Amenorrhea - Menstrual Abnormalities - Merck Manual Professional

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Amenorrhea: Menstrual Abnormalities: Merck Manual Professional
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> Menstrual Abnormalities
Amenorrhea
Amenorrhea (the absence of menstruation) can be primary or secondary.
Primary amenorrhea is failure of menses to occur by one of the
following:
Age 16 or 2 yr after the onset of puberty
About age 14 in girls who have not gone through puberty (eg, growth spurt,
development of secondary sexual characteristics)
If patients have had no menstrual periods by age 13 and have no signs of

puberty (eg, any type of breast development), they should be evaluated
for primary amenorrhea.
Secondary amenorrhea is cessation of menses after they have begun.
Usually, patients should be evaluated for secondary amenorrhea if
menses have been absent for 3 mo or 3 typical cycles because from
menarche until perimenopause, a menstrual cycle lasting > 90 days is
unusual.
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Pathophysiology
Normally, the hypothalamus generates pulses of gonadotropin-releasing
hormone (GnRH). GnRH stimulates the pituitary to produce gonadotropins
(follicle-stimulating hormone [FSH] and luteinizing hormone [LH]see
Menstrual Cycle), which are released into the bloodstream. Gonadotropins
stimulate the ovaries to produce estrogen (mainly estradiol), androgens
(mainly testosterone), and progesterone. These hormones do the
following:
FSH stimulates tissues around the developing oocytes to convert
testosterone to estradiol.
Estrogen stimulates the endometrium, causing it to proliferate.
LH, when it surges during the menstrual cycle, promotes maturation of the
dominant oocyte, release of the oocyte, and formation of the corpus
luteum, which produces progesterone.
Progesterone changes the endometrium into a secretory structure and
prepares it for egg implantation (endometrial decidualization).
If pregnancy does not occur, estrogen and progesterone production

decreases, and the endometrium breaks down and is sloughed during
menses. Menstruation occurs 14 days after ovulation in typical cycles.
When part of this system malfunctions, ovulatory dysfunction occurs; the
cycle of gonadotropin-stimulated estrogen production and cyclic
endometrial changes is disrupted, and menstrual flow does not occur,
resulting in anovulatory amenorrhea. Most amenorrhea, particularly
secondary amenorrhea, is anovulatory.
However, amenorrhea can occur when ovulation is normal, as occurs
when genital anatomic abnormalities (eg, congenital anomalies causing
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outflow obstruction, intrauterine adhesions [Asherman syndrome]) prevent

normal menstrual flow despite normal hormonal stimulation.
Etiology
Amenorrhea is usually classified as anovulatory (see Table 1: Some
Causes of Anovulatory Amenorrhea ) or ovulatory (see Table 2: Some
Causes of Ovulatory Amenorrhea ). Each type has many causes, but
overall, the most common causes of amenorrhea include
Pregnancy (the most common cause in women of reproductive age)
Constitutional delay of puberty
Functional hypothalamic anovulation (eg, due to excessive exercise, eating
disorders, or stress)
Use or abuse of drugs (eg, oral contraceptives, depoprogesterone,
antidepressants, antipsychotics)
Breastfeeding
Polycystic ovary syndrome
Contraceptives can cause the endometrium to thin, sometimes resulting in

amenorrhea; menses usually begin again about 3 mo after stopping oral
contraceptives. Antidepressants and antipsychotics can elevate prolactin,
which stimulates the breasts to produce milk and can cause amenorrhea.
Some disorders can cause ovulatory or anovulatory amenorrhea.
Congenital anatomic abnormalities cause only primary amenorrhea. All
disorders that cause secondary amenorrhea can cause primary
amenorrhea.
Anovulatory amenorrhea: The most common causes (see Table 1:
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) involve a disruption of the

hypothalamic-pituitary-ovarian axis. Thus, causes include
Some Causes of Anovulatory Amenorrhea
Hypothalamic
anovulation)
dysfunction
(particularly
functional
hypothalamic
Pituitary dysfunction
Premature ovarian failure
Endocrine disorders that cause androgen excess (particularly polycystic
ovary syndrome)
Anovulatory amenorrhea is usually secondary but may be primary if

ovulation never beginseg, because of a genetic disorder. If ovulation
never begins, puberty and development of secondary sexual
characteristics are abnormal. Genetic disorders that confer a Y
chromosome increase the risk of ovarian germ cell cancer.
Table 1
Some Causes of Anovulatory Amenorrhea

