Reproductive Endocrinology — MCQs

Reproductive Endocrinology Indian Medical PG Practice Questions and MCQs

Question 261: Which of the following findings is suggestive that ovulation has taken place?

A. Pseudostratification in endometrium
B. Presence of Spinnbarkeit Phenomenon in cervical mucous
C. Sudden reduction in size of follicle and free fluid in Pouch of Douglas on USG (Correct Answer)
D. Trilamilar endometrium on USG

Explanation: **Explanation:** The correct answer is **C: Sudden reduction in size of follicle and free fluid in Pouch of Douglas on USG.** **Why it is correct:** Ovulation is the release of an oocyte from a mature Graafian follicle. On serial Transvaginal Sonography (TVS), the most reliable signs that ovulation has occurred include the **sudden disappearance or collapse of the large pre-ovulatory follicle** (usually >18-20 mm) and the appearance of **free fluid in the Pouch of Douglas (POD)**, which results from the release of follicular fluid. Subsequently, the follicle transforms into a corpus luteum, which may appear as a smaller, irregular cystic structure with internal echoes and a "ring of fire" vascularity on Doppler. **Why other options are incorrect:** * **A. Pseudostratification in endometrium:** This is a histological feature of the **proliferative phase** (estrogen-dominant). After ovulation, progesterone causes the endometrium to transition to the secretory phase, characterized by subnuclear vacuolation. * **B. Spinnbarkeit Phenomenon:** This refers to the high elasticity and "stretchability" of cervical mucus under the influence of peak **estrogen** levels. It occurs **just before** ovulation. After ovulation, progesterone makes the mucus thick, tacky, and non-elastic. * **D. Trilaminar endometrium:** This "triple-line" appearance on USG is characteristic of the **late proliferative phase** (pre-ovulatory). Post-ovulation, the endometrium becomes homogenously hyperechoic (secretory phase). **NEET-PG High-Yield Pearls:** * **Gold Standard for timing ovulation:** Serial Transvaginal Ultrasound (Folliculometry). * **Earliest histological sign of ovulation:** Subnuclear vacuolation in the endometrial glands (seen on Day 16-17). * **LH Surge:** Occurs 32–36 hours before ovulation. It is the most reliable predictor of *impending* ovulation. * **Progesterone:** A mid-luteal phase (Day 21) serum progesterone level >3 ng/mL is indicative of ovulation.

Question 262: What is the first step in the management of hirsutism due to Stein-Leventhal syndrome?

A. Oral contraceptive pills (OCPs) (Correct Answer)
B. Human Menopausal Gonadotropin (HMG)
C. Spironolactone
D. Bromocriptine

Explanation: **Explanation:** **Stein-Leventhal Syndrome**, now more commonly known as **Polycystic Ovary Syndrome (PCOS)**, is characterized by hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology. **Why Option A is Correct:** **Oral Contraceptive Pills (OCPs)** are the **first-line pharmacological treatment** for hirsutism in PCOS patients who do not have immediate fertility goals. They work through three primary mechanisms: 1. **Suppression of LH:** By providing negative feedback, OCPs decrease LH secretion, which reduces ovarian androgen production. 2. **Increase in SHBG:** The estrogen component stimulates the liver to produce Sex Hormone Binding Globulin (SHBG), which binds free testosterone, making it biologically inactive. 3. **Inhibition of Adrenal Androgens:** They also cause a mild decrease in adrenal androgen production. **Why Other Options are Incorrect:** * **B. HMG:** This is a gonadotropin used for **ovulation induction** in patients seeking pregnancy. It would worsen the hormonal milieu in a patient primarily seeking treatment for hirsutism. * **C. Spironolactone:** This is an anti-androgen that blocks the androgen receptor and inhibits 5-alpha-reductase. While effective for hirsutism, it is considered **second-line** or an add-on therapy if OCPs are insufficient after 6 months. It is also teratogenic, necessitating concurrent OCP use. * **D. Bromocriptine:** This is a dopamine agonist used to treat **hyperprolactinemia**. While PCOS patients may have mildly elevated prolactin, it is not the primary treatment for hirsutism. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** Based on the **Rotterdam Criteria** (2 out of 3: Oligo/anovulation, Clinical/biochemical hyperandrogenism, PCO on ultrasound). * **First-line for Infertility:** Letrozole (Aromatase inhibitor) is now preferred over Clomiphene citrate. * **Hirsutism Timeline:** It takes at least **6 months** of OCP therapy to see clinical improvement in hair growth due to the long life cycle of terminal hair. * **Gold Standard for Hirsutism Assessment:** Modified Ferriman-Gallwey Score.

