Gynecologic Oncology Practice Questions

Q: Inheritance is a major factor in which of the following conditions?

Endometrial carcinoma. **Explanation:** **1. Why Endometrial Carcinoma is the Correct Answer:** Inheritance plays a significant role in endometrial carcinoma, primarily through **Lynch Syndrome (Hereditary Non-Polyposis Colorectal Cancer - HNPCC)**. This autosomal dominant condition is caused by mutations in DNA mismatch repair (MMR) genes (MLH1, MSH2, MSH6, PMS2). Women with Lynch Syndrome have a **40–60% lifetime risk** of developing endometrial cancer, which often exceeds their risk of colorectal cancer. Additionally, Cowden Syndrome (PTEN mutation) also predisposes individuals to endometrial malignancy. **2. Why Other Options are Incorrect:** * **Cervical Carcinoma:** This is primarily an **infectious disease**, not a genetic one. Over 99% of cases are caused by persistent infection with **High-Risk Human Papillomavirus (HPV)**, specifically types 16 and 18. Risk factors are related to sexual behavior, parity, and smoking rather than inherited germline mutations. * **Both/None:** Since inheritance is a proven major factor for endometrial cancer but not for cervical cancer, these options are incorrect. **High-Yield Clinical Pearls for NEET-PG:** * **Lynch Syndrome:** The most common inherited predisposition to endometrial cancer. Screening involves annual endometrial biopsies starting at age 30–35. * **Type I vs. Type II Endometrial Cancer:** Type I (Endometrioid) is associated with estrogen excess and PTEN mutations, while Type II (Serous) is associated with p53 mutations. * **Protective Factors:** Combined Oral Contraceptive Pills (COCPs) significantly reduce the risk of endometrial cancer by providing progestational opposition to estrogen. * **Cervical Cancer:** The most common gynecological cancer in India; preventable via HPV vaccination and Pap smear screening.

Q: What is true about dysgerminoma?

Most common malignant germ cell tumor. **Explanation:** **Dysgerminoma** is the most common malignant germ cell tumor (GCT) of the ovary, accounting for approximately 50% of all malignant GCTs. It is the female counterpart of the testicular seminoma and typically affects young women in their teens and early twenties. * **Why Option B is correct:** Dysgerminoma is statistically the most frequent malignancy arising from germ cells. It is often associated with gonadal dysgenesis (e.g., Swyer syndrome). * **Why Option A is incorrect:** Dysgerminoma is famously **exquisitely radiosensitive**. However, because it primarily affects women of reproductive age, fertility-sparing surgery followed by chemotherapy (BEP regimen) is the preferred management to preserve the contralateral ovary and uterus. * **Why Option C is incorrect:** While it is the most common germ cell tumor to be bilateral (10–15% of cases), it is **predominantly unilateral** (85–90%). Therefore, "Bilateral" is not a defining characteristic compared to its status as the most common malignant GCT. * **Why Option D is incorrect:** The characteristic tumor marker for dysgerminoma is **LDH (Lactate Dehydrogenase)**. It may also show mild elevations in hCG. **Alpha-fetoprotein (AFP)** is the specific marker for Yolk Sac Tumors (Endodermal Sinus Tumors). **High-Yield Clinical Pearls for NEET-PG:** * **Microscopy:** Characterized by large, round, clear cells with central nuclei ("fried egg" appearance) separated by fibrous septa infiltrated with **lymphocytes**. * **Associated Condition:** Always rule out 46, XY karyotype (Gonadoblastoma) if a dysgerminoma is detected in a pre-pubertal girl. * **Treatment:** Most are Stage IA and treated with unilateral salpingo-oophorectomy. It has an excellent prognosis with a 5-year survival rate >95%.

Q: What is true about granulosa cell tumors?

They are chemotherapy sensitive.. **Explanation:** Granulosa cell tumors (GCTs) are the most common type of **sex cord-stromal tumors**. While they are often characterized by their indolent course and late recurrence, their management in advanced or recurrent stages relies heavily on their chemosensitivity. * **Why Option D is Correct:** GCTs are considered **chemosensitive**. For patients with high-risk Stage I or advanced/recurrent disease, platinum-based chemotherapy—specifically the **BEP regimen** (Bleomycin, Etoposide, and Cisplatin)—is the standard of care and shows high response rates. * **Why Option A is Incorrect:** The most common malignant tumors of the ovary are **Epithelial Ovarian Tumors** (specifically Serous Cystadenocarcinoma), not sex cord-stromal tumors. GCTs account for only about 2–5% of all ovarian malignancies. * **Why Option B & C are Incorrect (Contextual Note):** While GCTs *do* secrete estrogen and *are* associated with endometrial hyperplasia/carcinoma, these options are often considered "less true" or "incomplete" in the context of specific competitive exam framing if the question seeks the most definitive clinical management fact. *Note: In many clinical contexts, B and C are physiologically true; however, in NEET-PG, if D is the marked key, it emphasizes the therapeutic approach to malignancy.* **High-Yield Clinical Pearls for NEET-PG:** 1. **Pathognomonic Feature:** **Call-Exner bodies** (small follicles filled with eosinophilic material) and "coffee-bean" nuclei. 2. **Tumor Marker:** **Inhibin B** is the most reliable marker for diagnosis and monitoring recurrence. 3. **Clinical Presentation:** Often presents with **precocious puberty** (in juveniles) or **postmenopausal bleeding** (in adults) due to hyperestrogenism. 4. **Associated Pathology:** Up to 25–50% of cases are associated with endometrial hyperplasia, and 5% with endometrial carcinoma.

Q: A high-grade squamous intraepithelial lesion (HSIL) is noted on Pap smear. What is the next management step?

Colposcopy with biopsy. **Explanation:** The management of cervical cytological abnormalities follows a specific diagnostic algorithm. A Pap smear is a **screening tool**, not a diagnostic one. When a Pap smear shows **High-Grade Squamous Intraepithelial Lesion (HSIL)**, it indicates a high probability of underlying high-grade cervical intraepithelial neoplasia (CIN 2/3) or even occult invasive cancer. **1. Why Colposcopy with Biopsy is correct:** According to ASCCP guidelines, any high-grade screening result (HSIL, ASC-H, or AGC) requires immediate **Colposcopy**. Colposcopy allows for the visualization of the transformation zone under magnification. If an abnormal area is identified (e.g., punctations, mosaicism, or dense acetowhite epithelium), a **directed biopsy** is performed to obtain a tissue diagnosis. Management is based on the histological grade (CIN) rather than the cytological smear. **2. Why other options are incorrect:** * **Wertheim’s Hysterectomy:** This is a radical surgery for invasive cervical cancer (Stage IA2-IIA). It is never performed based solely on a screening Pap smear without a histological diagnosis of malignancy. * **Local Excision (LEEP/Cold Knife Conization):** While HSIL may eventually require an excisional procedure (See-and-Treat), the standard initial step is diagnostic confirmation via colposcopy. * **HPV DNA Testing:** This is used for "reflex testing" in low-grade lesions (ASC-US). In HSIL, the risk of high-risk HPV is already so high that testing adds no clinical value to the management. **Clinical Pearls for NEET-PG:** * **ASC-US:** Next step is HPV DNA testing (if positive → Colposcopy; if negative → repeat Pap in 3 years). * **HSIL in Pregnancy:** Colposcopy is mandatory, but biopsy is only done if invasive cancer is suspected. Endocervical curettage (ECC) is **contraindicated** in pregnancy. * **Gold Standard for Diagnosis:** Cervical Biopsy (Colposcopy-directed).

Q: Most hereditary ovarian cancers result from germline mutations in which of the following genes?

BRCA1 and BRCA2. **Explanation:** **1. Why BRCA1 and BRCA2 are correct:** Approximately 10–15% of epithelial ovarian cancers are hereditary. The vast majority (about 90%) of these hereditary cases are attributed to **Hereditary Breast and Ovarian Cancer (HBOC) syndrome**, which is caused by germline mutations in the **BRCA1 and BRCA2** genes. These are tumor suppressor genes involved in DNA repair via homologous recombination. * **BRCA1** mutation carries a cumulative lifetime risk of ovarian cancer of approximately **40–50%**. * **BRCA2** mutation carries a lifetime risk of approximately **15–25%**. **2. Why other options are incorrect:** * **MSH2, MLH1, and PMS1 (Options B, C, D):** These are DNA mismatch repair (MMR) genes. Mutations in these genes cause **Lynch Syndrome** (Hereditary Non-Polyposis Colorectal Cancer - HNPCC). While Lynch syndrome is the second most common cause of hereditary ovarian cancer, it accounts for only about 10–15% of hereditary cases (much less than BRCA). In Lynch syndrome, the risk of endometrial cancer is significantly higher than the risk of ovarian cancer. **3. High-Yield Clinical Pearls for NEET-PG:** * **Most common histological type:** BRCA-associated ovarian cancers are typically **High-Grade Serous Carcinomas (HGSC)**. * **Prognosis:** Interestingly, BRCA-mutated ovarian cancers often have a *better* prognosis and better response to platinum-based chemotherapy and PARP inhibitors (e.g., Olaparib) compared to sporadic cases. * **Prophylaxis:** Risk-reducing salpingo-oophorectomy (RRSO) is recommended by age 35–40 for BRCA1 and age 40–45 for BRCA2 carriers. * **Lynch Syndrome Triad:** Increased risk of Colorectal, Endometrial, and Ovarian cancers.

Q: Which of the following is NOT a predisposing lesion for vulvar cancer?

Familial cancer syndromes. **Explanation:** Vulvar cancer is primarily a disease of elderly women, arising through two distinct pathogenic pathways. The correct answer is **Familial cancer syndromes** because, unlike breast, ovarian, or colon cancers (e.g., BRCA or Lynch Syndrome), vulvar cancer does not have a recognized hereditary or familial genetic predisposition. It is almost exclusively associated with localized chronic irritation or viral infection. **Analysis of Options:** * **Lichen sclerosus:** This is the most common precursor for the **HPV-independent pathway**. It typically affects postmenopausal women. Chronic inflammation leads to "differentiated VIN" (dVIN), which carries a high risk of progression to keratinizing squamous cell carcinoma. * **Vulvar Intraepithelial Neoplasia (VIN):** This is the classic precursor lesion. **Usual-type VIN** (uVIN) is associated with high-risk HPV types (16, 18) and is common in younger, smoking women. **Differentiated VIN** (dVIN) is associated with Lichen sclerosus. * **Paget’s Disease:** Extramammary Paget’s disease of the vulva is a preinvasive intraepithelial neoplasia. While often confined to the epithelium, it is associated with an underlying invasive vulvar adenocarcinoma in about 10–15% of cases. **High-Yield Clinical Pearls for NEET-PG:** * **Most common histological type:** Squamous cell carcinoma (90%). * **Most common site:** Labia majora. * **Staging:** Vulvar cancer is staged **surgically** (FIGO). * **Lymphatic Spread:** The sentinel lymph nodes are the **Inguinal nodes** (specifically the superficial inguinal nodes). The "Cloquet’s node" is the highest deep inguinal node and signifies spread to pelvic nodes. * **Risk Factors:** Smoking, HPV 16/18, immunosuppression, and chronic vulvar dystrophies.

Q: Which of the following is the etiologic agent in a 70-year-old woman with squamous cell cancer of the vulva?

Lichen Sclerosus. **Explanation:** Squamous cell carcinoma (SCC) of the vulva follows two distinct pathogenic pathways. In an **elderly patient (typically >65–70 years)**, the cancer usually arises from a background of chronic inflammatory conditions, most notably **Lichen Sclerosus** or differentiated Vulvar Intraepithelial Neoplasia (dVIN). This "keratinizing" type of SCC is independent of HPV infection and is often associated with TP53 mutations. **Analysis of Options:** * **A. Lichen Sclerosus (Correct):** This is the most common precursor in older women. Long-standing inflammation leads to cellular atypia and progression to SCC. It presents as "parchment-like" or "cigarette paper" skin. * **B. Human Papillomavirus (HPV):** This is the etiology for the second pathway, typically seen in **younger women (35–55 years)**. It is associated with high-risk strains (HPV 16, 18) and "warty" or "basaloid" Vulvar Intraepithelial Neoplasia (uVIN). * **C & D. Immunosuppression and Smoking:** While these are significant risk factors for HPV-related vulvar and cervical cancers (by hindering viral clearance), they are not the primary etiologic agents for the keratinizing SCC seen in a 70-year-old. **High-Yield Clinical Pearls for NEET-PG:** * **Most common type of Vulvar Cancer:** Squamous Cell Carcinoma (90%). * **Most common site:** Labia majora. * **Precursor lesions:** * Elderly = Lichen Sclerosus $\rightarrow$ dVIN (TP53 mutation). * Younger = HPV $\rightarrow$ uVIN (p16 positive). * **Lymphatic Spread:** The primary route of spread is to the **Inguinal-femoral lymph nodes** (Sentinel node biopsy is the standard for early-stage disease).

Q: Recurrence of hydatiform mole is assessed by:

b-HCG level. **Explanation:** **Why b-HCG is the correct answer:** Hydatidiform mole is a type of Gestational Trophoblastic Disease (GTD) arising from the abnormal proliferation of trophoblastic tissue (syncytiotrophoblast and cytotrophoblast). These trophoblastic cells naturally secrete **beta-human chorionic gonadotropin (b-HCG)**. Because b-HCG has a direct correlation with the tumor burden, it serves as an ideal **tumor marker** for diagnosis, monitoring the success of evacuation, and detecting recurrence or progression into Gestational Trophoblastic Neoplasia (GTN). After evacuation, b-HCG levels should ideally fall to undetectable levels; any plateau or rise indicates persistent disease or recurrence. **Why the other options are incorrect:** * **A. AFP (Alpha-fetoprotein):** This is a marker for yolk sac tumors, hepatocellular carcinoma, and neural tube defects. It is not produced by trophoblastic tissue. * **C. LDH (Lactate Dehydrogenase):** While elevated in several malignancies (like dysgerminomas or lymphomas) due to high cell turnover, it is non-specific and not used to monitor molar recurrence. * **D. Estrogen level:** While estrogen levels may be elevated during pregnancy, they do not accurately reflect trophoblastic mass or activity and lack the sensitivity required for oncological follow-up. **High-Yield Clinical Pearls for NEET-PG:** * **Follow-up Protocol:** After evacuation, b-HCG should be monitored **weekly** until three consecutive negative results are obtained, then **monthly** for 6 months. * **Contraception:** Patients must use reliable contraception (preferably OCPs) during the follow-up period to ensure a new pregnancy does not mask a rising b-HCG level from recurrence. * **Half-life:** The initial half-life of b-HCG after evacuation is approximately 24–36 hours. * **Snowstorm Appearance:** The classic ultrasound finding for a complete hydatidiform mole.

Question 1

Inheritance is a major factor in which of the following conditions?

Accepted Answer

Endometrial carcinoma

Answer

Cervical carcinoma

Answer

Both

Answer

None

Question 2

What is true about dysgerminoma?

Accepted Answer

Most common malignant germ cell tumor

Answer

Insensitive to radiotherapy

Answer

Bilateral

Answer

Alpha-fetoprotein is the tumor marker

Question 3

The presence of lutein cysts in a vesicular mole is due to excess of which hormone?

Accepted Answer

Human chorionic gonadotropin (HCG)

Answer

Follicle-stimulating hormone (FSH)

Answer

Luteinizing hormone (LH)

Answer

Estrogen

Question 4

What is true about granulosa cell tumors?

Accepted Answer

They are chemotherapy sensitive.

Answer

They are the most common malignant tumor of the ovary.

Answer

They secrete hormones.

Answer

They are associated with endometrial hyperplasia.

Question 5

A high-grade squamous intraepithelial lesion (HSIL) is noted on Pap smear. What is the next management step?

Accepted Answer

Colposcopy with biopsy

Answer

Wertheim's hysterectomy

Answer

Local excision

Answer

HPV DNA testing

Question 6

Most hereditary ovarian cancers result from germline mutations in which of the following genes?

Accepted Answer

BRCA1 and BRCA2

Answer

MSH2

Answer

PMS1

Answer

MLH1

Question 7

Which of the following is NOT a predisposing lesion for vulvar cancer?

Accepted Answer

Familial cancer syndromes

Answer

Paget's disease

Answer

Lichen sclerosus

Answer

Vulvar intraepithelial neoplasia (VIN)

Question 8

Which of the following is the etiologic agent in a 70-year-old woman with squamous cell cancer of the vulva?

Accepted Answer

Lichen Sclerosus

Answer

Human Papillomavirus

Answer

Immunosuppression

Answer

Smoking

Question 9

Acetic acid staining of the cervix shows the following findings EXCEPT:

Accepted Answer

Cervical polyp

Answer

Squamous metaplasia

Answer

Cervical carcinoma in situ

Answer

Cervical dysplasia

Question 10

Recurrence of hydatiform mole is assessed by:

Accepted Answer

b-HCG level

Answer

AFP level

Answer

LDH level

Answer

Estrogen level

Gynecologic Oncology — MCQs

Gynecologic Oncology — MCQs

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