Reproductive Endocrinology — MCQs

Reproductive Endocrinology Indian Medical PG Practice Questions and MCQs

Question 61: Which of the following is NOT a feature of polycystic ovarian disease?

A. Hirsutism
B. Polymenorrhea (Correct Answer)
C. Obesity
D. Infertility

Explanation: **Explanation:** Polycystic Ovarian Syndrome (PCOS) is a complex endocrine disorder characterized by hyperandrogenism and ovulatory dysfunction. **Why Polymenorrhea is the correct answer:** In PCOS, the fundamental pathology is **chronic anovulation**. Due to the lack of regular ovulation, there is no progesterone production to stabilize the endometrium. This leads to **Oligomenorrhea** (infrequent periods, >35 days apart) or **Amenorrhea** (absence of periods). **Polymenorrhea** (frequent cycles <21 days) is not a feature of PCOS; it is more commonly associated with endometriosis, PID, or perimenopause. **Analysis of Incorrect Options:** * **Hirsutism (A):** This is a hallmark feature caused by **hyperandrogenism**. Excess LH stimulates the ovarian theca cells to produce androgens, leading to male-pattern hair growth. * **Obesity (C):** Approximately 50-60% of PCOS patients are obese. Obesity exacerbates **insulin resistance**, which further stimulates androgen production and suppresses SHBG (Sex Hormone Binding Globulin). * **Infertility (D):** PCOS is the most common cause of **anovulatory infertility**. The lack of a dominant follicle prevents regular egg release. **High-Yield Clinical Pearls for NEET-PG:** * **Rotterdam Criteria (2 of 3):** 1. Clinical/biochemical hyperandrogenism, 2. Oligo/anovulation, 3. Polycystic ovaries on ultrasound ("String of pearls" appearance). * **LH:FSH Ratio:** Classically elevated to **3:1** (though no longer a diagnostic requirement). * **Metabolic Risks:** Increased risk of Type 2 Diabetes, Dyslipidemia, and **Endometrial Carcinoma** (due to unopposed estrogen). * **Drug of Choice:** **Clomiphene Citrate** (traditionally) or **Letrozole** (now preferred for ovulation induction).

Question 62: Which of the following best diagnoses the luteal phase?

A. Serum progesterone levels
B. Endometrial biopsy (Correct Answer)
C. Basal body temperature
D. Ultrasonography

Explanation: The diagnosis of the luteal phase depends on identifying the physiological changes induced by progesterone following ovulation. **Why Endometrial Biopsy is the Correct Answer:** Endometrial biopsy is considered the **gold standard** for diagnosing the luteal phase and assessing its functional adequacy. Under the influence of progesterone, the endometrium undergoes specific, predictable histological changes (secretory transformation). By performing a biopsy (traditionally on day 21–23 of a 28-day cycle), a pathologist can "date" the endometrium using **Noyes’ criteria**. If the histological date lags behind the menstrual date by more than 2 days, it indicates Luteal Phase Deficiency (LPD). **Analysis of Incorrect Options:** * **Serum Progesterone:** While a level >3 ng/mL confirms ovulation, a single mid-luteal measurement (Day 21) is often unreliable because progesterone is secreted in pulses. It reflects the presence of a corpus luteum but does not confirm if the end-organ (endometrium) is responding appropriately. * **Basal Body Temperature (BBT):** A rise of 0.4–0.8°F indicates the thermogenic effect of progesterone. However, it is retrospective, prone to user error, and only confirms that ovulation occurred, not the quality of the luteal phase. * **Ultrasonography:** USG can visualize the corpus luteum or a collapsed follicle, but it cannot provide functional or histological confirmation of the luteal phase. **High-Yield Clinical Pearls for NEET-PG:** * **Best time for biopsy:** 2–3 days before the expected onset of menstruation (Day 26 of a 28-day cycle) provides the most accurate dating. * **Fern Test:** Disappearance of the "fern pattern" and appearance of "cellular/beaded pattern" in cervical mucus also indicates the luteal phase. * **Progesterone Peak:** Occurs 7–8 days after the LH surge.

