Reproductive Endocrinology Practice Questions

Q: What is true about pure gonadal dysgenesis, except?

Decreased height. **Explanation:** The key to answering this question lies in differentiating **Pure Gonadal Dysgenesis (PGD)** from **Turner Syndrome (45,XO)**. 1. **Why "Decreased height" is the correct answer (the exception):** In Pure Gonadal Dysgenesis (such as **Swyer Syndrome, 46,XY** or **46,XX PGD**), patients typically have a **normal or even tall stature**. Short stature in gonadal dysgenesis is specifically linked to the loss of the **SHOX gene** located on the short arm of the X chromosome. Since patients with PGD have a normal karyotype (46,XX or 46,XY) and do not have the 45,XO chromosomal deletion, they do not exhibit the skeletal abnormalities or short stature characteristic of Turner Syndrome. 2. **Analysis of other options:** * **Dysgenetic ovaries:** By definition, gonadal dysgenesis involves the failure of the gonads to develop properly, resulting in "streak gonads" (fibrous tissue without germ cells). * **Delayed puberty & Primary amenorrhea:** Because the ovaries are dysgenetic, there is a lack of estrogen production. This leads to a failure of secondary sexual characteristic development (delayed puberty) and a failure to initiate menstruation (primary amenorrhea). **NEET-PG High-Yield Pearls:** * **Swyer Syndrome (46,XY PGD):** These patients have a female phenotype but carry a Y chromosome. They have a **high risk (approx. 25-30%) of developing gonadoblastoma**; therefore, prophylactic gonadectomy is indicated. * **Hormonal Profile:** Both Turner and PGD present with **Hypergonadotropic Hypogonadism** (High FSH/LH, Low Estrogen). * **Müllerian Structures:** In both Turner and Swyer syndrome, the uterus and fallopian tubes are **present** because there is no functional testicular tissue to produce Anti-Müllerian Hormone (AMH).

Q: What are the typical levels of sex hormone-binding globulin in Polycystic Ovary Syndrome (PCOS)?

Decreased. **Explanation:** In Polycystic Ovary Syndrome (PCOS), the level of **Sex Hormone-Binding Globulin (SHBG)** is typically **decreased**. **1. Why the correct answer (B) is right:** The primary driver for decreased SHBG in PCOS is **Hyperinsulinemia** (due to insulin resistance). High levels of insulin directly inhibit the hepatic synthesis of SHBG. Additionally, the **Hyperandrogenism** characteristic of PCOS further suppresses SHBG production in the liver. * **Clinical Consequence:** When SHBG levels fall, the "bound" fraction of testosterone decreases, leading to a significant rise in **Free Testosterone** (the biologically active form). This explains why a patient may have severe hirsutism even if their total testosterone levels are only mildly elevated. **2. Why incorrect options are wrong:** * **A. Increased:** SHBG increases in states of high estrogen (e.g., pregnancy, OCP use) or hyperthyroidism. In PCOS, the hyperinsulinemic state overrides any estrogenic effect on the liver. * **C & D. Unchanged/Variable:** SHBG reduction is a consistent biochemical hallmark of PCOS and serves as a key link between metabolic dysfunction and clinical hyperandrogenism. **High-Yield Clinical Pearls for NEET-PG:** * **The "Vicious Cycle":** Low SHBG → ↑ Free Androgens → ↑ Abdominal Adiposity → ↑ Insulin Resistance → ↓ SHBG. * **Diagnostic Utility:** The **Free Androgen Index (FAI)**, calculated as *(Total Testosterone / SHBG) x 100*, is a more sensitive marker for PCOS than total testosterone alone. * **Treatment Effect:** Combined Oral Contraceptive Pills (COCPs) are used in PCOS because the estrogen component **increases SHBG**, thereby lowering free testosterone and improving hirsutism.

Q: Which of the following statements is true regarding androgen insensitivity syndrome?

