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CHAPTER 22 System-Specific Pathology
401
• Long interval between menarche and menopause:
• early menarche and late menopause are each associated with an increased risk
• thought to be related to prolonged exposure to
oestrogen.
• Childbirth:
• nulliparous women have a greater risk of developing
breast carcinoma than parous women
• in parous women, protection is related to early age
for rst full-term pregnancy
• if rst birth is delayed to mid- or late thirties, the
woman is at greater risk of developing breast cancer
than a nulliparous woman.
• Family history of breast cancer:
• rst-degree female relatives of breast cancer patients
have an increased risk of developing breast cancer
• inherited mutations of a gene on the long arm of
chromosome 17 (BRCA1) are found in almost all
families with susceptibility to female breast and
ovarian cancer.
• Atypical hyperplasia in previous breast biopsy:
• women with benign breast disease whose breast
biopsies show atypical epithelial hyperplasia have a
denite increased risk of developing breast cancer.
• Previous chest wall radiotherapy:
• individuals who have undergone chest wall irradiation as a young adult, e.g. for lymphoma, have an
increased risk of developing breast cancer.
• Geographic factors:
• marked variation in breast cancer rates between different countries
• highest rates are in North America, North-West
Europe, Australia and New Zealand
• lowest rates in South East Asia and Africa
• this dierence may be due to age at menarche, age at
a full rst-time pregnancy, age at menopause.
• Lifestyle factors:
• some evidence to suggest that obesity and alcohol
consumption can increase risks of breast cancer
also, with weaker evidence for smoking and lack of
exercise.
Aetiological Mechanisms
• Overexposure to oestrogen and underexposure to
progesterone.
• Increased risk with hormone replacement therapy; debate over possibility of small risk with oral
contraceptives.
• Some tumours contain oestrogen and progesterone
receptors. Aected patients are more likely to respond
to some form of hormone manipulation.
Non-Invasive Carcinomas
• Tumour conned to ducts (ductal carcinoma in situ) or
acini (lobular carcinoma in situ).
• Ductal carcinoma in situ is unilateral, occurs in pre- and
post-menopausal women, has several forms and may
become invasive.
• Lobular carcinoma in situ occurs in premenopausal
women, has no clinical features (i.e. does not present as a
palpable lump and is usually found in biopsies removed
for other reasons), is oen bilateral, can be multifocal,
and is a risk factor for invasive carcinoma.
Invasive Carcinomas
• Occur in pre- and post-menopausal women.
• Most are inltrating ductal carcinomas of no special
type.
• Inltrating lobular carcinomas can be multifocal.
• Less common types include mucinous, medullary, papillary and tubular carcinomas.
Gross Features
Macroscopic appearances depend upon the amount of
stroma within the carcinoma.
• Scirrhous: implies prominent brous tissue reaction
resulting in the carcinoma having a dense, white appearance which grates when cut (like the surface of an unripe
pear).
• Medullary (encephaloid): like substance of brain,
tumour feels much soer; cellular with little stroma.
• Mucinous carcinomas: predominance of mucin or jellylike material.
Paget’s disease of the nipple
• Erosion of the nipple, clinically resembling eczema.
• Associated with underlying ductal carcinoma in situ or
invasive carcinoma.
• Eventually destroys the nipple.
• Dierentiated from eczema in that eczema is usually
bilateral, does not destroy the nipple and is not associated with an underlying lump.
Spread of Breast Carcinoma
• Directly into skin and muscle:
• tethering to skin
• skin dimpling
• ulceration
• fungation
• xity to pectoral muscles.
• Via lymphatics to axillary, cervical and internal mammary nodes.
• Via bloodstream to lungs, bone, liver and brain:
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SECTION III Pathology
• lungs: pleural eusion, lymphangitic carcinomatosa
• bone: pathological fractures, hypercalcaemia
• liver: jaundice
• brain: confusion, ts.
• May be considerable delay before metastases occur.
Prognostic Factors
• Presence of invasion: non-invasive tumours are curable
if all lesions are resected; multicentricity may require
mastectomy.
• Tumour size: the smaller the tumour, the higher the
survival.
• Tumour type: tubular, medullary, mucinous and papillary are associated with more favourable prognosis.
• Staging: outcome depends upon involvement of lymph
nodes and distant metastases.
• Degree of dierentiation.
• Expression of hormone receptors – an indication of
likely response to anti-oestrogens.
