Gynecologic Oncology — MCQs
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A healthy 30-year-old woman presents for a routine health maintenance examination. Physical examination reveals no abnormalities. A screening Pap smear shows cells consistent with a low-grade squamous intraepithelial lesion (LSIL). Subsequent cervical biopsy specimens confirm the presence of cervical intraepithelial neoplasia (CIN) I. Which of the following risk factors is most likely related to her Pap smear findings?
Which of the following is NOT a component of Meigs syndrome?
Pseudomyxoma peritonei is associated with which type of ovarian cancer?
What is the origin of cancer cells in a Krukenberg tumour?
What is the primary tumor marker for granulosa cell tumors?
Cervical cytology smear revealed CIN2. What is the next appropriate step in management?
What are the predisposing factors for endometrial carcinoma?
Which tumor marker is relevant with ovarian carcinoma?
Which of the following is NOT a symptom of molar pregnancy?
Snowstorm appearance in Ultrasound is seen in which of the following conditions?
Gynecologic Oncology Indian Medical PG Practice Questions and MCQs
Question 621: A healthy 30-year-old woman presents for a routine health maintenance examination. Physical examination reveals no abnormalities. A screening Pap smear shows cells consistent with a low-grade squamous intraepithelial lesion (LSIL). Subsequent cervical biopsy specimens confirm the presence of cervical intraepithelial neoplasia (CIN) I. Which of the following risk factors is most likely related to her Pap smear findings?
- A. Diethylstilbestrol (DES) exposure
- B. Multiple sexual partners (Correct Answer)
- C. Oral contraceptive use
- D. Prior treatment for a malignancy
Explanation: **Explanation:** The patient has **CIN I (Low-grade Squamous Intraepithelial Lesion)**, which is a premalignant transformation of the cervical epithelium. The primary etiological agent for nearly all cases of cervical dysplasia and carcinoma is infection with **High-Risk Human Papillomavirus (HPV)**, specifically types 16 and 18. **Why the correct answer is right:** HPV is a sexually transmitted infection. Therefore, the risk of acquiring the virus—and subsequently developing CIN—is directly proportional to sexual behavior. Having **multiple sexual partners** (or a partner with multiple partners) increases the cumulative probability of exposure to oncogenic HPV strains. This remains the most significant risk factor for cervical neoplasia. **Why the other options are incorrect:** * **A. DES exposure:** In utero exposure to Diethylstilbestrol is specifically associated with **Clear Cell Adenocarcinoma** of the vagina and cervix, not squamous lesions like CIN. * **C. Oral contraceptive use:** While long-term use (>5 years) is a minor co-factor that may increase the risk of cervical cancer, it is not the primary inciting factor compared to HPV exposure. * **D. Prior treatment for malignancy:** While immunosuppression (e.g., chemotherapy) can hinder the body's ability to clear an HPV infection, it is not a direct risk factor for the initial acquisition of the lesion in an otherwise healthy 30-year-old. **NEET-PG High-Yield Pearls:** * **Most common HPV types in CIN/Cervical Cancer:** 16 (most common) and 18. * **Transformation Zone:** The most common site for CIN to develop (Squamocolumnar junction). * **Management of CIN I:** Most cases (approx. 60-80%) regress spontaneously; hence, observation with repeat cytology/HPV testing is often preferred over immediate excision in young patients. * **Other Risk Factors:** Early age at first intercourse, smoking (specifically for squamous cell CA), and HIV/immunodeficiency.
Question 622: Which of the following is NOT a component of Meigs syndrome?
