BY MUNEEB HASAN KHAN
PLACENTA
DEVELOPMENT:
• Human placenta is an organ of fetomaternal origin and hemochorial type whose development
begins in 3rd week, and is well-established by around 4th
month.
• Its development involves:
|
Maternal Part |
Fetal Part |
|
·
In 2nd week, maternal endometrium
undergoes decidua reaction and
splits into 3 regions: 1. Parietalis – lines uterine wall apart from conceptus. 2. Capsularis – superficial part overlying the conceptus. 3. Basalis–lies deep to conceptus. Basalis forms maternal part of placenta i.e decidual plate. ·
Capsularis enlarges as fetus grows until it contacts
Parietalis, and then degenerates. This allows smooth chorion to fuse with
decidua parietalis, potentially obliterating
the uterine cavity. ·
Amniotic sac enlarges faster than chorionic sac
resulting in the fusion of 2 membranes into amniochorionic membrane, with obliteration of chorionic cavity as a result. |
·
Early development involves rapid growth of
trophoblast engulfing maternal lacunae
and development of tertiary chorionic villi. After 8th week, chorionic villi covering the entire
chorionic sac undergo 2 gradual changes: 1. Those at abembryonic pole become compressed by deciduas capsularis and
form smooth chorion (laevae). 2. Those at embryonic pole associated with deciduas basalis grow rapidly
to form bushy chorion (frondosum),
which serves as fetal part of placenta.
·
Part of chorion related to placenta is chorionic plate. |
• The 2 parts anchors to each other by
cytotrophoblastic shell i.e.
external layer of trophoblastic cells on maternal surface of placenta.
• Further on, erosion of endometrium
by villi creates 2 effects:
a) Enlargement of intervillous spaces
b) Wedge-shaped spokes of deciduas
basalis i.e. placental septas that
divide the space into incomplete, interconnected compartments (since the septas
project towards chorionic plate but do not fuse with it).
• This forms cotyledons in fetal placenta which appear separated by grooves on gross examination. Each
cotyledon shows following features:
I.
2 or more Stem villi (extend
from chorionic to decidual plates)
II.
Multiple Branch villi (free
extensions of stem villi into IV space)
III.
Branches of umbilical
vessels supplying the villi (develop from extraembryonic mesoderm)
IV.
Maternal vessels (spiral arteries/endometrial veins) opening into intervillous spaces
(formed by endovascular
invasion of cytotrophoblast EVT cells into vessel endothelium)
FUNCTIONS OF PLACENTA
1. Metabolism:
·
Synthesis of glycogen, cholesterol, fatty acids etc for nutrition
especially during early pregnancy.
2. Transport:
·
Occurs rapidly through large surface area provided by the
microvilli of placental membrane.
·
Four major mechanisms: simple
diffusion, facilitated diffusion, active transport, pinocytosis.
Transfer
of Gases
·
CO2, O2, CO cross rapidly by simple
diffusion.
·
Even small disruptions can result in fetal hypoxia &IUGR.
Transfer
of Nutrients
·
Water crosses by simple
diffusion.
·
Glucose passes by facilitated
diffusion through GLUT-1 carrier proteins. o Amino acids cross by active transport.
·
Fats cross in relatively small amounts (esp. long chain
polyunsaturated FFA)
·
Vitamins also cross, water-soluble more readily than fat-soluble
ones.
Transfer
of Maternal Hormones
·
Protein hormones (e.g. insulin) do not cross in significant amounts
except thyroid hormones.
·
Unconjugated steroid hormones (e.g. testosterone &progestins)
can cross freely.
Transfer
of Electrolytes
·
Rapid
exchange of electrolytes takes place, each at its own rate, often assisted by facilitated diffusion through channel
proteins.
Transfer of Maternal Antibodies/Proteins
·
Small antibodies i.e. IgG (of Rh system) cross placenta and confer
passive immunity to fetus.