Question 63: What is the karyotype in testicular feminisation syndrome?

A. XX
B. XY (Correct Answer)
C. XXY
D. VON

Explanation: **Explanation:** **Testicular Feminization Syndrome**, now more commonly known as **Androgen Insensitivity Syndrome (AIS)**, is a condition where a genetic male is resistant to androgenic hormones. 1. **Why XY is correct:** The underlying pathology is a mutation in the **Androgen Receptor (AR) gene** located on the X chromosome. Despite having a **46, XY karyotype** and functioning testes that produce normal or high male levels of testosterone, the body’s tissues cannot respond to these hormones. Consequently, the individual develops a female phenotype (external genitalia) but lacks female internal organs (uterus/tubes) because the testes still produce **Anti-Müllerian Hormone (AMH)**. 2. **Why other options are incorrect:** * **XX:** This is a normal female karyotype. In conditions like Müllerian Agenesis (MRKH), the karyotype is XX, but in AIS, the individual is genetically male. * **XXY:** This is the karyotype for **Klinefelter Syndrome**. These individuals have a male phenotype, small firm testes, and infertility, but they do not present with female external genitalia. * **VON:** This is not a recognized genetic karyotype. **High-Yield Clinical Pearls for NEET-PG:** * **Phenotype:** Tall, well-developed female with primary amenorrhea. * **Key Feature:** Scant or **absent axillary and pubic hair** (due to androgen insensitivity). * **Internal Anatomy:** Vagina is short/blind-ending; uterus, ovaries, and fallopian tubes are absent. * **Gonads:** Testes are present (undescended in the abdomen or inguinal canal) and must be removed after puberty to prevent **Gonadoblastoma**. * **Differential Diagnosis:** Always differentiate from **MRKH Syndrome** (which has 46, XX karyotype and normal pubic hair).

Question 64: For a patient with polycystic ovary disease, during which phase of the menstrual cycle should LH/FSH estimation be performed?

A. Days 1-4
B. Days 8-10 (Correct Answer)
C. Days 13-15
D. Days 24-26

Explanation: In Polycystic Ovary Syndrome (PCOS), the characteristic hormonal imbalance is an **elevated LH:FSH ratio** (typically >2:1 or 3:1). To accurately capture this baseline tonic elevation of LH, testing must be performed during the **early to mid-follicular phase**. ### Why Days 8-10 is Correct While many hormonal assays are traditionally done on Day 2 or 3, in PCOS, the LH levels are persistently elevated due to increased GnRH pulse frequency. Testing on **Days 8-10** is considered ideal because it avoids the very early follicular fluctuations and provides a stable representation of the "tonic" LH elevation before any potential pre-ovulatory surge (though ovulation is rare in PCOS). This window captures the steady-state hormonal environment characteristic of the disease. ### Why Other Options are Incorrect * **Days 1-4 (Early Follicular):** While often used for baseline FSH to check ovarian reserve, LH levels can be naturally low or fluctuating during menses, potentially masking the diagnostic LH:FSH ratio. * **Days 13-15 (Mid-cycle):** This is the periovulatory period. In a normal cycle, a physiological LH surge occurs here. Testing during this time would lead to a false-positive interpretation of high LH. * **Days 24-26 (Luteal Phase):** During this phase, progesterone is dominant, which suppresses LH secretion via negative feedback. This would obscure the high LH levels typical of PCOS. ### NEET-PG High-Yield Pearls * **Gold Standard Diagnosis:** Currently based on the **Rotterdam Criteria** (requires 2 out of 3: Hyperandrogenism, Oligo/Anovulation, and Polycystic ovaries on USG). * **LH:FSH Ratio:** While high-yield for exams, it is **no longer mandatory** for diagnosis under Rotterdam criteria but remains a classic biochemical marker. * **Best Initial Test for Hyperandrogenism:** Free testosterone levels. * **USG Hallmark:** "String of pearls" appearance (12 or more follicles measuring 2-9 mm).

Question 65: Regarding PCOS and hyperinsulinaemia, which of the following statements is/are true?

A. Hyperinsulinaemia is observed in about 40% to 50% of women with PCOS.
B. Hyperinsulinaemia stimulates hepatic synthesis of SHBG.
C. Metformin causes hypoglycemia in normoglycemic women.
D. Metformin has many other health benefits. (Correct Answer)

Explanation: **Explanation:** **1. Why Option D is Correct:** Metformin, a biguanide, is a cornerstone in managing PCOS-related metabolic dysfunction. Beyond improving insulin sensitivity, it offers several health benefits: it aids in **weight loss**, reduces the risk of developing **Type 2 Diabetes Mellitus**, improves lipid profiles, and may reduce the risk of endometrial hyperplasia by restoring regular ovulatory cycles. In pregnancy, it is also used to manage Gestational Diabetes (GDM). **2. Why the Other Options are Incorrect:** * **Option A:** Hyperinsulinemia is much more prevalent than 40-50%. It is observed in approximately **50-70%** of all women with PCOS, and the prevalence can be as high as **80-90% in obese PCOS patients**. * **Option B:** Insulin actually **inhibits** the hepatic synthesis of Sex Hormone Binding Globulin (SHBG). Lower SHBG levels lead to an increase in **Free Testosterone**, which worsens the clinical symptoms of hyperandrogenism (hirsutism, acne). * **Option C:** Metformin is an **"euglycemic"** agent, not a hypoglycemic one. It works by decreasing hepatic glucose production and increasing peripheral insulin sensitivity. Unlike sulfonylureas or insulin, it **does not cause hypoglycemia** in normoglycemic women. **NEET-PG High-Yield Pearls:** * **The "Two-Hit" Hypothesis:** Hyperinsulinemia contributes to hyperandrogenism by (1) stimulating ovarian theca cells to produce androgens and (2) suppressing hepatic SHBG production. * **LH:FSH Ratio:** Classically >2:1 or 3:1 (though no longer a diagnostic criterion in Rotterdam). * **First-line for Ovulation Induction:** Letrozole (Aromatase Inhibitor) is now preferred over Clomiphene Citrate. * **Gold Standard for Insulin Resistance:** Hyperinsulinemic-euglycemic clamp (though rarely used clinically).

Question 66: In precocious females, when does menstruation occur?

A. After 13 years of age
B. At 13 years of age
C. Less than 10 years of age (Correct Answer)
D. Below 12 years of age

Explanation: ### Explanation **Core Concept:** Precocious puberty is defined as the onset of secondary sexual characteristics before the age of 8 in girls. The sequence of pubertal development typically follows the order: **Thelarche** (breast development) → **Adrenarche/Pubarche** (axillary/pubic hair) → **Growth Spurt** → **Menarche** (menstruation). In normal development, menarche occurs approximately 2–2.5 years after thelarche, with an average age of 12.5 years. In the context of precocious puberty, menstruation is considered "precocious" if it occurs **before the age of 10**. **Analysis of Options:** * **Option C (Correct):** Medical literature and standard textbooks (like Williams Gynecology) define precocious menstruation as the onset of menses before age 10. This reflects an accelerated hypothalamic-pituitary-ovarian (HPO) axis maturation. * **Option A & B (Incorrect):** 13 years is the upper limit of the *normal* range for the onset of puberty. If a girl has not started any pubertal changes by age 13, it is classified as **Delayed Puberty**. * **Option D (Incorrect):** While 12 years is the average age for menarche in the general population, it does not meet the clinical criteria for "precocious." **High-Yield Clinical Pearls for NEET-PG:** * **True (Central) Precocious Puberty:** GnRH-dependent; follows the normal sequence of puberty but at an earlier age. Most cases in girls (80-90%) are **idiopathic**. * **Pseudo (Peripheral) Precocious Puberty:** GnRH-independent; often due to ovarian cysts, McCune-Albright syndrome, or adrenal tumors. * **Bone Age:** In precocious puberty, bone age is typically advanced beyond chronological age, leading to early epiphyseal closure and short adult stature. * **Treatment:** The gold standard for Central Precocious Puberty is **GnRH agonists** (e.g., Leuprolide) to desensitize the pituitary and halt premature maturation.

