Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Dermatology > Skin Cancer > Flashcards

Skin Cancer Flashcards

You may prefer our related Brainscape-certified flashcards:
Dermatology Board Prep flashcards
1
Q

Tx for actinic keratosis (pre-squamous)

A

Diclofenac (topical NSAID)
Imiquimoid
Trichloroacetic acid (peel)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

Imiquimod
Vosmedegib
5 FC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Tx of melanoma

A 
Aldesleukin (IL2)
Vemurafenib
Trametinib
sorafenib
Interferon alfa
Ipilimumab
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

only MAB used for skin cancer

A

ipilimumab (melanoma )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

common sites for skin mets

A

GI, Lungs, Brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

when BCC does met. whats the tx

A

no stndardized tx.

–> cisplatin is the best we have

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

topical treatment of BCC in most sites

A

5 florouracil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

advanced/metastatic BCC tx

A

vesmodegib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

BCC especially reliant on

A

HedgeHog Signalling pathway–>vesmodegib is a SMO inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what all does imiquimod treat

A

BCC, HPV, AL’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

HH signalling travels via a protein named

A

SMO-smoothened

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

why must small molecule inhibitors work at or below SMO

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Moa for Vismoedegib

A

oral smo inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

BBW’s for SMOE

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Targetted drugs for squamous cell

A

none

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

conventional drugs for squamous cell

A

cisplatin but not standard tx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

first line theray for squamous

A

sxical xision

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Immuntherapies for Melanoma

A

Aldesleukin
Interferon alpha
Ipilimumab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Signal transduction inhibitors for melanoma

A

sorafenib
trametinib
vemurafenib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

chemotherapy for advanced melanoma

again these don’t work well

A

dacarbazine, lomustine, carmustine (20% but repsonse short lived)
also taxanes, platinums, vincas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how does aldesleukin work?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

induces proliferation of B, T, Macrphages and NK cells

A

aldesleukin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

BBW’s with aldesleukin

A

Cardio, Pul, Renal, CNS deffieincies

*also contra in hepatic disease or post-trasnplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what do you have to have before putting someone on Aldesleukin

A

Thallium Stress Test
formal PFT
*daily on tx CXR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

unique side effect of aldesleukin

A

renail failure insufficiency by CAPILLARY LEAK SYNDROME

“all-dats-leakin”

31
Q

what to do Tregs do

A

tone down host anti-tumor, viral response

  • guards againts autimmunity in life
  • but hinders our anti-cancer efforts
32
Q

VLS (capillary leak syndrome)

A

hypotension, inc vasc, permeability, pulmonary edema, renal/liver failure

33
Q

what causes VLA

A

CD122hiNK cells–> releaisng pro-inflamm cytokines (TNF)
or
IL2 binding to CD25 endothelial cells increasing permeability

34
Q

Aldesleukin acivates which cell lines

A

CD4 and CD* (beefs up their antitumor response

Treg->accidentally beefs up host anti-antitumor repsone (BAD off target effect)

35
Q

MOA for interferon alpha2b

A

works like endogenous interferon

36
Q

BBW’s for interferon

A

worsening of auto-immune dz
cardiac dysfuntion
depression–> suicide

37
Q

routine tests for interferon

A

CBC’s, CXR, ECG, LFT’s

38
Q

CLTA4 recombinant antibody

A

Ipilimumab

39
Q

many BBW’s but no D-D interxn potention

A

Ipilimumab

40
Q

side effects of Ipilimumab

A

Severe and fatal immune-mediated adverse reactions
*can cause dermatitis/TEN
rash, dirrhea, tiredness, ithch

41
Q

MOA for ipilimumab

A

bind CLTA4 on the t cell and PREVENTS CLTA4 from binding to B7 (CD80/CD86)

42
Q

what does CTLTA4 do

A

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
Q

THIS DRUG FIGHTS MELANOMA INDIRECTLY BY INCREASING T CELL MEDIATE ANTI-TUMOR RESPONSE

A

IPILUMUMAB

44
Q

PROBLEM WITH IMMUNE THERAPY

A

UNWANTED IMMUNE-MEDIATED ADVERSE EFFECTS IN MANY ORGANS–> LIMITS CLINICAL UTILITY

45
Q

HEMORRHAGE POSIBLE–>rash (severe-desquamative),hepatic dysfunction high LFT’s,, heme toxic

A

sorafenib

46
Q

mutli-kinase inhibitor

A

sorafenib

47
Q

what kinases does sorafenib inhibit

A

VEGF, PDGFR< cKIT, RAF

48
Q

2 drugs that cause hand and foot syndrome

A

Sorafenib

Trametinib

49
Q

routine tests required with sorafenib

A

CBC’s–> anemia and nutropenia, BM supressed

50
Q

increased risk of brain/GI bleed

A

srafenib–> inhibits VEGF

51
Q

effects of sorafenib mutli-kinase inhibition

A
  1. antiproliferation

1. antiangiogenic

52
Q

recommended regimen for sorafenib right now

A

dacarbazine IV on day one

then sorafenib for 21 days

53
Q

MOA for tremtinib

A

reversible MEK inihib.

54
Q

how to remember tremetinib

A

treMEKinhib

55
Q

treats BRAF V600E or V600K muts

A

tremetinib

56
Q

severe skin toxiticities

A

tremetinib and sorafenib

57
Q

routine test for tremetinib

A

LVEF must be monitored, CBC’s and LFT’s

58
Q

side effects

A

cardiomyopathy, ILD, retinal pigment epithelial detachmet

59
Q

retinal epithelial dettachment

A

tremetinib

60
Q

requires genotyping for BRAF mutation

A

tremetinib and vemurafenib

61
Q

order of signal transduciton

A

RTK–> cKIT, NRAS< BRAF<proliferation and survival

62
Q

if MEK is mutant what will work

A

nothing or tremtinib?

63
Q

if mek is mutant what wont work

A

vemurafenib–> downstream

64
Q

works on BRAF V600E * not to be used in wild-type tumors

works only on mutant BRAF

A

vemurafenib

65
Q

may cause paradoxical ERK activation of RAS driven growth if used un wild type tumors

A

vemurafenib

66
Q

requires constituitively acitve BRAF mutation V600e

A

vemurafenib and trametinib

67
Q

patients receiving this drug are at a higher risk for developing SCC (25% of patients)

A

vemurafenib

68
Q

significant toxicities of vemurafeinib

A

skin-SJS and SCC possible
eye-uveitis, iritis, retinal vein occlusion
cardiac–> qt prolong
liver–>PGP and cyp interactions

69
Q

monitoring required with vemurafenib

A

EKG, electrolytes, creatinine, lft’s

70
Q

resistance to vemurafenib

A

alternative pathway selection (normal RAF, Araf, Craf, etc all have a greater presence if BRAF is inhibited)

71
Q

causes pradoxical RAS-driven proliferation of pre-exisiting and unrecognized malignancies

A

vemurafenib

72
Q

commonalities of toxicity in MEK/RAF inh.

A

liver, heart, eye, secondary malignancies

73
Q

all three raf/mek inhibitors have the potential to cause

A

possibly severe rash (SJS-desquamative)

74
Q

pregnancy

A

immune modulators C–>dont give

raf/mek inhibitors D–> teratogen associated

Dermatology (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions