The presentation contains all the information on Puberty with its applied clinical conditions. this presentation is helpful especially for students.

1. DR. D. Y. PATIL HOMOEOPATHIC MEDICAL
COLLEGE AND RESEARCH CENTRE
PRECOCIOUS PUBERTY
DR. RADHIKA KHANDELWAL
DEPARTMENT OF GYNAECOLOGY AND
OBSTETRICS

2. DEFINITION –
Puberty in girls is the period which links
childhood to adulthood. It is the period of
gradual development of secondary sexual
characters.
CHANGES DURING PUBERTY –
o Morphological changes
o Biological changes
o Psychological changes

3. GROWTH SPURT
BREAST BUDDING (THELARCHE)
PUBIC AND AXILLARY HAIR GROWTH
(ADRENARCHE)
PEAK GROWTH IN HEIGHT
MENSTRUATION (MENARCHE)

4. •The brain starts the process with the production of a hormone called gonadotropin-
releasing hormone (GnRH).
•When this hormone reaches the pituitary gland — a small bean-shaped gland at the
base of your brain — it leads to the production of more hormones in the ovaries for
females (estrogen) and the testicles for males (testosterone).
•Estrogen is involved in the growth and development of female sexual characteristics.
Testosterone is responsible for the growth and development of male sexual
characteristics.
•Why this process begins early in some children depends on whether they have central
precocious puberty or peripheral precocious puberty.

5. MENARCHE
• The onset of first
menstruation in life
is called menarche.
It may occur
anywhere between
10 – 16 years of
age, the peak time
being 13 years.
ADRENARCHE
• Adrenal glands
increases their
activity of sex
steroid synthesis
from about 7 years
of age. Increase
sebum formation,
pubic and axillary
hair and change in
voice.
THELARCHE
• Development of
breast tissue after
the age of 8 years
of age.
PUBARCHE
• Development of
pubic and axillary
hair after the age
of 10 years of age.

6. STAGE BREAST PUBIC HAIR
STAGE I
Prepubertal state, elevation of papilla
only.
No pubic hair present.
STAGE II
Breast buds and papilla slightly elevated,
and areola begins to enlarge. (Median age
: 9.8 years).
Sparse, long hair on either of labia majora.
(Median age : 10.5 years).
STAGE III
Further enlargement of entire breast
tissue.
Darker, coarser and curly hair over the mons
pubis.
STAGE IV
Secondary mound of areola and papilla
projecting above the breast tissue
(Median age : 12.1 years).
Adult type hair covering the mons only.
(Median age 12.0 years)
STAGE V
Areola recessed to general contour of
breast. (Median age : 14.6 years)
Adult hair with an inverse triangle distribution
(female escutcheon) covering the medial
thighs. (Median age : 13.7 years)

7. Precocious puberty
Delayed puberty
Menstrual abnormalities (amenorrhea,
menorrhagia, dysmenorrhea)
Others (infection, neoplasm, hirsutism
etc.)

8. Precocious puberty is when a child's body begins changing into that of an
adult (puberty) too soon.
OR
Is when puberty begins before age 8 in girls and before age 9 in boys.
Puberty includes rapid growth of bones and muscles, changes in body
shape and size, and development of the body's ability to reproduce

9. The term precocious puberty is reserved for girls
who exhibit any secondary sex characteristics
before the age of 8 or menstruate before the age
of 10.
Precocious puberty may be isosexual where the
features are due to excess production of
oestrogen or it may be heterosexual where the
features are due to excess production of
androgen (from ovarian and adrenal neoplasm).

10. GnRH
Dependent/Complete/Central/Isosexual/True
• Constitutional - commonest
• Juvenile primary hypothyroidism
• Intracranial lesions – trauma, tumor or
infection
• Incomplete
• Premature thelarche
• Premature puberche
• Premature menarche
GnRH Independent/ Precocious
Pseudopuberty/Peripheral/ Heterosexual
• Ovary
• Granulosa cell tumor
• Theca cell tumor
• Leydig cell tumor
• Chorionic epithelioma
• Androblastoma
• McCune – Albright syndrome
• Adrenal
• Hyperplasia
• Tumor
• Liver
• Hepatoblastoma
• Iatrogenic
• Oestrogen or androgen intake

11. CONSTITUTIONAL –
• It is due to premature activation of hypothalamopituitary ovarian axis.
• There is secretion of gonadotrophins and gonadal steroids due to
premature release of GnRH.
• Bone maturation is accelerated.
• If menstruation occurs it is ovulatory.
• The changes in puberty progress in an orderly sequence.

12. INTRACRANIAL LESIONS –
• Meningitis, encephalitis, craniopharyngioma, neurofibroma or any other
tumor – hypothalamic or pineal gland.
PREMATURE THELARCHE –
• It is isolated development of breast tissue before the age of 8 and
commonly between 2 – 4 years of age. Either one or both the breast may
be enlarged.
• There is no other feature of precocious puberty.
• It generally requires no treatment.

13. PREMATURE PUBARCHE–
• Isolated development of axillary and/or pubic hair prior to the age of 8
without other signs of precocious puberty.
PREMATURE MENARCHE –
• Isolated event of cystic vaginal bleeding without any other signs of
secondary sexual development.

