Lecture about placenta &fetal membrane development in human

1. Placenta& Fetal
membranes
Salah Roshdy,MD
Professor of Obstetrics & Gynecology
Sohag College of Medicine
Sohag University

2. Learning Objectives
Mention function of fetal membrane
Discuss origin of placenta
Describe normal placenta
Lists functions of placenta
Enumerate placental hormones
Discuss placental abnormalities
Describe normal & abnormal U.C

3. Early Human Development
Zygote
Morula
Blastocyst
Embryo
Fetus

4. Fetal membrane
•Originate from blastocyst, don’t
participate in the formation of
embryo
•Including:
1) Chorion
2) Amnion
3) Yolk sac
4) Allantois
5)Umbilical cord

5. Amnion
Thin but tough
Forms a fluid filled membranous amniotic
sac that surrounds the embryo and fetus
Is attached to the margins of the
embryonic disc

6. Amnion
•Amniotic membrane: amniotic epi.+ extraembryonic
mesoderm
•Amniotic fluid:
Produce:1)amniotic cells
2) infusion of fluid from maternal blood
3) urine output from the fetus
4) pulmonary secretions
Output: 1) absorbed by amniotic cells
2) fetus swallow

7. Amniotic Fluid
Plays a major role in fetal growth and
development.
Daily contribution of fluid from respiratory
tract is 300-400 ml.
500 ml of urine is added daily during the
late pregnancy.
Amniotic fluid volume is 30 ml at 10
weeks, 350 ml at 20 weeks, 700-1000 ml
at 37 weeks.

8. Composition of Amniotic
Fluid
99 % is water
Desquamated fetal epithelial cells
Organic & inorganic salts
Protein, carbohydrates, fats,
enzymes, hormones
Meconium & urine in the late stage

9. Significance of Amniotic Fluid
Permits symmetrical external growth of the embryo and
fetus
Acts as a barrier to infection
Permits normal fetal lung development
Prevents adherence of amnion to fetus
Cushions & protects the embryo and fetus
Helps maintain the body temperature
Enables the fetus to move freely

10. Yolk Sac
It is large at 32 days
Shrinks to 5mm pear shaped remnant
by 10th week & connected to the
midgut by a narrow yolk stalk
Becomes very small at 20 weeks
Usually not visible thereafter

11. Significance of Yolk Sac
Has a role in transfer of nutrients during
the 2nd and 3rd weeks
Blood development first occurs here
Incorporate into the endoderm of embryo
as a primordial gut
Primordial germ cells appear in the
endodermal lining of the wall of the yolk
sac in the 3rd week

12. Fate of Yolk Sac
At 10 weeks lies in the chorionic cavity
between chorionic and amniotic sac
Atrophies as pregnancy advances
Sometimes it persists throughout the
pregnancy but of no significance
In about 2% of adults the proximal intra-
abdominal part of yolk stalk persists as an
ileal diverticulum or Meckel diverticulum

13. Allantois
In the 3rd week it appears as a
sausagelike diverticulum from the
caudal wall of yolk sac that extends
into the connecting stalk
During the 2nd month, the
extraembryonic part of the allantois
degenerates

15. Functions of Allantois
Blood formation occurs in the wall during
the 3rd to 5th week
Its blood vessels persist as the umbilical
vein and arteries
Becomes Urachus and after birth is
transformed into median umbilical
ligament extends from the apex of the
bladder to the umbilicus

16. Chorion
The extraembryonic somatic mesoderm
and the two layers of trophoblast form the
chorion
Chorion forms the wall of chorionic sac
Embryo and its amniotic and yolk sacs are
suspended into it by connecting stalk

17. Chorion
Growth of these extensions are
caused by underlying extraembryonic
somatic mesoderm
The cellular projections form primary
chorionic villi

19. Chorion
Chorionic villi cover the entire chorionic
sac until the beginning of 8th week
As this sac grows, the villi associated with
decidua capsularis are compressed,
reducing the blood supply to them
These villi soon degenerates producing an
avascular bare area smooth chorion
(chorion laeve)

20. Chorion
As the villi disappear, those
associated with the decidua basalis
rapidly increase in number
Branch profusely and enlarge
This bushy part of the chorionic sac
is villous chorion

21. PRIMARY CHORIONIC
VILLI
At the end of 2nd
week, finger-like
processes formed of
outer
syncytiotrophoblast
& inner
cytotrophoblast
appear

22. SECONDARY CHORIONIC
VILLI
Early in 3rd
week,
extraembryonic
mesoderm
extends inside the
villi

23. TERTIARY CHORIONIC VILLI
During 3rd week,
arterioles, venules &
capillaries develop in
the mesenchyme of
villi & join umbilical
vessels
By the end of 3rd
week, embryonic
blood begins to flow
slowly through
capillaries in
chorionic villi

24. Decidua
The gravid endometrium is known as
decidua
It is the functional layer of
endometrium in a pregnant woman
This part of the endometrium
separates from the rest of the uterus
after parturition

25. DECIDUA  Decidua
basalis: It lies at
the site of
implantation ,it
forms the maternal
part of the placenta
 Decidua
capsularis: it
covers the
conceptus
 Decidua
parietalis: the
rest of the
endometrium
that lines the
body & the
fundus.
25

26. Decidua
The full significance of decidual cells is not
understood
They may protect the maternal tissue
against uncontrolled invasion by the
syncytiotrophoblast
They may be involved in hormonal
production

27. 27
PLACENTA
This is a fetomaternal organ.
It has two components:
 Fetal part – develops from the chorionic sac ( chorion
frondosum )
 Maternal part – derived from the endometrium ( functional
layer – decidua basalis )

29. During the 4th and 5th month, the decidua forms a
number of decidual septa, which project into the
intervillous space.
As a result of this septum formation, the placenta is
divided into a number of compartments (cotyledons).

30. PLACENTAL MEMBRANE
This is a composite
structure that separating
the fetal blood from the
maternal blood.
It has four layers:
 Syncytiotrophoblast
 Cytotrophoblast
 Connective tissue of
villus
 Endothelium of fetal
capillaries
After the 20th week, the
cytotrophoblastic cells
disappear and the
placental membrane
consists only of three
layers.
30

31. 31
It separates fetal from maternal blood.
It prevents mixing of them.
It is an incomplete barrier as it only prevents large
molecules to pass ( heparin & bacteria)
But cannot prevents passage of viruses(e.g.
rubella), micro-organisms(toxoplama, treponema
pallidum) drugs and hormones.

32. Functions of placental barrier:
1. It prevents most organisms from passing to
the fetus, so it acts as a protective
mechanism against damaging factors, many
viruses such as Rubella, Coxackie virus,
German measles and poliomylitis virus
traverse the placenta. These viruses may
result in congenital malformations.
2. Most of the drugs cross the placenta and
cause serious damage.

33. The full term
placenta
is discoid in shape.
 Diameter = 15-25 cm,
 2-3 cm thick,
 Weight = 0.5 kg.
 Umbilical cord is attached
to its center.
Position : in the upper uterine
segment (99.5%), either in
the posterior surface (2/3) or
the anterior surface (1/3).

34. Surfaces:
1- Fetal surface: which is
smooth and shinny because it is
covered by an amniotic
membrane. The umbilical cord
is attached centrally to this
surface.
2- Maternal surface: which
is rough, reddish, and has 15 –
20 elevated areas called
cotyledons with deep grooves
in between made by the
decidual septa.

35. Function of placenta:-
1. Respiratory function
2. Excretory function
3. Nutritional function
4. Endocrine function:- placenta acts as
endocrine gland
5. Barrier function:- prevents transfer of
maternal infection.
6. Enzymatic action-
7. Immunological function:- ig G.

