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Puberty and Adolescence
PUBERTY:
IS THE PROCESS OF PHYSICAL CHANGES BY
WHICH A CHILD'S BODY BECOMES AN ADULT
BODY CAPABLE OF REPRODUCTION
ADOLESCENCE:
IS THE AGE BETWEEN 10 -19 YEARSE
TRANSITIONAL STAGE OF PHYSICAL
AND MENTAL HUMAN DEVELOPMENT
GENERALLY OCCURRING BETWEEN
PUBERTY AND LEGAL ADULTHOOD
PHYSIOLOGY
• Puberty is initiated by hormone signals from the
brain to the gonads (the ovaries and testes).
• the gonads produce a variety of hormones that
stimulate the growth, function, or transformation.
THE NORMAL PUBERTY
• Physical changes.
• Hormonal changes.
Hair
distribution
Menstruation+
fertility
Physical
changes.
BMD
Body
composition
Reproductive
system maturation
PHYSICAL CHANGES.
• Puberty proceeds through five stages from
childhood to full maturity (P1 to P5) as described by
Marshall and Tanner.
• In both sexes, these stages reflect the progressive
modifications of the external genitalia and of sexual
hair.
PHYSICAL CHANGES FOR MALES
1-testicular enlargement is the first physical
manifestation of puberty
2-pubic hair often appears on a boy shortly
after the genitalia begin to grow
3- voice change and Adams apple
4-Male musculature and body shape and Body
odor and acne
TANNER STAGING OF PUBERTY IN MALES
Tanner I
prepubertal (testicular volume less than 3.5 ml; small penis of 3 cm or less)[
Tanner II
testicular volume 6 ml; skin on scrotum thins, reddenss and enlarges; penis
length unchanged
Tanner III
testicular volume between 6 and 12 ml; scrotum enlarges further; penis
begins to lengthen to about 6 cm
Tanner IV
testicular volume between 12 and 20 ml; scrotum enlarges further and
darkens; penis increases in length to 10 cm and circumference
Tanner V
testicular volume greater than 20 ml; adult scrotum and penis of 15 cm in
length
BREAST DEVELOPMENT
The first physical sign of puberty in girls
 occurring on average at about 10 years of age.
 Tanner staging of puberty.
TANNER BREAST DEVELOPMENT
Breasts (female)
Tanner I
no glandular tissue; areola follows the skin contours of the chest ( prepubertal)
Tanner II
breast bud forms, with small area of surrounding glandular tissue; areola begins to widen
Tanner III
breast begins to become more elevated, and extends beyond the borders of the areola,
which continues to widen but remains in contour with surrounding breast [
Tanner IV
increased breast size and elevation; areola and papilla form a secondary mound projecting
from the contour of the surrounding breast [
Tanner V
breast reaches final adult size; areola returns to contour of the surrounding breast, with a
projecting central papilla. [
PUBIC HAIR
• second noticeable change in puberty.
• usually within a few months of thelarche.
• Tanner staging.
TANNER PUBIC STAGING
Pubic hair (both male and female)
Tanner I
no pubic hair at all (prepubertal Dominic state) [typically age 10 and younger]
Tanner II
small amount of long, downy hair with slight pigmentation at the base of the penis
and scrotum (males) or on the labia majora (females) [10–11.5]
Tanner III
hair becomes more coarse and curly
Tanner IV
adult-like hair quality, extending across pubis but sparing medial thighs [13–15]
Reproductive system maturation
UTERINE DEVELOPMENT
The Prepubertal uterus
tear-drop shaped
neck and isthmus accounting for up to 2/3 of the uterine
volume.
Craniocaudal direction without the flextion of adult .
then, with the production of estrogens, it becomes pear
shaped, with the uterine body increasing in length and
thickness proportionately more than the cervix.
• The mucosal surface of the vagina also changes in
becoming thicker and duller pink in color.
• Whitish secretions (physiologic leukorrhea ).
• The ovaries usually contain small follicular cysts
visible by ultrasound.
OVARY DEVLOPMENT
• In prepuberty, the ovarian size volume extends from 0.3 - 0.9 TO
cm3.
• More than 1.0 cm3 indicates
that puberty has begin.
•
During puberty, the ovarian
size increases rapidly to a mean postpubertal volume of
cm3.
MENSTRUATION+ FERTILITY
• menarche ,and typically occurs about two years after
thelarche
• The average age of menarche in girls is 11. years
• The time between menstrual periods (menses) is not
always regular in the first two years after menarche
• Ovulation is necessary for fertility ,but may or may not
accompany the earliest menses
• Starting of ovulation? By production of progesteron
Bone mineral density
• 6-9 month after thelarche
• 11.5 y at Ts 2-3
• BMD
Peak menerlization 14-16 y.
Influence by
Genetic
Excersise
GH.
HORMONAL CHANGES OF PUBERTY
• Gonadotropin-Releasing Hormone
• •Gonadotropins
• •Adrenal steroids
•
•
•
•
•
GONADOTROPIN-RELEASING
HORMONE
GnRH is synthesized and released from
neurons within the hypothalamus.
Chromosome8.
