Exam 2 Antineoplastics Flashcards
(29 cards)
Mechlorethamine (Mustargen): class, MOA, SE
Antineoplastic: alkylating agent
Part of MOPP regimen; hodgkin
Cause miscoding, breakage and cross-linking
Not cell cycle phase specific
Most effect on rapidly proliferating cells: tumor, GI, hair, bone marrow
SE: vesicant, hematologic, hyperuricemia (tx with alllopurinol), renal damage (must hydrate), N/V, Sterility, teratogenesis
BURN, BLOOD, BARF, BUN, BABY
Alkylating Agent toxicity
Vesicant (site injection tissue damage), N/V (CTZ and local), bone marrow depression, immunosuppression, teratogenesis, infertility (incl sperm), alopecia
General: BURN, BLOOD, BARF, BALD, BABY
CYCLOPHOSPHAMIDE (cytoxan): MOA, use, SE
Anti neoplastic Alkylating agent NOT a vesicant Broad spectrum SE: immunosuppressive, alopecia, hematologic toxicity, HEMORRHAGIC CYSTITIS, SIADH Tx hemorrhagic cystitis with MESNA
List the 3 alkylating agents
Mechloerthamine (Mustargen)
Cyclophosphamide (Cytoxan)
Cisplatin (Platinol)
Cisplatin (Platinol): MOA, use, SE
Antineoplastic alkylating agent
Crosslinks DNA, sensitizes cells to radiation
Use: Broad spectrum (like Cyclophosphamide)
SE: Nephrotoxic, acoustic n damage, anaphylaxis
List the anti-metabolite agents
- Methotrexate
- Mercaptopurine (6MP, purinethol)
- 5-FU (adrucil)
Methotrexate: Class, MOA, how to decrease toxicity? Resistance, use?
Antineoplastic antimetabolite
Inhibits DHF reductase, no thymidylate
Blocks DNA, RNA and protein synthesis
Decrease toxicity with Leucovorin (bypass blockade)
Resistance: decrease uptake/increase amt enzyme
Wide use
How is Methotrexate toxic
- Precipitates in renal tubules – need to hydrate
- Hepatotoxic – esp with long term use (ie immunosuppressant for RA)
- Myelosuppression
- Alopecia
- GI
- Pulmonary
- Teratogenic, sterility
Purine Analogues: class, use, MOA
Antimetabolic antineoplastics Converted by HGPRT to nucleotide; inhibit synthesis of purine nucleotides (aka DNA, RNA) Resistance with decreased HGPRT Not cell cycle specific Myelosuppressive
6-MP: class, SE, metabolism
Antimetabolite antineoplastic
Purine analogue
Metab by xanthine oxidase
May cause hyperuricemia (tx with allopurinol, but will need to decrease 6MP dose)
Toxicity: Bone marrow depression, jaundice
5-FU class, MOA, use
Antimetabolite antineoplastic agent
Inhibits thymidylate synthase and thus blocks DNA synthesis (specific to G1 and S phase)
Response increased by leucovorin (FH4 needed to form thymidylate synthase complex
Broad use, topical BCC
Doxorubicin (adriamycin) class, MOA, use
Antibiotic antineoplastic
Intercalates/STICKS into DNA, generates free radicals, effect increased by iron
Cardiotoxic esp with herceptin
Wide use
Daunorubicin makes urine turn red/orange but less cardiotoxicity
Bleomycin (Blenoxane) class, MOA, efficacy, SE
Antibiotic Antineoplastic
Directly damages DNA
G2, M phase specific
Oral or into bladder
Highly Effective – testicular, ovarian
SE: little bone marrow depression, pulmonary fibrosis, anaphylactoid sx
*lance Armstrong wouldn’t take Bleo bc risk pulmonary fibrosis – BleNOXane – NO Oxygen
What are the various mechanisms of CA chemo
- Alkylate DNA
- Interfere with metab (antimetabolites)
- Bind to microtubules
- Block hormones
- Antibodies
Strategies for treating cancer include
- Destroy CA cells
- Remove CA (surgery)
- Prevent mets
- Convert tumor to normal cell
- Halt neoplastic cell division
What determines the likelihood of CA tx success?
Better if…
a) fast growing tumor
b) high % of cells in growth fraction
c) small tumors
d) early detection (less invasive, no mets)
How do CA cells becomes resistant to drugs
Changes in level/affinity of target enzymes
Decreased drug activation
Increased DNA repair
Increased salvage pathways for purines and pyrimidines
Decreased drug uptake
Increased drug efflux
Where does tx toxicity occur
Rapidly growing cells
a) bone marrow (common; may lead to increased bleeding after other procedures)
b) GI tract: N/V, irritation
c) Hair follicles: alopecia
d) Renal: nephrotoxicity
e) Reproduction: infertility and teratogenesis
Nitrogen mustard used to…
Treat lymphoma
Plant Alkaloids include
Vinblastine, Vincristine, Paclitaxel (Taxol)
Plant Alkaloids: MOA, use
Bind to tubulin, disrupt mitosis, prevent segregation of chromosomes lined up (Vinblastine and Vincristine block polymerization)
Cell cycle specific – M PHASE
Resistance due to increase P glycoprotein
Vincristine/Vinblastine class, MOA, SE
Plant alkaloid antineoplastic agent
Bind to tubulin M phase
Axonal transport also uses microtubules
*Vincristine: crisps the neurons, low myelosuppression
*Vinblastine: blasts the bone marrow, less neurotoxicity
Paclitaxel (Taxol) class MOA, use
Plant alkaloid antineoplastic agent
binds tubulin/microtubuline, arrests mitosis, disrupts axonal transport
Kaposis sarcoma
SE: myelosuppression, myalgias, peripheral neuropathy, hypersensitivity
Tax is toxic to tubulin
Imatinib (Gleevec) class, MOA, use, SE
Tyrosine Kinase inhibitor antineoplastic
inhibits Bcr-Abl fusion protein (tx for CML)
SE: NVD, edema, myalgia, can be immunosuppressive
No immunizations, avoid if recently immunized for polio