• Overexpression of products of proto-oncogene C-erb
B-2/HER-2.
Phylloides Tumour
• Can occur at any age, but mean age of presentation is 45.
• Can become very large (not to be confused with giant
broadenoma).
• Should be excised with wide margin of normal breast
tissue.
• Recurrence is a major problem.
• Risk of recurrence is less if tumours are small with low
mitotic rate and minimal cellular atypia, and have a
rounded rather than an inltrative edge.
• Chance of metastases increases with recurrence.
• Metastases occur in about 10% of cases of recurrence.
Inflammatory Conditions
ese include:
• acute pyogenic mastitis
• tuberculosis
• actinomycosis
• mammary duct ectasia
• fat necrosis.
Acute Pyogenic Mastitis
• Painful, acute inammatory condition due to S. aureus.
• Occurs in the rst few weeks aer delivery, during
breastfeeding.
• Usually associated with cracked nipple, although blockage of a duct may be a factor.
• Results in localized swelling and erythema.
• Responds to ucloxacillin, but if uctuation has
occurred indicating abscess, incision and drainage will
be required.
Tuberculosis
• Rare.
• Due to haematogenous spread.
• Caseous mass with marked brous reaction, mimicking
carcinoma.
Actinomycosis
• Rare.
• May be due to spread of infection from the lung through
the thoracic wall, or occur as primary infection.
• Usually presents with hard lump beneath the nipple,
which may be painful.
• Results in abscess formation with pus containing typical
‘sulfur granules’.
Mammary Duct Ectasia
• Usually aects ducts behind nipple.
• Usually occurs in h decade.
• ick, creamy nipple discharge, which may occasionally
be blood-stained.
• Fibrosis around ducts may cause nipple retraction, thus
mimicking carcinoma.
• Ducts are dilated and are lled with inspissated material.
• Condition sometimes known as periductal mastitis or
plasma cell mastitis because of the prevalence of plasma
cells on histological examination.
Fat Necrosis
• Caused by trauma, e.g. seat-belt injury, partner's teeth.
• Presents with hard lump that may mimic carcinoma.
• Macroscopically, yellow tissue with haemorrhagic areas
of calcication.
• Occurs more frequently in the obese.
Proliferative Conditions of the Breast
• Known by a variety of names including cystic mastitis,
brocystic disease and chronic mastitis.
• Causes severe discomfort in the breast before period.
• One component, i.e. epithelial hyperplasia, is associated
with an increased risk of cancer.
• Causes palpable lumps, mimicking breast cancer.
• Cysts occur in the breast and may require aspiration.
• Histological features are numerous and include:
• adenosis
• sclerosing adenosis
• epithelial hyperplasia
• cysts
• brous.
CHAPTER 22 System-Specific Pathology
403
Gynaecomastia
Breast tissue in men contains only ductular structures with
no evidence of acini. Gynaecomastia is the benign enlargement of male breast tissue. It occurs most commonly in
adolescent and older age groups.
Causes are shown in Box 22.3.
Breast Cancer in Men
• Rare: accounts for 1% of all breast carcinomas.
• Increased risk in patients with Klinefelter’s syndrome.
• Usually presents as a lump, but there can be nipple discharge or retraction.
• Prognosis aected by such factors as lymph node status
and size.
BOX 22.3 Causes of Gynaecomastia
Physiological
Neonates
Puberty
Old age
Pathological
Drugs
Oestrogens
Cyproterone
Spironolactone
Cimetidine
Digitalis
Griseofulvin
Amphetamines
Tricyclic antidepressants
Cannabis
Anabolic steroid abuse
Carcinoma of the male breast
Liver failure
Renal failure
Hyperthyroidism
Hypogonadism
Klinefelter’s syndrome
Agenesis
Testicular tumours
Other tumours
Bronchial carcinoma (inappropriate secretion of
hormones)
Pituitary tumours (e.g. prolactinoma)
Malnutrition
Idiopathic
CARDIOVASCULAR SYSTEM
Atherosclerosis
Atherosclerosis is by far the most common disorder leading to death and serious morbidity throughout the developed world. It is responsible for more deaths than all forms
of cancer.
Lesions of Atherosclerosis
Fatty streaks
• First visible lesion.
• Seen in young, even infants, and consist of intracellular
lipid deposits.
• Appear as raised subendothelial yellow streaks.
Gelatinous plaques
• Small, so, blister-like elevations.
• Occur more commonly in aorta and large vessels.