Question 263: Testicular feminization syndrome is associated with which of the following?

A. 46,XX karyotype
B. Presence of a vagina
C. Primary amenorrhea (Correct Answer)
D. Short stature

Explanation: **Explanation:** **Testicular Feminization Syndrome**, now more commonly known as **Complete Androgen Insensitivity Syndrome (CAIS)**, is a condition where a genetic male (46,XY) is resistant to the action of androgens due to a defect in the androgen receptor. **Why Primary Amenorrhea is Correct:** Patients with CAIS have functioning testes (usually intra-abdominal) that produce **Anti-Müllerian Hormone (AMH)**. AMH causes the regression of all Müllerian structures, meaning the patient has **no uterus, fallopian tubes, or upper third of the vagina**. Without a uterus, menstruation cannot occur, making primary amenorrhea the hallmark clinical presentation when these individuals reach puberty. **Analysis of Incorrect Options:** * **A. 46,XX karyotype:** Incorrect. The genotype is **46,XY**. They are phenotypically female but genetically male. * **B. Presence of a vagina:** This is partially incorrect/misleading. While there is a **blind-ending vaginal pouch** (derived from the urogenital sinus), the true anatomical vagina (upper 2/3) is absent. * **D. Short stature:** Incorrect. These patients are typically **tall** or have normal height for a male, as the Y chromosome carries genes for stature and there is no estrogen-induced early epiphyseal closure. **High-Yield Clinical Pearls for NEET-PG:** * **Phenotype:** Well-developed breasts (due to peripheral conversion of testosterone to estrogen) but **absent/scanty axillary and pubic hair** (due to androgen insensitivity). * **Gonads:** Testes are present (often in the inguinal canal or abdomen) and must be removed after puberty to prevent **gonadoblastoma/dysgerminoma**. * **Hormonal Profile:** High Testosterone, high LH, and normal to slightly high FSH. * **Differential:** Differentiate from **Müllerian Agenesis (MRKH)**, where the karyotype is 46,XX and ovaries are present.

Question 264: The Modified Ferriman Gallway score is used to grade which of the following conditions?

A. Hirsutism (Correct Answer)
B. Abnormal Uterine bleeding
C. Polycystic Ovarian Disease (PCOD)
D. Gestational Trophoblastic Neoplasia

Explanation: **Explanation:** The **Modified Ferriman-Gallway (mFG) score** is the gold standard clinical tool used to objectively quantify the severity of **Hirsutism** (Option A). **Why it is correct:** Hirsutism is defined as the presence of terminal hair in females in a male-pattern distribution. The mFG score evaluates **9 androgen-sensitive body areas**: upper lip, chin, chest, upper back, lower back, upper abdomen, lower abdomen, upper arms, and thighs. Each area is graded from 0 (no hair) to 4 (frankly virile), with a maximum score of 36. In most populations, a score of **≥8** is considered diagnostic of hirsutism. **Why other options are incorrect:** * **Abnormal Uterine Bleeding (AUB):** This is assessed using the **PALM-COEIN** classification for etiology and the **PBAC (Pictorial Blood Loss Assessment Chart)** or Higham’s chart to quantify blood loss. * **Polycystic Ovarian Disease (PCOD/PCOS):** While hirsutism is a common symptom of PCOS, the diagnosis of PCOS itself is based on the **Rotterdam Criteria** (Hyperandrogenism, Ovulatory dysfunction, and Polycystic ovaries on ultrasound). The mFG score only measures one clinical component (hirsutism). * **Gestational Trophoblastic Neoplasia (GTN):** This is staged using the **FIGO Staging** and the **WHO Modified Prognostic Scoring System** (which uses parameters like age, antecedent pregnancy, and hCG levels). **High-Yield Clinical Pearls for NEET-PG:** * **Commonest cause of Hirsutism:** Polycystic Ovarian Syndrome (PCOS). * **Drug of choice for Hirsutism:** Combined Oral Contraceptive Pills (OCPs) are first-line; Spironolactone is the most common anti-androgen added if OCPs are insufficient. * **Rapid onset hirsutism + Virilization:** Always suspect an androgen-secreting tumor (Adrenal or Ovarian). * **Areas NOT included in mFG score:** Forearms and lower legs (these are not strictly androgen-dependent).

