Amenorrhea Updated

Primary and Secondary
Amenorrhea
norrhea, FEU-NRMF Department of Obstetrics and Gynecology, 2012 1

Amenorrhea: absence of menses
during the reproductive years
Physiologic: Pregnancy, post partum
Pathologic: endocrine & anatomic disorders
Amenorrhea itself is not a pathologic
entity and should not be used as a final
diagnosis

Amenorrhea: absence of menses
during the reproductive years
Primary: absence of menses in a woman
who has never menstruated by the age of
16 years
Secondary: absence of menses for an
arbitrary time period, usually longer than 6
to 12 months.

Primary Amenorrhea
Criteria No period by age 14 in the
LEON absence of growth or
SPEROFF, MD
Professor of Obstetrics
and Gynecology, Oregon
development of secondary
Health Sciences
University School of
sexual characteristics
Medicine
A 14 year old showing

no breast budding
already needs further
evaluation.
Amenorrhea:
When to Failure to initiate breast
evaluate?
ASRM Practice Committee
development by age 13
2004

PUBERTY: Sequence of physical
events
Event Age Hormone
Breast development 10-11 Estradiol

(Thelarche)
Appearance of pubic and 10.5-11.5 Androgen
axillary hairs (Pubarche) s
Maximal growth velocity 11-12 GH
Menarche 11.5-13 Estradiol
Marshal
Marshal WA,
WA, Tanner
Tanner JM,
JM, Variations
Variations in
in the
the pattern
pattern of
of pubertal
pubertal
changes
changes in
in girls.
girls. Arch
Arch Dis
Dis Child
Child 1969;44-291
1969;44-291
Breast Growth:
B1 Prepubertal: elevation of papilla
only
B2 Breast budding
B3 Enlargement of breasts with
glandular tissue, without
separation of breast contours
B4 Secondary mound formed by
areola
Marshal WA, Tanner JM, Variations in the pattern of pubertal
B5 Single
changes in girls. Archcontour of breast and
Dis Child 1969;44-291
areola
Pubic Hair Growth:
PH1 Prepubertal: no pubic hair
PH2 Labial hair present
PH3 Labial hair spreads over mons
pubis
PH4 Slight lateral spread
PH5 Further lateral spread to form
inverse triangle and reach
Marshal WA, Tanner JM, Variations in the pattern of pubertal changes in
medial thighs
girls. Arch Dis Child 1969;44-291

PUBERTY: Sequence of physical
events
When PUBERTY begins, it
usually lasts for about 4-5
years ending in sexual
maturity. Lee, PA. Normal Ages of Pubertal
Events among American Males and Females.
Adolescent Health Care, 1980; 1: 26-29.
Mean interval is 2.3 years (SD

of 1 year)
A 14 year old showing no
breast budding already needs
further evaluation.
The H-P-O Environment
Compartment IV
Interactions Central
nervou
s
system
Sex Hormones Hypothalamus
during childhood
Compartment III GnRH
Anterio
Estrogen is Low
r
pituita
ry
LH & FSH are low Compartment II FSH LH
Ovary
CNS-HPO axis extremely

Compartment I Estrogen Progesterone
sensitive to negative feedback
effects of low levels of circulating
estrogen Uterus
Menses

The H-P-O
Interactions
Sex Hormones prior to puberty
When the critical weight or body
composition is achieved
CNShypothalamic axis becomes less

sensitive to the negative effect of estrogen.
GnRH is secreted in greater amounts.
This results in an increase in both LH and to
a lesser extent FSH.

The H-P-O
Interactions
Sex Hormones DURING puberty
Episodic pulses of LH during sleep and

awake periods.
The initial endocrinologic change in puberty.
After menarche.
Activation of positive gonadotropin

response to increasing estrogen levels.
Last endocrinologic event in puberty.
Results in midcycle gonadotrophic surge and ovulation.

Delayed Menarche
Onset of menses in
women older than
16.5 years who
have no
reproductive
abnormalities.
Factors Affecting
onset of
Menarche
1 Body fat composition
2 Strenuous exercise
3 Stress

Body composition & menarche
The mean time of onset of menarche was
previously thought to occur when a critical body
weight of about 48 kg (106 lb) was reached.
It is now believed that the ratio of fat to both

total body weight and lean body weight is
probably the most relevant factor that
determines the time of onset of puberty and
menstruation.

