Transcript Causes of Heavy Menstrual Bleeding

Menstrual disorders
Lentz GM, Lobo RA, Gershenson DM,
and Katz VL. Comprehensive
Gynecology 2012. 6th Edition.
Menstrual disorders
•
•
•
Abnormal uterine bleeding/ Heavy
uterine bleeding
Amenorrhea
Primary and Secondary
Dysmenorrhea, Premenstrual
Syndrome (PMS), Premenstrual
Dysphoric Disorder (PMDD)
Lentz GM, Lobo RA, Gershenson DM,
and Katz VL. Comprehensive
Gynecology 2012. 6th Edition.
ABNORMAL UTERINE
BLEEDING
Lentz GM, Lobo RA, Gershenson DM,
and Katz VL. Comprehensive
Gynecology 2012. 6th Edition.
Abnormal Uterine Bleeding
 defined
as changes in frequency of
menses, duration of flow or amount of
blood loss
Lentz GM, Lobo RA, Gershenson DM,
and Katz VL. Comprehensive
Gynecology 2012. 6th Edition.
Definition of terms

Mean interval between menses is 28 days
(±7 days)

Mean duration of menstrual flow is 4 days
(>7 days is menorrhagia)

Mean amount of MBL in normal women is
about 35 mL (>80 mL is menorrhagia)
Lentz GM, Lobo RA, Gershenson DM,
and Katz VL. Comprehensive
Gynecology 2012. 6th Edition.
DEFINITION OF MENSTRUAL CYCLE
IRREGULARITIES: NO LONGER USED
IRREGULARITY
DEFINITION
OLIGOMENORRHEA
Infrequent IRREGULARLY timed episodes of
bleeding usually occurring at intervals of more
than 35 days
POLYMENORRHEA
Frequent but REGULARLY timed episodes of
bleeding usually occuring at intervals of 21 days or
less
MENORRHAGIA
REGULARLY timed episodes of bleeding that are
EXCESSIVE in amount (> 80 ml) and duration of
flow (> 5 days)
METRORRHAGIA
Irregularly timed bleeding or bleeding between
periods
MENOMETRORRHAGIA
EXCESSIVE, PROLONGED bleeding that occurs at
IRREGULARLY timed frequent intervals
HYPOMENORRHEA
REGULARLY timed bleeding that is decreased in
amount
INTERMENSTRUAL
BLEEDING/SPOTTING
Bleeding usually not of an excessive amount that
occurs between otherwise normal menstrual cycles
Etiology

Two major categories
A. Organic
I. Systemic
II. Reproductive Tract disease
B. Dysfunctional
I. Anovulatory
II. Ovulatory
Lentz GM, Lobo RA, Gershenson DM,
and Katz VL. Comprehensive
Gynecology 2012. 6th Edition.
A. Organic: Systemic Disease
•
Chronic systemic diseases e.g. hepatitis, renal
disease, cardiac disease, and coronary vascular
disorders (usually from anovualtion due to hypothalamic
cause or problem with estrogen metabolism)
•
Disorders of blood coagulation e.g. von
Willebrand's disease and prothrombin deficiency
• Disorders producing platelet deficiency e.g
leukemia, severe sepsis, idiopathic thrombocytopenic
purpura (ITP), and hypersplenism
• Drugs e.g.anticoagulants
• Endocrine disorders e.g. hormonal disorders
involving thyroid, PRL, and cortisol
Lentz GM, Lobo RA, Gershenson DM, and Katz VL. Comprehensive Gynecology 2012. 6th Edition.
A. Organic: Reproductive Tract Disease

The most common cause: accidents of pregnancy

Other causes:
1) Malignancy of the genital tract
endometrial and cervical cancer – most common
vaginal, vulvar, fallopian tube cancer – less common
2) Anatomic uterine abnormalities
submucous myomas, endometrial polyps,
adenomyosis (probably d/t abnormal vasculature and blood
flow and increased inflammatory changes)
3) Cervical lesions
erosions, polyps, cervicitis (postcoital bleeding)
Lentz GM, Lobo RA, Gershenson DM,
and Katz VL. Comprehensive
Gynecology 2012. 6th Edition.
ABNORMAL UTERINE BLEEDING: WORKUP

History
– Timing of bleeding, quantity of bleeding, menstrual hx including menarche and
recent periods, associated sxs, family hx of bleeding disorders

