Reproductive Endocrinology — MCQs

Reproductive Endocrinology Indian Medical PG Practice Questions and MCQs

Question 111: Menarche usually occurs how much time after thelarche?

A. 1 year
B. 2 years (Correct Answer)
C. 6 months
D. 4 years

Explanation: **Explanation:** The sequence of female pubertal development follows a predictable chronological order, typically initiated by the activation of the HPO (Hypothalamic-Pituitary-Ovarian) axis. **1. Why Option B is Correct:** Thelarche (breast bud development) is usually the first clinical sign of puberty, occurring under the influence of rising estrogen levels (typically around age 10). **Menarche** (the onset of menstruation) is a late event in the pubertal sequence. On average, menarche occurs **2 to 2.5 years after thelarche**. By this time, the estrogen levels have sufficiently stimulated the endometrial lining to undergo shedding. **2. Why Other Options are Incorrect:** * **Option A (1 year):** This is too early. While the interval can vary, the physiological maturation required for the first menses generally takes longer than 12 months. * **Option C (6 months):** This is incorrect as the peak height velocity (PHV) usually occurs between thelarche and menarche, requiring more time for the hormonal milieu to stabilize. * **Option D (4 years):** If menarche has not occurred within 3 years of thelarche (or by age 15), it is clinically defined as primary amenorrhea and warrants investigation. **3. NEET-PG High-Yield Pearls:** * **Sequence of Puberty (Mnemonic: T-P-A-M):** 1. **T**helarche (Breast development - earliest sign) 2. **P**ubarche (Pubic hair development) 3. **A**daxarche/Growth Spurt (Peak Height Velocity) 4. **M**enarche (Last major event) * **Precocious Puberty:** Development of secondary sexual characteristics before age 8. * **Delayed Puberty:** No thelarche by age 13 or no menarche by age 15. * **Growth Spurt:** In girls, the peak height velocity occurs *before* menarche (Tanner Stage 2-3). Once menarche occurs, only about 2.5–5 cm of additional height is gained.

Question 112: Which of the following is true of testicular feminization syndrome?

A. Testes are present
B. Female habitus
C. XY genotype
D. Uterus is present (Correct Answer)

Explanation: **Explanation:** **Testicular Feminization Syndrome**, now more commonly known as **Complete Androgen Insensitivity Syndrome (CAIS)**, is a condition where a genetic male (46, XY) has a total resistance to androgen action due to a mutation in the androgen receptor gene. **Why the "Correct" Answer is actually the "Incorrect" statement (Understanding the Question Logic):** In NEET-PG and similar exams, questions often ask for the "True" statement, but based on the options provided, this specific question is likely asking which of the following is **NOT** true (a common source of confusion in older question banks). * **The Fact:** In CAIS, the **uterus is absent**. * **The Mechanism:** The testes are present (intra-abdominal or inguinal) and secrete **Anti-Müllerian Hormone (AMH)**. AMH causes the regression of Müllerian structures (uterus, fallopian tubes, and upper 1/3rd of the vagina). Therefore, a patient with CAIS will have a blind-ending vaginal pouch and no uterus. **Analysis of Other Options:** * **A. Testes are present:** True. Testes develop because the SRY gene on the Y chromosome is functional. * **B. Female habitus:** True. Due to androgen resistance, the body follows the default female pathway. Peripheral conversion of testosterone to estrogen leads to breast development (often excellent) and female body contours. * **C. XY genotype:** True. These individuals are genetically male (46, XY). **High-Yield Clinical Pearls for NEET-PG:** 1. **Presentation:** Primary amenorrhea in a girl with well-developed breasts but **absent/scanty axillary and pubic hair** (due to androgen insensitivity). 2. **Karyotype:** 46, XY. 3. **Gonads:** Risk of malignancy (Gonadoblastoma/Dysgerminoma) is 2-5%; gonadectomy is recommended **after puberty** to allow for natural breast development. 4. **Differential Diagnosis:** In **Müllerian Agenesis (MRKH Syndrome)**, the karyotype is 46, XX, and pubic/axillary hair is normal.

Question 113: A 35-year-old mother of two children, aged 5 and 6 years, has had amenorrhea and galactorrhea for the past 12 months. Her serum prolactin level is 450 ng/ml. What is the most likely diagnosis?

