البلوغ و اضطرابات التطور البلوغي DR HISHAM AL-HAMMAMI Puberty and Disorders of Pubertal Development DR.HISHAM AL HAMMAMI 2020 power point

1. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 1

2. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬‫غ‬ ‫ا‬
PUBERTY
& ‫ا‬ ‫ت‬ () ‫ا‬ ‫,طور‬
‫و‬ - ‫ا‬
./0 ‫3درة‬ ‫ا‬ ‫ب‬ ,5‫ا‬
6‫ا‬‫ب‬ &
‫,8د7ت‬ ‫ا‬ ‫ن‬ ‫ف‬ ‫ط‬ ; ‫,,را=ق‬
‫ا‬ ( ‫وا‬ ‫د‬ & ‫وا‬ ‫>د‬ ‫ا‬?,
‫ع‬ (,‫ار‬ ‫,را=ق‬‫ا‬‫دا‬ ‫رو‬ ,‫ت‬
& ‫ا‬
‫ن‬ 8 ً 8 B10-16
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 2

3. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬‫غ‬ ‫ا‬ ‫ء‬
ONSET OF PUBERTY
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 3
‫ط‬ ‫ا‬ F = ‫دث‬H ‫ذي‬ ‫ا‬ ‫ر‬ K ‫ا‬ ‫ط‬ ‫,و‬‫ث‬
‫ھو‬)12.4(
‫ورا‬ ‫ا‬ ‫ل‬ ‫وا‬K 8 ‫8د‬ ‫,3رر‬-
;R‫و‬ ‫ا‬
=‫&>را‬ ‫ا‬
H ‫ا‬
‫>ذا‬ ‫ا‬
S ‫ر‬ ‫ا‬
( K ‫ا‬
"‫8ت‬ - ‫ط‬ ‫,و‬ ‫وزن‬"‫ن‬48‫رام‬B‫/و‬ 5
‫ث‬ ‫ط‬ ‫ا‬ ‫8دء‬ ‫ث‬H ‫روري‬S( leptin)
( ‫ل‬ ‫0وا‬–8)0 ‫راض‬ ‫أ‬
‫دة‬ ‫د‬Z ( ‫ت‬ 8‫طرا‬S‫ا‬–
‫ز‬K ‫وا‬ ‫د‬ [‫ط‬S7‫وا‬‫ز‬ ‫ا‬

4. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
Figure 31-1 Decreasing age at menarche, 1840 to 1978, with inset from 1950 to 2008, indicating a leveling off (about 12.4 years
in the United States) since 1975. (Adapted from Styne DM, Grumbach MM: Disorders of puberty in the male and female. In Yen
SSC, Jaffe RB, Barbieri RL [eds]: Reproductive Endocrinology: Physiology, Pathophysiology, and Clinical Management, 4th ed.
Philadelphia, WB Saunders, 1999.)
Downloaded from: StudentConsult (on 19 July 2012 09:38 AM)
4D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y

5. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 5

6. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
‫ـ‬ ‫ا‬HPGA‫ج‬ , ‫إ‬ ./0 ‫در‬ R ? & ‫ا‬
‫ن‬ ‫ت‬ ‫,و‬‫ت‬ - H‫د‬ R ‫ا‬
‫دات‬ ‫رو‬ , ‫وا‬‫و‬ & ‫ا‬
_ 8 ‫ا‬ ‫د‬ 0 ‫ت‬ ‫,و‬ /.
‫8وع‬ ‫ا‬ ‫/ول‬H820‫ل‬ H ‫ا‬ ‫ن‬:
•;(,‫,ر‬‫ت‬ - H‫د‬ R ‫ا‬5 ‫5ل‬Z8‫ر‬ 8.
•‫ن‬ ? ‫0ظ‬ ‫ا‬ ‫دد‬K ‫ا‬ ‫ب‬ 5,
S 8 ‫ا‬ b ‫ا‬.
•‫ن‬ ‫رة‬ )R ‫8(,رة‬ ‫ر‬ ,cS
‫ت‬ 8 ‫&ر‬ ‫ا‬‫ج‬ , ‫وإ‬‫دات‬ ‫رو‬ , ‫ا‬
& ‫ا‬‫ت‬ - H ‫ا‬‫د‬ 3 ‫ا‬
‫ول‬ ‫,راد‬ 6‫ا‬.
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 6
‫دة‬ ‫ا‬ ‫و‬ ‫ا‬ ‫و‬ ‫ا‬ ‫ات‬ ‫ا‬
Figure 31-2 Changes in the concentration of
gonadotropins (LH and FSH), sex steroids (DHEA,
androstenedione, and estradiol), and the number of
oogonia throughout fetal life and pubertal development.

7. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
‫)در‬‫ول‬ ‫,راد‬ 6‫ا‬‫ر‬ ‫ا‬?
Z ‫ا‬ ‫و‬ ‫م‬ ‫ا‬ ‫ن‬.
‫و7دة‬ ‫ا‬ ‫د‬ 0‫زول‬3/, ‫ا‬‫م‬
?8/ ‫ا‬ ;&‫را‬ ‫ا‬‫ق‬b‫إط‬
‫ت‬ - H ‫ا‬‫د‬ 3 ‫ا‬:
•‫,وى‬ ‫)ل‬‫ت‬ - H ‫ا‬?=
‫/ول‬H8 F,‫ذرو‬ . ‫إ‬ ‫)ل‬ ‫ا‬
‫ث‬ - ‫ا‬ ‫[ر‬Z ‫ا‬.
•‫,وى‬ ‫)ل‬‫ت‬ - H ‫ا‬. ‫إ‬
‫ر‬ K8 R . ‫أد‬4‫وات‬.
•‫ت‬ ‫و‬ ‫[ر‬ ‫ا‬ ‫,وى‬ ‫(ض‬
. ‫إ‬ ; ‫ر‬ ‫5ل‬Z8 & ‫ا‬
‫ل‬b ‫8/وغ‬ ‫ا‬ ‫ل‬ 8R ‫,واه‬
‫د‬H‫وا‬ ‫8وع‬ ‫أ‬.
‫دة‬ ‫ا‬ ‫و‬ ‫ا‬ ‫ا‬
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 7

8. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬! ‫ا‬ "
CHILDHOOD
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 8
‫ور‬H ‫ا‬ ‫5ون‬HPGA‫ر‬ K8 ‫-8ط‬ ‫ط(ل‬ ‫ا‬ ‫د‬ 04-10‫وات‬.
•‫ظم‬ ‫ا‬ ّ H?/ ‫ا‬gonadostat‫ت‬ ‫,و‬ ?8/ ‫ا‬ ;&‫را‬ ‫ا‬ ‫م‬ 3/, ‫ا‬ ‫ر‬ -h, ‫0ظ‬ ‫ا‬
‫ـ‬ ‫ا‬estradiol، S( ‫ا‬ ‫دورا‬ ‫ا‬
•‫ـ‬ ‫ا‬ ‫ط‬ 8-,‫و‬CNS?/ ‫دا‬ ‫ا‬Intrinsic‫ـ‬GnRH.
•‫5ل‬Z8 ‫ط‬ 8-, ‫ا‬ ‫دث‬H‫ل‬ K= ?/ c ‫و&ود‬ ‫0ن‬ ‫,3ل‬.
‫ت‬ ‫,و‬ hZ ,)‫د‬ 3 ‫ا‬ ‫ت‬ - H ‫ا‬+& ‫ا‬ ‫ت‬ ‫و‬ ‫[ر‬ ‫ا‬(S( ‫ا‬‫0ن‬
‫ن‬ , ‫أ‬
‫م‬ّ‫ظ‬CNS?/ ‫دا‬ ‫ا‬‫ق‬b‫6ط‬GnRH‫ھو‬‫6=راز‬ ? ‫ر‬ ‫ا‬ ‫-8ط‬ ‫ا‬
gonadotropin‫ر‬ 0 ‫ن‬4‫(,رة‬ ‫ا‬ .,H ‫وات‬‫و‬H‫8/وغ‬ ‫ا‬ ‫ل‬.

9. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
‫ة‬ #$ ‫ا‬ ‫غ‬ ‫ا‬ % & " ‫ة‬ '
LATE PREPUBERTAL PERIOD
?‫ھ‬ ‫8/وغ‬ ‫ا‬ ; 3=‫,را‬ ‫ا‬ ‫و‬ ‫ا‬ ّ ‫>د‬ ‫ا‬ ‫,8د7ت‬ ‫ا‬:‫ت‬ &‫درو‬ ‫ا‬ ‫ج‬ , ‫إ‬+‫ر‬ZR ?= 58Z ‫ا‬ 3‫ط‬ ‫ا‬ ‫ز‬ ,‫5ظر‬ ‫ا‬.
‫ت‬ k‫,و‬ ;(,‫,ر‬DHEA،DHEA-S،androstenedione‫ر‬ 0 ‫ن‬ 88-11
‫وا68ط‬ K ‫ا‬ ‫ر‬ KZ‫أ‬ ‫و‬(adrenarche or pubarche)
‫5ل‬Z8 ‫دث‬H‫,3ل‬‫د‬ 3 ‫ا‬ ‫دات‬ ‫رو‬ , ‫ا‬ ‫ت‬ ‫,و‬ ‫او‬ ‫د‬ 3 ‫ا‬ ‫ت‬ - H ‫ا‬ ‫إ=راز‬ ‫0ن‬
R‫8د‬ =‫رو‬K ‫ر‬ B ‫ا‬.
‫8ـ‬ 8 )l S‫0ر‬ ‫أ5-ر‬ ‫ھن‬ ‫5ر‬ 8 ‫ا‬ K ‫ا‬ ‫ر‬KZ ‫ظ[ور‬ ‫ن‬ ‫ن‬ K ?,‫/وا‬ ‫ا‬ ‫ت‬ ,( ‫ا‬PCOS‫?>د‬‫8/وغ‬ ‫ا‬.
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 9

10. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
VARIATION IN OOCYTE NUMBER AND HORMONE LEVELS DURING PRENATAL AND POSTNATAL PERIODS. (DHEA =
DEHYDROEPIANDROSTERONE;
FSH = FOLLICLE-STIMULATING HORMONE; HCG = HUMAN CHORIONIC GONADOTROPIN; LH = LUTEINIZING
HORMONE.)
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 10

11. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬‫غ‬ ‫ا‬ ‫ء‬
PUBERTAL ONSET
‫/ول‬H811:
•‫,زول‬ّ Hgonadostat& ‫,در‬‫ـ‬
-Ve FB‫ـ‬SS‫ت‬ S8GnRH
•‫ع‬ (,‫ار‬leptin‫[ذا‬ ‫روري‬S‫و‬ ‫8ق‬
‫ر‬ >, ‫ا‬
•ّ H ?= ‫ر‬ m‫ا‬ ‫ض‬ ( 7‫ا‬
gonadostat،‫زوال‬ ‫را=ق‬‫ا‬ ‫ط‬ 8-,‫ـ‬
CNS‫ا‬?/ ‫دا‬‫ق‬b‫6ط‬GnRH
GnRH‫ا‬?/ /‫إ=راز‬ ‫ط‬[5/?
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 11
Figure 31-3 Changes in set point of the hypothalamic-pituitary unit (gonadostat) (solid lines) and the
maturation of the negative and positive feedback mechanisms from fetal life to adulthood in relation to the
normal changes of puberty. This figure does not illustrate the change in the sex steroid-independent intrinsic
central nervous system inhibitory mechanism that is observed from late infancy to puberty.

12. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬‫غ‬ ‫ا‬ ‫ء‬
PUBERTAL ONSET
•gonadotropin8‫&ر‬ ‫ا‬ cS
S 8 ‫ا‬SS‫ت‬ () ‫ا‬ ‫,طور‬
‫و‬ - ‫ا‬ & ‫ا‬.
•‫8/وغ‬ ‫ا‬ ‫ن‬ [ . ‫إ‬ ‫,)ف‬ ‫ن‬:
•‫ل‬ ,5cS;&‫را‬ ‫ا‬ ‫م‬ 3/, ‫ا‬ ‫آ‬8 & 6‫ا‬‫ـ‬
estradiol‫ق‬b‫إط‬ ./0LH‫س‬ h,,‫و‬
S 87‫ا‬ ‫دورات‬ ‫ا‬.
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 12
Figure 31-3 Changes in set point of the hypothalamic-pituitary unit (gonadostat) (solid lines) and the
maturation of the negative and positive feedback mechanisms from fetal life to adulthood in relation to the
normal changes of puberty. This figure does not illustrate the change in the sex steroid-independent intrinsic
central nervous system inhibitory mechanism that is observed from late infancy to puberty.

13. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 13
‫و‬ - ‫ا‬ & ‫ا‬ ‫ت‬ () ‫ا‬ ‫,طور‬
?‫ط‬ ‫ا‬ ‫و‬ ‫ا‬ ‫رع‬ ,)‫طول‬ ‫ا‬ ‫دة‬ ‫ز‬(
‫ف‬ ), ‫دم‬ ,Marshall and tanner‫و‬ ‫-دي‬ ‫ا‬ ‫,طور‬ ‫ل‬H‫را‬
) Z, ‫و‬ ()‫و‬ ‫ت‬ > K ‫را‬KZ.
SOMATIC CHANGES OF PUBERTY
‫غ‬ ‫ا‬ " ' ( ‫ا‬ ‫ات‬ ‫ا‬

14. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬SOMATIC CHANGES OF PUBERTY
‫غ‬ ‫ا‬ " ' ( ‫ا‬ ‫ات‬ ‫ا‬
the development of secondary sexual characteristics.
‫و‬ - ‫ا‬ & ‫ا‬ ‫ت‬ () ‫ا‬ ‫,طور‬ ‫ل‬H‫را‬
D R : H I S H A M A L H A M M A M I
14
Figure 31-4 Stages of breast development as defined by Marshall and Tanner. Stage 1: Preadolescent;
elevation of papilla only. Stage 2: Breast bud stage; elevation of breast and papilla as a small mound
with enlargement of the areolar region. Stage 3: Further enlargement of breast and areola without
separation of their contours. Stage 4: Projection of areola and papilla to form a secondary mound
above the level of the breast. Stage 5: Mature stage; projection of papilla only, resulting from recession
of the areola to the general contour of the breast.
Stage 1: Preadolescent;
elevation of papilla only.
Stage 2: Breast bud stage;
elevation of breast and papilla
as a small mound with
enlargement of the areolar
region.
Stage 3: Further enlargement
of breast and areola without
separation of their contours.
Stage 4: Projection of areola
and papilla to form a
secondary mound above the
level of the breast.
Stage 5: Mature stage;
projection of papilla only,
resulting from recession of the
areola to the general contour of
the breast.
;( ‫ا‬ ‫8ل‬R /H‫ر‬:(,‫ر‬ 7;
/H ‫ا‬ 7‫إ‬ ‫&/د‬ ‫ا‬ Š‫ط‬ ‫0ن‬
‫و‬K/ ‫ا‬ ‫و‬ ‫-دي‬ ‫ا‬ ‫و‬ ?= ‫دة‬ ‫ز‬‫ة‬
‫رة‬ 7‫ا‬ ‫رز‬ 8, ‫دون‬
‫رزة‬ 8 /H ‫ا‬ .38, ، cS ‫ا‬ /H‫ر‬;
‫-دي‬ ‫ا‬ ‫,وى‬ . ‫إ‬ ‫وة‬K/ ‫ا‬ ;&‫,را‬
‫5ل‬Z8 /H ‫ا‬ ‫و‬ ‫-دي‬ ‫ا‬ ‫,8ر0م‬ /H‫ر‬
‫وة‬K/ ‫ا‬ H ‫و‬ ; ‫ر‬ >) ‫رز‬ 8,.
, ‫ث‬ H8 /H ‫وا‬ ‫وة‬K/ ‫ا‬ ‫,وء‬‫5ل‬Z
‫-د‬ ‫ا‬ ‫,وى‬ ‫=وق‬ ‫وي‬ - ‫رز‬ 8,‫ي‬

15. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
SOMATIC CHANGES OF PUBERTY
the development of secondary
sexual characteristics.
D R : H I S H A M A L H A M M A M I
15
Figure 31-5 Stage of female pubic hair development according to Marshall and Tanner. Stage 1:
Preadolescent; absence of pubic hair. Stage 2: Sparse hair along the labia; hair downy with slight
pigment. Stage 3: Hair spreads sparsely over the junction of the pubes; hair is darker and coarser. Stage
4: Adult-type hair; there is no spread to the medial surface of the thighs. Stage 5: Adult-type hair with
spread to the medial thighs assuming an inverted triangle pattern.
Stage 1: Preadolescent; absence of
pubic hair.
Stage 2: Sparse hair along the labia; hair
downy with slight pigment.
Stage 3: Hair spreads sparsely over the
junction of the pubes; hair is darker and
coarser.
Stage 4: Adult-type hair; there is no spread
to the medial surface of the thighs.
Stage 5: Adult-type hair with spread to
the medial thighs assuming an inverted
triangle pattern.
‫8ل‬R /H‫ر‬‫ب‬ B،;( ‫ا‬K ‫ا‬ ‫ر‬KZ
( ‫و‬ 0 ‫,5ون‬ ‫و‬ ‫ن‬ ‫(ر‬Z ‫ا‬ ./0 ‫-رة‬ , ‫ر‬ KZ‫أ‬ ‫و&ود‬(
_8), ‫ا‬
K ‫ا‬ ‫ق‬ (,‫ار‬ ‫=وق‬ ‫-ر‬ , ‫5ل‬Z8 ‫ر‬KZ ‫ا‬ ‫ر‬Z,،Š8) ‫و‬
ً >8), ‫أ5-ر‬ ‫و‬ ‫و‬Z ‫أ5-ر‬.
? ‫ا‬ F&‫و‬ ‫ا‬ . ‫إ‬ ‫ر‬KZ ‫ا‬ ‫ر‬Z, 7 _ 8 ‫ا‬ ‫د‬ 0 ‫ر‬KZ ‫ا‬ ‫ط‬‫ن‬ ‫د‬ (/.
? ‫ا‬ F&‫و‬ ‫ا‬ . ‫إ‬ ‫ر‬KZ ‫ا‬ ‫,داد‬ ‫ا‬ ; _ 8 ‫ا‬ ‫د‬ 0 ‫ر‬KZ ‫ا‬ ‫ط‬‫ن‬ ‫د‬ (/
‫3/وب‬ ‫ا‬ ‫-/ث‬ ‫ا‬ ‫وذج‬ ‫5ل‬Z, . ‫إ‬ ‫ؤدي‬.

16. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
‫غ‬ ‫ا‬ ‫ة‬ ' ' ‫ر‬ ! ‫ا‬ % ‫ا‬ "
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 16
Figure 31-6 Sequence of physical changes during pubertal development.
‫[ود‬ ‫ا‬)‫-داء‬ ‫ا‬ ‫,8ر0م‬(Thelarche
K ‫ا‬ ‫ر‬KZPubarche‫ا68ط‬ ‫ر‬KZ ‫أو‬adrenarche
? ‫0ظ‬ ‫ا‬ ‫و‬ ‫ا‬Maximal growth‫طول‬ ‫ا‬ 0‫ر‬ ‫ذروة‬ ‫أو‬
peak height velocity
‫ث‬ ‫ط‬ ‫ا‬Menarche
‫,8د7ت‬ ‫ا‬‫د‬ & ‫ا‬somatic[ ‫ا‬
•K ‫ا‬ ‫ر‬KZ ‫,وزع‬‫ا‬?/[5
•‫ا‬ ‫-داء‬ ‫ا‬ ‫,طور‬?/[5
‫دى‬ ./0 ‫دث‬H ‫ل‬ / , ‫ا‬ ‫ھذا‬4.5ً ‫ط‬ ‫و‬

17. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬‫ت‬ *' ‫ا‬ ‫ا‬ +'‫د‬
ADOLESCENT GROWTH SPURT
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 17
‫و‬ ‫ا‬ ‫رع‬ , ‫دث‬H
‫8ل‬R ‫ت‬ ,( ‫ا‬ ‫د‬ 0
0 F/ - ‫ن‬ ‫ن‬ ,‫د‬
‫ذ5ور‬ ‫ا‬
‫ھم‬GH،
estradiol،‫و‬I-L
GF I(3=‫د‬ ?=
‫ا‬‫و‬‫د‬ 03‫راھ‬ ‫ا‬‫ت‬
‫دث‬H,‫ذروة‬0‫ر‬
‫8دء‬ ‫8ل‬R ‫طول‬ ‫ا‬
‫ث‬ ‫ط‬ ‫ا‬8? ‫وا‬H1
ّ?‫ط‬ ‫و‬ ‫و&د‬
‫د‬K8 ‫دود‬H
Menarche

18. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 18
‫7,و&د‬‫ت‬ =b, ‫إ‬‫وظ‬H/?=
‫ا‬ /,5 ‫ا‬‫ظ‬K،‫ا‬H/ ‫ا‬ /,5،
‫و‬ ‫ا‬ 8 ‫ا‬ ‫أو‬‫وم‬HZ& ‫ا‬‫م‬
‫ا‬ ‫ن‬ 8‫ذ5ور‬6‫وا‬‫ث‬‫8/و‬ ‫ا‬ ‫8ل‬R‫غ‬
‫د‬K8? & ‫ا‬ cS ‫ا‬ /H‫ر‬‫=•ن‬
‫,5ون‬ H/ ‫وا‬ ‫ظ‬K ‫ا‬ /,5 ‫ا‬‫ل‬R‫أ‬
‫و‬ ‫ا‬ 8 ‫ا‬ ‫أن‬ ‫ن‬ H ?=
, ‫م‬ & ‫ا‬ ?= ? HZ ‫ا‬ c /‫5ون‬
‫أ58ر‬; ‫ر‬ 3 ‫ت‬ ,( ‫ا‬ ?=
‫ذ5ور‬ ‫ا‬.
,* ‫ا‬ * ‫ا‬ ‫و‬ -( ‫ا‬ . / 0
BODY COMPOSITION AND BONE AGE

19. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 19
,* ‫ا‬ * ‫ا‬ ‫و‬ -( ‫ا‬ . / 0
BODY COMPOSITION AND BONE AGE
‫ر,8ط‬() ‫ا‬ ‫ظ[ور‬ ‫88دء‬ ‫ر‬ 85 ‫5ل‬Z8 ? ‫ظ‬K ‫ا‬ ‫ر‬ K ‫ا‬‫ت‬
‫ث‬ ‫ط‬ ‫ا‬ ‫8دء‬ ‫و‬ ‫و‬ - ‫ا‬ & ‫ا‬.
/ ?0 KZ ‫ا‬ ‫ر‬ ‫,)و‬ 8 ? ‫ظ‬K ‫ا‬ ‫ر‬ K ‫ا‬ ‫د‬ ‫د‬H, ‫5ن‬‫د‬
، ‫رى‬ ‫ا‬85‫ر‬ ‫وا‬ ، ‫ر=ق‬ ‫ا‬ ، _ ‫ر‬ ‫ا‬.
‫ا‬ ‫ر‬ h, ‫م‬ 3, ?= ‫ص‬ ‫5ل‬Z8 ? ‫ظ‬K ‫ا‬ cS ‫ا‬ ‫د‬ (‫8/وغ‬.

20. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 20

21. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
/ ‫ا‬ ‫غ‬ ‫ا‬
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 21
‫ظ[و‬ ‫ا‬‫ر‬‫ا‬‫5ر‬ 8b0 ّ‫ي‬‫ا‬ ‫ت‬ b0 ‫ن‬‫ر‬ K8 ‫وي‬ - ‫ا‬ ? & ‫ا‬ cS‫ل‬R‫أ‬‫ر‬ K ‫ا‬ ‫ن‬
‫8ـ‬ ‫8/وغ‬ ‫ا‬ ‫8دء‬ ;ّR‫,و‬ ‫ا‬2.5‫ري‬ K ‫راف‬H ‫ا‬
‫ر‬ 0 ‫ا‬:
8‫وات‬l‫ث‬
9‫/ذ5ور‬ ‫وات‬
8 ‫ا‬:1/10,000‫ط(ل‬.
‫8ـ‬ ; Z‫أ‬5‫ف‬ KS‫أ‬‫د‬ 06‫ا‬‫ذ5ور‬ ‫ا‬ ; ‫ر‬ 3 ‫ث‬.

22. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
/ ‫ا‬ ‫غ‬ ‫ا‬
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 22
75%?‫ھ‬ ‫5ر‬ 8 ‫ا‬ ‫8/وغ‬ ‫ا‬ ‫7ت‬ H ‫ن‬‫أ‬idiopathic
‫ل‬ Z ‫م‬ 3, ‫إ&راء‬ ‫&ب‬
•‫رة‬ ‫ط‬ S‫ر‬ ‫ت‬ =‫أ‬ ‫و&ود‬ ?(
•‫ل‬ ,H ‫5را‬ 8 ‫ا‬ ? ‫ظ‬K ‫ا‬ cS ‫ا‬ ‫ف‬ 3 ‫إ‬.
‫ت‬ ,( ‫ا‬ ‫ھؤ7ء‬ ‫,5ون‬‫أطول‬‫[ن‬ ‫را‬R‫ا‬ ‫ن‬peers‫ط(و‬ ‫ا‬ /H‫ر‬ ?=،[ ‫ا‬ ?= ‫[ن‬ 5 ‫و‬‫)ر‬R‫ا‬‫ت‬ > 85.

23. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
Central (GnRH dependent)
Idiopathic*
Central nervous system (CNS) tumors:
Astrocytomas, adenomas, gliomas,
germinomas
Congenital anomaly:
Hamartomas, hydrocephalus, arachnoid or
suprasellar cysts, septooptic dysplasia,
empty sella syndrome
CNS infection
Head trauma
Ischemia
Iatrogenic: Radiation, chemotherapy, surgical
Adoption from underdeveloped to developed
country
Peripheral (GnRH independent)
Estrogen- or testosterone-producing tumors:
Adrenal/ovarian carcinoma or adenoma
Ovarian germ cell tumor: granulosa cell tumor,
theca cell tumor, Leydig cell tumor
Gonadotropin- or hCG-producing tumors:
Choriocarcinoma, dysgerminoma, teratoma,
gonadoblastoma
Hepatoblastoma, chorioepithelioma
Congenital adrenal hyperplasia:
21-hydroxylase deficiency, 11-hydroxylase
deficiency
Exogenous exposure to androgen or estrogen
McCune-Albright syndrome
Ovarian follicular cysts
Primary hypothyroidism
Aromatase excess syndrome
Glucocorticoid resistance
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y
23
ETIOLOGIES OF PRECOCIOUS PUBERTY
* The most common cause of precocious
puberty is
idiopathic. CNS central nervous system;
GnRH gonadotropin releasing
hormone; hCG human chorionic gonadotropin.

24. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 24
‫س‬ & ‫ا‬ ‫ر‬ > ‫5ر‬ 8 ‫ا‬ ‫8/وغ‬ ‫ا‬
Heterosexual Precocious Puberty
•‫ذ5رة‬ ‫ا‬ ‫ورام‬ ‫ا‬Virializing neoplasm
•S 8Ovarian
•‫5ظر‬Adrenal
•?3/ ‫ا‬ ‫5ظر‬ ‫ا‬ ; ), ‫=رط‬Congenital adrenal hyperplasia ( adrenogenital syndrome )
•hZ ‫ا‬ &‫ر‬ ‫ت‬ &‫درو‬ “ ‫رض‬K, ‫ا‬Exogenous androgen exposure

25. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 25
‫ب‬ 0‫م‬ ‫ز‬ 7‫ا‬hydroxylase-21‫5ظري‬ ‫ا‬‫ج‬ , ‫إ‬ ‫دة‬ ‫ز‬
‫ن‬ &‫درو‬ ‫ا‬.
‫دة‬Z ‫5-ر‬ ‫ا‬ ‫ل‬ 5Z ‫ا‬:More severe forms
[8 ‫ا‬ / , ‫ا‬ ‫ء‬ S0 ‫ا‬Ambiguous genitalia
?R‫,ر‬ ‫ل‬ &‫,ر‬ ‫ا‬Progressive virilization
‫8/وغ‬ ‫ا‬ ‫د‬ 0 ‫رة‬ )R R
‫ج‬bK ‫ا‬
‫زول‬ ,‫5ور‬ ‫ا‬ S 0‫إ‬
?H‫&را‬ ‫ا‬ ‫ح‬b)‫إ‬Surgical correction
‫دة‬Z ‫ل‬R ‫ا‬ ‫ل‬ 5Z ‫ا‬:A less severe form
?5 b5 ‫ا‬ ‫ر‬ B ‫5ل‬Z ‫ا‬), ‫ا‬ ‫8دء‬ ‫ا‬ ‫ذو‬ ‫5ظر‬ ‫ا‬ ; ), ‫=رط‬‫ر‬ h(
‫5ر‬ 8 ‫ا‬ K ‫ا‬ ‫ر‬KZ ‫و‬Premature pubarche
‫ـ‬ ‫-ل‬ ‫طراب‬S‫ا‬PCOS‫8/وغ‬ ‫ا‬ ‫د‬ 0

26. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 26
/ ‫ا‬ ‫غ‬ ‫ا‬1 ‫ا‬ %2 "
ISOSEXUAL PRECOCIOUS PUBERTY
‫س‬ & ‫ا‬ ‫-ل‬ ‫5ر‬ 8 ‫ا‬ ‫8/وغ‬ ‫ا‬
‫ل‬ 5 ‫ا‬IPPComplete:
‫ل‬ 5 ‫,طور‬0‫و‬ &‫ت‬ () ‫ا‬
‫و‬ - ‫ا‬ & ‫ا‬.
‫ع‬ (,‫ار‬‫ت‬ ‫,و‬‫ا‬‫دات‬ ‫رو‬ ,
& ‫ا‬
•?3 3H ‫ا‬:True
•, ‫ا‬‫ل‬ K(/ K ‫5ر‬ 8 ‫ا‬‫ا‬‫,ط‬‫ور‬
K 8‫ط‬ ‫ا‬ ?B‫8/و‬ ‫ا‬‫و‬, ?, ‫ا‬Z‫ل‬
‫ور‬H ‫ا‬HPG.
•‫ذب‬ 5 ‫ا‬:Pseudo
•5Z8 ‫ن‬ &‫,رو‬ l ‫ض‬ّ‫ر‬K, ‫ا‬‫ل‬
‫,3ل‬‫ور‬H ‫ا‬ ‫0ن‬HPG.

27. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬1 ‫ا‬ %2 " / ‫ا‬ ‫غ‬ ‫ا‬+ +3 ‫ا‬
TRUE ISOSEXUAL PRECOCITY
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 27
75%‫ن‬‫و‬ 8 ‫7ت‬ H ‫ا‬
constitutional
‫ص‬ Z, ‫ا‬:GnRH
stimulation test
‫د‬ 010%‫ت‬ ,( ‫ا‬ ‫ن‬،
‫=•ن‬‫ھو‬ ?,H, ‫ا‬ ‫8ب‬ ‫ا‬
?= ‫طراب‬S‫ا‬CNS
‫0راض‬ ‫ا‬ ‫,ظ[ر‬
‫ظ[ور‬ ‫8ل‬R 8)K ‫ا‬
8 ‫ا‬ ? & ‫ا‬ cS ‫ا‬‫5ر‬
3, ‫ا‬ ‫ن‬ S, ‫أن‬ ‫&ب‬‫م‬
‫ن‬ ‫ر‬ ‫إ&راء‬MRI‫/رأس‬
‫5ر‬ 8 ‫ا‬ ‫8/وغ‬ ‫ا‬‫ل‬ 5 ‫ا‬ ‫س‬ & ‫ا‬ ‫-ل‬.
?3 3H ‫ا‬:
‫8ب‬ ‫ا‬ ‫&[ول‬Constitutional
(idiopathic)
‫وي‬S0 ?B ‫د‬ ‫رض‬Organic
brain disease
‫أورام‬CNS
‫رأس‬ ‫ا‬ ‫وض‬S‫ر‬
‫رأس‬ ‫ا‬ ‫ء‬ 3 , ‫ا‬
‫ن‬ , ‫إ‬CNS

28. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
1 ‫ا‬ %2 " / ‫ا‬ ‫غ‬ ‫ا‬‫ذب‬ 6 ‫ا‬
PSEUDOISOSEXUAL PRECOCITY
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 28
‫ت‬ ‫,و‬ ;=‫,ر‬ ‫د‬ 0 ‫دث‬H
‫ن‬ &‫,رو‬ ‫ا‬, ‫8دون‬‫ل‬ K(H ‫ا‬‫ور‬
& ‫ا‬ ‫ت‬ () ‫ا‬ cS ‫8ب‬ ,‫و‬
‫ض‬ ‫ر‬H, ‫ر‬ 8, ‫ا‬GnRH‫ؤدي‬ 7
. ‫إ‬‫دوث‬H‫ت‬ - H ‫ن‬ ‫ت‬ ‫,و‬
‫ن‬ > 8/ /- ‫د‬ R ‫ا‬.
‫س‬ & ‫ا‬ ‫-ل‬ ‫5ر‬ 8 ‫ا‬ ‫8/وغ‬ ‫ا‬‫ذب‬ 5 ‫ا‬
•‫ت‬ 5‫و‬ ‫أورام‬‫ض‬ 8 ‫ا‬
•‫5ظر‬ ‫ا‬ ‫اورام‬
•?&‫ر‬ ‫ن‬ &‫,رو‬ ‫رض‬K, ‫ا‬
•‫,3دم‬ ‫ا‬ ‫ن‬ ‫ز‬ ‫ا‬ ‫درق‬ ‫ا‬ ‫)ور‬R
•McCune-Albright syndrome
•Peutz-Jeghers syndrome

29. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 29
‫ز‬b,
( / ‫ا‬ ‫-ل‬H ‫ا‬?
? ‫ظ‬K ‫ا‬
‫دد‬K, ‫ا‬
‫-ل‬ ,5%‫ن‬BC‫ا‬ ‫وغ‬GBC‫ا‬ ‫ت‬IJKJ‫وي‬M>N‫ا‬ ‫ر‬P
‫ن‬ ‫,,5ون‬QR>C‫ا‬‫5ر‬ 8 ? &
‫0ظ‬ ‫وب‬ 05‫ددة‬K,
‫ب‬ /H 8 ‫[وة‬R ;38Café au lait spots
‫=رط‬‫زول‬ ,‫5ور‬‫5ظري‬ hZ ‫ن‬.
‫ت‬ [ ‫ا‬ S‫و‬ ‫درق‬ ‫ا‬ ‫ط‬ Z ‫=رط‬
S‫و‬C‫و‬T‫ز‬TVC‫ا‬JT
WTR‫ر‬XC‫ا‬:
Somatic mutation in affected postzygotic
tissues.
ُ َ َ‫ﱡ‬ َ ‫ﱠ‬ ‫ا‬‫م‬ ِ ‫ا‬ ُ‫د‬ِّ َ َ ُ ‫ا‬
MCCUNE-ALBRIGHT SYNDROME
(POLYOSTOTIC FIBROUS DYSPLASIA)

30. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
‫رق‬ ‫ا‬ ‫ر‬ &
HYPOTHYROIDISM
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 30
?R‫در‬ ‫ا‬ ‫ون‬ ‫[ر‬ ‫ا‬ ‫ض‬ ‫و‬K,8 & K ‫ا‬
‫د‬ ‫د‬ ‫ا‬ ‫د‬ ‫د‬Z ‫ا‬ ‫درق‬ ‫ا‬ ‫)ور‬R‫إ=راز‬‫ـ‬ ‫ر‬ , ‫5ل‬Z8 ;(,‫ر‬TRH‫د‬ R ‫ا‬ ‫ت‬ - H ‫ق‬b‫إط‬+‫ت‬ ‫,و‬ ‫ع‬ (,‫ار‬
‫ن‬ ,57‫8رو‬ ‫ا‬)‫ب‬ /H ‫-ر‬(
‫ض‬ 8 ‫ت‬ 5 ? ‫ظ‬K ‫ا‬ ‫ر‬ K ‫ا‬ ;&‫,را‬ ‫د‬Rretarded

31. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
PEUTZ-HEGHERS SYNDROME
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 31
‫ز‬b,
The peutz-jeghers :
‫ز‬b,
The peutz-jeghers :
; ‫,را=ق‬: ; ‫,را=ق‬:
•ِ َb— ‫ا‬ ُ‫ء‬‫دا‬?= ‫ل‬
S[ ‫ا‬ ‫ة‬ 3 ‫ا‬
•‫ت‬ >8),‫&/د‬
‫ط‬
•ِ َb— ‫ا‬ ُ‫ء‬‫دا‬?= ‫ل‬
S[ ‫ا‬ ‫ة‬ 3 ‫ا‬
•‫ت‬ >8),‫&/د‬
‫ط‬
•& ‫ا‬ ‫8ل‬H ‫ا‬ ‫8ورم‬?
‫در‬ ‫ا‬‫ذو‬‫ب‬ 8 ‫ا‬
‫ا‬3/H‫د‬R ‫ذي‬ ‫ا‬ ،
‫(رزا‬ ‫5ون‬
‫ن‬ &‫,رو‬ “
•8 8H ‫ا‬ / ‫ا‬ ‫ورم‬
R‫دو‬ ) ‫ا‬.
•& ‫ا‬ ‫8ل‬H ‫ا‬ ‫8ورم‬?
‫در‬ ‫ا‬‫ذو‬‫ب‬ 8 ‫ا‬
‫ا‬3/H‫د‬R ‫ذي‬ ‫ا‬ ،
‫(رزا‬ ‫5ون‬
‫ن‬ &‫,رو‬ “
•8 8H ‫ا‬ / ‫ا‬ ‫ورم‬
R‫دو‬ ) ‫ا‬.

32. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
8 ‫ا‬ ‫ظ[ور‬ ‫ا‬‫و‬ - & () ‫5ر‬‫و‬‫ا‬H‫دة‬: 8 ‫ا‬ ‫ظ[ور‬ ‫ا‬‫و‬ - & () ‫5ر‬‫و‬‫ا‬H‫دة‬:
‫5ر‬ 8 ‫ا‬ ‫[ود‬ ‫ا‬:>4‫وات‬ ‫5ر‬ 8 ‫ا‬ ‫[ود‬ ‫ا‬:>4‫وات‬
‫5ر‬ 8 ‫ا‬ ‫ن‬ ‫ا68ط‬ ‫ر‬KZ ‫ظ[ور‬:>7‫وات‬ ‫5ر‬ 8 ‫ا‬ ‫ن‬ ‫ا68ط‬ ‫ر‬KZ ‫ظ[ور‬:>7‫وات‬
•ً ‫رور‬S ‫س‬ ‫ج‬bK ‫ا‬
•‫ذ5ور‬ ‫ا‬ ‫ن‬ ‫ث‬ 6‫ا‬ ‫د‬ 0 ; Z‫أ‬
K ‫ا‬ ‫ر‬KZ ‫ظ[ور‬:>8‫وات‬ K ‫ا‬ ‫ر‬KZ ‫ظ[ور‬:>8‫وات‬
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 32
1 ‫ا‬ %2 " / ‫ا‬ ‫غ‬ ‫ا‬8& ‫ا‬
INCOMPLETE ISOSEXUAL PRECOCITY
‫5ر‬ 8 ‫ا‬ ‫[ود‬ ‫ا‬Premature thelarche

33. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 33
‫ءات‬ )3, 7‫ا‬0 KZ ‫ا‬Radiologic
•‫ل‬ / , ‫ا‬ ? ‫ظ‬K ‫ا‬ ‫ر‬ K ‫ا‬)‫س‬ & ‫ا‬ ‫-ل‬ ‫5ر‬ 8 ‫8/وغ‬(Serial bone age
•‫ن‬ ‫ر‬ ‫ا‬(MRI)‫وري‬H ‫ا‬ ?38‫ط‬ ‫ا‬ ‫أو‬(CT)? - ‫ر‬ [‫إظ‬ ; ‫غ‬ ‫/د‬optimal visualization?5‫,ر‬ ‫ا‬ ‫رج‬ ‫وا‬ ‫ء‬ ‫وط‬ ‫ا‬ 3‫ط‬)
?3 3H ‫س‬ & ‫ا‬ ‫-ل‬ ‫5ر‬ 8 ‫8/وغ‬.(
•‫5ظر‬ ‫ا‬ ‫أو‬ ‫وض‬H ‫ا‬ ‫و‬ ‫/8طن‬ ‫5و‬ 6‫ا‬ ‫و‬ ?38‫ط‬ ‫ا‬ ‫و‬ ‫ن‬ ‫ر‬ ‫ا‬)‫ذب‬ 5 ‫س‬ & ‫ا‬ ‫-ل‬ ‫5ر‬ 8 ‫و8/وغ‬ ، ‫س‬ & ‫ا‬ ‫ر‬ > ‫5ر‬ 8 ‫8/وغ‬.(
‫ءات‬ )3, 7‫ا‬‫8ر‬ ‫ا‬Laboratory
•(LH) and (FSH)
•(DHEA-S), testosterone)‫س‬ & ‫ا‬ ‫ر‬ > ‫5ر‬ 8 ‫8/وغ‬(
•17-OH progesterone, 11-deoxycortisol)‫8ـ‬ ‫ك‬Z ‫ا‬[CAH]‫8ب‬‫س‬ & ‫ا‬ ‫ر‬ > ‫5ر‬ 8 ‫8/وغ‬(
•‫درق‬ ‫ا‬ ‫ف‬ ‫وظ‬ ‫رات‬ 8, ‫ا‬]4free TTSH,[)‫س‬ & ‫ا‬ ‫-ل‬ ‫5ر‬ 8 ‫8/وغ‬(
•‫ض‬ ‫ر‬H, ‫ر‬ 8, ‫ا‬(GnRH):‫س‬ RLH‫ء‬ ‫إ0ط‬ ‫د‬K8100 μg‫ن‬GnRH‫د‬ ‫ور‬)./0 ‫د‬ ,K ‫ا‬ ‫ر‬ B‫و‬ ‫د‬ ,K ‫ا‬ ‫5ر‬ 8 ‫ا‬ ‫8/وغ‬ ‫ا‬ ‫ز‬ ,
‫ت‬ - H‫د‬ R ‫ا‬.(
‫وق‬ ‫ا‬31-2%6= ‫م‬ ? (0 ‫ا‬ ? ‫ا‬ ‫ص‬ 3 ‫ا‬? A‫إ‬‫ي‬ AD‫ا‬ / ‫ا‬ ‫غ‬ ‫ا‬ - +

34. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬+ +3 ‫ا‬ 1 ‫ا‬ %2 " ‫غ‬ ‫ا‬ ‫ج‬F
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 34
75%‫5ر‬ 8 ‫ا‬ ‫8/وغ‬ ‫ا‬ ‫7ت‬ H ‫ن‬‫و‬ 88 & K‫3/دات‬GnRH
‫ج‬b0 ‫8دون‬>50%‫ت‬ ,( ‫ا‬ ‫ن‬‫33ن‬H?B‫8/و‬ ‫طول‬152.4‫م‬.
‫3/دات‬GnRHLH‫و‬FSH‫ف‬R‫,و‬‫د‬ 3 ‫ا‬ & ‫ا‬ ‫دات‬ ‫رو‬ , ‫ا‬ ‫إ=راز‬
‫رع‬ , ‫ا‬ ‫ت‬ Z Z ‫ا‬ ‫م‬ H, ‫ا‬ ;

35. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 35
Figure 31-7 Scatter diagram of final height vs age at diagnosis of girls with gonadotropin-releasing hormone (GnRH)-dependent
precocious puberty who were treated with GnRH agonist therapy (top). The shaded area represents the range of normal adult
height for North American women. Bottom, Percentage target height (final target height/target height × 100) vs the age at
diagnosis. (Modified from Kletter GD, Kelch RP: Effects of gonadotropin-releasing hormone analogue therapy on adult stature in
precocious puberty. J Clin Endocrinol Metab 79:333, 1994.)

36. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 36

37. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬‫غ‬ ‫ا‬ #$0
DELAYED PUBERTY
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 37
‫ر‬ K8 ‫ت‬ ,( ‫ا‬ ‫ظم‬K ‫د‬ 0 ?B‫8/و‬ ‫ا‬ cS ‫ا‬ ‫8دأ‬13
‫ر‬ K8 ‫[ود‬ ‫ا‬ ‫دوث‬H ‫0دم‬14F •=‫ء‬ )3, 7‫ا‬ ?0‫,د‬
?&‫و‬ ‫و‬ ‫ز‬ ( ‫ا‬ ‫ر‬ h, ‫ا‬)10: (%
•/ 0
•3 R‫د‬ )R ‫ذ‬ ‫أ‬ ‫&ب‬:
•‫ا‬ H ‫ا‬H)‫ا‬ ّ K ‫ا‬38
•‫طول‬ ‫ا‬
•‫>ذا‬ ‫ا‬ ‫دات‬ K ‫ا‬
•S ‫ر‬ ‫ا‬ ‫ن‬ ‫ر‬ , ‫ا‬ ‫واع‬ ‫أ‬
•‫ء‬ 3Z“ ?B‫8/و‬ ‫ا‬ ‫,طور‬ ‫ا‬ ‫ل‬ ) (,‫ء‬ 8m‫وا‬.

38. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
Constitutional (physiologic delay) *
Chronic anovulation (polycystic ovarian syndrome)
Anatomic
Imperforate hymen
Transverse vaginal septum
Vaginal and/or cervical agenesis
Müllerian agenesis
Androgen insensitivity syndrome
(testicular feminization)
Hypergonadotropic hypogonadism
Gonadal dysgenesis (Turner syndrome)
Pure gonadal dysgenesis (46,XX or 46,XY)
Premature ovarian failure
Idiopathic
Resistant ovary syndrome
Autoimmune oophoritis
Chemotherapy
Radiation
17α-Hydroxylase deficiency
Aromatase deficiency
Galactosemia
Hypogonadotropic hypogonadism
Central nervous system etiologies
Tumors (i.e., craniopharyngioma)
Infection
Trauma
Chronic disease (i.e., celiac disease or Crohn
disease)
GnRH deficiency (Kallman syndrome)
Isolated gonadotropin deficiency
Hypothyroidism
Hyperprolactinoma
Adrenal
Congenital adrenal hyperplasia
Cushing syndrome
Addison disease
Psychosocial
Eating disorders
Excessive exercise
Stress, depression
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y
38
CAUSES OF DELAYED PUBERTY
* The most common cause of delayed puberty is
constitutional
delay. GnRH gonadotropin-releasing hormone.

39. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
‫غ‬ ‫ا‬ #$0
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 39
BOX 31-3 Radiologic and Laboratory Tests Used to Evaluate Female Delayed Puberty
ً 0 KZRadiologic
•‫ن‬ ‫ر‬MRI+‫غ‬ ‫/د‬ ‫وري‬H ?38‫ط‬CT?5‫,ر‬ ‫ا‬ ‫رج‬ ‫وا‬ ‫ء‬ ‫وط‬ ‫ا‬ 3‫ط‬ - ‫رؤ‬ ;)‫)ور‬R‫د‬ R‫أ‬
‫ص‬R‫ت‬ - H‫د‬ R ‫ا‬(
ً ‫8ر‬Laboratory
•FSH
•>8) > )Karyotype)‫ر‬ h, ‫8/وغ‬–[8 / , ‫ء‬ S0‫أ‬(
•‫رون‬ , &‫8رو‬)‫وز‬K ‫وي‬ - ‫5ل‬Z8 ‫ر‬ h, ‫8/وغ‬17-‫ز‬b 5‫درو‬ ‫ھ‬[P450c17](
•‫ن‬ ,57‫8رو‬)‫)ور‬R‫د‬ R‫أ‬‫ص‬R‫ت‬ - H‫د‬ R ‫ا‬(

40. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
‫غ‬ ‫ا‬ #$0
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 40
•‫)ور‬R‫د‬ R ‫ا‬‫ص‬R‫ت‬ - H‫د‬ R ‫ا‬:Hypogonadotropic hypogonadism
•‫وي‬ - ‫أو‬ ? ‫8د‬ ‫ث‬ ‫ط‬ ‫ع‬ ‫3ط‬ ‫ا‬ ‫8ب‬ , ‫د‬R ‫ت‬ 8‫طرا‬S‫ا‬
•?8)K ‫ا‬ ‫3[م‬ ‫ا‬Anorexia nervosa:
•‫)ور‬R‫د‬ R ‫ا‬‫ص‬R‫ت‬ - H‫د‬ R ‫ا‬
•‫8/وغ‬ ‫را‬ h,
•./0 ‫ؤ-ر‬0.5-1%‫ت‬ 8 Z ‫ا‬ ‫د‬ 0.
•‫)ور‬R‫د‬ R ‫ا‬;(,‫ر‬‫ت‬ - H‫د‬ R ‫ا‬Hypergonadotropic hypogonadism.
•‫ذوذات‬Z ‫ا‬>8) ‫ا‬
•H‫&را‬ ‫ا‬ ‫ن‬ S 8 ‫ا‬ ‫ت‬ ‫أذ‬
•‫وي‬ 5 ‫ج‬b0
•KZ‫أ‬
•?>8) ‫ا‬ ‫و&ود‬ ‫د‬ 0Y‫ل‬ ) , ‫ا‬ ‫&ب‬ F •=‫د‬ R ‫ا‬
‫ب‬ 8 ‫ا‬‫ب‬ 8 ‫ا‬

41. ‫ا‬ ‫راض‬ ‫ا‬–‫ا‬ ‫ا‬
"‫ز‬F "‫ن‬ /
KALLMANN SYNDROME
D R . H I S H A M A L - H A M M A M I P R O F E S S O R O F O B S T E T R I C S A N D G Y N E C O L O G Y
F A C U L T Y O F M E D I C I N E S Y R I A N P R I V A T E U N I V E R S I T Y 41
‫8ـ‬ ‫ھر‬ ‫,,ظ‬
•‫)ور‬R‫د‬ R ‫ا‬‫ص‬R‫ت‬ - H‫د‬ R ‫ا‬Hypogonadotropic
hypogonadism
•[)3 ‫أو‬ ‫م‬Z ‫ا‬ H ‫ب‬ BAnosmia or hyposmia
‫0ن‬ c, , ‫د‬R
•-‫ور‬ ‫ا‬ ?= ‫ط(رة‬ ‫0ن‬ &, ‫,5ون‬KAL?>8) ‫ا‬ ./0X
•‫ـ‬ ‫(رزة‬ ‫ا‬ ‫ت‬ ‫)8و‬K ‫ا‬ ‫ھ&رة‬ ; , ‫د‬ & ‫ط(رات‬ ‫او0ن‬GnRH. ‫إ‬
& ‫ا‬ ‫ة‬ H ‫ا‬ ?= ‫ء‬ ‫وط‬ ‫ا‬.
‫د‬R .S‫ر‬ ‫ا‬ ‫ھؤ7ء‬
‫ذوذات‬Z ‫ن‬ ‫ون‬ K
‫ب‬ 5‫,را‬ ‫ا‬ ?= ‫رى‬ ‫أ‬
‫)ف‬ ‫ا‬ ‫ط‬ ‫ا‬ ./0
‫/رأس‬
?= 8 )6‫ا‬ ‫ھد‬ Z,
‫5ل‬ ‫ن‬ ‫دة‬H‫وا‬50000
.- ‫أ‬