GnRH stimulates the synthesis and
secretion of the gonadotropins .
GnRH is secreted in pulses .
LH ,FSH
ROLE OF GONADOTROPINS
FSH
Stimulates the ovary
Involved in spermatogenesis in the testes
Induces receptors for LH
LH
Uses as substrate to produce estradiol in theca cells
Stimulates testosterone synthesis by Leydig cells
FSH is usually higher than LH in prepubertal stages, and this
reverses in pubertal stages
SEX STEROIDS
TESTOSTERONE
EXTERNAL GENITALIA.
MUSCLE GROWTH
ESTROGEN
BREAST
UTERINE
ADIPOSE TISSUE
BONE MINERALIZATION
EPIPHYSIEL PLATE
ABNORMAL PUBERTY
Precocious puberty.
Delayed puberty
PRECOCIOUS PUBERTY
the appearance of physical and hormonal signs of
pubertal development at an earlier age than is
considered normal.
girls < 7 years.
black girls 6-8 years.
boys< 8 years
PRECOCIOUS PUBERTY CAN BE DIVIDED INTO 2
DISTINCT CATEGORIES.
gonadotropin-independent
precocious puberty
gonadotropin-dependent
precocious puberty
in which the presence of
sex steroids is independent of
pituitary gonadotropin release.
involves the premature
activation of the
hypothalamic-pituitarygonadal (HPG) axis.
GIPP
GDPP
CAUSES
1.Constitutional or idiopathic:
• In most cases of precocious puberty (90%) , no
cause is found.
• For some unknown reason the hypothalamus
stimulates the pituitary gland to secrete its
gonadotrophic hormones.
• There is normal menstruation and ovulation.
• Pregnancy can occur at young age.
CAUSES
2. Organic lesions of the brain:
• The next common cause.
• Organic lesions affecting the midbrain, hypothalamus,
pineal body, or pituitary gland may lead to premature
release of pituitary gonadotrophins.
• Examples include traumatic brain injury, meningitis,
encephalitis, brain abscess, brain tumor as glioma,
craniopharyngioma, and hamartomas.
CAUSES
3. McCune-Albright syndrome.
4. Adrenal causes:
(a) Hyperplasia, adenoma, or carcinoma of
suprarenal cortex.
Congenital adrenal hyperplasia and lead to
precocious puberty in the male direction, i.e.
heterosexual precocious puberty;
(b) Estrogen secreting adrenal tumor which is very
rare.
CAUSES
5. 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.
6. Juvenile hypothyroidism:
Lack of thyroxine leads to increased production of thyroid stimulating hormone and
the secretion of pituitary gonadotrophins may also be increased.
7. Drugs:
•
latrogenic may follow oral or local administration of estrogen.
•
A long course of estrogen cream used for treatment of vulvovaginitis of children
may lead to breast development or withdrawal bleeding.
8. Silver syndrome: Small stature, retarded bone age and increased Gonadotrophin
levels.
SYMPTOMS
Girls.
*breast enlargement,
unilateral.
*Pubic and axillary hair.
*Axillary odor
*Menarche until 2-3
years after onset of
breast enlargement.
*The pubertal growth
spurt occurs early in
female puberty.
boys
*testicular enlargement
*Growth of the penis and
scrotum + appearance of
pubic hair typically occur at
least a year after testicular
enlargement.
*Accelerated linear growth
(the pubertal growth spurt)
occurs later in the course
of male puberty than in
female puberty
SIGNS
*breast enlargement
*breast diameter inc
*areola darkens +
thickens
*nipple becomes more
prominent
*enlargement of the
clitoris
*pubic hair
*deep-red color of vaginal
mucosa
*Mild acne
*enlargement of the testes
*penis growth,
*reddening+thinning of the
scrotum
*increased pubic hair
*the pubertal growth spurt,
acne,
*voice change,
*facial hair.
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.
FEMALE PRECOCIOUS PUBERTY
3. Special investigations:
These are done according to
the history and clinical
findings and include:
DIAGNOSIS
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.
DIAGNOSIS
b. Hormonal assay:
including serum FSH, LH,
prolactin, estradiol,
testosterone, 17α-hydroxy
progesterone, TSH, and
human chorionic
gonadotrophin to diagnose
Choriocarcinoma.
DIAGNOSIS
c. Ultrasonography
to diagnose ovarian or adrenal tumor.
d. CT or MRI :
to diagnose an organic lesion of the brain,
or adrenal tumor.
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.
TREATMENT OF PRECOCIOUS
PUBERTY
1. Treatment of the cause, e.g.,
thyroxin for hypothyroidism,
removal of ovarian and adrenal
tumors.
2. Incomplete forms of precocious
puberty do not require treatment,
as estrogen production is not
increased.
3. MCCUNE-ALBRIGHT SYNDROME
• is treated with testolactone oral tablets.
• The drug inhibits the formation of estrogen
from its precursors, so reduces estrogen
level.
• The dose is 20 mg/kg body weight in 4
divided doses and increased to 40 mg/kg
body weight during a 3 week interval.
4. IDIOPATHIC TYPE
is treated by explanation and reassurance and by giving one
of the following drugs which inhibit the secretion of
gonadotrophins:
(a)Gonadotrophin releasing hormone analogues
(b)Medroxyprogesterone acetate tablets (Provera tablets)
(c) Danazol capsules
(d) Cyproterone acetate tablets
Treatment is given till the age of 12 years (mean age of
pubertal development).
MCCUNE-ALBRIGHT SYNDROME:
•
The disease is found more frequently in girls.
•
It consists of a triad of :
1.
Precocious puberty,
2.
Cystic changes in bones, and
3.
Cafe-au lait patches of the skin.
•
The cause of precocious puberty is autonomous production of estrogen by the
ovaries.
•
FSH and LH levels are low.
•
The treatment is testolactone oral tablets which inhibit ovarian
steroidogenesis.
DELAYED PUBERTY
Delayed puberty is indicated if no signs of
puberty are observed in a girl by14 years in
age and in a boy by 15 years in age
Evaluation also indicated of an arrest of
pubertyal maturation occurs
ETIOLOGY OF DELAYED PUBERTY
1 - Constitutional
with +ve family history , short stature & normal fertility .
2 - Hypergonadotropic hypogonadism
Gonadal damage secondary to chemotherapy/radiation
Enzyme defects in the gonads
Androgen insensitivity
Ovarian/testicular dysgenesis
3 - Hypogonadtropic hypogonadism
A male has abnormal testicles that do not produce normal levels of the sex
hormone, testosterone.
A female has abnormal ovaries that do not produce normal levels of sex
hormone, estrogen.
4- Gonadal Failure (bilateral)
In these cases, circulating levels of LH & FSH are high (hypergonadotropic
hypogonadism)
*Congenital
Turner Syndrome
Klinefelter’s Syndrome
Complete androgen insensitivity
*Acquired
Chemotherapy/Radiation/Surgery
Postinfectious (ie. mumps orchitis, coxsackievirus infection, dengue, shigella, malaria,
varicella)
Testicular torsion
Autoimmune/metabolic (autoimmune polyglandular syndromes)
“Vanishing Testes syndrome”
“Resistant Ovaries syndomre” (gonadatropin receptor problems)
5- Eugonadotropic pubertal delay
*Congenital Anatomic Anomalies
Imperforate hymen
Vaginal atresia
Vaginal aplasia
*PCOS
*Hyperprolactinemia
6-Other Endocrine Causes
*Hypothyroidism
Interferes with gonadotropin secretion
*Hyperprolactinemia
Interfere with gonadotropin production
7- other causes
Malnutrition
Growth Hormone Deficiency
Brain tumors
Craniopharyngioma, astrocytomas, gliomas, histiocytosis X, germinomas,
prolactinomas
Iron overload (pituitary damage)
GnRH receptor abnormalities
INVESTIGATING 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 2ry sexual characteristics
in imperforate hymen .
INVESTIGATING DELAYED PUBERTY
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,testes, pubic & axillary
hair if present.
(C) Neurological examination for smell sense
(Kallman's syndrome), visual field & other cranial
nerve lesions .
1-Primary investigations
Routine first-line:
FBC and CRP or ESR to exclude anaemia, iron deficiency, malnutrition and hidden
inflammatory disease.
RFT and LFT to exclude renal and liver diseases.
Bone profile.
TSH and free T4 to exclude hypothyroidism (central hypothyroidism cannot be excluded on TSH
alone)
Second-line (endocrine):
FSH and LH - low levels are associated with central or constitutional delay. Elevated levels
are associated with primary testicular or ovarian disorder.
Prolactin - significant elevation is suggestive of pituitary microadenoma.
Early morning estradiol (girls) - low but detectable levels suggest pubertal development is
imminent.
Early morning testosterone (boys) - low but detectable levels suggest pubertal development is
imminent.
Elevated testosterone (female range) and LH:FSH ratio is suggestive of PCOS in girls.
INVESTIGATING DELAYED PUBERTY
2- secondary investigations
Chromosomal study if short stature or
hypergonadotropic type .
Radiological bone age study & radiologic study for
pituitary adenoma
TREATMENT OF DELAYED PUBERTY
Exclusion of a serious organic disease or a chromosome variation is the
primary goal in an adolescent presenting with true delayed sexual
development.
If all is normal, and puberty is just late, simple reassurance is all that is
needed.
Delay, especially when accompanied by short stature, can produce anxiety,
depression and low self-esteem, isolation and school refusal.
As this is almost always a problem for boys due to the difference in
physiological timing of events, a short-term course of around three to 12
months' treatment with low-dosage testosterone can boost growth,
pubertal progress and morale.
Treatment options include monthly depot testosterone esters or daily oral
capsules.
TREATMENT OF DELAYED PUBERTY
Testosterone is usually continued until there is clear evidence of
spontaneous puberty (testicular growth).
The duration and dosage of therapy should be monitored by a
paediatric endocrinologist as overdosage or excessively long
courses can reduce the period of pubertal growth.
Growth hormone is not necessary unless there is a proven
deficiency.
Therapeutic management of simple delayed puberty is rarely
required in girls, but very low doses of ethinyl estradiol are the
mainstay of treatment.
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