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.
Oxygen diffuses into the embryonic circulation and carbon dioxide diffuses out. Foetal haemoglobin (HbF) has a higher affinity for oxygen than adult haemoglobin.
For example, amino acids, lipids, glucose, cholesterol and water‐ soluble vitamins.
For example, urea, bilirubin and creatine.
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.
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.
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.