Pharmacology for NEET-PG
Anticancer Drugs for NEET-PG
Anticancer pharmacology links each cytotoxic and targeted agent to its mechanism, cell-cycle specificity, and dose-limiting toxicity, and it is a high-yield NEET-PG block. Questions frequently name a distinctive organ toxicity and ask for the drug, so the signature adverse effects of the major agents are the core deliverable. The topic covers alkylating agents, antimetabolites, antitumour antibiotics, plant alkaloids, platinum compounds, and the newer targeted and hormonal therapies. Examiners favour toxicities that are drug-specific and clinically important: doxorubicin cardiotoxicity, bleomycin pulmonary fibrosis, cisplatin nephrotoxicity, cyclophosphamide haemorrhagic cystitis, and vincristine neuropathy. Rescue and protective agents are equally testable, including leucovorin with methotrexate, mesna with cyclophosphamide, and dexrazoxane with anthracyclines. Targeted therapy adds imatinib, trastuzumab, rituximab, and the tyrosine kinase inhibitors with their own class effects. Common traps include confusing vincristine neuropathy with vinblastine myelosuppression, forgetting that methotrexate toxicity is rescued by folinic acid not folic acid, and overlooking the specific antidotes that make certain regimens safe.
MedNext Academy | 3 min read
Anticancer Drugs for NEET-PG
Anticancer pharmacology links each cytotoxic and targeted agent to its mechanism, cell-cycle specificity, and dose-limiting toxicity, and it is a high-yield NEET-PG block. Questions frequently name a distinctive organ toxicity and ask for the drug, so the signature adverse effects of the major agents are the core deliverable. The topic covers alkylating agents, antimetabolites, antitumour antibiotics, plant alkaloids, platinum compounds, and the newer targeted and hormonal therapies. Examiners favour toxicities that are drug-specific and clinically important: doxorubicin cardiotoxicity, bleomycin pulmonary fibrosis, cisplatin nephrotoxicity, cyclophosphamide haemorrhagic cystitis, and vincristine neuropathy. Rescue and protective agents are equally testable, including leucovorin with methotrexate, mesna with cyclophosphamide, and dexrazoxane with anthracyclines. Targeted therapy adds imatinib, trastuzumab, rituximab, and the tyrosine kinase inhibitors with their own class effects. Common traps include confusing vincristine neuropathy with vinblastine myelosuppression, forgetting that methotrexate toxicity is rescued by folinic acid not folic acid, and overlooking the specific antidotes that make certain regimens safe.
Anticancer pharmacology links each cytotoxic and targeted agent to its mechanism, cell-cycle specificity, and dose-limiting toxicity, and it is a high-yield NEET-PG block. Questions frequently name a distinctive organ toxicity and ask for the drug, so the signature adverse effects of the major agents are the core deliverable. The topic covers alkylating agents, antimetabolites, antitumour antibiotics, plant alkaloids, platinum compounds, and the newer targeted and hormonal therapies. Examiners favour toxicities that are drug-specific and clinically important: doxorubicin cardiotoxicity, bleomycin pulmonary fibrosis, cisplatin nephrotoxicity, cyclophosphamide haemorrhagic cystitis, and vincristine neuropathy. Rescue and protective agents are equally testable, including leucovorin with methotrexate, mesna with cyclophosphamide, and dexrazoxane with anthracyclines. Targeted therapy adds imatinib, trastuzumab, rituximab, and the tyrosine kinase inhibitors with their own class effects. Common traps include confusing vincristine neuropathy with vinblastine myelosuppression, forgetting that methotrexate toxicity is rescued by folinic acid not folic acid, and overlooking the specific antidotes that make certain regimens safe.
Key points
- **Doxorubicin:** Anthracycline causing dose-dependent dilated cardiomyopathy; dexrazoxane is cardioprotective and cumulative dose is limited.
- **Bleomycin:** Antitumour antibiotic causing pulmonary fibrosis; minimal myelosuppression, which is unusual for cytotoxics.
- **Cisplatin:** Nephrotoxic, ototoxic, and highly emetogenic; hydration and amifostine reduce renal injury.
- **Cyclophosphamide:** Alkylating agent whose metabolite acrolein causes haemorrhagic cystitis, prevented by mesna and hydration.
- **Vincristine and vinblastine:** Vincristine causes peripheral neuropathy with little marrow toxicity; vinblastine causes myelosuppression.
- **Methotrexate:** Antifolate whose toxicity is rescued by folinic acid, also called leucovorin, which bypasses the blocked dihydrofolate reductase step.
- **5-fluorouracil:** Antimetabolite causing mucositis, diarrhoea, and myelosuppression; hand-foot syndrome is characteristic.
- **Imatinib:** Tyrosine kinase inhibitor of BCR-ABL, transforming chronic myeloid leukaemia management; generally well tolerated.
- **Trastuzumab:** Anti-HER2 monoclonal antibody used in HER2-positive breast cancer; can cause reversible cardiotoxicity.
- **Rituximab:** Anti-CD20 monoclonal antibody used in B-cell lymphomas; infusion reactions and hepatitis B reactivation are concerns.
- **Tamoxifen:** Selective oestrogen receptor modulator in hormone-receptor-positive breast cancer; increases endometrial cancer and thromboembolism risk.
- **Cell-cycle specificity:** Antimetabolites act in S phase and vinca alkaloids in M phase, whereas alkylating agents are cell-cycle non-specific.
Frequently Asked Questions
Which anticancer drug causes which organ toxicity?
Doxorubicin harms the heart, bleomycin the lungs, cisplatin the kidneys and ears, cyclophosphamide the bladder, and vincristine the peripheral nerves. These pairings are the core recall targets.
Why is folinic acid, not folic acid, used to rescue methotrexate toxicity?
Methotrexate blocks dihydrofolate reductase. Folinic acid is already reduced and bypasses the blocked step, whereas folic acid cannot be converted while the enzyme is inhibited.
What is mesna used for?
Mesna binds acrolein, the toxic metabolite of cyclophosphamide and ifosfamide, in the urinary tract and prevents haemorrhagic cystitis.
How are targeted therapies different from classical cytotoxics?
Targeted agents such as imatinib and trastuzumab act on specific molecular abnormalities, giving more selective activity and different toxicity profiles than broad cytotoxic drugs.
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