• May be precursors of mature plaques.
Fibrolipid plaques (Fig. 22.1)
• Characteristic lesions of atherosclerosis.
• Most commonly, have a lipid-rich core with overlying
brous cap on the luminal surfaces.
• Great variations from the basal accumulation of lipid,
being very large with only a thin overlying cap to the
opposite extreme, where the cellular and connective tissue elements predominate.
• Plaques tend to be found at certain sites, but especially
the lower abdominal aorta, coronary arteries, renal
arteries, distal supercial femoral and popliteal arteries,
descending thoracic aorta, internal carotid and circle of
Willis. Arteries of the upper limb tend to be spared.
• Microscopically, plaques have three components:
• cells: mainly vascular smooth muscle cells, macro-
phages and lymphocytes
• connective tissue bres of collagen, elastin and
proteoglycans
• lipids, mainly cholesterol and oxidized cholesterol in
the form of low density lipoproteins. ese are quite
irritant and have been shown to cause severe inammatory reactions in connective tissue; may result in
periarterial inammation, brosis and lymphocyte
inltration.
Complicated plaques
Typical brolipid plaques may undergo several complications, as follows:
• Rupturing or ulceration of the luminal surface may
occur. is may result in fat in the fatty part discharging
into the bloodstream as so-called ‘cholesterol emboli’.
• rombosis may occur over ulcerated plaques, which
may extend, leading to arterial occlusion, particularly in
the coronary circulation.
404
Atheromatous core
Internal
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SECTION III Pathology
Foam cells
(lipid-rich
macrophages)
Smooth muscle cell
proliferation
Fig. 22.1 Typical fibrolipid atheromatous plaque.
• Haemorrhage may occur into a plaque because of breakdown of the overlying brous cap. is may balloon the
plaque, narrowing the lumen, or lead to its rupture.
• Calcication frequently occurs.
• Extensive necrosis of the plaque may occur, which may
cause embolism of plaque material, leaving large areas
of ulceration.
• May be thinning and weakening of media, which may
result in aneurysmal dilatation.
Risk Factors
Predisposing factors to atherosclerosis include:
• increasing age
• male sex
• race
• smoking
• diabetes mellitus
• obesity
• systemic hypertension
• hyperlipidaemia
• family history.
Pathogenesis
Pathogenesis must account for:
• focal nature of the lesion
• the place of risk factors in causation, especially
hyperlipidaemia
• the presence of lipids in most lesions
• smooth muscle proliferation, which is an early and
characteristic feature.
e various theories of pathogenesis are as follows:
• response to injury, e.g. chemicals from cigarette smoke,
cholesterol, hypertension
• increased permeability to lipids
Fibrous cap
Intima
elastic
lamina
• raised lipids: increased lipid absorption more likely
in hyperlipidaemia, and the low density lipoprotein is
likely to be oxidized by free radicals at the site of injury
where they are absorbed into the intima
• oxidized low density lipoprotein itself is toxic to
endothelial cells, and attracts monocytes and
macrophages
• smooth muscle proliferation: proliferates under the
inuence of PGDF
• thrombogenic theory: plaques arise from mural thrombi
formed at sites of endothelial injury with subsequent
organization.
ISCHAEMIC HEART DISEASE
Ischaemic heart disease (IHD) is the term used for several
closely related conditions where the supply of oxygenated
blood to the heart is inadequate. Atherosclerotic narrowing
is the main cause, but may be aggravated by:
• increased demand due to ventricular hypertrophy
• increased demand due to impaired oxygen transport,
e.g. severe anaemia, advanced lung disease, carbon
monoxide poisoning.
Four ischaemic syndromes may result, depending on the
severity and speed of onset:
• stable angina
• acute coronary syndromes (unstable angina and acute
myocardial infarction)
• sudden cardiac death
• ischaemic cardiomyopathy.
Angina of Effort
• Characterized by central chest pain, which may radiate
down the le arm, up and into the jaw.
CHAPTER 22 System-Specific Pathology
405
• Caused by a shortage of oxygenated blood supplying the
heart muscle, due to increased demand during exercise
in the presence of narrowed coronary arteries.
Acute Coronary Syndrome (Unstable Angina and
Acute Myocardial Infarction)
Myocardial infarction may be:
• subendocardial
• transmural.
Subendocardial (partial thickness or non-Q-wave
infarct)
• Inner third of heart muscle is least well perfused and
therefore more vulnerable to reduced coronary ow.
• In subendocardial infarct, although there is usually diffuse coronary arteriosclerosis, there is less commonly
superimposed thrombosis.
• Frequently S/T-wave changes but no Q-wave.
Transmural infarction (full thickness or Q-wave infarct)
• More common.
• More serious and usually involves le ventricle.
• May follow disruption of arteriosclerotic plaque with
superimposed thrombosis.
• Platelet activation and aggregation responsible for this
may be reduced if the patient is on antiplatelet drugs.
• Normally Q-waves on ECG.
Pathological consequences of acute transmural infarct
ese are:
• arrhythmia
• acute heart failure
• papillary muscle infarct, leading to rupture with acute
mitral regurgitation
• pericarditis
• mural thrombus: may result in peripheral arterial
embolus, causing stroke, acutely ischaemic limb or mesenteric ischaemia
• scarring of heart muscle with subsequent ventricular
aneurysm
• myocardial rupture, causing intraventricular septal defect,
bleeding into the pericardium with tamponade, depending
on site of rupture.
Sudden Cardiac Death
• Dened as unexpected death from cardiac cause within
an hour of onset of acute symptoms.
• Majority of cases are due to ischaemic heart disease.
• In a small percentage of cases, no cause is found.
• Final cause of death is almost always a lethal arrhythmia.
Ischaemic Cardiomyopathy
• Tends to occur in the elderly.
• Insidious and gradually deteriorating congestive cardiac
failure with ECG changes.
• Oen a history of angina or myocardial infarction.
• May be due to multiple small infarcts or chronic myocardial ischaemia or a combination of both.
• Histologically the main nding is diuse myocardial
atrophy and interstitial brosis.
ANEURYSMS
An aneurysm is abnormal dilatation of an artery.
Aneurysms may be classied as:
• true: where the wall is formed totally by the three normal elements of the arterial wall, i.e. intima, media and
adventitia
• false: a pulsating haematoma, the cavity of which is in
direct continuity with the lumen of an artery, i.e. where
the wall is formed by connective tissue which is not part
of the vessel wall.
e types of aneurysm are shown in Fig. 22.2.
True Aneurysms
ese may be:
• fusiform: dilatation due to a segment of the vessel wall
being aected around the whole circumference
• saccular: where only part of the circumference is
involved.
Congenital Aneurysms
‘Berry’ Aneurysms
• Due to congenital defect in media at junction of vessels
around the circle of Willis.
• Most common cause of subarachnoid haemorrhage.
• Commonest age of presentation is around 50 years.
• Increased incidence in patients with hypertension.
• Increased incidence in patients with adult polycystic
kidney disease.
Acquired Aneurysms
ese may be:
• atheromatous
• mycotic
• syphilitic
• dissecting (acute aortic dissection)
• false
• arteriovenous aneurysms (aneurysmal varices).
Atheromatous Aneurysms
ese are most common at:
• abdominal aorta
• popliteal artery
• femoral artery.
False
True
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406
Arteriovenous
(aneurysmal varix)
Fig. 22.2 Types of aneurysm.
SECTION III Pathology
Fusiform
Saccular
Vein
Artery
• May be due to any form of bacteraemia, e.g. Salmonella.
• Usually saccular.
Syphilitic Aneurysms
• Common many years ago but now rare.
• Tend to involve the thoracic aorta, especially the arch.
• Due to endarteritis of vasa vasorum with inammatory
process extending into the media and causing ischaemic
damage of the vessel wall.
Dissecting Aneurysm (Acute Aortic Dissection)
• Most common in thoracic aorta.
• Blood enters the diseased media, which splits into two
layers.
• Associated with Marfan’s syndrome.
• Associated with hypertension.
• Blood enters false lumen and then ruptures, either back
into the main lumen of the artery distally, in which case
the patient may survive for some time; or externally,
with sudden death.
• If it involves the ascending aorta, it may dissect across
a coronary ostium, leading to myocardial infarction; or
across the aortic valve, causing aortic regurgitation.
False Aneurysm (Pulsating Haematoma)
• Results from a small tear in an artery which is followed
by haematoma, the wall of which becomes organized
and holds the aneurysm in check for some time before
it ruptures.
• May follow stab wounds, intra-arterial injections or
intra-arterial radiological procedures.
• Repaired by controlling artery above and below, closing
the small defect and evacuating the haematoma.
Arteriovenous Aneurysms
• Sometimes known as aneurysmal varices.
