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Oncology Class > Final exam > Flashcards

Final exam Flashcards

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1
Q

What are opioid conversions?

A

Morphine - 10mgIV = 30mgPO
Oxycodone - 20mgPO
Hydromorphone - 1.5mgIV = 7.5mgPO

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2
Q

What is length time bias?

A

Asymptomatic patients are more likely to have less aggressive malignancies, so screening appears to increase survival time

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3
Q

What factors affect the number needed to screen?

A

Frequency of testing
Prevalence of disease
Duration of follow-up

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4
Q

Cervical cancer screening guidelines

A

<21: no screening
21-65: pap q3y OR pap/HPV q5y (age 30+)
>65: no screening unless high risk

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5
Q

Breast cancer screening guidelines

A

40-49: pt discussion
50-74: q2y mammo
>75: no mammo

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6
Q

Lung ca screening guidelines

A

50-80 AND >20py OR currently smoking OR smoking in last 15 yrs = q1y LDCT

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7
Q

Prostate ca screening guidelines

A

55-69: joint decision making
>70: no screening

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8
Q

Colon ca screening guidelines

A

45-75: q10y colonoscopy
76-85: pt discussion
>85: no screening

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9
Q

What is the difference between Sanger and NGS?

A

Sanger: sequences one fragment at a time, good for small analysis
NGS: sequences millions of fragments simultaneously

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10
Q

What is a diagnostic biomarker? Example?

A

Characteristic that indicates what disease the patient has. Melan-a

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11
Q

What is a prognostic biomarker? Example

A

A marker that indicates risk of disease recurrence. Oncotype DX DCIS score

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12
Q

What is a predictive biomarker? Example

A

marker that indicates what treatment will most likely benefit the patient. NGS for solid tumors

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13
Q

what is a pharmacokinetic biomarker? example?

A

marker that indicates what drug dose should be given to the patient. G6PD for rasburicase.

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14
Q

How do you treat MSI-high CRC?

A

PD-1 blockade (pembro)

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15
Q

What molecular markers should you check for stage IV CRC?

A

KRAS, NRAS, BRAF, MSI, HER2 (BRHNK mnemonic)

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16
Q

How do you treat BRAF V600E stage IV CRC?

A

BRAF/MEK (can lead to phenotype switch to MMR deficient)

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17
Q

How do you treat HER2 stage IV CRC?

A

trastuzumab + TKI (better than TKI alone)

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18
Q

Why has KRAS been considered undruggable?

A

binding pocket on GTPase is hard to access, approaches have had high toxicity

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19
Q

How do you treat KRAS+ stage IV CRC?

A

Can use adagrasib + chemo (cetuximab)

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20
Q

MOA enzalutamide, darolutamide, apalutamide

A

binds to the androgen receptor to prevent androgen signaling

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21
Q

MOA abiraterone

A

blocks 17alpha-hydroxylase, reduces production of T

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22
Q

docetaxel MOA

A

inhibits microtubule formation (S phase)

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23
Q

MOA PARPis

A

stabilizes single-stranded DNA breaks, this inhibition gives time for a double-stranded break to form and the cell to apoptose

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24
Q

when do you test for somatic/germline mutations in prostate cancer?

A

metastatic disease

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25
what is the ideal ratio of basal:demand for PCA?
2:1 (1:2 if prominent incident pain)
26
how do you determine basal rate for PCA?
determine total opioid in 24hr, convert to IV hourly rate, put 75% in basal considering cross-tolerance
27
what are three common mutations in AML?
DNMT3A (enzyme that catalyzes DNA methylation) FLT3 (TK cytokine receptor) IDH1
28
How does DNMT3A cause cells to be pre-leukemic?
biases fate decisions toward self-renewal rather than differentiation
29
what is 7+3 treatment?
common treatment for AML 7days cytarabine, 3 days daunorubicin
30
what is CPX-351?
a capsule containing both cytarabine and daunorubicin, delivers drug into the intracellular space, maintains ratio, does not rely on transporters
31
what is gemtuzimab? where does it bind?
a mab attached to chemotherapy (ozogamicin). binds CD33 --> brought into endosome, degraded by lysosome, chemo is released into the cytoplasm and can make its way to the nucleus
32
what is venetoclax?
blocks Bcl2, leading to cell death used in AML
33
What is azacitidine
a hypomethylating agent (typically reserved for patients ineligible for induction
34
What is quizartinib? AEs?
FLT3 blocker for AML, QT prolongation
35
What is ivosidenib? AEs?
IDH1 blocker, differentiation syndrome
36
what is differentiation syndrome?
increased cytokine release and rapid differentiation of myeloid precursor cells. leads to fever, weight gain, peripheral edema, hypotension, acute renal failure, interstitial pulmonary infiltrates
37
what are the stages of multiple myeloma?
initiation --> MGUS --> smoldering myeloma --> MM (intramedullary to extramedullary)
38
what is bortezomib?
treatment for MM binds proteosome, prevents degradation of pro-apoptotic factors, leads to programmed cell death
39
red flags for hereditary cancer
early age of diagnosis same types of cancer in close relatives, multiple generations less common cancers multiple cancers associated with same gene Ashkenazi Jewish
40
when is radiation therapy necessary post-mastectomy?
>=4LNs+ OR >=5cm
41
what patients are more likely to benefit from endocrine therapy than chemo?
lobular histology, low grade, strong ER expression, low oncotype score
42
list 4 actionable mutations in breast cancer
BRCA1/2 - PARPi ESR1 - elecestrant PIK3CA - alpelisib PI3K, PTEN, AKT1 - capivasertib
43
what is pancreatic cancer association with depression?
tumors make IDO1, shunts tryptophan away from serotonin synthesis, instead makes kynurenine
44
What do you have to keep in mind with fluoxetine, paroxetine, bupropion use?
CYP2D6 inhibitors, interfere with tamoxifen
45
what are the four steps of pre-clinical drug discovery?
target identification hit generation lead generation preclinical studies in animals
46
What are four characteristics important to be a successful drug candidate?
high potency favorable pharmocokinetics developability good toxicity profile
47
How does a PROTAC work?
binding of E3 ligase to target protein, ubiquitination and destruction of protein
48
which cancers have the most diverse somatic mutations?
lung adenocarcinoma, stomach, head and neck
49
What mechanisms contribute to the mutational spectra of melanoma, GI tumors, lung cancer?
melanoma- w/ and w/o UV factors GI tumors- w/ and w/o MMR lung cancer- w/ and w/o exposure to environmental carcinogens (cigarette smoke)
50
Why do BRAF inhibitors not work in CRC?
EGFR is upregulated at baseline, mediates MAPK signaling through RAS shortly after deactivation of BRAF
51
What are the phases of CML?
Chronic (<10% blasts) - luekocytosis, hypercellular marrow Advanced Accelerated (10-19% blasts, basophils, platelets, splemomegaly) Blast phase (<20% blasts)
52
what is the most frequent gatekeeper mutation in CML?
T315I
53
list mechanisms of acquired resistance to targeted therapy
gatekeeper mutations bypass pathways mutations in pathways downstream of oncogene morphological change persistence of cancer stem cells changes in microenvironment
54
three genes most commonly mutated in SCLC?
RB1, p53, KMT2d (small park)
55
lung adenocarcinoma most common mutations
p53, EGFR, KRAS (peak-ras)
56
lung SCC most common mutations
p53, CDKN2A, KMT2d (pecks)
57
indications for immunotherapy in NSCLC
advanced: PDL1>50% pembro, PDL1<50% pembro+chemo, stage III, N2 and N3
58
side effects of checkpoint inhibitors
pneumonitis, myocarditis, myositis, nephritis, colitis, hepatitis
59
what is the warburg effect?
cancer cells replace normal oxygen respiration with fermentation of sugar shunt pyruvate to lactate, foregoing the efficient oxidative phosphorylation for the quicker aerobic glycolysis
60
how does obesity lead to higher risk for cancer?
obesity causes chronic inflammation (oncogenic) tumors activate oncogenes that lead to inflammation, obese tissue is conducive high leptin:adiponectin ratio in adipose tissue creates an environment conducive to cell proliferation
61
how does estrogen drive ER+ breast cancer
ER dependent: binds to ER, acts as TF for genes including MYC, Bcl2, and FOXM1 ER independent: metabolism of estrogen in cytoplasm leads to metabolites with genotoxic effects
62
what are effects of phytoestrogens on the estrogen receptor?
low concentrations in vitro: promote tumor growth high concentrations in vitro: inhibit tumor growth
63
what are the steps involved in metastasis?
development of metastatic cell establishment of premetastatic niche motility and invasion intravasation dissemination and transport cellular arrest, vascular adhesion, extravasation colonization
64
name 3 ways surgery can induce inflammatory responses
immunosuppression (systemic) NETs - associated with metastatic risk neovascularization
65
nonsynonymous mutation that leads to cancer?
PTEN
66
common copy number variant?
HER2
67
common in/del?
EGFR exon 19 del
68
common frameshift mutation
PTEN c800delA (premature stop codon)
69
common splice site mutation
KIT in GIST
70
common structural variant
ALK fusion in NSCLC
71
how is sanger sequencing used in cancer (specific example)?
1790T>G in BRAF
72
primary goals of cancer phase I trials
identify DLT and MTD
73

Oncology Class (1 decks)

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