Gynecologic Oncology Practice Questions

Q: All of the following are known risk factors for the development of ovarian carcinoma except?

Use of oral contraceptives. ### Explanation The development of epithelial ovarian carcinoma is closely linked to the **"Incessant Ovulation Theory."** This theory suggests that repeated trauma to the ovarian surface epithelium during ovulation, followed by inflammatory repair processes, increases the risk of malignant transformation. **Why "Use of Oral Contraceptives" is the correct answer:** Oral Contraceptive Pills (OCPs) are **protective** against ovarian cancer, not a risk factor. By suppressing ovulation, OCPs provide "rest" to the ovarian epithelium. Using OCPs for 5 years reduces the lifetime risk of ovarian cancer by approximately 50%. This protective effect persists for up to 15–20 years after discontinuation. **Analysis of Incorrect Options:** * **Family History:** A first-degree relative with ovarian cancer significantly increases risk. About 10–15% of cases have a hereditary component. * **Use of Clomiphene:** Clomiphene citrate is an ovulation-inducing agent. Prolonged use (usually >12 cycles), especially in women who do not achieve pregnancy, is associated with an increased risk due to "super-ovulation." * **BRCA-1 Positive:** This is the strongest genetic risk factor. BRCA-1 mutation carriers have a 40–50% lifetime risk of developing ovarian cancer (compared to 1.3% in the general population). **NEET-PG High-Yield Pearls:** * **Protective Factors:** OCPs, Pregnancy (Multiparity), Breastfeeding, and Tubal Ligation/Salpingectomy (prevents migration of precursors from the fallopian tube). * **Risk Factors:** Nulliparity, Early menarche, Late menopause, Endometriosis (linked to Clear cell and Endometrioid types), and Lynch Syndrome (HNPCC). * **Most Common Type:** Serous cystadenocarcinoma is the most common epithelial ovarian malignancy.

Q: Gestational trophoblastic neoplasia includes all except?

Complete hydatidiform mole. **Explanation:** The core concept in this question lies in the distinction between **Gestational Trophoblastic Disease (GTD)** and **Gestational Trophoblastic Neoplasia (GTN)**. While GTD is an umbrella term encompassing all proliferative disorders of the placenta, GTN specifically refers to the subset that is **malignant** or has the potential for local invasion and metastasis. 1. **Why Option A is the Correct Answer:** A **Complete Hydatidiform Mole** is considered a benign form of GTD. Although it has a risk of progressing to malignancy (approx. 15-20%), the mole itself is not classified as a neoplasia until there is evidence of persistent elevation of hCG or clinical invasion. Therefore, it is excluded from the definition of GTN. 2. **Why Other Options are Incorrect:** * **Invasive Mole (Option B):** Characterized by the invasion of molar villi into the myometrium; it is the most common form of GTN following a hydatidiform mole. * **Choriocarcinoma (Option C):** A highly malignant, epithelial tumor that lacks chorionic villi and spreads hematogenously. It is a classic component of GTN. * **Placental Site Trophoblastic Tumor (PSTT) (Option D):** A rare GTN arising from intermediate trophoblasts at the placental site. It is unique because it produces low levels of hCG but high levels of Human Placental Lactogen (hPL). **High-Yield Clinical Pearls for NEET-PG:** * **FIGO Staging:** Only GTN (Invasive mole, Choriocarcinoma, PSTT, and Epithelioid Trophoblastic Tumor) is staged using the FIGO anatomical staging and WHO scoring system. * **Karyotype:** Complete Mole is usually **46,XX** (diploid, paternal origin), whereas Partial Mole is **69,XXY** (triploid). * **Management:** The primary treatment for GTN is chemotherapy (Methotrexate or Actinomycin-D), whereas the primary treatment for a Hydatidiform Mole is **Suction and Evacuation**.

Q: What is the primary management for a 25-year-old female diagnosed with choriocarcinoma?

Chemotherapy. **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.

Q: 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?

BRCA1. **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.

Q: Staging of carcinoma of the cervix is primarily done by which method?

Clinical findings. **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**.

