
capital fracture . It
may also occur in
decompression
sickness. in patients
on steroid therapy.
in alcoholics or
following renal
transplantation.
Even though the
articular cartilage is
spared , micro­
fractures and
collapse of the
affected bone often
lead to arthritis .
96
12 Osreoanicuiar System

Fig.12.15 AllkV" 1
Fig.12.13 Rheumatoid
spondylltill. /I ' ., ' ,
arthritis. The femoral condyles ,
th ese 11,,,,1 1. 11 VI'll , I ,
tibial head and patella show very
wid C ~ f)(t ', lCl t " lf" '/1 1
extensive cartilaginous destruc·
throuqll tll<',"I"I \I ' "
tion, particularly at the periphery
resulillHIIII, II iI' VI.,
of the articular surfaces .
sponlfyilll:, " , ,III " II'
Osteophytes are absent.
order , willi I" " , II I
Rheumatoid arthritis is a chronic
systemic inflammatory disease in youll" "" 'II ,11 11 II
assoC J;II('<I w,lI, III
which is commonest in the 3rd to
dis ea~u I:" 11, 1/ ,,' I,
5th decades and shows a
feature" :,111111.11 II, II
predilection for females . Small
rheum:II,,"I,I/1I11111
joints are principally affected,
usually symmetrically, but the add lill '"," ,,,I,,
progressive involvement of large ossificnll"" It " II. '
domin:llll1y tI,. " ,' 1. '
joints is common. The condition
Compll edll" II·. ,",1, 1
is thought to be autoimmune in
kyphoslf; , ',11111"1",,,
nature, is more frequent in
piraIOrY""II ldll ,I'
patients with HLA·DW4 and is
associated with the presence of
a serum immunoglobulin known
as the rheumatoid factor .

Fig .12.16 PrlU"!'

(Osteitis dOlor 111 1111
segmenl "I ,,,.11 I" ,'
shows Ill: III" II J, "',
thickenlllli (,I II" " "
and rCI)I:1( """ " Ii , ,1
bone by co, 11'" ' I" Ii
Pagei's d H,("" '(' Wi
thought to I '" , II " , I,
infectioll , :lIfl li t'. "I '
popul atll II I (11'.11,,11
and show:" II ", \, Iii,
older a(hllt: , It ,' " I,
initially I)y I 'XI '" ,'.IV'
Fig.12.12 Osteoarthrosis. This femoral head (top) is irregular in resorpilull ,111<11 011 1,
outline, shows eburnation of its superior aspect and also irregular markecl 1111 I fl iI '" II I
cystic defects at the sites of cartilaginous loss anteriorly. Below , bon e fOrl""II,,, , II"
another example seen in cross·section, shows a multilocular focus of skel etoll , 1',1111' 1I I" Ii
cystic degeneration in the subchondral bone associated with marked and sku ll, 1',111"' .1 "I
osteosclerosis and early osteophyte formation laterally. Osteo· Fig.12.14 Rheumatoid arthritis. This is the synovium from a knee althOlJol1 ti", II or III I I'
arthrosis is an extremely common, non·inflammatory, 'wear and tear' joint, which shows florid synovial villous hyperplasia (pannus for· commurlly IIIVi ,1 \1' 11 1
phenomenon, which affects mainly large weighl -bearing joints mation) Chronic synovial inflammation with hyperplasia are the
(usually asymmetrically). Recognised predisposing factors include cardinal features of this disease and precede destruction of the
increasing age, obesity and pre·existent conditions such as articular cartilage. Systemic features of rheumatoid arthritis may
congenital hip dislocation, genu varum, Perthes disease or previous include subcutaneous rheumatoid nodules , splenomegaly, Caplan's
fracture . Associaled findings in affected patients include cervical syndrome and secondary amyloidosis . Pathologically, the arthritis
spondylosis, hallux rigidus and Heberden's nodes (osteophytes over associated with psoriasis and ulcerative colitis is almost
the terminal interphalangeal joints). indistinguishable.

