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A normal menstrual cycle involves the hypothalamus, anterior pituitary
gland, ovaries, and endometrial lining of the uterus to create hormonal
release. This process results in follicle development, ovulation, and
either pregnancy or menstruation every 28 days (average) during
Polycystic ovary syndrome (PCOS) is a heterogeneous disorder that
presents with signs and symptoms of hyperandrogenism (e.g., acne,
hirsutism) or ovulatory dysfunction.
Long-term complications of PCOS may include impaired glucose
tolerance, diabetes, metabolic syndrome, infertility, endometrial cancer,
Treatment for PCOS involves nonpharmacologic and pharmacologic
management. Pharmacologic management targets the pathophysiologic
aspects of the syndrome and individual goals of treatment. Oral
contraceptives are preferred when contraception is desired; letrozole or
clomiphene citrate is warranted when pregnancy is desired.
Dysmenorrhea, or painful cramping that occurs with the onset and first
days of menstruation, can be categorized as either primary (without
underlying uterine pathology) or secondary as a result of uterine
conditions, including endometriosis, uterine polyps, or fibroids;
complications of intrauterine contraceptive device use; or pelvic
inflammatory disease. A careful history can distinguish most cases of
always be investigated further for its underlying etiology.
Dysmenorrhea is the single largest cause of lost productivity and school
absence among adolescent girls. Healthcare providers can play a
significant role in patient education and development of rational
symptoms and improve functionality.
Endometriosis is defined as the presence of functional endometrial tissue
occurring outside the uterine cavity. It is the most common cause of
secondary dysmenorrhea in young women and can result in chronic
pelvic pain, infertility, and dyspareunia. A significant delay in diagnosis
of endometriosis is common and can result in negative effects on
fertility and pain control. Recognition of the potential for a diagnosis of
endometriosis, through a careful history and physical examination, is a
key for clinicians to provide appropriate care.
Pain control in endometriosis is directed at suppression of endometrial
implants that respond to estrogen with bleeding, resulting in subsequent
inflammation and pain. Pharmacologic therapy is directed at reducing
inflammation (via use of NSAIDs) and reduction in estrogen (through
use of hormonal contraception), or the use of gonadotropin-releasing
hormone (GnRH) analogs to induce a pseudomenopausalstate. A
treatment plan should take into account cost, ease of use of therapy, and
the patient’s desire for future fertility.
Endometriosis treatment plans that include GnRH analogs or aromatase
inhibitors may also require the use of “add-back” therapy. Add-back
therapy is the addition of progestins or estrogens that may be used with
GnRH analogs and aromatase inhibitors to decrease menopausalside
effects including hot flashes, vaginal dryness, and decreases in bone
More than 200 premenstrualsymptoms (such as increased energy, libido,
ability to relax, abdominal distension, fatigue, headaches, and crying
spells) have been described as occurring during the days before
menstruation. It is not until the symptoms have a decidedly negative
influence on the physical, psychological, or social function of a woman
that premenstrualsyndrome (PMS) or premenstrual dysphoric disorder
(PMDD) exists. Both PMS and PMDD have symptoms that occur in
the luteal phase with resolution within a few days of menstruation,
lasting across at least two menstrual cycles, and disrupt normal
Nonprescription options that have been studied and have shown at least
minimal benefit in PMS and PMDD include calcium, magnesium,
pyridoxine, chaste tree or chasteberry, and some mind–body
Treatment for PMS and PMDD includes lifestyle modifications,
psychological interventions, selective serotonin reuptake inhibitors
(SSRIs), other psychotropic medications, oral contraceptives, GnRH
agonists, and danazol. Because serotonin is critical in the pathogenesis
of these disorders, SSRIs have become the treatment of choice for
Feedback biologic mechanisms involving the hypothalamus, anterior pituitary gland,
ovaries, and endometrial lining of the uterus control the average 28-day menstrual
1–3 The hypothalamus synthesizes gonadotropin-releasing hormone (GnRH) and
secretes the hormone in a pulse-like manner with varying frequencies throughout the
menstrual cycle (typically every 60–90 minutes). GnRH stimulates the anterior
pituitary to produce and release follicle-stimulating hormone (FSH) and luteinizing
hormone (LH). FSH is important for stimulating growth of ovarian follicles, and LH
is critical for ovulation and sex steroid production. FSH and LH act on the ovaries to
produce estrogen and progesterone. Estrogen in turn acts on the hypothalamus and
anterior pituitary, in a negative feedback manner, to stop FSH and LH secretion (Fig.
The menstrual cycle can be divided into three phases: the follicular phase,
ovulation, and the luteal phase (Fig. 50-2).