• May be traumatic, but more commonly follow formation of an AV stula for dialysis.
Abdominal aortic aneurysm
• Incidence is rising.
• Risk factors include smoking and hypertension.
• Main complication is rupture, which may be intraperitoneal, accompanied by rapid death, or retroperitoneal.
• May be a familial tendency.
• May be associated aneurysms of common iliac arteries.
• May also be increased incidence of femoral and popliteal artery aneurysms.
Mycotic Aneurysms
• Commonly associated with subacute infective
endocarditis.
General Complications of Aneurysms
• Rupture.
• rombosis with occlusion, e.g. in popliteal artery
aneurysms.
• Distal emboli from mural thrombus.
• Pressure on adjacent structure, e.g. abdominal aortic
aneurysm eroding vertebral bodies; femoral aneurysms
pressing on femoral nerve; popliteal artery aneurysm
compressing popliteal vein leading to DVT.
ENDOCRINE SYSTEM
See also Chapter 12.
CHAPTER 22 System-Specific Pathology
407
Thyroid Disease
Goitre
is is an enlargement of the thyroid gland. Causes range
from the physiological, when the gland increases in size
as result of increased demand for thyroid hormone, e.g. at
puberty, to frank malignant disease. e causes of goitres
are shown in Box 22.4.
Hyperthyroidism
Hyperthyroidism (thyrotoxicosis) is a clinical syndrome
resulting from the eects of excess circulating T3 and T4.
Hyperthyroidism results from three main pathological
lesions:
• Graves’ disease
• functioning adenoma
• toxic nodular goitre.
Clinical features of thyrotoxicosis
• Anxiety.
• Nervousness.
• Irritability.
• Sweating.
• Heat intolerance.
BOX 22.4 Causes of Goitres
Simple (non-toxic) goitre
Simple hyperplastic goitre
Multinodular goitre
Toxic goitre
Diffuse goitre (Graves’ disease)
Toxic nodule
Toxic multinodular goitre
Neoplastic goitre
Benign
Adenoma
Malignant
Papillary
Follicular
Anaplastic
Medullary
Inflammatory
De Quervain’s thyroiditis
Riedel's thyroiditis
Autoimmune
Hashimoto’s thyroiditis
• Insomnia.
• Hair loss.
• Palpitations.
• Menorrhagia.
• Diarrhoea.
• Tre mor.
• Eye signs: exophthalmos lid retraction, lid lag.
• Tachycardia.
• Atrial brillation.
• Proximal myopathy.
• Pretibial myxoedema.
• Warm, moist palms.
• Hyper-reexia.
• Osteoporosis.
Hypothyroidism
Hypothyroidism (myxoedema) is the clinical syndrome
resulting from inadequate levels of circulating T3 and T4.
Causes include:
• Hashimoto’s thyroiditis
• Iatrogenic:
• surgical removal of thyroid tissue
• drugs, e.g. sulfonylureas, lithium, amiodarone.
Clinical Features of Myxoedema
• Slowness of thought, speech and movement.
• Weight gain.
• Cold intolerance.
• Tiredness.
• Lethargy.
• Constipation.
• Loss of hair.
• Menstrual irregularities.
• Dry hair.
• Puy, swollen face.
• Loss of outer third of eyebrows.
• Ischaemic heart disease.
• Bradycardia.
• Carpal tunnel syndrome.
• Muscle weakness.
Hashimoto’s Thyroiditis
• Commonest cause of hypothyroidism.
• Disease of middle age occurring more oen in females.
• Association with human leucocyte antigen (HLA), DR5.
• Autoimmune.
• Microscopically, gland is inltrated by lymphocytes and
plasma cells.
• Presents with goitre; patient is usually euthyroid.
• Later, atrophy and brosis of gland with development of
myxoedema.
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SECTION III Pathology
Carcinoma of the Thyroid Gland
Carcinoma of the thyroid gland is uncommon, accounting
for less than 1% of all cancer deaths. It is associated with:
• radiation exposure, e.g. neck X-rays, or as a result of
nuclear fallout
• family history of multiple endocrine neoplasia syndromes IIa and IIb.
ere are four types of thyroid carcinoma, which are summarized in Table 22.1.
Clinical presentation
is includes:
• goitre
• dysphagia
• signs of local invasion, e.g. Horner’s syndrome,
hoarseness
• cervical lymphadenopathy
• pathological fractures due to bone secondaries
• cough due to lung metastases
• rarely, thyrotoxicosis.
