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Oncology APP > antineoplastic agents > Flashcards

antineoplastic agents Flashcards

1
Q

FOLFOX stands for

A

leucovorin calcium (folinic acid), fluorouracil, and oxaliplatin

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2
Q

CAPOX stands for

A

Oxaliplatin and capecitabine

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3
Q

cell cycle phase where organelles duplicate

A

G1

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4
Q

cell cycle phase where DNA replicates

A

S

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5
Q

cell cycle phase where cell prepares itself to divide

A

G2

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6
Q

cell cycle phase where centromeres and microtubules form

A

prophase

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7
Q

cell cycle phase where DNA aligns along the middle of the cell

A

metaphase

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8
Q

enzyme that fixes DNA coils as it is being unwound by DNA helicase

A

topoisomerase

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9
Q

class of drug that binds covalently to DNA to arrest the cell cycle

A

alkylating agents

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10
Q

an alkalating nitrogen mustard

A

cyclophosphamide

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11
Q

5-flourouricil MOA

A

inhibits thymidilate synthase, interfering with the production of thymine (one of the four constituent bases of nucleic acids)

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12
Q

methotrexate MOA

A

inhibits dihydrofolate reductase, which is key to producing thymidilate synthase and the production of thymine (one of the four constituent bases of nucleic acids)

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13
Q

6-mercaptopurine MOA

A

inhibits the production of the purine containing nucleotides, adenine and guanine thus halting DNA synthesis

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14
Q

doxorubicin and daunorubicin MOAs (hint: there are 3)

A

1- inhibit topoisomerase, which may break DNA coils during S phase replication 2- inhibits helicase so DNA can’t unwind 3-producing reactive oxygen species

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15
Q

camptothecin and etoposide MOA

A

inhibit topoisomerase, which may break DNA coils during S phase replication

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16
Q

vinchristine and vinblastine (vinca alkaloids) MOA

A

destabilize microtubules during assembly to disrupt the M phase

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17
Q

paclitaxel and docetaxel MOA

A

stabilize microtubules so they can’t break down and no telophase can occur

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18
Q

gemfitinib and erlotinib MOA

A

1st generation tyrosine kinase inhibitor, reversible binding to mutant EGFR receptor, inactive on the T790M mutation

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19
Q

afatinib and dacomitinib MOA

A

2nd generation tyrosine kinase inhibitor (TKI), irreversible covalent binding to all ErbB receptors (EGFR, ErbB2 and ErbB4), inactive on the T790M mutation

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20
Q

osimertinib MOA

A

3rd generation tyrosine kinase inhibitor (TKI), irreversabile covalent binding to EGFR receptor, active on the T790M mutation

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21
Q

osimertinib indication(s)

A

Third generation EGFR inhibitor indicated for NCSLC, may use when there are brain metastases, only approved TKI for T790M mutation

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22
Q

erlotinib indication(s)

A

pancreatic cancer, NCSLC

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23
Q

vandetanib MOA and indication(s)

A

EGFR, VEGF, RET thyroid cancer

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24
Q

cetuximab, panitumumab, and necitumumab MOA

A

Anti-EGFR monoclonal antibodies bind to the extracellular domain of EGFR in its inactive state; they compete for receptor binding by occluding the ligand-binding region, and thereby block ligand-induced EGFR tyrosine kinase activation

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25
Q

cetuximab indication(s)

A

colorectal cancer and head and neck cancer

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26
Q

panitumumab indication(s)

A

colorectal cancer

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27
Q

dabrafenib and trametinib inhibit what pathway?

