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The thyroid 405
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diameter in the absence of lymph node metastasis. In
addition, it may also be adequate for follicular
tumours with minimal capsular invasion, small
tumour size and no metastatic disease. Most other
patients with differentiated thyroid cancer will require
total thyroidectomy and possible radioiodine
therapy.
Radioiodine ablation (RAI)
Iodine- 131 ablation of the thyroid bed and remnant is
an essential component of the treatment of differentiated thyroid cancer. The majority of differentiated
thyroid cancers retain the capacity to take up and
concentrate iodine. This permits radioactive isotopes
of iodine to be used both for the localization and
treatment of residual or metastatic thyroid carcinoma. By removing and then ablating all thyroid tissue, followlater in this chapter).
Complications of
swelling, or thyroiditis in those patients with a large
thyroid remnant. In addition, radiation sialadenitis
affecting the parotid or submandibular glands may
present with painful swelling of the affected salivary
gland(s) after eating. There are few long- term sequelae from radioiodine providing that the cumulative
dose is kept to a minimum.
up using thyroglobulin is possible (see
131
I therapy include oedema and
TSH suppression
Recurrence rates are reduced by postoperative levothyroxine therapy. Patients who have not required
RAI do not need TSH suppression and the serum
TSH should be maintained in the low- normal range
between 0.3 and 2.0 mU/l. Following initial treatment with total thyroidectomy and RAI, and before
evaluation of the patient’s response to treatment
after 9–12 months, TSH should be suppressed to
below 0.1 mU/l in all patients. Following evaluation
of response after 9–12months after total thyroidectomy and RAI, the risk of thyroid cancer recurrence should be reclassified according to the criteria
for Dynamic Risk Stratification. This restratification
should enable the degree of TSH suppression to be
adjusted accordingly.
Thyroglobulin
Serum thyroglobulin is the best way of detecting the
presence of normal or malignant thyroid tissue and
most patients who are free of disease will have undetectable levels. In patients in whom the thyroglobulin
rises during followand wholelook for local or systemic recurrence.
up, careful clinical examination
body scanning should be performed to
Medullary carcinoma
Phaeochromocytoma and hyperparathyroidism should
be excluded. All patients with medullary carcinoma
require total thyroidectomy and central lymph node dissection. Radical neck dissection may be required when
cervical lymphadenopathy is present.
Prophylactic thyroidectomy is indicated in unaffected kindred members with the germline RET
mutation, even in childhood.
Anaplastic carcinoma
This condition has a very poor prognosis with a 1- year
survival of <15%. The main aim of treatment following
diagnosis is local control of the disease. Useful palliation may be achieved with external beam radiotherapy, and tracheostomy should be avoided if at all
possible.
Additional resources
Case 104: A lump in the neck that moves on
swallowing
Case 105: A woman with an obvious endocrine
disease
Case 106: A mass of cervical lymph nodes
Case 107: A rapidly enlarging mass in the neck
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The parathyroids
Ekpemi Irune
Learning objective
✓ To understand the presentations of both hypoparathyroidism and
hyperparathyroidism and their management.
of calcium (and magnesium) from the distal
Anatomy and
development
The parathyroids are four endocrine glands (sometimes three or five) about the size of peas, which usually lie in two pairs behind the lateral lobes of the
thyroid gland. The superior parathyroids arise from
the fourth branchial pouch and owing to their short
migration can usually be found posterior to the upper
two-
thirds of the thyroid. The inferior glands arise
from the third pouch in association with the developing thymus (see Figure 39.1). The inferior parathyroids may lie almost anywhere in the neck or superior
mediastinum although the majority lie within 1cm of
the lower thyroid pole.
tubules is reciprocally increased.
2
It activates the 1α- hydroxylase enzyme in the
kidney, which converts the inactive 25-hydroxycholecalciferol (25- hydroxy- vitamin D) into
1,25- dihydroxycholecalciferol. The resultant activated 1,25 form of vitamin D facilitates intestinal
absorption of calcium.
3
It stimulates osteoclastic activity in the bones,
resulting in the decalcification and liberation of
excessive amounts of calcium and phosphate in
the blood.
Effects ofincreased
PTHproduction
Physiology
The parathyroids produce parathormone (PTH),
which has a profound influence on calcium and
phosphate metabolism. There are three main
effects.
