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dermatology yr 2 > skin cancer > Flashcards

skin cancer Flashcards

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Dermatology Board Prep flashcards
1
Q

what is a melanoma

A

Malignant tumour arising from melanocytes

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2
Q

what proportion of skin cancer deaths is melanoma responsible for?

A

75%

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3
Q

where can melanoma arise?

A

on mucosal surfaces (e.g. oral, conjunctival, vaginal) and within uveal tract of eye

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4
Q

how is melanoma incidence changing (incr or decr)

A

increasing

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5
Q

genetic factors For melanoma

A

Family history (CDKN2A mutations), MC1R variants
DNA repair defects (e.g. xeroderma pigmentosum)
Lightly pigmented skin
Red hair

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6
Q

environmental factors for melanoma

A

Sun exposure – intense intermittent or chronic
Sunbeds
Immunosuppression

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7
Q

a risk factor of melanoma related to a skin feature

A

> 100 melanocytic nevi (mole/ spot)
atypical melanocytic nevi

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8
Q

what populations are at greater and lower risk of melanoma

A

predominantly in Caucasian populations
than darkly pigmented populations

more australia and NZ than europe

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9
Q

subtypes of melanoma

A

Superficial spreading
Nodular
Lentigo maligna
Acral lentiginous
Unclassifiable

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10
Q

which subtypes of melanoma are the first and second most common amongst fair skin?

A

superficial spreading, 60-70 of all melanomas

2nd: nodular 15-30% of all melanomas

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11
Q

where is the most common site to get superficial spreading melanoma and nodular melanoma in men and women

A

trunk in men and legs in women

trunk head and neck for nodular both sexes

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12
Q

is nodular melanoma more common in males or females?

A

males

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13
Q

what do nodular melanomas look like?

A

blue to black. but sometimes pink to red
nodule
may be ulcerated or bleeding

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14
Q

what is the growth rate of nodular melanoma (fast or slow)

A

develops rapidly

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15
Q

does superficial spreading melanoma arise on pre existing veni or de novo?

A

can be both

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16
Q

what is something that happens in 2/3 of superficial spreading tumours? which bodily system is responsible for this?

A

In ~2/3 of tumours, regression (visible as grey, hypo-or depigmentation )

a result of host immunity against tumour

(basically immune system fighting it and making it disappear/ fade a bit)

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17
Q

what are the two types of spreading of a melanoma and what melanoma type does each correspond to

A

horizontal (also called radial) growth in superficial spreading melanoma

and

vertical growth in nodular melanoma

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18
Q

which type of growth and by extension: melanoma subtype comes as a first phase and which one is the progressed phase

A

first horizontal growth and superficial spreading melanoma and then if progresses it will be vertical: nodular

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19
Q

what are some features that you (only) see in the superficial spreading melanoma?

A

asymmetry, boarder irregularity, colour variation

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20
Q

what is a sign that melanoma has moved from superficial spreading to nodular?

A

red nodule (san spiraki next to the superficial spreading lesion) see slide 12

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21
Q

what are the less common types of melanomas

A

acral lentiginous melanoma
and
non- classifiable melanomas: nail melanoma and amelanotic melanoma

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22
Q

why are non - classifiable melanomas called “non- classifiable”

A

because they don’t have a typical presentation of that allows them to fit into the other categories

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23
Q

explain the association between acral lentiginous melanoma and race

A

basically because darker skintones hardly ever get the other types of melanoma, 75% of afro caribbean people who have melanomas have this type just because ITS THE ONLY TYPE THEY CAN GET AS EASILY AS CAUCASIANS

similar vibes for asian but % = 45

REMEMBER this is what BOB MARLEY HAD

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24
Q

where does acral melanoma occur

A

in soles and palms ( akra!!)
OR
in/ around nail apparatus

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25
Q

what age group is acral melanoma more common in

A

7th decade of life

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26
Q

nail melanoma what is it

A

slide didnt have text but basically this black line on usually only one nail starts form cuticle till end of nail

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27
Q

what is amelanotic melanoma

A

when the lesion is pink - not black or blue as typical so can be tricky -
(when its pink stop and think)

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28
Q

what is the public awareness self detection campaign acronym for melanoma. explain it

A

ABCDE
asymmetry (two halves dont match)

border: uneven borders

color: variety of color in the spot

diameter: bigger than pencil eraser (1/4”)

Evolution: change in size shape colour ect.

