enrinology內(nèi)分泌總論-文庫吧資料
2025-05-22 01:40本頁面
【正文】 ease. ? ACTH then travels to the adrenal gland, where it stimulates the release of cortisol. ? Cortisol in turn inhibits both CRH and ACTH release（ feedback inhibition） . ? The brain establishes circadian rhythms and can trigger increased CRH release in response to stress. CRH ACTH cortisol Mechanisms of hormone action ? Peptide and catecholamine hormones and prostaglandins bind to receptors on the cell surface. ? Steroid and thyroid hormones act for the most part by binding to intracellular receptors. ? binding to receptors on the cell surface ? binding to intracellular receptors hormones bind to receptors on the cell surface ? Peptide and catecholamine hormones and prostaglandins bind to receptors on the cell surface, where the hormonereceptor interactions affect intracellular mediators, or second messengers. Second messengers ? cAMP: ? Glucagon, ACTH, PTH ? Protein kinase activity ? Insulin ? Calcium ? Alphaadrenergic agonists, AT II ? phospholipids ? ADH, GnRH, TRH. hormones bind to receptors on the cell surface binding to intracellular receptors intracellular receptors Disorders of the endocrine and metabolic system ? Most recognizable disorders of the endocrine system are due to an excess or a deficiency of particular hormones, whether caused by abnormalities of endocrine glands, ectopic production of hormones, abnormal conversion of prohormones to their active forms, or iatrogenic factors. Hypofunction of endocrine glands ? Endocrine glands may be injured or destroyed by neoplasia, infections, hemorrhage, autoimmune disorders, and other causes. Hormone deficiency secondary to extraglandular disorders ? Impaired conversion of a prohormone to a hormone occurs in chronic renal failure, in which there is defective conversion of 25hydroxycholecalciferol to 1,25dihydroxycholecalciferol. Hyporesponsiveness to hormones ? Hormone levels may be normal or even elevated in the presence of manifestations of endocrine deficiency. Hormone exess syndrome ?Hyperfunction of endocrine glands ?Ectopic hormone production ?Hormone administration ?Tissue hypersensitivity Hyperfuction of endocrine glands ?
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