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Addison’s Disease, Research Paper Example

Pages: 2

Words: 640

Research Paper

Addison’s Disease Mapping Pathophysiology

Addison’s disease is an endocrine disorder that affects individuals from all age groups. The disease is caused by insufficient production in the hormone cortisol. Even though the disease affects individuals from age groups, there is a considerable difference in the severity and manner in which adult and child patients experience

Etiology

In adults 70% of Addison’s disease cases are as a result of adrenal cortex idiopathic atrophy. This largely stems from the autoimmune process. The other 30% of the cases in adults are as a result of the adrenal gland suffering damage caused by amyloidosis, inflammatory necrosis, tumor, hemorrhage and granuloma (Huether, McCance, Brashers, & Rote, 2014). In adults, a patient with Addison’s disease may also be found with hypothyroidism in polyglandular deficiency syndrome or diabetes mellitus. However, in children, congenital adrenal hyperplasia (CAH) is the chief cause of primary adrenal insufficiency.

Pathogenesis

Patient experiences deficiencies in glucocorticoids and mineralocorticoids. Adrenal insufficiency usually depicts as a defect within the hypothalamic-pituitary-adrenal axis. The destruction of the adrenal cortex is the main cause of Addison’s disease.

Glucocorticoid deficiency: this deficiency has a severe effect on insulin sensitivity and the metabolism of protein, carbohydrate and fat. This stems from the fact that glucocorticoid deficiency is a contributory factor of hypotension. When there is an insufficiency or general lack of cortisol, the amount of carbohydrate derived from protein becomes insufficient. As a result of this, the patient’s resistance to trauma, infection and any other form of stress considerably depreciates. This is because the lacking neuromuscular function causes general physiological and biological weakness. In adults, the type II adrenal insufficiency results from an inadequacy in ACTH production (Falvo, 2014). In these cases, electrolyte levels are either mildly deranged or at the normal state.

Mineralocorticoid deficiency: the reabsorption of and is stimulated by mineralocorticoids. As such, this deficiency causes a considerable decrease in excretion and an inverse increase in excretion which can be mainly detected in urine. However, in severe cases, it can be traced in the GI tract, saliva and sweat.

Presenting Signs and Symptoms

Most of the symptoms of adrenal insufficiency are gradual and are particularly more severe in children when compared to adults. This is the underlying difference between the symptoms. This begins a gradual loss of appetite, muscle weakness and fatigues and weight loss. More than half of the reported cases have also recorded to have been suffering from diarrhea and/or vomiting. As a result of the gradual decrease in blood pressure, patients experience dizziness and at time faint (Brook, Clayton, & Brown, 2009). Children in particular experience a more sever effect of low blood sugar and salt loss. Children depict a craving for salty foods.

ACTH Stimulation Test

The most used test for Addison’s disease. Measurements of urine cortisol and/or blood cortisol are taken before and after the patient has received an injection of ACTH. Patients with normal adrenal function would depict an increase in the levels of blood cortisol and urine cortisol. However, for patients who have both types of adrenal insufficiency may depict poor responses to the test. Severe

Medical Treatment

Treatment mainly involves replacing the hormones not being produced by the adrenal glands. Hydrocortisone tablets which are taken orally are used to replace cortisol. In case of aldosterone deficiency, oral doses of Florinef (fludrocortisone acetate) can be taken. This is a mineralocorticoid that is taken to increase a patient’s intake. However, this therapy is most commonly used on children. Adults do not require aldosterone replacement therapy. This is because adults, who have secondary (type II) adrenal insufficiency, can maintain a constant production of aldosterone.

References

Brook, C. G., Clayton, P. E., & Brown, R. S. (2009). Brook’s clinical pediatric endocrinology. Hoboken: Wiley-Blackwell.

Falvo, D. R. (2014). Medical and psychosocial aspects of chronic illness and disability. Burlington: ones & Bartlett Learning.

Huether, S. E., McCance, K. L., Brashers, V. L., & Rote, N. S. (2014). Pathophysiology : the biologic basis for disease in adults and children. St. Louis: Elsevier.

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