Principles of Cancer Chemotherapy — MCQs
Which of the following antifungal agents is used in combination therapy for cryptococcal meningitis?
Which of the following is NOT a mechanism of antibiotic resistance?
All of these are G2 phase blockers except:
Multi drug resistant tuberculosis is defined as resistance to?
Which of the following antineoplastic drugs SHOULD NOT be given by rapid IV infusion?
Many drugs are used as rescue therapy for preventing the adverse effects of anticancer drugs. Folinic acid is used in:-
Secondary leukemias are caused by
Which is not seen in Tumour lysis Syndrome?
Which of the following is the platinum-based chemotherapeutic agent used as first-line treatment for ovarian carcinoma?
What is the most appropriate next step in management for a patient with a Stage III ovarian cancer with partial response to platinum-based chemotherapy?
Principles of Cancer Chemotherapy Indian Medical PG Practice Questions and MCQs
Question 1: Which of the following antifungal agents is used in combination therapy for cryptococcal meningitis?
- A. Flucytosine (Correct Answer)
- B. Nystatin
- C. Terbinafine
- D. Voriconazole
Explanation: **Flucytosine** - **Flucytosine** is commonly used in combination with **amphotericin B** for the initial treatment of **cryptococcal meningitis** [1][2][3]. - This combination therapy allows for synergy, improving efficacy and potentially reducing the dosage and toxicity of amphotericin B [1]. *Nystatin* - **Nystatin** is an antifungal agent primarily used for topical or oral treatment of **mucocutaneous candidiasis**. - It is not systemically absorbed and therefore ineffective for invasive infections like **cryptococcal meningitis**. *Terbinafine* - **Terbinafine** is an antifungal drug mainly used to treat **dermatophyte infections**, such as athlete's foot and onychomycosis [2]. - Its mechanism of action targets fungal ergosterol synthesis at an early stage, which is not suitable for treating **cryptococcal meningitis**. *Voriconazole* - **Voriconazole** is a broad-spectrum azole antifungal used for severe invasive fungal infections, including **aspergillosis** and **candidiasis** [2]. - While it has some activity against *Cryptococcus*, it is not the preferred or standard agent for initial combination therapy for **cryptococcal meningitis**, for which amphotericin B and flucytosine are typically used [2].
Question 2: Which of the following is NOT a mechanism of antibiotic resistance?
- A. Efflux pump activity
- B. Inactivation by enzymes such as beta-lactamase
- C. Modification of drug target sites
- D. Increased drug absorption (Correct Answer)
Explanation: ***Increased drug absorption*** - **Increased drug absorption** would lead to a higher intracellular concentration of the antibiotic, making it *more potent* against the bacteria rather than contributing to resistance. - Antibiotic resistance mechanisms aim to *reduce the effective concentration* of the drug at its target site or *alter the target itself*. *Efflux pump activity* - **Efflux pumps** are bacterial membrane proteins that actively pump antibiotics out of the bacterial cell [3]. - This mechanism *reduces the intracellular concentration* of the antibiotic, preventing it from reaching its therapeutic target [3]. *Inactivation by enzymes such as beta-lactamase* - Bacteria can produce enzymes like **beta-lactamase** that *chemically modify or degrade* the antibiotic molecule, rendering it inactive [2]. - This is a common mechanism of resistance against **beta-lactam antibiotics** (e.g., penicillin, cephalosporins) [2]. *Modification of drug target sites* - Bacteria can develop mutations that *alter the structure of the antibiotic's target site*, such as a bacterial ribosome or cell wall component [1]. - This change in the target means the antibiotic can no longer bind effectively or interfere with cellular processes, thus *losing its efficacy* [1].
