AMENORRHEA

AMENORRHEA
Absence of menses

Physiologic
Pregnancy
Lactation
Postpartum

Pathologic
Endocrine
Anatomic anomalies
 AMENORRHEA
TYPES OF AMENORRHEA

Primary amenorrhea
 No menses by 14 years of age and absence of secondary
sexual or secondary sex.
 No menses by age 16 years of age with presence of
secondary sex characteristics.
 Absence of menses in a woman who has never
menstruated by the age of 16.5 years.
 AMENORRHEA
Secondary Amenorrhea

 The absence of menses in a previously menstruating

woman.
 No menses for 3 months if previous menses were
regular.
 No menses for 6 months if previous menses were
irregular.
World Health Organization Amenorrhea Group
WHO Group I(Hypogonadotropic hypoestrogenic) has no
endogenous estrogen production, normal or low FSH levels,
normal PRL levels and no lesion in the hypothalamus or
pituitary.

WHO Group II (Normogonadotropic normoestrogenic) has

endogenous estrogen production, normal levels FSH and PRL.

WHO Group III (Hypergonadotropic hypoestrogenic) has

elevated FSH and low to absent estrogen, indicative of
premature ovarian failure (POF).
 AMENORRHEA
PRIMARY AMENORRHEA- Differential Diagnosis
Breast development present Breast development absent
Uterus present Consider secondary differential Gonadal dysgenensis
Hypothalamic cause 45XX
Pituitary cause 46X,abnormal X
Ovarian cause Mosaic X
Uterine cause 46XX or 46XY, pure gonadal
dysgenesis
17 hydroxylase deficiency with
46XX
Galactosemia

Hypothalamic or Pituitary
failure
Kallmann Syndrome
CNS congenital defect
HP tumors
CNS infection
Physiologic delay
 AMENORRHEA
PRIMARY AMENORRHEA- Differential Diagnosis

Breast development present Breast development absent

Uterus absent Mullerian agenesis 17, 20 desmolase deficiency (46

Androgen insensitivity XX)
syndrome Agonadism
17-hydoxylase deficiency (46
XY)
 AMENORRHEA
ABSENT BREAST, PRESENT UTERUS
HYPOgonatropic HYPOgonadism

GnRH

FSH,
LH
 AMENORRHEA
HYPERgonatropic HYPOgonadism

GnRH

FSH
LH
 AMENORRHEA
KALLMANN SYNDROME HYPOGONADOTROPIC
HYPOGONADISM-
Hypothalamic -Isolated gonadrotopin deficiency
failure associated with anosmia. suggests as hypothalamic
or pituitary problem

-Primary pituitary deficiency

-Secondary pituitary deficiency
Pituitary •kernicterus
failure •hypotharoidism
•Encepphalitis

HYPERGONADOTROPIC
HYPOGONADISM-
Gonadal failure TURNER SYNDROME
suggests ovarian failure to
produce estrogen
 AMENORRHEA
HYPO-GONADOTROPIC HYPER-
GONADOTROPIC

CAUSES •Hypothalamic failure Ovarian failure

•Anterior Pituitary failure

HYPOTHALAMUS Low GnRH High GnRH

ANTERIOR PITUITARY Low FSH High FSH

OVARIES Low estrogen No estrogen

SPECIFIC ETIOLOGY •Kallmann’s syndrome •Premature ovarian failure

•CNS tumor •Turner syndrome
 AMENORRHEA
KALLMAN’S SYNDROME
 Insufficient GnRH or pulsatile secretion of GNRH
 Deficiencies in GNRH may also be caused by developmental or
genetic defects, inflammatory processes, tumors, vascular lesion or
trauma.
 Accompanied by anosmia.

TURNER SYNDROME
 Short stature, webbed neck, short 4th metacarpal
 Diagnosis confirmed with high FSH, karyotyping
 Tx : estrogen therapy to induce secondary sex characteristic with
cycle progesterone to prevent endometrial hyperplasia.
 AMENORRHEA
PRIMARY AMENORRHEA
OVARIAN FAILURE SAVAGE SYNDROME Failure of the ovaries to respond to FSH
and LH secondary to receptor defect.
TURNER SYNDROME Due to ovarian atresia resulting in
depletion of oocytes
PREMATURE OVARIAN •Cessation of ovarian function in patients
FAILURE less than 40 years old
•Due to decreased follicular endowment or
accelerated follicular atresia
•Usually associated with mosaicism.

