Gynecologic Oncology — MCQs

A 42-year-old woman presents with menometrorrhagia for the past 2 months. She has no history of prior irregular menstrual bleeding and has not yet reached menopause. Physical examination reveals no vaginal or cervical lesions and a normal-sized uterus, but there is a right adnexal mass. An abdominal ultrasound scan shows a 7-cm solid right adnexal mass. Endometrial biopsy shows hyperplastic endometrium without cellular atypia. What is the most likely lesion underlying her menstrual abnormalities?

Q290Medium

Which of the following statements is not true regarding cervical cancer screening guidelines according to the WHO?

Gynecologic Oncology Indian Medical PG Practice Questions and MCQs

Question 281: Endometrial carcinoma with vaginal metastasis, what FIGO stage would it be?

A. Stage III a
B. Stage III b (Correct Answer)
C. Stage III c
D. Stage IV a

Explanation: **Explanation:** The FIGO staging for Endometrial Carcinoma was updated in 2023; however, for NEET-PG, the **FIGO 2009 staging** remains the primary reference for this specific classification. **Why Stage III B is correct:** Stage III represents the local and/or regional spread of the tumor. Specifically, **Stage III B** is defined by the involvement of the **vagina and/or the parametrium**. The presence of vaginal metastasis indicates that the tumor has extended beyond the uterus but remains within the pelvic cavity, fitting the criteria for III B. **Analysis of Incorrect Options:** * **Stage III A:** This stage involves the tumor invading the **serosa** of the corpus uteri and/or the **adnexa** (fallopian tubes/ovaries) by direct extension or metastasis. * **Stage III C:** This stage involves metastasis to the **pelvic and/or para-aortic lymph nodes**. It is further divided into III C1 (pelvic nodes) and III C2 (para-aortic nodes). * **Stage IV A:** This represents advanced spread where the tumor invades the **bladder mucosa and/or the bowel mucosa**. **High-Yield Clinical Pearls for NEET-PG:** 1. **Most Common Site of Distant Metastasis:** Lungs. 2. **Most Common Site of Local Recurrence:** Vaginal vault. 3. **Prognostic Factor:** The most important prognostic factor in endometrial cancer is the **histological grade and depth of myometrial invasion**. 4. **Lymphatic Spread:** The primary route of spread is via lymphatics; pelvic nodes are usually involved before para-aortic nodes. 5. **Risk Factor:** Unopposed estrogen (PCOS, Obesity, Tamoxifen use) is the classic precursor for Type I Endometrial Carcinoma.

Question 282: Which of the following is not seen in Cowden syndrome?

A. Diabetes mellitus
B. Hypertension
C. Obesity
D. Multiparity (Correct Answer)

Explanation: **Explanation:** **Cowden Syndrome** is an autosomal dominant condition caused by a mutation in the **PTEN gene** (a tumor suppressor gene). It is characterized by multiple hamartomas and an increased risk of various malignancies, most notably breast, thyroid, and **endometrial cancer**. **Why Multiparity is the correct answer:** The question asks for what is **not** typically associated with Cowden Syndrome in the context of endometrial cancer risk. **Multiparity** is a known **protective factor** against endometrial cancer because it reduces the lifetime exposure to "unopposed estrogen" through high levels of progesterone during pregnancy. In contrast, Cowden syndrome patients are at a significantly higher risk (up to 30% lifetime risk) of developing Type I endometrial carcinoma. **Why the other options are incorrect:** Options A, B, and C (**Diabetes mellitus, Hypertension, and Obesity**) constitute the classic **"Corpus Uteri Cancer Syndrome"** or the metabolic triad associated with endometrial cancer. * **Obesity:** Increases peripheral conversion of androstenedione to estrone in adipose tissue. * **Diabetes & Hypertension:** These are independent risk factors often co-existing with obesity that further predispose an individual to endometrial hyperplasia and malignancy. In a patient with Cowden Syndrome, these metabolic factors act synergistically with the PTEN mutation to further elevate the risk of gynecologic oncology. **High-Yield Clinical Pearls for NEET-PG:** * **PTEN Mutation:** Also associated with Bannayan-Riley-Ruvalcaba syndrome. * **Pathognomonic Sign:** Mucocutaneous lesions (Trichilemmomas, papillomatous papules, and acral keratoses). * **Cancer Risks:** Breast (85% risk), Thyroid (Follicular type), and Endometrium. * **Lhermitte-Duclos disease:** A rare cerebellar dysplastic gangliocytoma is a specific diagnostic criterion for Cowden Syndrome.

