Anticancer Drugs Practice Questions

Q: Which of the following anticancer drugs can cause a hypercoagulable state?

L-asparaginase. **Explanation:** **L-asparaginase** is the correct answer because its primary mechanism of action involves the depletion of asparagine, which is essential for protein synthesis in leukemic cells. However, this inhibition of protein synthesis is not selective and also affects the liver’s production of endogenous anticoagulants. Specifically, it leads to a significant **decrease in Protein C, Protein S, and Antithrombin III** levels. This deficiency shifts the hemostatic balance toward a **hypercoagulable state**, increasing the risk of venous thromboembolism (VTE) and sagittal sinus thrombosis. **Analysis of Incorrect Options:** * **A. 5-Fluorouracil (5-FU):** Primarily known for causing gastrointestinal toxicity (mucositis), myelosuppression, and a unique **hand-foot syndrome**. While it can cause cardiotoxicity (vasospasm), it is not classically associated with systemic hypercoagulability. * **C. Melphalan:** An alkylating agent (nitrogen mustard) used in multiple myeloma. Its dose-limiting toxicity is **bone marrow suppression**. * **D. Carmustine:** A nitrosourea that is highly lipid-soluble and crosses the blood-brain barrier. Its major toxicities include **delayed myelosuppression** and pulmonary fibrosis. **High-Yield Clinical Pearls for NEET-PG:** * **L-asparaginase** is a mainstay in **Acute Lymphoblastic Leukemia (ALL)** protocols. * **Key Side Effects:** Acute pancreatitis (high-yield), hyperglycemia (due to decreased insulin synthesis), and hypersensitivity reactions (anaphylaxis). * **Monitoring:** Patients on L-asparaginase should be monitored for signs of thrombosis and fibrinogen levels. * **Contrast:** While most anticancer drugs cause bleeding due to thrombocytopenia, L-asparaginase is unique for its **pro-thrombotic** potential.

Q: What is the primary reason for administering mesna along with cyclophosphamide?

To ameliorate hemorrhagic cystitis. **Explanation:** **1. Why Option C is Correct:** Cyclophosphamide and Ifosfamide are nitrogen mustards that are metabolized in the liver to form **Acrolein**, a toxic metabolite. Acrolein is excreted in the urine and causes direct irritation to the bladder mucosa, leading to **Hemorrhagic Cystitis** (characterized by hematuria and bladder pain). **Mesna** (2-MercaptoEthane Sulfonate Na) is a sulfhydryl compound that acts as a regional detoxifier. It concentrates in the bladder and reacts chemically with acrolein to form a non-toxic, water-soluble stable adduct, thereby preventing bladder damage. **2. Why Other Options are Incorrect:** * **Option A & D:** Mesna does not influence the pharmacokinetics (absorption or metabolism) of cyclophosphamide. Cyclophosphamide is a prodrug activated by hepatic CYP450 enzymes; Mesna does not interfere with this activation. * **Option B:** Mesna does not decrease the excretion of the drug. In fact, it is essential that both Mesna and the toxic metabolites are excreted together in the urine for the protective effect to occur. **3. High-Yield Clinical Pearls for NEET-PG:** * **Hydration:** Vigorous intravenous hydration is the first line of defense against hemorrhagic cystitis to dilute the acrolein. * **Ifosfamide:** While Mesna is optional for low-dose cyclophosphamide, it is **mandatory** when administering Ifosfamide due to higher acrolein production. * **Other Side Effects:** Apart from cystitis, cyclophosphamide is notorious for causing **SIADH** and **Alopecia**. * **Dose-Limiting Toxicity:** For cyclophosphamide, the dose-limiting toxicity is **Bone Marrow Suppression**.

Q: Which of the following drugs is widely used in the management of carcinoma of the breast?