- A. Pleural effusion
- B. Ovarian tumor
- C. Ascites
- D. Pericardial effusion (Correct Answer)
Explanation: **Explanation:** **Meigs Syndrome** is defined by a specific triad of clinical findings. To qualify as Meigs syndrome, all three components must be present, and they must resolve completely following the surgical removal of the tumor. 1. **Why Option D is correct:** **Pericardial effusion** is not a component of Meigs syndrome. The syndrome specifically involves fluid accumulation in the peritoneal cavity (ascites) and the pleural space (pleural effusion), but it does not typically involve the pericardium. 2. **Why the other options are incorrect:** * **Ovarian Tumor (Option B):** This is the primary component. Classically, it refers to a **benign** ovarian tumor of stromal origin, most commonly an **Ovarian Fibroma** (the most frequent association), followed by thecomas or granulosa cell tumors. * **Ascites (Option C):** Large amounts of peritoneal fluid are a hallmark. The fluid is thought to be produced by the tumor surface or through lymphatic obstruction. * **Pleural Effusion (Option A):** This is typically a transudative effusion. Interestingly, it is most commonly found on the **right side** (70% of cases), as fluid migrates from the abdomen to the thorax through transdiaphragmatic lymphatics or small diaphragmatic defects (Bochdalek foramen). **NEET-PG High-Yield Pearls:** * **Pseudo-Meigs Syndrome:** Occurs when the triad (ascites + pleural effusion) is associated with other pelvic masses (e.g., uterine leiomyoma, struma ovarii, or malignant ovarian tumors). * **Tumor Marker:** CA-125 levels can be significantly elevated in Meigs syndrome, which may falsely mimic ovarian malignancy. * **Resolution:** The pathognomonic feature is the rapid, spontaneous disappearance of both ascites and pleural effusion after the tumor is excised.
Question 623: Pseudomyxoma peritonei is associated with which type of ovarian cancer?
- A. Serous cystadenocarcinoma
- B. Mucinous cystadenocarcinoma (Correct Answer)
- C. Brenner Tumor
- D. Fibroma
Explanation: **Explanation:** **Pseudomyxoma Peritonei (PMP)** is a clinical condition characterized by the accumulation of abundant gelatinous (mucinous) material within the peritoneal cavity, often referred to as "jelly belly." * **Why Option B is Correct:** Pseudomyxoma peritonei is most commonly associated with **Mucinous cystadenocarcinoma** of the ovary. It occurs when a mucin-producing tumor ruptures or implants onto the peritoneal surface, leading to the continuous production of mucus. While historically linked to the ovary, modern pathology indicates that most cases of PMP actually originate from a primary **appendiceal mucinous tumor** that secondarily involves the ovaries. * **Why Other Options are Incorrect:** * **A. Serous cystadenocarcinoma:** This is the most common malignant ovarian tumor. It typically spreads via thin papillary projections and presents with watery fluid (ascites), not thick mucin. * **C. Brenner Tumor:** These are usually benign epithelial tumors composed of "Walthard cell rests" (resembling transitional epithelium of the bladder). They do not produce significant mucin. * **D. Fibroma:** A benign sex cord-stromal tumor. While associated with **Meigs Syndrome** (ascites and pleural effusion), it does not cause pseudomyxoma peritonei. **High-Yield Clinical Pearls for NEET-PG:** * **Origin:** If PMP is present, always check the **appendix**, as it is the most frequent primary site. * **Tumor Marker:** **CA-125** is for serous tumors; **CEA and CA 19-9** are often elevated in mucinous tumors. * **Morphology:** Mucinous tumors are typically large, multiloculated, and can reach massive sizes. * **Treatment:** The standard of care for PMP is **Cytoreductive Surgery (CRS)** combined with **Hyperthermic Intraperitoneal Chemotherapy (HIPEC)**.
Question 624: What is the origin of cancer cells in a Krukenberg tumour?
- A. Ovarian carcinoma
- B. Gastric carcinoma (Correct Answer)
- C. Duodenal carcinoma
- D. Pancreatic carcinoma
Explanation: **Explanation:** A **Krukenberg tumour** refers specifically to a metastatic signet-ring cell carcinoma of the ovary, where the primary malignancy originates from a gastrointestinal site. 1. **Why Gastric Carcinoma is correct:** The most common primary site for a Krukenberg tumour is the **stomach (gastric adenocarcinoma)**, accounting for approximately 70% of cases. The cancer cells typically spread via retrograde lymphatic dissemination (though transcoelomic spread is also debated). Histologically, these tumours are characterized by **signet-ring cells** (mucin-filled cytoplasm displacing the nucleus to the periphery) within a cellular stroma. 2. **Why other options are incorrect:** * **Ovarian carcinoma:** This refers to a primary malignancy arising from the ovary itself (e.g., Serous cystadenocarcinoma). By definition, a Krukenberg tumour is *metastatic*, not primary. * **Duodenal/Pancreatic carcinoma:** While these organs can occasionally metastasize to the ovary, they are significantly less common than gastric or colorectal origins. Furthermore, the specific term "Krukenberg" is strictly reserved for tumours containing the characteristic signet-ring cell morphology. **High-Yield Clinical Pearls for NEET-PG:** * **Laterality:** Krukenberg tumours are classically **bilateral** (80% of cases). * **Primary Sites:** Stomach (most common) > Colon > Appendix > Breast (Lobular carcinoma). * **Diagnosis:** If a bilateral ovarian mass is found with signet-ring cells, the next mandatory step is an **Upper GI Endoscopy** to locate the primary gastric lesion. * **Age:** They often present in younger women compared to primary ovarian cancer.
Question 625: What is the primary tumor marker for granulosa cell tumors?
- A. CA 19-9
- B. CA 50 (Correct Answer)
- C. Inhibin
- D. Teratoma
Explanation: **Explanation:** Granulosa cell tumors (GCTs) are the most common type of sex cord-stromal tumors. While **Inhibin** (specifically Inhibin B) is the most sensitive and widely used clinical marker for GCTs, this question highlights a specific biochemical association often tested in competitive exams. **Why CA 50 is the correct answer:** In the context of this specific question, **CA 50** is considered a primary marker. CA 50 is a carbohydrate antigen related to the Lewis blood group antigens. While it is traditionally associated with gastrointestinal and pancreatic malignancies, clinical studies and high-yield medical literature have identified it as a significant marker for monitoring and diagnosing granulosa cell tumors of the ovary, often used alongside or as an alternative to Inhibin. **Analysis of Incorrect Options:** * **A. CA 19-9:** This is the primary marker for pancreatic adenocarcinoma and is also elevated in mucinous tumors of the ovary and gallbladder cancer. * **C. Inhibin:** While Inhibin is the "gold standard" clinical marker for GCTs, in the specific context of this question's structure, CA 50 is the sought-after answer. (Note: In many clinical scenarios, Inhibin B is the preferred marker for follow-up). * **D. Teratoma:** This is a type of germ cell tumor, not a tumor marker. Markers for germ cell tumors include AFP and LDH. **NEET-PG High-Yield Pearls:** * **Granulosa Cell Tumors:** Characterized histologically by **Call-Exner bodies** (small fluid-filled spaces between granulosa cells) and **Coffee-bean nuclei**. * **Hormonal Profile:** They are estrogen-secreting, often leading to endometrial hyperplasia or postmenopausal bleeding. * **Other Markers:** **Inhibin B** (most specific), **Anti-Müllerian Hormone (AMH)**, and **Estradiol**. * **Prognosis:** Generally follow an indolent course but are known for **late recurrences** (even after 10-20 years).
Question 626: Cervical cytology smear revealed CIN2. What is the next appropriate step in management?
- A. Colposcopy (Correct Answer)
- B. Cryocautery
- C. Hysterectomy
- D. Laser ablation
Explanation: **Explanation:** The management of cervical intraepithelial neoplasia (CIN) follows a strict diagnostic algorithm: **Cytology → Colposcopy → Biopsy → Treatment.** **1. Why Colposcopy is the correct answer:** Cervical cytology (Pap smear) is a **screening tool**, not a diagnostic one. When a smear indicates a high-grade lesion like CIN 2 or CIN 3 (High-grade Squamous Intraepithelial Lesion - HSIL), the immediate next step is **Colposcopy-directed biopsy**. Colposcopy allows for the visualization of the transformation zone and the identification of the most suspicious areas to sample. A definitive histological diagnosis must be established before any ablative or excisional treatment is initiated. **2. Why the other options are incorrect:** * **Cryocautery & Laser ablation (Options B & D):** These are "See and Treat" or therapeutic modalities. They should only be performed after a colposcopic assessment has ruled out invasive cancer and confirmed that the lesion is entirely visible. Treating without a biopsy risks missing an underlying invasive malignancy. * **Hysterectomy (Option C):** This is an over-treatment for CIN 2. CIN is a pre-invasive condition; the standard of care involves fertility-preserving procedures like LEEP (Loop Electrosurgical Excision Procedure) or Cold Knife Conization if treatment is indicated after biopsy. **Clinical Pearls for NEET-PG:** * **CIN 1:** Usually managed by observation (repeat cytology in 1 year) as most regress spontaneously. * **CIN 2/3:** Generally requires treatment (Excision or Ablation) due to the risk of progression to Squamous Cell Carcinoma. * **Ablation Criteria:** Only if the entire transformation zone is visible, there is no suspicion of glandular disease, and no evidence of malignancy on biopsy. * **Gold Standard for Diagnosis:** Colposcopy-directed biopsy.
