Gynecologic Oncology — MCQs

Gynecologic Oncology Indian Medical PG Practice Questions and MCQs

Question 171: Which of the following is the most common type of ovarian tumors?

A. Granulosa cell tumor
B. Serous epithelial tumor (Correct Answer)
C. Mature teratoma
D. Dysgerminoma

Explanation: **Explanation:** Ovarian tumors are classified based on their cell of origin into three main categories: Surface Epithelial Tumors, Germ Cell Tumors, and Sex Cord-Stromal Tumors. **1. Why Serous Epithelial Tumor is correct:** Surface epithelial tumors are the most common type of ovarian neoplasms, accounting for approximately **60–70% of all ovarian tumors** and up to 90% of malignant ones. Among these, **Serous tumors** (both benign serous cystadenoma and malignant serous cystadenocarcinoma) are the most frequent subtype. Serous cystadenomas are the most common benign epithelial tumors, while High-Grade Serous Carcinoma (HGSC) is the most common primary ovarian malignancy. **2. Why other options are incorrect:** * **Granulosa cell tumor:** These are Sex Cord-Stromal tumors. They are rare (approx. 2–5% of ovarian tumors) and are known for producing estrogen, often presenting with postmenopausal bleeding or precocious puberty. * **Mature teratoma (Dermoid cyst):** This is a Germ Cell Tumor. While it is the **most common ovarian tumor in women under 30**, it is less frequent than epithelial tumors in the overall population. * **Dysgerminoma:** This is the most common **malignant** germ cell tumor, typically seen in young women/adolescents, but it represents only about 1% of all ovarian cancers. **High-Yield Clinical Pearls for NEET-PG:** * **Most common overall:** Serous Epithelial Tumor. * **Most common benign tumor in young females (<30 yrs):** Mature Cystic Teratoma. * **Most common malignant tumor in young females:** Dysgerminoma. * **Psammoma bodies:** Classically seen in Serous Papillary tumors. * **Tumor Marker:** CA-125 is the primary marker for epithelial ovarian tumors.

Question 172: Placental alkaline phosphatase is a marker of which of the following?

A. Theca cell tumor
B. Teratoma
C. Choriocarcinoma
D. Dysgerminoma (Correct Answer)

Explanation: **Explanation:** **Dysgerminoma** is the most common malignant germ cell tumor of the ovary, occurring primarily in young women. It is the female counterpart of the testicular seminoma. **Placental Alkaline Phosphatase (PLAP)** is a highly specific and sensitive cell-membrane marker for dysgerminoma. Other characteristic markers for this tumor include **LDH** (Lactate Dehydrogenase) and occasionally low levels of hCG. **Analysis of Incorrect Options:** * **Theca cell tumor:** These are sex cord-stromal tumors that are typically benign and often estrogen-producing. They do not express PLAP; their markers are more related to hormonal output (Inhibin is a more common marker for sex cord tumors like Granulosa cell tumors). * **Teratoma:** Mature teratomas usually do not have specific serum markers. Immature teratomas are associated with **AFP** (Alpha-fetoprotein), not PLAP. * **Choriocarcinoma:** This is a highly malignant gestational trophoblastic neoplasm or germ cell tumor characterized by the secretion of very high levels of **beta-hCG**. PLAP is not a diagnostic marker for this condition. **High-Yield Clinical Pearls for NEET-PG:** * **Dysgerminoma Trio:** The most common markers tested are **PLAP** (most specific), **LDH** (used for monitoring), and **c-KIT (CD117)**. * **Radiosensitivity:** Dysgerminoma is the most radiosensitive tumor of the ovary, though fertility-sparing surgery and chemotherapy are now preferred. * **Associated Conditions:** It is frequently associated with **gonadal dysgenesis** (e.g., Swyer syndrome, Turner syndrome). * **Fried-egg appearance:** Histologically, it shows large, clear cells with central nuclei and fibrous stroma infiltrated by lymphocytes.

