Reproductive Endocrinology Practice Questions

Q: Which of the following is true about Polycystic Ovarian Disease (PCOD)?

Hirsutism, oligomenorrhea, and hypertension. **Explanation:** Polycystic Ovarian Disease (PCOD/PCOS) is a complex endocrine disorder characterized by the classic triad of **hyperandrogenism, ovulatory dysfunction, and metabolic disturbances.** **Why Option C is Correct:** 1. **Hirsutism:** This is the clinical manifestation of hyperandrogenism (excessive terminal hair growth in a male-pattern distribution). It is a hallmark feature of PCOD. 2. **Oligomenorrhea:** Chronic anovulation leads to infrequent menstrual cycles (oligomenorrhea) or total absence of periods (amenorrhea). 3. **Hypertension:** PCOD is strongly associated with **Metabolic Syndrome**. Insulin resistance leads to hyperinsulinemia, which increases sympathetic activity and sodium retention, frequently resulting in hypertension and an increased risk of cardiovascular disease. **Analysis of Incorrect Options:** * **Options A & B:** While these contain correct elements, they are incomplete. Option C represents the most comprehensive clinical picture of the systemic nature of the disease. * **Option D (Polymenorrhea):** This refers to frequent menstrual cycles (intervals <21 days). PCOD is characterized by delayed cycles (Oligomenorrhea) due to the lack of regular ovulation. **NEET-PG High-Yield Pearls:** * **Rotterdam Criteria:** Diagnosis requires 2 out of 3: (1) Clinical/biochemical hyperandrogenism, (2) Oligo/anovulation, (3) Polycystic ovaries on USG ("String of pearls" appearance). * **LH:FSH Ratio:** Classically elevated to **3:1**. * **Gold Standard for Insulin Resistance:** Hyperinsulinemic-euglycemic clamp (though rarely used clinically). * **Drug of Choice:** Combined Oral Contraceptive Pills (OCPs) for cycle regulation; Clomiphene Citrate or Letrozole (current DOC) for infertility; Metformin for insulin resistance.

Q: What are the typical hormonal level changes observed in Polycystic Ovarian Disease (PCOD)?

Testosterone increases. **Explanation:** In Polycystic Ovarian Disease (PCOD/PCOS), the primary endocrine hallmark is **hyperandrogenism**. The correct answer is **Testosterone increases** because the high levels of Luteinizing Hormone (LH) stimulate the ovarian **theca cells** to overproduce androgens (testosterone and androstenedione). This excess testosterone is responsible for clinical features like hirsutism, acne, and male-pattern alopecia. **Analysis of Options:** * **Option A & B (LH/FSH changes):** In PCOD, there is an **increase in LH** and a **decrease or normal level of FSH**. This leads to a characteristic **LH:FSH ratio of >2:1 or 3:1**. LH is elevated due to increased GnRH pulse frequency, while FSH is relatively low, preventing follicular maturation and leading to anovulation. * **Option C (Insulin):** PCOD is strongly associated with **Insulin Resistance**. Consequently, the body compensates by producing more insulin, leading to **Hyperinsulinemia** (not a decrease). High insulin further stimulates theca cells to produce more testosterone and inhibits Sex Hormone Binding Globulin (SHBG) production in the liver, increasing free testosterone levels. **NEET-PG High-Yield Pearls:** * **Gold Standard Diagnosis:** Rotterdam Criteria (requires 2 out of 3: Oligo/anovulation, Hyperandrogenism, and Polycystic ovaries on USG). * **SHBG Levels:** Always **decreased** in PCOD, which increases the "Free Androgen Index." * **Estrogen Status:** There is a state of **chronic hyperestrogenism** (specifically Estrone, E1) due to peripheral conversion of androgens in adipose tissue. This increases the risk of endometrial hyperplasia/carcinoma. * **Metabolic Marker:** Acanthosis nigricans is a clinical sign of underlying insulin resistance.

Q: What is the typical Luteinizing Hormone (LH) to Follicle-Stimulating Hormone (FSH) ratio in women diagnosed with polycystic ovarian disease?