Karyotype is XY. **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. 1. **Why Option C is Correct:** Individuals with AIS have a **46, XY karyotype**. Because the SRY gene is present, testes develop intra-abdominally and produce normal male levels of testosterone and Anti-Müllerian Hormone (AMH). However, because the body cannot respond to androgens, the external phenotype develops as female. 2. **Why the Other Options are Incorrect:** * **Option A:** In AIS, AMH is produced by the testes, which causes regression of Müllerian structures (uterus, fallopian tubes, and upper 1/3 of the vagina). Therefore, the **vagina is short and blind-ending** (only the lower 2/3, derived from the urogenital sinus, is present). * **Option B:** The karyotype is **XY**, not XX. This distinguishes it from Müllerian Agenesis (Mayer-Rokitansky-Küster-Hauser syndrome), which presents similarly but with a 46, XX karyotype. * **Option D:** **Pubic and axillary hair are absent or scanty**. This is a hallmark clinical sign because the development of sexual hair is dependent on androgen action on hair follicles. **High-Yield Clinical Pearls for NEET-PG:** * **Presentation:** Primary amenorrhea in a phenotypically well-developed female with breast development (due to peripheral conversion of testosterone to estrogen). * **Gonads:** Testes are usually located in the labia majora, inguinal canal, or abdomen. * **Management:** Gonadectomy is performed **after puberty** (to allow natural completion of breast development) to prevent gonadoblastoma/dysgerminoma. * **Key Differentiator:** AIS (Absent hair, XY) vs. MRKH (Normal hair, XX).

Q: Corpus lutein cyst occurs due to:

HOG. **Explanation:** The correct answer is **hCG (Human Chorionic Gonadotropin)**. (Note: "HOG" in the question is a common typographical error for hCG in medical entrance exams). **Why hCG is correct:** The corpus luteum is formed from the ovarian follicle after ovulation. In a non-pregnant cycle, it regresses after 12–14 days. However, if pregnancy occurs, the syncytiotrophoblast of the developing embryo secretes **hCG**. hCG is structurally similar to Luteinizing Hormone (LH) and acts on the LH receptors of the corpus luteum to maintain it and stimulate progesterone production. A **Corpus Luteum Cyst** (specifically the *Theca Lutein Cyst*) occurs due to hypersensitivity or abnormally high levels of hCG, which causes overstimulation and cystic enlargement of the luteal cells. **Why other options are incorrect:** * **HPL (Human Placental Lactogen):** Produced by the placenta, its primary role is regulating maternal metabolism (anti-insulin effect) to ensure nutrient supply to the fetus; it has no luteotropic effect. * **Estrogen:** While produced by the corpus luteum, it does not cause the formation of the cyst; rather, it is a product of the follicular and luteal phases. * **Progesterone:** This is the primary hormone secreted *by* the corpus luteum to maintain the endometrium. It is the result of luteal activity, not the cause of cyst formation. **High-Yield Clinical Pearls for NEET-PG:** * **Theca Lutein Cysts** are classically associated with conditions of high hCG: **Gestational Trophoblastic Disease (Hydatidiform Mole)**, multiple pregnancies, and Ovulation Induction (OHSS). * They are usually **bilateral**, multiple, and disappear spontaneously once the source of hCG is removed. * **Luteoma of Pregnancy:** A benign tumor-like condition (not a true cyst) that can cause maternal virilization; also driven by hCG.

Q: What percentage of patients with Polycystic Ovary Syndrome (PCOS) also have diabetes mellitus?

10%. **Explanation:** Polycystic Ovary Syndrome (PCOS) is fundamentally a metabolic disorder characterized by insulin resistance and hyperinsulinemia. While approximately **50–70%** of women with PCOS exhibit insulin resistance, the progression to overt Type 2 Diabetes Mellitus (T2DM) occurs in a smaller subset. According to standard textbooks (like Williams Gynecology) and epidemiological studies, roughly **10%** of women with PCOS are diagnosed with Type 2 Diabetes by age 40. **Analysis of Options:** * **D (10%) - Correct:** This represents the prevalence of overt Diabetes Mellitus in the PCOS population. It is a high-yield figure often tested to differentiate between "impaired glucose tolerance" and "frank diabetes." * **B & C (30% & 20%):** These figures are more representative of the prevalence of **Impaired Glucose Tolerance (IGT)** or "Prediabetes" in PCOS patients, which is significantly more common than overt diabetes. * **A (50%):** This percentage correlates with the prevalence of **Metabolic Syndrome** or general **Insulin Resistance** in the PCOS population, rather than a diagnosis of diabetes itself. **Clinical Pearls for NEET-PG:** * **Screening:** All women diagnosed with PCOS should undergo a **75g Oral Glucose Tolerance Test (OGTT)**, as fasting glucose alone often misses the diagnosis. * **Risk Factor:** The risk of T2DM in PCOS is independent of, but exacerbated by, obesity. * **Gold Standard:** The Hyperinsulinemic-euglycemic clamp is the gold standard for measuring insulin resistance, though HOMA-IR is more commonly used in research. * **Management:** Metformin is the insulin sensitizer of choice, though lifestyle modification remains the first-line treatment for metabolic complications.

