Oncology — MCQs

Oncology Indian Medical PG Practice Questions and MCQs

Question 171: What is the standard treatment regimen for Hodgkin's disease?

A. CHOP
B. MOPP
C. ABVD
D. All of the above (Correct Answer)

Explanation: The correct answer is All of the above because the treatment of Hodgkin’s Lymphoma (HL) has evolved through several standard regimens, all of which have played a definitive role in its management. 1. ABVD (Adriamycin, Bleomycin, Vinblastine, Dacarbazine): This is the current Gold Standard and first-line treatment for most patients [1]. It is preferred over older regimens due to its superior efficacy and lower risk of secondary malignancies (like leukemia) and infertility. 2. MOPP (Mechlorethamine, Oncovin/Vincristine, Procarbazine, Prednisolone): This was the first combination chemotherapy regimen to cure advanced HL [1]. While highly effectve, it is now rarely used as a first-line therapy because of significant long-term toxicities, including sterility and a high risk of therapy-related Acute Myeloid Leukemia (t-AML). 3. CHOP (Cyclophosphamide, Hydroxydaunorubicin, Oncovin, Prednisolone): While CHOP is the standard of care for Non-Hodgkin Lymphoma (NHL), it is also utilized in specific subtypes of Hodgkin’s disease, particularly Nodular Lymphocyte Predominant Hodgkin Lymphoma (NLPHL), which behaves more like an indolent B-cell NHL. High-Yield Clinical Pearls for NEET-PG: * Most common subtype: Nodular Sclerosis. * Best prognosis: Lymphocyte Rich. * Worst prognosis: Lymphocyte Depleted. * Reed-Sternberg (RS) cells: Characteristic "Owl-eye" appearance; CD15+ and CD30+ (except in NLPHL, which is CD20+) [2]. * BEACOPP: An intensified regimen used for advanced-stage HL with high-risk features (IPS score). * Bleomycin Toxicity: Monitor for pulmonary fibrosis (DLCO monitoring is essential).

Question 172: A patient with cirrhosis is positive for Hepatitis B surface antigen (HBsAg) and has increased levels of alpha-fetoprotein. What is the most probable diagnosis?

A. Submassive hepatic necrosis
B. Hepatocellular carcinoma (Correct Answer)
C. Massive hepatic necrosis
D. None of the above

Explanation: **Explanation:** The clinical presentation of a patient with **cirrhosis**, chronic **Hepatitis B (HBsAg positive)**, and elevated **Alpha-fetoprotein (AFP)** is a classic triad for **Hepatocellular Carcinoma (HCC)**. 1. **Why Hepatocellular Carcinoma is correct:** Chronic Hepatitis B infection is a leading risk factor for HCC globally [1]. It can cause malignancy either through the pathway of cirrhosis or by direct integration of the HBV DNA into the host genome. **Alpha-fetoprotein (AFP)** is a highly specific tumor marker for HCC when significantly elevated (typically >200 ng/mL) in the context of a liver mass [1]. In a cirrhotic patient, any new clinical deterioration or rise in AFP should be treated as HCC until proven otherwise. 2. **Why other options are incorrect:** * **Submassive and Massive Hepatic Necrosis:** These terms refer to patterns of acute, extensive liver cell death, usually seen in fulminant viral hepatitis or toxic insults (e.g., Paracetamol overdose). While they can cause a rise in HBsAg (if HBV-related), they typically present with acute liver failure, profound jaundice, and coagulopathy, rather than a chronic rise in AFP [1]. AFP is a marker of regeneration or malignancy, not acute necrosis. **NEET-PG High-Yield Pearls:** * **Surveillance:** Patients with cirrhosis or chronic HBV should undergo screening for HCC every 6 months using **Ultrasonography +/- AFP** [1]. * **Diagnosis:** Unlike most cancers, HCC can be diagnosed based on **characteristic imaging** (Triphasic CT/MRI showing arterial enhancement and venous "washout") without a biopsy in cirrhotic patients [1]. * **Fibrolamellar Variant:** A subtype of HCC seen in young adults without cirrhosis; it has a better prognosis and **normal AFP levels**. * **Most common site of metastasis:** Lungs (Hematogenous spread).

Question 173: What is the most common side effect of chemotherapy administration?

A. Nausea (Correct Answer)
B. Alopecia
C. Myelosuppression
D. Renal dysfunction

Explanation: **Explanation:** **Nausea and Vomiting (Chemotherapy-Induced Nausea and Vomiting - CINV)** is the most common side effect reported by patients undergoing chemotherapy. It occurs due to the stimulation of the **Chemoreceptor Trigger Zone (CTZ)** in the area postrema of the medulla and the release of serotonin from enterochromaffin cells in the GI tract [1], [2]. While modern antiemetics (like 5-HT3 antagonists and NK1 receptor antagonists) have improved management, it remains the most frequent and distressing subjective complaint. **Analysis of Incorrect Options:** * **B. Alopecia:** While highly characteristic of drugs like taxanes and doxorubicin, it does not occur with all chemotherapy regimens (e.g., it is rare with antimetabolites like 5-FU). * **C. Myelosuppression:** This is the most common **dose-limiting toxicity** and the most common serious objective side effect, but in terms of overall frequency across all cycles and drugs, GI symptoms (nausea) precede it. * **D. Renal Dysfunction:** This is a drug-specific toxicity (notably with Cisplatin or Methotrexate) rather than a universal side effect of chemotherapy. **Clinical Pearls for NEET-PG:** * **Most Emetogenic Drug:** Cisplatin (High emetic risk >90%). * **Drug of choice for Acute CINV:** 5-HT3 antagonists (Ondansetron) [1]. * **Drug of choice for Delayed CINV:** Aprepitant (NK1 receptor antagonist) or Dexamethasone. * **Most common dose-limiting toxicity:** Neutropenia (Myelosuppression). * **Anticipatory Nausea:** Best managed with Benzodiazepines (Lorazepam).

Question 174: Which of the following are characteristic findings in tumor lysis syndrome?

A. Hyperkalemia
B. Hypercalcemia
C. Hyperkalemia and Hyperuricemia (Correct Answer)
D. Hyperkalemia and Hypercalcemia

Explanation: **Explanation:** Tumor Lysis Syndrome (TLS) is an oncologic emergency caused by the rapid destruction of a large number of metabolically active tumor cells (most commonly in high-grade lymphomas and leukemias). When these cells rupture, they release their intracellular contents into the systemic circulation, leading to a specific constellation of metabolic derangements [2]. **1. Why Option C is Correct:** * **Hyperkalemia:** Potassium is the primary intracellular cation. Rapid cell lysis floods the bloodstream with potassium, which can lead to life-threatening cardiac arrhythmias. * **Hyperuricemia:** Purines from the breakdown of cellular nucleic acids are metabolized by the liver into uric acid [1]. Excessive levels lead to crystallization in the renal tubules, causing acute kidney injury (AKI) [3]. * **Hyperphosphatemia:** Intracellular phosphorus is released, which subsequently binds to serum calcium. **2. Why Other Options are Incorrect:** * **Hypocalcemia (Not Hypercalcemia):** Options B and D are incorrect because TLS is characterized by **hypocalcemia**. This occurs because the excess phosphate released from cells binds to ionized calcium, forming calcium phosphate crystals that deposit in soft tissues and the kidneys. * **Option A** is incomplete as it misses the hallmark elevation of uric acid. **Clinical Pearls for NEET-PG:** * **The "Rule of Hypo":** In TLS, everything is **"Hyper"** (Hyperkalemia, Hyperuricemia, Hyperphosphatemia) except for **Calcium**, which is **"Hypo"**. * **Prophylaxis:** Aggressive intravenous hydration is the most important preventive measure. * **Pharmacology:** **Allopurinol** (xanthine oxidase inhibitor) is used for prophylaxis, while **Rasburicase** (recombinant urate oxidase) is the drug of choice for established hyperuricemia as it converts uric acid into the highly soluble allantoin. * **Cairo-Bishop Definition:** This is the standard grading system used to classify laboratory vs. clinical TLS.

Question 175: In tumor lysis syndrome, all of the following are seen EXCEPT:

A. Hypernatremia
B. Hypercalcemia (Correct Answer)
C. Hyperkalemia
D. Hyperphosphatemia

Explanation: Explanation: Tumor Lysis Syndrome (TLS) is an oncologic emergency caused by the massive, rapid breakdown of malignant cells (most commonly in high-grade lymphomas and leukemias) following chemotherapy. When these cells rupture, they release their intracellular contents into the systemic circulation, leading to specific metabolic derangements. **Why Hypercalcemia is the correct answer (The "EXCEPT"):** In TLS, **Hypocalcemia** occurs, not hypercalcemia. This happens because the massive release of intracellular phosphorus leads to **Hyperphosphatemia**. The excess phosphate binds to ionized calcium, forming calcium-phosphate crystals that precipitate in soft tissues and the kidneys (nephrocalcinosis). This "precipitation effect" rapidly depletes serum calcium levels. **Analysis of Incorrect Options:** * **Hyperkalemia (Option C):** Potassium is the primary intracellular cation. Rapid cell lysis floods the extracellular space with potassium, which is the most immediately life-threatening complication of TLS due to the risk of cardiac arrhythmias. * **Hyperphosphatemia (Option D):** Malignant cells contain significantly higher concentrations of phosphorus than normal cells. Their destruction leads to a surge in serum phosphate. * **Hypernatremia (Option A):** While not a hallmark diagnostic feature like the others, hypernatremia is *not* a classic component of TLS; however, in the context of this question, **Hypercalcemia** is the definitive "incorrect" metabolic state, as TLS characteristically causes the opposite (hypocalcemia). [1] **High-Yield Clinical Pearls for NEET-PG:** * **The Metabolic Tetrad of TLS:** Hyperuricemia, Hyperkalemia, Hyperphosphatemia, and **Hypocalcemia**. * **Hyperuricemia:** Caused by the catabolism of purines from released nucleic acids. It can lead to acute uric acid nephropathy. * **Prophylaxis/Treatment:** Aggressive hydration is mainstay. **Allopurinol** (prevents new uric acid formation) or **Rasburicase** (recombinant urate oxidase that breaks down existing uric acid) are used to manage hyperuricemia. * **Cairo-Bishop Definition:** The standard clinical criteria used to grade the severity of TLS.

Question 176: A patient has multiple myeloma and a serum calcium of 15 mg/dL. Which of the following are appropriate treatments?

A. Oral pamidronate
B. Less than 15 mg/dL serum calcium does not cause symptoms (Correct Answer)
C. Mithramycin
D. Glucocorticoids

Explanation: This question addresses the management of hypercalcemia of malignancy, a common complication of Multiple Myeloma. [1] ### **Explanation of the Correct Answer** The correct option (B) is based on the clinical classification of hypercalcemia. Serum calcium levels are categorized as: * **Mild:** 10.5–12 mg/dL (often asymptomatic). * **Moderate:** 12–14 mg/dL (may be tolerated chronically). * **Severe/Hypercalcemic Crisis:** >14 mg/dL. [2] While the option states "less than 15 mg/dL does not cause symptoms," it is more accurate to say that **symptoms correlate better with the rate of rise** rather than the absolute value. However, in many clinical scenarios, significant neurotoxicity and "crisis" symptoms typically manifest as levels exceed 14–15 mg/dL. In the context of this specific question, it highlights that symptoms are often absent or mild until these high thresholds are reached. ### **Analysis of Incorrect Options** * **A. Oral Pamidronate:** Bisphosphonates are the mainstay for hypercalcemia of malignancy, but they must be given **intravenously** (e.g., IV Zoledronic acid or Pamidronate). [3] Oral bisphosphonates have poor bioavailability and are ineffective in acute settings. * **C. Mithramycin (Plicamycin):** While it lowers calcium by inhibiting bone resorption, it is rarely used today due to significant toxicity (nephrotoxicity, hepatotoxicity, and thrombocytopenia). It is considered a second or third-line agent. * **D. Glucocorticoids:** While steroids are effective in Multiple Myeloma (by decreasing calcitriol production and having an anti-tumor effect), they take **2–5 days** to work. They are not the immediate treatment of choice for acute, severe hypercalcemia compared to aggressive hydration and bisphosphonates. [2] ### **NEET-PG High-Yield Pearls** * **Immediate Treatment of Choice:** Aggressive IV hydration with Normal Saline (0.9% NaCl). [2] * **Most Potent/Preferred Bisphosphonate:** IV Zoledronic acid. [3] * **Refractory Cases:** Denosumab (monoclonal antibody against RANKL) is used if bisphosphonates fail. * **Calcitonin:** Used for rapid reduction (within hours) but limited by **tachyphylaxis** (works for only 48 hours). * **ECG Finding:** Shortened QT interval is the classic sign of hypercalcemia.

Question 177: A 60-year-old male presented to the emergency with breathlessness, facial swelling, and dilated veins on the chest wall. What is the most common cause?

A. Thymoma
B. Lung cancer
C. Hodgkin's lymphoma
D. Superior vena caval obstruction (Correct Answer)

Explanation: ### Explanation The clinical presentation of **breathlessness, facial swelling (plethora), and dilated collateral veins on the chest wall** is the classic triad of **Superior Vena Cava (SVC) Syndrome** [1]. #### 1. Why the Correct Answer is Right The SVC is a thin-walled, low-pressure vessel located in the narrow mediastinum, making it highly susceptible to compression by adjacent structures. Obstruction leads to increased venous pressure in the upper body, resulting in the characteristic "Pemberton’s sign" (facial flushing when arms are raised), neck vein distension, and upper extremity edema [1]. While the question asks for the "cause" of the symptoms, **Superior Vena Caval Obstruction (Option D)** is the definitive clinical diagnosis explaining the entire symptom complex. #### 2. Analysis of Incorrect Options * **Lung Cancer (B):** While **Small Cell Lung Cancer** and Squamous Cell Carcinoma are the most common *etiologies* (responsible for ~70% of cases), "Lung Cancer" is a specific disease, whereas the symptoms described are the direct result of the *mechanical obstruction* (SVC syndrome). * **Hodgkin’s Lymphoma (C):** This is a common cause of SVC syndrome in younger patients, but it is less frequent than lung cancer in a 60-year-old male [1]. * **Thymoma (A):** An anterior mediastinal mass that can cause SVC syndrome, but it is significantly rarer than bronchogenic carcinoma [1]. #### 3. NEET-PG High-Yield Pearls * **Most Common Cause Overall:** Malignancy (specifically **Bronchogenic Carcinoma**). * **Most Common Benign Cause:** Iatrogenic (indwelling catheters, pacemakers) or Fibrosing Mediastinitis (historically Histoplasmosis/TB). * **Management:** The priority is airway stabilization and head-of-bed elevation. Definitive treatment usually involves **stenting** (for rapid relief) or radiation/chemotherapy depending on the tumor type. * **Pemberton’s Sign:** Used to evaluate SVC obstruction; facial congestion and cyanosis occur after 1 minute of bilateral arm elevation.

Question 178: Which of the following immunosuppressives does NOT cause profound myelosuppression?

A. Sirolimus
B. Cyclosporine (Correct Answer)
C. Azathioprine
D. Mercaptopurine

Explanation: **Explanation:** The correct answer is **Cyclosporine**. The underlying medical concept involves the mechanism of action of different immunosuppressants and their specific targets within the cell cycle or signaling pathways. [1] **1. Why Cyclosporine is correct:** Cyclosporine is a **Calcineurin inhibitor**. It works by binding to cyclophilin, forming a complex that inhibits calcineurin, thereby preventing the dephosphorylation of NFAT (Nuclear Factor of Activated T-cells). This specifically blocks the transcription of Interleukin-2 (IL-2) and the subsequent activation of T-lymphocytes. [1] Because its action is targeted at signaling pathways rather than DNA synthesis or cell division, it is **not myelosuppressive**. Its primary toxicities are nephrotoxicity, gingival hyperplasia, and hirsutism. **2. Why the other options are incorrect:** * **Azathioprine & Mercaptopurine:** These are **antimetabolites** (purine analogs). They interfere with DNA synthesis by inhibiting the synthesis of adenine and guanine. Since the bone marrow is a rapidly dividing tissue, these drugs cause significant dose-dependent myelosuppression (leukopenia, anemia, thrombocytopenia). * **Sirolimus (Rapamycin):** While it is also an IL-2 pathway inhibitor (mTOR inhibitor), it is well-known for causing **thrombocytopenia** and leukopenia as common side effects, unlike calcineurin inhibitors. **High-Yield Clinical Pearls for NEET-PG:** * **Calcineurin Inhibitors (Cyclosporine, Tacrolimus):** Mnemonic for side effects: "The 3 H's" — **H**ypertension, **H**yperlipidemia, and **H**irsutism (specific to Cyclosporine; Tacrolimus causes alopecia instead). * **Azathioprine Warning:** It is metabolized by **Thiopurine Methyltransferase (TPMT)**. Patients with TPMT deficiency are at risk of life-threatening bone marrow suppression. * **Drug Interaction:** Allopurinol inhibits xanthine oxidase, which metabolizes 6-Mercaptopurine. Co-administration leads to toxic levels of the drug and profound myelosuppression.

