menstruation Flashcards
primary amenorrhea:
-absence of menarche by age 15
secondary amenorrhea:
absence of menses for 6 mo or greater in a woman previously menstruating
Informally: denotes any missed menses in a woman previously menstruating
Dysfunction of any part of the HPO axis can cause amenorrhea.
Often it’s useful to think about causes as
- Hypothalamic
- Pituitary, or
- Uterine/vaginal in origin.
Primary amenorrhea etiology:
Chromosomal abnormalities Structural abnormalities: -Absence of the uterus, cervix, and/or vagina -Transverse vaginal septum or imperforate hymen Hypothalamic causes Pituitary causes Ovarian causes Other
most common chromosomal cause of amenorrhea:
Turner syndrome
45, XO aka turners:
1/2500 live births, but…
99% of 45, XO conceptions are lost prior to birth, usually in the first or second trimester
Turner syndrome includes:
- short stature
- infertility
- primary gonadal failure
- osteoporosis
Turner Syndrome and amenorrhea:
Ovaries are replaced by fibrous tissue (“streak gonads”)
Little or no estrogen production is possible
Managed with hormone replacement starting in teens
Normal uterus and vagina are usually present
Pregnancy possible with donated egg, IVF
Mosaic turners:
only missing X chromosome in some cells.
- soft signs of turners
- risk for premature menopause
Mullerian abnormalities:
Remember that the paramesonephric ducts fuse to form the primordial uterovaginal tissue, and subsequently the fallopian tubes, uterus and upper 1/3 of the vagina
-can cause amenorrhea by causing absence of uterus, cervix or vagina
Mayer-Rokitansky-Kuster-Hauser syndrome:
uterus does not fully develop and undeveloped vaginal canal
Transverse vaginal septum:
the result of abnormal apoptosis of the vaginal plate.
Can occur at multiple levels.
This can involve both Mullerian tissue and Urogenital (external genitalia) tissue.
Imperforate hymen:
Absence of appropriate apoptosis of the cells of the hymenal membrane, which originates from cells of the urogenital sinus (external tissue).
This finding is more common than Mullerian abnormalities, and can be partial or complete.
risk of hematometra or hematocolpos (blood back up into abd) is possible
presentation of structural causes of primary amenorrhea:
Congenital anomalies of the uterus and vagina present with cyclic pelvic pain, possible pelvic mass if functional endometrium is present.
If uterus, endometrium are absent then patient will be asymptomatic except for amenorrhea.
Management of structural causes of primary amenorrhea:
Resection if it’s an imperforate hymen, vaginal septum
Hysterectomy for absent cervix
Creation of neovagina if necessary
Hypothalamic causes of amenorrhea:
Functional hypothalamic amenorrhea Hypothalamic malfunction due to significant physical or psychological stressors, e.g.: -Eating disorders (e.g. anorexia nervosa) -Vigorous exercise -Very low body fat -High emotional or physical stress Treat by: - addressing behavioral issues/stressors -hormone supplementation -Weight gain if indicated
or
Kallmann syndrome
or
Infiltrative dz and tumors of hypothalamus
Kallmann syndrome:
congenital GnRH deficiency classically associated with anosmia
also associated with decreased tanner staging
- manage with E/P therapy
- GnRH can be used to induce ovulation
Pituitary causes of primary amenorrhea:
Hyperprolactinemia due to pituitary adenoma
May be associated with galactorrhea
This is more likely to present as secondary amenorrhea– will discuss later
Ovarian causes of primary amenorrhea
PCOS
Premature ovarian failure
These also are more likely to present as secondary amenorrhea
Androgen insensitivity syndrome (“testicular feminization”)
primary amenorrhea
46 XY karyotype with nonfunctional androgen receptors
Female phenotype
Genetic mutation causes severe impairment in androgen receptor function
Testes may be present in labia
No internal female organs (vagina, cervix, uterus, ovaries)
Removal of gonads after puberty recommended due to risk of malignant transformation
primary amenorrhea work-up:
History General health status (neonatal and childhood) Pubertal milestones Change in weight Exercise habits Medication history Family history Physical exam Height and weight Skin Breast development Pelvic examination (or rectal examination) to detect pelvic organs, masses Syndromic features Ultrasound may be needed to confirm presence or absence of ovaries, uterus, cervix, testes Diagnosis Labs If uterus/vagina present: B-HCG, FSH, karyotype if FSH elevated, prolactin If uterus is absent Karyotype, serum testosterone
*** most common cause of secondary amenorrhea?
pregos
excluding pregnancy from secondary amenorrhea:
Serum measurement of B-hCG is the most sensitive test for pregnancy
The only way to exclude pregnancy is by a pregnancy test
Don’t take sexual history at face value
Most common etiologies of secondary amenorrhea:
Ovarian and then hypothalamic
Secondary Amenorrhea can be iatrogenic!
