Amenorrhea Flashcards

1
Q

Amenorrhea

Primary vs secondary

A

Primary Amenorrhea -
No menses by age 13 without evidence of secondary sex characteristics
Lack of breast development, lack of pubic/axillary hair growth
No menses by age 15 with secondary sex characteristics

Secondary Amenorrhea -
No menses for 3 cycles or 3-6 months
Prevalence in US: Primary <0.1% vs Secondary 4%

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2
Q

Amenorrhea

causes

A

Most common - genetic disorders/gonadal dysgenesis (43%)
Pregnancy (trauma/abuse)
Hypogonadotropic hypogonadism *
Hypergonadotropic hypogonadism
Ovarian failure/ovarian insufficiency *
PCOS *
Anatomical defects
Müllerian anomaly (15%), transverse vagina or imperforate hymen
* = more likely cause secondary amenorrhea

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3
Q

Amenorrhea

Hypogonadotropic Hypogonadism

A

↓estradiol/FSH
“brain” (hypothalamus or pituitary)
Normal Karyotype (46, XX)
Constitutional Delay
Associated with stress, eating disorders, extreme exercise
Medications (antipsychotics), opioid drug abuse
Pituitary tumors

Kallmann syndrome - congenital GnRH deficiency
(anosmia - lack of sense of smell)

Endocrine disorders
Hyperprolactinemia
Hypothyroidism
Cushing Syndrome

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4
Q

Amenorrhea

Hypergonadotropic Hypogonadism

A

↑FSH/LH
Low estradiol ( = no biofeedback)
“Ovaries”

Gonadal agenesis/dysgenesis
45 XO Turner’s syndrome
Müllerian vs 46XY androgen insufficiency

Fragile X premutation
Chemotherapy/Radiation
Autoimmune oophoritis
Infection - Mumps
Surgery

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5
Q

Turner’s Syndrome

general

A

45 XO, mosaic 45X or 46XX (streak ovaries)
Short stature, webbed neck, shield chest with wide spaced nipples
Cardiac defects (bicuspid AV, coarctation aorta), aortic aneurysms
Horseshoe kidney
Increased incidence DM, autoimmune disorders, hypothyroidism

Growth hormone ages 2-5
HRT ages 12-50
Needs cardiology referral -due to possible heart defects
Referral to pediatric endocrine for GH

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6
Q

Primary Amenorrhea

labs

A

Labs/Tests:
HCG
TSH
Prolactin
FSH/LH
Free/total testosterone
PUS
Karotype

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7
Q

primary amenorrhea

Hypogonadotropic Hypogonadism – treatment

A

Correcting underlying pathology, if possible

Lifestyle Changes
Therapy

Provide estrogen/progesterone
Breast development
Closes epiphyses
Maintains bone density
Increases uterine size/proper endometrium

Ovulation Induction:
Exogenous FSH/LH
Monitor for weight - low birth weight, preterm birth

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8
Q

primary amenorrhea

Hypergonadotropic Hypogonadism - treatment

A

Provide estrogen/progesterone
Breast development
Maintains bone density
Increases uterine size/endometrium

If Y chromosome - needs gonadal removal
Germ cell tumors

Fertility - Egg donation, Adoption

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9
Q
A
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10
Q

Secondary Amenorrhea

causes

A

Most common cause - pregnancy

Anovulation
PCOS
Hypothyroidism
Hyperprolactinemia
physiologic = breastfeeding
Medications (OCP)

Estrogen Deficiency
Perimenopause
Premature Ovarian Failure (< 40 y/o) – aka primary ovarian insuffiency (POI)
Hypothalamic/Pituitary Insufficiency
Sheehan’s Syndrome

Tract Obstruction
Cervical stenosis - s/p conization
Asherman Syndrome - intrauterine adhesions s/p D&C

Hypogonadotropic Hypogonadism
Stress
Extreme exercise
Eating disorders

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11
Q

Polycystic Ovarian Syndrome

general and RF

A

Multisystem disorder that is based in androgen excess, ovulatory dysfunction and/or polycystic ovaries

Most common endocrine/metabolic disorder in females; 10-15%

Risk factors –
Genetics – first degree relative with PCOS – estimated about 70%
Premature menarche
Obesity? and/or insulin resistance (regretless of body weight)
Use of antiseizure medications – valproic acid

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12
Q

PCOS

Genetics

A

Genetics + Environment both play a role

Genome-wide association studies have determined certain susceptibility genes: loci at 2p16.3, 2p21, and 9q33.3, and involving the LH /human chorionic gonadotropin (HCG) receptor, a thyroid adenoma locus, DENND1A

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13
Q

PCOS

Patho

A

↑GnRH pulse frequency = ↑LH (>LH:FSH)

Hypersecretion of LH →↑androgen production by the ovarian theca cells

This impairs follicular development

There is also thought to be ovarian resistance to FSH due to high levels of AMH

Ovulation is inhibited and progesterone DOES NOT ELEVATE due to no corpus luteum formation

“vicious cycle”
Insulin reacts with thecal cells = ↑testosterone
Create negative feedback to hypothalamus/pituitary
Decrease insulin sensitivity which then leads to the pancreas releasing more insulin
More circulating insulin = more insulin to react with thecal cells to ↑testosterone

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14
Q

PCOS

Rotterdam criteria

A

2 out of the 3

Anovulation or oligo-ovulation
Hyperandrogenism – elevated free testosterone or clinical signs of this
Polycystic ovaries seen on PUS – “string of pearls”

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15
Q

PCOS

Signs of hyperandrogenism

A

Hirsutism
Excess in terminal hair (thick, pigmented) body hair
Male distribution: upper lip, chin, periareolar, midsternum, lower abdomen
Acne vulgaris – normally along jaw line

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16
Q

Polycystic Ovaries

US

A

Seen on PUS (usually both transabdominal and TVUS)

Presence of 12 or more follicles (small 2-9mm) or increased ovarian volume >10ml

“string of pearls”

17
Q

PCOS

Labs/imaging

A

Testing for hyperandrogenism: total and free testosterone
Ruling out other causes of oligomenorrhea:
TSH
Prolactin
HCG
17-hydroxyprogesterone – r/o non classical congenital adrenal hyperplasia (NCCAH)

PUS – transabdominal and TVUS

18
Q

PCOS

Tx

not desiring pregnancy/ post children/>35

A

Not desiring pregnancy:
Control bleeding with OCPs – usually either drospirenone or norgestimate progestin (most testosterone suppressing)
Yaz, Yasmin, Slynd; Ortho Cyclen, Ortho Tri Cyclen
Progesterone IUD – this will not help acne or hirsutism
Control hirsutism and acne by reducing testosterone
Metformin 850-1000mg BID
Spironolactone 100mg q day

Post childbearing/>35y/o
Same as ←: control bleeding and hirsutism
Manage uterine protection through perimenopause either with OCP, progestin IUD, cyclic progesterone

19
Q

PCOS

Tx for those desiring pregnancy

A

Desiring pregnancy:
Metformin 850-1000mg BID
Weight management – 5-10% can significantly reduce serum androgen levels

Letrozole (Femara) 5-7.5mg Days 3-7
now considered first line

Clomiphene citrate (Clomid)

Gonadotropin therapy – injectables; cost and multiples are a concern

20
Q

Secondary Amenorrhea

Sheehan’s Syndrome - s/p postpartum hemorrhage

A

Anterior pituitary becomes hypoxic during PPH then necrosis occurs

Results in difficulty of breastfeeding or absence of lactation

Loss of axillary/pubic hair

Acute symptoms: hypotension, tachycardia (hypovolemia) with hyponatremia and persistent hypoglycemia
Similar symptoms to hypothyroidism - fatigue, hypotension, wt gain, constipation
Hormones affected in order of severity - GH, prolactin/FSH/LH/ACTH and last TSH

MRI of pituitary to confirm diagnosis - empty sella 70%

21
Q

Sheehan’s syndrome- Secondary Amenorrhea

Tx

A

Treat hypothyroidism - levothyroxine
Cortisol deficiency - prednisone
Gonadotropin deficiency - HRT and growth hormone
Rarely, diabetes insipidus - desmopressin (DDAVP)

Referral to endocrine!

22
Q

Secondary Amenorrhea

Labs

A

Labs: HCG, prolactin, FSH/estradiol, TSH, free/total testosterone
PUS

If labs are normal, progesterone challenge
Prometrium 200mg nightly x 7-10 days, withdrawal with in 2 weeks (Provera 10mg as well)
Bleeding = estrogen present, lack of progesterone (PCOS)
No bleeding = low estrogen levels (Hypo/hypo), premature ovarian failure or outflow tract (Asherman’s or cervical stenosis)

Then give estrogen/progesterone together -
Bleeding = hypo/hypo or POF
No bleeding = outflow tract

Outflow tract -
Hysteroscope/HSG

23
Q
A