Plant Alkaloids — MCQs
Peripheral neuropathy as a side effect is caused by which of the following anticancer drugs?
All of these are G2 phase blockers except:
Which of the following drugs act by inhibiting DNA replication?
Many drugs are used as rescue therapy for preventing the adverse effects of anticancer drugs. Folinic acid is used in:-
Treatment of choice in intracranial ALL is:
Which chemotherapy agents are commonly used for the treatment of retinoblastoma?
Which is the most cardiotoxic anti-cancer drug among the following?
On chronic use, linezolid leads to which of the following?
All of the following are hormonal agents used in treatment of cancer EXCEPT:
Profound mitotic delay occurs when the doses of anticancer drugs are:
Plant Alkaloids Indian Medical PG Practice Questions and MCQs
Question 1: Peripheral neuropathy as a side effect is caused by which of the following anticancer drugs?
- A. Cyclophosphamide
- B. Etoposide
- C. Irinotecan
- D. Vincristine (Correct Answer)
Explanation: ***Vincristine*** - **Vincristine** is a **vinca alkaloid** that works by inhibiting **microtubule formation**, which is essential for cell division [1], [3]. - Its major dose-limiting toxicity is **peripheral neuropathy**, manifesting as paresthesias, weakness, and loss of reflexes due to damage to neuronal microtubules [1], [2]. *Cyclophosphamide* - **Cyclophosphamide** is an **alkylating agent** that forms cross-links in DNA, leading to cell death. - Its most common side effects include **myelosuppression**, hemorrhagic cystitis, and alopecia; **peripheral neuropathy** is generally not a prominent adverse effect. *Etoposide* - **Etoposide** is a **topoisomerase II inhibitor** that causes DNA strand breaks. - Key toxicities include **myelosuppression** and **gastrointestinal disturbances**, but it is not typically associated with significant peripheral neuropathy. *Irinotecan* - **Irinotecan** is a **topoisomerase I inhibitor** that causes DNA damage during replication. - Its primary dose-limiting toxicities are **diarrhea** and **myelosuppression**, not peripheral neuropathy.
Question 2: 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 3: Which of the following drugs act by inhibiting DNA replication?
- A. Mitomycin C
- B. 6-Mercaptopurine (Correct Answer)
- C. Actinomycin D
- D. Asparaginase
Explanation: ***6-Mercaptopurine*** - This drug is a **purine analog** that acts as an **antimetabolite**, directly interfering with the **synthesis of purine nucleotides** required for DNA replication. - By inhibiting enzymes like **PRPP amidotransferase** and getting incorporated into DNA as a fraudulent nucleotide, it blocks the **de novo synthesis** pathway, preventing normal DNA replication. - This represents **direct inhibition of DNA synthesis** at the nucleotide building block level. *Mitomycin C* - This agent is an **alkylating agent** that **cross-links DNA** strands, causing DNA damage that prevents strand separation. - While it does prevent DNA replication, its mechanism is through **DNA damage and structural disruption** rather than inhibition of the DNA synthesis machinery itself. - It acts by damaging already-formed DNA rather than preventing new DNA synthesis. *Actinomycin D* - Actinomycin D is an **intercalating agent** that inserts itself between DNA base pairs, primarily **inhibiting RNA synthesis** by blocking RNA polymerase movement. - While it binds to DNA, its primary therapeutic action is on **transcription (RNA synthesis)**, not direct inhibition of DNA replication. *Asparaginase* - Asparaginase is an enzyme that **depletes asparagine** from the blood, which is an essential amino acid for certain cancer cells (e.g., leukemic cells). - Its mechanism is to starve cancer cells of asparagine, leading to **inhibition of protein synthesis**, not DNA replication.
