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Skin & MSK > Dermatopathology: Blistering disorders > Flashcards

Dermatopathology: Blistering disorders Flashcards

1
Q

IHC marker for keratinocytes

A

Cytokeratin

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2
Q

Cytokeratin is an IHC marker for this

A

Keratinocytes

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3
Q

2 IHC markers for melanocytes

A

S100, HMB45

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4
Q

2 IHC markers for Langerhans cells

A

S100, CD1a

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5
Q

IHC marker for nerves

A

S100

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6
Q

2 IHC markers for vessels

A

Actin-muscle, CD34-endothelium

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7
Q

Flat, non-elevated, circumscribed, <5mm

A

Macule

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8
Q

Flat, non-elevated, circumscribed, >5mm

A

Patch

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9
Q

What is the difference between a macule and a patch?

A

Both are flat, non-elevated, and circumscribed
Macule is <5mm
Patch is >5mm

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10
Q

Elevated lesion, <5mm

A

Papule

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11
Q

What is the size of a macule?

A

<5mm

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12
Q

What is the size of a patch?

A

> 5mm

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13
Q

Elevated lesion, >5mm

A

Nodule

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14
Q

What is the difference between a papule and nodule?

A

Both are elevated lesions
Papule is <5mm
Nodule is >5mm

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15
Q

Elevated, flat-topped lesion, usually >5mm

A

Plaque

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16
Q

Lay term for vesicle or bulla

A

blister

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17
Q

Fluid-filled cavity, <5mm

A

Vesicle

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18
Q

Fluid-filled cavity, >5mm

A

Bulla

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19
Q

What is the difference between vesicle and bulla?

A

Both are blisters; fluid-filled cavity
Vesicle is <5mm
Bulla is >5mm

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20
Q

Purulent vesicle or bulla

A

Pustule

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21
Q

Dry, flaky area of impaired cornification on skin surface

A

Scale

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22
Q

Dried collection of blood, serum, or pus on skin surface

A

Crust

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23
Q

Thickening of skin with increased skin markings due to chronic rubbing/scratching

A

Lichenification

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24
Q

Thinned area of skin

A

Atrophy

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25
Q

Skin elevation caused by dermal edema
Often itchy, usually resolves quickly

A

Wheal

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26
Q

Separation of nail from nail bed

A

Onycholysis

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27
Q

Describes skin lesion that appears in lines of trauma (e.g. scratch lines)

A

Koebner phenomenon

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28
Q

Small distal dilated blood vessels that appear close to skin surface

A

Telangiectasia

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29
Q

A traumatic lesion causing epithelial disruption and bleeding (a deep scratch)

A

Excoriation

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30
Q

Increased thickness of stratum corneum

A

Hyperkeratosis

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31
Q

Hyperkeratosis is an increased thickness of this layer

A

Stratum corneum

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32
Q

Hyperkeratosis with retained keratinocyte nuclei

A

Parakeratosis

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33
Q

Hyperkeratosis with no retention of keratinocyte nuclei

A

Orthokeratosis

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34
Q

Hyperplasia of stratum granulosa
Prominent keratohyalin granules

A

Hypergranulosis

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35
Q

In hypergranulosis, these are prominent

A

Keratohyalin granules

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36
Q

Increased thickness of epidermis

A

Acanthosis

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37
Q

Intercellular edema in epidermis
Desmosomes easily seen due to fluid between epithelial cells
(intercellular bridges often indicate squamous cell involvement)

A

Spongiosis

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38
Q

Loss of intercellular keratinocyte adhesion

A

Acantholysis

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39
Q

Formation of spaces between cells, usually seen in basal cell-basement membrane zone

A

Vacuolization

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40
Q

Vacuolization is usually seen in this zone of the skin

A

Basal cell-basement membrane zone

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41
Q

Abnormal (premature) individual cell keratinization

A

Dyskeratosis

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42
Q

Linear pattern of melanocytic proliferation at dermal-epidermal junction

A

Lentiginous

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43
Q

Lentiginous is a linear pattern of melanocytic proliferation at this

A

Dermal-epidermal junction

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44
Q

Lentiginous is a linear pattern of proliferation of these cells at dermal-epidermal junction

A

Melanocytes

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45
Q

Infiltration of epidermis by inflammatory cells

A

Exocytosis

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46
Q

Complete loss of epidermis and exposure of dermis/subcutis

A

Ulceration

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47
Q

Incomplete loss of epithelium

A

Erosion

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48
Q

Desmosomes attach these

A

Suprabasal keratinocytes to each other

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49
Q

What attach suprabasal keratinocytes to each other?

