Gynecologic Oncology — MCQs
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What is the primary management for a 25-year-old female diagnosed with choriocarcinoma?
Lutein cysts are associated with all of the following except:
A 56-year-old woman presents with weight loss and abdominal enlargement over 5 months. She has a family history of breast and ovarian carcinoma. Physical examination reveals a normal-sized uterus and no cervical lesions, but a left adnexal mass is palpable. An abdominal ultrasound shows a 10-cm cystic mass in the left adnexal region, with scattered 1-cm peritoneal nodules and ascites. Cytologic studies of peritoneal fluid reveal malignant cells. Which of the following mutated genes is most likely a factor in the development of this neoplasm?
What is the most frequent epithelial tumor of the ovary?
Staging of carcinoma of the cervix is primarily done by which method?
All of the following are risk factors for the development of endometrial cancer, EXCEPT:
What is the most common uterine malignancy?
Which of the following agents is implicated in the development of carcinoma of the cervix?
Precocious puberty is associated with which ovarian tumor?
Which of the following is NOT a germ cell tumor?
Gynecologic Oncology Indian Medical PG Practice Questions and MCQs
Question 571: What is the primary management for a 25-year-old female diagnosed with choriocarcinoma?
- A. Chemotherapy (Correct Answer)
- B. Radiotherapy
- C. Hysterectomy
- D. Hysterectomy followed by radiotherapy
Explanation: **Explanation:** Choriocarcinoma is a highly malignant, epithelial tumor arising from the trophoblastic cells. It is characterized by its rapid growth and early hematogenous spread, most commonly to the lungs. Despite its aggressive nature, it is one of the most **chemosensitive** solid tumors known to medicine, which is why **Chemotherapy (Option A)** is the primary and definitive management. * **Why Chemotherapy is Correct:** Choriocarcinoma is exquisitely sensitive to cytotoxic drugs. Treatment is stratified based on the FIGO/WHO risk score. Low-risk cases (score <7) are typically treated with single-agent chemotherapy (e.g., Methotrexate or Actinomycin-D), while high-risk cases (score ≥7) require multi-agent regimens like EMA-CO. * **Why Radiotherapy (Option B) is Incorrect:** Choriocarcinoma is generally radioresistant. Radiotherapy is rarely used, except in specific cases of brain or liver metastases to control hemorrhage. * **Why Hysterectomy (Option C & D) is Incorrect:** Since choriocarcinoma often affects women of reproductive age (like the 25-year-old in this question), fertility preservation is a priority. Hysterectomy does not address the systemic/micro-metastatic nature of the disease and is reserved only for life-threatening uterine hemorrhage or chemoresistant localized nodules. **NEET-PG High-Yield Pearls:** * **Tumor Marker:** Serum **beta-hCG** is the most sensitive marker for diagnosis and monitoring response to treatment. * **Common Site of Metastasis:** The **Lungs** (80%), often presenting as "cannonball" lesions on X-ray. * **Characteristic Histology:** Absence of chorionic villi; presence of sheets of syncytiotrophoblasts and cytotrophoblasts with significant hemorrhage and necrosis. * **Prognosis:** Even in the presence of widespread metastasis, the cure rate remains high (>90%) with appropriate chemotherapy.
Question 572: Lutein cysts are associated with all of the following except:
- A. Gestational trophoblastic tumors
- B. Clomiphene administration
- C. Bilaterality
- D. Use of oral contraceptive pills (Correct Answer)
Explanation: **Explanation:** **Theca Lutein Cysts** are functional ovarian cysts caused by hyperstimulation of the ovaries due to excessively high levels of **human chorionic gonadotropin (hCG)** or increased sensitivity to gonadotropins. **Why Option D is the correct answer:** Oral contraceptive pills (OCPs) **suppress** the hypothalamic-pituitary-ovarian axis, leading to the inhibition of FSH and LH. By preventing follicular development and ovulation, OCPs actually **reduce** the risk of functional cysts (including lutein cysts) and are often used as a treatment to prevent their recurrence. They do not cause or associate with the formation of lutein cysts. **Analysis of Incorrect Options:** * **A. Gestational Trophoblastic Tumors:** Conditions like Hydatidiform mole or Choriocarcinoma produce massive amounts of hCG, which cross-reacts with LH receptors on theca cells, leading to the formation of multiple lutein cysts (Hyperreactio Luteinalis). * **B. Clomiphene Administration:** Clomiphene citrate is an ovulation-inducing agent. It increases endogenous FSH/LH, which can overstimulate the ovaries, leading to the development of multiple lutein cysts as part of Ovarian Hyperstimulation Syndrome (OHSS). * **C. Bilaterality:** Lutein cysts are characteristically **bilateral**, multiple, and filled with clear straw-colored fluid. This distinguishes them from most other functional cysts like follicular cysts, which are typically unilateral. **Clinical Pearls for NEET-PG:** * **Management:** Lutein cysts are benign and usually **regress spontaneously** once the source of hCG is removed (e.g., after evacuation of a molar pregnancy). Surgery is only indicated for complications like torsion or rupture. * **Association:** They are also seen in multiple pregnancies (twins/triplets) and Rh isoimmunization due to large placental mass and high hCG. * **Appearance:** On ultrasound, they present a "spoke-wheel" appearance due to multiple thin-walled septations.
