Brainscape's Knowledge GenomeTM

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


See full index

Dermatology > Pathophys/Path 2 > Flashcards

Pathophys/Path 2 Flashcards

You may prefer our related Brainscape-certified flashcards:
Dermatology Board Prep 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How do melanomas develop?

A

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

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

What are the three types of nevi?

A

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

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

What defines nevi?

A

Well circumscribed
Small
Symmetric
Uniformly pigmented

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why get melanoma?

A

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

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

Screening for melanoma?

A 
A asymmetry
B borders-irregular, scalloped
C color-mottled, variegated
D diameter >6mm
E elevation
"change" "ugly duckling"
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

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

Melanoma Treatment

A

Early, cut it out

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Solar Radiation

A

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

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

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

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

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

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

When sunlight hits skin…

A

reflected, absorbed by epidermis, dermis, DNA, proteins

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

Action spectrum is determined by?

A

UV absorbing properties of molecule that initiates response: chromophore

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

Major UVB chromophores in skin?

A

DNA, urocanic acid, aromatic amino acids

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

Photodamage

A

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

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

Suntan

A

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
Q

Chronic Effects of UVR

A

photoaging

BCC, SCC, melanoma

27
Q

chronologic aging

A

smooth, pale, finely wrinkled skin, benign growths

28
Q

photoaging

A

UVA(penetrate deeper)/UVB(more efficient)
dry, deep wrinkles, inelastic, leathery, atrophic, telangiectasias, irrugular pigmentation, comedone/cyst formation, actinic keratoses, malinancies, benign

29
Q

DNA damage

A

direct: UVB-obsorption of photons by bases of DNA
indirect: absorption of photons by other chromophores

30
Q

DNA photoproducts

A

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
Q

Skin defense against UVR

A 
stratum-reflection
melanin-absorption
tumor suppressor genes-patched, p53,016
DNA repair
apoptosis
32
Q

Immunosuppression and sun

A

langerhans cells disapear with sunburn

those and lymohocytes are sensitive to DNA damage

33
Q

Light used to treat?

A

Eczema, Psoriasis, Cutaneous lymphoma

34
Q

Tanning Beds

A

Mostly UVA, 5X normal amount, no protection, melanoma associated
>75% increase in those that use before 30s
carcinogenic by WHO

35
Q

Acral Lentiginous Melanoma

A

hands and feet

36
Q

Lentigo Maligna Melanoma

A

face

37
Q

nodular

A

nodular
sun exposed
“no preceding radical growth”
15%MM 2x more in men

38
Q

Superficial Spreading

A

not as aggressive

“red, white, blue”`

39
Q

Breslow’s thickness

A

distance of involvement from the stratum granulosum (top) to the deepest tumor cell (bottom) 4mm bad

40
Q

Nonmelanoma risk?

A

1 in 5 lifetime

rising in young females

41
Q

Basal Cell Carcinoma

A

-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
Q

RIsk of BCC

A 
UV
fair complexion
sunburns (blistering)
family history of BCC
immunosuppression
43
Q

Pathology of BCC

A
  • 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
Q

BCC Subtypes

A 
nodular (most common)
superficial
pigmented
morpheoform (cutaneous)
micronodular
cystic
infiltrative
45
Q

BS nevus syndrome (Gorlin Syndrome)

A 
auto dominant   1 in 56,000
mutation of PTCH1
BCC in 20's
MSK defects/jay cysts
increase other cancer risk (fibrosarcoma, medulloblastoma)
46
Q

BCC metastasis/treatment

A

rare 0.0028%-0.55%

surgery, radiation, topical (targated Vismodegib)-SMO inhibitor

47
Q

Squamous Cell C

A
  • epidermal keratinocytes (resembles spinous layer)
  • 2nd most common skin cancer
  • progress like cervical cancer, minimal atypia, full thickness epidermal atypia above BM, incasive
48
Q

Actinic Keratoses

A

thin non-indurated lesion
superficial
in epidermis

49
Q

SSC Pathology

A
  • hyperchromatic pleomorphic nuclei, disorganized growth, mitoses and invasion throughout basal layer
  • pink, keratinizing cells like stratum spinosum
50
Q

SSC Risks

A 
no mutation only p53
UV
HPV
Immunosuppression
-scars,inflammation,chemical,radiation,leukoplakia
51
Q

Cutaneous SCC metastasis risk?

A

size, depth, site, host immune status

1) larger than 2cm
2) greater than 4mm depth
3) on lips or ears

52
Q

SCC metastasis

A

<5%, mets to lymph nodes and lung

53
Q

Keratoacanthoma

A 
SCC related,
neoplasm of keratinocytes
rapidly grows over 2-6 weeks 
painful
involute spontaneously
54
Q

Marjolin’s Ulcer

A

ulcerative incasive SCC

chronic inflammation, scarring, radiation, trauma

55
Q

SCC Treatment

A

excision
actinic keratosis: topical/cryotherapy
topical

Dermatology (9 decks)

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