A

BRAF and MEK

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28
Q

necitumumab indication(s)

A

NSCLC

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29
Q

trastuzumab indication(s)

A

breast cancer, gastric cancer, and gastroesophageal junction cancer

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30
Q

trastuzumab MOA

A

HER2 inhibitor

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31
Q

pertuzumab MOA

A

HER2 inhibitor

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32
Q

lapatinib MOA

A

HER2 inhibitor

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33
Q

neratinib MOA

A

HER2 inhibitor

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34
Q

name 2 oral HER2 inhibitors

A

lapatinib and neratinib

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35
Q

ado-trastuzumab emtansine MOA

A

Antibody-Drug Conjugate

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36
Q

3 main adverse effects of HER2 inhibitors

A

cardiotoxicity, diarrhea, rash

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37
Q

which class of drugs requires a baseline and every 3 months echocardiogram

A

HER2 inhibitors

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38
Q

which HER2 inhibitor also inhibits EGFR and requires monitoring for liver toxicity?

A

lapatinib

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39
Q

cobimetinib MOA

A

MEK inhibitor

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40
Q

dabrafenib MOA

A

BRAF inhibitor

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41
Q

trametinib MOA

A

MEK inhibitor

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42
Q

encorafenib MOA

A

BRAF inhibitor

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43
Q

binimetinib MOA

A

MEK inhibitor

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44
Q

vemurafenib MOA, indication

A

BRAF inhibitor, melanoma

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45
Q

vemurafenib/cobimetinib indication(s)

A

Melanoma, Erdheim-Chester disease

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46
Q

dabrafenib/trametinib indication(s)

A

melanoma, thyroid cancer, NCLSC

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47
Q

encorafenib/binimetanib indication(s)

A

melanoma

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48
Q

what is the function of the interaction between PD-L1 on normal cells and PD-1 on CD8 positive (killer) t-cells?

A

keeps the killer T-Cell from destroying normal cells. Pembrolizumab interrupts this by inhibiting PD-L1 and enabling the T-Cell to respond to the foriegn antigen presented on the cancer cell

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49
Q

suffix -tinib indicates

A

tyrosine kinase inhibitor, example lapatinib

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50
Q

suffix -anib

A

angiogenesis inhibitor

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51
Q

suffix -zomib

A

proteosome inhibitor

52
Q

suffix -rafenib

A

BRAF inhibitor

53
Q

t or tu naming convention indicates which target

A

tumor

54
Q

ci naming convention indicates which target

A

circulatory system

55
Q

li or l naming convention indicates which target

A

immunomodulation

56
Q

mo naming convention indicates which source for monoclonal antibodies

A

mouse

57
Q

xi naming convention indicates which source for monoclonal antibodies

A

chimeric, combining genetic material from a non-human species and genetic material from a human being

58
Q

zu naming convention indicates which source for monoclonal antibodies

A

humanized, mostly derived from a human source, with small regions derived from non-human species

59
Q

u naming convention indicates which source for monoclonal antibodies

A

human

60
Q

HDAC stands for

A

histone deacetylase inhibitor

61
Q

HDAC inhibitors MOA

A

inhibites histone deacetylase, blocking chromatin closure and inhibiting transcription, which leads to cell cycle arrest and cell death

62
Q

PARP stands for

A

poly ADP ribose polymerase inhibitor

63
Q

PARP inhibitor MOA

A

block PARP enzyme, which normally repairs damaged DNA. This leads to cell death

64
Q

proteasome inhibitor MOA

A

block the degradation of excess or damaged proteins, leading to a variety of effects including apoptosis, migration, and decreased proliferation and angiogenesis

65
Q

class of drugs that target CTLA-4, PD-1, or PD-L1

A

immune checkpoint inhibitors

66
Q

cytotoxic lymphocyte associated protein 4 is targeted by what class of drugs

A

immune checkpoint inhibitors

67
Q

this class of drugs uses a single molecule to bind 2 different and unique antigen binding sites

A

bispecific antibodies

68
Q

One drug in this class takes advantage of increased CD-30 expression on Reed-Sternberg cells

A

ADCs (antibody drug conjugates)

69
Q

vorinostat MOA, route, indication(s)

