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NUR 326 > Chemotherapy > Flashcards

Chemotherapy Flashcards

1
Q

what are the goals of an anticancer regimen

A

kill every cancer cell and produce a cure

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2
Q

what are the next goals for anticancer treatment if a cure doesnt work

A

control growth
offer palliation

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3
Q

what is growth fraction

A

the ratio of proliferating cells to resting cells
- inc growth fraction when there are more cells proliferating than resting

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4
Q

malignant tumors typically have a ___ growth factor initially

A

high

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5
Q

as a tumor inc in size, the growth factor ___

A

slows down

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6
Q

why do larger tumors have a slower growth factor

A

they have a necrotic core
dec nutrient supply at core
more cells in resting phase
more difficult to treat

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7
Q

what are barriers to successful cancer treatment

A

100% kill is required
toxicity of the drugs used
late detection of many cancers
drug resistance
cell heterogeneity

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8
Q

why is chemo so hard on a pt

A

most toxic drug group
must use the same does throughout the whole treatment to reach 100% kill
using the right amount of drug to not kill the patient but able to cure the cancer

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9
Q

what are consequences of late detection

A

mets –> spread
less responsive –> low growth fracture
patient more debilitated by disease –> not strong enough for the meds

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10
Q

why do solid tumors respond poorly to chemo

A

low growth factor
limited blood supply

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11
Q

why is resistance a problem with chemo drug therapy

A

cancer cells are constantly mutating
- natural selection, the drug resistants will flourish

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12
Q

what is heterogeneity

A

ongoing mutations that allow cells to differ greatly so
- they can have different responses to drugs
- as tumors age, the heterogeneity increases

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13
Q

what are the strategies for chemo success

A

intermittent combo
combo therapy
optimal dosing
regional therapy

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14
Q

what is intermittent chemo goal

A

100% cancer kills with limited normal cell injury

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15
Q

what is intermittent chemo

A

balancing between letting the normal cells recover and then pumping the pt full of drugs again

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16
Q

what is combo therapy

A

using multiple drugs which help
- reduce drug resistance and normal cell injury
- inc cancer cell kills
- one drug causing problems here while the other drug causes problems there so you dont see a rapid dec in one thing

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17
Q

what is optimal dosing

A

using a dose schedule with cell cycle specific agents to keep active drugs in the body for when the cells finally enter the right stage

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18
Q

what is regional dose therapy

A

allows access to tumors which are difficult to target
- high conc
- dec systemic toxicity
- ex: intraarterial, intrathecal, intraperitoneal, intravesical

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19
Q

what are the usual toxicities associated with chemo

A

NV for several days after chemo
- dec WBC, RBC, platelets
- D
- alopecia
- fatigue

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20
Q

what are the major toxicities associated with chemo and bone marrow

A

neutropenia: infection
erythrocytopenia: anemia
thrombocytopenia: bleeding

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21
Q

what is the toxicity associated with the GI tract

A

stomatits

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22
Q

what is magic mouthwash

A

rx cocktail for stomatitis
- lidocaine, mylanta, diphenhydramine, nystatin, prednisone, distilled water
- swish gargle spit 5-10 ml q 6 hrs
not curative

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23
Q

what are reproductive toxicities of chemo

A

bad for developing fetus
germinal epithelial testes
no for pregnant women, could cause infertility in men

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24
Q

what toxicities are associated with the kidneys

A

hyperuricemia
- excessive levels of uric acid in the blood
- cause cell death/destruction of DNA

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25
Q

what are broad toxicity risks

A

extravasation
carcinogenesis
organ damage

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26
Q

what are the chemo agents

A

cytotoxic agents
- alkylating agents
- antimetabolites
- antitumor abx
- mitotic inhibitors
hormonal agents
biological agents
targeted drugs

27
Q

what do cytotoxic agents cause

A

cell death

28
Q

what do hormonal agents cause

A

block effects of hormones on tumor

29
Q

what do biological agents cause

A

alter the body’s response to cancer

30
Q

what is a cell cycle specific phase drug

A

drug that only works at a specific cell phase

31
Q

what is the problem with phase specific drugs

A

can’t interrupt cells that are in G0

32
Q

what are the implications of phase specific drugs

A

has to stay in the body a long time in order for the cells to enter into the correct stage

33
Q

what are cell cycle non specific drugs

A

drugs that work on cells in all phases even G0

34
Q

what is the disadvantage to non specific drug therapy

A

not as effective as injury to prliferating cells

35
Q

what are cell non specific often used with

A

combo with cell cycle specific agent

36
Q

what is the moa of cytotoxic agents

A

disrupt DNA synthesis
disrupt mitosis

37
Q

what class is cyclophosphamide

A

alkylating agents

38
Q

what type of cytotoxic agent is cylophosphamide

A

cell cycle nonspecific
* has some problems with resistance*

39
Q

what are the toxicities of cyclophosphamide

A

bone marrow suppression, N/V, hair loss
vesicant
hemorrhagic cystitis
sterility
discoloration of skin

40
Q

what is the class of methotrexate

A

antimetabolite
- resembles natural metabolites

41
Q

what type of cytotoxic agent is methotrexate

A

cell cycle specific
- usually S phase

42
Q

what is a problem associated with methotrexate

A

resistance

43
Q

what are the side effects of methotrexate

A

bone marrow suppression, N/V, hair loss
nephro/hepatoxicity
fetal death abnormalities

44
Q

what class is doxorubicin

A

anti tumor abx

45
Q

what type of cytotoxic agent is doxorubicin

A

cell cycle non specific

46
Q

what is the origin of doxorubicin

A

streptomyces

47
Q

what are the side effects of doxorubicin

A

bone marrow suppression, N/V, hair loss
cardiotoxicities –> dysrhythmias, heart failure
acute and delayed rxn

48
Q

what class is vincristine

A

vinca alkaloids

49
Q

what type of cytotoxic agent is vincristine

A

cell cycle specific
- M phase

50
Q

what are the toxicities of vincristine

A

some have no bone marrow suppression
peripheral neuropathy
vesicant

51
Q

what class is ondansetron

A

antiemetic, serotonin antagonist

52
Q

what is the moa of ondansetron

A

block serotonin receptors on vagal nerve in the CTZ
- chemo receptor zone

53
Q

what are adverse effects of ondansetron

A

h/a
D
dizzy

54
Q

how can ondansetron be improved

A

improved with use of steroids

55
Q

what class is promethazine

A

antiemetic, dopamine antagonist

56
Q

what are the uses for promethazine

A

chemo
post op
general N/V

57
Q

what is the moa of promethazine

A

blocks dopamine receptors in the CTZ
-both antiemetic and sedative effects

58
Q

what are the adverse effects of promethazine

A

respiratory depression
drowsy, sedation
black box: resp depression for those under 2, gangrenous extravasation

59
Q

what is the moa of biologics immunotherapy

A

uses body’s own immune system to kill cancer cells

60
Q

what are the different types of biologic immunotherapies

A

immune checkpoint inhibitors: allow immune cells to respond strongly
t cell transfer therapy: boosts natural abilities of T cell
monoclonal antibodies: mark cancer cells so better seen
treatment vaccines: boost immune system response
immune system modulators:inc immune response to prevent/slow cancer

61
Q

what are biologic immunotherapies used for

A

leukemia/lymphomas
breast
bladder
brain
colon
lung
pancreatic

62
Q

what are side effects of biologic immunosuppressants

A

pain, swelling, soreness
flu like symptoms
wt gain
D
risk of infection

63
Q

routes of biologic immunosupressants

A

IV
oral
topical
intravesical

NUR 326 (20 decks)

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