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year 5 > dermatology skin cancers > Flashcards

dermatology skin cancers Flashcards

1
Q

what causes skin cancer

A

most are due to interaction of

  • Exposure to UVR
  • relative absence of the protective pigment melanin

skin has DNA repair mechanisms which are efficient at repairing UVR skin damage but not perfect and sometimes a mutation can occur and creates mutated cells

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2
Q

risk factors for skin cancer

A
  • immunosuppressed
  • pale skin
  • living in sunny places
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3
Q

two groups of skin cancers

A
  • malignant melanoma 1.5%: melanocyte derived

- non melanoma skin cancers 20% -keratinocyte derived

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4
Q

two types of prevention

A

primary is stopping skin cancers developing

secondary is detecting early or minimising harm from early dysplastic lesions

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5
Q

minimising exposure to UVR

A

sun protection
avoiding exposure during middle three hrs of the day
shade
summer clothing

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6
Q

what is SPF a measure of

A

mostly protection against UVB

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7
Q

SPF 4 means

A

lets 25% through

blocks 75%

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8
Q

SPF 50 means

A

lets 2% through and blocks 98%

or takes 50 times as long to cause same amount of erythema

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9
Q

SPF of 10 and a broad brimmed hat cover

A

10x4 for the hat= 40

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10
Q

benefits of UVR

A

-vitamin D
20 minutes only
still adebated issue

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11
Q

what is sunburn

A

erythema dilatation of the dermis vasculature in response to damage from UVR
peaks at 8-24hrs before subsitiding

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12
Q

complications of sunburn

A

pain
allodynia- pain on light touch
oedema and blistering

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13
Q

what rx can be given for sunburn

A

indomethacin

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14
Q

what is xeroderma pigementosa

A 
autosomal recessive extreme photosensitivity
excessive sunburn to trivial exposure
freckling
risks of skin cancer from young age
DNA repair defect 
especially to UVB wavelengths
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15
Q

what part of UVR sunshine causes erythema and skin cacer

A

shorter wavelenths UVB are more potent at causing sunburn

  • for most skin cancers therefore UVB is the most important causative UVR waveband
  • but melanoma may be UVA and UVB
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16
Q

XP 2 main phenotypes

A
  1. more erythema- actively transcribed genes

2. more freckling- not actively transcribed

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17
Q

A to E approach for melanoma stands for

A 
A asymmetry
B border-irregular
C colour- often multiple colours
D diameter- OFTEN >1cm across
E evolution of elevation - most are changing
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18
Q

3 main surgical excisions

A

scalpel
punch biopsy
ring curette

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19
Q

what are shave biopsies

A

using a scalpel
aim to remove most of lesion but not all
NOT FOR SUSPECTED MELANOMA

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20
Q

PRIMARY VS SECONDARY HEALING

A
  • primary is pulling edge of wound sites close together to heal = primary closure
  • secondary is not possible to pull together as surgical defect too large - so especially at concave sites allow wound to heal from base up
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21
Q

grafts vs flaps

A

grafts= skin taken from elsewhere on the body and detached from the blood supply

flap= skin from donor areas of skin that keep their connection with their origin and therefore have a blood supply

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22
Q

anaesthesia used for derm surgery

A

1% lignocaine with adrenaline 1:20,000,000
adrenaline causes vasoconstriction
but not in patients with PVD or raynauds- digital necrosis
and not first term pregnancy

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23
Q

drawbacks of curetting a lesion

A

damages the normal architecture so pathologist cant comment on adequacy of margins
not for malignant

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24
Q

side effects of cryotherapy

A 
pain
inflammation
blistering
ulcers
scarring
tendon rupture
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25
Q

risk factors for skin cancer

A
  • age-age is a proxy for UVR exposure
  • ambient- body parts, where they live
  • human behaviour
  • pigmentary phenotype- pheomelanin-eumelanin
  • genetics- xeroderma pigmentosum, albinism, melanocortin 1 receptor
  • mutation of tumour suppressor gene-kudson two hit hypothesis - AR TSG inheritance and only neeeds one more hit then
  • immune system
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26
Q

basal cell nevus syndrome risks

A

-already have inherited mutation in one allele
knudson hit
so present at younger age

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27
Q

cancer assoc. to immunosuppression

A

squamous cell carcinoma

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28
Q

most common skin cancer in Europe

A

basal cell carcinoma

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29
Q

BCC what is it

A

malignant tumour of keratinocytes

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30
Q

behaviour of BCC

A

NEVER metastasises

but is locally destructive and can invade aggressively locally although slowly occurs

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31
Q

presentation of a BCC

A

-translucent quality
-often translucen papules
-pearly
which surround an ulcerated crater
telangiectasia
mostly middle third of face
1cm to >5cm
appear over months to years
can also ulcerate, discharge, bleed or weep

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32
Q

types of BCC

A

nodular
morphoeic
superficial
infiltrative

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33
Q

nodular BCC

A

classical BCC

clinical and tumour margins well defined

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34
Q

morphoeic BCC

A

defining the edge of these tumours is subject to considerble area as they can sometimes be several larger than first appear

moh’s surgery

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35
Q

superficial BCC

A

-relatively more common on backs and limbs
dont show any significant induration
cyrotherapy and chemotherapeutic agents may be more appropriate that ssurgery

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36
Q

infiltrative

A

morphoeic and nodular
insidious
grow haphazard
moh’s surgery

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37
Q

differentials BCC

A

sometimes people think

  • acne spots- but lasting >3-4 weeks
  • damage or trauma
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38
Q

bcc excision margin

A

4mm margin

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39
Q

moh’s surgery for BCC

A
  • middle third of face
  • irregular tumour eg morphoeic and infiltrative
  • take horizontal sections so can examine during surgery
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40
Q

risk factors for BCC

A

-immunosuppression
-rare inherited syndromes basal cell nevus syndrome
hx of BCC or skin cancer

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41
Q

what is basal cell nevus syndrome or gorlin’s

A

-autosomal dominant
mutation in PTCH gene
present with a large number of BCC at young age and show small pit like abnormalities on palms and other dysmorphic features
-not always fhx as can be new mutation
-first hit inherited and then second due to UVR

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42
Q

squamous cell carcinoma behaviour

A

agressive
3-5% mets
body sites strongly mirrors UVR exposure

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43
Q

two precursor lesions SCC

A

actinic keratoses

intra-epithelial carcinoma

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44
Q

presentation SCC

A

-keratinising nodule
-ulcerated
-ugly
-photodamage erythema around it - and changes to vasculature
-usually nodule
can have lost their keratinising appearance
keratin plug volcano
sometimes appear smooth

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45
Q

distribution of scc

A

bald heads
top of ears
face
back of hands

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46
Q

SCC signs more likely to have mets

A

> 2cm
depth >4mm
poorly differentiated
background immunosuppression

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47
Q

management SCC

A

-excision margin 4-6mm

radiotherapy only in some cases

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48
Q

RF for SCC

A
  1. immunosuppresison
  2. SCC related to continuous sun exposure so in outdoor workers
  3. UV related
  4. more common in XP
  5. PUVA
  6. areas with high levels of arsenic ingestion
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49
Q

differential SCC

A

fergus smith syndrome

similar looking but behave different

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50
Q

what is melanoma

A

malignant tumour of melanocytes

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51
Q

presentation of melanomas

A 
most are pigmented 
asymmetry
irregular border
multiple colours
diameter 
evolving
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52
Q

in situ melanoma is

A

melanoma in situ- aka only in epidermis not into dermis

still cancerous but cant spread

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53
Q

types of melanoma

A 
nodular
acral
lentigo melanoma
amelanotic 
superficial
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54
Q

risk factors for melanoma

A
  • UVR exposure but intermittent exposure eg australia untanned indoor worker
  • acral melanoma on palms and soles is not UVR related and more prevalent in some populations
  • familial melanoma -autosomal dominant
  • PUVA risk factor
  • immunosuppression
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55
Q

fhx of melanoma clues

A

-large number of nevi that look atypical

fhx of melanoma

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56
Q

behaviour of melanoma

A

metastasise early

57
Q

risk factors melanoma

A

-skin type
gender
men on trunk
women on legs

several episodes sun burn
atypical naevus syndrome
fhx and phx

58
Q

superficial melanoma

A

flat or almost flat lesions in which the malignant clones of cells have appeared to spread laterally from a central point

can resemble melanocytic nevi or freckles

59
Q

nodular melanoma

A

nodules
reflection of a large downward vertical collection of malignant cells
can be a later stage of SSM

60
Q

lentigo maligna melanoma

A

refers to melanoma on continually sun exposed sites such as face or back of hands
response to UVR
develop over many years

61
Q

lentigo maligna vs lentigo maligna melanoma

A

lentigo maligna is precursor so cells only in epidermis

62
Q

amelanotic melanoma

A

aka without melanin
not pigmented
hard to pick up

63
Q

acral melanomas

A 
melanoma on palms or soles 
rare
usually pigmented
not related to UVR
certain popualtions eg Africans
64
Q

two types of melanoma

A

melanoma de novo- new which is faster growing
or
melanoma on pre-existing lesion eg a mole

