day 2 oncology Flashcards

1
Q

MOA of epipodophyllotoxins

A

Act by inhibiting DNA topoisomerase II

prevents proper unwinding of DNA resulting in blockade of DNA synthesis and cell division

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2
Q

uses of epipodophyllotoxins

A

• Etoposide: lung cancer, germ cell cancer, gastric cancer

teniposide- pediatric leukemia***

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3
Q

2 types of epipodophyllotoxins

A

Etoposide

teniposide

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4
Q

3 adverse effects of epipodophyllotoxins

A

Myelosuppression
• Alopecia
• Hypotension

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5
Q

What are antitumor antibiotics?

A

Derived from microorganisms (bacteria)

compounds are produced and used by bacteria to compete with other microorganisms for resources

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6
Q

What are some examples of antitumor antibiotics?

A
Anthracyclines/Anthracenedione
Mitomycin
Doxorubicin
Bleomycin
Daunorubicin
Epirubicin
Idarubicin
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7
Q

MOA of anthracyclines

A

– Inhibit topoisomerase 2
generate free radicals
bind to DNA and intercalate DNA strands

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8
Q

DNA intercalation is what?

A

Drug binds to areas on both strands preventing DNA from being replicated

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9
Q

Free radical formation

A

Free radicals are very damaging to tissues by binding to metabolic products and disrupting cellular function

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10
Q

uses of anthracyclines

A

• Doxorubicin: breast CA, myeloma, leukemia, lymphoma
daunorubicin and idrarubicin- leukemia
epirubicin- breast, gastroesophageal CA
mitoxantrone- leukemia, lymphoma, prostate CA, multiple sclerosis

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11
Q

adverse effects of anthracyclines

A
• Myelosuppression
• Alopecia
• N/V
• Mucositis
• Vesicant if extravasated 
cardiotoxicity
mitoxantrone- turns urine blue/ green
doxo/ dauno/ ida/ epirubicin turn urine reddish/ orange
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12
Q

acute cardiotoxicity from anthracyclines

A

• Within 24-72 hours of admin
arrythmias, pericarditis, myocarditis
usually subclinical

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13
Q

chronic cardiotoxicity from anthracyclines

A

• Dose dependent
delayed by years
results in cardiomyopathy and heart failure

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14
Q

Cardiotoxicity of anthracycline

A

– 1 -2% risk for doxorubicin doses 500

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15
Q

Use of dexrazoxane

A

Reduces free radical formation in cardiac tissue

may reduce therapeutic effect of doxorubicin

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16
Q

Bleomycin MOA

A

Binds DNA and forms free radicals that destroy DNA and prevent DNA replication

17
Q

Bleomycin uses?

A

lymphoma, germ cell tumor, head and neck cancer, SCC

18
Q

What is a major concern with the use of bleomycin?

A

Pulmonary toxicity

symptoms include, cough, pnemonitis dyspnea

19
Q

Pleural effusion is what?

A

• Pleural is fluid build up around the lung
prevents normal expansion upon inhalation
risk factors = age >70
supplemental oxygen
cumulative doses >400
underlying pulmonary disease

20
Q

Tyrosine kinase inhibitors MOA

A

Inhibiting tyrosine kinases can target and block specific regulatory pathways and promote cancer cell death through apoptosis

21
Q

What are the differences between the TKI’s?

A

– Target different TK that vary in level activity in different cancers
differ in binding affinity to their targets making some more potent inhibitors than other
some bind with less restricition

22
Q

Resistance to TKI’s

A

Mutations in the amino acid sequence of tyrosine kinases could prevent the TKI from binding to the target site and make the drug inactive

23
Q

Adverse effects of TKIs

A
– Rash
– Myelosuppression 
– Fatigue
– Fluid
diarrhea
CHF
24
Q

Drug interactions of TKI’s

A

• Many metabolized by CYP450 enzyme system
enzyme inhibitors decrease metabolism and increase risk for side effects
enzyme inducers increase metabolism and decrease risk for side effects
reduced bioavailability with concomitant use of stomach acid reducers like PPI and H2 antagonists

25
Q

possible MOA of immunomodulators?

A

– May alter tumor necrosis factor
may increase activity of NK cells and interferons
may promote apoptosis

26
Q

immunomodulators MC used for what?

A

Mc used for multiple myeloma

in combo with dexamethazone

27
Q

3 examples of immunomodulators

A

Thalidomide
Lenalidomide
Pomalidomide

28
Q

adverse effects of immunomodulators

A
peripheral neuropathy
thromboembolism
fatigue
rash
dizziness
myelosuppression
29
Q

proteasomes inhibitors MOA

A

inhibit complexes of proteins that would otherwise breakdown unneeded or damaged proteins

30
Q

proteasomes inhibitors used to treat what?

A

used in treatment for multiple myeloma

31
Q

adverse effects of proteasome inhibitors

A
peripheral neuropathy
neuralgia
rash
N/V/D
heart failure
pulm toxicity
32
Q

monoclonal antibodies MOA

A

target specific proteions in cancer cells that block their standard function
(various sites on the surface of the cell)

33
Q

how mAb kill tumor cells

A

could block receptors required for activating cell functions
could bind to free protein ligands looking to bind to receptors
could bind to receptors and cause apoptosis
could bind to receptors and cause antibody dependent cellular cytotoxicity

34
Q

uses of mAb

A

rituximab- lymphoma
trastuzmab- HER2 breast cancer
panitumumab- colorectal cancer
cetuximab- colorectal, lung, head and neck CA
bevacizumab- colorectal, breast, lung, renal cell cancer

35
Q

adverse effects of mAb

A

infusion related reactions
heart failure
hypomagnesemia
delayed wound healing

36
Q

aspariginase MOA

A

breaks down asparagine to aspartate which will deprive the tumors of a vital amino acid leading to stress and apoptosis

37
Q

forms of aspariginase

A

Ecoli
PEG
erwinia

38
Q

use of aspariginase

A

part of combination chemo to treat ALL

39
Q

adverse effects of aspariginase

A

hypersensitivity
pancreatitis
neurologic toxicity
clotting bleeding d/o