It increases the excretion of phosphate from the
1
kidney by inhibiting its tubular reabsorption
(phosphaturic effect); active tubular reabsorption
Ellis and Calne’s Lecture Notes in General Surgery, Fourteenth Edition.
Edited by Christopher Watson and Justin Davies.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
Companion website: www.wiley.com/go/Watson/GeneralSurgery14
• A raised serum calcium and a lowered serum
phosphate.
• An increased excretion of phosphate in the urine
(phosphaturic effect of PTH).
An increased excretion of calcium in the urine.
•
The large amount of calcium filtered (owing to
the hypercalcaemia) exceeds the capacity of the
tubules to reabsorb it all, so increased calcium
excretion occurs.
•
In the longer term, it causes increased osteo-
clastic activity, with a raised serum alkaline
phosphatase associated with decalcification of
the bones.
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Hypoparathyroidism
Lack of PTH results in low serum calcium. This leads
initially to paraesthesiae (perioral and fingertips)
then hyperirritability of skeletal muscle with carpopedal spasms, the syndrome being called tetany. The
most common cause of this is removal or bruising
of the parathyroids during thyroidectomy (see
Chapter39). Tetany is liable to occur if the serum calcium falls below 1.5mmol/L.
Clinical features
Spasms may affect any part of the body, but typically
the hands and feet. The wrists flex and the fingers are
drawn together in extension, the sod’accoucheur’. This spasm may be induced by placing
a tourniquet around the arm for a few minutes
(Trousseau’s sign
muscles may be demonstrated by tapping over the
facial nerve, which results in spasm (Chvostek’s
2
sign
).
Note that clinical tetany may occur with a normal
level of serum calcium in alkalosis (e.g. overbreathing, excessive prolonged vomiting) because of a compensatory shift of ionized calcium to the unionized
form in the serum.
1
). Hyperirritability of the facial
called ‘main
either no symptoms or nonincluding fatigue, depression and weakness; less
commonly, it is detected during the investigation of
nephrolithiasis or osteopenia (e.g. on dual-
ray absorptiometry [DEXA] testing), the two
Xmain complications of hyperparathyroidism. Many
‘asymptomatic’ patients feel much better after
treatment. The annual incidence is highest among
women in the 5th and 6th decade of life (2 per 1000
population).
specific symptoms
energy
Pathology
In 85–90% of patients, primary hyperparathyroidism
is due to a solitary hyperfunctioning parathyroid
adenoma. The lower glands are affected more commonly than the upper ones. In 10% of cases, the cause
of primary hyperparathyroidism is familial with
thepresence of multiglandular hyperplasia. This may
be associated with multiple endocrine neoplasia
(MEN) type I, MEN type II and MEN type IV (Box40.1)
or may be sporadic or induced by longintake, radiotherapy to the neck and calcium supplementation. More rarely, hyperparathyroidismtumour syndrome is an inherited cause of hyperparathyroidism, which is also linked with maxillary and
antral fibrotumours.
osseous tumours and renal and uterine
term lithium
jaw
Hyperparathyroidism
There are four distinct types of pathologically
increased PTH secretion: primary, secondary, tertiary and that due to ectopic PTH production by
tumours.
Primary hyperparathyroidism
The diagnosis of primary hyperparathyroidism is
made following the detection of hypercalcaemia in
the presence of inappropriately normal or elevated
circulating PTH levels; the PTH should be low if calcium is raised. The hypercalcaemia is usually discovered on routine screening of patients who have
1
Armand Trousseau (1801–1867), Physician, Hôpital Necker,
Hôpital St Antoine and Hôpital Dieu, Paris, France. Also
described thrombophlebitis migrans associated with cancer.
2
Frantisek Chvostek (1835–1884), Physician, JosefsAkademie, Vienna, Austria.
Parathyroid carcinoma
Parathyroid carcinoma is a very rare condition and
accounts for less than 1% of all cases of primary
hyperparathyroidism. Patients often have higher
serum calcium and PTH levels and are more likely to
have a palpable neck mass than those with benign
hyperparathyroidism. There is an association with
previous neck irradiation and the MEN type 1
syndrome.
Surgery is the only effective treatment. Malignancy
should be considered with any gland that is firm, has
a grey appearance or that is adherent to surrounding
structures. If malignancy is confirmed, surgery may
involve simple excision or en bloc resection, including excision of local structures such as ipsilateral
thyroid, lymph nodes, thymus, strap muscles and the
recurrent laryngeal nerve. Approximately 30% of
tumours will metastasize, but death from the disease
is usually attributable to hypercalcaemia and its
effects on the heart, pancreas and kidney, rather
than metastatic tumour burden.
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Box 40.1 Multiple endocrine neoplasia (MEN)
syndromes
These syndromes are characterized by the
development of tumours in two or more endocrine structures in the same patient. These may
be endocrine adenomas or adenocarcinomas.
Some, such as medullary carcinoma of the
thyroid, may be familial, with autosomal dominant
inheritance.
MEN type I
•
Pancreatic tumour: islet cell tumours except β- cell
tumours (insulinoma).
•
Hyperparathyroidism.
•
Pituitary tumour, e.g. prolactinoma.
•
Adrenocortical tumour.
Secondary hyperparathyroidism
In some 10% of patients with hyperparathyroidism,
the condition is found to be due to hyperplasia of
all four parathyroid glands. This occurs most
commonly in patients with renal failure maintained
by dialysis, in whom renal conversion of
25-hydroxycholecalciferol (calcidiol) to 1,25-dihydroxycholecalciferol (calcitriol) is impaired. This
active form of vitamin D is required for absorption of
calcium from the gut; deficiency results in hypocalcaemia, which chronically stimulates PTH production. The parathyroid glands undergo hyperplasia in
response. To prevent this, dialysis patients are routinely given 1α-
hydroxycholecalciferol (alphacalcidol),
so bypassing renal 1α- hydroxylase.
Tertiary hyperparathyroidism
Prolonged secondary hyperparathyroidism leads to
autonomous PTH production, which continues even
after renal transplantation replaces the previously
deficient renal 1α- hydroxylase conversion step. Total
parathyroidectomy is required.
Ectopic PTH production
Hyperparathyroidism is occasionally due to ectopic
PTH production by tumours, such as squamous carcinoma of the bronchus.
MEN type II
•
Medullary carcinoma of the thyroid.
•
Phaeochromocytoma.
•
Hyperparathyroidism.
MEN type III (also known astype IIB)
•
Medullary carcinoma of the thyroid.
•
Phaeochromocytoma.
•
Neurofibromas of tongue, lips and eyelid.
•
Marfanoid appearance.
MEN type IV
•
Hyperparathyroidism.
•
Anterior pituitary tumours.
•
Adrenocortical tumours and renal tumours.
•
Tumours of the reproductive organs (e.g. neuroendocrine tumour of the cervix and uterine tumours).
Clinical features of
hyperparathyroidism
These depend on the results of excessive production
of PTH by the tumour (see earlier in this chapter).
Presenting symptoms may include the following.
Renal effects: renal stones, infection associated
•
with renal calculi, calcification in the renal substance (nephrocalcinosis) or uraemia. Urinary
tract calculi are the most common clinical manifestation of hyperparathyroidism. It is important
to remember that chronic renal disease with
impaired excretion of phosphate may result in
secondary hyperplasia of the parathyroid glands
with features similar to those of a primary
adenoma of the parathyroid.
• Bone changes: spontaneous fractures or pain in the
bones. X- ray will show decalcification of the bones
with cyst formation. The weakened bones may
be deformed; this condition is known as osteitis
fibrosa cystica or von Recklinghausen’s disease
bone. There may be metastatic calcification in soft
tissues, arterial walls and the kidneys.
•
Abdominal pain: constipation is common.
Dyspepsia or frank peptic ulceration is also
3
Friederich Daniel von Recklinghausen (1833–1910),
Professor of Pathology, successively at Königsberg,
Germany; Würzburg, Germany; and Strasbourg, France.
He also described neurobromatosis.
3
of
sometimes associated with parathyroid adenoma,
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as is pancreatitis. If ulcer symptoms persist after
treatment of the adenoma, the presence of a gastrinoma should be excluded by serum gastrin
assay (there is an MEN syndrome association).
• Vague ill health associated with high serum cal-
cium: the patient very often complains of lassitude,
mental disturbances, weakness, anorexia and loss
of weight. Thirst and polyuria are common.
