Dermatopathology Flashcards

1
Q

clinical word for freckles?

A

ephelis

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2
Q

acantholysis definition?

A

the breaking of intercellular connections between keratinocytes

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3
Q

acanthosis definition?

A

epidermal hyperplasia

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4
Q

dyskeratosis definition?

A

the atypical keratinization below the stratum granulosum

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5
Q

erosion definition?

A

focal incomplete epidermal loss

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6
Q

exocytosis definition?

A

epidermal inflammatory cells

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7
Q

hydropic swelling?

A

intracellular keratinocyte edema

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8
Q

hypergranulosis definition?

A

hyperplasia of the SG layer

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9
Q

hyperkeratosis definition?

A

hyperplasia of the SC layer

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10
Q

lentigenous definition?

A

linear (non-nested) melanocyte proliferation within SB layer

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11
Q

papillomatosis definition?

A

hyperplasia of dermal papillae; causes surface elevation

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12
Q

parakeratosis definition?

A

SC layer retains their nuclei

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13
Q

spongiosis definition?

A

epidermal intercellular edema

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14
Q

vaculoization defintion?

A

formation of vacuoles within keratinocytes

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15
Q

what is a melanocytic nevus?

A

it is a congenital or acquired melanocytic neoplasm

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16
Q

what are the three types of melanocytic nevi?

A

junctional, compound, and intradermal

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17
Q

what is a junctional nevus?

A

where there are nests of melanocytic cells/nevus cells at the dermoepidermal junction; they are usually flat and brown to black

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18
Q

what is a compound nevus?

A

when there are nests of nevus cells/melanocytes dipping into the dermis level as well as at the dermoepidermal junction; they are slightly raise and colored

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19
Q

what is an intradermal nevus?

A

it is one in which melanocytic nevus cells are located only in the dermis, they are raised and normally flesh colored

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20
Q

what types of mutation can cause nevi?

A

activating mutations in BRAF that cause proliferation of melanocytes

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21
Q

what is a dysplastic nevus?

A

often a compound nevus with atypical growth

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22
Q

what are three ways a dysplastic nevus is different from a regular nevus?

A
  1. basal cell layer replacement via lentigenous hyperplasia
  2. papillary dermal fibrosis
  3. pigment incontinence
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23
Q

what is pigment incontinence?

A

when dead melanocytes release melanin into dermis

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24
Q

what mutation can be attributed to some dysplastic nevi?

A

BRAF or NRAS - activating

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25
Q

what is dysplastic nevus syndrome?

A

an AD familial disorder characterized by hundres of nevi; strongly associated with melanoma and can result from familial mutation of CDK4
acquired mutations of BRAF and NRAS are commo

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26
Q

where can you get melanoma?

A

SMEMEA

skin, mucosal surfaces, esophagus, meninges, eyes, anogenital area

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27
Q

what is the microscopic histology of melanoma?

A

large nuclei with irregular contours, chromatin clumped at periphery of nuclear membrane; cherry red color to nuclei

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28
Q

what are the two types of growth you see with melanoma?

A

radial and vertical

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29
Q

what is radial growth?

A

horizontal spread of melanoma within the epidermal and superficial dermal layer, dont metastasize

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30
Q

what are some examples of radial growth?

A

lentigo maligna - an indolent lesion on the face that may not progress for decades
superficial spreading melanoma - sun-exposed skin; most common
acral/mucosal lentigenous - not from sun-exposure

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31
Q

what is vertical growth?

A

the invasion of the melanoma into the dermis, involving formation of a nodule
cells lack maturation and have the capability to metastasize

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32
Q

what is the Breslow thickness?

A

it is a measure of the melanoma from stratum granulosum to the deepest layer of penetration - it correlates with ability/likelihood of metastasis - the deeper, the more likely it is to metastasize

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33
Q

what are some mutations that may lead to melanoma?

A

BRAF, NRAS, PI3K/AKT
RB mutations that affect CDK inihibitors
telomerase activators (mutations of TERT promoter)

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34
Q

how does melanoma metastasize?

A

hematogenously

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35
Q

what is a seborrheic keratosis?

A

it is a uniform, round, brown lesion with keratin plugs or horn cysts

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36
Q

what mutation leads to seborrheic keratosis?

A

mutations in FGFR2 which increase the Ras and PI3K/AKT pathways - leading to epidermal proliferation

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37
Q

what can be one cause of seborrheic keratosis?

A

paraneoplastic syndrome indicative of a GI malignancy - the cancer produced TGF-alpha which stimulates epidermal proliferation

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38
Q

what is the microscopic morphology of seborrheic keratosis?

A

exophytic, monotonous sheets of small cells with variable pigmentation; hyperkeratosis

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39
Q

what is acanthosis nigricans?

A

it is a hyperpigmented velvety lesion that occurs in flexural areas

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40
Q

what are some microscopic morphologies of acanthosis nigricans?

A

prominent rete ridges and hyperkeratosis, basal cell hyperpigmentation (BUT no basal cell hyperplasia)

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41
Q

what are the two types of acanthosis nigricans?

A

benign and malignant

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42
Q

what is benign acanthosis nigricans?

A

it is familial AD and usually develops in childhood due to inheritance of FGFR-3 mutation
can also be related to obesity or endocrine disorders

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43
Q

what is malignant acanthosis nigricans?

A

it develops in adulthood and is usually associated with occult adenocarcinoma

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44
Q

what is the proper term for a skin tag?

A

fibroepithelial polyp

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45
Q

what is a fibroepithelial polyp?

A

it is a tumor with a fibrovascular stalk that is covered in benign epidermis

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46
Q

what is an epithelial cyst?

A

aka wen

it is a lesion filled with keratin, lipid, and sebaceous secretions

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47
Q

what are some types of epithelial cysts?

A

epithelial inclusion cyst, pilar (trichilemmal) cysts, dermoid cyst, streatocystoma multiplex

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48
Q

what is an epithelial inclusion cyst?

A

it contains keratin, wall is made of normal epidermis

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49
Q

what is a pilar (trichilemmal) cyst?

A

wall is made of follicular epithelium

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50
Q

what is a dermoid cyst?

A

wall is similar to epidermis but has lots of hair follicles

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51
Q

what is a steatocystoma multiplex

A

wall resembles sebaceous gland ductal epithelium with numerous compressed sebaceous lobules

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52
Q

what are adnexal tummors?

A

tumors arising from skin appendages like sebaceous glands, hair follicles etc

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53
Q

what is Cowden syndrome?

A

a malignancy that can have adnexal tumors as markers

54
Q

what is actinic keratosis?

A

a brown/red lesion due to sun-exposure and hyperkeratosis

55
Q

what is the morphology of actinic keratosis?

A

cutaneous horns, basal cell hyperplasia, dyskeratosis, parakeratosis; blue-gray elastic fibers due to abberant fibroblast action due to UV exposure

56
Q

what mutation causes actinic keratoses?

A

TP53 due to UV

57
Q

what is actinic keratosis a precursor for?

A

squamous cell carcinoma

58
Q

what is squamous cell carcinoma morphology?

A

red scaling plaques to more developed nodular ucleractions with complete epidermal atypia

59
Q

what is a keratocanthoma?

A

it is a type of SCC (maybe) that presents as a cup shaped nodule with keratin filled crater

60
Q

what mutations are responsible for scc?

A
TP53 mutation (with actinic keratosis precursor)
HRAS mutation (activating)
lof Notch signaling responsible for epidermal differentiation
61
Q

what genetic disease predisposes people to SCC?

A

xeroderma pigmentosa - involves loss of nucleotide base excision repair mechanism for pyrimidine dimers

62
Q

what are other potential causes of SCC?

A

immunosuppression (HPV infection?) and industrial carcinogens

63
Q

what is basal cell carcinoma?

A

hyperproliferation of basal cells

64
Q

what is the morphology of BCC?

A

pearly, telangiectatic nodules that dont metastasize and are locally invasive

65
Q

what are the two ways BCC can occur?

A

multifocal and nodular

66
Q

what is multifocal BCC?

A

it is only in the epidermis and consists of superficial spreading

67
Q

what is nodular BCC?

A

characterized by islands of basal cells in the dermis that are hyperchromatic and in a mucinous matrix with stroma retracting from the cells

68
Q

what is nevoid basal cell carcinoma syndrome?

A

aka Gorlin syndrome; an AD disorder consisting of multuple BCCs early in life

69
Q

what is the main mutation causing BCC?

A

unbridled Hedgehog signaling
SHH normally binds to its receptor PTCH which causes it to release SMO which goes on to activate GLI1 which increases cell proliferation - when SHH is unbridled, you get lots of cell proliferation

70
Q

what is dermatofibroma?

A

a benign neoplasm characterized by dermal fibroblast proliferation and trapping of collagen; it includes epidermal hyperplasia over the region and downward elongation of rete ridges because of this
spindle cells are characteristic of these too

71
Q

what is dermatofibrosarcoma protuberans?

