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Thyroid disease and epilepsy in pregnancy

الكلية كلية الطب     القسم  النسائية والتوليد     المرحلة 4
أستاذ المادة نادية مضر سلمان مرزة       23/05/2017 10:37:53
Thyroid Disease in Pregnancy: د.نادية مضر الحلي

Maternal physiology:
Thyroid disease is the commonest pre-existing endocrine disorder in pregnant women. Thyroid-stimulating hormone (TSH) is released from the anterior pituitary. It increases both the synthesis and release of thyroxin (T4) and triiodothyronine (T3). The T3 and T4 are mostly bounded to thyroid binding globulin. The unbound thy¬roid hormones have biological activity; only 0.04 % of T4 and 0.05 % of T3 are free.
Iodide is essential for the synthesis of thyroid hormones, and the thyroid gland actively traps iodine & produce T4. Circulating T3 is produced principally by peripheral deiodination of T4.
In pregnancy, there is increased TBG production as a result of increased oestrogen synthesis. This leads to an increase in the serum con¬centrations of total T4 and T3, but not the free circulating thyroid hor¬mones.
There is iodine deficiency in pregnancy as a result of loss through increased glomerular filtration. This results in increased uptake by the thyroid gland, which results in enlargement and the appearance of a goitre. Fetal thyroid activity also depletes the maternal iodide pool from the sec¬ond trimester.
As human chorionic gonadotrophin (hCG) and TSH share a common alpha subunit and have similar beta subunits, TSH receptors are prone to stimulation by hCG.

Fetal thyroid function
During the first trimester, the fetus requires thyroxin for normal fetal brain development. From 10 weeks gestation, the fetal thyroid gland produces both T4 and T3 and there is little relationship between maternal and fetal levels. Fetal levels reach those of the adult at 16 weeks gestation.
Congenital hyperthyroidism can occur through TSH receptor stimulating antibodies which cross the placenta.


Iodine Deficiency:
Women in areas of iodine deficiency may have goitres and reduced reproductive success. In iodine deficiency, the maternal thyroid gland has a greater affinity for iodide than the placenta and the fetuses are thus prone to cretinism, the leading preventable cause of mental retardation worldwide. The fetal cochlea, cerebral neocortex and basal ganglia are particularly sensitive to iodine deficiency. Iodine administration prior to conception and up to the 2nd trimester will improve neurological outcome by protecting the fetal brain. lodination of water, salt or flour can easily achieve this.


المادة المعروضة اعلاه هي مدخل الى المحاضرة المرفوعة بواسطة استاذ(ة) المادة . وقد تبدو لك غير متكاملة . حيث يضع استاذ المادة في بعض الاحيان فقط الجزء الاول من المحاضرة من اجل الاطلاع على ما ستقوم بتحميله لاحقا . في نظام التعليم الالكتروني نوفر هذه الخدمة لكي نبقيك على اطلاع حول محتوى الملف الذي ستقوم بتحميله .