Question 67: In which of the following conditions does hypogonadism and anosmia coexist?

A. Kallman syndrome (Correct Answer)
B. Mayer-Rokitansky-Kuster syndrome
C. Noonan Syndrome
D. Ashermann 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 during embryonic development. This results in: 1. **Hypogonadotropic Hypogonadism:** Low GnRH leads to low FSH/LH and subsequent low sex steroids (delayed puberty/amenorrhea). 2. **Anosmia or Hyposmia:** Due to the agenesis or hypoplasia of the olfactory bulbs. It is often associated with the *KAL-1* gene mutation (X-linked) or *FGFR1* mutations. **Analysis of Incorrect Options:** * **Mayer-Rokitansky-Küster-Hauser (MRKH) Syndrome:** Characterized by Müllerian agenesis (absent uterus and upper 2/3 of the vagina) in a 46,XX female. These patients have **normal ovarian function** and a normal sense of smell. * **Noonan Syndrome:** Often called "Male Turner Syndrome," it involves short stature, webbed neck, and pulmonary stenosis. While it can cause cryptorchidism and delayed puberty, it is not typically associated with anosmia. * **Asherman Syndrome:** An acquired condition involving intrauterine adhesions (synechiae) usually following over-vigorous curettage. It causes secondary amenorrhea but does not affect the hypothalamic-pituitary-ovarian axis or the sense of smell. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Most commonly X-linked recessive (KAL-1 gene). * **Clinical Presentation:** Primary amenorrhea, failure of secondary sexual characteristics, and "color blindness" (sometimes associated). * **Diagnosis:** Low FSH, Low LH, Low Estrogen/Testosterone + MRI showing absent olfactory bulbs. * **Treatment:** Pulsatile GnRH or exogenous gonadotropins to induce puberty and fertility.

Question 68: Diethylstilbesterol causes which of the following defects, except?

A. Renal anomalies (Correct Answer)
B. Perifimbrial cysts
C. T shaped uterus
D. Vaginal adenosis

Explanation: **Explanation:** Diethylstilbestrol (DES) is a synthetic non-steroidal estrogen that was historically used to prevent miscarriages. However, it is a potent **teratogen** that interferes with the development of the **Müllerian ducts** (Paramesonephric ducts). **1. Why Renal Anomalies is the Correct Answer:** Renal anomalies are typically associated with primary Müllerian duct agenesis (e.g., Mayer-Rokitansky-Küster-Hauser syndrome) because the urinary and reproductive systems develop simultaneously from the intermediate mesoderm. However, DES exposure does not cause renal defects; it causes **structural remodeling** of the already formed reproductive tract. Therefore, renal anomalies are NOT a feature of DES exposure. **2. Analysis of Incorrect Options:** * **Vaginal Adenosis:** This is the most common structural change in DES-exposed daughters. It involves the persistence of glandular columnar epithelium in the vagina (which should normally be stratified squamous). It is a precursor to **Clear Cell Adenocarcinoma** of the vagina. * **T-shaped Uterus:** DES interferes with the mesenchymal-epithelial interactions during uterine development, leading to a constricted, T-shaped uterine cavity, which increases the risk of preterm labor and ectopic pregnancy. * **Perifimbrial Cysts:** DES exposure is associated with various adnexal abnormalities, including perifimbrial cysts, paratubal cysts, and fimbrial deformity. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad of DES Exposure:** Vaginal adenosis, T-shaped uterus, and Clear Cell Adenocarcinoma (Vagina/Cervix). * **Cervical Changes:** "Coxcomb" cervix, cervical collars, and cervical hypoplasia. * **Male Offspring:** DES exposure can lead to epididymal cysts, cryptorchidism, and microphallus. * **Key Association:** Always link DES with **Clear Cell Adenocarcinoma**; it is a favorite "except" type question in exams.

Question 69: Which of the following is NOT a component of the Rotterdam criteria for diagnosing polycystic ovarian syndrome?