14. TRUE PRECOCIOUS – The diagnosis is made by –
• History of early menarche of mothers and sisters.
• The pubertal changes occur in orderly sequence.
• Tanner stages.
• No cause could be detected.
The investigations to confirm –
• X-ray hand and wrist for bone age. Acceleration of growth is one of the earliest
clinical feature of precocious puberty.
• Pelvic sonography to exclude ovarian pathology.
• Skull X-ray/CT – scan/MRI brain – to exclude intracranial lesion.
• Thyroid profile.
• Serum hCG, FSH, LH.

15. PREMATURE THELARCHE– The diagnosis is made by –
• Somatic growth pattern is not accelerated.
• Bone age is not advanced.
• Nipple development is absent.
• Vaginal smear shows negative estrogen effect.

16. PREMATURE PUBERCHE– The diagnosis is made by –
• It may be due to adrenal or ovarian mischief.
The investigations are –
• An ovarian enlargement may not be palpable clinically, examination under anesthesia or
sonography is helpful.
• IVP or CT scan is required to detect adrenal tumor.
• If nothing abnormal is detected, then the diagnosis of IDIOPATHIC PUBERCHE is made.

17. PREMATURE MENARCHE– The diagnosis is made by –
• The other cause of vaginal bleeding such as foreign body or injury has to be excluded.
• If the bleeding is cyclic, the diagnosis is confirmed.

18. The treatment depends upon the cause.
The goals are –
• To reduce gonadotrophin secretions.
• To suppress gonadal steroidogenesis or counteract the peripheral action of sex steroids.
• To decrease the growth rate to normal and slowing the skeletal maturation.
• To protect the girl from sex abuse.

19. The drugs used are –
• GnRH agonist therapy : arrests the pubertal precocity and growth velocity significantly.
Suppresses FSH, LH secretion, reverses the ovarian cycle, establishes amenorrhea, causes
regression of breast, pubic hair changes and other secondary sexual characteristics. This
drug is to be continued till the median age of puberty.
• Medroxy progesterone acetate – suppresses gonadal steroids, menstruation, breast
development, but cannot change the skeletal growth.
• Cyproterone acetate – it acts as a potent progestogen, having agonist affects on
progesterone receptors.
• Danazol – produces amenorrhea, arrests breast development.

20. • Prognosis vary considerably depending on the etiology.
• Overall prognosis is good with primary hypothyroidism, adrenal or ovarian tumors following
treatment.
• For the CNS group, prognosis depends on neurological involvement and treatment outcome.
• Apart from short stature due to accelerated bone maturation, the idiopathic group have got
a normal menstrual pattern in future and fertility rate is also expected to be normal.

21. Puberty is said to be delayed when the breast tissue and/or pubic hair have not appeared by
13-14 years or menarche appears to be late as 16 years.

22. • Gonadal dysgenesis, 45 XO
• Pure gonadal dysgenesis, 46 XX, 46 XY
• Ovarian failure, 46 XX
HYPERGONADOTROPHIC
HYPOGONADISM
• Constitutional delay
• Chronic illness, malnutrition
• Primary hypothyroidism
• Isolated gonadotrophin deficiency (Kallman’s syndrome)
• Intracranial lesions – tumors
HYPOGONADOTROPHIC
HYPOGONADISM
• Anatomical causes (Imperforate hymen, Transverse vaginal septum)
• Androgen insensitivity syndrome
EUGONADISM

23. • Treatment is directed according to the etiology.
• Assurance, improvement of general health and treatment of any illness may be of help in
non-endocrinal causes.
• Causes with hypogonadism may be treated with cyclic oestrogen.
• Combined oestrogen and progestin, sequential regimen is started.
• Cases of hypergonadotropic hypogonadism should have chromosomal study to exclude
intersexuality.

24. • Menstrual abnormality in adolescents are common.
• The periods may be heavy, irregular or scanty initially.
• Eventually the majority of these teenaged girls establish a normal cycle and are fertile.

25. DYSFUNCTIONAL
UTERINE BLEEDING
• Anovulatory cycles
ENDOCRINE
DYSFUNCTION
• Polycystic ovary syndrome
• Hypo or hyperthyroidism
HAEMATOLOGICAL
• Idiopathic thrombocytopenic purpura
• Von-Willebrands disease
• Leukemia
PELVIC TUMORS
• Fibroid uterus
• Sarcoma botryoides
• Osetrogen producing ovarian tumor
PREGNANCY
COMPLICATIONS
• Abortion

26. • Diagnosis is made by careful history taking and thorough clinical examination
• Evaluation is specially indicated if the menstrual interval is < 22 days or > 44 days, lasts
longer than one week or the bleeding is too heavy that anemia develops.

27. • INVESTIGATIONS INCLUDE
• Routine hematological examination including – bleeding time, clotting time, platelet
count.
• Thyroid profile (T3, T4, TSH).
• Clotting profile
• Ultrasonography

28. • The girl needs adequate explanation, reassurance and psychological support.
• Rest and correction of anemia are helpful.
• Therapy with haematinics or even blood transfusion may be needed.
• In refractory cases, progesterone is given till bleeding stops.
• Medication is continued till 21 days.
• Regular menstrual cycle will be established once the hypothalamo-pituitary-ovarian axis
is matured.