Reproductive Endocrinology Practice Questions

Q: All of the following are raised in PCOS except?

E2:E1 ratio. In Polycystic Ovary Syndrome (PCOS), the hormonal and metabolic profile is characterized by hyperandrogenism and insulin resistance. **Explanation of the Correct Answer:** * **A. E2:E1 ratio:** In PCOS, the ratio of **Estradiol (E2) to Estrone (E1) is decreased**, not raised. While E2 is the primary estrogen produced by the ovaries, PCOS involves significant peripheral aromatization of androstenedione into Estrone (E1) within adipose tissue. Consequently, **E1 levels become higher than E2**, leading to a reversal of the normal ratio. **Explanation of Incorrect Options:** * **B. LH:FSH ratio:** Raised. High-frequency GnRH pulses favor LH secretion over FSH. A ratio of **>2:1 or 3:1** is a classic (though not diagnostic) finding. * **C. LDL:HDL ratio:** Raised. Insulin resistance and hyperandrogenism lead to dyslipidemia, specifically increasing "bad" cholesterol (LDL) and decreasing "good" cholesterol (HDL). * **D. Fasting serum insulin:** Raised. Peripheral insulin resistance is a hallmark of PCOS, leading to compensatory hyperinsulinemia, which further stimulates ovarian androgen production. **High-Yield Clinical Pearls for NEET-PG:** * **Hyperestrogenism in PCOS:** It is a state of "chronic tonic estrogen" (mostly E1) without the progesterone surge, leading to an increased risk of **Endometrial Hyperplasia/Carcinoma**. * **SHBG:** Sex Hormone Binding Globulin is **decreased** in PCOS due to high insulin, leading to increased levels of **Free Testosterone**. * **Gold Standard for Insulin Resistance:** Hyperinsulinemic-euglycemic clamp (though rarely used clinically). * **AMH:** Anti-Müllerian Hormone levels are typically **raised** due to the high number of pre-antral follicles.

Q: What percentage of females with polycystic ovary syndrome (PCOS) experience oligomenorrhea?

80%. **Explanation:** Polycystic Ovary Syndrome (PCOS) is the most common endocrine disorder in women of reproductive age, characterized by a triad of hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology. **Why 80% is correct:** Menstrual irregularities, specifically **oligomenorrhea** (defined as 35 days) or amenorrhea, are the hallmark clinical features of PCOS. These occur due to chronic anovulation caused by an imbalance in the LH:FSH ratio and intra-ovarian hyperandrogenism, which arrests follicular development. Large-scale clinical studies and standard textbooks (such as Williams Gynecology) indicate that approximately **80%** of women diagnosed with PCOS present with these menstrual disturbances. **Analysis of Incorrect Options:** * **50% & 60%:** These figures significantly underestimate the prevalence. While some women with PCOS have "ovulatory PCOS" (regular cycles but with hyperandrogenism and PCO morphology), they represent a minority (approx. 20%). * **70%:** While closer, this value is statistically lower than the established clinical prevalence reported in high-yield medical literature for competitive exams like NEET-PG. **High-Yield Clinical Pearls for NEET-PG:** * **Rotterdam Criteria:** Diagnosis requires 2 out of 3: (1) Oligo/Anovulation, (2) Clinical/Biochemical Hyperandrogenism, (3) Polycystic ovaries on USG. * **LH:FSH Ratio:** Classically elevated to **>2:1 or 3:1**, though no longer a formal diagnostic criterion. * **Insulin Resistance:** Present in 50-70% of cases, leading to acanthosis nigricans. * **First-line treatment:** Lifestyle modification (weight loss). For infertility, **Letrozole** is now the drug of choice (superior to Clomiphene).

Q: Sexual infantilism is associated with which of the following conditions?

All of the above. **Explanation:** Sexual infantilism refers to the failure of secondary sexual characteristic development and the maintenance of prepubertal status beyond the expected age of puberty. This occurs due to a defect in the **Hypothalamic-Pituitary-Gonadal (HPG) axis**, resulting in either low gonadotropins (Hypogonadotropic Hypogonadism) or primary gonadal failure (Hypergonadotropic Hypogonadism). * **Pituitary Tumor (Option A):** Tumors like craniopharyngiomas or prolactinomas can compress or destroy gonadotroph cells in the anterior pituitary. This leads to a deficiency in FSH and LH, preventing the stimulation of ovaries/testes, thus causing sexual infantilism. * **Gonadal Aplasia (Option B):** The most common cause is **Turner Syndrome (45,XO)**. In these cases, the gonads fail to develop (streak gonads), leading to a lack of estrogen. Without estrogen, secondary sexual characteristics do not develop, despite high levels of FSH/LH. * **Dwarfism (Option C):** Panhypopituitarism (e.g., Lorain-Levi dwarfism) involves a deficiency in both Growth Hormone (leading to short stature/dwarfism) and Gonadotropins (leading to sexual infantilism). **Conclusion:** Since all three conditions disrupt the HPG axis at different levels, **Option D** is the correct answer. **High-Yield NEET-PG Pearls:** * **Most common cause of Sexual Infantilism with anosmia:** Kallmann Syndrome (Hypogonadotropic). * **Most common cause of Sexual Infantilism with short stature:** Turner Syndrome (Hypergonadotropic). * **Diagnostic Step:** The first step in evaluation is measuring serum **FSH levels** to differentiate between central (pituitary/hypothalamic) and peripheral (gonadal) causes.

