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Puberty dr-arshiyasultana-110312042731-phpapp02
Puberty is the transition period between childhood and adulthood that involves physical and hormonal changes. Precocious puberty refers to the onset of puberty before age 8 in girls and age 9 in boys. It can be classified as central, peripheral, or combined based on whether the cause is in the brain or peripheral organs. Diagnosis involves physical exams, hormone tests, imaging, and puberty staging. Treatment depends on the type but may include medication to delay puberty or surgery to remove tumors.
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Puberty dr-arshiyasultana-110312042731-phpapp02
- 1. PUBERTYPUBERTY 10/04/13 1 Arshiya Sultana Lecturer,Dept. of Obstetrics & Gynaecology NIUM, Bangalore, Karnataka.
- 2. Puber- marriageable age Pubertus– adulthood The period of transition between sexual immaturity and maturity Puberty is first phase of adolescence. How puberty occurs ? 10/04/13 2
- 3. Fetal and InfancyFetaland Infancy During the latter half of fetal life, the hypothalamus pituitary ovarian axis is functional completely. FSH levels are suppressed from 20 weeks gestation by the production of estrogen by the placenta and by the fetus itself. At birth, the fetus is separated from its placenta and therefore the major source of estrogen is removed. 10/04/13 3
- 4. Hypoestrogenic state of thefetus FSH level rises and remains elevated for 6-10 months After birth But FSH is suppressed by Central inhibition of production of GnRH Controlled by gene in the GnRH cell nucleus in the hypothalamus 10/04/13 4
- 5. FSH pulses are undetectable-8-9 yrs 1-2 yrs – spike of FSH increases in frequency Childhood 4-5 yrs – frequency of the FSH pulses increases in day light hours Fully functional production of GnRH with N adult frequency, amplitude and pulse s 5-10yrs ovulatory menstrual cycle 10/04/13 5
- 6. Pituitary glands All activitiesincreases At puberty – increase secretion of releasing factors by the hypothalamus Manifested by sudden spurt in height, enlargement of thyroid, adrenal cortex activity, skin pigmentation Cyclical production of gonadotrophin and estrogen in amount10/04/13 6
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- 9. STAGES OF PUBERTYSTAGESOF PUBERTY Growth spurt Breast development (thelarche) Pubic hair growth (Adrenarche) Menstruation (menarche) Axillary hair growth 70% of girls, variation often occur in Tanner Definite signs of puberty are usually present by the age 9 or 10 years 10/04/13 9
- 10. Growth spurtGrowth spurt It begins around the age of 11yrs in girls 6 to 10cms per year for around 2 years Effect of estrogen – fusion of end plate of the femur and growth ceases by the age of 15 yrs 10/04/13 10
- 11. Tanner staging ofbreastTanner staging of breast development –development – Marshall and Tanner (1969)Marshall and Tanner (1969) Elevation of papilla Elevation of papilla & breast on a small mount, increased in areola Further enlargement Secondary mound of areola and papilla Recession of areola to contour of breast prepubertal 9-13 yrs 10-14 yrs 11-15 yrs 12-17 yrs 10/04/13 11
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- 13. MenarcheMenarche occurs atany between 9 to 17 yrs In India -13.5 yrs Age of menarche varies family Race Social class Family size, birth order Environment Diet General health 10/04/13 13
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- 15. Axillary hairAxillary hair Appearslater During the 2yrs before the menarche the genital tract develops Menstrual phase itself often preceded by mucoid vaginal discharge 10/04/13 15
- 16. Other Changes duringpubertyOther Changes during puberty Apart from development of secondary sexual characters and growth spurt other changes are Gonads Sex organs Pelvis Skin changes Psychological changes Hormonal 10/04/13 16
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- 19. Precocious pubertyPrecocious puberty Tannerstage 2 of breast development prior the age of 8 yrs in white and 7 yrs in black Elevation of papilla & breast on a small mount, increased in areola 10/04/13 19
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- 21. PrecociousPrecocious PubertyPuberty Isosexual Heterosexual CompleteIncomplete Central Peripheral Combined Premature thelarche Premature adrenarche 10/04/13 21
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- 23. CompleteComplete Central isosexual pubertyCentralisosexual puberty Systemic estrogen effect True or gonadotrophin dependent 90% Cyclic release of gonadotrophin Classification: Idiopathic or organic brain disease Idiopathic : Most common 70% Underlying etiology unknown 10/04/13 23