KALLMAN SYNDROME Congenital absence of GnRH

associated with anosmia
HYPOTHALAMIC- TUMOR, TRAUMA, May result in disruption of GnRH
PITUITARY SARCOIDOSIS, transport.
DYSFUCNTION ENCEPHALITIS AND
IRRADIATION
 AMENORRHEA
ll. PRESENT BREAST, ABSENT UTERUS
 Genetically female MULLERIAN AGENESIS
 Genetically male ANDROGEN INSENSITIVITY
 AMENORRHEA

MULLERIAN AGENESIS
2nd most frequent cause of primary amenorrhea
Phenotypically and endocrinologically functioning
females
Short blind vaginal pouch with absent uterus
With normal female testosterone ; karyotype 46XX
Surgically created neovagina; cannot carry a pregnancy.
 AMENORRHEA
ANDROGEN INSENSITIVITY
 Testicular femiization
 46XY normally functioning male gonads
 Normal male levels of testerone
 Lack of receptors in the target organs
 Lack of male differentiation in the internal and external
genitalia
 Absent or scanty pubic hair, short vaginal pouch; testes
palpable at inguinal canal.
 Tx: at 18 years old, gonads should be removed to prevent
malignant transformation; neovagina creation.
 AMENORRHEA
BREAST ABSENT AND MULLERIAN AGENESIS ANDROGEN
UTERUS PRESENT INSENSIVITY

KARYOTYPE 46 XX 46XY

CAUSE OF ABSENCE OF Failure of Mullerian duct Mullerian inhibiting factor

UTERUS formation

SOURCE OF ESTROGEN Ovaries Testes

PRESENCE OF PUBIC Yes None

HAIR

TESTOSTERONE LEVEL Female level Male level

TREATMENT Creation of neovagina Removal of gonads

Creation of new vagina
 AMENORRHEA
OUTFLOW TRACT ABNORMALITIES
CAUSE PATHOLOGY CLINICAL FINDINGS TREATMENT

Hymen fails to canalize Bulging membranes on surgical correction

during fetal development
and a solid membrane
Imperforate remains across the vaginal
hymen septum
PE with purple red
discoloration.
Hematocolpos, pelvic
and abdominal pain
Hemtometra. Distend
during valsalva
maneuver
 AMENORRHEA
OUTFLOW TRACT AND UTERINE ABNORMALITIES
CAUSE PATHOLOGY CLINICAL FINDINGS TREATMENT
Failure of the mullerian duct to Hematocolpos, pelvic pain surgical correction
fuse with the urogenetal sinus and abdominal pain.
Normal vaginal orifice but
Transverse
vaginal no visible cervix. In some
cases, an MRI may be
septum required to distinguish an
imperforate hymen from a
transverse septum.
 AMENORRHEA
OUTFLOW TRACT AND UTERINE ABNORMALITIES
CAUSE PATHOLOGY CLINICAL FINDINGS MANAGEMENT
•Common form of •Present in their late teens with •MRI of the pelvis
primary amenorrhe. normally developing breasts, pubic and urinary tract
• 1 in 4000-10,000 hair and external genitalia as the •Vaginal dilator
Mullerian presence and function of the therapy.
agenesis and
ovaries are normal. •Surgical
hypoplasia • can present with no vagina, a construction of a
(Mayer- portion of a vagina, complete neovagina.
uterine agenesis or a portion of the
Rokitansky- uterus.
KusterHauser
syndrome) •Amenorrhea is generally the only
complaint.
•Skeletal abnormalities are also
common.
 AMENORRHEA
OUTFLOW TRACT AND UTERINE ABNORMALITIES

CAUSE PATHOLOGY CLINICAL FINDINGS MANAGEMENT

•Incidence is 32% •Testes are present and secrete •Testosterone level

•Gonadal malignancy normal male levels of testosterone. •Karyotype
22% • presents in later teens with •Gonad removal until
•X-linked recessive normal breast development and pubertal maturation
Complete disorder, occurs in primary ameorrhea.. •Vaginal dilator
Androgen 46XY individuals and •PE: normal external genitalia. A therapy
Insensitivity relts in phenotypic shortened or absent vagina, no
Syndrome women. cervix or uterus.
(CAIS) •AMH results in •Pubic and axillary hair is sparse.
(Testicular regression of mullerian
Feminization) structures.
Musculinization fails to
occur because of an
androgen receptor
defect.
 AMENORRHEA
OVARIAN ABNORMALITIES
(Hypergonadotropic Hypogonadism)

•Primary dysfunction at the level of the ovary.

