Let's talk about the hormone cycle. What happens physiologically?

Under the influence of gonadotropins (FSH and LH), a group of primary follicles (eggs) is recruited, and by day 6 to 8 of the menstrual cycle, one follicle becomes mature or "dominant," a process characterized by acceleerated growth of granulosa cells and enlargement of the fluid filled antrum. The recruited follicles not destined to ovulate begin to undergo degeneration, similar to the atresia observed in other follicles during embryogenesis. Just prior to ovulation, meiosis resumes in the ova of the dominant follicle, and the first meiotic division is completed with formatino of the first polar body. (okay enough with the medical talk). Rapid enlargement of the antrum (up to 10 to 25 mm in size) occurs with an associated increase in follicular fluid (we women feel pain!!). Ovulation from the dominant follicle occurs some 16 to 23 hours after the LH peak or 24 to 38 hours after the onset of the LH surge as the result of rupture of the follicular wall at the area of the stigma, followed by expulsion of the ovum together with a mass of surounding granulosa cells called cumulus cells. The rupture is believed to result from the action of hydrolyzing enzymes on the surface of the follicle, possibly under the control of prostaglandins. The second meiotic division begins after the egg is fertilized by a sperm.

Following ovulation, the formation of the corpus luteum begins in the retained remannt of the ovulated follicle (the corpus luteum produces the progesterone in the early stages of pregnancy). The principal estrogen secreted by the ovary and the most potent naturally occurring estrogen is estradiol. Estrone is also secreted by the ovary, but the principal source of estrone is from extraglandular conversion of androstenedione in peripheral tissues (aromatase in your abdominal fat cells). Estriol, is the most abundant estrogen in urine, arises form the 16-hydroxylation of estradiol and estrone.

Like other steroid hormones, ovarian steroids are derived from cholesterol. The ovary can synthesize cholesterol from circulating low density lipoproteins LDL. Virtually all ovarian cells are believed to possess the complete enzymatic complement required for the conversionm of cholesterol to estradiol; however, different cell types within the ovary contain different amounts of these enzymes so that the principal asteroids produced differ in the various compartments. For example, the corpus luteum forms progesterone and 17-hydroxyprogesterone predominantly, whereas theca and stromal cells convert cholesterol to the androgens androstenedione and testosterone. Granulosa cells are particularly rich in the aromatase (an enzyme) responsible for conversion of androgens to estrogen and utlize as substrates for this process from the androgens from the theca and stromal cells.

Estrogens promote development of the secondary sexual characteristics in women and cause uterine growth, thickening of the vaginal mucosa, thinning of the cervical mucus, and development of the ductular system of the breasts.

Progesterone is the principal hormone secreted by the corpus luteum and is responsible for progestational effects, namely, induction of secretory activity in the endometrium of the estrogen-primed uterus in preparation for implantation of the fertilized egg. Progesterone also induces a decidual reaction in endometrium. Other effects include inhibition of uterine contractions, increased viscosity of cervical mucus, glandular development of the breats, and increase in basal body temperature.

A normal menstrual cycle is usually divided into a follicular (or proliferative phase) and a luteal (or secretory phase). The secretion of FSH and LH is fundamentally under negative feedback control by ovarian steroids (particularly estradiol) and probably by inhibin (inhibits the release of FSH by the hypothalamic-pituitary unit), but the response of gonadotropins to different levels of estradiol varies;
FSH secretion is inhibited progressively as estrogen levels increase - typically negative feedback. In contrast, LH secretion is SUPPRESSED maximally by estrogen in low amounts and is ENHANCED in response to a rising and sustained elevation of estradiol - so called positive feedback control. Negative feedback of estrogen involves both the hypothalamus and pituitary, whereas positive feedback operates primarly at the level of the pituitary (both located in the brain).

The length of the normal menstrual cycle is defined as the time from the onset of one menstrual bleeding episode to onset of the next. In women of reproductive age, the menstrual cycle averages 28+-3 days, and the mean duration of flow is 4+-2 days. Longer menstrual cycles (usually due to anovulation) occur at the start of menarche (puberty) and prior to menopause (perimenopause). At the end of one menstrual cycle and in the face of a waning corpus luteum, plasma levels of estrogen and progesterone fall, and circulating levels of FSH increase concomitantly. Under the influence of increasing levels of FSH, follicular recruitment is initiated to effect development of the follicle that will be dominant during the next cycle.

Just prior to ovulation, estradiol secretion reaches a peak and then falls. Immediately thereafter, a further rise in the plasma level of LH mediates the final maturation of the follicle, followed by follicular rupture and ovulation 16 to 23 hours after the LH peak. Plasma progesterone also begins to rise just prior to midcycle and facilitates the positive feedback action of estradiol on LH secretion.

At the onset of the luteal phase, plasma gonadotropins decrease and plasma progesterone increases. A secondary rise in estrogens causes further gonadotropin suppresion. Near the end of the luteal phase, progesterone and estrogen levels fall, and FSH levels begin to rise to initiate the development of the next follicle (usually in the contralateral ovary) and the next menstrual cycle.

The endometrium lining the uterine cavity undergoes marked alterations in response to the changing plasma levels of ovarian hormones. Concomitant with the decrease in plasma estrogen and progesterone and the decline of corpus luteum function in the late lteal phase, intense vasospasm occurs in the spiral arterioles supplying blood to the endometrium, followed byan eschemic necrosis, endometrial desquamation, and bleeding. This vasospasm is caused by locally synthesized prostaglandins. (thus by taking motrin or advil can decrease prostaglandin synthesis and symptoms)





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