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Repro / GU > SM_207b: Endocrine Control Female Repro II > Flashcards

SM_207b: Endocrine Control Female Repro II Flashcards

1
Q

Amenorrhea is ____

A

Amenorrhea is absence of menses

  • Primary: no menarche
  • Secondary: abnormal cessation of menses (> 6 months)
  • Oligomenorrhea: infrequent menses
  • Generally associated with absent or irregular ovulation
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2
Q

Evaluation of primary and secondayr amenorrhea is the same EXCEPT ___ and ___

A

Evaluation of primary and secondayr amenorrhea is the same EXCEPT

  • If no breast development: no estrogen production, evaluation for delayed puberty
  • If breasts: assess anatomy prior to endocrine workup (15% with abnormal exam)
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3
Q

_____ is most common cause of secondary amenorrhea

A

Pregnancy is most common cause of secondary amenorrhea

  • Contraception can fail: pregnancy with tubal ligation or IUD increases ectopic risk
  • Early dating of pregnancy is critical
  • Workup: rule out pregnancy, rule out non-reproductive endocrine disorders (excess prolactin), thyroid disease, evaluate anatomy and outflow tract
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4
Q

Prolactin is responsible for ___

A

Prolactin is responsible for milk secretion

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5
Q

Lactation amenorrhea is ____

A

Lactation amenorrhea is a lack of menstrual cycles while lactating

  • Adaptive: avoid pregnancy while lactating
  • Role of prolactin
    • Hpothalamus: decreased GnRH pulses)
    • Pituitary: imhibits LH (inhibit positive estrogen feedback): no ovulation, inadequate corpus luteum
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6
Q

Describe symptoms of hyperprolactinemia

A

Hyperprolactinemia symptoms

  • Galactorrhea: milky breast discharge
  • Infertility: even when no menstrual abnormality
  • Menstrual disturbances: oligomenorrhea, amenorrhea
  • Hypogonadism: symptoms of low estrogen (hot flashes, vaginal dryness, decreased bone mineral density)
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7
Q

Prolactin is under ____

A

Prolactin is under tonic inhibition by dopamine

  • Dopamine: physiologic prolactin inhibiting factor, carried to pituitary from hypothalamus
  • Decreased dopamine levels -> increased prolactin secretion
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8
Q

Describe pharmacological causes of prolactin excess

A

Prolactin excess: pharmacological causes

  • Drugs affecting dopamine metabolism: antipsychotics, antidepressants, antihypertensives, opitates
  • Mechanisms: dopamine receptor blockers, CNS dopamine depleters
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9
Q

Describe intracranial causes of pathologic hyperprolactinemia

A

Pathologic hyperprolactinemia: intracranial causes

  • Prolactinoma: monoclonal expansion of prolactin-secreting cells
  • Interference with dopamine delivery: tumor (pituitary, hypothalamic), empty sella (compressed pituitary)
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10
Q

TRH is a ____

A

TRH is a prolactin releasing factor

  • Increases prolactin gene transcription
  • Primary hypothyroidism: increased TRH -> increased prolactin
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11
Q

Cabergoline and bromocriptin are ____

A

Cabergoline and bromocriptin are D2 dopamine agonists

(cabergoline is better)

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12
Q

Describe evaluation of anatomy and outflow tract in workup of amenorrhea and oligomenorrhea

A

Evaluation of anatomy and outflow tract in workup of amenorrhea and oligomenorrhea

  • Not pubertal: imaging
  • Pubertal: progestin challenge (will also assess estrogen status)
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13
Q

Describe progestational challenge

A

Progestational challenge

  • Progestin x 5-10 days
  • Positive withdrawal bleed 2-7 days later: implies estrogen-primed endometrium, normal anatomy with intact outflow tract, implies anovulation (lack of ovulation) with normal estrogen level
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14
Q

Describe endometrial changes in response to estrogen and progesterone

A

Endometrial changes in response to estrogen and progesterone

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15
Q

Polycystic ovary disease is caused by ____ and results in ____ and ____

A

Polycystic ovary disease is caused by excess androgen from the ovary and results in lack of selection of dominant follicle and no ovulation

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16
Q

Cyst is ____

A

Cyst is a closed sac having a distinct membrane and developing abnormally in a cavity or structure of the body

  • Polycystic ovary with multiple small follicles: eggs may degenerate
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17
Q

Describe diagnostic criteria for polycystic ovary syndrome

A

Polycystic ovary syndrome diagnostic criteria

  • Exclude other causes of hyperandrogenism
  • 2 of 3 of the following: oligo and/or anovulation, clinical and/or biochemical signs of hyperandrogenism, ultrasound with ≥ 12 follicles in each ovary 2-9 mm and/or increased ovarian volume (> 10 mL)
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18
Q

Describe pathophysiology of polycystic ovary syndrome

A

Polycystic ovary syndrome pathophysiology

  1. Excess androgen from ovary
  2. Follicles cannot convert from androgenic to estrogenic environment
  3. Dominant follicle is not selected
  4. No ovulation
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19
Q