Cardiovascular: hypertension may be noted at the
•
initial diagnosis and is often associated with left
ventricular hypertrophy. Although serum PTH
correlates strongly with left ventricular mass, the
reduction in left ventricular mass following parathyroidectomy is not associated with a similar
reduction in mean blood pressure. Primary hyperparathyroidism appears to be associated with an
increased rate of premature death owing to cardiovascular disease, although early surgical intervention may result in improved survival.
•
Asymptomatic: an increasing number of patients
with very few or no symptoms are now being diagnosed on routine biochemical screening. Despite
this, the majority of these patients feel better following parathyroidectomy and this, combined with
a recognition that up to 25% of patients will have
progressive disease, has led to support for early surgical intervention following initial diagnosis.
A careful family history should also be taken to
exclude MEN and this, or presentation of primary
hyperparathyroidism at an early age, should raise the
suspicion of hyperplasia rather than an adenoma.
The main effects have historically been summarized
as: ‘stones, bones, abdominal groans, mental moans’.
The parathyroids 409
Serum urea and creatinine should be measured to
•
assess renal function.
Tc99m- Sestamibi (methoxyisobutylisonitrile [MIBI])
•
parathyroid scintigraphy will identify a solitary parathyroid adenoma and highlight an ectopic retrosternal location. Sestamibi is technetiumMIBI and, following injection, is taken up by parathyroid glands and retained by adenomas.
•
Ultrasound of the neck is also effective in local-
izing an adenoma. In clinical practice, surgeons
look for concordance between two imaging
modalities to improve the preoperative localization of parathyroid tumours. This is often by
pooling ultrasound and sestamibi imaging
outcomes.
Renal ultrasound may be implemented to exclude
•
kidney stones.
Computed tomography (CT) scan, with images
•
before and repeated several times after contrast
administration, may also show up ectopic adenomas, which take up contrast rapidly.
• 4- Dimensional- CT (4D- CT) scanning is a modern
imaging technique that has higher reported sensitivity of up to 79.8% in detecting single, multiple
and ectopic parathyroid gland disease.
• Genetic Testing is an essential part of diagnostic
screening in all patients with a family history of
hyperparathyroidism, patients < 35 years of age
presenting with hyperparathyroidism or those
< 45 years with evidence of multigland disease,
suspected jaw tumour syndrome and/or gland
hyperplasia. There are specific national guidelines that underpin genetic testing in this
population.
99- labelled
Special investigations
Diagnostic investigations include the following.
• Serum calcium and PTH. A high serum calcium,
corrected for plasma albumin, in the presence of
detectable serum PTH should raise a strong suspicion of primary hyperparathyroidism. The PTH
may be normal or elevated but in either case is
inappropriately elevated for the level of serum
calcium.
• Serum phosphate may be low (hypophosphataemia) and phosphaturia may also be present.
• 24- hour urine collection for calcium should be
taken to exclude familial hypocalciuric hypercalcaemia (FHH).
Medical management
Patients with primary hyperparathyroidism may be
managed medically with oral medication such as
Cinacalcet. This is a calcimimetic that is a calcium
sensing receptor (CaSR) agonist. Stimulation of CaSR
results in inhibition of PTH synthesis and secretion
thus leading to a reduction in serum calcium
concentrations.
Fracture risks in patients can be managed using a
bisphosphonate taken orally. This approach is especially suitable in patients who are not medically fit for
surgery or where surgery has been unsuccessful.
Medical management must be directed under the
care of an endocrinologist.
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Indications forsurgery
Surgery should be considered in any patient once a
diagnosis of primary hyperparathyroidism has been
confirmed and even patients with mild hypercalcaemia get symptomatic benefit following surgery. This
is subject to the patient being medically fit enough to
undergo general anaesthesia.
Bilateral neck exploration
This procedure is normally carried out using endotracheal intubation and neck extension to facilitate access
to the neck. Bilateral neck exploration is carried out
through a transverse (Kocher’s
the clavicle to provide access to both retrothyroid
spaces to detect and remove one or more enlarged
glands.
If a single gland is enlarged, it is likely to be an adenoma and is removed once the remaining glands
have been visualized and confirmed to be normal.
Frozen section of the gland, or urgent ‘near patient’
estimation of PTH levels, will confirm the tissue
removed during surgery contains parathyroid tissue.
Frozen section will not distinguish between an adenoma or a carcinoma. Robust pathological assessment of the entire gland is required to achieve this.
