Reproductive Endocrinology — MCQs

Reproductive Endocrinology Indian Medical PG Practice Questions and MCQs

Question 41: In a 40-day menstrual cycle, at which day does ovulation typically occur?

A. 14th day
B. 20th day
C. 26th day (Correct Answer)
D. 30th day

Explanation: **Explanation:** The key to solving this question lies in understanding the phases of the menstrual cycle. A menstrual cycle consists of two main phases: the **Follicular Phase** (pre-ovulatory) and the **Luteal Phase** (post-ovulatory). 1. **The Concept of the Fixed Luteal Phase:** While the follicular phase varies in length among women, the **luteal phase is constant and lasts 14 days** (ranging from 12–16 days). This is because the lifespan of the *corpus luteum* is biologically predetermined. 2. **Calculation:** To determine the day of ovulation, subtract the fixed luteal phase from the total cycle length. * **Formula:** Day of Ovulation = Total Cycle Length – 14 days * **Calculation:** 40 – 14 = **26th Day**. **Analysis of Incorrect Options:** * **Option A (14th day):** This is only correct for a "textbook" 28-day cycle (28 – 14 = 14). It is a common misconception that ovulation always occurs on day 14. * **Option B (20th day):** This would be the ovulation day for a 34-day cycle. * **Option D (30th day):** This would imply a luteal phase of only 10 days, which is generally considered a "Luteal Phase Defect" and is not the physiological norm. **NEET-PG High-Yield Pearls:** * **Variable Phase:** The Follicular phase is the variable part of the cycle; its length determines the overall cycle length. * **Ovulation Marker:** The most reliable indicator that ovulation has occurred is a rise in **Basal Body Temperature (BBT)** due to the thermogenic effect of Progesterone. * **LH Surge:** Ovulation occurs **24–36 hours** after the onset of the LH surge and **10–12 hours** after the LH peak. * **Best Timing for Biopsy:** If performing an endometrial biopsy to check for ovulation, it is traditionally done on Day 21–23 of a 28-day cycle (Mid-luteal phase).

Question 42: What is the effect of GnRH agonists when given along with progestins on uterine fibroids?

A. Decrease in size of fibroid
B. Increase in growth of fibroid (Correct Answer)
C. No change in size of fibroid
D. Decrease size of only vascular fibroids

Explanation: ### Explanation The correct answer is **B. Increase in growth of fibroid.** **1. Underlying Medical Concept** Uterine fibroids (leiomyomas) are estrogen and progesterone-dependent tumors. While GnRH agonists are typically used to shrink fibroids by inducing a hypoestrogenic state (pseudomenopause), the addition of **progestins** counteracts this effect. Progesterone plays a critical role in the pathogenesis of fibroids by increasing the mitotic activity of the leiomyoma cells and upregulating growth factors like EGF (Epidermal Growth Factor). When progestins are administered alongside GnRH agonists (often as "add-back therapy" to reduce vasomotor symptoms), they can stimulate the growth of the fibroid or prevent the expected shrinkage, effectively neutralizing the therapeutic benefit of the GnRH agonist on tumor volume. **2. Analysis of Incorrect Options** * **Option A:** GnRH agonists *alone* decrease the size of fibroids. However, the addition of progestins reverses this effect. * **Option C:** There is a measurable change; the fibroid typically increases in size due to the mitogenic effect of progesterone. * **Option D:** The effect of progestins is mediated through cellular receptors and growth factors, not specifically limited to the vascularity of the tumor. **3. NEET-PG High-Yield Pearls** * **GnRH Agonists:** Used pre-operatively for 3 months to reduce fibroid volume (by ~35-60%) and decrease intraoperative blood loss. * **The "Flare Effect":** Initial administration of GnRH agonists causes a transient rise in FSH/LH before downregulation occurs. * **Progesterone Antagonists:** Drugs like **Mifepristone** and **Ulipristal acetate** (SPRM) are effective in reducing fibroid size because they block the stimulatory effect of progesterone. * **Add-back Therapy:** Usually involves low-dose estrogen or combined HRT to prevent bone loss and hot flashes without significantly affecting fibroid shrinkage, but pure progestins are generally avoided if volume reduction is the primary goal.

Question 43: A 23-year-old woman presents for evaluation of a 7-month history of amenorrhea. Examination discloses bilateral galactorrhea and normal breast and pelvic examinations. Pregnancy test is negative. Which of the following classes of medication is a possible cause of her condition?