- 24. Growth spurt israpid with short duration Rate of progression vary General health is not impaired USG- functional follicular ovarian cyst Incidence of POF and infertility is not increased Other causes are to be excluded before diagnosis – MRI, CT scan, etc 30% cases may have organic brain disease 10/04/13 24
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- 26. Peripheral precocious pubertyPeripheralprecocious puberty Pseudoprecocious puberty Gonadotrophin independent Classification: Ovarian tumour Adrenal tumour – estrogen secreting - rare Iatrogenic- exogenous administration of sex steroids Primary hypothyroidism MC Cune Albright syndrome Ovarian cyst- estrogen secreting can cause PPP 10/04/13 26
- 27. Ovarian tumourOvarian tumour Itis common cause for PPP Granulosa theca cell tumour – benign, estrogen secreting, confined to one ovary, Palpable rectal abdominal examination or USG Treatment : unilateral salpingoopherectomy 10/04/13 27
- 28. Mc Cune AlbrightsyndromeMc Cune Albright syndrome Rare – girls Triad 1. Precocious puberty 2. multiple area of fibrous dysplasia of bone 3. café au lait spots of the skin facial asymmetry or skeletal deformities X-ray shows dysplastic lesions Fluctuation of estrogen levels and low gonadotrophin- independent of GnRH stimulation 10/04/13 28
- 29. Café au laitskin pigmentationCafé au lait skin pigmentation 10/04/13 29
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- 31. X ray showingdysplastic lesionX ray showing dysplastic lesion Single view of the left hand demonstrates multiple large expansile "bubbly" lytic lesions with sharp transition zones and without an associated periosteal reaction ( arrows). The lesions are located in the phalanges, carpels, metacarpals, distal ulna and radial bones. The cortex is very thin in many areas overlying the expansile lytic lesion, making it difficult to determine if a fracture has occurred 10/04/13 31
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- 35. Incomplete precocious pubertyIncompleteprecocious puberty No systemic estrogen effect One pubertal change is clinically apparent Absence of superficial cell desquamated from vaginal mucosa or bone age 10/04/13 35
- 36. Premature thelarche –development ofPremature thelarche – development of breast < 8yrs in white and <7yrs in blackbreast < 8yrs in white and <7yrs in black 10/04/13 36 This is a bilateral enlargement of breasts in 1-2 yr olds that is common. There are no other signs of puberty development and the growth is normal. As long as the vulva, labia, vagina are normal infantile, and there is no pubic hair, then nothing is done.
- 37. 10/04/13 37 Benign andneeds no therapy Commonly occurs between 1and 4 yrs of age. No progression 1/3th regression 1/10 progression Estradiol level < 20 ng/ml GnRH stimulation: FSH increases and LH no response
- 38. Appearance of pubichair <8 yrs No other pubertal changes No evidence of systemic estrogen Other androgen mediated clinical findings- axillary hair growth, oily skin, and acne One half children have organic brain disease. 10/04/13 38 Premature AdrenarchePremature Adrenarche
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- 40. Premature AdrenarchePremature Adrenarche Adrenal androgen increases increase 17 hydroxyprogesterone – ACTH stimulation Shows 21 hydroxylase deficiency 10/04/13 40
- 41. DiagnosisDiagnosis To distinguished heterosexualand isosexual puberty- History Physical examination –identify Tanner staging Height Incomplete precocious puberty-serial observation for at least 6 months 10/04/13 41
- 42. Diagnosis contdDiagnosis contd Thyroiddysfunction can be evaluated by thyroid profile. Serum HCG concentrations are elevated in the presence of trophoblastic disease. Iatrogenic sources of estrogen – medical history Mc Cune Albright – clinical features 10/04/13 42
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- 44. To distinguish incomplete(PrematureTo distinguish incomplete (Premature thelarche) from complete precociousthelarche) from complete precocious pubertypuberty Serum estradiol Prolactin LH GnRH stimulation test 10/04/13 44
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- 46. Incomplete precocious puberty-Incomplete precocious puberty - Premature adrenarchePremature adrenarche Cranial CT scan, 17 alpha hydroxyprogesterone level at baseline and following intravenous ACTH stimulation 10/04/13 46
- 47. To distinguish PeripheralPP fromTo distinguish Peripheral PP from central precocious pubercentral precocious pubertyty GnRH stimulation test - In PPP no change in gonadotrophin levels whereas True PP FSH increases more than LH advanced bone age in both Increase in ovarian volume and uterine size in TPP 10/04/13 47
