Gynecologic Oncology — MCQs

Gynecologic Oncology Indian Medical PG Practice Questions and MCQs

Question 121: Which of the following malignant ovarian germ cell tumor variants has the best prognosis?

A. Yolk sac tumor
B. Dysgerminoma (Correct Answer)
C. Immature teratoma
D. Mature teratoma

Explanation: **Explanation:** **Dysgerminoma** is the most common malignant ovarian germ cell tumor (OGCT) and carries the **best prognosis** among all malignant variants. The primary reason for its excellent survival rate (over 95% in early stages) is its extreme **radiosensitivity** and **chemosensitivity**. Unlike other germ cell tumors, dysgerminomas are often diagnosed at Stage I and respond exceptionally well to the BEP (Bleomycin, Etoposide, Cisplatin) regimen. **Analysis of Incorrect Options:** * **Yolk Sac Tumor (Endodermal Sinus Tumor):** This is highly aggressive and spreads rapidly. While chemotherapy has improved outcomes, it historically had a much poorer prognosis than dysgerminoma. It is characterized by elevated **AFP** and **Schiller-Duval bodies**. * **Immature Teratoma:** The prognosis depends strictly on the **histological grade** (amount of immature neural tissue). While treatable, Grade 2 and 3 tumors are more aggressive than dysgerminomas. * **Mature Teratoma (Dermoid Cyst):** This is a **benign** tumor. The question specifically asks for the "malignant" variant with the best prognosis. While its prognosis is technically "best" because it is non-cancerous, it does not fit the category of malignant germ cell tumors. **High-Yield Clinical Pearls for NEET-PG:** * **Tumor Marker:** Dysgerminoma is associated with elevated **LDH** and sometimes hCG. * **Association:** It is the most common malignancy found in patients with **gonadal dysgenesis** (e.g., Swyer syndrome). * **Microscopy:** Look for "Fried egg appearance" (clear cytoplasm, central nuclei) and **lymphocytic infiltration** of the stroma. * **Management:** Fertility-sparing surgery (Unilateral Salpingo-oophorectomy) is the standard of care for young patients.

Question 122: Attacks of flushing and cyanosis occur in which type of ovarian tumors?

A. Struma ovarii
B. Krukenberg's tumor
C. Arrhenoblastoma
D. Carcinoid tumors of ovary (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Carcinoid tumors of ovary**. **Mechanism:** Ovarian carcinoid tumors are rare germ cell tumors (often arising within a mature cystic teratoma). They secrete vasoactive substances, primarily **serotonin (5-HT)**, bradykinin, and histamine, directly into the systemic circulation. Unlike intestinal carcinoids, which must metastasize to the liver to cause symptoms (due to the "first-pass effect" where the liver inactivates serotonin), **primary ovarian carcinoids** bypass the portal circulation. This allows the secretagogues to reach the systemic circulation directly, leading to **Carcinoid Syndrome**, characterized by episodic **flushing, cyanosis, diarrhea, and bronchospasm.** **Analysis of Incorrect Options:** * **A. Struma ovarii:** This is a specialized teratoma composed primarily of thyroid tissue. It presents with features of **hyperthyroidism** (tachycardia, tremors, weight loss), not carcinoid flushing. * **B. Krukenberg's tumor:** This is a metastatic signet-ring cell carcinoma, usually originating from the stomach. It typically presents with bilateral ovarian enlargement and ascites, not hormonal flushing. * **C. Arrhenoblastoma (Sertoli-Leydig Cell Tumor):** These are sex cord-stromal tumors that secrete androgens. They lead to **virilization** (hirsutism, clitoromegaly, deepening of voice), not vasomotor symptoms. **High-Yield Clinical Pearls for NEET-PG:** * **Primary vs. Secondary:** Primary ovarian carcinoid can cause carcinoid syndrome **without liver metastasis**, whereas GI carcinoids require liver metastasis to manifest the syndrome. * **Histology:** Look for "Insular" or "Trabecular" patterns and Argentaffin/Argyrophil positivity. * **Diagnostic Marker:** Elevated 24-hour urinary **5-HIAA** (5-Hydroxyindoleacetic acid). * **Cardiac Involvement:** Long-standing cases can lead to right-sided heart valve fibrosis (Tricuspid regurgitation/Pulmonary stenosis).

