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293 Cards in this Set
- Front
- Back
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What is clinical use of Oxaliplatin (Eloxatin)
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Colorectal cancer in combination with 5-FU, leucovorin
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What are the toxicities of Oxaliplatin (Eloxatin)
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Hematologic toxicity, mucositis, pulmonary fibrosis, pharnygolaryngodysesthesias, nausea/vomiting, renal toxicity, neurotoxicity - particulary sensitivity to cold; rare hepatic venoocculsive disease.
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For which drug is it important to counsel patients to avoid touching cold objects or drinking cold beverages?
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Oxaliplatin (Eloxatin)
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What drugs are mixed in Sodium chloride?
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Cisplatin
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why is cisplatin mixed in sodium chloride?
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to prevent the chloride groups from leaving.
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What are antimetabolites?
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resemble naturally occuring nuclear structural components "metabolites" such as nucleotide bases.
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What are the specific pyrimidine analogues?
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thymidine, uracil, cytidine
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What are the pharmacology of pyridimidine analogues?
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incorporated into DNA as false base pairs after being metabolized to active forms. This prevents DNA replication.
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What are the 5-fluorouracil?
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resembles uracil; enters cells and is phosphorylated to F-dUMP which inhibits thymidylate synthase, which leads to the depletion of TTP (thymidine triphosphate), a necessary consitituent of DNA.
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What is the clinical use for 5-fluorouracil (Adrucil)?
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Colon, gastric cancer, esophageal, breast cancer, pancreatic cancer, gynecologic cancers, head and neck cancer.
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What are the toxicities for 5-fluorouracil (Adrucil)?
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Nausea/vomiting, anorexia, alopecia, mucositis, diarrhea, myelosuppression, neurologic toxicity, coronary vasospasm/angina.
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What can be combined to stabilizes the complex of F-dUMP with thymidylate synthase to enhance efficacy of 5-FU?
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leucovorin
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What is Floxuridine (FUDR)'s clinical use?
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Local therapy for metastatic colon cancer
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What is the toxicity for Floxuridine (FUDR)?
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Nausea/vomiting, anorexia alopecia, mucositis, diarrhea, myelosuppression, neurologic toxicity, coronary vasospasm/angina.
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What is the common administration for Floxuridine (FUDR)?
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via intra-arterial infusions.
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What is the clinical use for Capecitabine (Xeloda)?
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Colon cancer, breast cancer
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What is the toxicities for Capecitabine (Xeloda)?
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Diarrhea, palmar plantar erythrodysesthesia + nausea/vomiting, anorexia, alopecia, mucositis, diarrhea, myelosuppression, neurologic toxicity, coronary, vasospasm/angina.
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What is the dosing scedule of Capecitabine (Xeloda)?
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Given orally for two weeks of therapy then one week off.
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What is the pharmacology of sytidine analogs?
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phosphorylated to its active triphosphate form (ara-CTP) within tumor cells. This causes inhibition f DNA polymerase which is needed for DNA strand elongation. It is also incorporated directly into DNA inhibiting replication of DNA.
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What is the clinical use for Cytarabine (Ara-C) (Cytosar - U)?
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Acute myeloid leukemia, acute lymphocytic leukemia, lymphoma.
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What are the toxicities for Cytarabine (Ara-C) (Cytosar - U)?
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Myelosuppression, nausea/vomiting, alopecia, hand-foot syndrome, diarrhea, hepatic dysfunction, neurologic toxicity (cerebellar toxicity), chemical conjunctivitis.
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Dose high or low dose of Ctarabine (Ara-C) (Cytosar-U) has distinct toxicity especially neurologic toxicity?
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High-dose Ara-C has distinct toxicities relative to low dose.
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What is given with Cytarabine (Ara-C) (Cytosar-U) to prevent conjunctivitis?
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ophthalmic: dexamethasone is given to prevent conjunctivitis.
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What is the clinical use for Cytarabine liposomal (Depocyt)?
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Central nervous system leukemia/ lymphoma.
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What are the toxicities of Cytarbine liposomal (Depocyt)?
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Chemical arachnoiditis (treat with steroids), headache
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What is the treatment for Cytarabine liposomal (Depocyt) chemical arachnoiditis?
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treat with steroids.
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What is the dosage form for Cytarabine liposomal (Depocyt)?
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Encased in a liposomal dosage form for intrathecal administration.
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What is Gemcitabine (Gemzar)?
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fluorine substituted deoxycytidine analog similar to cytarabine. It is incorporated into the DNA which leads to inhibition of DNA polymerase activity.
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What is the clinical use for Gemcitabine (Gemzar)?
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Lung caner, breast cancer, ovarian cancer, pancreatic cancer.
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What are the toxicities of gemcitabine (Gemzar)?
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Nausea/ Vomiting, myelosuppression, edema, flu like symptoms, fatigue, transient elevations in LFTs.
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How do Azacytidien and decitabine exert their effects?
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direct incorporation into the DNA and inhibition of DNA methyltransferase which causes hypomethylation of DNA ultimately apoptosis.
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What is the clinical use for Azacytidine?
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Myelodysplastic syndrome.
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What is the toxicities for Decitabine (Dacogen)?
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Myelosuppression, Nausea/vomiting, constipation, diarrhea, edema,
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What is the administration for Azacytidine?
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SQ or IV injection daily for 7 days.
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What is the administration for Decitabine (Dacogen)?
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IV given every 8 hours * 3 days.
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What are the purine analogues (guanine, adenine)?
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Similar to pyrimidine analogues, act as false nucleoside base pairs and cause diruption of normal DNA synthesis.
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What is the clinical use for 6-mercaptopurine-6MP (Purinethol)?
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Acute and chronic leukemia, lymphoma.
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What are the toxicities of 6-mercaptopurine-6MP (Purinethol)?
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Myelosuppression, nausea/vomiting, hepatotoxicity.
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Which drug has severe nausea/vomiting?
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Cisplatin, CDDP - (Platinol)
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How is 6-mercaptopurine-6MP (Purinethol) metabolized?
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metabolized to an inactive metabolite via xanthine oxidase.
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What must be done to 6-mercaptopurine-6MP (Purinethol) if given with allopurinol?
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Must reduce dose of 6-MP if given together with allopurinol.
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What is the clinical use for 6-thioguanine-6TG (Tabloid Thoguanine)?
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Acute leukemia.
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What are the toxicities for 6-thioguanine-6TG (Tabloid Thioguanine)?
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Myelosuppression, GI toxicity.
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What are the clinical uses for Fludarabine (Fludara)?
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CLL, low-grade non-Hodgkin's lymphoma.
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What is the toxicities of Fludarabine (Fludara)?
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Prolonged myelosuppression, renal insufficiency, opportunistic infection.
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What drug is used mostly for mainenance therapy for ALL?
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Fludarabine (Fludara).
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What drug is used with Bactrim prophylaxis?
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Fludarabine (Fludara).
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What is Cladribine (Leustatin) used for?
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Hairy cell leukemia (HCL).
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What are the purine analogues?
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6-mercaptopurine-6MP (purinethol), 6-thioguanine-6TG(Tabloid Thioguanine), Fludarabine (Fludara), Cladribine (Leustatin), Pentostatin.
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What is patinet at risk for after completion of Cladribine (Leustatin)?
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Patient may be at risk for opportunistic infections after completion of therapy.
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What is is the dosage of Cladribine (Leustatin)?
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Given as a continuous infusion for 7 days.
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What is the clinical use for Pentostatin?
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hairy cell leukemia (HCL), graft versus host disease.
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What is the toxicities for Pentostatin?
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Myelosuppression, opportunistic infections, renal failure, hepatic toxicity.
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What is the 2 nd or 3 rd line for HCL due to inreased toxicity vs. Cladribine (Leustatin)?
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Pentostatin.
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What is the pharmacology for Antifolate agents?
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Folic acid is an essential dietary cofactor for the production of purine precursors of DNA. Inhibition of dihydrofolate reductase (enzyme responsible for reducing folic acid to folinic acid) results in the depletion of tetrahydrofolate precursors required for the synthesis fo purines and thymidylate.
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What is the clinical use for Methotrexate?
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Breast cancer, leukemia, choriocarcinoma, lymphoma
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What are the toxicities for Methotrexate?
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Mucositis, myelosuppression, nausea/vomiting, pneumonitis, hepatotoxicity, renal failure.
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What is "leucovorin rescue" used for?
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Methotrexate.
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Why is "leucovorin rescue" used with Methotrexate?
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Use "leucovorin resuce", a reduced form of folic acid averts the need for dihydrofolate reductase to reduce exogenous folic acid.
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What is the clinical use of Pemetrexed (Alimta)?
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Mesothelioma, non-small cell lung cancer.
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What are the toxicities of Pemetrexed (Alimta)?
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Mucositis, myelosuppression, nausea/vomiting.
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What drug must be given with vitamin B12, folic acid and dexamethasone?
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Pemetrexed (Alimta).
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Why is vitamin B12, folic acid and dexamethasone given with Pemetrexed (Alimta)?
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To decrease infections risk and rash.
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What is the pharmacology fo Vinca Alkaloids?
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Cell-cycle specific agents which block cells in mitosis.
Bind specifically to the alpha and beta subunits of tubulin, inhibiting its polymerization. Polymerization of tubulin is responsible for the formation of the mitotic spindle during the metaphase period of mitosis. Thus, vinca alkalodis inhibit cell dividion it the M phase of the cell cycle. |
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What is the clinical use of Vinblastine (Velban)?
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Testicular cancer, lymphoma, Kapsosi's sarcoma, neuroblastoma
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What are the toxicities for Vinblastine (Velban)?
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Myelosuppression, peripheral neuropathy, constipation, nausea/vomiting, alopecia, SIADH, mucositis, extravasation, ischemic cardiac toxcity.
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what does vinblastin (Velban) cause more of: myelosuppression or neurotoxicity?
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Causes more myelosuppression relative to neurotoxicity; vesicant.
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What is Vincristine (Oncovin) used for?
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Leukemia, lymphoma, Wilm's tumor, neuroblastoma, brain tumors, rhabdomyosarcoma, bladder cancer.
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What is Vincristine's toxicity?
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Myelosuppression, peripheral neuropathy, consitpation, nausea/vomiting, slopecia, SIADH, mucositis, extravasation, ischemic cardiac toxicity.
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What is more pronounced in Vincristine (Oncovin): neurologic toxicity or myelosuppression?
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Causes more neurotoxicity relative to myelosuppression.
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Which drug is capped at 2mg?
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Vincristine (Oncovin).
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Why is Vincristine (Oncovin) capped dosed at 2 mg?
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dose empirically capped at 2 mg because of dose-related neurotoxicity, vesicant.
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What is Vinorelbine (Navelbine) used for?
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Non small cell lung cancer, breast cancer.
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What are the side effects of Vinorelbine (Navelbine)?
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Myleosuppression, peripheral neurophathy, consitpation, nausea/vomiting, alopecia, SIADH, mucositis, extravasation, ischemic cardiac toxicity.
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Does Vinblastine or Vinorelbine (Navelbine) have more myelosuppression?
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Vinorelbine.
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Which agent is a vesicant: an agent that causes tissue blistering?
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Vinorelbine (Navelbine).
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What are the four mechanisms for Anthracycline antibiotics?
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1. Topoisomerase II inhibition: stabilizes the topoisomerase complex after it has broken the DNA chain for replication and prevents the DNA helix from being resealed thus stoppping replication.
2. DNA intercalation causing single and double strand DNA breaks. 3. Freee radical generation by doxorubicin metabolites. 4. Disruption of cell membranes. |
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What is the clinical use of Doxorubicin (Adriamycin)?
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Lymphoma, leukemia, multiple myeloma, breast cancer, sarcoma, small cell lung cancer, ovarian cancer, endometrial cancer, head and neck cancer, bladder cancer, thyroid cancer.
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What is the toxicities for Doxorubicin (Adriamycin)?
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Cardiac toxicity, nausea/vomiting, mucositis, alopecia, myelosuppression, extravasation, red/orange urine, radiation recall.
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What is the color of Doxorubicin (Adriamycin)?
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drug has a red/orange color.
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What drug has dose-related cardiomyopathy at cumulative dose fo 550mg/m2 lifetime exposure?
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Doxorubicin (Adriamycin).
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What dose dose Doxorubicin (Adriamycin) have cardiomyopathy?
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At a cumulative dose of 550mg/m2.
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What is clinical use for Liposomal doxorubicin (Doxil)?
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Ovarian cancer, breast cancer, multiple myeloma.
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What is the toxicity for Liposomal doxorubicin (Doxil)?
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Cardiac toxicity, nausea/vomiting, mucositis, alopecia (less), hand foot syndrome, myelosuppression, extravasation, red/orange urine, radiation recall.
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What color is Liposomal doxorubicin (Doxil)?
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Drug has a red/orange color.
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What is Epirubicin (Ellence) clinically used for?
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Breast cancer
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What are the toxicities of Epirubicin (Ellence)?
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Cardiac toxicity, nausea/vomiting, mucositis, alopecia (less), hand foot syndrome, myelosuppression, extravasation, red/orange urine, radiation recall.
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What drug is the Epimer of doxorubicin?
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Epirubicin (Ellence).
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What is the clinical use for Daunorubicin (Cerubidine)?
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Breast cancer.
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What are the toxicities for Daunorubicin (Cerubidine)?
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Cardiac toxcity, nausea/vomiting, mucositis, alopecia (less), hand foot syndrome, myelosuppression, extravasation, red/orange urine, radiation recall.
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What is the clinical use for Idarubicin (Idamycin)?
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Acute myeloid leukemia.
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What are the toxicities of Idarubicin (Idamycin)?
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Cardiac toxicity, nausea/vomiting, mucositis, alopecia (less), hand foot syndrome, myelosuppression, extravasation, red/orange urine, radiation recall.
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What drugs has risk of cardiac toxcitiy increase with cumulative doses?
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Anthracycline antibiotics: Liposomal doxorubicin (Doxil), Epirubicin (Ellence), Daunorubicin (Cerubidine), Idarubicin (Idamycin).
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What is the pharmacology of Anthracendione antibiotics?
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Topoisomerase II inhibition induced strand breakage and DNA intercalation; minimal generation of free radicals which contributes to less cardiac toxicity.
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What is the clinical use of Mitoxantrone (Novantrone)?
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Acute myeloid leukemia, breast cancer, prostate cancer.
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What is the toxicity of Mitoxantrone (Novantrone)?
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Less cardiac toxicity than doxorubicin, nausea/vomiting, mucositis, alopecia, myelosuppression, extravasation, red/orange urine, radiation recall.
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Which drug has less cardio toxicity: Doxorubicin (Adriamycin) or Mitoxantrone (Novantrone)?
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Mitoxantrone (Novantrone) has less cardiac toxicity.
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What is the pharmacology of Topoisomerase I inhibitors?
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Inhibits the enzyme topoisomerase I resulting int he stabilization of the "cleavable complexes" causeing reversible single strand DNA breaks.
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What is the drug color for Mitoxantrone (Novantrone)?
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Blue color.
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What is the clinical use for Irinotecan - CPt - 11 (Camptosar)?
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Colon cancer, rectal cancer, small cell lung cancer.
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what is the toxcities for Irinotecan - CPT - 11 (Campotosar)?
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Diarrhea, myelosuppression, nausea/vomiting, cholinergic syndrome.
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What is the metabolism of Irinotecan - CPT - 11 (Camptosar)?
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A prodrug, the active moiety is SN-38.
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what is associated with the infusion of Irinotecan - CPT -11 (Camptosar)?
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cholinergic mediated diarrhea associated with infusion can be reversed with atropine.
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How to reverse Irinotecan-CPT-11 (Camptosar) infusion associated cholinergic mediated diarrhea?
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can be reversed with atropine.
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How to control Irinotecan - CPT-11 (Camptosar) delayed diarrhea?
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delayed diarrhea may be controlled with loperamide 4 mg PO * 1 then 2mg PO Q2H until formed BM (more stringent directions than what is on the OTC box)
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Patients with UGT1A1 deficiencies have worse toxicities with what drug?
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Irinotecan - CPT - 11 (Camptosar).
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What is the clinical use of Topotecan (Hycamtin)?
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Ovarian cancer, small cell lung cancer, myelodysplastic syndrome.
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What are the side effects of Topotecan (Hycamtin)?
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Myelosuppression, fatigue.
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What is the pharmacology of the Topoisomerase II inhibitors?
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Forms ternary complexes with topoisomerase II and DNA and results in double-stranded DNA breaks. Strand passage and resealing that follows topoisomerase binding to DNA is inhibited. Cells in S and G2 phase are most sensitve to this phenomenon.
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Cells in what phase are sensitive to Topoisomerase II inhibitor double-strand DNA break?
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Cells in S and G2 phase are most sensitive to this phenomenon.
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What is the clinical use for Etoposide - VP - 16 (Vepesid)?
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Testicular cancer, acute leukemia, lymphoma, lung cancer, breast cancer, Kaposi's sarcoma, ovarian cancer.
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What are the toxicities for Etoposide - VP - 16 (Vepesid)?
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Myelosuppression, secondary nausea/vomiting, hepatotoxicity, flushing, mucositis, acute myeloid leukemia, infusion related reactions.
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What is the dosage form of Etoposide - VP - 16 (Vepesid)?
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50 mg capsules available; bioavilibility is 50%.
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What is the clinical use of Tenoposide - VM - 26 (Vumon)?
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Childhood leukemia
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What are the toxicities of Tenoposide - VM - 26 (Vumon)?
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Myelosuppression, secondary, nausea/vomiting, hepatotoxicity, flushing, mucositis, acute myeloid leukemia, infusion related reactions.
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What is the pharmacology of the Taxanes?
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Stabilizes the micortubule complexes by preventing depolymerization and halting mitosis - "mitotic inhbitors".
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What is the clinical use for Paclitaxel (Taxol)?
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Breast cancer, ovarian cancer, lung cancer, bladder cancer, head and neck cancer.
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What are the toxicities of Paclitaxel (Taxol)?
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Myelosuppression, infusion-related reactions (related to Cremophor vehicle); neuropathy, mucositis, myalgias, heaptototxicity, alopecia.
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What are the premedication regimen for Paclitaxel (Taxol)?
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dexamethasone, H2-antagonist, and diphenhydramine.
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What is the clinical use for Docetaxel?
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Breast cancer, ovarian cancer, non-small cell lung cancer, prostate cancer.
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What are the toxicities for Docetaxel (Taxotere)?
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Myelosuppression, neuropathy, peripheral edema, myalgias, fatigure, haptotoxicity, alopecia, infusion related reactions.
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What is administered with 3days of dexamethasone to prophylaxis against edema starting the day before, the day of and the day after chemotherapy?
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Docetaxel
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What is the dose related edema problem with Docetaxel (Taxotere)?
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Edema problem with cumulative doses of > 400 mg.
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What is the clinical use for Albumin bound paclitaxel (Abraxane)?
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Breast cancer.
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What are the toxicities for Albumin Bound Paclitaxel (Abraxane)?
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Myelosuppression, alopecia, neuropathy, myalgias, haptoxicity.
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What drug has no cremaphor, so risk of hypersensitivity reactions is very low?
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Albumin Bound Paclitaxel (Abraxane).
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Does Albumin Bound Paclitaxel (Abraxane) need traditional premedications?
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No because of no cremaphor, so risk of of hypersensitivity.
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What is the pharmacology fo Epothilones?
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Binds to the Beta tubulin subunit of the microtubule, stabilizing microtubular function, thus arresting the cell cycle and inducing apoptosis. Used in patients with taxane resistant disease.
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What is the clinical use for Ixabepilone (Ixempra)?
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Breast cancer.
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What are the toxicities for Ixabepilone?
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Nausea/vomiting, alopecia, myelosuppression, peripheral neuropathy, mucositis.
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What does Ixabepilone (Ixempra) requires prior to receiving?
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Not formulated in cremaphor. Only requires H1 and H2 antagonists prior to receiving.
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What is the pharmacology for Estramustine (Emcyt)?
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Estradiol molecule linked to anor-nitrogen mustard through a carbamate ester group. Inhibition of microtubule assemby and disassembly.
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What is the pharmacology of Estramustine (Emcyt)?
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Originally developed as an Alkylating agent, it is an estradiol molecule linked to a nor-nitrogen mustard through a carbamate ester group. It is the main mechanism of actions seems to be through the inhibition of microtubule assemby and disassembly.
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What is the clinical use of Estramustine (Emcyt)?
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prostate cancer.
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What is the toxicities of Estramustine (Emcyt)?
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GI disturbances, edema, cardiovascular toxicity, thromboembolic events, gynecomastia.
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What is the pharmacology of Gemtuzumab oxogamicin (Mylotarg)?
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Monoclonal antibody directed agaisnt CD33. The binding of hte antibody portion of Gemtuzumab ozogamicin with CD33 antigen results in the formation of a complex tha tis internalized by the cell. Upon internalization, the calicheamicin derivative is released inside the lysosomes of the cell. Calicheamicin binds to DNA in the minor groove resulting in DNA double stradn breaks and cell death.
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What is the pharmacology of Rituximab (Rituxan)?
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1st monoclonal antibody approved by thte FDA. It is a chimeric humanized murine monoclonal antibody to B-cell surface marker CD20. CD20 regulates cell cycle initiation. Rituximab binds to the antigen on the cell surface, activation complement-dependent B-cell sytotoxicity and believed to mediate cell killing through an antibody-dependent cellular toxicity.
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What is the pharmacology of Ibritumomab tiuxetan (Zevalin)?
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Recombinanat humanized murine monoclonal antibody to B-cell surface marker CD20. Antibody is comprised of Ibritumomab and tiuxetan, a linker chelator that allows the attachment of indium-111 and yttrium-90. The beta emission from Y-90 induces cellular damage by the formation of free radicals in the target and neighboring cells.
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What is the pharmacology of Tositumomab (Bexxar)?
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Tositumomab is a murine monoclonal antibody which binds to the CD20 antigen, similar to ibritumomab. Iodine I-131 tositumomab is a radio-iodinated derivative of tositumomab covalently linked to iodine 121. The possilbe actions fo regimen include apoptosis, complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and cell death. Administration resluts in depletion of CD20 posibive cells.
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What is the pharmacology of Alemtuzumab (Campath)?
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Recombinanat DNA-derived humanized monoclonal antibody to CD52, an antigen expressed on B- and T-cells. The antibody depletes B- and T- cell counts rapidly and is highly immunosuppressive.
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What is the pharmacology of Cetuximab (Erbitux)?
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Recombinanat humanized monoclonal antibody to Her-2-neu, a protein that is overexpressed ont he surface fo breast carcinomas in about 25% of cases. The antibody results in antibody dependent cellular cytotoxicity (ADCC) and complement dependent cytotoxicity.
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What is the pharmacology of Trastuzumab (Herceptin)?
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Recombinant humanized monoclonal antibody to Her-2-neu, a proetin that is overexpressed on the surface of breast carcinomas in about 25% of cases. The antibody results in antibody dependent cellular cytotoxicity (ADCC) and complement dependent cyctotoxicity.
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What is the pharmacology of Bevacizumab (Avastin)?
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Bevacizumab is a recombinant, humanized monoclonal antibody which binds to, and neutralizes, vascular endothelial growth factor (VEGF). VEGF binding initiates angiogenesis (endothelial proliferation and the formation of new blood vessels). The inhibition of microvascular growth is believed to retard the growth of all tissues (including metastatic tissue).
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What is the clinical use for Gemtuzumab ozogamicin (Mylotarg)?
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Acute myeloid leukemia.
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What is the toxicities for Gemtuzumab ozogamicin (Mylotarg)?
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infusion reactions, mucositis, profound myelosuppression, hepatic toxicity including venoocculsive disease.
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For what population is Gemtuzumab ozogamicin (Mylotarg) typically reserved for?
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Typically reserved fro elderly patients or refractory AML.
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What is the clinical use for Rituximab (Rituxan)?
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Non-hodgkin's lymphoma, CLL, several immunologically mediated diseases (ITP).
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What are the toxicities for Rituximab (Rituxan)?
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infusion reactions, mild myelosuppression (most reactsion happen with 1st dose).
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For what forms of Non-Hodgkin's lymphoma is Rituximab (Rituxan)?
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Active in both indolent and aggressive NHL.
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How to infuse Rituximab (Rituxan)?
|
Start infusion slow and increase over time.
|
|
|
What is ibritumomab tiuxetan (Zevalin) used for?
|
Non-Hodgkin's lymphoma.
|
|
|
What is the toxicity for Ibritumomab tiuxetan (Zevalin)?
|
Infusion reactions, myelosuppression.
|
|
|
What is the clinical use for Tositumomab (Bexxar)?
|
Non-Hodgkin's lymphoma.
|
|
|
What is the toxicity for Tositumomab (Bexxar)?
|
Infusion reactions, myelosuppression, secondar malignanancies.
|
|
|
What is the clinical use for cetuximab (Erbitux)?
|
Colorectal cancer.
|
|
|
What is the clinical use for Alemtuzumab (Campath)?
|
Chronic lymphocytic leukemia.
|
|
|
What is the toxicities for Alemtuzumab (Campath)?
|
Infusion reactions, opportunistic infectsion, prolonged myelosuppression.
|
|
|
What is Alemtuzumab (Campath) typically reserved for?
|
refractory cases due to infectious morbidity.
|
|
|
What is Cetuximab (Erbitux) clinically used for?
|
Colorectal cancer.
