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11/11/2014 Amenorrhea: Menstrual Abnormalities: Merck Manual Professional

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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 ofpuberty (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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PathophysiologyNormally, 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 thedominant 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 occurswhen 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.

EtiologyAmenorrhea 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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Some Causes of Anovulatory Amenorrhea ) involve a disruption of the

hypothalamic-pituitary-ovarian axis. Thus, causes include

Hypothalamic dysfunction (particularly functional hypothalamic

anovulation)

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 Ychromosome increase the risk of ovarian germ cell cancer.

Some Causes of Anovulatory Amenorrhea

Cause Examples

Hypothalamic

dysfunction,

structural

Genetic disorders (eg, congenital gonadotropin-

releasing hormone deficiency, GnRH receptor

gene mutations that result in low FSH and

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

Table 1

estradiol
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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 adult-

onset adrenal virilism

Cushing syndrome,


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Some Causes of OvulatoryAmenorrhea

Drug-induced virilization (eg, by androgens,

antidepressants, , or high-dose

progestins)

Hyperthyroidism

Hypothyroidism

Obesity (which causes excess extraglandularproduction of estrogen)


True hermaphroditism

Tumors producing androgens (usually ovarian or

adrenal)

Tumors producing estrogens or tumors producing

human chorionic gonadotropin (gestationaltrophoblastic disease)

*Hyperprolactinemia due to other conditions (eg, hypothyroidism, use of certain drugs) may also causeamenorrhea.

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

usually accompanied by normal

hormonal function. Such

danazol

Table 2
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Cause Examples

Congenital

genital

abnormalities

Cervical stenosis (rare)

Imperforate hymen

Pseudohermaphroditism

Transverse vaginal

septum

Vaginal or uterine

aplasia (eg, Mllerian

agenesis)

Acquired

uterine

abnormalities

Asherman syndrome

Endometrial TB

Obstructive fibroids andpolyps

obstruction may result in

hematocolpos (accumulation of

menstrual blood in the vagina),

which can cause the vagina to

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

develop normally. Some

congenital disorders (eg, thoseaccompanied by vaginal aplasia

or a vaginal septum) also cause

urinary tract and skeletal

abnormalities.

Some acquired anatomic abnormalities, such as endometrial scarring

after instrumentation for postpartum hemorrhage or infection (Asherman

syndrome), cause secondary ovulatory amenorrhea.

EvaluationGirls 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 3typical cycles.

They have < 9 menses a year.

They have a sudden change in menstrual pattern.

History: History of present illnessincludes 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. Historyshould 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 systemsshould 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 historyshould 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, ,

, ), and sex hormones that can cause

virilization (eg, androgens, estrogens, high-dose progestins) and

questions about recent use of contraceptives.

Family historyshould 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 byapplying 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

busulfan

chlorambucil cyclophosphamide


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Pearls & Pitfalls

If amenorrhea occurs in girls with secondary sexualcharacteristics or in women of reproductive age, do apregnancy test regardless of sexual and menstrual history.

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. Skindiscoloration (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

characteristics usually reflects normal

hormonal function; amenorrhea is


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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.

Findings Suggesting Possible Causes of Amenorrhea

Finding Other Possible

Findings

Possible Cause

Use of certain drugs

Drugs that affect

dopamine (which

helps regulate

prolactin secretion):

Antihypertensi ves (eg,, ,

)

Galactorrhea Hyperprolactinemia

Table 3

methyldopa rese rp ine

verapamil
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Antipsychotics, 2nd generation(eg, ,

, )

Antipsychotics, con ventional(eg, ,

phenothiazines, )

Cocaine

GI drugs (eg, ,

)Hallucinogens

Opioids (eg, ,

)

Tricyclic antidepressants (eg,,

)

Hormones and certain

other drugs that affect

the balance of

estrogenic and

androgenic effects

(eg, androgens,

antidepressants,

, high-dose

progestins)