14
LEPTIN and its Role in
Puberty
Peptide secreted in adipose tissue
Circulates in the blood bound to a protein
Acts on CNS neurons that regulate eating habits and
energy balance
Increases during childhood until onset of puberty
level of leptin the earlier onset of menarche
1 GnRH
2 LH

Strenuous exercise &
menarche
Young women with strenuous exercise programs
that have sufficient estrogen to produce some
breast development do not need extensive
endocrinologic evaluation if concern arises about
lack of onset of menses.
They should be counseled that they will usually
have a delayed onset of menses, but it is not a
health problem.
Menarche is delayed about 0.4 year for each year
of premenarcheal athletic training.

Strenuous exercise &
menarche
Metabolic features of amenorrheic athletes:
1 elevated serum FSH
2 elevated serum IGFBP-1
3 Lowered IGF

Stress & menarche
Stress per se can lead to inhibition of the
GnRH axis.
Stress
(-)
CRH GnRH
ACTH, Cortisol
(-)

PRIMARY AMENORRHEA: Classification
Breast (-) Breast (+) Breast (-) Breast (+)
Uterus (+) Uterus (-) Uterus (-) Uterus (+)
Hypothalamic Failure secondary to Hypothalamic
inadequate GnRH release
(Hypogonadotropic Hypogonadism)
Insufficient GnRH synthesis (Kallmans Syndrome)
Insufficient GnRH secretion
Congenital Anatomic defects in the CNS (stenosis of
the aqueduct, absence of sellar floor)
CNS neoplasm
Pituitary Failure Pituitary

Isolated Gonadotropin insufficiency (Thalassemia
major, retinitis pigmentosa)
Pituitary neoplasia (pituitary adenoma, chromophobe
adenomas)
Mumps encephalitis
Newborn Kernicterus
Prepubertal Hypothyroidism
Gonadal Failure (Hypergonadotropic Androgen resistance Agonadism Ovarian

Hypogonadism) (testicular 17,20 desmolase
45,X Anomalies (Turners Syndrome, Mosaicism) feminization) deficiency
Structurally Abnormal X Chromosome
Pure gonadal dysgenesis (46 XX, 46 XY with gonad 17-hydroxylase Uterine
streaks, Gonadal agenesis) Congenital absence deficiency, 46 XY
46 xx, 17-hydroxylase deficiency
of uterus (RKH)
Diagnosis & Management Diagnosis &
Diagnosis & Diagnosis &
Management
Management Management
19
Environment
Breasts (-) Uterus (+)Compartment IV Central
nervou
s
Lack of breast system
development is the Hypothalamus
most sensitive indicator

that the ovaries never Compartment III GnRH
Anterio
secreted estradiol. r
pituita
ry
FSH LH
Compartment II
Ovary
Compartment I
X
Estrogen
Uterus
Progesterone
Menses

Environment
nervou
s
If the lack of estradiol is system
because of gonadal Hypothalamus
(ovarian) failure
Estradiol
Anterio
r
Progesterone pituita
Compartment II FSH
ry
LH
LH and FSH
Ovary
HYPERGONADOTRO
PIC
HYPOGONADISM
Compartment I
X
Estrogen
Uterus
Progesterone
Menses

Environment
nervou
s
Since estrogen is not system
necessary for mllerian Hypothalamus
duct development or
wolffian duct Compartment III GnRH
Anterio
regression, the internal r
pituita
ry
and external genitalia Compartment II FSH LH
are phenotypically Ovary
X
normal female.
Uterus
Menses

Environment
nervou
s
When ovarian follicles system
are absent, synthesis of Hypothalamus
ovarian steroids and

inhibin does not occur. Compartment III GnRH
Anterio
Breast development r
pituita
ry
does not occur Compartment II FSH LH
because of the very low Ovary
X
circulating E2 levels.
Uterus
Menses

45X Turners syndrome
Accompanying somatic anomalies
Short stature {<60 in) CVS: coarctation of the aorta
Webbing of neck MVP
Short 4th metacarpal aortic aneursyms
Cubitus valgus Bicuspid aortic valve
Broad shield-like chest Renal horseshoe kidney
Low set hairline & ears unilateral pelvic kidney
No 20 sex characteristics Pigmented nevi
Wide spaced nipples Edema of the feet & hands

45X Turners syndrome
Chances of menstruation and future pregnancy:
Rarely may have a few follicles that develop under endogenous
gonadotropin stimulation early in puberty and may synthesize enough
estrogen to induce breast development and a few episodes of uterine
bleeding.
However, they will have premature ovarian failure; usually before age
25. Rarely, ovulation and pregnancy can occur.

