08.26 - Pharmacology of Lung Cancer (Sweatman) - Questions Flashcards

(58 cards)

1
Q

Drug used for non-squamous NSCLC only

A

Bevacizumab

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2
Q

Which subtype harbors EGFR mutation

A

Adenocarcinoma

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3
Q

Why no Bevacizumab in Squamous Cell

A

High risk of bleeding

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4
Q

KRAS mutation can render __ drugs ineffective

A

Anti-EGFR

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5
Q

In what subtype is EML4-ALK more prevalent

A

2-7% of NSCLC, more in adeno

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6
Q

What type of patients are likely to have EML4-ALK

A

Nonsmokers, Light Smoking, Adeno

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7
Q

EML4-ALK produces activation of

A

MEK/ERK Pathway

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8
Q

Inhibitor of EML4-ALK

A

Crizotinib

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9
Q

Problem in TKI administration

A

Orally administered - Must be absorbed

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10
Q

Mutations (4) more common in Non-smokers

A

EGFR, EML4-ALK, HER2, hMSH2

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11
Q

What percent of patients have actionable mutations

A

60%

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12
Q

Top 3 mutations, in order, in adenocarcinomas

A

KRAS, EGFR, ALK

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13
Q

Which subtype of tumor should have mutation testing

A

Adenocarcinoma

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14
Q

Test for EGFR

A

DNA seq

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15
Q

Test for EML4-ALK

A

FISH

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16
Q

Treatment rationale for SCLC

A

Met occurs early so chemo/radiation is only option

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17
Q

Treatment rationale for NSLC

A

Surgical recision if early stage, Genetic testing if adeno

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18
Q

Standard treatment for SCLC

A

Etoposide + Cisplatin or Carboplatin

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19
Q

Standard treatment for NSCLC

A

Cisplatin + Taxel or other; Maintenance w/ Pemetrexed; Targeted; Bevacizumab if non-squamous

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20
Q

General MOA of Pemetrexed

A

DHFR inhibitor

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21
Q

General MOA of -platins

A

Form DNA intrastrand crosslinks and adducts

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22
Q

General MOA of Cyclophosphamide

A

Alkylating

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23
Q

General MOA of - Taxels

A

Microtubule stabilizer inhibiting de-polymerization

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24
Q

General MOA of Doxorubicin

A

Intercalator, Free Radicals, Topo 2 inhibition

25
General MOA of Etoposide
DNA Topo 2 stabilizer
26
General MOA of Gemcitabine
DNA polymerase inhibitor
27
General MOA of Isfosfamide
Cross linker
28
General MOA of -Tecans
DNA Topo 1 stabilizer
29
General MOA of Vinca Alkyloids
Microtubule inhibitor
30
Toxicity of Carboplatin
Blood chemistry dyscrasia
31
Toxicity of Cisplatin
Nephro- and Oto-toxicity
32
Toxicity of Cyclophosphamide
Hemorrhagic Cystitis (Mesna is protective), Pulmonary Fibrosis
33
Toxicity of Docataxel
Sensory neuropathy
34
Toxicity of Doxorubicin
CHF - Cardiotoxicity
35
Toxicity of Etoposide
Infection, Alopecia
36
Toxicity of Gemcitabine
Arthralgia
37
Toxicity of Ifosfamide
Neurotoxicity, Renal failure (<10%)
38
Toxicity of Irinotecan
Typical
39
Toxicity of Paclitaxel
Myalgia and Arthralgia
40
Toxicity of Pemetrexed
Elevated LFTs and Creatinine
41
Toxicity of Topotecan
Hyperbilirubinemia
42
Toxicity of Vinblastine
Neuropathic; Never give intrathecal
43
Toxicity of Vinorelbine
Neutropenia; Never give intrathecal
44
2 notable toxicities of Erlotinib
Rash; Interstitial lung-disease-type events
45
General MOA of Afatinib
Covalent inhibitor of EGRF, HER2, and HER4
46
2 most notable toxicities of Afatinib
Diarrhea, Rash
47
Covalent inhibitor of EGRF, HER2, and HER4
Afatinib
48
Advantage of Afatinib
Less toxic than Erlotinib
49
Mutation that confers resistance of EGFR to TKI's
T790M
50
T790M mutation restores
ATP affinity of EGFR to WT levels
51
2 notable toxicites of Crizotinib
GI, Visual Disorders
52
General MOA of Crizotinib
Multi-kinase inhibitor, including ALK
53
Sims and Diffs in toxicities of Erlotinib and Crizotinib
Both liver and eye; erlotinib rash, much less rash in crizotinib
54
TKI's that are CYP substrates
Crizotinib, Erlotinib
55
Mutation that confers resistance to Crizotinib
G2032R ROS1
56
MOA of Bevacizumab
Receptor of VEGFR fused to Fc fragment of an antibody - Prevents VEGF from binding its endogenous receptor sites
57
2 notable toxicities of Bevacizumab
HTN/Thromboembolism; Fistula
58
What subtype has highest adverse effects with Bevacizumab
Squamous - don’t use