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- 2021-03-24 发布于上海
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第十二章
内分泌系统疾病
;内分泌系统的组成:
内分泌腺:
内分泌组织:
内分泌细胞(APUD细胞,amine precursor uptake and decarboxylation):能摄取胺前体并将其脱羧形成相应的胺和多肽。
;Homeostasis in the hypothalamus-pituitary-thyroid axis and mechanism of action of thyroid hormones. Secretion of thyroid hormones (T3 and T4) is controlled by trophic factors secreted by both the hypothalamus and the anterior pituitary. Decreased levels of T3 and T4 stimulate the release of thyrotropin-releasing hormone (TRH) from the hypothalamus and thyroid-stimulating hormone (TSH) from the anterior pituitary, causing T3 and T4 levels to rise. Elevated T3 and T4 levels, in turn, feed back to suppress the secretion of both TRH and TSH. TSH binds to the TSH receptor on the thyroid follicular epithelium, which causes activation of G proteins, and cAMP-mediated synthesis and release of thyroid hormones (T3 and T4). In the periphery, T3 and T4 interact with the thyroid hormone receptor (TR) to form a hormone-receptor complex that translocates to the nucleus and binds to so-called thyroid response elements (TREs) on target genes to initiate transcription.;Disorders Associated with Thyrotoxicosis;
甲状腺的正常解剖与组织结构
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;
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;甲状腺素的形成过程: 合成,贮存,碘化,重吸收,分解释放;(3) 甲状腺球蛋白的酪氨酸残基+I2O
碘化的甲状腺球蛋白(碘化)
(4) 滤泡腔内 滤泡
上皮细胞胞质内(重吸收) 胶质小泡
甲状腺球蛋白分解 甲状腺素(T4,四碘甲状腺原氨酸)+T3
(分解释放); 甲 状 腺 肿
(goiter)
是由于缺碘或某些致甲状腺肿因子所引起的甲状腺非肿瘤性增生性疾病。
;分类
根据增生情况:弥漫性甲状腺肿
结节性甲状腺肿
;弥漫性非毒性甲状腺肿
Diffuse nontoxic goiter
(又称: 单纯性甲状腺肿
Simple goiter
地方性甲状腺肿
Endemic goiter )
; 病 因
1.缺碘
缺碘时甲状腺对脑垂体的反馈抑制??弱,促甲状腺素增高,使甲状腺素分泌增高,甲状腺增大,充血,滤泡上皮增生,胶样物质减少,当贮存碘用完,碘与酪氨酸结合↓ 甲状腺素↓ 促甲状腺素分泌↑ 上皮合成大量的甲状腺球蛋白贮存在滤泡腔内,压迫上皮萎
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