65
Q

Breslow thickness

A

measured in mm from granular layer to deepest part of the tumour

66
Q

management of suspicious pigmented lesions

A
  • treat like melanoma
  • excise with 2mm margin and send to pathology
  • they measure breslow thickness
  • and a wide local excision may then be done determined by breslow thickness
67
Q

management of <1mm v >1mm breslow thickness

A
  • wide local excision is when original scar is excised and a margin of normal skin taken

if BT <1mm then margin of 1cm on all sides of scar taken

if BT >1mm then margin of 2cm on all sides taken

68
Q

other rx option for melanoma

A

-may give vemurafenib (braf) signal or ipilimumab for metastatic disease

69
Q

pre-malignant lesions of SCC

A

actinic keratoses

70
Q

actinic keratoses what are they

A

focal areas of dysplasia

71
Q

presentation of AK

A 
-erythema - can be hard to tell between 
and scale
-feel rough
-scaly lesions
-often at sites of UVR exposure eg tops of ears 
-common in syn sensitive
72
Q

prognosis AK

A

low rate of progression to SCC

73
Q

management of AK decision

A

based on

  • cosmetic
  • progression to SCC- hard to determine
  • diagnostic unsure whether a AK or SCC
74
Q

options for AK management

A
  • liquid nitrogen

- background change have efedex- hydrofluoracil cream

75
Q

intra-epithelial carcinoma

A

also bowen’s disease or in situ

76
Q

pathology IE carcinoma

A

full thickness of dysplasia of epidermis

but not breached basement membrane

77
Q

management of intra-epithelial carcinoma

A

histopathology confirmation of dx may be required with an incisionall biopsy to assay for any invasion (SCC)

78
Q

differentiating intra-epithelial carcinoma and AK

A
  • Ak smaller and focal

- IEC tends to be plaque like and larger

79
Q

management options for IEC and AK

A 
-both lower progression rate
so can just destroy superficial skin
surgical excision
cryo-dont use if unsure about dx 
curette
cautery
topical chemo agents
80
Q

topical chemo agents for IEC or AK

A

-imiquimod -simulates immune system
-5 fluorouracil- inhibits DNA and RNA synthesis
-ingenol mebutate- induces cell death
topical NSAID eg diclofenac
photdynamic therapy with topicla porphyrins

81
Q

SE topical chemo agents

A

inflammation

malaise

82
Q

rarer skin cancers

A 
merkel cell
appendage tumours
kaposi sarcoma
cutaneous lymphomas
sarcomas
cutaneous secondaries
83
Q

merkel cell pathology

A
  • neuroendocrine carcinoma
  • merkel cell polyomavirus
  • UVR related
84
Q

RF for merkel cell

A

immunosuppressed as virus

85
Q

behaviour of MCC

A

-metastatic spread so poorer 70% at 5 yrs prognosis

86
Q

management MCC

A

excision +/- radiotherapy

87
Q

appendageal carcinomas pathology

A

due to benign keratinocyte tumours related to hair follicles and sweat glands

  • also cna be malignant
  • can metastasise
  • managed as SCC
88
Q

cutaneous lymphoma T cell presentation

A
  • usually present as widespread rash that resembles psoriasis
  • as lesion progresses becomes more nodular
  • progresses very slowly
89
Q

cutaneous B cell lymphoma presentation

A

-erythematous nodules or plaques

90
Q

most common primary cutaneous sarcoma is

A

dermatofibrosarcoma protuberans

91
Q

presentation dermatofibrosarcoma protuberans

A

-firm nodule or plaque reminiscent of ann odd dermatofibroma
over shoulder girdle in young adult
-can mets
-recurrence locally common

92
Q

management of DFP

A

-wide excision +/- radiotherapy

93
Q

leiomyosarcoma

A
  • cutaneous sarcoma

- firm indolent nodule

94
Q

kaposi sarcoma pathology

A

-spindle cell malignancy from vascular endothelium
-seen in untreated HIV/ AIDS
virus= herpes 8

95
Q

cutaneous secondaries causes

A
  • rare from internal malignancies-sister mary joseph -adenocarcinoma of umbilicus
  • from primary skin cancers mostly seen in melanoma
96
Q

keratoacanthoma presentation

A

looks like a fast growing SCC

  • grows for 6 weeks then involutes and falls off
  • if left when it regresses leaves a scar
97
Q

management of keratoacanthoma

A

-often managed as for SCC and completely excised and biopsied

98
Q

mimics of skin cancer

A 
-freckles
solar lentigines
blue nevi
meyerson's nevi
melanocytic macule mucosa
neurofibromas
cafe au lait macule
halo nevi
melanocytic nevi
congenital nevi
sebhorreic keratosis 
vascular- angioma, P granuloma, venous lake
viral warts
comedones
epidermal cyst
molluscum
skin tags
sebaceous hypreplasia
dermatofibromsa
99
Q

cherry angiomas presentation

A

dont blanch
increase with age
also called cambell de morgan

100
Q

angiomas presentation

A

some blanch others dont
not worrying
can mimic melanomas
if blanch dont need to worry as means vascular

