Causes of Amenorrhea
When endocrine function along the
hypothalamic– pituitary–ovarian axis is disrupted or an abnormality devel-ops
in the genital outflow tract (obstruction of the uterus, cervix, or vagina or
scarring of the endometrium), menstru-ation ceases. Causes of amenorrhea are
divided into those arising from (1) pregnancy, (2) hypothalamic–pituitary
dys-function, (3) ovarian dysfunction, and (4) alteration of the genital
outflow tract.
Because
pregnancy is the most common cause of amenorrhea, it is essential to exclude
pregnancy in the evaluation of amenorrhea.
A history of breast fullness,
weight gain, and nausea suggest the diagnosis of pregnancy, which is confirmed
by a positive human chorionic gonadotropin (hCG) assay. It is important to rule
out pregnancy to allay the patient’s anxiety and to avoid unnecessary testing.
Also, some treatments for other causes of amenorrhea can be harmful to an
ongoing pregnancy. Lastly, the diag-nosis of ectopic pregnancy should be
entertained in the presence of abnormal menses and a positive preg-nancy test,
as this would necessitate medical or surgical intervention.
Box 35.1
Polymenorrhea—frequent
menstrual bleeding
(frequency,
21 days or less) Menorrhagia—prolonged or excessive uterine
bleeding
that occurs at regular intervals (the loss of 80 mL or more of blood that lasts
for more than 7 days)
Metrorrhagia—irregular
menstrual bleeding or bleeding between periods
Menometrorrhagia—frequent
menstrual bleeding that is excessive and irregular in amount and duration
American College of Obstetricians and
Gynecologists. Manage-ment of anovulatory bleeding. ACOG Practice Bulletin 14.
Washington, DC: American College of Obstetricians and Gyne-cologists; 2000.
Release of hypothalamic
gonadotropin-releasing hor-mone (GnRH) occurs in a pulsatile fashion, modulated
by catecholamine secretion from the central nervous system and by feedback of
sex steroids from the ovaries. When this pulsatile secretion of GnRH is
disrupted or altered, the anterior pituitary gland is not stimulated to secrete
follicle-stimulating hormone (FSH) and luteinizing hor-mone (LH). The result is
an absence of folliculogenesis despite estrogen production, no ovulation, and
lack of corpus luteum with its usual production of estrogen and progesterone.
Because of the lack of sex hormone produc-tion with no stimulation of the
endometrium, there is no menstruation.
Alterations in catecholamine
secretion and metabo-lism in sex steroid hormone feedback or an alteration of
blood flow through the hypothalamic–pituitary portal plexus can disrupt the
signaling process that leads to ovu-lation. This latter disruption can be
caused by tumors or infiltrative processes that impinge on the pituitary stalk
and alter blood flow.
The most common causes of
hypothalamic–pituitary dysfunction are presented in Box 35.2. Most hypothalamic–
pituitary amenorrhea is of functional origin and can be corrected by modifying
causal behavior, by stimulating gonadotropin secretion, or by giving exogenous
human menopausal gonadotropins.
The physician cannot differentiate hypothalamic– pituitary causes of amenorrhea from ovarian or genital outflow causes by medical history or even physical exam-ination alone. However, there are some clues in the med-ical history and physical examination that would suggest a hypothalamic–pituitary etiology for amenorrhea. A his tory of any condition listed in Box 35.2 should cause the physician to consider hypothalamic–pituitary dysfunction.
Box 35.2
Functional Causes
Weight
loss
Excessive
exercise
Obesity
Drug-Induced Causes
Marijuana
Psychoactive
drugs, including antidepressants
Neoplastic Causes
Prolactin-secreting
pituitary adenomas Craniopharyngioma Hypothalamic hamartoma
Psychogenic Causes
Chronic
anxiety
Pseudocyesis
Anorexia
nervosa
Other Causes
Head
injury
Chronic
medical illness
The definitive method to identify hypothalamic–pituitary dysfunction is to measure FSH, LH, and prolactin levels in the blood. In these conditions, FSH and LH levels are in the low range. The prolactin level is normal in most conditions, but is elevated in prolactin-secreting pituitary adenomas.
In ovarian failure, the ovarian
follicles are either exhausted or are resistant to stimulation by pituitary FSH
and LH. Asthe ovaries cease functioning,
blood concentrations of FSH and LH increase. Women with ovarian failure
experience thesymptoms and signs of estrogen deficiency. A summary of causes is
presented in Box 35.3.
Obstruction of the genital
outflow tract prevents overt menstrual bleeding even if ovulation occurs.
Box 35.3
Turner
syndrome (45,X gonadal dysgenesis)
X
chromosome long-arm deletion (46,XX q5)
Gonadotropin-resistant
ovary syndrome (Savage syndrome)
Premature
natural menopause
Autoimmune
ovarian failure (Blizzard syndrome)
Most
cases ofoutflow obstruction result from congenital abnormalities in the development and canalization of the müllerian
ducts. Imperforatehymen and no uterus or vagina are the most
common anomalies that result in primary amenorrhea. Surgical cor-rection of an
imperforate hymen allows for menstruation and fertility. Less-commonly
encountered anomalies, such as a transverse vaginal septum, are more difficult
to correct, and even with attempted surgical correction, menstruation and
fertility are often not restored.
Scarring
of the uterine cavity (Asherman syndrome) is the most frequent anatomic cause
of secondary amenorrhea (Fig. 35.1). Women who undergo
dilation and curettage (D&C) for retained products of pregnancy (especially
when infection is present) are at risk for developing scar-ring of the
endometrium. Cases of mild scarring can be corrected by surgical lysis of the
adhesions performed by hysteroscopy and D&C. However, severe cases are
often refractory to therapy. Estrogen therapy should be added to the surgical
treatment postoperatively to stimulate endometrial regeneration of the denuded
areas. In some cases, a balloon or intrauterine (contraceptive) device may be
placed in the uterine cavity to help keep the uterine walls apart during
healing.
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