•The ovaries no longer respond to gonadotropin stimulation limiting follicular
development and production of E2.
 AMENORRHEA
OVARIAN ABNORMALITIES
(Hypergonadotropic Hypogonadism)
CAUSE DESCRIPTION/ CLINICAL FINDINGS
PATHOLOGY
Gonadal Dysgenesis
•Aneuploidy involving X •Internal and external genitalia develop
chromosome normally
•60%-45X, 40%-45X/46XX •The cohort of primordial follicles undergoes
mosaics, 46XXqi accelerated atresia so that oocytes are
isochromosome and 46XXp depleted prior to the onset of puberty.
Turner Syndrome short arm deletion. •Cardinal features: webbed neck, shield-
shaped chest, short stature and sexual
infatilism.
•Some TS wih mosaic karyotypes can undergo
spontaneous puberty and conception (16%
and 3.6%)
 AMENORRHEA
OVARIAN ABNORMALITIES
(Hypergonadotropic Hypogonadism)
CAUSE DESCRIPTION/ MANAGEMENT
PATHOLOGY
Gonadal Dysgenesis
•Partial deletions and rearrangements •Determining whether a Y
of 1 X chromosome, can cause wide chromosome is present in a
range of gonadal dysfunctions ranging mosaic is important because the
from gonadal dysgenesis to POF. presence of the SRY portion of the
Mosaicism Y chromosome predisposes to
tumor formation.
•Presence of Y chromosome
requires gonadectomy or removal
of the gonadal streaks.
 AMENORRHEA
OVARIAN ABNORMALITIES
(Hypergonadotropic Hypogonadism)
CAUSE DESCRIPTION/ CLINICAL FINDINGS MANAGEMENT
PATHOLOGY
Gonadal
Dysgenesis
•46XX or XY individuals •Phenotypic women of normal •Require removal of
who experience height who fail to undergo puberty their gonadal streaks
dysgenesis of genital to preventmalignant
tissue early in transformation.
embryonic
Pure Gonadal development.
Dysgenesis •Results from geetic,
environmental or
infectious insults
•SWYER SYNDROME-
patients with 46XY
gonadal dysgenesis
 AMENORRHEA
OVARIAN ABNORMALITIES
(Hypergonadotropic Hypogonadism)

CAUSE DESCRIPTION/ CLINICAL FINDINGS

PATHOLOGY

•Autosomal recessive •Phenotypic women but also lack uterus

•Rare disorder that can affect because AMH was secreted early in fetal life.
46XY or XX individuals • hypertension , hypokalemia,
•The lack of 17ꭤ-hydroxylse and hypergonadotropic hypogonadism
17,20-lyase activities results in
both gonadal and adrenal
CYP17 Deficiency insufficiencies.
 AMENORRHEA
OVARIAN ABNORMALITIES
(Hypergonadotropic Hypogonadism)

CAUSE DESCRIPTION/ CLINICAL FINDINGS

PATHOLOGY

•Very rare condition. •Present with varying levels of secondary

•Identified to be preventing sexual development
the ovaries from responding to •Primary amenorrhea
gonadotropin stimulation and
resulting in POF.
LH and FSH
receptor mutations
 AMENORRHEA
OVARIAN ABNORMALITIES
(Hypergonadotropic Hypogonadism)
CAUSE DESCRIPTION/
PATHOLOGY
• can manifest as primary or secondary amenorrhea.
•For patients who previously menstruated, amenorrhea
associated with a depletion of oocytes and cessation of
Premature Ovarian Failure menses before age 40years.
•In those with primary amenorrhea, 50% will have an
abnormal karyotype.
•Up to 90% remain unexpalined following evaluation.
 AMENORRHEA
OVARIAN ABNORMALITIES
(Hypergonadotropic Hypogonadism)