Physical
– Speculum exam to R/o vaginal or cervical source of bleeding
– Bimanual exam may reveal bulky uterus/discrete fibroids
– Assess for obesity, hirsutism, stigmata of thyroid disease (hypothyroidism
associated with anovulation), signs of hyperprolactinemia (visual field testing,
galactorrhea)
– Pap smear
– Endometrial biopsy, if appropriate


Pregnancy Test
Imaging
– Pelvic ultrasound
– Sonohystogram (SIS) or hysterosalpingogram (HSG)

Surgical
– Endometrial biopsy (>35 y/o, long history of excessive bleeding, EM >8mm)
– Hysteroscopy
– D&C
Lentz GM, Lobo RA, Gershenson DM, and Katz VL. Comprehensive Gynecology 2012. 6th Edition.
AUB: TREATMENT STRATEGIES

Medical vs Surgical
– Depends on the ff. patient characteristic:
age, desire to preserve fertility, coexisting medical conditions, and patient preference

Anovulatory DUB
– For adolescents:
Cyclic progestogen (MPA 10mg OD for10 days/month x 6 mos) – 1st line
COCs – only 2nd line used if DUB persists beyond 6 mos. on cyclic progestogen,
because it does not allow HPO to mature
– For perimenopausal women:
Low dose COCs (20ug EE) – 1st line
Cyclic progestogen – only 2nd line, this will help the endometrium but not
reliably control bleeding because of unpredictability of the hormonal
situation
Lentz GM, Lobo RA, Gershenson DM, and Katz VL. Comprehensive Gynecology 2012. 6th Edition.
AUB: TREATMENT STRATEGIES

Ovulatory DUB
Cyclic progestogen (MPA 10mg OD for 3 weeks/mo. ) – shorter duration do not work
Local progesterone exposure (LNG-IUS) –  80% MBL by 3 mos (lasts >5 yrs)
NSAIDs – Mefenamic acid 500mg TID, Ibuprofen 400mg TID, Meclofenamate Na
100mg TID, Naproxen Na 550mg LD then 275mg q6
Antifibrinolytic agents – 50% MBL
EACA (ε-aminocaproic acid)18g/d x 3 days then 12g ,9g ,6g, 3g = total 48g
AMCA (tranexamic acid) 6/d x 3 days then 4g, 3g, 2g, 1g,= total 22g
PAMBA (para-amino methylbenzoic acid)
COCs –  50% MBL
Androgenic steroids – Danazol 200-400mg/day x 12 weeks 60% MBL
GnRH Agonists – given for 3 months, reserved for women with severe MBL with failed
with other medication
Lentz GM, Lobo RA, Gershenson DM, and Katz VL. Comprehensive Gynecology 2012. 6th Edition.
AUB: TREATMENT STRATEGIES

Acute Bleeding
Pharmacologic Agents vs. Surgical Therapy
Dilatation and curettage – fastest way, best when EM is thick >10-12 mm and px
is >35 y/o
Estrogens – best when EM is thin <5mm
Oral CEE 10mg/day in 4 divided doses
IV CEE 25mg q4-6 hrs.
High dose OCPs(50ug EE) 4tabs OD, continued for 1week after bleeding stops
Progestogens – no evidence in stopping acute bleeding, and can only be used after
stabilization of the endometrium (after 2-3 days of estrogen)
MPA 10mg/day x 10 days/month
Norethindrone acetate 2.5-5mg/day in 4 divided doses
Endometrial ablation – used if medical therapy is not effective
22-55% amenorrhea success rate
86-99% satisfaction rate
only 25% proceed to hysterectomy w/in 4 years
Hysterectomy – used to treat persistent ovulatory DUB when medical therapy has failed
Lentz GM, Lobo RA, Gershenson DM, and Katz VL. Comprehensive Gynecology 2012. 6th Edition.
The “MOST COMMON”
Most common cause
of vaginal bleeding in
CHILDHOOD
• FOREIGN BODY IN THE
VAGINA
Most common cause
of vaginal bleeding in
REPRODUCTIVE age
women
• ACCIDENTS OF
PREGNANCY
Most common cause
of vaginal bleeding in
POSTMENOPAUSAL
women
• ATROPHIC
ENDOMETRIUM
Characteristics
Descriptive
Terms
Normal limits
Frequent
Normal
Infrequent
<24
24-38
>38
Regularity of menses in
days (cycle to cycle variation in a
Absent
Regular
Irregular
±2-20
>20
Duration of flow in days
Prolonged
Normal
Shortened
>8
4.5-8
<4.5
Heavy
Normal
Light
>80
5-80
<5
Frequency of menses in days
year)
Volume of monthly blood
loss in mL
Fraser. International definitions of abnormal menstrual bleeding.
Fertil Steril 2007 & Hum Reprod 2007
•
Chronic AUB
– bleeding from the uterine corpus that is abnormal in
volume, regularity, and/or timing that has been present
for the majority of the last 6 months
•
Acute AUB
– episode of heavy bleeding that, in the opinion of the
clinician, is of sufficient severity to require immediate
intervention to prevent further blood loss
• Intermenstrual bleeding (IMB)
• occurs between clearly defined cyclic and predictable
menses and includes both randomly occurring
episodes as well as those that manifest predictably at
the same time in each cycle
• Breakthrough bleeding (BTB)
• unscheduled bleeding that occurs during the use of
exogenous gonadal steroid therapy
PALM group
– discrete structural abnormalities that can
be seen and measured by imaging
techniques such as ultrasound or
hysteroscopy
 COEIN group
– non-structural entities, not defined by
imaging or histopathology

