Female Puberty

Puberty:

Is the period when the endocrine and gametogenic functions of the

gonads have first developed to the point where reproduction is
possible including physiological , morphological and behavioral
changes.
During the period from birth to puberty, a
neural mechanism is operating to prevent the
normal pulsatile release of GnRH, the
secretion of GnRH is inhibited by neurons
that release the neurotransmitter GABA.
In children between the ages of 7 and 10, a
slow increase in estrogen secretion precedes
the more rapid rise in the early teens.
The hypothalamic-
pituitary ovarian axis
The Hypothalamus Controls
the Gonads and Sexual
Activity . secretion of most of
the anterior pituitary
hormones is controlled by
“releasing hormones” formed
in the hypothalamus and
transported to the anterior
pituitary gland , the
hypothalamus does not
secrete significant quantities
of GnRH during childhood.
During the prepubertal period, the
hypothalamic-pituitary-ovarian axis
becomes activated—an event known as
Gonadarche.
The onset of puberty is initiated by some
maturation process that occurs elsewhere in the
brain in (the limbic system) (the system for
psychic control) transmit signals into the arcuate
nuclei to modify both the intensity of GnRH release
and the frequency of the pulses :
(1) the increasing levels of estrogen secretion at
puberty,
(2) the cyclical variation during the monthly sexual
cycle,
(3) the further increase in estrogen secretion
during the first few years of reproductive life.
And others related to menopause.
Onset of Puberty:
 Secretion of FSH and LH is elevated at birth and
remains relatively high for the first six months of
postnatal life, but then declines to very low levels
until puberty.
 Secretion of LH is pulsatile, and both the
frequency and amplitude of the LH pulses increase
at puberty (secretion is greater at night than
during the day).Night and sleeping!
 Because of the increased pulses of LH at puberty,
the gonads secrete increased amounts of sex
steroid hormones.
 (estradiol is the major estrogen)from the ovaries
during puberty, in turn, produce body changes
characteristic ,and progesterone control menstual
cycle and period.
Female Secondary Sex Characteristics:
Estrogen have the majer role in female sex characteristics including:

Breast:During the pubertal period, the development of breasts, is

known as thelarche.

Bone:Estrogens also regulate the growth spurt at puberty, induce

closure of the epiphyses, have a positive effect in maintaining bone
formation, and can antagonize the degrading actions of parathyroid
hormone on bone.
Body shape:Estradiol induces the increased fat in the hips.
Women have narrow shoulders and broad hips, thighs that
converge, and arms that diverge (wide carrying angle).
• Voice:, the larynx retains its prepubertal proportions and the
voice stays high-pitched.

• Hair distrubition:Women have less body hair and more scalp hair,
and the pubic hair generally has a characteristic flat-topped
pattern.

However, growth of pubic and axillary hair in both sexes is due

primarily to androgens rather than estrogens. The adrenals begin to
produce significant amounts of androgens 4 to 5 years prior to
menarche, and this event is called adrenarche.
 Menarche
 Means the beginning of the cycle of menstruation.
 Usually culminating in the onset of puberty and menstruation
between ages 11 and 16 years in girls (average, 13 years).
 In the female, the infantile pituitary gland and ovaries are capable
of full function if they are appropriately stimulated.
The first ovulation does not occur until 6 to 9
months after menarche because the
hypothalamic-pituitary axis is not fully
responsive to the feedback effects of
estrogen.
Anovulatory Cycle:

 AT Puberty - If the preovulatory surge of LH is not of

sufficient magnitude, ovulation will not occur and the cycle
is said to be “anovulatory.” The phases of the sexual cycle
continue, but they are altered in the following ways:
 First: lack of ovulation causes failure of development of the
corpus luteum, so there is almost no secretion of
progesterone during the latter portion of the cycle.
 Second: the cycle is shortened by several days, but the
rhythm continues. Therefore, it is likely that progesterone is
not required for maintenance of the cycle itself, although it
can alter the cycle’s rhythm.
 Some condition effect the onset of
puberty

