Gynecologic Oncology Practice Questions

Q: What is the percentage of complete moles that progress to persistent Gestational Trophoblastic Neoplasia (GTN)?

15-20%. **Explanation:** Gestational Trophoblastic Neoplasia (GTN) refers to the malignant subset of gestational trophoblastic diseases. The risk of malignant transformation is significantly higher in complete hydatidiform moles compared to partial moles. **Why 15-20% is correct:** In a **Complete Hydatidiform Mole (CHM)**, there is a total absence of fetal tissue and a 46,XX or 46,XY diploid karyotype (entirely paternal). Due to the higher proliferation of trophoblastic tissue, approximately **15-20%** of patients with a complete mole will develop persistent GTN (most commonly invasive mole, and less frequently, choriocarcinoma). **Analysis of Incorrect Options:** * **A, B, and C (1-12%):** These percentages are too low for complete moles. However, it is important to note that for **Partial Hydatidiform Moles (PHM)**, the risk of progression to GTN is much lower, typically cited as **1-5%**. Options A and B would be more representative of the risk associated with partial moles. **High-Yield Clinical Pearls for NEET-PG:** * **Karyotype:** Complete Mole is 46,XX (90%) or 46,XY (10%); Partial Mole is Triploid (69,XXX or 69,XXY). * **Risk Factors for Malignancy in CHM:** Pre-evacuation hCG >100,000 mIU/mL, excessive uterine size for dates, and large theca lutein cysts (>6 cm). * **Follow-up:** Post-evacuation, weekly β-hCG levels are monitored until three consecutive normal values are obtained, then monthly for 6 months. * **Diagnosis of GTN:** Based on FIGO criteria—hCG plateau (4 values over 3 weeks), hCG rise (3 values over 2 weeks), or histological diagnosis of choriocarcinoma.

Q: Which of the following statements regarding hydatidiform mole is correct?

All of the above. ### Explanation Hydatidiform mole (molar pregnancy) is a part of Gestational Trophoblastic Disease (GTD) characterized by abnormal proliferation of trophoblastic tissue and hydropic degeneration of chorionic villi. **Why "All of the above" is correct:** * **Conversion to Carcinoma:** Approximately **2% of complete hydatidiform moles** progress to choriocarcinoma (a highly malignant epithelial tumor). While the risk of developing persistent Gestational Trophoblastic Neoplasia (GTN) is higher (15–20%), the specific conversion rate to frank choriocarcinoma is historically cited around 2-3%. * **Diploid Nature:** A **Complete Mole** is typically **diploid (46,XX or 46,XY)**. It is androgenetic in origin, usually formed when a "blighted" ovum (no maternal nucleus) is fertilized by a single sperm that duplicates its chromosomes (90%) or by two sperm (10%). Note: Partial moles are triploid (69,XXX/XXY). * **Increased beta-hCG:** Trophoblastic hyperplasia leads to excessive production of human chorionic gonadotropin. In molar pregnancies, **beta-hCG levels are disproportionately high** for the period of gestation (often >100,000 mIU/mL), which is a key diagnostic marker. **High-Yield Clinical Pearls for NEET-PG:** 1. **Snowstorm Appearance:** The classic ultrasound finding due to multiple hydropic villi. 2. **Theca Lutein Cysts:** Occur in 25-30% of cases due to extreme ovarian stimulation by high hCG. 3. **Management:** Suction evacuation is the treatment of choice regardless of uterine size. 4. **Follow-up:** Weekly beta-hCG monitoring until three consecutive negative results, then monthly for 6 months to ensure no malignant transformation. 5. **Karyotype Distinction:** Complete Mole = 46,XX (Diploid); Partial Mole = 69,XXY (Triploid).

Q: Carcinoma of the cervix stage IA1 is defined by which of the following depth of invasion?

Less than 3 mm depth of stromal invasion. **Explanation:** The staging of Cervical Cancer is based on the **FIGO (International Federation of Gynecology and Obstetrics) classification**. Stage I is defined as carcinoma strictly confined to the cervix. Stage IA represents **microscopically diagnosed** invasive carcinoma, where the lesion is not visible to the naked eye. * **Stage IA1:** Defined as measured stromal invasion **less than 3.0 mm** in depth. * **Stage IA2:** Defined as measured stromal invasion **between 3.0 mm and less than 5.0 mm** in depth. **Why the other options are incorrect:** * **Option B & D:** The "7 mm" horizontal spread criterion was removed in the **2018 FIGO update**. Previously, Stage IA required a lateral extent of <7 mm, but current staging relies solely on the **depth of invasion**. * **Option C:** Invasion greater than 3 mm (but less than 5 mm) would categorize the disease as **Stage IA2**. If the invasion exceeds 5 mm, it is classified as Stage IB. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** Stage IA1 and IA2 are diagnosed via **microscopy** (usually through a cone biopsy or LEEP), not clinical examination. * **Management:** For Stage IA1 without lymphovascular space invasion (LVSI), **Extra-fascial Hysterectomy** (Type A) or even **Conization** (if fertility preservation is desired) is sufficient. * **Lymphovascular Space Invasion (LVSI):** The presence of LVSI does not change the FIGO stage but significantly influences the choice of surgical radicality. * **Stage IB1:** Now defined as invasion ≥ 5 mm depth and < 2 cm in greatest dimension.

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: Which tumor marker is elevated in dysgerminoma?

Lactate dehydrogenase (LDH). **Explanation:** **Dysgerminoma** is the most common malignant germ cell tumor of the ovary, typically occurring in young women and adolescents. It is the female counterpart of the testicular seminoma. **Why LDH is the correct answer:** Lactate dehydrogenase (LDH) is the classic, highly sensitive tumor marker for dysgerminoma. It reflects the high turnover rate of the undifferentiated germ cells. While not entirely specific, it is used for both initial diagnosis and monitoring treatment response/recurrence. Occasionally, dysgerminomas may also show mild elevations in **Alkaline Phosphatase (ALP)**. **Analysis of Incorrect Options:** * **A. Alpha-fetoprotein (AFP):** This is the characteristic marker for **Yolk Sac Tumors** (Endodermal Sinus Tumors). It is also elevated in immature teratomas and Sertoli-Leydig cell tumors. * **C. Human chorionic gonadotropin (HCG):** This is the primary marker for **Choriocarcinoma**. While 5% of dysgerminomas contain syncytiotrophoblastic giant cells that can produce low levels of HCG, it is not the primary diagnostic marker. * **D. CA-19-9:** This is a marker primarily associated with **pancreatic and biliary tract cancers**, as well as some mucinous ovarian tumors, but has no specific association with dysgerminoma. **High-Yield Clinical Pearls for NEET-PG:** * **Most common** malignant germ cell tumor in pregnancy: Dysgerminoma. * **Radiosensitivity:** Dysgerminomas are exquisitely radiosensitive (though surgery and chemotherapy are preferred to preserve fertility). * **Associated Condition:** Often associated with **gonadal dysgenesis** (Swyer Syndrome); if a dysgerminoma is found in a pre-menarcheal girl, a karyotype should be performed. * **Summary Table:** * Dysgerminoma → LDH * Yolk Sac Tumor → AFP (Schiller-Duval bodies) * Choriocarcinoma → hCG * Granulosa Cell Tumor → Inhibin B

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 stage of vaginal carcinoma when there is involvement of the pelvis?

Stage III. **Explanation:** The staging of vaginal carcinoma follows the **FIGO (International Federation of Gynecology and Obstetrics)** classification system. The correct answer is **Stage III** because this stage specifically denotes the extension of the tumor beyond the primary site to involve the pelvic structures. * **Stage III (Correct):** This stage is defined by the carcinoma extending to the **pelvic wall** and/or involving the **lower third of the vagina**. It also includes cases with biopsy-proven metastatic **pelvic or inguinal lymph nodes**, regardless of the primary tumor size. * **Stage I (Incorrect):** The carcinoma is strictly limited to the **vaginal wall**. There is no extension into the surrounding tissues or lymph nodes. * **Stage II (Incorrect):** The carcinoma has involved the **paravaginal tissues** (subvaginal tissues) but has **not** reached the pelvic wall. * **Stage IV (Incorrect):** This represents advanced disease. **Stage IVA** involves the mucosa of the bladder or rectum, or extension beyond the true pelvis. **Stage IVB** involves distant metastasis (e.g., lungs, liver). **High-Yield Clinical Pearls for NEET-PG:** * **Primary vs. Secondary:** Primary vaginal cancer is rare. Most vaginal cancers are metastatic (secondary), most commonly from the cervix or endometrium. * **Histology:** The most common histological type is **Squamous Cell Carcinoma (SCC)**, often associated with high-risk HPV (16 and 18). * **Location:** The most common site for primary vaginal cancer is the **upper third of the posterior vaginal wall**. * **Lymphatic Drainage:** This is a frequent exam topic. The **upper 2/3** drains to the pelvic (iliac) nodes, while the **lower 1/3** drains to the inguinal and femoral nodes.

Question 1

What is the percentage of complete moles that progress to persistent Gestational Trophoblastic Neoplasia (GTN)?

Accepted Answer

15-20%

Answer

1-4%

Answer

4-8%

Answer

8-12%

Question 2

A 25-year-old married nullipara undergoes laparoscopic cystectomy for an ovarian cyst, which on histopathology reveals ovarian serous cystadenocarcinoma. What should be the next management?

Accepted Answer

Serial Ca-125 measurement and follow-up

Answer

Hysterectomy and bilateral salpingo-oophorectomy

Answer

Hysterectomy with radiotherapy

Answer

Radiotherapy

Question 3

Which of the following statements regarding hydatidiform mole is correct?

Accepted Answer

All of the above

Answer

2% of cases may convert to carcinoma

Answer

It is diploid

Answer

There is an increase in beta-hCG levels

Question 4

Carcinoma of the cervix stage IA1 is defined by which of the following depth of invasion?

Accepted Answer

Less than 3 mm depth of stromal invasion

Answer

Less than 7 mm depth of stromal invasion

Answer

Greater than 3 mm depth of stromal invasion

Answer

Greater than 7 mm depth of stromal invasion

Question 5

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 6

A 55-year-old nulliparous black woman has a large, fungating tumor projecting from her cervix. A biopsy reveals a background of spindle-shaped cells with over 10 mitoses per high power field. Many of the mitoses have abnormal mitotic spindles. What is the most likely diagnosis?

Accepted Answer

Well-differentiated cervical carcinoma

Answer

Sarcomatous transformation of a uterine leiomyoma

Answer

Malignant mixed mullerian tumor

Answer

Well-differentiated endometrial carcinoma

Question 7

Which tumor marker is elevated in dysgerminoma?

Accepted Answer

Lactate dehydrogenase (LDH)

Answer

Alpha-fetoprotein (AFP)

Answer

Human chorionic gonadotropin (HCG)

Answer

Carbohydrate antigen 19-9 (CA-19-9)

Question 8

Suburethral metastasis is seen in which of the following?

Accepted Answer

Carcinoma endometrium

Answer

Carcinoma cervix

Answer

Choriocarcinoma

Answer

Vaginal carcinoma

Question 9

Gestational trophoblastic neoplasia includes all except?

Accepted Answer

Complete hydatidiform mole

Answer

Invasive mole

Answer

Choriocarcinoma

Answer

Placental site trophoblastic tumor

Question 10

What is the stage of vaginal carcinoma when there is involvement of the pelvis?

Accepted Answer

Stage III

Answer

Stage I

Answer

Stage II

Answer

Stage IV

Gynecologic Oncology — MCQs

Gynecologic Oncology — MCQs

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