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ADDISON’S DISEASE 
PREPARED BY 
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. 
PREPARED BY 
AIJIN.A.MOHAN
ETIOLOGY 
TUBERCULOSIS-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 
PREPARED BY 
AIJIN.A.MOHAN
PATHOGENESIS 
ACTH 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 features 
Signs 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 
PREPARED BY 
AIJIN.A.MOHAN
PIGMENTATION OF BUCCAL MUCOSA
HYPERPIGMENTATION OF THE LIPS 
PREPARED BY 
AIJIN.A.MOHAN
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. 
PREPARED BY 
AIJIN.A.MOHAN
DIFFERENTIAL DIAGNOSIS 
Hyper 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 
PREPARED BY 
AIJIN.A.MOHAN
VON RECKLINGHAUSENS DISEASE 
PREPARED BY 
AIJIN.A.MOHAN
ALBRIGHTS SYNDROME 
PREPARED BY 
AIJIN.A.MOHAN
MANAGEMENT 
It is done by adequate corticosteroid 
maintenance therapy provided by an 
average daily dose of 25-40 mg 
cortisone. 
PREPARED BY 
AIJIN.A.MOHAN
THANK YOU 
PREPARED BY 
AIJIN.A.MOHAN

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

  • 1. ADDISON’S DISEASE PREPARED BY AIJIN.A.MOHAN
  • 2. 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.
  • 3. Addison’s disease is an un common condition estimated to occur in 1 in 100000 of the population. PREPARED BY AIJIN.A.MOHAN
  • 4. ETIOLOGY TUBERCULOSIS-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
  • 5. 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 PREPARED BY AIJIN.A.MOHAN
  • 6. PATHOGENESIS ACTH 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..
  • 8. Clinical features Signs 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
  • 9. 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.
  • 10.
  • 13. HYPERPIGMENTATION OF THE LIPS PREPARED BY AIJIN.A.MOHAN
  • 14. 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. PREPARED BY AIJIN.A.MOHAN
  • 15. DIFFERENTIAL DIAGNOSIS Hyper 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
  • 16. PEUTZ JEGHERS SYNDROME PREPARED BY AIJIN.A.MOHAN
  • 17. VON RECKLINGHAUSENS DISEASE PREPARED BY AIJIN.A.MOHAN
  • 18. ALBRIGHTS SYNDROME PREPARED BY AIJIN.A.MOHAN
  • 19. MANAGEMENT It is done by adequate corticosteroid maintenance therapy provided by an average daily dose of 25-40 mg cortisone. PREPARED BY AIJIN.A.MOHAN
  • 20. THANK YOU PREPARED BY AIJIN.A.MOHAN