A. Antiestrogens
B. Gonadotropins
C. Phenothiazines (Correct Answer)
D. Prostaglandins

Explanation: **Explanation:** The clinical presentation of **secondary amenorrhea** associated with **bilateral galactorrhea** (and a negative pregnancy test) is classic for **Hyperprolactinemia**. **Why Phenothiazines are correct:** Phenothiazines (e.g., Chlorpromazine) are typical antipsychotics that act as **Dopamine (D2) receptor antagonists**. Under normal physiological conditions, dopamine is secreted by the hypothalamus and acts as the primary "prolactin-inhibiting factor." By blocking dopamine receptors in the tuberoinfundibular pathway, phenothiazines remove this inhibition, leading to increased prolactin secretion from the anterior pituitary. Elevated prolactin inhibits the pulsatile release of **GnRH**, leading to decreased FSH/LH and subsequent amenorrhea. **Analysis of Incorrect Options:** * **Antiestrogens (e.g., Clomiphene):** These block estrogen receptors in the hypothalamus, leading to an *increase* in GnRH and gonadotropins. They are used to induce ovulation, not cause galactorrhea. * **Gonadotropins (FSH/LH):** These stimulate the ovaries directly. While they can cause Ovarian Hyperstimulation Syndrome (OHSS), they do not cause hyperprolactinemia or galactorrhea. * **Prostaglandins:** These are primarily used for cervical ripening, induction of labor, or abortion (e.g., Misoprostol). They do not affect the prolactin-dopamine axis. **High-Yield Clinical Pearls for NEET-PG:** * **Drug-induced hyperprolactinemia** is a common cause of galactorrhea. Other culprits include Metoclopramide, Methyldopa, Reserpine, and TCAs. * **Hook Effect:** In cases of very large prolactinomas, lab results may show falsely low prolactin levels; serial dilution is required for diagnosis. * **First-line treatment** for symptomatic hyperprolactinemia (prolactinoma) is medical management with Dopamine agonists (**Cabergoline** > Bromocriptine), not surgery. * **TSH Check:** Always rule out primary hypothyroidism, as elevated **TRH** acts as a prolactin-releasing factor.

Question 44: Primary amenorrhea with anosmia is seen in which of the following conditions?

A. Kallmann syndrome (Correct Answer)
B. Mayer-Rokitansky-Kuster-Hauser syndrome
C. Reifenstein syndrome
D. Turner syndrome

Explanation: **Explanation:** **Kallmann Syndrome** is the correct answer. It is a form of **hypogonadotropic hypogonadism** caused by the failure of GnRH-secreting neurons to migrate from the olfactory placode to the hypothalamus. This migration defect is often associated with the hypoplasia or aplasia of the olfactory bulbs, leading to the pathognomonic clinical dyad of **primary amenorrhea** (due to low FSH/LH) and **anosmia** (loss of smell). It is most commonly inherited as an X-linked recessive trait (KAL1 gene mutation). **Analysis of Incorrect Options:** * **Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome:** Characterized by Müllerian agenesis (absent uterus and upper 2/3 of the vagina). Patients have a female karyotype (46,XX), normal ovaries, and normal secondary sexual characteristics, but **no anosmia**. * **Reifenstein syndrome:** This is a form of Partial Androgen Insensitivity Syndrome (46,XY). It presents with ambiguous genitalia, gynecomastia, and infertility, but is not a classic cause of primary amenorrhea with anosmia. * **Turner syndrome (45,XO):** The most common cause of primary amenorrhea. It is a form of **hypergonadotropic hypogonadism** (streak ovaries, high FSH). While it features short stature and webbed neck, it does **not** involve anosmia. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** Low FSH, Low LH, and Low Estrogen (Hypo-Hypo). * **MRI Finding:** Absent or hypoplastic olfactory bulbs. * **Management:** Pulsatile GnRH therapy is used to induce ovulation/fertility; hormone replacement therapy (HRT) is used for secondary sexual characteristics. * **Key Distinction:** Unlike Turner syndrome, patients with Kallmann syndrome usually have **normal stature** (or are slightly tall due to delayed epiphyseal closure).

Question 45: Inhibin B levels as a test of ovarian reserve are best measured on which day of menstruation?

