Placenta
- Dimensions:
- Weight: 500 gm & 500 mL
- Diameter: 15-20 cm
- Placental weight = Fetal weight at 17 weeks
- Central thickness: 2.5-4 cm
- Placentomegaly:
- Placental thickness ≥4 cm
- Causes:
- Diabetes, GDM
- GTD
- Twin pregnancy, TTTS
- Rh negative pregnancy
- Small Placenta
- Pre eclampsia
- IUGR
GA | Placental Wt |
At 17 weeks | Placental Weight = Fetal weight |
At term | Ratio of placental weight to fetus = 1:6 |
- Formation:
ㅤ | Fetal side | Maternal side |
Placenta formation | Chorion frondosum | Decidua basalis |
Appearance | Smooth, shiny | Dull |
During Placental separation | Central separation | Peripheral separation |
Method | Schultze method | Duncan method |
ㅤ | Better, M/c ↳ Retroplacental clot formed ↳ Decreased bleeding | ㅤ |

- Features:
- Discoidal
- Deciduate: Shed off after delivery
- Hemochorial: Lies in contact with maternal blood
Umbilical cord:
- 3 vessels
- a. Right umbilical artery
- b. Left umbilical artery
- c. Left umbilical vein
- Mnemonic: Are you Very Lost (RUV lost)
- Presence of a single umbilical artery
- A/w congenital anomalies
- Like Renal agenesis
- Normal average length is 50-60 cms
- contains a gelatinous substance called Wharton's jelly
- Shed off by 7 - 10 days
Placental Hormones
- M/c site of production : Syncytiotrophoblast.
- hCG
- HPL
- Cause: Insulin Resistance
- Fasting Hypoglycemia
- Postprandial Hyperglycemia
- Progesterone
- From DHEA-S produced by fetal adrenal gland.
- Estriol (E3)
Maintaining Pregnancy by Progesterone
- β hCG from Syncytiotrophoblast
- Maintains Corpus luteum till 8 weeks
- Corpus luteum → secrete progesterone till 8 weeks
- After 8 weeks → Syncytiotrophoblast secrete Progestogen
Human Chorionic Gonadotropin (hCG)
- Type: Glycoprotein hormone
- Also AMH/MIS → Glycoprotein hormone
- Secreted by Syncytiotrophoblast from implantation onwards
- Subunits:
- α-subunit: Similar to LH, FSH, TSH
- β-subunit:
- Similar to LH
- Specific
- Tested in UPT
- So structurally similar to LH
- Function:
- Maintains corpus luteum up to 6 weeks of pregnancy
- First stimulus for release of testosterone from fetal testis
- Doubling time: 48 hours
- Levels:
- Appears in blood: Day 8-9 after fertilization (D22 of cycle)
- Peak levels: 9-10 weeks
- Plateau: 16-20 weeks
- T1/2: 36 hours
Feature | hCG | LH |
T½ | 37 hours | 30 minutes |
Potency | 80X | X |
- Functions:
- Stimulate the maternal thyroid gland during pregnancy.
- Stimulates Leydig cells → Testosterone production
- Stimulates corpus luteum → Relaxin production
- Exhibits immunosuppressive activity → Prevents fetal rejection
- Maintains corpus luteum up to 6 weeks of pregnancy
Subtype | Source | Clinical Use / Significance |
Intact hCG | Syncytiotrophoblast | Normal pregnancy. Basis of routine pregnancy tests. |
Free β-hCG | Trophoblastic tissue | ↑ in Down syndrome screening. Marker of GTN, testicular tumors. |
Hyperglycosylated hCG (hCG-H) | Invasive cytotrophoblast | Early pregnancy. Marker of trophoblastic invasion. ↑ in invasive mole, choriocarcinoma. |
Nicked hCG (hCGn) | Trophoblastic tumors, late pregnancy | Partially degraded form. Seen in trophoblastic neoplasia. |
β-core fragment | Urinary metabolite of β-hCG | Present in urine. Used in urine tumor marker assays. |
