CHAPTER 65

Menopause

Andréa Sonenberg, PhD, WHNP, CNM-BC

The period leading up to the cessation of the menstrual cycle is called the climacteric, or menopause, and can last 10 to 15 years, usually beginning between 35 and 40 years of age (Beckmann et al., 2014; Carcio & Secor, 2012; Hawkins, Roberto-Nichols, & Stanley-Haney, 2012; Melmed, Polonsky, Reed, & Kronenberg, 2012). Menopause is the cessation of ovarian function, production of ovarian hormones, and consequently the discontinuation of the menstrual cycle. Estrogen previously produced by the ovaries is nearly absent. This cessation may be a natural occurrence as part of the female life process, or surgically induced (oophorectomy). There is variation in number and severity of symptoms experienced by women. Therapies are offered after individual assessment of a woman’s personal experience of menopausal symptoms, distinct risk factors for the long-term effects of menopause, potential side effects of the therapeutic agents, and her own preferences. Management of menopause can be a combination of medicinal, nutritional, and lifestyle change therapies.

Due to the lengthening of the female lifecycle, long-term sequelae of estrogen depletion after menopause have been identified, along with potential short-term menopausal symptoms. The shorter-term symptoms include: vasomotor hot flashes; urogenital dryness and atrophy; integumentary, hair, and nail changes; osteoclast resorption; weight changes; joint pain and arthritis; dental and oral changes; visual changes; hearing changes; mood swings and depression; cognitive changes; sexual concerns; and sleep disturbances (Beckmann et al., 2014; Carcio & Secor, 2012; Hawkins et al., 2012). There is ethnic and regional variability in how women experience vasomotor symptoms, such as hot flashes. For example, only 10% of women in Hong Kong and 69% of Australian women experience short-term symptoms, whereas 75% of American women report experiencing them (Beckmann et al., 2014). Additionally, in the United States, there are racial and ethnic disparities in the prevalence of vasomotor symptoms, with the rate being most prevalent in African Americans (45.6%), then Latin Americans (35.4%), White Caucasian Americans (31.2%), Chinese Americans (20.5%), followed by Japanese Americans (17.6%; Beckmann et al., 2014; Carcio & Secor, 2012). Beckmann et al. (2014) also note that recent study findings support the theory that body mass index (BMI) may be a more reliable indicator in predicting the incidence of vasomotor symptoms in perimenopausal women. Long-term sequelae, which may not occur until years after menopause, include osteoporosis, cancers, coronary heart disease (CHD), and risk of stroke. Understanding which patients are at risk for developing these complications is important in undertaking the management of menopause in primary care.

With cessation of primary ovarian function, menopause also includes termination of production of the potent estrogen estradiol. However, the organ does not remain entirely dormant; therefore, the total production of estrogen does not cease entirely; the hormone’s production continues in the form of estrone, a weaker form of estrogen. Under the stimulation of 1 uteinizing hormone (LH) in the ovarian stroma, androstenedione is converted to estrone in the extraglandular tissue, particularly fat tissue. This extragonadal estrogen concentration is therefore directly proportional to body weight. Due to this relationship and estrogen’s effect on endometrial lining, obese women are at a higher risk for endometrial hyperplasia during menopause, while women with a lower BMI are at a lower risk of experiencing estrogenic symptoms (Beckmann et al., 2014; Melmed et al., 2012).

Before menopause, the ovary is very responsive to the two pituitary gonadotropins, follicle-stimulating hormone (FSH), and LH. In high-enough concentrations, there is a negative feedback loop in which estrogen produced by the ovary signals the pituitary not to release FSH and LH. As the ovaries age and the follicles they produce diminish, estrogen concentrations decline, and the release of FSH and LH is no longer blocked. In response to the feedback loop, and in an attempt to stimulate the ovary, the concentrations of FSH and LSH rise. This period of diminishing estrogen production and increasing concentrations of FSH and LH begins occurring several years before the woman’s final menses (Beckmann et al., 2014; Melmed et al., 2012). This period is referred to as the perimenopause (Beckmann et al., 2014; Melmed et al., 2012).