Question 265: What is the treatment for a hirsute patient with Polycystic Ovary Syndrome (PCOS)?

A. Ethinyl estradiol + Levonorgestrel
B. Ethinyl estradiol + Desogestrel (Correct Answer)
C. Levonorgestrel
D. None of the above

Explanation: **Explanation:** The management of hirsutism in Polycystic Ovary Syndrome (PCOS) focuses on reducing circulating free testosterone and inhibiting its peripheral action. Combined Oral Contraceptive Pills (COCPs) are the first-line treatment for this purpose. **Why Option B is Correct:** Ethinyl estradiol (EE) combined with **Desogestrel** is preferred because Desogestrel is a **third-generation progestin**. Unlike older progestins, third-generation progestins have **low androgenic activity** and higher selectivity. Furthermore, the estrogen component (EE) increases the production of **Sex Hormone Binding Globulin (SHBG)** in the liver, which binds free testosterone, while the progestin component suppresses LH secretion, reducing ovarian androgen production. This dual action effectively treats hirsutism and acne. **Why Other Options are Incorrect:** * **Option A & C:** **Levonorgestrel** is a second-generation progestin. It is highly **androgenic** (derived from 19-nortestosterone) and can actually worsen hirsutism and acne by decreasing SHBG levels and binding to androgen receptors. Therefore, it is generally avoided in PCOS patients with hyperandrogenism. **High-Yield Clinical Pearls for NEET-PG:** * **Best Progestins for PCOS:** Desogestrel, Gestodene, and Norgestimate (3rd gen) or **Cyproterone acetate** and **Drospirenone** (anti-androgenic progestins). * **Timeframe:** It takes at least **6 months** of COCP therapy to see a clinical improvement in hirsutism due to the long hair growth cycle. * **Mechanism:** COCPs work by: 1) Suppressing LH (decreasing ovarian androgens), 2) Increasing SHBG (decreasing free testosterone), and 3) Inhibiting 5α-reductase activity in the skin.

Question 266: What is the cause for luteal phase defect?

A. Progesterone is inadequately secreted (Correct Answer)
B. Excess estrogen is secreted
C. Excess progesterone is secreted
D. Both estrogen and progesterone are in excess

Explanation: **Explanation:** Luteal Phase Defect (LPD) is a clinical condition characterized by an endometrial lining that is out of phase with the menstrual cycle, primarily due to an environment that is insufficient to support embryo implantation or early pregnancy. **1. Why Option A is Correct:** The fundamental pathology of LPD is **inadequate progesterone secretion** by the corpus luteum. Progesterone is essential for the "secretory transformation" of the endometrium. If progesterone levels are low or the duration of its secretion is short (less than 10 days), the endometrium fails to mature appropriately, leading to implantation failure or early spontaneous abortion. **2. Why the other options are incorrect:** * **Options B, C, and D:** Excess estrogen or progesterone do not define LPD. While an imbalance in the estrogen-to-progesterone ratio can affect the endometrium, LPD is specifically a state of **deficiency**, not excess. Excess progesterone would actually support the secretory phase, and excess estrogen (without progesterone) would lead to endometrial hyperplasia, not a luteal phase defect. **NEET-PG High-Yield Pearls:** * **Diagnostic Gold Standard:** Historically, a **timed endometrial biopsy** (showing a lag of >2 days by Noyes criteria) was the gold standard, though it is now less commonly used in routine practice. * **Clinical Presentation:** Often presents as infertility or recurrent pregnancy loss (RPL). * **Short Luteal Phase:** A luteal phase lasting **<10 days** (from ovulation to menses) is a classic indicator of LPD. * **Associated Conditions:** LPD is frequently seen in cases of hyperprolactinemia, thyroid dysfunction, and extreme exercise/stress, which disrupt the pulsatile release of GnRH and LH. * **Treatment:** Progesterone supplementation (vaginal or oral) during the luteal phase and treatment of the underlying cause (e.g., Bromocriptine for hyperprolactinemia).

Question 267: A 30-year-old athlete complains of amenorrhea for 1 year. Her BMI is 20 kg/m2. Luteinizing hormone (LH) and follicle-stimulating hormone (FSH) are in the low normal range. Clinical and ultrasonography (USG) findings are normal. What is the most likely cause of her amenorrhea?

A. Depression
B. Excessive exercise (Correct Answer)
C. Premature menopause
D. Anorexia nervosa

Explanation: **Explanation:** The patient presents with **Functional Hypothalamic Amenorrhea (FHA)**, a condition characterized by the suppression of the Hypothalamic-Pituitary-Ovarian (HPO) axis due to energy deficits. **Why "Excessive Exercise" is correct:** In female athletes, intense physical activity combined with inadequate caloric intake leads to a decrease in **GnRH pulsatility** from the hypothalamus. This results in "low-normal" or low levels of LH and FSH (hypogonadotropic hypogonadism) and subsequent low estrogen. The patient’s history as an athlete and a BMI on the lower end of normal (20 kg/m²) strongly point toward exercise-induced FHA. **Why other options are incorrect:** * **Depression:** While psychological stress can cause FHA, the specific mention of the patient being an athlete makes exercise the more definitive clinical trigger. * **Premature Menopause (POI):** This would present with **elevated** gonadotropins (High FSH/LH) due to the loss of negative feedback from the ovaries, not low-normal levels. * **Anorexia Nervosa:** While this also causes FHA, it typically presents with a BMI <17.5 kg/m², severe body image distortion, and more profound metabolic disturbances than described here. **High-Yield Clinical Pearls for NEET-PG:** * **Female Athlete Triad:** Consists of (1) Low energy availability/Disordered eating, (2) Menstrual dysfunction (Amenorrhea), and (3) Low bone mineral density (Osteoporosis). * **Diagnosis of Exclusion:** FHA is diagnosed only after ruling out organic causes (e.g., pregnancy, prolactinoma, thyroid dysfunction). * **Progesterone Challenge Test:** Patients with FHA usually have a **negative** withdrawal bleed because of low endogenous estrogen levels (thin endometrium). * **Management:** The primary treatment is lifestyle modification (increasing caloric intake and reducing exercise intensity).

Question 268: Mifepristone is not used in which of the following conditions?

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

Explanation: **Explanation:** **Mifepristone** is a potent **competitive progesterone receptor antagonist**. Since progesterone is the "hormone of pregnancy" essential for maintaining the decidua and uterine quiescence, blocking its receptors leads to decidual breakdown, cervical softening, and increased uterine contractility. 1. **Why Threatened Abortion is the correct answer:** In a threatened abortion, the goal of management is to **preserve the pregnancy**. Progesterone supplementation is often used to support the pregnancy. Administering Mifepristone (an anti-progesterone) would actively promote the detachment of the embryo and induce uterine contractions, leading to an inevitable or complete abortion. Therefore, it is strictly contraindicated. 2. **Analysis of other options:** * **Fibroid:** Mifepristone is used to reduce the size of leiomyomas by inhibiting progesterone-dependent growth of the fibroid tissue. * **Ectopic Pregnancy:** While Methotrexate is the primary medical management, Mifepristone is sometimes used as an adjunct to increase the success rate of tubal resolution by sensitizing the tissue. * **Molar Pregnancy:** Mifepristone can be used as a pre-evacuation cervical priming agent to facilitate suction and evacuation. **High-Yield Clinical Pearls for NEET-PG:** * **Medical Abortion Protocol:** 200 mg Mifepristone (oral) followed 36–48 hours later by 800 mcg Misoprostol (vaginal/oral/buccal) is effective up to 9 weeks (63 days) of gestation. * **Cushing’s Syndrome:** Mifepristone is also FDA-approved for controlling hyperglycemia in patients with endogenous Cushing’s syndrome (due to its glucocorticoid receptor antagonistic effect at high doses). * **Emergency Contraception:** A single dose of 10 mg Mifepristone is highly effective if taken within 120 hours of unprotected intercourse.