PALM
–
–
–
–
Polyp
Adenomyosis
Leiomyoma
Malignancy/Hype
rplasia
COEIN
 Coagulopathy
 Ovulatory Disorders
 Endometrial Disorders
 Iatrogenic Causes
 Not Classified
*FIGO classification system for causes of abnormal uterine bleeding in the reproductive years
P olyp
A denomyosis
L eiomyoma
M alignancy and
hyperplasia
P olyp
A denomyosis
L eiomyoma
M alignancy and
hyperplasia
P
olyp
A denomyosis
Submucousal
L
eiomyoma
M
alignancy and hyperplasia
Other
Leiomyoma Subclassification System
SM Submucosal
(Wamsteker 1993)
O - Other
0
Pedunculated
intracavitary
1
<50% intramural
2
≥50% intramural
3
Contacts endometrium;
100% intramural
4
Intramural
5
Subserosal; ≥50%
intramural
6
Subserosal; <50%
intramural
7
Subserosal
pedunculated
8
Other (e.g. cervical,
Intramural,Subserous,
Transmural
P
A
L
M
olyp
denomyosis
eiomyoma
alignancy and hyperplasia
C
O
E
I
N
oagulopathy
vulatory dysfunction
ndometrial
atrogenic
ot yet classified
Causes of Ovulatory
Dysfunction
Luteal out of phase cycles
Endocrinopathies
PCOS
Hypothyroidism
Hyperprolactinemia
Mental stress
Obesity
Anorexia
Weight loss
Extreme exercise
C
O
E
I
N
oagulopathy
vulatory dysfunction
ndometrial
atrogenic
ot yet classified
C
O
E
I
N
oagulopathy
vulatory dysfunction
ndometrial
Causes of Ovulatory
Dysfunction
Systemic Pharmacotherapy
atrogenic
Phenothiazines
ot yet classified
Tricyclic antidepressants
C
O
E
I
N
oagulopathy
vulatory dysfunction
ndometrial
atrogenic
ot yet classified
Primary disorder of local
endometrial hemostasis
Endometrial
inflammation/infection
Abnormalities in the local
inflammatory response
Aberrations in endometrial
vasculogenesis
C
O
E
I
N
oagulopathy
vulatory dysfunction
ndometrial
Gonadal Steroids
atrogenic
LNG-IUS
ot yet classified
C
O
E
I
N
oagulopathy
vulatory dysfunction
ndometrial
Arteriovenous
malformations
Myometrial hypertrophy
atrogenic
Associations with some
systemic diseases
ot yet classified
Others
PALM
–
–
–
–
Polyp
Adenomyosis
Leiomyoma
Malignancy/Hype
rplasia
COEIN
 Coagulopathy
 Ovulatory Disorders
 Endometrial Disorders
 Iatrogenic Causes
 Not Classified