Question 173: In what percentage of patients with hydatidiform mole is the height of the uterus more than expected for the period of amenorrhea?

A. 10%
B. 30%
C. 50%
D. 70% (Correct Answer)

Explanation: In a Hydatidiform Mole (molar pregnancy), the characteristic clinical finding is a discrepancy between the uterine size and the period of amenorrhea. **Explanation of the Correct Answer (D):** In approximately **70%** of cases of complete hydatidiform mole, the height of the uterus is **greater than expected** for the gestational age. This occurs due to the rapid proliferation of trophoblastic tissue and the accumulation of retained intrauterine blood (clots). The classic "snowstorm appearance" on ultrasound represents these multiple hydropic villi filling the enlarged uterine cavity. **Explanation of Incorrect Options:** * **A (10%) & B (30%):** These percentages are too low. While some patients may present with a uterus smaller than expected (about 20-25% of cases, often due to the expulsion of molar tissue or missed abortion), the vast majority present with an enlarged uterus. * **C (50%):** While a significant number, it underestimates the prevalence. Standard textbooks (like Williams Obstetrics and Dutta) cite that roughly 70% of patients exhibit a uterus "large for dates." **High-Yield Clinical Pearls for NEET-PG:** * **Uterine Size:** 70% are larger than dates, 20-25% are smaller than dates, and the remainder are equal to dates. * **Theca Lutein Cysts:** Found in 25-30% of cases due to extremely high hCG levels causing ovarian hyperstimulation. * **Vaginal Bleeding:** The most common presenting symptom (95% of cases), often described as "white currant in red currant juice" appearance. * **Hyperemesis Gravidarum:** More severe in molar pregnancies due to excessively high serum β-hCG levels. * **Preeclampsia:** If preeclampsia occurs in the first trimester or early second trimester, always suspect a hydatidiform mole.

Question 174: What is the primary treatment for a lutein cyst associated with a hydatidiform mole?

A. Ovarian cystectomy
B. Ovariectomy
C. Suction evacuation (Correct Answer)
D. Ovariotomy

Explanation: **Explanation:** The correct answer is **C. Suction evacuation**. **Medical Concept:** Theca lutein cysts are functional ovarian cysts that develop due to hypersensitivity or excessively high levels of **hCG (human Chorionic Gonadotropin)**, which shares an alpha subunit with LH. In cases of a hydatidiform mole, the massive proliferation of trophoblastic tissue leads to pathologically high hCG levels, causing bilateral ovarian enlargement. The primary treatment strategy is to **remove the source of the hCG**. Once the molar pregnancy is managed via **suction evacuation**, the stimulus for the cysts is removed. Consequently, the theca lutein cysts undergo spontaneous regression, usually within 8–12 weeks post-evacuation. **Why other options are incorrect:** * **A & B (Ovarian cystectomy/Ovariectomy):** Surgical removal of the cyst or the ovary is contraindicated. These cysts are benign, physiological responses to hormonal stimulation and are not neoplastic. Surgery increases the risk of hemorrhage and unnecessary loss of ovarian reserve. * **D (Ovariotomy):** This refers to an incision into the ovary. It is unnecessary and carries a high risk of bleeding due to the increased vascularity of the ovaries in molar pregnancies. **NEET-PG High-Yield Pearls:** * **Appearance:** Theca lutein cysts are typically **bilateral**, multicystic, and can reach sizes >10 cm ("soap bubble" appearance on USG). * **Management:** Always **conservative**. Surgery is only indicated in rare complications like torsion or rupture with internal hemorrhage. * **Association:** Besides molar pregnancy, they are seen in multiple gestations, Rh isoimmunization, and Ovulation Induction (OHSS). * **Complication:** If they persist after hCG levels become undetectable, consider an alternative diagnosis like a true ovarian neoplasm.

Question 175: BRCA1 gene mutation is not associated with which of the following cancers?

