antineoplastic agents Flashcards

(126 cards)

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
cetuximab indication(s)
colorectal cancer and head and neck cancer
26
panitumumab indication(s)
colorectal cancer
27
dabrafenib and trametinib inhibit what pathway?
BRAF and MEK
28
necitumumab indication(s)
NSCLC
29
trastuzumab indication(s)
breast cancer, gastric cancer, and gastroesophageal junction cancer
30
trastuzumab MOA
HER2 inhibitor
31
pertuzumab MOA
HER2 inhibitor
32
lapatinib MOA
HER2 inhibitor
33
neratinib MOA
HER2 inhibitor
34
name 2 oral HER2 inhibitors
lapatinib and neratinib
35
ado-trastuzumab emtansine MOA
Antibody-Drug Conjugate
36
3 main adverse effects of HER2 inhibitors
cardiotoxicity, diarrhea, rash
37
which class of drugs requires a baseline and every 3 months echocardiogram
HER2 inhibitors
38
which HER2 inhibitor also inhibits EGFR and requires monitoring for liver toxicity?
lapatinib
39
cobimetinib MOA
MEK inhibitor
40
dabrafenib MOA
BRAF inhibitor
41
trametinib MOA
MEK inhibitor
42
encorafenib MOA
BRAF inhibitor
43
binimetinib MOA
MEK inhibitor
44
vemurafenib MOA, indication
BRAF inhibitor, melanoma
45
vemurafenib/cobimetinib indication(s)
Melanoma, Erdheim-Chester disease
46
dabrafenib/trametinib indication(s)
melanoma, thyroid cancer, NCLSC
47
encorafenib/binimetanib indication(s)
melanoma
48
what is the function of the interaction between PD-L1 on normal cells and PD-1 on CD8 positive (killer) t-cells?
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
49
suffix -tinib indicates
tyrosine kinase inhibitor, example lapatinib
50
suffix -anib
angiogenesis inhibitor
51
suffix -zomib
proteosome inhibitor
52
suffix -rafenib
BRAF inhibitor
53
t or tu naming convention indicates which target
tumor
54
ci naming convention indicates which target
circulatory system
55
li or l naming convention indicates which target
immunomodulation
56
mo naming convention indicates which source for monoclonal antibodies
mouse
57
xi naming convention indicates which source for monoclonal antibodies
chimeric, combining genetic material from a non-human species and genetic material from a human being
58
zu naming convention indicates which source for monoclonal antibodies
humanized, mostly derived from a human source, with small regions derived from non-human species
59
u naming convention indicates which source for monoclonal antibodies
human
60
HDAC stands for
histone deacetylase inhibitor
61
HDAC inhibitors MOA
inhibites histone deacetylase, blocking chromatin closure and inhibiting transcription, which leads to cell cycle arrest and cell death
62
PARP stands for
poly ADP ribose polymerase inhibitor
63
PARP inhibitor MOA
block PARP enzyme, which normally repairs damaged DNA. This leads to cell death
64
proteasome inhibitor MOA
block the degradation of excess or damaged proteins, leading to a variety of effects including apoptosis, migration, and decreased proliferation and angiogenesis
65
class of drugs that target CTLA-4, PD-1, or PD-L1
immune checkpoint inhibitors
66
cytotoxic lymphocyte associated protein 4 is targeted by what class of drugs
immune checkpoint inhibitors
67
this class of drugs uses a single molecule to bind 2 different and unique antigen binding sites
bispecific antibodies
68
One drug in this class takes advantage of increased CD-30 expression on Reed-Sternberg cells
ADCs (antibody drug conjugates)
69
vorinostat MOA, route, indication(s)
oral HDAC inhibitor indicated for CTCL
70
romidepsin MOA, route, indication(s)
IV HDAC inhibitor indicated for CTCL, PTCL
71
belinostat MOA, route, indication(s)
IV HDAC inhibitor indicated for PTCL
72
panobinostat MOA, route, indication(s)
oral HDAC inhibitor indicated for multiple myeloma
73
common HDAC inhibitor adverse effects (there are 6)
hematologic, GI, QTc prolongation, hepatotoxicity, infection, hyperglycemia
74
which HDAC carries a boxed warning for diarrhea
panobinostat
75
only PARP inhibitor not approved for ovarian cancer
talazoparib
76
primary indication for PARP therapy
BRCA1/2 mutated breast cancer
77
olaparib MOA and indication(s)
PARP inhibitor, breast, ovarian, pancreatic, and prostate cancer
78
rucaparib MOA and indication(s)
PARP inhibitor. breast, ovarian, pancreatic, and prostate cancer
79
niraparib MOA and indications(s)
PARP inhibitor. ovarian cancer
80
talazoparib MOA and indication(s)
PARP inhibitor, breast cancer
81
When the ANC drops below 1,000 it is called
neutropenia
82
normal ANC is
between 2500-6000
83
bevacizumab, ramucirumab, and ziv-aflibercept MOA
VEGF/VEGFR inhibitors
84
when taking a VEGF inhibitor, what level proteinuria should prompt a 24 hour urine protein exam?
2+ protein on dipstick or urine protein/creatinine ratio of >1.
