Reproductive Endocrinology — MCQs

Reproductive Endocrinology Indian Medical PG Practice Questions and MCQs

Question 11: A 30-year-old married female diagnosed with prolactinoma, showing a 5 mm microadenoma on pituitary MRI, is currently taking bromocriptine. Her urine pregnancy test has turned positive. What is the best advice for her?

A. Start cabergoline
B. Advise trans-sphenoidal surgery anticipating increase in tumor size during pregnancy
C. Advise abortion considering the teratogenic potential of bromocriptine
D. Stop bromocriptine (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Stop bromocriptine** The primary goal of treating a microprolactinoma (<10 mm) in a woman desiring pregnancy is to restore ovulation. Once pregnancy is confirmed, the standard management is to **discontinue dopamine agonists (Bromocriptine or Cabergoline)**. The underlying medical concept is that the risk of clinically significant tumor enlargement during pregnancy for a **microadenoma** is very low (<1–2%). While the pituitary gland naturally enlarges during pregnancy due to lactotroph hyperplasia, it rarely causes compressive symptoms in microadenomas. Therefore, the potential (though minimal) fetal exposure to the drug outweighs the risk of tumor growth. **Why other options are incorrect:** * **Option A:** Cabergoline is more effective for shrinking tumors, but it is not started once pregnancy is confirmed. If a patient was already on it, it is still stopped. * **Option B:** Trans-sphenoidal surgery is reserved for patients who fail medical therapy or those with **macroadenomas** showing progressive visual field defects despite medical treatment. It is not indicated for a 5 mm microadenoma. * **Option C:** Bromocriptine is not considered teratogenic. Extensive data shows no increase in congenital malformations or miscarriages in women who took it during the first few weeks of gestation. **High-Yield Clinical Pearls for NEET-PG:** * **Microadenoma (<10 mm):** Risk of growth in pregnancy is **<2%**. Stop drug; no routine MRI or visual field testing needed unless symptomatic (headache/visual loss). * **Macroadenoma (>10 mm):** Risk of growth is higher (**~20–30%**). Management involves either continuing Bromocriptine throughout pregnancy or stopping it with monthly visual field monitoring. * **Drug of Choice:** Bromocriptine is preferred over Cabergoline in women seeking pregnancy due to a longer track record of safety data, though Cabergoline is increasingly used. * **Breastfeeding:** Is **not contraindicated** in patients with prolactinomas.

Question 12: All of the following are diagnoses of PCOS except?

A. Elevated LH
B. Reversed estradiol:estrone ratio
C. Reduced SHBG level
D. Reduced serum insulin level (Correct Answer)

Explanation: **Explanation:** Polycystic Ovary Syndrome (PCOS) is a complex metabolic and endocrine disorder. The hallmark of its metabolic profile is **insulin resistance**, which leads to **compensatory hyperinsulinemia** (elevated serum insulin levels). Therefore, **Option D (Reduced serum insulin level)** is incorrect and the right answer for this "except" question. **Analysis of Options:** * **Elevated LH (Option A):** In PCOS, there is an increased frequency of GnRH pulses, leading to high LH levels and a high LH:FSH ratio (typically >2:1 or 3:1). This stimulates theca cells to produce excess androgens. * **Reversed Estradiol:Estrone Ratio (Option B):** In a normal cycle, Estradiol (E2) is the dominant estrogen. In PCOS, peripheral aromatization of excess androgens in adipose tissue leads to high levels of **Estrone (E1)**. This results in a reversed E2:E1 ratio (E1 > E2). * **Reduced SHBG level (Option C):** Hyperinsulinemia and high androgens suppress the hepatic production of Sex Hormone Binding Globulin (SHBG). Low SHBG increases the fraction of **free (active) testosterone**, worsening hirsutism and acne. **NEET-PG High-Yield Pearls:** * **Rotterdam Criteria (2 of 3):** 1. Hyperandrogenism (clinical/biochemical), 2. Ovulatory dysfunction (Oligo/Anovulation), 3. Polycystic ovaries on ultrasound (≥12 follicles or volume >10cc). * **Gold Standard for Insulin Resistance:** Hyperinsulinemic-euglycemic clamp (though rarely used clinically). * **Key Hormone Change:** Hyperinsulinemia is the primary driver that decreases SHBG and increases ovarian androgen production.

