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M K AM K A R TI
VAC LAM
P A N G U M LA N G H A YA T
G IR IM
Y A T K R IP T A M A H A M
VAN D
Name of the disease & terminologies
Etiology
History, signs and symptoms
Physical examination
Investigation
Treatment according to allopathic medicine
Other therapies
Yoga practices
Books and journals for reference
ALTERNATIVE NAMES
Addison disease
Adrenocortical hypofunction
Chronic adrenocortical insufficiency
Adrenal insufficiency
INTRODUCTION
Either of two small, dissimilarly shaped
endocrine glands, one located above each
kidney, consisting of the cortex, which
secretes several steroid hormones, and the
medulla, which secretes epinephrine.
Also called suprarenal gland.
The adrenal glands, located on the cephalad
portion of each kidney, consist of a cortex and
medulla, each with separate endocrine
functions.
The adrenal cortex produces glucocorticoids
(primarily cortisol), mineralocorticoids
(primarily aldosterone), and androgens
(primarily dehydroepiandrosterone and
androstenedione).
Glucocorticoids promote and inhibit gene
transcription in many cells and organ systems.
Prominent effects include anti-inflammatory
actions and increased hepatic
gluconeogenesis.
Mineralocorticoids regulate electrolyte
transport across epithelial surfaces,
particularly renal conservation of Na in
exchange for K.
Adrenal androgens' chief physiologic activity
occurs after conversion to testosterone
Physiology of the pituitary-corticoadrenal
system is further discussed in Principles of
Endocrinology and discussed in Pituitary
Disorders.
The adrenal medulla is composed of
chromaffin cells, which synthesize and secrete
catecholamines (mainly epinephrine and lesser
amounts of norepinephrine
Chromaffin cells also produce bioactive
amines and peptides (eg, histamine, serotonin,
chromogranins, neuropeptide hormones).
Epinephrine and norepinephrine the major
effector amines of the sympathetic nervous
system, are responsible for the flight or fight
response (ie, chronotropic and inotropic
effects on the heart; bronchodilation;
peripheral and splanchnic vasoconstriction
with skeletal muscular vasodilation; metabolic
effects including glycogenolysis, lipolysis, and
renin release).
Most deficiency syndromes affect output of all
adrenocortical hormones.
Hypofunction may be primary (malfunction of
the adrenal gland itself, as in Addison's
disease) or secondary (due to lack of adrenal
stimulation by the pituitary or hypothalamus,
although some experts refer to hypothalamic
malfunction as tertiary).
Hyperfunction produces distinct clinical
syndromes.
Hypersecretion of androgens results in adrenal
virilism; of glucocorticoids, Cushing's
syndrome; and of aldosterone,
hyperaldosteronism (aldosteronism).
These syndromes frequently have overlapping
features.
Hyperfunction may be compensatory, as in
congenital adrenal hyperplasia, or due to
acquired hyperplasia, adenomas, or
adenocarcinomas.
Excess quantities of epinephrine and
norepinephrine are produced in
pheochromocytoma
Addison's disease is a hormone deficiency
caused by damage to the outer layer of the
adrenal gland (adrenal cortex).
Addison's disease is a disorder that results in
the body producing insufficient amounts of
certain hormones produced by the adrenal
glands.
The adrenal glands are located just above each
of two kidneys.
These glands are part of the endocrine system,
and they produce hormones that give
instructions to virtually every organ and tissue
in the body.
In Addison's disease, adrenal glands produce too
little cortisol, which is one of the hormones in a
group called the glucocorticoids.
Sometimes, Addison's disease also involves
insufficient production of aldosterone, one of the
mineralocorticoid hormones.
Addison's disease can be life-threatening.
Also called adrenal insufficiency or
hypocortisolism, Addison's disease can occur at
any age, but is most common in people ages 30 to
50.
Treatment for Addison's disease involves taking
hormones to replace the insufficient amounts being
made by adrenal glands.
ETIOLOGY
About 70% of cases in the US are due to idiopathic
atrophy of the adrenal cortex, probably caused by
autoimmune processes.
The remainder result from destruction of the adrenal
gland by granuloma (eg, TB), tumor, amyloidosis,
hemorrhage, or inflammatory necrosis.
Hypoadrenocorticism can also result from
administration of drugs that block corticosteroid
synthesis (eg, ketoconazole, the anesthetic
etomidate).
Addison's disease may coexist with diabetes mellitus
or hypothyroidism in polyglandular deficiency
syndrome.
SIGNS AND SYMPTOMS
Signs and symptoms of Addison's disease usually
develop slowly, often over several months, and may
include:
Muscle weakness and fatigue
Weight loss and decreased appetite
Darkening of the skin (hyperpigmentation)
Low blood pressure, even fainting
Salt craving
Low blood sugar (hypoglycemia)
Nausea, diarrhea or vomiting
Irritability
Depression
Sometimes, however, the signs and symptoms of
Addison's disease may appear suddenly.
Addisonian crisis
Addisonian crisis may be provoked by
physical stress (such as injury, infection or
illness), if Addison's disease is untreated
WHEN TO SEEK MEDICAL ADVICE
If severe fatigue, unintentionally lost weight,
feel progressively weaker, experience
abdominal pain, fainting spells and the skin
has become darker, see the doctor to
determine whether Addison's disease or some
other medical condition may be the cause.
Adrenal glands, located above each of kidneys, produce a number of
hormones, among them the glucocorticoids and the mineralocorticoids.
SCREENING AND DIAGNOSIS
Doctor will talk first about the medical history
and the signs and symptoms.