36. Nutritive function
Fetus obtains its nutrients from the maternal blood
Glucose- transferred to the fetus by facilitated diffusion
Lipids for fetal growth and development has dual origin. They
are transferred across the fetal membrane or synthesised in the
fetus
Amino acids are transferred by active transport
Water and electrolytes- Na, K ,Cl cross by simple diffusion, Ca ,
P, and Fe cross by active transport
Water soluble vitamins are transferred by active transport but
the fat soluble vitamins are transferred slowly

37. Respiratory function
Although fetal respiratory movement occurs,
no active exchange of gases takes place
Intake of oxygen and output of carbon dioxide
take place by simple diffusion across the fetal
membrane
O2 delivery to the fetus is at the rate of 8
ml/kg which is achieved by cord blood flow of
160-320ml/min

38. Excretory function
Waste products from the fetus such as
urea, uric acid, cretinine are excreted to
the maternal blood by simple diffusion

39. Barrier Function
Substances with large molecular weight or size like
insulin or heparin are transferred minimally
Only IgG ( not IgA or Ig M )antibodies and antigens
can cross the placental barrier
Most drugs can cross the placental barrier and some
can be teratogenic
Various viruses, bacteria, protozoa can cross the
placenta and affect the fetus in utero

40. Immunological function
Inspite of foreign paternally inherited
antigens in the fetus and placenta, there
is no graft rejection due to
immunological protection provided by
the placenta

41. Endocrine and Enzymatic
function
Placenta secretes various hormones –
Protein hormones like HCG, human
placental lactogen,pregnancy specific beta 1
glycoprotein,,pregnancy associated plasma
protein, steroidal hormones like estrogen and
progestrone
Enzymes secreted are diamine oxidase-
which activates the circulatory pressor
amines,oxytocinase which neutralizes
oxytocin, phospholipase A2 which
synthesizes arachidonic acid

42. Placenta

43. PLACENTAL PROTEIN
HORMONES
1. placental lactogen (hPL)
2. chorionic gonadotropin
(hCG)
3. Adenocorticotropin (ACTH)
4. Growth hormone variant
(hGH-V)
5. Parathyroid hormone-related
protein (PTH-rP)
6. Calcitonin
7. Relaxin
8. Inhibins
9. Activins
10. Atrial natriuretic peptide

44. PLACENTAL PROTEIN
HORMONES
11. Hypothalamic-like releasing and
inhibiting hormones
 Thyrotropin releasing hormone
(TRH)
 Gonadotropin releasing hormone
(GnRH)
 Corticotropin-releasing hormone
(CRH)
 Growth hormone-releasing
hormone (GHRH)
12. fetal compartment – alpha feto-
protein
13. Maternal compartment – prolactin,
relaxin and other decidual proteins

45. • Glycoprotein with biological activity similar to luteinizing
hormone
• Both act via the plasma membrane LH-hCG receptor
• Produced in the placenta, but also synthesized in fetal
kidney and a number of fetal tissues may produce the β-
subunit or intact hCG molecule .
• Also produced by malignant tumors
• Presence of hCG in blood and urine of reproductive age
women is almost indicative of the presence of fetal
trophoblasts either in pregnancy or in neoplastic disease
Human chorionic gonadotropin (hCG)

46. Chemical Characteristics of hCG
Carbohydrate component protects the molecule from catabolism
Plasma half life of the intact molecule: 36-hour
Composed of 2 dissimilar subunits (α and β)
No biological activity of either separated subunit
Bioactivity which is binding to the LH receptor is only present if the
two units are combined
Structurally identical to 3 other glycoprotein hormones: LH, FSH and
TSH
Amino acid sequences of the beta subunit of hCG is distinctively
dissimilar from those of LH, FSH, and TSH

47. Biosynthesis of hCG
Plasma levels of free β-subunits increase steadily
until the 36th week of pregnancy and then plateaus till
the end of pregnancy
Secretion of β-hCG corresponds roughly to the
placental mass
Rate of secretionof the complete hCG molecule is
maximal at 8 to 10 weeks of gestation
Placental GnRH, produced in cytotrophoblast, acts in
paracrine manner on syncitiotrophoblast to stimulate
hCG production