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29
Q

what is Garbe’s rule (concerning presentation of worried patient with skin lesion)

A

If a patient is worried about a single skin lesion, do not ignore their suspicion and have a low threshold for performing a biopsy

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30
Q

what are some things that may look like melanomas and therefore constitute differentials for melanoma?

A

basal cell carcinoma

seborrhoeic keratosis

dermatofibroma

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31
Q

what are some poor prognostic factors for melanoma

A

ANATOMY of an OLD THICK MAN with ULCER and LYMPH NODES
(way to remember)

Increased Breslow thickness >1mm
Ulceration
Increasing Age
Male gender
Anatomical site – trunk, nhead, neck
Lymph node involvement

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32
Q

what is the 10 year survival rate for stage 1A vs thick (>4mm) and ulceration (pT4b) melanomas?

A

> 95% of people get 10 yr surv with the first thing
vs
the other: 50% survival rate

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33
Q

what is berslow thickness of melanoma

A

its thickness measurement from granular layer (stratum granulosum) to BOTTOM of tumour

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34
Q

what investigations to do if suspecting melanoma, and what is their role/ significance.

A

1) dermoscopy can improve correct diagnosis of melanoma by nearly 50%

BUT
Dermoscopic findings should not be considered n isolation
History and risk factor status are important

if still in doubt
2) Excise lesion for histological assessment if in any doubt
(if in doubt take it out)

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35
Q

what is the management of melanoma

A

primary excision down to subcutaneous fat
with a 2mm peripheral margin
(do this to send the lesion to biopsy and investigaitons - ex. determine breslow depth)
then
wide excision determined by berslow depth
-5mm for in situ (Only on top layer of skin)
-10 mm for </=1 mm invasion below top skin layer

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36
Q

why is it important to lece magins in melanoma excision

A

to prevent recurrence or persistent disease

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37
Q

what are the staging methods for melanoma and why do we care about staging

A

pathological (breslow depth and other stuff from analyses) and TNM

important because different excision extent for each

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38
Q

in melanoma, other than the local lesion biopsy what other part should you biopsy + why?

A

biopsy sentinel lymph nodes (a lymph node that contains lymph that drains into a particular skin area)

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39
Q

for what TNM staging of melanoma is sentimel lymph node biopsy currently offered for?

A

for pT1b + (dont need to know what that is)

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40
Q

when do you dissect a sentimel lymph node?

A

when theres extracapsular spread seen on lymph node biopsy (you also do immunotherapy probs)

41
Q

for which melanoma stages do you need to do smth more after extraction? and what in particular?

A

for stage III and IV and IIc w/o SLNB you do imaging :
PET CT
AND MRI BRAIN
and check LDH - major prognostic indicator in melanoma

42
Q

what is a major prognostic indicator in melanoma

A

LDH

43
Q

state the types of treatments for unresectable or metastatic melanoma?

A

Immunotherapy

mutated oncogene targeted therapy

44
Q

what are two mechanisms of 2 types of drugs + names of drugs

A

1)immunotherapy:
CTLA-4 inhibition (eg ipilimumab) - used in unresectable or metastatic
BRAF negative melanoma

2)mutated oncogene targeted therapy:

combination of BRAF inhibitor (e.g. encorafenib, vemurafenib, dabrafenib) andMEK inhibitor (e.g. trametinib)

45
Q

what is the pathology before a carcinoma called

A

actinic keratoses - there are dysplastic keratinocytes

46
Q

what are the risk factors for keratinocyte dysplasia and by extension carcinomas?

A

solar induced and PUVA induced (a treatment with UV) - UV damage

pale skin types

genetic syndromes

birth associated lesions

prokeratosis (abnormal thickening of epidermis)

immunosupression from organ transplant

chronic non healing wounds eg ulcers

ionising radiation- ariline pilots

occupational chem exposures

47
Q

some genetic syndromes risk factors of carcinomas

A
  • Xeroderma pigmentosum (Most important!!)
    • Oculocutaneous albinism
    • Muir Torre syndrome
    • Nevoid basal cell carcinoma syndrome*
48
Q

one birth associated lesion risk of carcinoma>?