Question 3: All of these are G2 phase blockers except:
- A. Paclitaxel (Correct Answer)
- B. Daunorubicin
- C. Etoposide
- D. Topotecan
Explanation: ***Paclitaxel*** - **Paclitaxel** is a **microtubule-stabilizing drug** that acts predominantly in the **M phase** of the cell cycle by inhibiting microtubule depolymerization, thereby blocking cell division [1]. - It is known as a **mitotic inhibitor**, specifically preventing the progression from **metaphase to anaphase** [2]. - **NOT a G2 phase blocker** - this is the correct answer. *Etoposide* - **Etoposide** is a **topoisomerase II inhibitor** that causes DNA strand breaks, predominantly acting in the **late S and G2 phases** of the cell cycle [3]. - Its primary effect is to arrest cells in the **G2 phase**, making it a classic **G2 phase blocker** [2]. *Daunorubicin* - **Daunorubicin** is an **anthracycline antibiotic** that intercalates into DNA, leading to DNA damage and inhibition of DNA and RNA synthesis. - It primarily acts in the **S phase** but the resulting DNA damage activates checkpoints leading to **G2 phase arrest**, thus functioning as a G2 blocker [3]. *Topotecan* - **Topotecan** is a **topoisomerase I inhibitor**, which prevents DNA unwinding and replication by stabilizing the topoisomerase I-DNA complex, leading to DNA strand breaks. - Its main effect is in the **S phase**, but the DNA damage induces cell cycle arrest in the **G2 phase** through checkpoint activation [3].
Question 4: Multi drug resistant tuberculosis is defined as resistance to?
- A. Rifampicin and Pyrazinamide
- B. INH and Rifampicin (Correct Answer)
- C. Resistance to all first line drugs
- D. INH and Pyrazinamide
Explanation: ***INH and Rifampicin*** - **Multidrug-resistant tuberculosis (MDR-TB)** is specifically defined by resistance to at least **isoniazid (INH)** and **rifampicin** [1], which are the two most potent first-line anti-TB drugs. - This dual resistance makes treatment significantly more challenging and prolonged compared to drug-susceptible TB. *Rifampicin and Pyrazinamide* - While resistance to these drugs is serious, it does not specifically define MDR-TB unless resistance to **isoniazid** is also present. - **Pyrazinamide** is another first-line drug, but its resistance pattern alone with rifampicin does not meet the MDR-TB criteria. *Resistance to all first-line drugs* - Resistance to all four first-line drugs (isoniazid, rifampicin, pyrazinamide, and ethambutol) [1] is classified as **Extensively Drug-Resistant TB (XDR-TB)**, a more severe form of resistance than MDR-TB. - MDR-TB specifically refers to resistance to **INH and rifampicin**, not necessarily all first-line drugs. *INH and Pyrazinamide* - While resistance to both **isoniazid** and **pyrazinamide** is a concern, it does not meet the definition of MDR-TB. - The definition requires resistance to **rifampicin** in addition to isoniazid.
Question 5: Which of the following antineoplastic drugs SHOULD NOT be given by rapid IV infusion?
- A. Cyclophosphamide
- B. Cytosine arabinoside
- C. Cisplatin (Correct Answer)
- D. Bleomycin
Explanation: ***Cisplatin*** - **Cisplatin** is highly nephrotoxic and emetogenic; rapid IV infusion can exacerbate these adverse effects, leading to severe renal damage and intractable nausea/vomiting. - It typically requires **prolonged infusion times** (e.g., 6-8 hours) with extensive pre- and post-hydration to reduce kidney toxicity and ensure patient tolerance. *Cyclophosphamide* - While cyclophosphamide can cause **hemorrhagic cystitis**, this is managed by adequate hydration and mesna, and its infusion rate is generally not as critically prolonged as cisplatin's. - It is often administered as a **relatively quick IV infusion** over 30-60 minutes, emphasizing hydration. *Bleomycin* - **Bleomycin** is known for pulmonary toxicity and hypersensitivity reactions, but these are not primarily linked to its infusion rate. - It is commonly given via **slow IV push or short infusion**, sometimes with a test dose to assess for hypersensitivity. *Cytosine arabinoside* - **Cytosine arabinoside** can cause myelosuppression and cerebellar toxicity, but these toxicities are not typically exacerbated by a rapid infusion rate. - It is often administered via a **continuous infusion** over several days or as a rapid IV bolus.