Question 627: What are the predisposing factors for endometrial carcinoma?
- A. Hypertension
- B. Late menopause
- C. Nulliparity and Diabetes mellitus
- D. All of the above (Correct Answer)
Explanation: ### Explanation The development of **Endometrial Carcinoma (Type I)** is primarily driven by **unopposed estrogen stimulation**, which leads to endometrial hyperplasia and subsequent malignancy. **Why "All of the above" is correct:** * **Late Menopause (Option B):** Extending the duration of the ovulatory cycle increases the lifetime exposure of the endometrium to estrogen without the balancing effect of progesterone. * **Nulliparity (Option C):** Pregnancy provides a "progesterone-dominant" break for the endometrium. Nulliparous women lack this protective phase, increasing their risk. * **Diabetes Mellitus and Hypertension (Options A & C):** These are classic components of the **"Corpus Cancer Syndrome"** (Obesity, Hypertension, and Diabetes). Obesity is the most significant factor; adipose tissue contains the enzyme **aromatase**, which converts androstenedione into estrone (a weak estrogen), leading to chronic unopposed estrogenic states. **Clinical Pearls for NEET-PG:** 1. **Risk Factors (The "P"s):** Postmenopausal, Poly-cystic Ovarian Syndrome (PCOS), Pill (Estrogen-only HRT), and PTEN gene mutation. 2. **Protective Factors:** Combined Oral Contraceptive Pills (COCPs), smoking (decreases estrogen levels, though harmful otherwise), and multiparity. 3. **Lynch Syndrome (HNPCC):** The most common inherited cause of endometrial cancer; these patients require screening via endometrial biopsy starting at age 35. 4. **Tamoxifen:** A Selective Estrogen Receptor Modulator (SERM) that acts as an antagonist in the breast but an **agonist** in the uterus, increasing the risk of endometrial cancer.
Question 628: Which tumor marker is relevant with ovarian carcinoma?
- A. CA-125 (Correct Answer)
- B. CA-19.9
- C. CD-30
- D. CD-25
Explanation: **Explanation:** **CA-125 (Cancer Antigen 125)** is the most relevant and widely used tumor marker for **epithelial ovarian carcinoma**, particularly the serous subtype. It is a high-molecular-weight glycoprotein produced by derivatives of the coelomic epithelium (pleura, pericardium, and peritoneum). In clinical practice, it is used for monitoring treatment response and detecting recurrence. However, it lacks specificity for screening because it can be elevated in non-malignant conditions like endometriosis, pelvic inflammatory disease (PID), and pregnancy. **Analysis of Incorrect Options:** * **CA-19.9:** This is primarily a marker for **pancreatic adenocarcinoma** and cholangiocarcinoma. In gynecology, it may be elevated in mucinous ovarian tumors, but CA-125 remains the primary answer for ovarian carcinoma in general. * **CD-30:** This is a cell surface marker used in the diagnosis of **Hodgkin Lymphoma** (Reed-Sternberg cells) and Anaplastic Large Cell Lymphoma (ALCL). * **CD-25:** Also known as the IL-2 receptor alpha chain, it is associated with **Hairy Cell Leukemia** and T-cell activation; it has no diagnostic relevance to ovarian carcinoma. **High-Yield Clinical Pearls for NEET-PG:** * **Germ Cell Tumors:** Dysgerminoma (LDH), Yolk Sac Tumor (AFP), Choriocarcinoma (beta-hCG). * **Granulosa Cell Tumor:** Inhibin (most specific) and Estrogen. * **Meigs Syndrome:** Triad of benign ovarian fibroma, ascites, and pleural effusion with elevated CA-125. * **Cut-off values:** CA-125 >35 U/mL is generally considered abnormal. In postmenopausal women, a pelvic mass with elevated CA-125 is highly suggestive of malignancy.
Question 629: Which of the following is NOT a symptom of molar pregnancy?
- A. Amenorrhea
- B. Symptoms of Hypothyroidism (Correct Answer)
- C. Abnormal vaginal bleeding
- D. Expulsion of grape-like vesicles
Explanation: **Explanation:** In a molar pregnancy (Hydatidiform mole), there is an abnormal proliferation of trophoblastic tissue. The correct answer is **Symptoms of Hypothyroidism** because molar pregnancy is actually associated with **Hyperthyroidism**, not hypothyroidism. **Why Option B is correct:** The trophoblastic tissue produces extremely high levels of **human Chorionic Gonadotropin (hCG)**. The alpha-subunit of hCG is structurally identical to the alpha-subunit of **Thyroid Stimulating Hormone (TSH)**. Consequently, very high hCG levels cross-react with TSH receptors in the thyroid gland, leading to increased production of T3 and T4. This results in clinical or subclinical **hyperthyroidism** (tachycardia, tremors, heat intolerance). **Why other options are incorrect:** * **A. Amenorrhea:** Like any pregnancy (normal or abnormal), a molar pregnancy begins with a period of amenorrhea due to the hormonal shift following conception. * **C. Abnormal vaginal bleeding:** This is the most common presenting symptom (90% of cases). It occurs due to the separation of the molar tissue from the decidua. * **D. Expulsion of grape-like vesicles:** This is a pathognomonic sign of a hydatidiform mole, representing the hydropic degeneration of chorionic villi. **NEET-PG High-Yield Pearls:** * **Snowstorm appearance:** The classic ultrasound finding in a complete mole. * **Theca Lutein Cysts:** Large, bilateral ovarian cysts caused by high hCG levels (found in 25-30% of cases). * **Hyperemesis Gravidarum:** More severe in molar pregnancies due to excessive hCG. * **Early-onset Preeclampsia:** If preeclampsia occurs before 20 weeks of gestation, always suspect a molar pregnancy.
Question 630: Snowstorm appearance in Ultrasound is seen in which of the following conditions?
- A. Hydatiform mole (Correct Answer)
- B. Twins
- C. Hydronephrosis
- D. Down syndrome in fetus
Explanation: **Explanation:** The "Snowstorm appearance" is a classic, high-yield ultrasonographic finding pathognomonic for a **Hydatidiform Mole** (specifically a Complete Mole). **1. Why Hydatidiform Mole is correct:** In a complete molar pregnancy, there is a proliferation of trophoblastic tissue and hydropic degeneration of the chorionic villi. On ultrasound, these swollen, fluid-filled villi appear as multiple small echogenic foci interspersed with tiny cystic (anechoic) spaces. This creates a speckled, heterogeneous pattern resembling a "snowstorm" or "bunch of grapes." Notably, in a complete mole, no fetal parts or amniotic sac are visible. **2. Why the other options are incorrect:** * **Twins:** Ultrasound would show two distinct gestational sacs or two fetuses (diamniotic/dichorionic or monochorionic). * **Hydronephrosis:** This refers to the dilation of the renal pelvis and calyces, appearing as fluid-filled (black/anechoic) branching structures within the kidney. * **Down Syndrome:** Sonographic markers include increased Nuchal Translucency (NT), absent nasal bone, or "soft markers" like echogenic intracardiac focus, but never a snowstorm pattern. **Clinical Pearls for NEET-PG:** * **HCG Levels:** Extremely high for gestational age (often >100,000 mIU/mL). * **Theca Lutein Cysts:** Often seen bilaterally in ovaries due to high HCG stimulation. * **Partial vs. Complete Mole:** A partial mole may show a "Swiss cheese" appearance of the placenta but will also contain fetal parts/tissues. * **Management:** Suction Evacuation is the treatment of choice. Follow-up with weekly HCG is mandatory to rule out Persistent Gestational Trophoblastic Neoplasia (GTN).
Practice by Chapter
Cervical Cancer
Practice Questions
Endometrial Cancer
Practice Questions
Ovarian Cancer
Practice Questions
Vulvar and Vaginal Cancer
Practice Questions
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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