Human Reproduction Set-3

Serum progesterone remains near luteal values, $LH$ and $FSH$ stay suppressed, and the secretory endometrium does not begin breakdown.

Serum progesterone remains high, but $LH$ and $FSH$ do not change, and the endometrium continues to stay secretory.

Serum progesterone concentration remains near luteal values but loss of progesterone action raises $GnRH$‑driven $LH$ and $FSH$, and the secretory endometrium begins to break down causing menstrual bleeding.

Serum progesterone falls rapidly due to luteolysis; however $LH$ and $FSH$ remain largely unchanged during the first 48 hours and bleeding does not start.

Woman B has a short luteal phase (~10 days), suggesting insufficient luteal progesterone and a reduced chance of successful implantation.

Woman B has a longer luteal phase (>14 days) and therefore a higher probability of conception.

Both women have identical luteal phase adequacy because the date of menstruation (day 28) fixes luteal length at 14 days irrespective of BBT.

Woman A is more likely to have luteal phase deficiency because her BBT rise is earlier.

GnRH agonist triggers a short LH rise that still has enough time to sustain VEGF release from multiple corpora lutea, so OHSS risk is similar to $hCG$.

Exogenous $hCG$ produces only a brief LH-like effect (short half-life), so it causes less OHSS than GnRH agonist.

GnRH agonist reduces ovarian VEGF production directly, so luteinized follicles become less vascular and OHSS is prevented.

A GnRH agonist induces a short endogenous $LH$ (and $FSH$) surge, whereas exogenous $hCG$ has a much longer half‑life and prolonged luteinrophic action that sustains VEGF release from luteinized follicles, increasing vascular permeability and risk of OHSS.

Both A and R are true but R does not correctly explain A.

Both A and R are true and R correctly explains A.

A is true but R is false.

A is false but R is true.

PGT‑A will likely report a euploid embryo (false‑negative for ICM mosaicism), and transfer could result in an aneuploid fetus or developmental problems because the $ICM$ (future embryo) carries the abnormal cells.

PGT‑A will reliably detect the ICM mosaicism because chromosomal status of the $TE$ always mirrors that of the $ICM$.

A euploid $TE$ guarantees a chromosomally normal fetus because $TE$ and $ICM$ derive from identical, uniformly distributed lineages.

ICM‑restricted mosaicism cannot occur; mosaicism must be present equally in both $TE$ and $ICM$.

$1.2\times10^8$

$6\times10^8$

$3.6\times10^8$

$1.2\times10^9$

$2$

$20\times0.6\times0.7\times0.4 =\;3.36$

$4$

$6$

$n+1$

$2n-1$

$2n$

$2n+1$

Phenotypically female external genitalia, well-developed breasts at puberty, scant or absent pubic/axillary hair, absence of uterus and fallopian tubes, presence of undescended testes

Phenotypically female external genitalia with normal pubic hair, presence of uterus and functioning ovaries, testes absent

Ambiguous external genitalia with virilization at puberty, presence of uterus, ovaries absent, undescended testes

Phenotypically male external genitalia with micropenis, presence of uterus, undescended testes

Splitting at days $1$–$3$ (early cleavage) → dichorionic diamniotic; not predisposed to TTTS

Splitting at days $8$–$13$ (after amnion formation) → monochorionic monoamniotic; no increased risk of TTTS

Splitting at days $4$–$8$ (blastocyst/early implantation) → monochorionic diamniotic; yes, increased risk of TTTS due to placental vascular anastomoses

Splitting after day $13$ → conjoined twins; TTTS risk is not the primary concern