A. Menopause
B. Pituitary adenoma (Correct Answer)
C. Intraductal papilloma of the breasts
D. Sheehan's syndrome

Explanation: **Explanation:** The clinical presentation of **amenorrhea** and **galactorrhea** (the classic "Amenorrhea-Galactorrhea Syndrome") in a reproductive-age woman is highly suggestive of **Hyperprolactinemia**. Prolactin inhibits the pulsatile release of GnRH from the hypothalamus, leading to low FSH/LH levels and subsequent amenorrhea. **Why Pituitary Adenoma is correct:** The serum prolactin level is the diagnostic key here. While physiological causes (pregnancy, stress) or drugs usually cause mild elevations (<100 ng/ml), a level **>200 ng/ml** is highly specific for a **Prolactinoma** (a pituitary adenoma). A level of 450 ng/ml strongly indicates a macroprolactinoma (>10 mm), necessitating an MRI of the Sella Turcica. **Why other options are incorrect:** * **Menopause:** While it causes amenorrhea, it is characterized by high FSH levels and does not cause galactorrhea or massive prolactin elevation. * **Intraductal papilloma:** This presents with unilateral, bloody nipple discharge from a single duct, without systemic endocrine symptoms like amenorrhea or elevated prolactin. * **Sheehan's syndrome:** This is postpartum pituitary necrosis resulting in *hypopituitarism*. It leads to a failure to lactate (due to prolactin deficiency) and secondary amenorrhea, rather than hyperprolactinemia. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of choice:** Dopamine agonists like **Cabergoline** (preferred due to better efficacy and fewer side effects) or Bromocriptine. * **Hook Effect:** In cases of extremely high prolactin, lab assays may show falsely low levels; serial dilution is required. * **Visual Field Defect:** Large adenomas can compress the optic chiasm, leading to **bitemporal hemianopia**. * **Rule of thumb:** Prolactin >200 ng/ml = Prolactinoma until proven otherwise.

Question 114: A woman with secondary amenorrhea has a negative progesterone challenge test but a positive combined estrogen and progesterone challenge test. What is the probable cause?

A. Ovarian failure (Correct Answer)
B. Polycystic ovarian disease
C. Asherman syndrome
D. Pregnancy

Explanation: This question tests the systematic approach to secondary amenorrhea using hormonal challenge tests. ### **Mechanism & Interpretation** 1. **Negative Progesterone Challenge Test:** This indicates that the withdrawal of progesterone did not result in bleeding. This happens because either the **endometrium was not primed with estrogen** (low estrogen states) or there is an **outflow tract obstruction**. 2. **Positive Combined Estrogen-Progesterone Test:** The administration of exogenous estrogen followed by progesterone resulted in withdrawal bleeding. This confirms that the **outflow tract (uterus and cervix) is patent** and the endometrium is functional. **Conclusion:** Since the uterus is functional but didn't bleed with progesterone alone, the patient lacks endogenous estrogen. In the context of the options provided, **Ovarian Failure** (Premature Ovarian Insufficiency) is the cause of this hypoestrogenic state. ### **Why Other Options are Incorrect** * **Polycystic Ovarian Disease (PCOS):** Characterized by "unopposed estrogen." These patients have a **positive** progesterone challenge test because their endometrium is already primed. * **Asherman Syndrome:** This involves intrauterine adhesions. Patients will have a **negative** combined estrogen-progesterone test because the outflow tract is obstructed or the endometrium is destroyed. * **Pregnancy:** The most common cause of secondary amenorrhea, but it would result in a negative result for both tests (no bleeding). ### **NEET-PG High-Yield Pearls** * **Next Step:** After a positive combined test confirms a functional uterus, the next step is to check **Serum FSH levels** to differentiate between Hypogonadotropic Hypogonadism (Low FSH) and Ovarian Failure (High FSH). * **Step-1 (Progesterone Test):** Uses Medroxyprogesterone acetate (10mg for 5–10 days). * **Step-2 (Combined Test):** Uses Conjugated Estrogen (1.25mg for 21 days) + Progesterone (last 10 days).

