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

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BRIEF DESCRIPTION ABOUT ADDISONS DISEASE FOR DENTAL AND MEDICAL STUDENTS AND FOR GRADUATES AND FOR UNDERGRADUATES WHO FIND IT DIFFICULT TO UNDERSTAND FROM THE MEDICAL PUBLICATONS ABOUT THIS DISEASE AND ITS DIAGNOSIS AND ALSO DIFFERENTIAL DIAGNOSIS.

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

  1. 1. ADDISON’S DISEASE PREPARED BY AIJIN.A.MOHAN
  2. 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. 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. 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. 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. 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..
  7. 7. 1- ADRENAL GLANDS
  8. 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. 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. 10. HYPERPIGMENTATION PREPARED BY AIJIN.A.MOHAN
  11. 11. PIGMENTATION OF BUCCAL MUCOSA
  12. 12. HYPERPIGMENTATION OF THE LIPS PREPARED BY AIJIN.A.MOHAN
  13. 13. 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
  14. 14. 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
  15. 15. PEUTZ JEGHERS SYNDROME PREPARED BY AIJIN.A.MOHAN
  16. 16. VON RECKLINGHAUSENS DISEASE PREPARED BY AIJIN.A.MOHAN
  17. 17. ALBRIGHTS SYNDROME PREPARED BY AIJIN.A.MOHAN
  18. 18. 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
  19. 19. THANK YOU PREPARED BY AIJIN.A.MOHAN

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