{"title":"Adrenal gland disorders","authors":"G. Butler, J. Kirk","doi":"10.1093/med/9780199232222.003.0068","DOIUrl":null,"url":null,"abstract":"\n\n\n • The fetal adrenal gland has an additional cortex which atrophies after birth.\n \n\n • Postnatally, there are three zones to the cortex:\n \n\n\n ◦ glomerulosa producing mineralocorticoids\n \n\n ◦ fasciculata producing cortisol\n \n\n ◦ reticularis producing androgens.\n \n\n • Adrenarche is a maturation process from age 6 years with an increase in androgens.\n \n\n • Acute adrenal crisis presents with:\n \n\n\n ◦ low sodium\n \n\n ◦ high potassium\n \n\n ◦ cortisol low/undetectable.\n \n\n • ACTH raised in primary causes, low in secondary.\n \n\n • Primary insufficiency may be congenital dysplasia (adrenal hypoplasia congenita) and enzyme blocks: congenital adrenal hyperplasia (CAH).\n \n\n • Acquired causes include autoimmune adrenalitis (Addison’s disease) and tuberculosis.\n \n\n • Secondary insufficiency arises due to adrenocorticotropic hormone deficiency from hypopituitarism (congenital or acquired).\n \n\n • CAH, e.g. 21-hydroxylase deficiency (commonest), can present with virilization of a newborn female, hyperandrogenism, or salt-wasting adrenal crisis.\n \n\n • Iatrogenic treatment is commonest cause of adrenal steroid excess.\n \n\n • Other causes are adrenal adenoma/carcinoma (Cushing syndrome) or pituitary adenoma (Cushing disease).","PeriodicalId":217485,"journal":{"name":"Paediatric Endocrinology and Diabetes","volume":"22 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2020-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Paediatric Endocrinology and Diabetes","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1093/med/9780199232222.003.0068","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
• The fetal adrenal gland has an additional cortex which atrophies after birth.
• Postnatally, there are three zones to the cortex:
◦ glomerulosa producing mineralocorticoids
◦ fasciculata producing cortisol
◦ reticularis producing androgens.
• Adrenarche is a maturation process from age 6 years with an increase in androgens.
• Acute adrenal crisis presents with:
◦ low sodium
◦ high potassium
◦ cortisol low/undetectable.
• ACTH raised in primary causes, low in secondary.
• Primary insufficiency may be congenital dysplasia (adrenal hypoplasia congenita) and enzyme blocks: congenital adrenal hyperplasia (CAH).
• Acquired causes include autoimmune adrenalitis (Addison’s disease) and tuberculosis.
• Secondary insufficiency arises due to adrenocorticotropic hormone deficiency from hypopituitarism (congenital or acquired).
• CAH, e.g. 21-hydroxylase deficiency (commonest), can present with virilization of a newborn female, hyperandrogenism, or salt-wasting adrenal crisis.
• Iatrogenic treatment is commonest cause of adrenal steroid excess.
• Other causes are adrenal adenoma/carcinoma (Cushing syndrome) or pituitary adenoma (Cushing disease).