OG28.1-4,OG30.1-2 | Infertility and Endocrine Gynaecology — Graded Quiz

Correct. A normal AMH (2.1 ng/mL implies adequate ovarian reserve), regular cycles (presumed ovulatory), and a near-normal semen analysis (count 18 million/mL is mildly low but motility and morphology are within normal range) with no structural history = unexplained infertility. This diagnosis requires that all standard investigations (ovulatory status, semen analysis, tubal patency) return essentially normal results.

Unexplained infertility is diagnosed when all standard investigations (semen analysis, ovulatory confirmation, tubal patency) yield essentially normal results. It represents 10–30% of infertile couples.

The semen parameters here are near the WHO 2021 reference ranges (count ≥16 million/mL, motility ≥42%, morphology ≥4%). Regular cycles with normal AMH suggest normal ovulation. Without pelvic pathology history, the combination points to unexplained infertility. A tubal assessment has not yet been done but does not by itself change the working diagnosis at this stage.

Correct. A smooth filling defect at the lower uterine segment in a woman with multiple Caesarean sections is characteristic of a Caesarean scar defect (isthmocele). The pouch at the scar can accumulate debris, alter cervical mucus, and impair implantation. This is a distinct entity from Asherman's syndrome (which produces irregular adhesion-type defects throughout the cavity).

Caesarean scar defect (isthmocele) is an emerging cause of secondary infertility and abnormal uterine bleeding in women with previous CS — look for a smooth lower-segment niche on HSG or ultrasound.

Asherman's syndrome typically follows curettage and shows irregular intrauterine defects with poor cavity fill. A Caesarean scar defect (isthmocele) presents as a smooth niche at the lower segment after repeat CS — recognisable because the defect is at the isthmus, smooth-edged, and correlates with the scar location. Fibroids and polyps can be distinguished by their echogenicity and morphology on ultrasound.

Correct. A dilated, blocked tube (likely hydrosalpinx given the prior ectopic + beaded pattern) exerts a deleterious effect on IVF endometrial receptivity via retrograde fluid flow and toxic embryotoxic mediators. Salpingectomy before IVF significantly improves live birth rates (Cochrane evidence). Reanastomosis is not appropriate for an ampullary-isthmic ectopic repair site with confirmed re-occlusion. Proximal catheterisation is for proximal, not distal, occlusion.

A blocked/dilated tube (hydrosalpinx) halves IVF success rates. Salpingectomy before IVF is recommended to improve endometrial receptivity and live birth rates.

Hydrosalpinx (or any dilated blocked tube) reduces IVF pregnancy rates by ~50%. Salpingectomy (or proximal ligation if salpingectomy is not feasible) prior to IVF is the evidence-based recommendation. Reanastomosis is reserved for bilateral distal disease in women where IVF is not available or affordable. Selective catheterisation addresses proximal spasm/debris, not distal damage.

Correct. WHO Group I anovulation (hypogonadotrophic hypogonadism — low FSH, LH, and oestradiol) results from absent pulsatile GnRH drive and does not have a functioning pituitary-ovarian axis to stimulate with clomiphene or letrozole. These oral agents work by blocking oestrogen negative feedback — which presupposes an intact HPO axis. Only exogenous gonadotrophins (or pulsatile GnRH) can substitute for the absent pituitary stimulation. Gonadotrophins with careful monitoring are the practical first-line option.

WHO Group I anovulation (hypogonadotrophic) requires exogenous gonadotrophins (or pulsatile GnRH) for ovulation induction — clomiphene and letrozole are ineffective because the pituitary axis is absent.

Clomiphene and letrozole both work by modulating oestrogen feedback at the hypothalamus/pituitary — they require a functioning pituitary that can respond by secreting FSH. In WHO Group I (low FSH/LH), the pituitary is not secreting enough FSH to respond to these agents. Exogenous gonadotrophins provide the FSH directly. Pulsatile GnRH is an option but is less available; gonadotrophins are the standard practical first-line.

Correct. This is severe OHSS: haematocrit ≥45%, hypoalbuminaemia, oliguria, tense ascites, and rising creatinine — all hallmarks of the third-space fluid shift that defines severe OHSS. Management requires hospitalisation, IV albumin (expands intravascular volume and scavenges VEGF), strict fluid balance, and LMWH thromboprophylaxis (haemoconcentration + venous stasis = high VTE risk). Laparoscopy is avoided unless torsion is confirmed.