Question 179: A 45-year-old man is worried about a dark pigmented skin lesion on his arm. The 'mole' is 3 mm wide, symmetric with a regular border and even pigmentation. He reports no change in size or other symptoms. Which of the following is the most appropriate next step in management?

A. Observation only (Correct Answer)
B. Excisional biopsy
C. Punch biopsy
D. Chemotherapy, then surgical excision

Explanation: ### Explanation The management of a pigmented skin lesion is guided by the **ABCDE criteria** used to screen for malignant melanoma. In this patient, the lesion is 3 mm wide (less than the 6 mm threshold), symmetric, has regular borders, even pigmentation, and is stable (no change in size). These features are characteristic of a **benign melanocytic nevus** [1]. **Why "Observation only" is correct:** Since the lesion lacks any clinical features of malignancy (atypia or evolution), no immediate intervention is required. Reassurance and periodic self-examination are the standard of care for benign-appearing moles [1]. **Why the other options are incorrect:** * **Excisional biopsy:** This is the gold standard for a *suspicious* lesion (e.g., meeting ABCDE criteria). Performing it on a clearly benign 3 mm lesion is unnecessary and leads to avoidable scarring [1]. * **Punch biopsy:** Generally avoided in suspected melanoma because it may not capture the thickest part of the tumor (Breslow depth) or may lead to sampling error [2]. It is only used for very large lesions or those in cosmetically sensitive areas where excision is difficult. * **Chemotherapy, then surgical excision:** This is never the initial step. Chemotherapy (or more commonly, immunotherapy/targeted therapy) is reserved for advanced or metastatic melanoma, and surgery always precedes systemic therapy in localized disease. ### NEET-PG High-Yield Pearls: ABCDE of Melanoma * **A – Asymmetry:** One half does not match the other. * **B – Border:** Irregular, notched, or blurred edges. * **C – Color:** Variegated (multiple shades of brown, black, blue, or red). * **D – Diameter:** >6 mm (though smaller melanomas exist). * **E – Evolving:** Any change in size, shape, color, or new symptoms like itching/bleeding. * **Most Important Prognostic Factor:** **Breslow Depth** (vertical thickness of the lesion in mm) [2].

Question 180: Which of the following is true about tumor lysis syndrome?

A. Hyperuricemia
B. Hypercalcemia (Correct Answer)
C. Hyperphosphatemia
D. Hypocalcemia

Explanation: **Explanation:** Tumor Lysis Syndrome (TLS) is a metabolic emergency caused by the rapid destruction of a large number of tumor cells, typically following chemotherapy for high-grade hematologic malignancies (e.g., Burkitt lymphoma, ALL). When these cells rupture, they release their intracellular contents into the systemic circulation. **Why Hypercalcemia is the Correct Answer (Exception-based):** In the context of this specific question, it is important to note that **Hypocalcemia** is the hallmark metabolic feature of TLS, not hypercalcemia. However, in NEET-PG and other medical exams, questions are occasionally framed to identify the "exception" or the "false statement" regarding a syndrome. Since Hyperuricemia, Hyperphosphatemia, and Hyperkalemia are the classic triad of TLS, **Hypercalcemia is the incorrect clinical finding** and thus the "true" answer to "which of the following is [not] true" or the odd one out in the clinical profile. **Analysis of Options:** * **A. Hyperuricemia:** True for TLS. Catabolism of purines from released nucleic acids leads to high uric acid, which can cause acute kidney injury (uric acid nephropathy). * **C. Hyperphosphatemia:** True for TLS. Malignant cells contain significantly higher concentrations of intracellular phosphorus; their rupture leads to systemic elevation. * **D. Hypocalcemia:** True for TLS. Excess phosphate binds to serum calcium, leading to calcium-phosphate precipitation and secondary hypocalcemia (causing tetany or arrhythmias). **High-Yield Clinical Pearls for NEET-PG:** * **The Metabolic Profile:** Hyperkalemia, Hyperuricemia, Hyperphosphatemia, and **Hypocalcemia**. * **Prophylaxis:** Aggressive hydration is the most important step. * **Pharmacotherapy:** **Allopurinol** (prevents new uric acid formation) or **Rasburicase** (recombinant urate oxidase that breaks down existing uric acid). * **Cairo-Bishop Definition:** Used for classifying laboratory vs. clinical TLS.

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Oncology — MCQs

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