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Dermatology > skin cancer drugs > Flashcards

skin cancer drugs Flashcards

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Dermatology Board Prep flashcards
1
Q

what are the conventional chemo drugs used for tx of basal cell carcinoma? (6)

A

cisplatin, cyclophosphamide
doxorubicin,fluorouracil
methtrexate, vinblasatine

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2
Q

conventional chemo drugs for squamous cell carcinoma?(1)

A

cisplatin

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3
Q

conventional chemo drugs for melanoma?(6)

A

think: D-drugs except doxo, microtubule inhibitors
carmustine
dacarbazine, dactinomycin, docetaxel
lomustine, vinblastine

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4
Q

conventional drugs for actinic keratosis?(1)

A

fluorouracil

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5
Q

targeted and other therapeutics for basal cell carcinoma?(2)

A

imiquimod and vismodegib

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6
Q

targeted therapies for squamous cell carcinoma?

A

NONE

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7
Q

targeted therapies for melanoma?(6)

A 
aldesleukin
interferon
ipilimumab
sorafenib
trametinib
vemurafenib
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8
Q

targeted therapy for actinic keratosis?(3)

A

diclofenac
imiquimod
trichloroacetic acid

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9
Q

conventional chemo most commonly used for which two cancers?

A

BCC and melanoma

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10
Q

t/f. most skin cancers are cured if found and treated early

A

true

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11
Q

two topical treatments for localized BCC?

A

fluorouracil and imiquimod

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12
Q

BCC advanced or metastatic disease is rare. What is the most common standard chemo for this disease? targeted drug?

A

standard: cisplatin
targeted: vismodegib

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13
Q

imiquimod MOA?

A

Immunostimulant

  • TLR7 and/or TLR8 agonist–>Th1 immune response by activating sentinel cells in the vicinity of the tumor
  • involvement of adenosine receptor blockade
  • activation of NF-KappaB-upregulation of cytokines like TNFalpha and interleukins
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14
Q

imiquimod indications

A

BCC, also actinic keratosis and HPV

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15
Q

Imiquimod ADME:

A

topical agent; limited systematization

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16
Q

imiquimod ADE? pregancy category?

A

photosensivity; contact can compromise condom and diaphragm integrity
Category C

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17
Q

Imiquimod MOA independent of TLR7/8 activation?

A

hedgehog singaling repressor

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18
Q

what is hedgehog signaling?

A

pathway that regulated body patterning and organ development (mainly quiescent by adulthood except for a role in tissue repair)

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19
Q

MOA of vismodegib

A

oral SMO(smoothened = protein by which HH signals travel) inhibitor

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20
Q

ADME of vismodegib

A

lipohillic agent with extensive metabolism

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21
Q

the 3 black box warnings of vismodegib

A

BBB: intrauterine fetal death, male-mediated teratogenicity, pregnancy

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22
Q

t/f. male and females need to practice contraception while on vismodegib.

A

true

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23
Q

how long do restrictions of blood donation last for after tx with vismodegib?

A

7 months

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24
Q

other common ADEs of vismodegib?

A

Alopecia most common
GI toxicities, weight loss, fatigue
Category D pregancy

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25
Q

T/F. SCC does not involve drugs in initial therapy and there are targeted tx for this cancer.

A

false.
True - no drugs at initial tx
False - no targeted therapy

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26
Q

most common standard chemo drug used for tx in SCC?

A

cisplatin

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27
Q

Aldesleukin MOA?

A

IL-2 receptor agonist. binds to IL-2 receptor surface–> proliferation of B and T cells, monocytes, macrophages, and CTLs inlcuding NK cells

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28
Q

Admin for aldesleukin?

A

IV or SC

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29
Q

BBW for which conditions and using aldesleukin?

A

CNS - diminshed mental status, speech difficulties, corcial blindness, limb or gait ataxia, hallucinations, agitations

cardiac - hypotension, S-TACH, peripheral vasodilation, SVT

pulmonary disease- dyspnea, pulmonary congesion, rales, rhonchi

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30
Q

except for BBW, contradindicated in which other diseases?

A

renal or hepatic disease, and/or organ translplant recipeint

31
Q

aldesleukin BBW for which side effect?

A

capillary leak syndrome (causes renal disease)

32
Q

aldesleukin has significant ADEs at every organ system. Which pts can it be given to?

A

patients with normal cardiac and pulmonary function as determined by thallium stress testing and PFTs.

33
Q

interferon MOA?

A

IV or SC administered immunomodulator; acts like endogenous interferon

34
Q

BBW for interferon use in which 3 conditions?

A

autoimmune disease
cardiac disease
depression - may increase risk of suicidal ideation
also infection (no BBW)

35
Q

most common ADE for interferon?

A

flu, flu-like symptoms (fever, fatigue)
alson: neutropenia, leukopenia, anemia, alopecia
elevated hepatic enzymes(routine LFTs required)
cough and dyspnea(pulmonary infiltrates, pneumonitis, and pneumonia)

36
Q

Ipilimumab MOA?

A

CTLA4 recombinant antibody–> bolsters antitumor response of immune system

CTLA4 is a negative regulator of T-cell activation

37
Q

Ipilimumab ADE?