Severe OHSS features: haematocrit ≥45%, significant ascites, oliguria, hypoalbuminaemia, elevated creatinine. Requires hospitalisation, IV albumin, strict fluid balance, and LMWH thromboprophylaxis.

The clinical features — haematocrit ≥45%, oliguria, tense ascites, rising creatinine, and hypoalbuminaemia — fulfil criteria for severe (not moderate) OHSS. Moderate OHSS has abdominal discomfort and mild ascites but no renal impairment or haemoconcentration requiring inpatient management. Ruptured cyst would have peritonism and haemodynamic instability; PID would have fever and cervical motion tenderness.

Correct. The primary reason for freeze-all in incipient OHSS is that early OHSS is driven by exogenous hCG (used for trigger), and if a pregnancy implants, the resulting endogenous hCG from the trophoblast sustains and worsens the OHSS into 'late OHSS' — which is more severe and prolonged. By deferring transfer to a frozen-thawed cycle, the ovaries recover, OHSS resolves, and the transfer occurs in a non-stimulated uterus.

Freeze-all strategy in OHSS risk: defers transfer to prevent late OHSS driven by implantation-derived endogenous hCG, which would sustain and worsen the ovarian hyperstimulation response.

Frozen embryo transfer does NOT universally outperform fresh transfer — outcomes are comparable in most patients (and in some protocols, fresh transfer is preferred). The specific indication for freeze-all here is OHSS prevention: avoiding the endogenous hCG of early implantation that would escalate early OHSS to late severe OHSS. PGT is a separate indication for freeze-all and is not the driver here.

Correct. She satisfies all three Rotterdam criteria: (1) oligo-ovulation — 4 periods/year, well below the threshold of ≤8 periods/year; (2) clinical/biochemical hyperandrogenism — moderate acne plus elevated free testosterone; (3) PCOM on ultrasound — ≥12 follicles per ovary (she has 14), peripheral arrangement, increased stromal echogenicity. With TSH and prolactin normal, other causes are excluded. Rotterdam requires 2 of 3, so she more than qualifies.

Rotterdam 2003: 2 of 3 required. PCOM threshold is ≥12 follicles per ovary (2003 criteria; updated 2018 threshold is ≥20 follicles per ovary on modern high-resolution ultrasound). Clinical acne counts as clinical hyperandrogenism.

Rotterdam 2003 criteria: (1) oligo/anovulation — 4 periods/year confirms this; (2) hyperandrogenism — moderate acne is clinical hyperandrogenism, and elevated free testosterone is biochemical confirmation; (3) PCOM — 14 follicles/ovary with peripheral arrangement. All three are present. A GnRH test is not part of the Rotterdam diagnostic workup.

Correct. Chronic anovulation in PCOS leads to unopposed oestrogen exposure of the endometrium — no progesterone withdrawal means the endometrium proliferates continuously without shedding. This dramatically increases the risk of endometrial hyperplasia and endometrial carcinoma over time. Women with PCOS have a 3-fold increased risk of endometrial cancer. Metabolic syndrome (borderline glucose, hypertension, elevated BMI) compounds this risk.

Chronic anovulation in PCOS = unopposed oestrogen = 3-fold increased risk of endometrial hyperplasia/carcinoma. Regular progestogen withdrawal (or COCP) is mandatory to protect the endometrium in women with PCOS and fewer than 4 periods/year.

The key risk here is unopposed oestrogen from chronic anovulation. In PCOS, follicles do not complete ovulation, so no corpus luteum forms and no progesterone is produced. Without progesterone's protective effect, the endometrium undergoes progressive, unchecked proliferation — the substrate for hyperplasia and malignancy. PCOS does not increase ovarian or cervical cancer risk. Premature ovarian insufficiency is the opposite of PCOS's typical presentation.

Correct. Elevated 17-OHP (3.8 ng/mL — the stimulated level above 10 ng/mL would be definitive, but elevated basal 17-OHP is strongly suggestive) combined with mildly elevated DHEAS (adrenal androgen), gradual onset hirsutism without virilisation, and normal testosterone indicates non-classical CAH (21-hydroxylase deficiency). The enzyme block causes accumulation of 17-OHP and diversion to adrenal androgens. PCOS usually shows normal or mildly elevated testosterone, NOT significantly elevated 17-OHP.