Free α-subunit | Pituitary, tumors | Nonspecific. Seen in pituitary hCG, ovarian and testicular tumors, some thyroid cancers.B |
The adrenal cortex of the fetus releases
- In early pregnancy:
- Cortisol
- In 2nd trimester:
- DHEA
The fetal adrenal gland primarily produces
- Dehydroepiandrosterone sulfate (DHEA-S)
- crucial for growth and development.
Fetal growth
- D/t Fetal Insulin / IGF
- Not d/t Maternal Insulin / GH
- Insulin do not cross Placenta
- Normal Newborn
- Fetal Hyperglycemia
- Stimulates Insulin → Fetal growth
- In Newborn of Diabetic mother
- Maternal hyperglycemia → ↑↑↑ Fetal insulin → Macrosomia
- Fetal Hypoglycemia
Estrogen
- Synthetic
- EE
- CEE
- Physiological
- E1, E2, E3
Potency
- Ethinyl Estradiol (EE) >
- Conjugated Equine Estrogen (CEE) >
- Estradiol (E2) >
- Estrone (E1) >
- Estriol (E3)
Common Estrogen Types
Condition | Estrogen Most Common/Specific |
Most common synthetic Estrogen in OCP | EE |
Most common synthetic Estrogen in HRT | 17-beta estradiol |
Most common in reproductive age female | E2 (Estradiol) |
Most common in pregnancy | E2 |
Most specific in pregnancy, Synthesised by Placenta [From DHEA from fetal adrenal gland] | E3 |
Most common in menopausal female, PCOS | E1 (Estrone) |
Low Estrogen
- POI
- Menopause
- Gonadal dysgenesis
- Sheehan’s Syndrome
- Kallman’s syndrome
Progesterone challenge test is Negative
- If Low Estrogen
- Progesterone can only act on Estrogen primed endometrium
- Normal Estrogen
- Ascherman syndrome
- d/t no endometrium
- [Positive in PCOS]
Source of Estrogen + Progesterone :
- Before 8 weeks:
- Corpus luteum of pregnancy
- Made and maintained by LH
- After 8 weeks:
- Placenta
Estrogen
Target Organ | Actions |
Uterus (Estrogen dominant) | • Increases blood flow. • Increases contractility, increases excitability. • Menstruation |
Vagina | • Vaginal Cornification |
Cervix | • Cervical mucus production |
Secondary sexual characteristics | • Creates female body contour. • Promotes fat distribution in breast & buttocks. • DO NOT CAUSE PUBIC OR AXILLARY HAIR GROWTH |
Breast | • Promotes growth. • Aids ductal proliferation. |
Bone | • Produces Osteoprotegerin (inhibitor of RANK ligand). • ↓↓ osteoclast differentiation → ⛔ bone resorption → Protects bone |
Liver | • ↓↓ plasma LDL cholesterol |
CVS | • ⛔ platelet activation → ↓ Clot formation • Promotes vasodilation by increasing NO |
CNS | Neuroprotective: • ⛔ neuronal cell death |
Kidneys | • Causes salt & water retention |
Progesterone
Target Organ | Actions |
Uterus | Anti-estrogenic action: • Makes uterus less active, less excitable, less contractile |
Breast | • Promotes lobulo-alveolar (gland) growth |
CNS | Thermogenic action: • ↑↑ Basal Body Temperature (BBT) by 0.5-1°C during ovulation. |
Respiration | • Stimulates respiration → Leads to CO2 washout → ↓↓ alveolar PCO2 levels |
Kidneys | Causes Natriuresis: • Promotes salt & water excretion • (Only steroid hormone → cause Natriuresis) |
NOTE
- Androgens are formed in Ovary
- In Theca Interna cells
- Not DHT, DHEA
- Testosterone → 5α reductase enzyme→ Di-hydro testosterone (DHT) (more potent).
- Aromatase from granulosa cells
- convert to Estradiol (E2) → most potent
- Aromatase from peripheral fat
- convert to Estrone (E1)
Hormonal Changes in Pregnancy


