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Pharmacology > Cancer Chemotherapy > Flashcards

Cancer Chemotherapy Flashcards

1
Q

what is tumor lysis syndrome

A

increased uric acid production leading to gout

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2
Q

are alkylating agents cell cycle specific or non-specific

A

non specific

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3
Q

alkylating agents can be classified as nitrogen mustards, nitrosoureas, or other. what is an example of a nitrogen mustard

A

cyclophosphamide

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4
Q

alkylating agents can be classifies as nitrogen mustards, nitrosoureas, or other. what is an example of a nitrosourcea

A

carmustine

*-mustine ending

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5
Q

what is the suffix used for alkylating agents that aren’t nitrogen mustards or nitrosoureas

A

-platin
-carbazine

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6
Q

what is the mechanism of action of alkylating agents

A

alkylation of nucleophilic group on DNA at the N7 position of guanine

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7
Q

cyclophosphamide is metabolized into a phosphoramide mustard and acrolein. what are the effects of each

A

phosphoramide mustard allows for the cytotoxic effects
acrolein causes toxicity

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8
Q

cyclophosphamide metabolizes into a toxin called __. what does this toxin cause

A

acrolein
hemorrhagic cystitis

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9
Q

what is MENSA-2 used for

A

decrease the effect of cyclophosphamide metabolite acrolein affect that causes hemorrhagic cystitis

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10
Q

Busulfan is what class of chemo drug

A

alkylating agent

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11
Q

how does busulfan work

A

depresses granulocytosis

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12
Q

how does the alkylating agent procarbazine work

A

it has monoamine oxidase like activity

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13
Q

what is an important consideration when giving someone procarbazine

A

since it has monoamine oxidase activity, patients should be educated to avoid tyramine containing foods to avoid the cheese reaction (hypertensive crisis)

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14
Q

what are the 2 main adverse effects of cisplatin

A

emesis
nephrotoxicity (will show as elevated creatinine and urea level)
ototoxicity

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15
Q

what are the 3 main classes or antimetabolite chemo drugs

A

folate analog
purine analog
pyrimidine analog

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16
Q

at what stage of the cell cycle do antimetabolites including folate analogs, purine analogs, and pyrimidine analogs act

A

S phase

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17
Q

what is the mechanism of action of methotrexate

A

it inhibits DHFR leading to inhibition of THF synthesis, which inhibits synthesis of deoxynucleotides/DNA synthesis

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18
Q

what is the main toxicity of methotrexate. what is another toxicity

A

megaloblastic anemia
renal toxicity

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19
Q

what can be given to reverse the effects of methotrexate leading to megaloblastic anemia

A

leucovorin (AKA folinic acid)

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20
Q

what are 2 examples of purine analogs

A

6-mercaptopurine
6-thioguanine

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21
Q

6-mercaptopurine and 6-thioguanine are metabolized to __ and __ by the enzyme __

A

6-mercaptopurine–>thio-IMP
6-thioguanine–>thio-GMP
HGPRT

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22
Q

how do 6-mercaptopurine and
6-thioguanine work

A

their metabolites inhibit enzymes involved in purine synthesis

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23
Q

besides HGPRT, what other enzyme metabolizes thiopurine such as 6-mercaptopurine and 6-thioguanine

A

thiopurine methyltransferase

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24
Q

what is the mechanism of action of the pyrimidine analog 5-gluorouracil

A

it is converted into 5-FdUMP which inhibits thymidylate synthase, decreasing synthesis of dTMP/DNA synthesis, leading to apoptosis

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25
Q

what can be administered with leucovorin to enhance its effect

A

5-fluorouracil

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26
Q

what are the adverse effects of 5-fluorouracil

A

hand foot syndrome
coronary artery spasm
angina pectoris

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27
Q

what is the mechanism of action of the cytosine analog cytarabine

A

inhibition of DNA polymerase

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28
Q

what is the main toxicity of cytarabine

A

cerebral and cerebellar dysfunction

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29
Q

what are the 2 classes of antimitotic drugs

A

vinca alkaloids
taxanes

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30
Q

what is the mechanism of action of the antimitotic drug class vinca alkaloids

A

inhibition of tubulin polymerization which prevents microtubule assembly

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31
Q

what is the mechanism of action of the antimitotic drug class taxanes

A

promote assembly of microtubules and prevent microtubule disassembly

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32
Q

vincristine and vinblastine are what class of chemo drugs

A

antimitotic vinca alkaloids

33
Q

-taxel drugs are what class of chemo drugs

A

antimitotic taxanes

34
Q

vincristine and vanblastine act on what stage of the cell cycle

A

M

35
Q

what is the 4 main toxicities of vincristine

A

peripheral neuropathy
alopecia
constipation
SIADH

36
Q

what is the main toxicity of vinblastine

A

myelosuppression

37
Q

does vincristine or vinblastine cause more myelosuppression

A

vinblastine

38
Q

-taxel drugs act in what stage of the cell cycle

A

M

39
Q

what is the main toxicity of -taxel drugs

A

neutropenia

40
Q

what is the difference between topoisomerase I and topoisomerase II

A

I-breaks and seals single DNA strands
II-breaks and reseals both DNA strands

41
Q

topoisomerase inhibitors act in what stage of the cell cycle

A

early G2/late S

42
Q

-tecan drugs are what class of drugs

A

topoisomerase I inhibitors

43
Q

-poside drugs are what class of drugs

A

topoisomerase II inhibitors

44
Q

what is the mechanism of action of irinotecan

A

it undergoes hydrolysis to form SN-38 which is an greater inhibitor of topoisomerase I

