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Terms in this set (39)

D. The temperature of the testes must be considerably below that of the internal body temperature for spermatogenesis to occur. The testes are normally maintained at a temperature of about 32°C (89.6°F) and are kept cool by a countercurrent heat exchange between the spermatic arteries and veins and by air circulating around the scrotum.

The testes develop in the abdomen, but normally descend into the scrotum during fetal and neonatal development.

In approximately 10% of newborn infants, one or, less commonly, both testes remain in the abdominal cavity or inguinal canal. Although most (98%) of undescended testes (cryptorchidism) spontaneously descend by 1 year, and all but 0.3% spontaneously descend by puberty, early surgical treatment is recommended because abdominal temperatures can
cause irreversible damage to the spermatogenic epithelium. Also, the incidence of malignant tumors is higher in undescended than in scrotal testes.

Maturation of spermatogonia, the primitive germ cells, into primary spermatocytes does not begin until adolescence. Throughout the reproductive life of the human male, 100 to 200 million sperms are produced daily. Of critical importance to the hormonal regulation of spermatogenesis is the pulsatile release of GnRH and the subsequent involvement of FSH and LH at their target cells.

FSH acts directly on the Sertoli cells of the seminiferous tubules to regulate mitotic and meiotic activity of germ cells.

LH effects are mediated via stimulation of testosterone secretion by the Leydig cells.

GnRH must be released in a pulsatile manner in order to stimulate FSH and LH secretion. Continuous release of GnRH results in down-regulation of GnRH receptors on gonadotropes and inhibition of FSH and LH synthesis and secretion.
D. Estrogen has a primary role in stimulating endometrial proliferation and regeneration after menses (D).

The direct effect of estrogen on the cervix (A) is to stimulate secretion of a thin, elastic, alkaline mucus. All of these effects facilitate enhanced sperm transport through the cervix.

Estrogen stimulates vaginal secretion of fluid with a high pH (B).

Estrogen helps to maintain bone density, by increasing osteoblast activity and decreasing osteoclast activity (C).

Growth of the breast alveoli and lobules is stimulated by progesterone; growth of the ductal elements is stimulated by estrogen (E).

Symptoms of estrogen deficiency include decreased bone density, decreased vaginal secretions and thus decreased vaginal lubrication and associated pain during sexual intercourse (dyspareunia). Estrogen deficiency is associated with problems at the level of the ovary (depletion of ovarian follicles in menopause, premature ovarian failure) or problems at the levels of the hypothalamus/pituitary leading to lack of follicle development and thus, reduced ovarian estrogen production (e.g. hypothalamic amenorrhea, excess prolactin secretion both of which inhibit GnRH and, thus LH and FSH release).

Symptoms of estrogen deficiency often accompany secondary amenorrhea and are most common in menopausal women, in premature ovarian failure (POF), in women who are underweight (anorexic, bulimic), in women who exercise a lot (hypothalamic amenorrhea), in women who are stressed (increased CRH decreases GnRH), and in women with excess prolactin secretion (excessively high prolactin levels inhibits GnRH).

The number of follicles recruited to enter the growing stage is dependent on the number of follicles left in the ovarian reserve. Like-wise, the number of antral follicles that are cyclically recruited into the cohort from which a dominant follicle will be selected depends on the number of preantral follicles available. Thus, a reduced number of follicles in the reserve means fewer follicles will be growing.

As women age, the number of growing follicles declines. Thus, estimating the number of growing follicles gives an indirect measurement of the number of follicles left in the ovarian reserve. Anti-müllerian hormone (AMH) (also known as müllerian inhibiting substance - MIS - the Sertoli cell hormone that is responsible for regression of müllerian ducts in males and thus responsible for the absence of female internal reproductive organs in males) is released from granulosa cells of growing follicles. Serum levels of AMH decline with age owing to loss of follicles from the reserve and an associated reduction in the number of growing follicles. Reduced AMH = reduced ovarian reserve.

Inhibin B is released from granulosa cells of antral follicles under FSH stimulation and the serum levels of inhibin B indicate the size of the cohort of follicles from which a dominant follicle will be selected. As the follicle pool declines, the number of follicles recruited during each menstrual cycle also declines. Thus, serum levels of inhibin B slowly decline with age and with deletion of the ovarian reserve.

Serum levels of FSH during the early follicular phase are controlled primarily by estrogen from the large antral follicles. Estrogen inhibits FSH in a negative feedback fashion. If follicles are not present or are of poor quality (as occurs as women progress towards menopause), estrogen is not produced in sufficient quantities to inhibit FSH secretion. Thus, FSH levels increase. In fact, increased early follicular phase (day 3 of menstrual cycle) FSH level is one of the earliest clinical markers of menopause. LH levels rise also (owing to reduced negative feedback from reduced estrogen and progesterone), but to a lesser extent.

Antral follicle count (AFC) or basal antral follicle count is another test for checking a females ovarian reserve. Antral follicles can be viewed by transvaginal ultrasound and counted. A count of ~13 antral follicles (diameter 2-10 mm) in the early follicular phase (Day 2-5 of the menstrual cycle) is considered normal and indicative of a sufficient ovarian reserve. Such a number would be expected in reproductive aged women with regular menstrual cycles. The number declines in relation to depletion of the ovarian reserve and is often < 4 antral follicles in women > 40 years. Increased number of antral follicles (>30) is indicative of PCOS
B. The placenta produces all of the hormones listed in the five answers at various times during pregnancy. During the first trimester, the corpus luteum secretes estrogens and progesterone which are essential for pregnancy maintenance. Corpus luteum functions begins to decline at 6-7 weeks gestation, and its function is completely taken over by the placenta by about week 7-9. This is known as the lutealplacental shift. It is marked by an increase in estriol secretion (estriol is not secreted by the corpus luteum) and by a reduction in 17-hydroxy-progesterone secretion (17-OH-progesterone is secreted by the corpus
luteum and not the placenta). Note that during pregnancy, placental progesterone precursors (cholesterol) comes solely from the maternal circulation and thus placental progesterone secretion is not a good indicator of fetal health. Estrogen precursors (androgens) are of fetal adrenal origin and therefore placental estrogen secretion is an indicator of fetal (and placental) health. DHEA is the primary fetal androgen precursor for placental estrogen production. DHEA is produced in fetal adrenals and is sent to the placenta in the sulfated form (DHEAS) where it is converted to estradiol (mainly) and (some) estrone.
DHEAS is also transported to fetal liver where it is converted to 16-alpha-OH-DHEAS. 16-alpha-OH-DHEAS
is then sent to the placenta where it is converted to Estriol. Once the placenta takes over as the primary source of estrogen and progesterone at around weeks 7-9 of gestation, the ovary can be removed and pregnancy will be maintained.