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LEIOMYOMATOUS UTERUS 23
11. Can leiomyomas be treated with medication?
Yes, although medical therapy directed at reducing abnormal uterine bleeding (progestin analogues,
oral contraceptives, the levonorgestrel-releasing intrauterine device, or depot medroxyprogesterone
acetate) does not directly affect the leiomyomas. Gonadotropin-releasing hormone (GnRH) agonists
can reduce leiomyoma size by inducing a menopausal-like state of reduced estrogen levels; maxi-
mum reduction in tumor size (30% to 64%) occurs within 3 to 6 months. GnRH agonists have also
been shown to improve preoperative and postoperative hemoglobin and hematocrit levels signifi-
cantly. Use of these agents is generally considered to be a short-term solution because side effects
can be severe, and drug cessation often results in a return of symptoms.
12. What are the indications for surgical treatment?
• Persistent abnormal bleeding unresponsive to medical therapy
• Excessive pain or pressure
• Cases in which fertility is believed to be affected
• Case in which tumor growth occurs after menopause (malignancy should also be considered)
13. What surgical and nonmedical treatment options are available?
• Uterine artery embolization (UAE): This procedure disrupts the blood supply to the uterus, which
can decrease leiomyoma size and improve symptoms. Efficacy is limited when leiomyomas are
large. Potential complications include premature ovarian failure, chronic vaginal discharge, and
pelvic infection.
• Hysteroscopic resection: This procedure is appropriate for submucosal leiomyomas, and it can
allow many patients to avoid hysterectomy.
• Myomectomy: This surgical removal of only the leiomyoma is most commonly offered to women
who would like to preserve the ability to have children.
• Hysterectomy: The only definitive treatment, hysterectomy is appropriate for women who do not
wish to have children. It can be performed by several different routes: vaginally, laparoscopically,
by laparotomy, or with use of a robotic surgical system.
BiBliography
1. Aharoni A, Reiter A, Golan D, et al. Patterns of growth of uterine leiomyomas during pregnancy: a prospective longitu-
dinal study. Br J Obstet Gynaecol. 1988;95:510–513.
2. Candiani GB, Fedele L, Parazzini F, Villa L. Risk of recurrence after myomectomy. Br J Obstet Gynaecol. 1991;98:
385–389.
3. Cook JD, Walker CL. Treatment strategies for uterine leiomyoma: the role of hormonal modulation. Semin Reprod
Med. 2004;22:105–111.
4. Cramer SF, Patel A. The frequency of uterine leiomyomas. Am J Clin Pathol. 1990;94:435–438.
5. Day Baird D, Dunson DB, Hill MC, Cousins D, Schectman JM. High cumulative incidence of uterine leiomyoma in black
and white women: ultrasound evidence. Am J Obstet Gynecol. 2003;188:100–107.
6. Evans P, Brunsell S. Uterine fibroid tumors: diagnosis and treatment. Am Fam Physician. 2007;75:1503–1507.
7. Fernandez H, Sefrioui O, Virelizier C, et al. Hysteroscopic resection of submucosal myomas in patients with infertility.
Hum Reprod. 2001;16:1489–1492.
8. Friedman AJ, Haas ST. Should uterine size be an indication for surgical intervention in women with myomas? Am J
Obstet Gynecol. 1993;168:751–755.
9. Gupta S, Jose J, Manyonda I. Clinical presentation of fibroids. Best Pract Res Clin Obstet Gynaecol. 2008;22:615–626.
10. Hurskainen R, Teperi J, Rissanen P, et al. Quality of life and cost effectiveness of levonorgestrel releasing intrauterine
system versus hysterectomy for treatment of menorrhagia: a randomised trial. Lancet. 2001;35:273–277.
11. Kjerulff KH, Langenberg P, Seidman JD, Stolley PD, Guzinski GM. Uterine leiomyomas: racial differences in severity,
symptoms and age at diagnosis. J Reprod Med. 1996;41:483–490.