Mosaicism (X/XX. X/XXX. XXX)
Clinical features:
Primary amenorrhea and normal female external genitalia, taller and
have fewer anatomic abnormalities than individuals with a 45,X
karyotype.
Chances of menstruation and future pregnancy:

Occasionally may have a few follicles that develop under endogenous
gonadotropin stimulation early in puberty and may synthesize enough
estrogen to induce breast development .
20% may have sufficient estrogen production to menstruate

Rarely, ovulation and pregnancy may occur. However, they will have
premature ovarian failure; usually before age 25.

Structurally abnormal X chromosome
46 XX but part of X is abnormal
1. Deletion of the long arm of the X chromosome (Xq)
2. Deletion of the short arm of the X chromosome (Xp)
3. Isochrome of the long arm of the X chromosome
4. Ring X and minute fragmentation of the X chromosome

Pure Gonadal Dysgenesis
Genetic disorder and has been reported in siblings.
46 XX and 46 XY
Manifestations: normal stature and phenotype,
absence of secondary sexual characteristics, and
primary amenorrhea.
Some may have a few ovarian follicles,
develop breasts, and may even menstruate
spontaneously for a few years.

17 -hydroxylase deficiency 46 XX
Rare Cause
Normal female internal genitalia
Clinical Features
primary amenorrhea without breast development, normal female
internal genitalia
elevated serum progesterone level (>3 ng/mL)
elevated serum deoxycorticosterone level (>17 ng/100 mL)
low 17-hydroxyprogesterone level (<0.2 ng/mL)
low cortisol
high ACTH
high mineralocorticoid
hypernatremia, hypokalemia, hypertension

17 -hydroxylase deficiency 46 XX
Chances of menstruation & future pregnancy
They have cystic ovaries and viable oocytes.
Individuals with 17-hydroxylase deficiency do have
primordial follicles but cannot synthesize sex steroids.
Pregnancies have been documented following in vitro
fertilization/embryo transfer (IVF-ET) despite low levels
of endogenous sex steroids.

GONADAL STEROIDOGENESIS
Speroff L, et al.
Clinical Gynecologic Cholester Acetate
Endocrinolgy and
Infertility, ed 6, Lip- ol P450scc
pincott, 1999
X
5 pathway 4 pathway
Pregnenolo
DHEA Progesterone 3-OHSD
P450c17 pathway ne pathway
17OHlase 5,4 isomerase
X
17- Progesterone
Hydroxypregnenolone
P450c17, 20 lyase P450c17
17OHlase
Dehydroepidandrosterone 17-
3-OHSD P450c17 Hydroxyprogesterone
5,4
isomerase 17, 20 lyase
17-OHSD
Androstenedio Testosteron
ne e
P450arom P450arom
Estrone
17HSD
norrhea, FEU-NRMF Department of Obstetrics and Gynecology, 2012

X
Estradiol
31
Cholestero ADRENAL STEROIDOGENESIS
P450c17
P450c17
X
P450scc
DHEA
Pregnenolo 17-OH
ne pregnenolone
3-OHSD 5,4 isomerase
C17,20 lyase
Progesteron 17 OH lase 17- Androstenedio
e OHprogesterone ne
21-OH lase 17-HSD
11 deoxycortisone
(DOC)
11-OH lase
11
deoxycortisol
X
Testosteron
e
Corticosteron
e
18-OH lase, 19-
OHdehydrogenase
X
Cortisol
Aldosteron Harding BW: In: Endocrinology, vol 2 De

Environment
nervou
s
because of Hypothalamus
hypothalamic failure
Estradiol
Anterio
r
Compartment II FSH
ry
LH
LH and FSH
Ovary
HYPOGONADOTROP
IC HYPOGONADISM
Compartment I
X
Estrogen
Uterus
Progesterone
Menses

