Reproductive Endocrinology Practice Questions

Q: Time taken for capacitation of sperms is?

6-8 hours. **Explanation:** **Capacitation** is the final stage of sperm maturation that occurs within the female reproductive tract (primarily in the uterus and fallopian tubes). It involves the removal of the protective glycoprotein coat and seminal plasma proteins from the plasma membrane overlying the acrosome. This process is essential because it increases sperm motility (hyperactivation) and allows the sperm to undergo the acrosome reaction upon reaching the oocyte. 1. **Why 6-8 hours is correct:** Standard medical textbooks (including Williams Obstetrics and Dutta’s Textbook of Gynecology) state that the physiological process of capacitation takes approximately **7 hours** on average. Therefore, the range of **6-8 hours** is the most accurate representation of the time required for these biochemical changes to complete. 2. **Why other options are incorrect:** * **2-4 and 4-6 hours:** These durations are too short for the complete removal of the decapacitation factors and the necessary influx of calcium ions required for hyperactivation. * **8-10 hours:** While sperm can survive in the female tract for up to 48–72 hours, the specific process of becoming "capacitated" is usually completed well before 10 hours. **High-Yield Clinical Pearls for NEET-PG:** * **Site of Capacitation:** Female reproductive tract (Uterus and Fallopian tube). * **Key Change:** Increase in membrane permeability to **Calcium (Ca²⁺)**, leading to increased cAMP levels and hypermotility. * **In-Vitro Fertilization (IVF):** In IVF, capacitation is artificially induced by washing the sperm in special media to remove inhibitory seminal proteins. * **Sequence of Events:** Capacitation → Acrosome Reaction → Fusion with Oocyte (Zona Pellucida).

Q: The luteinizing hormone (LH) surge typically occurs at what point in relation to ovulation?

24-36 hours before ovulation. **Explanation:** The menstrual cycle is governed by a complex feedback loop between the ovaries and the pituitary gland. The **LH surge** is the critical hormonal trigger for ovulation. **Why Option C is correct:** Ovulation is triggered by a rapid rise in Luteinizing Hormone (LH). This surge is initiated by a sustained rise in estradiol (reaching >200 pg/mL for approximately 48 hours). * **LH Surge onset:** Occurs **32–36 hours** before ovulation. * **LH Peak:** Occurs **10–12 hours** before ovulation. Therefore, the window of **24–36 hours** accurately represents the interval between the initiation of the surge and the release of the oocyte. **Why other options are incorrect:** * **Option A:** While LH is high during ovulation, the *surge* must precede the event to induce follicular rupture and the resumption of meiosis I. * **Option B:** 5–6 days before ovulation corresponds to the mid-follicular phase, where estrogen is rising but has not yet triggered the positive feedback mechanism required for the LH surge. * **Option D:** After ovulation, LH levels drop significantly as the follicle transforms into the corpus luteum, which primarily secretes progesterone. **High-Yield NEET-PG Pearls:** * **Meiosis:** The LH surge triggers the completion of **Meiosis I** (arrested in prophase) and the start of **Meiosis II** (arrested in metaphase). * **Urine LH Kits:** These detect the LH surge and are used to predict the "fertile window," typically indicating ovulation will occur within the next 24 hours. * **Prostaglandins & Proteolytic Enzymes:** LH induces these substances to physically rupture the follicular wall (stigma). * **Mittelschmerz:** This refers to the mid-cycle pelvic pain associated with ovulation.

Q: What is the germinal cell layer surrounding the oocyte before ovulation called?

Cumulous oophorus. **Explanation:** The correct answer is **Cumulus oophorus**. In the developing ovarian follicle (Graafian follicle), the oocyte is surrounded by a specialized cluster of granulosa cells. As the antrum (fluid-filled cavity) enlarges, the oocyte is pushed to one side and remains connected to the peripheral granulosa cells by a mound or "pedicle" of cells known as the **cumulus oophorus**. The innermost layer of these cells, which are in direct contact with the zona pellucida, is termed the *corona radiata*. **Analysis of Incorrect Options:** * **A. Zona pellucida:** This is a thick, transparent, acellular glycoprotein membrane secreted by the oocyte itself. While it surrounds the oocyte, it is not a "germinal cell layer." * **B. Zona reticularis:** This is the innermost layer of the **adrenal cortex**, responsible for producing androgens (e.g., DHEA). It is unrelated to ovarian folliculogenesis. * **D. Zona glomerulosa:** This is the outermost layer of the **adrenal cortex**, responsible for the synthesis of mineralocorticoids (aldosterone). **NEET-PG High-Yield Pearls:** * **Stigma:** The small area on the ovarian surface that thins out and ruptures during ovulation to release the oocyte. * **Meiotic Status:** At the time of ovulation, the oocyte is arrested in **Metaphase of Meiosis II**. It only completes meiosis II if fertilization occurs. * **Call-Exner Bodies:** Small fluid-filled spaces between granulosa cells, characteristic of Granulosa Cell Tumors (and seen in normal developing follicles). * **Theca Interna:** The vascularized layer of the follicle that produces androstenedione under the influence of LH.

