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oncology > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

difference between cancer and abnormal growth

A

abnormal growth only becomes cancerous when it spreads out to its surrounding environment

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2
Q

phases of carcinogenesis

A
  1. initiation
  2. promotion
  3. progression
  4. metastasis
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3
Q

naming cancer: prefixes

A

benign is prefix + “oma”
malignant is prefix + “carcinoma, sarcoma, or blastoma”e

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4
Q

exceptions to naming cancer: prefixes

A

lymphoma is malignant tumor from lymphocyte
mesothelioma is malignant tumor from mesothelium
seminoma is malignant germ cell tumor

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5
Q

prefix for fat

A

lipo

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6
Q

prefix for bone

A

osteo

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7
Q

prefix for fibrous tissue

A

fib

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8
Q

prefix for cartilage

A

chondro

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9
Q

prefix for blood vessel

A

hemangio

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10
Q

prefix for smooth muscle

A

leiomyo

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11
Q

prefix for striated muscle

A

rhabdomyo

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12
Q

prefix for gland

A

adeno

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13
Q

what is carcinoma

A

malignant neoplasm of epithelial origin/cancer of the internal or external lining of the bodyw

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14
Q

what is sarcoma

A

cancer that originates in supportive & connective tissues such as bones, tendons, cartilage, muscle, fat

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15
Q

what is myeloma

A

cancer that originates in the plasma cells of the bone marrow

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16
Q

what is blastoma

A

cancer derived from premature precursor cells or embryonic tissue

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17
Q

what is leukemia

A

cancer of the bone marrow

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18
Q

what is lymphoma

A

solid cancers that develop in the glands or nodes of the lymphatic system

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19
Q

TNM stages?

A

T(1-4) the size and extent of the main tumor
N (0-3) the number of nearby lymph nodes that have cancer
m (0-1) metastasis

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20
Q

overall stage grouping system

A

stages 0-4

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21
Q

stage 0

A

carcinoma in situ, abnormal cells growing in their normal place

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22
Q

stage 1

A

tumor is contained within organs

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23
Q

stage 2

A

larger tumor within organ, little lymph node involvement

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24
Q

stage 3

A

tumor has spread to lymph nodes

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25
Q

stage 4

A

metastasis

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26
Q

germline vs somatic genetic variants

A

germline can be passed on to offspring (present in egg/sperm, all cells carry the variant)

somatic arise during an individual’s lifetime, are not passed on (only the tumor carries the variant, occur in non-germline tissue)

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27
Q

oncogenes

A

promote unregulated cell growth

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28
Q

types of oncogenes

A

growth factors
receptor tyrosine kinases
cytoplasmic tyrosine kinases
serine/threonine kinases
GTPase signaling
transcription factors

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29
Q

tumor suppressor genes

A

regulate and inhibit inappropriate cell growth

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30
Q

TSP functions

A

cell cycle arrest/apoptosis
protein phosphatase
inhibit growth-promoting signal transduction
ubiquitin ligase
master brake of cell cycle
cell adhesion & migration
DNA repair

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31
Q

difference btwn oncogene and TSP

A

a single genetic event can activate an oncogene (dominant)
multiple mutations are required to inactivate a TSP (recessive)

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32
Q

knudson hypothesis

A

cancer is the result of accumulated mutations to a cell’s DNA

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33
Q

cancer cells favor ____>_______

A

glycolysis > oxidative phosphorylation

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34
Q

cancers exhibit increased demand for _____ which can be therapeutic targets

A

specific amino acids

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35
Q

treatment modality that is local and non-targeted

A

radiation

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36
Q

treatment modality that is local and targeted

A

surgery

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37
Q

treatment modality that is systemic and non-targeted

A

chemotherapy

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38
Q

treatment modality that is systemic and targeted

A

targeted therapies

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39
Q

adjuvant therapy

A

to eradicate residual cancer after primary surgery

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40
Q

neoadjuvant therapy

A

to shrink large, locally advanced disease to enable surgical resection

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41
Q

induction therapy

A

1st treatment for a disease, aims to achieve a rapid reduction in tumor burden or disease activity

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42
Q

consolidation therapy

A

post-remission therapy to eradicate any remaining disease

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43
Q

maintenance therapy

A

to prevent cancer from recurring

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44
Q

palliative therapy

A

to increase survival and improve quality of life by symptom control for advanced, incurable cancer

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45
Q

cycle

A

a period of chemo treatment followed by a period of rest

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46
Q

what dictates cycles

A

cancer, stage, individual, toxicity risk
balance with toxicities (more frequent cycles enhances tumor effects but increases toxicities)
also determined by PK of drug

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47
Q

inhibition of HDAC or DNMT does what

A

restores tumor suppressor gene expression

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48
Q

mechanism of CDK4/6 inhibitors

A

prevent Rb protein phosphorylation which prevents cell transition from G1 to S, leads to cell cycle arrest and apoptosis

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49
Q

generic naming formula of targeted therapies

A

prefix (variable) + substem + stem

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50
Q

substem cir

A

circulatory system is target

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51
Q

substem lim

A

immune system is target

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52
Q

substem tu

A

tumor is target

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53
Q

substem ximab

A

chimeric human mouse

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54
Q

substem zumab

A

humanized mouse

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55
Q

substem mumab

A

fully human

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56
Q

stem mAb

A

monoclonal antibody

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57
Q

stem ib

A

small molecule w/ inhibitory properties

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58
Q

tinib

A

tyrosine kinase inhibitor

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59
Q

zomib

A

proteasome inhibitor

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60
Q

ciclib

A

cyclin-dependent kinase inhibitor

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61
Q

parib

A

poly-ADP-ribose polymerase inhibitor

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62
Q

anti CTLA-4 targets _____

A

CD28 pathway

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63
Q

anti PD-1 targets _____

A

TCR pathway

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64
Q

anti-CTLA-4 primarily affects ____

A

CD4+ T cells

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65
Q

anti PD-1 primarily affects _____

A

CD8+ T cells

66
Q

which (anti-CTLA-4 or PD-1) can move T cells into tumors

A

anti-CTLA-4

67
Q

which (anti-CTLA-4 or PD-1) expands clonal diversity

A

anti CTLA-4

68
Q

______ is required before CAR T cell infusion

A

lymphodepleting conditioning therapy

69
Q

what does lymphodepleting conditioning therapy consist of

A

fludarabine 30 mg/m2 IV daily x 4 days
cyclophosphamide 500 mg/m2 IV daily x 2 days (starting w/ first dose of fludarabine)

70
Q

what are the common complications of CAR T cell infusion

A

Cytokine release syndrome (CRS) and neurotoxicity

71
Q

how is prodromal CRS managed

A

observe, antibiotics per local guidelines if neutropenic, and symptom management

72
Q

how is overt CRS managed

A

antipyretics, O2, IV fluids, low dose vasopressors

73
Q

how is severe CRS managed

A

high dose/multiple vasopressors, O2/mechanical ventilation, tocilizumab

74
Q

how is grade 2-3 neurotoxicity managed

A

dexamethasone 10 mg IV q6h
until grade 1 then taper x 3 days

75
Q

how is grade 4 neurotoxicity managed

A

methylprednisolone 1000 mg IV x 3 days, then manage as 2/3

76
Q

which classes of cancer drugs work by DNA damage

A

alkylating agents and antitumor antibiotics

77
Q

which drugs are alkylating agents

A

cyclophosphamide
carmustine
cisplatin

78
Q

how do alkylating agents work

A

via crosslinking of guanine bases

79
Q

which drugs are antitumor antibiotics

A

doxorubicin
daunorubicin
bleomycin

80
Q

how do the antitumor antibiotics work

A

via DNA intercalation

81
Q

which classes of cancer drugs work by interfering with DNA synthesis

A

topoisomerase inhibitors and antimetabolites

82
Q

which drugs are topoisomerase inhibitors

A

irinotecan
topotecan
etoposide

83
Q

how do topoisomerase inhibitors work

A

by blocking DNA strand re-ligation during DNA synthesis

84
Q

which drugs are antimetabolites

A

methotrexate
mercaptopurine
5-fluorouracil
cytarabine
capecitabine
gemcitabine
trifluridine and tipiracil

