Monthly Endometrial Cycle and Menstruation
Associated with the monthly cyclical production of estrogens and progesterone by the ovaries is an endometrial cycle in the lining of the uterus that oper-ates through the following stages: (1) proliferation of the uterine endometrium; (2) development of secre-tory changes in the endometrium; and (3) desqua-mation of the endometrium, which is known as menstruation. The various phases of this endometrialcycle are shown in Figure 81–7.
Proliferative Phase (Estrogen Phase) of the Endometrial Cycle, Occurring Before Ovulation. At the beginning of eachmonthly cycle, most of the endometrium has been desquamated by menstruation. After menstruation, only a thin layer of endometrial stroma remains, and the only epithelial cells that are left are those located in the remaining deeper portions of the glands and crypts of the endometrium.Under the influence ofestrogens, secreted in increasing quantities by theovary during the first part of the monthly ovarian cycle, the stromal cells and the epithelial cells proliferate rapidly. The endometrial surface is re-epithelialized within 4 to 7 days after the beginning of menstruation.
Then, during the next week and a half—that is, before ovulation occurs—the endometrium increases greatly in thickness, owing to increasing numbers of stromal cells and to progressive growth of the endome-trial glands and new blood vessels into the endo-metrium. At the time of ovulation, the endometrium is 3 to 5 millimeters thick.
The endometrial glands, especially those of the cer-vical region, secrete a thin, stringy mucus. The mucus strings actually align themselves along the length of the cervical canal, forming channels that help guide sperm in the proper direction from the vagina into the uterus.
Secretory Phase (Progestational Phase) of the Endometrial Cycle, Occurring After Ovulation. During most of the latterhalf of the monthly cycle, after ovulation has occurred, progesterone and estrogen together are secreted in large quantities by the corpus luteum. The estrogens cause slight additional cellular proliferation in the endometrium during this phase of the cycle, whereas progesterone causes marked swelling and secretory development of the endometrium. The glands increase in tortuosity; an excess of secretory substances accu-mulates in the glandular epithelial cells. Also, the cyto-plasm of the stromal cells increases; lipid and glycogen deposits increase greatly in the stromal cells; and the blood supply to the endometrium further increases in proportion to the developing secretory activity, with the blood vessels becoming highly tortuous. At the peak of the secretory phase, about 1 week after ovulation, the endometrium has a thickness of 5 to 6 millimeters.
The whole purpose of all these endometrial changes is to produce a highly secretory endometrium that con-tains large amounts of stored nutrients to provide appropriate conditions for implantation of a fertilized ovum during the latter half of the monthly cycle. From the time a fertilized ovum enters the uterine cavity from the fallopian tube (which occurs 3 to 4 days after ovulation) until the time the ovum implants (7 to 9 days after ovulation), the uterine secretions, called “uterine milk,” provide nutrition for the early dividing ovum. Then, once the ovum implants in the endometrium, the trophoblastic cells on the surface of the implanting ovum (in the blastocyst stage) begin to digest the endometrium and absorb the endometrial stored substances, thus making great quantities of nutrients available to the early implanting embryo.
Menstruation. If the ovum is not fertilized, about 2 daysbefore the end of the monthly cycle, the corpus luteum in the ovary suddenly involutes, and the ovarian hormones (estrogens and progesterone) decrease to low levels of secretion, as shown in Figure 81–3. Menstruation follows.
Menstruation is caused by the reduction of estro-gens and progesterone, especially progesterone, at the end of the monthly ovarian cycle. The first effect is decreased stimulation of the endometrial cells by these two hormones, followed rapidly by involution of the endometrium itself to about 65 per cent of its previous thickness. Then, during the 24 hours preceding the onset of menstruation, the tortuous blood vessels leading to the mucosal layers of the endometrium become vasospastic, presumably because of some effect of involution, such as release of a vasoconstric-tor material—possibly one of the vasoconstrictor types of prostaglandins that are present in abundance at this time.
The vasospasm, the decrease in nutrients to the endometrium, and the loss of hormonal stimulation initiate necrosis in the endometrium, especially of the blood vessels. As a result, blood at first seeps into the vascular layer of the endometrium, and the hemor-rhagic areas grow rapidly over a period of 24 to 36 hours. Gradually, the necrotic outer layers of the endometrium separate from the uterus at the sites of the hemorrhages until, about 48 hours after the onset of menstruation, all the superficial layers of the endometrium have desquamated. The mass of desquamated tissue and blood in the uterine cavity, plus contractile effects of prostaglandins or other substances in the decaying desquamate, all acting together, initiate uterine contractions that expel the uterine contents.
During normal menstruation, approximately 40 milliliters of blood and an additional 35 milliliters of serous fluid are lost. The menstrual fluid is normally nonclotting because a fibrinolysin is released along with the necrotic endometrial material. If excessive bleeding occurs from the uterine surface, the quantity of fibrinolysin may not be sufficient to prevent clot-ting.The presence of clots during menstruation is often clinical evidence of uterine pathology.
Within 4 to 7 days after menstruation starts, the loss of blood ceases because, by this time, the endometrium has become re-epithelialized.
Leukorrhea During Menstruation. During menstrua-tion, tremendous numbers of leukocytes are released along with the necrotic material and blood. It is prob-able that some substance liberated by the endometrial necrosis causes this outflow of leukocytes. As a result of these leukocytes and possibly other factors, the uterus is highly resistant to infection during men-struation, even though the endometrial surfaces are denuded. This is of extreme protective value.
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