Heavy menstrual bleeding (HMB)
– volume of monthly blood loss of more
than 80 ml
– management may be either medical or
surgical
MEDICAL MANAGEMENT
Acute HMB
SURGICAL MANAGEMENT
Chronic HMB
High dose Estrogen
LNG-IUS
Dilatation and curettage
High dose COCs
Antifibrinolytic agents
Endometrial ablation
Progestins
NSAIDs
Hysterectomy
Tranexamic acid
COCs
Cyclic progestogen
Danazol
AMENORRHEA
Lentz GM, Lobo RA, Gershenson DM,
and Katz VL. Comprehensive
Gynecology 2012. 6th Edition.
Amenorrhea



May be physiologic or pathologic which may include primary
and secondary causes
Primary amenorrhea.
No menses by age 14 in the absence of growth or
development of secondary sexual characteristics.
Or
No menses by age 16 with the appearance of secondary
sexual characteristics.
Secondary amenorrhea.
In a menstruating women, the absence of menstruation for three
previous cycle intervals or 6 months.
Lentz GM, Lobo RA, Gershenson DM,
and Katz VL. Comprehensive
Gynecology 2012. 6th Edition.
Evaluation of
Amenorrhea
1.
2.
3.
History
Physical examination
Diagnostics
Diagnostic Evaluation for Secondary Amenorrhea
Causes of Amenorrhea
1.
2.
Primary Amenorrhea
Secondary Amenorrhea
Primary causes initially classified on whether absent uterus and/or
breast development are also found
Amenorrhea
Primary causes initially classified on whether absent uterus and/or
breast development are also found
BREASTS
UTERUS
CONDITION
ABSENT
PRESENT
With pituitary masses
TURNER’S SYNDROME
PRESENT
ABSENT
TESTICULAR FEMINIZATION (XY) AND
CONGENITAL ABSENCE OF THE UTERUS
ABSENT
ABSENT
MALE KARYOTYPE EITHER ENZYME
DEFICIENCY OR AGONADISM
PRESENT
PRESENT
HYPOTHALAMIC CAUSES, PITUITARY,
OVARIAN, UTERINE OR OUTFLOW TRACT
PROBLEMS
Lentz GM, Lobo RA, Gershenson DM,
and Katz VL. Comprehensive
Gynecology 2012. 6th Edition.
Amenorrhea

Secondary amenorrhea may be physiologic or
pathologic. Pathologic lesions include intrauterine adhesions after curettage. Work up
include: HYPOTHALAMIC CAUSES,
PITUITARY, OVARIAN, UTERINE OR
OUTFLOW TRACT PROBLEMS
Lentz GM, Lobo RA, Gershenson DM,
and Katz VL. Comprehensive
Gynecology 2012. 6th Edition.
Compartmental Systems

Compartment I
– Disorders of the outflow tract

Compartment II
– Disorders of the ovary

Compartment III
– Disorders of the anterior pituitary

Compartment IV
– Disorders of CNS (hypothalamic factors)
Compartment I: Disorders of the
Outflow Tract or Uterus

Mullerian Anomalies
– Imperforate hymen
– Transverse vaginal septum
Mullerian agenesis (Mayer-RokitanskyKuster-Hauser syndrome)
 Androgen insensitivity
 Ashermans syndrome

Imperforate Hymen
•The hymen itself is formed from
the proliferation of the sinovaginal
bulbs, becoming perforate before
or shortly after birth.
•Results when this sheet of tissue
fails to completely canalize
•Translucent thin membrane just
inferior to the urethral meatus
that bulges with valsalva
maneuver
Transverse vaginal septum
•Horizontal wall of tissue that
has formed during
embryologic development and
essentially creates a blockage
in the vagina
• Occurs between the upper
one-third and lower two-thirds
of the vaginal canal.
•Resection of septum
Mayer-Rokitansky-Kuster-Hauser Syndrome
(utero-vaginal agenesis)






•
15% of primary amenorrhea
Normal secondary
development & external
female genitalia
Normal female range
testosterone level (20-80
ng/dl)
Absent uterus and upper
vagina & normal ovaries
Karyotype 46XX
15-30% renal, skeletal and
middle ear anomalies
Treatment: Progressive
vaginal
dilatation/vaginoplasty
Androgen Insensitivity






