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PY9.1-10 | Reproductive Physiology — Gate Quiz

Graded 10 questions · 20 min · 3 attempts

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Q1 PY9.1 1 pt

Ovulation in a normal 28-day menstrual cycle occurs on approximately which day?

A Day 7
B Day 14
C Day 21
D Day 28

Correct! Ovulation occurs on Day 14 of a 28-day cycle, triggered by the LH surge (mid-cycle LH peak, ~36 hours before ovulation). The follicular phase (Days 1–14) is variable; the luteal phase (Days 14–28) is constant at 14 days. This is why cycle length variation affects the pre-ovulatory timing.

Key concept: Menstrual cycle — Follicular phase (variable, Days 1–14): FSH → follicle maturation; Ovulation (Day 14): LH surge triggers; Luteal phase (constant 14 days, Days 14–28): corpus luteum produces progesterone + oestrogen. If no pregnancy: corpus luteum regresses → progesterone falls → menstruation. Fertile window: 5 days before + 1 day after ovulation (sperm survives 5 days; egg lives 12–24 hrs).

Incorrect. In a standard 28-day cycle, ovulation occurs on Day 14, triggered by a mid-cycle LH surge. The luteal phase is always 14 days; the follicular phase varies.

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Q2 PY9.2 1 pt

The mid-cycle LH surge that triggers ovulation is caused by:

A Progesterone positive feedback on the hypothalamus-pituitary axis
B Rising oestrogen levels (above 200 pg/mL for >36 hours) causing positive feedback on the pituitary
C FSH negative feedback on LH release
D Inhibin B from granulosa cells stimulating LH

Correct! When oestradiol rises above ~200 pg/mL (threshold) and remains elevated for >36 hours (temporal requirement), it switches from negative to positive feedback on the pituitary, triggering the massive mid-cycle LH surge (10-fold increase) that causes follicular rupture and ovulation ~36 hours later.

Key concept: Oestrogen dual feedback — Low oestrogen (most of cycle): NEGATIVE feedback on pituitary → ↓FSH, ↓LH; High oestrogen (mid-cycle threshold: >200 pg/mL for >36h): POSITIVE feedback → LH surge → ovulation. This is unique — the only positive hormone feedback loop in the HPG axis. Combined OCP prevents this surge by maintaining constant low oestrogen + progestin.

Incorrect. The LH surge is caused by high oestradiol (>200 pg/mL for >36h) switching to POSITIVE feedback on the pituitary gonadotrophs — the only example of oestrogen positive feedback in the HPG axis.

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Q3 PY9.3 1 pt

The corpus luteum primarily secretes which hormone to prepare the endometrium for implantation?

A FSH
B Oestradiol
C Progesterone
D Prolactin

Correct! The corpus luteum (formed from the ruptured follicle after ovulation) primarily secretes progesterone. Progesterone converts the proliferative endometrium to the secretory (decidualised) phase, creating an optimal environment for implantation. It also raises basal body temperature (~0.5°C).

Key concept: Corpus luteum of menstruation (lifespan 14 days) → secretes progesterone + oestrogen. If pregnancy: hCG from trophoblast rescues corpus luteum → continues progesterone production until placenta takes over at ~10 weeks (luteoplacental shift). Progesterone: ↑secretory glands, ↑spiral arteries, ↑uterine receptivity, ↑BBT, ↓uterine contractility, ↑cervical mucus viscosity (prevents sperm entry).

Incorrect. The corpus luteum primarily secretes progesterone (with some oestrogen). Progesterone maintains the secretory endometrium for implantation and, if pregnancy occurs, supports early gestation until the placenta takes over at 8–10 weeks.

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Q4 PY9.5 1 pt

Spermatogenesis requires a temperature 2–3°C below core body temperature. This is maintained by:

A The blood-testis barrier preventing heat entry
B Countercurrent heat exchange between the pampiniform plexus and testicular artery
C Cremasteric muscle reflexes that keep the testis permanently outside the body
D High testosterone levels locally that reduce testicular temperature

Correct! The pampiniform plexus is a network of veins draining the testis that surrounds the testicular artery. Warm arterial blood is cooled by the adjacent cooler venous blood (countercurrent heat exchange) before reaching the testis, maintaining scrotal temperature ~2–3°C below core body temperature (~34°C vs 37°C).

Key concept: Testicular thermoregulation — Pampiniform plexus (countercurrent exchanger) + scrotal position + cremasteric reflex (↑temperature → cremasteric muscle relaxes → testis descends). Cryptorchidism (undescended testis): temperature too high → impaired spermatogenesis → infertility if bilateral; also ↑risk of testicular germ cell tumours. Varicocoele (dilated pampiniform plexus) → impairs heat exchange → common cause of male infertility.

Incorrect. The pampiniform plexus (venous network surrounding the testicular artery) acts as a countercurrent heat exchanger — cooling arterial blood before it reaches the testis.

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Q5 PY9.6 1 pt

hCG is produced by the early embryo/trophoblast and serves as the basis for pregnancy tests. Its primary physiological role is:

A Initiating labour by stimulating uterine contractions
B Rescuing the corpus luteum to continue progesterone production
C Stimulating milk production in mammary glands
D Triggering ovulation in the first trimester

Correct! hCG (structurally similar to LH, binds LH receptors) is produced by trophoblast cells from implantation (~7–8 days after fertilisation). Its primary function is to "rescue" the corpus luteum, preventing its regression and maintaining progesterone production until the placenta takes over at 8–10 weeks. This prevents menstruation and maintains the pregnancy.

Key concept: hCG — Produced by syncytiotrophoblast; peaks at 8–10 weeks then falls; detected in blood 8 days after ovulation (when pregnancy test first positive). hCG subunit: α identical to LH/FSH/TSH; β-hCG is unique (basis of pregnancy tests). hCG used clinically: trigger ovulation (surrogate LH surge), treat male hypogonadism, diagnose gestational trophoblastic disease. Levels >100,000 mIU/mL with hyperemesis gravidarum (molar pregnancy).

Incorrect. hCG's primary function is to rescue (maintain) the corpus luteum, which continues producing progesterone essential for early pregnancy maintenance until the placenta takes over (~8–10 weeks).

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Q6 PY9.7 1 pt

The placenta transfers oxygen from maternal to fetal blood despite fetal Hb having higher O₂ affinity than adult Hb. This is explained by:

A The double Bohr effect — fetal CO₂ shifts maternal ODC left while maternal CO₂ shifts fetal ODC right
B Active transport of O₂ molecules across the trophoblast membrane
C The double Bohr effect — fetal CO₂ shifts maternal ODC right (releases O₂) while fetal Hb has higher affinity (left-shifted ODC)
D Higher fetal blood pressure driving O₂ across the concentration gradient

Correct! The double Bohr effect: (1) Fetal CO₂ diffuses to maternal blood → maternal ODC shifts RIGHT (Bohr effect) → maternal Hb releases O₂; (2) Maternal CO₂ diffuses to fetal blood → fetal blood becomes more acidic → fetal HbF ODC shifts slightly right, but HbF is inherently left-shifted (higher affinity) → net: fetal blood picks up the O₂ released by maternal Hb.

Key concept: O₂ transfer at placenta — HbF (2α2γ) has higher O₂ affinity than HbA (left-shifted ODC) because γ chains bind 2,3-DPG weakly. Double Bohr effect amplifies transfer. Haldane effect: oxygenation of maternal Hb at lungs decreases CO₂ binding, facilitating CO₂ transfer from fetus. Placenta also: nutrition transport, hormone production (progesterone, oestrogen, hCG, hPL), waste removal.

Incorrect. Double Bohr effect: fetal CO₂ shifts maternal ODC right (↑O₂ release by maternal Hb) while HbF remains left-shifted relative to HbA (higher O₂ affinity) → facilitates O₂ transfer from mother to fetus.

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Q7 PY9.8 1 pt

A new mother notices that her milk lets down (ejects) whenever she hears her baby cry. This is mediated by:

A Prolactin release triggered by the sound stimulus causing milk production
B Oxytocin release from the posterior pituitary causing myoepithelial cell contraction and milk ejection
C Oestrogen suppression allowing milk flow
D FSH/LH suppression reducing inhibition of mammary glands

Correct! The milk ejection (let-down) reflex: sensory stimuli (sound/sight of baby, or suckling) → hypothalamus → posterior pituitary releases oxytocin → contracts myoepithelial cells surrounding alveoli → milk ejection. Prolactin maintains milk PRODUCTION (synthesis) — oxytocin triggers EJECTION.

Key concept: Lactation — Prolactin (anterior pituitary): maintains milk SYNTHESIS; stimulated by suckling, suppressed by dopamine, inhibited by oestrogen (explains why lactation only begins post-delivery). Oxytocin (posterior pituitary): MILK EJECTION; triggered by suckling, conditioned (sight/sound of baby), positive feedback. Suckling → ↑prolactin + ↑oxytocin + ↓GnRH → lactational amenorrhoea (contraceptive). Progesterone and oestrogen inhibit lactation during pregnancy.