Due to the varied locations of estrogen receptors throughout the body, diminished estrogen production with relative elevation in concentration of other hormones (including FSH, LH, gonadotropin-releasing hormone [GnRH], dehydroepiandrostenedione, epinephrine, corti-cotropin, beta-endorphin, growth hormone, and calcitonin gene-related peptide) results in wide-ranging, multisystem sequelae (Beckmann et al., 2014; Porth & Matfin, 2009). Table 65.1 presents the manifestations of menopause due to diminished estrogen and relative increase in other hormones.

Sources: Beckmann et al. (2014); Carcio and Secor (2012); Hawkins et al. (2012); Porth and Matfin (2009)

SIGNS, SYMPTOMS, AND SEQUELAE

Early manifestations of menopause begin in the perimeno-pausal period. Among the most common are vasomotor symptoms, including hot flashes and night sweats. These symptoms may persist for years; urogenital atrophy, another sequela of estrogen depletion, may last an indefinite period of time.

Vasomotor Symptoms

The true etiology of the vasomotor symptoms of menopause is unknown (Beckmann et al., 2014; Porth & Matfin, 2009). These symptoms are experienced by the majority of menopausal women, although as previously noted, the prevalence has great cultural variation (Beckmann et al., 2014; Carcio & Secor, 2012; Harlow et al., 2012). Of American women, 75% experience these symptoms. Without hormonal replacement therapy, symptoms last on average 2 to 3 years, with some women experiencing them for 10 years or more (Beckmann et al., 2014; Harlow et al., 2012). Symptoms range in frequency and severity from mild annoyances to significant disruptions in everyday life, contributing to mood swings, anxiety, and depression. Some women experience them only occasionally; others are affected more than three times daily. Difficulty sleeping and concentrating are some of the most disabling symptoms of menopause. This may be related to mood changes and perceived changes in energy level, as well as the annoyance of nocturnal vasomotor symptoms (Porth & Matfin, 2009). All of these indicators have the potential to affect a woman’s quality of life, including her relationships with family, close friends, and even coworkers (Beckmann et al., 2014; Carcio & Secor, 2012).

Variations in women’s experience of symptomatology can be attributed to a variety of factors (Table 65.2)

Urogenital Atrophy

Unlike the variability in women’s experience of vasomotor symptoms, urogenital atrophy is sequelae of menopause that is difficult to avoid. Such atrophy normally first occurs within 2 or 3 years after menopause, with increasing symptomatology by late menopause (Harlow et al., 2012). Estrogen receptors are located throughout the urogenital system in the vagina, urethra, and bladder. Urogenital atrophy occurs in the absence of estrogen stimulation. However, not all women will report to the provider the related symptoms, which include thinning and drying of the vaginal epithelium and loss of its elasticity, resulting in pruritus and dyspareunia (Beckmann et al., 2014; Carcio & Secor, 2012; Huether & McCance, 2008; Porth & Matfin, 2009). Urinary incontinence is a symptom that is more likely to be reported. Any of these symptoms alone or in combination can have serious effects on a woman’s quality of life and especially sexuality (Carcio & Secor, 2012; Nappi & Lachowsky, 2009).

BMI, body mass index; PMDD, premenstrual dysphoric disorder; PMS, premenstrual syndrome.
Source: Carcio and Secor (2012).

Hypoestrogenism also contributes to a decrease in cellular glycogen, with a resultant decrease in lactic acid production, and increase in vaginal pH. The increased alkalinity of the vaginal environment predisposes women to bacterial vaginoses after menopause (Melmed et al., 2012; Porth & Matfin, 2009).

In addition to the early symptoms of perimenopause and menopause, there are later sequelae as well, including CHD and osteoporosis.

