Reproductive Endocrinology — MCQs

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?

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What is the Spinnbarkeit phenomenon?

Reproductive Endocrinology Indian Medical PG Practice Questions and MCQs

Question 181: What is true about pure gonadal dysgenesis, except?

A. Dysgenetic ovaries
B. Decreased height (Correct Answer)
C. Delayed puberty
D. Primary amenorrhea

Explanation: **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).

Question 182: What are the typical levels of sex hormone-binding globulin in Polycystic Ovary Syndrome (PCOS)?

A. Increased
B. Decreased (Correct Answer)
C. Unchanged
D. Variable

Explanation: **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.

Question 183: Which of the following statements is true regarding androgen insensitivity syndrome?

A. A vagina is formed
B. Karyotype is XX
C. Karyotype is XY (Correct Answer)
D. Pubic hair is normally present

Explanation: **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).

Question 184: 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?

A. 1 in 1
B. 1 in 2
C. 1 in 3 (Correct Answer)
D. 1 in 4

Explanation: ### Explanation **1. Why the Correct Answer (C) is Right:** In a Robertsonian translocation involving chromosome 21 and another acrocentric chromosome (e.g., 14), the carrier mother has 45 chromosomes. During meiosis, the translocated chromosome (14;21) and the normal chromosomes (14 and 21) can segregate in six possible gametic combinations. However, only **three** result in potentially viable pregnancies: 1. **Normal:** One normal 14 and one normal 21. 2. **Balanced Carrier:** One translocated (14;21) chromosome. 3. **Trisomy 21 (Down Syndrome):** One translocated (14;21) chromosome plus a normal 21. The other three combinations (Monosomy 21, Monosomy 14, and Trisomy 14) are lethal and result in early spontaneous abortion. Therefore, among the **viable** gametes, the theoretic risk of functional trisomy 21 is **1 in 3**. **2. Why the Incorrect Options are Wrong:** * **Option A (1 in 1):** This occurs only if the translocation is **21;21 (homologous)**. In that case, 100% of surviving offspring would have Down Syndrome because the gamete will always contain either two 21s or none. * **Option B (1 in 2):** This does not account for the balanced carrier state or the elimination of non-viable monosomic/trisomic zygotes. * **Option D (1 in 4):** This is a common distractor based on simple Mendelian inheritance, but it fails to account for the specific segregation patterns of acrocentric translocations. **3. NEET-PG High-Yield Pearls:** * **Theoretical vs. Actual Risk:** While the *theoretical* risk is 1 in 3 (33%), the *actual* clinical risk for a female carrier is approximately **10–15%** and for a male carrier is only **1–2%** (due to selective disadvantage of abnormal sperm). * **Most Common Translocation:** The most common Robertsonian translocation is **13;14**. * **Down Syndrome Etiology:** 95% are due to meiotic non-disjunction, 3-4% due to Robertsonian translocation, and 1-2% due to mosaicism. * **Recurrence Risk:** Unlike non-disjunction (related to maternal age), translocation Down Syndrome has a high recurrence risk, necessitating parental karyotyping.

Question 185: Corpus lutein cyst occurs due to:

A. HOG (Correct Answer)
B. HPL
C. Estrogen
D. Progesterone

Explanation: **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.

Question 186: What percentage of patients with Polycystic Ovary Syndrome (PCOS) also have diabetes mellitus?

A. 50%
B. 30%
C. 20%
D. 10% (Correct Answer)

Explanation: **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.

Question 187: Polycystic ovarian disease is associated with which of the following conditions?

A. Ovarian cancer
B. Endometrial carcinoma (Correct Answer)
C. Congenital adrenal hyperplasia
D. Vaginal carcinoma

Explanation: **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.

Question 188: All are true about ectopic pregnancy EXCEPT:

A. The most common cause is pelvic inflammatory disease.
B. It can be diagnosed by human chorionic gonadotropin (hCG) levels.
C. A negative pregnancy test excludes the diagnosis. (Correct Answer)
D. Methotrexate is used as a part of medical management.

Explanation: **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.

Question 189: 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?

A. Oral contraceptive pills (Correct Answer)
B. Corticosteroids
C. GnRH analog
D. Wedge resection of ovary

Explanation: ### Explanation **Diagnosis:** The clinical presentation of obesity, acne, hirsutism, and an elevated **LH:FSH ratio (4:1)** is classic for **Polycystic Ovary Syndrome (PCOS)**. The normal DHEAS level helps rule out adrenal causes of hyperandrogenism. **1. Why Oral Contraceptive Pills (OCPs) are the Correct Choice:** OCPs are the **first-line treatment** for PCOS in women not seeking pregnancy. They address the condition through three mechanisms: * **Cycle Regulation:** Progestin induces regular shedding of the endometrium, preventing endometrial hyperplasia. * **Suppression of LH:** By providing negative feedback, OCPs decrease LH secretion, which in turn reduces ovarian androgen production. * **Increased SHBG:** The estrogen component increases **Sex Hormone Binding Globulin (SHBG)**, which binds free testosterone, thereby improving acne and hirsutism. **2. Why Other Options are Incorrect:** * **B. Corticosteroids:** These are used for Congenital Adrenal Hyperplasia (CAH). Since DHEAS is normal, an adrenal source is unlikely. * **C. GnRH Analogs:** While they suppress the pituitary-ovarian axis, they are not first-line due to side effects (bone loss, vasomotor symptoms) and are typically reserved for severe, refractory cases. * **D. Wedge Resection:** This is an obsolete surgical procedure due to the high risk of pelvic adhesions. Laparoscopic Ovarian Drilling (LOD) is the modern surgical alternative, but only for infertility cases resistant to Clomiphene. **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 >2:1 or 3:1 in PCOS. * **Gold Standard for Hirsutism:** OCPs + Spironolactone (if OCPs alone are insufficient after 6 months). * **Metabolic Risk:** PCOS is strongly associated with **Insulin Resistance**; Metformin is used if glucose intolerance is present, but OCPs remain first-line for menstrual and androgenic symptoms.

Question 190: What is the Spinnbarkeit phenomenon?

A. Elasticity of cervical mucus (Correct Answer)
B. Clue cells of cervical mucosa
C. Vaginal secretions with numerous leucocytes
D. Dependent on serum progesterone

Explanation: **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.

Practice by Chapter

Hypothalamic-Pituitary-Ovarian Axis

Practice Questions

Disorders of Puberty

Practice Questions

Hirsutism and Virilization

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Primary Ovarian Insufficiency

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Hyperprolactinemia

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Hyperandrogenism

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Metabolic Dysfunction in PCOS

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Neuroendocrine Disorders and Reproduction

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Hormonal Evaluation and Testing

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Ovulation Induction

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