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Pathology Flashcards

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Dermatology Board Prep flashcards
1
Q

what is the epidermis mainly maid up of?

A

mainly maturing squamous cells

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2
Q

where is the mitotic pool located?

A

in the basal layer

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3
Q

where are melanocytes found?

A

at the DEJ

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4
Q

what is epidermis?

A

stratified keratinising squamous epithelium

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5
Q

what are prominent in prickle cells?

A

desmosomes

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6
Q

what is the granular layer rich in?

A

keratohyalin granules

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7
Q

what type of cells are present in the corneal layer?

A

differentiated keratinised cells

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8
Q

where are corneocytes shed from & what does this create?

A

shed from the surface of the epidermis to form house dust

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9
Q

what do melanocytes do?

A

synthesise melanin pigment

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10
Q

how is melanin pigment transferred to keratinocytes?

A

via dendritic processes

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11
Q

where are Langerhans cells found?

A

in upper & mid epidermis

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12
Q

what kind of cell are Langerhans cells?

A

dendritic

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13
Q

what do Langerhans cells do?

A

act as sentiniels monitoring environment for antigens

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14
Q

what’s the difference between black people’s melanocytes & white people’s?

A

black people’s melanocytes make more melanin

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15
Q

what is the dermis made up of?

A

matrix of type 1 & type 111 collagen

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16
Q

what is present in the dermis?

A

elastic fibres

ground substance

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17
Q

what is ground substance?

A

hyaluronic acid & chondroitin sulphate

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18
Q

describe papillary dermis & where it is found?

A

thin layer just beneath the epidermis

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19
Q

describe reticular dermis

A

thicker bundles of type 1 collagen

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20
Q

what does reticular dermis contain?

A

appendage structures e.g. sweat glands, pilosebaceous units

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21
Q

what is the epidermal BM made of?

A

laminin & collagen 4

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22
Q

can you see Langerhan’s cells using a normal stain?

A

no

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23
Q

what is hyperkeratosis?

A

increased thickness of keratin layer

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24
Q

what is parakeratosis?

A

persistence of nuclei in the keratin layer

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25
Q

what does parakeratosis indicate?

A

skin is turning over too quickly

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26
Q

what is acanthuses?

A

increased thickness of the epithelium

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27
Q

what is papillomatosis?

A

irregular epithelial thickening

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28
Q

what is spongiosis?

A

oedema fluid between squares appears to increase the prominence of intercellular prickles

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29
Q

what does severe spongiosis cause?

A

vesicles filled by oedema fluid

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30
Q

what are the 4 main inflammatory reaction patterns?

A
  • spongiotic
  • psoriasiform
  • lichenoid
  • vesiculobullous
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31
Q

describe what happens in the spongiotic inflammatory reaction pattern & give an example

A

intraepidermal oedema

e.g. eczema

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32
Q

describe what happens in the psoriasiform inflammatory reaction pattern & give an exampl

A

elongation of the rate ridges

e.g. psoriasis

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33
Q

describe what happens in the lichenoid inflammatory reaction pattern & give an exampl

A

basal layer damage

e.g. lichen planus & lupus

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34
Q

describe what happens in the vesiculobullous inflammatory reaction pattern & give an exampl

A

blistering

e.g. bullous pemphigoid, pemphigus & dermatitis herpetiforms

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35
Q

what happens in psoriasis?

A

pathogenesis remains elusive

  • epidermal hyperplasia
  • hereditary factors?
  • new lesions at sites of trauma
  • complement mediated attack on keratin layer
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36
Q

if you were to scrape a scale of a psoriasis plaque, what would happen?

A

pinprick bleeding

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37
Q

what are crumbly nails in psoriasis due to?

A

dystrophy due to increased turnover in their epithelial nail beds

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38
Q

what does the distribution of acne vulgarise reflect?

A

sebaceous gland sites

- face, upper back, anterior chest

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39
Q

what is released when acne spots burst?

A

sebum & keratin which is very irritating for the skin

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40
Q

what can you stain for in acne vulgaris?

A

androgen receptors

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41
Q

what does keratin plugging of pilosebaceous units cause?

A

distension 7 then infection of the unit

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42
Q

where is sebum produced?

A

by the sebaceous gland

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43
Q

what is an open comedone?

A

blackhead

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44
Q

what is a closed comedone?

A

whitehead

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45
Q

in which sex is rosacea more common?

A

females

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46
Q

what is rosacea?

A

recurrent facial flushing, visible blood vessels, pustules, thickening of skin

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47
Q

what is rhinophyma?

A

thickening of skin

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48
Q

namesake known triggers of rosacea

A

sunlight
alcohol
spicy foods
stress

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49
Q

which antibiotics does some rosacea respond to?

A

tetracyclines

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50
Q

what pathology is found in rosacea?