Environment
nervou
s
If defect is system
hypothalamic, patients Hypothalamus
will respond to a GnRH

bolus/stimulation. Compartment III GnRH
Anterio
r
pituita
ry
FSH LH
Compartment II
Ovary
Compartment I
X
Estrogen
Uterus
Progesterone
Menses

Insufficient GnRH synthesis (Kallmans Syndrome)
Clinical features
Anosmia
Normal height
Increased growth of long bones
Greater wing span to height ratio

Environment
nervou
s
because of Pituitary Hypothalamus
failure
Estradiol
Anterio
r
Compartment II FSH
ry
LH
LH and FSH
Ovary
HYPOGONADOTROP
IC HYPOGONADISM
Compartment I
X
Estrogen
Uterus
Progesterone
Menses

Environment
nervou
s
If defect is in the system
pituitary, patients will Hypothalamus
NOT respond to a
GnRH Compartment III GnRH
Anterio
bolus/stimulation. r
pituita
ry
FSH LH
Compartment II
Ovary
Compartment I
X
Estrogen
Uterus
Progesterone
Menses

PRIMARY AMENORRHEA: Breast (-)
Uterus (+)
Serum FSH NV: 5-20IU/L
HIGH (FSH > 30mIU/ml ) LOW (FSH < 30mIU/ml )

Hypergonadotropic Hypogonadotropic
hypogonadism hypogonadism
GONADAL CNS H-P
BP MONITORING Karyotyping ??
Karyotyping (peripheral ?
WBC)
XY XX
Excise Any sign of Serum Electrolytes

gonads Hyper- (Na, K)
Serum progesterone
androgenism 17OH progesterone,
? DOC
YES NO
38
norrhea, Excise gonads
FEU-NRMF Department ofLeave
Obstetrics and Gynecology, 2012 38
Uterus (+)
HIGH Serum FSH
Hypergonadotropic hypogonadism
BP Measurements
NORMAL HYPERTENSION
Gonadal dysgenesis
17 -hydroxylase
deficiency 46,XX
Karyotyping
Hypernatremia
Hypokalemia
45,X; 46,X/abnormal X; Mosaicism
Serum progesterone > 3 ng/ml
Pure gonadal dysgenesis; 17 OH Progesterone (0.2 ng/ml)
45,X/46,XY DOC (>17 ng/100ml)
45,X/45Xi (Yq); 45,X Testicular
determinant position
39
39
Uterus (+)
Serum FSH NV: 5-20IU/L
HIGH (FSH > 30mIU/ml ) LOW (FSH < 30mIU/ml )

Hypergonadotropic Hypogonadotropic
hypogonadism hypogonadism
GONADAL CNS H-P
BP MONITORING All are XX
Prolactin, CT Scan,
Karyotyping (peripheral MRI
WBC)
Lesion No lesion
XY XX
GnRH stimulation test
Excise Any sign of Serum
gonads Hyper- Electrolytes (Na,
K) Normal FSH, Absent
androgenism Serum LH response response
? progesterone Hypothalam Pituitary
17OH ic failure failure
NO progesterone,
YES DOC
40
norrhea, Excise gonads
FEU-NRMF Department ofLeave
Obstetrics and Gynecology, 2012 40
Environment
Breasts (+) Uterus (-)Compartment IV Central
nervou
s
The presence of the system
breasts indicates Hypothalamus
biologically active
estrogen. Compartment III GnRH
Anterio
Thus, this assures an
?
r
pituita
ry
intact HP-gonadal axis. Compartment II FSH LH
However, the patient GONADS
can be a male or Compartment I Estrogen Progesterone
female.
Uterus
Menses

Androgen Resistance (Testicular Feminization)
Genetically transmitted: X-linked recessive or sex-limited autosomal
dominant disorder with transmission through the mother
Androgen receptor synthesis or action DOES NOT occur

XY karyotype: normally functioning male gonads that produce normal
male levels of testosterone and dihydrotestosterone
Why (-) Uterus?

Why (+) Breast?