Cause
Examples
Hypothalamic
dysfunction,
structural
Genetic disorders (eg, congenital gonadotropinreleasing hormone deficiency, GnRH receptor

gene mutations that result in low FSH and
estradiol levels and a high LH level, Prader-Willi
syndrome)
Infiltrative disorders of the hypothalamus (eg,
Langerhans cell granulomatosis, lymphoma,
sarcoidosis, TB)
Irradiation to the hypothalamus
Traumatic brain injury
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Tumors of the hypothalamus

Hypothalamic
dysfunction,
functional
Cachexia
Chronic disorders, particularly respiratory, GI,
hematologic, renal, or hepatic (eg, Crohn's
disease, cystic fibrosis, sickle cell disease,
thalassemia major)
Dieting
Drug abuse (eg, of alcohol, cocaine, marijuana, or
opioids)
Eating disorders (eg, anorexia nervosa, bulimia)
Exercise, if excessive
HIV infection
Immunodeficiency
Psychiatric disorders (eg, stress, depression,
obsessive-compulsive disorder, schizophrenia)
Psychoactive drugs
Undernutrition
Pituitary
dysfunction
Aneurysms of the pituitary

Hyperprolactinemia*
Idiopathic hypogonadotropic hypogonadism
Infiltrative disorders of the pituitary (eg,
hemochromatosis, Langerhans cell
granulomatosis, sarcoidosis, TB)
Isolated gonadotropin deficiency
Kallmann syndrome (hypogonadotropic
hypogonadism with anosmia)
Postpartum pituitary necrosis (Sheehan's
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syndrome)
Traumatic brain injury
Tumors of the brain (eg, meningioma,
craniopharyngioma, gliomas)
Tumors of the pituitary (eg, microadenoma)
Ovarian
dysfunction
Autoimmune disorders (eg, autoimmune oophoritis

as may occur in myasthenia gravis, thyroiditis, or
vitiligo)
Chemotherapy (eg, high-dose alkylating drugs)
Genetic abnormalities, including chromosomal
abnormalities (eg, congenital thymic aplasia,
Fragile X syndrome, Turner syndrome [45,X],
idiopathic accelerated ovarian follicular atresia)
Gonadal dysgenesis (incomplete ovarian
development, sometimes secondary to genetic
disorders)
Irradiation to the pelvis
Metabolic disorders (eg, Addison disease,
diabetes mellitus, galactosemia)
Viral infections (eg, mumps)
Other endocrine
dysfunction
Androgen insensitivity syndrome (testicular

feminization)
Congenital adrenal virilism (congenital adrenal
hyperplasiaeg, due to 17-hydroxylase
deficiency or 17,20-lyase deficiency) or adultonset adrenal virilism
Cushing syndrome,
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Drug-induced virilization (eg, by androgens,

antidepressants, danazol , or high-dose
progestins)
Hyperthyroidism
Hypothyroidism
Obesity (which causes excess extraglandular
production of estrogen)
True hermaphroditism
Tumors producing androgens (usually ovarian or
adrenal)
Tumors producing estrogens or tumors producing
human chorionic gonadotropin (gestational
trophoblastic disease)
*Hyperprolactinemia due to other conditions (eg, hypothyroidism, use of certain drugs) may also cause
amenorrhea.
Females with these disorders may have virilization or ambiguous genitals.
Virilization may occur in Cushing syndrome secondary to an adrenal tumor.
Ovulatory amenorrhea: The most common causes (see Table 2: Some

Causes of Ovulatory Amenorrhea ) include
Chromosomal abnormalities
Congenital anatomic genital abnormalities that obstruct menstrual flow
Obstructive abnormalities are

