Management of the Menopausal Patient, Part I
Management of the Menopausal Patient, Part I
Authors: Redonda Miller, MD, Assistant Professor of Medicine, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD; and Katherine K. Chang, MD, Resident, Osler Housestaff, Department of Medicine, Johns Hopkins Hospital, Baltimore, MD.
Peer Reviewer: Felice Milan, MD, Associate Professor of Clinical Medicine, Montefiore Medical Center, Albert Einstein College of Medicine, Irvington, NY.
Editor’s Note—While health care maintenance, prevention, and management of common medical conditions are often thought of as the "bread and butter" of primary care medicine, a significant portion of most physicians’ practices also involves attention to the normal physiologic changes associated with aging. Menopause falls into this realm, and its effects on women are numerous. The hormonal changes that are the hallmark of menopause result in the physical and psychological symptoms that may prompt a visit to the doctor.
Vasomotor symptoms, often referred to as "hot flashes," are one of the most common problems of perimenopausal women. Up to 75% of women may experience these sensations. Less recognized (and reported) are urogenital symptoms, including pruritis, dyspareunia, and urinary incontinence. Psychological manifestations, including depression, decreased libido, and cognitive changes, are some of the most distressing symptoms for women. A familiarity with the various options for treatment of each of these problems, including appropriate use of hormone replacement therapy (HRT), is crucial for effective patient management.
Beyond the self-reported symptoms are systemic changes that are not immediately apparent to patients. Physicians must counsel women on the effect of menopause on the development of osteoporosis and cardiovascular disease. Again, there are varied approaches to treatment, ranging from dietary modification to HRT to exciting new drugs that are revolutionizing women’s health, including newer generation bisphosphonates and selective estrogen-receptor modulators (SERMs).
This two-part article will take a comprehensive clinical approach to menopause. In Part I, Drs. Miller and Chang focus on the physiologic changes of menopause, many of the resultant clinical manifestations, and options for treatment. Part II will be published in the next issue of Primary Care Reports and will discuss the cardiovascular effects of menopause, the special case of premature ovarian failure, and the general approach to use of HRT, including the controversy over its advantages and disadvantages.
Background
Menopause affects every woman at some point in her life. The average age of menopause is 51, but it commonly occurs anytime between the ages of 45 and 55. As the lifespan of women continues to increase into the 80s, they can expect to live more than a third of their lives after menopause. Women experience the symptoms and sequelae of menopause in varying degrees of severity, and they pose a significant source of morbidity (see Table 1). Many of these consequences can be alleviated by HRT. While not every woman is a candidate for HRT, many eligible women remain reluctant to use it. Recent data suggest that, in the United States, only 20% of postmenopausal women with an intact uterus and 38% who have undergone hysterectomy are current users of HRT.1
| Table 1. Symptoms and Sequelae of Menopause |
| Vasomotor Symptoms |
| • hot flashes |
| Breast Changes |
| Urogenital Symptoms |
| • vaginal dryness |
| • incontinence |
| • frequent UTIs |
| Cognitive Effects |
| • irritability |
| • depression |
| • decreased libido |
| Loss in Bone Density |
| Cardiovascular Effects |
| • decrease in HDL |
| • increase in LDL |
| • loss of vasodilation |
Physiology
"The menopause" is technically defined as the last menses and cannot be dated with certainty until periods have been absent for 12 months. Menopause is often used more colloquially to refer to the time period between the initial prolongation and irregularity of a woman’s menstrual cycle and the complete cessation of menses with its consequent symptoms. Hormone levels may fluctuate for 2-5 years prior to the last menses. This antecedent period, together with the first 12 months after the menopause, is better termed "the perimenopause."