- 48. A rectal abdominalexamination and pelvic USG – identify ovarian tumours and ovarian cysts. Adrenal tumours –adrenal sonograms CNS diseases is confirmed with the use of neurologic and ophthalmologic examination, skull x – ray, EEG and CT cranial scan or MRI study of the brain. 10/04/13 48
- 49. TreatmentTreatment Incomplete forms –self limiting Hypothyroid –thyroid replacement therapy Iatrogenic Ovarian and adrenal tumours – removed 10/04/13 49
- 50. Mc Cune Albrightsyndrome- Testolactone – total daily oral dose of 20 mg/kg body in four divided doses- over a 3 weeks interval the total daily dose is increased to 40 mg/kg body wt Continue till the sign regress Side effects: diarrhoea, abdominalcramping 10/04/13 50
- 51. Idiopathic – GnRHanalogs are reported as being sucessful in the treatment of IPP and central nervous system . Therapy – early – increase the height Long acting GnRH agonist Deslorelin 4-8 ug/kg Leuprolide acetate 20-60ug/kg Buserelin 20-30 ug/kg Leuprolide acetate IM 60ug/kg every 4 weeks Buserelin 1200-1800 ug/kg intranasally 10/04/13 51 Once daily SC injection
- 52. GnRH agonist arenot useful in PPP Side effects: allergic reactions allergy symptoms of lungs with intranasal GnRH should be continued TPP till the mean age of pubertal development. 10/04/13 52
- 53. Precocious puberty canbe differentiated from premature adrenarche by the concomitant appearance of pubic hair with breast development in girls and with testicular enlargement in boys. Other differential diagnoses include virilization caused by congenital adrenal hyperplasia and an adrenocortical or gonadal tumor. In premature adrenarche, serum concentrations of dehydroepiandrosterone, dehydroepiandrosterone sulfate (DHEAS), androstenedione, and testosterone and urinary 17-ketosteroids are usually increased for chronological age and in the range of those found in early puberty. 10/04/13 53
- 54. The bone ageis usually within 2 standard deviations of the chronological age. Moderately elevated levels of serum androgen other than DHEAS, bone age advancement, or signs of atypical premature pubarche (such as cystic acne or symptoms of systemic virilization) indicate the need for a corticotropin test to rule out late-onset congenital adrenal hyperplasia. Marked elevation of serum androgen levels and advanced bone age suggest the possibility of an adrenocortical or gonadal tumor. 10/04/13 54
- 55. Delayed pubertyDelayed puberty breast tissue and/or pubic hair have not appeared by 13-14 yrs of age Or menarche appears as late as 16 yrs The normal upper age limit of menarche is 15 yrs. 15% cases – constitutional delay – PCOD, cryptamenorrhoea. 10/04/13 55
- 56. CausesCauses 10/04/13 56 Hypergonadotrophic hypogonadism Hypogonadotrophic hypogonadism Anatomic causes • Gonadaldysgenesis • Pure gonadal dysgenesis (46xx, 46xy) • Ovarian failure • constitutional delay • chronic illness • Malnutrition • primary hypothyoidism • isolated gonadotrophin deficiency • Intracranial lesions • Pure gonadal dysgenesis (46xx, 46xy) • Ovarian failure • mullerian • imperforate hymen • transerve vaginal septum
- 57. DiagnosisDiagnosis Thorough history Previous illness Physicalexamination: Height and weight secondary sexual characters growth pattern 10/04/13 57
- 58. heightheight Short stature (<147cm) – chronic illness turner syndrome Hypothalamic or pituitary lesions hypothyroidism laurence moon biedl syndrome 10/04/13 58
- 59. Weight:Weight: Underweight : 1. malnutrition 2.malabsorption syndrome 3. aneroxia nervosa 4. Excessive dieting 5. other psychiatric diseases Normal weight or obese : 1. constitutional delay, 2. XY gonadal dysgenesis 3. Kallman syndrome 4. pituitary tumours, PCOS, 5. Adrenal abnormalities and other causes of secondary amenorrhoea. 10/04/13 59
- 60. InvestigationsInvestigations Physical examination karyotyping FSH level – Increased in ovarian failure Decreased in hypopituitarism Thyroid and prolactin Ultrasound X ray pituitary MRI CT scan Laparoscopy 10/04/13 60
- 61. TreatmentTreatment Treatment is directedaccording to the etiology Assurance, improvement of general health and treatment of any illness may be of help in non endocrinal causes cases with hypogonadism may be treated with cyclic estrogen Unopposed estrogen 0.3 mg (conjugated estrogen) daily is given for first 6 months 10/04/13 61
- 62. combined estrogenand progestin sequential regimen is started cases of hypergonadotrophic hypogonadism should have chromosomal study to exclude intersexuality. 10/04/13 62
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