Question 283: What is the primary treatment for stage III carcinoma of the ovary?

A. Total hysterectomy
B. Total hysterectomy and bilateral salpingo-oophorectomy
C. Debulking surgery with tumor removal (Correct Answer)
D. None of the above

Explanation: **Explanation:** The primary treatment for advanced epithelial ovarian cancer (Stage III and IV) is **Cytoreductive Surgery (Debulking)** followed by systemic chemotherapy. **Why Option C is Correct:** In Stage III ovarian cancer, the disease has spread beyond the pelvis to the peritoneum and/or regional lymph nodes. The goal of surgery is not just organ removal, but **maximal cytoreduction**—removing as much visible tumor mass as possible. Reducing the tumor burden to "optimal" levels (residual nodules <1 cm) improves the efficacy of subsequent platinum-based chemotherapy and significantly enhances overall survival. **Why Options A and B are Incorrect:** * **Options A and B:** While a Total Abdominal Hysterectomy (TAH) and Bilateral Salpingo-Oophorectomy (BSO) are *components* of the surgery, they are insufficient on their own for Stage III. These options ignore the metastatic deposits on the omentum, bowel, and peritoneal surfaces. Simply removing the uterus and ovaries without addressing the extrapelvic spread (debulking) would result in a poor prognosis. **High-Yield Clinical Pearls for NEET-PG:** * **Standard of Care:** The "Gold Standard" is primary cytoreductive surgery + adjuvant chemotherapy (Paclitaxel + Carboplatin). * **Optimal Debulking:** Defined as residual disease <1 cm in maximum diameter. "Complete" debulking (no visible disease) offers the best prognosis. * **Interval Debulking:** If the patient is too ill or the tumor is unresectable initially, Neoadjuvant Chemotherapy (NACT) is given for 3 cycles, followed by surgery. * **Tumor Marker:** **CA-125** is the most important marker for monitoring treatment response and recurrence in epithelial ovarian cancer.

Question 284: An elderly female is diagnosed to have Ca cervix stage III B. What is the management of choice in this patient?

A. Wertheim hysterectomy
B. Shautas procedure
C. Chemotherapy
D. Intracavitary brachytherapy with external beam radiation (Correct Answer)

Explanation: **Explanation:** The management of Carcinoma Cervix is primarily determined by the FIGO stage. Stage III B is defined by the involvement of the pelvic wall and/or presence of hydronephrosis or a non-functioning kidney. **1. Why Option D is Correct:** For **locally advanced cervical cancer (LACC)**, which includes Stages II B through IV A, the standard of care is **Concurrent Chemoradiotherapy (CCRT)**. This involves External Beam Radiation Therapy (EBRT) to treat the primary tumor and pelvic nodes, followed by Intracavitary Brachytherapy (ICBT) to deliver a high dose to the central tumor. Cisplatin is typically used as a radiosensitizer. In this question, Option D represents the definitive radiotherapy component of this management. **2. Why the other options are incorrect:** * **Options A & B (Wertheim and Schauta’s Hysterectomy):** These are radical surgical procedures. Surgery is generally reserved for **early-stage disease (Stage I to II A)**. In Stage III B, the disease has spread to the pelvic side walls, making it impossible to achieve clear surgical margins. * **Option C (Chemotherapy):** While chemotherapy is used concurrently with radiation in Stage III B, it is not used as a standalone primary treatment (except in palliative settings for Stage IV B). **Clinical Pearls for NEET-PG:** * **Stage II B** is the earliest stage where surgery is no longer the primary treatment (Parametrial involvement). * **Most common cause of death** in Ca Cervix: Uremia due to bilateral ureteric obstruction (Stage III B). * **Investigation of choice for staging:** MRI Pelvis (though FIGO staging remains clinical). * **Standard Radiosensitizer:** Weekly Cisplatin.