Question 123: A patient presents with 22 weeks of pregnancy (Gravida 4, Para 1) and carcinoma in situ. What is the preferred treatment?

A. Conization of the cervix
B. Medical termination of pregnancy (MTP) and hysterectomy
C. Medical termination of pregnancy (MTP) and radiotherapy
D. Allow delivery followed by hysterectomy (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Allow delivery followed by hysterectomy** The management of cervical neoplasia during pregnancy is guided by the stage of the disease and the gestational age. **Carcinoma in situ (CIN III/Stage 0)** is a pre-invasive condition. In such cases, the primary goal is to allow the pregnancy to reach term because CIN III does not progress rapidly to invasive cancer during the short duration of pregnancy. The standard protocol for CIN III diagnosed during pregnancy is **expectant management**. The patient is monitored with colposcopy and cytology every 10–12 weeks. Definitive treatment (like hysterectomy or conization) is deferred until 6–12 weeks postpartum, as the lesion may even regress after vaginal delivery. **Analysis of Incorrect Options:** * **A. Conization of the cervix:** While conization is the treatment for CIN III in non-pregnant women, it is avoided during pregnancy unless invasive cancer is strongly suspected. It carries high risks of life-threatening hemorrhage, preterm labor, and pregnancy loss. * **B & C. MTP and Hysterectomy/Radiotherapy:** These are aggressive interventions reserved for **invasive cervical cancer** diagnosed in early pregnancy (usually <20–24 weeks). Since CIN III is non-invasive, terminating a viable 22-week pregnancy is medically and ethically unnecessary. **Clinical Pearls for NEET-PG:** * **Mode of Delivery:** Vaginal delivery is generally safe and preferred for CIN (all grades) and Stage IA1. Cesarean section is reserved for advanced invasive stages to avoid hemorrhage and cervical dystocia. * **Biopsy in Pregnancy:** If a suspicious lesion is seen, a **punch biopsy** is safe, but **endocervical curettage (ECC)** is strictly contraindicated due to the risk of rupturing the membranes. * **Regression:** Up to 60–70% of CIN II/III lesions may regress or remain stable postpartum; hence, re-evaluation at 6 weeks postpartum is mandatory before definitive surgery.

Question 124: What percentage of ovarian tumors of non-epithelial origin occur in childhood?

A. 20%
B. 30%
C. 40%
D. 50% (Correct Answer)

Explanation: **Explanation:** The correct answer is **50% (Option D)**. **Understanding the Concept:** Ovarian tumors in children and adolescents differ significantly from those in adults. While epithelial tumors are the most common type in adult women (representing ~90% of cases), they are rare in the pediatric population. In children and adolescents, **Germ Cell Tumors (GCTs)**—a subset of non-epithelial tumors—are the most prevalent. Specifically, approximately **50% of all ovarian tumors occurring in childhood and adolescence are of non-epithelial origin**, with Germ Cell Tumors being the dominant histological type. **Analysis of Options:** * **Option A, B, and C (20%, 30%, 40%):** These percentages underestimate the prevalence. While non-epithelial tumors are rare in the general population (only about 10% of all ovarian cancers), their relative frequency is dramatically higher in the pediatric age group due to the near-absence of epithelial surface tumors before puberty. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common Ovarian Tumor in Children:** Mature Cystic Teratoma (Dermoid cyst). * **Most Common Malignant Ovarian Tumor in Children:** Dysgerminoma. * **Tumor Markers:** Always correlate non-epithelial tumors with markers: * **Dysgerminoma:** LDH and hCG. * **Yolk Sac Tumor:** Alpha-fetoprotein (AFP). * **Choriocarcinoma:** beta-hCG. * **Granulosa Cell Tumor:** Inhibin. * **Management:** Unlike epithelial cancers, most malignant non-epithelial tumors in children are highly chemosensitive (e.g., BEP regimen) and are often treated with fertility-sparing surgery (unilateral salpingo-oophorectomy).

Question 125: The performance of a prophylactic salpingo-oophorectomy reduced the risk of BRCA-related gynaecologic cancer by what percentage?