12. Leibsohn S, d’Ablaing G, Mishell Jr DR. Leiomyosarcoma in a series of hysterectomies performed for presumed
uterine leiomyomas. Am J Obstet Gynecol. 1990;162:968–974.
13. Lethaby A, Vollenhoven B, Sowter M. Pre-operative GnRH analogue therapy before hysterectomy or myomectomy for
uterine fibroids. Cochrane Database Syst Rev. 2000;2. CD000547.
KEY POINTS: LEIOMYOMATOUS UTERUS
1. Fibroids are hormone-sensitive, fibromuscular benign tumors that are thought to originate from a
monoclonal cell line.
2. Leiomyomas can cause abnormal uterine bleeding, dysmenorrhea, pelvic pressure, and even blad-
der and bowel symptoms.
3. Fibroids can be treated medically, surgically, or with uterine artery embolization.
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24 GENERAL GYNECOLOGY
14. Marshall LM, Spiegelman D, Barbieri RL, et al. Variation in the incidence of uterine leiomyoma among premenopausal
women by age and race. Obstet Gynecol. 1997;90:967–973.
15. Maruo T, Ohara N, Matsuo H, et al. Effects of levonorgestrel-releasing IUS and progesterone receptor modulator PRM
CDB-2914 on uterine leiomyomas. Contraception. 2007;75:S99–S103.
16. Munro MG. Abnormal Uterine Bleeding. Cambridge: Cambridge University Press; 2010.
17. Parker WH. Etiology, symptomatology, and diagnosis of uterine myomas. Fertil Steril. 2007;87:725–736.
18. Practice Committee of the American Society for Reproductive Medicine. Myomas and reproductive function. Fertil
Steril. 2004;82(Suppl. 1):S111–S116.
19. Qidwai GI, Caughey AB, Jacoby AF. Obstetric outcome in women with sonographically detected uterine leiomyomata.
Obstet Gynecol. 2006;107:376–382.
20. Quade BJ, Wang TY, Sornberger K, Dal Cin P, Mutter GL, Morton CC. Molecular pathogenesis of uterine smooth
muscle tumors from transcriptional profiling. Genes Chromosomes Cancer. 2004;40:97–108.
21. Sankaran S, Manyonda SI. Medical management of fibroids. Best Pract Res Clin Obstet Gynaecol. 2008;22:655–676.
22. Smith RP. Uterine leiomyomata. In: Netter’s Obstetrics and Gynecology. 2nd ed. Philadelphia: Saunders; 2008:304.
23. Stenchever MA, Droegemueller W, Herbst AL, Mishell DR, eds. Comprehensive Gynecology. 4th ed. St. Louis: Mosby;
2001.
24. Stewart EA, Friedman AJ, Peck K, Nowak RA. Relative overexpression of collagen type I and collagen type III messen-
ger ribonucleic acids by uterine leiomyomas during the proliferative phase of the menstrual cycle. J Clin Endocrinol
Metab. 1994;79:900–906.
25. Walker CL, Stewart EA. Uterine fibroids: the elephant in the room. Science. 2005;308:1589–1592.
26. Wallach EE, Vlahos NF. Uterine myomas: an overview of development, clinical features, and management. Obstet
Gynecol. 2004;104:393–406.
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25
1. What is anovulation, and what is the general cause?
Anovulation is the absence of ovulation from the ovary. It is referred to as either primary (when the
patient has no earlier history of normal ovulation) or secondary (when normal ovulation was previously
present). Generally speaking, the cause of anovulation is dysfunction at any level of the hypothalamic-
pituitary-ovarian (HPO) axis. Because the HPO axis involves a complex interaction of multiple organ
systems, more precise causes are not always identifiable.
2. What are primary disruptions of the HPO axis that cause anovulation?
• Hypothalamic dysfunction
• Gonadal dysgenesis
• Weight-related issues
• Early-onset hypothyroidism
3. What are common causes of secondary anovulation?
• Obesity
• Hyperprolactinemia
• Hypothyroidism or hyperthyroidism
• Adrenal disorders
• Stress
• Pregnancy
• Primary ovarian insufficiency (POI)
• PCOS (polycystic ovarian syndrome)
4. What are common symptoms of anovulation?
Amenorrhea, abnormal uterine bleeding, signs of androgen excess, and infertility are common
symptoms.
5. How does anovulation lead to abnormal uterine bleeding?
The absence of normal cycles leads to a state of unopposed estrogen, which destabilizes the endome-
trium and leads to irregular, noncyclic shedding.
6. How does obesity cause anovulation?
Androgens are converted to estrogen in adipose tissue, a process that leads to an elevated estrogen-
to-progesterone ratio. In turn, this change can suppress progesterone production and result in a state
of unopposed estrogen. High levels of estrogen suppress gonadotropin-releasing hormone (GnRH)
release from the hypothalamus; result is suppression of follicle-stimulating hormone (FSH). Numerous
studies have shown that weight loss in an obese female patient with PCOS helps restore ovulation
and subsequent normal menses. (For more detailed information on the normal menstrual cycle, see
Chapter 1.)
7. How does hyperprolactinemia affect the HPO axis?
Hyperprolactinemia decreases GnRH release through negative feedback on the hypothalamus.
8. What are common causes of hyperprolactinemia?
• Prolactinoma
• Breastfeeding
• Hypothyroidism
• Medications
• Stress
9. How is hyperprolactinemia treated?
Dopamine agonists are the mainstays of treatment.
CHAPTER 6
ANOVULATION
Jacob Casey, MD, and Judy H. Chen, MD
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26 GENERAL GYNECOLOGY
Prolactinomas are benign and are the most common tumors of the pituitary gland. Treatment
depends on size; microadenomas (<10 mm) that are asymptomatic can be followed with medical
therapy and follow-up imaging. Macroadenomas (>10 mm) may require surgical intervention in addi-
tion to medical therapy.
10. How does thyroid dysfunction cause anovulation?
Hypothyroidism can lead to overproduction of thyroid-releasing hormone (TRH) and thyroid-stimulating
hormone (TSH), as well as disrupting the release of GnRH. In experimental models, TRH is a stimulus
for prolactin release, which, in turn, exerts negative feedback on GnRH and results in anovulation.
However, hypothyroidism leads to menstrual irregularities more frequently than to anovulation.
Hyperthyroidism can increase the production of sex hormone–binding globulin (SHBG), the con-
version of androgens to estrogens, and baseline levels of gonadotropins. This can result in menstrual
irregularities and, less frequently, anovulation.
11. How do adrenal disorders cause anovulation?
In conditions such as congenital adrenal hyperplasia and Cushing syndrome, abnormal corticosteroid
production leads to androgen excess. This condition disrupts the HPO axis and results in anovulation.
12. What are some factors that affect GnRH release from the hypothalamus?
• Weight loss: Significant weight loss and loss of body fat in particular are associated with hypo-
thalamic anovulation and amenorrhea. Extreme weight loss such as that associated with eating
disorders can also be associated with other endocrine abnormalities. These conditions carry a
mortality rate as high as 5% to 15%. Therefore, this condition requires careful assessment; patients
require intensive psychotherapy for both mental and physical health.
• Exercise: Increased opioid production from excess exercise, in combination with the loss of weight
and body fat that accompany strenuous exercise, may inhibit ovulation through positive effects on
norepinephrine or leptin inhibition on the release of GnRH.
• Stress: Extreme stress may induce anovulation by the opioid pathways similar to those noted with
exercise.
13. What is the female athlete triad?
The female athlete triad is a hypoestrogenic state consisting of insufficient caloric intake, amenorrhea,
and decreased bone mineral density. Elevated cortisol centrally inhibits the release of gonadotropins,
thus resulting in decreased estrogen production and suppression of ovulation.
14. What is Kallmann syndrome?
Kallmann syndrome is characterized by primary amenorrhea and anosmia. It results from failed neu-
ronal migration of GnRH neurons and can be inherited in an X-linked or autosomal recessive pattern.