A. Ovarian carcinoma
B. Breast carcinoma
C. Endometrial carcinoma (Correct Answer)
D. Fallopian tube cancer

Explanation: **Explanation:** The BRCA1 (Breast Cancer 1) gene is a tumor suppressor gene located on **chromosome 17q21**. It plays a critical role in DNA repair via homologous recombination. Mutations in this gene significantly increase the lifetime risk of specific cancers, primarily those of the breast and the female reproductive tract (ovary and fallopian tube). * **Why Endometrial Carcinoma (Option C) is the correct answer:** While some recent studies suggest a potential minor increase in the risk of rare, aggressive serous-like endometrial cancers in BRCA1 carriers, it is **not** traditionally considered part of the core BRCA1 clinical syndrome. Standard screening and prophylactic guidelines for BRCA1 mutation carriers focus on breast and ovarian/tubal health, not the endometrium. * **Why other options are incorrect:** * **Breast Carcinoma (Option B):** This is the most common association. BRCA1 mutations carry a lifetime risk of breast cancer up to 65–80%. * **Ovarian Carcinoma (Option A):** BRCA1 is strongly associated with epithelial ovarian cancer (specifically high-grade serous carcinoma), with a lifetime risk of approximately 40%. * **Fallopian Tube Cancer (Option D):** Modern pathology suggests that many "ovarian" cancers actually originate in the fimbrial end of the fallopian tube (STIC lesions). BRCA1 is a major risk factor for primary fallopian tube carcinoma. **High-Yield Clinical Pearls for NEET-PG:** 1. **Chromosome Location:** BRCA1 is on **17q**, while BRCA2 is on **13q**. 2. **Associated Cancers (BRCA1):** Breast (often Triple Negative), Ovary, Fallopian tube, and Prostate (lower risk than BRCA2). 3. **Associated Cancers (BRCA2):** Breast (including male breast cancer), Ovary, **Pancreas**, and Prostate. 4. **Prophylaxis:** Risk-reducing salpingo-oophorectomy (RRSO) is recommended for BRCA1 carriers between ages 35–40.

Question 176: What is the most common cause of postmenopausal bleeding?

A. Endometrial cancer
B. Endometrial polyps
C. Endometrial atrophy (Correct Answer)
D. Endometrial hyperplasia

Explanation: **Explanation:** **1. Why Endometrial Atrophy is Correct:** Endometrial atrophy is the **most common cause** of postmenopausal bleeding (PMB), accounting for approximately 60–80% of cases. In the postmenopausal state, low estrogen levels lead to a thin, friable endometrial lining. The lack of structural support causes the thin epithelium to shed or the underlying microvasculature to rupture easily, resulting in light spotting or bleeding. **2. Analysis of Incorrect Options:** * **Endometrial Cancer (A):** While this is the most **concerning** cause that must be ruled out, it accounts for only about 10% of PMB cases. * **Endometrial Polyps (B):** These are common benign growths and a frequent cause of PMB (approx. 10–15%), but they are less common than atrophy. * **Endometrial Hyperplasia (D):** This is a precursor to malignancy caused by unopposed estrogen. While significant, it is statistically less frequent than atrophic changes. **3. Clinical Pearls for NEET-PG:** * **Gold Standard Investigation:** Fractional Curettage (historically) or Office Endometrial Biopsy (Pipelle). * **First-line Screening:** Transvaginal Ultrasound (TVUS). * **Cut-off Value:** An endometrial thickness (ET) of **≤ 4 mm** in a postmenopausal woman has a high negative predictive value for malignancy. If ET is > 4 mm, a biopsy is mandatory. * **Most common cause of PMB worldwide:** Endometrial Atrophy. * **Most common gynecological malignancy in developed countries:** Endometrial Cancer (In India, it is traditionally Cervical Cancer, though Endometrial Cancer is rising in urban populations).

Question 177: Which of the following is associated with BRCA mutation carrier status?

