ADDISON’S DISEASE
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ADDISON’S DISEASE
Addison’s disease is also called adrenal insufficiency
Addison’s disease is a hormonal disorder resulting from
a severe or total deficiency of the hormones made in the
adrenal cortex.
Clinically the disease is characterized by bronzing of the skin
and a pigmentation of the mucous membrane.
Both oral and skin pigmentation are thought to be result from
melanocytes stimulating hormonal activity.
Addison’s disease is an un common condition
estimated to occur in 1 in 100000 of the population.
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ETIOLOGYTUBERCULOSIS-It was a leading cause of addison’s
disease until the antibiotics were introduced that
successfully treated T.B.
Autoimmune disorders-Here the body’s immune
system makes antibiotics which cells of the adrenal
cortex and slowly destroys them.
Adrenocortical destruction-Bilateral adrenocortical
destruction after T.B or fungal infection and an
idiopathic atrophy are the most frequent causes .PREPARED BY
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Others- Occasionally , bilateral tumor metastasis
leukemic infiltration and amyloidosis of the
adrenal cortex have been found to be responsible
,other less common causes include cancer ,
chronic infection , Cytomegalovirus , surgical
removal of adrenal glands.
Whatever may be the cause the loss of adrenal
cortex results in deficiency in both glucocoticoids
and mineralocorticoids
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AIJIN.A.MOHAN
PATHOGENESISACTH and MSH are similar in structure and ACTH is
believed to have some degree of melanocyte stimulating
activity.
Normally pituitary gland produces ACTH which causes
adrenal cortex to produce glucocorticoids which inturn
secreted into the circulation .When glucocorticoids reach
a certain concentration in the blood they cause the
anterior pituitary to cease the production of the ACTH . In
Addison’s disease however the defective cortex is unable
to produce much glucocorticoid , so this feedback
mechanism is not activated and the pituitary continues to
produce ACTH .As a result increased production of
melanin changes the colour of skin in a smoky tan or
chestnut brown..
1- ADRENAL GLANDS
Clinical featuresSigns and symptoms - Fatigue , weakness , weight
loss , abdominal pain , vomiting and mood
disturbances (maniac,deppressive) . These
symptoms worsen overtime due to the slowly
progressive loss of cortisol and aldosterone
production.
Skin signs :
HYPER PIGMENTATION- It is most evident in areas
exposed to light, but also affects the body folds, the
sites of pressure and friction and in the areas of palm
and soles.
It is also prominent on the gums , buccal mucosa
,nipple , armpits , genitals
Women may have loss of androgen stimulated hair such as pubic and under arm hair.
PIGMENTATION : Pigmentation usually appears early and is one of the most prominent signs of the disease.
The more usual being deep tanning of the skin and mucous membrane with heavier deposits of melanin over pressure points such as cheek . The increased melanocytic activity is expressed by the development of distinct brownish macule on the oral mucosa and the skin.
COLOUR OF PIGMENTATION : Bluish black to pale brown or deep chocolate spreading over buccal mucosa from the angle of mouth or developing on the gingiva tongue and lips.
HYPERPIGMENTATION
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PIGMENTATION OF BUCCAL MUCOSA
HYPERPIGMENTATION OF THE LIPS
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DIAGNOSIS`
Test’s measuring cortisol and aldosterone blood
and urine levels must be performed to make a
definite diagnosis.
The diagnosis of addison’s disease is
based on the clinical sign as well as on
characteristic changes in the blood
sodium and chloride levels.
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DIFFERENTIAL DIAGNOSISHyper pituitarism- It can be distinguished by the
use of urine test levels of 17-ketosteroid in the urine
are decreased in the former but elevated in the latter
condition . A history of silver ingestion identifies
argyra.
Peutz-jeghers syndrome , Albrights syndrome
and Recklinhausens disease- The macular type of
discolouration that occasionally develop in place of
more generalized tanning might be mistaken for
peutz jegher’s syndrome , albrights syndrome or von
recklinghausens disease.PREPARED BY
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PEUTZ JEGHERS SYNDROME
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VON RECKLINGHAUSENS DISEASE
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ALBRIGHTS SYNDROME
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MANAGEMENT
It is done by adequate corticosteroid
maintenance therapy provided by an
average daily dose of 25-40 mg
cortisone.
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AIJIN.A.MOHAN
THANK YOUPREPARED BY
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