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Pulmonology > Rx for Lung Cancer- Sweatman > Flashcards

Rx for Lung Cancer- Sweatman Flashcards

1
Q

Name 3 mechanisms of resistance to TKIs

A

1) Drug binding site mutation (highly conserved ATP binding site)
2) Compensatory Tyrosine phosphorylation by MET
3) MET assumes an independent role in the proliferative signaling process

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2
Q

What are the 2 common downstream mutations in the EGFR/Tyrosine Kinase complex pathway?

A

Constitutive activation of KRAS or BRAF

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3
Q

What effect does downstream mutation have on drug therapy?

A

It renders it useless

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4
Q

What is the effect of the EML4-ALK oncogene?

A

Activation of MEK/ERK, subsequent proliferation

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5
Q

Who is the EML4-ALK mutation seen in?

A

Non-smokers and those with adenocarcinomas

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6
Q

What is the mechanism for VEGF release?

A

Hypoxia is sensed by the cell–> induces HIF-1–>HIF-1 translates to the nucleus–>VEGF is transcribed–>Angiogenesis

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7
Q

What TKI is used against EML4-ALK?

A

Crizotinib

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8
Q

What TKI is used against EGFR?

A

Erlotinib

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9
Q

What is the gold standard CONVENTIONAL chemo treatment for SCLC?

A

Etoposide + cisplatin or carboplatin

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10
Q

When is Erlotinib first line therapy?

A

Treatment of locally advanced or metastatic NSCLC after failure of at least one prior chemo regimen

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11
Q

Mechanism of 6-Mercaptopurine, 6-Thioguanine, and Methotrexate therapy?

A

Inhibits purine ring synthesis; the first 2 interrupt elongation after incorporation into the strand; MTX is a DHFR antagonist

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12
Q

Mechanism of Hydroxyurea?

A

Inhibits ribonucleotide reductase

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13
Q

Mechanism of 5-Fluorouracil?

A

Inhibits dTMP synthesis

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14
Q

Mechanism of Cytarabine?

A

Inhibits DNA synthesis (antimetabolite)

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15
Q

Mechanism of Bleomycin?

A

Acts as molecular scissors to cut DNA strands

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16
Q

Mechanism of the Anthracyclines?

A

Intercalate DNA; also produces free radicals (where the cardiomyopathy comes from)

17
Q

Mechanism of the alkylating agents, Nitrosureas, and Platinum drugs?

A

Cross-link DNA

18
Q

Mechanism of L-aspariginase?

A

Inhibits protein synthesis

19
Q

Mechanism of Taxanes and Vincas?

A

Inhibit microtubule function; Taxanes stabilize and Vincas prevent formation

20
Q

Unique toxicities of the platinum drugs?

A

Ototoxicity and Nephrotoxicity

21
Q

Unique toxicity of cyclophosphamide and ifosfamide? What is given with it to prevent this?

A

Hemorrhagic cystitis (more so cyclophosphamide); mesna protects the bladder

22
Q

Unique toxicities seen in the taxanes and vincas? What clinical finding helps you diagnose this?

A

Peripheral neuropathy; loss of deep tendon reflex

23
Q

Unique toxicity of the anthracylcines (doxorubicin, daunorubicin, and idrarubicin)? What is given to protect against it?

A

Cardiomyopathy–>CHF; co-administer with dexrazoxane

24
Q

What are some downsides to oral therapy (TKIs)?

A

Interactions with CYP, P-gp efflux pumps, first-pass metabolism, and drug drug interactions

25
Q

Are TKIs used for NSCLC or SCLC?

A

NSCLC

26
Q

Name the common ADEs of TKIs

A

1) EGFR antagonists cause skin rash
2) All TKIs cause GI symptoms like nausea, vomiting, diarrhea (EGFR important in maintenance of GI cells)
3) Endocrine dysfunction and QT prolongation

27
Q

Why are there so many ADEs associated with TKIs?

A

The target is very nonspecific and it plays an important homeostatic role in multiple tissues throughout the body

28
Q

What is the definition of a pharmacodynamic change? what are some examples?

A

A change in the level of drug in the body; protein binding, efflux pumps

29
Q

What is the definition of pharmacokinetic change?

A

Alteration of the molecular target

30
Q

What is the role of CTLA-4?

A

plays an important role in T cell activation at initial antigen presentation

31
Q

What is PD1?

A

Don’t you mean PD-L1? What a fucking douche

32
Q

What is the significance of PD-L1 expression by cancer cells?

A

It binds T-cells and tells the lymphocyte it is a friendly cell; evades the immune system

33
Q

What is Nivolumab?

A

A recently approved drug; only for metastatic disease after platinum drug based therapy

34
Q

Mechanism of action of Bevacizumab?

A

Inhibits VEGF–> inhibits angiogenesis

35
Q

What are a couple life threatening toxicites of Bevacizumab?

A

Thromboembolism, fistula formation, hemorrhage

36
Q

Why does Bevacizumab cause nephrotoxicity?

A

Because VEGF plays an important homeostatic role in maintaing the glomerular basement membrane

37
Q

Why is bevacizumab not recommended for treatment of squamous cell lung carcinoma?

A

Because it commonly causes fatal hemorrhage

Pulmonology (31 decks)

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