Oncology Practice Questions

Q: In humoral hypercalcemia of malignancy, what serum calcium level indicates severe hypercalcemia, which may present with symptoms such as fatigue, mental status changes, dehydration, or nephrolithiasis?

14 mg/dl. ### Explanation **Core Concept:** Hypercalcemia of malignancy is primarily driven by the secretion of **Parathyroid Hormone-related Protein (PTHrP)**, which mimics PTH action on bones and kidneys. In clinical practice, hypercalcemia is categorized by total serum calcium levels: * **Mild:** 10.5 – 11.9 mg/dL * **Moderate:** 12.0 – 13.9 mg/dL * **Severe (Hypercalcemic Crisis):** **≥ 14.0 mg/dL** [1] **Why Option A is Correct:** A serum calcium level of **14 mg/dL** is the threshold for **severe hypercalcemia**. At this level, patients are frequently symptomatic and require urgent inpatient management. Symptoms include profound dehydration (due to nephrogenic diabetes insipidus), altered mental status (lethargy/coma), and cardiac arrhythmias (shortened QT interval) [1]. **Analysis of Incorrect Options:** * **Option B (12 mg/dl):** This falls into the **moderate** range. While patients may be symptomatic, it does not represent the threshold for "severe" hypercalcemia or a medical emergency unless the rise is very acute. * **Option C (11 mg/dl):** This represents **mild** hypercalcemia. Most patients at this level are asymptomatic or have vague symptoms like mild fatigue. * **Option D (10 mg/dl):** This is within the **normal range** (typically 8.5–10.5 mg/dL). **NEET-PG High-Yield Pearls:** 1. **Most Common Cause:** In hospitalized patients, malignancy is the #1 cause of hypercalcemia; in outpatients, it is Primary Hyperparathyroidism [2]. 2. **Mechanism:** PTHrP is most commonly associated with **Squamous Cell Carcinomas** (Lung, Head/Neck) [2]. 3. **Treatment Priority:** The immediate first step in managing severe hypercalcemia (≥14 mg/dL) is **aggressive IV hydration with Normal Saline**, followed by Bisphosphonates (Zoledronic acid) or Denosumab [1]. 4. **ECG Finding:** Look for a **shortened QT interval**; this is a classic board-style question.

Q: What is the primary treatment for Superior Vena Cava (SVC) syndrome caused by Small Cell Lung Carcinoma?

Chemotherapy. **Explanation:** Superior Vena Cava (SVC) syndrome is a clinical emergency characterized by the obstruction of blood flow through the SVC. The choice of treatment depends primarily on the **histological type** of the underlying malignancy [1]. **1. Why Chemotherapy is Correct:** Small Cell Lung Carcinoma (SCLC) is a highly **chemosensitive** tumor. In cases of SVC syndrome caused by SCLC (or Lymphomas), chemotherapy is the treatment of choice because it induces a rapid systemic response, leading to tumor shrinkage and decompression of the vena cava. Relief of symptoms typically occurs within 7 to 10 days of starting treatment. **2. Why Other Options are Incorrect:** * **Radiotherapy:** While radiotherapy is the treatment of choice for **Non-Small Cell Lung Carcinoma (NSCLC)** causing SVC syndrome [1] (as NSCLC is less sensitive to chemotherapy), it is reserved as a second-line or palliative option for SCLC if chemotherapy fails. * **Surgery:** Surgical bypass or resection is rarely indicated in malignant SVC syndrome due to the high morbidity and the effectiveness of medical management [2]. It is generally reserved for benign causes (e.g., retrosternal goiter). * **No treatment:** SVC syndrome is a medical emergency that can lead to cerebral edema or airway compromise; leaving it untreated is life-threatening. **Clinical Pearls for NEET-PG:** * **Most common cause overall:** Lung Cancer (NSCLC > SCLC). * **Most common benign cause:** Iatrogenic (Indwelling catheters/pacemaker wires). * **Pemberton’s Sign:** Facial flushing and inspiratory stridor upon raising both arms (indicates SVC obstruction). * **Immediate Management:** Elevate the head of the bed, oxygen, and loop diuretics to reduce hydrostatic pressure while awaiting definitive diagnosis.

Q: What is the standard treatment regimen for metastatic testicular carcinoma?