2:01. **Explanation:** In Polycystic Ovarian Syndrome (PCOS), the characteristic endocrine hallmark is an **elevation in the LH:FSH ratio**. This occurs due to an increased frequency and amplitude of Gonadotropin-Releasing Hormone (GnRH) pulses, which preferentially stimulates the anterior pituitary to secrete LH over FSH. 1. **Why 2:1 is correct:** While a ratio of **>2:1 or 3:1** is classically associated with PCOS, the most commonly tested threshold in medical examinations is **2:1**. High LH levels stimulate the ovarian theca cells to produce excess androgens (androstenedione and testosterone). Meanwhile, relatively low FSH levels result in poor follicular recruitment and a failure to convert these androgens into estrogens (via aromatase), leading to follicular atresia and the "necklace appearance" of cysts on ultrasound. 2. **Why other options are incorrect:** * **1:1:** This is the normal physiological ratio during the early follicular phase of a healthy menstrual cycle. * **1:2:** An inversion where FSH is higher than LH is typically seen in states of ovarian failure (Menopause) or Premature Ovarian Insufficiency. * **3:1:** While this ratio is highly suggestive of PCOS, **2:1** is the standard diagnostic benchmark used in most clinical textbooks and NEET-PG patterns. **High-Yield Clinical Pearls for NEET-PG:** * **Rotterdam Criteria:** Diagnosis requires 2 out of 3: (1) Oligo/Anovulation, (2) Hyperandrogenism (Clinical/Biochemical), (3) Polycystic ovaries on USG. * **Gold Standard:** The LH:FSH ratio is **no longer** a mandatory part of the Rotterdam criteria but remains a classic "textbook" biochemical marker. * **Insulin Resistance:** Hyperinsulinemia decreases Sex Hormone Binding Globulin (SHBG), further increasing free testosterone levels.

Q: What is the typical hormonal status in Polycystic Ovarian Disease (PCOD)?

LH Increased, FSH Normal to Low. **Explanation:** In Polycystic Ovarian Disease (PCOD/PCOS), the primary endocrine hallmark is a disruption of the hypothalamic-pituitary-ovarian axis. The correct answer is **A (LH Increased, FSH Normal to Low)**. **Why Option A is Correct:** In PCOS, there is an increase in the **GnRH pulse frequency**, which preferentially stimulates the anterior pituitary to secrete **Luteinizing Hormone (LH)**. High LH levels act on the ovarian theca cells to increase androgen production. Conversely, **Follicle Stimulating Hormone (FSH)** levels remain normal or low due to the negative feedback from high levels of estrone (converted from androgens in peripheral fat) and inhibin. This leads to the characteristic **LH:FSH ratio of >2:1 or 3:1**. **Why Other Options are Incorrect:** * **B (LH Decreased):** LH is characteristically elevated in PCOS, driving hyperandrogenism. * **C (FSH Increased):** FSH is typically low or at the lower end of the normal range. High FSH is seen in Premature Ovarian Failure (POF) or Menopause. * **D (17-OH Progesterone Normal):** While 17-OHP can be normal in PCOS, it is often **mildly elevated** (but <200 ng/dL). This option is less definitive than the LH/FSH imbalance which defines the core pathophysiology. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Rotterdam Criteria (requires 2 out of 3: Oligo/anovulation, Hyperandrogenism, and Polycystic ovaries on USG). * **The "String of Pearls" sign:** Seen on USG (12 or more follicles, 2-9 mm in diameter). * **Metabolic Link:** Hyperinsulinemia and Insulin Resistance are central to the pathogenesis, often leading to Acanthosis Nigricans. * **DOC for Ovulation Induction:** Letrozole (Aromatase inhibitor) is now preferred over Clomiphene Citrate.

Q: A tall adolescent presents with primary amenorrhea. On examination, she has normal breast development, absent axillary and pubic hair, and an inguinal hernia. What is the probable diagnosis?

Androgen insensitivity syndrome. ### Explanation The clinical presentation points toward **Androgen Insensitivity Syndrome (AIS)**, specifically the complete form. **1. Why Androgen Insensitivity Syndrome (AIS) is correct:** AIS is an X-linked recessive condition where a genotypic male (46, XY) has a functional mutation in the androgen receptor. * **Breast development:** Occurs because the testes produce testosterone, which is peripherally converted to estrogen (aromatization). * **Absent hair:** Axillary and pubic hair growth is dependent on androgen action; since receptors are non-functional, hair is absent or sparse. * **Inguinal hernia:** This is a classic sign in AIS, representing the undescended testes (cryptorchidism) located in the inguinal canal. * **Tall stature:** Due to the presence of the Y chromosome and the lack of androgen-mediated epiphyseal closure. **2. Why other options are incorrect:** * **Complete Gonadal Dysgenesis (Swyer Syndrome):** These patients have a 46, XY karyotype but streak gonads. They lack estrogen, so they present with **no breast development** (sexual infantilism). * **MRKH Syndrome:** These are genotypic females (46, XX) with normal ovaries. They have **normal pubic and axillary hair** because their androgen receptors function normally. * **Congenital Adrenal Hyperplasia (CAH):** This typically presents with ambiguous genitalia and **virilization** (excess hair/clitoromegaly) in females, not normal breast development with absent hair. **3. NEET-PG High-Yield Pearls:** * **AIS vs. MRKH:** The most common "differentiating" factor in exams is **hair distribution** (Absent in AIS, Normal in MRKH) and **Karyotype** (46, XY in AIS, 46, XX in MRKH). * **Management of AIS:** Gonadectomy is performed **after puberty** to allow for natural breast development (via aromatization), followed by estrogen replacement to prevent osteoporosis. * **Vagina:** In both AIS and MRKH, the vagina is a short, blind-ended pouch.