Hormone | Pattern in Pregnancy | Near Term / Parturition |
Estrogen | Rises steadily throughout pregnancy | ㅤ |
Progesterone | Increases initially, then constant after 7th month | Estrogen : Progeserone ratio ↑ near term |
Prolactin | Gradual rise | Peaks just before delivery |
Cervical Mucous Study
ㅤ | Estrogen | Progesterone |
Consistency | Profuse, watery, elastic | Thick, scanty, viscous |
Known as | Spinnbarkeit (Stretching ⊕) Spin → Loose | Tack (Stretching ⊝) Tack → katti |
ㅤ | ㅤ | ㅤ |
Ferning


- Seen under microscope on D8
- ↳ Proliferative phase
- Disappears by D18 of cycle
- If ferning persist by D18, indicates Anovulation
Endometrial Glands
- Endometrial Biopsy → Not commonly done for ovulation.
- Timing: D26 (Pre-menstrual phase).






• Glands shrink
• Prominent vessels and Hemorrhagic spots
Stages | Features |
Early proliferative ↳ Estrogen | • Simple tubular glands • Telescoping of gland • Pseudostratification (Nuclei at different levels) |
Early secretory ↳ Progesterone | • Subnuclear vacuolation: First sign of ovulation on biopsy (D17 - D18) |
Late secretory ↳ Progesterone | • Corkscrew glands • Sawtooth appearance • Secretions in gland |
Placental Anomalies


- Maternal side larger than fetal side
- Equal size lobes
- Unequal lobes
- Connected by blood vessels.
- After delivery
- Placenta shows an oval defect in chorion
- with torn blood vessels ending abruptly at margins
- Complications
- Retained placenta
- PPH
- Increased size of placenta
- Increased risk of placenta previa → Antepartum hemorrhage (APH).
Placenta bilobata
Placenta succenturiata

- Single umbilical cord
- Battledore placenta:
- Marginal insertion of cord
- Circumvallate placenta:
- Valve-like thickening
- A/w
- IUGR
- Placenta Previa
- Preterm labor
- Circummarginate placenta:
- No valve-like thickening
Velamentous Cord Insertion




Pathophysiology
- Cord attaches to membranes, not directly to placenta
- Wharton's jelly absent in membrane part
- Vessels run freely in membranes before reaching placenta
Complications
Vasa previa

- Unprotected vessels may rupture
- After ARM: Fetal distress + bleed.
- Less blood loss + marked fetal distress
- Leads to fetal blood loss → life-threatening
Types | A/w | Notes |
1 | Velamentous cord | ㅤ |
2 | Placenta Succinturiata | • Umbilical cord attached only to bigger lobe • Smaller lobe if left behind → cause PPH |
IOC
Condition | Screening | IOC | ㅤ |
Vasa Previa | ㅤ | USG Doppler | ㅤ |
Placenta Previa | TAS (PP vs. AP) | TVS | Best Time for USG • T3 (32 - 36 weeks) |
Placenta accreta | TVS | MRI | ㅤ |
Placental Transfer:
✅ Can Cross the Placenta
Nutrients
- Glucose – facilitated diffusion
- Amino acids – active transport
- Fatty acids – esp. long-chain
- Water-soluble Vitamins (e.g., B, C)
- Minerals – calcium, iron
Gases
- O₂ – maternal to fetal
- CO₂ – fetal to maternal
Water & Electrolytes
- Water, Na⁺, K⁺, Cl⁻ – passive/facilitated
Antibodies
- IgG – receptor-mediated (passive immunity)
- IgG2:
- Does not cross placenta
- protects against capsulated organisms
Hormones
- Cortisol, Thyroid hormones – limited crossing, regulated
Drugs
- Lipid-soluble, low MW (<500 Da)
- Examples: alcohol, nicotine, caffeine, some anesthetics, anticonvulsants, antidepressants
Toxins
- Alcohol, mercury, lead, pesticides
Pathogens
- Viruses: rubella, CMV, Zika
- Bacteria: Treponema pallidum
- Parasites: Toxoplasma gondii
❌Cannot / Limited Passage
Large Molecules
- Proteins – albumin, Hb
- IgM – too large
Hormones
- Insulin, LH, FSH, GH, TSH, HCG
- Peptide hormones – limited
- Catecholamines – degraded/metabolized
Some Drugs
- High MW (>1000 Da), polar
- Example: heparin
- Efflux by P-glycoprotein
Blood Cells
- RBCs, WBCs – normally blocked
- Rare: microtransfusion in placental injury
Most Bacteria
- Generally blocked
- Exception: Listeria
Placenta Accreta Spectrum (PAS)IOC →

