Which Type Of Skin Glands Are Most Affected By The Hormonal Changes That Occur During Puberty?

Introduction

Puberty is a vital process in the development of all individuals—the series of hormonal changes during puberty results in the physical evolution of sexually mature adults. In addition to sexual maturity, children besides go through other physical and emotional changes such as pilus growth, phonation changes, and acne. In this article, the evolution, organ systems involved, physiological machinery, evaluation and testing, pathophysiology, and clinical significance of puberty volition be discussed.

Cellular

GnRH neurons of the hypothalamus control the initiation of puberty. The pulsatile secretion of GnRH by these neurons causes the changes of puberty. Currently, there are increasing amounts of evidence showing that kisspeptin neurons in the arcuate nucleus release neurokinin B and dynorphin to generate the pulsatile secretion of GnRH.[ane] GnRH causes the release of LH and FSH from the gonadotropic cells of the anterior pituitary gland. FSH and LH affect the Leydig and Sertoli cells in the testes and the theca and granulosa cells of the ovary. The zona reticularis of the adrenal cortex produced the hormones responsible for adrenarche and office separately from the hypothalamic-pituitary-gonadal axis.

Development

Puberty typically begins around 6 for African American girls and 7 years of age in white girls but tin range between 8 and 13 years of historic period. The first sign of puberty is linear growth, just examiners practice not usually notice this growth. The most notable and reliable first sign of puberty in girls is chest development. Other signs of puberty include enlargement of the labia majora and labia minora and clear to white vaginal discharge. The pubertal growth spurt occurs betwixt 9 and 10 years old. Chest development (thelarche) typically occurs between 8 to 12 years old with a mean age of ten years. Menarche follows soon subsequently thelarche about two.five years later with a mean historic period of 12.five years but tin range from 9 to 15 years old.[2] Pubic hair development unremarkably follows along with breast development and occurs due to the product of adrenal androgens. Product of dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEAS) by the adrenal gland increases around age 6 to vii years and is independent of thelarche and menarche. DHEA and DHEAS influence pubic hair development equally well as axillary pilus development and trunk odor. Tanner staging is the all-time way to appraise the stage a child may be in; the categorization of each stage tin can be seen in Table 1.

Puberty in boys begins with testicular enlargement to greater than 2.5 cm in length or greater than 4 mL in volume; this occurs between ix.5 and 14 years of age with an boilerplate of eleven.5 years of age. Pubic hair development in males is controlled by both adrenal androgens DHEA and DHEAS besides as androgens produced by the testicles and usually occurs between seven and 8 years old.[2] These androgens also assist in the development of axillary and facial pilus and voice changes. Male person growth spurts typically occur between 11 and 12 years old. Other pubertal changes seen in males include a decrease in total torso fat, vocalization break and change, and an increase in muscle mass. The unlike stages of pubertal development and what qualifies for each phase can exist seen in Tabular array ii.

Organ Systems Involved

The reproductive system is the main organ system involved in puberty. The changes of puberty let the reproductive system to become fully functional. Past the end of puberty, both males and females are fertile and able to reproduce. The endocrine organization is the other major office player in puberty. The hypothalamus, pituitary gland, adrenal glands, ovaries, and testes all produce hormones involved in the changes of puberty. The hormones produced affect multiple systems within the body. The specific hormones and their involvement in the procedure of puberty are discussed further in the mechanism section.

Function

The main role of puberty is to produce sexually mature adults. The hormonal changes of puberty allow children to get reproductively viable. Puberty is likewise a flow of increased linear growth; a large portion of an individual's height is achieved from the growth occurring in puberty.

Mechanism

The mechanism of the initiation of puberty is not entirely understood; however, it is known that the GnRH neurons are the chief player in the initiation of puberty. The GnRH neurons develop in the olfactory placode and then drift to the area of the hypothalamus during the gestational period. Puberty begins with the pulsatile secretion of GnRH from these neurons; other neurotransmitters, GABA and NMDA, are as well linked with this process. Additionally, the genes KISS1 and neurokinin B have recently been shown to exist involved in the regulation of GnRH release. The increased levels of GnRH increase the release of LH and FSH from the inductive pituitary. During puberty, the negative feedback machinery is less sensitive, allowing for college FSH and LH levels to circulate within the body.

