Reproductive Endocrinology — MCQs

Reproductive Endocrinology Indian Medical PG Practice Questions and MCQs

Question 91: Moebius syndrome in a fetus occurs due to maternal intake of which of the following teratogens?

A. Mifepristone
B. Misoprostol (Correct Answer)
C. Diethylstilbestrol (DES)
D. Methotrexate

Explanation: **Explanation:** **Misoprostol** is a synthetic prostaglandin E1 (PGE1) analogue frequently used for medical abortion and labor induction. When used unsuccessfully for first-trimester abortion, it is associated with a specific pattern of malformations known as **Moebius Syndrome**. **Pathophysiology:** The underlying mechanism is **Vascular Disruption**. Misoprostol causes intense uterine contractions, leading to transient uterine ischemia and fetal hypoxia. This disrupts the development of the cranial nerve nuclei (specifically CN VI and VII) and limb buds. Moebius syndrome is clinically characterized by congenital facial paralysis and impaired ocular abduction, often accompanied by limb defects (like clubfoot). **Analysis of Incorrect Options:** * **Mifepristone (A):** An anti-progestogen used in medical abortion. While it is the first step in the regimen, it is not specifically linked to Moebius syndrome. * **Diethylstilbestrol (DES) (C):** A synthetic estrogen formerly used to prevent miscarriages. It is classically associated with **Clear Cell Adenocarcinoma of the vagina** and T-shaped uterine anomalies in the female offspring (DES daughters). * **Methotrexate (D):** A folate antagonist. Exposure in the first trimester leads to **Fetal Methotrexate Syndrome**, characterized by craniosynostosis, wide-set eyes (hypertelorism), and limb abnormalities, but not the specific cranial nerve palsies of Moebius syndrome. **High-Yield Clinical Pearls for NEET-PG:** * **Misoprostol triad:** Moebius syndrome, Terminal transverse limb defects, and Equinovarus (clubfoot). * **Safe use:** Misoprostol is safe for labor induction at term in appropriate doses; the teratogenic risk is specific to failed early pregnancy termination. * **Other Vascular Disruption defects:** Gastroschisis and intestinal atresia are also linked to early pregnancy vascular insults (e.g., cocaine or nicotine).

Question 92: A woman treated for infertility presents with 6 weeks of amenorrhea and urinary retention. What is the most likely etiology?

A. Retroverted uterus
B. Pelvic hematocele
C. Impacted cervical fibroid (Correct Answer)
D. Carcinoma cervix

Explanation: **Explanation:** The clinical presentation of **6 weeks of amenorrhea** (suggesting early pregnancy) combined with **acute urinary retention** is a classic "high-yield" scenario in reproductive endocrinology and obstetrics. **Why "Impacted Cervical Fibroid" is correct:** In early pregnancy, the uterus enlarges. If a fibroid is present in the cervix or the lower uterine segment, the increasing size of the gravid uterus can cause the fibroid to become **impacted in the pouch of Douglas**. This impaction displaces the cervix anteriorly and upwards against the pubic symphysis. This displacement stretches and compresses the **internal urethral orifice** and the bladder neck, leading to acute urinary retention. While a retroverted gravid uterus is a more common cause of this phenomenon, among the given options, an impacted fibroid is a definitive mechanical cause of such retention. **Analysis of Incorrect Options:** * **A. Retroverted uterus:** While a retroverted gravid uterus is the most common cause of urinary retention at 12–14 weeks (when the uterus rises out of the pelvis), at 6 weeks, the uterus is usually not large enough to cause impaction unless a fibroid is also present. * **B. Pelvic hematocele:** Usually associated with ruptured ectopic pregnancy. While it causes pelvic pain and shock, it rarely presents primarily as acute urinary retention. * **D. Carcinoma cervix:** While it can cause urinary symptoms via direct invasion of the bladder or ureters (leading to hydronephrosis), it does not typically cause acute urinary retention triggered by 6 weeks of amenorrhea. **NEET-PG Clinical Pearls:** * **The "12-week rule":** Acute urinary retention in pregnancy most commonly occurs between **10–14 weeks** due to a retroverted gravid uterus. * **Mechanism:** The cervix is pushed against the sub-pubic angle, lengthening and compressing the urethra. * **Management:** Immediate catheterization followed by manual correction of the uterine position (if retroverted) or surgical consideration (if fibroid).