Virilization Drug-induced virilization

Body habitus

High body mass index

(eg, > 30 kg/m2)

Estrogen excess

Virilization Polycystic ovary

syndrome

Low body mass index

(eg, < 18.5 kg/m2)

Risk factors

such as a

chronic

disorder,

Functional hypothalamic

anovulation

molindone

olanzapine r isperidone

haloperidol

pimozide

Estrogens

cimetidine

metoclopramide

codeine

morphine

clomipramine

desipramine

danazol


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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

Short stature Primary

amenorrhea,

webbed neck,

widely spaced

nipples

Turner syndrome

Skin abnormalities

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 toPolycystic ovary syndrome


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An and rogen -secreti ng tumor

Cushing syndrome

Adrenal viril ism

Drugs (eg, androgens,antidepressants, ,

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

Androgen excess due to



Cushing syndrome

Adrenal viril ism

Drugs (eg, androgens,

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antidepressants, ,

high-dose progestins)

Primary

amenorrhea


True hermaphroditism



Adrenal viril ism

Gonadal dysgenesis

A gene tic diso rder

Enlarged

ovaries


17-Hydroxylase deficiency


An and rogen -secreti ng ova riantumor

Breast and genital abnormalities

Galactorrhea Hyperprolactinemia

Nocturnal

headache,

visual field

defects

Pituitary tumor

Absence or incomplete

development ofbreasts (and of

secondary sexual

characteristics)

Normal

adrenarche

Primary anovulatory

amenorrhea due toisolated ovarian failure

Absence of

adrenarche

Primary anovulatory

amenorrhea due to

hypothalamic-pituitary

dysfunction

Absence of

adrenarche

Kallmann syndrome

danazol


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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 True hermaphroditism


Virilization

Fused labia, clitoral

enlargement at birth

Androgen exposure

during the 1st

trimester, possibly

indicating

Congenital adrenal virilismTrue hermaphroditism

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 pubichair)

absence of

cervix and

uterus

syndrome

Ovarian enlargement

(bilateral)

Symptoms of

estrogen

deficiency

Premature ovarian

failure due to

autoimmune oophoritis

Virilization 17-Hydroxylase

deficiency

Polycystic ovarysyndrome

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 bedone 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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Evaluation of primary amenorrhea.a

aNormal values areDHEAS: 250300 ng/dL (0.70.8 mol/L)

FSH: 520 IU/L

LH: 540 IU/L

Karyotype (female): 46,XXProlactin: 100 ng/mL

Testosterone: 2080 ng/dL (0.72.8 nmol/L)

bSome clinicians measure LH levels when they measure FSH levels or when FSH levels areequivocal.

cConstitutional delay of growth and puberty is possible.

dPossible diagnoses include functional hypothalamic chronic anovulation and genetic disorders

(eg, congenital gonadotropin-releasing hormone deficiency, Prader-Willi syndrome).

Fig. 1


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ePossible diagnoses include Cushing syndrome, exogenous androgens, congenital adrenalvirilism, and polycystic ovary syndrome.

fPossible diagnoses include Turner syndrome and disorders characterized by Y chromosomematerial.

gPubic hair may be sparse.

DHEAS = dehydroepiandrosterone sulfate; FSH = follicle-stimulating hormone; LH = luteinizing

hormone; TSH = thyroid-stimulating hormone.

Evaluation of secondary amenorrhea.

Fig. 2


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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 serumprolactin 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 ofestrogen and a progestin to try to stimulate withdrawal bleeding can be

done (progesterone challenge test). The trial begins by giving

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

medroxyprogesterone
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estrogen excess.

If bleeding does not occur, an estrogen (eg, conjugated equine estrogen

1.25 mg, 2 mg) once/day is given for 21 days, followed by

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.

TreatmentTreatment 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.

estradiol

medroxyprogesterone

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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 sexualcharacteristics 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-secretingtumor, 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, MDContent last modified October 2013

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