Women with Kallmann syndrome have normal ovaries and can undergo successful ovulation induction
(for more detailed information on ovulation induction, see Chapter 24.)
15. What is POI?
POI is a condition in which the resting pool of primordial follicles in a female patient is prematurely
depleted before 40 years of age, with resulting early menopause. Although the exact mechanism of
primordial follicle depletion is unknown, causes include genetic factors, chemotherapy, radiotherapy,
and surgical intervention.
16. What are dysgenetic gonads?
The term dysgenetic gonads refers to limited gonadal development. This includes patients with abnor-
mal karyotypes (e.g., 45 XO, phenotypic female patients with 46 XY karyotype), gonadal agenesis, or
rudimentary gonads.
KEY POINTS: ANOVULATION
1. Anovulation commonly manifests as infrequent, irregular menses or amenorrhea.
2. Common causes of anovulation are pregnancy, thyroid disease, hyperprolactinemia, PCOS, and
weight extremes.
3. Ovarian failure is normal at menopause (average age, 51 years) and is premature, referred to as
Premature Ovarian Insufficiency, when it occurs before 40 years of age.
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ANOVULATION 27
BiBliography
1. American College of Obstetricians and Gynecologists. Management of Abnormal Uterine Bleeding Associated With
Ovulatory Dysfunction. ACOG practice bulletin 136. Washington, DC: American College of Obstetricians and Gynecologists;
2013.
2. De Vos M, Devroey P, Fauser BC. Primary ovarian insufficiency. Lancet. 2010;376:911–921.
3. ESHRE/ASRM PCOS Consensus Workshop Group. Consensus on infertility treatment related to polycystic ovary
syndrome. Hum Reprod. 2008;23:462–477.
4. Lash MM, Armstrong A. Impact of obesity on women’s health. Fertil Steril. 2009;91:1712–1716.
5. Lentz GM, Lobo RA, Gershenson DM, Katz VL, eds. Comprehensive Gynecology. 6th ed. Philadelphia: Mosby; 2013.
6. Poppe K, Velkeniers B. Female infertility and the thyroid. Best Pract Res Clin Endocrinol Metab. 2004;18:153–165.
7. Practice Committee of the American Society for Reproductive Medicine. Practice guidelines: use of exogenous
gonadotropins in anovulatory women. A technical bulletin. Fertil Steril. 2008;90:S7–S12.
8. Practice Committee of the American Society for Reproductive Medicine and the Practice Committee of the Society
for Assisted Reproductive Technology. Criteria for number of embryos to transfer: a committee opinion. Fertil Steril.
2013;99:44–46.
9. Practice Committee of the American Society for Reproductive Medicine. Use of clomiphene citrate in infertility
women: a committee opinion. Fertil Steril. 2013;100:341–348.
10. Speroff L, Fritz MA. Clinical Gynecologic Endocrinology and Infertility. 7th ed. Philadelphia: Lippincott Williams
&Wilkins; 2005.
11. Unuane D, Tournaye H, Velkeniers B, Poppe K. Endocrine disorders and female infertility. Best Pract Res Clin Endocri-
nol Metab. 2011;25:861–873.
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28
1. With which aspects of sexuality should a gynecologist be familiar?
Gynecologists should be familiar with the physiology of sexual response and phases of the
sexual response cycle. They should be able to obtain a thorough sexual history, which includes
screening for sexual dysfunction, abuse, number of partners, use of barrier protection methods,
sexually transmitted infection (STI) history, and current method of birth control. They should also
be familiar with disorders of the genital tract that may hinder sexual responsiveness.
2. What are the phases of the sexual response cycle?
Masters and Johnson originally described four physiologic stages of sexual response: excite-
ment, plateau, orgasm, and resolution. Kaplan and colleagues subsequently modified these
stages to desire, arousal, and orgasm.
3. List the normal physiologic changes seen in desire and arousal.
• Increased blood flow to the labia and vagina
• Lubrication of the genital tract (subepithelial transudate resulting from engorgement)
• Clitoral engorgement and protrusion
• Vaginal expansion
• Breast enlargement
• Nipple erection
The dopamine system is thought to be responsible for sexual desire, and the noradrenergic
system is thought to be responsible for sexual arousal.
4. What characterizes orgasm in women?
Simultaneous rhythmic contractions of the orgasmic platform, uterus, and rectal sphincter occur
at 0.8-second intervals and then diminish in intensity, duration, and regularity. Generalized
myotonia occurs, as well as tachycardia, tachypnea, and an elevation in blood pressure. This
response is not affected by hysterectomy, and it is possible for women to be multiorgasmic.
Resolution of vasocongestion results in a return to normal anatomy and physiology.
5. What is sexual dysfunction?
In general, sexual dysfunction is a heterogeneous group of disorders that hinder a person’s
ability to experience sexual pleasure. For women, this can encompass problems in the sexual
response cycle (e.g., Kaplan’s stages of desire, arousal, or orgasm), as well as pain, discomfort,
or stress associated with sexual activity.
6. What is the prevalence of sexual dysfunction?
The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-V) estimates
the prevalence of female orgasmic problems to be greater than 40%, but not all women who
report orgasmic problems report associated distress. In other words, some women with orgas-
mic problems still report high sexual satisfaction.
7. What are the types of disorders seen in female sexual dysfunction?
The DSM-V describes the following types of sexual dysfunctions in women:
• Female orgasmic disorder
• Female sexual interest/arousal disorder
• Genitopelvic pain/penetration disorder
• Substance/medication-induced sexual dysfunction
8. How does the DSM-V define the different sexual dysfunction disorders?
• Female orgasmic disorder: Marked delay, infrequency, reduction in intensity, or absence
of orgasm that is distressing to the patient. It is critical in this diagnosis that this is not the
result of relationship stressors that may cause these symptoms. The prevalence of this
CHAPTER 7
FEMALE SEXUAL DYSFUNCTION
Whitney Sigala, MD
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FEMALE SEXUAL DYSFUNCTION 29
condition varies widely depending on age, culture, and severity of symptoms. A medication review
should be undertaken to ensure that this disorder is not medication induced (e.g., selective sero-
tonin reuptake inhibitors [SSRIs] are known to cause difficulties with orgasm).
• Female sexual interest/arousal disorder: A persistent or recurrent deficiency or absence of
sexual desire or receptivity to sexual activity that causes marked distress or interpersonal difficulty.
Imbalanced sexual desire between partners is not sufficient to make the diagnosis. This was
previously termed hypoactive sexual desire disorder but was broadened to female sexual interest/
arousal disorder in the DSM-V. If this condition is secondary to a mood disorder or interpersonal
issues, this diagnosis should not be made.
• Genitopelvic pain/penetration disorder: Persistent difficulty or pain with penetration during inter-
course that may be associated with fear, anxiety, or tensing of the pelvic muscles during attempts
at penetration. This disorder ranges from total inability to have vaginal penetration to minimal
symptoms, but to fit the diagnosis the condition must be distressing to the patient. Approximately
15% of women in North America report recurrent pain during intercourse, and this complaint is a
frequent cause for referral to specialists in sexual dysfunction.
• Substance/medication-induced sexual dysfunction: Any sexual dysfunction that has a temporal
relationship or should be attributed to a substance or medication change.
These disorders must persist for approximately 6 months or more and must be present during almost
all occasions of sexual activity. They should also not be attributable to a medical comorbidity (e.g.,
SSRI use, endometriosis) or personal issue (e.g., relationship problems, life stressors).
9. What is the etiology of sexual dysfunction?
Sexual dysfunction is multifactorial; causes can include abuse, psychologic factors, racial and
religious influences, comorbid conditions (e.g., hypertension, dyslipidemia, spinal cord dysfunction,
premature ovarian insufficiency), earlier surgical history, and medication history (e.g., SSRIs, antihy-
pertensives, antihistamines, hormonal medications).