|
|
|
What are the toxicities of Cetuximab (Erbitux)?
|
Infusion reactions, acneform rash, diarrhea, asthenia, malaise, interstitial lung disease.
|
|
|
what is Trastuzumab (Herceptin) used clinically for?
|
her-2-neu overexpressing breast cancer.
|
|
|
What are the side effects for Trastuzumab (herceptin)?
|
Infusion reations, cardiomyopathy (with anthracyclines), diarrhea.
|
|
|
What is the clinical use with Bevacizumab (Avastin)?
|
Colon cancer; non-small cell lung cancer, non-Hodgkin's lymphoma, breast cancer, ovarian cancer.
|
|
|
What is the toxicities for Bevacizumab (Avastin)?
|
Bleeding, thrombosis, hypertension, infusion reactions, nephrotic syndrome, impaired wound healing, gastrointestinal perforations.
|
|
|
What is the pharmacology of Imatinib (Gleevec)?
|
Inhibits Bcr-Abl tyrosine kinase, the constitutive abnormal gene product of the Philadelphia chromosome in chronic myeloid leukemia (CML). Binds to the kinase binding site of the BCR-ABL gene competitively blocking access to adenosine triphosphate which ultimately leads to apoptosis.
|
|
|
What is the pharmacology of Dasatinib (Sprycel)?
|
Newer generation tyrosine kinase inhibitor which shares the same biding site on the BCR-ABL tyrosine kinase. This agent has been found to be effective in patients resistant to imatinib.
|
|
|
What is the pharmacology of Gefitinib (Iressa) and erlotinib (Tarceva)?
|
They act as inhibitors of the tyrosine kinase associated with the EGFR receptor that is overexpressed in certain epithelial cancers such as lung cancer. This ultimately leads to inhibition of cell proliferation and survival.
|
|
|
What is the pharmacology of the Sorafenib (Nexavar) and Sunitinib (Sutent)?
|
Tyrosine kinase inhibitors of multiple receptors including: platelet derived growth factor, vascular endothelial growth factors, and stem cell factor receptors.
|
|
|
What is the pharmacology of Lapatinib (Tykerb)?
|
Small molecule kinase inhibitor that inhibits both EGFR and HER-2. (Dual inhibitor).
|
|
|
What is the clinical use for Imatinib (Gleevec)?
|
CML, ALL (Philadelphia chromosome positive). GIST (Gastrointestinal stromal tumors).
|
|
|
What is the toxicities of Dasatinib (Sprycel)?
|
Myelosuppression, nausea, edema, hepatic toxicity.
|
|
|
What is the drug interactions of Imatinib (Gleevec)?
|
CYP3A4
|
|
|
What is done to minimize nausea with Imatinib (Gleevec)?
|
take with food to minimize nausea.
|
|
|
What is the clinical use of Dasatinib (Sprycel)?
|
CML resistant to imatinib or other therapies.
|
|
|
What is the toxicities of Dasatinib (Sprycel)?
|
Myelosuppression, nausea/vomiting, headache, fluid retention.
|
|
|
What are the drug interactions of Dasatinib (Sprycel)?
|
CYP3A4
|
|
|
What is the clinical use of Gefitinib (Iressa)?
|
Non-small cell lung cancer.
|
|
|
What is the toxicities for Gefitinib (Iressa)?
|
Diarrhea, rash, nausea, pneumonitis.
|
|
|
What drug has mild benefit in patinets that have failed standard chemotherapy?
|
Gefitinib (Iressa).
|
|
|
What is the clinical use of Erlotinib (Tarceva)?
|
Non small cell lung cancer (2nd line agent), pancreatic cancer.
|
|
|
What are the toxicities for Erlotinib (Tarceva)?
|
Diarrhea, rash, nausea, pneumonitis.
|
|
|
What is the drug interactions of Erlotinib (Tarceva)?
|
CYP3A4
|
|
|
What is the clinical use for Sorafenib (Nexavar)?
|
Renal cell carcinoma.
|
|
|
What is the clinical use for Sunitinib (Sutent)?
|
Renal cell carcinoma, GIST tumors
|
|
|
What is the toxicities for Soprafenib (Nexavar)?
|
Nausea, vomiting, diarrhea, hand foot syndrome, anorexia, fatigue, rash, hypertension
|
|
|
What is the toxicities for Sunitinib (Sutent)?
|
Nauea, vomiting, diarrhea, hand foot syndrome, anorexia, fatigue, rash, hyerptension, skin discoloration.
|
|
|
What is the drug interactions for Sorafenib (Nexavar)?
|
CYP3A4
|
|
|
What is the drug interactions for sunitinib (Sutent)?
|
CYP3A4
|
|
|
What is Lapatinib (Tykerb) clinically used for?
|
Breast cancer.
|
|
|
What is the pharmacology for Tamoxifen (Nolvadex), Raloxifene (Evista), Toremifene (Fareston) - SERMs (Selective estrogen receptor modulators?
|
Acts as an estrogenic antagonist as certain tissues (breast, uterus) and estrogenic agonist at other tissues (bone). Use in patients with estrogen receptor (ER) and/or progesterone receptor (PR) positive disease.
|
|
|
What is the Toxicity for Tamoxifen (Nolvadex), Raloxifene (Evista), Toremifene (Fareston) -SERMs (Selective estrogen receptor modulators)?
|
DVT, increease risk of endometrial cancer, hot flashes.
|
|
|
What is the pharmacology for Pure Antiestrogen - Fulvestrant (Faslodex)?
|
Steroidal compound which competitively binds to estrogen receptors ontumors and other tissue targets. Causes dwon-reulation of estrogen receptors and inhibits tumor growth.
|
|
|
What is the toxicity for the Pure Antiestrogen - Fulvestrant (Faslodex)?
|
Pain at the injection site,hot flashes, nausea.
|
|
|
What is thepharmacology for Aromatase inhibitors: Anastrozole (Arimidex), Letroxzole (Femara), and Exemestane (Aromasin)?
|
Inhibits thearomataseenzymeresponsible fo rhte conversion of androgens to estrogens.
|
|
|
What are the Aromatase inhibitors clinically used for?
|
Breast cancer.
|
|
|
What is the toxicitis for the Aromatase inhibitors - Anastrozole (Arimidex), Letrozole (Femara),and Exemestane (Aromasin)?
|
Lack the estrogenic toxicities (endometrial cancer), hot flashes, joint pains. Prolonged use can cause osteoporosis and arthralgias.
|
|
|
What are the antiandrogens used for?
|
Prostate cancer.
