ADOLESCENT SEXUAL AND

REPRODUCTIVE HEALTH INCLUDING

PUBERTAL CHANGES

DR. ASIRIFI AMOAKO S.K.

• Stages of life
• Infant < 1 yr
• Childhood 1 – 13 yrs
• ADOLESCENT transition
• Adult > 18 years

These terms according to WHO

 PUBERTAL CHANGES
• Have implications for adolescent sexual and RH
• Puberty describes the entire period
• Pubertal changes constitute
– a series of changes involving the development of body
and 20 sexual characteristics and the attainment of
reproductive capability

• Child reproductive incapability

• ADOLESCENT pubertal changes
• Adult reproductive capability
 Changes in Genital organs in Adolescence
• Mons pubis, labia majora & minora: increase in size.
• Vagina:
1. length: increase, appearance of the rugae
2. Epithelium: thick, stratified squamous cells containing
glycogen
3. pH: acidic.
• Uterus:
enlarges, Uterus / Cervix :2 / 1
• Ovaries:
1. Increase in size, almond shape
2. 300 thousand primary follicles at menarche ( 2 million at birth)
 Adolescence therefore:
• Is the period of life during which the
child becomes an adult person
i.e. the physical , sexual and
psychological development are
complete .
• PUBERTY first part of adolescence .
 Puberty and its disorders

PUBERTY
It is a physiological phase lasting 2 to 5
years, during which the genital organs
mature
 Puberty

A stage of human development when sexual maturation

and growth are completed and result in the ability to reproduce.
What happens?
 Accelerated somatic growth
 Maturation of primary sexual characteristics (gonads and
genitals)
 Appearance of secondary sexual characteristics (pubic and
axillary hair, female breast development, male voice
changes,...)
 Menstruation and spermatogenesis begin
 Manifestations of puberty

• Menarche,
• Secondary sex characters,
• Physical development
• Psychological changes.
 Secondary sex characters
• dev’ t of the breast
• appearance of pubic hair
• axillary hair.
• The first sign of pubertal development is
usually breast growth (thelarche),
followed by appearance of pubic hair
(pubarche), then (axillary hair), then
(menarche).
• The mean interval between breast
budding and menarche is 2.5 years with a
standard deviation of about one year.
 Adrenarche

means increased activity of the suprarenal

cortex at puberty with increased
production of adrenal androgens which
lead to appearance of pubic and
axillary hair.
Adrenarche usually precedes gonadarche.
 Hormonal Changes that initiate puberty

• During childhood , the hypothalamus is

extremely sensitive to the negative feedback
exerted by the small quantities of estradiol
& testosterone produced by the child's
ovaries .
• As puberty approaches , the sensitivity of
the hypothalamus is decreased and
subsequently , it increase the pulsatile
GnRH secretion .
The anterior pituitary responds by progressive secretion
of FSH and LH associated with increased secretion of
growth hormone .
The gonads (ovaries or testes) respond to the increase in
Gonadotropin secretion by growing(follicular
development & estrogen secretion) and beginning to
produce testosterone and estradiol.
The rising levels of testosterone and estradiol produce the
body changes of female and male puberty.
• Estrogen causes development of the genital organs and
the appearance of the secondary sexual characters .
• With increased estrogen secretion , menarche and cyclic
estrogen secretion occurs .
 Factors affecting the initiation
of pubertal development :

1 - Height and weight ratio (nutritional

factors).
2 - Maturation of the hypothalamus .
3 - Increased neurotransmitter output
in CNS .
4 - Onset of adrenal androgen activity
 Puberty – hormonal changes -Summary

Hormonal changes precede physical changes

Increased stimulation of hypothalamo-pituitary-
gonadal axis
– gradual activation of the GnRH (LHRH)
– increases frequency and amplitude of LH pulses.
– gonadotropins stimulate secretion of sexual steroids
(estrogenes and androgenes)
– extragonadal hormonal changes (elevation of Insulin-
like Growth Factor-1, and adrenal steroids)
Extrahypothalamic region - neurotransmitters, stress, nutrition
serotonin, dopamin, GABA norepinephrin, neuropeptide Y, glutamic acid

Ventromedial region
of hypothalamus LH-RH (gonadoliberin)

Adenohypophysis LH FSH

Gonads Inhibin

Estrogens Estrogens

Androgens Androgens
 Staging of pubertal development
(Tanner)

Pubertal development is classified according to the

Tanner standard – 5 different stages
– Girls: breast (B1-5), pubic hair (Pu1-5), axillary hair (A1-5), menarche
– Boys: testicular volume > 4 ml (Te), penis enlargement (G1-5), pubic hair
(Pu1-5), axillary hair (A1-5), spermarche