Q: Which of the following is true regarding Savage syndrome?

Receptor defect to gonadotrophic hormones. **Savage Syndrome**, also known as **Resistant Ovary Syndrome**, is a rare cause of hypergonadotropic hypogonadism. ### **Explanation of the Correct Answer** The fundamental defect in Savage syndrome is a **resistance of the ovarian follicles to gonadotropins (FSH and LH)**. This is typically due to a **receptor defect** or a post-receptor signaling abnormality. Because the ovaries do not respond to FSH, there is no follicular development or estrogen production. The lack of negative feedback leads to a compensatory **elevation of FSH and LH** levels. ### **Analysis of Incorrect Options** * **B. Short stature:** This is a classic feature of **Turner Syndrome (45,XO)**, not Savage syndrome. Patients with Savage syndrome usually have a normal 46,XX karyotype and normal stature. * **C. Ovaries do not contain follicles:** This is the key histological differentiator. In Savage syndrome, the ovaries **do contain numerous primordial follicles**, but they fail to mature. In contrast, "Pure Gonadal Dysgenesis" or Turner syndrome is characterized by "streak ovaries" devoid of follicles. * **D. FSH is normal:** In this condition, FSH is **markedly elevated** (Hypergonadotropic) because the pituitary is trying to overcome the ovarian resistance. ### **High-Yield Clinical Pearls for NEET-PG** * **Karyotype:** Usually 46,XX (Normal female). * **Clinical Presentation:** Primary or secondary amenorrhea with normal secondary sexual characteristics. * **Diagnosis:** Requires an **ovarian biopsy** to demonstrate the presence of primordial follicles (distinguishes it from Premature Ovarian Failure/Menopause). * **Management:** Hormone Replacement Therapy (HRT) for bone health; pregnancy usually requires oocyte donation, though spontaneous remissions are rarely reported.

Q: All are true about the pathogenesis of Ovarian Hyperstimulation Syndrome, EXCEPT?

Increase in intravascular volume. **Explanation:** Ovarian Hyperstimulation Syndrome (OHSS) is a serious iatrogenic complication of ovulation induction. The hallmark of its pathogenesis is **increased capillary permeability**, not an increase in intravascular volume. **1. Why Option B is the Correct Answer (The False Statement):** In OHSS, there is a massive shift of fluid from the intravascular space into the extravascular space (third-spacing) due to leaky capillaries. This leads to **intravascular volume depletion (hypovolemia)**, hemoconcentration, and decreased organ perfusion. This can result in complications like acute kidney injury and thromboembolism. **2. Analysis of Other Options:** * **Option A:** OHSS is characterized by massive **ovarian enlargement** due to multiple follicular cysts. These ovaries become extremely **fragile** and are at high risk for torsion or rupture. * **Option C:** The primary mediator is **Vascular Endothelial Growth Factor (VEGF)**, along with cytokines like IL-6 and IL-8. These are released in response to hCG (human Chorionic Gonadotropin) and cause the characteristic increase in vascular permeability. * **Option D:** OHSS is almost exclusively **secondary to infertility treatments**, specifically following the administration of hCG (the "trigger" shot) during IVF or ovulation induction. **High-Yield Clinical Pearls for NEET-PG:** * **Trigger:** hCG is the most common trigger; OHSS rarely occurs without it. * **Clinical Features:** Ascites, pleural effusion, electrolyte imbalance, and hypercoagulability. * **Classification:** Based on Golan’s criteria (Mild, Moderate, Severe, Critical). * **Management:** Fluid resuscitation (crystalloids/albumin), thromboprophylaxis, and paracentesis if needed. Diuretics should generally be avoided as they worsen intravascular depletion.

Q: Preimplantation genetic diagnosis is used for which of the following?

