Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 2 Heme lymph > DSA antineoplastic agents, Linger, Part I > Flashcards

DSA antineoplastic agents, Linger, Part I Flashcards

1
Q

What are the alkylating agents

A

cyclophosphamide
ifosfamide
busulfan
cisplatin

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

What are the antimetabolites

A

methotrexate
fluorouracil 5
mercaptopurine

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

what are the vinca alkaloids

A

vinblastine and vincristine

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

what are the taxanes

A

paclitaxel

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

what are the epipodophyllotoxins

A

etoposide

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

what are the antibiotic natural products

A

doxorubicin and danuorubicin

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

what are the anthracenediones

A

belomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the enzymes used for anit-neoplasia

A

L asparaginase

pegaspargase

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

What are the “-nibs”

A

protein tyrosine kinase inhibitors

like imatinib

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

what are the monoclonal Ab

A

rastuzumab

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

what are the rescue agents

A

leucovorin and mesna

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

what are the drugs to minimize neutropnia

A

filgrastim and pegfilgrastin

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

What is the serotonin antagonist

A

ondansetron

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

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

What is Primary Induction therapy

A

1st Tx given

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

Neoadjuvant therapy

A

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

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

what is adjuvant therapy

A

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

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

When do you use primary induction chemotherapy

A

with advanced cancer with no other alternative Tx options

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

why is chemo commonly used as an adjuvant therapy

A

to reduce incidence of both local and systemic recurrence

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

What is G1 phase cell cycle

A

precedes DNA synthesis

cell makes components to make DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is S phase cell cylce

A

DNA synthesis

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

What is the G2 phase

A

synthesis of components for cell division

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What controls the transitions in cell cycle

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What does cell cycle specific mean

A

agents that are cytotoxic for cells during specific phases of the cell cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what does cell cycle nonspecific mean

A

agents that are cytotoxic regardless of whether the cells are cycling or resting in G0 compartment

28
Q

what drug classes are cell cycle specific

A 
antimetabolites
epipodophyllotoxins
antitumor antibodies
taxanes
vinca alkaloids
camptothecins
29
Q

what are the cell cycle nonspecific drug classes

A 
alkylating agents
antimetabolites (cladribine)
antracyclines
antitumor antibiotics
platinum analogs
30
Q

What are the S phase metabolites

A 
antimetabolites:
capecitabine
clofarabine
cytarabine
fludarabine
5-fluoro uracil
gemcitabine
6- merccaptopurine
methotrexate
6-thioguanine
31
Q

what drug inhibits S-G2 phase

A

etoposide

32
Q

What drug and its class inhibits G2-M phase

A

bleomycin (antibiotic)

33
Q

what are the taxanes and what phase do they inhibit

A

paclitaxel
docetaxel
M phase

34
Q

what are the vinca alkaloids and what phase do they inhibit

A

vinblastine
vincristine
vinorelbine
M phase

35
Q

what are the camptothecins and what phase do they inhibit

A

S phase

36
Q

which antitumoe antibiotics are not cell cycle specific

A

dactinomycin and mitomycin

37
Q

majority of cells in center of solid tumor are in what phase and why

A

G0 because of bad vascularization and absence of nutrients

low growth fraction

38
Q

antineoplastic tumors work better on high or low growth fraction

A

high

39
Q

why is chemo effective for burkitt lymphoma

A

because have high growth fractions close to 100% so drugs work

40
Q

when is antineoplastic chemo indicated

A

disseminated neoplasms that are not ammenable via surgery

41
Q

how do antineplastic drugs kill (kinetics)

A

log

first order kinetcs that a given dose will kill a constant fraction of cells

42
Q

what are pharmacologic sanctuaries

A

regions where tumor cells are less susceptible to antineoplastic agents

43
Q

what are the main sheculdes of administration chemo drugs

A

intermittent high dose therpay and continuous infusion

44
Q

why is intermittent high dose therapy most ocmmon form of anticancer agent administration

A

allows recovery of normal tissues

45
Q

when is continuous infusion used

A

when the drugs are rapidly metabolized or excreted

cell cycle specific more useful this way

46
Q

what are common routes administration of the antineoplastic drugs

A

IV and PO

47
Q

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

A

efficacy

48
Q

what is optimum scheduling in administration

A

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
Q

what is repeated exposure

A

several cycles of treatment should be given

50
Q

What are problems with chemo

A

drug resistance
toxicity
tolerance adverse effects

51
Q

what is primary resistance and how did that occur

A

absence of response on first expousre form resitance thought to be due to genomic instability assoc with development of most cancers

52
Q

what are mech of resistance to single agents

A

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
Q

What causes an multi-drug resistant phenotype

A

increased expression MDR1 gene which encodes cell surface transporter glycoprotein (P glycoprotein)
P glycoprotein pump is ATP dependent

54
Q

What drugs may inhibit the P glycoprotein transporter

A

Ca Ch blockers like verapamil

55
Q

what areas of normal cells are attacked by chemo drugs

A

high growth areas

bone marrow, GI, hair follicles, buccal mucosa, sperm forming cells

56
Q

what are common adverse effects of chemo

A

severe vomiting, nausea, stomatis, alopecia
myelosuppression, predisposition to infection and impaired wound healing
azoospermia sometimes
developmental growth of children may be depressed

57
Q

when do blood counts reach their low post Tx? cycle timing?

A

10-14 days and recover by day 21 and normal by 28

treatment is every 21-28 days

58
Q

how is neturopenia, thrombocytopenia and anemia Tx from Tx with chemo drugs

A

the GM CSF and G CSF drugs
oprelvekin- thrombocytes
erythropoeitin- RBC

59
Q

where is vomitin controlled

A

2 medullary centers

comiting center and chemoR trigger zone

60
Q

Which drugs cause severe emesis

A

cisplatin, dacarbazine, doxorubicin, mechlorethamine

61
Q

what drugs have minimal emesis

A

methotrexate and fluorouracil

62
Q

what are the main anti-emetics used to depress vomiting adverse effect

A

ondansetron, serotonin antagonist

63
Q

the chemo drugs work on what vomiting medullary center

A

the chemoR trigger zone which releases NT that act on vomiting center

64
Q

what is stomatitis

A

inflammation of oral mucosa

65
Q

what drugs cause most profound alopecia

A

cyclophosphamide, dactinomycin, doxorubicin, paclitaxel and vincristine

66
Q

what agent is used to decreased bone destrcution in metastatic diseases in the bones

A

bisphosphonates inhibit osteoclast action and bone resorption and may be used to delay time to first skeletal complication

Year 2 Heme lymph (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions