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PT3 Oncology > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

classes that are alkylating agents

A
  • nitrogen mustards
  • nitrosoureas
  • platinum compounds
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2
Q

alkylating agents general MoA

A

-electrophilic molecules that covalently modify nucleophilic molecules in cell, particularly DNA

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3
Q

monofunctional alkylating agents cause

A

single strand DNA breaks

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4
Q

bifunctional alkylating agents cause

A

inhibition of DNA replication and transcription by crosslinking DNA

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5
Q

nitrogen mustards specific MoA

A
  • get activated into a aziridine ring

- nucleophilic attack of unstable aziridine ring on DNA

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6
Q

nitrogen mustard drugs

A
  • mechlorethamine
  • cyclophosphamide (used more)
  • procarbazine (atypical)
  • dacarbazine (atypical)
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7
Q

mechlorethamine recovery rate

A

delayed, very slow

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8
Q

cyclophosphamide recovery rate

A

rapid

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9
Q

nitrogen mustards dose limiting toxicity

A

myelosuppression

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10
Q

nitrogen mustards common resistance pathway

A

increase in DNA repair

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11
Q

toxic metabolite of cyclophosphamide

A

acrolein

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12
Q

acrolein toxicity

A
  • nephrotoxic and urotoxic

- causes severe hemorrhagic cystitis

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13
Q

drug to reduce acrolein toxicity

A

MESNA

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14
Q

procarbazine main action

A

methylator

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15
Q

dacarbazine is given with what

A

temozolomide

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16
Q

dacarbazine and temozolomide are metabolized to what

A

5-imidizole-4 caroxamide, the active alkylating species

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17
Q

platinum compounds

A
  • cisplatin
  • carboplatin
  • oxaliplatin
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18
Q

cisplatin feature

A

non-cell cycle specific

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19
Q

carboplatin feature

A

less toxic than cisplatin, but less active

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20
Q

oxaliplatin feature

A

little cross resistance with other Pt compounds, less toxic too

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21
Q

notable ADME of platinum compounds

A

Cl diuresis reduces toxicity so the drug doesn’t get activated until it is in the cell

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22
Q

cisplatin DLT

A

nephrotoxicity
neurotoxicity
ototoxicity

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23
Q

carboplatin DLT

A

myelosuppression - thrombocytopenia

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24
Q

oxaliplatin DLT

A

peripheral neuropathy

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25
Q

bifunctional alkylating agents

A

nitrogen mustards

platinums

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26
Q

monofuctional alkylating aget

A

nitrosoureas

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27
Q

general metabolite/antimetabolite MoA

A

interfere with DNA synthesis or synthesis of precursors

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28
Q

the classical cell cycle specific drugs

A

metabolites/antimetabolites

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29
Q

folate antimetabolite drugs

A

methotrexate

amethopterin

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30
Q

folate antimetabolite MoA

A

inhibit dihydrofolate reductase and dTMP synthesis

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31
Q

unique ADME of methotrexate

A

polyglutamation concentrates drug in the cell

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32
Q

folate antimetabolite toxicity

A

bone marrow
GI
renal
teratogen

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33
Q

folate antimetabolite resistance

A

increased/altered DHFR

decreased uptake

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34
Q

nucleotide analog (antimetabolite) drug

A

5-FU

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35
Q

5-FU MoA

A

irreversible inhibition of thymidylate synthase and incorporation into DNA/RNA

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36
Q

phsases of cell cycle 5-FU can kill cells

A

G1 and S

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37
Q

5-FU DLT

A

bone marrow suppression

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38
Q

5-FU resistance

A

increased/altered thymidylate synthase

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39
Q

pharmacogenetic issue with 5-FU

A

dihydropyrimidine dehydrogenase deficiency

-could lead to extreme toxicity

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40
Q

leucovorin use

A
  • rescues cells exposed to folate antagonists

- given with high dose methotrexate

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41
Q

antimetabolite resistance

A

most are prodrugs so alterations in metabolic pathway alterations

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42
Q

antibiotic anticancer drugs

A

doxorubicin

bleomycin

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43
Q

doxorubicin MoA

A

DNA intercalator and topoisomerase-II interference

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44
Q

bleomycin MoA

A

DNA & metal binding via free radical damage in G2 stage

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45
Q

doxorubicin DLT

A

cardiotoxicity

myelosuppresison

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46
Q

bleomycin DLT

A

lung and skin fibrosis

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47
Q

etoposide MoA

A

stabilized topo-II DNA complex to cause double strand breaks

prevents religation

48
Q

etoposide DLT

A

bone marrow

49
Q

etoposide resistance

A

P-glycoprotein activity which decreases accumulation

50
Q

irinotecan MoA

A

topoisomerase I inhibition

51
Q

irinotecan DLT

A

bone marrow suppression

52
Q

other side effects of note in irinotecan

A

severe diarrhea, which lets you know its working

53
Q

two groups of antimitotic agents

A

stabilizers

destabilizers

54
Q

stabilizing antimitotic drug groups

A

taxanes

epothilones

55
Q

destabilizing antimitotic drug groups

A

vinca alkaloids

56
Q

vinca alkaloid drugs

A

vincristine

vinblastin

57
Q

vinca alkaloids MoA

A

destabilize microtuble assembly so sister chromatids can’t be pulled apart, causing too much DNA to accumulate and cell dies

