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Pulmonary > PHARM: Lung Cancer > Flashcards

PHARM: Lung Cancer Flashcards

1
Q

MOA of Carboplatin and Cisplatin.

A

DNA intrastrand crosslinking and adducts

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2
Q

MOA of Cyclophosphamide.

A

pro-drug of active alkylating moiety

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3
Q

MOA of docetaxel.

A

microtubule stabilizer inhibiting depolymerization

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4
Q

MOA of doxorubicin.

A

Intercalator, free radical generator, topo II inhibitor

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5
Q

MOA of etoposide.

A

DNA-topo II complex stabolizer

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6
Q

MOA of gemcitabine.

A

DNA polymerase inhibitor via incorporation of triphosphate form during DNA synthesis

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7
Q

MOA of ifosfamide.

A

intra-and inter-strand cross linker

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8
Q

MOA of irinotecan.

A

DNA-topo I complex stabilizer

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9
Q

MOA of paclitaxel.

A

microtubule stabilizer inhibiting depolymerization

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10
Q

MOA of pemetrexed.

A

DHFR inhibitor

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11
Q

MOA of topotecan.

A

DNA-topo I complex stabilizer

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12
Q

MOA of vincristine and vinorelbine.

A

Microtubule inhibitor (tubules disintegrate into spiral aggregates/protofilaments)

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13
Q

AE of carboplatin.

A

Allergy
Blood dyscrasia
Increased hepatic enzymes, BUN,a nd creatinine

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14
Q

AE of cisplatin

A

Allergy
Nephrotoxicity
Ototoxicity

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15
Q

AE of cyclophosphamide.

A

Hemorrhagic cystitis (MESNA protective)
Pulmonary fibrosis
Amenorrhea/infertility
Secondary malignancies

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16
Q

AE of docetaxel.

A

Increased mortality in NSCLC
Edema (steroids protective)
Sensory Neuropathy

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17
Q

AE of doxorubicin.

A

CHF
Hepatic Disease
Extravasational necrosis
Secondary malignancy

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18
Q

AE of etoposide.

A

Hematologic Toxicity

Alopecia

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19
Q

AE of gemcitabine.

A

arthralgia
alopecia
sensory peripheral neuropathy

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20
Q

AE of ifosfamide.

A

Alopecia
Blood dyscrasia
neurotoxicity
Hematuria renal failure

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21
Q

AE of irinotecan.

A

Weakness, pain, weight loss

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22
Q

AE of paclitaxel.

A

taxane hypersensitivity

myalgia and arthralgia

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23
Q

AE of pemetrexed.

A 
GI toxicity (worse when combined with cipslatin in NSCLC)
Elevated LFT and serum creatinine
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24
Q

AE of topotecan.

A

Hyperbilirubinemia

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25
Q

AE of vinblastine.

A

Neuropathic toxicity

FATAL (if intrathecal administration)

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26
Q

AE of vinorelbine.

A

Neutropenia

less neuropathic toxicity than vinblastine

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27
Q

MOA of methotrexate.

A

inhibits folic acid metabolism

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28
Q

AE of methotrexate.

A

stomatitis, pulmonary fibrosis, kidney failure

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29
Q

In which type of pulmonary neoplasm should histologic subtype be explicitly reported?

A

NSCLC

30
Q

Which type of pulmonary neoplasm has the largest amount of mutations that have targeted therapy available?

A

adenocarcinomas

31
Q

In which type of pulmonary neoplasm should you NEVER use bevacizumab?

A

squamous cell lung cancer

32
Q

What is the result of inactivating “driver” genes?

A

cell death

33
Q

What is the result of inactivating “passenger” genes?

A

no effect on tumor cells

34
Q

What is synthetic lethality?

A

occurs when inactivation of two or more genes leads to cell death whereas inactivation of either gene alone does not affect viability of the cell as the remaining gene acts in a compensatory manner

35
Q

What happens when a ligand binds to a TK receptor?

A

receptor dimerization and trans-phosphorylation of two tyrosine residues (ultimately transduce the signal to the nucleus where nuclear transcription is modified)

36
Q

What are three mechanisms that may stimulate constant proliferative signaling pathways in cancer cells?

A

1) Amplification of receptor
2) Mutation of the receptor
3) Translocation

37
Q

List some examples of ways in which resistance to TKIs can occur?

A

1) ATP binding site mutaiton
2) Mutations that occur downstream of drug target
3) Compensatory phosphorylation by MET (HGFR)
4) Parallel signaling processes get activated

38
Q

What is the consequence of a mutation in BIM?

A

Absence of the pro-apoptotic BH3 domain of BIM will prevent apoptosis (because it will not be able to stimulate BAX and BAK)

39
Q

Why do people with KRAS and BRAF mutations not respond to TKIs targeting EGFR?