97
 12 Osteoarticular System

Rheumatoid Fig.12.15 Ankylosing Fig.12.17 Paget's disease.

femoral condyles ,
patella show ve ry
ilaginous destruc­
rly at the periphery
surfaces .
re absent.
and shows a
for females. Small
ipallyaffec ted ,
rically, but
invol vement of large
on . The condition
spondylitis. A section through
these lumbar verte brae shows
widespread osseous fusion
throug h th e intervert ebral discs,
resulting in ankylosis. Ankylcsing
spondylitis is an idiopathic dis­
order, whic h occurs most often
in young men and is strong ly
associated with HLA-B27 . The
disease is charact erised by
features similar to those of
rheumatOid arthriti s, except for
the addition of articular
ossific ation. It aff ects pre­
domi nantl y the axial skeleton.
Comp lica tions include seve re
kyphosis, sometimes with res­
plratoryembarra ssment.
This proximal portion of femur,
whil e showing simil ar featu res to
Fig . 12.16, also demonstrates
residual foci of porotic bone and
typical marked hype raemia. Th is
latt er, acting as a multifocal
arteriovenous shunt. may give
rise to congestive ca rd iac
failure . Other complications of
Pag et's d isease inc lude bony
deformi ty, a predisposition to
fractures (th e thick but irregular
new bone is weaker than normal)
and the development of
osteosarcoma or c hondro­
sarcoma in 1 % of cases .

,.
Fig .12.18
Charcot's joint.
Fig.12.16 Paget's disease
This corona l se ction
(Osteitis deformans). This
through a knee jOint
segment of macerated femur
demonstrates gross
shows marked, irregutar
distortion by
thickeni ng of the co rtica l bone
subluxation and
and replacement of cance ll ous
des tructi on of the
bon e by coarse trabecu lae .
arti cular cartilage
Pag et's disease, which is
These features have
thought to be due to a sl ow viral
developed as a
infection, affects up to 2% of th e
complication of
population (usually subclinically)
neurological disease
and shows a predilection for
associa ted with loss
older adults. It is c haracterise d
of pain sensation or
initially by excessive bone
proprioception .
resorption and latterly by a
Classical ca uses
marked increase in irregular new
include tabes
bone fo rmat ion. The axia l
dorsali s, peripheral
skeleton , particu larly the spine
neuropathy (often
and skull, is most often affected
diabetic) and
althou gh the long bones are
syringomye lia.
commonly involved .

ritis may
, Caplan's
ca lly, the arthritis
almost

98
12 Osteoarticular System

Fig.12.19 Hyper­
ostosis frontalis
interna. Projec tin g
from the inner
surface o f the frontal
bones is a we ll
circumscribed mass
of extensi vely
ridged. rather
greyish bone.
Hyperostosis
frontalis interna is a
not uncommon idio­
pathic le sion, which
is usually seen in
late adulthood and is Fig.12.21 Ivory osteoma . Projecting from the superior surfac e of
rather more common thiS skull is a smooth, rounded nodule. Ivory osteomas are benign
in women. It is rarely tumours, composed of densely sclerotic mature bone, which usually Fig.12.23 Cartilage-capped exostosis. 11,1: , " ", I' ii, V.I
of any clin ical sig ­ arise only from the sku ll or facial bones. They may present at any age, projected from the surface of a femur , S II OW~ " I JlIII.·, 'III
nificance . Localised show a slight predi lec tion for males and never undergo malignant cartilage overlying a nodule of cortical bOllu II " ", " " II I
reactive hyper­ change. They are some times a feature of Gardner's syndrome known as os teochondromas o r ecchondro' lIil'.i) .,,,, 11 ,1]0
ostosis of the skull (familial polyposis co li with epidermoid cysts, fibromatoses and bone deve lopmental le sions, derived Irom lalc r:llly ,Il l''''. "",
may also sometim es tumours) ca rtil age, wh ic h then undergoes endoc honrll , II, ".·.iI,' .
be seen overlyi ng present mos t often in the lower femur or IIPI" " Iii ,I.' "I , I
a meningi oma young adult s. Rarely, they may be mult iple (:'111111 " " Ii " , I
known as diaphyseal ac lasis), in whic h Clrc, 1111' ,1.1 111 " II"
20 % risk of developing chondrosarco rJ'l ;)

Fig.12.24 rndll""
Thi s CUI (111. Ii ' .• " I" " I
10we r (:llIl " III" . I, .,I'
multilJlt ! 11111.' \l II 'Y "
carlilacJ" III III,·. "1 "1 1'
p h ys l ~: :li ll i , It, '1111
d rollla~: :111 ' I lltlll'"1 1
whic ll lll ol ylli ' '" 011 101'
ariSlnq 1111 1", 1. "",1 "
yOUII Cj :111 1111'0) 1111111 '
preSCIIGi' "I 1111 iii 'I Ii,
(kno wllil:,I )lh. ,, '· ,I ,
thouqllll< l 11I' 1llIllI, 1
Fig.12.20 Fibrous dysplasia. Thi s segmen t of rib is markedly Fig.12.22 Osteoid osteoma. Arising from the co rtex of thi s segment may 11( ' ,1'"lIl' 1,11 .. , 1'
expanded b y a well ci rc umscribed , pale mass . Fibrous dysplasia is of bone is a well circumscribed, vascular nodule . There is adjacent t1 55 tH! l': Ii'II " II II II< ", I
regarded as a hamartomatous lesion, composed of fibrous tissue bony sclerosis . Os teoid os teomas are benign tumours which present syn<'lfoll" ') I\II Y 1'>1 1
and woven bone, and may take three forms : (1) the monostotic most often in childhood or adolescence, are commoner in males and rntfltl"I.· Ii "." '"' , 110 1
variant (commonest), which is seen at any age and usually affect s are typically very painful (espec ially at night). They arise pre­ ri!::ik of I II -V I ,I, 'I 111111 i
t

long bones or the ribs; (2) the polyostoti c variant, which typically.
present s in c hild hood, is often unilateral and may also affect the sku ll ;
and (3) the polyostotic variant as sociated with cafe-au-Iait spots and
end oc rine abno rmalities (Albright' s synd rome). Sarcomatous change
occurs in about 1 % of cases.
dominantly in the shaft of long bones, particularly the leg , and sarCOl1 1.1
class ically the associated pain is relieved by aspirin . They do not
undergo malignant c hange.

99
 12 Osteoarticular System

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
Fig.12.23 Cartilage-capped exostosis. This lesion. which !t'0-o::;,t'!5' -.L!l uncertain histogenesis .
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 Fig.12.26 Osteoclastoma (giant cell tumour of bone). Arising in
syndrome). Any patient with the epiphysis of this femur and extending into the metaphysis is a
multiple lesions has a significant reasonably circumscribed. haemorrhagic mass. Giant cell tumours
risk of developing chondro­ of bone are uncommon lesions which tYP ically present in young
sarcoma. 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 I II i ,' jl ,d lt
(particularly the femur or tibia). A Ill f 111 1111

small proportion of cases are I II'Y' IH

seen in the elderly, secondary to ' " I1 I" i" 11
Paget's disease (see Figs. 12.16 '" Vlllv" I
and 12.17). They tend to c 11I ' j' I ,IH
extensive local invasion and ';,,, ,11 01
early haematogenous spread. .11 ,' I . 111 !

the overall 5-year-survival being I H h d '.1 1 i,

about 20% I H I r .lil lt
III Yl i d! I

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 Fig.12.29 Multiple myeloma. This portion of skull (top) shows
(although proximal multiple punched-out lesions containing haemorrhagic tumour.
long bone involve­ Below, a segment of the spine demonstrates ill demarcated,
ment is not haemorrhagic, osteolytic lesions in the lower cervical vertebral
uncommon). It tends bodies. Multiple myeloma typically presents in late adulthood and is
to be slow-growing. characterised by a neoplastic proliferation of plasma cells, which
often attaining a classically gives rise to osteolytic lesions in the marrow of the axial
considerable size.. skeleton. Excessive immunoglobulin production by the tumour cells
and 5-year-survival allows detection of the light chain Bence-Jones protein in the urine. a
is about 75% useful diagnostic aid. Complications include a predisposition to
infection. renal damage and amyloidosis The prognosis is very
variable.