Question 573: A 56-year-old woman presents with weight loss and abdominal enlargement over 5 months. She has a family history of breast and ovarian carcinoma. Physical examination reveals a normal-sized uterus and no cervical lesions, but a left adnexal mass is palpable. An abdominal ultrasound shows a 10-cm cystic mass in the left adnexal region, with scattered 1-cm peritoneal nodules and ascites. Cytologic studies of peritoneal fluid reveal malignant cells. Which of the following mutated genes is most likely a factor in the development of this neoplasm?
- A. BRCA1 (Correct Answer)
- B. ERBB2 (HER2)
- C. MYC
- D. KRAS
Explanation: **Explanation:** The clinical presentation of a postmenopausal woman with a large adnexal mass, ascites, peritoneal nodules (omental caking), and malignant cytology is highly suggestive of **High-Grade Serous Ovarian Carcinoma (HGSOC)**. **Why BRCA1 is correct:** The patient’s strong family history of breast and ovarian cancer points toward **Hereditary Breast and Ovarian Cancer (HBOC) syndrome**. Mutations in **BRCA1** (located on chromosome 17q) and **BRCA2** (chromosome 13q) are the most significant genetic risk factors for epithelial ovarian cancer. BRCA1 mutations carry a lifetime risk of ovarian cancer of approximately 40-50%. These genes are involved in DNA repair via homologous recombination; their loss leads to genomic instability and malignant transformation. **Why the other options are incorrect:** * **ERBB2 (HER2):** While amplified in some breast and gastric cancers, it is not a primary driver or a hereditary marker for the development of epithelial ovarian cancer. * **MYC:** This oncogene is frequently amplified in various cancers (like Burkitt lymphoma), but it is a somatic change rather than a germline mutation associated with the specific family history described. * **KRAS:** Mutations in KRAS are typically associated with **Low-Grade Serous Carcinoma** and **Mucinous Ovarian Tumors**, rather than the aggressive, hereditary high-grade serous type suggested here. **NEET-PG High-Yield Pearls:** * **Most common ovarian cancer:** Serous Cystadenocarcinoma. * **Psammoma bodies:** Characteristic microscopic finding in serous tumors. * **Tumor Marker:** CA-125 is used for monitoring treatment response in epithelial ovarian cancer. * **Prophylaxis:** Risk-reducing bilateral salpingo-oophorectomy (RRBSO) is recommended for BRCA1 carriers by age 35–40.
Question 574: What is the most frequent epithelial tumor of the ovary?