A. Mucinous borderline ovarian tumor
B. High grade pelvic serous carcinoma (Correct Answer)
C. Endometrioid ovarian cancer
D. Sertoli-Leydig ovarian tumor

Explanation: **Explanation:** **Correct Answer: B. High grade pelvic serous carcinoma** **Medical Concept:** BRCA1 and BRCA2 mutations are primarily associated with the **High-Grade Serous Carcinoma (HGSC)** pathway. These mutations involve defects in homologous recombination DNA repair. Most "ovarian" cancers in BRCA carriers actually originate from the fimbrial end of the fallopian tube as **Serous Tubal Intraepithelial Carcinoma (STIC)**, which then spreads to the ovary and peritoneum. Therefore, the term "High-grade pelvic serous carcinoma" encompasses these etiologies. **Analysis of Incorrect Options:** * **A. Mucinous borderline ovarian tumor:** These are typically associated with KRAS mutations and are **not** linked to BRCA. In fact, mucinous and germ cell tumors are rarely seen in BRCA carriers. * **C. Endometrioid ovarian cancer:** While some cases are associated with Lynch Syndrome (HNPCC), they are not the classic presentation for BRCA mutations. Endometrioid tumors often arise from endometriosis (ARID1A mutations). * **D. Sertoli-Leydig ovarian tumor:** These are sex cord-stromal tumors often associated with **DICER1** mutations, not BRCA. **NEET-PG High-Yield Pearls:** * **BRCA1** carries a higher lifetime risk of ovarian cancer (approx. 40-50%) compared to **BRCA2** (approx. 15-25%). * **Prophylactic Surgery:** Risk-reducing salpingo-oophorectomy (RRSO) is recommended by age 35–40 for BRCA1 and 40–45 for BRCA2. * **OCPs:** Combined oral contraceptives are **protective** and reduce the risk of ovarian cancer in BRCA carriers. * **Treatment:** BRCA-mutated tumors are highly sensitive to platinum-based chemotherapy and **PARP inhibitors** (e.g., Olaparib).

Question 178: What is the risk of recurrence of a hydatidiform mole in a future pregnancy?

A. 1-4% (Correct Answer)
B. 4-8%
C. 8-10%
D. 10-12%

Explanation: **Explanation:** The risk of recurrence for a hydatidiform mole (HM) after one molar pregnancy is approximately **1–2%**, with most clinical guidelines and textbooks (like Williams Obstetrics) citing a range of **1–4%**. This represents a 10 to 40-fold increase compared to the general population risk (0.1%). **1. Why Option A is Correct:** The underlying medical concept is that while most molar pregnancies are sporadic events due to abnormal fertilization (dispermy or fertilization of an empty egg), a small subset of patients has a genetic predisposition. After one mole, the risk remains low (1–4%). However, if a woman has **two** prior molar pregnancies, the risk of recurrence jumps significantly to **15–20%**. **2. Why Other Options are Incorrect:** * **Options B, C, and D (4–12%):** These values overestimate the risk after a single molar event. While the risk is significantly higher than the baseline population, it does not reach these double-digit percentages until a patient has had at least two consecutive molar pregnancies. **3. NEET-PG High-Yield Clinical Pearls:** * **Follow-up:** After evacuation, weekly serum β-hCG levels are monitored until they are undetectable for three consecutive weeks, then monthly for 6 months. * **Contraception:** Combined Oral Contraceptive Pills (OCPs) are the preferred method during follow-up to prevent pregnancy, which would otherwise confuse β-hCG monitoring. * **Future Pregnancies:** In subsequent pregnancies, an early ultrasound (first trimester) is mandatory to confirm normal fetal development, and the placenta should be sent for histopathology after delivery. * **Genetic Link:** Recurrent familial moles are often associated with mutations in the **NLRP7** or **KHDC3L** genes.

Question 179: Which of the following can cause endometrial cancer?

