Ebook Pathology for surgeons in training (3/E): Part 1

Pathology for Surgeons in Training
An A–Z Revision Text
Third Edition

Dugald L. Gardner, MD FRCP FRCPed FRCPath FRCSEd
Honorary Fellow, Department of Pathology, University of Edinburgh;
Emeritus Conservator, the Royal College of Surgeons of Edinburgh,
Emeritus Professor of Histopathology, University of Manchester
and
David E. F. Tweedle ChM FRCS FRCSEd
Consultant Surgeon, University Hospital of
South Manchester and the Christie Hospital, Manchester,
Examiner, the Royal College of Surgeons of Edinburgh

A member of the Hodder Headline Group
LONDON ● NEW YORK ● NEW DELHI


CRC Press
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This book is dedicated to Helen and to Fiona,
without whose indulgence and understanding
tolerance it could not have been completed.



CONTENTS

Foreword
Preface
Acknowledgements

vii

viii
ix

A
B
C
D
E
F
G
H
I
J
K
L
M
N
O
P
Q
R
S
T
U
V
W
X
Y
Z

1
30
73
116
123
128
136
145
164
189
195
202
225
238
250
262
284
284
287
315
334
343
354
362
362
363
v


Contents

Appendix tables
Brief biographies
Further reading
Index

vi

365
369
378
379


FOREWORD

The third edition of Pathology for Surgeons in Training indicates that the unusual format of this book has found a
real niche in the ever expanding surgical literature available to young surgeons.That it is specifically directed to
this group of doctors is important because they are faced with a wide range of pressures in their professional lives
and yet have to find the time and the stimulus to acquire knowledge rapidly.This format with its focus specifically on the knowledge required for surgical examinations set by the Royal Colleges, provides a most useful
learning and reference foundation.The previous editions of this book enjoyed considerable success and there is
no doubt the new and revised addition which has been brought thoroughly up to date but has maintained the
original style, will be equally well received.
Pathology is the foundation stone of surgical knowledge for clinical application. All subjects are extensively
cross-referenced but also include where appropriate historical notes and suggestions for further reading which
are most useful.The student is provided with the base knowledge and the opportunity to extend this as interest
or necessity dictates.The very fact that the volume does not need to be read from cover to cover but acts much
more as an anthology of Pathology only adds to its usefulness.The text is clear, well laid out and the knowledge
contained is accurate.
I commend Pathology for Surgeons in Training not only to young surgeons but to established teachers, trainers

and examiners as a certain way to ensure that they also keep their knowledge base up to date. Passing examinations is a means to an end but this revision text should not be considered simply as an examination crammer. It
serves a much wider, more useful and longer lasting function.
Professor J G Temple
President, Royal College
of Surgeons of Edinburgh

vii


PREFACE

Candidates preparing for the examinations for the diplomas of MRCS or AFRCS often feel a need for a
compact guide allowing quick and highly selective revision of Pathology. The present volume is intended to
meet this requirement. The subjects chosen include not only classical Surgical Pathology but a substantial
component of Microbiology, Haematology, Immunology, Clinical Chemistry and Blood Transfusion
as well as brief notes on such issues as Audit, Computers, Imaging and Telepathology.
This is not a textbook nor should it be read from cover-to-cover. The book has been prepared as an A to Z
guide to the knowledge demanded by College examiners. It is planned so that postgraduate students can
approach their chosen topics easily. To meet these aims, the contents, based on the syllabuses issued by the four
surgical Colleges of Great Britain and Eire, are assembled for rapid, selective reference.
There is extensive Cross-referencing so that a candidate, wishing to revise Ischaemia, for example, is advised
also to read Anoxia, Gangrene and Necrosis while an examinee, seeking rapid help with Cancer of the Colon, is
referred to Carcinogenesis, Cancer Genetics and Tumours. For the same reasons, there is a comprehensive Index,
arranged so that the major topics are clearly distinguished from those that have been given only incidental mention.
A difficulty that all recent surgical texts face is how to deal with the advances taking place in Molecular
Biology, Immunology and Genetics and other subjects dominated by highly specialised techniques, a problem compounded by the jargon used by experts in these subjects. Here, we have compromised. All surgeons in
training require to know that a susceptibility to colon and breast cancer, retinoblastoma and Wilms’ tumour,
chronic myelocytic leukaemia and xeroderma pigmentosa, may be inherited.They may be interested in the frequency of the heritable defects, the mode of inheritance and the chromosomal abnormalities that underlie some
cancers.They cannot be expected to know the exact location and designation of the mutant gene loci associated
with these tumours or even the number and location of any chromosomal defect.

The text includes 56 Tables. Further summary Tables of normal haematological and chemical values are
appended.There are 58 explanatory Diagrams selected to illuminate points of importance and difficulty.The
relevance of History to contemporary surgical practice may be denied but the authors believe that short comments on the founding fathers of Surgery and related subjects, add interest and assist candidates to place examination topics in context. Brief biographies of pioneers whose names are quoted in the text are therefore retained.
No modern work can fail to take proper account of the impact made by the Internet. Consequently, a short
note is included indicating how additional information can be obtained from Web sites.
D. L. Gardner
D. E. F. Tweedle
January 2002

viii


ACKNOWLEDGEMENTS

We owe a particular debt to Mr P. K. Datta FRCSEd, Consultant Surgeon, Caithness General Hospital, whose
long experience as an Examiner for the Royal College of Surgeons of Edinburgh has proved invaluable in
designing this Edition, and to Dr. Stephanie J. Dancer FRCPath, Department of Laboratory Medicine,Vale of
Leven District General Hospital, whose advice and guidance in this, as in the previous Edition, has enabled us to
deal with the complex problems of Clinical Microbiology.
Our colleagues, Professor T.J. Anderson FRCPath.,Western General Hospital, Edinburgh (Breast cancer); Mr
A. Bleetman FRCSEd., Birmingham Heartlands Hospital (Accident and Emergency Surgery); Dr Jan
Cullingworth, Ph.D. University of Edinburgh (Carcinogenesis); Mr. I D Gardner FRCS., Derbyshire Royal
Infirmary (Surgery); Dr T Hewson PhD, University of Edinburgh (Immunology); Dr S. J. Howell MRCP,
Christie Hospital, Manchester (Cancer studies); Dr. A. S. Krajewski FRCPath, Northampton General Hospital
(Immunology); Dr A. M. Lessells, FRCPath, Western General Hospital, Edinburgh (Biopsy diagnosis); Dr D. F.
Martin FRCP, University Hospital of South Manchester (Imaging); Mr. R. K. Tandon FRCSEd, Royal
Wolverhampton Hospital (Orthopaedics); Professor W. A. Wallace, FRCSEd., Department of Orthopaedic
Surgery, University of Nottingham (Internet), have given unstintingly of their time and energy in ensuring the
accuracy of the text.
We acknowledge the expert advice of the Departments of Haematology and of Clinical Biochemistry