Question 285: Which tumour marker is specific for choriocarcinoma?

A. CA 125
B. HCG (Correct Answer)
C. AFP
D. LDH

Explanation: **Explanation:** **Human Chorionic Gonadotropin (hCG)** is the definitive tumor marker for Gestational Trophoblastic Neoplasia (GTN), including **choriocarcinoma**. Choriocarcinoma arises from the syncytiotrophoblast cells, which are physiologically responsible for secreting hCG. In this malignancy, hCG levels are typically markedly elevated and correlate directly with tumor burden, making it an ideal marker for diagnosis, monitoring treatment response, and detecting recurrence. **Analysis of Incorrect Options:** * **CA 125 (Cancer Antigen 125):** The primary marker for **epithelial ovarian tumors** (especially serous cystadenocarcinoma). It is non-specific and can be elevated in endometriosis, PID, or menstruation. * **AFP (Alpha-Fetoprotein):** The characteristic marker for **Yolk Sac Tumors** (Endodermal Sinus Tumors) and Hepatocellular Carcinoma. * **LDH (Lactate Dehydrogenase):** A non-specific marker often elevated in **Dysgerminomas**. It reflects high cell turnover. **High-Yield Clinical Pearls for NEET-PG:** * **Beta-hCG Subunit:** Always measure the $\beta$-subunit specifically, as the $\alpha$-subunit is identical to LH, FSH, and TSH. * **The "Hook Effect":** Extremely high hCG levels (as seen in choriocarcinoma) can sometimes cause a false-negative result in undiluted samples during immunoassays. * **Metastasis:** Choriocarcinoma is highly vascular and spreads hematogenously. The **lungs** are the most common site of metastasis ("cannonball" appearance on X-ray). * **Treatment:** Unlike most solid tumors, choriocarcinoma is highly sensitive to chemotherapy (e.g., Methotrexate or EMA-CO regimen), even in advanced stages.

Question 286: Which of the following is related to prophylactic chemotherapy in molar pregnancy?

A. It may be given in 'at risk' patients (Correct Answer)
B. Multiple agents are preferred
C. Malignant sequelae becomes nil
D. Follow-up is not required

Explanation: **Explanation:** Prophylactic chemotherapy in molar pregnancy is a controversial but recognized clinical strategy aimed at reducing the risk of progression to Gestational Trophoblastic Neoplasia (GTN). **Why Option A is Correct:** Prophylactic chemotherapy (usually with Methotrexate or Actinomycin-D) is indicated for patients categorized as **'high risk'** for malignant transformation, especially when reliable follow-up is unavailable. High-risk criteria include: * Pre-evacuation hCG levels >100,000 mIU/mL. * Excessive uterine size for gestational age. * Theca lutein cysts >6 cm. * Age >40 years. **Why Other Options are Incorrect:** * **Option B:** Single-agent chemotherapy (Methotrexate or Actinomycin-D) is the standard for prophylaxis. Multiple agents are reserved for high-risk metastatic GTN (e.g., EMA-CO regimen). * **Option C:** While it reduces the incidence of post-molar GTN (from ~15-20% down to 3-8%), it **does not eliminate** the risk entirely. Malignant sequelae can still occur. * **Option D:** Follow-up is **mandatory**. Prophylactic chemotherapy may actually mask the early rise of hCG or select for chemo-resistant trophoblastic cells, making strict serial hCG monitoring even more critical. **High-Yield Clinical Pearls for NEET-PG:** * **Standard Management:** The primary treatment for a hydatidiform mole is **Suction and Evacuation**, regardless of the risk profile. * **Follow-up Gold Standard:** Weekly serum β-hCG levels until three consecutive normal values are obtained, followed by monthly levels for 6 months. * **Contraception:** Combined Oral Contraceptive Pills (COCs) are the preferred method during the follow-up period to avoid confusing a new pregnancy with GTN.

Question 287: What are the predisposing factors for carcinoma of the cervix?

A. Multiple sexual partners (Correct Answer)
B. Genital warts
C. Late menarche
D. Nulliparity

Explanation: **Explanation:** Carcinoma of the cervix is primarily caused by persistent infection with high-risk strains of **Human Papillomavirus (HPV)**, most commonly types 16 and 18. Since HPV is a sexually transmitted infection (STI), the risk of developing cervical cancer is directly proportional to the risk of exposure to the virus. * **Why Option A is Correct:** Having **multiple sexual partners** (or a partner who has had multiple partners) significantly increases the probability of exposure to HPV. This is considered the most significant behavioral risk factor for cervical neoplasia. * **Why the other options are incorrect:** * **Genital Warts (Option B):** These are caused by **low-risk HPV types (6 and 11)**. While they indicate sexual activity and exposure to HPV, these specific strains are non-oncogenic and do not lead to cervical cancer. * **Late Menarche (Option C):** Early menarche and late menopause are risk factors for estrogen-dependent cancers (like endometrial or breast cancer), but they have no significant association with cervical cancer. * **Nulliparity (Option D):** High parity (having many children) is actually a risk factor for cervical cancer due to hormonal changes and cervical trauma during delivery. Nulliparity is a protective factor for cervical cancer but a risk factor for endometrial and ovarian cancers. **High-Yield Clinical Pearls for NEET-PG:** * **Most common histological type:** Squamous cell carcinoma (80-85%). * **Other Risk Factors:** Early age at first intercourse (<18 years), smoking (specifically for squamous cell), long-term oral contraceptive use, and immunosuppression (HIV). * **Screening:** The transformation zone is the most common site of origin; screening is done via Pap smear and HPV DNA testing. * **Vaccination:** The ideal age for HPV vaccination is 9–14 years (before sexual debut).

Question 288: The risk of sarcoma developing in a fibroid uterus is approximately:

A. <1% (Correct Answer)
B. <10%
C. >30%
D. >50%

Explanation: **Explanation:** The correct answer is **A. <1%**. **Why it is correct:** Uterine leiomyosarcoma (LMS) is a rare malignant tumor of the smooth muscle of the uterus. While leiomyomas (fibroids) are the most common benign tumors in women, their malignant transformation into sarcoma is extremely rare. Large-scale clinical studies and pathological reviews consistently show that the risk of a pre-existing fibroid harboring an occult malignancy is approximately **0.1% to 0.3%** (or roughly 1 in 500 to 1 in 1000 cases). Therefore, the risk is significantly less than 1%. **Why incorrect options are wrong:** * **B (<10%):** This overestimates the risk by a factor of ten. While 10% might represent the prevalence of fibroids in the general population, it does not represent the rate of sarcomatous change. * **C and D (>30% and >50%):** These values are clinically inaccurate. If the risk were this high, every fibroid would require radical surgical intervention (hysterectomy) rather than conservative management or observation. **High-Yield Clinical Pearls for NEET-PG:** * **Pathogenesis:** Most leiomyosarcomas are believed to arise *de novo* rather than from the malignant transformation of a pre-existing benign leiomyoma. * **Red Flags:** Rapid growth of a "fibroid" in a **postmenopausal woman** is a classic warning sign for sarcoma. In premenopausal women, rapid growth is less predictive of malignancy but still warrants close monitoring. * **Diagnosis:** Definitive diagnosis is **histopathological**, characterized by high mitotic index, cellular atypia, and coagulative tumor cell necrosis. * **Management Caution:** The risk of occult sarcoma is the primary reason why the use of **power morcellation** during laparoscopic surgery is controversial, as it can disseminate malignant cells throughout the peritoneal cavity.

Question 289: A 42-year-old woman presents with menometrorrhagia for the past 2 months. She has no history of prior irregular menstrual bleeding and has not yet reached menopause. Physical examination reveals no vaginal or cervical lesions and a normal-sized uterus, but there is a right adnexal mass. An abdominal ultrasound scan shows a 7-cm solid right adnexal mass. Endometrial biopsy shows hyperplastic endometrium without cellular atypia. What is the most likely lesion underlying her menstrual abnormalities?

A. Corpus luteum cyst
B. Endometrioma
C. Granulosa-theca cell tumor (Correct Answer)
D. Mature cystic teratoma

Explanation: ### Explanation The clinical presentation of **menometrorrhagia** (heavy, irregular bleeding) associated with a **solid adnexal mass** and **endometrial hyperplasia** in a 42-year-old woman strongly points toward an estrogen-secreting ovarian tumor. **1. Why Granulosa-Theca Cell Tumor is Correct:** Granulosa cell tumors (GCTs) are the most common **sex cord-stromal tumors**. They are functionally active and characteristically secrete **estrogen**. This excess estrogen leads to endometrial stimulation, resulting in endometrial hyperplasia (as seen in this patient) or even endometrial carcinoma. In premenopausal women, this manifests as menstrual irregularities like menometrorrhagia. On ultrasound, they typically appear as large, solid, or complex cystic masses. **2. Why the Other Options are Incorrect:** * **Corpus Luteum Cyst:** These are functional cysts that secrete progesterone. While they can cause a delayed period followed by spotting, they are usually small (<3 cm), transient, and do not cause endometrial hyperplasia. * **Endometrioma:** Also known as "chocolate cysts," these are associated with dysmenorrhea and pelvic pain rather than menometrorrhagia. On ultrasound, they show characteristic "ground-glass" internal echoes, not a solid mass. * **Mature Cystic Teratoma (Dermoid Cyst):** These are the most common germ cell tumors. While they are solid/cystic masses, they are hormonally inactive and would not cause endometrial hyperplasia. **3. NEET-PG High-Yield Pearls:** * **Pathognomonic Finding:** **Call-Exner bodies** (small follicles filled with eosinophilic material) are seen on histology. * **Tumor Marker:** **Inhibin B** is the most sensitive marker for diagnosis and monitoring recurrence. * **Associated Pathology:** Always perform an endometrial biopsy in patients with GCT, as 5–10% have coexisting endometrial carcinoma due to prolonged estrogen exposure. * **Age Distribution:** Adult GCT (most common) peaks at 50–54 years; Juvenile GCT occurs in children/adolescents and causes precocious puberty.

Question 290: Which of the following statements is not true regarding cervical cancer screening guidelines according to the WHO?

A. Pap smear should be repeated yearly in women of reproductive age group. (Correct Answer)
B. HPV test should be done every five years in women between the ages of 30 to 49 years.
C. Visual inspection with acetic acid is more reliable at older age as it becomes easier to identify the transformation zone with age.
D. Pap smear can be repeated less frequently if it comes out negative for 3 consecutive years.

Explanation: **Explanation:** The WHO guidelines for cervical cancer screening emphasize cost-effective, high-impact strategies, moving away from annual testing toward longer intervals and more sensitive primary tests. **1. Why Option A is the Correct Answer (The False Statement):** Annual Pap smears are **not recommended** by the WHO. For the general population, the WHO recommends screening starting at age 30 with a high-performance test (like HPV DNA). Even when using cytology (Pap smear), the recommended interval is every 3 to 5 years, not yearly. Annual screening leads to over-diagnosis of transient HPV infections and unnecessary invasive procedures without significantly increasing the detection of invasive cancer. **2. Analysis of Other Options:** * **Option B:** In the general population, the WHO recommends **HPV DNA testing** as the primary screening tool every 5 to 10 years for women aged 30–49. * **Option C:** This statement is technically **incorrect** in clinical reality (VIA is actually *less* reliable in older women because the transformation zone recedes into the endocervical canal), but in the context of this specific question, Option A is the most definitive "not true" statement regarding standard screening frequency. * **Option D:** Traditional cytology-based programs often allow for an extension of the screening interval (e.g., every 5 years) if a woman has a history of consecutive negative smears, aligning with the goal of reducing the burden on healthcare systems. **High-Yield Clinical Pearls for NEET-PG:** * **Primary Screening Tool (WHO):** HPV DNA test is preferred over VIA or Cytology. * **Screening Age:** Start at **30 years** for the general population; start at **25 years** for women living with HIV. * **Frequency for HIV+:** Screen every 3 to 5 years using HPV DNA. * **Screen-and-Treat:** WHO promotes the "screen-and-treat" approach (treating based on a positive screening test without biopsy confirmation) to reduce loss to follow-up in low-resource settings.

Practice by Chapter

Cervical Cancer

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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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