Puberty :
-it is the rendering of the Latin word
(pubertas) meaning (Grown up).it is the
stage of physical maturation in which an
individual becomes physiologically
capable of sexual reproduction and is
defind by WHO as the age between 10
and 19 years.
*usually it takes 3-4 years for the
completion of the secondary sexual
characteristics.
Factors affecting the onset of puberty:
1-gentic , a major influence.
2-Nutritional state.
3-General health.
4-Geographic location.
5-Exposure to light.
6-psychological state
Pubertal events:
*Thelarche
*Adrenarche
*Axillary hair
8- 13 years
9- 13years
10- 14years
*peak height
10- 14years
*Menarche
11- 15years
*Mature sexual hair and breasts
14- 15years
Pubertal changes before the age of 8years are
regarded as precocious puberty
Classification
1--Gonadotrop independent p.p. (True p.p.) (central)
due to premature & early activation of the
hypothalamic – pituitary – gonadal axis:a—idiopathic or constitutional
b—CNS lesions:
a-Hypothalamic tumor
b- infection
c-head injury
d-congenital defects
2--Gonadotropin – Independent p.p.
*Adrenal tumors , McCune-Albr.ght syndrome
*Endocrinopathies – congenital adrenal
Hyperplasia , primary hypothyroidism
*Accidental exposure to steroids
*Aromatase excess syndrome
3—Intermediate type p.p.
*Gonadotropin – secreating tumors – teratomas
hepatoblastoma , dysgerminoma , ovarian
granulosa cell tumor , thecoma
Diagnosis
history:-events of growth, behavioral changes , drug usage,
history of intracranial lesion ,symptoms of hypothyroidism
physical examination:general,neurological,endocriological
Visual fields assessment .
height measurements
investigation:- T3 T4 TSH , FSH , LH , E2
,Testosterone , u/s ,MRI
If normal investigation ,then assess the bone age
a-normal i.e.:- chronological age then asses E2
&DHEAS TO exclude ectopic source / ovarian / adrenal
pathology
b-low i.e.:- bone age less than
chronological age .then do T3 T4 TSH
c- higher: then we asses E2 ,LH
response to GnRH
mangment : aim:1-to identify the correctable
2-to arrest pubertal
causes
development
3-to suppress linear
growth and further
4acceleration of skeletal maturation
to prevent sexual abuse and pregnancy
5- surgery reassurance the parents
for tumors / chemo /radiotherapy
-replacement
therapy in case cah in hepothyrodism -in Mc Cune –AL
bright syndrome treatment by testolactone 40
mg/kg/day to suppress conversion of testosterone to
estrogen
- with gonadotrophines dependent giving
medroxyprogesterone acetate 100-700m im every 24weeks ,cyproterone acetate (has anti;-androgenic
gonadotropic ).or to give LHRH analogues 0.2-0.3
mg/kg maximum 7.5 mg in every 4 weeks