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cancer chemotherapy
cancer chemotherapy drugs
| Question | Answer |
|---|---|
| CYCLOPHOSPAMIDE | Nitrogen mustard |
| CYCLOPHOSPAMIDE MECHANISM | Reactive carbon forms covalent bond with DNA Results in: DNA replication arrest DNA damage and chromosome breaks Mutagenic |
| CYCLOPHOSPAMID toxicity | BONE MARROW TOXICITY- Most cause dose-limiting myelosuppression MUCOUSAL TOXICITY- Oral blister, intestinal denudation HAIR FOLLICLES- Hair loss NEUROTOXICITY- N/V, ALTERED MENTAL STATUS CARCINOGENIC MUTAGENIC |
| CARMOSTINE | Nitrosourea |
| CARMOSTINE MECHANISM | Reactive carbon forms covalent bond with DNA Nonenzymatic activation step Can cause G-C cross-links Highly lipid soluble (BCNU and CCNU) |
| CISPLATIN discription | Platinum compounds No activated carbon moieties Spontaneous formation of reactive molecule Intra- and Inter-strand DNA cross-links |
| CISPLATIN Mechanism | All enter cells via a Cu++ transporter CTR1 Are actively exported from the cell via Cu++ transporter ATP7A and ATP7B and by the multi-drug resistance protein 1 (MDR-1) |
| CISPLATIN toxicity | Acute: N/V Delayed: nephrotoxicity, ototoxicity, peripheral neuropathy |
| CYTARABINE | DEOXYCYTIDINE ANALOG |
| CYTARABINE MOA | Mechanism: Biochemical pharmacology mirrors the uptake and metabolism of normal nucleosides Insertion into DNA stops cells cycle INDUCES APOPTOSIS |
| CYTARABINE Toxicity | N/V, myelosuppression |
| 5-FLUOROURACIL | PYRIMIDINE ANALOGUES FLUOROPYRIMIDINES |
| FLUOROURACIL MOA | Mechanism: Inhibits thymidine synthesis Covalently binds to thymidilate synthase Stops DNA synthesis Incorporates into RNA |
| FLUOROURACIL toxicity | SEVERE N/V MYELOSUPPRESSION |
| MERCAPTOPURINE | PURINE ANTAGONISTS 6-THIOPURINES |
| MERCAPTOPURINE Mechanism | 6-MP: INHIBITS ADENOSINE AND GUANOSINE SYNTHESIS 6-TG: INHIBITS GUANOSINE SYNTHESIS |
| MERCAPTOPURINE Toxicity | IMMUNOSUPPRESSION MYELOSUPPRESSION HEPATOTOXICITY |
| METHOTREXATE description and effects | FOLIC ACID ANALOG Essential dietary factor Transformed enzymatically into FH4 Cofactor for methyl group transfer in synthesis of thymidine |
| METHOTREXATE Mechanism | Inhibition of dihydrofolate reductase |
| METHOTREXATE Toxicity | MYELOSUPPRESSION mucositis diarrhea RESCUE THERAPY: TOXICITY CAN BE REVERSED WITH L-LEUCOVORIN (REDUCED FOLATE) |
| VINCRISTINE | VINCA ALKALOIDS ANTIMITOTICS: drugs that inhibit mitosis |
| VINCRISTINE Mechanism | INHIBITION of microtubule POLYMERIZATION INHIBITS MITOSIS |
| VINCRISTINE Toxicity | MYELOSUPPRESSION, HAIR LOSS, NEUROTOXICITY |
| TAXOL | ANTIMITOTICS: drugs that inhibit mitosis TAXANE |
| TAXOL Mechanism | ENHANCES microtubule POLYMERIZATION Metaphase arrest INHIBITS MITOSIS |
| ETOPISIDE | EPIPODOPHYLOTOXINS TOPIOISOMERASE INHIBITORS |
| ETOPISIDE Mechanism | Inhibits DNA TOPIOISOMERASE II Inhibits DNA TOPIOISOMERASE II BLOCK Cells in G2 and S-PHASE |
| ETOPISIDE Toxicity | ACUTE: N/V , hypotension DELAYED: Myelosuppression, Hair Loss |
| TOPTECAN | CAMPTOTHECINS TOPIOISOMERASE INHIBITORS |
| TOPTECAN Mechanism | Inhibits DNA TOPIOISOMERASE I BLOCK Cells in G2 and S-PHASE |
| TOPTECAN Toxicity | ACUTE: N/V DELAYED: Myelosuppression |
| DOXORUBACIN | TOPIOISOMERASE INHIBITORS ANTITUMOR ANTIBIOTICS ANTHRACYCLINES |
| DOXORUBACIN Mechanism | INHIBITION OF TOPIOSOMERASE II BINDING W/ DNA AND RNA RELEASE OF FREE RADICALS BINDING TO CELL MEMBRANES AND ALTERING FLUID/ION TRANSPORT |
| DOXORUBACIN Toxicity | ACUTE: MYELOSUPPRESSION, NAUSEA, RED URINE DELAYED: CARDIOTOXICITY, MOST LIKELY DUE TO THE RELEASE OF FREE RADICALS RESULT IN Heart Failure |
| MITOMYCIN C Mechanism | ANTITUMOR ANTIBIOTICS |
| MITOMYCIN C | DOES NOT INHIBIT TOPIOISOMERASES Cross-links w/ DNA Forms free radicals, results in DNA damage |
| MITOMYCIN C Toxicity | N/V DELAYED: MYELOSURESSION, ANOREXIA, HEMOLYSIS |
| IMATINIB | Tyrosine and other Kinase Inhibitors |
| IMATINIB mechanism | Stops the active kinase from binding to substrate therefore the malignant phenotype is not expressed |
| IMATINIB resistance | 3 different POINT mutation in the kinase domain of ABL-B Prevents drug from binding |
| IMATINIB interactions | Ketoconazole (inhibts Cyp3A4) increases half life Rifampin (induces Cyp3A4) decreases half life |
| ERLOTINIB | EGFR Tyrosine Kinase inhibitors |
| ERLOTINIB Mechanism | Competes with ATP-binding site |
| ERLOTINIB Resistance | Mutation in kinase domain |
| CETUXIMAB | Monoclonal Antibodies |
| CETUXIMAB mechanism | monoclonal Ab to EGFR binding domain |
| CETUXIMAB Main Adverse Effects | Diarrhea, acneiform rash, nail changes, headaches, possible anaphylactic reactions |
| BEVACIZUMAB | Inhibitors of Angiogenesis HUMANIZED monoclonal Ab Vascular Endothelial Growth Factor-a (an isoform of VEGF-a |
| BEVACIZUMAB mechanism | Delays progression of renal cancer, glioblastoma Available via infusions |
| BEVACIZUMAB Main Adverse Effects | Excessive bleeding, dec wound healing, HT, proteinuria, thromboembolic events. |
| SORAFENIB | Inhibitors of Angiogenesis COMPETITIVE inhibitors of ATP-binding site of VEGF-R2 Also effects activation of other RTKs (e.g. PDGF-Rβ) |
| SORAFENIB Main Adverse Effects | Excessive bleeding Dec wound healing Hypertension Proteinuria Thromboembolic events |
Created by:
ksoul6
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