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Νόσος Αdisson, Hypoadrenocorticism

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Νόσος Αdisson, Hypoadrenocorticism Empty Νόσος Αdisson, Hypoadrenocorticism

Post  Admin 9/4/2009, 9:41 am

Hypoadrenocorticism

Naturally occurring hypoadrenocorticism (also known as primary hypoadrenocorticism or Addison's disease) is caused by destruction of the adrenal cortices. The resultant deficiency of both glucocorticoids and mineralocorticoids causes the clinical signs observed. Primary hypoadrenocorticism is a rare disease in the cat.

The most common clinical signs of primary hypoadrenocorticism in the cat are lethargy, inappetance, and weight loss. Vomiting and diarrhea are less frequently encountered. in some cats, the symptoms may wax and wane. Physical examination may reveal depression, weakness, dehydration, and low body temperature.

Primary hypoadrenocorticism should be suspected in a cat with appropriate clinical features and laboratory abnormalities. Classic laboratory findings in a cat with Addison's disease include low blood sodium and high blood potassium concentrations (resulting from the lack of mineralocorticoids), as well as hyperphosphatemia, azotemia, (excess urea in the blood), and mild anemia. However, these laboratory findings also can be seen with other diseases. The most accurate screening test for hypoadrenocorticism is the ACTH stimulation test, in which the response of the adrenal glands to a test dose of commercial ACTH is evaluated.

Therapy for the cat with primary hypoadrenocorticism consists of lifelong glucocorticoid and mineralocorticoid supplementation, either oral or injectable. Initial treatment also may require fluid administration. The dosage of mineralocorticoid replacement is adjusted based on the results of serial blood sodium and potassium concentrations.

Secondary hypoadrenocorticism develops when pituitary ACTH secretion is deficient, resulting in inadequate stimulation of adrenal glucocorticoid production. Certain drugs containing glucocorticoids or progesterone can inhibit pituitary ACTH secretion. The resultant deficiency in glucocorticoid production may result in clinical signs similar to those observed in primary hypoadrenocorticism, except the electrolyte (sodium and potassium) disturbances associated with mineralocorticoid deficiency arc absent.

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