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Puberty & precotious puberty
PUBERTY & PRECOTIOUS
PUBERTY
Dickson Cv BNS3 {BISHOP STUART UNIVERSITY}
Physiologic Changes with
Puberty
physiologic transition from
childhood to sexual and
reproductive maturity.
10 sexual characteristics of
the hypothalamus, pituitary,
and ovaries initially undergo
an intricate maturation
process 20 sexual x-tics
Hypothalamic-Pituitary-Ovarian
Axis
 A cascade of events unfolds in the neuro-endocrine system .
 In utero, GnRH neurons develop in the olfactory placode.These
neurons migrate through the forebrain to the arcuate nucleus of the
hypothalamus by 11 weeks of gestation.
 They form axons that extend to the median eminence and to the
capillary plexus of the pituitary portal system.
 Gonadotropin-releasing hormone is influenced by higher cortical
centers .
 Released in a pulsatile fashion into the pituitary portal plexus .
Cont…
 GnRH "pulse generator" stimulates
secretion of gonadotropins, FSH and LH,
from the anterior pituitary by mid-
gestation
 stimulates ovarian synthesis and release of
gonadal steroid hormones.
 Concurrently, accelerated germ cell
division and follicular development begins,
6 to 7 million oocytes by 5 months'
gestation.
Cont…
 By late gestation, gonadal steroids exert a
negative feedback upon both the pituitary
gonadotropins and hypothalamic GnRH
secretion.
 During this time, the oocyte number
decreases through a process of gene-
related apoptosis to reach 1 to 2 million by
birth.
Cont…
 At birth, FSH and LH levels rise abruptly in
response to the fall in placental estrogen.
 And gradually decline within the first few
months of life to reach prepubertal levels by age
1 to 4 years.
 This transient rise in gonadotropin levels vs
gonadal steroid levels, is thought to explain
instances of neonatal breast budding and minor
bleeding from endometrial shedding.
Cont…
 Childhood years are thus characterized by
low plasma levels of FSH, LH, and estradiol.
However, studies suggest that the GnRH
pulse generator is exquisitely sensitive to
minute amounts of gonadal steroids.
 True central precocious puberty may develop
as a result of premature activation of the
GnRH pulse generator.
Cont…
 During childhood, the ovary
increases in size and undergoes
active follicular growth and
atresia.
 As a result of this attrition, by
puberty only 300,000 to 500,000
oocytes remain.
Pubertal Changes
 Initial pubertal changes occur between the ages of 8 and 13 years
in North America.
 Changes before or after are categorized as either precocious or
delayed puberty and warrant evaluation.
 At approximately age 10 to 12 years, breast budding, termed
thelarche.
 This is followed by pubic hair growth, known as pubarche and then
Menarche.
 Following breast and pubic hair growth, adolescents, during a 3-
year span from ages 10.5 to 13.5 years, undergo an accelerated
increase in height, termed a growth spurt.
Precocious Puberty
 Early pubertal development may be seen
in both sexes.
 For girls, precocious puberty has
historically been defined as the
development of breast or pubic hair in
girls younger than 8 years.
Cont…
 Premature pubertal development may
result from a variety of etiologies.
 These causes have been categorized based
on the site of pathogenesis and include:
 central precocious puberty
peripheral precocious puberty
 heterosexual precocious puberty
 variations of normal puberty.
Central/true Precocious Puberty
(Gonadotropin-Dependent)
 Early activation of the hypothalamic-pituitary-
ovarian axis leads to GnRH secretion, increased
gonadotropin formation, and in turn increased
gonadal sex steroid levels.
 Central precocious puberty is rare and affects one in
5,000 to 10,000 individuals in the general population.
 The most common cause of central precocious
puberty is idiopathic, however, central nervous
systems lesions must be excluded.
