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Dermatology > Skin Pathology > Flashcards

Skin Pathology Flashcards

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Dermatology Board Prep flashcards
1
Q

Where is the mitotic pool in normal skin?

A

basal layer

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2
Q

What type of epithelium is the normal epidermis made up of?

A

stratified keratinising squamous epithelium

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3
Q

What are the granules found in the granular layer?

A

keratohyalin

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4
Q

What is the main feature in prickle cell layer?

A

prominent desmosomes

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5
Q

How is pigment transfered to keratinocytes from the melanocytes?

A

dendritic processes

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6
Q

Where are the langerhan cells found?

A

upper and mid-epidermis

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7
Q

What are the 2 layers of the dermis?

A

papillary dermis

reticular dermis

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8
Q

What is found in the reticular dermis?

A

appendage structures- sweat glands and pilosebaceous units

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9
Q

What is hyperkeratosis?

A

increased thickness of keratin layer

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10
Q

What is parakeratosis?

A

persistence of nuclei in the keratin layer

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11
Q

What is acanthosis?

A

increased thickness of epithelium

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12
Q

What is papillomatosis?

A

irregular epithelial thickening

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13
Q

What is spongiosis?

A

oedema fluid between squames appears to increase prominence of intercellular prickles

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14
Q

What can develop is the spongiosis is sever?

A

vesicles filled oedema fluid develop

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15
Q

What are the 4 main reaction patterns of inflammatory skin disease?

A

spongiotic-intraepidermal oedema
psoriasiform
lichenoid
vesiculobullous

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16
Q

What is psoriasiform?

A

elongation of the rete ridges (the squiggly line of the DEJ)

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17
Q

What is lichenoid?

A

basal layer damage

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18
Q

Give examples vesiculobullous blistering diseases?

A

pemphigoid; pemphigus and dermatits herpetiformis

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19
Q

What is the Koebner phenomenon?

A

new lesions arising at the sites of trauma

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20
Q

How is complement involved in psoriasis?

A

complement attracts neutrophils to the keratin layer which creates munro microabscesses

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21
Q

How do lichenoid disorders appear?

A

itchy, flat topped violaceous papules

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22
Q

What disease has irregular sawtooth acanthosis with basal damage?

A

lichen planus

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23
Q

What are other lichenoid disorders aside from lichen planus?

A

erythema multiforme and toxic epidermal necrolysis

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24
Q

What is the most common type of pemphigus?

A

pemphigus vulgaris

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25
Q

What happens histologically during pemphigus?

A

loss of integrity of epidermal cell adhesion

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26
Q

What drugs can be used to treat pemphigus?

A

steroid

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27
Q

What causes the loss of integrity of the epidermal cell adhesion in pemphigus vulgaris?

A

IgG auto-antibodies are made against desmoglien which disrupts the desmosomes and results in acantholysis (loss of intercellular adhesion)

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28
Q

What is acantholysis?

A

lysis of intercellular adhseion sites

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29
Q

What are the main areas of skin that pemphigus vulgaris affects?

A

scalp, face, axillae, groin and trunk

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30
Q

How does pemphigus vulgaris appear?

A

fliud filled blisters which rupture to form shallow erosions-dont really see bullae

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31
Q

Where are the blisters in terms of skin layers in bullous pemphigoid?

A

sub-epidermally

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32
Q

What is the pathogenesis of bullous pemphigoid?

A

IgG react with antigens on hemidesmosomes which anchor basal cells to the BM so epidermis floats away from BM and fliud and inflam cells go into that space (esp. eosinophils)

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33
Q

What disease is dermatitis herpetiformis associated with?

A

coeliac disease

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34
Q

Where does dermatitis herpetiformis typically affect?

A

elbows, knees and buttocks symmetrically

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35
Q

What is histological hallmark of dermatitis herpetiformis?

A

papillary dermal microabscesses

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36
Q

How does dermatitis herpetiformis present?

A

intensly itchy lesions which are often excoriated

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37
Q

What immunoglobulin is involved with dermatitis herpetiformis?

A

IgA- the IgA which targets the gliadin cross reacts with connective tissue matrix proteins

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38
Q

Why does acne appear at puberty?

A

androgen levels increase

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39
Q

What are the symptoms in rosacea?

A

recurrent facial flushing
visible blood vessels
pustules
thickening of skin-rhinophyma

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40
Q

What are the triggers for rosacea?

A

sunlight
alcohol
spicy foods
stress

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41
Q

What drug does rosacea respond to?

A

tetracyclines

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42
Q

What is often seen on pathology of rosacea?

A

follicular demodex mites

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43
Q

What is the Breslow thickness?

A

from the granular layer down to the deepest point of invasion

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44
Q

What is the ABCDE rule for diagnosing melanoma?