48. Biosynthesis of hCG
Other agents that believed to influence
hCG secretion in trophoblast:
 Interleukin-6
 Epidermal growth factor
 Cyclic AMP
Activin stimulates and inhibin inhibits
production of GnRH and hCG

49. Cellular Origin of hCG
< 5 weeks hCG is expressed in both
syncytiotrophoblasts and
cytotrophoblast cells
At the peak of maternal levels later in
gestation
hCG is produced almost exclusively in
the syncitiotrophoblast

50. Concentration of hCG in
Serum and Urine
• Intact hCG molecule is detectable in plasma of
pregnant women about 7 to 9 days after ovulation
• hCG enters maternal blood at time of blastocyst
implantation
• Blood levels increase rapidly, doubling every 2
days
• Maximal levels attained at about 8 to 10 weeks’
gestation
• Between the 60th and 80th days after the last
menses - peak levels reach about 100,000 mIU/mL

51. Concentration of hCG in Serum
and Urine
• When the hCG titers exceeds 1,000-1,500 IU/L,
vaginal ultrasonography should identify an
intrauterine gestation
• 10-12 weeks gestation – maternal plasma
levels begin to decline
• Nadir - about 20 weeks
• Plasma levels are maintained at this lower level
for the rest of the pregnancy
• Urine concentration of hCG follows the pattern
of maternal plasma

53. Metabolic Clearance of
hCG
30 percent through the kidneys
the rest cleared by the liver and other
pathways

54. Biological Functions of
hCG
1. Rescue and maintenance of function of
the corpus luteum (continued
progesterone production)
• progesterone producing life span of the corpus
luteum of menstruation could be prolonged for
2 weeks by hCG administration
• about the 8th day after ovulation or 1 day after
implantation- hCG takes over for the corpus
luteum
• Continued survival of the corpus luteum is
totally dependent on hCG

55. Biological Functions of
hCG
• Survival of the pregnancy is dependent on
corpus luteum progesterone until the 7th
week of pregnancy
• Progesterone luteal synthesis begins to
decline at about 6 weeks despite continued
and increasing hCG production
• Down regulation of hCG-LH receptors in
the corpus luteum when trophoblasts
produce sufficient progesterone for
pregnancy maintenance

56. 2. Stimulation of fetal testicular testosterone
secretion
• Before 110 days – no fetal anterior pituitary LH
• At a critical time in sexual differentiation of the
male fetus, hCG enters fetal plasma from the
syncitiotrophoblast, acts as an LH surrogate
and stimulates replication of testicular Leydig
cells and testosterone synthesis to promote
male sexual differentiation
Biological Functions of
hCG

57. 3. Stimulation of maternal thyroid activity
hCG binds to the TSH receptors of thyroid
cells
LH-hCG receptor is expressed in the thyroid
Possibly, hCG stimulates thyroid activity via
the LH-hCG receptor and by the TSH
receptor
hCG has intrinsic thyroid activity and maybe
the 2nd placental thyrotropic substance
Biological Functions of hCG

58. 4. Promotion of relaxin secretion by the
corpus luteum
5. Promote uterine vascular vasodilatation
and myometrial smooth muscle
relaxation via LH-hCG receptors.
6.Suppresses maternal immune function
& reduces possibility of fetus
immunorejection.
Biological Functions of
hCG

59. Human Chorionic
Somammotropin (hCS)
or Placental Lactogen
Structure similar to growth hormone
Produced by the placenta
Levels throughout pregnancy
Large amounts in maternal blood but
DO NOT reach the fetus

60. - single non-glycosylated polypeptide chain
- similar to hPRL (prolactin)
1. Chemical Characteristics
potent lactogenic and GH-like bioactivity
HUMAN PLACENTAL LACTOGEN

61. - hPL – on chromosome 17
2. Gene Structure
3. Serum Concentration
• demonstrable in placenta within 5 to 10 days
after conception
• detected as early as 3 weeks after fertilization
• rises until about 34 to 36 weeks
HUMAN PLACENTAL LACTOGEN