Common Etiologies of
Precocious Puberty
 Central(GnRH-dependent)
 Idiopathic
 Central nervous system (CNS) tumors
 CNS infection
 Head trauma
 Iatrogenic
 Radiation
 Chemotherapy
 Surgical

Cont…
 Malformations of the CNS
 Arachnoid or suprasellar cysts
 Septo-optic dysplasia
 Hydrocephalus
 Empty sella syndrome
Peripheral (GnRH-
independent)
 Congenital adrenal hyperplasia
 Testosterone/estrogen-producing tumors
 Adrenal/ovarian carcinoma or adenoma
 Granulosa cell tumor
 Theca cell tumor
 Leydig cell tumor
 Gonadotropin/hCG-producing tumors
 Choriocarcinoma
 Dysgerminoma
 Hepatoblastoma

Cont…
Exogenous exposure to androgen or
estrogen
 Familial male-limited precocious puberty
 McCune-Albright syndrome
 Ovarian cysts
 Hypothyroidism (VanWyk-Grumbach
syndrome)
 Aromatase excess syndrome
 Symptoms of central precocious
puberty are similar to those of
normal puberty, with breast
development, growth spurt, and
eventual menses.
 However, these are seen at an
earlier age
.
DIAGNOSIS
Signs of sexual maturation
Blood and urine levels
Hormone levels
X-ray to show Bone maturation
CT/MRI to detect tumors in the
brain/ovary/testicle.
TREATMENT
 There are 2 approaches
1) Treat the underlying cause or disease
2) Lowering the high levels of sex hormones
with medication to stop the progression of
sexual development
 LHRH- synthetic hormones that block the
body production of sex hormones.
LHRH
 Synthetic hormones
 Dramatic results and no side effects
 In boys penis and testicles shrink back to
the normal size or no further development.
 In girls breast size may decrease / at least
there is no further development seen
 Growth and behavior of the child will return
to normal and will reach an appropriate
level.
CARING
 More compulsory than treatment and is very
necessary for the emotional support of the
child.
 Important points at school
1. Poor grades
2. Problems at school
3. Loss of interest in daily activities
4. Depression
SUPPORT
To create a supportive environment,
try not to focus your comments on
your child's appearance; instead,
offer praise for achievements in
school or sports and support your
child's participation in other
activities.
Puberty & precotious puberty

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Puberty & precotious puberty

  • 2. PUBERTY & PRECOTIOUS PUBERTY Dickson Cv BNS3 {BISHOP STUART UNIVERSITY}
  • 3. Physiologic Changes with Puberty physiologic transition from childhood to sexual and reproductive maturity. 10 sexual characteristics of the hypothalamus, pituitary, and ovaries initially undergo an intricate maturation process 20 sexual x-tics
  • 4. Hypothalamic-Pituitary-Ovarian Axis  A cascade of events unfolds in the neuro-endocrine system .  In utero, GnRH neurons develop in the olfactory placode.These neurons migrate through the forebrain to the arcuate nucleus of the hypothalamus by 11 weeks of gestation.  They form axons that extend to the median eminence and to the capillary plexus of the pituitary portal system.  Gonadotropin-releasing hormone is influenced by higher cortical centers .  Released in a pulsatile fashion into the pituitary portal plexus .
  • 5. Cont…  GnRH "pulse generator" stimulates secretion of gonadotropins, FSH and LH, from the anterior pituitary by mid- gestation  stimulates ovarian synthesis and release of gonadal steroid hormones.  Concurrently, accelerated germ cell division and follicular development begins, 6 to 7 million oocytes by 5 months' gestation.
  • 6. Cont…  By late gestation, gonadal steroids exert a negative feedback upon both the pituitary gonadotropins and hypothalamic GnRH secretion.  During this time, the oocyte number decreases through a process of gene- related apoptosis to reach 1 to 2 million by birth.
  • 7. Cont…  At birth, FSH and LH levels rise abruptly in response to the fall in placental estrogen.  And gradually decline within the first few months of life to reach prepubertal levels by age 1 to 4 years.  This transient rise in gonadotropin levels vs gonadal steroid levels, is thought to explain instances of neonatal breast budding and minor bleeding from endometrial shedding.