A 
A-asymmetry
B-border irregularity
C-colour variation
D-diameter greater than 6mm
E-evolution/change
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45
Q

What is the ugly duckling sign?

A

Comparing a mole to see if it is similar to other moles on a patient as all naevi on one individual should all look similar, if not-suggests melanoma

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46
Q

What do basal cell carcinomas arise from?

A

the keratinocytes withing the basal layer of the epidermis

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47
Q

What do SCCs come from?

A

the suprabasal layers

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48
Q

What breslow thickness gives a 5 year survival of 50%?

A

greater than 4mm

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49
Q

How do BCCs usually present?

A

a translucent, slow-growing lump or non-healing ulcer

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50
Q

Are BCCs usually painful?

A

no

51
Q

What are the visible features of a BCC?

A 
pearly or translucent with a rolled edge
telaniectasia
central ulceration "rodent ulcer" 
scaly plaque "superficial"
infiltrative "morphoeic"
52
Q

What are the types of BCC?

A 
nodular
rodent ulcer
superficial
morphoiec (infiltrative)
pigmented
53
Q

Where do SCCs tend to arise?

A

sun-damaged skin

54
Q

How do SCCs present?

A

warty or crusted lump or non-healing ulcer

55
Q

Do SCCs tend to be painful?

A

yes

56
Q

What are the precursor lesions for SCCs?

A

actinic keratoses and Bowen’s disease (carcinoma-in-situ)

57
Q

How does Bowen’s disease appear?

A

erythematous plaque

58
Q

What is Naevoid basal cell carinoma syndrome?

A

an autosomal dominant familial cancer syndrome that results in early onset and multiple BCCs

59
Q

What leads to tumour cells not all being homogenous?

A

When cells have mulitple mutations, they are more unstable and so acquire mutations in parralel clonal expansion giving lots of cell types within a tumour

60
Q

What are the hallmarks of cancer?

A 
sustaining proliferation signalling
evading growth suppressors
activiating invasion and metastases
enabling replicative immortality (telomerase)
inducing angiogenesis
resisting cell death
61
Q

What happens in oncogenic Ras signalling?

A

Ras does not need growth factors to be activated and so cell division and proliferation happen constantly. Ras is an oncogene.

62
Q

What xeroderma pigmentosum?

A

A genetic condition where genes involved in the repair of DNA damage are mutated leading to extrememly increased risk of skin cancer

63
Q

What chemicals increase the risk of non-melanoma skin cancer?

A 
coal tar pitch
soot
creosote
petroleum products
shale oils
arsenic
64
Q

What diseases increase the risk of malignant melanoma?

A

ulcerative colitis

Crohn’s disease

65
Q

What UV radiation wavelengths are most implicated in skin cancer and aging?

A

UVB and UVA

66
Q

How does UVB cause skin damage?

A

through direct DNA damage

67
Q

How does UVA cause skin damage?

A

indirect oxidative damage of DNA bases- penetrates more deeply into the skin than UVB

68
Q

What type of DNA damage does UV cause?

A

pyrimidine dimer (two adjacent bases bond on the same DNA strand) which leads to distortion of the DNA helix

69
Q

What is the problem with unrepaired UV induced photoproducts?

A

Interfere iwth base pariing during DNA replication leading to mutations- polymerase usually will correctly guess the right bases but is error prone and may insert the wrong bases

70
Q

What is the problem with having oxidised DNA bases?

A

It can mispair with bases causing point mutations

71
Q

How is direct DNA daamge repaired?

A

nucleotide excision repair

72
Q

What is the UV signiture mutation in direct DNA damage?

A

TT becomes CC

73
Q

What base is oxidised in indirect DNA damage?

A

deoxyguanosine becomes 8-oxo-deoxyguanosine

74
Q

How is indirect DNA damage repaired?

A

base excision repair

75
Q

What is the typical mutation in indirect DNA damage?

A

C becomes A (point mutation)

76
Q

How does UV radiation induce immunosuppression?

A

depletes langerhan cells
generates regulatroty T cells which have an immune suppressive activity
causes secretion of anti-inflam cytokines by macrohpages and keratinocytes

77
Q

What is the other name for freckles

A

ephilides

78
Q

What do freckles reflect about melanocytes in the skin?

A

Their clumpy distribution

79
Q

What causes actinic lentigenes?

A

UV exposure

80
Q

Where are actinic lentigenes found mainly?

A

face ; forearms; dorsum of hands

81
Q

What is seen pathologically in actinic lentigines?

A

elongated rete ridges and increased melanin and melanocytes

82
Q

What type of congenital melanocytic naevi have a 10-15% risk of melanoma?

A

large lesions (>20cm)- giant garment type

83
Q

How are large congenital naevi treated?

