Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

PHARM 2 > anti-cancer > Flashcards

anti-cancer Flashcards

(151 cards)

Start Studying
1
Q

primary chemotherapy

A

primary tx in pt with adv CA without alternative tx possible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

neoadjuvant chemo

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

site directed chemo

A

direct instillation - into sanctuary sites

regional perfusion - of tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

common AE

A

nausea/vomiting

stomatitis
alopecia
myelosupression (tx with filgrastim)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

drugs with STRONG myelosuppression

A 
cytarabine
alkylating agents
doxorubicin
danunorubicin
vinblastine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

drugs with MODERATE myelosuppression

A

carboplatin
MTX
5-FU

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

drugs with MILD myelosuppression

A

bleomycin
vincristine
asparaginase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

which drug causes cardiotoxicity

A

doxorubicin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

which drug(s) causes hemorrhagic cystitis

A

cyclophosphamide

ifosphamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

which drug causes pulmonary fibrosis

A

bleomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

which drug is most likely cause cause tx-induced neoplasms

A

aklylating agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

which drug rescues BM from MTX

A

leucovorin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

which drug reduces hemorrhagic cystitis caused by cyclophosmaide and ifosfamide

A

mesna

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

which drug reduces anthracycline-induced cardiotoxicity

A

dexrazoxane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

which drug reverses neutropenia caused by many anti-CA agents

A

filgrastim

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

amifostine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

primary resistance

A

no response to drug on first exposure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

acquired resistance - single drug resistance

A

due to inc expression of 1 or more genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

acquired resistance - MDR

A

emerges to several drugs after exposure to a single agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

cell cycle specific - assoc with high growth fraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