A

a well-defined fibrosarcoma characterized by closely packed fibroblasts in a pinwheel shape

72
Q

what mutations can cause dermatofibrosarcoma protuberans?

A

a translocation of the collagen 1A1 gene and PDGFbeta genes in which the collagen promoter is put in front of the PDGFbeta gene, overexpressing it, leading to tumor cell growth

73
Q

what is mycosis fungoides?

A

a cutaneous CD4+ cell lymphoma characterized by red scaling plaques, fungating nodules

74
Q

what is Sezary syndrome?

A

a type of mycosis fungoides that involves diffuse erythema and scaling across entire body

75
Q

what are histologic characteristics of mycosis fungoides?

A

the presence of Sezary-Lutzner cells which form band-like aggregates in the superficial dermis; they can invade into the epidermis, forming Pautrier microabscesses

76
Q

what is mastocytosis?

A

an accumulation of mast cells in the skin causing a brown-pink nodule that may be prurituc

77
Q

what causes the symptoms of mastocytosis?

A

release of histamine and heparin; systemic symptoms include gi bleeding, nasal discharge, and osteoporosis)

78
Q

what stains would you use to visualize mastocytosis microscopically?

A

Giemsa or toludine blue (in case the mast cells are degranulated)

79
Q

what mutation causes mastocytosis?

A

activating mutation in the Kit receptor tyrosine kinase which drives cell growth and survival

80
Q

what is urticaria?

A

the formation of hives due to introduction of something into body; get edmeatous wheals often due to mast cell degranulaiton

81
Q

what layer of skin does the urticaria edema occur in?

A

the dermis

82
Q

what are the three types of urticaria?

A

IgE and mast cell dependent
IgE independent and mast cell dependent
IgE and mast cell independent

83
Q

how do you get IgE and mast cell dependent urticaria?

A

type 1 hypersensitivity reaction to allergens like food, drugs, pollen

84
Q

how do you get IgE independent, mast cells dependent urticaria?

A

direct stimulation of mast cells without IgE by things like antibiotics, opiates, and curare

85
Q

how do you get IgE and mast cell independent urticaria?

A

local increase of vascular permeability by things like aspirin which inhibits the cyclooxygenase pathway

86
Q

what is acute eczematous dermatitis?

A

a type IV hypersensitivity that involves reactive chemicals reacting with self-proteins to make haptens that act as neoantigens and cause an inflammatory response via Langerhans cells - then upon reexposure you get a reaction

87
Q

what is allergic contact dermatitis?

A

when you additionally have spongiosis (intercellular epidermal edema) that splays apart keratinocytes via desomosomes in SS

88
Q

what do lesions in acute eczematous dermatitis look like?

A

oozing, crusting, red, vesicles that can eventually become scaling red plaques

89
Q

what is erythema multiforme?

A

a type IV hypersensitivity reaction that is CD8+ T cell mediated and causes blisters and targetoid lesions

90
Q

what are some causes of erythema multiforme?

A

infections like HSV and typhoid, antibiotics (sulfonamides, penicillin, etc) or cancer and collagen vascular diseases (lupus and dermatomyositis)

91
Q

what are the three types of erythema multiforme?

A

EM minor, EM major (Steven’s Johnson syndrome), and toxic epidermal necrolysis

92
Q

what are the manifestations of EM minor?

A

blisters and targetoid lesions, dermoepidermal lymphocytic infiltrate, dermal edema; self-limiting

93
Q

what are the manifestations of Stevens-Johnson syndrome (EM major)?

A

febrile form with diffuse blisters all over skin and other surfaces like conjunctiva, mucosal surface, and genitals

94
Q

what are the manifestations of toxic epidermal necrolysis?

A

full thickness, diffuse necrosis and sloughing of cutaneous and mucosal epithelia

95
Q

what does psoriasis look like?

A

salmon-pink lesions with silvery scales; often get nail dysfiguration

96
Q

what are some diseases associated with psoriasis?

A

arthritis, myopathy, enteropathy, joint diseases, AIDS

97
Q

what can psoriasis lead to increased risks of?

A

CV disease and stroke

98
Q

what are microscopic manifestations of psoriasis?

A
acanthosis and increases rete ridges
increased mitoses above SB
parakeratosis
auspitz sign
spongiosis in SS layer
munro microabscesses
99
Q

what is the Auspitz sign?

A

due to epidermal thinning over dermal papillae, you get pinpoint bleeding from dermal bv’s when scale is removed

100
Q

what is a munro microabscess?