A

staged surgical excision

84
Q

What is the developmental stages in naevus growth?

A

junctional naevus
compound naevus
intradermal naevus

85
Q

What happens in the junctional naevus?

A

meloancytes proliferate leading to clusters of cells at the DEJ

86
Q

What is found in the compound naevus?

A

junctional clusters as well as groups of cells in the dermis

87
Q

What is found in the intradermal naevus?

A

all junctional activity has caesed and all the cells are entirely dermal

88
Q

What do dysplastic naevi look like?

A

generall >6mm diameter
variegated pigment
border asymmetry

89
Q

What are the 2 types of dysplastic naevi?

A

sporadic and familial

90
Q

What happens pathologically with dysplastic naevi?

A

architectural atypia and cellular atypia with a host reaction of fibrosis and inflammation

91
Q

What is the difference between dysplastic naevi and melanoma histologically?

A

the epidermis is not effaced in dysplasia although severe dysplasia may be difficulat to differenciate from melaonma in situ

92
Q

What is a halo naevi?

A

have a peripheral halo of depigmentation which show inflammatory regression and are overrun by lymphocytes

93
Q

What is a blue naevi?

A

entirely dermal and consist of pigment rich dendirtitic spindle cells

94
Q

What is a Spitz naevus?

A

a naevus that occurs in the under 20s and closely mimic melanoma but are usually entirely benign

95
Q

What do Spitz naevi look like?

A

pink lumps due to the prominent vasculature, epidermal hyperplasia

96
Q

Where is melanoma most commonly found?

A

sun-exposed sites: scalp, face, neck, arm, trunk. leg

97
Q

What are some signs of melanoma?

A 
change in shape; irregular pigmentation
bleeding
development of satellite nodules
ulceration
new pigmented lesion deveoped in adulthood
98
Q

What are the 4 main types of melanoma?

A

superficial spreading
acral/muscosal lentiginous
lentigo maligna
nodular

99
Q

What are the 2 phases of growth in melanoma?

A

radial growth phase (RGP) and vertical growth phase (VGP)

100
Q

What happens during the radial growth phase?

A

grow as macules when either entirely in-situ or with dermal microinvasion

101
Q

What happens during the vertical growth phase?

A

the melanoma cells invade the dermis forming an expansile mass with mitoses

102
Q

What is there an absense of in nodular melanoma?

A

no clinical or microscopic evidence of RGP

103
Q

What are the adverse prognostic indicators in melanoma?

A

breslows thickness
ulceration
high mitotic rate; lymphovascular invasion; satellites ; sentinel lymph node involvement

104
Q

What causes satellite deposits of MM?

A

invasion of local dermal lmyphatics

105
Q

What defines a small naevus?

A

less than 1.5cm

106
Q

What is atypical or dysplasatic naevus syndrom?

A

relative risk of melanoma increases with number of atypical naevi (2x if 2; 6x if >6)

107
Q

What is the most common type of melanoma?

A

superficial spreading

108
Q

How does superficial spreading melanoma progress?

A

a macule with irregular border and colour which may have been increasing in size for years before developing a nodule (slow horizontal growth phase and rapid vertical growth phase)

109
Q

How does nodular melanoma appear

A

blue-black or redskin coloured nodule which may be ulcerated or bleeding

110
Q

How can you differentiate nodular from superficial spreading?

A

nodular medlanoma do not have any significant surrounding macular pigmentation

111
Q

What is a lentigo maligna melanoma?

A

an invasive melanom developing within a lentigo maligna

112
Q

What areas of the body does acral lentiginous melanoma affect?

A

palms, soles or nails

113
Q

What is amelanotic melanoma?

A

absent or minimal visible pigment

114
Q

How do seborrheic keratoses?

A

brown/black greasy lesions
that have a “stuck on” appearance
often “warty but may be flat”

115
Q

How do dermatofirbroma appear?

A

deep (dermal), brown/grey, firm nodule (can be red)

116
Q

What can cause dermatofibromas?

A

insect bites

117
Q

What margin is given in excising melanoma?

A

1cm lateral margin for every 1mm depth invasion

118
Q

What is a seborrhoeic keratosis?

A

benign proliferation of epidermal keratinocytes

119
Q

What is seen on pathology of seborrhoeic keratosis?

A

epidermal acanthosis; hyperkeratosis; horn cysts

120
Q

What are 3 precursors of SCC?

A

bowens disease
actinic keratosis
viral lesions

121
Q

What do precursors of SCC show?

A

squamous dysplasia

122
Q

What type of HPV is associated with dysplasia?

A

type 16

123
Q

What sites are associated with worse prognosis with SCC?

A

scalp, ear, nose; perineural spread

Dermatology (15 decks)

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