A

nonspecific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
cell cycle specific drugs
``` antimetabolites microtubule inhibitors epipodophyllotoxins camptothecins bleomycin ```
26
cell cycle nonspecific drugs
alkylating agents platinum coordination complexes antitumor abx
27
anti-metabolites drugs
active against S phase of cell cycle - mainly affect DNA synthesis folate analogs purine analogs pyrimidine analogs
28
folate analog
MTX
29
MTX
inhibits DHFR enzyme - inhibits purine nucleotides and deoxythymidylate nucleotide synthesis DNA and RNA synthesis inhibited
30
leucovorin
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
31
MTX AE
``` stomatitis mucositis myelosuppression alopecia n/v ``` Renal damage - uncommon (complic of high dose MTX) hepatic fibrosis and cirrhosis pneumonitis neurologic toxicities
32
Purine analogs
6-mercaptopurine | 6-thioguanine
33
6-mercaptopurine
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
34
6-mercaptopurine use
ALL (childhood)
35
6-mercaptopurine AE
n/v/d hepatotoxicity BM suppresion
36
6-mercaptopurine metabolism
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
37
pt on MTX, now reports gouty like arthritis, what drug should be avoided?
allopurinol | hyperuricemia is common in anti-CA tx because of buildup of purine/pyrimidine building blocks
38
6-thioguanine
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
39
6-thioguanine use
nonlymphocytic leukemias | compare to 6-MP
40
6-thioguanine AE
n/v/d hepatotoxicity BM suppression
41
6-thioguanine metabolism
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
42
pyrimidine analogs
5-FU capecitabine deoxycytidine analogs: cytarabine, gemcitabine
43
5-fluorouracil MOA
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
44
what enzyme metabolizes 5-FU
dihydropyrimidine dehydrogenase deficiency can result in severe toxicity = myelosuppression, neurotoxicity, life threatening diarrhea
45
5'fluorouracil administrated with what
leucovorin
46
colorectal CA tx
5-FU + leucovorin also for solid tumors topical for keratoses and superficial basal cell CA
47
5-FU AE
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]
48
capecitabine
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
49
first line tx for metastatic colorectal cancer
capecitabine also used for metastatic breast cancer (b/c of specific activation in cancer cells)
50
capecitabine AE
diarrhea hand food syndrome myelosuppresion, n/v = incidence is a lot less than IV 5-FU
51
cytarabine
deoxycytidine analog
52
gemcitabine
deoxycytidine analog
53
cytarabine MOA
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
54
cytarabine use
hematological malignancies NOT solid tumors
55
cytarabine AE
myelosuppression mucositis n/v neurotoxicity
56
Gemcitabine
prodrug - phosphorylated to nucleoside di and tri phosphate = inhibits DNA synthesis (ribonucleotide reductase) incorporation of gemcitabine triphosph into DNA = chain termination
57
Gemcitabine use
solid tumors | hematological malignancies
58
gemcitabine AE
flu like n/v myelosuppresion renal microangiopathy syndromes
59
vinca alkaloids
(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
60
taxanes
(microtubule inhibitors) paclitaxel docetaxel
61
vinblastine use
hodgkins nonhodgkins breast CA germ cell CA
62
vinblastine AE
BM suppression***** alopecia peripheral neuropathy n/v potent vesicant (causes nearby tissue damage)
63
vincristine
hematological tumors | pediatric tumors
64
vincristine AE
neurotoxicity - peripheral neuropathy** worry about this SIADH **mild myelosuppression
65
taxanes
paclitaxel docetaxel PK: liver metabolism, dose reduction in liver dysf pt
66
taxanes MOA
bind beta tubulin at dif site than vinca binding side PROMOTE microtubule polymerization, inhibits epolym and promotes microtubule polymerization
67
paclitaxel use
solid tumors
68
paclitaxel AE
HS, myelosuppression, peripheral neuroatphy Abraxane can act as albumin form= no HS,no premedication, less incidence of myelosuppresion
69
Docetaxel
2nd line for adv breast CA and NSLC
70
Docetaxel AE
myelosuppresion fluid retention - t with dexamethasone - neurotoxicity - dec chance to cause nephrotoxicity as paclitaxel does
71
epipodophyllotoxins
etoposide teniposide MOA: inhibits topoisomeriase II - DNA damage. blocks cells in late S-G2 phase
72
etoposide indication
testicular CA | SCLC
73
teniposide indication
refractory ALL
74
camptothecin
topotecan irinotecan inhibits topoisomerase I = DNA damage
75
topotecan
2nd line for advanced ovarian CA following inital tx with platinum based chemo 2nd line for SCLC
76
topotecan PK
renal excretion | adjust with pt with renal impairment
77
irinotecan PK
prodrug converted in liver to active metabolite eliminated in bile and feces dose reduction in liver dysfunction
78
irinotecan application
metastatic colorectal CA + 5-FU + leucovorin
79
antitumor Abx
bleomycin | anthracyclines
80
bleomycin MOA
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
bleomycin PK
excretion is renal excretion dose reduction in renal failure pt
82
bleomycin application
hodgkin/non hodgkins | germ cell tumor, head, neck, squamous skin, cervix and vulva
83
bleomycin AE
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
anthracyclines MOA
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
anthracycline AE
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
what drug can reduce cardiotoxicity of anthracyclines
dexrazoxane
87
anthracyclines
doxorubicin | daunorubicin
88
doxorubicin
childhood CA, hematological malignancies, solid cancers
89
daunorubicin
AML limited use against solid tumors