Table 2
usually accompanied by normal Some Causes of Ovulatory
hormonal
function.
Such Amenorrhea
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obstruction
may
result
in Cause
hematocolpos (accumulation of
Congenital
menstrual blood in the vagina), genital
which can cause the vagina to abnormalities
bulge,
or
in
hematometra
(accumulation of blood in the
uterus), which can cause uterine
distention, a mass, or bulging of
the cervix. Because ovarian
function is normal, external
genital
organs
and
other
secondary sexual characteristics Acquired
develop
normally.
Some uterine
abnormalities
congenital disorders (eg, those
accompanied by vaginal aplasia
or a vaginal septum) also cause
urinary
tract
and
skeletal
abnormalities.
Examples
Cervical stenosis (rare)

Imperforate hymen
Pseudohermaphroditism
Transverse vaginal
septum
Vaginal or uterine
aplasia (eg, Mllerian
agenesis)
Asherman syndrome
Endometrial TB
Obstructive fibroids and
polyps
Some acquired anatomic abnormalities, such as endometrial scarring

after instrumentation for postpartum hemorrhage or infection (Asherman
syndrome), cause secondary ovulatory amenorrhea.
Evaluation
Girls are evaluated if
They have no signs of puberty (eg, breast development, growth spurt) by
age 13.
Pubic hair is absent at age 14.
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Menarche has not occurred by age 16 or by 2 yr after the onset of puberty

(development of secondary sexual characteristics).
Women of reproductive age should have a pregnancy test after missing

one menses. They are evaluated for amenorrhea if
They are not pregnant and have missed menstrual cycles for 3 mo or 3
typical cycles.
They have < 9 menses a year.
They have a sudden change in menstrual pattern.
History: History of present illness includes whether menses have ever

occurred (to distinguish primary from secondary amenorrhea) and, if so,
how old patients were at menarche, whether periods have ever been
regular, and when the last normal menstrual period occurred. History
should also include duration and flow of menses; presence or absence of
cyclic breast tenderness and mood changes; and growth, development,
and age at thelarche (development of breasts at puberty).
Review of systems should cover symptoms suggesting possible causes,
including galactorrhea, headaches, and visual field defects (pituitary
disorders); fatigue, weight gain, and cold intolerance (hypothyroidism);
palpitations, nervousness, tremor, and heat intolerance (hyperthyroidism);
acne, hirsutism, and deepening of the voice (androgen excess); and, for
patients with secondary amenorrhea, hot flushes, vaginal dryness, sleep
disturbance, fragility fractures, and decreased libido (estrogen deficiency).
Patients with primary amenorrhea are asked about symptoms of puberty
(eg, breast development, growth spurt, presence of axillary and pubic
hair) to help determine whether ovulation has occurred.
Past medical history should note risk factors for functional hypothalamic
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anovulation, such as stress; chronic illness; new drugs; a recent change in

weight, diet, or exercise intensity; and, in patients with secondary
amenorrhea, risk factors for Asherman syndrome (eg, D & C, endometrial
ablation, endometritis, obstetric injury, uterine surgery).
Drug history should include specific questions about use of drugs that
affect dopamine (eg, antihypertensives, antipsychotics, opioids, tricyclic
antidepressants), cancer chemotherapy drugs (eg,
busulfan ,
chlorambucil , cyclophosphamide ), and sex hormones that can cause
virilization (eg, androgens, estrogens, high-dose progestins) and
questions about recent use of contraceptives.
Family history should include height of family members and any cases of
delayed puberty or genetic disorders in family members.
Physical examination: Clinicians should note vital signs and body
composition and build, including height and weight, and should calculate
body mass index (BMI). Secondary sexual characteristics are evaluated;
breast and pubic hair development are staged using Tanner's method. If
axillary and pubic hair is present, adrenarche has occurred.
With the patient seated, clinicians should check for breast secretion by
applying pressure to all sections of the breast, beginning at the base and
moving toward the nipple. Galactorrhea (breast milk secretion not
temporally associated with childbirth) may be observed; it can be
distinguished from other types of nipple discharge by finding fat globules
in the fluid using a low-power microscope.
Pelvic examination is done to detect anatomic genital abnormalities; a
bulging hymen may be caused by hematocolpos, which suggests genital
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outflow obstruction. Pelvic examination findings also help determine