Adrenal Disorders
Medulla
Commonest adrenal medullary tumour is a phaeo chromocytoma.
• Peak incidence at 30–50 years.
• Male/female ratio is 1 : 1.
• Derived from adrenal medullary chroman cells.
• 10–20% of cases are familial and associated with other
conditions:
• MEN IIa
• MEN IIb
• neurobromatosis
• Von Hippel–Lindau syndrome
• tuberous sclerosis
• Sturge–Weber syndrome.
• 10% are extra-adrenal associated with paraganglia.
• Clinical features include:
• hypertension (occasionally intermittent)
• pallor
• headaches
• sweating and nervousness
• palpitations
• abdominal pain.
• Occasionally malignant.
• Curable cause of secondary hypertension.
• Laboratory diagnosis depends on elevated 24 h urine
vanillylmandelic acid (VMA) estimation.
Cortex
e adrenal cortex produces the following steroid hormones:
• glucocorticoids (zona fasciculata)
• mineralocorticoids (zona glomerulosa)
• sex steroids (zona reticularis).
Hyperfunction of the Adrenal Cortex
Hyperfunction of the adrenal cortex produces generalized
eects, the nature of which depends on whether it is glucocorticoids, mineralocorticoids or sex steroids that are
produced in excess.
Cushing’s syndrome
• Due to excess glucocorticoids.
• Causes include:
• iatrogenic: therapeutic administration of gluco -
corticoids
• excess ACTH secretion from the pituitary gland
• adrenal cortical neoplasms
• ectopic ACTH secretion.
TABLE 22.1 Types of Thyroid Carcinoma
Proportion of
Type
Papillary 65 16–40 Lymphatic Excellent
Follicular 20 40–60 Blood Good
Anaplastic 10 Old age Locally aggressive Very poor
Medullary 5 Over 40 Local, lymph nodes, blood Variable: poor if bone
all Cases (%) Age (Years) Spread Prognosis
Local nodes
Especially bone
Lymph nodes
Younger in familial cases
metastases; more
aggressive in familial
cases
CHAPTER 22 System-Specific Pathology
409
Systemic features of Cushing’s syndrome:
• Moon face.
• Bualo hump.
• Central obesity.
• Avascular necrosis of bone.
• Stunted growth.
• Proximal myopathy.
• Hypertension.
• Peptic ulceration.
• Hyperglycaemia.
• Menstrual disturbances.
• Stria on the abdomen.
• Acne.
• Cataracts.
• Osteoporosis: pathological fractures.
• Predisposition to infection.
• inning of the hair.
• inning of the skin.
• Psychosis.
Hyperaldosteronism
Conn’s syndrome (primary hyperaldosteronism)
• Due to autonomous secretion of excess aldosterone.
• Usually caused by an adenoma of the zona glomerulosa.
• Increased renal retention of sodium and water leads to
hypertension.
• Potassium loss leads to muscular weakness and cardiac
arrhythmias.
• Hypokalaemia associated with metabolic alkalosis causing tetany and paraesthesia.
• Diagnosis rests on raised plasma aldosterone while
renin is low.
Secondary hyperaldosteronism
• Reduction in renal glomerular perfusion activates the
renin–angiotensin system.
• is stimulates aldosterone secretion in an attempt to
correct renal glomerular perfusion.
• is is the commonest type of hyperaldosteronism.
• Aldosterone levels raised but are appropriate response
to high renin levels.
Hypersecretion of Sex Steroids
• Some adrenal cortical adenomas secrete sex steroids,
most commonly androgens.
Hypofunction of the Adrenal Cortex
Adrenocortical hypofunction can be primary, due to
lesions within the adrenal gland, or secondary, due to failure of ACTH secretion by the pituitary gland. Causes of
chronic primary insuciency include:
• tuberculosis
• autoimmune disease
• amyloidosis
• haemochromatosis
• metastatic tumours
• atrophy due to prolonged steroid therapy.
Acute insufficiency
• Waterhouse–Friderichsen syndrome: acute haemorrhagic necrosis of the adrenals associated with meningococcal septicaemia.
• Other acute septicaemias, e.g. Gram-negative septicaemia, may cause similar eects.
• May be due to disseminated intravascular coagulation
within the adrenal gland.
