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Addison’s disease
Addison’s disease
Addison’s disease
Addison’s disease
Addison’s disease
Addison’s disease
Addison’s disease
Addison’s disease
Addison’s disease
Addison’s disease
Addison’s disease
Addison’s disease
Addison’s disease
Addison’s disease
Addison’s disease
Addison’s disease
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Addison’s disease

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  • 1. Addison’s Disease:The insufficiency of adrenal glands
  • 2. IntroductionAddison’s Disease is a rare and chronicdisease that is characterized by adrenalinsufficiencyThere is a decrease in hormones in theadrenal cortex such as glucocorticoids andmineralocorticoids6-110 cases diagnosed per 100,000 in theworld per year.1.4 million deaths per year around theworld.Usually effects 30-50 year-olds, but can beseen in all ages
  • 3. HistoryFirst discovered by Thomas Addison in 1855First described as an infection of the adrenal gland- mostcommonly TB.Now instead of infection, its most commonly characterizedby an autoimmune destruction of the adrenal glands
  • 4. Causes of the DiseaseThree different causes of the diseaseAdrenal Dysgenesis:Genetic CausesImparied Steriodiogensis:Congenital Adrenal HyperplasiaAdrenal Destruction:Autoimmune destruction
  • 5. Causes of DiseaseAdrenal Destruction:Most common type in industrialized worldAffects humoral and cell-mediated responsesImmune reaction against enzyme 21-hydroxylase, acytochrome P450 enzyme.Normal functioning 21-hydroxylase catalyzes the additionof an “-OH” on carbon 21 in steroidsAddison’s Disease has an enormous amount ofautoantibodies attack this enzyme and slowly kill off theadrenal cortex.82.5% of autoantibodies are adrenal antibodies
  • 6. SymptomsChronic fatigueMuscle WeaknessWeight loss, Nausea, DiarrheaHyperpigmentationHypercalcemia, Hypoglycemia, Hypoatremia, andHyperkalemiaEsinophilia and LymphocytosisMetabolic acidosisAddisonian Crisis:Severely low blood pressure and potential coma or death
  • 7. How Are the Hormones Affected?When Addison’s disease goes into affect, the Anteriorpituitary produces excessive but ineffective amounts ofAdrenocorticotropic (ACTH) to the adrenal cortex thushindering its ability to produce and release hormones(Glucocorticoids and Mineralocorticoids).Since there is no ACTH to stimulate the adrenal cortexto release its hormones, the adrenal cortex can notrelease hormones to regulate processes in the body.
  • 8. Normal Negative FeedbackThe hypothalamus releases hypothalamic inhibitory orreleasing hormones to the anterior pituitary.The anterior pituitary then releases ACTH to the adrenalcortex.The adrenal cortex will then release Glucocorticoids (toraise blood glucose levels or to replenish glucose duringor after stressful situations) or Mineralocorticoids (toreabsorb sodium and excrete potassium in order tobalance water in the body).When their functions are completed, the target tissuesof the hormones will release their own hormones back tothe hypothalamus in order to stop the release ofhormones to affect the body.
  • 9. Normal negative feedback loopsTarget tissueHormone of targettissue
  • 10. Disrupted Negative Feedback The anterior pituitary releases excessive yet ineffective amountsof ACTH which is supposed to stimulate the adrenal cortex. The adrenal cortex as a result is affected negatively and does notrelease Glucocorticoids or Mineralocorticoids. Since Glucocorticoids are not produced, glucose cannot bereplenished when stressful situations occur. Since Mineralocorticoids are not produced, there is a lack ofsodium and water in the body thus leading to severe dehydration. Also, because ACTH exists in excessive yet ineffective amounts,bronzing of the skin occurs because ACTH is linked to melaninproduction.
  • 11. Diagram of disrupted negativefeedbackExcessive and ineffectiveamounts ofAdrenal cortexhormones are notreleased
  • 12. DiagnosisDetermined by low level of adrenal hormone afterstimulation with synthetic ACTH hormone tetercosactideShort Test:Compares blood cortisol levels before and after250 micrograms of tetracosactide if abnormal go to long testLong Test:1 mg of tetracosactide is administered and blood taken at 1, 4, 8,and 24 hours later
  • 13. Current TreatmentReplacement corticoidsteroids or fludrocortisoneacetateDoses change according to lifestyle, i.e. stress, infectionor injuryHave to carry emergency injection of hydrocortisoneand card/bracelet indentifying their condition
  • 14. Clinical TrialsRevival of Stem Cells in Addison’s StudyAims to regenerate adrenocorticolsteroidogenic cell functions by stimulationproliferation and differentiation of progenitorcells in order to replace damaged adrenalcortex cells
  • 15. Conclusion and Future StudiesIt’s a rare but detrimental disease if left untreatedManageable disease through hormone therapy and helpsindividuals lead a normal lifeFuture StudiesDeveloping a time release capsule to better mimic thenatural fluctuations of the cortisol production

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