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EndoRepro 2 Exam 1 > Clin: Puberty Disorders - Moulton > Flashcards

Clin: Puberty Disorders - Moulton Flashcards

1
Q

what 6 hormones are produced by the anterior pituitary gland?

A

FSH, LH, TSH, prolactin, GH, ACTH

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2
Q

what 2 neuro-hormones are produced by the posterior pituitary?

A

vasopressin and oxytocin

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3
Q

the FOLLICULAR phase of the ovarian cycle begins with what?

A

the onset of menstruation and culminates in the preovulatory surge of LH

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4
Q

the LUTEAL phase of the ovarian cycle begins with what?

A

the onset of preovulatoy LH surge and ends with the first day of menses

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5
Q

decreasing levels of estradiol and progesterone from the regressing corpus luteum of the preceding cycle initiate what?

A

an increase in FSH by a negative feedback mechanism, which stimulates follicular growth and estradiol secretion

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6
Q

what does LH stimulate?

A

theca cells

- produce androgens (androstenedione and testosterone)

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7
Q

what does FSH stimulate?

A

granulosa cells

- convert androgens into estrogens (E1 and E2)

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8
Q

during the luteal phase, LH and FSH are significantly suppressed through negative feedback effect of what?

A

elevated circulating estradiol and progesterone

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9
Q

if conception does NOT occur during the luteal phase, what happens?

A

progesterone and estradiol levels decline as a result of corpus luteal regression

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10
Q

after corpus luteal regression, levels of what will rise, initiating new follicular growth for the next cycle?

A

FSH

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11
Q

what are the 5 peptides of the hypothalamus that have an affect on the reproductive cycle?

A

GnR, TRH, SRIF, CRF, PIF (prolactin release-inhibiting factor)

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12
Q

which peptide is responsible for the release of LH and FSH?

A

gonadotropin-releasing hormone

- acts on anterior pituitary to stimulate release of LH/FSH

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13
Q

what are the levels of estrogen during early follicular development?

A

LOW

- approx 1 week before ovulation, estradiol levels begin to increase

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14
Q

when do estrogen levels reach their maximum?

A

1 day before the midcycle LH peak

  • after peak and before ovulation, there is marked and precipitous fall
  • during luteal phase, estradiol rises to a maxim 5-7 days after ovulation and returns to baseline before menstruation
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15
Q

when does secretion of progesterone by the corpus luteum reach a maximum?

A

5-7 days after ovulation

- returns to baseline before menstruation

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16
Q
  • disruption and disitegration of the endometrial glands and stroma, leukocyte infiltration and RBC extravasion
  • sloughing of the functionalis layer and compression of the basalis layer
A

menstrual phase

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17
Q

endometrial growth secondary to estrogenic stimulation

- increase in length of the spiral arteries and numerous mitoses can be seen in the tissues

A

proliferative phase

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18
Q

following ovulation, progesterone secretion by the corpus luteum stimulates the glandular cells to secrete mucus, glycogen and other substance

  • grands become tortuous and lumens are dilated, filled with these substances
  • stroma becomes edematous
  • mitoses are rare
  • spiral arteries continue to extend into superficial layer of the endometrium and become convoluted
  • endometrial lining reaches it’s maximal thickness
A

secretory phase

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19
Q

what happens if conception does not occur by day 23?

A

the corpus luteum begins to regress, secretion of progesterone and estradiol declines, and the endometrium undergoes involution

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20
Q

1 day prior to the onset of menstruation, marked constriction of the spiral arteries occurs resulting in what?

A

ischemia of the endometrium, leukocyte infiltration and RBC extravasion
- results in necrosis that causes sloughing of the endometrium -> menstruation

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21
Q

why is an intact coagulation pathway important in regulating menstruation?

A

restoration of blood vessels requires successful interaction of platelets and clotting factors
- meds like warfarin, aspirin, and clopidogrel can impair the coagulation system and be associated with heavy bleeding

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22
Q

what is the median age of menarche?