Question 4: 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 5: Treatment of choice in intracranial ALL is:
- A. Intrathecal methotrexate (Correct Answer)
- B. Intrathecal vincristine
- C. Vincristine and prednisolone
- D. Prednisolone
Explanation: ***Intrathecal methotrexate*** - **Intrathecal methotrexate** is the cornerstone of central nervous system (CNS) prophylaxis and treatment for **intracranial acute lymphoblastic leukemia (ALL)** due to its ability to reach high concentrations in the cerebrospinal fluid (CSF). - It is highly effective in eradicating leukemic cells in the **CNS**, preventing leptomeningeal relapse, and is often combined with other intrathecal agents or cranial radiation. *Intrathecal vincristine* - **Vincristine** is primarily an intravenous chemotherapeutic agent and is **neurotoxic** when administered intrathecally, potentially causing severe and irreversible neurological damage, including paralysis and death. - Therefore, **intrathecal vincristine** is contraindicated due to its severe adverse effects on the CNS. *Vincristine and prednisolone* - **Vincristine** and **prednisolone** are systemic agents typically administered intravenously and orally, respectively, and are crucial components of **induction and consolidation therapy** for ALL. - However, their ability to penetrate the **blood-brain barrier** is limited, making them ineffective for directly treating or preventing intracranial ALL. *Prednisolone* - **Prednisolone** is a corticosteroid used systemically for its **anti-inflammatory** and **cytotoxic effects** on leukemic cells, particularly in inducing remission in ALL. - While it can partially penetrate the **blood-brain barrier**, its concentration in the CSF is usually insufficient to effectively treat or prevent established **intracranial ALL** on its own.
Question 6: Which chemotherapy agents are commonly used for the treatment of retinoblastoma?
- A. vincristine, carboplatin and etoposide (Correct Answer)
- B. vinblastine, etoposide and bleomycin
- C. vinblastine, vincristine and etoposide
- D. vinblastine, vincristine and cisplatin
Explanation: ***Vincristine, carboplatin and etoposide*** - This combination is a well-established and commonly used **chemotherapy regimen** for the systemic treatment of retinoblastoma, particularly when there is significant intraocular disease or extraocular extension. - **Vincristine** targets microtubules, **carboplatin** is an alkylating agent, and **etoposide** is a topoisomerase inhibitor, working together to achieve a synergistic antineoplastic effect. *Vinblastine, etoposide and bleomycin* - While etoposide is used, **vinblastine** is not a primary agent for retinoblastoma, and **bleomycin** is more commonly associated with germ cell tumors or lymphomas, not retinoblastoma. - This combination lacks the broad spectrum of activity and specific targeting for retinoblastoma that is present in the standard regimen. *Vinblastine, vincristine and etoposide* - Although vincristine and etoposide are used, **vinblastine** is not typically included in the first-line systemic chemotherapy for retinoblastoma. - The absence of a platinum agent like carboplatin would make this regimen less effective for retinoblastoma, which often requires a strong alkylating agent. *Vinblastine, vincristine and cisplatin* - While vincristine is appropriate, **vinblastine** is not a standard component, and **cisplatin** is an alkylating agent but **carboplatin** is generally preferred in retinoblastoma due to its similar efficacy and a more favorable toxicity profile, especially regarding nephrotoxicity. - The use of cisplatin can lead to more significant **renal toxicity** and potentially ototoxicity compared to carboplatin, which is often avoided in a pediatric population when alternatives exist.
Question 7: Which is the most cardiotoxic anti-cancer drug among the following?
- A. Cyclophosphamide
- B. Tamoxifen
- C. Imatinib
- D. Anthracyclines (Correct Answer)
Explanation: ***Anthracyclines*** - **Anthracyclines** (e.g., doxorubicin, daunorubicin) are notorious for causing **dose-dependent cardiotoxicity**, leading to **irreversible dilated cardiomyopathy** and **heart failure**. - Their cardiotoxic effect is primarily due to the generation of **reactive oxygen species** and interference with cardiac topoisomerase IIβ. *Cyclophosphamide* - Cyclophosphamide can cause cardiotoxicity, particularly at **high doses**, manifesting as **hemorrhagic myocardial necrosis** or **pericarditis**. - However, its cardiotoxicity is generally considered **less frequent and severe** than that of anthracyclines. *Tamoxifen* - Tamoxifen is primarily associated with an **increased risk of thromboembolic events** and **endometrial cancer**. - While some cardiac effects like **QT prolongation** can occur, it is not considered a primary cardiotoxic agent leading to cardiomyopathy. *Imatinib* - Imatinib, a **tyrosine kinase inhibitor**, has been linked to **cardiac dysfunction** including heart failure in some patients. - However, the incidence and severity of cardiotoxicity with imatinib are **lower** compared to anthracyclines, which are broadly cardiotoxic.