10. How is sexual dysfunction evaluated?
By systematically evaluating the causes of sexual dysfunction, gynecologists can offer targeted
solutions that may resolve a frustrating issue. A complete sexual history should be obtained, including
questions about sexual orientation, type and frequency of sexual activity, information on previous and
current partners, and sexual satisfaction. A pelvic examination can be used to evaluate pelvic pain
disorders. Based on the patient’s history, further diagnostic studies (e.g., gonorrhea or Chlamydia
cultures, ultrasound) may be indicated. Androgen levels should not be used to diagnose sexual
dysfunction.
11. What are potential barriers to treatment?
• Reluctance to discuss this topic with health care providers
• Perception that few or no treatment options exist
• Inadequate provider training
• Inadequate time to obtain a complete sexual history
• Underestimation of the prevalence of sexual dysfunction
12. Does hysterectomy affect sexual function?
No. Hysterectomy does not affect sexual function or the ability to achieve orgasm.
13. What treatment options exist for female sexual dysfunction?
• Dyspareunia: Topical estrogens may improve symptoms, especially in postmenopausal women. If
estrogen is contraindicated (e.g., a history of hormone-sensitive cancer), nonestrogen lubricants
may be helpful. Systemic estrogen with or without progestin therapy has not been shown to
improve sexual function.
• Orgasmic disorders: Studies on the benefit of sildenafil have been inconclusive.
• Female sexual interest/arousal disorder: Transdermal testosterone can be an effective short-
term treatment; however, it should not be used for longer than 6 months. Treatment should also be
balanced with the risks of androgen replacement therapy, which include hirsutism, acne, viriliza-
tion, possible cardiovascular effects, and a potential increased risk of breast cancer.
The safety and efficacy of herbal supplements for treating female sexual dysfunction are unproven.
In many cases a multidisciplinary approach should be used, which may include a primary care
physician, a gynecologist, a psychiatrist, a psychotherapist, a sex therapist, and a pelvic physical
therapist. Partner and couples therapy may also be of benefit. Any identifiable underlying disorders
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30 GENERAL GYNECOLOGY
should be treated; for example, a patient with dyspareunia that is thought to be secondary to endome-
triosis should have either laparoscopy or hormonal medication.
14. What devices can be used to treat female sexual dysfunction?
The Food and Drug Administration (FDA) has approved a battery-powered device that is applied to the
clitoris to increase blood flow and engorgement. It has been shown to benefit patients with arousal
and orgasm dysfunction.
BiBliography
1. American College of Obstetricians and Gynecologists. Female sexual dysfunction. ACOG practice bulletin number 119.
Obstet Gynecol. 2011;117:996–1007.
2. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Washington, DC:
American Psychiatric Association; 2013.
3. Basson R. Female sexual response: the role of drugs in the management of sexual dysfunction. Obstet Gynecol.
2001;98:350–353.
4. Basson R, Berman J, Burnett A, et al. Report of the International Consensus Development Conference on Female Sexual
Dysfunction: definitions and classifications. J Urol. 2000;163:888–893.
5. Berman JR, Goldstein I. Female sexual dysfunction. Urol Clin North Am. 2001;28:405–416.
6. Kaplan H. Disorders Of Sexual Desire And Other New Concepts And Techniques In Sex Therapy. New York: Simon and
Schuster; 1979.
7. Laumann EO, Paik A, Rosen RC. Sexual dysfunction in the US: prevalence and predictors. JAMA. 1999;281:537–554.
8. Masters W, Johnson V. Human Sexual Response. Boston: Little, Brown and Company; 1966.
KEY POINTS: FEMALE SEXUAL DYSFUNCTION
1. In general, sexual dysfunction is a heterogeneous group of disorders that hinder a person’s ability to
experience sexual pleasure.
