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Puberty & adolescence by Pandian M, Tutor, Dept of Physiology, DYPMCKOP,MH

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Introduction
Components of puberty
Sudden spurt of physical growth
Appearance of secondary sex characters
Stages of development of secondary sex characters.
Types of secondary sex characters.
Hormonal changes during puberty
Control of onset of puberty
Applied aspects

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Puberty & adolescence by Pandian M, Tutor, Dept of Physiology, DYPMCKOP,MH

  1. 1. PUBERTY & ADOLESCENCE Pandian M Dept of Physiology DYPMCKOP
  2. 2. •What changes occur in males and females at puberty? •What do the terms menarche and menopause mean?
  3. 3. SLO •Introduction •Components of puberty •Sudden spurt of physical growth •Appearance of secondary sex characters • Stages of development of secondary sex characters. • Types of secondary sex characters. •Hormonal changes during puberty •Control of onset of puberty •Applied aspects
  4. 4. INTRODUCTION •Puberty and adolescence are the phases of growth between childhood and adulthood. •Puberty refers to the stage of gonadal development •Maturation to the point where reproduction is possible for the first time. •Adolescence refers to the period of sudden spurt of physical growth between childhood and adulthood
  5. 5. CONT…. • Two phases (adolescence and puberty) of growth are overlapping, hence the terms are interchangeable. • The total period of growth spurt ranges between 3 and 5 years. • It starts from the age of 8 years. • The average age of onset of puberty is 12 years in girls and 14 years in boys.
  6. 6. FEMALE •In girls, the first event is thelarche , the development of breasts •Followed by pubarche , the development of axillary and pubic hair, and •Then by menarche , the first menstrual period.
  7. 7. COMPONENTS OF PUBERTY The two principal components of puberty are: 1. Sudden spurt of physical growth 2. Appearance of secondary sex characters.
  8. 8. 1. SUDDEN SPURT OF PHYSICAL GROWTH • During sudden spurt of physical growth, there is increase in height, muscle mass and muscle strength of an individual. • The height increases by 7–12 cm in boys and about 6–11 cm in girls. • The increase in height is mainly of the trunk part rather than of limbs. • The muscle mass and muscle strength also increases in both the sexes but the increase is far greater in boys as compared to in girls.
  9. 9. 2. APPEARANCE OF SECONDARY SEX CHARACTERS •Stages of development of secondary sex characters. •The sequence of events of puberty which occurs in 3–5 years •Period have five stages.
  10. 10. TYPES OF SECONDARY SEX CHARACTERS. •The secondary sex characters are almost fully developed by the stage 5 of the puberty both in male and females. •These can be grouped as: - Structural, - Functional and - Psychological.
  11. 11. HORMONAL CHANGES DURING PUBERTY • Besides ovaries and testes, other endocrinal glands (adrenal, thyroid and anterior pituitary) also grow in size. • Their activity increases at the onset of puberty. • The hormonal changes noticed at the time of puberty are: 1. Gonadotropins. 2. Adrenal androgens. 3. Growth hormone. 4. Thyroid gland secretions 5. Gonadal hormones
  12. 12. 1. GONADOTROPINS. • In both sexes, the levels of gonadotropins: • The anterior pituitary gland secrete follicle stimulating hormone (FSH) and luteinizing hormone (LH) • The secretion rise slowly from birth of the child up to pre- adolescent age. • At the time of puberty (early teen age) their levels suddenly increase. • In pre-pubertal stage, the gonadrotropin secretion is not under the check of gonadal hormones (oestrogen and testosterone).
  13. 13. 2. ADRENAL ANDROGENS. • There is an increase in the secretion of adrenal androgens at puberty. • The onset of this stage of increase or activation is called adrenarche. • It occurs at 8–10 years of age in girls and at 10–12 years of age in boys. • Functions :- • subserved by adrenal androgens at puberty are: • Growth of pubic and axillary hair in both sexes, and growth of muscle mass and its strength.
  14. 14. 3. GROWTH HORMONE • Normally from birth up to pre-pubertal stage, the growth hormone secretion is intermittent (a few peaks every 24 h) • but at the time of puberty, though basal level of growth hormone does not rise but there is an increase in the frequency and amplitude of the peaks. • It is responsible for generalized growth spurt at adolescence. • The anabolic actions of sex hormones, adrenal androgens, growth hormone and IGF-I seem to potentiate each other producing a marked growth spurt during puberty
  15. 15. 4. THYROID GLAND SECRETIONS •Thyroxine also increase during puberty. •Thyroxine is necessary for normal growth and development •Main role in normal body growth and skeletal maturation. •TH exert their effect directly by increasing protein synthesis and enzymes; •Indirectly by increasing production of growth hormone and somatomedins.
  16. 16. •Some important effects are on: •Bone development, •Teeth development, •Normal cycle of growth and maturation and •Subcutaneous tissues.
  17. 17. 5. GONADAL HORMONES •Sex hormones - •There is slow increase in secretion of sex hormones in children between the age of 7 and 10 years. •But, there is a rapid rise in oestrogen secretion (in girls) and testosterone in boys in early teenage.
  18. 18. CONTROL OF ONSET OF PUBERTY •The exact mechanism of onset of puberty is still not fully understood, but experimental and clinical observations •Hypothalamus play a major role in this stage •Awakening of Hypothalamus •Role of Leptin
  19. 19. • The gonads of children can be stimulated by gonadotropins; • Their pituitaries contain gonadotropins and their hypothalamic contain gonadotropin-releasing hormone (GnRH) • However, their gonadotropins are not secreted. • In immature monkeys, normal menstrual cycles can be brought on by pulsatile injection of GnRH, • They persist as long as the pulsatile injection is continued. • Thus, it seems clear that pulsatile secretion of GnRH brings on puberty.
  20. 20. •During the period from birth to puberty, a neural mechanism is operating to prevent the normal pulsatile release of GnRH. •The nature of the mechanism inhibiting the GnRH pulse generator is unknown. •However, one or more genes produce products that stimulate secretion of GnRH, and inhibition of these genes before puberty is an interesting possibility
  21. 21. LEPTIN • It has been argued for some time that a critical body weight must normally be reached for puberty to occur. • Thus, for example, young women who engage in strenuous athletics lose weight and stop menstruating, as do girls with anorexia nervosa. • If these girls start to eat and gain weight, they menstruate again, that is, they “go back through puberty”. • It now appears that leptin, the satiety-producing hormone secreted by fat cells, may be the link between body weight and puberty.
  22. 22. CONT…. •Obese ob/ob mice that cannot make leptin are infertile, and their fertility is restored by injections of leptin. •Leptin treatment also induces precocious puberty in immature female mice. •However, the way that leptin fits into the overall control of puberty remains to be determined.
  23. 23. Changes in plasma hormone concentrations during puberty in boys
  24. 24. SECONDARY SEXUAL DEVELOPMENT •First signs of puberty •Testicular volume of 4mls •Slight progressive increase in scrotal folds •Slight increase in scrotal pigmentation
  25. 25. TESTICULAR VOLUME
  26. 26. Changes in plasma hormone concentrations during puberty in girls
  27. 27. APPLIED PHYSIOLOGY
  28. 28. EFFECTS OF EXTIRPATION OF TESTES •Extirpation (removal) of testes is called castration. •Effects of castration depend upon the age when testes are removed.
  29. 29. 1. EFFECTS OF EXTIRPATION OF TESTES BEFORE PUBERTY – EUNUCHISM •If a boy looses the testes before puberty, he continues to have infantile sexual characters throughout his life and this condition is called eunuchism. •Height of the person is slightly more but the bones are weak and thin. •Muscles become weak and shoulder remains narrow. •Sex organs do not increase in size
  30. 30. •The secondary sexual characters do not develop. •The voice remains like that of a child. •There is abnormal deposition of fat on buttocks, hip, pubis and breast, resembling the feminine distribution.
  31. 31. 2. EFFECTS OF EXTIRPATION OF TESTES IMMEDIATELY AFTER PUBERTY • If testes are removed after puberty, some of the male secondary sexual characters revert to those of a child and other masculine characters are retained. • Sex organs are depressed. Seminal vesicles and prostate undergo atrophy. • Penis remains smaller. • Voice remains mostly masculine but other secondary sexual characters like masculine hair distribution, musculature and thickness of bones are lost. • There may be loss of sexual desire and sexual activities.
  32. 32. 3. EFFECT OF EXTIRPATION OF TESTES IN ADULTS •Removal of testes in adults does not cause loss of secondary sexual characters. •But, accessory sex organs start degenerating. •The sexual desire is not totally lost. •Erection occurs but ejaculation is rare because of degeneration of accessory sex organs and lack of sperms.
  33. 33. HYPERGONADISM IN MALES •Hypergonadism is the condition characterized by hypersecretion of sex hormones from gonads. •Cause •Hypergonadism in males is mainly due to the tumor of Leydig cells. •It is common in prepubertal boys who develop precocious pseudopuberty.
  34. 34. •Symptoms •There is a rapid growth of musculature and bones. •But, the height of the person is less because of early closure of epiphysis. •There is excess development of sex organs and secondary sexual characters. •The tumors also secrete estrogenic hormones, which cause gynecomastia (the enlargement of breasts).
  35. 35. HYPOGONADISM IN MALES • Hypogonadism is a condition characterized by reduction in the functional activity of gonads. Causes • Hypogonadism in males is due to various abnormalities of testes: 1. Congenital nonfunctioning of testes 2. Under-developed testes due to absence of human chorionic gonadotropins in fetal life 3. Cryptorchidism, associated with partial or total degeneration of testes
  36. 36. CRYPTORCHIDISM • The failure of descent of the testis into the scrotal sac is an extremely common disorder. • 1-4% `newborn male baby • Testicular descent usually begins at approximately the 28th week of gestation. • The disorder usually is detected at birth • Corrected by about 3 months of age. Surgical corrections (Orchidopexy) is necessary for the remainder of the infants, young children, adults.
  37. 37. •Surgery should be performed after diagnosis to try to preserve spermatogonial stem cells and obviate neoplastic changes. •Cryptochidism may be unilateral or bilateral •If the testis are in the inguinal canal, stimulation with hCG or gonodotrophin releasing hormone (GnRH)-via stimulation of hypothalamic pituitary axis-stimulate the testicular descent.
  38. 38. 4. Castration 5. Absence of androgen receptors in testes 6. Disorder of the gonadotropes (cells secreting gonadotropins) in anterior pituitary 7. Hypothalamic disorder.
  39. 39. •Signs and Symptoms •Clinical picture of male hypogonadism depends upon whether the testicular deficiency develops before or after puberty.
  40. 40. DISORDERS OF PUBERTY (APPLIED ) •They are related to the time of its onset Examples 1. Early onset of puberty (precocious puberty) 2. Late onset of puberty (delayed or absent puberty)
  41. 41. 1. EARLY ONSET OF PUBERTY (PRECOCIOUS PUBERTY) It refers to the onset of puberty in a child before 8 yrs •It is more commonly seen in girls •There is early development of secondary sex characters & gametogenesis also starts earlier. Precocious puberty is of two types : 1. True precocious puberty 2. Pseudoprecocious puberty
  42. 42. 1. TRUE PRECOCIOUS PUBERTY •There is early increased secretion of gonadotropins either due to decreased inhibition of release of GnRH from the pulse generator (Hypothalamus) or •Due to chronic stimulation of hypothalamic cells by some irritative focus. •Hence the condition is also called gonadotropin- dependent precocious puberty
  43. 43. 2. PSEUDOPRECOCIOUS PUBERTY •Early development of secondary sex characters without gametogenesis •It occurs due to abnormal exposure of sex hormone to immature child. •In this type of precocious puberty , child may not remain isosexual & normal sequence of events of puberty is also altered.
  44. 44. CAUSES OF PSEUDOPRECOCIOUS PUBERTY •Following conditions involving adrenal or gonads result in pseudoprecocious puberty are: *Congenital virilizing hyperplasia **Androgen-secreting tumours in males and ***Oestrogen-secreting tumours in females.
  45. 45. CONGENITAL ADRENAL HYPERPLASIA • Causes. Congenital adrenal hyperplasia is caused by congenital deficiency of 21-hydroxylase deficiency and deficiency of 11- hydroxylase enzymes. • Characteristic features are virilism and excessive body growth. • In boys, it is characterized by: • Precocious body growth leading to stocky appearance called infant hercules. • Precocious sexual development with enlarged penis even at age of 4 years.
  46. 46. •Hypogonadism can arise through failure of testicular function (primary hypogonadism) – failure •Pituitary function (secondary hypogonadism) •Hypothalamic failure (tertiary hypogonadism)
  47. 47. KLINEFELTER SYNDROME • Disorder of gonadal development • Non – disjunction in male germ cells is thought to account for 50% of the cases • By screening for sex chromatin positive – phenotypic males, the syndrome has been found in 1 in 400 or 500 new borns • Dominants chromosomal feature in almost all patients is at least an XXY chromosome pattern • Classic form of K syndrome is characterized by small, firm testes with hyalinization of seminiferous tubules -
  48. 48. •Azoospermia •Gynecomastia •Elevated serum and urinary gonadotropin •Mental retardation •Impairment of social and mental function.
  49. 49. • Primary hypogonadism: Disorder of testicular function itself in the pressure of normal hypothalamus – hypophyseal function- called hypergonodotropic hypogonadism is Klinefelter’s Syndrome. • Klinefelter’s Syndrome is a chromosomal abnormality that results in small testes and failure of secondary sex characteristics. 1. Incidence of 1 in 500 births. 2. Duplication of the X chromosome resulting in the abnormal karyotype 47XXY. 3. Testosterone replacement to improve bone to prevent fracture & male development.
  50. 50. • Bilateral gynacomastia • Hyperplasia of interductal tissue • Secondary to estrogen excess • Ducts themselves usually hyperplastic • Decreased intellectual function • Aberrant social behaviour • Personality disorder • Delayed emotional development • Defective gross motor control • Increased incidence of major and minor congenital abnormalities • Lower birth weight in patients with this syndrome compared with control individuals. • Decreased thyroid function • Chronic pulmonary disease • Venous varicosities • Abnormal glucose tolerance • Increased risk of breast cancer
  51. 51. Other’s causes: • Mumps orchitis, Cryptorchidism (failure of testes to descend into scrotum), Testicular damage from radiation or chemotherapy. Treatment: • Steroid replacement therapy • Maintain only secondary sexual characters only normal growth of public/axillary hair sexual function – No fertility. FSH 65U/L (<10 U/L normal) LH 35U/L (<10U/L normal) T 4n mol/L (9-41 n mol/L) Sperm very low count Leydig cells/ST – not working
  52. 52. • Secondary hypogonadism: • Hypogonadotrophic hypogonadism • Failure of pituitary gland function • FSH/LH secretion↓ • Uncommon and generally associated and general hypopituitarism. • Tertiary hypogonadism: • Failure of GnRH secretion from the hypothalamus • Kallmann’s Syndrome: hereditary disorder • Anosmia (impaired sense of smell)
  53. 53. • Gonadal Dysgenesis (Turner’s Syndrome) A group of phenotypic females with short stature primary amenorrhea and sexual infantilism was described by Turner in 1938. Less than 58 inches tall Idiopathic short stature Webbed neck (pterggium colli -wing like structure extended on cornea) which is a consequence of failed formation of the Jugular lymphatic system High arched palate (roof of the mouth) Low set prominent ears Low posterior hairline
  54. 54. REFERENCES•Text book of Medical Physiology • Guyton & Hall •Human Physiology •Vander •Text book of Medical Physiology •Indukurana •William’s textbook of Endocrinology 12th Edition •Net source
  55. 55. THANK YOU . . .

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