DSA antineoplastic agents, Linger, Part I Flashcards

1
Q

What are the alkylating agents

A

cyclophosphamide
ifosfamide
busulfan
cisplatin

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2
Q

What are the antimetabolites

A

methotrexate
fluorouracil 5
mercaptopurine

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3
Q

what are the vinca alkaloids

A

vinblastine and vincristine

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4
Q

what are the taxanes

A

paclitaxel

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5
Q

what are the epipodophyllotoxins

A

etoposide

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6
Q

what are the antibiotic natural products

A

doxorubicin and danuorubicin

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7
Q

what are the anthracenediones

A

belomycin

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8
Q

what are the enzymes used for anit-neoplasia

A

L asparaginase

pegaspargase

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9
Q

What are the “-nibs”

A

protein tyrosine kinase inhibitors

like imatinib

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10
Q

what are the monoclonal Ab

A

rastuzumab

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11
Q

what are the rescue agents

A

leucovorin and mesna

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12
Q

what are the drugs to minimize neutropnia

A

filgrastim and pegfilgrastin

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13
Q

What is the serotonin antagonist

A

ondansetron

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14
Q

what cancers are curable with chemo

A
ALL, AML, Ewing Sarcoma
Gestational trophoblastic carcinoma
Hodgkin, non hodgkin, burkitt, diffuse large cell
follcular mixed cell
lymphoblastic
rhabdomyosarcoma
testicular carcinoma
Wilms tumor
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15
Q

what viruses can lead to what types cancer

A

Hep B and C– hepatocellular
HIV– hodgkins and non-hodgkins
HPV– cervical and head and neck
Ebstein-barr virus – nasopharyngeal

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16
Q

What is Primary Induction therapy

A

1st Tx given

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17
Q

Neoadjuvant therapy

A

Tx as first step to shrink tumor beofre primary treatment is given
(type of induction therapy)

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18
Q

what is adjuvant therapy

A

additional cancer Tx given after primary Tx to lower the risk that the cancer will come back

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19
Q

When do you use primary induction chemotherapy

A

with advanced cancer with no other alternative Tx options

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20
Q

why is chemo commonly used as an adjuvant therapy

A

to reduce incidence of both local and systemic recurrence

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21
Q

What is G1 phase cell cycle

A

precedes DNA synthesis

cell makes components to make DNA

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22
Q

What is S phase cell cylce

A

DNA synthesis

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23
Q

What is the G2 phase

A

synthesis of components for cell division

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24
Q

What is the M phase

A

cell divides into 2 daughter G1 cells

each daughter cell may re-enter cell cycle or pass into nonproliferative stage

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25
What controls the transitions in cell cycle
activity of specific cyclin dependent kinases (CDKs) which ar activated by small regulatory proteins called cyclins and can be inhibited by other proteins like p16 and p53 (tumor suppressors)
26
What does cell cycle specific mean
agents that are cytotoxic for cells during specific phases of the cell cycle
27
what does cell cycle nonspecific mean
agents that are cytotoxic regardless of whether the cells are cycling or resting in G0 compartment
28
what drug classes are cell cycle specific
``` antimetabolites epipodophyllotoxins antitumor antibodies taxanes vinca alkaloids camptothecins ```
29
what are the cell cycle nonspecific drug classes
``` alkylating agents antimetabolites (cladribine) antracyclines antitumor antibiotics platinum analogs ```
30
What are the S phase metabolites
``` antimetabolites: capecitabine clofarabine cytarabine fludarabine 5-fluoro uracil gemcitabine 6- merccaptopurine methotrexate 6-thioguanine ```
31
what drug inhibits S-G2 phase
etoposide
32
What drug and its class inhibits G2-M phase
bleomycin (antibiotic)
33
what are the taxanes and what phase do they inhibit
paclitaxel docetaxel M phase
34
what are the vinca alkaloids and what phase do they inhibit
vinblastine vincristine vinorelbine M phase
35
what are the camptothecins and what phase do they inhibit
S phase
36
which antitumoe antibiotics are not cell cycle specific
dactinomycin and mitomycin
37
majority of cells in center of solid tumor are in what phase and why
G0 because of bad vascularization and absence of nutrients | low growth fraction
38
antineoplastic tumors work better on high or low growth fraction
high
39
why is chemo effective for burkitt lymphoma
because have high growth fractions close to 100% so drugs work
40
when is antineoplastic chemo indicated
disseminated neoplasms that are not ammenable via surgery
41
how do antineplastic drugs kill (kinetics)
log | first order kinetcs that a given dose will kill a constant fraction of cells
42
what are pharmacologic sanctuaries
regions where tumor cells are less susceptible to antineoplastic agents
43
what are the main sheculdes of administration chemo drugs
intermittent high dose therpay and continuous infusion
44
why is intermittent high dose therapy most ocmmon form of anticancer agent administration
allows recovery of normal tissues
45
when is continuous infusion used
when the drugs are rapidly metabolized or excreted | cell cycle specific more useful this way
46
what are common routes administration of the antineoplastic drugs
IV and PO
47
what term describes: " each drug used in combination therapy should hace some individual therapeutic activity and should be used at maximal toelration based on individual
efficacy
48
what is optimum scheduling in administration
intensitve intermittent schedules of drug treatment should allow the shortest time required for recovery of most sensitive target tissue (usually bone marrow) from the acute toxic effects of antineoplastic agents
49
what is repeated exposure
several cycles of treatment should be given
50
What are problems with chemo
drug resistance toxicity tolerance adverse effects
51
what is primary resistance and how did that occur
absence of response on first expousre form resitance thought to be due to genomic instability assoc with development of most cancers
52
what are mech of resistance to single agents
decreased drug transport into cells reduced drug affinity increased expression of enzyme that inactivates drug increased expression of DNA repair enzymes for drugs that damange DNA
53
What causes an multi-drug resistant phenotype
increased expression MDR1 gene which encodes cell surface transporter glycoprotein (P glycoprotein) P glycoprotein pump is ATP dependent
54
What drugs may inhibit the P glycoprotein transporter
Ca Ch blockers like verapamil
55
what areas of normal cells are attacked by chemo drugs
high growth areas | bone marrow, GI, hair follicles, buccal mucosa, sperm forming cells
56
what are common adverse effects of chemo
severe vomiting, nausea, stomatis, alopecia myelosuppression, predisposition to infection and impaired wound healing azoospermia sometimes developmental growth of children may be depressed
57
when do blood counts reach their low post Tx? cycle timing?
10-14 days and recover by day 21 and normal by 28 | treatment is every 21-28 days
58
how is neturopenia, thrombocytopenia and anemia Tx from Tx with chemo drugs
the GM CSF and G CSF drugs oprelvekin- thrombocytes erythropoeitin- RBC
59
where is vomitin controlled
2 medullary centers | comiting center and chemoR trigger zone
60
Which drugs cause severe emesis
cisplatin, dacarbazine, doxorubicin, mechlorethamine
61
what drugs have minimal emesis
methotrexate and fluorouracil
62
what are the main anti-emetics used to depress vomiting adverse effect
ondansetron, serotonin antagonist
63
the chemo drugs work on what vomiting medullary center
the chemoR trigger zone which releases NT that act on vomiting center
64
what is stomatitis
inflammation of oral mucosa
65
what drugs cause most profound alopecia
cyclophosphamide, dactinomycin, doxorubicin, paclitaxel and vincristine
66
what agent is used to decreased bone destrcution in metastatic diseases in the bones
bisphosphonates inhibit osteoclast action and bone resorption and may be used to delay time to first skeletal complication