Q: Polycystic ovarian disease is associated with which of the following conditions?

Endometrial carcinoma. **Explanation:** Polycystic Ovarian Syndrome (PCOS) is characterized by chronic anovulation, which leads to a state of **unopposed estrogen**. In a normal menstrual cycle, ovulation is followed by the production of progesterone, which stabilizes and eventually sheds the endometrium. In PCOS, the lack of ovulation means progesterone is not produced, leaving the endometrium exposed to continuous estrogenic stimulation. This results in endometrial hyperplasia, which significantly increases the long-term risk of **Endometrial Carcinoma** (specifically Type I, endometrioid adenocarcinoma). **Analysis of Options:** * **A. Ovarian cancer:** While some studies suggest a marginal increase in risk, the association is not as strong or direct as that with endometrial cancer. In fact, the use of Combined Oral Contraceptive Pills (COCPs) to treat PCOS actually *reduces* the risk of ovarian cancer. * **C. Congenital adrenal hyperplasia (CAH):** Non-classic CAH is a **differential diagnosis** for PCOS (as it presents with similar hyperandrogenism), but it is not caused by or "associated" with PCOS as a complication. * **D. Vaginal carcinoma:** There is no known pathophysiological link between PCOS and vaginal malignancy. **NEET-PG High-Yield Pearls:** * **The "PCOS Triad":** Hyperandrogenism, Ovulatory dysfunction, and Polycystic ovaries on ultrasound (Rotterdam Criteria). * **Metabolic Risks:** PCOS is strongly associated with Insulin Resistance, Type 2 Diabetes Mellitus, and Metabolic Syndrome. * **LH:FSH Ratio:** Classically >2:1 or 3:1 (though no longer a primary diagnostic criterion). * **Protective Factor:** Cyclic progestogens or COCPs are prescribed in PCOS specifically to induce withdrawal bleeds and protect the endometrium from hyperplasia.

Q: All are true about ectopic pregnancy EXCEPT:

A negative pregnancy test excludes the diagnosis.. **Explanation:** The correct answer is **C (A negative pregnancy test excludes the diagnosis)** because this statement is clinically inaccurate. While a urine pregnancy test (UPT) is highly sensitive, it has a threshold (usually 20–25 mIU/mL). In cases of chronic ectopic pregnancy or very early gestations, the hCG levels may fall below this threshold, leading to a "false negative" UPT. Therefore, a negative urine test cannot 100% exclude an ectopic pregnancy; a serum beta-hCG test is the gold standard for confirmation. **Analysis of other options:** * **Option A:** Pelvic Inflammatory Disease (PID), specifically caused by *Chlamydia trachomatis*, is the **most common risk factor** because it causes tubal scarring and cilia dysfunction. * **Option B:** Serial hCG levels are crucial for diagnosis. In a normal pregnancy, hCG doubles every 48 hours; a suboptimal rise (less than 35-53%) suggests an ectopic or failing intrauterine pregnancy. * **Option D:** Methotrexate (a folate antagonist) is the standard medical management for hemodynamically stable patients meeting specific criteria (e.g., hCG <5000 mIU/mL, no fetal heart tone, mass <4cm). **High-Yield Clinical Pearls for NEET-PG:** * **Most common site:** Ampulla of the Fallopian tube (70%). * **Most common site for rupture:** Isthmus (due to narrow lumen). * **Discriminatory Zone:** The serum hCG level (usually 1500–2000 mIU/mL) at which a gestational sac should be visible on Transvaginal Sonography (TVS). If hCG is above this and the uterus is empty, suspect ectopic pregnancy. * **Arias-Stella Reaction:** Hypersecretory endometrium seen on biopsy, which is suggestive of pregnancy but not specific to ectopic.

Q: What is the Spinnbarkeit phenomenon?