Question 115: A 35-year-old mother of two children is suffering from amenorrhea for the last 12 months. She has a history of failure of lactation following her second delivery but remained asymptomatic thereafter. Skull X-ray shows an empty sella. What is the diagnosis?

A. Menopause
B. Pituitary tumor
C. Sheehan's syndrome (Correct Answer)
D. Intraductal papilloma of the breast

Explanation: ### Explanation **Correct Answer: C. Sheehan's syndrome** **Medical Concept:** Sheehan’s syndrome is **postpartum pituitary necrosis** caused by severe obstetric hemorrhage and hypotension. During pregnancy, the pituitary gland enlarges (hypertrophy of lactotrophs), making it highly susceptible to ischemia if blood pressure drops. In this clinical scenario, the key diagnostic clues are: 1. **Failure of lactation:** This is often the earliest sign, indicating a deficiency in Prolactin. 2. **Secondary Amenorrhea:** Indicates a deficiency in Gonadotropins (FSH/LH). 3. **Empty Sella on X-ray:** Over time, the necrotic pituitary tissue is resorbed and replaced by cerebrospinal fluid, leading to an "empty sella" appearance on imaging. --- **Why the other options are incorrect:** * **A. Menopause:** While it causes amenorrhea, it does not explain the failure of lactation following delivery or the radiological finding of an empty sella. Menopause is characterized by high gonadotropins (FSH >40 IU/L). * **B. Pituitary tumor:** A functional tumor (like a Prolactinoma) would typically cause galactorrhea, not a failure of lactation. On X-ray, a tumor would show **sellar enlargement or erosion**, rather than an empty sella. * **D. Intraductal papilloma:** This is a localized breast pathology causing bloody nipple discharge. It has no association with amenorrhea or pituitary imaging findings. --- **NEET-PG High-Yield Pearls:** * **Earliest sign:** Failure of lactation (Prolactin deficiency). * **Most common initial symptom:** Failure to resume menses (Gonadotropin deficiency). * **Most serious complication:** Secondary adrenal insufficiency (ACTH deficiency), which can be life-threatening during stress. * **Gold Standard Investigation:** MRI of the pituitary (shows a small, shrunken gland or empty sella in chronic cases). * **Treatment:** Lifelong hormone replacement therapy (Cortisol, Thyroxine, and Estrogen/Progesterone). Always replace glucocorticoids *before* thyroxine to avoid adrenal crisis.

Question 116: What is true about Swyer syndrome?

A. Gonads are ovaries
B. Mullerian ducts develop normally (Correct Answer)
C. External genitalia appear male
D. Excess testosterone

Explanation: **Explanation:** **Swyer Syndrome (Pure Gonadal Dysgenesis)** is a condition characterized by a **46,XY karyotype** in a phenotypic female. It occurs due to a mutation in the **SRY gene** or other genes involved in testis determination (like SOX9). 1. **Why Option B is correct:** In a normal male fetus, the testes produce **Anti-Müllerian Hormone (AMH)**, which causes the regression of Müllerian structures. In Swyer syndrome, the gonads fail to develop into testes and remain as non-functional **"streak gonads."** Because no testes are formed, no AMH is produced. In the absence of AMH, the Müllerian ducts (uterus, fallopian tubes, and upper vagina) develop normally. 2. **Why other options are incorrect:** * **Option A:** The gonads are not ovaries; they are fibrous **streak gonads** that lack germ cells. * **Option C:** Since there are no functioning testes, there is no testosterone or Dihydrotestosterone (DHT). Without androgens, the default pathway is female; thus, external genitalia appear **completely female**. * **Option D:** There is a **deficiency of testosterone**, not an excess, leading to a lack of secondary sexual characteristics (delayed puberty). **High-Yield Clinical Pearls for NEET-PG:** * **Presentation:** Primary amenorrhea with tall stature (due to delayed epiphyseal closure) and normal female internal/external genitalia. * **Malignancy Risk:** There is a high risk (approx. 30%) of developing **Gonadoblastoma** in the streak gonads. * **Management:** Immediate **prophylactic bilateral gonadectomy** upon diagnosis, followed by Hormone Replacement Therapy (HRT) for secondary sexual characteristics and bone health. * **Fertility:** Patients can achieve pregnancy through **oocyte donation** because they have a functional uterus.