A. 15%
B. 28%
C. 54%
D. 96% (Correct Answer)

Explanation: **Explanation:** The correct answer is **96% (Option D)**. Risk-reducing Salpingo-oophorectomy (RRSO) is the gold standard for preventing gynecologic cancers in women with **BRCA1 and BRCA2** mutations. Since most "ovarian" cancers in these patients actually originate in the fimbrial end of the fallopian tube (Serous Tubal Intraepithelial Carcinoma - STIC), removing both the tubes and ovaries drastically reduces the risk. Large-scale clinical studies (such as those by Rebbeck et al.) have demonstrated that RRSO reduces the risk of BRCA-related ovarian and fallopian tube cancers by approximately **80% to 96%**. **Analysis of Options:** * **Option A (15%) & B (28%):** These values are far too low. RRSO is highly effective because it removes the primary tissue at risk before malignant transformation occurs. * **Option C (54%):** This figure is more closely associated with the reduction in **breast cancer risk** if the oophorectomy is performed pre-menopausally (approximately 50% reduction), but it underestimates the protection against gynecologic cancers. * **Option D (96%):** This represents the upper limit of efficacy reported in literature. The risk does not drop to 0% because of the residual risk of **Primary Peritoneal Carcinoma (PPC)**, which can arise from the peritoneal lining even after the ovaries are removed. **High-Yield Clinical Pearls for NEET-PG:** * **Timing of Surgery:** For BRCA1, RRSO is recommended between ages **35–40**. For BRCA2 (which has a later onset of cancer), it can be delayed until ages **40–45**. * **Breast Cancer Link:** RRSO in pre-menopausal BRCA carriers also reduces the risk of breast cancer by ~50%. * **OCPs:** Combined Oral Contraceptive Pills reduce ovarian cancer risk in BRCA carriers by ~50% if used for 5 years or more. * **Screening:** For those deferring surgery, screening with **TVUS and CA-125** every 6 months is often done, though its efficacy in detecting early-stage disease is limited.

Question 126: All of the following are prognostic factors of carcinoma endometrium, EXCEPT:

A. Pelvic node involvement
B. Deep myometrial involvement
C. Enlarged uterine cavity (Correct Answer)
D. Poor differentiation

Explanation: In endometrial carcinoma, prognosis is primarily determined by factors that reflect the **surgical-pathological stage** and the biological aggressiveness of the tumor. **Why "Enlarged uterine cavity" is the correct answer:** While an enlarged uterus may be a clinical finding during examination, the **size of the uterine cavity** is no longer considered a significant prognostic factor in modern FIGO staging. Historically, it was part of the 1971 clinical staging, but it has been replaced by more precise pathological markers that correlate better with survival and recurrence. **Explanation of incorrect options (Prognostic Factors):** * **Pelvic node involvement:** This is one of the most critical prognostic factors. Lymph node metastasis automatically upgrades the disease to Stage IIIC, significantly decreasing the 5-year survival rate. * **Deep myometrial involvement:** Invasion into the outer half of the myometrium (Stage IB) increases the risk of lymphovascular space invasion (LVSI) and lymph node metastasis. * **Poor differentiation (Grade 3):** Histological grade is a major predictor of outcome. High-grade tumors are more likely to be aggressive, non-endometrioid (like serous or clear cell), and have a higher propensity for distant spread. **High-Yield Clinical Pearls for NEET-PG:** * **Most important prognostic factor:** Histological type and grade. * **Most common site of distant metastasis:** Lungs. * **Staging:** Endometrial cancer is **surgically staged** (FIGO). * **Risk Factors:** Obesity (most common), nulliparity, late menopause, and Lynch Syndrome (HNPCC). * **Protective Factors:** Combined oral contraceptives and smoking (due to anti-estrogenic effects, though not recommended for health).

Question 127: What is the primary group of lymph nodes affected in cervical carcinoma?

A. Common iliac group
B. Inguinal nodes
C. Obturator nodes (Correct Answer)
D. Para-aortic nodes

Explanation: ### Explanation **1. Why Obturator nodes are correct:** Cervical carcinoma primarily spreads via the lymphatic system in an orderly, stepwise fashion. The **Obturator nodes** (part of the external iliac group) are considered the **primary/sentinel station** for cervical drainage. The cervix drains first into the primary group, which includes the paracervical, obturator, external iliac, and internal iliac nodes. Among these, the obturator nodes are the most frequently involved early in the disease process. **2. Analysis of incorrect options:** * **A. Common iliac group:** These are considered **secondary nodes**. They receive drainage from the primary groups (external/internal iliacs). Involvement usually indicates more advanced disease (Stage IIIB/IVA). * **B. Inguinal nodes:** These nodes typically drain the lower third of the vagina, the vulva, and the skin below the umbilicus. They are not a primary site for cervical cancer unless there is significant vaginal extension. * **C. Para-aortic nodes:** These are **tertiary nodes**. Involvement of para-aortic nodes represents distant metastasis (Stage IVB in FIGO 2018, though now specifically noted in surgical staging). They receive drainage from the common iliac nodes. **3. NEET-PG High-Yield Pearls:** * **Order of Spread:** Primary (Obturator/External/Internal Iliac) → Secondary (Common Iliac) → Tertiary (Para-aortic). * **Most common site of distant metastasis:** Lungs. * **Ureteric involvement:** The most common cause of death in cervical cancer is **Uremia** due to bilateral ureteric obstruction (post-renal failure). * **FIGO Staging:** Remember that cervical cancer staging is now primarily **clinical** but allows for imaging (MRI/CT) and pathological findings where available. * **Sentinel Lymph Node (SLN) Mapping:** Usually uses Technetium-99 or Indocyanine Green (ICG) to identify the first node (often the obturator) to avoid complete lymphadenectomy morbidity.

Question 128: What is the recommended initial management for atypical hyperplasia?

A. Cyclical progestogens
B. Continuous progestogens
C. Levonorgestrel-releasing intrauterine system (MIRENA)
D. Hysterectomy (Correct Answer)

Explanation: **Explanation:** **Atypical Hyperplasia (AH)**, also known as Endometrioid Intraepithelial Neoplasia (EIN), is a premalignant condition with a high risk of progressing to or harboring coexistent malignancy. **Why Hysterectomy is the Correct Answer:** The definitive management for atypical hyperplasia is **Total Hysterectomy** (usually with bilateral salpingo-oophorectomy in postmenopausal women). This is because approximately **40% of women** diagnosed with AH on a biopsy are found to have a concurrent, undiagnosed endometrial carcinoma in the final hysterectomy specimen. Surgery eliminates the risk of progression and provides a definitive diagnosis. **Why Other Options are Incorrect:** * **Options A & B (Cyclical/Continuous Progestogens):** While progestogens can reverse hyperplasia without atypia, they are not the first-line treatment for atypical hyperplasia due to the high failure rate and the risk of underlying malignancy. * **Option C (LNG-IUS/Mirena):** The LNG-IUS is highly effective for *non-atypical* hyperplasia. In atypical cases, it is only reserved for patients who strongly desire **fertility preservation** or those who are **medically unfit** for surgery. It is not the "recommended initial management" for the general population. **NEET-PG High-Yield Pearls:** * **Risk of Malignancy:** Hyperplasia *without* atypia has a <3% risk of progression; Hyperplasia *with* atypia has a ~29-40% risk. * **Fertility Sparing:** If a patient with AH desires pregnancy, management involves high-dose oral progestogens or LNG-IUS with mandatory endometrial sampling every 3 months. * **Postmenopausal Bleeding:** Always the first symptom to rule out endometrial hyperplasia/carcinoma. * **Gold Standard Diagnosis:** Endometrial biopsy or D&C (Dilatation and Curettage).

Question 129: What is the standard treatment for Stage II carcinoma of the endometrium?