whether estrogen has been deficient. In postpubertal females, thin, pale
vaginal mucosa without rugae and pH > 6.0 indicate estrogen deficiency.
The presence of cervical mucus with spinnbarkeit (a stringy, stretchy
quality) usually indicates adequate estrogen.
General examination focuses on evidence of virilization, including
hirsutism, temporal balding, acne, voice deepening, increased muscle
mass, clitoromegaly (clitoral enlargement), and defeminization (a
decrease in previously normal secondary sexual characteristics, such as
decreased breast size and vaginal atrophy). Hypertrichosis (excessive
growth of hair on the extremities, head, and back), which is common in
some families, is differentiated from true hirsutism, which is characterized
by excess hair on the upper lip and chin and between the breasts. Skin
discoloration (eg, yellow due to jaundice or carotenemia, black patches
due to acanthosis nigricans) should be noted.
Red flags: The following findings are of particular concern:
Delayed puberty
Virilization
Visual field defects
Interpretation of findings: Pregnancy should not be excluded based on

history; a pregnancy test is required.
In primary amenorrhea, the presence
of
normal
secondary
sexual Pearls & Pitfalls
characteristics usually reflects normal
If amenorrhea occurs in girls with secondary sexual
characteristics or in women of reproductive age, do a
hormonal function; amenorrhea is
pregnancy test regardless of sexual and menstrual history.
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usually ovulatory and typically due to a

congenital anatomic genital tract obstruction. Primary amenorrhea
accompanied by abnormal secondary sexual characteristics is usually
anovulatory (eg, due to a genetic disorder).
In secondary amenorrhea, clinical findings sometimes suggest a
mechanism (see Table 3: Findings Suggesting Possible Causes of Amenorrhea
):
Galactorrhea suggests hyperprolactinemia (eg, pituitary dysfunction, use of
certain drugs); if visual field defects and headaches are also present,
pituitary tumors should be considered.
Symptoms and signs of estrogen deficiency (eg, hot flushes, night sweats,
vaginal dryness or atrophy) suggest premature ovarian failure.
Virilization suggests androgen excess (eg, polycystic ovary syndrome,
androgen-secreting tumor, Cushing syndrome, use of certain drugs). If
patients have a high BMI, acanthosis nigricans, or both, polycystic ovary
syndrome is likely.
Table 3
Findings Suggesting Possible Causes of Amenorrhea

Finding
Other Possible
Findings
Possible Cause
Galactorrhea
Hyperprolactinemia
Use of certain drugs
Drugs that affect

dopamine (which
helps regulate
prolactin secretion):
Antihypertensives (eg,
methyldopa , reserpine ,
verapamil )
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Antipsychotics, 2nd generation

(eg, molindone ,
olanzapine , risperidone )
Antipsychotics, conventional
(eg, haloperidol ,
phenothiazines, pimozide )
Cocaine
Estrogens
GI drugs (eg, cimetidine ,
metoclopramide )
Hallucinogens
Opioids (eg, codeine ,
morphine )
Tricyclic antidepressants (eg,
clomipramine ,
desipramine )
Hormones and certain

other drugs that affect
the balance of
estrogenic and
androgenic effects
(eg, androgens,
antidepressants,
danazol , high-dose
progestins)
Virilization
Drug-induced virilization
Estrogen excess
Virilization
Polycystic ovary
syndrome
Risk factors
such as a
chronic
disorder,
Functional hypothalamic
anovulation
Body habitus
High body mass index

(eg, > 30 kg/m2)
Low body mass index

(eg, < 18.5 kg/m2)
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dieting, or an
eating disorder
Hypothermia,
bradycardia,
hypotension
anovulation due to
anorexia nervosa or
starvation
Reduced gag
reflex, palatal
lesions,
subconjunctival
hemorrhages
anovulation due to
bulimia with frequent
vomiting
Primary
amenorrhea,
webbed neck,
widely spaced
nipples
Turner syndrome
Warm, moist skin
Tachycardia,
tremor
Hyperthyroidism
Coarse, thick skin; loss

of eyebrow hair
Bradycardia,
delayed deep
tendon
reflexes,
weight gain,
constipation
Hypothyroidism
Acne
Virilization
Androgen excess due to
Short stature
Skin abnormalities