101
 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
Charcot's joint, 98 ~ L t, II
Achalasia , 25 stenosis , 4-5 fat embolism , 89
,

Acoustic neuroma, 93 Aortitis, syphilitic, 5, 10 general paresis, 89

Chemodectoma, 61 II , I
Adenocarcinoma Appendicitis, acute , 31 haemorrhages, 89-90
Cholangiocarcinoma,43 1111. 11

breast, 46-49
Appendix , carcinoid tumour, 30 hydrocephalus, 87
Cholecystitis li t "!

duodenum, 28
Asbestos and lung disease , 22 infarction , 91
acute, 42 IVI"
gallbladder, 43
Atheroma, 1, 9 meningitis, 88
chronic, 42 IIII,l il

Cholelithiasis, 42, "3 ,; , .,

kidney, 68
complicated , 10
raised intracranial pressure, 89

large bowel , 34-35

risk factors , 9
tumours, 92-93
Cholesterolosis , 43
lung , 20-21
ulcerated , 10
Breast Chondrosarcoma, 100, 101 " tl ill
ovary , 74-75
Atrium , left, myxoma of, 8 carcinoma, 46-49 Choriocarcinoma 111/,1'
pancreas , 44
duct papillomata, 46 testis , 84 IIIl i ll'

prostate, 85
Barrett's ulcer, 24 fibroadenoma, 45-46 uterus , 81 f it 1" 1

stomach,27-28
Bileducts fibrocystic disease, 45 Cirrhosis, 39-40 II VI"j
uterUS , 80
carcinoma, 43 gynaecomastia,49 Coalminers, lung diseases, 17-18 , 1!) 1",ly
Addison 's disease, 59 , 60 gallstones in , 42 male, 49 Colon/Colitis see Bowel, large 11t 1l " 1
Adenomyoma, 79 Bladder mammillary fistula, 45 Conn's syndrome, 60 I lq ll,i

Adenomyosis , 79 diverticulum , 71 non-Hodgkin 's lymphoma , 49 Coronary artery thrombosis, 1 I,ll \I I

Adrenal gland transitional cell carcinoma, 71 peau d'orange , 48 Corpora albicantia, 72 1,1,1111
Addison 's disease, 59 Bones Brenner tumour, 75 Corpus luteum , 72 ," lI~'
haemorrhage, 59 fibrous dysplasia, 99 Bronchi , tumours, 20-21 Craniopharyngioma , 55 Ilil l

nodular hyperplasia, 60 necrosis, 96 Bronchiectasis , 15,21 Crohn 's disease, 29 Ilii n

tumours, 60-61 tumours, 99-102 causes , 15 Cushing 's syndrome , 60 ," II

Alzheimer'sdisease , 91 see a/so Fractures and specific Bronchopneumonia , 13, 15 Cystadenocarcinoma (ovary)
Amyloidosis disorders of bones with bronchial carcinoma, 21 mucinous, 75 . 111, 11
renal,68 Bowel, large tuberculous , 16 serous, 74 111 , i"

spleen, 51 amoebic dysentery, 33 Budd-Chiari syndrome, 38 Cystadenoma (ovary) , V'II

Aneurysmal bone cyst , 100 chronic ischaemic colitis, 32 Burkitt's lymphoma, 52 mucinous , 74 1\.1 1

Aneurysms Crohn 's disease , 29 serous, 73 IIV"II

aortic , 11-12 diverticular disease, 32 Caecum, carcinoma of, 35 1,.,ll l
berry, 90 diverticulitis , 32 Calculi Duke's staging of large bowel tumOllr~: . : 1'1 IIV' '
cerebral artery, 90 pseudomembranous colitis , 33 bile duct, 42 Duodenum li ll y,
dissecting , 11-12 tumours, 33-35 gallbladder, 42 , 43 periampullary carcinoma, 28 I l' h l
left ventricular, 2 ulcerative colitis , 31-32 renal , 64 ulcers , 28 li l/ d l

splenic artery, 12 Bowel , small stag horn , 64 Dysentery, amoebic, 33 1 IIIIilil

true, classification of, 11 Crohn's disease , 29 Candidiasis , oesophageal , 24 Dysgerminoma, 76 11 111 III
Ankylosing spondylitis, 98 infarction, 30 Carcinoma III" h
Aorta ischaemia, 30 see sites of carcinoma Ecchondromas, 100 11,,1 ,
aneurysms, 11-12 tuberculosis, 30 Cardiomyopathy EctopiC pregnancy, 77 il',1
atheroma, 9-1 0 tumours, 30 congestive, 7 Emphysema
fatty streaks ,9 typhoid infection, 29 hypertrophic obstructive , 6 centriacinar, 19 I 'illi ll
syphilis, 10 ulcers, 29 types of, 6 classification, 19 ) II.

