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At 6-8 weeks there is
transfer of functions of corpus
luteum to the placenta-which
acts temporarily as a new
endocrine organ or powerhouse
of hormone production.
Protein hormones
Steroid hormones
HYPOTHALAMIC-                  CYTOCHEMICAL
  LIKE(RELEASING)                   ORIGINE
     HORMONES
Corticotrophin releasing      Cytotrophoblast
(CRH)                                  +
Gonadotrophin releasing
                                       +
(GnRH)
Thyrotrophin releasing(TRH)            +
Growth hormone
releasing(GHRH)
PITUITAEY LIKE      CYTOCHEMICAL
     HORMONES          ORIGIN
•Adenocorticotrophic   Syncytiotrophoblast
hormone(ACTH)
•Human chorionic                     +
gonadotrophin (hCG)
•Human chorionic                     +
thyrotrophin (hCT)
•Human placental                         +
lactogen (hPL)
Protein hormones are similar
but not necessarily identical with
those produced by the pituitary. For
example placental lactogen is
chemicaly similar to both pituitary
growth hormone and prolactin, but
biological activity of    placental
lactogen is much inferior than
prolactin    or   growth   hormone
produced by pituitary.
Human  chorionic gonadotrophin
Human placental lactogen
Pregnancy       specific     β-1
 glycoprotein (PSβ-1G)
 hCG  is a glycoprotein
 Molecular weight is 36000-40000 daltons
 It consists of a hormone non-specific α(92
  amino acids) and a hormone specific β(145
  amino acids) subunit
 The α subunit is biochemically similar to LH,
  FSH and TSH
 Β subunit is relatively unique to hCG
 It act as a stimulus for the secretion
  of progesteron by the corpus luteum
  of pregnancy
 The rescue and maintenance of
  corpus luteum       till 6 weeks of
  pregnancy
 It stimulate Leyding cells of the
  male fetus to produce testosterone
 It   has got immuno-suppressive
  activity
It inhibit the maternal process
 of immunorejection of the fetus
 as a homograft
Stimulates both adrenal and
 placental steroidogenesis
Stimulates    maternal thyroid
 because of its thyrotrophic
 activity
   The half life of hCG is about 24 hours
   By radioimmunoassay it can be detected in the
    maternal serum or urine as early as 8-9 days
    following ovulation
   The doubling time of hCG concentration in plasma is
    1.4-2 days
   It reach maximum levels ranging 100IU and 200IU/ml
    between 60-70 days of pregnancy
   The concentration falls slowly reaching a low level of
    10-20IU/ml between 100-130 days
   There after it remains constant throughout pregnancy
   Slight secondary peak occur at 32 weeks
   Hormone disappears from the circulation within
    2weeks following delivery
Multiple pregnancy
Hydatidiform    mole or
 choriocarcinoma
Pregnancy     with   a21
 trisomy fetus
 Itis synthesised by the syncytiotrophoblat of
  the placenta.
 Chemically and immunologically similar to
  pituitary growth hormone and prolactin.
 HPL in maternal serum is first detected
  during the 5th week.
 The level rises progressively from 5micro
  gms/ml to 25micro gms/ml until about 36
  weeks.
 The plasma concentration of HPL is
  proportional to placental mass.
Antagonizes  insulin action
High level of maternal insulin
 helps protein synthesis
HPL causes lipolysis and
 proteolysis
Promotes transfer of glucose
 and amino acids to the fetus.
 Produced  by the trophoblast cells
 It can be detected in the maternal serum
  18—20 days ovulation.
  PS β– 1 G is a potent immunosupressor of
  lymphocyte proliferation
 It prevents the rejection of the conceptus
 Early  pregnancy factor (EPF)is a protein
  ,produced by the activated platelets and
  other maternal tissues.
 It is detected in the circulation 6 to 24 hours
  after conception.
 It is an immunosupressant and prevents
  rejection of the conceptus.
 Inhibin
        , activin, insulin like growth factor,
 transmitting growth factor β and epidermal
  growth factors are produced by the
  syncytiotrophoblast cells.
Functios include,
 Immunosupressive
 Paracrine
 Steroidogenic.
A  (PAPP-A) is secreted by the
 syncytiotrophoblast
It act as an immunosupressant in
 pregnancy
OESTROGEN:    The site of
 production is in the
 syncytiotrophoblast
Chemical nature: Estrogens are
 phenolic steroids with 18 carbon
 atoms, charecterized by an
 atomic ring.
Estriol is produced in large
 amounts during pregnancy.
      Maternal cholesterol is converted in by
    placenta to pregnenolone and later to
    progesterone.      Placental      pregnenolone
    toghether with fetal adrenal pregnenolone is
    partly converted to pregnenolone sulphate .
    pregnenolone sulphate is then coverted by fetal
    adrenals to dehydroepiandrosterone sulphate or
    DHEA SO4 ,the most important percurser of
    placental oestrogens. This biochemical changes
    is produced by hydrolysis of the sulphate to
    dehydroepiandrosterone     and conversion to
    androsterone, followed by aromatization of
    oestrogen.
 DHEA  SO4 of fetal adrenal origin is converted
  in the fetal liver to 16- alpha hydroxy DHEA
  SO4 which is then converted by placenta to
  oestriol in two steps.
 Step 1: Sulphatase removes the so4 radical.
 Step 2: Aromatase converts the A ring to the
  phenolic stucture characteristics of
  oestrogens.
 Thus the production of oestriol involves the
  integration of maternal , fetal and placental
  pathways.
Oestriol is first detectable at
 9weeks     (0.05ng/ml)     and
 increases gradually to about
 30ng/ml at term.
 Normal oestriol value values signify fetal well-
  being.
 Oestriol levels reflects placental functioning
  ability.
 Low oestriol level indicates , fetal death, fetal
  anomalies (adrenal atrophy, anencephaly, down
  syndrome), hydatidiform moles, placental
  sulphatase or aromatase deficiency.
 High levels are often associated with multiple
  pregnancy and Rh-isoimmunization.
 Declining oestriol levels or their failure to rise on
  serial examinations are indicative of placental
  insuffiency causing IUGR, PIH, maternal renal
  disease.
Before 6weeks of       pregnancy the
corpus     luteum     secretes    17-hydroxy
progesterone. Following the development of
trophoblast it is synthesised and secreted
form placenta. The placenta can utilise
cholesterole as a precuser derived from the
mother for the production of pregnenolone
and ultimatly progesterone.
 The   average levels of progesterone at
  12week ,28week, and term approximate
  25ng/ml, 80ng/ml, 300ng/ml respectively.
 Low progesterone levels are observed in
  ectopic pregnancy and abortion.
 High values are observed in , hydatidiform
  mole, Rh-isoimmunization.
 After delivery plasma progesterone level
  decreases rapidly and is not detectable after
  24 hours.
 Oestrogen      causes     hypertrophy    and
  hyperplasia of the uterine myometrium.
 Progesterone in conjunction with oestrogen
  stimulates growth of the uterus
 It   causes decidual changes in the
  endometrium and inhibits myometrial
  contraction.
 Hypertrophy and proliferation of breat ducts
  are due to oestrogen
 Both steroids are required for the adaptation
  of the maternal organs to the constantly
  increasing demands of the growing fetus.
 Oestrogen   sensitises the myometrium to
  oxytocin and prostaglandins. Oestrogen ripen
  the cervix.
 Progesterone along with hCG and decidual
  cortisol inhibits T-lymphocyte mediated
  tissue rejection and protects the conceptus.
 Together they cause inhibition of cyclic
  fluctuating activity of gonandotropin-gonadal
  axis ther by preserving gonannnnndal
  function
 Diagnosisof pregnancy
 Follow up cases who had trophoblastic
  tumours
 Detection of functions of feto-placental unit
 Main  source of production is the corpus
  luteum of overy,but part of it may be
  produced by the placenta and decidua.
