Placenta
Introduction
As the human
embryo grows its need for nutrition increases, requiring a connection to the
mother for nutrient, gas and waste exchange. The placenta develops to meet
these needs.
The trophoblast
develops from the outer layer of the blastocyst before implantation into
the endometrium. Trophoblast cells produce human chorionic gonadotrophin (hCG).
Around 6–7 days after fertilisation the trophoblast begins to invade the
endometrium, triggering the decidual reaction (see Chapter 12) and the process
that will form the placenta from both embryonic and maternal tissues (see
Figure 12.3).
The
trophoblast layer has important roles in implantation and placental
development, and protects the embryo from maternal immunological attack. With
implantation the trophoblast divides into two layers (Figure 13.1): the inner cytotrophoblast
(mononuclear cells) and the outer syncytiotrophoblast (multinucleated).
After 2
weeks the front line of invading trophoblasts of the syncytiotrophoblast reach
the endometrial blood vessels and erode them, forming pools of maternal blood
within trophoblastic lacunae that have formed (Figure 13.2). At the same time chorionic
villi begin to grow from embryonic tissue, and will grow, branch and become
more complex until the end of the second trimester.
Initially,
chorionic villi cover the whole surface of the chorion and by the end of the
third week embryonic blood begins to flow through the capillaries within the
villi. A week after the chorionic villi appear the basic structure of the
placenta has formed and the embryo has developed a primitive circulatory system
(see Chapter 27).
Development
of the placenta continues to give a mature placental structure at 12–13 weeks.
Villi become
restricted to just one region of the chorion. Linked pools of maternal blood
are filled by spiral arteries of the endometrium, themselves branches of the
uterine arteries. Foetal blood enters the placenta through the two umbilical
arteries, which branch and continually divide until they reach the looping
capillaries of the chorionic villi. These branching blood vessels form 15–25
units called cotyledons (Figure 13.3).
In the villi
the syncytiotrophoblasts and endothelium create the barrier between maternal
and fetal blood. Due to the syncytiotrophoblasts’ multinucleated structure the
nuclei gather in certain places (proliferation knots) leaving other areas free
of nuclei. These are exchange zones and they create an extremely thin
and efficient selective barrier through which nutrients, gas, waste products
and antibodies may pass.
The villi
are bathed in maternal blood, and exchange takes place. Blood returns to the
mother through the uterine veins, and the blood within these maternal pools is
replaced 2–3 times per minute. Oxygen‐rich blood is returned to the foetus by
the umbilical vein (see Chapter 31).
The placenta
has vital roles in hormone production, nutrient, metabolite and gas exchange,
and in protecting the foetus from immune attack by maternal cells and
pathogens, and in enabling the passage of antibodies from mother to foetus.
Gas
exchange
Oxygen
diffuses into the embryonic circulation and carbon dioxide diffuses out. Foetal
haemoglobin (HbF) has a higher affinity for oxygen than adult haemoglobin.
Nutrients
For example,
amino acids, lipids, glucose, cholesterol and water‐ soluble vitamins.
Waste
removal
For example,
urea, bilirubin and creatine.
Hormones
HCG is
produced by the placenta for the first 2 months of pregnancy, maintaining the
corpus luteum, which in turn produces progesterone to maintain the endometrium.
By week 16 the placenta takes on the task of progesterone production.
The placenta
also produces oestrogens that aid development of the uterus and mammary glands,
and human chorionic somatomammotrophin (hCS, or placental lactogen), an
insulin antagonist, that modulates maternal carbohydrate metabolism,
prioritises foetal access to maternal blood glucose and aids breast development
for lactation.
Antibodies
Maternal
immunoglobulins are selectively transferred from about 14 weeks, and the foetus
gains passive immunity that persists in the newborn infant for several months.
Other maternal proteins are degraded by the trophoblast.
Late in the
third trimester the syncytiotrophoblast layer develops grape‐like nucleated
clusters within its cytoplasm called syncytial knots which break off and
pass into the maternal circulatory system. Shortly before birth fibrinoid deposits
appear on the villi.
After birth
blood flow ceases through the umbilical arteries and veins, and blood flow to
the lungs increases as they fill with air. The lungs are about 15 times better
at gas exchange than the placenta. The placenta is extruded as the afterbirth.
Clinical relevance
Most drugs
(infamously, thalidomide), antibiotics and corticoids, some viruses (e.g.
toxoplasma, HIV) and other pathogens can pass across the placenta into foetal
blood.
Rhesus (Rh) factors are red blood cell surface
molecules that will provoke an immune response (against Rh factors). If an Rh–
mother bears an Rh+ child her immune system is likely to only see
the Rh factors during birth when foetal blood may cross the placenta to meet
maternal blood. The mother will develop anti‐Rh antibodies. If she bears a
second Rh+ child those anti‐Rh antibodies will cross the placenta
and destroy foetal red blood cells causing erythroblastosis fetalis.
Pre‐eclampsia is often diagnosed by
increased blood pressure and proteinuria. It occurs in up to 10% of pregnancies
and is more common in first‐time mothers. It may arise from a shallowly
implanted placenta becoming hypoxic and initiating an immune response from the
mother. Birth of the baby is the only treatment option.
Placenta accreta, placenta increta and placenta percreta
involve the placenta attaching too firmly to the wall of the uterus.
Accreta is too firmly attached, increta is even more firmly attached (into the
myometrium) and percreta is attached through the uterine wall sometimes to
internal organs, even as far as the bladder. Manual exploration and the removal
of the retained placental tissue are necessary.
Placental insufficiency and intrauterine
growth restriction (IUGR) describe conditions in which the placenta cannot
supply the necessary nutrients to the foetus. Drug or alcohol abuse, smoking,
preclampsia, long‐term high blood pressure, infections, diabetes, problems wit
h incompatibility are all thought to be related.