Androgen resistance
XY
AMH
MIS

Mullerian DuctRegresses
TESTESMALE Internal
Wolfiaan Duct Develop genitalia
s
Eternal Genitalia
TESTOSTER
Develops in the
absence of sex
steroids

ONE
X
Feminine
Short or absent
Penis vagina
Pubic & axillary
hair scanty
Normal breast
development
Why (+) breasts? Breast development is normal or
enhanced
Estrogen levels here are in the
male range but are sufficient for
breast proliferative activity.
Testosterone inhibits breast
proliferation. The absence of
androgen action allows even
low levels of estrogen to cause
unabated breast stimulation.

Congenital absence of uterus
Uterine Agenesis, Uterovaginal Agensis, Rokitansky Kuster
Hauser Syndrome
Second most frequent cause of primary amenorrhea
46 XX: Normal endocrinologic females
Normal FSH and LH, Female Estrogen, Progesterone
and testosterone
Normal breast, normal pubic and axillary hair
Shortened vagina
Possible associated findings: Renal, skeletal, cardiac and
other abnormalities

Breast (+) Uterus (-) Diagnosis
Serum testosterone
+
Observation of pubic
and axillary hair
Normal female testosterone Normal male testosterone

Normal pubic and axillary Absent pubic and axillary
hair hair
Congenital absence of Androgen insensitivity

uterus (testicular feminization)
MRKH syndrome
Confirm ovulation Confirm with karyotype

weekly serum progesterone x 4 Exceise Gonads after 18 yo
NO NEED for HT
Estrogen therapy thereafter
Renal scan
Vaginal Reconstruction Can not have offspring
May have offspring thru Surrogacy IVF
Testes that are intraabdominal or that occur in the inguinal
canal have an increased risk of developing a malignancy
(gonadoblastoma or dysgerminoma), with an incidence
reported to be about 20%
Rare before age 20

it is usually recommended that the gonads be left in place
until after puberty is completed, to allow full breast
development and epiphyseal closure to occur.
At around age 18, the gonads should be removed.

Patients should be informed that they have an abnormal sex
chromosome, without specifically mentioning a Y
chromosome.
Use term gonads instead of testes.
They should also be informed that they can never become
pregnant because they do not have a uterus and that their
gonads (not testes) need to be removed after age 18
because of their high potential for malignancy.
Patients should be informed that they have an abnormal sex

chromosome, without specifically mentioning a Y
chromosome.

PRIMARY AMENORRHEA: Breast (+) Uterus
(-)
Breast (+) Androgen resistance Congenital absence of uterus
Uterus (-) (testicular feminization) (RKH)
Karyotype 46 XY 46 XX
Heredity Maternal X-linked recessive; 25% risk of Not known

affected child, 25% risk of carrier
Axillary and pubic hair absent to sparse, Scanty Normal female body hair, ovulatory.
+/- ovulatory and PMS- None Normal ovulatory female.

Biphasic basal temperature
like symptoms
Hormone levels Endocrinologically Normal male, Endocrinologically Normal female,
Other anomalies Rare Frequent
Management Remove gonads after breast development Mechanical dilatation of vagina

epiphyseal closure (usually at 18 yo) Surgical reconstruction of vagina
Counselling (McIndoe)
ERT No hormonal therapy needed

Other anomalies rare. No need to evaluate. Evaluate for additional renal, skeletal
cardiac and other congenital
abnormalities.
Pregnancy and Will never menstruate. Will never menstruate.

Cannot have children. May have their own genetic children via
Menstruation ART using a surrogate recepient.

Environment
Breasts (-) Uterus (-) Compartment IV Central
nervou
s
The absence of the system
breast development Hypothalamus
and uterus suggests

that we are dealing with Compartment III GnRH

Anterio
a male phenotype. r
pituita
ry
FSH LH
Compartment II
GONADS
Uterus
Menses

17 -hydroxylase deficiency (in XY)
Why (-) Uterus? XY, (+) testes, (+) AMH/MIS, mullerian
duct regresses
Why (-) breasts? Enzyme deficient thus no sex steroids
No estrogen
No breasts

Breast (-) Uterus (-)
Primary Amenorrhea
Breast (-), Uterus (-)
Karyotype (46,XY)
Enzyme deficiency Agonadism

Vanishing Testes
Syndrome
Refer to an endocrine center for the extensive evaluation necessary to
establish the diagnosis.
If gonads are present, they should be removed