(Dr S. W. Walker) of the Royal Infirmary, Edinburgh, and the guidance of the staff of the Scottish Blood
Transfusion Service.We express our thanks to Mr I. Lennox, MMAA, formerly of the Department of Medical
Illustration of the University of Edinburgh, who prepared the drawings with his customary skill and
understanding, and to Mrs S. Jones M A of the Royal College of Surgeons of Edinburgh whose critical help with
the manuscript has proved indispensable.

ix



HOW TO USE THIS BOOK
THIS IS AN A TO Z REVISION TEXT FOR
EXAMINATION CANDIDATES
IT IS FOR SIMPLE, QUICK REFERENCE, NOT FOR SYSTEMATIC READING
Using the A to Z headings and the Index, select the topic you want to revise, e.g. Embolism
READ IT
Then follow the guides to related topics.They are shown
at right of column margins in the form:
Now read Coagulation (p. 95), Thrombus (p. 320)

READ THEM
Persuade your friends to ask you questions from the book.
Check the Tables e.g. for evaluation of coagulation factors prior to surgery.
Check the Appendix.
Read the snapshot Biographies when a name is given in the text.
Learning about the history of a topic helps you to remember it.
When you have exhausted what this book tells you about a topic, look at the
Further Reading list. It will guide you to larger references on the subject.
Search the Web sites recommended by your Internet tutor.

xi



A
ABSCESS
An abscess is a localised collection of pus. Diseases
dominated by abscess formation are suppurative.

Causes
There is a wide range of causes.They include physical
and chemical injury, irritation and infection. The
necrotic tissue of malignant tumours may resemble an
abscess. Infection may be direct, indirect or bloodborne. Foreign bodies provoke abscess formation and
stitch abscesses appear within the tracks of sutures.
Abscesses form in infected surgical wounds and at
sites of injuries that penetrate skin or other lining
epithelia.

Infective agents
Every variety of extracellular, infective microorganism may cause abscess. Cutaneous abscesses
are usually due to Staphylococcus aureus. Intraabdominal abscesses are initiated by gastro-intestinal
commensals such as Klebsiella pneumoniae, Escherichia
coli, Enterobacter spp., Bacterioides spp., Proteus
spp., Clostridia spp., Streptococcus intermedius group
and Enterococcus faecalis. Aerobic micro-organisms
thrive at abscess margins but anaerobes such as
Actinomyces israelii and micro-aerophilic organisms
proliferate centrally. ‘Cold’ abscesses are caused by
Mycobacterium tuberculosis: necrotic material accumulates without signs of acute inflammation. Abscesses

attributable to protozoa, metazoa (worms) and
fungi are described on pp. 282, 356 and 135,
respectively.
Now read Bacteria (p. 30)

Structure
Abscesses form when persistent inflammation
results in the accumulation of cell and tissue debris.

An inflammatory exudate includes many dead and
some living polymorphs but, occasionally,
macrophages predominate. The causative microorganisms, parasites or foreign bodies can often be
recognised within the pus. Some may survive inside
or outside phagocytic cells (p. 225, 270) in spite of
antibiotic treatment.
The contents of an abscess may be fluid, semi-fluid,
caseous or granular.The appearances are much influenced by the nature of the causal organism.
Tuberculous pus, for example, appears like cream
cheese and is caseous. Amoebic pus resembles
orange–brown anchovy sauce. Staphylococcal pus is
yellow, thick and viscous. Haemolytic streptococcal
pus is thin, watery and blood-stained while the pus in
Pseudomonas aeruginosa infections is green. Pus resulting from anaerobic infection is thin and often foulsmelling.
Pyogenic abscesses are common in the skin, subcutaneous tissues, mouth, peritoneal cavity and anorectal tissues. Perinephric, pelvic and subphrenic
abscesses are also frequent. Those that derive from
blood-borne infection are most frequent in the brain
(p. 63), liver (p. 210), lung (p. 217) and bone (p. 54).
Less commonly, abscesses develop in the pancreas and
fallopian tubes.

Behaviour
Abscesses swell as the large molecules liberated by
tissue destruction attract water by osmosis.
Extension of the lesion, continued irritation and
the persistence of infection contribute to the disorganisation and death of increasing numbers of cells.
Their proteins are denatured. Overlying tissue dies.
Abscesses ‘point’ and rupture through epithelial surfaces. Without this escape or effective surgical treatment, they resolve slowly. Granulation tissue forms
a surrounding, pyogenic membrane. Finally, fibrosis
leads to encapsulation and even to dystrophic calcification.
1


Acquired Immunodeficiency Syndrome (AIDS)

ACQUIRED
IMMUNODEFICIENCY
SYNDROME (AIDS)
AIDS (Acquired ImmunoDeficiency Syndrome) is a
generalised disorder of immunity. It is caused by a
human immunodeficiency virus (HIV).
The syndrome of AIDS is a growing, worldwide,
health problem. The greatest number of cases is
encountered in Africa. Here, more than 25% of some
populations is infected. In South Africa, where there
are 4 ¥ 106 cases, the incidence of new cases is
~1600/day.

Prevention is complicated.Antibody tests occasionally yield false-negative results because of delay in
antibody formation, so-called ‘seroconversion’.
Occupational exposure rarely leads to infection in

doctors, dentists and other health workers (p. 159).
● Transplacental infection. Intra-uterine infection
of the fetus may occur.
● Neonatal infection. Blood, amniotic fluid and
breast milk convey the virus. Maternal IgM antibodies cross the placenta so that serological tests in
the neonate are ambiguous.

