Chemo drugs Flashcards by Michael Steinbacher

cell cycle non specific agents

alkylating agents, anthracyclines, nitrosureas, platinum agents

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cell cycle specific

antimetabolites, vincas, taxanes

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2 main alkylating agents

cyclophosphamide, ifosfamide

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alkylating agents MoA

direct crosslinking of DNA base pairs

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alkylator toxicities

myelosuppression, nausea vomiting, 2 malignancies, infertility, *hemorrhagic cystitis from acrolein metabolite (worse w/ ifosfamide, treated w/ Mesna)

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3 main Pt compounds

cisplatin, carboplatin, oxaliplatin

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Pt compound general toxicities

peripheral neuropathy, nephrotoxicity, nausea/vomiting, thrombocytopenia, ototoxicity

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oxaliplatin toxicity

cold sensitivity

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cisplatin toxicity

extra nephrotoxic, gauranteed nausea vomiting

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carboplatin toxicitiy

thrombocytopenia

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nitrosureas toxicity

CNS, pulmonary, myelosuppression, nausea vomiting, phelbitis

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general MoA antimetabolites

DNA replication/repair analogues, S phase specific

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2 main folate antagonists

methotrexate, pemtrexed

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MTX MoA

inhibits DHFR- tumor cells rely on endogenous folate for growth

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MTX toxicity

mucositis, myelosuppression are characteristic

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“rescue” of normal cells w/ MTX?

normal cells can use exogenous folate for growth unlike tumors

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3 pyrimidine analogues

flurouracil and capecitabine (oral prodrug of flurouracil), cytarabine

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toxicity of fluorouracil

w/ bolus: myelosuppression;
w/ continuous IV:
GI mucositis & diarrhea
Hand foot syndrome (esp w/ capecitabine)

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fn of leucovorin w/ 5FU

potentiation: raises 5FU binding affinity to thymidylate synthase

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fn of leucovorin w/ MTX

inhibits MTX, can be given a couple hours after to rescue

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MoA of cytarabine

pyrimidine analog/antagonist

toxicity of cytarabine

cerebellar toxicity, conjunctivitis w/ continous infusion and high dose

6-mercaptopurine Moa

purine analog/antagonist, lowers de novo purine synthesis

microtubule inhibitors

taxanes (paclitaxel) and vincas (vincristine and vinblastine)

Vincas Moa

microtubule destruction- M phase specific

vinca toxicity

cumulative neurotoxicity (peripheral neuropathy), variable myelosuppression: more in vinblastine

what never to do w/ vincas

adminster intrathecally- fatal!!!!

taxane moa

microtubule stabilization- M phase specific

taxane toxicity

myelosuppression, peripheral neuropathy, hypersensitivty

topo I fn

relaxing supercoil before transcription

topo II fn

recoil DNA after transcription

topo I inhibitors

camptothecins: topotecan and irinotecan

topo I toxicities

myelosuppression, diarrhea (irinotecan)- early tx w/ atropine, late is life threatening and tx w/ loperamide aggressively

topo II inhibitors

etoposide, teniposide

topo II toxicities

myelosuppression, 2 malig, mucositis-dose dependent

etoposide extra toxicity

formulated in agent that causes hypotension

anthracycline examples

doxorubicin, daunorubicin, idarubicin, epriubicin, mitoxantrone

primary and secondary moa of anthracyclines (original purpose?)

originally antibiotics; moa- intercalate DNA and inhibit topo; secondary is free radical damage and some alkylation

anthracycline toxicity

dose dependent biventricular heart failure, myelosuppression, mucositis, extravasation

most dangerous anthracycline

doxorubicin- highest cardiac risk

anthracycline extravasation

drug administerd into peripheral tissue rather than vessels- can lead to blistering and necrosis

bleomycin toxicity

pulmonary: interstitial pneumonitis, pulmonary fibrosis, hypersensitivity

mechanism of bleomyciin toxicity

cytokine release, free radicals, lipid peroxidation, interstitial edema, stumulation of fibroblasts- collagen

breast cancer hormonal therapies

antiestrogens: tamoxifen, fulvestrant, megestrol acetate aromatase inhibitors: anastrozole, letrozole, exemestane

hormonal therapy for prostate cancer

antiandrogens: flutamide, bicalutamide, nilutamide LHRH agonists: leuprolide, gosrelin GnRH antagonist: degarelix CYP17 inhib: abiratone

bevacizumab target/toxcitiy

VEGF-R; proteinuria and G perforation

cetuximab target/toxicity

EGFR; severe hypersensitivity, acneiform rash (can be good Px)

imatinib moa

tyrosine kinase inhibitor for bcr-abl TK, inhibits prolif and induces apop in bcr-abl cell lines

imatinib use/ brand name

CML mainly, Gleevac

ipilimumab moa

CTLA-4 inhibitor- keeps T cells active to fight tumors