Obstetrics and Gynaecology chapters
Placenta: development, structure, functions and hormones
How the trophoblast implants and forms the placenta, how the villi, intervillous space, cord and membranes are built, how oxygen, nutrients and antibodies cross, which hormones the placenta makes and what they do, and the shape and cord anomalies that matter clinically.
- The syncytiotrophoblast invades the decidua and remodels the spiral arteries into wide, low-resistance vessels; poor remodelling underlies pre-eclampsia and FGR. Maternal blood bathes the villi in the intervillous space; the cord has two arteries and one vein.
- The placenta transfers oxygen by diffusion (helped by fetal haemoglobin), glucose by facilitated diffusion, and IgG only among antibodies; it removes CO2, urea and unconjugated bilirubin.
- Hormones come from the syncytiotrophoblast: hCG rescues the corpus luteum (peaks at 10-12 weeks), hPL raises maternal insulin resistance, oestriol needs the fetal adrenal and liver, and progesterone keeps the uterus quiet after the luteo-placental shift at about 8 weeks.
On this page
Overview
The placenta is a temporary organ shared by mother and fetus. It acts as the fetal lung, gut, kidney and endocrine gland, and as a partial barrier. Its fetal part is the chorion frondosum (villous chorion) and its maternal part is the decidua basalis.
Most PGET questions test: the trophoblast layers, spiral artery remodelling, the cord vessels, what crosses (oxygen, glucose, IgG, drugs) and the hormones (hCG, hPL, oestrogens, progesterone).
Development
Fertilisation to implantation
- Fertilisation occurs in the ampulla of the tube. The zygote divides into a morula (about day 3) and becomes a blastocyst (about day 4-5) as it enters the uterus.
- The blastocyst has an inner cell mass (embryo) and an outer trophoblast (placenta and membranes).
- Implantation happens about 7 days after ovulation, into endometrium prepared by progesterone (decidualisation). The window of implantation is short.
- The trophoblast splits into two layers:
| Layer | Features |
|---|---|
| Cytotrophoblast | Inner layer of single cells that divide (the stem layer); thins out later in pregnancy |
| Syncytiotrophoblast | Outer multinucleated layer without cell borders; invades the decidua; makes hCG, hPL, oestrogens, progesterone, PAPP-A |
Villi and the intervillous space
- Spaces (lacunae) open in the syncytiotrophoblast and fill with maternal blood from eroded vessels, forming the intervillous space.
- Trophoblast projections grow into this space as villi; mesoderm grows into them and then fetal capillaries form inside, linking to the embryo's circulation. The embryonic heart starts pumping around the third week after fertilisation.
- Villi over the decidua basalis keep growing (chorion frondosum, which becomes the placenta); those over the capsularis wither (chorion laeve, the smooth chorion of the membranes).
| Decidua | Position |
|---|---|
| Decidua basalis | Under the implantation site; maternal part of the placenta |
| Decidua capsularis | Covers the conceptus on the cavity side |
| Decidua parietalis (vera) | Lines the rest of the cavity |
Spiral artery remodelling
- Extravillous trophoblast invades the maternal spiral arteries and replaces their muscular, elastic wall.
- The arteries become wide, low-resistance, high-flow channels that no longer constrict, so the intervillous space fills at low pressure.
- In pre-eclampsia and FGR, invasion is shallow and patchy: the spiral arteries keep their muscle, flow is poor and the placenta becomes ischaemic, releasing factors that damage maternal endothelium. A notch on uterine artery Doppler reflects this high resistance.
Failed trophoblast invasion of the spiral arteries is the first step in pre-eclampsia. Too-deep invasion, through absent decidua (for example over a caesarean scar), causes the placenta accreta spectrum.
Luteo-placental shift
- hCG from the trophoblast keeps the corpus luteum alive, so it continues to make progesterone and oestrogen.
- The corpus luteum supports the pregnancy for about 8 weeks; after that the placenta makes enough progesterone (the luteo-placental shift). Removing the corpus luteum before about 7 weeks usually causes miscarriage unless progesterone is given.
Structure of the mature placenta
- A disc with two surfaces:
- Fetal surface (chorionic plate): smooth, shiny, covered by amnion, with cord vessels branching over it; the cord usually inserts near the centre.
- Maternal surface (basal plate): rough, dark red, divided by grooves (septa) into cotyledons.
- Blood flow: maternal blood spurts from the spiral arteries into the intervillous space, bathes the villi and drains into uterine veins. Fetal blood flows in the villous capillaries. The two do not mix (this human type is called haemochorial: maternal blood touches the chorion directly).
- Placental barrier (villous membrane): syncytiotrophoblast, cytotrophoblast (sparse later), basement membrane, villous connective tissue and fetal capillary endothelium. It becomes thinner and larger as pregnancy advances, so transfer rises greatly in late pregnancy.
Umbilical cord
- Two umbilical arteries carry deoxygenated blood from the fetus (branches of the internal iliac arteries) to the placenta.
- One umbilical vein carries oxygenated blood to the fetus, through the liver and the ductus venosus to the IVC.
- The vessels are cushioned in a jelly-like connective tissue (Wharton's jelly) and covered by amnion.
- Single umbilical artery occurs in about 0.5% of fetuses and is linked with slower growth and congenital anomalies (especially renal and cardiac): it prompts a detailed scan.
In the cord the vein carries oxygenated blood and the arteries carry deoxygenated blood, the opposite of the adult naming rule.
Membranes
- Amnion (inner) and chorion (outer) touch by about 12 weeks and stick together but never truly fuse.
- Neither contains vessels or nerves. The choriodecidua makes prostaglandins E2 and F2-alpha, which help start labour.
- Amniotic fluid is first made by the amnion, later mainly by fetal urine and lung fluid, and removed by fetal swallowing.
Functions
| Function | How |
|---|---|
| Respiration | O2 and CO2 cross by simple diffusion |
| Nutrition | Glucose by facilitated diffusion (main fetal fuel); amino acids by active transport; fatty acids, water, electrolytes, vitamins |
| Excretion | Urea, creatinine and unconjugated bilirubin pass to the mother (the reason for neonatal jaundice once this route is lost) |
| Immunity | IgG crosses by receptor-mediated transfer, giving passive immunity |
| Endocrine | hCG, hPL, oestrogens, progesterone, relaxin, PAPP-A, inhibin A, PlGF, CRH |
| Barrier | Partial only: many drugs, alcohol, nicotine and some infections cross |
How the fetus gets enough oxygen
Near term the mean PO2 in the maternal intervillous blood is about 50 mmHg and in the oxygenated fetal blood about 30 mmHg, a gradient of about 20 mmHg. The fetus still gets enough oxygen because:
- Fetal haemoglobin (HbF) has a curve shifted to the left: at low PO2 it holds 20-50% more oxygen than adult haemoglobin.
- Fetal haemoglobin concentration is about 50% higher than the mother's.
- The Bohr effect works in both directions: fetal blood loses CO2 (raising its oxygen affinity) while maternal blood gains CO2 (releasing oxygen). Carbon dioxide crosses about 20 times faster than oxygen.
Maternal intervillous PO2 about 50 mmHg; oxygenated fetal PO2 about 30 mmHg
Gradient = 50 − 30 = 20 mmHg → drives simple diffusion of oxygen to the fetus
IgG is the only immunoglobulin that crosses the placenta. IgM and IgA do not cross, so IgM in a newborn means the fetus made it: congenital infection. Maternal anti-D (IgG) crosses and causes haemolytic disease; most anti-A and anti-B are IgM and do not.
Heparin, including low molecular weight heparin, does not cross the placenta, so it is the anticoagulant of choice in pregnancy. Warfarin does cross and is teratogenic.
Placental hormones
All the major hormones are made by the syncytiotrophoblast.
Human chorionic gonadotrophin (hCG)
- A glycoprotein very like LH (shares the alpha subunit with LH, FSH and TSH; the beta subunit is specific and is what tests detect).
- Appears in maternal blood about 8-9 days after ovulation; urine tests can be positive 1-2 days before the missed period.
- In a healthy intrauterine pregnancy it doubles about every 48 hours early on.
- Peaks at about 10-12 weeks, then falls to a lower plateau by 16-20 weeks.
- Actions:
- rescues the corpus luteum and keeps progesterone and oestrogen coming until the placenta takes over;
- stimulates fetal Leydig cells to make testosterone (male genital development);
- has a weak TSH-like effect (very high levels in molar pregnancy and hyperemesis can cause hyperthyroidism).
- Clinical: pregnancy tests, ectopic and miscarriage follow-up, molar pregnancy and choriocarcinoma (very high), and raised in Down syndrome screening.
Human placental lactogen (hPL, human chorionic somatomammotropin)
- A protein hormone made from about 5 weeks, rising steadily in proportion to placental mass; made in larger amounts than all other placental hormones together.
- Anti-insulin (diabetogenic): lowers maternal insulin sensitivity and glucose use, leaving more glucose for the fetus; drives lipolysis so the mother burns fatty acids instead.
- Weak growth hormone-like and lactogenic actions; helps prepare the breast.
hPL (with progesterone, cortisol and other hormones) explains the insulin resistance of late pregnancy and why gestational diabetes appears in the second half.
Oestrogens
- The placenta cannot make oestrogen from scratch (it lacks a key enzyme for androgen synthesis). It converts DHEA (DHEA sulphate) from the maternal and fetal adrenal glands into oestradiol, oestrone and oestriol.
- Oestriol is the main pregnancy oestrogen and needs the fetal adrenal cortex and fetal liver: the fetoplacental unit. Low unconjugated oestriol (uE3) is part of the quadruple test (low in Down syndrome).
- Actions: growth of the uterus, breast ducts and external genitalia; softening of pelvic ligaments and the cervix; increased uterine blood flow.
Progesterone
- From the corpus luteum at first, then mainly from the placenta (made from maternal cholesterol).
- Actions: maintains the decidua; keeps the myometrium quiet (prevents contractions); increases secretions of the tube and uterus for the early embryo; prepares the breast lobules and alveoli; relaxes smooth muscle elsewhere (heartburn, constipation, ureteric dilatation).
Other placental products
| Product | Point to remember |
|---|---|
| PAPP-A | From syncytiotrophoblast; low in Down syndrome (combined test); low levels linked with FGR |
| Inhibin A | Placental; raised in Down syndrome (quadruple test) |
| PlGF (placental growth factor) | Angiogenic; low in pre-eclampsia, used as a test |
| Relaxin | Corpus luteum and placenta; ligament softening (weak in humans) |
| CRH | Rises towards term; thought to help time labour |
| Human chorionic thyrotropin | Weak thyroid stimulation |
Second-trimester screening markers in Down syndrome
| Marker | Source | Direction |
|---|---|---|
| hCG (beta) | Syncytiotrophoblast | Up |
| Inhibin A | Placenta | Up |
| AFP | Fetal yolk sac and liver | Down |
| Unconjugated oestriol | Placenta and fetal adrenal | Down |
| PAPP-A (first trimester) | Syncytiotrophoblast | Down |
"HI up, AOP down": hCG and Inhibin go up; AFP, Oestriol and PAPP-A go down in Down syndrome.
Anomalies of shape, cord and attachment
| Anomaly | Description | Risk |
|---|---|---|
| Succenturiate lobe | Extra lobe joined to the main placenta by vessels in the membranes | Retained lobe → PPH, infection; vessels may lie over the os (vasa praevia) |
| Velamentous cord insertion | Cord inserts into the membranes; vessels run unprotected to the placenta | Vasa praevia; fetal bleeding when membranes rupture |
| Battledore (marginal) insertion | Cord inserts at the edge | Usually harmless |
| Circumvallate placenta | Membranes fold back to form a thick ring on the fetal surface | Antepartum bleeding, preterm birth, FGR |
| Placenta praevia | Placenta in the lower segment | Painless bleeding |
| Placenta accreta spectrum | Villi attach to or invade myometrium where decidua is lacking (previous caesarean scar, praevia) | Massive haemorrhage; may need hysterectomy |
After every third stage, inspect the placenta and membranes. Missing cotyledons or torn vessels running to a gap in the membranes (succenturiate lobe left behind) mean retained tissue and a high risk of postpartum haemorrhage; arrange examination under anaesthesia and manual removal.
Expect: syncytiotrophoblast as the hormone-making invasive layer and cytotrophoblast as the dividing layer; implantation about 7 days after ovulation; decidua basalis as the maternal part; spiral artery remodelling and its failure in pre-eclampsia and FGR; two umbilical arteries and one vein, single umbilical artery; haemochorial placenta with the intervillous space; oxygen transfer helped by HbF, higher fetal haemoglobin and the Bohr effect; glucose by facilitated diffusion; IgG as the only crossing antibody and IgM as a sign of fetal infection; heparin not crossing; hCG timing, peak at 10-12 weeks, rescue of the corpus luteum, luteo-placental shift at 8 weeks; hPL and insulin resistance; oestriol and the fetoplacental unit; Down syndrome marker directions; succenturiate lobe, velamentous insertion and vasa praevia.
Quick revision
- Syncytiotrophoblast: invades and makes hormones; cytotrophoblast: divides.
- Spiral arteries remodelled to low resistance; failure = pre-eclampsia, FGR.
- Cord: two arteries (to placenta), one vein (to fetus); single artery 0.5%.
- Oxygen by diffusion; HbF left shift; glucose by facilitated diffusion.
- Only IgG crosses; IgM in newborn = congenital infection.
- hCG: 8-9 days after ovulation, doubles every 48 hours, peak 10-12 weeks; keeps corpus luteum.
- Luteo-placental shift about 8 weeks.
- hPL: insulin resistance; oestriol: fetoplacental unit; progesterone: quiet uterus.
Written by The House Job from standard references (Obstetrics by Ten Teachers; Gynaecology by Ten Teachers; Guyton and Hall Textbook of Medical Physiology).
FAQ
Why does a woman miscarry if the corpus luteum is removed very early?
Until about 8 weeks the corpus luteum, kept alive by hCG, makes the progesterone that holds the decidua; after the luteo-placental shift the placenta makes enough on its own.
Do maternal and fetal blood mix in the placenta?
No. Maternal blood fills the intervillous space and fetal blood stays inside the villous capillaries; they are separated by the thin villous membrane, which only rarely leaks.
What is the main metabolic effect of human placental lactogen?
It reduces the mother's insulin sensitivity and increases fat breakdown, so she uses fatty acids and more glucose is left for the fetus.
Why is a velamentous cord insertion dangerous?
The cord vessels run through the membranes without the protection of Wharton's jelly; if they cross the cervix (vasa praevia) they can tear when the membranes rupture and the fetus can bleed to death quickly.