Reproductive Endocrinology — MCQs

Reproductive Endocrinology Indian Medical PG Practice Questions and MCQs

Question 81: In Polycystic Ovarian Disease (PCOD), which of the following statements is true?

A. Increased FSH and decreased LH
B. Increased LH and decreased estrogen
C. Increased FSH/LH ratio and decreased estrogen
D. Increased LH and increased estrogen (Correct Answer)

Explanation: In Polycystic Ovarian Disease (PCOD/PCOS), the core pathophysiology involves a disruption of the Hypothalamic-Pituitary-Ovarian (HPO) axis. ### **Why Option D is Correct** 1. **Increased LH:** There is an increased frequency and amplitude of GnRH pulses, which preferentially stimulates the anterior pituitary to secrete **Luteinizing Hormone (LH)**. This leads to a characteristic **LH:FSH ratio of >2:1 or 3:1**. 2. **Increased Estrogen:** High LH levels stimulate the ovarian **theca cells** to produce excess androgens (androstenedione). These androgens are then converted into **estrone (E1)** via peripheral aromatization in adipose tissue. This results in a state of hyperestrogenism (specifically acyclic estrone), which further sensitizes the pituitary to GnRH, creating a vicious cycle. ### **Why Other Options are Incorrect** * **Option A & C:** In PCOD, **FSH is typically low or normal**, never increased. The FSH/LH ratio is decreased (because the denominator, LH, is high). * **Option B:** While LH is increased, **estrogen is also increased** (not decreased). Low estrogen is seen in conditions like premature ovarian failure or menopause, not PCOD. ### **NEET-PG High-Yield Pearls** * **The "Two-Cell" Theory in PCOD:** LH acts on Theca cells (Androgens ↑); FSH acts on Granulosa cells (but is insufficient to aromatize all androgens, leading to follicular arrest). * **Gold Standard for Diagnosis:** Rotterdam Criteria (requires 2 out of 3: Hyperandrogenism, Oligo/anovulation, and Polycystic ovaries on USG). * **Insulin Resistance:** This is a key driver; hyperinsulinemia decreases Sex Hormone Binding Globulin (SHBG), further increasing free testosterone levels. * **String of Pearls:** Classic USG finding (12 or more follicles measuring 2–9 mm).

Question 82: Premature ovarian insufficiency is defined as hypogonadotropic hypogonadism and amenorrhea arising before the age of?

A. 40 years (Correct Answer)
B. 45 years
C. 50 years
D. 55 years

Explanation: **Explanation:** **Premature Ovarian Insufficiency (POI)**, formerly known as premature ovarian failure, is defined by the loss of ovarian activity before the age of **40 years**. It is characterized by a triad of: 1. **Amenorrhea** (primary or secondary) for at least 4 months. 2. **Hypergonadotropic hypogonadism** (Elevated FSH > 25 IU/L on two occasions, 4 weeks apart). 3. **Hypoestrogenism.** **Why 40 years is correct:** The average age of natural menopause is approximately 51 years. POI affects about 1% of the female population. The cutoff of 40 years is a standardized clinical definition used to distinguish pathological early loss of ovarian function from the normal climacteric period. **Why other options are incorrect:** * **45 years:** Menopause occurring between 40 and 45 years is termed **"Early Menopause."** While earlier than average, it is not classified as POI. * **50 and 55 years:** These ages fall within the **normal physiological range** for menopause (average 45–55 years). **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause:** Most cases are idiopathic. However, the most common chromosomal cause is **Turner Syndrome (45,XO)** or Fragile X premutation. * **Hormonal Profile:** High FSH, High LH, and **Low Estradiol**. (Note: The question stem mentions "hypogonadotropic," but POI is actually **hypergonadotropic**; the pituitary secretes more FSH to stimulate failing ovaries). * **Management:** Hormone Replacement Therapy (HRT) is mandatory until at least the age of natural menopause (50–51 years) to prevent osteoporosis and cardiovascular disease. * **Fertility:** Unlike menopause, POI is not permanent in all cases; there is a 5–10% chance of spontaneous conception.

Question 83: Which of the following is recommended for a woman with antiphospholipid antibodies and a history of prior abortions or stillbirth?