A

oral HDAC inhibitor indicated for CTCL

70
Q

romidepsin MOA, route, indication(s)

A

IV HDAC inhibitor indicated for CTCL, PTCL

71
Q

belinostat MOA, route, indication(s)

A

IV HDAC inhibitor indicated for PTCL

72
Q

panobinostat MOA, route, indication(s)

A

oral HDAC inhibitor indicated for multiple myeloma

73
Q

common HDAC inhibitor adverse effects (there are 6)

A

hematologic, GI, QTc prolongation, hepatotoxicity, infection, hyperglycemia

74
Q

which HDAC carries a boxed warning for diarrhea

A

panobinostat

75
Q

only PARP inhibitor not approved for ovarian cancer

A

talazoparib

76
Q

primary indication for PARP therapy

A

BRCA1/2 mutated breast cancer

77
Q

olaparib MOA and indication(s)

A

PARP inhibitor, breast, ovarian, pancreatic, and prostate cancer

78
Q

rucaparib MOA and indication(s)

A

PARP inhibitor. breast, ovarian, pancreatic, and prostate cancer

79
Q

niraparib MOA and indications(s)

A

PARP inhibitor. ovarian cancer

80
Q

talazoparib MOA and indication(s)

A

PARP inhibitor, breast cancer

81
Q

When the ANC drops below 1,000 it is called

A

neutropenia

82
Q

normal ANC is

A

between 2500-6000

83
Q

bevacizumab, ramucirumab, and ziv-aflibercept MOA

A

VEGF/VEGFR inhibitors

84
Q

when taking a VEGF inhibitor, what level proteinuria should prompt a 24 hour urine protein exam?

A

2+ protein on dipstick or urine protein/creatinine ratio of >1.

85
Q

when using a VEGF inhibitor, why avoid using nsaids?

A

bleeding concerns, hypertension

86
Q

what syndrome presents with headache, seizures, lethargy, confusion, blindness, or other neurologic disturbances?

A

posterior reversible encephalopathy syndrome (PRES)

87
Q

T or F: VEGF inhibitors are contraindicated for those with a history of a thrombotic event

A

F: patients with such a history may take VTE prevention medications concurrently if otherwise not contraindicated

88
Q

what grade hemorrhage should prompt discontinuation of a VEGF inhibitor?

A

grade 3-4

89
Q

sorafenib, regorafenib, sunitinib, axitinib MOA

A

VEGF inhibitors

90
Q

pazopanib, lenvatinib, vandetanib, caboztanib MOA

A

VEGF inhibitors

91
Q

what TKI has a boxed warning for QTc prolongation and requires a REMS program enrollment for prescribers?

A

vandetanib

92
Q

regorafenib, cabozantinib, sorafenib, axitinib, and sunitinib cause what dose-limiting toxicity?

A

hand-foot skin reaction

93
Q

what organ is at special risk for adverse effects with TKI inhibitors of angiogenesis?

A

thyroid, thought to be because it is a highly vascular organ

94
Q

what VEGF TKI carries a boxed warning for perforations, fistulas, and hemorrhage

A

cabotazantinib

95
Q

minor adverse effect that occurs more often with sorafenib, axitinib, regorafenib, and lenvantinib

A

voice changes, often described as hoarseness

96
Q

what grade of hand-foot skin reaction should prompt reduction of VEGF TKI for at least a week

A

grade 2, painful skin changes that limit ADLs

97
Q

what grade of hand-foot skin reaction should prompt interruption of a VEGF TKI for at least a week

A

grade 2, skin changes that limit self-care ADLs

98
Q

what measures should be taken for grade 1 VEGF TKI related hand foot skin reaction?

