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Dermatology > Pathophys/Path 2 > Flashcards

Pathophys/Path 2 Flashcards

1
Q

Melanoma Epidemeology

A 
est. 138,000 new cases in 2013
Highest risk: caucasian men >50
Most common cancer in: 25-29y/o
2nd most common: 15-29y/o
1 American dies every hour from melanoma
Rising: young women with tanning
           older men
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2
Q

How do melanomas develop?

A

80% is denovo
20% from nevi
Must be in dermis to metastasize

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3
Q

What are the three types of nevi?

A

1) Junctional - epidermis
2) Compound - epidermis/dermis
3) Intradermal Melanocytic

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4
Q

What defines nevi?

A

Well circumscribed
Small
Symmetric
Uniformly pigmented

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5
Q

Nevi and Melanoma Relationship?

A
  • compromised by melanocytes
  • share some mutations (BRAF)
  • more nevi (>50) increase chance of melanoma
  • melanoma can develop from pre-exisiting nevi
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6
Q

Why get melanoma?

A

Multifactorial: Genetic (CDNK2, BRAF)
Environment (UV)
Underlying immune status

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7
Q

Melanoma risk factors?`

A
  • Large # of nevi (>50)
  • giant congenital nevi
  • atypical nevi
  • history of blistering sunburns
  • family history of melanoma
  • light complexing
  • tanning bed use
  • underlying immune dysfunction
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8
Q

Screening for melanoma?

A 
A asymmetry
B borders-irregular, scalloped
C color-mottled, variegated
D diameter >6mm
E elevation
"change" "ugly duckling"
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9
Q

Melanoma Metastasis

A

Often lymphatics
#1 site is skin
most common cause of death: CNS involvement
Most important prognostic factor: lymph node involvement
Most important histologic prognostic: Breslow thickness and ulceration

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10
Q

Melanoma Treatment

A

Early, cut it out

Metastatic: no proof that anything increases survival (late 2011)

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11
Q

Vemurafenib

A

attacks MAPK kinase signaling pathway
-Small molecular inhibitor of BRAF (V600E mut.)
-good for unresectable/metastatic melanoma
survival benefit for 50% of patients with mutation
-modest in duration (6 month survival)

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12
Q

Sunlight and Cancer

A

UVB forms dimers b/w neighboring thymine pairs in DNA, repaired by endonucleases and other repair

  • Squamous: cumulative
  • Basal: not relate to cumulative?
  • Melanoma: role with genetic and immune
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13
Q

Xeroderma Pigmentosum

A

Autosomal recessive 1 in 1 million
deficient repair of UV-induced DNA damage (nucleotide excision repair of thymine dimers)
-freckles, wrinkling, skin atrophy
first cancer at 8, at 20 risk is 10,000 higher (2,000 for melanoma)
eyes, CNS, death 32y/o

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14
Q

Solar Radiation

A

5% is between 100-400nm, lots of diseases

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15
Q

UVC

A

200-290nm don’t penetrate ozone layer, most potent, when artificially produced it’s absorbed by DNA, RNA, proteins and can be lethal to epidermal cells

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16
Q

UVB

A

290-320nm, window glass filters out <320nm, sunburn/photochemical rxns in skin
SPF against this one
2-5% of what reaches earth surface

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17
Q

UVA

A

320-400nm then its visible
least potent, penetrates glass and deeper than UVB-cause of wrinkles
98% of what reaches us from sun

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18
Q

what modifies UVR?

A

atmosphere, latitude, altitude (1000ft is 4% increase), reflection (water-7%, sand-25%, snow-80%), clouds (scatter not absorb), time of day, season

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19
Q

When sunlight hits skin…

A

reflected, absorbed by epidermis, dermis, DNA, proteins

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20
Q

Action spectrum is determined by?

A

UV absorbing properties of molecule that initiates response: chromophore

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21
Q

Major UVB chromophores in skin?