IOC
Condition | Screening | IOC | ㅤ |
Vasa Previa | ㅤ | USG Doppler | ㅤ |
Placenta Previa | TAS (PP vs. AP) | TVS | Best Time for USG • T3 (32 - 36 weeks) |
Placenta accreta | TVS | MRI | ㅤ |

Signs on USG Placenta Accreta Spectrum:
- Placental lakes/moth-eaten appearance.
- Heterogenous Placenta
- Thinning of myometrium behind Placenta
- Loss of clear space behind Placenta
- Loss of Bladder line
- Absence Of hypoechoic area
- behind placenta representing decidua basalis
- Absence Of Continuous white line reflecting
- bladder - uterine serosa interface.

Types:
Types | Featuures |
Placenta accreta (M/c) | Chorionic villi superficially attached to myometrium |
Placenta increta | Villi invade myometrium |
Placenta percreta | Villi penetrate → attached to serosa |
Amniotic Fluid
- pH : 7 - 7.5
- Maximum at
- 32-34 weeks
- 1000 mL
- At term/40 weeks:
- 800 mL
- ≥42 weeks:
- 200 mL
Normal values
- AFI (Amniotic Fluid Index): 5 - 25 cm
- SVP (Single Largest Vertical Pocket): 2 - 8 cm
Source
- Gestational age: Source
- First trimester: Maternal plasma
- 12-20 weeks: Fetal skin
- 20 weeks: Fetal urine
- Mnemonic: Amniotic fluid → AFP → ammede blood, fetal skin, Peee
Appearance
- Straw coloured: Term
- Clear to pale yellow
- Without white specks
- White specks → indicate meconium staining
- Cloudy → Infection
Gestational age | Amniotic fluid appearance |
32nd week | • Clear • No flakes |
36th week | • Some flakes present • Traces of cloudiness |
42nd week (term / post-term) | • Very cloudy + ↑↑ flakes |
Colour
- Colour: Seen in
- Saffron colour, yellowish green:
- Post term pregnancy
- Green colour (Due to biliverdin in meconium):
- Fetal distress
- Transverse lie/Breech
- Listeria infection
- Mnemonic: Green → GB → Liver → LFT
- Golden colour (Due to bilirubin):
- Rh incompatibility
- Mnemonic: Gold (golden), Ruby (rubin) → Rich (Rh)
- Tobacco juice/Brown:
- Intrauterine fetal death
- Mnemonic: Tobacco brings death
- Dark red:
- Concealed hemorrhage
Listeria infection
- Cross placenta
- Make Amniotic fluid Green
- Shows differential motility
Amniotic Fluid Disorders


