Addison’s disease important DR. Aijin.A.Mohan

ADDISON’S DISEASE

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AIJIN.A.MOHAN

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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AIJIN.A.MOHAN

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

AIJIN.A.MOHAN

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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AIJIN.A.MOHAN

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

AIJIN.A.MOHAN

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

AIJIN.A.MOHAN