A 
vascular ectasia
pachy inflammation with plasma cells 
pustules
perifollicular granulomas 
follicular demodex mites
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51
Q

where are demodex mites usually found?

A

in sebaceous duct

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52
Q

what happens around the mites?

A

lots of granulomatous inflammation

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53
Q

what is the primary feature of immunobullous disease?

A

blisters

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54
Q

what is pemphigus?

A

rare autoimmune bullous disease of variable severity

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55
Q

what causes pemphigus?

A

loss of integrity of epidermal cell adhesion

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56
Q

which drugs does pemphigus respond to?

A

steroids

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57
Q

how many distinct subtypes are there of pemphigus?

A

4, separable clinically & histologically

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58
Q

which is the most common subtype of pemphigus?

A

pemphigus vulgaris

59
Q

what happens in pemphigus vulgaris?

A

IgG auto-antibodies are made against desmogelin 3

60
Q

what does desmoglein 3 normally do?

A

maintains desmosomal attachments

61
Q

what is the end result of pemphigus vulgaris?

A

acantholysis

62
Q

where is pemphigus vulgaris affect in particular?

A

scalp, face, axillae, groin trunk

63
Q

where can pemphigus vulgaris affect aside from the skin?

A

mucosa

e.g. motuh, resp. tract

64
Q

when the blisters of pemphigus vulgaris rupture, what’s left?

A

shallow erosions

65
Q

what is common to all variants of pemphigus?

A

the process of acantholysis

66
Q

what is pacantholysis?

A

lysis of intercellular adhesion sites

67
Q

what kind of blisters are found in bullous pemphigoid?

A

subepidermal

68
Q

what is the difference between bullous pemphigoid & pemphigus?

A

no acantholysis in bullous pemphigoid

69
Q

what happens in bullous pemphigoid?

A

Circulating antibodies (IgG) react with a major and/or minor antigen of the hemidesmosomes anchoring basal cells to basement membrane

70
Q

what does bullous pemphigoid result in?

A

local complement activation & tissue damage

71
Q

what do older lesions of bullous pemphigoid show & what does this mimic?

A

show re-epithelialisation of their floor, mimicking pemphigus vulagris

72
Q

what is dermatitis herpetiforms?

A

autoimmune bullous disease

73
Q

which GI disease is dermatitis herpetiforms strongly associated with?

A

coeliac disease

74
Q

what do the lesions in dermatitis herpetiforms look & feel like?

A

intensely itchy symmetrical lesions

found on elbows, knees & buttocks, often excoriated

75
Q

what is the hallmark of dermatitis herpitforms?

A

papillary dermal microabscesses

76
Q

in dermatitis herpetiforms, what forms in dermal papillae & what does this cause?

A

immune complexes

activates complement & generates neutrophil chemotaxins

77
Q

where are melanocytes derived from?

A

the neural crest

78
Q

where do the the melanoblasts migrate from & to during embryogenesis?

A

from neural crest to skin, uveal tract & leptomeninges

79
Q

when do melanoblasts form melanocytes?

A

once they settle in the skin

80
Q

where are the melanocytes situated?

A

basally situated

81
Q

what is the ratio of melanocytes to basal keratinocytes?

A

1:5 - 1:10

in all races

82
Q

what does the MC1R gene encode?

A

MC1R protein which sits on cell surface?

83
Q

what does the MC1R protein do?

A

determines balance of pigment in skin & hair

turns phaeomelanin into eumelanin

84
Q

which protein causes red hair?

A

phaeomelanin

85
Q

which protein is found in hair colours other than red?

A

eumelanin

86
Q

what does one defective copy of MC1R cause?

A

freckling

87
Q

what does two defective copy of MC1R cause?

A

red hair & freckling

88
Q

when do freckles (ephilides) occur?

A

after UV exposure

89
Q

what do freckles reflect?

A

clumpy distribution of melanocytes

90
Q

what are actinic lentigines also known as?

A

solar lentigines

age/liver spots

91
Q

what are actinic lentigines related to?

A

UV exposure

92
Q

where are actinic lentigines usually found?

A

race, forearms & dorsal hands

93
Q

what are actiniclentigines?

A

epidermis elongated with rite ridges & increased melanin & basal melanocytes

94
Q

what are melanocytic naevi?

A

broad range of lesions which are either congenital or acquired

95
Q

when are most naevi acquired?

A

in the first 2 decades of life

96
Q

why do melanocytic naevi often have a hairy surface?

A

due to proliferation of hair follicles

97
Q

what happens during infancy that allows the formation of simple naevi?

A

the melanocytes:keratinocyte ratio breaks down at a number of cutaneous sites

98
Q

what are simple naevi?

A

very common being lesions with low malignant potential

99
Q

which children have more naevi?

A

immunosuppressed/leukaemic

100
Q

generally how big are dysplastic naevi?

