In addition to and in concert with the changes in maternal fuel metabolism already discussed, virtually every aspect of maternal physiology is affected by pregnancy. Table 1 summarizes many of these. The fetus, placenta, and amniotic fluid account for just under 40% of the average weight gain during pregnancy, with the rest attributable to uterine and breast growth (11%), blood and extravascular fluid (23%), and maternal fat stores (26%). To maintain the needed rate of delivery of oxygen, nutrients, and other molecules to the fetus and the removal of CO2 and waste from it, both the volume of blood and the rate at which it flows are dramatically increased; these changes are attributable to the high capacity and low resistance of the utero-placental vessels (Figure 1).

Table1. Changes in Maternal Physiology During Pregnancy

Fig1. Fetal-maternal circulation in the placenta. The transfer of gasses, nutrients, waste products, and other molecules between the maternal and fetal circulation takes place in the maternal blood pools which have arisen from the spiral arteries of the endometrium. Freshly oxygenated blood from the mother enters the pools through the maternal arteries (left side, red). Blood that is poor in oxygen and nutrients leaves the fetus through the umbilical arteries (right side, blue), enters the capillaries of the chorionic villus where it is oxygenated and gains nutrients before it returns to the fetus in the umbilical vein (right side, red). Oxygen-depleted blood leaves the maternal blood pool through the maternal veins (left side, blue). Note that in fetal life, the situation is reversed from that after birth, when oxygenated blood is carried by the arteries.

Pituitary size increases by 35–40%, due primarily to the increase and size of the prolactin secreting lactotrophs. Changes in other pituitary hormones are seen as outlined in Table 1. Increased estrogen and progesterone levels are probably responsible for the suppression of the pituitary gonadotrophins.

In the thyroid gland, both the size of the follicles and the colloid content contribute to a modest increase in the gland’s size. Although increased synthesis of the thyroid hormones leads to their increased total amounts in the blood, the amounts of free T4 and T3 are unchanged. This is due to the stimulation by estrogens of the liver synthesis of the thyroid hormone serum binding protein, thyroid binding globulin (TBG). The rise in total blood cortisol levels is due to increased ACTH secretion but also in part to estrogen-induced increase in the hepatic synthesis of cortisol binding globulin, the specific serum binding protein for this steroid hormone.

Free cortisol in the blood also rises, in parallel with the increase in ACTH.

اخر الاخبار

اخبار العتبة العباسية المقدسة

قسم الشؤون الفكرية يصدر عددين جديدين من نشرتي الكفيل والخميس

متحف الكفيل يستعرض حاملَ شموعٍ يعود إلى العصر القاجاري

ذوو شهداء مدرسة ميناب الإيرانية يتشرفون بزيارة مرقد أبي الفضل العباس (عليه السلام)

قسم الصناعات ينجز 75‎%‎ من أعمال إنشاء سور حديدي في شركة عين الحياة

المزيد

الآخبار الصحية

السجائر الإلكترونية والإقلاع عن التدخين.. نتائج متباينة تثير الجدل العلمي

مصر تحقق إنجازاً دولياً جديداً في منظمة الصحة العالمية

دراسة: السباحة فعّالة أكثر من الجري في الحفاظ على صحة القلب

عامل خطر في بداية الحمل يؤخر تطور الكلام والمهارات الحركية لدى الرضع

المزيد

الآخبار التكنلوجية

أحلامك ليست عشوائية.. إليك ما يفعله دماغك أثناء نومك

روسيا.. العلماء يضاعفون الاستقرار الحراري للألواح الشمسية ثلاث مرات

علماء يكشفون سر سرعة الدلافين في السباحة

سلمي أو دموي.. هكذا تنتقل السلطة في مجتمع الجرذان

المزيد

مواضيع ذات صلة

Placental Lactogen and Placental Growth Hormone

Human Chorionic Gonadotrophin

Polycystic Ovary Syndrome (PCOS)

Estrogen and the Cardiovascular System

Effects of Estrogen on Bone

Uterine Effects of Estrogen and Progesterone

Menopause

Chemistry and Metabolism of Female Steroid Hormones: Feedback Effects on the Hypothalamus and Pituitary

Control of the Ovary by the Hypothalamus and Pituitary

Synthesis of Progesterone and Estrogens

Female Steroid Hormones

The Androgen Receptor