dermatology skin cancers Flashcards
what causes skin cancer
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
risk factors for skin cancer
- immunosuppressed
- pale skin
- living in sunny places
two groups of skin cancers
- malignant melanoma 1.5%: melanocyte derived
- non melanoma skin cancers 20% -keratinocyte derived
two types of prevention
primary is stopping skin cancers developing
secondary is detecting early or minimising harm from early dysplastic lesions
minimising exposure to UVR
sun protection
avoiding exposure during middle three hrs of the day
shade
summer clothing
what is SPF a measure of
mostly protection against UVB
SPF 4 means
lets 25% through
blocks 75%
SPF 50 means
lets 2% through and blocks 98%
or takes 50 times as long to cause same amount of erythema
SPF of 10 and a broad brimmed hat cover
10x4 for the hat= 40
benefits of UVR
-vitamin D
20 minutes only
still adebated issue
what is sunburn
erythema dilatation of the dermis vasculature in response to damage from UVR
peaks at 8-24hrs before subsitiding
complications of sunburn
pain
allodynia- pain on light touch
oedema and blistering
what rx can be given for sunburn
indomethacin
what is xeroderma pigementosa
autosomal recessive extreme photosensitivity excessive sunburn to trivial exposure freckling risks of skin cancer from young age DNA repair defect especially to UVB wavelengths
what part of UVR sunshine causes erythema and skin cacer
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
XP 2 main phenotypes
- more erythema- actively transcribed genes
2. more freckling- not actively transcribed
A to E approach for melanoma stands for
A asymmetry B border-irregular C colour- often multiple colours D diameter- OFTEN >1cm across E evolution of elevation - most are changing
3 main surgical excisions
scalpel
punch biopsy
ring curette
what are shave biopsies
using a scalpel
aim to remove most of lesion but not all
NOT FOR SUSPECTED MELANOMA
PRIMARY VS SECONDARY HEALING
- 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
grafts vs flaps
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
anaesthesia used for derm surgery
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
drawbacks of curetting a lesion
damages the normal architecture so pathologist cant comment on adequacy of margins
not for malignant
side effects of cryotherapy
pain inflammation blistering ulcers scarring tendon rupture
risk factors for skin cancer
- 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
basal cell nevus syndrome risks
-already have inherited mutation in one allele
knudson hit
so present at younger age
cancer assoc. to immunosuppression
squamous cell carcinoma
most common skin cancer in Europe
basal cell carcinoma
BCC what is it
malignant tumour of keratinocytes
behaviour of BCC
NEVER metastasises
but is locally destructive and can invade aggressively locally although slowly occurs
presentation of a BCC
-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
types of BCC
nodular
morphoeic
superficial
infiltrative
nodular BCC
classical BCC
clinical and tumour margins well defined
morphoeic BCC
defining the edge of these tumours is subject to considerble area as they can sometimes be several larger than first appear
moh’s surgery
superficial BCC
-relatively more common on backs and limbs
dont show any significant induration
cyrotherapy and chemotherapeutic agents may be more appropriate that ssurgery
infiltrative
morphoeic and nodular
insidious
grow haphazard
moh’s surgery
differentials BCC
sometimes people think
- acne spots- but lasting >3-4 weeks
- damage or trauma
bcc excision margin
4mm margin
moh’s surgery for BCC
- middle third of face
- irregular tumour eg morphoeic and infiltrative
- take horizontal sections so can examine during surgery
risk factors for BCC
-immunosuppression
-rare inherited syndromes basal cell nevus syndrome
hx of BCC or skin cancer
what is basal cell nevus syndrome or gorlin’s
-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
squamous cell carcinoma behaviour
agressive
3-5% mets
body sites strongly mirrors UVR exposure
two precursor lesions SCC
actinic keratoses
intra-epithelial carcinoma
presentation SCC
-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
distribution of scc
bald heads
top of ears
face
back of hands
SCC signs more likely to have mets
> 2cm
depth >4mm
poorly differentiated
background immunosuppression
management SCC
-excision margin 4-6mm
radiotherapy only in some cases
RF for SCC
- immunosuppresison
- SCC related to continuous sun exposure so in outdoor workers
- UV related
- more common in XP
- PUVA
- areas with high levels of arsenic ingestion
differential SCC
fergus smith syndrome
similar looking but behave different
what is melanoma
malignant tumour of melanocytes
presentation of melanomas
most are pigmented asymmetry irregular border multiple colours diameter evolving
in situ melanoma is
melanoma in situ- aka only in epidermis not into dermis
still cancerous but cant spread
types of melanoma
nodular acral lentigo melanoma amelanotic superficial
risk factors for melanoma
- 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
fhx of melanoma clues
-large number of nevi that look atypical
fhx of melanoma
behaviour of melanoma
metastasise early
risk factors melanoma
-skin type
gender
men on trunk
women on legs
several episodes sun burn
atypical naevus syndrome
fhx and phx
superficial melanoma
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
nodular melanoma
nodules
reflection of a large downward vertical collection of malignant cells
can be a later stage of SSM
lentigo maligna melanoma
refers to melanoma on continually sun exposed sites such as face or back of hands
response to UVR
develop over many years
lentigo maligna vs lentigo maligna melanoma
lentigo maligna is precursor so cells only in epidermis
amelanotic melanoma
aka without melanin
not pigmented
hard to pick up
acral melanomas
melanoma on palms or soles rare usually pigmented not related to UVR certain popualtions eg Africans
two types of melanoma
melanoma de novo- new which is faster growing
or
melanoma on pre-existing lesion eg a mole
Breslow thickness
measured in mm from granular layer to deepest part of the tumour
management of suspicious pigmented lesions
- 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
management of <1mm v >1mm breslow thickness
- 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