Normal breasts but no sexual
hair
Normal looking female external
genitalia
Absent uterus and upper
vagina
Karyotype 46, XY
Testes present, male range
testosterone level (300 ng/dL
to 800 ng/dL)
Treatment : gonadectomy after
puberty + ERT
Androgen Insensitivity
(Testicular feminization)
22% with Dysgerminoma or
Gonadoblastoma
 Gonadectomy once patient undergoes
spontaneous and complete natural breast
development
 Estrogen monotherapy to prevent
osteoporosis and cardiovascular disease
 Vaginal dilatation or create neovagina
once sexually active

Differences between Mullerian
agenesis and Androgen
Insensitivity
Mullerian Agenesis
Androgen
Insensitivity
Karyotype
46, XX
46, XY
Heredity
Not known
Maternal X-linked
recessive;
25% risk of affected
child, 25% risk of carrier
Sexual hair
Normal female
Absent to sparse
Testosterone level
Normal female
Normal to slightly
elevated male
Other anomalies
Frequent
Rare
Gonadal neoplasia
Normal incidence
5% incidence of
malignant tumors
Compartment II: Disorders of the
Ovary
Gonadal Dysgenesis


Chromosomally abnormal
- Classic turner’s syndrome (45XO)
- Turner variants (45XO/46XX),(46X-abnormal X)
- Mixed gonadal dygenesis (45XO/46XY)
Chromosomally normal
- 46XX (Perrault)
- 46XY (Swyer’s syndrome)
Gonadal Dysgenesis



Gonadal dysgenesis associated with a normal
karyotype is also linked to neurosensory
deafness (Perrault syndrome)
Pure gonadal dysgenesis indicates the
presence of bilateral streak gonads,
regardless of karyotype.
Mixed gonadal dysgenesis indicates testicular
tissue on one side and a streak gonad on the
other.
Typical features of Turner Syndrome
XY Gonadal Dysgenesis

Swyer’s syndrome
– Female patient with XY karyotype
– Palpable mullerian system
– Normal female testosterone level
– Lack of sexual development
Mosaicism
Multiple cell lines of varying sex
chromosome composition
 Appear normal, attaining normal stature
before premature menopause is
experienced (accelerated atresia)
 Patients are short

Gonadal Agenesis
No complicated clinical problems
accompany the gonadal failure due to
agenesis
 Viral and metabolic influences in early
gestation or undiscovered genetic
mutations are suspected
 Surgical removal of the gonadal streaks is
necessary to avoid the possibility of
neoplasia

Premature Ovarian Failure
Early depletion of ovarian follicles before
the age of 40
 Etiology : unknown but maybe due to
genetic disorder with an increased rate of
follicle disappearance
 Most common abnormalities: 45,X and 47,
XXY followed by mosaicism
 Hormonal therapy recommended

Radiation
Ovarian dose
Sterilization effect
60 rads
No effect
150 rads
Some risk over age 40
250-500 rads
Ages 15-40: 60% sterilized
500-800 rads
Ages 15-40: 60-70% sterilized
Over 800 rads
100% permanently sterilized
Chemotherapy

Alkylating agents – very toxic to the
gonads

Inverse relationship between the dose
required for ovarian failure and age at the
start of therapy.
Compartment III: Disorders of the
Anterior Pituitary
Hypogonadism and delayed puberty warrant
brain evaluation by MRI
 Nonfunctioning adenoma: microadenoma
 Pituitary prolactin secreting adenomas
 Sheehan’s syndrome

– Acute infarction and necrosis of the pituitary
gland due to post partum hemorrhage and shock
– Failure of lactation and loss of pubic and axillary
hair
Constitutional Delayed Puberty

10-30% of cases with delayed puberty

Physiologic variant in development

Short stature, appropriate bone maturation delay

Delayed secondary sexual characteristics

Familial pattern

Late but otherwise normal growth pattern and adult
reproductive function
Compartment IV: Central Nervous
System Disorders

Hypothalamic amenorrhea
(hypogonadotropic hypogonadism)
– Deficiency in GnRH pulsatile secretion
– Frequently associated with stress
– Higher proportion of underweight women and
previous menstrual irregularity
– Displays the endocrine, metabolic, and
psychological characteristics suggesting the
presence of a subclinical eating disorder
Compartment IV: Central Nervous
System Disorders
– Chronic hypothalamic anovulation
 Stress
 Increased exercise levels
 Anorexia nervosa
– Head trauma
– Space-occupying lesions
Exercise and Female
Athlete Triad

Disordered eating, amenorrhea,
and osteoporosis
↑ endogenous opioids, ACTH, prolactin, adrenal
androgens, cortisol, and melatonin
 Minimum of 17% body fat required for the
initiation of menses and 22% body fat for the
maintenance of menses (Frisch. Science 1974)

Exercise and Female Athlete Triad

Low caloric intake during strenuous exercise
more important than body fat (Laughlin. J. Clin
Endocrinol Metab 1997)

Suboptimal amount of body fat→ estrogens to
inactivate catecholestrogens
Stress-induced Hypothalamic
Amenorrhea

Potential mediators:
– Opioid (β-endorphins)
– Dopaminergic (Prolactin)

Activation of H-P-A axis and the stress
inhibition of the H-P-G axis

↑ CRF→ ↑ ACTH → ↓ GnRH-LH secretion
→ ↓steroid biosynthesis
Space-Occupying Lesions
Craniopharyngiomas, gliomas, dermoid
cysts
 Peak incidence: ages 6 and 14
 Disruption of tonic inhibition of dopamine
on PRL release
 Neurological symptoms (headache, visual
field defects)
 Cranial imaging: Abnormal sella and
calcifications

Kallman’s Syndrome
Rare (1:50,000)
 Autosomal dominant or x-linked recessive
 Congenital absence of GnRH neurons,
partial or complete agenesis of olfactory
bulb
 Sexual infantilism, primary amenorrhea,
anosmia
 Normal height for their age

Anorexia Nervosa

Affects 1-3% of adolescents and young
adults

Diagnostic criteria:
– Refusal to maintain body weight at or above
normal weight for height and age
– Intense fear of gaining weight or being fat, even
though underweight
– Denial of seriousness of current low body weight
– Amenorrhea
Anorexia Nervosa

Restrictive Type
– W eight is mainly controlled by restricting
oral intake

B inge-eating/Purging subtype
– Self-induced vomiting
– Misuse of laxative
Anorexia Nervosa (Physical examination)






B radycardia, hypothermia, abnormal response
to heat and cold
Dry skin, yellow skin (hypercarotenemia)
Scaphoid abdomen, loss of subcutaneous fat
Submandibular adenopathy or parotid gland
enlargement
Cardiac murmur
Prepubertal appearing vaginal mucosa
(hypoestrogenemia)
Anorexia Nervosa (Laboratory Findings)
Low
Normal
High
FSH
TSH
Serum total
cortisol
LH
Prolactin
Serum free cortisol
Estradiol
ACTH
24 hour urinary
free cortisol
Leptin
IGF-I
DHEAS
Anorexia Nervosa and Leptin
Ideal sensor of energy deficiency
 Concentration increases with obesity and
decreases rapidly during fasting
 Regulates the synthesis and secretion of
GnRH, gonadotropins, and sex steroids
 Low leptin levels in anorexia nervosa
significantly correlated with low IGF-I
levels

Anorexia Nervosa and Skeletal System
Decreased bone formation and increased
resorption → increased rates of
osteopenia and osteoporosis
 44-92% patients with osteopenia with
amenorrhea of < 24 months
 Normalization of B MD with weight
recovery noted in some cross-sectional
studies

Anorexia Nervosa and Skeletal System
Osteopenia improves but does not resolve
with weight gain in recent prospective
studies
 OC and recombinant human IGF-I with
significant positive effect on B MD

Hypothalamic Amenorrhea
(Hypothalamic hypogonadism)

Most common cause of primary and
secondary amenorrhea

Abnormalities of GnRH secretion and
disruption of H-P-O axis

Low levels of FSH, LH, estrogen

Diagnosis by exclusion of pituitary lesions
Hypothalamic Amenorrhea
(Hypogonadotropic hypogonadism)

Mild suppression: marginal effect on
reproduction, inadequate luteal phase

Moderate suppression: anovulation with
menstrual irregularity

Profound suppression: Hypothalamic
amenorrhea
–W
eight loss, exercise, stress
Hypothalamic Amenorrhea
(Hypogonadotropic hypogonadism)