Immunological changes
Cell-mediated

Causes
The HIV are retroviruses that infect the lymphocytes, macrophages and monocytes of body fluids. In
North America, Europe and sub-Saharan and
Central Africa the agent is HIV-1. In West Africa, a
second strain, HIV-2, is found. Helper T lymphocytes (p. 173) are destroyed. The loss of these T-cells
accounts for most features of the syndrome.
Macrophages and monocytes remain virus reservoirs
and HIV binds to the cells of the intestinal tract and
central nervous system.
Now read Retroviruses (p. 350)

Transmission
The human immunodeficiency viruses are transmitted by venereal contact or parenterally, before or after
birth. In Western countries, the infection is common
among homosexual adults and intravenous drug
abusers; in Africa, Latin America and the Caribbean,
heterosexual adults and infants are implicated; in Asia,
India, Eastern Europe and the Pacific rim, heterosexual and homosexual adults and drug abusers are the
common targets.
● Venereal infection. This mode of transmission is

principally by anal intercourse among homosexual
and bisexual adults; the virus is conveyed in seminal
lymphocytes. Heterosexual infection is becoming
more frequent in Europe as are other sexually
related diseases.
● Parenteral infection. This mode of transmission
is commonplace in addicts who inject drugs intravenously. It may also afflict haemophiliacs given
factor VIII from contaminated, pooled plasma.
2

Failure of cell-mediated immunity caused by the
destruction of T-helper (Th) lymphocytes is the
key to understanding AIDS.
Now read Immunity (p. 171), Lymphocytes (p. 206)

HI virus envelopes bind to lymphocyte surface receptors, allowing virus particles to enter the cells (Figs 1
and 56). Within the lymphocytes, a viral enzyme,
reverse transcriptase, writes (‘transcribes’) viral RNA
onto lymphocyte DNA, conveying information
about the structure of the virus to the host. The
altered host DNA is integrated into the lymphocyte
genome. However, HIV may remain in infected lymphocytes, unintegrated and dormant.When these cells
are activated, often by coincidental infections such as
cytomegalovirus (CMV), hepatitis B virus (HBV),
Epstein–Barr virus (EBV) or a herpes virus, HIV
replicates and kills them.
As AIDS progresses, there is a therefore a fall in
the number of CD4 lymphocytes. As a result, Tcells no longer proliferate in response to other bacterial and viral antigens and cell-mediated immune
reactions are progressively impaired. Diminished
natural killer (NK) cell activity (p. 231) is also

observed.

Antibody-mediated
In response to HIV, all infected persons form antiHIV antibodies (p. 19). The antibodies may appear
within days of exposure to the virus but the response
can be delayed for as long as 6 months.Antibodies are
against the HIV envelope glycoprotein that provokes
polyclonal B-cell activity. Detecting anti-HIV


Acquired Immunodeficiency Syndrome (AIDS)

Impaired
(C) immune
response

Macrophage

HIV

Uncontrolled
latent virus
CD
4
(B)

(F)
Clinical
AIDS

(A)

Th-cell

Good early
Tc-cell response

Passage of time

CD
8

Tc-cell
response
reduces
viraemia

(D)
Infection
not
eliminated

Virus
persists:
CD
cells
decrease

(E)

Tc-cell

Figure 1 Pathogenesis of Acquired Immunodeficiency Syndrome (AIDS).
(A) CD8 T cytotoxic/cytolytic lymphocytes (Tc-cells) respond early and positively to HIV infection. Antivirus antibodies
are also formed and viraemia lessens. (B) However, there is simultaneous destruction of T helper (CD4) lymphocytes (Thcells) and virus gains entry to them causing (C) a failure of the cell-mediated immune response and (D) progressive inability to eliminate HIV. Virus persists (E) and patient remains permanently infectious. Eventually, impaired immunity provides
opportunity for onset (F) of life-threatening opportunistic viral, bacterial or protozoal infections.

After a latent period that may be very long, secondary,
opportunistic infection or cancer often progress
rapidly, leading to death.

are also frequent. AIDS may encourage molluscum
contagiosum and anogenital condylomata.
Many central nervous system and lung disorders are
due to opportunistic infection.They include streptococcal, staphylococcal and Haemophilus infections.
Oral candidiasis and hairy cell leukoplakia occur, the
latter attributable to Epstein–Barr virus. Oesophageal
ulceration due to Candida, cytomegalovirus and
Herpes virus accompany diarrhoea, malabsorption,
anorectal ulceration and proctitis.

Opportunistic infection

Tumours

Impaired immunity encourages opportunistic infection by viral, bacterial, protozoal and parasitic
agents. Many of these organisms are not normally
pathogenic. The most frequent are cytomegalovirus,
Mycobacterium tuberculosis, and Pneumocystis carinii.
herpes simplex and herpes zoster infections

AIDS is often complicated by cancer. Kaposi’s sarcoma (p. 49) is the most common malignant tumour.
Squamous carcinoma of the mouth and cloacogenic
anorectal carcinoma are unusually frequent and
oesophageal carcinoma in-situ is encountered. The
frequency of extranodal, B-cell non-Hodgkin’s

antibodies clinically allows infection to be confirmed
but does not prove conclusively that the full syndrome
will develop. Later, with the onset and increased
severity of disease, antibody levels fall.

Structure

3


Acquired Immunodeficiency Syndrome (AIDS)

lymphoma (p. 223) is raised. Multiple myeloma may
develop and brain cancer is increasingly common.
Now read Kaposi’s sarcoma (p. 49)

Regional disease
Persistent generalised lymphadenopathy is the result
of massive viral replication.The lymph nodes may be
the site of bacillary angiomatosis (p. 222). Brain atrophy is associated with late, advancing immunosuppression. If intravenous drug abuse is continued,
embolic infection and endocarditis often occur.When
hepatitis B or syphilis co-exist, their effects are potentiated by HIV. Liver granulomas are due to mycobacteria.