Question 93: A female patient presents with secondary amenorrhea and a serum prolactin level of 75 ng/ml. What is the most appropriate treatment?

A. Cabergoline (Correct Answer)
B. Ganirelix
C. Clomiphene
D. Estradiol

Explanation: ### Explanation **Correct Answer: A. Cabergoline** The patient presents with **secondary amenorrhea** and **hyperprolactinemia** (Prolactin >25 ng/ml). Elevated prolactin levels inhibit the pulsatile release of GnRH from the hypothalamus, leading to decreased FSH and LH, which results in anovulation and amenorrhea. **Cabergoline** is a long-acting **Dopamine Agonist** with a high affinity for D2 receptors. Since dopamine is the primary physiological inhibitor of prolactin secretion, dopamine agonists are the first-line treatment for hyperprolactinemia (both idiopathic and prolactinomas). Cabergoline is preferred over Bromocriptine due to its superior efficacy and better side-effect profile (less nausea/dizziness). **Why Incorrect Options are Wrong:** * **B. Ganirelix:** This is a GnRH antagonist used primarily in IVF cycles to prevent premature LH surges. It would further suppress the reproductive axis. * **C. Clomiphene:** A Selective Estrogen Receptor Modulator (SERM) used for ovulation induction. While it treats infertility, it does not address the underlying cause (hyperprolactinemia) and is usually ineffective until prolactin levels are normalized. * **D. Estradiol:** This is used for hormone replacement therapy (HRT). While it may induce withdrawal bleeding, it does not treat the hyperprolactinemia and can potentially stimulate prolactin-secreting cells. **High-Yield NEET-PG Pearls:** * **Normal Prolactin:** <25 ng/ml. * **Drug of Choice:** Cabergoline is the DOC for prolactinomas and hyperprolactinemia. * **Hook Effect:** In cases of very large macroadenomas, prolactin levels may appear falsely low; a 1:100 serum dilution is required for accurate measurement. * **Imaging:** If prolactin is >100 ng/ml, an MRI of the sella turcica is mandatory to rule out a prolactinoma.

Question 94: Mifepristone is used in the management of which of the following conditions?

A. Threatened abortion
B. Fibroid
C. Ectopic pregnancy (Correct Answer)
D. Molar pregnancy

Explanation: **Explanation:** **Mifepristone** is a potent synthetic anti-progestogen. It acts by competitively binding to progesterone receptors, leading to the breakdown of the decidua and sensitization of the myometrium to prostaglandins. **Why Ectopic Pregnancy is Correct:** In the management of **unruptured ectopic pregnancy**, Mifepristone is used as an adjunct to **Methotrexate**. Progesterone is essential for the maintenance of early pregnancy; by blocking its receptors, Mifepristone impairs the viability of the trophoblastic tissue, thereby increasing the success rate of medical management and accelerating the resolution of the ectopic mass. **Analysis of Incorrect Options:** * **A. Threatened Abortion:** Progesterone is vital for maintaining pregnancy. Using an anti-progestogen like Mifepristone would induce uterine contractions and cervical ripening, potentially converting a threatened abortion into an inevitable or complete abortion. * **B. Fibroid:** While Mifepristone can be used to reduce the size of leiomyomas (by inhibiting progesterone-dependent growth), it is **not** the standard or first-line management compared to GnRH analogues or Ulipristal acetate. In the context of this specific question, its role in ectopic pregnancy is a more frequently tested clinical application. * **D. Molar Pregnancy:** The primary treatment for hydatidiform mole is **Suction and Evacuation**. Medical induction (including Mifepristone) is contraindicated due to the high risk of heavy hemorrhage and the theoretical risk of trophoblastic embolization. **NEET-PG High-Yield Pearls:** * **Medical Abortion Regimen:** 200 mg Mifepristone (oral) followed by 800 mcg Misoprostol (vaginal/sublingual) after 24–48 hours. * **Cushing’s Syndrome:** Mifepristone is also FDA-approved for hyperglycemia secondary to endogenous Cushing’s syndrome (acting as a glucocorticoid receptor antagonist). * **Emergency Contraception:** A single dose of 10–25 mg Mifepristone is highly effective if taken within 120 hours of unprotected intercourse.

