Puberty and Adolescence

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Puberty and Adolescence
OTHMAN MOHAMED OMAIR ALI ALFAQIRI
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Pubertyis the process of physical changes by
which a child's body becomes an adult body
capable of reproduction
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Adolescence is the age between 10 -19
yearse transitional stage of physical and mental
human development generally occurring between
puberty and legal adulthood
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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.

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The normal puberty

• Physical changes.
• Hormonal changes.

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Hair distribution
Physical changes.
Menstruation fertility
Reproductive system maturation
Body composition
BMD
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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.

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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

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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

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Breast development

• The first physical sign of puberty in girls
• occurring on average at about 10 years of age.
• Tanner staging of puberty.

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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.

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Pubic hair

• second noticeable change in puberty.
• usually within a few months of thelarche.
• Tanner staging.

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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)
  1011.5
• Tanner III 
• hair becomes more coarse and curly
• Tanner IV 
• adult-like hair quality, extending across pubis
  but sparing medial thighs 1315

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UTERINE DEVELOPMENT
Reproductive system maturation

• 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.

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• 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.

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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.

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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

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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.

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HORMONAL CHANGES OF PUBERTY

• Gonadotropin-Releasing Hormone
• Gonadotropins
• Adrenal steroids

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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

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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

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Sex steroidsTestosterone external
genitalia.Muscle growth estrogenbreast
uterineadipose tissuebone mineralization
epiphysiel plate
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Abnormal puberty

• Precocious puberty.
• Delayed puberty

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Precocious puberty

• the appearance of physical and hormonal signs of
  pubertal development at an earlier age than is
  considered normal.
• girls lt 7 years.
• black girls 6-8 years.
• boyslt 8 years

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Precocious puberty can be divided into 2 distinct
categories.
gonadotropin-dependent precocious puberty
involves the premature activation of the
hypothalamic-pituitary-gonadal (HPG) axis. GDPP
gonadotropin-independent precocious
puberty in which the presence of sex
steroids is independent of pituitary gonadotropin
release. GIPP
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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.

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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.

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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.

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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.

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• 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.

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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
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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,
reddeningthinning of the scrotum increased
pubic hair the pubertal growth spurt, acne,
voice change, facial hair.
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Diagnosis of precocious puberty

• 1. History
• It excludes iatrogenic source of estrogen or
  androgen.
• It differentiates between isosexual and
  heterosexual precocious puberty.

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• 2. Physical examination
• It diagnoses McCune-Albright syndrome.
• Neurologic and ophthalmologic examinations
  exclude organic lesions of the brain.

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FEMALE PRECOCIOUS PUBERTY

• 3. Special investigations
• These are done according to the history and
  clinical findings and include

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DIAGNOSIS

• 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.

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DIAGNOSIS

• b. Hormonal assay including
  serum FSH, LH, prolactin, estradiol,
  testosterone, 17a-hydroxy progesterone, TSH, and
  human chorionic gonadotrophin to diagnose
  Choriocarcinoma.

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DIAGNOSIS

• c. Ultrasonography
• to diagnose ovarian or adrenal tumor.
• d. CT or MRI
• to diagnose an organic lesion of the brain, or
  adrenal tumor.

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

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Idiopathic precocious puberty

• is diagnosed after excluding all other causes.

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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.

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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.

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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).

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McCune-Albright Syndrome

• The disease is found more frequently in girls.
• It consists of a triad of
• Precocious puberty,
• Cystic changes in bones, and
• 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.

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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

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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.

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• 4- Gonadal Failure (bilateral)
• In these cases, circulating levels of LH FSH
  are high (hypergonadotropic hypogonadism)
• Congenital
• Turner Syndrome
• Klinefelters 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)

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• 5- Eugonadotropic pubertal delay
• Congenital Anatomic Anomalies
• Imperforate hymen
• Vaginal atresia
• Vaginal aplasia
• PCOS
• Hyperprolactinemia

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• 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

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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 .

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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 .

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• 1-Primary investigations
• Routine first-lineFBC 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 LHFSH
  ratio is suggestive of PCOS in girls.

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Investigating Delayed Puberty

• 2- secondary investigations
• Chromosomal study if short stature or
  hypergonadotropic type .
• Radiological bone age study radiologic study
  for pituitary adenoma

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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.

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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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• Thank you