Question 13: Which of the following is NOT a sonographic criterion for diagnosing Polycystic Ovarian Disease (PCOD)?

A. Enlarged ovaries with a volume greater than 10 mL
B. Presence of more than 20 cysts in the ovary (Correct Answer)
C. Cyst size ranging from 2 to 9 mm
D. Cysts identified in either one or both ovaries

Explanation: The diagnosis of Polycystic Ovarian Syndrome (PCOS) is primarily based on the **Revised Rotterdam Criteria (2003)**. To meet the sonographic criteria, only one ovary needs to satisfy the requirements. ### Why Option B is the Correct Answer The original Rotterdam criteria defined PCO morphology as the presence of **12 or more follicles** (measuring 2–9 mm) in either ovary. While newer guidelines (ESHRE 2018) have increased this threshold to **≥20 follicles** when using high-frequency endovaginal transducers (≥8 MHz), the standard textbook definition and the one most commonly tested in NEET-PG still revolve around the classic Rotterdam threshold of **≥12 follicles**. Therefore, "more than 20" is not the standard diagnostic cutoff in traditional criteria. ### Analysis of Other Options * **Option A:** An **ovarian volume >10 mL** (calculated using the formula $0.5 \times \text{length} \times \text{width} \times \text{thickness}$) in either ovary is a core diagnostic criterion. * **Option C:** The follicles must be small, typically **2–9 mm** in diameter, representing arrested follicular development. * **Option D:** The criteria are met if the morphology is present in **either one or both** ovaries. ### NEET-PG High-Yield Pearls * **Rotterdam Criteria (2/3 required):** 1. Oligo/Anovulation, 2. Clinical/Biochemical Hyperandrogenism, 3. Polycystic ovaries on USG. * **"String of Pearls" Appearance:** Classic description where follicles are arranged peripherally around a dense, echogenic stroma. * **Exclusion:** If a dominant follicle (>10 mm) or corpus luteum is present, the scan should be repeated during the next cycle for accuracy. * **LH:FSH Ratio:** Often >2:1 or 3:1 (though no longer a primary diagnostic criterion).

Question 14: Which side effect of clomiphene necessitates its immediate discontinuation?

A. Hot flashes
B. Multiple pregnancy
C. Teratogenic effects
D. Visual symptoms (Correct Answer)

Explanation: **Explanation:** **Clomiphene Citrate (CC)** is a Selective Estrogen Receptor Modulator (SERM) and the first-line drug for ovulation induction in PCOS. **Why Visual Symptoms are the Correct Answer:** Visual symptoms (blurring of vision, scotomas, or flashes) occur in approximately 1.5% of patients. These are thought to be due to the drug’s anti-estrogenic effect on the pituitary gland or direct effects on the retina/optic nerve. Unlike other side effects, visual disturbances are a **mandatory indication for immediate discontinuation** of the drug and a referral to an ophthalmologist, as continued use may lead to permanent visual impairment. **Analysis of Incorrect Options:** * **A. Hot Flashes:** This is the **most common** side effect (approx. 10%) due to the anti-estrogenic effect on the hypothalamus. While uncomfortable, it is transient and does not require stopping the drug. * **B. Multiple Pregnancy:** CC increases the risk of twins (approx. 7–10%) and triplets (0.5%). This is a known risk/complication of therapy, not a reason to abort the current cycle once it has occurred. * **C. Teratogenic Effects:** Clomiphene is cleared from the body before the period of organogenesis begins. Large-scale studies have shown no significant increase in congenital anomalies compared to the general population. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Action:** It blocks estrogen receptors in the hypothalamus, inhibiting negative feedback. This increases GnRH pulse frequency, leading to increased FSH and LH. * **Dose:** Usually started at 50 mg/day for 5 days (Day 2 to Day 6 or Day 3 to Day 7 of the cycle). * **Ovarian Hyperstimulation Syndrome (OHSS):** Rare with Clomiphene compared to Gonadotropins. * **Anti-estrogenic effect:** It may cause thinning of the endometrium and thickening of cervical mucus, which can sometimes lead to a "conception-ovulation gap."