Aortic valve Bowen 'sdisease, vulval, 82 Cerebral see Brain focal dust , 19 ( 1,1;
incompetence , causes , 5 Brain Cerebral artery , aneurysms , 90 panacinar, 19 t l ill
infective endocarditis , 5-6 abscess , 88 Cerebrospinal fluid , normal circulation, 87 paraseptal,20 ~ I!il
non-infective endocarditis, 6 atrophy, 91 CerebrovaSCular accident, causes, 90, 91 Enchondromatosis, 100 , ,4, ... 111

103
Charcot's joint, 98
Endoci Irdill•. acute, 26

Chemodectoma, 61
aculOdl(Jlll llllli. , I ·1 chronic atrophic, 27

Cholangiocarcinoma,43
infe(;tivu, ~ , Ghon focus, 15

Cholecystitis
non-lf1feCliv" II". ",il lI/ Iii: , () Glioblastoma multiforme, 92

acute, 42
types or , ~ , Gliomas, 92

chronic, 42
Endocrine NI '''II IiI'd, I : 'Y 'IIII' l1Tl O , Multiple Glomerulonephritis

Cholelithiasis, 42, .13

see Mulli plt l I 11I 1"l lil l' I N' H!plasia acute proliferative, 66

CholesterolosiS,43
Synd"""" chronic, 67

Chondrosarcoma, 100,101
Endometri0111c: membranous, 66

Choriocarcinoma
ovarian, 7: \ Glomus jugulare tumours, 61

testis, 84
Endometriulll
Goitre

uterus, 81
adenocar,:11 11 1111(1.1\( I
colloid, 56

Cirrhosis, 39-40
hyperplaSil l, IH)
diffuse toxic, 56

Coalminers, lung diseases, 17-18, 19

polyp, 79
multinodular, 56, 57

Colon/Colitissee Bowel, large

Endomyoca rdl lllll, 1,1,14 1'11:1 , /
Gout, tophaceous, 96

Conn'ssyndrome, 60
EpendymOlTlu , Oil
Granulosa cell tumour, 75

Coronary artery thrombosis, 1

Epicardium, tllulll(\llIlil ' dUpOSltS, 8
Graves' disease, 56

Corpora albicantia, 72
Epididymitis
Grawitztumour, 68

Corpus luteum, 72
abscess,8!)
Gynaecomastia,49

Craniopharyngioma, 55
chronic, 85

Crohn's disease, 29
tuberculous, 8
Haemochromatosis, 39, 40

Cushing's syndrome, 60
Exostosis, carlil ago cappeu, 100
Haemopericardium, 2,12

Cystadenocarcinoma (ovary)
Haemorrhages

mucinous, 75
Fallopian tubes
intracerebral,90

serous, 74
abscess,72
pontine, 90

Cystadenoma (ovary)
cysts, 77
subarachnoid, 90

mucinous, 74
ectopic pregnancy, 77
subdural, 89

serous, 73
hydrosalpinx, 78
Haemosiderosis, pulmonary, causes, 17

inflammation, 72, 78
Hamartoma, pulmonary, 20

Duke's staging of large bowel tumours, 35

pyosalpinx, 78
Hashimoto'sdisease, 56, 57

Duodenum
Fatty change
Heart

periampullary carcinoma, 28
heart, 9
brown atrophy, 9

ulcers, 28
liver, 38-39
see a/so specific parts and diseases of

Dysentery, amoebic, 33
Fibroids,79 heart