 Relaxin relaxes the symphysis and sacroiliac
  joints during pregnancy and also helps in
  cervical ripening by its biochemical effect.
Placental endocrinology

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Placental endocrinology

  • 1.
  • 2.
  • 3. At 6-8 weeks there is transfer of functions of corpus luteum to the placenta-which acts temporarily as a new endocrine organ or powerhouse of hormone production.
  • 5. HYPOTHALAMIC- CYTOCHEMICAL LIKE(RELEASING) ORIGINE HORMONES Corticotrophin releasing Cytotrophoblast (CRH) + Gonadotrophin releasing + (GnRH) Thyrotrophin releasing(TRH) + Growth hormone releasing(GHRH)
  • 6. PITUITAEY LIKE CYTOCHEMICAL HORMONES ORIGIN •Adenocorticotrophic Syncytiotrophoblast hormone(ACTH) •Human chorionic + gonadotrophin (hCG) •Human chorionic + thyrotrophin (hCT) •Human placental + lactogen (hPL)
  • 7. Protein hormones are similar but not necessarily identical with those produced by the pituitary. For example placental lactogen is chemicaly similar to both pituitary growth hormone and prolactin, but biological activity of placental lactogen is much inferior than prolactin or growth hormone produced by pituitary.
  • 8. Human chorionic gonadotrophin Human placental lactogen Pregnancy specific β-1 glycoprotein (PSβ-1G)
  • 9.  hCG is a glycoprotein  Molecular weight is 36000-40000 daltons  It consists of a hormone non-specific α(92 amino acids) and a hormone specific β(145 amino acids) subunit  The α subunit is biochemically similar to LH, FSH and TSH  Β subunit is relatively unique to hCG
  • 10.  It act as a stimulus for the secretion of progesteron by the corpus luteum of pregnancy  The rescue and maintenance of corpus luteum till 6 weeks of pregnancy  It stimulate Leyding cells of the male fetus to produce testosterone  It has got immuno-suppressive activity
  • 11. It inhibit the maternal process of immunorejection of the fetus as a homograft Stimulates both adrenal and placental steroidogenesis Stimulates maternal thyroid because of its thyrotrophic activity
  • 12. The half life of hCG is about 24 hours  By radioimmunoassay it can be detected in the maternal serum or urine as early as 8-9 days following ovulation  The doubling time of hCG concentration in plasma is 1.4-2 days  It reach maximum levels ranging 100IU and 200IU/ml between 60-70 days of pregnancy  The concentration falls slowly reaching a low level of 10-20IU/ml between 100-130 days  There after it remains constant throughout pregnancy  Slight secondary peak occur at 32 weeks  Hormone disappears from the circulation within 2weeks following delivery
  • 13. Multiple pregnancy Hydatidiform mole or choriocarcinoma Pregnancy with a21 trisomy fetus
  • 14.  Itis synthesised by the syncytiotrophoblat of the placenta.  Chemically and immunologically similar to pituitary growth hormone and prolactin.  HPL in maternal serum is first detected during the 5th week.  The level rises progressively from 5micro gms/ml to 25micro gms/ml until about 36 weeks.  The plasma concentration of HPL is proportional to placental mass.
  • 15. Antagonizes insulin action High level of maternal insulin helps protein synthesis HPL causes lipolysis and proteolysis Promotes transfer of glucose and amino acids to the fetus.
  • 16.  Produced by the trophoblast cells  It can be detected in the maternal serum 18—20 days ovulation.  PS β– 1 G is a potent immunosupressor of lymphocyte proliferation  It prevents the rejection of the conceptus
  • 17.  Early pregnancy factor (EPF)is a protein ,produced by the activated platelets and other maternal tissues.  It is detected in the circulation 6 to 24 hours after conception.  It is an immunosupressant and prevents rejection of the conceptus.
  • 18.  Inhibin , activin, insulin like growth factor, transmitting growth factor β and epidermal growth factors are produced by the syncytiotrophoblast cells. Functios include,  Immunosupressive  Paracrine  Steroidogenic.
  • 19. A (PAPP-A) is secreted by the syncytiotrophoblast It act as an immunosupressant in pregnancy
  • 20. OESTROGEN: The site of production is in the syncytiotrophoblast Chemical nature: Estrogens are phenolic steroids with 18 carbon atoms, charecterized by an atomic ring. Estriol is produced in large amounts during pregnancy.
  • 21. Maternal cholesterol is converted in by placenta to pregnenolone and later to progesterone. Placental pregnenolone toghether with fetal adrenal pregnenolone is partly converted to pregnenolone sulphate . pregnenolone sulphate is then coverted by fetal adrenals to dehydroepiandrosterone sulphate or DHEA SO4 ,the most important percurser of placental oestrogens. This biochemical changes is produced by hydrolysis of the sulphate to dehydroepiandrosterone and conversion to androsterone, followed by aromatization of oestrogen.
  • 22.  DHEA SO4 of fetal adrenal origin is converted in the fetal liver to 16- alpha hydroxy DHEA SO4 which is then converted by placenta to oestriol in two steps.  Step 1: Sulphatase removes the so4 radical.  Step 2: Aromatase converts the A ring to the phenolic stucture characteristics of oestrogens.  Thus the production of oestriol involves the integration of maternal , fetal and placental pathways.
  • 23. Oestriol is first detectable at 9weeks (0.05ng/ml) and increases gradually to about 30ng/ml at term.
  • 24.  Normal oestriol value values signify fetal well- being.  Oestriol levels reflects placental functioning ability.  Low oestriol level indicates , fetal death, fetal anomalies (adrenal atrophy, anencephaly, down syndrome), hydatidiform moles, placental sulphatase or aromatase deficiency.  High levels are often associated with multiple pregnancy and Rh-isoimmunization.  Declining oestriol levels or their failure to rise on serial examinations are indicative of placental insuffiency causing IUGR, PIH, maternal renal disease.
  • 25. Before 6weeks of pregnancy the corpus luteum secretes 17-hydroxy progesterone. Following the development of trophoblast it is synthesised and secreted form placenta. The placenta can utilise cholesterole as a precuser derived from the mother for the production of pregnenolone and ultimatly progesterone.
  • 26.  The average levels of progesterone at 12week ,28week, and term approximate 25ng/ml, 80ng/ml, 300ng/ml respectively.  Low progesterone levels are observed in ectopic pregnancy and abortion.  High values are observed in , hydatidiform mole, Rh-isoimmunization.  After delivery plasma progesterone level decreases rapidly and is not detectable after 24 hours.
  • 27.  Oestrogen causes hypertrophy and hyperplasia of the uterine myometrium.  Progesterone in conjunction with oestrogen stimulates growth of the uterus  It causes decidual changes in the endometrium and inhibits myometrial contraction.  Hypertrophy and proliferation of breat ducts are due to oestrogen  Both steroids are required for the adaptation of the maternal organs to the constantly increasing demands of the growing fetus.
  • 28.  Oestrogen sensitises the myometrium to oxytocin and prostaglandins. Oestrogen ripen the cervix.  Progesterone along with hCG and decidual cortisol inhibits T-lymphocyte mediated tissue rejection and protects the conceptus.  Together they cause inhibition of cyclic fluctuating activity of gonandotropin-gonadal axis ther by preserving gonannnnndal function
  • 29.  Diagnosisof pregnancy  Follow up cases who had trophoblastic tumours  Detection of functions of feto-placental unit
  • 30.  Main source of production is the corpus luteum of overy,but part of it may be produced by the placenta and decidua.  Relaxin relaxes the symphysis and sacroiliac joints during pregnancy and also helps in cervical ripening by its biochemical effect.