|
|
|
what isthe pharmacology for the Antiandrogens: Flutamide (Eulexin), Bicalutamide (Casodex), Nilutamide (nilandron)?
|
Non-steroidal antiandrogens which competitively inhibit the binding of androgens (testosterone) to the peripheral receptors.
|
|
|
What is the toxicity for Antiandrogens: Flutamide (Eulexin), Bicalutamide (Casodex), Nilutamide (Nilandron)?
|
gynecomastia, hot flshes, increased liver function tests, nausea, vomiting, diarrhea, and visual distrubances, tumor flare (pain): Can be used in combination with an LHRH antagonist.
|
|
|
What is the clinical use for leuteinizing Hormone Releasing Hormone Analogs (LHRH)?
|
Breast and Prostate cancer.
|
|
|
What is the phamracology for Leuteinizing hormone Releasing Hormone Analogs (LHRH)?
|
FSH-LH-RH binds to receptors int he hypothalamus causing the release of FSH and LH, which in turn increases the production of androgens and estrogens capable of stimulating the adrenal glands, testes, and ovaries. LHRH competes for binding to the hypothalamus causing an initial surge in release of LH and FSH followed by dwon reulation of the receptor through a negative feedback loop.
|
|
|
What is the toxicity for LHRH: Goserelin (Zoladex), Leuprolide (Lupron), Triptorelin (Trelstar)?
|
hot flashes, diarrhea, decreased libido, impotence, gynecomastia, GI disturbance, peripheral edema.
|
|
|
What may be seen in LHRH: Goserelin (Zoladex), Leuprolide (Lupron), Triptorelin (Trelstar) if patients are not treated with antiandrogens prior to treatment?
|
Because of the initial surge in LH, FSH and ultimately testosterone an initial disease flare (manifested as bone pain) may be seen if patients who are not treated with antiandrogens prior to treatment.
|
|
|
What is the pharmacology for the All-trans-retinoic acid (Tretinoin)?
|
binds with the retinoic acid-1 alpha recepotr in promyelocytes in acutre promyelocytic leukemia, resulting in differentiation of the leukemic blast into a more mature form which undergoes normal cell death.
|
|
|
What is the toxicity for the all-trans-retinoic acid (Tretinoin)?
|
Retinoic acid syndrome (respiratory failure, fever, weight gain, peripheral edema), hyperleucocytosis, headache, CNS toxicity, multiple drug interactions with cytochrome P-450 system.
|
|
|
What is the clinical use for All-tran-retinoic acid (Tretinoin)?
|
Acute promyelocytic leukemia.
|
|
|
What is the pharmacology for Bexarotene (Targretin)?
|
Binds with the retinoic acid-1 X receptor in lymphocytes.
|
|
|
What is the toxicity for Bexartene (Targretin)?
|
hyperlipidemia, myelosuppression, headache.
|
|
|
What is the clinical use for Bexarotene (Targretin)?
|
Used in cutaneous T-cell lymphoma.
|
|
|
What is the Pharmacology for Arsenic trioxide (Trisenox)?
|
Induces apoptosis in malignant promyelocytes in acute promyelocytic leukemia.
|
|
|
What is the toxicity for Arsenic trioxide (Trisenox)?
|
APL syndrome, myelosuppression, neuropathy, QT interval prolongation, tachycardia, fatigue, nausea.
|
|
|
What is the pharmacology for the G1 phase specific: L-asparaginase?
|
enzyme which lyses asparagine into aspartic acid and ammonia. leukemia cells require asparagine for normal cell processes and L-asparaginase depletes the exogenous pool of asparagine thereby depriving the leukemia cellsand causing cell death. Normal cells can synthesize their own asparagine, and are thus unaffected.
|
|
|
What is the Clinical Use for L-asparaginase (Elsapr)?
|
Acute lymphocytic leukemai.
|
|
|
What are the toxicities for L-asparaginase (Elspar)?
|
Anaphylaxis, pancreatitits, DIC.
|
|
|
What dosage form of L-asparaginase (Elspar) is available for patinets intolerant to conventional dosage form?
|
Available in a pegylated dosage form (pegasparaginase) for patients that are intolerant to the conventional dosage form.
|
|
|
What is the pharmacology for G2 phase specific Bleomycin?
|
Causes fragmentation of DNA via interactions with oxygen and iron which generates free radicals leading to single and double strand DNA breaks.
|
|
|
What is the clinical use for Bleomycin (Blenoxane)?
|
Testis cancer, head and neck cancer, lymphoma, germ cell tumors of the ovary.
|
|
|
What is the toxicity for Bleomycin (Blenoxane)?
|
Pulmonary fibrosis, cutaneous toxicity, hypersensitivity rreactions, Raynoud's syndrome.
|
|
|
What is the exposure to Bleomycin (Blenoxane) that may lead to Pulmonary toxicity?
|
Pulmonary toxicity is dose related and appears to increase with a total lifetime exposure of 400units or 400 mg.
|
|
|
What is Pharmacology for Hydroxyurea?
|
Inhibits ribonucleotide reductase. Cells accumulate in the S phase because DNA synthesis is inhibited and only abnormally short DNA strands are produced.
|
|
|
What is Pharmacology for Arsenic trioxide?
|
Acts as a differentiating agent inducing the growth progression of cancerous cells into mature more normalcells. used in thetreatment of acute promyelocytic leukemia.
|
|
|
What is Pharmacology for Mitomycin C?
|
Sometimes classified as an antitumor antibiotic. It has similarities to nitrogen mustard and may function as an alkylating agent. Known to cause prolonged myelosupppresssion which limits theamount of doses that can be given.
|
|
|
What is Pharmacology for Bortezomib (Velcade)?
|
Specific inhibitor of the 26S proteasome, a large intracellular adenosine triphosphate-dependent protease responsible for protein catabolism in all eurkaryotic cells. Ultimately leads to the inhibition of NF-kB leading to decrease in various growth, survival, and angiogenic factors. it also promotes apoptosis.
|
|
|
What are the toxicities of Bortezomib (Velcade)?
|
Thrombocytopenia, fatigue, peripheral neuropathy, and neutropenia, nausea/vomiting.
|
|
|
What si the Use of Bortezomib (Velcade)?
|
relapsed multiplemyeloma and relapsed or refractory mantle cell lymphoma.
|
|
|
What is the pharmacology for Thalidomide/lenalidomide?
|
May be related to immune modulation (Increase
T-helper cells), cytokine inhbition (TNF-a), anti-antiogensesis (basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF)). |
|
|
What is the toxicities for Thalidomide?
