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ThoughtfulSparrow

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sergeenko

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reproductive biology pregnancy stages hormones of pregnancy reproductive system

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This document provides an overview of pregnancy and menopause, detailing the stages of fetal development, hormone levels, and parturition. It's a valuable resource for understanding the reproductive system. Key concepts like estrogen, progesterone, and human chorionic gonadotropin (hCG) are discussed.

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Pregnancy menopause sergeenko Pregnancy If the ovum is fertilized by a sperm, the fertilized ovum begins to divide and will become the fetus. pregnancy lasts approximately 40 weeks. During pregnancy, the levels of estrogen and progesterone increase steadily. Their functions include ma...

Pregnancy menopause sergeenko Pregnancy If the ovum is fertilized by a sperm, the fertilized ovum begins to divide and will become the fetus. pregnancy lasts approximately 40 weeks. During pregnancy, the levels of estrogen and progesterone increase steadily. Their functions include maintenance of the endometrium, development of the breasts for lactation after delivery, and suppression of the development of new ovarian follicles. In early pregnancy (the first trimester), the source of steroid hormones is the corpus luteum; in mid-to-late pregnancy (the second and third trimesters), the source is the placenta Events of Early Pregnancy The events of early pregnancy are summarized in Table 10.4. The timetable is based on the number of days after ovulation and includes the following steps: 1. Fertilization of the ovum takes place within 24 hours of ovulation, in a distal portion of the oviduct called the ampulla. Four days after ovulation the fertilized ovum, the blastocyst, with approximately 100 cells, arrives in the uterine cavity -- 2. Implantation. The blastocyst floats freely in the uterine cavity for 1 day and then implants in the endometrium 5 days after ovulation. The receptivity of the endometrium to the fertilized ovum is critically dependent on a low estrogen/progesterone ratio and corresponds to the period of highest progesterone output by the corpus luteum. At the time of implantation, the blastocyst consists of an inner mass of cells, which will become the fetus, and an outer rim of cells called the trophoblast. The trophoblast invades the endometrium and forms an attachment to the maternal membranes. Thus the trophoblast contributes the fetal portion of the placenta. At the point of implantation, under stimulation by progesterone, the endometrium differentiates into a specialized layer of decidual cells. Eventually, the decidua will envelop the entire conceptus. Trophoblastic cells proliferate and form the syncytiotrophoblast, whose function is to allow the blastocyst to penetrate deep into the endometrium -- 3. Secretion of HCG and “rescue” of the corpus luteum. The trophoblast, which will become the placenta, begins secreting HCG approximately 8 days after ovulation. HCG, which has biologic activity similar to LH, it “informs” the corpus luteum that fertilization has occurred. The corpus luteum, now under the direction of HCG, continues to synthesize progesterone and estrogen, which maintain the endometrium for implantation. (Without fertilization and the stimulation by HCG, the corpus luteum regresses 12 days after ovulation, at which point it stops producing steroid hormones, and menses occurs.) The high levels of estrogen and progesterone also suppress the development of the next ovarian follicles. Production of HCG increases dramatically during the first weeks of pregnancy. The pregnancy test is based on the excretion of large amounts of HCG in urine, which are measurable. HCG is detectable in maternal urine 9 days after ovulation, even before the next expected menses. Hormones of Pregnancy Hormone levels during pregnancy are depicted in Figure 10.11. ♦ First trimester. HCG is produced by the trophoblast, beginning about 8 days after fertilization. To “rescues” the corpus luteum from regression and, with an LH-like action, stimulates corpus luteal production of progesterone and estrogen. HCG levels are maximal at approximately gestational week 9 and then decline. Although HCG continues to be produced for the duration of pregnancy, its function beyond the first trimester is unclear. ♦ Second and third trimesters. During the second and third trimesters, the placenta assumes responsibility for production of steroid hormones. The pathways for the synthesis of progesterone and estrogen are shown in Figure 10.12. Progesterone is produced by the placenta as follows: Cholesterol enters the placenta from the maternal circulation. In the placenta, cholesterol is converted to pregnenolone, which then is converted to progesterone.. Estriol, the major form of estrogen during pregnancy,. 1. cholesterol is supplied to the placenta from the maternal circulation and is 2. converted to pregnenolone in the placenta. 3. Pregnenolone then enters the fetal circulation and is converted to dehydroepiandrosterone- sulfate (DHEAsulfate) in the fetal adrenal cortex. 4. DHEA-sulfate is hydroxylated to 16-OH DHEA-sulfate in the fetal liver. 5. 