62. - stimulated : insulin, cAMP
- inhibited : PGE2, PGF2α
4. Regulation of hPL Biosynthesis
5. Metabolic Actions
① lipolysis and increase FFA
② anti-insulin action
HUMAN PLACENTAL LACTOGEN

63. Human Chorionic
Somammotropin (hCS)
or Placental Lactogen
Biological effects are reverse of those of
insulin: utilization of lipids;
make glucose more readily available to
fetus, and for milk production.
hCS levels proportionate to placental size
hCS levels placental
insuffiency

64. PLACENTAL STEROID
HORMONE

65. Progesterone
• After 6 to 7 weeks of gestation ovarian
progesterone production is minimal
• After about 8 weeks – placenta replaces
the ovary as the source of progesterone &
continues to increase production
throughout pregnancy
• daily production rate is 250 mg
• In pregnancies with multiple fetuses, daily
production rate may be >6000 mg/day

66. Source of Cholesterol for Placental
Progesterone Biosynthesis
• Progesterone - synthesized from cholesterol in
a two-step enzymatic reaction
• 1st  cholesterol is converted to pregnenolone
within the mitochondria.
• Pregnenolone leaves the mitochondria and
converted to progesterone in the endoplasmic
reticulum by 3β-hydroxysteroid dehydrogenase
• Progesterone is released immediately through
a process of diffusion

67. Source of Cholesterol for Placental
Progesterone Biosynthesis
• limited capacity for the biosynthesis of
cholesterol in trophoblast
• maternal plasma cholesterol was the
principal precursor (90 %) of progesterone
biosynthesis in the placenta
• trophoblast preferentially uses LDL
cholesterol for progesterone biosynthesis

68. Source of Cholesterol for
Placental Progesterone
Biosynthesis
• Hydrolysis of LDL releases essential amino acids
and cholesterol esters, which in turn yield fatty
acids and cholesterol
• Essential amino acids and fatty acids are
transported to the fetus and cholesterol is used for
placental progesterone biosynthesis
• Fetus contributes essentially no precursor
• Pregnenolone sulfate may be the most important
precursor for synthesis and metabolism of
progesterone in human decidua and fetal
membranes

69. Progesterone and Fetal
Well-Being
No relationship between placental
progesterone synthesis and fetal well
being
Progesterone biosynthesis may persist
several weeks after fetal death

70. Progesterone Metabolism
During Pregnancy
• Same as in men and nonpregnant women
• During pregnancy - a disproportionate increase in the
plasma concentration of 5α-dihydroprogesterone as a
result of synthesis in syncytiotrophoblast from both
placenta-produced progesterone and fetal-derived
precursor
• 5α-reduced metabolite contributes to the resistance in
pregnancy against the vasopressor action of angiotensis II
• Progesterone is also converted to the potent
mineralocorticoid deoxycorticosterone in pregnant women
and in the fetus, thus an increase in deoxycorticosterone
in the maternal and fetal compartments

71. Role of Progesterone
• Prepares and maintains the endometrium
to allow implantation
• Has a role in suppressing the maternal
immunologic response to fetal antigens
thereby preventing maternal rejection of
the trophoblast and has a role in
parturition
• serves as a substrate for fetal adrenal
gland production of glucocorticoids and
mineralocorticoids

72. Support of the endometrium to provide an
environment conducive to fetal survival. If the
endometrium is deprived of progestins, the
pregnancy will inevitably be terminated.
Suppression of contractility in uterine
smooth muscle, which, if unchecked, would
clearly be a disaster. This is often called the
"progesterone block" on the myometrium.
Toward the end of gestation, this myometrial-
quieting effect is antagonized by rising levels
of estrogens, thereby facilitating parturition.

73. Progesterone potently inhibit
secretion of the pituitary
gonadotropins LH and FSH.
This effect almost always
prevents ovulation from
occuring during pregnancy.