DESCRIPTION/
CAUSE CLINICAL FINDINGS
PATHOLOGY
Premature Ovarian
Failure

•Short or long arm deletions or •Not very severe enough to cause primary
mosaicism gonadal dysgenesis.
X chromosome
abnormalities
 AMENORRHEA
OVARIAN ABNORMALITIES
(Hypergonadotropic Hypogonadism)
CAUSE DESCRIPTION/ MANAGEMENT
PATHOLOGY
Premature Ovarian
Failure

•Induced by chemothearpy, •Karyotype

radiation or surgery •Adrenal and thyroid antibody testing
•Majority of cases are •Inclusion of any Y chromosomal material is
idiopathic an indication for gonadectomy.
Spontaneous POF •6% have premutations in the
gene responsible for fragile X
syndrome
•4% steroidogenic cell
autoimmunity.
 AMENORRHEA
OVARIAN ABNORMALITIES
(Hypergonadotropic Hypogonadism)

DESCRIPTION/
CAUSE MANAGEMENT
PATHOLOGY
Premature Ovarian
Failure

•Follicular depletion by •Oophoropexy

radiation, chemotherapy •GnRH agonist or antagonist
(alkalyting agents) or surgical •Ovarian tissue cryopserevation
Iatrogenic POF manipulation or removal of
ovarian tissue
 AMENORRHEA
OVARIAN ABNORMALITIES
(Hypergonadotropic Hypogonadism)
CAUSE MANAGEMENT
•Estrogen replacement
•If the uterus is intact, adjunct cyclic treatment with progestins is
required to prevent endometrial hyperplasia

Premature Ovarian Failure •PREGNANCY

•Spontaneous pregnancy is possible, although unlikely (5%)
•Infertility treatment classically requires oocyte donation, however in
some cases, high doses of gonadotropinscan achieve follicular
development.
•Can be associated with psychological distress and appropriate
counselling and emotional support should be initiated.
 AMENORRHEA
HYPOTHALAMIC DYSFUNCTION
(Hypogonadotropic Hypogonadism)
•Underlying etiology is a decrease in GnRH release and stimulation of the
pituitary to release gonadotropins resulting in failure of folliculogenesis and
production of E2

•The term hypothalamic amenorrhea applies to condition in which GnRH

secretion is diminished in the absence of any organic pathology.

•Physical or psychological stress, anorexia nervosa, exercise and weight loss can
contribute to dysfunctional hypothalamic GnRH secretion.
 AMENORRHEA
HYPOTHALAMIC DYSFUCNTION
(Hypogonadotropic Hypogonadism)

DESCRIPTION/
CAUSE CLINICAL FINDINGS
PATHOLOGY
•Inherited X-linked disorder •Primary amenorrhea
resulting from genetic •Absent breast developmet
mutation that causes failure of •Presence of cervix and uterus
olfactory and GnRH neuronal •anosmia
Kallmann syndrome migration from the olfactory
placode.
•Absence of GnRH pulses to
stimulate gonadotropin release
from the pituitary
 AMENORRHEA
HYPOTHALAMIC DYSFUCNTION
(Hypogonadotropic Hypogonadism)

DESCRIPTION/
CAUSE CLINICAL FINDINGS
PATHOLOGY
• not associated with anosmia
•Absence of functional
Congenital GnRH hypothalamic neurons.
deficiency

•Inhibit signaling of GnRH to •Broad range of phenotypes, depending on the

release gonadotropins from the particular mutation.
GnRH receptor anterior pituitary
mutations

•Hypothalamic neoplasm,
trauma, hemorrhage, cranial
Other CNS irradiation.
pahtologies •Craniopharyngioma- most
common causing delayed
puberty.
 AMENORRHEA
HYPOTHALAMIC DYSFUCNTION
(Hypogonadotropic Hypogonadism)

Management •Correcting the underlying causative behavior if identified

•The primary treatment is estrogen/progestin replacement as with POF.
 AMENORRHEA
PITUITARY DISORDERS