Chronic insufficiency (Addison’s disease)
• Eects of chronic adrenal insuciency include:
• anorexia, weight loss, vomiting
• weakness
• lethargy
• hypertension
• skin pigmentation
• hyponatraemia with hyperkalaemia
• chronic dehydration
• sexual dysfunction.
• During acute illnesses patients may undergo an acute
Addisonian crisis with vomiting, dehydration, electrolyte disturbances and circulatory collapse.
• Plasma cortisol levels are low.
• Estimation of ACTH levels enables a distinction to be
made between primary adrenocortical insuciency
(ACTH raised) and secondary insuciency (ACTH low).
Tumours of the Adrenal Cortex
ese are:
• adenoma
• carcinoma.
Adenoma
• ‘Functioning’ adenomas cause Cushing’s syndrome or
Conn’s syndrome.
• Clinically unsuspected ‘non-functioning’ adenomas
may be found in about 2% of adult autopsies or picked
up incidentally on CT scans for other conditions.
Carcinoma
• Rare.
• Usually hormone-secreting with a tendency to produce
androgens.
• May be extremely large and exhibit invasive growth.
GENITOURINARY SYSTEM
Gynaecological Causes of Acute Abdominal Pain
ese include:
• ruptured ectopic pregnancy
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SECTION III Pathology
• torsion of ovarian cyst
• ruptured ovarian cyst
• salpingitis
• severe dysmenorrhoea
• mittelschmerz
• endometriosis
• torsion or degeneration of a broid.
Pelvic Inflammatory Disease
Infection of the fallopian tubes usually involves the ovaries
and peritoneum, and the combined infection is called pelvic inammatory disease (PID).
• Results from ascending infection of organisms from
vagina or cervix.
• Most episodes are associated with traditional sexually transmitted disease pathogens, i.e. Chlamydia and
gonorrhoea.
• Predominantly disease of young, sexually active women.
• Secondary invasion with anaerobes is common, so that
a combination of antibiotics is required to cover the
spectrum of likely pathogens.
• Associated with tubule damage, leading to ectopic pregnancy or infertility.
• Partner notication is important in management.
Acute Pelvic Inflammatory Disease
Causes are:
• Primary:
• sexually transmitted diseases
• Escherichia coli, Bacteroides or other gut organisms
• iatrogenic, e.g. following D&C, termination of preg-
nancy, insertion of an intrauterine contraceptive
device
• aer delivery or miscarriage.
• Secondary:
• direct spread from nearby pelvic organs, e.g. appen-
dicitis or schistosomiasis.
• Pathological consequences of acute pelvic inammatory
disease include:
• salpingitis
• pyosalpinx
• hydrosalpinx
• acute pelvic peritonitis
• salpingo-oophoritis
• tubo-ovarian abscess
• adhesions.
Sequelae
ese include:
• chronic pelvic pain
• subfertility
• ectopic pregnancy
• recurrent PID with:
• heavy periods
• dysmenorrhoea
• dyspareunia
• chronic pelvic pain due to adhesions
• infertility.
Chronic Pelvic Inflammatory Disease
is may be due to:
• inadequately treated, recurrent, acute pelvic inammatory disease
• tuberculosis (rare).
Ovarian Disease
Ovarian lesions present either with pain, due to inammation, or swelling of the organ. Rarely do they present with
the remote eects of endocrine secretion.
Ovarian Cysts
• Both normal follicles and corpus luteum are cystic.
• Retention cysts form frequently and by denition must
be >2 cm.
• Luteal cysts may rupture with slight haemorrhage into
the peritoneal cavity.
• Follicular cysts have an inner layer of granulosa cells
and contain clear uid; they may be multiple.
• ‘Chocolate’ cysts of the ovary are a feature of endometriosis.
• Ovarian cysts cause symptoms by either rupture or
torsion.
Ovarian Tumours
Ovarian tumours may be divided into ve main categories:
• epithelial
• germ cell
• sex-cord stromal
• metastatic
• miscellaneous.
Epithelial tumours
• Majority of ovarian tumours are derived from surface
epithelium.
• Several varieties, which depend upon embryonic
dierentiation.
• Mucinous type may be benign or malignant.
• Benign mucinous cystadenoma may grow to be a very
large size, lling the peritoneal cavity, and may be mistaken for ascites.
• Benign tumours may rupture, releasing tumour cells
which seed onto the peritoneum and continue to produce mucus (pseudomyxoma peritonei).
• Some tumours are borderline between cystadenoma
and cystadenocarcinoma.
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