Lung Cancer Pharm Flashcards

1
Q

EGFR mutations are evident in a significant number of what types of cancer?

A

Adenocarcinoma

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2
Q

High risk of bleeding in squamous cell lung cancer associtated with what drug?

A

Bevacizumab

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3
Q

What is the significance of activating a tyrosine kinase receptor in a cancer cell

A

If the ligand is bound by the receptor, transphosphorylation of two tyrosine residues occurs and this signal can be transduced to the nucleus where it effects transcription that can cause uncontrollable growth/avoidance of apoptosis.
TKIs try to prevent this

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4
Q

Resistance to Tyrosine Kinase Inhibitors can occur how

A

Via EGFR mutation which leads to

  • Change in binding site receptor
  • compensatory phosphorylation of the Tyr Kinase binding site via MET, HGFR
  • or HGF taking assuming an independent role in signaling
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5
Q

What are some other ways that cells can be insensitive to TKI

A

Via proliferative signals arising from downstream events via KRAS or BRAF mutations

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6
Q

EML4-ALK Translocation

A

Fuses the EML4 and ALK genes leads to activation of the Mek/Erk pathway and cell proliferation

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7
Q

Why is VEGF a good drug target?

A

Prevents good vasculature from reaching the tumor site

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8
Q

Genetic testing for KRAS, EGFR, and ALK rearrangement have become necessary for adherence to treatment guidelines

A

truth

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9
Q

EGFR and ALK testing only recommended for ppl with what type of tumors

A

Adenocarcinoma

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10
Q

The US preventative service task force recently suggested what

A

smokers age 55-80 with over 30 pack year history of smoking should receive low dose CT scans to look for possible tumors

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11
Q

What process is sued to test for EGFR mutations

A

DNA sequencing

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12
Q

What process is used to test for ALK gene rearrnagement

A

FISH

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13
Q

ALK rearrangements are more common in smokers or non-smokers

A

non-smokers

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14
Q

Treatment plan for SCLC

A

Metastasis ocurs early in small cell lung cancer to chemotherapy is the only option

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15
Q

NSCLC treatment

A

surgical resection if there has been no metastasis. Use chemo in adjuvant role when you need to reduce the bulk of the tumor prior to surgery and eradiate micrometastasis
Prevent growth and metastasis

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16
Q

Standard chemo for SCLC

A

Etoposide + Cisplatin or Carboplatin

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17
Q

NSCLC treatment

A

Cisplatin and Paclitaxel

AND EGFR TKI’s for pts with +EGFR genetic test

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18
Q

Maintenance therapy for NSCLC pts who have responsive tumors

A

Pemetrexed

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19
Q

What are the two nitrogen mustards?

A

Cyclophosphamide and Ifosfamide

20
Q

Mechanism of action for cyclophosphamide/Ifosfamide

A

Bind to the N7 of Guanine and Alkylate DNA producing inter/intra strand crosslinks that prevent DNA replication

21
Q

Ifosfamide differs from cyclophosphamide in regards to adverse effects how?

A

No risk of pulmonary fibrosis and less renal toxicity

22
Q

WHAT MUST BE GIVEN WITH Cyclophosphamide

A

Mesna…protects against acrolein product and prevents bladder tumors and urotoxicity

23
Q

Platinum drugs are

A

Cisplatin and Carboplatin

24
Q

Platinum drugs MOA

A

Same as Nitrogen Mustards (cyclophosphamide and Ifosfamide)

25
Q

Cisplatin Toxicity

A

Renal, ototoxic, peripheral neuropathy

26
Q

Carboplatin toxicity

A

myelosuppresive, ANEMIA, INFECTION

27
Q

Folic Acid Analogs

A

Methotrexate, Pemetrexed

28
Q

How do methotrexate and pemetrexed work?

A

Dihydrofolate reductase inhibition, inhibits DNA synthesis

29
Q

Give what with methotrexate and pemetrexed?

A

Leucovorin- causes metabolic rescue

30
Q

What kind of drug is Gemcitabine and how does it work>

A

Pyrimidine analog, DNA polymerase inhibitor causing inhibition of chain elongation

31
Q

Toxicity associated with Gemcitabine?

A

“Hand-Foot” syndrome

32
Q

The two vinca alkyloids are

A

Vincristine and Vinorelbine

33
Q

Vinca alkyloids MOA

A

bind to beta tubulin to cause metaphase arrest and apoptosis. Prevent microtubule assembly.

34
Q

Vincristine adverse effects

A

GI stasis, impaction

Intrathecal admin can be fatal, neurotoxicity

35
Q

Camptothecin analogs

A

irinotecan and topoteca

36
Q

How do irinotecan and topotecan work?

A

They stabilize DNA topoisomerase I cleavable complex causing single and double strand DNA breaks

37
Q

Toxicity of Camptothecin analogs

A

extrvasational toxicity (fluid leaking), GI toxicity,

38
Q

Etoposide mechanism

A

form complex with topoisomerase II and DNA

39
Q

BBW for Etoposide

A

myelosuppression, bleeding, opportunistic infection

40
Q

Paclitaxel

A

Bind to beta tubulin to prevent microtubule disassembly.

41
Q

Bevacizumab

A

anti-VEGF, binds to VEGF, prevents receptor activation, anti angiogenesis/neovascularization

42
Q

Big side effect for Bevacizumab

A

hemorrhage (can be life threatening esp with squamous cell

43
Q

Erlotinib

A

Reversible inhibitor for EGFR

44
Q

WHat do you always give with Doxorubicin to relieve cardiotoxicity

A

Dexroxazone…iron chelator

45
Q

What do you give with Cisplatin and carboplatin q

A

Amifostine