DESCRIPTION/
CAUSE CLINICAL FINDINGS
PATHOLOGY

•Prolactinoma-most common •Amenorrhea

•Adenomas •Low or normal levels of gonadotropins
•Empty sella syndrome
Pituitary Lesions
 AMENORRHEA
PITUITARY DISORDERS

DESCRIPTION/
CAUSE
PATHOLOGY
• 14% of secondary amenorrhea and small portion of primary
amenorrhea
•Pregnancy and breastfeeding
Hyperprolactinemia •Prolactinomas
•Sheehan syndrome
•Isolated gonadotropin (FSH/LH) deficiency- rare condition
associated with thalassemia major, retinitis pigmentosa or
prepubertal hypothyroidism.
 AMENORRHEA
NORMOGONADOTROPIC AMENORRHEA

•Heterogenous group with normal levels of gonadotropins and Estradiol

•Normal secondary sexual development.
•The underlying etiology of amenorrhea is chronic anovulation.
 AMENORRHEA
NORMOGONADOTROPIC AMENORRHEA

CAUSE DESCRIPTION/ CLINICAL FINDINGS MANAGEMENT

PATHOLOGY

•Most common cause of •Nornal levels of gonadotropins •Weight reduction

amenorrhea associated and estradiol •COC, cyclic
with •Chronic an/oligoovulation, progesterone
hyperandrogenism. androgen excess and/or •Treatment of other
•Increased risk for DM polycysticovaries on ultrasound. underlying medical
type 2, insulin comorbidities.
resistance,hypertension
, lipid abnormalities,
obesity,metabolic
PCOS syndrome and
endometrial
cancer/hyperplasia
 AMENORRHEA
NORMOGONADOTROPIC AMENORRHEA

DESCRIPTION/
CAUSE PATHOLOGY MANAGEMENT

•Presents similarly to PCOS with •17-hydroxyprogesterone

amenorrhea and •ACTH stimulation test
hyperandrogenism •Glucocorticoid replacement
•Most have autosomal recessive •COC
disorder resulting in 21-
hydroxylase deficiency

Late-onset congenital
adrenal hyperplasia
 AMENORRHEA
NORMOGONADOTROPIC AMENORRHEA

DESCRIPTION/
CAUSE PATHOLOGY MANAGEMENT

•Prolonged, inappropriate •diagnostics: late night

hypercortisolism salivary cortisol, 24 hr urinary
•Etiology: pituitary tumor, adrenal free cortisol and
hypersecretion of cortisol, dexamethsone suppression
iatrogenic. testing.
•Loss of normal hypothalamic-
pituitary-adrenal feedback
mechanisms and loss of the
Cushing Syndrome normal circadian rhythm of
cortisol secretion
 AMENORRHEA
NORMOGONADOTROPIC AMENORRHEA

DESCRIPTION/
CAUSE PATHOLOGY
•Normal gonadotropin levels and normal to mildly
depressed E2

Hyperprolactinemia
 AMENORRHEA
NORMOGONADOTROPIC AMENORRHEA

DESCRIPTION/
CAUSE PATHOLOGY MANAGEMENT

•1-2% of primary and •TSH and PRL routinely evaluated

secondary amenorrhea •↑TSH and ↓T4=hypothyroidism
•Can lead to •↑TSH and NT4=sublinical
hyperprolactinemia hypothyroisim
•TRHTSH and PRL •Levothyroxine 25-50ug/day TSH
assessment q4-6wks until TSH
normalize.
Thyroid disease
 AMENORRHEA
MENOPAUSE

DESCRIPTION/
PATHOLOGY MANAGEMENT

• genetically programmed loss of ovarian • elevated FSH and low E2

follicles
•12 months of amenorrhea after the final
menstrual period.
•Reflects complete or near complete,
ovarian follicular depletion and the
absence of ovarian E2 secretion.
•Mean age -51yo (43-57)(American)
 AMENORRHEA

PRESENT BREAST , PRESENT UTERUS

Second largest category of individuals with primary
amenorrhea, accounting for about one third of them.