Bleomycin, Etoposide, Cisplatin. The standard of care for metastatic germ cell tumors (GCTs), including testicular carcinoma, is the **BEP regimen** (Bleomycin, Etoposide, and Cisplatin). This combination is highly effective, making testicular cancer one of the most curable solid malignancies. 1. **Why Option A is Correct:** * **Cisplatin:** The backbone of treatment; it causes DNA cross-linking. * **Etoposide:** A topoisomerase II inhibitor that prevents DNA replication. * **Bleomycin:** An antitumor antibiotic that induces DNA strand breaks. Depending on the risk stratification (IGCCCG criteria), patients receive either 3 or 4 cycles of BEP. 2. **Why Other Options are Incorrect:** * **Option B (VeIP):** Vinblastine, Ifosfamide, and Cisplatin is a second-line (salvage) regimen used if BEP fails. * **Option C & D:** These combinations (containing 5-FU, Doxorubicin, or Methotrexate) are used for gastrointestinal, breast, or hematological malignancies but have no role in the primary management of testicular GCTs. **High-Yield Clinical Pearls for NEET-PG:** * **Toxicity Profile:** * **Bleomycin:** Associated with **pulmonary fibrosis**. Avoid in patients over 40 or those with pre-existing lung disease. * **Cisplatin:** Highly emetogenic; causes **nephrotoxicity** (prevented by aggressive hydration) and **ototoxicity**. * **Etoposide:** Can lead to secondary leukemia (AML). * **Tumor Markers:** Always monitor **AFP, beta-hCG, and LDH** for diagnosis, staging, and response to treatment. (Note: AFP is never elevated in pure seminoma). * **Residual Mass:** If a mass >1 cm remains after chemotherapy in non-seminomatous GCTs, **Retroperitoneal Lymph Node Dissection (RPLND)** is indicated.

Q: A young man with leukemia is treated with methotrexate. What is the mechanism of action of this drug?

Inhibiting dihydrofolate reductase. **Explanation:** **Mechanism of Action:** Methotrexate (MTX) is a folate antagonist and a cell cycle-specific antimetabolite (acting in the **S-phase**). It works by competitively and irreversibly inhibiting the enzyme **Dihydrofolate Reductase (DHFR)** [1]. Under normal conditions, DHFR converts dihydrofolate into tetrahydrofolate (THF), which is a critical one-carbon carrier required for the synthesis of thymidylate and purine nucleotides [2]. By blocking DHFR, MTX leads to a depletion of THF, thereby inhibiting DNA synthesis and cell replication [1]. **Analysis of Incorrect Options:** * **Option A:** MTX does not interfere with the intestinal absorption of dietary folic acid; it interferes with its intracellular metabolism. * **Option C:** While DNA synthesis is the primary target, MTX does not directly prevent the formation of mRNA (which is the mechanism of drugs like Actinomycin D or certain RNA polymerase inhibitors). * **Option D:** This describes drugs like 6-Mercaptopurine or 5-Fluorouracil, which are prodrugs converted into active cytotoxic metabolites [2]. MTX is active in its parent form, though it undergoes intracellular polyglutamation which enhances its potency. **High-Yield Clinical Pearls for NEET-PG:** * **Rescue Therapy:** **Leucovorin (Folinic acid)** is used to "rescue" normal cells from MTX toxicity by bypassing the inhibited DHFR enzyme. * **Resistance:** Most commonly occurs due to decreased drug uptake or an increase in DHFR enzyme levels within the cell. * **Adverse Effects:** Nephrotoxicity (prevented by hydration and urinary alkalinization), hepatotoxicity (cirrhosis), and pulmonary fibrosis. * **Antidote:** **Glucarpidase** can be used in cases of toxic plasma MTX concentrations in patients with delayed clearance.

Q: What is the drug of choice for chronic myeloid leukemia?

Imatinib Mesylate. **Explanation:** **Correct Answer: A. Imatinib Mesylate** Chronic Myeloid Leukemia (CML) is characterized by the **Philadelphia chromosome [t(9;22)]**, which creates the **BCR-ABL1** fusion gene. This gene encodes a constitutively active tyrosine kinase protein that drives uncontrolled granulocyte proliferation. **Imatinib Mesylate** is a selective **Tyrosine Kinase Inhibitor (TKI)** that binds to the ATP-binding site of the BCR-ABL protein, inhibiting its activity [1], [2]. It is the first-line "Standard of Care" (Drug of Choice) for CML in the chronic phase, significantly improving 10-year survival rates [1]. **Why other options are incorrect:** * **B. Fludarabine:** A purine analog primarily used in the treatment of **Chronic Lymphocytic Leukemia (CLL)** and certain non-Hodgkin lymphomas. * **C. Cladribine (2-CdA):** The drug of choice for **Hairy Cell Leukemia**. It is a purine nucleoside analog that is resistant to degradation by adenosine deaminase. * **D. Pentostatin:** Another adenosine deaminase inhibitor used as an alternative treatment for Hairy Cell Leukemia, but not for CML. **High-Yield Clinical Pearls for NEET-PG:** * **Cytogenetics:** CML is associated with a decrease in **Leukocyte Alkaline Phosphatase (LAP) score**, which helps differentiate it from a leukemoid reaction (where LAP is high). * **Side Effects of Imatinib:** Most common side effects include **periorbital edema**, muscle cramps, and skin rashes. * **Resistance:** If resistance to Imatinib develops (often due to the T315I mutation), second-generation TKIs like **Dasatinib** or **Nilotinib** are used [1]. **Ponatinib** is specifically used for the T315I mutation. * **Monitoring:** Therapeutic response is monitored via quantitative PCR for BCR-ABL1 transcripts (Molecular Response) [1].