4
) incision just above
Unilateral neck exploration
Most (95%) patients with primary hyperparathyroidism have a single affected gland. Preoperative
localization of the adenoma by ultrasound of the neck
and/or sestamibi scanning (or where available 4DCT) enables unilateral neck exploration. Patients with
multigland disease, MEN- related hyperplasia, FHH
and renal disease are not suitable for this approach.
In addition, patients with a short neck and previous
neck surgery or irradiation may also not be suitable.
formed under either general anaesthesia or local
anaesthetic cervical block as a day case. This technique
can be combined with intraoperative PTH measurement, a fall of at least 50% indicating removal of all
hyperfunctioning parathyroid tissue.
Minimally invasive
parathyroidectomy
This relies on the use of an incision of about 2.5cm in
the neck. In some cases, access is gained through a
remote site such as in the transaxillary approach.
Specially designed ports are inserted in strategic locations to avoid placing a scar in the neck and endoscopes may be used in the case of video- assisted
parathyroidectomy. These procedures are comparable to open procedures in terms of achieving curative
outcomes in parathyroid surgery. Patient selection
and surgeon experience are crucial to success. In
some cases, a minimally invasive procedure may be
converted to an open neck procedure when challenges that cannot be remedied using a minimally
invasive approach arise intraoperatively.
Complications ofparathyroid
surgery
The main complications of parathyroid surgery include:
•
Recurrent laryngeal nerve palsy: occurs in under
1% of patients.
Hypocalcaemia: the remaining parathyroid glands
•
are suppressed by the high PTH levels and may
take some time to recover.
•
Persistent hypercalcaemia: residual parathyroid
tissue remains, possibly a fifth gland or an ectopic
gland within the anterior mediastinum.
Focused parathyroidectomy
Following accurate preoperative localization of single
gland disease, exploration is carried out through a
small incision lateral in the neck which may be per-
4
eodore Kocher (1841–1917), Professor of Surgery, Bern,
Switzerland. He won a Nobel Prize in 1909 for work on the
thyroid gland. In addition to the thyroid incision, he also
described a subcostal incision for open cholecystectomy
and a posterior approach to the hip.
Management ofpersistent
or recurrent primary
hyperparathyroidism
Despite careful initial surgery, a number of patients
will not be cured following initial surgery or will
relapse at a later stage. This is most often due to a
failure to diagnose multigland disease or the presence
of an ectopic parathyroid gland. Failure of primary
surgery often raises the prospect of revisional surgery.
These patients require extensive imaging (ultrasound,
sestamibi, CT and MRI scans) prior to surgery to
The parathyroids 411
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localize and remove the abnormal gland(s). Selective
venous sampling, with PTH measurement by catheterization of the venous tributaries in the neck, may
also help localization and is often combined with
arteriography.
Additional resources
Case 108: A patient with colic and its underlying
endocrine cause
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The thymus
Christopher Watson
Learning objective
✓ To have knowledge of the tumours of the thymus and their association
with myasthenia gravis.
The thymus gland controls the development of
T lymphocytes in the embryo and neonate and lies in
the anterior mediastinum between the sternum in
front and great vessels and pericardium posteriorly.
Following puberty, the thymus involutes and
becomes a fat- infiltrated remnant but to the surgeon,
it is of importance in having an illnection with myasthenia gravis and being a rare site
of mediastinal tumour.
understood con-
Tumours
Tumours of the thymus are of complex pathology; they
may arise either from the epithelium (Hassall’s corpus-
1
cles
) and are termed ‘thymomas’, or from lymphoid
tissue, or a mixture of both. Thymic tumours typically
have solid and cystic components, and may be benign
thymomas, or malignant and rapidly invasive thymic
carcinomas. Peak incidence is between the fifth and
seventh decades. The thymus may also be involved in
cases of lymphoma, particularly Hodgkin’s disease.
Neuroendocrine tumours may occasionally originate
1
Arthur Hassall (1817–1894), Physician, Royal Free Hospital,
London, UK. He published the rst textbook on histology in
English.
Ellis and Calne’s Lecture Notes in General Surgery, Fourteenth Edition.
Edited by Christopher Watson and Justin Davies.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
Companion website: www.wiley.com/go/Watson/GeneralSurgery14
in the thymus and may produce vasoactive substances
akin to those produced in carcinoid syndrome.