Q: Which statement is true regarding Androgen Insensitivity Syndrome?

Phenotype may be completely female.. **Explanation:** **Androgen Insensitivity Syndrome (AIS)**, formerly known as Testicular Feminization Syndrome, is an X-linked recessive condition where a mutation in the androgen receptor gene prevents target tissues from responding to testosterone. 1. **Why Option A is correct:** In **Complete AIS (CAIS)**, the body is entirely unresponsive to androgens. Despite having a 46,XY karyotype and functioning testes, the external genitalia develop along female lines due to the default pathway. At puberty, peripheral conversion of testosterone to estrogen leads to breast development (thelarche), resulting in a **completely female phenotype**, though they lack internal female pelvic organs. 2. **Why other options are incorrect:** * **Option B:** The gonads are **testes**, not ovaries. SRY gene expression on the Y chromosome ensures testicular development. * **Option C:** It affects **genotypic males (46,XY)**. While the phenotype is female, the genetic sex is male. * **Option D:** The **testes are formed normally** (producing normal/high levels of testosterone and Anti-Müllerian Hormone); the defect lies in the **androgen receptors**, which are either absent or non-functional. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Presentation:** Primary amenorrhea in a tall, well-developed female with scant/absent pubic and axillary hair (due to androgen resistance). * **Internal Anatomy:** Vagina is short/blind-ending. Uterus, fallopian tubes, and upper 1/3 of the vagina are **absent** due to normal AMH production by the testes. * **Management:** Gonadectomy is performed **after puberty** (to allow natural completion of growth and breast development) to prevent gonadoblastoma/dysgerminoma. * **Differential:** In **Müllerian Agenesis (MRKH)**, pubic hair is normal and ovaries are present (46,XX).

Question 1

Menstruation is defined as precocious if it starts before the child reaches the age of:

Accepted Answer

10 years

Answer

8 years

Answer

14 years

Answer

20 years

Question 2

Which of the following statements regarding insulin resistance in women with PCOS is false?

Accepted Answer

Although insulin resistance is highly prevalent in PCOS, progression to type 2 diabetes is uncommon.

Answer

Both lean and obese women with PCOS can exhibit insulin resistance.

Answer

Beta-cell dysfunction, independent of obesity, can be observed in PCOS.

Answer

Acanthosis nigricans and skin tags are dermatologic manifestations of insulin resistance.

Question 3

Which of the following is true about Polycystic Ovarian Disease (PCOD)?

Accepted Answer

Hirsutism, oligomenorrhea, and hypertension

Answer

Hirsutism and hypertension

Answer

Oligomenorrhea and hypertension

Answer

Polymenorrhea

Question 4

What are the typical hormonal level changes observed in Polycystic Ovarian Disease (PCOD)?

Accepted Answer

Testosterone increases

Answer

Luteinizing Hormone (LH) decreases

Answer

Luteinizing Hormone (LH) increases, Follicle-Stimulating Hormone (FSH) increases

Answer

Insulin decreases

Question 5

What is the typical Luteinizing Hormone (LH) to Follicle-Stimulating Hormone (FSH) ratio in women diagnosed with polycystic ovarian disease?

Accepted Answer

2:01

Answer

1:02

Answer

1:01

Answer

3:01

Question 6

A patient presents with amenorrhea and galactorrhea, and has elevated prolactin levels. She is not pregnant. In addition to evaluating for a prolactinoma, what other investigations can assess the cause of hyperprolactinemia?

Accepted Answer

Thyrotropin-releasing hormone (TRH) stimulation test

Answer

Corticotropin-releasing hormone (CRH) stimulation test

Answer

Dopamine challenge test

Answer

Histamine type II receptor antagonist challenge

Question 7

Withdrawal bleeding occurs when progestin is administered continuously?

Accepted Answer

Estrogen concentration is sufficient

Answer

Structural abnormality in the pelvis

Answer

Associated with endocrine disorder

Answer

Atrophic endometrium

Question 8

What is the typical hormonal status in Polycystic Ovarian Disease (PCOD)?

Accepted Answer

LH Increased, FSH Normal to Low

Answer

LH Decreased

Answer

FSH Increased

Answer

17 OH Progesterone Normal

Question 9

A tall adolescent presents with primary amenorrhea. On examination, she has normal breast development, absent axillary and pubic hair, and an inguinal hernia. What is the probable diagnosis?

Accepted Answer

Androgen insensitivity syndrome

Answer

Complete gonadal dysgenesis

Answer

Mayer-Rokitansky-Küster-Hauser syndrome

Answer

Congenital adrenal hyperplasia

Question 10

Which statement is true regarding Androgen Insensitivity Syndrome?

Accepted Answer

Phenotype may be completely female.

Answer

There is a predominant ovarian component in the gonads.

Answer

It always affects females.

Answer

Testes are formed abnormally and receptors are normal.

Reproductive Endocrinology — MCQs

Reproductive Endocrinology — MCQs

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