Adrenal Gland

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The adrenal gland has two distinct endocrine components: the cortex and the medulla
The adrenal cortex synthesizes, stores and secretes three main groups of hormone, all of which are steroid hormones synthesized from cholesterol:

Glucocorticoid hormones, e.g. hydrocortisone from zona fasciculata.
Mineralocorticoid hormone (aldosterone), from the zona glomerulosa.
Sex steroids, from zona reticularis.

The adrenal medulla is derived embryologically from neural crest ectoderm and is part of the sympathetic nervous system.
It synthesizes and secretes the vasoactive amines, adrenaline and noradrenaline (epinephrine and norepinephrine).
Excessive production of adrenal cortical hormones usually results from hyperplasia or a tumour.
Excessive ACTH production, for example by an ACTH-secreting adenoma of the pituitary, stimulates an increase in the number, size and secretory activity of the adrenal cortical cells, leading to adrenal cortical hyperplasia.
The uncontrolled excessive production of adrenal cortical hormones may produce Cushing's syndrome.


Adrenal cortical adenoma is a well-circumscribed, yellow tumour in the adrenal cortex, which is usually 2-5 cm in diameter.
The colour of the tumour, as with the adrenal cortex as a whole, is due to the stored lipid (mainly cholesterol), from which the cortical hormones are synthesized.
These tumours are frequent incidental findings at post mortem examination, and appear to have produced no significant metabolic disorder; only a very small percentage produce Cushing's syndrome.
Nevertheless, these apparently 'non-functioning' adenomata are most often encountered in elderly obese people.
There is some debate that they may really represent nodules in diffuse nodular cortical hyperplasia.
Very occasionally, a true adrenal cortical adenoma is associated with the clinical manifestations of Conn's syndrome, and can be shown to be excreting mineralocorticoids.

Adrenal cortical carcinoma is rare, and virtually every case is associated with excessive production of hormones, usually gluco-corticoids and sex steroids.
As a result the patients usually have features of Cushing's syndrome mixed with androgenic effects, which are particularly noticeable in women.
The tumours are usually large and yellowish white, and local invasion and metastatic spread are common.

Ectopic ACTH secretion may be associated with non-adrenal tumours, particularly oat-cell carcinoma of the bronchus and some carcinoid tumours.
In cases of the highly malignant bronchial tumour the symptoms are mainly metabolic, with hypokalaemia, alkalosis and impaired glucose tolerance.
The patient rarely survives long enough to develop the physical features of Cushing's syndrome, although these and hypertension may develop if the inappropriate secretion is due to a less rapidly fatal tumour.


Chronic adrenal cortical insufficiency produces Addison's disease

Addison's disease is caused by chronic adrenal cortical insufficiency due to lack of glucocorticoids and mineralocorticoids.
The main features of the disease are: low serum sodium and high serum potassium, with chronic dehydration; hypotension, often markedly postural; lethargy and weakness; vomiting and loss of appetite; and brownish pigmentation of skin and buccal mucosa.

The most common cause is destruction of the cortex of both adrenals by autoimmune adrenalitis often associated with autoimmune thyroid disease and autoimmune gastritis and other endocrine organ autoimmune disease.
Other causes are bilateral adrenal tuberculosis, fungal infections and adrenal destruction by tumour, but all are rare.

The adrenal is reduced in size and there is a heavy lymphocytic infiltrate, a manifestation of autoimmune adrenalitis.


Acute adrenal cortical failure is usually due to haemorrhagic infarction, but may be iatrogenic

Bilateral haemorrhagic necrosis of the adrenals is usually associated with disseminated intravascular coagulation.
It is a feature of severe septicaemia, particularly meningococcal septicaemia, in which it is known as the 'Waterhouse-Friderichsen syndrome'.
There is hypovolaemic and hypotensive shock, with hypoglycaemia, and high risk of sudden death.

Iatrogenic acute adrenal cortical failure may occur when prolonged high-dose therapeutic corticosteroid therapy is abruptly stopped.
Prolonged corticosteroid therapy leads to suppression of normal endogenous steroid production by the adrenal cortex, which becomes markedly atrophied.
Cessation of exogenous steroid therapy produces acute adrenal cortical failure (adrenal crisis), with hypovolaemic and hypotensive shock, hypoglycaemia, and risk of sudden death.

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Revised: 02-11-2014.