FSH increases estrogen product by the ovaries in girls, and in boys triggers testicular growth and supports maturing spermatozoa. LH initiates ovulation and creates the corpus luteum in females, and in males acts on Leydig cells in the testes to increment testosterone production. The Increased production of adrenal androgens leading to the development of acne, axillary hair, body odor, and pubic hair is also taking place during the onset of puberty. The linear growth of puberty results from pulsatile increases in growth hormone (GH) secretion, which is secreted by the pituitary gland. Increases in insulin-like growth gene ane are also present. Estrogen increases the rates of GH secretion and is involved in growth plate dispatch and fusion. Testosterone increases insulin-similar growth factor 1 levels and bursts of GH secretion.[three]

Related Testing

The first-line cess for any child experiencing issues with pubertal development is a thorough history and physical test. The history will let the healthcare practitioner to gain insight into any possibility of a genetic cause. The history will also provide vital data almost the child's growth pattern and development to appointment. Information technology may also betoken out clues to other causes of pubertal disorders such equally poor diet, underlying illness, excessive exercise, or the use of exogenous steroids. The physical exam should include examining the genitalia and the breasts in girls to determine tanner staging. Tanner staging is a standard arrangement used to categorize the different stages of pubertal development a child has accomplished. For boys, Tanner staging includes testes and penile growth, pubic hair distribution, and linear growth. In girls, Tanner staging includes breast evolution, pubic hair distribution, and linear growth. In add-on to tanner categorizations, test of the optic fundus and determining if the sense of smell is intact can be helpful. Standardized growth charts tracking the child'southward growth over time are likewise helpful in determining if a child is developing appropriately.[iv]

Peel lesions noted on the physical exam can as well betoken toward certain causes of abnormal puberty, such as McCune-Albright Syndrome. An 10-ray of the left wrist is commonly used to decide bone age and whether the child's bone maturation is more advanced than their age, suggesting they might exist going through premature puberty. In addition to an ten-ray of the left wrist, primal nervous system (CNS) imaging may exist performed if there are signs of CNS involvement. Measurement of hormone levels may also be helpful in the presence of abnormal puberty. Levels of estradiol, testosterone, FSH, and LH can be measured by checking for the presence of pubertal or prepubertal levels. A GnRH stimulation examination is too helpful to determine a central or peripheral crusade. The test involves administering 100 micrograms of GnRH after overnight fasting and observing the levels of FSH, LH, estradiol, and testosterone at 15, 30, 45, and 60 minutes post-injection. The stimulation test will cause activation of the hypothalamic-pituitary-gonadal centrality in central causes resulting in increased levels of the hormones; a peripheral cause volition not increase hormone levels.[2]

Additional testing may include thyroid hormone levels (TSH, T3, T4), blood glucose levels, a consummate blood count, liver enzymes, and an erythrocyte sedimentation rate. Another type of testing is a karyotype which will show the child's chromosomal blueprint and is helpful if there is a suspicion of Turner or Klinefelter syndromes. Although the clinician may evaluate many other factors later on a history and physical, the testing should be tailored individually for each kid's presentation and towards the about likely crusade of their abnormal puberty.

Pathophysiology

The pathophysiology of puberty tin be broken down into three master categories premature puberty, delayed puberty, and contrasexual development.

Premature Puberty

Precocious puberty or early evolution of secondary sexual characteristics is defined equally pubertal development before age 6 in African American girls and earlier 7 years in all other girls; however, an historic period of annihilation younger than 8 years is also used. Precocious puberty is defined in boys as the development of secondary sexual characteristics before historic period 9. Many of the causes of early pubertal development are shared; however, some causes of early on puberty are unique to each of the sexes.[5]

The causes of precocious puberty shared by either gender include benign premature adrenarche, fundamental nervous system and pituitary lesions, ramble and idiopathic precocious puberty, McCune-Albright syndrome, and exogenous sex hormones.

• Premature adrenarche correlates with the premature presence of pubic or axillary hair and possibly increased sebaceous gland activeness without other signs of puberty present, usually earlier 6 years of historic period. This is normally an isolated aberration, and most children go on to develop the other signs of puberty at a normal age. Plasma DHEAS is usually elevated to pubertal levels. Other sex hormones such every bit FSH, LH, estradiol, and testosterone are typically at levels found in children earlier puberty. Other studies, such as a GnRH stimulation exam, will show prepubertal results. An ACTH stimulation test may exist used to exclude congenital adrenal hyperplasia, which can have similar presenting symptoms.[two]

• CNS and pituitary lesions volition typically present with normal stages of puberty but occurring prematurely. Children may have a bone age greater than their chronological age. Additionally, these lesions may come up with other problems, such as visual field defects. If a central nervous organisation lesion or a pituitary lesion is suspected, an MRI of the brain can determine the presence of a lesion in these areas.