Describe evaluation of androgen excess

A

Evaluation of androgen excess

  • Testosterone: elevation consistent with PCOS, very high levels (> 150 ng/mL suggest tumor)
  • DHEAS: elevated levels indicate adrenal source
  • 17-hydroxyprogesterone: assess in morning during follicular phase, elevated levels indicate CAH
  • 24 hour urinary free cortisol: elevated in Cushing’s syndrome
  • Rule out tumor: mostly by history
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20
Q

PCOS is associated with ____

A

PCOS is associated with insulin resistance

  • Insulin increases androgen production from ovary
  • Insulin sensitizers induce ovulation
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21
Q

Most patients with polycystic ovarian syndrome are ____

A

Most patients with polycystic ovarian syndrome are obese

  • Obesity -> insulin resistance -> increased insulin -> increased ovarian androgen
  • Weight loss leads to ovulation
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22
Q

PCOS may result in ____

A

PCOS may result in persistent anovulation

  • Loss of hormonal cycling
  • Normal estrogen levels: small follicles each make estrogen, aromatase in fat converts androgen to estrogen
  • Estrogen leads to decreased FSH via negative feedback -> promote early follicle (cyst) growth -> no dominant follicle selection
  • No ovulation: estrogen levels too low for LH surge
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23
Q

PCOS has ___ LH/FSH ratio in some

A

PCOS has increased LH/FSH ratio in some

  • Androgen overproduction
24
Q

Eugonadotropic anovulation clinical consequences are ___, ___, and ___

A

Eugonadotropic anovulation clinical consequences are

  • Infertility
  • Menstrual disturbances: 50% amenorrhea, 30% dysfunctionla uterine bleeding
  • Continuous estrogen without periodic progesterone increases risk for endometrial cancer
25
Q

PCOS treatment involves ____

A

PCOS treatment involves inducing ovulation

  • Change follicle
    • Androgenic -> estrogenic
    • Increased FSH -> increased aromatase -> increased estrogen
    • Decreased insulin -> decreased androgens
26
Q

Combination oral contraceptives for PCOS ____

A

Combination oral contraceptives for PCOS reduce ovarian androgen production

  • Decrease FSH and LSH -> decreased ovarian steroidogenesis
  • Estrogen -> increased sex hormone binding globulin -> less free testosterone
  • Benefits: reduce acne and hirsutism, cycle control to reduce risk of endometrial hyperplasia
27
Q

Describe WHO classification of amenorrhea / anovulation

A

WHO classification of amenorrhea / anovulation

  • WHO I (hypogonadotropic hypogonadism): decreased estrogen and decreased or similar FSH, hypothalamic failure
  • WHO II (eugonadotropic, most cases): constant estrogen and FSH, ovulatory disorder
  • WHO III (hypergonadotropic hypogonadism): decreased estrogen and increased FSH, ovarian failure
28
Q

Withdrawal bleed on progestin challenge in post-pubertal female indicates ____

A

Withdrawal bleed on progestin challenge in post-pubertal female indicates normal estrogen and anatomy

(PCOS: WHO II)

29
Q

Describe the estrogen-progestin challenge

A

Estrogen-progestin challenge

  • Prime endometrium with estrogen x 21 days
  • Induce progestational withdrawal bleed: progestin x 10 days
  • Positive withdrawal bleed: normal anatomy, lack of estrogen
    • High FSH: ovarian failure (WHO 3)
    • Low FSH: hypothalamic failure (WHO 1)
30
Q

Follicles ____ with age

A

Follicles age with age

31
Q

Menopause is ____ with ____ and involves ____ and later ____

A

Menopause is 1 year after final menses with ovarian failure and involves FSH elevated and later LH elevation

  • FSH elevates b/c of lack of inhibin and lack of estrogen negative feedback
32
Q

Gonadal dysgenesis involves ____

A

Gonadal dysgenesis involves streak gonads due to accelerated atresia of germ cells

  • Replacement of gonad with fibrous tissue
33
Q

Gonadal dysgenesis presents with ___, ___, and ___

A

Gonadal dysgenesis presents with lack of puberty, primary amenorrhea, and premature ovarian failure

  • Most common cause of primary amenorrhea
  • Premature ovarian failure: no estrogen produced -> increased FSH and LH
34
Q

Turner Syndrome is ____ that usually involves ____

A

Turner Syndrome is 45 XO that usually involves lack of puberty

  • Webbed neck
  • High arched palate
  • Cubitus valgus
  • Broad shield-like chest with widely spaced nipples
  • Low hairline on neck
  • Short 4th metacarpal bones
  • Disproportionately short legs
35
Q

Premature ovarian failure genetic causes are ____ and ____

A

Premature ovarian failure genetic causes are Turner Syndrome (45XO) and fragile X premutation carriers

  • Fragile X premutation carriers: > 200 CGG repeats, early menopause, carry gene for mental retardation
36
Q

____ can result in premature ovarian failure

A

Polyglandular autoimmune disease can result in premature ovarian failure

  • Auto-antibodies to endocrine organs: associated with other autoimmune disorders
  • 3% have premature ovarian failure: oocytes still present, antibodies to ovary disrupt ovulation
  • Hypothyroidism and other endocrine failure are also common
37
Q

Describe treatment of premature ovarian failure

A

Pemature ovarian failure treatment

  • Hormone replacement: induce puberty, relieve hypoestrogenic symptoms (maintain bone mineral density)
  • Fertility: oocyte donation is needed, intermittent ovulation can occur in autoimmune ovarian failure but not reliably
38
Q

Hypogonadotropic hypogonadism is ____ and occurs when ____

A

Hypogonadotropic hypogonadism is central failure and occurs when the hypothalamus and pituitary do not respond to low estrogen levels

  • Low or normal gonadotropin levels
  • Low estrogen: lack of progestin withdrawal bleeding, scant progestin withdrawal bleed
39
Q

Central factors in amenorrhea involve ____ or ____

A

Central factors in amenorrhea involve disorders of GnRH deficiency / resistance or disorders of aberrant GnRH secretion

  • Disorders of GnRH deficiency / resistance: genetic defects -> lack of puberty, destructive lesions may cause amenorrhea
  • Disorders of aberrant GnRH secretion: nutritional, environmental, or behavioral factors
40
Q

____, ____, and ____ are reversible causes of hypothalamic amenorrhea

A

Nutritional stress, physical stress, or emotional stress are reversible causes of hypothalamic amenorrhea

41
Q

LH secretion reflects ____

A

LH secretion reflects GnRH secretion

  • GnRH is released in pulses every 60-90 minutes
  • GnRH cannot be measured in the blood
42
Q

LH pulses are ____ with fasting and weight loss

A

LH pulses are lost with fasting and weight loss

  • LH pulses are restored when fasting period is over
43
Q

LH secretion ____ in anorexia nervosa

A

LH secretion decreases in anorexia nervosa

44
Q

Functional hypothalamic amenorrhea has ____ LH secretion

A

Functional hypothalamic amenorrhea has decreased LH secretion

45
Q

Describe functional hypothalamic amenorrhea traits

A

Functional hypothalamic amenorrhea traits

  • Behavioral traits: subclinical depression, subclinical eating disorder (fewer calories, lower fat, more exercise)
  • Personality traits: perfectionists
46
Q

Cortisol levels are ____ in hypothalamic amenorrhea

A

Cortisol levels are higher in hypothalamic amenorrhea

47
Q

Menarche requires ____, while menstrual cyclicity requires ____

A

Menarche requires 17% body fat, while menstrual cyclicity requires 22% body fat

  • Boys and girls have similar body fat until puberty, but girls have an increase in body fat at puberty
48
Q

Leptin is produced by ____ and signals ____

A

Leptin is produced by adipocytes and signals satiety to hypothalamus

  • Without leptin: continued eating results in obesity
  • Leptin restores normal hormone levels when fasting
49
Q

Anorexia nervosa and functional hypothalamic amenorrhea have ____ leptin

A

Anorexia nervosa and functional hypothalamic amenorrhea have low leptin

50
Q

Describe modulators of GnRH expression and release

A

Modulators of GnRH expression and release

  • Pheromones
  • Photoperiod
  • Physical stress
  • Nutritional state
  • Body fat
  • Emotional stress
51
Q

Kisspeptin ___ GnRH release

A

Kisspeptin stimulates GnRH release

  • Administration: induce puberty
  • May convey metabolic signals to GnRH neurons
52
Q

Describe treatment of hypothalamic amenorrhea

A

Hypothalamic amenorrhea treatment

  • Hormone replacement: relieve hypoestrogenic symptoms, maintain bone mineral density
  • Fertility: oral medications usually do not work, injectable medication needed
  • Behavioral therapy
53
Q

Asherman’s syndrome is ___

A

Asherman’s syndrome is intrauterine synechiae (usually multiple scars)

  • Typical history: D&C associated with infection, pregnancy
    Risk factors: prior uterine surgery (myomectomy - entering uterine cavity)
54
Q

Acquired outflow tract abnormalities causing amenorrhea are ____ and ____

A

Acquired outflow tract abnormalities causing amenorrhea are Asherman’s syndrome and cervical stenosis

  • Cervical stenosis is history of cone biopsy
55
Q

Congenital outflow tract abnormalities causing amenorrhea are ____ and ____

A

Congenital outflow tract abnormalities causing amenorrhea are urogenital anomalies and absence of Mullerian structures

  • Urogenital anomalies: usually present with pain (transverse vaginal septum, imperforate hymen)
  • Absence of Mullerian structures: androgen insensitivity, Mullerian agenesis

Repro / GU (46 decks)

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