Behaviour and prognosis
The clinical signs of infection at first resemble glandular fever.There is then a latent period that may be
as long as 10 years. Prognosis in AIDS is related to the
number of viral particles in the circulating plasma.
Transmission is rare from persons with levels of less
than 1500 viral copies of HIV-1/mL serum. Many
antiviral drugs (Table 6) are available. They may be
given alone or in double or triple combination.They
slow the progression of HIV and AIDS but there is
not yet any single drug that can effect a cure.
Now read Antiviral agents (p. 23)

Intensive HIV retroviral therapy has led to a decline
in the morbidity of AIDS and the frequency of perinatal infection has been reduced. That immunity can
be acquired has been suggested by recent studies of prostitutes in an African population.Vaccines are therefore
under trial but none offers certain protection.There are
separate treatments for the common bacterial,viral,fungal and parasitic infections that complicate AIDS.In the
absence of treatment, death is the inevitable outcome.
Male circumcision offers some protection.

HIV AND SURGERY
Virus is present in all body fluids. Surgeons and nurses
are exposed whenever they operate on seropositive
cases, and patients are at risk when examined or cared
for by seropositive surgeons or health workers. Blood
and blood products that have not been screened for
virus must be avoided.
4

Patients as a threat to hospital staff

Great care is needed in the management of patients
who have been exposed to HIV, whether seropositive
or not.There is no entirely reliable drug for the treatment of staff who have been exposed. However, the
overall risk to surgeons of acquiring needle-stick and
other sharp instrument injury is relatively small,
occurring in ~0.4% of operations. Saliva is of low
infectivity.
Now read Needle stick injury (p. 362)

All HIV-positive patients are assumed to be
infectious. Theatre procedures must be scrupulous.
One theatre is selected for high-risk cases.
Anaesthesia is induced in theatre. The anaesthetist
wears protective clothing. All body fluids may contain virus so glasses, goggles and masks are worn.
Impenetrable gowns and drapes are used. The risk
of glove penetration during surgery (p. 142) varies
according to the type and length of operation but
may be as high as 30%. ‘Double-gloving’ (p. 143) is
advisable. Occasionally, the use of steel-mail gloves
is recommended. Instruments are passed only in
containers, but disposable instruments may be
adopted. Staples and diathermy are preferred to
sutures. The increasing use of closed drainage
systems has lessened the risk.
After an operation, gowns, shoes and gloves are discarded in reverse order and all instruments placed in a
bag for return to the central sterilising unit.
Endoscopic instruments are freed from virus by
cleaning in detergent, followed by a minimum of 4
minutes exposure to 2% gluteraldehyde. For endoscopic retrograde cholangiopancreatography (ERCP)
and colonoscopy, 10 minutes exposure to gluteraldehyde between all cases, is recommended. However,

the elimination of coincidental hepatitis B virus and
Cryptosporidium requires at least 30 minutes treatment and Mycobacterium tuberculosis 60 minutes. In
cases of injury from high risk donors, individuals are
expected to complete a 6 week course of prophylactic
chemotherapy.
Now read Disinfection (p. 118), Sterilisation (p. 304)

Surgeons as a threat to patients
There is a small risk that surgical and dental
patients may acquire HIV from hospital staff. The


Adrenal Glands

probability of transmitting HIV by needle-stick
injury is ~0.14%. A doctor or nurse discovered to
be HIV-positive is required by English law to
report to the hospital manager and to colleagues
and is banned from undertaking further invasive
procedures.

ACTINOMYCOSIS
Actinomycosis is a bacterial disease caused by a variety of Gram-positive anaerobic or micro-aerophilic
rods from the genus Actinomyces.

Causes
The species implicated in the majority of human
infections is Actinomyces israelii. Many actinomycotic infections are, however, polymicrobial.
Organisms such as Actinobacilli, Bacteroides spp.,
Staphylococcus spp. and Streptococcus spp. can be

isolated in varying combinations, depending upon
the site of infection.

on a microscope slide, these aggregates of microorganisms stain to show characteristic Gram-positive branching bacilli. Their isolation from a site
other than the tonsils implies a pathological state.
Surgical incision and drainage is still advocated
despite the advent of efficacious antimicrobial therapy. Long-term intravenous treatment with penicillin followed by oral antibiotics (p. 17) cures
extensive disease.

Nocardiosis
Nocardiosis has many features in common with actinomycosis. The infection is caused by the aerobic
organism, Nocardia asteroides.

ADRENAL GLANDS
Each of the paired adrenal (suprarenal) glands comprises a cortex and a medulla. Although contiguous,
these components function as separate organs.

Structure
Actinomycosis begins with a disruption of the
mucosal barrier. Oral and cervico-facial infections
develop after dental procedures or trauma.
Pulmonary lesions follow aspiration (p. 217).
Abdominal disease succeeds the surgical treatment
of appendicitis or the ingestion of foreign bodies
such as fishbones. Pelvic actinomycosis is associated with neglected intra-uterine contraceptive
devices.
The lesions of actinomycosis are deep-seated, indolent and destructive. An acute inflammatory phase is
soon superseded by a chronic reaction. Single or multiple indurated swellings develop and eventually suppurate centrally to yield abscesses that are often
followed by sinus formation. Actinomyces israelii proliferates in the centre of the abscess. Fibrotic walls surround the lesions and sinus tracts close and re-form
spontaneously.The rupture of a liver abscess through

the diaphragm into the pleural cavity is one mechanism of spread.

Behaviour and prognosis
The diagnosis of actinomycosis rests upon the
identification of sulphur granules in pus: crushed

Biopsy diagnosis of adrenal disease
Many adrenal diseases can be diagnosed by high resolution CT and MRI, and by isotopic scanning.
Nodules as small as 5.0 mm in diameter can be
detected. Fine needle aspiration under radiological
guidance can sometimes be performed. The identity
of functioning tumours is confirmed by adrenal vein
catheterisation when blood and urine are collected
for analysis.