Oligohydramnios vs. Polyhydramnios
- Conditions leading to both oligo & polyhydramnios:
- TTTS
- TORCH infections
Oligohydramnios
- AFI: <5 cm
- Single largest vertical pocket (SVP): <2 cm
- M/c cause of mild oligohydramnios: Idiopathic
- M/c cause of severe oligohydramnios:
Fetal renal anomalies | Notes |
Renal agenesis / anomalies | • m/c |
Posterior Urethral valve | ㅤ |
UPI / PIH | • Decreased transudation across placenta (Small placenta) • Oligo in T3 |
Ruptured membranes | • Best: P/s examination |
TORCH | • Early onset Oligohydramnios |
IUD/ Post term baby | ㅤ |
- Other causes:
- Decreased urine output:
- Renal disorders
- Drugs: ACE inhibitors/Indomethacin
- Decreased volume of Amniotic fluid:
- Post term pregnancy
- PROM
- Leaking after amniocentesis
- Chromosomal Anomaly:
- (69 chr) Triploidy
- May lead to compression defects
- CTEV
- Potter’s syndrome / sequence
Polyhydramnios
- AFI: >25 cm
- SVP: >8 cm
- Mild Polyhydramnios: Idiopathic
- M/c cause of severe Polyhydramnios:
- Fetal GIT anomalies
- Esophageal atresia
- Duodenal atresia
- Cleft lip/Cleft palate
- Anencephaly
- CDH
- Other causes:
- Increased transudation across placenta:
- Placentomegaly
- Placental thickness ≥4 cm
- Causes:
- Diabetes, GDM
- GTD
- Twin pregnancy, TTTS
- Rh negative pregnancy
- Increased urine output:
- Hydrops Fetalis
- Twin pregnancy, Diabetes, Bartter syndrome
- Fetal anemia (Thalassemia, Rh negative pregnancy, Parvo virus infection)
- Increased transudation from fetal skin:
- NTD, Abdominal wall defect
- Chromosomal anomaly:
- Trisomy
Approach to a Case of Polyhydramnios/Oligohydramnios

Note:
- PSV of MCA
- ≥ 1.5 MOM: Fetal anemia.
- < 0.8 MOM: Fetal polycythemia.
- Indomethacin:
- Can be used to treat polyhydramnios
- S/E: Premature closure of ductus arteriosus
- C/I: >32 weeks of pregnancy
Note:
- M/c CTG Finding in oligohydramnios:
- Variable deceleration → Due to cord compression
- Persistent variable deceleration:
- Only indication for amnioinfusion
Syndromes related to Oligohydramnios
Potters syndrome:

- Severe oligohydramnios due to kidney defects
- Renal agenesis
- B/L renal agenesis (incompatible with life).
- PCKD
- C/f:
- Lung hypoplasia
- most common cause of mortality in Potter syndrome
- Typical flat facies
- Potters sequence
- Severe oligohydramnios due to non renal causes
- Extremities anomaly.
- Wrinkled skin.
- Facial dysmorphism.
- Renal agenesis B/L (primary anomaly).
- Oligohydramnios.
- Eyes widely separated.
- Epicanthic folds.
- Flat facies.
- High forehead.
- Receding chin.
- Washer man's hand.
- Potter facies.
Clinical features:

Amniotic band syndrome
- Severe oligohydramnios due to PPROM
- C/f:
- Distal digit amputation
- Craniofacial abnormalities
Note:
- Proximal limb amputation:
- Phocomelia due to Thalidomide
- Mnemonic: Melathe (melia) kayyi poi (Proximallimb) → thali kettan (thalidomide) pattanilla
- Distal digit amputee
- Amniotic band syndrome
- Oligohydramnios

Presentation Of Oligohydramnios
- Early pregnancy:
- Lung hypoplasia,
- Limb amputation

- Late pregnancy:
- Cord compression
- Fetal distress
- Meconium aspiration syndrome
- Club foot/CTEV
Amniotic Fluid Embolism
- Diagnosis: Clinical diagnosis, no confirmatory test.
- Prognosis: Can lead to maternal mortality within 30-40 mins.
- Time of Occurrence: At the time of labour/within 30 mins of labour.
Phases:
- 1st Phase:
- Cardiorespiratory arrest (Difficulty breathing, ↑PR, ↓BP).
- pulmonary vasoconstriction and right ventricular failure.
- 2nd Phase:
- DIC + excessive bleeding.
Diagnostic Criteria:
- Unexplained shock + less bleeding.
- Clinical onset within 30 mins of labour.
- Abrupt cardiorespiratory arrest.
- Overt DIC.
- No fever.