74. Placental Estrogen
Production
• produces huge amounts of estrogens
using blood-borne steroidal precursors
from the maternal and fetal adrenal glands
• Normal human pregnancy is
hyperestrogenic state, continually
increasing as pregnancy progresses
terminating abruptly after birth

75. Placental Estrogen
Production
• first 2 to 4 weeks of pregnancy - rising levels of
hCG maintain production of estradiol in the
maternal corpus luteum
• seventh week of pregnancy – maternal corpus
luteum production of both progesterone and
estrogen decreases significantly
• there is a luteal–placental transition by the
seventh week, more than 50 percent of
estrogen entering the maternal circulation is
produced in the placenta

76. Placental Estrogen
Biosynthesis
• pathways for estrogen synthesis in the human
placenta differ from those in the ovary of non
pregnant women
• production occurs in the follicular and luteal
• Ovarian theca cells synthesize
androstenedione  granulosa cells  estradiol
• Androstenedione is produced de novo from
acetate and cholesterol, catalyzed by
aromatase 450  estrone, acted upon by
estradiol dehydrogenase  estradiol

77. Schematic presentation of the
biosynthesis of estrogens in the
human placenta
• DHEA-S secreted in large amounts by the fetal
adrenal glands is converted to 16 α
hydroxydehydroepiandrosterone sulfate (16 α
OHDHEA-S) in the fetal liver
• DHEAS and 16 α OHDHEA-S are converted in the
placenta to estrogens viz., 17 β estradiol (E2) and
estriol (E3)
• Near term, half of E2 is derived from fetal adrenal
DHEA-S and half from maternal DHEA-S
• 90 % of E3 in the placenta arises from fetal 16 α
OHDHEA-S and only 10 % from other sources

78. Two of the principle effects of placental
estrogens are:
Stimulate growth of the myometrium and
antagonize the myometrial-suppressing
activity of progesterone. In late gestation
induces myometrial oxytocin receptors,
thereby preparing the uterus for parturition.
Stimulate mammary gland development.

79. Relaxin
• Expressed in: human corpus luteum, decidua, and
placenta
• structurally similar to insulin and insulin-like growth
factor
• relaxin along with rising progesterone levels acts
on myometrial smooth muscle to promote uterine
relaxation and the quiescence observed in early
pregnancy
• relaxin and relaxin-like factors in the placenta and
fetal membranes may play an autocrine–paracrine
role in regulation of extracellular matrix degradation
in the puerperium

80. Leptin
• normally secreted by adipocytes
• initially believed to be an anti-obesity hormone
• now regulates bone growth and immune function
• secreted by both cytotrophoblast cells and
syncytiotrophoblast and maternal levels are
significantly higher than in non pregnant women
and that in the fetal circulation
• Fetal leptin levels
– correlated positively with fetal birthweight
• play an important role in fetal development and
growth

81. Inhibin
• glycoprotein hormone, inhibit pituitary FSH release
• produced by the testis, ovarian granulosa cells and
the corpus luteum
• placenta produces inhibin alpha-, and beta A and
beta B-subunits
• Inhibin A – principal bioactive inhibin secreted
during pregnancy
• Highest level is at term
• Placental inhibin production together with large
amounts of placental sex steroids  inhibit FSH
secretion and preclude ovulation during pregnancy

82. Inhibin
Trophoblastic inhibin synthesis
 inhibited by activin A
 stimulated by hCg, GnRH, epidermal
growth factor, transforming growth factor-
alpha and PGF 2 β and PGE 2
 may act via GnRH to regulate hCG
synthesis and secretion in the placenta

83. Activin
• closely related to inhibin
• enhances FSH synthesis and secretion and
participates in the regulation of the menstrual
cycle
• roles in cell proliferation, embryogenesis,
osteogenesis, differentiation, apoptosis,
metabolism, homeostasis, immune response,
wound repair and endocrine function
• nerve cell survival factors
• has 3 forms: A, B and AB