83% resumed menses once precipitating
cause of amenorrhea is reversed
(Perkins et al. Hum Reprod 16: 2198, 2001)
The “MOST COMMON”
Most common cause
of amenorrhea in
adolescents
• ANOREXIA NERVOSA
Most common cause
of PRIMARY
amenorrhe
• GONADAL FAILURE
Test to confirm
gonadal failure
• SERUM FSH
Lentz GM, Lobo RA, Gershenson DM,
and Katz VL. Comprehensive
Gynecology 2012. 6th Edition.
DYSMENORRHEA
Lentz GM, Lobo RA, Gershenson DM,
and Katz VL. Comprehensive
Gynecology 2012. 6th Edition.
Dysmenorrhea

Primary Dysmenorrhea – pain with no obvious pathologic disease
(usually <20 y.o)

Secondary Dysmenorrhea – associated with pelvic conditions or
pathology causing pelvic pain in conjunction with menses (most
often >20 y/o)
CAUSES OF SECONDARY DYSMENORRHEA
Gynecologic Pathology
Non-gynecologic Disorders
Causing Pelvic Pain
Cervical stenosis
Endometriosis and adenomyosis
Pelvic infection and adhesions
Uterine polyps or fibroids
Ovarian cyst or mass
Pelvic congestion
Congenital obstructed mullerian
malformations
Conditioned behavior
Bowel disease
Irritable bowel syndrome
Inflammatory bowel disease
Celiac sprue (?)
Lactose intolerance (?)
Urinary tract disease
Ureteral obstruction
Interstitial cystitis
Nephrolithiasis
Lentz GM, Lobo RA, Gershenson DM, and Katz VL. Comprehensive Gynecology 2012. 6th Edition.
Differences between Primary and
Secondary Dysmenorrhea
Primary Dysmenorrhea
Secondary Dysmenorrhea
Cause
Effects of endogenous prostaglandin
Secondary to pelvic pathology
Hx
Midline crampy lower abdominal pain w/c
gradually resolves over 12-72 hrs and does
Pain not responding to NSAIDs and OCs
Occur after many years of painless menses
Associated
symptom
Diarrhea
Headache
Fatigue or Malaise
+/- Urinary and Bowel symptoms
PE
Normal pelvic exam
Adolescents with dysmenorrhea in first 6
months of menarche – consider obstructive
genital tract malformation
(+) physical finding associated with:
cervical stenosis, endometriosis,
adenomyosis, fibroids, ovarian cyst,
nongynecologic disorders (bowel disease or
urinary tract disease)
Treatment
NSAIDs (Fenamates>ibuprofen, naproxen, Treat underlying disease
not occur at times other than menses
indomethacin)
COX-2 inhibitors
OCs, LNG-IUS, TENS, Nifedipine,
Narcotic analgesic - last resort
Lentz GM, Lobo RA, Gershenson DM, and Katz VL. Comprehensive Gynecology 2012. 6th Edition.
Primary Dysmenorrhea: Pathogenesis
Arachidonic acid
 PGF2α
 uterine hypercontractility
 uterine blood flow
 Ischemia
 Sensitization of pain fibers