A. Surgery
B. Radiotherapy followed by surgery (Correct Answer)
C. Chemotherapy
D. Progesterone followed by surgery

Explanation: **Explanation:** **Stage II Endometrial Carcinoma** is defined by the involvement of the **cervical stroma**, but the tumor does not extend beyond the uterus. **Why Option B is Correct:** The management of Stage II endometrial cancer is traditionally controversial, but for NEET-PG purposes, the standard approach involves **preoperative radiotherapy followed by surgery** (Extra-fascial Hysterectomy or Radical Hysterectomy). * **Radiotherapy (Brachytherapy or External Beam):** Shrinks the tumor and sterilizes the cervical parametria and vaginal vault, reducing the risk of local recurrence. * **Surgery:** Performed 6 weeks post-radiation to remove the primary source. * *Note:* Modern FIGO guidelines also allow for primary Radical Hysterectomy (Wertheim’s) followed by tailored adjuvant radiation, but the "Radiation + Surgery" sequence remains a classic academic answer. **Why Other Options are Incorrect:** * **Option A (Surgery alone):** Insufficient for Stage II because cervical involvement significantly increases the risk of parametrial spread and vaginal vault recurrence. * **Option C (Chemotherapy):** Primarily used for advanced stages (Stage III/IV) or high-risk histological types (e.g., serous or clear cell). * **Option D (Progesterone):** Used for fertility-sparing treatment in Stage IA (Grade 1) or as palliative care in metastatic disease; it is not a curative modality for Stage II. **High-Yield Clinical Pearls:** * **FIGO Staging:** Stage I (Uterus only), **Stage II (Cervical stroma)**, Stage III (Local/Regional spread), Stage IV (Bladder/Bowel/Distant). * **Most Common Type:** Endometrioid adenocarcinoma (Type I). * **Risk Factors:** Obesity, Nulliparity, Early menarche/Late menopause, and Tamoxifen use. * **Investigation of Choice:** Fractional Curettage or Pipelle biopsy; **Transvaginal Ultrasound (TVS)** is the initial screening tool (Endometrial thickness >4mm in postmenopausal women requires biopsy).

Question 130: What is true about a complete hydatidiform mole?

A. Its chromosome pattern is XX.
B. It is associated with preeclampsia.
C. Enlarged ovarian cysts occur.
D. All of the above. (Correct Answer)

Explanation: A **Complete Hydatidiform Mole (CHM)** is a gestational trophoblastic disease characterized by the proliferation of trophoblastic tissue and hydropic degeneration of chorionic villi. **Explanation of Options:** * **Option A (Chromosome pattern is XX):** CHM is typically diploid (46,XX). It occurs through **androgenesis**, where an "empty" egg (lacking maternal chromosomes) is fertilized by a single sperm that duplicates its DNA (90%) or, less commonly, by two sperm (dispermy, 46,XY). 46,XX is the most common karyotype. * **Option B (Associated with Preeclampsia):** CHM is a classic cause of **early-onset preeclampsia** (occurring before 20 weeks of gestation). This is due to the massive release of anti-angiogenic factors from the hyperplastic trophoblastic tissue. * **Option C (Enlarged ovarian cysts):** High levels of hCG (human chorionic gonadotropin) have an $\alpha$-subunit identical to LH and FSH. This leads to hyperstimulation of the ovaries, resulting in bilateral **Theca Lutein Cysts**. These typically resolve after the mole is evacuated. **Conclusion:** Since all statements are clinically accurate features of a complete mole, **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Snowstorm Appearance:** The classic ultrasound finding for CHM. * **HCG Levels:** Markedly elevated (often >100,000 mIU/mL), unlike partial moles. * **Fetal Parts:** Absent in complete moles; present in partial moles (which are usually triploid, 69,XXX/XXY). * **Risk of Malignancy:** CHM has a higher risk (15-20%) of progressing to Gestational Trophoblastic Neoplasia (GTN) compared to partial moles (<5%). * **Treatment:** Suction and evacuation is the treatment of choice.

Practice by Chapter

Cervical Cancer

Practice Questions

Endometrial Cancer

Practice Questions

Ovarian Cancer

Practice Questions

Vulvar and Vaginal Cancer

Practice Questions

Gestational Trophoblastic Disease

Practice Questions

Screening for Gynecologic Cancers

Practice Questions

Principles of Gynecologic Oncology Surgery

Practice Questions

Radiation Therapy in Gynecologic Malignancies

Practice Questions

Chemotherapy in Gynecologic Oncology

Practice Questions

Palliative Care in Gynecologic Oncology

Practice Questions

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