A
  1. 43 years
    - 10% of females menstruate at 11.11 years
    - 90% are menstruating by 13.75
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23
Q

menarche occurs how long after thelarche?

A

within 2-3 years after thelarche

  • at Tanner stage IV
  • rare before Tanner stage III
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24
Q

what is primary amenorrhea?

A

no menstruation by 13 without secondary sexual development

- OR by the age of 15 WITH secondary sex characteristics

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25
Q

what was the range of most normal cycles during the first gynecologic year?

A

21-45 days

- by third year, 80% of menstrual cycles are 21-35 days long

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26
Q

what is the mean cycle interval during the first gynecologic year?

A

32.2 days

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27
Q

what was the menstrual flow length during the first gynecologic year?

A

7 days or less

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28
Q

what is the mean blood loss per menstrual period?

A

30cc

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29
Q

blood loss greater than 80cc is associated with what?

A

anemia

- changing pas q 1-2 hours is considered excessive, especially if bleeding is lasting > 7 days

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30
Q

what is the mean age of puberty?

A

12.4 (between 11-16 years)

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31
Q

onset of puberty determined by:

A
  • genetic factors
  • geographic location (metropolitan areas, near sea level began puberty earlier)
  • nutritional status (obese children have earlier onset, malnourished had later onset)
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32
Q

female infant acquires the lifetime pear number of oocytes by when?

A

16-20 weeks gestation

- 6-7 million oocytes!

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33
Q

what is termed the gonadostat?

A

the HPA regulating gonadotropin release

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34
Q

what causes low levels of gonadotropins and sex steroid during the prepubertal period?

A
  1. gonadostat sensitivity to negative feedback of low circulating estradiol
  2. intrinsic CNS inhibition of hypothalamic gonadotropin-releasing hormone (GnRH) secretion
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35
Q

between the ages of 8-11, there is an increase in what?

A

serum concentrations of DHEA, DHEA-S and androstenedione

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36
Q

what are the initial endocrine changes associated with puberty?

A

adrenal androgen production and differentiation by the zona reticularis of the adrenal cortex

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37
Q

what causes growth of axillary and pubic hair? (adrenarche, pubarche)

A

rise in adrenal androgens

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38
Q

around 11 years old, there is a gradual loss of sensitivity of what?

A

gonadostat to the negative feedback of sex steroids

- in combination with intrinsic loss of CNS inhibition of hypothalamic GnRH release

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39
Q

increase in GnRH promotes what?

A

ovarian follicular maturation and sex steroid production, which leads to the development of secondary sex characteristics

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40
Q

first physical sign of puberty

  • unilateral development in first 6 months in not uncommon
  • required estrogen
A

thelarche (breast development)

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41
Q

pubic har/axillary hair development

- required androgens

A

pubarche/adrenarche

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42
Q

onset of menses
- required pulsatile GnRH from the hypothalamus, FSH, and LH from the pituitary, estrogen and progesterone from the ovaries, normal outflow tract

A

menarche

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43
Q

when does maximal growth or peak height velocity happen?

A

about 1 year before onset of menses

- 2 years earlier in girls that boys

44
Q

thelarche, adrenarche, and menarche for white, black, and hispanic girls

A

white: 10.3, 10.5, 12.7
black: 9.5, 9.5, 12.3
hispanic: 9.8, 10.3, 12.5

45
Q

preadolescent, elevation of papilla only

A

Tanner stage 1

46
Q

breast bug stage, elevation of breast and papilla as a small mound with enlargement of the areolar region

A

Tanner stage 2

47
Q

further enlargement of breast and areola without separation of their contours

A

Tanner stage 3

48
Q

projections of areola and papilla to form secondary mound above the level of the breast

A

Tanner stage 4

49
Q

mature stage, projection of papilla only, resulting from recession of the areola to the general contour of the breast