Clinical features
There are three modes of presentation:
1
A mediastinal mass: Incidental finding on chest
imaging.
Local symptoms of a mass in the mediastinum:
2
Chest pain, breathlessness, phrenic nerve palsy or
obstruction of the superior vena cava.
3
Paraneoplastic syndromes: Autoimmune conditions
such as myasthenia gravis and pure red cell aplasia, or immunodeficiency syndromes.
Treatment
Treatment is by thymectomy via median sternotomy,
combined with radiotherapy and/or chemotherapy if
malignant, to prevent mediastinal recurrence.
Early invasion, with no more than pleural and
mediastinal fat involvement (stage 1), carries a good
prognosis (90% at 5 years); involvement of the pericardium, great vessels or lung has a poor prognosis.
Myasthenia gravis
This condition is characterized by weakness of skeletal muscle caused by autoantibodies directed against
the postsynaptic nicotinic acetylcholine receptors at
the neuromuscular junction, as a consequence of
The thymus 413
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which the motor endplate becomes refractory to the
action of acetylcholine. About 15% of cases are associated with a tumour of the thymus, whereas thymic
hyperplasia is present in most of the remaining cases.
Clinical features
Women are twice as commonly affected as men, and
the disease usually commences in early adult life. The
extrinsic ocular muscles are most often affected and
may indeed be the only ones involved, with ptosis,
diplopia and squint. The affected muscles become
weak with use and recover, partially or completely,
after rest. The voice is weak and death may eventually
occur from respiratory muscle failure.
Treatment
The majority of cases are controlled by choline esterase
inhibitors, for example pyridostigmine, with immunosuppression also having a role in resistant cases.
If a thymoma is present, it is excised, although such
tumours are often locally invasive. Thymectomy is
otherwise indicated if the disease is progressive and
the prognosis is best in young women (under the age
of 40 years) with a history of 5 years or less.
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The adrenal glands
Vasilis Kosmoliaptsis
Learning objective
✓ To know the physiology of the adrenal (suprarenal) glands and
functional and nonparts of the gland, and their management.
functional tumours that derive from the separate
The adrenal glands are paired glands situated above
and medial to the upper pole of each kidney. The cortex derives from the mesoderm of the urogenital
ridge, while the medulla derives from neural crest
ectoderm. These different origins account for the
different physiology of medulla and cortex, and the
different pathology encountered surgically.
Physiology
Adrenal cortex
The adrenal cortex secretes three groups of steroids:
Glucocorticoids (from the zona fasciculata), which
1
regulate carbohydrate metabolism, protein breakdown and fat mobilization.
2 Androgenic corticoids (from the zona reticularis),
which are virilizing.
3 Mineralocorticoids (from the zona glomerulosa),
which regulate mineral and water metabolism.
Aldosterone acts to retain sodium and water and
to excrete potassium.
Glucocorticoids and androgens are under hypothalamic control via adrenocorticotrophic hormone
(ACTH) secreted by the anterior pituitary gland;
Ellis and Calne’s Lecture Notes in General Surgery, Fourteenth Edition.
Edited by Christopher Watson and Justin Davies.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
Companion website: www.wiley.com/go/Watson/GeneralSurgery14
mineralocorticoids are under the control of the
renin–angiotensin system (see Chapter 13). As the
steroids share a similar biochemical structure, it is
not surprising that there is some overlap in actions;
thus, hydrocortisone (cortisol), a glucocorticoid, also
affects salt and water metabolism and has sex steroid
effects (acne, hirsutism) if given in large amounts.
Adrenal medulla
The adrenal medulla is richly innervated with sympathetic preganglionic fibres, and produces the catecholamines adrenaline (epinephrine) and noradrenaline
(norepinephrine) in response to autonomic stimulation.
Pathology
The main pathologies affecting the adrenal gland can
be categorized based on whether they lead to increased
function, owing to tumour or hyperplasia; decreased
function, owing to atrophy, infarction or removal; or
abnormal function, owing to enzyme disorders.
Increased function
• Glucocorticoids (Cushing’s syndrome): adrenocortical adenoma; ACTH- producing pituitary ad enoma;
ectopic ACTH production (paraneoplastic).
• Androgenic corticoids: virilism (the adrenogenital
syndrome).
• Mineralocorticoids: primary hyperaldosteronism
(Conn’s syndrome).
• Catecholamines: phaeochromocytoma.
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