A. Day 2
B. Day 3 (Correct Answer)
C. Day 4
D. Day 5

Explanation: **Explanation:** **Inhibin B** is a glycoprotein hormone produced by the **granulosa cells** of early antral follicles. It functions primarily to provide negative feedback on the pituitary gland to suppress the secretion of Follicle Stimulating Hormone (FSH). **Why Day 3 is the Correct Answer:** In the early follicular phase, Inhibin B levels reflect the size and quality of the "resting" follicle pool. Its levels peak during the early follicular phase (Days 1–3) as the cohort of follicles begins to grow. **Day 3** is the standardized clinical window for measuring ovarian reserve markers (including FSH and Estradiol) because it represents the "baseline" of the menstrual cycle. A decline in Day 3 Inhibin B levels is one of the earliest biochemical markers of a diminishing ovarian reserve, often occurring before a significant rise in FSH is detected. **Analysis of Incorrect Options:** * **Day 2:** While levels are rising, Day 3 is the globally accepted clinical standard for baseline endocrine testing to ensure consistency in results. * **Day 4 & 5:** By this stage, the selection of the dominant follicle may have already begun. Measuring later in the follicular phase may result in higher Inhibin B levels that reflect the growth of specific follicles rather than the total "reserve" or resting pool. **High-Yield Clinical Pearls for NEET-PG:** * **Inhibin A vs. B:** Remember **"B for Before"** (Early follicular phase/Ovarian reserve) and **"A for After"** (Luteal phase/Dominant follicle). * **Best Marker:** While Inhibin B is a marker of reserve, **AMH (Anti-Müllerian Hormone)** is currently considered the most reliable and sensitive biochemical marker because it remains stable throughout the cycle. * **Inhibin B in Men:** It is produced by **Sertoli cells** and serves as a marker of spermatogenesis.

Question 46: In Swyer syndrome, what is typically found?

A. Testes are present (Correct Answer)
B. Ovaries are present
C. Short stature
D. Decreased FSH and LH

Explanation: **Explanation:** **Swyer Syndrome (Pure Gonadal Dysgenesis)** is a condition characterized by a **46,XY karyotype** in individuals who present with a female phenotype. 1. **Why the correct answer is right (Option A):** In Swyer syndrome, there is a mutation in the **SRY gene** (or other genes like SOX9). Because the SRY gene is non-functional, the primitive gonads fail to differentiate into functional testes. Instead, they persist as **undifferentiated "streak gonads."** Histologically, these are fibrous tissue remnants of the gonadal stroma. In the context of NEET-PG questions, "testes are present" refers to the fact that the individual possesses the XY genotype and gonadal tissue that failed to become ovaries, though they are non-functional streaks. These streak gonads carry a high risk (approx. 30%) of developing **gonadoblastoma**, necessitating prophylactic gonadectomy. 2. **Why the incorrect options are wrong:** * **Option B:** Ovaries require two functional X chromosomes (46,XX). In Swyer syndrome, the lack of germ cells leads to streak gonads, not functional ovaries. * **Option C:** Short stature is a hallmark of **Turner Syndrome (45,XO)** due to SHOX gene haploinsufficiency. Patients with Swyer syndrome typically have **normal or tall stature** because they lack the SHOX deletion. * **Option D:** Because there is no functional gonadal tissue to produce estrogen or inhibin, there is no negative feedback on the pituitary. This results in **Hypergonadotropic Hypogonadism** (Elevated FSH and LH). **High-Yield Clinical Pearls for NEET-PG:** * **Phenotype:** Female external genitalia, well-developed Müllerian structures (Uterus/Fallopian tubes present) because no Anti-Müllerian Hormone (AMH) was produced. * **Presentation:** Primary amenorrhea with delayed puberty (lack of secondary sexual characteristics). * **Key Distinction:** Unlike AIS (Androgen Insensitivity Syndrome), Swyer syndrome patients **have a uterus** and **pubic/axillary hair** (though sparse due to low adrenal androgens). * **Management:** Hormone Replacement Therapy (HRT) for puberty induction and bone health; early gonadectomy.

Question 47: A girl presents with primary amenorrhea, normal breast development, hirsutism, and acne. What is the most probable diagnosis?

A. Klinefelter syndrome
B. Polycystic Ovarian Disease (PCOD) (Correct Answer)
C. Turner's syndrome
D. Gonadal dysgenesis

Explanation: ### Explanation The correct answer is **Polycystic Ovarian Disease (PCOD)**. **1. Why PCOD is the correct diagnosis:** The clinical triad of **primary amenorrhea**, **normal breast development**, and **signs of hyperandrogenism** (hirsutism and acne) strongly points toward PCOD. * **Normal breast development** indicates a functional Hypothalamic-Pituitary-Ovarian (HPO) axis with sufficient estrogen production (Tanner Stage 2+). * **Hyperandrogenism** (hirsutism/acne) is a hallmark of PCOD, caused by elevated LH levels and insulin resistance leading to excess ovarian androgen production. * While PCOD typically presents as secondary amenorrhea, it is a recognized cause of primary amenorrhea in adolescents who have undergone normal thelarche (breast development) but fail to achieve menarche due to chronic anovulation. **2. Why the other options are incorrect:** * **Klinefelter Syndrome (47, XXY):** This affects phenotypic males. They present with small testes, gynecomastia, and infertility, not primary amenorrhea in a female phenotype. * **Turner’s Syndrome (45, XO):** Characterized by "streak gonads" and estrogen deficiency. Patients typically present with **absent breast development** (sexual infantilism), short stature, and webbed neck. * **Gonadal Dysgenesis:** Similar to Turner’s, the lack of functional ovarian tissue leads to low estrogen, resulting in **absent secondary sexual characteristics** (no breast development). **3. NEET-PG High-Yield Pearls:** * **Most common cause of primary amenorrhea with breast development:** Müllerian Agenesis (MRKH Syndrome), but it lacks hirsutism/acne. * **Rotterdam Criteria for PCOS:** Requires 2 out of 3: (1) Hyperandrogenism, (2) Oligo/anovulation, (3) Polycystic ovaries on USG. * **LH:FSH Ratio:** Classically > 2:1 or 3:1 in PCOD. * **First-line treatment for hirsutism in PCOD:** Combined Oral Contraceptive Pills (COCPs).

Question 48: A 20-year-old girl presents with a history of rapidly developing hirsutism and amenorrhea. Which of the following blood tests would be most appropriate to establish the diagnosis?

A. 17-hydroxyprogesterone
B. Dehydroepiandrosterone (DHEA)
C. Testosterone (Correct Answer)
D. Luteinizing hormone (LH): Follicle-stimulating hormone (FSH) ratio

Explanation: **Explanation:** The clinical presentation of **rapidly developing hirsutism** (virilization) and amenorrhea in a young woman is a "red flag" that strongly suggests an **androgen-secreting tumor** (ovarian or adrenal), rather than a functional disorder like PCOS. 1. **Why Testosterone is correct:** Serum **Total Testosterone** is the most appropriate initial test to screen for ovarian tumors (like Sertoli-Leydig cell tumors). A testosterone level **>200 ng/dL** is highly suggestive of a malignancy. In cases of rapid onset virilization, testosterone is the most potent androgen responsible for the clinical symptoms and is the primary marker for ovarian sources of androgen excess. 2. **Why other options are incorrect:** * **17-hydroxyprogesterone:** This is the screening test for **Congenital Adrenal Hyperplasia (CAH)**, specifically the 21-hydroxylase deficiency. While CAH causes hirsutism, it is usually present from childhood/puberty and is rarely "rapidly progressive." * **DHEA/DHEAS:** DHEAS is a marker for **adrenal tumors**. While it should be measured alongside testosterone, testosterone is generally considered the first-line marker for overall androgen excess in this clinical context. (Note: DHEAS >7000 µg/dL suggests an adrenal tumor). * **LH:FSH ratio:** An elevated ratio (>2:1 or 3:1) is characteristic of **PCOS**. However, PCOS typically presents with a slow, chronic progression of symptoms since puberty, not a rapid onset of virilization. **High-Yield Clinical Pearls for NEET-PG:** * **Slow onset hirsutism:** Think PCOS or Idiopathic. * **Rapid onset + Virilization:** Think Androgen-secreting tumors. * **Source Localization:** If Testosterone is markedly elevated but DHEAS is normal, the source is likely **Ovarian**. If DHEAS is markedly elevated, the source is **Adrenal**. * **Ferriman-Gallwey Score:** Used to clinically quantify hirsutism (Score ≥8 is significant).

Question 49: All are true about hormonal levels in Polycystic Ovarian Disease except?

A. Increased androstenedione
B. Reduced FSH/LH ratio
C. Increased oestrone
D. Decreased testosterone level (Correct Answer)

Explanation: **Explanation:** Polycystic Ovarian Syndrome (PCOS) is characterized by a state of **hyperandrogenism** and chronic anovulation. The correct answer is **D (Decreased testosterone level)** because, in PCOS, testosterone levels are typically **elevated** or at the high end of the normal range, rather than decreased. **Why the other options are incorrect (True for PCOS):** * **A. Increased androstenedione:** The ovaries and adrenal glands produce excess androgens. Androstenedione is a key precursor that is elevated, contributing to hirsutism and acne. * **B. Reduced FSH/LH ratio:** In PCOS, there is an increased frequency of GnRH pulses, leading to **increased LH** and relatively **low/normal FSH**. This results in a classic **LH:FSH ratio of >2:1 or 3:1**. Since the denominator (FSH) is lower than the numerator (LH), the FSH/LH ratio is mathematically reduced. * **C. Increased oestrone (E1):** Due to peripheral aromatization of excess androstenedione in adipose tissue, levels of oestrone (E1) are elevated. This leads to a state of "unopposed estrogen," increasing the risk of endometrial hyperplasia. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard for Diagnosis:** Rotterdam Criteria (requires 2 out of 3: Hyperandrogenism, Ovulatory dysfunction, Polycystic ovaries on USG). * **SHBG Levels:** Sex Hormone Binding Globulin is **decreased** in PCOS (often due to hyperinsulinemia), which further increases the "Free Testosterone Index." * **Insulin Resistance:** Hyperinsulinemia stimulates the ovarian theca cells to produce more androgens and inhibits hepatic SHBG production. * **USG Hallmark:** "String of pearls" appearance (12 or more follicles measuring 2–9 mm).

Question 50: Which of the following is an ovarian cause of hirsutism?

A. Polycystic Ovarian Disease (PCOD) (Correct Answer)
B. Ovarian carcinoma
C. Dysgerminoma
D. Endometriotic cyst

Explanation: **Explanation:** **Polycystic Ovarian Disease (PCOD/PCOS)** is the most common cause of hirsutism in women. The underlying pathophysiology involves an increase in the pulse frequency of Gonadotropin-Releasing Hormone (GnRH), leading to an elevated **LH:FSH ratio**. High levels of Luteinizing Hormone (LH) stimulate the ovarian **theca cells** to produce excess androgens (androstenedione and testosterone). These androgens are converted to dihydrotestosterone (DHT) in the skin, which stimulates terminal hair growth in male-pattern areas. **Analysis of Incorrect Options:** * **Ovarian Carcinoma:** Most ovarian cancers (like epithelial tumors) are non-functional and do not produce hormones. While specific "Sertoli-Leydig cell tumors" can cause virilization, they are rare compared to PCOD. * **Dysgerminoma:** This is a germ cell tumor that typically produces **LDH** or occasionally hCG. It does not produce androgens and therefore does not cause hirsutism. * **Endometriotic Cyst:** Also known as a "chocolate cyst," this is a benign condition where endometrial tissue grows on the ovary. It is associated with pelvic pain and infertility, not androgen excess. **High-Yield Clinical Pearls for NEET-PG:** * **Ferriman-Gallwey Score:** Used to clinically quantify hirsutism (Score ≥8 is significant). * **Hyperthecosis:** A more severe form of PCOD characterized by nests of luteinized theca cells, often leading to frank virilization. * **HAIR-AN Syndrome:** A subset of PCOS characterized by **H**irsutism, **A**canthosis nigricans, **I**nsulin **R**esistance, and **A**ndrogen excess. * **First-line Treatment:** Combined Oral Contraceptive Pills (OCPs) are the first-line medical management for hirsutism in PCOS.

Practice by Chapter

Hypothalamic-Pituitary-Ovarian Axis

Practice Questions

Disorders of Puberty

Practice Questions

Hirsutism and Virilization

Practice Questions

Primary Ovarian Insufficiency

Practice Questions

Hyperprolactinemia

Practice Questions

Hyperandrogenism

Practice Questions

Metabolic Dysfunction in PCOS

Practice Questions

Neuroendocrine Disorders and Reproduction

Practice Questions

Hormonal Evaluation and Testing

Practice Questions

Ovulation Induction

Practice Questions

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