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PHARM 2 > anti-cancer > Flashcards

anti-cancer Flashcards

1
Q

primary chemotherapy

A

primary tx in pt with adv CA without alternative tx possible

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2
Q

neoadjuvant chemo

A

given before sx. goal is to dec size of primary tumor so surgical resection can be made easier

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3
Q

adjuvant chemo

A

after local tx modalities (surgery) has been perforemd.

destroyed microscopic cells that may be present after local tx modalities.

dec incidence of both local and systemic recurrence and improve overall survival of pt

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4
Q

site directed chemo

A

direct instillation - into sanctuary sites

regional perfusion - of tumor

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5
Q

log kill hypothesis

A

action of cytotoxic drugs follows FIRST ORDER KINETICS

given dose kills a constant fraction of tumor cell population (rather than constant number)

repeat doses are required to eradicate

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6
Q

common AE

A

nausea/vomiting

stomatitis
alopecia
myelosupression (tx with filgrastim)

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7
Q

drugs with STRONG myelosuppression

A 
cytarabine
alkylating agents
doxorubicin
danunorubicin
vinblastine
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8
Q

drugs with MODERATE myelosuppression

A

carboplatin
MTX
5-FU

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9
Q

drugs with MILD myelosuppression

A

bleomycin
vincristine
asparaginase

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10
Q

which drug causes cardiotoxicity

A

doxorubicin

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11
Q

which drug(s) causes hemorrhagic cystitis

A

cyclophosphamide

ifosphamide

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12
Q

which drug causes pulmonary fibrosis

A

bleomycin

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13
Q

which drug is most likely cause cause tx-induced neoplasms

A

aklylating agents

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14
Q

which drug rescues BM from MTX

A

leucovorin

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15
Q

which drug reduces hemorrhagic cystitis caused by cyclophosmaide and ifosfamide

A

mesna

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16
Q

which drug reduces anthracycline-induced cardiotoxicity

A

dexrazoxane

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17
Q

which drug reverses neutropenia caused by many anti-CA agents

A

filgrastim

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18
Q

which drugs is a cytoprotective agent that reduces renal toxicity cauesd by cisplatin

A

amifostine

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19
Q

primary resistance

A

no response to drug on first exposure

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20
Q

acquired resistance - single drug resistance

A

due to inc expression of 1 or more genes

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21
Q

acquired resistance - MDR

A

emerges to several drugs after exposure to a single agent

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22
Q

cell cycle specific vs cell cycle nonspecific drugs

A

specific: exert action only on cells traversing cell cycle
nonspecific: exert action whether they are cycling or resting in G0

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23
Q

what is more effective in hematological malignancies: cell cycle specific or nonspecific

A

cell cycle specific - assoc with high growth fraction

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24
Q

what is more useful in solid tumors with low growth fraction: cell cycle specific or nonspecific

A

nonspecific

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25
Q

cell cycle specific drugs

A 
antimetabolites
microtubule inhibitors
epipodophyllotoxins
camptothecins
bleomycin
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26
Q

cell cycle nonspecific drugs

A

alkylating agents
platinum coordination complexes
antitumor abx

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27
Q

anti-metabolites drugs

A

active against S phase of cell cycle - mainly affect DNA synthesis

folate analogs
purine analogs
pyrimidine analogs

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28
Q

folate analog

A

MTX

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29
Q

MTX

A

inhibits DHFR enzyme
- inhibits purine nucleotides and deoxythymidylate nucleotide synthesis

DNA and RNA synthesis inhibited

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30
Q

leucovorin

A

activated folate - bypasses action of MTX - “provides normal tissues with reduced folate”

cells are immune to toxic effects of MTX with leucovorin. “antidote to drugs that decrease levels of folic acid to rescue BM”

if excessive amts are given, can enter tumor cells and counteract actions of MTX

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31
Q

MTX AE

A 
stomatitis
mucositis
myelosuppression
alopecia
n/v

Renal damage - uncommon (complic of high dose MTX)

hepatic fibrosis and cirrhosis

pneumonitis

neurologic toxicities

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32
Q

Purine analogs

A

6-mercaptopurine

6-thioguanine

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33
Q

6-mercaptopurine

A

pro-drug

hypoxanthine analog

converted to thio-IMP via salvage pathway with HGPRT

thio-IMP inhibits first step of de novo purine synthesis (amidotransferase) - and formation of AMP and GMP (from IMP)

thio-IMP –> TGTP (can incorp self into RNA) and TdGTP (can incorporate self into DNA) = terminate synthesis

