80 terms

Chemo MOA and AE

Fludarabine MOA
s-phase specific. inhibits DNA polymerase causing chain termination and inhibits ribonucleotide reductase
Fludarabine AE
myelosuppresion, T cell suppresion, N/V, PN, edema, pulmonary toxicity
Mercaptopurine MOA
s-phase specific. incorporates metabolites into DNA causing miscoding during DNA replication. inhibits de novo purine synthesis
Mercaptopurine AE
Myelosupression, mild GI, hepatotoxicity, immunosupression
Mercaptopurine DI/FI
allopurinol, milk
Fluorouriacil MOA
s-phase specific. binds to and inhibits thymidylate synthetase.
Fluorouriacil AE
mucositis, Diarrhea, hand-foot syndrome, myelosuppression, N/V
Fluorouriacil DI
leucovorin, cimetidine, MTX
Capecitabine MOA
s-phase specific. binds to and inhibits thymidylate synthetase
Capecitabine AE
D/N/V hand-foot syndrome, myelosuppresion
Capecitabine DI
cytarabine MOA
s-phase specific, inhibits DNA polymerase, inhibits replication of DNA and causes chain termination
cytarabine AE
dose dependent: cerebellar toxicity, conjunctivitis, myelosuppression
other- mucositis, N/V, rash, "ara-C syndrome"
gemcitabine MOA
s-phase specific. inhibits dna polymerase and ribonucleotide reductase. terminates chain elongation
gemcitabine AE
flu-like syndrome, myelosuppresion, peripheral edema
5-azacitidine/Decitabine MOA
AZA- inh DNA and RNA
DAC- incorporates into DNA and inh methylation
methotrexate MOA
s-phase specific. inhibits DHFR
methotrexate AE
depends on +/- leucovorin rescue: mucositis, renal dysfunction, myelosuppresion, CNS toxicity, hepatic toxicity, GI toxicity
methotrexate DI
PCN, Ibu, sulfonamides, nephrotoxic meds, PPI
Pemetrexed MOA
s-phase specific. disrupts folate-dependent processes for cell replication. inh DHFR, thymidylate synthase and GARFT. inh purine and thymidine synthesis
Pemetrexed AE
myelosuppression (give folic acid and vitamine B12 to reduce
rash- give dexamethasone 4mg PI BID x 3 days starting 1 day before treatment
pralatrexate MOA
competes for DHFR-folate binding site to inhibit DHFR.
vinca alkaloid MOA
vincristine, vinblastine, vinorelbine- binds to tubulin, inh of microtubule assembly. m-phase specific
Vincristine AE
PN, C, SIADH, jaw pain (lethal if IT)
Vinblastine AE
myelosupression, PN, C, alopecia, N/V
Vinorelbine AE
myelosuppresion, N/V/C, PN, alopecia, low back pain
Taxane MOA
docetaxel, paclitaxel- bind to tubulin, inhibit tubulin depolymerization. induce tubulin polymerization->inappropriate, stable, nonfunctional microtubules. m-phase specific
docetaxel AE
myelosuppresion, fluid retention syndrome (give dexamethasone 8mg PO BID x3 days starting the day before), alopecia, PN, myalgias/arthralgias
Paclitaxel AE
myelosuppresion, PN, myalgias/arthralgias, alopecia, hypersens rxn (give dexamethaxone 20mg IV or PO 12 adn 6 hrs proir to dose, diphenhydramine 50mg IV and ranitidine 50mg IV 30 mins before
Cabazitaxel MOA
binds to tubulin and promotes microtubule assembly and inh disassembly. pre-med with diphenhydramine 25mg, dexamethasone 8mg and ranitidine 50mg
Epothilones MOA (ixabepilone
bind to b-tubulin subunit leading to stabilization of microtubule function- m-phase specific. premed with diphenhydramine 50mg PO and ranitidine 150mg PO 1 hr prior
Eribulin MOA
inhibits growth phase of microtubules-sequesters tubulin into non productive aggregates. G2/M cell-cycle block
camptotecin MOA
irinotecan, topotecan- cell cycle non specific, but require ongoing DNA synthesis. binds Topo I, interfers with DnA synthesis.