Incorrect. Milk ejection is mediated by oxytocin (posterior pituitary), not prolactin. Prolactin maintains milk synthesis; oxytocin (triggered by conditioned stimuli or suckling) causes myoepithelial contraction and milk let-down.

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Q8 PY9.9 1 pt

Testosterone in males is produced primarily by:

A Sertoli cells under FSH stimulation
B Leydig (interstitial) cells under LH stimulation
C The adrenal cortex under ACTH stimulation
D Peritubular myoid cells in the seminiferous tubules

Correct! Testosterone is produced by Leydig cells (interstitial cells of the testis) in response to LH (which acts on Leydig cell LH receptors → cAMP → testosterone synthesis from cholesterol). Sertoli cells respond to FSH and support spermatogenesis (ABP, inhibin, aromatase) but produce very little testosterone.

Key concept: Male gonadal regulation — LH → Leydig cells → testosterone (negative feedback on LH/GnRH); FSH → Sertoli cells → ABP (maintains high local testosterone for spermatogenesis) + inhibin B (selective FSH negative feedback); testosterone → spermatogenesis (via Sertoli ARs). Actions of testosterone: spermatogenesis, secondary sex characteristics, anabolic, libido, erythropoiesis, bone density.

Incorrect. Testosterone is produced by Leydig (interstitial) cells in response to LH. Sertoli cells respond to FSH and produce androgen-binding protein (ABP), inhibin, and support spermatogenesis.

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Q9 PY9.10 1 pt

A 23-year-old woman presents with oligomenorrhoea, hirsutism, acne, and infertility. Investigations show elevated LH/FSH ratio (>2), elevated androgens, and polycystic ovaries on ultrasound. This is consistent with PCOS. The primary hormonal abnormality is:

A Elevated FSH causing excessive follicle stimulation
B Elevated prolactin suppressing ovulation
C Insulin resistance → hyperinsulinaemia → ↑ovarian and adrenal androgen production + ↑LH pulse frequency
D Low oestradiol causing anovulation

Correct! PCOS pathophysiology: insulin resistance (70–80% of cases) → compensatory hyperinsulinaemia → ↑ovarian androgen synthesis (theca cells) + ↑adrenal DHEA + ↑GnRH pulse frequency → ↑LH/FSH ratio → LH stimulates androgen production > FSH stimulates follicle maturation → androgen excess → anovulation, hirsutism, acne.

Key concept: PCOS (Rotterdam criteria: 2 of 3 — oligoanovulation, clinical/biochemical hyperandrogenism, polycystic ovaries on USS). Most common endocrinopathy in women of reproductive age (5–10%). Insulin resistance is central. Treatment: lifestyle (weight loss), metformin (insulin sensitiser), OCP (reduce androgens), clomiphene/letrozole (ovulation induction). Long-term risks: T2DM, cardiovascular disease, endometrial cancer (from anovulatory oestrogen unopposed by progesterone).

Incorrect. The primary driver in PCOS is insulin resistance → hyperinsulinaemia → ↑androgen production + ↑LH pulse frequency → ↑LH/FSH ratio → anovulation.

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Q10 PY9.4 1 pt

A pregnant woman in the third trimester has a lower haemoglobin level than before pregnancy. The most likely explanation is:

A Reduced erythropoiesis due to high progesterone levels
B Dilutional anaemia — plasma volume increases (50%) more than red cell mass (25%)
C Iron deficiency from reduced dietary intake in pregnancy
D Haemolysis of RBCs due to placental antibodies

Correct! In pregnancy, plasma volume increases by ~50% while red cell mass increases by only ~25%. This disproportionate increase in plasma causes dilutional anaemia (physiological anaemia of pregnancy) — Hb falls to ~10.5–11 g/dL. This is not true anaemia but a normal adaptation that reduces blood viscosity and improves uteroplacental perfusion.

Key concept: Physiological changes in pregnancy — Haematological: ↑plasma volume (50%) > ↑RBC mass (25%) = dilutional anaemia (normal Hb ~10.5–11 g/dL); ↑WBC, ↑platelets (mild), ↑clotting factors (hypercoagulable state). Cardiovascular: ↑CO (40%), ↑HR, ↓SVR, ↓BP (first/second trimester). Respiratory: ↑TV, ↑minute ventilation, ↓PaCO₂ (mild respiratory alkalosis), ↑O₂ consumption. Renal: ↑GFR (50%), ↑RPF, physiological glycosuria possible.

Incorrect. The physiological fall in Hb during pregnancy is due to dilutional anaemia — plasma volume expands more (~50%) than red cell mass (~25%), diluting the Hb concentration.

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