A

DNA, urocanic acid, aromatic amino acids

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22
Q

Photodamage

A

UVB majority of effects on skin
acute/chronic response depends on phototype
Types I-VI burning, tanning, cancer

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23
Q

Acute effects of UVR

A 
inflammation
immunomodulation
tanning
epidermal hyperplasia (skin thickening)
Vit D photosynthesis
DNA damage -apoptosis, cell cycle arrest to repair
24
Q

Sunburn

A 
mostly UVB
erythema-vasodilation
heat-increased blood flow
pain/pruritus - cytokine release
intracellular edema/perivascular edema
hyperkeratosis, acenthosis >72hrs
25
Suntan
UVA/visible: immediate, fades in hour, oxidation/redistribution of existing melanin, no protection -Delayed is UVB, >72hrs, increased melanin synthesis and transfer, some protection
26
Chronic Effects of UVR
photoaging | BCC, SCC, melanoma
27
chronologic aging
smooth, pale, finely wrinkled skin, benign growths
28
photoaging
UVA(penetrate deeper)/UVB(more efficient) dry, deep wrinkles, inelastic, leathery, atrophic, telangiectasias, irrugular pigmentation, comedone/cyst formation, actinic keratoses, malinancies, benign
29
DNA damage
direct: UVB-obsorption of photons by bases of DNA indirect: absorption of photons by other chromophores
30
DNA photoproducts
dimers formed by covalent binding of 2 adjacent pyrimidines in the same polynucleotide chain - cyclobutane - 6,4 photoproducts * **signature mutations C to T or CC to TT
31
Skin defense against UVR
``` stratum-reflection melanin-absorption tumor suppressor genes-patched, p53,016 DNA repair apoptosis ```
32
Immunosuppression and sun
langerhans cells disapear with sunburn | those and lymohocytes are sensitive to DNA damage
33
Light used to treat?
Eczema, Psoriasis, Cutaneous lymphoma
34
Tanning Beds
Mostly UVA, 5X normal amount, no protection, melanoma associated >75% increase in those that use before 30s carcinogenic by WHO
35
Acral Lentiginous Melanoma
hands and feet
36
Lentigo Maligna Melanoma
face
37
nodular
nodular sun exposed "no preceding radical growth" 15%MM 2x more in men
38
Superficial Spreading
not as aggressive | "red, white, blue"`
39
Breslow's thickness
distance of involvement from the stratum granulosum (top) to the deepest tumor cell (bottom) 4mm bad
40
Nonmelanoma risk?
1 in 5 lifetime | rising in young females
41
Basal Cell Carcinoma
-germinative keratinocytes "picket fence" blue -most common invasive neoplasm in US 2million/year PTCH mutation in 30% (tumor suppressor of basal epidermal cell proliferation)
42
RIsk of BCC
``` UV fair complexion sunburns (blistering) family history of BCC immunosuppression ```
43
Pathology of BCC
- basophilic hyperchormatic cells that form nodules, extending from surface of epidermis - peripheral cells form palisade - tumor nodule set in mucinous stroma with retraction from that stroma (clefting)
44
BCC Subtypes
``` nodular (most common) superficial pigmented morpheoform (cutaneous) micronodular cystic infiltrative ```
45
BS nevus syndrome (Gorlin Syndrome)
``` auto dominant 1 in 56,000 mutation of PTCH1 BCC in 20's MSK defects/jay cysts increase other cancer risk (fibrosarcoma, medulloblastoma) ```
46
BCC metastasis/treatment
rare 0.0028%-0.55% | surgery, radiation, topical (targated Vismodegib)-SMO inhibitor
47
Squamous Cell C
- epidermal keratinocytes (resembles spinous layer) - 2nd most common skin cancer - progress like cervical cancer, minimal atypia, full thickness epidermal atypia above BM, incasive
48
Actinic Keratoses
thin non-indurated lesion superficial in epidermis
49
SSC Pathology
- hyperchromatic pleomorphic nuclei, disorganized growth, mitoses and invasion throughout basal layer - pink, keratinizing cells like stratum spinosum
50
SSC Risks
``` no mutation only p53 UV HPV Immunosuppression -scars,inflammation,chemical,radiation,leukoplakia ```
51
Cutaneous SCC metastasis risk?
size, depth, site, host immune status 1) larger than 2cm 2) greater than 4mm depth 3) on lips or ears
52
SCC metastasis
<5%, mets to lymph nodes and lung
53
Keratoacanthoma
``` SCC related, neoplasm of keratinocytes rapidly grows over 2-6 weeks painful involute spontaneously ```
54
Marjolin's Ulcer
ulcerative incasive SCC | chronic inflammation, scarring, radiation, trauma
55
SCC Treatment
excision actinic keratosis: topical/cryotherapy topical

Dermatology (9 decks)

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