A

because KRAS and BRAF are located downstream of EGFR

40
Q

What fusion gene is common in lung cancers and activates the MEK/ERK pathway and cell proliferaiton?

A

EML4-ALK translocation

41
Q

In what groups of patients is EML4-ALK translocation most common?

A

nonsmokers
light smokers
patient with adenocarcinoma

42
Q

How does VEGF work?

A

Hypoxia stimulates HIF-1 (hypoxia inducible factor 1) and this stimulates the release of VEGF which promotes angiotenesis and will decrease hypoxia

43
Q

What are the potential down-sides for blocking VEGF (and formation of new blood vessels) with bevacizumab?

A
  • Reduce distribution of concurrent chemotherapy

- INcrease accumulation of more aggressive cells that have an increased capacity to spread to other organs

44
Q

True or false: because TKIs are targeted drugs, there is not inter-patient variation in drug pharmacokinetics.

A

FALSE: these drugs are administered orally and must be absorbed by the stomach and small intesting before entering the circulation (this is VERY dependent on host pharmacogenetics)

45
Q

Are EGFR mutations more common in people who smoke or never smoke?

A

people who NEVER smoke

46
Q

Are KRAS mutations more common in people who smoke or never smoke?

A

people who smoke

47
Q

For what type of pumonary neoplasm is routine testing for EGFR mutations and ALK rearrangements strongly suggested?

A

adenocarcinomas

48
Q

How can you detect an EGFR mutations?

A

DNA sequencing

49
Q

How can you detect the ALK fusion gene?

A

FISH analysis

50
Q

True or False: all heavy smokers should undergo routine low dose CT scans to look for very small/highly treatable lung tumors.

A

TRUE! (for patient with >30 pack year history)

51
Q

What should the treatment plan be for SCLC?

A

metastasis occurs early so chemo/radiation is the only option

52
Q

What should the treatment plan be for NSCLC?

A

surgical resection if there has been no metastasis (best if the primary tumor is small!)

53
Q

What is the standard chemo combination for SCLC?

A

Etoposide + cisplatin/carboplatin

54
Q

What is the standard chemo combination for NSCLC?

A

Cisplatitn + (pacitaxel, gemcitabine, docetaxel, vinorelbine, irinotecan, or pemetrexed)

+ EGFR TKIs
+ Bevacizumab

55
Q

What drug is used in “maintenance treatment” of NSCLC?

A

Pemetrexed maintenance (a DHFR inhibitor like methotrexate)

56
Q

What is erlotinib?

A

reversible TKI selective for EGRF (ErbB1)

57
Q

True or false: you should eat food when you take erlotinib.

A

FALSE: food increases variability in drug bioavailabiltiy so you should not eat (or smoke)

58
Q

What is interesting about the metabolism of erlotinib?

A

CYP C3A4 substrate!

59
Q

What are the major adverse effects of erlotinib?

A

-Rash
-Corneal perforation/ulceration
-Stomach/intestinal perforation
Liver/kidney problems

60
Q

True or False: erlotinib provides long-term survival in patients expressing the EGFR mutation.

A

FALSE: short term!

61
Q

What is afatinib?

A

COVALENT inhibitor of EGFR (ErbB1), HER2 (ErbB2) and HER4 (ErbB4)

62
Q

What are the major side effects of afatinib?

A

Diarrhea (100%)
Rash (90%)
But has lower incidence of other side effects (except for pulmonary toxicity in Asians)

63
Q

What can you use to treat the rash due to afatinib or erlotinib?

A

steroids
antimicrobials
colloid oatmeal lotion

64
Q

How is the rash due to afatinib and erlotinib useful for physicians?

A

they can gauge whether clinically effective drug levels are being achieved by the specific dosing regimen

65
Q

Do mutations in the ATP binding site of EGFR occur due to the administration of erlotinib and afatinib?

A

NO- these drugs just allow resistant clones to become the predominant cell in the tumor because they kill all the susceptible cells

66
Q

What is crizotinib?

A

reversible multi-kinase inhibitor (that affects ALK)

67
Q

What are the common adverse effects of crizotinib?

A 
GI toxicity
Visual disorders common
Edema (sometimes)
QT prolongaiton (rarely)
Rash (rarely)
68
Q

What is bevacizumab?

A

Chimeric soluble receptor of VEGFR fused to an Fc fragment of an antibody that prevents VEGF from binding to its endogenous cellular receptor sites

69
Q

How is bevacizumab administered?

A

IV infusion

70
Q

What are the major toxicities of bevacizumab?

A

thromboembolism
hemorrhage
fistulas
Alopecia

71
Q

Why does bevacizumab lead to hemorrhages?

A

it blocks endothelial cell regeneration leading to underlying matrix exposure and also promotes non-physiologic apoptosis of endothelial cells (so vasculature is more prone to bleeding)

Pulmonary (34 decks)

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