A

Desmosomes

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50
Q

Protein in desmosomes that is more superficial

A

Desmoglein 1

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51
Q

Protein in desmosomes that is found in deeper skin

A

Desmoglein 3

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52
Q

Problem with this structure results in intraepidermal splits

A

Desmosomes

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53
Q

Structures that attach basal keratinocytes to basement membrane

A

Hemidesmosomes

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54
Q

Hemidesmosomes attach these

A

Basal keratinocytes to basement membrane

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55
Q

Problem with this structure results in subepidermal splits

A

Hemidesmosomes

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56
Q

Anchoring filaments that provide stability to the dermal-epidermal adhesion

A

Collagen VII

57
Q

Disorders with formation of blisters and vesicles as their primary manifestation

A

Bullous disorders

58
Q

Blister filled with acute inflammation

A

Pustule

59
Q

Describes blistering disorders due to loss of keratinocyte intercellular attachment

A

Pemphigus

60
Q

Most common form of Pemphigus

A

Pemphigus Vulgaris

61
Q

What age does Pemphigus Vulgaris present?

A

40-60 year old

62
Q

Bullous disorder with this typical patient:
40-60 year old
Male = female
May be life threatening

A

Pemphigus Vulgaris

63
Q

What causes Pemphigus Vulgaris?

A

IgG Autoantibodies against desmoglein 3

64
Q

Pemphigus Vulgaris is caused by IgG autoantibodies against this

A

Desmoglein 3

65
Q

What type of split is present in Pemphigus vulgaris?

A

Suprabasal

66
Q

Condition characterized by row of “tombstones”

A

Pemphigus Vulgaris
(due to basal cells remaining attached)

67
Q

Condition where IgG produces “fishnet” pattern in direct immunofluorescence

A

Pemphigus Vulgaris

68
Q

Type of bullae in Pemphigus Vulgaris

A

Flaccid; easily ruptured; painful

69
Q

Phenomenon where a blister expands when pressure is applied

A

Nikolsky sign

70
Q

Nikolsky sign in Pemphigus Vulgaris

A

Positive

71
Q

Common initial site of Pemphigus Vulgaris

A

Oral mucosa

72
Q

Pemphigus Vulgaris affects these sites

A

Mucosal sites and skin
(oral mucosa, esophagus, skin - head, trunk)

73
Q

Who is more likely to have Pemphigus Vulgaris, male or female?

A

Equal

74
Q

Bullous disorder caused by IgG autoantibodies against desmoglein 3

A

Pemphigus Vulgaris

75
Q

Type of Pemphigus that is an endemic in Brazil

A

Pemphigus Foliaceus

76
Q

Pemphigus Foliaceus involves antibodies against this

A

Desmoglein 1

77
Q

Type of split in Pemphigus Foliaceus

A

Subcorneal

78
Q

Is there mucosal involvement in Pemphigus Foliaceus?

A

No
There is no desmoglein 1 in mucosa

79
Q

Is there mucosal involvement in Pemphigus Vulgaris?

A

Yes
Oral mucosa is common initial site

80
Q

Pemphigus involving erosions rather than bullae

A

Pemphigus Foliaceus

81
Q

What causes Pemphigus Foliaceus?

A

Antibodies against desmoglein 1

82
Q

Bullous disorder caused by antibodies against desmoglein 1

A

Pemphigus Foliaceus

83
Q

What causes Paraneoplastic Pemphigus?

A

IgG against pemphigus and pemphigoid antigens

84
Q

Type of Pemphigus caused by IgG against pemphigus and pemphigoid antigens

A

Paraneoplastic Pemphigus

85
Q

Bullous disorder with same appearance as Pemphigus Vulgaris, may have band of lymphocytes in dermis

A

Paraneoplastic Pemphigus

86
Q

Paraneoplastic Pemphigus is most common with this neoplasm

A

Lymphomas

87
Q

Bullous disorder most common with lymphomas

A

Paraneoplastic Pemphigus

88
Q

Paraneoplastic Pemphigus can have the same appearance as Pemphigus Vulgaris, but may have a band of these

A

Lymphocytes in the dermis

89
Q

Blistering disease due to autoantibodies against BPA of hemidesmosomes

A

Bullous Pemphigus

90
Q

What causes Bullous Pemphigus?

A

IgG autoantibodies against BPA (Bullous Pemphigus Antigen) of hemidesmosomes

91
Q

Is acantholysis present in Bullous Pemphigus?

A

No

92
Q

Is acantholysis present in Pemphigus Vulgaris?

A

Yes

93
Q

The pathogenesis of Bullous Pemphigus involves IgG against GPA of this structure

A

Hemidesmosomes

94
Q

Split in Bullous Pemphigus

A

Subepidermal
with eosinophils

95
Q

What shows on direct immunofluorescence in Bullous Pemphigus?

