Amenorrhea is absence of menstruation. Amenorrhea is a normal feature in prepubertal, pregnant, and postmenopausal females. Amenorrhea can be caused by any number of changes in the organs, glands, and hormones involved in menstruation. Stress due to internal or situational concerns can cause secondary amenorrhea, because stress interferes with the brain’s control (through hormones) of the ovaries. Amenorrhea may be classified as primary or secondary. primary amenorrhea - from the beginning and usually lifelong; menstruation never begins at puberty. Primary amenorrhea is defined as the failure of menses to occur by age 16 years. Secondary amenorrhea - due to some physical cause and usually of later onset; a condition in which menstrual periods which were at one time normal and regular become increasing abnormal and irregular or absent. Secondary amenorrhea is defined as the cessation of menses once they have begun. This problem is seen in about 1% of women of reproductive age. Amenorrhea occurs if the hypothalamus and pituitary fail to provide appropriate gonadotropin stimulation to the ovary, resulting in inadequate production of estradiol or in failure of ovulation and progesterone production. Amenorrhea can also occur if the ovaries fail to produce adequate amounts of estradiol despite normal and appropriate gonadotropin stimulation by the hypothalamus and pituitary. Chronic conditions (eg, starvation, excessive exercise, depression, psychological stress, marijuana use, Crohn disease, cystic fibrosis, sickle cell disease, thalassemia major, HIV infection, renal disease, thyroid disease, diabetes mellitus, anorexia nervosa)
Physiologic states of amenorrhoea are seen during pregnancy and lactation (breastfeeding). The hypothalamus is the initiator of the follicular phase. The gonadotropin-releasing hormone (GnRH) pump located in the hypothalamus releases GnRH in a pulsatile fashion into the portal vessel system surrounding the anterior pituitary gland. GnRH interacts with the anterior pituitary gland to release follicle-stimulating hormone (FSH) in the follicular phase. FSH is secreted into the circulation and interacts with the granulosa cells surrounding the developing oocytes. As levels of progesterone, estradiol, and inhibin decline 2-3 days before menses, the hypothalamus begins to release higher levels of FSH, which recruits oocytes for the next menstrual cycle. As FSH increases during the early portion of the follicular phase, it interacts with granulosa cells to stimulate the aromatization of androgens into estradiol. Early in the follicular phase, both estradiol and FSH increase the FSH-receptor content of the developing follicles. Over the next several days, the steady increase of estradiol (E2) levels exerts a progressively greater suppressive influence on pituitary FSH release. Only one selected lead follicle, with the largest reservoir of estrogen, can withstand the declining FSH environment. The remaining oocytes that initially were recruited with the lead follicle undergo atresia. Immediately prior to ovulation, the combination of E2 and FSH leads to the production of luteinizing-hormone (LH) receptors on the granulosa cells surrounding the lead follicle.
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