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Dermatology pharm > Drugs to treat skin cancer > Flashcards

Drugs to treat skin cancer Flashcards

MOA, derm indication; ADE; contraindication; genotyping

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Dermatology Board Prep flashcards
1
Q

What CTX can be given for basal cell carcinoma?

A

cisplatin; cyclophosphamide; imiquimod; vismodegib

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2
Q

What is the CTX agent for squamous cell carcinoma?

A

cisplatin

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3
Q

What CTX can be given for melanoma?

A

carmustine; dacarbazine; docetaxel; aldesluekin; interferon; ipilimumab; sorafenib; trametinib; vemurafenib

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4
Q

What CTX can be given for actinic keratosis?

A

imiquimod; trichloroacetic acid

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5
Q

Conventional and targeted CTX are commonly used in what diseases?

A

BCC and melanoma

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6
Q

Unusual agents like an NSAID and TCA treat for what?

A

actinic keratosis

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7
Q

T/F most skin cancers are cured if found and Tx begins early

A

true

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8
Q

If localized BCC Tx with fluoruracil does not work or the lesion is small and in a low risk site, what is the Tx?

A

topical imiquimod

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9
Q

If BCC is metastatic, what is the most effective Tx?

A

cisplatin

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10
Q

If BCC is metastatic and ADEs are too risky, what is the Tx of choice?

A

Vismodegib

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11
Q

What is the main MOA of imiquimod?

A

smal molecule tumor directed immune response initiator (immune stimulator)

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12
Q

How does imiquimod work? (3)

A

direct activation of TLR7 and/or TLR8; involvement of adenosine receptor blockade; activation of NFkB

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13
Q

What does the activation of NFkB cause?

A

upregulation of cytokines like TNFa and interleukins

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14
Q

Other than BCC, what can imiquimod be used for?

A

actinic keratinosis and HPV

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15
Q

How is imiquimod applied?

A

topical agent for limited systematization

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16
Q

What are associated ADE with imiquimod?

A

Benzyl alcohol, paraben (components of drug) allergenic; localized skin rxn; increased photosensitivity; compromise condom and diaphragm integrity

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17
Q

If imiquimod is given in high concentrations, what is the effect?

A

apoptosis due to mitochondria begin damaged leading to caspase activation and Bcl-2/Bax shift

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18
Q

What is significant about hedgehog signaling?

A

body patterning and organ development but in adults is associated in tissue maintenance and repair

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19
Q

BCC is linked to what pathway?

A

inappropriate reactivation of the hedgehog pathway

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20
Q

What is the consequence of abberant signaling of the Hh pathway?

A

upregulation of anti-apoptotic Bcl-2, VEGF induction, angiopoietins

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21
Q

What is key for the action of clinical inhibitors of Hh? What is the drug used to accomplish this?

A

act at or below level of transmembrane protein SMO=> Vismodegib

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22
Q

What is the MOA of vismodegib?

A

oral SMO inhibitor

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23
Q

How is vismodegib metabolized?

A

extensively via a lipophilic agent

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24
Q

What are the main 3 ADEs associated with vismodegib?

A

intrauterine fetal death; male mediated teratogenicity; pregnancy and blood donating

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25
Q

What is significant in using vismodegib while pregnancy is in question?

A

both male and female need contraception

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26
Q

What are mild ADEs of vismodegib?

A

alopecia; GI tox (common); weight loss and fatigue

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27
Q

What is the initial Tx for squamous cell carcinoma?

A

surgery and/or radiation => no drug tx

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28
Q

If squamous cell carcinoma is metastatic, what is the regimen?

A

no standard but cisplatin tx is most effective

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29
Q

In what 3 ways can melanoma be treated?

A

immunotherapy, signal transduction inhibitors, CTX

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30
Q

What are the drugs for immunotherapy of melanoma?

A

Aldesleukin (IL-2); IFN-a-2B; Ipilmumab

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31
Q

What are 3 drugs for signal tranduction inhibitors for melanoma?

A

sorafenib; trametinib; vemurafenib

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32
Q

What are the best CTX agents for melanoma?

A

dacarbazine; carmustine

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33
Q

What is the MOA of aldesleukin?

A

binds to cell surface IL-2 receptor

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34
Q

What is the effect of aldesleukin?

A

induces proliferation and differentiation of B and T cells, monocytes, macs, and CTLs including NKs

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35
Q

What is Aldesleukin contraindicated in?

A

BBW in CNS; cardiac; pulmonary; renal; hepatic diseases or organ transplant

36
Q

What is an ADE associated with giving aldeleukin with renal failure patients?

A

capillary leak syndrome *** BBW

37
Q

What is an IV or SC administered immnomodulator?

A

Interferon-a 2B

38
Q

When should Interferon-a 2B be used with caution?

A

* BBW in autoimmune diseases; cardiac diseases; depression;* infection

39
Q

What is the most common ADE in Interferon-a 2B use?

A

flu like Sx

40
Q

Interferon are associated with what pulmonary Sx?

A

cough and dyspnea; pulm infiltrates, pneumonitis, pneumonia

41
Q

What common pathway does the INF-a 2b work on?

A

JAK-STAT pathway leading to upregulation of transcriptional genes

42
Q

What is the MOA of ipilimumab?

A

CTLA-4 recombinant Ab (encourages B7 binding to CTLA-4) for T cell activation

43
Q

What reason is ipilimumab administered?

A

bolsters antitumor response of immune system

44
Q

What are the ADEs of ipilimumab associated with?

A

severe and fatal immune mediated adverse rxns due to T cell activation and proliferation

45
Q

What is a common severe ADE of ipilimumab?

A

dermatitis including toxic epidermal necrolysis

46
Q

What are severe ADEs associated other diseases when given ipilimumab?

A

adrenal insufficiency; diarrhea; Guillain-Barre syndrome; hepatitis; hyper/hypothyroidism; hypopituitarism; myasthenia gravis; peripheral neuropathy; pregnancy; serious rash

47
Q

What is the multi-kinase inhibitor of VEGF, PDGF-r, KIT, Raf kinase?

A

Sorafenib

48
Q

How does the metabolism of sorafenib cause problems?

A

hepatic metabolism that may elevate LFTs in patients with hepatitis

49
Q

What are the most common ADEs with sorafenib?

A

Hand and foot syndrome; rash desquamation; anemia

50
Q

Why are routine CBCs required with sorafenib Tx?

A

bone marrow suppression and neutropenia

51
Q

What is increased that could lead to death in patients?

A

increased GI, respiratory and brain bleeding

52
Q

Does sorafenib affect pregnancy?

A

yes=> birth control required

53
Q

How does sorafenib utilize the RAF/MEK/ERK pathway?

A

inhibits tumor cell proliferation by targeting the pathway at the level of RAF kinase

54
Q

How does sorafenib exert an anti-angiogenic effect?

A

targeting the receptor tyrosine kinases VEGF-R and PDGF-r and associated cascades

55
Q

What is the MOA for Trametinib?

A

oral reversible MEK inhibitor

56
Q

What type of patients is trametinib indicated for? who is not included?

A

patients with BRAF V600E or V600K mutations => cannot give to patients previously receiving BRAF inhibitors

57
Q

What are common ADEs in patients receiving trametinib?

A

skin toxicity (dermatitis, erythema, hand-foot syndrome); GI tox; Decreased LVEF; HTN; hemorrhage

58
Q

What are rare ADEs associated with trametinib?

A

cardiomyopathy; interstitial lung disease; retinal pigment epithelial detachment

59
Q

What is the MOA of vemurafenib?

A

oral inhibitor of mutated BRAF (includes BRAFV600E)

60
Q

What is required to treat with vemurafenib? why?

A

genotyping=> cannot use in wild type tumors

61
Q

Why can vemurafenib not be used in wild type tumors?

A

paradoxical ERK activation of mutated RAS-driven growth

62
Q

How does resistance occur when using vemurafenib?

A

alternative pathway activation

63
Q

vemurafenib metabolism?

A

hepatic, PGP and CYP interactions possible; elevated serum creatinine

64
Q

How does vemurafenib affect the heart? what must be done while taking it?

A

QT prolongation => electrolyte monitoring

65
Q

What cancer is increased with vemurafenib use? why?

A

cutaneous SCC=> increased photosensitivity=> must avoid sunlight

66
Q

What severe issues are associated with vemurafenib that is not as common with other drugs?

A

uveitis, iritis, retinal vein occlusion

67
Q

What are the common toxicities of BRAF/MEK inhibitors?

A

liver; heart; eye; secondary malignancies

68
Q

What do all BRAF-MEK inhibitors require?

A

BRAF genotyping

69
Q

Which drugs are considered category C drugs?

A

aldesleukin; ipilimumab; IFN-a 2b

70
Q

Which drugs are considered category D drugs?

A

sorafenib; trametinib; vemurafenib

71
Q

What is the MOA of carmustine?

A

alkylation and carbamoylation of amino acids

72
Q

What drugs are typically used topically in actinic keratosis?

A

imiquimod

73
Q

What is the dose limitation of cisplatin?

A

renal tubular damage and failure

74
Q

What is the dose limitation of docetaxel?

A

neutropenia

75
Q

What is the dose limitation of most of the other cancer drugs?

A

myelosuppression

76
Q

How does trichloroacetic acid work?

A

chemical peel that rapidly penetrates and cauterizes skin, keratin

77
Q

What are ADEs associated with trichloroacetic acid?

A

burning; inflammation; localized tenderness

78
Q

What do interferon, sorafenib and trametinib have in common?

A

blood dyscrasias

79
Q

Which targeted drug will cause bleeding in the GI, lung and brain?

A

sorafenib

80
Q

Which targeted drug will cause HTN?

A

sorafenib

81
Q

What do Trametinib and Vemurafenib have in common?

A

eye damage

82
Q

What targeted drug is associated with secondary tumors?

A

vemurafenib

83
Q

Which targeted drugs may lead to a rash?

A

imiquimod; ipilimumab; sorafenib; trametinib; vemurafenib

84
Q

Which targeted drugs are associated with the need for genetic testing?

A

trametinib and vemurafenib

85
Q

MOA for cisplatin

A

forms DNA intrastrand crosslinks and adducts

86
Q

MOA for cyclophosphamide

A

pro-drug of active alkylating moiety

87
Q

MOA for decarbazine

A

pro drug of active alkylating moiety

Dermatology pharm (10 decks)

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