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Block 7 Week 2 > Fung: Dermatopathology > Flashcards

Fung: Dermatopathology Flashcards

1
Q

What are the four layers of the epidermis from the basement membrane to the surface?

A

stratum basale
stratum spinosum
stratum granulosum
stratum corneum

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2
Q

Which layer of the epidermis has keratohyalin granules?

A

stratum granulosum

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3
Q

What are two cell types in the epidermis? What do these cells do?

A
  1. melanocytes: protect the skin from UV injury

2. Langerhan cells: antigen recognition and immune response

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4
Q

What are two layers found in the dermis?

A

papillary vs reticular layer

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5
Q

What is found in the dermis?

A

sebaceous glands, apocrine, and eccrine glands too

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6
Q

How do the palms of the hands and soles of the feet differ in terms of their epidermal layer?

A

thicker layer of keratin bc these areas undergo a lot of trauma and sheering forces daily

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7
Q

Circumscribed, flat lesion <5mm distinguished from surrounding skin by color

A

macule

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8
Q

Circumscribed, flat lesion >5mm distinguished from surrounding skin by color

A

patch

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9
Q

Elevated dome-shaped or flat-topped lesion <5mm

A

papule

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10
Q

Elevated dome-shaped or flat-topped lesion >5mm

A

nodule

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11
Q

Elevated flat-topped lesion >5mm

A

plaque

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12
Q

discrete, pus-filled, raised lesion

A

pustule

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13
Q

dry, horny, platelike excrescence, usu the result of imperfect cornification

A

scale

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14
Q

fluid-filled raised lesion <5mm, also called a blister

A

vesicle

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15
Q

fluid-filled raised lesion >5mm; also called a blister

A

bulla

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16
Q

traumatic lesion breaking the epidermis and causing a raw linear area

A

excoriation

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17
Q

itchy, transient, elevated lesion with variable blanching and erythema formed as the result of edema

A

wheal

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18
Q

thickened, rough skin; usu the result of repeated rubbing

A

lichenification

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19
Q

What’s the difference bw a vesicle and a bulla?

A

a vesicle is 5mm

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20
Q

What is a notable feature of a wheal?

A

blanching

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21
Q

diffuse epidermal hyperplasia

A

acanthosis

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22
Q

abnormal, premature keratinization w/i cells below the stratum granulosum

A

dyskeratosis

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23
Q

hyperplasia of the stratum granulosum

A

hypergranulosis

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24
Q

thickening of the stratum corneum

A

hyperkeratosis

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25
Q

a linear pattern of melanocyte proliferation w/i the epidermal basal cell layer

A

lentiginous

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26
Q

surface elevation caused by hyperplasia and enlargement of contiguous dermal papillae

A

papillomatosis

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27
Q

keratinization w retained nuclei in the stratum corneum

A

parakeratosis

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28
Q

intercellular edema of the epidermis

A

spongiosis

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29
Q

Where is hyperkeratosis seen?

A

in the palms and soles of the feet

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30
Q

What is the difference between hyperkeratosis and parakeratosis?

A

hyperkeratosis: thick layer of keratin above the granulosum
parakeratosis: thick layer of keratin, but it retains the nucleus

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31
Q

What is the difference between acanthosis and papillomatosis?

A

both are epidermal hyperplasia, but papillomatosis produces distinct papillary fragments

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32
Q

In spongiosis, what happens to the cells due to the intracellular edema?

A

they get pushed apart

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33
Q

Where is dyskeratosis seen?

A

within cells BELOW the stratum granulosum

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34
Q

Last from days to weeks

Characterized by lymphocytic and macrophage inflammatory infiltrate and edema

A

acute inflammatory dermatoses

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35
Q

Persist for months to years
Associated with changes in epidermal growth (atrophy or hyperplasia) or dermal fibrosis
The skin is roughened due to excess or abnormal scale formation and shedding

A

chronic inflammatory dermatoses

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36
Q

Common disorder characterized by localized mast cell degranulation and dermal microvascular hyperpermeability
Patients present with pruritic edematous plaques (wheals)
Angioedema is a related condition with edema of the deeper dermis and subcutaneous fat
Can be acute (less than 6 weeks) or chronic

A

urticaria

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37
Q

How do patients with urticaria present?

A

w pruritic (itchy) edematous plaques (wheals)

38
Q

Urticaria is a common disorder characterized by localized (blank) degranulation and dermal microvascular (blank)

A

mast cell; hyperpermeability

39
Q

In urticaria (hives), which layer of the skin will have edema and sparse inflammation?

A

papillary dermis

40
Q

Causes of urticaria?

A 
immunological mechanisms
non-immuno mechanisms
physical stimuli
skin contact
small vessel vasculitis
41
Q

Treatment for urticaria?

A 
avoid specific allergens
oral H1 (histamine) antagonists
epi
42
Q

One of the most common skin disorders

Can be subdivided into 5 categories

Results from T-cell mediated inflammatory reactions (type IV hypersensitivity)

A

acute eczematous dermatitis (eczema)

43
Q

What type of immune reaction occurs in eczema?

A

T-cell mediated inflammatory reaction (type 4 hypersensitivity)

44
Q

What will you see microscopically in cases of eczema?

A

spongiosis
intraepidermal vesicles
hemorrhage
lymphocytes invading

45
Q

What causes eczema?

A

internal or external antigen

46
Q

Treatment for eczema?

A

remove offending agent

topical steroids

47
Q 
Self-limited hypersensitivity reaction 
Associated with infections from
Virus: Herpes simplex 
Bacteria: Mycoplasma, leprosy, typhoid
Fungus: Histoplasma, Coccidioides
Exposure to drugs: sulfonamides, penicillin, barbiturates, salicylates, antimalarials
Cancer
Collagen vascular disease
A

Erythema multiforme

48
Q

How does erythema multiforme present clinically?

A

with classical target-oid lesions with crust in the center; different shapes and sizes of lesions

49
Q

How does erythema multiforme look microscopically?

A

spongiosis
dermal edema
necrotic keratinocytes
parakeratosis

50
Q

A febrile form of erythema multiforme with extensive skin involvement
Also involves oral mucosa, conjunctiva, urethra, genital and perianal areas
May lead to sepsis
Often seen in children

A

Stevens Johnson syndrome

51
Q

A form of erythema multiforme
Characterized by diffuse necrosis and sloughing of cutaneous and mucosal epithelial surfaces
Clinical picture similar to that of burn patients

A

Toxic epidermal necrolysis

52
Q

Treatment for erythema multiforme?

A 
observe
oral antihistamines
topical steroids
acyclovir (herpes simplex)
prednisone

chronic: antibiotics

53
Q

Common disorder affecting 1-2% of the US population

Chronic inflammatory dermatosis that results from interactions of genetic and environmental factors
Associated with HLA-C

Results from activated T cells in the skin stimulating the secretion of cytokines and growth factors that induce keratinocyte proliferation

15% of patients have associated arthritis

A

psoriasis

54
Q

What kind of immune reaction is occurring in psoriasis?

A

activated T cells in the skin stimulate cytokines and growth factors that induce keratinocyte proliferation

55
Q

What might patients with psoriasis also present with?

A

arthritis

56
Q

What does psoriasis look like microscopically?

A 
acanthosis in epidermis
spongiosis
lymphocyte invasion
can have suprapapillary thinning
spongiform pustules
57
Q

Treatment for psoriasis

A

topical steroids
intralesional steroid injection
UVB and tar
drugs

58
Q

Common chronic inflammatory dermatosis that affects up to 5% of the general population

Involves regions with high density of sebaceous glands

Scalp
Forehead
External auditory canal
Retroauricular area
Nasolabial folds
Presternal area
A

Seborrheic dermatitis

59
Q

What are two causes of sebhorreic dermatitis?

A

increased sebum production

colonization of the skin by Malassezia (fungus)

60
Q

Severe form of sebhorreic dermatitis seen in (blank) patients with low CD4 count

A

HIV+

61
Q

Treatment of sebhorreic dermatitis?

A

frequent washing of the affected area with antisebhorreic soaps
topical steroids
anti-yeast meds
oral antifungals

62
Q

Self-limited condition most commonly resolving spontaneously 1-2 years after onset

“Six Ps”
Pruritic, purple, polygonal, planar, papules and plaques

Resolution of lesions may leave postinflammatory hyperpigmentation

Squamous cell carcinoma may develop in oral lesions

A

Lichen planus

63
Q

What does lichen planus look like microscopically?

A

contact hyperkeratosis
hypergranulosis
lichenoid lymphocytes (thick band of lymphocytic infiltration of dermal/epidermal junction)

64
Q

Treatment for lichen planus?