Dysgerminoma, 76
Fractures, 94
Hodgkin's disease

malunion, 94
breast, 49

Ecchondromas, 100 ,
non-union with false joint, 94
hepatic involvement, 41

Ectopic pregnancy, 77
osteoporosis and, 95
lymph nodes, 53

Emphysema
spleen in, 52

centriacinar, 19
Gallbladder
Honeycomb lung, 18

classification, 19
carcinoma, 43
Hydatid cyst, hepatic, 37

focal dust, 19
cholecystitis, 42
Hydatidiform mole, 81

panacinar,19
cholesterolosiS,43
Hydrocephalus, 87, 89

paraseptal,20
stones, 42
causes, 87

Enchondromatosis, 100
Gastritis Hydronephrosis, 68, 69, 70, 71

104

Hydrosalpinx, 78
Hyperaldosteronism, 60
Lambl's excrescence , 8
Larynx, carcinoma, 13
hepatic involvement, 41
intestinal , 31
Multiple sclerosis, 9 1 " ,
Myeloma , multiple, 10 1 ti l "
Hyperostosis frontalis interna, 99 Leiomyoma lymph nodes , 53-54 Myocardial infarct, 1, 2 I! ,1' 111
Hyperparathyroidism, 58, 96 gastric, 28 thyroid gland, 58 causes , 1 1101 1,,, ,
Hypothyroidism, 56, 57 uterine , 79 see also Hodgkin 's disease ; Non­ complications, 2 I I '~ II tj
Leiomyosarcoma, uterine , 80 Hodgkin 's lymphoma Myocardial rupture , 2 1 1',1" 1
Infarct Leukaemias , spleen and , 51-52 Myocardium 'v, "
bone,96 Leukoplakia, oral , 23 Maffucci syndrome, 100 brown atrophy, 9 ' Ih l
cerebral,91 Linitis plastica, 28 Malignant melanoma, lymph nodes, 54 fatty degeneration , 9 I I'j h u
hepatic, 37 Lipids, cardiovascular deposition, 9 Mallory- Weiss tear, 24 Myxoedema, 57 ( h*h H
intestinal , 30 Liver Meckel 's diverticulum , 29 Myxoma, left atrial , 8 , I",
myocardial, 1, 2 abscesses, 36 Mendelson's syndrome, 14 1111 ,
pulmonary, 17 amoebiasis, 36 Meningioma, 92 Nabothian cysts, 79 , Jrl l' Ii '
renal,65 amyloidosis, 39 Meningitis Nephritis , chronic interstitial , 64 ( '""II h.
testicular, 83 Budd-Chiari syndrome, 38 bacterial,88
Intestines see Bowel cirrhosis, 39-40 tuberculous , 88
Nephroblastoma,69 ( " ~" "
Nephrotic syndrome , causes of, 67 \ 'V' " V
Islet cell tumours, 44 fatty change , 38-39 Mesenteric artery, embolism , 30 Neurilemmoma, 93 .,1 .
hydatid disease , 37 Mesothelioma, 22 Neuroblastoma, 61 I I I! I
Joints, 96, 97, 98 necrosis, 36 Metastatic carcinoma Neurofibroma, plexiform , 93 "II I
polycystic, 36 adrenal , 60 Neuroma, acoustic, 93
Kidney portal vein thrombosis, 37 bone , 102
'v
Nipple IH ll t
acute pyelonephritis , 63 tumours, 38, 40-41 brain , 93 Paget's disease, 48 1. 1\

