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.
Hormonal contraceptives that contain only progestogen like the oral contraceptive Circulating estradiol stimulates growth of the endometrium. Progesterone, produced by the corpus luteum formed after ovulation, transforms proliferating endometrium into secretory endometrium. During the late follicular phase, estrogen positively influences LH secretion, instead of suppressing pituitary LH secretion as it does early in the follicular phase. To have this positive effect, the E2 level must achieve a sustained elevation for several days. The LH surge promotes maturation of the dominant oocyte, the release of the oocyte and then the luteinization of the granulosa cells and the surrounding theca cells of the dominant follicle resulting in progesterone production. The appropriate level of progesterone arising from the maturing dominant follicle contributes to the precise timing of the mid-cycle surge of LH. E2 promotes uterine endometrial gland growth, which allows for future implantation. Other signs or symptoms along with the absence of periods, such as milky nipple discharge, headache, vision changes, or excessive hair growth on your face and torso (hirsutism).
Treatments of Amenorrhea based on the condition. Medical care needs are defined by the etiology of the menstrual cycle disturbance and the desires of the patient. Progesterone supplements (hormone treatment). Gonadotropin therapy or the use of pulsatile GnRH therapy is required to induce ovulation for patients with infertility whose underlying pathology cannot be reversed. Dopamine agonists are effective in treating hyperprolactinemia. Oral contraceptives (ovulation inhibitors). Dietary modifications (to include increased caloric and fat intake). Hormone replacement therapy is required to maintain bone density in patients whose underlying pathology cannot be reversed to restore normal endocrine function. In most cases, physicians will induce menstruation in non-pregnant females who have missed two or more consecutive menstrual periods, because of the danger posed to the uterus if the non-fertilized egg and endometrium lining are not expelled. Without this monthly expulsion, the risk of uterine cancer increases.Women with evidence of hyperandrogenism and disordered menses have many other medical issues that must be addressed. Specific treatment for amenorrhea is your opinion or preference and expectations for the course of the condition.