Hormonal therapy should be administered

Breasts (+) Uterus Environment
Compartment IV
(+) Central
nervou
s
Genetic Female. system
Second largest Hypothalamus
category.
Profile similar to Anterio

r
secondary amenorrhea. pituita
ry
FSH LH
Compartment II
Ovary
Uterus
Menses

Secondary Amenorrhea
1. CNS-Hypothalamic Causes 62%
2. Pituitary Causes 16%
3. Ovarian Causes 12%
4. Uterine Cause 7%

CNS-Hypothalamic Causes
Etiology
1 Lesions in the hypothalamus
2 Drugs
3 Stress and exercise
4 Weight loss
5 Polycystic Ovary Disease/Syndrome
6 Functional hypothalamic amenorrhea

Lesions in the hypothalamus
Craniopharyngiomas,
granulomatous diseases,
etc.
Low gonadotrophin
levels low estradiol
levels

Drugs
Phenothiazines, some antihypertensives, other
drugs
OCPs persistent HP inhibition postpill
amenorrhea
This oral contraceptive-induced suppression
should not last more than 6 months.

Stress & Exercise
FACTS strenuous activity LH and FSH
endorphins and catechol
estrogens
lowered body fats catechol
estrogens
catechol dopamine (-) GnRH no LH
estrogen
endorphins endorphins (-) NE effect on GnRH

(-) GnRH

Weight Loss
Amenorrhea associated with weight loss appears to
be due mainly to failure of normal GnRH release,
with the lack of a pituitary response under extreme
conditions.
Hypoleptinemia as well as GH and thyroid
dysfunction contribute to these findings.
1. Simple weight loss: hypothalamic dysfunction
2. Severe weight loss: possible additional pituitary
disorder

Anorexia Nervosa
A severe psychiatric disorder
Uncommon in men and rare in blacks and Asians
Patients have a hypothalamic disorder interfering
with normal GnRH. Pituitary dysfunction also occurs
when the weight loss becomes severe.
1 normal T4, abnormally low T3
2 elevated GH
3 high cortisol
4 low ACTH and DHEA-S
5 LH pattern similar to pre-pubertal girls

PCOS: Diagnostic criteria
1990 NIH: requires both 2003 ESHRE/ASRM:
criteria1 requires 2 of 3 criteria2,3
1 Chronic anovulation 1 Oligo- and/or anovulation
(OA) (OA)
2 Clinical and/or 2 Clinical and/or
biochemical signs of biochemical signs of
hyperandrogenism (HA) hyperandrogenism (HA)
3 Polycystic ovaries (PCO)
With exclusion of other etiologies (AED)4
AED androgen excess disorders.
Zawadzki
Zawadzki JK,
11
JK, Dunaif
Dunaif A.
A. In:
In: Dunaif
Dunaif A,
A, et
et al,
al, eds.
eds. Polycystic
Polycystic Ovary
Ovary Syndrome.
Syndrome.
Boston:
Boston: Blackwell
Blackwell Scientific
Scientific Publications,
Publications, 1992,
1992, pp.
pp. 377-384.
377-384. The
22
The Rotterdam
Rotterdam
ESHRE/ASRM-Sponsored PCOS consensus workshop group. Fertil
ESHRE/ASRM-Sponsored PCOS consensus workshop group. Fertil Steril. Steril.
2004;81:19-25.
2004;81:19-25. 33The
The Rotterdam
Rotterdam ESHRE/ASRM-Sponsored
ESHRE/ASRM-Sponsored PCOS PCOS consensus
consensus
workshop
workshop group.
group. Hum
Hum Reprod.
Reprod. 2004;19:41-47.
2004;19:41-47. Ehrmann
44
Ehrmann DA.
DA. N
N Engl
Engl JJ Med.
Med.
2005;352:1223-36.
2005;352:1223-36.
Functional hypothalamic amenorrhea
No underlying pituitary, hypothalamic or ovarian
causes
No cyclic alterations in LH pulsatility no pulses or
only one pattern seen throughout menstrual cycle
(persistent luteal pattern)
Possibly due to CNS neurotransmitter abnormality,
increase opioid acitivity