Elasticity of cervical mucus. **Explanation:** The **Spinnbarkeit phenomenon** refers to the elasticity or "stretchability" of cervical mucus. This physiological change is a hallmark of the **periovulatory phase** (late follicular phase) of the menstrual cycle. **1. Why Option A is correct:** Under the influence of peak **estrogen** levels just before ovulation, the cervical mucus becomes thin, clear, watery, and highly elastic. This elasticity allows the mucus to be stretched into a long thread (usually 8–12 cm) between two glass slides or fingers. This change facilitates sperm penetration and survival, serving as a clinical marker for the "fertile window." **2. Why the other options are incorrect:** * **Option B:** Clue cells are epithelial cells covered with bacteria (*Gardnerella vaginalis*), a diagnostic feature of **Bacterial Vaginosis**, not a property of mucus elasticity. * **Option C:** Vaginal secretions with numerous leukocytes indicate an inflammatory or infectious process (e.g., Trichomoniasis or Cervicitis), whereas ovulatory mucus is typically acellular. * **Option D:** The Spinnbarkeit phenomenon is **estrogen-dependent**. Progesterone, dominant in the luteal phase, makes the mucus thick, tacky, and non-elastic, effectively "plugging" the cervix. **3. High-Yield Clinical Pearls for NEET-PG:** * **Ferning Pattern:** Estrogen causes the crystallization of sodium chloride in cervical mucus, creating a "fern-like" pattern under the microscope. * **Insler Score:** A clinical scoring system (0-12) used to assess the quality of cervical mucus (volume, Spinnbarkeit, ferning, and cervical os appearance) to predict ovulation. * **Progesterone Effect:** Post-ovulation, the mucus becomes thick (low Spinnbarkeit) and loses the ferning pattern, which is a sign that ovulation has occurred.

Question 1

What is true about pure gonadal dysgenesis, except?

Accepted Answer

Decreased height

Answer

Dysgenetic ovaries

Answer

Delayed puberty

Answer

Primary amenorrhea

Question 2

What are the typical levels of sex hormone-binding globulin in Polycystic Ovary Syndrome (PCOS)?

Accepted Answer

Decreased

Answer

Increased

Answer

Unchanged

Answer

Variable

Question 3

Which of the following statements is true regarding androgen insensitivity syndrome?

Accepted Answer

Karyotype is XY

Answer

A vagina is formed

Answer

Karyotype is XX

Answer

Pubic hair is normally present

Question 4

A 20-year-old woman has a Robertsonian translocation involving chromosome 21 and a second acrocentric chromosome. What is the theoretic likelihood of a functional trisomy 21 if one of her ova is fertilized by a normal sperm?

Accepted Answer

1 in 3

Answer

1 in 1

Answer

1 in 2

Answer

1 in 4

Question 5

Corpus lutein cyst occurs due to:

Accepted Answer

HOG

Answer

HPL

Answer

Estrogen

Answer

Progesterone

Question 6

What percentage of patients with Polycystic Ovary Syndrome (PCOS) also have diabetes mellitus?

Accepted Answer

10%

Answer

50%

Answer

30%

Answer

20%

Question 7

Polycystic ovarian disease is associated with which of the following conditions?

Accepted Answer

Endometrial carcinoma

Answer

Ovarian cancer

Answer

Congenital adrenal hyperplasia

Answer

Vaginal carcinoma

Question 8

All are true about ectopic pregnancy EXCEPT:

Accepted Answer

A negative pregnancy test excludes the diagnosis.

Answer

The most common cause is pelvic inflammatory disease.

Answer

It can be diagnosed by human chorionic gonadotropin (hCG) levels.

Answer

Methotrexate is used as a part of medical management.

Question 9

A 22-year-old obese woman presents with facial acne and hirsutism. Her serum LH level is 36 mIU/mL and FSH is 9 mIU/mL. Androstenedione and testosterone levels are mildly elevated, but serum DHEAS is normal. The patient does not wish to conceive at this time. Which of the following is the most appropriate treatment for her condition?

Accepted Answer

Oral contraceptive pills

Answer

Corticosteroids

Answer

GnRH analog

Answer

Wedge resection of ovary

Question 10

What is the Spinnbarkeit phenomenon?

Accepted Answer

Elasticity of cervical mucus

Answer

Clue cells of cervical mucosa

Answer

Vaginal secretions with numerous leucocytes

Answer

Dependent on serum progesterone

Reproductive Endocrinology — MCQs

Reproductive Endocrinology — MCQs

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