Single gene mutation analysis. **Explanation:** **Preimplantation Genetic Testing (PGT)** is a technique used to identify genetic defects in embryos created through In-Vitro Fertilization (IVF) before pregnancy is established. **Why Option B is correct:** The primary clinical indication for PGT-M (formerly known as PGD) is the detection of **Single Gene Mutations** (monogenic disorders). It is used for couples who are known carriers of specific inherited conditions such as Cystic Fibrosis, Thalassemia, Sickle Cell Anemia, or Huntington’s disease. By testing a biopsy from the trophectoderm (blastocyst stage), clinicians can select and transfer only those embryos that are unaffected by the specific mutation. **Analysis of Incorrect Options:** * **A. Fetal gender determination:** While technically possible, using PGT solely for social sex selection is ethically controversial and legally prohibited in many regions (including India under the PCPNDT Act). * **C. HLA typing:** While PGT can be used for HLA matching (to create a "savior sibling"), it is a specialized application and not the primary diagnostic use of the technology compared to mutation analysis. * **D. Karyotyping:** Traditional karyotyping requires a large number of dividing cells (metaphase). For embryos, we use **PGT-A** (Aneuploidy screening) via NGS (Next-Generation Sequencing) or FISH, rather than standard karyotyping, to detect chromosomal imbalances. **High-Yield Clinical Pearls for NEET-PG:** * **Timing of Biopsy:** Usually performed at the **Blastocyst stage (Day 5)** by sampling the trophectoderm (5-10 cells), which is safer for the embryo than the cleavage stage (Day 3) biopsy. * **PGT-A:** Screens for aneuploidy (e.g., Down Syndrome); recommended for advanced maternal age. * **PGT-SR:** Screens for structural rearrangements (e.g., balanced translocations). * **Legal Note:** In India, PGT is governed by the ART (Regulation) Act, 2021.

Q: What is the sequence of development of pubertal changes in girls?

Thelarche, Pubarche, linear growth spurt, Menarche. ### Explanation The sequence of pubertal changes in girls follows a predictable chronological order driven by the activation of the Hypothalamic-Pituitary-Gonadal (HPG) axis. **1. Why Option A is Correct:** The physiological sequence is governed by increasing levels of estrogen and adrenal androgens. * **Thelarche (Breast development):** Usually the first sign of puberty (around age 8–10), triggered by rising estrogen. * **Pubarche/Adrenarche (Pubic/Axillary hair):** Follows shortly after, due to increasing adrenal androgens. * **Linear Growth Spurt:** Occurs mid-puberty. Peak height velocity in girls typically happens *before* the onset of menstruation. * **Menarche (First menstruation):** The final milestone, occurring approximately 2–2.5 years after thelarche (average age 12.5 years). **2. Why Other Options are Incorrect:** * **Options B & C:** These suggest Pubarche precedes Thelarche. While this can occur in some individuals, the standard physiological sequence taught for exams identifies Thelarche as the first event. * **Option D:** This suggests Menarche is the first event. Menarche is a late-stage pubertal event; if it occurs before breast development, it is considered pathological (e.g., precocious puberty or vaginal bleeding). **3. High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic:** **T**all **P**eople **G**et **M**oney (**T**helarche → **P**ubarche → **G**rowth Spurt → **M**enarche). * **Precocious Puberty:** Development of secondary sexual characteristics before age 8. * **Delayed Puberty:** Absence of thelarche by age 13 or absence of menarche by age 15. * **Growth:** Once menarche occurs, epiphyseal closure begins due to high estrogen levels, and girls usually grow only 2–5 cm further. * **Marshall and Tanner Staging:** Used to clinically grade the progression of thelarche and pubarche (Stages 1–5).

Q: What is the most common cause of hirsutism in a teenage girl?

Ovarian disease. **Explanation:** The most common cause of hirsutism in women, including teenage girls, is **Polycystic Ovary Syndrome (PCOS)**, which falls under the category of **Ovarian disease**. PCOS accounts for approximately 70-80% of all cases of clinical androgen excess. The underlying pathophysiology involves an increase in LH pulse frequency, leading to ovarian theca cell hyperplasia and excessive production of androgens (primarily testosterone). **Analysis of Options:** * **A. Ovarian disease (Correct):** As mentioned, PCOS is the leading cause. Other ovarian causes include rare androgen-secreting tumors (e.g., Sertoli-Leydig cell tumors), but PCOS remains the statistical majority. * **B. Pheochromocytoma:** This is a catecholamine-secreting tumor of the adrenal medulla. It presents with the "classic triad" of episodic headaches, sweating, and tachycardia, but it does not cause hirsutism. * **C. Obesity:** While obesity is frequently associated with PCOS and can worsen hirsutism by decreasing Sex Hormone Binding Globulin (SHBG) levels (increasing free testosterone), it is a contributing factor rather than the primary etiology. * **D. Adrenogenital syndrome:** Also known as Congenital Adrenal Hyperplasia (CAH). While Non-Classic CAH (late-onset) is a significant cause of hirsutism, it is much less common than PCOS. **High-Yield Clinical Pearls for NEET-PG:** * **Ferriman-Gallwey Score:** Used to quantify hirsutism; a score of ≥8 is generally considered significant in the Indian population. * **First-line Investigation:** Total and Free Testosterone levels. If rapid onset or >200 ng/dL, suspect an androgen-secreting tumor. * **DHEAS:** A specific marker for adrenal causes of hirsutism. * **Treatment of Choice:** Combined Oral Contraceptive Pills (OCPs) are the first-line pharmacological treatment for PCOS-related hirsutism.