Question 269: What is the most common cause of primary amenorrhea with ambiguous genitalia in a 46XX individual?

A. 21-hydroxylase deficiency (Correct Answer)
B. 17-hydroxylase deficiency
C. 11-hydroxylase deficiency
D. Desmolase hydrolase deficiency

Explanation: **Explanation:** The clinical presentation of **primary amenorrhea with ambiguous genitalia** in a 46,XX individual is most commonly due to **Congenital Adrenal Hyperplasia (CAH)**. **1. Why 21-hydroxylase deficiency is correct:** This is the most common cause of CAH (accounting for >90% of cases). A deficiency in the 21-hydroxylase enzyme impairs the conversion of progesterone to deoxycorticosterone (mineralocorticoid pathway) and 17-OH progesterone to 11-deoxycortisol (glucocorticoid pathway). The resulting lack of negative feedback leads to an excess of ACTH, which shunts precursors into the **androgen pathway**. In a 46,XX fetus, these high levels of adrenal androgens cause virilization of the external genitalia (ambiguity), while the internal female organs (uterus/ovaries) remain intact. **2. Why the other options are incorrect:** * **11-hydroxylase deficiency:** While it also causes virilization and CAH, it is much rarer. It is uniquely characterized by **hypertension** due to the buildup of 11-deoxycorticosterone (a mineralocorticoid). * **17-hydroxylase deficiency:** This leads to a decrease in both androgens and cortisol. A 46,XX individual would have normal female external genitalia (not ambiguous) but would fail to undergo puberty (primary amenorrhea) and present with **hypertension and hypokalemia**. * **Desmolase deficiency:** This is a rare, severe form of CAH where no steroid hormones are produced. It typically results in female external genitalia regardless of genetic sex and is often fatal in infancy due to salt wasting. **Clinical Pearls for NEET-PG:** * **Most common cause of Ambiguous Genitalia:** 21-hydroxylase deficiency. * **Diagnostic Marker:** Elevated levels of **17-hydroxyprogesterone (17-OHP)**. * **Salt-wasting type:** Presents with hyponatremia, hyperkalemia, and hypotension. * **Internal Genitalia:** In CAH, the uterus and tubes are always present because there is no Anti-Müllerian Hormone (AMH).

Question 270: Which of the following is FALSE regarding Polycystic Ovary Syndrome (PCOS)?

A. High FSH/LH ratio (Correct Answer)
B. Bilateral ovarian cysts
C. Hirsutism
D. Increased risk of diabetes mellitus

Explanation: **Explanation:** In Polycystic Ovary Syndrome (PCOS), the characteristic hormonal imbalance is a **Reversed FSH/LH ratio**, typically >2:1 or 3:1. Therefore, Option A is false because PCOS is characterized by **High LH** and **Low/Normal FSH**. The increased pulse frequency of GnRH favors LH production over FSH. Low FSH levels result in poor follicular recruitment and a lack of aromatase activity, leading to an accumulation of androgens. **Analysis of other options:** * **Bilateral ovarian cysts:** According to the **Rotterdam Criteria**, one of the diagnostic features is the presence of polycystic ovaries on ultrasound (≥12 follicles measuring 2–9 mm or ovarian volume >10 mL). This is typically a bilateral finding. * **Hirsutism:** This is a clinical manifestation of hyperandrogenism, another pillar of the Rotterdam Criteria. It is often assessed using the **Modified Ferriman-Gallwey score**. * **Increased risk of diabetes mellitus:** PCOS is strongly associated with **peripheral insulin resistance** and compensatory hyperinsulinemia. This significantly increases the long-term risk of Type 2 Diabetes and Metabolic Syndrome. **High-Yield Clinical Pearls for NEET-PG:** * **Rotterdam Criteria (2 out of 3):** 1. Oligo/Anovulation, 2. Hyperandrogenism (Clinical/Biochemical), 3. Polycystic ovaries on USG. * **Gold Standard Investigation:** Transvaginal Ultrasound (TVS). * **DOC for Ovulation Induction:** Letrozole (Aromatase inhibitor) is now preferred over Clomiphene Citrate. * **Long-term risks:** Endometrial hyperplasia/carcinoma (due to unopposed estrogen), Dyslipidemia, and OSA.

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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