90
akylating agents
@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
alkylating agents (5)
``` nitrogen mustards nitrosoureas alkyl sulfonates methylhydrazines triazines ```
92
alkylating agents AE
carcinogenic in nature - inc risk of AML
93
nitrogen mustards
cyclophosphamide ifosfamide mechlorethamine melphalan
94
cyclophoshpamide AE
***hemorrhagic cystitis - prevent with adequate hydration and admin of mesna aldophsophamide - excreted as acrolein = causing hemorrhagic cystitis mesna binds acrolein sterility
95
cyclophosphamide use
solid ca and hemotlogical cancers
96
ifosfamide
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
ifosfamide AE
hemorrhagic cystitis (prevented with mesna) same reasons platelet suppression neurotoxicity urinary tract toxicity
98
mechlorethamine
powerful vesicant replaced by cyclophasmide and other alkylating agnets severe n/v
99
melphalan
useful for **multiple myeloma breast CA ovarian CA
100
melphalan AE
oral ulceration hepatotoxicity pulmonary fibrosis
101
nitrosoureas
carmustine IV lomustine oral lipid soluble - cross BBB - tx brain tumors and lymphomas
102
nitrosoureas AE
pulmonary fibrosis myelosuppression renal failure
103
alkyl sulfonate
busulfan
104
busulfan use
CML
105
busulfan AE
pulmonary fibrosis
106
methylhydrazines
procarbazine
107
procarbazine use
hodgkin/non hodgkins lymphoma brain tumors
108
procarbazine AE
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
which drug has a metabolite that is a weak MAOI
procarbazine
110
triazines
dacarbazine
111
dicarbazine use
malignant melanoma hodgkins soft tissue sarcoma neuroblastoma
112
dacarbazine AE
potent vesicant - avoid extravasation n/v
113
platinum coordination complexes
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
platinum analogs
cisplatin | carboplatin
115
cisplatin use
testicular tumor** ovarian and bladder cancer cisplastin + vinblastine + bleomycin = advancement of testicular cancers***
116
what triple combo therapy is used with testicular cancer********
vinblastine + bleomycin + cisplastin
117
cisplastin AE
peripheral sensory neuropathy (via apoptosis of DRG) ototoxicity nephrotoxicity electrolyte disturbances: low Mg, Ca, K, and PO4 anaphylactic rxns
118
cisplastin nephrotoxicity prevention
prevented by hydration and diuresis (loops) OR amifostine: thiophosphate cytoprotective agent - reduce renal toxicity
119
carboplatin
ovarian nonsmall cell SCLC breast, head/neck/bladder CA
120
carboplatin
less AE than cisplastin dose limiting toxicity is myelosuppression
121
hormonal agents
glucocorticoids estrogen inhibitors androgen inhibitors
122
prednisone
induces lymphocyte apoptosis lymphocyte derived neoplasms: lymphomas, leukemias, multiple myeloma AND autoimmune hemolytic anemia, thrombocytopenia assoc with CLL
123
estrogen inhibitors
selective estrogen receptor modulators selective estrogen receptor downregulators aromatase inhibitors
124
SERMs
tamoxifen | raloxifene
125
tamoxifen
SERM ANTAGONIST @ breast CA AGONST @ nonbreast tissue used for receptor + breast CA ***risk of endometrial hyperplasia
126
raloxifene
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
which drug can cause endometrial hyperplasia: raloxifene or tamoxifen
tamoxifen
128
SERD
fulvestrant
129
fulvestrant
pure estrogen antagonist - NO AGONIST ACTIVITY inc ER degradation useful in tamoxifen resistant breast CA
130
aromatase inhibitors
anastrozole letrozol exemstane used in ER + breast CA (adjuvant) anastrozole and letrozole: NOT steroid and is a competitive inhibitor
131
androgren inhibitors
androgen receptor blockers: flutamide gonadotropin releasing hormone analgos: goserelin, leuprolide
132
flutamide
nonsteroid competitive antagonist tx: prostatic CA causes gynecomastia reversible hepatic toxicity
133
GNRH analogs
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
signal transduction inhibitors
EGFR and HER2/neu inhibitors (ErbB1 and ErbB2) BCR-ABL & C-KIT inhibitors RAS/MAP Kinase inhibitors Proteasome inhibitors angiogenesis inhibitors
135
EGFR inhibitors
tyrosine kinase gefitinib erlotinib cetuximab
136
gefitinib
NSCLC
137
erlotinib
NSCLC | pancreatic CA
138
cetuximab
colorectal CA - restricted to KRAS expressing head/neck CA
139
lapatinib
EGFR and ErbB2 inibitor Tx: NSCLC, pancreatic CA
140
trastuzumab
humanized monoclonal ab against ErbB2 (HER2) tx: breast ca with inc HER2 cardiotoxic**
141
imatinib
Bcr-ABL inhibitor = CML tx inhibits C-kit = tx GIST tx idiopathic hypereosinophilic syndrome
142
sorafenib
inhibits RAF serine/threonine kinase inhibits VEGF-R2, VEGF-R3, PDGFR-beta = stopping angiogenesis - stopping blood supply to tumor RCC
143
bortezomib
proteasome inhibitor = induce growth inhibition and apoptosis of tumor cells use: multiple myeloma, mantle cell lymphoma
144
sunitinib
inhibits angiogenesis inhibits VEGFR-1, VEGFR-2, PDGFR Use: RCC, GIST
145
asparaginase
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
asparaginase AE
HS dec in clotting factors liver abnl pancreatitis seizures, coma
147
hydroxyurea MOA
kills cells in S phase inhibits ribonucleotide reductase = depletion of deoxyribonucleoside triphosphate pool = DNA synthesis is inhibited
148
hydroxyurea use
malignant melanoma CML ovarian CA primary squamous CA of head/neck (not including lip) adult sickle cel ldisease
149
hydroxyurea AE
**macrocytosis = inc MCV rash, hyperpigmentation
150
IFN-alpha MOA
stimulatse NK to kil ltransformed cells inc expression of HLA on tumor cells
151
IFN-alpha use
kaposi sarcoma hairy cell RCC HPV, HBV, HCV

PHARM 2 (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions