Addison S Disease

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ADDISON´S

DISEASE

ROJAS MARTINEZ CHRISTIAN DE JESUS. 8 B


DRA. SALCEDO OROZCO THANIA.
DEFINITION

• Addison’s disease, the traditional term for primary adrenal


insufficiency, is defined as the clinical manifestation of chronic
glucocorticoid- and/or mineralocorticoid deficiency due to failure of
the adrenal cortex which may result in an adrenal crisis with
potentially life-threatening consequences.
ETIOLOGY AND CLASSIFICATION

• This is caused by an inability of the adrenal cortices to produce adequate


adrenocortical hormones. Adrenal insufficiency is classified as primary or
secondary.
• Primary Adrenal Insufficiency
• Any disease process which causes direct injury to the adrenal cortex can
result in primary adrenal insufficiency (Addison disease).
• Secondary Adrenal Insufficiency
• Secondary insufficiency occurs most commonly due to exogenous steroid
administration resulting in the suppression of ACTH synthesis.

• Primary = autoimmune-mediated intrinsic adrenal gland dysfunction


(both cortisol and aldosterone deficiency).
• Secondary = chronic glucocorticoid administration resulting in hypothalamic-
pituitary dysfunction (only cortisol deficiency).
EPIDEMIOLOGY

• Addison disease is rare. The incidence is 0.6 per 100,000 of the


population per year.
• The total number of people affected by this condition at a
given time ranges from 4 to 11 per 100,000 of the population. In
adults, the common age of presentation is 30 to 50 years.
PATHOPHYSIOLOGY

• Adrenal failure in Addison disease results in decreased cortisol


production initially followed by that of aldosterone, both of which will
eventually result in an elevation of adrenocorticotropic (ACTH)
and melanocyte-stimulating hormone (MSH) hormones due to the
loss of negative feedback inhibition
MANIFESTATIONS

• The dramatic consequences of adrenal failure with weakness,


weight loss, anorexia, orthostatic hypotension due to
dehydration, salt craving, hyperpigmentation, musculoskeletal
and abdominal pain, nausea, and vomiting.
DIAGNOSIS

• The diagnosis is established by demonstrating low cortisol and aldosterone levels,


high renin level, and a blunt cortisol response with ACTH stimulation. The approach
for the evaluation s as follows;
• An inappropriately low cortisol level.
• Assessing the adrenal cortex's functional capacity to synthesize cortisol and
determine whether the cortisol deficiency is related to a corticotropin (ACTH)
deficiency.
• Determining whether a treatable cause is present.
TREATMENT

• Early recognition is critical for the management of adrenal insufficiency.


• Acute Phase
• Patients with an adrenal crisis require the following:
• Fluid resuscitation to restore the intravascular volume with intravenous (IV) normal saline
• Dextrose to correct hypoglycemia
• Correction of the hormone deficiency, both glucocorticoid and mineralocorticoid

• The immediate hormonal treatment is the administration of hydrocortisone.


REFERENCES

• Munir, S., Quintanilla Rodriguez, B. S., & Waseem, M. (2021). Addison Disease. In StatPearls. StatPearls
Publishing.
• Barthel, A., Benker, G., Berens, K., Diederich, S., Manfras, B., Gruber, M., Kanczkowski, W., Kline, G.,
Kamvissi-Lorenz, V., Hahner, S., Beuschlein, F., Brennand, A., Boehm, B. O., Torpy, D. J., & Bornstein, S. R.
(2019). An Update on Addison's Disease. Experimental and clinical endocrinology & diabetes : official journal,
German Society of Endocrinology [and] German Diabetes Association, 127(2-03), 165–175.
https://doi.org/10.1055/a-0804-2715
• Pearce, S., Gan, E. H., & Napier, C. (2021). MANAGEMENT OF ENDOCRINE DISEASE: Residual adrenal
function in Addison's disease. European journal of endocrinology, 184(2), R61–R67.
https://doi.org/10.1530/EJE-20-0894

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