Menopause results from the fall in estradiol (the main form of estrogen produced by the ovaries) that accompanies the progressive atresia of ovarian follicles. This atresia also results in decreased levels of inhibin, a glycoprotein produced by the ovaries. The loss of negative feedback of inhibin on the pituitary gland causes an elevation in the pituitary gonadotropin, follicle-stimulating hormone (FSH). The level of the other pituitary gonadotropin, luteinizing hormone (LH), also increases, but FSH levels rise more quickly and to a higher level. An FSH level greater than 30 mIU/mL is supportive of menopause in a nonmenstruating woman, but clinicians should be aware that FSH can intermittently fluctuate to high levels in the perimenopause as well. Measurement of the FSH can be helpful in certain clinical situations when the diagnosis is unclear, such as in an amenorrheic woman who lacks other symptoms or in a woman with premature menopause. Most often, however, menopause remains a clinical diagnosis.
Clinical Manifestations
Vasomotor Symptoms
Vasomotor symptoms are the most common reasons women seek medical attention during menopause.2 Symptoms are most frequent during the first 2-3 postmenopausal years.3 Among postmenopausal women, the reported prevalence of vasomotor symptoms varies widely across cultures, ranging from 70-75% in the United States and Europe to 20% in Asian cultures.4-6 In addition, marked variability exists in the frequency, duration, and intensity of vasomotor symptoms. The majority of affected women experience mild symptoms that do not significantly interfere with daily activities,7 while about 20-45% seek medical help for more troubling symptoms.4,8 Studies have found that women who have undergone surgical menopause have an increased number, duration, and severity of vasomotor complaints compared with those who have undergone natural menopause.3,5 Vasomotor symptoms typically last 0.5-5 years after natural menopause, although in some women they may persist for more than 15 years.3
Etiology. While the cause of vasomotor disturbances is likely multifactorial, involving hormonal, psychogenic, and metabolic components, estrogen withdrawal has been shown to be the precipitating factor, acting directly or indirectly to alter the body’s thermoregulatory center in the hypothalamus. It is hypothesized that a sudden downward shift of the body’s setpoint temperature triggers vasomotor symptoms. Evidence suggests that b-endorphin, an endogenous opioid, and calcitonin gene-related peptide (CGRP), a potent vasodilator, may be key mediators.9,10
Vasomotor Signs and Symptoms. The hot flash is a subjective sensation of intense warmth, beginning in the head and neck and spreading downward into the upper arms and torso. A prodromal syndrome of nausea, headache, lightheadedness, vertigo, or palpitations may precede the episode. It is often accompanied by sweating, which may be drenching, as well as visible flushing over the affected areas. Finally, chills or shakes may occur, with the entire episode lasting 30 seconds to five minutes.8 The term "hot flush" refers to the objective events that occur during the hot flash. These events include an increase in skin conductance, rise in peripheral temperature, and subsequent decrease in central temperature.11 Women who have hot flashes are more than twice as likely to report insomnia,12 possibly reflecting the fact that hot flashes occur most commonly at night. Indeed, secondary effects of sleeplessness and early morning awakenings are particularly troubling for many, contributing to the fatigue, irritability, and forgetfulness associated with sleep deprivation. Caffeine, alcohol, spicy foods, sexual activity, a hot and humid environment, and psychological stress have been identified as potential trigger factors for hot flashes.7
Treatment Options. Short-term conventional HRT has been shown to be effective in treating both vasomotor symptoms and secondary insomnia in most postmenopausal women (see Table 2).11,13 Various oral preparations of estrogen may be used, with a linear relationship between dose and symptom reduction.14 In a woman who still has her uterus, progestin (synthetic progesterone) can be given sequentially or continuously. Recently, low-dose (0.025 mg) transdermal estrogens have also been shown to be effective in ameliorating vasomotor complaints.15 Vasomotor symptoms are usually relieved during the first cycle of treatment, and up to four weeks may be needed to evaluate maximal therapeutic efficacy.16,17 Estrogen replacement therapy also significantly improves self-reported sleep measures in both symptomatic and asymptomatic postmenopausal women.13
| Table 2. Therapies for Vasomotor Symptoms | |||
| Agents | Side Effects | ||
| Estrogen-based preparations | • Estrogen compounds (oral, transdermal) | Nausea, headaches, breast tenderness, bleeding | |
| • Estrogen/progestin combinations (oral, transdermal) | |||
| Progestin-only preparations | • Oral medroxyprogesterone acetate | Breast tenderness, irritability, depression, headaches | |
| • Depomedroxyprogesterone acetate (depot injectable) | |||
| • Transdermal cream | |||
| a-adrenergics | • Clonidine | Dizziness, fatigue, headaches, irritability | |
| Dopamine antagonists | • Veralipride | Breast discharge, increased prolactin levels | |
| Synthetic steroids | • Tibolone | Venous and leg disorders | |
| Phytoestrogens | • Soy protein | Unknown | |
Besides HRT, several other therapies have shown success in relieving vasomotor symptoms (see Table 2). Clonidine (0.1, 0.2, or 0.4 mg p.o. b.i.d.) is one such option, although its efficacy is not as high as HRT, and its usage may be limited by side effects such as dizziness, fatigue, headaches, and irritability.18 For those with persistent, severe symptoms, combination estrogen-androgen therapies may benefit those women who have failed estrogen-alone therapy.19 Veralipride (100 mg p.o. q.d.), a dopamine antagonist, is another alternative. Side effects include mild breast discharge and an increased serum prolactin level, and seems to be safe for short-term use.20 A relatively new drug, tibolone (2.5 mg p.o. q.d.), has shown promising results in relieving hot flashes in European studies but is currently not available in the United States. A synthetic steroid analogue with mixed estrogenic, progestogenic, and androgenic effects, tibolone has the advantage of a low rate of vaginal bleeding (7% in one study), but it also has rare side effects of venous and leg problems.21 Progestins alone, in oral (medroxyprogesterone acetate 10 mg q.d.),22 long-acting injectable (depomedroxyprogesterone acetate 50, 100, or 150 mg q month),23 or transdermal (20 mg q.d.)24 forms, is also effective. Other alternative medicine approaches, such as soy supplementation (20 g/d), have been promoted, but more studies will be needed to prove their efficacy.25
Breast Changes
With the loss of estrogen at menopause, glandular tissue of the breast undergoes involution. Replacement of supporting collagen by adipose tissue leads to sagging and drooping. Both breast density and fibrocystic changes decrease, making mammography easier to interpret. Most women report a loss in breast size. HRT can increase epithelial call proliferation and density of the postmenopausal breast26 but can also cause significant breast pain and tenderness, particularly in breasts that have not been exposed to estrogen in years. Likewise, an increase in breast density from HRT can be detected mammographically, which can hamper early breast cancer diagnosis.27
Urogenital Symptoms
Urogenital Changes. In postmenopausal women, urogenital atrophy is often underreported, underdiagnosed, and undertreated. Women may not bring up urogenital issues with their physicians due to embarrassment, or they may believe that symptoms are simply inevitable products of aging. Yet, urogenital symptoms are prevalent in postmenopausal women and contribute significantly to lower quality of life. In a study of 1200 postmenopausal women, nearly half experienced some form of lower genital tract disorder (vaginal dryness, difficulty with intercourse, itching, discharge, or smarting pain), and nearly 30% reported some degree of urinary incontinence.28 Symptom onset can be varied, occurring during the perimenopause or developing insidiously, up to 10 or more years after the cessation of menses. Early recognition and treatment of these problems in women can provide a great deal of comfort, as well as preclude the development of more serious consequences in the future.
Pathophysiology. While urogenital aging is attributed to both estrogen deficiency and the aging process, the exact role of estrogen in the pathogenesis of symptoms is incompletely understood. Estrogen is known to help maintain the health and integrity of genital and urinary structures29; estrogen receptors are found throughout the female genital tract and the lower urinary tract,30 reflecting their common embryonic origin, the urogenital sinus. These receptors are not only limited to the urogenital tract but are also found in supporting pelvic muscles and ligaments.31 Thus, urogenital structures may deteriorate in part because of the loss of estrogen’s stimulation during menopause.