A

accumulation of neutrophils in the stratum corneum

101
Q

what is the pathogenesis of psoriasis?

A

type IV hypersensitivity mediated by CD4+ Th1 cells, Th17 cells and CD8+ cells

102
Q

what cytokines cause hyperkeratosis in psoriasis?

A

INF-gamma, IL-17, and TNF

103
Q

what is the Koebner phenomenon?

A

genesis of new lesions at sites of trauma

104
Q

what is seborrheic dermatitis?

A

CID common in areas with lots of sebaceous glands - macules and papules on erythematous-yellow, greasy base

105
Q

what are the six P’s of Lichen Planus?

A

pruritic, purple, polygonal, planar, papules, plaques

106
Q

what are other characteristics of Lichen Planus?

A

self-limited, can cause SCC if chronic, koebner happens, wickham striae; dense continuous infiltrate of lymphocytes at DE jxn

107
Q

what is pemphigous?

A

an inflammatory blistering disorder that is a type II hypersensitivity rxn

108
Q

what are morphologic hallmarks of pemphigous?

A

acantholysis with intercellular clefting and intraepithelial blisters

109
Q

what is the morphology of pemphigous vulgaris?

A

involves places other than skin inlcuing mucosa; have easily ruptured blisters due to separation occurring right above basal layer (suprabasal blister)

110
Q

against what is the antibody against in pemphigous vulgaris?

A

desmoglein 1 and 3

111
Q

what is the morphology of pemphigous foliaceus?

A

superficial blisters that present at erythema and crusting - subcorneal blister (desmoglein 1 antibody)

112
Q

what class of antibodies is involved in pemphigous?

A

IgG - it disrupts cellular adhesion and activates intercellular proteases

113
Q

what do you see in immunofluorescence with pemphigous?

A

netlike structures composed of desmoglein antibodies

114
Q

what is bullous pemphigoid?

A

an autoimmune disorder characterized by tense blisters that arent easily ruptured that are sub-epidermal (i.e. at DE jxn)

115
Q

what are the autoantibodies in bollus pemphigoid against?

A

BPAG2 autoantibodies (hemidesmosomes - which is what holds epidermis to dermis)

116
Q

what is the Nikolsky sign?

A

when you rub the skin and you get immediate exfoliation and blister formation - positive in P. vulgaris and negative in bullous pemphigoid

117
Q

what is dermatitis herpetiformis?

A

a rare disorder characterized by urticaria and grouped vesciles - people develop IgA ab’s to gluten and these cross-react with reticulin in epidermal basement memrbane - subdermal blister,

118
Q

what is epidermolysis bullosa?

A

inherited disorders in structural proteins - when you rub the skin you get blisters

119
Q

what are the three types of epidermylosis bullosa?

A

simplex, junctional, dystrophic

120
Q

what is simplex epidermylosis bullosa?

A

defects in the basal layer (mutation in keratin 14 or 5) dominant negative

121
Q

what is junctional epidermylosis bullosa?

A

lamina lucida level blisters, AR defects in laminin which normally binds to hemidesmosomes

122
Q

what is dystrophic epidermylosis bullosa?

A

blisters develop beneath lamina densa in association with rudimentary or defective anchoring fibrils - mutation in type VII collagen

123
Q

what are the two types of acne vulgaris?

A

noninflamm and inflamm

124
Q

what are open comedones?

A

small follicular papules containing a central black keratin plug

125
Q

what are closed comedones?

A

follicular papules without visible central plaques

126
Q

what is rosacea?

A

non-specific perifollicular infiltrate with dermal edema due to high cutaneous levels of antimicrobial peptide cathelicidin

127
Q

what is panniculitis?

A

inflammation of subcutaneous fat

128
Q

what are two types of panniculitis?

A

erythema nodosum (very painful); erythema induratum

129
Q

what is erythema nodosum?

A

veyr tender erythematous nodules that affects connective tissues between fat lobules and lobules themselves

130
Q

what is erythema induratum?

A

primary vasculitis of subcutaneous fat with subsequent inflammation and necrosis of adipose tissue

131
Q

what is molluscum contagiousum?

A

a poxvirus that causes firm, prurituc, pink umbilicated papules that has a cheesy material containg molluscum bodies; microscopically see lots of virions

132
Q

what is impetigo?

A

superficial bacterial infection (s. aureus and Group A step) that is super contagious and can be bollus in kids
“honey colored crust” - pustules have lots of neutrophils and G+ cocci