medication induced amenorrhea:
Hormonal contraceptives Progestin IUD Metoclopramide (Reglan) Causes hyperprolactinemia Antipsychotic drugs (e.g. Thorazine, Haldol, Risperdal) Cause hyperprolactinemia; see above
Hypothalamic causes of secondary amenorrhea:
Functional hypothalamic amenorrhea (see prior slides)
Decreased GnRH secretion
commonly associated with anorexia nervosa, low body weight, low body fat, excessive exercise, emotional stress, acute severe illness
Risk of osteoporosis due to low estrogen levels
Infiltrative lesions of the hypothalamus
Lymphoma, sarcoidosis, etc.
Celiac disease
Nutritional deficiency can impact hypothalamic function
Pituitary causes of secondary amenorrhea:
Pituitary Adenomas
90 % are prolactinomas
10% other pituitary masses and disease
Thyroid: hyper or hypo can cause it through interactions with pituitary
Ovarian causes of secondary amenorrhea:
Polycystic ovarian syndrome (PCOS) Cause of 20% of amenorrhea Associated with hyperandrogenism, infrequent or absent menses, polycystic ovaries on ultrasound , obesity Diagnosis of exclusion You’ll have a lecture on this.
Premature ovarian failure (primary ovarian insuffiency)
Depletion of functional oocytes before age 40
Causes: genetic, autoimmune, cancer treatment, unknown
secondary amenorrhea and uterine disorders:
Asherman’s syndrome
Acquired scarring of the endometrial lining, due to prior surgery or intrauterine infection
See yesterday’s lecture
Diagnosing secondary amenorrhea:
-* first B-hCG to rule out prego
-History
Stress
Weight loss / changes in diet
Exercise
Medications
Acne, hirsutism, voice changes
Headaches, vision changes, polydipsia, polyuria
Hot flashes, vaginal dryness, disturbed sleep
Galactorrhea
History of uterine surgery or infection
-Physical exam
Height, weight
BMI
>30 suspect PCOS
<18.5 suspect functional hypothalamic amenorrhea
Skin (acne, hirsutism, striae, vitiligo, etc)
Breasts (galactorrhea)
Pelvic exam (signs of estrogen deficiency)
-Labs:
B-hCG
Prolactin
FSH
TSH
Serum testosterone (if signs of androgen excess)
A useful tool: the Progestin withdrawal test
Provera 10 mg/d x 10 d, then stop.
Withdrawal bleeding indicates presence of estrogen
Failure to bleed indicates inadequate estrogen or endometrial scarring
If no menses occurs: Supplement with estrogen, then repeat progestin withdrawal.
No bleeding indicates Asherman’s syndrome
Bleeding indicates an intact uterus/endometrium that is not receiving estrogen/progesterone– POF, hypothalamic amenorrhea, etc
For functional hypothalamic amenorrhea:
Lifestyle changes (adequate caloric intake, moderate exercise, stress reduction)
Intervention for eating disorders
Consider combined OCs for osteoporosis prevention
For Hyperprolactinemia:
Dopamine agonist (cabergoline, bromocriptine) Surgery for selected macroadenomas (large, poor response to medication)
For Premature Ovarian Failure:
Estrogen/progestin therapy to prevent bone loss, manage menopausal sxs
For Asherman’s syndrome:
Hysteroscopic lysis of adhesions
Long-term estrogen supplementation for endometrial growth
primary Dysmenorrhea:
Pelvic pain that occurs during menstruation in the absence of pelvic pathology
Secondary dysmenorrhea:
Pain with menses that results from pathologic changes in the pelvic viscera
Primary Dysmenorrhea
Begins with the onset of regular ovulatory cycles (usually 1-3 years post-menarche)
Cramps may be accompanied by nausea, vomiting, diarrhea, back pain, headache, dizziness
Symptoms start just prior to flow onset and may last several days
Present in 60% of teens
15% will seek medical attention
what is primary dysmenorrhea caused by?
Caused by excess production of endometrial prostaglandins
Increased uterine contractions
Dysrhythmic or tetanic uterine contractions
Increased uterine muscle tone
GI tract stimulation
dx of primary dysmenorrhea:
Get a thorough medical history; rule out other pathologies
Age at menarche
Details of menstrual cycles (frequency, regularity, duration)
LMP
Onset and duration of cramps
Presence of associated sxs (nausea, vomiting, headache, etc)
Severity / impact on daily activities
Treatment history
Sexual history, especially hx of STIs
You need to include a pelvic exam if:
Sxs are severe
Pt is sexually active
Pelvic exam can be omitted if pt is not sexually active and symptoms are mild
Transabdominal ultrasound may be a useful alternative to rule out other pelvic/ abdominal pathologies
Managing primary dysmenorrhea:
NSAIDs, NSAIDs, NSAIDs!
Ibuprofen, naproxen, mefenamic acid
Start with onset of menses, continue until sxs abate
May need to start 1-2 days prior to menses if sxs severe
May need maximum dosage (e.g. ibuprofen 800 mg q8h)
Take with food to minimize GI upset
-because NSAID are antiprostaglandins
what do you do if nsaids for dysmenorrhea don’t work or if pt is sexually active?
Combined OCP’s
If NSAIDs fail or are not tolerated, OR in a sexually active patient!
Suppression of ovulation decreases prostaglandin production
Long-term use decreases menstrual flow
Allows for scheduled or deferred menses
Modality of choice if patient
is sexually active
-can combine with NSAIDs
-if failed rule out secondary causesWatch for these “Red flags” of primary dysmenorrhea – should warn you that it may be deeper than initially thought…
Failure to improve with NSAIDs + OCs Symptoms that worsen on treatment Onset of sxs with menarche (rather than 1-2 y later) Pelvic pain outside of menses History of STI Consider referral for laparoscopy
secondary dysmenorrhea etiologies:
Endometriosis Adenomyosis Uterine leiomyomata Ovarian cysts Pelvic adhesions Chronic PID Obstructive uterovaginal anomalies Cervical stenosis Copper IUD IBS Inflammatory bowel disease Interstitial cystitis
secondary dysmenorrhea diagnostic clues:
The prevalence of secondary dysmenorrhea increases with age
The prevalence of primary dysmenorrhea decreases with age, and may remit after a term pregnancy
suggestive hx of secondary dysmenorrhea:
Onset after age 25 Abnormal uterine bleeding Non-midline pelvic pain Absence of other menstrual sxs (nausea, vomiting, headache, etc.) Presence of dyspareunia or dyschezia Progressive sxs
diagnosis of secondary dysmenorrhea:
Pelvic exam findings are critical
Purulent cervical discharge
Cervical motion and/or adnexal tenderness
Nodularity of uterosacral ligaments
Uterine enlargement or irregularity
Adnexal mass
Pelvic ultrasound may be useful to clarify above findings
Labs- screen for G/Chl
-laparoscopy or hysteroscopy may be needed
management of secondary dysmenorrhea:
NSAIDs, analgesics, etc. OCs, medicated IUD Treat the underlying disorder, e.g. Antibiotics for pelvic infection Cautery of endometrial implants Hormonal tx for endometriosis Resection of symptomatic fibroids Ovarian cystectomy Hysterectomy Drug tx for inflammatory bowel disease Drug tx for interstitial cystitis
Menorrhagia:
prolonged and or heavy menses
- blood loss >80 ml
prolonged menses:
> 7 days
metrorrhagia:
irregular bleeding, especially between menses
menometrorrhagia
excessive and irregular uterine bleeding
dysfunctional uterine bleeding (DUB)
Abnormal bleeding not from anatomic abnormality, generally anovulatory bleeding.
polymenorrhea
-cycle length less than 24 days
DUB causes:
Common in adolescence, perimenopause, PCOS, thyroid disorders
Anatomic abnormalities
Endometrial polyp
Uterine leiomyomata, especially submucosal
Adenomyosis
Uterine malignancy