Estrogen also promotes relatively more acidic conditions in the vagina through colonization with lactic-acid-producing lactobacilli. This environment is more resistant to infection.32 Without estrogen, women have a drier, less acidic vaginal environment and, subsequently, more frequent infections. The vaginal flora shifts toward a predominance of Escherichia coli and other fecal gram-negative bacteria that can serve as a potential reservoir for urinary tract infections (UTIs).
Signs and Symptoms of Urogenital Aging. With the withdrawal of estrogen during menopause, atrophic changes occur. In the vagina, this leads to itching, burning, and dryness, which occurs most frequently 4-6 years after menopause.3 Dyspareunia and secondary loss of interest in sexual activity may follow. Since both the thickness and vascularity of the vaginal wall are estrogen dependent,32 postmenopausal women have thinner vaginal walls that are more susceptible to trauma and have less ability to heal. Vaginitis occurs with greater frequency, and weakened support muscles may lead to prolapse.
In the urinary tract, atrophic changes lead to dysuria and urinary incontinence. Recurrent UTIs also occur.
Treatment. Estrogen replacement therapy is effective in improving the signs and symptoms of urogenital atrophy. While estrogen has been known to improve vaginal dryness, itching, atrophic vaginitis, and dyspareunia, its effects on urinary symptoms have only recently been investigated. Estrogen subjectively improves urinary incontinence in postmenopausal women.33,34 Combining estrogen therapy with a-adrenergic drugs may provide significantly more benefit than estrogen alone.33 Estrogen also prolongs the time to recurrence among postmenopausal women with recurrent UTIs.35 (Interestingly, cranberry juice was found to reduce the incidence of bacteriuria and pyuria in elderly women, although clinical correlation with symptoms of UTI in this study was lacking.)36
Local vaginal estrogen therapy results in higher tissue levels in the urogenital tract compared to oral administration, and thus may be an important mode of delivery for treatment of associated conditions (see Table 3). In general, much lower doses of estrogen are needed to relieve urogenital atrophy than are needed to treat vasomotor symptoms,37 opening the door to treatment with unopposed estrogen without eliciting a proliferative endometrium. Local estrogen treatment is available in a variety of forms, including vaginal creams (containing conjugated equine estrogen, micronized estradiol, or diethylstilbestrol), vaginal estriol pessaries, estradiol vaginal rings, and intravaginal estradiol tablets. Since all forms have good safety profiles and are comparably effective in relieving symptoms, individual preferences may dictate choice of administration. The estradiol vaginal ring has been shown to be a well-tolerated option,38 with the most frequent side effect of leukorrhea (whitish discharge).39 Patients seem to prefer the ring over both the vaginal pessary, which can be messy to administer and may cause increased vaginal discharge,38 and estriol vaginal cream.40 The intravaginal tablet, an easy and hygienic alternative, is effective at relieving symptoms at a dose as low as 25 mg without systemic effects or stimulation of the endometrium.41
| Table 3. Vaginal Estrogen Preparations | |
| Vaginal Preparation | Comments |
| cream | messy administration |
| estriol pessary | increased vaginal discharge messy administration discomfort |
| estradiol ring | leukorrhea |
| intravaginal estradiol tablet | disposable applicator applied once or twice weekly |
Unfortunately, none of the low-dose estrogens used in vaginal delivery systems confers benefit on bone mineral metabolism or cardiovascular disease when used alone. Postmenopausal women who are receiving systemic HRT and continue to have urogenital symptoms may benefit from the addition of local treatment. However, the primary care physician must keep in mind that local estrogen preparations may have systemic effects as well.
As for nonhormonal therapies, vaginal dryness can also be addressed through over-the-counter vaginal lubricants or a moisturizing vaginal gel. The gel, while superior in efficacy to other lubricants,42 is not as effective as estrogen in treating vaginal dryness.43 It remains an alternative to local estrogen therapy or as an adjunct to systemic HRT.
Cognitive Effects
Psychological Symptoms. Many women report psychological symptoms at the time of menopause, including irritability, inability to concentrate, memory loss, anxiety, and depression. Whether these symptoms are direct consequences of menopause or are simply secondary effects of sleep deprivation (from nocturnal hot flashes), other physical symptoms, or changing life roles remains controversial. HRT can have a placebo effect that makes the issue even murkier. A recent longitudinal analysis of more than 2500 women did not find an association between depression and natural menopause unless the women had a long perimenopausal period with increased symptoms or had a prior history of depression.44 While efficacy data are inconclusive, most experts would recommend a trial of HRT for amelioration of minor psychological symptoms, such as irritability and difficulty with concentration, particularly if other indications for HRT are present. A supportive familial environment is probably most helpful. Physicians should ensure that the patient is not suffering from major depression, as this is more serious and usually warrants other therapies, such as selective serotonin reuptake inhibitors.
Libido. A decrease in libido is a common symptom reported by perimenopausal women. Lack of sexual interest is often multifactorial in nature and may be related to psychological factors, such as depression and low self-image, and physical effects, such as dyspareunia secondary to vaginal dryness. A decline in the ovarian androgens, androstenedione and testosterone, may also play a role. Many authors have suggested that the supplementation of standard HRT with androgens has beneficial effects on sexual functioning, although large, well-controlled studies are lacking. One study involving 34 postmenopausal women with low libido found significantly improved sexual activity and satisfaction when testosterone was added.45 Other benefits of estrogen-androgen therapy have been touted, including improvement in vasomotor symptoms, cognition, and bone density. The long-term safety of testosterone in women is unknown, but further research is ongoing in this area.
Dementia. Recently, there has been interest in the possibility that estrogen use may prevent or delay the development of dementia, particularly Alzheimer’s disease. Several epidemiological studies have suggested a preventive role for HRT, and a recent meta-analysis estimated a 29% decline in the risk of dementia among estrogen users.46 Proposed mechanisms include the abilities of estrogen to serve as an antioxidant, inhibit neuronal apoptosis, and possibly affect metabolism of b-amyloid. Estrogen’s effect, however, appears to be mainly preventive, as a large, randomized, controlled trial resulted in no benefit to women with already established disease.47 Definite conclusions regarding HRT and the prevention of dementia are difficult to draw at this time, and prevention of dementia should not be the sole indication for HRT in a postmenopausal woman.
Bone Loss
Background. Osteoporosis is a huge health problem that is frequently underrecognized by physicians. It is estimated to affect more than 25 million people and cost roughly $13.8 billion annually in the United States.48 Much of this cost is due to the significant morbidity and mortality from the most serious complication of osteoporosis, hip fractures. Patients who suffer a hip fracture have a 20% chance of dying within one year, a 50% chance of requiring assistance to ambulate, and a 25% chance of requiring permanent nursing home placement.49 Postmenopausal women are particularly susceptible to osteoporosis, as bone loss occurs most rapidly in the first five years after menopause. During this time, up to 15% of bone density may be lost. In addition to menopause, other risk factors include white or Asian race, low body weight, family history, and smoking.
Osteoporosis is the result of an imbalance between bone formation and bone resorption. Estrogen plays an antiresorptive role, the exact mechanism of which is unknown. Estrogen receptors have been localized on both osteoblasts and osteoclasts. Postmenopausal bone loss is thus related to the decline in estrogen, with an ensuing increase in bone resorption. This bone loss may occur at a rate of 2-5% per year for up to five years and then decreases to about 1% per year.50 Cancellous bone found in the spine and wrist is predominantly affected.
Screening. Screening for osteoporosis should begin at the first office visit in a perimenopausal woman. A thorough history of all risk factors should be obtained. The physician should also measure height on an annual basis, as loss of height is often an early sign of osteoporosis. A loss of a half inch or more is an indication for concern.
Measurement of bone mineral density (BMD) is an important tool for assessing the risk of future fracture for a woman. Dual-energy X-ray absorptiometry (DEXA) scanning is the most common method used for this measurement. The test is easy to perform, uses little radiation, is cheap (on the order of $200), and takes approximately 10 minutes. According to World Health Organization criteria, BMD is classified according to the DEXA T-score as normal (T-score > -1), osteopenic (T-score between -1 and -2.5), or osteoporotic (T-score £ -2.5).51 While appealing in thought, DEXA scanning has not yet been proven to be cost-effective for the universal screening of women. Most experts recommend measuring BMD in women at menopause if they have one or more risk factors for osteoporosis, if they are undecided about HRT, if incidental osteopenia is found by x-ray, or if they present with a fracture (see Table 4). A study looking at the influence of bone densitometry on women’s decisions about HRT found that women who were diagnosed with low BMD were more likely than normal women to begin some measure to prevent fractures (94% vs 56%; P < 0.01) and more likely to start HRT (38% vs 8%; P < 0.01).52
Management. Perimenopausal women should be counseled about the rapid bone loss associated with menopause. Since osteoporosis is a clinically silent disease until fracture occurs, most women do not pay enough attention to its prevention. Physicians should advise women about the bone-preserving effects of exercise. Weight-bearing exercises, such as jogging or stair-climbing, are most beneficial. Other modifiable risk factors, such as smoking or heavy alcohol use, should also be addressed.
Ensuring that perimenopausal women are receiving enough calcium is critical. According to National Osteoporosis Foundation (NOF) guidelines, all women (pre- and postmenopausal) should consume 1000 mg of elemental calcium a day. Postmenopausal women not taking estrogen, women older than 65 years, and women with a diagnosis of osteoporosis should receive 1500 mg of calcium per day. Foods rich in calcium include dairy products, dark green vegetables, sardines, salmon, and nuts. If a woman’s diet is inadequate, calcium supplements should be prescribed. Calcium carbonate is least expensive, but for women who have chronic gastrointestinal illnesses or who are taking antacids, calcium citrate is better absorbed.
Recommendations regarding dietary intake of vitamin D suggest that perimenopausal women should receive at least 400 IU per day. Supplementation is generally not necessary in most women but should be considered in patients with malabsorption syndromes or who lack adequate exposure to sunlight (housebound or nursing home residents). Women with diagnosed osteoporosis should have 800 IU of vitamin D per day.
Further management of perimenopausal bone loss must take into account other risk factors, including the BMD if measured. Preventive therapy should be administered in any woman at significant risk. A T-score of -1.5 or less on DEXA scanning is no longer an indication for prevention, but for active treatment (NOF guidelines). This discussion will focus primarily on prevention.
For prevention in a high-risk woman, strong consideration should be given to estrogen replacement, as it prevents bone loss and may even increase bone mass by a few percentage points when started at menopause. Long-term use (at least 7-10 years) results in a decrease in the osteoporotic fracture rate by 50%.53 All forms of estrogen seem to be effective. For women who cannot tolerate usual doses of esterified estrogens (0.625 mg), smaller doses (0.3 mg) were recently shown to be effective in preserving BMD.54 Unfortunately, if estrogen is discontinued, its protective effect on bone slowly wanes.
For women unable to take HRT but at significantly high risk of osteoporosis, other preventive therapies are available. Raloxifene, a selective estrogen-receptor modulator, is a promising alternative. When given at 60 mg per day, it has been shown to result in a 2.5% greater BMD compared to placebo at two years.55 Other useful agents are the bisphosphonates, which act by inhibiting bone resorption. These medications are effective and are usually considered second-line therapies in women who cannot tolerate estrogens. A 5 mg daily dose of alendronate was shown to prevent bone loss and actually increase BMD by up to 3.5% at two years.56 In osteoporotic patients, a 10 mg dose of alendronate will increase bone density up to 9% at three years with a concomitant decrease in vertebral fractures by 44%.57 Risedronate is a newer bisphosphonate that appears to be equally efficacious, but FDA approval is pending at the time of this writing. Finally, calcitonin administered nasally at a dose of 200 IU q.d. is a safe and well-tolerated alternative. Although considered somewhat weaker than the other agents discussed above, postmenopausal women experienced an increase in BMD of 2% at two years.58 It is reasonable to combine HRT with bisphosphonates or calcitonin in patients at significant risk, but definitive data have not yet been published documenting additive benefits.
Additional Information
Patients frequently request additional sources of information for further reading. The following are several resources particularly helpful to patients:
1. Menopause Guidebook. Obtained through: The North American Menopause Society, P.O. Box 94527, Cleveland, OH 44101-4527.
2. www.menopause.org
3. www.discoveryhealth.com
4. www.drkoop.com
5. www.nof.com
6. www.mediconsult.com
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50. Riggs BL, et al. Differential changes in bone mineral density of the appendicular and axial skeleton with aging: Relationship to spinal osteoporosis. J Clin Invest 1981;67:328-335.
51. WHO Study Group. Assessment of fracture risk and its application to screening for postmenopausal osteoporosis: Report of a WHO Study Group. WHO Technical Report Series 843, Geneva, Switzerland: World Health Organization. 1994;1-129.
52. Rubin SM, Cummings SR. Results of bone densitometry affect women’s decisions about taking measures to prevent fractures. Ann Intern Med 1992;166:990-995.
53. Weiss NS, et al. Decreased risk of fractures of the hip and lower forearm with postmenopausal use of estrogen. N Engl J Med 1980;303:1195-1198.
54. Genant HK, et al. Low-dose esterified estrogen therapy: Effects on bone, plasma estradiol concentrations, endometrium, and lipid levels. Arch Intern Med 1997;157:2609-2615.
55. Delmas PD, et al. Effects of raloxifene on bone mineral density, serum cholesterol concentrations, and uterine endometrium in postmenopausal women. N Engl J Med 1997;337:1641-1647.
56. Hosking D, et al. Prevention of bone loss with alendronate in postmenopausal women under 60 years of age. N Engl J Med 1998;338:485-492.
57. Cummings SR, et al. Effect of alendronate on risk of fracture in women with low bone density but without vertebral fractures: Results from the Fracture Intervention Trial. JAMA 1998; 280:2077-2082.
58. Reginster JY, et al. A double-blind, placebo-controlled, dose-finding trial of intermittent nasal salmon calcitonin for prevention of postmenopausal lumbar spine bone loss. Am J Med 1995;98:452-458.
Physician CME Questions
25. The leading cause of death for women in the United States is:
a. lung cancer.
b. breast cancer.
c. coronary artery disease.
d. cerebrovascular accident.
e. colon cancer.
26. Which of the following can provide relief for vasomotor symptoms in a woman who is not a candidate for HRT?
a. Reserpine
b. Tibolone
c. Clonidine
d. a and c
e. b and c
27. Which of the following statements is false regarding urogenital symptoms in menopause?
a. Estrogen receptors are found on pelvic muscles and ligaments.
b. The vagina becomes less acidic after menopause.
c. Significant differences in efficacy exist between the various forms of local estrogen treatment.
d. Vaginal gels and lubricants have lower efficacy in relieving vaginal dryness compared to topical estrogen therapy.
e. Many women may not bring up urogenital symptoms with their physicians due to embarrassment.
28. Which of the following is true regarding the DEXA scan for measurement of bone mineral density?
a. It is fairly expensive, at more than $500 per test.
b. It is a lengthy test that takes more than one hour to perform.
c. It is currently indicated in every postmenopausal woman.
d. It is indicated in women with one or more risk factors for osteoporosis.
e. It results in significant radiation exposure to the patient.
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