Irinotecan AE
diarrhea (acute-w/in 1 hr- atropin. delayed- antimotility agents)
myelosuppresion, alopecia, hyperbilirubinemia
bleomycin MOA
inhibits DNA synthesis by generation of activated oxygen free radicals
epipodophyllotoxinc (etoposide) MOA
s and G2-phase specific. inhibits topo II by stabilizing the topoisomerase ii- DNA complex- prevents DNA unwind
etoposide AE
myelosuppresion, alopecia, N/V hypersensitivity, radiation recall
antracyclines MOA
doxorubicin, daunorubicin, epirubicin, adarubicin- topo II inh, DNA intercalation, free-radical formation
antracycline AE
doxorubicin, daunorubicin, epirubicin, adarubicin- myelosuppresion, discolor urine, radiation recall, cardiac toxicities- acute: arrhythmias, pericarditis. chronic: cumulative injury to myocardium
antracenedione MOA
mitoxantrone- topo II inhibitor, dna intercalation, low incidince of free-radical formation. cell cycle non specific
alkylating agent MOA
cyclophosphamide, ifosfamide, temozolomide, bendamustine
covalent bonding of highly reactive alkyl groups wwith nucleophilic groups of proteins and nucleic acids.
cyclophosphamide AE
hemorrhagic cystisis, N/V, secondary malignancies, myelosuppresion, infertility, SIADH
ifosfamide AE
hemorrhagic cystitis (give with mesna), hematuria, N/V, electrolyte wasting, alopecia, myelosuppresion, CNS toxicity (somnolence, confusion, hallucinations)
platinum analogues MOA
cisplatin, carboplatin, oxaliplatin
binds to DNA and forms intra- and inter-strand cross-links
cisplatin AE
nephrotoxicity, PN, ototoxicity, electrolyte wasting, acute and delayed N/V, SIADH
carboplatin AE
myelosuppresion, N/V, electrolyte wasting, nephrotoxicity
oxaliplatin AE
PN, myelosuppresion, n/v/d, pharyngolaryngeal dysesthesia- prolong duration of infusion
l-asparaginase MOA
depletes plasma asparagine which is essential for leukemia cell survival.
l-asparaginase AE
hypersensitivty rxn (epinephrine, IV CCS, diphenhydramine), hyperglycemia, pancreatitis, coagulopahty and bleeding problems, inc BUN, dec alb
imatinib MOA
inhibits the message for cell division sent fromteh abnormal tyrosine kinase encoded by the philadelphia chromosome, prevening cell proliferation and inducing apoptosis
imatinib AE
myelosuppresion, edema, rash, N
dasatinib MOA
inhibits multiple protein kinases.
dasatinib AE
myelosuppresion, fluid retention, diarrhea, bleeding, rash, qt prolong
nilotinib MOA
inh bcr-abl tyrosine kinase activity
nilotinib AE
fluid retention/peripheral edema, rash, myelosuppresion, hepatotoxicity, N/V
erlotinib MOA
inhibits EGFR tyrosine kinase, leading to inhibition of EGFR autophosphorylation and signaling
erlotinib AE
rash, dry skin, diarrhea, conjunctivitis, fatigue
lapatinib MOA
inhibits EGFR and HER2
lapatinib AE
rash, D/N/V, myelosuppresion, dec LVEF
multikinase inhibitors MOA
target multiple kinases to inhibit cancer cell proliferation and cause apoptosis. Sunitinib, sorafenib, pazopanib
sunitinib MOA
inh PDGF, VEGF, and KIT receptors
inhibits PDGF, VEGF, KIT, intracellular kinases, angiogenesis
ihn VEGFR-1,2,3, PDGF, KIT, interleukin-2 receptor inducible kinase
vorinostat and romidepsin- histone deacetylase inhibitor
MTOR inh
temisirolimus, everlimus- binds to intracellular protein and inhibits mTOR that controls cell division
Monoclonal antibodies
induce apoptosis, block growth factor receptors or induce anti-idotype antibodies
alemtuzumab MOA
binds to CD52 + B and T lymphocytes
alemtuzumab AE
myelosuppresion, rash, infection, hypotension, N/V, leukopenia
Bevacizumab MOA
binds to VEGF
bevacizumab AE
bleeding, GI perforation, hypertension, thrombolic event, proteinuria, arterial thrombosis
cetuximab MOA
blocks EGFR receptor
cetuximab AE
acne type rash, d, nail cracking, low Mg
panitumumab MOA
blocks egfr receptor
panitumumab AE
ance type rash, d, nail cracking low mg
rituximab MOA
binds to CD20 +b cells
rituximab AE
infusion reactions, myalgias, hep B reactivation
ofatumumab MOA
binds to CD20 + b cells
ofatumumab AE
infusion reactions, hep b reactivation
trastuzumab MOA
binds to HER2+ cells
trastuzumab AE
cardiac toxicity, infusion reactions