{"title":"肾上腺紊乱","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":"{\"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}","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}
• 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).