Puberty

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APGO educational topic number 42 puberty
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meet Tina Tanner this video will discuss
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puberty the endocrine process that will
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involve Tina’s physical emotional and
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sexual transition from childhood to
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adulthood the objectives of this video
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to describe the changes in the
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hypothalamic pituitary ovarian axis and
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target organs during normal puberty
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explain the normal sequence of pubertal
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events and ages at which these changes
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occur discuss the psychological issues
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associated with puberty and finally
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define precocious and delayed puberty
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and describe the steps the initial
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evaluation of these conditions let’s
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start our discussion with the
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hypothalamic pituitary ovarian or hpo
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axis this has been quiet and all
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throughout Tina’s childhood and it
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starts to become active during puberty
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the arcuate nucleus and the hypothalamus
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releases GnRH this will stimulate the
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anterior pituitary to release the
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gonadotropins FSH and LH these will
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stimulate the ovary to produce estradiol
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and progesterone the ovary is not the
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only source of sex hormone production
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and women adren are key the production
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of androgens from the adrenal glands
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begins at approximately six to eight
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years for girls this involves the
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increased production of
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dehydroepiandrosterone which can be
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converted to the more potent and Rajan’s
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testosterone and dihydrotestosterone
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Tina’s sexual maturation will take
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approximately four years and occurs in a
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predictable sequence first there is
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growth acceleration then the larkey or
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breast development puberty or pubic hair
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development a period of maximum growth
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rate and then menarchy the onset of
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menses and ovulation estradiol from the
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ovaries will stimulate the larkey and
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androgens from the adrenal gland will
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stimulate pube Archy there is a strong
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relationship between body fat content
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and the onset of puberty mild to
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moderate obesity results in an earlier
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puberty there is also ethnic variation
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in the onset of puberty this table
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demonstrates the mean ages of theall our
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key pew bar key and monarchy and African
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American Mexican American and white
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girls the United States note that the
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mean ages for theall are key and puberty
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are almost a full year earlier for
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african-american girls compared to white
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girls the mean age for men our key is
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closer for the three different
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ethnicities the sequence of breast and
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pubic hair development
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/ the Tanner classification of sexual
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maturity this quantifies five stages
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starting with stage one being
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pre-pubertal to stage 5 which is adult
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development let’s now move to
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psychological changes prior to puberty
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there is no gender difference in
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depression rates between boys and girls
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during puberty however the prevalence of
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depression is twice as great in girls
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compared to boys during puberty girls
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can become less satisfied with their
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physical appearance and develop a
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diminished self-worth these tendencies
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have been reported to be more pronounced
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in white adolescents and this transition
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is especially difficult if there is an
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early onset of puberty let’s move now to
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precocious puberty this is the onset of
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secondary sexual development prior to
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age 6 for african-american girls and age
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7 for white girls let’s quickly diagram
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the hpo axis again here is the
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hypothalamus which secretes GnRH which
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stimulates the pituitary which will then
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stimulate the ovary to make sex hormones
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there are GnRH dependent and G and Rh
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independent causes of early sex hormone
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production GnRH dependent causes result
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from early activation of the HPA axis
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this is most commonly idiopathic other
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ideologies are infection or inflammation
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of the central nervous system and rarely
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a tumor of the hypothalamic pituitary
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stalk will cause this for the gnrh
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independent causes there is sex hormone
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production independent of HP o axis
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stimulation MacEwan albright syndrome
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results from a defect in cellular
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regulation that results in the ovary
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producing estrogen without FSH
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stimulation this syndrome is also
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characterized by multiple bone fractures
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and cafe au lait spots other causes of
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GnRH independent precocious puberty
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include ovarian tumors such as a
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granulosa cells 2 mer adrenal tumors or
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enzyme secreting defects such as
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congenital adrenal hyperplasia and
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antigenic causes such as ingestion of
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oral contraception the evaluation of
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precocious puberty should start with a
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careful history and first ask
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specifically how quickly puberty is
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progressing a rapid progression of
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puberty symptoms suggest the GnRH
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independent cause such as an ovarian
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tumor the history can also help you
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discern if the symptoms seem to be more
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from estrogen or androgen stimulation
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the next step will be physical
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examination with pubertal staging they
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should also be radiographic evaluation
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of bone age the next step will be to
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check a serum LH level first you check a
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baseline knowledge if this level is
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markedly high then the diagnosis of GnRH
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dependent precocious puberty can be made
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for an elevated LH shows that the hpo
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axis is active if the baseline LH level
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is lower intermediate the next step is
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to administer a gnrh agonist if the
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level increases then you know that you
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have a gnrh dependent etiology for the
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precocious puberty if there is no
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increase in the LH level with GnRH
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stimulation then a gnrh independent
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cause of the precocious puberty can be
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made the next step in the evaluation of
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a GnRH dependent cause of precocious
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puberty will be brain imaging the
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evaluation with a GnRH independent cause
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involves looking for a peripheral cause
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of the precocious puberty with
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laboratory testing and pelvic ultrasound
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let’s now discuss the opposite spectrum
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with delayed puberty this is when there
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is no secondary sex characteristic
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development by age 13 no evidence of
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menarche by age 15 to 16 or if menses
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have not occurred within five years of
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theall Archy there are hyper
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gonadotropic and hypokinetic tropic
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ideologies for the hypogonadism as
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associated with delayed puberty with
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hyper gonadotropic ideologies there will
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be an elevated FSH level for the hpo
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axis is activated the most common causes
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Turner syndrome the abnormality in our
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absence of one of the X chromosomes
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patients with Turner syndrome can
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present with primary amenorrhea and
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streak ovaries they can often have
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associated short stature web neck and a
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solid chest treatment in this situation
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will involve administration of estrogen
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which will stimulate breast development
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and genital tract maturation in
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hypokinetic tropic hypogonadism the
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arcuate nucleus does not secrete GnRH
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the most common etiology is
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constitutional delay which accounts for
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20% of all cases of delayed puberty this
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tends to be familial with calman
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syndrome there is hypoplastic olfactory
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tracks and the arcuate nucleus does not
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secrete gnrh young women will have
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little or no sense of smell and will
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have delayed puberty
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other ideologies include anorexia
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exercise or stress
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and craniopharyngioma is the most common
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tumor associated with delayed puberty
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lastly there are anatomic causes that
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can result in primary amenorrhea in
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girls with normal breast development
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mullerian a Genesis or Myer rokitansky
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kustra Hauser syndrome is congenital
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absence of the vagina and often uterus
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and fallopian tubes there are normal
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ovaries since the ovaries are not
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derived from mullerian structures and if
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a patient has an imperforate hymen there
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is obstruction of menstrual blood
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patients will present with uterine pain
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and a bulging vaginal introitus this
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concludes the aapko video on puberty we
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have discussed Tina’s transition through
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this process and ideologies for why she
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could have precocious or delayed puberty