Placenta

The human placenta is haemochorial: maternal blood directly bathes the fetal chorionic villi. Villi develop in week 2–3 — primary (cytotrophoblast core), secondary (mesodermal core) and tertiary (with fetal capillaries, by the end of week 3). Those facing the decidua basalis proliferate as the chorion frondosum (fetal part of the placenta), while the rest regress to the smooth chorion laeve. The decidua basalis forms the maternal part. At term the placenta is ≈20 cm in diameter and 2–3 cm thick. Its fetal surface is smooth, covered by amnion, with the umbilical cord inserting near the centre; its maternal surface is divided by septa into 15–20 cotyledons — checked for completeness after delivery.

Maternal circulation: ≈80–100 spiral arteries open into the intervillous space; at term ≈500–700 mL/min of maternal blood flows through it. In the first half of pregnancy, extravillous trophoblast invades and remodels the spiral arteries into wide, low-resistance vessels — essential for adequate flow. Fetal circulation: two umbilical arteries carry deoxygenated blood to the villous capillaries; oxygenated blood returns in the single umbilical vein. The placental barrier — syncytiotrophoblast, cytotrophoblast (sparse after ≈4–5 months), villous connective tissue and fetal capillary endothelium — thins as pregnancy advances, increasing diffusion.

Functions: gas exchange (simple diffusion, helped by the higher O₂ affinity of fetal haemoglobin); nutrient transfer (glucose by facilitated diffusion via GLUT1, amino acids by active transport, fatty acids); removal of urea, CO₂ and bilirubin; transfer of maternal IgG by FcRn-mediated transcytosis (passive immunity — the only antibody class to cross); and endocrine output of hCG, progesterone, estrogens (estriol from fetal adrenal DHEA-S), hPL, placental GH and CRH. It is an imperfect barrier: lipid-soluble drugs, alcohol, some microorganisms (TORCH) and anti-RhD antibodies cross.