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
what are broad toxicity risks
extravasation carcinogenesis organ damage
26
what are the chemo agents
cytotoxic agents - alkylating agents - antimetabolites - antitumor abx - mitotic inhibitors hormonal agents biological agents targeted drugs
27
what do cytotoxic agents cause
cell death
28
what do hormonal agents cause
block effects of hormones on tumor
29
what do biological agents cause
alter the body's response to cancer
30
what is a cell cycle specific phase drug
drug that only works at a specific cell phase
31
what is the problem with phase specific drugs
can't interrupt cells that are in G0
32
what are the implications of phase specific drugs
has to stay in the body a long time in order for the cells to enter into the correct stage
33
what are cell cycle non specific drugs
drugs that work on cells in all phases even G0
34
what is the disadvantage to non specific drug therapy
not as effective as injury to prliferating cells
35
what are cell non specific often used with
combo with cell cycle specific agent
36
what is the moa of cytotoxic agents
disrupt DNA synthesis disrupt mitosis
37
what class is cyclophosphamide
alkylating agents
38
what type of cytotoxic agent is cylophosphamide
cell cycle nonspecific * has some problems with resistance*
39
what are the toxicities of cyclophosphamide
bone marrow suppression, N/V, hair loss vesicant hemorrhagic cystitis sterility discoloration of skin
40
what is the class of methotrexate
antimetabolite - resembles natural metabolites
41
what type of cytotoxic agent is methotrexate
cell cycle specific - usually S phase
42
what is a problem associated with methotrexate
resistance
43
what are the side effects of methotrexate
bone marrow suppression, N/V, hair loss nephro/hepatoxicity fetal death abnormalities
44
what class is doxorubicin
anti tumor abx
45
what type of cytotoxic agent is doxorubicin
cell cycle non specific
46
what is the origin of doxorubicin
streptomyces
47
what are the side effects of doxorubicin
bone marrow suppression, N/V, hair loss cardiotoxicities --> dysrhythmias, heart failure acute and delayed rxn
48
what class is vincristine
vinca alkaloids
49
what type of cytotoxic agent is vincristine
cell cycle specific - M phase
50
what are the toxicities of vincristine
some have no bone marrow suppression peripheral neuropathy vesicant
51
what class is ondansetron
antiemetic, serotonin antagonist
52
what is the moa of ondansetron
block serotonin receptors on vagal nerve in the CTZ - chemo receptor zone
53
what are adverse effects of ondansetron
h/a D dizzy
54
how can ondansetron be improved
improved with use of steroids
55
what class is promethazine
antiemetic, dopamine antagonist
56
what are the uses for promethazine
chemo post op general N/V
57
what is the moa of promethazine
blocks dopamine receptors in the CTZ -both antiemetic and sedative effects
58
what are the adverse effects of promethazine
respiratory depression drowsy, sedation black box: resp depression for those under 2, gangrenous extravasation
59
what is the moa of biologics immunotherapy
uses body's own immune system to kill cancer cells
60
what are the different types of biologic immunotherapies
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
what are biologic immunotherapies used for
leukemia/lymphomas breast bladder brain colon lung pancreatic
62
what are side effects of biologic immunosuppressants
pain, swelling, soreness flu like symptoms wt gain D risk of infection
63
routes of biologic immunosupressants
IV oral topical intravesical