2. Sexual dysfunction is multifactorial, and a multidisciplinary approach should be used for treatment.
3. A complete sexual history should include questions about sexual orientation, type and frequency of
sexual activity, information on previous and current partners, and sexual satisfaction.
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31
1. What are the differences between menopause and perimenopause?
Perimenopause is the period immediately before menopause and is characterized by irregular
menstrual cycles and hormonal fluctuations. It is associated with hot flashes, vaginal dryness, sleep
disturbances, and mood symptoms. The average age for perimenopause to start is 47.5 years, and an
average of 4 years will pass before the final menstrual period.
Menopause is a retrospective diagnosis after a woman has experienced 12 months of amenor-
rhea without any other obvious pathologic or physiologic cause. It is a reflection of complete ovarian
follicular depletion resulting in high follicle-stimulating hormone (FSH) concentrations and hypoestro-
genemia. In the United States, the average age for menopause is 51.4 years. Menopause that occurs
before the age of 40 years is called premature ovarian failure or primary ovarian insufficiency.
2. What causes menopause to occur? What endocrine changes are seen?
Menopause is caused by a gradual depletion of functioning ovarian follicles. Declining inhibin B levels
from the granulosa cells lead to increased FSH production from the pituitary that accelerates the
follicular phase of the menstrual cycle. High basal estradiol levels can be seen during menses, often in
association with follicular cysts. As the granulosa cells gradually lose their ability to produce estradiol,
FSH levels rise (as do luteinizing hormone [LH] levels, to a lesser extent). After menopause, androgen
levels decline by 50%. The greater decline of estradiol, however, favors a higher androgen-to-estrogen
ratio. This change can lead to signs of hirsutism and alopecia in some women. Estrogen production
after menopause is principally in the form of estrone and results from aromatization of androstenedi-
one in adipose tissues.
3. What are common symptoms of perimenopause and menopause?
Shorter follicular and luteal phases result in shortened, irregular menstrual cycles. Anovulation then
occurs and results in “skipped” menstrual periods, oligomenorrhea, and eventually amenorrhea.
Vasomotor symptoms, also known as hot flashes, occur in approximately 80% of women and can
persist for 5 to 15 years after menopause. Over time, symptoms of urogenital atrophy can develop;
these include dyspareunia, vulvar pruritus, and incontinence. Other associated symptoms are sleep
and mood disturbances, as well as new-onset depression. Although not a symptom of menopause,
accelerated bone loss also occurs.
4. What are the available treatments for menstrual irregularities associated with
menopause?
In the absence of contraindications (e.g., tobacco use, hypertension, or vascular disease), irregular
menstrual cycles can be treated with low-dose oral contraceptive pills. Another effective way to
control irregular bleeding while reducing the risk of endometrial hyperplasia is monthly withdrawal
bleeding induced by progestins. When patients do not experience bleeding after withdrawal of the pro-
gestin, hypoestrogenism is diagnosed, and estrogen replacement therapy can be considered. Another
treatment option is continuous progestin use, but breakthrough bleeding is a common undesired side
effect.
5. What is a hot flash?
A hot flash is a sudden sensation of warmth, often accompanied by a flushed sensation of the upper
body and face that quickly becomes generalized. Typically lasting from 1 to 5 minutes, it is often
associated with profuse perspiration. Palpitations or feelings of anxiety can also occur. Hot flashes
result from alterations in the hypothalamic thermoregulatory center caused by fluctuations in steroid
and peptide hormone levels.
6. How can vasomotor symptoms be treated?
For women with moderate to severe hot flashes, the most effective therapy is estrogen. This treatment
can stop hot flashes completely in approximately 80% of women and reduce the frequency and sever-
ity of hot flashes in the remainder.
CHAPTER 8
MENOPAUSE
Rachel Rosenheck, MD, and Judy H. Chen, MD
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32 GENERAL GYNECOLOGY
7. What are the health risks and benefits of hormone therapy (HT) in perimenopausal
and menopausal women?