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An androgen-secreting tumor
Cushing syndrome
Adrenal virilism
Drugs (eg, androgens,
antidepressants, danazol ,
high-dose progestins)
Striae
Moon facies,
buffalo hump,
truncal obesity,
thin
extremities,
virilization,
hypertension
Cushing syndrome
Acanthosis nigricans
Obesity,
virilization
Polycystic ovary
syndrome
Vitiligo or
hyperpigmentation of
the palm
Orthostatic
hypotension
Addison's disease
General findings suggesting estrogenic or androgenic abnormalities
Symptoms of estrogen
deficiency (eg, hot
flushes, night sweats,
particularly with
vaginal dryness or
atrophy)
Risk factors
such as
oophorectomy,
chemotherapy,
or pelvic
irradiation
Premature ovarian
failure
Hirsutism with
virilization

Cushing syndrome
Adrenal virilism
Drugs (eg, androgens,
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antidepressants, danazol ,
high-dose progestins)
Primary
amenorrhea

Adrenal virilism
Gonadal dysgenesis
A genetic disorder
Enlarged
ovaries

17-Hydroxylase deficiency
An androgen-secreting ovarian
tumor
Breast and genital abnormalities
Galactorrhea
Absence or incomplete
development of
breasts (and of
secondary sexual
characteristics)
Hyperprolactinemia
Nocturnal
headache,
visual field
defects
Pituitary tumor
Normal
adrenarche
Primary anovulatory
amenorrhea due to
isolated ovarian failure
Absence of
adrenarche
Primary anovulatory
amenorrhea due to
hypothalamic-pituitary
dysfunction
Absence of
adrenarche
Kallmann syndrome
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with impaired
sense of smell
Delay of breast
development and
secondary sexual
characteristics
Family history of
delayed
menarche
Constitutional delay of
growth and puberty
Normal breast
development and
secondary sexual
characteristics with
primary amenorrhea
Cyclic
abdominal
pain, bulging
vagina, uterine
distention
Genital outflow
obstruction
Ambiguous genitals
Virilization
Fused labia, clitoral

enlargement at birth
Androgen exposure
during the 1st
trimester, possibly
indicating
Congenital adrenal virilism
Drug-induced virilization
Clitoral enlargement
after birth
Virilization
Androgen-secreting
tumor (usually ovarian)
Adrenal virilism
Use of anabolic steroids
Normal external
Apparent
Androgen insensitivity
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genitals with
incompletely
developed secondary
sexual characteristics
(sometimes with
breast development
but minimal pubic
hair)
Ovarian enlargement
(bilateral)
absence of
cervix and
uterus
syndrome
Symptoms of
estrogen
deficiency
Premature ovarian
failure due to
autoimmune oophoritis
Virilization
17-Hydroxylase
deficiency
Polycystic ovary
syndrome
Lesions
Pelvic mass (unilateral)
Pelvic pain
Pelvic tumors
Testing: History and physical examination help direct testing.

If girls have secondary sexual characteristics, a pregnancy test should be
done to exclude pregnancy and gestational trophoblastic disease as a
cause of amenorrhea. Women of reproductive age should have a
pregnancy test after missing one menses.
The approach to primary amenorrhea (see Fig. 1: Evaluation of primary
amenorrhea. ) differs from that to secondary amenorrhea (see Fig. 2:
Evaluation of secondary amenorrhea. ), although no specific general
approaches or algorithms are universally accepted.
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Fig. 1
Evaluation of primary amenorrhea.a
a Normal
values are
DHEAS: 250300 ng/dL (0.70.8 mol/L)

FSH: 520 IU/L
LH: 540 IU/L
Karyotype (female): 46,XX
Prolactin: 100 ng/mL
Testosterone: 2080 ng/dL (0.72.8 nmol/L)
b Some
clinicians measure LH levels when they measure FSH levels or when FSH levels are
equivocal.
cConstitutional
delay of growth and puberty is possible.
d Possible
diagnoses include functional hypothalamic chronic anovulation and genetic disorders

