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
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
26
basal cell nevus syndrome risks
-already have inherited mutation in one allele knudson hit so present at younger age
27
cancer assoc. to immunosuppression
squamous cell carcinoma
28
most common skin cancer in Europe
basal cell carcinoma
29
BCC what is it
malignant tumour of keratinocytes
30
behaviour of BCC
NEVER metastasises | but is locally destructive and can invade aggressively locally although slowly occurs
31
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
32
types of BCC
nodular morphoeic superficial infiltrative
33
nodular BCC
classical BCC | clinical and tumour margins well defined
34
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
35
superficial BCC
-relatively more common on backs and limbs dont show any significant induration cyrotherapy and chemotherapeutic agents may be more appropriate that ssurgery
36
infiltrative
morphoeic and nodular insidious grow haphazard moh's surgery
37
differentials BCC
sometimes people think - acne spots- but lasting >3-4 weeks - damage or trauma
38
bcc excision margin
4mm margin
39
moh's surgery for BCC
- middle third of face - irregular tumour eg morphoeic and infiltrative - take horizontal sections so can examine during surgery
40
risk factors for BCC
-immunosuppression -rare inherited syndromes basal cell nevus syndrome hx of BCC or skin cancer
41
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
42
squamous cell carcinoma behaviour
agressive 3-5% mets body sites strongly mirrors UVR exposure
43
two precursor lesions SCC
actinic keratoses | intra-epithelial carcinoma
44
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
45
distribution of scc
bald heads top of ears face back of hands
46
SCC signs more likely to have mets
>2cm depth >4mm poorly differentiated background immunosuppression
47
management SCC
-excision margin 4-6mm | radiotherapy only in some cases
48
RF for SCC
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
49
differential SCC
fergus smith syndrome | similar looking but behave different
50
what is melanoma
malignant tumour of melanocytes
51
presentation of melanomas
``` most are pigmented asymmetry irregular border multiple colours diameter evolving ```
52
in situ melanoma is
melanoma in situ- aka only in epidermis not into dermis still cancerous but cant spread
53
types of melanoma
``` nodular acral lentigo melanoma amelanotic superficial ```
54
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
55
fhx of melanoma clues
-large number of nevi that look atypical | fhx of melanoma
56
behaviour of melanoma
metastasise early
57
risk factors melanoma
-skin type gender men on trunk women on legs several episodes sun burn atypical naevus syndrome fhx and phx
58
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
59
nodular melanoma
nodules reflection of a large downward vertical collection of malignant cells can be a later stage of SSM
60
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
61
lentigo maligna vs lentigo maligna melanoma
lentigo maligna is precursor so cells only in epidermis
62
amelanotic melanoma
aka without melanin not pigmented hard to pick up
63
acral melanomas
``` melanoma on palms or soles rare usually pigmented not related to UVR certain popualtions eg Africans ```
64
two types of melanoma
melanoma de novo- new which is faster growing or melanoma on pre-existing lesion eg a mole
65
Breslow thickness
measured in mm from granular layer to deepest part of the tumour
66
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
67
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
68
other rx option for melanoma
-may give vemurafenib (braf) signal or ipilimumab for metastatic disease
69
pre-malignant lesions of SCC
actinic keratoses
70
actinic keratoses what are they
focal areas of dysplasia
71
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 ```
72
prognosis AK
low rate of progression to SCC
73
management of AK decision
based on - cosmetic - progression to SCC- hard to determine - diagnostic unsure whether a AK or SCC
74
options for AK management
- liquid nitrogen | - background change have efedex- hydrofluoracil cream
75
intra-epithelial carcinoma
also bowen's disease or in situ
76
pathology IE carcinoma
full thickness of dysplasia of epidermis | but not breached basement membrane
77
management of intra-epithelial carcinoma
histopathology confirmation of dx may be required with an incisionall biopsy to assay for any invasion (SCC)
78
differentiating intra-epithelial carcinoma and AK
- Ak smaller and focal | - IEC tends to be plaque like and larger
79
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 ```
80
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
81
SE topical chemo agents
inflammation | malaise
82
rarer skin cancers
``` merkel cell appendage tumours kaposi sarcoma cutaneous lymphomas sarcomas cutaneous secondaries ```