Question 6: Many drugs are used as rescue therapy for preventing the adverse effects of anticancer drugs. Folinic acid is used in:-
- A. Cyclophosphamide toxicity
- B. Doxorubicin toxicity
- C. Methotrexate toxicity (Correct Answer)
- D. Cisplatin toxicity
Explanation: ***Methotrexate toxicity*** - **Folinic acid (leucovorin)** is a reduced folate that bypasses the metabolic block caused by **methotrexate** on dihydrofolate reductase. - It replenishes the body's **folate stores** and protects healthy cells from methotrexate's cytotoxic effects, particularly in the bone marrow and gastrointestinal tract. *Cyclophosphamide toxicity* - **Cyclophosphamide** toxicity, primarily hemorrhagic cystitis, is prevented by **mesna** (2-mercaptoethane sulfonate). - Mesna inactivates the urotoxic metabolite **acrolein** in the urine, preventing bladder damage. *Doxorubicin toxicity* - **Doxorubicin** causes cardiotoxicity, which can be mitigated by the iron-chelating agent **dexrazoxane**. - Dexrazoxane reduces the formation of **free radicals** that contribute to doxorubicin-induced myocardial damage. *Cisplatin toxicity* - **Cisplatin** toxicity, especially nephrotoxicity, is largely prevented by **aggressive hydration** and administration of **diuretics**. - **Amifostine** is another agent that can reduce cisplatin-induced nephrotoxicity, neurotoxicity, and ototoxicity by acting as a cytoprotectant.
Question 7: Secondary leukemias are caused by
- A. Antimetabolites
- B. Vinca alkaloids
- C. Actinomycin D
- D. Alkylating agents (Correct Answer)
Explanation: ***Alkylating agents*** - **Alkylating agents**, such as **cyclophosphamide**, **chlorambucil**, **melphalan**, and **busulfan**, are highly associated with the development of secondary leukemias, particularly **acute myeloid leukemia (AML)** and **myelodysplastic syndrome (MDS)**. - They cause **DNA damage** by forming covalent bonds with DNA, leading to mutations and chromosomal aberrations (especially deletions of chromosomes 5 and 7) that can promote leukemogenesis. - The latency period is typically **5-7 years** after exposure, and the risk is dose-dependent. *Antimetabolites* - **Antimetabolites**, like **methotrexate** and **5-fluorouracil**, interfere with **DNA replication** and repair but are less frequently linked to secondary leukemias compared to alkylating agents. - While they can cause bone marrow suppression, their mechanism of action typically involves disrupting nucleotide synthesis rather than directly inducing the specific chromosomal changes seen in secondary leukemias. *Vinca alkaloids* - **Vinca alkaloids**, such as **vincristine** and **vinblastine**, primarily target **microtubule formation** and inhibit cell division, often used in cancer chemotherapy. - They are not a significant cause of secondary leukemias; instead, they primarily cause **neurotoxicity** and bone marrow suppression as side effects. *Actinomycin D* - **Actinomycin D** (dactinomycin) acts by intercalating into **DNA** and inhibiting RNA synthesis, making it an **antitumor antibiotic**. - While it is a potent chemotherapy agent with various side effects, it is not a primary cause of **secondary leukemias**, which are predominantly associated with alkylating agents and topoisomerase II inhibitors.
Question 8: Which is not seen in Tumour lysis Syndrome?
- A. Hyperkalemia
- B. Hypophosphatemia (Correct Answer)
- C. Hyperuricemia
- D. Hypocalcemia
Explanation: ***Hypophosphatemia*** - **Tumor lysis syndrome (TLS)** is characterized by the rapid breakdown of tumor cells, leading to the release of intracellular components into the bloodstream. - This process typically results in **acute hyperphosphatemia**, not hypophosphatemia, due to the high phosphate content within tumor cells. *Hyperkalemia* - **Hyperkalemia** is a hallmark of TLS because potassium, a major intracellular cation, is released in large quantities as tumor cells lyse. - Excess potassium can lead to potentially life-threatening cardiac arrhythmias. *Hyperuricemia* - **Hyperuricemia** occurs in TLS because nucleic acids (DNA and RNA) released from dying tumor cells are metabolized into purines, which are then converted to uric acid [1]. - High uric acid levels can precipitate in the renal tubules, leading to **acute kidney injury** [1]. *Hypocalcemia* - **Hypocalcemia** develops in TLS secondary to the acute hyperphosphatemia. - The excess phosphate binds with serum calcium to form **calcium-phosphate precipitates**, effectively lowering the concentration of free ionized calcium.
Question 9: Which of the following is the platinum-based chemotherapeutic agent used as first-line treatment for ovarian carcinoma?
- A. Cyclophosphamide
- B. Methotrexate
- C. Cisplatin (Correct Answer)
- D. Dacarbazine
Explanation: ***Cisplatin*** - **Cisplatin** is a platinum-based chemotherapy drug that forms **DNA cross-links**, inhibiting DNA synthesis and leading to the death of rapidly dividing cells, making it highly effective against **ovarian carcinoma**. - It is a cornerstone of chemotherapy regimens for ovarian cancer, often used in combination with other agents such as paclitaxel. *Methotrexate* - **Methotrexate** is an **antimetabolite** that inhibits dihydrofolate reductase, thereby interfering with DNA synthesis. - While it is used in various cancers like leukemia, lymphoma, and some solid tumors (e.g., breast cancer, gestational trophoblastic disease), it is **not a primary recommended drug for ovarian carcinoma**. *Cyclophosphamide* - **Cyclophosphamide** is an **alkylating agent** that causes DNA damage, leading to cell death. - It is used in many cancers, including lymphoma, breast cancer, and some leukemias, but it is **not a first-line or primary agent for ovarian carcinoma** in contemporary treatment guidelines. *Dacarbazine* - **Dacarbazine** is an **alkylating agent** primarily used in the treatment of **malignant melanoma** and Hodgkin lymphoma. - It is **not indicated for the treatment of ovarian carcinoma**.
Question 10: What is the most appropriate next step in management for a patient with a Stage III ovarian cancer with partial response to platinum-based chemotherapy?
- A. Bevacizumab
- B. Perform surgery (Correct Answer)
- C. Switch to radiotherapy
- D. Continue regimen
Explanation: ***Perform surgery (Interval Debulking Surgery)*** - In **Stage III ovarian cancer**, after an initial partial response to **platinum-based chemotherapy**, **interval debulking surgery** is the standard next step to remove residual disease. - This approach aims to reduce tumor burden to an optimal level (< 1 cm residual disease), which has been shown to improve overall survival in multiple trials (EORTC 55971, GOG-152). - Performed after 3-4 cycles of neoadjuvant chemotherapy when the patient has demonstrated response and is medically fit for surgery. *Bevacizumab* - **Bevacizumab** is an **anti-angiogenic agent** used in ovarian cancer, typically as part of frontline maintenance therapy or for recurrent disease, not as the immediate next step after partial response to primary chemotherapy when surgery is feasible. - While it can be incorporated into maintenance treatment post-surgery, it's not the primary next step after partial response when interval debulking surgery is indicated. *Switch to radiotherapy* - **Radiotherapy** has a limited role in the primary treatment of advanced ovarian cancer due to its widespread peritoneal nature. - It is sometimes used for localized recurrence or symptom palliation, but not as a standard next step after partial response to chemotherapy in Stage III disease. *Continue regimen* - Continuing the same regimen after only a **partial response** is generally not the most effective strategy when further tumor reduction via surgery is possible. - The goal in advanced ovarian cancer is **maximal cytoreduction**, and if residual disease is present after neoadjuvant chemotherapy, interval debulking surgery is preferred over continued chemotherapy alone.
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