Question 95: A 20-year-old young girl presents with a history of rapidly developing hirsutism and amenorrhea with a change in voice. Which of the following blood tests would you perform to establish a diagnosis?

A. 17-OH progesterone
B. DHEA
C. Testosterone (Correct Answer)
D. LH + FSH estimation

Explanation: ### Explanation The clinical presentation of **rapidly developing hirsutism**, **amenorrhea**, and **virilization** (deepening of voice) in a young woman is a "red flag" for an **androgen-secreting tumor**. **1. Why Testosterone is the correct answer:** In cases of rapid-onset virilization, the primary goal is to rule out a tumor of the ovary or adrenal gland. **Serum Testosterone** is the most important initial marker. A level **>200 ng/dL** is highly suggestive of an ovarian androgen-secreting tumor (e.g., Sertoli-Leydig cell tumor). While DHEAS is used to screen for adrenal tumors, Testosterone is the more common and sensitive marker for the potent androgens causing frank virilization like voice changes. **2. Why other options are incorrect:** * **17-OH Progesterone:** This is the screening test for **Congenital Adrenal Hyperplasia (CAH)**. While CAH causes hirsutism, it is usually present from childhood/puberty and rarely presents with such a sudden, rapid onset of virilization in a 20-year-old. * **DHEA/DHEAS:** DHEAS is a marker for **adrenal** sources of androgens. While it would be measured if an adrenal tumor (like Adrenal Carcinoma) was suspected (levels >7000–8000 µg/dL), Testosterone remains the broader initial step to identify significant hyperandrogenism. * **LH + FSH estimation:** These are used to diagnose PCOS (LH:FSH ratio >2:1) or Premature Ovarian Failure. PCOS causes *gradual* hirsutism and rarely causes voice changes or clitoromegaly. **Clinical Pearls for NEET-PG:** * **Gradual onset + Obesity + Irregular periods:** Think **PCOS** (Most common cause of hirsutism). * **Rapid onset + Virilization (Voice change/Clitoromegaly):** Think **Androgen-secreting tumor**. * **Testosterone >200 ng/dL:** Suspect Ovarian Tumor (Sertoli-Leydig). * **DHEAS >7000 µg/dL:** Suspect Adrenal Tumor. * **Ferriman-Gallwey Score:** Used to clinically quantify hirsutism (Score ≥8 is significant).

Question 96: The phase of the ovarian cycle can be correlated with all of the following EXCEPT:

A. Endometrial sampling
B. Vaginal cytology
C. Blood hormonal levels
D. Estrous cycle (Correct Answer)

Explanation: The ovarian cycle (comprising the follicular and luteal phases) is a physiological process specific to primates, including humans. The correct answer is **D. Estrous cycle**, as it is a distinct reproductive cycle found in non-primate mammals. ### Why "Estrous Cycle" is the Correct Answer: The **Estrous cycle** occurs in animals like dogs, cows, and rodents. Unlike the human menstrual cycle, where the endometrium is shed (menstruation), the endometrium in the estrous cycle is reabsorbed if fertilization does not occur. Furthermore, females are only sexually receptive during the "estrus" (heat) phase, whereas human females can be receptive throughout the cycle. Therefore, the ovarian cycle of a human cannot be correlated with an estrous cycle. ### Why the Other Options are Incorrect: * **A. Endometrial sampling:** The endometrium undergoes predictable changes (proliferative vs. secretory) in response to ovarian steroids (estrogen and progesterone). A biopsy can accurately date the phase of the ovarian cycle. * **B. Vaginal cytology:** The vaginal epithelium is sensitive to hormones. High estrogen (follicular phase) causes an increase in **superficial cells** (high Karyopyknotic Index), while progesterone (luteal phase) increases **intermediate cells**. * **C. Blood hormonal levels:** Measuring FSH, LH, Estradiol, and Progesterone provides a direct correlation. For example, high Progesterone (>3 ng/mL) definitively indicates the luteal phase (post-ovulation). ### NEET-PG High-Yield Pearls: * **Karyopyknotic Index (KI):** The percentage of superficial cells in a vaginal smear; it peaks at ovulation due to maximum estrogen. * **Fern Test:** Estrogen causes cervical mucus to "fern"; Progesterone (luteal phase) disappears this pattern. * **Spinnbarkeit Effect:** Maximum elasticity of cervical mucus occurs just before ovulation (follicular phase).

