Anti-CA Pharm Flashcards
(24 cards)
antimetabolites
- bone marrow cell replication PROFOUNDLY inhibited
- highly cell cycle specific
MTX (methotrexate)
- folic acid analog
- binds DHFR = inhibits formation of MTHF which is needed for dTMP synthesis
- works on cells in S phase mostly
- result = decrease in nucleic acid synthesis
what step of DNA synthesis is inhibited by 5-FU? hydroxyurea?
- 5-FU = step taking dUMP –> dTMP
- hydroxyurea = UMD –> dUMP & CTP –> dCTP
taxanes carry the risk of what s/e? why?
risk of hypersensitivity rxn b/c they are natural agents
what are paclitaxel and docetaxel made from?
- paclitaxel = PACIFIC yew tree bark
- docetaxel = ENGLISH yew tree bark
taxane MOA
- interfere w/ mitosis
- bind to microtubules = inhibits microtubule disassembly to tubulin = cell prevented from finishing mitosis
how is the MOA of taxanes different from colchicine?
- colchicine blocks mitosis by preventing the formation of the spindles in the first place
- taxanes prevent the spindles from being broken down
paclitaxel
- used for solid tumors
- given IV
- irritates skin and mucous membranes on contact
docetaxel
- first line tx for breast CA
- 2nd line for non-small cell lung CA
- 1st line for prostate CA when combined w/ prednisone
- skin and mucous memb irritant; given IV
s/e of taxanes
- myelosupression & hypersensitivity rxns
- paclitaxel = neurotoxicity; can reduce dose but that also lowers chance of curing the CA; usually reversible so can consider switching meds
- docetaxel = fluid retention –> usually can be minimized by taking steroids night before and morning of tx
vinca alkaloid MOA/effect on mitosis
- binds tubulin = prevents spindles from forming
vinca alkaloid - route of administration; why is it so important?
- only given IV
- FATAL if given intrathecally
- the pt won’t die immediately; they will have progressive neurotoxicity and die in a few weeks/months
vinca alkaloid s/e
- vincristine = neurotoxicity
- vinblastine & vinorelbine = myelosuppression
podophyllotoxin MOA & effect on mitosis
- blocks cell cycle in 2 places = G1 phase & S-phase (DNA replication)
podophyllotoxin s/e & admin routes
- s/e = hypotension, alopecia, n/v, myelosuppression
- admin = IV (more common) or orally as liquid capsule
- have to give IV over 60 minutes b/c any longer than that will cause more hypotension
indications for podophyllotoxin
- genital warts assoc w/ squamous cell carcinomas (when in the cream form)
- testicular CA that didn’t respond to other tx plans (etoposide form)
antitumor antibiotics
- from Streptomyces spp.
- interact w/ DNA and/or RNA usually
- less phase specific
- s/e = tissue necrosis
- all given IV
what is the only antitumor antibiotic that can be given in other forms besides IV?
- bleomycin
- can be given IV, IM, subQ, intrapleural
alkylating agents: take home points
- directly damages DNA
- broad spectrum of antitumor activity & immunosuppression
- active vs. proliferating & nonproliferating cells
- cause dose-limiting myelosuppression
- genotoxic & assoc w/ increased risk of leukomogenesis
MOA of doxorubicin; what is the effect on cell membranes?
- MOA = DNA topoisomerase II inhibitor (blocks DNA replication and transcription)
- leads to generation of free radicals = membrane damage = DNA strand breaks
s/e of antracyclines (including doxorubicin)
- dose cumulative cardiotoxicity
- red discoloration of urine
- myelosuppression
- amenorrhea
- n/v
MOA of cisplatin
- C1-moieties react w/ N7 of guanine causing intrastrand & interstrand crosslinks in DNA
- cell cycle non-specific but may be most active in G phase
s/e of cisplatin
- platinum analogs overall cause myelosuppresion, n/v, neurotoxicity
- cisplatin specifically = NEPHROtoxicity
what platinum analog has less nephrotoxicity than cisplatin? how is it dosed?
- carboplatin
- dosed based on area under curve (AUC)