A

> 6 mm diameter

101
Q

what kind of pigment do dysplastic naevi usually have?

A

variegated pigment

102
Q

what are dysplastic naevi borders normally like?

A

asymmetrical

103
Q

which 2 clinical settings are dysplastic naevi usually found in?

A
  • sporadic

- familial

104
Q

describe the sporadic clinical setting

A

not inherited
one to several atypical naevi
risk of malignant melanocyte slightly raised

105
Q

describe the familial clinical setting

A

strong FH of melanoma
autosomal inheritance
high penetrance
lots of atypical naevi

106
Q

what kind of atypia do dysplastic naevi exhibit?

A

architectural & cellular

107
Q

what will be seen pathologically in a dysplastic naevi?

A

host-reaction fibrosis & inflammation, epidermis will not be affected

108
Q

what do halo naevi look like?

A

brown with a peripheral halo of depigmentation

109
Q

what do halo naevi look like pathologically?

A

inflammatpry regressioon & overrun by lymphocytes

110
Q

describe blue naevi pathologically

A

entierly dermal & consist of pigment rich dendritic spindle celss

111
Q

what cellular variant can blue naevi have?

A

may have mitoses & mimic melanoma

112
Q

what do Spitz naevi consist of?

A

spindle and/pr epitheloid cells

113
Q

what can Spitz naevi mimic?

A

melanoma

114
Q

are malignant melanoma more common in males or females?

A

females

115
Q

what age group does incidence of malignant melanoma peak in?

A

middle-age

116
Q

what sites of the body are malignant melanoma usually found?

A

sun exposed sites

117
Q

what factors would make you suspect a malignant melanoma?

A
  • change in shape
  • irregular pigmentation
  • bleeding
  • development of satellite nodules
  • ulceration
  • new pigmented lesion develops in adulthood
118
Q

what are the 4 main types of melanoma?

A
  • superficial spreading
  • acral/mucosal lentignous
  • lentigo maligna
  • nodular
119
Q

what is the commonest type of melanoma?

A

superficial spreading

120
Q

where is superficial spreading melanoma usually found?

A

trunk & limbs

121
Q

where are lentigo maligna usually found?

A

sun-damaged face/neck/scalp

122
Q

where are nodular malignant melanoma usually found?

A

varied sites but often trunk

123
Q

if a tumour regresses because of a host’s immune system, what is there still a risk of?

A

metastases

124
Q

what is the radial growth phase (RGP)?

A

malignant melanoma grows as a macule when either entirely in-situ or with dermal micro invasion, does not invade blood vessels at this point

125
Q

what is vertical growth phase (VGP)?

A

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

126
Q

in which growth phase can malignant melanoma metastasise?

A

VGP

127
Q

what is nodular melanoma?

A

simple nodule of VGP tumour, some consider this more aggressive

128
Q

what does melanoma prognosis relate to?

A

Breslow depth & ulceration

129
Q

what is the Breslow depth?

A

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

130
Q

how melanoma treated?

A
  • primary excision to give clear margins
  • some receive a sentinel node biopsy
  • chemo, immunotherapy, genetic therapies
131
Q

what are the epidermal tumours?

A
  • seborrheic keratosis
  • Bowen’s disease
  • actinic keratosis
  • viral lesions
  • basal & squamous cell carcinoma
132
Q

what is a seborrheic keratosis?

A

benign proliferation of epidermal keratinocytes

133
Q

what is the Leser-Trelat sign?

A

eruptive appearance of many lesions may indicate internal malignancy

134
Q

what is a horn cyst?

A

not acutely a cyst but some fluid encased under the epidermis

135
Q

what are the 3 main subtypes of BCC?

A
  • nodular
  • superficial
  • infiltrative (morphoeic)
136
Q

what does a BCC look like?

A

stuck
shiny & pearly
telangiectasis

137
Q

what are the precursors of SCC?

A
  • Bowen’s disease (legs)
  • Actinic keratosis (head/neck)
  • Viral lesions (anogenital skin)
138
Q

wha do precursors show?

A

squamous dysplasia

139
Q

what does Bowen’s disease look like?

A

scaly patch/plaque, irregular border, no dermal invasion

140
Q

what is the commonest clinical setting for a SCC?

A

elderly, sun exposed sites, UV implicated

141
Q

how can an SCC occasionally arise?

A
  • chronic leg ulcers e.g. stasis ulcers
  • sites of burns; sinuses e.g. chronic osteomyelitis
  • chronic lupus vulgaris
142
Q

what are the rare associations an SCC can arise?

A
  • xeroderma pigmentosum
  • dystrophic variant
  • epidermolysis bullosa
143
Q

what is the normal behaviour of an SCC?

A

generally good prognosis, locally invasive, low but definite risk of metastasis

Dermatology (16 decks)

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