A

continue current dose level, initiate supportive care measures

99
Q

pembrolizumab, nivolumab, cemiplimab MOA

A

anti-PD-1

100
Q

atezolimab, avelumab, durvalumab, ipilimumab MOA

A

anti-PD-L1

101
Q

typical timeframe for dermatologic AEs with immune checkpoint inhibitors

A

2 weeks

102
Q

typical timeframe for GI AEs with immune checkpoint inhibitors

A

7 weeks

103
Q

typical timeframe for endocrine related AEs with immune checkpoint inhibitors

A

9 weeks

104
Q

typical timeframe for hepatic AEs with immune checkpoint inhibitors

A

12 weeks

105
Q

which immune checkpoint inhibitor class had a 72% incidence of any grade toxicicity, and 24% incidence of high grade toxicity?

A

CTLA-4 inhibitors

106
Q

which immune checkpoint inhibitor class had a 30% incidence of any grade toxicicity, and 5-8% incidence of high grade toxicity?

A

PD-1/PD-L1 inhibitors

107
Q

what was the toxicity rate (any grade) for combined CTLA-4 and PD-1/PD-L1 inhibitor therapy?

A

96%

108
Q

what is the toxicity rate (high grade) for CTLA-4 inhibitor therapy?

A

55-60%

109
Q

starting prednisone dose for grade 2 dermatologic AE for an ICI

A

0.5 mg/kg/day

110
Q

starting prednisone dose for general grade 2 AE for an ICI

A

1 mg/kg/day

111
Q

starting prednisone dose for grade 3 or 4 AE for an ICI

A

2 mg/kg/day or use IV methylprednisolone

112
Q

what is the threshold dose and duration of prednisone to use prophylaxis for pneumocystis jiroveci pneumonia?

A

20 mg daily or more for 4 or more weeks

113
Q

what is the threshold dose and duration of prednisone to use prophylaxis for fungal infections? What agent may be considered?

A

20 mg daily or more for 6-8 or more weeks, fluconazole

114
Q

when should h2 blocker or a PPI be used for prophylaxis for GI side effects from steroids?

A

anticoagulation, NSAID use, PUD, or other GI bleeding risk

115
Q

what is the threshold duration of prednisone to use prophylaxis for osteoporosis? What agent may be considered?

A

6-8 weeks, calcium and vitamin D

116
Q

agent used in several autoimmune diseases that can be used in steroid refractory colitis but not refractory hepatitis?

A

infliximab

117
Q

what organization publishes guidance on immunotherapy related toxicities?

A

NCCN

118
Q

what combination therapy uses 6 drugs and is divided into small doses to be given more than once a day

A

hyperCVAD (hyper stands for hyperfractionated)

119
Q

targets CD3 and CD19 receptors, indicated for B-cell ALL.

A

blinatumomab, a bispecific antibody

120
Q

inotuzumab ozogamicin targets the CD22 receptor. What is its MOA and initial indication?

A

ADC, B-Cell ALL

121
Q

ado-trastuzumab emtansine
gemtuzumab ozogamicin
brentuximab vedotin
inotuzumab ozogamicin
polatuzumab vedotin

are all what class of drug?

A

antibody-drug conjugates (ADCs)

122
Q

what potentially life threatening condition may present with hypotension, fever, and o2 desaturation?

A

cytokine release syndrome (CRS)

123
Q

cytokine release syndrome (CRS) is managed with what measures?

A

infusion cessation, fluid resuscitation, broad spectrum antibiotics, and moderate doses of dexamethasone for severe cases.

124
Q

IL6-receptor blockade with tocilizumab can be cautiously considered to treat refractory cases of what clinical syndrome?

A

cytokine release syndrome (CRS)

125
Q

what syndrome presents with tremor, aphasia, confusion, LOC, seizure, and global encephalopathy

A

immune effector cell (IEC) associated neurotoxicity syndrome (ICANS)

126
Q

How to manage immune effector cell (IEC) associated neurotoxicity syndrome (ICANS)?

A

infusion cessation, moderate doses of dexamethasone for severe cases, potentially anti-epileptic drugs. Tocilizumab not utilized, theoretically could exacerbate neurologic complications.

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