Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
84 Cards in this Set
- Front
- Back
|
What is the log kill hypothesis
|
a theory that given a certain amount of medication a a certain number of cells are killed. so every dose = specific # of cells death.
|
|
|
In what situation is the log kill hypothesis accepted as true and what situations is it thought to not be true
|
Log kill is true most often in small tumors where all are actively growing. it is not true in larger solid tumers
|
|
|
What hypothis is used to explain how effective a drug will be against a large solid tumor?
|
Gompertzian kinetics which states that each dose of medication does not kill a set number but it is dependent on on the size of the tumor and the amount of active proliferation taking place. with a reduced effectness of the drug on cells that are no longer actively proliferating.
|
|
|
What phase of the cell cycle are vinca alkaloids targeting
|
Mitosis
|
|
|
What phase of the cell cycle does cytarabine target?
|
S phase, targets DNA replication
|
|
|
give an example of a cell cycle non specific drug
|
alkylating agents.bc they dont target a specific phase of the cell cycle they can be used against actively proliferating tumors and non proliferating ones.
|
|
|
What was the drug regimen once used against hodgkins disease
|
MOPP,
Mechlorethimine Vincrisitin (Oncovin) Prednisone Procarbazine |
|
|
What is adjuvent therapy?
|
When drugs are used as therapy after a primary therapy has been used. IE, using chemo after surgury to prevent another tumor
|
|
|
What is neoadjuvent therapy?
|
When a drug is used before another therapy to make the other therapy more viable. IE chemo to shrink a tumor small enough that it can be removed surgically.
|
|
|
What drugs fall in the alkylating group
|
bis(chloroethyl)amines
nitrosoreas alkyl sulfinate ethylinamine triazines methlyhydrazine derivatives platinum analogs |
|
|
What are some drugs in the antimetabolite catagory
|
folic acid analogs
purine and purimidine analogs |
|
|
What are 4 drugs that fall under the catagory of bis(chloroethyl)amines?
|
mechlorethamine
cyclophosphamide chlorambucil melphalon |
|
|
What drugs fall under the catagory of nitrosoreas
|
carmustine
lomustine streptozicin |
|
|
what drugs fall under the catagory alkyl sulfonate
|
busulfan
|
|
|
What drugs fall under the catagory of ethylenimines
|
thiotepa
|
|
|
what is the mech of action for alkylating agents
|
alkylates DNA residues and causes various changes such as crosslinking. this damage the tumor cell. BUT DNA HAS MECHS TO REPAIR DAMAGE.
|
|
|
What are some adverse effects of the alkylating agents
|
meylosuppression: causes anemia, thrombocytopenia, low white count-infection.
gastorintesinal damage mucosa-nausea and vomiting very common in these drugs more so than others. reproductive effects:decreased sperm count carcinogenicity |
|
|
methylchlorethamine adverse effects
|
strong vesicant does a lot of damage to skin, and mucosa
must be given through IV not orally. used in hodgkins |
|
|
cyclophosphamide adverse effects
|
immunosuppressant some times used for this effect
hemorrahagic cystitis-bleeding from urinary bladder |
|
|
nitrosoureas adverse efffects
|
crosses blood brain barriers used often to treat brain tumors
delayed myelosuppression as opposed to other alkylating agents. for up to 4 weeks. |
|
|
streptozocin adverse effects
|
causes myelosuppression less frequently. but can case renal damage.
|
|
|
Non-classical alkylating agents:
procarbazine adverse effects |
myelosuppression
neurotoxicity makes u sick when u drink alcohol increased BP after tyramine carcinogenic |
|
|
platinum analogs adverse effects
|
renal toxicity
myelosuppresion highly emetogenic: vomiting ototoxicity peripheral neuropathy electrolight imbalances anaphalatic like reactions |
|
|
Folic acid analogs drugs:
|
methotrexate
pemetrexed |
|
|
methotrexate mech of action
|
interferes with DNA synthasis. by interefering dihydrofolate reductase, which is responible for remaking the cofactor for thymidilate sulfate.