25% has hyperprolactinemis and prolactenomas

The remaining women had profile similar to those with

secondary amenorrhea and thus should be
subcategorized and treated similarly to women with
secondary amenorrhea.
 AMENORRHEA
SECONDARY AMENORRHEA: Differential
Diagnosis

Physiologic:
Pregnancy
Menopause
Postpartum lactation
 AMENORRHEA
SECONDARY AMENORRHEA: Differential Diagnosis

Etiology Causal Factor

Reproductive tract
Cervical stenosis Surgical procedure (ie: LEEP, CKC)
Asherman Syndrome Endometrial scarring

Ovarian
Premature ovarian failure
PCOS
Pituitary
Hyperprolactinemia
Pituitary adenomas
Sheehan Syndrome
Idiopathic, chromosomal abnormality,
autoimmune disease, infection
Inappropriate gonadotropin secretion, insulin
resistance
Lactotroph hyperplasia +/- prolactinoma, drugs
Thyrotroph , corticotroph or other hyperplasia
Postpartum hemorrhage
 AMENORRHEA
SECONDARY AMENORRHEA: Differential Diagnosis

Etiology Causal Factor

Reproductive tract
Cervical stenosis Surgical procedure (ie: LEEP, CKC)
Asherman Syndrome Endometrial scarring

Ovarian
Premature ovarian failure
PCOS
Pituitary
Hyperprolactinemia
Pituitary adenomas
Sheehan Syndrome
Idiopathic, chromosomal abnormality,
autoimmune disease, infection
Inappropriate gonadotropin secretion, insulin
resistance
Lactotroph hyperplasia +/- prolactinoma, drugs
Thyrotroph , corticotroph or other hyperplasia
Postpartum hemorrhage
 AMENORRHEA
SECONDARY AMENORRHEA: Differential Diagnosis

Etiology Causal Factor

CNS
Hypothalamic amenorrhea Stress, eating disorders, weight loss, excessive
exercise
Brain injury Interruption of HPOA
Inflammatory or infiltrative process Interruption of HPOA
Other endocrinopathies
Hypothyroidism
Cushing syndrome
Late onset adrenal hyperplasia
 AMENORRHEA
SECONDARY AMENORRHEA: Differential Diagnosis

Etiology Causal Factor

CNS
Hypothalamic amenorrhea Stress, eating disorders, weight loss, excessive
exercise
Brain injury Interruption of HPOA
Inflammatory or infiltrative process Interruption of HPOA
Other endocrinopathies
Hypothyroidism
Cushing syndrome
Late onset adrenal hyperplasia
 AMENORRHEA

CNS-Hypothalamic Causes

POLYCYSTIC OVARIAN SYNDROME

(STEIN-LEVENTHAL SYNDROME)
 AMENORRHEA
TRIAD: Minor criteria
 Hirsutism 1. Insulin resistance
 Amenorrhea 2. Perimenarchal onset of
 Obesity hersutism and obesity
3. Elevated LH-FSM ratio
4. Intermittent anovulation
Major criteria associated with
1. Chronic anovulation hyperandrogenemia (free
2. Hyperandrogenemia testerons, DHEAS)
(clinical/ lab) 5. Ultrasonographic evidence of
3. Other etiology excluded PGOS
 AMENORRHEA
Pituitary causes
May be associated with decreased secretion of other
pituitary hormones, particularly ACTH and TSH, in
addition to LH and FSH.
May have secondary hypothyroidism or adrenal
insuficiency.

SHEEHAN’S SYNDROME
Pituitary cell destruction as a result of a hypotensive
episode during pregnancy.
 AMENORRHEA
SIMMOND’S DEISEASE
Pituitary cell destruction unrelated to pregnancy

Hyperprolactinemia- cause anovulation by inhibiting

GnRH; may be due to the following:
Medications: dopamine antagonists- leading to reduced
dopamine levels (e.g. metoclopromide, domperidone);
antipsychotic medications
Tumor- prolactinoma (pituitary hypersecretion)
Idiopatic
 AMENORRHEA
Ovarian causes
1. PREMATURE OVARIAN FAILURE
 Cessation of ovarian function before the age of 40
 Irradiation , chemotheraphy or autoimmunity
 If less then 25 years old, do karyotyping (mosaicism)