Aside from reducing vasomotor symptoms and improving urogenital atrophy, HT is associated with
a 2% to 5% increase in bone mineral density (BMD) and a 25% to 50% decreased risk of vertebral
and hip fractures. Observational studies found HT to be cardioprotective, but this finding was not
replicated in randomized controlled trials. In 2002, a large, randomized controlled study showed an
increased risk of stroke, thromboembolic events, and breast cancer in women who used HT. Reduc-
tions in colon cancer and fracture risk, however, were also seen. The absolute risks and benefits for
any individual woman are small. Because of these findings, the long-term risks are considered to
exceed the benefits of HT use in healthy postmenopausal women; this treatment should be reserved
for symptomatic women and used for as short a duration as possible.
8. What are the different types of estrogen preparations available for HT?
Box 8-1 contains a list of currently available preparations for HT. All routes of administration appear
to be equally effective for symptomatic relief, but their metabolic effects differ. Oral estrogen has a
more favorable effect on lipid profiles, but it is associated with an increase in serum triglycerides and
C-reactive protein. Use of transdermal or vaginal estrogen appears to have a higher risk of venous
thromboembolism and stroke.
9. What progestins are available for use in perimenopausal and menopausal women,
and what is the key benefit of these hormones?
Currently available progestins used for HT include medroxyprogesterone acetate, norethindrone, and
micronized progesterone. Progestins reduce the risk of endometrial hyperplasia and endometrial cancer
in women who receive estrogen therapy and must always be given in patients who still have a uterus.
10. What are the contraindications to HT?
HT is contraindicated in pregnancy, active thromboembolic disease, chronic liver impairment, undiag-
nosed genital bleeding, or estrogen-dependent neoplasms.
11. What are selective estrogen receptor modulators (SERMs), and what are their
indications?
SERMs comprise a class of drugs that have differential estrogen agonistic and antagonistic properties
in various tissues. They have no proven benefits in preventing cardiovascular disease and carry an
increased risk of thrombotic events. Raloxifene is currently approved for the prevention and treatment
of osteoporosis; it does not improve hot flashes or urogenital atrophy. The side effect profile of raloxi-
fene is similar to that of tamoxifen, and it does not have established benefits in breast cancer therapy.
Bazedoxifene is an SERM that has been marketed for the control of hot flashes.
12. Does HT increase the risk of breast cancer?
More than 50 epidemiologic studies and more than a half-dozen meta-analyses have tried to answer
this question. With few exceptions, these studies were observational and subject to bias. In addition,
the types of hormones used, their respective doses, and their duration of administration varied, as did
the criteria for the diagnosis of breast cancer. The majority of meta-analyses did not find compelling
evidence for an association between estrogen-only HT and breast cancer.
The Women’s Health Initiative Study was halted prematurely because of an increased relative hazard
for breast cancer of 1.24 (or 8 in 10,000 women/year more breast cancers) after 5.6 years of follow-up in
patients treated with combination estrogen-progestin versus placebo. Women in the estrogen-progestin
arm of the study were also diagnosed with later stage cancer and more aggressive types of tumors.
13. Define osteoporosis and how it is diagnosed.
Osteoporosis is a progressive bone disease characterized by a decrease in bone mass and density that
leads to an increase risk of fracture. BMD is best assessed by a dual-energy x-ray absorptiometry (DEXA)
study. The World Health Organization (WHO) defines osteoporosis as a BMD that is greater than 2.5 SD
below the young adult mean (called a T-score). Osteopenia is a BMD greater than 1.0 to less than 2.5
standard deviations (SD) below the young adult mean. A Z-score is the BMD of the patient compared with
the expected mean at her own age, with greater than 1 SD below the mean considered abnormal.
Although not diagnostic of osteoporosis, biochemical markers of bone remodeling exist and
include serum markers of bone formation (osteocalcin, bone specific alkaline phosphatase, and
procollagen extension peptides) and urinary markers of bone resorption (pyridinoline cross-linked
peptides, N-telopeptides, hydroxyproline, and hydroxylysine).
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