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Heme Midterm 3 > Chemotherapeutics > Flashcards

Chemotherapeutics Flashcards

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1
Q

what is the growth fraction and will it be higher or lower in tumor cells?

A

growth fraction is the number of cells cycling compared to those in Go…it will be higher in tumors as more are growing

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2
Q

what is the log kill hypothesis for chemo

A

states that 1 round of chemo will kill 99% of cells around

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3
Q

what are two reasons we use combined chemo against tumors?

A
  1. tumors are often hetergenous and will have different genetic problems leading to the tumor
  2. different parts of the tumor can have different resistances
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4
Q

primary chemotherapy

A

palliative therapy…cancer progressed and chemo only option

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5
Q

adjuvant chemo

A

small tumor…surgery first them chemo to follow

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6
Q

neoadjuvant chemo

A

huge tumor…so chemo first then surgery

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7
Q

radiosensitization chemo

A

some chemo drugs make cancer more susceptible to radiation so administer chemo then radiation

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8
Q

three general types of chemos in increasing order of toxicity

A

biologics, targeted inhibitors, traditional

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9
Q

three general types of chemos in increasing order of specificity of target

A

traditional, targeted inhibitors, biologics

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10
Q

how do phase non specific drugs work and what are they called?

A

they cross link DNA, so it cannot unwind and replicate or make RNA
alkylating agents

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11
Q

what do alkylating agents have to help cross link?

A

bifunctional structure to bind at two different spots on the DNA strand and crosslink it

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12
Q

how to get resistance to alkylating agents with repair systems?

A

increased DNA repair will notice the cross link and lead to ridding of it

two modes are base excision repair and nucleotide excision repair

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13
Q

what is another way to get alkylating agent resistance?

A

glutathione can bind the agent before it is even able to act on the cell and render it ineffective

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14
Q

cyclophosphamide/Ifosphamide type of chemo drug

A

alkylating or DNA cross link agent…non specific cell cycle

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15
Q

cyclophosphamide/Ifosphamide toxicity

A

hemorrhagic cystitis…bladder bleeding

myelosuppression

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16
Q

how does cyclophosphamide/Ifosphamide cause hemorrhagic cystitis?

A

given in inactive form that is broken down into active form and acrolein…the acrolein causes the bladder bleeding

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17
Q

how to treat toxicity of cyclophosphamide/Ifosphamide?

A

can give Mensa that will inhibit the acrolein and yield no toxic effects of cyclophosphamide/Ifosphamide

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18
Q

Bleomycin and Busulfan type of chemo drug

A

alkylating agents…DNA cross link…phase non specific

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19
Q

Bleomycin and Busulfan toxicities

A

pulmonary fibrosis and myelosuppression

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20
Q

Carmustine type of chemo agent

A

alkylating…DNA cross link…phase non specific

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21
Q

carmustine side effect/drug interaction

A

made with alcohol…so alcohol abusers on Antabuse will lead to high levels of acetaldehyde and BAD hangovers

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22
Q

Cisplatin and Carboplatin type of chemo drug

A

alkylating agent…DNA cross link…stage non specific

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23
Q

Cisplatin and Carboplatin toxicities

A

renal toxicity

ototoxicity

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24
Q

mechanism of Cisplatin and Carboplatin renal toxicity? treatment?