A 
topical steroids
intralesional steroids
systemic steroids
drugs
light therapy
65
Q

(blank) disorders are a group of diseases in which blisters are the primary and most distinctive feature

A

bullous

66
Q

4 conditions in which blisters are a feature

A

herpes virus
spongiotic dermatitis
erythema multiforme
thermal burns

67
Q

3 types of blistering disorders

A

subcorneal (beneath the stratum corneum)
suprabasal (above the stratum basale)
subepidermal (beneath the epidermis at the level of the basement membrane)

68
Q

Corneal blisters affect which protein in the skin?

A

desmoglin 1

69
Q

Superbasal blisters affect which protein in the skin?

A

desmoglin 3

70
Q

In inflammatory blistering disorder caused by autoantibodies that result in the dissolution of intercellular attachments within the epidermis and mucosal epithelium
IgG autoantibodies to desmoglein 1 and 3 disrupt intercellular adhesions of desmosomes

A

pemphigus

71
Q

This form of pemphigus accounts for 80% of cases

A

pemphigus vulgaris

72
Q

This form of pemphigus is rare and forms plaques around the groin

A

pemphigus vegetans

73
Q

This form of pemphigus forms subcorneal blisters

A

pemphigus foliaceus

74
Q

What is unique about the blisters in pemphigus?

A

they crust and break open

75
Q

Treatment of pemphigus

A

immunosuppressive agents to decrease the titers of the pathogenic antibodies

76
Q

In pemphigus, the body forms autoantibodies to what? What does this cause?

A

desmoglin 1 and 3; disruption of intercellular adhesions of desmosomes

77
Q

A blistering disorder caused by autoantibodies directed to the proteins that bind basal keratinocytes to the basement membrane
Antibody deposition occurs in a linear pattern at the dermoepidermal junction
The proteins BPAGs are part of the hemidesmosomes that link basal keratinocytes to the basement membrane

A

bullous penphigoid

78
Q

In bullous pemphigoid, what is the body making autoanitbodies to?

A

BPAG - proteins that bind basal keratinocytes to the basement membrane

79
Q

What is one characteristic feature of bullous pemphigoid?

A

subepidermal blister (the whole epidermis is raised above the blister)

80
Q

What can be used to detect bullous pemphigoid?

A

immunofluorescence to look for linear IgG on the roof of the blister

81
Q

What is a characteristic immunofluorescence feature of pemphigus?

A

swiss cheese pattern of intra-epidermal IgG

82
Q

Treatment of bullous pemphigoid?

A

topical steroids
systemic steroids
drugs

83
Q

Rare disorder characterized by urticaria and grouped vesicles

Strong association with HLA-B8, HLA-DR3 and HLA-DQw2

Genetically predisposed individuals develop IgA antibodies to dietary gluten

These antibodies cross-react with reticulin which is a component of the anchoring fibrils that attaches the epidermal basement membrane to the superficial papillary dermis

The injury results in subepidermal blisters

A

dermatitis herpetiformis

84
Q

In dermatitis herpetiformis, what do individuals develop IgA antibody against? These antibodies can cross-react with what protein?

A

dietary gluten; reticulin

85
Q

Classic presentation of dermatitis herpetiformis?

A

blisters occurring on the elbows and knees

86
Q

What would you look for on immunofluorescence staining in dermatitis herpetiformis?

A

granular IgA

87
Q

What does dermatitis herpetiformis look like microscopically?

A

subepidermal blister
eos
neutrophils

88
Q

Treatment for dermatitis herpetiformis?

A

dapsone

sulfapyridine

89
Q

Inherited defect in structural proteins that cause mechanical instability to the skin

Clinical manifestations soon after birth with blister formation at sites of pressure, rubbing or trauma

4 types
Simplex – suprabasalar blister
Junctional – subepidermal blister
Dystrophic – subepidermal blister
Mixed
A

Epidermolysis bullosa

90
Q

Autosomal dominant inheritance of defects in keratin 14 or keratin 5 resulting in defects in the basal cell layer of the epidermis

A

Epidermolysis bullosa - simplex type

91
Q

Autosomal recessive inheritance of defects in laminin, a protein at the lamina lucida
The lamina lucida binds to both hemidesmosomes and anchoring filaments
Blisters are seen at the level of the lamina lucida

A

Epidermolysis bullosa - junctional type

92
Q

Autosomal dominant or recessive inheritance of defects in type VII collagen (a major component of the basement membrane anchoring fibrils)
Defects causes blisters at the level of the lamina densa
This is a scarring disorder

A

Epidermolysis bullosa - dystrophic type

Block 7 Week 2 (9 decks)

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