Monitoring of the pubertal growth acceleration

– growth velocity is 2-3 times greater than prepubertal
– sexual dimorfism in pubertal growth
 Stages of Tanner
BREAST GROWTH PUBIC HAIR GROWTH
1 Elevation of papillae only, no breast 1 No pubic hair. (Pre-adolescent)
buds: (Pre-adolescent)

2 Slightly elevated breast buds and
papillae. (About 8 – 13 years).
3 Enlargement and elevation of breast
and areola, no separation of contours .
2 Sparse growth along the labia of long,
slightly pigmented hair (About 8 – 14
years)
3 Dark, coarse, curly hair over the pubic
area

4 Areola and papillae project from breast 4 Adult type hair but covers pubic area
and form a secondary mound only

5 Projection of papillae only with 5 Lateral extension

recession of areola into general contour.
Mature breast.
Staging of pubertal development in boys
(Tanner)

G1-5, Pu 1-5, A 1-5, testicular volume > 4 ml – first sign of male puberty
Staging of pubertal development in girls
(Tanner)

B 1-5, Pu 1-5, A 1-5. (B2 – first sign of female puberty)

 Normal pubertal development

Boys Girls

Age of start 12,5 11,5

(yrs) (10 - 14) (9 - 13)

First sign of puberty G2 B2

(testicular volume
up to 4 ml)

Growth velocity 10,3 9,0

(cm/yr) (Tanner III-IV) (Tanner II-III)

Duration of puberty 3,2  1,8 2,4  1,1

(yrs) (adult size of testis ) (menarché)
 Pubertal disorders

A. Precocious puberty

B. Delayed puberty

C. Child with ambiguous genitalia (intersex)

 FEMALE PRECOCIOUS PUBERTY

Definition:
It means menarche or appearance of any of the
secondary sexual characters before the age of
8 years.

Accepted limits for PP:

the age of 8 or before in girls
the age of 9 or before in boys
 Types:
1 - True precocious puberty .
2 - False
(pseudo-precocious puberty).
3 - Incomplete precocious
puberty .
 Classification
Central (true)/complete, gonadotropin-dependent

Early stimulation of hypothalamic-pituitary-gonadal

axis.

Periferal, GnRH independent (precocious pseudopuberty)

The source of sex steroid may be endogenous or exogenous,

gonadal or extragonadal, independent of gonadotropins
stimulation.
 General terminology

Complete PP
Incomplete PP (isolated pubertal sign)

Isosexual precocity
early pubertal development appropriate for sex
Contrasexual (heterosexual) precocity
inappropriate for sex or appropriate for opposite sex
 Etiology of precocious puberty
1. McCune-Albright syndrome.
• Autonomous endocrine hormone excess,
• Polyostotic fibrous dysplasia
• Unilateral Café-au-lait spots
The presence of any two of the above

2. Adrenal causes:
(a) Hyperplasia, adenoma, or carcinoma of suprarenal
cortex.
Congenital adrenal hyperplasia and Cushing syndrome
lead to precocious puberty in the male direction, i.e.
heterosexual precocious puberty;
(b) Estrogen secreting adrenal tumor which is very rare.
 Etiology of precocious puberty
3. Ovarian causes :
(a) Estrogen producing tumors as granulosa and theca cell tumor;
(b) Androgen producing tumors as androblastoma;
(c) Choriocarcinoma because it secretes human chorionic gonadotrophin (HCG) which
may stimulate the ovaries to secrete estrogen;
(d) Dysgerminoma if it secretes HCG.
4. Juvenile hypothyroidism:
Lack of thyroxine leads to increased production of thyroid stimulating hormone and the
secretion of pituitary gonadotrophins may also be increased.
5. Drugs:
• latrogenic may follow oral or local administration of estrogen.
• A long course of estrogen cream used for treatment of vulvovaginitis in children
may lead to breast development or withdrawal bleeding.
6. Silver syndrome: Small stature, retarded bone age and increased Gonadotropin
levels.
 Diagnosis of precocious puberty
1. History:
• It excludes iatrogenic source of estrogen or androgen.
• It differentiates between isosexual and heterosexual precocious puberty.
2. Physical examination:
• It diagnoses McCune-Albright syndrome.
• Neurologic and ophthalmologic examinations exclude organic lesions of the
brain.
3. Special investigations:
a. X-ray examination of the hand and wrist
to determine bone age.
• Estrogen stimulates growth of bone but causes early fusion of the epiphysis.
So the child is taller than her peers during childhood, but she is short during adult
life.
b. Hormonal assay:
including serum FSH, LH, prolactin, estradiol, testosterone, 17α-hydroxy
progesterone, TSH, and human chorionic gonadotrophin to diagnose
Choriocarcinoma.
 3. Special investigations cont’d:

Hypothyroidism
retards bone age, and is the only condition of precocious
puberty in which bone age is retarded
 Idiopathic precocious puberty:

is diagnosed after excluding all other

causes.
 True precocious puberty
(central, gonadotropin-dependent)

Always isosexual!
Bone age is accelerated

FSH and LH elevation after LH-RH is diagnostic test

(LH/FSH > 2)

MRI of CNS is necessary to exclude the neoplasia

Heterosexual pubertal development in girls

Clinical findings
Hirsutisms, acne, virilisation of external genitalia, amenorrhoea or menstrual
cycle disturbance

Elevation of androgens
- Adrenal (congenital adrenal hyperplasia, tumors)
- Ovarian (polycystic ovary syndrome, tumors)
- Exogenous (anabolic steroids – doping?)

Bone age is accelerated

Elevation of testosterone or adrenal androgens
 Heterosexual pubertal development in boys

Clinical findings
Gynecomastia, hypogenitalism, eunuchoid body proportions

Elevation of estrogens
Adrenal or testiscular tumors
Administration of
Exogenous estrogens
Drugs – amfetamin, canabis, tricyclic antidepresives

Primary hypogonadism or syndromes with androgen insensitivity

or testosteron synthesis disorders (related to ambigous genitalia)
 Variants of normal development
Premature thelarche (isolated breast enlargement)
– exclude the start of precocious puberty!
Premature adrenarche (pubic and axillary hairs)
– exclude simple virilising form of congenital adrenal hyperplasia(CAH)!
Premature menarche
exclude vaginal bleeding due to trauma or rare ovarian cyst!

Bone age is not accelerated!

FSH and LH levels after LH-RH are normal
Gonadal and adrenal steroid levels are normal
Pelvic and adrenal ultrasonography is normal
 Gynaecomastia

Breast enlargement in boys

Physiologic
(Testosterone is being converted to estrogenes in the liver. Increased
sensitivity of E receptors in breast to slightly elevated E level)
– in 40 – 50% boys at the start of puberty
– unilateral or bilateral
Pathologic
– Unilateral – breast tumor (very rare)
– Billateral
• elevated prolactin (PRL) – prolactinoma or subclinical hypothyreosis
with elevation of TSH
• elevated estrogen/testosterone (47,XXY)
 Precocious puberty-treatment
Gonadotropin-dependent PP
• Idiopathic
– GnRH (LH-RH) analog (triptorelin) to block LH-RH receptor in
gonadotroph of pituitary gland
• Organic – tumor or cysts
– Surgery
Gonadotropin independent (pseudopuberty)
- testicular, ovarian or adrenal tumors –surgery
- CAH – substitution of corticosteroids
- autonomous steroid secretion-estrogens receptor antagonists
(tamoxifen), steroid synthesis inhibitors (ketoconazol), aromatase
inhibitors (testolacton)
 Treatment of precocious puberty
Objectives:
1. Arrest maturation until normal pubertal age.
2. Attenuate & diminish established precocious
characteristics.
3. Maximize adult height.
4. Avoid abuse, reduce emotional & social problems
 Delayed Puberty

It is when Secondary Sexual Characters do not develop by the age

of 14yrs or no menstruation till age of 16yrs

It is either :
* Delayed onset: Breast bud does not appear till 13 years or
menarche does not occur till 16 years . or
* Delayed progression : Menarche does not occur within 5 years
after breast bud .
 Etiology of delayed puberty
1 - Constitutional
with +ve family history , short stature & normal fertility .
2 - Hypergonadotropic hypogonadism
(FSH > 40) = ovarian causes of I-ry amenorrhea = primary ovarian
failure & 2-ry ovarian failure (if occurs before puberty).
3 - Hypogonadtropic hypogonadism
= hypothalamic & pituitary causes of I-ry amenorrhea e.g. Kallman's
syndrome , Anorexia nervosa .
4 - Normogonadotropic hypogonadism = end organ defects =
uterine causes (Mullerian agenesis and testicular feminization
syndrome), imperforate hymen (c/o = delayed menarche + normal
other aspects of puberty), PCOD and Virilizing ovarian adrenal
tumors .
5 - General causes of amenorrhea (endocrinal or non-endocrinal
especially malnutrition) if occurred before puberty &↓GH & steroid
synthesis defects .
 Investigations of delayed puberty
History :
1 - Family history , nutritional history , any systemic diseases
(e.g. history of endocrinal disturbance).
2 - Clinical picture of space occupying lesion in the ovary , adrenal,
pituitary & hypothalamus.
3 - Periodic pain and +ve 2-ry sexual characteristics in imperforate
hymen .
Examination :
(A) Body measurement for causes of amenorrhea + ↑or ↓weight, short or
tall stature , proportions (upper / lower segment ratio & arm span /
height ratio).
(B) Tanner staging of breast, pubic & axillary hair if present.
(C) Clinical picture of Turner ,Mullerian agenesis & imperforate
hymen .
(D) Neurological examination for sense of smell (Kallman's syndrome),
visual field & other cranial nerve lesions .
Special Investigations :
1 - FSH & LH assay important to differentiate level of the lesion & progesterone
assay in 17-OH(17-hydroxylase) deficiency .
2 - Chromosomal study if short stature or hypergonadotropic type .
3 - Radiological bone age study & radiologic study for pituitary adenoma

Treatment of delayed puberty

* Constitutional : Reassurance .
• Treatment of the cause (if treatable) or cyclic estrogen-progesterone hormone
replacement therapy if the cause is not treatable , for 3 cycles:
Norethistrone acetate 5 mg twice daily for 21 d or OCP
* Patient with Y chromosome cell line : Gonadectomy + hormone replacement therapy
 General Diagnostic evaluation of Puberty
Dx
History
- pubertal history of other family members
- prenatal and perinatal (exposure to exogenous sex steroids in
intrauterine period; birth weight, lenght, mechanism of delivery,
perinatal pathology - resuscitation,..)
- concomitant illnesses, postnatal exposure to sex steroids
- time of first sign of puberty

Physical examination
- auxologic parameters (height, weight, arm span, upper/lower
segment ratio,...)
- skin, hair, thyreoid, neurologic findings
- staging of pubertal signs, inspection of external genitalia
Growth charts
 Diagnostic evaluation

Laboratory
- gonadotropins (FSH, LH) basal and peak after LHRH stimulation
(prepubertal LH/FSH<1)
- estradiol
- testosterone (basal value and value after LH stimulation)
- adrenal androgens (17-OHP, A-dion,...) and ACTH

Skeletal maturity (bone age)

Pelvic sonography (ovarian and uterine size)
CT or MRI of adrenals, CNS
Vaginoscopy and vaginal cytology
Genetic – karyotype, DNA analysis
 Bone age
(Assessment of biologic maturation)

X-ray film of the left hand and wrist

– Radius Ulna Small bones (RUS)
(X-ray of knee – important examination for final height
prediction)

Different methods of bone age evaluation – radiographic

atlas of skeletal development
- Greulich Pyle
- Tanner-Whitehouse II
- Tanner-Whitehouse III
- Sempé
 Bone age

2 yrs 6 m. 10 yrs 12 yrs

 Adolescent Sexual and Reproductive Health
• Refers to the physical and
emotional well-being of
adolescents and includes their
ability to remain free from
• Unwanted pregnancy
• Unsafe abortion
• STIs including HIV/AIDS, and
• All forms of sexual violence
and coercion.
 The need for Adolescent SRH
• Worldwide majority of men and women, married and unmarried become sexually active
during adolescence.

• Most adolescents lack accurate knowledge about reproduction and sexuality and do not
have access to RH information and services including contraception
• Approximately 14 m children are born to adolescent women each year. (10% of all births)

• The physical immaturity of young mothers increase their risk of death or serious disability

• Pregnancy related complications are among the major causes of death fro girls 15 – 19
worldwide
• 5 m unsafe abortions take place among adolescent girls annually

• Globally, 1 out of 20 adolescents get STI each year and half of all new HIV cases are among
young people aged 10 – 24 years
• Girls and young women often miss or are denied the formal education and employment
opportunities which enhance decision-making skills and that empower them to delay
marriage and pregnancy, and refuse unwanted sex.
 In Ghana
• Adolescents fertility (GDHS 2008)
• 10% already mothers
• 3% pregnant with 1st child
• 11% urban adolescents have started child bearing
• 16% rural adolescents have started child bearing
• 14% of births at KATH (2007)

Interventions for adolescent SRH (ICPD Action 7.41)

• Information and services should be made available to adolescents to help them to
understand their sexuality and protect them from unwanted pregnancies, STIs and
subsequent risk of infertility, harmful behaviours (drug abuse, smoking, unsafe sex etc)

• This should be combined with the education of young men to respect women’s self
determination and to share responsibility in matters of sexuality and reproduction
 Promotion of adolescent sexual rights
• Deciding freely and responsibly on all aspects of their sexuality

• Being free of discrimination, coercion or violence in their sexual lives and

in all sexual decisions

• Expecting and demanding equality, full consent, mutual respect and

shared responsibility in sexual relationships.
Thank you