- A. Papillary serous cystadenoma (Correct Answer)
- B. Brenner tumor
- C. Endometrioid tumor
- D. Mucinous cystadenoma
Explanation: **Explanation:** Surface epithelial-stromal tumors are the most common type of ovarian neoplasms, accounting for approximately 65–70% of all ovarian tumors. Among these, **Serous tumors** are the most frequent. 1. **Why A is correct:** Serous tumors represent about 30% of all ovarian neoplasms. **Serous cystadenomas** (specifically the papillary variety) are the most common benign epithelial tumors. They are frequently bilateral (15–25%) and are characterized histologically by psammoma bodies in approximately 30% of cases. 2. **Why B is incorrect:** **Brenner tumors** are uncommon epithelial tumors composed of transitional epithelium (similar to bladder epithelium). They are usually benign and often incidental findings. 3. **Why C is incorrect:** **Endometrioid tumors** account for about 10–15% of ovarian surface epithelial tumors. They are significant because they are frequently malignant and are associated with endometriosis in 15–30% of cases. 4. **Why D is incorrect:** **Mucinous cystadenomas** are the second most common epithelial tumors (approx. 20–25%). They are known for reaching massive sizes and can be associated with *Pseudomyxoma peritonei* if a malignant mucinous tumor ruptures. **High-Yield Clinical Pearls for NEET-PG:** * **Most common ovarian tumor overall:** Benign Cystic Teratoma (Dermoid cyst) in young women; Serous Cystadenoma in the general population. * **Most common malignant ovarian tumor:** Serous Cystadenocarcinoma. * **Psammoma bodies:** Characteristic of Serous tumors and Meningiomas. * **Bilateralism:** Serous tumors are the most likely epithelial tumors to be bilateral. * **Tumor Marker:** CA-125 is the primary marker for monitoring epithelial ovarian cancers.
Question 575: Staging of carcinoma of the cervix is primarily done by which method?
- A. CT scan
- B. MRI scan
- C. Clinical findings (Correct Answer)
- D. Histopathology
Explanation: **Explanation:** The staging of **Carcinoma Cervix** is unique among gynecological malignancies because it is primarily **Clinical**. This approach is maintained by FIGO (International Federation of Gynecology and Obstetrics) to ensure that staging can be performed consistently worldwide, including in resource-limited settings where advanced imaging is unavailable. **Why Clinical Findings is Correct:** According to the **FIGO 2018 staging system**, the stage is determined based on physical examination (inspection, palpation, and vaginal/rectal exam), colposcopy, biopsy, and basic procedures like cystoscopy or proctoscopy (if advanced disease is suspected). While the 2018 update *allows* the use of imaging and pathology to refine the stage, the fundamental framework remains clinical to allow for global comparability. **Why Other Options are Incorrect:** * **CT and MRI Scans:** While these are excellent for assessing lymph node involvement and parametrial spread, they are considered "optional" adjuncts. They are used to *supplement* the clinical stage rather than define the primary staging method. * **Histopathology:** While a biopsy is mandatory to **diagnose** cervical cancer, the **staging** is not surgical (unlike endometrial or ovarian cancer). Histopathology of the radical hysterectomy specimen may provide "pathological staging," but the official FIGO stage assigned for treatment planning is clinical. **High-Yield Clinical Pearls for NEET-PG:** * **Cervical Cancer:** Clinical Staging (FIGO). * **Endometrial & Ovarian Cancer:** Surgical Staging. * **Vulvar Cancer:** Surgical Staging. * **Key Update:** In FIGO 2018, Stage IB is now divided into 5mm increments of depth, and **lymph node status** (determined by imaging or pathology) can now upgrade a patient to **Stage IIIC**.
Question 576: All of the following are risk factors for the development of endometrial cancer, EXCEPT:
- A. Fibromyoma
- B. Endometrial hyperplasia
- C. Dysgerminoma (Correct Answer)
- D. Granulosa cell tumor
Explanation: **Explanation:** The development of Type I Endometrial Carcinoma is primarily driven by **unopposed estrogen** stimulation, which leads to endometrial proliferation. **Why Dysgerminoma is the Correct Answer:** Dysgerminoma is a germ cell tumor of the ovary. Unlike sex cord-stromal tumors, germ cell tumors are generally **hormonally inactive** (or may produce LDH/hCG). They do not secrete estrogen and, therefore, do not contribute to the hormonal milieu required for endometrial hyperplasia or malignancy. **Analysis of Other Options:** * **Granulosa Cell Tumor:** This is a sex cord-stromal tumor known for secreting high levels of **estrogen**. This chronic estrogenic state is a classic risk factor for endometrial hyperplasia and subsequent carcinoma. * **Endometrial Hyperplasia:** Specifically atypical hyperplasia (EIN), this is the direct **precursor lesion** for Type I endometrial cancer. The risk of progression to malignancy is approximately 29% if left untreated. * **Fibromyoma (Leiomyoma):** While fibroids themselves are benign, they are **estrogen-dependent** tumors. Their presence often indicates a hyperestrogenic state or prolonged exposure to estrogen, which correlates with an increased risk of endometrial cancer. **NEET-PG High-Yield Pearls:** * **Risk Factors (The "Rule of Estrogen"):** Obesity (peripheral conversion of androstenedione to estrone), Nulliparity, Early menarche/Late menopause, PCOS, and Tamoxifen use. * **Protective Factors:** Combined Oral Contraceptive Pills (COCPs), smoking (decreases estrogen levels, though harmful otherwise), and multiparity. * **Lynch Syndrome (HNPCC):** The most common genetic predisposition; these patients require prophylactic hysterectomy by age 40-45.
Question 577: What is the most common uterine malignancy?
- A. Leiomyosarcoma of uterus
- B. Endometroid adenocarcinoma (Correct Answer)
- C. Serous uterine carcinoma
- D. Clear cell carcinoma
Explanation: **Explanation:** **Endometrial carcinoma** is the most common gynecological malignancy in developed countries and the most common uterine malignancy worldwide. It is broadly classified into two types: Type I and Type II. 1. **Why Endometroid Adenocarcinoma is correct:** **Endometroid adenocarcinoma** is the classic **Type I endometrial carcinoma**. It accounts for approximately **75–80%** of all endometrial cancers. It is typically associated with "unopposed estrogen" stimulation (e.g., obesity, PCOS, nulliparity, or HRT), arises from endometrial hyperplasia, and generally carries a favorable prognosis as it is often diagnosed at an early stage. 2. **Why other options are incorrect:** * **Leiomyosarcoma (Option A):** This is a mesenchymal tumor (sarcoma). While it is the most common primary uterine sarcoma, sarcomas overall represent only about 3–5% of all uterine malignancies. * **Serous Uterine Carcinoma (Option C):** This is a **Type II** endometrial cancer. It is highly aggressive, estrogen-independent, and typically occurs in older, thin, postmenopausal women. It accounts for only about 10% of cases. * **Clear Cell Carcinoma (Option D):** Also a **Type II** cancer, it is rare (<5% of cases) and carries a poor prognosis compared to the endometrioid type. **High-Yield Clinical Pearls for NEET-PG:** * **Most common symptom:** Postmenopausal bleeding (PMB). * **Most common histological type:** Endometrioid adenocarcinoma. * **Precursor lesion:** Atypical Endometrial Hyperplasia (now termed Endometrial Intraepithelial Neoplasia - EIN). * **Protective factors:** Combined oral contraceptive pills (OCPs), smoking (decreases estrogen levels, though not a health recommendation), and multiparity. * **Lynch Syndrome (HNPCC):** Associated with a significantly increased risk of endometrioid adenocarcinoma.
Question 578: Which of the following agents is implicated in the development of carcinoma of the cervix?
- A. Herpes simplex virus
- B. Human papilloma virus (Correct Answer)
- C. Epstein-Barr virus
- D. Adenovirus
Explanation: **Explanation:** The primary etiological factor in the development of cervical carcinoma is persistent infection with high-risk strains of the **Human Papillomavirus (HPV)**. HPV types 16 and 18 are responsible for approximately 70% of all cervical cancer cases globally. The oncogenic potential of HPV lies in its early proteins, **E6 and E7**, which inhibit the host’s tumor suppressor proteins **p53 and pRb**, respectively. This leads to uncontrolled cell cycle progression and genomic instability. **Analysis of Options:** * **Option A (HSV):** While Herpes Simplex Virus Type 2 was once considered a potential candidate, it is now viewed only as a possible co-factor that may increase the risk of HPV persistence, but it does not cause cervical cancer independently. * **Option C (EBV):** Epstein-Barr Virus is associated with Burkitt lymphoma, Nasopharyngeal carcinoma, and Hodgkin lymphoma, but not cervical cancer. * **Option D (Adenovirus):** Adenoviruses typically cause respiratory, ocular, and gastrointestinal infections and have no established link to human malignancies. **High-Yield Clinical Pearls for NEET-PG:** * **Most common strain:** HPV 16 is the most common strain associated with Squamous Cell Carcinoma; HPV 18 is more frequently associated with Adenocarcinoma. * **Screening:** The Pap smear looks for cytological changes (koilocytes), while HPV DNA testing (HC2 or PCR) detects the virus itself. * **Vaccination:** The 9-valent vaccine (Gardasil 9) provides the broadest protection. The ideal age for vaccination is 9–14 years (before sexual debut). * **Transformation Zone:** Most cervical cancers arise in the Squamocolumnar Junction (Transformation Zone).