45
Q

what is the main toxicity of topoisomerase I inhibitor irinotecan

A

life threatening diarrhea (this drug has a cholinergic effect acting on the bowel mucosa to cause diarrhea)

46
Q

topoisomerase I inhibitor irinotecan is contradicted in patients with what syndrome

A

Gilberts

47
Q

what class of drug are -rubicin drugs such as doxorubicin and daunorubicin

A

cytotoxic antibiotics

48
Q

what is the mechanism of action of doxorubicin and daunorubicin, both cytotoxic antibiotics (3)

A

intercalation into DNA
inhibition of topoisomerase II (causes DNA fragmentation)
generation of free radicals

49
Q

what enzyme protects tissues from free radicals generated from drugs such as doxorubicin and daunorubin

A

glutathione peroxidase

50
Q

what is the main toxic effect of doxorubicin and daunorubicin

A

cardiotoxicity due to free radical generation and lipid peroxification

51
Q

what drug can reverse the effect of free radical formation that occurs as a result of doxorubicin or daunorubicin administration

A

dexrazoxane (an iron chelating agent)

52
Q

radiation recall reaction may occur after administration of __, which prevents free radical formation following doxorubicin or daunorubicin administration

A

dexrazoxane

53
Q

what is the mechanism of action of bleomycin

A

it combines with iron and generates free radicals, causing breakage in DNA

54
Q

bleomycin affects what stage of the cell cycle

A

G2 and M

55
Q

Bcr-Abl tyrosine kinase is used for what cellular process

A

signal transduction

56
Q

imantinib is an example of what drug class

A

Bcr-Abl tyrosine kinase inhibitor

57
Q

what is the mechanism of action of Bcr-Abl tyrosine kinase inhibitor

A

they bind to ATP binding side of the BCR-ABL fusion gene so it is unable to convert to its active form

58
Q

Erlotinib is an example of what type of drug

A

epidermal growth factor receptor kinase inhibitor

59
Q

epidermal growth factor inhibitor targets what stage of the cell cycle

A

G1

60
Q

-zomib is used for what class of drugs

A

proteosome inhibitors

61
Q

what stage of the cell cycle do proteosome inhibitors act in

A

G2/S

62
Q

do proteosome inhibitors (-zomim)upregulate or downregulated MHC I

A

downregulate

(this leads to alteration of presentation of antigens to CD8+ cells, ultimately making the patient more prone to infection)

63
Q

what is the function of Bcl-2

A

prevent the release of cytochrome C from the mitochondria, inhibiting apoptosis

64
Q

what is the mechanism of Bcl-2 inhibitors

A

they make the cell more sensitive to stress signals (such as chemotherapy) by increasing activation of caspases, leading to cell death

65
Q

what is the mechanism of action of riruximab

A

antibody dependent cytotoxicity mediated by NK cells

66
Q

what is the mechanism of action of bevacizumab

A

its an angiogenesis inhibitor that is directed against vascular endothelial growth factor

67
Q

what is the mechanism of action of Cetuximab

A

it targets epidermal growth factor, interfering with cancer cell growth

68
Q

what is the mechanism of action of trastuzumab

A

it binds to the extracellular portion of HER-2, preventing activation of transmembrane tyrosine kinase

69
Q

what are the toxic effects of the monoclonal antibody trastuzumab

A

cardiomyopathy with decreased myocardial contractility

70
Q
A
71
Q

what is the mechanism of action of L-asparaginase

A

it destroys asparagine outside the cell, depriving cancer cells from asparagine and inhibiting protein synthesis

(*leukemic cells can not synthesize asparagine due to their low level of asparagine synthase)

72
Q

what are the 3 main toxic effects of L-asparaginase

A

hepatotoxicity
hypersensitivity
pancreatitis

73
Q

hydroxyurea acts in what stage of the cell cycle

A

S

74
Q

what is the function of hydroxyurea

A

inhibition of ribonucleotide reductase of purines and pyrimidines during the S phase

75
Q

what is the function of filgrastim (granulocyte colony stimulating factor) or sargramostim (granulocyte-monocyte colony stimulating factor)

A

prevention of chemo-induced neutropenia

76
Q

what is the function of ondansetron

A

anti-emetic drug

77
Q

what is the function of amifostine

A

it acts as a free radical scavenger to reduce nephrotoxicity (it is used with cisplatin)

78
Q

what is the function of amifostine

A

it is used to reduce the incidence of neutropenia-related fever and infection by alkylating agents

79
Q
A

Pharmacology (16 decks)

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