Question 117: Which of the following serum values is not associated with the diagnosis of Polycystic Ovary Syndrome (PCOS)?

A. Elevated LH
B. Rise in oestrone/estradiol level
C. Reduced SHBG level
D. Reduced serum fasting insulin level (Correct Answer)

Explanation: **Explanation** Polycystic Ovary Syndrome (PCOS) is a complex endocrine disorder characterized by hyperandrogenism, ovulatory dysfunction, and metabolic disturbances. **Why Option D is Correct:** The hallmark metabolic feature of PCOS is **Insulin Resistance**. To compensate for the body's decreased sensitivity to insulin, the pancreas produces more insulin, leading to **Hyperinsulinemia**. Therefore, serum fasting insulin levels are typically **elevated**, not reduced. Hyperinsulinemia plays a central role in pathogenesis by stimulating ovarian theca cells to produce androgens and inhibiting the hepatic synthesis of SHBG. **Analysis of Incorrect Options:** * **A. Elevated LH:** In PCOS, there is an increased frequency of GnRH pulses, leading to a preferential secretion of Luteinizing Hormone (LH). This often results in a characteristic **LH:FSH ratio > 2:1 or 3:1**. * **B. Rise in Oestrone/Estradiol:** Peripheral conversion of androstenedione (produced by theca cells) occurs in adipose tissue, leading to elevated **Oestrone (E1)** levels. This "unopposed estrogen" state increases the risk of endometrial hyperplasia. * **C. Reduced SHBG level:** High levels of insulin and androgens suppress the production of **Sex Hormone Binding Globulin (SHBG)** in the liver. Low SHBG levels result in higher concentrations of **Free Testosterone**, which is responsible for clinical hirsutism and acne. **NEET-PG High-Yield Pearls:** * **Rotterdam Criteria (2 of 3):** 1. Clinical/biochemical hyperandrogenism; 2. Oligo/Anovulation; 3. Polycystic ovaries on USG (≥12 follicles or volume >10ml). * **Gold Standard for Insulin Resistance:** Hyperinsulinemic-euglycemic clamp (though rarely used clinically). * **Drug of Choice for Ovulation Induction:** Letrozole (Aromatase inhibitor) is now preferred over Clomiphene Citrate.

Question 118: Persistent untreated anovulation leads to all of the following EXCEPT?

A. Hirsutism
B. Increased risk of cardiovascular disease
C. Increased risk of ovarian tumors (Correct Answer)
D. Increased risk of endometrial carcinoma

Explanation: **Explanation:** The core pathophysiology of persistent anovulation (most commonly seen in Polycystic Ovary Syndrome - PCOS) involves a state of **"unopposed estrogen."** In a normal cycle, ovulation is followed by the formation of the corpus luteum, which produces progesterone. In chronic anovulation, the absence of a corpus luteum means no progesterone is produced to counteract the proliferative effects of estrogen on the endometrium. **Why Option C is the Correct Answer:** Persistent anovulation is actually associated with a **decreased** or neutral risk of epithelial ovarian cancer. According to the "Incessant Ovulation Theory," the repeated scarring and repair of the ovarian surface during ovulation increase the risk of malignancy. Since anovulation prevents this repetitive trauma, it does not increase the risk of ovarian tumors. **Analysis of Incorrect Options:** * **A. Hirsutism:** Anovulation is frequently linked to hyperandrogenism (as seen in PCOS). Elevated LH levels stimulate ovarian theca cells to produce excess androgens, leading to clinical hirsutism. * **B. Cardiovascular Disease:** Chronic anovulation is often part of a metabolic syndrome involving insulin resistance, dyslipidemia, and obesity, all of which significantly increase long-term cardiovascular risk. * **D. Endometrial Carcinoma:** This is a classic association. Unopposed estrogen leads to endometrial hyperplasia, which can progress to adenocarcinoma. **High-Yield Clinical Pearls for NEET-PG:** * **PCOS Triad:** Hyperandrogenism, Anovulation, and Polycystic ovaries on USG (Rotterdam Criteria). * **Protective Factors for Ovarian Cancer:** Pregnancy, Lactation, and OCPs (all of which suppress ovulation). * **Drug of Choice for Ovulation Induction:** Letrozole (Aromatase inhibitor) is now preferred over Clomiphene Citrate.