Q: A patient presents with obesity and hirsutism. Laboratory investigations reveal high levels of LH and androgens. What is the likely diagnosis?

Polycystic Ovary Syndrome (PCOS). **Explanation:** The clinical presentation of **obesity and hirsutism**, combined with elevated **LH and androgens**, is the classic biochemical and clinical hallmark of **Polycystic Ovary Syndrome (PCOS)**. **Why Option A is correct:** In PCOS, there is a characteristic derangement of the Hypothalamic-Pituitary-Ovarian (HPO) axis. Increased GnRH pulse frequency leads to **preferential secretion of LH** over FSH. High LH levels stimulate the **theca cells** of the ovary to produce excess androgens (androstenedione and testosterone), resulting in hirsutism and acne. Obesity further exacerbates the condition through insulin resistance, which decreases Sex Hormone Binding Globulin (SHBG), increasing the bioavailability of free androgens. **Why the other options are incorrect:** * **Exogenous steroid ingestion:** While this can cause hirsutism, it typically results in the suppression of endogenous gonadotropins (Low LH/FSH) due to negative feedback. * **Turner Syndrome (45, XO):** This presents with primary amenorrhea, short stature, and streak ovaries. Laboratory findings show **Hypergonadotropic Hypogonadism** (High FSH/LH but very low estrogen/androgens). * **Klinefelter Syndrome (47, XXY):** This affects males, presenting with small testes, gynecomastia, and infertility. While LH is high, testosterone is typically low. **High-Yield Clinical Pearls for NEET-PG:** * **Rotterdam Criteria:** Diagnosis requires 2 out of 3: (1) Hyperandrogenism (clinical/biochemical), (2) Oligo/anovulation, (3) Polycystic ovaries on USG. * **LH:FSH Ratio:** Classically >2:1 or 3:1 (though no longer a mandatory diagnostic criterion). * **Gold Standard Treatment:** Lifestyle modification (weight loss). For hirsutism, OCPs are first-line; for infertility, **Letrozole** is now the drug of choice.

Question 1

Time taken for capacitation of sperms is?

Accepted Answer

6-8 hours

Answer

2-4 hours

Answer

4-6 hours

Answer

8-10 hours

Question 2

The luteinizing hormone (LH) surge typically occurs at what point in relation to ovulation?

Accepted Answer

24-36 hours before ovulation

Answer

At the time of ovulation

Answer

5-6 days before ovulation

Answer

24-72 hours after ovulation

Question 3

All of the following are true regarding precocious puberty, except:

Accepted Answer

Development of secondary sexual characteristics before the age of 6 years

Answer

Development of secondary sexual characteristics before the age of 8 years

Answer

Menstruation before the age of 10 years

Answer

The most common cause is constitutional

Question 4

What is the germinal cell layer surrounding the oocyte before ovulation called?

Accepted Answer

Cumulous oophorus

Answer

Zona pellucida

Answer

Zona reticularis

Answer

Zona glomerulosa

Question 5

Which of the following is true regarding Savage syndrome?

Accepted Answer

Receptor defect to gonadotrophic hormones

Answer

Short stature

Answer

Ovaries do not contain follicles

Answer

FSH is normal

Question 6

All are true about the pathogenesis of Ovarian Hyperstimulation Syndrome, EXCEPT?

Accepted Answer

Increase in intravascular volume

Answer

Due to ovarian enlargement and fragility

Answer

Role of VEGF and inflammatory cytokines

Answer

Secondary to infertility treatment

Question 7

Preimplantation genetic diagnosis is used for which of the following?

Accepted Answer

Single gene mutation analysis

Answer

Fetal gender determination

Answer

HLA typing

Answer

Karyotyping

Question 8

What is the sequence of development of pubertal changes in girls?

Accepted Answer

Thelarche, Pubarche, linear growth spurt, Menarche

Answer

Pubarche, Thelarche, Menarche, linear growth spurt

Answer

Pubarche, Menarche, Thelarche, linear growth spurt

Answer

Menarche, Thelarche, Pubarche, linear growth spurt

Question 9

What is the most common cause of hirsutism in a teenage girl?

Accepted Answer

Ovarian disease

Answer

Pheochromocytoma

Answer

Obesity

Answer

Adrenogenital syndrome

Question 10

A patient presents with obesity and hirsutism. Laboratory investigations reveal high levels of LH and androgens. What is the likely diagnosis?

Accepted Answer

Polycystic Ovary Syndrome (PCOS)

Answer

Exogenous steroid ingestion

Answer

Turner syndrome

Answer

Klinefelter syndrome

Reproductive Endocrinology — MCQs

Reproductive Endocrinology — MCQs

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