Q: Which of the following is NOT a typical symptom or sign of Polycystic Ovarian Disease (PCOD)?

Weight loss. **Explanation:** **Polycystic Ovarian Disease (PCOD/PCOS)** is a complex endocrine disorder characterized by insulin resistance, hyperandrogenism, and chronic anovulation. **Why Weight Loss is the Correct Answer:** Weight loss is **not** a feature of PCOD; instead, **obesity** (specifically central/android obesity) is a hallmark sign, seen in approximately 50-60% of patients. Obesity exacerbates the condition because adipose tissue decreases Sex Hormone Binding Globulin (SHBG) and increases peripheral conversion of androgens to estrogens, further disrupting the hypothalamic-pituitary-ovarian axis. **Analysis of Incorrect Options:** * **Alopecia:** High levels of circulating free androgens (testosterone) lead to "male-pattern" hair loss (androgenetic alopecia) and hirsutism. * **Theca Cell Hyperplasia:** In PCOD, elevated Luteinizing Hormone (LH) levels cause hyperplasia of the ovarian theca cells. These cells are responsible for the overproduction of androgens (androstenedione and testosterone). * **Hyperandrogenism:** This is a core diagnostic criterion (Rotterdam Criteria). It manifests clinically as acne, hirsutism, and biochemically as elevated serum testosterone levels. **High-Yield Clinical Pearls for NEET-PG:** * **Rotterdam Criteria (2 out of 3):** 1. Oligo/Anovulation, 2. Clinical/Biochemical Hyperandrogenism, 3. Polycystic ovaries on Ultrasound ("String of pearls" appearance). * **LH:FSH Ratio:** Classically elevated to **>2:1 or 3:1**. * **Insulin Resistance:** Leads to **Acanthosis Nigricans** (velvety hyperpigmentation in skin folds). * **First-line Management:** Weight loss and lifestyle modification. For infertility, **Letrozole** is now the drug of choice (DOC), surpassing Clomiphene Citrate.

Q: All of the following statements about Androgen Insensitivity Syndrome are true except?

Pubic hair are abundant. **Explanation:** **Androgen Insensitivity Syndrome (AIS)**, formerly known as Testicular Feminization Syndrome, is an X-linked recessive condition where there is a functional defect in the androgen receptors. **Why Option B is the correct answer (The False Statement):** In AIS, although the body produces high levels of testosterone, the peripheral tissues cannot respond to it due to receptor resistance. Since the development of **pubic and axillary hair** is dependent on androgen action, these patients typically have **absent or very sparse** pubic and axillary hair. Therefore, the statement that pubic hair is "abundant" is incorrect. **Analysis of Incorrect Options:** * **Option A (XY Genotype):** True. These individuals are genetically male (46, XY). * **Option C (Blind Vagina):** True. Due to the presence of the Y chromosome, the SRY gene leads to the development of testes which secrete **Müllerian Inhibiting Substance (MIS)**. MIS causes regression of the Müllerian ducts (uterus, fallopian tubes, and upper 1/3rd of the vagina). The lower 2/3rd of the vagina (derived from the urogenital sinus) develops but ends blindly. * **Option D (Ovaries are absent):** True. These patients have undescended testes (often located in the labia majora or inguinal canal) rather than ovaries. **High-Yield Clinical Pearls for NEET-PG:** * **Phenotype:** Phenotypically female with well-developed breasts (due to peripheral conversion of testosterone to estrogen). * **Primary Amenorrhea:** AIS is a leading cause of primary amenorrhea with breast development. * **Management:** Gonadectomy is performed **after puberty** (to allow natural breast development) to prevent the risk of gonadoblastoma/dysgerminoma. * **Differential Diagnosis:** Differentiate from **Müllerian Agenesis (MRKH Syndrome)** where the genotype is 46, XX, ovaries are present, and pubic hair is normal.

Q: What is the best agent for premenstrual syndrome management?