Pituitary Causes
Hypoestrogenic amenorrhea
Neoplasms e.g. chromophobe adenoma
Non-neoplastic lesion
1 Anoxia, thrombosis, hemorrhage pituitary cell damage
2 Sheehan syndrome hypotensive episode during

pregnancy
3 Simmond disease hypotension unrelated to pregnancy

Ovarian Causes
Hypo-gonadotrophic hypogonadism
Infection, interference of blood supply, bilateral
cystectomies that deplete follicles insufficient
estrogen
Cystic degeneration of the ovaries
PREMATURE OVARIAN FAILURE: (<40 years old)
1 ovarian Sclerosis
2 Gonadal irradiation
3 Chemotherapy
4 Autoimmune associations e.g. thyroid disease

Uterine Causes
The likelihood of the diagnosis is strengthened if a
sound cannot be passed into the uterine cavity.
1 Intrauterine adhesions (IUAs) or synechiae (Asherman's
syndrome)
A Postabortal curettage (30%)
B D&C in non-pregnant patient

C severe endometritis or fibrosis following a myomectomy,
metroplasty, or cesarean delivery
2 Missed abortion or endometrial tuberculosis

Secondary Amenorrhea
Diagnostic Evaluation
1 History & PE
2 Ancillary diagnostic tools
CBC, Urinalysis
TSH assay
Serum E2, Progesterone challenge test, Endometrial
imaging (TVS)
Serum FSH, Prolactin

E2 above 30 40 pg/ml
plus PCO by ultrasound
Diagnosis: PCOS
no PCO by ultrasound
(+) history of drug ingestion, stress, weight loss,
exercise
Diagnosis: Hypothalamic pituitary dysfunction
Self limiting, not life threatening

E2 low
plus LOW FSH
Diagnosis: CNS lesion or HP failure
If history of drug ingestion, stress, weight loss,
exercise NOT present, CT or MRI waranted
plus HIGH FSH

Diagnosis: POF
Anti-thyroid and Antinuclear antibodies
karyotype

Diagnostic Evaluation
AMENORRHEA
TSH, FSH, Prolactin, Serum Estradiol
Progestational Challenge
Elevated TSH
+ withdrawal bleed after - withdrawal bleed after
PCT PCT
E2 30-40pg/mL E2 low
HYPO
THYROIDISM Prl > 100ng/ml
ANOVULATION
PCOS FSH assay
HYPER-
Ptolactinemia
LOW HIGH
HYPOTHALAMIC
AMENORRHEA
OVARIAN
FAILURE
CT SCAN or MRI

Secondary amenorrhea
Management depends on:
1 Diagnosis
2 Desire for pregnancy

Non-prolactin
secreting tumors
should be excised if
possible
Primary and Secondary
Amenorrhea
END OF LECTURE

Amenorrhea Updated

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Primary and Secondary

norrhea, FEU-NRMF Department of Obstetrics and Gynecology, 2012 1

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A 14 year old showing

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Breast development 10-11 Estradiol

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Mean interval is 2.3 years (SD

Sex Hormones Hypothalamus

LH & FSH are low Compartment II FSH LH

CNS-HPO axis extremely

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CNShypothalamic axis becomes less

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Episodic pulses of LH during sleep and

Activation of positive gonadotropin

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It is now believed that the ratio of fat to both

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Pituitary Failure Pituitary

Gonadal Failure (Hypergonadotropic Androgen resistance Agonadism Ovarian

development is the Hypothalamus

most sensitive indicator

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because of gonadal Hypothalamus

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necessary for mllerian Hypothalamus

are phenotypically Ovary

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are absent, synthesis of Hypothalamus

ovarian steroids and

because of the very low Ovary

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Chances of menstruation and future pregnancy:

20% may have sufficient estrogen production to menstruate

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norrhea, FEU-NRMF Department of Obstetrics and Gynecology, 2012

Aldosteron Harding BW: In: Endocrinology, vol 2 De

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hypothalamic, patients Hypothalamus

will respond to a GnRH

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because of Pituitary Hypothalamus

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pituitary, patients will Hypothalamus

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HIGH (FSH > 30mIU/ml ) LOW (FSH < 30mIU/ml )

Excise Any sign of Serum Electrolytes

HIGH (FSH > 30mIU/ml ) LOW (FSH < 30mIU/ml )

breasts indicates Hypothalamus

Thus, this assures an