|
|
|
methotrexate adverse effects
|
myelosuppression
gastrointestinal: nausea and vomiting hepatic with long term therapy |
|
|
what is N5-formyl-FH4(leucovorin) used for?
|
it is an antidote to methyltrexate. used if over medicated or if using methotrexate at high doses to kill cancer and then giving this to prevent major system damage.
|
|
|
What is mech of action for pemetrexed?
|
inhibit thymidilate synthase and dihydrofolate reductase.
|
|
|
what are adverse effects of pemetrexed?
|
bone marrow suppression
GI issues rashes adverse effects are mitigated by giving folic acid and b12 suppliments. this does not effect the effectiveness of the drug |
|
|
6-mercaptopurine mech of action
|
hypoxanthine nucleotide analog, interferes with multiple reactions and incorperates itself into the DNA and RNA which causes damage
|
|
|
6-mercaptopurine metabolism
|
methylation by TPMT, some people have a polymorphism that reduces TPMT which leads to a increased reaction to this drug.
oxidation: by xanthine oxidase. allopurinal given for gout inhibits this enzyme which would cause increased toxicity form this drug. |
|
|
6-mercaptopurine adverse effects
|
myelsuppression
liver toxicity immunosuppression |
|
|
6-thioguianin mech of action
|
guanine analog, can be put in DNA to cause damage etc
|
|
|
6-thioguianin metabolism
|
methylation by TPMT, some people have a polymorphism that reduces TPMT which leads to a increased reaction to this drug.
deaminated to 6thioxanthine |
|
|
fludaribine phosphate mech of action
|
only purine analog that is a nucleotide which means has the sugar backbone.
inhibition of DNA synthesis inhibition of ribonucleotide reductase can be incorporated into DNA and RNA induces apoptosis |
|
|
fludaribine phosphate adverse effects
|
myelsuppression
imunosupression |
|
|
Cladribine mech of action
|
inhibition of DNA sysnthesis/repair
incorperation into DNA/RNA |
|
|
Cladribine adverse effects
|
bm suppression
immunosupression |
|
|
5-flourouracil mech of action
|
Uracil analog,
inhibits thymidialt synthase which inhibits DNA synthesis also incorperates into DNA/RNA |
|
|
5-flourouracil adverse effects
|
myelosuppression
GI Neurotoxicity |
|
|
cytarabine mech of action
|
S phase specific
inhibition DNA synthesis inhibtion of DNA elongation incorperation into DNA |
|
|
cytarabine adverse effects
|
myelosuppression
GI Neurotoxicity |
|
|
gemcitobine mech of action
|
inhibition DNA synthesis
inhibtion of ribonucleotide reductase, which is the enzyme that changes ribonucleotides to deoxyribonucleotides incorperation into DNA |
|
|
gemcitobine adverse effects
|
myelosuppression
GI |
|
|
dactinomyocin mech of action
|
antitumor antibiotic
binds DNA reduces RNA synthesis |
|
|
dactinomyocin adverse effects
|
BM
GI alopecia tissue damage is extravascated |
|
|
donarubicin
doxorubicin mech of action |
antitumor antibiotic
inhibits topoisomerase II intercalates into DNA generates free radicals that damage cell membrane |
|
|
donarubicin
doxorubicin adverse effects |
BM
GI alopecia tissue damage is extravascated cardiotoxicity |
|
|
describe the chronic cardio toxictiy of Doxorubicin
|
cardiomyopathy that leads to heart failure damage is related to cumilitave doses above 500mg/m2 can have as high as 20% experience this. thought to be result of the free radical generation.
can be treated with a kelating compound to reduce Fe free radicals |
|
|
describe the cardio toxicity acute form of doxirubicin
|
ECg abnormalities
arythmeias pericarditis/mycarditis |
|
|
bleomyocin mech of action
|
anti tumor antibiotic
binds DNA free radical generation DNA strand breaking |
|
|
bleomyocin adverse effects
|
lung conditions can cause cough and dyspenia, pulmonary infiltrate, increased risk with age and cumilitive dose
Skin reactions allergic reactions |
|
|
mitomyocin mech of action
|
anti tumor antibiotic
reduced to form an alkylating agent |
|
|
mitomyocin adverse effects
|
BM
nausea hemolytic uremic syndrome pulmonary toxicity |
|
|
wat is the MOA of vinblastine and vincristine?
|
bind tubulin inhibit polymerazation of microtubules, which inhibits mitiosis
|
|
|
What is the major toxicity of vinblastine?
|
BM loss
nausea alopecia irratation with extravasation |
|
|
What is the major toxicity of vincristine?
|
less BM loss than vinblastine
neurotoxicity- peripheral neuropathy and constipation alopecia irratation with extravasation |
|
|
MOA of paclitaxil?
|
binds tubulin and enchances polymerazation, this also causes problems with mitosis.
|
|
|
Major tox of paclitaxil?
|
BM suppression
hypersensitivity peripheral neuropathy arrythmeias |
|
|
MOA of podophylotoxins (etoposide)
|
inhibits topoisomerase II causes DNA to breakdown
|
|
|
Major tox of podophylotoxins (etoposide)
|
BM suppression
GI problems allopecia allergic reactions leukemia |
|
|
MOA of camptothecin? (topotecan)
|
inhibit topoisomerase I cause DNA breakdown
|
|
|
major tox of camptothecin (topotecan)
|
BM suppression
GI problems |
|
|
MOA asparginase
|
decreases asparagine in cells which leads to decreased protien synthesis.
|
|
|
Major tox of Apseriginase
|
allergic reactiona
hepatotoxicity clotting issues Neurotox pancreatitis elevated glucose |
|
|
BCR-ABL tyrosine kinase inhibitor MOA
|
tyrosine kinase inhibitor
|
|
|
BCR-ABL tyrosine kinase inhibitor major toxicity
|
GI
anemia,neurtopenia, thrombocytopenia edema liver issues |
|
|
what are the tyrosine kinase inhibitor
|
imatinib
desantinib nilotinib |
|
|
What are the growth factor receptor inhibitors that bind the extracellular region?
|
cetuximab
panitumumab |
|
|
What are the major tox of cetuximab and
panitumumab? |
infusion reaction
rash interstitial lung disease. |
|
|
What are the growth factor receptor inhibitors that bind teh tyrosine kinase portion?
|
gefitinib
erlotinib |
|
|
What are the major tox of gefitinib and
erlotinib |
diarrehia
rash interstitial lung disease |
|
|
MOA of beviczumab
|
vascular endothelium growth factor receptor inhibitors.
|
|
|
major tox of beviczumab
|
infusino Rx
hypertension GI perforation bleeding wound healing complications arterial thromboembolic events protienuria |
|
|
sorefinib and sunitinib MOA
|
multiple tyrosine kinase receptor inhibitors espeacially on the vascular endothelial growth receptors.
|
|
|
sorefinib and sunitinib major tox
|
fatigue
hypertension bleeding sorefinib- hand foot syndrome sunitinib- cardic issues |
|
|
MOA hydroxyurea?
|
inhibits ribonucleotide reductase
decrease DNA sysnthesis |
|
|
major tox for hydroxyurea
|
BM suppression
GI problems skin issues |
|
|
What is the ending on the name of all the monoclonal antibodies
|
MAB
|
|
|
What is B-raf
|
a mutated gene in the RAS pathway that is present in most melanomas
the mutation is at the 600th aa and is a V to E change that instead of being regulated by RAS to be turned on and off its just turned on all the time. |
|
|
what is plx4032?
|
a drug that was developed that reacts with mutant B-RAF but not wild type B-RAF. it is used in the treatment of melanoma.
|
|
|
Is plx4032 a cure?
|
no it increases survival time but ultimately genetic mutations lead to resistance.
|
|
|
What does CTLE 4 do?
|
it turns off T-cells
|
|
|
what does ipilimumab do
|
it is a humanized antibody that interferes with CTLE 4 and causes increased immune response used against melanoma.
|