16-OH DHEA-sulfate then crosses back to the placenta, 6 6.where a sulfatase enzyme removes sulfate and aromatase converts it to estriol. ♦ Second and third trimesters. The placenta also produces the peptide hormone human placental lactogen (hPL), which is structurally related to GH and prolactin. hPL helps to coordinate fuel economy in the fetoplacental unit via conversion of glucose to fatty acids and ketones. Parturition Parturition, the delivery of the fetus,. The mechanism of parturition is unclear, although roles for estrogen, progesterone, cortisol, oxytocin, prostaglandins, relaxin , and catecholamines have been proposed. The following events occur near term and may contribute to parturition: ♦ Once the fetus reaches a critical size, distention of the uterus increases its contractility. Uncoordinated contractions, known as Braxton Hicks contractions, begin approximately 1 month before parturition. ♦ Near term, the fetal adrenal cortex produces significant amounts of cortisol. Cortisol increases the estrogen/progesterone ratio, which increases the sensitivity of the uterus to contractile stimuli. Estrogen increases contractility, and progesterone decreases it. Parturition… ♦ Estrogen stimulates (and progesterone inhibits) local production of the prostaglandins PGE2 and PGF2α. Thus the increasing estrogen/progesterone ratio stimulates local prostaglandin production, (1) Prostaglandins increase the intracellular Ca concentration of uterine smooth muscle, thereby increasing its contractility. (2) Prostaglandins also promote gap junction formation between uterine smooth muscle cells to permit synchronous contraction of the uterus. (3) Prostaglandins cause softening, thinning and dilation of the cervix early in labor. ♦ The role that oxytocin. Oxytocin is a powerful stimulant of uterine contractions (indeed, it is used to induce labor). Evidence indicates that the uterine oxytocin receptors are up-regulated toward the end of gestation. It is also known that dilation of the cervix, as occurs during the progression of labor, stimulates oxytocin secretion. Yet maternal blood levels of oxytocin do not increase near term, leaving the physiologic role of oxytocin uncertain. There are three stages of normal labor. In the first stage, uterine contractions originating at the fundus and sweeping downward move the head of the fetus toward the cervix and progressively widen and thin the cervix. In the second stage, the fetus is forced through the cervix and delivered through the vagina. In the third stage, the placenta separates from the uterine decidual tissue and is delivered. During this last stage, powerful contractions of the uterus also serve to constrict uterine blood vessels and limit postpartum bleeding. After delivery of the placenta, hormone concentrations return to their prepregnant levels, except for prolactin Fig. 10.11). Lactation Throughout pregnancy, estrogen and progesterone stimulate the growth and development of the breasts, preparing them for lactation. Estrogen also stimulates prolactin secretion by the anterior pituitary, and prolactin levels steadily increase over the course of pregnancy (see Fig. 10.11). However, although prolactin levels are high during pregnancy, lactation does not occur because estrogen and progesterone block the action of prolactin on the breast. After parturition, when estrogen and progesterone levels fall precipitously, their inhibitory effects on the breast are removed and lactation can proceed. lactation is maintained by suckling, which stimulates the secretion of both oxytocin and prolactin. As long as lactation continues, there is suppression of ovulation because prolactin inhibits GnRH secretion by the hypothalamus and FSH and LH secretion by the anterior pituitary. Although not 100% effective, Hormonal Contraception Oral contraceptives contain combinations of estrogen and progesterone or progesterone alone. The combination preparations exert contraceptive effects primarily through negative feedback effects on the anterior pituitary (i.e., by inhibiting FSH and LH secretion, they prevent ovulation). The contraceptive effect of progesterone alone is based primarily on its effects on cervical mucus and tubal motility. Higher-dose preparations of estrogen and progesterone inhibit ovulation and may interfere with implantation; these preparations can be used as postcoital contraceptives, or “morning after” pills. Menopause Menopause, or the climacteric, is the cessation of menstrual cycles in women, and it occurs at approximately 50 years of age. For several years preceding menopause, anovulatory cycles estrogen secretion gradually declines and eventually ceases. Because of the decreased level of estrogen, there is reduced negative feedback on the anterior pituitary and, accordingly, increased secretion and pulsatility of FSH and LH at menopause. Increase FSH characteristic of menopause because of loss of negative feedback The symptoms of menopause are caused by the loss of the ovarian source of estrogen and include thinning of the vaginal epithelium, decreased vaginal secretions, decreased breast mass, accelerated bone loss, vascular instability (“hot flashes”), and emotional lability. (Because estrogen can be produced from androgenic precursors in adipose tissue, obese women tend to be less symptomatic than nonobese women.) Estrogen replacement therapy is aimed at replacing the ovarian source of estrogen, thus minimizing or preventing the symptoms of menopause.

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