Q: A 64-year-old man is admitted to the hospital for the assessment of hematuria after being involved in a motor vehicle accident. His physical examination is normal. A CT scan of the abdomen is shown in Figure below. Which of the following is the most likely diagnosis?

renal cell carcinoma. ***Renal cell carcinoma*** - **Heterogeneous enhancing mass** on CT with areas of **necrosis** and **calcification** is classic for renal cell carcinoma in a 64-year-old male. - The **motor vehicle accident** led to incidental discovery of a pre-existing tumor, as **traumatic hematuria** would show different CT findings like fluid collections or lacerations. *Kidney contusion and laceration* - Would show **perinephric hematoma**, **fluid collections**, and **parenchymal disruption** on CT imaging following trauma. - **Acute traumatic injury** typically presents with obvious signs of tissue damage and bleeding around the kidney, not a solid enhancing mass. *Transitional cell carcinoma* - Arises from the **urothelium** lining the **renal pelvis** or **collecting system**, appearing as filling defects on imaging. - CT would show **hydronephrosis** and **ureteral obstruction** rather than a solid parenchymal mass with enhancement patterns. *Renal hamartoma* - Also known as **angiomyolipoma**, contains **fat**, **smooth muscle**, and **blood vessels** visible as low-density areas on CT. - Appears as a **well-circumscribed lesion** with **fat attenuation** (negative Hounsfield units), unlike the heterogeneous enhancement seen here.

Question 1

Tumor lysis syndrome is associated with all of the following laboratory features except?

Accepted Answer

Hypercalcemia

Answer

Hyperkalemia

Answer

Hyperuricemia

Answer

Hyperphosphatemia

Question 2

In humoral hypercalcemia of malignancy, what serum calcium level indicates severe hypercalcemia, which may present with symptoms such as fatigue, mental status changes, dehydration, or nephrolithiasis?

Accepted Answer

14 mg/dl

Answer

12 mg/dl

Answer

11 mg/dl

Answer

10 mg/dl

Question 3

What is the primary treatment for Superior Vena Cava (SVC) syndrome caused by Small Cell Lung Carcinoma?

Accepted Answer

Chemotherapy

Answer

Radiotherapy

Answer

Surgery

Answer

No treatment

Question 4

What is the standard treatment regimen for metastatic testicular carcinoma?

Accepted Answer

Bleomycin, Etoposide, Cisplatin

Answer

Vinblastine, Etoposide, Cisplatin

Answer

Doxorubicin, 5-Fluorouracil, Mercaptopurine

Answer

Methotrexate, 5-Fluorouracil, Vincristine

Question 5

A 74-year-old man presents with fatigue, shortness of breath on exertion, and back and rib pain worsened by movement. Investigations reveal anemia, elevated calcium, urea, and creatinine. X-rays show multiple lytic lesions in long bones and ribs, and protein electrophoresis is positive for an immunoglobulin G (IgG) paraprotein. What is the most likely mechanism for the renal injury?

Accepted Answer

Tubular damage by light chains

Answer

Plasma cell infiltrates

Answer

Glomerular injury

Answer

Vascular injury by light chains

Question 6

A young man with leukemia is treated with methotrexate. What is the mechanism of action of this drug?

Accepted Answer

Inhibiting dihydrofolate reductase

Answer

Preventing absorption of folic acid

Answer

Preventing formation of messenger ribonucleic acid (mRNA)

Answer

Forming a cytotoxic metabolite

Question 7

Which of the following are symptoms of carcinoid syndrome?

Accepted Answer

Wheezing, Flushing, Cyanosis, Clubbing, Diarrhoea

Answer

Wheezing, Flushing

Answer

Wheezing, Cyanosis

Answer

Flushing, Cyanosis

Question 8

What is the drug of choice for chronic myeloid leukemia?

Accepted Answer

Imatinib Mesylate

Answer

Fludarabine

Answer

Cladribine

Answer

Pentostatin

Question 9

A 64-year-old man is admitted to the hospital for the assessment of hematuria after being involved in a motor vehicle accident. His physical examination is normal. A CT scan of the abdomen is shown in Figure below. Which of the following is the most likely diagnosis?

Accepted Answer

renal cell carcinoma

Answer

kidney contusion and laceration

Answer

transitional cell carcinoma

Answer

renal hamartoma

Question 10

A 62-year-old woman with a family history of breast cancer (her mother died of breast cancer at age 63) is concerned about her future risk. Which of the following features is a recognized risk factor for breast cancer?

Accepted Answer

Early onset of menarche

Answer

Late onset of menopause

Answer

Late-life radiation exposure

Answer

Nulliparity

Oncology — MCQs

Oncology — MCQs

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