A. Multiple cysts in ovaries seen on ultrasound
B. Anovulation
C. Clinical or biochemical hyperandrogenism
D. Hyperinsulinism (Correct Answer)

Explanation: The **Rotterdam Criteria (2003)** is the current gold standard for diagnosing Polycystic Ovarian Syndrome (PCOS). To make a diagnosis, at least **two out of the three** specific criteria must be present, after excluding other etiologies (like CAH or Cushing’s). ### Why Hyperinsulinism is the Correct Answer: While **hyperinsulinism** and insulin resistance are central to the pathophysiology of PCOS (driving the ovaries to produce excess androgens), they are **not** part of the formal diagnostic criteria. A patient can be diagnosed with PCOS even if they have normal insulin sensitivity, provided they meet the other criteria. ### Explanation of Incorrect Options: * **A. Multiple cysts in ovaries (PCO morphology):** Defined as ≥12 follicles (measuring 2–9 mm) in either ovary or an increased ovarian volume (>10 mL). *Note: Newer guidelines suggest ≥20 follicles if using high-frequency probes.* * **B. Anovulation:** Specifically, oligo-ovulation or anovulation, usually manifesting as irregular periods (cycles >35 days or <8 per year). * **C. Hyperandrogenism:** This can be **clinical** (hirsutism, acne, male-pattern baldness) or **biochemical** (elevated serum testosterone or DHEAS). ### High-Yield NEET-PG Pearls: * **LH:FSH Ratio:** Classically 3:1, but no longer used for diagnosis. * **Hirsutism Scoring:** The **Modified Ferriman-Gallwey score** is used (Score ≥8 is significant in most populations). * **Gold Standard Treatment:** Lifestyle modification (weight loss) is the first-line management. * **Drug of Choice:** **Clomiphene citrate** (traditionally) or **Letrozole** (now preferred) for ovulation induction; **Metformin** for insulin resistance.

Question 70: Which of the following best describes male pseudohermaphroditism?

A. XX genotype with male external genitalia
B. XY genotype with female external genitalia (Correct Answer)
C. Presence of both testis and ovary
D. Presence of male external genitalia and an ovary

Explanation: ### Explanation **1. Understanding the Concept (Why B is correct):** In medical terminology, "pseudohermaphroditism" is defined by the **mismatch between the genetic sex (gonads) and the phenotypic sex (external genitalia)**. * **Male Pseudohermaphroditism** (now termed 46,XY Disorder of Sexual Development or DSD) occurs when an individual has a **46,XY genotype** and testes, but the external genitalia are female or ambiguous. * This happens due to either a failure in androgen synthesis or a failure in androgen action (e.g., **Androgen Insensitivity Syndrome** or 5-alpha reductase deficiency). Because the body cannot respond to or produce testosterone effectively, the default female phenotype develops externally despite the presence of a Y chromosome. **2. Analysis of Incorrect Options:** * **Option A (XX with male genitalia):** This describes **Female Pseudohermaphroditism** (46,XX DSD). The most common cause is Congenital Adrenal Hyperplasia (CAH), where excess fetal androgens virilize an XX fetus. * **Option C (Both testis and ovary):** This defines **True Hermaphroditism** (Ovotesticular DSD). It requires the histological presence of both ovarian and testicular tissue in the same individual. * **Option D (Male genitalia and an ovary):** This is a variation of female pseudohermaphroditism or ovotesticular DSD, but it does not define the specific clinical entity of male pseudohermaphroditism. **3. High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of Male Pseudohermaphroditism:** Androgen Insensitivity Syndrome (AIS). * **Most common cause of Female Pseudohermaphroditism:** Congenital Adrenal Hyperplasia (21-hydroxylase deficiency). * **Key Diagnostic Feature:** In AIS (Male Pseudohermaphroditism), there is a **blind-ending vagina** and absent uterus (due to Anti-Müllerian Hormone production by the testes). * **Rule of Thumb:** The "Pseudo" prefix refers to the **gonad**. A *Male* pseudohermaphrodite has *testes* (XY) but looks like a female. A *Female* pseudohermaphrodite has *ovaries* (XX) but looks like a male.

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

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free