Anti-neoplastic drugs Flashcards
what are chemotherapeutic drugs?
destroy or injure invading organisms or tissues
include: antimicrobial, antiparasitic and antineoplastic drugs
objective is “level the playing field” so body’s own mechanisms have an opportunity to prevail against invaders
what % of CAs are cured? what % are cured using radiation and surgery? using antineoplastic drugs?
50% of CA pts are cured
35% are cured using radiation and surgery
15% are cured using antineoplastic drugs
3 ways antineoplastic drugs may distinguish CA cells from normal cells?
- rate of growth and proliferation
- consumption of selected nutrients
- consumption of O2
what types of cells are generally affected by antineoplastic drugs and why?
bone marrow cells (anemia, leukopenia, infxns)
hair follicles (alopecia)
buccal mucosa (stomatitis)
gonads (impotence)
embryonic tissue (teratogenicity)
all affected b/c they divide rapidly and consume lg amounts of nutrients and O2
what two reasons are antineoplastic drugs administered?
for purpose of curing the disease
if cure is unattainable, then goal is palliation and increased longevity
3 times when antineoplastic drugs are indicated?
neoplasm is known to be sensitive to the drug
neoplasm has metastasized to the point that surgery and radiation are not practical
surgery and radiation require chemo supplementation
why do treatments sometimes involve following surgery and radiation with chemo?
b/c by reducing tumor burden the remaining CA cells enter the proliferation stage and then are more susceptible to antineoplastic drugs
are antineoplastic drugs subject to resistance?
YES resistance can develop
how are most antineoplastics delivered?
most delivered via IV so as to optimize concentration
primary resistance vs acquired resistance?
primary: absence of response on 1st exposure to contemporary antineoplastic drugs among specific CAs (malignant melanoma, brain CA, renal cell CA)
acquired: develops in response to repeated exposure to selected antineoplastic drugs (CA cell mutation mitigate drug effects, enhanced drug efflux via P-glycoprotein)
what is tumor lysis syndrome?
when is it esp common? complications? prevented by/treated by? if not precipitated by antineoplastic drugs what is it called?
SEs caused by debris from dead CA cells
common when treating leukemia and lymphoma
complications: hyperkalemia, hyperphosphatemia, hypocalcemia, hyperuricemia, hyperuricosuria
may be prevented/treated with allopurinal (inhibit uric acid synthesis) and IV fluids
referred to as Spontaneous Tumor Lysis Syndrome if not precipitated by antineoplastics
how many CA cell are there usu by the time dx? what is the MC outcome if untreated? outcome of infrequent chemo? outcome of aggressive and prolonged chemo? combo of what two things hastens cure?
usu abundant CA cells by the time dx no treatment usu = death infrequent chemo may delay death aggressive and prolonged chemo may result in cure chemo + surgery may hasten cure
3 methods of antineoplastic classification?
- cell cycle
- MOA
- chemical classification
what are cell cycle antineoplastics?
cell cycle specific agents which selectively inhibit one or more phases in the CA cell reproductive cycle
what are the MOAs which some antineoplastics may utilize?
alkylating agents
microtubule inhibitors
antimetabolites
what are two chemical classifications of antineoplastics?
platinum analogues
steroid inhibitors
7 common MOAs of antineoplastics?
alkylating agents platinum analogs antimetabolites microtubule inhibitors antibiotic-like drugs hormonal inhibitors monoclonal antibodies
how do alkylating agents work?
introduce alkyl group to DNA which prevents replication (chlorambucil, procarbazine)
how do antimetabolites work?
interfere w/formation of DNA or RNA by preventing access to key metabolic components
how do microtubule inhibitors work?
prevent separation of chromosomes (methotrexate- folic acid antagonist; 6 mercaptopurine, 5-fluorouracil)
how do antibiotic-like drugs work?
break DNA during replication (doxorubicin)
how do hormonal inhibitors work?
reduce natural stimulation of tissue growth and proliferation (tamoxifen- estrogen antagonist)
additional emerging antineoplastic MOAs?
signal transduction inhibitors differentiation agents anti-angiogenic drugs hypoxia inducing drugs cytoprotective drugs biologic response modifiers genetic modifiers
how do signal transduction inhibitors work?
inhibit chem signals to cell for growth and proliferation
how do differentiation agents work?
hasten cell maturation past reproductive stage
how do anti-angiogenic drugs work?
inhibit vascularization of tumors
how do hypoxia inducing drugs work?
increase O2 consuming rxns in tumors
how do biologic response modifiers work?
enhance immunologic and other self-defense mechanisms