amyloidosis, 68 venous congestion , 37 heart, 8 retraction , 47 Iq l ll

chronic interstitial nephritis , 64 Zahn infarct, 37 liver, 41 Non-Hodgkin 's lymphoma
cortical lobulation, 62 Lobar pneumonia, 13 lung , 21 , 22 adrenal gland, 61 1' "1 1' ' '
cortical necrosis , 65 Lung ovary, 77 breast, 49 "I! ,
cyst, simple, 63 abscesses, 14 spleen , 53 Burkitt's, 52 "I"
dysplasia, 63 acini,19 Miners, lung disease , 17-18, 19 hepatic involvement, 41 , 52 1' 1111 ; I
essential hypertension, 66 emphysema, 19-20 Mitral valve intestines , 31 , VIII
glomerulonephritis, 66-67 occupational disease , 17-18,19, 22 incompetence , causes of, 4 lymph nodes , 54 Illi ll
horseshoe, 62 sarcoidosis, 51 infective endocarditis, 5 spleen , 52 1 ' . 1111 I
hydronephrosis, 68, 69 , 70, 71 tuberculosis, 15-16, 18 mixed disease , 4 thyroid gland , 58 II I ii
infarction , 65 tumours, 20-22 non-infective endocarditis, 6
lobulation , 62 Lymph node in rheumatic endocarditis, 3 Oesophagus
, ""
I 'H i 0111 ,
medullary sponge, 63 Hodgkin 's disease, 53 stenosis, 3 achalasia , 25 1" " ,, 11
nephrotic syndrome, causes of, 67 malignant melanoma, 54 Mbnckeberg 's sclerosis, 12 candidiasis , 24 I'VI '
papillary necrosis, 68 non-Hodgkin 's lymphoma, 54 Mouth carcinoma, 25 110 11
polycystic, 62 sarcoidosis, 53 leukoplakia, 23 Mallory- Weiss tear, 24 i 'li iv
renal vein thrombosis, 65 secondary carcinoma, 54 squamous carcinoma, 23 peptic ulcer, 24 ! '1l1V
stones, 64 tuberculosis, 53 Mullerian tumour, malignant mixed , 80 stricture, 24 ' ii i
transplant rejection, 65-66 Lymphoma Multiple Endocrine Neoplasia Syndrome, varices, 25 ".,,11
tuberculosis, 64 adrenal gland, 61 58 Oilier's, disease, 100 "HIlt ,
tumours, 68-69 breast, 49 typel,55 Oophoritis, pyogenic, 72 I II I
Krukenberg tumour, 77 Burkitt 's, 52 type II, 58, 61 Osteitis Iil il