Question 97: Which of the following statements regarding prolactin levels is TRUE?

A. Lowest in pregnancy and increases after delivery
B. Highest during pregnancy and fall during lactation (Correct Answer)
C. Unaffected by pregnancy and lactation
D. Variable in every pregnancy

Explanation: **Explanation:** **Understanding Prolactin Dynamics** The correct answer is **B**. During pregnancy, prolactin levels rise progressively, reaching their peak (up to 10–20 times non-pregnant levels) at term. This increase is driven by high levels of circulating **estrogen**, which stimulates the lactotrophs in the anterior pituitary to undergo hyperplasia and hypertrophy. Post-delivery, estrogen levels plummet. In non-breastfeeding women, prolactin returns to baseline within 2–3 weeks. In breastfeeding women, while basal prolactin remains elevated, it gradually **falls** over several months of lactation, though it spikes transiently during each episode of suckling (the neuroendocrine reflex). **Analysis of Incorrect Options:** * **Option A:** Incorrect. Prolactin is at its highest during pregnancy, not lowest. It does not increase *after* delivery; rather, the *action* of prolactin (lactogenesis) begins after delivery once the inhibitory effect of progesterone is removed. * **Option C:** Incorrect. Both pregnancy and lactation are the primary physiological states that significantly alter prolactin secretion. * **Option D:** Incorrect. Prolactin follows a highly predictable physiological pattern in all normal pregnancies. **High-Yield Clinical Pearls for NEET-PG:** * **The Progesterone Paradox:** Even though prolactin is high during pregnancy, milk secretion is inhibited by high **Progesterone** levels. Lactation only begins after the placenta is delivered and progesterone levels drop. * **Amniotic Fluid:** Prolactin is found in high concentrations in amniotic fluid, where it aids in fetal osmoregulation. * **Lactational Amenorrhea:** High prolactin inhibits **GnRH pulsatility**, leading to suppressed FSH/LH and subsequent anovulation. * **Drug of Choice:** For pathological hyperprolactinemia (Prolactinoma), the drug of choice is **Cabergoline** (a dopamine agonist).

Question 98: What is a primary medical application of Gonadotropin-releasing hormone (GnRH) analogues?

A. Ovulation induction
B. Endometriosis management
C. Uterine fibroid treatment
D. All of the above (Correct Answer)

Explanation: ### Explanation The therapeutic utility of **GnRH analogues** (agonists and antagonists) is based on their ability to manipulate the hypothalamic-pituitary-ovarian axis. Their effect depends entirely on the **mode of administration**: * **Pulsatile administration:** Mimics the natural physiological release of GnRH, stimulating the pituitary to release FSH and LH. This is used for **ovulation induction** (Option A) in patients with hypogonadotropic hypogonadism. * **Continuous (Non-pulsatile) administration:** Initially causes a "flare effect," but subsequently leads to **downregulation and desensitization** of GnRH receptors. This results in a state of "pseudomenopause" or medical oophorectomy. This hypoestrogenic state is the cornerstone for treating estrogen-dependent conditions like **Endometriosis** (Option B) and **Uterine Fibroids** (Option C), where it reduces lesion size and symptoms. **Why "All of the above" is correct:** GnRH analogues are versatile. While continuous administration is more common clinically for suppressing estrogen, pulsatile administration remains a valid (though less frequent) method for inducing ovulation. **High-Yield NEET-PG Pearls:** * **Flare Effect:** Occurs in the first 7–10 days of agonist therapy; prevented by using GnRH **antagonists** (e.g., Cetrorelix), which provide immediate suppression. * **Add-back Therapy:** When using GnRH agonists for >6 months (e.g., for endometriosis), low-dose estrogen/progesterone is added to prevent bone mineral density loss and vasomotor symptoms. * **Fibroids:** GnRH analogues are typically used **pre-operatively** for 3 months to reduce tumor volume and correct anemia before myomectomy or hysterectomy.

Question 99: Which hormone level is most commonly assessed to evaluate ovarian reserve?

