We will now proceed to follow the further development of the placenta
and its relationship to the membranes that surround the developing fetus.
Once the placenta is in place,
we have a situation where uterine arteries travel into placenta
bringing oxygen in blood to the embryo.
This maternal oxygen and blood fills intervillous spaces
and allows gas exchange to occur across the villi.
Maternal blood interacts with deoxygenated blood
coming from the umbilical arteries of the fetus,
and even if though blood does not directly mingle,
gas exchange and nutrients exchange occur across the villi.
Thereafter, umbilical veins take oxygenated blood back to the embryo
and maternal veins take deoxygenated maternal blood from the intervillous space
back into maternal circulation to be replenished.
Typically, the blood of the fetus and the mother should never directly connect.
One problem that arises with this situation
is that as maternal blood enters the intervillous space,
it necessarily mixes with blood that's already there;
meaning that the oxygenated blood from the mother
is mixing with the deoxygenated blood already present in the intervillous space
that has not yet left through maternal vein.
What this means is that the oxygen content of the blood
in the intervillous space is lower than pure arterial blood.
To compensate for this, the fetus produces a fetal hemoglobin
which binds to oxygen much more strongly than mature hemoglobin.
In physiology, we can say that the O2 P50 value of fetal hemoglobin
is 19 millimeters of mercury,
meaning it's about 50% saturated at a partial pressure of 19 millimeters
compared with 26.8 millimeters of mercury for adult hemoglobin.
Long story short, it binds to oxygen much more strongly than mature hemoglobin
and allows the fetal hemoglobin to actually take the oxygen
away from the maternal circulation
even though we've got mixture of maternal oxygenated
and deoxygenated blood in the intervillous space.
Now, one problem that can also occur is that a fetal blood does contact maternal blood
due to a rupture of a villus or another problem,
there can be immune reactions on the maternal blood to fetal blood.
In particular, if the fetal blood produces the D antigen and is therefore Rh positive,
then it can create an immune reaction in a mother who is Rh negative
so she has not got that antigen on her own blood,
she will produce antibodies against the D antigen and these IgG antibodies
can cross the placenta and attack fetal red blood cells.
Attacking the fetal red blood cells causes a condition known as erythroblastosis fetalis.
That's going to mean that we have an excessive creation
of new red blood cells, erythroblasts,
in the fetus to compensate for the red blood cells
that are being attacked by the maternal antibodies.
This can progress to a condition called fetal hydrops or the tissues of the fetus swell
in response to the immune attack from the mother's antibodies,
and in less severe but still serious forms you can have breakdown of fetal blood cells
producing excessive bilirubin leading to jaundice as development proceeds further.
This response becomes more and more severe for subsequent pregnancies
because the maternal immune system is already primed to produce those antibodies
against the D antigen in Rh positive blood.
The placenta, initially, is going to form as a spherical object
surrounding the developing embryo in the uterine lining,
but as the embryo and placenta enlarge
it starts to push its way into the cavity of the uterus.
As this occurs, the placenta thins on one side and will eventually form
more or less a pancake shape structure on its attachment to the uterus
and not be present outside the fetus beyond that.
As the embryo enlarges, the chorionic cavity which contains the yolk sac will thin
and the amniotic cavity, shown here in blue, will expand outward tremendously
giving buoyancy to the fetus and supporting it as it moves but also helping it resist gravity.
The portion of the endometrium, the lining of the uterus that's pushed outward
as the embryo grows on the uterine wall is gonna be known as the decidua capsularis
and the lining of the endometrium everywhere else is called the decidua parietalis.
At the point where the decidua parietalis of the uterine wall
meets the decidua capsularis covering the developing fetus,
we have an area called the decidua basalis
and that's just marking the subdivisions
of the endometrial lining as the fetus continues to develop.
As it develops, the fetus becomes larger and larger.
The placenta is more or less pushed to one side, and as I said before,
from the relatively pancake-shaped structure,
most likely on the posterior wall of the uterus.
It's connected to the developing fetus by the umbilical cord,
which is full of a loose mesenchyme
called Wharton's jelly that surrounds the vessels
that are travelling in the umbilical cord to and from the placenta.
The membrane that supports the fetus consist of the amniotic membrane
and then a smooth layer of the chorion, a very thin layer of the endometrium
that was present when the fetus grew out of the uterine wall
and then another smooth layer of the chorion.
This amniochorionic membrane is what ruptures when delivery is imminent
and is known as the water breaking
that allows the amniotic fluid to exit the birth canal
and set the stage for a hopefully smooth delivery.
By the 14th or 15th week of pregnancy,
there's enough amniotic fluid surrounding the developing fetus
that we can safely sample some of it via amniocentesis.
This is generally done in order to check some genetic issues that may be arising in the fetus
and looking for chromosomal abnormalities,
markers of neural tube defects such as alpha-fetoprotein
and other possible issues that might be anticipated.
Alternatively, the chorionic villi can be sampled and then taken for a genetic analysis.
This can be done either through the anterior body wall using ultrasound or vaginally,
to harvest some of the chorionic villi.