A

wasting of K+/Mg2+ leads to renal failure…

treat with hydration and K+/Mg2+

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25
mechanism of Cisplatin and Carboplatin ototoxicity?
accumulates in the cochlear duct fluid...causing inflammatory response also enters nerves and can kill the hair cells that aid hearing
26
three treatments for Cisplatin and Carboplatin ototoxicity?
uptake inhibitors for ear canal anti inflammatories anti oxidants
27
methotrexate mechanism and target stage as chemo drug
S phase...is a folate antagonist
28
What does methotrexate target and inhibit? what does this not allow to be made?
target dihydorfolate reductase DHFR | does not allow purine ring to be made or transformation of UMP into TMP (thymidine)
29
3 modes of methotrexate resistance
decreased uptake increase DHFR production DHFR mutations
30
methotrexates main toxicity
myelosuppression
31
methotrexate secondary toxicity
mucositis...inflammation and breakdown of GI mucosa
32
what is a risk with methotrexate?
if a patient has a 3rd space, pleural effusion of ascites, then methotrexate will enter this area and be stored until released later...can cause late toxicities
33
how is methotrexate cleared?
renally..why 3rd space is such an issue because it doesnt get cleared
34
what is a 3rd space?
pleural effusion or ascite
35
leucovorins effects on methotrexate?
it is a folate replacement and is actually only taken up by normal cells rescuing them from effects of methotrexate but still letting methotrexate screw with cancerous cells
36
name all six DNA alkylating non stage specific drugs?
``` cyclophosphamide ifosfamide Busulfan Carmustine Cisplatin Carboplatin ```
37
purine analogs (4)
mercaptopurine azathioprine Cladribine Pentostatin
38
6-mercaptopurine toxicity
myelosuppression and T cell supression so more susceptible to bad infections like PJP
39
cytarabine MOA | fluorouracil MoA
pyrimidine analog
40
cytarabine toxicity
acute cerebellar neurotoxic | also see conjunctivitis because of being clearing in eyes
41
topoisomerase inhibitors (4)
irinonectan topotecan etoposide teniposide
42
doxorubicin and daunorubicin MOA | and class
inserts into DNA and blocks unwinding for replication by making oxygen free radicals that damage DNA anthracyclines
43
what do doxorubicin and daunorubicin need to work?
iron
44
irinotecan and topotecan toxicity
diarrhea...life threatening
45
etoposide toxicity
myelosuppression and secondary malignancy...AML
46
doxorubicin and daunorubicin toxicity
cardiac myocyte death | and extravasation injury
47
agent to prevent doxorubicin and daunorubicin toxicity
dexrazoxane...prevents it by picking up iron that the drugs need
48
Bleomycin MOA and stage
G2 phase and gets into helix and makes oxygen radicals
49
dactinomycin MOA and stage
inhibits transcription and G2
50
G2 drugs
bleomycin and dactinomycin
51
bleomycin toxiciity
pulmonary fibrosis
52
M phase drugs
vincristine, vinblastine, paclitaxel
53
vincristine, vinblastine and paclitaxel MOA
messes with microtubules so mitosis is not effective
54
vincristine and vinblastine toxicity
microtubules needed in nerves...can lead to peripheral neuropathy
55
name of drugs that target the Raf kinase inhibitor
vemurafenib and dabrafenib
56
HER2 inhibitors
cetuximab. erlotinib and trastuzumab
57
trastuzomab toxicity
cardio toxicity
58
unique allergy to cetuximab
from lone star tick bite...can see anaphylactic shock
59
VEGF inhibitor and what is this important for
Bevacizumab...kidney angiogenesis
60
what class of chemos is the most emetic agent?
alkylating agents, specifically the platins
61
what other treatment do you need to consider when giving chemo
you must have an anti emitic plan that is intensive
62
two drugs to treat anemia from chemo
epoietin alfa | darbepoietin alfa
63
what is risk of giving EPO for chemo treatment
tumor growth
64
two thrombocytopenia drugs that can cause lower thrombocytopenia due to an immune response
rTPO and PEG-rTPO
65
two thrombocytopenia drugs for chemo that do not have immune response
romiplosim | eltromobopag
66
name two drugs for neutropenia treatment with chemo
filgastrim (neulasta) pegfilgastrim these are artificial GCSFs
67
side effects of filgastrim and pegfilgastrim and how do we treat it
moderate to severe bone pain | claritin
68
what is a common oral side effect that causes eating problems of chemotherapy?
taste buds turnover every 10 days...dysgeusia
69
what happens to parietal gland with chemo and what drug to treat it?
leads to dry mouth...treat with pilocarpine (parasympathetic agonist)
70
how to treat neuropathy pain in the mandible/maxillary
make sure its not dental then manage with NSAIDs

Heme Midterm 3 (10 decks)

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