  • 8. Cont…  Childhood years are thus characterized by low plasma levels of FSH, LH, and estradiol. However, studies suggest that the GnRH pulse generator is exquisitely sensitive to minute amounts of gonadal steroids.  True central precocious puberty may develop as a result of premature activation of the GnRH pulse generator.
  • 9. Cont…  During childhood, the ovary increases in size and undergoes active follicular growth and atresia.  As a result of this attrition, by puberty only 300,000 to 500,000 oocytes remain.
  • 10. Pubertal Changes  Initial pubertal changes occur between the ages of 8 and 13 years in North America.  Changes before or after are categorized as either precocious or delayed puberty and warrant evaluation.  At approximately age 10 to 12 years, breast budding, termed thelarche.  This is followed by pubic hair growth, known as pubarche and then Menarche.  Following breast and pubic hair growth, adolescents, during a 3- year span from ages 10.5 to 13.5 years, undergo an accelerated increase in height, termed a growth spurt.
  • 11. Precocious Puberty  Early pubertal development may be seen in both sexes.  For girls, precocious puberty has historically been defined as the development of breast or pubic hair in girls younger than 8 years.
  • 12. Cont…  Premature pubertal development may result from a variety of etiologies.  These causes have been categorized based on the site of pathogenesis and include:  central precocious puberty peripheral precocious puberty  heterosexual precocious puberty  variations of normal puberty.
  • 13. Central/true Precocious Puberty (Gonadotropin-Dependent)  Early activation of the hypothalamic-pituitary- ovarian axis leads to GnRH secretion, increased gonadotropin formation, and in turn increased gonadal sex steroid levels.  Central precocious puberty is rare and affects one in 5,000 to 10,000 individuals in the general population.  The most common cause of central precocious puberty is idiopathic, however, central nervous systems lesions must be excluded.
  • 14. Common Etiologies of Precocious Puberty  Central(GnRH-dependent)  Idiopathic  Central nervous system (CNS) tumors  CNS infection  Head trauma  Iatrogenic  Radiation  Chemotherapy  Surgical 
  • 15. Cont…  Malformations of the CNS  Arachnoid or suprasellar cysts  Septo-optic dysplasia  Hydrocephalus  Empty sella syndrome
  • 16. Peripheral (GnRH- independent)  Congenital adrenal hyperplasia  Testosterone/estrogen-producing tumors  Adrenal/ovarian carcinoma or adenoma  Granulosa cell tumor  Theca cell tumor  Leydig cell tumor  Gonadotropin/hCG-producing tumors  Choriocarcinoma  Dysgerminoma  Hepatoblastoma 
  • 17. Cont… Exogenous exposure to androgen or estrogen  Familial male-limited precocious puberty  McCune-Albright syndrome  Ovarian cysts  Hypothyroidism (VanWyk-Grumbach syndrome)  Aromatase excess syndrome
  • 18.  Symptoms of central precocious puberty are similar to those of normal puberty, with breast development, growth spurt, and eventual menses.  However, these are seen at an earlier age .
  • 19. DIAGNOSIS Signs of sexual maturation Blood and urine levels Hormone levels X-ray to show Bone maturation CT/MRI to detect tumors in the brain/ovary/testicle.
  • 20. TREATMENT  There are 2 approaches 1) Treat the underlying cause or disease 2) Lowering the high levels of sex hormones with medication to stop the progression of sexual development  LHRH- synthetic hormones that block the body production of sex hormones.
  • 21. LHRH  Synthetic hormones  Dramatic results and no side effects  In boys penis and testicles shrink back to the normal size or no further development.  In girls breast size may decrease / at least there is no further development seen  Growth and behavior of the child will return to normal and will reach an appropriate level.
  • 22. CARING  More compulsory than treatment and is very necessary for the emotional support of the child.  Important points at school 1. Poor grades 2. Problems at school 3. Loss of interest in daily activities 4. Depression
  • 23. SUPPORT To create a supportive environment, try not to focus your comments on your child's appearance; instead, offer praise for achievements in school or sports and support your child's participation in other activities.