Chemo MOA and AE

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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

warfarin

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
fatigue

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

sorafenib

inhibits PDGF, VEGF, KIT, intracellular kinases, angiogenesis

pozopanib

ihn VEGFR-1,2,3, PDGF, KIT, interleukin-2 receptor inducible kinase

HDAC inh MOA

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

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