A. Metropathia hemorrhagica (Correct Answer)
B. Gynandroblastoma
C. Dysgerminoma
D. Teratoma

Explanation: **Explanation:** The development of endometrial cancer is primarily driven by **unopposed estrogen stimulation**, which leads to endometrial hyperplasia and eventual malignant transformation. **Why Metropathia Hemorrhagica is correct:** Metropathia hemorrhagica (Schroeder’s disease) is a specialized form of Dysfunctional Uterine Bleeding (DUB) typically seen in perimenopausal women. It is characterized by **anovulatory cycles** where a persistent unruptured follicle leads to a state of hyperestrogenism without the protective, differentiating effect of progesterone. This chronic, unopposed estrogen causes the endometrium to become hyperplastic (cystic glandular hyperplasia), significantly increasing the risk of progressing to endometrial carcinoma. **Why the other options are incorrect:** * **Gynandroblastoma:** This is a rare sex cord-stromal tumor containing both granulosa cell and Sertoli-Leydig cell components. While granulosa cells produce estrogen, this specific mixed tumor is not the classic association for endometrial cancer compared to pure Granulosa Cell Tumors. * **Dysgerminoma:** This is a germ cell tumor (the female counterpart of seminoma). It is hormonally inert (though it may rarely produce hCG) and does not cause endometrial hyperplasia. * **Teratoma:** Most commonly presenting as Mature Cystic Teratomas (Dermoid cysts), these are germ cell tumors containing tissues from all three germ layers. They do not typically secrete estrogen. **High-Yield Clinical Pearls for NEET-PG:** * **Risk Factors:** Obesity (peripheral conversion of androstenedione to estrone), PCOS, Nulliparity, Early menarche/Late menopause, and Lynch Syndrome (HNPCC). * **Protective Factors:** Combined Oral Contraceptive Pills (OCPs), Multiparity, and Smoking (decreases estrogen levels, though harmful otherwise). * **Precursor Lesion:** Atypical Endometrial Hyperplasia (now termed Endometrial Intraepithelial Neoplasia or EIN) carries the highest risk (up to 30-40%) of progressing to cancer.

Question 180: What is the stage of an ovarian tumor if only one ovary is involved, without surface involvement or rupture?

A. Stage IA (Correct Answer)
B. Stage IB
C. Stage IC1
D. Stage IC2

Explanation: **Explanation:** The staging of ovarian cancer follows the **FIGO (International Federation of Gynecology and Obstetrics)** classification. This question tests the specific criteria for Stage I, where the tumor is strictly limited to the ovaries or fallopian tubes. **Why Stage IA is correct:** * **Stage IA** is defined as a tumor limited to **one ovary** (capsule intact) or one fallopian tube. * Crucially, there must be **no tumor on the external surface**, no rupture of the capsule, and no malignant cells in the ascites or peritoneal washings. **Why the other options are incorrect:** * **Stage IB:** The tumor involves **both ovaries** or fallopian tubes, but the capsules are still intact, and there is no surface involvement or malignant cells in washings. * **Stage IC:** The tumor is limited to one or both ovaries/tubes but with specific complications: * **Stage IC1:** Surgical spill (intraoperative rupture). * **Stage IC2:** Capsule ruptured **before surgery** or tumor present on the ovarian/tubal surface. * **Stage IC3:** Malignant cells present in the ascites or peritoneal washings. **High-Yield NEET-PG Pearls:** 1. **Most common type:** Epithelial Ovarian Cancer (Serous is the most frequent subtype). 2. **Staging Method:** Ovarian cancer is **surgically staged**. 3. **Prognostic Factor:** The integrity of the capsule (Stage IA vs. IC) is a major prognostic factor and determines the need for adjuvant chemotherapy. 4. **CA-125:** While used for monitoring, it is not part of the FIGO staging criteria.

Practice by Chapter

Cervical Cancer

Practice Questions

Endometrial Cancer

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Ovarian Cancer

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Vulvar and Vaginal Cancer

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Gestational Trophoblastic Disease

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Screening for Gynecologic Cancers

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Principles of Gynecologic Oncology Surgery

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Radiation Therapy in Gynecologic Malignancies

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Chemotherapy in Gynecologic Oncology

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Palliative Care in Gynecologic Oncology

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