 Factors stimulating the secretion of GnRH:

 norepinephrine, and neuropeptide Y
emanating from synaptic inputs to GnRH-
producing neurons.
Body fat and level of physical activity
 The age at which puberty begins is related to the
amount of body fat and level of physical activity of the
child.
 The average age of menarche is later (age 15) in girls
who are very active physically than in the general
population (age 12.6).
 This appears to be due to a requirement for a minimum
percentage of body fat for menstruation to begin;
 Recent evidence suggests that the secretion of leptin
from adipocytes is required for puberty.
Women who are very lean and physically active may
have irregular cycles and amenorrhea .
Young women who engage in strenuous athletics lose
weight and stop menstruating, as do girls with
anorexia nervosa.,may also be related to the
percentage of body fat.
However, there is also evidence that physical exercise
may act to inhibit GnRH and gonadotropin secretion
Precocious puberty:
Precocious puberty : defined as sexual maturation
before the age of 8 years,
True precocious puberty - no cause can be determined
results from premature activation of the hypothalamic-
pituitary-gonadal axis, leading to the development of
secondary sex characteristics as well as gametogenesis.
The most frequent causes are :
• CNS lesions or infections,
• Hypothalamic disease, and
• Hypothyroidism.
PRECOCIOUS PUBERTY:

 Precocious pseudopuberty :Early development of secondary

sexual characteristics without gametogenesis is caused by
abnormal exposure of immature females to estrogen.
 This syndrome distinguish it from true precocious puberty
due to an early but otherwise normal pubertal pattern of
gonadotropin secretion from the pituitary.
 Excess androgen secretion causes masculinization
(adrenogenital syndrome) and precocious pseudopuberty or
female pseudohermaphroditism.
 Classification of the causes of precocious
sexual development in humans
.
 True precocious puberty
 Constitutional
 Cerebral: Disorders involving posterior hypothalamus
 Tumors
 Infections
 Developmental abnormalities
 Gonadotropin-independent precocity
 Precocious pseudopuberty (no spermatogenesis or ovarian development)
 Adrenal
 Congenital virilizing adrenal hyperplasia
 Estrogen-secreting tumors (in females)
Delayed or Absent Puberty:
The normal variation in the age at which adolescent
changes occur is so wide that puberty cannot be
considered to be pathologically delayed until the
menarche has failed to occur by the age of 17.
causes:
 Hypogonadism: primary defect in gonads or
secondary defect in hypothalamic pituitary axis.
 Failure of maturation due to panhypopituitarism
is associated with dwarfing and evidence of other
endocrine abnormalities.
 Puberty is delayed even though the gonads are
present and other endocrine functions are called
primary amenorrhea.
 Hypogonadism-Reduced Secretion by the
Ovaries:
 When ovaries are absent from birth or when they
become nonfunctional before puberty, female
eunuchism occurs.

 In this condition the usual secondary sexual

characteristics do not appear, and the sexual
organs remain infantile. Especially characteristic
of this condition is prolonged growth of the long
bones because the epiphyses do not unite with the
shafts as early as they do in a normal women.
Genetic Defects:

Examples include
(1) GnRH resistance, FSH resistance, and LH
resistance, which are due to defects in the GnRH, FSH,
or LH receptors, respectively,
(2) aromatase deficiency, which prevents the formation
of estrogens.
(3) mutations, somatic mutation after initial cell
division has occurred in the embryo. It is associated
with multiple endocrine abnormalities, including
precocious puberty and amenorrhea with galactorrhea.
REFERENCE:

 HALL, J. E., & GUYTON, A. C. (2011). Guyton and

Hall textbook of medical physiology. Philadelphia,
PA, Saunders Elsevier.
 FOX, S. I. (2011). Human physiology. New York,
McGraw-Hill.
 BARRETT, K. E., BARMAN, S. M., BOITANO, S.,
BROOKS, H. L., WEITZ, M., KEARNS, B. P., GANONG,
W. F., & GANONG, W. F. (2016). Ganong's review of
medical physiology. New York, McGraw-Hill
Medical.