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AN77.1-6 | Gametogenesis and fertilization — Gate Quiz

Graded 10 questions · 20 min · 3 attempts

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Q1 AN77.1 1 pt

Which is the correct sequence of spermatogenesis from stem cell to mature gamete?

A Spermatogonium → spermatid → primary spermatocyte → secondary spermatocyte → spermatozoon
B Spermatogonium → primary spermatocyte → secondary spermatocyte → spermatid → spermatozoon
C Primary spermatocyte → spermatogonium → spermatid → secondary spermatocyte → spermatozoon
D Spermatogonium → secondary spermatocyte → primary spermatocyte → spermatid → spermatozoon

Correct. Spermatogonium (2n) → primary spermatocyte (2n, 4C after DNA replication) → meiosis I → secondary spermatocyte (n, 2C) → meiosis II → spermatid (n, 1C) → spermiogenesis → spermatozoon.

Spermatogenesis sequence: Spermatogonium (2n) → [DNA replication] → Primary spermatocyte (2n, 4C) → [Meiosis I] → Secondary spermatocyte (n, 2C) → [Meiosis II] → Spermatid (n, 1C) → [Spermiogenesis] → Spermatozoon. Total: ~74 days.

The correct sequence: spermatogonium → primary spermatocyte (meiosis I) → secondary spermatocyte (meiosis II) → spermatid (spermiogenesis) → spermatozoon.

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Q2 AN77.2 1 pt

At what stage of meiosis is the secondary oocyte arrested at the time of ovulation?

A Prophase I (diplotene/dictyotene)
B Metaphase I
C Metaphase II
D Anaphase II

Correct. The secondary oocyte is arrested at Metaphase II at the time of ovulation. It remains in this state until fertilisation, when meiosis II is completed and the second polar body is extruded.

Oocyte meiotic arrests: (1) Prophase I (dictyotene) — from foetal life/birth, maintained by inhibitory signals in follicle; (2) Metaphase II — triggered by LH surge just before ovulation, maintained until fertilisation. These are clinically important for ART — egg retrieval must be timed after LH surge.

Two meiotic arrests in oogenesis: (1) Prophase I diplotene (dictyotene) from birth until puberty; (2) Metaphase II from just before ovulation until fertilisation.

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Q3 AN77.1 1 pt

A man with raised FSH, normal LH, and small soft testes has no sperm in his ejaculate. Testicular biopsy shows Sertoli cells only (no germ cells). Which statement BEST explains the elevated FSH?

A Absence of germ cells → absence of inhibin B from Sertoli cells → no negative feedback on FSH
B Sertoli cells produce testosterone which normally suppresses FSH
C LH stimulates Sertoli cells which normally suppress FSH secretion
D Absence of androgen receptor on Sertoli cells causes FSH rise

Correct. Sertoli cells produce inhibin B (in response to FSH and in the presence of active spermatogenesis). Inhibin B provides negative feedback on FSH from the pituitary. Without germ cells, inhibin B is absent → FSH rises (Sertoli cell only pattern).

FSH negative feedback: Sertoli cells → inhibin B → pituitary. Elevated FSH = Sertoli cell dysfunction or germ cell absence. LH negative feedback: Leydig cells → testosterone → hypothalamus/pituitary. Sertoli cell-only syndrome (Del Castillo): azoospermia + elevated FSH + normal LH/testosterone.

FSH feedback: Sertoli cells produce inhibin B → negative feedback on pituitary FSH. Without spermatogenesis/germ cells, inhibin B falls → FSH rises. LH/testosterone axis controls LH feedback, not FSH.

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Q4 AN77.3 1 pt

Where does normal fertilisation occur?

A Isthmus of the uterine tube
B Ampulla of the uterine tube
C Fundus of the uterus
D Infundibulum/fimbriae of the uterine tube

Correct. Fertilisation normally occurs in the AMPULLA of the uterine tube — specifically the ampullary-isthmic junction is the most common site. The ampulla is the widest, longest part of the tube.

Journey: Ovulation (from follicle) → fimbriae pick up oocyte → ampulla (fertilisation) → isthmus → uterine cavity (implantation, days 6–10). Ectopic pregnancy most commonly occurs in the ampulla (same site as fertilisation) when the embryo fails to travel to the uterus.

Fertilisation site: ampulla of the uterine tube (widest part). Ovum is picked up by fimbriae → transported to ampulla where sperm fertilise it → then travels to uterus for implantation.

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Q5 AN77.3 1 pt

What triggers the acrosome reaction, allowing sperm to penetrate the zona pellucida?

A Contact with the cumulus oophorus
B Binding to ZP3 glycoprotein on the zona pellucida
C Depolarisation of the oocyte membrane
D Capacitation in the uterine cavity

Correct. Binding of sperm to ZP3 (zona pellucida glycoprotein 3) triggers the acrosome reaction — exocytosis of acrosomal contents (acrosin, hyaluronidase) that digest the zona pellucida, allowing sperm penetration.

Steps in zona penetration: Sperm approaches zona → ZP3 binds sperm receptor → acrosome reaction (ZP3-triggered) → acrosin + hyaluronidase released → zona dissolves locally → sperm penetrates. After penetration: cortical reaction (zona hardening) prevents polyspermy.

ZP3 on the zona pellucida binds to sperm receptor → triggers acrosome reaction → enzyme release → zona penetration. Capacitation enables the acrosome reaction but does not trigger it directly.

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Q6 AN77.4 1 pt

What is the mechanism of the PERMANENT block to polyspermy after fertilisation?

A Depolarisation of the oocyte membrane (fast block)
B Cortical granule exocytosis → zona reaction → zona hardening
C Progesterone secretion from the corpus luteum
D Meiosis II completion and second polar body extrusion

Correct. The permanent (slow) block to polyspermy: cortical granules beneath oocyte membrane fuse with plasma membrane → exocytose enzymes into perivitelline space → zona pellucida hardens (zona reaction) → prevents additional sperm from binding/penetrating.

Polyspermy blocks: (1) Fast/electrical: immediate membrane depolarisation — temporary; (2) Slow/permanent: cortical granule exocytosis → zona pellucida hardens (zona reaction) — within 60 seconds. Clinical relevance: IVF uses ICSI to bypass natural fertilisation barriers; polyspermy in IVF leads to triploid embryos which are discarded.

Two blocks to polyspermy: Fast (immediate, electrical) = membrane depolarisation. Slow/permanent = cortical granule exocytosis → zona reaction (hardening). The permanent block is the cortical/zona reaction.

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Q7 AN77.2 1 pt

How many functional gametes are produced from one primary oocyte completing meiosis?

A 1 oocyte + 1 polar body
B 1 oocyte + 3 polar bodies
C 2 oocytes + 2 polar bodies
D 4 equal oocytes

Correct. One primary oocyte → meiosis I → 1 secondary oocyte + 1 first polar body → meiosis II → 1 mature oocyte + 1 second polar body (+ the first polar body may divide → total 3 polar bodies). Net: 1 functional oocyte + 3 polar bodies.

Key contrast: Spermatogenesis → 4 equal functional sperm. Oogenesis → 1 large functional oocyte + 3 small non-functional polar bodies. The asymmetry conserves cytoplasm/organelles for the oocyte to support early embryo development.

Oogenesis: 1 primary oocyte → 1 mature ovum + 3 polar bodies (unequal division conserves cytoplasm for the oocyte). Compare: spermatogenesis → 4 equal functional sperm.

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Q8 AN77.4 1 pt

A 23-year-old woman treated for pelvic inflammatory disease (PID) 2 years ago now presents with a positive pregnancy test and lower abdominal pain. TVS shows no intrauterine sac with a small left adnexal mass. Which risk factor from her history MOST directly explains her presentation?

A Young age at first intercourse
B Prior PID causing tubal damage and impaired ciliary transport
C Use of combined oral contraceptive pill
D Regular menstrual cycles

Correct. PID (from Chlamydia, Gonorrhoea) causes tubal scarring, ciliary damage, and peritubal adhesions. This impairs the transport of the fertilised egg from the ampulla to the uterus → egg implants in the tube → ectopic pregnancy.

PID (Chlamydia trachomatis, Neisseria gonorrhoeae) → tubal scarring → ectopic pregnancy risk ×6–10. In India, high prevalence of untreated STIs contributes to the burden of ectopic pregnancy. Screen all pregnant women with prior PID history; have low threshold for TVS and serial beta-hCG monitoring.

PID is the most important risk factor for tubal ectopic pregnancy. Chlamydial and gonococcal salpingitis scar the tubes → impaired ciliary transport → fertilised egg cannot reach uterus.

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Q9 AN77.3 1 pt

Capacitation of sperm occurs in the female reproductive tract. Which of the following changes occurs during capacitation?

A Formation of the acrosome from the Golgi apparatus
B Development of the flagellum from the centriole
C Removal of glycoprotein coat enabling acrosome reaction potential
D Formation of the midpiece with mitochondria

Correct. Capacitation (6–8 hours in female tract): removal of cholesterol and glycoproteins from the sperm plasma membrane, destabilising it, allowing hypermotility (hyperactivation) and enabling the subsequent acrosome reaction when ZP3 is encountered.

Capacitation vs spermiogenesis: Spermiogenesis (testis, before ejaculation) = structural transformation (acrosome, flagellum, midpiece). Capacitation (female tract, after ejaculation) = functional activation (glycoprotein removal, hypermotility, acrosome reaction potential). Both are needed for fertilisation.

Capacitation occurs in the female reproductive tract: glycoprotein coat removal, membrane changes → hypermotility, enables acrosome reaction. The acrosome, flagellum, and midpiece form during spermiogenesis (in the testis), not capacitation.

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Q10 AN77.1 1 pt

FSH acts on which testicular cells, and what is its primary effect?

A Leydig cells → stimulates testosterone production
B Sertoli cells → stimulates spermatogenesis and inhibin B production
C Spermatogonia → directly stimulates mitotic division
D Peritubular myoid cells → stimulates sperm transport

Correct. FSH acts on Sertoli cells → stimulates spermatogenesis (by creating a supportive environment for germ cells), produces inhibin B (negative feedback on FSH), and produces androgen-binding protein (concentrates testosterone in tubule).

Testis dual regulation: FSH → Sertoli cells → spermatogenesis support + inhibin B (negative feedback). LH → Leydig cells → testosterone → local effect on tubules + systemic androgen effects. Elevated FSH = Sertoli/germ cell dysfunction. Elevated LH = Leydig cell dysfunction.

FSH → Sertoli cells (spermatogenesis support + inhibin B). LH → Leydig cells (testosterone). This is the classic dual-hormone regulation of the testis.

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