Question 15: Which type of abnormality in sexual development has the best prognosis?

A. Congenital adrenal hyperplasia (Correct Answer)
B. Mixed gonadal dysgenesis
C. Androgen insensitivity syndrome
D. True hermaphroditism

Explanation: **Explanation:** **Congenital Adrenal Hyperplasia (CAH)**, specifically the 21-hydroxylase deficiency variant, has the best prognosis among Disorders of Sexual Development (DSD) because it is a **purely hormonal/enzymatic defect** rather than a structural or chromosomal one. These patients are genetically female (46,XX) with normal internal female reproductive organs (uterus, fallopian tubes, and ovaries). With early diagnosis, glucocorticoid/mineralocorticoid replacement, and corrective surgery for virilized external genitalia, they can achieve **normal puberty, regular menstruation, and successful pregnancy (fertility is preserved).** **Why other options are incorrect:** * **Mixed Gonadal Dysgenesis (45,X/46,XY):** These patients have a high risk of developing gonadoblastoma (up to 25%) and usually require gonadectomy. They have streak gonads and impaired fertility. * **Androgen Insensitivity Syndrome (46,XY):** While these patients have a female phenotype, they lack a uterus and ovaries (due to AMH production) and have undescended testes. They are **permanently infertile** and require gonadectomy due to malignancy risk. * **True Hermaphroditism (Ovotesticular DSD):** This involves the presence of both ovarian and testicular tissue. Management is complex, and achieving normal fertility is rare and highly dependent on the functionality of the existing gonadal tissue. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of ambiguous genitalia** in a newborn: CAH (21-hydroxylase deficiency). * **Gold standard for diagnosis of CAH:** Elevated 17-hydroxyprogesterone (17-OHP) levels. * **Malignancy Risk:** Highest in DSDs containing a Y-chromosome and dysgenetic gonads (e.g., Mixed Gonadal Dysgenesis). * **Fertility:** CAH is the only condition among the options where natural conception and childbirth are routinely possible.

Question 16: Which of the following is an ovarian reserve test?

A. Luteinizing hormone (LH)
B. Follicle-stimulating hormone (FSH) (Correct Answer)
C. Plasma progesterone
D. Endometrial biopsy

Explanation: **Explanation:** Ovarian reserve refers to the quantity and quality of the remaining oocytes in the ovaries. Testing is crucial for assessing fertility potential and predicting response to controlled ovarian stimulation. **Why FSH is the Correct Answer:** Day 3 (early follicular phase) **Follicle-stimulating hormone (FSH)** is a classic biochemical marker of ovarian reserve. As the pool of follicles declines with age, the production of Inhibin B and estradiol decreases. This loss of negative feedback causes the pituitary gland to secrete higher levels of FSH to stimulate the remaining follicles. Therefore, an **elevated basal FSH level (>10–12 mIU/mL)** is indicative of diminished ovarian reserve (DOR). **Analysis of Incorrect Options:** * **A. Luteinizing hormone (LH):** While LH is involved in ovulation and androgen production, it is not a primary marker for oocyte quantity. It is more relevant in diagnosing PCOS (LH:FSH ratio) or detecting the mid-cycle surge. * **C. Plasma progesterone:** This is used to confirm that **ovulation** has occurred (measured on Day 21 of a 28-day cycle). It does not reflect the total remaining egg supply. * **D. Endometrial biopsy:** Historically used to diagnose "Luteal Phase Defect" or endometrial dating, it assesses the response of the uterus to hormones, not the ovarian reserve. **High-Yield Clinical Pearls for NEET-PG:** * **Best Marker:** **Anti-Müllerian Hormone (AMH)** is currently considered the most reliable biochemical marker because it is cycle-independent (can be tested any day). * **Best Imaging Marker:** **Antral Follicle Count (AFC)** via transvaginal ultrasound (TVUS) on Day 2–5. * **Clomiphene Citrate Challenge Test (CCCT):** A provocative test where FSH is measured before and after Clomiphene; an exaggerated FSH rise indicates poor reserve. * **Poor Prognosis:** FSH >20 mIU/mL usually suggests a very poor response to IVF.