A

nevus sebaceous

49
Q

some occupational chemical exposures that are risks of carcinoma

A

Tar, polycyclic aromatic hydrocarbons

50
Q

state the different types of carcinoma

A

Bowen’s disease (squamous cell carcinoma in situ)

Squamous cell carcinoma

Basal cell carcinoma

51
Q

explain difference between Bowen’s disease, SSC and BCC

A

(Squamous cell carcinoma in situ)- if it’s the full thickness of the epidermis

But not INVADING the dermis

SCC: has invaded the dermis,
AND has potential for metastasis/ death

BCC: can ALSO be locally invasive like SCC but the difference to SCC is that IT NEVER METASTASISES

52
Q

what is the most common type of skin cancer

A

Basal cell carcinoma

53
Q

what is the ration BCC: SCC

A

4:1

54
Q

what are the demographics of BCC and ACC (ADENOID cystic carcinoma)

A

both ore common in men
men:women
2-3: 1

both more common in pale skin types

median age diagnosis of BCC is 68

55
Q

where (in skin leayers) are actinic keratoses found and what are they

A

Atypical keratinocytes confined to epidermis

56
Q

where in body is actininc keratoses most prominent?

A

Develop on sun-damaged skin - usually head, neck, upper trunk and extremities

57
Q

what do actininc keratoses lesions look like on skin and how do you distinguish from SSC

A

Macules or papules
Red or pink
Usually some scale – may be thick scale
Distinction from squamous cell carcinoma sometimes difficult – requiring biopsy

58
Q

risk of progression of actinic keratoses to SCC?

A

0.025–16% per year for any single lesion

59
Q

WHAT does Bowen’s disease look like on skin

A

Erythematous scaly patch or slightly elevated plaque

May resemble actinic keratoses, psoriasis, chronic eczema

60
Q

what does Bowens disease arise from? (not in sense of cause in sense of preceding “phase”)

A

May arise de novo or from pre-existing AK

61
Q

what does SCC arise from? (not in sense of cause in sense of preceding “phase”)

A

Arises within background of sun-damaged skin

62
Q

WHAT DOES scc LOOK LIKE on skin

A
  • Erythematous to skin coloured
    • Papule
    • Plaque-like
    • Exophytic (protrudes sortof- slide 44)
    • Hyperkeratotic
    • Ulceration
63
Q

clniical high risk features of SCC

A

Localisation and size:
- Trunk and limbs > 2cm
- Head / neck > 1cm
- Periorificial zones
Margins: Ill-defined
Rapidly growing
Immunosuppressed patients
Previous radiotherapy or site of chronic inflammation

64
Q

HIstological high risk signs for SCC

A

Histology:
- Grade of differentiation: poorly differentiated
- Acantholytic, adenosquamous, demosplastic subtypes
- Tumour thickness - Clark level: >6mm, Clark IV, V
- Invasion beyond subcutaneous fat
- Perineural, lymphatic or vascular invasion

65
Q

WHAT IS a keratoacanthoma

A

Rapidly enlarging papule that evolves into a sharply circumscribed, crateriform nodule with keratotic core-( see it slide 48 its hard to imagine )

66
Q

how long does Keratoacanthoma take to resolve

A

slowly over months

67
Q

where does Keratoacanthoma typically occur

A

head and neck/ sun exposed areas

68
Q

what is Keratoacanthoma commonly mistaken for?