(eg, congenital gonadotropin-releasing hormone deficiency, Prader-Willi syndrome).
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e Possible
diagnoses include Cushing syndrome, exogenous androgens, congenital adrenal

virilism, and polycystic ovary syndrome.
fPossible
diagnoses include Turner syndrome and disorders characterized by Y chromosome
material.
g Pubic
hair may be sparse.
DHEAS = dehydroepiandrosterone sulfate; FSH = follicle-stimulating hormone; LH = luteinizing

hormone; TSH = thyroid-stimulating hormone.
Fig. 2
Evaluation of secondary amenorrhea.
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If symptoms or signs suggest a specific disorder, specific tests may be

indicated regardless of what an algorithm recommends. For example,
patients with abdominal striae, moon facies, a buffalo hump, truncal
obesity, and thin extremities should be tested for Cushing syndrome (see
Cushing Syndrome). Patients with headaches and visual field defects or
evidence of pituitary dysfunction require brain MRI.
If clinical evaluation suggests a chronic disease, liver and kidney function
tests are done, and ESR is determined.
Often, testing includes measurement of hormone levels; total serum
testosterone or dehydroepiandrosterone sulfate (DHEAS) levels are
measured only if signs of virilization are present. Certain hormone levels
should be remeasured to confirm the results. For example, if serum
prolactin is high, it should be remeasured; if serum FSH is high, it should
be remeasured monthly at least twice. Amenorrhea with high FSH levels
(hypergonadotropic hypogonadism) suggests ovarian dysfunction;
amenorrhea with low FSH levels (hypogonadotropic hypogonadism)
suggests hypothalamic or pituitary dysfunction.
If patients have secondary amenorrhea without virilization and have
normal prolactin and FSH levels and normal thyroid function, a trial of
estrogen and a progestin to try to stimulate withdrawal bleeding can be
done (progesterone challenge test). The trial begins by giving
medroxyprogesterone 5 to 10 mg po once/day or another progestin for 7
to 10 days.
If bleeding occurs, amenorrhea is probably not caused by an endometrial
lesion (eg, Asherman syndrome) or outflow tract obstruction, and the
cause is probably hypothalamic-pituitary dysfunction, ovarian failure, or
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estrogen excess.
If bleeding does not occur, an estrogen (eg, conjugated equine estrogen
1.25 mg, estradiol 2 mg) once/day is given for 21 days, followed by
medroxyprogesterone 10 mg po once/day or another progestin for 7 to
10 days. If bleeding does not occur after estrogen is given, patients may
have an endometrial lesion or outflow tract obstruction. However, bleeding
may not occur in patients who do not have these abnormalities (eg,
because the uterus is insensitive to estrogen); thus, the trial using estrogen
and progestin may be repeated for confirmation.
However, because this trial takes weeks and results can be inaccurate,
diagnosis of some serious disorders may be delayed significantly; thus,
brain MRI should be considered before or during the trial.
Mildly elevated levels of testosterone or DHEAS suggest polycystic ovary
syndrome, but levels can be elevated in women with hypothalamic or
pituitary dysfunction and are sometimes normal in hirsute women with
polycystic ovary syndrome. The cause of elevated levels can sometimes
be determined by measuring serum LH. In polycystic ovary syndrome,
circulating LH levels are often increased, increasing the ratio of LH to
FSH.
Treatment
Treatment is directed at the underlying disorder; with such treatment,
menses sometimes resume. For example, most abnormalities obstructing
the genital outflow tract are surgically repaired.
If a Y chromosome is present, bilateral oophorectomy is recommended
because risk of ovarian germ cell cancer is increased.
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Problems associated with amenorrhea may also require treatment,

