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Placenta, Fetal Membranes & Fetal Circulation

Anatomy · Embryology · lean revision notes

Placenta, Fetal Membranes & Fetal Circulation

The placenta is the fetomaternal interface for gas exchange, nutrition, excretion and hormone production, while the fetal membranes enclose the protective amniotic fluid. Fetal circulation, with its three physiological shunts, is uniquely adapted to oxygenate the fetus through the placenta — and rearranges itself dramatically at the first breath. This is a perennial NEET PG favourite spanning Anatomy, Embryology and Physiology.

Development & basic structure of the placenta

The placenta is discoid, haemochorial (haemomonochorial at term), deciduate and villous. It derives from two components:

  • Foetal part — the chorion frondosum (villous chorion).
  • Maternal part — the decidua basalis.

At term the placenta is ~15–20 cm in diameter, 3 cm thick centrally, weighs ~500 g, and the fetoplacental weight ratio is about 1:6.

From trophoblast to villi

After implantation, the trophoblast differentiates into an inner cytotrophoblast (Langhans layer) and outer syncytiotrophoblast. Lacunae in the syncytiotrophoblast coalesce to form the intervillous space, into which maternal spiral arteries open.

The chorionic villi mature in three stages:

  1. Primary villi — cytotrophoblast core covered by syncytiotrophoblast.
  2. Secondary villi — extraembryonic mesoderm invades the core.
  3. Tertiary villi — blood vessels develop within the mesoderm (definitive villus).

High-yield: Tertiary villus = the definitive functional unit of the placenta because it contains fetal blood vessels. Appearance of blood vessels in the villous core marks the tertiary stage.

Anchoring villi attach the villous tree to the decidua via the cytotrophoblastic shell; floating (free) villi project into the intervillous space and perform exchange.

Cotyledons and septa

Decidual (placental) septa partition the maternal surface into 15–20 cotyledons (lobes), each containing a main stem villus and its branches. Each cotyledon is supplied by a spiral artery. The maternal surface is rough and lobulated; the fetal surface is smooth, shiny and covered by amnion, with the umbilical cord typically attached centrally/eccentrically.

The placental (membrane) barrier

The structures separating maternal blood (intervillous space) from fetal blood form the placental barrier. In early pregnancy it has 4 layers; by term it thins to facilitate exchange.

Layer (early pregnancy) Status at term
Syncytiotrophoblast Persists (thinned)
Cytotrophoblast (Langhans) Largely disappears / discontinuous
Connective tissue of villus core Reduced
Endothelium of fetal capillary Persists

High-yield: Early placenta = haemochorial with 4 layers; at term effectively haemomonochorial (cytotrophoblast lost) → thinner barrier → better exchange.

Circulation through the placenta

Spiral arteries → intervillous space (maternal blood bathes villi) → exchange across barrier → collected by endometrial veins. Fetal side: two umbilical arteries (deoxygenated blood from fetus) → villous capillaries → one umbilical vein (oxygenated blood to fetus).

High-yield: The umbilical VEIN carries OXYGENATED blood, the umbilical ARTERIES carry DEOXYGENATED blood — the reverse of the usual rule. A single umbilical artery is associated with congenital anomalies (notably renal/cardiac).

Functions & hormones of the placenta

  • Respiratory — O₂/CO₂ exchange (placenta is the "fetal lung").
  • Nutritive & excretory — transfer of glucose (facilitated diffusion via GLUT), amino acids (active), waste removal.
  • Barrier — incomplete; many agents cross (see below).
  • Endocrine — produces both peptide and steroid hormones.
Hormone Source / role
hCG Syncytiotrophoblast; maintains corpus luteum; peaks ~8–10 weeks; basis of pregnancy test
hPL (human placental lactogen) Syncytiotrophoblast; diabetogenic, lipolytic; marker of placental mass
Progesterone Maintains pregnancy; placenta takes over from corpus luteum by ~8–12 weeks (luteo-placental shift)
Oestrogens (estriol) Needs fetal adrenal + liver (DHEAS) + placental aromatase — fetoplacental unit

High-yield: Oestriol synthesis requires the fetoplacental unit — placenta lacks 17α-hydroxylase, so it depends on fetal adrenal DHEAS. Falling maternal estriol historically signalled fetal compromise.

Placental transfer of drugs/agents (frequently tested)

  • Cross readily: lipid-soluble, low-molecular-weight substances, gases, alcohol, warfarin, antithyroid drugs, most anaesthetics, viruses (TORCH), Rh antibodies (IgG).
  • Do NOT cross appreciably: heparin (large, polar), insulin (minimal), IgM, most muscle relaxants.

High-yield: Heparin does NOT cross the placenta → anticoagulant of choice in pregnancy. Warfarin crosses and is teratogenic (fetal warfarin syndrome).

Fetal membranes & amniotic fluid

The conceptus is enclosed by the amnion (inner) and chorion (outer), which fuse by ~12 weeks obliterating the chorionic cavity. The amnion is the innermost, avascular membrane lining the amniotic cavity.

Amniotic fluid dynamics

Early in gestation the fluid is largely a transudate of maternal/fetal plasma; later, fetal urine becomes the major source, balanced by fetal swallowing and absorption. Lung secretions contribute.

Parameter Value
Volume at term ~800–1000 mL (peaks ~34–36 wks)
Polyhydramnios > 2000 mL (or AFI > 24–25 cm)
Oligohydramnios < 300–500 mL (AFI < 5 cm)
pH Alkaline (~7.0–7.5) — basis of nitrazine test for PROM

Functions: cushions the fetus, allows movement & symmetrical growth, maintains temperature, prevents adhesions, aids lung development, antibacterial, acts as a hydrostatic wedge during labour.

High-yield: Polyhydramnios → think oesophageal/duodenal atresia, anencephaly (impaired swallowing). Oligohydramnios → think renal agenesis (Potter sequence), PROM, IUGR, posterior urethral valves (impaired urine output).

Potter sequence flow: Renal agenesis → no fetal urine → oligohydramnios → fetal compression → pulmonary hypoplasia + limb deformities + characteristic facies.

Fetal circulation

In utero the lungs are non-functional and the placenta is the organ of oxygenation. Three shunts divert blood away from the lungs and liver.

The pathway (trace it stepwise)

Placenta → umbilical vein (oxygenated) → ductus venosus (bypassing liver) → IVC → right atrium → foramen ovale → left atrium → left ventricle → ascending aorta (best-oxygenated blood to coronaries & brain) → ...

Meanwhile: SVC → right atrium → right ventricle → pulmonary artery → ductus arteriosus → descending aorta → internal iliac → umbilical arteries → back to placenta.

High-yield: The crista dividens (lower edge of septum secundum) splits IVC blood — well-oxygenated stream is preferentially directed across the foramen ovale to the left side, ensuring the brain and heart get the best-oxygenated blood.

The three shunts

Shunt Connects Function Postnatal remnant
Ductus venosus Umbilical vein → IVC Bypasses liver Ligamentum venosum
Foramen ovale RA → LA Bypasses lungs (R→L) Fossa ovalis
Ductus arteriosus Pulmonary trunk → aorta Bypasses lungs Ligamentum arteriosum

Other obliterated structures

Fetal structure Adult remnant
Umbilical vein Ligamentum teres hepatis (round ligament of liver)
Umbilical arteries (distal) Medial umbilical ligaments
Urachus (allantois) Median umbilical ligament

High-yield: Most-oxygenated fetal blood (SaO₂ ~80%) is in the umbilical vein; least-oxygenated returns via umbilical arteries. Highest O₂ delivery in the body → liver and the brain.