Non-classical CAH (21-hydroxylase deficiency) mimics PCOS but is distinguished by elevated basal 17-OHP (confirmed by ACTH stimulation test showing post-ACTH 17-OHP >10 ng/mL). Up to 8% of apparent PCOS cases are actually non-classical CAH.

The key discriminating feature here is the elevated 17-OHP, which is NOT elevated in PCOS. Adrenal Cushing's syndrome would show elevated cortisol, central adiposity, striae, and hypertension. Idiopathic hirsutism has normal androgens and normal cycles. Non-classical CAH mimics PCOS clinically but is distinguished by elevated 17-OHP, which warrants ACTH stimulation testing for confirmation.

Correct. In a woman with PCOS-related hirsutism who does not want pregnancy, a COCP with anti-androgenic progestogen (such as cyproterone acetate 2 mg + ethinyl oestradiol) is first-line pharmacological treatment. It suppresses LH-driven ovarian androgen production via oestrogen-mediated gonadotrophin suppression, increases SHBG (reducing free testosterone), and the anti-androgenic progestogen directly blocks the androgen receptor at the hair follicle. Contraception is provided simultaneously.

For hirsutism in PCOS: anti-androgenic COCP (e.g., cyproterone acetate-ethinyloestradiol) suppresses LH-driven ovarian androgens, increases SHBG, and directly blocks the androgen receptor. Note: full hair reduction takes 6–9 months.

Finasteride is a 5-alpha reductase inhibitor used for hirsutism but is not used in women of reproductive age without reliable contraception due to teratogenicity. Dexamethasone is used for adrenal-source androgen excess (CAH), not PCOS. Spironolactone in high doses is effective for hirsutism but must not be used as monotherapy in women of reproductive potential without concomitant contraception — it causes feminisation of a male foetus. An anti-androgenic COCP addresses both menstrual regulation and hirsutism simultaneously.

Correct. Vasectomy reversal success rates are strongly time-dependent. With an interval under 10 years and no anti-sperm antibodies detected, patency rates after reversal are approximately 70–90% and pregnancy rates 40–55% — comparable to or better than IVF/ICSI outcomes in a young female partner. The couple can then attempt natural conception repeatedly without further intervention. When the interval exceeds 10 years, anti-sperm antibodies are more likely and patency rates fall, making ICSI more cost-effective.

Vasectomy reversal has 70–90% patency with interval < 10 years and absent anti-sperm antibodies. This compares favourably to ICSI and is the preferred option when the interval is short. Beyond 15 years, ICSI is more cost-effective.

An older female partner (38 years) or diminished ovarian reserve would favour ICSI (shorter time-to-treatment). A wish to avoid multiple pregnancy does not differentiate between the two options meaningfully. The key predictor of vasectomy reversal success is the obstructive interval: under 10 years with no antibodies favours reversal; over 15 years significantly favours ICSI.

Correct. AMH 0.4 ng/mL and AFC of 3 are consistent with severely diminished ovarian reserve (DOR). Elevated FSH (18 IU/L) reflects compensatory pituitary upregulation in response to failing follicular recruitment — it is a marker of DOR, not its cause. DOR significantly reduces the ovarian response to stimulation and lowers live birth rates in IVF. At 36 with DOR, delaying treatment is harmful. Early IVF referral is warranted; if ovarian response is very poor, donor egg IVF is the most effective option.

Diminished ovarian reserve markers: AMH <1 ng/mL, AFC <5–7, day-3 FSH >10 IU/L. At age 36, DOR warrants urgent IVF referral — expectant management is inappropriate because further age-related decline will only worsen prognosis.

DOR (AMH <1 ng/mL, AFC <5–7, FSH >10 IU/L) does not equal premature ovarian insufficiency (which requires FSH >25 IU/L on two occasions). However, DOR substantially reduces treatment success. Expectant management in a 36-year-old with DOR wastes irreplaceable time. Gonadotrophins do not restore ovarian reserve — FSH elevation here reflects diminished reserve (fewer follicles producing inhibin B), not pituitary failure.