including
Inducing ovulation if pregnancy is desired
Treating symptoms and long-term effects of estrogen deficiency (eg,
osteoporosis)
Treating symptoms and managing long-term effects of estrogen excess
(eg, prolonged bleeding, persistent or marked breast tenderness, risk of
endometrial hyperplasia and cancer)
Minimizing hirsutism and long-term effects of androgen excess (eg,
cardiovascular disorders, hypertension)
Key Points
Primary amenorrhea in patients without normal secondary sexual
characteristics is usually anovulatory (eg, due to a genetic disorder).
Always exclude pregnancy by testing rather than by history.
Primary amenorrhea is evaluated differently from secondary amenorrhea.
If patients have primary amenorrhea and normal secondary sexual
characteristics, do pelvic ultrasonography to check for congenital anatomic
genital tract obstruction.
If patients have signs of virilization, check for conditions that cause
androgen excess (eg, polycystic ovary syndrome, an androgen-secreting
tumor, Cushing syndrome, use of certain drugs).
If patients have symptoms and signs of estrogen deficiency (eg, hot
flushes, night sweats, vaginal dryness or atrophy), check for premature
ovarian failure.
If patients have galactorrhea, check for conditions that cause
hyperprolactinemia (eg, pituitary dysfunction, use of certain drugs). .
Last full review/revision August 2012 by JoAnn V. Pinkerton, MD
Content last modified October 2013
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> SEE ALL MERCK MANUALS

If patients have had no menstrual periods by age 13 and have no signs of

Amenorrhea: Menstrual Abnormalities: Merck Manual Professional

If pregnancy does not occur, estrogen and progesterone production

Amenorrhea: Menstrual Abnormalities: Merck Manual Professional

outflow obstruction, intrauterine adhesions [Asherman syndrome]) prevent

Contraceptives can cause the endometrium to thin, sometimes resulting in

Amenorrhea: Menstrual Abnormalities: Merck Manual Professional

) involve a disruption of the

Anovulatory amenorrhea is usually secondary but may be primary if

Some Causes of Anovulatory Amenorrhea

Genetic disorders (eg, congenital gonadotropinreleasing hormone deficiency, GnRH receptor

Amenorrhea: Menstrual Abnormalities: Merck Manual Professional

Tumors of the hypothalamus

Aneurysms of the pituitary

Amenorrhea: Menstrual Abnormalities: Merck Manual Professional

Autoimmune disorders (eg, autoimmune oophoritis

Androgen insensitivity syndrome (testicular

Amenorrhea: Menstrual Abnormalities: Merck Manual Professional

Drug-induced virilization (eg, by androgens,

Females with these disorders may have virilization or ambiguous genitals.

Virilization may occur in Cushing syndrome secondary to an adrenal tumor.

Ovulatory amenorrhea: The most common causes (see Table 2: Some

Obstructive abnormalities are

Amenorrhea: Menstrual Abnormalities: Merck Manual Professional

Cervical stenosis (rare)

Some acquired anatomic abnormalities, such as endometrial scarring

Amenorrhea: Menstrual Abnormalities: Merck Manual Professional

Menarche has not occurred by age 16 or by 2 yr after the onset of puberty

Women of reproductive age should have a pregnancy test after missing

History: History of present illness includes whether menses have ever

Amenorrhea: Menstrual Abnormalities: Merck Manual Professional

anovulation, such as stress; chronic illness; new drugs; a recent change in

Amenorrhea: Menstrual Abnormalities: Merck Manual Professional

outflow obstruction. Pelvic examination findings also help determine

Interpretation of findings: Pregnancy should not be excluded based on

Amenorrhea: Menstrual Abnormalities: Merck Manual Professional

usually ovulatory and typically due to a

Findings Suggesting Possible Causes of Amenorrhea

Use of certain drugs

Drugs that affect

Amenorrhea: Menstrual Abnormalities: Merck Manual Professional

Antipsychotics, 2nd generation

Hormones and certain

High body mass index

Low body mass index

Amenorrhea: Menstrual Abnormalities: Merck Manual Professional

Warm, moist skin

Coarse, thick skin; loss

Androgen excess due to

Polycystic ovary syndrome

Amenorrhea: Menstrual Abnormalities: Merck Manual Professional

General findings suggesting estrogenic or androgenic abnormalities

Androgen excess due to

Amenorrhea: Menstrual Abnormalities: Merck Manual Professional

Androgen excess due to

Androgen excess due to

Breast and genital abnormalities

Amenorrhea: Menstrual Abnormalities: Merck Manual Professional

Fused labia, clitoral

Amenorrhea: Menstrual Abnormalities: Merck Manual Professional