Antineoplastic therapy – Flashcards
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antineoplastic
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drugs used to treat cancers
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4 types
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-cytotoxic (chemotherapy) -targeted antineoplastic (target specific types of cancer cells without widespread systemic effects) -hormones & hormone antagonists -bioloiogcal response modifers (immunomodulators) -different types effective against different types of cancers
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characteristics of cancer cells
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multiple mutations or epigenetic changes enable them to evade apoptosis, proliferate excessively, indefinitely, & other characteristics that make them malignant
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cytotoxic antineoplastics
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cyclophosphamide, cisplatin, methotrexate, fluorouracil, doxorubicin, vincristine, vinblastine
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imatinib
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targeted antineoplastic
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hormones & hormone antagonists
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-hormones can influence growth of cancer -glucocorticoids (high dose)- prednisone -antiestrogens- tamoxifen -aromatase inhibitors -antiandrogens, estrogens, other agents
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biological response modifers
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-filgrasin- granulocyte stimulating factor -epoetin alfa- erythropoetin- stimulate bone marrow to make RBCs
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principles of chemotherapy
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-kills rapidly dividing cells including cancer, GI tract, bone marrow, hair follicles, tastebuds, sperm/ova -several phases of cell cycle, drugs are cycle phase specific/nonspecific -kill cells during active phases of cell cycles, not dormant
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Why are chemotherapy drugs given in combo regimens?
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target cells in different phases of cycle,different mechanisms of action, tumor may have multiple types of cells/mutations
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tissue growth fraction
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ratio of dividing cells to dormant ones, chemotherapy more effective against high tissue growth faction
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Why is chemotherapy given in cycles w/2 week rest breaks?
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to allow patient to recover, not kill patient, allow mucous membranes and bone marrow to recover
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circadian cycle/side effects
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timing it right may decrease severity of side effects
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alkylating agents
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bind to DNA, interfere with DNA functions, stop DNA replication if crosslinks form, prevent cell division
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platinum compounds
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bind to DNA form crosslinks, stop DNA replication, prevent cell division
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antimetabolites
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substitute for normal chemicals and stop metabolic processes
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antitumor antibiotics
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bind to DNA & block transcription, may have additional actions
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mitotic inhibitors
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disrupt microtubules, preventing cell division
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What actually kills the cells?
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our own immune system! cytotoxic T cells also apoptotic action of drugs but immune system must clean it all up!
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toxicities of chemotherapies
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refers to damage to normal cells at therapeutic drug levels rapidly dividing cells at highest risk alopecia, anorexia, nausea & vomiting, diarrhea, mucositis/stomatitis, bone marrow suppression, sterility in men, amennorhea in women, teratogenesis, organ toxicity (nephro, hepato, cardiac (heart failure), neuro (peripheral neuropathy), carcinogenesis- ↑risk of developing cancer later
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targeted antineoplastics
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-interfere with molecules that are important for tumor growth -examples: inhibit cell enzymes not found in normal cells or are overexpressed in cancer cells, antibodies against tumor-specific antigens, aniogenesis inhibitors, antibodies against specific receptors on cancer cells -These drugs may be tolerated better, less systemic effects, still serious side effects
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high dose glucocorticoids
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prednisone cause apoptosis of lymphoid cells→metatastic cancers also used to manage side effects of cancer therapy & cancer such as chemo induced NV or cerebral edema
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aniestrogens
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-tamoxifen -block estrogen receptors -SERMS selective estrogen receptor modulators block some estrogen receptors and stimulate others
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aromatase inhibitors
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block synthesis of estrogens
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antiandrogens
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block androgen receptors
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biological response modifiers
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don't target cancer cells directly but alter biological responses by stimulating bone marrow (hematopoietic growth factors) or affect immune function by stimulating or suppressing certain components of the immune system to destroy cancer cells or promote immune function during therapy (immunomodulators)
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methotrexate
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also used as a antirheumatic (in lower doses) -highly protein bound! huge risk for toxicity with other highly protein bound drugs (NSAIDS, aspirin)