85
Q

how do antimetabolites work

A

incorporated into DNA/RNA and inhibit nucleic acid synthesis

86
Q

which classes of cancer drugs work on translation/cell division

A

microtubule inhibitors & nutrient deprivation

87
Q

which drugs are microtubule inhibitors

A

paclitaxel
cabazitaxel
docetaxel
vincristine
eribulin

88
Q

how do microtubule inhibitors work

A

inhibit tubulin polymerization or function

89
Q

which drug works by nutrient deprivation

A

asparaginase

90
Q

how does asparaginase work

A

inhibition of protein synthesis

91
Q

which drug classes work as targeted therapies on the “go” signals

A

hormonal agents and epigenetic agents

92
Q

which drug classes fall under hormonal agents

A

SERMs
aromatase inhibitors
LHRH agonist
LHRH antagonist
antiandrogens

93
Q

which drug is a SERM

A

tamoxifen

94
Q

which drug is an aromatase inhibitor

A

anastrazole

95
Q

which drug is a LHRH agonist

A

leuprolide

96
Q

which drug is a LHRH antagonist

A

degarelix

97
Q

which drug is an antiandrogen

A

bicalutamide

98
Q

how do SERMs work

A

block the effects of estrogen in the breast tissue

99
Q

how do aromatase inhibitors work

A

inhibiting aromatase, which is an enzyme that converts androgens into estrogens

100
Q

how do LHRH agonists and antagonists work

A

lower androgen levels by decreasing LH formation or release by the pituitary gland

101
Q

how do antiandrogens work

A

block androgen receptor

102
Q

which drug classes are epigenetic agents

A

HDAC inhibitors and DNMT inhibitors

103
Q

which drug is a HDAC inhibitor

A

vorinostat

104
Q

which drug is a DNMT inhibitor

A

azacitidine

105
Q

how do HDAC inhibitors work

A

blocks deacetylation by HDAC and restores expression of tumor suppressor genes

106
Q

how do DNMT inhibitors work

A

blocks methylation of promoters & restores expression of tumor suppressor genes

107
Q

which drug classes are targeted therapies NOT for “go” signals i.e. other random targets

A

angiogenesis inhibitors, proteasome inhibitors, CDK4/6 inhibitors, PARP inhibitors

108
Q

which drug is an angiogenesis inhibitor

A

bevacizumab

109
Q

how do angiogenesis inhibitors work

A

targeting VEGF

110
Q

which drug is a proteasome inhibitor

A

carfilzomib

111
Q

how do proteasome inhibitors work

A

lead to accumulation of misfolded proteins leading to induction of cancer cell apoptosis

112
Q

which drugs are CDK4/6 inhibitors

A

ribociclib
palbociclib
abemaciclib

113
Q

how do CDK4/6 inhibitors work

A

prevent phosphorylation of Rb

114
Q

which drugs are PARP inhibitors

A

olaparib
niraparib
rucaparib

115
Q

how do PARP inhibitors work

A

prevent double-stranded DNA damage repair in BRCA-deficient cells

116
Q

what are two major classes of immunotherapies

A

checkpoint inhibitor antibodies
CAR T cell therapy

117
Q

which checkpoint inhibitor targets CTLA-4

A

ipilimumab

118
Q

which checkpoint inhibitors target PD-1

A

nivolumab
pembrolizumab
dostarlimab
cemiplimab

119
Q

which checkpoint inhibitors target PD-L1

A

atezolizumab
avelumab
durvalumab

120
Q

which checkpoint inhibitor targets LAG3

A

relatlimab

121
Q

which CAR therapy
targets CD19
costimulatory 4-1BB

A

kymirah
breyanzi

122
Q

which CAR therapy
targets CD19
costimulatory CD28

A

yescarta
tecartus

123
Q

which CAR therapy
targets BCMA
costimulatory 4-1BB

A

abecma

124
Q

which CAR therapy
targets BCMAx2
costimulatory 4-1BB

A

carvykti

125
Q

what are the types of abnormal cell growth

A

hypertrophy (size)
hyperplasia (number)
metaplasia (change)
dysplasia (disordered)

126
Q

6 cancer hallmarks

A
  1. produce go signals
  2. override stop signals
  3. angiogenesis
  4. evade immune surveillance
  5. resist cell death
  6. energy metabolism
127
Q

what is the difference between chemotherapy vs targeted therapy target-wise

A

chemo targets rapidly dividing cells
targeted acts on cancer-specific molecular targets

128
Q

chemo is cyto___ while targeted therapy is cyto___

A

chemo cytotoxic
targeted cytostatic

129
Q

what is the difference between chemotherapy vs targeted therapy specificity-wise

A

chemo is specific for rapidly dividing cells
targeted has a higher specificity for cancer cells

130
Q

what is the difference between chemotherapy vs targeted therapy toxicity-wise

A

chemo is toxic to any fast growing cell
targeted is toxic to normal cells with the specific target

131
Q

anti-CTLA-4 vs anti-PD-1: which one has a significant recurrence after response

A

PD-1

132
Q

common immune side effects to see with immune checkpoint blockers?

A

colitis
dermatitis
hepatitis
endocrinopathy

133
Q

how do you monitor dermatitis

A

exam, biopsy skin

134
Q

first line dermatitis

A

topical/oral steroids

135
Q

how do you monitor endocrinopathy

A

signs are fatigue, hypotension, metabolic changes
monitor TSH, T4, cortisol, ACTH

136
Q

first line endocrinopathy

A

hormone replacement

137
Q

how do you monitor hepatitis

A

usually asymptomatic, monitor AST/ALT

138
Q

first line hepatitis

A

oral steroids

139
Q

how do you monitor colitis

A

clinical, endoscopy
signs are diarrhea, abdominal pain

140
Q

first line colitis

A

oral steroids

141
Q

BCR-ABL inhibitor

A

Imatinib
Dasatinib
Ponatinib
Nilotinib

142
Q

BRAF inhibitors

A

Dabrafenib
Vemurafenib

143
Q

EGFR inhibitors

A

Erlotinib
Afatinib
Gefitinib
Lapatinib
Cetuximab
Osimertinib
Panitumamib

144
Q

what is micromedex good for

A

off label indications
dose adjustments
drug interactions
ADME

145
Q

what is NCCN good for

A

chemo regimen recs
diagnosis & stage specific
tumor marker-directed
evidence-based
frequent updates

146
Q

what is hemonc.org good for

A

chemo regimen compendium
diagnosis & stage specific
tumor marker directed
evidence based
frequently updated

147
Q

what is NIH daily med good for

A

package insert PDFs- generic and tradename
boxed warnings
inactive ingredients– excipients & preservatives

148
Q

when do you need to recalculate BSA

A

when weight loss or gain of >10%

149
Q

how to calculate % change in weight

A

change in weight/initial weight x 100%

150
Q

which body weight do you use to calculate BSA for chemo

A

actual body weight (using ideal/adjusted risks treatment failure)

151
Q

ANC level you want to ensure patients are at for chemotherapy

A

> 1500

152
Q

platelets level you want to ensure patients are at for chemotherapy

A

> 100k

153
Q

calvert formula

A

dose (mg)= target AUC x (GFR+25)

154
Q

AST upper limit normal

A

36

155
Q

ALT upper limit normal

A

56

156
Q

CrCL formula

A

[(140-age) x IBW]/(SCr x 72) x 0.85 if female

157
Q

IBW

A

women: 45.5 + 2.3 per every inch >5 feet
men: 50 + 2.3 per every inch >5 feet

158
Q

Adjusted body weight

A

IBW + 0.4(ABW-IBW)

159
Q

when do you use adjusted body weight

A

when their actual body weight is 25% or more over IBW

160
Q

BSA

A

square root of [(cm x kg) / 3600]

oncology (19 decks)

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