Question 579: Precocious puberty is associated with which ovarian tumor?
- A. Dermoid
- B. Gynandroblastoma
- C. Granulosa cell tumor (Correct Answer)
- D. Arrhenoblastoma
Explanation: **Explanation:** **Granulosa Cell Tumor (GCT)** is the correct answer because it is a functional **Sex Cord-Stromal Tumor** that secretes high levels of **Estrogen**. In prepubertal girls, this excess estrogen triggers **Isosexual Precocious Puberty**, characterized by early breast development (thelarche), growth of pubic hair, and vaginal bleeding. GCTs are the most common estrogen-secreting ovarian tumors and are histologically identified by the presence of **Call-Exner bodies** and "coffee-bean" nuclei. **Analysis of Incorrect Options:** * **Dermoid (Mature Cystic Teratoma):** This is a germ cell tumor containing tissues from all three germ layers (ectoderm, mesoderm, endoderm). It is usually asymptomatic or causes torsion but does not secrete hormones that trigger precocity. * **Gynandroblastoma:** An extremely rare sex cord-stromal tumor containing both male (Sertoli-Leydig) and female (Granulosa) elements. While it can be hormonal, it is not the classic or most common association for precocious puberty. * **Arrhenoblastoma (Sertoli-Leydig Cell Tumor):** These are androgen-secreting tumors. Instead of precocious puberty, they cause **virilization** (hirsutism, clitoromegaly, and voice deepening). **High-Yield Clinical Pearls for NEET-PG:** * **Tumor Marker:** Inhibin (specifically Inhibin B) is the gold standard marker for monitoring GCT. * **Histology:** Look for the "Coffee Bean" appearance of nuclei and Call-Exner bodies (rosette-like structures). * **Age Distribution:** The **Adult GCT** is more common (postmenopausal), while the **Juvenile GCT** is the subtype specifically associated with precocious puberty. * **Risk:** Due to high estrogen, GCT is often associated with endometrial hyperplasia or endometrial carcinoma.
Question 580: Which of the following is NOT a germ cell tumor?
- A. Dysgerminoma
- B. Teratoma
- C. Granulosa theca cell tumor (Correct Answer)
- D. Embryonal cell carcinoma
Explanation: **Explanation:** Ovarian tumors are classified based on their tissue of origin. To answer this question, one must distinguish between **Germ Cell Tumors (GCTs)** and **Sex Cord-Stromal Tumors (SCSTs)**. **Why Option C is correct:** **Granulosa theca cell tumor** is a **Sex Cord-Stromal Tumor**, not a germ cell tumor. These tumors arise from the ovarian stroma or the specialized cells surrounding the oocyte (granulosa and theca cells). They are clinically significant because they are often hormonally active, typically secreting **estrogen**, which can lead to endometrial hyperplasia or precocious puberty. **Why the other options are incorrect:** * **A. Dysgerminoma:** The most common malignant germ cell tumor. It is the female counterpart of the testicular seminoma and is highly radiosensitive. * **B. Teratoma:** The most common germ cell tumor overall. It can be mature (benign/dermoid cyst) or immature (malignant), containing tissues from all three germ layers (ectoderm, mesoderm, endoderm). * **C. Embryonal cell carcinoma:** A rare, highly aggressive malignant germ cell tumor that often secretes both Alpha-fetoprotein (AFP) and human Chorionic Gonadotropin (hCG). **NEET-PG High-Yield Pearls:** 1. **Most common Ovarian Tumor:** Surface Epithelial Tumor (Serous Cystadenoma). 2. **Tumor Markers for GCTs:** * **Dysgerminoma:** LDH (Lactate Dehydrogenase). * **Yolk Sac Tumor:** AFP (Alpha-fetoprotein) – look for *Schiller-Duval bodies*. * **Choriocarcinoma:** β-hCG. 3. **Granulosa Cell Tumor Marker:** Inhibin (specifically Inhibin B). Look for *Call-Exner bodies* on histology. 4. Germ cell tumors are typically seen in younger women (adolescents and young adults), whereas epithelial tumors are more common in postmenopausal women.
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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