83
merkel cell pathology
- neuroendocrine carcinoma - merkel cell polyomavirus - UVR related
84
RF for merkel cell
immunosuppressed as virus
85
behaviour of MCC
-metastatic spread so poorer 70% at 5 yrs prognosis
86
management MCC
excision +/- radiotherapy
87
appendageal carcinomas pathology
due to benign keratinocyte tumours related to hair follicles and sweat glands - also cna be malignant - can metastasise - managed as SCC
88
cutaneous lymphoma T cell presentation
- usually present as widespread rash that resembles psoriasis - as lesion progresses becomes more nodular - progresses very slowly
89
cutaneous B cell lymphoma presentation
-erythematous nodules or plaques
90
most common primary cutaneous sarcoma is
dermatofibrosarcoma protuberans
91
presentation dermatofibrosarcoma protuberans
-firm nodule or plaque reminiscent of ann odd dermatofibroma over shoulder girdle in young adult -can mets -recurrence locally common
92
management of DFP
-wide excision +/- radiotherapy
93
leiomyosarcoma
- cutaneous sarcoma | - firm indolent nodule
94
kaposi sarcoma pathology
-spindle cell malignancy from vascular endothelium -seen in untreated HIV/ AIDS virus= herpes 8
95
cutaneous secondaries causes
- rare from internal malignancies-sister mary joseph -adenocarcinoma of umbilicus - from primary skin cancers mostly seen in melanoma
96
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
97
management of keratoacanthoma
-often managed as for SCC and completely excised and biopsied
98
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 ```
99
cherry angiomas presentation
dont blanch increase with age also called cambell de morgan
100
angiomas presentation
some blanch others dont not worrying can mimic melanomas if blanch dont need to worry as means vascular
101
venous lake is
- commonly seen on the lips - easily compressible - often confused with melanotic macules of the lips which are not compressible
102
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
103
vascular nevus and port wine stain
present at birth or appear soon after
104
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 ```
105
dx clue for dermatofibromas
much firmer and feel bigger than they look
106
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
107
skin tags are
focal overgrowth of epidermis and dermis
108
who and where gets skin tags
obese | flexural areas
109
viral warts cause
HPV
110
viral warts diff dx
easier to dx in children | but in adults can look like AK, SK, scc
111
who is at risk of viral warts
immunosuppressed
112
molluscum contagiosum cause
pox virus infection
113
who gets molluscum contagiosum
common in children tend to resolve 6months | if multiple in adults suggesst underlying immunosuppression
114
clinical dx of molluscum
central umbilication
115
epidermal cyst presentation
may contain a punctum- which is an opening of the surface and remains of follicualr infundibulum which has become obstructed
116
what are epidermal cyst
-epithelium lined | punctum
117
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
118
what are freckles
macular focal areas of overproduction of melanin sun exposure on sensitive skin face shoulder and arms
119
seb k are
benign keratinocyte tumours | some of which harbour somatic mutations
120
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 ```
121
symptoms of seb k
itchy | break off q
122
what are solar lentigines
also called liver spots | flat or almost flat brown marks
123
where are solar lentigines most common
back of hands forearms face
124
cause of solar lentigines
reflect previous sun exposure so surrounding skin can show other features of sun damage -no proliferation of melanocytes
125
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
126
melanocytic nevi what are they
focal collection of melanocytes clustered in a nest that may or may not produce pigment benign melanocytic tumours
127
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
128
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
129
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
130
dermal nevus
melanocytic nevis with no pigment
131
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
132
what causes a blue nevi
melanin deep in dermis causes a blue colour due to light scattering more common asian popualtions childhood
133
new onset blue nevi in adulthood management
suspcious for melanoma
134
halo nevi pathology
-melanocytic nevi that are under immune attack with destruction of melanocytes -
135
meaning of halo nevi
- mostly common in childhood and harmless | - no clinical significance but can appear in a patient with a melanoma elsewhere
136
meyerson's nevi presentation
melanocytic nevi surrounded by a patch of eczema
137
mucosal melanotic macules are
macular areas of increased pigmentation on the lips usually multiple pigmented macules if solitary can be a melanoma
138
cafe au lait spots >5 signify
neurofibromatosis?