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Dermatology > Skin Cancer > Flashcards

Skin Cancer Flashcards

1
Q

Tx for actinic keratosis (pre-squamous)

A

Diclofenac (topical NSAID)
Imiquimoid
Trichloroacetic acid (peel)

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2
Q

Tx of Basal cell carcinoma (albinos with severe peeling sunburns)

A

Imiquimod
Vosmedegib
5 FC

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3
Q

Tx of melanoma

A 
Aldesleukin (IL2)
Vemurafenib
Trametinib
sorafenib
Interferon alfa
Ipilimumab
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4
Q

only MAB used for skin cancer

A

ipilimumab (melanoma )

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5
Q

common sites for skin mets

A

GI, Lungs, Brain

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6
Q

basal cell clinical course

A

slow growing, greater ability to eb locally invasive (bone)–> but least likley to metastasize (reason is because it has a very fastidious strome that it can growht in and it carries this stroma with it as it locally invades–>less likley for distant mets)

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7
Q

when BCC does met. whats the tx

A

no stndardized tx.

–> cisplatin is the best we have

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8
Q

topical treatment of BCC in most sites

A

5 florouracil

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9
Q

topical tx of BCC is small and at low risk sites in pt’s who are bad candidates for conventional therapy

A

imiquimod-topical with limited systematization

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10
Q

advanced/metastatic BCC tx

A

vesmodegib

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11
Q

BCC especially reliant on

A

HedgeHog Signalling pathway–>vesmodegib is a SMO inhibitor

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12
Q

MOA for Imiquimod

A

immuno-stimulant
>activates TLR7 and TLR 8 (activating a TH1 respone in sentinel cells around the tumor)whilst inhibiting Adenosine receptors
>also activates NFkB-causing upreg of TNF and IL’s
>also negatuvely modulates GLI ligand-independent signalling
>adora’s?

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13
Q

what all does imiquimod treat

A

BCC, HPV, AL’s

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14
Q

define the mutations in most BCC

A

HH driven malignancy with an activating mutation in GLI oncogene–> which signals in a ligand-independent manner

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15
Q

HH signalling travels via a protein named

A

SMO-smoothened

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16
Q

consequence of upregulaiton of HH signalling–> what molecules wind up being over-produced

A

BCL2 (anti-apoptotic)
VEGF
angiopoetins
*therfore HHinihbition from imiquimod, vesmodigib reduces all of these

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17
Q

why must small molecule inhibitors work at or below SMO

A

pathway is ligand independent, so blocking PTCH! receptor is inneffective

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18
Q

Moa for Vismoedegib

A

oral smo inhibitor

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19
Q

BBW’s for SMOE

A

intrauterine fetal death
male-related teratogenicity
*must confirm no pregnancy and use 2 forms of BC

