Ch 45 Flashcards
cytotoxic agents
nonspecifically inhibit DNA replication or mitosis
targeted anticancer drugs
inhibit specific proteins involved in tumor cell growth
induction therapy
rapidly decrease tumor burden and symptoms
consolidation therapy
complete or extend initial remission
maintenance therapy
sustain remission as long as possible
cancer Tx dosing schedule driven by
- drug/host kinetics
- tumor cell kinetics
- drug toxicity
cell cycle specific
act during a specific phase of the cell cycle
cell cycle nonspecific
act throughout the whole cell cycle
drug resistance
- major cause of cancer treatment failure
- innate resistance or acquired resistance
host toxicity
- nausea and vomiting
- alopecia
- target organ toxicities
- myelosuppression
methotrexate
- ADE mitigated by leucovorin
- hepatotoxicity and renal injury
pemetrexed
- myelosuppression is major toxicity
- folic acid and B12 minimize ADE
purine analogues
- impair DNA synthesis
- used in leukemias
- myelosuppression is dose limiting
- allopurinol prescribed in conjunction
pyrimidine analogues
- inhibit DNA synthesis
- fluorouracil used for solid tumors
- ADE: myelosuppression, N/V, oral/GI ulceration, alopecia
ribonucleotide reductase inhibitor (hydroxyurea)
-also used to increase fetal hemoglobin levels in sickle cell anemia
nitrogen mustards
- cyclophosphamide is most widely used
- DNA alkylating: cross link DNA strands
- ADE: hemorrhagic cystitis
nitrosurea drugs
- DNA alkylating
- highly lipophilic with good CNS penetration
- used for brain tumors
- delayed, prolonged myelosuppression
- pulmonary damage with high doses
platinum compounds
- DNA alkylating
- cisplatin first line for testicular, ovarian, cervical, and bladder cancer
- severe N/V and renal toxicity
- N/V severe enough to need pretreatment
busulfan
- similar to nitrogen mustard
- used for chronic myeloid leukemia
- pulmonary fibrosis in small subset of long term use patients
dacarbazine
used in hodgkin disease
mitomycin
- used for stomach and pancreatic cancer
- can cause severe extravasation necrosis
anthracycline MOA
intercalation of DNA to cause inhibition of topoisomerase which results in deformation and uncoiling of DNA
anthracycline ADE
- extravasation
- cardiac toxicity
- dexrazoxane is cardioprotective
DNA topoisomerase inhibitor MOA
cause permanent DNA strand breaks by preventing resealing after uncoiling for replication
ironotectan
DNA topoisomerase inhibitor that causes diarrhea in significant number of cases
mitotic inhibitor MOA
-interfere with microtubule function and block cell division
vincristine
- vinca alkaloid mitotic inhibitor
- dose limiting neurotoxicity and cranial nerve damage
protein kinase inhibitor MOA
inhibits enzymatic activation of growth factor receptors and other regulatory proteins thus impeding malignant cell transformation and proliferation
antineoplastic monoclonal antibody MOA
bind to specific cancer cell antigen