A

Tanner stage 5

50
Q

preadolescent, absence of pubic hair

A

Tanner stage 1

51
Q

sparse hair along the labia, hair downy with slight picment

A

Tanner stage 2

52
Q

hair spreads sparsely over the junction of the pubes, hair is darker and coarses

A

Tanner stage 3

53
Q

adult-type hair, there is no spread to the medial surface of the thigh

A

Tanner stage 4

54
Q

adult-type hair with spread to the medial thighs assuming an inverted triangle pattern

A

Tanner stage 5

55
Q

development of any sign of secondary sexual characteristics prior to an age 2.5 standard deviations earlier than the expected age of pubertal onset

A

precocious puberty

  • 8 years old for girls (5x more likely in girls)
  • 9 years old for boys

NOTE: do a thorough evaluation to eliminate serious disease, and arrest potential osseous maturation that can affect normal growth patterns (can lead to premature fusion of long bones of the epiphyses)

56
Q

what are the two major subgroups of precocious puberty?

A
  1. heterosexual: develop opposite sex characteristics

2. isosexual: premature sexual maturation that is appropriate for the phenotype

57
Q

can be caused by viralizing neoplasms, congenital adrenal hyperplasia, or exposure to exogenous androgens

  • androgen secreting neoplasms (usually in ovaries)
  • congenital adrenal hyperplasia (CAD)
A

heterosexual precocity

58
Q

congenital adrenal hyperplasia most commonly results from a defect in what enzyme?

A

adrenal enzyme 21-hydroxylase

  • leads to excessive androgen production
  • classical: most severe form can cause birth of female w/ ambiguous genitalia
  • nonclassical: can cause premature pubarche and an adult disorder resembling PCOS
59
Q

results in development of the full complement of secondary sexual characteristics and increased levels of sex steroids

A

complete isosexual precocious puberty

60
Q

true isosexual precocity

A

arises from premature activation of the normal process of pubertal development involving the hypothalamic-pituitary-ovarian axis

61
Q

pseudoisosexual precocity

A

exposure of estrogens independent of the H-P-O axis

- estrogen producing tumors

62
Q

how do you diagnose true isosexual precocious puberty?

A

administration of exogenous GnRH and see a resultant rise in LH levels consistent with older girls who are undergoing normal puberty

63
Q

what is the tx of true isosexual precocious puberty?

A 
GnRH agonist (leuprolide acetate)
- suppresses pituitary release of FSH and LH, resulting in the decline of gonadotropins to prepubertal levels and arrest of gonadal sex steroid secretion
64
Q

ovarian tumor, exogenous estrogenic compound use, McCune-ALbright syndrome and Peutz-Jeghers syndrome
- increased estrogen levels that cause sexual characteristic maturation WITHOUT activation of H-P-O axis

A

pseudoisosexual precocity

65
Q

somatic mutation during embryogenesis which causes them to function independent of their normal stimulating hormones

A

McCune-Albright syndrome (Polyostotic fibrous dysplasia)

66
Q

associated with a sex cord tumor that secretes estrogen

- gastrointestinal polyposis and mucocutaneous pigmentation

A

Peutz-Jeghers syndrome

67
Q

when is puberty considered delayed?

A
  • secondary sexual characteristics have not appeared by age of 13
  • if thelarche has not occurred by 14
  • no menarche by age 15-16
  • when menses has not begun 5 years after onset of thelarche
68
Q
  • gonadal dysgenesis (Turner syndrome)
A

hypergonadotropic hypogonadism (FSH > 30mIU/mL)

69
Q
  • constitutional (physiologic delay)
  • Kallmann syndrome
  • anorexia/extreme exercise
  • pituitary tumors
A

hypogonadotropic hypogonadism (FSH + LH < 10mIU/mL)

70
Q

no spontaneous uterine bleeding by age 13, without secondary sexual characteristics
- no menstruation by 15 years with secondary sex development

A

primary amenorrhea

71
Q

patient with prior menses has absent menses for 6 months or more

A

secondary amenorrhea

72
Q

what are the diagnostic findings of primary amenorrhea with ABSENCE of secondary sex characteristics?

A

FSH, LH < 5 IU/L

  • hypogonadotropic hypogonadism
  • MRI
73
Q

mutation of KAL gene on x chromosome that prevents the migration of GnRH neurons into the hypothalamus
- patients will often have anosmia (lose sense of smell) or hyposmia

A

Kallmann syndrome

74
Q

most common form of female gonadal dysgenesis (1 in 250 births)

  • majority show no signs of secondary sex characteristics
  • mosaicism: 25%
  • webbing of neck
  • broad flat chest
  • short stature
  • streaked ovaries
  • coarctation of aorta
A

Turners syndrome, 45 XO

75
Q

46 XY

  • male levels of testosterone
  • defect in androgen receptor
  • testes in abdominal wall: secrete normal amounts of antimullerian hormones (so no uterus forms)
  • external female genitalia
  • breast development with smaller than normal areola/nipples (caused by estrogen secretion in testes and conversion of androgens to estrogen in the liver)
A

androgen insensitivity syndrome (AIS)

- tx: gonadectomy after puberty to avoid neoplasm (gonadoblastoma and dysgerminomas)

76
Q

primary amenorrhea, breast development, levels of testosterone consistent with females and karyotype 46XX

  • mullerian defects that cause obstruction of vaginal canal
  • imperforate hymen or transverse septum
  • absence of normal uterus: failure of the mullerian ducts to fuse distally and to form the upper genital tract (will have a vaginal dimple)
A

mullerian dysgenesis or agenesis

77
Q

15% of primary amenorrhea, 46XX

  • normal secondary development and external female genitalia
  • normal FEMALE range testosterone
  • absent uterus and upper vagina
  • normal ovaries
  • renal anomalies are common
  • most common cause primary amenorrhea in women with normal breast development
A

Mayter-Rokitanksky-Kuster-Hauser syndrome

mullerian agenesis

78
Q

normal uterus on US

  • imperforate hymen
  • suspect in adolescents if they present complaining of monthly dysmenorrhea without vaginal bleeding
  • vaginal bulge and midline cystic mass
A

outflow tract obstruction

- tx: hymenectomy

79
Q

these patients present with similar sx to outflow tract obstruction, but will NOT have vaginal bulge

A

transverse vaginal septum

80
Q

diagnostic evaluation of pt with secondary amenorrhea d/t:

- thyroid disease

A
  • normal prolactin

- abnormal TSH

81
Q

diagnostic evaluation of pt with secondary amenorrhea d/t:

- mild hypothyroidism

A

more often associated with hypermenorrhea or oligomenorrhea (NOT amenorrhea)
- tx should restore menses, may take several months

82
Q

what is the tx for microadenomas (<10mm) found on MRI

- typically are slow growing and rarely malignant

A

can be monitored with repeat prolactin measurements and imaging

  • tx should focus on management of infertility, glactorrhea, and breast discomfort
  • consideration for dopamine agonist
83
Q

what is the tx for macroadenoma (>10mm)

A

may be treated with dopamine agonist

- transphenoidal resection or craniotomy

84
Q

secondary amenorrhea

  • normal TSH and prolactin -> progesterone challenge test (PCT)
  • if PCT positive?
  • if PCT negative?
A

if positive: positive bleeding (normogonadotropic -> PCOS most common)
in negative: no withdrawal bleeding (indicates inadequate estrogenization or an outflow tract abnormality)

85
Q

what is performed after a progesterone challenge test?

A

estrogen/progesterone challenge test

86
Q

what does a negative estrogen/progesterone challenge test indicate?

A

outflow tract obstruction

87
Q

what does a positive estrogen/progesterone challenge test indicate?

A

abnormality with the hypothalamic-pituitary axis or ovaries

  • if FSH/LH is elevated = ovarian abnormality
  • if FSH/LH normal or low = pituitary or hypothalamic abnormality -> ORDER MRI
88
Q

what does it indicated if an MRI shows no tumor after positive estrogen/progesterone challenge test and normal/low FSH/LH?