A

severe and fatal immune-mediated adverse reaction due to T-cell activation and proliferation
dermatitis including toxic epidermal necrolysis (amonst most common severe immune rxns)

38
Q

BBW for ipillimumab posted for many ADEs such as____?

A

adrenal insufficiency, Guillain-Barre syndrome, hepatitis, hyperthyroidism, hypopituitarism, hypothryoidism, mayasthenia gravis, peripheral neuropathy, pregnancy, serious rash

39
Q

most common ADEs of ipilimumab?

A

tiredness, rash diarrhea

40
Q

sorafenib MOA?

A

oral multi-kinase inhibitor (VEGF, PDGFR, KIT, raf kinase)

41
Q

how is sorafenib metabolized?

A

hepatic metabolism - hepatitis elevated LFTs?

42
Q

some ADEs of sorafenib?

A

most common: hand and foot syndrome, rash/desquamation, anemia

others: BM suppression, neutropenia–> use CBCs to monitor
increased risk of bleeding(possbily fatal) in GI, respiratory system, and brain

43
Q

is sorafenib safe to use during pregnancy?

A

NO!!! category D

44
Q

trametinib MOA

A

oral reversible MEK inhibitor for patients with BRAF V600E or V600K mutations. (not for pts who have previously received BRAF inhibitors)

45
Q

most severe ADE of trametinib

A

rapid onset of skin toxicity(dermatitis, erythema, hand-foot sydrome); severe in 12% of patients

46
Q

what are other ADEs of trametinib?

A

GI toxicity: diarrhea, stomatitis, anemia
decreased LVEF, HTN, hemorrhage

rarely: cardiomyopathy, interstitial lung disease, RETINAL PIGMENT EPITHELIAL DETACHMENT

47
Q

MOA of vemurafenib?

A

oral inhibitor of mutated BRAF, including BRAF V600E

48
Q

vemurafenib: is genotyping required? which type of tumors can it not be used in? how does resistance develop?

A

genotyping required
not be used in wild type tumors
resistance via alternate pathway activation

49
Q

how is vemurafenib metabolized?

A

hepatic metabolism: PGP and CYP interactions possible, elevated serum creatinine –> LFTs required

50
Q

ADEsof vemurafenib?

A

QT prolongation and TP–> LFTs required
increased photosensitivy–>avoid sunlight
cutaneous SCC in 1/4th patients (perform regular dermatologic examinations)
SEVERE dermatologic reactions possible(SJS) possible

51
Q

which ADE does vemurafenib have in common with trametinib?

A

both cause opthalmologic issues

vemurafenib ADEs: uveitis, iritis, retinal vein occlusion

52
Q

drugs with pregnancy category C status?

A

Aldesleukin, ipilimumab,

53
Q

pregnancy category D status?

A

sorafenib, trametinib, vemurafenib

54
Q

carmustine MOA?

A

both alkylation and carbamoylation of amino acids

55
Q

cisplatin MOA?

A

forms DNA intrastrand crosslinks and adducts

56
Q

cyclophosphamide MOA?

A

pro-drug of active alkylating moiety

57
Q

dacarbazine MOA?

A

pro-drug of active alkylating moiety

58
Q

dactinomycin MOA?

A

DNA intercalator

59
Q

docetaxel MOA?

A

microtubule stabilizer; inhibits depolymerization

60
Q

doxorubicin MOA?

A

intercalator, free radical generator, topoi II inhibitor

61
Q

fluorouracil MOA?

A

thymidylate synthase(TS) inhibitor; interferes with RNA&RNA synthesis/function

62
Q

lomustine MOA?

A

alkylating agent

63
Q

methotrexate MOA?

A

DHFR inhibitor

64
Q

vinblastine MOA?

A

microtubule formation inhibitor

65
Q

dose limitation and routine care of cisplatin?

A

renal tubular damage and failure; myelosuppression; associated with development of secondary malignancies

66
Q

dose limitation and routine care of docetaxel?

A

neutropenia; associated with development of secondary malignancies

67
Q

all the following drugs have which dose limitation and routine care.
carmustine, cyclophosphamide, dactinomycin, doxorubicin,lomustine, methotrexate

A

myelosuppression and development of secondary malingancies

68
Q

all of the following drugs have which dose limitation and routine care?
dacarbazine, fluorouracil, vinblastine

A

myelosuppresion

routine care: CBCs

69
Q

what is actinic keratosis?

A

non-invasive lesion in sun-exposed skin (early epithelial transformation that is extremely unlikely to progress to SCC (1/1000 per annum)

70
Q

diclofenac MOA?

A

an NSAID. inhibitor of inflammatory mediators including, PGE2.

71
Q

diclofenac ADE?

A

Adverse reactions include itchy rash, dry skin, and skin peeling and redness

72
Q

trichloroacetic acid MOA?

A

acetic acid; rapidly penetrates and cauterize skin, keratin, and otehr tissue

73
Q

ADE of trichloroacetic acid?

A

burning, inflammation and localized tenderness

Dermatology (18 decks)

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