• Constitutional/idiopathic precocious puberty tends to present more often in females merely tin occur in both boys and girls. Precocious or premature puberty is considered idiopathic when a child has no familial links to premature development, and there is no other cause that explains the premature evolution of puberty. Constitutional precocious puberty can exist linked to a familial tendency toward early evolution. Children with these disorders will respond to a GnRH stimulation test with pubertal levels of sex hormones, including FSH and LH. These children may take a bone age that is much college than their chronological age. Additionally, all other causes of premature puberty must be ruled out, such as CNS pathology and elevated adrenal hormones.[ii]

• McCune-Albright syndrome is associated with cafe-au-lait spots, polyostotic fibrous dysplasia, and precocious puberty. McCune-Albright syndrome is likewise associated with other endocrine disorders. The cafe-au-lait spots tin exist large and have been described every bit resembling the coast of Maine.

• Exogenous sex activity hormones in substances such equally oral contraceptives and anabolic steroids tin can cause secondary sexual characteristics to develop. These causes can usually be ruled in or out as a crusade rather quickly by running a urinalysis. The metabolites of exogenous hormones tin be constitute in the urine. Additionally, children who take an exogenous hormone source and are not undergoing natural puberty will lack pubic pilus. Girls may have darkened areolae, and boys will have small testicles of a prepubertal child.[2]

Causes of premature puberty unique to males include gonadotropin secreting tumors, benign gynecomastia of adolescence, and familial gynecomastia.

• Gonadotropin secreting tumors are tumors that typically secrete hCG-like components that can have a similar function in signaling to LH, resulting in an incomplete type of premature puberty in boys. Girls, however, need FSH to increase estrogen production in the ovaries and thus, volition non have premature development due to this type of tumor lone. Examples of tumors that might produce hCG are hepatomas, teratomas, and germinomas of the pineal gland.[2]

• Benign gynecomastia of boyhood is gynecomastia in boys in mid to late puberty is very mutual. The breasts will oftentimes be tender. If the history and physical examination fall within normal limits, reassurance and monitoring are all that are necessary. The gynecomastia will ordinarily resolve on its own.[ii]

• Familial gynecomastia appears during puberty and has a genetic link, usually either x-linked recessive or sex-linked dominant. Some boys may need cosmetic surgery; withal, about will non require further evaluation unless hypogonadism is suspected.[two]

The causes of the signs of premature puberty unique to females include premature menarche and premature thelarche.

• Menarche typically occurs 2-and-a-half years after breast development begins with an average age of kickoff menses being 12.5, any menses occurring earlier the onset of breast development, without any other signs of puberty, or in a child under the age of 8 is concerning for premature menarche.[four] Premature menarche is non entirely understood; however, it is idea to exist due to transient activity by the ovaries. Premature menarche can too be the result of exogenous estrogens. Girls with premature menarche are usually merely monitored frequently to ensure at that place are no signs of underlying pathology.

• Premature thelarche is the development of breast tissue in either or both breasts without other signs of puberty present or before viii years of historic period.[two] The breast tissue does not form that of a mature breast. DHEAS is elevated to phase ii pubertal levels. Premature thelarche ordinarily can be left to resolve on its own, and biopsying this tissue is non recommended; it could completely alter the tissue and its futurity development if done.

Delayed Puberty

Delayed puberty is the lack of physical evidence of puberty past 2 to 2.5 standard deviations higher up the mean age for the initiation of puberty. In boys, this is considered a flow longer than iv years between the kickoff signs of testicular enlargement and the terminate of puberty, or the absence of testicular growth past 14 years erstwhile. Delayed puberty in girls is considered the absence of breast growth by 13 years old or more than than four years between thelarche and menarche. The causes of delayed puberty include hypogonadotropic hypogonadism, hypopituitarism, constitutional delay, chromosomal abnormalities, and hypothalamic dysfunction due to secondary causes.[6]

• Hypergonadotropic hypogonadism is the failure of the gonads to produce sexual activity hormones. FSH and LH will be elevated because at that place is no negative feedback on the hypothalamic-pituitary-gonadal axis. There can be many causes of gonadal failure, including genetics and concrete trauma. In boys, Noonan syndrome and myotonic dystrophy have been known to cause gonadal failure. Additionally, there take been cases of LH beta-receptor mutations reported in boys resulting in a lack of a gonadal response. Trauma to the testes by testicular torsion or cryptorchidism is also a cause of gonadal failure in boys. In females, autoimmune ovarian failure is a possible cause, and the kid will likely have signs or symptoms of other autoimmune weather condition. Interestingly, half of the girls with galactosemia have been shown to develop ovarian failure, probably due to toxic metabolites.[half dozen]

• Hypopituitarism is a lack of release of hormones from the pituitary gland. Delayed puberty is not the only sign of hypopituitarism. Other endocrine dysfunctions such equally hypothyroidism, os growth, and adrenal insufficiency may also be nowadays. Kallmann syndrome is a specific disorder falling under hypopituitarism where neurons in the developing brain fail to migrate, resulting in the absence of a sense of smell or anosmia and a lack of gonadotropin-releasing hormone cells in the hypothalamus.[4]