A. Aspirin only
B. Aspirin plus low molecular weight heparin (Correct Answer)
C. Aspirin plus low molecular weight heparin plus prednisolone
D. No treatment

Explanation: **Explanation:** The management of Antiphospholipid Syndrome (APS) in pregnancy is a high-yield topic for NEET-PG. The primary goal is to prevent placental thrombosis and pregnancy loss. **Why Option B is Correct:** The standard of care for a pregnant woman with APS and a history of prior pregnancy loss (recurrent abortions or stillbirth) is **combination therapy with Low-Dose Aspirin (LDA) and Low Molecular Weight Heparin (LMWH)**. * **Aspirin (75–150 mg):** Inhibits thromboxane A2, reducing platelet aggregation. * **LMWH (Prophylactic dose):** Prevents thrombosis and has additional anti-inflammatory and anti-complement effects that aid trophoblastic invasion. Studies show that combination therapy significantly improves live birth rates compared to aspirin alone. **Why Other Options are Incorrect:** * **Option A (Aspirin only):** While used for "obstetric APS" in some guidelines, it is less effective than combination therapy for patients with a definitive history of pregnancy loss. * **Option C (Aspirin + LMWH + Prednisolone):** Steroids were used in the past but are no longer recommended. They do not improve live birth rates and significantly increase the risk of maternal complications like gestational diabetes and hypertension. * **Option D (No treatment):** Untreated APS in pregnancy carries a high risk (up to 80-90%) of recurrent loss, IUGR, and preeclampsia. **High-Yield Clinical Pearls for NEET-PG:** 1. **Diagnosis (Sapporo Criteria):** Requires at least one clinical (vascular thrombosis or pregnancy morbidity) and one laboratory criterion (Lupus anticoagulant, Anticardiolipin, or Anti-β2 glycoprotein-I antibodies) positive on two occasions, 12 weeks apart. 2. **Timing:** Aspirin is ideally started pre-conception; LMWH is started as soon as pregnancy is confirmed. 3. **Warfarin:** It is **contraindicated** in pregnancy (teratogenic) but can be used postpartum. 4. **Postpartum:** Prophylaxis should continue for 6 weeks after delivery to prevent maternal thromboembolism.

Question 84: A 23-year-old female presents with a history of recurrent abortions. Which of the following tests is NOT indicated in the investigation of recurrent abortions?

A. Parental cytogenetics
B. Thyroid profile
C. Antiphospholipid antibodies
D. TORCH infection screening (Correct Answer)

Explanation: **Explanation:** Recurrent pregnancy loss (RPL) is defined as the loss of two or more consecutive pregnancies. The investigation of RPL focuses on identifying chronic or structural causes rather than sporadic events. **Why TORCH screening is NOT indicated:** TORCH infections (Toxoplasmosis, Other, Rubella, CMV, Herpes) are known to cause **sporadic** pregnancy loss or congenital malformations. However, they do not cause **recurrent** abortions because the mother typically develops lasting immunity after the primary infection, preventing subsequent pregnancy losses from the same pathogen. Therefore, routine TORCH screening is no longer recommended in the workup of RPL. **Why the other options are indicated:** * **Parental Cytogenetics:** Indicated to rule out balanced reciprocal or Robertsonian translocations in either parent, which can lead to unbalanced gametes and recurrent miscarriages. * **Thyroid Profile:** Endocrine disorders, specifically uncontrolled hypothyroidism or the presence of anti-thyroid antibodies, are established risk factors for RPL. * **Antiphospholipid Antibodies (APLA):** Antiphospholipid Syndrome is the most important treatable causes of RPL. Testing for Lupus anticoagulant, Anticardiolipin, and Anti-β2 glycoprotein I antibodies is mandatory. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of sporadic abortion:** Fetal chromosomal anomalies (Autosomal trisomy). * **Most common cause of RPL:** Often remains "unexplained" (approx. 50%), but among identifiable causes, APLA and uterine anomalies are frequent. * **Uterine factor:** Hysterosalpingography (HSG) or Hysteroscopy is indicated to rule out a septate uterus (the uterine anomaly most associated with RPL). * **Progesterone:** Luteal phase deficiency is a controversial but often tested endocrine cause of RPL.

Question 85: A 28-year-old obese woman presents with infertility and amenorrhea, accompanied by significant facial hair in a male distribution. Laboratory studies show increased serum LH, total serum testosterone, and dehydroepiandrosterone sulfate. What pelvic ultrasound finding would likely be observed?

A. A mass resembling a bunch of grapes projecting into the vagina
B. Blood-filled cysts in the ovary
C. Fluid accumulation in the fallopian tubes
D. Multiple small follicular cysts on the ovary (Correct Answer)

Explanation: This patient presents with the classic triad of **Polycystic Ovary Syndrome (PCOS)**: obesity, menstrual irregularities (amenorrhea), and hyperandrogenism (hirsutism). ### **Explanation of the Correct Answer** In PCOS, the fundamental pathology involves a hormonal imbalance characterized by an **increased LH:FSH ratio** (often >2:1 or 3:1). High LH levels stimulate the ovarian theca cells to produce excess androgens (testosterone and DHEAS). However, the relatively low FSH levels are insufficient to stimulate the maturation of follicles. This leads to **follicular arrest**, where multiple follicles begin to develop but fail to reach ovulation. On ultrasound, these arrested follicles appear as **multiple small subcortical follicular cysts** (typically 2–9 mm in diameter), often described as a "string of pearls" appearance. ### **Why Other Options are Incorrect** * **Option A:** Describes **Hydatidiform mole** (specifically Sarcoma botryoides if in a child), characterized by a "snowstorm" appearance on ultrasound, not PCOS. * **Option B:** Refers to **Endometriomas** (Chocolate cysts), which are associated with endometriosis and chronic pelvic pain, not typically primary hyperandrogenism. * **Option C:** Describes **Hydrosalpinx**, which is a consequence of pelvic inflammatory disease (PID) and a cause of tubal factor infertility, unrelated to the endocrine profile described. ### **NEET-PG High-Yield Pearls** * **Rotterdam Criteria (2 out of 3):** 1. Clinical/biochemical hyperandrogenism; 2. Oligo/anovulation; 3. Polycystic ovaries on USG (≥12 follicles or ovarian volume >10cc). * **Gold Standard Diagnosis:** Clinical + Biochemical; Ultrasound is supportive but not always mandatory. * **Metabolic Association:** Strong link with **Insulin Resistance** and Acanthosis Nigricans. * **First-line Treatment:** Weight loss (lifestyle) is first; **Clomiphene citrate** or Letrozole for infertility; OCPs for cycle regulation.

Question 86: Which of the following is NOT a major source of androgens in females?

A. Adrenals
B. Ovaries
C. Peripheral conversion from androgen precursors in the liver, gastrointestinal tract, and adipose tissue
D. Corpus luteum (Correct Answer)

Explanation: In the female body, androgens are produced through three primary pathways. Understanding the distribution of these sources is high-yield for NEET-PG. ### **Why "Corpus Luteum" is the Correct Answer** The **corpus luteum** is a temporary endocrine structure formed after ovulation. Its primary physiological role is the secretion of **progesterone** (to maintain the secretory endometrium) and some estrogen. While it produces small amounts of androstenedione as a precursor to estrogen, it is **not** considered a "major source" of systemic androgens. Its function is specialized for pregnancy maintenance rather than androgen contribution. ### **Analysis of Incorrect Options** * **A. Adrenals:** The adrenal glands (specifically the *zona reticularis*) contribute approximately **25%** of circulating testosterone and are the primary source of DHEA-S (95-100%). * **B. Ovaries:** The ovarian theca cells produce androgens under the influence of LH. The ovaries contribute roughly **25%** of circulating testosterone. * **C. Peripheral Conversion:** This is a significant source, accounting for the remaining **50%** of circulating testosterone. Precursors like androstenedione are converted into testosterone in the liver, skin, gastrointestinal tract, and adipose tissue. ### **Clinical Pearls for NEET-PG** * **The 25-25-50 Rule:** Remember that Testosterone in females comes 25% from Adrenals, 25% from Ovaries, and 50% from Peripheral conversion. * **DHEA-S Marker:** DHEA-S is almost exclusively produced by the adrenals. If a patient has virilization and elevated DHEA-S, the source is likely an adrenal tumor. * **Hyperandrogenism:** In PCOS (the most common cause of female hyperandrogenism), the excess androgens primarily originate from the ovarian theca cells due to elevated LH levels.

Question 87: Primary amenorrhea with anosmia is seen in which condition?

A. Kallman syndrome (Correct Answer)
B. Laurence-Moon-Biedl syndrome
C. Foster-Kennedy syndrome
D. Sheehan's syndrome

Explanation: **Explanation:** **Kallmann Syndrome** is the correct answer because it is characterized by the failure of GnRH-secreting neurons to migrate from the olfactory placode to the hypothalamus. This results in **Hypogonadotropic Hypogonadism** (low FSH/LH, low estrogen) leading to primary amenorrhea, combined with **Anosmia** (loss of smell) or hyposmia due to the agenesis of the olfactory bulbs. It is most commonly inherited as an X-linked recessive trait (KAL-1 gene mutation). **Analysis of Incorrect Options:** * **Laurence-Moon-Biedl Syndrome:** A rare genetic disorder characterized by obesity, retinitis pigmentosa, polydactyly, mental retardation, and hypogonadism. While it causes primary amenorrhea, it is **not** typically associated with anosmia. * **Foster-Kennedy Syndrome:** A clinical triad caused by an olfactory groove meningioma or frontal lobe tumor. It presents with ipsilateral optic atrophy, contralateral papilledema, and anosmia. It does not cause primary amenorrhea. * **Sheehan’s Syndrome:** This is postpartum pituitary necrosis due to severe obstetric hemorrhage. It presents as **secondary amenorrhea** and failure of lactation; it is an acquired condition, not a cause of primary amenorrhea or anosmia. **High-Yield Clinical Pearls for NEET-PG:** * **Genetics:** Most common cause of hypogonadotropic hypogonadism. * **Diagnosis:** Low GnRH, low FSH/LH, and low Estrogen/Testosterone. * **Associated features:** Color blindness, cleft lip/palate, and renal agenesis (in 30% of cases). * **MRI Finding:** Absence or hypoplasia of olfactory bulbs and sulci. * **Treatment:** Pulsatile GnRH therapy or exogenous gonadotropins to induce ovulation/fertility.

Question 88: Which of the following is not increased in Polycystic Ovary Syndrome (PCOS)?

A. Estrogen
B. Luteinizing hormone
C. Sex hormone-binding globulin (Correct Answer)
D. Insulin

Explanation: **Explanation:** In Polycystic Ovary Syndrome (PCOS), the core pathophysiology involves hyperandrogenism and insulin resistance. **Why SHBG is decreased:** **Sex Hormone-Binding Globulin (SHBG)** is a protein produced by the liver that binds to testosterone. In PCOS, high levels of **Insulin** (due to insulin resistance) and elevated **Androgens** directly inhibit the hepatic synthesis of SHBG. Consequently, SHBG levels **decrease**. This reduction is clinically significant because lower SHBG leads to an increase in the "Free Androgen Index," meaning more unbound, biologically active testosterone is available to cause symptoms like hirsutism and acne. **Analysis of incorrect options:** * **Estrogen:** Levels are typically increased (specifically **Estrone/E1**). Peripheral conversion of androstenedione in adipose tissue leads to "unopposed estrogen," which increases the risk of endometrial hyperplasia. * **Luteinizing Hormone (LH):** There is a characteristic increase in LH pulse frequency and amplitude, often resulting in an **LH:FSH ratio > 2:1 or 3:1**. * **Insulin:** Most PCOS patients exhibit **Hyperinsulinemia** due to peripheral insulin resistance. This excess insulin stimulates the ovarian theca cells to produce more androgens. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Rotterdam Criteria (requires 2 out of 3: Oligo/anovulation, Hyperandrogenism, and Polycystic ovaries on ultrasound). * **String of Pearls:** Ultrasound appearance showing 12 or more follicles (2-9 mm) or increased ovarian volume (>10 ml). * **Best Initial Treatment:** Lifestyle modification (Weight loss). * **Drug of Choice for Infertility:** Letrozole (Aromatase inhibitor) is now preferred over Clomiphene citrate.

Question 89: Clomiphene citrate is not known to produce which of the following effects in a 30-year-old female of reproductive age?