105
Multiple sclerosis , 91
deformans, 98
tuberculous, 7

Myeloma, multiple, 101

fibrosa cystica, 96
Periostitis, syphilitic, 95

Myocardial infarct, 1, 2
Osteoarthrosis,97
Perisplenitis, chronic, 50

causes, 1
Osteochondritis , syphilitic , 95
Phaeochromocytoma , 61

complications, 2
Osteochondromas, 100
Pharyngeal pouch , 23

Myocardial rupture, 2
Osteoma
Phyllodes tumour, 46

Myocardium
ivory , 99
Pituitary tumours, 55

brown atrophy, 9
osteoid , 99
Pleomorphic adenoma, parotid , 23

fatty degeneration , 9
Osteomalacia, 96
Pleura

Myxoedema,57
Osteomyelitis
hyaline plaques, 22

Myxoma , left atrial, 8

chronic, 95
mesothelioma , 22

tuberculous, 95
Plummer-Vinson syndrome , 25

Nabothian cysts, 79
Osteoporosis, 95
Pneumoconiosis, 17

Nephritis, chronic interstitial, 64

Osteosarcoma , 101
Pneumonia

Nephroblastoma,69
Ostoclastoma, 100
aspiration , 14

Nephrotic syndrome, causes of, 67

Ovary
broncho- , 13, 15, 16, 21

Neurilemmoma, 93
abscess , 72
Klebsiella, 14

Neuroblastoma, 61
corpora albicantia , 72
lipid , 14

Neurofibroma, plexiform , 93
corpus luteum, 72
10':>ar,13

Neuroma, acoustic, 93
cystic follicles , 72
staphylococcal , 14

Nipple
endometriosis, 73
Polyarteritis nodosa, 10

Paget's disease , 48
torsion , 77
Polycystic disease

retraction , 47
tumours, 73-77
kidney, 62

Non-Hodgkin 's lymphoma

liver, 36

adrenal gland, 61
Paget 's disease
Polyposis coli, familial, 34

breast, 49
ofbone,98
Polyps

Burkitt 's, 52
of nipple, 48
breast, 46

hepatic involvement, 41 , 52
Pancreas
cervix, 81

intestines, 31
cysts, 44
endometrium, 79

lymph nodes, 54
tumours, 44
large bowel, 33-34

spleen , 52
Pancreatitis
stomach,27

thyroid gland , 58
acute, 43
Portal vein, thrombosis, 37

chronic, 44
Polt's disease , 95

Oesophagus
Papillary muscle, rupture of, 2, 4
Pregnancy, ectopic, 77

achalasia , 25
Parathyroid glands
Prostate gland

candidiasis, 24
hyperplasia, 58
benign hypertrophy, 86

carcinoma, 25
tumours, 58
carcinoma, 85

Mallory-Weiss tear, 24
Pelvi-ureteric junction obstruction, 70
Pulmonary

peptic ulcer, 24
Pelvis, renal, transitional cell carcinoma,
embolism , 16

stricture, 24
69
haemosiderosis, 17

varices, 25
Penis, carcinoma , 86
infarct, 17

Oilier's, disease, 100

Pericarditis
Pyelonephritis, acute, 63

Oophoritis , pyogenic , 72
constrictive, 8
Pylorus , congenital stenosis, 25

Osteitis
fibrinous, 1, 7,8
Pyonephrosis, 64

106
Pyosalpinx, 78 vulva, 82 epididymis , 85

Stomach
heart, 7, 8

Rectum
gastritis, 26, 27
intestinal , 30

tumours, 34-35
'leather-bottle ', 28
lymph nodes, 53

ulcerative colitis, 31
pyloric stenosis , 25
and meningitis , 88

Renal vein thrombosis , 65

tumours, 27-28
miliary, 16, 51

Rheumatic heart disease , 3-5

ulcers, 26-27
pulmonary , 15-16, 18

Rheumatoid arthritis , 97
Stroke , causes, 90 , 91
renal,64

Rickets, 96
Struma ovarii , 76
spinal,95

Syphilis
spleen, 51

Salivary glands, mixed tumour, 23

and aortitis, 5, 10
Tumours see sites and specific types of

Salpingitis
and general paresis, 89
tumour

acute, 72, 78
and periostitis, 95
Typhoid, small intestine, 29

chronic, 78
Syringomyelia, 87

Sarcoidosis
Ulcerative colitis, 31-32

lymph nodes, 53
Teratoma
Ureter

spleen , 51
differentiated,84
duplication of, 69

Schwannoma , benign, 93
malignant intermediate (MTI), 84
transitional cell carcinoma, 70

Seminoma, 84
malignant trophoblastic (MTT) , 84
ureteritis cystica , 70

Silicosis, 18
mature cystic, 76
Urethral valve , 71

Spermatic cord, torsion, 83

ovarian, 76
Uterus

Spinal cord, ependymoma, 92

testicular, 84
bicornuate, 79

Spine, tuberculosis, 95
Testis
cervical carcinoma, 82

Spleen
atrophy, 83, 85
cervical 'erosion ', 81

amyloidosis, 51
torsion , 83 , 84
endocervical polyp , 81

'cricket ball', 50
tumours, 83-84
tumours , 79-81

enlargement, 50, 51 , 52
Thecoma, 76
see also Endometrium

Hodgkin's disease, 52
Thrombosis

infarction , 50
coronary artery, 1
Vagina, carcinoma, 82

leukaemias and, 51-52

deep venous, 11
Ventricle,lef1

myelofibrosis, 51
portal vein , 37
aneurysms, 2

non-Hodgkin 's lymphoma, 52

Thrombus, mural, 1,2
hypertrophy, 3, 4, 6

passive venous congestion, 50

Thymoma, 54
Vulva

sarcoidosis , 51
Thyroglossal cyst, 55
Bowen'sdisease, 82

secondary carcinoma, 53
Thyroid gland
carcinoma, 82

'sugar-icing ', 50
carcinoma, 57-58

tuberculosis, 51
enlargement, classification, 55
Waterhouse--Friderichsen syndrome, 59

Splenic artery aneurysm, 12

gOitre, 56
Wilm's tumour, 69

Squamous carcinoma
Graves' disease, 56

cervix , 82
Hashimoto's disease, 56

larynx, 13
lymphoma, ?8

lung,20
myxoedema,57

oesophagus, 25
Tongue, carcinoma, 23

penis, 86
Tuberculosis

vagina, 82
adrenal gland , 59

107