A

Complement
Linear IgG along dermal-epidermal junction (DEJ)

96
Q

Linear IgG along dermal-epidermal junction is seen on DIF in this blistering disease

A

Bullous Pemphigus

97
Q

Blistering disease associated with celiac disease

A

Dermatitis Herpetiformis

98
Q

Dermatitis Herpetiformis is associated with this

A

Celiac disease

99
Q

Age at presentation in Dermatitis Herpetiformis

A

Peak teens to 20s

100
Q

Who is more likely to have Dermatitis Herpetiformis, male or female?

A

Males
(2:1 male to female ratio)

101
Q

Dermatitis Herpetiformis is more common in this population

A

Scandinavian

102
Q

Blistering disease more common in Scandinavian populations

A

Dermatitis Herpetiformis

103
Q

Bullous disorder that is an endemic in Brazil

A

Pemphigus Foliaceus

104
Q

When wheat is digested, this is produced that is deamidated, binds to transglutaminase, and becomes a neoantigen

A

Gliadin

105
Q

Form of transglutaminase in the intestine

A

Tissue translutaminase (TTG, TG2)

106
Q

Form of transglutaminase in the skin

A

Epidermal transglutaminase (eTG, TG3)

107
Q

In Dermatitis Herpetiformis, anti-eTG IgA deposits here

A

Tips of dermal papilla

108
Q

What causes Dermatitis Herpetiformis?

A

Anti-eTG IgA deposits at tips of dermal papilla
(complement is fixed, leading to patches of vesicles on erythematous base)

109
Q

Split in Dermatitis Herpetiformis

A

Subepidermal at tips of dermal papilla
Split is filled with neutrophils (pustules)

110
Q

What is seen on DIF in Dermatitis Herpetiformis?

A

Granular IgA at dermal papillary tips

111
Q

Granular Iga at dermal papillary tips is seen on DIF in this bullous disorder

A

Dermatitis Herpetiformis

112
Q

Blistering disorder involving a subepidermal split at tips of dermal papilla

A

Dermatitis Herpetiformis

113
Q

Blistering disorder involving a subepidermal split filled with neutrophils (pustules)

A

Dermatitis Herpetiformis

114
Q

Blistering disorder when clusters of vesicles/pustules are formed on an erythematous base
Very pruritic

A

Dermatitis Herpetiformis

115
Q

Locations on the body where clusters of vesicles/pustules are found in Dermatitis Herpetiformis

A

elbows, knees, buttocks

116
Q

Group of hereditary bullous disorders

A

Epidermolysis Bullosa

117
Q

What causes Epidermolysis Bullosa?

A

Defective proteins at dermis-epidermal junction result in mechanical fragility

118
Q

Bullous disorder caused by defective proteins at DEJ, resulting in mechanical fragility

A

Epidermolysis Bullosa

119
Q

Bullous disorder where friction blisters form easily

A

Epidermolysis Bullosa

120
Q

Form of Epidermolysis Bullosa that is mild with no scarring

A

EB simplex

121
Q

2 gene mutations in EB simplex

A

Keratin 14 and 5

122
Q

Most severe form of Epidermolysis Bullosa, forms scars

A

Dystrophic EB

123
Q

Dystrophic EB is due to defective this

A

Anchoring filaments (type VII collagen)

124
Q

Split in Epidermolysis Bullosa

A

Most forms have subepidermal split

125
Q

DIF appearance of Epidermolysis Bullosa

A

Negative

126
Q

Bullous disorder characterized by friction blisters

A

Epidermolysis Bullosa

127
Q

Autoimmune form of Epidermolysis Bullosa

A

Epidermolysis bullosa acquisita

128
Q

Onset of Epidermolysis bullosa acquisita

A

Adult onset

129
Q

Bullous disorder where friction blisters are produced at sites of trauma (fingers, feet, oral)

A

Epidermolysis bullosa acquisita

130
Q

What causes Epidermolysis bullosa acquisita?

A

IgG autoantibodies against type VII collagen

131
Q

Bullous disorder caused by IgG autoantigens against type VII collagen

A

Epidermolysis bullosa acquisita

132
Q

Split in Epidermolysis bullosa acquisita

A

Subepidermal

133
Q

DIF appearance of Epidermolysis bullosa acquisita

A

Linear IgG along basement membrane

134
Q

Linear IgG along basement membrane is seen on DIF in this bullous disorder

A

Epidermolysis bullosa acquisita

135
Q

In Dermatitis herpetiformis, the subepidermal split at the tips of dermal papilla are filled with these

A

Neutrophils

136
Q

Bullous disorder with a subepidermal split filled with neutrophils, forming pustules

A

Dermatitis herpetiformis

137
Q

Bullous disorder with a subepidermal blister with eosinophils

A

Bullous pemphigus

138
Q

Bullous pemphigus involves a subperidermal blister with these

A

Eosinophils

Skin & MSK (8 decks)

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