A

Difficult to distinguish clinically and histologically from squamous cell carcinoma

69
Q

investigations for keratoacanthoma

A

Often clinical diagnosis sufficient

Diagnostic biopsy may be taken if diagnostic uncertainty

Ultrasound of regional lymph nodes ± FNA if concerns regarding regional lymph node metastasis

70
Q

differentials for SCC

A

BCC
viral wart
merkel cell carcinoma

71
Q

what is typical treatment of SCC

A

(supper similar to melanomas)

Examination of rest of skin and regional lymph nodes
Excision

Secondary prevention
- Skin monitoring advice
- Sun protection advice

72
Q

when do you do radiotherapy for SCC

A

Unresectable
- High risk features e.g. perineural invasion

73
Q

WHAT TO DO FOR METASTATIC SCC

A

GIVE CEMIPLIMAB

74
Q

BCC subtypes

A

Nodular
micronodular

Superficial
Morpheic

Infiltrative
Basisquamous

75
Q

what is the most common type of BCC

A

NODULAR Accounts for approximately 50% of all Basal cell carcinomas

76
Q

what DOES Nodular BCC look like

A

Typically presents as shiny, pearly papule or nodule

77
Q

superficial BCC appearance

A

Well-circumscribed, erythematous, macule / patch or thin papule /plaque

78
Q

morphoeic BCC, how common? how aggressive? and characteristics

A

Less common
Slightly elevated or depressed area of induration
Usually light-pink to white in colour
More aggressive behaviour
- Extensive local destruction

79
Q

what are the histological features of basisquamous BCC

A

Histological features of both basal cell carcinoma and squamous cell carcinoma

80
Q

compare and contrast nodular BCC and micronodular

A

Micronodular basal cell carcincoma
Resembles nodular basal cell carcinoma clinically
More destructive behaviour – high rates of recurrence and subclinical spread

81
Q

BCC investigations

A

Often clinical diagnosis sufficient

Diagnostic biopsy may be taken

82
Q

differentials for BCC

A

SCC

Adnexal (Sebaceous) carcinoma

Merkel cell carcinoma

83
Q

treat of BCC

A

Standard surgical excision

84
Q

WHEN do we do mohs micrographic surgery

A
  • Recurrent basal cell carcinoma
    • Aggressive subtype (morpheic / infiltrative / micronodular)
    • Critical site
85
Q

for people not suitable for excision what ar eother options for BCC treat

A

(if superficial) Topical therapy e.g. 5-Fluorouracil, Imiquimod
Photodynamic therapy
Curettage (scraping)
Radiotherapy ( in elederly who surgery not good option for)
Vismodegib –genetic treatment that selectively inhibits abnormal signalling in Hedgehog (Hh) pathway

86
Q

describe the origin cells of merkel cell carcinoma

A

NOT MERKEL CELLS

ORIGIN CELLS are highly anaplastic cells which share features with neuroectodermally derived cells (including Merkel cells)

87
Q

aetiological factors of merkel cell carcinoma

A

80% are associated with polyomavirus
UV exposure is also an aetiological factor

88
Q

where in body does merkel cell carcinoma most occur

A

Predilection for the head and neck region of older adults

89
Q

appearance of merkel cell carcinoma

A

Solitary, rapidly growing nodule- pink-red to violaceous, firm, dome shaped,
- Ulceration can occur

90
Q

how agressive is merkel cell carcinoma

A

Aggressive, malignant behaviour
>40% develop advanced disease

91
Q

TRUE OR FALSE Nodular melanoma has a rapid radial growth phase

A

FALSE : Nodular melanoma lacks a radial growth phase

92
Q

T or F: ABCDE rule is helpful for early detection of nodular melanoma

A

false

Asymmetry, border irregularity, colour variation and diameter >5-6mm are products of the radial growth phase, absent in nodular MM

93
Q

what is the ugly ducking sign?

A

a mole that does not resemble other nevi - may indicate an MM (malignant melanoma)

94
Q

t/f suspected melanoma should undergo punch biopsy

A

false, should undergo complete excision and biopsy form that

95
Q

t/f confirmed melanoma shou undergo sentinel lymph node biopsy

A

false - only offered for pT1b melanomas currently

96
Q

t/f BCC never metastasises, and thus treatment is usually desirable rather than essential

A

Untreated basal cell carcinomas may become highly destructive to local structures and if left untreated over many years, may eventually become metastatic

97
Q

is melanoma or merkel cell carcinoma more aggressive?

A

merkel

98
Q

when can radiation therapy be used anf not be used in carcinoma related stuff

A

Radiation therapy may be used in treatment of BCC, SCC, MCC but not actinic keratoses

dermatology yr 2 (2 decks)

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