ADRENAL CORTEX
The adrenal cortex has three zones, each secreting a
distinct population of steroid hormones (corticosteroids). An outer zona glomerulosa synthesises
mineralocorticoids, an intermediate zona fasiculata
secretes glucocorticoids and an inner zona reticularis liberates weak adrenal androgens. The cortex is
also a source of oestrogens.The synthesis of corticosteroids from adrenal or plasma cholesterol begins in
the mitochondria of the cortical cells.
Now read Endocrine system (p. 126)

5


Adrenal Glands

Cortisol

The most important corticosteroid in man is cortisol
(hydrocortisone).This hormone comprises half of the
total steroid production by the adrenal cortex. Cortisol
stimulates gluconeogenesis from glycogen and from
protein, raising the blood glucose concentration. It also
promotes the renal retention of sodium and the loss of
potassium but much less effectively than aldosterone.
Cortisol modulates the correction of fluid imbalance
in dehydration and the intracellular over-hydration of
adrenocortical insufficiency. It facilitates the vasoconstrictive effects of catecholamines on arterioles, leading
to an increase in systemic blood pressure.Erythropoiesis
with leucocytosis and eosinophilia are stimulated.
Lymphoid tissue atrophies. Antibody production falls
and allergic responses are diminished.There is a reduction in the severity of inflammatory reactions and in
the speed and adequacy of wound healing. In shock
(p. 290), cortisol can stabilise lysosomal membranes if it
is given before any further damaging stimulus.
The secretion of cortisol is modulated by adrenocorticotrophic hormone (ACTH - corticotrophin), a
39-amino acid polypeptide released from the corticotrophic cells of the anterior pituitary gland. In turn,
these pituitary cells are regulated by a corticotrophinreleasing hormone (CRH) that passes to the anterior
pituitary gland from the hypothalamus.

Aldosterone
Aldosterone increases renal tubular Na+ re-absorption
and K+ and H+ excretion. Comparable effects are
recognised in the ileum and colon and the loss of Na+
in sweat and saliva is diminished.
Aldosterone secretion is regulated by the reninangiotensin system (p. 201). In response to lowered
renal arteriolar blood pressure, juxtaglomerular cells
liberate the enzyme renin which converts the prohormone protein angiotensinogen to angiotensin I.

Angiotensin-converting enzyme (ACE) abbreviates
this decapeptide to active angiotensin II. This molecule is an octapeptide acting directly upon the cells of
the zona glomerulosa. It stimulates aldosterone secretion the release of which is influenced by potassium
and by sodium.

Androgens
The principal androgen secreted by the adrenal cortex
is dehydro-epi-androsterone (DHEA) but smaller
6

amounts of androstenedione and testosterone are also
liberated.

Adrenal cortical hyperfunction
Three syndromes of excess adrenal cortical activity
(hyperadrenocorticalism) correspond to the three
main classes of corticosteroid: Cushing’s syndrome
(excess glucocorticoid), Conn’s syndrome (excess
mineralocorticoid), and the adrenogenital syndromes
(excess androgen).

Cushing’s syndrome
Cushing’s syndrome is encountered more often in
women than men. Moon face, virilisation and the
abnormal deposition of fat in sites such as the back of
the neck attract attention and the individual may be
described as resembling a ‘lemon on a stick’.There is
a proximal myopathy with muscle atrophy, abdominal
striae and osteoporosis. Hypertension is characteristic.
Abnormal collagen metabolism and maturation result

in defective wound healing.The lowered glucose tolerance simulates diabetes mellitus.
The causes of excess glucocorticoid secretion are:
● Cushing’s disease (p. 273).
● A functioning tumour of the adrenal cortex
(p. 247). There is depressed ACTH secretion and
atrophy of the remaining, normal adrenal tissue.
● The secretion of corticotrophin-releasing factor
(CRF) from an ectopic source such as small cell
bronchogenic carcinoma, islet cell tumour of the
pancreas or thymic carcinoid tumour. Adrenal cortical hyperplasia may be extreme.
Changes closely similar to Cushing’s syndrome are
caused by therapeutic corticosteroid treatment when
the bodily changes are said to be ‘cushingoid’

Hyperaldosteronism
Excess aldosterone enhances sodium retention and
potassium excretion. There is systemic hypertension
but usually no dependent oedema. The muscles
become weak and there may be flaccid paralysis.
Hyperaldosteronism may be primary or secondary.
Conn’s syndrome is primary hyperaldosteronism.
It is usually caused by an adenoma of the adrenal cortex. However, the syndrome may be due to unilateral
or bilateral adrenal cortical hyperplasia or, rarely, to
primary adrenal cortical carcinoma.
Inappropriate secretion of excess aldosterone may


Adrenal Glands

be secondary to cardiac failure or hepatic cirrhosis.

The secretion of aldosterone is increased following
injury or operation. The magnitude and duration of
this increase are proportional to the severity of the
accident or procedure; they are exaggerated if there
are postoperative complications, particularly local or
systemic sepsis. Secondary hyperaldosteronism may
also be a consequence of increased secretion of renin
from a kidney affected by renal artery stenosis or from
a renin-secreting renal tumour. It is a component of
Cushing’s syndrome.

non-functional tumours are usually malignant as are
those secreting androgens.

Benign

Adenoma
Adenomas are formed of clear or of compact cells,
resembling those of the zona fasciculata and zona
reticularis, respectively. Those that are functional
secrete cortisol, aldosterone or sex steroids.

Malignant

Adrenogenital syndrome

Carcinoma

This rare disorder is attributable to a functioning
tumour of cortical cells. It may also be due to an

inherited disorder of steroid synthesis, the most frequent of which is 21-hydroxylase deficiency.
Virilisation is one result.

Carcinoma is distinguished from adenoma with difficulty.
Indeed,the malignant behaviour of the neoplastic cells may
not be suspected until metastases have been recognised.

Adrenal cortical hypofunction

The secretions of the adrenal medulla exercise a less
critical influence on surgical homeostasis than those
of the cortex but they occupy central roles in
responses to stress (p. 313) and sepsis (p. 178).

Glucocorticoid hypofunction (hypo-adrenocorticalism) may be acute or chronic.

Acute
This uncommon disorder is exemplified by the
haemorrhagic adrenal cortical necrosis of the
Waterhouse–Friderichsen syndrome, a complication
of meningococcal bacteraemia. It is also an occasional
feature of other septicaemic or bacteriaemic states in
which endotoxic shock is contributory.A closely similar condition of haemorrhagic adrenal infarction may
follow episodes of hypotension during major abdominal surgery. Clinical signs include the acute onset of
vomiting with resultant dehydration, hyponatraemia,
hyperkalaemia, hypoglycaemia and hypotension.

Chronic (Addison’s disease)
Chronic insufficiency is usually attributable to autoimmune adrenalitis (p. 28) but may be due to metastatic carcinoma.Tuberculosis is another cause.

Tumours
The adrenal cortex is a frequent site for metastases
from carcinoma of the bronchus, breast, stomach, kidney and other sources.
Primary adrenal cortical tumours are uncommon.
They may be functional or non-functional. Large,

ADRENAL MEDULLA

Tumours
Metastases from common primary sites, such as the
bronchus, are frequent. Primary tumours are very
uncommon.

Benign

Phaeochromocytoma
This is a rare tumour of the chromaffin cells of the
adrenal medulla or of the extra-adrenal chromaffin
cells of the organ of Zuckerkändl.The tumour may
be bilateral and is occasionally part of a multiple
endocrine neoplasia 2 (MEN 2) syndrome.
Phaeochromocytomas are usually but not always
benign. The neoplastic cells secrete the catecholamines, adrenaline and noradrenaline, as well as
inappropriate hormones that include ACTH and
vaso-intestinal polypeptide (VIP). The tumour is
usually associated with hypertension and hyperglycaemia. Diagnosis is confirmed by the detection of
high levels of vanillyl mandelic acid (VMA) in urinary samples collected over 24 hours. VMA is a
metabolite of the catecholamines.
Now read Multiple endocrine neoplasia (p. 126)

7


Adrenal Glands

Myelolipoma
Myelolipoma is a name for the uncommon finding of
an island of haemopoietic and adipose tissue within
the adrenal medulla.

Ganglioneuroma and neurofibroma
These are occasional benign tumours of the adrenal
medulla and of the organ of Zuckerkändl.

Malignant

Neuroblastoma
This malignant tumour accounts for ~15% of cancer
deaths in children.Although neuroblastoma may originate in any part of the sympathetic nervous system,
the majority are intra-abdominal. Half of these
tumours derive from the adrenal medulla.There may
be a selective distribution of metastases so that those
from a left adrenal tumour pass to the lung, those from
a right-sided tumour to the liver. Chromosomal and
genetic analyses (p. 91) assist prognosis.

AGEING
Ageing is the process of growing old. It is the aggregate of the degenerative changes in cells, tissues and
organs that decides the life span. Age changes are
both intrinsic and extrinsic.Together, they result in a

decreased capacity to respond to environmental
stress. They therefore exercise a significant influence
on the results of surgery.

Intrinsic changes
There is a failure to replace effete cells in numbers
sufficient to maintain normal tissue function and a
time-dependent, irreversible deterioration in cell
structure. Cells have a finite life span. Although
clones of cells that appear ‘immortal’ can be
selected in the laboratory, this is not the natural
condition. Normally, cultured cells are restricted by
a ‘Hayflick limit’ to a sequence of 48 divisions, after
which death occurs. One explanation is that there
is a continual accumulation of genetic errors on
the basis of somatic mutation: the errors that occur
invariably in DNA replication (p. 140) are not
wholly repaired. A further view invokes programmed ageing, apoptosis (p. 89).
In progeria, premature ageing, there are many
fewer cell divisions than normal before cell death.
8

Extrinsic changes
Another explanation for the changes of ageing is the
gradual aggregation of free radical damage, the
‘cumulative error’ hypothesis. Such injury is caused,
for example, by ionising radiation or by failed antioxidant defence mechanisms. Free radicals (p. 133)
can lead to mitochondrial and nuclear DNA damage.
Cells affected in this way cannot repair DNA. They
form insoluble material like lipofuscin in heart muscle

and secrete inadequate amounts of endocrine and
paracrine molecules.A second, extrinsic cause may be
the modification of tissue proteins by the accumulation of products such as those of glycosylation that
cross-link and inactivate adjacent proteins.

AGEING AND SURGERY
Surgery is greatly influenced by problems created
by the processes of ageing and by the altered
responses of senescent tissues to disease. The aged
are susceptible to cancer and atheroma. Morbidity
and mortality are increased by comparison with
younger individuals. Amyloid (p. 9) accumulates and
osteoporosis is commonplace.
In operative surgery, the most common difficulties
are nutritional and metabolic. Old persons are prone
to protein malnutrition and often suffer from deficiencies of vitamins A, B and D. They are frequently
anaemic. In the face of large changes in blood pressure
and tissue perfusion, myocardial ischaemia may culminate in infarction.
Postoperatively, deep vein thrombosis and
embolism are constant threats. Skeletal muscle atrophy
prejudices survival. Immobility encourages thrombosis. It also diminishes respiratory movements and facilitates bronchopneumonia. Senescent tissues may be
incapable of mounting normal defence reactions
against infection. Respiratory capacity is limited.
There is an impairment of renal function and inadequate urinary concentration. Cerebral function is
often altered and episodes of hypotension may precipitate cerebral infarction.

AMOEBIASIS
Amoebiasis is a colonic infection caused by the
intestinal protozoon, Entamoeba histolytica.

Amyloid

Cause

OTHER AMOEBAE

The disease follows faecal contamination of food or
water but flies can convey amoebic cysts to foodstuffs.
There is also a well-recognised risk of transmission
between homosexual males: amoebiasis is a cause of
diarrhoea in patients with AIDS. After ingestion, the
vegetative amoebae that evolve may live for long periods in the gut without invading this tissue. Dysentery
results when invasion begins. Infection may spread to
the liver by the portal vein and ultimately to the lung
and brain. Amoebic liver abscess is a common sequel;
it is much more frequent in males than females.
Abscess is usually single.
In diagnosis, free E. histolytica are sought in specimens of fresh, warm stool. However, they are often
not detectable. To allow identification of the organism, secretions or biopsy specimens are stained by the
periodic-acid/Schiff (PAS) method. Serological confirmation of diagnosis is sought by applying an
enzyme-linked immunosorbent assay (ELISA) to the
sample but indirect haemagglutination and polymerase chain reactions (p. 139) can also be used.The
diagnosis of liver abscess is assisted by ultrasonic and
CT scans, ultrasonically guided needle aspiration and
serum haemagglutination tests.

Structure
Characteristic transverse ulcers with overhanging
edges form in the wall of the colon (Fig. 53d, p. 334).

They may be confused with those of Crohn’s disease
or ulcerative colitis. However, biopsy reveals unicellular amoebae with four small, darkly staining nuclei.
Amoebic abscesses, such as those that frequently
develop in the liver, contain orange–red pus resembling ‘anchovy sauce’. Unlike other hepatic abscesses
(p. 210), those of amoebiasis do not possess a welldeveloped pyogenic membrane although they are
bounded by a thin wall of granulation tissue. Abscess
formation may also occur in the lung and brain.
Now read Abscess (p. 1)

Behaviour and prognosis
Amoebic abscesses may rupture into the pleural, pericardial or peritoneal cavities. Unusual or rare complications of amoebiasis include toxic dilatation of the
colon; perforation; and the formation of an amoeboma the appearances of which can be mistaken for
those of cancer.

Acanthamoeba spp. can cause disseminated infection
in immunocompromised individuals, for example
after renal transplantation. Free-living amoebae such
as Naegleria fowleri have been found in freshwater baths
and tanks.This organism is capable of causing meningitis and can harbour Legionella pneumophila (p. 216).

AMYLOID
Amyloids are insoluble glycoproteins that cause organ
failure when laid down in excess.The disorder caused
by this process is amyloidosis (b-fibrillosis).
The amyloids are chemically distinct but have
identical physical properties. Each molecule consists
of an individual protein molecule and a smaller antigenic P-substance that is common to all the amyloids.
The amyloids are divided into categories according to
the chemical structure of the individual proteins.
All amyloids have a molecular arrangement

described as a folded, beta-pleated sheet. This means
that the dyes used in staining amyloid are incorporated in a similar laminar fashion between the sheets
of the protein, giving a doubly refractile appearance
when viewed with plane-polarised light. Congo red is
one of the stains most commonly employed to identify amyloid: the red-stained material is seen in
polarised light to be apple green, not red.

AMYLOIDOSIS
Excessive deposition of amyloids in tissues is amyloidosis (Table 1). When a cause for amyloidosis can be
demonstrated, the condition is secondary.When no
demonstrable cause can be found, the term idiopathic
or primary amyloidosis is used. In Western countries,
the commonest cause of secondary amyloidosis is
rheumatoid arthritis but the disorder is also encountered in other chronic inflammatory conditions,
bronchiectasis and chronic osteomyelitis. In less
privileged countries, the chronic inflammatory causes
of amyloidosis include tuberculosis and leprosy.

Biopsy diagnosis
In systemic amyloidosis, needle biopsy of the rectal
mucosa or the kidney establishes the diagnosis.
9


Amyloid
Table 1 Types of amyloid of significance in surgery
Type of amyloid

Characteristics

Amyloid A (AA)

Deposited in blood vessel walls in chronic inflammatory diseases such as rheumatoid arthritis
(p. 191) and Crohn’s disease (p. 165)

Amyloid L (AL)

Laid down during the development of some immunocytic diseases and in plasma cell
myeloma (p. 237).The material is an aggregate of Ig light chains or fragments of them

Amyloid b2-microglobulin
(Ab2M)

Accumulates in selected sites such as bone and carpal tunnel connective tissue after longterm renal dialysis using membranes of low permeability. In sporadic cerebral amyloid
angiopathy the amyloid is b4 peptide. It is found around blood vessels and in nearby giant
cells

Amyloid calcitonin (ACAL)
and amyloid intestinal
vaso-active polypeptide
(AVAPP)

Molecules that accumulate locally at sites of functioning endocrine tumours (p. 126, 247)

Autopsy diagnosis
With time, the spleen, kidneys, liver and other viscera
become enlarged and pale. Iodine gives affected tissues a mahogany brown colour that resists decolorisation with sulphuric acid.

ANAEMIA
Anaemia is a reduction below normal (Appendix

Table) in the concentration of haemoglobin in the
circulating blood. However, account must be taken of
the age, sex and race of an individual before measurements such as haemoglobin concentration become
meaningful.
In anaemia, there is a diminution in the number
of circulating red blood cells; in the concentration
of haemoglobin in each cell; or in both. When the
red blood cells retain their normal size, the anaemia
is normocytic. An increase in red cell size is
macrocytosis, a decrease microcytosis. When the
haemoglobin concentration within the cell is
raised, the term hyperchromasia is used. The converse condition is hypochromasia.
There are three main classes of anaemia: dyserythropoietic, haemolytic and haemorrhagic.

DYSERYTHROPOIETIC (DYSHAEMOPOIETIC)
ANAEMIA
Dyserythropoiesis indicates a defect in the formation
of haemoglobin.
10

Iron deficiency anaemia, usually microcytic
and hypochromic, is commonplace in countries
where parasitic disease and malnutrition are rife. It
affects 30% of the world’s population. However,
there is a lower prevalence among those cooking in
iron utensils. Iron deficiency anaemia is still surprisingly frequent in the UK and is often recognised in patients admitted for surgery. It is
attributable to insidious blood loss and the escape
of 10–20 mL/day soon results in a negative iron
balance and the depletion of iron stores. Iron
deficiency anaemia is characteristic of the

Plummer–Vinson syndrome (p. 257, 375).
Now read Iron (p. 271)

Megaloblastic anaemia is a particular form of
dyshaemopoiesis. It is common in vegans in whom
it may lead to blindness. There is a defect both in
the numbers and in the maturation of red blood
cells due to a deficiency of cyanocobalamin (vitamin B12, p. 352). Megaloblasts are large, haemoglobinised, red blood cells that retain an immature
nucleus. There is an imbalance between nuclear
and cytoplasmic maturation. In diseases of the
proximal part of the small intestine, such as multiple diverticulosis, a blind loop syndrome with a
change in gut flora leads both to iron deficiency
and to megaloblastosis. Megaloblastic anaemia is
also common after resection of the distal part of
the small intestine. There is defective vitamin B12
absorption.


Anal Canal

HAEMOLYTIC ANAEMIA
In haemolytic anaemia, there is excessive red blood
cell destruction (p. 301). There are genetic and
acquired causes. Hereditary spherocytosis is an example of the former, malaria of the latter. Micro-angiopathic haemolytic anaemia is described on p. 100.