other rx option for melanoma
-may give vemurafenib (braf) signal or ipilimumab for metastatic disease
pre-malignant lesions of SCC
actinic keratoses
actinic keratoses what are they
focal areas of dysplasia
presentation of AK
-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
prognosis AK
low rate of progression to SCC
management of AK decision
based on
- cosmetic
- progression to SCC- hard to determine
- diagnostic unsure whether a AK or SCC
options for AK management
- liquid nitrogen
- background change have efedex- hydrofluoracil cream
intra-epithelial carcinoma
also bowen’s disease or in situ
pathology IE carcinoma
full thickness of dysplasia of epidermis
but not breached basement membrane
management of intra-epithelial carcinoma
histopathology confirmation of dx may be required with an incisionall biopsy to assay for any invasion (SCC)
differentiating intra-epithelial carcinoma and AK
- Ak smaller and focal
- IEC tends to be plaque like and larger
management options for IEC and AK
-both lower progression rate so can just destroy superficial skin surgical excision cryo-dont use if unsure about dx curette cautery topical chemo agents
topical chemo agents for IEC or AK
-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
SE topical chemo agents
inflammation
malaise
rarer skin cancers
merkel cell appendage tumours kaposi sarcoma cutaneous lymphomas sarcomas cutaneous secondaries
merkel cell pathology
- neuroendocrine carcinoma
- merkel cell polyomavirus
- UVR related
RF for merkel cell
immunosuppressed as virus
behaviour of MCC
-metastatic spread so poorer 70% at 5 yrs prognosis
management MCC
excision +/- radiotherapy
appendageal carcinomas pathology
due to benign keratinocyte tumours related to hair follicles and sweat glands
- also cna be malignant
- can metastasise
- managed as SCC
cutaneous lymphoma T cell presentation
- usually present as widespread rash that resembles psoriasis
- as lesion progresses becomes more nodular
- progresses very slowly
cutaneous B cell lymphoma presentation
-erythematous nodules or plaques
most common primary cutaneous sarcoma is
dermatofibrosarcoma protuberans
presentation dermatofibrosarcoma protuberans
-firm nodule or plaque reminiscent of ann odd dermatofibroma
over shoulder girdle in young adult
-can mets
-recurrence locally common
management of DFP
-wide excision +/- radiotherapy
leiomyosarcoma
- cutaneous sarcoma
- firm indolent nodule
kaposi sarcoma pathology
-spindle cell malignancy from vascular endothelium
-seen in untreated HIV/ AIDS
virus= herpes 8
cutaneous secondaries causes
- rare from internal malignancies-sister mary joseph -adenocarcinoma of umbilicus
- from primary skin cancers mostly seen in melanoma
keratoacanthoma presentation
looks like a fast growing SCC
- grows for 6 weeks then involutes and falls off
- if left when it regresses leaves a scar
management of keratoacanthoma
-often managed as for SCC and completely excised and biopsied
mimics of skin cancer
-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
cherry angiomas presentation
dont blanch
increase with age
also called cambell de morgan
angiomas presentation
some blanch others dont
not worrying
can mimic melanomas
if blanch dont need to worry as means vascular
venous lake is
- commonly seen on the lips
- easily compressible
- often confused with melanotic macules of the lips which are not compressible
pyogenic granuloma
-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
vascular nevus and port wine stain
present at birth or appear soon after
dermatofibromas are
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
dx clue for dermatofibromas
much firmer and feel bigger than they look
sebaceous hyperplasia are
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
skin tags are
focal overgrowth of epidermis and dermis
who and where gets skin tags
obese
flexural areas
viral warts cause
HPV
viral warts diff dx
easier to dx in children
but in adults can look like AK, SK, scc
who is at risk of viral warts
immunosuppressed
molluscum contagiosum cause
pox virus infection
who gets molluscum contagiosum
common in children tend to resolve 6months
if multiple in adults suggesst underlying immunosuppression
clinical dx of molluscum
central umbilication
epidermal cyst presentation
may contain a punctum- which is an opening of the surface and remains of follicualr infundibulum which has become obstructed
what are epidermal cyst
-epithelium lined
punctum
comedones are
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
what are freckles
macular focal areas of overproduction of melanin
sun exposure on sensitive skin
face shoulder and arms
seb k are
benign keratinocyte tumours
some of which harbour somatic mutations
presentation of seb K
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
symptoms of seb k
itchy
break off q
what are solar lentigines
also called liver spots
flat or almost flat brown marks
where are solar lentigines most common
back of hands
forearms
face
cause of solar lentigines
reflect previous sun exposure
so surrounding skin can show other features of sun damage
-no proliferation of melanocytes
diff dx of solar lentigines
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
melanocytic nevi what are they
focal collection of melanocytes clustered in a nest that may or may not produce pigment
benign melanocytic tumours
timeline melanocytic nevi
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
significance of melanocytic nevi
-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
diff dx of melanocytic nevi
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
dermal nevus
melanocytic nevis with no pigment
congenital melanocytic nevi presentation
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
what causes a blue nevi
melanin deep in dermis causes a blue colour due to light scattering
more common asian popualtions
childhood
new onset blue nevi in adulthood management
suspcious for melanoma
halo nevi pathology
meaning of halo nevi
- mostly common in childhood and harmless
- no clinical significance but can appear in a patient with a melanoma elsewhere
meyerson’s nevi presentation
melanocytic nevi surrounded by a patch of eczema
mucosal melanotic macules are
macular areas of increased pigmentation on the lips
usually multiple pigmented macules
if solitary can be a melanoma
cafe au lait spots >5 signify
neurofibromatosis?
