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

1. PUBERTY
&
ADOLESCENCE
Pandian M
Dept of Physiology
DYPMCKOP

2. •What changes occur in males and females at
puberty?
•What do the terms menarche and menopause
mean?

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. 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. 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. 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. COMPONENTS OF PUBERTY
The two principal components of puberty are:
1. Sudden spurt of physical growth
2. Appearance of secondary sex characters.

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. 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.

11. 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.

15. 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

16. 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).

19. 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.

20. 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

21. 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.

22. •Some important effects are on:
•Bone development,
•Teeth development,
•Normal cycle of growth and maturation
and
•Subcutaneous tissues.

23. 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.

24. 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

25. • 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.

26. •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

27. 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.

28. 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.

30. Changes in plasma hormone concentrations
during puberty in boys

32. SECONDARY SEXUAL
DEVELOPMENT
•First signs of puberty
•Testicular volume of
4mls
•Slight progressive
increase in scrotal folds
•Slight increase in
scrotal pigmentation

33. TESTICULAR VOLUME

34. Changes in plasma hormone concentrations
during puberty in girls

35. APPLIED PHYSIOLOGY

36. EFFECTS OF EXTIRPATION OF
TESTES
•Extirpation (removal) of testes is called
castration.
•Effects of castration depend upon the age
when testes are removed.

37. 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

38. •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.

39. 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.

40. 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.

41. 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.

42. •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).

43. 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

44. 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.

45. •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.

46. 4. Castration
5. Absence of androgen receptors in testes
6. Disorder of the gonadotropes (cells secreting
gonadotropins) in anterior pituitary
7. Hypothalamic disorder.

47. •Signs and Symptoms
•Clinical picture of male hypogonadism
depends upon whether the testicular
deficiency develops before or after puberty.

48. 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)

49. 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

50. 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

51. 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.

52. 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.

53. 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.

56. •Hypogonadism can arise through failure of
testicular function (primary hypogonadism) –
failure
•Pituitary function (secondary hypogonadism)
•Hypothalamic failure (tertiary hypogonadism)

58. 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 -

59. •Azoospermia
•Gynecomastia
•Elevated serum and urinary gonadotropin
•Mental retardation
•Impairment of social and mental function.

60. • 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.

63. • 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

64. 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

65. • 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)

66. • 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

70. 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

71. THANK YOU . . .