101
Q

venous lake is

A
  • commonly seen on the lips
  • easily compressible
  • often confused with melanotic macules of the lips which are not compressible
102
Q

pyogenic granuloma

A

-vascular proliferation in response to wounding
common on hands and around mouth
occur in children and adults
because they bleed with minimal trauma they are often curetted
-can mimic amelanotic melanomas/pigmented- therefore if suspicious dont currette
hx of trauma not always apparent

103
Q

vascular nevus and port wine stain

A

present at birth or appear soon after

104
Q

dermatofibromas are

A 
firm nodules
tend to appear early in adult life
more common proximal legs or arms
reactive to earlier insults such as insect bites
proliferation of fibroblasts in dermis
105
Q

dx clue for dermatofibromas

A

much firmer and feel bigger than they look

106
Q

sebaceous hyperplasia are

A

enlarged sebaceous glands most common on the face
vary 2-6mm

characteristic translucent and yellow colour and an umbilicated or rosette like shape around a central follicular orifice

often multiple ones

107
Q

skin tags are

A

focal overgrowth of epidermis and dermis

108
Q

who and where gets skin tags

A

obese

flexural areas

109
Q

viral warts cause

A

HPV

110
Q

viral warts diff dx

A

easier to dx in children

but in adults can look like AK, SK, scc

111
Q

who is at risk of viral warts

A

immunosuppressed

112
Q

molluscum contagiosum cause

A

pox virus infection

113
Q

who gets molluscum contagiosum

A

common in children tend to resolve 6months

if multiple in adults suggesst underlying immunosuppression

114
Q

clinical dx of molluscum

A

central umbilication

115
Q

epidermal cyst presentation

A

may contain a punctum- which is an opening of the surface and remains of follicualr infundibulum which has become obstructed

116
Q

what are epidermal cyst

A

-epithelium lined

punctum

117
Q

comedones are

A

giant comedones are epidermal cyst with a prominent opening
refer for review as suspected melanomas
also seen in people with high UVR exposure
elastotic UVR damage to Dermis

118
Q

what are freckles

A

macular focal areas of overproduction of melanin
sun exposure on sensitive skin
face shoulder and arms

119
Q

seb k are

A

benign keratinocyte tumours

some of which harbour somatic mutations

120
Q

presentation of seb K

A 
usually >30
stuck on appearance like wax
warty-irregular surface
greasy
most common on trunk
well circumscribed
plaque and pigmented
comedo like openings and milia cysts
often black brown but can be pink
121
Q

symptoms of seb k

A

itchy

break off q

122
Q

what are solar lentigines

A

also called liver spots

flat or almost flat brown marks

123
Q

where are solar lentigines most common

A

back of hands
forearms
face

124
Q

cause of solar lentigines

A

reflect previous sun exposure
so surrounding skin can show other features of sun damage
-no proliferation of melanocytes

125
Q

diff dx of solar lentigines

A

can be difficult to tell vs lentigo maligna (melanoma)

-if they have lots of them unlikely to be a melanoma
but if in doubt refer to derm

126
Q

melanocytic nevi what are they

A

focal collection of melanocytes clustered in a nest that may or may not produce pigment

benign melanocytic tumours

127
Q

timeline melanocytic nevi

A

start to appear in childhood- reach a max in third or fourth decade

in early life often flat and dark before becoming raised whilst still being pigmented before losing their pigment but remaining raised

128
Q

significance of melanocytic nevi

A

-many harbour mutation of genes known to be implicated in tumours eg BRAF
but rate of progression of benign melanocytic nevi to a melanoma is very low 1/200,000 per yr

129
Q

diff dx of melanocytic nevi

A

melanoma-so in in doubt treat as melanoma
low rate progress to melanomas
but
conversely a significant fraction of melanomas are derived from moles
cos we have lots of moles

130
Q

dermal nevus

A

melanocytic nevis with no pigment

131
Q

congenital melanocytic nevi presentation

A

some pigmented nevi are present at birth or soon after
-harmless unless very large >10cm and can undergo malignant change

many also contain hair follicles and sweat glands

132
Q

what causes a blue nevi

A

melanin deep in dermis causes a blue colour due to light scattering
more common asian popualtions
childhood

133
Q

new onset blue nevi in adulthood management

A

suspcious for melanoma

134
Q

halo nevi pathology

A
135
Q

meaning of halo nevi

A
  • mostly common in childhood and harmless

- no clinical significance but can appear in a patient with a melanoma elsewhere

136
Q

meyerson’s nevi presentation

A

melanocytic nevi surrounded by a patch of eczema

137
Q

mucosal melanotic macules are

A

macular areas of increased pigmentation on the lips
usually multiple pigmented macules

if solitary can be a melanoma

138
Q

cafe au lait spots >5 signify

A

neurofibromatosis?

year 5 (9 decks)

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