1–3 The day bleeding begins is referred to
as the first day (or day 1) of the menstrual cycle. Bleeding usually occurs from days 1
to 5 of the cycle, although may be longer in some women. The follicular phase begins
at the onset of menstruation and lasts approximately 10 to 14 days (see Fig. 50-2). At
the beginning of this phase, several follicles begin to develop within the ovary. In the
second half of the follicular phase most of the developing follicles atrophy, while the
dominant follicle develops further and produces estrogen in increasing amounts.
Elevated estradiol levels during the ovulatory phase lead to a surge in LH and FSH.
The LH surge is responsible for final-stage growth and maturation of the follicle,
ovulation, and the formation of the corpus luteum. Ovulation usually occurs 14 days
before the last day of the cycle and is followed by the luteal phase. The luteal phase
is 13 to 15 days in duration and is the least variable part of the human reproductive
1 During this progesterone-dominant phase, the corpus luteum produces
progesterone and estrogen. Progesterone prepares the endometrium for implantation
of a fertilized ovum. If implantation does not occur, corpus luteum regression causes
a decrease in the levels of estrogen and progesterone. When these hormone levels
decrease, the endometrium cannot be maintained and is sloughed off (menstrual
phase). Using the average 28-day cycle as an example, day 28 is the last day of the
cycle and is the day before bleeding begins again for the next menstrual cycle.
hormone; LH, luteinizing hormone. (Adapted with permission from Premkumar K. The Massage Connection:
Anatomy and Physiology. Baltimore, MD: Lippincott Williams & Wilkins; 2004.)
Polycystic ovary syndrome (PCOS) affects approximately 6% to 15%, or
approximately 1 in 10, women of reproductive age, making it the leading cause of
anovulatory infertility and the most common endocrine abnormality for this age
4 This syndrome, or constellation of symptoms, was first described in 1935 by
Stein and Leventhal when they reported infertility and amenorrhea in seven women
5 Excessive male-patterned hair growth and obesity
were added later to the description of this syndrome.
to as Stein-Leventhal syndrome, polycystic ovary, polycystic ovarian disease,
hyperandrogenic chronic anovulatory syndrome, and functional ovarian
hyperandrogenism. The name polycystic ovary syndrome has been most widely
accepted because “syndrome” best describes the heterogeneous nature of this
disorder. However, there have been recommendations to change the name because it
focuses on the polycystic ovarian morphology, which is not necessary for diagnosis.
It has been suggested that the name should include the complex metabolic,
hypothalamic, pituitary, ovarian, and adrenal interactions of the syndrome.
The diagnosis of PCOS is complicated by variations among women presenting signs
and symptoms of PCOS and because precise and uniform criteria for diagnosis have
not been firmly established. Three major diagnostic criteria for PCOS have been
proposed by different organizations.
The initial diagnostic criteria were developed in 1990 during an expert conference
sponsored by the US National Institutes of Health and US National Institute of Child
Health and Human Development. The panel concluded that the major criteria for
PCOS should include (in order of importance) the following: (a) hyperandrogenism
(clinical signs of hyperandrogenism such as hirsutism) or hyperandrogenemia
(biochemical signs of hyperandrogenism such as elevated testosterone levels), (b)
oligo-ovulation (infrequent or irregular ovulation with fewer than nine menses/year),
and (c) exclusion of other known disorders such as hyperprolactinemia, thyroid
abnormalities, and congenital adrenal hyperplasia.
8 The second set of criteria was
proposed at an expert conference in Rotterdam sponsored by the European Society
for Human Reproduction and Embryology and the American Society for
Reproductive Medicine in 2003.
9 They concluded that the presence of two of these
three features, after exclusion of related disorders, confirmed diagnosis of PCOS: (a)
oligo-ovulation or anovulation, (b) clinical or biochemical signs of
hyperandrogenism, or (c) polycystic ovaries. The third set of criteria was developed
by a task force of the Androgen Excess Society in 2006 with a complete report
including phenotyping in 2009.
10,11 Their criteria include hyperandrogenism
(hirsutism or hyperandrogenemia), ovarian dysfunction (oligo-ovulation or polycystic
ovaries), and exclusion of other androgen excess or related disorders. Recent
practice guidelines support the Rotterdam criteria for diagnosing PCOS.
Criteria for diagnosis of PCOS in adolescence can be difficult to assess due to
typical changes during puberty and are different from those used for older women of
4 Specifically, all three Rotterdam criteria should be present or
oligomenorrhea or amenorrhea should be present for at least 2 years after menarche
(or primary amenorrhea at age 16 years), the diagnosis of polycystic ovaries on
ultrasound should include increased ovarian size (>10 cm3
rather than just signs of androgen excess should be documented.
Common clinical signs of hyperandrogenism in PCOS include hirsutism, acne, and
alopecia. Hirsutism, the most common of these characteristics, occurs in 60% to 75%
It is defined as an excess of thickly pigmented body hair in a male pattern
distribution and commonly found on the upper lip, lower abdomen, and around the
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