Puberty and Adolescence. OTHMAN MOHAMED OMAIR ALI ALFAQIRI. Puberty : is the process of physical changes by which a child 's body becomes an adult body capable of reproduction.
Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.
Puberty and Adolescence
OTHMAN MOHAMED OMAIR
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
Reproductive system maturation
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
prepubertal (testicular volume less than 3.5 ml; small penis of 3 cm or less)[
testicular volume 6 ml; skin on scrotum thins, reddenss and enlarges; penis length unchanged
testicular volume between 6 and 12 ml; scrotum enlarges further; penis begins to lengthen to about 6 cm
testicular volume between 12 and 20 ml; scrotum enlarges further and darkens; penis increases in length to 10 cm and circumference
testicular volume greater than 20 ml; adult scrotum and penis of 15 cm in length
no glandular tissue; areola follows the skin contours of the chest (prepubertal)
breast budforms, with small area of surrounding glandular tissue; areola begins to widen
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 [
increased breast size and elevation; areola and papilla form a secondary mound projecting from the contour of the surrounding breast [
breast reaches final adult size; areola returns to contour of the surrounding breast, with a projecting central papilla. [
Pubic hair (both male and female)
no pubic hair at all (prepubertal Dominic state) [typically age 10 and younger]
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]
hair becomes more coarse and curly
adult-like hair quality, extending across pubis but sparing medial thighs [13–15]
Reproductive system maturation
The Prepubertal uterus
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.
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.
Bone mineral density
Peak menerlization 14-16 y.
Stimulates the ovary
Involved in spermatogenesis in the testes
Induces receptors for 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
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
gonadotropin-independent precocious puberty
in which the presence of sex steroids is independent of pituitary gonadotropin release.
gonadotropin-dependent precocious puberty
involves the premature activation of the hypothalamic-pituitary-gonadal (HPG) axis.
1.Constitutional or idiopathic:
2. Organic lesions of the brain:
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.
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) Dysgerminomaif 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.
8. Silver syndrome: Small stature, retarded bone age and increased Gonadotrophin levels.
*breast enlargement, unilateral.
*Pubic and axillary hair.
*Menarche until 2-3 years after onset of breast enlargement.
*The pubertal growth spurt occurs early in female puberty.
*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
*breast diameter inc
*areola darkens + thickens
*nipple becomes more prominent
*enlargement of the clitoris
*deep-red color of vaginal mucosa
*enlargement of the testes
*reddening+thinning of the scrotum
*increased pubic hair
*the pubertal growth spurt, acne,
2. Physical examination:
3. Special investigations:
These are done according to the history and clinical findings and include:
to determine bone age.
b. Hormonal assay: including serum FSH, LH, prolactin, estradiol, testosterone, 17α-hydroxy progesterone, TSH, and human chorionic gonadotrophinto diagnose Choriocarcinoma.
to diagnose ovarian or adrenal tumor.
d.CT or MRI :
to diagnose an organic lesion of the brain, or adrenal tumor.
retards bone age, and is the only condition of precocious puberty in which bone age is retarded
is diagnosed after excluding all other causes.
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.
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)
(d) Cyproterone acetate tablets
Treatment is given till the age of 12 years (mean age of pubertal development).
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
with +ve family history , short stature & normal fertility .
Gonadal damage secondary to chemotherapy/radiation
Enzyme defects in the gonads
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 (hypergonadotropichypogonadism)
Complete androgen insensitivity
Postinfectious (ie. mumps orchitis, coxsackievirus infection, dengue, shigella, malaria, varicella)
Autoimmune/metabolic (autoimmune polyglandular syndromes)
“Vanishing Testes syndrome”
“Resistant Ovaries syndomre” (gonadatropin receptor problems)
5- Eugonadotropic pubertal delay
*Congenital Anatomic Anomalies
6-Other Endocrine Causes
Interferes with gonadotropin secretion
Interfere with gonadotropin production
7- other causes
Growth Hormone Deficiency
Craniopharyngioma, astrocytomas, gliomas, histiocytosis X, germinomas, prolactinomas
Iron overload (pituitary damage)
GnRH receptor abnormalities
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 .
(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 .
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.
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.
2- secondary investigations
Chromosomal study if short stature or hypergonadotropic type .
Radiological bone age study & radiologic study for pituitary adenoma
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.
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.