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Results for “ADRENAL CORTEX HYPERFUNCTION”

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At least 595 records · Page 33Linked to original sources
PubMed1986

Evaluation of canine hyperadrenocorticism, using computed tomography.

Abdominal computed tomography was performed in 9 dogs with hyperadrenocorticism and in 2 healthy dogs. Both adrenal glands were identified in all dogs. Computed tomography allowed accurate identification of the sites of adrenal gland dysfunction, when interpreted in combination with a biochemical diagnosis of canine hyperadrenocorticism. This accuracy permitted the retroperitoneal approach to be used for all adrenalectomies. Use of contrast medium (although not essential) was helpful in the computed tomographic identification of blood vessels, kidneys, and other abdominal organs.

Adrenal Cortex Neoplasms↗
PubMed1988

Polycystic ovarian disease and congenital and late-onset adrenal hyperplasia.

This article surveys the congenital and late-onset forms of the common steroidogenic enzyme defects of the adrenal cortex--steroid 21-hydroxylase, steroid 11 beta-hydroxylase, and 3 beta-hydroxysteroid dehydrogenase deficiencies--in connection with the occurrence of polycystic ovarian disease.

3-Hydroxysteroid Dehydrogenases↗
PubMed1987

Hyperadrenocorticism in a ferret.

A 7-year-old adult male ferret had progressive hair loss that was bilaterally symmetric. Also clinically evident were severe dehydration, polydipsia, muffled heart sounds, weak femoral pulses, hepatomegaly, lethargy, weakness, temporal muscular atrophy, dyspnea, and weakness. The blood profile of the ferret indicated profound leukopenia, eosinopenia, and high phosphorus, BUN, creatinine, and potassium concentrations, as well as high aspartate transaminase activity; the albumin concentration was low. The serum cortisol concentration was 8.1 micrograms/dl. Necropsy and histologic findings confirmed a diagnosis of hyperadrenocorticism, complicated by dilatative cardiomyopathy, chronic active hepatitis, and renal disease.

Adrenal Cortex Neoplasms↗
PubMedDate not supplied

[Severe essential arterial hypertension; the physiopathogenic role of the adrenal medulla. I. Population studies and experimental research].

The authors have carried out a populational study by performing psychomorphological and blood determinations, and have detected the presence of a chronic hyperactivity syndrome of the adrenals in 12,5 percent of the healthy young subjects engaged in various activities that they have investigated. In an experimental study the oxydative processes in the enzymatic cycle of Krebs were cut off by injecting the adrenal medullary area with a 40% solution of sodium salicylate, while the secretion of the adrenal cortex was maintained, as was demonstrated by the unaffected activity of the hexose monophosphate shunt in this tissue. The experimental results demonstrated that the adrenal medullary tissue represents a major pathogenetic link in the complex etiopathogeny of essential arterial hypertension, and this invalidates the role attributed by Volhard (in 1931) to the renal tissue, explaining the failure of haemodialysis, bilateral nephrectomy and kidney transplantation in preventing the recurrence of essential arterial hypertension.

Adrenal Cortex Hormones↗