91 terms

WH-Ch. 31 & 32

puberty age (mean age in US)
10-16 yo (12.4 yo)
factors that influence
1) geographic
2) nutritional
3) psychological
F weight during puberty
106 lbs
thelarche (sign of & tanner stage)
breast bud (1st sign of puberty-tanner stage 2)
early sexual maturation
first appearance of pubic hair
1st mentrual period
what regulates the release of gonadotropin
hypothalmic-pituitary system (gonadostat)
when are levels of gonadotropins & estradiol low & inhibition of GnRH
what happens as puberty approaches
loss of sensitivity by gonadostat to neg. feedback of sex steroids
what does decreased sensitivity of gonadostat & loss of inhibition of GnRH lead to
1) sleep-assoc. increases in GnRH secretions
2) pulsatile release of LH/FSH
what does increase in gonadotropin release promote
1) ovarian follicular maturation
2) sex steroid production
3) dev. of secondary sex characteristics
know tanner staging
who dev. earlier
growth spurt seen earlier in who
what does sex steroid production accelerate
fusion of long bone epiphyses
when does peak height velocity occur
1 year prior to menarche
T/F there is no significant diff. in male & female body composition prior to puberty
girls body after puberty
1) less lean body mass
2) greater % of body fat
bone age correlates w/ onset of
secondary sexual characteristics
so what to use to evaluate adolescents w/ delayed onset of puberty
osseous maturation
precocious puberty
dev. of secondary sexual characteristics at an age earlier than 2.5 standard deviations less than expected age of puberty
age for boys & girls in N. America
girls-8 yo
boys-9 yo
incidence in N American
how much more common in girls
heterosexual precocious puberty d/t
1) virilizing neoplasm
2) congenital adrenal hyperplasia
3) exogenous androgen exposure
how many cases of true isosexual precocious puberty are idopathic
other 10% are d/t
CNS d/o
children w/ precocious puberty secondary to CNS condition often exhibit what sx
neuro sx before premature puberty sx are seen
pseudoisosexual precocious puberty
elevated estrogen levels w/out activation of hypothalamic-pituitary axis
1) ovarian/adrenal neoplasm
2) exogenous estrogen exposure
3) hypothyroidism
4) McCune-Albright syndrome
5) Peutz-Jeghers syndrome
labs for precocious puberty
1) FSH
2) LH
4) Testosterone
5) 17-OH progesterone
6) 11-deoxycortisol
7) thyroid function test
8) GnRH stimulation test
radiologic eval
1) serial bone age
2) MRI or CT of brain
3) MRI, CT, US of abdomen
1) r/o organic cause
2) GnRH agonist (ex. Luprelide)
1) suppresses pituitary release of LH & FSH=arrest of gonadal steroid secretion
2) temp menopause to suspend dev. of puberty
when will N gonadotropin release & pubertal maturation resume
3-12 mo after discont.
what should behavior expectations by family members & teachers be based on
child's age (not presence of secondary sexual characteristics)
delayed puberty
failure to undergo thelarche by age 14
10% d/t (ex.)
physiologic & familial (ex. all girls in family are "late bloomers")
90% d/t
1) hypogonadotropic hypogonadism (lack of)
2) hypergonadotropic hypogonadism (increase in gonadotropin but no response in sexual organs)
testing to eval delayed puberty
radiologic & lab
1) FSH
2) karyotype
3) progesterone
4) prolactin
what does it mean if increase in FSH
ovaries fail
types of amenorrhea (def.)
1) primary
-never had period before
2) secondary
-absent >6mo
MC cause of amenorrhea
primary amenorrhea w/ sexual infantilism d/t
1) hypogonadotropic hypogonadism
2) gonadal angenesis/dysgenesis
3) 17-hydroxylase deficiency
how to determine with cause it is
measure FSH
hypogonadotropic hypogonadism d/t
1) lesion of hypothalamus or pituitary gland
2) pituitary failure
3) decrease in GnRH synthesis & release
4) CNS tumor
evaluate w/
1) MRI
2) TSH
3) GH
gonadal agenesis/dysgenesis d/t
1) karyotype abnormality
2) N karyotype w/ failure of N gonads to develop
types of karyotype abnormality
1) 45XO
2) abnormal X
3) mosaicism w/ or w/out Y chromo.
primary amenorrhea w/ N breast dev. w/ structural abnormalities categories
1) 46XX-N female karyotype
2) 46XY-complete androgen insensitivity
breast dev. in complete androgen insensitivity is d/t
conversion of male levels of androgen to estrogen
N karyotype amenorrhea cause
1) imperforate hymen
2) transverse obstructing vaginal septum
3) cervical agenesis
4) meyer-rokitansky-kuster-hauser syndrome
amenorrhea/oligomenorrhea w/ N breast dev. & uterine structure dev. d/t (MC)
1) prego*
2) asherman's syndrome
3) hypoestrogenism
asherman's syndrome
no opening in cavity
hypoestrogenism d/t
1) hypothalamic-pituitary dysfunction
2) premature ovarian failure
3) hyperprolactinemia
hypothalamic-pituitary dysfunction (ex.)
1) decreased FSH
2) decreased prolactin level
ex. athletes
premature ovarian failure (labs look like)
1) increased FSH
2) N prolactin
(looks like menopause but not)
1) decreased FSH
2) elevated prolactin
drugs that effect prolactin level
1) tranquilizers
2) antidepressants
3) antiHTN
4) narcotics
5) metaclopramide
6) estrogen
secondary amenorrhea/oligiomenorrhea common condition
1) mild hypothalamic dysfunction
2) N estrogen levels but anovulation occurs
3) have period then stops or irregular
1) nutrition/exercise
2) psychological stress
3) depo provera use
4) recent prego/lactation
1) reasurrance (w/ prego test)
2) contraception
3) fertility tx
4) periodic progestin WD
congenital adrenal hyperplasia
inborn glandular deficiency resulting in overproduction of steroids
type of inheritance
aut. rec.
cushing's syndrome
moon face, truncal obesity, HTN, osteoporosis, glucose intolerance
1) adrenal gland tumor
2) pituitary overproduction
remove steroid-producing tumor
adrenal neoplasm sx
increased steroid production
polycystic ovarian syndrome (PCOS) % in women
1) chronic anovulation or oligoovulation
2) w/ clinical or lab evidence of hyperandrogenism
time of puberty
increased risk for
metabolic syndrome
test to see how bad
FSH:LSH ratio
1) hyperandrogenic d/o
2) acranosis nigrans (brown folds)
ovarian neoplasm is what type of d/o
hyperandrogenic d/o
idiopathic hirsutism
1) androgen levels N
2) hirsutism
3) ovulation N
various hair removal
seen w/ hx
1) functional d/o appear w/ puberty & evolve over time
2) neoplastic conditions occur at any time
3) sx may be sudden
seen w/ PE
1) functional d/o
2) neoplastic condition
labs results w/ functional d/o
1) increase DHEA-S, serum 17-hyroxyprogesterone, serum cortisol
2) derease in prolactin
lab results w/ neoplastic condition
1) DHEA-S >8,000ng/mL
2) increase in testosterone (>200)
3) pelvic US
4) MRI or CT of abdomen
1) cause
2) risks (ex. DM)
if tumor
if congenital/karyotype anomaly
genetics team
if pituitary
do they want to be prego?-tx according to that