·
Large antibodies e.g. IgM (of ABO system) cannot cross into fetus.
·
Antibodies against certain diseases in mother can immunize fetus as
well e.g. diphtheria, measles & smallpox – and sometimes they do not e.g.
pertussis.
·
Other proteins (e.g. transferrin, an iron transport protein) may
also pass by transcytosis.
Transfer
of Waste Products
·
Urea/Uric acid pass by simple
diffusion.
·
Conjugated bilirubin passes rapidly by transport from placenta.
Transfer
of Drugs
·
Drugs or their metabolites can pass through simple diffusion or active
transport, depending on amount circulating in maternal blood.
o Some drugs act as teratogens. o Consumption
of narcotics/alcohol may also affect fetus e.g. fetal addiction and fetal
alcohol syndrome.
o Labour management drugs e.g
sedatives, analgesics etc may affect fetus leading to fetal respiratory
depression.
Transfer
of Infection
·
Infections can pass to fetus through microdefects in the membrane
or of their own accord e.g.
Tryponema pallidum(syphilis) –destructive
changes in brain and eyes
Rubella – cataracts in eye
Ø Toxoplasma gondii(toxoplasmosis)
– mental retardation and eye defects
Ø Cytomegalovirus, varicella, measles, herpes, poliomyelitis viruses can all cause birth defects in fetus
3. Hormonal synthesis:
·
Protein hormones are:
1. Human chorionic gonadotropin
2. Human chorionic somatomammotropin
(placental lactogen)
3. Human chorionic thyrotropin 4. Human
chorionic corticotropin
·
Steroid hormones are:
1. Progesterone
2. Estrogen
PLACENTA AS ALLOGRAFT
Fetal part of placenta has a genome distinct from mother since half
of its chromosomes are paternally inherited; but it does not activate the
mother’s immune system. To acquire immunity the fetus must
a.
Evade T cells
b.
Evade NK cells
c.
Protect itself from the complement cascade. These may occur by:
1) Immunosuppressant molecules – e.g. early pregnancy factor,
prostaglandin E2, transforming growth factors (TGF), interleukin 10,
indoleamine 2,3-deoxygenase etc.
2) Lack of MHC complex
e.g. on syncytiotrophoblast.
3) Expression of non-polymorphic HLA-G antigen e.g. on extra villous
trophoblastic cells (EVT) that invade spiral artery endothelium, which is
not detected by T cells.
4) Tolerance of maternal B
and T cells towards fetus.
5) Apoptosis of activated maternal
leukocytes by receptors on placenta.
6) Membrane cofactor protein (CD46) which blocks C3 component of complement cascade, preventing its
activation.
PLACENTAL MEMBRANE
·
Refers to the structures lining the villi that separate the fetal
& maternal circulations from each other.
·
Microdefects can allow non-transferable entities e.g. infectious
agents & RBCs to intermingle.
·
Undergoes changes as placenta develops:
o Until 20th week, consists
of 4 layers from periphery to core
i.e. syncytiotrophoblast, cytotrophoblast, connective tissue of villus,
endothelium of fetal capillaries.
o After 20th week, it
contains 3 layers and starts thinning as a result of:
a) Disappearance of cytotrophoblastic layer causing only a loose
covering of syncytium on villus containing multiple microvilli
b) Reduction in C.T. of the core
c) Movement of capillaries towards
periphery o All these changes allow a rapid exchange across the membrane. o Multinucleated syncytial
knots can form on the syncytium, which may break off and enter maternal
circulation. Usually they are destroyed by enzymatic action in maternal lungs. o Hoffbauer cells are
also present which are phagocytic.
o Towards end of pregnancy, many
changes occur that cause reduced
exchange between the 2 circulations:
a) Increase in fibrous tissue in core of villus
b) Thickening of basement membrane in capillaries
c) Obliteration of
small capillaries
d) Deposition of fibrinoid on surface of villi which reduces exchange.
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