2. MENOPAUSE
3. Uterine causes
4. Intrauterine adhesions
5. Asherman’s syndrome
 AMENORRHEA
ASHERMAN’S SYNDROME
The most frequent antecedent factor is endometrial
curettage associated with pregnancy
Confirmation of the diagnosis is usually made by
hysterography or hysteroscopy

Clinical approach to secondary amenorrhea

 History and physical Examination
 Rule out pregnancy (hCG)

 Rule out correctable causes of an ovulation – measure E2, FSH,

PRL,TSH levels
 AMENORRHEA
Progesterone challenge test
Estrogen progesterone challenge test
HSG or Hysteroscopy to rule out flow tract obstruction
Secondary amenorrhea

Pregnancy test

Progesterone challenge test

Estrogen progesterone challenge test

HSG
EVALUATION OF AMENORRHEA
When to evaluate for amenorrhea?
 Rule out pregnancy
 Use clinical judgment
 Do not overlook gross evidence of a disease process:
Turner syndrome, frank virilization, obstructed vagina
or other evidences of a disease process.
 Use a systematic approach, evaluating each critical
component of menstruation: hypothalamus, pituitary,
ovaries, uterus and genital outflow tract.
EVALUATION OF AMENORRHEA
Present illness*
Past medical history*
Development
Social
Family history
EVALUATION OF AMENORRHEA
Important PE for amenorrhea
 Height, weight,BMI,waist-to-hip ratio if obese, BP and PR
 General body habitus
 Vision changes or peripheral loss of vision
 Mouth and teeth for tooth enamel erosion
 Skin evaluated for hyperpigmentation, acanthosis nigricans,
abdominal striae, acne, hirsutism and balding
 Thyroid gland palpated for size, shape and nodules
 Breast development, galactorrhea or other breast discharge
 Abdominal exam for masses, fat distribution and virilization
(clitoromegaly), imperforate hymen or labial fusion
 Internal genitalia examined for transverse vaginal septum, lateral
vaginal obstruction, estrogenized vaginal mucosa and the presence of a
cervix with visible patent external cervical os.
 Rectal exam to evaluate the extent of hematocolposand presence of
uterus beyond a vaginal obstruction or absent vaginal orifice.
EVALUATION OF AMENORRHEA
Laboratory
hCG to evaluate pregnancy
FSH, E2, TSH, PRL
17-hydroxyprogesterone, testosterone and
dehydroepiandrosterone sulfate (DHEAS) for patients
with virilization, hirsutism or androgen excess
Testosterone if concern for complete androgen
insensitivity.
karyotype
EVALUATION OF AMENORRHEA
Imaging
Pelvic ultrasound
Hysterosalpingogram (HSG) or sonohysterography
EVALUATION OF AMENORRHEA
Follow-up laboratory and Imaging studies for initial
evaluation
Fragile X (FMR1) premutation for patients with POF
Antiadrenal and antithyroid antibodies
Karyotype
Cortisol level
Insulin-like growth factor (IGF-1)
ACTH
MRI of pituitary
MRI of pelvis
Renal UTZ and radiograph
Endometrial biopsy
 AMENORRHEA
PROGESTERONE CHALLENGE TEST
 Indirectmeans of determining sufficient estrogen to produce
endometrial growth that will slough after the progesterone levels fall

 Interpretation:
o Withdrawal bleeding with in 7 days
 Almost always due to anovulation

 Correctable causes of anovulation such as prolactinoma and

hypothyroidism------measure prolactin and TSH
 Endometrial CA with unopposed estrogen

o No withdrawal bleeding
 Inadequate estrogen (endometrium is not estrogen primed)

----perform estrogen –progesterone challenge test

 Outflow tract obstruction
 AMENORRHEA
ESTROGEN–PROGESTERONE CHALLENGE TEST:
 Done if no withdrawal bleeding after progesterone challenge test.
 Interpretation :
o Positive EPCT (+ bleeding)
 No estrogen

-determine FSH level

 If low FSH: HP failure

 If high FSH: ovarian failure

o Negative EPCT (no bleeding)

 Outflow tract obstruction

-obtain hysterosalphimngogram
 Cervical stenosis, and endometrial adhesion (Ashersman’s

Syndrome)
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