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34
Q

6-mercaptopurine use

A

ALL (childhood)

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35
Q

6-mercaptopurine AE

A

n/v/d
hepatotoxicity
BM suppresion

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36
Q

6-mercaptopurine metabolism

A

Xanthine oxidase (check if taking allopurinol)

Thiopurine methyltransferase (check for genetic deficiency)

if either are inhibited, must dec 6-MP dose to prevent AE with accumulation of drug

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37
Q

pt on MTX, now reports gouty like arthritis, what drug should be avoided?

A

allopurinol

hyperuricemia is common in anti-CA tx because of buildup of purine/pyrimidine building blocks

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38
Q

6-thioguanine

A

guanine analog

converted to TGMP by HGPRT

TGMP is able to:
- inhibit purine synthesis (PRPP amidotransferase inhibited)

  • inhibits phosphorylation of GMP –> GDP (guanylate kinase enzyme inhibited)
  • can convert to TGTP and dTGTP = both incorporate into RNA and DNA respectively
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39
Q

6-thioguanine use

A

nonlymphocytic leukemias

compare to 6-MP

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40
Q

6-thioguanine AE

A

n/v/d
hepatotoxicity
BM suppression

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41
Q

6-thioguanine metabolism

A

1) thiopurine methyltransferase: check for genetic deficiency
2) deamination

NO allopurinol interaction - no need to reduce 6-TG dose

DO need to reduce 6-TG dose if genetic deficiency is present

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42
Q

pyrimidine analogs

A

5-FU
capecitabine
deoxycytidine analogs: cytarabine, gemcitabine

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43
Q

5-fluorouracil MOA

A

converted to deoxyribonucleotide 5-FdUMP

5-FdUMP inhibits thymidylate synthase = DNA synthesis is inhibited

“thymineless death”

5-FU also is converted to 5’FUTP - incorporated into RNA = interfere with RNA fxn

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44
Q

what enzyme metabolizes 5-FU

A

dihydropyrimidine dehydrogenase

deficiency can result in severe toxicity = myelosuppression, neurotoxicity, life threatening diarrhea

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45
Q

5’fluorouracil administrated with what

A

leucovorin

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46
Q

colorectal CA tx

A

5-FU + leucovorin

also for solid tumors

topical for keratoses and superficial basal cell CA

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47
Q

5-FU AE

A

n/v alopecia, BM depression

“HAND FOOT SYNDROME” - erythematous desquamation of palms and soles

[eccrine sweat glands excrete 5-FU. highest concentration of eccrine sweat glands are in palms and soles - lots of 5-FU excreted here]

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48
Q

capecitabine

A

ORAL prodrug of 5-FU

activated by 3 step enzymatic conversion to 5-FU (1st two steps in liver, then in tumor cells with thymidine phosphorylase)

expression of enzyme is higher in tumor cells than normal cells

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49
Q

first line tx for metastatic colorectal cancer

A

capecitabine

also used for metastatic breast cancer

(b/c of specific activation in cancer cells)

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50
Q

capecitabine AE

A

diarrhea
hand food syndrome
myelosuppresion, n/v = incidence is a lot less than IV 5-FU

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51
Q

cytarabine

A

deoxycytidine analog

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52
Q

gemcitabine

A

deoxycytidine analog

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53
Q

cytarabine MOA

A

converted to cytarabine triphosphosphate

  • competitively inhibits DNA Pol-alpha (blocks DNA synthesis)
  • competively inhibtis DNA Pol-beta (blocks DNA repair)
  • incorporated into DNA, RNA = interference with chain elongation and ligation of fragments
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54
Q

cytarabine use

A

hematological malignancies

NOT solid tumors

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55
Q

cytarabine AE

A

myelosuppression
mucositis
n/v
neurotoxicity

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56
Q

Gemcitabine

A

prodrug - phosphorylated to nucleoside di and tri phosphate = inhibits DNA synthesis (ribonucleotide reductase)

incorporation of gemcitabine triphosph into DNA = chain termination

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57
Q

Gemcitabine use

A

solid tumors

hematological malignancies

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58
Q

gemcitabine AE

A

flu like
n/v
myelosuppresion
renal microangiopathy syndromes

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59
Q

vinca alkaloids

A

(microtubule inhibitors)

vinblastine
vincristine

metabolized by liver P450

dose modific required in liver dysfunction

MOA: binds b-tubulin = disrupts assembly
- mitotic arrest in metaphase

AE - neurotoxicity, may disrupt functions that require microtubules

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60
Q

taxanes

A

(microtubule inhibitors)

paclitaxel
docetaxel

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61
Q

vinblastine use

A

hodgkins
nonhodgkins
breast CA
germ cell CA

62
Q

vinblastine AE

A

BM suppression*****
alopecia
peripheral neuropathy
n/v

potent vesicant (causes nearby tissue damage)

63
Q

vincristine

A

hematological tumors

pediatric tumors

64
Q

vincristine AE

A

neurotoxicity - peripheral neuropathy** worry about this
SIADH

**mild myelosuppression

65
Q

taxanes

A

paclitaxel
docetaxel

PK: liver metabolism, dose reduction in liver dysf pt

66
Q

taxanes MOA

A

bind beta tubulin at dif site than vinca binding side

PROMOTE microtubule polymerization, inhibits epolym and promotes microtubule polymerization

67
Q

paclitaxel use

A

solid tumors

68
Q

paclitaxel AE

A

HS, myelosuppression, peripheral neuroatphy

Abraxane can act as albumin form= no HS,no premedication, less incidence of myelosuppresion

69
Q

Docetaxel

A

2nd line for adv breast CA and NSLC

70
Q

Docetaxel AE

A

myelosuppresion
fluid retention - t with dexamethasone
- neurotoxicity
- dec chance to cause nephrotoxicity as paclitaxel does

71
Q

epipodophyllotoxins

A

etoposide
teniposide

MOA: inhibits topoisomeriase II - DNA damage. blocks cells in late S-G2 phase

72
Q

etoposide indication

A

testicular CA

SCLC

73
Q

teniposide indication

A

refractory ALL

74
Q

camptothecin

A

topotecan
irinotecan

inhibits topoisomerase I = DNA damage

75
Q

topotecan

A

2nd line for advanced ovarian CA following inital tx with platinum based chemo

2nd line for SCLC

76
Q

topotecan PK

A

renal excretion

adjust with pt with renal impairment

77
Q

irinotecan PK

A

prodrug converted in liver to active metabolite

eliminated in bile and feces

dose reduction in liver dysfunction

78
Q

irinotecan application

A

metastatic colorectal CA + 5-FU + leucovorin

79
Q

antitumor Abx

A

bleomycin

anthracyclines

80
Q

bleomycin MOA

A

G2 phase specific! 1 binding site for DNA, another for iron

binds DNA = single and double strand breaks

once iron reduces - Fe3+ = forms free radicals

81
Q

bleomycin PK

A

excretion is renal excretion

dose reduction in renal failure pt

82
Q

bleomycin application

A

hodgkin/non hodgkins

germ cell tumor, head, neck, squamous skin, cervix and vulva

83
Q

bleomycin AE

A

dose limiting = acute pulm toxicity: pneumonitis, fibrosis

***skin hyperpigmentation

**minimal BM suppression (toxic to lung and skin)

[bleomycin hydrolase is found everywhere besides lung and skin]

84
Q

anthracyclines MOA

A

binds cellular membranes to alter fluidity and ions transport

inhibits topo II

binding to DNA through intercalation - blockade of DNA/RNA synthesis = DNA breakage

free radicals form via iron dependent enzyme

85
Q

anthracycline AE

A

mainly myelosuppression

**cardiotoxicity

dose dependent cardiomyopathy
d/t free radicals

dexrazoxane can reduce cardiotoxicity = iron chelating agent

erythema and desquamation of skin at sites of prior radiation

86
Q

what drug can reduce cardiotoxicity of anthracyclines

A

dexrazoxane

87
Q

anthracyclines

A

doxorubicin

daunorubicin

88
Q

doxorubicin

A

childhood CA, hematological malignancies, solid cancers

89
Q

daunorubicin

A

AML

limited use against solid tumors

90
Q

akylating agents

A

@N7 position of guanine within DNA

lead to cell death

can occur on a single strand or both strands of DNA through cross linking/”intrastrand linking”