84. Activin
• Chorionic activin and inhibin - regulators
within the placenta for the production of GnRH,
hCG and steroids
• Inhibin – inhibitory, Activin - stimulatory
• may serve functions in placental metabolic
processes other than GnRH synthesis, but are
still under study
• Placental and decidual inhibin and activin early
in pregnancy – indicate their possible roles in
embryogenesis and local immune responses
• Activin levels actively decline after delivery

85. Fetomaternal circulation
2 umbilical arteries
 deoxygenated, or "venous-like" blood flows to the
placenta
1 umbilical vein
 with a significantly higher oxygen content(80%
saturation)

86. As fetal lungs are not functioning, the fetus obtains
oxygen and nutrients from the mother through the
placenta and the umbilical cord
The core concept behind fetal circulation is that fetal
hemoglobin has a higher affinity for oxygen than does
adult hemoglobin, which allows a diffusion of oxygen from
the mother's circulatory system to the fetus.
Circulatory system of the mother is not directly connected
to that of the fetus .
Water, glucose, amino acids, vitamins, and inorganic
salts freely diffuse across the placenta along with oxygen

87. Circulation
Blood from the placenta is
carried to the fetus by the
umbilical vein.
About half of this enters the
fetal ductus venosus and is
carried to the inferior vena
cava, while the other half
enters the liver proper from
the inferior border of the
liver. The branch of the
umbilical vein that supplies
the right lobe of the liver first
joins with the portal vein

88. The blood then moves to the right atrium of the heart.
Between the right and left atrium, the foramen ovale
allow most of the blood flows through it directly into
the left atrium from the right atrium, thus bypassing
pulmonary circulation.
The continuation of this blood flow is into the left
ventricle, and from there it is pumped through the
aorta into the body.

89. Some of the blood entering the right atrium does not
pass directly to the left atrium through the foramen ovale,
but enters the right ventricle and is pumped into the
pulmonary artery.
In the fetus, connection between the pulmonary artery
and the aorta, called the ductus arteriosus, which directs
most of this blood away from the fluid filled, non
functioning lungs

90. Changes of fetal circulation
at birth
1. Closure of umbilical arteries: Functionally, soon
after birth, but actual obliteration takes by 2-3
months
2. Closure of umbilical vein: little later than arteries and
allows few extra volume of blood to go to fetus from
placenta
3. Closure of ductus arteriosus: within few hrs of
respiration
4. Closure of foramen ovale: functionally , soon after
birth but anatomically, closes in about 1 year

91. Changes of fetal circulation at
birth
Fetal Structure
Foramen ovale
Ductus arteriosus
Left umbilical vein
 Extra-hepatic portion
 Intra-hepatic portion
(ductus venosus)
Left and right umbilical
arteries
 Proximal portions
 Distal portions
Adult Remnant
Fossa ovalis of the heart
Ligamentum arteriosum
Ligamentum teres hepatis
Ligamentum venosum
Superior vesical arteries
Medial umbilical ligaments

92. Abnormalities Of The
Placenta
(A) Abnormal Shape
(B) Abnormal Diameter
(C) Abnormal Weight
(D) Abnormal Position
(E) Abnormal Adhesion

93. Abnormalities of placenta
1- Abnormal position: Placenta Praevia
the placenta is attached to the lower uterine segment (due
to low level of implantation of the blastocyst). It causes
severe antepartum haemorrhage. There are three types:

95. 1- Placenta accreta: due to
abnormal adhesion between
the chorionic villi and the
uterine wall.
2- Placenta percreta: The
chorionic villi penetrate the
myometrium all the way to
the perimetrium.
- the placenta fails to
separate from the uterus
after birth and may cause
severe postpartum
hemorrhage.
2- Abnormal adhesion:

96. 3- Abnormal attachment of umbilical
cord:
a- Velamentous attachment:
The cord does not reach the placenta itself but
is attached to amniotic membrane over the
fetal surface of placenta. The umbilical vessels
pass in the membrane to reach the placenta. It
is easly torn.

97. (4) Abnormal Shape:
1. Placenta Bilobate
2. Placenta Bipartite
3. Placenta Succenturiate
4. Placenta Circumvallate
5. Placenta Fenestrate

98. The placenta
consists of two
equal lobes
connected by
placental tissue
1. Placenta Bilobate:

99. 2. Placenta Bipartite:
The placenta consists of two equal parts
connected by membranes.
The umbilical cord is inserted in one lobe and
branches from its vessels cross the
membranes to the other lobe.
Rarely, the umbilical cord divides into two
branches, each supplies a lobe.

100. The placenta consists of a large lobe and a
smaller one connecting together by
membranes.
The umbilical cord is inserted into the large
lobe and branches of its vessels cross the
membranes to the small succenturiate
(accessory) lobe.
3. Placenta Succenturiate:

101. 3. Placenta Succenturiata:
The accessory lobe may be retained in
the uterus after delivery leading to
postpartum haemorrhage.
This is suspected if a circular gap is
detected in the membranes from which
blood vessels pass towards the edge of
the main placenta.

102. A whitish ring composed of decidua, is seen
around the placenta from its foetal surface.
This may result when the chorion
frondosum is two small for the nutrition of
the foetus, so the peripheral villi grow in
such a way splitting the decidua basalis
into a superficial layer ( the whitish ring)
and a deep layer.
4. Placenta Circumvallate:

103. 4. Placenta Circumvallate:

104. It can be a cause of :
1. Abortion,
2. Ante partum haemorrhage,
3. Preterm labour and
4. Intrauterine foetal death.
4. Placenta Circumvallate:

105. 5. Placenta Fenestrata:
A gap is seen in the placenta
covered by membranes giving the
appearance of a window.

106. Placenta membranacea:
A great part of the chorion develops
into placental tissue.
The placenta is large, thin and may
measure 30-40 cm in diameter.
It may encroach on the lower uterine
segment i.e. placenta praevia.
(4) Abnormal Diameter:

107. The Umbilical Cord
Anatomy
•Origin :
It develops from the connecting stalk.
•Length:
At term, it measures about 50 cm.
•Diameter:
2 cm.

108. Structure: It consists of mesodermal connective
tissue called Wharton's jelly, covered by
amnion.
It contains:
1. One umbilical vein carries oxygenated blood
from the placenta to the foetus
2. Two umbilical arteries carry deoxygenated
blood from the foetus to the placenta,
3. Remnants of the yolk sac and allantois.
The Umbilical Cord

109. Insertion:
The cord is inserted in the foetal
surface of the placenta near the
center "eccentric insertion" (70%)
Or at the center "central insertion"
(30%).
The Umbilical Cord

110. Abnormalities
Of The
Umbilical Cord

111. 1. Marginal insertion :
in the placenta ( battledore insertion).
2. Velamentous insertion:
in the membranes and vessels connect
the cord to the edge of the placenta.
If these vessels pass at the region of the
internal os , the condition is called "
Vasa praevia".
(A) Abnormal cord insertion:

112. Vasa praevia
Vasa praevia can occur also
when the vessels connecting
a succenturiate lobe with the
main placenta pass at the
region of the internal os

113. Velamentous insertion

114. 1. Short cord which may lead to :
i-Intrapartum haemorrhage due to
premature separation of the placenta,
ii-Delayed descent of the foetus druing
labour,
iii-Inversion of the uterus.
(B) Abnormal cord length:

115. 2. Long cord which may lead to:
i-Cord presentation and cord
prolapse,
ii-Coiling of the cord around the neck,
iii-True knots of the cord.
(B) Abnormal cord
length:

116. (C) Knots of the cord:
1. True knot:
when the foetus passes through a loop of
the cord.
If pulled tight, foetal asphyxia may result.
2. False knot:
localized collection of Wharton’s jelly
containing a loop of umbilical vessels.

117. A long umbilical cord may more
easily become twisted, or even
form a knot