Circulatory changes at birth

The first breath and clamping of the cord trigger a cascade:

  1. Lungs expand → fall in pulmonary vascular resistance → increased pulmonary blood flow → increased left atrial pressure.
  2. Cord clamped/placenta removed → loss of low-resistance circuit → rise in systemic vascular resistance → increased left-sided pressures.
  3. LA pressure > RA pressure → functional closure of foramen ovale (septum primum pressed against septum secundum).
  4. Rising PaO₂ and falling prostaglandins (PGE₂) → ductus arteriosus constricts.
Structure Functional closure Anatomical closure
Foramen ovale Minutes–hours (at birth) ~3 months–1 year
Ductus arteriosus ~10–15 h (functional) ~1–3 months (ligamentum arteriosum)
Ductus venosus Within days ~1 week–3 months

High-yield: Increased PaO₂ closes the ductus arteriosus; PGE₂ keeps it open. Therefore: PGE₁/PGE₂ infusion maintains a patent DA in duct-dependent congenital heart disease; indomethacin/ibuprofen (NSAID = PG synthase inhibitors) close a PDA in preterms.

PDA pharmacology one-liner: To OPEN → PGE; to CLOSE → indomethacin.

Clinical correlates & placental abnormalities

  • Placenta praevia — placenta over/near the internal os → painless APH.
  • Abruptio placentae — premature separation → painful APH, "couvelaire uterus".
  • Placenta accreta/increta/percreta — abnormal decidual invasion (accreta = adherent to myometrium; increta = into myometrium; percreta = through serosa); risk factor = previous LSCS scar + praevia.
  • Velamentous cord insertion / vasa praevia — fetal vessels traverse membranes unsupported → can rupture during ROM → fetal exsanguination.
  • Hydatidiform mole — abnormal trophoblastic proliferation (complete mole = 46,XX, all paternal, "snowstorm" on USG, ↑↑hCG).
  • Single umbilical artery — associated congenital anomalies.

High-yield: Complete mole = diploid, entirely paternal genome (46,XX), no fetal parts, highest risk of choriocarcinoma. Partial mole is usually triploid (69,XXX/XXY) with fetal parts.

Recently asked / exam angle

  • "Definitive (functional) unit of placenta" → tertiary chorionic villus.
  • "Which carries oxygenated blood in the fetus" → umbilical vein (and ductus venosus/IVC stream to LA).
  • Remnant matching: ductus venosus → ligamentum venosum, ductus arteriosus → ligamentum arteriosum, foramen ovale → fossa ovalis, umbilical vein → ligamentum teres.
  • "Drug keeping ductus arteriosus patent" → PGE₁ (alprostadil); "closes PDA" → indomethacin/ibuprofen.
  • "Anticoagulant of choice in pregnancy" → heparin / LMWH (does not cross placenta).
  • Polyhydramnios vs oligohydramnios associations (atresia vs renal agenesis) — image/clinical vignettes.
  • Estriol and the fetoplacental unit; enzyme deficiency (placenta lacks 17α-hydroxylase).
  • "Layers of the placental barrier at term" → effectively haemomonochorial (cytotrophoblast lost).
  • Crista dividens directing oxygenated IVC blood through foramen ovale.
  • Type of placenta in humans → haemochorial, discoid, villous, deciduate.

Rapid revision

  1. Human placenta = discoid, haemochorial, deciduate, villous; ~500 g at term, 15–20 cotyledons.
  2. Tertiary villus is the definitive unit (has fetal vessels).
  3. Maternal part = decidua basalis; fetal part = chorion frondosum.
  4. Umbilical vein = oxygenated; umbilical arteries (2) = deoxygenated.
  5. Three shunts: ductus venosus, foramen ovale, ductus arteriosus.
  6. Remnants: DV → ligamentum venosum; DA → ligamentum arteriosum; FO → fossa ovalis; umbilical vein → ligamentum teres.
  7. Heparin does not cross placenta → anticoagulant of choice; warfarin is teratogenic.
  8. PGE keeps DA open; indomethacin/↑PaO₂ closes it.
  9. Amniotic fluid at term ~800–1000 mL; major source late = fetal urine.
  10. Polyhydramnios → oesophageal/duodenal atresia, anencephaly; oligohydramnios → renal agenesis (Potter), PROM.
  11. Estriol needs the fetoplacental unit; placenta lacks 17α-hydroxylase.
  12. Crista dividens shunts best-oxygenated IVC blood across foramen ovale to brain/heart.