91
Q

alkylating agents (5)

A 
nitrogen mustards
nitrosoureas
alkyl sulfonates
methylhydrazines
triazines
92
Q

alkylating agents AE

A

carcinogenic in nature - inc risk of AML

93
Q

nitrogen mustards

A

cyclophosphamide
ifosfamide
mechlorethamine
melphalan

94
Q

cyclophoshpamide AE

A

***hemorrhagic cystitis - prevent with adequate hydration and admin of mesna

aldophsophamide - excreted as acrolein = causing hemorrhagic cystitis

mesna binds acrolein

sterility

95
Q

cyclophosphamide use

A

solid ca and hemotlogical cancers

96
Q

ifosfamide

A

prodrug
IV
activated in liver with 3A4

more toxic than cyclophosphamide - b/c can be metabolized to lots metabolites including CHLOROACETALDEHYDE = nephro and neurotoxicity

97
Q

ifosfamide AE

A

hemorrhagic cystitis (prevented with mesna) same reasons

platelet suppression
neurotoxicity
urinary tract toxicity

98
Q

mechlorethamine

A

powerful vesicant

replaced by cyclophasmide and other alkylating agnets

severe n/v

99
Q

melphalan

A

useful for **multiple myeloma

breast CA
ovarian CA

100
Q

melphalan AE

A

oral ulceration
hepatotoxicity
pulmonary fibrosis

101
Q

nitrosoureas

A

carmustine IV
lomustine oral

lipid soluble - cross BBB - tx brain tumors and lymphomas

102
Q

nitrosoureas AE

A

pulmonary fibrosis
myelosuppression
renal failure

103
Q

alkyl sulfonate

A

busulfan

104
Q

busulfan use

A

CML

105
Q

busulfan AE

A

pulmonary fibrosis

106
Q

methylhydrazines

A

procarbazine

107
Q

procarbazine use

A

hodgkin/non hodgkins lymphoma

brain tumors

108
Q

procarbazine AE

A

CNS depression

leukopenia – potent immunosuppressive

*disulfiram like rxn

one metabolite = weak MAOI - AE when given with other MAOI and tyramine containing foods –> HTN CRISIS

high carcinogenic potential is higher

109
Q

which drug has a metabolite that is a weak MAOI

A

procarbazine

110
Q

triazines

A

dacarbazine

111
Q

dicarbazine use

A

malignant melanoma
hodgkins
soft tissue sarcoma
neuroblastoma

112
Q

dacarbazine AE

A

potent vesicant - avoid extravasation

n/v

113
Q

platinum coordination complexes

A

PK: kidney excretion (requires dose modification)

MOA: formation of intrastrand and interstrand cross links = inhibition of DNA synthesis and function
N7 position of guanine

114
Q

platinum analogs

A

cisplatin

carboplatin

115
Q

cisplatin use

A

testicular tumor**

ovarian and bladder cancer

cisplastin + vinblastine + bleomycin = advancement of testicular cancers***

116
Q

what triple combo therapy is used with testicular cancer**

A

vinblastine + bleomycin + cisplastin

117
Q

cisplastin AE

A

peripheral sensory neuropathy (via apoptosis of DRG)

ototoxicity

nephrotoxicity

electrolyte disturbances: low Mg, Ca, K, and PO4

anaphylactic rxns

118
Q

cisplastin nephrotoxicity prevention

A

prevented by hydration and diuresis (loops)

