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PY9.1-10 | Reproductive Physiology — Part 4

Parturition and Lactation

Parturition (labour/childbirth) is a coordinated process involving hormonal, mechanical, and inflammatory signals to transition from uterine quiescence (maintained throughout pregnancy by progesterone) to active contractions.

Figure: Parturition and Lactation

Trigger for labour (not fully understood in humans, but key factors):
• Falling progesterone:oestrogen ratio near term → myometrium becomes responsive to oxytocin
• Oxytocin (from posterior pituitary) → stimulates myometrial contractions
• Positive feedback loop: fetal head distends cervix → more oxytocin → stronger contractions (Ferguson's reflex)
• Prostaglandins (from fetal membranes, cervix) → enhance uterine contractility + cervical ripening
• Cortisol (from fetal adrenals near term) → stimulates placental oestrogen synthesis + lung maturation

Stages of labour:
1. First stage — cervical dilatation from 0 to 10 cm (latent + active phases; 6–18 hours in primigravidae)
2. Second stage — expulsion: from full dilatation to delivery of baby (up to 2 hours in primigravidae)
3. Third stage — delivery of placenta and membranes (within 30 minutes)

Lactation:
• Prolactin (from anterior pituitary) → stimulates milk synthesis (alveolar cells of breast)
• Oxytocin → stimulates milk ejection (let-down reflex: baby's suckling → neural signal → hypothalamus → posterior pituitary → oxytocin release → myoepithelial cells contract → milk expressed)
• High prolactin → suppresses GnRH → suppresses FSH/LH → lactational amenorrhoea (natural contraception; not reliable after 6 months or if not exclusively breastfeeding)
• Breast milk: colostrum (days 1–3, rich in IgA), then transitional milk, then mature milk
• Benefits: passive immunity (IgA), optimal nutrition, bonding, reduced maternal risk of breast/ovarian cancer

Physiological Basis of Pregnancy Tests

Home and laboratory pregnancy tests detect human chorionic gonadotrophin (hCG) in urine or serum.

Figure: Physiological Basis of Pregnancy Tests

Why hCG?
• hCG is produced exclusively by the trophoblast (early placental tissue) from ≈Day 8 after fertilisation.
• Serum hCG is detectable as early as 8–10 days post-conception.
• Urine hCG is detectable from ≈10–14 days (threshold ≈20–25 mIU/mL).
• hCG doubles approximately every 48 hours in normal early pregnancy (used to confirm viability).

Types of pregnancy tests:

Type	Principle	Sensitivity	Use
Urine lateral flow (home test)	Antibody sandwich — anti-hCG antibody + coloured particles	20–25 mIU/mL	Home use, from Day 1 of missed period
Quantitative serum β-hCG	ELISA or chemiluminescence	1–2 mIU/mL	Early detection, monitoring viability
Qualitative serum	Positive/negative	5–10 mIU/mL	Hospital use

Clinical uses of β-hCG levels:
• Ectopic pregnancy: hCG rises but slower than expected; no intrauterine sac on ultrasound
• Gestational trophoblastic disease (hydatidiform mole, choriocarcinoma): very high hCG levels, disproportionate to gestational age
• Down syndrome screening: lower hCG in T18, higher in T21 (part of triple/quadruple test)

False positives are rare: hook effect (very high hCG saturates antibodies in urine strip tests, giving false negative — suspect in molar pregnancy with negative home test but clinical features).

Menopause and Perimenopause: The End of Reproductive Years

Menopause is defined as the permanent cessation of menstruation for 12 consecutive months, resulting from loss of ovarian follicular function. The average age in India is 46–48 years (slightly earlier than Western populations at 51 years).

Figure: Menopause and Perimenopause: The End of Reproductive Years

Why does menopause occur?
Women are born with a finite stock of primordial follicles (≈2 million at birth). This stock declines continuously throughout life — through atresia (programmed follicular death), regardless of ovulation. By the mid-40s, so few follicles remain that they can no longer respond adequately to FSH → oestrogen production falls → the HPG axis loses its target → FSH and LH rise sharply (no negative feedback).

Perimenopause = the transitional period (typically 4–6 years before and 1 year after the final period). Characterised by:
• Irregular cycles (anovulatory cycles, shortened or lengthened cycles)
• Fluctuating oestrogen levels
• Beginning of vasomotor symptoms

Hormonal changes at menopause:
• Oestradiol (E₂): falls dramatically (from 100–200 pg/mL to <20 pg/mL)
• Oestrone (E₁): becomes the predominant oestrogen (produced by peripheral aromatisation of adrenal androgens in adipose tissue)
• FSH: rises markedly (>30–40 IU/L; often >100 IU/L) — the most reliable hormonal marker
• LH: also rises (but less dramatically)
• Progesterone: essentially absent (no ovulation = no corpus luteum)
• Inhibin: falls → removes inhibitory feedback on FSH

Clinical effects of oestrogen deficiency:
• Vasomotor symptoms (hot flushes, night sweats) — 75% of women; due to instability of the thermoregulatory centre
• Urogenital atrophy: vaginal dryness, dyspareunia (painful intercourse), recurrent UTIs
• Osteoporosis: accelerated bone loss in first 5–10 years post-menopause (oestrogen normally inhibits osteoclasts)
• Cardiovascular: loss of oestrogen's cardioprotective effect → increased LDL, decreased HDL → increased atherosclerosis risk
• Mood changes, sleep disturbance, reduced libido

Hormone Replacement Therapy (HRT):
• Replaces oestrogen (± progestogen if uterus intact — to prevent endometrial hyperplasia)
• Relieves vasomotor symptoms, prevents osteoporosis
• Risks: slightly increased breast cancer risk (oestrogen + progestogen combination), VTE
• In India: underused due to awareness gaps; doctors must discuss benefits vs. risks individualised for each patient