Hypoadrenalism-Addison’s Disease
Addison’s disease results from failure of the adrenal cortices to
produce adrenocortical hormones, and this in turn is most frequently caused by primary atrophy of the adrenal cortices.
In about 80 per cent of the cases, the atrophy is caused by autoimmunity
against the cor-tices. Adrenal gland hypofunction is also frequently caused by
tuberculous destruction of the adrenal glands or invasion of the adrenal
cortices by cancer. The dis-turbances in Addison’s disease are as follows.
Mineralocorticoid Deficiency. Lack of aldosterone
secre-tion greatly decreases renal tubular sodium reabsorp-tion and
consequently allows sodium ions, chloride ions, and water to be lost into urine
in great profusion. The net result is a greatly decreased extracellular fluid
volume. Furthermore, hyponatremia, hyperkalemia, and mild acidosis develop
because of failure of potassium and hydrogen ions to be secreted in exchange
for sodium reabsorption.
As the extracellular fluid becomes depleted, plasma volume falls,
red blood cell concentration rises markedly, cardiac output decreases, and the
patient dies in shock, death usually occurring in the untreated patient 4 days
to 2 weeks after cessation of mineralo-corticoid secretion.
Glucocorticoid Deficiency. Loss of cortisol secretion
makesit impossible for a person with Addison’s disease to maintain normal blood
glucose concentration between meals because he or she cannot synthesize
significant quantities of glucose by gluconeogenesis. Furthermore, lack of
cortisol reduces the mobilization of both proteins and fats from the tissues,
thereby depressing many other metabolic functions of the body. This
sluggishness of energy mobilization when cortisol is not available is one of
the major detrimental effects of glu-cocorticoid lack. Even when excess
quantities of glucose and other nutrients are available, the person’s muscles
are weak, indicating that glucocorticoids are needed to maintain other
metabolic functions of the tissues in addition to energy metabolism.
Lack of adequate glucocorticoid secretion also makes a person with
Addison’s disease highly susceptible to the deteriorating effects of different
types of stress, and even a mild respiratory infection can cause death.
Melanin Pigmentation. Another characteristic of
mostpeople with Addison’s disease is melanin pigmentation of the mucous
membranes and skin. This melanin is not always deposited evenly but
occasionally is deposited in blotches, and it is deposited especially in the
thin skin areas, such as the mucous membranes of the lips and the thin skin of
the nipples.
The cause of the melanin deposition is believed to be the
following: When cortisol secretion is depressed, the normal negative feedback
to the hypothalamus and anterior pituitary gland is also depressed, therefore
allowing tremendous rates of ACTH secretion as well as simultaneous secretion
of increased amounts of MSH. Probably the tremendous amounts of ACTH cause most
of the pigmenting effect because they can stimulate formation of melanin by the
melanocytes in the same way that MSH does.
Treatment of People with Addison’s Disease. An untreatedperson with total
adrenal destruction dies within a few days to a few weeks because of weakness
and usually circulatory shock. Yet such a person can live for years if small
quantities of mineralocorticoids and glucocorti-coids are administered daily.
Addisonian Crisis. As noted earlier,
greatquantities of glucocorticoids are occasionally secreted in response to
different types of physical or mental stress. In a person with Addison’s
disease, the output of glucocorticoids does not increase during stress. Yet
whenever different types of trauma, disease, or other stresses, such as
surgical operations, supervene, a person is likely to have an acute need for
excessive amounts of glucocorticoids and often must be given 10 or more times
the normal quantities of glucocorticoids to prevent death.
This critical need for extra glucocorticoids and the associated
severe debility in times of stress is called an addisonian crisis.
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