Question 8: On chronic use, linezolid leads to which of the following?
- A. Thrombocytopenia (Correct Answer)
- B. Deranged LFT
- C. Nephrotoxicity
- D. Ototoxicity
Explanation: ***Thrombocytopenia*** - **Linezolid** is known to cause **myelosuppression**, particularly **thrombocytopenia**, with prolonged use (typically >2 weeks). - This adverse effect is usually **reversible** upon discontinuation of the drug. - This is the **most characteristic** and **dose-limiting** hematologic toxicity of chronic linezolid therapy. *Deranged LFT* - While **linezolid** can occasionally cause **elevated liver enzymes**, this is a **less common** adverse effect compared to myelosuppression. - **Thrombocytopenia** is far more characteristic of **chronic linezolid use** and is the primary concern requiring monitoring. - Hepatotoxicity with linezolid is typically mild and less dose-limiting than hematologic effects. *Nephrotoxicity* - **Linezolid** is generally considered to have a low risk of **nephrotoxicity** and does not typically cause significant kidney damage. - **Aminoglycosides** or **vancomycin** are examples of antibiotics more commonly associated with nephrotoxic effects. *Ototoxicity* - **Ototoxicity**, characterized by hearing loss or tinnitus, is not a common or recognized side effect of **linezolid** therapy. - This adverse effect is more frequently associated with drugs like **aminoglycosides** or high-dose **loop diuretics**.
Question 9: All of the following are hormonal agents used in treatment of cancer EXCEPT:
- A. Cabergoline
- B. Leuprolide
- C. Irinotecan (Correct Answer)
- D. Anastrozole
Explanation: ***Irinotecan*** - **Irinotecan** is a **chemotherapeutic agent** that acts as a **topoisomerase I inhibitor**, interfering with DNA replication and repair. - It works through a **cytotoxic mechanism** directly killing cancer cells, rather than modulating hormonal pathways. *Cabergoline* - **Cabergoline** is a **dopamine agonist** primarily used to treat **prolactinomas**, which are prolactin-producing pituitary tumors. - While it treats a tumor, its mechanism is **hormonal modulation** by reducing prolactin secretion, not direct cytotoxicity. *Anastrozole* - **Anastrozole** is an **aromatase inhibitor** used in estrogen receptor-positive breast cancer. - It works by **blocking the conversion of androgens to estrogens**, thereby reducing estrogen levels that fuel cancer growth. *Leuprolide* - **Leuprolide** is a **GnRH agonist** used in prostate cancer, breast cancer, and other hormone-sensitive conditions. - It initially stimulates, then continuously downregulates, the **pituitary gland's production of LH and FSH**, leading to reduced testosterone or estrogen levels.
Question 10: Profound mitotic delay occurs when the doses of anticancer drugs are:
- A. No dose effect
- B. Smaller
- C. Intermediate
- D. Larger (Correct Answer)
Explanation: ***Larger*** - **Larger doses** of anticancer drugs cause extensive DNA damage, leading to prolonged activation of cell cycle checkpoints (G2/M checkpoint) [1] - This extensive damage results in **profound mitotic delay** as the cell attempts DNA repair or undergoes apoptosis [1] - High-dose chemotherapy maximally activates checkpoint mechanisms, causing significant and prolonged mitotic arrest [1] *No dose effect* - This option is incorrect because mitotic delay is a well-established dose-dependent phenomenon - Even minimal doses of cytotoxic agents can trigger checkpoint activation and affect mitotic progression *Smaller* - **Smaller doses** cause less severe DNA damage, leading to minimal or transient mitotic delay - Cells can efficiently repair minor damage and resume mitosis relatively quickly - The delay is present but not "profound" *Intermediate* - **Intermediate doses** cause moderate mitotic delay, falling between minimal and profound effects - The checkpoint activation is noticeable but not maximal - This would not be characterized as "profound," which implies extensive and prolonged cell cycle arrest
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