Question 119: All of the following are indications for the use of Mifepristone, EXCEPT:

A. Abortion
B. Cushing syndrome
C. Postpartum hemorrhage (PPH) (Correct Answer)
D. Cervical ripening

Explanation: **Explanation:** Mifepristone is a potent **synthetic steroid** that acts primarily as a **progesterone receptor antagonist** (and at higher doses, a glucocorticoid receptor antagonist). **Why Postpartum Hemorrhage (PPH) is the correct answer:** Mifepristone is **not** used in the management of PPH. PPH requires uterotonic agents (like Oxytocin, Carboprost, or Misoprostol) to cause uterine contraction. Mifepristone, by blocking progesterone, actually increases uterine sensitivity to prostaglandins but does not provide the immediate, sustained contraction needed to stop acute bleeding. **Analysis of other options:** * **Abortion:** Mifepristone is the drug of choice for medical termination of pregnancy (MTP) up to 7 weeks (often used up to 9-10 weeks) in combination with Misoprostol. It causes decidual necrosis and cervical softening. * **Cushing Syndrome:** Due to its anti-glucocorticoid properties, Mifepristone is FDA-approved for controlling hyperglycemia secondary to hypercortisolism in patients with endogenous Cushing syndrome. * **Cervical Ripening:** It is used for pre-induction cervical ripening and in the management of intrauterine fetal death (IUFD) to facilitate labor induction. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Competitive antagonist at Progesterone (PR-A and PR-B) and Glucocorticoid receptors. * **MTP Protocol:** 200 mg Mifepristone orally, followed 36-48 hours later by 800 mcg Misoprostol (vaginal/sublingual/buccal). * **Other Uses:** Emergency contraception (10 mg dose), management of uterine fibroids (reduces size), and endometriosis. * **Key Contraindication:** Chronic adrenal failure and ectopic pregnancy.

Question 120: Which of the following biochemical changes is NOT seen in established cases of Stein-Leventhal syndrome?

A. Marked elevation of LH in contrast to FSH
B. Insulin resistance
C. Elevation of plasma testosterone
D. Elevation in the level of sex hormone binding globulin (SHBG) (Correct Answer)

Explanation: **Stein-Leventhal Syndrome**, now commonly known as Polycystic Ovary Syndrome (PCOS), is a complex endocrine disorder characterized by hyperandrogenism, ovulatory dysfunction, and metabolic disturbances. ### **Explanation of the Correct Option** **D. Elevation in the level of sex hormone binding globulin (SHBG)** In PCOS, SHBG levels are **decreased**, not elevated. This reduction is primarily driven by hyperinsulinemia and high androgen levels, both of which suppress SHBG production in the liver. Low SHBG is clinically significant because it leads to an increase in the **Free Androgen Index (FAI)**, meaning more testosterone is biologically active in the bloodstream, worsening hirsutism and acne. ### **Analysis of Incorrect Options** * **A. Marked elevation of LH in contrast to FSH:** A classic biochemical hallmark is an **increased LH:FSH ratio** (often >2:1 or 3:1). High GnRH pulse frequency favors LH secretion, while FSH is relatively suppressed by high levels of estrone and inhibin. * **B. Insulin Resistance:** Peripheral insulin resistance and compensatory hyperinsulinemia are central to the pathogenesis of PCOS (seen in both obese and lean phenotypes). Insulin acts synergistically with LH to increase androgen production by theca cells. * **C. Elevation of plasma testosterone:** Hyperandrogenism is a core diagnostic criterion. The ovaries (theca cells) overproduce androstenedione, which is converted to testosterone. ### **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 ultrasound. * **The "Estrone" Factor:** In PCOS, androstenedione is converted to **Estrone (E1)** in peripheral adipose tissue. This chronic "unopposed estrogen" state increases the risk of **Endometrial Hyperplasia/Carcinoma**. * **Gold Standard Treatment for Ovulation Induction:** Letrozole (Aromatase inhibitor) is 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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