Auto-immune haemolytic anaemia
In auto-immune haemolytic anaemia, anti-red blood
cell auto-antibodies are formed.
Antibody binding is usually optimal at 37°C. The
anaemia is of a ‘warm antibody type’. Occasionally,

antibody binds to the red cells best at low temperature; the anaemia is then of a ‘cold antibody type’.
Auto-immune haemolytic anaemia may complicate
systemic lupus erythematosus (p. 29) or lymphoma
(p. 223) and can be provoked by mycoplasmal
pneumonia and by viral infections. In a further category, anaemia becomes severe in cold weather.

Iso-immune haemolytic anaemia
Iso-immune haemolytic anaemia is exemplified by
haemolytic disease of the newborn (p. 46).
The red blood cells of a fetus may bear antigens,such
as those of the Rhesus blood groups (p. 46), distinct
from those of the mother. Some fetal red blood cells
invariably cross the placental barrier,entering the maternal circulation. If anti-fetal red blood cell antibodies are
then formed by the mother, they may pass back across
the placenta.Entering the fetal circulation,they bind to
fetal red blood cells and lead to haemolysis.

HAEMORRHAGIC ANAEMIA
Haemorrhagic anaemia is caused by acute or chronic
blood loss for example in menorrhagia or in the presence of haemorrhoids (p. 12).
Now read Blood loss (p. 42)

OTHER FORMS OF ANAEMIA
Particular forms of anaemia accompany liver disease
(macrocytic), renal failure and rheumatoid arthritis
(hypochromic, normocytic), and pregnancy (hypochromic, normocytic or macrocytic).

Leuco-erythroblastic anaemia
In this condition, immature red and white blood cells
and their precursors appear in the circulating blood.

The cause is usually the presence of extensive
metastatic tumour deposits in the bone marrow.

ANAL CANAL
The anal canal (Fig. 2a) is the distal end of the intestine. Most of the upper third of the anal canal is lined
by large bowel mucosa. The middle third, the transitional zone, is lined mainly by transitional epithelium.
The lower part is lined solely by squamous epithelium
but unlike the skin of the peri-anal region, is devoid
of hair follicles, sweat glands and sebaceous glands.
These histological distinctions, originating embryologically, ensure that there are significant differences
in the pathological responses of the various parts.

Biopsy diagnosis of anal disease
Anal disease outwith the canal may be apparent naked
eye or at proctoscopy.Fungal infections can be diagnosed
by the microscopy of cell scrapings.Anal warts are excised
under local anaesthesia,but samples of suspected tumours
are obtained under general anaesthesia.

DEVELOPMENTAL AND CONGENITAL
DISORDERS
● If there is defective development of the anal canal
above the levator ani muscle, there is no anal
sphincter. In males the rectum usually opens into
the urethra, in females into the posterior vagina.
The lack of a sphincter results in incontinence.
● When there is anomalous development of the midpart of the anal canal,there is an imperforate anal membrane,the rupture of which may lead to fibrous stenosis.
● Defects of the lower part of the anal canal, below
the levator ani muscle, result in the opening of the
anal canal onto the surface of the vulva or perineum,

effectively constituting an ectopic anus.An opening
below the levator ani muscle maintains continence.

Fissure
Anal fissure is a vertical, slit-like ulcer in the epithelium
of the lower part of the canal.The majority of fissures
11


Anal Canal

occurs posteriorly, in a position designated 6 o’clock. In
time, a so-called sentinel skin tag develops at the outer
end of the fissure.The anal papilla at the inner end may
hypertrophy, with the development of a fibrous polyp.
Most fissures have no obvious cause although patients
are usually constipated. Fissures are more common in
parous than in nulliparous women and may be sited anteriorly (‘12 o’clock’). Fissures are particularly common
in Crohn’s disease, less frequent in ulcerative colitis.

Rectum
Large intestinal
epithelium
Transitional
epithelium
Squamous
epithelium
Anal skin

Haemorrhoids

Haemorrhoids are the dilated vascular spaces of the
mucosa and skin of the anal canal.The spaces develop
from naturally-occurring fusiform and saccular dilatations of the arteriovenous plexus that lies beneath the
anal epithelium. The plexuses form cushions that aid
continence. Haemorrhoids are a consequence of prolapse of these cushions due to episodic, increased pressure within the anal canal.They are more common in
individuals who consume a typical low-fibre Western
diet, particularly in those who are constipated and
strain at stool.
● Internal haemorrhoids arise in the upper
two thirds of the anus and are lined by columnar epithelium with an intestinal sensory innervation.
● External haemorrhoids are a late manifestation
of internal haemorrhoids but can arise de novo.
They are lined by modified squamous epithelium
with a cutaneous innervation and are often exquisitely painful, particularly if haemorrhage produces
a peri-anal haematoma. Thrombosis then occurs.
In the absence of surgical intervention, the superficial component shrivels to become a painless
skin tag.

INFECTION AND INFLAMMATION
Abscess
Anorectal abscesses are very common.They are classified anatomically (Fig. 2b) as peri-anal, ischiorectal,
submucosal, intersphincteric or pelvirectal.
Peri-anal abscesses and other septic phenomena are
common in patients suffering from AIDS. Anorectal
sepsis is also frequent in patients with Crohn’s disease.
However, there is usually no demonstrable cause and
it is assumed that abscess develops from a focus of
infection in an anal gland, between the internal and
12

Dentate line

(a)

Peri-rectal
Submucosal

Ischiorectal
(b)

Peri-anal

Intersphincteric

Figure 2 Anal canal.
(a) Anatomy of the anal canal. (b) Location of peri-anal and
peri-rectal abscesses.

external sphincters. Some anorectal abscesses originate from Staphylococcus aureus infection of a sebaceous gland.
Bacteria isolated from anorectal abscesses include
Escherichia coli, Bacteroides fragilis, Enterococcus faecalis
and/or streptococci of groups A, C, G and, occasionally, B. The Streptococcus intermedius group may be
implicated.The infection tends to extend downwards
between the sphincters into the peri-anal region.
Fistula formation (p. 132) may occur.

Fistula
The majority of fistulas in ano are not associated with
gastro-intestinal disease but are a consequence of
anorectal abscesses. However, they are a common