Antineoplastic agents I

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Antineoplastic agents I
2012-02-29 00:28:43
HUSOP DA EXAM2 Antineoplastic agents

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  1. What is the difference between treating local tumors vs. metastatic tumors?
    One can treat local tumor growth with radiation and surgery.
  2. What are the 5 heterogeneous classes of anti-cancer drugs?
    Alkylating agents, antimetabolites, natural products, hormones and antagonists, and miscellaneous
  3. The most appropriate molecular target for cancer treatment varies with what three characteristics?
    Tumor cell type, degree of metastasis, and susceptibility to cytotoxicity
  4. Why is adjunctive chemotherapy not a primary treatment modality?
    Excess toxicity due to effects on non-neoplastic, but rapidly dividing cells like epithelium.
  5. With what diseases state would one use chemotherapy as a primary treament modality?
    Various leukemias
  6. T/F Anticancer drugs are most effective when combining different MOA's and toxicities.
  7. Cytotoxic drugs should be given as close as possible to their __________ to prevent tumor regrowth.
    Maximum individualdose and frequency
  8. Antimetabolites act at the _____ phase of the cell cycle to block production of __________.
    G1, nucleotides
  9. __________ & platinum compounds act at the _____ phase of the cell cyle to block __________
    Alkylating agents, S, DNA synthesis
  10. Agents acting at the G2 phase of the cell cycle inhibit __________.
  11. What is the most appropriate method to use when dosing cytotoxic drugs?
    PK monitoring to determine AUC
  12. What are the 5 types of alkylating agents?
    Nitrogen mustards, ethyleneimines, alkyl sulfonates, nitrosoureas, and triazenes
  13. The biological activity of alkylating agents is based on __________.
    bis-(2-chlorethyl) group
  14. T/F Cyclophosphamide undergoes in vivo activation.
  15. Cyclophosphamide is __________ by CYP2Bwith transport to the site of action.
  16. What is one proposed mechanism for cyclophosphamide selectivity?
    Normal cells possess ability to neutralize the activated intermediate by EtOH dehydrogenase or glutathione.
  17. How does alkylation cause cell death?
    DNA repair mechanisms can recognize alkylated DNA, create strand breaks, and induce apoptosis
  18. If alkylating agents can produce a DNA __________, it can be more effective at killing cells.
  19. Why is DNA cross-linking are more efficient way of cytotoxicity?
    The repair mechanisms are part of a more error-prone pathway
  20. How will use of single alkylating agents cause tumor resistance?
    Decreased permeation of drug, increased cellular content of nucleophiles, increased activity of DNA repair pathways, andincreased rates of metabolism to inactive forms
  21. T/F The primary toxicity of alkylating agents is nephrotoxicity.
    False, it's bone marrow toxicity
  22. Besides mone marrow toxicity, what are some other primary toxicites of alkylating agents?
    Mucosal toxicity and neurotoxicity
  23. Alkylating agents have the ability to produce __________.
  24. __________ can severely damage the skin if not properly injected into a vein.
  25. Cyclophophamide is actived in the _____ by CYP2B to __________. The metabolite sponaneously cleaves in the target tissue to form the reactive __________.
    liver, 4hydroxycyclophosphamide, phosphoramide mustard and acrolein.
  26. Cyclophosphamide is commonly indicated for what cancer?
    Breast cancer, lymphomas, and chronic lymphocytic leukemias
  27. Ifosphamide is a __________ analog and can produce severe _____ toxicity.
    cyclophosphamide, CNS
  28. Melphalan is given for _____ days then a ______ rest period.
    4, 4 week
  29. Chlorambucil is commonly used to treat what?
    Chronic lymphocytic leukemia
  30. __________ is