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20
Q

Targetted drugs for squamous cell

A

none

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21
Q

conventional drugs for squamous cell

A

cisplatin but not standard tx

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22
Q

first line theray for squamous

A

sxical xision

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23
Q

Immuntherapies for Melanoma

A

Aldesleukin
Interferon alpha
Ipilimumab

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24
Q

Signal transduction inhibitors for melanoma

A

sorafenib
trametinib
vemurafenib

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25
chemotherapy for advanced melanoma | again these don't work well
dacarbazine, lomustine, carmustine (20% but repsonse short lived) also taxanes, platinums, vincas
26
how does aldesleukin work?
IL2 agonist whose effects are identical to endogenous IL2--> BINDS to IL3 surface receptor-creates a cytokine cascade-whereby TNF IL's and IFN's are rleased
27
induces proliferation of B, T, Macrphages and NK cells
aldesleukin
28
BBW's with aldesleukin
Cardio, Pul, Renal, CNS deffieincies | *also contra in hepatic disease or post-trasnplant
29
what do you have to have before putting someone on Aldesleukin
Thallium Stress Test formal PFT *daily on tx CXR
30
unique side effect of aldesleukin
renail failure insufficiency by CAPILLARY LEAK SYNDROME | "all-dats-leakin"
31
what to do Tregs do
tone down host anti-tumor, viral response * guards againts autimmunity in life * but hinders our anti-cancer efforts
32
VLS (capillary leak syndrome)
hypotension, inc vasc, permeability, pulmonary edema, renal/liver failure
33
what causes VLA
CD122hiNK cells--> releaisng pro-inflamm cytokines (TNF) or IL2 binding to CD25 endothelial cells increasing permeability
34
Aldesleukin acivates which cell lines
CD4 and CD* (beefs up their antitumor response | Treg->accidentally beefs up host anti-antitumor repsone (BAD off target effect)
35
MOA for interferon alpha2b
works like endogenous interferon
36
BBW's for interferon
worsening of auto-immune dz cardiac dysfuntion depression--> suicide
37
routine tests for interferon
CBC's, CXR, ECG, LFT's
38
CLTA4 recombinant antibody
Ipilimumab
39
many BBW's but no D-D interxn potention
Ipilimumab
40
side effects of Ipilimumab
Severe and fatal immune-mediated adverse reactions *can cause dermatitis/TEN rash, dirrhea, tiredness, ithch
41
MOA for ipilimumab
bind CLTA4 on the t cell and PREVENTS CLTA4 from binding to B7 (CD80/CD86)
42
what does CTLTA4 do
negative regulator of t cell activation (thus blockade prevents t cells from being toned down...you can only turn them up, their proliferaiton and acitvation is augmented..and HOST MORE ABLE TO FIGHT OF TUMOR
43
THIS DRUG FIGHTS MELANOMA INDIRECTLY BY INCREASING T CELL MEDIATE ANTI-TUMOR RESPONSE
IPILUMUMAB
44
PROBLEM WITH IMMUNE THERAPY
UNWANTED IMMUNE-MEDIATED ADVERSE EFFECTS IN MANY ORGANS--> LIMITS CLINICAL UTILITY
45
HEMORRHAGE POSIBLE-->rash (severe-desquamative),hepatic dysfunction high LFT's,, heme toxic
sorafenib
46
mutli-kinase inhibitor
sorafenib
47
what kinases does sorafenib inhibit
VEGF, PDGFR< cKIT, RAF
48
2 drugs that cause hand and foot syndrome
Sorafenib | Trametinib
49
routine tests required with sorafenib
CBC's--> anemia and nutropenia, BM supressed
50
increased risk of brain/GI bleed
srafenib--> inhibits VEGF
51
effects of sorafenib mutli-kinase inhibition
1. antiproliferation | 1. antiangiogenic
52
recommended regimen for sorafenib right now
dacarbazine IV on day one | then sorafenib for 21 days
53
MOA for tremtinib
reversible MEK inihib.
54
how to remember tremetinib
treMEKinhib
55
treats BRAF V600E or V600K muts
tremetinib
56
severe skin toxiticities
tremetinib and sorafenib
57
routine test for tremetinib
LVEF must be monitored, CBC's and LFT's
58
side effects
cardiomyopathy, ILD, retinal pigment epithelial detachmet
59
retinal epithelial dettachment
tremetinib
60
requires genotyping for BRAF mutation
tremetinib and vemurafenib
61
order of signal transduciton
RTK--> cKIT, NRAS< BRAF
62
if MEK is mutant what will work
nothing or tremtinib?
63
if mek is mutant what wont work
vemurafenib--> downstream
64
works on BRAF V600E * not to be used in wild-type tumors | works only on mutant BRAF
vemurafenib
65
may cause paradoxical ERK activation of RAS driven growth if used un wild type tumors
vemurafenib
66
requires constituitively acitve BRAF mutation V600e
vemurafenib and trametinib
67
patients receiving this drug are at a higher risk for developing SCC (25% of patients)
vemurafenib
68
significant toxicities of vemurafeinib
skin-SJS and SCC possible eye-uveitis, iritis, retinal vein occlusion cardiac--> qt prolong liver-->PGP and cyp interactions
69
monitoring required with vemurafenib
EKG, electrolytes, creatinine, lft's
70
resistance to vemurafenib
alternative pathway selection (normal RAF, Araf, Craf, etc all have a greater presence if BRAF is inhibited)
71
causes pradoxical RAS-driven proliferation of pre-exisiting and unrecognized malignancies
vemurafenib
72
commonalities of toxicity in MEK/RAF inh.
liver, heart, eye, secondary malignancies
73
all three raf/mek inhibitors have the potential to cause
possibly severe rash (SJS-desquamative)
74
pregnancy
immune modulators C-->dont give | raf/mek inhibitors D--> teratogen associated

Dermatology (12 decks)

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