• Constitutional filibuster of puberty happens to children who have had normal development up until that point. These children then begin to fall to the bottom of the growth curve, and their growth significantly slows down. These children will have prepubertal levels of FSH, LH, estradiol, and testosterone on a GnRH stimulation exam. Eventually, puberty will spontaneously occur, resulting in the progression of development in these children. [6]

• Chromosomal abnormalities are a cause of delayed puberty shared past both males and females; however, unlike abnormalities are found as the cause in each sex. For girls, Turner syndrome is a common cause of ovarian failure where there is a trouble with one of the 10 chromosomes. These girls will often exist 45 Ten or 45 Ten/46 20. Along with ovarian failure, Turner syndrome has many other identifying characteristics, including but not limited to a webbed neck, brusk stature or delayed growth, coarctation of the aorta, a shield chest, and widely spaced nipples. Although in that location are many possible physical signs of Turner syndrome, sometimes these females are not identified until there is an absenteeism of menses or a fertility problem. This is considering some of these girls with Turner syndrome volition show the development of pubic hair and chest development. I of the most common disorders for boys is Klinefelter syndrome, which tin can take a multitude of chromosomal patterns, including 48, XXXY, 48, XXYY, and 49 XXXYY. Klinefelter syndrome typically presents with pocket-sized testes, gynecomastia, tall stature, long legs, and brusque arms. This disorder volition crusade puberty to not come to completion rather than a complete filibuster.[iv]

• In addition to the above causes of delayed puberty, pubertal delay can also occur in several illnesses where hypothalamic dysfunction tin occur. Some examples are hypothyroidism, cystic fibrosis, sickle cell disease, celiac disease, and diabetes mellitus, to proper noun a few.[6] Additionally, poor nutrition and the use of long-term glucocorticoids have been linked to delayed puberty.

Contrasexual Evolution

Contrasexual development occurs when male or female children develop physical features of the contrary gender. This condition tends to exist more common in girls and is commonly caused past polycystic ovaries and increased responses by the adrenal gland. Girls volition have a male-like distribution of hair and may develop hirsutism. Girls can also develop clitoromegaly and lose the contour of the breast mass. The possible causes include Cushing syndrome, acromegaly, exogenous androgens, adrenal tumor, ovarian tumor, and hyperprolactinemia. Although contrasexual development is less common in boys, the crusade is typically estrogen-secreting tumors.[ii]

Clinical Significance

Puberty is an extremely meaning process and a function of all children'due south evolution into functional adults. During this time, children begin to gain the capacity for reproduction, which is essential to discuss with children as they progress through puberty. Discussion of sexual practices is an important aspect of well-child visits and is pertinent to identifying children with unsafe or high-risk sexual encounters. The discussion of sexuality by pediatricians or other medical caregivers with young teens as they progress into machismo provides a hazard for them to speak to someone under confidentiality and ask specific questions to sympathize amend their sexuality as well as what is considered safe sexual practices.[vii]

Puberty likewise coincides with a child'southward psychosocial development. Children who may exist early or behind in attaining puberty milestones compared to their peers are at a much higher risk of emotional distress and depression self-esteem. The ability to monitor the progression of puberty in the pediatric population is vital as it is essential to their reproductive development but likewise because of the many physical and psychological risks children confront during this time in their development.

Review Questions

Figure

tanner staging. Created past Logen Breehl utilizing articles referenced in physiology of puberty article

References

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Loomba-Albrecht LA, Styne DM. The physiology of puberty and its disorders. Pediatr Ann. 2012 Apr;41(4):e1-9. [PubMed: 22494212]

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Klein DA, Emerick JE, Sylvester JE, Vogt KS. Disorders of Puberty: An Approach to Diagnosis and Management. Am Fam Doc. 2017 Nov 01;96(9):590-599. [PubMed: 29094880]

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Carel JC, Léger J. Clinical practice. Precocious puberty. N Engl J Med. 2008 May 29;358(22):2366-77. [PubMed: 18509122]

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Dye AM, Nelson GB, Diaz-Thomas A. Delayed Puberty. Pediatr Ann. 2018 January 01;47(i):e16-e22. [PubMed: 29323692]

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Breuner CC, Mattson G., Committee ON Boyhood. Committee ON PSYCHOSOCIAL ASPECTS OF Kid AND FAMILY HEALTH. Sexuality Education for Children and Adolescents. Pediatrics. 2016 Aug;138(2) [PubMed: 27432844]

Source: https://www.ncbi.nlm.nih.gov/books/NBK534827/

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