Coronary Heart Disease

CHD is the leading cause of death among postmenopausal women in the United States (U.S. Department of Health and Human Services [USDHHS], Centers for Disease Control and Prevention [CDC], 2013). In women 30.3% of deaths were secondary to cardiovascular disease (heart disease and stroke); this figure is 29.5% for men (USDHHS, CDC, 2013). Several mechanisms of cardioprotection are afforded by estrogen. They include: improved lipid metabolism, vasodilation, and positive effects on platelet function, endothelial-derived relaxing factor, prostacyclin, and others (Melmed et al., 2012). Some of these functions are related to estrogen receptor stimulation. Estrogen receptors are located throughout the cardiovascular system. Estrogen receptor stimulation may contribute to vasodilation. In the absence of estrogen and estrogen receptor stimulation, vasodilation may not occur to the greatest extent possible.

Studies have reported a clear association between the loss of ovarian function and CHD. Because menopause is a progressive process, this increased CHD risk is generally gradual and will be influenced by other risk factors, as listed in Table 65.3. It commonly takes several years for the ovaries to cease functioning completely. The evidence is inconclusive as to whether abrupt cessation of estrogen production in women who have undergone bilateral oophorectomy puts them at increased risk of developing CHD than those experiencing a natural menopause (Jacoby, Grady, & Sawaya, 2009; Melmed et al., 2012).

Source: Carcio and Secor (2012); Hawkins et al. (2012).

Osteoporosis

Osteoporosis is another later sequelae of menopause. Increased bone loss and the subsequent development of symptomatic osteoporosis are directly related to diminished estrogen production. The effect of estrogen on bone is direct. It is the decrease in estrogen associated with menopause rather than aging in general that is responsible for 75% of the bone loss in women during the 15 years after menopause (Melmed et al., 2012). With the increased rate of osteoporosis comes an associated increased risk of fracture. For a more in-depth discussion of osteoporosis please refer to Chapter 45.

EPIDEMIOLOGY

The average age of menopause in the United States is 50 to 52 years, with 95% of women experiencing it between the ages of 44 and 55 years (Beckmann et al., 2014). Due to the average female life expectancy being 81.1 years (Hoyert & Xu, 2012), a woman can expect to spend one third of her life in the postmenopausal stage. Baby boomers are now entering their sixth decade of life, with 36,829,148 women between the ages of 50 and 70 years in 2010 (Howden & Meyer, 2011). Evidence indicates that race, socioeconomic status, education, and height do not affect the age of menopause (Beckmann et al., 2014).

The diagnosis of menopause is based on multiple components. The occurrence of irregular cycles, followed by amenorrhea for 1 year, is a hallmark symptom. It is also essential to rule out other potential causes for amenorrhea. Differential diagnoses are listed in Table 65.4. Within an age-related context, the presence of perimenopausal or menopausal symptoms of estrogen deficiency is classic. Age, however, is not always indicative of menopause; menopause may occur before 40 or as late as 60 years (Beckmann et al., 2014; Melmed et al., 2012). In addition to symptoms and age, laboratory evaluations may also be performed to help confirm the diagnosis, although are not absolutely necessary unless there is indication for confirmation (Carcio & Secor, 2012).

Patient history is of paramount importance in the diagnosis of menopause. Topic areas to be explored by the provider are listed in Table 65.3. The physical examination includes a Pap smear and pelvic examination. These can assist in the evaluation of the physiological changes, which occur secondary to menopause. Routine screening for perimenopausal cervical cancer screening is essential and should be done according to guidelines.

DIAGNOSTIC STUDIES

Ovarian failure is detected by rises in FSH and LH levels (Beckmann et al., 2014; Carcio & Secor, 2012; Melmed et al., 2012). The concentrations of these hormones rise in response to decreased estrogen levels secondary to the increasingly hypoactive ovaries. These hormones increase in an attempt to stimulate the ovaries to produce a dominant follicle. The rise in FSH is 10- to 20-fold; the increase in LH is approximately three times the concentration found before menopause (Beckmann et al., 2014; Melmed et al., 2012). With regard to the diagnosis of osteoporosis, it is recommended that a bone density scan be done for all women older than 65 years (Beckmann et al., 2014; U.S. Preventive Services Task Force [USPSTF], 2012). Table 65.5 lists the indications to screen for os teoporosis in postmenopausal women younger than 65 years.

Source: Hawkins et al. (2012).

 

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