Endometrial PGF2α and PGE2
correlates with severity of
dysmenorrhea and may affect
other organs (bowel causing N/V
and diarrhea)
Lentz GM, Lobo RA, Gershenson DM,
and Katz VL. Comprehensive
Gynecology 2012. 6th Edition.
PREMENSTRUAL
DISORDERS:
Premenstrual Syndrome (PMS)
Premenstrual Dysphoric Disorder (PMDD)
Lentz GM, Lobo RA, Gershenson DM,
and Katz VL. Comprehensive
Gynecology 2012. 6th Edition.
Premenstrual Disorders: PMS and PMDD
Premenstrual Syndrome
(PMS)
Definition
is defined as a group of mild to moderate
symptoms, physical and behavioral, that
occur in the 2nd half of the menstrual cycle
Premenstrual Disphoric
Disorder (PMDD)
represents a more severe disease, with
marked behavioral and emotional
symptoms.
and that may interfere with work and personal
relationships, followed by an entirely symptomfree period.
Similarity
Differences
Manifest in the LUTEAL PHASE of menstrual cycle
Resolve during menses
Severity of symptom
Must have one severe affective symptom
which occur regularly during the last week
of the luteal phase:
Markedly depressed mood or hopelessness
Anxiety or tension
Affective lability
Persistent anger
5 of 11 symptom in the DSM-IV criteria
Lentz GM, Lobo RA, Gershenson DM,
and Katz VL. Comprehensive
Gynecology 2012. 6th Edition.
Premenstrual Disorders: PMS and PMDD
Key symptoms of PMS AND PMDD
Somatic symptoms
Affective symptoms
Abdominal bloating, swelling, weight gain
Aches
Increased appetite, food cravings Breast
pain or tenderness
Headache
Dizziness, poor coordination, clumsiness
Cramps, change in bowel habits Fatigue
Depressed mood+
Irritability, persistent anger+
Mood lability, crying, social withdrawal+
Anxiety, tension+
Feeling hopeless or guilty
Poor impulse control or feeling out of
control Decreased interest, change in libido
Insomnia
Loss of concentration, confusion
being severe before menstruation starts and mild or absent after menstruation
Modified from the American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders,
4th ed, text revision (DSM-IV-TR). Washington, DC, 2000, American Psychiatric Association, pp. 771-774.
+
Severe PMS or PMDD is based on at least five symptoms, including one
of four core psychological symptoms
Lentz GM, Lobo RA, Gershenson DM, and Katz VL. Comprehensive Gynecology 2012. 6th Edition.
Premenstrual Disorders: PMS and PMDD
PROPOSED CAUSES OF PMS AND PMDD
In summary, the cause of PMS and PMDD is associated with ovarian steroids and ovulation, which
seems to produce alterations in neurohormones and neurotransmitters that lead to a reduction of
serotonergic function during the luteal phase. Beta-endorphin, GABA, the autonomic nervous
system, and social expectations may also play a role in these complex disorders.
Lentz GM, Lobo RA, Gershenson DM, and Katz VL. Comprehensive Gynecology 2012. 6th Edition.
Premenstrual Disorders: PMS and PMDD
Premenstrual Syndrome (PMS)
Premenstrual Disphoric Disorder (PMDD)
Diagnosis
Made by history of 2 consecutive menstrual cycles demonstrating luteal phase symptoms
Medical problems influencing symptomatology must be ruled out (by history and PE)
Differential
Diagnosis
Endometriosis
Dysmenorrhea
Physical disorders with premenstrual exacerbations
Autoimmune disorders
Diabetes mellitus
Anemia
Treatment
1.
2.
3.
Hypothyroidism
Psychiatric disorders with luteal phase exacerbation
Depression
Anxiety
Dysthymic disorder
Bipolar disorder
Diet, Exercise, and Lifestyle Changes - complex CHO diet (tryptophan as source of serotonin), low fat
vegetable diet (SHBG to decrease active estrogen), high-intensity aerobic exercise, Calcium (1200mg/day x
3 months), Vit B6 (50mg/d), Mg (200-400mg/d)
Cognitive Behavioral Therapy – less effective as primary therapy, usually as supportive adjunct to managing
symptoms of PMS through group psychoeducation and relaxation therapy
Pharmacologic agents
Diuretics – for bloating, fluid retention and perceived change in body habitus; use K-sparing diuretic
(Spirinolactone 100mg/d)
Psychoactive drugs – SSRIs are extremely effective (luteal phase or continuous) – caution if px
has anxiety symptoms (FDA approved for PMDD: Fluoxetine HCl/Sarafem 20mg/d, Sertraline
HCl/Zoloft 50mg/d, Paroxetine HCl/ Paxil CR 12.5mg/d); Alprazolam 025mg TID Day 20-28/cycle;
Buspirinone less addictive potential vs Alprazolam
Oral Contraceptives – mainly for physical symptoms: breast pain, bloating, acne, and appetite.
(Monophasic OCs with shortened hormone-free interval (3-4 days) – better; FDA approved for PMDD:
Ethinyl estradiol 20 ug, drosperinone 3mg/ YAZ
NSAIDs – for cramping and other systemic symptoms (i.e. aches, diarrhea, or heat intolerance)
Danazol – for premenstrual mastalgia 200mg/day Day 20-28/cycle
Bromocriptine – for cyclic mastalgia at 2.5-5 mg/day during the luteal phase
GnRH agonists – ovulation suppression, treatment of PMS and physical symptoms of PMDD
4. Surgical Treatment: Total Hysterectomy and Bilateral oophorectomy – if all other treatment regimens
have failed.
Thank you !