OR

amifostine: thiophosphate cytoprotective agent - reduce renal toxicity

119
Q

carboplatin

A

ovarian
nonsmall cell
SCLC
breast, head/neck/bladder CA

120
Q

carboplatin

A

less AE than cisplastin

dose limiting toxicity is myelosuppression

121
Q

hormonal agents

A

glucocorticoids
estrogen inhibitors
androgen inhibitors

122
Q

prednisone

A

induces lymphocyte apoptosis

lymphocyte derived neoplasms: lymphomas, leukemias, multiple myeloma

AND autoimmune hemolytic anemia, thrombocytopenia assoc with CLL

123
Q

estrogen inhibitors

A

selective estrogen receptor modulators

selective estrogen receptor downregulators

aromatase inhibitors

124
Q

SERMs

A

tamoxifen

raloxifene

125
Q

tamoxifen

A

SERM

ANTAGONIST @ breast CA

AGONST @ nonbreast tissue

used for receptor + breast CA

***risk of endometrial hyperplasia

126
Q

raloxifene

A

antiestrogen in uterus and breast

promotes estrogenic effects in bone to inhibit resporption

Tx and prevention of post menopausal osteoporosis

prophylaxis against breast CA in high risk post menop women

NO RISK OF ENDOMETRIAL HYPERPLASIA

NOT USED IN BREAST CA TX

127
Q

which drug can cause endometrial hyperplasia: raloxifene or tamoxifen

A

tamoxifen

128
Q

SERD

A

fulvestrant

129
Q

fulvestrant

A

pure estrogen antagonist - NO AGONIST ACTIVITY

inc ER degradation
useful in tamoxifen resistant breast CA

130
Q

aromatase inhibitors

A

anastrozole
letrozol
exemstane

used in ER + breast CA (adjuvant)

anastrozole and letrozole: NOT steroid and is a competitive inhibitor

131
Q

androgren inhibitors

A

androgen receptor blockers: flutamide

gonadotropin releasing hormone analgos: goserelin, leuprolide

132
Q

flutamide

A

nonsteroid
competitive antagonist

tx: prostatic CA

causes gynecomastia

reversible hepatic toxicity

133
Q

GNRH analogs

A

pulsatile administration stimulates FSH and LH from AP – stimulating gonadal hormone release

prostate CA

biphasic response:

initial - inc LH, FSH, testosterone; counteract with flutamide

delayed - downregulation of GnRH receptors: dec LH, FSH, testosterone

134
Q

signal transduction inhibitors

A

EGFR and HER2/neu inhibitors (ErbB1 and ErbB2)

BCR-ABL & C-KIT inhibitors

RAS/MAP Kinase inhibitors

Proteasome inhibitors

angiogenesis inhibitors

135
Q

EGFR inhibitors

A

tyrosine kinase

gefitinib

erlotinib

cetuximab

136
Q

gefitinib

A

NSCLC

137
Q

erlotinib

A

NSCLC

pancreatic CA

138
Q

cetuximab

A

colorectal CA - restricted to KRAS expressing

head/neck CA

139
Q

lapatinib

A

EGFR and ErbB2 inibitor

Tx: NSCLC, pancreatic CA

140
Q

trastuzumab

A

humanized monoclonal ab against ErbB2 (HER2)

tx: breast ca with inc HER2

cardiotoxic**

141
Q

imatinib

A

Bcr-ABL inhibitor = CML tx

inhibits C-kit = tx GIST

tx idiopathic hypereosinophilic syndrome

142
Q

sorafenib

A

inhibits RAF serine/threonine kinase

inhibits VEGF-R2, VEGF-R3, PDGFR-beta = stopping angiogenesis - stopping blood supply to tumor

RCC

143
Q

bortezomib

A

proteasome inhibitor = induce growth inhibition and apoptosis of tumor cells

use: multiple myeloma, mantle cell lymphoma

144
Q

sunitinib

A

inhibits angiogenesis

inhibits VEGFR-1, VEGFR-2, PDGFR

Use: RCC, GIST

145
Q

asparaginase

A

breaks down asparagine –> aspartate + NH3

No asparagine synthase in tumor cells - therefore tumor cells deprived of asparagine = apoptose and die

SPECIFIC FOR ALL

inhibition of protein synthesis

normal cells have asparagine synthase - minimum toxicity

146
Q

asparaginase AE

A

HS

dec in clotting factors

liver abnl

pancreatitis

seizures, coma

147
Q

hydroxyurea MOA

A

kills cells in S phase

inhibits ribonucleotide reductase = depletion of deoxyribonucleoside triphosphate pool = DNA synthesis is inhibited

148
Q

hydroxyurea use

A

malignant melanoma

CML

ovarian CA

primary squamous CA of head/neck (not including lip)

adult sickle cel ldisease

149
Q

hydroxyurea AE

A

**macrocytosis = inc MCV

rash, hyperpigmentation

150
Q

IFN-alpha MOA

A

stimulatse NK to kil ltransformed cells

inc expression of HLA on tumor cells

151
Q

IFN-alpha use

A

kaposi sarcoma
hairy cell
RCC
HPV, HBV, HCV

PHARM 2 (18 decks)

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