A. Hot flushes
B. Ovulation
C. Decreased FSH and LH secretion (Correct Answer)
D. Polycystic ovaries

Explanation: **Explanation:** **Mechanism of Action & Correct Answer:** Clomiphene Citrate (CC) is a Selective Estrogen Receptor Modulator (SERM). Its primary action is to act as a **competitive antagonist** at the estrogen receptors in the hypothalamus and pituitary gland. By blocking the negative feedback of endogenous estrogen, the brain perceives a "hypoestrogenic state." This triggers the hypothalamus to increase the pulse frequency of GnRH, which subsequently **increases the secretion of FSH and LH** from the anterior pituitary. Therefore, Option C is the correct answer because CC increases, rather than decreases, gonadotropin levels to stimulate follicular development. **Analysis of Other Options:** * **A. Hot flushes:** This is the most common side effect (occurring in ~10% of patients). It occurs because CC blocks estrogen receptors in the thermoregulatory center of the hypothalamus, mimicking menopausal symptoms. * **B. Ovulation:** This is the intended therapeutic effect. The rise in FSH stimulates follicular growth, leading to a dominant follicle and a subsequent LH surge. * **D. Polycystic ovaries:** Overstimulation of the ovaries by increased FSH can lead to the development of multiple follicles or ovarian enlargement. In severe cases, this can progress to Ovarian Hyperstimulation Syndrome (OHSS). **High-Yield Clinical Pearls for NEET-PG:** * **First-line indication:** WHO Group II Anovulation (e.g., PCOS). * **Structural similarity:** It is structurally related to Diethylstilbestrol (DES). * **Anti-estrogenic effect on Endometrium:** While it helps ovulation, its peripheral anti-estrogenic effect can result in thin endometrium and thick cervical mucus, sometimes leading to a "conception-ovulation gap." * **Multiple Pregnancy Risk:** Approximately 8–10% (predominantly twins). * **Isomer:** Enclomiphene is the active isomer responsible for the ovulation-inducing effect.

Question 90: Which hormone level is typically elevated in polycystic ovarian syndrome?

A. 17-alpha-hydroxyprogesterone
B. FSH (Follicle-Stimulating Hormone)
C. LH (Luteinizing Hormone) (Correct Answer)
D. TSH (Thyroid-Stimulating Hormone)

Explanation: **Explanation:** In Polycystic Ovarian Syndrome (PCOS), the primary endocrine hallmark is a disruption of the hypothalamic-pituitary-ovarian axis. The correct answer is **LH (Luteinizing Hormone)** because PCOS is characterized by an increased frequency and amplitude of GnRH pulses, which preferentially stimulates the anterior pituitary to secrete LH over FSH. This results in an **elevated LH:FSH ratio (typically >2:1 or 3:1)**. High LH levels act on the ovarian theca cells to increase androgen production, leading to hyperandrogenism and follicular arrest. **Analysis of Incorrect Options:** * **17-alpha-hydroxyprogesterone:** This is a marker for **Congenital Adrenal Hyperplasia (CAH)**. While it may be mildly elevated in some PCOS cases, a significant elevation is used to rule out CAH, which is a common differential diagnosis for PCOS. * **FSH (Follicle-Stimulating Hormone):** In PCOS, FSH levels are typically **low or low-normal**. The lack of sufficient FSH prevents the aromatization of androgens to estrogens and hinders the development of a dominant follicle. * **TSH (Thyroid-Stimulating Hormone):** TSH levels are usually normal in PCOS. Thyroid dysfunction is a separate endocrine disorder, though hypothyroidism can mimic some PCOS symptoms (like irregular cycles) and should be ruled out during workup. **Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Rotterdam Criteria (requires 2 out of 3: Oligo/anovulation, Hyperandrogenism, and Polycystic ovaries on ultrasound). * **Insulin Resistance:** Hyperinsulinemia is a key driver in PCOS; it decreases Sex Hormone Binding Globulin (SHBG), further increasing free testosterone levels. * **Ultrasound Finding:** "String of pearls" appearance (12 or more follicles measuring 2–9 mm). * **First-line for Ovulation Induction:** Letrozole (now preferred over Clomiphene Citrate).

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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