Puberty In Girls - pediagenosis
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Monday, October 8, 2018

Puberty In Girls

Puberty In Girls
Puberty is the process by which the immature individual will acquire the physical and behavioral attributes that allow him or her to reproduce. In girls, puberty is largely the response of the body to the widespread actions of estrogens, secreted by the newly awakened plural-ovaries under the influence of gonadotropins secreted by the anterior pituitary. While the progression of pubertal changes is predictable, age of onset differs dramatically in different areas of the world and even among children of different ethnic backgrounds within a particular region. Economic disparities may also be reflected in the age of pubertal onset.

 Physical changes of puberty
In North American and European girls, puberty visibly begins with breast development between the ages of 8 and 10. Other secondary sexual characteristics appear over the ensuing 2.5 years. Puberty culminates with onset of menstruation. The average age of menarche in Caucasian girls is 12.8 ± 1.2 years and, on average, 4–8 months earlier in African-American girls.
The physical changes of puberty in girls have been divided into five stages using a system developed by Marshall and Tanner, who examined groups of English girls as they went through sexual maturation (Fig. 12.1). They then classified the relative and absolute changes in the sexual characteristics of the participants. Although they did not regard their findings as universal, their system has been widely used to describe the timing and progression of typical pubertal changes. Their descriptions must be recognized as specific to the demographics of their study population and to the years covered by the study. Pat- terns persist, but the characteristics and timing of these changes are affected by race, nutrition and other genetic and environmental factors.
This describes the contribution of the adrenal gland to puberty in both girls and boys. It is a developmentally programmed increase in adrenal synthesis and secretion of the weak androgens: androstenedione, dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S). Adrenarche begins at about ages 6–8 years in girls. Secretion of weak adrenal androgens precedes the visible onset of puberty by about 2 years. DHEA and DHEA-S are responsible for initiating growth of pubic and axillary hair as well as growth of and secretion by axillary sebaceous glands. Axillary and pubic hair appear in parallel with the beginning of breast development and visibly mark the onset of puberty in girls.
The exact trigger for adrenarche is not known. It is independent of adenocorticotropic hormone (ACTH) release, gonadotropin release and ovarian function, and appears to be an intrinsic, programmed event within the adrenal gland. Adrenarche is distinct from the other events of puberty (pubarche) and either may occur in the absence of its counterpart.

Breast development (thelarche)
The mammary gland, or breast, is an ectodermal derivative. The breast tissues are remarkably sensitive to hormones. Such hormonal effects are most notable during embryonic development and after puberty. The basic structure of the breast is common to all mammals although there exist wide variations in the number of mammary glands, their size, location and shape. Each mammary gland comprises lobulated masses of glandular tissue. Glandular tissues are embedded in adipose tissue and separated by fibrous connective tissues. Each of the lobes contains lobules of alveoli, blood vessels and lactiferous ducts. See Chapter 23 for a more detailed description of the structure and function of the human breast.
At birth, the breasts consist almost entirely of lactiferous ducts with few, if any, alveoli. These rudimentary mammary glands are capable of a small degree of secretory function (“witch’s milk”) within a few days of birth. Breast secretion in the neonatal period occurs in response to the high prolactin levels in the newborn infant following prior exposure of the fetal breast to high concentrations of placental estrogen during gestation. After placental estrogens are cleared from the neonatal circulation, the breast enters a dormant phase until puberty. With the onset of puberty, ovarian estrogens induce growth of the lactiferous duct system. The ducts branch as they grow and their ends form into small, solid, spheroidal cell masses. These structures will form the lobular alveoli. The breast and alveoli enlarge. With menarche, cyclic estrogen and progesterone secretion begin and an extra phase of ductal and rudimentary lobular growth will occur. Adrenal corticosteroids further enhance duct development. The breasts continue to increase in size for some time after menarche due to deposition of fat and additional connective tissue. Final breast differentiation and growth will not occur until pregnancy.

Secondary sexual characteristics
Ovarian estrogens also produce the following changes in pubertal girls:
               Pubic hair.
               Keratinization (cornification) of the vaginal mucosa.
               Enlargement of labia minora and majora.
               Uterine enlargement.
               Increased fat deposition in hips and thighs.

Somatic growth
The pubertal growth spurt in girls typically begins 2 years before it begins in boys, accounting for about 50% of the 12 cm difference in average height between men and women. The other 50% results from a slower rate of growth during the spurt in girls compared with boys. The mechanisms by which sex steroids induce bone growth in girls are the same as in boys (Chapter 11). Structural growth ceases at a median age of 17 years in girls.

The term used to describe the onset of menstrual cycles. It is the culmination of a complex sequence of events that involves maturation of the hypothalamic–pituitary–ovarian (HPO) axis to produce both mature ova and an endometrium that can support a zygote if fertilization should occur. The three stages of maturation of the HPO axis include: (i) an increase in the release of follicle-stimulating hormone
(FSH) and luteinizing hormone (LH) from the pituitary gland; (ii) ovarian recognition of, and response to these gonadotropins, allowing production of ovarian steroids (estrogen and progesterone); (iii) establishment of positive feedback regulation of the hypothalamus and pituitary gland by estrogens. The combination of these maturational events permits ovulation.
Throughout childhood, FSH and LH concentrations within the pituitary gland and plasma of boys and girls are low. As described in Chapter 11, the pulse amplitude and frequency of FSH and LH release are also low, suggesting the gonadotropin-releasing hormone (GnRH) pulse generator is cycling slowly. This characteristic pattern has been called the juvenile pause. The first endocrinologic manifestation of puberty is an increase in FSH and LH pulse amplitude. At its initiation, this increase is most notable during sleep, although the diurnal sleep– awake difference in FSH and LH secretion is almost obliterated by the end of puberty.
The initiation of puberty remains incompletely understood. Still, most agree it must be related to a release of the hypothalamic GnRH pulse generator from CNS inhibition.
There has been much interest in the observation that the age of menarche decreased by 2–3 months per decade during the 150 years preceding World War II and then stabilized over the next 50 years. A decrease was again noted in recent studies, thought to represent the influence of optimal nutrition. Onset of menarche is closely related to attainment of a crucial percentage of body fat. Two metabolic signals have been recently identified that can act centrally and may be causal in pubertal events: insulin-like growth factor 1 (IGF-1) and leptin. Serum IGF-1 levels increase during childhood and peak at puberty: the increase parallels that of DHEA-S, the marker of adrenarche. Leptin, a hormone signaling satiety, inhibits neuropeptide Y (NPY). NPY is a mediator of food intake, but also controls GnRH neuronal activity in the hypothalamus. Serum leptin levels increase in both sexes prior to onset of puberty. Rising leptin levels inhibit NPY. This, in turn, releases GnRH from its prepubertal inhibition. Leptin levels continue to rise throughout puberty among healthy females, but fall fairly rapidly after pubertal initiation in males.
Maturation of the ovary at puberty allows initiation of estrogen production by the granulosa cells surrounding the ova. Waves of granulosa cells undergo development and sub sequentatresia as puberty progresses. Ova begin to mature under the influence of ovarian estrogen produced by these granulosa cells. In addition to oocyte maturation, estrogen from the granulosa cells will regulate production of gonadotropins by the pituitary gland. With complete maturation of the HPO axis, this estrogen will drive maturation of a dominant ovarian follicle, culminating in ovulation. With ovulation of the first ovum, the collapsing ovarian follicle reconfigures itself as a corpus luteum and begins to produce progesterone. The endometrium responds to estrogen by proliferating and to progesterone by converting to a secretory tissue capable of supporting embryo implantation. In the first years after menarche many menstrual cycles will be anovulatory, reflecting the incomplete maturation of the hypothalamic positive feedback response to ovarian estrogen. The menstrual bleeding patterns often encountered soon after menarche represent continuous exposure of the endometrium to estrogen and sloughing of proliferative or hyperplastic endometrium. Because no corpus luteum forms in the absence of ovulation, the endometrium cannot exhibit the progesterone effect that makes menstruation a self-limited phenomenon. This anovulatory bleeding can be very unpredictable and quite heavy. By 5 years after onset of menarche, 90% of girls have regular, ovulatory menstrual cycles.

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