Question 17: What is the most common cause of hirsutism?

A. Polycystic ovary disease (Correct Answer)
B. Arrhenoblastoma
C. Cushing syndrome
D. Congenital adrenal hyperplasia

Explanation: **Explanation:** **1. Why Polycystic Ovary Syndrome (PCOS) is Correct:** PCOS is the most common cause of hirsutism, accounting for approximately **70–80% of all cases**. The underlying pathophysiology involves a state of functional ovarian hyperandrogenism. Elevated 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 hair follicles, leading to the transformation of fine vellus hair into coarse terminal hair in androgen-sensitive areas. **2. Analysis of Incorrect Options:** * **Arrhenoblastoma (Sertoli-Leydig Cell Tumor):** While this is a potent source of androgens, it is a rare ovarian tumor. It typically presents with **virilization** (clitoromegaly, voice deepening) and a rapid onset of symptoms, rather than simple hirsutism. * **Cushing Syndrome:** This results from chronic glucocorticoid excess. While it can cause hirsutism due to adrenal androgen co-secretion, it is much less common than PCOS and is usually accompanied by systemic features like moon facies, truncal obesity, and striae. * **Congenital Adrenal Hyperplasia (CAH):** Specifically the Non-Classic (Late-onset) form, CAH is a significant cause of hirsutism but is statistically less frequent than PCOS. It is caused by a partial deficiency of the 21-hydroxylase enzyme. **3. Clinical Pearls for NEET-PG:** * **Ferriman-Gallwey Score:** Used to clinically quantify hirsutism (Score ≥8 is significant in the Indian population). * **Idiopathic Hirsutism:** The second most common cause; characterized by hirsutism with normal menses and normal androgen levels. * **First-line Treatment:** Combined Oral Contraceptive Pills (OCPs) are the mainstay for PCOS-related hirsutism. * **Rapid Onset:** Always suspect an androgen-secreting tumor if hirsutism is sudden in onset and associated with virilization.

Question 18: Time of ovulation is detected by all EXCEPT:

A. Urine LH
B. Urine FSH (Correct Answer)
C. Serum progesterone
D. Basal body temperature

Explanation: **Explanation:** The detection of ovulation is based on identifying the physiological changes triggered by the hypothalamic-pituitary-ovarian axis. **Why Urine FSH is the correct answer:** While Follicle Stimulating Hormone (FSH) does show a small peak just before ovulation (concomitant with the LH surge), it is **not** used clinically to detect or predict the time of ovulation. FSH levels are primarily used to assess ovarian reserve (Day 3 FSH) or to diagnose menopause. Because the FSH surge is less pronounced and less specific than the LH surge, urine FSH kits do not exist for ovulation monitoring. **Why the other options are incorrect:** * **Urine LH:** This is the "gold standard" for home prediction. The **LH surge** occurs 24–36 hours before ovulation. Detecting the surge in urine is highly predictive of the fertile window. * **Serum Progesterone:** A mid-luteal phase (Day 21) serum progesterone level >3 ng/mL is a reliable retrospective indicator that ovulation has occurred. Progesterone rises immediately after the rupture of the follicle and the formation of the corpus luteum. * **Basal Body Temperature (BBT):** Due to the thermogenic effect of progesterone, there is a slight rise in body temperature (0.5–1.0°F) following ovulation. This creates a **biphasic pattern** on a temperature chart. **Clinical Pearls for NEET-PG:** * **Earliest indicator of ovulation:** The LH surge (starts ~32–36 hours before ovulation). * **Most accurate single-day test for ovulation:** Mid-luteal serum progesterone. * **Best ultrasound method:** Serial Transvaginal Sonography (TVS) showing the disappearance of a mature follicle (Folliculometry). * **Cervical Mucus:** Becomes thin, watery, and shows **"Spinnbarkeit"** (high elasticity) and **ferning** under the influence of peak estrogen just before ovulation.

Question 19: Ovulation is presumed to have occurred if the progesterone level is __________ on day 21?

A. 0.3 ng/mL
B. 3 ng/mL (Correct Answer)
C. 30 ng/mL
D. 300 ng/mL

Explanation: **Explanation:** The assessment of serum progesterone levels during the mid-luteal phase (Day 21 of a 28-day cycle) is a gold-standard biochemical marker to confirm that ovulation has occurred. **Why 3 ng/mL is correct:** After ovulation, the collapsed follicle transforms into the **corpus luteum**, which secretes progesterone. A serum progesterone level of **>3 ng/mL** is the widely accepted threshold to provide presumptive evidence of ovulation. While levels >10 ng/mL are often considered optimal for supporting a pregnancy, any value above 3 ng/mL indicates that luteinization has taken place. **Analysis of Incorrect Options:** * **0.3 ng/mL:** This is a typical level found during the **follicular phase** (pre-ovulatory). It indicates that the corpus luteum has not yet formed. * **30 ng/mL:** While possible in a healthy pregnancy or a very robust luteal phase, this is significantly higher than the minimum diagnostic threshold required to simply "presume" ovulation. * **300 ng/mL:** This is a pathologically high or physiological impossibility for a standard Day 21 check; such levels are not seen in normal menstrual cycles. **NEET-PG High-Yield Pearls:** * **Timing:** Progesterone should be measured 7 days before the expected menses. In a 28-day cycle, this is **Day 21**. * **Peak Secretion:** Progesterone levels peak approximately 7–8 days after the LH surge. * **Anovulation:** A level **<3 ng/mL** on Day 21 suggests anovulation, requiring further workup (e.g., PCOS, thyroid dysfunction, or hyperprolactinemia). * **Other signs of ovulation:** Spinnbarkeit (thin, stretchy cervical mucus), Mittelschmerz (mid-cycle pain), and a 0.5°F rise in Basal Body Temperature (BBT).

Question 20: All of the following are true regarding the use of GnRH analogues in the treatment of endometriosis, EXCEPT?

A. Continuous administration leads to downregulation of pituitary gonadotropins.
B. The risk of osteoporosis decreases with prolonged use because estrogen-mediated osteoblastic activity continues. (Correct Answer)
C. Add-back therapy typically includes estrogens.
D. Discontinuation of therapy can result in recurrence.

Explanation: ### Explanation **1. Why Option B is the Correct Answer (The Exception):** GnRH analogues (like Leuprolide or Goserelin) induce a state of **"pseudomenopause"** by creating a hypoestrogenic environment. Estrogen is crucial for bone health as it inhibits osteoclast activity. Prolonged use of GnRH analogues leads to significant **hypoestrogenism**, which increases bone resorption and **increases the risk of osteoporosis**, rather than decreasing it. Bone mineral density (BMD) loss is a major limiting factor, restricting the solo use of these drugs to 6 months. **2. Analysis of Other Options:** * **Option A:** GnRH is naturally secreted in a pulsatile manner. **Continuous (non-pulsatile) administration** leads to the downregulation of GnRH receptors in the pituitary, causing a decrease in LH and FSH (medical oophorectomy). * **Option C:** To mitigate side effects like hot flashes and bone loss, **"Add-back therapy"** is used. This involves giving low doses of estrogen (with or without progestogens) or Tibolone, which is sufficient to protect bones but not enough to stimulate endometrial implants. * **Option D:** GnRH analogues suppress the disease but do not cure it. Upon discontinuation, the pituitary-ovarian axis resumes, estrogen levels rise, and **recurrence of symptoms** is common. **3. NEET-PG High-Yield Pearls:** * **Initial Flare Effect:** In the first 7–10 days of GnRH analogue therapy, there is a transient rise in gonadotropins before downregulation occurs. * **The "Estrogen Threshold Hypothesis":** There is a window of estrogen levels (30–45 pg/mL) that is low enough to prevent endometriosis growth but high enough to prevent bone loss. * **Duration:** Without add-back therapy, use is limited to **6 months**. With add-back therapy, it can be extended to **12 months** or more.

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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