pharmacology Flashcards
(22 cards)
what are the three treatment options in cancer
surgery, radiotherapy, pharmacological therapy
what are general toxic effects of cytostatic drugs
myelosuppression, impaired wound healing, loss of hair, damage to gastointestinal epithelium, nausea and vomiting, depression of growth in children, sterility, tetragenicity
how do alkylating cytostatics work
alkylating cytostatics are able to form a crosslink with the DNA and thus prevent unwinding of DNA done by helicases. they are not phase dependent
what is the most frequently used alkylating cytostatic
cyclophosphamide (nitrogen)
what is a downside to cisplatin
higher toxixity and acute nephrotoxic and neurotoxic things.
how do antimetabolites work
inhibit activity of enzymes duo to competition with the natural substrate for the active site of an enzyme. they then reduce DNA synthesis and result in cell death.
in which face do work and what is the most frequently used one
S phase, methotrexate
what is the active form of 5FU
5 FDMP
what does cytarabine do
blocks the funciton of DNA polymerase and thus causes inhibition of DNA replicaiton
how do antimitotics work
taxenes are formed that make the microtubules rigid and non funcitonal. thus cell shape cahnges occur which cause inhibition of cell division
what is the most frequently used antimitotics and in which phase they work
M phase, paclitaxel
how do topo-isomerase inhibitors work
they inhibit top isomerases which causes inhibition of unwinding, cutting and ligation of DNA.
what is the most frequently used topo-isomerase inhibitor and in which phase do they act
doxorubicine, G2 phase
how can emesis occur
directly by stimulation of the CTZ and indirectly by the release of serotonin in the GI tract
ondansetron, granisetron and metoclopramide are drugs to target emesis. what kind of drugs are this
ondansetron and granisetron are 5HT3 receptor antagonis
metoclopramide is a D2 antagonist
which two types of resistance to cytostatics are there
primary (present when drug is first given) or required (developed during treatment by adaption or mutation of tumor cells)
on which three factors depends the effectiveness of therapy
dose related plateau, duration of exposure, combinations of cytostatic drugs
synergy
some combinations of drugs are more effective
trastuzamb
monoclonal antibdoy against HER2, inhibits tumor cell prilferation and mediates antibody dependent cellular cytoxicity (ADCC)
cetuximab
monoclonal antibody directed against the epidermal growth factor receptor (EGF). blocking EGF-R reults in inhibition of cell growth, cell division, migration, angiogenises and induces apoptosis
bevacizumab
monoclonal antibody directed agaisnt the vascular endothelial growth factor (VEGF)
imatinib
inhibitor or protein tyrosine kinases and thus inhibition of cell proliferation, induces apoptosis