Doxorubicin. **Explanation:** **Doxorubicin** (an Anthracycline antibiotic) is a cornerstone in the management of breast cancer. Its primary mechanism of action involves inhibiting **Topoisomerase II**, intercalating between DNA base pairs, and generating free radicals that cause DNA strand breaks. It is a key component of standard chemotherapy regimens such as **AC** (Adriamycin/Doxorubicin + Cyclophosphamide) and **FAC** (5-FU + Adriamycin + Cyclophosphamide). **Analysis of Incorrect Options:** * **Actinomycin–D (Dactinomycin):** Primarily used for pediatric solid tumors like **Wilms’ tumor**, Ewing’s sarcoma, and Rhabdomyosarcoma, as well as Gestational Choriocarcinoma. It is not a first-line agent for breast carcinoma. * **Bleomycin:** Known for causing pulmonary fibrosis, it is mainly used in **Germ cell tumors** (Testicular cancer), Hodgkin’s lymphoma, and squamous cell carcinomas of the head and neck. * **Dacarbazine:** An alkylating agent that is the drug of choice for **Malignant Melanoma** and is used in the ABVD regimen for Hodgkin’s Lymphoma. **High-Yield Clinical Pearls for NEET-PG:** * **Cardiotoxicity:** The most significant side effect of Doxorubicin is dose-dependent dilated cardiomyopathy. **Dexrazoxane** is an iron-chelating agent used to prevent this toxicity. * **Red Urine:** Doxorubicin can cause a harmless reddish discoloration of urine (not hematuria). * **Other Breast Cancer Drugs:** Remember that **Tamoxifen** (SERM) is used for ER/PR positive cases, and **Trastuzumab** is used for HER2/neu positive cases.

Q: Which of the following blocks DNA replication by getting incorporated into the DNA strand?

Cytarabine. **Explanation:** **Correct Option: A. Cytarabine** Cytarabine (Ara-C) is a pyrimidine analog (antimetabolite) that acts specifically during the **S-phase** of the cell cycle. Its mechanism involves two primary steps: 1. It is phosphorylated intracellularly into its active form, **cytarabine triphosphate**. 2. This active form competes with deoxycytidine triphosphate to be **incorporated into the DNA strand**. Once incorporated, it acts as a DNA chain terminator and inhibits **DNA polymerase**, thereby blocking DNA synthesis and repair. **Incorrect Options:** * **B & C (Nalidixic acid and Ciprofloxacin):** These are Quinolone/Fluoroquinolone antibiotics. They inhibit **DNA Gyrase** (Topoisomerase II) and **Topoisomerase IV** in bacteria. They do not get incorporated into the DNA strand. * **D (Paclitaxel):** This is a Taxane that acts on microtubules. It **stabilizes microtubules** by preventing depolymerization (freezing them in the polymerized state), leading to cell cycle arrest in the **M-phase**. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Cytarabine is a cornerstone in the induction therapy of **Acute Myeloid Leukemia (AML)**. * **Specific Toxicity:** High-dose Cytarabine is associated with **Cerebellar toxicity** (ataxia, dysarthria) and **conjunctivitis** (prophylactic steroid drops are often used). * **Resistance:** Resistance to Cytarabine often occurs due to a decrease in the activating enzyme **deoxycytidine kinase**.

Q: Which of the following is the most emetogenic anticancer drug?

Cisplatin. **Explanation:** The emetogenicity of chemotherapy is categorized based on the percentage of patients who experience vomiting without antiemetic prophylaxis. **Cisplatin** is the prototype of **High Emetogenic Chemotherapy (HEC)**, with an emetic risk of >90%. **1. Why Cisplatin is the correct answer:** Cisplatin induces nausea and vomiting through two distinct pathways: * **Acute Phase (<24 hours):** Primarily due to the release of serotonin (5-HT) from enterochromaffin cells in the GI tract, stimulating 5-HT3 receptors. * **Delayed Phase (24–72 hours):** Primarily mediated by Substance P acting on Neurokinin-1 (NK1) receptors in the brainstem. Because it triggers both pathways intensely, it is considered the most emetogenic conventional agent. **2. Why the other options are incorrect:** * **Carboplatin:** While related to cisplatin, it is significantly less emetogenic (Moderate Emetogenic Risk, 30–90%) and has less renal and ototoxicity. * **High-dose Cyclophosphamide:** This is classified as HEC (especially >1500 mg/m²), but statistically, Cisplatin remains the gold standard for the highest emetic potential in clinical pharmacology. * **High-dose Methotrexate:** This is generally classified as having **Moderate to Low** emetogenic potential (30–60% risk). **3. Clinical Pearls for NEET-PG:** * **Drug of Choice for Cisplatin-induced vomiting:** A combination of a **5-HT3 antagonist** (e.g., Ondansetron), a **Corticosteroid** (Dexamethasone), and an **NK1 antagonist** (e.g., Aprepitant). * **Other HEC agents:** Dacarbazine, Mechlorethamine, and Streptozocin. * **Cisplatin Toxicity Profile:** Remember the mnemonic "3 Os" — **O**totoxicity, **O**ne (Nephrotoxicity), and **O**mited (Vomiting/Emesis). Amifostine is used to reduce cisplatin-induced nephrotoxicity.

Q: What is the primary toxicity of busulfan?

Severe myeloid suppression. **Explanation:**Busulfan is a bifunctional alkylating agent (alkyl sulfonate) primarily used in the treatment of Chronic Myeloid Leukemia (CML) and as a part of conditioning regimens prior to bone marrow transplantation [1].**Why Option B is Correct:**The hallmark and dose-limiting toxicity of busulfan is **severe and prolonged myeloid suppression** [1]. It specifically targets hematopoietic stem cells, leading to profound leucopenia, thrombocytopenia, and anemia. This property makes it highly effective for "ablating" the bone marrow before a transplant, but it requires careful monitoring to avoid irreversible marrow failure.**Analysis of Incorrect Options:** * **Option A (Lung Fibrosis):** While busulfan is famous for causing "Busulfan Lung" (interstitial pulmonary fibrosis), this is a chronic, dose-dependent side effect. In the context of "primary" or most common acute toxicity, myeloid suppression takes precedence.* **Option C (Cystitis):** Hemorrhagic cystitis is the classic toxicity associated with **Cyclophosphamide** and **Ifosfamide** due to the metabolite acrolein.* **Option D (Hyperuricemia):** This is a common feature of **Tumor Lysis Syndrome**, seen with many rapidly acting cytotoxic drugs (like Vincristine or Cytarabine), but it is not the specific primary toxicity defining busulfan's profile.**High-Yield Clinical Pearls for NEET-PG:** * **Skin Hyperpigmentation:** Busulfan often causes a characteristic "tan" or Addisonian-like skin darkening (without adrenal insufficiency).* **Seizures:** At high doses (conditioning regimens), busulfan can cross the blood-brain barrier and cause seizures; prophylactic **phenytoin** or benzodiazepines are often administered.* **Veno-occlusive disease (VOD):** Busulfan is a major risk factor for hepatic VOD (Sinusoidal Obstruction Syndrome).

Q: Which anti-cancer drug affects both DNA and RNA?

Actinomycin-D. **Explanation:** **Correct Answer: C. Actinomycin-D (Dactinomycin)** Actinomycin-D is an antitumor antibiotic derived from *Streptomyces*. Its primary mechanism of action involves **intercalating between guanine-cytosine (G-C) base pairs** of the DNA double helix. This physical binding creates a stable complex that inhibits the enzyme **DNA-dependent RNA polymerase**, thereby blocking the synthesis of messenger RNA (mRNA). At higher concentrations, it also inhibits **DNA polymerase**, leading to the inhibition of DNA replication. Because it disrupts both the template function (DNA replication) and the transcription process (RNA synthesis), it is the correct choice. **Analysis of Incorrect Options:** * **A. 5-Fluorouracil (5-FU):** An antimetabolite (pyrimidine analog) that primarily inhibits **thymidylate synthase**, leading to "thymineless death" of DNA. While it can be incorporated into RNA, its hallmark action is DNA synthesis inhibition. * **B. Methotrexate:** A folate antagonist that inhibits **dihydrofolate reductase (DHFR)**. This depletes tetrahydrofolate, which is essential for purine and thymidylate synthesis, primarily affecting DNA synthesis. * **C. Etoposide:** A plant alkaloid that acts specifically by inhibiting **Topoisomerase II**, leading to DNA strand breaks. It does not directly affect RNA synthesis. **High-Yield NEET-PG Pearls:** * **Clinical Use:** Actinomycin-D is a component of the "VAC" regimen used for **Wilms’ tumor** and **Rhabdomyosarcoma**. It is also highly effective in **Gestational Choriocarcinoma**. * **Toxicity:** It is a potent vesicant (causes tissue necrosis on extravasation) and causes significant bone marrow suppression. * **Cell Cycle:** It is cell-cycle non-specific but most active in the G1 phase.

Q: Cisplatin is known to cause several adverse effects. Which of the following is NOT a typical side effect of cisplatin therapy?

Cardiomyopathy. **Explanation:** **Cisplatin** is a potent platinum-based alkylating agent used for various solid tumors. The correct answer is **Cardiomyopathy**, as this is not a characteristic side effect of Cisplatin. Instead, cardiomyopathy is the classic dose-limiting toxicity associated with **Anthracyclines** (e.g., Doxorubicin and Daunorubicin). **Analysis of Options:** * **Nephrotoxicity (Option B):** This is the most significant dose-limiting toxicity of Cisplatin [1]. It causes acute tubular necrosis. It is managed with aggressive **Amifostine** (a cytoprotective agent) and vigorous hydration with chloride diuresis [1]. * **Neuropathy (Option C):** Cisplatin frequently causes a sensory peripheral neuropathy (stocking-glove pattern) due to its accumulation in the dorsal root ganglia [1]. * **Tinnitus/Ototoxicity (Option D):** Cisplatin is highly ototoxic, leading to high-frequency hearing loss and tinnitus [1]. This is often irreversible and more common in the pediatric population. **High-Yield Clinical Pearls for NEET-PG:** 1. **Mnemonic for Cisplatin Toxicity:** Remember the **"3 Ns"** — **N**ephrotoxicity, **N**eurotoxicity, and **N**ausea/vomiting (it is highly emetogenic) [1]. 2. **Ototoxicity:** Unlike many other drugs, Cisplatin-induced hearing loss is bilateral and permanent [1]. 3. **Electrolyte Imbalance:** It characteristically causes **Hypomagnesemia** and hypokalemia due to renal tubular damage. 4. **Carboplatin:** A related drug that is less nephrotoxic and ototoxic but causes significant **Myelosuppression** (thrombocytopenia) [1].

Question 1

Which of the following is an aromatase inhibitor used in breast cancer therapy?

Accepted Answer

Letrozole

Answer

Anastrozole

Answer

Exemestane

Answer

Tamoxifen

Question 2

Which of the following anticancer drugs can cause a hypercoagulable state?

Accepted Answer

L-asparaginase

Answer

5-FU

Answer

Melphalan

Answer

Carmustine

Question 3

What is the primary reason for administering mesna along with cyclophosphamide?

Accepted Answer

To ameliorate hemorrhagic cystitis

Answer

To increase absorption

Answer

To decrease excretion

Answer

To decrease metabolism

Question 4

Which of the following drugs is widely used in the management of carcinoma of the breast?

Accepted Answer

Doxorubicin

Answer

Actinomycin–D

Answer

Bleomycin

Answer

Dacarbazine

Question 5

Which of the following blocks DNA replication by getting incorporated into the DNA strand?

Accepted Answer

Cytarabine

Answer

Nalidixic acid

Answer

Ciprofloxacin

Answer

Paclitaxel

Question 6

Fulvestrant is used in the treatment of which of the following conditions?

Accepted Answer

HR positive metastatic breast cancer in postmenopausal women

Answer

Male breast cancer

Answer

Paget's disease

Answer

Acute myeloid leukemia associated with Down's syndrome

Question 7

Which of the following is the most emetogenic anticancer drug?

Accepted Answer

Cisplatin

Answer

Carboplatin

Answer

High dose cyclophosphamide

Answer

High dose methotrexate

Question 8

What is the primary toxicity of busulfan?

Accepted Answer

Severe myeloid suppression

Answer

Lung fibrosis

Answer

Cystitis

Answer

Hyperuricemia

Question 9

Which anti-cancer drug affects both DNA and RNA?

Accepted Answer

Actinomycin-D

Answer

5-Fluorouracil

Answer

Methotrexate

Answer

Etoposide

Question 10

Cisplatin is known to cause several adverse effects. Which of the following is NOT a typical side effect of cisplatin therapy?

Accepted Answer

Cardiomyopathy

Answer

Nephrotoxicity

Answer

Neuropathy

Answer

Tinnitus

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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