MENOPAUSE - pediagenosis
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Saturday, November 13, 2021




Menopause is the loss of normal ovarian steroidogenesis because of age, chemotherapy (alkylating agents), radiation, or surgical therapy. (Menopause may be viewed as an endocrinopathy: the loss of an endocrine function with adverse health consequences.) Menopause naturally occurs at a median age of 51.5, with 95% of women going through this transition between ages 44 and 55. Menopause may occur at a younger age in smokers, those with poor nutrition or chronic illness, or those who have a loss of genetic material from the long arm of the X chromosome.

When ovarian steroidogenesis is lost, menstrual function (if the uterus is present) ceases. Up to 85% of women will also experience hot flashes, flushes, and night sweats, with the most severe symptoms associated with the steepest or most abrupt declines in hormone levels (e.g., surgical menopause). Vaginal atrophy, vulvodynia, dysuria, urinary urgency, and urgency incontinence, urinary frequency, nocturia, and an increased incidence of stress urinary incontinence are also common with the loss of estrogen. For many women, there is a decrease in libido, independent of that caused by vaginal dryness and the attendant dyspareunia. Around the time of menopause, there is an estrogendependent accelerated loss of bone mass. There is a suggestion of an increased risk of cardiovascular disease associated with natural menopause and strong evidence of this in premature surgical menopause.

During the natural transition from ovulatory func- tion to postmenopause ovarian activity (the “climacteric period”), many women will experience irregular vaginal bleeding and may experience the beginnings of hot flashes or flushes. Following menopause, the ovary is not truly quiescent: luteinizing hormone (LH) stimulation of theca cell islands in the ovarian stroma results in testosterone and androstenedione production. Although these are produced at a much lower level than before menopause, androgens become the primary hormonal product of the ovaries.

Although the timing and symptoms of menopause are sufficiently characteristic to allow a diagnosis to be made by history and physical findings alone, when the symptoms are atypical or the timing other than expected, alternative causes for the symptoms such as pregnancy, hypothyroidism, polycystic ovary syndrome (PCOS), a prolactin-secreting tumor, or hypothalamic dysfunction should all be considered. When the diagnosis of ovarian failure must be confirmed, measurement of serum follicle-stimulating hormone (FSH) can help support the diagnosis. FSH levels higher than 100 mIU/mL are diagnostic. Although lower levels (40 to 50 mIU/mL) may be sufficient to establish a diagnosis when symptoms are also present, a single measure of an elevation at these lower levels is not a reliable indicator of menopause. Serum estradiol levels may be determined (generally less than 15 pg/mL) but are less reliable as a marker of ovarian failure. A pregnancy test is always indicated in sexually active perimenopausal women who are not using contraception. A vaginal maturation index may be obtained but is generally not required for diagnosis. Bone densitometry may be indicated for those at special risk for bone loss. When noncyclic bleeding occurs in these patients, pelvic examination, Pap smear, and endometrial biopsy should be strongly considered. Women who have ovarian failure below age 30 should have a karyotype performed.

The management of menopause and its symptoms has become controversial in recent years. Estrogen replacement therapy is still indicated when symptoms such as vasomotor or urogenital symptoms warrant, but most suggest that this therapy should be time-limited. Hormone replacement therapy targeted primarily toward the prevention of bone loss or to reduce the risk of heart disease has generally been replaced by more specific osteoporosis therapies and cardiac risk–reduction strategies. When estrogens are used, progestins are usually added to the regimen if the patient has a uterus present to reduce the risk of endometrial hyperplasia or cancer. (Continuous estrogen exposure without periodic or concomitant progestins increases the risk of endometrial carcinoma six- to eightfold.)

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