|
somnolence/drowsiness, constipation, dizziness/orthostatic, hypotension,rash, and peripheral neuropathy. Most serious toxicity is teratogenicity.
|
|
|
What is the toxicities for Lenalidomide?
|
neutropenia, thrombocytopenia and thrombotic issues are most prevalent with lenalidomide (much less somnolence, neuropatheis compared to thalidomide.
|
|
|
What are the clinical uses of Thalidomide?
|
mulitple myeloma.
|
|
|
What is required to use Thalidomide?
|
Must be enrolled int he S.T.E.P.S program to use thalidomide.
|
|
|
What is the clinical use for Lenalidomide?
|
myelodysplastic syndrome and multiplemyeloma.
|
|
|
What is required to use lenalidomide?
|
Must be enrolled in the Revassist program to use Lenalidomide.
|
|
|
What is the pharmacology of Temsirolimus?
|
Mammalian target of Rapamycin (mTOR) inhibitor. This inhibits protein synthesis and protein degradationand angiogenesis.
|
|
|
What is the toxicities of Temsirolimus?
|
rash, fatigue, mucositis, nausea, edema, loss of appetite. Rare problems with interstitial lung disease, immunosuppression, and renal failure.
|
|
|
What is the uses for Temsirolimus?
|
metatatic renal cell carcinoma.
|
|
|
What is the pharmacology for IL-2 (aldesleukin, Proleukin)?
|
Lymphokine produced by recombinant technology which promotes an immunologic response to cancer; unfortunately the immune respoonse is non-specific and significant toxicity from capillary leak syndrome can result.
|
|
|
What is the clinical use for IL-2 (aldesleukin, Proleukin)?
|
Renal cell carcinoma, melanoma.
|
|
|
What are the toxicities for IL-2 (aldesleukin, Proleukin)?
|
Vascular leak syndrome, hypotension, cardiac toxicity, prerenal azotemia, hepatotoxicity, myelosuppression, CNS toxicity.
|
|
|
What drug must be administered in controlled settings?
|
IL-2 (aldesleukin, Proleukin).
|
|
|
What drugs are required with IL-2 (aldesleukin, Proleukin)?
|
most patients will require IV pressor support with dopamine and/or norepinephrine.
|
|
|
What is the clinical use for Interferon alfa (2a-Roferon A; 2b - Intron A)?
|
Renal cell carcinoma, chronic myeloid leukemia, multiple myeloma, melanoma.
|
|
|
What are the toxicities for Interferon alfa (2a-Roferon A; 2b-Intron A)?
|
Fatigue, flu-like symptoms, depression.
|
|
|
What is the administration frequency for Interferon alfa (2a - Roferon A; 2b - Intron A)?
|
Usually given several times per week sub-Q.
|
|
|
What is the clinical use for Denileukin diftitox (Ontak)?
|
Cutaneosu T cell lymphoma which expresses CD25.
|
|
|
What are the toxicities of Denileukin diftitox (Ontak)?
|
Capillary leak syndrome, hypersensitivity reactions,flu like symptoms.
|
|
|
What is Deniluekin diftitox (Ontak) fusion of?
|
Recombinant fusion protein that combines both IL-2 and diphtheria toxin.
|
|
|
What factors affect response to chemotherapy?
|
Tumor burden + drug resistance.
|
|
|
What are the mechanisms of resitance?
|
1. decreased drug accumulation.2.alteration in levels of "target" enzyme. 3. Altered drug catabolism/metabolism. 4. Increase glutathione/glutathione S- transferase. 5. Increased drug efflux (multidrug resistance).
|
|
|
What is Glutathione (GSH)?
|
ubiquitous thiol that plays a central role in a wide range of cellular functions. In cancer,it protects by free radical scavengin of radiation induced lesions and detoxicfication of alkylating agents via glutathione S transferase.
|
|
|
What is Glutathione S transferase (GST)?
|
enzyme involved in detoxification,distributed in all organs but primarily in the liver and kidney. GST mediates the activity between GSH and anticancer agents.
|
|
|
What cancers has an excess of GST and GSH?
|
lung, head and neck, esophageal, adenocarcinomas, colon, bladder, ovarian, and stomach.
|
|
|
What is the P-glycoprotein (PGP)?
|
P-glycoprotein (PGP) the hallmark of MDR, a 170 kD proetin that acts as a transmembrane efflux pump.
|
|
|
What chemotherapy agents are affected by MDR?
|
vinca alkaloids - Vincristine, vinblastine, vinorelbine. Epipodophyllotoxins - etoposide, teniposide. Anthracyclines - Doxorubicin, daunorubicin, mitoxantrone. Taxanes - Paclitaxel, docetaxel.
|
|
|
What is UDP-glucuronosyltransferase (UGT1A1)?
|
enzyme responsible for the glucuronidation of SN-38 to inactive metabolites. The UGT1A1 enzyme exists in polymorphic states and reduced or deficient levels fo this enzyme are observed in Gilbert's syndrome, a familial hyperbilirubinemia disorder, and correlateswith irinotecan-induced diarrhea and neutropenia.
|
|
|
What is Dihydropyrimidine dehydrogenase (DPD) defiiciency?
|
DPD is responsible for the breakdwon of 5-FU; deficiency leads to severe neuroteoxicty with 5- FU.
|
|
|
What is Thiopurine methyltransferase (TPMT)?
|
TPMT is a cytosolic enzyme that catalyzes the S-methylation of aromatic and heterocyclic culfhydryl agents, including mercaptopurine and thioguanine. The gene responsible for TPMT exhibits polymorphoism wiht TPMT activity inheritedas an autosomal codominant trait. Most patinets (90%) inherit hight TPMT activity, but 10% inherit intermediate acitivity and 1/300 inherits low acitvity.
|
|
|
What does TPMT activity determines?
|
TPMT activity determines how much mercaptopurine or thioguanine is inactived to methylated metabolites, or remains available for activation. Severe hematopoietic toxicity will result if conventional doses of thiopurines are given to TPMT-deficient patients, and these patients require significant dosage reductions (patients with low TPMT activity can tolerate only approximately 10% of the normal dose of mercaptopurine).
|
|
|
What agents are dose modified in renal dysfunction?
|
Bleomycin, Capecitabine, Carboplatin, Cisplatin,Cyclophosphamide, Etoposide, Fludarabine, Hydroxyurea, Ifosfamide, Methotrexate, Pnetostatin, Streptozocin, Topotecan.
|
|
|
What agents are dose adjusted in hepatic dysfunction?