85
when using a VEGF inhibitor, why avoid using nsaids?
bleeding concerns, hypertension
86
what syndrome presents with headache, seizures, lethargy, confusion, blindness, or other neurologic disturbances?
posterior reversible encephalopathy syndrome (PRES)
87
T or F: VEGF inhibitors are contraindicated for those with a history of a thrombotic event
F: patients with such a history may take VTE prevention medications concurrently if otherwise not contraindicated
88
what grade hemorrhage should prompt discontinuation of a VEGF inhibitor?
grade 3-4
89
sorafenib, regorafenib, sunitinib, axitinib MOA
VEGF inhibitors
90
pazopanib, lenvatinib, vandetanib, caboztanib MOA
VEGF inhibitors
91
what TKI has a boxed warning for QTc prolongation and requires a REMS program enrollment for prescribers?
vandetanib
92
regorafenib, cabozantinib, sorafenib, axitinib, and sunitinib cause what dose-limiting toxicity?
hand-foot skin reaction
93
what organ is at special risk for adverse effects with TKI inhibitors of angiogenesis?
thyroid, thought to be because it is a highly vascular organ
94
what VEGF TKI carries a boxed warning for perforations, fistulas, and hemorrhage
cabotazantinib
95
minor adverse effect that occurs more often with sorafenib, axitinib, regorafenib, and lenvantinib
voice changes, often described as hoarseness
96
what grade of hand-foot skin reaction should prompt reduction of VEGF TKI for at least a week
grade 2, painful skin changes that limit ADLs
97
what grade of hand-foot skin reaction should prompt interruption of a VEGF TKI for at least a week
grade 2, skin changes that limit self-care ADLs
98
what measures should be taken for grade 1 VEGF TKI related hand foot skin reaction?
continue current dose level, initiate supportive care measures
99
pembrolizumab, nivolumab, cemiplimab MOA
anti-PD-1
100
atezolimab, avelumab, durvalumab, ipilimumab MOA
anti-PD-L1
101
typical timeframe for dermatologic AEs with immune checkpoint inhibitors
2 weeks
102
typical timeframe for GI AEs with immune checkpoint inhibitors
7 weeks
103
typical timeframe for endocrine related AEs with immune checkpoint inhibitors
9 weeks
104
typical timeframe for hepatic AEs with immune checkpoint inhibitors
12 weeks
105
which immune checkpoint inhibitor class had a 72% incidence of any grade toxicicity, and 24% incidence of high grade toxicity?
CTLA-4 inhibitors
106
which immune checkpoint inhibitor class had a 30% incidence of any grade toxicicity, and 5-8% incidence of high grade toxicity?
PD-1/PD-L1 inhibitors
107
what was the toxicity rate (any grade) for combined CTLA-4 and PD-1/PD-L1 inhibitor therapy?
96%
108
what is the toxicity rate (high grade) for CTLA-4 inhibitor therapy?
55-60%
109
starting prednisone dose for grade 2 dermatologic AE for an ICI
0.5 mg/kg/day
110
starting prednisone dose for general grade 2 AE for an ICI
1 mg/kg/day
111
starting prednisone dose for grade 3 or 4 AE for an ICI
2 mg/kg/day or use IV methylprednisolone
112
what is the threshold dose and duration of prednisone to use prophylaxis for pneumocystis jiroveci pneumonia?
20 mg daily or more for 4 or more weeks
113
what is the threshold dose and duration of prednisone to use prophylaxis for fungal infections? What agent may be considered?
20 mg daily or more for 6-8 or more weeks, fluconazole
114
when should h2 blocker or a PPI be used for prophylaxis for GI side effects from steroids?
anticoagulation, NSAID use, PUD, or other GI bleeding risk
115
what is the threshold duration of prednisone to use prophylaxis for osteoporosis? What agent may be considered?
6-8 weeks, calcium and vitamin D
116
agent used in several autoimmune diseases that can be used in steroid refractory colitis but not refractory hepatitis?
infliximab
117
what organization publishes guidance on immunotherapy related toxicities?
NCCN
118
what combination therapy uses 6 drugs and is divided into small doses to be given more than once a day
hyperCVAD (hyper stands for hyperfractionated)
119
targets CD3 and CD19 receptors, indicated for B-cell ALL.
blinatumomab, a bispecific antibody
120
inotuzumab ozogamicin targets the CD22 receptor. What is its MOA and initial indication?
ADC, B-Cell ALL
121
ado-trastuzumab emtansine gemtuzumab ozogamicin brentuximab vedotin inotuzumab ozogamicin polatuzumab vedotin are all what class of drug?
antibody-drug conjugates (ADCs)
122
what potentially life threatening condition may present with hypotension, fever, and o2 desaturation?
cytokine release syndrome (CRS)
123
cytokine release syndrome (CRS) is managed with what measures?
infusion cessation, fluid resuscitation, broad spectrum antibiotics, and moderate doses of dexamethasone for severe cases.
124
IL6-receptor blockade with tocilizumab can be cautiously considered to treat refractory cases of what clinical syndrome?
cytokine release syndrome (CRS)
125
what syndrome presents with tremor, aphasia, confusion, LOC, seizure, and global encephalopathy
immune effector cell (IEC) associated neurotoxicity syndrome (ICANS)
126
How to manage immune effector cell (IEC) associated neurotoxicity syndrome (ICANS)?
infusion cessation, moderate doses of dexamethasone for severe cases, potentially anti-epileptic drugs. Tocilizumab not utilized, theoretically could exacerbate neurologic complications.