A. Luteinizing Hormone (LH)
B. LH/FSH ratio
C. Follicle-Stimulating Hormone (FSH) (Correct Answer)
D. Estradiol

Explanation: **Explanation:** **Ovarian reserve** refers to the quantity and quality of the remaining oocytes in the ovaries. As a woman ages, the number of follicles decreases, leading to a decline in **Inhibin B** and **Estradiol** levels. Since these hormones normally provide negative feedback to the pituitary, their decline results in a compensatory rise in **Follicle-Stimulating Hormone (FSH)**. **Why FSH is the Correct Answer:** Basal FSH, measured on **Day 2 or 3** of the menstrual cycle, is the traditional "gold standard" screening test for ovarian reserve. A high FSH level (typically >10-12 mIU/mL) indicates a diminished ovarian reserve (DOR), as the pituitary is "working harder" to stimulate the depleted follicles. **Analysis of Incorrect Options:** * **LH (A):** LH levels are primarily used to detect the mid-cycle surge for ovulation or to diagnose PCOS; they do not independently reflect the oocyte pool. * **LH/FSH Ratio (B):** An elevated ratio (>2:1 or 3:1) is a classic diagnostic marker for **Polycystic Ovary Syndrome (PCOS)**, not ovarian reserve. * **Estradiol (D):** While often measured alongside FSH, isolated estradiol is not a reliable marker. However, a very high early-cycle estradiol (>60-80 pg/mL) can falsely suppress FSH, masking a diminished reserve. **High-Yield NEET-PG Pearls:** * **Most Sensitive/Earliest Marker:** Anti-Müllerian Hormone (**AMH**). Unlike FSH, AMH is cycle-independent (can be tested any day). * **Best Ultrasound Marker:** Antral Follicle Count (**AFC**), measured via TVS. * **Day 3 FSH >20 mIU/mL:** Usually indicates poor response to stimulation and very low pregnancy potential. * **Inhibin B:** Produced by granulosa cells; its decline is one of the earliest biochemical changes in reproductive aging.

Question 100: Which of the following hormones is known to play a role in the development of ovarian hyperstimulation syndrome?

A. Luteinizing hormone
B. HCG (Correct Answer)
C. FSH
D. Progesterone

Explanation: **Explanation:** Ovarian Hyperstimulation Syndrome (OHSS) is an iatrogenic complication of ovulation induction. The central pathophysiology involves increased capillary permeability, leading to a fluid shift from the intravascular space to the "third space" (peritoneal, pleural, and pericardial cavities). **Why HCG is the correct answer:** Human Chorionic Gonadotropin (HCG) is the primary trigger for OHSS. It stimulates the ovarian follicles to produce various vasoactive substances, most notably **Vascular Endothelial Growth Factor (VEGF)**. VEGF increases vascular permeability, leading to the clinical manifestations of OHSS. This is why OHSS typically occurs after the "HCG trigger" injection or during early pregnancy (due to endogenous HCG production). **Why the other options are incorrect:** * **FSH (Follicle Stimulating Hormone):** While FSH is used for follicular recruitment and growth, it does not directly cause the massive increase in capillary permeability seen in OHSS. It sets the stage by creating a multi-follicular environment, but HCG is the actual "trigger." * **Luteinizing Hormone (LH):** LH has a similar structure to HCG and binds to the same receptor (LH/hCG receptor). However, HCG has a much longer half-life (>24 hours) compared to LH (approx. 60 minutes), leading to the sustained overstimulation required to develop OHSS. * **Progesterone:** Progesterone is a product of the corpus luteum. While levels are high in OHSS due to multiple corpora lutea, it is a consequence of the syndrome rather than the causative agent. **High-Yield Clinical Pearls for NEET-PG:** * **Key Mediator:** VEGF (Vascular Endothelial Growth Factor). * **Risk Factors:** Young age, low BMI, PCOS, and high anti-Müllerian hormone (AMH) levels. * **Prevention:** Use of GnRH agonists instead of HCG for the "trigger" in high-risk patients (only in antagonist cycles) and "coasting" (withholding gonadotropins). * **Classification:** Severe OHSS is characterized by ascites, pleural effusion, hemoconcentration (Hct >55%), and electrolyte imbalances.

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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