SSRI. **Explanation:** Premenstrual Syndrome (PMS) and its more severe form, Premenstrual Dysphoric Disorder (PMDD), are characterized by cyclic physical and emotional symptoms occurring during the luteal phase. **Why SSRIs are the Correct Answer:** Selective Serotonin Reuptake Inhibitors (SSRIs) are considered the **first-line pharmacological treatment** for PMS/PMDD. The underlying pathophysiology involves a maladaptive response to normal fluctuations in gonadal steroids (estrogen and progesterone), which leads to a functional deficiency in **serotonin**. SSRIs rapidly increase synaptic serotonin levels, effectively alleviating both emotional (irritability, depression) and physical symptoms. Unlike in major depression, SSRIs for PMS can be administered either continuously or restricted to the luteal phase (starting on day 14). **Analysis of Incorrect Options:** * **Progesterone (A):** While PMS occurs during the progesterone-dominant luteal phase, clinical trials have shown that progesterone supplementation is no more effective than a placebo. * **Anxiolytics (B):** Benzodiazepines (like Alprazolam) may be used as a second-line adjunct for severe anxiety but are not first-line due to the risk of dependence and side effects. * **Vitamin E (D):** While sometimes suggested for cyclical mastalgia (breast pain), it lacks robust evidence for treating the global symptoms of PMS. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Symptoms must be documented prospectively for at least **two consecutive menstrual cycles** using a daily symptom diary. * **Symptom-Free Interval:** Symptoms must resolve within 4 days of the onset of menses and must not be present during the follicular phase (Days 4–12). * **Severe Cases:** If SSRIs fail, the next step is often **GnRH agonists** (to induce "medical oophorectomy") or COCPs (specifically those containing **Drospirenone**).

Q: A patient presents with a history of amenorrhea and hirsutism. Ultrasound of the ovary is provided. What is the most likely diagnosis?

Polycystic Ovary Syndrome (PCOS). ***Polycystic Ovary Syndrome (PCOS)*** - **Amenorrhea** and **hirsutism** are classic presenting symptoms of PCOS, part of the **Rotterdam criteria** for diagnosis. - Ultrasound typically shows **multiple peripheral follicles** arranged in a "**string-of-pearls**" pattern around the ovarian cortex. *Endometriosis* - Primarily presents with **cyclical pelvic pain** and **dysmenorrhea**, not amenorrhea or hirsutism. - Ultrasound would show **endometriomas** (chocolate cysts) rather than multiple peripheral follicles. *Adenomyomatosis* - This is a **benign gallbladder condition** characterized by **hyperplasia of the gallbladder wall**, not an ovarian pathology. - Would not cause **amenorrhea** or **hirsutism** as it doesn't affect reproductive hormones. *Choriocarcinoma* - A **malignant gestational trophoblastic neoplasm** that presents with **irregular bleeding** and elevated **β-hCG levels**. - Would not typically cause **hirsutism** or the characteristic ovarian ultrasound findings described.

Question 1

All of the following are raised in PCOS except?

Accepted Answer

E2:E1 ratio

Answer

LH:FSH ratio

Answer

LDL:HDL ratio

Answer

Fasting serum insulin

Question 2

Which of the following is NOT a feature of Stein-Leventhal syndrome?

Accepted Answer

Galactorrhoea

Answer

Increased androgens

Answer

Increased or normal oestrogens

Answer

Increased LH

Question 3

What percentage of females with polycystic ovary syndrome (PCOS) experience oligomenorrhea?

Accepted Answer

80%

Answer

50%

Answer

60%

Answer

70%

Question 4

Sexual infantilism is associated with which of the following conditions?

Accepted Answer

All of the above

Answer

Pituitary tumor

Answer

Gonadal aplasia

Answer

Dwarfism

Question 5

Which of the following is NOT a typical symptom or sign of Polycystic Ovarian Disease (PCOD)?

Accepted Answer

Weight loss

Answer

Alopecia

Answer

Theca cell hyperplasia

Answer

Hyperandrogenism

Question 6

All of the following statements about Androgen Insensitivity Syndrome are true except?

Accepted Answer

Pubic hair are abundant

Answer

Patients have an XY genotype

Answer

A blind vagina may be present

Answer

Ovaries are absent

Question 7

Determination of serum progesterone level to document ovulation. For the evaluation, select the most appropriate day of a normal 28-day menstrual cycle for a woman with 5-day menstrual periods.

Accepted Answer

Day 21

Answer

Day 3

Answer

Day 8

Answer

Day 14

Question 8

What is the best agent for premenstrual syndrome management?

Accepted Answer

SSRI

Answer

Progesterone

Answer

Anxiolytics

Answer

Vitamin E

Question 9

A patient presents with a history of amenorrhea and hirsutism. Ultrasound of the ovary is provided. What is the most likely diagnosis?

Accepted Answer

Polycystic Ovary Syndrome (PCOS)

Answer

Endometriosis

Answer

Choriocarcinoma

Answer

Adenomyosis

Question 10

A 16-year-old female has not yet started having menstrual cycles. Her secondary sex characteristics appear normal, as does external examination of her genitalia. She is given an intramuscular injection of progesterone, and 5 days later she has her first period. What is the most likely mechanism responsible for the delay in menses?

Accepted Answer

A normal constitutional delay in menarche

Answer

Hypoestrogenism

Answer

Hypopituitarism

Answer

An end-organ abnormality

Reproductive Endocrinology — MCQs

Reproductive Endocrinology — MCQs

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