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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)

adrenarche

early sexual maturation

pubarche

first appearance of pubic hair

menarche

1st mentrual period

what regulates the release of gonadotropin

hypothalmic-pituitary system (gonadostat)

when are levels of gonadotropins & estradiol low & inhibition of GnRH

pre-puberty

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

h&p

who dev. earlier

blacks

growth spurt seen earlier in who

boys

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

true

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

1:10,000

how much more common in girls

5x

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

75%

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

d/t

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
3) DHEA-S
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

tx

1) r/o organic cause
2) GnRH agonist (ex. Luprelide)

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

radiologic

MRI

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

prego

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
4) ACTH

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)

hyperprolactinemia

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

d/t

1) nutrition/exercise
2) psychological stress
3) depo provera use
4) recent prego/lactation

tx

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

types

-complete
-partial

type of inheritance

aut. rec.

cushing's syndrome

hypercortisolism

sx

moon face, truncal obesity, HTN, osteoporosis, glucose intolerance

d/t

1) adrenal gland tumor
2) pituitary overproduction

tx

remove steroid-producing tumor

adrenal neoplasm sx

increased steroid production

polycystic ovarian syndrome (PCOS) % in women

6-10%

PCOS

1) chronic anovulation or oligoovulation
2) w/ clinical or lab evidence of hyperandrogenism

onset

time of puberty

increased risk for

metabolic syndrome

test to see how bad

FSH:LSH ratio

HARN-AN

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

tx

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

tx

1) cause
2) risks (ex. DM)

if tumor

remove

if congenital/karyotype anomaly

genetics team

if pituitary

meds

if PCOS

do they want to be prego?-tx according to that

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