58
Q

vincristine DLT

A

peripheral neuropathy

59
Q

vinblastin DLT

A

bone marrow suppression

60
Q

Taxane drug

A

paclitaxel

61
Q

paclitaxel MoA

A

stabilizes microtubule assembly, preventing the spindle from being broken down

62
Q

paclitaxel DLT

A

myelosuppression

peripheral neuropathy

63
Q

Epothilone drug

A

ixabepilone

64
Q

ixabepilone mechanism

A

stabilizes microtubule assembly, preventing the spindle from being broken down

65
Q

L-asparaginase MoA

A

hydrolyzes L-asparagine to deplete it, inhibiting protein synthesis

66
Q

L-asparaginase use

A

treatment of ALL

67
Q

hormonal agent drugs

A 
tamoxifen
anastrozole
degarelix
bicalutamide
prednisone
68
Q

tamoxifen MoA

A
  • blocks estrogen response
  • inhibits G1 to S transition
  • antiestrogen SERM
69
Q

tamoxifen toxicity

A
  • rarely severe
  • n/v
  • hot flashes
  • vaginal bleeding
70
Q

tamoxifen cancer risk

A

2-3 fold increase in endometrial cancer risk

71
Q

anastrozole MoA

A
  • significantly suppress serum estradiol levels

- inhibits aromatase, which catalyzes the final step in estrogen production

72
Q

anastrozole toxicity

A
  • rare severe

- some musculoskeletal

73
Q

anastrozole use

A

ER positive breast cancer

74
Q

tamoxifen use

A

breast cancer

75
Q

leuprolide MoA

A

acts on pituitary to inhibit FSH and LH release (via negative feed back because it is an AGONIST)

76
Q

Degarelix MoA

A

GnRH antagonist

77
Q

leuprolide and degarelix use

A

prostate cancer

leuprolide needs antiandrogens with it

78
Q

benefit of degarelix over leuprolide

A

no initial testosterone surge

79
Q

bicalutamide MoA

A

inhibits uptake and/or binding of testosterone by prostate tissue
(antiandrogen)

80
Q

bicalutamide use

A
  • metastatic prostatic carcinoma

- combined with LHRH agonists

81
Q

bicalutmide toxicity

A

rarely severe adverse reactions

82
Q

prednisone use

A
  • hodgkins
  • acute lymphocytic leukemia
  • lymphoma
83
Q

trastuzumab target and use

A
  • HER2/neu

- breast cancer

84
Q

cetuximab target and use

A
  • EGFR

- colon cancer

85
Q

rituximab target and use

A
  • CD20

- B cell lymphoma

86
Q

bevacizumab target and use

A
  • VEGF

- colon and breast

87
Q

ipilimumab target and use

A
  • CTLA-4

- melanoma and lung

88
Q

anti cancer antibody that targets the immune system

A

ipilimumab

89
Q

potential mechanisms for how antibodies work in breast cancer

A
  • prevent cleavage of HER2
  • prevent dimerization
  • activate immune response
  • endocytosis
90
Q

imatinib main target

A

Bcr-Abl

91
Q

imatinib toxicity

A

usually mild
N/V
edema
some bone marrow

92
Q

signal transduction inhibitors

A 
imatinib
nilotinib
dasatinib
bosutinib
ponatinib
sorafenib tosylate
vemurafenib
*all kinases*
93
Q

sunitinib features

A

broad spectrum kinase inhibitor that is used after others have failed

94
Q

sorafenib tosylate MoA

A

inhibits raf/MEK/ERK and VEGFR pathways

95
Q

sorafenib tosylate uses

A

carcinomas

melanoma

96
Q

sorafenib tosylate ADME

A

metabolized by 3A4

inhibits other cyps

97
Q

sorafenib tosylate DLT

A

bone marrow suppression

*skin rash most common

98
Q

vemurafenib MoA

A

inhibits Raf/MEK/ERK

99
Q

vemurafenib use

A

metastatic melanoma

some lung cancers

100
Q

vemurafenib toxicity

A

30% develop cutaneous squamous sell carcinoma

101
Q

bortezomib MoA

A
  • 26S proteasome inhibitor in mammalian cells

- inhibits NFkB

102
Q

bortezomib uses

A

multiple myeloma

103
Q

bortezomib toxicity

A

GI
peripheral neuropathy
hematological toxicities

104
Q

tretinoin use

A

acute promyelocytic leukemia

105
Q

arsenic trioxide use

A

acute promyelocytic leukemia

106
Q

arsenic trioxide mechanism

A

damages PML/RAR fusion protein

107
Q

arsenic trioxide toxicity

A

tachycardia

prolonged QT

108
Q

thalidomide use

A

multiple myeloma

109
Q

thalidomide mechanism

A
  • angiogenesis inhibitor

- TNF blocking

110
Q

thalidomide toxicity

A
  • CV events
  • neuropathy
  • teratogen
111
Q

vorinostat MoA

A

histone deacetylase inhibitor

112
Q

vorinostat use

A

cutaneous t-cell lymphoma

113
Q

biologics used to bolster immune system

A

IL-2

interferons

114
Q

IL-2 use

A

metastatic melanoma

115
Q

Interferons use

A

hairy cell leukemia

PT3 Oncology (9 decks)

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