Puberty
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puberty
Transcript of Puberty
Define
Transitional stage from childhood to adulthood manifested
by physiological changes & development of SSC .
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Timing
Usually occurs between the ages of 10 & 16 years .
Major determination is genetic. Other factor .
1. Geographic location
2. Exposure to light.
3. General health & nutrition:
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A. Critical body weight of 47.8 Kg (Frisch hypothesis).
B. A greater percentage of body fat (16% to 23.5%) may
serve as initiating signal.
Moderately obese girls have earlier menarche.
Anorectics have delayed menarche.
Puberty is delayed in morbid obesity, other factors are
involved.
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What When How
1. Thelarche Development of
breast, 5Taner
stages
±10 yrs, first
sign of
puberty
E2
2. Adrenarche Development of
pubic hair, 5 Taner
stages & axillary
hair, 3Taner stages
PH: 1yr after
Thelarche
AH is the
final SCC
Adrenal
androgen
3. Spurt of
growth
Accelerated
growth, 6-11cm/yr
With
adrenarche
GH & E2
4. Menarche The first
menstruation
±12yr
(9-17.7)
Midpuber
tal E2
Stages (Physiological changes)
The pubertal sequence requires 4.5 yrs. (range, 1.5-6 yrs)
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5. Deposition of SC fat: 17% to menstruate & 22% to
ovulate
6. Genital organs changes:
Mons pubes, labia maiora & minora: increase in size.
Vagina:
.length: increase, appearance of the rugae
.Epithelium: thick, stratified squamous., containing glycogen
.pH: acidic.
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Uterus: enlarge, U/C:2/1
Ovaries:
.increase in size, almond shape
.300 thousands primary follicle at menarche (2 million at
birth)
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Summary of pubertal events
1.FSH & LH rise moderately before the age of 10 yrs,
followed by a rise in E2. LH pulse frequency increases
are first seen in sleep but then are extended throughout
the day. The final adult pattern is 1.5 to 2 hrs intervals
between pulse.
2.Increased levels of E2 (gonadarche) results in
Maturation of SSC.
Increased skeletal growth at low levels of E2.
Increased GH & IGF-1
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3. Adrenal androgen cause adrenarche (pelvic & axillary
hair). No major role in growth. It is an independent event.
4. Midpuberty levels of E2 are sufficient to induce
menstruation.
5. Postmenarchal periods are irregular for 12-18 mo {LH
surge is late pubertal event}
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Leptin & puberty
Leptin is a peptide secreted by adipose tissues; it acts on
CNS neurons, regulating eating behavior & energy balance.
Higher levels of leptin correspond to earlier menarche. Girls
with idiopathic precocious puberty have higher leptin levels.
Leptin levels decrease with increasing Tanner stage. They
have increased sensitivity to leptin. The decrease may allow
greater food intake.
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Growth hormone:
At puberty its secretion is critically dependent on sex steroid.
It stimulates IGF-1 in cartilage & IGF-1 production in liver.
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Define
Breast development <8 y or menstruation <9 y.
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Etiology, Classification
A. True, GnRH dependent, complete, central,
isosexual: Activation of the HPO axis, development of the
gonads, SSC & ovulation
1.Constitutional, idiopathic: (85%)diagnosed by exclusion.
2.CNS: Meningitis, encephalitis, hydrocephalus
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B. Pseudo, GnRH independent, incomplete, peripheral,
iso or hetrosexual :
No activation of the HPO axis, but extrapituitary HCG or
sex steroid exposure.
No developments of the gonads, No ovulation but
development of SSC.
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1. Isosexual:
Feminizing T (Granulosa-Theca cell, malignant teratoma).
Estrogen intake.
Albright S (precocious puberty, café-au-lait skin patches,
cystic bony changes).
Hypothyroidism (Short stature & retarded bone age).
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The small cyst like
space is similar to the
Call-Exner bodies
normally seen in
granulosa cells
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2. Hetrosexual:
Virilizing T: virilization but no uterine bleeding.
Androgen intake.
CAH
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C. Partial: premature thelarche or adrenarche.
It is due to end-organ increased sensitivity to normal
circulating low E or A.
Follow-up
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Diagnosis
History
Examination
i. Growth: Tanner stage, height & weight percentile
ii. External genitalia changes
iii. Abdominal, pelvic & neurological examination.
IV. Signs of androgenization
v. Other findings: signs of Albright S, hypothyroidism
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d. X ray of the lower ends of radius & ulna:bone age
a. Retarded: hypothyroidism b. Normal: Partial
c. Advanced:
FSH: Low (<2 IU/ml) ---- pseudo-----follow up
Normal (> 2 mIU/ml) ----- true:
CT or MRI --------Normal (idiopathic)
Abnormal (CNS lesion) Aboubakr Elnashar
Treatment
Objectives:
•Arrest maturation until normal pubertal age.
•Attenuate & diminish established precocious
characteristics.
•Maximize adult height.
•Avoid abuse, reduce emotional & social problems
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Treatment of the cause:
• Albright S ( MPA or Testolactone, aromatase inhibitor).
• Ovarian or CNS tumor (excision).
• Hypothyriodism, CAH
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Constitutional: GnRh analogue
Drug of choice because it achieves all objectives.
It acts by binding to the anterior pituitary receptors causing
down-regulation & desensitization of the pituitary.
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Regression of symptoms occurs in the first year {Regression
of pubertal characteristics, amenorrhea & decreased growth
velocity}.
Delayed epiphyseal fusion; treatment more effective if begun
before bone age >12 yrs.
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Maintain E2 at <10 pg/mL.
Children require higher doses than adults for suppression.
Adrenarche will continue.
Treatment is continued until the epiphyses are fused or the
appropriate pubertal & chronological ages are matched.
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SSC do not develop by the age of 14 y or no menstruation
till age of 16y
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It is either :
* Delayed onset: Breast bud does not appear till
13 years or menarche does not occur till 16
years . or
* Delayed progreession : Menarche does not
occur within 5 years after breast bud .
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Causes
Early cycles are anovulatory E unopposed by
P endometrial hyperplasia
Treatment
for 3 cycles:
Norethistrone acetate 5mg twice daily for 21 d or
OCP Aboubakr Elnashar