Q: All of the following are risk factors for the development of endometrial cancer, EXCEPT:

Dysgerminoma. **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.

Q: Precocious puberty is associated with which ovarian tumor?

Granulosa cell tumor. **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.

Q: Prophylactic chemotherapy in hydatidiform mole should preferably be given:

In selected cases following evacuation. **Explanation:** The primary management for a hydatidiform mole is **suction evacuation** followed by serial monitoring of serum β-hCG levels. Prophylactic chemotherapy is **not recommended as a routine practice** because it can mask the development of persistent gestational trophoblastic neoplasia (GTN), increase the risk of drug resistance, and expose patients to unnecessary toxicity. **Why Option C is correct:** Prophylactic chemotherapy (usually with Methotrexate or Actinomycin D) is reserved for **selected high-risk cases** where the risk of malignant transformation is high and the patient is likely to be lost to follow-up. High-risk criteria include: * Pre-evacuation β-hCG >100,000 mIU/mL. * Excessive uterine enlargement for gestational age. * Theca lutein cysts >6 cm. * Age >40 years. **Analysis of Incorrect Options:** * **Options A, B, and D:** Routine use (whether before, immediately after, or 6 weeks post-evacuation) is contraindicated. In 80–90% of cases, evacuation alone is curative. Routine administration leads to over-treatment and potential development of chemo-resistant trophoblastic cells. **Clinical Pearls for NEET-PG:** * **Gold Standard Treatment:** Suction evacuation is the treatment of choice regardless of uterine size. * **Follow-up:** Weekly β-hCG until three consecutive normal values are obtained, then monthly for 6 months. * **Contraception:** Combined Oral Contraceptive Pills (COCPs) are preferred during the follow-up period to prevent pregnancy (which would confuse hCG monitoring). * **Risk of Malignancy:** Approximately 15–20% for complete moles and <5% for partial moles.

Question 1

All of the following are known risk factors for the development of ovarian carcinoma except?

Accepted Answer

Use of oral contraceptives

Answer

Family history of ovarian carcinoma

Answer

Use of Clomiphene

Answer

BRCA-1 positive individual

Question 2

Suburethral metastasis is seen in which of the following?

Accepted Answer

Carcinoma endometrium

Answer

Carcinoma cervix

Answer

Choriocarcinoma

Answer

Vaginal carcinoma

Question 3

Gestational trophoblastic neoplasia includes all except?

Accepted Answer

Complete hydatidiform mole

Answer

Invasive mole

Answer

Choriocarcinoma

Answer

Placental site trophoblastic tumor

Question 4

What is the primary management for a 25-year-old female diagnosed with choriocarcinoma?

Accepted Answer

Chemotherapy

Answer

Radiotherapy

Answer

Hysterectomy

Answer

Hysterectomy followed by radiotherapy

Question 5

Lutein cysts are associated with all of the following except:

Accepted Answer

Use of oral contraceptive pills

Answer

Gestational trophoblastic tumors

Answer

Clomiphene administration

Answer

Bilaterality

Question 6

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?

Accepted Answer

BRCA1

Answer

ERBB2 (HER2)

Answer

MYC

Answer

KRAS

Question 7

Staging of carcinoma of the cervix is primarily done by which method?

Accepted Answer

Clinical findings

Answer

CT scan

Answer

MRI scan

Answer

Histopathology

Question 8

All of the following are risk factors for the development of endometrial cancer, EXCEPT:

Accepted Answer

Dysgerminoma

Answer

Fibromyoma

Answer

Endometrial hyperplasia

Answer

Granulosa cell tumor

Question 9

Precocious puberty is associated with which ovarian tumor?

Accepted Answer

Granulosa cell tumor

Answer

Dermoid

Answer

Gynandroblastoma

Answer

Arrhenoblastoma

Question 10

Prophylactic chemotherapy in hydatidiform mole should preferably be given:

Accepted Answer

In selected cases following evacuation

Answer

Prior to evacuation as a routine

Answer

Following evacuation as a routine

Answer

As a routine 6 weeks postevacuation

Gynecologic Oncology — MCQs

Gynecologic Oncology — MCQs

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