|
Anthracyclines,Docetaxel, Etoposide, Imatinib, Paclitaxel, Thiotepa, Vinblastine,Vincreistine, Vinorelbine.
|
|
|
What is a general requirement to administer chemotherapy safely?
|
WBC of>3000/mm3 or an ANC of > 1500/mm3 and a platelet count of >100,000/mm3.
|
|
|
How to calculate patient's body surface area (BSA)?
|
BSA (m2) =(Ht (cm) * Wt (kg))^1/2/3600
|
|
|
How to cure Anemmia?
|
use of blood transfusions. Use of erythropoietic stimulating agents.
|
|
|
How to treat neutropenia?
|
patient is considered neutropenic when aboslute neutrophil drops < 500/mm3. use of colony stimulating factors.
|
|
|
How to treat for Thrombocytopnia?
|
Use of platelet transfusions. Use of oprelvekin (IL-11). Not recommended due to side effects.
|
|
|
What are the principles of combination chemotherapy?
|
1. provides maximum cell kill within the range of toxicity that a patinet can tolerate. 2. The thought behind combination therapy should be that the drug have activity as single agents. 3 Use combination therapy that has different mechanisms of action fro potential additive or synergisticeffects. 4. use combination therapy with non-overlapping dose limiting toxicities. 5. use of combination therapy can broaden coverage to have additive activity against resistant cell lines. 6. combination therapy helps prevent hte development of reistance.
|
|
|
What is Complete respnose (CR)?
|
percentage of patients who demonstrate a complete disappearance of tumor mass or disease and no nw appearance of the disease for a least one month after treatment. Not necessarily that patient is cured.
|
|
|
What is Partial response (PR)?
|
percentage of patients who dmeostrated at least a 50% rduction in measurable tumor mass with no new areas of disease and no shows progression of disease for at least 1 month after treatment.
|
|
|
Wha tis the Overall response rate (ORR)?
|
summation of PR + CR.
|
|
|
What agents are dose adjusted in hepatic dysfunction?
|
Anthracyclines,Docetaxel, Etoposide, Imatinib, Paclitaxel, Thiotepa, Vinblastine,Vincreistine, Vinorelbine.
|
|
|
What is a general requirement to administer chemotherapy safely?
|
WBC of>3000/mm3 or an ANC of > 1500/mm3 and a platelet count of >100,000/mm3.
|
|
|
How to calculate patient's body surface area (BSA)?
|
BSA (m2) =(Ht (cm) * Wt (kg))^1/2/3600
|
|
|
How to cure Anemmia?
|
use of blood transfusions. Use of erythropoietic stimulating agents.
|
|
|
How to treat neutropenia?
|
patient is considered neutropenic when aboslute neutrophil drops < 500/mm3. use of colony stimulating factors.
|
|
|
How to treat for Thrombocytopnia?
|
Use of platelet transfusions. Use of oprelvekin (IL-11). Not recommended due to side effects.
|
|
|
What are the principles of combination chemotherapy?
|
1. provides maximum cell kill within the range of toxicity that a patinet can tolerate. 2. The thought behind combination therapy should be that the drug have activity as single agents. 3 Use combination therapy that has different mechanisms of action fro potential additive or synergisticeffects. 4. use combination therapy with non-overlapping dose limiting toxicities. 5. use of combination therapy can broaden coverage to have additive activity against resistant cell lines. 6. combination therapy helps prevent hte development of reistance.
|
|
|
What is Complete respnose (CR)?
|
percentage of patients who demonstrate a complete disappearance of tumor mass or disease and no nw appearance of the disease for a least one month after treatment. Not necessarily that patient is cured.
|
|
|
What is Partial response (PR)?
|
percentage of patients who dmeostrated at least a 50% rduction in measurable tumor mass with no new areas of disease and no shows progression of disease for at least 1 month after treatment.
|
|
|
Wha tis the Overall response rate (ORR)?
|
summation of PR + CR.
|
|
|
What agents are dose adjusted in hepatic dysfunction?
|
Anthracyclines,Docetaxel, Etoposide, Imatinib, Paclitaxel, Thiotepa, Vinblastine,Vincreistine, Vinorelbine.
|
|
|
What is a general requirement to administer chemotherapy safely?
|
WBC of>3000/mm3 or an ANC of > 1500/mm3 and a platelet count of >100,000/mm3.
|
|
|
How to calculate patient's body surface area (BSA)?
|
BSA (m2) =(Ht (cm) * Wt (kg))^1/2/3600
|
|
|
How to cure Anemmia?
|
use of blood transfusions. Use of erythropoietic stimulating agents.
|
|
|
How to treat neutropenia?
|
patient is considered neutropenic when aboslute neutrophil drops < 500/mm3. use of colony stimulating factors.
|
|
|
How to treat for Thrombocytopnia?
|
Use of platelet transfusions. Use of oprelvekin (IL-11). Not recommended due to side effects.
|
|
|
What are the principles of combination chemotherapy?
|
1. provides maximum cell kill within the range of toxicity that a patinet can tolerate. 2. The thought behind combination therapy should be that the drug have activity as single agents. 3 Use combination therapy that has different mechanisms of action fro potential additive or synergisticeffects. 4. use combination therapy with non-overlapping dose limiting toxicities. 5. use of combination therapy can broaden coverage to have additive activity against resistant cell lines. 6. combination therapy helps prevent hte development of reistance.
|
|
|
What is Complete respnose (CR)?
|
percentage of patients who demonstrate a complete disappearance of tumor mass or disease and no nw appearance of the disease for a least one month after treatment. Not necessarily that patient is cured.
|
|
|
What is Partial response (PR)?
|
percentage of patients who dmeostrated at least a 50% rduction in measurable tumor mass with no new areas of disease and no shows progression of disease for at least 1 month after treatment.
|
|
|
Wha tis the Overall response rate (ORR)?
|
summation of PR + CR.
|
|
|
What is the stable disease (SD)?
|
measurable tumor that does not meet the criteria for a response, but has not progressed. Mass neither grows nor shrinks by more than 35%.
|
|
|
What is the Progressive Disease (PD)?
|
increase intumor size by ate least 20 - 25% or the appearance of new disease.
|
|
|
What is the Time to treatment progression (TTP)?
|
period of time that the disease remains stable, without advancing in stage or size.
|
|
|
Wha is Disease Free Survival (DFS)?
|
time the patients who achieved a complete response are alive without the disease recurring.
|
|
|
What is the overall suvival (OS)?
|
usually reported as a median.
|