A

hypothalamic cause of amenorrhea

89
Q
  • *leading cause of female anovulatory infertility**
  • 60-70% of patients have insulin sensitivity
  • elevated insulin and androgen levels reduce the hepatic production of sex hormone binding globulins(SHBG)
A

PCOS

  • anovulation
  • y=hyperandrogenism
  • hirsuitism
  • acne
  • menstrual dysfunction
  • hyperinsulinemia
  • LH hypersecretion
  • elevated testosterone
  • obesity, sleep disorders, acanthosis nicrigans, lipid abnormalities
90
Q

what are the 3 criteria for diagnosing PCOS (need 2/3)?

A
  • oligomenorrhea or amenorrhea
  • biochemical or clinical signs of hyperandrogenism (LH to FSH 2:1)
  • US revealing multiple small cysts beneath the cortex of the ovary
91
Q

what are the tx for PCOS?

A
  • weight loss
  • oral contraceptives (suppress gonadotropins FSH/LH, estrogen also stimulates the sex hormone binding globulin)
  • clomiphene citrate (can induce ovulation)
  • ovarian diathermy/laser tx
  • spironolactone and/or electrolysis (competes for testoterone-binding sites)
  • insulin sensitizing agents (metformin)
92
Q

excess terminal hair in a male pattern distribution
- represents exposure to hair follicles to androgen excess
0 can be familial, not always pathological
- Ferrima-Galloway scale

A

hirsutism

93
Q

masculinization of a female associated with marked increase in circulating testosterone

  • enlargement of the clitoris, temporal balding, deepening of the voice, decreased breast size, loss of female body fat distribution, and hirsutism
  • usually results from excessive male hormone production or exogenous hormone use
A

virilization

94
Q

polymenorrhagia

A

abnormally frequent menses at intervals <21 days

95
Q

menorrhadia (hypermenorrhea)

A

excessive or prolonged bleeding (>80mL and > 7 days)

- occurs at normal intervals

96
Q

metrorrhagia

A

irregular episodes of uterine bleeding

97
Q

menometrorrhagia

A

heavy and irregular uterine bleeding

98
Q

intermenstrual bleeding

A

scant bleeding at ovulation for 1 or 2 days

99
Q

oligomenorrhea

A

menstrual cycles occurring >35 days but less than 6 months

100
Q

abnormal uterine bleeding that cannot be attributed to:

  • meds
  • blood dyscrasias (thrombocytopenia, leukemia, autoimmune)
  • systemic disease
  • trauma
  • organic conditions (pregnancy, fibroids, polyps)
  • usually caused by aberrations in the HPO axis
  • most often occurs around years of menarche (11-14) or perimenopause (45-50)
A

dysfunctional uterine bleeding (DUB)

101
Q

what are the structural causes of abnormal bleeding? (PALM)

A

polyps
adenomyosis
leiomyoma
malignancy and hyperplasia

102
Q

what are the nonstructural cause of abnormal bleeding? (COEIN)

A

coagulopathy (associated with heavy flow)
ovulatory dysfunction (unpredictable menses w/variable flow)
endometrial (infection)
iatrogenic (exogenous hormones)
not yet classified (arteriovenous malformations)

103
Q

what is the workup for abnormal uterine bleeding (AUB)?

A
  • pregnancy test
  • CBC
  • targeted screening for vWF, PT/PTT
  • TSH
  • chlamydia trachomatic
104
Q

what is the tx for AUB if massive bleeding?

A

hospitalization and transfusion if unstable

- 25mg IV conjugated estrogens then normal treatment (combination hormonal therapy, mirena)

105
Q

what is the tx for AUB if moderate bleeding?

A

combination OCP’s, Mirena

106
Q

wht is the tx for AUB if unresponsive to conservative therapy?

A

D&C, polypectomy, myomectomy, endometrial ablation, hysterectomy

EndoRepro 2 Exam 1 (25 decks)

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